EPA815-Z-02-004
Monday,
June 3,2002
Part in
Environmental
Protection Agency
40 CFR Part 141
Announcement of Preliminary Regulatory
Determinations for Priority Contaminants
on the Drinking Water Contaminant Candidate List
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Please be aware the comments should be addressed to the W-01-03
Comments Clerk (instead of the W-01-14 Comments Clerk as
incorrectly cited in the June 03,2002 Federal Register)
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38222
Federal Register/Vol. 67, No. 106/Monday, June 3, 2002 / Proposed Rules
/. .Does Anchorage Have an Inspection
and Maintenance (I/M) Program in
Place That Meets EPA Requirements in
Section 182(a)(2)(B) of the Act?
Yes. Anchorage's I/M program was
initially implemented in 1985. Since
then, Anchorage has continued to
improve its performance. Improved
program elements include: test
equipment and procedures, quality
assurance and quality control
procedures, vehicle repair requirements
and enforcement/The Anchorage I/M
program, improvements and
amendments, have been adopted
through previous SIP revisions (51 FR
8203, September 15,1986; 54 FR 31522,
July 31,1989; 60 FR 17232, April 5,
1995; 64 FR 72940, December 29,1999,
67 FR 822, January 8, 2002).
K. Are There Controls on Stationary
Sources of CO as Required by Section
172(c)(5)oftheAct?
Yes. Section 172 (c) (5) of the Act
requires States with nonattainment
areas to include in their SIPs a permit
program for the construction and
operation of new or modified major
stationary sources in nonattainment
areas. In a separate, prior action, we
approved the new source review permit
program for Alaska. (See 60 FR 8943,
February 16,1995.)
L. Has Anchorage Implemented an
Oxygenated Fuel Program as Described
in Section 187(b)(3)?
Yes. In a separate, prior action, we
approved the oxygenated gasoline
program for Anchorage (61 FR 24712,
May 16,1996).
m. Summary of EPA's Proposal
We are proposing approval of the
following elements of the Anchorage CO
Attainment Plan, as submitted on
January 4, 2002:
A. Procedural requirements, under
section 110(a)(l) of the Act;
B. Base year emission inventory,
periodic emission inventory and
commitments under sections 187(a)(l)
and!87(a)(5)oftheAct;
C. Attainment demonstration, under
section 187(a)(7) of the Act;
D. The TCM programs under 182(d)(l)
and 108(fJ(l)(A) of the Act
E. Contingency measures under
section 187(a)(3) of the Act.
F. RFP demonstration, under sections
171(1) and 172(c)£2) of the Act; and
H. The conformity budget under
section 176(c)(2)(A) of the Act and
§93.118 of the transportation
conformity rule (40 CFR part 93, subpart
A).
IV. Administrative Requirements
Under Executive Order 12866 (58 FR
51735, October 4,1993), this proposed
action is not a "significant regulatory
action" and therefore is not subject to
review by the Office of Management and
Budget. For this reason, this action is
also not subject to Executive Order
13211, "Actions Concerning Regulations
That Significantly Affect Energy Supply,
Distribution, or Use" (66 FR 28355, May
22, 2001). This proposed action merely
proposes to approve state law as
meeting Federal requirements and
imposes no additional requirements
beyond those imposed by state law.
Accordingly, the Administrator certifies
that this proposed rule will not have a
significant economic impact on a
substantial number of small entities
under the Regulatory Flexibility Act (5
U.S.C. 601 et seq.). Because this rule
proposes to approve pre-existing
requirements under state law and does
not impose any additional enforceable
duty beyond that required by state law,
it does not contain any unfunded
mandate or significantly or uniquely
affect small governments, as described
in the Unfunded Mandates Reform Act
of 1995 (Public Law 104-4).
