[Federal Register Volume 67, Number 106 (Monday, June 3, 2002)]
[Proposed Rules]
[Pages 38222-38244]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 02-13796]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 141

[FRL-7221-8]
RIN 2040-AD61


Announcement of Preliminary Regulatory Determinations for 
Priority Contaminants on the Drinking Water Contaminant Candidate List

AGENCY: Environmental Protection Agency.

ACTION: Notice of preliminary regulatory determination.

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SUMMARY: The Safe Drinking Water Act (SDWA), as amended in 1996, 
directs the Environmental Protection Agency (EPA) to publish a list of 
contaminants (referred to as the Contaminant Candidate List, or CCL) to 
assist in priority-setting efforts. SDWA also directs the Agency to 
select five or more contaminants from the current CCL and determine by 
August 2001 whether or not to regulate these contaminants with a 
National Primary Drinking Water Regulation (NPDWR). Today's action 
presents the preliminary regulatory determinations for nine 
contaminants and describes the supporting rationale for each.

DATES: Comments must be received on or before August 2, 2002.

[[Page 38223]]


ADDRESSES: Please send your comments to the W-01-14 Comments Clerk. 
Submit electronic comments to: [email protected]. Written comments 
should be mailed to: Water Docket (MC-4101), U.S. Environmental 
Protection Agency, 1200 Pennsylvania Avenue, NW., Washington, DC, 
20460. Hand deliveries should be delivered to EPA's Water Docket at 
East Tower Basement (EB Room 57), Waterside Mall, 401 M Street, SW., 
Washington, DC, 20460. You may contact the docket at (202) 260-3027 
between 9 a.m. and 3:30 p.m. Eastern Time, Monday through Friday. 
Comments may be submitted electronically. See SUPPLEMENTARY INFORMATION 
for file formats and other information about electronic filing and 
docket review.

FOR FURTHER INFORMATION CONTACT: For information regarding today's 
action, contact Karen Wirth, Office of Ground Water and Drinking Water, 
EPA, 1200 Pennsylvania Avenue, NW. (MC 4607M), Washington, DC 20460; 
telephone 202-564-5246, e-mail: [email protected]. General 
information may also be obtained from the EPA Safe Drinking Water 
Hotline, phone: (800) 426-4791 or its local number (703) 412-3330, e-
mail: [email protected]. The Hotline is open Monday through Friday, 
excluding Federal holidays, from 9 a.m. to 5:30 p.m. Eastern Time.

SUPPLEMENTARY INFORMATION:

Submission of Comments

    EPA will accept written or electronic comments (please do not send 
both). EPA prefers electronic comments. Commenters should use a 
separate paragraph for each issue discussed. No facsimiles (faxes) will 
be accepted. Commenters who want EPA to acknowledge receipt of their 
comments should also send a self-addressed, stamped envelope. If you 
submit written comments, please submit an original and three copies of 
your comments and enclosures (including references).
    Electronic comments must be submitted in WordPerfect 8 (or an older 
version) or ASCII file format. Compressed or zipped files will not be 
accepted. You may file electronic comments on this action online at 
many Federal Depository Libraries.
    The Agency's response-to-comments document for the final decision 
will address the comments received on this action. The response-to-
comments document will be made available in the docket.

Obtaining Docket Materials

    The docket is available for inspection from 9 a.m. to 4 p.m. 
Eastern Time, Monday through Friday, excluding legal holidays, at the 
Water Docket, East Tower Basement (EB Room 57), Waterside Mall, USEPA, 
401 M Street, SW; Washington, D.C. For access to docket (Docket Number 
W-01-03) materials, please call (202) 260-3027 between 9 a.m. and 3:30 
p.m., Eastern Time, Monday through Friday, to schedule an appointment.

Abbreviations and Acronyms

<--Less than
--Greater than
[mu]--Microgram, one-millionth of a gram
[mu]g/L--Micrograms per liter
AIDS--Acquired immunodeficiency syndrome
ATSDR--Agency for Toxic Substances and Disease Registry
AWWA--American Water Works Association
AWWARF--American Water Works Association Research Foundation
BW--Body weight for an adult, assumed to be 70 kilogram (kg)
CASRN--Chemical Abstract Services Registry Number
CCL--Contaminant Candidate List
CDC--Centers for Disease Control and Prevention
CFR--Code of Federal Regulations
CMR--Chemical Monitoring Reform
DASH--Dietary Approaches to Stop Hypertension
DW--Drinking water consumption, assumed to be 2 L/day
EPA--U.S. Environmental Protection Agency
FR--Federal Register
g/day--Grams of contaminant per day g/L--Grams of the contaminant per 
liter
G6PD--Glucose-6-phosphate dehydrogenase
GAE--Granulomatous amoebic encephalitis
HIV--Human immunodeficiency virus
HRL--Health reference level
IOC--Inorganic compound
IRIS--Integrated Risk Information System
kg--Kilogram
L--Liter
LD50--Lethal Dose 50; the dose at which 50% of the test 
animals died; a calculated value (LD50)
LOAEL--Lowest-observed-adverse-effect level
MCLG--Maximum contaminant level goal
mg--Milligram, one-thousandth of a gram
mg/kg--Milligrams of contaminant per kilogram body weight
mg/L--Milligrams of the contaminant per liter
mg/m\3\--Milligrams per cubic meter
NAS--National Academy of Sciences
NDWAC--National Drinking Water Advisory Council
NIH--National Institute of Health
NIRS--National Inorganic and Radionuclide Survey
NOAEL--No-observed-adverse-effect level
NPDWR--National Primary Drinking Water Regulation
NRC--National Research Council
NTP--National Toxicology Program
OW--Office of Water
PWS--Public Water System
RfD--Reference dose
RSC--Relative source contribution
SDWA--Safe Drinking Water Act
SDWIS/FED--Safe Drinking Water Information System, Federal version
SOC--Synthetic organic compound
TRI--Toxic Release Inventory
UCM--Unregulated Contaminant Monitoring
UF--Uncertainty factor
URIS--Unregulated Contaminant Information System
U.S.--United States of America
USGS--United States Geological Survey
VOC--Volatile organic compound
WHO--World Health Organization

Table of Contents

I. Background and Summary of Today's Action
    A. What is the Purpose of Today's Action?
    B. What is EPA's Preliminary Determination, and What Happens 
Next?
    C. What is the CCL?
    D. Does Today's Action Apply to My Public Water System?
II. What Criteria and Approach Did EPA Use to Make the Preliminary 
Regulatory Determinations?
    A. Recommended Criteria and Approaches
    1. The National Research Council's recommended approach
    2. The National Drinking Water Advisory Council's recommended 
criteria and approach
    B. EPA's Criteria and Approach
III. What Analysis Did EPA Use to Support the Preliminary Regulatory 
Determinations?
    A. Evaluation of Adverse Health Effects
    B. Evaluation of National Occurrence and Exposure
    1. The Unregulated Contaminant Monitoring Program
    2. National Inorganic and Radionuclide Survey and Supplementary 
IOC Occurrence Data
    3. Supplemental Data
IV. Preliminary Regulatory Determinations
    A. Summary
    B. Contaminant Profiles
    1. Acanthamoeba
    2. Aldrin and Dieldrin
    3. Hexachlorobutadiene
    4. Manganese
    5. Metribuzin
    6. Naphthalene
    7. Sodium
    8. Sulfate
V. Specific Requests for Comment, Data or Information
VI. References

[[Page 38224]]

I. Background and Summary of Today's Action

A. What Is the Purpose of Today's Action?

    Section 1412(b)(1)(A) of the SDWA, as amended in 1996, directs EPA 
to make determinations by August 2001 of whether or not to regulate at 
least five contaminants from EPA's Contaminant Candidate List of 
unregulated contaminants. For those contaminants that EPA determines to 
regulate, EPA has 24 months to propose Maximum Contaminant Level Goals 
(MCLGs) and National Primary Drinking Water Regulations (NPDWRs) and 
has 18 months following proposal to publish final MCLGs and promulgate 
NPDWRs. Today's action presents EPA's preliminary regulatory 
determinations for nine CCL contaminants together with the 
determination process, rationale, and supporting technical information 
for each.
    The contaminants discussed in today's action include: Three 
inorganic compounds (IOCs) (manganese, sodium, and sulfate); three 
synthetic organic compounds (SOCs) (aldrin, dieldrin, and metribuzin); 
two volatile organic compounds (VOCs) (hexachlorobutadiene and 
naphthalene); and one microbial contaminant, Acanthamoeba.

B. What Is EPA's Preliminary Determination, and What Happens Next?

    EPA's preliminary determination is that no regulatory action is 
appropriate for the contaminants Acanthamoeba, aldrin, dieldrin, 
hexachlorobutadiene, manganese, metribuzin, naphthalene, sodium, and 
sulfate.
    EPA will make final determinations on these contaminants after a 
60-day comment period and a public meeting. The public meeting will be 
held in the spring of 2002 in the Washington, D.C. area, to provide an 
information exchange with stakeholders on issues related to today's 
action. Further information about this meeting will be given in a 
future Federal Register Notice and will be available from the Drinking 
Water Hotline at 1-800-426-4791.
    EPA is making preliminary regulatory determinations on CCL 
contaminants that have sufficient information to support a regulatory 
determination at this time. The Agency continues to conduct research 
and/or to collect occurrence information on the remaining CCL 
contaminants. EPA has been aggressively conducting research to fill 
identified data gaps and recognizes that stakeholders may have a 
particular interest about the planned timing for future regulatory 
determinations for other contaminants on the CCL. The Agency is not 
precluded from taking action when information becomes available and 
will not necessarily wait until the end of the next regulatory 
determination cycle before making other regulatory determinations.

C. What Is the CCL?

    SDWA, as amended in 1996, directs EPA to publish a list of 
contaminants to assist in priority setting for the Agency's drinking 
water program. This list is called the Contaminant Candidate List or 
CCL. Section 1412(b)(1)(B) states that the EPA Administrator shall 
publish a list of contaminants which `` * * * are not subject to any 
proposed or promulgated national primary drinking water regulation, 
which are known or anticipated to occur in public water systems, and 
which may require regulation under this title [SDWA].''
    The CCL was developed with considerable input from the scientific 
community and stakeholders. A draft CCL requesting public comment was 
published on October 6, 1997 (62 FR 52193). The first CCL was published 
on March 2, 1998 (63 FR 10273). The SDWA requires that a new CCL will 
be published every five years thereafter (e.g., February 2003). The 
1998 CCL contained 60 contaminants, including 50 chemicals or chemical 
groups and 10 microbiological contaminants or microbial groups. Many of 
these contaminants lacked some of the information necessary to support 
a regulatory determination and were identified as having data needs. 
CCL contaminants were divided into categories to represent next steps 
and data needs associated with each contaminant. The categories were: 
(1) Regulatory determination priorities (i.e., no data needs); (2) 
health effects research priorities; (3) treatment research priorities; 
(4) analytical methods research priorities; and (5) occurrence 
priorities. Twenty contaminants were classified as regulatory 
determination priorities on the 1998 CCL because EPA believed in 1998 
that there were sufficient data to evaluate both exposure and risk to 
public health, and to support a determination of whether or not to 
proceed to promulgation of a NPDWR.
    Since the March 1998 CCL, EPA found that there was insufficient 
information to support a regulatory determination for 12 of the 20 
priority contaminants (see Table 1). In addition, sodium was added to 
the list of eight remaining regulatory determination priorities 
primarily as a means of reassessing the current guidance level. Thus, 
EPA is now presenting preliminary regulatory determinations for nine 
priority contaminants that have sufficient information to support a 
regulatory determination at this time: Acanthamoeba, aldrin, dieldrin, 
hexachlorobutadiene, manganese, metribuzin, naphthalene, sodium, and 
sulfate.

    Table 1.--1998 Priority Contaminants Which Are Now Judged to Lack
      Information Sufficient To Support a Regulatory Determination
------------------------------------------------------------------------
     Chemical contaminant                    Research needs
------------------------------------------------------------------------
Boron........................  Treatment technology and finalization of
                                a health risk assessment (reference dose-
                                -RfD).
Bromobenzene.................  Non-cancer health effects data including
                                subchronic toxicity tests,
                                immunotoxicity, neurotoxicity, and
                                structure-activity analyses. Further
                                work to identify an appropriate
                                treatment technology.
1,1-dichloroethane...........  Health effects data--cancer,
                                reproductive, developmental, and
                                pharmacokinetic studies. Further work to
                                identify an appropriate treatment
                                technology.
1,3-dichloropropene..........  Occurrence information using revised
                                sample preservation method.
2,2-dichloropropane..........  Health effects data--mutagenicity and
                                carcinogenicity screening tests, and
                                structure-activity analysis. Further
                                work to identify an appropriate
                                treatment technology.
p-isopropyltoluene...........  Health effects data--subchronic, chronic,
                                cancer, neurodevelopmental,
                                reproductive, and developmental.
                                Evaluate related findings on cumene and
                                other alkylbenzenes.
Metolachlor, s-metolachlor,    Analysis of health effects of metolachlor
 and metolachlor degradation    degradation degradates and occurrence
 products: ethane sulfonic      information.
 acid, and oxanilic acid.

[[Page 38225]]

 
Organotins...................  Non-cancer health effects data--
                                developmental and reproductive toxicity,
                                neurotoxicity, and immunotoxicity.
                                Pharmacokinetic studies and structure-
                                activity analysis recommended. Further
                                work needed to identify appropriateness
                                of treatment technology and analytical
                                methods. Additional occurrence
                                information.
1,1,2,2-tetrachloroethane....  Non-cancer health effects data--
                                developmental and reproductive toxicity,
                                neurotoxicity, and immunotoxicity.
                                Carcinogenicity studies. Further work to
                                identify an appropriate treatment
                                technology.
Triazines & degradation        Analytical methods data and occurrence
 products.                      information. Finalize list of degradates
                                to evaluate.
1,2,4-trimethylbenzene.......  Health effects data--neurotoxicity
                                screening tests. Further work to
                                identify an appropriate treatment
                                technology.
Vanadium.....................  Health effects data on neurotoxicity and
                                toxicokinetics of inhalation and oral
                                routes. Further work to identify an
                                appropriate treatment technology.
------------------------------------------------------------------------

    The Agency continues to conduct research and/or to collect 
occurrence information for all other contaminants on the CCL. The 
overall research approach is closely aligned with the 1983 National 
Research Council (NRC) risk assessment/risk management paradigm, which 
involves a systematic evaluation of data on health effects, exposure, 
and risk management options (NRC 1983) and is detailed in the Draft CCL 
Research Plan (USEPA 2001a). The plan was drafted in close consultation 
with outside stakeholders including the American Water Works 
Association (AWWA), the AWWA Research Foundation (AWWARF), other 
governmental agencies, universities, as well as other public and 
private sector groups. EPA and the AWWARF jointly sponsored a 
conference, in late September of 1999, to review all aspects of the 
proposed CCL Research Plan and to make suggestions for future research 
activities. The three-day meeting was attended by representatives from 
the water utility industry, State and Federal health and regulatory 
agencies, professional associations, academia, and public interest 
groups. The recommendations and results from this meeting have been 
incorporated into the draft research plan (USEPA 2001a).
    EPA's Science Advisory Board reviewed the research plan in August 
of 2000 and again in June of 2001. The plan is targeted for completion 
in 2002. It will be available to the public at that time and will be 
posted on EPA's web site. Implementation of the research plan will 
require the coordinated efforts of both governmental and non-
governmental entities. EPA intends to make all aspects of CCL research 
planning, implementation, and communication a collaborative process.

D. Does Today's Action Apply to My Public Water System?

    Today's action itself does not impose any requirements on anyone. 
Instead, it notifies interested parties of EPA's preliminary 
determination not to regulate nine CCL contaminants.

