[Federal Register: May 1, 2007 (Volume 72, Number 83)]
[Proposed Rules]
[Page 24015-24058]
[DOCID:fr01my07-20]

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Part III

Environmental Protection Agency

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40 CFR Part 141

 Drinking Water: Regulatory Determinations Regarding Contaminants on
the Second Drinking Water Contaminant Candidate List--Preliminary
Determinations; Proposed Rule

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 141

[EPA-HQ-OW-2007-0068 FRL-8301-3]
RIN 2040-AE58

Drinking Water: Regulatory Determinations Regarding Contaminants
on the Second Drinking Water Contaminant Candidate List--Preliminary
Determinations

AGENCY: Environmental Protection Agency (EPA).

ACTION: Notice.

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SUMMARY: The Safe Drinking Water Act (SDWA), as amended in 1996,
requires the Environmental Protection Agency (EPA) to make regulatory
determinations on at least five unregulated contaminants and decide
whether to regulate these contaminants with a national primary drinking
water regulation (NPDWR). SDWA requires that these determinations be
made every five years. These unregulated contaminants are typically
chosen from a list known as the Contaminant Candidate List (CCL), which
SDWA requires the Agency to publish every five years. EPA published the
second CCL (CCL 2) in the Federal Register on February 24, 2005 (70 FR
9071 (USEPA, 2005a)). This action presents the preliminary regulatory
determinations for 11 of the 51 contaminants listed on CCL 2 and
describes the supporting rationale for each. The preliminary
determination is that an NPDWR is not appropriate for any of the 11
contaminants considered for regulatory determinations. The Agency seeks
comment on these 11 preliminary determinations. While the Agency has
not made a preliminary determination for perchlorate, this action
provides an update on the Agency's evaluation of perchlorate. The
Agency requests public comment on the information and the options that
the Agency is considering in evaluating perchlorate and welcomes the
submission of relevant, new information and/or data that may assist the
Agency in its regulatory determination.

DATES: Comments must be received on or before July 2, 2007.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-OW-
2007-0068, by one of the following methods:
     http://www.regulations.gov: Follow the online instructions

for submitting comments.
     Mail: Water Docket, Environmental Protection Agency,
Mailcode: 2822T, 1200 Pennsylvania Ave., NW., Washington, DC 20460.
     Hand Delivery: Water Docket, EPA Docket Center (EPA/DC).
Such deliveries are only accepted during the Docket's normal hours of
operation, and special arrangements should be made for deliveries of
boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-HQ-OW-2007-
0068. EPA's policy is that all comments received will be included in
the public docket without change and may be made available online at
http://www.regulations.gov, including any personal information

provided, unless the comment includes information claimed to be
Confidential Business Information (CBI) or other information whose
disclosure is restricted by statute. Do not submit information that you
consider to be CBI or otherwise protected through http://www.regulations.gov The http://www.regulations.gov. Web site is an

``anonymous access'' system, which means EPA will not know your
identity or contact information unless you provide it in the body of
your comment. If you send an e-mail comment directly to EPA without
going through http://www.regulations.gov your e-mail address will be

automatically captured and included as part of the comment that is
placed in the public docket and made available on the Internet. If you
submit an electronic comment, EPA recommends that you include your name
and other contact information in the body of your comment and with any
disk or CD-ROM you submit. If EPA cannot read your comment due to
technical difficulties and cannot contact you for clarification, EPA
may not be able to consider your comment. Electronic files should avoid
the use of special characters, any form of encryption, and be free of
any defects or viruses. For additional instructions on submitting
comments, go to Unit I.B of the SUPPLEMENTARY INFORMATION section of
this document.
    Docket: All documents in the docket are listed in the http://www.regulations.gov
 index. Although listed in the index, some

information is not publicly available, e.g., CBI or other information
whose disclosure is restricted by statute. Certain other material, such
as copyrighted material, will be publicly available only in hard copy.
Publicly available docket materials are available either electronically
in http://www.regulations.gov or in hard copy at the Water Docket, EPA/

DC, EPA West, Room 3334, 1301 Constitution Ave., NW., Washington, DC.
The Public Reading Room is open from 8:30 a.m. to 4:30 p.m., Monday
through Friday, excluding legal holidays. The telephone number for the
Public Reading Room is<PHONE_NUMBER>, and the telephone number for the
EPA Docket Center is<PHONE_NUMBER>.

FOR FURTHER INFORMATION CONTACT: Wynne Miller, Office of Ground Water
and Drinking Water, Standards and Risk Management Division, at (202)
564-4887 or e-mail<EMAIL_ADDRESS>For general information
contact the EPA Safe Drinking Water Hotline at<PHONE_NUMBER> or e-
mail<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

Abbreviations and Acronyms

a. i.--active ingredient
< --less than
< =--less than or equal to
>--greater than
>=--greater than or equal to
[mu]--microgram, one-millionth of a gram
[mu]g/g--micrograms per gram
[mu]g/kg--micrograms per kilogram
[mu]g/L--micrograms per liter
ATSDR--Agency for Toxic Substances and Disease Registry
AWWARF--American Water Works Association Research Foundation
BMD--bench mark dose
BMDL--bench mark dose level
BW--body weight for an adult, assumed to be 70 kilograms (kg)
CASRN--Chemical Abstract Services Registry Number
CBI--confidential business information
CDC--Centers for Disease Control and Prevention
ChE--cholinesterase
CCL--Contaminant Candidate List
CCL 1--EPA's First Contaminant Candidate List
CCL 2--EPA's Second Contaminant Candidate List
CFR--Code of Federal Regulations
CMR--Chemical Monitoring Reform
CWS--community water system
1,3-DCP--1,3-dichloropropene
DCPA--dimethyl tetrachloroterephthalate (dacthal)
DDE--1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene
DDT--1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane
DNT--dinitrotoluene
DW--dry weight
DWEL--drinking water equivalent level
DWI--drinking water intake, assumed to be 2 L/day
EPA--United States Environmental Protection Agency
EPCRA--Emergency Planning and Community Right-to-Know Act
EPTC--s-ethyl dipropylthiocarbamate
ESA--ethane sulfonic acid
FDA--United States Food and Drug Administration
FQPA--Food Quality Protection Act
FR--Federal Register
FW--fresh weight
g--gram
g/day--grams per day

HRL--health reference level
IOC--inorganic compound
IRIS--Integrated Risk Information System
kg--kilogram
L--liter
LD50--an estimate of a single dose that is expected to
cause the death of 50 percent of the exposed animals; it is derived
from experimental data.
LOAEL--lowest-observed-adverse-effect level
MAC--mycobacterium avium intercellulare
MCL--maximum contaminant level
MCLG--maximum contaminant level goal
mg--milligram, one-thousandth of a gram
mg/kg--milligrams per kilogram body weight
mg/kg/day--milligrams per kilogram body weight per day
mg/L--milligrams per liter
mg/m3--milligrams per cubic meter
MRL--minimum or method reporting limit (depending on the study or
suvey cited)
MTBE--methyl tertiary butyl ether
MTP--monomethyl-2,3,5,6-tetrachloroterephthalate
N--number of samples
NAS--National Academies of Sciences
NAWQA--National Water Quality Assessment (USGS Program)
NCEH--National Center for Environmental Health (CDC)
NCFAP--National Center for Food and Agricultural Policy
NCI--National Cancer Institute
NCWS--non community water system
ND--not detected (or non detect)
NDWAC--National Drinking Water Advisory Council
NHANES--National Health and Nutrition Examination Survey (CDC)
NIRS--National Inorganic and Radionuclide Survey
NIS--sodium iodide symporter
NOEL--no-observed-effect-level
NOAEL--no-observed-adverse-effect level
NPS--National Pesticide Survey
NQ--not quantifiable (or non quantifiable)
NRC--National Research Council
NPDWR--National Primary Drinking Water Regulation
NTP--National Toxicology Program
OA--oxanilic acid
OW--Office of Water
OPP--Office of Pesticide Programs
PCR--Polymerase Chain Reaction
PGWDB--pesticides in ground water data base
PWS--public water system
RED--Reregistration Eligibility Decision
RfC--reference concentration
RfD--reference dose
RSC--relative source contribution
SAB--Science Advisory Board
SDWA--Safe Drinking Water Act
SOC--synthetic organic compound
SVOC--semi-volatile organic compound
T3--triiodothyronine
T4--thyroxine
TDS--Total Diet Study (FDA)
Tg-DNT--technical grade DNT
TPA--2,3,5,6-tetrachchloroterephthalic acid
TRI--Toxics Release Inventory
TSH--thyroid stimulating hormone
TT--treatment technique
UCM--Unregulated Contaminant Monitoring
UCMR 1--First Unregulated Contaminant Monitoring Regulation
UF--uncertainty factor
US--United States of America
USDA--United States Department of Agriculture
USGS--United States Geological Survey
UST--underground storage tanks
VOC--volatile organic compound
I. General Information
    A. Does This Action Impose Any Requirements on My Public Water
System?
    B. What Should I Consider as I Prepare My Comments for EPA?
II. Purpose, Background and Summary of This Action
    A. What Is the Purpose of This Action?
    B. Background on the CCL and Regulatory Determinations
    C. Summary of the Approach Used To Identify and Evaluate
Candidates for Regulatory Determination 2
    D. What Are EPA's Preliminary Determinations and What Happens
Next?
    E. Supporting Documentation for EPA's Preliminary Determinations
III. What Analyses Did EPA Use To Support the Preliminary Regulatory
Determinations?
    A. Evaluation of Adverse Health Effects
    B. Evaluation of Contaminant Occurrence and Exposure
IV. Preliminary Regulatory Determinations
    A. Summary of the Preliminary Regulatory Determination
    B. Contaminant Profiles
    1. Boron
    2. and 3. Mono- and Di-Acid Degradates of Dimethyl
Tetrachloroterephthalate (DCPA)
    4. 1,1-Dichloro-2,2-bis(p-chlorophenyl) ethylene (DDE)
    5. 1,3-Dichloropropene (1,3-DCP; Telone)
    6. and 7. 2,4- and 2,6-Dinitrotoluenes (2,4- and 2,6-DNT)
    8. s-Ethyl dipropylthiocarbamate (EPTC)
    9. Fonofos
    10. Terbacil
    11. 1,1,2,2-Tetrachloroethane
V. What Is the Status of the Agency's Evaluation of Perchlorate?
    A. Sources of Perchlorate
    B. Health Effects
    C. Occurrence in Water, Food, and Humans.
    D. Occurrence Studies on Perchlorate in Human Urine, Breast
Milk, and Amniotic Fluid
    E. Status of the Preliminary Regulatory Determination for
Perchlorate
    F. What Are the Potential Options for Characterizing Perchlorate
Exposure and Proceeding With the Preliminary Regulatory
Determination for Perchlorate?
    G. Next Steps
VI. What About the Remaining CCL 2 Contaminants?
    A. Metolachlor
    B. Methyl tertiary-butyl ether
    C. Microbial Contaminants
VII. EPA's Next Steps
VIII. References

I. General Information

A. Does This Action Impose Any Requirements on My Public Water System?

    None of these preliminary regulatory determinations or the final
regulatory determinations, when published, will impose any requirements
on anyone. Instead, this action notifies interested parties of the
availability of EPA's preliminary regulatory determinations for 11 of
the 51 contaminants listed on CCL 2 and seeks comment on these
preliminary determinations. This action also provides an update on the
Agency's review of perchlorate and methyl tertiary butyl ether (MTBE).

B. What Should I Consider as I Prepare My Comments for EPA?

    You may find the following suggestions helpful for preparing your
comments:
    1. Explain your views as clearly as possible.
    2. Describe any assumptions that you used.
    3. Provide any technical information and/or data you used that
support your views.
    4. If you estimate potential burden or costs, explain how you
arrived at your estimate.
    5. Provide specific examples to illustrate your concerns.
    6. Offer alternatives.
    7. Make sure to submit your comments by the comment period
deadline.
    8. To ensure proper receipt by EPA, identify the appropriate docket
identification number in the subject line on the first page of your
response. It would also be helpful if you provided the name, date, and
Federal Register citation related to your comments.

II. Purpose, Background and Summary of This Action

    This section briefly summarizes the purpose of this action, the
statutory requirements, previous activities related to the Contaminant
Candidate List and regulatory determinations, and the approach used and
outcome of these preliminary regulatory determinations.