This proposed rule also does not have
tribal implications because it will not
have a substantial direct effect on one or
more Indian tribes, on the relationship
between the Federal Government and
Indian tribes, or on the distribution of
power and responsibilities between the
Federal Government and Indian tribes,
as specified by Executive Order 13175
(65 FR 67249, November 9, 2000). This
action also does not have Federalism
implications because it does not have
substantial direct effects on the States,
on the relationship between the national
government and the States, or on the
distribution of power and
responsibilities among the various
levels of government, as specified in
Executive Order 13132 (64 FR 43255,
August 10,1999). This action merely
proposes to approve a state rule
implementing a Federal standard, and
does not alter the relationship or the
distribution of power and
responsibilities established in the Clean
Air Act. This proposed rule also is not
subject to Executive Order 13045
"Protection of Children from
Environmental Health Risks and Safety
Risks" (62 FR 19885, April 23,1997),
because it is not economically
significant.
In reviewing SIP submissions, EPA's
role is to approve state choices,
provided that they meet the criteria of
the Clean Air Act. In this context, in the
absence of a prior existing requirement
for the State to use voluntary consensus
standards (VCS), EPA has no authority
to disapprove a SIP submission for
failure to use VCS. It would thus be
inconsistent with applicable law for
EPA, when it reviews a SIP submission,
to use VCS in place of a SIP submission
that otherwise satisfies the provisions of
the Clean Air Act. Thus, the
requirements of section 12(d) of the
National Technology Transfer and
Advancement Act of 1995 (15 U.S.C.
272 note) do not apply. This proposed
rule does not impose an information
collection burden under the provisions
of the Paperwork Reduction Act of 1995
(44 U.S.C. 3501 etseq.).
List of Subjects in 40 CFR Part 52
Environmental protection, Air
pollution control; Carbon monoxide,
Incorporation by reference,
Intergovernmental relations, Reporting
and recordkeeping requirements.
Dated: May 22, 2002.
Elbert Moore, '
Acting Regional Administrator, Region 10.
[FRDoc. 02-13698 Filed 5-31-02; 8:45 am]
BILLING CODE 6560-50-P
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.
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.
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Federal Register/Vol. 67, No. 106/Monday, June 3, 2002/Proposed Rules
38223
ADDRESSES: Please send your comments
to the W-01-14 Comments Clerk.
Submit electronic comments to: ow-
docket@epa.gov. 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:
wirth.karen@epa.gov. 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:
hotline.sdwa@epa.gov. The Hotline is
open Monday through Friday, excluding
Federal holidays, from 9:00 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 9:00 a.m. to 4:00 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 9:00 a.m.. and 3:30 p.m.,
Eastern Time, Monday through Friday,
to schedule an appointment.
Abbreviations and Acronyms
<—Less than
>—Greater than
jx—Microgram, one-millionth of a gram
Hg/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
LD5o—Lethal Dose 50; the dose at which
50% of the test animals died; a
calculated value (LDso)
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/m3—Milligrams per cubic meter
NAS—National Academy of Sciences
NDWAC—National Drinking Water
Advisory Council
NTH—National Institute of Health
MRS—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
RED—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
VL References
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Federal Register/Vol. 67, No. 106/Monday, June 3, 2002/Proposed Rules
I. Background and Summary of Today's
Action
A. What Is the Purpose of Today's
Action?
Section 1412(b)(l)(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 (lOCs) (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 1-800^26-
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)(l)(B) states that
the EPA Administrator shall publish a
list of contaminants which " * * * are
not subject to any proposed or
promulgated national primary drinking
water regulation, which are known or
anticipated to occur in public water
systems, and which may require
regulation under this title [SDWA]."
