[Federal Register Volume 59, Number 65 (Tuesday, April 5, 1994)]
[Unknown Section]
[Page 0]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 94-7619]


[[Page Unknown]]

[Federal Register: April 5, 1994]


_______________________________________________________________________

Part II





Department of Labor





_______________________________________________________________________



Occupational Safety and Health Administration



_______________________________________________________________________



29 CFR Parts 1910, 1915, 1926, and 1928 
Indoor Air Quality; Proposed 
Rule
DEPARTMENT OF LABOR

Occupational Safety and Health Administration

29 CFR Parts 1910, 1915, 1926, 1928

[Docket No. H-122]
RIN 1218-AB37

 
Indoor Air Quality

AGENCY: Occupational Safety and Health Administration (OSHA), Labor.

ACTION: Notice of proposed rulemaking; notice of informal public 
hearing.

-----------------------------------------------------------------------

SUMMARY: By this notice, the Occupational Safety and Health 
Administration (OSHA) proposes to adopt standards addressing indoor air 
quality in indoor work environments. The basis for this proposed action 
is a preliminary determination that employees working in indoor work 
environments face a significant risk of material impairment to their 
health due to poor indoor air quality, and that compliance with the 
provisions proposed in this notice will substantially reduce that risk.
    The provisions of the standard are proposed to apply to all indoor 
``nonindustrial work environments.'' In addition, all worksites, both 
industrial and nonindustrial within OSHA's jurisdiction are covered 
with respect to the proposed provisions addressing control of 
environmental tobacco smoke. The proposal would require affected 
employers to develop a written indoor air quality compliance plan and 
implement that plan through actions such as inspection and maintenance 
of building systems which influence indoor air quality.
    Provisions under the standard also propose to require employers to 
implement controls for specific contaminants and their sources such as 
outdoor air contaminants, microbial contamination, maintenance and 
cleaning chemicals, pesticides, and other hazardous chemicals within 
indoor work environments. Designated smoking areas which are to be 
separate, enclosed rooms exhausted directly to the outside are proposed 
to be required in buildings where the smoking of tobacco products is 
not prohibited. Specific provisions are also proposed to limit the 
degradation of indoor air quality during the performance of renovation, 
remodeling and similar activities. Provisions for information and 
training of building system maintenance and operation workers and other 
employees within the facility are also included in this notice.
    Finally, proposed provisions in this notice address the 
establishment, retention, availability, and transfer of records such as 
inspection and maintenance records, records of written compliance 
programs, and employee complaints of building-related illness.
    The Agency invites the submission of written data, views and 
comments on all regulatory provisions proposed in this notice, and on 
all relevant issues pertinent to those provisions. OSHA is also 
scheduling an informal public hearing where persons may orally submit 
their views. It is noted here that subsequent Federal Register notices 
may be published subsequent to this notice, if the public presents 
views leading to a substantial change in focus or it is otherwise 
determined to be appropriate.

DATES: Comments on the proposed standard must be postmarked by June 29, 
1994. Notices of intention to appear must be postmarked by June 20, 
1994. Testimony and evidence to be submitted at the hearing must be 
postmarked by July 5, 1994. The hearing will commence at 9:30 a.m. on 
July 12, 1994.

ADDRESSES: Comments are to be submitted in quadruplicate or 1 original 
(hardcopy) and 1 disk (5\1/4\ or 3\1/2\) in WP 5.0, 5.1, 6.0 or Ascii 
to: The Docket Office, Docket No. H-122, Room N-2625, U.S. Department 
of Labor, 200 Constitution Avenue, NW., Washington, DC 20210, Telephone 
No. (202) 219-7894. (Any information not contained on disk, e.g., 
studies, articles, etc., must be submitted in quadruplicate.)
    Notices of intention to appear and testimony and evidence are to be 
submitted in quadruplicate to: Mr. Tom Hall, Division of Consumer 
Affairs, Occupational Safety and Health Administration, 200 
Constitution Avenue, NW., room N3649, Washington, DC 20210; (202) 219-
8615.
    The hearing will be held in the auditorium of the U.S. Department 
of Labor, 200 Constitution Avenue, NW., Washington, DC.

FOR FURTHER INFORMATION CONTACT: Proposal: Mr. James F. Foster, 
Director of Information and Consumer Affairs, Occupational Safety and 
Health Administration, 200 Constitution Avenue, NW., room N3641, 
Washington, DC 20210; (202) 219-8151.
    Informal Hearing Information: Mr. Tom Hall, Division of Consumer 
Affairs, Occupational Safety and Health Administration, 200 
Constitution Avenue, NW., room N3649, Washington, DC 20210; (202) 219-
8615.

Table of Contents

I. Supplementary Information
    A. Events Leading to This Action
II. Health Effects
    A. Sick Building Syndrome
    B. Building-Related Illness
    1. Indoor Air Contaminants
    2. Microbial Contaminants
    C. Environmental Tobacco Smoke
    1. Pharmacokinetics
    (a) Absorption and Distribution
    (b) Metabolism
    2. Irritation
    3. Pulmonary Effects
    4. Cardiovascular Effects
    (a) Thrombus Formation
    (b) Vascular Wall Injury
    (c) Possible Mechanisms of Effect
    (d) Acute Heart Effects
    (e) Chronic Heart Effects
    5. Reproductive Effects
    6. Cancer
    (a) Evidence of Association
    (b) Epidemiological and Experimental Studies
    7. Genotoxicity
    8. Conclusions
    D. Case Reports
    1. Sick Building Syndrome and Building-Related Illness
    2. Environmental Tobacco Smoke
III. Exposure
    A. Sources of Indoor Air Contaminants
    B. Microbial Contamination
    C. Exposure Studies
    1. Low-level Contaminants
    2. Bioaerosols
    3. Environmental Tobacco Smoke
    (a) Chemistry
    (b) Human Activity Pattern Studies Used to Assess Workplace 
Exposure
    (c) Indoor Levels of Environmental Tobacco Smoke Constituents
    (d) Levels of Respirable Suspended Particulates and Nicotine 
Found in Field Studies
    (e) Biomarkers of Environmental Tobacco Smoke Exposure
    (f) Inadequacy of General Dilution Ventilation to Address 
Environmental Tobacco Smoke Exposure Control
IV. Preliminary Quantitative Risk Assessment
    A. Introduction
    B. Review of Epidemiologic Studies and Published Risk Estimates
    C. Data Sources
    D. OSHA's Estimates of Risk-Environmental Tobacco Smoke Exposure
    E. OSHA's Risk Estimates--Indoor Air Quality
    F. Pharmacokinetic Modeling of Environmental Tobacco Smoke 
Exposure
    1. Considerations for Selection of a Biomarker for Environmental 
Tobacco Smoke
    2. Cardiovascular Effects
    3. Carcinogenicity
    4. Evaluation of Cotinine as a Biomarker for Environmental 
Tobacco Smoke
    5. Description of Pharmacokinetic Models for Nicotine and 
Cotinine
    6. Application of Pharmacokinetic Modeling for Environmental 
Tobacco Smoke Exposure Estimation
    7. Analysis of Uncertainty
    (a) Physiological Parameters
    (b) Distribution Parameters
    (c) Kinetic Parameters
V. Significance of Risk
    A. Environmental Tobacco Smoke
    B. Indoor Air Quality
VI. Preliminary Regulatory Impact Analysis
    A. Introduction
    B. Industry Profile
    1. Affected Industries
    2. Indoor Contaminants-Sources
    3. Controlling Indoor Air
    4. Building Characteristics
    5. Profile of Affected Buildings
    6. Buildings with Indoor Air Problems
    7. Number of Employees Affected
    8. Environmental Tobacco Smoke
    (a) Smoking Ordinances and Policies
    (b) Number of Nonsmokers Working Indoors
    C. Nonregulatory Alternatives
    1. Introduction
    2. Market Imperfections
    3. Alternative Nonregulatory Options
    (a) Tort Liability
    (b) Workers' Compensation
    4. Conclusion
    D. Benefits
    1. Indoor Air Quality
    2. Environmental Tobacco Smoke
    3. Cost Savings
    (a) Worker Productivity
    (b) Property Damage, Maintenance and Cleaning Costs
    E. Technological Feasibility and Compliance Costs
    1. Technological Feasibility
    2. Compliance Costs
    (a) Developing Indoor Air Quality Compliance Programs
    (b) Indoor Air Quality Operation and Maintenance Program
    (c) Training for HVAC Maintenance Workers and Informing 
Employees About the Indoor Air Quality Standard
    (d) Compliance with Related Standards
    (e) Air Contaminant-Tobacco Smoke
    (f) Air Quality During Renovation and Remodeling
    F. Economic Impact and Regulatory Flexibility Analysis
    1. Economic Feasibility
    2. Regulatory Flexibility Analysis
    3. Environmental Impact
VII. Summary and Explanation
    A. Scope and Application: Paragraph (a)
    B. Definitions: Paragraph (b)
    C. Indoor Air Quality Compliance Program: Paragraph (c)
    D. Compliance Program Implementation: Paragraph (d)
    E. Controls for Specific Contaminant Sources: Paragraph (e)
    F. Air Quality During Renovation and Remodeling: Paragraph (f)
    G. Employee Information and Training: Paragraph (g)
    H. Recordkeeping: Paragraph (h)
    I. Dates: Paragraph (i)
    J. Appendices: Paragraph (j)
    K. Specific Issues
VIII. State-Plan Standards
IX. Federalism
X. Information Collection Requirements
XI. Public Participation
XII. List of Subjects in 29 CFR Parts 1910, 1915, 1926, and 1928
XIII. Authority and Signature
XIV. Part 1910, 1915, 1926, 1928--Proposed Occupational Safety and 
Health Standards

Supplementary Information

A. Events Leading to This Action

    Concern about the health hazards posed by occupational exposure to 
environmental tobacco smoke (ETS) prompted three public interest groups 
to petition the Agency in May 1987 for an Emergency Temporary Standard 
under section 6(c) of the Occupational Safety and Health (OSH) Act, 29 
U.S.C. 655(c). The American Public Health Association and Public 
Citizen submitted a joint petition; Action on Smoking and Health (ASH) 
also submitted a petition. The petitions requested the prohibition of 
smoking in most indoor workplaces.
    OSHA determined, that available data with respect to exposures were 
insufficient to demonstrate the existence of a ``grave danger,'' within 
the meaning of section 6(c) of the OSH Act, from workplace exposure to 
ETS. OSHA denied the petitions in September 1989 but continued to 
investigate regulatory options.
    In October 1989 ASH filed suit in the U.S. Court of Appeals for the 
District of Columbia Circuit for review of OSHA's denial of its 
petition for an Emergency Temporary Standard. The court denied ASH's 
petition for review in May 1991, finding that OSHA has reasonably 
determined that it could not sufficiently quantify the workplace risk 
associated with tobacco smoke to justify an Emergency Temporary 
Standard.
    OSHA issued on September 20, 1991, a Request for Information (RFI) 
(56 FR 47892) on indoor air quality problems, in order to obtain 
information necessary to determine whether it would be appropriate and 
feasible to pursue regulatory action concerning Indoor Air Quality 
(IAQ). Issues on which comments were requested in the RFI included 
health effects attributable to poor IAQ, ventilation systems 
performance, exposure assessment, and abatement methods. Information 
concerning specific contaminants such as ETS and bioaerosols was also 
requested.
    In March 1992, the AFL-CIO petitioned OSHA to promulgate an overall 
IAQ standard. OSHA responded in May 1992 that such a standard was under 
consideration.
    In response to the RFI, over 1,200 comments were submitted by 
interested persons, groups, unions, and industries. Issues of 
particular concern identified in the comments, in addition to health 
effects considerations, include the lack of ventilation performance 
standards; the lack of worker training on the operation and maintenance 
of Heating Ventilation and Air Conditioning (HVAC) systems; the lack of 
pollutant source control; and the lack of available technical guidance 
on IAQ issues and control techniques.
    Of the comments that specifically addressed the question of whether 
OSHA should regulate IAQ, a majority (75%) indicate support for 
regulation. Of those that commented on the need for regulation, 
approximately 21% were explicitly in favor of a regulation on ETS, more 
than 41% were in favor of an overall IAQ regulation, and approximately 
13% were in favor of a combined IAQ regulation.
    Numerous comments focused on the adverse health effects of tobacco 
smoke and of general indoor air pollution. The health effects of 
concern relevant to both tobacco smoke and indoor air pollutants ranged 
from the acute irritant effects to cancer.
    Comments submitted in response to the RFI indicated wide support 
for a regulatory approach that would focus on the design, operation and 
maintenance of building ventilation systems, source reduction 
methodology, and worker information and training programs. Commenters 
also recommended that provisions should require that employers receive 
training about the regulation and the need for compliance, and that 
their training regarding building HVAC maintenance and operation be 
tailored to the level of complexity of the HVAC system and their 
personal degree of involvement.
    Many commenters particularly felt that regulation of IAQ was 
necessary to eliminate exposures to ETS in the workplace. Commenters 
urged the Agency to either ban smoking completely from the workplace or 
allow smoking only in separately ventilated, designated smoking areas 
that were separate from work areas.
    OSHA believes that data submitted to the record, and other 
evidence, support the conclusion that air contaminants and other air 
quality factors can act to present a significant risk of material 
impairment to employees working in indoor environments. Adverse health 
effects associated with poor IAQ may include sensory irritation, 
respiratory allergies, asthma, nosocomial infections, humidifier fever, 
hypersensitivity pneumonitis, Legionnaires' disease, and the signs and 
symptoms characteristic of exposure to chemical or biologic substances 
such as carbon monoxide, formaldehyde, pesticides, endotoxins, or 
mycotoxins.
    The Agency believes that available data support proposing 
regulation of IAQ, including exposure to ETS. Further stimulus for this 
determination was provided by conclusions reached in a report published 
in December, 1992 by the Environmental Protection Agency, addressing 
hazards associated with exposure to ETS. In that study, Respiratory 
Health Effects of Passive Smoking: Lung Cancer and Other Disorders [Ex. 
4-311], EPA concluded that exposure to ETS presents an excess risk of 
induction of cancer in humans. OSHA has submitted this proposed 
standard to the U.S. Environmental Protection Agency which is reviewing 
it in detail for purposes of submitting detailed comments to the 
docket.
    For the reasons noted above, and discussed in the following 
sections, OSHA is proposing to address indoor air quality problems, 
including exposure to ETS, as set forth in this notice.

II. Health Effects

    Indoor air quality problems can occur in all types and ages of 
buildings; in newly constructed buildings, in renovated or remodeled 
buildings, and in old buildings. Problems in new, clean buildings are 
rarely, if ever, related to microbial growth, since the physical 
structures are new [Ex. 3-61]. Older buildings that have not been 
adequately maintained and operated may have problems with bioaerosols 
if parts of the building have been allowed to become reservoirs for 
microbial growth. Also, if inadequate outside air is provided, 
regardless of the age of the building, chemical and biological 
contaminants will build up to levels that can cause health effects in 
some workers. In addition, other physical factors such as lack of 
windows, noise, and inadequate lighting, and ergonomic factors 
involving uncomfortable furniture and intensive use of video display 
units, etc., will cause discomfort in occupants that may be 
inaccurately attributed to air quality.
    Some information contained in the docket indicates that these 
chronic health complaints are psychological, however, OSHA believes 
that chronic health complaints related to poor indoor air quality are 
unlikely to be due to mass psychogenic illness, even though a 
psychological overlay is common. It is true that poor management, 
boring work, poor lighting conditions, temperature variations, poor 
ergonomic design, and noise may all lower the threshold for complaint. 
Nevertheless, air quality complaints usually have some basis, although 
they are often difficult to assess with specificity [Exs. 3-61C, 4-
144].
    Indoor air quality problems are generally classified as Sick 
Building Syndrome (SBS) or Building-related Illness (BRI). However, a 
very important constituent of poor indoor air quality is ETS because of 
the serious health effects that result from exposure. The following 
discussion will first identify the health effects associated with SBS 
and BRI. A discussion of the health effects associated with exposure to 
ETS will follow.
    It is important to note that OSHA considers these health effects to 
be material impairments of health when the worker is clinically 
diagnosed with a condition that is either caused or aggravated by poor 
indoor air quality in the workplace. For example, in the formaldehyde 
standard (29 CFR 1910.1048) [Ex. 4-107] OSHA determined that a 
physician's diagnosis of irritation met the requirement of material 
impairment of health. In addition, OSHA considers all the other health 
effects discussed, which are more clinically severe than irritation, to 
be material impairments of health as well.

A. Sick Building Syndrome

    Typically, health effects caused by poor indoor air quality have 
been categorized as SBS or BRI. In 1983, the World Health Organization 
published a list of eight non-inclusive symptoms that characterize Sick 
Building Syndrome [Ex. 4-325]. These include irritation of the eyes, 
nose and throat; dry mucous membranes and skin; erythema; mental 
fatigue and headache; respiratory infections and cough; hoarseness of 
voice and wheezing; hypersensitivity reactions; and nausea and 
dizziness. Generally, these conditions are not easily traced to a 
specific substance, but are perceived as resulting from some 
unidentified contaminant or combination of contaminants. Symptoms are 
relieved when the employee leaves the building and may be reduced or 
eliminated by modifying the ventilation system. Comments to the docket 
indicate that such symptoms have been observed in and reported by 
workers [Exs. 3-446, 4-87].
    In some instances, outbreaks of SBS are identified with specific 
pollutant exposures, but in general only general etiologic factors 
related to building design, operation and maintenance can be identified 
[Ex. 4-274]. In 1987, Woods et al. [Ex. 3-745] conducted a stratified 
random telephone survey of 600 U.S. office workers across the national. 
Twenty four percent reported that they were dissatisfied with the air 
quality at the office; while 20% perceived their performance to be 
hampered by poor indoor air quality. Women were nearly twice as likely 
to report a productivity effect of poor indoor air quality than men 
(28% versus 15%). Based on this, Woods et al. [Ex. 3-745] hypothesized 
that 20% of U.S. office workers are exposed to indoor conditions which 
manifest as SBS. In fact, complaints about SBS have become so numerous 
that 37 out of 53 states and territories have designated a building 
complaints investigation contact person [Ex. 4-310].
    Breysse [Ex. 4-32] reported on symptoms associated with new 
carpeting in a state office building, in order of prevalence: headache, 
eye and throat irritation, nausea, dizziness, eye tearing, chest 
tightness, diarrhea, cough, muscle aches, burning nose, fatigue, dark 
urine, and rashes. Twenty out of 35 persons were affected. Air sampling 
was conducted before and after carpet removal; a similar range of 
aliphatic hydrocarbons was found after removal, but in much lower 
concentrations. Many individuals who believe the building they work in 
is implicated in SBS, have described similar effects. Symptoms usually 
include one or more of the following: mucous membrane (eye, nose, or 
throat) irritation, dry skin, headache, nausea, fatigue, and lethargy 
[Ex. 4-293]. These symptoms are generally believed to result from 
indoor air pollution. There is no secondary spread of symptoms to 
others outside the building who are exposed to the occupants (unlike 
the situation faced by many chemical and asbestos workers). Anderson 
[Ex. 4-10] suggested the possible causes for SBS as related to 
psychosocial, chemical, physical, or biological factors.
    Anderson [Ex. 4-10] distinguished SBS symptoms as different from 
mass psychogenic illness; although in general the causes of SBS are 
unknown, he suggested that most SBS symptoms could be explained by 
stimulation of sensory nerve fibers in the upper airways and the face 
(referred to as common chemical sense). Because these fibers can 
respond in only one way, SBS cases largely have the same symptoms 
irrespective of the cause [Ex. 4-10].
    It is now known that there is a variety of important health effects 
from indoor air pollution. In addition to the indoor environmental 
disease caused by infectious agents, carcinogens or toxins; the indoor 
environment may create conditions that can produce skin and mucosal 
allergy and hyperactivity reactions, sensory effects (odors and 
irritations), airways effects (from both acute and chronic exposures), 
neuropsychological effects, and psychosocial effects, especially due to 
the lack of social support [Ex. 4-200].
    Indoor air pollution may be caused by physical, chemical, or 
microbiological agents, and is aggravated by poor ventilation. The 
causation of SBS by indoor air pollution was first objectively 
demonstrated in 1984 in a study of 62 Danish subjects suffering from 
``indoor climate symptoms'' [Ex. 4-20]. These subjects reported 
primarily eye and upper respiratory irritation, but were otherwise 
healthy individuals, and did not suffer from asthma, allergy, or 
bronchitis. The subjects were exposed to a mixture of 22 volatile 
organic chemicals commonly found in the indoor environment at 
concentrations of 0, 5, and 25 mg/m3. These concentrations 
corresponded respectively to ``clean'' air, average polluted air in 
Danish houses, and maximum polluted air in Danish houses. After 
exposure, the Digit Span test was administered. The Digit Span test 
consists of the subject being allowed to view a series of random digits 
for a short period of time; the numbers are then covered up and the 
subject asked to repeat the sequence backwards. This test is reported 
to be sensitive to situational anxiety and alertness, and therefore a 
measure of stress and ability to concentrate. Bach et al. found 
significant declines in performance on the digit span test following 
exposure to these low levels of volatile organic chemicals, 
demonstrating objectively the existence of SBS [Ex. 4-20].
    Molhave et al. [Ex. 4-228], in reporting on the same 62 subjects, 
found that subjects exposed for 2\3/4\ hrs did not adapt, and that the 
subjects reacted to irritation of the mucous membranes and not to odor 
intensity. The exposure was doubled-blind, and neither the subjects nor 
the testers knew the exposure.
    Although these problems have been demonstrated to be real, they may 
affect only a small percentage of building occupants. Also, there are 
various degrees of problems which may occur. Some individuals who 
experience relatively mild and treatable symptoms such as headache, may 
be able to cope with the sick building environment for extended 
periods, although suffering from increased stress. Other individuals, 
more seriously affected, may find symptoms so severe that they may be 
unable to be in the building for extended periods, or at all. Still 
others may become temporarily or permanently disabled.
    It has been suggested that SBS may not be one syndrome but a number 
of sub-syndromes [Ex. 4-170]. This hypothesis suggests that the 
symptoms particularly associated with chemical exposure include 
fatigue; headache; dry and irritated eyes, nose, and throat; and 
sometimes include nausea and dizziness. Those symptoms most related to 
microbial exposures would result in itchy, congested, or runny nose; 
itchy watery eyes; and sometimes include wheezing, tight chest, or flu-
like symptoms. The overlapping symptoms in each case are eye, nose, and 
throat irritation, perhaps making the two sub-syndromes, chemical and 
microbial, difficult to distinguish. Jones concludes that there is a 
need for a treatment protocol as well as a diagnostic protocol, which, 
in addition to describing corrective actions available in response to 
different diagnostic findings, would also provide guidelines for the 
design and implementation of follow-up studies of buildings and 
individuals in order to assess treatment effectiveness [Ex. 3-170].
    Randolph and Moss [Ex. 4-258] have written about a number of 
problems ascribed to indoor air pollution in the chemically sensitive 
patient. These problems include irritability from natural gas fumes, 
allergy to dust from forced air ventilation systems, intoxication and 
even hallucination from paint fumes. Randolph describes chemical 
sensitivity to dry cleaning chemicals, and rug shampoo, and implicates 
moldy carpets in producing allergenic substances. He also describes 
joint pain, malaise, and fatigue due to pesticide exposure; and skin 
rashes from exposure to plasticizers. Randolph further describes 
intolerance to highly scented products such as deodorant soaps, toilet 
deodorants, and disinfectants, especially pine-scented ones. Other 
patients have reported reacting to strong perfumes and other cosmetics. 
So-called air fresheners often prove to be particularly troublesome. He 
also describes that some patients are sensitive to the odors from hot 
plastic-coated wires in electronic equipment.
    There is little data on the perceptions of victims of SBS. Shapiro 
[Ex. 4-282] has complied a summary of 16 case-histories of SBS in the 
victims' own words. It is useful to review these for insight into the 
problems from the victims' point of view.
    One episode that Shapiro [Ex. 4-282] reported on was in a building 
occupied by a government agency. As a result of problems related to 
carpeting and other suspected causes, five workers were reported to 
have left the agency, 11 were relocated to alternative workspace or 
worked at home, and 100 reported to the agency's medical officer that 
they had SBS related problems. The range of self-reported symptoms 
included a variety of moderate and acute respiratory problems; 
headache; sore throat; burning of the eyes, lungs, and skin; rashes; 
fatigue; laryngitis; clumsiness; disorientation; loss of balance; 
nausea; numbness in extremities and face; and difficulty with mental 
tasks.
    The patient's reported that the diagnoses of the occupational 
health physicians they visited included upper and lower respiratory 
irritation, intoxication-type syndrome, occupational asthma, and 
chronic hypersensitivity pneumonitis.
    The central nervous system effects reported by many do not lend 
themselves to ready diagnosis [Ex. 4-282]. Some of the lesser affected 
individuals either saw no physician at all or saw a family doctor or 
allergist who was not familiar with occupational or environmental 
health [Ex. 4-282].
    The Air Force Procedural Guide [Ex. 4-199] on dealing with SBS 
takes a practical view: ``* * * in most cases the sick building 
syndrome does not have a clearly understood etiology and many of the 
SBS studies and investigations were inconclusive. The significance of 
exposure that [what chemical or physical agent concentrations cause 
symptoms] can be pathogenic remains unanswered, but the realities of 
worker complaints and discomfort are valid reasons to seriously address 
this problem.''
    In summary, SBS is not a well-defined disease with well-defined 
causes. It appears to be a reaction, at least in part due to 
stimulation of the common chemical sense, to a variety of chemical, 
physical or biological stimuli. Its victims display all or some of a 
pattern of irritation of the mucous membranes, and the worst affected 
individuals have neurological symptoms as well.

B. Building-Related Illness

    Building-related illness (BRI) describes specific medical 
conditions of known etiology which can often be documented by physical 
signs and laboratory findings. Such illnesses include sensory 
irritation when caused by known agents, respiratory allergies, 
nosocomial infections, humidifier fever, hypersensitivity pneumonitis, 
Legionnaires' disease, and the symptoms and signs characteristic of 
exposure to chemical or biologic substances such as carbon monoxide, 
formaldehyde, pesticides, endotoxins, or mycotoxins [Exs. 3-61, 4-144]. 
Some of these conditions are caused by exposure to bioaerosols 
containing whole or parts of viruses, fungi, bacteria, or protozoans. 
These illnesses are often potentially severe and, in contrast to SBS 
complaints, are often traceable to a specific contaminant source, such 
as mold infestation and/or microbial growth in cooling towers, air 
handling systems, and water-damaged furnishings. Symptoms may or may 
not disappear when the employee leaves the building. Susceptibility is 
influenced by host factors, such as age and immune system status. 
Mitigation of building-related illnesses requires identification and 
removal of the source, especially in cases involving hypersensitivity 
responses.
1. Indoor Air Contaminants
    Comments submitted to the docket in response to the RFI and 
contained in the literature indicate that specific substances or 
classes of substances have been implicated as contributing to poor 
indoor air quality problems. These substances, either alone or in 
synergy, have produced health effects that OSHA believes can be 
considered material impairment [Ex. 4-124]. In most cases, people 
likely to be at risk have specific susceptibility.
    But such susceptibility is common and adverse effects can arise 
suddenly following exposure. The relevant effects can be categorized 
into six categories: irritation, pulmonary, cardiovascular, nervous 
system, reproductive, and cancer.
    Common chemical sense or irritation perception is mediated through 
receptors found not only throughout the nasal, pharyngeal, and 
laryngeal areas of the respiratory system but also on the surface of 
the eyes, specifically the conjunctiva and cornea [Ex. 4-239]. It is 
partially through the stimulation of these receptors that exposed 
persons perceive irritation. Many comments to the docket, from 
citizens, researchers, and indoor air consultants, raised the issue 
about the irritating effects related to known indoor air contaminants. 
The air contaminants of concern include formaldehyde [Exs. 3-14, 3-32, 
3-38, 3-188, 3-440a, 3-446, 3-575, 4-125, 4-144, 4-214], volatile 
organic compounds (VOCs) [Exs. 3-32, 3-446, 3-500, 4-145, 4-243, 4-
320], ozone [Exs. 3-14, 4-42, 4-134, 4-236, 4-237], carpet-associated 
chemicals [Exs. 3-25, 3-444D, 3-576, 4-144, 4-214], vehicle exhausts 
[Exs. 3-6, 3-63, 3-206, 3-238, 3-360, 3-437, 3-444D, 3-631, 3-659], 
combustion gases [Ex. 3-32], particulates [Exs. 3-32, 3-446, 3-500], 
man-made mineral fibers (fiberglass, glasswool and rockwool) [Ex. 4-
33], and pesticides [Ex. 3-446]. The irritation effects present as 
sensory irritation of the skin and upper airways, irritation of eye, 
nose and throat, dry mucous membranes, erythema, headache, and abnormal 
taste [Ex. 3-14, 4-33]. The pulmonary effects include upper and lower 
respiratory tract effects such as rapid breathing, fatigue, increased 
infection rate, broncho-constriction, pulmonary edema, asthma, 
allergies and flu-like symptoms. Acute exposure to low level of air 
contaminants results in primarily reversible effects, while chronic 
exposure may result in pulmonary fibrosis that can result in 
irreversible damage [Exs. 3-14, 4-33].
    These health effects were associated, as reported in many comments 
to the docket, with specific contaminants, including asbestos [Exs. 3-
38, 3-440A, 3-500], combustion gases [Exs. 3-14, 3-34, 3-440A, 3-446, 
3-500], formaldehyde [Exs. 3-32, 3-38, 3-188, 3-440A, 4-124], ozone 
[Exs. 4-42, 4-237], VOCs [Ex. 3-32], vehicular exhaust [Ex. 3-63], and 
particulates [Exs. 3-32, 3-38, 3-440A, 3-500].
    Individuals with underlying pulmonary disease, such as asthma, are 
more susceptible than others to acute exposure to these indoor air 
contaminants and experience coughing and wheezing at low levels of 
exposure. Synergism may occur between chemical contaminants, such as 
ozone and VOCs, in aggravating asthma [Ex. 4-33]. These affected 
individuals may also be at increased risk of pulmonary infections due 
to the synergistic effect between chemical and microbial contaminants 
[Ex. 4-33].
    Cardiovascular effects have also been associated with poor indoor 
air quality. These effects are presented as headache, fatigue, 
dizziness, aggravation of existing cardiovascular disease, and damage 
to the heart. These effects are associated with exposure to combustion 
gases such as carbon monoxide [Exs. 3-38, 3-440A], VOCs [Ex. 3-500], 
and particulates [Ex. 3-500].
    Nervous system effects have also been produced due to exposure to 
poor indoor air quality. These effects include headache, blurred 
vision, fatigue, malaise with nausea, ringing in the ears, impaired 
judgement, and polyneuritis. These effects are associated with exposure 
to carbon dioxide [Ex. 3-14], carbon monoxide [Exs. 3-32, 3-38, 3-446, 
3-500], formaldehyde [Exs. 3-32, 3-38, 3-446, 3-500], and VOCs [Exs. 3-
32, 3-446, 3-500].
    Relevant reproductive effects include menstrual irregularities and 
birth defects and are associated with exposure to formaldehyde [Exs. 3-
446, 3-500] and VOCs [Exs. 3-446, 3-500].
    The occurrence of cancer has also been attributed to exposures 
associated with poor indoor air quality. In particular, cancer of the 
lung, including mesothelioma, esophagus, stomach, and colon have been 
associated with exposure to asbestos [Exs. 3-6, 3-14, 3-38, 3-188, 3-
440A, 3-500], radon [Exs. 3-35, 3-38, 3-188, 3-440A, 3-500], vehicular 
exhausts [Exs. 3-84, 3-206, 3-360H], combustion gases [Ex. 3-500], VOCs 
[Exs. 3-446, 3-500, 4-294], and particulates [Ex. 3-500].
2. Microbial Contamination
    Building-related illnesses can result in serious illness and death. 
Indoor transmission of disease caused by obligate pathogens (microbes 
that require a living host) is common in indoor environments, 
especially those that are overcrowded and inadequately ventilated [Ex. 
4-33]. Diseases in this category include influenza, rhinovirus or 
colds, and measles. Indoor transmission of disease caused by 
opportunistic microorganisms usually affects compromised individuals, 
those with existing conditions that make them more susceptible to 
infection, such as pulmonary disease or immunodeficiency. Legionnaires' 
disease, pulmonary tract infections, and humidifier fever are diseases 
that fall into this category. Diseases that affect the immune system 
include allergic reactions, as seen in antibody-mediated responses 
(asthma and rhinitis) and interstitial lung disease, as seen in cell-
mediated reactions (hypersensitivity pneumonitis) [Ex. 4-33]. All of 
these diseases produce substantial amounts of illness each year [Exs. 
4-33, 4-41, 4-214].
    In the U.S., Legionnaires' disease is considered to be a fairly 
common, serious form of pneumonia. The Legionella bacterium is one of 
the top three bacterial agents in the U.S. which causes sporadic 
community-acquired pneumonia. Because of the difficulty in clinically 
distinguishing this disease from other forms of pneumonia, many cases 
go unreported. Although approximately 1,000 cases are reported to the 
Centers for Disease Control and Prevention annually, it has been 
estimated that over 25,000 cases of the illness actually occur. This 
disease burden is estimated to result in over 5,000 to 7,000 deaths per 
year [Ex. 4-41]. Brooks et al. [Ex. 4-33] reported that as many as 
116,000 cases occur each year. Of these cases, it is estimated that 
between 35,000 and 40,000 die. The attack rate for L. pneumophila 
ranges from 0.1 to 5%. The case fatality rate ranges from 15 to 20% 
[Ex. 4-214].
    Two serious allergic or hypersensitivity diseases are asthma and 
hypersensitivity pneumonitis (extrinsic allergic alveolitis). An 
estimated 3% of the U.S. population suffers from asthma (approximately 
9,000,000 people) [Ex. 4-41]. These individuals may be more susceptible 
to bioaerosol contamination or chemical contamination of the indoor 
environment.
    Hypersensitivity pneumonitis is triggered by recurrent exposure to 
microbials, fumes, vapors, and dusts [Ex. 4-33]. The lung interstitium, 
terminal bronchioles, and alveoli react in an inflammatory process that 
can organize into granulomas and progress to fibrosis. The symptoms of 
acute episodes of this disease are malaise, fever, chills, cough and 
dyspnea. The symptoms of chronic episodes are serious respiratory 
symptoms such as progressive dyspnea. Chronic disease can lead to 
irreversible pulmonary structural and functional changes [Ex. 4-33].
    Approximately 15% (20,250) of 135,000 hospital admissions per year 
that last an average of more than eight days are due to allergic 
disease [Ex. 4-41]. Burge and Hodgson estimate that these 
hospitalizations cost five million work days per year. The prevalence 
of symptoms consistent with hypersensitivity pneumonitis, an 
interstitial lung disease caused by organic dusts or by aerosols has 
been examined in subpopulations at well-defined, increased risk, such 
as farmers (0.1-32%) or pigeon breeders (0.1-21%) [Exs. 4-41, 4-214]. 
The only unbiased source of complaint rates in unselected office 
workers are control buildings used in the study of hypersensitivity 
pneumonitis in the U.S. Arnow et al. [Ex. 4-15] reported complaints 
consistent with hypersensitivity pneumonitis in 1.2 percent and Gamble 
et al. [Ex. 4-116] in 4 percent of these populations. Since no clinical 
data are available, it is not known how these complaints are related to 
actual disease, and it is unknown whether these complaints are 
associated with lost work time, doctor visits or hospital admissions 
[Ex. 4-41].
    Humidifier fever, a less serious variant of hypersensitivity 
pneumonitis, also is caused by exposure to microorganisms contained in 
an aerosol. Attack rates in building epidemics have been as high as 
75%, whereas complaint rates are usually 2-3% in nonepidemic situations 
[Ex. 4-41]. Because of the similarity of the individual symptoms to 
other diseases (fever, headache, polyuria, weight loss and joint pain), 
it is often difficult to separate actual disease from complaints 
related to the common cold in nonepidemic situations [Exs. 4-33, 4-41]. 
While rare, a workplace epidemic of humidifier fever can virtually shut 
down an entire building, and only removal of the contamination will end 
the epidemic [Exs. 4-41, 4-144, 4-214].
    Microbial contamination of building structures, furnishings, and 
HVAC system components contribute to poor indoor air quality problems, 
especially those related to building-related illnesses. OSHA believes 
that consequent health effects constitute material impairment of health 
[Exs. 3-61, 4-41]. These can be categorized as irritation, pulmonary, 
cardiovascular, nervous system, reproductive, and cancer effects.
    Irritation effects, either from the physical presence of 
bioaerosols or from exposure to VOCs released by biologicals, have been 
demonstrated in susceptible workers [Ex. 3-32]. In addition, water 
leakage on furnishings or within building components can result in the 
proliferation of microorganisms that can release acutely irritating 
substances into the air. Typically, where microorganisms are allowed to 
grow, a moldy smell develops. This moldy smell is often associated with 
microbial contamination and is a result of VOCs released during 
microbial growth on environmental substrates [Ex. 4-41].
    Pulmonary effects which have been associated with exposure to 
bioaerosols include rhinitis, asthma, allergies, hypersensitivity 
diseases, humidifier fever, spread of infections including colds, 
viruses, and tuberculosis, and the occurrence of Legionnaire's disease 
[Exs. 3-17, 3-32, 3-38, 3-61B, 3-188, 3-440A, 3-446, 3-500, 4-41, 4-
144, 4-214].
    Building-related asthma has also recently been documented in office 
workers [Exs. 3-61, 4-43] and some case reports show it to be 
associated specifically with humidifier use. Biocides used in 
humidification systems are suspected causes of office-associated asthma 
[Ex. 4-103].
    Cardiovascular effects manifested as chest pain, and nervous system 
effects manifested as headache, blurred vision, and impaired judgment, 
have occurred in susceptible people following exposure to bioaerosols 
[Exs. 3-32, 3-446]. It has been suggested that these effects may be 
caused by VOCs released by the microbiologicals, or they may be a 
complication of related pulmonary effects.
    The development of cancer in susceptible people is possible 
following exposure to certain types of toxigenic fungi and mycotoxins. 
However, the probability of such exposures occurring in workplaces 
covered by this standard is probably limited. Mycotoxins (toxins 
produced as secondary metabolites by many fungi) are among the most 
carcinogenic of known substances, and are also acutely toxic. The 
American Conference of Governmental and Industrial Hygienists wrote 
``[t]he toxigenic fungi are common contaminants of stored grain and 
other food products and have caused well-described outbreaks of acute 
systemic toxicosis as well as specific organ carcinogenesis when such 
food is consumed * * * It appears clear that massive contamination with 
a highly toxigenic fungus strain of a site in which aerial dispersion 
of metabolic products occurred would be necessary to induce acute 
symptoms. However, considering the carcinogenicity of many fungal 
toxins, an examination of the risks of chronic inhalation exposure 
appears justified'' [Ex. 3-61].
    In summary, most of the health effects associated with SBS and BRI 
occur in indoor environments were concentrations of pollutants are much 
less than the OSHA Permissible Exposure Levels (PELs) (29 CFR 
1910.1000) [Ex. 4-3]. It is important to point out that the PELs are 
chemical-specific standards that are not only based on health effects 
but also on technological feasibility, cost restraints and a 
``healthy'' worker exposed for a 40-hour work week. In the industrial 
workplace, hazards are minimized by the use of administrative and 
engineering controls and the use of personal protective equipment. The 
nonindustrial environment, however, does not have these controls. 
Ventilation systems are designed only to remove occupant-generated 
contaminants, such as carbon dioxide and odors. These types of systems 
were not designed to dilute multiple point sources of contaminants that 
are typically found in nonindustrial workplaces (see section III). 
Unless adequate ventilation and source controls are utilized and 
adequately maintained, many of the chemical contaminants can 
concentrate to levels that induce symptoms. The possibility exists that 
synergistic effects occur. These effects occur not only between 
substances to enhance their toxicity but also by lowering the 
resistance to lung infection in susceptible persons.

C. Environmental Tobacco Smoke

    ETS is composed of exhaled mainstream and sidestream smoke. The 
chemical composition and exposure sources of ETS are described in the 
Exposure section of this preamble (see Section III). The 
pharmacokinetics of ETS have been widely studied and are described in 
the following section.
    A wide spectrum of health effects have been associated with 
exposure to ETS. These effects include mucous membrane irritation, 
decrease in respiratory system performance, adverse effects on the 
cardiovascular system, reproductive effects, and cancer. The following 
section also presents more detailed information on these health 
effects.
1. Pharmacokinetics
    Whether a chemical elicits toxicity or not depends not only on its 
inherent potency and site specificity but also on how the human system 
can metabolize and excrete that particular chemical. To produce health 
effects, the constituents of ETS must be absorbed and must be present 
in appropriate concentration at the sites of action. After absorption, 
some of these contaminants are metabolized to less toxic metabolites 
while some carcinogens are activated by metabolism in the body. 
Available biomarkers of ETS, such as nicotine, clearly show that 
nonsmoker exposure is of sufficient magnitude to be absorbed and to 
result in measurable levels of these biomarkers. There is sufficient 
evidence in the literature to indicate that several components of 
sidestream smoke are rapidly absorbed and widely distributed within the 
body. However, the extent of absorption, distribution, retention and 
metabolism of these contaminants in the body depends upon various 
physiological and pharmacokinetic parameters that are influenced by 
gender, race, age and smoking habits of the exposed individuals. These 
parameters and others may result in differences in susceptibility among 
exposed subpopulations. Nicotine is one of the most widely studied 
constituents of tobacco smoke. There have been numerous studies on the 
pharmacokinetics of nicotine in both animals and man.
    (a) Absorption and distribution. Absorption and distribution of 
tobacco smoke constituents are usually measured by using surrogate 
markers. A correlation between nicotine absorption and exposure to 
tobacco smoke has between demonstrated, thus making nicotine an 
appropriate marker for tobacco smoke in pharmacokinetic studies. The 
steady state volume of distribution for nicotine is large indicating 
that it is widely distributed within the body [Ex. 4-185]. Nicotine has 
been shown to bind with plasma proteins which may interfere with 
elimination and thereby prolong retention in the body. The studies in 
the docket clearly indicate that nicotine and other constituents of 
tobacco smoke are readily absorbed and distributed throughout the body 
thereby increasing the potential of producing adverse effects at more 
then one target site.
    (b) Metabolism. Nicotine is rapidly eliminated, primarily via 
metabolism and urinary excretion. The investigation of metabolism in 
vivo and in vitro, has resulted in the identification of more than 20 
metabolic products in the plasma and urine of humans and animals. The 
principle metabolic pathways of nicotine appear to involve oxidation of 
the pyrrolidine ring to yield nicotine-1'-N-oxide and cotinine, the 
latter being the major metabolite and the precursor of many of the 
metabolic products of nicotine. Some of the metabolites detected in the 
urine of rats after intravenous administration in a study by Kyerematen 
et al. [Ex. 4-185] are listed in Table II-1. In humans, cotinine is the 
major degradation product of nicotine metabolism and has a serum half-
life of about 17 hours compared to two hours for the parent compound, 
nicotine [Exs. 4-27, 4-253]. Trans-3'-hydroxycotinine in the free form 
constitutes the largest single metabolite in smokers' urine accounting 
for 35-40% of the urinary nicotine metabolite [Exs. 4-48, 4-241].
    Smokers and nonsmokers differ in their metabolism of nicotine and 
cotinine [Exs. 4-133, 4-184, 4-279]. The half-life values for urinary 
elimination of nicotine and cotinine were found to be significantly 
shorter in smokers than nonsmokers [Ex. 4-186]. Plasma nicotine 
clearance was faster in smokers than in nonsmokers in this study. More 
rapid elimination of nicotine and cotinine has been attributed to the 
inductive effects of chronic cigarette smoking on the hepatic 
metabolism of many xenobiotic agents. However, Benowitz et al. [Ex. 4-
29] were unable to confirm published research suggesting that smokers 
metabolize nicotine and cotinine more rapidly than nonsmokers.
    Variations in nicotine metabolism occur among individuals. 
Variations also occur due to differences in gender and race [Exs. 4-26, 
4-186, 4-314]. It has also been suggested that the metabolism of 
nicotine between smokers and nonsmokers may differ. Male smokers have 
been shown to metabolize nicotine faster than do female smokers after 
intravenous infusion of nicotine and active smoking. However, this 
difference was not observed by Benowitz and Jacob [Ex. 4-23] during a 
study of daily intake of nicotine in smokers versus nonsmokers. The 
metabolism of nicotine has also been studied in animals. Male rats (4 
strains) were shown to metabolize nicotine faster than did females [Ex. 
4-185].
    In summary, the potential effect of nicotine, and other ETS 
constituents in the body, is governed by interactions between several 
physiological and pharmacokinetics parameters. These interactions may 
lead to longer retention of toxic constituents, thus prolonging the 
effects on the target organs resulting in tissue injury.
2. Irritation
    Exposure to ETS is capable of inducing eye and upper respiratory 
tract irritation. Common chemical sense or irritation perception is 
mediated through receptors in the fifth, ninth, and tenth cranial 
nerves. These receptors are found throughout the nasal, pharyngeal, and 
laryngeal areas of the respiratory system and also on the surface of 
the eyes [Ex. 4-239]. It is partially through the stimulation of these 
receptors that exposed persons perceive irritation.

      Table II-1.--Urinary Excretion of Nicotine and Metabolites in Male and Female Rats After Intravenous      
                                 Administration of [\14\C]Nicotine (0.5 mg/kg)                                  
----------------------------------------------------------------------------------------------------------------
                                                               Male                           Female            
                                                 ---------------------------------------------------------------
                                                    Recovery of                     Recovery of                 
                   Metabolite                      administered    t1/2   administered    t1/2
                                                   radioactivity       (Hr)        radioactivity       (Hr)     
                                                   (percentage)                    (percentage)                 
----------------------------------------------------------------------------------------------------------------
Nicotine........................................      10.8 plus-                                                
                                                     minuse> 1.5       2.5 plus-                                
                                                                     minuse> 0.4   \1\24.0 plus-                
                                                                                     minuse> 4.6    \2\5.6 plus-
                                                                                                     minuse> 0.5
Cotinine........................................       9.3 plus-                                                
                                                     minuse> 0.8       6.0 plus-                                
                                                                     minuse> 0.6    \1\5.7 plus-                
                                                                                     minuse> 0.7    \2\6.8 plus-
                                                                                                     minuse> 0.8
Nicotine-N-oxide................................      10.8 plus-                                                
                                                     minuse> 0.9       1.6 plus-                                
                                                                     minuse> 1.4       7.8 plus-                
                                                                                     minuse> 1.4       2.6 plus-
                                                                                                     minuse> 0.3
Cotinine-N-oxide................................       8.5 plus-                                                
                                                     minuse> 1.6       7.5 plus-                                
                                                                     minuse> 0.8    \1\3.7 plus-                
                                                                                     minuse> 1.0       6.8 plus-
                                                                                                     minuse> 0.6
3-Pyridylacetic acid............................       1.8 plus-                                                
                                                     minuse> 0.3       5.8 plus-                                
                                                                     minuse> 0.3       1.2 plus-                
                                                                                     minuse> 0.2           \3\ND
3-(3-Pyridyl)--oxobutyric acid       2.7 plus-                                                
                                                     minuse> 0.6       5.3 plus-                                
                                                                     minuse> 0.9       2.4 plus-                
                                                                                     minuse> 0.7       6.0 plus-
                                                                                                     minuse> 0.6
3-Hydroxycotinine...............................       5.7 plus-                                                
                                                     minuse> 0.5       6.7 plus-                                
                                                                     minuse> 0.8       5.6 plus-                
                                                                                     minuse> 1.5       9.9 plus-
                                                                                                      minuse>1.5
-(3-Pyridyl)--                                                                                
 methylaminobutyric acid........................       4.2 plus-                                                
                                                     minuse> 0.6       5.9 plus-                                
                                                                     minuse> 0.8    \1\1.4 plus-                
                                                                                     minuse> 0.4              ND
Nornicotine.....................................       8.1 plus-                                                
                                                     minuse> 0.9       4.1 plus-                                
                                                                     minuse> 0.6       8.1 plus-                
                                                                                     minuse> 1.8    \1\8.3 plus-
                                                                                                      minuse>1.3
Demethylcotinine................................       0.8 plus-                                                
                                                     minuse> 0.1              ND            <0.3              ND
-(3-Pyridyl)--oxo-N-                                                                          
 Methylbutramide................................       1.8 plus-                                                
                                                     minuse> 0.3       3.5 plus-                                
                                                                     minuse> 0.6    \1\0.6 plus-                
                                                                                     minuse> 0.3              ND
Isomethylnicotinium ion.........................       2.1 plus-                                                
                                                         minuse>       4.5 plus-                                
                                                                     minuse> 0.7            <0.3              ND
Allohydroxydemethylcotinine.....................       2.8 plus-                                                
                                                     minuse> 0.4       9.8 plus-                                
                                                                     minuse> 1.4       1.9 plus-                
                                                                                     minuse> 0.6      10.0 plus-
                                                                                                     minuse>1.6 
                                                 ---------------------------------------------------------------
    Total.......................................      69.4 plus-                                                
                                                     minuse> 3.0  ..............      65.0 plus-                
                                                                                     minuse> 3.6  ..............
----------------------------------------------------------------------------------------------------------------
\1\0.01 0.05.                                                                                      
\2\p  0.01.                                                                                          
\3\ND, not determined; concentration too low to estimate t1/2 accurately.                              