A. What Is the Purpose of This Action?

    The Safe Drinking Water Act (SDWA), as amended in 1996, requires
EPA to publish a list of currently unregulated contaminants that may
pose risks for drinking water (referred to as the Contaminant Candidate
List, or CCL) and to make determinations on whether to regulate at
least five contaminants from the CCL with a national primary drinking
water regulation (NPDWR)

(section 1412(b)(1)). The 1996 SDWA requires the Agency to publish both
the CCL and the regulatory determinations every five years. The purpose
of this action is to present (1) EPA's preliminary regulatory
determinations for 11 candidates selected from the 51 contaminants
listed on the second CCL (CCL 2), (2) the process and the rationale
used to make these determinations, and (3) a brief summary of the
supporting documentation. This action also includes a request for
comment(s) on the Agency's preliminary determinations.
    The 11 regulatory determination contaminants candidates discussed
in this action are boron, the dacthal mono- and di-acid degradates,
1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE), 1,3-
dichloropropene, 2,4-dinitrotoluene, 2,6-dinitrotoluene, s-ethyl
propylthiocarbamate (EPTC), fonofos, terbacil, and 1,1,2,2-
tetrachloroethane.

B. Background on the CCL and Regulatory Determinations

    1. Statutory Requirements for CCL and Regulatory Determinations.
The specific statutory requirements for the CCL and regulatory
determinations can be found in SDWA section 1412(b)(1). The 1996 SDWA
Amendments require EPA to publish the CCL every five years. The CCL is
a list of contaminants that are not subject to any proposed or
promulgated NPDWRs, are known or anticipated to occur in public water
systems (PWSs), and may require regulation under SDWA. The 1996 SDWA
Amendments also direct EPA to determine whether to regulate at least
five contaminants from the CCL every five years (within three and one-
half years after publication of the final list). In making regulatory
determinations, SDWA requires EPA to publish a Maximum Contaminant
Level Goal \1\ (MCLG) and promulgate an NPDWR \2\ for a contaminant if
the Administrator determines that:
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    \1\ The MCLG is the ``maximum level of a contaminant in drinking
water at which no known or anticipated adverse effect on the health
of persons would occur, and which allows an adequate margin of
safety. Maximum contaminant level goals are nonenforceable health
goals'' (40 CFR 141.2).
    \2\ An NPDWR is a legally enforceable standard that applies to
public water systems. An NPDWR sets a legal limit (called a maximum
contaminant level or MCL) or specifies a certain treatment technique
(TT) for public water systems for a specific contaminant or group of
contaminants.
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    (a) The contaminant may have an adverse effect on the health of
persons;
    (b) the contaminant is known to occur or there is a substantial
likelihood that the contaminant will occur in public water systems with
a frequency and at levels of public health concern; and
    (c) 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.
    If EPA determines that all three of these statutory criteria are
met and makes a final determination that a national primary drinking
water regulation is needed, the Agency has 24 months to publish a
proposed MCLG and NPDWR. After the proposal, the Agency has 18 months
to publish and promulgate a final MCLG and NPDWR (SDWA section
1412(b)(1)(E)).\3\
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    \3\ The statute authorizes a nine month extension of this
promulgation date.
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    2. The First Contaminant Candidate List (CCL 1). Following the 1996
SDWA Amendments, EPA sought input from the National Drinking Water
Advisory Council (NDWAC) on the process that should be used to identify
contaminants for inclusion on the CCL. For chemical contaminants, the
Agency developed screening and evaluation criteria based on
recommendations from NDWAC. For microbiological contaminants, NDWAC
recommended that the Agency seek external expertise to identify and
select potential waterborne pathogens. As a result, the Agency convened
a workshop of microbiologists and public health experts who developed
criteria for screening and evaluation and subsequently developed an
initial list of potential microbiological contaminants.
    The first CCL process benefited from considerable input from the
NDWAC, the scientific community, and the public through stakeholder
meetings and the public comments received on the draft CCL published on
October 6, 1997 (62 FR 52193 (USEPA, 1997a)). EPA published the final
CCL, which contained 50 chemical and 10 microbiological contaminants,
on March 2, 1998 (63 FR 10273 (USEPA, 1998a)). A more detailed
discussion of how EPA developed CCL 1 can be found in the 1997 and the
1998 Federal Register notices (62 FR 52193 (USEPA, 1997a) and 63 FR
10273 (USEPA, 1998a)).
    3. The Regulatory Determinations for CCL 1. EPA published its
preliminary regulatory determinations for a subset of contaminants
listed on CCL 1 on June 3, 2002 (67 FR 38222 (USEPA, 2002a)). The
Agency published its final regulatory determinations on July 18, 2003
(68 FR 42898 (USEPA, 2003a)). EPA identified 9 contaminants from the 60
contaminants listed on CCL 1 that had sufficient data and information
available to make regulatory determinations. The 9 contaminants were
Acanthamoeba, aldrin, dieldrin, hexachlorobutadiene, manganese,
metribuzin, naphthalene, sodium, and sulfate. The Agency determined
that a national primary drinking water regulation was not necessary for
any of these 9 contaminants. The Agency issued guidance on Acanthamoeba
and health advisories for magnesium, sodium, and sulfate.
    The decision-making process that EPA used to make its regulatory
determinations for CCL 1 was based on substantial expert input and
recommendations from different groups including stakeholders, the
National Research Council (NRC) and NDWAC. In June 2002, EPA consulted
with the Science Advisory Board (SAB) Drinking Water Committee and
requested its review and comment on whether the protocol EPA developed,
based on the NDWAC recommendations, was consistently applied and
appropriately documented. SAB provided verbal feedback regarding the
use of the NRC and NDWAC recommendations in EPA's decision criteria for
making its regulatory determinations. SAB recommended that the Agency
provide a transparent and clear explanation of the process for making
regulatory determinations. The Agency took SAB's recommendation into
consideration and further explained the CCL 1 regulatory determination
evaluation process in the July 18, 2003 (68 FR 42898 (USEPA, 2003a))
notice and in the supporting documentation.
    EPA has used the same approach to develop the regulatory
determinations discussed in this action. While this action includes a
short description of the decision process used to make regulatory
determinations (section II.C), a more detailed discussion can be found
in the 2002 and the 2003 Federal Register notices (67 FR 38222 (USEPA,
2002a) and 68 FR 42898 (USEPA, 2003a)).
    4. The Second Contaminant Candidate List (CCL 2). The Agency
published its draft CCL 2 Federal Register notice on April 2, 2004 (69
FR 17406 (USEPA, 2004a)) and the final CCL 2 Federal Register notice on
February 24, 2005 (70 FR 9071 (USEPA, 2005a)). The CCL 2 carried
forward the 51 remaining chemical and microbial contaminants that were
listed on CCL 1.
    5. The Regulatory Determinations for CCL 2. This current action
discusses EPA's preliminary determinations for 11 of the 51
contaminants listed on the CCL 2.

C. Summary of the Approach Used To Identify and Evaluate Candidates for
Regulatory Determination 2

    Figure 1 provides a brief overview of the process EPA used to
identify which CCL 2 contaminants are candidates for regulatory
determinations and the SDWA statutory criteria considered in making the
regulatory determinations.
BILLING CODE 6560-50-P
[GRAPHIC] [TIFF OMITTED] TP01MY07.050

BILLING CODE 6560-50-C
    In identifying which CCL 2 contaminants are candidates for
regulatory determinations, the Agency considered whether sufficient
information and/or data were available to characterize the potential
health effects and the known/likely occurrence in and exposure from
drinking water. With regards to sufficient health effects information/
data, the Agency considered whether an Agency-approved health risk
assessment \4\ was available to identify any potential adverse health
effect(s) and derive an estimated level at which adverse health
effect(s) are likely to occur. With regards to sufficient occurrence
information/data, the Agency considered whether information/data were
available to

evaluate and give a generally representative idea of known and/or
likely occurrence in public water systems. If sufficient information/
data were available to characterize adverse human health effects and
known/likely occurrence in public water systems, the Agency identified
the contaminant as a potential candidate for regulatory determinations.
In addition to information/data for health and occurrence, EPA also
considered the availability and adequacy of analytical methods (for
monitoring) and treatment.
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    \4\ Health information used for the regulatory determinations
process includes but is not limited to health assessments available
from the Agency's Integrated Risk Information System (IRIS), the
Agency's Office of Pesticide Programs (OPP) in a Reregistration
Eligibility Decision (RED), the National Academy of Sciences (NAS),
and/or the Agency for Toxic Substances and Disease Registry (ATSDR).
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    If EPA chose a contaminant as a candidate for regulatory
determination, the Agency used an approach similar to the first
regulatory determination process to answer the three statutory criteria
(listed in section II.B.1).
    For the current regulatory determination process, the Agency
considered the following in evaluating each of the three statutory
criteria.
    (1) First statutory criterion--Is the contaminant likely to cause
an adverse effect on the health of persons? The Agency evaluated the
best available, peer-reviewed assessments and studies to characterize
the human health effects that may result from exposure to the
contaminant when found in drinking water. Based on this
characterization, the Agency estimated a health reference level (HRL)
for each contaminant. Section III.A provides more detailed information
about the approach used to evaluate and analyze the health information.
    (2) Second statutory criterion--Is the contaminant known or likely
to occur in public water systems at a frequency and level of concern?
To evaluate known occurrence in PWSs, the Agency compiled, screened,
and analyzed data from several occurrence data sets to develop
representative occurrence estimates for public drinking water systems.
EPA used the HRL estimates for each contaminant as a benchmark against
which to conduct an initial evaluation or screening of the occurrence
data. For each contaminant, EPA estimated the number of PWSs (and the
population served by these PWSs) with detections greater than one-half
the HRL (> 1/2 HRL) and greater than the HRL (> HRL). To evaluate the
likelihood of a contaminant to occur in drinking water, the Agency
considered information on the use and release of a contaminant into the
environment and supplemental information on occurrence in water (e.g.,
ambient water quality data, State ambient or finished water data, and/
or special studies performed by other agencies, organizations and/or
entities). Section III.B provides more details on the approach used to
analyze the occurrence information/data.
    (3) Third statutory criterion--In the sole judgment of the
Administrator, does regulation of the contaminant present a meaningful
opportunity for health risk reduction for persons served by public
water systems? EPA evaluated the potential health effects and the
results of the occurrence and exposure estimates (i.e., the population
exposed and the sources of exposure) at the health level of concern to
determine if regulation presents a meaningful opportunity for health
risk reduction. EPA has made a preliminary determination regarding the
meaningful opportunity for health risk reduction for 11 contaminants
based upon the population exposed to these contaminants at levels of
concern.
    If the answers to all three statutory criteria are affirmative for
a particular contaminant, then the Agency makes a determination that a
national drinking water regulation is necessary and proceeds to develop
an MCLG and a national primary drinking water regulation for that
contaminant. It should be noted that this regulatory determination
process is independent of the more detailed analyses needed to develop
a national primary drinking water regulation. Thus, a decision to
regulate is the beginning of the Agency regulatory development process,
not the end.
    If the answer to any of the three statutory criteria is negative,
then the Agency makes a determination that a national drinking water
regulation is not necessary for that contaminant.

D. What Are EPA's Preliminary Determinations and What Happens Next?

    EPA has made preliminary determinations that no regulatory actions
are appropriate for the 11 contaminants evaluated for this second round
of regulatory determinations. EPA will make final determinations on
these 11 contaminants after a 60-day comment period. EPA is making
preliminary regulatory determinations only on those CCL 2 contaminants
that have sufficient information to support such a determination at
this time. The Agency continues to conduct research and/or to collect
information on the remaining CCL 2 contaminants to fill identified data
gaps. 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.

E. Supporting Documentation for EPA's Preliminary Determinations

    For this action, EPA prepared several support documents that are
available for review and comment in the EPA Water Docket and at http://www.regulations.gov.
 These support documents include:

     A comprehensive regulatory support document entitled,
``Regulatory Determinations Support Document for Selected Contaminants
from the Second Drinking Water Contaminant Candidate List'' (CCL 2)
(USEPA, 2006a). This support document summarizes the information and
data on the physical and chemical properties, uses and environmental
release, environmental fate, potential health effects, occurrence and
exposure estimates, the preliminary determination for each contaminant
candidate, and the Agency's rationale for its determination. The
technical health and occurrence support documents listed next served as
the basis for the health information and the drinking water occurrence
estimates summarized in this comprehensive regulatory support document.
     Technical health support documents. These documents
address exposure from drinking water and other media, toxicokinetics,
hazard identification, and dose-response assessment, and provide an
overall characterization of the risk from drinking water for the
contaminants considered for regulatory determination. These documents
are listed in the reference section as ``USEPA, 2006j'' through
``USEPA, 2006r.''
     Technical occurrence support documents (USEPA, 2006b and
USEPA, 2006c). These documents include more detailed information about
the sources of the data, how EPA assessed the data quality,
completeness, and representativeness, and how the data were used to
generate estimates of drinking water contaminant occurrence in support
of these regulatory determinations. Section III.B.3 provides more
information about the title and content of these technical support
documents.

