[Federal Register Volume 66, Number 13 (Friday, January 19, 2001)]
[Rules and Regulations]
[Pages 5527-5706]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 01-995]
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Part II
Department of Labor
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Mine Safety and Health Administration
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30 CFR Part 72
Diesel Particulate Matter Exposure of Underground Coal Miners; Final
Rule
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30 CFR Part 57
Diesel Particulate Matter Exposure of Underground Metal and Nonmetal
Miners; Final Rule
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Federal Register / Vol. 66, No. 13 / Friday, January 19, 2001 / Rules
and Regulations
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DEPARTMENT OF LABOR
Mine Safety and Health Administration
30 CFR Part 72
RIN 1219-AA74
Diesel Particulate Matter Exposure of Underground Coal Miners
AGENCY: Mine Safety and Health Administration (MSHA), Labor.
ACTION: Final rule.
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SUMMARY: This rule establishes new health standards for underground
coal mines that use equipment powered by diesel engines.
This rule is designed to reduce the risks to underground coal
miners of serious health hazards that are associated with exposure to
high concentrations of diesel particulate matter (dpm). DPM is a very
small particle in diesel exhaust. Underground miners are exposed to far
higher concentrations of this fine particulate than any other group of
workers. The best available evidence indicates that such high exposures
put these miners at excess risk of a variety of adverse health effects,
including lung cancer.
The final rule for underground coal mines would require that the
dpm emissions from certain pieces of equipment be restricted to
prescribed levels. Underground coal mine operators would also be
required to train miners about the hazards of dpm exposure.
By separate notice, MSHA will publish a rule to reduce dpm
exposures in underground coal mines.
DATES: The provisions of the final rule are effective March 20, 2001.
However, Sec. 72.500(b) will not apply until July 19, 2002;
Sec. 72.501(b) will not apply until July 21, 2003; and, Sec. 72.501(c)
will not apply until January 19, 2005.
FOR FURTHER INFORMATION CONTACT: David L. Meyer, Director, Office of
Standards, Regulations, and Variances, MSHA, 4015 Wilson Boulevard,
Arlington, VA 22203-1984. Mr. Meyer can be reached at [email protected]
(Internet E-mail), 703-235-1910 (voice), or 703-235-5551 (fax). You may
obtain copies of the final rule in alternative formats by calling this
number. The alternative formats available are either a large print
version of the final rule or the final rule in an electronic file on
computer disk. The final rule also is available on the Internet at
http://www.msha.gov/REGSINFO.HTM.
SUPPLEMENTARY INFORMATION:
I. Key Features of MSHA's Final Rule Limiting the Concentration of
Diesel Particulate Matter (DPM) in Underground Coal Mines
(1) What are the requirements for permissible equipment?
Permissible equipment must not emit more than 2.5 grams per hour of
dpm, as measured in a laboratory test. Any permissible equipment that
is added to a mine's inventory underground more than 60 days after the
date this rule is published will have to meet this standard upon
introduction. This includes newly purchased equipment, used equipment,
or a piece of equipment receiving a replacement engine with a different
serial number than the engine it is replacing, including engines or
equipment coming from one mine into another. It does not include a
piece of equipment whose engine was previously part of the mine's
inventory and rebuilt.
Within 18 months from the date the rule is issued, the entire
permissible fleet must meet this standard.
The rule leaves the choice of controls used to achieve the
emissions limit to operators. Operators may use any combination of
controls (e.g., cleaner engine, OCC, filter) to meet the emissions
standard specified in this section.
As a practical matter, MSHA expects that to comply with this
standard, most permissible equipment will be equipped with a paper
filter. As explained in Part IV of this preamble, MSHA has verified
that there are commercially available paper filters which will allow
99% of the existing 541 units in the permissible fleet to meet this
requirement--including permissible units powered by the Deutz MWM 916,
the Caterpillar 3304 and the Caterpillar 3306. Commercially available
paper filters capable of bringing the emissions of these units into
compliance include a model which can be installed directly on the
exhaust coming from a water scrubber or on the exhaust coming from a
heat exchanger, as well as the integrated DST system. Other
filters which use paper with the same performance characteristics will
also be acceptable. Control devices whose dpm removal efficiency has
not been demonstrated by laboratory testing on a diesel engine can be
evaluated following the procedures in 30 CFR 72.503 of this part added
by this rulemaking. Moreover, the rule provides that MSHA may rely upon
the test results of other organizations who perform equivalent tests.
MSHA will publish on its web site a list of tested control devices
and their performance. Compliance will be determined by reference to
this data--there will be no in-mine testing.
The only engine which might not be able to meet these requirements
for dpm emissions from permissible equipment with a paper filter is the
Isuzu QD-100. MSHA's inventory indicates there are currently only two
units of permissible equipment using this engine; however, these two
units can comply at a derated power setting.
The engines currently approved for permissible use are generally
high in particulate emissions. MSHA is committed to taking actions
which will facilitate the approval for permissible use of the lower-
emission engines which have become available in recent years. These
actions could include waiving test fees, contracting for the
performance of such tests, or on an interim basis permitting the use of
an engine approved for nonpermissible use in a permissible package.
MSHA will solicit input from the mining community, through a Federal
Register notice as it considers how to proceed in this regard.
(2) What are the requirements for heavy-duty non-permissible equipment?
Non-permissible heavy duty equipment will ultimately not be
permitted under the final rule to emit more than 2.5 grams per hour of
dpm. For reasons of feasibility, this requirement will be implemented
in phases.
Any heavy duty equipment added to a mine's inventory more than 60
days after the date of publication of this rule will have to comply
with an interim emissions limit for that machine of 5.0 gr/hr. This
includes newly purchased equipment, used equipment, or a piece of
equipment receiving a replacement engine with a different serial number
than the engine it is replacing, including engines or equipment coming
from one mine into another. It does not include a piece of equipment
whose engine was previously part of the mine's inventory and rebuilt.
All heavy duty equipment in the fleet must meet the interim
standard of 5.0 grams per hour of dpm in 30 months.
Finally, another 18 months later (4 years in all), all
nonpermissible heavy duty equipment in the fleet will have to meet the
final standard of 2.5 grams per hour of dpm.
As with permissible equipment, the rule leaves the choice of
controls used to achieve the emissions limit to operators. Any
combination of controls (e.g., cleaner engine, OCC, filter) can be used
as long as compliance with the standard specified in this section is
met.
[[Page 5527]]
As a practical matter, MSHA believes that most existing heavy duty
equipment will utilize commercially available hot gas filters (e.g.,
ceramic cell, wound fiber, sintered metal, etc.) to comply with the
final limit. All the existing fleet can reach the interim limit with
such a filter; some will not need one. MSHA determined that all but a
few can reach the final limit with such a filter.
The rule provides that MSHA may rely upon the test results of
organizations who perform filtration efficiency tests. In this regard,
MSHA will accept the results of filter tests performed by VERT. VERT is
an acronym for Verminderung der Emissionen von Realmaschinen in
Tunnelbau, a consortium of several European agencies conducting diesel
emission research in connection with major planned tunneling projects
in Austria, Switzerland and Germany. VERT was established to advance
hot gas filter technology due to concerns in Europe about dpm levels.
This gave VERT the opportunity to acquire the necessary filter
evaluation expertise. A wide range of commercially available hot gas
filters have been tested by VERT and the filtration efficiency
determined. The Secretary may also accept filter efficiency test
results from other testing organizations that can demonstrate a high
level of expertise in filter evaluation (see Sec. 72.503(c) of the
final rule).
Operators using the DST'' system with the catalytic convertor on
heavy duty equipment, or the Jeffrey dry exhaust system, will also be
deemed in compliance with the final rule, since test results conducted
in the same manner as the requirement in the final rule demonstrate
that those systems can reduce the emissions from all existing heavy
duty engines to below the limit. Filtration devices whose filter
efficiency has not been demonstrated by testing on a diesel engine can
be evaluated following the procedures in 30 CFR 72.503 of this part
added by this rulemaking.
MSHA will publish on its web site a list of tested control devices
and their performance. Compliance will be determined by reference to
this data--there will be no in-mine testing.
The standard may also be met through the use of newer, cleaner
engines in some heavy duty equipment with low horsepower engines. There
are already many engines approved for non-permissible use in
underground coal mines that will enable heavy duty equipment to limit
emissions, thus allowing the use of lower efficiency filters. MSHA is
also considering approaches that would expedite the approval of
additional engines based on evidence that such engines meet EPA
standards which ensure the engines are at least as clean as required
under MSHA approval standards.
(3) What are the requirements for generators and compressors?
The final rule provides that generators and compressors meet the
same dpm emissions standards as heavy duty equipment. Thus, generators
and compressors will ultimately not be permitted to emit more than 2.5
grams per hour of dpm. Generators and compressors introduced into the
fleet of an underground coal mine more than 60 days after the final
rule is published will have to meet an interim emissions limit of 5.0
g/hr. Generators and compressors in the existing fleet will have 30
months to meet the interim standard of 5.0 grams per hour of dpm. After
an additional 18 months (4 years in all), all generators and
compressors underground will have to meet the final standard of 2.5
grams per hour of dpm.
Although the proposed rule would not have covered generators and
compressors, MSHA explicitly asked the mining community if there were
types of light duty equipment that should, because of operating
characteristics, be treated like heavy duty equipment. Generators and
compressors generate more dpm emissions than other light-duty equipment
based on their known duty cycle and type of work for which they are
designed; indeed, they use engines whose horsepower often exceeds that
in permissible equipment. Accordingly, MSHA has determined they should
be covered by this rulemaking.
MSHA's inventory indicates that the 34 generators and 29
compressors constitute less than 3% of the underground light duty
diesel fleet. The existing compressors are using engines which should
meet the standard's interim and final requirements with a commercially
available hot gas filter.
Generators and compressors will be able to utilize the same
technologies as heavy duty machines to comply with this standard. This
will include hot gas filters or paper filters, as appropriate. Smaller
generators and compressors may utilize the clean engine technologies.
(4) What are the requirements for other nonpermissible equipment?
The final rule provides that any piece of nonpermissible light-duty
equipment introduced into an underground coal mine more than 60 days
after the date of publication of the rule must not emit more than 5.0
grams per hour of dpm. This includes newly purchased equipment, used
equipment, or a piece of equipment receiving a replacement engine with
a different serial number than the engine it is replacing, including
engines or equipment coming from one mine into another, but it does not
include a piece of equipment whose engine was previously part of the
mine's inventory and rebuilt.
The final rule does not impose any new requirements on the existing
nonpermissible light-duty fleet (except for generators and compressors
as noted above).
While new light duty equipment would not have been covered by the
proposed rule, MSHA explicitly asked the mining community if it would
be feasible to cover such new light duty equipment, even if it were not
feasible to set limits for all light duty equipment. MSHA has
determined that it is feasible to require that newly introduced light
duty equipment meet the same 5 gr/hr standard as new heavy duty
equipment.
To facilitate compliance with this standard, light duty equipment
which uses an engine meeting certain EPA standards listed in the MSHA
rule will be deemed to automatically meet the MSHA dpm standard for
newly introduced light-duty equipment. For example, any ``heavy duty
highway engine'' produced after 1994 will be deemed to meet this dpm
standard. The agency has determined that there are already MSHA
approved engines available in a full range of horsepower sizes that can
meet the EPA standards listed in this final rule.
In practice, what this rule does is simply ensure that very old
engines with few, if any, emission controls are not added to a mine's
current light duty fleet, thus accelerating the turnover to a newer
generation of technology.
(5) Is there a summary of the applicable requirements and effective
dates?
All of the emissions standards established by MSHA's final rule are
summarized in Table I-1.
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(6) What other requirements are contained in the final rule for
underground coal mines?
Miners have to be trained annually in the risks of dpm exposure and
in control methods being used at the mine. Also, certain information
about diesel engines and aftertreatment devices has to be added to the
mine ventilation plan. The paperwork requirements added by this rule
are small--on average, less than 7 hours in the first year and 4 hours
per year thereafter for a mine operator that uses diesel powered
equipment. Furthermore, manufacturers of diesel powered equipment will
incur burden hours only during the first year that the rule is in
effect in order to amend existing MSHA approvals. During the first year
that the rule is in effect the average manufacturer will incur 70
paperwork burden hours.
(7) Will the final rule eliminate any health risks to miners resulting
from the use of diesel powered equipment underground?
Although the Agency expects that health risks will be substantially
reduced by this rule, the best available evidence indicates that a
significant risk of adverse health effects due to dpm exposures will
remain after the rule is fully implemented.
MSHA considered establishing stricter standards for certain types
of equipment, and covering more light duty equipment, but concluded
that such actions would either be technologically or economically
infeasible for the coal mining industry as a whole at this time. As
MSHA takes actions to facilitate the introduction of newer and cleaner
engines underground, and as control technologies continue to develop,
additional reductions in dpm levels may become feasible for the
industry as a whole. MSHA will continue to monitor developments in this
area.
(8) What are the costs and benefits of the final rule?
Costs
Table I-2 summarizes the compliance costs to mine operators that
use diesel powered equipment for each section of the rule; total
compliance costs are about $7 million a year. Table I-3 summarizes the
compliance costs to mine operators that use diesel powered equipment by
mine size (i.e., mines employing fewer than 20 workers, mines employing
between 20 and 500 workers, and mines employing more than 500 workers).
In addition, there is a total annualized cost to diesel equipment
manufacturers of $30,030.
MSHA's full Regulatory Economic Analysis, (REA) from which Tables
I-2 and I-3 are derived, provides considerable detail on the
assumptions MSHA used in developing these cost estimates, and on the
costs associated with the controls required for particular engines in
the current fleet. For example, MSHA is estimating that for a
Caterpillar 3304 PCNA in a heavy duty piece of equipment, an operator
will have to spend about $4,500 a year to achieve compliance with the
limits for that equipment (hot gas filter, cost annualized, plus annual
costs of regeneration). Copies of MSHA's full (REA) analysis are in the
record and are available to the mining community upon request.
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Benefits
Benefits of the rule include reductions in lung cancer. In the long
run, as the mining population turns over, MSHA estimates that a minimum
of 1.8 lung cancer deaths will be avoided per year.\1\
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\1\ This lower bound figure could significantly underestimate
the magnitude of the health benefits. For example, the estimate
based on the mean value of all the studies examined is 13 lung
cancer deaths avoided per year.
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Benefits of the rule will also include reductions in the risk of
death from cardiovascular, cardiopulmonary, or respiratory causes and
in sensory irritation and respiratory symptoms. MSHA does not believe
that the available data can support reliable or precise quantitative
estimates of these benefits. Nevertheless, the expected reductions in
the risk of death from cardiovascular, cardiopulmonary, or respiratory
causes appear to be significant, and the expected reductions in sensory
irritation and respiratory symptoms appear to be rather large.
(9) What actions has MSHA taken, and what additional actions does it
plan to take, to facilitate compliance with this rule?
This rule is a continuation of efforts by MSHA to help the mining
community deal with the use of diesel engines in mining. The diesel
equipment rule, now in effect, has itself contributed to the reduction
of diesel exhaust emissions through the use of low sulfur diesel fuel,
the requirement that all engines underground be approved, and improved
maintenance. In one case, testimony was presented by a mine operator
that timely engine maintenance, triggered by the weekly undiluted
exhaust emissions test required by the new regulation, has greatly
reduced carbon monoxide emissions from diesel equipment. These properly
tuned engines will generate less particulate. MSHA has devoted
workshops specifically to dpm control, issued a Toolbox of control
methods to assist the mining community in this regard, and developed a
computerized Estimator to help individual mines evaluate the impact of
alternative approaches of controlling dpm emissions. The agency has
verified the efficiency of the current generation of paper filters, and
has sponsored work on the measurement of dpm in ambient mine
atmospheres.
This final rule includes certain provisions to facilitate
compliance--e.g., authorizing MSHA to rely on the testing requirements
of organizations like VERT, and permitting compliance with certain EPA
requirements to be deemed as compliance with the requirements in this
rule for newly introduced light duty equipment. The agency is, as
described above, planning to take action in consultation with the
mining community to facilitate the approval, and in particular the
approval for permissible use, of a newer, cleaner generation of diesel
engines. The agency will be preparing a compliance guide for this rule,
and posting a variety of useful information on its web site. If
necessary, additional workshops may be scheduled. In addition, MSHA is
ready to provide special technical assistance to those who are planning
to bring new engines or equipment underground in the next few months.
(10) Are surface mines addressed in this rule?
Surface areas of underground mines, and surface mines, are not
covered by this rule. In certain situations the concentrations of dpm
at surface mines may be a cause for concern: e.g., production areas
where miners work in the open air in close proximity to loader-haulers
and trucks powered by older, out-of-tune diesel engines, shops, or
other confined spaces where diesel engines are running. The Agency
believes, however, that these problems are currently limited and
readily controlled through education and technical assistance. The
Agency would like to emphasize, however, that surface miners are
entitled to the same level of protection as other miners; and the
Agency's risk assessment indicates that even short-term exposures to
concentrations of dpm like those observed may result in serious health
problems. Accordingly, in addition to providing education and technical
assistance to surface mines, the Agency will also continue to evaluate
the hazards of diesel particulate exposure at surface mines and will
take any necessary action, including regulatory action if warranted, to
help the mining community minimize any hazards.
II. Background Information
This part provides the context for this preamble. The nine topics
covered are:
(1) The role of diesel-powered equipment in underground coal mining
in the United States;
(2) The composition of diesel exhaust and diesel particulate matter
(dpm);
(3) The difficulties in measuring ambient dpm in underground coal
mines;
(4) Limiting the public's exposure to diesel and other fine
particulates--ambient air quality standards;
(5) The impact on emissions of MSHA approval standards and
environmental tailpipe standards;
(6) Methods for controlling dpm emissions in underground coal
mines;
(7) Existing standards for underground coal mines that limit miner
exposure to diesel emissions;
(8) Information on how certain states are restricting occupational
exposure to diesel particulate matter; and
(9) A history of this rulemaking.
Material on these subjects which was available to MSHA at the time
of the proposed rulemaking was included in Part II of the preamble that
accompanied the proposed rule (63 FR 17501 et seq.). This version has
been updated to reflect the record, to discuss certain issues relevant
to underground coal mines in more detail, and reorganized as
appropriate.
(1) The Role of Diesel-Powered Equipment in Underground Coal Mining in
the United States
Diesel engines, first developed about a century ago, now power a
full range of mining equipment. However at this time, less than 20% of
underground coal mines (fewer than 150 underground coal mines) utilize
this technology. Equipment powered by other sources (electrical power
delivered by cable or trolley, and battery power) continues to
predominate in this mining sector. Moreover, unlike in other mining
sectors, most of the current diesel fleet in underground coal mines
consists of light-duty support vehicles, and only limited numbers of
the equipment used in digging or hauling coal is powered by diesel
engines.
Many in the mining industry believe that diesel-powered equipment
has productivity and safety advantages over equipment powered by other
sources. Others cite evidence to the contrary, and several key
underground coal mining states continue to ban or significantly
restrict the use of diesel-powered equipment in underground coal mines.
The use of diesel engines to power equipment in underground coal mining
is increasing and appears likely to continue to do so absent
significant improvement in other power technologies.
Historical Overview of Diesel Power Use in Mining. As discussed in
the notice of proposed rulemaking, the diesel engine was developed in
1892 by the German engineer Rudolph Diesel. It was originally intended
to burn coal dust with high thermodynamic efficiency. Later, the diesel
engine was modified to burn middle distillate petroleum (diesel fuel).
In diesel engines, liquid fuel droplets are injected
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into a prechamber or directly into the cylinder of the engine. Due to
compression of air in the cylinder the temperature rises high enough in
the cylinder to ignite the fuel.
The first diesel engines were not suited for many tasks because
they were too large and heavy (weighing 450 lbs. per horsepower). It
was not until the 1920's that an efficient lightweight diesel power
unit was developed. Since diesel engines were built ruggedly and had
few operational failures, they were used in the military, railway,
farm, construction, trucking, and busing industries. The U.S. mining
industry was slow to begin using these engines. Thus, when in 1935 the
former U.S. Bureau of Mines published a comprehensive overview on metal
mine ventilation (McElroy, 1935), it did not mention ventilation
requirements for diesel-powered equipment. By contrast, the European
mining community began using these engines in significant numbers, and
various reports on the subject were published during the 1930's.
According to a 1936 summary of these reports (Rice, 1936), the diesel
engine had been introduced into German mines by 1927. By 1936, diesel
engines were used extensively in coal mines in Germany, France, Belgium
and Great Britain. Diesel engines were also used in potash, iron and
other mines in Europe. Their primary use was in locomotives for hauling
material.
It was not until 1939 that the first diesel engine was used in the
United States mining industry, when a diesel haulage truck was used in
a limestone mine in Pennsylvania, and not until 1946 was a diesel
engine used in coal mines. Today, however, diesel engines are used to
power a wide variety of equipment in all sectors of U.S. mining.
Production equipment includes vehicles such as haultrucks and shuttle
cars, load-haul-dump units, face drills, and explosives trucks. Diesel
engines are also used in support equipment including generators and air
compressors, ambulances, crane trucks, ditch diggers, foam machines,
forklifts, graders, locomotives, longwall component carriers, lube
units, mine sealant machines, personnel carriers, hydraulic power
units, rock dusting machines, roof drills, tractors, utility trucks,
water spray units, and welders.
Current Patterns of Diesel Power Use in Underground Coal Mining.
The underground coal mining sector is not as reliant upon diesel power
as are other mining sectors. While nearly all underground metal and
nonmetal mines, and nearly all surface mines, use diesel-powered
equipment, less than 20% of underground coal mines use it. Table II-1
provides further information on the current inventory.
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The great majority of the diesel engines used in underground coal
mines are used to power support equipment, rather than production
equipment. This is in sharp contrast to other sectors. For example, in
underground metal and nonmetal mines, of the approximate 4,100 pieces
of diesel equipment normally in use at the time of MSHA's proposal,
nearly half of the units were estimated to be used for loading and
hauling. By contrast, of the approximately 3,000 pieces of diesel
equipment in use in underground coal mines, MSHA estimates that fewer
than 10% are used for coal loading and haulage. Moreover, because of
space constraints and other operating conditions in underground coal
mines, virtually all coal loading and hauling equipment has engines
less than 200 horsepower; by contrast, virtually all such equipment in
metal and nonmetal mines has engines greater than 200 horsepower and
ranging to more than 750 horsepower or greater. As a result, the
average horsepower of diesel engines powering equipment in underground
coal mines is much less than the average engine in underground metal
and nonmetal mines and all surface mines. This is significant because,
other things being equal, lower horsepower engines are going to produce
less dpm emissions by mass than higher horsepower engines.
The engines in underground coal mines can be divided into three
categories recognized under existing MSHA regulations: ``permissible'',
``heavy-duty nonpermissible'', and ``light-duty nonpermissible.'' In
this final dpm rule, MSHA is establishing different requirements for
each of these categories. Accordingly, some background on this
categorization is needed.
Use of Diesel Engines in Permissible Equipment. Under existing
regulations, equipment, whether powered by diesel engines or
electricity, that is used in areas of the mine where methane gas is
likely to be present in dangerous concentrations must be MSHA-approved
``permissible'' equipment.
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Permissible diesel powered equipment for use in coal mines is provided
with special equipment to prevent the ignition of methane. This special
equipment includes flame arresters and special treatment of flanges and
joints. Since diesel engines normally have very hot surface
temperatures and hot exhaust gas that can constitute an ignition
source, permissible diesels must be provided with a means to maintain
the temperatures of surfaces and the exhaust gas below 302 deg.F.
MSHA regulations are very specific in defining those areas of the
mine where permissible equipment is required. Generally, permissible
equipment is required where the coal mining is actually being
performed, because the mining process typically liberates methane.
These areas are commonly referred to as ``inby'' areas. In some cases,
however, permissible equipment is required to be used in other areas of
the mine. For example, only permissible diesel-powered equipment may be
used in return aircourses. The permissible equipment provides an
additional level of fire protection because of the strict temperature
controls on the equipment surface and exhaust. This increased
protection is required because of the potential for the accumulation of
dangerous levels of methane in these aircourses.
MSHA's January 2000 inventory indicates that of the 3,121 diesel
powered pieces of equipment in underground coal mines, 528 units are
permissible pieces. The emissions generated by permissible equipment
make a significant contribution to dpm concentrations in the mines
where they are functioning. This is because the equipment has large
engines, works hard and continuously in locations generally far from
ventilation sources, and in close quarters with miners.
Moreover, the engines which have to date been approved for
permissible use are among those which emit the highest levels of dpm
(in grams/hour): the Caterpillar 3304, Caterpillar 3306 (available in
two horsepower sizes), the Deutz D916-6, and the Isuzu QD-100. The
Deutz D916-6 is still used in underground coal mines, however, it is no
longer in production. MSHA recently approved the Caterpillar 3306PCTA
permissible, the first approved turbocharged engine.
Diesel engines in the horsepower ratings required to power
permissible equipment are now available in new low emissions technology
engines. However, none of them has been approved for use on permissible
equipment because no applications for MSHA approval have been received.
This situation may reflect a lack of adequate incentives for engine and
equipment manufacturers to incur the development costs to meet MSHA
permissibility requirements or to pay the fees required for approval.
MSHA is developing programs that would facilitate the availability
of engines that utilize the latest technologies to reduce gaseous and
particulate emissions for use in permissible equipment. Current engine
designs that utilize low emissions technologies are currently approved
by MSHA in nonpermissible form.
One of the programs that MSHA is considering would follow the
precedent established in the recently published diesel equipment rule.
To facilitate compliance with this dpm rule, MSHA is considering
funding the additional emissions testing needed to gain permissibility
approval, previously approved, non-permissible engines that utilize low
emissions technology engines, or waiving the normal fees that the
Agency charges for the administrative and technical evaluation portion
of the approval process.
Alternatively, MSHA may relax, as an interim measure, the
requirement that engine approvals be issued only to engine
manufacturers. Under this program an equipment manufacturer could
utilize an engine, approved by MSHA as nonpermissible, in a permissible
power package. MSHA would ensure that the additional emissions tests
required for permissible engines are conducted as part of the power
package approval process. Provisions of the two programs could be
combined.
While the availability of cleaner engines would help reduce the dpm
emissions from the permissible fleet, there are aftertreatment filters
available for such equipment that are both highly efficient and
relatively low cost. As discussed in more detail in section 6 of this
part, because the exhaust temperature of these permissible pieces of
equipment must be cooled for safety reasons, aftertreatment devices
whose filtration media consists of paper can be directly installed on
this equipment. Paper filters exposed to uncooled exhaust pose a fire
and ignition hazard.
Use of Diesel Engines in Nonpermissible Equipment. In those areas
of an underground coal mine where methane concentrations can be limited
through the control of ventilation air, permissible equipment is not
required. Generally, this is the case in areas away from the face,
often referred to as ``outby'' areas. Most equipment operating in
underground coal mines is ``nonpermissible'' equipment.
Nonpermissible equipment is divided into several categories for
purposes of the diesel equipment rules that currently apply in
underground coal mines (30 CFR part 75). In pertinent part, those rules
provide:
Sec. 75.1908 Nonpermissible diesel-powered equipment; categories
(a) Heavy-duty diesel-powered equipment includes--
(1) Equipment that cuts or moves rock or coal;
(2) Equipment that performs drilling or bolting functions;
(3) Equipment that moves longwall components;
(4) Self-propelled diesel fuel transportation units and self-
propelled lube units; or
(5) Machines used to transport portable diesel fuel
transportation units or portable lube units.
(b) Light-duty diesel-powered equipment is any diesel-powered
equipment that does not meet the criteria of paragraph (a) * * *
(c) * * *.
(d) Diesel-powered ambulances and fire fighting equipment are a
special category of equipment that may be used underground only in
accordance with the mine fire fighting and evacuation plan * * *.
MSHA's inventory indicates that of the 3,121 diesel powered pieces
of equipment, 497 are heavy duty nonpermissible pieces, 66 are
generators and air compressors, and 2,030--that is, about two-thirds of
the total underground coal diesel fleet at present--are other light
duty nonpermissible pieces.
The rationale for the division of nonpermissible dieselized
equipment into these classes requires some background here because in
this rulemaking on dpm, MSHA proposed making a significant distinction
between the requirements applicable to each class.
The division resulted from MSHA's 1996 regulation establishing
safety rules for the use of dieselized equipment in underground coal
mines (the general history and purpose of which are summarized in
section 9 of this Part). As discussed in the preamble to the final
diesel safety rule (61 FR 55459-61), the purpose of the categorization
was to take the diversity of nonpermissible equipment into account in
establishing regulatory requirements relevant to safety. The final
categorization scheme for nonpermissible equipment developed over the
course of time in response to public comments to the proposed rule.
Equipment falling within the heavy duty category is typically used
for extended periods during a shift on a continuous, rather than an
intermittent,
[[Page 5534]]
basis. Heavy duty equipment also moves heavy loads or performs
considerable work. Accordingly, to ensure such equipment could operate
in a safe manner, the safety rule required that each piece of heavy
duty equipment:
* * * has to be equipped with an automatic fire suppression system
addressing the additional fire risks resulting from the way this
equipment is used. Heavy-duty equipment also produces greater levels
of gaseous contaminants, and under the final rule is therefore
subject to weekly undiluted exhaust emissions tests * * * and is
included in the air quantity calculation of ventilation of diesel-
powered equipment * * *. (61 FR 55461)
It is important to note that there are other types of underground
coal mining equipment which, although they have operating
characteristics much like heavy duty equipment, were not designated as
such under the diesel equipment rule. That is because such equipment
(e.g., generators and compressors) is considered as portable equipment
and special requirements were established in that rule to address the
hazards presented by that equipment.
Ambulances and fire-fighting equipment which use diesel engines
have operating characteristics like light-duty equipment, but under the
diesel equipment rule are considered a special category of equipment
that does not have to meet the requirements of that rule. The equipment
in this category must only be used in emergencies or fire drills and in
compliance with fire fighting and evaluation plan requirements.
Consequently, such equipment is not required to have an approved engine
or power package or comply with the design and performance requirements
of Secs. 75.1909 and 75.1910 (61 FR 55461).
Under the diesel equipment rule, heavy-duty equipment may be used
to perform light-duty work; but equipment that is classified as light-
duty may not be used, even intermittently, to perform the functions
listed in paragraphs (a)(1) through (a)(5) of 30 CFR 75.1908 because it
is not required to have the automatic fire suppression system that MSHA
determined was necessary for such kinds of work. (Id.) As noted in the
preamble, two machines of the same model could fall into different
equipment categories depending on how they are used. Although of the
same design, they do not present the same risk of fire because of the
way in which they are used, nor do they produce the same quantities of
exhaust contaminants:
``* * * machines that are operated for extended periods of time
under heavy load generate more contaminants than machines that are
not.'' (Id.)
It was for this reason--the rate of contaminant generation--that in
proposing a rule to limit the concentration of dpm in underground coal
mines, MSHA proposed making a distinction between heavy-duty equipment
and light-duty equipment. MSHA proposed requiring heavy-duty
nonpermissible equipment and permissible equipment to be equipped with
filters capable of removing 95% of the dpm emitted by the engines in
those pieces of equipment. The proposal did not include any controls
for the dpm emitted from light-duty equipment nor for ambulances and
fire-fighting equipment. As noted in section 9 of this part, the Agency
asked the mining community to comment on the Agency's assumptions and
consider some options in this regard. The record on this matter and
MSHA's final decision are discussed in Part IV.
Whether categorized as heavy-duty or light-duty, the engine exhaust
from nonpermissible equipment is not required to be cooled for safety
reasons like exhaust from permissible equipment. Accordingly, this
means that paper-type filters cannot be added directly to
nonpermissible equipment without first adding a water scrubber or heat
exchanger; otherwise, the paper would burn. As a result, control
devices that are designed to filter hot exhaust gases (e.g., ceramic
filters) provide a cost effective alternative for dpm control with
nonpermissible equipment.
Does Diesel Power Have Advantages Over Alternative Sources of Power
for Equipment Used in Underground Coal Mines? As pointed out by a
commenter, a number of power sources for mining equipment have been
tried in the mining industry only to be rejected for various reasons
(e.g., gasoline engines, cables, and compressed air). Today, this
commenter continued, there are three general ways of powering mining
equipment: electric power (delivered by electric trailing cables or by
trolley wires), on-board battery power, and diesel. Table II-2
reproduces a list provided by this commenter as to his view of some of
the ``advantages and challenges'' of these power sources; MSHA is
reproducing this list as a convenient summary, but does not necessarily
agree or disagree with each specific entry.
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[[Page 5536]]
Some in the mining industry strongly favor the use of diesel
engines to power equipment in underground coal mines. A representative
of a company with four underground coal mines testified that it has 200
pieces operated by diesel power, and is continuing to add more. Another
commenter stated that diesel is the power source of choice for moving
personnel and supplies in large underground mines where coal is moved
by conveyor belt.
A number of commenters asserted that diesel-powered equipment has
productivity and safety advantages over electrically-powered and
battery-powered equipment.
One commenter argued that diesel reduces the risks associated with
the use of electrical equipment by eliminating the need for trolley
wires, trolley poles and trailing cables that cause injuries, accidents
and fatalities--shocks, electrocutions, burns, fires, tripping or being
struck by trolley poles, and also reduce the number of material
handling injuries. This commenter also argued that unlike electrical
power, diesel use does not restrict mining plans or the mining cycle
because operations are not hampered by cable length or time consuming
power moves, provide greater flexibility in underground travel routes,
and make equipment moves from one area of a mine to another more
efficient. This commenter further claimed that compared to battery-
powered mining equipment (which arguably provides the same
flexibility), diesels can haul coal more efficiently over longer
distance, provide more power, and eliminate time-consuming battery
change-out time.
Another commenter noted the increased potential for fatalities and
injuries in underground coal mines when trolley wires are present, and
further that trolley wires restrict ventilation in one entry.
Another commenter noted the difficulties of evacuating miners in
the event of emergencies over the large distances in some underground
mines using sources of power that were more prone to failure than
diesel.
Another commenter asserted that all of the 18 employees who had
died since 1972 as a result of exposed overhead direct current trolley
lines could have lived if diesel power had been in use, and pointed to
examples of fires initiated by trolley wires with associated loss of
productivity. This commenter also noted that battery powered equipment
has been known to cause injuries, and explosions both from its
production of hydrogen gas and from sparks igniting methane in the mine
atmosphere.
Commenters also note that many asserted safety risks associated
with the use of diesel powered equipment in underground coal mines have
now been addressed as a result of MSHA's safety rules.
Other commenters, however, pointed out that there are a number of
the nation's most productive underground coal mines (including both
those using longwall and those using room and pillar mining techniques)
which do not use this technology. These commenters challenged industry
claims that diesel power is necessary for business to survive. Some
also noted that miners are trained to protect themselves better from
safety hazards that accompany the use of electrical power, like
tripping on cables and electrical hazards, but are not able to protect
themselves from health hazards they cannot see. In this regard, the
hearing transcripts are replete with reminders by underground coal
miners of their concern about what they are breathing in light of the
tragic experience with black lung disease.
As indicated by MSHA in the preamble to the proposed rule (63 FR
17503), not many studies done recently address the contentions that
diesel power provides safety and/or productivity advantages, and the
studies which have been reviewed by MSHA do not clearly support this
hypothesis.
Outlook for Use of Diesel Engines To Power Equipment in Underground
Coal Mines
The use of diesel engines to power equipment in underground coal
mining is increasing. In fact, since this rulemaking was proposed,
MSHA's inventory has recorded an increase of about 5% in the number of
diesel-powered pieces of equipment at the roughly 145 coal mines using
diesel power underground. This trend appears likely to continue, absent
significant improvement in other power technologies.
Several key underground coal mining states--Ohio, Pennsylvania and
West Virginia--continue to ban or significantly restrict the use of
diesel-powered equipment in underground coal mines (as discussed in
section 8 of this Part). There are 339 underground coal mines in these
states. If the current restrictions in these States were relaxed, in
accordance with the expressed interest of industry groups toward this
end, many of these underground coal mines are likely to begin using
diesel to power some equipment.
Full implementation of MSHA's recent rules for the safe use of
diesel-powered equipment in underground coal mines (discussed in
section 7 of this part), is also likely to lead to increased diesel use
because they resolve certain safety concerns that discouraged the
mining community from using such equipment more widely. Another factor
suggesting that the use of diesel power will expand is that both miners
and mine operators are concerned about the future of their industry.
On the other hand, operators as well as miners have acknowledged
that potential health hazards associated with the use of diesel power
must be addressed if its use is to become widespread. Although the
Agency expects that health risks will be substantially reduced by this
rule, the best available evidence indicates that a significant risk of
adverse health effects due to dpm exposures will remain after the rule
is fully implemented. As explained in Part V of this preamble, however,
MSHA has concluded that the underground coal mining sector as a whole
cannot feasibly reduce dpm concentrations further at this time.
Nevertheless, the efforts by US and overseas environmental regulators
to restrict dpm and other diesel emissions into the environment,
discussed in sections 4, 5 and 6 of this Part, are leading to
technological improvements in engines, fuel and filters that will help
reduce this risk.
Currently, diesel power faces only a limited number of competitive
power sources. It is unclear how quickly new ways to generate energy to
run mobile vehicles will be available for use in underground mining
activities. New hybrid electric automobiles have been introduced this
year by two manufacturers (Honda and Toyota); these vehicles combine
traditional internal combustion power sources (in this case gasoline)
with electric storage and generating devices that can take over during
part of the operating period. By reducing the time the vehicle is
directly powered by combustion, such vehicles reduce emissions. Further
developments in electric storage devices (batteries), and chemical
systems that generate electricity (fuel cells) are being encouraged by
government-private sector partnerships. For further information on
recent developments, see the Department of Energy alternative fuels web
site at http://www.afdc.doe.gov/altfuels.html., and ``The Future of
Fuel Cells'' in the July 1999 issue of Scientific American. Until such
new technologies mature, and are reviewed for safe use underground,
MSHA assumes that the mining community's interest in the use
underground of diesel-power as an
[[Page 5537]]
alternative to direct electric power is likely to continue.
(2) The Composition of Diesel Exhaust and Diesel Particulate Matter
(DPM)
The emissions from diesel engines are actually a complex mixture of
compounds, containing gaseous and particulate fractions. The specific
composition of the diesel exhaust in a mine will vary with the type of
engines used and how they are used. Factors such as type of fuel, load
cycle, engine maintenance, tuning, and exhaust treatment will affect
the composition of both the gaseous and particulate fractions of the
exhaust. This complexity is compounded by the multitude of
environmental settings in which diesel-powered equipment is operated.
Nevertheless, there are a few basic facts about diesel emissions that
are of general applicability.
The gaseous constituents of diesel exhaust include oxides of
carbon, nitrogen and sulfur, alkanes and alkenes (e.g., butadiene),
aldehydes (e.g., formaldehyde), monocyclic aromatics (e.g., benzene,
toluene), and polycyclic aromatic hydrocarbons (e.g., phenanthrene,
fluoranthene). The oxides of nitrogen (NOX) merit particular
mention because in the atmosphere they can precipitate onto particulate
matter. Thus, reducing the emissions of NOX is a way that
engine manufacturers can control particulate production indirectly.
(See section 5 of this part).
The particulate components of the diesel exhaust gas include the
so-called diesel soot and solid aerosols such as ash particulates,
metallic abrasion particles, sulfates and silicates. Most of these
particulates are in the invisible sub-micron range of 100nm.
The main particulate fraction of diesel exhaust is made up of very
small individual particles. These particles have a solid core
consisting mainly of elemental carbon. They also have a very surface-
rich morphology. This extensive surface absorbs many other toxic
substances, that are transported with the particulates, and can
penetrate deep into the lungs. More than 1,800 different organic
compounds have been identified as absorbed onto the elemental carbon
core. A portion of this hydrocarbon material results from incomplete
combustion of fuel; however, most is derived from engine lubrication.
In addition, the diesel particles contain a fraction of non-organic
adsorbed materials. Figure II-1 illustrates the composition of dpm.
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Diesel particles released to the atmosphere can be in the form of
individual particles or chain aggregates (Vuk, Jones, and Johnson,
1976). In underground coal mines, more than 90% of these particles and
chain aggregates are submicrometer in size--i.e., less than 1
micrometer (1 micron) in diameter. Dust generated by mining and
crushing of material--e.g., silica dust, coal dust, rock dust--is
generally not submicrometer in size. Figure II-2 shows a typical size
distribution of the particles found in the environment of a mine using
equipment powered by diesel engines (Cantrell and Rubow, 1992). The
vertical axis represents relative dpm concentration, and the horizontal
axis the particle diameter.
As can be seen, the distribution is bimodal, with dpm generally
less than 1 m in size, and dust generated by the mining
process greater than 1 m.
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[[Page 5538]]
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As shown on Figure II-3 diesel particulates have a bimodal size
distribution which includes small nuclei mode particles and larger
accumulation mode particles. As further shown, most of diesel particle
mass is contained in the accumulation mode but most of the particle
number can be found in the nuclei mode.
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[[Page 5539]]
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BILLING CODE 4510-43-C
The particles in the nuclei mode, also know as nanoparticles, are
being investigated for their health hazard relevance. Interest in these
particles has been sparked by the finding that newer ``low polluting''
engines emit higher numbers of small particles than the old engine
technology engines. Although the exact composition of diesel
nanoparticles is not known, it is thought that they may be composed of
condensates (hydrocarbons, water, sulfuric acid). The amount of these
condensates and the number of nanoparticles depends very significantly
on the particulate sampling conditions, such as dilution ratios, which
were applied during the measurement.
Both the maximum particle concentration and the position of the
nuclei and accumulation mode peaks, however, depend on which
representation is chosen. In mass distributions, the majority of the
particulates (i.e., the particulate mass) is found in the accumulation
mode. The nuclei mode, depending on the engine technology and particle
sampling technique, may be as low as a few percent, sometimes even less
than 1%. A different picture is presented when the number distribution
representation is used. Generally, the number of particles in the
nuclei mode contributes to more than 50% of the total particle count.
However, sometimes the nuclei mode particles represent as much as 99%
of the total particulate number. The topic of dpm, with particular
reference to very tiny particles known as nanoparticles, is discussed
further in section 5 of this Part.
(3) The Difficulties of Measuring Ambient DPM in Underground Coal
Mines.
As it indicated in its notice of proposed rulemaking to limit the
concentrations of dpm in underground coal mines (63 FR 17498, 17500),
MSHA decided not to propose a rule to require the measurement of
ambient dpm levels in underground coal mines in order to determine
compliance. The Agency observed that while there are a number of
methods which can measure ambient dpm at high concentrations in
underground coal mines with reasonable accuracy. When the purpose is
exposure assessment, MSHA does not believe any of these methods provide
the accuracy that would be required to measure ambient dpm levels in
underground coal mines at lower concentrations.
In particular, MSHA expressed concern about potential difficulties
in using the available methods to distinguish between dpm and submicron
coal mine dust (63 FR 17506-17507). While the use of an available
impactor device can prevent larger particles from entering the sampler
(e.g., carbonates), albeit at the expense of eliminating the larger
fraction of dpm as well, there are limits on the extent to which it can
help MSHA distinguish how much of the fine particulate reaching the
sampler is coal dust and how much is dpm. To make the distinction
analytically, NIOSH method 5040 would have to be adjusted so that only
the elemental carbon is determined. However, as MSHA noted, there are
no established relationships between the concentration of elemental
carbon and total dpm under various operating conditions. The organic
carbon component of dpm can vary with engine type and duty cycle;
hence, the amount of whole dpm present for a measured amount of
elemental carbon may vary. Accordingly, MSHA concluded that it was
``not confident that there is a measurement method for dpm that will
provide accurate, consistent and verifiable results at lower
concentration levels in underground coal mines'' (63 FR 17500).
Since there has been no disagreement with MSHA's initial conclusion
about the current availability of an accurate, consistent and
verifiable method of measuring dpm concentration levels in underground
coal mines, the final rule is not dependent on ambient air
measurements. MSHA has proposed using such a method for underground
metal and nonmetal mines, and the validity of the measurement was the
subject of much comment; accordingly, a more complete discussion of
this topic will be found in the preamble of the final rule for
underground metal and nonmetal mines.
[[Page 5540]]
(4) Limiting the Public's Exposure to Diesel and Other Fine
Particulates--Ambient Air Quality Standards
Pursuant to the Clean Air Act, the Federal Environmental Protection
Agency (EPA) is responsible for setting air pollution standards to
protect the public from toxic air contaminants. These include standards
to limit exposure to particulate matter. The pressures to comply with
these limits have an impact upon the mining industry, which emits
various types of particulate matter into the environment during mining
operations, and a special impact on the coal mining industry whose
product is used extensively in emission-generating power facilities.
But those standards hold interest for the mining community in other
ways as well, for underlying some of them is a large body of evidence
on the harmful effects of airborne particulate matter on human health.
Increasingly, that evidence has pointed toward the risks of the
smallest particulates--including the particles generated by diesel
engines.
This section provides an overview of EPA's rulemaking efforts to
limit the ambient air concentration of particulate matter, including
its recent particular focus on diesel and other fine particulates.
Additional and up-to-date information about the most current rulemaking
in this regard is available on an EPA's Web site, http://www.epa.gov/ttn/oarpg/naaqsfin/.
EPA is also engaged in other work of interest to the mining
community. Together with some state environmental agencies, EPA has
actually established limits on the amount of particulate matter that
can be emitted by diesel engines. This topic is discussed in the next
section of this Part (section 5). Environmental regulations also
establish the maximum sulfur content permitted in diesel fuel used in
highway vehicles, and such sulfur content can be an important factor in
dpm generation. This topic is discussed in section 6 of this Part. In
addition, EPA and some state environmental agencies have also been
exploring whether diesel particulate matter is a carcinogen or a toxic
material at the concentrations in which it appears in the ambient
atmosphere; discussion of these studies can be found in Part III of
this preamble.
Background. Air quality standards involve a two-step process:
Standard setting by EPA, and implementation by each State.
Under the law, EPA is specifically responsible for reviewing the
scientific literature concerning air pollutants, and establishing and
revising National Ambient Air Quality Standards (NAAQS) to minimize the
risks to health and the environment associated with such pollutants.
This review is to be conducted every five years. Feasibility of
compliance by pollution sources is not supposed to be a factor in
establishing NAAQS. Rather, EPA is required to set the level that
provides ``an adequate margin of safety'' in protecting the health of
the public.
Implementation of each national standard is the responsibility of
the states. Each must develop a state implementation plan that ensures
air quality in the state consistent with the ambient air quality
standard. Thus, each state has a great deal of flexibility in targeting
particular modes of emission (e.g., mobile or stationary, specific
industry or all, public sources of emissions vs. private-sector
sources), and in what requirements to impose on polluters. However, EPA
must approve the state plans pursuant to criteria it establishes, and
then take measurements of pollution to determine whether all counties
within the state are meeting each ambient air quality standard. An area
not meeting an NAAQS is known as a ``nonattainment area''.
Total Suspended Particulates (TSP). Particulate matter originates
from all types of stationary, mobile and natural sources, and can also
be created from the transformation of a variety of gaseous emissions
from such sources. In the context of a global atmosphere, all these
particles mix together, and both people and the environment are exposed
to a ``particulate soup,'' the chemical and physical properties of
which vary greatly with time, region, meteorology, and source category.
The first ambient air quality standards dealing with particulate
matter did not distinguish among these particles. Rather, the EPA
established a single NAAQS for ``total suspended particulates'', known
as ``TSP.'' Under this approach, the states could come into compliance
with the ambient air requirement by controlling any type or size of
TSP. As long as the total TSP was under the NAAQS--which was
established based on the science available in the 1970s--the state met
the requirement.
Particulates Less than 10 Microns in Diameter (PM10).
When the EPA completed a new review of the scientific evidence in the
mid-eighties, its conclusions led it to revise the particulate NAAQS to
focus more narrowly on those particulates less than 10 microns in
diameter, or PM10. The standard issued in 1987 contained two
components: an annual average PM10 limit of 50 g/
m3, and a 24-hour PM10 limit of 150 g/
m3. This new standard required the states to reevaluate
their situations and, if they had areas that exceeded the new
PM10 limit, to refocus their compliance plans on reducing
the levels of particulates smaller than 10 microns in size. Sources of
PM10 include power plants, iron and steel production,
chemical and wood products manufacturing, wind-blown and roadway
fugitive dust, secondary aerosols and many natural sources.
Some state implementation plans required surface mines to take
actions to help the state meet the PM10 standard. In
particular, some surface mines in Western states were required to
control the coarser particles--e.g., by spraying water on roadways to
limit dust. The mining industry has objected to such controls, arguing
that the coarser particles do not adversely impact health, and has
sought to have them excluded from the EPA ambient air standards (Shea,
1995; comments of Newmont Gold Company, March 11, 1997, EPA docket
number A-95-54, IV-D-2346).
Particulate Less than 2.5 Microns in Diameter (PM2.5).
The next EPA scientific review was completed in 1996. A proposed rule
was published in November of 1996, and, after public hearings and
review by the Office of Management and Budget, a final rule was
promulgated on July 18, 1997 (62 FR 38651).
The new rule further modifies the standard for particulate matter.
Under the new rule, the existing national ambient air quality standard
for PM10 remains basically the same--an annual average limit
of 50 g/m3 (with some adjustment as to how this is
measured for compliance purposes), and a 24-hour ceiling of 150
g/m3. In addition, however, the new rule would
establish a NAAQS for ``fine particulate matter'' that is less than 2.5
microns in size. The PM2.5 annual limit was set at 15
g/m3, with a 24-hour ceiling of 65 g/
m3.
The basis for the PM2.5 NAAQS was a large body of
scientific data indicating that particles in this size range are
responsible for the most serious health effects associated with
particulate matter. The evidence was thoroughly reviewed by a number of
scientific panels through an extended process. The proposed rule
resulted in considerable public attention, and hearings by Congress, in
which the scientific evidence was further discussed. Moreover,
challenges to the EPA's determination that this size category warranted
rulemaking were rejected by a three-judge panel of the DC Circuit
Court. (ATA v. EPA, 175 F.3d 1027, D.C. Circuit 1999).
[[Page 5541]]
A majority of the DC Circuit Court, however, agreed with challenges
to the EPA's determination to keep the existing requirements on
PM10 as a surrogate for the coarser particulates in this
category (those particulates between 2.5 and 10 microns in diameter);
instead, the Court ordered EPA to develop a new standard for this size
category.
Implications for the Mining Community. As noted earlier in this
part, diesel particulate matter is mostly less than 1.0 micron in size.
It is, therefore, a fine particulate; in some regions of the country,
diesel particulate generated by highway and off-road vehicles
constitutes a significant portion of the ambient fine particulate (June
16, 1997, PM-2.5 Composition and Sources, Office of Air Quality
Planning and Standards, EPA). As noted in Part III of this preamble,
some of the scientific studies of health risk from fine particulates
used to support the EPA rulemaking were conducted in areas where the
major fine particulate was from diesel emissions. Accordingly, MSHA has
concluded that it must consider the body of evidence of human health
risk from environmental exposure to fine particulates in assessing the
risk of harm to miners of occupational exposure to diesel particulate,
and did so in its risk assessment (see part III of this preamble).
Comments on the appropriateness of this conclusion by MSHA, are
reviewed in Part III.
(5) The impact on emissions of MSHA approval standards and
environmental tailpipe standards.
MSHA requires that the gaseous emissions from all diesel engines
used in underground coal mines meet certain minimum standards of
cleanliness; only engines which meet those standards are ``approved''
for use in underground coal mines. The 1996 diesel equipment safety
rule required that all engines in the underground mining fleet be
approved engines. Thus, these rules set a ceiling for various types of
diesel gas emissions. But diesel engines do not have to meet a dpm
emissions standard to be ``approved'' for underground use.
Engine emissions of dpm are however, restricted by Federal
environmental regulations, supplemented in some cases by State
restrictions. Over time, these regulations have required, and are
continuing to require, that new diesel engines meet tighter and tighter
standards on dpm emissions. As these cleaner engines replace or
supplement older engines in underground coal mines, they can lead to a
significant reduction in the amount of dpm emitted by the underground
fleet.
This section reviews developments in this area. Although this
subject was discussed in the preamble of the proposed dpm rule (63 FR
17507), this review here updates the relevant information.
MSHA Approval Requirements for Engines Used in Underground Coal
Mines. MSHA requires that all diesel engines used in underground coal
mines be ``approved'' by MSHA for such use, and be maintained by
operators in approved condition. Among other things, approval of an
engine by MSHA ensures that engines exceeding certain pollutant
standards are not used in underground coal mines. MSHA sets the
standards for such approval, establishes the testing criteria for the
approval process, and administers the tests. The costs to obtain
approval of an engine are usually borne by the engine manufacturer or
equipment manufacturer.
MSHA's 1996 diesel equipment rule (discussed in more detail in
section 7 of this Part) made significant changes to diesel engine
requirements for underground coal mines. The new rule required the
entire underground coal fleet to convert to approved engines no later
than November 1999. Accordingly, by the time this rule to limiting dpm
exposure goes into effect, all diesel engines in underground coal mines
are expected to be approved engines.
The new rule also required that during the approval process the
agency determine the particulate index (PI) for the engine. The
particulate index (or PI), calculated under the provisions of 30 CFR
7.89, indicates the air quantity necessary to dilute the diesel
particulate in the engine exhaust to 1 milligram of diesel particulate
matter per cubic meter of air.
Unlike the ventilation rate set for each engine, the PI does not
appear on the engine's approval plate (61 FR 55421). Furthermore, the
particulate index of an engine is not, under the diesel equipment rule,
used to determine whether or not the engine can be used in an
underground coal mine.
At the time the diesel equipment rule was issued, MSHA explicitly
deferred the question of whether to require engines used in mining
environments to meet a specific PI (61 FR 55420-21, 55437). While the
matter was discussed during the diesel equipment rulemaking, the
approach taken in the final rule was to adopt the multi-level aproach
recommended by the Diesel Advisory Committee. This multi-level approach
included the requirement to use clean fuel, low emission engines,
equipment design, maintenance, and ventilation, all of which are
included in the final rule. The requirement for determining the
particulate index was included in the diesel equipment rule in order to
provide information to the mining community in purchasing equipment--so
that mine operators can compare the particulate levels generated by
different engines. Mine operators and equipment manufacturers, can use
the information along with consideration of the type of machine the
engines would power and the area of the mine in which it would be used
to make decisions concerning the engine's contribution of diesel
particulate to the mine's total respirable dust. Equipment
manufacturers can use the particulate index to design and install
exhaust after-treatments (61 FR 55421). So that the PI for any engine
is known to the mining community, MSHA reports the index in the
approval letter, posts the PI and ventilating air requirement for all
approved engines on its website, and publishes the index containing its
lists of approved engines.
In the proposed dpm rule, MSHA indicated that given that the
equipment rule was recently promulgated, it did not yet have enough
information to determine the feasibility of a requirement that certain
engines meet a specific PI in order to be used underground (63 FR
17564). MSHA received comments on this subject during the hearings and
thereafter; the Agency's response to these comments is included in Part
IV of this preamble.
Authority for Environmental Engine Emission Standards. The Clean
Air Act authorizes the federal Environmental Protection Agency (EPA) to
establish nationwide standards for mobile sources of air pollution,
including those powered by diesel engines (often referred to in
environmental regulations as ``compression ignition'' or ``CI''
engines). These standards are designed to reduce the amount of certain
harmful atmospheric pollutants emanating from mobile sources: the mass
of particulate matter, nitrogen oxides (which as previously noted, can
result in the generation of particulates in the atmosphere),
hydrocarbons and carbon monoxide.
California has its own engine emission standards. New engines
destined for use in California must meet these standards. The standards
are issued and administered by the California Air Resources Board
(CARB). In many cases, the California standards are the same as the
national standards; as noted herein, the EPA and CARB have worked on
certain agreements with the industry toward that end. In other
[[Page 5542]]
situations, the California standards may be more stringent than federal
standards.
Regulatory responsibility for implementation of the Clean Air Act
is vested in the Office of Transportation and Air Quality (formerly the
Office of Mobile Sources), part of the Office of Air and Radiation of
the EPA. Some of the discussion which follows was derived from
materials which can be accessed from the agency's home page on the
World Wide Web at (http://www.epa.gov/omswww/omshome.htm). Information
about the California standards may be found at the CARB home page at
(http://www.arb.ca.gov/homepage.htm).
Diesel engines are generally divided into three broad categories
for purposes of engine emissions standards, in accordance with the
primary use for which the type of engine is designed: (1) Light duty
vehicles and light duty trucks (i.e., trucks under 8500 lbs GVWR, which
include pick-up trucks and SUVs. EPA has also established a class of
``medium duty passenger vehicles'' which include passenger vehicles
over 8500 lbs. These vehicles, mostly large SUVs, are treated like
light-duty trucks for the purposes of emission standards; (2) heavy
duty highway engines (i.e., those designed primarily to power trucks)
greater than 8500 lbs GVWR) which range from the largest pick-up trucks
to over the road trucks); and (3) nonroad vehicles (i.e., those engines
designed primarily to power small equipment, construction equipment,
locomotives, farm equipment and other non-highway uses).
The terms ``heavy duty'' and ``light duty'' are used differently by
EPA and MSHA. The category of an engine for purposes of environmental
regulations is not the same as the category of mining equipment in
which it is used. The engine categories used by EPA have been
established with reference to normal transportation uses. But as
explained in section 1 of this Part, MSHA has established a
classification system for underground coal mining equipment based on
how that equipment is used in mining. This system includes
``permissible'' equipment (required where explosive methane gas may be
present in significant quantities) and two categories of
``nonpermissible'' equipment known as ``heavy duty nonpermissible'' and
``light duty nonpermissible''. Accordingly, ``heavy duty'' engines
might be used in ``light duty'' nonpermissible equipment.
The exact emission standards which a new diesel engine must meet
varies with engine category and the date of manufacture. Through a
series of regulatory actions, EPA has developed a detailed
implementation schedule for each of the three engine categories. The
schedule generally forces technology while taking into account certain
technological realities.
Detailed information about each of the three engine categories is
provided below; a summary table of particulate matter emission limits
is included at the end of the discussion.
EPA Emission Standards for Light-Duty Vehicles and Light Duty
Trucks. Although vehicle engines in these categories are not currently
approved for use in underground coal mines, it might be sought in the
future. Accordingly, some information about the applicable
environmental regulations is provided here.\2\
---------------------------------------------------------------------------
\2\ The discussion focuses on the particulate matter
requirements for light duty trucks, although the current pm
requirement for all light duty vehicles is the same. The EPA
regulations for these categories apply to the unit, rather than just
to the engine itself; for heavy-duty highway engines and nonroad
engines, the regulations attach to the engines.
---------------------------------------------------------------------------
Current light-duty vehicles generally comply with the Tier 1 and
National LEV emission standards. Particulate-matter emission limits are
found in 40 CFR part 86. In 1999, EPA issued new Tier 2 standards that
will be applicable to light-duty cars and trucks beginning in 2004.
With respect to pm, the new rules phase in tighter emissions limits to
parts of production runs for various subcategories of these engines
over several years; by 2009, all light duty trucks must limit pm
emissions to a maximum of 0.02 g/mi (40 CFR 86.1811-04(c)). Engine
manufacturers may, of course, produce complying engines before the
various dates required.
EPA Emissions Standards for Heavy-Duty Highway Engines. In 1988, a
standard limiting particulate matter emitted from the heavy duty
highway diesel engines went into effect, limiting dpm emissions to 0.6
g/bhp-hr. The Clean Air Act Amendments of 1990 and associated
regulations provided for phasing in even tighter controls on
NOX and particulate matter through 1998. Thus, engines had
to meet ever tighter standards for NOX in model years 1990,
1991 and 1998; and tighter standards for PM in 1991 (0.25 g/bhp-hr) and
1994 (0.10 g/bhp-hr). The latter remains the standard for PM from these
engines for current production runs (40 CFR 86.094-11(a)(1)(iv)(B)).
Since any heavy duty highway engine manufactured since 1994 must meet
this standard, there is a supply of engines available today which meet
this standard. These engines are used in commercial mining pickup
trucks.
New standards for this category of engines are gradually being put
into place. On October 21, 1997, EPA issued a new rule for certain
gaseous emissions from heavy duty highway engines that will take effect
for engine model years starting in 2004 (62 FR 54693). The rule
establishes a combined requirement for NOX and Non-methane
Hydrocarbon (NMHC). The combined standard is set at 2.5 g/bhp-hr, which
includes a cap of 0.5g/bhp-hr for NMHC. EPA promulgated a rulemaking on
December 22, 2000 (65 FR 80776) to adopt the next phase of new
standards for these engines. EPA is taking an integrated approach to:
(a) Reduce the content of sulfur in diesel fuel; and thereafter, (b)
require heavy-duty highway engines to meet tighter emission standards,
including standards for PM. The purpose of the diesel fuel component of
the rulemaking is to make it technologically feasible for engine
manufacturers and emissions control device makers to produce engines in
which dpm emissions are limited to desired levels in this and other
engine categories. The EPA's rule will reduce pm emissions from new
heavy-duty engines to 0.01 g/bhp-hr, a reduction from the current 0.1
g/bhp-hr. MSHA assumes it will be some time before there is a
significant supply of engines that can meet this standard, and the fuel
supply to make that possible.
EPA Emissions Standards for Nonroad Engines. Nonroad engines are
those designed primarily to power small portable equipment such as
compressors and generators, large construction equipment such as haul
trucks, loaders and graders, locomotives and other miscellaneous
equipment with non-highway uses. Engines of this type are used most
frequently in the underground coal mines to power equipment.
Nonroad diesel engines were not subjected to emission controls as
early as other diesel engines. The 1990 Clean Air Act Amendments
specifically directed EPA to study the contribution of nonroad engines
to air pollution, and regulate them if warranted (Section 213 of the
Clean Air Act). In 1991, EPA released a study that documented higher
than expected emission levels across a broad spectrum of nonroad
engines and equipment (EPA Fact Sheet, EPA420-F-96-009, 1996). In
response, EPA initiated several regulatory programs. One of these set
Tier 1 emission standards for larger land-based nonroad engines (other
than for rail use). Limits were established for engine emissions of
[[Page 5543]]
hydrocarbons, carbon monoxide, NOX, and dpm. The limits were
phased in over model years from 1996 to 2000. With respect to
particulate matter, the rules required that starting in model year
1996, nonroad engines from 175 to 750 hp meet a limit on pm emissions
of 0.4 g/bhp-hr, and that starting in model year 2000, nonroad engines
over 750 hp meet the same limit.
Particulate matter standards for locomotive engines were set
subsequently (63 FR 18978, April, 1998). The standards are different
for line-haul duty-cycle engine and switch duty-cycle engines. For
model years from 2000 to 2004, the standards limit pm emissions to 0.45
g/bhp-hr and 0.54 g/bhp-hr respectively; after model year 2005, the
limits drop to 0.20 g/bhp-hr and 0.24 g/bhp-hr respectively.
In October 1998, EPA established additional standards for nonroad
engines (63 FR 56968). Among these are gaseous and particulate matter
limits adopted for the first time (Tier 1 limits) for nonroad engines
under 50 hp. Tier 2 emissions standards for engines between 50 and 175
hp include pm standards for the first time. Further, they establish
Tier II particulate matter limits for all other land-based nonroad
engines (other than locomotives which previously had Tier II
standards). Some of the non-particulate emissions limits set by the
1998 rule are subject to a technology review in 2001 to ensure that the
required levels are feasible; EPA has indicated that in the context of
that review, it intends to consider further limits for particulate
matter. Because of the phase-in of these Tier II pm standards, and the
fact that some manufacturers will produce engines meeting the standard
before the requirements go into effect, there are or soon will be some
Tier II pm engines in some sizes available, but it is likely to be a
few years before a full size range of Tier II pm nonroad engines is
available.
Table II-3 provides a full list of the EPA required particulate
matter limitations on nonroad diesel engines for tier 1 and 2. For
example, a nonroad engine of 175 hp produced in 2001 must meet a
standard of 0.4 g/hp-hr; a similar engine produced in 2003 or
thereafter must meet a standard of 0.15 g/hp-hr.
Table II-3.--EPA Nonroad Engine PM Requirements
----------------------------------------------------------------------------------------------------------------
Year first PM limit (g/
kW range Tier applicable kW-hr)
----------------------------------------------------------------------------------------------------------------
kW8............................................................. 1 2000 1.00
2 2005 0.80
8kW19................................................ 1 2000 0.80
19kW37............................................... 1 1999 0.80
2 2004 0.60
37kW75............................................... 1 1998 ..............
2 2004 0.40
75kW130.............................................. 1 1997 ..............
2 2003 0.30
130kW225............................................. 1 1996 0.54
2 2003 0.20
225kW450............................................. 1 1996 0.54
2 2001 0.20
450kW560............................................. 1 1996 0.54
2 2002 0.20
kW>560.......................................................... 1 2000 0.54
2 2006 0.20
----------------------------------------------------------------------------------------------------------------
The Impact of MSHA and EPA Engine Emission Standards on the
Underground Coal Mining Fleet. In the mining industry, engines and
equipment are often purchased in used condition, and frequently
rebuilt. Thus, many of the diesel engines in an underground coal mine's
fleet today may only meet older environmental emission standards, or no
environmental standards at all. Although the environmental tailpipe
requirements on dpm are already bringing about a reduction in the
overall contribution of dpm to the general atmosphere, the beneficial
effects of the EPA regulations on mining atmospheres will be slower
absent incentive or regulatory actions that accelerate the turnover of
mining fleets to engines that emit less dpm. Moreover, while the
requirement that all underground coal mine engines be ``MSHA approved''
is leading to a less polluting fleet than would otherwise be the case,
there are many approved engines that do emit significant levels of
pollution, and in particular dpm. As noted in the discussion of MSHA's
approval requirements, the Agency is taking internal actions to ensure
that these requirements do not inadvertently slow the introduction of
cleaner engine technology.
It should be noted that in theory, underground mines can still
purchase certain types of new engines that do not have to meet EPA
standards. For example, the current rules on nonroad diesel engines
state that they do not apply to engines intended to be used in
underground coal and metal and nonmetal mines (40 CFR 89.1(b)).
Moreover, it is not uncommon for engine manufacturers to take a model
submitted for EPA testing and adjust the horsepower or other features
for use in a mining application. In recent years, however, engine
manufacturers have significantly cut back on such adjustments because
the mining community is not a major market. Accordingly, MSHA believes
that most of the diesel engines that will be available for underground
mines in the future will meet the applicable EPA standard. In addition,
many of the recently approved engines by MSHA currently meet the tier
II nonroad pm standards.
The Question of Nanoparticles. Comments received from several
commenters on the proposed rule for diesel particulate matter exposure
of underground coal miners raised questions relative to
``nanoparticles;'' i.e., particles found in the exhaust of diesel
engines that are less than 50 nanometers (nm) in diameter.
One commenter was concerned about recent indications that
nanoparticles may pose more of a health risk than the larger particles
that are emitted from a diesel engine. This commenter submitted
information demonstrating
[[Page 5544]]
that nanoparticles emitted from the engine could be removed effectively
from the exhaust using aftertreatment devices such as ceramic traps.
Another commenter was concerned that MSHA's proposed rule for
underground coal mines is based on removing 95% of the particulate by
mass. He believed that this reduction in mass was attributed to those
particles greater than 0.1m but less than 1m and did
not address the recent scientific hypothesis that it may be the very
small nanopaticles that are responsible for adverse health effects.
Based on the recent scientific information on the potential health
effects resulting from exposure to nanoparticles, this commenter did
not believe that potential the risk of cancer would be reduced if
exposure levels to nanoparticles increased. He indicated that studies
suggest that the increase in nanoparticles will exceed 6 times their
current levels.
Current environmental emission standards established by EPA and
CARB, and the particulate index calculated by MSHA, focus on the total
mass of diesel particulate matter emitted by an engine--for example,
the number of grams per some unit of measure (i.e. grams/brake-
horsepower). Thus, the technology under development by the engine
industry to meet the standards accordingly focuses on reducing the mass
of dpm emitted from the engine. There is some evidence, however, that
some aspects of this new technology, particularly fuel injection, is
resulting in an increase in the number of nanoparticles emitted from
the engine.
Figure II-3, repeated here from section 2 of this Part, illustrates
this situation (Majewski, W. Addy, Diesel Progress, June, 1998).
BILLING 4510-43-P
[GRAPHIC] [TIFF OMITTED] TR19JA01.007
BILLING CODE 4510-43-C
The formation of particulates starts with particle nucleation
followed by subsequent agglomeration of the nuclei particles into an
accumulation mode. Thus, as illustrated in Figure II-3, the majority of
the mass of dpm is found in the accumulation mode, where the particles
are generally between 0.1 and 1 micron in diameter. However, when
considering the number of particles emitted from the engine, more than
half and sometimes almost all of the particles (by number) are in the
nuclei mode.
A number of studies have demonstrated that the size of the
particles emitted from the newer low emission diesel engines, has
shifted toward the generation of nuclei mode particles. One study
(cited by Majewski) compared a 1991 engine to its 1988 counterpart. The
total PM mass in the newer engine was reduced by about 80%; but the new
engine generated thousands of times more particles than the older
engine (3000 times as much at 75 percent load and about 14,000 times as
much at 25 percent load). One hypothesis offered for this phenomenon is
that the cleaner engines produce less soot particles on which
particulates can condense and accumulate, and hence they remain in
nuclei mode. The accumulation particles act as a ``sponge'' for the
condensation and/or adsorption of volatile materials. In the absence of
that sponge, gas species which are to become liquid or solid will
nucleate to form large numbers of small particles (see diesel.net
technology guide). Mayer, while pointing out that nanoparticle
production was a problem with older engines as well, concurs that the
technology used to clean up pollution in newer engines is not having
any positive impact on nanoparticle production. While there is
scientific evidence that the newer engines, designed to reduce the mass
of pollutants emitted from the diesel engine, emit more particles in
the nuclei mode, quantifying the magnitude of these particles has been
difficult. This is because as dpm is released into the
[[Page 5545]]
atmosphere the diesel particulate undergoes very complex changes. In
addition, current sampling procedures produce artificial particulates,
which otherwise would not exist under atmospheric conditions.
Experimental work conducted at West Virginia University (Bukarski)
indicate that nanoparticles are not generated during the combustion
process, but rather during other physical and chemical processes which
the exhaust undergoes in aftertreatment systems.
While current medical research findings indicate that small
particulates, particularly those below 2m in diameter, may be
more harmful to human health than the larger ones, much more medical
research and diesel emission studies are needed to fully characterize
diesel nanoparticles emissions and their influence on human health. If
nanoparticles are found to have an adverse health impact by virtue of
size or number, it could require significant adjustments in
environmental engine emission regulation and technology. It could also
have implications for the type of controls utilized, with some
asserting that aftertreatment filters are the only effective way to
limit the emission of nanoparticles and others asserting that
aftertreatment filters can increase the number of nanoparticles.
As discussed in Part III, the available evidence on the risks for
dpm exposure do not currently include enough data to draw conclusions
about the risks of exposure to significant numbers of very small
particles. Research on nanoparticles and their health effects is
currently a topic of investigation. As there have been few measurements
of the number of particles emitted (as opposed to mass), it will be
very difficult for epidemiologists to extrapolate information in this
regard.
Based on the comments received and a review of the literature
currently available on the nanoparticle issue, MSHA believes that
promulgation of the final rules for underground coal and metal and
nonmetal mines is necessary to protect miners. The nanoparticle issues
discussed above will not be answered for some time because of the
extensive research required to address the questions raised. MSHA's
rules will require the application of exhaust aftertreatment devices on
nearly all of the most polluting engines. The application of these
measures will reduce the number of nanoparticles as well as the mass of
the larger particles to which a miner will be exposed--miners wanted
aftertreatment on all machines for this purpose.
(6) Other Methods for Controlling DPM in Underground Coal Mines
As discussed in the last section, the introduction of new engines
underground will play a significant role in reducing the concentration
of dpm in underground coal mines. There are, however, other approaches
to reducing dpm concentrations in underground coal mines. Among these
are: use of aftertreatment devices to eliminate particulates emitted by
an engine; altering fuel composition to minimize engine particulate
emission; use of maintenance practices and diagnostic systems to ensure
that fuel, engine and aftertreatment technologies work as intended to
minimize emissions; enhancing ventilation to reduce particulate
concentrations in a work area; enclosing workers in cabs or other
filtered areas to protect them from exposure; and use of work and fleet
practices that reduce miner exposures to emissions.
As noted in section 9 of this Part, information about these
approaches was solicited from the mining community in a series of
workshops in 1995, and highlights were published by MSHA as an appendix
to the proposed rule on dpm ``Practical Ways to Control Exposure to
Diesel Exhaust in Mining--a Toolbox.'' During the hearings and in
written comments on this rulemaking, these control methods were
discussed.
This section provides updated information on two methods for
controlling dpm emissions: aftertreatment devices and diesel fuel
content. There was considerable comment on aftertreatment devices
because MSHA's proposed rule would have required that certain equipment
be equipped with high-efficiency particulate filters; the efficiency of
such devices remains an important issue in determining the
technological and economic feasibility of the final rule. Moreover,
some commenters strongly favored the use of oxidation catalytic
converters, a type of aftertreatment device used to reduce gaseous
emission but which can also lessen dpm levels. Accordingly, information
about them is reviewed here. With respect to diesel fuel composition, a
recent rulemaking initiative by EPA, and actions taken by other
countries in this regard, are discussed here because of their
implications for the mining community.