The CCL was developed with
considerable input from the scientific
community and stakeholders. A draft
CCL requesting public comment was
published on October 6,1997 (62 FR
52193). The first CCL was published on
March 2,1998 (63 FR 10273). The
SDWA requires that a new CCL will be
published every five years thereafter
(e.g., February 2003). The 1998 CCL
contained 60 contaminants, including
50 chemicals or chemical groups and 10
microbiological contaminants or
microbial groups. Many of these
contaminants lacked some of the
information necessary to support a
regulatory determination and were
identified as having data needs. CCL
contaminants were divided into
categories to represent next steps and
data needs associated with each
contaminant. The categories were: (1)
Regulatory determination priorities (i.e.,
no data needs); (2) health effects
research priorities; (3) treatment
research priorities; (4) analytical
methods research priorities; and (5)
occurrence priorities. Twenty
contaminants were classified as
regulatory determination priorities on
the 1998 CCL because EPA believed in
1998 that there were sufficient data to
evaluate both exposure and risk to
public health, and to support a
determination of whether or not to
proceed to promulgation of a NPDWR.
Since the March 1998 CCL, EPA
found that there was insufficient
information to support a regulatory
determination for 12 of the 20 priority
contaminants (see Table 1). In addition,
sodium was added to the list of eight
remaining regulatory determination
priorities primarily as a means of
reassessing the current guidance level.
Thus, EPA is now presenting
preliminary regulatory determinations
for nine priority contaminants that have
sufficient information to support a
regulatory determination at this time:
Acanthamoeba, aldrin, dieldrin,
hexachlorobutadiene, manganese,
metribuzin, naphthalene, sodium, and
sulfate.
TABLE 1.—1998 PRIORITY CONTAMINANTS WHICH ARE Now JUDGED To LACK INFORMATION SUFFICIENT To SUPPORT A
REGULATORY DETERMINATION
Chemical contaminant
Research needs
Boron
Bromobenzene .
1,1-dlchloroe thane
1,3-dlchloropropene
2,2-dlchloropropane
p-lsopropyltoluene.
Metolachlor, s-metolachlor, and metolachlor
degradation products: ethane sulfonio acid,
and oxanilic add.
Treatment technology and finalization of a health risk assessment (reference dose—RfD).
Non-cancer health effects data including subchronic toxicity tests, immunotoxicity,
neurotoxicity, and structure-activity analyses. Further work to identify an appropriate treat-
ment technology.
Health effects data—cancer, reproductive, developmental, and pharmacokinetic studies. Fur-
ther work to identify an appropriate treatment technology.
Occurrence information using revised sample preservation method.
Health effects data—mutagenicity and carcinogenicity screening tests, and structure-activity
analysis. Further work to identify an appropriate treatment technology.
Health effects data—subchronic, chronic, cancer, neurodeveloprhental, reproductive, and de-
velopmental. Evaluate related findings on cumene and other alkylbenzenes.
Analysis of health effects of metolachlor degradation degradates and occurrence information.
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38225
TABLE 1.—1998 PRIORITY CONTAMINANTS WHICH ARE Now JUDGED To LACK INFORMATION SUFFICIENT To SUPPORT A
REGULATORY DETERMINATION—Continued
Chemical contaminant
Research needs
Organotins
1,1,2,2-tetrachloroethane
Triazines & degradation products
1,2,4-trimethylbenzene
Vanadium
Non-cancer health effects data—developmental and reproductive toxicity ~ neurotoxicity, and
immunotoxicity. Pharmacokinetic studies and structure-activity analysis recommended. Fur-
ther work needed to identify appropriateness of treatment technology and analytical meth-
ods. Additional occurrence information.
Non-cancer health effects data—developmental and reproductive toxicity, neurotoxicity, and
immunotoxicity. Carcinogenicity studies. Further work to identify an appropriate treatment
technology.
Analytical methods data and occurrence information. Finalize list of degradates to evaluate.
Health effects data—neurotoxicity screening tests. Further work to identify an appropriate
treatment technology.
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)(l)(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
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Federal Register/Vol. 67, No. 106/Monday, June 3, 2002 / Proposed Rules
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(bXl)(AHiMiiU (specified in
section n 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(bKl)(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](l)(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)(l)(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 l412(b)(lKAXi)-(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
m.A. of today's action, EPA
characterized the human health effects
that may result from exposure to a
contaminant found in (kinking water.