II. What Criteria and Approach Did EPA Use To Make the Preliminary 
Regulatory Determinations?

    Section 1412(b)(1)(A) of SDWA directs that EPA shall publish a MCLG 
and promulgate a NPDWR for a contaminant if the Administrator 
determines that (i) the contaminant may have adverse effects on the 
health of persons; (ii) the contaminant is known to occur, or there is 
substantial likelihood that the contaminant will occur, in public water 
systems with a frequency, and at levels of public health concern; and 
(iii) in the sole judgment of the Administrator, regulation of such 
contaminant presents a meaningful opportunity for health risk reduction 
for persons served by public water systems.
    This section presents the decision-making framework for selecting 
contaminants from a CCL for future action. It also discusses criteria 
that EPA used for making the preliminary regulatory determinations 
announced in today's action.
    The process of making preliminary regulatory determinations 
benefitted from substantial expert input and reflects major 
recommendations and themes suggested by different groups including 
stakeholders, the NRC, and the National Drinking Water Advisory Council 
(NDWAC).

A. Recommended Criteria and Approaches

    The Agency held a stakeholders meeting on November 16-17, 1999. The 
purpose of the meeting was to provide an update and to seek comment 
from stakeholders on the following: The regulatory determination 
process, specific factors to consider when making regulatory 
determinations, the draft CCL research plan, and the process for 
developing future CCLs. Participants at the meeting included 
representatives of public water utilities, State drinking water 
programs, public health and environmental groups, local government, the 
private sector, EPA and other Federal agencies. EPA intends to hold an 
additional stakeholders meeting in the spring of 2002 to solicit input 
on the preliminary regulatory determinations that are outlined in 
today's action.
1. The National Research Council's Recommended Approach
    EPA asked the NRC for assistance in developing a scientifically 
sound approach for deciding whether or not to regulate contaminants on 
the current and future CCLs. In response to the request, the NRC's 
Committee on Drinking Water Contaminants published the report, Setting 
Priorities for Drinking Water Contaminants (NRC 1999). This report 
evaluated various existing schemes for setting priorities among 
environmental contaminants and recommended a framework to guide EPA in 
deciding which contaminants on the CCL to regulate.
    The recommended framework applies to both chemical and microbial 
contaminants and would proceed as follows: (1) Gather and analyze 
health effects, exposure, treatment, and analytical methods data for 
each contaminant; (2) conduct a preliminary risk assessment for each 
contaminant based on the available data; and (3) issue a decision 
document for each contaminant describing the outcome of the preliminary 
risk assessment. The NRC notes that in using this decision framework, 
EPA should keep in mind the importance of involving all interested 
parties, recognize that the

[[Page 38226]]

process requires considerable expert judgment to address uncertainties 
from gaps in information about exposure potential and/or health 
effects, evaluate the many different effects that contaminants can 
cause, and interpret available data in terms of statutory requirements.
2. The National Drinking Water Advisory Council's Recommended Criteria 
and Approach
    One of the formal means by which EPA works with its stakeholders is 
through the NDWAC. The Council comprises members from the general 
public, State and local agencies, and private groups concerned with 
safe drinking water. It advises the EPA Administrator on key aspects of 
the Agency's drinking water program. The NDWAC provided specific 
recommendations to EPA on a protocol to assist the Agency in its 
efforts to make regulatory determinations for current and future CCL 
contaminants. These recommendations were the result of a working group 
formed by the NDWAC charged with developing regulatory determination 
criteria and protocols. Separate but similar protocols were developed 
for chemical and microbial contaminants. These protocols are intended 
to provide a consistent approach to evaluating contaminants for 
regulatory determinations.
    The NDWAC protocol uses the three statutory requirements of SDWA 
section 1412(b)(1)(A)(i)-(iii) (specified in section II of today's 
action) as the foundation for guiding EPA in making regulatory 
determination decisions. For each statutory requirement, evaluation 
criteria were developed and are summarized later in this section for 
the chemical contaminants only.
    To address whether a contaminant may have adverse effects on the 
health of persons (a statutory requirement in section 
1412(b)(1)(A)(i)), the NDWAC recommended that EPA characterize the 
health risk and estimate a health reference level for evaluating the 
occurrence data for each contaminant.
    To evaluate the known or likely occurrence of a contaminant, 
(required by statute 1412(b)(1)(A)(ii)), the NDWAC recommended that EPA 
consider: (1) The actual and estimated national percent of public water 
systems (PWSs) reporting detections above half the health reference 
level; (2) the actual and estimated national percent of PWSs with 
detections above the health reference level; and (3) the geographic 
distribution of the contaminant.
    To address whether regulation of a contaminant presents a 
meaningful opportunity for health risk reduction (a statutory 
requirement in section 1412(b)(1)(A)(iii)), the NDWAC recommended that 
EPA consider estimating the national population exposed above half the 
health reference level and the national population exposed above the 
health reference level.

B. EPA's Criteria and Approach

    EPA developed its evaluation approach based on the recommendations 
from NRC and NDWAC. For the nine contaminants addressed in today's 
action, EPA evaluated the following: the adequacy of current analytical 
and treatment methods; the best available peer reviewed data on health 
effects; and approximately seven million analytical data points on 
contaminant occurrence. For those contaminants with adequate monitoring 
methods, as well as health effects and occurrence data, EPA employed an 
approach to assist in making preliminary regulatory determinations that 
follows the themes recommended by the NRC and NDWAC to satisfy the 
three SDWA requirements under section 1412(b)(1)(A)(i)-(iii). The 
process was independent of many of the more detailed and comprehensive 
risk management factors that will influence the ultimate regulatory 
decision making process. Thus, a decision to regulate is the beginning 
of the Agency regulatory development process, not the end.
    Specifically, as described in section III.A. of today's action, EPA 
characterized the human health effects that may result from exposure to 
a contaminant found in drinking water. Based on this characterization, 
the Agency estimated either a health reference level (HRL) or a 
benchmark value for each contaminant.
    As described in section III.B., for each contaminant EPA estimated 
the number of PWSs with detections greater than one-half the HRL 
(\1/2\ HRL) and greater than the HRL (HRL); the 
population served at these benchmark values; and the geographic 
distribution using a large number of State occurrence data 
(approximately seven million analytical points) that broadly reflect 
national coverage. If a benchmark value was used instead of a HRL, the 
same process was carried out with \1/2\ the benchmark value and the 
full benchmark value. Use and environmental release information, as 
well as ambient water quality data were used to augment the State data 
and to evaluate the likelihood of contaminant occurrence.
    The findings from these evaluations were used to determine if there 
was adequate information to evaluate the three SDWA statutory 
requirements and to make a preliminary determination of whether to 
regulate a contaminant.
    EPA prepared Regulatory Determination Support Documents that are 
available for review and comment in the EPA Water Docket. These 
documents present summary information and data on a contaminant's 
physical and chemical properties, uses and environmental release, 
environmental fate, health effects, occurrence, and exposure. The 
documents discuss in detail the rationale used to support the 
preliminary regulatory determination.
    As a parallel effort during the comment period, EPA intends to have 
the Science Advisory Board review the analysis, the approach used for 
making regulatory determinations, and the preliminary regulatory 
determinations.

III. What Analysis Did EPA Use To Support the Preliminary Regulatory 
Determinations?

    Sections III.A. and B. of today's action outline the evaluation 
steps EPA used to support the preliminary determinations.

A. Evaluation of Adverse Health Effects

    The purpose of this section is to discuss the health effects 
information evaluated, the approach used to derive a HRL for evaluating 
the occurrence data, and to briefly describe the support documents that 
provide detailed information on adverse health effects and their dose 
response.
    As discussed previously, section 1412(b)(1)(A)(i) directs EPA to 
determine whether each candidate contaminant has an adverse effect on 
public health. The potential for adverse health effects for each 
contaminant are presented in section IV.B. of today's action.
    For those contaminants considered to be human carcinogens or likely 
to be human carcinogens, EPA evaluated data on the mode of action of 
the chemical to determine the method of low dose extrapolation. When 
this analysis indicates that a low dose extrapolation is needed and 
when data on the mode of action are lacking, EPA uses a default low 
dose linear extrapolation to calculate risk specific doses. These are 
estimated oral exposures associated with risk levels that range from 
one cancer in ten thousand (10-4) to one cancer in a million 
(10-6). These risk specific doses are combined with drinking 
water consumption data to estimate drinking water concentrations 
corresponding to this risk range, which are then used as HRLs for these 
contaminants. Of the nine contaminants discussed in today's action, 
only aldrin,

[[Page 38227]]

dieldrin, and hexachlorobutadiene had data to consider them to be 
likely or possible human carcinogens. They are also the only 
contaminants for which linear low dose extrapolation was done. The 
Agency selected the 10-6 risk specific concentration as the 
HRL for these three contaminants.
    For those chemicals not considered to be carcinogenic to humans, 
EPA generally calculates a reference dose (RfD). An RfD is an estimate 
of a daily oral exposure to the human population (including sensitive 
subgroups) that is likely to be without an appreciable risk of 
deleterious effects during a lifetime. It can be derived from a ``no-
observed-adverse-effect level (NOAEL),'' ``lowest-observed-adverse-
effect level (LOAEL),'' or benchmark dose, with uncertainty factors 
generally applied to reflect limitations of the data used.
    The Agency uses an uncertainty factor (UF) to address uncertainty 
resulting from incompleteness of the toxicological database. Generally, 
the UFs are factors ranging from 3 to 10-fold that are multiplied 
together and used in deriving the RfD from experimental data. UFs are 
intended to account for: (1) The variation in sensitivity among the 
members of the human population (i.e., intraspecies variability); (2) 
the uncertainty in extrapolating animal data to humans (i.e., 
interspecies variability); (3) the uncertainty in extrapolating from 
data obtained in a study with less-than-lifetime exposure to lifetime 
exposure (i.e., extrapolating from subchronic to chronic exposure); (4) 
the uncertainty in extrapolating from a LOAEL rather than from a NOAEL; 
and (5) the uncertainty associated with extrapolation from animal data 
when the data base is incomplete.
    For manganese, metribuzin and naphthalene EPA derived the HRLs 
using the RfD approach as follows:
HRL = (RfD x BW)/DW x RSC.

Where:

RfD = Reference Dose
BW = Body weight for an adult, assumed to be 70 kilograms (kg)
DW = Drinking water consumption, assumed to be 2 L/day (90th 
percentile)
RSC = The relative source contribution, or the level of exposure 
believed to result from drinking water when compared to other sources 
(e.g., air). The RSC is assumed to be 20% unless noted otherwise.

    The HRL for sulfate was not established using the RfD approach. The 
available data do not provide the necessary dose-response information 
to support the derivation of an RfD for sulfate. However, 500 
milligram/liter (mg/L) is a concentration at which adverse effects did 
not occur in any of the reported studies. This value was used as the 
HRL. Further details on the sulfate HRL are included in section IV.B.8.
    In the case of sodium, the benchmark value used to evaluate the 
occurrence data is not designated as an HRL because of the lack of 
suitable dose-response data and the considerable controversy regarding 
the role of sodium in the etiology of hypertension. The benchmark value 
for sodium of 120 mg/L was derived from the recommended daily dietary 
intake of 2.4 grams/day (g/day). Additional information regarding the 
sodium benchmark value is included in section IV.B.7.
    Monitoring data are not available from PWSs for Acanthamoeba. 
Accordingly, an HRL was not established.
    EPA has prepared Health Effects Support Documents for each 
contaminant that are available for review and comment at the EPA Water 
Docket. These documents address the following: exposure from drinking 
water and other media; toxicokinetics; hazard identification; dose-
response assessment; and an overall characterization of risk from 
drinking water. The Acanthamoeba health effects support document 
addresses the details of the following: occurrence in water and soil, 
exposure, populations at risk, association with contact lenses and poor 
hygiene, symptoms of keratitis eye infections, incidence, diagnosis and 
treatment of granulomas amoebic encephalitis (GAE), risk factors and 
prevention.
    EPA used the best available peer reviewed data and analyses in 
evaluating adverse health effects. Health effects information is 
available for aldrin, dieldrin, hexachlorobutadiene, manganese, 
metribuzin, and naphthalene in the Integrated Risk Information System 
(IRIS) database. IRIS is an electronic EPA data base (www.epa.gov/iris/index.htm) containing peer reviewed information on human health effects 
that may result from exposure to various chemicals in the environment. 
These chemical files contain descriptive and quantitative information 
on hazard identification and dose response, RfDs for chronic 
noncarcinogenic health effects; as well as slope factors and unit risks 
for carcinogenic effects. In all cases, the IRIS information was 
supplemented with more recent data from peer reviewed publications. In 
cases where the new data impacted the IRIS evaluation, the Office of 
Water (OW) Health Effects Support Documents are being independently 
peer reviewed.

B. Evaluation of National Occurrence and Exposure

    As noted previously in today's action, section 1412(b)(1)(A)(ii) 
directs EPA to determine whether each candidate for regulation is known 
to occur, or is substantially likely to occur, in PWSs with a 
frequency, and at levels, of public health concern. A substantial 
amount of State finished drinking water occurrence data for unregulated 
contaminants are provided under the Agency's Unregulated Contaminant 
Monitoring (UCM) program. These data form part of the Agency's basis 
for its estimates of national occurrence. The UCM program was initiated 
in 1987 to fulfill a SDWA requirement of the 1986 amendments that PWSs 
monitor for specified ``unregulated'' contaminants to gather scientific 
information on their occurrence for future regulatory decision making 
purposes. An additional EPA study conducted in the mid-1980s, the 
National Inorganic and Radionuclide Survey (NIRS), provides a 
statistically representative sample of the national occurrence of many 
regulated and unregulated inorganic contaminants in ground water CWSs.
    EPA prepared a report entitled Analysis of National Occurrence of 
the 1998 Contaminant Candidate List (CCL) Regulatory Determination 
Priority Contaminants in Public Water Systems (USEPA 2001b) that 
provides detailed reviews of the State monitoring data for each CCL 
regulatory determination priority contaminant. This report includes 
detailed information regarding how the data were assessed for quality, 
completeness, and representativeness, how the data were aggregated into 
national cross-sections, and presents summary occurrence findings. In 
EPA's contaminant-specific Regulatory Determination Support Documents 
described earlier (see section II.B. of today's action), additional 
information is included that presents an analysis of the occurrence 
data for special trends as well as populations served by PWSs with 
detections. EPA also reviewed information on the use, environmental 
release, and ambient occurrence of each contaminant to augment the 
State drinking water data (UCM and supplemental State monitoring data) 
and aid in the evaluation of occurrence. Summary descriptions of these 
data and analyses for each regulatory determination priority 
contaminant are presented in section IV. of today's action.
    Section III.B. describes how the drinking water data sets were used 
to evaluate the occurrence of the regulatory determination priority

[[Page 38228]]

contaminants, including data sources, data quality, and analytical 
methods. Also included are summary descriptions of the ambient 
occurrence data, as well as the use and environmental release 
information that were considered.
    The primary drinking water occurrence data for the regulatory 
determination priority contaminants are from the UCM program and the 
NIRS (see Table 2). The sources of these data, their quality, national 
aggregation, and the approach used to estimate a given contaminant's 
occurrence are discussed in the following sections.