Emissions aftertreatment devices. One of the most discussed
approaches to controlling dpm emissions involves the use of devices
placed on the end of the tailpipe to physically trap diesel particulate
emissions and thus limit their discharge into the mine atmosphere.
These aftertreatment devices are often referred to as ``particle
traps'' or ``soot traps,'' but the term filter is also used. The two
primary categories of particulate traps are those composed of ceramic
materials (and thus capable of handling uncooled exhaust), and those
composed of paper materials (which require the exhaust to first be
cooled). Typically, the latter are designed for conventional
permissible equipment which have water scrubbers installed which cool
the exhaust. However, another alternative that is now used in coal
mines is ``dry system technology'' which cools the diesel exhaust with
a heat exchanger and then uses a paper filter. In addition, ``oxidation
catalytic converters,'' devices used to limit the emission of diesel
gases, and ``water scrubbers,'' devices used to cool the emission of
diesel gases, are discussed here as well, because they also can have
effect on limiting particle emission.
Water Scrubbers. Water scrubbers are devices added to the exhaust
system of diesel equipment. Water scrubbers are essentially metal boxes
containing water through which the diesel exhaust gas passes. The
exhaust gas is cooled, generally to below 170 degrees F. A small
fraction of the unburned hydrocarbons is condensed and remains in the
water with some of the dpm. Tests conducted by the former Bureau of
Mines and others indicate that no more than 20 to 30 percent of the dpm
is removed. However, MSHA has no definitive evidence on the amount of
dpm reduction that can be achieved with a particular water scrubber.
The water scrubber does not remove the carbon monoxide, the oxides of
nitrogen, or other gaseous emission that remains a gas at room
temperature, so their effectiveness as aftertreatment devices is
limited.
The water scrubber serves as an effective spark and flame arrester
and as a means to cool the exhaust gas. Consequently, it is used in
most of the permissible diesel equipment in mining as part of the
safety components needed to gain MSHA approval.
The water scrubber has several operating characteristics which keep
it from being a candidate for an aftertreatment device on
nonpermissible equipment. The space required on the vehicle to store
sufficient water for an 8 hour shift is not available on some
equipment. Furthermore, the exhaust contains a great deal of water
vapor which condenses under some mining conditions creating a fog which
can adversely effect visibility. Also, operation of the equipment on
slopes can cause the water level in the scrubber
[[Page 5546]]
to change resulting in water blowing out the exhaust pipe. Control
devices can be placed within the scrubber to maintain the appropriate
water level. Because these devices are in contact with the water
through which the exhaust gas has passed, they need frequent
maintenance to insure that they are operating properly and have not
been corroded by the acidic water created by the exhaust gas. The water
scrubber must be flushed frequently to remove the acidic water and the
dpm and other exhaust residue which forms a sludge that adversely
effects the operation of the unit. These problems, coupled with the
relatively low dpm removal efficiency, have prevented widespread use of
water scrubbers as a primary dpm control device on nonpermissible
equipment.
Oxidation Catalytic Converters (OCCs). Oxidation catalytic
converters (OCCs) were among the first devices added to diesel engines
in mines to reduce the concentration of harmful gaseous emissions
discharged into the mine environment. OCCs began to be used in
underground mines in the 1960's to control carbon monoxide,
hydrocarbons and odor (Haney, Saseen, Waytulonis, 1997). Their use has
been widespread. It has been estimated that more than 10,000 OCCs have
been put into the mining industry over the last several years
(McKinnon, dpm Workshop, Beckley, WV, 1995).
Several of the harmful emissions in diesel exhaust are produced as
a result of incomplete combustion of the diesel fuel in the combustion
chamber of the engine. These include carbon monoxide and unburned
hydrocarbons including harmful aldehydes. Catalytic converters, when
operating properly, remove significant percentages of the carbon
monoxide and unburned hydrocarbons. Higher operating temperatures,
achieved by hotter exhaust gas, improve the conversion efficiency.
Oxidation catalytic converters operate, in effect, by continuing
the combustion process outside the combustion chamber. This is
accomplished by utilizing the oxygen in the exhaust gas to oxidize the
contaminants. A very small amount of material with catalytic
properties, usually platinum or a combination of the noble metals, is
deposited on the surfaces of the catalytic converter over which the
exhaust gas passes. This catalyst allows the chemical oxidation
reaction to occur at a lower temperature than would normally be
required.
For the catalytic converter to work effectively, the exhaust gas
temperature must be above 370 degrees Fahrenheit for carbon monoxide
and 500 degrees Fahrenheit for hydrocarbons. Most converters are
installed as close to the exhaust manifold as possible to minimize the
heat loss from the exhaust gas through the walls of the exhaust pipe.
Insulating the segment of the exhaust pipe between the exhaust manifold
and the catalytic converter extends the portion of the vehicle duty
cycle in which the converter works effectively.
The earliest catalytic converters for mining use consisted of
alumina pellets coated with the catalytic material and enclosed in a
container. The exhaust gas flowed through the pellet bed where the
exhaust gas came into contact with the catalyst. Designs have evolved,
and now the most common design is a metallic substrate, formed to
resemble a honeycomb, housed in a metal shell. The catalyst is
deposited on the surfaces of the honeycomb. The exhaust gas flows
through the honeycomb and comes into contact with the catalyst.
Soon after catalytic converters were introduced, it became apparent
that there was a problem due to the sulfur found in diesel fuels in use
at that time. Most diesel fuels in the United States contained anywhere
from 0.25 to 0.50 percent sulfur or more on a mass basis. In the
combustion chamber, this sulfur was converted to SO2,
SO3, or SO4 in various concentrations, depending
on the engine operating conditions. In general, most of the sulfur was
converted to gaseous SO2. When exhaust containing the
gaseous sulfur dioxide passed through the catalytic converter, a large
proportion of it was converted to solid sulphates which are in fact,
diesel particulate. Sulfates can ``poison'' the catalyst, severely
reducing its life.
Recently, as described elsewhere in this preamble, the EPA required
that diesel fuel used for over the road trucks contain no more than 500
ppm (0.05 percent) sulfur. This action made low sulfur fuel available
throughout the United States. MSHA, in its recently promulgated
regulations for the use of diesel powered equipment in underground coal
mines required that this low sulfur fuel be used. When the low sulfur
fuel is burned in an engine and passed through a converter with a
moderately active catalyst, only small amounts of SO2 and
additional sulfate based particulate are created. However, when a very
active catalyst is used, to lower the operating temperature of the
converter or to enhance the CO removal efficiency, even the low sulfur
fuel has sufficient sulfur present to create an SO2 and
sulfate based particulate problem. Consequently, as discussed later in
this section, the EPA has notified the public of its intentions to
promulgate regulations that would limit the sulfur content of future
diesel fuel to 15 ppm (0.0015 percent) for on-highway use in 2006.
The particulate removal capabilities of some OCCs are significant
in gravimetric terms. In 1995, the EPA implemented standards requiring
older buses in urban areas to reduce the dpm emissions from rebuilt bus
engines (40 CFR 85.1403). Aftertreatment manufacturers developed
catalytic converter systems capable of reducing dpm by 20%. Such
systems are available for larger diesel engines common in the
underground metal and nonmetal sector. However, as has been pointed out
by Mayer, the portion of particulate mass that seems to be impacted by
OCCs is the soluble component, and this is a smaller percentage of
particulate mass in utility vehicle engines than in automotive engines.
Moreover, some measurements indicate that more than 40% of NO is
converted to more toxic NO2, and that particulate mass
actually increases using an OCC at full load due to the formation of
sulfates. In summation, Mayer concluded that the OCCs do not reduce the
combustion particulates, produce sulfate particulates, or have
unfavorable gaseous phase reactions increasing toxicity, and that the
positive effects are irrelevant for construction site diesel engines.
He concludes that the negative effects outweigh the benefits (Mayer).
The Phase 1 interim data report of the Diesel Emission Control-
Sulfur Effects (DECSE) Program (a joint government-industry program
established to explore lower sulfur content that is discussed in more
detail later in this section) similarly indicates that testing of OCCs
under certain operating conditions can increase dpm emissions due to an
increase in the sulfate fraction. (DECSE Program Summary, Dec. 1999)
Another commenter also notes that oxidation catalytic activity can
increase sulfates under certain operating temperatures, and that
oxidation is a part of aftertreatment systems approaches like the
DST and some ceramic traps. But this commenter asserts that
the sulfate production occurs at an operating mode that is seldom seen
in real operation.
Other commenters during the rulemaking strongly supported the use
of OCCs to reduce particulate and other diesel emissions. They argue
that the OCCs result in significant reductions in dpm and in dpm
generating gases. One commenter noted that with a clean engine, an OCC
might well reduce particulates enough to meet any requirements
established by MSHA.
[[Page 5547]]
However, another commenter noted that OCCs and ceramic traps can
fail when used at higher altitude mines due to the lower oxygen content
in the exhaust system. Another commenter asserted that OCCs are not
effective at low temperature, although they are improving. Accordingly,
this commenter indicated that OCCs have an impact only on light duty
equipment when the equipment is working, not when it is idling, and are
virtually useless on permissible equipment because of the low exhaust
temperatures achieved through cooling. Despite a specific request from
MSHA at the rulemaking hearings, no data were provided by OCC advocates
to demonstrate that they can perform well at the lower temperatures
normally found in light duty equipment.
Hot gas particulate traps. Throughout this preamble, MSHA is
referring to the particulate traps (filters) that can be used in the
undiluted hot exhaust stream from the diesel engine as hot gas filter.
Hot gas filter refers to the current commercially available particulate
filters such as ceramic cell, woven fiber filter, sintered metal
filter, etc.
Following publication of EPA rules in 1985 limiting diesel
particulate emissions from heavy duty diesel engines, development of
aftertreatment devices capable of more significant reductions in
particulate levels began to be developed for Comerica applications.
The wall flow type ceramic honeycomb diesel particulate filter
system was initially the most promising approach (SAE, SP-735, 1988).
This consisted of a ceramic substrate encased in a shock-and vibration-
absorbing material covered with a protective metal shell. The ceramic
substrate is arranged in the shape of a honeycomb with the openings
parallel to the centerline. The ends of the openings of the honeycomb
cells are plugged alternately. When the exhaust gas flows through the
particulate trap, it is forced by the plugged end to flow through the
ceramic wall to the adjacent passage and then out into the mine
atmosphere. The ceramic material is engineered with pores in the
ceramic material sufficiently large to allow the gas to pass through
without placing excessive back pressure on the engine, but small enough
to trap the particulate on the wall of the ceramic material.
Consequently, these units are called wall flow traps.
Work with ceramic filters in the last few years has led to the
development of the ceramic fiber wound filter cartridge (SAE, SP-1073,
1995). The ceramic fiber has been reported by the manufacturer to have
dpm reduction efficiencies up to 80 percent. This system has been used
on vehicles to comply with German requirements that exhaust from all
diesel engines used in confined areas be filtered. Other manufacturers
have made the wall flow type ceramic honeycomb dpm filter system
commercially available to meet the German standard. One commenter noted
that a total exhaust, wall-flow, ceramic filter developed in Canada in
collaboration with a US firm has been successfully demonstrated
underground with a reduction of between 60% and 90% of particulate
matter.
The development of these devices has proceeded in response to
international and national efforts to regulate dpm emissions. However,
due to the extensive work performed by the engine manufacturers on new
technological designs of the diesel engine's combustion system, and the
use of low sulfur fuel, particulate traps were found to be unnecessary
for compliance with the EPA standards of the time for vehicle engines.
These devices proved to be quite effective in removing particulate,
achieving particulate removal efficiencies of greater than 90 percent.
It was quickly recognized that this technology, while not
immediately required for most vehicles, might be useful in mining
applications. The former Bureau of Mines investigated the use of
catalyzed diesel particulate filters in underground mines in the United
States (BOM, RI-9478, 1993). The study demonstrated that filters could
work, but that there were problems associated with their use on
individual unit installations, and the Bureau made recommendations for
installation of ceramic filters on mining vehicles.
Canadian mines also began to experiment with ceramic traps in the
1980's with similar results (BOM, IC 9324, 1992). Work in Canada today
continues under the auspices of the Diesel Emission Evaluation Program
(DEEP), established by the Canadian Centre for Mineral and Energy
Technology in 1996 (DEEP Plenary Proceedings, November 1996). The goals
of DEEP are to: (1) evaluate aerosol sampling and analytical methods
for dpm; and (2) evaluate the in-mine performance and costs of various
diesel exhaust control strategies.
Reservations regarding their usefulness and practicality remain.
One commenter stated at one of the MSHA workshops in 1995, ``while
ceramic filters give good results early in their life cycle, they have
a relatively short life, are very expensive and unreliable.'' Another
commenter reported unsuccessful experiments with ceramic filters in
1991 due to their inability to regenerate at low temperatures, lack of
reliability, high cost of purchase and installation, and short life.
Another reported that ceramics would not work at higher altitudes
because of lower oxygen content in the exhaust system. Another
commenter pointed out that elevated operating temperatures in certain
engine modes can result in sulfates adding as much as 50% to total
particulate mass, and asserted that ceramic traps alone were unable to
offset this effect on their own.
In response to the proposed rule, MSHA received information and
claims about the current efficiency of such technologies. One
commenter, representing those who manufacture emissions controls, and
referring to technologies other than low temperature paper filters--
such as higher temperature disposable paper filters, ceramic monolith
diesel particulate filters, wound ceramic fiber filters, and metal
fiber filters--asserted that there were technologies which could
achieve in excess of 95% filtration efficiency under ``many operating
conditions.'' Another commenter submitted copies of information
provided to that commenter by individual manufacturers of emission
control systems, many of which made similar claims. Another commenter,
however, questioned manufacturer claims, asserting big differences had
been observed between such claims an independent 8-mode tests.
It appears that two groups in particular have been doing some
research comparing the efficiency of recent ceramic models: the
University of West Virginia, as part of that State's efforts to develop
rules on the use of diesel-powered equipment underground; and VERT
(Verminderung der Emissionen von Realmaschinen in Tunnelbau), a
consortium of several European agencies conducting research in
connection with major planned tunneling projects in Austria,
Switzerland and Germany to protect occupational health and subsequent
legislation in each of the three countries restricting diesel emissions
in tunneling (in both cases, background on the regulatory efforts of
the jurisdictions involved is discussed in section 8 of this part).
The legislature of the State of West Virginia enacted the West
Virginia Diesel Act, which created the West Virginia Diesel Commission
and set forth an administrative vehicle to allow and regulate the use
of diesel equipment in underground coal mines in that state. West
Virginia University was appropriated funds to test diesel exhaust
controls, as well as an array of
[[Page 5548]]
diesel particulate filters. The University was asked to provide
technical support and data necessary for the Commission to make
decisions on standards for emission controls.
The University provided data on four different engines and an
assortment of configurations of available control devices, both hot gas
filters and the DST system (a system which, first cools the
exhaust, then runs it through a paper filter). The range of collection
efficiencies reported for the ceramic filters and oxidation catalysts
combined fell between 65% and 78%. The highest collection efficiency
obtained using the ISO 8 mode test cycle (test cycle described in rule)
was 81% on the DST system. The University reported problems
with this system that would account for the lower than expected
efficiency for a paper filter type system. A commenter who spoke for
the Commission at MSHA's public hearing expressed serious reservations
of the 95% collection efficiency of MSHA's proposed rule and believed
it was not achievable with technology based on the University's current
work. The WV Commission also provided MSHA a detailed proposal for
setting a laboratory diesel particulate standard of 0.5 milligram per
cubic meter. As discussed in part IV, this is similar to the
Pennsylvania standard, but without a strict filter efficiency value,
and as further discussed in part IV, MSHA's approach in this final rule
is similar.
VERT's studies of particulate traps are detailed in two articles
published in 1999 which have been widely disseminated to the diesel
community here through www.DieselNet.com (Mayer et al., March 1999, and
Mayer, April 1999). The March article focuses on the efficiency of the
traps; the April article compares the efficiency of other approaches
(OCCs, fuel reformulation, engine modifications to reduce ultra-fine
particulates) with that of the traps. Here we focus only on the
information about particulate traps.
The authors of the March article report that 29 particulate trap
systems were tested using various ceramic, metal and fiber filter media
and several regeneration systems. The authors of the March article
summarize their conclusions as follows:
The results of the 4-year investigations of construction site
engines on test rigs and in the field are clear: particulate trap
technology is the only acceptable choice among all available
measures. Traps proved to be an extremely efficient method to
curtail the finest particles. Several systems demonstrated a
filtration rate of more than 99% for ultra-fine particulates.
Specific development may further improve the filtration rate.
A two-year field test, with subsequent trap inspection,
confirmed the results pertaining to filtration characteristics of
ultra-fine particles. No curtailment of the ultra-fine particles is
obtained with any of the following: reformulated fuel, new
lubricants, oxidation catalytic converters, and optimization of the
engine combustion.
Particulate traps represent the best available technology (BAT).
Traps must therefore be employed to curtail the particulate
emissions that the law demands are minimized. This technology was
implemented in occupational health programs in Germany, Switzerland
and Austria.
On the bench tests, it appears that the traps reduce the overall
particulate matter by between 70 and 80%, with better results for solid
ultrafine particulates; under hot gas conditions, it appears the non-
solid components of particulate matter cannot be dependably retained by
these traps. Consistent with this finding, it was found that polycyclic
aromatic hydrocarbons (PAHs) decreased proportionately to the
gravimetric decrease of carbon mass. The tests also explored the impact
of additives on trap efficiency, and the impact of back pressure.
The field tests confirmed that the traps were easy to mount and
retained their reliability over time, although regeneration using an
external power source was required when low exhaust temperatures failed
to do this automatically. Electronic monitoring of back pressure was
recommended. In general, the tests confirmed that a whole series of
trap systems have a high filtration rate and stable long time
properties and are capable of performing under difficult construction
site conditions. Again, the field tests indicated a very high reduction
(97-99%) by particulate count, but a lower rate of reduction in terms
of mass.
Subsequently, VERT has evaluated additional commerically available
filter systems. A list of recently evaluated hot gas filters are shown
in Table II-4. The filtration efficiency, expressed on a gravimetric
basis is shown in the column headed ``PMAG--without additive''. The
filtration efficiencies determined by VERT for these 6 filter systems
range from 80.7% to 94.5%. The average efficiency of these filters is
87%. MSHA will be updating the list of VERT's evaluated systems as they
become available.
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Some commenters asserted that the VERT work was for relatively
small engines and not for large engines, i.e. 600-700 hp, and hence
could not be relied upon to demonstrate the availability of filters of
such high efficiencies for the larger equipment used in some
underground mines. MSHA believes this comment is misplaced. The
efficiency of a filter is attributable to the design of the filter and
not the size of the engine. VERT is documenting filter efficiencies of
commercially available filters. It is customary in the industry,
however, for the filter manufacturer to size the filter to fit the size
of the engine. The mine operator must work with the filter manufacturer
to verify that the filter needed will work for the intended machine.
MSHA believes that this is no different for other types of options
installed on machines for underground mining use.
More information about the results of the VERT tests on specific
filters, and how MSHA intends to use this information to aid the mining
industry in complying with the requirements of the standards for heavy
duty equipment, generators and compressors, are discussed in Part IV of
this preamble.
The accumulated dpm must be removed from particulate traps
periodically. This is usually done by burning off the accumulated
particulate in a controlled manner, called regeneration. If the diesel
equipment on which the trap is installed has a duty cycle which creates
an exhaust gas temperature greater than about 650 degrees Fahrenheit
for more than 25 percent of the operating time, the unit will be self
cleaning. That is, the hot exhaust gas will burn off the particulate as
it accumulates. Unfortunately, only hard working equipment, such as
load, haul, dump and haulage equipment usually satisfies the exhaust
gas temperature and duration requirements to self regenerate.
Techniques are available to lower the temperature needed to
initiate the regeneration. One technique under development is to use a
fuel additive. A comparatively small amount of a chemical is added to
the diesel fuel and burns along with the fuel in the combustion
chamber. The additive is reported to lower the required regeneration
temperature significantly. The additive combustion products are
retained as a residue in the particulate trap. The trap must be removed
from the equipment periodically to flush the residue. Another technique
used to lower the regeneration temperature is to apply a catalyst to
the surfaces of the trap material. The action of the catalyst is
similar to that of the fuel additive. The catalyst also lowers the
concentration of some gaseous emissions in the same manner as the
oxidation catalytic converter described earlier.
A very active catalyst applied to the particulate trap surfaces and
a very active catalyst in a catalytic converter installed upstream of
the trap can create a situation in which the trap performs less
efficiently than expected. Burning low sulfur diesel fuel, containing
less than 500 ppm sulfur, will result in the creation of significant
quantities of sulfates in the exhaust gas. These sulfates will still be
in the gaseous state when they reach the ceramic trap and will pass
through the trap. These sulfates will condense later forming diesel
particulate. Special care must be taken in the selection of the
catalyst formulation to ensure that sulfate formation is avoided. This
problem does not occur in systems designed with a catalytic converter
upstream of a water scrubber. The gaseous phase sulfates will condense
when contacting the water in the scrubber and will not be discharged
into the mine atmosphere. Thus far, no permissible diesel packages have
been approved which incorporate a catalytic converter upstream of the
water scrubber. One research project conducted by the former Bureau of
Mines which attempted this arrangement was unsuccessful. In attempting
to maintain a surface temperature less than the 300 degrees Fahrenheit
(required for permissibility purposes) the exhaust gas was be cooled to
the point that the catalytic converter did not reach the necessary
operating temperature. It would appear that a means to isolate the
catalytic converter from the exhaust gas water jacket is necessary for
the arrangement to function as intended.
If the machine on which the particulate trap is installed does not
work hard enough to regenerate the trap with the hot exhaust gas and
the option to use a fuel additive or catalyzed trap is not appropriate,
the trap can still be regenerated while installed on the machine.
Systems are available whereby air is heated by an externally applied
heat source and caused to flow through the particle trap when the
engine is stopped. The heat can be supplied by an electrical resistance
element installed in front of the trap. The heat can also be supplied
by a burner installed into the exhaust pipe in front of the trap. The
burner is fueled by an auxiliary fuel line. The fuel is ignited
creating large quantities of hot gas. With both systems, an air line is
also connected to the exhaust pipe to create a flow of hot gases
through the particulate trap. Both systems utilize operator panels to
control the regeneration process.
Equipment owners may choose to remove the particle trap from the
machine to perform the regeneration. Particle traps are available with
quick release devices. The trap is then placed on a specially designed
device that creates a controlled flow of heated air that is passed
through the filter burning off the accumulated particulate.
The selection of the most appropriate means to regenerate the trap
is dependent on the equipment type, the equipment duty cycle, and the
equipment utilization practices at the mine.
A program under the Canadian DEEP project is field testing dpm
filter systems in a New Brunswick Mine. Investigators are testing four
filter systems on trucks and scoops. The initial feedback from Canada
is very favorable concerning the performance of filters. Operators are
very positive and are requesting the vehicles equipped with the filters
because of the noticeable improvement in air quality and an absence of
smoke even under transient load conditions. One system undergoing
testing utilizes an electrical heating element installed in the filter
system to provide the heated air for regeneration of the filter. This
heating element requires connection of the filter to an external
electrical source at the end of the shift. Initial tests have been
successful.
VERT has also published information on the extent of dpm filter
usage in Europe as evidence that the filter technology has attained
wide spread acceptance. MSHA believes this information is relevant to
coal and metal/nonmetal mining because the tunneling equipment on which
these filters are installed is similar to metal/nonmetal equipment and
can be applied to heavy duty equipment in coal mining operations. VERT
stated that over 4,500 filter systems have been deployed in England,
Scandinavia, and Germany. Deutz Corporation has deployed 400 systems
(Deutz's design) with full flow burners for regeneration of filters
installed on engines between 50-600kw. The Oberland-Mangold company has
approximately 1,000 systems in the field. They have accumulated an
average of 8,400 operating hours in forklift trucks, 10,600 operating
hours in construction site engines, and 19,200 operating hours in
stationary equipment. The Unikat company has introduced in Switzerland
over 250 traps since 1989 and 3,000 worldwide with some operating more
than 20,000 hours. In German industry,
[[Page 5551]]
approximately 1,500 traps in forklifts are installed annually.
Paper filters. In 1990, the former Bureau of Mines conducted a
project to develop a means to reduce the amount of dpm emitted from
permissible diesel powered equipment using technologies that were
available commercially and that could be applied to existing equipment.
The project was conducted with the cooperation of an equipment
manufacturer, a mine operator, and MSHA. In light of the fact that all
permissible diesel powered equipment, at that time, utilized water
scrubbers to meet the MSHA approval requirements, the physical
characteristics of the exhaust from that type of equipment were the
basis for the selection of candidate technologies. The technology
selected for development was the pleated media filter or paper filter
as it came to be called. The filter selected was an intake air cleaner
normally used for over the road trucks. That filter was acceptable for
use with permissible diesel equipment because the temperature of the
exhaust gas from the water scrubber was less than 170 degrees F, well
below the ignition point of the filter material. Recognizing that under
some operating modes, water would be discharged along with the exhaust,
a water trap was installed in the exhaust stream before it passed
through the filter. After MSHA conducted a thorough permissibility
evaluation of the modified system, this filter was installed on a
permissible diesel coal haulage vehicle and a series of in-mine trials
were conducted. It was determined, by in mine ambient gravimetric
sampling, that the particulate filter reduced dpm emissions by 95
percent compared with the same machine without the filter. The test
results showed that the filters would last between one and two shifts,
depending on how hard the equipment worked. (BOM, IC 9324).
Following the successful completion of the former Bureau of Mines
mine trial, several equipment manufacturers applied for and received
MSHA approval to offer the paper filter kits as options on a number of
permissible diesel machines. These filter kits were installed on other
machines at the mine where the original tests were conducted, and
later, on machines at other mines.
Despite the initial reports on the high efficiency of paper
filters, during the hearings and in the comments on this rulemaking a
number of commenters questioned whether, in practice, paper filters
could achieve efficiencies on the order of 95% when used on existing
permissible equipment. In order to determine whether it could verify
those concerns, MSHA contracted with the Southwest Research Institute
to verify the ability of such a paper filter to reduce the dpm
generated by a typical engine used in permissible equipment. The
results of this verification investigation are reviewed in Part IV of
this preamble. They confirmed that commercially available paper filters
are capable of achieving very high efficiencies.
Another commenter noted that the volatile fraction of particulate
is not trapped by hot gas filters, but rather passes through the filter
in gaseous form. The volatile fraction consists of, among other
components, gaseous forms of sulfur compounds, lube oil and the high
boiling point fraction of unburned fuel. These components condense in
the mine atmosphere as diesel particulate. The commenter asserted that
the process of volatilization is reduced in the water cooled exhaust,
but it is present nevertheless.
MSHA recognizes that the volatile fraction of dpm passes through
hot gas filters. This volatile fraction later condenses in the mine
atmosphere and is collected on particulate samplers. This is not the
case with hot gas filters that utilize a catalytic converter. The
volatile fraction is oxidized in the catalytic converter and the gases
produced do not condense as particulate. Paper filters are typically
used with water scrubbers or heat exchangers, both of which condense
the volatile fraction into dpm before the exhaust gas reaches the paper
filter. This allows the paper filter to trap the condensed volatile
fraction.
Dry systems technology. The recently developed means of achieving
permissibility with diesel powered equipment in the United States is
the dry exhaust conditioning system or dry system. This system combines
several of the concepts described above as well as new, innovative
approaches. The system also solves some of the problems encountered
with older technologies.
The dry system in its most basic form consists of a heat exchanger
to cool the exhaust gas, a mechanical flame arrestor to prevent the
discharge of any flame from within the engine into the mine atmosphere,
and a spark arrestor to prevent sparks from being discharged. The
surfaces of these components and the piping connecting them are
maintained below the 300 degrees F required by MSHA approval
requirements. A filter, of the type normally used as an intake air
filter element, is installed in the exhaust system as the spark
arrestor. In terms of controlling dpm emissions, the most significant
feature of the system is the use of this air filter element as a
particulate filter. The filter media has an allowable operating
temperature rating greater than the 300 degree F exhaust gas
temperature allowed by MSHA approval regulations. These filters are
reported to last up to sixteen hours, depending on how hard the machine
operates.
The dry system can operate on any grade without the problems
encountered by water scrubbers. Furthermore, there is no problem with
fog created by operation of the water scrubber. Dry systems have been
installed and are operating successfully on diesel haulage equipment,
longwall component carriers, longwall component extraction equipment,
and in nonpermissible form, on locomotives. However, as pointed out by
commenters, requiring the use of a dry system on all mining equipment
would be expensive, cumbersome, and in many cases would require
considerable engineering measures that might render them infeasible.
Although the dry systems were originally designed for permissible
equipment applications, they can also be used directly on outby
equipment (whose emissions are not already cooled), or to replace water
scrubbers used to cool most permissible equipment with a system that
includes additional aftertreatment.
Two manufacturers have received approval for diesel power packages
that are configured as described above; Paas Technologies, (under
various corporate designations including Minecraft and a registered
trade name, Dry Systems Technology, or DST ) and Jeffrey
Mining Equipment Company (currently Long-Airdox-Jeffrey).
The design of the dry system manufactured by DST
includes a catalytic converter. However, with respect to the basic Paas
Technologies system, without a catalytic converter, the initial
reported laboratory reductions in dpm were dramatic: up to 98%.
During the hearings, however, there were many questions about the
applicability of the early results to MSHA's proposed requirement that
emissions of certain equipment be reduced 95% by mass. It was indicated
by a commenter that the original Paas Technology dry system tests with
a paper filter were performed at West Virginia University used high
sulfur fuel which is currently prohibited in underground coal mines.
The commenter stated that the University tested different fuels
containing varying sulfur contents and the results indicated a
fluctuation in overall dpm emission results. The commenter stated the
[[Page 5552]]
difference in dpm collection efficiency by the filter was on the order
of 12 to 15%. Another commenter stated the difference in dpm reduction
using a 0.37 percent fuel sulfur and a 0.04 percent fuel sulfur was
about 22 percent. This commenter further stated that other published
papers from Europe report the same dpm reductions with varying fuel
sulfur levels, approximately 15 to 20 percent reduction.
As was stated ealier, Paas Technologies has further developed its
system by the adding a catalytic converter in the exhaust before the
particulate paper filter. Paas Technologies have developed a technique
whereby the catalytic converter is mounted so that the exhaust gas
temperature remains high enough for the converter to operate
effectively while complying with the MSHA surface temperature
requirement. In addition to removing most of the carbon monoxide, the
catalytic converter removes most of the unburned hydrocarbons before
they are cooled and condensed. This feature extends the operating life
of the filter. Any sulfate formed in the catalytic converter or in the
engine combustion process condenses to a solid form as the exhaust gas
passes through the heat exchanger and is collected in the particulate
filter.
Paas Technologies submitted a detailed set of test results on a
94hp MWM D-916-6 test engine equipped with a Model M38 DST
Management System, which included the catalytic converter, for the
rulemaking record. These tests were conducted by Southwest Research
Institute using an 8-mode test, with ASTM No. 2-D diesel fuel. Both the
test cycle and test fuel (low sulfur) conformed with the test procedure
detailed in the proposed rule and in this final rule. In idle mode, the
dpm emissions were reduced about 90%; in mode 5, the dpm emissions were
down 99%; on average of the 8 modes, the dpm emissions were reduced by
97%.
The Jeffrey system, which does not utilize a catalytic converter,
was the subject of the MSHA verification initiative, noted in part IV.
The verification was conducted in such a way as to test filter
efficiency separately from whole system, with the low sulfur fuel
required for coal mine use and without a catalytic converter. The
verification confirmed that the paper filter has a dpm removal
efficiency greater than 95 percent.
This data submitted to the rulemaking record demonstrates that
paper filters used on dry systems can achieve a filtration efficiency
that allows equipment to meet the 2.5 gm/hr standard with low sulfur
diesel fuel both with and without a catalytic converter in the system.
Reformulated fuels. It has long been known that sulfur content can
have a big effect on dpm emissions. In the diesel equipment rule, MSHA
requires that fuel used in underground coal mines have less than 0.05%
(500 ppm) sulfur. EPA regulations requiring that such low-sulfur fuel
(less than 500 ppm) be used in highway engines, in order to limit air
pollution, have in practice ensured that this is the type of diesel
fuel available to mine operators, and they currently use this type of
fuel for all engines.
EPA has proposed a rule which would require further reductions in
the sulfur content of highway diesel fuel. Such an action was taken for
gasoline fuel on December 21, 1999.
On May 13, 1999 (64 FR 26142) EPA published an Advance Notice of
Proposed Rulemaking (ANPRM) relative to changes for diesel fuel. In
explaining why it was initiating this action, EPA noted that diesel
engines ``contribute greatly'' to a number of serious air pollution
problems, and that diesel emissions account for a large portion of the
country's particulate matter and nitrogen oxides-a key precursor to
ozone. EPA noted that while these emissions come mostly from heavy-duty
truck and nonroad engines, they expected the contribution to dpm
emissions from light-duty equipment to grow due to manufacturers' plans
to greatly increase the sale of light duty trucks. These vehicles are
now subject to Tier 2 emission standards, whether powered by gasoline
or diesel fuel. Such standards may be difficult to meet without
advanced catalyst technologies that in turn are likely to require
sulfur reductions in the fuel.
Moreover, planned Tier 3 standards for nonroad vehicles would
require similar action (64 FR 26143). (For more information on the EPA
planned engine standards, see section 5 of this Part). The EPA noted
that the European Union has adopted new specifications for diesel fuel
that would limit it to 50 ppm by 2005, (an interim limit of 350 ppm by
this year), that the entire diesel fuel supply in the United Kingdom
should soon be at 50 ppm, and that Japan and other nations were working
toward the same goal (64 FR 26148).
In the ANPRM, EPA specifically noted that while continuously
regenerating ceramic filters have shown considerable promise for
limiting dpm emissions even at fairly low exhaust temperatures, the
systems were fairly intolerant of fuel sulfur. Accordingly, the agency
hopes to gather information on whether or not low sulfur fuel was
needed for effective PM control (64 FR 26150). EPA's proposed rule was
published in May 2000 and EPA issued final regulations addressing
emissions standards (December 2000) for new model year 2007 heavy-duty
diesel engines and the low-sulfur fuel rule. The regulations require
ultra-low sulfur fuel be phased in during 2006-2009.
A joint government-industry partnership is also investigating the
relationship between varying levels of sulfur content and emissions
reduction performance on various control technologies, including
particulate filters and oxidation catalytic convertors. This program is
supported by the Department of Energy's Office of Heavy Vehicles
Technologies, two national laboratories, the Engine Manufacturers
Association, and the Manufacturers of Emission Controls Association. It
is known as the Diesel Emission Control-Sulfur Effects (DECSE) Program;
more information is available from its web site, http://www.ott.doe.gov/decse.
MSHA expects that once such cleaner fuel is required for
transportation use, it will in practice become the fuel used in mining
as well--directly reducing engine particulate emissions, increasing the
efficiency of aftertreatment devices, and eventually through the
introduction of new generation of cleaner equipment. Mayer states that
reducing sulfur content, decreasing aromatic components and increasing
the Cetane index of diesel fuel can generally result in a 5% to 15%
reduction in total particulate emissions.
Several commenters in this rulemaking suggested other fuel
formulations which could have a beneficial effect on dpm emissions. One
commenter encouraged the use of FRF, Fire Resistant Fuel, which has
various safety features as well as lower NOX and PM, and
noted it is under study for use by the military.
Another commenter noted the development of a catalytic ignition
system that permits the engines to operate on alternative fuels which
greatly reduce harmful emissions. For example, using a water-methanol
mix, the commenter noted dramatic reductions in harmful emissions of
NOX, CO and HC over a gasoline, spark ignition engine. This
commenter also noted that the ignition system could operate on a diesel
engine, but provided no information about emissions reductions by its
use.
Meyer reports the results of a test by VERT of a special synthetic
fuel containing neither sulfur nor bound nitrogen nor aromatics, with a
very high
[[Page 5553]]
Cetane index. The fuel performed very well, but produced only abut 10%
fewer particulates than low sulfur diesel fuel, nor did it show any
improvement in diminishing nonparticulate emissions.
Cabs. Even though cabs are not the type of control device that is
attached to the exhaust of the diesel engine to reduce emissions, cabs
can protect miners from environmental exposures to dpm. Both cabs and
control booths are discussed in the context of reducing miners
exposures to dpm.
A cab is an enclosure around the operator installed on a piece of
mobile equipment. It can provide the same type of protection as a booth
at a crusher station as found in some surface operations. While cabs
are not available for all mining equipment, they are available for much
of the larger equipment that also has application in the construction
industry.
To be effective, a cab should be tightly sealed with windows and
doors closed. Rubber seals around doors and windows should be in good
condition. Door and window latches must operate properly. In addition
to being well sealed, the cab should have an air filtration and
pressurizing system. Air intake should be located away from engine
exhaust. The airflow should provide one air change per minute for the
cab and should pressurize the cab to 0.20 inches of water. While these
are not absolute requirements, they do provide a guideline of how a cab
should be designed. If a cab does not have an air filtration and
pressurizing system, the diesel particulate concentration inside the
cab will be similar to the diesel particulate concentration outside the
cab.
MSHA has evaluated the efficiency of cab filters for diesel
particulate reduction. Several different types of filter media have
been tested in underground mines. These include standard filter paper
and high efficiency filter paper. Filter papers can reduce diesel
particulate exposures by 60 percent to 90 percent. When changing filter
media, it is necessary to make sure that the airflow into the cab is
not reduced and that the airflow through an air conditioning system is
not reduced.
Although the installation of a cab does not relieve the mine
operator from the responsibility of complying with the equipment dpm
limits, cabs provide assistance in complying with noise and respirable
dust regulations. Cabs protect the equipment operator protection from
dpm, respirable dust and noise exposures.
(7) Existing Standards for Underground Coal Mines That Assist in
Limiting Miner Exposure to Diesel Emissions
MSHA already has in place various requirements that indirectly help
to control miner exposure to diesel emissions in underground mines--
including exposure to diesel particulate. The first such requirements
were developed in the 1940's; the most recent went into full effect
only in November, 1999. It is important to understand these
requirements because they form the base upon which this new rule is
overlaid.
Early developments. In 1944, part 31 established procedures for
limiting the gaseous emissions from diesel powered equipment and
establishing the recommended dilution air quantity for mine locomotives
that use diesel fuel. In 1949, part 32 established procedures for
testing of mobile diesel-powered equipment for non-coal mines. In 1961,
part 36 was added to provide requirements for the use of diesel
equipment in gassy noncoal mines, in which engines must be temperature
controlled to prevent explosive hazards. These rules were drafted in
response to research conducted by the former Bureau of Mines.
Continued research by the former Bureau of Mines in the 1950s and
1960s led to refinements of its ventilation recommendations,
particularly when multiple engines are in use. An airflow of 100 to 250
cfm/bhp for engines that have a properly adjusted fuel to air ratio was
recommended (Holtz, 1960). An additive ventilation requirement was
recommended for operation of multiple diesel units, which could be
relaxed based on the mine operating procedures. This approach was
subsequently refined to become a 100-75-50 percent guideline (MSHA
Policy Memorandum 81-19MM, 1981). Under this guideline, when multiple
pieces of diesel equipment are operated, the required airflow on a
split of air would be the sum of: (a) 100 percent of the approval plate
quantity for the vehicle with the highest approval plate air quantity
requirement; (b) 75 percent of the approval plate air quantity
requirement of the vehicle with the next highest approval plate air
quantity requirement; and (c) 50 percent of the approval plate airflow
for each additional piece of diesel equipment.
Limitations on Diesel Gasses. MSHA has limits on some of the gasses
produced in diesel exhaust. These are listed in Table II-5, for both
coal mines and metal/nonmetal mines, together with information about
the recommendations in this regard of other organizations. As indicated
in the table, MSHA requires mine operators to comply with gas specific
threshold limit values (TLVs) recommended by the American
Conference of Governmental Industrial Hygienists (ACGIH) in 1972 (for
coal mines) and in 1973 (for metal and nonmetal mines).
BILLING CODE 4510-43-P
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BILLING CODE 4510-43-C
To change an MSHA exposure limit, regulatory action is required
because the rule does not provide for their automatic updating. In
1989, MSHA proposed changing some of these gas limits in the context of
a proposed rule on air quality standards (54 FR 35760). Following
opportunity for comment and hearings, a portion of that proposed air
quality rule (concerning control of drill dust and blasting) was
promulgated. As a result of a recent legal action, MSHA's efforts to
revise the specific limits for those gases emitted by diesel engines
have been placed under the continued supervision of a federal court of
appeals. This action is discussed in more detail in section 9 of this
Part.
Diesel Equipment Rule for Underground Coal Mines. On October 25,
1996, MSHA promulgated standards for the ``Approval, Exhaust Gas
Monitoring, and Safety Requirements for the Use of Diesel-Powered
Equipment in Underground Coal Mines'' (61 FR 55412). The history of
this ``diesel equipment rule'' (sometimes referred to here as the
``diesel safety rule'' to help distinguish it from this rulemaking
which is oriented toward health) is set forth as part of the history of
this rulemaking (see section 9 of this part).
The diesel equipment rule focuses on the safe use of diesels in
underground coal mines. Integrated requirements are established for the
safe storage, handling, and transport of diesel fuel underground,
training of mine personnel, minimum ventilating air quantities for
diesel powered equipment, monitoring of gaseous diesel exhaust
emissions, maintenance requirements, incorporation of fire suppression
systems, and design features for nonpermissible machines.
Certain requirements were included in the diesel equipment rule
that are directly related to reducing diesel emissions. For example,
the diesel equipment rule requires that the emissions of permissible
and heavy duty equipment be tested weekly. The tests are conducted
using instrumentation and the tests are conducted with the engines
operated at a loaded condition which is representative of actual
operation. The results are monitored and recorded. Higher than normal
emissions readings indicate that the engines and equipment are not
being maintained in approved condition. Although some of these
requirements help reduce dpm emissions, they were not included in the
rule for that specific purpose.
Lower-emission engines. The diesel equipment rule requires that
virtually all diesel-powered engines used in underground coal mines be
approved by MSHA; see 30 CFR part 7, (approval requirements), part 36
(permissible machines defined), and part 75 (use of such equipment in
underground coal mines). The approval requirements, among other things,
require clean-burning engines in diesel-powered equipment (61 FR
55417). In promulgating the final rule, MSHA recognized that clean-
burning engines are ``critically important'' to reducing toxic gasses
to levels that can be controlled through ventilation. To achieve the
objective of clean-burning engines, the rule sets performance standards
which must be met by virtually all diesel-powered equipment in
underground coal mines.
[[Page 5555]]
As noted in section 5 of this part, the technical requirements for
approved diesel engines focus on limiting the amount of various gases
that an engine can emit, including undiluted exhaust limits for carbon
monoxide and oxides of nitrogen (61 FR 55419). The limits for these
gasses are derived from existing 30 CFR part 36.
The diesel equipment rule also provides that the particulate matter
emitted by approved engines be determined during the testing required
to gain approval. The particulate index (or PI), calculated under the
provisions of 30 CFR 7.89, indicates what air quantity is necessary to
dilute the diesel particulate in the engine exhaust to 1 milligram of
diesel particulate matter per cubic meter of air. The purpose of the PI
requirement is discussed in more detail in section 5 of this part.
Gas Monitoring. The diesel equipment rule also addresses the
monitoring and control of gaseous diesel exhaust emissions (30 CFR part
70; 61 FR 55413). In this regard, the rule requires that mine operators
take samples of carbon monoxide and nitrogen dioxide as part of
existing onshift workplace examinations (61 FR 55413, 55430-55431).
Samples exceeding an action level of 50 percent of the threshold limits
set forth in 30 CFR 75.322 trigger corrective action by the mine
operator (30 CFR part 70, 61 FR 55413).
Engine Maintenance. The diesel equipment rule requires that diesel-
powered equipment be maintained in safe and approved condition (30 CFR
75.1914; 61 FR 55414). As explained in the preamble, maintenance
requirements were included because of MSHA's recognition that
inadequate equipment maintenance can, among other things, result in
increased levels of harmful gaseous and particulate components from
diesel exhaust (61 FR 55413-55414).
The rule also requires the weekly examination of diesel-powered
equipment (30 CFR 75.1914(g)). To determine if more extensive
maintenance is required, the rule further requires a weekly check of
the gaseous CO emission levels on permissible and heavy duty outby
machines. The CO check requires that the engine be operated at a
repeatable loaded condition and the CO measured. The carbon monoxide
concentration in the exhaust provides a good indication of engine
condition. If the CO measurement increases to a higher concentration
than what was normally measured during the past weekly checks, then a
maintenance person would know that a problem has developed that
requires further investigation.
In addition, operators are required to establish programs to ensure
that those performing maintenance on diesel equipment are qualified (61
FR 55414).
Fuel. The diesel equipment rule also requires that underground coal
mine operators use diesel fuel with a sulfur content of 0.05% (500 ppm)
or less (30 CFR 75.1910(a); 61 FR 55413). Some types of exhaust
aftertreatment technology designed to lower hazardous diesel emissions
work more effectively when the sulfur content of the fuel is low. More
effective aftertreatment devices will result in reduced hydrocarbons,
carbon monoxide, and particulate levels. Low sulfur fuel also greatly
reduces the sulfate production from the catalytic converters currently
in use in underground coal mines thereby decreasing exhaust
particulate. To further reduce miners' exposure to diesel exhaust, the
final rule prohibits operators from unnecessarily idling diesel-powered
equipment (30 CFR 75.1916(d).
Ventilation. The diesel equipment rule requires that as part of the
approval process, ventilating air quantities necessary to maintain the
gaseous emissions of diesel engines within existing required ambient
limits be set. The ventilating air quantities are required to appear on
the engine's approval plate. The rule also requires generally that mine
operators maintain the approval plate quantity minimum airflow in areas
of underground coal mines where diesel-powered equipment is operated.
The engine's approval plate air quantity is also used to determine the
minimum air quantity in areas where multiple units of diesel powered
equipment are being operated. The minimum ventilating air quantity
where multiple units of diesel powered equipment are operated on
working sections and in areas where mechanized mining equipment is
being installed or removed, must be the sum of 100 percent of the
approval plate quantities of all of the equipment. As stated in the
preamble of the diesel equipment rule, MSHA believes that effective
mine ventilation is a key component in the control of miners' exposure
to gasses and particulate emissions generated by diesel equipment.
Impact of the diesel equipment rule on dpm. The diesel equipment
rule is helping the mining community use diesel-powered equipment more
safely in underground coal mines. Moreover, the diesel equipment rule
has many features which reduce the emission and concentration of
harmful diesel emissions in underground coal mines--including the
particulate component of these emissions.
During the public hearings on the equipment rule, miners complained
about the high concentrations of diesel emissions at the section
loading point and in the areas of the mine where longwall equipment is
being installed or removed. Accordingly, MSHA established, in that
rule, provisions which would address miners' concerns.
The equipment rule required that the approval plate ventilation
quantity be provided at the section loading point. The loading point is
also identified as a location where regular air quality samples are
required to be taken. Corrective action is required if the samples of
CO and NO2 exceeded more than one half the allowable
concentration limit of these gases.
Longwall equipment installations and removals are handled in a
similar manner. The diesel emissions from all of the equipment in the
area of the mine where the longwall move is being made are required to
be considered in establishing the amount of ventilation air to be
provided. A specific location where that quantity is to be measured is
established. Additionally, the same air quality sampling program
required for section loading points is required for areas of the mine
where the longwall move is to take place.
Permissible haulage vehicles contribute the largest quantities of
emissions at the section loading point. Longwall moves are typically
carried out by permissible and heavy duty equipment such as shield
carriers, mules, and locomotives which produce large quantities of
diesel emissions. Emissions from these vehicles are reduced by the use
of approved engines, low sulfur fuel, the loaded repeatable engine
condition testing, regular maintenance by trained personnel and the
ventilation and sampling provisions of the diesel equipment rule.
Because the effective dates for provisions of the diesel equipment
regulations are staggered, the full impact of the new rules was not
known at the time the dpm hearings were held. MSHA expects that the
concentrations of diesel emissions at the section loading point and
during longwall moves will be reduced as these provisions are fully
implemented.
In developing the diesel equipment rule, however, MSHA did not
explicitly consider the risks to miners of a working lifetime of dpm
exposure at very high levels, nor the actions that could be taken to
specifically reduce dpm exposure levels in underground coal mines. It
was understood that the agency would be taking a separate look
[[Page 5556]]
at the health risks of dpm exposure. (61 FR 55420).
(8) Information on How Certain States Are Restricting Occupational
Exposure to DPM
As noted earlier in this part, the Federal government has long been
involved in efforts to restrict diesel particulate emissions into the
environment--both through ambient air quality standards, and through
restrictions on diesel engine emissions. While MSHA's actions to limit
the concentration of dpm in underground mines are the first effort by
the Federal government to deal with the special risks faced by workers
exposed to diesel exhaust on the job, several states have already taken
actions in this regard with respect to underground coal mines.
This section reviews some of these actions, as they were the
subject of considerable discussion and comment during this rulemaking.
Pennsylvania. As indicated in section 1, Pennsylvania essentially
had a ban on the use of diesel-powered equipment in underground coal
mines for many years. As noted by one commenter, diesel engines were
permitted provided the request was approved by the Secretary of the
Department of Environmental Protection but no request was ever
approved.
In 1995, one company in the State submitted a plan for approval and
started negotiations with its local union representatives. This led to
statewide discussions and the adoption of a new law in the State that
permits the use of diesel-powered equipment in deep coal mines under
certain circumstances specified in the law (Act 182). As further noted
by this commenter, the drafters of the law completed their work before
the issuance of MSHA's new regulation on the safe use of diesel-powered
equipment in underground coal mines. The Pennsylvania law, unlike
MSHA's diesel equipment rule, specifically addresses diesel
particulate. The State did not set a limit on the exposure of miners to
dpm, nor did it establish a limit on the concentration of dpm in deep
coal mines. Rather, it approached the issue by imposing controls that
will limit dpm emissions at the source.
First, all diesel engines used in underground deep coal mines in
Pennsylvania must be MSHA-approved engines with an ``exhaust emissions
control and conditioning system'' that meets certain tests. (Article
II-A, Section 203-A, Exhaust Emission Controls). Among these are dpm
emissions from each engine no greater than ``an average concentration
of 0.12 mg/m 3 diluted by fifty percent of the MSHA approval
plate ventilation for that diesel engine.'' In addition, any exhaust
emissions control and conditioning system must include a ``Diesel
Particulate Matter (DPM) filter capable of an average of ninety-five
percent or greater reduction of dpm emissions.'' It also requires the
use of an oxidation catalytic converter. Thus, the Pennsylvania statute
requires the use of low-emitting engines, and then the use of
aftertreatment devices that significantly reduce the particulates
emitted from these engines.
The Pennsylvania law also has a number of other requirements for
the safe use of diesel-powered equipment in the particularly hazardous
environments of underground coal mines. Many of these parallel the
requirements in MSHA's diesel equipment rule. Like MSHA's requirements,
they too can result in reducing miner exposure to diesel particulate--
e.g., regular maintenance of diesel engines by qualified personnel and
equipment operator examinations. The requirements in the Pennsylvania
law take into account the need to maintain the aftertreatment devices
required to control diesel particulate.
While both mine operators and labor supported this approach, it
remains controversial. During the hearings on this rulemaking, one
commenter indicated that at the time the standards were established, it
would have taken a 95% filter to reduce dpm from certain equipment to
the 0.12 mg/m 3 emissions standard because 0.25 sulfur fuel
was being utilized. This test reported by the commenter was completed
prior to MSHA promulgating the diesel equipment rule that required the
use of .05% sulfur fuel. Another commenter pointed out that as
operators in the state began considering the use of newer, less
polluting engines, achieving an efficiency of 95% reduction of the
emissions from any such engines would become even more difficult. There
was some disagreement among the commenters as to whether existing
technology would permit operators to meet the 0.12 mg/m 3
emission standard in many situations.
One commenter described the difficulty in efforts to get a small
outby unit approved under the current Pennsylvania law. Accordingly,
the industry has indicated that it would seek additional changes in the
Pennsylvania diesel law. Commenters representing miners indicated that
they were also involved in these discussions.
West Virginia. Until 1997, West Virginia law banned the use of
diesel-powered equipment in underground coal mines. In that year, the
State created the joint labor-management West Virginia Diesel Equipment
Commission (Commission) and charged it with developing regulations to
permit and govern diesel engine use in underground coal mines. As
explained by several commenters, the Commission, in collaboration with
West Virginia University (WVU), developed a protocol for testing diesel
engine exhaust controls, and the legislature appropriated more than
$150,000 for WVU to test diesel exhaust controls and an array of diesel
particulate filters.
There were a number of comments received by MSHA on the test
protocols and results. These are discussed in appropriate parts in this
preamble. One commenter noted that various manufacturers of products
have been very interested in how their products compare to those of
other manufacturers tested by the WVU. Another asserted that mine
operators had been slowing the scheduling of tests by WVA.
Pursuant to the West Virginia law establishing the Commission, the
Commission was given only a limited time to determine the applicable
rules for the use of diesel engines underground, or the matter was
required to be referred to an arbitrator for resolution. One commenter
during the hearings noted that the Commission had not been able to
reach resolution and that indeed arbitration was the next step. Other
commenters described the proposal of the industry members of the
Commission--0.5mg/m3 for all equipment, as configured,
before approval is granted. In this regard, the industry members of the
West Virginia Commission said:
``We urge you to accelerate the finalization of * * * these
proposed rules. We believe that will aid our cause, as well as the
other states that currently don't use diesel.'' (Id.)
Virginia. According to one commenter, diesel engine use in
underground mining was legalized in Virginia in the mid-1980s. It was
originally used on some heavy production equipment, but the haze it
created was so thick it led to a drop in production. Thereafter, most
diesel equipment has been used outby (805 pieces). The current state
regulations consist of requiring that MSHA approved engines be used,
and that the ``most up-to-date, approved, available diesel engine
exhaust aftertreatment package'' be utilized. There are no distinctions
between types of equipment. The commenter noted that more hearings were
planned soon. Under a directive from the governor of Virginia, the
state is reviewing its
[[Page 5557]]
regulations and making recommendations for revisions to sections of its
law on diesels.
Ohio. The record of this rulemaking contains little specific
information on the restrictions on the underground use of diesel-
powered equipment in Ohio. MSHA understands, however, that in practice
it is not used. According to a communication with the Division of Mines
and Reclamation of the Ohio Division of Natural Resources, this outcome
stems from a law enacted on October 29, 1995, now codified as section
1567.35 of Ohio Revised Code Title 15, which imposes strict safety
restrictions on the use of various fuels underground.
(9) History of this Rulemaking
As discussed throughout this part, the Federal government has
worked closely with the mining community to ascertain whether and how
diesel-powered equipment might be used safety and healthfully in this
industry. As the evidence began to grow that exposure to diesel exhaust
might be harmful to miners, particularly in underground mines, formal
agency actions were initiated to investigate this possibility and to
determine what, if any, actions might be appropriate. These actions,
including a number of non-regulatory initiatives taken by MSHA, are
summarized here in chronological sequence.
Activities Prior to Proposed Rulemaking on DPM. In 1984, the
National Institute for Occupational Safety and Health (NIOSH)
established a standing Mine Health Research Advisory Committee to
advise it on matters involving or related to mine health research. In
turn, that standing body established the Mine Health Research Advisory
Committee Diesel Subgroup to determine if:
* * * there is a scientific basis for developing a recommendation on
the use of diesel equipment in underground mining operations and
defining the limits of current knowledge, and recommending areas of
research for NIOSH, if any, taking into account other investigators'
ongoing and planned research. (49 FR 37174).
In 1985, MSHA established an Interagency Task Group with NIOSH and
the former Bureau of Mines (BOM) to assess the health and safety
implications of the use of diesel-powered equipment in underground coal
mines.
In April 1986, in part as a result of the recommendation of the
Task Group, MSHA began drafting proposed regulations on the approval
and use of diesel-powered equipment in underground coal mines. Also in
1986, the Mine Health Research Advisory Committee Diesel Subgroup
(which, as noted above, was created by a standing NIOSH committee)
summarized the evidence available at that time as follows:
It is our opinion that although there are some data suggesting a
small excess risk of adverse health effects associated with exposure
to diesel exhaust, these data are not compelling enough to exclude
diesels from underground mines. In cases where diesel equipment is
used in mines, controls should be employed to minimize exposure to
diesel exhaust.
On October 6, 1987, pursuant to section 102(c) of the Mine Act, 30
U.S.C. 812(c), which authorizes MSHA to appoint such advisory
committees as it deems appropriate, the agency appointed an advisory
committee ``to provide advice on the complex issues concerning the use
of diesel-powered equipment in underground coal mines.'' (52 FR 37381).
MSHA appointed nine members to this committee, officially known as The
Mine Safety and Health Administration Advisory Committee on Standards
and Regulations for Diesel-Powered Equipment in Underground Coal Mines
(hereafter the MSHA Diesel Advisory Committee). As required by section
101(a)(1) of the Mine Act, MSHA provided the MSHA Diesel Advisory
Committee with draft regulations on the approval and use of diesel-
powered equipment in underground coal mines. The draft regulations did
not include standards setting specific limitations on diesel
particulate, nor had MSHA at that time determined that such standards
would be promulgated.
In July 1988, the MSHA Diesel Advisory Committee completed its work
with the issuance of a report entitled ``Report of the Mine Safety and
Health Administration Advisory Committee on Standards and Regulations
for Diesel-Powered Equipment in Underground Coal Mines.'' It also
recommended that MSHA promulgate standards governing the approval and
use of diesel-powered equipment in underground coal mines. The MSHA
Diesel Advisory Committee recommended that MSHA promulgate standards
limiting underground coal miners' exposure to diesel exhaust.
With respect to diesel particulate, the MSHA Diesel Advisory
Committee recommended that MSHA ``set in motion a mechanism whereby a
diesel particulate standard can be set.'' (MSHA, 1988). In this regard,
the MSHA Diesel Advisory Committee determined that because of
inadequacies in the data on the health effects of diesel particulate
matter and inadequacies in the technology for monitoring the amount of
diesel particulate matter at that time, it could not recommend that
MSHA promulgate a standard specifically limiting the level of diesel
particulate matter in underground coal mines (Id. 64-65). Instead, the
MSHA Diesel Advisory Committee recommended that MSHA ask NIOSH and the
former Bureau of Mines to prioritize research in the development of
sampling methods and devices for diesel particulate.
The MSHA Diesel Advisory Committee also recommended that MSHA
request a study on the chronic and acute effects of diesel emissions
(Id.). In addition, the MSHA Diesel Advisory Committee recommended that
the control of diesel particulate ``be accomplished through a
combination of measures including fuel requirements, equipment design,
and in-mine controls such as the ventilation system and equipment
maintenance in conjunction with undiluted exhaust measurements.'' The
MSHA Diesel Advisory Committee further recommended that particulate
emissions ``be evaluated in the equipment approval process and a
particulate emission index reported.'' (Id. at 9).
In addition, the MSHA Diesel Advisory Committee recommended that
``the total respirable particulate, including diesel particulate,
should not exceed the existing two milligrams per cubic meter
respirable dust standard.'' (Id. at 9.) It should be noted that section
202(b)(2) of the Mine Act requires that coal mine operators maintain
the average concentration of respirable dust at their mines at or below
two milligrams per cubic meter which effectively prohibits diesel
particulate matter in excess of two milligrams per cubic meter (30
U.S.C. 842(b)(2)).
As noted, the MSHA Diesel Advisory Committee issued its report in
1988. During that year, NIOSH issued a Current Intelligence Bulletin
recommending that whole diesel exhaust be regarded as a potential
carcinogen and controlled to the lowest feasible exposure level (NIOSH,
1988). In its bulletin, NIOSH concluded that although the excess risk
of cancer in diesel exhaust exposed workers had not been quantitatively
estimated, it is logical to assume that reductions in exposure to
diesel exhaust in the workplace would reduce the excess risk. NIOSH
stated that ``[g]iven what we currently know, there is an urgent need
for efforts to be made to reduce occupational exposures to DEP [dpm] in
mines.''
Consistent with the MSHA Diesel Advisory Committee's research
recommendations, MSHA, in September 1988, formally requested NIOSH to
[[Page 5558]]
perform a risk assessment for exposure to diesel particulate. (57 FR
500). MSHA also requested assistance from NIOSH and the former BOM in
developing sampling and analytical methodologies for assessing exposure
to diesel particulate in mining operations. (Id.). In part, as a result
of the MSHA Diesel Advisory Committee's recommendation, MSHA also
participated in studies on diesel particulate sampling methodologies
and determination of underground occupational exposure to diesel
particulate.
On October 4, 1989, MSHA published a Notice of Proposed Rulemaking
on approval requirements, exposure monitoring, and safety requirements
for the use of diesel-powered equipment in underground coal mines. (54
FR 40950). The proposed rule, among other things, addressed, and in
fact followed, the MSHA Diesel Advisory Committee's recommendation that
MSHA promulgate regulations requiring the approval of diesel engines
(54 FR 40951), limiting gaseous pollutants from diesel equipment,
(Id.), establishing ventilation requirements based on approval plate
dilution air quantities (54 FR 40990), requiring equipment maintenance
(54 FR 40958), requiring that trained personnel work on diesel-powered
equipment, (54 FR 40995), establishing fuel requirements, (Id.),
establishing gaseous contaminant monitoring (54 FR 40989), and
requiring that a particulate index indicating the quantity of air
needed to dilute particulate emissions from diesel engines be
established. (54 FR 40953).
On January 6, 1992, MSHA published an Advance Notice of Proposed
Rulemaking (ANPRM) indicating it was in the early stages of developing
a rule specifically addressing miners exposure to diesel particulate
(57 FR 500). In the ANPRM, MSHA, among other things, sought comment on
specific reports on diesel particulate prepared by NIOSH and the former
BOM. MSHA also sought comment on reports on diesel particulate which
were prepared by or in conjunction with MSHA (57 FR 501). The ANPRM
also sought comments on the health effects, technological and economic
feasibility, and provisions which should be considered for inclusion in
a diesel particulate rule (57 FR 501). The notice also identified five
specific areas where the agency was particularly interested in
comments, and about which it asked a number of detailed questions: (1)
Exposure limits, including the basis thereof; (2) the validity of the
NIOSH risk assessment model and the validity of various types of
studies; (3) information about non-cancer risks, non-lung routes of
entry, and the confounding effects of tobacco smoking; (4) the
availability, accuracy and proper use of sampling and monitoring
methods for diesel particulate; and (5) the technological and economic
feasibility of various types of controls, including ventilation, diesel
fuel, engine design, aftertreatment devices, and maintenance by
mechanics with specialized training. The notice also solicited specific
information from the mining community on ``the need for a medical
surveillance or screening program and on the use of respiratory
equipment.'' (57 FR 500). The comment period on the ANPRM closed on
July 10, 1992.
While MSHA was completing a ``comprehensive analysis of the
comments and any other information received'' in response to the ANPRM
(57 FR 501), it took also several actions to encourage the mining
community to begin to deal with the problems identified.
In 1995, MSHA sponsored three workshops ``to bring together in a
forum format the U.S. organizations who have a stake in limiting the
exposure of miners to diesel particulate (including) mine operators,
labor unions, trade organizations, engine manufacturers, fuel
producers, exhaust aftertreatment manufacturers, and academia.''
(McAteer, 1995). The sessions provided an overview of the literature
and of diesel particulate exposures in the mining industry, state-of-
the-art technologies available for reducing diesel particulate levels,
presentations on engineering technologies toward that end, and
identification of possible strategies whereby miners' exposure to
diesel particulate matter can be limited both practically and
effectively.
The first workshop was held in Beckley, West Virginia on September
12 and 13, and the other two were held on October 6, and October 12 and
13, 1995, in Mt Vernon, Illinois and Salt Lake City, Utah,
respectively. A transcript was made. During a speech early the next
year, the Deputy Assistant Secretary for MSHA characterized what took
place at these workshops:
The biggest debate at the workshops was whether or not diesel
exhaust causes lung cancer and whether MSHA should move to regulate
exposures. Despite this debate, what emerged at the workshops was a
general recognition and agreement that a health problem seems to
exist with the current high levels of diesel exhaust exposure in the
mines. One could observe that while all the debate about the studies
and the level of risk was going on, something else interesting was
happening at the workshops: one by one miners, mining companies, and
manufacturers began describing efforts already underway to reduce
exposures. Many are actively trying to solve what they clearly
recognize is a problem. Some mine operators had switched to low
sulfur fuel that reduces particulate levels. Some had increased mine
ventilation. One company had tried a soy-based fuel and found it
lowered particulate levels. Several were instituting better
maintenance techniques for equipment. Another had hired extra diesel
mechanics. Several companies had purchased electronically
controlled, cleaner, engines. Another was testing a prototype of a
new filter system. Yet another was using disposable diesel exhaust
filters. These were not all flawless attempts, nor were they all
inexpensive. But one presenter after another described examples of
serious efforts currently underway to reduce diesel emissions.
(Hricko, 1996).
In March of 1997, MSHA issued, in draft form, a publication
entitled ``Practical Ways to Control Exposure to Diesel Exhaust in
Mining--a Toolbox''. The draft publication was disseminated by MSHA to
all underground mines known to use diesel equipment and posted on
MSHA's Web site.
As explained in the publication, the Toolbox was designed to
disseminate to the mining community information gained through the
workshops about methods being used to reduce miner exposures to dpm.
MSHA's Toolbox provided specific information about nine types of
controls that can reduce dpm exposures: low emission engines; fuels;
aftertreatment devices; ventilation; enclosed cabs; engine maintenance;
work practices and training; fleet management; and respiratory
protective equipment. Some of these approaches reduce emissions from
diesel engines; others focus on reducing miner exposure to whatever
emissions are present. Quotations from workshop participants were used
to illustrate when and how such controls might be helpful.
As it clearly stated in its introductory section entitled ``How to
Use This Publication,'' the Toolbox was not designed as a guide to
existing or pending regulations. As MSHA noted in that regard:
While the (regulatory) requirements that will ultimately be
implemented, and the schedule of implementation, are of course
uncertain at this time, MSHA encourages the mining community not to
wait to protect miners' health. MSHA is confident that whatever the
final requirements may be, the mining community will find this
Toolbox information of significant value.
On October 25, 1996, MSHA published a final rule addressing
approval, exhaust monitoring, and safety requirements for the use of
diesel-powered equipment in underground coal mines (61 FR 55412). The
final rule addresses, and in large part is consistent
[[Page 5559]]
with, the specific recommendations made by the MSHA Diesel Advisory
Committee for limiting underground coal miners' exposure to diesel
exhaust. As noted in section 7 of this part, the diesel safety rule was
implemented in steps concluding in late 1999. Aspects of this diesel
safety rule had a significant impact on this rulemaking.
In the Fall of 1997, following comment, MSHA's Toolbox was
finalized and disseminated to the mining community. At the same time,
MSHA made available to the mining community a software modeling tool
developed by the Agency to facilitate dpm control. This model enables
an operator to evaluate the effect which various alternative
combinations of controls would have on the dpm concentration in a
particular mine--before making the investment. MSHA refers to this
model as ``the Estimator''. The Estimator is in the form of a template
that can be used on standard computer spreadsheet programs. As
information about a new combination of controls is entered, the results
are promptly displayed.
Proposed Rulemaking on Dpm. On April 9, 1998, MSHA published a
proposed rule to ``reduce the risks to underground coal miners of
serious health hazards that are associated with exposure to high
concentrations of diesel particulate matter'' (63 FR 17492).
MSHA went to some lengths to ensure the mining community would be
able to review and comment on the proposed rule. The agency made copies
of the proposal available for review by the mining community at each
district and field office location, at the National Mine Safety and
Health Academy, and at each technical support center. MSHA also
provided the opportunity for comments to be accepted from the mining
community at each of those locations, as well as through mail,
e-mail and fax to the national office. MSHA also distributed the
proposal to all underground mines, to mining associations and other
interested parties. A copy was also posted on MSHA's website.
In order to further facilitate participation by the mining
community, MSHA developed as an introduction to its preamble explaining
the proposed rule a ``plain language'' questions and answers section.
The notice of proposed rulemaking reviewed and discussed the
comments received in response to the ANPRM, including information on
such control approaches as fuel type, fuel additives, and maintenance
practices (63 FR 17512-17514). For the convenience of the mining
community, a copy of MSHA's Toolbox was also reprinted as an Appendix
at the end of the notice of proposed rulemaking (63 FR 17580 et seq.).
A complete description of the Estimator, and several examples, were
also presented in the preamble of the proposed dpm rule (63 FR 17565 et
seq.).
The proposed dpm rule was fairly simple. In addition to miner
training, the proposed rule would have required aftertreatment filters
on all permissible equipment and, subsequently, on all heavy duty
nonpermissible equipment.
Throughout the preamble, MSHA discussed a number of other approaches
that might have merit in limiting the concentration of dpm in
underground coal mines. MSHA made it very clear to the mining community
that the rule being proposed represented only one of the approaches
which might ultimately be required by the final rule and on which
comment was being solicited by the proposed rulemaking notice.
For example, the agency noted the following:
``MSHA recognizes that a specification standard does not allow
for the use of future alternative technologies that might provide
the same or enhanced protection at the same or lower cost. MSHA
welcomes comment as to whether and how the proposed rule can be
modified to enhance its flexibility in this regard * * *. (There
are) two alternative specification standards which would provide
somewhat more flexibility for coal mine operators. Alternative 1
would treat the filter and engine as a package that has to meet a
particular emission standard. Instead of requiring that all engines
be equipped with a high-efficiency filter, this approach would
provide some credit for the use of lower-polluting engines.
Alternative 2 would also provide credit for mine ventilation beyond
that required.'' (63 FR 17498)
These alternatives were further discussed in a separate Question and
Answer (#12). The agency was also clear it would welcome comment on
``whether there are some types of light-duty equipment whose dpm
emissions should, and could feasibly, be controlled'', and ``whether it
would be feasible for this sector to implement a requirement that any
new light-duty equipment added to a mine's fleet be filtered'' Question
and Answer (#6) (63 FR 17556).
MSHA also discussed and welcomed comment on a number of other
alternatives: e.g., restricting the exposure of underground coal mines
to all fine particulates regardless of source (63 FR 17495); and the
use of administrative controls (e.g., rotation of personnel) and
personal protective equipment (e.g., respirators) to reduce the dpm
exposure of miners. The Agency also sought comments on its risk
assessment, presented in full in the preamble to the proposed rule
(Part III). As noted therein, this was the first risk assessment ever
performed by the agency to be peer reviewed. Such a review is not
required under the agency's statute, but MSHA took the time to obtain
such a review in this instance due to significant disagreement within
the mining community about the health risks of exposure to dpm (63 FR
17521).
MSHA also asked for comment on its economic assumptions in the
preamble. Two of the Questions and Answers (#5 and #7) were
specifically devoted to cost impacts, including those on small mines.
MSHA also specifically requested all members of the mining community to
consider using the Estimator in developing comments on the proposed
rulemaking (63 FR 17565).
On July 14, 1998, in accordance with the National Environmental
Protection Act, MSHA published a notice in the Federal Register seeking
comment on its preliminary determination that the proposed rule would
not have a significant environmental impact (63 FR 37796).
The initial comment period was scheduled to last for 120 days until
August 7, 1998. In response to requests from the public, on August 5,
1998, MSHA extended the initial comment period on the proposed rule
(and the comment period on its preliminary determination of no
significant environmental impact) for an additional 60 days, until
October 9, 1998 (63 FR 41755). That notice also announced MSHA's intent
to hold public hearings on the proposal.
On October 19, 1998, MSHA announced in the Federal Register
locations of four public hearings on the proposed rule. The agency
further announced that the close of the post-hearing comment period and
rulemaking record would be on February 16, 1999 (63 FR 55811).
In November 1998, MSHA held hearings in Salt Lake City, Utah and
Beckley, West Virginia. In December 1998, hearings were held in Mt.
Vernon, Illinois, and Birmingham, Alabama.
These hearings were well attended. Testimony was presented by
individual miners, representatives of miners, individual coal
companies, mining industry associations, representatives of engine and
equipment manufacturers and one individual manufacturer. Members of the
mining community participating had an extensive opportunity to hear and
respond to alternative views; some participated in several hearings.
They also had an opportunity to engage in direct dialogue
[[Page 5560]]
with members of MSHA's rulemaking committee-responding to questions and
asking questions on their own. There was extensive comment not only
about the provisions of the proposed rule itself, but also about the
need for diesel powered equipment in this sector, the risks associated
with its use, the need for regulation in this sector, alternative
approaches (including but not limited to those on which MSHA
specifically sought comment), and the technological and economic
feasibility of various alternatives.
During the hearings, MSHA made a number of requests that
information provided at the hearing be supplemented by submission of
cited sources, additional data, and in particular for data to support
assertions made about various control technologies. MSHA again
solicited information concerning the agency's cost assumptions, for the
results of studies using MSHA's Estimator model, and also asked for any
data on a number of other points. For example, the agency requested
further information on the size distribution of particles from cleaner
engines, on the viability of a fine particulate standard in lieu of a
dpm standard, for a list of any studies concerning the risks of dpm or
lack thereof, and data on equipment upgrades.
