[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
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Chemical contaminant Research needs
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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
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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
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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