    The ability of tobacco smoke to elicit irritation may be enhanced 
by low relative humidity and varies according to concentration [Ex. 4-
239]. Irritating components of ETS are contained in both the vapor 
phase and the particulate phase (see Tables III-6 and III-7). These 
effects have been studied in both experimental (e.g., animals studies; 
clinical and chamber studies on humans) and field (e.g., surveys and 
epidemiological studies) studies. The NRC report [Ex. 4-239] summarized 
these studies and concluded that even though the specific components of 
ETS that cause irritation were not identified, the overall effects were 
eye and throat irritation and immunological responses. Weber [Ex. 4-
317] reported the results of a field study that included 44 workrooms 
where smoking was taking place. Eye irritation was reported by 52 out 
of 167 workers. Nonsmokers reacted more than smokers to the ETS; 36 of 
the 52 workers who reported eye irritation at work were nonsmokers [Ex. 
4-317]. Asano et al. [Ex. 4-18] reported significant eye irritation, as 
measured by blinking rates, in both healthy smoking and nonsmoking 
adults following exposure to ETS. Nonsmokers reported more eye 
irritation than smokers did. Effects such as eye irritation and nasal 
stuffiness were reported to OSHA in comments to the docket [Exs. 3-38, 
3-58, 3-59, 3-188, 3-438D, 3-440A].
3. Pulmonary Effects
    Much of the literature relevant to the association between non-
cancerous health effects and ETS has focused on children. Because 
children are undergoing development and maturation, they are not 
physiologically equivalent to adults exposed to the same conditions. 
Therefore, findings in studies conducted with respect to ETS and 
children may not be directly applicable to adults. However, a number of 
studies have investigated the relationship between ETS and pulmonary 
health effects in adults.
    Studies which are restricted to adults vary by numerous factors, 
such as the population studied, the measures used to estimate exposure 
to ETS, and the physiologic and health outcomes examined. The studies 
also varied in the consideration of potential confounders. A number of 
studies have found relationships between ETS exposure and pulmonary 
health effects. These studies have: (1) used pulmonary function tests, 
which may be more sensitive than methods used in other studies, to 
detect physiological changes occurring in the small airways of the 
lungs (e.g., forced mid-expiratory flow rate (FEF25-75), and 
forced end-expiratory flow rate (FEF75-85)); (2) studied older 
populations with a longer history of exposure to ETS; (3) stratified 
the level of ETS exposure with significant findings more likely to 
occur in persons with higher exposures; and (4) more frequently found 
significant changes in lung function in men, although adverse pulmonary 
effects to ETS have also been shown in women. The following discussion 
summarizes the results of these studies [Exs. 4-18, 4-37, 4-62, 4-148, 
4-173, 4-176, 4-178, 4-180, 4-209, 4-210, 4-278, 4-295, 4-321].
    Asano et al. [Ex. 4-18] demonstrated the acute physiologic changes 
which occur as a result of exposure to ETS. Nonsmokers had more 
pronounced changes in eye blinking rates (a measure of eye irritation), 
expired carbon monoxide, increased heart rate and systolic blood 
pressure.
    Studies of ETS and chronic health effects in adults differ by how 
they define ``never smokers'', ``exsmokers'', and how other various 
levels of ETS exposure are defined, either in nominal, ordinal or 
interval scales; and whether or not they take into account exposure 
both in the workplace and at home. The potential for misclassification 
bias occurs when ``nonsmokers'' are loosely defined and used as the 
comparative group to passive smokers. Several studies considered the 
confounding impact of environmental air pollution [Ex. 4-278], indoor 
cooking fuels [Exs. 4-37, 4-62] or occupational exposures to dusts and 
fumes [Exs. 4-176, 4-178, 4-209, 4-210, 4-321].
    There have been fewer longitudinal studies [Exs. 4-148, 4-278, 4-
295] as compared to the majority which have been cross-sectional 
studies. The duration of exposure, which is critical to producing a 
measurable health effect, was quantified by number of years directly in 
several studies [Exs. 4-37, 4-148, 4-173, 4-295, 4-321], or indirectly 
by the age of the population under study [Exs. 4-176, 4-209, 4-210]. In 
those studies which had carefully assessed for level of exposure and 
had specified a duration of at least 10 years, significant pulmonary 
function decrements were noted in both men and women [Exs. 4-37, 4-148, 
4 176, 4-321]. Overall, changes in pulmonary indices are more likely to 
occur in men than in women, however, several studies have documented 
statistically significant physiological changes in pulmonary function 
occurring in women [Exs. 4-37, 4-176, 4-178, 4-321].
    Understanding the significance of findings is complicated because 
studies used a variety of measures from spirometry. Although most 
studies evaluated FVC (forced vital capacity) and FEV1 (forced 
expiratory volume in one second), fewer studies have measured 
FEF25-75 or FEF75-85 [Exs. 4-176, 4-180, 4-209, 4-210, 4-
321]. These later measures have been suggested as being more sensitive 
to detecting changes in the small airways where effects of ETS are most 
likely to occur [Exs. 4-46, 4-216, 4-230, 4-231]. However, there is no 
clear consensus in the medical literature as to the routine clinical 
use of FEF25-75 or FEF75-85, or their diagnostic value in 
independently detecting small airway disease [Ex. 4-8].
    Estimates of the decrement in FEV1 due to ETS exposure in 
passive smokers as compared to never smokers, ranges from 80 
milliliters (ml) [Ex. 4-148] to 190 ml [Ex. 4-37]. When this decrement 
is expressed as a percent of FEV1, it has been estimated to be 
5.7% in males, or 7.3% when these same subjects were matched for age 
[Ex. 4-210]. As a means of comparison, the average loss in lung volume 
per year due to aging alone is estimated to be 25 to 30 ml [Ex. 4-329]. 
The American Thoracic Society [Ex. 4-8] specifies that spirometry 
equipment have a level of accuracy within 50 ml. Since pulmonary 
function maneuvers are very effort dependent, intra-individual 
variation between the three best efforts should be within 5% to be 
acceptable. The importance of these spirometry criteria is emphasized 
by the fact that the FEV1 may result in being 100 to 200 ml lower 
than when a maximal effort is given by the subject. Furthermore, a 
decrease of 15% must be achieved before certain pulmonary indices are 
considered outside of normal limits. Given this perspective, although 
changes in pulmonary function tests may truly occur as a result of 
exposure to ETS over a number of years, the actual clinical impact may 
not be apparent in the healthy, young individual. Older individuals and 
those with preexisting pulmonary disease are more susceptible to the 
pulmonary effects of exposure to ETS.
    Outside of respiratory changes being documented through pulmonary 
function testing, other symptoms have been found to be significantly 
associated with ETS exposure. Hole et al. [Ex. 4-148] found a 
significant increase in the prevalence of infected sputum, persistent 
sputum, dyspnea and hypersecretion in passive smokers as compared to 
controls. Furthermore, rates increased as those exposed were stratified 
by level of exposure to passive smoke from low to high. Kauffmann et 
al. [Ex. 4-178] noted a significant increased risk for dyspnea in 
American (Odds Ratio (OR)=1.42) and French women (OR=1.43), and an 
increased risk for wheeze in American women (OR=1.36). Schwartz and 
Zeger [Ex. 4-278] found an increased risk for phlegm or sputum in a 3-
year longitudinal study (OR=1.41). This risk was raised to 1.76 when 
asthmatics, who may be medicated, were excluded from the analysis.
    As small airway disease progresses to chronic obstructive pulmonary 
disease (COPD) (also referred to as chronic obstructive lung disease 
(COLD)), the impact of ETS becomes more detectable. Kalandidi et al. 
[Ex. 4-173] reported an adjusted odds ratio of 2.5 (90% Confidence 
Interval (CI), 1.3 to 5.0) for Greek women never smokers exposed to 
their husbands' tobacco smoke.
    While there is a clear trend, and in several studies a 
statistically significant finding of a demonstrated decrease in 
pulmonary function indices, or an increase in respiratory symptoms in 
passive smokers, the impairment nonsmokers suffer by the exposure may 
not be immediately obvious. It is important to note that these findings 
have been demonstrated in otherwise healthy individuals. Based upon the 
finding of White and Froeb [Ex. 4-321], Fielding and Phenow [Ex. 4-102] 
have described such changes as being equivalent to those found in light 
smokers, who smoke from 1 to 10 cigarettes per day. Where a decrease of 
100 to 200 ml of FVC or FEV1 may be clinically insignificant in 
healthy persons, such a change may be significant for workers with 
already impaired pulmonary function [Exs. 3-438D, 3-440A, 4-76, 4-182]. 
These changes may be the pivotal point at which a worker becomes unable 
to continue to work.
    Cellular effects on the pulmonary tissue have also been observed in 
animals exposed to ETS during experimental studies. Several studies 
reviewed by OSHA have demonstrated that chronic cigarette smoke 
exposure produces an accumulation of alveolar macrophages (AM) (the 
presence of AM indicates a body's response to environmental insults), 
within the respiratory bronchioles of many animals species. This effect 
is similar to that seen in human smokers [Exs. 4-31, 4-58, 4-109, 4-
110, 4-140, 4-147, 4-150, 4-179, 4-212, 4-249]. Increased elastase 
secretion by alveolar macrophages from mice chronically exposed to 
cigarette smoke has also been observed [Ex. 4-322].
    Accumulation of polymorphonuclear leucocytes (PMNs) is also an 
indication of the body's response to environmental insults. PMNs were 
found in the alveolar septum of cigarette smoke-exposed hamsters, 
similar to the PMNs observed in the lungs of human smokers [Ex. 4-204]. 
In contrast to the focal nature of the alveolar macrophages 
accumulation, the accumulation of PMN is diffuse. Studies of PMN 
leukocyte function have not been systematically evaluated in smoke-
exposed animals.
    Other studies also show effects of ETS exposure at the cellular 
level. For example, young lambs exposed to ETS for one month did not 
develop detectable pulmonary system effects or alteration in lung 
mechanics or airway responsiveness. However, the lambs did develop 
inflammation of pulmonary cells [Ex. 4-290]. A cytotoxic effect of 
tobacco smoke was also demonstrated by decreased intracellular 
adenosine triphosphate (ATP) content in guinea pig alveolar macrophages 
and lowered cell bacteriocidal activity in a study by Firlik [Ex. 4-
104]).
    Exposure to tobacco smoke has been shown to increase the 
permeability of the respiratory epithelial membrane to macromolecules. 
Burns et al. [Ex. 4-45] have shown that exposure of guinea pigs to 
tobacco smoke followed by fluorescein isothiocyanate-dextran (FITC-D, 
molecular weight 10,000) increased the amount of intact FITC-D that 
crossed the respiratory epithelium into the vascular space. 
Transmission electron-microscopic studies showed that the FITC-D 
diffused across damaged type I pneumocyte membranes and cytoplasm to 
reach the basal lamina and entered the alveolar capillaries through the 
endothelial junction. Damage to alveolar epithelium was more frequent 
for the smoke-exposed animals than the room air-exposed animals.
    Aryl hydrocarbon hydroxylase (AHH) participates in the activation 
of various carcinogens, such as benzo(a)pyrene. This is one of the many 
carcinogens found in ETS. Both mainstream and sidestream smoke are 
capable of inducing pulmonary AHH activity. Gairola [Ex. 114] has 
demonstrated the induction of pulmonary AHH activity in Sprague-Dawley 
rats and male C57BL mice after exposure to either mainstream or 
sidestream smoke from University of Kentucky Reference cigarettes (2R1) 
for seven days per week for 16 weeks. However, no such induction was 
noted in Hartley guinea-pigs under similar conditions, indicating a 
species difference. The mainstream and the sidestream smoke were 
equally effective in inducing the AHH activity.
    There is consistent evidence that decrements in pulmonary function 
and increases in respiratory symptoms occur in current smokers and in 
exsmokers. However, in passive smokers these health effects are not as 
easily demonstrated. The Environmental Protection Agency's December 
1992 report, Respiratory Health Effects of Passive Smoking: Lung Cancer 
and Other Disorders [Ex. 4-311], reviewed an abundance of evidence 
showing persistent physiologic changes in children's respiratory 
function and related health effects as a result of exposure to ETS. 
Studies evaluating these same effects are not as plentiful in adults. 
However, the EPA concluded, ``recent evidence suggests that passive 
smoking has subtle but statistically significant effects on the 
respiratory health of adults'' [Ex. 4-311].
    The weight of the evidence shows that exposure to ETS results in 
decreases in pulmonary function indices and increases in respiratory 
symptoms in otherwise healthy men and women who are exposed to ETS for 
periods of 10 or more years. The risk of developing COPD appears to be 
increased in passive smokers with lifelong exposures to ETS. Whether 
these changes impact upon respiratory function to a degree that 
impairment occurs may be dependent upon the individual's pulmonary 
status and overall health condition.
4. Cardiovascular Effects
    A developing body of research indicates that the cardiovascular 
effects of ETS exposure on the health of nonsmokers include acute 
effects, such as exacerbation of angina, as well as chronic effects, 
such as atherosclerosis [Exs. 4-123, 4-291, 4-330].
    Cardiovascular diseases [Exs. 4-91, 4-136] such as myocardial 
infarction [Ex. 4-12], sudden death, and arterial thrombosis occur more 
frequently in cigarette smokers as opposed to nonsmokers [Exs. 4-86, 4-
233]. The same chemicals which produce these effects in active smokers 
are present in ETS. These include nicotine, carbon monoxide, polycyclic 
aromatic hydrocarbons (PAHs) and tobacco glycoproteins.
    The following discussion on cardiovascular effects covers thrombus 
formation, vascular wall injury and the possible mechanisms of these 
effects in nonsmokers. Discussion of the acute and chronic health 
effects follows.
    (a) Thrombus Formation. Blood clots in the coronary arteries are an 
important component of an acute myocardial infarction (MI). An 
additional component of the acute MI is the presence of atherosclerotic 
plaques in the walls of the coronary arteries. Platelets are involved 
in both the acute formation of blood clots and the chronic formation of 
atherosclerotic plaques.
    There is evidence that ETS exposure can cause platelets to become 
more easily activated thus predisposing the platelets to become 
involved in forming clots and atherosclerotic plaques. For example, 
evidence exists that demonstrates that the platelets of nonsmokers 
exposed to ETS are more easily activated [Exs. 4-40, 4-80]. The study 
by Burghuber [Exs. 4-40] demonstrates that the platelet activating 
capabilities of ETS are more prominent in nonsmokers than in smokers. 
The results of this study suggest that nonsmokers are at a greater risk 
of blood clot formation secondary to ETS exposure than smokers.
    Acute ETS exposure also results in an increased platelet 
aggregation, which is an initial stage of the development of coronary 
thrombosis or vasoconstriction. This vasoconstriction can lead to the 
development of coronary atherosclerosis after chronic exposure [Exs. 4-
111, 4-123, 4-272]. Environmental smoke exposure also can increase 
platelet-activating factor (PAF), platelet factor 4, beta-
thromboglobulin, and fibrinogen concentration which provides a marker 
of its effect on coronary heart disease [Exs. 4-85, 4-157, 4-224].
    (b) Vascular Wall Injury. Atherosclerotic plaque formation is a 
complicated chronic process that can lead to constriction of the lumen 
of the blood vessels, resulting in reduced blood supply to the 
myocardial tissues. It is thought that an essential step in plaque 
formation is injury to the endothelial lining of the arterial wall. ETS 
has been implicated in causing injury to the endothelial cells which 
line the arterial walls. This was demonstrated in the study by Davis et 
al. [Ex. 4-80] which identified an increase in the number of 
endothelial cell carcasses in the circulation of healthy people after 
being exposed to ETS.
    ETS has also been implicated in stimulating smooth muscle cell 
proliferation and in altering blood lipids. Each of these can 
contribute to plaque formation which leads to an increased 
susceptibility to heart attacks.
    (c) Possible Mechanisms of Effect. At least three mechanisms are 
described in the literature by which ETS may place stress on the heart 
by increasing myocardial oxygen demand, decreasing myocardial oxygen 
supply or interfering with the cell's ability to utilize oxygen for 
energy production.
    One mechanism by which ETS may reduce oxygen supply is through the 
formation of carboxyhemoglobin. Carboxyhemoglobin is formed when a 
person is exposed to carbon monoxide, a component of ETS. The carbon 
monoxide effectively competes with oxygen for the heme group of the 
hemoglobin molecule in the red blood cell (RBC). In fact, carbon 
monoxide has a much greater affinity for hemoglobin than does oxygen 
and binds very strongly with hemoglobin making it unavailable for the 
transport of oxygen. The heart muscle (myocardium) can experience 
injury at the cellular level when the oxygen demanded by the heart 
muscle exceeds the oxygen supplied by the blood. Therefore, the 
formation of carboxyhemoglobin can decrease the ability of the blood to 
deliver oxygen to the myocardium and can cause injury to the heart if 
myocardial oxygen demand exceeds supply.
    A number of studies have suggested that ETS exposure adversely 
affects the myocardial oxygen supply-demand relationship; this would 
predispose the heart to develop ischemia or exacerbate preexisting 
ischemia. Direct or indirect exposure to tobacco smoke has been shown 
to increase the hemodynamic determinants of myocardial oxygen demand 
[Exs. 4-13, 4-242] at the same time that it potentially reduces both 
myocardial oxygen supply and delivery by enhancing the development of 
coronary atherosclerosis [Exs. 4-242, 4-323], causing coronary 
vasoconstriction [Exs. 4-323, 4-324] and reducing the oxygen carrying 
capacity of blood through increased carboxyhemoglobin levels [Ex. 4-
13]. As a result, fewer red blood cells are available to transport 
oxygen to the body, and to the heart muscle itself. To compensate for 
this reduced oxygen carrying capacity of the blood, the heart must work 
harder, for example, by increasing the heart rate. This is an example 
of one mechanism by which ETS may place even further stress on the 
heart by increasing myocardial oxygen demand, precisely at a time when 
the oxygen delivery capabilities of the blood are reduced.
    A second mechanism by which ETS may increase myocardial oxygen 
demand is via the direct effect of nicotine. The nicotine in ETS may 
cause an increased resting heart rate and blood pressure in exposed 
individuals.
    One study examined the effects of ETS on healthy individuals during 
exercise, and found that healthy individuals experienced fatigue at 
lower work levels when exercising in the presence of ETS [Ex. 4-123]. 
The authors concluded that ETS exposure interfered with the heart 
muscle cells' ability to utilize oxygen for energy production.
    Consequently, ETS exposure may have an adverse impact on myocardial 
metabolism and expose the heart muscle to an increased susceptibility 
to injury. These mechanisms of cardiac stress and potential injury to 
the heart are in agreement with accepted theories of cardiac injury.
    (d) Acute Heart Effects. An acute effect of exposure to ETS is the 
aggravation of existing heart conditions, such as angina. The National 
Research Council (1986) reported, based on the effects of studies by 
Anderson et al. [Ex. 4-9] and Aronow et al. [Exs. 4-14, 4-16, 4-17], 
that angina patients are especially sensitive at carboxyhemoglobin 
levels between 2 and 4%. Guerin et al. [Ex. 4-129] report that 
physiologically adverse effects occur in humans at 2.5% 
carboxyhemoglobin blood content. Cumulative carbon monoxide levels, due 
to ETS that result in such an effect are not uncommon in work 
environments [Ex. 4-129]. Acute exposure to ETS has been reported to 
increase heart rate, elevate blood pressure, and increase 
carboxyhemoglobin levels in both angina patients [Exs. 3-38, 4-222] and 
in healthy subjects [Exs. 4-18, 4-217]. Acute exposure has also been 
associated with slight changes in blood components thought to be 
involved in the pathogenesis of atherosclerosis, such as endothelial 
cell count, platelet aggregate ratio, and platelet sensitivity to 
prostacyclin [Exs. 4-40, 4-80]. Many effects of ETS exposure, such as 
ischemia, may be additionally aggravated by simultaneous exposure to 
other compounds, such as solvents [Exs. 3-446, 4-99].
    (e) Chronic Heart Effects. The occurrence of coronary heart disease 
in ETS-exposed nonsmokers has been studied by various epidemiological 
researchers [Exs. 4-85, 4-120, 4-122, 4-138, 4-139, 4-142, 4-148, 4-
154, 4-191, 4-277, 4-295]. Small, but statistically significant (at p 
 0.05), increases in coronary heart disease mortality [Exs. 
4-85, 4-138, 4-139, 4-142, 4-277] indicate a modest impact of long-term 
ETS tobacco smoke exposure on the cardiovascular health of nonsmokers. 
The relative risks calculated in these studies ranged from 1.3 to 2.7.
    The ability of ETS exposure to induce coronary heart disease has 
also been studied in animals. Zhu et al. [Ex. 4-330] exposed rats to 
ETS and showed a dose-related increase in myocardial infarct size and a 
decrease in bleeding time. But there were no significant differences in 
serum triglycerides, high density lipoprotein and cholesterol. This 
study showed that air nicotine, carbon monoxide, and total particulate 
concentrations increased with ETS exposure, and this increased exposure 
led to a continuous increase in plasma carboxyhemoglobin, nicotine, and 
cotinine levels in ETS-exposed rats. There was a positive relationship 
between the infarct size and air nicotine, carbon monoxide, total 
particulate concentrations and plasma carboxyhemoglobin, nicotine, and 
cotinine levels. The average concentrations of air nicotine, carbon 
monoxide and particulates, according to the authors, were 30-fold, 3-
fold and 10- fold higher, respectively, than in a heavy smoking 
environment. The duration of exposure, however, was short compared to 
even a rat's lifetime. Infarct size nearly doubled following only 180 
hours of ETS exposure distributed over a six week period.
    In the same study, the effect of ETS exposure on platelet function 
and aortic and pulmonary artery atherosclerosis in New Zealand male 
rabbits was demonstrated. The increase of atherosclerosis after 
exposure to ETS was shown to be independent of changes in serum lipids 
and exhibited a dose-response relationship in this study. Average air 
nicotine, carbon monoxide and total particulate concentrations were 
1,040 g/m\3\, 60.2 ppm and 32.8 mg/m\3\ for high dose group 
and 30 g/m\3\, 18.8 ppm and 4.0 mg/m\3\ for low dose group and 
<1 g/m\3\, 3.1 ppm and 0.13 mg/m\3\ for the control group. 
Atherosclerosis in this study was significantly increased in the high 
dose group.
    Olsen [Ex. 245] exposed rats daily to smoke from University of 
Kentucky 2R1 Reference cigarettes for 10 minutes, 7 times a week for 4, 
8 or 20 weeks. Sidestream (SS) smoke was collected by a moving column 
of air spiked every minute with a puff of fresh mainstream (MS) smoke. 
Rats were exposed to this SS smoke collected in a 2 L/min air flow 
using a glass container placed over a burning cigarette. A fraction of 
this air flow containing SS smoke was diluted with fresh room air and 
continuously diverted to the rats as follows: 50%, 25% and 10% SS 
smoke. Carboxyhemoglobin content for each treatment group was 
determined immediately after the last smoke exposure and percent 
carboxyhemoglobin for each group was found to be: 4 week exposure-
mainstream=7.2plus-minuss>1.2 and 25% 
sidestream=11.8plus-minuss>0.7; 8 week exposure 
mainstream=6.1plus-minuss>1.2 and 25% 
sidestream=11.9plus-minuss>0.9; 20 week exposure 
mainstream=8.3plus-minuss>0.9, 10% 
sidestream=6.30plus-minuss>0.5, 25% 
sidestream=10.8plus-minuss>0.8 and 50% 
sidestream=18.3plus-minuss>1.2. This indicates a tobacco smoke-
related detrimental effect on blood components, thus increasing the 
probability that coronary disease would develop over a longer exposure 
period.
    Research has shown that passive exposure to tobacco smoke damages 
endothelial cells and increases the number of circulating anuclear 
carcasses of endothelial cells [Ex. 4-80]. ETS appears to alter cardiac 
cellular metabolism in such a way that renders the myocyte less capable 
of producing adenosine triphosphate (ATP). Reduced oxidative 
phosphorylation in cardiac mitochondrial fractions taken from rabbits 
exposed to ETS has been demonstrated [Ex. 4-130]. Studies have 
indicated that the reduction in mitochondrial respiration secondary to 
ETS exposure is likely due to decreased cytochrome oxidase activity 
[Exs. 4-130, 4-131].
    Nicotine, a component of tobacco smoke, has been shown in in vitro 
studies, to inhibit the release of prostacyclin, through inhibition of 
cyclooxygenase, from the rings of rabbit or rat aorta. Nicotine could 
also affect platelets by releasing catecholamines which lead to 
increased thromboxane A2 [Ex. 4-25]. Passive smoke also increases blood 
viscosity and hematocrit due to relative hypoxia induced by chronic 
carbon monoxide exposure [Ex. 4-25]. Nicotine, contained in cigarette 
smoke can lead to catecholamine release, which enhances platelet 
adhesiveness and decreases the ventricular fibrillation threshold. This 
threshold is also affected by carbon monoxide levels [Exs. 4-25, 4-
196]. Cigarette smoke also increases the lipolysis that increases 
levels of plasma free fatty acids, which result in enhanced synthesis 
of LDL [Ex. 4-234].
    In conclusion, there are multiple pathways by which ETS may damage 
the heart. ETS exposure has been demonstrated to both increase 
myocardial oxygen demand and decrease myocardial oxygen supply. If 
oxygen demand exceeds supply for a long enough period of time, then 
myocardial cell injury or even cell death can occur. In addition, ETS 
exposure may cause platelets to become less sensitive to the anti-
clotting regulatory substances in the blood and therefore increase the 
tendency of the blood to clot. An increased tendency for the blood to 
clot may lead to an increased susceptibility to heart attacks.
    ETS exposure may also contribute to the chronic formation of 
arterial wall plaques which are implicated in the event of an acute 
myocardial infarction. The two mechanisms described by which ETS 
exposure may stimulate plaque formation are endothelial cell injury and 
increased platelet activation.
    Different people will have different abilities to deal with the 
increased stress on the heart and the increased tendency of the blood 
to clot as a result of ETS exposure. For example, a young, otherwise 
healthy individual may be able to tolerate short-term ETS exposure 
without apparent difficulty, although asymptomatic arterial wall injury 
may occur which can contribute to cardiac injury in the future. 
However, an older person with pre-existing coronary artery disease and 
therefore minimum cardiac reserve may not be able to tolerate short-
term ETS exposure, due to the increased stress on the heart.
5. Reproductive Effects
    Data on the reproductive effects due to the exposure of nonsmoking 
pregnant women to ETS has been presented in many studies [Exs. 3-438, 
4-92, 4-132, 4-174, 4-208, 4-273, 4-285, 4-287, 4-299]. This is 
important since many nonsmoking women continue to work throughout their 
pregnancies. Pregnant women working in indoor environments without 
tobacco smoking restrictions, as in restaurants, comprise one of the 
most heavily ETS-exposed groups [Exs. 4-151, 4-287].
    Low birthweight has also been shown to be associated with paternal 
smoking, implying passive exposure to tobacco smoke by the nonsmoking 
mother [Exs. 4-92, 4-273]. Passive exposure to tobacco smoke is 
estimated to double the risk of low birthweight in a full-term baby 
[Ex. 4-208]. Nonsmoking pregnant women who are exposed to ETS have been 
reported to deliver neonates that range 24 to 120 grams lighter in 
weight than those babies delivered by nonexposed pregnant women [Exs. 
4-132, 4-174, 4-208, 4-273]. This relationship between passive smoking 
and low birthweight remains statistically significant even after 
accounting for mother's age, parity, social class, sex of baby, and 
alcohol consumption. This effect is more apparent in neonates born to 
actively smoking women who deliver babies that weigh, on average, 200 
grams less than those of nonsmoking women [Ex. 4-101]. The reduction in 
birthweight is clinically significant at the low end of the birthweight 
distribution. These infants have higher perinatal mortality [Ex. 4-
239].
    Other reproductive effects that have been ascribed to maternal ETS 
exposure include miscarriage, an increase in congenital abnormalities 
[Exs. 4-239, 4-299], and numerous other physiological effects [Ex. 4-
297]. It was reported that these effects may be part of a general 
immunosuppressive condition associated with the occurrence of low 
birthweight [Ex. 4-299]. This effect may predispose the baby to 
respiratory tract infections.
    The effects of environmental smoke exposure on the fetus may have 
long-term sequelae into childhood and adulthood [Exs. 4-53, 4-181, 4-
213, 4-225, 4-239, 4-51, 4-297]. There is limited evidence which 
suggests that growth retardation observed in the fetus is reflected in 
the growing child as reductions in lung development [3-438]. This is 
especially relevant if that child continues to be exposed to ETS 
throughout childhood and into adulthood [Exs. 4-177, 4-297]. Prenatal 
exposure to ETS and exposure to ETS as a child may also increase an 
individual's cancer risk, perhaps by a factor of two (2) [Exs. 4-65, 4-
164, 4-252].
    Experimental research on the adverse reproductive effects 
associated with ETS exposure in animals is limited. However, one study 
[Ex. 4-6] demonstrated such effects. Sciatic nerve tissue taken from 
the offspring of ETS-exposed female mice revealed definite toxic 
effects on the neonatal tissue [Ex. 4-6]. Pregnant female mice (C57BL/
KsJ) were exposed to low-tar cigarette smoke in a special smoking 
chamber. Cigarette smoke was blown into the chamber for 4 minutes, 5 
times daily, except on weekends when this was done 3 times daily. At 18 
days of gestation, blood samples were taken and carbon monoxide levels 
were measured. Ultrastructural abnormalities of fetal tissue revealed 
swollen mitochondria with distorted cristae, some indication of 
deformed mitochondria, darkened nuclei with condensations of nuclear 
material, lamellar bodies, granules and myelin bodies similar to those 
found in human toxicity studies. The blood samples from pregnant mice 
revealed a mean carbon monoxide saturation in the hemoglobin of 9% 
which is equivalent to that found in humans who actively smoke 10-20 
cigarettes per day.
6. Cancer
    Concern over the carcinogenic effects of ETS was expressed in many 
comments submitted to the docket, such as Exs. 3-32, 3-35, 3-38, 3-207, 
3-438, 3-440A, and 3-449. The results of epidemiological and 
experimental studies indicate that exposure to ETS is causally 
associated with cancer of the lung in chronically-exposed nonsmokers. A 
discussion of this evidence follows.
    (a) Evidence of Association.--The results of epidemiological 
studies taken in the aggregate suggest that nonsmoker exposure to ETS 
is causally-related to the development of lung cancer.
    Evidence of specificity of effect is provided by active smoking 
studies that report a causal association with lung cancer [Ex. 4-311]. 
It was therefore logical to examine nonsmokers with passive exposure to 
tobacco smoke, since the chemicals found in passive smoke are 
qualitatively similar to those in mainstream smoke. Active smoking 
induces all four major histological types of human lung cancer--
squamous-cell carcinomas, small-cell carcinomas, large-cell carcinomas, 
and adenocarcinomas [Ex. 4-311]. The results of lung cancer studies 
that examined the variation in tumor cell type induced by ETS exposure 
indicate that mostly adenocarcinomas and squamous cell carcinomas are 
produced by ETS exposure. Some studies have reported an excess of 
adenocarcinomas, while others have reported excesses in squamous cell 
and small-cell carcinomas. From this information, it is apparent that 
similar tumor cell types are induced by ETS exposure as are induced by 
active smoking.
    The unequivocal causal association between active tobacco smoking 
and lung cancer in humans, as well as the corroborative evidence of the 
carcinogenicity of tobacco smoke provided by animal bioassays and in 
vitro studies and the chemical similarity between mainstream smoke and 
ETS, clearly establish the plausibility that ETS is also a human lung 
carcinogen (Table II-2). In addition, biomarker studies verify that ETS 
exposure results in detectable uptake of tobacco constituents by 
nonsmokers [Exs. 4-50, 4-311].

Table II-2.--43 Chemical Compounds Identified in Tobacco Smoke for 
Which There is ``Sufficient Evidence'' of Carcinogenicity in Humans or 
Animals [Ex. 4-160]


Acetaldehyde
Acylonitrile
Arsenic
Benz (a)anthracene
Benzene
Benzo (a)pyrene
Benzo(b)fluoranthene
Benzo (k)fluoranthene
Cadmium
Chromium VI
DDT
Dibenz(a,h)acridine
Dibenz(a,j)acridine
Dibenz(a,h)anthracene
Dibenzo (a,i)pyrene
Dibenzo (a,e)pyrene
Dibenzo (a,l)pyrene
Dibenzo (a,h)pyrene
Formaldehyde
Hydrazine
Lead
Nickel
N-nitrosodiethanolamine
N-nitrosodiethylamine
N'-nitrosodimethylamine
N'-nitrosonornicotine
N-nitrosopiperidine
N-nitrosodi-n-propylamine
N-nitrosopyrrolidine
N-nitrosodi-n-butylamine
ortho-toluidine
Styrene
Urethane
Vinyl chloride
1,1-dimethylhydrazine
2-nitropropane
2-napthylamine
4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
4-aminobiphenyl
5-methylchrysene
7H-dibenzo(c,g)carbazole
Indeno (1,2,3,-cd)pryene

    (b) Epidemiological and Experimental Studies. There are at least 32 
epidemiological studies that have attempted to evaluate the 
carcinogenic potential of ETS. OSHA analyzed these studies and 
determined that 14 were positive for an association [Exs. 4-36, 4-65, 
4-106, 4-119, 4-121, 4-142, 4-143, 4-153, 4-158, 4-187, 4-252, 4-275, 
4-276, 4-292, 4-300], 5 were equivocal with a positive trend [Exs. 4-4, 
4-47, 4-117, 4-122, 4-171], and 13 were equivocal [Exs. 4-35, 4-38, 4-
52, 4-118, 4-148, 4-164, 4-175, 4-183, 4-192, 4-283, 4-286, 4-296, 4-
326]. [See the Risk Assessment section for further discussion.]
    OSHA considered the consistency of the association to determine if 
the finding of the same exposure effect occurred in different 
populations and different types of studies. The great number of 
epidemiological studies available on ETS were conducted by different 
researchers, on different populations, in various countries with 
diverse study designs. This extensive amount of data increases 
confidence that the associations seen between ETS exposure and the 
development of lung cancer is externally consistent and is not due to 
artifacts or a product of some unidentified, indirect factors unlikely 
to be common to all of the studies. The fact that exposure to ETS is 
common dilutes the risk estimates derived from these studies because 
the comparison group has some exposure to ETS. A recent Centers for 
Disease Control and Prevention (CDC) report [Ex. 4-50] found that 100% 
of a subset of the National Health and Nutrition Evaluation Survey 
(NHANES) III conducted by the National Center for Health Statistics had 
detectable levels of cotinine in their bodies indicating that everyone 
in the sample had detectable exposure to tobacco smoke [Ex. 4-50]. 
Cotinine is a metabolite of nicotine and is used as a surrogate of 
exposure to tobacco smoke. This indicates that the cancer risk may 
indeed be greater since the relationship in these studies has been more 
exposed versus less exposed instead of exposed versus nonexposed.
    Many potential sources of bias, such as publication bias (the 
tendency of scientific journals to publish studies with positive 
results), misclassification bias (smokers or former smokers claiming to 
be nonsmokers), and recall bias (the reliance on self-reporting of both 
personal smoking habits and exposure to others' tobacco smoke) can not 
account for the elevation in risks seen in these various studies. Also, 
the relative risks that were estimated from prospective study data are 
similar to those estimated from case/control study data. Biases that 
may be problematic to case-control studies are not a problem in 
prospective studies. Since the results from both types of studies are 
similar it is apparent that these biases are not important in the case-
control studies (e.g., misclassification bias and recall bias). This 
information strengthens the confidence of a causal connection.
    Animal studies have shown the carcinogenicity of cigarette smoke. 
Limited existing data suggest that sidestream smoke may contain more 
carcinogenic activity per milligram of cigarette smoke concentrate than 
does mainstream smoke [Ex. 3-689D]. Currently, OSHA is aware of only a 
few experimental inhalation studies with sidestream smoke or ETS 
reported in the literature. A discussion of these studies follows.
    Otto and Elmenhorst [Ex. 4-247] have shown that there are 
carcinogenic constituents in the vapor phase of tobacco smoke. They 
exposed C57B1 and BLH mice to the gas phase of cigarette mainstream 
smoke of 12 cigarettes for 90 minutes daily over 27 months. The 
particulate matter was removed by passing the smoke through a Cambridge 
filter. The percentages of mice with lung adenomas were 5.5% and 32% in 
the smoke-exposed C57B1 and BLH mice, as compared to 3.4% and 22% for 
their respective controls. Leuchtenberger and Leuchtenberger [Ex. 4-
197] have also shown that the rate of tumors among mice exposed to the 
gas phase was greater than animals exposed to the whole smoke. 
Pulmonary adenomas and adenocarcinomas were induced in Snell's mice by 
the gas phase but not by the whole smoke in this study. These studies 
demonstrate that the carcinogenicity of tobacco smoke is not limited to 
the particulate phase.
    Studies have also reported hyperplasia and metaplasia in the 
trachea and bronchi of mice exposed to cigarette smoke by the 
inhalation route [Exs. 4-226, 4-327]. Four lung tumors and emphysema 
were detected in 100 male and female C57B1 mice exposed, nose only, to 
fresh mainstream smoke [Ex. 4-135].
    Pulmonary squamous neoplasms were detected in female Wistar rats 
exposed to a 1:5 smoke-to-air mixture for 15 seconds of every minute 
during an 11 minute exposure twice a day, 5 days per week, for the 
lifespan of the animals [Ex. 4-79]. Respiratory tumors were also 
observed in Fischer-344 rats exposed, nose only, to a 1:10 smoke to air 
mixture for approximately 30 seconds every minute, 7 hours per day, 5 
days per week for 128 weeks [Ex. 4-77]. The incidence of laryngeal 
leukoplakias in Syrian golden hamsters ranged from 11.3% for the 
animals that received the low dose to 30.6% of those animals that 
received the highest dose. These animals were exposed to a 1:7 smoke-
to-air mixture for 10 to 30 minutes, 5 days a week, nose only, for a 
period of up to 52 weeks [Ex. 4-88]. Exposing hamsters twice a day, 5 
days a week for up to 100 weeks resulted in almost 90% of the exposed 
hamsters having hyperplastic or neoplastic changes in the larynx in a 
study by Bernfeld et al. [Ex. 4-30]. Lung tumors have been reported in 
beagle dogs exposed to the smoke from nonfilter cigarettes [Ex. 4-19]. 
However, no tumors were seen in rabbits exposed to cigarette smoke for 
up to 5\1/2\ years [Ex. 4-149].
    Sidestream condensates have also been shown to cause 
carcinogenicity when implanted into female Osborne-Mendel rat lungs 
[Ex. 4-127]. Cigarette smoke condensate fraction from sidestream smoke 
was implanted at a dose level of one cigarette per animal in this 
study.
    Coggins et al. [Ex. 4-59] reported epithelial hyperplasia in the 
nasal cavity of high-dosed rats exposed to environmental tobacco smoke. 
They exposed Sprague-Dawley rats of both sexes, nose only, to ``aged 
and diluted sidestream smoke'' (ADSS) at 0.1, 1 or 10 mg of 
particulates per meter for 14 days and found ``slight to mild'' 
epithelial hyperplasia and inflammation in the most rostral part of the 
nasal cavity in the 10 mg group only. They also found that these 
changes were reversible if the animals were kept without further 
exposure for an additional 14 days. No effects in the lung were 
reported. Similar results of mild hyperplasia were also obtained when 
male rats were exposed to the same concentrations for up to 13 weeks 
[Ex. 4-60]. In this study the authors reported hypercellularity and the 
thickening of the respiratory epithelium of the dorsal nasal conchae 
and adjacent wall of the middle meatus.
    Rats are obligatory nose-breathers, and the anatomy and physiology 
of the respiratory tract and the biochemistry of the lung differ 
between rodents and humans. Because of these distinctions, laboratory 
animals and humans are likely to have different deposition and exposure 
patterns for the various cigarette smoke components in the respiratory 
system. For example, rodents have extensive and complex nasal 
turbinates where significant particle deposition could occur, 
decreasing exposure to the lung. These anatomical and physiological 
differences, aside from the subchronic exposure, may partially account 
for absence of any lung tumors in the study by Coggins et al.
    The application of cigarette smoke condensate (CSC) to mouse skin 
is a widely employed assay for the evaluation of carcinogenic 
potential. CSC assays may not, however, reveal all of the carcinogenic 
activity of actual cigarette smoke, because these condensates lack most 
of the volatile and semi-volatile components of whole smoke. Benign 
skin tumors and carcinomas were seen in Swiss-ICR mice exposed to 
cigarette tar from the sidestream smoke of nonfilter cigarettes 
suspended in acetone and applied to skin for 15 months [Ex. 4-327]. In 
lifetime rat studies, intrapulmonary implants of mainstream smoke 
condensate in a lipid vehicle caused a dose-dependent increase in the 
incidence of lung carcinomas [Exs. 4-75, 4-289].
    The polyamines contained in tobacco smoke, spermidine, spermine, 
and their diamine precursor, putrescine, are believed to have an 
essential role in cellular proliferation and differentiation. Formation 
of putrescine from ornithine is catalyzed by ornithine decarboxylase 
(ODC), the rate-limiting enzyme in polyamine biosynthesis. A 
significant increase in lung and trachea ornithine decarboxylase 
activity was observed by Olsen [Ex. 4-245] after an eight week exposure 
of male Sprague-Dawley rats to MS smoke. All dilutions of SS smoke 
exposure caused significant increase in trachea ODC activity but did 
not influence the lung ODC activity.
    Environmental tobacco smoke induced carcinogenicity is also 
supported by a case-control study of lung cancer in pet dogs [Ex. 4-
259]. The study compared the incidence of lung cancer in pet dogs 
exposed to their owners' smoking versus dogs whose owners did not 
smoke. Dogs have a very low natural incidence of lung cancer. There was 
an elevated risk of lung cancer (Relative Risk = 1.6) observed in pets 
with smoking owners. However, the analysis was statistically 
insignificant, perhaps in part due to small sample size.
7. Genotoxicity
    Short-term mutagenicity tests have gained widespread acceptance as 
an initial step in the identification of potential carcinogens. 
Extensive use of these tests has come about because they are easy to 
perform and are inexpensive and also because of the reported high 
positive correlations between short-term mutagenicity tests and 
carcinogenicity. It has been reported that 90 percent of the 
carcinogens tested are mutagens and 90 percent of the noncarcinogens 
are nonmutagens.
    Several short-term bioassays have been performed to evaluate the 
genotoxicity of cigarette smoke. While most of them have evaluated the 
effect of cigarette smoke condensate, some have attempted to evaluate 
either the gas phase or the whole smoke.
    The most commonly employed assay for mutagenic activity employs 
various strains of Salmonella typhimurium. Whole smoke as well as 
cigarette smoke condensate of tobacco have been shown to be mutagenic 
in Salmonella typhimurium strain TA 1538 [Ex. 4-21]. Sidestream smoke 
was also found to be mutagenic in a system where the smoke was tested 
directly on the bacterial plates [Ex. 4-246]. Sidestream smoke and 
extracts of ETS collected from indoor air [Exs. 4-202, 4-5, 4-198, 4-
201, 4-203] also exhibited mutagenic activity in this bacterial strain. 
Claxton et al. [Ex. 4-55] found that sidestream smoke accounted for 
approximately 60% of the total S. typhimurium mutagenicity per 
cigarette, 40% from the sidestream smoke particulates and 20% from the 
semi-volatiles. The highly volatile fraction, from either mainstream or 
sidestream smoke was not mutagenic.
    Condensates from both mainstream [Exs. 4-89, 4-193] and sidestream 
smoke [Ex. 4-90] have also been reported to have mutagenic activity. 
Doolittle et al. [Ex. 4-89] demonstrated the genotoxicity of the 
sidestream smoke from the Kentucky Reference cigarette (1R4F) by 
employing several different assays. In their study, sidestream smoke 
produced positive results in Salmonella typhimurium strains TA98, 
TA100, TA1537, and TA1538 in the presence of S9 mix from aroclor-
induced rat liver but produced negative results in strain TA1535. They 
also showed that sidestream smoke produced positive results in the 
Chinese hamster ovary cells chromosomal aberration assay and in the 
Chinese hamster ovary cell sister-chromatid exchange assay both with 
and without metabolic activation. They demonstrated that the sidestream 
smoke was weakly positive in inducing DNA repair in cultured rat 
hepatocytes. However, sidestream smoke was nonmutagenic in the Chinese 
hamster ovary cell-HGPRT assay both with and without metabolic 
activation but it was found to be cytotoxic in this system.
    In their further studies, Doolittle et al. [Ex. 4-90] observed 
similar responses when they measured the genotoxic activity of 
mainstream cigarette smoke condensate (CSC) from Kentucky reference 
research cigarette (1R4F). As seen with sidestream smoke, CSC in this 
study was mutagenic in Salmonella typhimurium strain TA98, TA100, 
TA1537, and TA1538 in the presence of S9 mix but was negative in strain 
TA1535. CSC was also positive in the Chinese hamster ovary (CHO) cells-
chromosomal aberration assay and in the CHO-sister-chromatid exchange 
assay both with and without metabolic activation. CSC was weakly 
positive in inducing DNA repair in cultured rat hepatocytes. However, 
again as seen with sidestream smoke, CSC was nonmutagenic in the CHO-
HGPRT assay, with or without metabolic activation but was found to be 
cytotoxic in this system. The results from these two studies appear to 
indicate that sidestream smoke behaves very much like mainstream smoke 
in these assays.
    Mohtashamipur et al. [Ex. 4-227] demonstrated significant mutagenic 
activity in the urine of rats exposed to sidestream smoke. In this 
study, cigarettes were machine smoked under standardized laboratory 
conditions and the sidestream smoke of two cigarettes was directed 
through metabolism cages containing rats. The urine of these rats was 
collected 24 hours prior to the SS exposure and 24 hours after the 
onset of the exposure. The individual urine samples of all (10) rats 
after exposure showed significantly higher activity for direct-acting 
mutagens (in strain TA1538) than the urine samples of the same rats 
before the exposure.
    The formation of DNA adducts is widely accepted as an initial step 
in the carcinogenesis process. The measurement of DNA adducts by the 
\32\P-postlabeling assay has been used as a way to assess DNA damage 
following exposure to cigarette smoke. Lee et al. [Ex. 4-194] exposed 
Sprague-Dawley rats to 0.1, 1.0 and 10 mg total particulate matter/m\3\ 
of aged and diluted sidestream smoke (ADSS) for 6 hours per day for 14 
consecutive days. They examined the DNA from lung, heart, larynx and 
liver after 7 and 14 days of exposure and after 14 days of recovery. 
They also examined alveolar macrophages for chromosomal aberrations. 
Exposure related DNA adducts were found in the highest dose test. 
However, no elevation in chromosomal aberrations was observed in 
alveolar macrophages in this study. Similar results were also obtained 
when animals were exposed to the same three concentrations for up to 90 
days. DNA adducts were seen in lung, heart and larynx DNA of the 
animals exposed to the highest concentration of ADSS [Ex. 4-195]. The 
adduct levels were highest after 90 days of exposure and were 
significantly reduced in all target tissues 90 days after cessation of 
exposure. Again, chromosomal aberrations in alveolar macrophages were 
not elevated in any group after 90 days of exposure. The authors 
concluded that the concentration of DNA adducts formed in the lung 
tissue did not increase linearly as the ADSS concentration was 
increased from 1 to 10 mg.
    Several short-term tests have been performed in eukaryotic systems. 
A solution of the gas phase of mainstream cigarette smoke has been 
shown to induce reciprocal mitotic recombination in Saccharomyces 
cerevisiae D3 and petite mutants in an isolate of strain D3 [Ex. 4-
163]. Whole mainstream cigarette smoke induced mitotic gene conversion, 
reverse mutation, and reciprocal mitotic recombination in strain D7 of 
Saccharomyces cerevisiae [Ex. 4-113]. Transformation of mammalian cells 
was induced in several cell systems using the cigarette smoke 
condensate from mainstream cigarette smoke [Exs. 4-22, 4-161, 4-188, 4-
267, 4-268, 4-298].
    Another in vitro assay that measures the number of sister-chromatid 
exchanges (SCEs) induced has been employed widely to determine the 
mutagenic activity of cigarette smoke. Valadand-Berrieu and Izard [Ex. 
4-313] used a solution of the gas phase from cigarette mainstream smoke 
and showed that this solution induced a significant dose-related 
increase in sister-chromatid exchanges. Putman et al. [Ex. 4-257] have 
also demonstrated dose-dependent increases in sister chromatid exchange 
frequencies in bone-marrow cells of mice exposed to cigarette smoke for 
2 weeks.
    Review of the literature clearly demonstrates that MS smoke and ETS 
exposure causes cancer in humans. These results are supported not only 
by animal studies but also by studies that show SS smoke to be both 
genotoxic and clastogenic.
8. Conclusions
    The epidemiological and clinical studies, taken in aggregate, 
indicate that exposure to environmental tobacco smoke may produce 
mucous membrane irritation, pulmonary, cardiovascular, reproductive, 
and carcinogenic effects in nonsmokers. Exposure to ETS may aggravate 
existing pulmonary or cardiovascular disease in nonsmokers. In 
addition, animal studies show that both mainstream and sidestream 
tobacco smoke produce similar adverse effects.

D. Case Reports

1. Sick Building Syndrome and Building-Related Illness
    Many case reports of material impairment of health due to 
occupational exposure to poor IAQ have been reported to OSHA through 
submission to the indoor air quality docket [H-122]. These adverse 
health effects range from irritation effects to more severe, life-
threatening building-related illnesses, such as Legionnaire's disease, 
and cancer.
    Ford Motor Company responded in docket comment 3-447, that 
``[p]resently, at Ford, we investigate an average of two IAQ complaints 
per month which are predominantly classified as Sick Building Syndrome. 
We have seen Building-Related Illness, but these incidents have been 
rare and associated with specific contaminant episodes. The IAQ 
complaints we generally investigate are characterized by general 
malaise, headache, and flu-like symptoms that are said to disappear 
when the occupants leave the building * * * Of the IAQ problems 
investigated, about 20 percent can be attributed to PTS [passive 
tobacco smoke]/ETS. Upper respiratory irritation or eye irritation 
typically are associated with these complaints.'' Similar types of 
health effects were reported to the agency in docket comments 3-1, 3-
22, 3-58, 3-142C, 3-367, 3-413, 3-529, 3-632, 3-634, 3-642, 3-659, and 
3-698.
    One comment [Ex. 3-433 reported that ``based upon approximately 30 
IAQ investigations in a member company over the past two and one-half 
years, the following adverse health effects have been reported in 
office environments: eye, nose, and throat irritations; headaches, 
nausea, dizziness, fatigue; cough, shortness of breath, chest 
tightness. These so-called ``sick building syndrome (SBS)'' symptoms 
often disappear when the person leaves the building environment. These 
symptoms are usually subjective and non-specific, lacking a physician's 
diagnosis of a definite illness.'' Others have reported [Ex. 3-377] 
that ``as air flow and ventilation are cut back, our workers are 
becoming sick. Many are exposed to contaminants or other harmful 
substances; and, without ventilation, these sources linger and cause 
nausea, skin irritations and other unhealthy symptoms of illness. In 
severe cases, these contaminants and bacteria have been known to 
contribute to upper respiratory infections.'' Comment 3-570 reported 
similar health effects due to poor indoor air quality.
    More serious health conditions have been reported ranging from 
severe asthma to central nervous systems disorders. For example, 
Comment 3-158 responded that ``I have developed a serious asthma 
condition due to indoor air quality problems. Besides, three of the 
remaining five employees at the branch office have been diagnosed with 
chronic fatigue syndrome. In conversations with various health care 
professionals, I have come to the conclusion that the diagnoses of 
chronic fatigue syndrome were actually sick building syndrome. Of the 
six employees at the branch office, four of the six are moderate to 
heavy smokers. This does not take into consideration the other factors 
that could be causing poor indoor air quality problems in the office.''
    Comment 3-631 was a collection of reports from the workers in one 
building that illustrate the poor conditions of a building that can 
lead to serious health effects in workers. Health problems experienced 
by workers in this building included chronic sinus infections; 
headaches; fatigue; eye, nose and throat irritations; difficulty 
breathing and congestion; allergies; and asthma. These health problems 
seem to clear up when the workers were out of the building over a 
weekend or a vacation.
    The physical condition of this building was obviously in disrepair 
since the commenters reported pails of stagnant water, collected from 
leaks in the roof, were left in hallways. Water in ``[t]hese pails 
ha[d] overflowed and run down the stairs. What [wa]s left in the pails 
evaporate[d] leaving a gross residue of who knows what.'' The water 
leaks from the roof caused mold infestation and water damage. Water 
logged insulation hung in the ceiling out in a hallway. There was an 
obvious lack of routine, sufficient cleaning. Dust and particulate 
matter were visible in the air. The bathrooms were dirty. Smells of 
sewer gas, mold, and diesel and other vehicular fumes permeated the 
office space. Ventilation problems were evident since paint or varnish 
fumes lingered whenever part of the inside physical structure of the 
building was painted. Tar fumes were evident from constant patching of 
the leaky roof. Insect infestation of the building was evident. 
Pesticide fumes lingered whenever the building was spray[ed] for 
roaches and steam bugs. Workers sighted cockroaches, silverfish, and 
steam bugs near the coffee shop and on back stairs. The comment 
continued that ``a sink faucet in the lunch room has been leaking for 
years and water runs on the counter under the toaster and microwave. 
The water heater had leaked for about 2 months before it was fixed. At 
that time the carpet was soaked and water was running under the wall 
into a supervisor's office. There is a moldy odor from this carpet and 
the floor below.''
    Cancer has also been reported to be associated with poor indoor air 
quality. A courthouse in San Diego, California [Ex. 3-55], ``is 
notorious for poor air quality and employee respiratory illness and 
cancer.'' It was reported to OSHA that many long-term employees have 
cancer (stomach and lung cancer), terminal lung disease, chronic ear 
and throat infections, and bronchial problems'' [Exs. 3-585, 3-635, 3-
637, 3-68].
    Comment 3-630 from a union reported that ``[a]fter surveying 
thousands of workers across the country, SEIU compiled actual survey 
responses that list adverse health effects caused by indoor air 
pollution. These include headaches, nose congestion or irritation, 
throat irritation, dry cough, dry or itchy skin, dizziness, nausea, 
lethargy or fatigue, colds, asthma/wheezing, chest tightness, runny 
nose/post nasal drip, eye or contact lens irritation, respiratory 
difficulties. In addition, EPA estimates that pollutants found in 
indoor air are responsible for 2,500 to 6,500 cancer deaths each year'' 
[refer to Ex. 3-630L].
    These concerns are not just relevant to office workers but also to 
maintenance and other nonindustrial workers that work in indoor 
environments. For example, comment 3-347 responded that ``[i]n our 
closed, indoor work environments, air quality is a very real health and 
safety concern to professional painters. I have seen firsthand 
otherwise healthy men and women pass out or get violently ill as a 
result of being exposed to indoor air contaminants.'' Comment 3-412 
responded ``[o]ur locals have encountered air-pollution problems 
ranging from ink mist and photocopier emissions to asbestos and 
microbial disease. The level of toxic chemical contaminants is often 
alarmingly high in our darkrooms, and carbon-monoxide emissions from 
trucks at newspaper loading docks frequently penetrate the ventilation 
system. In 1985 microbial contamination from a water tower infected six 
New York Times employees with Legionnaires' Disease and 34 others with 
less serious respiratory infections.''
    Operation engineers are also affected by poor indoor air quality. 
Comment 3-452 responded that ``[t]his is particularly important for the 
operation engineers who appear healthy and then suffer from respiratory 
problems, much like allergic reactions, after working in a building 
with poor ventilation.''
2. Environmental Tobacco Smoke
    Many case reports of severe material impairment of health due to 
occupational exposure to ETS have been reported to OSHA through 
submission to the indoor air quality docket [H-122]. Information 
contained in these comments indicate that adverse health effects in 
workers due to environmental tobacco smoke exposure while at work range 
from mucous membrane irritation (eye, nose, and throat effects) to more 
severe, life-threatening conditions, such as status asthma, other 
chronic lung diseases and heart diseases. For example, comment 3-309 
responded [Regarding ETS exposure in a cafeteria], ``By the time I have 
finished lunch my eyes are tearing, my nose is plugged, and I have a 
headache'' as well as comment 3-315, ``I had fewer headaches and fewer 
respiratory ailments; my chronic sore throat disappeared [after a 
company-wide no smoking policy was implemented]''. Comment 3-22 
responded ``[m]y patients find it hard to obtain smoke free workplaces. 
I have seen patients who have suffered status asthma from workplace 
smoking, patients who have had to quit their jobs because of ETS in the 
workplace. Recently, one of my never smoking patients sustained vocal 
cord lesions seen almost entirely in smokers.'' Comment 3-104 continued 
that ``[p]assive tobacco smoke (PTS) is the principal indoor air 
contaminant in my office building in Rockefeller Center. While smoking 
is limited to `private offices', the smoke flows freely from these 
private offices throughout the entire general office areas since the 
smokers will not keep their doors closed, and even when they do, they 
have to come out sometime. And, as soon as the door is opened, the 
dense smoke accumulation within the office is diffused to all adjacent 
work areas. Because office buildings have closed ventilation systems, 
only a `smoke free' office policy can be effective. Half measures only 
cause further stress, frustration and irritation to both smokers and 
nonsmokers.'' Comment 3-289 responded that ``I have been exposed to 
asbestos culminating in my getting asbestosis (plural plaque) of the 
lungs. The combination of asbestos exposure plus second-hand smoke from 
my smoking co-workers has posed and is currently posing a health risk 
to me.''