      Table 2.--Primary Drinking Water Occurrence Data Sources Used in the Regulatory Determination Process
----------------------------------------------------------------------------------------------------------------
                                                               UCM round 1       UCM round 2
                        Contaminant                           cross section     cross section         NIRS
----------------------------------------------------------------------------------------------------------------
Aldrin....................................................  ................                X   ................
Dieldrin..................................................  ................                X   ................
Hexachlorobutadiene.......................................                X                 X   ................
Manganese.................................................  ................  ................                X
Metribuzin................................................  ................                X   ................
Naphthalene...............................................                X                 X   ................
Sodium....................................................  ................  ................                X
Sulfate...................................................  ................                X   ................
----------------------------------------------------------------------------------------------------------------

1. The Unregulated Contaminant Monitoring Program
    Occurrence data for most of the regulatory determination priority 
contaminants (aldrin, dieldrin, hexachlorobutadiene, metribuzin, 
naphthalene, and sulfate) are from the monitoring results of the UCM 
program. This program was implemented in two phases, or ``rounds.'' The 
first round of UCM monitoring began in 1987, and the second in 1993. 
EPA reviewed and edited the data for the purposes of this analysis.
    a. UCM Rounds 1 and 2. The 1987 UCM (52 FR 25720, July 8, 1987) 
contaminants include 34 VOCs including the regulatory determination 
priority contaminants hexachlorobutadiene and naphthalene. The UCM 
(1987) contaminants were first monitored during the period 1988-1992. 
This period is referred to as ``Round 1'' monitoring. The Round 1 data 
were put into a database called the Unregulated Contaminant Information 
System (URIS).
    The 1993 UCM contaminants included 34 VOCs (including naphthalene 
and hexachlorobutadiene), 13 SOCs, and sulfate (52 FR 25720, July 8, 
1987). Aldrin, dieldrin, and metribuzin were among the 13 SOCs 
monitored. Monitoring for the UCM (1993) contaminants began in 1993 and 
continued through 1999. This is referred to as ``Round 2'' monitoring. 
The UCM (1987) contaminants (the 34 VOCs monitored in Round 1) were 
also included in the Round 2 monitoring. As with other monitoring data, 
PWSs reported these results to the States. During the past several 
years, States have submitted Round 2 data to EPA's Safe Drinking Water 
Information System (Federal version; SDWIS/FED) database.
    The details of the actual individual monitoring periods are 
complex. The timing and procedures for required monitoring are outlined 
in the report entitled Analysis of National Occurrence of the 1998 
Contaminant Candidate List (CCL) Regulatory Determination Priority 
Contaminants in Public Water Systems (USEPA 2001b). Round 1 and Round 2 
data were analyzed separately because they represent different time 
periods, include different States (only eight States are represented in 
the data from both rounds), and only two CCL priority contaminants are 
common to both rounds.
    b. Development of occurrence data cross-sections. The Round 1 
database contains contaminant occurrence data from 38 States, 
Washington, D.C. and the United States (U.S.) Virgin Islands. The Round 
2 database contains data from 34 States and Tribes. Therefore, neither 
database contains data from all States. Also, data from some of the 
States in the databases are incomplete. As a result, unadjusted 
national results could be skewed to low-occurrence or high-occurrence 
settings (e.g., some States only reported detections). To address this 
lack of representativeness, national cross-sections from the Round 1 
and Round 2 State data were established using a similar approach 
developed for the EPA report entitled A Review of Contaminant 
Occurrence in Public Water Systems (USEPA 1999a). The cross-section 
approach in this report was developed to support occurrence analyses 
for EPA's Chemical Monitoring Reform (CMR) evaluation, and was 
supported by scientific peer reviewers and stakeholders.
    For SOCs and VOCs on the CCL, two national cross-sections were 
developed from the UCM data. The Round 1 national cross-section 
consists of data from 24 States with approximately 3.3 million 
analytical data points from approximately 22,000 unique PWSs. The Round 
2 national cross-section consists of data from 20 States with 
approximately 3.7 million analytical data points from slightly more 
than 27,000 unique PWSs. The actual number of systems and records 
varies for each contaminant according to the number of reported records 
for a particular contaminant. The support document, Analysis of 
National Occurrence of the 1998 Contaminant Candidate List (CCL) 
Regulatory Determination Priority Contaminants in Public Water Systems 
(USEPA 2001b), provides a summary description of how the national 
cross-sections for the Round 1 and Round 2 data sets were developed.
    All samples in the Round 1 and Round 2 State data sets were taken 
from finished drinking water, representing the product delivered to the 
public. Data were limited to samples with confirmed water source and 
sampling type information. Only routine monitoring samples were used; 
``special'' samples, ``investigation'' samples (investigating a 
contaminant problem, that would likely bias the results), and samples 
of unknown type were excluded from the data set. Various quality 
control and review checks were made of the results, including follow-up 
questions to the States providing the data to clarify potential 
reporting inconsistencies, records with invalid codes, or use of 
analytical units. The State data sets were then compiled into single 
database in a unified format.
    While the national cross-sections of States provides a good picture 
of

[[Page 38229]]

national occurrence, there are limitations in the data in that the 
original monitoring data were not collected by a statistical random 
sample. Since the data sets do not include the entire U.S., they cannot 
capture all local variations in contaminant occurrence. However, EPA 
believes the cross-sections do provide a reasonable estimate of the 
overall distribution, including the central tendency, of contaminant 
occurrence across the U.S.
    c. Occurrence analysis. The summary descriptive statistics 
presented in section IV of today's action for each contaminant 
generally include the following: The number of samples, the total 
number of systems, the percent of samples with at least one observed 
detection that has a concentration above the HRL (the HRL is an 
estimated health effect level used for the purposes of this analysis), 
and the 99th percentile concentration and median concentration of the 
observed detections. As described in section III. A, in the case of 
sodium, the benchmark was used to evaluate the occurrence data rather 
than a designated HRL. The 99th percentile concentration is commonly 
used to characterize upper bound data to avoid maximum values that are 
often problematic outlier observations. Because most of the regulatory 
determination priority contaminants have very low occurrence (<1% of 
samples with detections), these statistics are presented for the 
detections only. One exception is sulfate, for which the median and 
99th percentile concentrations are presented for all samples (i.e., the 
entire universe of samples) because of its relatively high occurrence. 
The percentages of PWSs, and population served, having at least one 
detected concentration above \1/2\HRL and HRL are 
also presented. As noted, the occurrence values and summary statistics 
presented are the actual data from the aggregated State cross-sections. 
EPA considered this the most straightforward and accurate way to 
present the data that were available for the determination process. EPA 
extrapolated values for national occurrence (based on the actual cross-
section data). However, because the State data used for the cross-
section are not a statistical sample, national extrapolations can be 
problematic, especially for contaminants with such low occurrence as 
was the case for many of these CCL contaminants. National 
extrapolations based on peak concentrations, such as the percent of 
systems with at least one observed concentration above the HRL, may 
also be misleading, since peak concentrations are highly variable from 
one location to another. For these reasons, the nationally extrapolated 
estimates of occurrence and exposure are not presented in today's 
action and are not used as the basis for the preliminary regulatory 
determinations. However, to provide additional perspective, the 
nationally extrapolated occurrence and exposure values are presented in 
the support documents and are available for review and comment.
    At this phase of consideration, more involved statistical modeling 
of the data was not performed. The presentation of the actual results 
of the cross-section analysis provides a straight-forward presentation 
and demonstrates the integrity of the data available for stakeholder 
review. As noted, however, the cross-section analysis should provide a 
reasonable estimate of the central tendency of occurrence for these 
contaminants because of the large number of States included with 
complete monitoring data sets for the intended purposes (Round 1 
consists of approximately 3.3 million analytical data points from 
22,000 PWSs in 24 States; and Round 2 consists of approximately 3.7 
million analytical data points from 27,000 PWSs in 20 States) that are 
representative of the range of pollution potential indicators and 
spatial/hydrogeologic diversity in the nation. EPA believes that the 
current approach is appropriate and protective but is seeking comments 
on the necessity of applying a further, more rigorous statistical 
modeling effort that could be conducted on the cross-section data. This 
additional effort could use probabilistic modeling to estimate the 
distribution of mean contaminant concentrations in PWSs in the U.S. 
Because this approach is based on estimating mean concentrations, 
instead of peaks as in the current approach, the results would be more 
statistically robust and more suitable to national extrapolation. This 
approach allows for better quantification of estimation error. It would 
also allow an assessment of systems with mean, rather than peak 
concentrations which exceed the HRL and \1/2\ the HRL, which may be 
more appropriate for chronic health effects. However, EPA does not 
believe that such an undertaking would fundamentally change the 
conclusions drawn from the data for these nine contaminants or the 
resulting preliminary regulatory determinations. The approach is 
currently being peer reviewed for use by the Agency to review and 
revise, if necessary, existing NPDWRs (i.e., the ``six-year review''). 
The model is described in the report entitled, Occurrence in Estimation 
Methodology and Occurrence Findings Report for Six-Year Regulatory 
Review (USEPA 2001c).
    d. Comparison to the Six-Year Review. EPA is using a similar 
methodology for occurrence analysis for the six-year review of existing 
NPDWRs. For this effort, EPA compiled a separate and different 
contaminant occurrence database and constructed a cross-section that 
consists of 13 million compliance monitoring results from approximately 
41,000 PWSs in 16 States. Also, as for the CCL, contaminant occurrence 
is reported in terms of the number of PWSs having at least one sample 
concentration above the levels of regulatory interest. For the six-year 
review effort, however, the Agency has also performed the more detailed 
statistical modeling as previously described, in order to estimate, for 
a certain number of the regulated contaminants, the number of PWSs with 
mean concentrations over time that exceed the levels of interest. This 
effort is driven by the underlying nature of the data and the type of 
data analysis it can support (i.e., the data base has a significant 
number of detections) as contrasted with the CCL data set.
2. National Inorganic and Radionuclide Survey and Supplementary IOC 
Occurrence Data
    The NIRS database includes 36 IOCs (including 10 now-regulated 
IOCs), two regulated radionuclides, and four unregulated radionuclides. 
Manganese and sodium were two of the IOCs monitored. The NIRS provides 
contaminant occurrence data from 989 community water systems served by 
ground water. The NIRS does not include surface water systems. The 
selection of CWSs included in NIRS was designed so that the contaminant 
occurrence results are statistically representative of national 
occurrence at CWSs using ground water sources (the survey was focused 
on ground water systems, in part, because ground water has a higher 
occurrence and concentrations of naturally occurring IOCs). Most of the 
NIRS data are from smaller systems (based on population served) and 
each of the 989 statistically randomly selected CWSs was sampled at a 
single time between 1984 and 1986.
    The NIRS data were collected from ground water CWSs in 49 States. 
Data were not available for the State of Hawaii. NIRS data were 
designed to be stratified based on system size (population served by 
the system), and uniform analytical detection limits were employed.
    The summary descriptive statistics presented in section IV of 
today's action

[[Page 38230]]

for manganese and sodium are derived from NIRS data analyses and 
generally include the total number of systems and samples, the percent 
systems with detections, the 99th percentile concentration of all 
samples, the 99th percentile concentration of samples with detections, 
and the median concentration of samples with detections. The 
percentages of PWSs, and population served, with detections 
\1/2\ HRL and HRL are also presented. Because the 
NIRS data were collected in a statistically designed sample survey, 
these summary statistics are representative of national occurrence in 
ground water PWSs. The actual values for the NIRS analyses are also 
reported, similar to the treatment for the cross-section data.
    One limitation of the NIRS study is a lack of occurrence data for 
surface water systems. To provide perspective on the occurrence of the 
CCL determination priority contaminants in surface water systems 
relative to ground water systems, additional State monitoring data were 
reviewed. These State ground water and surface water PWS occurrence 
data were available to EPA from an independent review of the occurrence 
of regulated contaminants in PWSs and published in the report A Review 
of Contaminant Occurrence in Public Water Systems (USEPA 1999a). The 
review contains data from Alabama, California, Illinois, New Jersey, 
and Oregon for manganese (approximately 38,700 samples from 5,500 
systems total) and sodium (approximately 36,000 samples from 6,500 PWSs 
total). The data were subject to the same quality review and editing 
process as the Round 1 and Round 2 data described previously. The data 
analysis, and presentation of results, were similar as well. However, 
because State surface water and ground water data were available from 
only a few States for manganese and sodium, the State data were 
analyzed individually. National cross-sections could not be developed 
for them.
3. Supplemental Data
    EPA collected supplemental data for each contaminant, including use 
and environmental release information (e.g., EPA's Toxic Release 
Inventory, academic and private sector publications) and ambient water 
quality data (i.e., source water existing in surface waters and 
aquifers before extraction and treatment as drinking water), to augment 
the drinking water data and better characterize the contaminant's 
presence in the environment. Data from the U.S. Geological Survey's 
National Water Quality Assessment program, the most comprehensive and 
nationally consistent data describing ambient water quality in the U.S. 
were included when available. A detailed discussion of the supplemental 
data collected for each contaminant can be found in the respective 
Regulatory Determination Support Document.

IV. Preliminary Regulatory Determinations

A. Summary

    The Agency is soliciting public comment on whether a preliminary 
determination that nine contaminants do not meet all three SDWA 
requirements is appropriate and thus no NPDWRs should be considered for 
those nine contaminants, identified by chemical abstract service 
registry number (CASRN) in Table 3.

             Table 3.--Preliminary Regulatory Determinations
------------------------------------------------------------------------
                                                        Preliminary
          Contaminant                 CASRN              Regulatory
                                                       Determination
------------------------------------------------------------------------
Acanthamoeba..................  N/A..............  Do not regulate.
Aldrin........................  309-00-2.........  Do not regulate.
Dieldrin......................  60-57-1..........  Do not regulate.
Hexachlorobutadiene...........  87-68-3..........  Do not regulate.
Manganese.....................  7439-96-5........  Do not regulate.
Metribuzin....................  21087-64-9.......  Do not regulate.
Naphthalene...................  91-20-3..........  Do not regulate.
Sodium........................  7440-23-5........  Do not regulate.
Sulfate.......................  14808-79-8.......  Do not regulate.
------------------------------------------------------------------------

    As previously stated, EPA is only making regulatory determinations 
on CCL contaminants that have sufficient information to support a 
regulatory determination at this time. The Agency continues to conduct 
research and/or to collect occurrence information on the remaining CCL 
contaminants. EPA has been aggressively conducting research to fill 
identified data gaps and recognizes that stakeholders may have a 
particular interest in the timing of future regulatory determinations 
for other contaminants on the CCL. Stakeholders may be concerned that 
regulatory determinations for such contaminants should not necessarily 
wait until the end of the next regulatory determination cycle.
    In this regard, it is important to recognize that the Agency is not 
precluded from monitoring, conducting research, developing guidance, or 
regulating contaminants not included on the CCL to address an urgent 
threat to public health (see SDWA section 1412(b)(1)(D)); or taking 
action on CCL contaminants when information becomes available. As 
previously mentioned, the Agency continues to conduct research and/or 
to collect occurrence information for contaminants on the CCL (except 
the nine mentioned in today's action) and may proceed with regulatory 
determination prior to the end of the next regulatory determination 
cycle. EPA solicits comment on which of the remaining CCL contaminants 
stakeholders believe should have the highest priority for future 
regulatory determinations and their reasons in support of such 
comments.
    The following sections summarize the data and rationale used by the 
Agency to reach these preliminary decisions.

B. Contaminant Profiles

    This section discusses the following background information for 
each regulatory priority contaminant: The available human and 
toxicological data; how the drinking water data sets were used to 
evaluate occurrence in PWSs; and the population served at levels of 
public health concern. The findings from these evaluations were used to 
determine if the three SDWA statutory requirements were satisfied for 
each contaminant, and in making preliminary determinations whether to 
regulate the contaminants. Table 4 presents summary statistics 
describing the occurrence of the regulatory determination priority 
contaminants. Monitoring data are not available from PWSs for 
Acanthamoeba, therefore, summary statistics are not represented in 
Table 4. In reviewing these statistics it is important to keep in mind 
that they are based on peak rather than mean concentrations at the 
sampled systems. In general, the percentages of systems with mean 
concentrations exceeding the HRL and \1/2\ the HRL would be lower.