On February 12, 1999, (64 FR 7144) MSHA published a notice in the
Federal Register announcing: (1) The availability of three additional
studies discussed in the preamble of the proposed rule but not
available at the time of publication; and (2) the extension of the
post-hearing comment period and close of record for 60 additional days,
until April 30, 1999.
On April 27, 1999, in response to requests from the public, MSHA
extended the post-hearing comment period and close of record for 90
additional days, until July 26, 1999 (64 FR 22592).
On July 8, 1999, MSHA published a notice in the Federal Register
correcting technical errors in the preamble discussion on the Diesel
Emission Control Estimator formula in the Appendix to Part V of the
proposed rulemaking notice, and correcting Figure V-5 of the preamble.
Comments on these changes were solicited by July 26, 1999, the close of
the rulemaking record (64 FR 36826). The Estimator model was
subsequently published in the literature.
The rulemaking record closed on July 26, 1999, fifteen months after
the date the proposed rule was published for public notice. The
comments, like the hearings, reflected extensive participation in this
effort by the full range of interests in the mining community and
covered a full range of ideas and alternatives.
On June 30, 2000, the rulemaking record was reopened for 30 days in
order to obtain public comment on certain additional documents which
the agency determined should be placed in the rulemaking record. Those
documents were MSHA's paper filter verification studies and the recent
information from VERT on the performance of hot gas filters mentioned
in section 6 of this Part. In addition, the notice provided an
opportunity for comment on additional documents being placed in the
rulemaking record for a related rulemaking for underground metal and
nonmetal mines, and an opportunity to comment on some additional
documents on risk being placed in both records. In this regard, the
notice reassured the mining community that any comments filed on risk
in either rulemaking proceeding would be placed in both records, since
the two rulemakings utilize the same risk assessment.
Other Related Activity. On September 3, 1999, the United States
Court of Appeals for the District of Columbia Circuit issued its
decision on writ of mandamus sought by the United Mine Workers to
compel MSHA to issue final regulations controlling gaseous emissions in
the exhaust of diesel engines used in underground coal mines. (190 F.3d
545.) The UMWA argued that such action should have been completed some
years before as part of MSHA's air quality rulemaking to update
emissions limits on hundreds of exposure limits. The Court found that
the Agency was in violation of the statute's requirement that the
Secretary must either promulgate final regulations, or explain her
decision not to promulgate them, within ninety days of the
certification of the record of a hearing if one is held or the close of
the public comment period if a hearing is not held 30 U.S.C. 811(a)(4).
However, the Court declined to immediately issue the mandamus order
sought in this case because, among other factors: (a) The UMWA agreed
that the diesel equipment rules alone may have the desired effect of
reducing exposure to these gases; (b) the UMWA further agreed that the
control of diesel particulate matter and respirable mine dust rank as
higher rulemaking priorities for MSHA; and (c) MSHA submitted a
tentative schedule for such rulemaking that the court found to be
reasonable. However, the court retained jurisdiction of the case to
ensure MSHA would move forward on this matter, and ordered several
reports by the agency on its progress on December 31, 1999, June 30,
2000, December 31, 2000, and December 31, 2001.
III. Risk Assessment
Introduction
1. Exposures of U.S. Miners
a. Underground Coal Mines
b. Underground Metal and Nonmetal Mines
c. Surface Mines
d. Miner Exposures Compared to Exposures of Other Groups
2. Health Effects Associated with Dpm Exposures
a. Relevancy Considerations
i. Animal Studies
ii. Reversible Health Effects
iii. Health Effects Associated with PM2.5 in Ambient
Air
b. Acute Health Effects
i. Symptoms Reported by Exposed Miners
ii. Studies Based on Exposures to Diesel Emissions
iii. Studies Based on Exposures to Particulate Matter in Ambient
Air
c. Chronic Health Effects
i. Studies Based on Exposures to Diesel Emissions
(1) Chronic Effects other than Cancer
(2) Cancer
(a) Lung Cancer
(i) Evaluation Criteria
(ii) Studies Involving Miners
(iii) Best Available Epidemiologic Evidence
(iv) Counter-Evidence
(v) Summation
(b) Bladder Cancer
ii. Studies Based on Exposures to PM2.5 in Ambient
Air
d. Mechanisms of Toxicity
i. Agent of Toxicity
ii. Deposition, Clearance, and Retention
iii. Effects other than Cancer
iv. Lung Cancer
(1) Genotoxicity Studies
(2) Animal Inhalation Studies
3. Characterization of Risk
a. Material Impairments to Miners' Health or Functional Capacity
i. Sensory Irritations and Respiratory Symptoms (including
allergenic responses)
ii. Premature Death from Cardiovascular, Cardiopulmonary, or
Respiratory Causes
iii. Lung Cancer
(1) Summary of Collective Epidemiologic Evidence
(a) Consistency of Epidemiologic Results
(b) Best Available Epidemiologic Evidence
(c) Studies with Quantitative or Semiquantitative Exposure
Assessments
(d) Studies Involving Miners
(2) Meta-Analyses
(3) Potential Systematic Biases
(4) Causality
(5) Other Interpretations of the Evidence
b. Significance of the Risk of Material Impairment to Miners
i. Meaning of Significant Risk
(1) Legal Requirements
(2) Standards and Guidelines for Risk Assessment
ii. Significance of Risk for Underground Miners Exposed to DPM
[[Page 5561]]
(1) Sensory Irritations and Respiratory Symptoms (including
allergenic responses)
(2) Premature Death from Cardiovascular, Cardiopulmonary, or
Respiratory Causes
(3) Lung Cancer
(a) Risk Assessment Based on Studies Involving Miners
(b) Risk Assessment Based on Miners' Cumulative Exposure
(i) Exposure-Response Relationships from Studies Outside Mining
(ii) Exposure-Response Relationships from Studies on Miners
(iii) Excess Risk at Specific DPM Exposure Levels
c. The Rule's Expected Impact on Risk
4. Conclusions
Introduction
MSHA has reviewed the scientific literature to evaluate the
potential health effects of occupational dpm exposures at levels
encountered in the mining industry. This part of the preamble presents
MSHA's review of the currently available information and MSHA's
assessment of health risks associated with those exposures. All
material submitted during the public comment periods was considered
before MSHA drew its final conclusions.
The risk assessment begins in Section III.1, with a discussion of
dpm exposure levels observed by MSHA in the mining industry. This is
followed by a review, in Section III.2, of information available to
MSHA on health effects that have been studied in association with dpm
exposure. Finally, in Section III.3 entitled ``Characterization of
Risk,'' the Agency considers three questions that must be addressed for
rulemaking under the Mine Act and relates the available information
about risks of dpm exposure at current levels to the regulatory
requirements.
A risk assessment must be technical enough to present the evidence
and describe the main controversies surrounding it. At the same time,
an overly technical presentation could cause stakeholders to lose sight
of the main points. MSHA is guided by the first principle the National
Research Council established for risk characterization, that the
approach be:
[a] decision driven activity, directed toward informing choices and
solving problems * * * Oversimplifying the science or skewing the
results through selectivity can lead to the inappropriate use of
scientific information in risk management decisions, but providing
full information, if it does not address key concerns of the
intended audience, can undermine that audience's trust in the risk
analysis.
Although the final rule covers only one sector, this portion of the
preamble was intended to enable MSHA and other interested parties to
assess risks throughout the coal and M/NM mining industries.
Accordingly, the risk assessment includes information pertaining to all
sectors of the mining industry. All public comments on the exposures of
miners and the health effects of dpm exposure--whether submitted
specifically for the coal rulemaking or for the metal/nonmetal
rulemaking--were incorporated into the record for each rulemaking and
have been considered for this assessment.
MSHA had an earlier version of this risk assessment independently
peer reviewed. The risk assessment as proposed incorporated revisions
made in accordance with the reviewers' recommendations, and the final
version presented here contains clarifications and other responses to
public comments. With regard to the risk assessment as published in the
proposed preamble, the reviewers stated that:
* * * principles for identifying evidence and characterizing risk
are thoughtfully set out. The scope of the document is carefully
described, addressing potential concerns about the scope of
coverage. Reference citations are adequate and up to date. The
document is written in a balanced fashion, addressing uncertainties
and asking for additional information and comments as appropriate.
(Samet and Burke, Nov. 1997).
Some commenters generally agreed with this opinion. Dr. James
Weeks, representing the UMWA, found the proposed risk assessment to be
``balanced, thorough, and systematic.'' Dr. Paul Schulte, representing
NIOSH, stated that ``MSHA has prepared a thorough review of the health
effects associated with exposure to high concentrations of dpm, and
NIOSH concurs with the published [proposed] characterization of risks
associated with these exposures.'' Dr. Michael Silverstein,
representing the Washington State Dept. of Labor and Industries, found
MSHA's ``regulatory logic * * * thoroughly persuasive.'' He commented
that ``the best available scientific evidence shows that diesel
particulate exposure is associated with serious material impairment of
health * * * the evidence * * * is particularly strong and certainly
provides a sufficient basis for regulatory action.''
Many commenters, however, vigorously criticized various aspects of
the proposed assessment and some of the scientific studies on which it
was based. MSHA's final assessment, published here, was modified to
respond to all of these criticisms. Also, in response to commenters'
suggestions, this assessment incorporates some research studies and
literature reviews not covered or inadequately discussed in the
previous version.
Some commenters expressed the opinion that the proposed risk
assessment should have been peer-reviewed by a group representing
government, labor, industry, and independent scientists. Since the
rulemaking process included a pre-hearing comment period, eight public
hearings (four for coal and four for M/NM), and two post-hearing
comment periods, these constituencies had ample opportunity to review
and comment upon MSHA's proposed risk assessment. The length of the
comment period for the Coal Dpm proposal was 15 months. The length of
the comment period for the Metal/Nonmetal Dpm proposal was nine months.
1. Exposures of U.S. Miners
Information about U.S. miner exposures comes from published studies
and from additional mine investigations conducted by MSHA since
1993.\3\ Previously published studies of exposures to dpm among U.S.
miners are: Watts (1989, 1992), Cantrell (1992, 1993), Haney (1992),
and Tomb and Haney (1995). MSHA has also conducted investigations
subsequent to the period covered in Tomb and Haney (1995), and the
previously unpublished data through mid-1998 are included here. Both
the published and unpublished studies were placed in the record with
the proposal, giving MSHA's stakeholders the opportunity to analyze and
comment on all of the exposure data considered.
---------------------------------------------------------------------------
\3\ MSHA has only limited information about miner exposures in
other countries. Based on 223 personal and area samples, average
exposures at 21 Canadian noncoal mines were reported to range from
170 to 1300 g/m 3 (respirable combustible dust),
with maximum measurements ranging from 1020 to 3100 g/m
3 (Gangel and Dainty, 1993). Among 622 full shift
measurements collected since 1989 in German underground noncoal
mines, 91 (15%) exceeded 400 g/m 3 (total
carbon) (Dahmann et al., 1996). As explained elsewhere in this
preamble, 400 g/m 3 (total carbon) corresponds
to approximately 500 g/m 3 dpm.
---------------------------------------------------------------------------
MSHA's field studies involved measuring dpm concentrations at a
total of 50 mines: 27 underground metal and nonmetal (M/NM) mines, 12
underground coal mines, and 11 surface mining operations (both coal and
M/NM). At all surface mines and all underground coal mines, dpm
measurements were made using the size-selective method, based on
gravimetric determination of the amount of submicrometer dust collected
with an impactor. With few exceptions, dpm measurements at underground
M/NM mines were made using the Respirable Combustible Dust (RCD) method
(with
[[Page 5562]]
no impactor). At two of the underground M/NM mines, measurements were
made using the total carbon (TC) method, and at one, RCD measurements
were made in one year and TC measurements in another. Measurements at
the two remaining underground M/NM mines were made using the size-
selective method, as in coal and surface mines.\4\ Weighing errors
inherent in the gravimetric analysis required for both size-selective
and RCD methods become statistically insignificant at the relatively
high dpm concentrations observed.
---------------------------------------------------------------------------
\4\ The various methods of measuring dpm are explained in
section 3 of Part II of the preamble to the proposed rule. This
explanation, along with additional information on these methods, is
also provided in section 3 of Part II of the preamble to the final
M/NM rule.
---------------------------------------------------------------------------
According to MSHA's experience, the dpm samples reflect exposures
typical of mines known to use diesel equipment for face haulage in the
U.S. However, they do not constitute a random sample of mines, and care
was taken in the proposed risk assessment not to characterize results
as necessarily representing conditions in all mines. Several commenters
objected to MSHA's use of these exposure measurements in making
comparisons to exposures reported in other industries and, for M/NM, in
estimating the proposed rule's impact. These objections are addressed
in Sections III.1.d and III.3.b.ii(3)(c) below. Comments related to the
measurement methods used in underground coal and M/NM mines are
addressed, respectively, in Sections III.1.b and III.1.c.
Each underground study typically included personal dpm exposure
measurements for approximately five production workers. Also, area
samples were collected in return airways of underground mines to
determine diesel particulate emission rates.\5\ Operational information
such as the amount and type of equipment, airflow rates, fuel, and
maintenance was also recorded. Mines were selected to obtain a wide
range of diesel equipment usage and mining methods. Mines with greater
than 175 horsepower and less than 175 horsepower production equipment
were sampled. Single and multiple level mines were sampled. Mine level
heights ranged from eight to one-hundred feet. In general, MSHA's
studies focused on face production areas of mines, where the highest
concentrations of dpm could be expected; but, since some miners do not
spend their time in face areas, samples were collected in other areas
as well, to get a more complete picture of miner exposure. Because of
potential interferences from tobacco smoke in underground M/NM mines,
samples were not collected on or near smokers.
---------------------------------------------------------------------------
\5\ Since area samples in return airways do not necessarily
represent locations where miners normally work or travel, they were
excluded from the present analysis. A number of area samples were
included, however, as described in Sections III.1.b and III.1.c. The
included area samples were all taken in production areas and
haulageways.
---------------------------------------------------------------------------
Table III-1 summarizes key results from MSHA's studies. The higher
concentrations in underground mines were typically found in the
haulageways and face areas where numerous pieces of equipment were
operating, or where airflow was low relative to the amount of equipment
operating. In production areas and haulageways of underground mines
where diesel powered equipment was used, the mean dpm concentration
observed was 644 g/m3 for coal and 808 g/
m3 for M/NM. In travelways of underground mines where diesel
powered equipment was used, the mean dpm concentration (based on 112
area samples not included in Table III-1) was 517 g/
m3 for M/NM and 103 g/m3 for coal. In
surface mines, the higher concentrations were generally associated with
truck drivers and front-end loader operators. The mean dpm
concentration observed was less than 200 g/m3 at
all eleven of the surface mines in which measurements were made. More
information about the dpm concentrations observed in each sector is
presented in the material that follows.
Table III-1.--Full-Shift Diesel Particulate Matter Concentrations Observed in Production Areas and Haulageways of 50 Dieselized U.S. Mines
--------------------------------------------------------------------------------------------------------------------------------------------------------
Standard error of
Mine type Number of mines Number of samples Mean exposure mean (g/ Exposure range
(g/m\3\) m\3\) (g/m\3\)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Surface.................................................. 11 45 88 11 9-380
Underground Coala........................................ 12 226 644 41 0-3.650
Underground Metal and Nonmetal........................... 27 355 808 39 10-5.570
--------------------------------------------------------------------------------------------------------------------------------------------------------
Note: Intake and return area samples are excluded.
a. Underground Coal Mines
Approximately 145 out of the 910 existing underground coal mines
currently utilize diesel powered equipment. Of these 145 mines, 32
mines currently use diesel equipment for face coal haulage. The
remaining mines use diesel equipment for transportation, materials
handling and other support operations. MSHA focused its efforts in
measuring dpm concentrations in coal mines on mines that use diesel
powered equipment for face coal haulage. Twelve mines using diesel-
powered face haulage were sampled. Mines with diesel powered face
haulage were selected because the face is an area with a high
concentration of vehicles operating at a heavy duty cycle at the
furthest end of the mine's ventilation system.
Diesel particulate levels in underground mines depend on: (1) The
amount, size, and workload of diesel equipment; (2) the rate of
ventilation; and, (3) the effectiveness of whatever diesel particulate
control technology may be in place. In the dieselized mines studied by
MSHA, the sections used either two or three diesel coal haulage
vehicles. In eastern mines, the haulage vehicles were equipped with a
nominal 100 horsepower engine. In western mines, the haulage vehicles
were equipped with a nominal 150 horsepower engine. Ventilation rates
ranged from the approval plate requirement, based on the 100-75-50
percent rule (Holtz, 1960), to ten times the approval plate
requirement. In most cases, the section airflow was approximately twice
the approval plate requirement. Other control technology included
aftertreatment filters and fuel. Two types of aftertreatment filters
were used. These filters included a disposable diesel emission filter
(DDEF) and a Wire Mesh Filter (WMF). The DDEF is a commercially
available product; the WMF was developed by and only used at one mine.
Both low sulfur and high sulfur fuels were used.
Figure III-1 displays the range of exposure measurements obtained
by MSHA in the field studies it conducted in underground coal mines. A
study
[[Page 5563]]
normally consisted of collecting samples on the continuous miner
operator and coal haulage vehicle operators for two to three shifts,
along with area samples in the haulageways. A total of 142 personal
samples and 84 area samples were collected, excluding any area samples
taken in intake or return airways.
BILLING CODE 4510-43-P
[GRAPHIC] [TIFF OMITTED] TR19JA01.010
BILLING CODE 4510-43-C
As stated in the proposed risk assessment, no statistically
significant difference was observed in mean dpm concentration between
the personal and area samples.\6\ A total of 19 individual measurements
exceeded 1500 g/m3, still excluding intake and
return area samples. Although the three highest of these were from area
samples, nine of the 19 measurements exceeding 1500 g/
m3 were from personal samples.
---------------------------------------------------------------------------
\6\ One commenter (IMC Global) noted that MSHA had provided no
data verifying this statement. For the 142 personal samples, the
mean dpm concentration measurement was 608 g/m3,
with a standard error of 42.5 g/m3. For the 84
area samples, the mean was 705 g/m3, with a
standard error of 82.1 g/m3. The significance
level (p-value) of a t-test comparing these means is 0.29 using a
separate-variance test or 0.25 using a pooled-variance test.
Therefore, a difference in population means cannot be inferred at
any confidence level greater than 75%. Here, and in other sections
of this risk assessment, MSHA has employed standard statistical
methods described in textbooks on elementary statistical inference.
---------------------------------------------------------------------------
In six mines, measurements were taken both with and without use of
disposable after-treatment filters, so that a total of eighteen
studies, carried out in twelve mines, are displayed. Without use of
after-treatment filters, average observed dpm concentrations exceeded
500 g/m3 in eight of the twelve mines and exceeded
1000 g/m3 in four.\7\ At five of the twelve mines,
all dpm measurements were 300 g/m3 or greater in
the absence of after-treatment filters.
---------------------------------------------------------------------------
\7\ In coal mine E, the average as expressed by the mean
exceeded 1000 g/m3, but the median did not.
---------------------------------------------------------------------------
The highest dpm concentrations observed at coal mines were
collected at Mine ``G.'' Eight of these samples were collected during
employment of WMFs, and eight were collected while filters were not
being employed. Without filters, the mean dpm concentration observed at
Mine ``G'' was 2052 g/m3 (median = 2100 g/
m3). With
[[Page 5564]]
employment of WMFs, the mean dropped to 1241 g/m3
(median = 1235 g/m3).
Filters were employed during three of the four studies showing
median dpm concentration at or below 200 g/m3.
After adjusting for outby sources of dpm, exposures were found to be
reduced by up to 95 percent in mines using the DDEF and by
approximately 50 percent in the mine using the WMF.
The higher dpm concentrations observed at the mine using the WMF
(Mine ``G*'') are attributable partly to the lower section airflow. The
only study without filters showing a median concentration at or below
200 g/m3 was conducted in a mine (Mine ``A'') which
had section airflow approximately ten times the nameplate requirement.
The section airflow at the mine using the WMF was approximately the
nameplate requirement.
Some commenters [e.g., WV Coal Assoc and Energy West] objected to
MSHA's presentation of underground coal mine exposures based on
measurements made using the size-selective method (gravimetric
determination of the amount of submicrometer dust collected with an
impactor). These commenters argued that the data were `` * * *
collected with emissions monitoring devices discredited by MSHA itself
in the preamble * * *'' and that these measurements do not reliably ``*
* * distinguish it [dpm] from other particles in coal mine dust, at the
critical upper end range of submicron particles.''
MSHA did not ``discredit'' use of the size-selective method for all
purposes. As discussed elsewhere in this preamble, the size-selective
method of measuring dpm was designed by the former BOM specifically for
use in coal mines, and the size distribution of coal mine dust was
taken into account in its development. Despite the recognized
interference from a small fraction of coal mine dust particles, MSHA
considers gravimetric size-selective measurements to be reasonably
accurate in measuring dpm concentrations greater than 200 g/
m3, based on a full-shift sample, when coal mine dust
concentrations are not excessive (i.e., not greater than 2.0 mg/
m3). Interference from submicrometer coal mine dust is
counter-balanced, to some extent, by the fraction of larger size,
uncaptured dpm. Coal mine dust concentrations were not excessive when
MSHA collected its size-selective samples. Therefore, even if as much
as 10 percent of the coal mine dust were submicrometer, this fraction
would not have contributed significantly to the high concentrations
observed at the sampled mines.
At lower concentrations, or shorter sampling times, random
variability in the gravimetric determination of weight gain becomes
significant, compared to the weight of dust accumulated on the filter.
For this reason, MSHA has rejected the use of the gravimetric size-
selective method for enforcement purposes.\8\ This does not mean,
however, that MSHA has ``discredited'' this method for other purposes,
including detection of very high dpm concentrations at coal mines
(i.e., greater than 500 g/m3) and estimation of
average dpm concentrations, based on multiple samples, when coal mine
dust concentrations are not excessive. On the contrary, MSHA regards
the gravimetric size-selective method as a useful tool for detecting
and monitoring very high dpm concentrations and for estimating average
exposures.
---------------------------------------------------------------------------
\8\ MSHA has concluded that random weighing variability would
make it impractical to use the size-selective method to enforce
compliance with any dpm concentration limit less than about 300
g/m3. MSHA believes that, at such levels,
single-sample noncompliance determinations based on the size-
selective method could not be made at a sufficiently high confidence
level.
---------------------------------------------------------------------------
b. Underground Metal and Nonmetal Mines
Currently there are approximately 265 underground M/NM mines in the
United States. Nearly all of these mines utilize diesel powered
equipment, and 27 of those doing so were sampled by MSHA for dpm.\9\
The M/NM studies typically included measurements of dpm exposure for
dieselized production equipment operators (such as truck drivers, roof
bolters, haulage vehicles) on two to three shifts. A number of area
samples were also collected. None of the M/NM mines studied were using
diesel particulate afterfilters.
---------------------------------------------------------------------------
\9\ The proposal discussed data from 25 underground M/NM mines.
Studies at two additional mines, carried out too late to be included
in the proposal, were placed into the public record along with the
earlier studies. During the proceedings, MSHA provided copies of all
of these studies to stakeholders requesting them.
---------------------------------------------------------------------------
Figure III-2 displays the range of dpm concentrations measured by
MSHA in the 27 underground M/NM mines studied. A total of 275 personal
samples and 80 area samples were collected, excluding intake and return
area samples. Personal exposures observed ranged from less than 100
g/m3 to more than 3500 g/m3.
Exposure measurements based on area samples ranged from less than 100
g/m3 to more than 3000 g/m3.
With the exception of Mine ``V'', personal exposures were for face
workers. Mine ``V'' did not use dieselized face equipment.
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[[Page 5566]]
As stated in the proposed risk assessment, no statistically
significant difference was observed in mean dpm concentration between
the personal and area samples.\10\ A total of 45 individual
measurements exceeded 1500 g/m\3\, still excluding intake and
return area samples. The three highest of these, all exceeding 3500
g/m\3\, were from personal samples. Of the 45 measurements
exceeding 1500 g/m\3\, 30 were from personal samples and 15
were from area samples.
---------------------------------------------------------------------------
\10\ One commenter (IMC Global) noted that MSHA had provided no
data verifying this statement. For the 275 personal samples, the
mean dpm concentration measurement was 770 g/m\3\, with a
standard error of 42.8 g/m\3\. For the 80 area samples, the
mean was 939 g/m\3\, with a standard error of 86.6
g/m\3\. The significance level (p-value) of a t-test
comparing these means is 0.08 using a separate-variance test or 0.07
using a pooled-variance test. Therefore, a difference in population
means cannot be inferred at a 95% confidence level.
---------------------------------------------------------------------------
Average observed dpm concentrations exceeded 500 g/m\3\ in
18 of the 27 underground M/NM mines and exceeded 1000 g/m\3\
in 12.\11\ At eight of the 27 mines, all dpm measurements exceeded 300
g/m\3\. The highest dpm concentrations observed at M/NM mines
were collected at Mine ``E''. Based on 16 samples, the mean dpm
concentration observed at Mine ``E'' was 2008 g/m\3\ (median =
1835 g/m\3\). Twenty-five percent of the dpm measurements at
this mine exceeded 2400 g/m\3\. All four of these were based
on personal samples.
---------------------------------------------------------------------------
\11\ At M/NM mines C, I, J, P, and Z the average as expressed by
the mean exceeded 1000 g/m\3\ but the median did not. At M/
NM mines H and S, the median exceeded 1000 g/m\3\ but the
mean did not. At M/NM mine K, the mean exceeded 500 g/m\3\,
but the median did not.
---------------------------------------------------------------------------
As with underground coal mines, dpm levels in underground M/NM
mines are related to the amount and size of equipment, to the
ventilation rate, and to the effectiveness of the diesel particulate
control technology employed. In the dieselized M/NM mines studied by
MSHA, front-end-loaders were used either to load ore onto trucks or to
haul and load ore onto belts. Additional pieces of diesel powered
support equipment, such as bolters and mantrips, were also used at the
mines. The typical piece of production equipment was rated at 150 to
350 horsepower. Ventilation rates in the M/NM mines studied mostly
ranged from 100 to 200 cfm per horsepower of equipment. In only a few
of the mines inventoried did ventilation exceed 200 cfm/hp. For single-
level mines, working areas were ventilated in series (i.e., the exhaust
air from one area became the intake for the next working area). For
multi-level mines, each level typically had a separate fresh air
supply. One or two working areas could be on a level. Control
technology used to reduce diesel particulate emissions in mines
inventoried included oxidation catalytic converters and engine
maintenance programs. Both low sulfur and high sulfur fuel were used;
some mines used aviation grade low sulfur fuel.
Some commenters argued that, because of the limited number of
underground M/NM mines sampled by MSHA, ``* * * results of MSHA's
admittedly non-random sample cannot be extrapolated to other mines.''
[MARG] More specifically, IMC Global claimed that since only 25 [now
27] of about 260 underground M/NM mines were sampled,\12\ then ``if the
* * * measurements are correct, this information shows at best
potential exposure problems to diesel particulate in only 10% of the
miners working in the metal-nonmetal mining sector and then only for
certain unlisted commodities.'' \13\ IMC Global went on to suggest that
MSHA should ``perform sufficient additional exposure monitoring * * *
to show that the diesel particulate exposures are representative of the
entire industry before promulgating regulations that will be applicable
to the entire industry.''
---------------------------------------------------------------------------
\12\ Three underground M/NM mine surveys, carried out too late
to be included in the discussion, were placed into the public record
and provided to interested stakeholders. These surveys contained
data from two additional underground M/NM mines (``Z'' and ``aa'')
and additional data for a mine (``d'') that had previously been
surveyed. The risk assessment has now been updated to include these
data, representing a total of 27 underground M/NM mines.
\13\ A breakdown by commodity is given at the end of this
subsection.
---------------------------------------------------------------------------
As mentioned earlier, MSHA acknowledges that the mines for which
dpm measurements are available do not comprise a statistically random
sample of all underground M/NM mines. MSHA also acknowledges that the
results obtained for these mines cannot be extrapolated in a
statistically rigorous way to the entire population of underground M/NM
mines. According to MSHA's experience, however, the selected mines (and
sampling locations within those mines) represent typical diesel
equipment use conditions at underground M/NM mines. MSHA believes that
results at these mines, as depicted in Figure III-2, in fact fairly
reflect the variety of diesel equipment used by the industry,
regardless of type of M/NM mine. Based on its extensive experience with
underground mines, MSHA believes that this body of data better
represents those diverse diesel equipment use conditions, with respect
to dpm exposures, than any other body of data currently available.
MSHA strongly disagrees with IMC Global's contention that, ``* * *
this information shows at best potential exposure problems to diesel
particulate in only 10% of the miners working in the metal-nonmetal
mining sector.'' IMC Global apparently drew this conclusion from the
fact that MSHA sampled approximately ten percent of all underground M/
NM mines. This line of argument, however, depends on an unwarranted and
highly unrealistic assumption: Namely, that all of the underground M/NM
mines not included in the sampled group of 25 experience essentially no
``potential [dpm] exposure problems.'' MSHA certainly did not go out
and, by chance or design, pick for sampling just exactly those mines
experiencing the highest dpm concentrations. IMC Global's argument
fails to recognize that the sampled mines could be fairly
representative without being randomly chosen.
MSHA also disagrees with the premise that 27 [or 25 as in the
proposal] is an inherently insufficient number of mines to sample for
the purpose of identifying an industry-wide dpm exposure problem that
would justify regulation. The between-mine standard deviation of the 27
mean concentrations observed within mines was 450 g/m\3\.
Therefore, the standard error of the estimated grand mean, based on the
variability observed between mines, was
[GRAPHIC] [TIFF OMITTED] TR19JA01.012
MSHA considers this degree of uncertainty to be acceptable, given that
the overall mean concentration observed exceeded 800 g/m\3\.
---------------------------------------------------------------------------
\14\ This quantity, 87 g/m\3\, differs from the
standard error of the mean of individual measurements for
underground M/NM mines, presented in Table III-1. The tabled value
is based on 355 measurements whose standard deviation is 727
g/m\3\. Therefore, the standard error of the mean of all
individual measurements is 727/355 =
39 g/m\3\, as shown in the table. Similarly, the mean of
all individual measurements (listed in Table III-1 as 808
g/m\3\) differs from the grand mean of individual mean
concentrations observed within mines, which is 838 g/m\3\.
---------------------------------------------------------------------------
Several commenters questioned MSHA's use of the RCD and size-
selective methods for measuring dpm exposures at underground M/NM
mines. IMC Global indicated that MSHA's RCD measurements might
systematically inflate the dpm concentrations presented in this
section, because ``* * * estimates for the non-diesel particulate
component of RCD actually vary between 10% to 50%, averaging 33%.''
[[Page 5567]]
MSHA considers the size-selective, gravimetric method capable of
providing reasonably accurate measurements when the dpm concentration
is greater than 200 g/m3, interferences are
adequately limited, and the measurement is based on a full-shift
sample. Relatively few M/NM measurements were made using this method,
and none at the mines showing the highest dpm concentrations. No
evidence was presented that the size distribution of coal mine dust
(for which the impactor was specifically developed) differs from that
of other mineral dusts in a way that significantly alters the
impactor's performance. Similarly, MSHA considers the RCD method, when
properly applied, to be capable of providing reasonably accurate dpm
measurements at concentrations greater than 200 g/
m3. As with the size selective method, however, random
weighing errors can significantly reduce the precision of even full-
shift RCD measurements at lower dpm concentrations. For this reason, in
order to maintain a sufficiently high confidence level for its
noncompliance determinations, MSHA will not use the RCD method for
enforcement purposes. This does not mean, however, that MSHA has
``discredited'' the RCD measurements for all other purposes, including
detection of very high dpm concentrations (i.e., greater than 300
g/m3) and estimation of average concentrations
based on multiple samples. On the contrary, MSHA considers the RCD
method to be a useful tool for detecting and monitoring very high dpm
concentrations in appropriate environments and for estimating average
exposures when those exposures are excessive.
MSHA did not employ an impactor in its RCD measurements, and it is
true that some of these measurements may have been subject to
interference from lubrication oil mists. However, MSHA believes that
the high estimates sometimes made of the non-dpm component of RCD
(cited by IMC Global) do not apply to the RCD measurements depicted in
Figure III-2. MSHA has three reasons for believing these RCD
measurements consisted almost entirely of dpm:
(1) MSHA took special care to sample only environments where
interferences would not be significant. No samples were taken near
pneumatic drills or smoking miners.
(2) There was no interference from carbonates. The RCD analysis was
performed at 500 deg. C, and carbonates are not released below
1000 deg. C. (Gangel and Dainty, 1993)
(3) Although high sulphur fuel was used in some mines, thereby
adding sulfates to the RCD measurement, these sulfates are considered
part of the dpm, as explained in section 2 of Part II of this preamble.
Sulfates should not be regarded as an interference in RCD measurements
of dpm.
Commenters presented no evidence that there were substantial
interferences in MSHA's RCD measurements, and, as stated above, MSHA
was careful to avoid them. Therefore, MSHA considers it reasonable, in
the context of this risk assessment, to assume that all of the RCD was
in fact dpm. Moreover, in the majority of underground M/NM mines
sampled, even if the RCD measurements were reduced by \1/3\, the mine's
average would still be excessive: it would still exceed the maximum
exposure level reported for non-mining occupations presented in Section
III.1.d.
The breakdown, as suggested by IMC Global, of sampled underground
M/NM mines by commodity is as follows:
------------------------------------------------------------------------
Number
Commodity of
mines
------------------------------------------------------------------------
Copper......................................................... 2
Gold........................................................... 1
Lead/Zinc...................................................... 6
Limestone...................................................... 6
Potash......................................................... 2
Salt........................................................... 6
Trona (soda ash)............................................... 2
Other Nonmetal................................................. 2
--------
Total...................................................... 27
------------------------------------------------------------------------
c. Surface Mines
Currently, there are approximately 12,620 surface mining operations
in the United States. The total consists of approximately 1,550 coal
mines and 11,070 M/NM mines. Virtually all of these mines utilize
diesel powered equipment.
MSHA conducted dpm studies at eleven surface mining operations:
eight coal mines and three M/NM mines. MSHA deliberately directed its
surface sampling efforts toward occupations likely to experience high
dpm concentrations. To help select such occupations, MSHA first made a
visual examination (based on blackness of the filter) of surface mine
respirable dust samples collected during a November 1994 study of
surface coal mines. This preliminary screening of samples indicated
that relatively high surface mine dpm concentrations are typically
associated with front-end-loader operators and haulage-truck operators;
accordingly, sampling focused on these operations. A total of 45
samples was collected.
Figure III-3 displays the range of dpm concentrations measured at
the eleven surface mines. The average dpm concentration observed was
less than 200 g/m3 at all mines sampled. The
maximum dpm concentration observed was less than or equal to 200
g/m3 in 8 of the 11 mines (73%). The surface mine
studies suggest that even when sampling is performed at the areas of
surface mines believed most likely to have high exposures, dpm
concentrations are generally likely to be less than 200 g/
m3.
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[[Page 5569]]
d. Miner Exposures Compared to Exposures of Other Groups
Occupational exposure to diesel particulate primarily originates
from industrial operations employing equipment powered with diesel
engines. Diesel engines are used to power ships, locomotives, heavy
duty trucks, heavy machinery, as well as a small number of light-duty
passenger cars and trucks. NIOSH has estimated that approximately 1.35
million workers are occupationally exposed to the combustion products
of diesel fuel in approximately 80,000 workplaces in the United States.
(NIOSH 1988) Workers who are likely to be exposed to diesel emissions
include: mine workers; bridge and tunnel workers; railroad workers;
loading dock workers; truck drivers; fork-lift drivers; farm workers;
and, auto, truck, and bus maintenance garage workers (NIOSH, 1988).
Besides miners, groups for which occupational exposures have been
reported and health effects have been studied include loading dock
workers, truck drivers, and railroad workers.
As estimated by the reported geometric mean,\15\ the median site-
specific occupational exposures for loading dock workers operating or
otherwise exposed to unfiltered diesel fork lift trucks ranged from 23
to 55 g/m3, as measured by submicrometer elemental
carbon (EC) (NIOSH, 1990). Reported geometric mean concentrations of
submicrometer EC ranged from 2.0 to 7.0 g/m3 for
truck drivers and from 4.8 to 28 g/m3 for truck
mechanics, depending on weather conditions (Zaebst et al., 1991).
---------------------------------------------------------------------------
\15\ Median concentrations were not reported. The geometric mean
provides a smoothed estimate of the median.
---------------------------------------------------------------------------
Because these exposure averages, unlike those for railroad workers
and miners, were reported in terms of EC, it is necessary, for purposes
of comparison, to convert them to estimates of total dpm. Watts (1995)
states that ``elemental carbon generally accounts for about 40% to 60%
of diesel particulate mass.'' Therefore, in earlier versions of this
risk assessment, a 2.0 conversion factor was assumed for dock workers,
truck drivers, and truck mechanics, based on the midpoint of the 40-60%
range proposed by Watts.
Some commenters objected to MSHA's use of this conversion factor.
IMC Global, for example, asserted that Watts' ``* * * 40 to 60%
relationship between elemental carbon and diesel particulate mass * * *
applies only to underground coal mines where diesel haulage equipment
is used.'' IMC Global, and other commenters, also objected to MSHA's
use of a single conversion factor for ``* * * different types of diesel
engines under different duty cycles with different fuels and different
types of emission control devices (if any) subjected to varying degrees
of maintenance.''
MSHA's quotation from Watts (1995) was taken from the ``Summary''
section of his paper. That paper covers a variety of occupational
environments, and the summary makes no mention of coal mines. The
sentence immediately preceding the quoted passage refers to the
``occupational environment'' in general, and there is no indication
that Watts meant to restrict the 40- to 60-percent range to any
specific environment. It seems clear that the 40-to 60-percent range
refers to average values across a spectrum of occupational
environments.
IMC Global mistakenly attributed to MSHA ``the blanket statement''
that the same ratio of elemental carbon to dpm applies ``for all diesel
engines in different industries for all patterns of use.'' MSHA made no
such statement. On the contrary, MSHA agrees with Watts (and IMC
Global) that ``the percentage of elemental carbon in total diesel
particulate matter fluctuates'' depending on ``engine type, duty cycle,
fuel, lube oil consumption, state of engine maintenance, and the
presence or absence of an emission control device.'' (Watts, op cit.)
Indeed, MSHA acknowledges that, because of these factors, the
percentage on a particular day in a particular environment may
frequently fall outside the stated range. But MSHA is not applying a
single conversion factor to individual elemental carbon measurements
and claiming knowledge of the total dpm corresponding to each separate
measurement. Instead, MSHA is applying an average conversion factor to
an average of measurements in order to derive an estimate of an average
dpm exposure. Averages are always less widely dispersed than individual
values.
[[Page 5570]]
Still, MSHA agrees with IMC Global that better estimates of dpm
exposure levels are attainable by applying conversion factors more
specifically related to the separate categories within the trucking
industry: dock workers, truck drivers, and truck mechanics. Based on a
total of 63 field measurements, the mean ratios (in percent) of EC to
total carbon (TC) reported for these three categories were 47.3, 36.6,
and 34.2, respectively (Zaebst et al., 1991).\16\ As explained
elsewhere in this preamble, TC amounts to approximately 80 percent, by
weight, of total dpm. Therefore, each of these ratios must be
multiplied by 0.8 in order to estimate the corresponding percentage of
EC in dpm.
---------------------------------------------------------------------------
\16\ MSHA calculated the ratio for truck drivers by taking a
weighted average of the ratios reported for ``local drivers'' and
``road drivers.''
---------------------------------------------------------------------------
It follows that the median mass concentration of dpm can be
estimated as 2.64 (i.e., 1/(0.473 x 0.8)) times the geometric mean EC
reported for dock workers, 3.42 times the geometric mean EC for truck
drivers, and 3.65 times the geometric mean EC for truck mechanics.
Applying the 2.64 conversion factor to the range of geometric mean EC
concentrations reported for dock workers (i.e., 23 to 55 g/
m3) results in an estimated range of 61 to 145 g/
m3 in median dpm concentrations at various docks. Similarly,
the estimated range of median dpm concentrations is calculated to be
6.8 to 24 g/m3 for truck drivers and 18 to 102
g/m3 for truck mechanics. It should be noted that
MSHA is using conversion factors only for those occupational groups
whose geometric mean exposures have been reported in terms of EC
measurements.
Average exposures of railroad workers to dpm were estimated by
Woskie et al. (1988) and Schenker et al. (1990). As measured by total
respirable particulate matter other than cigarette smoke, Woskie et al.
reported geometric mean concentrations for various occupational
categories of exposed railroad workers ranging from 49 to 191
g/m3.
For comparison with the exposures reported for these other
industries, median dpm exposures measured within sampled mines were
calculated directly from the data described in subsections a, b, and c
above. The median within each mine is shown as the horizontal ``belt''
plotted for the mine in Figures III-1, III-2, and III-3.
Figure III-4 compares the range of median dpm concentrations
observed for mine workers within different mines to a range of dpm
exposure levels estimated for urban ambient air and to the ranges of
median dpm concentrations estimated for loading dock workers operating
or otherwise exposed to diesel fork lift trucks, truck drivers, truck
mechanics, and railroad workers. The range for ambient air, 1 to 10
g/m\3\, was obtained from Cass and Gray (1995). For dock
workers, truck drivers, truck mechanics, and railroad workers, the
estimated ranges of median dpm exposures are, respectively: 61 to 145
g/m\3\, 6.8 to 24 g/m\3\, 18 to 102 g/m\3\
and 49 to 191 g/m\3\. The range of median dpm concentrations
observed at different underground coal mines is 55 to 2100 g/
m\3\, with filters employed at mines showing the lower
concentrations.\17\ For underground M/NM mines, the corresponding range
is 68 to 1835 g/m\3\, and for surface mines it is 19 to 160
g/m\3\. Since each range plotted is a range of median values
or (for ambient air) mean values, the plots do not encompass all of the
individual measurements reported.
---------------------------------------------------------------------------
\17\ One commenter misinterpreted the tops of the ranges plotted
in Figure III-4. This commenter apparently mistook the top of the
range depicted for underground coal mines as the mean or median dpm
exposure concentration measured across all underground coal mines.
The top of this range (at 2100 g/m\3\, actually represents
the highest median concentration at any of the coal mines sampled.
It corresponds to the ``belt'' plotted for Mine ``G'' (with no
after-filters) in Figure III-1. The bottom of the same bar, at 55
g/m\3\, corresponds to the ``belt'' plotted for Mine H *
(with after-filters) in Figure III-1.
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[[Page 5572]]
As shown in Figure III-4, some miners are exposed to far higher
concentrations of dpm than are any other populations for which exposure
data have been reported. Indeed, median dpm concentrations observed in
some underground mines are up to 200 times as high as mean
environmental exposures in the most heavily polluted urban areas,\18\
and up to 10 times as high as median exposures estimated for the most
heavily exposed workers in other occupational groups.
---------------------------------------------------------------------------
\18\ It should be noted, however, that 24-hour environmental
exposures for a full lifetime are not directly comparable with
workday exposures over an occupational lifetime. If it is assumed
that air inhaled during a work shift comprises half the total air
inhaled during a 24-hour day, then the amount of air inhaled over
the course of a 70-year lifetime is approximately 4.7 times the
amount inhaled over a 45-year occupational lifetime with 240 working
days per year.
---------------------------------------------------------------------------
Several commenters objected to Figure III-4 and, more generally, to
MSHA's comparison of dpm exposure levels for miners against the levels
reported for other occupations. The objections to MSHA's method of
estimating ranges of median dpm exposure for job categories within the
trucking industry have already been discussed and addressed above.
Other objections to the comparison were based on claims of insufficient
accuracy in the RCD and gravimetric size selective measurements MSHA
used to measure dpm levels for miners. MSHA considers its use of these
methods appropriate for purposes of this comparison and has responded
to criticisms of the dpm measurements for miners in Subsections 1.a and
1.b of this risk assessment.\19\
---------------------------------------------------------------------------
\19\ One commenter pointed out that the measurements for miners
included both area and personal samples but provided no evidence
that this would invalidate the comparison. As pointed out in
Subsections 1.a and 1.b, area samples did not dominate the upper end
of MSHA's dpm measurements. Furthermore, Figure III-4 presents a
comparison of medians rather than means or individual measurements,
so inclusion of the area samples has very little impact on the
results.
---------------------------------------------------------------------------
Some commenters objected to MSHA's basing a characterization of dpm
exposures to miners on data spanning a ten-year period. These
commenters contended that, in at least some M/NM mines, dpm levels had
improved substantially during that period. No data were submitted,
however, to support the premise that dpm exposures throughout the
mining industry have declined to the levels reported for other
occupations. As stated in the proposal and emphasized above, MSHA's dpm
measurements were not technically designed as a random or statistically
representative sample of the industry. They do show, however, that very
high exposures have recently occurred in some mines. For example, as
shown in Figure III-2, more than 25 percent of MSHA's dpm measurements
exceeded 2000 g/m\3\ at underground M/NM mines ``U'' and
``Z''--and these measurements were made in 1996-7. In M/NM mines where
exposures are actually commensurate with other industries already,
little or nothing would need to be changed to meet the exposure limits.
IMC Global further objected to Figure III-4 on the grounds that ``*
* * the assumptions that MSHA used to develop that figure are grossly
inaccurate and do not make sense in the context of a dose-response
relationship between lung cancer and Dpm exposure.'' IMC Global
suggested that the comparison in Figure III-4 be deleted for this
reason. MSHA believes that the comparison is informative and that
empirical evidence should be used, when it is available, even though
the evidence was not generated under ideal, theoretical dose-response
model conditions. The issue of whether Figure III-4 is consistent with
an exposure-response relationship for dpm is addressed in Subsection
3.a.iii(4) of this risk assessment.
2. Health Effects Associated With Dpm Exposures
This section reviews the various health effects (of which MSHA is
aware) that may be associated with dpm exposures. The review is divided
into three main sections: acute effects, such as diminished pulmonary
function and eye irritation; chronic effects, such as lung cancer; and
mechanisms of toxicity. Prior to that review, however, the relevance of
certain types of information will be considered. This discussion will
address the relevance of health effects observed in animals, health
effects that are reversible, and health effects associated with fine
particulate matter in the ambient air.
Several commenters described medical surveillance studies that
NIOSH and/or the former Bureau of Mines had carried out in the late
1970s and early 1980s on underground miners employed in western,
dieselized coal mines. These commenters urged MSHA to make these
studies available and to consider the results in this rulemaking. Some
of these commenters also suggested that these data would provide a
useful baseline for pulmonary function and lung diseases among miners
exposed to dpm, and recommended that follow-up examinations now be
conducted to evaluate the possible effects of chronic dpm exposure.
In response to such comments presented at some of the public
hearings, another commenter wrote:
First of all, MSHA is not a research agency, it is a regulatory
agency, so that it would be inappropriate for MSHA to initiate
research. MSHA did request that NIOSH conduct a risk assessment on
the health effects of diesel exhaust and encouraged NIOSH and is
currently collaborating with NIOSH (and NCI) on research of other
underground miners exposed to diesel exhaust. And third, research on
the possible carcinogenicity of diesel particulate matter was not
undertaken on coal miners in the West or anywhere else because of
the confounding exposure to crystalline silica, also considered a
carcinogen, because too few coal miners have been exposed, and for
too short a time to conduct a valid study. It was not arbitrariness
or indifference on MSHA's part that it did not initiate research on
coal miners; it was not within their mandate and it is inappropriate
in any event. [UMWA]
Three reports summarizing and presenting results from these medical
surveillance studies related to dpm exposures in coal mines were, in
fact, utilized and cited in the proposed risk assessment (Ames et al.,
1982; Reger et al., 1982; Ames et al., 1984). Ames et al. (1982)
evaluated acute respiratory effects, and their results are considered
in Subsection 2.b.ii of this risk assessment. Reger et al. (1982) and
Ames et al. (1984) evaluated chronic effects, and their results are
considered in Subsection 2.c.i(1).
A fourth report (Glenn et al., 1983) summarized results from the
overall research program of which the coal mine studies were a part.
This health and environmental research program included not only coal
miners, but also workers at potash, trona, salt, and metal mines. All
subjects were given chest radiographs and spirometric tests and were
questioned about respiratory symptoms, smoking and occupational
history. In conjunction with these medical evaluations, industrial
hygiene surveys were conducted to characterize the mine environments
where diesel equipment was used. Diesel exhaust exposure levels were
characterized by area and personal samples of NO2 (and, in some cases,
additional gasses), aldehydes, and both respirable and total dust. For
the evaluations of acute effects, exposure measures were based on the
shift concentrations to which the examined workers were exposed. For
the evaluations of chronic effects, exposures were usually estimated by
summing the products of time spent in various locations by each miner
by concentrations estimated for the various locations. Results of
studies on acute effects in salt mines were reported by Gamble et al.
(1978) and are considered
[[Page 5573]]
in Subsection 2.b.ii of this risk assessment. Attfield (1979), Attfield
et al. (1982), and Gamble et al. (1983) evaluated effects in M/NM
mines, and their results are considered in Subsection 2.c.i(1). The
general summary provided by Glenn et al. (1983) was among the reports
that one commenter (MARG) listed as having received inadequate
attention in the proposed risk assessment. In that context, the general
results summarized in this report are discussed, under the heading of
``Counter-Evidence,'' in Subsection 2.c.i(2)(a) of this risk
assessment.
a. Relevancy Considerations
i. Animal Studies
Since the lungs of different species may react differently to
particle inhalation, it is necessary to treat the results of animal
studies with some caution. Evidence from animal studies can
nevertheless be valuable--both in helping to identify potential human
health hazards and in providing a means for studying toxicological
mechanisms. Respondents to MSHA's ANPRM who addressed the question of
relevancy urged consideration of all animal studies related to the
health effects of diesel exhaust.
Unlike humans, laboratory animals are bred to be homogeneous and
can be randomly selected for either non-exposure or exposure to varying
levels of a potentially toxic agent. This permits setting up
experimental and control groups of animals that exhibit relatively
little biological variation prior to exposure. The consequences of
exposure can then be determined by comparing responses in the
experimental and control groups. After a prescribed duration of
deliberate exposure, laboratory animals can also be sacrificed,
dissected, and examined. This can contribute to an understanding of
mechanisms by which inhaled particles may exert their effects on
health. For this reason, discussion of the animal evidence is placed in
the section entitled ``Mechanisms of Toxicity'' below.
Animal evidence also can help isolate the cause of adverse health
effects observed among humans exposed to a variety of potentially
hazardous substances. If, for example, the epidemiologic data are
unable to distinguish between several possible causes of increased risk
of disease in a certain population, then controlled animal studies may
provide evidence useful in suggesting the most likely explanation--and
provide that information years in advance of definitive evidence from
human observations.
Furthermore, results from animal studies may also serve as a check
on the credibility of observations from epidemiologic studies of human
populations. If a particular health effect is observed in animals under
controlled laboratory conditions, this tends to corroborate
observations of similar effects in humans.
One commenter objected to MSHA's reference to using animal studies
as a ``check'' on epidemiologic studies. This commenter emphasized that
animal studies provide far more than just corroborative information and
that researches use epidemiologic and animal studies ``* * * to help
understand different aspects of the carcinogenic process.'' \20\ MSHA
does not dispute the utility of animal studies in helping to provide an
understanding of toxicological processes and did not intend to belittle
their importance for this purpose. In fact, MSHA places the bulk of its
discussion of these studies in a section entitled ``Mechanisms of
Toxicity.'' However, MSHA considers the use of animal studies for
corroborating epidemiologic associations to be also important--
especially with respect to ruling out potential confounding effects and
helping to establish causal linkages. Animal studies make possible a
degree of experimental design and statistical rigor that is not
attainable in human studies.
---------------------------------------------------------------------------
\20\ This risk assessment is not limited to cancer effects, but
the commenter's point can be generalized.
---------------------------------------------------------------------------
Other commenters disputed the relevance of at least some animal
data to human risk assessment. For example, The West Virginia Coal
Association indicated the following comments by Dr. Peter Valberg:
* * * scientists and scientific advisory groups have treated the
rat bioassay for inhaled particles as unrepresentative of human
lung-cancer risks. For example, the Presidential/Congressional
Commission on Risk Assessment and Risk Management (``CCRARM'') noted
that the response of rat lungs to inhaled particulate in general is
not likely to be predictive of human cancer risks. More specific to
dpm, the Clean Air Scientific Advisory Committee (``CASAC''), a
peer-review group for the U.S. EPA, has commented on two drafts
(1995 and 1998) of the EPA's Health Assessment Document on Diesel
Exhaust. On both occasions, CASAC emphasized that the data from rats
are not relevant for human risk assessment. Likewise, the Health
Effects Institute also has concluded that rat data should not be
used for assessing human lung cancer risk.
Similarly, the NMA commented that the 1998 CASAC review ``makes it
crystal clear that the rat studies cited by MSHA should not be relied
upon as a legitimate indicators of the carcinogenicity of Dpm in
humans.'' The Nevada Mining Association, endorsing Dr. Valberg's
comments, added:
* * * to the extent that MSHA wishes to rest its case on rat
studies, Dr. Valberg, among others, has impressively demonstrated
that these studies are worthless for human comparison because of
rats' unique and species-specific susceptibility to inhaled
insoluble particles.
However, neither Dr. Valberg nor the Nevada Mining Association provided
evidence that rats' susceptibility to inhaled insoluble particles was
``unique'' and that humans, for example, were not also susceptible to
lung overload at sufficiently high concentrations of fine particles.
Even if (as has apparently been demonstrated) some species (such as
hamsters) do not exhibit susceptibility similar to rats, this by no
means implies that rats are the only species exhibiting such
susceptibility.
These commenters appear at times to be saying that, because studies
of lung cancer in rats are (in the commenters' view) irrelevant to
humans, MSHA should completely ignore all animal studies related to
dpm. To the extent that this was the position advocated, the
commenters' line of reasoning neglects several important points:
1. The animal studies under consideration are not restricted to
studies of lung cancer responses in rats. They include studies of
bioavailability and metabolism as well as studies of immunological and
genotoxic responses in a variety of animal species.
2. The context for the determinations cited by Dr. Valberg was risk
assessment at ambient levels, rather than the much higher dpm levels to
which miners are exposed. The 1995 HEI report to which Dr. Valberg
alludes acknowledged a potential mechanism of lung overload in humans
at dpm concentrations exceeding 500 g/m\3\ (HEI, 1995). Since
miners may concurrently be exposed to concentrations of mineral dusts
significantly exceeding 500 g/m\3\, evidence related to the
consequences of lung overload has special significance for mining
environments.
3. The scientific authorities cited by Dr. Valberg and other
commenters objected to using existing animal studies for quantitative
human risk assessment. MSHA has not proposed doing that. There is an
important distinction between extrapolating results from the rat
studies to human populations and using them to confirm epidemiologic
[[Page 5574]]
findings and to identify and explore potential mechanisms of toxicity.
MSHA by no means ``wishes to rest its case on rat studies,'' and it
has no intention of doing so. MSHA does believe, however, that
judicious consideration of evidence from animal studies is appropriate.
The extent to which MSHA utilizes such evidence to help draw specific
conclusions will be clarified below in connection with those
conclusions.
ii. Reversible Health Effects
Some reported health effects associated with dpm are apparently
reversible--i.e., if the worker is moved away from the source for a few
days, the symptoms dissipate. A good example is eye irritation.
In response to the ANPRM, questions were raised as to whether so-
called ``reversible'' effects can constitute a ``material'' impairment.
For example, a predecessor constituent of the National Mining
Association (NMA) argued that ``it is totally inappropriate for the
agency to set permissible exposure limits based on temporary,
reversible sensory irritation'' because such effects cannot be a
``material'' impairment of health or functional capacity within the
definition of the Mine Act (American Mining Congress, 87-0-21,
Executive Summary, p. 1, and Appendix A).
MSHA does not agree with this categorical view. Although the
legislative history of the Mine Act is silent concerning the meaning of
the term ``material impairment of health or functional capacity,'' and
the issue has not been litigated within the context of the Mine Act,
the statutory language about risk in the Mine Act is similar to that
under the OSH Act. A similar argument was dispositively resolved in
favor of the Occupational Safety and Health Administration (OSHA) by
the 11th Circuit Court of Appeals in AFL-CIO v. OSHA, 965 F.2d 962, 974
(1992).
In that case, OSHA proposed new limits on 428 diverse substances.
It grouped these into 18 categories based upon the primary health
effects of those substances: e.g., neuropathic effects, sensory
irritation, and cancer. (54 FR 2402). Challenges to this rule included
the assertion that a ``sensory irritation'' was not a ``material
impairment of health or functional capacity'' which could be regulated
under the OSH Act. Industry petitioners argued that since irritant
effects are transient in nature, they did not constitute a ``material
impairment.'' The Court of Appeals decisively rejected this argument.
The court noted OSHA's position that effects such as stinging,
itching and burning of the eyes, tearing, wheezing, and other types of
sensory irritation can cause severe discomfort and be seriously
disabling in some cases. Moreover, there was evidence that workers
exposed to these sensory irritants could be distracted as a result of
their symptoms, thereby endangering other workers and increasing the
risk of accidents. (Id. at 974). This evidence included information
from NIOSH about the general consequences of sensory irritants on job
performance, as well as testimony by commenters on the proposed rule
supporting the view that such health effects should be regarded as
material health impairments. While acknowledging that ``irritation''
covers a spectrum of effects, some of which can be minor, OSHA had
concluded that the health effects associated with exposure to these
substances warranted action--to ensure timely medical treatment, reduce
the risks from increased absorption, and avoid a decreased resistance
to infection (Id. at 975). Finding OSHA's evaluation adequate, the
Court of Appeals rejected petitioners' argument and stated the
following:
We interpret this explanation as indicating that OSHA finds that
although minor irritation may not be a material impairment, there is
a level at which such irritation becomes so severe that employee
health and job performance are seriously threatened, even though
those effects may be transitory. We find this explanation adequate.
OSHA is not required to state with scientific certainty or precision
the exact point at which each type of sensory or physical irritation
becomes a material impairment. Moreover, section 6(b)(5) of the Act
charges OSHA with addressing all forms of ``material impairment of
health or functional capacity,'' and not exclusively ``death or
serious physical harm'' or ``grave danger'' from exposure to toxic
substances. See 29 U.S.C. 654(a)(1), 655(c). [Id. at 974].
In its comments on the proposed rule, the NMA claimed that MSHA had
overstated the court's holding. In making this claim, the NMA
attributed to MSHA an interpretation of the holding that MSHA did not
put forth. In fact, MSHA agrees with the NMA's interpretation as stated
in the following paragraph and takes special note of the NMA's
acknowledgment that transitory or reversible effects can sometimes be
so severe as to seriously threaten miners' health and safety:
NMA reads the Court's decision to mean (as it stated) that
``minor irritation may not be a material impairment'' * * * but that
irritation can reach ``a level at which [it] becomes so severe that
employee health and job performance are seriously threatened even
though those effects may be transitory.'' * * * AMC in 1992 and NMA
today are fully in accord with the view of the 11th Circuit that
when health effects, transitory or otherwise, become so ``severe''
as to ``seriously threaten'' a miner's health or job performance,
the materiality threshold has been met.
The NMA, then, apparently agrees with MSHA that sensory irritations
and respiratory symptoms can be so severe that they cross the material
impairment threshold, regardless of whether they are ``reversible.''
Therefore, as MSHA has maintained, such health effects are highly
relevant to this risk assessment--especially since impairments of a
miner's job performance in an underground mining environment could
seriously threaten the safety of both the miner and his or her co-
workers. Sensory irritations may also impede miners' ability to escape
during emergencies.
The NMA, however, went on to emphasize that ``* * * federal appeals
courts have held that `mild discomfort' or even `moderate irritation'
do not constitute `significant' or `material' health effects'':
In International Union v. Pendergrass, 878 F. 2d 389 (1989), the
D.C. Circuit upheld OSHA's formaldehyde standard against a challenge
that it did not adequately protect against significant
noncarcinogenic health effects, even though OSHA had found that, at
the permissible level of exposure, ``20% of workers suffer `mild
discomfort', while 30% more experience `slight discomfort'.'' Id. at
398. Likewise, in Texas Independent Ginners Ass'n. v. Marshall, 630
F, 2d 398 (1980), the Fifth Circuit Court of Appeals held that minor
reversible symptoms do not constitute material impairment unless
OSHA shows that those effects might develop into chronic disease.
Id. at 408-09.
MSHA is fully aware of the distinction that courts have made
between mild discomfort or irritation and transitory health effects
that can seriously threaten a miner's health and safety. MSHA's
position, after reviewing the scientific literature, public testimony,
and comments, is that all of the health effects considered in this risk
assessment fall into the latter category.
iii. Health Effects Associated with PM2.5 in Ambient Air
There have been many studies in recent years designed to determine
whether the mix of particulate matter in ambient air is harmful to
health. The evidence linking particulates in air pollution to health
problems has long been compelling enough to warrant direction from the
Congress to limit the concentration of such particulates (see part II,
section 5 of this preamble). In recent years, the evidence of harmful
effects due to airborne particulates has increased, suggesting that
``fine'' particulates (i.e., particles less than 2.5
[[Page 5575]]
m in diameter) are more strongly associated than ``coarse''
respirable particulates (i.e., particles greater than 2.5 m
but less than 10 m in diameter) with the adverse health
effects observed (EPA, 1996).
MSHA recognizes that there are two difficulties involved in
utilizing the evidence from such studies in assessing risks to miners
from occupational dpm exposures. First, although dpm is a fine
particulate, ambient air also contains fine particulates other than
dpm. Therefore, health effects associated with exposures to fine
particulate matter in air pollution studies are not associated
specifically with exposures to dpm or any other one kind of fine
particulate matter. Second, observations of adverse health effects in
segments of the general population do not necessarily apply to the
population of miners. Since, due to age and selection factors, the
health of miners differs from that of the public as a whole, it is
possible that fine particles might not affect miners, as a group, to
the same degree as the general population.
Some commenters reiterated these two points, recognized by MSHA in
the proposal, without addressing MSHA's stated reasons for including
health effects associated with fine particulates in this risk
assessment. There are compelling reasons why MSHA considered this body
of evidence in this rulemaking.
Since dpm is a type of respirable particle, information about
health effects associated with exposures to respirable particles, and
especially to fine particulate matter, is certainly relevant, even if
difficult to apply directly to dpm exposures. Adverse health effects in
the general population have been observed at ambient atmospheric
particulate concentrations well below the dpm concentrations studied in
occupational settings. The potency of dpm differs from the total fine
particulate found in ambient air. This makes it difficult to establish
a specific exposure-response relationship for dpm that is based on fine
particle results. However, this does not mean that these results should
be ignored in a dpm risk assessment. The available evidence of adverse
health effects associated with fine particulates is still highly
relevant for dpm hazard identification. Furthermore, as shown in
Subsection 3.c.ii of this risk assessment, the fine particle research
findings can be used to construct a rough exposure-response
relationship for dpm, showing significantly increased risks of material
impairment among exposed miners. MSHA's estimates are based on the best
available epidemiologic evidence and show risks high enough to warrant
regulatory action.
Moreover, extensive scientific literature shows that occupational
dust exposures contribute to the development of Chronic Obstructive
Pulmonary Diseases (COPD), thereby compromising the pulmonary reserve
of some miners. Miners experience COPD at a significantly higher rate
than the general population (Becklake 1989, 1992; Oxman 1993; NIOSH
1995). In addition, many miners also smoke tobacco. This places
affected miners in subpopulations specifically identified as
susceptible to the adverse health effects of respirable particle
pollution (EPA, 1996). Some commenters (e.g., MARG) repeated MSHA's
observation that the population of miners differs from the general
population but failed to address MSHA's concern for miners' increased
susceptibility due to COPD incidence and/or smoking habits. The Mine
Act requires that standards ``* * * most adequately assure on the basis
of the best available evidence that no miner suffer material impairment
of health or functional capacity * * *'' (Section 101(a)(6), emphasis
added). This most certainly authorizes MSHA to protect miners who have
COPD and/or smoke tobacco.
MARG also submitted the opinion that if ``* * * regulation of fine
particulate matter is necessary, it [MSHA] should propose a rule
dealing specifically with the issue of concern, rather than a rule that
limits total airborne carbon or arbitrarily singles out diesel exhaust
* * *.'' MSHA's concern is not with ``total airborne carbon'' but with
dpm, which consists mostly of submicrometer airborne carbon. At issue
here, however, are the adverse health effects associated with dpm
exposure. Dpm is a type of fine particulate, and there is no evidence
to suggest that the dpm fraction contributes less than other fine
particulates to adverse health effects linked to exposures in ambient
air.
For this reason, and because miners may be especially susceptible
to fine particle effects, MSHA has concluded, after considering the
public comments, that the body of evidence from air pollution studies
is highly relevant to this risk assessment. The Agency is, therefore,
taking the evidence fully into account.
b. Acute Health Effects
Information pertaining to the acute health effects of dpm includes
anecdotal reports of symptoms experienced by exposed miners, studies
based on exposures to diesel emissions, and studies based on exposures
to particulate matter in the ambient air. These will be discussed in
turn. Subsection 2.a.iii of this risk assessment addressed the
relevance to dpm of studies based on exposures to particulate matter in
the ambient air.
Only the evidence from human studies will be addressed in this
section. Data from genotoxicity studies and studies on laboratory
animals will be discussed later, in Subsection 2.d on mechanisms of
toxicity. Section 3.a and 3.b contain MSHA's interpretation of the
evidence relating dpm exposures to acute health hazards.
i. Symptoms Reported by Exposed Miners
Miners working in mines with diesel equipment have long reported
adverse effects after exposure to diesel exhaust. For example, at the
dpm workshops conducted in 1995, a miner reported headaches and nausea
experienced by several operators after short periods of exposure (dpm
Workshop; Mt. Vernon, IL, 1995). Another miner reported that smoke from
poorly maintained equipment, or from improper fuel use, irritates the
eyes, nose, and throat. ``We've had people sick time and time again * *
* at times we've had to use oxygen for people to get them to come back
around to where they can feel normal again.'' (dpm Workshop; Beckley,
WV, 1995). Other miners (dpm Workshops; Beckley, WV, 1995; Salt Lake
City, UT, 1995), reported similar symptoms in the various mines where
they worked.
At the 1998 public hearings on MSHA's proposed dpm rule for coal
mines, one miner, with work experience in a coal mine utilizing diesel
haulage equipment at the face, testified that
* * * unlike many, I have not experienced the headaches, the
watering of the eyes, the cold-like symptoms and walking around in
this cloud of smoke. Maybe it's because of the maintenance programs.
Maybe it's because of complying with ventilation. * * * after 25
years, I have not shown any effects. [SLC, 1998]
Other miners working at dieselized coal mines testified at those
hearings that they had personally experienced eye irritation and/or
respiratory ailments immediately after exposure to diesel exhaust, and
they attributed these ailments to their exposure. For example, one
miner attributed a case of pneumonia to a specific episode of unusually
high exposure. (Birm., 1998) The safety and training manager of the
mining company involved noted that ``there had been a problem
recognized in review with that exhaust system on that particular piece
of equipment'' and that the pneumonia may have
[[Page 5576]]
developed due to ``idiosyncracy of his lungs that respond to any type
of a respiratory irritant.'' The manager suggested that this incident
should not be generalized to other situations but provided no evidence
that the miner's lungs were unusually susceptible to irritation.\21\
---------------------------------------------------------------------------
\21\ MSHA realizes the incidents related in this subsection are
anecdotal and draws no statistical conclusions from them. Since they
pertain to specific experiences, however, they can be useful in
identifying a potential hazard.
---------------------------------------------------------------------------
Another miner, who had worked at the same underground mine before
and after diesel haulage equipment was introduced, indicated that he
and his co-workers began experiencing acute symptoms after the diesel
equipment was introduced. This miner suggested that these effects were
linked to exposure, and referring to a co-worker stated:
* * * had respiratory problems, after * * * diesel equipment was
brought into that mine--he can take off for two weeks vacation, come
back--after that two weeks, he felt pretty good, his respiratory
problems would straighten up, but at the very instant that he gets
back in the face of diesel-powered equipment, it starts up again,
his respiratory problems will flare up again, coughing, sore throat,
numerous problems in his chest. (Birm., 1998).
Several other underground miners asserted there was a correlation
between diesel exposure levels and the frequency and/or intensity of
respiratory symptoms, eye irritations, and chest ailments. One miner,
for example, stated:
I've experienced [these symptoms] myself. * * * other miners
experience the same kind of distresses * * * Some of the stresses
you actually can feel--you don't need a gauge to measure this--your
burning eyes, nose, throat, your chest irritation. The more you're
exposed to, the higher this goes. This includes headaches and nausea
and some lasting congestion, depending on how long you've been
exposed per shift or per week.
The men I represent have experienced more cold-like symptoms,
especially over the past, I would say, eight to ten years, when
diesel has really peaked and we no longer really use much of
anything else. [SLC, 1998]
Kahn et al. (1988) conducted a study of the prevalence and
seriousness of such complaints, based on United Mine Workers of America
records and subsequent interviews with the miners involved. The review
involved reports at five underground coal mines in Utah and Colorado
between 1974 and 1985. Of the 13 miners reporting symptoms: 12 reported
mucous membrane irritation, headache and light-headiness; eight
reported nausea; four reported heartburn; three reported vomiting and
weakness, numbness, and tingling in extremities; two reported chest
tightness; and two reported wheezing (although one of these complained
of recurrent wheezing without exposure). All of these incidents were
severe enough to result in lost work time due to the symptoms (which
subsided within 24 to 48 hours).
In comments submitted for this rulemaking, the NMA pointed out, as
has MSHA, that the evidence presented in this subsection is anecdotal.
The NMA, further, suggested that the cited article by Kahn et al.
typified this kind of evidence in that it was ``totally devoid of any
correlation to actual exposure levels.'' A lack of concurrent exposure
measurements is, unfortunately, not restricted to anecdotal evidence;
and MSHA must base its evaluation on the available evidence. MSHA
recognizes the scientific limitations of anecdotal evidence and has,
therefore, compiled and considered it separately from more formal
evidence. MSHA nevertheless considers such evidence potentially
valuable for identifying acute health hazards, with the understanding
that confirmation requires more rigorous investigation.\22\
With respect to the same article (Kahn et al., 1988), and
notwithstanding the NMA's claim that the article was totally devoid of
any correlation to exposure levels, the NMA also stated that MSHA:
* * * neglects to include in the preamble the article's
description of the conditions under which the ``overexposures''
occurred, e.g., ``poor engine maintenance, poor maintenance of
emission controls, prolonged idling of machinery, engines pulling
heavy loads, use of equipment during times when ventilation was
disrupted (such as during a move of longwall machinery), use of
several pieces of equipment exhausting into the fresh-air intake,
and use of poor quality fuel.
---------------------------------------------------------------------------
\22\ MSHA sees potential value in anecdotal evidence when it
relates to immediate experiences. MSHA regards anecdotal evidence to
be less appropriate for identifying chronic health effects, since
chronic effects cannot readily be linked to specific experiences.
Accordingly, this risk assessment places little weight on anecdotal
evidence for the chronic health hazards considered.
---------------------------------------------------------------------------
The NMA asserted that these conditions, cited in the article, ``have
been addressed by MSHA's final standards for diesel equipment in
underground coal mines issued October 25, 1996.''\23\ Furthermore,
despite its reservations about anecdotal evidence:
---------------------------------------------------------------------------
\23\ The 1996 regulations to which the NMA was referring do not
apply to M/NM mines.
NMA is mindful of the testimony of several miners in the coal
proceeding who complained of transient irritation owing to exposure
to diesel exhaust. * * * the October 1996 regulations together with
the phased-in introduction of catalytic converters on all outby
equipment and the introduction of such devices on permissible
equipment when such technology becomes available will address the
---------------------------------------------------------------------------
complaints raised by the miners.
The NMA provided no evidence, however, that elimination of the
conditions described by Kahn et al., or implementation of the 1996
diesel regulations for coal mines, would reduce dpm levels sufficiently
to prevent the sensory irritations and respiratory symptoms described.
MSHA completed an analysis of the impact of the 1996 diesel regulations
for underground coal mines (See Part II, Section 7). We do expect that
the concentrations of diesel emissions at the section loading point and
during longwall moves will be reduced as these provisions are fully
implemented. These dpm levels, though reduced, are still above the
exposures expected to cause sensory irritations and respiratory
symptoms (See Section 3(d)(5)). MSHA did not explicitly consider the
risks to miners of a working lifetime of dpm exposure at very high
levels, nor the actions that could be taken to specifically reduce dpm
exposure levels in underground coal mines when developing the 1996
underground coal diesel regulations. It was understood that the agency
would be taking a separate look at the health risks of dpm exposure. In
addition, the NMA did not provide evidence that these are the only
conditions under which complaints of sensory irritations and
respiratory symptoms occur, or explain why eliminating them would
reduce the need to prevent excessive exposures under other conditions.