III. Exposure

    Contaminants which contribute to poor indoor air quality can be 
attributed to both outside air and inside air. Outside air contaminants 
can be introduced into a building through the ventilation intakes, 
doors, building envelope, and windows. Outside air contaminants include 
vehicular exhausts, industrial emissions, microbiologicals, and pollen. 
Inside air contaminants are emitted from building materials and 
furnishings, appliances, office equipment and supplies, biological 
organisms, and of course, pollutants introduced by the building 
occupants themselves. Inside air contaminants include tobacco smoke, 
volatile organic compounds, combustion gases such as carbon monoxide, 
and occupant-generated bioeffluents. The concentration of these 
contaminants in buildings can increase if ventilation systems are 
inadequately designed, maintained and operated or if strong local 
contaminant sources are not controlled.

A. Sources of Indoor Air Contaminants

    A wide variety of substances are emitted by building construction 
materials and interior furnishings, appliances, office equipment, and 
supplies, human activities, and biological agents. For example, 
formaldehyde is emitted from various wood products, including particle 
board, plywood, pressed-wood, paneling, some carpeting and backing, 
some furniture and dyed materials, urea-formaldehyde insulating foam, 
some cleaners and deodorizers, and from press textiles. Volatile 
organic compounds, including alkanes, aromatic hydrocarbons, esters, 
alcohols, aldehydes, and ketones are emitted from solvents and cleaning 
compounds, paints, glues, caulks, and resins, spray propellants, fabric 
softeners and deodorizers, unvented combustion sources, dry-cleaning 
fluids, arts and crafts, some fabrics and furnishings, stored gasoline, 
cooking, building and roofing materials, waxes and polishing compounds, 
pens and markers, binders and plasticizers. Pesticides also contain a 
variety of toxic organic compounds.
    Building materials are point sources of emissions that include a 
variety of VOCs (Table III-1). Some of these materials have been linked 
to indoor air quality problems. The probability of a source emitting 
contaminants is related to the age of the material. The newer the 
material, the higher the potential for emitting contaminants. These 
materials include adhesives, carpeting, caulks, glazing compounds, and 
paints [Ex. 4-33]. These materials, as well as furnishings can act as a 
sponge or sink in which VOCs are absorbed and then re-emitted later.
    Appliances, office equipment, and supplies can emit VOCs and also 
particulates [Ex. 4-33]. Table III-2 lists the many contaminants that 
can be emitted from these point sources. There is an indirect 
relationship between the age of the point source and the potential rate 
of contaminant emission [Ex. 4-33].

 Table III-1.--Emissions From Building Materials or Interior Furnishings
------------------------------------------------------------------------
              Material                    Typical pollutants emitted    
------------------------------------------------------------------------
Adhesives..........................  Alcohols.                          
                                     Amines.                            
                                     Benzene.                           
                                     Decane.                            
                                     Dimethylbenzene.                   
                                     Formaldehyde.                      
                                     Terpenes.                          
                                     Toluene.                           
                                     Xylenes.                           
Caulking Compounds.................  Alcohols.                          
                                     Alkanes.                           
                                     Amines.                            
                                     Benzene.                           
                                     Diethylbenzene.                    
                                     Formaldehyde.                      
                                     Methylethylketone.                 
                                     Xylenes.                           
Carpeting..........................  Alcohols.                          
                                     Formaldehyde.                      
                                     4-Methylethyl- benzene.            
                                     4-Phenylcyclohexene.               
                                     Styrene.                           
Ceiling Tiles......................  Formaldehyde.                      
Clipboard/Particle Board...........  Alcohols.                          
                                     Alkanes.                           
                                     Amines.                            
                                     Benzene.                           
                                     3-Carene.                          
                                     Formaldehyde.                      
                                     Terpenes.                          
                                     Toluene.                           
Floor and Wall Coverings...........  Acetates.                          
                                     Alcohols.                          
                                     Alkanes.                           
                                     Amines.                            
                                     Benzenes.                          
                                     Formaldehyde.                      
                                     Methyl styrene.                    
                                     Xylenes.                           
Paints, Stains & Varnishes.........  Acetates.                          
                                     Acrylates.                         
                                     Alcohols.                          
                                     Alkanes.                           
                                     Amines.                            
                                     Benzenes.                          
                                     Formaldehyde.                      
                                     Limonene.                          
                                     Polyurethane.                      
                                     Toluene.                           
------------------------------------------------------------------------


      Table III-2.--Emissions From Appliances, Office Equipment and     
                               Supplies\1\                              
Appliances.........................  Carbon Monoxide.                   
                                     Nitrogen Dioxide.                  
                                     Sulfur Dioxide.                    
                                     Polyaromatic hydrocarbons.         
Carbonless Copy Paper..............  Chlorobiphenyl.                    
                                     Cyclohexane.                       
                                     Dibutylphthalate.                  
                                     Formaldehyde.                      
Computers/Video Display Terminals..  n-Butanol.                         
                                     2-Butanole.                        
                                     2-Butoxyethanol.                   
                                     Butyl-2-Methylpropyl phthalate.    
Computer/Video Display Terminals...  Caprolactam.                       
                                     Cresol.                            
                                     Diisooctyl phthalate.              
                                     Dodecamethyl cyclosiloxane.        
                                     2-Ethoxyethyl acetate.             
                                     Ethylbenzene.                      
                                     Hexanedioic acid.                  
                                     3-Methylene-2-pentanone.           
                                     Ozone.                             
                                     Phenol.                            
                                     Phosphoric Acid.                   
                                     Toluene.                           
                                     Xylene.                            
Duplicating Machines...............  Ethanol.                           
                                     Methanol.                          
                                     1,1,1-Trichloroethane.             
                                     Trichloroethylene.                 
Electrophotographic Printers,        Ammonia.                           
 Photocopiers & Related Supplies.    Benzaldehyde.                      
                                     Benzene.                           
                                     Butyl methacrylate.                
                                     Carbon black.                      
                                     Cyclotrisiloxane.                  
                                     Ethylbenzene.                      
                                     Isopropanol.                       
                                     Methylmethacrylate.                
                                     Nonanal.                           
                                     Ozone.                             
                                     Styrene.                           
                                     Terpene.                           
                                     Toluene.                           
                                     1,1,1-Trichloroethane.             
                                     Trichloroethylene.                 
                                     Xylenes.                           
                                     Zinc stearate combustion Products. 
Microfiche Developers/Blueprint      Ammonia.                           
 Machines.                                                              
Preprinted Paper Forms.............  Acetaldehyde.                      
                                     Acetic Acid.                       
                                     Acetone.                           
                                     Acrolein.                          
                                     Benzaldehyde.                      
                                     Butanal.                           
                                      1,5-Dimethylcyclopentene.         
                                     2-Ethyl furan.                     
                                     Heptane.                           
                                     Hexamethyl cyclosiloxane.          
                                     Hexanal.                           
                                     4-Hydroxy-4-methyl pentanone.      
                                     Isopropanol.                       
                                     Paper dust.                        
                                     Propionaldehyde.                   
                                     1,1,1-Trichloroethane.             
Typewriter Corrections Fluid.......  Acetone.                           
                                     1,1,1-Trichloroethane.             
\1\Source: [Ex. 4-33]                                                   

    Emissions from equipment, such as computers, will decrease over 
time compared to emissions from equipment that continually use 
chemicals. Emissions from such equipment (e.g., laser printers) that 
use chemicals continually, will obtain a steady state concentration 
dependent upon the chemicals used and frequency of equipment use.

B. Microbial Contamination

    Three conditions must exist in buildings before microbial 
contamination can occur: high humidity (over 60%), appropriate 
temperatures (varies according to microbe), and appropriate growth 
media [Exs. 3-61, 4-33]. These conditions are found in heating, 
ventilating, and air conditioning (HVAC) systems. HVAC systems provide 
multiple sites for microbes to grow (reservoir) and also the means to 
disperse the microbes throughout the ventilated space. These reservoirs 
of microbial growth, if allowed to proliferate unchecked, can lead to 
indoor air quality problems once the microbes or microbe-related 
products, such as endotoxins, are dispersed.
    Building materials that have been soaked with water, such as 
fiberglass insulation in air handlers, furnishings and fabrics, ceiling 
tiles, and carpeting are excellent media for microbial growth. 
Biological organisms, including fungal spores, bacteria, viruses, 
pollens, and protozoa derived from mold growth have been identified in 
humidifiers with stagnant water, water damaged surfaces and materials, 
condensing coils and drip-pans in HVAC systems, drainage pans in 
refrigerators, dirty heating coils, and are also associated with 
mammals, arthopods and insects. Table III-3 gives examples of 
biologicals found in indoor environments.
    Various allergens have been associated with the development of 
allergic rhinitis, asthma, or airway hyperresponsiveness (Table III-3) 
[Ex. 4-33]. Many of these allergens are common to the nonindustrial 
work environment. These include chemical volatiles and dusts, 
arthropods, and dusts, particulates & fibers.

                                         Table III-3.--Examples of Biologicals Found in Indoor Environments\1\                                          
--------------------------------------------------------------------------------------------------------------------------------------------------------
                     Class                                        Agent or component                                        Origin                      
--------------------------------------------------------------------------------------------------------------------------------------------------------
Arthopods and Insects...........................  Whole organism, body parts, feces.................  Furnishings, building materials, food.            
Microbes:                                                                                                                                               
    Algae.......................................  Whole organism, cellular components...............  Outdoor air, HVAC (rare).                         
    Bacteria....................................  Whole organism, spores and cell walls, endotoxin..  Stagnant water, floods, cooling towers, industrial
                                                                                                       processes.                                       
    Fungi.......................................  Whole organism spores and hyphae toxins and         Moist surfaces, HVAC system, bird droppings,      
                                                   volatiles.                                          outdoor air.                                     
    Protozoa....................................  Whole organism cellular components................  Water reservoirs, pets (rare).                    
    Viruses.....................................  Whole organism....................................  Humans and pets (rare).                           
Pets............................................  Skin, scales danders, urine, saliva, feces........  Pets, pet litter, pet cages, pet toys, pet        
                                                                                                       bedding.                                         
Plants..........................................  Stems, leaves and pollens.........................  Outdoor and indoor air.                           
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\Adapted from Ex. 4-33.                                                                                                                               


      Table III-4.--Indoor Air Allergens Associated With Asthma\1\      
------------------------------------------------------------------------
          Class                           Typical examples              
------------------------------------------------------------------------
Animal:                                                                 
    Avian................  High and low molecular weight proteins from  
                            feathers and droppings.                     
    Canine and Feline....  High and low molecular weight proteins from  
                            dander, saliva, and feces.                  
Arthropods:                                                             
    Mites, Cockroaches,    Structural proteins, carbohydrates and       
     Crickets and Moths.    metabolites.                                
Dusts, Particulates and                                                 
 Fibers:                                                                
    Household............  Pollens, fungi, danders and mites.           
    Metal................  Chromium, cobalt, nickel, platinum, and      
                            vanadium.                                   
    Plant................  Castor bean, coffee, cotton, flour, and      
                            grain.                                      
    Wood.................  Oak, mahogany, redwood, red cedar.           
Chemical Volatiles and     Acrylates, amines, anhydrides, colophony,    
 Dusts.                     enzymes, epoxy resins, freon, furfuryl      
                            alcohol, resins, isocyanates, latex,        
                            organophosphates, polyvinyl chloride,       
                            vegetable gums.                             
Microbes and Microbial                                                  
 Products:                                                              
    Bacteria.............   Bacillus spp.                               
    Fungi................  Alternaria spp., Aspergillus spp., Botrytis  
                            spp., Cladosporium spp., Penicillium spp.,  
                            Pullularia spp.                             
Pollens..................  Agrostis spp., Alopecurus spp., Anthoxanthum 
                            spp. Cynosurus spp., Dactylis spp., Holcus  
                            spp., Lolium spp., Secale spp.              
------------------------------------------------------------------------
\1\Source: Ex. 4-33.                                                    

    Exposures that cause hypersensitivity reactions include 
microorganisms, fumes, vapors, and dusts (Table III-5). These exposures 
are associated with the development of hypersensitivity pneumonitis or 
a less serious variant, humidifier fever [Ex. 4-33]. Many of these 
contaminants are found in the nonindustrial workplace. Birds and 
rodents are common pests. Air intakes can be contaminated with bird 
droppings and other avian-associated problems when used as nesting 
sites. These problems can affect the quality of the air being brought 
into the ventilation system through these air intakes. Rodent 
infestations affect work areas directly. Many of the chemicals listed 
in Table III-5 are commonly found in most workplaces.
    In summary, exposure to contaminants in nonindustrial workplaces 
will vary according to the characteristics of the building. These 
include its age, types of materials used in construction and the type 
of equipment and supplies that are used by building occupants. The 
design, maintenance, and operation of the building's HVAC system as 
well as the general housekeeping of the building, can greatly influence 
the levels of contaminants that exist.
    OSHA requests data on the levels of these contaminants in 
nonindustrial workplaces.

 Table III-5.--Indoor Air Contaminants Associated With Hypersensitivity 
                             Pneumonitis\1\                             
------------------------------------------------------------------------
          Class                           Typical examples              
------------------------------------------------------------------------
Animals:                                                                
    Avian................  High and low molecular weight proteins from  
                            feathers and droppings.                     
    Rodent...............  Low molecular weight proteins from urine and 
                            feces.                                      
Arthropods:                                                             
    Weevils..............  Sitophilus spp.                              
    Mites................  Ascaris spp.                                 
Altered Host Proteins or   Amines, anhydrides, epoxy resins vegetable   
 Chemical Hapten-Carrier    gums, and isocyanates.                      
 Conjugates.                                                            
Microbes:                                                               
    Bacteria.............  Thermoactinomycetes spp., Bacillus spp.      
    Fungi................  Aspergillus spp., Auerobasillium spp.,       
                            Cephalosporium spp., Penicillium spp.       
Organic Dusts &                                                         
 Particulates:                                                          
    Wood.................  Bark, Sawdust and Pollen.                    
    Grain................  Arthropod- and microbially-contaminated      
                            grains and flours.                          
    Cleaning Products....  Dust residues from carpet cleaning agents.   
------------------------------------------------------------------------
\1\Source: Ex. 4-33.                                                    

C. Exposure Studies

1. Low-level Contaminants
    Experimental studies have demonstrated that exposure of susceptible 
people to low level mixtures of VOCs have induced mucous membrane 
irritation and pulmonary effects. Some of these studies are discussed 
below.
    The potential of indoor air contamination to produce adverse 
effects in humans was demonstrated by Molhave et al. in Denmark [Ex. 4-
20]. These researchers studied 62 subjects suffering from ``indoor 
climate symptoms''. These subjects reported primarily eye and upper 
respiratory tract irritation, but were otherwise healthy individuals 
that did not suffer from asthma, allergy, or bronchitis. The subjects 
were exposed to a mixture of VOCs in concentrations of 0, 5, or 25 mg/
m3. These concentrations respectively represented ``clean'' air, 
average polluted air, and the maximum polluted air in Danish 
households. After exposure, a Digit Span test was administered. The 
study found significant declines in performance on this test; 
demonstrating that low-level exposures to volatile organic compounds 
had an adverse effect on the ability to concentrate [Ex. 4-20].
    Otto et al. [Ex. 4-248], repeating the Molhave et al. (1984) 
experiment, studied 66 healthy subjects with no history of eye and 
upper respiratory tract irritation. These subjects were exposed at 0 
and 25 mg/m3 VOC-contaminated air. Otto et al. reported that while 
subjects found the odor of chemicals unpleasant, to degrade indoor air 
quality, to increase headache, and produce general discomfort, VOC 
exposure for 2.75 hours duration did not affect performance on any 
behavioral tests. These results imply that persons who experience 
symptoms of SBS may have a lower threshold for certain health effects 
compared to nonreactive people. This suggests that those with 
compromised immune response (e.g. allergy sufferers) may be at elevated 
risk of SBS.
    Ahlstrom, et al. [Ex. 4-2] found that synergistic effects may occur 
when one strong indoor irritant interacts with other indoor 
contaminants present at low-level concentrations. Ahlstrom et al. found 
that there was almost a 4-fold increase in the perceived odor strength 
of formaldehyde at low concentration (0.08 ppm) when mixed with 100% 
indoor air from a building where SBS was reported, relative to 10% 
indoor air from the same building.
    The Report of the Canadian Interministerial Committee on Indoor Air 
Quality [Ex. 4-264] adopts the World Health Organization's definition 
of health: ``Health refers to a state of complete physical, mental, and 
social well being, and not just the absence of disease or infirmity.'' 
This definition was adopted to allow the setting of indoor air quality 
guidelines based on ``comfort'' as well as ``health''. The report 
observes that the symptoms of SBS are sufficiently general or 
subjective that they may be indicative of several other medical 
conditions. Therefore, perhaps the best indicator that workplace 
exposure may play a role in the symptoms reported by an individual is 
the observation that symptoms worsen during the work day, and disappear 
shortly after leaving work. They state that because there is a wide 
variation in individual susceptibility, based on genetics, age, 
medication, previous exposure to pollutants, gender, and state of 
health, especially those with allergies, that certain individuals may 
be more sensitive to SBS than others.
2. Bioaerosols
    The levels of bioaerosols in the indoor environment should reflect 
those found in the outdoor environment. A rank order assessment, 
comparing the abundance of microorganisms in the outdoor versus indoor 
environment is one way of assessing this relationship [Exs. 3-61, 4-
229]. If indoor and outdoor sampling results are not comparable, then 
it is possible that a reservoir of a particular microbe may be 
amplifying in the indoor environment; especially if moisture and a 
nutrient-rich substrate are available [Ex. 4-229]. An example of this 
would be Legionella. Commonly found in the outdoor environment, the 
bacteria are as expected, commonly found in untreated potable and 
nonpotable water. Situations can occur that allow these reservoirs to 
amplify not only in potable water and hot water service systems but 
also water used in cooling towers and evaporative condensers [Ex. 4-
229]. Infection occurs if the bacteria are disseminated, either through 
the HVAC system or potable water system (e.g., showers) to the 
breathing zone of a susceptible person. A healthy individual may 
develop the less severe Pontiac Fever. An individual that smokes or is 
older may develop the more serious pneumonia [Exs. 4-33, 4-229].
3. Environmental Tobacco Smoke
    The burning of tobacco in enclosed workplaces releases an aerosol 
containing a large variety of solid, liquid, and gas phase chemical 
compounds. Generation of tobacco smoke is governed by the source 
emission characteristics of smokers and their tobacco products, whereas 
removal is primarily determined by the rate of replacement of building 
air by outside air, with re-emission of surface-sorbed compounds 
playing a minor role. Natural and mechanical ventilation systems are 
designed primarily to limit the accumulation of the products of human 
respiratory metabolism, and secondarily to limit odor; not to control 
the byproducts of biomass combustion. Thus, smoking indoors creates air 
pollution which is not adequately abated by customary ventilation 
systems.
    Exposure to tobacco smoke primarily occurs through the inhalation 
route. Such an exposure can be measured by the determination of the 
absorption, distribution, metabolism and excretion of tobacco smoke 
constituents and/or their metabolites. However, relatively few of these 
individual constituents have been identified and characterized. Also, 
measurement of all components in tobacco smoke is not feasible. 
Therefore, it becomes necessary to identify a marker which, when 
measured, will accurately represent the frequency, duration and 
magnitude of the exposure to environmental tobacco smoke.
    This discussion reviews available data for the purposes of 
assessing exposure to ETS in the workplace. Nonsmokers are exposed to 
mainstream smoke after it has been exhaled by smokers, and to diluted 
sidestream smoke. Issues covered include activity patterns affecting 
the duration of nonsmokers' exposures, the concentrations of ETS in 
buildings, the comparison of ETS components in indoor workplaces, 
levels of biomarkers in workers, and the inadequacy of general dilution 
ventilation to address ETS exposure control. This discussion will 
indicate not only that exposure occurs, but that nonsmokers absorb ETS 
components.
    (a) Chemistry. Pipe, cigar, and cigarette smoke all contribute to 
environmental tobacco smoke (ETS) but cigarette smoke is of principal 
interest because it is by far the most common. Tables III-6 and III-7 
list some of the known constituents of tobacco smoke.
    The combustion of tobacco leads to the formation of mainstream 
smoke (MS) and sidestream smoke (SS). MS is generated during puff-
drawing in the burning cone and hot zones; it travels through the 
tobacco column and is inhaled by the smoker. The smoke which is exhaled 
by the smoker, while different from the inhaled smoke, is also 
considered ``mainstream.'' SS is formed in between puff-drawing and is 
emitted directly from the smoldering tobacco product into the ambient 
air.

                                   Table III-6.--Vapor Phase Constituents of Tobacco Smoke and Related Health Effects                                   
--------------------------------------------------------------------------------------------------------------------------------------------------------
                        Constituent                              Amount in MS        Ratio in SS/MS                     Health effects                  
--------------------------------------------------------------------------------------------------------------------------------------------------------
Carbon monoxide............................................  10-23 mg.............           2.5-4.7  Nervous system, cardiovascular system.\1\         
Carbon dioxide.............................................  20-40 mg.............              8-11  Nervous system, cardiovascular system.\1\         
Carbonyl sulfide...........................................  12-42 g.....         0.03-0.13  Irritant, cardiovascular, and nervous systems.\1\ 
Benzene....................................................  12-48 g.....              5-10  Known human\3\ carcinogen.                        
Toluene....................................................  100-200 g...           5.6-8.3  Irritant, nervous system.\1\                      
Formaldehyde...............................................  70-100 g....  0.1-  Probable human carcinogen.\3\                     
                                                                                                  50                                                    
Acrolein...................................................  60-100 g....              8-15  Irritant, pulmonary.\1\                           
Acetone....................................................  100-250 g...               2-5  Irritant.\1\                                      
Pyridine...................................................  16-40 g.....            6.5-20  Irritant, nervous system, liver, kidney.\1\       
3-methylpyridine...........................................  12-36 g.....              3-13  Irritant.\2\                                      
3-vinylpyridine............................................  11-30 g.....             20-40  Irritant.\2\                                      
Hydrogen cyanide...........................................  400-500 g...          0.1-0.25  Irritant, nervous, cardiovascular and pulmonary   
                                                                                                       system.\1\                                       
Hydrazine..................................................  32 ng................                 3  Probable human carcinogen.\3\                     
Ammonia....................................................  50-130 g....           3.7-5.1  Irritant.\1\                                      
Methylamine................................................  11.5-28.7 g.           4.2-6.4  Irritant.\1\                                      
Dimethylamine..............................................  7.8-10 g....           3.7-5.1  Irritant\1\.                                      
Nitrogen oxides............................................  100-600 g...              4-10  Pulmonary and cardiovascular system.\1\           
N-nitrosodimenthylamine....................................  10-40 ng.............            20-100  Probable human carcinogen.\3\                     
N-nitrodiethylamine........................................  ND-25 ng.............               <40  Probable human carcinogen.\3\                     
N-nitrosopyrrolidine.......................................  6-30 ng..............              6-30  Probable human carcinogen.\3\                     
Formic acid................................................  210-490 g...           1.4-1.6  Irritant, skin, kidney, liver\1\.                 
Acetic acid................................................  330-810 g...           1.9-3.6  Irritant.\1\                                      
Methyl chloride............................................  150-600 g...           1.7-3.3  Nervous system.\1\                                
1,3-butadiene..............................................  69.2 g......               3-6  Probable human carcinogen.\3\                     
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\NIOSH Pocket Guide to Chemical Hazards. U.S. Department of Health and Human Services. Public Health Services, 1990. Ex. 4-238.                       
\2\Hazards in the Chemical Laboratory. Ed: L. Bretherick, The Royal Society of Chemistry, 1986. [Ex. 4-137]                                             
\3\EPA: Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders, 1992. [Ex. 4-311]                                               


                                Table III-7.--Particulate Phase Constituents of Tobacco Smoke and Related Health Effects                                
--------------------------------------------------------------------------------------------------------------------------------------------------------
                        Constituent                               Amount in MS       Ratio in SS/MS                     Health effects                  
--------------------------------------------------------------------------------------------------------------------------------------------------------
Particulate matter contains di- and polycyclic aromatic      15-40 mg.............           1.3-1.9  Animal carcinogen.\4\                             
 hydrocarbon.                                                                                                                                           
Nicotine...................................................  1-2.5 mg.............           2.6-3.3  Nervous and cardiovascular system.\1\             
Anatabine..................................................  2-20 g......         <0.01-0.5  N/A.\5\                                           
Phenol.....................................................  60-140 g....           1.6-3.0  Irritant.\1\                                      
Catechol...................................................  100-360 g...           0.6-0.9  Irritant.\3\                                      
Hydroquinone...............................................  110-300 g...           0.7-0.9  N/A.\5\                                           
Aniline....................................................  360 ng...............                30  Probable human carcinogen.\4\                     
2-Toluidine................................................  160 ng...............                19  Irritant, cardiovascular system.\1\               
2-Naphthylamine............................................  1.7 ng...............                30  Known human carcinogen.\4\                        
4-Aminobiphenyl............................................  4.6..................                31  Known human carcinogen.\4\                        
Benz[a]anthracene..........................................  20-70 ng.............               2-4  Animal carcinogen.\4\                             
Benzo[a]pyrene.............................................  20-40 ng.............           2.5-3.5  Probable human carcinogen.\4\                     
Cholesterol................................................  22 g........               0.9  N/A.\5\                                           
-butyrolactone....................................  10-22 g.....           3.6-5.0  Animal carcinogen.\4\                             
Quinoline..................................................  0.5-2 g.....              3-11  Irritant.\3\                                      
Harman [1-methyl-9H-pyrido[3,4-b]-indole...................  1.7-3.1 g...           0.7-1.7  N/A.\5\                                           
N-nitrosonornicotine.......................................  200-3000 ng..........             0.5-3  Animal carcinogen.\4\                             
NNK [4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone]..  100-1000 ng..........               1-4  N/A.\5\                                           
N-nitrosodiethanolamine....................................  20-70 ng.............               1.2  Probable human carcinogen.\4\                     
Cadmium....................................................  110 ng...............               7.2  Probable human carcinogen.\4\                     
Nickel.....................................................  20-80 ng.............             13-30  Known human carcinogen.\4\                        
Zinc.......................................................  60 ng................               6.7  Irritant, nausea, vomiting.\2\                    
Polonium-210...............................................  0.04-0.1 pCi.........            1.04.0  Known human carcinogen.\4\                        
Benzoic acid...............................................  14-28 g.....         0.67-0.95  Irritant.                                         
Lactic acid................................................  63-174 g....           0.5-0.7  Irritant.\3\                                      
Glycolic acid..............................................  37-126 g....           0.60.95  Irritant.\2\                                      
Succinic acid..............................................  110-140 g...         0.43-0.62  N/A.\5\                                           
PCDD's and PCDF's\6\.......................................  1 pg.................                 2  N/A.\5\                                           
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\NIOSH Pocket Guide to Chemical Hazards. U.S. Department of Health and Human Services. Public Health Services, 1990. Ex. 4-238.                       
\2\The Merck Index, 10th Edition, Merck & Co., Inc., 1983. Ex. 4-220.                                                                                   
\3\Hazards in the Chemical Laboratory. Ed: L. Bretherick, The Royal Society of Chemistry, 1986. [Ex. 4-137]                                             
\4\EPA: Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders, 1992. [Ex. 4-311]                                               
\5\N/A--Relevant information not available.                                                                                                             
\6\PCDDs--Polychlorinated dibenzo-p-dioxins; PCDFs--Polychlorinated dibenzofurans.                                                                      

    MS and SS cigarette smoke are chemically and physically complex 
mixtures consisting of electrically charged submicron liquid particles 
at very high concentration consisting of permanent gases, reactive 
gases, and a large variety of organic chemicals. The composition of the 
smoke and especially the total quantities of individual constituents 
delivered are dependent on the conditions of smoke generation [Ex. 4-
311].
    Nicotine, while found in the particulate phase in MS, is found 
predominantly in the gas phase in ETS [Ex. 4-100]. The differences in 
size distribution for MS and SS particles, as well as the different 
breathing patterns of smokers and nonsmokers, affect deposition of the 
produced particle contaminants in various regions of the respiratory 
tract.
    There are substantial similarities and some differences between MS 
and SS emissions from cigarettes [Exs. 3-689D, 4-129, 4-239]. 
Differences in MS and SS emissions are due to differences in the 
temperature of the combustion of tobacco, pH, and degree of dilution 
with the air, which is accompanied by a correspondingly rapid decrease 
in temperature. SS is generated at a lower temperature (approximately 
600 deg.C between puffs versus 800 to 900 deg.C for MS during puffs) 
and at a higher pH (6.7-7.5 versus 6.0-6.7) than MS. Being slightly 
more alkaline, SS contains more ammonia, is depleted of acids, contains 
greater quantities of organic bases, and contains less hydrogen cyanide 
than MS. Differences in MS and SS are also ascribable to differences in 
the oxygen concentration (16% in MS versus 2% in SS). SS contaminants 
are generated in a more reducing environment than those in MS, which 
will affect the distribution of some compounds. Nitrosamines, for 
example, are present in greater concentrations in SS than in MS.
    Many of the compounds found in MS, which were identified as human 
carcinogens, are also found in SS emissions [Exs. 3-689D, 4-93, 4-129, 
4-239, 4-269] and at emission rates considerably higher than for MS. SS 
contains ten times more polycyclic aromatic hydrocarbons, aza-arenes 
and amines as compared with MS [Ex. 4-126]. All of the five known 
carcinogens, nine probable human carcinogens, and three animal 
carcinogens are emitted at higher levels in SS than in MS, several by 
an order of magnitude or more. Several toxic compounds found in MS are 
also found in SS (carbon monoxide, ammonia, nitrogen oxides, nicotine, 
acrolein, acetone, etc.), in some cases by an order of magnitude or 
higher (Tables III-6 and III-7).
    SS emissions, quantitatively, show little variability as a function 
of a number of variables (puff volume, filter versus nonfilter 
cigarette, and filter ventilation [Exs. 4-1, 4-34, 4-54, 4-128, 4-129, 
4-141]. The lack of substantial variability in SS emissions is related 
to the fact that they are primarily related to the weight of tobacco 
and paper consumed during the smoldering period, with little influence 
exerted by cigarette design [Ex. 4-129].
    (b) Human Activity Pattern Studies Used to Assess Workplace 
Exposure. Human activity pattern studies utilize random samples of 
human activity patterns using questionnaires and time-diary data to 
provide detailed generalizable data about human behavior. Such studies 
have been used to assess exposure to ETS. In 1987-1988, the California 
Air Resources Board sponsored a probability-based cross-sectional 
sample of 1,579 Californians aged 18 years and older, called the 
California Activity Pattern Survey (CAPS) [Exs. 4-168, 4-271]. The 
study was designed to provide information on time spent in various 
locations, including indoors, outdoors, and in transit, as well as 
specific microenvironments, such as living rooms, kitchens, 
automobiles, or buses. The study focused on time spent in activities 
such as cooking or playing sports, but more specifically targeted 
activities and environments that had implications for air pollution 
exposure, such as the presence of smokers, use of cooking equipment or 
solvents.
    In analyzing the data from CAPS, Jenkins et al. [Ex. 4-168] and 
Robinson et al. [Ex. 4-271] found that time spent at work had a high 
correlation with exposure to ETS. This association of ETS exposure with 
work settings remained strong after controlling for the length of the 
activity episode, and hence was not simply a function of longer time 
intervals at work. Robinson et al. [Ex. 4-271] also found that men 
reported higher levels of exposure than women, even after controlling 
for age, employment status, shorter working hours, etc. This finding 
suggests that the epidemiological studies of passive smoking and lung 
cancer, which have focussed on women, may be underestimating the effect 
of ETS on lung cancer.
    Further analysis of the CAP study [Ex. 4-169] verifies the high 
percentage of nonsmokers who are exposed to ETS while at work. This is 
indicated when the data are analyzed by employed nonsmoker status. As 
indicated in Table III-8, 51% of male and 38% of female nonsmokers 
reported ETS exposure at work. The average duration of this exposure 
was 313 minutes for males and 350 minutes for females. When the group 
that reported exposure at the workplace is analyzed further it becomes 
apparent that the overwhelming exposure location for these employed 
nonsmokers is the workplace (Table III-9). As indicated in Table III-9, 
77% of males and 85% of females were exposed an average of 313 minutes 
and 350 minutes, respectively.
    One other finding is that the more time spent at work, the higher 
the likelihood of greater ETS exposure. For example, the average 
duration of exposure to homemakers was approximately 2 hours a day, for 
workers the average duration of exposure was approximately 3 hours a 
day.

   Table III-8.--Percentage of Employed Nonsmokers Exposed to ETS and   
             Average Minutes of Exposure (in Parentheses)\1\            
------------------------------------------------------------------------
        Exposure location             Males       Females       Total   
------------------------------------------------------------------------
Home.............................       9(134)      13(109)      11(123)
Work.............................      51(313)      38(350)      46(324)
Other indoor.....................      28(89)       35(77)       31(85) 
Outdoor..........................      12(118)      14(79)       13(104)
------------------------------------------------------------------------
\1\Source: [Ex. 4-169].                                                 


   Table III-9.--Percentage of Employed Nonsmokers Exposed to ETS and   
 Average Minutes of Exposure (in Parentheses) of Those Who Reported ETS 
                           Exposure at Work\1\                          
------------------------------------------------------------------------
        Exposure location             Males       Females       Total   
------------------------------------------------------------------------
Home.............................       1(147)       2(180)       2(158)
Work.............................      77(313)      85(350)      80(324)
Other indoor.....................      15(92)        9(102)      13(94) 
Outdoor..........................       6(176)       4(140)       5(166)
------------------------------------------------------------------------
\1\Source: [Ex. 4-169].                                                 

    Work breaks and meals at work were the work activities most closely 
associated with ETS exposure, 51% and 35% respectively versus 27% for 
work per se [Ex. 4-271]. In other words, nonsmokers experienced ETS 
exposure in break areas more than in general work areas.
    When white collar versus blue collar workplaces were compared, 37% 
of factories/plants versus 22% of offices had episodes of ETS exposure, 
suggesting that blue collar nonsmoking workers have a greater exposure 
to ETS than white collar workers. For the CAP population, twice as many 
workers were employed in offices as were in factories [Ex. 4-271]. The 
most ETS exposed nonsmokers were those with 10 or more hours per day of 
work (especially at plants/factories), more than 2 hours per day of 
restaurant time, and more than 1 hour per day of bar or nightclub time.
    Robinson et al. [Ex. 4-271] concluded that the probability of 
passive smoking is highest for a combination of various social and work 
activities, consistent with the notion that activities that involve 
more people involve a greater chance of contact with people who smoke. 
A limitation of the CAP survey is that the data do not provide 
information on the intensity of exposure in the various 
microenvironments [Ex. 4-271].
    In summary, the CAP study showed that the most powerful predictor 
of potential exposure to ETS was being employed. Respondents who spent 
more than ten hours a day at the workplace were found to report more 
ETS exposure than those working less than 10 hours a day or not at all. 
Further data from this study show that the workplace is the location 
with the highest reported exposure to ETS in enclosed environments, and 
such exposure is on average nearly three times more prevalent at work 
than at home.
    Another relevant data source for assessing ETS exposure in the 
workplace is the National Health Interview Survey (NHIS) conducted by 
the Centers for Disease Control and Prevention (CDC). In its Health 
Promotion and Disease Prevention (NHIS-HPDP) supplement, CDC collected 
self-reported information on smoking from a representative sample of 
the U.S. population [Ex. 4-51]. The results suggest that at least 19% 
of employed nonsmokers experience ETS exposure at work. The CDC study 
results represent the prevalence of occupational exposure among 
nonsmoking adults [see section IV for further discussion of this 
study].
    In a smaller study, Cummings et al. [Ex. 4-67] studied the 
prevalence of exposure to ETS in 663 (44% male) never- and exsmokers 
aged 18-84 years, who attended a cancer clinic in Buffalo, New York in 
1986 (see Table IV-9). The study employed questionnaires and analysis 
of urinary cotinine levels. The subjects were asked if they were 
exposed to passive smoke either at home or at work in the four days 
preceding the interview. A further analysis of this data focusing on 
workers from this survey determined that overall, 339 subjects were 
currently employed. Of these 264 (77%) reported ETS exposure at work. 
The percentage of subjects exposed to ETS at both work and the home was 
29% (n=99). The percentage of subjects exposed at home, but not at work 
was 7% (n=23). The percentage of subjects exposed at work, but not at 
home was 49% (n=165). The percentage of subjects exposed neither at 
home or work was 15% (n=52). This further analysis indicates that the 
workplace is a significant source of ETS exposure for nonsmoking, 
employed people.
    Emmons et al. [Ex. 4-98] reported on a study of 186 nonsmoking 
volunteers from workplace settings selected to have a wide range of 
exposure to ETS. The subjects were asked to keep a 7-day exposure 
diary. The worksites ranged from those with minimal restrictions and 
high levels of exposure (long-term care and psychiatric facilities, 
chemical dependency and treatment centers, and a VA Hospital) to those 
with extensive restrictions and low exposure (e.g., state health 
department and community hospitals). Seventy-six percent of the 
subjects reported being regularly exposed to ETS in the workplace. The 
percentage of subjects reporting exposure at work is similar to that 
found by Cummings et al. [Ex. 4-67]. Nonsmokers encountered 
significantly more exposure to ETS at work (50%) as compared to home 
(10%). When the data set was examined by the presence or absence of 
smokers in the home, however, subjects who lived with smokers had 
virtually equivalent exposures across all three settings: work (34%), 
home (36%), and ``other'' (31%). Nonsmokers living with smokers 
received 29 minutes per day of exposure at work and 31 minutes per day 
at home and 27 minutes per day in other settings. On the other hand, 
subjects who did not live with smokers had the majority of their 
exposure at work (36 minutes per day) and very little at other 
settings.
    Additional studies verify that the workplace is an important source 
of exposure to ETS, particularly for nonsmokers unexposed at home [Exs. 
4-172, 4-262, 4-315]. A U.K. study of exposure to ETS in 20 nonsmoking 
men whose wives smoked showed that 78% of the men's reported hours of 
exposure came from outside the home; by contrast, 90% of the ETS 
exposure of 101 nonsmoking men whose wives did not smoke was reported 
to come from non-domestic microenvironments [Ex. 4-315]. Repace and 
Lowrey [Ex. 4-262] estimated that 86% of the U.S. population was 
exposed to ETS, and that the workplace was more important than the home 
as a source of ETS exposure, when weighted by the duration, exposure 
intensity, and probability of exposure. Kabat and Wynder [Ex. 4-172], 
in a study of 215 sixty-year-old U.S. women nonsmokers, found that 65% 
reported exposure to ETS at home and 67% reported exposure at work, 
averaged over adulthood.
    The conclusion that can be made from the activity surveys is that 
the workplace is a major location of ETS-exposure to nonsmokers. Human 
activities that involve contact with a greater number of people 
increase the probability of contact with smokers, and thus with ETS. 
These studies indicate that the workplace, with its high person 
densities relative to other microenvironments, including the home, 
appears to be a major factor in the working nonsmoking population's ETS 
exposure.
    (c) Indoor Levels of Environmental Tobacco Smoke Constituents. 
Personal monitoring studies have confirmed the role of the workplace as 
an important microenvironment of ETS exposure to nonsmokers. Spengler 
et al. [Ex. 4-288] and Sexton et al. [Ex. 4-280] demonstrated by 
personal monitoring of respirable suspended particulates (RSP) and the 
use of time-activity questionnaires that exposures to ETS both at home 
and at work are significant contributors to personal RSP exposures. 
Coultas et al. [Ex. 4-66], in a pilot study of 15 nonsmokers in 
Albuquerque, New Mexico, collected questionnaires and samples of saliva 
and urine to determine workplace ETS exposure. Personal air samples 
were obtained pre- and post-workshift. Exposure to ETS was reported by 
13 of the 15 subjects. The mean number of hours of exposure was 3.4 
(2.1). Basically, although the levels of cotinine, 
respirable particles, and nicotine varied with self-reports of ETS 
exposure, the general trend was a direct relationship between 
increasing incidence of self-reporting of exposure and actual biomarker 
data. Coghlin, Hammond, and Gann [Ex. 4-61] found similar results for 
53 nonsmoking volunteers studied by use of personal nicotine monitors, 
diaries, and questionnaires. They also found that the closer a 
nonsmoker was to a smoker, the higher the probability that the 
nonsmoker would report exposure.
    Presently, vapor phase nicotine and respirable suspended 
particulate matter (ETS-RSP) are the most commonly used markers for ETS 
because of their ease of measurement, knowledge of their emission rate 
from tobacco combustion, and their relationship to other ETS 
contaminants [Ex. 4-311]. Controlled experiments have shown that vapor 
phase nicotine varies with the source strength, and shows little 
variation among brands of cigarettes. Field studies have also shown 
that vapor phase nicotine concentrations are correlated with the number 
of cigarettes smoked, and further that weekly average nicotine 
concentrations are correlated with ETS-RSP [Ex. 4-311].
    (d) Levels of Respirable Suspended Particulates and Nicotine Found 
in Field Studies. Respirable suspended particulates (RSP) and nicotine 
are the most commonly used surrogates for ETS exposure [Ex. 4-239]. 
Both chamber and field studies have demonstrated that tobacco 
combustion has a major impact on indoor RSP mass when particle size is 
under 2.5 microns [Ex. 4-239]. A few examples illustrating the impact 
of ETS on nicotine and RSP concentrations in workplace and domestic 
microenvironments are shown in Tables III-10 and III-11. Studies of RSP 
in public access buildings by Leaderer et al. [Ex. 4-190], First [Ex. 
4-105], and Repace and Lowrey [Exs. 4-260, 4-261] (a total of 42 
smoking buildings and 21 nonsmoking buildings) showed that the weighted 
average RSP level during smoking in the smoking buildings was 262 
g/m\3\, while in the nonsmoking buildings the RSP level 
average 36 g/m\3\.
    Leaderer and Hammond [Ex. 4-189] measured weekly average vapor 
phase nicotine and RSP concentrations in 96 residences. Vapor phase 
nicotine measurements were found to be closely related to number of 
cigarettes smoked and highly predictive of RSP generated by tobacco 
combustion. The mean RSP background in the absence of measurable 
nicotine was found to be 15.27 g/m\3\. The mean 
RSP value in the presence of nicotine was 44.130 
g/m\3\. The weekly mean nicotine concentration in the 47 
residences with detectable nicotine values was 2.17 g/m\3\ 
(Table III-10).
    Summary statistics of additional studies on personal monitoring for 
nicotine are shown in Table III-11 [Ex. 4-263]. These studies show that 
the median exposures ranged from 5 to 20 g/m\3\.
    Summary nicotine data analyzed by the U.S. EPA [Ex. 4-311] suggest 
that average nicotine values in residences where smoking is occurring 
will average 2 to approximately 10 g/m\3\, with peak values of 
0.1 to 14 g/m\3\ as shown in Table III-10. Offices with 
smoking occupants show a range of average nicotine concentrations 
similar to that of residences, but with considerably higher peak 
values. RSP mass concentrations in smoker-occupied residences show 
average increases of from 18 to 95 g/m\3\, with individual 
increases as high as 560 g/m\3\ or as low as 5 g/
m\3\. ETS-RSP concentrations in offices with smoking occupants on 
average appear to be about the same as in residences. Restaurants, 
transportation, and other indoor spaces with smoking occupants have a 
generally wider range of increases in particle mass concentrations due 
to ETS than residential or office environments [Ex. 4-311].
    In summary, field data show that RSP is elevated by one to two 
orders of magnitude during smoking, and that nicotine released during 
smoking is easily detectable in both homes and workplaces by area or 
personal monitors. Offices with smoking occupants show a range of 
average nicotine concentrations similar to that of residences (2 to 10 
g/m\3\), but with considerably higher maximum values. ETS-RSP 
concentrations in offices with smoking occupants on average appear to 
be about the same as residences (18 to 95 g/m\3\). 
Restaurants, transportation, and other indoor spaces with smoking 
occupants have a generally wider range of particle mass concentrations 
due to ETS than residential or office environments [Ex. 4-311]. It must 
be noted that measurements of nicotine and ETS-RSP in indoor spaces do 
not constitute a direct measure of total exposure. Concentrations 
measured in all microenvironments have to be combined with human 
activity pattern studies to determine the time-weighted sum of various 
exposures.
    (e) Biomarkers of Environmental Tobacco Smoke Exposure. Nicotine, 
and its metabolite, cotinine, and other tobacco smoke constituents in 
the saliva, blood and urine have been used as biomarkers of active and 
passive smoking. Nicotine and cotinine can be used to determine the 
integrated short-term exposure of ETS across all microenvironments [Ex. 
4-311].