Based on this characterization, the
Agency estimated either a health
reference level (HKL) or a benchmark
value for each contaminant.
As described in section HLB., for each
contaminant EPA estimated the number
of PWSs with detections greater than '
one-half the HRL (>Vz 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 Vz 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 of 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.
ni. 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)(l)(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 FV.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,
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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 pase 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.htin)
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)(l)(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 H.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 m.B. describes how the
drinking water data sets were used to
evaluate the occurrence of the
regulatory determination priority
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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 N1RS
(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 SOURCE'S USED IN THE REGULATORY DETERMINATION
PROCESS
Contaminant
AWrin
Sulfate
UCM round 1
cross section
X
X
UCM round 2
cross section
X
X
X
X
X
X
NIRS
X
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
Eriority contaminants
exachlorobutadiene 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
xvith 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
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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 HI. 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
>V2HRL 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 Vz 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 lOCs
(including 10 now-regulated lOCs), two
regulated radionuclides, and four
unregulated radionuclides. Manganese
and sodium were two of the lOCs
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
lOCs). 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 rv of today's action
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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
>Vi 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 P.WS
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
Contaminant
a.
Aldrin
Dieldrin
Hexachlorobu-
tadiene.
Manganese
Metribuzin ...
Naphthalene
Sodium
Sulfate
CASRN
N/A
309-00-2
60-57-1 ...
87-68-3 ...
7439-96-5
21087-64-
9.
91-20-3 ...
7440-23-5
14808-79-
8.
Preliminary
Regulatory
Determination
Do not regulate.
Do not regulate.
Do not regulate.
Do not regulate.
Do not regulate.
Do not regulate.
Do not regulate.
Do not regulate.
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 tie 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)(l)(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 rattier than mean
concentrations at the sampled systems.
In general, the percentages of systems
with mean concentrations exceeding the
HRL and Vz the HRL would be lower.
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38231
TABLE 4.—OCCURRENCE SUMMARY FOR THE CHEMICAL REGULATORY DETERMINATION PRIORITY CONTAMINANTS
Contaminant
Aldrin (R2)
HRL = 0.002 ng/L
Dieldrin (R2) .. ...
HRL = 0.002 ug/L
Hexachlorobutadiene
(R1 & R2)
HRL = .9 (ig/L
Manganese (NIRS)
HRL = 300 ng/L
Metribuzin (R2)
HRL = 91 ng/L
Naphthalene
(R1 & R2)
HRL = 140 (ig/L
Sodium (NIRS) . .. :.
Benchmark = 120,000
H9/L
Sulfate (R2)
HRL = 5000,000 ng/L
Systems
>1/2HRt
0.02%
(2 of 12,165)
0 09%
(11 of 11,788)
Round 1- 0 16%
(20 of 12,284)
Round 2: 0.08%
(18 of 22,736)
6.1%
(60 of 989)
0% '
(Oof 13,512)
Round 1'001%
(2 of 13,452)
Round 2- 001%
(2 of 22,923)
22 6% .. . .
(224 of 989)
497%
(819 of 16,495)
Actual cross-sectic
Systems
>HRL
0.02%
(2 of 12,165)
0 09%
(11 of 11,788)
Round 1- 0 11%
(14 of 12,284)
Round 2: 0.02% :
(4 of 22,736)
3.2%
(32 of 989)
0% . ...
(0 of 13,512)
Round 1 • 0 01 %
(2 of 13,452)
Round 2' 0%
(0 of 22,923)
132%
(131 of 989)
1 8%
(295 of 16,495)
n and NIRS data
Population
>1/2HRL
0.02%
(8,700 of 47.7 M)
007%
(32,200 of 45.8 M)
Round 1- 057%
(407,600 of 71.6 M)
Round 2: 2.3%
(1 .6 M of 67.1 M)
4.6%
(68,100 of 1.5 M)
0%
(0 of 50.6 M)
Round 1- 0007%
(5,600 of 77.2 M)
Round 2- 0 002%
(1,700 of 67.5 M)
18.5% .. .