In the proposal for the present rule, MSHA requested additional
information about such effects from medical personnel who have treated
miners. IMC Global submitted letters from four healthcare practitioners
in Carlsbad, NM, including three physicians. None of these
practitioners attributed any cases of respiratory problems or other
acute symptoms to dpm exposure. Three of the four practitioners noted
that they had observed respiratory symptoms among exposed miners but
attributed these symptoms to chronic lung conditions, smoking, or other
factors. One physician stated that ``[IMC Global], which has used
diesel equipment in its mining operations for over 20 years, has never
experienced a single case of injury or illness caused by exposures to
diesel particulates.''
ii. Studies Based on Exposures to Diesel Emissions
Several experimental and statistical studies have been conducted to
investigate acute effects of exposure to
[[Page 5577]]
diesel emissions. These more formal studies provide data that are more
scientifically rigorous than the anecdotal evidence presented in the
preceding subsection. Unless otherwise indicated, diesel exhaust
exposures were determined qualitatively.
In a clinical study (Battigelli, 1965), volunteers were exposed to
three concentrations of diluted diesel exhaust and then evaluated to
determine the effects of exposure on pulmonary resistance and the
degree of eye irritation. The investigators stated that ``levels
utilized for these controlled exposures are comparable to realistic
values such as those found in railroad shops.'' No statistically
significant change in pulmonary function was detected, but exposure for
ten minutes to diesel exhaust diluted to the middle level produced
``intolerable'' irritation in some subjects while the average
irritation score was midway between ``some'' irritation and a
``conspicuous but tolerable'' irritation level. Diluting the
concentration by 50% substantially reduced the irritation. At the
highest exposure level, more than 50 percent of the volunteers
discontinued the experiment before 10 minutes because of
``intolerable'' eye irritation.
A study of underground iron ore miners exposed to diesel emissions
found no difference in spirometry measurements taken before and after a
work shift (Jorgensen and Svensson 1970). Similarly, another study of
coal miners exposed to diesel emissions detected no statistically
significant relationship between exposure and changes in pulmonary
function (Ames et al. 1982). However, the authors noted that the lack
of a statistically significant result might be due to the low
concentrations of diesel emissions involved.
Gamble et al. (1978) observed decreases in pulmonary function over
a single shift in salt miners exposed to diesel emissions. Pulmonary
function appeared to deteriorate in relation to the concentration of
diesel exhaust, as indicated by NO2; but this effect was
confounded by the presence of NO2 due to the use of
explosives.
Gamble et al. (1987a) assessed response to diesel exposure among
232 bus garage workers by means of a questionnaire and before- and
after-shift spirometry. No significant relationship was detected
between diesel exposure and change in pulmonary function. However,
after adjusting for age and smoking status, a significantly elevated
prevalence of reported symptoms was found in the high-exposure group.
The strongest associations with exposure were found for eye irritation,
labored breathing, chest tightness, and wheeze. The questionnaire was
also used to compare various acute symptoms reported by the garage
workers and a similar population of workers at a lead acid battery
plant who were not exposed to diesel fumes. The prevalence of work-
related eye irritations, headaches, difficult or labored breathing,
nausea, and wheeze was significantly higher in the diesel bus garage
workers, but the prevalence of work-related sneezing was significantly
lower.
Ulfvarson et al. (1987) studied effects over a single shift on 47
stevedores exposed to dpm at particle concentrations ranging from 130
/m\3\ to 1000 /m\3\. Diesel particulate
concentrations were determined by collecting particles on glass fiber
filters of unspecified efficiency. A statistically significant loss of
pulmonary function was observed, with recovery after 3 days of no
occupational exposure.
To investigate whether removal of the particles from diesel exhaust
might reduce the ``acute irritative effect on the lungs'' observed in
their earlier study, Ulfvarson and Alexandersson (1990) compared
pulmonary effects in a group of 24 stevedores exposed to unfiltered
diesel exhaust to a group of 18 stevedores exposed to filtered exhaust,
and to a control group of 17 occupationally unexposed workers. The
filters used were specially constructed from 144 layers of glass fiber
with ``99.97% degrees of retention of dioctylphthalate mist with
particle size 0.3 m.'' Workers in all three groups were
nonsmokers and had normal spirometry values, adjusted for sex, age, and
height, prior to the experimental workshift.
In addition to confirming the earlier observation of significantly
reduced pulmonary function after a single shift of occupational
exposure, the study found that the stevedores in the group exposed only
to filtered exhaust had 50-60% less of a decline in forced vital
capacity (FVC) than did those stevedores who worked with unfiltered
equipment. Similar results were observed for a subgroup of six
stevedores who were exposed to filtered exhaust on one shift and
unfiltered exhaust on another. No loss of pulmonary function was
observed for the unexposed control group. The authors suggested that
these results ``support the idea that the irritative effect of diesel
exhausts [sic] to the lungs is the result of an interaction between
particles and gaseous components and not of the gaseous components
alone.'' They concluded that ``* * * it should be a useful practice to
filter off particles from diesel exhausts in work places even if
potentially irritant gases remain in the emissions'' and that ``removal
of the particulate fraction by filtering is an important factor in
reducing the adverse effect of diesel exhaust on pulmonary function.''
Rudell et al. (1996) carried out a series of double-blind
experiments on 12 healthy, non-smoking subjects to investigate whether
a particle trap on the tailpipe of an idling diesel engine would reduce
acute effects of diesel exhaust, compared with exposure to unfiltered
exhaust. Symptoms associated with exposure included headache,
dizziness, nausea, tiredness, tightness of chest, coughing, and
difficulty in breathing. The most prominent symptoms were found to be
irritation of the eyes and nose, and a sensation of unpleasant smell.
Among the various pulmonary function tests performed, exposure was
found to result in significant changes only as measured by increased
airway resistance and specific airway resistance. The ceramic wall flow
particle trap reduced the number of particles by 46 percent, but
resulted in no significant attenuation of symptoms or lung function
effects. The authors concluded that diluted diesel exhaust caused
increased irritant symptoms of the eyes and nose, unpleasant smell, and
bronchoconstriction, but that the 46-percent reduction in median
particle number concentration observed was not sufficient to protect
against these effects in the populations studied.
Wade and Newman (1993) documented three cases in which railroad
workers developed persistent asthma following exposure to diesel
emissions while riding immediately behind the lead engines of trains
having no caboose. None of these workers were smokers or had any prior
history of asthma or other respiratory disease. Asthma diagnosis was
based on symptoms, pulmonary function tests, and measurement of airway
hyperreactivity to methacholine or exercise.
Although MSHA is not aware of any other published report directly
relating diesel emissions exposures to the development of asthma, there
have been a number of recent studies indicating that dpm exposure can
induce bronchial inflammation and respiratory immunological allergic
responses in humans. Studies published through 1997 are reviewed in
Peterson and Saxon (1996) and Diaz-Sanchez (1997).
Diaz-Sanchez et al. (1994) challenged healthy human volunteers by
spraying
[[Page 5578]]
300 g dpm into their nostrils.\24\ Immunoglobulin E (IgE)
binds to mast cells where it binds antigen leading to secretion of
biologically active amines (e.g., histamine) causing dilation and
increased permeability of blood vessels. These amines are largely
responsible for clinical manifestations of such allergic reactions as
hay fever, asthma, and hives. Enhanced IgE levels were found in nasal
washes in as little as 24 hours, with peak production observed 4 days
after the dpm was administered.\25\ No effect was observed on the
levels of other immunoglobulin proteins. The selective enhancement of
local IgE production was demonstrated by a dramatic increase in IgE-
secreting cells. The authors suggested that dpm may augment human
allergic disease responses by enhancing the production of IgE
antibodies. Building on these results, Diaz-Sanchez et al. (1996)
measured cytokine production in nasal lavage cells from healthy human
volunteers challenged with 150 g dpm sprayed into each
nostril. Based on the responses observed, including a broad increase in
cytokine production, along with the results of the 1994 paper, the
authors concluded that dpm exposure contributes to enhanced local IgE
production and thus plays a role in allergic airway disease.
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\24\ Assuming that a working miner inhales approximately 1.25
m\3\ of air per hour, this dose corresponds to a 1-hour exposure at
a dpm concentration of 240 g/m\3\.
\25\ IgE is one of five types of immunoglobulin, which are
proteins produced in response to allergens. Cytokine (mentioned
later) is a substance involved in regulating IgE production.
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Salvi et al. (1999) exposed healthy human volunteers to diluted
diesel exhaust at a dpm concentration of 300 g/m\3\ for one
hour with intermittent exercise. Although there were no changes in
pulmonary function, there were significant increases in various markers
of allergic response in airway lavage fluid. Bronchial biopsies
obtained six hours after exposure also showed significant increases in
markers of immunologic response in the bronchial tissue. Significant
increases in other markers of immunologic response were also observed
in peripheral blood following exposure. A marked cellular inflammatory
response in the airways was reported. The authors concluded that ``at
high ambient concentrations, acute short-term DE [diesel exhaust]
exposure produces a well-defined and marked systemic and pulmonary
inflammatory response in healthy human volunteers, which is
underestimated by standard lung function measurements.''
iii. Studies Based on Exposures to Particulate Matter in Ambient Air
Due to an incident in Belgium's industrial Meuse Valley, it was
known as early as the 1930s that large increases in particulate air
pollution, created by winter weather inversions, could be associated
with large simultaneous increases in mortality and morbidity. More than
60 persons died from this incident, and several hundred suffered
respiratory problems. The mortality rate during the episode was more
than ten times higher than normal, and it was estimated that over 3,000
sudden deaths would occur if a similar incident occurred in London.
Although no measurements of pollutants in the ambient air during the
episode are available, high PM levels were obviously present (EPA,
1996).
A significant elevation in particulate matter (along with
SO2 and its oxidation products) was measured during a 1948
incident in Donora, PA. Of the Donora population, 42.7 percent
experienced some acute adverse health effect, mainly due to irritation
of the respiratory tract. Twelve percent of the population reported
difficulty in breathing, with a steep rise in frequency as age
progressed to 55 years (Schrenk, 1949).
Approximately as projected by Firket (1931), an estimated 4,000
deaths occurred in response to a 1952 episode of extreme air pollution
in London. The nature of these deaths is unknown, but there is clear
evidence that bronchial irritation, dyspnea, bronchospasm, and, in some
cases, cyanosis occurred with unusual prevalence (Martin, 1964).
These three episodes ``left little doubt about causality in regard
to the induction of serious health effects by very high concentrations
of particle-laden air pollutant mixtures'' and stimulated additional
research to characterize exposure-response relationships (EPA, 1996).
Based on several analyses of the 1952 London data, along with several
additional acute exposure mortality analyses of London data covering
later time periods, the U.S. Environmental Protection Agency (EPA)
concluded that increased risk of mortality is associated with exposure
to combined particulate and SO2 levels in the range of 500-
1000 g/m3. The EPA also concluded that relatively
small, but statistically significant increases in mortality risk exist
at particulate (but not SO2) levels below 500 g/
m3, with no indications of a specific threshold level yet
indicated at lower concentrations (EPA, 1986).
Subsequently, between 1986 and 1996, increasingly sophisticated
techniques of particulate measurement and statistical analysis have
enabled investigators to address these questions more quantitatively.
The studies on acute effects carried out since 1986 are reviewed in the
1996 EPA Air Quality Criteria for Particulate Matter, which forms the
basis for the discussion below (EPA, 1996).
At least 21 studies have been conducted that evaluate associations
between acute mortality and morbidity effects and various measures of
fine particulate levels in the ambient air. These studies are
identified in Tables III-2 and III-3. Table III-2 lists 11 studies that
measured primarily fine particulate matter using filter-based optical
techniques and, therefore, provide mainly qualitative support for
associating observed effects with fine particles. Table III-3 lists
quantitative results from 10 studies that reported gravimetric
measurements of either the fine particulate fraction or of components,
such as sulfates, that serve as indicators or surrogates of fine
particulate exposures.
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A total of 38 studies examining relationships between short-term
particulate levels and increased mortality, including nine with fine
particulate measurements, were published between 1988 and 1996 (EPA,
1996). Most of these found statistically significant positive
associations. Daily or several-day elevations of particulate
concentrations, at average levels as low as 18-58 g/
m3, were associated with increased mortality, with stronger
relationships observed in those with preexisting respiratory and
cardiovascular disease. Overall, these studies suggest that an increase
of 50 g/m3 in the 24-hour average of
PM10 is associated with a 2.5 to 5-percent increase in the
risk of mortality in the general population, excluding accidents,
suicides, and homicides. Based on Schwartz et al. (1996), the relative
risk of mortality in the general population increases by about 2.6 to
5.5 percent per 25 g/m3 of fine particulate
(PM2.5) (EPA, 1996). More specifically, Schwartz et al.
(1996) reported significantly elevated risks of mortality due to
pneumonia, chronic obstructive pulmonary disease (COPD), and ischemic
heart disease (IHD). For these three causes of death, the estimated
increases in risk per incremental increase of 10 g/
m3 in the concentration of PM2.5 were 4.0
percent, 3.3 percent, and 2.1 percent, respectively. Each of these
three results was statistically significant at a 95-percent confidence
level.
A total of 22 studies were published on associations between short-
term particulate levels and hospital admissions, outpatient visits, and
emergency room visits for respiratory disease, Chronic Obstructive
Pulmonary Disease (COPD), pneumonia, and heart disease (EPA, 1996).
Fifteen of these studies were focused on the elderly. Of the seven that
dealt with all ages (or in one case, persons less than 65 years old),
all showed positive results. All of the five studies relating fine
particulate measurements to increased hospitalization, listed in Tables
III-2 and III-3, dealt with general age populations and showed
statistically significant associations. The estimated increase in risk
ranges from 3 to 16 percent per 25 g/m3 of fine
particulate. Overall, these studies are indicative of acute morbidity
effects being related to fine particulate matter and support the
mortality findings.
Most of the 14 published quantitative studies on ambient
particulate exposures and acute respiratory diseases were restricted to
children (EPA, 1996, Table 12-12). Although they generally showed
positive associations, and may be of considerable biological relevance,
evidence of toxicity in children is not necessarily applicable to
adults. The few studies on adults have not produced statistically
significant evidence of a relationship.
Thirteen studies since 1982 have investigated associations between
ambient particulate levels and loss of pulmonary function (EPA, 1996,
Table 12-13). In general, these studies suggest a short term effect,
especially in symptomatic groups such as asthmatics, but most were
carried out on children only. In a study of adults with mild COPD, Pope
and Kanner (1993) found a 29 10 ml decrease in 1-second
Forced Expiratory Volume (FEV1) per 50 g/
m3 increase in PM10, which is similar in
magnitude to the change generally observed in the studies on children.
In another study of adults, with PM10 ranging from 4 to 137
g/m3, Dusseldorp et al. (1995) found 45 and 77 ml/
sec decreases, respectively, for evening and morning Peak Expiratory
Flow Rate (PEFR) per 50 g/m3 increase in
PM10 (EPA, 1996). In the only study carried out on adults
that specifically measured fine particulate (PM2.5), Perry
et al. (1983) did not detect any association of exposure with loss of
pulmonary function. This study, however, was conducted on only 24
adults (all asthmatics) exposed at relatively low concentrations of
PM2.5 and, therefore, had very little power to detect any
such association.
c. Chronic Health Effects
During the 1995 dpm workshops, miners reported observable adverse
health effects among those who have worked a long time in dieselized
mines. For example, a miner (dpm Workshop; Salt Lake City, UT, 1995),
stated that miners who work with diesel ``have spit up black stuff
every night, big black--what they call black (expletive) * * * [they]
have the congestion every night * * * the 60-year-old man working there
40 years.'' Similarly, in comments submitted in response to MSHA's
proposed dpm regulations, several miners reported cancers and chronic
respiratory ailments they attributed to dpm exposure.
Scientific investigation of the chronic health effects of dpm
exposure includes studies based specifically on exposures to diesel
emissions and studies based more generally on exposures to fine
particulate matter in the ambient air. Only the evidence from human
studies will be addressed in this section of the risk assessment. Data
from genotoxicity studies and studies on laboratory animals will be
discussed later, in Subsection 2.d on mechanisms of toxicity.
Subsection 3.a(iii) contains MSHA's interpretation of the evidence
relating dpm exposures to one chronic health hazard: lung cancer.
i. Studies Based on Exposures to Diesel Emissions
The discussion will (1) summarize the epidemiologic literature on
chronic effects other than cancer, and then (2) concentrate on the
epidemiology of cancer in workers exposed to dpm.
(1) Chronic Effects Other Than Cancer
A number of epidemiologic studies have investigated relationships
between diesel exposure and the risk of developing persistent
respiratory symptoms (i.e., chronic cough, chronic phlegm, and
breathlessness) or measurable loss in lung function. Three studies
involved coal miners (Reger et al., 1982; Ames et al., 1984; Jacobsen
et al., 1988); four studies involved metal and nonmetal miners
(Jorgenson & Svensson, 1970; Attfield, 1979; Attfield et al., 1982;
Gamble et al., 1983). Three studies involved other groups of workers--
railroad workers (Battigelli et al., 1964), bus garage workers (Gamble
et al., 1987), and stevedores (Purdham et al., 1987).
Reger et al. (1982) examined the prevalence of respiratory symptoms
and the level of pulmonary function among more than 1,600 underground
and surface U.S. coal miners, comparing results for workers (matched
for smoking status, age, height, and years worked underground) at
diesel and non-diesel mines. Those working at underground dieselized
mines showed some increased respiratory symptoms and reduced lung
function, but a similar pattern was found in surface miners who
presumably would have experienced less diesel exposure. Miners in the
dieselized mines, however, had worked underground for less than 5 years
on average.
In a study of 1,118 U.S. coal miners, Ames et al. (1984) did not
detect any pattern of chronic respiratory effects associated with
exposure to diesel emissions. The analysis, however, took no account of
baseline differences in lung function or symptom prevalence, and the
authors noted a low level of exposure to diesel-exhaust contaminants in
the exposed population.
In a cohort of 19,901 British coal miners investigated over a 5-
year period, Jacobsen et al. (1988) found increased work absence due to
self-reported chest illness in underground workers exposed to diesel
exhaust, as compared to surface workers, but found
[[Page 5582]]
no correlation with their estimated level of exposure.
Jorgenson & Svensson (1970) found higher rates of chronic
productive bronchitis, for both smokers and nonsmokers, among Swedish
underground iron ore miners exposed to diesel exhaust as compared to
surface workers at the same mine. No significant difference was found
in spirometry results.
Using questionnaires collected from 4,924 miners at 21 U.S. metal
and nonmetal mines, Attfield (1979) evaluated the effects of exposure
to silica dust and diesel exhaust and obtained inconclusive results
with respect to diesel exposure. For both smokers and non-smokers,
miners occupationally exposed to diesel for five or more years showed
an elevated prevalence of persistent cough, persistent phlegm, and
shortness of breath, as compared to miners exposed for less than five
years, but the differences were not statistically significant. Four
quantitative indicators of diesel use failed to show consistent trends
with symptoms and lung function.
Attfield et al. (1982) reported on a medical surveillance study of
630 white male miners at 6 U.S. potash mines. No relationships were
found between measures of diesel use or exposure and various health
indices, based on self-reported respiratory symptoms, chest
radiographs, and spirometry.
In a study of U.S. salt miners, Gamble and Jones (1983) observed
some elevation in cough, phlegm, and dyspnea associated with mines
ranked according to level of diesel exhaust exposure. No association
between respiratory symptoms and estimated cumulative diesel exposure
was found after adjusting for differences among mines. However, since
the mines varied widely with respect to diesel exposure levels, this
adjustment may have masked a relationship.
Battigelli et al. (1964) compared pulmonary function and complaints
of respiratory symptoms in 210 U.S. railroad repair shop employees,
exposed to diesel for an average of 10 years, to a control group of 154
unexposed railroad workers. Respiratory symptoms were less prevalent in
the exposed group, and there was no difference in pulmonary function;
but no adjustment was made for differences in smoking habits.
In a study of workers at four diesel bus garages in two U.S.
cities, Gamble et al. (1987b) investigated relationships between job
tenure (as a surrogate for cumulative exposure) and respiratory
symptoms, chest radiographs, and pulmonary function. The study
population was also compared to an unexposed control group of workers
with similar socioeconomic background. After indirect adjustment for
age, race, and smoking, the exposed workers showed an increased
prevalence of cough, phlegm, and wheezing, but no association was found
with job tenure. Age- and height-adjusted pulmonary function was found
to decline with duration of exposure, but was elevated on average, as
compared to the control group. The number of positive radiographs was
too small to support any conclusions. The authors concluded that the
exposed workers may have experienced some chronic respiratory effects.
Purdham et al. (1987) compared baseline pulmonary function and
respiratory symptoms in 17 exposed Canadian stevedores to a control
group of 11 port office workers. After adjustment for smoking, there
was no statistically significant difference in self-reported
respiratory symptoms between the two groups. However, after adjustment
for smoking, age, and height, exposed workers showed lower baseline
pulmonary function, consistent with an obstructive ventilatory defect,
as compared to both the control group and the general metropolitan
population.
In a review of these studies, Cohen and Higgins (1995) concluded
that they did not provide strong or consistent evidence for chronic,
nonmalignant respiratory effects associated with occupational exposure
to diesel exhaust. These reviewers stated, however, that ``several
studies are suggestive of such effects * * * particularly when viewed
in the context of possible biases in study design and analysis.'' Glenn
et al (1983) noted that the studies of chronic respiratory effects
carried out by NIOSH researchers in coal, salt, potash, and trona mines
all ``revealed an excess of cough and phlegm in the diesel exposed
group.'' IPCS (1996) noted that ``[a]lthough excess respiratory
symptoms and reduced pulmonary function have been reported in some
studies, it is not clear whether these are long-term effects of
exposure.'' Similarly, Morgan et al. (1997) concluded that while there
is ``some evidence that the chronic inhalation of diesel fumes leads to
the development of cough and sputum, that is chronic bronchitis, it is
usually impossible to show a cause and effect relationship * * *.''
MSHA agrees that these dpm studies are not conclusive but considers
them to be suggestive of adverse chronic, non-cancerous respiratory
effects.
(2) Cancer
Because diesel exhaust has long been known to contain carcinogenic
compounds (e.g., benzene in the gaseous fraction and benzopyrene and
nitropyrene in the dpm fraction), a great deal of research has been
conducted to determine if occupational exposure to diesel exhaust
actually results in an increased risk of cancer. Evidence that exposure
to dpm increases the risk of developing cancer comes from three kinds
of studies: human studies, genotoxicity studies, and animal studies. In
this risk assessment, MSHA has placed the most weight on evidence from
the human epidemiologic studies and views the genotoxicity and animal
studies as lending support to the epidemiologic evidence.
In the epidemiologic studies, it is generally impossible to
disassociate exposure to dpm from exposure to the gasses and vapors
that form the remainder of whole diesel exhaust. However, the animal
evidence shows no significant increase in the risk of lung cancer from
exposure to the gaseous fraction alone (Heinrich et al., 1986, 1995;
Iwai et al., 1986; Brightwell et al., 1986). Therefore, dpm, rather
than the gaseous fraction of diesel exhaust, is usually assumed to be
the agent associated with any excess prevalence of lung cancer observed
in the epidemiologic studies. Subsection 2.d of this risk assessment
contains a summary of evidence supporting this assumption.
(a) Lung Cancer
MSHA evaluated 47 epidemiologic studies examining the prevalence of
lung cancer within groups of workers occupationally exposed to dpm.
This includes four studies not included in MSHA's risk assessment as
originally proposed.\26\ The earliest of these studies was published in
1957 and the latest in 1999. The most recent published reviews of these
studies are by Mauderly (1992), Cohen and Higgins (1995), Muscat and
Wynder (1995), IPCS (1996), Stober and Abel (1996), Cox (1997), Morgan
et al. (1997), Cal-EPA (1998), ACGIH (1998), and U.S. EPA (1999). In
response to both the ANPRM and the 1998 proposals, several commenters
also provided MSHA with
[[Page 5583]]
their own reviews of many of these studies. In arriving at its
conclusions, MSHA considered all of these reviews, including those of
the commenters, as well as the 47 source studies available to MSHA.
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\26\ One of these studies (Christie et al., 1995) was cited in
the discussion on mechanisms of toxicity but not considered in
connection with studies involving dpm exposures. Several commenters
advocated that it be considered. The other three were published in
1997 or later. Johnston et al. (1997) was introduced to these
proceedings in 64 FR 7144. Saverin et al. (1999) is the published
English version of a Germany study submitted as part of the public
comments by NIOSH on May 27, 1999. The remaining study is Bruske-
Hohlfeld et al. (1999).
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In addition, MSHA relied on two comprehensive statistical ``meta-
analyses'' \27\ of the epidemiologic literature: Lipsett and Campleman
(1999) thru \28\ and Bhatia et al. (1998).\29\ These meta-analyses,
which weight, combine, and analyze data from the various epidemiologic
studies, were themselves the subject of considerable public comment and
are discussed primarily in Subsection 3.a.iii of this risk assessment.
The present section tabulates results of the studies and addresses
their individual strengths and weaknesses. Interpretation and
evaluation of the collective evidence, including discussion of
potential publication bias or any other systematic biases, is deferred
to Subsection 3.a.iii.
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\27\ MSHA restricts the term ``meta-analysis'' to formal,
statistical analyses of the pooled data taken from several studies.
Some commenters (and Cox in the article itself) referred to the
review by Cox (op.cit.) as a meta-analysis. Although this article
seeks to identify characteristics of the individual studies that
might account for the general pattern of results, it performs no
statistical analysis on the pooled epidemiologic data. For this
reason, MSHA does not regard the Cox article as a meta-analysis in
the same sense as the two studies so identified. MSHA does, however,
recognize that the Cox article evaluates and rejects the collective
evidence for causality, based on the common characteristics
identified. In that context, Cox's arguments and conclusions are
addressed in Subsection 3.a.iii. Cox also presents a statistical
analysis of data from one of the studies, and that portion of the
article is considered here, along with his observations about other
individual studies.
\28\ MSHA's risk assessment as originally proposed cited an
unpublished version, attributed to Lipsett and Alexexeff (1998), of
essentially the same meta-analysis. Both the 1999 and 1998 versions
are now in the public record.
\29\ Silverman (1998) reviewed the meta-analysis by Bhatia et
al. (op cit.) and discussed, in general terms, the body of available
epidemiologic evidence on which it is based. Some commenters stated
that MSHA had not sufficiently considered Silverman's views on the
limitations of this evidence. MSHA has thoroughly considered these
views and addresses them in Subsection 3.a.(iii).
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Tables III-4 (27 cohort studies) and III-5 (20 case-control
studies) identify all 47 known epidemiologic studies that MSHA
considers relevant to an assessment of lung cancer risk associated with
dpm exposure.\30\ These tables include, for each of the 47 studies
listed, a brief description of the study and its findings, the method
of exposure assessment, and comments on potential biases or other
limitations. Presence or absence of an adjustment for smoking habits is
highlighted, and adjustments for other potentially confounding factors
are indicated when applicable. Although MSHA constructed these tables
based primarily on its own reading of the 48 source publications, the
tables also incorporate strengths and weaknesses noted in the
literature reviews and/or in the public comments submitted.
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\30\ For simplicity, the epidemiologic studies considered here
are placed into two broad categories. A cohort study compares the
health of persons having different exposures, diets, etc. A case-
control study starts with two defined groups known to differ in
health and compares their exposure characteristics.
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Some degree of association between occupational dpm exposure and an
excess prevalence of lung cancer was reported in 41 of the 47 studies
reviewed by MSHA: 22 of the 27 cohort studies and 19 of the 20 case-
control studies. Despite some commenters' use of conflicting
terminology, which will be addressed below, MSHA refers to these 41
studies as ``positive.'' The 22 positive cohort studies in Table III-4
are identified as those reporting a relative risk (RR) or standardized
mortality ratio (SMR) exceeding 1.0. The 19 positive case-control
studies in Table III-5 are identified as those reporting an RR or odds
ratio (OR) exceeding 1.0. A study does not need to be statistically
significant (at the 0.05 level) or meet all criteria described, in
order to be considered a ``positive'' study. The six remaining studies
were entirely negative: they reported a deficit in the prevalence of
lung cancer among exposed workers, relative to whatever population was
used in the study as a basis for comparison. These six negative studies
are identified as those reporting no relative risk (RR), standard
mortality ratio (SMR), or odds ratio (OR) greater than 1.0.\31\
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\31\ The six entirely negative studies are: Kaplan (1959);
DeCoufle et al. (1977); Waller (1981); Edling et al. (1987); Bender
et al. (1989); Christie et al. (1995).
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MSHA recognizes that these 47 studies are not of equal importance
for determining whether dpm exposure leads to an increased risk of lung
cancer. Some of the studies provide much better evidence than others.
Furthermore, since no epidemiologic study can be perfectly controlled,
the studies exhibit various strengths and weaknesses, as described by
both this risk assessment and a number of commenters. Several
commenters, and some of the reviewers cited above, focused on the
weaknesses and argued that none of the existing studies is conclusive.
MSHA, in accordance with other reviewers and commenters, maintains: (1)
That the weaknesses identified in both negative and positive studies
mainly cause underestimation of risks associated with high occupational
dpm exposure; (2) that it is legitimate to base conclusions on the
combined weight of all available evidence and that, therefore, it is
not necessary for any individual study to be conclusive; and (3) that
even though the 41 positive studies vary a great deal in strength,
nearly all of them contribute something to the weight of positive
evidence.
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(i) Evaluation Criteria
Several commenters contended that MSHA paid more attention to
positive studies than to negative ones and indicated that MSHA had not
sufficiently explained its reasons for discounting studies they
regarded as providing negative evidence. MSHA used five principal
criteria to evaluate the strengths and weaknesses of the individual
studies:
(1) power of the study to detect an exposure effect;
(2) composition of comparison groups;
(3) exposure assessment;
(4) statistical significance; and
(5) potential confounders.
These criteria are consistent with those proposed by the HEI Diesel
Epidemiology Expert Panel (HEI, 1999). To help explain MSHA's reasons
for valuing some studies over others, these five criteria will now be
discussed in turn.
Power of the Study
There are several factors that contribute to a study's power, or
ability to detect an increased risk of lung cancer in an exposed
population. First is the study's size--i.e., the number of subjects in
a cohort or the number of lung cancer cases in a case-control study. If
few subjects or cases are included, then any statistical relationships
are likely to go undetected. Second is the duration and intensity of
exposure among members of the exposed group. The greater the exposure,
the more likely it is that the study will detect an effect if it
exists. Conversely, a study in which few members of the exposed group
experienced cumulative exposures significantly greater than the
background level is unlikely to detect an exposure effect. Third is the
length of time the study allows for lung cancer to exhibit a
statistical impact after exposure begins. This involves a latency
period, which is the time required for lung cancer to develop in
affected individuals, or (mainly pertaining to cohort studies) a
follow-up period, which is the time allotted, including latency, for
lung cancers in affected individuals to show up in the study. It is
generally acknowledged that lung cancer studies should, at the very
minimum, allow for a latency period of at least 10 years from the time
exposure begins and that it is preferable to allow for latency periods
of at least 20 years. The shorter the latency allowance, the less power
the study has to detect any increased risk of lung cancer that may be
associated with exposure.
As stated above, six of the 47 studies did not show positive
results: One of these studies (Edling et al.) was based on a small
cohort of 694 bus workers, thus having little statistical power. Three
other of these studies (DeCoufle, Kaplan, and Christie) included
exposed workers for whom there was an inadequate latency allowance
(i.e., less than 10 years). The entire period of follow-up in the
Kaplan study was 1953-1958. The Christie study was designed in such a
way as to provide for neither a minimum period of exposure nor a
minimum period of latency: the report covers lung cancers diagnosed
only through 1992, but the ``exposed'' cohort includes workers who may
have entered the work force (and thus begun their exposure) as late as
Dec. 31, 1992. Such workers would not be expected to develop lung
cancer during the study period. The remaining two negative studies
(Bender, 1989 and Waller, 1981) appear to have included a reasonably
adequate number of exposed workers and to have allowed for an adequate
latency period.
Some of the 41 positive studies also had little power, either
because they included relatively few exposed workers (e.g., Lerchen et
al., 1987, Ahlman et al., 1991; Gustavsson et al., 1990) or an
inadequate latency allowance or follow-up period (e.g., Leupker and
Smith (1978); Milne, 1983; Rushton et al., 1983). In those based on few
exposed workers, there is a strong possibility that the positive
association arose merely by chance.\32\ The other studies, however,
found increased prevalence of lung cancer despite the relatively short
periods of latency and follow-up time involved. It should be noted
that, for reasons other than lack of power, MSHA places very little
weight on the Milne and Rushton studies. As mentioned in Table III-4,
the Rushton study compared the cohort to the national population, with
no adjustment for regional or socioeconomic differences. This may
account for the excess rate of lung cancers reported for the exposed
``general hand'' job category. The Milne study did not control for
potentially important ``confounding'' variables, as explained below in
MSHA's discussion of that criterion.
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\32\ As noted in Table III-4, the underground sulfide ore miners
studied by Ahlman et al. (1991) were exposed to radon in addition to
diesel emissions. The total number of lung cancers observed,
however, was greater than what was attributable to the radon
exposure, based on a calculation by the authors. Therefore, the
authors attributed a portion of the excess risk to diesel exposure.
---------------------------------------------------------------------------
Composition of Comparison Groups
This criterion addresses the question of how equitable is the
comparison between the exposed and unexposed populations in a cohort
study, or between the subjects with lung cancer (i.e., the ``cases'')
and the subjects without lung cancer (i.e., the ``controls'') in a
case-control study. MSHA includes bias due to confounding variables
under this criterion if the groups differ systematically with respect
to such factors as age or exposure to non-diesel carcinogens. For
example, unless adequate adjustments are made, comparisons of
underground miners to the general population may be systematically
biased by the miners' greater exposure to radon gas. Confounding not
built into a study's design or otherwise documented is considered
potential rather than systematic and is considered under a separate
criterion below. Other factors included under the present criterion are
systematic (i.e., ``differential'') misclassification of those placed
into the ``exposed'' and ``unexposed'' groups, selection bias, and bias
due to the ``healthy worker effect.''
In several of the studies, a group identified with diesel exposure
may have systematically included workers who, in fact, received little
or no occupational diesel exposure. For example, a substantial
percentage of the ``underground miner'' subgroup in Waxweiler et al.
(1973) worked in underground mines with no diesel equipment. This would
have diluted any effect of dpm exposure on the group of underground
miners as a whole.\33\ Similarly, the groups classified as miners in
Benhamou et al. (1988), Boffetta et al. (1988), and Swanson et al.
(1993) included substantial percentages of miners who were probably not
occupationally exposed to diesel emissions. Potential effects of
exposure misclassification are discussed further under the criterion of
``Exposure Assessment'' below.
---------------------------------------------------------------------------
\33\ Furthermore, as pointed out in comments submitted by Dr.
Peter Valberg through the NMA, the subgroup of underground miners
working at mines with diesel engines was small, and the exposure
duration in one of the mines with diesel engines was only ten years.
Therefore, the power of the study was inadequate to detect an excess
risk of lung cancer for that subgroup by itself.
---------------------------------------------------------------------------
Selection bias refers to systematic differences in characteristics
of the comparison groups due to the criteria and/or methods used to
select those included in the study. For example, three of the cohort
studies (Raffle, 1957; Leupker and Smith, 1976; Waller, 1981)
systematically excluded retirees from the cohort of exposed workers--
but not
[[Page 5593]]
from the population used for comparison. Therefore, cases of lung
cancer that developed after retirement were counted against the
comparison population but not against the cohort. This artificially
reduced the SMR calculated for the exposed cohort in these three
studies.
Another type of selection bias may occur when members of the
control group in a case-control study are non-randomly selected. This
happens when cases and controls are selected from the same larger
population of patients or death certificates, and the controls are
simply selected (prior to case matching) from the group remaining after
those with lung cancer are removed. Such selection can lead to a
control group that is biased with respect to occupation and smoking
habits. Specifically, `` * * * a severely distorted estimate of the
association between exposure to diesel exhaust and lung cancer, and a
severely distorted picture of the direction and degree of confounding
by cigarette smoking, can come from case-control studies in which the
controls are a collection of `other deaths' '' when the cause of most
``other deaths'' is itself correlated with smoking or occupational
choice (HEI, 1999). This selection bias can distort results in either
direction.
MSHA judged that seven of the 20 available case-control studies
were susceptible to this type of selection bias because controls were
drawn from a population of ``other deaths'' or ``other patients.'' \34\
These control groups were likely to have over-represented cases of
cardiovascular disease, which is known to be highly correlated with
smoking and is possibly also correlated with occupation. The only case-
control study not reporting a positive result (DeCoufle et al., 1977)
fell into this group of seven. The remaining 13 case-control studies
all reported positive results.
---------------------------------------------------------------------------
\34\ These were: Buiatti et al. (1985), Coggan et al. (1984),
DeCoufle et al. (1977), Garshick et al. (1987), Hayes et al. (1989),
Lerchen et al. (1987), and Steenland et al. (1990).
---------------------------------------------------------------------------
It is ``well established that persons in the work force tend to be
`healthier' than persons not employed, and therefore healthier than the
general population. Worker mortality tends to be below average for all
major causes of death.'' (HEI, 1999) Because workers tend to be
healthier than non-workers, the prevalence of disease found among
workers exposed to a toxic substance may be lower than the rate
prevailing in the general population, but higher than the rate
occurring in an unexposed population of similar workers. This
phenomenon is called the ``healthy worker effect.''
All five cohort studies reporting entirely negative results drew
comparisons against the general population and made no adjustments to
take the healthy worker effect into account. (Kaplan, 1959; Waller
(1981); Edling et al. (1987); Bender et al. (1989); Christie et al.
(1995)). The sixth negative study (DeCoufle, 1977) was a case-control
study in which vehicle drivers and locomotive engineers were compared
to clerical workers. As mentioned earlier, this study did not meet the
criterion for a minimum 10-year latency period. All other studies in
which exposed workers were compared against similar but unexposed
workers reported some degree of elevated lung cancer risk for exposed
workers.
Many of the 41 positive studies also drew comparisons against the
general population with no compensating adjustment for the healthy
worker effect. But the healthy worker effect can influence results even
when the age-adjusted mortality or morbidity rate observed among
exposed workers is greater than that found in the general population.
In such studies, comparison with the general population tends to reduce
the excess risk attributable to the substance being investigated. For
example, Gustafsson et al. (1986), Rushton et al. (1983), and Wong et
al. (1985) each reported an unadjusted SMR exceeding 1.0 for lung
cancer in exposed workers and an SMR significantly less than 1.0 for
all causes of death combined. Since the SMR for all causes is less than
1.0, there is evidence of a healthy worker effect. Therefore, the SMR
reported for lung cancer was probably lower than if the comparison had
been made against a more similar population of unexposed workers.
Bhatia et al. (1998) constructed a simple estimate of the healthy
worker effect evident in these studies, based on the SMR for all causes
of death except lung cancer. This estimate was then used to adjust the
SMR reported for lung cancer. For the three positive studies mentioned,
the adjustment raised the SMR from 1.29 to 1.48, from 1.01 to 1.23, and
from 1.07 to 1.34, respectively. \35\
---------------------------------------------------------------------------
\35\ A similar adjustment was applied to the SMR for lung cancer
reported in one of the negative studies (Edling et al., 1987). This
raised the SMR from 0.67 to 0.80. Because of insufficient data,
Bhatia et al. did not carry out the adjustment for the three other
studies they considered with potentially important healthy worker
effects. (Bhatia et al., 1998)
---------------------------------------------------------------------------
Exposure Assessment
Many commenters suggested that a lack of concurrent exposure
measurements in available studies limits their utility for quantitative
risk assessment (QRA). MSHA is fully aware of these limitations but
also recognizes that less desirable surrogates of exposure must
frequently be employed out of practical necessity. As stated by HEI's
expert panel on diesel epidemiology:
Quantitative measures of exposures are important in any
epidemiologic study used for QRA. The greater the detail regarding
specific exposure, including how much, for how long, and at what
concentration, the more useful the study is for this purpose.
Frequently, however, individual measurements are not available, and
surrogate measures or markers are used. For example, the most
general surrogate measures of exposure in occupational epidemiologic
studies are job classification and work location. (HEI, 1999)
It is important to distinguish, moreover, between studies used to
identify a hazard (i.e., to establish that dpm exposure is associated
with an excess risk of lung cancer) and studies used for QRA (i.e., to
quantify the amount of excess risk corresponding to a given level of
exposure). Although detailed exposure measurements are desirable in any
epidemiologic study, they are more important for QRA than for
identifying and characterizing a hazard. Conversely, epidemiologic
studies can be highly useful for purposes of hazard identification and
characterization even if a lack of personal exposure measurements
renders them less than ideal for QRA.
Still, MSHA agrees that the quality of exposure assessment affects
the value of a study for even hazard identification. Accordingly, MSHA
has divided the 47 studies into four categories, depending on the
degree to which exposures were quantified for the specific workers
included. This ranking refers only to exposure assessment and does not
necessarily correspond to the overall weight MSHA places on any of the
studies.
The highest rank, with respect to this criterion, is reserved for
studies having quantitative, concurrent exposure measurements for
specific workers or for specific jobs coupled with detailed work
histories. Only two studies (Johnston et al., 1997 and Saverin et al.,
1999) fall into this category.\36\ Both of these recent cohort studies
took smoking habits into account. These
[[Page 5594]]
studies both reported an excess risk of lung cancer associated with dpm
exposure.
---------------------------------------------------------------------------
\36\ The study of German potash miners by Saverin et al. was
introduced by NIOSH at the Knoxville public hearing prior to
publication. The study, as cited, was later published in English.
Although the dpm measurements (total carbon) were all made in one
year, the authors provide a justification for assuming that the
mining technology and type of machinery used did not change
substantially during the period miners were exposed (ibid., p.420).
---------------------------------------------------------------------------
The second rank is defined by semi-quantitative exposure
assessments, based on job history and an estimated exposure level for
each job. The exposure estimates in these studies are crude, compared
to those in the first rank, and they are subject to many more kinds of
error. This severely restricts the utility of these studies for QRA
(i.e., for quantifying the change in risk associated with various
specified exposure levels). For purposes of hazard identification and
characterization, however, crude exposure estimates are better than no
exposure estimates at all. MSHA places two cohort studies and five
case-control studies into this category.\37\ All seven of these studies
reported an excess risk of lung cancer risk associated with diesel
exposure. Thus, results were positive in all nine studies with
quantitative or semi-quantitative exposure assessments.
---------------------------------------------------------------------------
\37\ The cohort studies are Garshick et al. (1988) and
Gustavsson et al. (1990). The case-control studies are Emmelin et
al. (1993), Garshick et al.(1997), Gustavsson et al. (1990),
Siemiatycki et al. (1988), and Steenland et al. (1990, 1992).
---------------------------------------------------------------------------
The next rank belongs to those studies with only enough information
on individual workers to construct estimates of exposure duration.
Although these studies present no data relating excess risk to specific
exposure levels, they do provide excess risk estimates for those
working a specified minimum number of years in a job associated with
diesel exposure. One cohort study and five case-control studies fall
into this category, and all six of them reported an excess risk of lung
cancer.\38\ With one exception (Benhamou et al. 1988), these studies
also presented evidence of increased age-adjusted risk for workers with
longer exposures and/or latency periods.
---------------------------------------------------------------------------
\38\ The cohort study is Wong et al. (1985). The case-control
studies are Bruske-Hohlfeld et al. (1999), Benhamou et al. (1988),
Boffetta et al. (1990), Hayes et al. (1989), and Swanson et al.
(1993).
---------------------------------------------------------------------------
The bottom rank, with respect to exposure assessment, consists of
studies in which no exposure information was collected for individual
workers. These studies used only job title to distinguish between
exposed and unexposed workers. The remaining 32 studies, including five
of the six with entirely negative results, fall into this category.
Studies basing exposure assessments on only a current job title (or
even a history of job titles) are susceptible to significant
misclassification of exposed and unexposed workers. Unless the study is
poorly designed, this misclassification is ``nondifferential'' i.e.,
those who are misclassified are no more and no less likely to develop
lung cancer (or to have been exposed to carcinogens such as tobacco
smoke) than those who are correctly classified. If workers are
sometimes misclassified nondifferentially, then this will tend to mask
or dilute any excess risk attributable to exposure. Furthermore,
differential misclassification in these studies usually consists of
systematically including workers with little or no diesel exposure in a
job category identified as ``exposed.'' This too would generally mask
or dilute any excess risk attributable to exposure. Therefore, MSHA
assumes that in most of these studies, more rigorous and detailed
exposure assessments would have resulted in somewhat higher estimates
of excess risk.
IMC Global, MARG, and some other commenters expressed special
concern about potential exposure misclassification and suggested that
such misclassification might be partly responsible for results showing
excess risk. IMC Global, for example, quoted a textbook observation
that, contrary to popular misconceptions, nondifferential exposure
misclassification can sometimes bias results away from the null. MSHA
recognizes that this can happen under certain special conditions.
However, there is an important distinction between ``can sometimes''
and ``can frequently.'' There is an even more important distinction
between ``can sometimes'' and ``in this case does.'' As noted by the
HEI Expert Panel on Diesel Epidemiology (HEI, 1999, p.48), ``* * *
nondifferential misclassification most often leads to an overall
underestimation of effect.'' Similarly, Silverman (1998) noted,
specifically with respect to the diesel studies, that ``* * * this
[exposure misclassification] bias is most likely to be nondifferential,
and the effect would probably have been to bias point estimates [of
excess risk] toward the null value.''
Statistical Significance
A ``statistically significant'' finding is a finding unlikely to
have arisen by chance in the particular group, or statistical sample,
of persons being studied. An association arising by chance would have
no predictive value for exposed workers outside the sample. However, a
specific epidemiologic study may fail to achieve statistical
significance for two very different reasons: (1) there may be no real
difference in risk between the two groups being compared, or (2) the
study may lack the power needed to detect whatever difference actually
exists. As described earlier, a lack of sufficient power comes largely
from limitations such as a small number of subjects in the sample, low
exposure and/or duration of exposure, or too short a period of latency
or follow-up time. Therefore, a lack of statistical significance in an
individual study does not demonstrate that the results of that study
were due merely to chance--only that the study (viewed in isolation) is
statistically inconclusive.
As explained earlier, MSHA classifies a reported RR, SMR, or OR
(i.e., the point estimate of relative risk) as ``positive'' if it
exceeds 1.0 and ``negative'' if it is less than or equal to 1.0. By
common convention, a positive result is considered statistically
significant if its 95-percent confidence interval does not overlap 1.0.
If all other relevant factors are equal, then a statistically
significant positive result provides stronger evidence of an underlying
relationship than one that is not statistically significant. On the
other hand, a study must meet two requirements in order to provide
statistically significant evidence of no positive relationship: (1) the
upper limit of its 95-percent confidence interval must not exceed 1.0
by an appreciable amount \39\ and (2) it must have allowed for
sufficient exposure, latency, and follow-up time to have detected an
existing relationship.
---------------------------------------------------------------------------
\39\ As a matter of practicality, MSHA places the threshold at
1.05.
---------------------------------------------------------------------------
As shown in Tables III-4 and III-5, statistically significant
positive results were reported in 25 of the 47 studies: 11 of the 19
positive case-control studies and 14 of the 22 positive cohort studies.
In 16 of the 41 studies showing a positive association, the association
observed was not statistically significant. Results in five of the six
negative studies were not statistically significant. One of the six
negative studies (Christie et al., 1995, in full version), reported a
statistically significant deficit in lung cancer for miners. This
study, however, provided for no minimum period of exposure or latency
and, therefore, lacked the power necessary to provide statistically
significant evidence.\40\
---------------------------------------------------------------------------
\40\ More detailed discussion of this study appears later in
this subsection.
---------------------------------------------------------------------------
Whether or not a study provides statistically significant evidence
is dependent upon many variables, such as study size, adequate follow-
up time (to account for enough exposure and latency), and adequate case
ascertainment. In the ideal world, a
[[Page 5595]]
sufficiently powerful study that failed to demonstrate a statistically
significant positive relationship would, by its very failure, provide
statistically significant evidence that an underlying relationship
between an exposure and a specific disease was unlikely. It is
important to note that MSHA regards a real 10-percent increase in the
risk of lung cancer (i.e., a relative risk of 1.1) as constituting a
clearly significant health hazard. Therefore, ``sufficiently powerful''
in this context means that the study would have to be of such scale and
quality as to detect a 10-percent increase in risk if it existed. The
outcome of such a study could plausibly be called ``negative'' even if
the estimated RR slightly exceeded 1.0--so long as the lower confidence
limit did not exceed 1.0 and the upper confidence limit did not exceed
1.05. Rarely does an epidemiological study fall into this ``ideal''
study category. MSHA reviewed the dpm epidemiologic studies to
determine which of them could plausibly be considered to be negative.
For example, one study (Waxweiller et al., 1973) reported positive
but statistically non-significant results corresponding to an RR of
about 1.1. Among the studies MSHA counts as positive, this is the one
that is numerically closest to being ``negative''. This study, however,
relied on a relatively small cohort containing an indeterminate but
probably substantial percentage of occupationally unexposed workers.
Furthermore, there was no minimum latency allowance for the exposed
workers. Therefore, even if MSHA were to use 1.1 rather than 1.05 as a
threshold for significant relative risk, the study had insufficient
statistical power to merit ``negative'' status.
One commenter (Dr. James Weeks, representing the UMWA) argued that
``MSHA's reliance on * * * statistical significance is somewhat
misplaced. Results that are not significant statistically * * * can
nevertheless indicate that the exposure in question caused the
outcome.'' MSHA agrees that an otherwise sound study may yield positive
(or negative) results that provide valuable evidence for (or against)
an underlying relationship but fail, because of an insufficient number
of exposed study subjects, to achieve statistical significance. In the
absence of other evidence to the contrary, a single positive but not
statistically significant result could even show that a causal
relationship is more likely than not. By definition, however, such a
result would not be conclusive at a high level of confidence. A finding
of even very high excess risk in a single, well-designed study would be
far from conclusive if based on a very small number of observed lung
cancer cases or if it were in conflict with evidence from toxicity
studies.
MSHA agrees that evidence should not be ignored simply because it
is not conclusive at a conventional but arbitrary 95-percent confidence
level. Lower confidence levels may represent weaker but still important
evidence. Nevertheless, to rule out chance effects, the statistical
significance of individual studies merits serious consideration when
only a few studies are available. That is not the case, however, for
the epidemiology literature relating lung cancer to diesel exposure.
Since many studies contribute to the overall weight of evidence, the
statistical significance of individual studies is far less important
than the statistical significance of all findings combined. Statistical
significance of the combined findings is addressed in Subsection
3.a.iii of this risk assessment.
Potential Confounders
There are many variables, both known and unknown, that can
potentially distort the results of an epidemiologic study. In studies
involving lung cancer, the most important example is tobacco smoking.
Smoking is highly correlated with the development of lung cancer. If
the exposed workers in a study tend to smoke more (or less) than the
population to which they are being compared, then smoking becomes what
is called a ``confounding variable'' or ``confounder'' for the study.
In general, any variable affecting the risk of lung cancer potentially
confounds observed relationships between lung cancer and diesel
exposure. Conspicuous examples are age, smoking habits, and exposure to
airborne carcinogens such as asbestos or radon progeny. Diet and other
lifestyle factors may also be potential confounders, but these are
probably less important for lung cancer than for other forms of cancer,
such as bladder cancer.
There are two ways to avoid distortion of study results by a
potential confounder: (1) Design the study so that the populations
being compared are essentially equivalent with respect to the
potentially confounding variable; or (2) allow the confounding to take
place, but adjust the results to compensate for its effects. Obviously,
the second approach can be applied only to known confounders. Since no
adjustment can be made for unknown confounders, it is important to
minimize their effects by designing the comparison groups to be as
similar as possible.
The first approach requires a high degree of control over the two
groups being compared (exposed and unexposed in a cohort study; with
and without lung cancer in a case-control study). For example, the
effects of age in a case-control study can be controlled by matching
each case of lung cancer with one or more controls having the same year
of birth and age in year of diagnosis or death. Matching on age is
never perfect, because it is generally not feasible to match within a
day or even a month. Similarly, the effects of smoking in a case-
control study can be imperfectly controlled by matching on smoking
habits to the maximum extent possible.\41\ In a cohort study, there is
no confounding unless the exposed cohort and the comparison group
differ with respect to a potential confounder. For example, if both
groups consist entirely of never-smokers, then smoking is not a
confounder in the study. If both groups contain the same percentage of
smokers, then smoking is still an important confounder to the extent
that smoking intensity and history differ between the two groups. In an
attempt to minimize such differences (along with potentially important
differences in diet and lifestyle) some studies restrict comparisons to
workers of similar socioeconomic status and area of residence. Studies
may also explicitly investigate smoking habits and histories and forego
any adjustment of results if these factors are found to be
homogeneously distributed across comparison groups. In that case,
smoking would not actually appear to function as a confounder, and a
smoking adjustment might not be required or even desirable.
Nevertheless, a certain amount of smoking data is still necessary in
order to check or verify homogeneity. The study's credibility may also
be an important consideration. Therefore, MSHA agrees with the HEI's
expert panel that even when smoking appears not to be a confounder,
* * * a study is open to criticism if no smoking data are
collected and the association between exposure and outcome is weak.
* * * When the magnitude of the association of interest is weak,
uncontrolled confounding, particularly from a strong confounder such
as cigarette smoking, can have a major impact on the study's results
and on the credibility of their use. [HEI, 1999]
However, this does not mean that a study cannot, by means of an
efficient study design and/or statistical verification of homogeneity,
[[Page 5596]]
demonstrate adequate control for smoking without applying a smoking
adjustment.
---------------------------------------------------------------------------
\41\ If cases and controls cannot be closely matched on smoking
or other potentially important confounder, then a hybrid approach is
often taken. Cases and controls are matched as closely as possible,
differences are quantified, and the study results are adjusted to
account for the differences.
---------------------------------------------------------------------------
The second approach to dealing with a confounder requires knowledge
or estimation both of the differences in group composition with respect
to the confounder and of the effect that the confounder has on lung
cancer. Ideally, this would entail specific, quantitative knowledge of
how the variable affects lung cancer risk for each member of both
groups being compared. For example, a standardized mortality ratio
(SMR) can be used to adjust for age differences when a cohort of
exposed workers with known birth dates is compared to an unexposed
reference population with known, age-dependent lung cancer rates.\42\
In practice, it is not usually possible to obtain detailed information,
and the effects of smoking and other known confounders cannot be
precisely quantified.
---------------------------------------------------------------------------
\42\ Since these rates may vary by race, geographic region, or
other factors, the validity of this adjustment depends heavily on
choice of an appropriate reference population. For example,
Waxweiler et al. (1973) based SMRs for a New Mexico cohort on
national lung cancer mortality rates. Since the national age-
adjusted rate of lung cancer is about \1/3\ higher than the New
Mexico rate, the reported SMRs were roughly \3/4\ of what they would
have been if based on rates specific to New Mexico.
---------------------------------------------------------------------------
Stoaber and Abel (1996) argue, along with Morgan et al. (1997) and
some commenters, that even in those epidemiologic studies that are
adjusted for smoking and show a statistically significant association,
the magnitude of relative or excess risk observed is too small to
demonstrate any causal link between dpm exposure and cancer. Their
reasoning is that in these studies, errors in the collection or
interpretation of smoking data can create a bias in the results larger
than any potential contribution attributable to diesel particulate.
They propose that studies failing to account for smoking habits should
be disqualified from consideration, and that evidence of an association
from the remaining, smoking-adjusted studies should be discounted
because of potential confounding due to erroneous, incomplete, or
otherwise inadequate characterization of smoking histories.
It should be noted, first of all, that five of the six negative
studies neither matched nor adjusted for smoking.\43\ But more
importantly, MSHA concurs with IARC (1989), Cohen and Higgins (1995),
IPCS (1996), CAL-EPA (1998), ACGIH (1998), Bhatia et al. (1998), and
Lipsett and Campleman (1999) in not accepting the view that studies
should automatically be disqualified from consideration because of
potential confounders. MSHA recognizes that unknown exposures to
tobacco smoke or other human carcinogens can distort the results of
some lung cancer studies. MSHA also recognizes, however, that it is not
possible to design a human epidemiologic study that perfectly controls
for all potential confounders. It is also important to note that a
confounding variable does not necessarily inflate an observed
association. For example, if the exposed members of a cohort smoke less
than the reference group to which they are compared, then this will
tend to reduce the apparent effects of exposure on lung cancer
development. In the absence of evidence to the contrary, it is
reasonable to assume that a confounder is equally likely to inflate or
to deflate the results.
---------------------------------------------------------------------------
\43\ The exception is DeCoufle et al. (1977), a case-control
study that apparently did not match or otherwise adjust for age.
---------------------------------------------------------------------------
As shown in Tables III-4 and III-5, 18 of the published
epidemiologic studies involving lung cancer did, in fact, control or
adjust for exposure to tobacco smoke, and five of these 18 also
controlled or adjusted for exposure to asbestos and other carcinogenic
substances (Garshick et al., 1987; Boffetta et al., 1988; Steenland et
al., 1990; Morabia et al., 1992; Bruske-Hohlfeld et al., 1999). These
results are less likely to be confounded than results from most of the
studies with no adjustment. All but one of these 18 studies reported
some degree of excess risk associated with occupational exposure to
diesel particulate, with statistically significant results reported in
eight.
In addition, several of the studies with no smoking adjustment took
the first approach described above for preventing or substantially
mitigating potential confounding by smoking habits: they drew
comparisons against internal control groups or other control groups
likely to have similar smoking habits as the exposed groups (e.g.,
Garshick et al., 1988; Gustavsson et al., 1990; Hansen, 1993; and
Saverin et al., 1999). Therefore, MSHA places more weight on these
studies than on studies drawing comparisons against dissimilar groups
with no smoking controls or adjustments. This emphasis is in accordance
with the conclusion by Bhatia et al. (1998) that smoking homogeneity
typically exists within cohorts and is associated with a uniform
lifestyle and social class. Although it was not yet available at the
time Bhatia et al. performed their analysis, an analysis of smoking
patterns by Saverin et al. (op cit.) within the cohort they studied
also supports this conclusion.
IMC Global and MARG objected to MSHA's position on potential
confounders and submitted comments in general agreement with the views
of Morgan et al. (op cit.) and Stobel and Abel (op cit.). Specifically,
they suggested that studies reporting relative risks solely between 1.0
and 2.0 should be discounted because of potential confounders. Of the
41 positive studies considered by MSHA, 22 fall into this category (16
cohort and 6 case-control). In support of their suggestion, IMC Global
quoted Speizer (1986), Muscat and Wynder (1995), Lee (1989), WHO
(1980), and NCI (1994). These authorities all urged great caution when
interpreting the results of such studies, because of potential
confounders. MSHA agrees that none of these studies, considered
individually, is conclusive and that each result must be considered
with due caution. None of the quoted authorities, however, proposed
that such studies should automatically be counted as ``negative'' or
that they could not add incrementally to an aggregate body of positive
evidence.
IMC Global also submitted the following reference to two Federal
Court decisions pertaining to estimated relative risks less than 2.0:
The Ninth Circuit concluded in Daubert v. Merrell Dow
Pharmaceuticals'' that ``for an epidemiologic study to show
causation * * * the relative risk * * * arising from the
epidemiologic data will, at a minimum, have to exceed 2.''
Similarly, a District Court stated in Hall v. Baxter Healthcare
Corp.49: The threshold for concluding that an agent was more likely
the cause of the disease than not is relative risk greater than 2.0.
Recall that a relative risk of 1.0 means that the agent has no
affect on the incidence of disease. When the relative risk reaches
2.0. the agent is responsible for an equal number of cases of
disease as all other background causes. Thus a relative risk of 2.0
implies a 50% likelihood that an exposed individual's disease was
caused by the agent. [IMC Global]
In contrast with the two cases cited, the purpose of this risk
assessment is not to establish civil liabilities for personal injury.
MSHA's concern is with reducing the risk of lung cancer, not with
establishing the specific cause of lung cancer for an individual miner.
The excess risk of an outcome, given an excessive exposure, is not the
same thing as the likelihood that an excessive exposure caused the
outcome in a given case. To understand the difference, it may be
helpful to consider two analogies: (1) The likelihood that a given
death was caused by a lightning strike is relatively low, yet exposure
to lightning is rather hazardous; (2) a specific smoker may not be able
to prove that his or her lung cancer was
[[Page 5597]]
``more likely than not'' caused by radon exposure, yet radon exposure
significantly increases the risk--especially for smokers. Lung cancer
has a variety of alternative causes, but this fact does not reduce the
risk associated with any one of them.
Furthermore, there is ample precedent for utilizing epidemiologic
studies reporting relative risks less than 2.0 in making clinical and
public policy decisions. For example, the following table contains the
RR for death from cardiovascular disease associated with cigarette
smoking reported in several prospective epidemiologic studies:
------------------------------------------------------------------------
Estimate of RR
of death from
Study on cigarette smoking cardiovascular
disease
------------------------------------------------------------------------
British doctors......................................... 1.6
Males in 25 states: ..............
Ages 45-64.......................................... 2.08
Ages 65-79.......................................... 1.36
U.S. Veterans........................................... 1.74
Japanese study.......................................... 1.96
Canadian veterans....................................... 1.6
Males in nine states.................................... 1.70
Swedish males........................................... 1.7
Swedish females......................................... 1.3
California occupations.................................. 2.0
------------------------------------------------------------------------
Source: U.S. Department of Health and Human Services (1989).
By IMC Global's rule of thumb, all but one or two of these studies
would be discounted as evidence of increased risk attributable to
smoking. These studies, however, have not been widely discounted by
scientific authorities. To the contrary, they have been instrumental in
establishing that cigarette smoking is a principal cause of heart
disease.
A second example is provided by the increased risk of lung cancer
found to be caused by residential exposure to radon progeny. As in the
case of dpm, tobacco smoking has been an important potential confounder
in epidemiological studies used to investigate whether exposures to
radon concentrations at residential levels can cause lung cancer. Yet,
in the eight largest residential epidemiological studies used to help
establish the reality of this now widely accepted risk, the reported
relative risks were all less than 2.0. Based on a meta-analysis of
these eight studies, the combined relative risk of lung cancer
attributable to residential radon exposure was 1.14. This elevation in
the risk of lung cancer, though smaller than that reported in most
studies of dpm effects, was found to be statistically significant at a
95-percent confidence level (National Research Council, 1999, Table G-
25).
(ii) Studies Involving Miners
In the proposed risk assessment, MSHA identified seven
epidemiologic studies reporting an excess risk of lung cancer among
miners thought to have been exposed occupationally to diesel exhaust.
As stated in the proposal, two of these studies specifically
investigated miners, and the other five treated miners as a subgroup
within a larger population of workers.\44\ MSHA placed two additional
studies specific to exposed coal miners (Christie et al., 1995;
Johnston et al.,1997) into the public record with its Feb. 12, 1999
Federal Register notice. Another study,\45\ investigating lung cancer
in exposed potash miners, was introduced by NIOSH at the Knoxville
public hearing on May 27, 1999 and later published as Saverin et al.,
1999. Finally, one study reporting an excess risk of lung cancer for
presumably exposed miners was listed in Table III-5 as originally
published, and considered by MSHA in its overall assessment, but
inadvertently left out of the discussion on studies involving miners in
the previous version of this risk assessment.\46\ There are, therefore,
available to MSHA a total of 11 epidemiologic studies addressing the
risk of lung cancer for miners, and five of these studies are specific
to miners.
---------------------------------------------------------------------------
\44\ In the proposed risk assessment, the studies identified as
specifically investigating miners were Waxweiler et al. (1973) and
Ahlman et al. (1991). At the Albuquerque public hearing, Mr. Bruce
Watzman, representing the NMA, asked a member of the MSHA panel (Mr.
Jon Kogut) to list six studies involving miners that he had cited
earlier in the hearing and to identify those that were specific to
miners. In both his response to Mr. Watzman, and in his earlier
remarks, Mr. Kogut noted that the studies involving miners were
listed in Tables III-4 and III-5. However, he inadvertently
neglected to mention Ahlman et al. (op cit.) and Morabia et al.
(1992). (The latter study addressed miners as a subgroup of a larger
population.)
In his response to Mr. Watzman, Mr. Kogut cited Swanson et al.
(1993) but not Burns and Swanson (1991), which he had mentioned
earlier in the hearing in connection with the same study. These two
reports are listed under a single entry in Table III-5 (Swanson et
al.) because they both report findings based on the same body of
data. Therefore, MSHA considers them to be two parts of the same
study. The 5.03 odds ratio for mining machine operators mentioned by
Mr. Kogut during the hearing was reported in Burns and Swanson
(1991).
Only the six studies specified by Mr. Kogut in his response to
Mr. Watzman were included in separate critiques by Dr. Peter Valberg
and Dr. Jonathan Borak later submitted by the NMA and by MARG,
respectively. Dr. Valberg did not address Burns and Swanson (1991),
and he addressed a different report by Siemiatycki than the one
listed in Table III-5 and cited during the hearing (i.e.,
Siemiatycki et al., 1988). Neither Dr. Valberg nor Dr. Borak
addressed Ahlman et al. (op cit.) or Morabia et al. (op cit.). Also
excluded were two additional miner-specific studies placed into the
record on Feb. 12, 1999 (Fed Reg. 64:29 at 59258). Mr. Kogut did not
include them in his response to Mr. Watzman, or in his prior
remarks, because he was referring only to studies listed in Tables
III-4 and III-5 of the published proposals. Mr. Kogut also did not
include a study specific to German potash miners submitted by NIOSH
at a subsequent public hearing, and this too was left out of both
critiques. A published version of the study (Saverin et al., 1999)
was placed into the record on June 30, 2000. All of the studies
involving miners are in the public record and have been available
for comment by interested parties throughout the posthearing comment
periods.
\45\ Some commenters suggested that MSHA ``overlooked'' a
recently published study on NSW miners, Brown et al., 1997. This
study evaluated the occurrence of forms of cancer other than lung
cancer in the same cohort studied by Christie et al. (1995).
\46\ This study was published in two separate reports on the
same body of data: Burns and Swanson (1991) and Swanson et al.
(1993). Both published reports are listed in Table III-5 under the
entry for Swanson et al.
---------------------------------------------------------------------------
Five cohort studies (Waxweiler et al.,1973; Ahlman et al., 1991;
Christie et al., 1996; Johnston et al., 1997; Saverin et al., 1999)
were performed specifically on groups of miners, and one (Boffetta et
al., 1988) addressed miners as a subgroup of a larger population.
Except for the study by Christie et al., the cohort studies all showed
elevated lung cancer rates for miners in general or for the most highly
exposed miners within a cohort. In addition, all five case-control
studies reported elevated rates of lung cancer for miners (Benhamou et
al.,1988; Lerchen et al., 1987; Siemiatycki et al.,1988; Morabia et
al., 1992; Burns and Swanson, 1991).
Despite the risk assessment's emphasis on human studies, some
members of the mining community apparently believed that the risk
assessment relied primarily on animal studies and that this was because
studies on miners were unavailable. Canyon Fuels, for example,
expressed concerns about relying on animal studies instead of studies
on western diesel-exposed miners:
Since there are over a thousand miners here in the West that
have fifteen or more years of exposure to diesel exhaust, why has
there been no study of the health status of those miners? Why must
we rely on animal studies that are questionable and inconclusive?
Actually, western miners were involved in several studies of health
effects other than cancer, as described earlier in this risk
assessment. With respect to lung cancer, there are many reasons why
workers from a particular group of mines might not be selected for
study. Lung cancer often takes considerably more than 15 years to
develop, and a valid study must allow not only for adequate duration of
exposure but also for an adequate period of latency following exposure.
Furthermore, many mines contain radioactive gases and/or
[[Page 5598]]
respirable silica dust, making it difficult to isolate the effects of a
potential carcinogen.
Similarly, at the public hearing in Albuquerque on May 13, 1999, a
representative of Getchell Gold stated that he thought comparing miners
to rats was irrational and that ``there has not been a study on these
miners as to what the effects are.'' To correct the impression that
MSHA was basing its risk assessment primarily on laboratory animal
studies, an MSHA panelist pointed out Tables III-4 and III-5 of the
proposed preamble and identified six studies pertaining to miners that
were listed in those tables. However, he placed no special weight on
these studies and cited them only to illustrate the existence of
epidemiologic studies reporting an elevated risk of lung cancer among
miners.
With their post-hearing comments, the NMA and MARG submitted
critiques by Dr. Peter Valberg and Dr. Jonathan Borak of six reports
involving miners (see Footnote 42). Drs. Valberg and Borak both noted
that the six studies reviewed lacked information on diesel exposure and
were vulnerable to confounders and exposure misclassification. For
these reasons, Dr. Valberg judged them ``particularly poor in
identifying what specific role, if any, diesel exhaust plays in lung
cancer for miners.'' He concluded that they do not ``implicate diesel
exposure per se as strongly associated with lung cancer risk in
miners.'' Similarly, Dr. Borak suggested that, since they do not relate
adverse health effects in miners to any particular industrial exposure,
``the strongest conclusion that can be drawn from these six studies is
that the miners in the studies had an increased risk of lung cancer.''
MSHA agrees with Drs. Valberg and Borak that none of the studies
they reviewed provides direct evidence of a link between dpm exposure
and the excess risk of lung cancer reported for miners. (A few
disagreements on details of the individual studies will be discussed
below). As MSHA said at the Albuquerque hearing, the lack of exposure
information on miners in these studies led MSHA to rely more heavily on
associations reported for other occupations. MSHA also noted the
limitations of these studies in the proposed risk assessment. MSHA
explicitly stated that other epidemiologic studies exist which, though
not pertaining specifically to mining environments, contain better
diesel exposure information and are less susceptible to confounding by
extraneous risk factors.
Inconclusive as they may be on their own, however, even studies
involving miners with only presumed or sporadic occupational diesel
exposure can contribute something to the weight of evidence. They can
do this by corroborating evidence of increased lung cancer risk for
other occupations with likely diesel exposures and by providing results
that are at least consistent with an increased risk of lung cancer
among miners exposed to dpm. Moreover, two newer studies pertaining
specifically to miners do contain dpm exposure assessments based on
concurrent exposure measurements (Johnston et al., op cit.; Saverin et
al.,op cit.). The major limitations pointed out by Drs. Valberg and
Borak with respect to other studies involving miners do not apply to
these two studies.
Case-Control Studies
Five case-control studies, all of which adjusted for smoking, found
elevated rates of lung cancer for miners, as shown in Table III-5. The
results for miners in three of these studies (Benhamou et al., 1988;
Morabia et al., 1992; Siemiatycki et al., 1988) are given little
weight, partly because of possible confounding by occupational exposure
to radioactive gasses, asbestos, and silica dust. Also, Benhamou and
Morabia did not verify occupational diesel exposure status for the
miners. Siemiatycki performed a large number of multiple comparisons
and reported that most of the miners ``were exposed to diesel exhaust
for short periods of time,'' Lerchen et al. (1987) showed a marginally
significant result for underground non-uranium miners, but cases and
controls were not matched on date of birth or death, and the frequency
of diesel exposure and exposure to known occupational carcinogens among
these miners was not reported.
Burns and Swanson (1991) \47\ reported elevated lung cancer risk
for miners and especially mining machine operators, which the authors
attributed to diesel exposure. Potential confounding by other
carcinogens associated with mining make the results inconclusive, but
the statistically significant odds ratio of 5.0 reported for mining
machine operators is high enough to cause concern with respect to
diesel exposures, especially in view of the significantly elevated
risks reported in the same study for other diesel-exposed occupations.
The authors noted that the ``occupation most likely to have high levels
of continuous exposure to diesel exhaust and to experience that
exposure in a confined area has the highest elevated risks: mining
machine operators.''
---------------------------------------------------------------------------
\47\ This report is listed in Table III-5 under Swanson et al.
(1993), which provides further analysis of the same body of data.
---------------------------------------------------------------------------
Cohort Studies
As shown in Table III-4, MSHA identified six cohort studies
reporting results for miners likely to have been exposed to dpm. An
elevated risk of lung cancer was reported in five of these six studies.
These results will be discussed chronologically.
Waxweiller (1973) investigated a cohort of underground and surface
potash miners. The authors noted that potash ore ``is not embedded in
siliceous rock'' and that the ``radon level in the air of potash mines
is not significantly higher than in ambient air.'' Contrary to Dr.
Valberg's review of this study, the number of lung cancer cases was
reported to be slightly higher than expected, for both underground and
surface miners, based on lung cancer rates in the general U.S.
population (after adjustment for age, sex, race, and date of death).
Although the excess was not statistically significant, the authors
noted that lung cancer rates in the general population of New Mexico
were about 25 percent lower than in the general U.S. population. They
also noted that a higher than average percentage of the miners smoked
and that this would ``tend to counterbalance'' the adjustment needed
for geographic location. The authors did not, however, consider two
other factors that would tend to obscure or deflate an excess risk of
lung cancer, if it existed: (1) A healthy worker effect and (2) the
absence of any occupational diesel exposure for a substantial
percentage of the underground miners.
MSHA agrees with Dr. Valberg's conclusion that ``low statistical
power and indeterminate diesel-exhaust exposure render this study
inadequate for assessing the effect of diesel exhaust on lung-cancer
risk in miners.'' However, given the lack of any adjustment for a
healthy worker effect, and the likelihood that many of the underground
miners were occupationally unexposed, MSHA views the slightly elevated
risk reported in this study as consistent with other studies showing
significantly greater increases in risk for exposed workers.