[[Page 38231]]



                              Table 4.--Occurrence Summary for the Chemical Regulatory Determination Priority Contaminants
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                          Actual cross-section and NIRS data
                             ---------------------------------------------------------------------------------------------------------------------------
         Contaminant                                                                          Population  \1/
                               Systems  \1/2\HRL     Systems  HRL                 2\HRL                Population  HRL
--------------------------------------------------------------------------------------------------------------------------------------------------------
Aldrin (R2).................  0.02%........................  0.02%........................  0.02%........................  0.02%
HRL = 0.002 [mu]g/L.........  (2 of 12,165)................  (2 of 12,165)................  (8,700 of 47.7 M)............  (8,700 of 47.7 M)
Dieldrin (R2)...............  0.09%........................  0.09%........................  0.07%........................  0.07%
HRL = 0.002 [mu]g/L.........  (11 of 11,788)...............  (11 of 11,788)...............  (32,200 of 45.8 M)...........  (32,200 of 45.8 M)
Hexachlorobutadiene.........  Round 1: 0.16%...............  Round 1: 0.11%...............  Round 1: 0.57%...............  Round 1: 0.37%
(R1 & R2)...................  (20 of 12,284)...............  (14 of 12,284)...............  (407,600 of 71.6 M)..........  (262,500 of 71.6 M)
HRL = .9 [mu]g/L............
                              Round 2: 0.08%...............  Round 2: 0.02%...............  Round 2: 2.3%................  Round 2: 0.005%
                              (18 of 22,736)...............  (4 of 22,736)................  (1.6 M of 67.1 M)............  (3,100 of 67.1 M)
Manganese (NIRS)............  6.1%.........................  3.2%.........................  4.6%.........................  2.6%
HRL = 300 [mu]g/L...........  (60 of 989)..................  (32 of 989)..................  (68,100 of 1.5 M)............  (39,000 of 1.5 M)
Metribuzin (R2).............  0%...........................  0%...........................  0%...........................  0%
HRL = 91 [mu]g/L............  (0 of 13,512)................  (0 of 13,512)................  (0 of 50.6 M)................  (0 of 50.6M)
Naphthalene.................  Round 1: 0.01%...............  Round 1: 0.01%...............  Round 1: 0.007%..............  Round 1: 0.007%
(R1 & R2)...................  (2 of 13,452)................  (2 of 13,452)................  (5,600 of 77.2 M)............  (5,600 of 77.2 M)
HRL = 140 [mu]g/L...........
                              Round 2: 0.01%...............  Round 2: 0%..................  Round 2: 0.002%..............  Round 2: 0%
                              (2 of 22,923)................  (0 of 22,923)................  (1,700 of 67.5 M)............  (0 of 67.5 M)
Sodium (NIRS)...............  22.6%........................  13.2%........................  18.5%........................  8.3%
Benchmark = 120,000.........  (224 of 989).................  (131 of 989).................  (274,300 of 1.5 M)...........  (123,600 of 1.5 M)
[mu]g/L.....................
Sulfate (R2)................  4.97%........................  1.8%.........................  10.2%........................  0.9%
HRL = 5000,000 [mu]g/L......  (819 of 16,495)..............  (295 of 16,495)..............  (5.2 M of 50.4 M)............  (446,200 of 50.4 M)
--------------------------------------------------------------------------------------------------------------------------------------------------------

1. Acanthamoeba
    After reviewing the best available public health and occurrence 
information, EPA has made a preliminary determination not to regulate 
Acanthamoeba with a National Primary Drinking Water Regulation (NPDWR). 
EPA's finding is that Acanthamoeba does have adverse effects on the 
health of persons primarily as a result of infections affecting the 
eye, lung, brain, and skin. EPA has no national monitoring data for 
Acanthamoeba occurrence in PWSs. The Agency, however, believes that 
filtration practices commonly used to treat drinking water in the U.S. 
have a high removal rate for Acanthamoeba cysts. Moreover, EPA finds 
that the disease incidence for Acanthamoeba is extremely low and that 
exposure to Acanthamoeba-related infections are not typically produced 
by ingestion of drinking water, inhalation during showering, or other 
standard uses of drinking water. Rather, Acathamoeba related infections 
are typically associated with poor hygiene practices among contact lens 
wearers. Thus, EPA finds that regulation of Acanthamoeba does not 
present a meaningful opportunity for health risk reduction for persons 
served by PWSs. The Agency believes issuing guidance targeted to 
individuals at risk is a more appropriate action at this time. Detailed 
information supporting EPA's finding and tentative determination is 
provided in the Health Effects Support Document for Acanthamoeba, and 
is summarized later in this section.
    a. Background. Acanthamoeba is a common free-living microbe found 
in water, soil, and air. The protozoa exists in two stages: an active 
infective trophozoite form, and a dormant cyst form. The cyst stage 
also has potential to cause infection as it reverts to a trophozoite 
under appropriate conditions (Ferrante 1991). The cysts are resistant 
to inactivation by the levels of chlorine routinely used to disinfect 
municipal drinking water, swimming pools, and hot tubs and can survive 
for many years in the environment. However, because the cysts are 
fairly large (larger than Giardia and Cryptosporidium), they are very 
likely removed by filtration practices commonly used to treat drinking 
water.
    b. Health effects. Acanthamoeba species have been associated with 
human infections affecting the eye, lung, brain, and skin. There are 
two major clinically distinct human infections: Acanthamoeba keratitis 
and GAE.
    Acanthamoeba keratitis infection is a chronic ulceration and 
perforation of the cornea. Infection occurs predominantly in 
individuals who wear soft contact lenses and is thought to be a 
consequence of improper storage, handling, and disinfection of the 
lenses or lense case (Stehr-Green et al. 1989, Seal et al. 1992); 
wearing lenses in hot tubs and during swimming; and the formation of 
bacterial biofilms on contact lenses and lens storage cases 
(Schaumberg, et al. 1998). Acanthamoeba keratitis does not result from 
ingestion of contaminated drinking water.
    GAE can be caused by some species of Acanthamoeba. GAE is diagnosed 
more frequently in people with compromised immune systems including 
individuals with human immunodeficiency virus (HIV) and acquired 
immunodeficiency syndrome (AIDS) (Martinez and Visvesvera 1997). 
Reports indicate that possible routes of entry of Ancanthamoeba in 
immunocompromised individuals may be through the respiratory tract and 
skin lesions. Once inside the body, it spreads throughout the 
bloodstream to other parts of the body, and the central nervous system 
and may cause personality changes, cranial nerve palsies, nausea and 
headaches (Martinez and Visvesvera 1997, Marshall et al. 1997).
    c. Occurrence and exposure. i. Acanthamoeba occurrence. Members of 
the genus Acanthamoeba are widespread in nature and have been isolated 
worldwide from brackish and sea water, tap water, bottled water, 
airborne dust, swimming pools, hot springs, thermal effluents of power 
plants, ocean sediments, vegetables, and hot tubs. Acanthamoeba has 
also been recovered from the nose and throat of humans with impaired 
respiratory function and from apparently healthy persons, suggesting 
that the amoeba is

[[Page 38232]]

commonly inhaled. There are no monitoring data for Acanthamoeba under 
the UCMR or other programs. There is a published report on a presumed 
Acanthamoeba contamination of municipal drinking water supply occurring 
after a flooding incident in Iowa during 1993-1994 (Meier et al. 1998). 
The report suggests that increase in the incidence of Acanthamoeba 
keratitis in areas affected by flooding was associated with a higher 
than normal concentration of Acanthamoeba in surface water supplies. 
However, the overall risk of keratitis in the U.S., even with the Iowa 
flooding, is less than the 1:10,000 risk of infection per year that EPA 
has set as a goal for surface water supplies.
    ii. Acanthamoeba keratitis disease incidence. The Centers for 
Disease Control and Prevention (CDC) published a survey identifying 208 
cases of Acanthamoeba keratitis (between 1973 and 1988) in the U.S. 
based on requests made to their laboratories for analysis of samples 
from individuals affected with ocular keratitis and from a limited 
survey of eye health care practitioners in four States. The data 
indicate that keratitis has been reported from 34 States and the 
District of Columbia. While most cases were reported from California, 
Texas, Florida, and Pennsylvania (Stehr-Green et al. 1989), there were 
no distinct regional patterns of occurrence. Because keratitis is not a 
disease which is required to be reported to CDC, these reports may 
underestimate a national occurrence.
    Between 1973 and 1996 an estimated 700 Acanthamoeba keratitis cases 
have occurred in the U.S. (Martinez and Visvesvera 1997, Stehr-Green et 
al. 1989). There appears to be an increased keratitis incidence over 
the past decade that may be attributed to the increase in the number of 
contact lens wearers. The available published data on incidence from 
1985 to 1987 (Schaumberg et al. 1998) was used to conservatively 
estimate incidence at 1.65 to 2.01 cases per million contact-lens 
wearers. This would forecast a total of 64 cases per year for the U.S. 
contact-lens wearing population (about 34 million people wear contact 
lenses). The estimated number of Acanthamoeba keratitis cases is small 
compared to the population at risk.
    iii. GAE Disease Incidence. GAE is not a reportable disease in the 
U.S. Between 1957 and 1998 about 110 cases of GAE have been reported 
world-wide; 64 of the 110 cases were reported in the U.S., of which 30 
cases were diagnosed in AIDS patients. GAE has been reported to occur 
predominantly in patients who are immunocompromised, those with 
diabetes or alcoholism, and those receiving radiation therapy 
(Visvesvera and Stehr-Green 1990). Based on an EPA demographic 
distribution of sensitive population groups, there are approximately 
two million people in the U.S. who are considered immunocompromised 
from cancer chemotherapy, genetic factors, and HIV/AIDS (CDC 1997 and 
USEPA 1998a). Diabetics are also more vulnerable to GAE (Visvesvera and 
Stehr-Green 1990). Because the number of diabetics in the U.S. is about 
eight million (USEPA 1998a), the total population group more vulnerable 
to GAE because of preexisting disease is about 10 million. Note that 
cases in these populations are more likely to be diagnosed since the 
individuals are under a degree of medical surveillance not typical of 
the general population. The number of cases of GAE is very small when 
compared to the population of the U.S. even considering the more 
vulnerable subgroups.
    d. Preliminary determination. The Agency has made the preliminary 
determination not to regulate Acanthamoeba with a NPDWR since 
regulation would not present a meaningful opportunity for health risk 
reduction for the people served by public drinking water systems. 
Several species of Acanthamoeba infect humans and can be found 
worldwide in a range of environmental media (e.g., soil, dust, and 
fresh water). Because of this, it is assumed that finished drinking 
water may be a source of exposure. However, Acanthamoeba keratitis is 
not known to be produced by ingestion of drinking water, inhalation 
during showering, or other standard uses of drinking water. Rather, 
keratitis is associated with poor hygiene practices among contact lens 
wearers. GAE has been reported in a very small number of individuals 
known to be at risk for developing this disease; there have been a 
total of 64 U.S. cases which is a low incidence even considering the 
possible vulnerability of an estimated number of immunocompromised and 
diabetic individuals of 10 million. Reports indicate that the possible 
routes of entry of Acanthamoeba in immunocompromised individuals are 
through the respiratory tract and from skin lesions. Thus, it is 
unlikely that any of the 64 U.S. cases were associated with ingestion 
of Acanthamoeba in drinking water.
    EPA does not believe that there is an opportunity for meaningful 
public health protection through issuance of a drinking water 
regulation for Acanthamoeba. An effective means to protect public 
health is to identify those groups of individuals who may be at risk or 
more sensitive than the general population to the harmful effects of 
Acanthamoeba in drinking water and target them with protective measures 
(e.g., encourage contact lens wearers to follow manufacturers' or 
health care practitioners' instructions for cleaning and rinsing their 
contact lens). EPA intends to release a guidance document addressing 
the risks of Acanthamoeba infection.
2. Aldrin and Dieldrin
    After reviewing the best available public health and occurrence 
information, EPA has made a preliminary determination not to regulate 
the contaminants aldrin and dieldrin with National Primary Drinking 
Water Regulations (NPDWRs). EPA's findings are that aldrin and dieldrin 
may have adverse effects on the health of persons, and both are 
classified by EPA as likely to be carcinogenic to humans. EPA also 
finds that aldrin and dieldrin occur in PWSs, but not at a frequency or 
level of public health concern. Aldrin at \1/2\ health 
reference level (HRL) was found at approximately 0.02% of PWS surveyed, 
affecting approximately 0.02% of the population served; dieldrin at 
\1/2\ HRL was found at approximately 0.09% of PWS surveyed, 
affecting approximately 0.07% of the population served. As discussed 
later, EPA does not consider exposure to aldrin and dieldrin to be 
widespread nationally. Most uses of these compounds were canceled in 
1987. Thus, EPA finds that regulating aldrin and dieldrin would not 
present a meaningful opportunity for health risk reduction for persons 
served by PWSs.
    Detailed information supporting our findings and preliminary 
determinations is provided in the Health Effect Support Document for 
Aldrin and Dieldrin, the Analysis of National Occurrence of the 1998 
Contaminant Candidate List (CCL) Regulatory Determination Priority 
Contaminant in Public Water Systems, and the Regulatory Determination 
Support Document for Aldrin and Dieldrin. This information is 
summarized later in this section.
    a. Background. Aldrin and dieldrin (CASRNs 309-00-2 and 60-57-1, 
respectively) are the common names of two structurally similar 
insecticides. They are discussed together in today's action because 
aldrin readily changes to dieldrin in the body and in the environment, 
and they cause similar adverse health effects.
    The Shell Chemical Company was the sole U.S. manufacturer and 
distributor of aldrin and dieldrin; although neither