(274,300 of 1.5 M)
10.2%
(5.2 M of 50.4 M)
Population
. >HRL
0.02%
(8,700 of 47.7 M)
0 07%
(32,200 of 45.8 M)
Round 1 • 0 37%
(262,500 of 71. 6 M)
Round 2: 0 005%
(3,100 of 67.1 M)
2.6%
(39,000 of 1.5 M)
0%
(0 of 50.6M)
Round V 0007%
(5,600 of 77.2 M)
Round 2' 0%
(0 of 67.5 M)
83%
(1 23,600 of 1.5 M)
09%
(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 tjhe 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
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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.
li. 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 age
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 >Vz health reference
level (HRL) was found at approximately
0.02% of PWS surveyed, affecting
approximately 0.02% of the population
served; dieldrin at >Vz 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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38233
compound has been produced in the
U.S. since 1974 (ATSDR 1993). From
1950-1970, aldrin and dieldrin were
popular pesticides used for crops such
as corn and cotton. Because of concerns
about damage to the environment and
the potential harm to human health,
EPA banned most uses of aldrin and
dieldrin in 1974 except for the control
of termites. In 1987, EPA banned all
uses.
b. Health effects. EPA issued health
advisories for aldrin and dieldrin in
1992 and 1988, respectively. These
chemicals caused liver tumors in mice,
but not in rats, and are classified as
Group B2, probable human carcinogens,
under the 1986 cancer guidelines.
Under EPA's 1999 proposed Guidelines
for Carcinogen Risk Assessment (USEPA
1999b), aldrin and dieldrin are
classified as likely to be carcinogenic to
humans.
In animals, oral exposure to aldrin
and dieldrin has produced a variety of
dose-dependent systemic, neurological,
immunological, endocrine,
reproductive, developmental, genotbxic
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 disrupters (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 lO"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 (UP) of 1,000 [USEPA
1988, see section HI.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 hi
extrapolating from a LOAEL rather than
from a NOAEL.
EPA derived the RfD of 5 xlO"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
Hg/L at the theoretical cancer risk of
10~4-10~5, and 10~6, respectively (j'.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 |J.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 disrupters the HKL
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 |j.g/
L and 0.69 |ig/L.
The cross-section analysis shows that
0.02% of the reporting PWSs (2 out of
12,165) experienced detections of aldrin
at both >Vz 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
|ig/L and 1.36 Hg/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 >Vz 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 ug/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 ug/L and 0.04 |ig/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 >Vz 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 >Vz 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
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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 >Vz 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 >Vz 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 Semen 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 HI. 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 ug/L as a
benchmark against which to evaluate
the occurrence data as described in
section m.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
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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 ug/L
and 10 ug/L, respectively. For Round 2
cross-section samples with detections,
the median and the 99th percentile
concentrations are 0.30 ug/L and 1.5 ug/
L, respectively.
For Round 1, the cross-section
analysis shows that 0.16% of the.
reporting PWSs (20 out of 12,284) had
detections >Vz 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 >V2 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 >% HRL-are
influenced by the inclusion i>f one PWS
serving a very large population (1.5
million people). While the'percentages
of systems •with detections of
hexachlorobutadiene >Vz HRL are low
for both rounds, the difference in
population served is larger.
a. 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 >Vz 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
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manganese intake data from other
routes/sources (i.e., dietary intake,
inhalation from air, etc.), precluding its
use as a basis for the RED.
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) (USEPA1996).