Boffetta et al. (1988) investigated mortality in a cohort of male
volunteers who enrolled in a prospective study conducted by the
American Cancer Society. Lung cancer mortality was analyzed in relation
to self-reported diesel exhaust exposure and to employment in various
occupations
[[Page 5599]]
identified with diesel exhaust exposure, including mining. After
adjusting for smoking patterns,\48\ there was a statistically
significant excess of 167 percent (RR = 2.67) in lung cancers among
2034 workers ever employed as miners, compared to workers never
employed in occupations associated with diesel exposure. No analysis by
type of mining was reported. Other findings reported from this study
are discussed in the next subsection.
---------------------------------------------------------------------------
\48\ During the public hearing on May 25, 1999, Mr. Mark
Kaszniak of IMC Global incorrectly asserted that ``smoking was
treated in a simplistic way in this study by using three categories:
smokers, ex-smokers, and non-smokers.'' The study actually used five
categories, dividing smokers into separate categories for 1-20
cigarettes per day, 21 or more cigarettes per day, and exclusively
pipe and/or cigar smoking.
---------------------------------------------------------------------------
Although an adjustment was made for smoking patterns, the relative
risk reported for mining did not control for exposures to radioactive
gasses, silica dust, and asbestos. These lung carcinogens are probably
present to a greater extent in mining environments than in most of the
occupational environments used for comparison. Self-reported exposures
to asbestos and stone dusts were taken into account in other parts of
the study, but not in the calculation of excess lung cancer risks
associated with specific occupations, including mining.
Several commenters reiterated two caveats expressed by the study's
authors and noted in Table III-4. These are (1) that the study is
susceptible to selection biases because participants volunteered and
because the age-adjusted mortality rates differed between those who
provided exposure information and those who did not; and (2) that all
exposure information was self-reported with no quantitative
measurements. Since these caveats are not specific to mining and
pertain to most of the study's findings, they will be addressed when
this study's overall results are described in the next subsection.
One commenter, however (Mr. Mark Kaszniak of IMC Global), argued
that selection bias due to unknown diesel exposure status played an
especially important role in the RR calculated for miners. About 21
percent of all participants provided no diesel exposure information.
Mr. Kaszniak noted that diesel exposure status was unknown for an even
larger percentage of miners and suggested that the RR calculated for
miners was, therefore, inflated. He presented the following argument:
In the miner category, this [unknown diesel exposure status]
accounted for 44.2% of the study participants, higher than any other
occupation studied. This is important as this group experienced a
higher mortality for all causes as well as lung cancer than the
analyzed remainder of the cohort. If these persons had been included
in the ``no exposure to diesel exhaust group,'' their inclusion
would have lowered any risk estimates from diesel exposure because
of their higher lung cancer rates. [IMC Global post-hearing
comments]
This argument, which was endorsed by MARG, was apparently based on
a misunderstanding of how the comparison groups used to generate the RR
for mining were defined.\49\ Actually, persons with unknown diesel
exposure status were included among the miners, but excluded from the
reference population. Including sometime miners with unknown diesel
exposure status in the ``miners'' category would tend to mask or reduce
any strong association that might exist between highly exposed miners
and an increased risk of lung cancer. Excluding persons with unknown
exposure status from the reference population had an opposing effect,
since they happened to experience a higher rate of lung cancer than
cohort members who said they were unexposed. Therefore, removing
``unknowns'' from the ``miner'' group and adding them to the reference
group could conceivably shift the calculated RR for miners in either
direction. However, the RR reported for persons with unknown diesel
exposure status, compared to unexposed persons, was 1.4 (ibid., p.
412)--which is smaller than the 2.67 reported for miners. Therefore, it
appears more likely that the RR for mining was deflated than inflated
on account of persons with unknown exposure status.
---------------------------------------------------------------------------
\49\ During the public hearing on May 25, 1999, Mr. Kaszniak
stated his belief that, for miners, the ``relative risk calculation
excluded that 44% of folks who did not respond to the questionnaire
with regards to diesel exposure.'' Contrary to Mr. Kaszniak's
belief, however, the ``miners'' on which the 2.67 RR was based
included all 2034 cohort members who had ever been a miner,
regardless of whether they had provided diesel exposure information
(see Boffetta et al., 1988, p. 409).
Furthermore, the 44.2-percent nonrespondent figure is not
pertinent to potential selection bias in the RR calculation reported
for miners. The group of 2034 ``sometime'' miners used in that
calculation was 65 percent larger than the group of 1233 ``mainly''
miners to which the 44-percent nonrespondent rate applies. The
reference group used for comparison in the calculation consisted of
all cohort members ``with occupation different from those listed
[i.e., railroad workers, truck drivers, heavy equipment operators,
and miners] and not exposed [to diesel exhaust].'' The overall
nonrespondent rate for occupations in the reference group was about
21 percent (calculated by MSHA from Table VII of Boffetta et al.,
1988).
---------------------------------------------------------------------------
Although confounders and selection effects may have contributed to
the 2.67 RR reported for mining, MSHA believes this result was high
enough to support a dpm effect, especially since elevated lung cancer
rates were also reported for the three other occupations associated
with diesel exhaust exposure. Dr. Borak stated without justification
that ``[the] association between dpm and lung cancer was confounded by
age, smoking, and other occupational exposures * * *.'' He ignored the
well-documented adjustments for age and smoking. Although it does not
provide strong or direct evidence that dpm exposure was responsible for
any of the increased risk of lung cancer observed among miners, the RR
for miners is consistent with evidence provided by the rest of the
study results.
Ahlman et al. (1991) studied cohorts of 597 surface miners and 338
surface workers employed at two sulfide ore mines using diesel powered
front-end loaders and haulage equipment. Both of these mines (one
copper and one zinc) were regularly monitored for alpha energy
concentrations (i.e., due to radon progeny), which were at or below the
Finish limit of 0.3 WL throughout the study period. The ore in both
mines contained arsenic only as a trace element (less than 0.005
percent). Lung cancer rates in the two cohorts were compared to rates
for males in the same province of Finland. Age-adjusted excess
mortality was reported for both lung cancer and cardiovascular disease
among the underground miners, but not among the surface workers. None
of the underground miners who developed lung cancer had been
occupationally exposed to asbestos, metal work, paper pulp, or organic
dusts. Based on the alpha energy concentration measurements made for
the two mines, the authors calculated that not all of the excess lung
cancer for the underground miners was attributable to radon exposure.
Based on a questionnaire, the authors found similar underground and
surface age-specific smoking habits and alcohol consumption and
determined that ``smoking alone cannot explain the difference in lung
cancer mortality between the [underground] miners and surface workers.
Due to the small size of the cohort, the excess lung cancer mortality
for the underground miners was not statistically significant. However,
the authors concluded that the portion of excess lung cancer not
attributable to radon exposure could be explained by the combined
effects of diesel exhaust and silica exposure. Three of the ten lung
cancers reported for underground miners were experienced by conductors
of diesel-powered ore trains.
Christie et al. (1994, 1995) studied mortality in a cohort of
23,630 male Australian (New South Wales, NSW)
[[Page 5600]]
coal mine workers who entered the industry after 1972. Although the
majority of these workers were underground miners, most of whom were
presumably exposed to diesel emissions, the cohort included office
workers and surface (``open cut'') miners. The cohort was followed up
through 1992. After adjusting for age, death rates were lower than
those in the general male population for all major causes except
accidents. This included the mortality rate for all cancers as a group
(Christie et al., 1995, Table 1). Lower-than-normal incidence rates
were also reported for cancers as a group and for lung cancer
specifically (Christie et al., 1994, Table 10).
The investigators noted that the workers included in the cohort
were all subject to pre-employment physical examinations. They
concluded that ``it is likely that the well known `healthy worker'
effect * * * was operating'' and that, instead of comparing to a
general population, ``a more appropriate comparison group is Australian
petroleum industry workers.'' (Christie et al., 1995) In contrast to
the comparison with the population of NSW, the all-cause standardized
mortality ratio (SMR) for the cohort of coal miners was greater than
for petroleum workers by a factor of over 20 percent--i.e., 0.76 vs.
0.63 (ibid., p. 20). However, the investigators did not compare the
cohort to petroleum workers specifically with respect to lung cancer or
other causes of death. Nor did they adjust for a healthy worker effect
or make any attempt to compare mortality or lung cancer rates among
workers with varying degrees of diesel exposure within the cohort.
Despite the elevated SMR relative to petroleum workers, several
commenters cited this study as evidence that exposure to diesel
emissions was not causally associated with an increased risk of lung
cancer (or with adverse health effects associated with fine
particulates). These commenters apparently ignored the investigators'
explanation that the low SMRs they reported were likely due to a
healthy worker effect. Furthermore, since the cohort exhibited lower-
than-normal mortality rates due to heart disease and non-cancerous
respiratory disease, as well as to cancer, there may well have been
less tobacco smoking in the cohort than in the general population.
Therefore, it is reasonably likely that the age-adjusted lung cancer
rate would have been elevated, if it had been adjusted for smoking and
for a healthy worker effect based on mortality from causes other than
accidents or respiratory disease. In addition, the cohort SMR for
accidents (other than motor vehicle accidents) was significantly above
that of the general population. Since the coal miners experienced an
elevated rate of accidental death, they had a lower-than-normal chance
to die from other causes or to develop lung cancer. The investigators
made no attempt to adjust for the competing, elevated risk of death due
to occupational accidents.
Given the lack of any adjustment for smoking, healthy worker
effect, or the competing risk of accidental death, the utility of this
study in evaluating health consequences of Dpm exposure is severely
limited by its lack of any internal comparisons or comparisons to a
comparable group of unexposed workers. Furthermore, even if such
adjustments or comparisons were made, several other attributes of this
study limit its usefulness for evaluating whether exposure to diesel
emissions is associated with an increased risk of lung cancer. First,
the study was designed in such a way as to allow inadequate latency for
a substantial portion of the cohort. Although the cohort was followed
up only through 1992, it includes workers who entered the workforce at
the end of 1992. Therefore, there is no minimum duration of
occupational exposure for members of the cohort. Approximately 30
percent of the cohort was employed in the industry for less than 10
years, and the maximum duration of employment and latency combined was
20 years. Second, average age for members of the cohort was only 40 to
50 years (Christie et al., p. 7), and the rate of lung cancer was based
on only 29 cases. The investigators acknowledged that ``it is a
relatively young cohort'' and that ``this means a small number of
cancers available for analysis, because cancer is more common with
advancing age * * *.'' They further noted that ``* * * the number of
cancers available for analysis is increasing very rapidly. As a
consequence, every year that passes makes the cancer experience of the
cohort more meaningful in statistical terms.'' (ibid., p. 27) Third,
miners's work history was not tracked in detail, beyond identifying the
first mine in which a worker was employed. Some of these workers may
have been employed, for various lengths of time, in both underground
and surface operations at very different levels of diesel exposure.
Without detailed work histories, it is not possible to construct even
semi-quantitative measures of diesel exposure for making internal
comparisons within the cohort.
One commenter (MARG) claimed that this (NSW) study ``* * * reflects
the latest and best scientific evidence, current technology, and the
current health of miners'' and that it ``is not rational to predicate
regulations for the year 2000 and beyond upon older scientific studies
* * *.'' For the reasons stated above, MSHA believes, to the contrary,
that the NSW study contributes little or no information on the
potential health effects of long-term dpm exposures and that whatever
information it does contribute does not extend to effects, such as
cancer, expected in later life.
Furthermore, three even more recent studies are available that MSHA
regards as far more informative for the purposes of the present risk
assessment. Unlike the NSW study, these directly address Dpm exposure
and the risk of lung cancer. Two of these studies (Johnston et al.,
1997; Saverin et al., 1999), both incorporating a quantitative Dpm
exposure assessment, were carried out specifically on mining cohorts
and will be discussed next. The third (Bruske-Hohlfeld et al., 1999) is
a case-control study not restricted to miners and will be discussed in
the following subsection. In accordance with MARG's emphasis on the
timeliness of scientific studies, MSHA places considerable weight on
the fact that all three--the most recent epidemiologic studies
available--reported an association between diesel exposure and an
increased risk of lung cancer.
Johnston et al. (1997) studied a cohort of 18,166 coal miners
employed in ten British coal mines over a 30-year period. Six of these
coal mines used diesel locomotives, and the other four were used for
comparison. Historical NOX and respirable dust concentration
measurements were available, having routinely been collected for
monitoring purposes. Two separate approaches were taken to estimate dpm
exposures, leading to two different sets of estimates. The first
approach was based on NOX measurements, combined with
estimated ratios between dpm and NOX. The second approach
was based on complex calculations involving measurements of total
respirable dust, ash content, and the ratio of quartz to dust for
diesel locomotive drivers compared to the ratio for face workers
(ibid., Figure 4.1 and pp 25-46). These calculations were used to
estimate dpm exposure concentrations for the drivers, and the estimates
were then combined with traveling times and dispersion rates to form
estimates of dpm concentration levels for other occupational groups. In
four of the six dieselized mines, the NOX-based and dust-
based estimates of dpm were in generally good agreement, and they
[[Page 5601]]
were combined to form time-independent estimates of shift average dpm
concentration for individual seams and occupational groups within each
mine. In the fifth mine, the PFR measurements were judged unreliable
for reasons extensively discussed in the report, so the NOX-
based estimates were used. There was no NOX exposure data
for the sixth mine, so they used dust-based estimates of dpm exposure.
Final estimates of shift-average dpm concentrations ranged from 44
g/m\3\ to 370 g/m\3\ for locomotive drivers and from
1.6 g/m\3\ to 40 g/m\3\ for non-drivers at various
mines and work locations (ibid.,Tables 8.3 and 8.6, respectively).
These were combined with detailed work histories, obtained from
employment records, to provide an individual estimate of cumulative dpm
exposure for each miner in the cohort. Although most cohort members
(including non-drivers) had estimated cumulative exposures less than 1
g-hr/m\3\, some members had cumulative exposures that ranged as high as
11.6 g-hr/m\3\ (ibid., Figure 9.1 and Table 9.1).
A statistical analysis (time-dependent proportional hazards
regression) was performed to examine the relationship between lung
cancer risk and each miner's estimated cumulative dpm exposure
(unlagged and lagged by 15 years), attained age, smoking habit, mine,
and cohort entry date. Smoking habit was represented by non-smoker, ex-
smoker, and smoker categories, along with the average number of
cigarettes smoked per day for the smokers. Pipe tobacco consumption was
expressed by an equivalent number of cigarettes per day.
In their written comments, MARG and the NMA both mischaracterized
the results of this study, apparently confusing it with a preliminary
analysis of the same cohort. The preliminary analysis (one part of what
Johnston et al. refer to as the ``wider mortality study'') was
summarized in Section 1.2 (pp 3-5) of the 105-page report at issue,
which may account for the confusion by MARG and the NMA.\50\
---------------------------------------------------------------------------
\50\ Since MARG and the NMA both stressed the importance of a
quantitative exposure assessment, it is puzzling that they focused
on a crude SMR from the preliminary analysis and ignored the
quantitative results from the subsequent analysis. Johnston et al.
noted that SMRs from the preliminary analysis were consistent ``with
other studies of occupational cohorts where a healthy worker effect
is apparent.'' But even the preliminary analysis explored a possible
surrogate exposure-response relationship, rather than simply relying
on SMRs. Unlike the analysis by Johnston et al., the preliminary
analysis used travel time as a surrogate measure of dpm exposure and
made no attempt to further quantify dpm exposure concentrations.
(ibid.,p.5)
---------------------------------------------------------------------------
Contrary to the MARG and NMA characterization, Johnston et al.
found a positive, quantitative relationship between cumulative dpm
exposure (lagged by 15 years) and an excess risk of lung cancer, after
controlling for age, smoking habit, and cohort entry date. For each
incremental g-hr/m\3\ of cumulative occupational dpm exposure, the
relative risk of lung cancer was estimated to increase by a factor of
22.7 percent. Adjusting for mine-to-mine differences that may account
for a portion of the elevated risk reduced the estimated RR factor to
15.6 percent. Therefore, with the mine-specific adjustment, the
estimated RR was 1.156 per g-hr/m\3\ of cumulative dpm exposure. It
follows that, based on the mine-adjusted model, the estimated RR for a
specified cumulative exposure is 1.156 raised to a power equal to that
exposure. For example, RR = (1.156)\3.84\ = 1.74 for a cumulative dpm
exposure of 3.84 g-hr/m\3\, and RR = (1.156)\7.68\ = 3.04 for a
cumulative dpm exposure of 7.68 g-hr/m\3\.\51\ Estimates of RR based on
the mine-unadjusted model would substitute 1.227 for 1.156 in these
calculations.
---------------------------------------------------------------------------
\51\ Assuming an average dpm concentration of 200 g/
m\3\ and 1920 work hours per year, 3.84 g-hr/m\3\ and 7.68 g-hr/m\3\
correspond to 10 and 20 years of occupational exposure,
respectively.
---------------------------------------------------------------------------
Two limitations of this study weaken the evidence it presents of an
increasing exposure-response relationship. First, although the exposure
assessment is quantitative and carefully done, it is indirect and
depends heavily on assumptions linking surrogate measurements to dpm
exposure levels. The authors, however, analyzed sources of inaccuracy
in the exposure assessment and concluded that ``the similarity between
the estimated * * * [dpm] exposure concentrations derived by the two
different methods give some degree of confidence in the accuracy of the
final values * * *.'' (ibid., pp. 71-75) Second, the highest estimated
cumulative dpm exposures were clustered at a single coal mine, where
the SMR was elevated relative to the regional norm. Therefore, as the
authors pointed out, this one mine greatly influences the results and
is a possible confounder in the study. The investigators also noted
that this mine was ``* * * found to have generally the higher exposures
to respirable quartz and low level radiation.'' Nevertheless, MSHA
regards it likely that the relatively high dpm exposures at this mine
were responsible for at least some of the excess mortality. There is no
apparent way, however, to ascertain just how much of the excess
mortality (including lung cancer) at this coal mine should be
attributed to high occupational dpm exposures and how much to
confounding factors distinguishing it (and the employees working there)
from other mines in the study.
The RR estimates based on the mine-unadjusted model assume that the
excess lung cancer observed in the cohort is entirely attributable to
dpm exposures, smoking habits, and age distribution. If some of the
excess lung cancer is attributed to other differences between mines,
then the dpm effect is estimated by the lower RR based on the mine-
adjusted model.
For purposes of comparison with the findings of Saverin et
al.(1999), it will be useful to calculate the RR for a cumulative dpm
exposure of 11.7 g-hr/m\3\ (i.e., the approximate equivalent of 4.9 mg-
yr/m\3\ TC).\52\ At this exposure level, the mine-unadjusted model
produces an estimated RR = (1.227) \11.7\ = 11, and the mine-adjusted
model produces an estimated RR = (1.156) \11.7\ = 5.5.
---------------------------------------------------------------------------
\52\ This value represents 20 years of cumulative exposure for
the most highly exposed category of workers in the cohort studied by
Saverin et al.
As explained elsewhere in this preamble, TC constitutes
approximately 80 percent of total dpm. Therefore, the TC value of
4.9 mg-yr/m\3\ presented by Saverin et al. must first be divided by
0.8 to produce a corresponding dpm value of 6.12 mg-yr/m\3\. To
convert this result to the units used by Johnston et al., it is then
multiplied by 1920 work hours per year and divided by 1000 mg/g to
yield 11.7 g-hr/m\3\. This is nearly identical to the maximum
cumulative dpm exposure estimated for locomotive drivers in the
study by Johnston et al. (See Johnston et al., op cit., Table 9.1.)
---------------------------------------------------------------------------
Saverin et al. (1999) studied a cohort of male potash miners in
Germany who had worked underground for at least one year after 1969,
when the mines involved began converting to diesel powered vehicles and
loading equipment. Members of the cohort were selected based on company
medical records, which also provided bi-annual information on work
location for each miner and, routinely after 1982, the miner's smoking
habits. After excluding miners whose workplace histories could not be
reconstructed from the medical records (5.5 percent) and miners lost to
follow-up (1.9 percent), 5,536 miners remained in the cohort. Within
this full cohort, the authors defined a sub-cohort consisting of 3,258
miners who had ``worked underground for at least ten years, held one
single job during at least 80% of their underground time, and held not
more than three underground jobs in total.''
The authors divided workplaces into high, medium, and low diesel
exposure categories, respectively corresponding
[[Page 5602]]
to production, maintenance, and workshop areas of the mine. Each of
these three categories was assigned a representative respirable TC
concentration, based on an average of measurements made in 1992. These
averages were 390 g/m\3\ for production, 230 g/m\3\
for maintenance, and 120 g/m\3\ for workshop. Some commenters
expressed concern about using average exposures from 1992 to represent
exposure throughout the study. The authors justified using these
measurement averages to represent exposure levels throughout the study
period because ``the mining technology and the type of machinery used
did not change substantially after 1970.'' This assumption was based on
interviews with local engineers and industrial hygienists.
Thirty-one percent of the cohort consented to be interviewed, and
information from these interviews was used to validate the work history
and smoking data reconstructed from the medical records. The TC
concentration assigned to each work location was combined with each
miner's individual work history to form an estimate of cumulative
exposure for each member of the cohort. Mean duration of exposure was
15 years. As of the end of follow-up in 1994, average age was 49 years,
average time since first exposure was 19 years, and average cumulative
exposure was 2.70 mg-y/m\3\.
The authors performed an analysis (within each TC exposure
category) of smoking patterns compared with cumulative TC exposure.
They also analyzed smoking misclassification as estimated by comparing
information from the interviews with medical records. From these
analyses, the authors determined that the cohort was homogeneous with
respect to smoking and that a smoking adjustment was neither necessary
nor desirable for internal comparisons. However, they did not entirely
rule out the possibility that smoking effects may have biased the
results to some extent. On the other hand, the authors concluded that
asbestos exposure was minor and restricted to jobs in the workshop
category, with negligible effects. The miners were not occupationally
exposed to radon progeny, as documented by routine measurement records.
As compared to the general male population of East Germany, the
cohort SMR for all causes combined was less than 0.6 at a 95-percent
confidence level. The authors interpreted this as demonstrating a
healthy worker effect, noting that ``underground workers are heavily
selected for health and sturdiness, making any surface control group
incomparable.'' Accordingly, they performed internal comparisons within
the cohort of underground miners. The RR reported for lung cancer among
miners in the high-exposure production category, compared to those in
the low-exposure workshop category, was 2.17. The corresponding RR was
not elevated for other cancers or for diseases of the circulatory
system.
Two statistical methods were used to investigate the relationship
between lung cancer RR and each miner's age and cumulative TC exposure:
Poisson regression and time-dependent proportional hazards regression.
These two statistical methods were applied to both the full cohort and
the subcohort, yielding four different estimates characterizing the
exposure-response relationship. Although a high confidence level was
not achieved, all four of these results indicated that the RR increased
with increasing cumulative TC exposure. For each incremental mg-yr/m\3\
of occupational TC exposure, the relative risk of lung cancer was
estimated to increase by the following multiplicative factor: \53\
---------------------------------------------------------------------------
\53\ MSHA determined these values by calculating the antilog, to
the base e, of each corresponding estimate of reported by
Saverin et al. (op cit.) in their Tables III and IV. The cumulative
exposure unit of mg-yr/m \3\ refers to the average TC concentration
experienced over a year's worth of 8-hour shifts.
------------------------------------------------------------------------
RR per mg-yr/m3
-------------------
Method Full
cohort Subcohort
------------------------------------------------------------------------
Poisson............................................. 1.030 1.139
Proportional Hazards................................ 1.112 1.225
------------------------------------------------------------------------
Based on these estimates, the RR for a specified cumulative TC
exposure (X) can be calculated by raising the tabled value to a power
equal to X. For example, using the proportional hazards analysis of the
subcohort, the RR for X = 3.5 mg-yr/m3 is
(1.225)3.5 = 2.03.\54\ The authors calculated the RR
expected for a cumulative TC exposure of 4.9 mg-yr/m3, which
corresponds to 20 years of occupational exposure for miners in the
production category of the cohort. These miners were exposed for five
hours per 8-hour shift at an average TC concentration of 390
g/m3. The resulting RR values were reported as
follows:
---------------------------------------------------------------------------
\54\ This is the estimated risk relative not to miners in the
workshop category but to a theoretical age-adjusted baseline risk
for cohort members accumulating zero occupational TC exposure.
------------------------------------------------------------------------
RR for 4.9 mg-yr/
m3
Method -------------------
Full
cohort Subcohort
------------------------------------------------------------------------
Poisson............................................. 1.16 1.89
Proportional Hazards................................ 1.68 2.70
------------------------------------------------------------------------
This study has two important limitations that weaken the evidence
it presents of a positive correlation between cumulative TC exposure
and the risk of lung cancer. These are (1) potential confounding due to
tobacco smoking and (2) a significant probability (i.e., greater than
10 percent) that a correlation of the magnitude found could have arisen
simply by chance, given that it were based on a relatively small number
of lung cancer cases.
Although data on smoking habits were compiled from medical records
for approximately 80 percent of the cohort, these data were not
incorporated into the statistical regression models. The authors
justified their exclusion of smoking from these models by showing that
the likelihood of smoking was essentially unrelated to the cumulative
TC exposure for cohort members. Based on the portion of the cohort that
was interviewed, they also determined that the average number of
cigarettes smoked per day was the same for smokers in the high and low
TC exposure categories (production and workshop, respectively).
However, these same interviews led them to question the accuracy of the
smoking data that had been compiled from medical records. Despite the
cohort's apparent homogeneity with respect to smoking, the authors
noted that smoking was potentially such a strong confounder that ``even
small inaccuracies in smoking data could cause effects comparable in
size to the weak carcinogenic effect of diesel exhaust.'' Therefore,
they excluded the smoking data from the analysis and stated they could
not entirely rule out the possibility of a smoking bias. MSHA agrees
with the authors of this report and the HEI Expert Panel (op cit.) that
even a high degree of cohort homogeneity does not rule out the
possibility of a spurious correlation due to residual smoking effects.
Nevertheless, because of the cohort's homogeneity, the authors
concluded that ``the results are unlikely to be substantially biased by
confounding,'' and MSHA accepts this conclusion.
The second limitation of this study is related to the fact that the
results are based on a total of only 38 cases of lung cancer for the
full cohort and 21 cases for the subcohort. In their description of
this study at the May 27, 1999, public
[[Page 5603]]
hearing, NIOSH noted that the ``lack of [statistical] significance may
be a result of the study having a small cohort (approximately 5,500
workers), a limited time from first exposure (average of 19 years), and
a young population (average age of 49 years at the end of follow-up).''
More cases of lung cancer may be expected to occur within the cohort as
its members grow older. The authors of the study addressed statistical
significance as follows:
* * * the small number of lung cancer cases produced wide confidence
intervals for all measures of effect and substantially limited the
study power. We intend to extend the follow-up period in order to
improve the statistical precision of the exposure-response
relationship. [Saverin et al., op cit.]
Some commenters stated that due to these limitations, data from the
Saverin et al. study should not be the basis of this rule. On the other
hand, NIOSH commented that ``[d]espite the limitations discussed * * *
the findings from the Saverin et al. (1999) study should be used as an
alternative source of data for quantifying the possible lung cancer
risks associated with Dpm exposures.'' As stated earlier, MSHA is not
relying on any single study but, instead, basing its evaluation on the
weight of evidence from all available data.
(iii) Best Available Epidemiologic Evidence
Based on the evaluation criteria described earlier, and after
considering all the public comment that was submitted, MSHA has
identified four cohort studies (including two from U.S.) and four case-
control studies (including three from U.S.) that provide the best
currently available epidemiologic evidence relating dpm exposure to an
increased risk of lung cancer. Three of the 11 studies involving miners
fall into this select group. MSHA considers the statistical
significance of the combined evidence far more important than
confidence levels for individual studies. Therefore, in choosing the
eight most informative studies, MSHA placed less weight on statistical
significance than on the other criteria. The basis for MSHA's selection
of these eight studies is summarized as follows:
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Six entirely negative studies were identified earlier in this risk
assessment. Several commenters objected to MSHA's treatment of the
negative studies, indicating that they had been discounted without
sufficient justification. To put this in proper perspective, the six
negative studies should be compared to those MSHA has identified as the
best available epidemiologic evidence, with respect to the same
evaluation criteria. (It should be noted that the statistical
significance of a negative study is best represented by its power.) In
accordance with those criteria, MSHA discounts the evidentiary
significance of these six studies for the following reasons:
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Other studies proposed as counter-evidence by some commenters will
be addressed in the next subsection of this risk assessment.
The eight studies MSHA identified as representing the best
available epidemiologic evidence all reported an elevated risk of lung
cancer associated with diesel exposure. The results from these studies
will now be reviewed, along with MSHA's response to public comments as
appropriate.
Boffetta et al., 1988
The structure of this cohort study was summarized in the preceding
subsection of this risk assessment. The following table contains the
main results. The relative risks listed for duration of exposure were
calculated with reference to all members of the cohort reporting no
diesel exposure, regardless of occupation, and adjusted for age,
smoking pattern, and other occupational exposures (asbestos, coal and
stone dusts, coal tar and pitch, and gasoline exhausts). The relative
risks listed for occupations were calculated for cohort members that
ever worked in the occupation, compared to cohort members never working
in any of the four occupations listed and reporting no diesel exposure.
These four relative risks were adjusted for age and smoking pattern
only. Smoking pattern was coded by 5 categories: never smoker; current
1-20 cigarettes per day; current 21 or more cigarettes per day; ex-
smoker of cigarettes; current or past pipe and/or cigar smoker.
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[[Page 5608]]
In addition to comments (addressed earlier) on the RR for miners in
this study, IMC Global submitted several comments pertaining to the RR
calculated for persons who explicitly stated that they had been
occupationally exposed to diesel emissions. This RR was 1.18 for
persons reporting any exposure (regardless of duration) compared to all
subjects reporting no exposure. MSHA considers the most important issue
raised by IMC Global to be that 20.6 percent of all cohort members did
not answer the question about occupational diesel exhaust exposure
during their lifetimes, and these subjects experienced a higher age-
adjusted mortality rate than the others. As the authors of this study
acknowledged, this ``could introduce a substantial bias in the estimate
of the association.'' (Boffetta et al., 1988, p.412).
To show that the impact of this bias could indeed be substantial,
the authors of the study addressed one extreme possibility, in which
all ``unknowns'' were actually unexposed. Under this scenario,
excluding the ``unknowns'' would have biased the calculated RR upward
by a sufficient amount to explain the entire 18-percent excess in RR.
This would not, however, explain the higher RR for persons reporting
more than 16 years exposure, compared to the RR for persons reporting 1
to 15 years. Moreover, the authors did not discuss the opposite
extreme: if all or most of the ``unknowns'' who experienced lung cancer
were actually exposed, then excluding them would have biased the
calculated RR downward. There is little basis for favoring one of these
extremes over the other.
Another objection to this study raised by IMC Global was:
All exposure information in the study was self-reported and not
validated. The authors of the study have no quantitative data or
measurements of actual diesel exhaust exposures.
MSHA agrees with IMC Global and other commenters that a lack of
quantitative exposure measurements limits the strength of the evidence
this study presents. MSHA believes, however, that the evidence
presented is nevertheless substantial. The possibility of random
classification errors due to self-reporting of exposures does not
explain why persons reporting 16 or more years of exposure would
experience a higher relative risk of lung cancer than persons reporting
1 to 15 years of exposure. This difference is not statistically
significant, but random exposure misclassification would tend to make
the effects of exposure less conspicuous. Nor can self-reporting
explain why an elevated risk of lung cancer would be observed for four
occupations commonly associated with diesel exposure.
Furthermore, the study's authors did perform a rough check on the
accuracy of the cohort's exposure information. First, they confirmed
that, after controlling for age, smoking, and other occupational
exposures, a statistically significant relationship was found between
excess lung cancer and the cohort's self-reported exposures to
asbestos. Second they found no such association for self-reported
exposure to pesticides and herbicides, which they considered unrelated
to lung cancer (ibid., pp. 410-411).
IMC Global also commented that the ``* * * study may suffer from
volunteer bias in that the cohort was healthier and less likely to be
exposed to important risk factors, such as smoking or alcohol.'' They
noted that this possibility ``is supported by the U.S. EPA in their
draft Health Assessment Document for Diesel Emissions.''
The study's authors noted that enrollment in the cohort was
nonrandom and that participants tended to be healthier and less exposed
to various risk factors than the general population. These differences,
however, would tend to reduce any relative risk for the cohort
calculated in comparison to the external, general population. The
authors pointed out that external comparisons were, therefore,
inappropriate; but ``the internal comparisons upon which the foregoing
analyses are based are not affected strongly by selection biases.''
(ibid.)
Although the 1999 EPA draft notes potential volunteer bias, it
concludes: ``Given the fact that all diesel exhaust exposure
occupations * * * showed elevated lung cancer risk, this study is
suggestive of a causal association.'' \55\ (EPA, 1999, p. 7-13) No
objection to this conclusion was raised in the most recent CASAC review
of the EPA draft (CASAC, 2000).
---------------------------------------------------------------------------
\55\ In his review of this study for the NMA, Dr. Peter Valberg
stated: ``This last sentence reveals EPA's bias; the RRs for truck
drivers and railroad workers were not statistically elevated.''
Contrary to Dr. Valberg's statement, the RRs were greater than 1.0
and, therefore, were ``statistically elevated.'' Although the
elevation for these two occupations was not statistically
significant at a 95-percent confidence level, the EPA made no claim
that it was. Under a null hypothesis of no real association, the
probability should be \1/2\ that the RR would exceed 1.0 for an
occupation associated with diesel exposure. Therefore, under the
null hypothesis, the probability that the RR would exceed 1.0 for
all four such occupations is (1/2) 4 = 0.06. This
corresponds to a 94-percent confidence level for rejecting the null
hypothesis.
---------------------------------------------------------------------------
Boffetta et al., 1990
This case-control study was based on 2,584 male hospital patients
with histologically confirmed lung cancer, matched with 5099 male
patients with no tobacco-related diseases. Cases and controls were
matched within each of 18 hospitals by age (within two years) and year
of interview. Information on each patient, including medical and
smoking history, occupation, and alcohol and coffee consumption, was
obtained at the time of diagnosis in the hospital, using a structured
questionnaire. For smokers, smoking data included the number of
cigarettes per day. Prior to 1985, only the patient's usual job was
recorded. In 1985, the questionnaire was expanded to include up to five
other jobs and the length of time worked in each job. After 1985,
information was also obtained on dietary habits, vitamin consumption,
and exposure to 45 groups of chemicals, including diesel exhaust.
The authors categorized all occupations into three groups,
representing low, possible, and probable diesel exhaust exposure. The
``low exposure'' group was used as the reference category for
calculating odds ratios for the ``possible'' and ``probable'' job
groups. These occupational comparisons were based on the full cohort of
patients, enrolled both before and after 1985. A total of 35 cases and
49 controls (all enrolled after the questionnaire was expanded in 1985)
reported a history of diesel exposure. The reference category for self-
reported diesel exposure consisted of a corresponding subset of 442
cases and 897 controls reporting no diesel exposure on the expanded
questionnaire. The authors made three comparisons to rule out bias due
to self-reporting of exposure: (1) No difference was found between the
average number of jobs reported by cases and controls; (2) the
association between self-reported asbestos exposure was in agreement
with previously published estimates; and (3) no association was found
for two exposures (pesticides and fuel pumping) considered unrelated to
lung cancer (ibid., p. 584).
Stober and Abel (1996) identified this study as being ``of eminent
importance owing to the care taken in including the most influential
confounding factors and analyses of dose-effect relationships.'' The
main findings are presented in the following table. All of these
results were obtained using logistic regression, factoring in the
estimated effects of age, race, years of
[[Page 5609]]
education, number of cigarettes per day, and asbestos exposure (yes or
no). An elevated risk of lung cancer was reported for workers with more
than 30 years of either self-reported or ``probable'' diesel exposure.
The authors repeated the occupational analysis using ``ever'' rather
than ``usual'' employment in jobs classified as ``probable'' exposure,
with ``remarkably similar'' results (ibid., p. 584).
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The study's authors noted that most U.S. trucks did not have diesel
engines until the late 1950s or early 1960s and that many smaller
trucks are still powered by gasoline engines. Therefore, they performed
a separate analysis of truck drivers cross-classified by self-reported
diesel exposure ``to compare presumptive diesel truck drivers with
nondiesel drivers.'' After adjusting for smoking, the resulting OR for
diesel drivers was 1.25, with a 95-percent confidence interval of 0.85
to 2.76 (ibid., p. 585).
Bruske-Hohlfeld et al., 1999
This was a pooled analysis of two case-control studies on lung
cancer in Germany. The data pool consisted of 3,498 male cases with
histologically or cytologically confirmed lung cancer and 3,541 male
controls randomly drawn from the general population. Cases and controls
were matched for age and region of residence. For the pooled analysis,
information on demographic characteristics, smoking, and detailed job
and job-task history was collected by personal interviews with the
cases and controls, using a standardized questionnaire.
Over their occupational lifetimes, cases and controls were employed
in an average of 2.9 and 2.7 different jobs, respectively. Jobs
considered to have had potential exposure to diesel exhaust were
divided into four groups: Professional drivers (including trucks,
buses, and taxis), other ``traffic-related'' jobs (including switchmen
and operators of diesel locomotives or diesel forklift trucks), full-
time drivers of farm tractors, and heavy equipment operators. Within
these four groups, each episode of work in a particular job was
classified as being exposed or not exposed to diesel exhaust, based on
the written description of job tasks obtained during the interview.
This exposure assessment was done without knowledge of the subject's
case or control status. Each subject's lifetime duration of
occupational exposure was compiled using only the jobs determined to
have been diesel-exposed. There were 264 cases and 138 controls who
accumulated diesel exposure exceeding 20 years, with 116 cases and 64
controls accumulating more than 30 years of occupational exposure.
For each case and control, detailed smoking histories from the
questionnaire were used to establish smoking habit, including
consumption of other tobacco products, cumulative smoking exposure
(expressed as pack-years), and years since quitting smoking. Cumulative
asbestos exposure (expressed as the number of exposed working days) was
assessed based on 17 job-specific questionnaires that supplemented the
main questionnaire.
[[Page 5610]]
The main findings of this study, all adjusted for cumulative
smoking and asbestos exposure, are presented in the following table.
Although the odds ratio for West German professional drivers was a
statistically significant 1.44, as shown, the odds ratio for East
German professional drivers was not elevated. As a possible
explanation, the authors noted that after 1960, the number of vehicles
(cars, busses, and trucks) with diesel engines per unit area was about
five times higher in West Germany than in East Germany. Also, the
higher OR shown for professional drivers first exposed after 1955,
compared to earlier years of first exposure, may have resulted from the
higher density of diesel traffic in later years.
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As the authors noted, a strength of this study is the good
statistical power resulting from having a significant number of workers
exposed to diesel emissions for more than 30 years. Another strength is
the statistical treatment of potential confounders, using quantitative
measures of cumulative smoking and asbestos exposures.
Although they did not rely solely on job title, and differentiated
between diesel-exposed and unexposed work periods, the authors
identified limitations in the assessment of diesel exposure, ``under
these circumstances leading to an odds ratio that is biased towards one
and an underestimation of the true [relative] risk of lung cancer.'' A
more quantitative assessment of diesel exposure would tend to remove
this bias, thereby further elevating the relative risks. Therefore, the
authors concluded that their study ``showed a statistically significant
increase in lung cancer risk for workers occupationally exposed to
[diesel exhaust] in Germany with the exception of professional drivers
in East Germany.''
Garshick et al., 1987
This case-control study was based on 1,256 primary lung cancer
deaths and 2,385 controls whose cause of death was not cancer, suicide,
accident, or unknown. Cases and controls were drawn from records of the
U.S. Railroad Retirement Board (RRB) and matched within 2.5 years of
birth date and 31 days of death date. Selected jobs, with and without
regular diesel exposure, were identified by a review of job titles and
duties and classified as ``exposed'' or ``unexposed'' to diesel
exhaust. For 39 jobs, this exposure classification was confirmed by
personal sampling of current respirable dust concentrations, adjusted
for cigarette smoke, at four different railroads. Jobs for which no
personal sampling was available were classified based on similarities
in location and activity to sampled jobs.
A detailed work history for each case and control was obtained from
an annual report filed with the RRB. This was combined with the
exposure classification for each job to estimate the lifetime total
diesel exposure (expressed as ``diesel-years'') for each subject. Years
spent not working for a railroad, or for which a job was not recorded,
were considered to be unexposed. This amounted to 2.4% of the total
worker-years from 1959 to death or retirement.
Because of the transition from steam to diesel locomotives in the
1950s, occupational lifetime exposures were accumulated beginning in
1959. Since many of the older workers retired not long after 1959 and
received little or no diesel exposure, separate analyses were carried
out for subjects above and below the age of 65 years at death. The
group of younger workers was considered to be less susceptible to
exposure misclassification.
Detailed smoking histories, including years smoked, cigarettes per
day, and years between quitting and death, were obtained from next of
kin. Based on job history, each case and control was also classified as
having had regular, intermittent, or no occupational asbestos exposure.
The main results of this study, adjusted for smoking and asbestos
exposure, are presented in the following table for workers aged less
than 65 years at the time of their death. All of these results were
obtained using logistic regression, conditioned on dates of birth and
death. The odds ratio presented in the shaded cell for 20 years of
unlagged exposure was derived from an analysis that modeled diesel-
years as a continuous variable. All of the other odds ratios in the
table were derived from analyses that modeled cumulative exposure
categorically, using workers with less than five diesel-years of
exposure as the reference group. Statistically significant elevations
of lung cancer risk were reported for the younger workers with at least
20 diesel-years of exposure or at least 15 years accumulated five years
prior to death. No elevated risk of lung cancer was observed for the
older workers, who were 65 or more years old at the time of their
death. The authors attributed this to the fact, mentioned above, that
many of these older workers retired shortly after the transition to
diesel-powered locomotives and, therefore, experienced little or no
occupational diesel exposure. Based on the results for younger workers,
they concluded that ``this study supports the hypothesis that
occupational exposure to diesel exhaust increases lung cancer risk.''
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In its 1999 draft Health Assessment Document for Diesel Emissions,
the U.S. EPA noted various limitations of this study but concluded that
``compared with previous studies [i.e., prior to 1987] * * *, [it]
provides the most valid evidence that occupational diesel exhaust
emission exposure increases the risk of lung cancer.'' (EPA, 1999, p.
7-33) No objection to this conclusion was raised in the most recent
CASAC review of the EPA draft (CASAC, 2000).
The EMA objected to this study's determination of smoking frequency
based on interviews with next of kin, stating that such determination
``generally results in an underestimate, as it has been shown that
cigarette companies manufacture 60% more product than public surveys
indicate are being smoked.''
A tendency to mischaracterize smoking frequency would have biased
the study's reported results if the degree of under- or over-estimation
varied systematically with diesel exposure. The EMA, however, submitted
no evidence that the smoking under-estimate, if it existed at all, was
in any way correlated with cumulative duration of diesel exposure. In
the absence of such evidence, MSHA finds no reason to assume
differential mis-reporting of smoking frequency.
Even more importantly, the EMA failed to distinguish between
``public surveys'' of the smokers themselves (who may be inclined to
understate their habit) and interviews with next of kin. The
investigators specifically addressed the accuracy of smoking data
obtained from next of kin, citing two studies on the subject. Both
studies reported a tendency for surrogate respondents to overestimate,
rather than underestimate, cigarette consumption. The authors concluded
that ``this could exaggerate the contribution of cigarette smoking to
lung cancer risk if the next of kin of subjects dying of lung cancer
were more likely to report smoking histories than were those of
controls.'' (ibid, p.1246)
IMC Global, along with Cox (1997) objected to several
methodological features of this study. MSHA's response to each of these
criticisms appears immediately following a summary quotation from IMC
Global's written comments:
(A) The regression models used to analyze the data assumed
without justification that an excess risk at any exposure level
implied an excess risk at all exposure levels.
The investigators did not extrapolate their regression models
outside the range supported by the data. Furthermore, MSHA is using
this study only for purposes of hazard identification at exposure
levels at least as high as those experienced by workers in the study.
Therefore, the possibility of a threshold effect at much lower levels
is irrelevant.
(B) The regression model used did not specify that the exposure
estimates were imperfect surrogates for true exposures. As a result,
the regression coefficients do not bear any necessary relationship
to the effects that they try to measure.
As noted by Cox (op cit.), random measurement errors for exposures
in an univariate regression model will tend to bias results in the
direction of no apparent association, thereby masking or reducing any
apparent effects of exposure. The crux of Cox's criticism, however, is
that, for statistical analysis
[[Page 5614]]
of the type employed in this study, random errors in a multivariate
exposure (such as an interdependent combination of smoking, asbestos,
and diesel exposure) can potentially bias results in either direction.
This objection fails to consider the fact that a nearly identical
regression result was obtained for the effect of diesel exposure when
smoking and asbestos exposure were removed from the model: OR = 1.39
instead of 1.41. Furthermore, even with a multivariate exposure,
measurement errors in the exposure being evaluated typically bias the
estimate of relative risk downward toward a null result. Relative risk
is biased upwards only when the various exposures are interrelated in a
special way. No evidence was presented that the data of this study met
the special conditions necessary for upward bias or that any such bias
would be large enough to be of any practical significance.
C) The * * * analysis used regression models without presenting
diagnostics to show whether the models were appropriate for the
date.
MSHA agrees that regression diagnostics are a valuable tool in
assuring the validity of a statistical regression analysis. There is
nothing at all unusual, however, about their not having been mentioned
in the published report of this study. Regression diagnostics are
rarely, if ever, published in epidemiologic studies making use of
regression analysis. This does not imply that such diagnostics were not
considered in the course of identifying an appropriate model or
checking how well the data conform to a given model's underlying
assumptions. Evaluation of the validity of any statistical analysis is
(or should be) part of the peer-review process prior to publication.
D) The * * * risk models assumed that 1959 was the effective year
when DE exposure started for each worker. Thus, the analysis ignored
the potentially large differences in pre-1959 exposures among
workers. This modeling assumption makes it impossible to interpret
the results of the study with confidence.
MSHA agrees that the lack of diesel exposure information on
individual workers prior to 1959 represents an important limitation of
this study. This limitation, along with a lack of quantitative exposure
data even after 1959, may preclude using it to determine, with
reasonable confidence, the shape or slope of a quantitative exposure-
response relationship. Neither of these limitations, however,
invalidates the study's finding of an elevated lung cancer risk for
exposed workers. MSHA is not basing any quantitative risk assessment on
this study and is relying on it, in conjunction with other evidence,
only for purposes of hazard identification.
E) The risk regression models * * * assume, without apparent
justification, that all exposed individuals have identical dose-
response model parameters (despite the potentially large differences
in their pre-1959 exposure histories). This assumption was not
tested against reasonable alternatives, e.g., that individuals born
in different years have different susceptibilities * * *
Cases and controls were matched on date of birth to within 2.5
years, and separate analyses were carried out for the two groups of
younger and older workers. Furthermore, it is not true that the
investigators performed no tests of reasonable alternatives even to the
assumption that younger workers shared the same model parameters. They
explored and tested potential interactions between smoking intensity
and diesel exposure, with negative results. The presence of such
interactions would have meant that the response to diesel exposure
differed among individuals, depending on their smoking intensity.
One other objection that Cox (op. cit.) raised specifically in
connection with this study was apparently overlooked by IMC Global. To
illustrate what he considered to be an improper evaluation of
statistical significance when more than one hypothesis is tested in a
study, Cox noted the finding that for workers aged less than 65 years
at time of death, the odds ratio for lung cancer was significantly
elevated at 20 diesel-years of exposure. He then asserted that this
finding was merely
* * * an instance of a whole family of statements of the form
``Workers who were A years or younger at the time of death and who
were exposed to diesel exhaust for Y years had a significantly
increased relative odds ratios for lung cancer. The probability of
at least one false positive occurring among the multiple hypotheses
in this family corresponding to different combinations of A (e.g.,
no more than 54, 59, 64, 69, 74, 79, etc. years old at death) and
durations of exposure (e.g., Y = 5, 10, 15, 20, 25, etc. years) is
not limited to 5% when each combination of A and Y values is tested
at a p = 5% significance level. For example, if 30 different (A, Y)
combinations are considered, each independently having a 5%
probability of a false positive (i.e., a reported 5% significance
level), then the probability of at least one false positive
occurring in the study as a whole is p = 1 - (1 - 0.05) 30 = 78%.
This p-value for the whole study is more than 15 times greater than
the reported significance level of 5%.
MSHA is evaluating the cumulative weight of evidence from many
studies and is not relying on the level of statistical significance
attached to any single finding or study viewed in isolation.
Furthermore, Cox's analysis of the statistical impact of multiple
comparisons or hypothesis tests is flawed on several counts, especially
with regard to this study in particular. First, the analysis relies on
a highly unrealistic assumption that when several hypotheses are tested
within the same study, the probabilities of false positives are
statistically independent. Second, Cox fails to distinguish between
those hypotheses or comparisons suggested by exploration of the data
and those motivated by prior considerations. Third, Cox ignores the
fact that the result in question was based on a statistical regression
analysis in which diesel exposure duration was modeled as a single
continuous variable. Therefore, this particular result does not depend
on multiple hypothesis-testing with respect to exposure duration.
Fourth, and most importantly, Cox assumes that age and exposure
duration were randomly picked for tested from a pool of interchangeable
possibilities and that the only thing distinguishing the combination of
``65 years of age'' and ``20 diesel-years of exposure'' from other
random combinations was that it happened to yield an apparently
significant result. This is clearly not the case. The investigators
divided workers into only two age groups and explained that this
division was based on the history of dieselization in the railroad
industry--not on the results of their data analysis. Similarly, the
result for 20 diesel-years of exposure was not favored over shorter
exposure times simply because 20 years yielded a significant result and
the shorter times did not. Lengthy exposure and latency periods are
required for the expression of increased lung cancer risks, and this
justifies a focus on the longest exposure periods for which sufficient
data are available.
Garshick et al., 1988; Garshick, 1991
In this study, the investigators assessed the risk of lung cancer
in a cohort of 55,407 white male railroad workers, aged 40 to 64 years
in 1959, who had begun railroad work between 1939 and 1949 and were
employed in one of 39 jobs later surveyed for exposure. Workers whose
job history indicated likely occupational exposure to asbestos were
excluded. Based on the subsequent exposure survey, each of the 39 jobs
represented in the cohort was classified as either exposed or unexposed
to diesel emissions. The cohort was followed through 1980, and
[[Page 5615]]
1,694 cases of death due to lung cancer were identified.
As in the 1987 study by the same investigators, detailed railroad
job histories from 1959 to date of death or retirement were obtained
from RRB records and combined with the exposure classification for each
job to provide the years of diesel exposure accumulated since 1959 for
each worker in the cohort. Using workers classified as ``unexposed''
within the cohort to establish a baseline, time-dependent proportional
hazards regression models were employed to evaluate the relative risk
of lung cancer for exposed workers. Although the investigators believed
they had excluded most workers with significant past asbestos exposures
from the cohort, based on job codes, they considered it possible that
some workers classified as hostlers or shop workers may have been
included in the cohort even if occupationally exposed to asbestos.
Therefore, they carried out statistical analyses with and without shop
workers and hostlers included.
The main results of this study are presented in the following
table. Statistically significant elevations of lung cancer risk were
found regardless of whether or not shop workers and hostlers were
included. The 1988 analysis adjusted for age in 1959, and the 1991
analysis adjusted, instead, for age at death or end of follow-up (i.e.,
end of 1980).\56\ In the 1988 analysis, any work during a year counted
as a diesel-year if the work was in a diesel-exposed job category, and
the results from the 1991 analysis presented here are based on this
same method of compiling exposure durations. Exposure durations
excluded the year of death and the four prior years, thereby allowing
for some latency in exposure effects. Results for the analysis
excluding shop workers and hostlers were not presented in the 1991
report, but the report stated that ``similar results were obtained.''
Using either method of age adjustment, a statistically significant
elevation of lung cancer risk was associated with each exposure
duration category. Using ``attained age,'' however, there was no strong
indication that risk increased with increasing exposure duration. The
1991 report concluded that ``there appears to be an effect of diesel
exposure on lung cancer mortality'' but that ``because of weaknesses in
exposure ascertainment * * *, the nature of the exposure-response
relationship could not be found in this study.''
\56\ Also, the 1991 analysis excluded 12 members of the cohort
due to discrepancies between work history and reported year of
death, leaving 55,395 railroad workers included in the analysis.
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Some commenters noted that removing the shop workers and hostlers
from the analysis increased the relative risk estimates. Dr. Peter
Valberg found this ``paradoxical,'' since workers in these categories
had later been found to experience higher average levels of diesel
exposure than other railroad workers.
This so-called paradox is likely to have resulted simply from
exposure misclassification for a significant portion of the shop
workers. The effect was explained by Garshick (1991) as follows:
[[Page 5616]]
* * * shop workers who worked in the diesel repair shops shared job
codes with workers in non-diesel shops where there was no diesel
exhaust * * *. Apparent exposure as a shop worker based on the job
code was then diluted with workers with the same job code but
without true exposure, making it less likely to see an effect in the
shop worker group. In addition, workers in the shop worker group of
job codes tended to have less stable career paths * * * compared to
the other diesel exposure categories.
So although many of the shopworkers may have been exposed to
relatively high dpm concentrations, many others were among the lowest-
exposed workers or were even unexposed because they spent their entire
occupational lifetimes in unexposed locations. This could readily
account for the increase in relative risks calculated when shop workers
were excluded from the analysis.
Dr. Valberg also noted that, according to Crump 1999), mortality
rates for cirrhosis of the liver and heart disease were significantly
elevated for ``train riders,'' who were exposed to diesel emissions, as
compared to other members of the cohort, who were less likely to be
exposed. It is also the train riders who account, primarily, for the
elevated risk of lung cancer associated with diesel exposure in the
overall cohort. Dr. Valberg interpreted this as suggesting that
``lifestyle'' factors such as diet or smoking habits, rather than
diesel exposure, were responsible for the increased risk of lung cancer
observed among the diesel-exposed workers.
Dr. Valberg presented no evidence that, apart from diesel exposure,
the train riders differed systematically from the other workers in
their smoking habits or in other ways that would be expected to affect
their risk of lung cancer. Therefore, MSHA views the suggestion of such
a bias as speculative. Even if lifestyle factors associated with train
ridership were responsible for an increased risk of cirrhosis of the
liver or heart disease, this would not necessarily mean that the same
factors were also responsible for the increased risk of lung cancer.
Still, it is hypothetically possible that systematic differences, other
than diesel exposure, between train riders and other railroad workers
could account for some or even all of the increased lung cancer risk.
That is why MSHA does not rely on this, or any other, single study in
isolation.
Some commenters, including the NMA, objected to this study on
grounds that it failed to control for potentially confounding factors,
principally smoking. The NMA stated that this ``has rendered its
utility questionable at best.'' As explained earlier, there is more
than one way in which a study can control for smoking or other
potential confounders. One of the ways is to make sure that groups
being compared do not differ with respect to the potential confounder.
In this study, workers with likely asbestos exposure were excluded from
the cohort, stability of workers within job categories was well
documented, and similar results were reported when job categories
subject to asbestos exposure misclassification were excluded. In their
1988 report, the investigators provided the following reasons to
believe that smoking did not seriously affect their findings:
* * * the cohort was selected to include only blue-collar
workers of similar socioeconomic class, a known correlate of
cigarette smoking * * *, in our case-control study [Garshick et
al.,1987], when cigarette smoking was considered, there was little
difference in the crude or adjusted estimates of diesel exhaust
effects. Finally, in the group of 517 current railroad workers
surveyed by us in 1982 * * *, we found no difference in cigarette
smoking prevalence between workers with and without potential diesel
exhaust exposure. [Garshick et al.,1988]
Since relative risks were based on internal comparisons, and the
cohort appears to have been fairly homogeneous, MSHA regards it as
unlikely that the association of lung cancer with diesel exposure in
this study resulted entirely from uncontrolled asbestos or smoking
effects. Nevertheless, MSHA recognizes that differential smoking
patterns may have affected, in either direction, the degree of
association reported in each of the exposure duration categories.
Cox (1997) re-analyzed the data of this study using exploratory,
nonparametric statistical techniques. As quoted by IMC Global, Cox
concluded that ``these methods show that DE [i.e., dpm] concentration
has no positive causal association with lung cancer mortality risk.''
MSHA believes this quotation (taken from the abstract of Cox's article)
overstates the findings of his analysis. At most, Cox confirmed the
conclusion by Garshick (1991) that these data do not support a positive
exposure-response relationship. Specifically, Cox determined that
inter-relationships among cumulative diesel exposure, age in 1959, and
retirement year make it ``impossible to prove causation by eliminating
plausible rival hypotheses based on this dataset.'' (Cox, 1997; p.826)
Even if Cox's analysis were correct, it would not follow that there is
no underlying causal connection between dpm exposure and lung cancer.
It would merely mean that the data do not contain internal evidence
implicating dpm exposure as the cause, rather than one or more of the
variables with which exposure is correlated. Cox presented no evidence
that any ``rival hypotheses'' were more plausible than causation by dpm
exposure. Furthermore, it may simply be, as Garshick suggested, that an
underlying exposure-response relationship is not evident ``because of
weaknesses in exposure ascertainment.'' (Garshick, 1991, op cit.) None
of this negates the fact that, after adjusting for either age in 1959
or ``attained'' age, lung cancer was significantly more prevalent among
the exposed workers.
Along similar lines, many commenters pointed out that an HEI expert
panel examined the data of this study (HEI, 1999) and found that it had
very limited use for quantitative risk assessment (QRA). Several of
these commenters mischaracterized the panel's findings. The NMA, for
example, drew the following unjustified conclusion from the panel's
report: ``In short, * * * the correct interpretation of the Garshick
study is that any occupational increase in lung cancer among train
workers was not due to diesel exposures.''
Contrary to the NMA's characterization, the HEI Expert Panel's
report stated that the data are
* * * consistent with findings of a weak association between death
from lung cancer and occupational exposure to diesel exhaust.
Although the secondary exposure-response analyses * * * are
conflicting, the overall risk of lung cancer was elevated among
diesel-exposed workers. [ibid., p.25]
The panel agreed with Garshick (1991) and Cox (1997) that the data
of this study do not support a positive exposure-response relationship.
Like Garshick and unlike Cox, however, the panel explicitly recognized
that problems with the data could mask such a relationship and that
this does not negate the statistically significant finding of elevated
risk among exposed workers. Indeed, the panel even identified several
factors, in addition to weak exposure assessment as suggested by
Garshick, that could mask a positive relationship: unmeasured
confounding variables such as cigarette smoking, previous occupational
exposures, or other sources of pollution; a ``healthy worker survivor
effect''; and differential misclassification or incomplete
ascertainment of lung cancer deaths. (HEI, 1999; p.32)
Positive exposure-response relationships based on these data were
reported by the California EPA (OEHHA, 1998). MSHA recognizes that
those findings were sensitive to various assumptions and that other
investigators
[[Page 5617]]
have obtained contrary results. The West Virginia Coal Association,
paraphrasing Dr. Peter Valberg, concluded that although the two studies
by Garshick et al. `` * * * may represent the best in the field, they
fail to firmly support the proposition that lung cancer risk in workers
derives from exposure to dpm.'' At least one commenter (IMC Global)
apparently reached a considerably stronger conclusion that they were of
no value whatsoever, and urged MSHA to ``discount their results and not
consider them in this rulemaking.'' On the other hand, in response to
the ANPRM, a consultant to the National Coal Association who was
critical of all other studies available at the time acknowledged that
these two:
* * * have successfully controlled for severally [sic] potentially
important confounding factors * * * Smoking represents so strong a
potential confounding variable that its control must be nearly
perfect if an observed association between cancer and diesel exhaust
is * * * [inferred to be causal]. In this regard, two observations
are relevant. First, both case-control [Garshick et al., 1987] and
cohort [Garshick et al., 1988] study designs revealed consistent
results. Second, an examination of smoking related causes of death
other than lung cancer seemed to account for only a fraction of the
association observed between diesel exposure and lung cancer. A high
degree of success was apparently achieved in controlling for smoking
as a potentially confounding variable. [Robert A. Michaels, RAM TRAC
Corporation, submitted by National Coal Association].
To a limited extent, MSHA agrees with Dr. Valberg and the West
Virginia Coal Association: these two studies--like every real-life
epidemiologic study--are not ``firmly'' conclusive when viewed in
isolation. Nevertheless, MSHA believes that they provide important
contributions to the overall body of evidence. Whether or not they can
be used to quantify an exposure-response relationship, these studies--
among the most comprehensive and carefully controlled currently
available--do show statistically significant increases in the risk of
lung cancer among diesel-exposed workers.
Johnston et al. (1997)
Since it focused on miners, this study has already been summarized
and discussed in the previous subsection of this risk assessment. The
main results are presented in the following table. The tabled relative
risk estimates presented for cumulative exposures greater than 1000 mg-
hr/m3 (i.e., 1 g-hr/m3) were calculated by MSHA
based on the regression coefficients reported by the authors. The
conversion from mg-hr/m3 to mg-yr/m3 assumes
1,920 occupational exposure hours per year. Although 6.1 mg-yr/
m3 Dpm roughly equals the cumulative exposure estimated for
the most highly exposed locomotive drivers in the study, the relative
risk associated with this exposure level is presented primarily for
purposes of comparison with findings of Saverin et al. (1999).
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In its post-hearing comments, MARG acknowledged that this study
``found a `weak association' between lung cancer and respiratory diesel
particulate exposure'' but failed to note that the estimated relative
risk increased with increasing exposure. MARG also stated that the
association was ``deemed non-significant by the researchers'' and that
``no association was found among men with different exposures working
in the same mines.'' Although the mine-adjusted model did not support
95-percent confidence for an increasing exposure-response relationship,
the mine-unadjusted model yielded a statistically significant positive
slope at this confidence level. Furthermore, since the mine-adjusted
model adjusts for differences in lung cancer rates between mines, the
fact that relative risk increased with increasing exposure under this
model indicates (though not at a 95-percent confidence level) that the
risk of lung cancer increased with exposure among men with different
exposures working in the same mines.
Saverin et al. (1999)
Since this study, like the one by Johnston et al., was carried out
on a cohort of miners, it too was summarized and discussed in the
previous subsection of this risk assessment. The main results are
presented in the following table. The relative risk estimates and
confidence intervals at the mean exposure level of 2.7 mg-yr/
m3 TC (total carbon) were calculated by MSHA, based on
values of and corresponding confidence intervals presented in
Tables III and IV of the
[[Page 5618]]
published report (ibid., p.420). The approximate equivalency between
4.9 mg-yr/m3 TC and 6.1 mg-yr/m3 dpm assumes
that, on average, TC comprises 80 percent of dpm.
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These results are not statistically significant at the conventional
95-percent confidence level. However, the authors noted that the
relative risk calculated for the subcohort was consistently higher than
that calculated for the full cohort. They also considered the subcohort
to have a superior exposure assessment and a better latency allowance
than the full cohort. According to the authors, these factors provide
``some assurance that the observed risk elevation was not entirely due
to chance since improving the exposure assessment and allowing for
latency effects should, in general, enhance exposure effects.''
Steenland et al., (1990, 1992, 1998)
The basis for the analyses in this series was a case-control study
comparing the risk of lung cancer for diesel-exposed and unexposed
workers who had belonged to the Teamsters Union for at least twenty
years (Steenland et al., 1990). Drawing from union records, 996 cases
of lung cancer were identified among more than 10,000 deaths in 1982
and 1983. For comparison to these cases, a total of 1,085 controls was
selected (presumably at random) from the remaining deaths, restricted
to those who died from causes other than lung cancer, bladder cancer,
or motor vehicle accident. Information on work history, duration and
intensity of cigarette smoking, diet, and asbestos exposure was
obtained from next of kin. Detailed work histories were also obtained
from pension applications on file with the Teamsters Union.
Both data sources were used to classify cases and controls
according to a job category in which they had worked the longest. Based
on the data obtained from next of kin, the job categories were diesel
truck drivers, gasoline truck drivers, drivers of both truck types,
truck mechanics, and dock workers. Based on the pension applications,
the principal job categories were long-haul drivers, short-haul or city
drivers, truck mechanics, and dock workers. Of the workers identified
by next of kin as primarily diesel truck drivers, 90 percent were
classified as long-haul drivers according to the Teamster data. The
corresponding proportions were 82 percent for mechanics and 81 percent
for dock workers. According to the investigators, most Teamsters had
worked in only one exposed job category. However, because of the
differences in job category definitions, and also because the next of
kin data covered lifetimes whereas the pension applications covered
only time in the Teamsters Union, the investigators found it
problematic to fully evaluate the concordance between the two data
sources.
In the 1990 report, separate analyses were conducted for each
source of data used to compile work histories. The investigators noted
that ``many trucking companies (where most study subjects worked) had
completed most of the dieselization of their fleets by 1960, while
independent drivers and nontrucking firms may have obtained diesel
trucks later. * * * '' Therefore, they specifically checked for
associations between increased risk of lung cancer and occupational
exposure after 1959 and, separately, after 1964. In the 1992 report,
the investigators presented, for the Union's occupational categories
used in the study, dpm exposure estimates based on subsequent
measurements of submicrometer elemental carbon (EC) as reported by
Zaebst et al. (1991). In the 1998 report, cumulative dpm exposure
estimates for individual workers were compiled by combining the
individual work histories obtained from the Union's records with the
subsequently measured occupational exposure levels, along with an
evaluation of historical changes in diesel engine emissions and
patterns of diesel usage. Three alternative sets of cumulative exposure
estimates were considered, based on alternative assumptions about the
extent of
[[Page 5619]]
improvement in diesel engine emissions between 1970 and 1990. A variety
of statistical models and techniques were then employed to investigate
the relationship between estimated cumulative dpm exposure (expressed
as EC) and the risk of lung cancer. The authors pointed out that the
results of these statistical analyses depended heavily on ``very broad
assumptions'' used to generate the estimates of cumulative dpm
exposure. While acknowledging this limitation, however, they also
evaluated the sensitivity of their results to various changes in their
assumptions and found these changes to have little impact on the
results.
The investigators also identified and addressed several other
limitations of this study as follows:
(1) possible misclassification smoking habits by next of kin,
(2) misclassification of exposure by next of kin, (3) a relatively
small non-exposed group (n = 120) which by chance may have had a low
lung cancer risk, and (4) lack of sufficient latency (time since
first exposure) to observe a lung cancer excess. On the other hand,
next-of-kin data on smoking have been shown to be reasonably
accurate, non-differential misclassification of exposure * * * would
only bias our findings toward * * * no association, and the trends
of increased risk with increased duration of employment in certain
jobs would persist even if the non-exposed group had a higher lung
cancer risk. Finally, the lack of potential latency would only make
any positive results more striking. (Steenland et al., 1990)
The main results from the three reports covering this study are
summarized in the following table. All of the analyses were controlled
for age, race, smoking (five categories), diet, and asbestos exposure
as reported by next of kin. Odds ratios for the occupations listed were
calculated relative to the odds of lung cancer for occupations other
than truck driver (all types), mechanic, dock worker, or other
potentially diesel exposed jobs (Steenland et al., 1990, Appendix A).
The exposure-response analyses were carried out using logistic
regression. Although the investigators performed analyses under three
different assumptions for the rate of engine emissions (gm/mile) in
1970, they considered the intermediate value of 4.5 gm/mile to be their
best estimate, and this is the value on which the results shown here
are based. Under this assumption, cumulative occupational EC exposure
for all workers in the study was estimated to range from 0.45 to 2,440
g-yr/m\3\, with a median value of 373 g-yr/m\3\. The
estimates of relative risk (expressed as odds ratios) presented for EC
exposures of 373 g-yr/m\3\, 1000 g-yr/m\3\, and 2450
-yr/m\3\ were calculated by MSHA based on the regression
coefficients reported by the authors for five-year lagged exposures
(Steenland et al. 1998, Table II).
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[[Page 5621]]
Under the assumption of a 4.5 gm/mile emissions rate in 1970, the
cumulative EC exposure of 2450 g-yr/m\3\ ( 6.1 mg-
yr/m\3\ Dpm) shown in the table closely corresponds to the upper limit
of the range of data on which the regression analyses were based
(Steenland et al., 1998, p. 224). However, the relative risks (i.e.,
odds ratios) calculated for this level of occupational exposure are
presented primarily for purposes of comparison with the findings of
Johnston et al. (1997) and Saverin et al. (1999). At a cumulative Dpm
exposure of approximately 6.1 mg--yr/m\3\, it is evident that the
Johnston models predict a far greater elevation in lung cancer risk
than either the Saverin or Steenland models. A possible explanation for
this is that the Johnston data included exposures of up to 30 years in
duration, and the statistical models showing an exposure-response
relationship allowed for a 15-year lag in exposure effects. The other
two studies were based on generally shorter diesel exposures and
allowed less time for latent effects. In Subsection 3.b.ii(3) of this
risk assessment, the quantitative results of these three studies will
be further compared with respect to exposure levels found in
underground mines.
Several commenters noted that the HEI Expert Panel (HEI, 1999) had
identified uncertainties in the diesel exposure assessment as an
important limitation of the exposure-response analyses by Steenland et
al. (1998) and had recommended further investigation before the
quantitative results of this study were accepted as conclusive. In
addition, Navistar International Transportation (NITC) raised a number
of objections to the methods by which diesel exposures were estimated
for the period between 1949 and 1990 (NITC, 1999). In general, the
thrust of these objections was that exposures to diesel engine
emissions had been overestimated, while potentially relevant exposures
to gasoline engine emissions had been underestimated and/or unduly
discounted.\57\
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\57\ Many of the issues NITC raised in its critique of this
study depend on a peculiar identification of Dpm exclusively with
elemental carbon. For example, NITC argued that ``more than 65
percent of the total carbon to which road drivers (and mechanics)
were exposed consisted of organic (i.e., non-diesel) carbon, further
suggesting that some other etiology caused or contributed to excess
lung cancer mortality in these workers.'' (NITC, 1999, p. 16) Such
lines of argument, which depend on identifying organic carbon as
``non-diesel,'' ignore the fact that Dpm contains a large measure of
organic carbon compounds (and also some sulfates), as well as
elemental carbon. Any adverse health effects due to the organic
carbon or sulfate constituents of Dpm would nonetheless be due to
Dpm exposures.
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As mentioned above, the investigators recognized that these
analyses rely on ``broad assumptions rather than actual [concurrent]
measurements,'' and they proposed that the ``results should be regarded
with appropriate caution.'' While agreeing with both the investigators
and the HEI Expert Panel that these results should be interpreted with
appropriate caution, MSHA also agrees with the Panel ``* * * that
regulatory decisions need to be made in spite of the limitations and
uncertainties of the few studies with quantitative data currently
available.'' (HEI, 1999, p. 39) In this context, MSHA considers it
appropriate to regard the 1998 exposure-response analyses as
contributing to the weight of evidence that dpm exposure increases the
risk of lung cancer, even if the results are not conclusive when viewed
in isolation.
Some commenters also noted that the HEI Expert Panel raised the
possibility that the method for selecting controls in this study could
potentially have biased the results in an unpredictable direction. Such
bias could have occurred because deaths among some of the controls were
likely due to diseases (such as cardiovascular disease) that shared
some of the same risk factors (such as tobacco smoking) with lung
cancer. The Panel presented hypothetical examples of how this might
bias results in either direction. Although the possibility of such bias
further demonstrates why the results of this study should be regarded
with ``appropriate caution,'' it is important to distinguish between
the mere possibility of a control-selection bias, evidence that such a
bias actually exists in this particular study, and the further evidence
required to show that such bias not only exists but is of sufficient
magnitude to have produced seriously misleading results. Unlike the
commenters who cited the HEI Expert Panel on this issue, the Panel
itself clearly drew this distinction, stating that ``no direct evidence
of such bias is apparent'' and emphasizing that ``even though these
examples [presented in HEI (1999), Appendix D] could produce misleading
results, it is important to note that they are only hypothetical
examples. Whether or not such bias is present will require further
examination.'' (HEI, 1999, pp. 37-38) As the HEI showed in its
examples, such bias (if it exists) could lead to underestimating the
association between lung cancer and dpm exposure, as well as to
overestimating it. Therefore, in the absence of evidence that control-
selection bias actually distorted the results of this study one way or
the other, MSHA considers it prudent to accept the study's finding of
an association at face value.
One commenter (MARG) noted that information on cigarette smoking,
asbestos exposure, and diet in the trucking industry study was obtained
from next of kin and stated that such information was ``likely to be
unreliable.'' By increasing random variability in the data, such errors
could widen the confidence intervals around an estimated odds ratio or
reduce the confidence level at which a positive exposure-response
relationship might be established. However, unless such errors were
correlated with diesel exposure or lung cancer in such a way as to bias
the results, they would not, on average, inflate the estimated degree
of association between diesel exposure and an increased risk of lung
cancer. The commenter provided no reason to suspect that errors with
respect to these factors were in any way correlated with diesel
exposure or with the development of lung cancer.