                 Table III-10.--Mean Nicotine Levels in Home and Workplace Air: Area Monitors\1\                
----------------------------------------------------------------------------------------------------------------
                                                                 g/                                    
                Study and location                    Sample        m\3\                    Comment             
----------------------------------------------------------------------------------------------------------------
Leaderer and Hammond 1991, homes, NY State........           47        2.17   7-day average smoking.            
Hammond [3-1096] Mass., industrial................  ...........       24      9-hour average workshift          
                                                                               (nonsmoker's air; smoking allowed
                                                                               on premises).                    
    White collar..................................           60       21.5    ..................................
    Blue collar...................................          123        8.9    ..................................
    Food service..................................           51       10.3    ..................................
Carson (1988), offices, Canada....................           31       11      Workday samples.                  
Miesner (1989) workplaces, MA.....................           11        6.6    Workweek average.                 
Oldaker (1990), restaurants, NC...................           33       10.5    1-hour average (range).           
Jenkins (1991), Knoxville, TN, metro..............  ...........  ...........  1-hour average.        
    Restaurants...................................            7        3.4    ..................................
    Cocktail lounges..............................            8       17.6    ..................................
    Bowling alleys................................            4       10.7    ..................................
    Gaming parlors................................            2       10.7    ..................................
    Laundromats...................................            3        2.0    ..................................
    Airport gates.................................            2        6.0    ..................................
    Office........................................            1        6.0    ..................................
Nagda (1989), U.S. aircraft--in-flight average:                                                                 
    All flights...................................           69       13.4    Smoking section.                  
    Domestic......................................           61        0.11   Nonsmoking section.               
    International.................................            8        0.33   Nonsmoking section.               
Vaughn (1990), highrise office building...........            1        2.0    Nonsmoking air; 9-hour average.   
----------------------------------------------------------------------------------------------------------------
\1\Adapted from Repace and Lowrey 1993 [Ex. 4-263].                                                             


                         Table III-11.--Nicotine in Nonsmokers' Air: Personal Moitors\1\                        
----------------------------------------------------------------------------------------------------------------
                                                                 g/                                    
                Study and Location                    Sample         m3                    Comment              
----------------------------------------------------------------------------------------------------------------
Schenker (1990), railroad clerks, NE..............           40         6.9   Workshift median.                 
Coultas (1990), white collar, NM..................           15        20.4   Workshift mean  SD.   
Mattson (1989); flight attendants.................            4         4.7   4 flights, mean  SD.  
----------------------------------------------------------------------------------------------------------------
\1\Adapted from Repace and Lowrey 1993 [Ex. 4-263].                                                             

    Both nicotine and cotinine are tobacco-specific. Cotinine in 
saliva, blood, and urine is the most widely accepted biomarker for 
integrated exposure to both active smoking and ETS by virtue of its 
longer half-life than nicotine in body fluids. The half-life of 
cotinine in nonsmokers is of the order of a day, making it a good 
indicator of integrated ETS exposure over the previous day or two [Ex. 
4-311]. Although intersubject variability exists for both nicotine 
absorption and cotinine metabolism [Exs. 4-156, 4-162], cotinine is a 
good indicator that ETS exposure has taken place [Ex. 4-311]. Further, 
studies show that cotinine levels correlate with levels of recent ETS 
exposure [Ex. 4-311].
    In summary, nonsmokers' exposure to ETS has been characterized by a 
database of widely used atmospheric and biological markers which have 
been measured in a number of workplaces, such as offices, restaurants, 
commercial buildings, and on trains and in planes. OSHA believes that 
this database is sufficient to support the risk assessment which 
follows. ETS-nicotine exposures of the average worker appear to be of 
the order of 5 to 10 micrograms per cubic meter (g/m\3\), and 
for the most-exposed workers, 50 to 100 g/m\3\). For ETS-RSP, 
exposures are about tenfold that of the nicotine levels. The 
concentrations of various ETS atmospheric markers to which nonsmokers 
are exposed in the workplace, such as nicotine, respirable suspended 
particulate matter (RSP) and carbon monoxide, are linearly correlated 
with the amount of tobacco burned. Studies of human activity patterns 
show that the workplace is the largest single contributor to ETS 
exposure. Air exchange rates in nonindustrial workplaces are not 
designed to control the risks of ETS exposure.
    (f) Inadequacy of General Dilution Ventilation to Address 
Environmental Tobacco Smoke Exposure Control. A primary function of 
heating, ventilating, and air-conditioning (HVAC) systems is to 
circulate air throughout a building to achieve thermal and sensory 
comfort for the building occupants. The general ventilation function of 
the HVAC system is to dilute and remove occupant generated bioeffluents 
and other contaminants from the space. However, from the industrial 
hygiene perspective, general ventilation as delivered by a HVAC system, 
is not an acceptable engineering control measure for controlling 
occupational exposures to ETS.
    Dilution ventilation offers no protection in those cases where, due 
to the close proximity to a smoker (e.g., contaminant point source), 
the nonsmoking employee may be exposed to large amounts of sidestream 
smoke and exhaled mainstream smoke (ETS). Due to the limitations of 
general ventilation, the smoke cannot be removed from the air before 
reaching the breathing zone of nearby employees. The carcinogenicity of 
ETS discounts the use of general ventilation as an engineering control 
for this contaminant.
    The major ventilation guidance document available to HVAC 
practioners (e.g., designers, maintenance, and operators), is Standard 
62-1989 titled ``Ventilation for Acceptable Indoor Air Quality'' [Ex. 
4-333]. The standard is published by the American Society of Heating, 
Refrigerating and Air-Conditioning Engineers, Inc. (ASHRAE) and it 
specifies recommended minimum design outside air ventilation rates for 
91 different applications. Based on this current ventilation standard, 
a typical commercial HVAC system serving general office space should 
prescriptively deliver 20 cubic feet per minute per person (cfm/person) 
of outside air to the occupied space to dilute occupant generated 
contaminants like carbon dioxide (CO2) and body odors. This 
ventilation rate would provide what ASHRAE defines as ``acceptable 
indoor air quality'' (e.g., sensory comfort) to satisfy at least 80% of 
the building occupants. The prescribed ventilation rates in ASHRAE 
Standard 62-1989 are proportional to the occupants in the space (e.g., 
cfm/PER PERSON) because of the presumption that the contamination 
produced is in proportion to the occupant density.
    The foreword of ASHRAE Standard 62-1989 states ``with respect to 
tobacco smoke and other contaminants, this standard does not, and 
cannot, ensure the avoidance of all possible adverse health effects, 
but it reflects recognized consensus criteria and guidance.'' As 
published, ASHRAE Standard 62-1989 did not include any summary and/or 
explanation documentation which would explain the basis of the 
consensus standard. Without this documentation, it can only be inferred 
that the standard was mostly based on satisfaction of sensory comfort 
rather than based on the control of contaminants like ETS which may 
contribute to adverse health effects like lung cancer and heart 
disease.
    The method of room air distribution found in most HVAC systems is a 
mixing system that attempts to create an environment of uniform air 
velocities, temperatures and humidities in the occupied zone of a room 
(e.g.; floor to 6 feet above floor). In this occupied zone, air 
velocities less than 50 feet per minute (fpm) and minimization of 
temperature gradients will promote occupant comfort. In a conventional 
mixing system where the supply air diffusers (outlets) and the return 
air grilles are both located in the ceiling, the air motion in the 
occupied zone could be characterized as ``gentle drift'' toward the 
ceiling where the room air is then mixed with the conditioned air being 
delivered to the room through the supply air diffusers [1993 ASHRAE 
Handbook, Ch.31]. Because of natural convection currents and thermal 
buoyancy forces it is common, especially during heating season, to have 
stagnant zones. In a mixing room air distribution system, the emphasis 
is on comfort.
    There are other room air distribution schemes which consider 
contaminant control and have been used in the industrial environment 
like displacement ventilation and unidirectional (plug-flow) airflow 
ventilation. In these schemes, there is an attempt to move contaminants 
directionally along a clean to less clean gradient. These schemes are 
seldom used in conventional HVAC systems due to their cost, feasibility 
and compromise of comfort issues.
    From the industrial hygiene perspective, local exhaust ventilation, 
specific to each source, would be the preferred and recommended method 
for controlling occupational exposures to contaminant point sources 
like ETS. Such specific ventilation is effective because the 
contaminant is captured or contained at its source before it is 
dispersed into the work environment where only ineffective general 
dilution ventilation is available to control exposures.
    A designated smoking area which is enclosed, exhausted directly to 
the outside, and maintained under negative pressure is sufficient to 
contain tobacco smoke within the designated area. Such areas could be 
considered an application of local exhaust ventilation because the 
contaminant is being exhausted from a confined source without dispersal 
into the general workspace.

IV. Preliminary Quantitative Risk Assessment

A. Introduction

    The determining factor in the decision to perform a quantitative 
risk assessment is the availability of suitable data for use in such an 
assessment. A wide spectrum of health effects have been associated with 
exposure to indoor air pollutants and ETS. These effects range from 
acute irritant effects to cancer. In the case of ETS, OSHA has 
determined that data are available to quantify two types of risk: lung 
cancer and heart disease. For this risk assessment, OSHA defines 
``heart disease'' to be coronary heart disease excluding strokes, as 
defined in the Framingham study [Ex. 4-108]. In the case of indoor air 
pollutants, the only data available to OSHA were on specific acute 
health effects, such as severe headaches, excluding migraines, and 
other respiratory conditions, such as ``stuffy nose'', ``runny nose'', 
etc. OSHA is aware that there are more serious conditions such as 
legionellosis and hypersensitivity diseases associated with poor indoor 
air and suspected to be potential occupational hazards. However, the 
Agency currently does not have adequate data to conduct a quantitative 
risk assessment addressing these risks in the workplace. OSHA is 
continuing to develop appropriate methodology to address risk 
estimations for conditions related to poor indoor air quality in the 
workplace and is requesting input on data sources relevant to these 
efforts.
    There is uncertainty associated with the quantification of any kind 
of risk. In this risk assessment, OSHA has tried to describe many of 
the sources of uncertainty and to address their implications for OSHA's 
estimates of risk.
    For the purpose of this rulemaking and for deriving a quantitative 
estimate of occupational risk, OSHA has concentrated on information and 
data concerning heart disease and lung cancer as potential effects 
associated with exposure to ETS.

B. Review of Epidemiologic Studies and Published Risk Estimates

    As a first step in this risk assessment, OSHA critically reviewed 
epidemiologic studies associating exposure to ETS or indoor air 
pollutants with adverse health effects. The purpose of such a critical 
evaluation was to determine whether exposure to ETS is a causal factor 
in cancer and heart disease and whether exposure to indoor air 
pollutants has caused a significant increase in acute irritant effects. 
The critical review also enables OSHA to select those studies that have 
potential for use in a quantitative risk assessment. Tables IV-1 and 
IV-2 contain a summary of OSHA's assessment of several epidemiologic 
studies of ETS exposed individuals.
    OSHA evaluated studies on exposure to ETS to determine the 
importance and weight of each study in the overall hazard 
identification process. Of those, it was determined that fourteen 
showed a statistically strong association between exposure to ETS and 
lung cancer and four showed a significant association between ETS 
exposure and heart disease. Studies that were determined to be 
``positive'' by OSHA's review standards met standard epidemiologic and 
statistical criteria to support causation.
    Overall, on the basis of the studies reviewed, OSHA concludes that 
the relative risk of lung cancer in nonsmokers due to chronic exposure 
to ETS ranges between 1.20 and 1.50 and the relative risk for heart 
disease due to ETS exposure ranges between 1.24 and 3.00. 

                        Table IV-1.--Epidemiologic Studies Reviewed by OSHA--Lung Cancer                        
----------------------------------------------------------------------------------------------------------------
                 Positive                        Equivocal positive trend                  Equivocal            
----------------------------------------------------------------------------------------------------------------
Brownson et al. (1992).....................  Akiba et al.....................  Brownson et al. (1987).          
Correa et al...............................  Butler..........................  Buffler et al.                   
Fontham et al..............................  Gao et al.......................  Chan and Fung.                   
Garfinkel et al............................  Gillis et al....................  Hole et al.                      
Geng et al.................................  Kabat and Wynder................  Janerich et al.                  
Hirayama 1984a.............................  ................................  Katada et al.                    
Humble.....................................  ................................  Koo et al.                       
Inoue et al................................  ................................  Lee et al.                       
Kalandidi et al............................  ................................  Shimizu et al.                   
Lam et al..................................  ................................  Sobue et al.                     
Pershagen et al............................  ................................  Svenson et al.                   
Sandler et al..............................  ................................  Wu et al.                        
Stockwell et al............................  ................................  .................................
Trichopoulos et al.........................  ................................  .................................
----------------------------------------------------------------------------------------------------------------


                        Table IV-2.--Epidemiologic Studies Reviewed by OSHA Heart Disease                       
----------------------------------------------------------------------------------------------------------------
                  Positive                       Equivocal positive trend                  Equivocal            
----------------------------------------------------------------------------------------------------------------
Dobson et al...............................  Gillis et al....................  Garland et al.                   
He 1989....................................  Hole et al......................  Lee et al.                       
Helsing et al..............................  Humble et al....................  .................................
Sandler et al..............................  Svendsen et al..................  .................................
Hirayama 1964..............................  ................................  .................................
----------------------------------------------------------------------------------------------------------------

    Other relative risk estimates based on summaries of studies on ETS 
exposure performed by independent scientists and other government 
agencies are found in Tables IV-3 and IV-4. OSHA is not aware of any 
published risk assessments for overall exposure to indoor air 
pollutants. 

         Table IV-3.--Published Risk Estimates for Lung Cancer          
------------------------------------------------------------------------
                                                Estimates of relative   
                  Study                                risk\1\          
------------------------------------------------------------------------
Daleger et al. [Ex. 4-78].................               1.47(.076-2.83)
NRC 1986 [Ex. 4-239]......................               1.34(1.18-1.53)
Repace and Lowry [Ex. 4-263]..............                           2.4
Vainio and Partanen [Ex. 4-312]...........                     1.25-1.30
Wald et al. [Ex. 4-315]:                                                
    Case-control studies..................               1.27(1.05-1.53)
    Prospective studies...................               1.44(1.20-1.72)
    Combined..............................               1.55(1.19-1.54)
Wells [Ex. 4-319].........................               2.10(1.30-3.20)
EPA 1992 [Ex. 4-311]......................                      \2\1.19 
------------------------------------------------------------------------
\1\Numbers in parenthesis indicate published 95 percent confidence      
  intervals.                                                            
\2\Pooled studies.                                                      


        Table IV-4.--Published Risk Estimates for Heart Disease         
------------------------------------------------------------------------
                  Study                      Estimates of relative risk 
------------------------------------------------------------------------
Steenland [Ex. 4-292].....................                       \1\1.51
                                                                 \2\1.37
Wells [Ex. 4-319].........................                      \3\1.32 
------------------------------------------------------------------------
\1\Represents risk to nonsmoking men with spousal exposure.             
\2\Represents risk to nonsmoking women with spousal exposure.           
\3\Women.                                                               

    Most published risk assessments are based on spousal exposure to 
ETS. These studies have examined the lung cancer risk in nonsmoking 
housewives, using spousal smoking as a surrogate for the wife's 
exposure to ETS. The size of the association between these health 
effects and ETS exposure in the workplace is expected to be at least as 
large as the association seen between these health effects and ETS 
exposure in residential settings or public places. As noted by Meridian 
Research in their 1988 report, ``. . . it is the exposure to 
environmental tobacco smoke, and not the environment in which that 
exposure occurs, that is the important risk factor'' [Ex. 4-221]. 
Therefore, health effects observed and the risk estimates calculated 
from studies of the general population, or of selected subgroups, such 
as nonsmoking wives of smoking husbands, are relevant to the working 
nonsmoking population.
    In developing risk estimates for disease attributable to 
occupational exposure, reliance is placed on exposure encountered in 
the workplace to the extent possible. However, in the absence of purely 
occupational data, information derived in environments other than work 
sites is also considered. OSHA believes that there is no physiological 
difference related to exposure (or its outcome) regardless of where it 
is experienced. This is true regardless of whether the endpoint is lung 
cancer, heart disease, or indoor air related acute irritant effects. 
The only difference is that the degree of exposure may be greater in 
one place than in the other. Available information which uses nicotine 
concentration as an index of exposure suggests that the differences in 
exposure between office workplaces and residences lie well within the 
uncertainties of the determinations and for some workplaces, such as 
restaurants and transportation facilities, exposures are significantly 
higher than the average exposures found in residences. Thus, risk 
estimates based on residential exposures are expected to accurately 
reflect occupational risks in most workplaces and possibly 
underestimate the risk in some workplaces.
    In developing its risk assessment for lung cancer, the EPA reviewed 
19 studies which investigated nicotine concentrations in various 
environments [Ex. 4-311]. EPA's analysis showed that the range of 
average nicotine concentrations in office workplaces is very similar to 
that of homes. However, in some workplaces, such as restaurants and 
transportation facilities, exposures are significantly higher. It is 
true that there are many complicating factors in such determinations 
which could affect any final conclusions. For example, it is important 
to consider the duration of exposure, the intensity of exposure, the 
distance from the sources and other factors as well. However, EPA's 
analysis suggests that risk assessments based on home exposures are 
relevant to workplaces as well and, in comparison to some workplaces, 
may even result in an underestimate of the true occupational risk.
    In addition, other studies substantiate the magnitude of workplace 
exposures. For example, Emmons et al. [Ex. 4-98] found that the 
majority of ETS exposure occurred in the workplace. Study subjects were 
selected from workplace settings with a wide range of ETS exposure. The 
work sites ranged from those with minimal restriction of smoking and 
high levels of exposure to work sites with extensive smoking 
restrictions and low exposure. Ninety percent of the subjects worked 
outside the home. Eighty-four percent of those who worked outside the 
home (75.6% of the total sample) reported being regularly exposed to 
smoking in the workplace. While the most highly exposed individuals in 
the study were those who had both home and work exposures, it is clear 
that workplace exposure constituted a significant component of overall 
exposure. Subjects who did not live with smokers reported that the 
majority of their exposure was in the workplace (mean=36.1 min/day), 
home (mean=1.4 min/day) or in other locations (mean=13.1 min/day). 
Subjects who lived with smokers reported receiving slightly more 
exposure at home than the workplace, however the difference between 
home exposure and workplace exposure was not substantial (work: 
mean=29.4 min/day, home: mean=31.2 min/day, other: mean=27.1 min/day). 
These results are shown in Table IV-5. The importance of the findings 
from this study is twofold. First, it indicates that the workplace is 
the primary source of ETS exposure for nonsmokers, who do not live with 
smokers. Secondly, it shows that for nonsmokers living with smokers, 
even though their household environment becomes their primary source of 
exposure, the workplace still contributes a substantial amount of 
exposure, comparable to that experienced by the nonsmoker living with 
nonsmokers (29.4 min/day v. 36.1 min/day). 

               Table IV-5.--Exposure to ETS by Location\1\              
------------------------------------------------------------------------
                                      Exposure    95 percent confidence 
         Subject Category            (min/day)          interval        
------------------------------------------------------------------------
Living with a smoker:                                                   
    Workplace.....................         29.4             (7.01-51.80)
    Home..........................         31.2            (21.60-40.80)
    Other.........................         27.1            (15.10-39.10)
Living without a smoker:                                                
    Workplace.....................         36.1            (22.70-49.50)
    Home..........................          1.4              (0.05-2.75)
    Other.........................         13.1            (8.75-17.40) 
------------------------------------------------------------------------
\1\Source: Emmons et al. [Ex. 4-98]                                     

    Cummings et al. [Exs. 4-67], Hudgafvel-Pursiainen et al. [Ex. 4-
152], and Marcus et al. [Ex. 4-205] also present results to show 
significant workplace exposures to ETS. A re-analysis of the CAPS data 
(a detailed description of this study is found in the EXPOSURE section) 
shows that the workplace contributes on the average 46 percent to the 
total ETS exposure experienced by a nonsmoking worker.

C. Data Sources

    As mentioned previously, only diseases that have been reported to 
be significantly associated with ETS exposure and for which OSHA has 
access to data will be used in calculating health risk due to 
occupational exposure to ETS. These will be referred to as the 
``diseases of interest'' and include coronary heart disease (excluding 
strokes) as defined in the Framingham study and lung cancer.
    Ideally, data on the incidence of the diseases of interest in the 
U.S. population were needed to estimate the number of cases of disease 
in employed nonsmokers. Since nationwide incidence data were not 
available for nonsmokers, several survey sources were used to estimate 
the mortality rates for heart disease (Framingham Community Study) [Ex. 
4-108], and lung cancer (Cancer Prevention Survey conducted by the 
American Cancer Society) [Ex. 4-7]. Data on the U.S. workforce were 
obtained from the Bureau of Labor Statistics [Ex. 4-39]. Based on the 
1993 annual averages, as estimated by the Household Survey, BLS reports 
that the U.S. workforce for sectors covered by this standard is 
estimated to be 101,631,300 (men: 54.36%, women: 45.64%). Information 
on the proportion of employed adults who smoke was obtained from the 
National Health Interview Survey and is found in Table IV-7 [Ex. 4-
235]. It is estimated that 74,201,000 adults (73.01% of the U.S. labor 
force), employed in sectors covered by this standard, are nonsmokers.

    [Editorial note: No Table IV-6 is included in this preamble.] 

 Table IV-7.--Percent Estimates of Adults Employed in the United States 
                          by Smoking Status\1\                          
------------------------------------------------------------------------
                                                      Smoker   Nonsmoker
------------------------------------------------------------------------
Currently employed................................      26.99      73.01
Unemployed........................................      40.38      59.62
Not in labor force................................      21.50     78.50 
------------------------------------------------------------------------
\1\National Health Interview Survey [Ex. 235].                          

    In an effort to characterize prevalence of occupational exposure, 
OSHA considered several sources. To determine the prevalence of smoking 
among U.S. adults during 1991, the National Health Interview Survey-
Health Promotion and Disease Prevention (NHIS-HPDP) supplement 
collected self-reported information on smoking exposure at work from a 
representative sample of the U.S. civilian, non-institutionalized 
population greater than 18 years of age [Ex. 4-51]. In particular, 
employed individuals were asked whether, during the past two weeks, 
anyone had smoked in their immediate work area. Based on results 
adjusted for nonresponse and weighted to reflect national estimates, 
18.81 percent of nonsmokers reported exposure to smoke in their 
immediate work area as shown in Table IV-8. OSHA believes that 18.81 
percent may be an underestimate of frequency of exposure in the 
workplace because it is based solely on self-reported information and 
the question was not very specific in defining immediate work area. 

 Table IV-8.--Percent Estimates of Responses to Question 6a in the NHIS 
                          by Smoking Status\1\                          
------------------------------------------------------------------------
                                                      Smoker   Nonsmoker
------------------------------------------------------------------------
Yes...............................................      37.58      18.81
No................................................      60.81      79.79
Unknown...........................................       1.61      1.39 
------------------------------------------------------------------------
\1\Question 6a was: ``During the past 2 weeks, has anyone smoked in your
  immediate work area?''                                                

    Another source considered by OSHA for defining nonsmoker ETS 
exposure in the workplace was the work published by Cummings et al. 
[Ex. 4-67]. A recent re-analysis of the data file showed that among the 
nonsmoking, currently employed subjects, 48.67 percent (165 out of 339) 
reported exposure to ETS at work and not at home (Table IV-9) [Ex. 4-
69]. Based on the data sources mentioned above, OSHA assumes that the 
percent of nonsmoking workers who are potentially exposed to ETS at 
their worksite ranges between 18.81 and 48.67.

   Table IV-9.--Prevalence of ETS Exposure for Nonsmoking Workers\1\    
------------------------------------------------------------------------
                 Subject category                     Count     Percent 
------------------------------------------------------------------------
Exposed at work and home..........................         99      29.22
Exposed at home, not at work......................         23       6.78
Exposed at work, not at home......................        165      48.67
Not exposed at work or home.......................         52     15.34 
------------------------------------------------------------------------
\1\Data source: Cummings reanalysis [Ex. 4-69].                         

D. OSHA's Estimates of Risk--Environmental Tobacco Smoke Exposure

    The incidence of disease due to occupational exposure in nonsmokers 
was estimated using the following methodology: The expected number of 
cases, Ne, in nonsmoking workers who are occupationally exposed to 
ETS is expressed by:

Ne=Nd - N * Iu = N * (Ip - Iu)

where:
Ne is the cases in nonsmoking exposed workers attributable to ETS 
per year
Nd is the estimated number of cases per year in nonsmoking workers
N is the number of nonsmoking workers in the U.S.
Iu is the incidence rate of disease among the unexposed workers
Ip is the U.S. population incidence rate for nonsmokers

    The number of nonsmoking workers (N) was estimated by multiplying 
the percent of currently employed adults who report to be nonsmokers by 
the number of adult, employed, civilian noninstitutional population, as 
reported by BLS.
    The number of nonsmoking workers with disease per year (Nd) 
was estimated as Nd=N * Ip. The U.S. population incidence 
rate of lung cancer for nonsmoking women is reported to be 0.121 per 
one thousand nonsmoking women. The lung cancer incidence for nonsmoking 
males is estimated to be higher. For the purpose of this risk 
assessment, OSHA used 0.121 as the population incidence rate of lung 
cancer for nonsmokers. This will most likely result in an underestimate 
of the true risk for male workers. The average annual incidence rate 
for death from coronary heart disease excluding strokes for nonsmokers 
age 35 to 64 is estimated to be 4 per one thousand men and 2 per one 
thousand women, as reported by the Framingham study. This results in an 
overall weighted average of 3 deaths per one thousand individuals.
    The incidence rate of disease (Iu) among the unexposed workers 
is estimated using the relationship:

Iu = Ip / [RR * pe + (1-pe)]

where:
RR is the observed relative risk of disease for nonsmokers exposed to 
ETS
pe is the proportion of nonsmoking workers exposed to ETS while at 
work.

    OSHA used 1.34 as an observed estimate of relative risk (RR) for 
lung cancer among nonsmokers with occupational exposure as reported by 
Fontham et al. [Ex. 4-106]. Estimates of observed relative risk for 
heart disease in nonsmokers, as reported by Helsing et al. (1.24 for 
females and 1.31 for males), were used in calculating an overall 
adjusted relative risk estimate of 1.28 [Ex. 4-139]. The adjusted 
relative risk was a weighted average of the reported relative risks 
using the gender composition of the U.S. workforce as weights 
((1.24*45.64 + 1.31*54.36/100) = 1.28). The proportion of nonsmoking 
workers exposed to ETS while at work (pe) was assumed to range 
from 18.81 to 48.67 as stated previously.
    OSHA chose to rely on the Fontham and Helsing studies for estimates 
of the observed relative risks for several reasons. Both studies were 
conducted in the U.S. Both are large, population-based studies whose 
results can be generalized to the general public. Both studies, by 
design, controlled for misclassification to a large degree. The Helsing 
study, which was done in the 60's--a time when smoking was more 
acceptable than more recently, and being a prospective cohort study, 
was less prone to misclassification and other sources of bias. The 
Fontham study used multiple sources to ascertain nonsmoking status and 
validate subject response. Study subjects were questioned twice; the 
self-reported nonsmoking status was corroborated by urinary cotinine 
measurements; and medical records were cross-referenced with the 
physician's assessment. In addition, in the Fontham study, information 
on occupational exposure was collected and an estimate of lung cancer 
risk attributable to the workplace exposure was ascertained.
    The annual risk of disease attributable to occupational exposure to 
ETS was estimated by dividing the expected number of cases (Ne) by 
the number of nonsmoking workers in the U.S. population. Table IV-10 
presents the annual risk attributable to occupational exposure to ETS 
per 1,000 exposed employees. Because section (6)(b)(5) of the OSH Act 
states that no employee shall suffer ``material impairment of health or 
functional capacity even if such an employee has regular exposure to 
the hazard dealt with * * * for the period of his working life'', OSHA 
has converted the attributable annual risk into an attributable 
lifetime risk on the assumption that a worker is employed in his or her 
occupation for 45 years. Lifetime estimates of risk attributable to 
occupational ETS are presented in Table IV-10. Information contained in 
Table IV-10 indicates that for every 1,000 workers exposed to ETS, 
approximately 1 will most likely develop lung cancer and 7 to 16 will 
develop heart disease if they are exposed to ETS at their workplace in 
the course of a 45-year working lifetime. The formula used to calculate 
lifetime risk estimates the probability of at least one occurrence of 
disease in 45 years of continuous exposure and assumes independence of 
events from year to year. It also assumes that the worker's exposure 
profile and working conditions that may affect the level and intensity 
of exposure remain constant throughout a working lifetime.

Table IV-10.--Estimates of Risk For Nonsmoking Workers Exposed to ETS at
                            the Workplace1,2                            
------------------------------------------------------------------------
                                                              Lifetime  
                                                  Annual    occupational
                                                 risk\2\       risk\3\  
------------------------------------------------------------------------
Lung cancer..................................    0.01-0.02         0.4-1
Heart disease................................    0.15-0.36          7-16
------------------------------------------------------------------------
\1\Risks are expressed as number of cases per 1,000 workers at risk.    
\2\The annual risk for nonsmoking workers is estimated assuming the     
  proportion of nonsmoking workers exposed to ETS at the workplace      
  ranges from 18.81 to 48.67.                                           
\3\Assumes 45 years of occupational exposure and is calculated as 1-(1- 
  p)\45\, where p is the annual risk.                                   

E. OSHA's Risk Estimates--Indoor Air Quality

    Adverse health effects associated with poor IAQ are described as 
Building-Related Illness (BRI) and Sick Building Syndrome (SBS). SBS 
related conditions are not easily traced to a single specific 
substance, but are perceived as resulting from some unidentified 
contaminant or combination of contaminants. Symptoms are relieved when 
the employee leaves the building and may be reduced by modifying the 
ventilation system.
    Research in Britain [Ex. 4-44], Denmark [Ex. 4-284] and the United 
States [Ex. 3-745] indicates that about 20% of all office workers are 
afflicted with such symptoms. If the 20% level were to be considered as 
``background'', a simple approach would be to determine that any 
building, more than 20% of whose occupants report the symptoms, would 
be considered to be ``sick''. However, the question then arises as to 
how much greater than 20% would the incidence have to be to be 
considered excess and how would one address such issues as statistical 
significance for any one building. Furthermore, the definition used in 
assessing symptom occurrence can cause substantial variations in 
estimating symptom prevalence, even in the same building. The problem 
with many investigations of ``sick'' buildings is that rarely have 
``non-sick'' or control buildings been used to determine background 
prevalence of the symptoms. Until now, it appears that limited research 
has been done to address the issue of background levels of symptoms. 
OSHA seeks input on data sources to address expected background levels 
of SBS related conditions.
    Mendell and Smith [Ex. 4-218] examined symptom reports compiled in 
a number of individual studies for a number of buildings which had 
different types of ventilation. On the basis of the information 
gathered in the individual studies, Mendell and Smith compared the 
prevalence of sick building symptoms in buildings with five types of 
ventilation: natural only; fans only; air conditioned with no 
humidification; air conditioned with steam humidification; and air 
conditioned with water-based humidification. Overall, they found the 
prevalence of work-related headache, lethargy, upper respiratory/mucous 
membrane, lower respiratory and skin symptoms significantly increased 
in buildings with any type of air conditioning as compared to buildings 
with no air conditioning. Thus, according to this analysis, a basic 
problem with SBS appears to reside in the air conditioning system or, 
in some building aspect associated with the presence of air-
conditioning.
    Building-related illness (BRI) describes those specific medical 
conditions of known etiology which can often be documented by physical 
signs and laboratory findings. Symptoms may or may not disappear when 
the employee leaves the building. Currently, OSHA does not have any 
data on BRI related symptoms to conduct a quantitative risk assessment.
    The number of cases of illness in the United States related to poor 
indoor air quality has not yet been quantified; however OSHA has made 
an attempt to develop a preliminary risk estimate of SBS using a 
similar methodology as was done for ETS. The National Health Interview 
Survey was the primary data source for U.S. population frequency rates 
for acute upper respiratory symptoms other than the common cold, 
influenza, acute bronchitis, and pneumonia and frequency rates on 
severe headaches other than migraines. For this preliminary risk 
assessment, OSHA used the reported frequency rates as representative of 
population incidence rates for upper respiratory conditions and severe 
headaches. OSHA seeks comment on the use of frequency data in place of 
incidence data.
    Observed relative risks for comparable conditions were estimated by 
Mendell [Ex. 4-219]. Mendell's data source was the California Healthy 
Building Study. This study surveyed a representative sample of 12 
public office buildings in Northern California to ascertain the 
occurrence of work-related symptoms associated with air-conditioned 
office buildings. All buildings were either smokefree or had separately 
ventilated designated smoking areas. The sample included 6 buildings 
with air- conditioning systems, 3 buildings with mechanical ventilation 
and no air-conditioning, and 3 buildings with natural ventilation. The 
study included 880 workers. Mendell estimated relative risks for 
several building related symptoms and a subset of these estimates are 
shown in Table IV-11. In an effort to define comparable symptoms 
between the reported national statistics from NHIS and Mendell's study 
and for computational ease OSHA grouped ``runny nose'', ``stuffy 
nose'', ``dry/irritated throat'', and ``dry/irritated/itching eyes'' as 
upper respiratory/mucous membrane symptoms. Mendell reported relative 
risks for upper respiratory conditions and frequent headaches in air-
conditioned buildings as compared to naturally ventilated buildings. 
The relative risk for frequent headaches was reported to be 1.5. For 
upper respiratory conditions, such as ``stuffy nose'', ``runny nose'', 
etc., the relative risks ranged from 1.4 to 1.8. OSHA used 1.4 as an 
observed relative risk for upper respiratory conditions.
    CDC reports in the ``Current Estimates from the National Health 
Interview Survey, 1992'' that the annual rate for severe headaches, 
requiring medical attention or activity restriction, is at least 5 per 
thousand and the rate for upper respiratory conditions is at least 9 
per thousand. In addition, it is estimated that the proportion of 
office buildings in the U.S. with air-conditioning is 70 percent (see 
Preliminary Regulatory Impact Analysis section). Using the above 
information and the same methodology as described in section IV-D, OSHA 
estimated that the lifetime excess burden for severe headaches 
experienced in air-conditioned office buildings is 57 per one thousand 
exposed employees and the lifetime risk for acute upper respiratory 
conditions is 85 per one thousand exposed employees. OSHA's risk 
estimates for indoor air are shown in Table IV-12. OSHA used data 
derived from a study of air-conditioned office buildings to make an 
assessment of the occupational risk in all air-conditioned buildings. 
Furthermore, OSHA made an implicit assumption that an increase in work-
related headaches associated with an air-conditioned office environment 
occurs in the same proportion as headaches which can be severe enough 
to affect work activity. OSHA seeks comment on the applicability of the 
Mendell study for estimating occupational risk in air-conditioned 
buildings due to poor indoor air quality. In addition, OSHA seeks 
comment on its methodology of developing annual and lifetime risk 
estimates attributable to occupational exposures.

Table IV-11.--California Healthy Building Study Comparing Buildings With
        Natural Ventilation to Buildings With Air-Conditioning\1\       
------------------------------------------------------------------------
                                                   Relative   Confidence
                 Health outcome                      risk      interval 
------------------------------------------------------------------------
Upper respiratory symptoms:                                             
  Runny nose.....................................      1.5     (0.9-2.5)
  Stuffy nose....................................      1.8     (1.2-3.7)
  Dry/irritated throat...........................      1.6     (0.9-2.7)
  Dry/irritated/itchy eyes.......................      1.4     (0.9-2.2)
Frequent headaches...............................      1.5     (0.9-0.3)
------------------------------------------------------------------------
\1\Study subjects were asked whether the symptoms were occurring often  
  or always at work and improving when away from work.                  


  Table IV-12.--OSHA's Estimates of Risk for Workers in Air-Conditioned 
                              Buildings\1\                              
------------------------------------------------------------------------
                                                    Annual    Lifetime  
                                                   risk\2\  occupational
                                                               risk\3\  
------------------------------------------------------------------------
Severe headaches\4\..............................    1.296         57   
Upper respiratory symptoms\5\....................    1.969         85   
------------------------------------------------------------------------
\1\Risks are expressed as number of cases per 1,000 workers at risk.    
\2\The annual risk is estimated assuming that the prevalence of air-    
  conditioned office buildings in the U.S. is 70 percent.               
\3\Assumes 45 years of occupational exposure and is calculated as 1-(1- 
  p45, where p is the annual risk.                                      
\4\Defined as headaches that either require medical attention or        
  restrict activity.                                                    
\5\Defined as runny nose, stuffy nose, dry/irritated throat and dry/    
  irritated/itchy eyes and being severe enough to either require medical
  attention or restrict activity.                                       

F. Pharmacokinetic Modeling of ETS Exposure

    In developing a final rule, OSHA would like to consider the use of 
a physiologically based pharmacokinetic (PBPK) model in an effort to 
develop a clear and complete picture of factors that may affect 
environmental exposure measurements, internal dose estimates and 
ultimately estimates of expected risk attributed to ETS exposure at the 
workplace. OSHA is seeking comment on appropriate methodology, 
available data, etc. The following discussion offers an explanation of 
OSHA's approach to this issue and an opportunity for the Agency to 
solicit comment on specific points of concern as they relate to the use 
of pharmacokinetics in estimating occupational risk from exposure to 
ETS.
    Estimating the risk from exposure to ETS requires the use of some 
measure of the extent of exposure. Possible measures, or metrics, can 
range from categorical ranking based on survey responses to direct 
measurement of ETS-related chemicals in the body fluids of exposed 
individuals. In general, the use of an internal measure of individual 
exposure would be preferred over measurements of environmental 
contamination, such as airborne chemical or particulate concentrations. 
In particular, considerable attention has been given in the scientific 
literature to the possible use of cotinine concentrations in body 
fluids as a biomarker of ETS exposure [Exs. 4-24, 4-146, 4-165, 4-263, 
4-316]. However, obtaining a dependable estimate of exposure from 
measurements of a chemical's concentration in body fluids requires a 
quantitative understanding of the chemical's pharmacokinetics; its 
uptake, distribution, metabolism, and excretion. Following is a review 
of the evidence concerning the suitability of cotinine as an internal 
biomarker for ETS exposure.
1. Considerations for Selection of a Biomarker for ETS
    A biomarker should, to the greatest extent possible, accurately 
represent the individual's exposure to the substance of concern and 
have relevance to a specific endpoint. In the case of ETS, there are 
several relevant endpoints, with principal attention being given to 
heart disease and lung cancer. Each different endpoint may be mediated 
by a different subset of the components of ETS, and therefore the 
appropriate biomarker(s) for each endpoint could be different.
2. Cardiovascular Effects
    Cardiovascular effects resulting from exposure to ETS have been 
associated with carbon monoxide (CO), nicotine, and more recently with 
polycyclic aromatic hydrocarbons (PAHs) [Ex. 4-123]. Each of these is 
associated with a different fraction of ETS; CO is a gas phase 
constituent, nicotine is a low volatility vapor, and PAHs are absorbed 
on particulates. Because of the significant differences in physical 
fate and transport, a strategy for the use of biomarkers for 
cardiovascular effects of ETS would ideally make use of separate 
markers for CO, nicotine, and PAHs.
    The most common internal measure of CO exposure is blood 
carboxyhemoglobin (HbCO). Blood HbCO provides a useful measure of 
exposure to CO, and can be related to the cardiovascular effects of CO. 
A way to determine the occupational component of one's total CO 
exposure is to measure workplace CO levels and predict blood HbCO with 
a physiologically based pharmacokinetic model for CO [Ex. 4-11]. A 
difficulty associated with the use of CO or HbCO as a biomarker for ETS 
effects is the presence of other sources of CO in the workplace.
    Nicotine can be measured directly in body fluids and the 
circulating concentration can be related to physiological effects, such 
as heart rate [Ex. 4-26]. Alternatively, measurements of nicotine in 
air or cotinine in body fluids can be measured, and the circulating 
concentration of nicotine can be inferred using a pharmacokinetic 
model. The use of a pharmacokinetic model to relate inhaled nicotine to 
circulating nicotine and cotinine levels is the main focus of this 
section.
    PAHs are inhaled in the form of particulates on which they are 
adsorbed. Developing an appropriate biomarker for ETS-associated PAHs 
is complicated by the presence of PAHs on particulates not associated 
with ETS, and by the low, and variable, composition of PAHs adsorbed to 
particulate matter. One candidate material which has been suggested as 
an environmental marker for ETS-associated particulates is solanesol, a 
non-volatile tobacco constituent. However, the pharmacokinetic 
information necessary for use of solanesol as an internal biomarker is 
not currently available.
    The use of these three different biomarkers (CO, PAHs, and 
solanesol) does not appear to be practical. It appears that the most 
effective strategy currently achievable would be to rely on nicotine 
(or cotinine) measurement as a specific marker of ETS exposure as well 
as a direct measure of nicotine exposure.
3. Carcinogenicity
    The mechanism of carcinogenicity from exposure to ETS is not known, 
but it has been established that ETS includes a number of chemicals 
which have been identified as carcinogens (see Tables II-2, III-6, and 
III-7), although most of the identified carcinogenic components of ETS 
are not unique to ETS. Therefore, direct measurement of the 
carcinogenic components or related biomarkers in biological fluids 
would not provide a unique measure of exposure from ETS. The 
potentially carcinogenic components of ETS include highly volatile 
chemicals such as formaldehyde and benzene, lower volatility chemicals 
such as the nitrosamines, and non-volatile chemicals such as PAHs and 
metal compounds, which are bound to particulates. Given the current 
lack of information on the mechanism of carcinogenicity of ETS it is 
impossible to identify which components of ETS should be targeted for 
exposure estimation. The most prudent choice for a biomarker in this 
case would be one which provides the most general representation of all 
the components of ETS, and which is itself unique to ETS. In an 
experimental study of potential ETS-unique environmental markers of 
exposure, only nicotine was found to represent both the gas phase and 
particulate phase organic constituent of ETS [Ex. 4-97]. Several 
studies have shown a strong correlation between measurements of 
nicotine in the air and the mutagenicity of ETS [Exs. 4-198, 4-215]. In 
these studies, the relationship of nicotine to mutagenicity was as good 
as or better than the relationship of RSP to mutagenicity (RSP is 
assumed to be the major contributor of the carcinogenic effects of 
ETS). Therefore, since measurements of nicotine in the air correlate 
better than measurements of RSP to mutagenicity of ETS, and there is a 
positive correlation between short-term mutagenicity tests and 
carcinogenicity, the use of nicotine as an exposure marker for the 
carcinogenic effects of ETS appears to be justified.
4. Evaluation of Cotinine as a Biomarker for ETS
    The purpose of this section is to discuss the use of cotinine, a 
metabolite of nicotine, as an internal biomarker for inhalation 
exposure to nicotine, and, as such, its usefulness as a metric for the 
health effects of ETS. Cotinine is preferred over nicotine as an 
internal biomarker because of its slower clearance from the body [Ex. 
4-71].
    There is a strong correlation between nicotine intake and plasma 
cotinine levels [Ex. 4-115]. There is also a strong correlation between 
cotinine measured in body fluids and ETS exposure. In a controlled 
study, urinary cotinine was found to be a reliable marker for long-term 
ETS exposure, and plasma and salivary cotinine were found to be good 
indicators of short- as well as long-term exposure [Ex. 4-73]. Several 
studies have also demonstrated a positive relationship between self-
reported exposure to ETS and cotinine in serum [Exs. 4-166, 4-250, 4-
301], saliva [Ex. 4-166], and urine [Exs. 4-166, 4-211, 4-316]. In 
general, the currently available data support the assumption that 
nicotine and cotinine kinetics parameters for smokers can be 
extrapolated to nonsmokers for estimating exposures to ETS in 
nonsmokers [Ex. 4-24]. Studies have also demonstrated that salivary 
levels of cotinine are directly proportional to plasma levels [Ex. 4-
73], and that urinary excretion of cotinine is linearly related to 
plasma levels [Ex. 4-82]. Thus all three biological fluids provide a 
reasonable metric for nicotine intake, and thus can serve as biomarkers 
of ETS exposure in nonsmokers.
    There are two potential difficulties associated with the use of 
cotinine as a biomarker for ETS. The first is the presence of nicotine 
in the diet. Several foods, including tea, tomatoes, and potatoes, have 
been shown to contain nicotine in measurable quantities [Exs. 4-49, 4-
81, 4-281]. However, a study of 3,383 nonsmokers was unable to 
substantiate an effect of tea drinking on serum cotinine levels for 
self-reported daily tea consumption [Ex. 4-301]. The same study did 
find a strong correlation between self-reported ETS exposure and serum 
cotinine level.
    OSHA seeks comment and data on whether dietary intake of nicotine 
should be considered a significant factor in modelling nicotine 
metabolism for assessing risk due to ETS exposure.
    The second issue associated with the use of cotinine as a biomarker 
is the possibility that there is a longer half-life for the elimination 
of cotinine at very low biological concentrations, associated with the 
slow release of nicotine from binding sites [Exs. 4-28, 4-24, 4-167, 4-
254]. This longer half-life at very low concentrations could have the 
effect of overestimating exposure to ETS in the lowest exposed 
population. At this time there is not sufficient evidence to quantify 
the potential magnitude of this effect, but it is likely to be small. 
OSHA seeks comment on this issue.
5. Description of Pharmacokinetic Models for Nicotine and Cotinine
    For many purposes, an essentially first order process such as the 
kinetics of cotinine can be effectively modeled with a simple 
compartmental kinetic analysis [Exs. 4-27, 4-24, 4-73, 4-82]. The 
compartmental approach has been used to relate steady-state urinary 
cotinine levels to atmospheric nicotine concentrations [Ex. 4-263]. For 
investigating some of the concerns associated with the use of cotinine 
as a biomarker, however, a physiologically based pharmacokinetic (PBPK) 
description would be preferred. The advantage of the PBPK approach 
stems from its biologically motivated structure, which permits the 
direct incorporation of biochemical data and the biologically 
constrained comparison of model predictions with experimental 
timecourses to investigate such issues as dose-rate effects, exposure-
route differences, pharmacodynamic processes, and other potential 
nonlinearities [Ex. 4-57]. PBPK models of nicotine and cotinine have 
been described for both rats [Exs. 4-112, 4-255] and humans [Exs. 4-
254, 4-270].
    A physiological model of cotinine disposition [Ex. 4-112] was 
developed to analyze intravenous infusion of nicotine and cotinine and 
bolus dosing of cotinine in rats. In general, the observed cotinine 
time profiles in blood and tissues were consistent with linear 
kinetics, but the distribution of cotinine into all tissues appeared to 
be roughly three-fold greater following infusion of nicotine than 
following infusion of cotinine, and the clearance of cotinine following 
bolus and infusion dosing was significantly different.
    A more recent rat model [Ex. 255] featured a physiologically based 
description of nicotine kinetics and a compartmental description of 
cotinine. This model provided a successful description of the plasma 
kinetics of both nicotine and cotinine for intraarterial or intravenous 
bolus dosing of nicotine. The timecourse of nicotine in most tissues 
was also consistent with first order kinetics; however, it was 
necessary to include a description of saturable nicotine binding in the 
brain, heart, and lung to adequately reproduce nicotine concentration 
profiles in these tissues. This rat model has also been scaled for use 
in predicting mouse and human pharmacokinetics [Ex. 4-254]. The human 
model has recently been expanded to include a physiological description 
of cotinine as well as a forearm compartment, and is now able to 
describe nicotine and cotinine kinetics following intravenous infusion 
of nicotine in humans [Ex. 4-266]. Another human model [Ex. 4-270] has 
also been developed which includes physiological descriptions of both 
nicotine and cotinine. This model, which assumes linear kinetics, 
predicts results which agree with published data on the kinetics of 
nicotine and cotinine in blood following nicotine infusion as well as 
cotinine in the blood following the infusion of cotinine.
6. Application of Pharmacokinetic Modeling for ETS Exposure Estimation
    Both of the human models described above possess a reasonable 
biologically based structure, and either model would provide a useful 
starting point for the development of a PBPK model which could be of 
use in examining the relationship between cotinine concentrations in 
body fluids and inhaled nicotine. However, neither of the models 
currently possesses all of the features which would be necessary for 
such an analysis. The most useful application of PBPK modeling would 
appear to be to support an analysis of four issues related to the use 
of cotinine as a biomarker of ETS exposure: (1) Estimation of the 
contribution of dietary intake of nicotine to cotinine levels in the 
plasma, saliva and urine of nonsmokers; (2) Estimation of a plausible 
upper bound for cotinine concentrations in plasma, saliva and urine 
associated with ETS exposure (to identify individuals wrongfully 
identifying themselves as nonsmokers). This can be viewed as a way to 
validate misclassification results derived from surveys; (3) Evaluation 
of the potential impact of high affinity, low capacity binding of 
nicotine and cotinine in nonsmokers with low exposure to ETS; and (4) 
Evaluation of the potential impact of pharmacokinetic uncertainty and 
variability on the use of cotinine concentrations in plasma, saliva or 
urine to infer an individual's ETS exposure. The necessary features for 
accomplishing these analyses include both inhalation and oral routes of 
nicotine exposure, a salivary compartment, and a description of 
nicotine binding in the brain, heart and lung.
    In evaluating the use of cotinine as a biomarker of ETS exposure, 
two kinds of uncertainty must be considered. The first kind of 
uncertainty embraces those factors which could tend to bias a risk 
estimate. Two such factors are dietary intake of nicotine and nicotine 
binding. In both of these cases, the impact of ignoring the effect, if 
it were significant, would be to overestimate exposure (and therefore 
risk) for the least exposed individuals. The second kind of uncertainty 
includes those factors which tend to broaden the confidence interval 
for the risk estimate. The most significant factors in this category 
are uncertainty in the fraction of nicotine converted to free cotinine, 
and the rates of metabolic and urinary clearance of nicotine and 
cotinine. An example of such uncertainty is results reported for half-
lives of cotinine in nonsmokers [Ex. 4-24, 4-73, 4-82, 4-184, 4-186], 
showing a mean of 16.2 hours, with a coefficient of variation of 0.22.
7. Analysis of Uncertainty
    It is useful in this evaluation to distinguish uncertainty from 
variability. As it relates to the issue of using pharmacokinetic 
modeling in risk assessment, uncertainty can be defined as the possible 
error in estimating the ``true'' value of a parameter for a 
representative (``average'') individual. Variability, on the other 
hand, represents differences from individual to individual.
    For the purpose of evaluating the usefulness of pharmacokinetic 
modeling for estimating exposure, the uncertainty and variability in 
the various parameters for the pharmacokinetic models can be grouped 
into four classes: the physiological parameters (volumes and flows), 
the tissue distribution parameters (partitioning and binding), and the 
kinetic parameters (absorption, metabolism, and clearance).
    (a) Physiological Parameters. The physiological parameters include 
(1) the body weight and the weights of the individual organs or tissue 
groups, (2) the total blood flow and flows to each organ or tissue 
group, and (3) the alveolar ventilation rate. These quantities have 
been reasonably well established for the human [Exs. 4-155, 4-309] and 
the chief effort associated with pharmacokinetic model parameterization 
in the human is the determination of the necessary level of detail for 
the physiological description, grouping of the tissues not meriting a 
separate description into pharmacokinetically similar groups, and the 
association of the proper volume and flow data with the selected 
groupings. Existing models for nicotine and cotinine contain a fairly 
detailed physiological structure and differ only slightly in their 
assignment of tissues. The model of Plowchalk and deBethizy [Ex. 4-254] 
includes separate compartments for the brain, heart, and skin. The 
first two of these tissues are lumped into a ``vessel-rich'' tissue 
compartment in the model of Robinson et al. [Ex. 4-270], and the skin 
is lumped in with the muscle. Conversely, the gastrointestinal tract is 
given a separate compartment in the Robinson model but is lumped into a 
``slowly perfused'' tissue compartment in the Plowchalk model. These 
differences mainly reflect the different interests of the modeling 
groups in terms of target organs and routes of exposure. The Robinson 
model contains a venous infusion compartment to accommodate the mixing 
time for arterial administration. The published Plowchalk model does 
not include this feature, but a forearm compartment has since been 
added to provide a similar function [Ex. 4-83]. Neither model appears 
to contain an explicit description of inhalation or oral exposure, but 
the necessary equations could easily be added to the existing 
physiological structures. A salivary fluid compartment could also be 
added to either model if desired. Experience with other chemicals has 
shown that uncertainty in the physiological parameters generally has 
much less impact on overall model uncertainty because they are known 
relatively well and are not as influential on model behavior as the 
distribution and kinetic parameters [Ex. 4-56].
    (b) Distributional Parameters. In both of the published human 
models, the tissue partitioning was initially estimated on the basis of 
steady-state tissue/blood concentration ratios measured in animals. The 
partitioning parameters in the Robinson model were then iteratively 
adjusted to fit other timecourse data. The resulting partition 
coefficients in the two models differ by a factor from two to five in 
corresponding tissues. The partitioning data for cotinine, determined 
by Gabrelsson and Bondesson [Ex. 4-112], show a similar level of 
uncertainty; partitions for cotinine following infusion of nicotine 
were two- to five-fold higher than the same partitions following 
infusion of cotinine. The lack of reproducibility of these data 
represents a deficiency in the development of PBPK modeling for these 
chemicals. Fortunately, the partition coefficients tend to be less 
important than the kinetic parameters in terms of overall model 
performance. To a large extent, as long as the volume of distribution 
associated with the physiological structure and partition coefficients 
is in agreement with the apparent pharmacokinetic volume of 
distribution for each chemical, the model will perform adequately in 
terms of timecourses in blood and urine. This was evidenced by the 
ability of the Robinson model to reproduce published nicotine and 
cotinine pharmacokinetic data [Ex. 4-270]. A potentially more 
significant uncertainty associated with distribution is the possibility 
of pharmacokinetically significant tissue binding of nicotine. 
Satisfactory description of the timecourse of nicotine in the brain, 
lung, and heart of the rat required the inclusion of binding in these 
tissues [Ex. 4-255]. Clearly, the relatively low capacity, high 
affinity binding associated with nicotine is unlikely to effect total 
systemic clearance except at very low concentrations. However, the 
existence of nonlinear pharmacokinetics at low concentrations could 
lead to a miscalculation of exposure for the least exposed individuals. 
It has been suggested that there is a longer clearance half-life for 
nicotine, and therefore cotinine, associated with low circulating 
concentrations, and that this longer half-life is due to the slower 
release of nicotine bound to tissues [Exs. 4-28, 4-24, 4-167]. To date, 
no careful pharmacokinetic investigation of this possibility has been 
performed in the human model, and adequate nicotine-specific tissue 
binding information does not appear to have been collected except 
perhaps in the brain.
    (c) Kinetic Parameters. By far the most significant parameters in 
the models are those describing the absorption, metabolism, and 
clearance of nicotine and cotinine. The Robinson model uses reported 
human hepatic and renal clearance values for nicotine and cotinine. The 
sensitivity of this model to these input parameters was investigated by 
varying them within the range of reported clearance values from 
infusion studies in humans. The resulting model predictions for post-
infusion blood levels, urinary output, and the elimination half-lives 
of both nicotine and cotinine were found to be well within the ranges 
of those observed in human studies. Thus the model structure does not 
produce an exaggerated response to variation of the input parameters, 
and reflects the natural interaction between measures of clearance, 
volume of distribution, and rates of elimination. In the case of the 
physiological parameters, variability dominates over uncertainty, while 
for the distributional parameters, uncertainty dominates. In the case 
of the kinetic parameters describing clearance, it appears that 
variability again dominates. For example, the mean values for the 
terminal half-life of cotinine reported in different studies range from 
12 to 21 hours in non-smokers [Exs. 4-24, 4-73, 4-82, 4-184, 4-186]. 
The coefficient of variation in these same studies, a measure of 
interindividual variability, ranges from 17-22%, and the coefficient of 
variation for the entire collection of reported individual values is 
similar: 22% (N=35, mean=16.2). A review of the published data on 
infusion of nicotine and cotinine in humans [Ex. 4-270] found a 3-fold 
variation in reported half-lives for cotinine. For comparison, the 
variation in the volume of distribution for cotinine was 5-fold, while 
for the half-life and volume of distribution of nicotine, the variation 
was 8-fold and 6-fold, respectively. An even greater level of 
variability can be expected for the kinetic parameters for the renal 
clearance of nicotine and cotinine.
    OSHA considers the use of pharmacokinetics and specifically PBPK 
models an important tool in characterizing and quantifying internal 
dose for evaluation potential exposures and seeks comment on the 
applicability of this approach in ascertaining the relationship between 
adverse health effects and exposure to ETS.