[[Page 38233]]

compound has been produced in the U.S. since 1974 (ATSDR 1993). From 
1950-1970, aldrin and dieldrin were popular pesticides used for crops 
such as corn and cotton. Because of concerns about damage to the 
environment and the potential harm to human health, EPA banned most 
uses of aldrin and dieldrin in 1974 except for the control of termites. 
In 1987, EPA banned all uses.
    b. Health effects. EPA issued health advisories for aldrin and 
dieldrin in 1992 and 1988, respectively. These chemicals caused liver 
tumors in mice, but not in rats, and are classified as Group B2, 
probable human carcinogens, under the 1986 cancer guidelines. Under 
EPA's 1999 proposed Guidelines for Carcinogen Risk Assessment (USEPA 
1999b), aldrin and dieldrin are classified as likely to be carcinogenic 
to humans.
    In animals, oral exposure to aldrin and dieldrin has produced a 
variety of dose-dependent systemic, neurological, immunological, 
endocrine, reproductive, developmental, genotoxic and tumorigenic 
effects over a collective dose range of at least three orders of 
magnitude (<0.05-50 mg/kg body weight), depending on the specific 
endpoint and the duration of exposure.
    In general, animal studies have provided only mixed evidence that 
exposures to aldrin and dieldrin at moderate-to-high levels can result 
in adverse reproductive or developmental effects such as reduced 
fertility or litter size, reduced pup survival, fetotoxicity, or 
teratogenicity. Various in vivo and in vitro studies have provided 
evidence that aldrin and dieldrin may be weak endocrine disruptors 
(ATSDR 2000a), that is to say, they may weakly disrupt the hormones 
responsible for the maintenance of normal body function and the 
regulation of developmental processes.
    EPA derived the RfD of 3 x 10-5 mg/kg/day for aldrin by 
dividing the LOAEL for liver toxicity from a lifetime study on rats of 
0.025 mg/kg/day by an uncertainty factor (UF) of 1,000 (USEPA 1988, see 
section III.A. of today's action). The UF is a product of three 10-fold 
factors that account for the variation in sensitivity among the members 
of the human population, the uncertainty in extrapolating animal data 
to humans, and the uncertainty in extrapolating from a LOAEL rather 
than from a NOAEL.
    EPA derived the RfD of 5 x 10-5 mg/kg/day for dieldrin 
by dividing the NOAEL for liver toxicity from a lifetime study on rats 
of 0.005 mg/kg/day by a UF of 100 (10 to extrapolate from rats to 
humans, and 10 to protect sensitive humans) (USEPA 1990).
    The most sensitive endpoint of concern is cancer for both aldrin 
and dieldrin. The Agency used a linearized multi-stage model to 
extrapolate from effects seen at high doses in animal studies to 
predict tumor response at low doses. This model is based on the 
biological theory that a single exposure to a carcinogen can initiate 
tumor formation, and it assumes that a threshold does not exist for 
carcinogenicity. Based on this approach, it is estimated that aldrin 
and dieldrin carcinogenic potencies are 17 per mg/kg-day and 16 per mg/
kg-day, respectively. Using these cancer potencies, the concentrations 
associated with a specific risk levels for both contaminants are 0.2, 
0.02, and 0.002 [mu]g/L at the theoretical cancer risk of 
10-4, 10-5, and 10-6, respectively 
(i.e., 1 case in 10,000; 1 case in 100,000; and 1 case in 1,000,000) 
(USEPA 1993a and 1993b). EPA adopted the dose level of 0.002 [mu]g/L 
for both contaminants as the HRL, or the benchmark against which to 
evaluate the occurrence data.
    Potential susceptibility of life-stages and other sensitive 
populations. Aldrin and dieldrin are found as residues in food and 
mother's milk; however, no long-term studies demonstrating adverse 
effects on children are available. Although these chemicals are thought 
to be weak endocrine disruptors the HRL should adequately protect 
sensitive individuals from this and other adverse effects because 
cancer is assumed to be the most sensitive endpoint of concern.
    No other sensitive subpopulations were identified that may be 
affected by exposure to these contaminants.
    c. Occurrence and exposure. For most people, exposure to aldrin and 
dieldrin occurs when people eat contaminated foods. Contaminated foods 
might include fish or shellfish from contaminated lakes or streams, 
root crops, dairy products, and meats. Exposure to aldrin and dieldrin 
also occurs when you drink water, breathe air, or touch contaminated 
soil at hazardous waste sites containing these contaminants.
    Aldrin was monitored under Round 2 of the Unregulated Contaminant 
Monitoring (UCM). Cross-section occurrence estimates are very low with 
only 0.006% of the samples (2 out of 31,083) showing detections at 0.58 
[mu]g/L and 0.69 [mu]g/L.
    The cross-section analysis shows that 0.02% of the reporting PWSs 
(2 out of 12,165) experienced detections of aldrin at both 
\1/2\ HRL and HRL, affecting 0.02% of the 
population served (8,600 out of 47.8 million people).
    Dieldrin was also monitored under Round 2 of the UCM. The cross-
section occurrence estimates are also very low with only 0.064% of 
samples (19 out of 29,603) showing detections. For samples with 
detections, the median and the 99th percentile concentrations are 0.16 
[mu]g/L and 1.36 [mu]g/L, respectively.
    The cross-section analysis shows that 0.09% of the reporting PWSs 
(11 out of 11,788) have detections of dieldrin at both \1/2\ 
HRL and HRL, affecting 0.07% of the population served 
(32,000 out of 45.8 million).
    To augment SDWA drinking water data analysis, and to provide 
additional coverage of the corn belt States where aldrin and dieldrin 
use as agricultural insecticides was historically high but not 
represented in the Round 2 data, independent analyses of SDWA drinking 
water data from the States of Iowa, Illinois, and Indiana were 
undertaken. There were no detections of aldrin in Iowa or Indiana 
surface or ground water PWSs (Hallberg et al. 1996, USEPA 1999a). While 
Illinois had no detections in ground water, aldrin was detected in 2 
out of 109 (1.8%) surface water PWSs, the maximum concentrations of 
aldrin was 2.4 [mu]g/L. A survey of Illinois community water supply 
wells during the mid-1980s also showed very low occurrence of aldrin.
    Dieldrin was not reported in Iowa surface or ground water PWSs 
(Hallberg et al. 1996). While Illinois and Indiana also had no 
detections of the compound in ground water PWSs, dieldrin was detected 
in surface water PWSs in those States (USEPA 1999a). Dieldrin 
occurrence was relatively low in both States: 2 out of 109 (1.8%) 
surface water systems showed detections in Illinois and 1 out of 47 
(2.1%) surface water systems showed detections in Indiana. For Illinois 
and Indiana surface water PWSs, the maximum concentrations of dieldrin 
were 0.1 [mu]g/L and 0.04 [mu]g/L, respectively (USEPA 1999a).
    Even the data from all Round 2 reporting States, including States 
with incomplete or potentially skewed data, show very low occurrence of 
aldrin and dieldrin. Approximately 0.21% (32 out of 15,123) of the 
reporting PWSs have detections of aldrin at both \1/2\ HRL 
and HRL, affecting approximately 291,000 of the population 
served (out of 59 million). For dieldrin, approximately 0.21% (31 out 
of 14,725) of the reporting PWSs have detections at both \1/
2\ HRL and HRL, affecting about 212,000 of the population 
served (out of 57 million).
    d. Preliminary determination. The Agency has made a preliminary 
determination not to regulate aldrin or dieldrin with a NPDWR. Since 
the

[[Page 38234]]

contaminants occur in PWSs at a very low frequency and at low levels, a 
regulation would not present a meaningful opportunity for health risk 
reduction for the people served by public drinking water systems. EPA 
recognizes that aldrin and dieldrin are probable human carcinogens, but 
the chemicals have been banned for most uses since 1974, and have 
relatively low levels of occurrence in drinking water supplies. It is 
likely that there will be so few people exposed to aldrin and dieldrin 
in their drinking water that a national regulation to control these two 
pesticides in drinking water would not provide a meaningful opportunity 
to reduce risk.
    EPA will work closely with those few States that show aldrin and 
dieldrin contamination and encourage them to work with affected systems 
to evaluate site specific protective measures and to consider State-
level regulation.
3. Hexachlorobutadiene
    After reviewing the best available public health and occurrence 
information, EPA has made a preliminary determination not to regulate 
hexachlorobutadiene with a National Primary Drinking Water Regulation 
(NPDWR). EPA's finding is that hexachlorobutadiene may have adverse 
effects on the health of persons. It is classified by EPA as likely to 
be carcinogenic to humans. EPA also finds that hexachlorobutadiene 
occurs in PWSs, but not at a frequency or level of public health 
concern. Hexachlorobutadiene at \1/2\ health reference level 
(HRL) was found at approximately 0.16% of PWS surveyed in Round 1 cross 
section samples and 0.08% of Round 2 cross section samples, affecting 
approximately 0.57% of the population served in Round 1 and 2.3% in 
Round 2. (The Round 2 affected population percentage is strongly 
influenced by a \1/2\ HRL detection at one PWS serving 1.5 
million people.) Thus, EPA finds that regulating hexachlorobutadiene 
with a NPDWR would not present a meaningful opportunity for health risk 
reduction for persons served by PWSs.
    Detailed information supporting our finding and tentative 
determination is provided in the Health Effects Support Document for 
Hexachlorobutadiene, the Analysis of National Occurrence of the 1998 
Contaminant Candidate List (CCL) Regulatory Determination Priority 
Contaminant in Public Water Systems, and the Regulatory Determination 
Support Document for Hexachlorobutadiene. These findings are summarized 
later in this section.
    a. Background. Hexachlorobutadiene (CASRN 87-68-3) is a VOC that is 
relatively insoluble in water (solubility of 2-2.55 mg/L) and has never 
been manufactured as a commercial product in the U.S. However, 
significant quantities of the chemical are generated in the U.S. as a 
waste by-product from the chlorination of hydrocarbons, and lesser 
quantities are imported mostly from Germany as a commercial product. 
Hexachlorobutadiene is mainly used to make rubber compounds. It is also 
used as a solvent, to make lubricants, in gyroscopes, as a heat 
transfer liquid, and as a hydraulic fluid.
    Eight million pounds of hexachlorobutadiene were generated as a 
waste by-product in the U.S. in 1975, with 100,000 pounds released into 
the environment. By 1982, the annual U.S. by-product generation of the 
chemical increased to 28 million pounds. In contrast, the annual import 
rate of hexachlorobutadiene dropped from 500,000 pounds per year 
imported annually in the late 1970's, to 145,000 pounds per year 
imported in 1981 (ATSDR 1994, Howard 1989).
    Hexachlorobutadiene is listed by EPA as a toxic release inventory 
(TRI) chemical. Air emissions constitute most of the on-site releases. 
Also, over a 10-year period (1988-1998), surface water discharges 
generally increased, peaked in 1992-93, and then decreased 
significantly through the late-1990s. The TRI data for 
hexachlorobutadiene are reported from eight States (USEPA 2001d).
    b. Health effects. There are no reliable data of human health 
effects following exposure to hexachlorobutadiene. Hexachlorobutadiene 
is classified by EPA as a Group C, Possible Human Carcinogen, (USEPA 
1991) in accordance with EPA's 1986 Guidelines for Carcinogen Risk 
Assessment (USEPA 1986), and is considered likely to be a carcinogen to 
humans by the 1999 Proposed Guidelines for Carcinogen Risk Assessment 
(USEPA 1999b). Studies in animals show the selective effect of 
hexachlorobutadiene on the proximal tubule of the kidney. Subchronic 
(NTP 1991) and chronic (Kociba et al. 1977) studies in rodents present 
a clear picture of dose-related renal (kidney) damage at 2 mg/kg/day 
and above. Progressive events over time include changes in kidney 
weight, altered renal function (as shown by increased excretion of 
coproporhyrin), renal tubular degeneration and regeneration, 
hyperplasia (abnormal growth of cells), and renal tumor formation. 
Developmental effects were also observed in the offspring of 
hexachlorobutadiene exposed female rats (Harleman and Seinen 1979). 
However, these effects were observed at higher doses than for renal 
toxicity. Pups with lower birth weights and reduced growth were 
reported at maternal dose of 8.1-15 mg/kg/day in rats (Badaeva 1983, 
Harleman and Seinen 1979).
    Only one study of lifetime oral exposure to hexachlorobutadiene has 
been reported in peer reviewed literature (Kociba et al. 1977). At the 
highest dose of 20 mg/kg/day in the study, benign and malignant tumors 
were seen in approximately 23% (9/39) of the male rats, and 15% (6/40) 
of the female rats. This dose exceeded the maximum tolerated dose at 
which increased mortality, severe renal toxicity, and significant 
weight loss were also observed. There were no tumors found in rats at 
the second highest dose of 2 mg/kg/day. The conclusion from the dose 
response analysis is that hexachlorobutadiene is a weak carcinogen with 
its demonstrated carcinogenicity only at a cytotoxic dose.
    EPA divided the NOAEL for damage to kidney cells (specifically, 
renal tubular epithelial cell degeneration and regeneration) in rats 
from the Kociba et al. (1977) study and in mice from the National 
Toxicology Program (NTP 1991) study of 0.2 mg/kg/day by an uncertainty 
factor (UF) of 1000 (see section III.A. of today's action). The UF is a 
product of four factors, and rounded from 900 to 1000, that account 
for: the uncertainty in extrapolating animal data to humans (UF=10), 
the variation in sensitivity among the members of the human population 
(UF=10), using a minimum effect NOAEL, that may be a minimal LOAEL 
(UF=3), and the uncertainty associated with extrapolation from an 
incomplete animal data base (UF=3, the data base lacks chronic oral 
exposure studies and 2-generation reproductive toxicity studies) to 
arrive at an RfD of 2 x 10-\4\ mg/kg/day (USEPA 1998b). The 
RfD was used to develop the HRL of 1 [mu]g/L as a benchmark against 
which to evaluate the occurrence data as described in section III.A. of 
today's action.
    The nonlinear approach for low dose extrapolation (i.e., point of 
departure of 0.054 mg/kg/day divided by a margin of exposure 300), 
gives a result equal to the RfD. Thus, the RfD of 2 x 10-\4\ 
mg/kg/day which protects against damage to kidney tubule cells will 
also be protective against tumor formation in the kidney.
    Potential susceptibility of life-stages and other sensitive 
populations. Individuals with preexisting kidney damage may be more 
sensitive to

[[Page 38235]]