The Agency applied an uncertainty
factor (UF) of 1 (see section HI. 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
HI. 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 >Vz 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 Vz 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 LD5o values, are
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38237
indicative of low toxicity (USEPA
1998c). Subchronic studies in rats and
dogs suggest that metribuzin causes
decreased body weight gain, increased
organ weight (liver, thyroid and brain)
and small decreases in blood serum
activities. Chronic effects of metribuzin
exposure at high doses, in rats and dogs,
include changes in body weight gain,
mortality, elevated liver enzyme activity
and histopathological changes in the
liver. There are a few studies available
on metribuzin exposure and
reproductive and developmental effects.
Developmental studies in rabbits and
rats show that maternal toxicity occurs
at or above doses of 1.3 mg/kg/day in
the diet (USEPA 1998c). In general,
effects to the fetus occur only as a result
of maternal toxic effects. Similarly, in
reproductive studies in rats, systemic
toxicity was observed at mid- and high-
doses (7.5 mg/kg/day and 37.5 mg/kg/
day) in both parental animals and pups.
Effects were expressed as slightly
decreased body weights, decreased body
weight gain and exaggerated liver cell
growth (USEPA 1998c). Metribuzin
exposure can also produce some
endocrine effects in vivo as seen in the,
principal study used to derive the RfD.
A few inhalation studies are available
on metribuzin exposure and the effects
are comparable to the existing oral
exposure studies. At high exposure (720
mg/m3), increases in organ weights as
well as liver enzyme activities were
reported (USEPA 1998c).
The RfD for metribuzin is 0.013 mg/
kg/day based on a two-year feeding
study in rats where statistically
significant increases in blood levels of
T4 (thyroxine), decreases in blood levels
of T3 (triiodothyronine), increased
absolute and relative weight of the
thyroid and decreased lung weight were
observed at 1.3 mg/kg/day (LOAEL).
However, these effects were of marginal
biological significance and the 1.3 mg/
kg/day dose was regarded as a NOAEL
in the derivation of the RfD. The Agency
applied an uncertainty factor (UF) of
100 (see section III. A. of today's action).
The UF is a product of two 10-fold
factors that account for the variation in
sensitivity among the members of the •
human population and the uncertainty
in extrapolating animal data to humans
(USEPA 1998c).
EPA derived a HRL for evaluating the
occurrence data'of 91 ug/1 using the RfD
approach (described in section IILA. 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 ug/L). No
cross-section PWSs had, detection >Vz
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 >Vz
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
(ATSDR1995).
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
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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 HI. 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 ug/L as
a benchmark against which to evaluate
the occurrence data as described in
section HI. 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
(ATSDR1995). 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 ug/L and 900 ug/
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 ug/L). For Round 2 samples
with detections, the median and the
99th percentile concentrations are 0.73
ug/L and 73 ug/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 >Vz 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 >Vz 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 >Vz benchmark
value (60 mg/L) was found at
approximately 22.6% of PWS in the
National Inorganic and Radioriuclides
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,
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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 NRG 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 increalses in blood pressure
(NAS 1977, WHO 1979). High blood
pressure is a multi-factorial disorder
with dietary sodium as o_ne 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, Nffl
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 universa^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 genotoxiciry 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 (NRG 1989).
It is important to note that the
recommended intake is not related
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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 Vz 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 NRG dietary guideline (NRG 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 > Vz 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 lie
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 >Vz 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
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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 lOCs 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 (SO,,-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 ho
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
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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 lie
reporting PWSs have detections >Vz
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 Hie 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.
a. 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 die 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.
VI. References
Abraham, S. and M.D. Carroll. 1981. Fats,
cholesterol, and sodium intake in the diet
of persons 1-74 years: United States.
Advance data From Vital and Health
Statistics of the National Center for Health
Statistics, no. 54, pp. 1-11.
Agency for Toxic Substances and Disease
Registry (ATSDR). 1993. Toxicological
Profile for Aldrin/Dieldrin (Update).