V. Significance of Risk

    Before the Secretary can promulgate any permanent health or safety 
standard, he must find that a significant risk of harm is present in 
the workplace and that the new standard is reasonably necessary to 
reduce or eliminate that risk. Industrial Union Department, AFL-CIO v. 
American Petroleum Institute, 444 U. S. 607, 639-642 (1980) (Benzene). 
In the Benzene case, the Supreme Court held that section 3(8) of the 
Act, which defines a ``occupational safety and health standard'' as a 
``requirement reasonably necessary or appropriate'' to promote safety 
or health requires that, before promulgating a standard, the Secretary 
must find, ``on the basis of substantial evidence, that it is at least 
more likely than not that long-term exposure to [the hazard without new 
regulation] presents a significant risk of material health 
impairment.'' 444 U. S. at 653.
    In the Benzene decision, the Supreme Court indicated when a 
reasonable person might consider the risk significant and take steps to 
decrease it. The Court stated:

    It is the Agency's responsibility to determine in the first 
instance what it considers 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% benzene will be fatal, a reasonable person might well 
consider the risk significant and take the appropriate steps to 
decrease or eliminate it. (IUD v. API, 448 U. S. at 655).

A. Environmental Tobacco Smoke

    Two of the adverse health effects associated with exposure to ETS 
are lung cancer and heart disease (coronary heart disease, excluding 
strokes). Clinically, lung cancer is almost always fatal. However, 
heart disease runs the gamut from severe to disabling to fatal. Both of 
these diseases then constitute the type of ``material impairment of 
health or functional capacity'' which the Act seeks to reduce or 
eliminate. Therefore a standard aimed at reducing the incidence of 
these impairments is an appropriate exercise of the Secretary's 
regulatory authority.
    In the case before us the Agency estimates that there will be 
approximately between 144 and 722 cases of lung cancer per year among 
nonsmoking American workers exposed to ETS in the workplace. When 
considered over a working lifetime, this translates into an excess lung 
cancer rate in the workplace of one per thousand. As noted above, the 
Benzene court clearly indicated that a risk of one in a thousand could 
be considered significant and that the Agency would be justified in 
prescribing reasonable efforts to reduce such a risk.
    Therefore, the risk from lung cancer associated with worker 
exposure to ETS in the workplace meets the Benzene court's 
characterization of what could be considered significant.
    In addition, in evaluating the significance of the risk posed by 
any particular workplace hazard, the Secretary is entitled to take into 
consideration not only the rate of risk but the total number of workers 
exposed to such risk and the absolute magnitude of effects. In this 
case, evidence in the record shows that approximately between 144 and 
722 lung cancer deaths per year are attributable to ETS and that there 
are presently over 74 million nonsmoking American workers exposed to 
ETS in their places of employment. On the basis of these data, it would 
also be reasonable to conclude that Agency action is warranted to 
reduce this widespread and significant risk, although the Agency would 
reach this conclusion even without the great magnitude of effects.
    As noted above, cancer is not the only serious adverse health 
effect associated with exposure to ETS. Preliminary estimates indicate 
that the risk of mortality from heart disease due to ETS exposure is 
even greater than that of cancer. The Agency estimates that there will 
be between 2,094 and 13,000 deaths from heart disease per year among 
nonsmoking American workers exposed to ETS in the workplace. When 
considered over a working lifetime, this translates into an excess 
death rate of approximately between 7 and 16 cases of heart disease per 
thousand attributed to workplace exposure to ETS. Clearly, this risk is 
significant in itself and combined with the lung cancer risk, the 
significance of risk is very great.
    The proposal seeks to protect nonsmoking employees from the hazards 
of exposure to ETS in the workplace. It does this by prescribing the 
conditions under which employees would be allowed to smoke in the 
workplace, that is, only in separately enclosed designated areas which 
are separately ventilated. No employee can be required to work in an 
area where there will be contamination from ETS. This in OSHA's view 
reduces significant risk to only a small percentage of the current 
risk. To the extent that there are failures of enforcement of the 
smoking limitation and of the ventilation system, the risk will not be 
totally eliminated. Since there is no definition of, nor an established 
method for quantifying, exposure, it is not possible to determine a 
``dose limit'' that would eliminate significant risk. Even if that were 
possible, it is not clear it would be the correct policy approach.
    29 CFR Part 1990--Identification, Classification and Regulation of 
Potential Occupational Carcinogens sets forth certain procedures for 
regulating occupational carcinogens. Those procedures may not allow for 
the level of public input and policy review that is appropriate for 
this rulemaking, involving many different types of health effects and a 
broad range of employers and workers. Accordingly, the Assistant 
Secretary finds pursuant to 29 CFR Section 1911.4 that ``in order to 
provide greater procedural protections to interested persons or for 
other good cause consistent with the applicable laws'' ``it is found 
necessary or appropriate'' to adopt different procedures here.

B. Indoor Air Quality

    Poor indoor air quality creates a variety of material impairments 
of health, two aspects of which are Building-Related Illness and Sick 
Building Syndrome.
    One of the most severe health effects associated with Building-
Related Illness is legionellosis, a disease associated with microbial 
contamination of water sources which is commonly found in the water 
present in heating and cooling systems of buildings. Legionnaire's 
disease, caused by the Legionella organism, results in pneumonia which 
is fatal in approximately 20% of the cases. Even when not fatal, it is 
usually very severe, requiring substantial treatment or 
hospitalization. As many as 5% of those exposed to Legionella will get 
sick1. Legionnaire's disease and other illnesses associated with 
microbial contamination due to poor indoor air quality are serious 
health effects that constitute material impairment. Compliance with the 
indoor air quality provisions set forth in the proposal will 
substantially reduce these illnesses.
---------------------------------------------------------------------------

    \1\Raw figures from 1992 show approximately 1300 cases of 
Legionella reported although this is most certainly a gross under-
estimation of the scope of the problem, since the disease resembles 
others and is frequently misdiagnosed.
---------------------------------------------------------------------------

    There are numerous other adverse health effects such as nausea, 
dizziness, fatigue, pulmonary edema, asthma and aggravation of existing 
cardiovascular disease, which have been associated with poor indoor air 
quality. Evidence in the record indicates that between 20 and 30% of 
office buildings are ``sick'', having environments which may lead to a 
variety of these effects. Unfortunately, quantitative data are not 
systematically available on all of these effects.
    For purposes of risk evaluation, however, as explained more fully 
in the risk assessment discussion, the Agency has primarily focussed on 
two health effects commonly associated with poor indoor air quality: 
upper respiratory symptoms and severe headaches. The upper respiratory 
symptoms associated with poor indoor air quality (sick building 
syndrome) include stuffy nose, runny nose, dry itchy eyes, nose and 
throat. For purposes of our evaluation, ``severe headaches'' are 
defined as those serious enough to require medical attention or 
restrict activity, but excludes migraines.
    Unlike lung cancer and heart disease (health effects associated 
with exposure to ETS), these effects will not lead to death. There is 
no doubt, however, that OSHA does have the authority to regulate 
working conditions that lead to the type of upper respiratory effects 
and severe headaches described herein.
    Clearly the upper respiratory effects and severe headaches 
associated with poor indoor air quality are of the type that interfere 
with the performance of work. The severe headaches were such that 
medical treatment had to be sought; certainly such headaches were 
impairing at the time they occurred, even though they were not 
permanent. The upper respiratory symptoms were also severe enough to 
either require medical attention or restrict activity.
    There is ample precedent in OSHA rulemaking proceedings for the 
regulation of working conditions to avoid health impairments that are 
material but not life threatening. The Supreme Court in the cotton dust 
case,2 concluded that OSHA had the authority to promulgate 
regulations that would avoid Byssinosis, a respiratory disease which in 
the large majority of cases is not deadly or disabling, and is 
reversible if the employee left the cotton mills. Stage \1/2\ 
byssinosis, the most frequent type, has relatively mild symptoms. In 
the case of occupational exposure to formaldehyde, the regulation was 
designed to avoid, among other things, sensory irritation.3
---------------------------------------------------------------------------

    \2\AFL-CIO v. Marshall, 452 U. S. 490 (1981)
    \3\ See 52 FR 46168, 46235 (12/4/87)
---------------------------------------------------------------------------

    Moreover in the ``Air Contaminants'' standard, OSHA regulated many 
chemicals, such as acetone, gypsum and limestone which caused less 
severe impairments of health.4 In promulgating the final air 
contaminant rule OSHA analyzed which sorts of conditions would 
constitute material impairment, concluding that ``. . . the OSH Act is 
designed to be protective of workers and is to protect against 
impairment with less impact than severe impairment.''5 The less 
severe conditions, such as upper respiratory symptoms and severe 
headaches, caused by poor indoor air quality are the same type as the 
PELs preamble concluded were material impairments. These specific 
conclusions of the Agency with respect to what constitutes material 
impairments were upheld by the Court of Appeals on review6 
although the Court disagreed with OSHA on other matters.
---------------------------------------------------------------------------

    \4\See 54 FR 2332, 2361 (1/19/89)
    \5\ See discussion, 54 FR at 2361-2362
    \6\See AFL-CIO v. OSHA, 965 F. 2d 962, 975 (11th Cir., 1992). 
The Court noted that ``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' . . 
. from exposure to toxic substances.''
---------------------------------------------------------------------------

    Therefore OSHA concludes that the adverse health effects caused by 
poor indoor air quality, which range from legionellosis to severe 
headaches to upper respiratory symptoms are material impairments of 
health which the Act allows the Agency to regulate.
    The effects of the pneumonia caused by Legionella are deadly or 
severe. Although the rate of risk may not be as large as 1/1000 because 
the number of employees at risk is large. This effect alone makes a 
substantial contribution to a finding of significant risk, especially 
when taking into account the large number of cases.
    As to the severe headaches, the Agency estimates that the excess 
risk of developing the type of non-migraine headache which may need 
medical attention or restrict activity which has been associated with 
poor indoor air quality is 57 per 1,000 exposed employees. In addition 
the excess risk of developing upper respiratory symptoms which are 
severe enough to require medical attention or restrict activity is 
estimated to be 85 per 1,000 exposed employees. These numbers are 
extrapolated from actual field studies and therefore show the magnitude 
of the problem at present. There is no doubt that better maintenance of 
ventilation systems such as required in the proposal will improve the 
quality of air in covered workplaces and reduce the number of cases. In 
addition the types of good practices prescribed in the proposal will 
substantially reduce the type of microbial contamination associated 
with Legionnaire's disease. Therefore, OSHA concludes that this number 
of less severe effects along with the severe effects from Legionnaire's 
disease, together, constitute a significant risk. Accordingly, OSHA 
preliminarily concludes that, the proposal will substantially reduce a 
significant risk of material impairment of health from poor indoor air 
quality.

VI. Preliminary Regulatory Impact Analysis

A. Introduction

    Executive Order 12886 requires a Regulatory Impact Analysis and 
Regulatory Flexibility Analysis to be prepared for any regulation that 
meets the criteria for a ``significant regulatory action.'' One of 
these criteria, relevant to this rulemaking is that the rule have an 
effect on the economy of $100 million or more per year. Based upon the 
preliminary analysis presented below, OSHA finds that the proposed 
standard will constitute a significant regulatory action.
    The estimates presented in this Phase 1 Preliminary Regulatory 
Impact Analysis demonstrate technological and economic feasibility of 
the proposed standard. The analysis provides a non-detailed preliminary 
count of the affected employees and buildings, the associated costs, 
and benefits of the proposed standard provisions.
    OSHA estimates the annual cost of compliance with the IAQ standard 
to be $8.1 billion, of which the most costly provision will be for the 
building systems operation and maintenance, $8.0 billion. The cost for 
eliminating exposure to ETS may range from $0 to $68 million depending 
on whether establishments ban smoking or allow smoking in designated 
areas. In order to assess the overall economic impact of the rule, OSHA 
also estimated the cost savings to employers, or cost savings that will 
result from the implementation of the proposed standard. The major 
forms of these savings are efficiency and productivity improvements, 
cost reductions in operations and maintenance, and reduced incidence of 
property damage. Cost savings associated with productivity improvements 
are estimated to be $15 billion annually.
    OSHA preliminarily estimates that the proposed standard will 
prevent 3.0 million severe headaches and 4.5 million upper respiratory 
symptoms over the next 45 years. This is, approximately, 69,000 severe 
headaches and 105,000 upper respiratory symptoms per year. These 
estimates understate the prevalence of building-related symptoms since 
they reflect excess risk in only air conditioned buildings. In 
addition, 5,583 to 32,502 lung cancer deaths and 97,700 to 577,818 
coronary heart disease deaths related to occupational exposure to ETS 
will be prevented over the next 45 years. This represents 140 to 722 
lung cancer deaths per year and 2,094 to 13,001 heart disease deaths 
per year.

B. Industry Profile

    The environmental concern for air pollution has been largely 
focussed on questions of outdoor air contamination. Recently, however, 
attention has begun to shift to concerns about the quality of air 
within buildings since people spend 80 to 90 percent of their time 
indoors [Ex. 3-1075H].
    Indoor air is a variable complex mixture of chemicals and airborne 
particles. Its composition largely depends on the outdoor environment 
(urban or rural area), the shelter itself (age, construction material, 
electric equipment, heating, cooling, and ventilation systems), the 
activities of the occupants (smoking, nonsmoking, cooking by gas, oil 
or electricity) and the presence of plants and animals.
    The Industry Profile chapter characterizes the building stock and 
describes the factors that affect indoor air quality. This section also 
presents the number of employees who work in buildings whose indoor air 
will be affected by the proposed standard.
1. Affected Industries
    The standard covers all OSHA regulated industries: Agriculture, Oil 
and Gas Extraction (SIC 13), Manufacturing, Transportation, 
Communications, Wholesale Trade, Retail Trade, Finance, Insurance and 
Real Estate and Services. The scope of the proposal is twofold. The 
proposed indoor air quality compliance provisions would only cover 
employers with non-industrial work environments. This includes public 
and private buildings, schools, healthcare facilities, offices and 
office areas. Coverage also applies to nonindustrial work environments 
that are part of industrial worksites (e.g., an office, cafeteria, or 
break room located at a manufacturing facility).
    The provisions for protecting the nonsmoking employees from 
exposure to ETS apply to all indoor or enclosed work environments, in 
industrial and nonindustrial establishments. This would include 
maritime, construction, and agricultural workplaces.
2. Indoor Contaminants-Sources
    Indoor air contaminants emanate from a broad array of sources that 
can originate both outside of structures as well as from within a 
building. When a building is new, some contaminants are given off 
quickly and soon disappear. Others continue off-gassing at a slow pace 
for years. Common office supplies and equipment have been found to 
release hazardous chemicals--especially duplicators and copiers. Bulk 
paper stores have been found to release formaldehyde [Ex. 3-1087A20]. 
Some typical contaminants are listed below:

(a) Gases and Vapors (organic/inorganic):
    --Radon
    --Sulfur dioxide
    --Ammonia
    --Carbon Monoxide
    --Carbon Dioxide
    --Nitrous Oxides
    --Formaldehyde
(b) Fibers:
    --Asbestos
    --Fiberglass/Mineral Wools
    --Textiles/Cotton
(c) Dusts:
    --Allergens
    --Household dust (mites)
    --Pollens:
    --Feathers
    --Danders
    --Spores
    --Smoke/Fume
    --Environmental Tobacco Smoke
    --Coal
    --Wood
(d) Microbes:
    --Bacteria
    --Fungi
    --Viruses

    People contribute millions of particles to the indoor air primarily 
through the shedding of skin scales. Many of these scales carry 
microbes, most of which are short lived and harmless. Clothing, 
furnishings, draperies, carpets, etc. contribute fibers and other 
fragments. Cleaning processes, sweeping, vacuuming, dusting normally 
remove the larger particles, but often increase the airborne 
concentrations of the smaller particles. Cooking, broiling, grilling, 
gas and oil burning, smoking, coal and wood generate vast numbers of 
airborne indoor pollutants in various classifications.
3. Controlling Indoor Air
    Control of pollutants at the source is the most effective strategy 
for maintaining clean indoor air. However, control or mitigation of all 
sources is not always possible or practical. In the case of ETS, this 
means restricting smoking to separately ventilated spaces. General 
ventilation is, therefore, the second most effective approach to 
providing acceptable indoor air [Exs. 3-1061G, 3-1075J].
    Outside air dilutes and removes contaminants through natural 
ventilation, mechanical ventilation or through infiltration and 
exfiltration. Natural ventilation occurs when desired air flows occur 
through windows, doors, chimneys and other building openings. 
Mechanical ventilation is the mechanically induced movement of air 
through the building. Mechanical systems usually condition and filter 
the air and allow for the entry of outdoor air through outdoor dampers. 
Infiltration is the unwanted movement of air through cracks and 
openings into the building shell.
    The outside air ventilation rate of a building affects indoor air 
quality. It determines the extent to which contaminants are diluted and 
removed from the indoor environment. The extent to which outside air 
ventilation is effective in diluting indoor contaminants depends on how 
well outside air is mixed with indoor air and is reflected by 
ventilation efficiency. Ventilation efficiency can be reduced by air 
short-circuiting from the supply diffusers to the return inlets, by 
modular furniture partitions, and differences between the supply air 
temperature and the room air temperature.
    The rate at which outside air is supplied to a building is 
specified by the building code at the design stage. Outside air 
ventilation rates are based primarily on the need to control odors and 
carbon dioxide levels (e.g., occupant-generated contaminants or 
bioeffluents). Carbon dioxide is a component of outdoor air whose 
excessive accumulation indoors can indicate inadequate ventilation.
    Lack of adequate ventilation contributes to indoor air related 
health complaints. Specific deficiencies that produce air quality 
problems include inadequate outside air supply, poor air distribution, 
poor air mixing (and therefore poor ventilation efficiency), inadequate 
control of humidity, insufficient maintenance of the ventilation 
system, inadequate HVAC system capacity and inadequate exhaust from 
occupied areas. Inadequate outdoor air supply and distribution and 
insufficient control of thermal conditions can result from strategies 
to control energy consumption. In approximately 500 indoor air quality 
investigations conducted in the late 1970's and early 1980's, the 
National Institute for Occupational Safety and Health (NIOSH) found 
that the primary causes of indoor air quality problems were inadequate 
ventilation (52%), contamination from outside the building (10%), 
microbial contamination (5%), contamination from building fabric (4%) 
and unknown sources (13%) [56 FR 47892]. To date, NIOSH has conducted 
over 1,100 IAQ related investigations, but has not yet evaluated them 
to provide updated estimates.
    OSHA, therefore, believes that it is necessary to require 
maintenance of the HVAC system components that directly affect IAQ, 
since failure to do so results in the degradation of IAQ. Standards of 
HVAC maintenance vary and sometimes are deficient where untrained 
personnel are designated to maintain complex systems. It is, also, 
customary for companies to defer maintenance for economic and budgetary 
reasons, with adverse impacts on IAQ. Some examples of maintenance 
deficiencies include: plugged drains on cooling coil condensate drip 
pans (resulting in microbial contamination); failed exhaust fans in 
underground parking garages; microbial fouling of cooling tower water 
from lack of water treatment with biocides resulting in legionellosis 
cases; and failure of the automatic temperature control system 
resulting in lack of outside ventilation air.
4. Building Characteristics
    During the last 25 years, technical and socioeconomic changes have 
profoundly influenced the methods employed to plan, design, construct 
and operate buildings. Buildings system design, maintenance and 
operation can, and regularly do, provide acceptable indoor 
environments. However, neglect or disregard of the sources of indoor 
air contaminants, or of the proper design, operation and maintenance of 
building system components which influence indoor air quality can 
create an uncomfortable and unhealthy indoor atmosphere [Ex. 3-1075H2].
    The oil embargo of 1973 brought about the realization that 
considerable savings could be made in reducing the consumption of 
energy used to heat and cool buildings. Prior to 1973, the energy to 
heat and cool buildings was much cheaper and the buildings reflected 
that reality. Building enclosures had lower insulating values and 
allowed more infiltration. More air was circulated to the occupied 
spaces and more outdoor air was provided for ventilation. This resulted 
in a lower concentration of pollutants and higher velocities of air 
motion in indoor air. Office buildings were divided into individual 
rooms with their own walls as opposed to the current practice of open 
spaces with movable screens [Ex. 4-74].
    The centralization of services and the expanding economy have led 
to concentration of office space in the cities. The cost of land has 
shaped buildings into high-rise structures. The cost of materials and 
popularity of mirror glass has led to the sprouting of hundreds of what 
may be termed ``glass boxes''. These boxes are sealed to keep out noise 
and pollution--mainly from traffic.
    Buildings designed after 1973 have incorporated many energy 
conservation measures that range from adjusting thermal comfort zones 
to increased awareness of lighting efficiency, to designing new 
operating methods for ``sealed building'' [Ex.3-1159, p.1]. In large 
buildings, outside air ventilation rates were also reduced by closing 
outside air dampers in mechanical ventilation systems at nights, on 
weekends and sometimes even during occupancy. As a result of these 
measures, which primarily reduced costs for conditioning outdoor air as 
opposed to increasing energy efficiency, considerable energy savings 
have been achieved in buildings.
    In addition, during the 1970's variable air volume (VAV) HVAC 
systems became widely accepted. VAV systems condition supply air to a 
constant temperature and insure thermal comfort by varying the airflow. 
Early VAV systems did not allow control of the outside air quantity, so 
that a decreasing amount of outside air was provided as the flow of 
supply air was reduced.
    In some cases, building design flaws contribute to the poor quality 
of indoor air, such as locating air intake vents near to a loading dock 
or parking garage. Design flaws of interior space also contribute to 
indoor air problems. Most building cooling systems are designed to 
remove the heat generated by office machines, employees and light. The 
heat generated by these sources often exceeds the capacity of the HVAC 
system to remove it [Ex.3-1159C1]. Ideally with effective filtration 
and management systems, the air indoors should be cleaner than the air 
outdoors.
5. Profile of Affected Buildings
    Estimates of the number of buildings potentially affected by the 
indoor air standard were developed by OSHA based on Department of 
Energy's commercial building energy consumption survey (CBEC) 1989\7\ 
[Ex. 4-303]. There is a total of 4.5 million commercial buildings in 
the United States. Commercial buildings are defined as all non-
manufacturing/industrial and non-residential structures. Table VI-1 
presents the distribution of buildings by use, occupancy and thermal 
conditioning. Approximately 28 percent of all buildings are for 
mercantile or services. Other uses include offices (15 percent), 
assembly and warehouses (14 percent each), food service (5 percent), 
lodging (3 percent) and food sales and healthcare (2 percent each). The 
``other'' category (1 percent) covers buildings such as public 
restrooms and buildings that are 50 percent or more commercial but 
whose principal activity is agricultural, industrial/manufacturing or 
residential.
---------------------------------------------------------------------------

    \7\The commercial building and energy consumption survey is a 
triennial national sample survey of commercial buildings and their 
energy suppliers. This survey is the only source of national level-
data on both commercial building characteristics and energy 
consumption.
---------------------------------------------------------------------------

    On average, the largest types of buildings are for education and 
health care. Mercantile and service buildings account for the greatest 
number and floorspace of any single activity category. Office buildings 
account for nearly as much floorspace, but far fewer buildings. 
Together office and mercantile buildings represent almost 40 percent of 
all buildings and floorspace. Warehouses and assembly buildings both 
are almost as numerous as office buildings, but account for less 
floorspace. Over 62 percent of buildings have only one floor and 13 
percent have three or more floors. Most buildings (69%) house single 
establishments. Government occupied buildings represent 13 percent. 

                 Table VI-1.--Employees Working in Buildings and Other Building Characteristics                 
----------------------------------------------------------------------------------------------------------------
                                                                                   Percent of                   
                 Principle building activity                       Number of          all         Total number  
                                                                   buildings       buildings       employees    
----------------------------------------------------------------------------------------------------------------
Principal building activity:                                                                                    
    Assembly.................................................            615,000           14          4,012,000
    Education................................................            284,000            6          7,204,000
    Food sales...............................................            102,000            2            844,000
    Food service.............................................            241,000            5          1,943,000
    Health care..............................................             80,000            2          4,225,000
    Lodging..................................................            140,000            3          3,092,000
    Mercantile and service...................................          1,278,000           28         12,414,000
    Office...................................................            679,000           15         27,780,000
    Parking garage...........................................             45,000            1            332,000
    Public order and safety..................................             50,000            1            861,000
    Warehouse................................................            618,000           14          4,377,000
    Other....................................................             62,000            1          2,111,000
    Vacant\1\................................................            333,000            7         1,472,000 
                                                              --------------------------------------------------
      Total..................................................          4,527,000  ...........         70,667,000
Building occupants:                                                                                             
    Single establishments--owner occupied....................          2,445,000           54                   
    Multiple establishments--owner occupied..................            369,000            8                   
    Single establishments--nonowner occupied.................            672,000           15                   
    Multiple establishments--nonowner occupied...............            259,000            6                   
    Vacant...................................................            206,000            5                   
    Government buildings.....................................            577,000           13                   
Thermal conditioning:                                                                                           
    Heated...................................................          3,865,000           85                   
                                                              --------------------------------                  
        Entire building......................................          2,739,000           60                   
        Part of building.....................................          1,126,000           25                   
    Cooled...................................................          3,184,000           70                   
                                                              --------------------------------                  
        Entire building......................................          1,550,000           34                   
        Part of building.....................................          1,634,000           36                   
----------------------------------------------------------------------------------------------------------------
\1\Vacant buildings may contain occupants who are using up to 50 percent of the floorspace.                     
                                                                                                                
Source: U.S. Energy Information Administration, Commercial Buildings Characteristics 1989. Washington, DC. June 
  1991.                                                                                                         

    The survey also provides information on the number of buildings 
with heating and air conditioning systems. Total number of heated 
buildings is estimated to be 3.9 million. Heating systems include 
boilers, furnaces, individual space heaters, and packaged heating 
units. Almost one-half of all the buildings are heated by forced-air 
central systems. Air-distributing heat and cooling systems are most 
prevalent in office, mercantile and service buildings. The survey 
reveals that 70 percent of the buildings have air conditioning. It also 
shows that 80 percent of the buildings have heat and air conditioning, 
and 12 percent have heat, but no air conditioning.
    Over 40 percent of the floorspace built since 1986 was in a 
building with a computerized energy management and control systems 
(EMCS). EMCS is an energy conservation feature that uses mini/micro 
computers, instrumentation, control equipment and software to manage a 
building's use of energy for heating, ventilation, air conditioning, 
lighting and/or business related processes. These systems can also 
manage fire control, safety and security. Overall, EMCS are present in 
buildings accounting for 23 percent of floorspace. EMCS controls HVAC 
in only 251,000 buildings or 6 percent of total number of buildings.
    However, the DOE survey [Ex. 4-303] does not provide data by two-
digit Standard Industrial Classification (SIC). The number of buildings 
by SIC will determine subsequent costs. OSHA applied the DOE estimates 
of the number of buildings by type of occupancy (single or multi-
tenant) to the number of establishments by two-digit SIC given by the 
Bureau of Labor Statistics. First, OSHA allocated non-government single 
tenant buildings (estimated at 3.1 million) across the relative two-
digit SIC using the relative two-digit SIC distribution of the number 
of establishments. Then, OSHA allocated the 0.8 million non-government 
multi-establishment buildings across two-digit SIC using the relative 
two-digit SIC distribution of the number of establishments in multi-
establishment buildings (2.8 million). All government buildings were 
considered single tenant buildings. OSHA recognizes that this 
methodology of classification of buildings by two-digit SIC code may 
not reflect the fact that establishments in multi-tenant buildings 
should be allocated across several SICs or the fact that some single 
establishment buildings may be concentrated in certain SICs instead of 
all SICs. This is particularly true for the agricultural sector for 
which farms and farm buildings (silos, grain elevators and barns) are 
outside the scope of the IAQ portion of the proposal. However, OSHA 
does not have the data to provide such delineation at this point. Table 
VI-2 presents OSHA's estimate of the number of buildings by two-digit 
SIC and by characteristics of occupancy and ventilation system.

              Table VI-2.--Number of Buildings and Establishments Affected by IAQ Proposed Standard             
----------------------------------------------------------------------------------------------------------------
                                                                                                      Number of 
                             Buildings with  Buildings with     Total      Number of    Number of     naturally 
        SIC industry             single         multiple      number of      heated       cooled     ventilated 
                             establishments  establishments   buildings    buildings    buildings   buildings\1\
----------------------------------------------------------------------------------------------------------------
Agriculture, forestry,                                                                                          
 fishing...................        136,629          36,557       173,186      147,806      124,312        10,564
Mining.....................         11,976           3,204        15,181       12,956       10,897           926
Construction...............        336,841          90,127       426,968      364,398      306,475        26,045
Manufacturing..............        203,995          54,582       258,577      220,684      185,605        15,773
Transportation.............        127,706          34,170       161,876      138,154      116,193         9,874
Wholesale and retail trade.      1,011,035         270,518     1,281,553    1,093,747      919,889        78,175
Finance, insurance, real                                                                                        
 estate....................        275,760          73,784       349,544      298,320      250,900        21,322
Services...................      1,013,057         271,058     1,284,115    1,095,934      921,729        78,331
Government.................        577,000   ..............      577,000      505,000      348,000        35,197
                            ------------------------------------------------------------------------------------
      Total................      3,694,000         834,000     4,528,000    3,877,000    3,184,000       276,208
----------------------------------------------------------------------------------------------------------------
\1\Based on estimate of 6.1 percent of floorspace without HVAC.                                                 
                                                                                                                
Source: OSHA, Office of Regulatory Analysis, 1994.                                                              

6. Buildings With Indoor Air Problems
    Many published reports on building wellness describe buildings in 
terms of two general categories, sick or well buildings. Some of the 
published categories, in addition to the terms sick or well are: 
problem buildings and non-problem buildings, healthy buildings; 
buildings with high and low rates of IAQ related complaints; sick 
building syndrome (SBS).
    The SBS symptom complex is characterized by a range of symptoms 
including but not limited to, eye, nose and throat irritation, dryness 
of mucous membranes and skin, nose bleeds, skin rash, mental fatigue, 
headache, cough, hoarseness, wheezing, nausea and dizziness [Ex. 4-
159]. Within a given building there will usually be some commonality 
among the symptoms manifested as well as temporal association between 
occupancy in the building and appearance of symptoms. Many people who 
work in buildings characterized as having SBS typically exhibit health 
symptoms that disappear when the person is no longer in the building. 
In most cases, a physical basis for the occurrence of the SBS can be 
found: lack of proper maintenance, changes in thermal or contaminant 
loads imposed during the building's life, changes in control strategies 
to meet new objectives (e.g., energy conservation) or inadequate 
design.
    Building-related illnesses (BRI), on the other hand, are medically 
diagnosed diseases that present symptoms that can last for weeks, 
months, years or even a lifetime. Examples include nosocomial 
infections, humidifier fever, hypersensitivity pneumonitis, and 
legionellois. BRI can develop as a result of poor building systems 
operation and maintenance and uncontrolled point sources of 
contaminants.
    No building has a complete absence of problems, but those that 
function with minimal occupant complaints and comply with acceptable 
criteria for occupant exposure, system performance, maintenance 
procedures and economic objectives may be characterized as healthy 
buildings. Figure VI-1 below presents the classification of buildings 
by stages of performance.
    Based on the information submitted to the docket, OSHA assumed that 
30 percent of the buildings have indoor air quality problems [Ex. 3-
745].
BILLING CODE 4510-26-P


TP05AP94.000


BILLING CODE 4510-26-C

    Therefore, as presented in Table VI-3, the total number of problem 
buildings is estimated to be 1.4 million buildings.
7. Number of Employees Affected
    The commercial building energy consumption survey estimates that 
there are 70.7 million employees. However, survey data do not provide 
information by two-digit SIC. OSHA examined data obtained through the 
Bureau of Labor Statistics to estimate the number of employees by two-
digit SIC affected by the proposed standard. The data from the Bureau 
provided occupational breakdown of the labor force by detailed industry 
categories (two-digit SIC) and major occupational groupings.

   Table VI-3.--Number of Problem Buildings and Number of Employees Exposed to Indoor Air Quality Problems\1\   
----------------------------------------------------------------------------------------------------------------
                                                                                                     Number of  
                                                                     Employees       Number of       employees  
                                                                      working     buildings with  exposed to IAQ
                                                                    indoors\2\     IAQ problems     problems\3\ 
----------------------------------------------------------------------------------------------------------------
Agriculture, forestry, fishing..................................         279,050          51,956          83,715
Mining..........................................................         180,700           4,554          54,210
Construction....................................................       1,643,750         128,091         493,125
Manufacturing...................................................       5,748,000          77,573       1,724,400
Transportation..................................................       3,412,350          48,563       1,023,705
Wholesale and retail trade......................................      15,744,000         384,466       4,723,200
Finance, insurance, real estate.................................       7,248,150         104,863       2,174,445
Services........................................................      26,926,000         385,235       8,077,800
Government......................................................       9,473,561         173,100       2,842,068
                                                                 -----------------------------------------------
      Total.....................................................      70,655,561       1,358,400      21,196,668
----------------------------------------------------------------------------------------------------------------
\1\Exclusive of exposure to ETS.                                                                                
\2\OSHA estimate based upon BLS's 1993 employed persons by detailed industry and major occupation.              
\3\Based on OSHA estimate of 30 percent employee exposure to poor IAQ.                                          
                                                                                                                
Source: OSHA, Office of Regulatory Analysis, 1994.                                                              

    OSHA classified employees according to whether or not they work 
primarily in indoor areas, e.g., areas with possible exposures, by 
developing percentages of employees in each occupational category who 
might be working indoors. For example, personnel in the transportation 
industries were apportioned according to those potentially exposed to 
indoor air pollution (office workers) and those who are not (truck 
drivers). Table VI-3 presents the distribution of the 70.7 million 
employees who work indoors.
    No data are available as to the number of employees exposed to poor 
indoor air quality. Based on OSHA's percentage of problem buildings (30 
percent), OSHA assumed that 30 percent of employees working indoors are 
exposed to poor indoor air quality. Therefore, the number of employees 
potentially affected is 21 million.
8. Environmental Tobacco Smoke
    Environmental Tobacco Smoke (ETS) represents one of the strongest 
sources of indoor air contaminants in buildings where smoking is 
permitted. ETS is a mixture of irritating gases and carcinogenic tar 
particles and is considered one of the most widespread and harmful 
indoor air pollutants.
    (a) Smoking ordinances\8\ and policies. State and Local Governments 
have adopted an increasing number of ordinances and regulations 
limiting smoking in public and private worksites. The restrictiveness 
of these laws varies from simple, limited prohibitions to laws that ban 
smoking. Forty-five states and the District of Columbia restrict 
smoking in public workplaces and 19 states and the District of Columbia 
restrict smoking in private workplaces.
---------------------------------------------------------------------------

    \8\A smoking ordinance may mean any local law which addresses 
public smoking in some fashion to protect non-smokers.
---------------------------------------------------------------------------

    There are 397 city and county smoking ordinances covering 22 
percent of the total population [Ex. 4-305]. A total of 297 cities and 
counties mandate the adoption of workplace smoking policies. Typically 
these provisions require employers (private and public) to maintain a 
written smoking policy. Ordinances range from requirements for written 
smoking policies to the total elimination of smoking in the workplace. 
A total of 505 cities and counties limit smoking, specifically in 
restaurants. The requirements range from a nonsmoking section of 
unspecified size to the banning of all smoking [Ex. 4-305].
    A 1991 survey of company smoking policies shows that of the 85 
percent of firms with smoking policies, 34 percent have complete bans 
and another 34 percent prohibit smoking in all open work areas. Over 90 
percent of non-manufacturing establishments have smoking policies [H-
030 Ex. 77].
    Workplace smoking policies are more common in larger businesses. In 
a survey of personnel managers, 63 percent of those with 1,000 or more 
employees reported having a smoking policy compared with 52 percent of 
companies with fewer employees. In the same survey, smaller companies 
were half as likely as larger ones to have a policy under 
consideration. Similar findings were reported by the National Survey of 
Worksite Health Promotion Activities, in which larger worksites were 
more likely than smaller ones to report smoking control activities. In 
a survey of private New York city businesses, only 4 percent of 
companies with fewer than 100 employees had a written smoking policy 
[Ex. 3-1030Q].
    (b) Number of nonsmokers working indoors. Based on the National 
Health Interview Survey, OSHA estimated that 74.2 million employees or 
73.01 percent of the U.S. labor force covered by OSHA are nonsmokers. 
Table VI-4 presents the distribution of nonsmoking employees by two 
digit SIC.
    Results of population based surveys show that 88 percent of 
nonsmokers are aware of the negative health consequences of ETS. 
Despite this general awareness, exposure to ETS is pervasive [Ex. 4-
98]. To determine the occupational exposure of nonsmoking employees to 
ETS, OSHA used the estimate provided by the 1991 National Health 
Interview Survey. The survey, requested information from employed 
individuals on whether during the past two weeks anyone smoked in their 
immediate work area. Based on results adjusted for non-response and 
weighted to reflect national estimates, 18.81 percent reported exposure 
to ETS. OSHA believes that the 18.8 percent is an underestimate since 
it is based solely on self reported information and the question was 
not very specific in defining ``immediate'' work area. A recent 
reanalysis of a study by Cummings et al. [Ex. 4-68] shows that 48.67 
percent of currently employed nonsmokers reported ETS exposure at work 
and not at home [Ex. 3-442F].

                          Table VI-4.--Employees Exposed to Environmental Tobacco Smoke                         
----------------------------------------------------------------------------------------------------------------
                                                                                  Number of employees exposed to
                                                                                                ETS             
                          SIC industry                               Nonsmoker   -------------------------------
                                                                   employees\1\     Lower bound     Upper bound 
                                                                                     (18.81%)        (48.67%)   
----------------------------------------------------------------------------------------------------------------
Agriculture, forestry, fishing..................................       1,008,007         189,606         490,597
Mining..........................................................         249,256          46,885         121,313
Construction....................................................       3,479,876         654,565       1,693,655
Manufacturing...................................................      13,050,099       2,454,724       6,351,483
Transportation..................................................       3,953,337         743,623       1,924,089
Wholesale and retail trade......................................      19,041,884       3,581,778       9,267,685
Finance, insurance, real estate.................................       3,995,180         751,493       1,944,454
Services........................................................      21,687,986       4,079,510      10,555,543
Government......................................................       7,735,393       1,455,027       3,764,816
                                                                 -----------------------------------------------
      Total.....................................................      74,201,019      13,957,212      36,113,636
----------------------------------------------------------------------------------------------------------------
\1\Based on 73.01 percent nonsmoking employees.                                                                 
                                                                                                                
Source: OSHA, Office of Regulatory Analysis, 1994.                                                              

    By applying the lower and upper ranges of exposure, OSHA estimates 
that the number of nonsmoking employees exposed to ETS to be 13.9 to 
36.1 million employees.

C. Nonregulatory Alternatives

(1) Introduction
    The declared purpose of the Occupational Safety and Health (OSH) 
Act of 1970 is ``* * * to assure so far as possible every working man 
and woman in the Nation safe and healthful working conditions and to 
preserve our human resources. * * *'' Thus, the Act requires the 
Secretary of Labor, when promulgating occupational safety and health 
standards for toxic materials or harmful physical agents, to set the 
standard ``* * * that most adequately assures, to the extent feasible, 
on the basis of the best available evidence, that no employee will 
suffer material impairment of health or functional capacity. * * *'' It 
is on the basis of this congressional directive that OSHA has initiated 
regulatory actions to reduce the adverse health effects associated with 
occupational exposure to indoor air pollutants.
    The discussion below assesses the requisite preconditions for 
optimal safety in the context of a free market economy, and real world 
economic factors are compared with the free market paradigm to 
illustrate the shortcoming of the nonregulatory environment.
(2) Market Imperfections
    Economic theory suggests that the need for government regulation is 
greatly reduced where private markets work efficiently and effectively 
to allocate health and safety resources. The theory typically assumes 
perfectly competitive labor markets where employees, having perfect 
knowledge of job risks and being perfectly mobile among jobs, command 
wage premiums that fully compensate for any risk of future harm. Thus, 
theoretically, the costs of occupational injury and illness are borne 
initially by the firms responsible for the hazardous workplace 
conditions and ultimately by the consumers who pay for the final goods 
and services produced by these firms. With all costs internalized, 
private employers have an incentive to reduce hazards wherever the cost 
of hazard abatement is less than the total cost to the firm, the work 
force, and society of the expected injury or illness.
    The conditions of perfect competition do not need to be completely 
satisfied in order for the forces of the market to approximate an 
efficient outcome. However, some market imperfections can produce sub-
optimal results that can be improved upon with regulatory action. In 
the case of this rulemaking, employees face a significant health risk 
which is not adequately addressed by current nonregulatory 
alternatives. OSHA, therefore, believes that it must take appropriate 
actions to provide greater health protection for workers exposed to 
toxic substances.
    Although OSHA believes that adequate job safety and health could 
exist in the private market under perfect conditions, the private 
market often fails to provide acceptable levels of safety and health in 
instances where these conditions are not met. It appears that at least 
two of several conditions traditionally considered essential components 
of perfect markets are absent from the environment in which employees 
are exposed to hazards associated with exposure to indoor pollutants: 
(1) Perfect employee knowledge of risks and (2) perfect employee 
mobility between jobs.
    First, evidence on occupational health hazards in general suggests 
that in the absence of immediate or clear-cut danger, employees and 
employers have little incentive to seek or provide information on the 
potential long-term effects of exposure. Employers faced with 
potentially high compensatory payments may, in fact, have a 
disincentive to provide information to employees. When relevant 
information is provided, however, employers and employees might still 
find informed decisionmaking a difficult task, especially where long 
latency periods precede the development of chronic disabling disease. 
Moreover, if signs and symptoms are nonspecific--that is, if an illness 
could be job-related or could have other causes--employees and 
employers may not link disease with such occupational exposure.
    Second, even if workers were fully informed of the health risks 
associated with exposure to hazardous substances, many face limited 
employment options. Nontransferability of occupational skills and high 
national unemployment rates sharply reduce a worker's expectation of 
obtaining alternative employment quickly or easily.
    In many regions of the country, the practical choice for workers is 
not between a safe job and a better paying but more hazardous position, 
but simply between employment and unemployment at the prevailing rates 
of pay and risk. In addition to the fear of substantial income loss 
from prolonged periods of unemployment, the high costs of relocation, 
the reluctance to break family and community ties, and the growth of 
institutional factors such as pension plans and seniority rights serve 
to elevate the cost of job transfer. Thus, especially where wages are 
more responsive to the demands of more mobile workers who tend to be 
younger and perhaps less aware of job risks, hazard premiums for the 
average worker will not be fully compensated. Where this is the case, 
labor market negotiations are unlikely to reflect accurately the value 
that workers place on health.
    In addition to these market imperfections, externalities occur if 
employers and employees settle for an inefficiently low level of 
protection from hazardous substances. For the competitive market to 
function efficiently, only workers and their employers should be 
affected by the level of safety and health provided in market 
transactions. In the case of occupational safety and health, however, 
society shares part of the financial burden of occupationally induced 
diseases, including the costs of premature death, chronic illness, and 
disability. Those individuals who suffer from occupationally related 
illnesses are cared for and compensated by society through taxpayer 
support of social programs, including welfare, Social Security, and 
Medicare.
    If private employers do not have to pay the full cost of 
production, they have no economic incentive to reduce hazards whenever 
the cost of hazard abatement is greater than the cost of the expected 
illness. In this way, the private market fails to produce optimal 
levels of safety.
(3) Alternative Non-regulatory Options
    Based on the above evidence, OSHA has concluded that the private 
market has failed to provide optimal levels of safety to employees. 
Consequently, some form of intervention that fosters safer work 
environments must be used to reduce occupational exposure. Because such 
intervention need not occur through government regulation, OSHA has 
considered the effectiveness of other non-regulatory options: (1) 
relying on tort litigation and (2) relying on workers' compensation 
programs.
    (a) Tort Liability. The use of liability under tort law is one 
nonregulatory alternative that has been increasingly used in litigation 
concerning occupationally related illnesses. Prosser [Ex. 4-256] 
describes a tort, in part, as a ``civil wrong, other than a breach of 
contract, for which the court will provide a remedy in the form of an 
action for damages''.
    If the tort system applies, it would allow a worker whose health 
has been adversely affected by occupational exposure to a hazardous 
substance to sue and recover damages from the employer. Thus, if the 
tort system is effectively applied, it might shift the liability of 
direct costs of occupational disease from the worker to the firm under 
certain specific circumstances.
    With very limited exceptions, however, the tort system is not a 
viable alternative in dealings between employees and employers. All 
states have legislation providing that Workers' Compensation is either 
the exclusive or principal remedy available to employees against their 
employers. Thus, under tort law, workers with an occupational disease 
caused by exposure to a hazardous substance can only file a product 
liability suit against a third party manufacturer, processor, 
distributor, sales firm, or contractor. It is often difficult, however, 
to demonstrate a direct link between an exposure to a hazardous 
substance and the illness.
    In order to pursue litigation successfully, there must be specific 
knowledge of the magnitude and duration of a worker's exposure to a 
hazardous substance, as well as the causal link between the disease and 
the occupational exposure. Usually, it is extremely difficult to 
isolate the role of occupational exposures in causing the disease, 
especially if workers are exposed to many toxic substances and the 
exposure is not necessarily limited to the workplace such as the case 
for ETS. This difficulty is further compounded by the long latency 
periods that are frequently involved. In addition, the liable party 
must be identifiable, but workers may have several employers over a 
working lifetime. The burden of proof that an occupational exposure to 
a hazardous substance occurred, that a specific employer is the liable 
party, and that the exposure level was significant may prohibit the 
individual from initiating the suit.
    There are an increasing number of lawsuits that are related to 
health effects to building occupants from poor indoor air quality. 
These lawsuits are typically filed after the illness or health effect 
has been diagnosed. In this sense, increasing pressure is being placed 
on businesses. However, the legal pressure currently does not relate to 
the implementation of a clean indoor air policy (e.g., legal action is 
not currently being taken just because a company does not have a clean 
indoor air policy. These actions are event related as opposed to being 
policy related). IAQ litigation is growing rapidly and the focus is 
shifting from residential to commercial facilities. Examples to 
emphasize that are the recent $12.5 million claims against the Social 
Security Administration for the Richmond, California episode of 
Legionnaire's disease, the Call versus Prudential case in which 
building tenants settled with the defendants in what may have been the 
first jury trial in sick building litigation, and a suit by Hamilton, 
Ohio, county employees against their office building owners alleging 
exposure to fumes, bacteria, fungi, dust and irritants [Ex. 3-575].
    Legal proceedings do not internalize occupational illness costs 
because they involve substantial legal fees associated with bringing 
about court action. In deciding whether to sue, the tort victim must be 
sure that the size of the claim will be large enough to cover legal 
expenses. In effect, the plaintiff is likely to face substantial 
transaction costs in the form of a contingency fee, commonly 33 
percent, plus additional legal expenses. The accused firm must also pay 
for its defense. The high costs and uncertainties associated with tort 
law make it an inefficient mechanism for ensuring adequate protection 
of workers' health.
    Insurance and liability costs are not borne in full by the specific 
employer responsible for the risk involved. For firms that are insured, 
the premium determination process is such that premiums only partially 
reflect changes in risk associated with changes in exposure to 
hazardous substances. This lack of complete adjustment is the so-called 
``moral hazard'' problem, which is the risk that arises from the 
possible imprudence of the insured. As the insured firm has paid an 
insurance company to assume some of the risks, that firm has less 
reason to exercise the diligence necessary to avoid losses. Transfer of 
risk is a fundamental source of imperfection in markets.
    There is a growing number of state and local laws and ordinances 
controlling smoking. Armed with new data that show health effects from 
indoor air pollutants, plaintiffs who believe that they have been 
injured by the air inside their workplaces are beginning to take the 
offensive. They are lobbying on the local, state and federal levels for 
protective legislation, and in the absence of such legislation, they 
are suing for damages to their health. These cases are complex not only 
in the nature of the technical proof that must be developed and 
presented, but also in the number of parties involved. Suits have been 
filed against architects, builders, contractors, building product 
manufacturers and realtors [Ex. 3-662].
    (b) Workers' Compensation. The Workers' Compensation system is a 
result of the perceived inadequacies in liability or insurance systems 
to compel employers to prevent occupational disease or compensate 
workers fully for their losses. The system was designed to internalize 
some of the social costs of production, but in reality it has fallen 
short of compensating workers adequately for occupationally related 
disease. Thus, society shares the burden of occupationally related 
health effects, premature mortality, excess morbidity, and disability 
through taxpayer support of social programs such as welfare, Social 
Security disability payments, and Medicare.
    Compensation tends to be inadequate especially in permanent 
disability cases, in view of the expiration of benefit entitlement and 
the failure to adjust benefits for changes in a worker's expected 
earnings over time. As of January 1987, eight states restricted 
permanent disability benefits either by specifying a maximum number of 
weeks for which benefits could be paid or by imposing a ceiling on 
dollar payments [Ex. 4-302].
    At present, time and dollar restrictions on benefit payments are 
even more prevalent in the area of survivor benefits. The duration of 
survivor benefits is often restricted to 10 years, and dollar maximums 
on survivor payments range from $7,000 to $60,000. In addition, it 
should be noted that if the employee dies quickly from the occupational 
illness and has no dependents, the employer need pay only nominal 
damages under Workers' Compensation (e.g., a $1,000 death benefit).
    Finally, in spite of current statutory protection, disability from 
occupational diseases represents a continuing, complex problem for 
Workers' Compensation programs. Occupational diseases may take years to 
develop, and more than one causal agent may be involved in their onset. 
Consequently, disabilities resulting from occupationally induced 
illness often are less clearly defined than those from occupationally 
induced injury. As a result, Workers' Compensation is often a weak 
remedy in the case of occupational disease. Indeed, there is some 
evidence indicating that the great majority of occupationally induced 
illnesses are never reported or compensated [Ex. 4-84].
    The insurance premiums paid by a firm under the Workers' 
Compensation system are generally not experience rated; that is, they 
do not reflect the individual firm's job safety and health record. 
About 80 percent of all firms are ineligible for experience rating 
because of their small size. Such firms are class rated, and rate 
reductions are granted only if the experience of the entire class 
improves. Even when firms have an experience rating, the premiums paid 
may not accurately reflect the true economic losses. Segregation of 
loss experience into classes is somewhat arbitrary, and an individual 
firm may be classified with other firms that have substantially 
different normal accident rates. An experience rating is generally 
based on the benefits paid to workers, not on the firm's safety record. 
Thus, employers may have a greater incentive to reduce premiums by 
contesting claims than by initiating safety measures.
    In summary, the Workers' Compensation system suffers from several 
shortcomings that seriously reduce its effectiveness in providing 
incentives for firms to create safe and healthful workplaces. The 
scheduled benefits are significantly less than the actual losses to the 
injured workers, and recovery is often very difficult in the case of 
occupational diseases. Thus, the existence of a Workers' Compensation 
system limits an employer's liability significantly below the actual 
costs of the injury. In addition, premiums for individual firms are 
unlikely to be specifically related to that firm's risk environment. 
The firm, therefore, does not receive the proper economic signals and 
consequently fails to invest sufficient resources in reducing workplace 
injuries and illnesses. The economic costs not borne by the employer 
are borne by the employee or, as is often the case, by society through 
public insurance and welfare programs.
(4) Conclusion
    OSHA believes that there are no nonregulatory alternatives that 
adequately protect workers from the adverse health effects associated 
with exposure to indoor air pollution. Tort liability laws and Workers' 
Compensation provide some protection, but due to market imperfections 
they have not been sufficient. Some employers have not complied 
voluntarily with standards recommended by professional organizations. 
The deleterious health effects resulting from continued exposure to 
hazardous substances require a regulatory solution.