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

    Sections III.A and B of this action outline the health effects and
occurrence/exposure evaluation process EPA used to support these
preliminary determinations.

A. Evaluation of Adverse Health Effects

    Section 1412(b)(1)(A)(i) of SDWA requires EPA to determine whether
each

candidate contaminant may have an adverse effect on public health. This
section describes the overall process the Agency used to evaluate
health effects information, the approach used to estimate a contaminant
HRL (a benchmark against which to conduct the initial evaluation of the
occurrence data), and the approach used to identify and evaluate
information on hazard and dose-response for the contaminants under
consideration. More specific information about the potential for
adverse health effects for each contaminant is presented in section
IV.B of this action.
    There are two different approaches to the derivation of an HRL. One
approach is used for chemicals that cause cancer and exhibit a linear
response to dose and the other applies to noncarcinogens and
carcinogens evaluated using a non-linear approach.
    1. Use of Carcinogenicity Data for the Derivation of a Health
Reference Level. For those contaminants considered to be likely or
probable 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 linear low dose extrapolation is
appropriate or when data on the mode of action are lacking, EPA uses a
low dose linear extrapolation to calculate risk-specific doses. The
risk-specific doses are the estimated oral exposures associated with
lifetime excess risk levels that range from one cancer in ten thousand
(10-4) to one cancer in a million (10-6). The
risk-specific doses (expressed as mg/kg of body weight per day) are
combined with adult body weight and drinking water consumption data to
estimate drinking water concentrations corresponding to this risk
range. EPA generally used the one-in-a-million (10-6) cancer
risk in the initial screening of the occurrence data for carcinogens
evaluated using linear low dose extrapolation. Five of the eleven
contaminants discussed in this action had data available to classify
them as likely or probable human carcinogens. These five are also the
only contaminants for which low dose linear extrapolations were
performed. These five are p,p-dichlorodiphenyldichloroethylene (DDE),
1,3-dichloropropene (1,3-DCP or Telone), 2,4-dinitrotoluene, 2,6-
dinitrotoluene, and 1,1,2,2-tetrachloroethane. The remaining 6
contaminants have not been identified as known, likely or probable
carcinogens.
    2. Use of Non-carcinogenic Health Effects Data for Derivation of an
HRL. For those chemicals not considered to be carcinogenic to humans,
EPA generally calculates a reference dose (RfD). A 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 either a
``no-observed-adverse-effect level'' (NOAEL), a ``lowest-observed-
adverse-effect level'' (LOAEL), or a benchmark dose, with uncertainty
factors applied to reflect limitations of the data used.
    The Agency uses uncertainty factors (UFs) to address uncertainty
resulting from incompleteness of the toxicological database. The
individual UFs (usually applied as integers of 1, 3, or 10) are
multiplied together and used to derive the RfD from experimental data.
Individual 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/or
    (5) the uncertainty associated with an incomplete database.
    For boron, the dacthal (DCPA) mono and di acid degradates, s-ethyl
dipropylthiocarbamate (EPTC), fonofos and terbacil, EPA derived the
HRLs using the RfD approach as follows:

HRL = [(RfD x BW)/DWI] x RSC

Where:

RfD = Reference Dose
BW = Body Weight for an adult, assumed to be 70 kilograms (kg)
DWI = Drinking Water Intake, assumed to be 2 L/day (90th percentile)
RSC = Relative Source Contribution, or the level of exposure
believed to result from drinking water when compared to other
sources (e.g., food, ambient air). A 20 percent RSC is being used to
estimate the HRL and screen the occurrence data because it is the
lowest and most conservative RSC used in the derivation of an MCLG
for drinking water. For each of the 6 aforementioned non-
carcinogenic compounds for which the Agency has made a preliminary
regulatory determination in this action, EPA used the RfD in
conjunction with a 20 percent RSC to derive a conservative HRL
estimate and perform an initial screening of the drinking water
occurrence data. Since the initial screening of the occurrence data
at this conservative HRL value resulted in a preliminary negative
determination for each of these 6 compounds, the Agency determined
that it was not necessary to further evaluate the RSC in making the
regulatory determination.

    As discussed in section IV.B.2 and 3, the HRL for the two dacthal
degradates is based on the HRL value derived for the DCPA parent
following the guidance provided by EPA's Office of Pesticide Programs.
    3. Sources of Data/Information for Health Effects. EPA used the
best available peer-reviewed data and analyses in evaluating adverse
health effects. Peer-reviewed health-risk assessments were available
for all chemicals considered for regulatory determinations from the
Agency's Integrated Risk Information System (IRIS) Program\5\ and/or
the Office of Pesticide Programs (OPP) Reregistration Eligibility
Decisions (RED).\6\ Table 1 summarizes the sources of the health
assessment data for each chemical under regulatory determination
consideration. The Agency performed a literature search for studies
published after the IRIS or OPP health-risk assessment was completed to
determine if new information suggested a different outcome. The Agency
collected and evaluated any peer-reviewed publications identified
through the literature search for their impact on the RfD and/or cancer
assessment. In cases where the recent data indicated that a change to
the existing RfD or cancer assessment was needed, the updated OW
assessment, as described in the health effects support document, was
independently peer-reviewed. All quantitative cancer assessments
conducted under the Guidelines for Carcinogen Risk Assessment (51 FR
33992 (USEPA, 1986)) were updated using the Guidelines for Carcinogen
Risk Assessment (USEPA, 1999a) as directed in the November 2001 (66 FR
59593 (USEPA, 2001a)) Federal Register notice.
---------------------------------------------------------------------------

    \5\ IRIS is an electronic EPA database (http://www.epa.gov/iris/index.html
) 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.
    \6\ The OPP is required under the Federal Insecticide Fungicide
and Rodenticide Act (FIFRA) to review all pesticides registered
prior to 1984 and determine whether to reregister them for continued
use. The results of the reregistration analysis are included in the
REDs. Copies of the REDs are located at the following Web site:
http://cfpub.epa.gov/oppref/rereg/status.cfm?show=rereg.

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

    In March 2005, EPA updated and finalized the Cancer Guidelines and
a Supplementary Children's Guidance,

which include new considerations for mode of action and added
guidelines related to potential risks due to early childhood exposure
(USEPA, 2005b; USEPA, 2005c). EPA updated the earlier assessments
(based on the 1986 Guidelines) for DDE, the dinitrotoluenes (2,4 and
2,6 as a mixture), and 1,1,2,2-tetrachloroethane following the 1999
Guidelines. None of these chemicals have been determined to have a
mutagenic mode of action, which would require an extra factor of safety
for children's health protection. Therefore, conducting the cancer
evaluation using the 2005 Cancer Guidelines would not result in any
change from the assessment updated following the 1999 Guidelines.
    The cancer assessment for 1,3-dichloropropene was done by OPP and
IRIS (USEPA, 1998b and 2000a) under the Proposed Guidelines for
Carcinogen Risk Assessment (61 FR 17960 (USEPA, 1996a)). The
Administrator (USEPA, 2005d) has directed that current completed
assessments can be considered to be scientifically sound based on the
guidance used when the assessment was completed until a new assessment
is performed by one of the responsible program offices.

                           Table 1.--Sources and Dates of EPA Health Risk Assessments
----------------------------------------------------------------------------------------------------------------
                         Chemical                               IRIS          Date        OPP RED        Date
----------------------------------------------------------------------------------------------------------------
Boron.....................................................            X          2004  ............  ...........
Dacthal and its mono- and di-acid degradates..............            X          1994            X          1998
1,3-Dichloropropene.......................................            X          2000            X          1998
DDE.......................................................            X          1988  ............  ...........
2,4-Dinitrotoluene........................................            X     1990/1992  ............  ...........
2,6-Dinitrotoluene........................................          * X          1990  ............  ...........
EPTC......................................................            X          1990            X          1999
Fonofos...................................................            X          1991         ** X          1996
Terbacil..................................................            X          1989            X          1998
1,1,2,2-Tetrachloroethane.................................            X          1986  ............  ...........
----------------------------------------------------------------------------------------------------------------
* Applies to a mixture of 98 percent 2,4-dinitrotoluene and 2 percent 2,6-dinitrotoluene.
** Health Risk Assessment; RED not completed due to pesticide cancellation.

    As noted in section II.E, EPA has prepared several technical health
effects support documents for the contaminants considered for this
round of regulatory determinations. These documents address the
exposure from drinking water and other media, toxicokinetics, hazard
identification, and dose-response assessment, and provide an overall
characterization of risk from drinking water.

B. Evaluation of Contaminant Occurrence and Exposure

    EPA used data from several sources to evaluate occurrence and
exposure for the 11 contaminants considered in these regulatory
determinations. The major or primary sources of the drinking water
occurrence data used to support these determinations include the
following sources:
     The first Unregulated Contaminant Monitoring Regulation
(UCMR 1),
     The Unregulated Contaminant Monitoring (UCM) program, and
     The National Inorganic and Radionuclide Survey (NIRS).
    In addition to these primary sources of occurrence data, the Agency
also evaluated supplemental sources of occurrence information. Section
III.B.1 of this action provides a brief summary of the primary sources
of drinking water occurrence data and section III.B.2 provides brief
summary descriptions of the supplemental sources of occurrence
information and/or data. A summary of the occurrence data and the
results or findings for each of the 11 contaminants considered for
regulatory determination is presented in Section IV.B, the contaminant
profiles section.
    1. Primary Data Sources. As previously mentioned, the primary
sources of the drinking water occurrence data used to support this
action are the UCMR 1, the UCM program, and NIRS. The following
sections provide a brief summary of the data sources and the approach
used to estimate a given contaminant's occurrence. Table 2 lists the
primary data sources the Agency used for each of the 11 contaminants
considered for regulatory determinations.

                        Table 2.--Primary Sources of Drinking Water Occurrence Data Used in the Regulatory Determination Process
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                Primary data sources
                                                                             ---------------------------------------------------------------------------
                                                                                UCMR 1                              UCM
                   Number                               Contaminant          --------------------------------------------------------------------
                                                                                List 1           List 2                                         NIRS
                                                                                assessment       screening      Round 1  cross   Round 2  cross
                                                                                monitoring         survey          section          section
--------------------------------------------------------------------------------------------------------------------------------------------------------
1...........................................  Boron.........................                                                                        1 X
2...........................................  Dacthal mono- and
3...........................................  di-acid degradates............               X
4...........................................  DDE...........................               X
5...........................................  1,3-Dichloropropene...........             2 X                                 X                X
6...........................................  2,4-Dinitrotoluene............               X
7...........................................  2,6-Dinitrotoluene............               X
8...........................................  EPTC..........................               X
9...........................................  Fonofos.......................                                X
10..........................................  Terbacil......................               X

11..........................................  1,1,2,2-Tetrachloroethane.....                                                 X                X
--------------------------------------------------------------------------------------------------------------------------------------------------------
1 For boron, EPA also considered the results of a study funded by AWWARF (Frey et al., 2004).
2 1,3-Dichloropropene was sampled as a UCM Round 1 and 2 analyte but due to sample degradation concerns the contaminant was re-analyzed using the
  samples provided by the small systems that participated in the UCMR 1 List 1 Assessment Monitoring.

    a. The Unregulated Contaminant Monitoring Regulation. In 1999, EPA
developed the UCMR program in coordination with the CCL and the
National Drinking Water Contaminant Occurrence Database (NCOD) to
provide national occurrence information on unregulated contaminants
(September 17, 1999, 64 FR 50556 (USEPA, 1999b); March 2, 2000, 65 FR
11372 (USEPA, 2000b); and January 11, 2001, 66 FR 2273 (USEPA, 2001b)).
EPA used data from the UCMR 1 program to evaluate occurrence for 9 of
the 11 contaminants considered for these regulatory determinations.
These 9 contaminants include the dacthal mono- and di-acid degradates,
DDE, 1,3-dichloropropene, 2,4-dinitrotoluene, 2,6-dinitrotoluene, EPTC,
fonofos, and terbacil.
    EPA designed the UCMR 1 data collection with three parts (or tiers)
primarily based on the availability of analytical methods. Occurrence
data for 8 of the 9 contaminants listed in the preceding paragraph are
from the first tier of UCMR (also known as UCMR 1 List 1 Assessment
Monitoring). Occurrence data for fonofos are from the second tier of
UCMR 1 (also known as the UCMR 1 List 2 Screening Survey). EPA has not
collected data as part of the third tier due to the lack of adequate
analytical methods.
    The UCMR 1 List 1 Assessment Monitoring was performed for a
specified number of chemical contaminants for which analytical methods
have been developed. EPA required all large\7\ PWSs, plus a
statistically representative national sample of 800 small \8\ PWSs to
conduct Assessment Monitoring.\9\ Approximately one-third of the
participating small systems were scheduled to monitor for these
contaminants during each calendar year from 2001 through 2003. Large
systems could conduct one year of monitoring anytime during the 2001-
2003 UCMR 1 period. EPA specified a quarterly monitoring schedule for
surface water systems and a twice-a-year, six-month interval monitoring
schedule for ground water systems. The objective of the UCMR 1 sampling
approach for small systems was to collect contaminant occurrence data
from a statistically selected, nationally representative sample of
small systems. The small system sample was stratified and population-
weighted, and included some other sampling adjustments such as
allocating a selection of at least 2 systems from each State. With
contaminant monitoring data from all large PWSs and a statistical,
nationally representative sample of small PWSs, the UCMR 1 List 1
Assessment Monitoring program provides a contaminant occurrence data
set suitable for national drinking water estimates.
---------------------------------------------------------------------------