Some commenters pointed out that EC concentrations measured in 1990
for truck mechanics were higher, on average, than for truck drivers,
but the mechanics, unlike the drivers, showed no evidence of increasing
lung cancer risk with increasing duration of employment. NITC referred
to this as a ``discrepancy'' in the data, assuming that ``cumulative
exposure increases with duration of employment such that mechanics who
have been employed for 18 or more years would have greater cumulative
exposure than workers who have been employed for 1-11 years.'' (NITC,
1999)
Mechanics were included in the logistic regression analyses
(Steenland et al., 1998) showing an increase in lung cancer risk with
increasing cumulative exposure. These analyses pooled the data for all
occupations by estimating exposure for each worker based on the
worker's occupation and the particular years in which the worker was
employed. There are at least three reasons why, for mechanics viewed as
a separate group, an increase in lung cancer risk with increasing dpm
exposure may not have been reflected by increasing duration of
employment.
First, relatively few truck mechanics were available for analyzing
the relationship between length of employment and the risk of lung
cancer. Based on the union records, 50 cases and 37 controls were so
classified; based on the next-of-kin data, 43 cases and 41 controls
were more specifically classified as diesel truck mechanics
[[Page 5622]]
(Steenland et al., 1990). In contrast, 609 cases and 604 controls were
classified as long-haul drivers (union records). This was both the
largest occupational category and the only one showing statistically
significant evidence of increasing risk with increasing employment
duration. The number of mechanics included in the study population may
simply not have been sufficient to detect a pattern of increasing risk
with increasing length of employment, even if such a pattern existed.
The second part of the explanation as to why mechanics did not
exhibit a pattern similar to truck drivers could be that the data on
mechanics were more subject to confounding. After noting that ``the
risk for mechanics did not appear to increase consistently with
duration of employment,'' Steenland et al. (1990) further noted that
the mechanics may have been exposed to asbestos when working on brakes.
The data used to adjust for asbestos exposure may have been inadequate
to control for variability in asbestos exposure among the mechanics.
Third, as noted by NITC, the lung cancer risk for mechanics
(adjusted for age, race, tobacco smoking, asbestos exposure, and diet)
would be expected to increase with increasing duration of employment
only if the mechanics' cumulative dpm exposure corresponded to the
length of their employment. None of the commenters raising this issue,
however, provided any support for this assumption, which fails to
consider the particular calendar years in which mechanics included in
the study were employed. In compiling cumulative exposure for an
individual worker, the investigators took into account historical
changes in both diesel emissions and the proportion of trucks with
diesel engines--so the exposure level assigned to each occupational
category was not the same in each year. In general, workers included in
the study neither began nor ended their employment in the same year.
Consequently, workers with the same duration of employment in the same
occupational category could be assigned different cumulative exposures,
depending on when they were employed. Similarly, workers in the same
occupational category who were assigned the same cumulative exposure
may not have worked the same length of time in that occupation.
Therefore, it should not be assumed that duration of employment
corresponds very well to the cumulative exposure estimated for workers
within any of the occupational categories. Furthermore, in the case of
mechanics, there is an additional historical variable that is
especially relevant to actual cumulative exposure but was not
considered in formulating exposure estimates: the degree of ventilation
or other means of protection within repair shops. Historical changes in
shop design and work practices, as well as differences between shops,
may have caused more exposure misclassification among mechanics than
among long-haul or diesel truck drivers. Such misclassification would
tend to further obscure any relationship between mechanics' risk of
lung cancer and either duration of employment or cumulative exposure.
(iv) Counter-Evidence
Several commenters stated that, in the proposal, MSHA had dismissed
or not adequately addressed epidemiology studies showing no association
between lung cancer and exposures to diesel exhaust. For example, the
EMA wrote:
MSHA's discussion of the negative studies generally consists of
arguments to explain why those studies should be dismissed. For
example, MSHA states that, ``All of the studies showing negative or
statistically insignificant positive associations * * * lacked good
information about dpm exposure * * *'' or showed similar
shortcomings. 63 Fed. Reg. at 17533. The statement about exposure
information is only partially true, for, in fact, very few of any of
the cited studies (the ``positive'' studies as well) included any
exposure measurements, and none included concurrent exposures.
It should, first of all, be noted that the statement in question on
dpm exposure referred to the issue of any diesel exposure--not to
quantitative exposure measurements, which MSHA acknowledges are lacking
in most of the available studies. In the absence of quantitative
measurements, however, studies comparing workers known to have been
occupationally exposed to unexposed workers are preferable to studies
not containing such comparisons. Furthermore, two of the studies now
available (and discussed above) utilize essentially concurrent exposure
measurements, and both show a positive association (Johnston et al.,
1997; Saverin et al., 1999).
MSHA did not entirely ``dismiss'' the negative studies. They were
included in both MSHA's tabulation (see Tables III-4 and III-5) and (if
they met the inclusion criteria) in the two meta-analyses cited both
here and in the proposal (Lipsett and Campleman, 1999, and Bhatia et
al., 1998). As noted by the commenter, MSHA presented reasons (such as
an inadequate latency allowance) for why negative studies may have
failed to detect an association. Similarly MSHA gave reasons for giving
less weight to some of the positive studies, such as Benhamou et al.
(1988), Morabia et al. (1992), and Siemiatycki et al., 1988. Additional
reasons for giving less weight to the six entirely negative studies
have been tabulated above, under the heading of ``Best Available
Epidemiologic Evidence.'' The most recent of these negative studies
(Christie et al., 1994, 1995) is discussed in detail under the heading
of ``Studies Involving Miners.''
One commenter (IMC Global) listed the following studies (all of
which MSHA had considered in the proposed risk assessment) as
``examples of studies that reported negative associations between [dpm]
exposure and lung cancer risk'':
Waller (1981). This is one of the six negative studies
discussed earlier. Results were likely to have been biased by excluding
lung cancers occurring after retirement or resignation from employment
with the London Transit Authority. Comparison was to a general
population, and there was no adjustment for a healthy worker effect.
Comparison groups were disparate, and there was no adjustment for
possible differences in smoking frequency or intensity.
Howe et al. (1983). Contrary to the commenter's
characterization of this study, the investigators reported
statistically significant elevations of lung cancer risk for workers
classified as ``possibly exposed'' or ``probably exposed'' to diesel
exhaust. MSHA recognizes that these results may have been confounded by
asbestos and coal dust exposures.
Wong et al. (1985). The investigators reported a
statistically insignificant deficit for lung cancer in the entire
cohort and a statistically significant deficit for lung cancer in the
less than 5-year duration group. However, since comparisons were to a
general population, these deficits may be the result of a healthy
worker effect, for which there was no adjustment. Because of the
latency required for development of lung cancer, the result for ``less
than 5-year duration'' is far less informative than the results for
longer durations of employment and greater latency allowances. Contrary
to the commenter's characterization of this study, the investigators
reported statistically significant elevations of lung cancer risks for
``normal'' retirees (SMR = 1.30) and for ``high exposure'' dozer
operators with 15-19 years of union membership and a latency allowance
of at least 20 years (SMR = 3.43).
Edling et al. (1987). This is one of the six negative
studies discussed
[[Page 5623]]
earlier. The cohort consisted of only 694 bus workers and, therefore,
lacked statistical power. Furthermore, comparison was to a general,
external population with no adjustment for a healthy worker effect.
Garshick (1988). The reason the commenter (IMC Global)
gave for characterizing this study as negative was: ``That the sign of
the association in this data set changes based on the models used
suggests that the effect is not robust. It apparently reflects modeling
assumptions more than data.'' Contrary to the commenter's
characterization, however, the finding of increased lung cancer risk
for workers classified as diesel-exposed did not change when different
methods were used to analyze the data. What changed, depending on
modeling assumptions, was the shape and direction of the exposure-
response relationship among exposed workers (Cal-EPA, 1998; Stayner et
al., 1998; Crump, 1999; HEI, 1999). MSHA agrees that the various
exposure-response relationships that have been derived from this study
are highly sensitive to data modeling assumptions. This includes
assumptions about historical patterns of exposure, as well as
assumptions related to technical aspects of the statistical analysis.
However, as noted by the HEI Expert Panel, the study provides evidence
of a positive association between exposure and lung cancer despite the
conflicting exposure-response analyses. Even though different
assumptions and methods of analysis have led to different conclusions
about the utility of this study for quantifying an exposure-response
relationship, ``the overall risk of lung cancer was elevated among
diesel-exposed workers'' (HEI, 1999, p. 25).
Another commenter (MARG) cited a number of studies (all of which
had already been placed in the public record by MSHA) that, according
to the commenter, ``reflect either negative health effects trends among
miners or else failed to demonstrate a statistically significant
positive trend correlated with dpm exposure.'' It should be noted that,
as explained earlier, failure of an individual study to achieve
statistical significance (i.e., a high confidence level for its
results) does not necessarily prevent a study from contributing
important information to a larger body of evidence. An epidemiologic
study may fail to achieve statistical significance simply because it
did not involve a sufficient number of subjects or because it did not
allow for an adequate latency period. In addition to this general
point, the following responses apply to the specific studies cited by
the commenter.
Ahlman et al. (1991). This study is discussed above, under
the heading of ``Studies Involving Miners.'' MSHA agrees with the
commenter that this study did not ``establish'' a relationship between
diesel exposure and the excess risk of lung cancer reported among the
miners involved. Contrary to the commenter's characterization, however,
the evidence presented by this study does incrementally point in the
direction of such a relationship. As mentioned earlier, none of the
underground miners who developed lung cancer had been occupationally
exposed to asbestos, metal work, paper pulp, or organic dusts. Based on
measurements of the alpha energy concentration at the mines, and a
comparison of smoking habits between underground and surface miners,
the authors concluded that not all of the excess lung cancer for the
underground miners was attributable to radon daughter exposures and/or
smoking. A stronger conclusion may have been possible if the cohort had
been larger.
Ames et al. (1984). MSHA has taken account of this study,
which made no attempt to evaluate cancer effects, under the heading of
``Chronic Effects other than Cancer.'' The commenter repeated MSHA's
statement (in the proposed risk assessment) that the investigators had
not detected any association of chronic respiratory effects with diesel
exposure, but ignored MSHA's observation that the analysis had failed
to consider baseline differences in lung function or symptom
prevalence. Furthermore, as acknowledged by the investigators, diesel
exposure levels in the study population were low.
Ames et al. (1983). As discussed later in this risk
assessment, under the heading of ``Mechanisms of Toxicity,'' this study
was among nine (out of 17) that did not find evidence of a relationship
between exposure to respirable coal mine dust and an increased risk of
lung cancer. Unlike the Australian mines studied by Christie et al.
(1995), the coal mines included in this study were not extensively
dieselized, and the investigators did not relate their findings to
diesel exposures.
Ames et al. (1982). As noted earlier under the heading of
``Acute Health Effects,'' this study, which did not attempt to evaluate
cancer or other chronic health effects, detected no statistically
significant relationship between diesel exposure and pulmonary
function. However, the authors noted that this might have been due to
the low concentrations of diesel emissions involved.
Armstrong et al. (1979). As discussed later in this risk
assessment, this study was among nine (out of 17) that did not find
evidence of a relationship between exposure to respirable coal mine
dust and an increased risk of lung cancer. As pointed out by the
commenter, comparisons were to a general population. Therefore, they
were subject to a healthy worker effect for which no adjustment was
made. The commenter further stated that ``diesel emissions were not
found to be related to increased health risks.'' However, diesel
emissions were not mentioned in the report, and the investigators did
not attempt to compare lung cancer rates in exposed and unexposed
miners.
Attfield et al. (1982). MSHA has taken the results of this
study into account, under the heading of ``Chronic Effects other than
Cancer.''
Attfield (1979). MSHA has taken account of this study,
which did not attempt to evaluate cancer effects, under the heading of
``Chronic Effects other than Cancer.'' Although the results were not
conclusive at a high confidence level, miners occupationally exposed to
diesel exhaust for five or more years exhibited an increase in various
respiratory symptoms, as compared to miners exposed for less than five
years.
Boffetta et al. (1988). This study is discussed in two
places above, under the headings ``Studies Involving Miners'' and
``Best Available Epidemiologic Evidence.'' The commenter stated that
``the study obviously does not demonstrate risks from dpm exposure.''
If the word ``demonstrate'' is taken to mean ``conclusively prove,''
then MSHA would agree that the study, viewed in isolation, does not do
this. As explained in the earlier discussion, however, MSHA considers
this study to contribute to the weight of evidence that dpm exposure
increases the risk of lung cancer.
Costello et al. (1974). As discussed later in this risk
assessment, this study was among nine (out of 17) that did not find
evidence of a relationship between exposure to respirable coal mine
dust and an increased risk of lung cancer. Since comparisons were to a
general population, they were subject to a healthy worker effect for
which no adjustment was made. Diesel emissions were not mentioned in
the report.
Gamble and Jones (1983). MSHA has taken account of this
study, which did not attempt to evaluate cancer effects, under the
heading of ``Chronic Effects other than Cancer.'' The commenter did not
address MSHA's observation that the method of
[[Page 5624]]
statistical analysis used by the investigators may have masked an
association of respiratory symptoms with diesel exposure.
Glenn et al. (1983). As summarized by the commenter, this
report reviewed NIOSH medical surveillance on miners exposed to dpm and
found that ``* * * neither consistent nor obvious trends implicating
diesel exhaust in the mining atmosphere were revealed.'' The authors
noted that ``results were rather mixed,'' but also noted that ``levels
of diesel exhaust contaminants were generally low,'' and that ``overall
tenure in these diesel equipped mines was fairly short.'' MSHA
acknowledges the commenter's emphasis on the report's 1983 conclusion:
``further research on this subject is needed.'' However, the authors
also pointed out that ``all four of the chronic effects analyses
revealed an excess of cough and phlegm among the diesel exposed group.
In the potash, salt and trona groups, these excesses were
substantial.'' The miners included in the studies summarized by this
report would not have been exposed to Dpm for sufficient time to
exhibit a possible increase in the risk of lung cancer.
Johnston et al. (1997). This study is discussed in two
places above, under the headings ``Studies Involving Miners'' and
``Best Available Epidemiologic Evidence.'' MSHA disagrees with the
commenter's assertion that ``the study does not support a health risk
from dpm.'' This was not the conclusion drawn by the authors of the
study. As explained in the earlier discussion, this study, one of the
few containing quantitative estimates of cumulative dpm exposures,
provides evidence of increasing lung cancer risk with increasing
exposure.
Jorgenson and Svensson (1970). MSHA discussed this study,
which did not attempt to evaluate cancer effects, under the heading of
``Chronic Effects other than Cancer.'' Contrary to the commenter's
characterization, the investigators reported higher rates of chronic
productive bronchitis, for both smokers and nonsmokers, among the
underground iron ore miners exposed to diesel exhaust as compared to
surface workers at the same mine.
Kuempel (1995); Lidell (1973); Miller and Jacobsen (1985).
As discussed later in this risk assessment, under the heading of
``Mechanisms of Toxicity,'' these three studies were among the nine
(out of 17) that did not find evidence of a relationship between
exposure to respirable coal mine dust and an increased risk of lung
cancer. The extent, if any, to which workers involved in these studies
were occupationally exposed to diesel emissions was not documented, and
diesel emissions were not mentioned in any of these reports.
Morfeld et al. (1997). The commenter's summary of this
study distorted the investigators' conclusions. Contrary to the
commenter's characterization, this is one of eight studies that showed
an increased risk of lung cancer for coal miners, as discussed later in
this risk assessment under the heading of ``Mechanisms of Toxicity.''
For lung cancer, the relative SMR, which adjusts for the healthy worker
effect, was 1.11. (The value of 0.70 cited by the commenter was the
unadjusted SMR.) The authors acknowledged that the relative SMR
obtained by the ``standard analysis'' (i.e., 1.11) was not
statistically significant. However, the main object of the report was
to demonstrate that the ``standard analysis'' is insufficient. The
investigators presented evidence that the 1.11 value was biased
downward by a ``healthy-worker-survivor-effect,'' thereby masking the
actual exposure effects in these workers. They found that ``all the
evidence points to the conclusion that a standard analysis suffers from
a severe underestimate of the exposure effect on overall mortality,
cancer mortality and lung cancer mortality.'' (Morfeld et al., 1997, p.
350)
Reger (1982). MSHA has taken account of this study, which
made no attempt to evaluate cancer effects, under the heading of
``Chronic Effects other than Cancer.'' As summarized by the commenter,
``diesel-exposed miners were found to have more cough and phlegm, and
lower pulmonary function,'' but the author found that ``the evidence
would not allow for the rejection of the hypothesis of health equality
between exposed and non-exposed miners.'' The commenter failed to note,
however, that miners in the dieselized mines, had worked underground
for less than 5 years on average.
Rockette (1977). This is one of eight studies, discussed
under ``Mechanisms of Toxicity,'' showing an increased risk of lung
cancer for coal miners. As described by the commenter, the author
reported SMRs of 1.12 for respiratory cancers and 1.40 for stomach
cancer. MSHA agrees with the commenter that ``the study does not
establish a dpm-related health risk,'' but notes that dpm effects were
not under investigation. Diesel emissions were not mentioned in the
report, and, given the study period, the miners involved may not have
been occupationally exposed to diesel exhaust.
Waxweiler (1972). MSHA's discussion of this study appears
earlier in this risk assessment, under ``Studies Involving Miners.'' As
noted by the commenter, the slight excess in lung cancer, relative to
the general population of New Mexico, was not statistically
significant. The commenter failed to note, however, that no adjustment
was made for a healthy worker effect and that a substantial percentage
of the underground miners were not occupationally exposed to diesel
emissions.
(v) Summation
Limitations identified in both positive and negative studies
include: lack of sufficient power, inappropriate comparison groups,
exposure misclassification, statistically insignificant results, and
potential confounders. As explained earlier, under ``Evaluation
Criteria,'' weaknesses of the first three of these types can reasonably
be expected, for the most part, to artificially decrease the apparent
strength of any observed association between diesel exposure and
increased risk of lung cancer. Statistical insignificance and potential
confounders may, in the absence of evidence to the contrary, be
regarded as neutral on average. The weaknesses that have been
identified in these studies are not unique to epidemiologic studies
involving lung cancer and diesel exhaust. They are sources of
uncertainty in virtually all epidemiologic research.
Even when there is a strong possibility that the results of a study
have been affected by confounding variables, it does not follow that
the effect has been to inflate rather than deflate the results or that
the study cannot contribute to the weight of evidence supporting a
putative association. As cogently stated by Stober and Abel (op cit.,
p. 4), ``* * * associations found in epidemiologic studies can always
be, at least in part, attributed to confounding.'' Therefore, an
objection grounded on potential confounding can always be raised
against any epidemiologic study. It is well known that this same
objection was, in the past, raised against epidemiologic studies
linking lung cancer and radon exposure, lung cancer and asbestos dust
exposure, and even lung cancer and tobacco smoking.
Some commenters have now proposed that virtually every existing
epidemiologic study relating lung cancer to dpm exposure be summarily
discredited because of susceptibility to confounding or other perceived
weaknesses. Given the practical difficulties of designing and executing
an epidemiologic study, this is not so much an objection to any
specific study
[[Page 5625]]
as it is an attack on applied epidemiology in general. Indeed, in their
review of these studies, Stober and Abel (1996) conclude that.
In this field * * * epidemiology faces its limits (Taubes,
1995). * * * Many of these studies were doomed to failure from the
very beginning.
For important ethical reasons, however, tightly controlled lung cancer
experiments cannot be performed on humans. Therefore, despite their
inherent limitations, MSHA must rely on the weight of evidence from
epidemiologic studies, placing greatest weight on the most carefully
designed and executed studies available.
(b) Bladder Cancer
With respect to cancers other than lung cancer, MSHA's review of
the literature identified only bladder cancer as a possible candidate
for a causal link to dpm. Cohen and Higgins (1995) identified and
reviewed 14 epidemiologic case-control studies containing information
related to dpm exposure and bladder cancer. All but one of these
studies found elevated risks of bladder cancer among workers in jobs
frequently associated with dpm exposure. Findings were statistically
significant in at least four of the studies (statistical significance
was not evaluated in three).
These studies point quite consistently toward an excess risk of
bladder cancer among truck or bus drivers, railroad workers, and
vehicle mechanics. However, the four available cohort studies do not
support a conclusion that exposure to dpm is responsible for the excess
risk of bladder cancer associated with these occupations. Furthermore,
most of the case-control studies did not distinguish between exposure
to diesel-powered equipment and exposure to gasoline-powered equipment
for workers having the same occupation. When such a distinction was
drawn, there was no evidence that the prevalence of bladder cancer was
higher for workers exposed to the diesel-powered equipment.
This, along with the lack of corroboration from existing cohort
studies, suggests that the excessive rates of bladder cancer observed
may be a consequence of factors other than dpm exposure that are also
associated with these occupations. For example, truck and bus drivers
are subjected to vibrations while driving and may tend to have
different dietary and sleeping habits than the general population. For
these reasons, MSHA does not find that convincing evidence currently
exists for a causal relationship between dpm exposure and bladder
cancer. MSHA received no public comments objecting to this conclusion.
ii. Studies Based on Exposures to PM2.5 in Ambient Air
Prior to 1990, the relationship between mortality and long-term
exposure to particulate matter was generally investigated by means of
cross-sectional studies, but unaddressed spatial confounders and other
methodological problems inherent in such studies limited their
usefulness (EPA, 1996).\58\ Two more recent prospective cohort studies
provide better evidence of a link between excess mortality rates and
exposure to fine particulate, although some of the uncertainties here
are greater than with the short-term studies conducted in single
communities. The two studies are the ``Six Cities'' study (Dockery et
al., 1993), and the American Cancer Society (ACS) study (Pope et al.,
1995).\59\ The first study followed about 8,000 adults in six U.S.
cities over 14 years; the second looked at survival data for half a
million adults in 151 U.S. cities for 7 years. After adjusting for
potential confounders, including smoking habits, the studies considered
differences in mortality rates between the most polluted and least
polluted cities.
---------------------------------------------------------------------------
\58\ Unlike longitudinal studies, which examine responses at
given locations to changes in conditions over time, cross-sectional
studies compare results from locations with different conditions at
a given point in time.
\59\ A third such study, the California Seventh Day Adventist
study (Abbey et al., 1991), investigated only TSP, rather than fine
particulate. It did not find significant excess mortality associated
with chronic TSP exposures.
---------------------------------------------------------------------------
Both the Six Cities study and the ACS study found a significant
association between chronically higher concentrations of PM
2.5 (which includes dpm) and age-adjusted total
mortality.\60\ The authors of the Six Cities Study concluded that the
results suggest that exposures to fine particulate air pollution
``contributes to excess mortality in certain U.S. cities.'' The ACS
study, which not only controlled for smoking habits and various
occupational exposures, but also, to some extent, for passive exposure
to tobacco smoke, found results qualitatively consistent with those of
the Six Cities Study.\61\ In the ACS study, however, the estimated
increase in mortality associated with a given increase in fine
particulate exposure was lower, though still statistically significant.
In both studies, the largest increase observed was for cardiopulmonary
mortality.
---------------------------------------------------------------------------
\60\ The Six Cities study also found such relationships at
elevated levels of PM10 and sulfates. The ACS study was
designed to follow up on the fine particle results of the Six Cities
Study, and also investigated sulfates separately. As explained
earlier in this preamble, sulfates may be a significant constituent
of dpm, depending on the type of diesel fuel used.
\61\ The Six Cities study did not find a statistically
significant increase in risk among non-smokers, suggesting that non-
smokers might be less sensitive than smokers to adverse health
effects from fine particulate exposures; however, the ACS study,
with more statistical power, did find significantly increased risk
even for non-smokers.
---------------------------------------------------------------------------
Both studies also showed an increased risk of lung cancer
associated with increased exposure to fine particulate. Although the
lung cancer results were not statistically significant, they are
consistent with reports of an increased risk of lung cancer among
workers occupationally exposed to diesel emissions (discussed above).
The few studies on associations between chronic PM 2.5
exposure and morbidity in adults show effects that are difficult to
separate from measures of PM 10 and measures of acid
aerosols. The available studies, however, show positive associations
between particulate air pollution and adverse health effects for those
with pre-existing respiratory or cardiovascular disease. This is
significant for miners occupationally exposed to fine particulates such
as dpm because, as mentioned earlier, there is a large body of evidence
showing that respiratory diseases classified as COPD are significantly
more prevalent among miners than in the general population. It also
appears that PM exposure may exacerbate existing respiratory infections
and asthma, increasing the risk of severe outcomes in individuals who
have such conditions (EPA, 1996).
d. Mechanisms of Toxicity
Four topics will be addressed in this section of the risk
assessment: (i) the agent of toxicity, (ii) clearance and deposition of
dpm, (iii) effects other than cancer, and (iv) lung cancer. The section
on lung cancer will include discussions of the evidence from (1)
genotoxicity studies (including bioavailability of genotoxins) and (2)
animal studies.
i. Agent of Toxicity
As described in Part II of this preamble, the particulate fraction
of diesel exhaust is made up of aggregated soot particles, vapor phase
hydrocarbons, and sulfates. Each soot particle consists of an
insoluble, elemental carbon core and an adsorbed, surface coating of
relatively soluble organic compounds, such as polycyclic aromatic
hydrocarbons (PAHs). Many of these organic carbon compounds are
[[Page 5626]]
suspected or known mutagens and/or carcinogens. For example, nitrated
PAHs, which are present in dpm, are potent mutagens in microbial and
human cell systems, and some are known to be carcinogenic to animals
(IPCS, 1996, pp. 100-105).
When released into an atmosphere, the soot particles formed during
combustion tend to aggregate into larger particles. The total organic
and elemental carbon in these soot particles accounts for approximately
80 percent of the dpm mass. The remaining 20 percent consists mainly of
sulfates, such as H2SO4 (sulfuric acid).
Several laboratory animal studies have been performed to ascertain
whether the effects of diesel exhaust are attributable specifically to
the particulate fraction. (Heinrich et al., 1986, 1995; Iwai et al.,
1986; Brightwell et al., 1986). These studies compare the effects of
chronic exposure to whole diesel exhaust with the effects of filtered
exhaust containing no particles. The studies demonstrate that when the
exhaust is sufficiently diluted to nullify the effects of gaseous
irritants (NO2 and SO2), irritant vapors
(aldehydes), CO, and other systemic toxicants, diesel particles are the
prime etiologic agents of noncancer health effects. Exposure to dpm
produced changes in the lung that were much more prominent than those
evoked by the gaseous fraction alone. Marked differences in the effects
of whole and filtered diesel exhaust were also evident from general
toxicological indices, such as body weight, lung weight, and pulmonary
histopathology.
These studies show that, when the exhaust is sufficiently diluted,
it is the particles that are primarily responsible for the toxicity
observed. However, the available studies do not completely settle the
question of whether the particles might act additively or
synergistically with the gases in diesel exhaust. Possible additivity
or interaction effects with the gaseous portion of diesel exhaust
cannot be completely ruled out.
One commenter (MARG) raised an issue with regard to the agent of
toxicity in diesel exhaust as follows:
MSHA has not attempted to regulate exposure to suspected
carcinogens contained in dpm, but has opted instead, in metal/non-
metal mines, to regulate total carbon (``TC'') as a surrogate for
diesel exhaust, without any evidence of adverse health effects from
TC exposure. * * * Nor does the mere presence of suspected
carcinogens, in minute quantities, in diesel exhaust require a 95
percent reduction of total diesel exhaust [sic] in coal mines. If
there are small amounts of carcinogenic substances of concern in
diesel exhaust, those substances, not TC, should be regulated
directly on the basis of the risks (if any) posed by those
substances in the quantities actually present in underground mines.
[MARG]
First, it should be noted that the ``suspected carcinogens'' in
diesel exhaust to which the commenter referred are part of the organic
fraction of the total carbon. Therefore, limiting the concentration of
airborne total carbon attributable to dpm, or removing the soot
particles from the diesel exhaust by filtration, are both ways of
effectively limiting exposures to these suspected carcinogens. Second,
the commenter seems to have assumed that cancer is the only adverse
health effect of concern and that the only agents in dpm that could
cause cancer are the ``suspected carcinogens'' in the organic fraction.
This not only ignores non-cancer health effects associated with
exposures to dpm and other fine particles, but also the possibility
(discussed below) that, with sufficient deposition and retention, soot
particles themselves could promote or otherwise increase the risk of
lung cancer--either directly or by stimulating the body's natural
defenses against foreign substances.
The same commenter [MARG] also stated that ``* * * airborne carbon
has not been shown to be harmful at levels currently established in
MSHA's dust rules. If the problem is dpm, as MSHA asserts, then it is
not rationally addressed by regulating airborne carbon.'' MSHA's intent
is to limit dpm exposures in M/NM mines by regulating the submicrometer
carbon from diesel emissions--not any and all airborne carbon. MSHA
considers its approach a rational means of limiting dpm exposures
because most of the dpm consists of carbon (approximately 80 percent by
weight), and because using low sulfur diesel fuel will effectively
reduce the sulfates comprising most of the remaining portion. The
commenter offered no practical suggestion of a more direct, effective,
and rational way of limiting airborne dpm concentrations in M/NM mines.
Furthermore, direct evidence exists that the risk of lung cancer
increases with increasing cumulative occupational exposure to dpm as
measured by total carbon (Saverin et al., 1999, discussed earlier in
this risk assessment).
ii. Deposition, Clearance, and Retention
As suggested by Figure II-1 of this preamble, most of the
aggregated particles making up dpm are no larger than one micrometer in
diameter. Particles this small are able to penetrate into the deepest
regions of the lungs, called alveoli. In the alveoli, the particles can
mix with and be dispersed by a substance called surfactant, which is
secreted by cells lining the alveolar surfaces.
The literature on deposition of fine particles in the respiratory
tract was reviewed in Green and Watson (1995) and U.S. EPA (1996). The
mechanisms responsible for the broad range of potential particle-
related health effects varies depending on the site of deposition. Once
deposited, the particles may be cleared from the lung, translocated
into the interstitium, sequestered in the lymph nodes, metabolized, or
be otherwise chemically or physically changed by various mechanisms.
Clearance of dpm from the alveoli is important in the long-term effects
of the particles on cells, since it may be more than two orders of
magnitude slower than mucociliary clearance (IPCS, 1996).
IARC (1989) and IPCS (1996) reviewed factors affecting the
deposition and clearance of dpm in the respiratory tracts of
experimental animals. Inhaled PAHs adhering to the carbon core of dpm
are cleared from the lung at a significantly slower rate than
unattached PAHs. Furthermore, there is evidence that inhalation of
whole dpm may increase the retention of subsequently inhaled PAHs. IARC
(op cit.) suggested that this can happen when newly introduced PAHs
bind to dpm particles that have been retained in the lung.
The evidence points to significant differences in deposition and
clearance for different animal species (IPCS, 1996). Under equivalent
exposure regimens, hamsters exhibited lower levels of retained Dpm in
their lungs than rats or mice and consequently less pulmonary function
impairment and pulmonary pathology. These differences may result from a
lower intake rate of Dpm, lower deposition rate and/or more rapid
clearance rate, or lung tissue that is less susceptible to the
cytotoxicity of Dpm. Observations of a decreased respiration in
hamsters when exposed by inhalation favor lower intake and deposition
rates.
Retardation of lung clearance, called ``overload'' is not specific
to dpm and may be caused by inhaling, at a sufficiently high rate, dpm
in combination with other respirable particles, such as mineral dusts
typical of mining environments. The effect is characterized by (1) an
overwhelming of normal clearance processes, (2) disproportionately high
retention and loading of the lung with particles, compared to what
occurs at lower particle inhalation rates, (3) various pathological
responses; generally including chronic inflammation,
[[Page 5627]]
epithelial hyperplasia and metaplasia, and pulmonary fibrosis; and
sometimes including lung tumors.
In the proposed risk assessment, MSHA requested additional
information, not already covered in the sources cited above, on fine
particle deposition in the respiratory tract, especially as it might
pertain to lung loading in miners exposed to a combination of diesel
particulate and other dusts. In response to this request, NIOSH
submitted a study that investigated rat lung responses to chronic
inhalation of a combination of coal dust and diesel exhaust, compared
to coal dust or dpm alone (Castranova et al., 1985). Although this
report did not directly address deposition or clearance, the
investigators reported that another phase of the study had shown that
``particulate clearance, as determined by particulate accumulation in
the lung, is inhibited after two years of exposure to diesel exhaust
but is not inhibited by exposure to coal dust.''
iii. Effects Other Than Cancer
A number of controlled animal studies have been undertaken to
ascertain the toxic effects of exposure to diesel exhaust and its
components. Watson and Green (1995) reviewed approximately 50 reports
describing noncancerous effects in animals resulting from the
inhalation of diesel exhaust. While most of the studies were conducted
with rats or hamsters, some information was also available from studies
conducted using cats, guinea pigs, and monkeys. The authors also
correlated reported effects with different descriptors of dose,
including both gravimetric and non-gravimetric (e.g., particle surface
area or volume) measures. From their review of these studies, Watson
and Green concluded that:
(a) Animals exposed to diesel exhaust exhibit a number of
noncancerous pulmonary effects, including chronic inflammation,
epithelial cell hyperplasia, metaplasia, alterations in connective
tissue, pulmonary fibrosis, and compromised pulmonary function.
(b) Cumulative weekly exposure to diesel exhaust of 70 to 80
mghr/m\3\ or greater are associated with the presence of
chronic inflammation, epithelial cell proliferation, and depressed
alveolar clearance in chronically exposed rats.
(c) The extrapolation of responses in animals to noncancer
endpoints in humans is uncertain. Rats were the most sensitive animal
species studied.
Subsequent to the review by Watson and Green, there have been a
number of animal studies on allergic immune responses to dpm. Takano et
al. (1997) investigated the effects of dpm injected into mice through
an intratracheal tube and found manifestations of allergic asthma,
including enhanced antigen-induced airway inflammation, increased local
expression of cytokine proteins, and increased production of antigen-
specific immunoglobulins. The authors concluded that the study
demonstrated dpm's enhancing effects on allergic asthma and that the
results suggest that dpm is ``implicated in the increasing prevalence
of allergic asthma in recent years.'' Similarly, Ichinose et al.
(1997a) found that five different strains of mice injected
intratracheally with dpm exhibited manifestations of allergic asthma,
as expressed by enhanced airway inflammation, which were correlated
with an increased production of antigen-specific immunoglobulin due to
the dpm. The authors concluded that dpm enhances manifestations of
allergic airway inflammation and that `` * * * the cause of individual
differences in humans at the onset of allergic asthma may be related to
differences in antigen-induced immune responses * * *.''
The mechanisms that may lead to adverse health effects in humans
from inhaling fine particulates are not fully understood, but potential
mechanisms that have been hypothesized for non-cancerous outcomes are
summarized in Table III-6. A comprehensive review of the toxicity
literature is provided in U.S. EPA (1996).
BILLING CODE 4510-43-P
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[GRAPHIC] [TIFF OMITTED] TR19JA01.035
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Deposition of particulates in the human respiratory tract may
initiate events leading to increased airflow obstruction, impaired
clearance, impaired host defenses, or increased epithelial
permeability. Airflow obstruction can result from laryngeal
constriction or bronchoconstriction secondary to stimulation of
receptors in extrathoracic or intrathoracic airways. In addition to
reflex airway narrowing, reflex or local stimulation of mucus secretion
can lead to mucus hypersecretion and, eventually, to mucus plugging in
small airways.
Pulmonary changes that contribute to cardiovascular responses
include a variety of mechanisms that can lead to hypoxemia, including
bronchoconstriction, apnea, impaired diffusion, and production of
inflammatory mediators. Hypoxia can lead to cardiac arrhythmias and
other cardiac electrophysiologic responses that, in turn, may lead to
ventricular fibrillation and ultimately cardiac arrest. Furthermore,
many respiratory receptors have direct cardiovascular effects. For
example, stimulation of C-fibers leads to bradycardia and hypertension,
and stimulation of laryngeal receptors can result in hypertension,
cardiac arrhythmia, bradycardia, apnea, and even cardiac arrest. Nasal
receptor or pulmonary J-receptor stimulation can lead to vagally-
mediated bradycardia and hypertension (Widdicombe, 1988).
Some commenters mistakenly attributed the sensory irritant effects
of diesel exhaust entirely to its gaseous components. The mechanism by
which constituents of dpm can cause sensory irritations in humans is
much better understood than the mechanisms for other adverse health
effects due to fine particulates. In essence, sensory irritants are
``scrubbed'' from air entering the upper respiratory tract, thereby
preventing a portion from penetrating more deeply into the lower
respiratory tract. However, the sensory irritants stimulate trigeminal
nerve endings, which are located very close to the oro-nasal mucosa and
also to the watery surfaces of the eye (cornea). This produces a
burning, painful sensation. The intensity of the sensory irritant
response is related to the irritant concentration and duration of
exposure. Differences in relative potency are observed with different
sensory irritants. Acrolein and formaldehyde are examples of highly
potent sensory irritants which, along with others having low molecular
weights (acids, aldehydes), are often found in the organic fraction of
dpm (Nauss et al., 1995). They may be adsorbed onto the carbon-based
core or released in a vapor phase. Thus, mixtures of sensory irritants
in dpm may impinge upon the eyes and respiratory tract of miners and
produce adverse health effects.
It is also important to note that mixtures of sensory irritants in
dpm may produce responses that are not predicted solely on the basis of
the individual chemical constituents. Instead, these irritants may
interact at receptor sites to produce additive, synergistic, or
antagonistic effects. For example, because of synergism, dpm containing
a mixture of sensory irritants at relatively low concentrations may
produce intense sensory responses (i.e., responses far above those
expected for the individual irritants). Therefore, the irritant effects
of whole dpm cannot properly be evaluated by simply adding together the
known effects of its individual components.
As part of its public comments on the proposed preamble, NIOSH
submitted a study (Hahon et al., 1985) on the effects of diesel
emissions on mice infected with influenza virus. The object of this
study was to determine if exposure to diesel emissions (either alone or
in combination with coal dust) could affect resistance to pulmonary
infections. The investigators exposed groups of mice to either coal
dust, diesel emissions, a combination of both, or filtered air (control
group) for various durations, after which they were infected with
influenza. Although not reflected by excess mortality, the severity of
influenza infection was found to be more pronounced in mice previously
exposed to diesel emissions than in control animals. The effect was not
intensified by inhalation of coal dust in combination with those
emissions.
In addition to possible acute toxicity of particles in the
respiratory tract, chronic exposure to particles that deposit in the
lung may induce inflammation. Inflammatory responses can lead to
increased permeability and possibly diffusion abnormality. Furthermore,
mediators released during an inflammatory response could cause release
of factors in the clotting cascade that may lead to an increased risk
of thrombus formation in the vascular system (Seaton, 1995). Persistent
inflammation, or repeated cycles of acute lung injury and healing, can
induce chronic lung injury. Retention of the particles may be
associated with the initiation and/or progression of COPD.
Takenaka et al. (1995) investigated mechanisms by which dpm may act
to cause allergenic effects in human cell cultures. The investigators
reported that application of organic dpm extracts over a period of 10
to 14 days increased IgE production from the cells by a factor of up to
360 percent. They concluded that enhanced IgE production in the human
airway resulting from the organic fraction of dpm may be an important
factor in the increasing incidence of allergic airway disease.
Similarly, Tsien et al. (1997) investigated the effects of the organic
fraction of dpm on IgE production in human cell cultures and found that
application of the organic extract doubled IgE production after three
days in cells already producing IgE.
Sagai et al. (1996) investigated the potential role of dpm-induced
oxygen radicals in causing pulmonary injuries. Repeated intratracheal
instillation of dpm in mice caused marked infiltration of inflammatory
cells, proliferation of goblet cells, increased mucus secretion,
respiratory resistance, and airway constriction. The results indicated
that oxygen radicals, induced by intratracheally instilled dpm, can
cause responses characteristic of bronchial asthma.
Lovik et al (1997) investigated inflammatory and systemic IgE
responses to dpm, alone and in combination with the model allergen
ovalbumin (OA), in mice. To determine whether it was the elemental
carbon core or substances in the organic fraction of dpm that were
responsible for observed allergenic effects, they compared the effects
of whole dpm with those of carbon black (CB) particles of comparable
size and specific surface area. Although the effects were slightly
greater for dpm, both dpm and CB were found to cause significant,
synergistic increases in allergenic responses to the OA, as expressed
by inflammatory responses of the local lymph node and OA-specific IgE
production. The investigators concluded that both dpm and CB
synergistically enhance and prolong inflammatory responses in the lymph
nodes that drain the site of allergen deposition. They further
concluded that the elemental carbon core contributes substantially to
the adjuvant activity of dpm.
Diaz-Sanchez et al. (1994, 1996, 1997) conducted a series of
experiments on human subjects to investigate the effects of dpm on
allergic inflammation as measured by IgE production. The studies by
Takenaka et al. (op cit.) and Tsien et al. (op cit.) were also part of
this series but were based on human cell cultures rather than live
human volunteers. A principal objective of these experiments was to
investigate the pathways and mechanisms by which dpm induces allergic
inflammation. The investigators found that the organic fraction of dpm
can enhance IgE production, but that the major
[[Page 5630]]
polyaromatic hydrocarbon in this fraction (phenanthrene) can enhance
IgE without causing inflammation. On the other hand, when human
volunteers were sprayed intranasally with carbon particles lacking the
organic compounds, the investigators found a large influx of cells in
the nasal mucosa but no increase in IgE. These results suggest that
while the organic portion of dpm is not necessary for causing
irritation and local inflammation, it is the organic compounds that act
on the immune system to promote an allergic response.
Salvi et al. (1999) investigated the impact of diesel exhaust on
human airways and peripheral blood by exposing healthy volunteers to
diesel exhaust at a concentration of 300 g/m3 for
one hour with intermittent exercise. Following exposure, they found
significant evidence of acute inflammatory responses in airway lavage
and also in the peripheral blood. Some commenters expressed a belief
that the gaseous, rather than particulate, components of diesel exhaust
caused these effects. The investigators noted that the inflammatory
responses observed could not be attributed to NO2 in the
diesel exhaust because previous studies they had conducted, using a
similar experimental protocol, had revealed no such responses in the
airway tissues of volunteers exposed to a higher concentration of
NO2, for a longer duration, in the absence of dpm. They
concluded that ``[i]t therefore seems more likely that the particulate
component of DE is responsible.''
iv. Lung Cancer
(1) Genotoxicity Studies
Many studies have shown that diesel soot, or its organic component,
can increase the likelihood of genetic mutations during the biological
process of cell division and replication. A survey of the applicable
scientific literature is provided in Shirname-More (1995). What makes
this body of research relevant to the risk of lung cancer is that
mutations in critical genes can sometimes initiate, promote, or advance
a process of carcinogenesis.
The determination of genotoxicity has frequently been made by
treating diesel soot with organic solvents such as dichloromethane and
dimethyl sulfoxide. The solvent removes the organic compounds from the
carbon core. After the solvent evaporates, the mutagenic potential of
the extracted organic material is tested by applying it to bacterial,
mammalian, or human cells propagated in a laboratory culture. In
general, the results of these studies have shown that various
components of the organic material can induce mutations and chromosomal
aberrations.
One commenter (MARG) pointed out that ``even assuming diesel
exhaust contains particular genotoxic substances, the bioavailability
of these genotoxins has been questioned.'' As acknowledged in the
proposed risk assessment, a critical issue is whether whole diesel
particulate is mutagenic when dispersed by substances present in the
lung. Since the laboratory procedure for extracting organic material
with solvents bears little resemblance to the physiological environment
of the lung, it is important to establish whether dpm as a whole is
genotoxic, without solvent extraction. Early research indicated that
this was not the case and, therefore, that the active genotoxic
materials adhering to the carbon core of diesel particles might not be
biologically damaging or even available to cells in the lung (Brooks et
al., 1980; King et al., 1981; Siak et al., 1981). A number of more
recent research papers, however, have shown that dpm, without solvent
extraction, can cause DNA damage when the soot is dispersed in the
pulmonary surfactant that coats the surface of the alveoli (Wallace et
al., 1987; Keane et al., 1991; Gu et al., 1991; Gu et al., 1992). From
these studies, NIOSH concluded in 1992 that:
* * * the solvent extract of diesel soot and the surfactant
dispersion of diesel soot particles were found to be active in
procaryotic cell and eukaryotic cell in vitro genotoxicity assays.
The cited data indicate that respired diesel soot particles on the
surface of the lung alveoli and respiratory bronchioles can be
dispersed in the surfactant-rich aqueous phase lining the surfaces,
and that genotoxic material associated with such dispersed soot
particles is biologically available and genotoxically active.
Therefore, this research demonstrates the biological availability of
active genotoxic materials without organic solvent interaction.
[Cover letter to NIOSH response to ANPRM, 1992].
If this conclusion is correct, it follows that dpm itself, and not only
its organic extract, can cause genetic mutations when dispersed by a
substance present in the lung.
One commenter (IMC Global) noted that Wallace et al. (1987) used
aged dpm samples from scrapings inside an exhaust pipe and contended
that this was not a realistic representation of dpm. The commenter
further argued that the two studies cited by Gu et al. involved
``direct application of an unusually high concentration gradient'' that
does not replicate normal conditions of dpm exposure.
MSHA agrees with this commenter's general point that conditions set
up in such experiments do not duplicate actual exposure conditions.
However, as a follow-up to the Wallace study, Keane et al. (op cit)
demonstrated similar results with both exhaust pipe soot and particles
obtained directly from an exhaust stream. With regard to the two Gu
studies, MSHA recognizes that any well-controlled experiment serves
only a limited purpose. Despite their limitations, however, these
experiments provided valuable information. They avoided solvent
extraction. By showing that solvent extraction is not a necessary
condition of dpm mutagenicity, these studies provided incremental
support to the hypothesis of bioavailability under more realistic
conditions. This possibility was subsequently tested by a variety of
other experiments, including experiments on live animals and humans.
For example, Sagai et al. (1996) showed that whole dpm produced
active oxygen radicals in the trachea of live mice, but that dpm
stripped of organic compounds did not. Whole dpm caused significant
damage to the lungs and also high mortality at low doses. According to
the investigators, most of the toxicity observed appeared to be due to
the oxygen radicals, which can also have genotoxic effects.
Subsequently, Ichinose et al. (1997b) examined the relationship between
tumor response and the formation of oxygen radicals in the lungs of
mice injected with dpm. The mice were treated with sufficiently high
doses of dpm to produce tumors after 12 months. As in the earlier
study, the investigators found that the dpm generated oxygen radicals,
even in the absence of biologically activating systems (such as
macrophages), and that these oxygen radicals were implicated in the
lung toxicity of the dpm. The authors concluded that ``oxidative DNA
damage induced by the repeated DEP [i.e., dpm] treatment could be an
important factor in enhancing the mutation rate leading to lung
cancer.''
The formation of DNA adducts is an important indicator of
genotoxicity and potential carcinogenicity. Adduct formation occurs
when molecules, such as those in dpm, attach to the cellular DNA. These
adducts can negatively affect DNA transcription and/or cellular
duplication. If DNA adducts are not repaired, then a mutation or
chromosomal aberration can occur during normal mitosis (i.e., cell
replication) eventually leading to cancer cell formation. IPCS (1996)
contains a survey of animal experiments showing DNA adduct induction in
the lungs of experimental animals exposed to diesel
[[Page 5631]]
exhaust.\62\ MSHA recognizes that such studies provide limited
information regarding the bioavailability of organics, since positive
results may well have been related to factors associated with lung
particle overload. However, the bioavailability of genotoxic dpm
components is also supported by human studies showing genotoxic effects
of exposure to whole dpm. DNA adduct formation and/or mutations in
blood cells following exposure to dpm, especially at levels
insufficient to induce lung overload, can be presumed to result from
organics diffusing into the blood.
---------------------------------------------------------------------------
\62\ Some of these studies will be discussed in the next
subsection of this risk assessment.
---------------------------------------------------------------------------
Hemminki et al. (1994) found that DNA adducts were significantly
elevated in lymphocytes of nonsmoking bus maintenance and truck
terminal workers, as compared to a control group of hospital mechanics,
with the highest adduct levels found among garage and forklift workers.
Hou et al. (1995) reported significantly elevated levels of DNA adducts
in lymphocytes of non-smoking diesel bus maintenance workers compared
to a control group of unexposed workers. Similarly, Nielsen et al.
(1996) found that DNA adducts were significantly increased in the blood
and urine of bus garage workers and mechanics exposed to dpm as
compared to a control group.
One commenter (IMC Global) acknowledged that ``the studies
conducted by Hemminiki [Hemminiki et al, 1994] showed elevations in
lymphocyte DNA adducts in garage workers, bus maintenance workers and
diesel forklift drivers'' but argued that ``these elevations were at
the borderline of statistical significance.'' Although results at a
higher level of confidence would have been more persuasive, this does
not negate the value of the evidence as it stands. Furthermore,
statistical significance in an individual study becomes less of an
issue when, as in this case, the results are corroborated by other
studies.
IMC Global also acknowledged that the Nielsen study found
significant differences in DNA adduct formation between diesel-exposed
workers and controls but argued that ``the real source of genotoxins
was unclear, and other sources of exposure, such as skin contact with
lubricating oils could not be excluded.'' As is generally the case with
studies involving human subjects, this study did not completely control
for potential confounders. For this reason, MSHA considers it important
that several human studies--not all subject to confounding by the same
variables--found elevated adduct levels in diesel-exposed workers.
IMC Global cited another human study (Qu et al., 1997) as casting
doubt on the genotoxic effects of diesel exposure, even though this
study (conducted on Australian coal miners) reported significant
increases in DNA adducts immediately after a period of intense diesel
exposure during a longwall move. As noted by the commenter, adduct
levels of exposed miners and drivers were, prior to the longwall move,
approximately 50% higher than for the unexposed control group; but
differences by exposure category were not statistically significant. A
more informative part of the study, however, consisted of comparing
adducts in the same workers before and after a longwall move, which
involved ``intensive use of heavy equipment, diesel powered in these
mines, over a 2-3 week period.'' MSHA emphasizes that the comparison
was made on the same workers, because doing so largely controlled for
potentially confounding variables, such as smoking habits, that may be
a factor when making comparisons between different persons. After the
period of ``intensive'' exposure, statistically significant increases
were observed in both total and individual adducts. Contrary to the
commenter's characterization of this study, the investigators stated
that their analysis ``provides results in which the authors have a high
level of confidence.'' They concluded that ``given the * * * apparent
increase in adducts during a period of intense DEE [i.e., diesel
exhaust emissions] exposures it would be prudent to pay particular
attention to keeping exposures as low as possible, especially during
LWCO [i.e., ``longwall change out''] operations.'' Although the
commenter submitted this study as counter-evidence, it actually
provides significant, positive evidence that high dpm exposures in a
mining environment can produce genotoxic effects.
The West Virginia Coal Association submitted an analysis by Dr.
Peter Valberg, purporting to show that ``* * * the quantity of
particle-bound mutagens that could potentially contact lung cells under
human exposure scenarios is very small.'' According to Dr. Valberg's
calculations, the dose of organic mutagens deposited in the lungs of a
worker occupationally exposed (40 hours per week) to 500 g/
m\3\ of dpm would be equivalent in potency to smoking about one
cigarette per month.\63\ Dr. Valberg indicated that a person smoking at
this level would generally be classified a nonsmoker, but he made no
attempt to quantify the carcinogenic effects. Nor did he compare this
exposure level with levels of exposures to environmental tobacco smoke
that have been linked to lung cancer.
---------------------------------------------------------------------------
\63\ The only details provided for this calculation pertained to
ajusting 8-hour occupational exposures. Dr. Valberg adjusted the 500
g/m\3\ concentration for an 8-hour occupational exposure to
a supposedly equivalent 24-hour continuous concentration of 92
g/m\3\. This adjustment ignored differences in breathing
rates between periods of sleep, leisure activities, and heavy work.
Even under the unrealistic assumption of homogeneous breathing
rates, the calculation appears to be erroneous, since (500
g/m\3\) x (40 hours/week) is nearly 30 percent greater
than (92 g/m\3\) x (168 hours/week). Also, Dr. Valberg
stated that the calculation assumed a deposition fraction of 20
percent for dpm but did not state what deposition fraction was being
assumed for the particles in cigarette smoke.
---------------------------------------------------------------------------
Since the commenter did not provide details of Dr. Valberg's
calculation, MSHA was unable to verify its accuracy or evaluate the
plausibility of key assumptions. However, even if the equivalence is
approximately correct, using it to discount the possibility that dpm
increases the risk of lung cancer relies on several questionable
assumptions. Although their precise role in the analysis is unclear
because it was not presented in detail, these assumptions apparently
include:
(1) That there is a good correlation between genotoxicity dose-
response and carcinogenicity dose-response. Although genotoxicity data
can be very useful for identifying a carcinogenic hazard,
carcinogenesis is a highly complex process that may involve the
interaction of many mutagenic, physiological, and biochemical
responses. Therefore, the shape and slope of a carcinogenic dose-
response relationship cannot be readily predicted from a genotoxic
dose-response relationship.
(2) That only the organic fraction of dpm contributes to
carcinogenesis. This contradicts the findings reported by Ichinose et
al. (1997b) and does not take into account the contribution that
inflammation and active oxygen radicals induced by the inorganic carbon
core of dpm may have in promoting lung cancers. Multiple routes of
carcinogenesis may operate in human lungs--some requiring only the
various organic mutagens in dpm and others involving induction of free
radicals by the elemental carbon core, either alone or in combination
with the organics.
(3) That the only mutagens in dpm are those that have been
identified as mutagenic to bacteria and that the
[[Page 5632]]
mutagenic constituents of dpm have all been identified. One of the most
potent of all known mutagens (3-nitrobenzanthrone) was only recently
isolated and identified in dpm (Enya et al., 1997).
(4) That the mutagenic components of dpm have the same combined
potency as those in cigarette smoke. This ignores the relative potency
and amounts of the various mutagenic constituents. If the calculation
did not take into account the relative amounts and potencies of all the
individual mutagens in dpm and cigarette smoke, then it oversimplified
the task of making such a comparison.
In sum, unlike the experimental findings of dpm genotoxicity
discussed above, the analysis by Dr. Valberg is not based on empirical
evidence from dpm experiments, and it appears to rely heavily on
questionable assumptions. Moreover, the contention that active
components of dpm are not available in sufficient quantities to cause
significant mutagenic damage in humans appears to be directly
contradicted by the empirical evidence of elevated DNA adduct levels in
exposed workers (Hemminki et al., 1994; Hou et al., 1995; Nielsen et
al., 1996; Qu et al., 1997).
(2) Animal Inhalation Studies
When dpm is inhaled, a number of adverse effects that may
contribute to carcinogenesis are discernable by microscopic and
biochemical analysis. For a comprehensive review of these effects, see
Watson and Green (1995). In brief, these effects begin with
phagocytosis, which is essentially an attack on the diesel particles by
cells called alveolar macrophages. The macrophages engulf and ingest
the diesel particles, subjecting them to detoxifying enzymes. Although
this is a normal physiological response to the inhalation of foreign
substances, the process can produce various chemical byproducts
injurious to normal cells. In attacking the diesel particles, the
activated macrophages release chemical agents that attract neutrophils
(a type of white blood cell that destroys microorganisms) and
additional alveolar macrophages. As the lung burden of diesel particles
increases, aggregations of particle-laden macrophages form in alveoli
adjacent to terminal bronchioles, the number of Type II cells lining
particle-laden alveoli increases, and particles lodge within alveolar
and peribronchial tissues and associated lymph nodes. The neutrophils
and macrophages release mediators of inflammation and oxygen radicals,
which have been implicated in causing various forms of chromosomal
damage, genetic mutations, and malignant transformation of cells
(Weitzman and Gordon, 1990). Eventually, the particle-laden macrophages
are functionally altered, resulting in decreased viability and impaired
phagocytosis and clearance of particles. This series of events may
result in pulmonary inflammatory, fibrotic, or emphysematous lesions
that can ultimately develop into cancerous tumors.
IARC (1989), Mauderly (1992), Busby and Newberne (1995), IPCS
(1996), Cal-EPA (1998), and US EPA (1999) reviewed the scientific
literature relating to excess lung cancers observed among laboratory
animals chronically exposed to filtered and unfiltered diesel exhaust.
The experimental data demonstrate that chronic exposure to whole diesel
exhaust increases the risk of lung cancer in rats and that dpm is the
causative agent. This carcinogenic effect has been confirmed in two
strains of rats and in at least five laboratories. Experimental results
for animal species other than the rat, however, are either inconclusive
or, in the case of Syrian hamsters, suggestive of no carcinogenic
effect. In two of three mouse studies reviewed by IARC (1989), lung
tumor formation (including adenocarcinomas) was increased in the
exposed animals as compared to concurrent controls; in the third study,
the total incidence of lung tumors was not elevated compared to
historical controls. Two more recent mouse studies (Heinrich et al.,
1995; Mauderly et al., 1996) have both reported no statistically
significant increase in lung cancer rates among exposed mice, as
compared to contemporaneous controls. Monkeys exposed to diesel exhaust
for two years did not develop lung tumors, but the short duration of
exposure was judged inadequate for evaluating carcinogenicity in
primates.
Bond et al. (1990a) investigated differences in peripheral lung DNA
adduct formation among rats, hamsters, mice, and monkeys exposed to dpm
at a concentration of 8100 g/m3 for 12 weeks. Mice
and hamsters showed no increase of DNA adducts in their peripheral lung
tissue, whereas rats and monkeys showed a 60 to 80-percent increase.
The increased prevalence of lung DNA adducts in monkeys suggests that,
with respect to DNA adduct formation, the human lungs' response to dpm
inhalation may more closely resemble that of rats than that of hamsters
or mice.
The conflicting carcinogenic effects of chronic dpm inhalation
reported in studies of rats, mice, and hamsters may be due to non-
equivalent delivered doses or to differences in response among species.
Indeed, monkey lungs have been reported to respond quite differently
than rat lungs to both diesel exhaust and coal dust (Nikula, 1997).
Therefore, the results from rat experiments do not, by themselves,
establish that there is any excess risk due to dpm exposure for humans.
However, the human epidemiologic and genotoxicity (DNA adduct) data
indicate that humans comprise a species that, like rats, do suffer a
carcinogenic response to dpm exposure. This would be consistent with
the observation, mentioned above, that lung DNA adduct formation is
increased among exposed rats but not among exposed hamsters or mice.
Therefore, although MSHA recognizes that there are important
differences between rats and humans (as there are also between rats and
hamsters or mice), MSHA considers the rat studies relevant to an
evaluation of human health risks.
Reactions similar to those observed in rats inhaling dpm have also
been observed in rats inhaling fine particles with no organic component
(Mauderly et al., 1994; Heinrich et al., 1994, 1995; Nikula et al.,
1995). Rats exposed to titanium dioxide (TiO2) or pure
carbon (``carbon black'') particles, which are not considered to be
genotoxic, exhibited similar pathological responses and developed lung
cancers at about the same rate as rats exposed to whole diesel exhaust.
Carbon black particles were used in these experiments because they are
physically similar to the inorganic carbon core of dpm but have
negligible amounts of organic compounds adsorbed to their surface.
Therefore, at least in some species, it appears that the lung cancer
toxicity of dpm may result largely from a biochemical response to the
core particle itself rather than from specific, genotoxic effects of
the adsorbed organic compounds.\64\
---------------------------------------------------------------------------
\64\ NIOSH commented as follows: ``Data cited by MSHA in support
of this statement are not comparable. Rats were exposed to dpm at 4
mg/m3 for 2 years (Mauderly et al. 1987; Brightwell et
al. 1989), in contrast to rats exposed to Ti02 at 250 mg/
m3 for two years [reference to article (Lee et al. 1985)
not cited by MSHA]. It is not apparent that the overload mechanism
that is proposed to be responsible for tumors in the Ti02
exposed rats could also have been responsible for the tumors seen in
the dpm exposed rats at 62-fold lower exposure concentrations.'' In
the reports cited by MSHA, levels of Ti02 and/or carbon
black were commensurate with dpm levels.
---------------------------------------------------------------------------
One commenter stated that, in the proposed risk assessment, MSHA
had neglected three additional studies suggesting that lung cancer
risks in animals inhaling diesel exhaust are unrelated to genotoxic
mechanisms. One of these studies (Mauderly et al.,
[[Page 5633]]
1996) did not pertain to questions of genotoxicity but has been cited
in the discussion of mouse studies above. The other two studies
(Randerath et al., 1995 and Belinsky et al., 1995) were conducted as
part of the cancer bioassay described in the 1994 article by Mauderly
et al. (cited in the preceding paragraph). In the Randerath study, the
investigators found that no DNA adducts specific to either diesel
exhaust or carbon black were induced in the lungs of rats exposed to
the corresponding substance. However, after three months of exposure,
the total level of DNA adducts and the levels of some individual
adducts were significantly higher in the diesel-exposed rats than in
the controls. In contrast, multiple DNA adducts thought to be specific
to diesel exhaust formed in the skin and lungs of mice treated
topically with organic dpm extract. These results are consistent with
the findings of Mauderly et al. (1994, op cit.). They imply that
although the organic compounds of diesel exhaust are capable of
damaging cellular DNA, they did not inflict such damage under the
conditions of the inhalation experiment performed. The report noted
that these results do not rule out the possibility of DNA damage by
inhaled organics in ``other species or * * * [in] exposure situations
in which the concentrations of diesel exhaust particles are much
lower.'' In the Belinsky study, the investigators measured mutations in
selected genes in the tumors of those rats that had developed lung
cancer. This study did not succeed in elucidating the mechanisms by
which dpm and carbon black cause lung tumors in rats. The authors
concluded that ``until some of the genes involved in the
carcinogenicity of diesel exhaust and carbon black are identified, a
role for the organic compounds in tumor development cannot be
excluded.''
The carbon-black and TiO2 studies discussed above
indicate that lung cancers in rats exposed to dpm may be induced by a
mechanism that does not require the bioavailability of genotoxic
organic compounds adsorbed on the elemental carbon particles. Some
researchers have interpreted these studies as also suggesting that (1)
the carcinogenic mechanism in rats depends on massive overloading of
the lung and (2) that this may provide a mechanism of carcinogenesis
involving a threshold effect specific to rats, which has not been
observed in other rodents or in humans (Oberdorster, 1994; Watson and
Valberg, 1996). Some commenters on the ANPRM cited the lack of a link
between lung cancer and coal dust or carbon black exposure as evidence
that carbon particles, by themselves, are not carcinogenic in humans.
Coal mine dust, however, consists almost entirely of particles larger
than those forming the carbon core of dpm or used in the carbon black
and Ti02 rat studies. Furthermore, although there have been
nine studies reporting no excess risk of lung cancer among coal miners
(Liddell, 1973; Costello et al., 1974; Armstrong et al., 1979; Rooke et
al., 1979; Ames et al., 1983; Atuhaire et al., 1985; Miller and
Jacobsen, 1985; Kuempel et al., 1995; Christie et al., 1995), eight
studies have reported an elevated risk of lung cancer for those exposed
to coal dust (Enterline, 1972; Rockette, 1977; Howe et al., 1983;
Correa et al., 1984; Levin et al., 1988; Morabia et al., 1992; Swanson
et al., 1993; Morfeld et al., 1997). The positive results in five of
these studies (Enterline, 1972; Rockette, 1977; Howe et al., 1983;
Morabia et al., 1992; Swanson et al., 1993) were statistically
significant. Morabia et al. (op cit.) reported increased risk
associated with duration of exposure, after adjusting for cigarette
smoking, asbestos exposure, and geographic area. Furthermore, excess
lung cancers have been reported among carbon black production workers
(Hodgson and Jones, 1985; Siemiatycki, 1991; Parent et al., 1996).
After a comprehensive evaluation of the available scientific evidence,
the World Health Organization's International Agency for Research on
Cancer concluded: ``Carbon black is possibly carcinogenic to humans
(Group 2B).'' (IARC, 1996)
The carbon black and TiO2 animal studies cited above do
not prove there is a threshold below which dpm exposure poses no risk
of causing lung cancer in humans. They also do not prove that dpm
exposure has no incremental, genotoxic effects. Even if the genotoxic
organic compounds in dpm were biologically unavailable and played no
role in human carcinogenesis, this would not rule out the possibility
of a genotoxic route to lung cancer (even for rats) due to the presence
of the particles themselves. For example, as a byproduct of the
biochemical response to the presence of particles in the alveoli, free
oxidant radicals may be released as macrophages attempt to digest the
particles. There is evidence that dpm can both induce production of
reactive oxygen agents and also depress the activity of naturally
occurring antioxidant enzymes (Mori, 1996; Ichinose et al., 1997; Sagai
et al., 1996). Oxidants can induce carcinogenesis either by reacting
directly with DNA, or by stimulating cell replication, or both
(Weitzman and Gordon, 1990). Salvi et al. (1999) reported acute
inflammatory responses in the airways of human exposed to dpm for one
hour at a concentration of 300 g/m3. Such
inflammation is associated with the production of free radicals and
could provide routes to lung cancer with even when normal lung
clearance is occurring. It could also give rise to a ``quasi-
threshold,'' or surge in response, corresponding to the exposure level
at which the normal clearance rate becomes overwhelmed (lung overload).
Oxidant activity is not the only mechanism by which dpm could exert
carcinogenic effects in the absence of mutagenic activity by its
organic fraction. In its commentary on the Randerath study discussed
above, the HEI's Health Review Committee suggested that dpm could both
cause genetic damage by inducing free oxygen radicals and also enhance
cell division by inducing cytokines or growth hormones:
It is possible that diesel exhaust exerts its carcinogenic
effects through a mechanism that does not involve direct
genotoxicity (that is, formation of DNA adducts) but involves
proliferative responses such as chronic inflammation and hyperplasia
arising from high concentrations of particles deposited in the lungs
of the exposed rats. * * * Phagocytes (macrophages and neutrophils)
released during inflammatory reactions ``produce reactive oxygen
species that can damage DNA. * * * Particles (with or without
adsorbed PAHs) may thus induce oxidative DNA damage via oxygen free
radicals. * * * Alternatively, activated phagocytes may release
cytokines or growth factors that are known to increase cell
division. Increased cell division has been implicated in cancer
causation. * * * Thus, in addition to oxidative DNA damage,
increased cell proliferation may be an important mechanism by which
diesel exhaust and other insoluble particles induce pulmonary
carcinogenesis in the rat. [Randerath et al., 1995, p.55]
Even if lung overload were the primary or sole route by which dpm
induced lung cancer, this would not mean that the high dpm
concentrations observed in some mines are without hazard. It is
noteworthy, moreover, that dpm exposure levels recorded in some mines
have been almost as high as laboratory exposures administered to rats
showing a clearly positive response. Intermittent, occupational
exposure levels greater than about 500 g/m3 dpm may
overwhelm the human lung clearance mechanism (Nauss et al., 1995).
Therefore, concentrations at the even higher levels currently observed
in some mines could be expected to cause overload in some humans,
possibly
[[Page 5634]]
inducing lung cancer by a mechanism similar to what occurs in rats. In
addition, a proportion of exposed individuals can always be expected to
be more susceptible than normal to clearance impairments and lung
overload. Inhalation at even moderate levels may significantly impair
clearance, especially in susceptible individuals. Exposures to
cigarette smoke and respirable mineral dusts may further depress
clearance mechanisms and reduce the threshold for overload.
Consequently, even at dpm concentrations far lower than 500 g/
m3 dpm, impaired clearance due to dpm inhalation may provide
an important route to lung cancer in humans, especially if they are
also inhaling cigarette smoke and other fine dusts simultaneously.
(Hattis and Silver, 1992, Figures 9, 10, 11)
Furthermore, as suggested above, lung overload is not necessarily
the only route to carcinogenesis in humans. Therefore, dpm
concentrations too low to cause overload still may present a hazard. In
humans exposed over a working lifetime to doses insufficient to cause
overload, carcinogenic mechanisms unrelated to overload may operate, as
indicated by the human epidemiologic studies and the data on human DNA
adducts cited in the preceding subsection of this risk assessment. It
is possible that overload provides the dominant route to lung cancer at
high concentrations of fine particulate, while other mechanisms emerge
as more relevant for humans under lower-level exposure conditions.
The NMA noted that, in 1998, the US EPA's Clean Air Scientific
Advisory Committee (CASAC) concluded that there is ``no evidence that
the organic fraction of soot played a role in rat tumorigenesis at any
exposure level, and considerable evidence that it did not.'' According
to the NMA, this showed ``* * * it is the rat data--not the hamster
data--that lacks relevance for human health assessment.''
It must first be noted that, in MSHA's view, all of the
experimental animal data on health effects has relevance for human
health risk assessment--whether the evidence is positive or negative
and even if the positive results cannot be used to quantify human risk.
The finding that different mammalian species exhibit important
differences in response is itself relevant for human risk assessment.
Second, the passage quoted from CASAC pertains to the route for
tumorigenesis in rats and does not discuss whether this does or does
not have relevance to humans exposed at high levels. The context for
the CASAC deliberations was ambient exposure conditions in the general
environment, rather than the higher occupational exposures that might
impair clearance rates in susceptible individuals. Third, the comment
assumes that only a finding of tumorigenesis attributable to the
organic portion of dpm would elucidate mechanisms of potential health
effects in humans. This ignores the possibility that a mechanism
promoting tumors, but not involving the organics, could operate in both
rats and humans. Induction of free oxygen radicals is an example.
Fourth, although there may be little or no evidence that organics
contributed to rat tumorigenesis in the studies performed, there is
evidence that the organics contributed to increases in DNA adduct
formation. This kind of activity could have tumorigenic consequences in
humans who may be exposed for periods far longer than a rat's 3-year
lifetime and who, as a consequence, have more time to accumulate
genetic damage from a variety of sources.
Bond et al. (1990b) and Wolff et al. (1990) investigated adduct
formation in rats exposed to various concentrations of either dpm or
carbon black for 12 weeks. At the highest concentration (10 mg/
m3), DNA adduct levels in the lung were increased by
exposure to either dpm or carbon black; but levels in the rats exposed
to dpm were approximately 30 percent higher. Gallagher et al. (1994)
exposed different groups of rats to diesel exhaust, carbon black, or
TiO2 and detected no significant difference in DNA adduct
levels in the lung. However, the level of one type of adduct, thought
to be derived from a PAH, was elevated in the dpm-exposed rats but not
found in the control group or in rats exposed to carbon black or
TiO2.
These studies indicate that the inorganic carbon core of dpm is not
the only possible agent of genetic damage in rats inhaling dpm. After a
review of these and other studies involving DNA adducts, IPCS (1996)
concluded that ``Taken together, the studies of DNA adducts suggest
that some organic chemicals in diesel exhaust can form DNA adducts in
lung tissue and may play a role in the carcinogenic effects. * * *
however, DNA adducts alone cannot explain the carcinogenicity of diesel
exhaust, and other factors, such as chronic inflammation and cell
proliferation, are also important.''
Nauss et al. (1995, pp. 35-38) judged that the results observed in
the carbon black and TiO2 inhalation studies on rats do not preclude
the possibility that the organic component of dpm has important
genotoxic effects in humans. More generally, they also do not prove
that lung overload is necessary for dpm-induced lung cancer. Because of
the relatively high doses administered in some of the rat studies, it
is conceivable that an overload phenomenon masked or even inhibited
other potential cancer mechanisms. At dpm concentrations insufficient
to impair clearance, carcinogenesis may have followed other routes,
some possibly involving the organic compounds. At these lower
concentrations, or among rats for which overload did not occur, tumor
rates for dpm, carbon black, and TiO2 may all have been too
low to make statistically meaningful comparisons.
The NMA argued that ``MSHA's contention that lung overload might
``mask'' tumor production by lower doses of Dpm has been convincingly
rebutted by recognized experts in the field,'' but provided no
convincing explanation of why such masking could not occur. The NMA
went on to say:
The [CASAC] Panel viewed the premises that: a) a small tumor
response at low exposure was overlooked due to statistical power;
and b) soot-associated organic mutagens had a greater effect at low
than at high exposure levels to be without foundation. In the
absence of supporting evidence, the Panel did not view derivation of
a quantitative estimate of human lung cancer risk from the low-level
rat data as appropriate.
MSHA is not attempting to ``derive a quantitative estimate of human
lung cancer risk from the low-level rat data.''
Dr. Peter Valberg, writing for the West Virginia Coal Association,
provided the following argument for discounting the possibility of
other carcinogenic mechanisms being masked by overload in the rat
studies:
Some regulatory agencies express concern about the mutagens
bound to dpm. They hypothesize that, at high exposure levels,
genotoxic mechanisms are overwhelmed (masked) by particle-overload
conditions. However, they argue that at low-exposure concentrations,
these organic compounds could represent a lung cancer risk. Tumor
induction by mutagenic compounds would be characterized by a linear
dose-response and should be detectable, given enough exposed rats.
By using a ``meta-analysis'' type of approach and combining data
from eight long-term rat inhalation studies, the lung tumor response
can be analyzed. When all dpm-exposed rats from lifetime-exposure
studies are combined, a threshold of response (noted above) occurs
at approximately 600 g/m3 continuous lifetime
exposure (approximately 2,500 g/m3 of
occupational exposure). Additional statistical analysis of only
those rats exposed to low concentrations of dpm confirms the absence
of a tumorigenic effect below that threshold. Thus, even data in
rats (the most sensitive laboratory species) do not support the
hypothesis that particle-bound organics cause tumors.