D. Benefits

    In this chapter, OSHA presents its preliminary estimates of the 
expected reduction in fatalities and illnesses among the employees 
affected by the proposed IAQ standard. A qualitative description of the 
non-quantifiable additional cost savings to employers, is also 
provided.
1. Indoor Air Quality
    Health effects typically caused by poor IAQ have been categorized 
as Sick Building Syndrome (SBS) or Building-Related Illness (BRI). Some 
of the symptoms that characterize SBS include: irritation of eyes, nose 
and throat, dry mucous membranes and skin and coughs, hoarseness of 
voice and wheezing, hypersensitivity reaction, nausea and dizziness.
    BRI describes specific medical conditions of known etiology such 
as: Respiratory allergies, legionellosis, humidifier fever, nosocomial 
infections, sensory irritation when caused by known agents and the 
symptoms and signs characteristic of exposure to chemical or biologic 
substances such as carbon monoxide, formaldehyde, pesticides, 
endotoxins or mycotoxins. BRIs do not disappear when the person leaves 
the building.
    The Centers for Disease Control Prevention estimate that over 
25,000 cases of the pneumonia caused by Legionella occur each year with 
more than 4,000 deaths. It has been suggested that a large number of 
these cases occur as the result of workplace exposure [Exs. 4-33, 4-
318]. However, specific data on the occurrence of Legionella-related 
cases due to workplace exposure were not available.
    Some of the reductions attributable to the proposed standard, such 
as decreases in the number of upper respiratory symptoms (nose, throat 
and eye symptoms) and severe headaches have been estimated. Other 
reductions, however, have not been quantified at this time.
    OSHA's estimates are based upon the exposure profile (presented in 
Table VI-5) and OSHA's quantitative risk assessment discussed in detail 
in the preamble to the proposal). OSHA preliminarily estimates the risk 
of working in mechanically ventilated workplaces to be 57 severe 
headaches and 85 upper respiratory symptoms per 1,000 employees over a 
45 year work lifetime. By applying these rates to the affected 
population at risk, OSHA estimates that 3.8 million severe headaches 
and 5.6 million upper respiratory symptoms will develop in employees 
over the next 45 years who work in buildings with mechanical 
ventilation (with the worker population held constant).
    A common theme that runs through the literature and the OSHA docket 
indicates that the principal factor associated with indoor air quality 
complaints is inadequate ventilation. However, information available 
does not quantify the effectiveness of ventilation improvements. NEMI 
reports that: ``ventilation system modifications and improvements are 
key elements of solving existing IAQ problems and reducing IAQ 
complaints. In every case where recommended ventilation system 
modifications and improvements are implemented, the frequency and 
severity of complaints are reduced significantly'' [Ex. 3-1183].
    Some of the submissions base the effectiveness of ventilation 
improvements on the NIOSH analysis of indoor air quality investigations 
[Exs. 3-1183, 3-1090]. In approximately 500 indoor air quality 
investigations, NIOSH found that the primary causes of indoor air 
quality problems were inadequate ventilation (52%), contamination from 
outside the building (10%), microbial contamination (5%), contamination 
from building fabric (4%), and unknown sources (13%). Excluding 
contamination from building fabric and unknown sources, this suggests 
that 83 percent of complaints related to IAQ problems would be 
eliminated by the proposed OSHA standard. For purposes of this 
analysis, OSHA assumes that the overall effectiveness is, therefore, 80 
percent. As shown in Table VI-5, OSHA estimates that the proposed 
standard will prevent 3.0 million severe headaches and 4.5 million 
upper respiratory symptoms over the next 45 years. This is, 
approximately, 69,000 severe headaches and 105,000 upper respiratory 
symptoms per year. These estimates understate the prevalence of 
building-related symptoms since they only reflect excess risk in only 
air conditioned buildings. OSHA believes that the standard will also 
prevent severe headaches and upper respiratory symptoms in heated (but 
not air conditioned) buildings, and that it will prevent various other 
adverse health effects. OSHA is seeking additional information upon 
which to base quantifiable estimates of the other known adverse health 
effects.
    OSHA requests comment on the methodology of estimating the benefits 
for the IAQ portion of the proposal. Specifically, OSHA requests any 
studies which document (in quantitative terms) the effectiveness of 
HVAC maintenance on the decline of indoor air related ailments.
2. Environmental Tobacco Smoke
    Tobacco smoke has been classified as a carcinogen by the 
International Agency for Research on Cancer, the Surgeon General, 
NIOSH, and the U.S. Environmental Protection Agency. The National 
Health Interview Survey of Cancer Epidemiology and Control (NHIS-CEC) 
shows that the prevalence of cigarette smoking continues to decline in 
smoking among adults by approximately 0.50 percent per year. Despite 
these declines, smoking is responsible for an estimated 390,000 deaths. 
Exposure to ETS has been associated with the occurrence of many 
diseases, such as lung cancer and heart disease in nonsmokers and low 
birthweight in the offspring of nonsmokers.

 Table VI-5.--Cases and Cases Avoided of Occupationally Developed Upper 
Respiratory Symptoms and Headaches in Buildings With HVAC Systems Over a
                      Working Lifetime of 45 Years                      
------------------------------------------------------------------------
                              Headaches             Upper respiratory   
                     --------------------------         symptoms        
                                               -------------------------
                                      Cases                     Cases   
                        Baseline   avoided due    Baseline   avoided due
                       cases\1\       to IAQ     cases\2\       to IAQ  
                                     standard                 standard  
------------------------------------------------------------------------
Agriculture,                                                            
 forestry, fishing..       14,936       11,948       22,272       17,818
Mining..............        9,672        7,737       14,423       11,538
Construction........       87,978       70,383      131,196      104,957
Manufacturing.......      307,650      246,120      458,777      367,021
Transportation......      182,639      146,111      272,357      217,885
Wholesale and retail                                                    
 trade..............      842,666      674,133    1,256,607    1,005,286
Finance, insurance,                                                     
 real estate........      387,943      310,354      578,511      462,809
Services............    1,441,160    1,152,928    2,149,099    1,719,279
Government..........      507,053      405,643      756,132      604,906
                     ---------------------------------------------------
      Total.........    3,781,698    3,025,358    5,639,374   4,511,499 
------------------------------------------------------------------------
\1\Based on OSHA estimate of occupational headache risk of 57 per 1,000 
  employees over a working lifetime of 45 years.                        
\2\Based on OSHA estimate of occupational upper respiratory symptoms    
  risk of 85 per 1000 employees over a working lifetime of 45 years.    
  OSHA estimate for cases prevented through proposed standard is 80     
  percent.                                                              
                                                                        
Source: OSHA, Office of Regulatory Analysis, 1994.                      

    OSHA's estimates are based upon the exposure profile (presented in 
Table VI-3) and OSHA's quantitative risk assessment (discussed in 
detail in the preamble to the proposal). The OSHA estimates of lifetime 
risk of death attributable to exposure to ETS in the workplace range 
between 0.4 and 1 for lung cancer and between 7 and 16 for coronary 
heart disease, per 1,000 exposed employees. OSHA's estimate of the 
attributable risks suggest that all baseline cases of lung cancer and 
coronary heart disease will be prevented due to elimination of exposure 
of nonsmokers to ETS in the workplace.
    Table VI-6 presents estimates of the incidence of work-related 
cases avoided of lung cancer and heart disease following either the 
banning of smoking in the workplace or limiting smoking to designated 
smoking areas. OSHA estimates that approximately between 5,583 and 
32,502 cancer deaths and 97,700 to 577,818 coronary heart disease 
deaths related to occupational exposure to ETS will be prevented over 
the next 45 years. This represents 140 to 722 cancer deaths per year 
and 2,094 to 13,001 heart disease deaths per year.
3. Costs Savings
    OSHA has also preliminarily determined that the estimated number of 
deaths or illnesses prevented understates the actual benefits that 
would occur under the proposed standard. Significant additional 
economic benefits, apart from the lives saved and illnesses averted, 
are anticipated most of which can not be quantified at this time.

   Table VI-6.--Cases Avoided of Occupationally Developed Lung Cancer and Coronary Heart Disease Per Employees  
                               Exposed to ETS Over a Working Lifetime of 45 Years                               
----------------------------------------------------------------------------------------------------------------
                                     Number of non-smoking        Coronary heart\1\       Lung cancer\2\ deaths 
                                   employees exposed to ETS        disease avoided               avoided        
                                            at work          ---------------------------------------------------
                                 ----------------------------                                                   
                                   Lower bound   Upper bound  Lower bound  Upper bound  Lower bound  Upper bound
----------------------------------------------------------------------------------------------------------------
Agriculture, forestry, fishing..       189,606       490,597        1,327        7,850           76          442
Mining..........................        46,885       121,313          328        1,941           19          109
Construction....................       654,565     1,693,655        4,582       27,098          262        1,524
Manufacturing...................     2,454,724     6,351,483       17,183      101,624          982        5,716
Transportation..................       743,623     1,924,089        5,205       30,785          297        1,732
Wholesale and retail trade......     3,581,778     9,267,685       25,072      148,283        1,433        8,341
Finance, insurance, real estate.       751,493     1,944,454        5,260       31,111          301        1,750
Services........................     4,079,510    10,555,543       28,557      168,889        1,632        9,500
Government......................     1,455,027     3,764,816       10,185       60,237          582        3,388
                                 -------------------------------------------------------------------------------
      Total.....................    13,957,212    36,113,636       97,700      577,818        5,583       32,502
----------------------------------------------------------------------------------------------------------------
\1\OSHA estimate of occupational coronary heart disease risk for lower and upper bound exposure of 7 to 16 per  
  1,000 employees over a working life of 45 years.                                                              
\2\OSHA estimate of occupational lung cancer risk for lower and upper bound exposure of 0.4 to 0.9 per 1,000    
  employees over a working life of 45 years.                                                                    
                                                                                                                
Source: OSHA, Office of Regulatory Analysis, 1994.                                                              

    The major forms of these savings are efficiency and productivity 
improvements, cost reductions in operations and maintenance, and 
reduced incidence of property damage.
    (a) Worker Productivity. Productivity gains are realized when less 
labor input is required per unit of production. A productivity gain 
can, therefore, take the form of either a decrease in the labor hours 
needed to maintain the level of production or in the form of increased 
production and net income for the establishment.
    Productivity losses due to indoor air quality may take several 
forms: employees may be less effective because they feel fatigued or 
suffer from headaches, eye irritation or other effects. Employees may 
accomplish less per hour worked or may spend more time away from their 
work location (e.g., taking breaks or walks outdoor). One company 
indicated that ``since two of my employees have refrained from smoking 
while working . . ., their production has increased and their overall 
health seems better to say nothing of the health of those working 
around them'' [Ex. 3-192]. In addition to individual productivity, the 
quality of indoor air affects organizational productivity such as the 
visitor and customer satisfaction, impact on sales and revenue and 
repeat customers.
    Little data exist on productivity lost due to poor indoor air 
quality. A survey of 94 state government office buildings attributes an 
average productivity loss of 14 minutes per day or 3.0 percent to poor 
indoor air quality [Ex. 3-1075H2]. Based on information gathered from 
published resources, the National Energy Management Institute estimates 
that there is an increase in productivity of 3.5 percent or 
approximately 15 minutes per day for employees in a building that 
starts as an unhealthy building, and after IAQ improvements, becomes a 
healthy building [Ex. 4-240].
    To monetize the productivity improvements resulting from 
implementation of the proposed IAQ standard, OSHA multiplied the 
average employee payroll by 3.0 percent. As shown in Table VI-7, 
monetized productivity improvements is estimated at an annual $15 
billion.
    OSHA requests any studies relating to productivity effects relevant 
to the proposal be submitted.
    (b) Property Damage, Maintenance and Cleaning Costs. High 
concentrations of contaminants in indoor air can have adverse effects 
on materials and equipment. Damages may include corrosion of electronic 
components and electrical current leakage, which may eventually result 
in equipment malfunction. The costs of materials and equipment damage 
by indoor air pollutants include maintenance, repair, and/or 
replacement costs resulting from (1) soiling or deterioration of a 
materials's appearance, or (2) reduced service life for corroded or 
degraded appliances, furnishings, and equipment [Ex. 3-1075H2].
    Bell Communications Research reported that the seven regional 
telephone companies have spent large sums ranging from $10,000 to 
$380,000 per event to replace, clean and repair switches and other 
electronic equipment malfunctioning as a result of indoor air 
contaminants.

  Table VI-7.--Average Annual Cost Savings From Compliance With the IAQ 
               Proposed Standard Due to Productivity Gains              
------------------------------------------------------------------------
                               Number of      Average         Annual    
                               employees       annual    productivity\1\
                              exposed to    payroll per    improvements 
                               poor IAQ       employee      (million)   
------------------------------------------------------------------------
Agriculture, forestry,                                                  
 fishing..................          83,715      $16,290            $41  
Mining....................          54,210       32,375             53  
Construction..............         493,125       25,286            374  
Manufacturing.............       1,724,400       28,376          1,468  
Transportation............       1,023,705       29,655            911  
Wholesale and retail trade       4,723,200       20,405          2,891  
Finance, insurance, real                                                
 estate...................       2,174,445       28,377          1,851  
Services..................       8,077,800       20,811          5,043  
Government................       2,842,068       32,570          2,777  
                           ----------------             ----------------
      Total...............      21,196,668                     15,409   
------------------------------------------------------------------------
\1\Based on productivity loss of 3.0 percent.                           
                                                                        
Sources: U.S. Department of Labor, OSHA, Office of Regulatory Analysis, 
  1994. U.S. Department of Labor, Bureau of Labor Statistics. Employment
  and Wages Annual Averages, 1991. U.S. Bureau of the Census, County    
  Business Patterns, 1990. January 1993.                                

    Microbial contamination can cause significant damage to buildings 
and equipment and there is anecdotal evidence that damage can be so 
severe as to make a building unfit for human occupation. OSHA requests 
comment on the explicit or implicit rental value affected in buildings 
with such problems.
    No quantitative estimates are available on the effects of indoor 
air on equipment. OSHA requests more information on the effects of 
indoor air on materials and equipment.
    Indoor air pollutants and in particular ETS contribute to increased 
maintenance and cleaning expenses. Increased maintenance and cleaning 
costs include: the need to paint walls more frequently, need to clean, 
repair and replace furniture, upholstery, carpeting and curtains or 
drapes that have cigarette burns and or odors; the need to wash 
windows, showcases, and other surfaces that attract ash and dust; and 
the need to clean ashtrays. A survey of 2,000 companies that had 
adopted no-smoking policies found that 60 percent of these companies 
were able to reduce their cleaning and maintenance costs. The savings 
have been estimated at about $500 per smoker per year (3).
    If establishments decide to ban smoking in the workplace, the 
proposed standard would result in virtually eliminating all smoking 
related fires, fire fatalities and injuries and direct property damage. 
Smoking is a leading cause of fire related fatalities. During the 
1980's, the National Fire Protection Association reports that smoking 
materials were the cause of over 200,000 fires per year. This resulted 
in more than 1,000 civilian fatalities and 3,000 civilian injuries and 
approximately $300 million in direct property damage. During the period 
of 1989 to 1990, there was an average of $115 million in direct 
property damage due to non-residential smoking related fires which 
resulted in 36 fatalities and 3,212 injuries. OSHA will further 
investigate this issue and requests available data from the public.

E. Technological Feasibility and Compliance Costs

    This section presents OSHA's preliminary compliance cost estimates 
for the proposed standard on indoor air quality. The cost analysis 
covers the major proposed provisions for which data are available.
    OSHA requests more information on the consideration for the 
relationship of employers and facility owners. The decision to 
implement any IAQ improvements will be greatly influenced by the 
relationship between employers and landlords. Since changes in building 
ventilation systems will be made by landlords, employers may have to 
negotiate agreements to ensure that they can meet the OSHA standard. On 
the requirement for ETS, landlords in turn are likely to pressure 
employers to ban smoking; thereby, forestalling any need for 
construction of designated smoking rooms. This section also examines 
the technological feasibility of complying with proposed regulation.
1. Technological Feasibility
    As interpreted in the Benzene and Cotton Dust cases, the 
Occupational Safety and Health Act of 1970 requires that the Agency, 
with regard to exposure to toxic substances, is to reduce significant 
risk of material health impairment to the extent feasible. Accordingly, 
as part of the investigation of the potential effects of the OSHA 
proposal, OSHA has examined both the technological and economic 
feasibility of the proposal. The economic feasibility assessment 
appears later.
    OSHA's assessment of the technological feasibility is based on an 
examination of what would be required to comply with the proposal, 
along with a review of existing practices among affected 
establishments. With regard to this proposal, problems with 
technological feasibility, by and large, are not evident. Employers are 
required to operate their HVAC systems within those parameters 
originally designated for the equipment. While many employers may 
choose to provide separately ventilated smoking areas, this is an 
option, not a requirement, under the proposed regulation. This 
technology is widespread currently and can be used to achieve 
compliance with the proposed standard.
    For example, in some situations, such as hotels and prisons, 
employees have as their workplace the residence of others who live in 
that building. Restaurants, bars and other ``public'' places expose 
employees to customer's tobacco smoke. While it is technologically 
feasible to ban smoking in those establishments, there may be other 
problems, legal and economic. While it is theoretically possible to 
minimize employee exposure to ETS in such a work environment through 
special ventilation, in the absence of modified customer service 
arrangements, actually eliminating worker exposure to ETS would likely 
prove difficult. Consequently, the selection process for one of the 
smoking policy alternatives for a particular workplace must consider 
both the physical limitations of the building or firm and the 
building's use. In addition, some employers may be using their building 
facilities for purposes for which the original design did not intend, 
and for which retrofitting might prove difficult. OSHA requests comment 
on those workplaces for which compliance with the proposed standard 
would prove technologically challenging. OSHA will consider additional 
information on the ability of firms to implement IAQ programs.
2. Compliance Costs
    OSHA estimated preliminary costs of complying with the proposed 
standard. OSHA's cost assumptions and methodologies are based on 
information available from the rulemaking record. Further detailed 
industry analysis will be developed by the Agency.
    Table VI-8 contains OSHA's estimates of the annualized first-year 
and the annual recurring costs of full compliance with the proposed 
rule. The annualized first-year cost of compliance is $1.4 billion. The 
cost for eliminating exposure to ETS may range from $0 to $68 million 
depending on whether establishments shall ban smoking or allow smoking 
in designated areas. OSHA estimated that the annual cost of compliance 
with the IAQ standard will be $8.1 billion, of which the most costly 
provision will be for the building systems operation and maintenance, 
$8.0 billion.
    OSHA developed cost estimates for the affected industries using the 
following categories of information: (1) Provisions of the proposed 
standard requiring activities; (2) the number of potentially affected 
buildings, establishments and employees; (3) the percentage of 
establishments or buildings in each industry currently in compliance 
with each proposed requirement; and (4) the unit costs for bringing 
establishments into compliance with the various provisions of the 
proposed standard. These four items were combined to produce OSHA's 
estimated costs of compliance.
    Costs were estimated on an annual basis, with total annual costs 
calculated as the sum of annualized initial costs and annual recurring 
costs. All capital costs and non-recurring first year costs were 
annualized over the service life of the equipment or administrative 
activity, at a discount rate of 10 percent.
    (a) Developing Indoor Air Quality Compliance Programs. The proposed 
standard requires establishments to prepare written operations plans 
which would describe information required for the daily operation and 
management of the building systems9 and maintenance. The plan 
should provide an overview of the building and system, using a short 
text description and single-line schematics or as-built construction 
documents. The operations information would also describe how to 
operate the HVAC systems so that it performs with the reported design 
criteria. In addition, the operations information should include: (1) 
Special procedures like seasonal start-ups and shutdowns, and (2) a 
list of operating performance criteria such as minimum outside air 
ventilation rates, potable hot water storage and delivery temperatures, 
range of space relative humidities and any space pressurization 
requirements, (3) an evaluation of the need to retrofit the HVAC system 
when the design occupancy levels are exceeded, and (4) a checklist for 
visual inspection of building systems.
---------------------------------------------------------------------------

    \9\ Building systems include but are not limited to the heating 
and air conditioning (HVAC) system, the potable water systems, the 
energy management system and all other systems in a facility which 
may impact IAQ.

  Table VI-8.--Summary of Compliance Costs for Proposed OSHA Indoor Air 
                            Quality Standard                            
------------------------------------------------------------------------
                                      Annualized   Recurring    Annual  
                                         cost        cost        cost   
                                      ($million)  ($million)  ($million)
------------------------------------------------------------------------
IAQ written compliance program......       $21.1        --         $21.2
IAQ maintenance and operation                                           
 program............................     1,281.1    $6,697.4     7,978.5
Information and Training:                                               
    Maintenance workers.............         0.5         0.8         1.3
    All employees...................        --          --          --  
Controls for environmental tobacco                                      
 smoke\1\...........................      0-68.1        --        0-68.1
                                     -----------------------------------
      Total.........................     1,371.0     6,698.2     8,069.1
------------------------------------------------------------------------
\1\Costs incurred are dependent on whether establishments will totally  
  ban smoking or allow smoking in designated areas.                     
                                                                        
Source: U.S. Department of Labor, OSHA, Office of Regulatory Analysis,  
  1994.                                                                 

    The maintenance written plan will also include a description of the 
equipment to be maintained and the recommended maintenance procedures 
and frequency of performance. Preferably, the plan should contain the 
equipment maintenance manuals issued upon completion of facility 
construction. For establishments in buildings with natural ventilation, 
employers will develop a plan to assure that windows, doors, vents, 
stacks and other portals designed or used for natural ventilation are 
in operable condition.
    The cost associated with compiling such information will vary 
depending on the size of the establishment building, the complexity of 
the building system, the extent to which such information is already 
available, and type of occupancy (e.g., single establishment or multi-
establishment). In some cases some establishments especially the large 
ones may already have developed such information. For example, in 1986, 
IBM initiated a program by first evaluating building design, operation 
and maintenance and as a result, an IAQ program was devised to include: 
a model operation/maintenance and IAQ awareness program for building 
operation/maintenance personnel, an updated building commissioning 
document and appropriate building lease and contracted operation/
maintenance agreements [Ex. 3-904]. There are no data on the number of 
establishments with IAQ programs. Based on information in the docket, 
OSHA assumed that 95 percent of all establishments are required to 
develop the IAQ compliance program information.
    In addition, employers are required to: (1) identify a designated 
person who is given the responsibility of the IAQ compliance program, 
(2) keep written records of employee complaints of building-related 
illness and maintenance records, and (3) set up procedures to be 
utilized during renovation and modeling to minimize degradation of the 
indoor air quality of employees performing such activities and 
employees in other areas of the building.
    The cost equation for developing the written IAQ compliance 
program:

Co=En x Pc x ((Wt x T1)+(Wm x T2))


where

    Co=the cost of developing operation and maintenance 
information
    En=the number of establishments
    Pc=the percentage of establishments to develop operation 
and maintenance information (95%)
    Wt=the technician wage rate ($15.51 hourly compensation 
rate)
    T1=the technician time required to compile and develop 
building system operation and maintenance information (1 hour)
    Wm=the managerial wage rate ($30.48 hourly compensation 
rate)
    T2=the managerial time required to develop some 
requirements of the written plan (15 minutes)

    As presented in Table VI-9, the one time annualized cost of 
compiling and developing the written IAQ compliance program is $21.2 
million.

  Table VI-9.--Cost of Compliance for Developing a Written IAQ Program  
------------------------------------------------------------------------
                                                              Annualized
                                              Total no. of    first year
                                             establishments    cost\1\  
                                                              ($million)
------------------------------------------------------------------------
Agriculture, forestry, fishing.............        260,801         $0.91
Mining.....................................         22,861          0.08
Construction...............................        642,972          2.24
Manufacturing..............................        389,392          1.35
Transportation.............................        243,769          0.85
Wholesale and retail trade.................      1,929,891          6.71
Finance, insurance, real estate............        526,378          1.83
Services...................................      1,933,750          6.73
Government.................................        135,496          0.47
                                            ----------------------------
      Total................................      6,085,310         21.17
------------------------------------------------------------------------
\1\Based upon 15 minutes of managerial time estimated at $30.48/hr and  
  one hour of technician time estimated at $15.51/hour. Assumes 5       
  percent existing compliance. Cost is annualized over 10 years at a 10 
  percent interest rate.                                                
                                                                        
Source: U.S. Department of Labor, OSHA, Office of Regulatory Analysis,  
  1994.                                                                 

    (b) IAQ Operation and Maintenance Program. The proposed standard 
requires maintenance and inspection of the building system components 
that directly affect IAQ. Specifically, the HVAC system should provide 
at least the outside air ventilation rate based on actual occupancy, 
building code, mechanical code or ventilation code and that carbon 
dioxide concentration does not exceed 800 parts per million. In 
approximately 500 indoor air quality investigations, NIOSH found that 
the primary cause of indoor air quality problems is inadequate 
ventilation (52 percent).
    Other actions required include: (1) Control of humidity in 
buildings with mechanical cooling systems, (2) implementing the use of 
general or local exhaust ventilation where maintenance and housekeeping 
activities involve use of equipment or products which emit air 
contaminants in other areas of the facility, (3) maintain mechanical 
equipment rooms and any non-ducted air plenums or chases in a clean 
condition.
    OSHA recognizes that not every building will have to make all 
recommended changes to improve operation and maintenance of the HVAC 
system. In the majority of the cases, some improvements can be 
accomplished by changing the setting on a control device or centralized 
control system. Depending on the condition of the HVAC equipment, 
inspection and maintenance may include simple housekeeping of equipment 
and air transport pathways and/or catastrophic failure maintenance to 
repair/replace failed equipment. Also, there may be cases where a 
number of buildings will require major changes in the HVAC system such 
as enlarging the size of the outside air intake.
    The cost for providing maintenance first requires an estimate of 
the number of buildings without regular HVAC maintenance. The 1989 
Commercial Buildings Characteristics survey by the Department of Energy 
estimates that 46 percent of the buildings have regular HVAC 
maintenance. Therefore, the total number of buildings requiring 
maintenance is estimated at 2.3 million. OSHA then determined the 
number of problem buildings without HVAC maintenance by applying the 
OSHA estimate of 30 percent (presented in section B). The number of 
problem buildings without HVAC maintenance is estimated at 0.7 million.
    In general, the average cost per year to maintain a commercial HVAC 
system is a function of a number of factors. These factors include the 
type of system, the age of the system, the size of the system, layout 
of the system, reliability of the equipment installed. In addition to 
the physical characteristics of the system, the cost per year to 
maintain the system also depends on the operation of the system, the 
maintenance policies of the owner, the skill levels of the operating 
engineers and maintenance workers, and whether the maintenance is 
carried out by employees of the building owner or is the responsibility 
of an outside company.
    Bank of America's maintenance costs for its 2,000 worksites 
averaged $4 million per year or an average of $2,000 per worksite [Ex. 
3-552]. One facility, a high-rise office building, reported an annual 
cost of approximately $0.6 million [Ex. 3-448]. DOW Chemical Company's 
estimate for ventilation systems maintenance ranges from $0.17 to 
$0.25/sq.ft/yr [Ex. 3-502]. Therefore, OSHA used an average of $0.21/
sq.ft/yr to compute the cost of HVAC maintenance.
    In addition to regular HVAC maintenance, buildings with known IAQ 
problems will require other improvements such as (1) relocating air 
intakes and other pathways of building entry to restrict the entry of 
outdoor air contaminants, or (2) installing local source capture 
exhaust ventilation or substitution within workspaces where air 
contaminants are being emitted, or (3) increasing ventilation 
effectiveness, or (4) reduce unwanted infiltration, or (5) monitor 
outside air quantity to meet ventilation requirements. The National 
Energy Management Institute developed a cost model for implementing IAQ 
improvements which is based on the distribution of buildings with IAQ 
problems by climate zone, building activity and size, and 
characteristics of ventilation systems. The average cost to implement 
the actions listed above are estimated to be $1.14 per square foot. 
These improvements will only be required for the initial year.
    The cost equation for implementing the compliance program is as 
follows:

Cp=Ms 
(Nh x Ca+Np x Ca+Np x Ci x A20)

where
    Cp=cost for providing regular HVAC maintenance
    Ms=mean square footage per building (14,000)
    Nh=number of buildings without HVAC maintenance
    Ca=cost per square foot for providing HVAC maintenance 
($0.21)
    Np=number of problem buildings without HVAC maintenance
    Ci=cost per square foot for providing HVAC maintenance and 
IAQ improvement actions ($1.14)
    A20=Annualization factor at 10% over 20 years (0.117)
    Non-recurring first year costs were annualized over 20 years at 10 
percent interest rate. As presented in Table VI-10, the annualized 
first-year cost is estimated at $1.3 billion. OSHA anticipates total 
annual costs of $8.0 billion.
    (c) Training for HVAC Maintenance Workers and Informing Employees 
About the Indoor Air Quality Standard. The proposed standard requires 
training for all building maintenance workers involved in building 
system operation and maintenance. Standards of maintenance vary 
dramatically in the HVAC industry and sometimes are deficient where 
untrained personnel are designated to maintain very complex systems.
    Training programs for workers must include at least information on: 
(1) How to maintain adequate ventilation of air contaminants generated 
during building cleaning and maintenance, and (2) how to minimize 
adverse effects on indoor air quality during the use and disposal of 
chemicals and other agents.
    The exact cost of training will vary among establishments depending 
on whether employees are trained in-house or sent to outside training 
programs or consultants. OSHA estimated the costs for the trainer who 
must research, prepare and direct the sessions. For the time involved 
in the training session, a range of costs for the instructor could be 
developed. For example, the wage costs for the trainer could represent 
from 50 percent of the trainee labor costs (if there are only two in 
the class) to 5 percent if there are 20 trainees in a class. For the 
preparation time, OSHA judged that the trainer will require a special 
study seminar, such as that taught by the Building Owners and Managers 
Association International. 

                        Table VI-10.--Cost for System Operation and Maintenance Provision                       
----------------------------------------------------------------------------------------------------------------
                                        Buildings with IAQ problems and      Buildings without HVAC             
                                            without HVAC maintenance         maintenance and without            
                                    ---------------------------------------       IAQ problems           Total  
                                                 Annualized\1\             --------------------------   annual  
                                       No. of       cost to      Annual\2\                  Annual      cost ($ 
                                      buildings   improve IAQ     cost ($      No. of     cost\3\ ($   million) 
                                      with HVAC   ($ million)    million)     buildings    million)             
----------------------------------------------------------------------------------------------------------------
Agriculture, forestry, fishing.....      26,139           $49          $77        60,990        $179        $305
Mining.............................       2,291             4            7         5,346          16          27
Construction.......................      64,442           121          189       150,364         442         752
Manufacturing......................      39,027            73          115        91,062         268         456
Transportation.....................      24,432            46           72        57,007         168         285
Wholesale and retail trade.........     193,423           363          569       451,320       1,327       2,258
Finance, insurance, real estate....      52,756            99          155       123,098         362         616
Services...........................     193,810           363          570       452,222       1,330       2,263
Government.........................      87,086           163          256       203,200         597      1,017 
                                    ----------------------------------------------------------------------------
      Total........................     683,404         1,281        2,009     1,594,610       4,688      7,979 
----------------------------------------------------------------------------------------------------------------
\1\Number of problem buildings  x  $1.14 per sq. ft.  x  14,000 sq. ft. (mean floorspace/building), annualized  
  over 20 years at 10% interest rate.                                                                           
\2\Recurring cost estimated for number of problem buildings without HVAC maintenance using $0.21/sq. ft.        
\3\Number of non-problem buildings without maintenance  x  14,000 sq. ft. (mean floorspace per building)  x     
  $0.21 per square foot.                                                                                        
                                                                                                                
Source: OSHA, Office of Regulatory Analysis, 1994.                                                              

    OSHA assumed that the labor costs for the trainer and preparation 
time are approximately equal to 25 percent of the trainee's wage cost 
during the session. OSHA also assumed that 50 percent of the workers 
will require such training. The cost equation for maintenance workers 
training is as follows:

Ct=Nm x Pm x Wm x Tm

where

    Ct=the cost of training of maintenance workers
    Nm=the number of maintenance workers10
---------------------------------------------------------------------------

    \10\The number of maintenance workers is based on BLS's 
Occupational Employment Statistics survey of 1992 and includes all 
maintenance workers who perform work involving two or more 
maintenance skills to keep machines, mechanical equipment, or 
structure of an establishment in repair.
---------------------------------------------------------------------------

    Pm=the percentage of existing compliance as estimated by 
OSHA (50 percent)
    Wm=the hourly compensation wage rate for maintenance 
workers ($10.95)
    Tm=one-half hour of maintenance worker time plus 7.5 
minutes for trainer cost (37.5 minutes)

    The total cost of training is estimated at $6.84 per maintenance 
worker for a half hour program. Table VI-11, presents OSHA's estimate 
for the number of maintenance workers needing training and the 
associated costs. The annualized first year cost is estimated at $0.5 
million. It was assumed that job changes within establishments or 
buildings will require retraining. The annual new hire cost is 
estimated at $0.8 million, based upon industry turnover rates. Thus 
OSHA estimated annualized cost training to be $1.3 million.
    The proposed standard requires employers to inform all employees of 
the contents of the standard and its appendices. This could be 
accomplished by posting the proposed standard at a bulletin board; 
therefore, OSHA did not include a cost for this provision.
    (d) Compliance with Related Standards. The proposed standard 
requires employees performing work on HVAC systems to comply with 
several existing OSHA standards and therefore any costs associated with 
compliance with this provision have already been considered. This 
requirement is necessary to protect employees from exposure to indoor 
air pollutants and exposure to noise. This provision is considered to 
have a de minimus effect on all industries and OSHA believes that 
establishments are in full compliance with this requirement.
    (e) Air Contaminant-Environmental Tobacco Smoke. The primary 
objective of the tobacco smoke provision is to eliminate the 
nonsmoker's exposure to ETS. Under the proposed rule, firms will have 
the option of either banning smoking of tobacco products or permitting 
smoking only in designated areas.
    OSHA recognizes that not all establishments will make available 
designated smoking areas as there may be physical constraints on the 
option of providing separate ventilation. Such constraints are imposed 
by the building's design, the building's mechanical ventilation 
system's capabilities, by costs involved in providing adequate 
ventilation, by the occupant use of the building. In some cases, 
establishments located in severe climate zones may find it necessary to 
protect their smoking employees from weather exposure by providing 
designated smoking areas. 

                               Table VI-11.--Training Cost for Maintenance Workers                              
----------------------------------------------------------------------------------------------------------------
                                                                                         Annual new             
                                                   Building   Maintenance   Annualized      hire                
                                                 maintenance   employees     initial      training   Annual cost
                                                   workers       to be      cost\2\ ($    cost ($    ($ million)
                                                               trained\1\    million)     million)              
----------------------------------------------------------------------------------------------------------------
Agriculture, forestry, fishing.................       26,210       13,105       $0.015        $0.01        $0.01
Mining.........................................        5,460        2,730        0.003         0.00         0.01
Construction...................................       73,060       36,530        0.041         0.07         0.11
Manufacturing..................................      205,660      102,830        0.115         0.18         0.29
Transportation.................................       47,720       23,860        0.027         0.02         0.04
Wholesale and retail trade.....................      143,440       71,720        0.080         0.12         0.20
Finance, insurance, real estate................      172,350       86,175        0.096         0.17         0.26
Services.......................................      236,160      118,080        0.132         0.26         0.39
Government.....................................           NA           NA           NA           NA          NA 
                                                ----------------------------------------------------------------
      Total....................................      910,060      455,030        0.507         0.82         1.31
----------------------------------------------------------------------------------------------------------------
\1\Based on preliminary OSHA estimate of 50 percent existing compliance.                                        
\2\Initial costs are annualized over 10 years at a 10 percent interest rate. Training for maintenance workers is
  estimated to take one--half hour. Compensation wage rate is $10.95 per hour. Cost includes an additional 7.5  
  minutes per employee to cover trainer cost. Total training cost per employee is $6.84. NA: Data not available.
                                                                                                                
Source: OSHA, Office of Regulatory Analysis, 1994.                                                              

    Establishments in large high rise buildings may also find it 
desirable to provide such rooms to facilitate break periods. 
Consequently, in order to reflect the degree to which establishments 
will provide separate smoking areas, OSHA developed some estimates 
based on the characteristics of the stock of buildings and the 
percentage of companies currently banning smoking in the workplace.
    OSHA has no data on the number of establishments currently 
permitting smoking in designated smoking areas. OSHA estimated that 50 
percent of large establishments with floor space greater than 100,000 
square feet and with more than three floors will provide designated 
smoking areas. OSHA also assumed that 50 percent of all eating and 
drinking places and hotels and other lodging places may provide 
separate designated smoking areas. For these establishments, OSHA then 
applied the percentage of companies that will ban smoking based on the 
rates provided from a survey conducted by the Administrative Management 
Society Foundation (AMS) on current practices for smoking policies in 
the workplace. According to the survey, 25 percent of the companies 
completely ban smoking on their premises. However, the percentages 
varied by SIC as follows: manufacturing (23%), transportation and 
utilities (36%), banking and finance (28%), insurance (38%), retail and 
wholesale (7%), and services (18%). Also, 72 percent felt that smoking 
in the workplace should be either banned or restricted [H-030--Ex. 75].
    Firms opting to make available designated smoking areas are 
expected to incur initial capital costs. OSHA assumed that in many 
cases existing rooms or offices can be converted into a designated 
smoking area. Average cost estimates for retrofitting the HVAC system 
ranges from $4,000 for a 150 square feet room (which could accommodate 
up to 10 smokers) [Ex. 4-265] to $25,000 for 1,000 square feet (which 
could accommodate 30 to 65 smokers) [Ex. 3-643]. The HVAC retrofit 
represented in these estimates typically includes: (1) blocking off the 
return air inlet from the room, (2) providing a transfer air path, and 
(3) providing an exhaust fan and exhaust air pathway to the outside. 
The exhaust fan capacity would exceed air supplied to the room in 
sufficient quantity to create a negative pressure in the smoking room 
relative to surrounding areas to ensure containment of the contaminant. 
In order to achieve negative pressure some architectural modifications 
may be necessary to provide a tight enclosure. OSHA did not estimate an 
additional cost for housekeeping since such activities would have been 
performed prior to the promulgation of the proposed standard.
    Most facilities exhaust air from toilet rooms and also relieve air 
brought in for ventilation and economizer cooling10(a). The amount 
of exhaust air from a designated smoking area is inconsequential 
compared with the quantities of air leaving the building through toilet 
room exhaust and relief. Therefore, OSHA did not include recurring cost 
for the provision of a separately ventilated smoking area.
---------------------------------------------------------------------------

    \1\0(a)Use of outside air for cooling--``free cooling''.
---------------------------------------------------------------------------

    The equation for determining cost for allowing smoking in 
designated areas is as follows:

Cs = (Ne  x  (1-Ps) + Nd  x  (1-Psm)) 
Pc  x  Cr

where
    Cs = cost for providing designated areas
    Ne = number of establishments in buildings with 3 or more 
floors and floorspace greater than 100,000 sq.ft.
    Ps = percentage of establishments banning smoking
    Nd = 50 percent of establishments in Eating and Drinking 
Places (SIC 58), and Hotel (SIC 70)
    Psm = percentage of establishments in SIC 58 and SIC 70 
banning smoking
    Pc = percentage of establishments providing designated 
smoking areas (50%)
    Cr = cost for setting up a separate smoking area ($4,000 
for a 150 sq.ft. room that accommodates up to 10 smokers, 
furnishings existing)

    Initial costs are annualized over 20 years at 10 percent interest 
rate. As presented in Table VI-12, the total annual cost is estimated 
at $68 million. OSHA did not include a cost estimate for the government 
sector at this time.
    (f) Air Quality during Renovation and Remodeling. The proposed 
standard requires that during renovation and remodeling appropriate 
controls are utilized to minimize degradation of the indoor air quality 
of employees performing such activities and employees in other areas of 
the building. The basic characteristics of available control practices 
include: ventilation system/high efficiency particulate air (HEPA) 
vacuum; regulated areas, isolation or containment of work areas and 
appropriate negative pressure containment; outside air intakes, return/
recirculation air streams or plenums; notification of employees and 
contractors.
    For buildings with asbestos presence, the control practices under 
the OSHA asbestos standard are current industry practice. A survey 
developed for obtaining information on practices to control exposure to 
asbestos in buildings shows that asbestos-related work represents 16 
percent of renovation activities whereas general remodeling is 61 
percent and major repair and maintenance are 12 percent [Ex. 4-64].

    Table VI-12.--Optional Cost for Providing Separate Smoking Areas    
------------------------------------------------------------------------
                             Number of establishments                   
                           providing designated smoking                 
                                     areas\1\               Annualized  
                         --------------------------------   first-year  
                             In single       In multi-      cost\2\ ($  
                           establishment   establishment     million)   
                            buildings       buildings                   
------------------------------------------------------------------------
Agriculture, forestry,                                                  
 fishing................              43               8          $0.024
Mining..................               4               1           0.002
Construction............             105              21           0.059
Manufacturing...........              65              13           0.037
Transportation..........              34               7           0.019
Wholesale and retail                                                    
 trade..................          93,411          36,058          60.829
Finance, insurance, real                                                
 estate.................              83              16           0.046
Services................          11,188           3,968          7.121 
                         -----------------------------------------------
      Total.............         104,932          40,091          68.138
------------------------------------------------------------------------
\1\Number of establishments adjusted for percentage banning smoking as  
  follows: Manufacturing 23%; Transportation and Utilities 36%;         
  Wholesale and Retail 7%; average rate for all other industries 25%.   
  Number of establishments included represent 50 percent of large       
  establishments in buildings with 3 or more floors and with floor space
  greater than 100,000 sq. ft. Number of establishments include 50% of  
  all establishments in SIC 58 (Eating and Drinking places) and 70      
  (Hotels).                                                             
\2\Cost for making ventilation changes is estimated at $4,000/smoking   
  room which accommodates up to 10 smokers. Initial costs are annualized
  over 20 years at a 10 percent interest rate.                          
                                                                        
Source: U.S. Department of Labor, OSHA, Office of Regulatory Analysis,  
  1994.                                                                 

    More than half of the buildings sampled were occupied during 
renovation activities. However, all projects in which asbestos-related 
work was being performed were sealed off from the building occupants. A 
variety of renovation projects were performed in buildings ranging in 
project area from 15 to 900,000 square feet, in duration from one to 
156 weeks and in cost from $700 to more than $10 million. The average 
cost was approximately $0.3 million and the average duration for a 
project was 13 weeks.
    However, no data are available on the cost to provide controls 
required under the proposed IAQ standard or for current industry 
compliance for chemical exposure other than exposure to asbestos. OSHA 
assumed minimal cost due to the nature of these processes.

F. Economic Impact and Regulatory Flexibility Analysis

    The previous section presented the costs to all industries of 
complying with the proposed standard. This chapter examines projected 
economic and environmental impacts on those industries. OSHA developed 
quantitative estimates of the economic impact of the proposed standard 
on the affected industries. Data on profits are presented to illustrate 
the scale of profitability of affected industries and do not 
necessarily represent their ability to pay for proposed standard 
provisions.
    OSHA assessed the potential economic impacts and has preliminarily 
determined that the standard is economically feasible for each of the 
major industry groups that will be affected. OSHA conducted its 
analysis at the two digit SIC level. This has been OSHA's procedure for 
doing regulatory impact analyses for other proposed standards. OSHA 
preliminarily concludes that this is reflective of the actual impact on 
the average firm within each subsector. It does not appear that the 
affected groups will experience significant adverse economic impact as 
a result of the standard. However, if any interested person has 
information to show that the analysis at the two digit level is not 
representative of the potential economic impact of the proposal, OSHA 
requests the following information: Reasons why the preliminary 
regulatory analysis is not reflective of the actual anticipated costs 
in any particular sector; specific information as to why the analysis 
at the two digit level fails to adequately represent the economic 
impact; and specific information to help OSHA to better predict the 
impact on the sector in question. Such information should be included 
in the comments on the proposal.
    In accordance with the Regulatory Flexibility Act of 1980, OSHA 
additionally examined the potential for an unduly burdensome impact on 
small entities. OSHA believes that the standard will not have 
significant adverse effect on a substantial number of small entities. 
However, OSHA requests comment on those workplaces for which compliance 
with the proposed standard would prove economically and technologically 
challenging (e.g., restaurants, bars and other ``public'' places where 
employees are exposed to customer's tobacco smoke). While it is 
technologically feasible to ban smoking in those establishments, there 
may be other countervailing problems, legal and economic, which OSHA 
should consider.
(1) Economic Feasibility
    In order to determine the economic feasibility of the rule, OSHA 
compared estimated compliance costs with: (1) The value of sales and 
(2) before-tax profits. All financial data developed for this analysis 
are based on information from Dun and Bradstreet's annual credit 
survey. Aggregate sales data for 1991 were taken from the D&B Market 
Identifiers data base [Exs. 4-94, 4-95, 4-96]. Mean profit rates 
(profit as a percentage of sales) were taken from D&B's Insight data 
base; OSHA averaged data for 1990, 1991 and 1992.\11\
---------------------------------------------------------------------------

    \11\Dun's Insight computer data base presents data from their 
three most recent annual industry Norms and Key Business Ratios 
publications. For most industry groups, OSHA averaged data for three 
years.
---------------------------------------------------------------------------

    Using a conversion formula\12\ based on the federal corporate tax 
schedule, OSHA calculated pre-tax profits from its estimate for post-
tax profits. It should be noted that the sales and profit data, while 
the most recent available, reflect conditions during a cyclical trough; 
therefore, impacts may depict a worst case scenario. In the case of the 
federal government sector, price increases for services rendered may 
not apply. Budgets are usually fixed (in the short run) and compliance 
costs are paid by reducing funds for other items in the budget.
---------------------------------------------------------------------------

    \12\This conversion implicitly assumes individual business 
establishments are separate corporations. Because more than one 
establishment may be grouped together for tax purposes, the 
conversion will tend to underestimate pre-tax profits. State, local 
and other business taxes have not been factored into the conversion 
formula. Additionally, because average tax rates may decline as pre-
tax profits decline, the after-tax impact to the company may be less 
than suggested here.
---------------------------------------------------------------------------

    Where industry enjoys an inelastic demand for its product, an 
increase in operating costs can ordinarily be passed on to consumers. 
In this case, the maximum expected price increase is calculated by 
dividing the estimated compliance cost for each industry by the sales 
for that industry. Table VI-13 shows that the average price increase 
related to the cost of this proposed standard would be extremely small, 
0.07 percent, with the largest being 0.41 percent (Personal Services, 
SIC-72). The results in Table VI-13 indicate that even if all costs 
were passed on to consumers through price increases, the rule would 
have a negligible impact on prices.
    In many industries, however, establishments will not be able to 
pass along the entire cost of compliance through price increases since 
consumers may respond by reducing demand. Such establishments will have 
to absorb from profit the costs they cannot pass through. If all costs 
were absorbed from profit, the maximum expected decrease in profit can 
be calculated by dividing the estimated compliance cost for each 
industry by its estimated profit. Table VI-13 shows that the average 
decline in profits under this worst-case-elasticity assumption would be 
less than 0.94 percent. The largest potential decline in profits would 
be in Fishing at 4.5 percent (SIC-9).
    Because most establishments will not find it necessary to absorb 
all of the costs from profits and will be able to pass some of the 
costs on to consumers, average profits will not decline to the extent 
calculated in this analysis.