    \7\ Systems serving more than 10,000 people.
    \8\ Systems serving 10,000 people or fewer.
    \9\ Large and small systems that purchase 100% of their water
supply were not required to participate in the UCMR 1 Assessment
Monitoring or the UCMR 1 Screening Survey.
---------------------------------------------------------------------------

    In total, 370,312 sample results have been collected under the UCMR
1 List 1 Assessment Monitoring program at approximately 3,083 large
systems and 797 small systems. Approximately 33,600 samples were
collected for each contaminant. The UCMR 1 List 1 Monitoring program
included systems from all 50 States, the District of Columbia, 4 U.S.
Territories, and Tribal lands in 5 EPA Regions. An additional 3,719
samples were collected for 1,3-DCP at all small systems that conducted
UCMR 1 List 1 Assessment Monitoring.
    In addition to the UCMR 1 List 1 Assessment Monitoring, EPA
required monitoring for selected contaminants (including fonofos) for
which analytical methods were developed but not widely used. Known as
the UCMR 1 List 2 Screening Survey, EPA randomly selected 300 public
water systems (120 large and 180 small systems) from the pool of
systems required to conduct UCMR 1 List 1 Assessment Monitoring. In
total, 29,765 sample results have been collected under the UCMR 1 List
2 Screening Survey from the participating large and small systems.
Approximately 2,300 samples were collected for each contaminant. The
UCMR 1 List 2 Screening Survey included systems from 48 States, 2 U.S.
Territories, and Tribal lands in 1 EPA Region. EPA used the occurrence
data from this survey to evaluate fonofos.
    EPA analyzed the UCMR 1 List 1 Assessment Monitoring and List 2
Screening Survey data to generate the following initial occurrence and
exposure summary statistics:
     The total number of systems and the total population
served by these systems,
     The number and percentage of systems with at least 1
observed detection that has a concentration greater than \1/2\ the HRL
and greater than the HRL (or in some cases greater than or equal to the
minimum reporting limit or MRL), and
     The number of people and percentage of the population
served by systems with at least one observed detection greater than \1/
2\ the HRL and greater than the HRL (or in some cases greater than or
equal to the MRL).\10\
---------------------------------------------------------------------------

    \10\ EPA's support documents (USEPA, 2006a and 2006b) provide
summary statistics for the median and 99th percentile concentrations
of all analytical detections and detailed occurrence results based
on UCMR data according to source water type (surface versus ground
water), system size, and State.
---------------------------------------------------------------------------

    The initial UCMR 1 summary occurrence statistics for dacthal mono-
and di-acid degradates, DDE, 1,3-dichloropropene, 2,4-dinitrotoluene,
2,6-dinitrotoluene, EPTC, fonofos, and terbacil are presented in
section IV.B of this action.
    b. The Unregulated Contaminant Monitoring Program Rounds 1 and 2.
In 1987, EPA initiated the UCM program to fulfill a 1986 SDWA Amendment
that required monitoring of specified unregulated contaminants to
gather information on their occurrence in drinking water for future
regulatory decision-making purposes. EPA used data from the UCM program
to evaluate

occurrence for 2 of the 11 contaminants considered for these regulatory
determinations. These two contaminants are 1,3-dichloropropene and
1,1,2,2-tetrachloroethane.
    EPA implemented the UCM program in two phases or rounds. The first
round of UCM monitoring generally extended from 1988 to 1992 and is
referred to as UCM Round 1 monitoring. The second round of UCM
monitoring generally extended from 1993 to 1997 and is referred to as
UCM Round 2 monitoring.
    UCM Round 1 monitored for 34 volatile organic compounds (VOCs),
including 1,3-dichloropropene and 1,1,2,2-tetrachloroethane (52 FR
25720 (USEPA, 1987)). UCM Round 2 monitored for 13 synthetic organic
compounds (SOCs), sulfate and the same 34 VOCs from UCM Round 1
monitoring (57 FR 31776 (USEPA, 1992a)).
    The UCM Round 1 database contains contaminant occurrence data from
38 States, Washington, DC, and the U.S. Virgin Islands. The UCM Round 2
database contains data from 34 States and several Tribes. Due to
incomplete State data sets, national occurrence estimates based on raw
(unedited) UCM Round 1 or Round 2 data could be skewed to low-
occurrence or high-occurrence settings (e.g., some States only reported
detections). To address potential biases in the data,\11\ EPA developed
national cross-sections from the UCM Round 1 and Round 2 State data
using an approach similar to that used for EPA's 1999 Chemical
Monitoring Reform (CMR), the first Six Year Review, and the first CCL
Regulatory Determinations. This national cross-section approach was
developed to support occurrence analyses and was supported by
scientific peer reviewers and stakeholders. This approach identified 24
of the original 38 States from the UCM Round 1 database and 20 of the
original 34 States from the UCM Round 2 data base for the national
cross-section.
---------------------------------------------------------------------------

    \11\ The potential bias in the raw UCM data are due to lack of
representativeness (since not all States provided UCM data) and
incompleteness (since some States that provided data had incomplete
data sets).
---------------------------------------------------------------------------

    Because UCM Round 1 and Round 2 data represent different time
periods and include occurrence data from different States, EPA
developed separate national cross-sections for each data set. The UCM
Round 1 national cross-section consists of data from 24 States, with
approximately 3.3 million total analytical data points from
approximately 22,000 unique PWSs. The UCM 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
UCM Round 1 and 2 national cross-sections represent significantly large
samples of national occurrence data. Within each cross-section, the
actual number of systems and analytical records for each contaminant
varies. The support document, ``The Analysis of Occurrence Data from
the Unregulated Contaminant Monitoring (UCM) Program and National
Inorganics and Radionuclides Survey (NIRS) in Support of Regulatory
Determinations for the Second Drinking Water Contaminant Candidate
List'' (USEPA, 2006c), provides a description of how the national
cross-sections for the Round 1 and Round 2 data sets were developed.
    EPA constructed the national cross-sections in a way that provides
a balance and range of States with varying pollution potential
indicators, a wide range of the geologic and hydrologic conditions, and
a very large sample of monitoring data points. While EPA recognizes
that some limitations exist, the Agency believes that the national
cross-sections do provide a reasonable estimate of the overall
distribution and the central tendency of contaminant occurrence across
the United States.
    EPA analyzed the UCM Round 1 and 2 National Cross-Section data to
generate the following initial occurrence and exposure summary
statistics:
     The total number of systems and the total population
served by these systems,
     The number and percentage of systems with at least 1
observed detection that has a concentration greater than \1/2\ the HRL
and greater than the HRL (or in some cases greater than or equal to the
MRL), and
     The number of people and percentage of the population
served by systems with at least 1 observed detection that has a
concentration greater than \1/2\ the HRL and greater than the HRL (or
in some cases greater than or equal to the MRL).\12\
---------------------------------------------------------------------------

    \12\ EPA's support documents (USEPA, 2006a and 2006c) provide
summary statistics for the median and 99th percentile concentrations
of all analytical detections and detailed occurrence results based
on the UCM Round 1 and 2 Nationals Cross-Sectons according to source
water type (surface versus ground water), system size, and State.
---------------------------------------------------------------------------

    The initial UCM summary occurrence statistics for 1,3-
dichloropropene and 1,1,2,2-tetrachloroethane are presented in section
IV.B of this action.
    c. National Inorganic and Radionuclide Survey. In the mid-1980's,
EPA conducted the NIRS to provide a statistically representative sample
\13\ of the national occurrence of inorganic contaminants in community
water systems (CWSs) served by ground water. EPA used data from NIRS,
as well as a supplemental survey, to evaluate occurrence for boron.
---------------------------------------------------------------------------

    \13\ NIRS was designed to provide results that are statistically
representative of natioal occurrence at CWSs using ground water
sources and is stratified based on system size (population served by
the system). Most of the NIRS data are from smaller systems (92
percent from systems serving 3,300 persons or fewer).
---------------------------------------------------------------------------

    The NIRS database includes 36 radionuclides and inorganic compounds
(IOCs), including boron. The NIRS provides contaminant occurrence data
from 989 ground water CWSs covering 49 States (all except Hawaii) and
does not include surface water systems. The survey focused on ground
water systems, in part because IOCs tend to occur more frequently and
at higher concentrations in ground water than in surface water. Each of
the 989 randomly selected CWSs was sampled at a single time between
1984 and 1986.
    EPA analyzed the NIRS data to generate the following occurrence and
exposure summary statistics for boron:
     The total number of systems and the total population
served by these systems,
     The number and the percentage of systems with at least 1
detection that has a concentration greater than \1/2\ the HRL and
greater than the HRL,
     The number of people and percentage of the population
served by systems with at least 1 observed detection that has a
concentration greater than \1/2\ the HRL and greater than the HRL.\14\
---------------------------------------------------------------------------

    \14\ EPA's support documents (USEPA, 2006a and 2006c) provide
the number and percentage of 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.
---------------------------------------------------------------------------

    Similar to the treatment of the UCM cross-section data, the actual
values for the NIRS analyses of boron are reported in section IV.B.
Because the NIRS data were collected in a randomly designed sample
survey, these summary statistics are representative of national
occurrence in ground water CWSs.
    One limitation of the NIRS is a lack of occurrence data for surface
water systems. To provide perspective on the occurrence of boron in
surface water systems relative to ground water systems, EPA reviewed
and took into consideration a recent boron occurrence survey funded by
American Water Works Association Research Foundation (AWWARF) (Frey et
al., 2004). A short description of the AWWARF study is provided in the
supplemental section

(section III.B.2) and the results of the AWWARF survey are presented in
section IV.B of this action.
    d. Presentation of Occurrence Data and Analytical Approach. As
noted previously, the occurrence values and summary statistics
presented in this action are the actual data from the UCMR 1, UCM, and
NIRS data sets. These occurrence values represent direct counts of the
number and percent of systems, and population served by systems, with
at least 1 analytical detection above some specified concentration
threshold. EPA considered this to be the most straightforward and
accurate way to present these data for the regulatory determination
process.
    While both UCMR 1 and UCM data could support more involved
statistical modeling to characterize occurrence based on mean (rather
than peak) concentrations, EPA chose not to perform this step for the
regulatory determinations proposed in this action. EPA believes that
presenting the actual results of the occurrence monitoring is straight-
forward and the use of an analysis based on peak concentrations
provides conservative estimates of occurrence and potential exposure
from drinking water. Given that the preliminary determinations for the
11 contaminants discussed in this action are negative, it is not
necessary to go beyond the conservative (peak concentration) approach
used for this analysis.
    2. Supplemental Data. The Agency evaluated several sources of
supplemental occurrence information to augment the primary drinking
water occurrence data, to evaluate the likelihood of contaminant
occurrence, and/or to more fully characterize a contaminant's presence
in the environment. Sections II.B.2.a through II.B.2.f provide brief
descriptions of the main supplemental information/data sources cited in
this action. Summarized occurrence findings from these supplemental
sources are presented in Section IV.B, the contaminant profiles
section. While the following descriptions cover the more commonly
referenced supplemental sources of information/data, they do not
include every study and survey cited in the contaminant discussions. A
more detailed discussion of the supplemental sources of information/
data that EPA evaluated for each contaminant can be found in the
comprehensive regulatory determination support document (USEPA, 2006a).
    a. USGS NAWQA Information/Data. The United States Geological Survey
(USGS) collects long-term and nationally consistent data describing
water quality in ground water and surface water. In 1991, USGS
implemented the National Water-Quality Assessment (NAWQA) Program for
10-year cyclical data collection and data analyses. During the first
cycle (1991-2001), the NAWQA program monitored 51 major watersheds and
aquifers (study units), which supply more than 60% of the nation's
drinking water and water used for agriculture and industry in the U.S.
(Hamilton et al., 2004). NAWQA has collected data from over 6,400
surface water and 7,000 ground water sampling points. USGS National
Synthesis teams prepare comprehensive analyses of data on topics of
particular concern. EPA evaluated information/data from the following
USGS National Synthesis reports/projects:
    (1) The NAWQA Pesticide National Synthesis Project. In 2003, USGS
posted the preliminary results from the first cycle of monitoring for
pesticides in streams and ground water. USGS considers these results to
be provisional. The results and the data can be accessed at http://ca.water.usgs.gov/pnsp/.
 Data are presented separately for surface