adverse health effects from hexachlorobutadiene. Studies in animals 
showed that young rats and mice were more sensitive to the acute 
effects of hexachlorobutadiene (Hook et al. 1983, Lock et al. 1984), 
suggesting that infants may also be more susceptible to 
hexachlorobutadiene toxicity, perhaps as a result of immature organ 
systems.
    c. Occurrence and exposure. Most exposure to hexachlorobutadiene 
comes from breathing it in workplace air. People living near hazardous 
waste sites containing hexachlorobutadiene may be exposed to it by 
breathing air or by drinking contaminated water.
    Hexachlorobutadiene was monitored under both Rounds 1 and 2 of the 
Unregulated Contaminant Monitoring (UCM). The cross-section occurrence 
estimates are low for Round 1 and Round 2 with only 0.13% (54 of 
42,839) and 0.05% (43 of 93,585) of all samples showing detections, 
respectively. For Round 1 cross-section samples with detections, the 
median and the 99th percentile concentrations are 0.25 [mu]g/L and 10 
[mu]g/L, respectively. For Round 2 cross-section samples with 
detections, the median and the 99th percentile concentrations are 0.30 
[mu]g/L and 1.5 [mu]g/L, respectively.
    For Round 1, the cross-section analysis shows that 0.16% of the 
reporting PWSs (20 out of 12,284) had detections \1/2\ HRL, 
affecting 0.57% of the population served (407,000 out of 71.6 million). 
The percentage of reporting PWSs with detections HRL is 
0.11% (14 out of 12,284), affecting 0.37% of the population served 
(263,000 out of 71.6 million).
    For Round 2, the cross-section analysis shows that 0.08% of the 
reporting PWSs \1/2\ HRL (18 out of 22,736), affecting 2.3% 
of the population served (1.6 out of 67 million). The percentage of the 
reporting PWSs with detections HRL is 0.02% (4 out of 
22,736), affecting 0.005% of the population served (3,350 out of 67 
million).
    The Round 1 cross-section estimates of PWSs affected by 
hexachlorobutadiene are influenced by the State of Florida. Florida 
reports 5.4% of its PWSs experienced detections HRL, a value 
considerably greater than the next highest State (1.5%). In addition, 
only 13% of the PWSs in Florida (112 out of 855 PWSs) provided data, 
suggesting that only systems experiencing problems submitted data for 
hexachlorobutadiene, thereby biasing Florida's results for occurrence 
measures.
    The large values for the Round 2 cross-section estimates of 
population served with detections \1/2\ HRL are influenced 
by the inclusion of one PWS serving a very large population (1.5 
million people). While the percentages of systems with detections of 
hexachlorobutadiene \1/2\ HRL are low for both rounds, the 
difference in population served is larger.
    d. Preliminary determination. The Agency has made a preliminary 
determination not to regulate hexachlorobutadiene with a NPDWR since 
the contaminant occurs in PWSs at a very low frequency and at very low 
levels and would therefore not present a meaningful opportunity for 
health risk reduction for persons served by public drinking water 
supplies. Monitoring data indicate that hexachlorobutadiene is 
infrequently detected in public water supplies. It is important to note 
that when hexachlorobutadiene is detected, it very rarely exceeds the 
HRL or even a value of one-half the HRL.
4. Manganese
    After reviewing the best available public health and occurrence 
information, EPA has made a preliminary decision not to regulate 
manganese with a National Primary Drinking Water Regulation (NPDWR). 
EPA's finding is that manganese is essential for normal physiological 
functioning in humans and all animal species, however, several diseases 
are associated with both deficiencies and excess intake of manganese. 
Nonetheless, manganese is generally considered to have low toxicity 
when ingested orally. EPA also finds that manganese occurs in PWSs, 
with 6.1% of reporting ground water PWSs having detections above the 
\1/2\ health reference level (HRL) and 3.2% having 
detections above the HRL. But, because the toxicity of manganese by 
oral ingestion is low, EPA finds that regulation of manganese in 
drinking water does not present a meaningful opportunity for health 
risk reduction for persons served by PWSs.
    Detailed information supporting our finding and tentative 
determination is provided in the Health Effects Support Document for 
Manganese, the Analysis of National Occurrence of the 1998 Contaminant 
Candidate List (CCL) Regulatory Determination Priority Contaminant in 
Public Water Systems, and the Regulatory Determination Support Document 
for Manganese. These findings are summarized later in this section.
    a. Background. Manganese (CASRN 7439-96-5) is a naturally occurring 
element that constitutes approximately 0.1% of the earth's crust. It 
does not occur in the environment in its pure metal form, but is 
ubiquitous as a component of more than 100 minerals including many 
silicates, carbonates, sulfides, oxides, phosphates, and borates (ATSDR 
2000b). Manganese occurs naturally at low levels in soil, water, and 
food, and is essential for normal physiological functioning in humans 
and all animal species.
    EPA established a National Secondary Drinking Water Standard for 
manganese at 0.05 mg/L to prevent clothes from staining and to minimize 
taste problems. Secondary standards are non-enforceable Federal 
guidance for aesthetic effects (such as color, taste, or odor) or 
cosmetic effects (such as skin or tooth discoloration) and are provided 
as a guideline for States and PWSs.
    b. Health effects. Manganese is needed for normal growth and 
function; however, several diseases are associated with both 
deficiencies and excess intake of manganese.
    There is no information available on the carcinogenic effects of 
manganese in humans, and animal studies have reported mixed results. 
EPA considers manganese to be not classifiable with respect to 
carcinogenicity; Group D according to the Guidelines for Carcinogen 
Risk Assessment (1999b). Data from oral exposure suggest that manganese 
has a low developmental toxicity.
    There are several reports of toxicity to humans exposed to 
manganese by inhalation. Inhaled manganese can lead to neurological 
symptoms (e.g., tremor, gait disorders, etc.) as seen in miners exposed 
to manganese dusts or fumes. Much less is known about oral intake of 
manganese. The major source of manganese intake in humans (with the 
exception of possible occupational exposure) is dietary ingestion; 
however, manganese is not considered to be very toxic when ingested 
with food, and reports of adverse effects are rare.
    An epidemiological study performed in Peloponnesus, Greece 
(Kondakis et al. 1989) showed that lifetime consumption of drinking 
water containing naturally high concentrations of manganese oxides may 
lead to neurological symptoms and increased manganese retention as 
reflected in the concentration of manganese in hair for people over 50 
years old. For the group consuming the highest concentration (around 2 
mg/L) for more than 10 years, the authors suggested that some 
neurologic impairment might be present. The study raises concerns about 
possible adverse neurological effects following chronic ingestion from 
drinking water at doses within ranges deemed essential. However, the 
study did not examine

[[Page 38236]]

manganese intake data from other routes/sources (i.e., dietary intake, 
inhalation from air, etc.), precluding its use as a basis for the RfD.
    Another long-term drinking water study in Germany (Vieregge et al. 
1995) found no neurological effects in people older than 50 years of 
age who drank water containing 0.3 to 2.16 mg/L of manganese for more 
than 10 years. However, this study also lacks exposure data from other 
routes and sources, and the manganese concentration range in water is 
very wide. Thus, the study cannot be used for quantitative assessment.
    A small Japanese community (total 25 individuals) ingested high 
levels of manganese in contaminated well water (leaked from dry cell 
batteries buried near the wells) over a three-month period (Kawamura et 
al. 1941). Manganese intake was not determined at the time of 
intoxication, but was assayed months later; it was estimated to be 
close to 29 mg/L (i.e., 58 mg/day or 1.45 mg/kg/day). Symptoms included 
lethargy, increased muscle tonus (tension), tremor, mental 
disturbances, and even death. Autopsies revealed macroscopic and 
microscopic changes in the brain tissue. In contrast, six children (1 
to 10 years old) were not as affected as were the adults by this 
exposure. The elderly were more severely affected. Some effects may 
have resulted from factors other than manganese exposure.
    In various surveys, manganese intakes of adults eating western type 
and vegetarian diets ranged from 0.7 to 10.9 mg per day (Freeland-
Graves 1994, Gibson 1994). Depending on individual diets, a normal 
intake may be well over 10 mg/day, especially from a vegetarian diet. 
Thus, from the dietary surveys taken together, EPA concluded that an 
appropriate RfD for manganese is 10 mg/day (0.14 mg/kg/day) (USEPA 
1996). The Agency applied an uncertainty factor (UF) of 1 (see section 
III.A. of today's action) because the information used to determine the 
RfD was considered to be complete--it was taken from many large human 
populations consuming normal diets over an extended period of time with 
no adverse health effects. EPA derived a HRL for evaluating the 
occurrence data of 0.30 mg/L. The HRL is based on the dietary RfD and 
application of a modifying factor of 3 for drinking water as 
recommended by IRIS (USEPA 1996) (see the description of an RfD in 
section III.A. of today's action) and allocation of an assumed 20% 
relative source contribution from water ingestion. The modifying factor 
accounts for concerns raised by the Kondakis study (1989); the 
potential for higher absorption of manganese in water compared to food; 
consideration of fasting individuals; and the concern for infants with 
potentially higher absorption and lower excretion rates of manganese.
    Potential susceptibility of life-stages and other sensitive 
populations. There are no data to indicate that children are more 
sensitive to manganese than adults. Because manganese is an essential 
nutrient in developing infants, the potential adverse effects from 
manganese deficiency may be of greater concern than potential toxicity 
from over-exposure. Potential sensitive sub-populations include the 
elderly, pregnant women, iron-deficient individuals and individuals 
with impaired liver and bile duct function.
    c. Occurrence and exposure. Manganese has been detected in ground 
water PWS samples collected through the National Inorganics and 
Radionuclide Survey (NIRS). Approximately 68% (671 of 989) of the 
systems that were sampled, showed manganese above detection levels. 
However, for samples with detections, the median and the 99th 
percentile concentrations are 0.01 mg/L and 0.72 mg/L, respectively. 
NIRS samples show that 6.1% of the reporting ground water PWSs had 
detections \1/2\ HRL (60 out of 989), affecting about 4.6% 
of the population served (68,200 out of 1.5 million). The percentage of 
reporting ground water PWSs with detections HRL is 3.2% (32 
out of 989) affecting 2.6% of the population served (39,000 out of 1.5 
million).
    d. Preliminary determination. The Agency has made a preliminary 
determination not to regulate manganese with a NPDWR because it is 
generally not considered to be very toxic when ingested with the diet 
and because drinking water accounts for a relatively small proportion 
of manganese intake. Thus, regulation would not present a meaningful 
opportunity for health risk reduction for persons served by PWSs.
5. Metribuzin
    After reviewing the best available public health and occurrence 
information, EPA has made a preliminary determination not to regulate 
metribuzin with a National Primary Drinking Water Regulation (NPDWR). 
EPA's finding is that metribuzin is not classifiable as a human 
carcinogen, but there may be other adverse health effects related to 
metabolic activity from chronic exposure to high doses. EPA also finds 
that metribuzin has a very low occurrence in PWSs. Only one sample out 
of 34,507, in Round 2 of the Unregulated Contaminant Monitoring (UCM), 
was reported as having a detection and the concentration of that sample 
was below \1/2\ health reference level (HRL). Because metribuzin has 
such low occurrence, EPA finds that the regulation of metribuzin in 
drinking water does not present a meaningful opportunity for health 
risk reduction for persons served by PWSs.
    Detailed information supporting our findings and preliminary 
determinations is provided in the Health Effect Support Document for 
Metribuzin, the Analysis of National Occurrence of the 1998 Contaminant 
Candidate List (CCL) Regulatory Determination Priority Contaminant in 
Public Water Systems, and the Regulatory Determination Support Document 
for Metribuzin. These findings are summarized later in this section.
    a. Background. Metribuzin (CASRN 21087-64-9) is an SOC that does 
not volatilize readily, yet is very soluble in water. Metribuzin is 
relatively persistent in the environment and degrades primarily through 
exposure to sunlight.
    Metribuzin is used as an herbicide on crops and has limited non-
agricultural utility. Applications are primarily targeted to soybeans, 
potatoes, alfalfa, and sugar cane, and the geographic distribution of 
use largely reflects the distribution of these crops across the U.S. In 
terms of use, the herbicide is ranked 200th out of approximately 1,150 
active ingredients used in agricultural pesticides (USGS 1999). 
According to the U.S. Department of Agriculture's Agricultural 
Resources Management Study, the amount of metribuzin used annually and 
the number of acres treated appears to be modestly declining over the 
10-year survey period (1990-1999).
    b. Health effects. Metribuzin is not classifiable as to human 
carcinogenicity (Group D) (USEPA 1998c). This classification is based 
on the lack of evidence of carcinogenicity in the following studies: 
(1) A mouse study in which there were no increases in tumor incidences 
at dosing levels up to 438 mg/kg/day in the diet for males and 567 mg/
kg/day for females in the diet; (2) a rat study in which there were no 
statistically significant increases in tumor incidence at dosing levels 
up to 14.36 mg/kg/day for males and 20.38 mg/kg/day for females; and 
(3) a rat study which indicated no evidence for carcinogenicity at 
dosing levels up to 42.2 mg/kg/day for males and 53.6 mg/kg/day for 
females (USEPA 1998c).
    Acute exposures to metribuzin, as reflected in high LD50 
values, are

[[Page 38237]]

indicative of low toxicity (USEPA 1998c). Subchronic studies in rats 
and dogs suggest that metribuzin causes decreased body weight gain, 
increased organ weight (liver, thyroid and brain) and small decreases 
in blood serum activities. Chronic effects of metribuzin exposure at 
high doses, in rats and dogs, include changes in body weight gain, 
mortality, elevated liver enzyme activity and histopathological changes 
in the liver. There are a few studies available on metribuzin exposure 
and reproductive and developmental effects. Developmental studies in 
rabbits and rats show that maternal toxicity occurs at or above doses 
of 1.3 mg/kg/day in the diet (USEPA 1998c). In general, effects to the 
fetus occur only as a result of maternal toxic effects. Similarly, in 
reproductive studies in rats, systemic toxicity was observed at mid- 
and high-doses (7.5 mg/kg/day and 37.5 mg/kg/day) in both parental 
animals and pups. Effects were expressed as slightly decreased body 
weights, decreased body weight gain and exaggerated liver cell growth 
(USEPA 1998c). Metribuzin exposure can also produce some endocrine 
effects in vivo as seen in the principal study used to derive the RfD.
    A few inhalation studies are available on metribuzin exposure and 
the effects are comparable to the existing oral exposure studies. At 
high exposure (720 mg/m3), increases in organ weights as 
well as liver enzyme activities were reported (USEPA 1998c).
    The RfD for metribuzin is 0.013 mg/kg/day based on a two-year 
feeding study in rats where statistically significant increases in 
blood levels of T4 (thyroxine), decreases in blood levels of T3 
(triiodothyronine), increased absolute and relative weight of the 
thyroid and decreased lung weight were observed at 1.3 mg/kg/day 
(LOAEL). However, these effects were of marginal biological 
significance and the 1.3 mg/kg/day dose was regarded as a NOAEL in the 
derivation of the RfD. The Agency applied an uncertainty factor (UF) of 
100 (see section III.A. of today's action). The UF is a product of two 
10-fold factors that account for the variation in sensitivity among the 
members of the human population and the uncertainty in extrapolating 
animal data to humans (USEPA 1998c).
    EPA derived a HRL for evaluating the occurrence data of 91 [mu]g/1 
using the RfD approach (described in section III.A. of today's action).
    Potential susceptibility of life-stages and other sensitive 
populations. There is no evidence to suggest that children, or any 
other population subgroup, would be more sensitive than others when 
exposed to metribuzin. In addition, the UF applied for variation in 
sensitivity for humans adequately protects sensitive subgroups of the 
population.
    c. Occurrence and exposure. Metribuzin has been monitored under 
Round 2 of the UCM program. The cross-section shows that only 1 out of 
34,507 samples had detections from the 13,512 PWSs sampled (0.10 [mu]g/
L). No cross-section PWSs had detection \1/2\ HRL or 
HRL.
    The heaviest use of metribuzin is across the nation's corn-soybean 
production area. These States are not well represented in the Round 2 
database. Therefore, additional data from the Midwest corn belt were 
also evaluated. Drinking water data from Iowa, Indiana, Illinois, and 
Ohio also show very low occurrence of metribuzin.
    d. Preliminary determination. The Agency has made a preliminary 
determination not to regulate metribuzin with a NPDWR because it is not 
known to occur in PWSs at levels of public health concern. Monitoring 
data indicate that metribuzin is infrequently detected in public water 
supplies. When metribuzin is detected, it very rarely exceeds the HRL 
or a value of one-half of the HRL.
6. Naphthalene
    After reviewing the best available public health and occurrence 
information, EPA has preliminarily determined not to regulate 
naphthalene with a National Primary Drinking Water Regulation (NPDWR). 
EPA's finding is that there is inadequate data to support a conclusion 
about carcinogenicity of naphthalene by the oral route of exposure. 
But, there may be other adverse health effects from exposure to 
naphthalene such as hemolytic anemia from very high doses of 
naphthalene (e.g. ingestion of mothballs). EPA also finds that 
naphthalene has a very low occurrence in PWSs. Naphthalene at 
\1/2\ health reference level (HRL) was found at 
approximately 0.01% of public water supplies surveyed in Round 1 and 
Round 2 cross section samples, affecting less than 0.007% of the 
population served. Because naphthalene has such a low occurrence level, 
EPA finds that the regulation of naphthalene in drinking water does not 
present a meaningful opportunity for health risk reduction for persons 
served by PWSs.
    Detailed information supporting our findings and preliminary 
determination is provided in the Health Effect Support Document for 
Naphthalene, the Analysis of National Occurrence of the 1998 
Contaminant Candidate List (CCL) Regulatory Determination Priority 
Contaminant in Public Water Systems, and the Regulatory Determination 
Support Document for Naphthalene. These findings are summarized later 
in this section.
    a. Background. Naphthalene (CASRN 91-20-3) is a VOC that is 
naturally present in fossil fuels such as petroleum and coal and is 
formed when wood or tobacco are burned. Naphthalene is produced in 
commercial quantities from either coal tar or petroleum. Most of 
naphthalene use (60%) is as an intermediary in the production of 
phthalate plasticizers, resins, phthaleins, dyes, pharmaceuticals, and 
insect repellents. Crystalline naphthalene is used as a moth repellent 
and as a solid block deodorizer for diaper pails and toilets.
    Naphthalene production in the U.S. dropped from 900 million pounds 
per year in 1968 to 354 million pounds per year in 1982. Approximately 
seven million pounds of naphthalene were imported and nine million 
pounds were exported in 1978. By 1989, imports had dropped to four 
million pounds, and exports increased to 21 million pounds (ATSDR 
1995).
    b. Health effects. In inhalation studies (NTP 1992, 2000), rats and 
mice exposed to naphthalene developed tumors of the respiratory tract 
(nose, lungs). This appears to be a route-specific effect. Naphthalene 
is currently categorized as Group C, a possible human carcinogen, based 
on inadequate data in humans and limited evidence in animals (NTP 1992) 
via the inhalation route. According to the proposed 1999 cancer 
guidelines for carcinogen risk assessment, the carcinogenic potential 
of naphthalene cannot be determined via the oral or inhalation routes. 
A recent finding of clear evidence for nasal tumors in male and female 
mice (NTP 2000) suggests a need to reevaluate the carcinogenicity of 
naphthalene via the inhalation route of exposure.
    The data on naphthalene's ability to cause cancer by the oral route 
of exposure are inadequate to support a conclusion about its 
carcinogenicity by this route. The tumor data from the only long term 
oral exposure study (Schmahl 1955) indicates that naphthalene was not 
carcinogenic by the oral route, but the published study did not present 
quantitative data on tumor incidence. Most of the studies of 
naphthalene's ability to damage DNA are negative.
    Naphthalene can cause methemoglobinemia in humans, and humans are 
more sensitive to this effect than rats and mice. Methemoglobinemia is 
a condition where some of the red blood cells are chemically changed so