BILLING CODE: 4510-26-P

TP05AP94.001


BILLING CODE 4510-26-C
    OSHA believes that these impacts are not large enough to impair 
economic viability. While some marginal firms might be more seriously 
impacted, extensive economic dislocation is not expected to occur in 
any industry. OSHA has, therefore, preliminarily determined that the 
standard is economically feasible.
(2) Regulatory Flexibility Analysis
    The proposed IAQ standard will affect numerous small establishments 
and a portion of these establishments may have difficulty financing the 
compliance actions needed to comply depending on which alternative they 
choose. This section examines the potential for exceptional impacts 
among small establishments.
    The nature of compliance action limits the potential for 
exceptionally large compliance burdens on small businesses because most 
costs will be incurred on a per employee or per square foot basis. The 
number of buildings occupied with establishments with fewer than 20 
employees is estimated at 3.7 million or 82 percent of all buildings. 
Of these, 76 percent have floor space less than 10,000 square feet. 
Thus, small firms will incur low costs because they have small 
floorspace and few employees.
    To this point of the analysis, OSHA has not distributed the number 
of buildings across establishments since there are no data on which to 
describe the establishments in multi-tenant buildings. Therefore, OSHA 
developed establishment specific compliance costs based on the 
estimates presented in section E of this report. The economic impact by 
firm size is estimated with the assumption that all establishments will 
require HVAC maintenance. It was assumed that each establishment has a 
floor space of 10,000 square feet. To examine the potential regulatory 
burden that would be experienced by small establishments, OSHA 
calculated the ratio of their annual compliance cost to their sales and 
pre-tax profit for two scenarios for dealing with ETS: (1) provide 
designated smoking areas, or (2) totally ban smoking in the workplace. 
As shown in Table VI-14, for both scenarios, the average ratio of 
compliance costs to sales ranges from 0.44 percent to 0.52 percent. The 
highest impact (2.79 percent) for establishments not banning smoking 
would be in Personal Services (SIC-72). Estimates of compliance cost as 
a percentage of pre-tax profits were less than 7.05 percent for most 
sectors; Social Services establishments (SIC-83) would experience the 
largest reduction in profit (31 percent), if they allow smoking in 
designated rooms.
    These estimates apply to the average firm in each sector. The 
degree to which affected firms will either incur or shift compliance 
costs depends largely on the competitive environment in which the 
establishments operate and on the elasticity of demand for the 
establishment's services and commodities. OSHA requests information 
regarding compliance costs against indicators of the demand for and the 
costs of the types of services and commodities provided by 
establishments which would be affected by the proposed standard. OSHA 
specifically requests comments, including empirical data regarding the 
demand elasticity of such establishments' patrons who will not be 
permitted to smoke in the presence of employees at such establishments. 
If economic feasibility is shown to be an issue for establishments such 
as bars and restaurants, what methods of compliance would adequately 
protect workers in a feasible manner?
(3) Environmental Impact
    The provisions of the standard have been reviewed in accordance 
with the requirements of the National Environmental Policy Act (NEPA) 
of 1969 [42 U.S.C. 432, et seq.], the Council on Environmental Quality 
(CEQ) NEPA regulations [40 CFR Part 1500], and OSHA's DOL NEPA 
Procedures [29 CFR Part 11]. As a result of this review, OSHA concluded 
that this rule will have no significant environmental impact.

BILLING CODE 4510-26-P

TP05AP94.002


BILLING CODE 4510-26-C

VII. Summary and Explanation

    The requirements set forth in this notice are those which, based on 
currently available data, OSHA believes are necessary and appropriate 
to control conditions which may degrade indoor air and pose a 
significant risk of material impairment to employees in their work 
environments. The Agency considers that a broad approach to the control 
of IAQ problems, as proposed in this notice, will most effectively lead 
to a reduction in associated risk to employees [Exs. 3-2, 3-26, 3-37, 
3-41, 3-239, 3-287, 3-434, 3-500, 3-502]. OSHA has considered all data 
submitted in response to the Request for Information, as well as other 
scientific data which has been made a part of the record in this 
proceeding in arriving at these proposed provisions regarding 
regulation of indoor air quality.
    The following sections provide a summary of each provision of the 
proposal and a statement of their intent and purpose. Exhibit numbers 
included in this Summary and Explanation are citations to supporting 
comments and data submitted to the record in response to the RFI.
    The Agency solicits data, views, and comments on all provisions 
proposed in this notice. OSHA is interested in whether or not the 
proposed provisions are necessary, appropriate, and adequate to achieve 
the goals of the standard and why. Interested persons should also 
comment on whether or not the proposed provisions are technologically 
and economically feasible and why, and whether additional or 
alternative provisions addressing indoor air quality should be included 
in the standard and why.

Scope and Application: Paragraph (a)

    OSHA is proposing that these standards cover all employees under 
its jurisdiction, including employees in general industry, shipyards, 
longshoring, marine terminals, construction, and agriculture. To 
accomplish this, OSHA is proposing to publish an identical complete 
standard for general industry at 29 CFR 1910.1033, for shipyards at 29 
CFR 1915.1033, and for construction at 29 CFR 1926.1133. OSHA is 
proposing to amend section 1910.19 to make it clear that Sec. 1910.1033 
is a Subpart Z standard which is incorporated by cross reference into 
29 CFR parts 1917 and 1018 for longshoring and marine terminals. OSHA 
is proposing to amend 29 CFR 1928.21 to indicate that 1910.1033 will be 
applicable to agriculture. OSHA requests comments on the scope of the 
proposal and the formal manner by which the standard would be 
incorporated into the Code of Federal Regulations.
    Paragraph (a)(1) proposes to apply all provisions of the standard 
to ``nonindustrial work environments.'' In addition, paragraph (a)(2) 
proposes to further extend coverage of the provisions found in 
paragraph (e)(1), which address exposure to tobacco smoke, to all 
indoor work environments under OSHA's jurisdiction. This includes 
indoor work areas on construction sites, shipyards, and agricultural 
employments. The Agency believes that application of the proposed 
provisions under paragraph (e)(1) addressing exposure to tobacco smoke 
is necessary, appropriate, and feasible for any indoor or enclosed 
workplace covered by OSHA. Compliance with the tobacco smoke provisions 
essentially entails establishment of a separate enclosure, exhausted 
directly to the outside, and maintained under negative pressure where 
smoking is permitted. OSHA sees no feasibility obstacles in application 
of these provisions to industrial as well as nonindustrial work 
environments. It is not clear to OSHA, however, that the other indoor 
air quality provisions of the proposed standard can be feasibly or 
appropriately applied in typical industrial work environments. These 
provisions primarily address means to assure effective functioning of 
HVAC systems and actions felt necessary to be taken to maintain good 
general indoor air quality. Thus, it may not be feasible or appropriate 
to apply these provisions to industrial ventilation systems or 
industrial environments in which control of various industrial 
contaminant emissions rather than general air quality is the primary 
issue.

Definitions: Paragraph (b)

    The following terms are defined for the purpose of this proposal: 
``Air Contaminants'', ``Assistant Secretary'', ``Building systems'', 
``Building-related illness'', ``Designated person'', ``Designated 
smoking area'', ``Director'', ``Employer'', ``HVAC system'', ``Non-
industrial work environment'', and ``Renovation and remodeling''.
    The term ``Air contaminants'' refers to substances contained in the 
vapors from paint, cleaning chemicals, pesticides, solvents, 
particulates, outdoor air pollutants and other airborne substances 
which may cause material impairment to the health of employees working 
within the nonindustrial environment. The term ``air contaminants'' 
informs the employer that the provisions addressing control of air 
contaminants apply to airborne substances which may be within 
nonindustrial indoor work environments. For purposes of this proposal 
the definition of air contaminants may be broader than that used in 29 
CFR 1910.1000. Hazardous levels of air contaminants may arise from 
contaminant buildup due to inefficient or insufficient general dilution 
ventilation with outside air, the misapplication of general dilution 
ventilation to address strong point sources, indoor activities or 
operations such as renovation, remodeling, maintenance, etc. which lead 
to local source emissions, and entry of outdoor contaminants such as 
vehicle exhausts, wastes, stored materials, or pollutants from adjacent 
industrial facilities. Provisions are proposed in the standard which 
require the employer to take measures to address the avenues of 
contaminant buildup noted above.
    The term ``Assistant Secretary'' means the Assistant Secretary of 
Labor for Occupational Safety and Health, U.S. Department of Labor, or 
designee.
    The term ``Building systems'' applies to the heating, ventilation 
and air-conditioning (HVAC) system, the potable water system, the 
energy management system, and all other systems in a facility which may 
impact indoor air quality. This broad definition was necessary to avoid 
excluding non-HVAC systems which do impact indoor air quality. In the 
facilities industry, potable hot water systems are typically considered 
plumbing systems and not HVAC systems. Plumbing systems (potable hot 
water) have been implicated in Legionella episodes where the water is 
aerosolized, so excluding plumbing systems from the scope of this 
standard would have been unacceptable. This definition also intends to 
focus operation and maintenance efforts on those systems whose failure, 
degradation, or misuse would adversely impact indoor air quality.
    The term ``Building-related illness'' describes specific medical 
conditions of known etiology which can be documented by physical signs 
and laboratory findings. Such illnesses include sensory irritations 
when caused by known agents, respiratory allergies, nosocomial 
infections, asthma, humidifier fever, hypersensitivity pneumonitis, 
Legionnaires' disease, and the symptoms and signs characteristic of 
exposure to chemical or biologic substances such as carbon monoxide, 
formaldehyde, chlordane, endotoxins, or mycotoxins. ``Building-related 
illness'' defines the medical conditions that, if observed, require 
evaluation of the facility building systems to determine if they are 
functioning properly, and the taking of remedial action where 
warranted. Building-related illnesses are often potentially severe and 
are often traceable to a specific contaminant source such as ETS, 
microbial growth, and a host of other chemical or biologic substances 
which must be attended to mitigate degradation of indoor air quality.
    The term ``Designated person'' means a person who has been given 
the responsibility by the employer to take necessary measures to assure 
compliance with this section and who is knowledgeable in the 
requirements of this standard and the specific HVAC system servicing 
the affected building or office. As noted above a ``Designated person'' 
must be knowledgeable in HVAC system functioning. Provisions in the 
standard propose to require the ``Designated person'' to oversee the 
establishment and implementation of the IAQ compliance program, and 
oversee building systems inspection and maintenance activities, thus 
this person must have technical expertise in those areas. OSHA believes 
that there is a need for central responsibility in affected buildings 
and facilities [Exs. 3-434, 3-444b, 3-507]. Of course OSHA recognizes 
that in certain circumstances the ``Designated person'' may merely 
supervise or coordinate the activities of outside contractors or shift-
workers who have responsibility for maintaining parts of the building 
systems. Building systems and other factors affecting indoor air 
quality are sufficiently complex and unique to suggest the necessity of 
appointing a designated person who is on site to act on the employers 
behalf in this regard. For example, multiple employers may be engaging 
in different activities within a facility that affect building system 
functioning or air quality and actions by one employer may subject 
employees of other employers to environmental hazards. Fragmentation of 
responsibility and lack of communication has been observed by OSHA in 
the nonindustrial workplace. For example, when responding to an indoor 
air quality/building-related illness complaint, the OSHA Compliance 
Officer may need to gather information from a number of responsible 
facility groups like tenant leasing, facilities engineering, 
housekeeping, maintenance, operations, and energy management. These 
diverse groups may have little or no central authority and direction 
especially if they are outside contractors. The designated person would 
be in a position to mitigate the consequences of such diversity by 
being aware and responsible for the overall environmental conditions in 
the building or facility.
    Other OSHA health standards have adopted similar requirements with 
respect to those proposed in this Notice regarding the designated 
person. For example, final standards for chromium (57 FR 42102) and 
lead (58 FR 26590) require that a technically knowledgeable ``competent 
person'' be on site during construction activities, which often involve 
multiple employers. OSHA concluded in those standards that designating 
a person to act on the employers' behalf to ensure compliance with 
various provisions of those standards, was necessary because of the 
need for continual site characterization and analysis to identify the 
hazards present and the types of control measures and remedial actions 
that are effective. For these same reasons, OSHA proposes requirements 
for designated persons under this notice.
    The term ``Designated smoking area'' means a room in which smoking 
of tobacco products is permitted. The Agency believes that 
establishment of ``designated smoking areas'' is necessary to prevent 
employee exposure to ETS in workplaces where smoking is not prohibited. 
Provisions are included in this proposal addressing design, 
construction and operation of such areas to meet this purpose.
    The term ``Director'' means the Director, National Institute for 
Occupational Safety and Health (NIOSH), U.S. Department of Health and 
Human Services, or designee.
    The term ``Employer'' means all persons defined as employers by 
section 3(5) of the Occupational Safety and Health Act of 1970 
including employers (such as building owners or lessees) who control 
the ventilation or maintenance of premises where employees of other 
employers work. For purposes of the proposal, an employer is also 
defined as a person who exercises control over the ventilation systems 
in the workplace. Control over the ventilation systems is a multi-
faceted concept: it includes maintenance, recordkeeping and the 
development and implementation of the indoor air quality compliance 
plan. While responsibility for various aspects of the ventilation 
system encompasses many duties, the proposal does not necessarily 
contemplate that all of the duties will be performed by the same 
person. The proposal is flexible in that regard and responsibility for 
the various aspects can be shared by various persons depending on the 
circumstances.
    In many instances the employer will either be the owner of the 
building where the workplace is located or will be a long term lessee, 
responsible under the lease for the care and maintenance of the 
property. In these cases, the owner/employer would take care of the 
ventilation system by designating knowledgeable persons within his 
employ to the necessary tasks or by hiring competent contractors.
    In other cases, there will be a number of different businesses all 
located in separate leased space within the same building. In these 
instances the various employer/lessees would probably share 
responsibility for compliance with the proposed standard. For example, 
each individual lessee might be obligated to provide the building owner 
with a description of the work activity planned for within its 
particular leased space, including the number of employees or visitors 
expected, the hours of work operation and any situations where air 
contaminants may be released into the workplace air. Air contaminants 
might reasonably be expected to be released into the workplace air as a 
result of the installation of new furniture or wall coverings, any 
painting or remodeling scheduled to take place or any pest 
extermination activity within the premises. Each employer would, of 
course, be responsible for reporting to whoever is in charge of the 
ventilation system, any employee complaints or signs or symptoms that 
may be related to building-related illness.
    The building owners or whoever is in charge of the maintenance of 
the ventilation system would be in a position to develop standard 
operating procedures for the building systems as well as special 
procedures for emergencies and maintenance. In addition such a person 
would be in a position to know or develop an appropriate maintenance 
schedule and to gather relevant documents to assist in the care and 
maintenance of the ventilation system, such as diagrams of the system, 
manufacturers manuals, and inspection guidelines and schedules for the 
proper maintenance of such systems. The same person might also be 
responsible for maintaining and operating the HVAC system to provide 
the required air ventilation rate and desired relative humidity.
    The proposal is designed in this performance oriented manner to 
afford affected employers the flexibility to assure the establishment 
and maintenance of a system to provide healthful indoor air quality in 
the most sensible and efficient way possible considering their 
particular circumstances.
    The Occupational Safety and Health Act gives the Secretary the 
right to promulgate standards to assure employees safe and healthful 
working conditions. Employers must comply with the standards which the 
Secretary promulgates. The Act defines an employer expansively as a 
person with employees in a business affecting interstate commerce.
    The Agency believes that the proposal as written will protect 
employees from the risks of poor indoor air quality. Where the owner of 
a business is not the owner of the space where such business operates, 
the owner or landlord of the building will probably also be an employer 
within the meaning of the Act and the definition contained in this 
proposal. This is so because the building owner or operator will 
generally have employees (either on site or off site) and will be 
engaged in a business affecting interstate commerce. In such cases the 
situation will be construed to be a multi-employer worksite. Such 
situations are quite common in the context of construction sites. The 
Agency does not believe that there is any reason to treat nonindustrial 
multi-employer worksites differently from construction multi-employer 
worksites for purposes of compliance.
    OSHA has a long history of enforcing OSHA standards in multi-
employer worksites. Nothing in this proposed rule would change the 
position that the Agency has taken in cases such as Anning-Johnson (4 
OSH Cas. (BNA) 1193, Harvey Workover, Inc., 7 OSH Cas. (BNA) 1687 and 
in its Field Operations Manual (CPL 2.45 CH-1, Chapter V-9). As a 
general matter each employer is responsible for the health and safety 
of his/her own employees. However, under certain circumstances an 
employer may be cited for endangering the safety or health of another 
employer's employees. In determining who to hold responsible, OSHA will 
look at who created the hazard, who controlled the hazard, and whether 
all reasonable means were taken to deal with the hazard.
    It is contemplated that in those cases where there is a multi-
employer worksite that the affected employers will divide up the 
responsibilities in the manner in which they make the most sense. Those 
who have information at their disposal that is required to be kept 
under the proposal will make use of the information or make it 
available to whoever will need that information in the discharge of 
their duties. For example, the building engineer may have possession of 
the schematics of the ventilation system. The engineer would make them 
available to the person responsible for maintaining the system as well 
as the person responsible for developing the IAQ Compliance Plan (if 
that is not the same person). The proposal is designed to promote the 
efficient resolution of indoor air quality problems and will not result 
in duplicative efforts. There is nothing in the proposal, for example, 
that would prevent the building owner (who is an employer within the 
meaning of the Act) from gathering the required information from the 
various lessee/employers in the premises, developing, and implementing 
an IAQ Compliance Plan which would be shared with the various employers 
occupying the premises. In addition, it may be more efficient for the 
building owner to develop and maintain the records required by the 
proposal, again sharing them with the various employer-tenants. The 
Agency believes that the co-operative interrelationships which the 
performance oriented proposal permits will avoid duplication of 
compliance activities even within multi-employer worksites.
    The term ``HVAC system'' means the collective components of the 
heating, ventilation and air-conditioning system including, but not 
limited to, filters and frames, cooling coil condensate drip pans and 
drainage piping, outside air dampers and actuators, humidifiers, air 
distribution ductwork, automatic temperature controls, and cooling 
towers. This definition also intends to focus on those HVAC system 
components whose failure, degradation, or misuse would adversely impact 
indoor air quality.
    The term ``Nonindustrial work environment'' means an indoor or 
enclosed work space such as, but not limited to, offices, educational 
facilities, commercial establishments, and healthcare facilities, and 
office areas, cafeterias, and break rooms located in manufacturing or 
production facilities. Nonindustrial work environments do not include 
manufacturing and production facilities, residences, vehicles, and 
agricultural operations.
    The term ``Renovation and remodeling'' means building modification 
involving activities that include but are not limited to: removal or 
replacement of walls, ceilings, floors, carpet, and components such as 
moldings, cabinets, doors, and windows; painting, decorating, 
demolition, surface refinishing, and removal or cleaning of ventilation 
ducts.
    The terms ``HVAC system'', ``Nonindustrial work environment'', and 
``Renovation and remodeling'' are defined to clarify and illustrate the 
parameters under which obligations of the standard are incurred. For 
example, the definition of ``HVAC system'' lists what OSHA believes to 
be typical components of such systems which directly affect indoor air 
quality. These components are enumerated since provisions under the 
standard propose to require employers to perform routine inspection and 
maintenance on those components. ``Renovation and remodeling'' is 
defined to inform the employer of the situations under which the 
standard proposes to require the employer to take special precautions 
when those activities take place.

Indoor Air Quality Compliance Program: Paragraph (c)

    This paragraph proposes to require employers to obtain or develop 
certain written information that will facilitate implementation of 
measures necessary to prevent degradation of indoor air quality. 
Paragraph (c)(2) proposes to require the employer to identify a 
designated person to be given the responsibility of overseeing 
establishment and implementation of the written compliance program. 
Paragraph (c)(3) proposes to require the employer to establish a 
written IAQ compliance program to include at least the following 
information: a description of the facility building systems; schematics 
or construction documents locating building systems equipment; 
information on the daily operation and management of the building 
systems; a description of the building and its function; a written 
maintenance program; and a checklist for visual inspection of the 
building systems. Further, paragraph (c)(4) proposes to require that 
the following information also must be retained, if available, to 
assist in indoor air quality evaluations: as built construction 
documents; HVAC system commissioning reports; HVAC system testing, 
adjusting and balancing reports; operation and maintenance manuals; 
water treatment logs; and operator training materials. Paragraph (c)(5) 
proposes to require the establishment of records of employee complaints 
of building-related illnesses, as part of the written program.
    OSHA believes that written plans are an essential element of an 
overall compliance program since it will encourage employers to focus 
on indoor air quality and implement the necessary controls and measures 
to achieve compliance with the standard [Exs. 3-38, 3-85, 3-412, 3-434, 
3-500, 3-502, 3-505, 3-529]. The development of documented safety and 
health programs and procedures is a well-established and common 
practice in industry, and requirements for written programs are 
typically found in other OSHA standards dealing with exposure to toxic 
substances. Written plans provide information to allow OSHA, the 
employer, and employees to examine the control methods chosen and 
evaluate the extent to which these planned controls are being 
implemented.
    Paragraph (c)(3) proposes to require the employer to establish 
written plans for compliance. Specifically, paragraphs (c)(3)(i), 
(c)(3)(ii), and (c)(3)(iii) propose to require general, descriptive 
information about: the facility, building systems, building function 
and building use patterns. This general building description is 
believed to be essential information of a building profile which is 
necessary for a basic understanding of the building systems and which 
is necessary to set the foundation for the operations and maintenance 
information required in other paragraphs.
    Further, in paragraph (c)(3)(iv), OSHA believes that it is 
necessary to require written information which describes daily 
operation and management of the facility building systems which 
directly affects IAQ. When it comes to operations and management, 
organizational fragmentation within nonindustrial buildings may be 
further exacerbated by the lack of familiarity with the intent of the 
original design team whose assumptions and design intent for the HVAC 
system, are typically unknown. Over time, building use may differ from 
original design intent in ways not foreseen by the original designers. 
It is not uncommon for spaces to be loaded or used in ways beyond the 
original design intent which may adversely impact IAQ, such as putting 
up walls for private offices, exceeding intended occupant densities, 
and bringing into the space new contaminant sources. HVAC system total 
capacity may be able to handle these changes from original design loads 
but little is done to balance the available capacity among the 
individual zones that may be overused or underused.
    In addition, the employer may need to communicate design intent and 
performance criteria to building occupants whose expectations regarding 
their environment may exceed what is deliverable by the building 
systems.
    To address these issues, OSHA is proposing to require that each 
facility have written operations and management information whose aim 
is twofold. One purpose is to collect, summarize and translate design 
assumptions and intent into operating performance criteria that impact 
IAQ, such as minimum outside air ventilation rates and occupant 
densities.
    Secondly, the operations information should describe how to operate 
and manage the building systems so that they perform in conformance 
with the reported criteria. This written operations and management 
information replaces verbal communications and provides a training 
document whenever new personnel or new contractors are introduced to 
the site. Operating information should formally reflect changes in 
control strategies that typically occur in facilities to accommodate 
change in use or energy conservation efforts. This is an essential 
element because of the interdependence between outside air ventilation 
rate and the automatic temperature control system. In almost all 
buildings the performance of the ventilation system is affected by 
space temperature control needs.
    Paragraph (c)(3)(v) proposes to require a written maintenance 
program for those building system components that directly affect IAQ 
because failure to do so may result in the degradation of IAQ in the 
facility. A written maintenance program is believed to be necessary 
because levels of HVAC system maintenance vary dramatically and 
sometimes are deficient where untrained personnel are designated to 
maintain very complex systems. The following are examples of 
maintenance deficiencies which have been associated with IAQ problems: 
plugged drains on cooling coil condensate drip pans resulting in 
microbial contamination of pan; failed exhaust fans in underground 
parking garages which allow carbon monoxide to infiltrate into the 
building above; microbial fouling of cooling tower water from lack of 
water treatment with biocides resulting in legionellosis cases; and 
failure of automatic temperature control system resulting in lack of 
outside ventilation air.
    Maintenance of HVAC equipment, for example, may include simple 
housekeeping of equipment and air transport pathways, lube and 
adjustment programs for rotating machinery, and catastrophic failure 
maintenance to repair/replace failed equipment. There appears to be 
consensus among HVAC maintenance personnel that the most successful 
maintenance programs, gauged in terms of system performance and life-
cycle economics, are proactive rather than reactive. Consequently, OSHA 
is promoting preventive maintenance programs for those building system 
components which affect IAQ. At a minimum, the maintenance program 
should describe the equipment to be maintained, establish maintenance 
procedures and frequency of performance.
    Paragraph (c)(3)(vi) proposes to require a checklist to guide 
periodic inspections of building systems. This checklist should focus 
on those building system components whose failure, degradation, or 
misuse would adversely impact indoor air quality. The checklist shall 
include but not be limited to inspection of the following components 
and performance criteria: fibrous liner used for acoustics and 
insulation in airhandlers and ducts should be inspected for erosion and 
moisture; smoke-trails testing should be performed to verify design 
pressurization schemes like negative pressure smoking rooms; ceiling, 
floor and wall surfaces should be examined for signs of water leaks 
which could support and amplify microbial contamination; and outside 
air louvers, intake paths, dampers, actuators, and linkages should be 
checked for obstruction.
    Paragraph (c)(5) proposes to require the establishment of records 
of employee complaints of building-related illnesses as part of the 
written program. These records are believed to be necessary to expedite 
review and evaluation of the system and to support implementation and 
operation of an adequate IAQ program [Exs. 3-434, 3-444b, 3-502].
    The Agency believes that effective system operation and maintenance 
will necessarily rely upon written information and records such as 
those relating to design expectations, system capacities, code 
requirements, maintenance activities and system evaluations. As with 
other OSHA rulemakings, the written compliance plan is to be accessible 
to employees.

Compliance Program Implementation: Paragraph (d)

    This paragraph proposes to require that the employer take certain 
actions to maintain acceptable indoor air quality. These actions 
primarily address means that OSHA believes necessary to achieve 
continued adequate and proper functioning of building systems [Exs. 3-
10, 3-17, 3-26, 3-38, 3-41, 3-55, 3-56, 3-61, 3-85, 3-329, 3-364, 3-
412, 3-415, 3-434, 3-436, 3-444A, 3-479, 3-496, 3-500, 3-501, 3-502, 3-
505, 3-507, 3-529, 3-531].
    Paragraph (d)(1) proposes to require that employers maintain and 
operate the HVAC system to provide at least the minimum outdoor air 
ventilation rate, based on actual occupancy, required by the applicable 
building code, mechanical code, or ventilation code in effect at the 
time the facility was constructed, renovated, or remodelled, whichever 
was most recent [Ex. 3-18]. Paragraph (d)(2) proposes to require 
employers to conduct building system inspection and necessary 
maintenance activities as often as necessary to reduce the likelihood 
of indoor air quality problems related to the building systems [Ex. 3-
26]. Further requirements under paragraph (d) are: Assure that the HVAC 
system is operable during all work shifts, (d)(3) [Exs. 3-56, 3-226, 3-
347, 3-436]; implement the use of general or local ventilation where 
maintenance activities may result in hazardous chemical or particulate 
exposures in other areas of the building, (d)(4) [Exs. 3-347, 3-502]; 
maintain relative humidity below 60% in buildings with mechanical 
cooling systems, (d)(5) [Exs. 3-34, 3-61, 3-505B]; during regular 
maintenance, as described in subparagraph (d)(1), measure carbon 
dioxide levels. When they exceed 800 ppm, check to make sure the HVAC 
system is operating as it should and correct deficiencies if necessary, 
(d)(6) [Exs. 3-10, 3-34, 3-214]; assure that buildings without 
mechanical ventilation are maintained so that windows, doors, vents, 
etc., designed or used for natural ventilation are in operable 
condition, (d)(7); assure that mechanical equipment rooms and any non-
ducted air plenums or chases are maintained in a clean condition, free 
of hazardous substances, and asbestos, if friable, is encapsulated or 
removed so that it does not enter the air distribution system, (d)(8) 
[Exs. 3-29, 3-500]; assure that inspections and maintenance of the HVAC 
system are performed by or under the direction of the designated 
person, (d)(9) [Ex. 3-29]; establish a record of HVAC system 
inspections and maintenance, (d)(10) [Ex. 3-26]; assure that employees 
performing work on HVAC systems are provided with and use appropriate 
personal protective equipment, (d)(11) [Ex. 3-56]; evaluate the need to 
perform alterations of the HVAC system in response to employee reports 
of building-related illness, (d)(12); and take such remedial measures 
as the evaluation shows to be necessary, (d)(13).
    OSHA believes that implementation of each of the actions prescribed 
in this proposed paragraph are integral elements in the indoor air 
quality program. Provisions which address inspection, maintenance, 
alteration, and operation of building systems are believed to be 
essential to ensure successful functioning of system functioning.
    Paragraph (d)(1) proposes to require that employers operate and 
maintain the HVAC system to provide at least the minimum outside air 
ventilation rate. Available evidence in the literature supports this 
requirement. The literature which supports the case for ventilation 
with outside air falls into two categories. One category includes case 
studies which are generated when IAQ complaints require on-site 
responses and the investigators report their findings through IAQ 
forums sponsored by professional organizations like the American 
Society of Heating, Refrigerating and Air-Conditioning Engineers, Inc. 
and the American Industrial Hygiene Association. These studies report 
that the lack of outside ventilation air resulting from operational or 
maintenance deficiencies as one of the causes of IAQ complaints. Many 
of the studies include abatement recommendations to ventilate with 
outside air as feasible per the original design intent. The second 
category includes research projects which also support the case for 
ventilating buildings with at least the recommended minimum of outside 
air. Research in the areas of ventilation efficiency, tracer gas 
analysis, dilution/removal of internally generated contaminants, and 
environmental perceptions mostly support this contention.
    All three major building codes in the United States which are used 
in the design of new and retrofitted facilities mandate minimum outside 
air ventilation rates in mechanically-ventilated buildings. These three 
code bodies include the Building Officials and Code Administrators 
International, Inc. (BOCA), the International Conference of Building 
Officials (ICBO), and the Southern Building Code Congress 
International, Inc. (SBCCI). Per Section 102 of the 1991 Uniform 
Building Code as promulgated by the ICBO, the purpose of the building 
code is ``to offer minimum standards to safeguard life or limb, health, 
property and public welfare by regulating and controlling the design, 
construction, quality of materials, use and occupancy * * *''. Clearly, 
there is a significant commitment of resources by these code bodies to 
offer design guidance through the building codes to designers to insure 
that a facility is capable of delivering a minimum amount of outside 
air to its' occupants. This concept is supported by the efforts of plan 
reviewers and building inspectors in local governmental jurisdictions 
throughout the United States who ensure that facilities are constructed 
per the building codes. Considering the up-front efforts of these code 
officials, designers, and construction teams, it is reasonable from a 
standpoint of continuity, to require that buildings be operated and 
maintained to the same design intent.
    This provision is not meant to require rebuilding or retrofitting 
HVAC systems in response to minor work. For example, such steps would 
not be required for any renovation work that does not modify the 
building's configuration or the conditions that would be affected by 
the building code applicable at the time the system was installed or 
last modified.
    As part of maintenance, there should be a predictive element which 
periodically checks the HVAC system to evaluate conformance with 
paragraph (d). This check should conform with the proposals of 
paragraph (d)(2) which requires an inspection and maintenance of the 
building systems. This periodic visual inspection is focused by the 
checklist outlined in paragraph (c) and targets those components that 
directly impact indoor air quality. In the field of occupational safety 
and health, as practiced by industrial hygienists, it is common 
practice to perform walk-around inspections. On the other hand, the 
HVAC industry often relies heavily on remote sensing to characterize 
system performance. Therefore, this required visual inspection will 
help identify those deficiencies that would otherwise be missed, such 
as microbial contamination in cooling coil condensate drip pans.
    Paragraph (d)(3) requires that the facility HVAC system is 
operating during all workshifts. The employer must provide the minimum 
outside ventilation rate for contaminant dilution and removal whenever 
the building is occupied and used. OSHA understands that the minimum 
outside air ventilation rate may in practice only be provided when the 
building is fully occupied or utilized. It is not uncommon for office 
buildings to be occupied from 6 a.m. to 7 p.m. to accommodate flexible 
work schedules but the HVAC system may only be in operation from 8 a.m. 
to 5 p.m. to conserve energy. The technical rationale for this strategy 
is typically based on the recommendations of the American Society of 
Heating, Refrigerating and Air-Conditioning Engineers, Inc. (ASHRAE) in 
their Standard 62-1989 titled ``Ventilation for Acceptable Indoor Air 
Quality''. Section 6.1.3.4 and Appendix ``G'' of ASHRAE Standard 62-
1989 [Ex. 4-333] offers a rationale for the lead/lag operation of 
ventilation systems to accommodate transient occupancy. The basis for 
the rationale is that there is capacity in air to dilute contaminants 
if the space has been previously unoccupied for several hours. This 
strategy, however, applies only to occupant generated contaminants like 
carbon dioxide and odors. Housekeeping cleaning agents or pesticides 
are typical of contaminants that may be released which could not be 
absorbed by a non-ventilated space. Consequently, other contaminants 
must be diluted/removed by the ventilation system whenever the building 
is occupied. In addition, it is recognized that certain automatic 
temperature control strategies can also prevent a facility from 
receiving the minimum outside air ventilation rate. The obvious example 
is the early morning warm-up cycle wherein the outside air dampers are 
kept shut in the morning until the space temperature recovers from the 
setback temperature of the night before. These energy conservation and 
temperature control strategies must not interfere with providing 
minimum outside air ventilation when the building is occupied.
    Paragraph (d)(4) proposes to require the employer to utilize 
general or local exhaust ventilation, as provided by the existing HVAC 
system or auxiliary systems, to minimize the hazards associated with 
maintenance or housekeeping activities. The literature reports IAQ/BRI 
episodes that were initiated with activities like painting, carpet 
cleaning and floor resurfacing. If these activities occur during 
unoccupied periods then chemical vapors from paints and adhesives and 
excessive moisture from carpet cleaning may be diluted and removed by 
the outside air ventilation function of the HVAC system. During 
occupied periods, efforts should be made to restrict transportation of 
hazardous contaminants from these activities throughout the facility by 
the HVAC air distribution system.
    Paragraph (d)(5) proposes to require the employer to maintain 
occupied space relative humidities below 60% in buildings with 
mechanical cooling systems. Moisture in a building may support and 
amplify microbial contamination with potential for aerosolization. Both 
the American Society of Heating, Refrigerating and Air-Conditioning 
Engineers, Inc. (ASHRAE) in their Standard 62-1989 titled ``Ventilation 
for Acceptable Indoor Air Quality'', section 5.11 [Ex. 4-333] and the 
American Conference of Governmental Industrial Hygienists (ACGIH) in 
their 1989 ``Guidelines for the Assessment of Bioaerosols in the Indoor 
Environment'' [Ex. 3-61] recommend that relative humidity in the 
occupied space be maintained below 60%.
    OSHA is inviting comments on whether a relative humidity of 60% is 
the appropriate upper limit to inhibit microbial growth or if a higher 
limit is appropriate. In addition, OSHA would like comment on whether 
there should be a lower level of relative humidity as recommended by 
ASHRAE and ACGIH to reduce irritation effects due to low relative 
humidity. And finally, OSHA would like additional comment on whether it 
is feasible in hot and humid climates to achieve relative humidities of 
60% or less.
    Paragraph (d)(6) proposes to require the employer to monitor for 
carbon dioxide (CO2) in the occupied space as part of maintenance 
or employee complaint investigations. When the concentration exceeds 
800 ppm, the employer would be required to check the operation of the 
HVAC system. CO2 is frequently used as a gross surrogate indicator 
of indoor air quality. Ideally, by knowing the rate of accumulation of 
CO2 in the space and the rate of generation of CO2 by 
respiring occupants in the space, it would be possible to predict the 
rate of removal of CO2 from the space by the HVAC system. Because 
buildings have average occupant densities to generate CO2, the 
concentration is an indicator of the HVAC system's ability to dilute 
and remove occupant generated contaminants like CO2, water vapor, 
and odors (human bioeffluents). However, the CO2 concentration and 
the associated outside air ventilation rate offers no confidence as to 
the adequacy of dilution and removal of other contaminants released in 
the space. If the outside air ventilation rate is insufficient to 
dilute and remove CO2, then it can be assumed that other 
contaminant concentrations will also be elevated. The literature 
reports that CO2 concentrations in the space under 800 ppm will 
minimize health-related complaints [Exs. 3-34A, 4-331].
    Paragraph (d)(8) proposes to require the employer to restrict the 
presence of hazardous substances in air distribution systems. The HVAC 
air distribution system itself should not be the source of hazardous 
contaminants due to its' critical nature as a potential pathway to 
building occupants. Enclosed ducts are typically not used to store 
hazardous substances but non-ducted air transport pathways such as 
area-ways, plenums, chases, corridors, and mechanical rooms serving as 
return air plenums are sometimes used for storage. If these air 
transport pathways are used for storage, then the employer must be 
especially careful to make sure that no spillage or leakage of 
hazardous substances occurs. This will insure that the pathways are 
kept free of hazardous substances.
    Paragraph (d)(11) proposes to require that employees working on 
building systems are provided with and use personal protective 
equipment (PPE) as required by other OSHA standards including; 29 CFR 
1926, Subpart E, Personal Protective and Life Saving Equipment; 29 CFR 
1926.52, Occupational Noise Exposure; 29 CFR 1910, Subpart I, Personal 
Protective Equipment; and 29 CFR 1910.95 Occupational Noise Exposure.
    OSHA is aware, through its experience and through the literature 
and submissions to the docket, that HVAC Operations and Maintenance 
(O&M) personnel may often receive minimal training regarding existing 
relevant OSHA regulations and the hazards that they are exposed to in 
the performance of their duties. Sometimes, facilities are not viewed 
as industrial workplaces by either the management or employees. 
However, the hazards do exist and therefore compliance with existing 
regulations is necessary to protect the health and safety of O&M 
employees. Respirators may not normally be used in this industry due to 
the perceived lack of a substance-specific hazard. But situations may 
occur, for instance, such as chemical or microbial contamination, that 
would require compliance with 1910.134.
    Other provisions of this section require; that buildings without 
mechanical ventilation be operated and maintained to provide natural 
ventilation; that inspections and maintenance of building systems be 
performed by or under the supervision of the designated person; that 
the employer establish a written record of building system inspections 
and maintenance required under this section; that the employer evaluate 
the need to perform modifications to the building systems to meet the 
minimum requirements specified in paragraph (d) of this section in 
response to employee complaints of building-related illnesses.

Controls for Specific Contaminant Sources: Paragraph (e)

    This paragraph proposes to require employers to take specific 
protective measures to control employee exposure to specific agents 
such as tobacco smoke [Exs. 3-7, 3-10, 3-85, 3-291, 3-305, 3-409, 3-
449, 3-496, 3-505B], outdoor pollutants [Ex. 3-496, 3-500, 3-502, 3-
505], contaminant emissions from local indoor sources [Exs. 3-10, 3-17, 
3-26, 3-38, 3-412], microbial contaminants [Exs. 3-10, 3-26, 3-61, 3-
496, 3-500, 3-502, 3-505, 3-506], hazardous chemicals including 
cleaning and maintenance chemicals and pesticides [Exs. 3-56, 3-436, 3-
496, 3-500, 3-505].
    With respect to tobacco smoke in workplaces where smoking is not 
prohibited, paragraph (e)(1) proposes to require the establishment of 
designated smoking areas. Such areas must be enclosed and exhausted 
directly to the outside, and maintained under negative pressure 
sufficient to contain tobacco smoke within the designated area. Smoking 
is not permitted during cleaning and maintenance work in these 
designated smoking areas. Moreover, although cleaning and maintenance 
are specified in this paragraph, it is OSHA's intent that no work of 
any kind shall be performed in a designated smoking area when smoking 
is taking place. Designated smoking areas must be areas where employees 
do not have to enter in the performance of normal work activities. 
Signs must also be posted at designated smoking areas. Signs must be 
posted to inform anyone entering the building that smoking is 
restricted to designated areas. Finally, smoking within designated 
areas is not permitted during any time that the exhaust ventilation 
system servicing that area is not operating properly.
    The proposed provisions under paragraph (e)(1) addressing control 
of tobacco smoke are intended to ensure that employees outside of the 
designated smoking area will not be exposed to ETS. The Agency 
anticipates that the provisions as proposed will accomplish that goal. 
Enclosing smoking areas, exhausting them to the outside, maintaining 
them under negative pressure, and prohibiting smoking in designated 
areas even when the exhaust system is inoperable are believed to be 
necessary and sufficient to prevent tobacco smoke from migrating to 
other areas of the building.
    The designated smoking area must be under negative pressure 
compared to all surrounding spaces including adjoining rooms, 
corridors, plenums and chases. Negative pressure is achieved by 
exhausting more air from the space than is supplied to the space.
    Transfer air must enter the designated smoking room to make-up the 
volumetric flowrate differential between supply and exhaust air. It may 
be necessary to provide a tight architectural enclosure so as to 
achieve negative pressure and containment. Leakage through a lay-in 
ceiling tile system may occur if there is a return air plenum above it. 
Negative pressure will induce airflow into the room through the 
entrance door undercut. Containment may be checked by using smoke-
trails at the door undercut to verify direction of airflow.
    Contaminated exhaust air from a designated smoking room must be 
transported to the outside through exhaust ducts under negative 
pressure to avoid duct leakage into nonsmoking areas that the duct 
passes through.
    The provisions regarding posting of signs are intended to prevent 
inadvertent entry into smoking areas, and inadvertent smoking in areas 
other than designated smoking areas. To prevent involuntary exposure, 
designated smoking areas cannot be areas where employees perform normal 
work activities. For the same reason, smoking is not permitted in 
smoking areas during performance of work activities such as cleaning 
and maintenance of the designated smoking area.
    This provision will have special impact on establishments such as 
bars and restaurants. OSHA invites comments on feasibility 
considerations relative to such establishments and suggestions for 
alternative ways to assure that nonsmoking workers will not be exposed 
to tobacco smoke there.
    Proposed paragraph (e)(2) establishes requirements dealing with 
outdoor air pollutants and contaminants emitted locally within 
workspaces. This paragraph proposes to require the employer to 
implement measures to restrict the entry of outdoor air pollutants into 
the building and to control local indoor sources of air contaminant 
emissions by employing other control measures like substitution or 
local source capture exhaust ventilation.
    Proposed paragraph (e)(3) proposes to require the control of 
microbial contamination by routinely inspecting for and repairing water 
leaks that can promote growth of biologic agents, by promptly drying, 
replacing, removing, or cleaning damp or wet materials; and by taking 
measures to remove visible microbial contamination in ductwork, 
humidifiers, other HVAC system components, or on other building 
surfaces.
    Proposed paragraph (e)(4) addresses the use of cleaning and 
maintenance chemicals, pesticides and other hazardous chemicals. 
Pesticides must be used according to manufacturers' recommendations, 
and where chemicals are to be used, employees in those areas affected 
are to be informed, at least within 24 hours prior to use, of the type 
of chemical to be applied.
    The provisions proposed under (e)(2) are intended to ensure that 
indoor air quality is not degraded as a result of entry of outdoor 
contaminants, such as vehicle exhaust, or by circulation of 
contaminants generated within the building. The Agency believes that, 
where necessary, entry of outdoor air pollutants can be restricted by 
eliminating or repositioning entry points into the building.
    Indoor local contaminant emissions can be minimized where 
necessary, through application of control measures such as source 
substitution and engineering controls that may include local source 
capture exhaust ventilation. Collection of contaminants at their source 
of emission through engineering controls is an accepted basic principle 
of industrial hygiene. Equipment and processes which are located or 
take place in areas that may lead to contamination of other areas 
should be provided with engineering controls, where necessary and 
feasible.
    The provisions proposed in paragraph (e)(3) are intended to limit 
the opportunity for microbiological contamination of building systems 
and structures. Although individual microbes are not visible to the 
naked eye, colonies of microbes are. Moisture can lead to 
microbiological growth in indoor spaces, within HVAC systems, or within 
building structures, and thus to a variety of detrimental health 
effects. The employer therefore, is required to take preventive and 
corrective actions to minimize microbiological growth. Preventive 
action includes routine inspection for biological growth, with required 
corrective actions such as repairing water leaks, drying, replacing, or 
cleaning wet materials, and removal of visible microbiological growth 
(Exs. 3-61, 3-502).
    The provisions proposed in paragraph (e)(4) are intended to 
restrict indoor exposure to hazardous substances such as pesticides and 
chemicals used for cleaning and maintenance purposes. The Agency 
believes that proper use of such substances is important to limit 
incidental exposures to those performing cleaning and maintenance as 
well as to other employees who might be incidentally exposed. 
Manufacturers recommendations for use of these products often address 
aspects of ventilation, employee protection, occupancy limitations, and 
other protective measures. Thus, the Agency has proposed to require 
that chemicals covered under this paragraph must be used in accordance 
with manufacturer's recommendations. To further limit the potential for 
incidental exposures to these chemicals the standard proposes to 
require that employees in areas to be treated by such chemicals are to 
be notified within at least 24 hours prior to their application.

Air Quality During Renovation and Remodeling: Paragraph (f)

    Paragraph (f)(1) proposes to require implementation of specific 
procedures to minimize degradation of air quality during renovation and 
remodeling activities (Exs. 3-26, 3-38, 3-444B).
    Paragraph (f)(2) proposes to require development and implementation 
of a work plan to restrict entry of air contaminants into other work 
areas during remodeling, renovation, and similar activities (Ex. 3-
444b). Where appropriate, elements of the workplan to be considered are 
requirements of this standard, implementation of means to assure that 
HVAC systems continue to function effectively during remodeling and 
renovation activities, isolation or containment of work areas and 
appropriate negative pressure containment, air contaminant suppression 
controls or auxiliary air filtration, and controls to prevent air 
contaminant entry into HVAC systems. Finally, paragraph (e)(3), 
proposes to require 24 hour advance notification of employees, or 
promptly in emergency situations, of work to be performed on the 
building that may introduce air contaminants into their work area. Such 
notification must include anticipated adverse impacts on indoor air 
quality or workplace conditions.
    The provisions under proposed paragraphs (f)(1) and (f)(2) are 
intended to ensure that renovation, remodeling and similar activities 
are performed in a manner that will reduce the potential for air 
contaminants generated during those activities from entering other 
areas of the building. Such activities which may involve demolition, 
sanding, surface refinishing, component removal and replacement, etc. 
can result in hazardous substance emission from solvents, paints, 
carpets, etc. and can also produce high levels of particulate 
contamination. To control such emissions, the standard proposes to 
require employers to develop a workplan for the implementation of 
appropriate work procedures and controls such as exhaust ventilation, 
isolation, containment, or use of wet methods during renovation and 
remodeling activities.
    Finally, paragraph (f)(3) proposes to require notification of 
employees in the vicinity of renovation and remodeling activities who 
may be subject to incidental exposure to emissions produced during such 
activities (Ex. 3-444B). This notification must also apprise affected 
employees of the potential adverse impact on air quality. Informing 
employees of potential workplace hazards is felt by the Agency to be 
imperative for the success of any safety and health program. OSHA 
believes that employees can do much to protect themselves if they are 
informed of the nature of the hazards to which they are exposed.

Employee Information and Training: Paragraph (g)

    Paragraph (g) proposes to require employers to provide special 
training for workers involved in maintenance activities and those 
involved in HVAC system operations, and to provide certain pertinent 
information to all employees.
    Paragraph (g)(1) proposes to require that maintenance and HVAC 
operations personnel be trained in the use of personal protective 
equipment (PPE) required to be worn; training on how to maintain 
adequate ventilation of exhaust fumes during building cleaning and 
maintenance; and training of maintenance personnel on how to minimize 
adverse effects on indoor air quality during the use and disposal of 
chemicals and other agents [Exs. 3-26, 3-38, 3-41, 3-347, 3-415, 3-434, 
3-440, 3-444B, 3-500, 3-502].
    Paragraph (g)(2) proposes to require that all employees shall be 
informed of the contents of the standard and its appendices, signs and 
symptoms associated with building-related illness, and the requirement 
under proposed subparagraphs (d)(12) and (d)(13) which directs the 
employer to evaluate the effectiveness of the building systems, if 
necessary, upon receipt of complaints from employees of building-
related illness [Exs. 3-38, 3-347, 3-412, 3-415, 3-434, 3-444B, 3-500, 
3-529]. The information proposed to be provided under this subparagraph 
need not be conveyed to employees through formal training sessions or 
courses. Informing employees can be accomplished, for example, through 
written means such as fact sheets, memos, or posted bulletins. OSHA 
will provide in a non-mandatory appendix to the final rule an example 
illustrating what information is to be provided to employees.
    Paragraph (g)(3) proposes to require that the employer make 
training materials developed under these provisions, including the 
standard and its appendices, available for inspection and copying by 
employees, designated employee representatives, the Director, and the 
Assistant Secretary.
    Training and information requirements are routine components of 
OSHA health standards. The inclusion of training and information 
requirements reflects the Agency's conviction, as noted above, that 
informed employees are essential to the operation of any effective 
health program. OSHA believes that informing and training employees 
about the hazards to which they are exposed will contribute 
substantially to reducing the incidence of diseases caused by workplace 
conditions. Further, as noted earlier, it has been OSHA's experience 
that unacceptable indoor air quality is often the result of 
deficiencies in implementing effective HVAC system operation and 
maintenance programs. The Agency believes that specialized training of 
workers performing those activities is, therefore, necessary to ensure 
successful performance of their jobs.

Recordkeeping: Paragraph (h)

    Paragraph (h) proposes to require that employers maintain records 
of: All written information regarding the IAQ compliance program 
required to be established under paragraph (c); inspection and 
maintenance records required to be established under paragraph (d) [Ex. 
3-26], which must include the specific remedial or maintenance actions 
taken, the name and affiliation of the individual performing the work, 
and the date of the inspection or maintenance activity; and records of 
employee complaints of building-related illness required to be 
established under paragraph (c)(5) of this section [Ex. 3-502].
    Paragraph (h) also proposes to require the employer to retain these 
for at least the previous three years [Ex. 3-502], except that 
operation, maintenance, inspection, and compliance program records need 
not be retained for three years if rendered obsolete by the 
establishment and replacement of more recent records, or rendered 
irrelevant due to HVAC system replacement or redesign. The records 
required to be maintained by the employer are to be made available to 
employees and their designated representative and the Assistant 
Secretary for examination and copying.
    Finally, paragraph (h)(6) proposes to require that whenever the 
employer ceases to do business records that are required to be 
maintained by the employer are to be provided to and retained by the 
successor employer [Ex. 3-440B].
    Section 8 (c) of the Act authorizes OSHA to require employers to 
make, keep, and preserve, and make available to the Secretary or the 
Director records regarding their activities as prescribed by regulation 
as appropriate and necessary for the enforcement of the Act or for 
developing information regarding the causes and prevention of 
occupational illnesses. As noted earlier, the Agency believes that 
development of written compliance plans are essential to implementation 
of a successful IAQ program. The written compliance program, inspection 
and maintenance records, and operator and maintenance schedules which 
are required to be established under the proposal, are required to be 
retained under this paragraph. This information essentially documents 
the desired performance levels of HVAC systems, and the measures 
necessary to maintain those levels of performance, as well as other 
measures which should be followed to ensure acceptable indoor air 
quality. Such data must be available for use by designated persons, 
current employers, successor employers, and employees as a blueprint 
for program implementation. Without such data, air quality problems 
would likely arise due to ignorance of such elements as design occupant 
densities, equipment schedules, maintenance requirements and 
frequencies, etc. Records required to be established in response to 
employee complaints of building-related illness are also required to be 
retained under this paragraph. Such complaints require the employer to 
evaluate the need for, and to take if necessary, remedial action to 
correct observed problems [Ex. 3-1, 3-444B]. Information regarding 
employee illness is essential in identifying causal factors and trends 
in adverse health effects. Retention of this health data will aid in 
the recognition, evaluation and correction of indoor air quality 
deficiencies which lead to building-related illnesses. Records of 
building-related illness are proposed to be required to be retained for 
at least the previous 3 years. OSHA believes that requiring record 
retention for 3 years of building-related illnesses which occur in 
nonindustrial environments is reasonable. Such illnesses are not viewed 
in the same context as industrial illnesses which may be associated 
with long latency periods, and thus necessitate very long retention 
periods for health records. Establishment and maintenance of building-
related illness records is primarily for the purpose of documenting 
indoor air quality degradation, so that corrective action can be taken. 
Requiring records to be retained to preserve a 3 year history of 
building-related illness, is proposed as being reasonable to aid in the 
tracking of air quality trends and past experiences [Ex. 3-502].
    Other records are also required to be retained for at least the 
previous 3 years, except to the extent they become obsolete. OSHA does 
not believe that records such as maintenance and operating schedules 
which become irrelevant due to HVAC system modification or replacement 
need be retained further. The records required to be retained under 
this paragraph must be transferred to successor employers. Since these 
records contain information specific to the building or facility, as 
opposed to specific employers, such records should be maintained within 
affected buildings for future use.