water and ground water, as well as bed sediments and biota. In each
case, results are subdivided by land use category. Land use categories
include agricultural, urban, mixed (deeper aquifers of regional extent
in the case of ground water), and undeveloped. In this action, the
NAWQA pesticide data for surface water are referenced as Martin et al.
(2003) and the ground water data are referenced as Kolpin and Martin
(2003).
    (2) The National Survey of MTBE and Other VOCs in Community
Drinking Water Sources (part of the VOC National Synthesis Project). In
2003, USGS published the survey findings for MTBE, other ether gasoline
oxygenates, and other volatile organic compounds (VOCs) in source water
used by CWSs in the United States. The survey was funded by AWWARF and
performed by USGS in collaboration with the Metropolitan Water District
of Southern California and the Oregon Health and Science University.
USGS performed the survey in two independent stages designed to provide
representative sampling of all CWSs in the United States (Random
Source-Water Survey) and to improve understanding of the temporal
variability of MTBE and other compounds in selected water sources
(Focused Source-Water Survey). Participating water utilities provided
samples that were analyzed for 66 VOCs. The random survey design
selected 954 CWSs to be nationally representative of surface and ground
waters sources used by CWSs. The focused survey studied source waters
from 134 CWSs suspected or known to contain MTBE. The reports/results
and data sets from the survey can be accessed at http://sd.water.usgs.gov/nawqa/vocns/nat_survey.html.
 The random survey

results can be found in the USGS Water Resources Investigations Report
02-4079, referenced as Grady (2003). The focused survey results can be
found in the USGS Water Resources Investigations Report 02-4084,
referenced as Delzer and Ivahnenko (2003a).
    b. USGS National Highway Runoff Data and Methodology Synthesis. In
addition to the NAWQA project, USGS has prepared additional surveys of
national contaminant occurrence. For the National Highway Runoff Data
and Methodology Synthesis, USGS conducted a review of 44 studies of
semi-volatile organic compounds (SVOCs) and VOCs in runoff conducted
since 1970. The USGS Synthesis sought to evaluate data quality
parameters for comparison between and among these studies, including
documentation of sampling protocols and methods, limits of reporting
and detection, and protocols of quality-control and quality-assurance.
The complete USGS report is Open-File Report 98-409 and is referenced
as Lopes and Dionne (1998).
    c. Toxics Release Inventory. EPA established the Toxics Release
Inventory (TRI) in 1987 in response to section 313 of the Emergency
Planning and Community Right-to-Know Act (EPCRA). EPCRA section 313
requires facilities to report to both EPA and the States annual
information on toxic chemical releases from facilities that meet
reporting criteria. EPCRA section 313 also requires EPA to make this
information available to the public through a computer database. This
database is accessible through TRI Explorer, which can be accessed at
http://www.epa.gov/triexplorer. In 1990 Congress passed the Pollution

Prevention Act, which required that additional data on waste management
and source reduction activities be reported under TRI. The TRI database
details not only the types and quantities of toxic chemicals released
to the air, water, and land by facilities, but also provides
information on the quantities of chemicals sent to other facilities for
further management (USEPA, 2002b and 2003b).
    Facilities are required to report releases and other waste
management activities related to TRI chemicals if they manufacture,
process, or otherwise use more than established threshold quantities of
these chemicals. Currently

for most chemicals, the thresholds are 25,000 pounds for manufacturing
and processing and 10,000 pounds for use. Although TRI can provide a
general idea of release trends, it is far from exhaustive and should
not be used to estimate general public exposure to a chemical (USEPA,
2002b and 2003b).
    d. Pesticides in Ground Water Database. The Pesticides in Ground
Water Database (PGWDB) is a compilation of data from ground water
studies conducted by Federal, State, and local governments, the
pesticide industry, and other institutions between 1971 and 1991
(USEPA, 1992b). Data from 68,824 wells in 45 states are included. The
vast majority of the wells (65,865) were drinking water wells.
Monitoring was conducted for 258 pesticides and 45 degradates. Not all
studies tested for every compound.
    e. The National Pesticide Survey. In 1990, EPA completed a national
survey of pesticides in drinking water wells. The purpose of the
National Pesticide Survey (NPS) was to determine the national
occurrence frequencies and concentrations of select pesticides in the
nation's drinking water wells, and to improve EPA's understanding of
how pesticide occurrence in ground water correlates with patterns of
pesticide usage and ground water vulnerability. The survey included
approximately 1,300 CWS wells and rural domestic wells. Sampling was
conducted between 1988 and 1990. Wells were sampled for 101 pesticides,
25 pesticide degradates, and nitrate. The survey targeted areas
representing a variety of pesticide usage levels and ground water
vulnerability. The survey was designed to provide a statistically
reliable estimate of pesticide occurrence in the nation's drinking
water wells (USEPA, 1990a).
    f. The AWWARF Boron Study. The American Water Works Research
Foundation funded a survey to evaluate the occurrence of boron (as well
as hexavalent chromium) in drinking water sources (Frey et al., 2004).
The AWWARF study recruited 189 PWSs representing 407 source waters in
41 states. Of the 407 source water sample kits distributed in 2003,
approximately 342 were returned. Of these 342 samples, 341 were
analyzed for boron. Approximately 67 percent (or 228) represented
ground water sources and 33 percent (or 113) represented surface water
sources. The results of the AWWARF survey for boron are presented in
section IV.B of this action.
    3. Supporting Documentation for Occurrence. As mentioned in section
II.E, EPA prepared several technical occurrence documents to support
this action. These technical occurrence documents include the
following:
     ``The Analysis of Occurrence Data from the Unregulated
Contaminant Monitoring (UCM) Program and National Inorganics and
Radionuclides Survey (NIRS) in Support of Regulatory Determinations for
the Second Drinking Water Contaminant Candidate List'' (USEPA, 2006c),
which this action refers to as the ``UCM and NIRS Occurrence Report.''
     ``The Analysis of Occurrence Data from the First
Unregulated Contaminant Monitoring Regulation (UCMR 1) in Support of
Regulatory Determinations for the Second Drinking Water Contaminant
Candidate List'' (USEPA, 2006b), which this action refers to as the
``UCMR 1 Occurrence Report.''
    The ``UCM and NIRS Occurrence Report'' provides more detailed
information about the UCM and the NIRS data, how EPA assessed the data
quality, completeness, and representativeness, and how the data were
used to generate estimates of contaminant occurrence. The ``UCMR 1
Occurrence Report'' provides more detailed information about the UCMR 1
data, how EPA assessed the data quality, completeness,
representativeness, and how the data were used to generate estimates of
contaminant occurrence.
    The comprehensive regulatory support document (USEPA, 2006a)
provides a summary of the results from the drinking water occurrence
analyses discussed in the aforementioned technical support documents,
as well as information on production and use, environmental releases,
and/or occurrence in ambient water, potential health effects, the
Agency's preliminary determination, and the rationale for the
determination.

IV. Preliminary Regulatory Determinations

A. Summary of the Preliminary Regulatory Determination

    The Agency has made a preliminary determination that each of the 11
contaminants listed in Table 3 do not meet all three of the SDWA
criteria (discussed in section II.C) and thus do not warrant regulation
with an NPDWR. Table 3 also summarizes the primary information used to
make these regulatory determinations. Section IV.B of this action
provides a more detailed summary of the information and the rationale
used by the Agency to reach its preliminary decisions. The Agency
solicits public comment on the preliminary determinations for these 11
contaminants.
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BILLING CODE 6560-50-C

B. Contaminant Profiles

    This section provides further details on the background, health,
and occurrence information that the Agency used to evaluate each of the
11 candidate contaminants considered for regulatory determination. For
each candidate, the Agency evaluated the available human and
toxicological data, derived a health reference level, and evaluated the
potential and/or likely occurrence and exposed population for the
contaminant in public water systems. The Agency used the findings from
these evaluations to determine whether the three SDWA statutory
requirements were satisfied.
    As discussed in section II.E, the Agency has also prepared a
regulatory support document (USEPA, 2006a) that provides more details
on the background, health, and occurrence information/analyses used to
evaluate and make preliminary determinations for these 11 candidates.
1. Boron
    a. Background. Boron, a metalloid, tends to occur in nature in the
form of borates (e.g., boric acid, borax, boron oxide). Man-made
releases are typically in the form of borates or boron halides (e.g.,
boron trichloride, boron trifluoride). Boron compounds are used in the
production of glass, ceramics, soaps, fire retardants, pesticides,
cosmetics, photographic materials, and high energy fuels (USGS, 2004;
ATSDR, 1992).
    Natural processes such as the weathering of rocks, volcanic
activity, and geothermal steam contribute to the release of boron in
the environment. Releases to the environment from human activities
occur through the production, use, and disposal of boron-containing
compounds (e.g., industrial emissions, fertilizer and herbicide runoff,
hazardous waste deposits, and municipal sewage) (HSDB, 2004a; ATSDR,
1992).
    Although quantitative data are not available on the man-made
releases of most borates in the United States, two boron halide
compounds, boron trichloride and boron trifluoride, are listed as
Toxics Release Inventory (TRI) chemicals. TRI data for boron
trichloride and boron trifluoride are reported for the years 1995 to
2003 (USEPA, 2006d). The TRI data show boron trichloride releases from
facilities in 6 States and indicate that air emissions account for all
of the total releases of boron trichloride (on- and off-site), which
generally fluctuated in the range of hundreds of pounds per year during
the period of record. The TRI data show boron trifluoride releases from
facilities in 14 States and indicate that air emissions also account
for nearly all of the boron trifluoride releases, which ranged in the
tens of thousands of pounds annually.
    b. Health Effects. The Institute of Medicine (IOM, 2001) of the
National Academies categorizes boron as a possible trace mineral
nutrient for humans. Boron is essential for plant growth and deficiency
studies in animals and humans have provided some evidence that low
intakes of boron affects cellular function and the activity of other
nutrients. It may interact with Vitamin D and calcium homeostasis,
influence estrogen metabolism, and play a role in cognitive function
(IOM, 2001). Iyengar et al. (1988) reported an average dietary intake
of 1.5 mg/day for male adults based on the Food and Drug Administration
(FDA) Total Diet Study (TDS).
    Some human oral data are available from cases where boron was
ingested as a medical treatment. When the amount ingested was less than
3.68 mg/kg, subjects were asymptomatic, while doses of 20 and 25 mg/kg
resulted in nausea and vomiting. Case reports and surveys of accidental
poisonings indicate that the lethal doses of boron range from 15 to 20
grams (approximately 200 to 300 mg/kg) for adults, 5 to 6 grams
(approximately 70 to 85 mg/kg) for children, and 2 to 3 grams
(approximately 30 to 45 mg/kg) for infants (USEPA, 2004b).
    The primary adverse effects seen in animals after chronic exposure
to low doses of boron generally involve the testes and developing
fetus. Chronic effects of dietary boron exposure in two-year studies
included testicular atrophy and spermatogenic arrest in dogs, decreased
food consumption,