[[Page 38238]]

that they are not able to carry oxygen. It often leads to changes in 
the affected red blood cells so that they are broken down by the spleen 
(hemolysis) and removed from the bloodstream causing what is called 
hemolytic anemia. In the case of naphthalene, most of the data on 
methemoglobinemia and hemolysis come from cases in which large amounts 
of naphthalene (e.g., mothballs) were ingested causing significant 
hemolysis and requiring medical attention.
    In animal studies, high doses of naphthalene lead to cataracts in 
certain strains of rabbits, rats, and mice. The data on cataracts in 
humans are very limited and are confounded by exposure to other 
contaminants in addition to naphthalene. In the respiratory tract, 
naphthalene causes irritation, inflamation, and an increase in the 
number of cells (hyperplasia).
    To calculate the RfD, EPA divided the NOAEL of 71 mg/kg/day for 
impaired weight gain in rats from the Battelle Columbus Laboratory 
study (1980) by an uncertainty factor (UF) of 3,000 (see section III.A. 
of today's action) to arrive at an RfD of 0.02 mg/kg-day (USEPA 1998d). 
The UF is a product of four factors that account for: the variation in 
sensitivity among the members of the human population (UF=10), the 
uncertainty in extrapolating animal data to humans (UF=10), the 
uncertainty in extrapolating from data obtained in a study with less-
than-lifetime exposure to lifetime exposure (UF=10), and the 
uncertainty associated with extrapolation from an incomplete animal 
data set (UF=3, the data set lacks chronic oral exposure studies and 2-
generation reproductive toxicity studies). The RfD of 0.02 mg/kg/day 
was used to develop the HRL of 140 [mu]g/L as a benchmark against which 
to evaluate the occurrence data as described in section III.A. of 
today's action.
    Potential susceptibility of life-stages and other sensitive 
populations. Newborn infants with one or two copies of a defective gene 
for the enzyme, glucose-6-phosphate dehydrogenase (G6PD) are most 
sensitive to the hemolytic effects of naphthalene. There is evidence of 
naphthalene toxicity in infants who reportedly were exposed by dermal 
contact with diapers or clothing that had been stored with naphthalene 
mothballs or naphthalene flakes (ATSDR 1995). However, inhalation of 
the naphthalene vapors was likely a contributing route of exposure in 
each case (ATSDR 1995, EPA 1998d). Adults with the G6PD defect are also 
susceptible to naphthalene, but to a lesser extent than infants. In 
infants, production of the enzyme methemoglobin reductase is delayed 
rendering them more sensitive than adults to methemoglobinemia. Based 
on the available data the 10-fold UF for intraspecies differences 
(i.e., sensitivity among the members of the human population) used in 
developing the RfD will adequately protect individuals who are 
sensitive to naphthalene.
    c. Occurrence and exposure. The major source of human exposure to 
naphthalene is through the use of moth-balls containing naphthalene. 
This exposure can be from breathing the vapors or handling the 
mothballs. People also may be exposed by breathing tobacco smoke and 
air near industries that produce naphthalene. Usually naphthalene is 
not found in water because it evaporates or biodegrades quickly. When 
it is found in water, it is usually at levels lower than 0.01 mg/L 
(ATSDR 1995).
    Naphthalene was monitored under both Rounds 1 and 2 of the 
Unregulated Contaminant Monitoring (UCM). For Round 1 samples with 
detections, the median and the 99th percentile concentrations are 1.0 
[mu]g/L and 900 [mu]g/L, respectively. There are indications that two 
ground water systems in one cross-section State had outlier values 
(i.e., atypically high values not consistent with the rest of the data) 
and, thus, the 99th percentile value is suspect. Excluding these 
outliers from the analyses, no other State that contributed Round 1 
monitoring data had any detections that exceeded the HRL (140 [mu]g/L). 
For Round 2 samples with detections, the median and the 99th percentile 
concentrations are 0.73 [mu]g/L and 73 [mu]g/L, respectively.
    For Round 1, the cross-section analysis shows that 0.01% of the 
reporting PWSs (1 out of 13,452) had detections at both \1/
2\ HRL and HRL, affecting 0.007% of the population served 
(5,400 out of 77.2 million).
    For Round 2, the cross-section analysis shows that 0.01% of the 
reporting PWSs had detections \1/2\ HRL (2 out of 22,923), 
affecting 0.002% of the population served (1,300 out of 67.5 million). 
No Round 2 PWSs had detections HRL.
    d. Preliminary determination. The Agency has made a preliminary 
determination not to regulate naphthalene with a NPDWR because it is 
not known to occur in PWSs at levels of public health concern. 
Monitoring data indicate that naphthalene is infrequently detected in 
public water supplies. When naphthalene is detected, it very rarely 
exceeds the HRL or a value of one-half of the HRL.
7. Sodium
    After reviewing the best available public health and occurrence 
information, EPA has made a preliminary determination not to regulate 
sodium with a National Primary Drinking Water Regulation (NPDWR). 
Sodium is essential for normal physiological functioning in humans and 
all animal species; however, in humans several disorders are associated 
with excess intake of sodium, in particular, high blood pressure. EPA 
finds that sodium occurs in PWSs. Sodium at \1/2\ benchmark 
value (60 mg/L) was found at approximately 22.6% of PWS in the National 
Inorganic and Radionuclides Survey (NIRS) samples. Sodium at 
 the benchmark value (120 mg/L) was found at 13.2% of PWS. 
EPA believes that the contribution of drinking water to daily sodium 
intake is very small when compared to the total dietary intake and that 
short-term excursions beyond the benchmark values pose no adverse 
health risk for most individuals, including the majority of persons 
with hypertension. Because sodium in drinking water is a very small 
contributor to daily dietary intake and because the levels at which 
sodium intake can contribute to increasing the blood pressure of 
individuals with normal blood pressures is not clearly established, EPA 
does not believe that a NPDWR presents a meaningful opportunity for 
public health protection. Concurrent with today's action, EPA intends 
to issue an updated advisory to provide guidance to communities that 
may be exposed to drinking water with elevated levels of sodium 
chloride and other sodium salts, so that those individuals with 
restricted sodium intake may take appropriate actions.
    Detailed information supporting our finding and preliminary 
determination is provided in the Draft Drinking Water Advisory: 
Consumer Acceptability Advice and Health Effects Analysis on Sodium, 
Analysis of National Occurrence of the 1998 Contaminant Candidate List 
(CCL) Regulatory Determination Priority Contaminants in Public Water 
Systems, and Regulatory Determination Support Document for Sodium. 
These documents are available for review and comment at the EPA Water 
Docket.
    a. Background. Sodium (CASRN 7440-23-5) is the sixth most abundant 
element on Earth and is widely distributed in soils, plants, water, and 
foods. Most of the world has numerous deposits of sodium-containing 
minerals. The sodium ion is ubiquitous in water,

[[Page 38239]]

due to the high solubility of many sodium salts. Ground water typically 
contains higher concentrations of minerals and salts than do surface 
waters. In addition to naturally occurring sources of sodium, it is 
used in deicing roads, water treatment chemicals, and domestic water 
softeners; sewage effluents can also contribute significant quantities 
of sodium to water.
    Research indicates that the lower level of the taste threshold for 
sodium chloride in water is 30-60 mg/L (Pangborn and Pecore 1982). 
Individuals who are sensitive to the taste of sodium chloride can 
detect the taste in water at a concentration of 30 mg/L and recognize 
that taste as salty at a concentration of 60 mg/L. Accordingly, a 
moderate amount of sodium can be tolerated without any adverse impact 
on the aesthetic acceptability of the water. The taste threshold for 
sodium is influenced by a number of factors. It increases with the age 
of the consumer, in the presence of other dissolved minerals, and in 
waters with low chloride concentrations.
    Sodium consumption and source contribution of drinking water. 
Sodium is a normal component of the body, and adequate levels of sodium 
are required for good health. Food is the main source of daily human 
exposure to sodium, primarily in the form of sodium chloride (table 
salt). Most of the sodium in our diet is added to food during food 
processing and preparation. Various studies have reported dietary 
intakes of sodium that range from 1,800 to 5,000 mg/day (Abraham and 
Carroll 1981, Dahl 1960, Pennington et al. 1984). Discretionary sodium 
intake is variable and can be quite large. The Food and Drug 
Administration has found that most American adults tend to eat between 
4,000 and 6,000 mg/day. Sodium-restricted diets range from below 1,000 
to 3,000 mg/day (Kurtzweil 1995). The NRC recommended daily dietary 
intake for sodium is 2,400 mg/day.
    Drinking water generally accounts for a relatively small proportion 
of total sodium intake. An estimated 75% of dietary sodium comes from 
the sodium in processed foods, 15% is from discretional use of table 
salt during cooking and serving of foods, and 10% is from sodium 
naturally present in foods (Sanchez-Castillo et al. 1987). Drinking 
water is not considered in dietary intake surveys.
    b. Health end points. The primary health effect of concern from 
long term exposures to excess sodium is increased blood pressure 
(hypertension). A large body of evidence suggests that excessive sodium 
intake may contribute to age-related increases in blood pressure (NAS 
1977, WHO 1979). High blood pressure is a multi-factorial disorder with 
dietary sodium as one of a number of factors influencing its incidence.
    Frost et al. (1991) conducted an analysis of 14 published studies 
(12,773 subjects) from the U.S., Europe, and Asia, which measured blood 
pressure and sodium intake. The analysis indicated that there is a 
significant positive association between blood pressure and dietary 
sodium within populations. Elliot (1991) performed a similar analysis 
of 14 studies in 16 populations (12,503 subjects) relating 24-hour 
urinary sodium excretion and blood pressures. This analysis also showed 
a significant positive correlation between urinary sodium and both 
systolic and diastolic blood pressure for both males and females.
    Sullivan (1991) analyzed data on 183 subjects to determine sodium 
sensitivity, which was defined as an increase of mean blood pressure of 
more than five percent when progressing from low- to high-sodium 
intake. Using this criterion, sodium sensitivity was detected in 15% of 
Caucasian subjects with normal blood pressure, 29% of Caucasian 
borderline hypertensive subjects, 27% of African-American subjects with 
normal blood pressure and 50% of African-American borderline 
hypertensive subjects.
    Recent controlled studies of borderline hypertensive subjects 
called the Dietary Approaches to Stop Hypertension (DASH) trials 
demonstrated decreases in blood pressure with a diet that combined a 
moderate sodium intake (3,000 mg/day) with a high fruit and vegetable 
diet (DASH diet). The DASH diet was (two to three times) higher in 
potassium, calcium, magnesium, and fiber than the control diet. It 
reduced average blood pressures compared with the control diet in this 
clinical study (Vogt et al. 1999). When the study was repeated with 
differing degrees of salt restriction, small but additional decreases 
in blood pressure were observed for subjects on the sodium restricted 
DASH diet as opposed to subjects on the control diet (Sacks et al. 
2001). These results add to the weight-of-evidence that sodium is not 
the only factor in the diet to consider when managing blood pressure.
    Some clinical studies on the effect of decreased sodium intake on 
blood pressure have not detected convincing evidence of a protective 
effect of low sodium intake on the risk of cardiovascular disease 
(Muntzel and Drueke 1992, Salt Institute 2000, NIH 1993, Callaway 1994, 
Kotchen and McCarron 1998, McCarron 1998). Thus, it has been difficult 
to clearly define the role of sodium in the development of 
hypertension. Experts at the National Heart, Lung and Blood Institute, 
the scientific experts at the American Heart Association, American 
Society of Hypertension, and the European and International Societies 
of Hypertension do not feel that universal salt reduction is warranted 
for individuals with normal blood pressure (Taubes 1998). However, the 
National Institutes of Health, National Academy of Sciences, American 
Heart Association and U.S. Department of Agriculture all recommend 
restricting daily dietary sodium intake to 2.4 g/day or less, even 
though present average intake of most people exceed this value. The 
current outdated EPA guidance level for sodium in drinking water is 20 
mg/L. It was developed to protect those individuals restricted to a 
total sodium intake of 500 mg/day (EPA, 1976). The recently updated 
guidance document, Draft Drinking Water Advisory: Consumer 
Acceptability Advice and Health Effects Analysis on Sodium, is 
available for review and comment at the EPA Water Docket. It is based 
on current health effects and occurrence data, includes the taste 
effects of sodium in drinking water, and allows EPA to provide 
appropriate guidance to water suppliers.
    Ingestion of sodium ion is not believed to cause cancer. However, 
some studies suggest that sodium chloride may enhance risk of 
gastrointestinal tract cancer caused by other chemicals. Sodium salts 
have generally produced inconclusive results in in vitro or in vivo 
genotoxicity tests.
    Very high doses of sodium chloride (1,667 mg/kg) have been observed 
to cause reproductive effects in various strains of pregnant rats. 
Effects on the pregnant rats have included decreases in pregnancy rates 
and maternal body weight gain. Effects in offspring have included 
increased blood pressure and high mortality. No studies on 
developmental effects from exposure to sodium were identified.
    Benchmark Value. In the case of sodium, the value used to evaluate 
the occurrence data is not designated as an health reference level 
(HRL) because of the lack of suitable dose-response data and the 
considerable controversy regarding the role of sodium in the etiology 
of hypertension. Instead a benchmark value is used. The benchmark value 
for sodium was derived from the recommended daily dietary intake of 2.4 
g/day (NRC 1989). It is important to note that the recommended intake 
is not related