[[Page 5635]]
MSHA finds that this analysis relies on several questionable and
unsupported assumptions and that, for the following reasons, the
possibility remains that organic compounds in inhaled dpm may, under
the right exposure conditions, contribute to its carcinogenic effects:
(1) The absence of evidence for an organic carbon effect is not
equivalent to evidence of the absence of such an effect. Dr. Valberg
did not demonstrate that enough rats were exposed, at levels
insufficient to cause overload, to ensure detection of a 30- to 40-
percent increase in the risk of lung cancer. Also, the normal lifespan
of a rat whose lung is not overloaded with particles may, because of
the lower concentrations involved, provide insufficient time for the
organic compounds to express carcinogenic effects. Furthermore, low
bioavailability of the organics could further reduce the likelihood
that a carcinogenic sequence of mutations would occur within a rat's
relatively short lifespan (i.e., at particle concentrations too low to
cause overload).
(2) If the primary mechanism for carcinogenesis requires a reduced
clearance rate (due to overload), then acute exposures are important,
and it may not be appropriate to represent equivalent hazards by
spreading an 8-hour occupational exposures over a 24-hour period. For
example, eight hours at 600 g/m3 would have
different implications for lung clearance than 24 hours at 200
g/m3.
(3) Granting that the rat data cannot be used to extrapolate risk
for humans, these data should also not be used to rule out mechanisms
of carcinogenesis that may operate in humans but not in rats.
Clearance, for example, may operate differently in humans than in rats,
and there may be a gradual rather than abrupt change in human overload
conditions with increasing exposure. Also, at least some of the organic
compounds in dpm may be more biologically available to the human lung
than to that of the rat.
(4) For experimental purposes, laboratory rats are deliberately
bred to be homogeneous. This is done, in part, to deliberately minimize
differences in response between individuals. Therefore, individual
differences in the threshold for lung overload would tend to be masked
in experiments on laboratory rats. It is likely that human populations
would exhibit, to a far greater extent than laboratory rats, a range of
susceptibilities to lung overload. Also some humans, unlike the
laboratory rats in these experiments, place additional burdens on their
lung clearance by smoking.
One commenter (MARG) concluded that ``[t]here is * * * no basis for
extrapolating the rat results to human beings; the animal studies,
taken together, do not justify MSHA's proposals.''
MSHA is neither extrapolating the rat results to make quantitative
risk estimates for humans nor using them, in isolation, as a
justification for these regulations. MSHA does regard it as
significant, however, that the evidence for an increased risk of lung
cancer due to chronic dpm inhalation comes from both human and animal
studies. MSHA agrees that the quantitative results observed for rats in
existing studies should not be extrapolated to humans. Nevertheless,
the fact that high dpm exposures for two or three years can induce lung
cancer in rats enhances the epidemiologic evidence that much longer
exposures to miners, at concentrations of the same order of magnitude,
could also induce lung cancers.
3. Characterization of Risk
After reviewing the evidence of adverse health effects associated
with exposure to dpm, MSHA evaluated that evidence to ascertain whether
exposure levels currently existing in mines warrant regulatory action
pursuant to the Mine Act. The criteria for this evaluation are
established by the Mine Act and related court decisions. Section
101(a)(6)(A) provides that:
The Secretary, in promulgating mandatory standards dealing with
toxic materials or harmful physical agents under this subsection,
shall set standards which most adequately assure on the basis of the
best available evidence that no miner will suffer material
impairment of health or functional capacity even if such miner has
regular exposure to the hazards dealt with by such standard for the
period of his working life.
Based on court interpretations of similar language under the
Occupational Safety and Health Act, there are three questions that need
to be addressed: (a) Whether health effects associated with dpm
exposure constitute a ``material impairment'' to miner health or
functional capacity; (b) whether exposed miners are at significant
excess risk of incurring any of these material impairments; and (c)
whether the rule will substantially reduce such risks.
Some commenters argued that the link between dpm exposure and
material health impairments is questionable, and that MSHA should wait
until additional scientific evidence becomes available before
concluding that there are health risks due to such exposure warranting
regulatory action. For example, MARG asserted that ``[c]ontrary to the
suggestions in the [proposed] preamble, a link between dpm exposure and
serious illness has never been established by reliable scientific
evidence.'' \65\ MARG continued as follows:
---------------------------------------------------------------------------
\65\ MARG supported this assertion by claiming that ``[t]he EPA
reports which MSHA references in its preamble were found `not
scientifically adequate for making regulatory decisions concerning
the use of diesel-powered engines' by EPA's Clean Air Scientific
Advisory Committee. [reference to CASAC (1998)]'' Contrary to MARG's
claim, CASAC (1998) did not review any of the 20 EPA documents MSHA
cited in the proposed preamble. Instead, the document reviewed by
CASAC (1998) was an unpublished draft of a health risk assessment on
diesel exhaust (EPA, 1998), to which MSHA made no reference. Since
MSHA has not relied in any way on this 1998 draft document, its
``scientific adequacy'' is entirely irrelevant to this rulemaking.
In response to the 1998 CASAC review, EPA modified its draft
risk assessment (EPA, 1999), and CASAC subsequently reviewed the
1999 draft (CASAC, 2000). CASAC found the revised draft much
improved over the previous version and agreed that even
environmental exposure to diesel emissions is likely to increase the
risk of lung cancer (CASAC, 2000). CASAC endorsed this conclusion
for dpm concentrations in ambient air, which are lower, by a factor
of more than 100, than the levels observed in some mines (see Fig.
III-4).
Precisely because the scientific evidence * * * is inconclusive
at best, NIOSH and NCI are now conducting a * * * [study] to
determine whether diesel exhaust is linked to illness, and if so, at
what level of exposure. * * * MARG is also funding an independent
parallel study.
* * * Until data from the NIOSH/NCI study, and the parallel MARG
study, are available, the answers to these important questions will
not be known. Without credible answers to these and other questions,
MSHA's regulatory proposals * * * are premature * * *.''
For reasons explained below, MSHA does not agree that the
collective weight of scientific evidence is ``inconclusive at best.''
Furthermore, the criteria for evaluating the health effects evidence do
not require scientific certainty. As noted by Justice Stevens in an
important case on risk involving the Occupational Safety and Health
Administration, the need to evaluate risk does not mean an agency is
placed into a ``mathematical straitjacket.'' [Industrial Union
Department, AFL-CIO v. American Petroleum Institute, 448 U.S. 607, 100
S.Ct. 2844 (1980), hereinafter designated the ``Benzene'' case]. The
Court recognized that regulation may be necessary even when scientific
knowledge is not complete; and--
so long as they are supported by a body of reputable scientific
thought, the Agency is free to use conservative assumptions in
interpreting the data * * * risking error on the side of
overprotection rather than underprotection. [Id. at 656].
[[Page 5636]]
Moreover, the statutory criteria for evaluating health effects do
not require MSHA to wait for incontrovertible evidence. In fact, MSHA
is required to set standards based on the ``best available evidence''
(emphasis added).
a. Material Impairments to Miners' Health or Functional Capacity
MSHA recognizes that there is considerable disagreement, among
knowledgeable parties, in the interpretation of the overall body of
scientific research and medical evidence related to human health
effects of dpm exposures. One commenter for example, interpreted the
collective evidence as follows:
* * * the best available scientific evidence shows that diesel
particulate exposure is associated with serious material impairment
of health. * * * there is clear evidence that diesel particulate
exposure can cause lung cancer (as well as other serious non-
malignant diseases) among workers in a variety of occupational
settings. While no body of scientific evidence is ever completely
definitive, the evidence regarding diesel particulate is
particularly strong * * *. [Michael Silverstein, MD, State of
Washington Dept. of Labor and Industries]
Other commenters, including several national and regional
organizations representing the mining industry, sharply disagreed with
this interpretation. For example, one commenter stated that ``[i]n our
opinion, the best available evidence does not provide substantial or
credible support for the proposal.'' Several commenters argued that
evidence from within the mining industry itself was especially
weak.\66\ A representative of one mining company that had been using
diesel equipment for many years commented: ``[t]o date, the medical
history of our employees does not indicate a single case of lung
cancer, chronic illness, or material impairment of health due to
exposure to diesel exhaust. This appears to be the established norm
throughout the U.S. coal mining industry.'' This commenter, however,
submitted no evidence comparing the rate of lung cancer or other
material impairment among exposed miners to the rate for unexposed
miners (or comparable workers) of similar age, smoking habits, and
geographic location.
---------------------------------------------------------------------------
\66\ At the public hearing on May 11, 1999, a commenter
representing MARG suggested there is evidence that miners exposed to
dpm experience adverse health effects at lower-than-normal rates.
According to this commenter, ``[s]ignificantly, the human studies
conducted in the mining industry reveal a negative propensity for
diesel particulate matter-related health effects.'' These studies
drew comparisons against an external reference population and failed
to adjust for the ``healthy worker effect.'' (See MSHA's discussion
of this effect, especially as manifested in the study by Christie et
al., 1995, in Subsection 2.c.i(2)(a) of this risk assessment.)
---------------------------------------------------------------------------
With due consideration to all oral and written testimony, comments,
and evidence submitted during the rulemaking proceedings, MSHA
conducted a review of the scientific literature cited in Part III.2.
Based on the combined weight of the best available evidence, MSHA has
concluded that underground miners exposed to current levels of dpm are
at excess risk of incurring the following three kinds of material
impairment: (i) Sensory irritations and respiratory symptoms (including
allergenic responses); (ii) premature death from cardiovascular,
cardiopulmonary, or respiratory causes; and (iii) lung cancer. The next
three subsections will respectively explain MSHA's basis for linking
these effects with dpm exposure.
i. Sensory Irritations and Respiratory Symptoms (Including Allergenic
Responses)
Kahn et al. (1988), Battigelli (1965), Gamble et al. (1987a), and
Rudell et al. (1996) identified a number of debilitating acute
responses to diesel exhaust exposure. These responses included
irritation of the eyes, nose and throat; headaches, nausea, and
vomiting; chest tightness and wheeze. These symptoms were also reported
by miners at the 1995 workshops and the public hearings held on these
proceedings in 1998. In addition, Ulfvarson et al. (1987, 1990)
reported evidence of reduced lung function in workers exposed to dpm
for a single shift. The latter study supports attributing a portion of
the reduction to the dpm in diesel exhaust. After reviewing this body
of literature, Morgan et al. (1997) concluded ``it is apparent that
exposure to diesel fumes in sufficient concentrations may lead to
[transient] eye and nasal irritation'' and ``a transient decline of
ventilatory capacity has been noted following such exposures.''
One commenter (Nevada Mining Association) acknowledged there was
evidence that miners exposed to diesel exhaust experienced, as a
possible consequence of their exposure, ``acute, short-term or
`transitory' irritation, such as watering eyes, in susceptible
individuals * * *''; but asserted that ``[a]ddressing any such
transient irritant effects does not require the Agency's sweeping,
stringent PEL approach [in M/NM mines].''
Although there is evidence that such symptoms subside within one to
three days of no occupational exposure, a miner who must be exposed to
dpm day after day in order to earn a living may not have time to
recover from such effects. Hence, the opportunity for a so-called
``reversible'' health effect to reverse itself may not be present for
many miners. Furthermore, effects such as stinging, itching and burning
of the eyes, tearing, wheezing, and other types of sensory irritation
can cause severe discomfort and can, in some cases, be seriously
disabling. Also, workers experiencing sufficiently severe sensory
irritations can be incapacitated or distracted as a result of their
symptoms, thereby endangering themselves and other workers and
increasing the risk of accidents. For these reasons, MSHA considers
such irritations to constitute ``material impairments'' of health or
functional capacity within the meaning of the Act, regardless of
whether or not they are reversible. Further discussion of why MSHA
believes reversible effects can constitute material impairments can be
found above, in Subsection 2.a.2 of this risk assessment.
The best available evidence also points to more severe respiratory
consequences of exposure to dpm. Significant statistical associations
have been detected between acute environmental exposures to fine
particulates and debilitating respiratory impairments in adults, as
measured by lost work days, hospital admissions, and emergency room
visits (see Table III-3). Short-term exposures to fine particulates, or
to particulate air pollution in general, have been associated with
significant increases in the risk of hospitalization for both pneumonia
and COPD (EPA, 1996).
The risk of severe respiratory effects is exemplified by specific
cases of persistent asthma linked to diesel exposure (Wade and Newman,
1993). Glenn et al. (1983) summarized results of NIOSH health
evaluations among coal, salt, trona, and potash miners and reported
that ``all four of the chronic effects analyses revealed an excess of
cough and phlegm among the diesel exposed group.'' There is persuasive
evidence for a causal connection between dpm exposure and increased
manifestations of allergic asthma and other allergic respiratory
diseases, coming from recent experiments on animals and human cells
(Takenaka et al., 1995; Lovik et al., 1997; Takano et al., 1997;
Ichinose et al., 1997a). Based on controlled experiments on healthy
human volunteers, Diaz-Sanchez et al. (1994, 1996, 1997), Peterson and
Saxon (1996), and Salvi et al. (1999) reported significant increases in
various markers of allergic response resulting from exposure to dpm.
Peterson and Saxon (1996) reviewed the scientific literature on the
[[Page 5637]]
relationship between PAHs and other products of fossil fuel combustion
found in dpm and trends in allergic respiratory disease. They found
that the prevalences of allergic rhinitis (``hay fever'') and allergic
asthma have significantly increased with the historical increase in
fossil fuel combustion and that laboratory data support the hypothesis
that certain organic compounds found in dpm ``* * * are an important
factor in the long-term increases in the prevalence in allergic airway
disease.'' Similarly, much of the research on allergenic responses to
dpm was reviewed by Diaz-Sanchez (1997), who concluded that dpm
pollution in the ambient environment ``may play an important role in
the increased incidence of allergic airway disease.'' Morgan et al.
(1997) noted that dpm ``* * * may be partly responsible for some of the
exacerbations of asthma'' and that ``* * * it would be wise to err on
the side of caution.'' Such health outcomes are clearly ``material
impairments'' of health or functional capacity within the meaning of
the Act.
ii. Premature Death from Cardiovascular, Cardiopulmonary, or
Respiratory Causes
The evidence from air pollution studies identifies death, largely
from cardiovascular, cardiopulmonary, or respiratory causes, as an
endpoint significantly associated with acute exposures to fine
particulates (PM2.5-- see Table III-3). The weight of
epidemiologic evidence indicates that short-term ambient exposure to
particulate air pollution contributes to an increased risk of daily
mortality (EPA, 1996). Time-series analyses strongly suggest a positive
effect on daily mortality across the entire range of ambient
particulate pollution levels. Relative risk estimates for daily
mortality in relation to daily ambient particulate concentration are
consistently positive and statistically significant across a variety of
statistical modeling approaches and methods of adjustment for effects
of relevant covariates such as season, weather, and co-pollutants. The
mortality effects of acute exposures appear to be primarily
attributable to combustion-related particles in PM2.5 (such
as dpm) and are especially pronounced for death due to pneumonia, COPD,
and IHD (Schwartz et al., 1996). After thoroughly reviewing this body
of evidence, the U.S. Environmental Protection Agency (EPA) concluded:
It is extremely unlikely that study designs not yet employed,
covariates not yet identified, or statistical techniques not yet
developed could wholly negate the large and consistent body of
epidemiologic evidence * * *. [EPA, 1996]
There is also substantial evidence of a relationship between
chronic exposure to fine particulates (PM2.5) and an excess
(age-adjusted) risk of mortality, especially from cardiopulmonary
diseases. The Six Cities and ACS studies of ambient air particulates
both found a significant association between chronic exposure to fine
particles and excess mortality. In some of the areas studied,
PM2.5 is composed primarily of dpm; and significant
mortality and morbidity effects were also noted in those areas. In both
studies, after adjusting for smoking habits, a statistically
significant excess risk of cardiopulmonary mortality was found in the
city with the highest average concentration of PM2.5 as
compared to the city with the lowest. Both studies also found excess
deaths due to lung cancer in the cities with the higher average level
of PM2.5, but these results were not statistically
significant (EPA, 1996). The EPA concluded that--
* * * the chronic exposure studies, taken together, suggest
there may be increases in mortality in disease categories that are
consistent with long-term exposure to airborne particles and that at
least some fraction of these deaths reflect cumulative PM impacts
above and beyond those exerted by acute exposure events * * *. There
tends to be an increasing correlation of long-term mortality with PM
indicators as they become more reflective of fine particle levels.
[EPA, 1996]
Whether associated with acute or chronic exposures, the excess risk
of death that has been linked to pollution of the air with fine
particles like dpm is clearly a ``material impairment'' of health or
functional capacity within the meaning of the Act.
In a review, submitted by MARG, of MSHA's proposed risk assessment,
Dr. Jonathan Borak asserted that ``MSHA appears to regard all
particulates smaller than 2.5 g/m\3\ as equivalent.'' He
argued that ``dpm and other ultra-fine particulates represents only a
small proportion of ambient particulate samples,'' that ``chronic
cough, chronic phlegm, and chronic wheezing reflect mainly
tracheobronchial effects,'' and that tracheobronchial deposition is
highly dependent on particle size distribution.
No part of Dr. Borak's argument is directly relevant to MSHA's
identification of the risk of death from cardiovascular,
cardiopulmonary, or respiratory causes faced by miners exposed to high
concentrations of dpm. First, MSHA does not regard all fine
particulates as equivalent. However, dpm is a major constituent of
PM2.5 in many of the locations where increased mortality has
been linked to PM2.5 levels. MSHA regards dpm as presenting
a risk by virtue of its comprising a type of PM2.5. Second,
the studies MSHA used to support the existence of this risk
specifically implicate fine particles (i.e., PM2.5), so the
percentage of dpm in ``total suspended particulate emissions'' (which
includes particles even larger than PM10) is not relevant.
Third, the chronic respiratory symptoms listed by Dr. Borak are not
among the material impairments that MSHA has identified from the
PM2.5 studies. Much of the evidence pertaining to excess
mortality is based on acute--not chronic--ambient exposures of
relatively high intensity. In the preceding subsection of this risk
assessment, MSHA identified various respiratory symptoms, including
allergenic responses, but the evidence for these comes largely from
studies on diesel emissions.
As discussed in Section 2.a.iii of this risk assessment, many
miners smoke tobacco, and miners experience COPD at a significantly
higher rate than the general population. This places many miners in two
of the groups that EPA (1996) identified as being at greatest risk of
premature mortality due to particulate exposures.
iii. Lung Cancer
It is clear that lung cancer constitutes a ``material impairment''
of health or functional capacity within the meaning of the Act.
Therefore, the issue to be addressed in this section is whether there
is sufficient evidence (i.e., enough to warrant regulatory action) that
occupational exposure to dpm causes the risk of lung cancer to
increase.
In the proposed risk assessment, MSHA noted that various national
and international institutions and governmental agencies had already
classified diesel exhaust or particulate as a probable human
carcinogen. Considerable weight was also placed on two comprehensive
meta-analyses of the epidemiologic literature, which had both found
that the combined evidence supported a causal link. MSHA also
acknowledged, however, that some reviewers of the evidence disagreed
with MSHA's conclusion that, collectively, it strongly supports a
causal connection. As examples of the opposing viewpoint, MSHA cited
Stober and Abel (1996), Watson and Valberg (1996), Cox (1997), Morgan
et al. (1997), and Silverman (1998). As stated in the proposed risk
assessment, MSHA considered the opinions of these reviewers and agreed
that no individual study was perfect: Even the strongest of
[[Page 5638]]
the studies had limitations when viewed in isolation. MSHA nevertheless
concluded (in the proposal) that the best available epidemiologic
studies, supported by experimental data showing toxicity, collectively
provide strong evidence that chronic dpm exposure (at occupational
levels) actually does increase the risk of lung cancer in humans.
Although miners and labor representatives generally agreed with
MSHA's interpretation of the collective evidence, many commenters
representing the mining industry strongly objected to MSHA's
conclusion. Some of these commenters also expressed dissatisfaction
with MSHA's treatment, in the proposed risk assessment, of opposing
interpretations of the collective evidence--saying that MSHA had
dismissed these opposing views without sufficient explanation. Some
commenters also submitted new critiques of the existing evidence and of
the meta-analyses on which MSHA had relied. These commenters also
emphasized the importance of two reports (CASAC, 1998 and HEI, 1999)
that both became available after MSHA completed its proposed risk
assessment.
MSHA has re-evaluated the scientific evidence relating lung cancer
to diesel emissions in light of the comments, suggestions, and detailed
critiques submitted during these proceedings. Although MSHA has not
changed its conclusion that occupational dpm exposure increases the
risk of lung cancer, MSHA believes that the public comments were
extremely helpful in identifying areas of MSHA's discussion of lung
cancer needing clarification, amplification, and/or additional
supportive evidence.
Accordingly MSHA has re-organized this section of the risk
assessment into five subsections. The first of these provides MSHA's
summary of the collective epidemiologic evidence. Second is a
description of results and conclusions from the only two existing peer-
reviewed and published statistical meta-analyses of the epidemiologic
studies: Bhatia et al. (1998) and Lipsett and Campleman (1999). The
third subsection contains a discussion of potential systematic biases
that might tend to shift all study results in the same direction. The
fourth evaluates the overall weight of evidence for causality,
considering not only the collective epidemiologic evidence but also the
results of toxicity experiments. Within each of these first four
subsections, MSHA will respond to the relevant issues and criticisms
raised by commenters in these proceedings, as well as by other outside
reviewers. The final subsection will describe general conclusions
reached by other reviewers of this evidence, and present some responses
by MSHA about opposing interpretations of the collective evidence.
(1) Summary of Collective Epidemiologic Evidence
As mentioned in Section III.2.c.i(2)(a) and listed in Tables III-4
and III-5, MSHA reviewed a total of 47 epidemiologic studies involving
lung cancer and diesel exposure. Some degree of association between
occupational dpm exposure and an excess rate of lung cancer was
reported in 41 of these studies: 22 of the 27 cohort studies and 19 of
the 20 case-control studies. Section III.2.c.1(2)(a) explains MSHA's
criteria for evaluating these studies, summarizes those on which MSHA
places greatest weight, and explains why MSHA places little weight on
the six studies reporting no increased risk of lung cancer for exposed
workers. It also contains summaries of the studies involving miners,
addresses criticisms of individual studies by commenters and reviewers,
and discusses studies that, according to some commenters, suggest that
dpm exposure does not increase the risk of lung cancer.
Here, as in the earlier, proposed version of the risk assessment,
MSHA was careful to note and consider limitations of the individual
studies. Several commenters interpreted this as demonstrating a
corresponding weakness in the overall body of epidemiologic evidence.
For example, one commenter [Energy West] observed that ``* * * by its
own admission in the preamble * * * most of the evidence in [the
epidemiologic] studies is relatively weak'' and argued that MSHA's
conclusion was, therefore, unjustified.
It should first be noted that the three most recent epidemiologic
studies became available too late for inclusion in the risk assessment
as originally written. These three (Johnston et al., 1997; Saverin et
al., 1999; Bruske-Hohlfeld, 1999) rank among the strongest eight
studies available (see Section III.2.c.1(2)(a)) and do not have the
same limitations identified in many of the other studies. Even so, MSHA
recognizes that no single one of the existing epidemiologic studies,
viewed in isolation, provides conclusive evidence of a causal
connection between dpm exposure and an elevated risk of lung cancer in
humans. Consistency and coherency of results, however, do provide such
evidence. An appropriate analogy for the collective epidemiologic
evidence is a braided steel cable, which is far stronger than any of
the individual strands of wire making it up. Even the thinnest strands
can contribute to the strength of the cable.
(a) Consistency of Epidemiologic Results
Although no epidemiologic study is flawless, studies of both cohort
and case-control design have quite consistently shown that chronic
exposure to diesel exhaust, in a variety of occupational circumstances,
is associated with an increased risk of lung cancer. Furthermore, as
explained earlier in this risk assessment, limitations such as small
sample size, short latency, and (usually) exposure misclassification
reduce the power of a study. These limitations make it more difficult
to detect a relationship even when one exists. Therefore, the sheer
number of studies showing a positive association readily distinguishes
those studies criticized by Taubes (1995), where weak evidence is
available from only a single study. With only rare exceptions,
involving too few workers and/or observation periods too short to have
a good chance of detecting excess cancer risk, the human studies have
shown a greater risk of lung cancer among exposed workers than among
comparable unexposed workers.
Moreover, the fact that 41 out of 47 studies showed an excess risk
of lung cancer for exposed workers may itself be a significant result,
even if the evidence in most of those 41 studies is relatively weak.
Getting ``heads'' on a single flip of a coin, or two ``heads'' out of
three flips, does not provide strong evidence that there is anything
special about the coin. However, getting 41 ``heads'' in 47 flips would
normally lead one to suspect that the coin was weighted in favor of
heads. Similarly, results reported in the epidemiologic literature lead
one to suspect that the underlying relationship between diesel exposure
and an increased risk of lung cancer is indeed positive.
More formally, as MSHA pointed out in the earlier version of this
risk assessment, the high proportion of positive studies is
statistically significant according to the 2-tailed sign test. Under
the ``null hypothesis'' that there is no systematic bias in one
direction or the other, and assuming that the studies are independent,
the probability of 41 or more out of 47 studies being either positive
or negative is less than one per ten million. Therefore, the sign test
rejects, at a very high confidence level, the null hypothesis that each
study is equally likely to be positive or negative. This
[[Page 5639]]
means that the collective results, showing increased risk for exposed
workers, are statistically significant at a very high confidence
level--regardless of the statistical significance of any individual
study.
MSHA received no comments directly disputing its attribution of
statistical significance to the collective epidemiologic evidence based
the sign test. However, several commenters objected to the concept that
a number of inconclusive studies can, when viewed collectively, provide
stronger evidence than the studies considered in isolation. For
example, the Engine Manufacturers Association (EMA) asserted that--
[j]ust because a number of studies reach the same conclusion does
not make the collective sum of those studies stronger or more
conclusive, particularly where the associations are admittedly weak
and scientific difficulties exist in each. [EMA]
Similarly, IMC Global stated that--
* * * IMC Global does not consider cancer studies with a relative
risk of less than 2.0 as showing evidence of a casual relationship
between Dpm exposure and lung cancer.* * * Thus while MSHA states
[in the proposed risk assessment; now updated to 41 out of 47] that
38 of 43 epidemiologic studies show some degree of association
between occupational Dpm exposures and lung cancer and considers
that fact significant, IMC Global does not. [IMC Global]
Although MSHA agrees that even statistically significant
consistency of epidemiologic results is not sufficient to establish
causality, MSHA believes that consistency is an important part of
establishing that a suspected association is causal.\67\ Many of the
commenters objecting to MSHA's emphasis on the collective evidence
failed to distinguish the strength of evidence in each individual study
from the strength of evidence in total.
---------------------------------------------------------------------------
\67\ With respect to IMC Global's blanket rejection of studies
showing a relative risk less than 2.0, please see also the related
discussions in Subsection 2.c.i(2)(a) above, under the heading of
``Potential Confounders,'' and in Subsection 3.a.iii(3) below,
entitled ``Potential Systematic Biases.''
---------------------------------------------------------------------------
Furthermore, weak evidence (from just one study) should not be
confused with a weak effect. As Dr. James Weeks pointed out at the
public hearing on Nov. 19, 1998, a 40-percent increase in lung cancer
is a strong effect, even if it may be difficult to detect in an
epidemiologic study.
Explicable differences, or heterogeneity, in the magnitudes of
relative risk reported from different studies should not be confused
with inconsistency of evidence. For example, as described by Silverman
(1998), one of the available meta-analyses (Bhatia et al., 1998)
``examined the primary sources of heterogeneity among studies and found
that a main source of heterogeneity is the variation in diesel exhaust
exposure across different occupational groups.'' Figures III-9 and III-
10, taken from Cohen and Higgins (1995), respectively show relative
risks reported for the two occupations on which the most studies are
available: railroad workers and truck drivers.
Each of these two charts compares results from studies that
adjusted for smoking to results from studies that did not make such an
adjustment. For each study, the point plotted is the estimated relative
risk or odds ratio, and the horizontal line surrounding it represents a
95-percent confidence interval. If the left endpoint of a confidence
interval exceeds 1.0, then the corresponding result is statistically
significant at a 95-percent confidence level.
The two charts show that the risk of lung cancer has consistently
been elevated for exposed workers and that the results are not
significantly different within each occupational category. Differences
in the magnitude and statistical significance of results within
occupation are not surprising, since the groups studied differed in
size, average exposure intensity and duration, and the time allotted
for latent effects.
BILLING CODE 4510-43-C
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[GRAPHIC] [TIFF OMITTED] TR19JA01.036
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[GRAPHIC] [TIFF OMITTED] TR19JA01.037
BILLING CODE 4510-43-C
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As documented in Subsection 2.c.i(2)(a) of risk assessment, all of
the studies showing negative associations were either based on
relatively short observation or follow-up periods, lacked good
information about dpm exposure, involved low duration or intensity of
dpm exposure, or, because of inadequate sample size or latency
allowance, lacked the power to detect effects of the magnitude found in
the ``positive'' studies. Boffetta et al. (1988, p. 404) noted that, in
addition, studies failing to show a statistically significant
association--
* * * often had low power to detect any association, had
insufficient latency periods, or compared incidence or mortality
rates among workers to national rates only, resulting in possible
biases caused by the ``healthy worker effect.''
Some commenters noted that limitations such as insufficient
duration of exposure, inadequate latency allowance, small worker
populations, exposure misclassification, and comparison to external
populations with no adjustment for a healthy worker effect may explain
why not all of the studies showed a statistically significant
association between dpm exposure and an increased prevalence of lung
cancer. According to these commenters, if an epidemiologic study shows
a statistically significant result, this often occurs in spite of
methodological weaknesses rather than because of them. MSHA agrees that
limitations such as those listed make it more difficult to obtain a
statistically significant result when a real relationship exists.
(b) Best Available Epidemiologic Evidence
As explained above, it is statistically significant that 41 of the
47 available epidemiologic studies reported an elevated risk of lung
cancer for workers exposed to dpm. MSHA finds it even more informative,
however, to examine the collective results of the eight studies
identified in Section III.2.c.i(2)(a) as providing the best currently
available epidemiologic evidence. These studies, selected using the
criteria described earlier, are: Boffetta et al. (1988), Boffetta et
al. (1990), Bruske-Hohlfeld et al. (1999), Garshick et al. (1987),
Garshick et al. (1988,1991), Johnston et al. (1997), Steenland et al.
(1990,1992,1998), and Saverin et al. (1999). All eight of these studies
reported an increased risk of lung cancer for workers with the longest
diesel exposures and for those most likely to have been exposed,
compared to unexposed workers. Tables showing the results from each of
these studies are provided in Section III.2.c.1(2)(a).
The sign test of statistical significance can also be applied to
the collective results of these eight studies. If there were no
underlying association between exposure to diesel exhaust and an
increased risk of lung cancer, or anything else systematically favoring
a positive result, then there should be equal probabilities (equal to
one-half) that any one of these eight studies would turn out positive
or negative. Therefore, under the null hypothesis that positive and
negative results are equally likely, the probability that all eight
studies would show either a positive or a negative association is (0.5)
\8\ = 0.0039, or 0.39 percent. This shows that the collective results
of the eight studies comprising the best available epidemiologic
evidence are statistically significant at a confidence level exceeding
99 percent (i.e., 100-2 x 0.39).
When the risk of disease or death increases in response to higher
cumulative exposures, this is described by a ``positive'' exposure-
response relationship. Like consistency of results, the existence of a
positive exposure-response relationship is important in establishing
that the exposures in question actually cause an increase in risk.
Among the eight studies MSHA has identified as comprising the best
available epidemiologic evidence, there are five that provide evidence
of increasing lung cancer risk with increasing cumulative exposure:
Boffetta, et al. (1990), Bruske-Hohlfeld et al. (1999), Johnston et al.
(1997), Saverin et al. (1999), and Steenland et al. (1990, 1992, 1998).
The results supporting such a relationship are provided in the table
accompanying discussion of each of these studies in Section
III.2.c.i(2)(a).
Although some have interpreted the results from the two studies by
Garshick et al. as also providing evidence of a positive exposure-
response relationship (e.g., Cal-EPA, 1998), this interpretation is
highly sensitive to the statistical models and techniques used to
analyze the data (HEI, 1999; Crump 1999). Therefore, for purposes of
this risk assessment, MSHA is not relying on Garshick et al. (1987) or
Garshick et. al (1988, 1991) to demonstrate the existence of a positive
exposure-response relationship. MSHA used the study for purposes of
hazard identification only. The Garshick studies contributed to the
weight of evidence favoring a causal interpretation, since they show
statistically significant excesses in lung cancer risk for the exposed
workers.
The relative importance of the five studies identified in
demonstrating the existence of a positive exposure-response
relationship varies with the quality of exposure assessment. Boffetta
et al. (1990) and Bruske-Hohlfeld et al. (1999) were able to show such
a relationship based on the estimated duration of occupational exposure
for exposed workers, but quantitative measures of exposure intensity
(i.e., dpm concentration) were unavailable. Although duration of
exposure is frequently used as a surrogate of cumulative exposure, it
is clearly preferable, as many commenters pointed out, to base
estimates of cumulative exposure and exposure-response analyses on
quantitative measurements of exposure levels combined with detailed
work histories. Positive exposure-response relationships based on such
data were reported in all three studies: Johnston et al. (1997),
Steenland et al. (1998), and Saverin et al. (1999).
(c) Studies With Quantitative or Semiquantitative Exposure Assessments
Several commenters stressed the fact that most of the available
epidemiologic studies contained little or no quantitative information
on diesel exposures and that those studies containing such information
(such as Steenland et al., 1998) generated it using questionable
assumptions. Some commenters also faulted MSHA for insufficiently
addressing this issue. For example, one commenter stated:
* * * the Agency fails to highlight the lack of acceptable (or
any) exposure measurements concurrent with the 43 epidemiology
studies cited in the Proposed Rule.* * * the lack of concurrent
exposure data is a significant deficiency of the epidemiology
studies at issue and is a major factor that prevents application of
those epidemiology results to risk assessment. [EMA]
MSHA agrees that the nature and quality of exposure information
should be an important consideration in evaluating the strength of
epidemiologic evidence. That is why MSHA included exposure assessment
as one of the criteria used to evaluate and rank studies in Section
2.c.1(2)(a) of this risk assessment. Two of the most recent studies,
both conducted specifically on miners, utilize concurrent, quantitative
exposure data and are included among the eight in MSHA's selection of
best available epidemiologic evidence (Johnston et al., 1997 and
Saverin et al., 1999). As a practical matter, however, epidemiologic
studies rarely have concurrent exposure measurements; and, therefore,
the commenter's line of
[[Page 5643]]
reasoning would exclude nearly all of the available studies from this
risk assessment--including all six of the negative studies. Since
Section 101(a)(6) of the Mine Act requires MSHA to consider the ``best
available evidence'' (emphasis added), MSHA has not excluded studies
with less-than-ideal exposure assessments, but, instead, has taken the
quality of exposure assessment into account when evaluating them. This
approach is also consistent with the recognition by the HEI Expert
Panel on Diesel Emissions and Lung Cancer that ``regulatory decisions
need to be made in spite of the limitations and uncertainties of the
few studies with quantitative data currently available'' (HEI, 1999; p.
39).
The degree of quantification, however, is not the only relevant
consideration in evaluating studies with respect to exposure
assessment. MSHA also considered the likely effects of potential
exposure misclassification. As expressed by another commenter:
* * * [S]tudies that * * * have poor measures of exposure to
diesel exhaust have problems in classification and will have weaker
results. In the absence of information that misclassification is
systematic or differential, in which case study results would be
biased towards either positive or no-effect level, it is reasonable
to assume that misclassification is random or nondifferentiated. If
so,* * * study results are biased towards a risk ratio of 1.0, a
ratio showing no association between diesel exhaust exposure and the
occurrence of lung cancer. [Dr. James Weeks, representing UMWA]
In her review of Bhatia et al. (1998), Silverman (1998) proposed
that ``[o]ne approach to assess the impact of misclassification would
be to exclude studies without quantitative or semiquantitative exposure
data.'' According to Dr. Silverman, this would leave only four studies
among those considered by Dr. Bhatia: Garshick et al. (1988),
Gustavsson et al. (1990), Steenland et al. (1992), and Emmelin et al.
(1993).\68\ All four of these studies showed higher rates of lung
cancer for the workers estimated to have received the greatest
cumulative exposure, as compared to workers who had accumulated little
or no diesel exposure. Statistically significant results were reported
in three of these four studies. Furthermore, the two more recent
studies utilizing fully quantitative exposure assessments (Johnston et
al., 1997; Saverin et al., 1999) were not evaluated or otherwise
considered in the articles by Drs. Bhatia and Silverman. Like the other
four studies, these too reported elevated rates of lung cancer for
workers with the highest cumulative exposures. Specific results from
all six of these studies are presented in Tables III-4 and III-5.
---------------------------------------------------------------------------
\68\ Emmelin et al. (1993) was considered but excluded from the
meta-analysis by Bhatia et al. (1998) for reasons explained by the
authors.
---------------------------------------------------------------------------
Once again, the sign test of statistical significance can be
applied to the collective results of the four studies identified by Dr.
Silverman plus the two more recent studies with quantitative exposure
assessments. As before, under the null hypothesis of no underlying
effect, the probability would equal one-half that any one of these six
studies would turn out positive or negative. The probability that all
six studies would show either a positive or a negative association
would, under the null hypothesis, be (0.5) \6\ = 0.0156, or 1.56
percent. This shows that the collective results of these six studies,
showing an elevated risk of lung cancer for workers estimated to have
the greatest cumulative exposure, are statistically significant at a
confidence level exceeding 96 percent (i.e., 100-2 x 1.56).
As explained in the previous subsection, three studies showing
evidence of increased risk with increasing exposure based on
quantitative or semi-quantitative exposure assessments are included in
MSHA's selection of best available epidemiologic evidence: Johnston et
al. (1997), Steenland et al. (1998), and Saverin et al. (1999). Not
only do these studies provide consistent evidence of elevated lung
cancer risk for exposed workers, they also each provide evidence of a
positive exposure-response relationship--thereby significantly
strengthening the case for causality.
(d) Studies Involving Miners
Eleven studies involving miners are summarized and discussed in
Section 2.c.i(2)(a) of this risk assessment. Commenters' observations
and criticisms pertaining to the individual studies in this group are
also addressed in that section. Three of these studies are among the
eight in MSHA's selection of best available epidemiologic evidence:
(Boffetta et al., 1988; Johnston et al., 1997; Saverin et al., 1999).
All three of these studies provide evidence of an increased risk of
lung cancer for exposed miners. Although MSHA places less weight on the
remaining eight studies, seven of them show some evidence of an excess
lung cancer risk among the miners involved. The remaining study
(Christie et al., 1995) reported a greater all-cause SMR for the coal
miners involved than for a comparable population of petroleum workers
but did not compare the miners to a comparable group of workers with
respect to lung cancer.
The NMA submitted a review of six of these studies by Dr. Peter
Valberg, who concluded that ``[t]hese articles do not implicate diesel
exhaust, per se, as strongly associated with lung cancer in miners * *
* The reviewed studies do not form a consistent and cohesive picture
implicating diesel exhaust as a major risk factor for miners.''
Similarly, Dr. Jonathan Borak reviewed six of the studies on behalf of
MARG and concluded:
[T]he strongest conclusion that can be drawn from these six
studies is that the miners in those studies had an increased risk of
lung cancer. These studies cannot relate such increased [risk] to
any particular industrial exposure, lifestyle or combination of such
factors.
Apparently, neither Dr. Valberg nor Dr. Borak disputed MSHA's
observation that the miners involved in the studies they reviewed
exhibited, overall, an excess risk of lung cancer. It is possible that
any excess risk found in epidemiologic studies may be due to extraneous
unknown or uncontrolled risk factors (i.e., confounding variables).
However, neither Drs. Valberg or Borak, nor the NMA or MARG, offered
evidence, beyond a catalog of speculative possibilities, that the
excess lung cancer risk for these miners was due to anything other than
dpm exposure.
Nevertheless, MSHA agrees that the studies reviewed by Drs. Valberg
and Borak do not, by themselves, conclusively implicate dpm exposure as
the causal agent. Miners are frequently exposed to other occupational
hazards associated with lung cancer, such as radon progeny, and it is
not always possible to distinguish effects due to dpm exposure from
effects due to these other occupational hazards. This is part of the
reason why MSHA did not restrict its consideration of evidence to
epidemiologic studies involving miners. What implicates exposure to
diesel exhaust is the fact that diesel-exposed workers in a variety of
different occupations, under a variety of different working conditions
(including different types of mines), and in a variety of different
geographical areas consistently exhibit an increased risk of lung
cancer.
Drs. Valberg and Borak did not review the two studies that utilize
quantitative dpm exposure assessments: Johnston et al. (1997) and
Saverin et al. (1999). In recently received comments Dr. Valberg,
writing for the NMA brought up four issues on the Saverin et al. 1999.
These issues were potential exposure misclassification, potential flaws
in the sampling method, potential smoker
[[Page 5644]]
misclassification, and insufficient latency. Two of these issues have
already been extensively discussed in section 2.c.i.2.a.ii and
therefore will not be repeated here. Dr. Valberg suggested that the
potential flaw in the sampling method would tend to over-estimate
exposure and that there was insufficient latency. If, in fact, both of
these issues are relevant, they would act to UNDERESTIMATE the lung
cancer risk in this cohort instead of OVERESTIMATE it. MSHA regards
these, along with Boffetta et al. (1988), Burns and Swanson (1991),\69\
and Lerchen et al. (1987) to be the most informative of the available
studies involving miners. Results on miners from these five studies are
briefly summarized in the following table, with additional details
provided in Section 2.c.1(2)(a) and Tables III-4 and III-5 of this risk
assessment. The cumulative exposures at which relative risks from the
Johnston and Saverin studies are presented are equivalent, assuming
that TC constitutes 80 percent of total dpm. The cumulative dpm
exposure of 6.1 mg-yr/m3 is the multiplicative product of
exposure duration and dpm concentration for the most highly exposed
workers in each of these two studies.
\69\ Listed in Table III-5 under Swanson et al., 1993.
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BILLING CODE 4510-43-P
[GRAPHIC] [TIFF OMITTED] TR19JA01.038
Although MSHA places less weight on the studies by Burns and
Swanson and by Lerchen than on the other three, it is significant that
the five best available studies involving miners all support an
increased risk of lung cancer attributable to dpm exposure.
(2) Meta-Analyses
MSHA recognizes that simply tabulating epidemiologic studies as
positive or negative can sometimes be misleading. There are generally a
variety of outcomes that could render a study positive or negative,
some studies contain different analyses of related data sets, some
studies involve multiple
[[Page 5645]]
comparisons of various subgroups, and the studies differ widely in the
reliability of their results. Therefore, MSHA is not limiting its
assessment of the epidemiologic evidence to such a tabulation or
relying only on the sign test described above. MSHA has also considered
the results of two statistical meta-analyses covering most of the
available studies (Lipsett and Campleman, 1999; Bhatia et al., 1998).
These meta-analyses weighted and pooled independent results from those
studies meeting certain inclusion requirements to form overall
estimates of relative risk for exposed workers based on the combined
body of data. In addition to forming pooled estimates of the effect of
diesel exposure, both meta-analyses analyzed sources of heterogeneity
in the individual results and investigated but rejected publication
bias as an explanation for the generally positive results reported.
Both meta-analyses derived a statistically significant increase of 30
to 40 percent in the risk of lung cancer, attributable to occupational
dpm exposure.
Lipsett and Campleman (1999) systematically analyzed and combined
results from most of the studies summarized in Tables III-4 and III-5.
Forty-seven studies published between 1957 and 1995 were identified for
initial consideration. Some studies were excluded from the pooled
analysis because they did not allow for a period of at least 10 years
for the development of clinically detectable lung cancer. Others were
excluded because of bias resulting from incomplete ascertainment of
lung cancer cases in cohort studies or because they examined the same
cohort population as another study. One study was excluded because
standard errors could not be calculated from the data presented. The
remaining 30 studies, contributing a total of 39 separate estimates of
exposure effect (for distinct occupational groups within studies), were
analyzed using a random-effects analysis of variance (ANOVA) model.
Potential effects of publication bias (i.e., the likelihood that
papers with positive results may be more likely to be published than
those with negative results) were investigated by plotting the
logarithm of relative risk estimated from each study against its
estimated precision, as expressed by the inverse of its standard error.
According to the authors, the resulting ``funnel plot'' was generally
consistent with the absence of significant publication bias, although
there were relatively few small-scale, statistically insignificant
studies. The investigators performed a further check of potential
publication bias by comparing results of the included studies with the
only relevant unpublished report that became available to them during
the course of their analysis. Smoking-adjusted relative risks for
several diesel-exposed occupations in the unpublished study were,
according to the investigators, consistent with those found in the
studies included in the meta-analysis.
Each of the 39 separate estimates of exposure effect was weighted
by a factor proportional to its estimated precision. Sources of
heterogeneity in results were investigated by subset analysis--using
categorical variables to characterize each study's design, target
population (general or industry-specific), occupational group, source
of control or reference population, latency, duration of exposure,
method of ascertaining occupation, location (North America or Europe),
covariate adjustments (age, smoking, and/or asbestos exposure), and
absence or presence of a clear healthy worker effect (as manifested by
lower than expected all-cause mortality in the occupational population
under study).
Sensitivity analyses were conducted to evaluate the sensitivity of
results to inclusion criteria and to various assumptions used in the
analysis. This included (1) substitution of excluded ``redundant''
studies of the same cohort population for the included studies and (2)
exclusion of studies involving questionable exposure to dpm. An
influence analysis was also conducted to examine the effect of dropping
one study at a time, to determine if any individual study had a
disproportionate effect on results of the ANOVA.
The pooled relative risk from all 39 exposure effects (estimated
from 30 studies) was RR = 1.33, with a 95-percent confidence interval
(CI) extending from 1.21 to 1.46. For the subgroup of 13 smoking-
adjusted exposure effects (nine studies) from populations ``most likely
to have had substantial exposure'' to dpm, the pooled effect was RR =
1.47, with a CI from 1.29 to 1.67. Based on the all of the various
analyses they conducted, the authors concluded:
Although substantial heterogeneity existed in the initial pooled
analysis, stratification on several factors substantially reduced
heterogeneity, producing subsets of studies with increased relative
risk estimates that persisted through various influence and
sensitivity analyses. * * *
In studies that adjusted for confounding by cigarette smoking,
not only did the positive association between diesel exhaust
exposure and lung cancer persist but the pooled risk estimate showed
a modest increase, with little evidence of heterogeneity.
* * * [T]his meta-analysis provides quantitative evidence
consistent with several prior reviews, which have concluded that the
epidemiologic evidence supports a causal relationship between
occupational exposure to diesel exhaust and lung cancer. [Lipsett
and Campleman, 1999]
The other meta-analysis was conducted by Bhatia et al. (1998) on
epidemiologic studies published in peer-reviewed journals between 1957
and 1993. In this analysis, studies were excluded if actual work with
diesel equipment ``could not be confirmed or reliably inferred'' or if
an inadequate latency period was allowed for cancer to develop, as
indicated by less than 10 years from time of first exposure to end of
follow-up. Studies of miners were also excluded, because of potential
exposure to radon and silica. Likewise, studies were excluded if they
exhibited selection bias or examined the same cohort population as a
study published later. A total of 29 independent results on exposure
effects from 23 published studies were identified as meeting the
inclusion criteria.
To address potential publication bias, the investigators identified
several unpublished studies on truck drivers and noted that elevated
risks for exposed workers observed in these studies were similar to
those in the published studies utilized. Based on this and a ``funnel
plot'' for the included studies, the authors concluded that there was
no indication of publication bias.
After assigning each of the 29 separate estimates of exposure
effect a weight proportional to its estimated precision, Bhatia et al.
(1998) used a fixed-effects ANOVA model to calculate pooled relative
risks based on the following groupings: all 29 results; all case-
control studies; all cohort studies; cohort studies using internal
reference populations; cohort studies making external comparisons;
studies adjusted for smoking; studies not adjusted for smoking; and
studies grouped by occupation (railroad workers, equipment operators,
truck drivers, and bus workers). Elevated risks of lung cancer were
shown for exposed workers overall and within every individual group of
studies analyzed. A positive duration-response relationship was
observed in those studies presenting results according to employment
duration. The weighted, pooled estimates of relative risk were
identical for case-control and cohort studies and nearly identical for
studies with or without smoking adjustments.
The pooled relative risk from all 29 exposure effects (estimated
from 23 studies) was RR = 1.33, with a 95-percent confidence interval
(CI), adjusted for heterogeneity, extending
[[Page 5646]]
from 1.24 to 1.44. For just the smoking-adjusted studies, it was 1.35
(CI: 1.20 to 1.52); and for cohort studies making internal comparisons,
it was 1.43 (CI: 1.29 to 1.58). Based on their evaluation of the all
the analyses on various subgroups, Bhatia et al. (1998) concluded that
the elevated risk of lung cancer observed among exposed workers was
unlikely to be due to chance, that confounding from smoking was
unlikely to explain all of the excess risk, and that ``this meta-
analysis supports a causal association between increased risks for lung
cancer and exposure to diesel exhaust.''
The pooled relative risks estimated in both meta-analyses equal
1.33 and exceed 1.4 for studies making internal comparisons, or
comparisons to similar groups of workers. Both meta-analyses found
these results to be statistically significant, meaning that they cannot
be explained merely by random or unexplained variability in the risk of
lung cancer that occurs among both exposed and unexposed workers.
Although both meta-analyses relied, by necessity, on an overlapping
selection of studies, the inclusion criteria were different and some
studies included in one meta-analysis were excluded from the other.
They used different statistical models for deriving a pooled estimate
of relative risk, as well as different means of analyzing heterogeneity
of effects. Nevertheless, they derived the same estimate of the overall
exposure effect and found similar sources of heterogeneity in the
results from individual studies.\70\ One commenter observed that--
---------------------------------------------------------------------------
\70\ Several commenters suggested that because the two meta-
analyses both received direct or indirect funding from the same
governmental agency, they were not independently conducted. These
commenters speculated that Dr. Allan Smith, a co-author of Cal-EPA
(1998) and Bhatia et al. (1998), contributed to both meta-analyses.
Although an earlier version of Lipsett and Campleman (1999) appeared
as an appendix to Cal-EPA (1998), commenters provided no evidence
that Dr. Smith contributed anything to that appendix. Dr. Smith is
not listed as a co-author of Lipsett and Campleman (1999).
Lung cancer relative risks for occupational ``control groups''
vary over a range from 0.4 to 2.7 * * *. Therefore, the level of
relative risks being reported in the Dpm epidemiology fall within
---------------------------------------------------------------------------
this level of natural variation. [IMC Global]
This argument is refuted by the statistical significance of the
elevation in risk detected in both meta-analyses in combination with
the analyses accounting for heterogeneity of exposure effects.
The EMA objected that MSHA's focus on these two meta-analyses
``presents an incomplete picture because the counter-arguments of
Silverman (1998) were not discussed in the same detail.'' IMC global
also faulted MSHA for dismissing Dr. Silverman's views without adequate
explanation.
In her review,\71\ Dr. Silverman characterized Bhatia et al. (1998)
as a ``careful meta-analysis'' and acknowledged that it ``add[s] to the
credibility that diesel exhaust is carcinogenic * * *.'' She also
explicitly endorsed several of its most important conclusions. For
example, Dr. Silverman stated that ``[t]he authors convincingly show
that potential confounding by cigarette smoking is likely to have
little impact on the estimated RRs for diesel exhaust and lung
cancer.'' She suggested, however, that Bhatia et al. (1998)
``ultimately do not resolve the question of causality.'' (Silverman,
1998)
---------------------------------------------------------------------------
\71\ Silverman (1998) reviewed Bhatia et al. (1998) but not
Lipsett and Campleman (1999) or the earlier version of that meta-
analysis (Lipsett and Alexeeff, 1998) cited in MSHA's proposed
preamble.
---------------------------------------------------------------------------
Dr. Silverman imposed an extremely high standard for what is needed
to ultimately resolve the question of causality. The precise question
she posed, along with her answer, was as follows:
Has science proven causality beyond any reasonable doubt?
Probably not. [Silverman, 1998, emphasis added.]
Neither the Mine Act nor applicable case law requires MSHA to prove
causality ``beyond any reasonable doubt.'' The burden of proof that Dr.
Silverman would require to close the case and terminate research is not
the same burden of proof that the Mine Act requires to warrant
protection of miners subjected to far higher levels of a probable
carcinogen than any other occupational group. In this risk assessment,
MSHA is evaluating the collective weight of the best available
evidence--not seeking proof ``beyond any reasonable doubt.'' \72\
---------------------------------------------------------------------------
\72\ It is noteworthy that, in describing research underway that
might resolve the issue of causality, Dr. Silverman stressed the
need for studies with quantitative exposure measurements and stated
that ``underground miners may, in fact, be the most attractive group
for study because their exposure to diesel exhaust is at least five
times greater than that of previously studied occupational groups.''
(Silverman, 1998) She then mentioned a study on underground miners
in Germany that had recently been initiated. The study of German
underground potash miners (Saverin et al., 1999), published after
Dr. Silverman's article, utilizes quantitative exposure measurements
and is included in MSHA's selection of best available epidemiologic
evidence (see Section 3.a.iii(1)(a) of this risk assessment). MSHA
also includes in that selection another underground miner study
utilizing quantitative exposure measurements (Johnston et al.,
1997). The 1997 study was available prior to Dr. Silverman's article
but is not listed among her references.
---------------------------------------------------------------------------
The EMA objected to MSHA's reliance on the two meta-analyses
because of ``* * * serious deficiencies in each'' but did not, in
MSHA's opinion, identify any such deficiencies. The EMA pointed out
that ``most of the original studies in each were the same, and the few
that were not common to each were not of significance to the outcome of
either meta-analysis.'' MSHA does not regard this as a deficiency.
Since the object of both meta-analyses was to analyze the available
epidemiologic evidence linking dpm exposure with lung cancer, using
defensible inclusion criteria, it is quite understandable that they
would rely on overlapping information. The principal differences were
in the types and methods of statistical analysis used, rather than in
the data subjected to analysis; and MSHA considers it informative that
different approaches yielded very similar results and conclusions. It
is noteworthy, moreover, that both of the meta-analyses explicitly
addressed the EMA's concern by performing analyses on various different
sub-groupings of the available studies. The sensitivity of results to
the inclusion criteria was also explicitly investigated and considered.
MSHA believes that the conclusions of these meta-analyses did not
depend on unreasonable inclusion or exclusion criteria.
The EMA also argued that--
[a] meta-analysis cannot compensate for basic deficiencies in
the studies used to create the meta-analysis, and this fact is not
clearly stated by MSHA. Instead, MSHA follows the tack of the meta-
analysis authors, who claim that the meta-analysis somehow overcomes
deficiencies of the individual studies selected and presents a
stronger case. This is simply not true. [EMA]
MSHA agrees that a meta-analysis cannot correct for all
deficiencies that may be present in individual studies. It can,
however, correct for certain types of deficiencies. For example,
individual studies may lack statistical power because of small study
populations. By pooling results from several such studies, a meta-
analysis may achieve a level of statistical significance not attainable
by the individual studies. Furthermore, both of the meta-analyses used
well-defined inclusion criteria to screen out those studies with the
most severe deficiencies. In addition, they both found that it was the
more rigorous and technically more valid studies that reported the
strongest associations between excess lung cancer and dpm exposure.
They also performed separate analyses that ruled out inflationary
effects of such ``deficiencies'' as lack of a smoking adjustment. For
example,
[[Page 5647]]
Lipsett and Campleman (1999) reported a pooled RR = 1.43 for 20
smoking-adjusted results, as compared to a pooled RR = 1.25 for 19
results with no smoking adjustment.
IMC Global and MARG submitted five specific criticisms of the meta-
analyses, to which MSHA will respond in turn.
(1) publication bias
* * * both studies * * * rely only on published studies. * * *
the authors rely on statistical analysis in an attempt to uncover
possible publication bias.* * * the only safeguard to protect
against possible publication bias is to seek out unpublished results
* * *. [IMC Global]
Both meta-analyses compared the results of published and
unpublished studies and found them to be similar. Bhatia et al. (1998)
found several unpublished studies of lung cancer among truck drivers
that ``* * * were not included in our analysis; however the risk ratios
of these studies are similar to the [sic] those in published studies
among truck drivers.'' (Bhatia et al., p. 90) Lipsett and Campleman
(1999) checked ``[s]moking-adjusted relative risks for several diesel-
exposed occupations'' in an unpublished report on U.S. veterans and
found them ``* * * consistent with those reported here.'' They remarked
that ``although publication bias cannot be completely ruled out, it is
an unlikely explanation for our findings.'' (Lipsett and Campleman, p.
1015) In addition to comparing results directly against unpublished
studies, both meta-analyses used the statistical method of ``funnel
plots'' as an indirect means of checking for the existence of
significant publication bias. It should also be noted that MSHA did not
exclude unpublished studies from this risk assessment.
(2) Selection Bias
* * * [the] meta-analyses have to provide a much more convincing
rationale as to why all miners were excluded even when the
confounders that are mentioned are not likely or important, for
example in studies conducted in potash and salt mines. * * * IMC
Global sees no reason why the older studies of potash workers
[Waxweiler et al., 1973] and more recent studies on New South Wales
coal miners [Christie et al., 1995] should not be included * * *.
[IMC Global]
Studies were selectively included or excluded, without good or
sufficient explanation. [MARG]
Contrary to the commenters' characterization, both meta-analyses
listed each study excluded from the analysis of pooled relative risk
and gave a good reason for its exclusion. For example, both meta-
analyses excluded studies that failed to allow for a minimum 10-year
latency period for lung cancer to develop after first exposure. With
respect to the exclusion of all studies on miners, Bhatia et al. (1998)
pointed out that ``[s]ince studies of miners often indicate higher
relative risks for lung cancer than those considered in this meta-
analysis, this was a conservative exclusion.'' Even if studies on
miners had been considered, Waxweiler et al. (1973) and Christie et al.
(1995) would have been excluded from both meta-analyses because of
their failure to meet the 10-year minimum latency requirement.
(3) Lack of Actual Exposure Data
* * * [N]ondifferential exposure or disease misclassification
can sometimes produce bias away from the null * * * Thus, tests for
heterogeneity performed in both these meta-analyzes won't detect or
correct this problem. [IMC Global]
Lipsett and Campleman acknowledged that ``[e]xposure
misclassification is a problem common to all studies of cancer and
diesel emissions. In no case were there direct measurements of
historical diesel exhaust exposures of the subjects.'' However, as Dr.
Silverman pointed out in her review, ``* * * this bias is most likely
to be nondifferential, and the effect would probably have been to bias
point estimates toward the null value. Thus the summary RR of 1.33 may
be an underestimate of the true lung cancer effect associated with
diesel exposure.'' (Silverman, 1998)
(4) Smoking as a Confounder
* * * The use of data manipulation and modeling adjustments in
both these meta-analyses cannot rectify the flaws in the initial
studies. [IMC Global]
* * * misclassification of this exposure [cigarette smoking]
could result in residual confounding of individual studies and,
consequently, metaanalyses, of those studies. [MARG]
Contrary to the commenter's suggestion, neither of the meta-
analyses made any attempt to manipulate or adjust the data in order to
rectify what the commenter regards as ``flaws'' in the way smoking or
other potential confounders were treated in the initial studies. Both
meta-analyses, however, compared the pooled RR for studies with a
smoking adjustment to the pooled RR for studies without any such
adjustment. Both meta-analysis calculated a pooled RR for the smoking-
adjusted studies greater than or equal to that for the unadjusted
studies. In addition, Bhatia et al. (1998) analyzed the impact of the
smoking adjustment for the subgroup of studies reporting results both
with and without such an adjustment and found that the ``small
reduction in the pooled RR estimates would not be consistent with a
major effect from residual confounding.'' Dr. Silverman concluded that
``[t]he authors convincingly show that potential confounding by
cigarette smoking is likely to have little impact on the estimated RRs
for diesel exhaust and lung cancer.'' (Silverman, 1998)
(5) Inadequate Control in the Underlying Studies for Diet
As noted by Lipsett and Campleman, ``Diet may also confound the
diesel-lung cancer association.'' The researchers also caution that
this risk factor was not controlled for in the nearly 50 diesel
studies they examined. [MARG]
Since inhalation is the primary route of dpm exposure, and the lung
is the primary target organ, MSHA considers potential dietary
confounding to be of minor importance in the diesel-lung cancer
association. Lipsett and Campleman acknowledged that diet might be a
relevant consideration for long-haul truck drivers, but stated that
``diet would probably not be an important confounder in studies of
other occupations, particularly those using internal or other
occupationally active reference populations.'' Studies making internal
comparisons, or comparisons to similar groups of workers, are unlikely
to be seriously confounded by dietary differences, because the groups
of workers being compared are likely to have very similar dietary
habits, on average. The pooled relative risk for cohort studies making
comparisons internally or to other active workers was 1.48 (95% CI =
1.28 to 1.70). (Lipsett and Campleman, 1999, Table 3) This was
considerably higher than the pooled RRs for studies making comparisons
against regional or national populations, where dietary differences
(and also differences with respect to other potential confounders)
would be more important.
(3) Potential Systematic Biases
Citing failure to account for dietary differences as an example,
some commenters argued that the meta-analyses may simply propagate
weaknesses shared by the individual studies. These commenters contended
that many of the studies MSHA considered in this risk assessment share
methodological similarities and that, therefore, a ``deficiency''
causing bias in one study would probably also bias many other studies
in the same direction. According to these commenters, no matter how
great a majority of studies report a 30- to 40-percent increase in the
risk of lung cancer for exposed workers, the
[[Page 5648]]
possibility of systematic bias prevents the collective evidence from
being strong or sufficient.
Although this point has some theoretical foundation, it has no
basis in fact for the particular body of epidemiologic evidence
relating lung cancer to diesel exposure. The studies considered were
carried out by many different researchers, in different countries,
using different methods, and involving a variety of different
occupations. Elevated risk was found in cohort as well as case-control
studies, and in studies explicitly adjusting for potential confounders
as well as studies relying on internal comparisons within homogeneous
populations. The possibility that systematic bias explains these
results is also rendered less plausible by results from studies of a
radically different type: the elevated risk of lung cancer associated
with chronic environmental exposures to PM2.5 (Dockery et
al. 1993; Pope et al., 1995).
Furthermore, the commenters advancing this argument presented no
evidence that the studies shared any deficiencies of a type that would
systematically shift results in the direction of showing a spurious
association. As explained in Subsection 2.c.i(2)(a), exposure
misclassification, healthy worker effect, and low power due to
insufficient latency generally have the opposite effect--systematically
diluting and masking results. Although many studies may share a similar
susceptibility to bias by dietary differences or residual smoking
effects,\73\ there is no reason to expect that such effects will
consistently bias results in the same direction, across all occupations
and geographic regions.
---------------------------------------------------------------------------
\73\ The term ``residual smoking effects'' refers to the
potentially confounding effects of smoking that may remain after a
smoking adjustment has been made.
---------------------------------------------------------------------------
Associations between dpm exposure and excess lung cancer are
evident in a wide variety of occupational and geographical contexts,
and it is unlikely that all (or most) would be biased in the same
direction by lifestyle effects. There is no reason to suppose that, in
nearly all of these studies, exposed subjects were more likely than
unexposed subjects to have lifestyles (apart from their occupations)
that increased their risk of lung cancer. On the other hand, exposures
to other occupational carcinogens, such as asbestos dust, radon
progeny, and silica, could systematically cause studies in which they
are not taken into account to exhibit spurious associations between
lung cancer and occupational diesel exhaust exposures. Silica dust and
radon progeny are frequently present in mining environments (though not
usually in potash mines), and this was the reason that studies on
miners were excluded from the two meta-analyses.
IMC Global argued that because of the possibility of being misled
by systematic biases, epidemiologic evidence can be used to identify
only those hazards that, at a minimum, double the risk of disease
(i.e., RR 2.0). IMC Global explained this viewpoint by
quoting an epidemiologist as follows:
* * * [E]pidemiologic methods can only yield valid documentation
of large relative risks. Relative risks of low magnitude (say, less
than 2) are virtually beyond the resolving power of the
epidemiologic microscope. We can seldom demonstrably eliminate all
sources of bias, and we can never exclude the possibility of
unidentified and uncontrolled confounding. If many studies--
preferably based on different methods--are nevertheless congruent in
producing markedly elevated relative risks, we can set our
misgivings aside. If however, many studies produce only modest
increases, those increases may well be due to the same biases in all
the studies. [Dr. Samuel Shapiro, quoted by IMC Global]
It is important to note that, unlike IMC Global, Dr. Shapiro did
not suggest that results of RR 2.0 be counted as ``negative.'' He
contended only that low RRs do not completely rule out the possibility
of a spurious association due to unidentified or uncontrolled
confounding. More importantly, however, this restriction would allow
workers to be exposed to significant risks and is, therefore,
unacceptable for regulatory purposes. For purposes of protecting miners
from lung cancer, certainty is not required; and an increase in the
relative risk of less than 100 percent can increase the absolute risk
of lung cancer by a clearly unacceptable amount. For example, if the
baseline risk of lung cancer is six per thousand, then increasing it by
33 percent amounts to an increase of two per thousand for exposed
workers.
IMC Global went on to argue that--
* * * only a few of these studies have relative risks that
exceed 2.0, and some of the studies that do exceed 2.0 exhibit
biases that make them unsuitable for rulemaking purposes in our
opinion. * * * Thus, in IMC Global's opinion, the epidemiologic
evidence demonstrates an artificial association that can be
explained through common biases probably due to smoking habits and
lifestyle factors. [IMC Global]
This line of reasoning leaps from the possibility that systematic
biases might account for observed results to a conclusion that they
actually do so. Furthermore, after proposing to allow for possible
biases by requiring that only relative risks in excess of 2.0 be
counted as positive evidence, IMC Global has ignored its own criterion
and discounted results greater than 2.0 for the same reason. Contrary
to IMC Global's claim that ``only a few of the studies have relative
risks that exceed 2.0,'' Tables III-4 and III-5 show 23 separate
results greater than 2.0, applying to independent categories of workers
in 18 different studies.
According to Stober and Abel (1996), the potential confounding
effects of smoking are so strong that ``residual smoking effects''
could explain even statistically significant results observed in
studies where smoking was explicitly taken into account. MSHA agrees
that variable exposures to non-diesel lung carcinogens, including
relatively small errors in smoking classification, could bias
individual studies. However, the potential confounding effect of
tobacco smoke and other carcinogens can cut in either direction.
Spurious positive associations of dpm exposure with lung cancer would
arise only if the group exposed to dpm had a greater exposure to these
confounders than the unexposed control group used for comparison. If,
on the contrary, the control group happened to be more exposed to
confounders, then this would tend to make the association between dpm
exposure and lung cancer appear negative. Therefore, although smoking
effects could potentially distort the results of any single study, this
effect could reasonably be expected to make only about half the studies
that were explicitly adjusted for smoking come out positive. Smoking is
unlikely to have been responsible for finding an excess prevalence of
lung cancer in 17 out of 18 studies in which a smoking adjustment was
applied. Based on a 2-tailed sign test, this possibility can be
rejected at a confidence level greater than 99.9 percent.
Even in the 29 studies for which no smoking adjustment was made,
tobacco smoke and other carcinogens were important confounders only to
the extent that the populations exposed and unexposed to diesel exhaust
differed systematically with respect to these other exposures. Twenty-
four of these studies, however, reported some degree of excess lung
cancer risk for the diesel- exposed workers. This result could be
attributed to other occupational carcinogens only in the unlikely event
that, in nearly all of these studies, diesel-exposed workers happened
to be more highly exposed to these other carcinogens than the control
groups of workers unexposed to diesel.
Like IMC Global, Stober and Abel (1996) do not, in MSHA's opinion,
adequately distinguish between a possible bias and an actual one.
[[Page 5649]]
Potential biases due to extraneous risk factors are unlikely to account
for a significant part of the excess risk in all studies showing an
association. Excess rates of lung cancer were associated with dpm
exposure in all epidemiologic studies of sufficient size and scope to
detect such an excess. Although it is possible, in any individual
study, that the potentially confounding effects of differential
exposure to tobacco smoke or other carcinogens could account for the
observed elevation in risk otherwise attributable to diesel exposure,
it is unlikely that such effects would give rise to positive
associations in 41 out of 47 studies. As stated by Cohen and Higgins
(1995):
* * * elevations [of lung cancer] do not appear to be fully
explicable by confounding due to cigarette smoking or other sources
of bias. Therefore, at present, exposure to diesel exhaust provides
the most reasonable explanation for these elevations. The
association is most apparent in studies of occupational cohorts, in
which assessment of exposure is better and more detailed analyses
have been performed. The largest relative risks are often seen in
the categories of most probable, most intense, or longest duration
of exposure. In general population studies, in which exposure
prevalence is low and misclassification of exposure poses a
particularly serious potential bias in the direction of observing no
effect of exposure, most studies indicate increased risk, albeit
with considerable imprecision. [Cohen and Higgins (1995), p. 269].
Several commenters identified publication bias as another possible
explanation for the heavy preponderance of studies showing an elevated
risk of lung cancer for exposed workers. As described earlier, both of
the available meta-analyses investigated and rejected the hypothesis of
significant publication bias affecting the overall results. This was
based on both a statistical technique using ``funnel plots'' and a
direct comparison between results of published and unpublished studies.
Commenters presented no evidence that publication bias actually exists
in this case. After the 1988 NIOSH and 1989 IARC determinations that
diesel exhaust was a ``potential'' or ``probable'' human carcinogen,
negative results would have been of considerable interest, and, in the
absence of any evidence specifically applying to dpm studies, there is
no reason to assume they would not have been published.
(4) Causality
MSHA must draw its conclusions based on the weight of evidence. In
the absence of any statistical evidence for differential confounding or
significant publication bias, the weight of epidemiologic evidence
strongly favors a causal connection. On the one side, it is evident
that virtually all of the studies that adjusted for smoking and other
known confounders, or controlled for them by comparing against similar
groups of workers, showed positive associations (i.e., relative risk or
odds ratio > 1.0). Also on this side of the balance are all eight of
the studies MSHA identified as comprising the best available human
evidence. These include three studies reporting positive exposure-
response relationships based on quantitative dpm exposure assessments:
two recent studies specifically on underground miners (one coal and one
potash) and one on trucking industry workers.\74\ On the other side of
the balance is the possibility that publication bias or other
systematic biases may have been responsible for some unknown portion of
the overall 30- to 40-percent elevation in lung cancer risk observed--a
possibility that, while conceivable, is based on speculation. After
considering other viewpoints (addressed here and in the next
subsection), MSHA has accepted what in its view is the far more likely
alternative: that the vast majority of epidemiologic studies showed an
elevated risk in association with occupational exposures to diesel
exhaust because such exposures cause the risk of lung cancer to
increase. The toxicity experiments discussed in Subsection 2.d.iv of
this risk assessment support the causal interpretation that MSHA has
placed on the associations observed in epidemiologic studies.
---------------------------------------------------------------------------
\74\ These studies (respectively: Johnston et al., 1997; Saverin
et al., 1999; Steenland et al., 1998) are discussed in detail in
Subsection 2.c.i(2)(a) of this risk assessment.
---------------------------------------------------------------------------
In this risk assessment, MSHA is basing its conclusions primarily
on epidemiologic studies. However, the results obtained from animal
studies confirm that diesel exhaust can increase the risk of lung
cancer in some species and help show that dpm (rather than the gaseous
fraction of diesel exhaust) is the causal agent. The fact that dpm has
been proven to cause lung cancer in laboratory rats only under
conditions of lung overload does not make the rat studies irrelevant to
miners. The very high dpm concentrations currently observed in some
mines could impair or even overwhelm lung clearance for miners already
burdened by respirable mineral dusts, thereby inducing lung cancer by a
mechanism similar to what occurs in rats (Nauss et al., 1995). It must
also be noted, however, that most of the human studies show an
increased risk of lung cancer at dpm levels lower than what might be
expected to cause overload. Therefore, the human studies suggest that
overload is not a necessary condition for dpm to induce or promote lung
cancer among humans. Salvi et al. (1999) reported marked inflammatory
responses in the airways of healthy human volunteers after just one
hour of exposure to dpm at a concentration of 300 g/
m3. Animal studies provide evidence that inhalation of dpm
has related effects, such as induction of free oxygen radicals, that
could promote the development of human lung cancers by mechanisms not
requiring lung overload. (See Sec. III.2.d.iv(2).)
Similarly, the weight of genotoxicity evidence helps support a
causal interpretation of the associations observed in the epidemiologic
studies. This evidence shows that dpm dispersed by alveolar surfactant
can have mutagenic effects, thereby providing a genotoxic route to
carcinogenesis that is independent of overloading the lung with
particles. After a comprehensive review of the evidence, IPCS (1996)
concluded that both the particle core and the associated organic
materials have biological activity. The biological availability of
carcinogens present in the organic portion of dpm may, however, differ
significantly in different species. Chemical byproducts of
phagocytosis, which occurs even when the lung is not overloaded, may
provide another genotoxic route. Inhalation of diesel emissions has
been shown to cause DNA adduct formation in peripheral lung cells of
rats and monkeys, and increased levels of human DNA adducts have been
found in association with occupational exposures. (See Sec.