suppressed growth, and testicular atrophy in rats, and decreased
survival, testicular atrophy, and interstitial cell hyperplasia in
mice. Although researchers observed some increases in tumor incidences
in the liver and in subcutaneous tissues in mice, based on comparisons
to historic controls, these tumors were determined not to be associated
with exposure to boron from boric acid (USEPA, 2004b). Boron is not
considered mutagenic and the Agency determined that there are
inadequate data to assess the human carcinogenic potential for boron
(USEPA, 2004c).
    In developmental studies with rats, mice, and rabbits, oral
exposure to boric acid resulted in decreased pregnancy rate, increased
prenatal mortality, decreased fetal weights, and increased
malformations in fetuses and pups. However, these reproductive effects
were associated with maternal toxicity including changes in maternal
organ weights, body weights, weight gain, and increased renal tubular
dilation and/or regeneration (Price et al., 1990, 1994, 1996; Heindel
et al., 1992, 1994; Field et al., 1989). Reproductive effects in males
were noted in the subchronic and chronic studies described in the
preceding paragraphs.
    The EPA RfD for boron is 0.2 mg/kg/day (USEPA, 2004c) based on
developmental effects in rats from two studies (Price et al., 1996;
Heindel et al., 1992). The RfD was derived using the benchmark dose
(BMD) method (bench mark dose level or BMDL from Allen et al., 1996).
EPA calculated the HRL of 1.4 mg/L or 1,400 [mu]g/L for boron using the
RfD of 0.2 mg/kg-day and a 20 percent screening relative source
contribution.
    EPA also evaluated whether health information is available
regarding the potential effects on children and other sensitive
populations. Studies in rats, mice, and rabbits identify the developing
fetus as potentially sensitive to boron. Price et al. (1996) identified
a LOAEL of 13.3 mg/kg-day and an NOAEL of 9.6 mg/kg-day in the
developing fetus, based on decreased fetal body weight in rats.
Accordingly, boron at concentrations greater than the HRL might have an
effect on prenatal development. Individuals with severely impaired
kidney function might also be sensitive to boron exposure since the
kidney is the most important route for excretion.
    c. Occurrence Analyses. The National Inorganics and Radionuclides
Survey (NIRS) included boron as an analyte. Using data from NIRS, EPA
performed an initial evaluation of occurrence and exposure at levels
greater than 700 [mu]g/L (\1/2\ the HRL) and greater than 1,400 [mu]g/L
(the HRL for boron). The NIRS data indicate that approximately 4.3
percent (or 43) of the 989 ground water PWSs sampled had detections of
boron at levels greater than 700 [mu]g/L, affecting approximately 2.9
percent of the population served (or 42,700 people from 1.48 million).
Approximately 1.7 percent (or 17) of 989 ground water PWSs sampled had
detections of boron at levels greater than 1,400 [mu]g/L, affecting
approximately 0.4 percent of the population served (6,400 people from
1.48 million) (USEPA, 2006a and 2006c).
    Because NIRS did not contain data for surface water systems, the
Agency evaluated the results of a survey funded by the American Water
Works Association Research Foundation (Frey et al., 2004) to gain a
better understanding of the potential occurrence of boron in surface
water systems. The AWWARF study recruited 189 PWSs representing 407
source waters that covered 41 states. Of these 407 PWS source water
samples, 342 were returned and 341 were analyzed for boron. Of these
341 samples, approximately 67 percent (or 228) represented ground water
sources and 33 percent (or 113) represented surface water sources. None
of the 113 surface water sources exceeded the boron HRL of 1,400 [mu]g/
L and the maximum concentration observed in surface water was 345
[mu]g/L. Extrapolation of the data indicates that 95 percent of the
ground water detections had boron levels less than 1,054 [mu]g/L; the
maximum observed concentration in ground water was approximately 3,300
[mu]g/L. Seven of the 228 ground water sources (from 5 systems) had
boron concentrations greater than 1,400 [mu]g/L (Seidel, 2006).
    d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate boron with an NPDWR. While boron was
found at levels greater than the HRL (and \1/2\ the HRL) in several of
the ground water systems surveyed by NIRS, it was not found at levels
greater than the HRL (or \1/2\ the HRL) in the surface waters sources
evaluated in the AWWARF study. Taking this surface water information
into account, the Agency believes that the overall national occurrence
and exposure from both surface and ground water systems together is
likely to be lower than the values observed for the NIRS ground water
data. Because boron is not likely to occur at levels of concern when
considering both surface and ground waters systems, the Agency believes
that a national primary drinking water regulation does not present a
meaningful opportunity for health risk reduction.
    The Agency encourages those States with public water systems that
have boron at concentrations above the HRL to evaluate site-specific
protective measures and to consider whether State-level guidance (or
some other type of action) is appropriate. The Agency also plans to
update the Health Advisory for boron to provide more recent health
information. The updated Health Advisory will provide information to
any States with public water systems that may have boron above the HRL.
2 and 3. Mono- and Di-Acid Degradates of Dimethyl
Tetrachloroterephthalate (DCPA)
    a. Background. Dimethyl tetrachloroterephthalate (DCPA), a
synthetic organic compound (SOC) marketed under the trade name
``Dacthal,'' is a pre-emergent herbicide historically used to control
weeds in ornamental turf and plants, strawberries, seeded and
transplanted vegetables, cotton, and field beans. As of 1990, more than
80 percent of its use was for turf, including golf courses and home
lawns (USEPA, 1990b). On July 27, 2005, in response to concerns about
groundwater contamination (especially for one of the DCPA degradates),
the Agency published a Federal Register notice announcing that the
registrant for Dacthal had voluntarily terminated a number of uses for
products containing DCPA (70 FR 43408; USEPA, 2005f). The only uses
retained were those for use on sweet potatoes, eggplant, kale and
turnips.
    DCPA is not especially mobile or persistent in the environment.
Biodegradation and volatilization are the primary dissipation routes.
Degradation of DCPA forms two breakdown products, the mono-acid
degradate (or monomethyl tetrachloroterephthalate or MTP) and the di-
acid degradate (tetrachloroterephthalic acid or TPA). The di-acid,
which is the major degradate, is unusually mobile and persistent in the
field, with a potential to leach into water (USEPA, 1998c).
    Several studies and reports provide estimates of the amount of DCPA
used during the 1990s in the United States. The Agency estimated that
1.6 million pounds of DCPA active ingredient a.i. were used annually in
the early 1990s (USEPA, 1998c). USGS estimated that approximately 998
thousand pounds of DCPA a.i. were used annually circa 1992 (Thelin and
Gianessi, 2000). The National Center for Food and Agricultural Policy
(NCFAP, 2004) estimates that approximately 1.7 million

pounds of DCPA a.i. were used in 1992 and approximately 600 thousand
pounds a.i. were used in 1997 (NCFAP, 2004). The NCFAP data suggest a
decrease in the use of DCPA from the early to the late 1990s.
    b. Health Effects. Currently, no subchronic or chronic studies are
available to assess the toxicological effects of MTP (the mono-acid
degradate) and 3 studies in rats (30 and 90-day feeding studies and a
one-generation reproductive study) are available for TPA (the di-acid
degradate). The effects of exposure were mild (weight loss and
diarrhea) and occurred at doses greater than or equal to 2,000 mg/kg/
day. No reproductive effects were observed.
    The present toxicity database for MTP and TPA is not sufficient to
derive RfDs for these two chemicals. However, since the available data
indicate that neither MTP nor TPA are more toxic than their parent
compound, DCPA, the Agency suggests that the RfD for the DCPA parent
would be protective against exposure from these two DCPA metabolites
(USEPA, 1998c). Both compounds are formed in the body from the DCPA
parent and therefore, the toxicity of these degradates is reflected in
the toxicity of the parent. The RfD for DCPA is 0.01 mg/kg/day based on
a chronic rat study (ISK Biotech Corporation, 1993) with a NOAEL of 1.0
mg/kg/day and an uncertainty factor of 100 for rat to human
extrapolation and intra-species variability.
    No carcinogenicity studies have been performed using either TPA or
MTP. Based on the cancer data for the parent and lack of mutagenicity
for TPA and DCPA, the Agency (USEPA, 2004d) concludes that TPA is
unlikely to pose a cancer risk. Klopman et al. (1996) evaluated the
carcinogenic potential of TPA based on its chemical and biological
properties, as well as by a variety of computational tools, and
determined that it did not present any substantial carcinogenic risk.
There was suggestive evidence that DCPA could be carcinogenic based on
an increased incidence of thyroid and liver tumors in rats. The
presence of hexachlorobenzene and dioxin as impurities in the material
tested could have contributed to the cancer risk.
    Using the DCPA RfD of 0.01 mg/kg/day (USEPA, 1994) and a 20 percent
screening relative source contribution, the Agency calculated an HRL of
0.07 mg/L or 70 [mu]g/L for DCPA and used this HRL for TPA and MTP.
    EPA also evaluated whether health information is available
regarding the potential effects on children and other sensitive
populations. There are no data that identify a particular sensitive
population for DCPA exposure. Results of a single developmental study
indicate that exposure to pregnant dams with doses less than or equal
to 2,500 mg/kg/day of TPA via gavage did not have an adverse effect on
the fetus. EPA did not identify any data that suggest gender-related
differences in toxicity or sensitivity in the elderly.
    c. Occurrence. EPA included the DCPA mono- and di-acid degradates
(MTP and TPA) as analytes in the UCMR 1. The analysis results reported
for UCMR 1 are the sum of both the mono- and di-acid degradates. EPA
converted the analysis result for the degradates to the parent DCPA
equivalent and performed an initial evaluation of occurrence and
exposure at levels greater than 35 [mu]g/L (\1/2\ the HRL) and greater
than 70 [mu]g/L (the HRL). As previously discussed, EPA used the HRL
derived for the DCPA parent because it includes the toxicity for the
mono- and di-acid degradates. While the UCMR 1 data indicate that the
DCPA degradates were the most commonly reported analytes in the
monitoring survey (detected at an MRL of 1 [mu]g/L in 772 samples from
175 of the 3,868 PWSs sampled), very few systems exceeded the health
level of concern. PWSs with detections were found in 24 States and 1
Territory. The UCMR 1 data indicate that approximately 0.05 percent (or
2) of the 3,868 PWSs sampled had a detection of the DCPA degradates at
levels greater than 35 [mu]g/L, affecting approximately 0.33 percent of
the population served (or 739,000 people from 225 million).
Approximately 0.03 percent (or 1) of the 3,868 PWSs sampled have a
detection of the DCPA degradates at levels greater than 70 [mu]g/L,
affecting less than 0.01 percent of the population served (or 500
people from 225 million) (USEPA, 2006a and 2006b).
    EPA also evaluated several sources of supplemental occurrence
information for the DCPA parent, the mono-acid degradate and/or the di-
acid degradate. These supplemental sources include:
     The National Pesticide Survey (NPS),
     The provisional pesticide results from the 1992-2001 USGS
NAWQA survey of ambient surface and ground waters across the U.S., and
     Studies performed by the DCPA or dacthal registrant.
    As part of the National Pesticide Survey, EPA collected samples
from approximately 1,300 community water systems and rural drinking
water wells between 1988 and 1990. The NPS included monitoring for the
DCPA parent and the di-acid degradate. The DCPA parent was not detected
in any wells (using a detection limit of 0.06 [mu]g/L). While the di-
acid degradate was detected in 49 of 1,347 wells (using a detection
limit of 0.1 [mu]g/L), the maximum reported concentration of 7.2 [mu]g/
L did not exceed the HRL of 70 [mu]g/L (USEPA, 1990a).
    The USGS NAWQA program included the DCPA parent and the mono-acid
degradate as analytes in its 1992-2001 monitoring survey of ambient
surface and ground waters across the United States. EPA evaluated the
results of the provisional data, which are available on the Web (Martin
et al., 2003; Kolpin and Martin, 2003). While the USGS detected the
DCPA parent in both surface and ground waters, at least 95 percent of
the samples from the various land use settings were less than or equal
to 0.007 [mu]g/L. The estimated maximum surface water concentration, 40
[mu]g/L (agricultural setting), and the estimated maximum ground water
concentration, 10 [mu]g/L (agricultural setting), are both less than 70
[mu]g/L (the DCPA HRL). While the USGS detected the mono-acid degradate
in both surface waters and ground waters, at least 95 percent of the
samples from the various land use settings were less than 0.07 [mu]g/L
(the reporting limit for the mono-acid degradate). The maximum surface
water concentration, 0.43 [mu]g/L (agricultural setting), and the
maximum ground water concentration, 1.1 [mu]g/L (agricultural setting),
are both less than 70 [mu]g/L (the DCPA HRL, which includes the
toxicity of the degradates).
    Beginning in 1992, the registrant for DCPA performed two small-
scale ground water occurrence studies in New York and California over a
period of 17 and 22 months, respectively. The registrant monitored for
the DCPA parent and both of its degradates. The average reported
values, which are the sum of the parent and its degradates, were 50.36
[mu]g/L in New York and 12.75 [mu]g/L in California. Neither average
value exceeded the HRL of 70 [mu]g/L (USEPA, 1998c).
    d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate the DCPA mono-acid degradate and/or the
DCPA di-acid degradate with an NPDWR. Because these degradates appear
to occur infrequently at health levels of concern in PWSs, the Agency
believes that a national primary drinking water regulation does not
present a meaningful opportunity for health risk reduction. While the
Agency recognizes that these degradates have been detected in the PWSs
monitored under the UCMR 1, only 1 PWS had a detect above the HRL.