[[Page 38240]]

directly to dose-response information and is lower than most estimates 
of the present average daily intake of the U.S. population. A relative 
source contribution of 10% was applied in recognition that foods and 
other discretional use of table salt are the major source of sodium 
exposure. This results in a benchmark value of 120 mg/L, assuming 2 
liters of water per day (i.e., 2,400 mg/day/2L x 10% = 120 mg/L). The 
\1/2\ benchmark value coincides with the upper limit of the 
concentration at which those who are sensitive to the taste of sodium 
chloride in water are able to detect the salt taste. The EPA derived 
benchmark value of 120 mg/L was used as a means for evaluating the 
occurrence data. This value is more conservative than the values used 
for evaluating the other regulatory determination contaminants in 
today's action. It was derived from the NRC dietary guideline (NRC 
1989) for adults of 2,400 mg/day for sodium from salt rather than from 
the highest NOAEL in a toxicological study or even average dietary 
intake.
    Potential susceptibility of life-stages and other sensitive 
populations. Several studies have shown that children are more 
sensitive than adults to the acute effects of high sodium intake (Elton 
et al. 1963, DeGenaro and Nyhan 1971). This increased sensitivity is 
associated with a lower ability of the immature kidney to control 
sodium levels compared to the adult. The elderly may be sensitive to 
the hypertensive effects of sodium because they have a higher incidence 
of cardiovascular disease (including high blood pressure) than younger 
subjects (Sowers and Lester 2000). African-Americans may also be more 
susceptible to sodium-induced adverse health effects due to high 
prevalence of hypertension and increased salt sensitivity 
characteristics in this population (Sullivan 1991, Svetkey et al. 
1996). Individuals with decreased kidney function or kidney 
insufficiency are more sensitive to high sodium intake compared to 
individuals with healthy kidneys.
    c. Occurrence and exposure. Sodium was detected in 100% (989 of 
989) of the ground water PWS samples collected through the National 
Inorganics and Radionuclides Survey (NIRS). The median and the 99th 
percentile concentrations of all samples are 16.4 mg/L and 517 mg/L, 
respectively.
    Analysis of NIRS samples shows 22.6% of the reporting ground water 
PWSs have detections  \1/2\ the benchmark level (60 mg/L) 
(224 out of 989) affecting approximately 18.5% of the population served 
(274,000 out of 1.5 million people). The percentage of reporting ground 
water PWSs with detections  the benchmark level (120 mg/L) 
is 13.2% (131 out of 989), affecting approximately 8.3% of the 
population served (123,000 out of 1.5 million people).
    Additional SDWA data from the States of Alabama, California, 
Illinois, New Jersey, and Oregon, including both ground water and 
surface water PWSs, were examined through independent analyses and also 
show substantial sodium occurrence. These data add an additional 
perspective to the NIRS estimates that only include data for ground 
water systems. The supplemental State data show that all five States 
reported almost 100% detections in both ground water and surface water 
systems. For all PWSs in the five States, the median concentrations of 
all samples ranged from 5.26 to 31 mg/L and 99th percentile 
concentrations of all samples ranged from 150 to 370 mg/L. Surface 
water PWS detection frequencies  the benchmark value are 
slightly lower than those for ground water.
    d. Preliminary determination. The Agency has made a preliminary 
determination not to regulate sodium with a NPDWR since the relatively 
small amount of sodium in drinking water is not projected to cause 
adverse health effects in most individuals. This preliminary decision 
is based on the minor impact of sodium in drinking water. Drinking 
water generally accounts for a relatively small proportion of total 
sodium intake. Thus, restriction of the amount of sodium in drinking 
water would not present a meaningful opportunity for health risk 
reduction for persons served by PWSs.
    Sodium intake is a matter of concern for salt-sensitive individuals 
with hypertension. However, blood pressure is greatly influenced by 
other nutrients in the diet, lifestyle, and behavioral factors in 
addition to sodium itself, and is best treated under medical 
supervision giving consideration to the multiple factors that 
contribute to the blood pressure problems.
    EPA's Draft Drinking Water Advisory: Consumer Acceptability Advice 
and Health Effects Analysis for Sodium provides guidance to communities 
that may be exposed to elevated concentrations of sodium chloride or 
other sodium salts in their drinking water. The advisory provides 
appropriate cautions for individuals on low-sodium or sodium-restricted 
diets. It is based on current health effects and occurrence data, 
includes the taste effects of sodium in drinking water, and allows EPA 
to provide appropriate guidance to water suppliers.
    EPA presently requires periodic monitoring of sodium at the entry 
point to the distribution system. Monitoring is to be conducted 
annually for surface water systems and every three years for ground 
water systems (as defined in 40 CFR 141.41). The water supplier must 
report sodium test results to local and State public health officials 
by direct mail within three months of the analysis, unless this 
responsibility is assumed by the State. This requirement provides the 
public health community with information on sodium levels in drinking 
water to be used in counseling patients and is the most direct route 
for gaining the attention of the affected population.
8. Sulfate
    After reviewing the best available public health and occurrence 
information, EPA has made a preliminary determination not to regulate 
sulfate with a National Primary Drinking Water Regulation (NPDWR). 
EPA's finding is that sulfate may have adverse health affects on 
persons, primarily as a laxative effect following high acute exposures. 
EPA also finds that sulfate occurs in PWSs. Approximately 87% of the 
Round 2 Unregulated Contaminant Monitoring (UCM) samples showed 
detections of sulfate. Sulfate at \1/2\ health reference 
level (HRL) was found at 4.97% of PWS surveyed in the Round 2 cross 
section samples, affecting 10.2% of the population served; at 
HRL, it was found at 1.8% of the PWS, affecting 0.9% of the 
population served. EPA finds that the weight of evidence suggests that 
the risk of adverse health effects to the general population is 
limited, of short duration, and only occurs at high concentrations. 
Hence, the regulation of sulfate in drinking water does not present a 
meaningful opportunity for health risk reduction for persons served by 
PWSs. EPA is issuing a Drinking Water Advisory, with today's action, to 
provide guidance to communities that may be exposed to drinking water 
with high sulfate concentrations.
    Detailed information supporting our finding and preliminary 
determination is provided in the Draft Drinking Water Advisory: 
Consumer Acceptability Advice and Health Effects Analysis on Sulfate, 
the Analysis of National Occurrence of the 1998 Contaminant Candidate 
List (CCL) Regulatory Determination Priority Contaminant in Public 
Water Systems, and the Regulatory Determination Support

[[Page 38241]]

Document for Sulfate. These findings are summarized later in this 
section.
    a. Background. EPA was required by the 1986 SDWA amendments to 
issue a proposed and final standard for sulfate. EPA grouped sulfate 
with 23 other organic and IOCs in the ``Phase V'' regulatory package 
that was proposed in 1990 (55 FR 30371, July 25, 1990). The notice 
stated that the adverse health effect from ingesting high levels of 
sulfate is diarrhea and associated dehydration. Because local 
populations usually acclimate to high sulfate levels, the impact is 
primarily on infants, transient populations (e.g., business travelers, 
visitors, and vacationers), and new residents.
    In the 1990 notice, EPA proposed alternative MCLG levels for 
sulfate of 400 mg/L and 500 mg/L. Given the high cost of the rule, the 
relatively low risk, and the need to explore alternative regulatory 
approaches targeted at the transient consumer, EPA deferred the final 
regulatory decision on sulfate. A new schedule was established, in 
connection with litigation, that required EPA to finalize its 
regulatory action for sulfate by May 1996. In December of 1994, EPA re-
proposed the MCLG at 500 mg/L. Before the rule was promulgated, SDWA, 
as amended in 1996, directed EPA to determine by August 2001 whether to 
regulate sulfate in drinking water. In addition, section 1412(b)(12)(B) 
of SDWA directs EPA and the CDC to conduct a study, discussed in more 
detail later in this section, to establish a reliable dose-response 
relationship for the adverse human health effects from exposure to 
sulfate in drinking water, including the health effects that may be 
experienced by sensitive subpopulations (i.e., infants and travelers). 
SDWA specifies that the study be conducted using the best available 
peer-reviewed science in consultation with interested States, and 
completed by February 1999.
    Sulfate (SO4-2, CASRN 14808-79-8) exists in a 
variety of inorganic salts. Sulfate salts such as sodium, potassium and 
magnesium are very water soluble and are often found in natural waters. 
Sulfate salts of metals such as barium, iron, or lead have very low 
water solubility.
    Sulfate is found in soil, sediments and rocks and occurs in the 
environment as a result of both natural processes and human activities. 
Sulfate is used for a variety of commercial purposes, including pickle 
liquor (sulfuric acid) used in the steel and metal industries and as a 
reagent in the manufacturing of products such as copper sulfate (a 
fungicide/algicide). Specific data on the total production of all 
sulfates are not available, but production is expected to be in the 
thousands of tons per year.
    Sulfate may enter surface or ground water as a result of discharge 
or disposal of sulfate-containing wastes. In addition, sulfur oxides 
produced during the combustion of fossil fuels are transformed to 
sulfuric acid in the atmosphere. Through precipitation (acid rain), 
sulfuric acid can enter surface waters, lowering the pH and raising 
sulfate levels.
    Sulfate is present in the diet. A number of food additives are 
sulfate salts and most (such as copper sulfate and zinc sulfate) are 
approved for use as nutritional supplements.
    EPA established a National Secondary Drinking Water Regulation for 
sulfate at 250 mg/L based on aesthetic effects (i.e., taste and odor) 
in 1979 (40 CFR part 43.3). This value was adopted from the 1962 Public 
Health Service Drinking Water Standards. The taste threshold for 
sulfate is reported to range from 200 to 900 mg/L depending on the 
specific sulfate salt. The threshold for unpleasant taste for sodium 
sulfate is about 800 to 1,000 mg/L, based on the results of a study by 
Heizer et al. (1997) and a study conducted under a cooperative 
agreement by the CDC and EPA (USEPA 1999c).
    b. Health effects. Sulfate induces a laxative effect following high 
acute exposures (Anderson and Stothers 1978, Fingl 1980, Schofield and 
Hsieh 1983, Stephen et al. 1991, Cocchetto and Levy 1981, Gomez et al. 
1995, Heizer et al. 1997). The concentrations of sulfate that induced 
these effects varied, but all occurred at concentrations 500 
mg/L. A sulfate intake sufficient to produce a laxative effect when 
taken in one dose (5,400 mg) did not have the same effect when divided 
into four sequential hourly doses (Cocchetto and Levy 1981).
    Chronic exposure to sulfate may not have the same laxative effect 
as an acute exposure since humans appear to develop a tolerance to 
drinking water with high sulfate concentrations (Schofield and Hsieh 
1983). It is not known when this acclimation occurs; however in adults, 
acclimation is thought to occur within one to two weeks (USEPA 1999c).
    Evidence indicates that sulfate concentrations do not exert adverse 
reproductive or developmental effects at concentrations as high as 
5,000 mg/L (Andres and Cline 1989).
    Although several studies (Peterson 1951, Moore 1952, Cass 1953) 
have been conducted on the long-term exposure of humans to sulfate in 
drinking water, none of them can be used to derive the relationship 
between a quantified exposure and adverse health effects (a dose-
response characterization).
    As required by SDWA, and discussed previously in this section, EPA 
and the CDC completed a study, ``Health Effects from Exposure to High 
Levels of Sulfate in Drinking Water Study'', (CDC and USEPA 1999b) in 
January 1999. The overall purpose of the Sulfate Study was to examine 
the association between consumption of tap water containing high levels 
of sulfate and reports of osmotic diarrhea (an increase in stool 
volume) in susceptible populations (infants and transients). 
Specifically, the CDC researchers designed field investigations of 
infants naturally exposed to high levels of sulfate in the drinking 
water provided by PWSs and an experimental trial of exposure in adults.
    The CDC investigators were unable to study infants receiving their 
first bottles containing tap water with high levels of sulfate because 
the population of infants exposed to sulfate through their formula was 
not large enough to support the statistical requirements of such a 
study (USEPA 1999b). In the study of adult volunteers representing a 
transient population, the investigators did not find an association 
between acute exposure to sodium sulfate in tap water and reports of 
diarrhea. A total of 105 adult participants were randomly assigned to 
five sulfate-exposure groups (0, 250, 500, 800, and 1,200 mg/L) and 
were exposed to sulfate in bottled water over a period of six days. 
There was no significant dose-response association between acute 
exposure to sodium sulfate in water and reports of diarrhea. However, 
there was a weak (not statistically significant) increase in reports of 
increased stool volume at the highest dose level when it was compared 
to the combined lower doses.
    As a supplement to the Sulfate Study, the CDC, in coordination with 
EPA, convened an expert workshop (USEPA 1999d), open to the public, in 
Atlanta, Georgia, on September 28, 1998 (64 CFR 7028). The expert 
scientists reviewed the available literature and the Sulfate Study 
results. They favored a health advisory for sulfate-containing drinking 
water at levels greater than 500 mg/L (USEPA 1999d). The most sensitive 
endpoint was considered by the panelists to be osmotic diarrhea. The 
panel noted that none of the reported data for humans identify laxative 
effects at concentrations of 500 mg/L or below. In most situations 
where laxative effects were observed at concentrations below 800 mg/L, 
the water contained other osmotically active contaminants such as 
magnesium or had been mixed with powdered infant formula. These data

[[Page 38242]]

suggest that the total concentration of osmotically active contaminants 
needs to be significantly higher than the 500 mg/L health-based 
advisory. The Agency used an HRL of 500 mg/L for evaluating the 
occurrence data, based on the recommendations of the CDC and EPA Panel 
(USEPA 1999d).
    Potential susceptibility of life-stages and other sensitive 
populations. A potential sensitive population for dehydration resulting 
from diarrhea are infants receiving formula made with unfiltered tap 
water containing sulfate. Other groups include transient populations 
(i.e., tourists, hunters, students, and other temporary visitors) and 
people moving from areas with low sulfate drinking water concentrations 
into areas with high concentrations.
    The health-based advisory value of 500 mg/L will protect against 
sulfate's laxative effects, even in formula-fed infants, in the absence 
of high concentrations of other osmotically active chemicals in the 
water. In situations where the water contains high concentrations of 
total dissolved solids and/or other osmotically active ions, laxative-
like effects may occur if the water is mixed with concentrated infant 
formula or powdered nutritional supplements. In such situations, an 
alternate low-mineral-content water source is advised.
    c. Occurrence and exposure. Sulfate was monitored under Round 2 of 
the UCM program. The State cross-section occurrence estimate is very 
high with 87% of the samples (35,221 of 40,484) showing detections. The 
median and the 99th percentile concentrations of all samples are 24 mg/
L and 560 mg/L, respectively.
    The Round 2 cross-section analysis shows that approximately 5% of 
the reporting PWSs have detections \1/2\ HRL (820 out of 
16,495 PWSs), affecting about 10.2% of the population served (5.1 
million out of 50.4 million people). The percentage of the reporting 
PWSs with detections HRL is approximately 1.8% (300 out of 
16,495 PWSs), affecting about 0.9% of the population served (448,300 
out of 50.4 million people).
    Additional data from the States of Alabama, California, Illinois, 
Montana, New Jersey, and Oregon were examined. Of these States three 
had 99th percentile concentrations that exceeded the suggested HRL. A 
comparison between the 20-State cross-section data and the supplemental 
State data shows very similar results for sulfate detection frequencies 
in PWSs.
    d. Preliminary determination. The Agency has made a preliminary 
determination not to regulate sulfate with a NPDWR since regulation 
would not present a meaningful opportunity for health risk reduction 
for persons served by public drinking water systems. This preliminary 
decision is based on the weight of evidence suggesting that the risk of 
adverse health effects to the general population is limited and acute 
(a short duration laxative-related response) and occurs at high 
drinking water concentrations (500 mg/L, and in many cases 
1,000 mg/L). In addition, people either develop a tolerance 
for high concentrations of sulfate in drinking water, or they decrease 
the amount of water they drink at one time, most likely because of the 
taste of the water (the taste threshold is 250 mg/L).
    EPA intends to issue an advisory to provide guidance to communities 
that may be exposed to drinking water contaminated with high sulfate 
concentrations.

V. Specific Requests for Comment, Data or Information

    EPA is requesting public comment on today's action. EPA intends to 
respond to the public comments it receives and issue final regulatory 
determinations in late 2002. If the Agency determines that regulations 
are warranted, the regulations would then need to be formally proposed 
within 24 months of the determination to regulate, and promulgated 18 
months following the proposal.

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    Dated: May 24, 2002.
Christine Todd Whitman,
Administrator.
[FR Doc. 02-13796 Filed 5-31-02; 8:45 am]
BILLING CODE 6560-50-P