Atlanta, GA. U.S. Department of Health
and Human Services, Public Health
Service. 184 pp.
ATSDR. 1994. Toxicological Profile for
Hexachlorobutadiene. U.S. Department of
Health and Human Services, Public Health
Service. 135 pp. and Appendices.
ATSDR. 1995. Toxicological Profile for
Naphthalene (Update). Atlanta, GA. U.S.
Department of Health and Human Services,
Public Health Service. 200 pp.
ATSDR. 2000a. Toxicological Profile for
Aldrin and Dieldrin. Draft for public
comment. Atlanta, GA. U.S. Department for
Health and Human Services, Public Health
Service. Available on the Internet at: http:/
/www.atsdr.cdc.gov/toxprofiles/tpl.htmi.
ATSDR. 2000b Toxicological Profile for
Manganese (Update). Atlanta, GA. U.S.
Department of Health and Human Services,
Public Health Service. 466 pp. and
Appendices.
Anderson, D.M. and S.C. Stothers. 1978.
Effects of saline water high hi sulfates,
chlorides and nitrates on the performance
of young weanling pigs. Journal of Animal
Science, v. 47, no. 4, pp. 900-907.
Andres, C.J. and T.R. Cline. 1989. Influence
of sulfate in drinking water on mouse
reproduction during two parities. Journal
of Animal Science, v. 67, pp. 1313-1317.
Badaeva, L.N. 1983. Structural and metabolic
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Christine Todd Whitman,
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[FRDoc. 02-13796 Filed 5-31-02; 8:45 am]
BILLING CODE 6560-50-P
FEDERAL COMMUNICATIONS
COMMISSION
47 CFR PART 73
[DA 02-1158, MB Docket No. 02-110, RM-
10406]
Radio Broadcasting Services; Rose
Hill and La Grange, NC
AGENCY: Federal Communications
Commission.
ACTION: Proposed rule.
SUMMARY: This document requests
comments on a petition filed by Conner
Media, Inc. requesting the substitution
of Channel 284C3 for Channel 284A at
Rose Hill, North Carolina, reallotment of
Channel 284C3 from Rose Hill, North.
Carolina, to La Grange, North Carolina,
and modification of the license for
Station WZUP to specify operation on
Channel 284C3 at La Grange, North
Carolina, as its community of license.
The coordinates for Channel 284C3 at
Rose Hill are 35-16-00 and 77-58-00.
In accordance with Section 1.420(1) of
the Commission's Rules, we shall not
accept competing expressions of interest
in the use of Channel 284C3 at La
Grange.
DATES: Comments must be filed on or
before July 8, 2002, and reply comments
on or before July 23, 2002.
ADDRESSES: Federal Communications
Commission, 445 Twelfth Street, SW,
Washington, DC 20554. In addition to
filing comments with the FCC,
interested parties should serve the
petitioner's counsel, as follows: Peter
Gutmann, Pepper & Corazzini, 1776 K
Street, NW, Suite 200, Washington, DC
20006.
FOR FURTHER INFORMATION CONTACT:
Kathleen Scheuerle, Media Bureau,
(202) 418-2180.
SUPPLEMENTARY INFORMATION: This is a
summary of the Commission's Notice of
Proposed Rule Making, MB Docket No.
02-110, adopted May 1, 2002, and
released May 17, 2002. The full text of
this Commission decision is available
for inspection and copying during
regular business hours at the FCC's
Reference Information Center, Portals II,
445 12th Street, SW, Room CY-A257,
Washington, DC, 20554. The complete
text of this decision may also be
purchased from the Commission's
duplicating contractor, Qualex
International, Portals II, 445 12th Street,
SW, Room CY-B402, Washington, DC,
20554, telephone 202-863-2893,
facsimile 202-863-2898, or via e-mail
qualexint@aol.com. Provisions of the
Regulatory Flexibility Act of 1980 do
not apply to this proceeding. Members
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