    The Agency encourages those States with public water systems that
have detects for these degradates to evaluate site-specific protective
measures and to consider whether State-level guidance (or some other
type of action) is appropriate. The Agency also plans to update the
Health Advisory for the DCPA parent to include the mono and di acid
degradates, as well as any recent health information related to these
compounds. The updated Health Advisory will provide information to any
States with public water systems that may have DCPA degradates at
levels above the HRL.
4. 1,1-Dichloro-2,2-bis(p-chlorophenyl) ethylene (DDE)
    a. Background. DDE is a primary metabolite of DDT,\15\ a pesticide
once used to protect crops and eliminate disease-carrying insects in
the U.S. until it was banned in 1973. DDE itself has no commercial use
and is only found in the environment as a result of contamination and/
or breakdown of DDT. While DDE tends to adsorb strongly to surface soil
and is fairly insoluble in water, it may enter surface waters from
runoff that contains soil particles contaminated with DDE. In both soil
and water, DDE is subject to photodegradation, biodegradation, and
volatilization (ATSDR, 2002).
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    \15\ 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane.
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    b. Health Effects. DDE is not produced as a commercial product.
This has limited the numbers of conventional studies that have been
performed to assess toxicological properties. Limited data on DDE,
mostly from a National Cancer Institute (NCI) bioassay, suggest that
the liver is the primary target organ in mammalian species. However,
the NCI study did not evaluate a full array of noncancer endpoints.
There is an RfD of 0.0005 mg/kg/day for the parent pesticide DDT based
on a NOAEL of 0.05 mg/kg/day from a dietary subchronic study (USEPA,
1996b). In this study, liver lesions were identified at a LOAEL of 0.25
mg/kg/day. Data on DDT identify effects on the nervous and hormonal
systems as adverse effects that might also be seen with DDE because it
is one of DDT's primary metabolites. The limited data for DDE suggest
that any effects on the nervous system are less severe than those seen
with DDT. Endocrine effects from DDE are discussed in this section.
    Based on animal studies DDE is likely to be carcinogenic to humans.
This classification is based on increases in the incidence of liver
tumors, including carcinomas, in two strains of mice and in hamsters
after dietary exposure to DDE. Some epidemiological studies suggest a
possible association of the levels of DDE in serum with breast cancer.
However, other studies with similar methodologies do not show any
association. DDE was mutagenic in mouse lymphoma L5178Y and Chinese
hamster V79 cells but negative in the Ames assay. In the 1988 IRIS, EPA
calculated an oral slope factor of 0.34 (mg/kg/day)-1 for
DDE (USEPA, 1988a). For this regulatory determination, EPA calculated
an oral slope factor from the same data set (from the 1988 IRIS) using
the EPA 1999 Cancer Guidelines (USEPA, 1999a). The revised slope factor
is 1.67 x 10-1 (mg/kg/day)-1 resulting in a one-
in-a-million cancer-risk (HRL) of 0.2 [mu]g/L.
    There are some indications that DDE has an adverse impact on the
immune system (Banerjee et al., 1996). Oral exposures to 22 mg/kg/day
for 6 weeks suppressed serum immunoglobin levels and antibody titers.
Inhibition of leucocytes and macrophage migration were observed at the
cellular level. Considerable evidence exists that DDE can act as an
endocrine disruptor since it binds to the estrogen and androgen
receptors. DDE has a stronger affinity for the androgen receptor than
for the estrogen receptor. It competes with testicular hormones for the
androgen receptor leading to receptor-related changes in gene
expression (Kelce et al., 1995).
    EPA evaluated whether health information is available regarding the
potential effects on children and other sensitive populations. Children
and adolescents may be sensitive populations for exposure to DDE due to
its endocrine disruption properties. Some data suggest that DDE can
delay puberty in males (ATSDR, 2002).
    c. Occurrence. EPA included DDE as an analyte in the UCMR 1.
Because the HRL for DDE (0.2 [mu]g/L) is lower than the minimum
reporting limit (MRL) used for monitoring (0.8 [mu]g/L), EPA used the
MRL value to evaluate occurrence and exposure. The MRL is within the
10-4 to the 10-6 cancer risk range for DDE. In
evaluating the UCMR 1 data, EPA found that approximately 0.03 percent
(or 1) of the 3,867 PWSs sampled had a detection of DDE at the MRL of
0.8 [mu]g/L, affecting approximately 0.01 percent of the population
served (or 18,000 people from 226 million) (USEPA, 2006a and 2006b).
    The USGS NAWQA program included DDE as an analyte in its 1992-2001
monitoring survey of ambient surface and ground waters across the
United States. EPA evaluated the results of the provisional data, which
are available on the Web (Martin et al., 2003; Kolpin and Martin,
2003), as a supplemental source of occurrence information. While the
USGS detected DDE in both surface and ground waters, 95 percent of the
samples from the various land use settings were less than 0.006 [mu]g/L
(the USGS reporting limit). The maximum surface water concentration,
0.062 [mu]g/L (agricultural setting), and the maximum ground water
concentration, 0.008 [mu]g/L (agricultural setting), are both less than
0.2 [mu]g/L (the DDE HRL).
    d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate DDE with an NPDWR. Because DDE appears to
occur infrequently at levels of concern in PWSs, the Agency believes
that a national primary drinking water regulation does not present a
meaningful opportunity for health risk reduction. DDE was detected in
only one of the PWSs monitored under the UCMR 1 at a level greater than
the MRL (0.8 [mu]g/L), a concentration that is within the
10-4 to the 10-6 cancer risk range. In addition,
ambient water data from the USGS indicate that the maximum
concentrations detected in surface and ground water were less than the
HRL of 0.2 [mu]g/L.
    EPA recognizes that DDE is listed as a probable human carcinogen.
For this reason, the Agency encourages those States with public water
systems that might have DDE above the HRL to evaluate site-specific
protective measures and to consider whether State-level guidance (or
some other type of action) is appropriate.
5. 1,3-Dichloropropene (1,3-DCP; Telone)
    a. Background. 1,3-Dichloropropene (1,3-DCP), a synthetic volatile
organic compound, is used as a pre-plant soil fumigant to control
nematodes and other pests in soils to be planted with all types of food
and feed crops. 1,3-DCP is typically injected 12'' to 18'' beneath the
soil surface and can only be used by certified handlers (USEPA, 1998b).
To mitigate risks to drinking water, 1999 labeling requirements
restrict the use of 1,3-DCP:
     In areas with shallow ground water and vulnerable soils in
certain northern tier States (ND, SD, WI, MN, NY, ME, NH, VT, MA, UT,
and MT);
     In fields within 100 feet of a drinking water well; and
     In areas overlying karst \16\ geology.
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    \16\ Karst is a type of typography that is formed by the
dissolution and collapse of soluble rocks (typically limestone and
dolomite). According to the Karst Waters Institute, as excerpted by
USGS (2006), common geological characteristics of karst regions that
influence human use of its land and water resources include ground
subsidence, sinkhole collapse, ground water contamination, and
unpredictable water supply.

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    Estimates of national annual use during the 1990s vary widely, from
approximately 23 to 40 million pounds of active ingredient a.i. Based
on information from a 1991 data call-in and other sources, EPA
estimates that approximately 23 million pounds of 1,3-DCP a.i. were
used annually from 1990 to 1995 (USEPA, 1998b). NCFAP (2004) estimates
that approximately 40 million pounds a.i. were used in 1992 and
approximately 35 million pounds a.i. were used in 1997.
    1,3-Dichloropropene is listed as a TRI chemical and releases are
reported from facilities in 17 States over a time period covering 1988
to 2003 (although not all States had facilities reporting releases
every year) (USEPA, 2006e). Air emissions appear to account for most of
the on-site (and total) releases and generally declined between 1988
and 2003. A sharp decrease in air emissions is evident between 1995 and
1996. Surface water discharges are minor compared to air emissions and
no obvious trend is evident between 1988 and 2003. Reported underground
injection, releases to land, and off-site releases are generally
insignificant.
    b. Health Effects. Chronic and subchronic exposures to 1,3-DCP at
doses of 12.5 mg/kg/day and above in animal dietary studies indicate
that 1,3-DCP is toxic to organs involved in metabolism (liver),
excretion of conjugated metabolites (e.g., urinary bladder and the
kidney) and organs along the portals of entry (e.g., forestomach for
oral administration; mucous membrane of the nasal passage and lungs for
inhalation exposure). Exposure to 1,3-DCP has not been shown to cause
reproductive or developmental effects. Neither reproductive nor
developmental toxicity were observed in a two-generation reproductive
study in rats or in developmental studies in rats and rabbits at
maternal inhalation concentrations up to 376 mg/m\3\ (USEPA, 2000a).
Even concentrations that produced parental toxicity did not produce
reproductive or developmental effects (USEPA, 2000a).
    An RfD of 0.03 mg/kg/day for 1,3-DCP (USEPA, 2000a) has been
established using a benchmark dose (BMD) analysis based on a two-year
chronic bioassay (Stott et al., 1995) in which chronic irritation
(forestomach hyperplasia) and significant body weight reduction were
the critical and co-critical effects, respectively. A reference
concentration (RfC) of 0.02 mg/m\3\ was derived from a two-year
bioassay (Lomax et al., 1989), which observed histopathology in the
nasal epithelium.
    Under the proposed cancer risk assessment guidelines, the weight of
evidence for evaluation of 1,3-DCP's ability to cause cancer suggest
that it is likely to be carcinogenic to humans (USEPA, 2000a). This
characterization is supported by tumor observations in chronic animal
bioassays for both inhalation and oral routes of exposure.
    The oral cancer slope factors calculated from chronic dietary,
gavage and inhalation data ranged from 5 x 10-\2\ to 1 x
10-\1\ (mg/kg/day)-\1\. Due to uncertainties in
the delivered doses in some studies, EPA (IRIS) recommended using the
oral slope factor of 1 x 10-\1\ (mg/kg/day)-\1\
from an NTP (1985) study. Using this oral slope factor, EPA calculated
an HRL of 0.4 [mu]g/L at the 10-\6\ cancer risk level.
    EPA also evaluated whether health information is available
regarding the potential effects on children and other sensitive
populations. No human or animal studies are available that have
examined the effect of 1,3-DCP exposure on juvenile subjects.
Therefore, its effects on children are unknown. Developmental studies
in rats and rabbits show no evidence of developmental effects and
therefore it is unlikely that 1,3-DCP causes developmental toxicity.
    c. Occurrence. EPA included 1,3-DCP as an analyte in the UCM Round
1 and UCM Round 2 surveys. The MRLs for UCM Round 1 ranged from 0.02 to
10 [mu]g/L and the MRLs for UCM Round 2 ranged from 0.08 to 1 [mu]g/L.
EPA also analyzed for 1,3-DCP using the samples from the small systems
that were included in the UCMR 1 survey. The MRL used for the UCMR 1
survey was 0.5 [mu]g/L. Because some of these reporting limits exceeded
the thresholds of interest, the occurrence analyses may result in an
underestimate of systems affected (USEPA, 2006a, 2006b and 2006c).
However, the MRL values used for UCM Round 1 and UCM Round 2 as well as
UCMR 1 are within the 10-\4\ to the 10-\6\ cancer
risk range.
    The UCM Round 1 Cross Section data indicate that approximately 0.16
percent (or 15) of the 9,164 PWSs sampled had detections of 1,3-DCP at
levels greater than 0.2 [mu]g/L (\1/2\ the HRL), affecting
approximately 0.86 percent of the population served (or 438,000 of 51
million). The UCM Round 1 Cross Section data also indicate the same
values when the data are analyzed using 0.4 [mu]g/L (the HRL). That is,
0.16 percent (or 15) of 9,164 PWSs sampled had detections greater than
0.4 [mu]g/L (the HRL), affecting approximately 0.86 percent of the
population served (or 438,000 of 51 million people). The 99th
percentile of all detections is 2 [mu]g/L and the maximum reported
value is 2 [mu]g/L.
    The UCM Round 2 Cross Section data indicate that approximately 0.30
percent (or 50) of the 16,787 PWSs sampled had detections of 1,3-DCP at
levels greater than 0.2 [mu]g/L (\1/2\ the HRL), affecting
approximately 0.42 percent of the population served (or 193,000 of 46
million). The UCM Round 2 Cross Section data indicate that
approximately 0.23 percent (or 38) of the 16,787 PWSs sampled had
detections of 1,3-DCP at levels greater than 0.4 [mu]g/L (the HRL),
affecting approximately 0.33 percent of the population served (or
152,000 of 46 million). The 99th percentile of all detections is 39
[mu]g/L and the maximum reported value is 39 [mu]g/L.
    Because the sample preservative used may have resulted in potential
underestimates of occurrence for the UCM Rounds 1 and 2 data, EPA
subsequently analyzed for 1,3-DCP using the samples provided by 796 of
the small systems included in the recent UCMR 1 survey. None of the
3,719 samples from these 796 small systems (serving a population of 2.8
million) had detects of 1,3-DCP at levels greater than 0.5 [mu]g/L (the
minimum reporting limit used for the analysis of 1,3-DCP and a level
that is slightly higher than the HRL).
    EPA also evaluated several sources of supplemental information,
which included:
     The National Pesticide Survey,
     The Pesticides in Ground Water Database,
     A well water survey submitted by the registrant of Telone
(1,3-DCP),
     The USGS VOC National Synthesis Random Source Water
Survey, and
     The USGS VOC National Synthesis Focused Source Water
Survey.
    As part of the National Pesticide Survey, EPA collected samples
from approximately 1,300 community water systems and rural drinking
water wells between 1988 and 1990. The NPS included cis and trans 1,3-
DCP as analytes in the monitoring survey. Neither compound was detected
in the survey using a minimum reporting limit of 0.010 [mu]g/L (USEPA,
1990a).
    The Pesticides in Ground Water Database (USEPA, 1992b) indicates
that 1,3-DCP was found in 6 of 21,270 ground water wells sampled in 7
States. The 6 wells with positive detections for 1,3-DCP included 3
wells in California (at concentrations ranging from 0.890 to 31.0
[mu]g/L), 2 wells in Florida (at concentrations of 0.279 to 7.83 [mu]g/
L), and 1 well in Montana (at concentrations of 18 to 140 [mu]g/L).
While most or all of these 6 wells had