III.2.d.iv(1)) None of this evidence suggests that a lung cancer
threshold exists for humans exposed to dpm, despite its importance in
the rat model. Nor does this evidence suggest that lung overload is
necessary for dpm to induce lung cancer in humans. Indeed, lung
overload may be only one of many mechanisms through which lung cancer
is produced in humans.
Results from the epidemiologic studies, the animal studies, and the
genotoxicity studies are coherent and mutually supportive. After
considering all these results, MSHA has concluded that the
epidemiologic studies, supported by the experimental data establishing
the plausibility of a causal connection, provide strong evidence that
chronic occupational dpm exposure increases the risk of lung cancer in
humans.
In a review, submitted by MARG, of MSHA's proposed risk assessment,
Dr. Jonathan Borak asserted that MSHA's determination that results from
the
[[Page 5650]]
epidemiologic and toxicity studies were ``coherent and mutually
reinforcing'' involved circular reasoning. He supported this assertion
by incorrectly attributing to MSHA the view that ``most of the
individual [epidemiologic] studies are not very good'' and that their
suggestion of an association between dpm and lung cancer is ``made
credible in light of the animal data.'' To complete his argument that
MSHA relied on circular reasoning, Dr. Borak then suggested that the
epidemiologic data provided MSHA's sole basis for considering the
animal data relevant to humans. In a similar vein, Kennecott Minerals
claimed there was an ``absence of toxicological support for
epidemiologic findings that are themselves inconclusive.''
Contrary to Dr. Borak's assertion, MSHA has not characterized most
of the epidemiologic studies as ``not very good.'' Nor has MSHA
suggested that the epidemiologic evidence would not be credible or
plausible in the absence of supporting animal data. As Dr. Borak
correctly noted, MSHA acknowledged that ``none of the existing human
studies is perfect'' and that ``no single one of the existing
epidemiological studies, viewed in isolation, provides conclusive
evidence of a causal connection * * *.'' That a study is not
``perfect,'' however, does not imply that it is ``not very good.''
MSHA's position has consistently been that, as demonstrated by the two
available meta-analyses, the collective epidemiologic evidence is not
merely credible but statistically significant and indicative of a
causal association. Although MSHA views the toxicity data as supporting
and reinforcing the epidemiologic evidence, MSHA believes that the
collective epidemiologic evidence is highly credible in its own right.
Furthermore, MSHA does not consider the animal data relevant to
humans simply because of the positive epidemiologic evidence. The
animal evidence is also credible in its own right. As MSHA has
repeatedly pointed out, dust concentrations in some mines have been
measured at levels of the same order of magnitude as those found to
have caused lung cancer in rats. Such high exposures, especially when
combined with occupational exposures to respirable mineral dusts and
exposures to particles in tobacco smoke, could overload the human lung
and promote lung cancer by a mechanism similar to that hypothesized for
rats. (Hattis and Silver, 1992, Figures 9, 10, 11). Also, many of the
animal experiments have elucidated genotoxic effects that, while
apparently not responsible for the excess lung cancers observed for
rats, may be responsible for some or all of the excess risk reported
for humans.
MSHA has not relied on circular reasoning. If either the animal
data or the toxicity data had failed to show any link between dpm and
effects implicated in the induction or promotion of lung cancer, then
MSHA's conclusion would have been weakened. The existence of
experimental evidence confirming that there is such a link is not
imaginary and is logically independent of the epidemiologic evidence.
Therefore, contrary to Dr. Borak's characterization, the ``coherency
and reinforcement'' arising from the epidemiologic, animal, and
genotoxicity data are not the product of circular reasoning. A more apt
description is that the three sources of evidence, like three legs of a
tripod, support the same conclusion.
Many commenters argued that a causal connection between dpm
exposure and an increased human risk of lung cancer should not be
inferred unless there is epidemiologic evidence showing a positive
exposure-response relationship based on quantitative measures of
cumulative dpm exposure. MSHA does not agree that a quantitative
exposure-response relationship is essential in establishing causality.
Such a relationship is only one of several factors, such as consistency
and biological plausibility, that epidemiologists examine to provide
evidence of causality. As mentioned earlier, however, there are three
studies providing quantitative exposure-response relationships. One of
these studies (Steenland et al., 1998) controlled for age, race,
smoking, diet, and asbestos exposure, but relied on ``broad
assumptions'' to estimate historical exposure levels from later
measurements. Two of the studies, however, (Johnston et al., 1997, and
Saverin et al., 1999) utilized measurements that were either
contemporaneous with the exposures (Johnston) or that were made under
conditions very similar to those under which the exposures took place
(Saverin). Both of these studies were conducted on underground miners.
The Saverin study used exposure measurements of total carbon (TC). All
three of the studies combined exposure measurements for each job with
detailed occupational histories to form estimates of cumulative dpm
exposure; and all three reported evidence of increasing lung cancer
risk with increasing cumulative exposure.
Several commenters, expressing and endorsing the views of Dr. Peter
Valberg, incorrectly asserted that the epidemiologic results obtained
across different occupational categories were inconsistent with a
biologically plausible exposure-response relationship. For example,
MARG argued that--
It is biologically implausible that, if Dpm were (causally)
increasing lung cancer risk by 50% for a low exposure (say, truck
drivers), then the lung cancer risk produced by Dpm exposure in more
heavily exposed worker populations (railroad shop workers) would
fall in this same range of added risk. The added lung-cancer risk
for bus garage workers is half that of either railroad workers or
truck drivers, but Dpm concentrations are considerably higher.
[MARG]
Earlier, MARG had argued to the contrary that, due to their lack of
concurrent exposure measurements, these studies could not reliably be
used for hazard identification. MARG then attempted to use them to
perform the rather more difficult task of making quantitative
comparisons of relative risk. If cumulative exposures are unknown, as
MARG argued elsewhere, then there is little basis for comparing
responses at different cumulative exposures.
In an analysis submitted by the West Virginia Coal Association, Dr.
Valberg extended this argument to miners as follows:
* * * If dpm concentrations for truck drivers is in the range of
5-50 g/m\3\, then we can assign the 0.49 excess risk
(Bhatia's meta-analysis result) to the 5-50 g/m\3\
exposure. Hence, dpm concentrations for miners in the range of 100-
2,000 g/m\3\ should have yielded excess risks forty times
larger, meaning that the RR for exposed miners would be expected to
be about 21 (i.e., 1 + 19.6), whereas reported risk estimates are
less than 3 (range from 0.74 2.67). Such an utter lack of
concordance argues against a causal role for dpm in the reported
epidemiologic associations.
Based on a similar line of reasoning, IMC Global asserted that ``*
* * the assumptions that MSHA used to develop [Figure III-4] * * * do
not make sense in the context of a dose-response relationship between
lung cancer and Dpm exposure.'' This was one of the reasons IMC Global
gave for objecting to MSHA's comparison (in Section III.1.d) of
exposure levels measured for miners to those reported for different
occupations. IMC Global proposed that, as a consequence of this
argument, MSHA should delete this comparison from its risk assessment.
MSHA sees three major flaws in Dr. Valberg's argument and rejects
it for the following reasons:
(1) The argument glosses over the important distinction between
exposure concentrations (intensity) and cumulative exposure (dose).
Total
[[Page 5651]]
cumulative exposure is the product of intensity and duration of
exposure. Depending on duration, high intensity exposure may result in
similar (or even lower) cumulative exposure than low intensity
exposure. Furthermore, different industries, in different nations,
introduced diesel equipment at different times. The studies being
considered were carried out in a variety of different countries and
covered a variety of different historical periods. Therefore, the same
number of years in different studies can correspond to very different
durations of occupational exposure.
Many of the miners in the studies Dr. Valberg considered may have
been occupationally exposed to dpm for relatively short periods of time
or even not at all. Various forms of exposure misclassification would
tend to obscure any exposure-response relationship across industries.
Such obscuring would result from both exposure misclassification within
individual studies and also variability in the degree of exposure
misclassification in different industries.
Furthermore, the exposure levels or intensities assigned to the
various occupations would not necessarily be proportional to cumulative
exposures, even if the average number of years of exposure were the
same. Different job conditions, such as longer-than-average work hours,
could have major, variable impacts on cumulative exposures. For
example, lower dpm concentrations have been measured for truck drivers
than for other occupationally-exposed workers. However, the truck
drivers studied, due to their work conditions may have been in their
trucks for longer than the standard 40-hour work week and therefore
have larger cumulative dpm exposures. Truck drivers commonly congregate
in parking areas and sleep in their trucks with the engines idling,
thereby disproportionately increasing their cumulative dpm exposures
compared to miners and other types of workers.
(2) The commenters advancing this argument assumed that an
exposure-response relationship spanning occupations at different levels
of exposure intensity would take the form of a straight line. This
assumption is unwarranted, since carcinogens do not necessarily follow
such a simple pattern across a broad range of exposure levels. There is
little basis for assuming that the relationship between cumulative dpm
exposures and the relative risk of lung cancer would appear as a
straight line when plotted against exposure levels that may differ by a
factor of 100. Steenland et al. (1998) reported a better statistical
``fit'' to the data using a model based on the logarithm of cumulative
exposure as compared to simple cumulative exposure. Even across the
relatively limited range of exposures within the trucking industry, the
logarithmic exposure model exhibits pronounced curvature towards the
horizontal at the higher cumulative exposures (Steenland et al., 1998,
Fig. 5). If this model is extrapolated out to the much higher exposures
currently found in underground mining, then (as shown in Subsection
3.b.ii(3)(b) of this risk assessment) it diverges even more from a
straight-line model. Toxicological evidence of curvature in the dose-
response relationship has also been reported (Ichinose et al., 1997b,
p.190).
Furthermore, the exposure-response pattern may depend on other
aspects of exposure, besides how much is accumulated. For example, the
National Research Council (NRC) has adopted a risk model for radon-
induced lung cancer in which the relative risk (RR) at any age depends
on both accumulated exposure and the rate (reflecting the intensity of
exposure) at which total exposure was accumulated. In this model, which
was derived empirically from the epidemiologic data, exposures
accumulated over long time periods at relatively low rates result in a
greater risk of lung cancer than the same total exposures accumulated
over shorter time periods at relatively higher rates (NRC, 1999). A
similar effect for dpm could cause apparent anomalies in the pattern of
relative risks observed for occupations ranked simply with respect to
the intensity of their average exposures.
(3) Mean exposures and relative risks reported for miners involved
in the available studies were mischaracterized. Although dpm levels as
high as 2000 g/m\3\ have been measured in some mines, the
levels at most mines surveyed by MSHA were substantially lower (see
Figures III-1 and III-2). The average levels MSHA measured at
underground mines were 808 g/m\3\ and 644 g/m\3\ for
M/NM and coal mines using diesel equipment for face haulage,
respectively (Table III-1). However, these were not necessarily the
levels experienced by miners involved in the available studies. The
mean TC exposure concentration reported by Saverin et al. (1999), for
work locations having the highest mean concentration, was 390
g/m\3\--corresponding to a mean dpm concentration of about 490
g/m\3\. In the only other study involving miners for which
exposure measurements were available, Johnston et al. (1997) reported
dpm concentrations for the most highly exposed category of workers
(locomotive drivers), ranging from 44 g/m\3\ to 370
g/m\3\. Therefore, the mean dpm concentration experienced by
the most highly exposed miners involved in these two studies was not
``forty times larger'' than the level imputed to truck drivers, but
closer to seven times larger.\75\ Applying Dr. Valberg's procedure,
this yields an ``expected'' relative risk of about 4.4 for the
underground miners who happened to work at mines included in these
particular studies (1 + 7 x (0.49)). Miners exposed at higher levels
would, of course, face a greater risk.
---------------------------------------------------------------------------
\75\ The estimate of seven times larger dpm exposure in miners
is the result of averaging data from Saverin et al. (1999) with data
from Johnston et al. (1997) and comparing the combined average miner
exposure to the average truck driver dpm exposure.
---------------------------------------------------------------------------
Dr. Valberg asserted that the highest relative risk reported for
miners was 2.67 (from Boffetta et al., 1988). Dr. Valberg failed to
note, however, that the upper 95-percent confidence limit for miners'
relative risk in this study was 4.37, so that this result hardly
qualifies as an ``utter lack of concordance'' with the 4.4 ``expected''
value for miners. Furthermore, even higher relative risks for miners
have been reported in other studies. Burns and Swanson (1991) reported
5.0 for operators of mining machinery, with an upper 95-percent
confidence limit of 16.9. The relative risk estimated for the most
highly exposed miners in the study by Johnston et al. (1997) was either
5.5 or 11.0, depending on the statistical model used. These results
appear to be quite consistent with the data for truck drivers.
(5) Other Interpretations of the Evidence. After reviewing the same
body of scientific evidence as MSHA, Dr. Peter Valberg came to a very
different conclusion with respect to the likelihood of causality:
Flawed methodology (lack of adequate control for smoking);
values for relative risks (``RR'') that are low and often not
statistically elevated above 1.0; inadequate treatment of sources of
variability; reliance on multiple comparisons; and inadequate
control over how authors choose to define dpm exposure surrogates
(that is, job category within a profession, cumulative years of
work, age at time of exposure, etc.), all undermine the assignment
of causality to dpm exposure.
On the other hand, many scientific organizations and governmental
agencies have reviewed the available epidemiologic and toxicological
evidence for carcinogenicity and, in accordance with MSHA's conclusion,
identified dpm as a probable human carcinogen--at levels far lower than
those measured in some mines--or
[[Page 5652]]
placed it in a comparable category. These include:
Year
2000 National Toxicology Program (NTP);
1999 (tentative) U.S. Environmental Protection Agency (EPA);
1998 (tentative) (American Conference of Governmental Industrial
Hygienists (ACGIH); Currently on Y2K NIC list. Probable vote in 10/
2000;
1998 California Environmental Protection Agency (Cal-EPA);
1998 Federal Republic of Germany;
1996 International Programme on Chemical Safety (IPCS), a joint venture
of the World Health Organization, the International Labour
Organization, and the United Nations Environment Programme;
1989 International Agency for Research on Cancer (IARC);
1988 National Institute for Occupational Safety and Health (NIOSH)
Nevertheless, several commenters strongly objected to MSHA's
conclusion, claiming that the evidence was obviously inadequate and
citing scientific authorities who, they claimed, rejected MSHA's
inference of a causal connection. In some cases, views were
inaccurately attributed to these authorities, and misleading quotations
were presented out of context. For example, the Nevada Mining
Association stated that its own review of the scientific literature led
to--
* * * the only reasonable conclusion possible: there is no
scientific consensus that there is a causal link between dpm
exposure and lung cancer. The HEI [1999 Expert Panel] report
concludes that the causal link between diesel exhaust and lung
cancer remains unproven, and that further study and analysis are
clearly required. [Nevada Mining Assoc.]
Although HEI (1999) recommended further study and analysis for purposes
of quantitative risk assessment, the report contains no findings or
conclusions about the ``causal link.'' To the contrary, the report
explicitly states that the panel ``. . . was not charged to evaluate
either the broad toxicologic or epidemiologic literature concerning
exposure to diesel exhaust and lung cancer for hazard identification
purposes, which has been done by others.'' (HEI, 1999, p. 1)
Furthermore, the HEI panel ``. . . recognize[d] that regulatory
decisions need to be made in spite of the limitations and uncertainties
of the few studies with quantitative data currently available.'' (HEI,
1999, p. 20)
MARG, along with the Nevada Mining Association and several other
commenters, mischaracterized the Expert Panel's findings as extending
beyond the subject matter of the report. This report was limited to
evaluating the suitability of the data compiled by Garshick et al.
(1987, 1988) and Steenland et al. (1990, 1992, 1998) for quantitative
risk assessment. Contrary to the characterization by these commenters,
HEI's Expert Panel explicitly stated:
[The Panel] was not charged to evaluate the broad toxicologic or
epidemiologic literature for hazard identification purposes, which
has been done by others. State, national, and international agencies
have all reviewed the broader animal and human evidence for
carcinogenicity and, in either their draft or final reports, have
all identified diesel exhaust as [a] probable human carcinogen or
placed it in a comparable category.'' [HEI, 1999, p. 1]
[[Page 5653]]
The Panel then identified most of the organizations and governmental
institutions listed above (HEI, 1999, p. 8).
One commenter (MARG) also grossly misrepresented HEI (1999) as
having stated that ``the available epidemiologic work has `study design
flaws, including uncontrolled, confounding and lack of exposure
measures, leading to a lack of convincing evidence.' '' (MARG post-
hearing comments) The opinion falsely attributed to HEI was taken from
a sentence in which HEI's Diesel Epidemiology Expert Panel was
describing opinions expressed in ``[s]ome reviews critical of these
data.'' (HEI, 1999, p. 10) The Panel did not suggest that these
opinions were shared by HEI or by any members of the Panel. In fact,
the cited passage came at the end of a paragraph in which the Panel
cited a larger number of other review articles that had ``discusse[d]
this literature in depth'' and had expressed no such opinions. In the
same paragraph, the Panel confirmed that ``[t]he epidemiologic studies
generally show higher risks of lung cancer among persons occupationally
exposed to diesel exhaust than among persons who have not been exposed,
or who have been exposed to lower levels or for shorter periods of
time.'' (HEI, 1999, p. 10)
Several commenters noted that the U.S. EPA's Clean Air Scientific
Advisory Committee (CASAC) issued a report (CASAC, 1998) critical of
the EPA's 1998 draft Health Assessment Document for Diesel Emissions
(EPA, 1998) and rejecting some of its conclusions. After the HEI (1999)
Expert Panel report was published, the EPA distributed a revised draft
of its Health Assessment Document (EPA, 1999). In the 1999 draft, the
EPA characterized human exposures to diesel exhaust as ``highly
likely'' to be carcinogenic to humans at ambient (i.e., environmental)
exposure levels. After reviewing this draft, CASAC endorsed a
conclusion that, at ambient levels, diesel exhaust is likely to be
carcinogenic to humans. Although CASAC voted to recommend that the
designation in the EPA document be changed from ``highly likely'' to
``likely,'' this change was recommended specifically for ambient rather
than occupational exposures. The CASAC report states that ``[a]lthough
there was mixed opinion regarding the characterization of diesel
emissions as `highly likely' to be a human carcinogen, the majority of
the Panel did not agree that there was sufficient confidence (i.e.,
evidence) to use the descriptor `highly' in regard to environmental
exposures.'' (CASAC, 2000, emphasis added)
MSHA recognizes that not everyone who has reviewed the literature
on lung cancer and diesel exposure agrees about the collective weight
of the evidence it presents or about its implications for regulatory
decisions. IMC Global, for example, stated:
After independently reviewing most [of the] * * * epidemiologic
studies, the literature reviews and the two meta-analyzes, IMC
Global believes * * * MSHA has misrepresented the epidemiologic
evidence in the Proposed Rule. The best conclusion that we can reach
based on our review of this information is that different reputable
studies reach conflicting conclusions * * *. [IMC Global]
IMC Global continued by expressing concern that MSHA had ``dismissed''
opposing arguments critical of the positive studies, especially
``regarding lack of statistical significance; small magnitudes of
relative risk * * *; and the impact of confounding factors, especially
smoking * * * . [IMC Global]''
MSHA has addressed these three issues, as they relate to the
evaluation of individual studies, in Section 2.c.i(2)(a) of this
preamble. The argument that confounding factors such as smoking may
have been systematically responsible for the positive results was
discussed above, under the heading of ``Potential Systematic Biases.''
Statistical significance of the collective evidence is not the same
thing as statistical significance of individual studies. Application of
the sign test, as described Subsection 3.a.iii(1) above, is one way
that MSHA has addressed statistical significance of the collective
evidence. Another approach was also described above, under the heading
of ``Meta-Analyses.''
IMC Global quoted Morgan et al. (1997) as concluding that
``[a]lthough
[[Page 5654]]
there have been a number of papers suggesting that diesel fumes may act
as a carcinogen, the weight of the evidence is against this
hypothesis.'' This conclusion was based largely on the authors'
contention, shared by IMC Global, that the epidemiologic results were
inconsistent and of insufficient strength (i.e., RR 2.0) to rule out
spurious associations due to potential confounders. MSHA, on the other
hand, interprets the epidemiologic studies as remarkably consistent,
given their various limitations, and has argued that the strength of
evidence from individual studies is less important than the strength of
evidence from all studies combined. Dr. Debra Silverman has referred to
the ``striking consistency'' of this evidence. (Silverman, 1998)
Ironically, Morgan et al. point out many of the very limitations in
individual studies that may actually explain why the studies do not
yield entirely equivalent results. The 1997 Morgan article was written
before the meta-analyses became available and resolved many, if not
all, of the apparent inconsistencies in the epidemiologic results.
Since none of the existing human studies is perfect and many contain
important limitations, it is not surprising that reported results
differ in magnitude and statistical significance. The meta-analyses
described earlier showed that the more powerful and carefully designed
studies tended to show greater degrees of association. MSHA has
addressed the joint issues of consistency and strength of association
above, under the heading of ``Consistency of Epidemiologic Evidence.''
The Engine Manufacturers Association (EMA) quoted Cox (1997) as
concluding: ``* * * there is no demonstrated biological basis for
expecting increased risk at low to moderate levels of [diesel]
exposure.'' (Cox, 1997, as quoted by EMA] The EMA, however, prematurely
terminated this quotation. The quoted sentence continues: ``* * * low
to moderate levels of exposure (those that do not lead to lasting soot
deposits, chronic irritation, and perhaps GSH enzyme depletion in the
lung).'' MSHA does not regard concentrations of dpm exceeding 200
g/m\3\ as ``low to moderate,'' and the EMA presented no
evidence that the effects Dr. Cox listed do not occur at the high
exposure levels observed at some mines. Salvi et al. (1999) reported
marked inflammatory responses in the airways of healthy human
volunteers after just one hour of exposure to dpm at a concentration of
300 g/m\3\. The deleted caveat ending the quotation is
especially important in a mining context, since mine atmospheres
generally contain respirable mineral dusts that may diminish clearance
rates and contribute to meeting thresholds for chronic irritation and
inflammation leading to oxidative damage. Based on miners' testimony at
the public hearings and workshops, there is, in fact, reason to believe
that exposed miners experience lasting soot deposits and chronic
irritation as a result of their exposures.
With respect to the epidemiologic evidence, the EMA quoted Dr. Cox
as concluding: ``* * * among studies that demonstrate an increased
relative risk, it appears plausible that uncontrolled biases in study
design and data analysis methods can explain the statistical increases
in relative risk without there being a true causal increase.'' (Cox,
1997, quoted by EMA) Dr. Cox refers to non-causal explanations for
positive epidemiologic results as ``threats to causal inference.'' In
considering Dr. Cox's discussion of the evidence, it is important to
bear in mind that his purpose was ``* * * not to establish that any (or
all) of these threats do explain away the apparent positive
associations between [dpm] and lung cancer risk * * * but only to point
out that they plausibly could * * *.'' (Cox, 1997, p. 813) Dr. Cox's
stated intent was to identify non-causal characteristics of positive
studies that could potentially ``explain away'' the positive results.
This is a relatively simple exercise that could misleadingly be applied
to even the strongest of epidemiologic studies. As stated earlier, no
epidemiologic study is perfect, and it is always possible that unknown
or uncontrolled risk factors may have given rise to a spurious
association. Neither the EMA nor Dr. Cox pointed out however, that
there are characteristics common to the negative studies that plausibly
explain why they came out negative: insufficient latency allowance,
nondifferential exposure misclassification, inappropriate comparison
groups (including healthy worker effect, negative confounding by
smoking or other variables. A similar approach could also be used to
explain why many of the positive studies did not exhibit stronger
associations. As observed by Dr. Silverman, ``an unidentified negative
confounder may have produced bias across studies, systematically
diluting RRs.''
b. Significance of the Risk of Material Impairment to Miners
The fact that there is substantial and persuasive evidence that dpm
exposure can materially impair miner health in several ways does not
imply that miners will necessarily suffer such impairments at a
significant rate. This section will consider the significance of the
risk faced by miners exposed to dpm.
i. Meaning of Significant Risk
(1) Legal Requirements
The benzene case, cited earlier in this risk assessment, provides
the starting point for MSHA's analysis of this issue. Soon after its
enactment in 1970, OSHA adopted a ``consensus'' standard for exposure
to benzene, as authorized by the OSH Act. The standard set an average
exposure limit of 10 parts per million over an 8-hour workday. The
consensus standard had been established over time to deal with concerns
about poisoning from this substance (448 U.S. 607, 617). Several years
later, NIOSH recommended that OSHA alter the standard to take into
account evidence suggesting that benzene was also a carcinogen. (Id. at
619 et seq.). Although the ``evidence in the administrative record of
adverse effects of benzene exposure at 10 ppm is sketchy at best,''
OSHA was operating under a policy that there was no safe exposure level
to a carcinogen. (Id., at 631). Once the evidence was adequate to reach
a conclusion that a substance was a carcinogen, the policy required the
agency to set the limit at the lowest level feasible for the industry.
(Id. at 613). Accordingly, the Agency proposed lowering the permissible
exposure limit to 1 ppm.
The Supreme Court rejected this approach. Noting that the OSH Act
requires ``safe or healthful employment,'' the court stated that--
* * * `safe' is not the equivalent of `risk-free' * * * a
workplace can hardly be considered `unsafe' unless it threatens the
workers with a significant risk of harm. Therefore, before he can
promulgate any permanent health or safety standard, the Secretary is
required to make a threshold finding that a place of employment is
unsafe--in the sense that significant risks are present and can be
eliminated or lessened by a change in practices. [Id., at 642,
italics in original].
The court went on to explain that it is the Agency that determines how
to make such a threshold finding:
First, the requirement that a `significant' risk be identified
is not a mathematical straitjacket. It is the Agency's
responsibility to determine, in the first instance, what it
considered to be a `significant' risk. Some risks are plainly
acceptable and others are plainly unacceptable. If, for example, the
odds are one in a billion that a person will die from cancer by
taking a drink of chlorinated water, the risk clearly could not be
considered significant. On the other hand, if the odds are one in a
thousand that regular inhalation of gasoline vapors that are 2%
[[Page 5655]]
benzene will be fatal, a reasonable person might well consider the
risk significant and take appropriate steps to decrease or eliminate
it. Although the Agency has no duty to calculate the exact
probability of harm, it does have an obligation to find that a
significant risk is present before it can characterize a place of
employment as `unsafe.' [Id., at 655].
The court noted that the Agency's ``* * * determination that a
particular level of risk is `significant' will be based largely on
policy considerations.'' (Id., note 62).
Some commenters contended that the concept of significant risk, as
enunciated by the Supreme Court in the Benzene case, requires support
by a quantitative dose-response relationship. For example, one
commenter argued as follows:
* * * OSHA had contended in * * * [the benzene] case that
``because of the lack of data concerning the linkage between low-
level exposures and blood abnormalities, it was impossible to
construct a dose-response curve at this time''. 448 U.S. at 632-633.
The court rejected the Agency's attempt to support a standard based
upon speculation that ``the benefits to be derived from lowering''
the permissible exposure level from 10 to 1 ppm were `likely' to be
`appreciable'.'' 448 U.S. at 654.
One year after the Benzene case, the Court in American Textile
Mfr's Inst. v. Donovan, 452 U.S. 490 (1981), upheld OSHA's ``cotton
dust'' standard for which a dose-response curve had been established
by the Agency. The Court relied upon the existence of such data to
find that OSHA had complied with the Benzene mandate, stating: ``In
making its assessment of significant risk, OSHA relied on dose-
response curve data * * * It is difficult to imagine what else the
agency could do to comply with this Court's decision in the Benzene
case.'' Id. at 505, n. 25. See also Public Citizen Research Group v.
Tyson, 796 F. 2d 1479, 1496, 1499 (D.C. Cir. 1986) (where a dose
response curve was constructed for the ethylene oxide standard and
the agency [had] gone to great lengths to calculate, within the
bounds of available scientific data, the significance of the risk);
United Steelworkers of America v. Marshall, 647 F. 2d 1189, 1248
(D.C. Cir. 1980), cert. denied , 453 U.S. 913 (1981) (where in
promulgating a new lead standard ``OSHA amassed voluminous evidence
of the specific harmful effects of lead at particular blood levels
and correlated these blood lead levels with air lead levels'').
[NMA]
A dose-response relationship has been established between exposure
to PM2.5 (of which dpm is a major constituent) and the risk
of death from cardiovascular, cardiopulmonary, or respiratory causes
(Schwartz et al.,1996; EPA, 1996). Furthermore, three different
epidemiologic studies, including two carried out specifically on mine
workers, have reported evidence of a quantitative relationship between
dpm exposure and the risk of lung cancer (Johnston et al., 1997,
Steenland et al., 1998, Saverin et al., 1999). However, the Secretary
has carefully reviewed the legal references provided by the commenters
and finds there is no requirement in the law that the determination of
significant risk be based on such a relationship. The cited court
rulings appear to describe sufficient means of establishing a
significant risk, rather than necessary ones. Indeed, as stated earlier
in this section, the Benzene court explained that:
* * * the requirement that a `significant' risk be identified is
not a mathematical straitjacket. It is the Agency's responsibility
to determine, in the first instance, what it considered to be a
`significant' risk. * * * the Agency has no duty to calculate the
exact probability of harm * * *.
The Agency has set forth the evidence and rationale behind its
decision to propose a rule restricting miner exposure to dpm, obtained
an independent peer review of its assessment of that evidence,
published the evidence and tentative conclusions for public comment,
held hearings, kept the record open for further comments for months
after the hearings, and re-opened the record so that stakeholders could
comment on the most recent evidence available. Throughout these
proceedings, the Agency has carefully considered all public comments
concerning the evidence of adverse health effects resulting from
occupational dpm exposures. Based on that extensive record, and the
considerations noted in this section, the Agency is authorized under
the statute and relevant precedents to act on this matter--despite the
fact that a more conclusive or definitively established exposure-
response relationship might help address remaining doubts among some
members of the mining community.
As the Supreme Court pointed out in the benzene case, the
appropriate definition of significance also depends on policy
considerations of the Agency involved. In the case of MSHA, those
policy considerations include special attention to the history of
extraordinary occupational risks leading to the Mine Act. That history
is intertwined with the toll to the mining community of silicosis and
coal workers' pneumoconiosis (CWP or ``black lung''), along with
billions of dollars in Federal expenditures.
(2) Standards and Guidelines for Risk Assessment
Several commenters suggested that this risk assessment, as
originally proposed, deviated from established risk assessment
guidelines, because it did not provide a sufficiently quantitative
basis for evaluating the significance of miners's risks due to their
dpm exposures. One of these commenters (Dr. Jonathan Borak) maintained
that a determination of significant risk based on a ``qualitative''
assessment ``has no statistical meaning.''
MSHA recognizes that a risk assessment should strive to provide as
high a degree of quantification and certainty as is possible, given the
best available scientific evidence. However, in order to best protect
miners' health, it is not prudent to insist on a ``perfect'' risk
assessment. Nor is it prudent to delay assessing potentially grave
risks simply because the available data may be insufficient for an
ideal risk assessment. The need for regulatory agencies to act in the
face of uncertainty was recognized by the HEI's Diesel Epidemiology
Expert Panel as follows: ``The Panel recognizes that regulatory
decisions need to be made in spite of the limitations and uncertainties
of the few studies with quantitative data currently available.'' (HEI,
1999) When there is good, qualitative evidence--such as the sight and
smell of heavy smoke--that one's house is on fire, an inference of
significant risk may be statistically meaningful even without
quantitative measurements of the smoke's density and composition.
Moreover, as will be demonstrated below, the question of whether a
quantitative assessment is or is not essential is, in this case, moot:
this risk assessment does, in fact, provide a quantitative evaluation
of how significant the risk is for miners occupationally exposed to
dpm.
ii. Significance of Risk for Underground Miners Exposed to Dpm
An important measure of the significance of a risk is the
likelihood that an adverse effect actually will occur. A key factor in
the significance of risks that dpm presents to miners is the very high
dpm concentrations to which a number of those miners are currently
exposed--compared to ambient atmospheric levels in even the most
polluted urban environments, and to workers in diesel-related
occupations for which positive epidemiologic results have been
reported. Figure III-4 compared the range of median dpm exposure levels
measured for mine workers at various mines to the range of medians
estimated for other occupations, as well as to ambient environmental
levels. Figure III-11 presents a similar comparison, based on the
highest mean dpm level observed at
[[Page 5656]]
any individual mine, the highest mean level reported for any
occupational group other than mining, and the highest monthly mean
concentration of dpm estimated for ambient air at any site in the Los
Angeles basin.\76\ As shown in Figure III-11, underground miners are
currently exposed at mean levels up to 10 times higher than the highest
mean exposure reported for other occupations, and up to 100 times
higher than the highest mean environmental level even after adjusting
the environmental level upwards to reflect an equivalent occupational
exposure.
---------------------------------------------------------------------------
\76\ For comparability with occupational lifetime exposure
levels, the environmental ambient air concentration has been
multiplied by a factor of approximately 4.7. This factor reflects a
45-year occupational lifetime with 240 working days per year, as
opposed to a 70-year environmental lifetime with 365-days per year,
and assumes that air inhaled during a work shift comprises half the
total air inhaled during a 24-hour day.
---------------------------------------------------------------------------
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Given the significant increases in mortality and other acute health
effects associated with increments of 25 g/m\3\ in fine
particulate concentration (see Table III-3), the relative risk of acute
effects for some miners (especially those already suffering respiratory
problems) appears to be extremely high. Acute responses to dpm
exposures have been detected in studies of stevedores, whose exposures
were likely to have been less than one tenth the exposure of some
miners on the job. Likewise, the risk of lung cancer due to dpm
exposure would appear to be far greater for those underground miners
who are exposed at such high levels than for other workers or general
urban populations.
Several commenters asserted that current dpm exposures in
underground mines are lower than they were when MSHA conducted its
field surveys and that MSHA had not taken this into account when
assessing the significance of dpm risk to miners. A related comment was
that MSHA had not designed its sampling studies to provide a
statistically representative cross section of the entire industry but
had nevertheless used the results in concluding that the risk to
underground miners was significant.
In accordance with Sec. 101.(a)(6) of the Mine Act, MSHA is basing
this risk assessment on the best available evidence. None of the
commenters provided evidence that dpm levels in underground coal mines
had declined significantly since MSHA's field studies, or provided
quantitative estimates of any purported decline in average dpm
concentrations, or submitted data that would better represent the range
of dpm concentrations to which underground miners are typically exposed
at the present time. Although MSHA's field studies were not designed to
be statistically representative in a way that
[[Page 5657]]
can be readily quantified, they were performed at locations selected,
according to MSHA's best engineering judgement, to be typical of the
type of diesel equipment used. Furthermore, as will be shown below,
MSHA's evaluation of the significance of risks presented to underground
miners by their dpm exposures does not rely on the highest levels, or
even the average levels, that MSHA has measured. As documented in
Section 1.d of this risk assessment, some of the highest of MSHA's
measurements were made as recently as 1996-1997. In 1996 MSHA published
the diesel equipment safety rule that focused primarily on the safe
storage, handling, and transport of diesel fuel underground, training
of mine personnel, minimum ventilating air quantities for diesel
powered equipment, monitoring of gaseous diesel exhaust emissions,
maintenance requirements, incorporation of fire suppression systems,
and design features for nonpermissible machines. In developing this
diesel equipment safety rule for underground coal mines, however, MSHA
did not explicitly consider the health risks to miners of a working
lifetime of dpm exposure at very high levels, nor the actions that
could be taken to specifically reduce dpm exposure levels. It was
understood that the agency would be evaluating the health risks of dpm
exposure at a later date. (61 FR 55420). With the implementation of the
diesel safety rule in underground coal mines, MSHA believes that dpm
concentrations may have declined, in the past two to three years. It is
important to note, as is shown below, the cancer risks of dpm exposure
are clearly significant even at a concentration of 300 g/
m\3\--less than half of the average level that MSHA observed in its
field studies. However, MSHA also believes that a reduction in exposure
of more than 50 percent is highly implausible, even with the safety
standard implemented. It is also important to note that the diesel
equipment rule applied only to underground coal mines and not
underground metal/nonmetal mines.
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BILLING CODE 4510-43-C
Earlier in this risk assessment, MSHA identified three types of
material impairment that can result from occupational exposures to dpm.
The next three subsections present the Agency's evaluation of how much
of a risk there is that miners occupationally exposed to dpm will
actually incur such consequences. Each part addresses the risk of
incurring one of the three types of material impairment identified
earlier.
(1) Sensory Irritations and Respiratory Symptoms (including allergenic
responses)
It is evident from the direct testimony of numerous miners working
near diesel equipment that their exposures pose a significant risk of
severe sensory irritations and respiratory symptoms.
[[Page 5658]]
This was underscored during the workshops and public hearings by
several miners who noted that such effects occurred immediately and
consistently after episodes of intense exposure (Section 2.b.i). There
is also persuasive experimental evidence that exposure at levels found
in underground mines frequently cause eye and nose irritation (Rudell
et al., 1996) and pulmonary inflammation (Salvi et al., 1999). Section
2.a.ii and 3.a.i of this risk assessment explain why these effects
constitute ``material impairments'' under the Mine Act and why they
threaten miners' safety as well as health. Therefore, it is clear that
even short-term exposures to excessive concentrations of dpm pose
significant risks.
MSHA's quantitative evaluation of how significant the risks of
sensory irritations and respiratory symptoms are for miners is limited,
by the quantitative evidence available, to acute respiratory symptoms
linked to fine particulate exposures (PM2.5) in ambient air
pollution studies.MSHA recognizes that, for miners exposed to dpm, this
type of risk cannot be quantified with great confidence or precision
based on the available evidence. This is because PM2.5 is
not solely comprised of dpm and also because miners, as a group, have
different demographic and health characteristics from the general
populations involved in the relevant studies. However, MSHA believes
that the quantitative evidence suffices to establish a lower bound on
the significance of this type of risk to miners exposed to dpm. Even at
this lower bound, which is likely to substantially underestimate the
degree of risk, the probability that a miner's occupational exposure to
dpm will cause adverse respiratory effects is clearly significant.
As shown in Table III-3, the risk of acute lower respiratory tract
symptoms has been reported to increase, at a 95-percent confidence
level, by 15 to 82 percent (RR = 1.15 to 1.82) for each incremental
increase of 20 g/m3 in the concentration of
PM2.5 in the ambient air. This means that the relative risk
estimated for a given PM2.5 concentration ranges between
(1.15) k and (1.82) k, where k = the
concentration of PM2.5 divided by 20 g/
m3. For example, for a PM2.5 concentration of 40
g/m3, the RR is estimated to be between (1.15)
2 and (1.82) 2, or 1.32 to 3.31. MSHA believes
that part of the reason why the range is so wide is that the
composition of PM2.5 varied in the data from which the
estimates were derived.
MSHA acknowledges that there are substantial uncertainties involved
in converting 24-hour environmental exposures to 8-hour occupational
exposures. However, since mining often involves vigorous physical
activity (thereby increasing breathing depth and frequency) and sleep
is characterized by reduced respiration, it is highly likely that
miners would inhale at least one-third of their total 24-hour intake of
air during a standard 8-hour work shift. If it is assumed that the
acute respiratory effects of inhaling dpm at a concentration of 60
g/m3 over an 8-hour workshift are at least as great
as those at a concentration of 20 g/m3 over a 24-
hour period, then it is possible to estimate a lower bound on the
relative risk of such effects.
Based solely on the fact that dpm consists almost entirely of
particles much smaller than 2.5 micrometers in diameter, the dpm would
be expected to penetrate the lower respiratory tract at least as
effectively as PM2.5. Also, given the complex chemical
composition of dpm, and its generation within a confined space, there
is no reason to suspect that dpm in an underground mining environment
is less potent than ambient PM2.5 in inducing respiratory
symptoms. Under these assumptions, a short-term environmental exposure
to PM2.5 at a concentration of 20 g/m3
would correspond to a short-term occupational exposure to dpm at a
concentration of 60 g/m3. Consequently, the RR at
an occupational exposure level of Y g/m3 would
equal the RR calculated for an ambient exposure level of 20 x (Y/60)
g/m3. For example, the relative risk (RR) of acute
lower respiratory symptoms at an occupational exposure level of 300
g/m3 dpm would, at a minimum, correspond to the RR
at an ambient exposure level equal to 5 x 20 g/m3
PM2.5. (See Table III-3) A dpm concentration of 300
g/m3 happens to be the level at which Salvi et al.
(1999) found a marked pulmonary inflammatory response in healthy human
volunteers after just one hour of exposure.
Under these assumptions, the risk of lower respiratory tract
symptoms for a miner exposed to dpm for a full shift at a concentration
of 300 g/m3 or more, would be at least twice the
risk of ambient exposure (i.e., RR = (1.15) 5 = 2.01). This
would imply that for miners exposed to dpm at or above this level, the
risk of acute lower respiratory symptoms would double, at a minimum.
The Secretary considers such an increase in risk to be clearly
significant.
(2) Premature Death From Cardiovascular, Cardiopulmonary, or
Respiratory Causes
As in the case of respiratory symptoms, the nature of the best
available evidence limits MSHA's quantitative evaluation of how large
an excess risk of premature death, due to causes other than lung
cancer, there is for miners exposed to dpm. As before, this evidence
consists of acute effects linked to fine particulate exposures
(PM2.5) in ambient air pollution studies. Therefore, the
analysis is subject to similar uncertainties. However, also as before,
MSHA believes that the quantitative evidence suffices to place a lower
bound on the increase in risk of premature mortality for miners
occupationally exposed to dpm. As will be shown below, even this lower
bound, which is likely to substantially underestimate the degree of
increase, indicates that a miner's occupational exposure to dpm has a
clearly significant impact on the likelihood of premature death.
Schwartz et al. (1996) found an average increase of 1.5 percent in
daily mortality associated with each increment of 10 g/
m3 in the daily concentration of fine particulates. Higher
increases were estimated specifically for ischemic heart disease (IHD:
2.1 percent), chronic obstructive pulmonary disease (COPD: 3.3
percent), and pneumonia (4.0 percent). The corresponding 95-percent
confidence intervals for the three specific estimates were,
respectively, 1.4% to 2.8%, 1.0% to 5.7%, and 1.8% to 6.2%, per
increment of 10 g/m3 in daily PM2.5
exposure. Within the range of dust concentrations studied, the response
appeared to be linear, with no threshold. The investigators checked for
but did not find any consistent or statistically stable relationship
between increased mortality and the atmospheric concentration of
``coarse'' respirable particles--i.e., those with aerodynamic diameter
greater than 2.5 micrometers but less than 10 micrometers.
As explained earlier, it is highly likely that miners would inhale
at least one-third of their total 24-hour intake of air during a
standard 8-hour work shift. Therefore, under the same assumptions made
in the previous subsection, the 24-hour average concentrations of
PM2.5 measured by Schwartz et al. are no more potent, in
their impact on mortality risk, than eight-hour average concentrations
that are three times as high. As discussed in Section 2.a.iii of this
risk assessment, underground miners may be less, equally, or more
susceptible than the general population to the acute
[[Page 5659]]
mortality effects of fine particulates such as dpm. However, miners who
smoke tobacco and/or suffer various respiratory ailments fall into
groups identified as likely to be especially sensitive (EPA, 1996).
Consequently, for such miners occupationally exposed to dpm, the
relative risk of each type of premature mortality would be at least
equal to the corresponding lower 95-percent confidence limit specified
above.
Therefore, MSHA estimates that, on average, each increment of 30
g/m3 in the dpm concentration to which miners are
exposed increases the risk of premature death due to IHD, COPD, and
pneumonia by a factor of at least 1.4 percent, 1.0 percent, and 1.8
percent, respectively. A lower bound on the increased risk expected at
an occupational dpm concentration greater than 30 g/
m3, is obtained by raising the relative risks equivalent to
these factors (i.e., 1.014, 1.01, and 1.018) to a power, k, equal to
the ratio of the concentration to 30 g/m3. For a
concentration of 300 g/m3, k = 10; so MSHA
estimates the lower bounds on relative risk to be: (1.014)10
= 1.149 for IHD; (1.01)10 = 1.105 for COPD; and
(1.018)10 = 1.195 for pneumonia. This means that for miners
exposed to dpm at or above this level, MSHA expects the risks to
increase by at least 14.9 percent for IHD, 10.5 percent for COPD, and
19.5 percent for pneumonia. The Secretary considers increases of this
magnitude to be clearly significant, since the causes of death to which
they apply are not rare among miners.
(3) Lung Cancer
In contrast to the two types of risk discussed above, the available
epidemiologic data can be used to relate the risk of lung cancer
directly to dpm exposures. Therefore, the significance of the lung
cancer risk can be evaluated without having to make assumptions about
the relative potency of dpm compared to the remaining constituents of
PM2.5. This removes an important source of uncertainty
present in the other two evaluations.
There are two different ways in which the significance of the lung
cancer risk may be evaluated. The first way is based on the relative
risk of lung cancer observed in the best available epidemiologic
studies involving miners (identified as such in Subsections
3.a.iii(1)(b) and (d) of this risk assessment). As will be explained
below, this approach leads to an estimated tripling of lung cancer risk
for miners exposed to dpm, compared to a baseline risk for unexposed
miners. The second way is to calculate the lung cancer risk expected at
exposure levels MSHA has observed in underground mines, assuming a
specified occupational lifetime and using the exposure-response
relationships estimated for underground miners by Johnston et al.
(1997) and Saverin et al. (1999). As will be explained further below,
this second approach yields a wide range of estimates, depending on
which exposure-response relationship and statistical model is used. All
of the estimates, however, show at least a doubling of baseline lung
cancer risk, assuming dpm exposure for a 45-year occupational lifetime
at the average concentration MSHA has observed. Most of the estimates
are much higher than this. If the exposure-response relationship
estimated for workers in the trucking industry by Steenland et al.
(1998) is extrapolated to the much higher exposure levels for miners,
the resulting estimates fall within the range established by the two
mine-specific studies, thereby providing a degree of corroboration.
Since lung cancer is not a rare disease, the Secretary considers even
the very lowest estimate--a doubling of baseline risk--to represent a
clearly significant risk.
Both of these methods provide quantitative estimates of the degree
by which miners' risk of lung cancer is increased by their occupational
dpm exposures. The estimate based on exposure-response relationships is
more refined, in that it ties the increased risk of lung cancer to
specific levels of cumulative dpm exposure. However, this added
refinement comes at the price of an additional source of uncertainty:
the accuracy of the exposure-response relationship used to calculate
the estimate. This additional uncertainty is reflected, in MSHA's
evaluation, by a broad range of relative risk estimates, corresponding
to the range of exposure-response relationships derived using different
statistical models and epidemiologic data. The next two subsections
present the details of MSHA's two approaches to analyzing lung cancer
risk for miners exposed to dpm, along with MSHA's responses to the
relevant public comments.
(a) Risk Assessment Based on Studies Involving Miners
As one commenter pointed out, the epidemiologic evidence showing an
elevated risk of lung cancer for exposed workers is mostly based on
occupations estimated to experience far lower exposure levels, on
average, than those observed in many underground mines:
* * * [U]nderground coal, metal and non-metal miners face a
significant risk of lung cancer from occupational exposure to diesel
particulate. Numerous epidemiologic studies of workers exposed to
levels far below those experienced by coal, metal and non-metal
miners have found the risk for exposed workers to be 30-50% greater
than for unexposed workers. [Washington State Dept. of Labor and
Industries]
Indeed, although MSHA recognizes that results from animal studies
should be extrapolated to humans with caution, it is noteworthy that
dpm exposure levels recorded in some underground mines (see Figures
III-1 and III-2) have been well within the exposure range that produced
tumors in rats (Nauss et al., 1995).
Both existing meta-analyses of the human studies relating dpm
exposure and lung cancer excluded studies on miners but presented
evidence showing that, averaged across all other occupations, dpm
exposure is responsible for an increase of about 40 percent in lung
cancer risk (See Section 3.a.iii(2) of this risk assessment). Even a
40-percent increase in the risk of lung cancer would clearly be
significant, since this would amount to more than two cases of lung
cancer per year per thousand miners at risk, and to an even greater
risk for smoking miners. The best available evidence, however,
indicates (1) that exposure levels in underground mines generally
exceed exposures for occupations included in the meta-analyses and (2)
that lung cancer risks for exposed miners are elevated to a greater
extent than for other occupations.
As Dr. Valberg and other commenters pointed out, the epidemiologic
studies used in the meta-analyses involved much lower exposure levels
than those depicted for mines in Figures III-1 and III-2. The studies
supporting a 40-percent excess risk of lung cancer were conducted on
populations whose average exposure is estimated to be less than 200
g/m3--less than one tenth the average concentration
MSHA observed in some underground mines. More specifically, average
exposure levels in the two most extensively studied industries--
trucking (including loading dock workers) and railroads--have been
reported to be far below the levels observed in underground mining
environments. For workers at docks employing diesel forklifts--the
occupational group estimated to be most highly exposed within the
trucking industry--the highest average dpm concentration reported was
about 55 g/m3 EC at an individual dock (NIOSH,
1990). As explained in Subsection 1.d of this risk assessment, this
corresponds to
[[Page 5660]]
less than 150 g/m3 of dpm, on average. Published
dpm measurements for railworkers have generally also been less than 150
g/m3 (measured as respirable particulate matter
other than cigarette smoke). The reported mean of 224 g/
m3 for hostlers displayed in Figure III-11 represents only
the worst-case occupational subgroup (Woskie et al., 1988). In
contrast, in the study on underground potash miners by Saverin et al.
(1999), the mean TC concentration measured for production areas was 390
g/m3--corresponding to a mean dpm concentration of
about 490 g/m3. As shown in Table III-1, the mean
dpm exposure level MSHA observed in underground production areas and
haulageways was 644 g/m3 for coal mines and 808
g/m3 for M/NM.
In accordance with the higher exposure levels for underground
miners, the five studies identified in Section III.3.a.iii(1)(d) as
comprising the best available epidemiologic evidence on miners all show
that the risk of lung cancer increased for occupationally exposed
miners by substantially more than 40 percent. The following table
presents the relative risk (RR) of lung cancer for miners in these
studies, along with the geometric mean based on all five studies:
------------------------------------------------------------------------
Relative
risk of
Study lung
cancer
------------------------------------------------------------------------
Boffetta et al., 1988........................................ 2.67
Burns & Swanson, 1991........................................ 5.03
Johnston et al., 1997 (mine-adjusted model applied at highest 5.50
cumulative exposure)........................................
Lerchen et al., 1987......................................... 2.1
Saverin et al., 1999 (highest vs least exposed).............. 2.17
Geometric mean............................................... 3.2
------------------------------------------------------------------------
As shown in this table, the estimated RR based on these five
studies is 3.2 for miners exposed to dpm. In other words, the risk of
lung cancer for the highly exposed miners is estimated to be 3.2 times
that of a comparable group of occupationally unexposed workers. The
geometric mean RR remains 3.2 if the two studies on which MSHA places
less weight (by Burns & Swanson and by Lerchen) are excluded from the
calculation. This represents a 220-percent increase in the risk of lung
cancer for exposed miners, in contrast to the 40-percent increase
estimated, on average, for other occupationally exposed workers. The
Secretary believes that a 40-percent increase in the risk of lung
cancer already exceeds, by a wide margin, the threshold for a clearly
significant risk. However, a 220-percent increase to more than three
times the baseline rate is obviously of even greater concern.
Some commenters questioned whether increased lung cancer risks of
this magnitude were plausible, since they were not aware of any
unusually high lung cancer rates among workers at mines with which they
were familiar and which used diesel equipment. There are several
reasons why an elevated risk of lung cancer might not currently be
conspicuous among U.S. miners exposed to dpm. Lung cancer not only may
require a latency period of 30 or more years to develop, but it may
also not develop until beyond the normal retirement age of 65 years.
Cases of lung cancer developing after retirement may not all be known
to members of the mining community. Also, in a population that includes
many tobacco smokers, it may be difficult to discern cases of lung
cancer specifically attributable to dpm exposure when they first begin
to become prevalent. Two commenters expressed some of the relevant
considerations as follows. Although they were referring to coal miners,
the same points apply to M/NM miners.
Because the latency period for lung cancer is so long, and
diesel-powered equipment has only been used extensively in U.S. coal
mines for about 25 years, the epidemic may well be progressing
unnoticed. [UMWA]
If Dpm exposure will cause cancer, there is a huge population of
miners here in the West that have already been exposed. Considering
the latency periods indicated by MSHA, these miners should be
beginning to develop cancers. [Canyon Fuels]
(b) Risk Assessment Based on Miners' Cumulative Exposure
Although it is evident that underground miners currently face a
significant risk of lung cancer due to their occupational exposure to
dpm, there are certain advantages in utilizing an exposure-response
relationship to quantify the degree of risk at specific levels of
cumulative exposure. As some commenters pointed out, for example, dpm
exposure levels may change over time due to changes in diesel fuel and
engine design. The extent and patterns of diesel equipment usage within
mines also has changed significantly during the past 25 years, and this
has affected dpm exposure levels as well. Furthermore, exposure levels
at the mines involved in epidemiologic studies were not necessarily
typical or representative of exposure levels at mines in general. A
quantitative exposure-response relationship provides an estimate of the
risk at any specified level of cumulative exposure. Therefore, using
such a relationship to assess risk under current or anticipated
conditions factors in whatever differences in exposure levels may be
relevant, including those due to historical changes.
(i) Exposure-Response Relationships from Studies Outside Mining
Stayner et al. (1998) summarized quantitative risk assessments
based on exposure-response relationships for dpm published through
1998. These assessments were broadly divided into those based on human
studies and those based on animal studies. Depending on the particular
studies, assumptions, statistical models, and methods of assessment
used, estimates of the exact degree of risk varied widely even within
each broad category. However, as presented in Tables III and IV of
Stayner et al. (1998), all of the very different approaches and methods
published through 1998 produced results indicating that levels of dpm
exposure measured at some underground mines present an unacceptably
high risk of lung cancer for miners--a risk significantly greater than
the risk they would experience without the dpm exposure.\77\
---------------------------------------------------------------------------
\77\ In comments submitted by MARG, Dr. Jonathan Borak asserted
that MSHA had ``misrepresented the findings of a critical study'' by
stating that all methods showed an ``unacceptably high risk'' at
exposure levels found at some mines. Dr. Borak claimed that Stayner
et al. (1998) had described an analysis by Crump et al. ``that
reached an opposite conclusion.'' Dr. Borak failed to distinguish
between a finding of high risk and a finding of changes in that risk
corresponding to changes in estimated exposures. The findings to
which Dr. Borak referred pertained only to the exposure-response
relationship within the group of exposed workers. Garshick (1981),
Crump (1999), and HEI (1999) all noted that the risk of lung cancer
was nevertheless elevated among the exposed workers, compared to
unexposed workers in the same cohort, and they all identified
reasons why the data used in this study might fail to detect a
positive exposure-response relationship among the exposed workers.
---------------------------------------------------------------------------
Quantitative risk estimates based on the human studies were
generally higher than those based on analyses of the rat inhalation
studies. As indicated by Tables 3 and 4 of Stayner et al. (1998), a
working lifetime of exposure to dpm at 500 g/m 3
yielded estimates of excess lung cancer risk ranging from about 1 to
200 excess cases of lung cancer per thousand workers based on the rat
inhalation studies and from about 50 to 800 per thousand based on the
epidemiologic assessments. Stayner et al. (1998) concluded their report
by stating:
The risk estimates derived from these different models vary by
approximately three orders of magnitude, and there are substantial
uncertainties surrounding each of
[[Page 5661]]
these approaches. Nonetheless, the results from applying these
methods are consistent in predicting relatively large risks of lung
cancer for miners who have long-term exposures to high
concentrations of DEP [i.e., dpm]. This is not surprising given the
fact that miners may be exposed to DEP [dpm] concentrations that are
similar to those that induced lung cancer in rats and mice, and
substantially higher than the exposure concentrations in the
positive epidemiologic studies of other worker populations.
Restricting attention to the exposure-response relationships
derived from human data, Table IV of Stayner et al. (1998) presented
estimates of excess lung cancer risk based on exposure-response
relationships derived from four different studies: Waller (1981) as
analyzed by Harris (1983); Garshick et al. (1987) as analyzed by Smith
and Stayner (1991); Garshick et al. (1988) as analyzed by California
EPA (1998); and Steenland et al. (1998). Harris (1983) represented
upper bounds on risk; and all of the other estimates represented the
most likely value for risk, given the particular data and statistical
modeling assumptions on which the estimate was based. Three different
ranges of estimates were presented from the California EPA analysis,
corresponding to various statistical models and assumptions about
historical changes in dpm exposure among the railroad workers involved.
As mentioned above and in the proposed version of this risk assessment,
the low end of the range of estimates was 50 lung cancers per 1000
workers occupationally exposed at 500 g/m 3 for a
45-year working lifetime. This estimate was one of those based on
railroad worker data from Garshick et al. (1988).
Several commenters objected to MSHA's reliance on any of the
exposure-response relationships derived from the data compiled by
Garshick et al. (1987) or Garshick et al. (1988). These objections were
based on re-analyses of these data by Crump (1999) and HEI (1999),
using different statistical methods and assumptions from those used by
Cal-EPA (1998). For example, the NMA quoted HEI (1999) as concluding:
At present, the railroad worker cohort study * * * has very
limited utility for QRA [quantitative risk assessment] of lifetime
lung cancer risk from exposure to ambient levels of diesel exhaust *
* * [NMA, quoting HEI (1999)]
From this, the NMA argued as follows:
What then is the relevance of this data to the proceedings at
issue? Simply put, there is no relevance. The leading epidemiologist
[sic], including Dr. Garshick himself, now agree that the data are
inappropriate for conducting risk assessment. [NMA]
MSHA notes that the HEI (1999) conclusion cited by the NMA referred
to quantitative risk assessments at ambient, not occupational, exposure
levels. Also, HEI (1999) did not apply its approach (i.e.,
investigating the correlation between exposure and relative risk within
separate job categories) to the Armitage-Doll model employed by Cal-EPA
in some of its analyses. (Results using this model were among those
summarized in Table IV of Stayner et al., 1998). Therefore, the
statistical findings on which HEI (1999) based its conclusion do not
apply to exposure-response relationships estimated using the Armitage-
Doll model. Furthermore, although HEI concluded that the railroad
worker data have ``very limited utility for QRA * * * at ambient
levels'' [emphasis added], this does not mean, even if true, that these
data have ``no relevance'' to this risk assessment, as the NMA
asserted. Even if they do not reliably establish an exposure-response
relationship suitable for use in a quantitative risk assessment, these
data still show that the risk of lung cancer was significantly elevated
among exposed workers. This is the only way in which MSHA is now using
these data in this risk assessment.
In the proposed risk assessment, MSHA did not rely directly on the
railroad worker data but did refer to the lowest published quantitative
estimate of risk, which happened, as of 1998, to be based on those
data. MSHA's reasoning was that, even based on the lowest published
estimate, the excess risk of lung cancer attributable to dpm exposure
was clearly sufficient to warrant regulation. If risk assessments
derived from the railroad worker data are eliminated from
consideration, the lowest estimate remaining in Table IV of Stayner et
al. (1998) is obviously even higher than the one that MSHA used to make
this determination in the proposed risk assessment. This estimate
(based on one of the analyses performed by Steenland et al., 1998) is
89 excess cases of lung cancer per year per thousand workers exposed at
500 g/m 3 for a 45-year working lifetime.
HEI (1999) also evaluated the use of the Steenland data for
quantitative risk assessment, but did not perform any independent
statistical analysis of the data compiled in that study. Some
commenters pointed out HEI's reiteration of the cautionary remark by
Steenland et al. (1998) that their exposure assessment depended on
``broad assumptions.'' The HEI report did not rule out the use of these
data for quantitative risk assessment but suggested that additional
statistical analyses and evaluations were desirable, along with further
development of exposure estimates using alternative assumptions. MSHA
has addressed comments on various aspects of the analysis by Steenland
et al., including the exposure assumptions, in Section 2.c.i(2)(a) of
this risk assessment.
One commenter noted that Steenland et al. (1998) had recognized the
limitations of their analysis and had, therefore, advised that the
results ``should be viewed as exploratory.'' The commenter then
asserted that MSHA had nevertheless used these results as ``the basis
for a major regulatory standard'' and that ``[t]his alone is sufficient
to demonstrate that MSHA's proposal lacks the necessary scientific
support.'' [Kennecott Minerals]
The Secretary does not accept the premise that MSHA should exclude
``exploratory'' results from its risk assessment, even if it is granted
that those results depend on broad assumptions possibly requiring
further research and validation before they are widely accepted by the
scientific community. Steenland et al. (1998) estimated risks
associated with specific cumulative exposures, based on estimates of
historical exposure patterns combined with data originally described by
Steenland et al., 1990 and 1992. Regardless of whether the cumulative
exposure estimates used by Steenland et al. (1998) are sufficiently
reliable to permit pinpointing the risk of lung cancer at any given
exposure level, the quantitative analysis indicates that as cumulative
exposure increases, so does the risk. Therefore, the 1998 analysis adds
significantly to the weight of evidence supporting a causal
relationship. However, MSHA did not use or propose to use exposure-
response estimates derived by Steenland et al. (1998) as the sole basis
for any regulatory standard.
The exposure-response relationships presented by Steenland et al.
were derived from exposures estimated to be far below those found in
underground mines. As Stayner et al. (1998) point out, questions are
introduced by extrapolating an exposure-response relationship beyond
the exposures used to determine the relationship. The uncertainties
implicit in such extrapolation are demonstrated by comparing results
from two statistical models based on five-year lagged exposures--one
using simple cumulative exposure and the other using the natural
logarithm of cumulative exposure (Steenland et al., 1998, Table II).
[[Page 5662]]
Assuming that, on average, EC comprises 40 percent of total
dpm,\78\ the formula for calculating a relative risk (RR) using
Steenland's simple cumulative exposure model is
---------------------------------------------------------------------------
\78\ The assumption is that, on average, EC = TC/2 and TC =
0.8 x dpm.
---------------------------------------------------------------------------
RR = exp(0.4 x 0.389 x CumExp),
where CumExp is occupationally accumulated dpm exposure (expressed in
mg-yr/m\3\), ignoring the most recent five years. Again assuming
EC=0.4 x dpm, the corresponding formula using Steenland's Log(CumExp)
model is
RR = exp(0.1803 x (Log(0.4 x 1000 x CumExp + BG)-Log(BG))),
still ignoring occupational dpm exposure in the most recent five
years.\79\
---------------------------------------------------------------------------
\79\ BG, expressed in g-yr/m\3\, accounts for an
assumed background (i.e., non-occupational) EC exposure level of 1.0
g/m\3\. At age 70, after a 45-year worklife and an
additional 5-year lag after retirement, BG is assumed to equal 70
g-yr/m\3\. ``Log'' refers to the natural logarithm, and
``exp'' refers to the antilogarithm of the subsequent quantity.
---------------------------------------------------------------------------
The risk estimates from these two models are similar at the
cumulative exposure levels estimated for workers involved in the study,
but the projected risks diverge markedly at the higher exposures
projected for underground miners exposed to dpm for a 45-year
occupational lifetime. For example, a cumulative dpm exposure of 2.5
mg-yr/m\3\ (i.e., 45 years of occupational exposure at an average dpm
concentration of about 55.6 g/m\3\) is within the range of
cumulative exposures from which these exposure-response relationships
were estimated. At this level of cumulative exposure, the models (both
lagged five years) yield relative risk estimates of 1.48 (based on
simple cumulative exposure) and 1.64 (based on the logarithm of
cumulative exposure, with BG=70 g-yr/m\3\). On the other hand,
45 years of occupational exposure at an average dpm concentration of
808 g/m\3\ amounts to a cumulative dpm exposure of 36,360
g-yr/m\3\, or about 36.4 mg-yr/m\3\. At this level, which lies
well beyond the range of data used by Steenland et al. (1998), the
simple and logarithmic exposure models produce relative risk estimates
of about 300 and 2.6, respectively.
Despite the divergence of these two models at high levels of
cumulative exposure, they can provide a useful check of excess lung
cancer risks estimated using exposure-response relationships developed
from other studies. For highly exposed miners, the Steenland models
both produce estimates of lung cancer risk within the range established
by the two miner studies discussed below. This corroborates the upper
and lower limits on such risk as estimated by the various statistical
models used in those two studies.
(ii) Exposure-Response Relationships From Studies on Miners
As described in Section 2.c.i(2)(a) of this risk assessment, two
epidemiologic studies, both conducted on underground miners, provide
exposure-response relationships based on fully quantitative dpm
exposure assessments. Johnston et al. (1997) conducted their study on a
cohort of 18,166 underground coal miners, and Saverin et al. (1999)
conducted theirs on a cohort of 5,536 underground potash miners. Each
of these studies developed a number of possible exposure-response
relationships, depending on the statistical model used for analysis
and, in the case of Saverin et al. (1999), inclusion criteria for the
cohort analyzed. For purposes of this risk assessment, MSHA has
converted the units of cumulative exposure in all of these exposure-
response relationships to mg-yr/m\3\.
Two exposure-response relationships derived by Johnston et al.
(1997) are used in this risk assessment, based on a ``mine-adjusted''
and a ``mine-unadjusted'' statistical model. In both of these models,
cumulative dpm exposure is lagged by 15 years.\80\ This reflects the
long latency period required for development of lung cancer and means
that the most recent 15 years of exposure are ignored when the relative
risk of lung cancer is estimated. The exposure-response relationships,
as reported by the investigators, were expressed in terms of g-hr/m\3\
of cumulative dpm exposure. MSHA has converted the exposure units to
mg-yr/m\3\ by assuming 1920 work hours per year.
---------------------------------------------------------------------------
\80\ The 15-year lagged mine-unadjusted and mine-adjusted models
are respectively denoted by M/03 and M/06 in Table 11.2 of Johnston
et al. (1997). As explained earlier, the individual mines considered
in this study differed significantly with respect to both dpm
exposures and lung cancer experience. The investigators could not
determine exactly how much, if any, of the increased lung cancer
risk associated with dpm exposure depends on other, unknown factors
differentiating the individual mines. The mine-adjusted model
allocates a significant number of the lung cancers otherwise
attributable to dpm exposure to the ``norm'' for specific mines.
Therefore, if the differences in lung cancer prevalence between
mines is actually due to corresponding differences in mean dpm
exposure, then this model will mask a significant portion of the
risk due to dpm exposure. After adjusting for miners' age and
smoking habits, the mine-unadjusted model attributes differences in
the prevalence of lung cancer between mines to corresponding
differences in mean dpm exposure. However, the mine-adjusted model
has the advantage of taking into account differences between mines
with respect to potentially confounding factors, such as radon
progeny and silica levels.
---------------------------------------------------------------------------
Two different methods of statistical analysis were applied by
Saverin et al. (1999) to both the full cohort and to a subcohort of
3,258 miners who had worked underground, in relatively stable jobs, for
at least ten years. Thus, the investigators developed a total of four
possible exposure-response relationships from this study. Since they
were based on measurements of total carbon (TC), these exposure-
response relationships were expressed in terms mg-yr/m\3\ of cumulative
TC exposure. MSHA has converted the exposure units to mg-yr/m\3\ of
cumulative dpm exposure by assuming that, on average, TC comprises 80
percent of total dpm.
The following table summarizes the exposure-response relationships
obtained from these two studies. Each of the quantitative relationships
is specified by the unit relative risk (RR) per mg-yr/m\3\ of
cumulative dpm exposure. To calculate the relative risk estimated for a
given cumulative dpm exposure (CE), it is necessary to raise the unit
RR to a power equal to CE. For example, if the unit RR is 1.11 and CE =
20, then the estimated relative risk is (1.11)\20\ = 8.1. Therefore,
the estimated relative risk of lung cancer increases as CE increases.
For the two Johnston models, CE does not include exposure accumulated
during the 15 years immediately prior to the time in a miner's life at
which the relative risk is calculated.
Exposure-Response Relationships Obtained From Two Studies on Underground
Miners
------------------------------------------------------------------------
Unit RR
Study and statistical model per mg-yr/
m\3\ dpm
------------------------------------------------------------------------
Saverin et al. (1999):
Poisson, full cohort....................................... 1.024
Cox, full cohort........................................... 1.089
Poisson, subcohort......................................... 1.110
Cox, subcohort............................................. 1.176
Johnston et al. (1997):
15-year lag, mine-adjusted................................. 1.321
15-year lag, mine-unadjusted............................... 1.479
------------------------------------------------------------------------
Unit RR calculated from Tables III and IV, assuming TC = 0.8 x
dpm.
Unit RR calculated from Table 11.2, assuming 1920 work hours per year.
For example, suppose a miner is occupationally exposed to dpm at an
average level of 500 g/m\3\. Then each year of occupational
exposure would contribute 0.5 mg-yr/m\3\ to the miner's cumulative dpm
exposure. Suppose also that this miner's occupational exposure
[[Page 5663]]
begins at age 45 and continues for 20 years until retirement at age 65.
Consequently, at or above age 65, this hypothetical miner would have
accumulated a total of 10 mg-yr/m\3\ of occupational dpm exposure.
According to the Saverin-Cox-subcohort model, the relative risk
estimated for this miner after retirement is RR = (1.176)\10\ = 5.1.
This means that, at or above age 65, the retired miner's risk of lung
cancer is estimated (by this model) to be about five times that of
another retired miner having the same age and smoking history but no
occupational dpm exposure.
Since the two Johnston models exclude exposure within the last 15
years, it is instructive to calculate the relative risk using these
models for the same hypothetical retiree at age 75. Since this miner
retired at age 65, immediately after 20 years of occupational exposure,
the cumulative exposure used in applying the Johnston models must be
reduced by the 2.5 mg-yr/m\3\ accumulated from age 60 to age 65.
Therefore, according to the Johnston mine-adjusted model, the relative
risk estimated for this retired miner at age 75 is RR = (1.321)\7.5\ =
8.1. At age 80 or above, however, this model predicts that the relative
risk would increase to RR = (1.321)\10\ = 16.2.
The six exposure-response relationships obtained from these two
studies establish a range of quantitative risk estimates corresponding
to a given level of cumulative dpm exposure. This range provides lower
and upper limits on the risk of lung cancer for workers exposed at the
given level, relative to similar workers who were not occupationally
exposed. The lower limit of this range is established by Saverin's full
cohort Poisson model. Therefore, the lowest estimate of relative risk
after 45 years of occupational dpm exposure is RR = (1.024)\45x0.644\ =
2.0 at a mean concentration of 644 g/m\3\ or RR =
(1.024)\45x0.808\ = 2.4 at mean concentration of 808 g/m\3\.
These exposure levels correspond to the averages presented in Table
III-1 for underground coal and underground M/NM mines, respectively.
A relative risk of 2.0 amounts to a doubling of the baseline lung
cancer risk, and all of the models project relative risks of at least
2.0 after 45 years of exposure at these levels. Therefore, MSHA expects
that underground miners exposed to dpm at these levels for a full 45-
year occupational lifetime would, at a minimum, experience lung cancer
at a rate twice that of unexposed but otherwise similar miners. Five of
the six statistical models, however, predict a relative risk much
greater than 2.0 after 45 years at a mean dpm concentration of 644
g/m\3\. The second-lowest estimate of relative risk, for
example, is RR = (1.089)\45x0.644\ = 11.8, predicted by Saverin's full
cohort Cox model.\81\
---------------------------------------------------------------------------
\81\ Some commenters contended that MSHA cannot establish a
reliable exposure-response relationship because of potential
interferences in MSHA's dpm concentration measurements. More
specifically, some of these commenters claimed that MSHA's dpm
measurements in underground coal mines were significantly inflated
by submicrometer coal dust.
As explained in Subsection 1.a of this risk assessment, the
sampling device MSHA used to measure dpm in underground coal mines
was designed specifically to allow for the submicrometer fraction of
coal dust. Both the size-selective and RCD methods are reasonably
accurate when dpm concentrations exceed 300 g/m\3\.
Moreover, neither of these methods was used to establish the
exposure-response relationships presented by Saverin et al. (1999)
or Johnston et al. (1997).
---------------------------------------------------------------------------
In the next subsection of this risk assessment, relative risks will
be combined with baseline lung cancer and mortality data to estimate
the lifetime probability of dying from lung cancer due to occupational
dpm exposure.
(iii) Excess Risk at Specific Dpm Exposure Levels
The ``excess risk'' discussed in this subsection refers to the
lifetime probability of dying from lung cancer resulting from
occupational exposure to dpm for 45 years. This probability is
expressed as the expected excess number of lung cancer deaths per
thousand miners occupationally exposed to dpm at a specified level. The
excess is calculated relative to baseline, age-specific lung cancer
mortality rates taken from standard mortality tables. In order to
properly estimate this excess, it is necessary to calculate, at each
year of life after occupational exposure begins, the expected number of
persons surviving to that age with and without dpm exposure at the
specified level. At each age, standard actuarial adjustments must be
made in the number of survivors to account for the risk of dying from
causes other than lung cancer.
Table III-7 shows the excess risk of death from lung cancer
estimated across the range of exposure-response relationships obtained
from Saverin et al. (1999) and Johnston et al. (1997). Estimates based
on the 5-year lagged models from Steenland et al. (1998) fall within
this range and are included for comparison. Based on each of the eight
statistical models, the excess risk was estimated at four levels of dpm
exposure: 200