Dates: Paragraph (i)

    Paragraph (i) proposes to establish an effective date for this 
standard of sixty (60) days from publication in the Federal Register. A 
start-up date one year from the effective date is proposed as an 
adequate period of time for employers to achieve full compliance with 
all provisions under the rule. The Agency believes that affected 
employers can develop and implement compliance programs, establish 
designated smoking areas if smoking is not prohibited, and train 
employees as proposed under the standard within a one year period from 
the effective date.

Appendices: Paragraph (j)

    The appendices included with this regulation are intended to be 
informational and, unless otherwise expressly stated in this section, 
are not intended to create any additional obligations not otherwise 
imposed, or to detract or reduce any existing obligations.

K. Specific Questions Posed

    OSHA solicits data, views and comment on all provisions proposed in 
this notice. The Agency sets forth questions below to highlight 
specific areas in the proposal upon which comment is sought.
Regulatory Analysis Issues
    (1) Are there any comments on the method used by OSHA to estimate 
benefits resulting from IAQ provisions of the proposed standard?
    (2) Are there studies which document, in quantitative terms, the 
effectiveness of HVAC maintenance on the decline of indoor air related 
ailments?
    (3) OSHA has estimated a substantial productivity benefit resulting 
from this proposed standard. What additional studies and other 
information are available that demonstrate any effect on productivity?
    (4) OSHA has preliminarily determined that the direct costs of 
compliance with this standard will not unduly harm small entities. 
However, OSHA did not determine how the smoking restrictions in this 
regulation would affect demand, and therefore profitability, for 
establishments which provide services and commodities which would be 
affected by the proposal (e.g., restaurants and bars). OSHA requests 
comments, including empirical data regarding the demand elasticity of 
such establishments' patrons who will not be permitted to smoke in the 
presence of employees.
    If economic feasibility is shown to be an issue for establishments 
such as bars and restaurants, what alternative feasible methods of 
compliance would prevent workers from being exposed to tobacco smoke?
    What other workplaces have circumstances under which provisions of 
this standard may not be feasible?
    (5) During renovation and remodelling, what are the specific 
elements for implementing control measures to minimize degradation of 
the IAQ of employees performing such activities and employees in other 
areas of the building? What are the unit costs associated with the 
implementation of each control (capital and labor)?
    (6) Please describe practices in your workplace by providing 
answers to the following:

--Describe the business, SIC code number and number of employees in the 
establishment.
--What type of ventilation systems are presently being used?
--If carbon dioxide monitoring is conducted, how often is it being done 
and by whom and what are the associated costs?
--Does your establishment have a policy on IAQ? When and why was it 
implemented? What are the major components? How many employees are 
affected? What type of costs and cost savings have been associated with 
such a policy (e.g., operating, maintenance, retrofitting HVAC systems, 
property damage due to poor IAQ, employee productivity, cleaning, 
etc.)?
--Is smoking allowed in your establishment? If yes, is it limited to 
designated smoking areas with separate ventilation?
Scope and Application, Paragraph (a)
    (1) Is it necessary and feasible to extend coverage of the entire 
standard to industrial facilities as well as nonindustrial facilities? 
Why? Why not? Which provisions lend themselves to application to 
industrial environments?
    (2) Can coverage of the standard feasibly be extended to some 
industrial facilities but not others? If so, what characteristics 
distinguish those workplaces in which it is feasible or necessary to 
apply the standard from those in which it is not?
    (3) The regulation as drafted would require employers generally to 
prohibit smoking by their customers (such as in bars, restaurants, and 
stores) where not already banned by a government entity if employees 
would be exposed to ETS from customer smoking. Comment is requested on 
the appropriateness of this provision, possible alternatives, and 
feasibility issues.
Definitions, Paragraph (b)
    (1) Is the proposed definition of ``air contaminants'' sufficiently 
descriptive to inform employers of the hazards which may adversely 
affect indoor air quality? If not, what additional information should 
be included in the definition? Which elements included in the 
definition are not reflective of hazards which affect indoor air 
quality?
    Can employers reasonably be expected to be able to detect the 
presence of air contaminants, as defined, and determine whether they 
present a significant risk of material impairment of employee health? 
What methods are available to detect indoor air contaminants? What 
criteria should be used to evaluate the degree of risk that the 
presence of air contaminants pose to employees?
    (2) Is the proposed definition of ``building systems'' sufficiently 
descriptive to indicate which systems the employer must attend to in 
order to assure acceptable indoor air quality? Are the systems listed 
in the definition those that directly affect indoor air quality? If 
not, why not? What other systems affect indoor air quality that are not 
specifically cited in the definition, and how do they influence indoor 
air quality? How must such systems be maintained and operated in order 
to assure adequate indoor air quality?
    (3) Is the term ``building-related illness'' sufficiently 
descriptive and inclusive of the medical conditions that can arise from 
poor indoor air quality? If not, what other medical conditions should 
be addressed under the definition and why? Which conditions listed in 
the definition, if any, should not be considered as ``building-related 
illness'' and why?
    (4) Is it necessary and appropriate to require employers to 
authorize a ``designated person'' to be responsible for ensuring 
compliance with an indoor air quality standard? Why? Why not? If it is 
appropriate to require a designated person, what training should 
designated persons have in order to carry out their responsibilities 
under the proposed rule? Should the designated person be a person who 
is a full-time employee who is within the facility each day? Should a 
designated person be on-site during each shift? Is it unreasonable to 
expect that due to the complexity of building systems, a single 
designated person within a facility can successfully oversee and ensure 
adequate operation of all building systems that affect indoor air 
quality? Why? Why not? Would it be beneficial for the designated person 
to receive an inventory of chemical and physical agents used by all 
employers on site in order to track chemical usage and storage? 
Information collected could include date of receipt, amount applied or 
used, where and when in the facility it was used, and how the remainder 
is stored.
    (5) Does the definition of the term ``HVAC system'' identify all 
components of HVAC systems which can adversely affect indoor air 
quality if not properly operated and maintained? What other components 
should be included and why? What components designated in the 
definition do not affect indoor air quality and why?
    (6) Is the definition of ``nonindustrial work environment'' 
sufficiently descriptive to differentiate them from industrial work 
environments? If not, what other descriptors should be included in the 
definition? Which types of facilities and establishments proposed under 
the definition as nonindustrial work environments should not be subject 
to this standard and why?
    (7) Is the definition of ``renovation and remodeling'' 
appropriately descriptive of such activities? If not, what 
modifications to the definition would more reasonably reflect industry 
view of the characteristics of such activities?
Indoor Air Quality Compliance Program, Paragraph (c)
    (1) Is it necessary and appropriate to require employers to 
establish a written IAQ compliance program in order to assure the 
adequacy of indoor air quality in nonindustrial work environments? Why? 
Why not?
    (2) If establishment of a written compliance program is necessary, 
are the informational elements proposed to be developed under this rule 
appropriate and why? What is their function for successful 
implementation of the program? Which other written material should be 
made part of the IAQ compliance program and why?
    (3) Which informational elements proposed to be established as part 
of the IAQ program, if any, are irrelevant to successful building 
system operation and maintenance? Why?
    (4) Which informational elements proposed to be established as part 
of the IAQ program, if any, are not generally available to the employer 
and why?
Compliance Program Implementation, Paragraph (d)
    (1) Which of the implementation actions proposed under this 
paragraph are necessary and appropriate for maintenance of acceptable 
indoor air quality. Why? Which are not? Why not? In this regard, 
specific comment is particularly sought on the need for the following 
proposed elements of the implementation program:
    (a) Maintenance and operation of the HVAC system to provide at 
least a required minimum outside air ventilation rate;
    (b) Operation of the HVAC during all work shifts;
    (c) Use of exhaust ventilation during maintenance and housekeeping 
activities;
    (d) Maintenance of relative humidity to below 60%;
    (e) Requiring HVAC system evaluation where CO2 levels exceed 
800 ppm; and
    (f) Requiring building system evaluation in response to employee 
complaints of building related illness.
    (g) Should the regulation prohibit the storage of hazardous 
substances in air transport pathways serving as return air plenums? 
These areas may include area-ways, plenums, chases, corridors, and 
mechanical rooms serving as return air plenums.
Controls for Specific Contaminant Sources, Paragraph (e)
    (1) Will the proposed provisions addressing construction and 
operation of designated smoking areas assure that employees working 
outside designated areas will not be exposed to ETS? If so, which of 
the proposed provisions may be unnecessary to achieve this goal? If 
not, is it necessary to prohibit smoking within indoor workplaces to 
eliminate exposure to ETS or can the provisions as proposed be 
modified, or supplemented to prevent secondary exposure? If it is 
believed that designated smoking areas will effectively contain tobacco 
smoke, comment is particularly sought on the appropriateness of 
requiring designated smoking areas to be enclosed, exhausted directly 
to the outside and maintained under negative pressure.
    (2) Is the proposed provision requiring the use of measures such as 
local source capture exhaust ventilation or substitution to control air 
contaminants emitted from point sources where general ventilation is 
inadequate, feasible or effective?
    (3) Are the proposed provisions addressing control of microbial 
contamination effective, feasible, or necessary? Why? Why not? What 
additional provisions, if any, should be included to preclude microbial 
contamination for adversely affecting indoor air quality?
    (4) Where hazardous chemicals are used in the workplace, including 
cleaning and maintenance chemicals, is employee notification of their 
use 24 hours prior to their application, as proposed, necessary to 
mitigate potential incidental exposure to such chemicals? To what 
extent does the use of such chemicals in nonindustrial environments 
present a health risk to other employees, or to the acceptability of 
indoor air quality? Which chemicals and their uses are of particular 
concern in non-industrial indoor environments?
    (5) Are the proposed provisions specifically addressing renovation 
and remodeling activities necessary and appropriate and why? 
Particularly, are the proposed requirements to develop a work plan 
focusing special attention on HVAC systems, area isolation or 
containment, and air contaminant suppression controls necessary to 
limit the potential for degradation of air quality? Why? Why not? What 
other provisions, if any, should be included to limit the effects that 
renovation and remodeling activities may have on indoor environments?
Employee Information and Training, Paragraph (g)
    (1) Are the provisions proposing that building systems maintenance 
workers receive special training with respect to the use of personal 
protective equipment, use of ventilation during cleaning and 
maintenance activities, and on proper use and disposal of hazardous 
chemicals and other agents, necessary and appropriate to assure 
maintenance of acceptable indoor air quality? Why? Why not?
    (2) Should training of building maintenance and systems workers 
include additional specific elements not proposed in this notice? What 
should this additional training consist of and why? Which workers 
should this training be provided to--all maintenance and building 
systems workers, supervisors, crew leaders? Should such training be 
provided periodically, or would initial training suffice?
    (3) Is it necessary, as proposed, to require that all employees in 
the facility be informed of the contents of the standard and of signs 
and symptoms associated with building-related illness? Why? Why not?
Recordkeeping, Paragraph (h)
    (1) Will retention of records, as proposed, enhance the potential 
for reducing indoor air quality problems? Will retention of maintenance 
records, IAQ compliance program records, and records of employee 
complaints serve as necessary documentation upon which actions and 
decisions can be made to improve deficiencies found in facility air 
quality? If so, how will these records serve that purpose?
    (2) What length of time should the records required to be 
established under this proposal be required to be retained? Is OSHA's 
proposed 3-year retention period reasonable? Why? Why not? Should 
different retention periods be specified for each particular record, 
and if so, why?
    (3) Is it reasonable to require transfer of records from an 
employee to a successor employer? What other mechanisms are available 
to ensure that the facility-specific records remain at the building or 
facility in the event of tenant turnover?
Dates, Paragraph (i)
    Is it feasible for employees to fully implement the provisions of 
this notice within one year of the effective date, as proposed? Why? 
Why not? If not, which provisions present difficulties, technologic or 
economic, with respect to implementation? For which provisions should 
implementation periods be either decreased or increased and why? To 
what extent should implementation periods be decreased or increased for 
particular provisions?

VIII. State Plan Standards

    The 25 states and territories with their own OSHA-approved 
occupational safety and health plans must adopt a comparable standard 
within six months of the publication date of a final standard. These 25 
states are: Alaska, Arizona, California, Connecticut (for public 
employees only), New York (for state and local government employees 
only), Hawaii, Indiana, Iowa, Kentucky, Maryland, Michigan, Minnesota, 
Nevada, New Mexico, North Carolina, Oregon, Puerto Rico, South 
Carolina, Tennessee, Utah, Vermont, Virginia, Virgin Islands, 
Washington, and Wyoming. Until such time as a state standard is 
promulgated, Federal OSHA will provide interim enforcement assistance, 
as appropriate, in these states.

IX. Federalism

    This Notice of Proposed Rulemaking has been reviewed in accordance 
with Executive Order 12612 (52 FR 41685, October 30, 1987), regarding 
Federalism. This Order requires that agencies, to the extent possible, 
refrain from limiting state policy options, consult with states prior 
to taking any actions which would restrict state policy options, and 
take such actions only when there is clear constitutional authority and 
the presence of a problem of national scope. The Order provides for 
preemption of state law only if there is a clear Congressional intent 
for the Agency to do so. Any such preemption is to be limited to the 
extent possible.
    Section 18 of the Occupational Safety and Health Act (OSH Act) 
expresses Congress' intent to preempt state laws that establish 
occupational safety and health standards on issues on which Federal 
OSHA has promulgated standards. Under Section 18, a state can avoid 
preemption, however, if it submits, and obtains Federal approval of a 
plan for the development of such standards and their enforcement. 
Therefore states with occupational safety and health plans approved 
under Section 18 of the OSH Act will be able to develop their own state 
standards to deal with any special problems which might be encountered 
in a particular state.
    In addition, the Supreme Court has held that Section 18 does not 
preempt state or local laws of general applicability that do not 
conflict with OSHA standards and that regulate the conduct of workers 
and non workers alike. Gade v. National Solid Wastes Management 
Association, 112 S. Ct. 2374 (1992). Such laws regulate workers simply 
as members of the general public. OSHA recognizes that many state and 
local governments have enacted provisions designed to protect the 
health of their residents by addressing indoor air quality issues 
including the presence of ETS. It is OSHA's intent that state and local 
laws consistent with this standard shall remain in effect to the full 
extent permissible.

X. Information Collection Requirements

    5 CFR part 1320 sets forth procedures for agencies to follow in 
obtaining OMB clearance for information collection requirements under 
the Paperwork Reduction Act of 1980, 44 U.S.C. 3501 et seq. This 
proposed indoor air quality standard requires the employer to allow 
OSHA access to records. In accordance with the provisions of the 
Paperwork Reduction Act and the regulations issued pursuant thereto, 
OSHA certifies that it has submitted the information collection 
requirements for this proposal to OMB for review under section 3504(h) 
of that Act.
    Public reporting burden for this collection of information is 
estimated to average five minutes per response. Send any comments 
regarding this burden estimate, or any other aspect of this collection 
of information, including suggestions for reducing this burden, to the 
Office of Information Management, Department of Labor, room N-1301, 200 
Constitution Avenue, NW., Washington, DC 20210; and to the Office of 
Information and Regulatory Affairs, Office of Management and Budget, 
Washington, DC 20503.

XI. Public Participation

    Interested persons are requested to submit written data, views and 
arguments concerning this proposal. Responses to the questions raised 
at various places in the proposal are particularly encouraged. These 
comments must be postmarked by June 29, 1993. Comments are to be 
submitted in quadruplicate or 1 original (hardcopy) and 1 disk (5\1/4\ 
or 3\1/2\) in WP 5.0, 5.1, 6.0 or Ascii. Note: Any information not 
contained on disk, e.g., studies, articles, etc., must be submitted in 
quadruplicate to: The Docket Office, Docket No. H-122, room N-2625, 
U.S. Department of Labor, 200 Constitution Avenue, NW., Washington, DC 
20210, Telephone No. (202) 219-7894.
    All written comments received within the specified comment period 
will be made a part of the record and will be available for public 
inspection and copying at the above Docket Office address.

Notice of Intention To Appear at the Informal Hearing

    Pursuant to section 6(b)(3) of the OSH Act, informal public 
hearings will be held on this proposal in Washington, DC from July 12 
through July 26, 1994. If OSHA receives sufficient requests to 
participate in the hearing, the hearing period may be extended.
    The hearing will commence at 9:30 a.m. in the auditorium of the 
Frances Perkins Building, U.S. Department of Labor, 3rd Street and 
Constitution Avenue NW., Washington, DC 20210.
    Persons desiring to participate at the informal public hearing must 
file a notice of intention to appear by June 20, 1994. The notice of 
intention to appear must contain the following information:
    1. The name, address, and telephone number of each person to 
appear;
    2. The capacity in which the person will appear;
    3. The approximate amount of time required for the presentation;
    4. The issues that will be addressed;
    5. A brief statement of the position that will be taken with 
respect to each issue; and
    6. Whether the party intends to submit documentary evidence and, if 
so, a brief summary of it.
    The notice of intention to appear shall be mailed to Mr. Thomas 
Hall, OSHA Division of Consumer Affairs, Docket No. H-122, U.S. 
Department of Labor, room N-3647, 200 Constitution Avenue, NW., 
Washington, DC 20210, telephone (202) 219-8615.
    A notice of intention to appear also may be transmitted by 
facsimile to (202) 219-5986, by the same date provided the original and 
3 copies are sent to the same address and postmarked no later than 3 
days later.

Filing of Testimony and Evidence Before the Hearing

    Any party requesting more than ten (10) minutes for presentation at 
the informal public hearing, or who intends to submit documentary 
evidence, must provide in quadruplicate the testimony and evidence to 
be presented at the informal public hearing. One copy shall not be 
stapled or bound and be suitable for copying. These materials must be 
provided to Mr. Thomas Hall, OSHA Division of Consumer Affairs at the 
address above and be postmarked no later than June 29, 1994.
    Each submission will be reviewed in light of the amount of time 
requested in the notice of intention to appear. In instances where the 
information contained in the submission does not justify the amount of 
time requested, a more appropriate amount of time will be allocated and 
the participant will be notified of that fact prior to the informal 
public hearing.
    Any party who has not substantially complied with the above 
requirement may be limited to a ten-minute presentation and may be 
requested to return for questioning at a later time.
    Any party who has not filed a notice of intention to appear may be 
allowed to testify for no more than 10 minutes as time permits, at the 
discretion of the Administrative Law Judge, but will not be allowed to 
question witnesses.
    Notice of intention to appear, testimony and evidence will be 
available for inspection and copying at the Docket Office at the 
address above.

Conduct and Nature of Hearing

    The hearing will commence at 9:30 a.m. on the first day. At that 
time, any procedural matters relating to the proceeding will be 
resolved.
    The nature of an informal rulemaking hearing is established in the 
legislative history of section 6 of the OSH Act and is reflected by 
OSHA's rules of procedure for hearings (29 CFR 1911.15(a)). Although 
the presiding officer is an Administrative Law Judge and questioning by 
interested persons is allowed on crucial issues, the proceeding is 
informal and legislative in type. The Agency's intent, in essence, is 
to provide interested persons with an opportunity to make effective 
oral presentations which can proceed expeditiously in the absence of 
procedural restraints which impede or protract the rulemaking process.
    Additionally, since the hearing is primarily for information 
gathering and clarification, it is an informal administrative 
proceeding rather than an adjudicative one. The technical rules of 
evidence, for example do not apply. The regulations that govern 
hearings and the pre-hearing guidelines to be issued for this hearing 
will ensure fairness and due process and also facilitate the 
development of a clear, accurate and complete record. Those rules and 
guidelines will be interpreted in a manner that furthers that 
development. Thus, questions of relevance, procedure and participation 
generally will be decided so as to favor development of the record.
    The hearing will be conducted in accordance with 29 CFR part 1911. 
It should be noted that Sec. 1911.4 specifies the Assistant Secretary 
may upon reasonable notice issue alternatives procedures to expedite 
proceedings or for other good cause. The hearing will be presided over 
by an Administrative Law Judge who makes no decision or recommendation 
on the merits of OSHA's proposal. The responsibility of the 
Administrative Law Judge is to ensure that the hearing proceeds at a 
reasonable pace and in an orderly manner. The Administrative Law Judge, 
therefore, will have all the powers necessary and appropriate to 
conduct a full and fair informal hearing as provided in 29 CFR part 
1911 including the powers:
    1. To regulate the course of the proceedings;
    2. To dispose of procedural requests, objections and comparable 
matters;
    3. To confine the presentations to the matters pertinent to the 
issues raised;
    4. To regulate the conduct of those present at the hearing by 
appropriate means;
    5. In the Judge's discretion, to question and permit the 
questioning of any witness and to limit the time for questioning; and
    6. In the Judge's discretion, to keep the record open for a 
reasonable, stated time (known as the post-hearing comment period) to 
receive written information and additional data, views and arguments 
from any person who has participated in the oral proceedings.
    OSHA recognizes that there may be interested persons or 
organizations who, through their knowledge of the subject matter or 
their experience in the field, would wish to endorse or support the 
whole proposal or certain provisions of the proposal. OSHA welcomes 
such supportive comments, including any pertinent data and cost 
information which may be available, in order that the record of this 
rulemaking will present a balanced picture of the public response on 
the issues involved.

XII. List of Subjects

 29 CFR Parts 1910, 1915 and 1926

    Hazardous substances, Indoor air quality, Occupational Safety and 
Health, Reporting and recordkeeping requirements.

29 CFR Part 1928

    Occupational Safety and Health.

XIII. Authority and Signature

    This document was prepared under the direction of Joseph A. Dear, 
Assistant Secretary of Labor for Occupational Safety and Health, U.S. 
Department of Labor, 200 Constitution Avenue NW., Washington, DC 20210. 
Pursuant to sections 6(b) and 8(c) and 8(g)(2) of the Act, OSHA hereby 
proposes to amend 29 CFR by adding a new Sec. 1910.1033, 1915.1033, 
1926.1133 and revising of Sec. 1910.19 and 1928.21 as set forth below.

    Signed at Washington, DC, this 28th day of March, 1994.
Joseph A. Dear,
Assistant Secretary for Occupational Safety and Health.

    Part 1910, 1915, 1926, and 1928 of title 29 of the Code of Federal 
Regulations (CFR) are hereby proposed to be amended as follows:

XIV. Standards

Part 1910, 1915, 1926 [AMENDED]--OCCUPATIONAL SAFETY AND HEALTH 
STANDARDS

    1. The authority citation for subpart B of part 1910 would continue 
to read as follows:

    Authority: Secs. 4, 6, and 8 of the Occupational Safety and 
Health Act, 29 U.S.C. 653, 655, 657; Walsh-Healey Act, 41 U.S.C. 35 
et seq.; Service Contract Act of 1965, 41 U.S.C. 351 et seq., sec. 
107, Contract Work Hours and Safety Standards Act (Construction 
Safety Act), 40 U.S.C. 333; sec. 41, Longshore and Harbor Workers' 
Compensation Act, 33 U.S.C. 942; National Foundation of Arts and 
Humanities Act, 20 U.S.C. 951 et seq.; Secretary of Labor's Order 
No. 12-71 (36 FR 8754), 8-76 (41 FR 1911), 9-83 (48 FR 35736), or 1-
90 (55 FR 9033), as applicable.

    2. The authority citation for subpart Z of Part 1910 would continue 
to read as follows:

    Authority: Secs. 6, 8 of the Occupational Safety and Health Act, 
29 U.S.C. 653, 655, 657; Secretary of Labor's Order No. 12-71 (36 FR 
8754), 8-76 (41 FR 1911), 9-83 (48 FR 35736), or 1-90 (55 FR 9033), 
as applicable; and 29 CFR part 1911.
    All of subpart Z issued under section 6(b) of the Occupational 
Safety and Health Act, except those substances which have exposure 
limits listed in Tables Z-1, Z-2, and Z-3 of 29 CFR 1910.1000. The 
latter were issued under Section 6(a) (29 U.S.C. 655(a)).
    Section 1910.1000, Tables Z-1, Z-2, and Z-3 also issued under 5 
U.S.C. 533. Section 1910.1000, Tables Z-1, Z-2, and Z-3 were not 
issued under 29 CFR part 1911 except for the arsenic (organic 
compounds), benzene and cotton dust listings.
    Section 1910.1001 also issued under Sec. 107 of Contract Work 
Hours and Safety Standards Act, 40 U.S.C. 333.
    Section 1910.1002 not issued under 29 U.S.C. 655 or 29 CFR part 
1911; also issued under 5 U.S.C. 553.
    Section 1910.1025 also issued under 5 U.S.C. 553.
    Section 1910.1043 also issued under 5 U.S.C. 551 et seq. 
    Sections 1910.1200, 1910.1499, and 1910.1500 also issued under 5 
U.S.C. 553.

    3. The authority citation for part 1915 would continue to read as 
follows:

    Authority: Sec. 41, Longshore and Harbor Workers Compensation 
Act (33 U.S.C. 941); secs. 4, 6, 8 Occupational Safety and Health 
Act of 1970 (29 U.S.C. 653, 655, 657); sec. 4 of the Administrative 
Procedure Act (5 U.S.C. 553); Secretary of Labor's Order No. 12-71 
(36 FR 8754), 8-76 (41 FR 25059), 9-83 (48 FR 35736) or 1-90 (55 FR 
9033), as applicable; 29 CFR part 1911.

    4. The authority citation for subpart Z of part 1926 would be 
revised to read as follows:

    Authority: Sec. 107, Contract Work Hours and Safety Standards 
Act (Construction Safety Act) (40 U.S.C. 333); Secs. 6, 8 of the 
Occupational Safety and Health Act, 29 U.S.C. 653, 655, 657; 
Secretary of Labor's Order No. 12-71 (36 FR 8754), 8-76 (41 FR 
1911), 9-83 (48 FR 35736), or 1-90 (55 FR 9033), as applicable; and 
29 CFR part 1911.
    Section 1926.1102 not issued under 29 U.S.C. 655 or 29 CFR part 
1911; also issued under 5 U.S.C. 653.
    Section 1926.1103 through 1926.1118 also issued under 29 U.S.C. 
653.
    Section 1926.1128 also issued under 29 U.S.C. 653.
    Section 1926.1145 and 1926.1147 also issued under 29 U.S.C. 653.
    Section 1926.1148 also issued under 29 U.S.C. 653.

    5. Section 1910.19 of subpart B of part 1910 is proposed to be 
amended by adding a paragraph (l) to read as follows:


Sec. 1910.19  Special provisions for air contaminants

* * * * *
    (l) Indoor air quality. Section 1910.1033 shall apply to the 
exposure of every employee in every employment covered by Sec. 1910.16.
    6. Subpart Z of parts 1910, 1915, 1926 of Title 29 of the Code of 
Federal Regulations is proposed to be amended by adding identical new 
sections as 1910.1033, 1915.1033 and 1926.1133 to read as follows:


Sec. ________.____    Indoor air quality.

    (a) Scope and application. (1) The provisions set forth in this 
section apply to all nonindustrial work environments.
    (2) The provisions set forth in paragraph (e)(1) of this section, 
which address employee exposure to tobacco smoke, apply to all indoor 
or enclosed workplaces under OSHA jurisdiction.
    (b) Definitions.
    Air contaminants refers to substances contained in the vapors from 
paint, cleaning chemicals, pesticides, and solvents, particulates, 
outdoor air pollutants and other airborne substances which together may 
cause material impairment to employees working within the nonindustrial 
environment.
    Assistant Secretary means the Assistant Secretary of Labor for 
Occupational Safety and Health, U.S. Department of Labor, or designee.
    Building-related illness describes specific medical conditions of 
known etiology which can be documented by physical signs and laboratory 
findings. Such illnesses include sensory irritation when caused by 
known agents, respiratory allergies, asthma, nosocomial infections, 
humidifier fever, hypersensitivity pneumonitis, Legionnaires' disease, 
and the signs and symptoms characteristic of exposure to chemical or 
biologic substances such as carbon monoxide, formaldehyde, pesticides, 
endotoxins, or mycotoxins.
    Building systems include but are not limited to the heating, 
ventilation and air-conditioning (HVAC) system, the potable water 
systems, the energy management system and all other systems in a 
facility which may impact indoor air quality.
    Designated person means a person who has been given the 
responsibility by the employer to take necessary measures to assure 
compliance with this section and who is knowledgeable in the 
requirements of this standard and the specific building systems 
servicing the affected building or office.
    Designated smoking area means a room, in a non-work area, in which 
smoking of tobacco products is permitted.
    Director means the Director, National Institute for Occupational 
Safety and Health (NIOSH) U.S. Department of Health and Human Services 
or designee.
    Employer means all persons defined as employers by Sec. 3(5) of the 
Occupational Safety and Health Act of 1970 including employers (such as 
building owners or lessees) who control the ventilation or maintenance 
of premises where employees of other employers work.
    HVAC system means the collective components of the heating, 
ventilation and air-conditioning system including, but not limited to, 
filters and frames, cooling coil condensate drip pans and drainage 
piping, outside air dampers and actuators, humidifiers, air 
distribution ductwork, automatic temperature controls, and cooling 
towers.
    Nonindustrial work environment means an indoor or enclosed work 
space such as, but not limited to, offices, educational facilities, 
commercial establishments, and healthcare facilities, and office areas, 
cafeterias, and break rooms located in manufacturing or production 
facilities used by employees. Non-industrial work environments do not 
include manufacturing and production facilities, residences, vehicles, 
and agricultural operations.
    Renovation and remodeling means building modification involving 
activities that include but are not limited to: removal or replacement 
of walls, ceilings, floors, carpet, and components such as moldings, 
cabinets, doors, and windows; painting, decorating, demolition, surface 
refinishing, and removal or cleaning of ventilation ducts.
    (c) Indoor air quality (IAQ) compliance program.
    (1) All employers with workplaces covered by paragraph (a)(1) of 
this section shall establish a written IAQ compliance program.
    (2) The employer shall identify a designated person who is given 
the responsibility to assure implementation of the IAQ compliance 
program.
    (3) Written plans for compliance programs shall include at least 
the following:
    (i) A written narrative description of the facility building 
systems;
    (ii) Single-line schematics or as-built construction documents 
which locate major building system equipment and the areas that they 
serve;
    (iii) Information for the daily operation and management of the 
building systems, which shall include at least a description of normal 
operating procedures, special procedures such as seasonal start-ups and 
shutdowns, and a list of operating performance criteria including, but 
not limited to minimum outside air ventilation rates, potable hot water 
storage and delivery temperatures, range of space relative humidities, 
and any space pressurization requirements;
    (iv) A general description of the building and its function 
including but not limited to, work activity, number of employees and 
visitors, hours of operation, weekend use, tenant requirements and 
known air contaminants released in the space;
    (v) A written maintenance program for the maintenance of building 
systems which shall be preventive in scope and reflect equipment 
manufacturer's recommendations and recommended-good-practice as 
determined by the building systems maintenance industry. At a minimum, 
the maintenance program shall describe the equipment to be maintained, 
and establish maintenance procedures and frequency of performance;
    (vi) A checklist for the visual inspection of building systems.
    (4) The following additional information, if available, shall be 
retained by the employer to assist in potential indoor air quality 
evaluations:
    (i) As-built construction documents;
    (ii) HVAC system commissioning reports;
    (iii) HVAC systems testing, adjusting and balancing reports;
    (iv) Operations and maintenance manuals;
    (v) Water treatment logs; and
    (vi) Operator training materials.
    (5) The employer shall establish a written record of employee 
complaints of signs or symptoms that may be related to building-related 
illness to include at least information on the nature of the illness 
reported, number of employees affected, date of employee complaint, and 
remedial action, if any, taken to correct the source of the problem.
    (d) Compliance program implementation. Employers shall assure 
compliance with this section by implementing at least the following 
actions:
    (1) Maintain and operate the HVAC system to assure that it operates 
up to original design specifications and continues to provide at least 
the minimum outside air ventilation rate, based on actual occupancy, 
required by the building code, mechanical code, or ventilation code 
applicable at the time the facility was constructed, renovated, or 
remodeled, whichever is most recent;
    (2) Conduct building systems inspections and maintenance in 
accordance with paragraph (c) of this section;
    (3) Assure that the HVAC system is operating during all work 
shifts, except during emergency HVAC repairs and during scheduled HVAC 
maintenance;
    (4) Implement the use of general or local exhaust ventilation where 
housekeeping and maintenance activities involve use of equipment or 
products that could reasonably be expected to result in hazardous 
chemical or particulate exposures to employees working in other areas 
of the building or facility;
    (5) Maintain relative humidity below 60% in buildings with 
mechanical cooling systems;
    (6) The employer shall monitor carbon dioxide levels when routine 
maintenance under paragraph (d)(1) of this section is done. When the 
carbon dioxide level exceeds 800 ppm, the employer shall check to make 
sure the HVAC system is operating as it should. If it is not, the 
employer shall take necessary steps to correct deficiencies if they 
exist.
    (7) Assure that buildings without mechanical ventilation are 
maintained so that windows, doors, vents, stacks and other portals 
designed or used for natural ventilation are in operable condition;
    (8) Assure that mechanical equipment rooms and any non-ducted air 
plenums or chases that transport air are maintained in a clean 
condition, hazardous substances are properly stored to prevent 
spillage, and asbestos, if friable, is encapsulated or removed so that 
it does not enter the air distribution system;
    (9) Assure that inspections and maintenance of building systems are 
performed by or under the supervision of the designated person;
    (10) Establish a written record of building system inspections and 
maintenance required to be performed under this section;
    (11) Assure that employees performing work on building systems are 
provided with and use appropriate personal protective equipment as 
prescribed in 29 CFR part 1926, subpart E, Personal Protective and Life 
Saving Equipment; 29 CFR part 1926.52, Occupational Noise Exposure; 29 
CFR part 1910, subpart I, Personal Protective Equipment; and 29 CFR 
part 1910.95, Occupational Noise Exposure;
    (12) Evaluate the need to perform alterations of the building 
systems to meet the minimum requirements specified in paragraph (d) of 
this section in response to employee complaints of building-related 
illnesses; and
    (13) Take such remedial measures as the evaluation shows to be 
necessary.
    (e) Controls for specific contaminant sources.
    (1) Tobacco smoke.
    (i) In workplaces where the smoking of tobacco products is not 
prohibited, the employer shall establish designated smoking areas and 
permit smoking only in such areas;
    (ii) The employer shall assure that designated smoking areas are 
enclosed and exhausted directly to the outside, and are maintained 
under negative pressure (with respect to surrounding spaces) sufficient 
to contain tobacco smoke within the designated area;
    (iii) The employer shall assure that cleaning and maintenance work 
in designated smoking areas is conducted only when no smoking is taking 
place;
    (iv) The employer shall assure that employees are not required to 
enter designated smoking areas in the performance of normal work 
activities;
    (v) The employer shall post signs clearly indicating areas that are 
designated smoking areas;
    (vi) The employer shall post signs that will clearly inform anyone 
entering the workplace that smoking is restricted to designated areas; 
and
    (vii) The employer shall prohibit smoking within designated smoking 
areas during any period that the exhaust ventilation system servicing 
that area is not properly operating.
    (2) Other indoor air contaminants.
    (i) The employer shall implement measures such as the relocation of 
air intakes and other pathways of building entry, where necessary, to 
restrict the entry of outdoor air contaminants such as vehicle exhaust 
fumes, into the building;
    (ii) When general ventilation is inadequate to control air 
contaminants emitted from point sources within workspaces the employer 
shall implement other control measures such as local source capture 
exhaust ventilation or substitution.
    (3) Microbial contamination.
    (i) The employer shall control microbial contamination in the 
building by routinely inspecting for, and promptly repairing, water 
leaks that can promote growth of biologic agents;
    (ii) The employer shall control microbial contamination in the 
building by promptly drying, replacing, removing, or cleaning damp or 
wet materials; and
    (iii) The employer shall take measures to remove visible microbial 
contamination in ductwork, humidifiers, other HVAC and building system 
components, or on building surfaces when found during regular or 
emergency maintenance activities or during visual inspection.
    (4) Use of cleaning and maintenance chemicals, pesticides, and 
other hazardous chemicals in the workplace.
    (i) The employer shall assure that these chemicals are used and 
applied according to manufacturers' recommendations; and
    (ii) The employer shall inform employees working in areas to be 
treated with potentially hazardous chemicals, at least within 24 hours 
prior to application, of the type of chemicals intended to be applied.
    (f) Air quality during renovation and remodeling.
    (1) General. During renovation or remodeling, the employer shall 
assure that work procedures and appropriate controls are utilized to 
minimize degradation of the indoor air quality of employees performing 
such activities and employees in other areas of the building.
    (2) Work plan development.
    (i) Before remodeling, renovation, or similar activities are begun 
the employer shall meet with the contractor or individual(s) performing 
the work and shall develop and implement a work plan designed to 
minimize entry of air contaminants to other areas of the building 
during and after performance of the work; and
    (ii) The work plan shall consider all of the following where 
appropriate:
    (A) Requirements of this standard.
    (B) Implementation of means to assure that HVAC systems continue to 
function effectively during remodeling and renovation activities.
    (C) Isolation or containment of work areas and appropriate negative 
pressure containment.
    (D) Air contaminant suppression controls or auxiliary air 
filtration/cleaning.
    (E) Controls to prevent air contaminant entry into the HVAC air 
distribution system.
    (3) Prior notification of employees who work in the building.
    (i) The employer shall notify employees at least 24 hours in 
advance, or promptly in emergency situations, of work to be performed 
on the building that may introduce air contaminants into their work 
area;
    (ii) Notification shall include anticipated adverse impacts on 
indoor air quality or workplace conditions.
    (g) Employee information and training.
    (1) The employer shall provide training for maintenance workers and 
workers involved in building system operation and maintenance which 
shall include at least the following:
    (i) Training in the use of personal protective equipment (PPE) 
needed in operating and maintaining building systems;
    (ii) Training on how to maintain adequate ventilation of air 
contaminants generated during building cleaning and maintenance; and
    (iii) Training of maintenance personnel on how to minimize adverse 
effects on indoor air quality during the use and disposal of chemicals 
and other agents.
    (2) All employees shall be informed of:
    (i) The contents of the standard in this section and its 
appendices; and
    (ii) Signs and symptoms associated with building-related illness 
and the requirement under paragraphs (d)(12) and (d)(13) of this 
section directing the employer to evaluate the effectiveness of the 
HVAC system and to take remedial measures to the HVAC system if 
necessary, upon receipt of complaints from employees of building-
related illness.
    (3) Availability of training material. The employer shall make 
training materials developed in response to paragraph (g), including 
the standard in this section and its appendices, available for 
inspection and copying by employees, designated employee 
representatives, the Director, and the Assistant Secretary.
    (h) Recordkeeping.
    (1) Maintenance records. The employer shall maintain inspection and 
maintenance records required to be established under paragraph (d) of 
this section, which shall include the specific remedial or maintenance 
actions taken, the name and affiliation of the individual performing 
the work, and the date of the inspection or maintenance activity.
    (2) Written IAQ compliance program. The employer shall maintain the 
written compliance program and plan required to be established under 
paragraph (c) of this section.
    (3) Employee complaints. The employer shall maintain a record of 
employee complaints of signs or symptoms that may be associated with 
building-related illness required to be established under paragraph 
(c)(5) of this section. These complaints shall be promptly transmitted 
to the designated person for resolution.
    (4) Retention of records. The employer shall retain records 
required to be maintained under this section for at least the previous 
three years, except that records required to be maintained under 
paragraphs (h)(1) and (h)(2) of this section need not be retained for 
three years if rendered obsolete by the establishment and replacement 
of more recent records, or rendered irrelevant due to HVAC system 
replacement or redesign.
    (5) Availability. The records required to be maintained by this 
paragraph shall be available on request to employees and their 
designated representative and the Assistant Secretary for examination 
and copying.
    (6) Transfer of records. Whenever the employer ceases to do 
business, records that are required to be maintained by paragraph (h) 
of this section shall be provided to and retained by the successor 
employer.
    (i) Dates. (1) Effective date. This section is effective [DATE 60 
DAYS FROM PUBLICATION OF THE FINAL RULE]
    (2) Start-up dates.
    Employers shall have implemented all provisions of this standard no 
later than one year from [THE EFFECTIVE DATE OF THE FINAL RULE].

Appendix A to Sec. ________. ________--CARBON DIOXIDE MEASUREMENT 
PROTOCOL (NONMANDATORY)

    Carbon dioxide (CO2) sampling is one of the measurement 
tools used to characterize indoor air quality. Indoor CO2 air 
concentrations are indicator measures for effectiveness of building 
ventilation. Elevated carbon dioxide levels can be an indicator of 
inadequate outside air exchange rates. Carbon dioxide concentrations 
below 800 ppm generally indicate that the ventilation is adequate 
for diluting occupant-generated contaminants. The carbon dioxide 
concentration and the associated outside air ventilation rate offers 
no confidence as to the adequacy of dilution and removal of other 
contaminants released in the space. There is also no implication of 
health effects associated with this level of carbon dioxide, or any 
implication of a permissible exposure limit. Health effects have 
been observed in buildings where the carbon dioxide levels were 
below 800 ppm.
    OSHA recommends this procedure:
    (1) Design a program of air sampling that includes samples 
taken: (a) at least every three months to detect the effects of 
seasonal changes (summer/winter transition seasons); (b) after 
adjustments have been made to the HVAC system; and (c) at any time 
there is reason to believe air quality has deteriorated. At least 
once a year carbon dioxide levels should be monitored when the HVAC 
system is providing minimum outside air ventilation.
    (2) Measure carbon dioxide concentrations late in the morning 
(about 11:00 am) and late in the afternoon before workers leave for 
home (about 3:30 pm). These are the times when carbon dioxide levels 
should be closest to equilibrium levels and should give the best 
indication of effective air exchange rates. These normal use 
patterns may be altered by visitor frequency and should be accounted 
for in the monitoring scheme.
    (3) Conduct the sampling at a height of between 3 and 5 feet 
above the floor, or about the height of employees' heads. Make sure 
the samples are taken at least 2 feet from where people are 
breathing. Take the samples at a sufficient distance from any other 
sources of carbon dioxide so these sources do not affect the 
measurements.
    (4) Select sampling locations in normally-occupied areas where 
the ventilation mixing would be the least effective. These areas 
might include corners of a room farthest from supply ducts and 
exhaust vents, locations surrounded by barriers that might affect 
air movement, or rooms at the far end of a ventilation supply duct.
    (5) Measure the carbon dioxide levels outside the building for 
comparison with the indoor levels. Average outdoor carbon dioxide 
levels are typically 300 to 500 ppm.
    (6) Use colormetric detector tubes or other direct-reading 
instruments calibrated and operated according to the manufacturer's 
instructions for measuring carbon dioxide concentrations.
    Take sampling and analytical error into account before comparing 
results with the 800 ppm benchmark. All measuring devices have a 
degree of uncertainty associated with the results. An estimate of 
that uncertainty is called the sampling and analytical error. The 
uncertainty can be reduced by taking more samples with the same 
device. Table A-1 can be used to assure 95 percent confidence that 
the average of the results from a set of detector tube samples is 
less than 800 ppm. OSHA recommends these following steps:
    (1) Calculate the average of the measurements.
    (a) Add the detector tube results together.
    (b) Divide that total by the number of samples.
    (2) Compare the average of the results with the number of 
samples taken in the second column in the table. If the average is 
less than the number in the table, there is confidence that the 
CO2 levels are less than 800 ppm. Example: Three samples are 
taken and the results are 650 ppm, 710 ppm, and 680 ppm. The average 
of these three samples is 680 ppm (2,040 ppm divided by 3). The 
results indicate confidence that the carbon dioxide levels are less 
than 800 ppm since the 680 ppm average of the three samples is less 
than 695 ppm

 Table A-1.--Number of Samples Taken To Assure 95 Percent Confidence CO2
                  Concentrations Are Less Than 800 ppm                  
------------------------------------------------------------------------
                                                                  The   
                  Number of samples taken                     average\1\
                                                                (ppm)   
------------------------------------------------------------------------
2...........................................................        670 
3...........................................................        695 
4...........................................................        710 
5...........................................................        720 
6...........................................................        725 
7...........................................................       730  
------------------------------------------------------------------------
\1\The average must be less than.                                       

    Table A-2 shows how to determine if the indoor sample results 
are significantly different from the results taken outdoors. Use 
this table by following these steps:
    (1) Take the same number of samples indoors and outdoors.
    (2) Average the results of the outdoor and indoor samples.
    (a) Add the outdoor results together and divide by the number of 
samples taken.
    (b) Add the indoor results together and divide by the number of 
samples taken.
    (3) Compare the range of the outdoor and indoor samples.
    (a) Subtract the lowest sample result of the outdoor samples 
from the highest result for the outdoor samples.
    (b) Subtract the lowest sample result of the indoor samples from 
the highest result for the indoor samples.
    (4) Calculate Delta, which is a term derived by subtracting the 
difference between the indoor average and the outdoor average and 
then multiplying that result times 2.
    (5) Calculate the Sum of the Ranges. Add the outdoor Range and 
the indoor Range together.
    (6) Calculate the Test Statistic. Divide Delta by the Sum of the 
Ranges.
    (7) Compare the Test Statistic with the second column in the 
table below. If the Test Statistic is more than the number found in 
the column, the difference is significant.
    Example:
    (1) Three samples are taken indoors and three samples are taken 
outdoors. The results of the outdoor samples are 500 ppm, 580 ppm 
and 480 ppm. The results of the indoor samples are 650 ppm, 710 ppm, 
and 680 ppm.
    (2) The average of the outdoor samples is 520 ppm (1,560 ppm 
divided by 3) and the average of the indoor samples is 680 ppm 
(2,040 ppm divided by 3).
    (3) The Range of the outdoor samples is 100 (580-480=100) and 
the Range of the indoor samples is 60 ppm (710-650).
    (4) ``Delta'' is 320; (680-520) x 2=320.
    (5) The ``Sum of the Ranges'' is 160; (100+60)=160.
    (6) The ``Test Statistic'' is 2 (320 divided by 160=2).
    (7) Since the ``Test Statistic,'' 2, is greater the 0.974 found 
in the table for 3 samples, the indoor air levels of carbon dioxide 
are significantly more than the outdoor air levels. 

     Table A-2.--Determination of the Test Statistic (If Inside CO2     
 Concentration Testing Results Are Significantly Different From Outside 
                Concentrations (95 Percent Confidence))                 
------------------------------------------------------------------------
                                                                Test    
                 Number of samples taken                    statistic\1\
------------------------------------------------------------------------
2.........................................................        2.322 
3.........................................................        0.974 
4.........................................................        0.644 
5.........................................................        0.493 
6.........................................................        0.405 
7.........................................................       0.347  
------------------------------------------------------------------------
\1\Test statistic must be more than.                                    

    If the indoor sample results show levels that are greater than 
800 ppm or that the indoor levels are significantly more than the 
outdoor levels, initiate actions to investigate the functioning of 
the HVAC system and determine if the employees are affected.

APPENDIX B to Sec. ________. ________--INFORMATION SOURCES--
NONMANDATORY

    The following is a partial list of available data sources which 
building owners/agents of employers may wish to consult to help 
identify, characterize, and reduce sources of indoor air pollutants 
in office work environments. These sources also provide useful 
information concerning the operation, maintenance, and evaluation of 
mechanical ventilation systems.
    Building Air Quality: A Guide for Building Owners and Facility 
Managers. U.S. EPA/NIOSH. Dec. 1991. EPA/400/1-91/033. DHHS (NIOSH) 
Publication No. 91-114. Available from Superintendent of Documents, 
P.O. Box 371954, Pittsburgh, PA 15250-7954.
    Introduction to Indoor Air Quality: (1) Self-Paced Learning 
Module and (2) A Reference Manual. U.S. EPA, Office of Air and 
Radiation. EPA/400/3-91/00. July 1991.
    Managing Indoor Air Quality. 1991. Shirley J. Hansen. The 
Fairmont Press, Inc., 700 Indian Trail, Lilburn, GA 30247.
    ASHRAE Standard 62-1989. Ventilation for Acceptable Indoor Air 
Quality. American Society of Heating, Refrigeration, and Air-
conditioning Engineers, Inc. 1791 Tullie Circle, NE, Atlanta, GA 
30329.
    Washington State Ventilation and Indoor Air Quality Code, 
Chapter 51-13 WAC. Washington State Building Code Council.
    Indoor Air Quality Workbook. 1990. D. Jeff Burton. IVE, Inc., 
178 North Alta Street, Salt Lake City, Utah 84103.

APPENDIX C to Sec. ________. ________-- SMOKING CESSATION PROGRAM 
INFORMATION--NONMANDATORY

    The following organizations provide smoking cessation 
information and program material:
    (1) The National Cancer Institute operates a toll-free Cancer 
Information Service (CIS) with trained personnel to help you. Call 
1-800-4-CANCER to reach the CIS office serving your area, or write: 
Office of Cancer Communications, National Cancer Institute, National 
Institutes of Health, Building 31, Room 10A24, Bethesda, Maryland 
20892.
    (2) American Cancer Society, 1599 Clifton Road NE, Atlanta, 
Georgia 30062, (404) 320-3333. The American Cancer Society (ACS) is 
a voluntary organization composed of 58 divisions and 3,100 local 
units. Through ``The Great American Smokeout'' in November, the 
annual Cancer Crusade in April, and numerous educational material, 
ACS helps people learn about the health hazards of smoking and 
become successful exsmokers.
    (3) American Heart Association, 7320 Greenville Avenue, Dallas 
Texas 75231, (214) 750-5300. The American Heart Association (AHA) is 
a voluntary organization with 130,000 members (physicians, 
scientists, and laypersons) in 55 states and regional materials 
about the effects of smoking on the heart. AHA also has developed a 
guidebook for incorporating a weight-control component into smoking 
cessation programs.
    (4) American Lung Association, 1740 Broadway, New York, New York 
10019, (212) 245-8000. A voluntary organization of 7,500 members 
(physicians, nurses and laypersons), the American Lung Association 
(ALA) conducts numerous public information programs about the health 
effects of smoking. ALA has 59 state and 85 local units. The 
organization actively supports legislation and information campaigns 
for nonsmokers' rights and provides help for smokers who want to 
quit, for example through ``Freedom From Smoking,'' a self-help 
cessation program.
    (5) Office on Smoking and Health, United States Department of 
Health and Human Services, 5600 Fisher Lane, Park Building, Room 
110, Rockville, Maryland 20857. The Office of Smoking and Health 
(OSH) is the Department of Health and Human Services' lead agency in 
smoking control. OSH has sponsored distribution of publications on 
smoking-related topics, such as free flyers on relapse after initial 
quitting, helping a friend or family member quit smoking, the health 
hazards of smoking, and the effects of parental smoking on 
teenagers.

PART 1928--OCCUPATIONAL SAFETY STANDARDS FOR AGRICULTURE--AMENDED

    7. The authority citation for Part 1928 is proposed to continue to 
read as follows:

    Authority: Secs. 4, 6, 8, Occupational Safety and Health Act of 
1970 (29 U.S.C. 653, 655, 657); Secretary of Labor's order Nos. 12-
71 (36 FR 8754), 8-76 (41 FR 25059), 9-83 (48 FR 35736), or 1-90 (55 
FR 9033), as applicable; 29 CFR part 1911.

    8. Section 1928.21 is proposed to be amended by adding a new 
paragraph (a)(6) as follows:


Sec. 1928.21  Applicable standards in 29 CFR Part 1910.

    (a) ***
    (6) Indoor air quality--Section 1910.1033.

[FR Doc. 94-7619 Filed 4-4-94; 8:45 am]
BILLING CODE 4510-26-P