concentrations greater than the HRL for 1,3-DCP, the overall percentage
of positive wells detections was less than 0.1 percent.
    In 1998, the registrant for Telone (1,3-DCP) submitted a private
well water study to the Agency. The well water survey covered 5 regions
where Telone was used intensively and evaluated 518 wells (~5,800
samples) for the presence of 1,3-DCP. Of the 518 wells, 65 had
detectable levels of 1,3-DCP and/or its metabolites at levels greater
than 0.015 [mu]g/L (the detection limit for 1,3-DCP was 0.015 [mu]g/L
and the metabolites were 0.023 [mu]g/L). None of the wells exceeded 0.2
[mu]g/L (a level half the EPA-derived HRL for 1,3-DCP) (USEPA, 2004e
and 2004f).
    For the Random Source Water Survey, the USGS collected samples from
954 source waters that supply community water systems between 1999 and
2000. For the Focused Source Water Survey, the USGS collected 451
samples from 134 source waters that supply community water systems
between 1999 and 2001. The USGS included 1,3-DCP as an analyte in both
surveys. The USGS did not detect 1,3-DCP in any of the source water
samples from the Random Source Water Survey using a reporting limit of
0.2 [mu]g/L (a level that is one-half the HRL for 1,3-DCP). In
addition, the USGS did not detect 1,3-DCP in any of the source water
samples in the Focused Source Water Survey using a detection limit of
0.024 [mu]g/L for cis-1,3-dichloropropene and 0.026 [mu]g/L for trans-
1,3-dichloropropene (levels that are about 16 times lower than the HRL
for 1,3-DCP) (Ivahnenko et al., 2001; Grady, 2003; Delzer and
Ivahnenko, 2003a).
    d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate 1,3-DCP with an NPDWR. Because 1,3-DCP
appears to occur infrequently at health levels of concern in PWSs, the
Agency believes that a national primary drinking water regulation does
not present a meaningful opportunity for health risk reduction. While
1,3-DCP was detected in the UCM Round 1 (late 1980s) and the UCM Round
2 (mid 1990s) surveys, it was not detected in a subsequent evaluation
of 796 small systems from the UCMR 1 survey. In addition, the USGS did
not detect 1,3-DCP in two occurrence studies performed between 1999 and
2001 using monitoring levels that were lower than the HRL. EPA believes
the 1999 pesticide labeling requirements, which are intended to
mitigate risks to drinking water, may be one reason for the lack of
occurrence of 1,3-DCP at levels of concern in subsequent monitoring
surveys.
    EPA recognizes that 1,3-dichloropropene is listed as a probable
human carcinogen. For this reason, the Agency encourages those States
with public water systems that may have 1,3-dichloropropene above the
HRL to evaluate site-specific protective measures and to consider
whether State-level (or some other type of action) is appropriate. The
Agency also plans to update the Health Advisory document for 1,3-DCP to
provide more recent health information. The updated Health Advisory
will provide information to any States with public water systems that
may have 1,3-DCP above the HRL.
6 and 7. 2,4- and 2,6-Dinitrotoluenes (2,4- and 2,6-DNT)
    a. Background. 2,4- and 2,6-dinitrotoluene (DNT), semi-volatile
organic compounds, are two of 6 isomers of dinitrotoluene.
Dinitrotoluenes are used in the production of polyurethane foams,
automobile air bags, dyes, ammunition, and explosives, including
trinitrotoluene or TNT (HSDB, 2004b and 2004c; ATSDR, 1998). Neither
2,4-nor 2,6-DNT occur naturally. They are generally produced as
individual isomers or as a mixture called technical grade DNT (tg-DNT).
Technical grade DNT primarily contains a mixture of 2,4-DNT and 2,6-DNT
with the remainder consisting of the other isomers and minor
contaminants such as TNT and mononitrotoluenes (HSDB, 2004b).
    No recent quantitative estimates of DNT production or use are
available. The Hazardous Substances Data Bank (HSDB, 2004b) cites a
1980 EPA Ambient Water Quality Criteria Document that places combined
2,4- and 2,6-DNT production at 272,610,000 pounds in 1975.
    Both 2,4-DNT and 2,6-DNT are listed as TRI chemicals. TRI data for
2,4-DNT are reported from facilities in 21 States over a time period
covering 1988 to 2003. Total releases nationally in 2003 were 14,899
lbs. Releases of all kinds (off-site releases and on-site air, surface,
underground injection, and land releases) declined in the early 1990s,
and then peaked again around 1999-2001. On-site air emissions and
surface water releases of 2,4-DNT were generally the most consistent
(least fluctuating) types of releases, with surface water releases
generally declining over the period on record (USEPA, 2006f).
    TRI data for 2,6-DNT are reported from facilities in 10 States over
a time period covering 1988 to 2003 (with no more than 9 States having
reporting facilities in any one year). Total reported releases for 2003
were 10,937 lbs. Trends for 2,6-DNT are similar to those for 2,4-DNT.
The TRI data for 2,6-DNT show a trend of declining releases in the late
1980s and early 1990s, and a subsequent peak around 1999-2001. On-site
air emissions and surface water discharges are the most consistent
types of release for 2,6-DNT and surface water discharges exhibit a
declining trend (USEPA, 2006f).
    In addition, TRI lists mixed DNT isomer releases as a separate
category over the same time period (1990-2003). TRI releases of mixed
isomers were reported from facilities in 9 States, with no more than 7
States having reporting facilities in any one year. Total releases in
2003 were 13,790 lbs. Underground injections made up the bulk of on-
site releases during the 1990s, but diminished thereafter. Air
emissions remained relatively constant. Surface water discharges and
releases to land were generally insignificant but peaked in 2003. Off-
site releases varied widely. Total releases peaked in 1993 and 1997,
and generally diminished in recent years (USEPA, 2006f).
    b. Health Effects. In experimental animal studies, 2,4- and 2,6-DNT
appear to be acutely toxic at moderate to high levels
(LD50's \17\ ranging from 180 to 1,954 mg/kg) when
administered orally. In subacute studies (4 weeks) conducted by Lee et
al. (1978), dogs, rats, and mice were fed 2,4-DNT and studied for toxic
effects. A NOAEL of 5 mg/kg/day was established; decreased body weight
gain and food consumption, neurotoxic signs, and lesions in the brain,
kidneys, and testes occurred at 25 mg/kg/day (the highest dose tested).
---------------------------------------------------------------------------

    \17\ LD50 = An estimate of a single dose that is
expected to cause the death of 50% of the exposed animals. It is
derived from experimental data.
---------------------------------------------------------------------------

    Subchronic studies in mice, rats, and dogs that administered 2,4-
and 2,6-DNT in the diet produced similar effects in all species. All
species exposed to 2,4-DNT exhibited methemoglobinemia, anemia, bile
duct hyperplasia sometimes accompanied by hepatic degeneration, and
depressed spermatogenesis. Neurotoxicity and renal degeneration
occurred in dogs at a dose level of 20 mg/kg/day of 2,6-DNT (Lee et
al., 1976). At a dose level of 25 mg/kg/day of 2,4-DNT, male and female
dogs developed impaired muscle movement and paralysis,
methemoglobinemia, aspermatogenesis, hemosiderosis of the spleen and
liver, cloudy swelling of the kidneys, and lesions of the brain (Ellis
et al., 1985).

These doses were determined to be LOAELs for these studies.
    2,4-DNT has been shown to cause reproductive effects in rats, mice,
and dogs (Ellis et al., 1979; Lee et al., 1985; Hong et al., 1985;
Ellis et al., 1985). Ellis et al. (1979) observed effects in rats
following dietary exposure after a dose of 35 mg/kg/day but not 5 mg/
kg/day over 3 generations. Male mice fed 2,4-DNT for 13 weeks exhibited
testicular degeneration and atrophy and decreased spermatogenesis at 95
mg/kg/day (Hong et al., 1985). In another reproductive study, dogs
exhibited mild to severe testicular degeneration and reduced
spermatogenesis (Ellis et al., 1985) when administered 2,4-DNT in
capsules at 25 mg/kg/day. There are currently no studies of the
reproductive or developmental toxicity of 2,6-DNT although a subchronic
study in dogs identified atrophy of spermatogenic cells in males
suggesting a one- or two-generation study as a data need for 2,6-DNT.
    Some studies evaluated the effects of DNT in the form of a
technical mixture (tg-DNT). In a study by Price et al. (1985), the
teratogenic potential of tg-DNT (containing approximately 76 percent
2,4-DNT and 19 percent 2,6-DNT) was investigated in rats. The study was
conducted in two phases to evaluate the possible teratogenicity of DNT
as well as DNT effects on postnatal development. For the first phase,
rats were administered 0, 14, 35, 37.5, 75, 100, or 150 mg/kg/day of
DNT in corn oil by gavage. In the postnatal phase, rats were
administered 14, 35, 37.5, 75, or 100 mg/kg/day of DNT in corn oil by
gavage. The NOAEL and LOAEL for developmental toxicity were 14 and 35
mg/kg/day, respectively, based on significant increases in relative
liver and spleen weight in the fetuses of dams administered DNT at
levels of 35 mg/kg/day or greater. No teratogenic toxicity was seen in
the study rats.
    In chronic exposures, oral dietary administration of 2,4-DNT to
dogs primarily affected the nervous system, erythrocytes, and biliary
tract (Ellis et al., 1979, 1985). Based on neurotoxicity, hematologic
changes, and effects on the bile ducts in dogs, the LOAEL was
determined to be 1.5 mg/kg/day and the NOAEL was 0.2 mg/kg/day. EPA
established an RfD of 0.002 mg/kg/day for 2,4-DNT (USEPA, 1992c) based
on this study. An uncertainty factor of 100, to account for
interspecies and intraspecies variability, was applied to derive the
RfD.
    EPA established an RfD of 0.001 mg/kg/day for 2,6-DNT (USEPA,
1992c). This RfD was also based on neurotoxicity, Heinz body formation,
biliary tract hyperplasia, liver and kidney histopathology, and death
in beagle dogs that were fed gelatin capsules containing 2,6-DNT daily
for up to 13 weeks (Lee et al., 1976). The NOAEL for this study was 4
mg/kg/day, and an uncertainty factor of 3,000 (100 for inter- and
intra-species variability, 10 for the use of a subchronic study, 3 to
account for the limited database) was applied to derive the RfD.
    DNT is likely to be carcinogenic to humans (classified as a B2
carcinogen; USEPA, 1990c). This is based on significant increases in
hepatocellular carcinoma and mammary gland tumors in female rats fed
DNT (98 percent 2,4-DNT with 2 percent 2,6-DNT) in the diet in a two-
year study (Ellis et al., 1979). The tumor incidence in the female rats
was used to establish a slope factor of 6.67 x 10-1
according to the 1999 EPA guidelines. Concentrations of 5 [mu]g/L, 0.5
[mu]g/L, and 0.05 [mu]g/L are associated with carcinogenic risks of
10-4, 10-5, and 10-6 respectively.
There were no studies found in the literature that evaluated the
effects of 2,4- or 2,6-DNT on children. There is evidence that the pups
and fetuses from dams administered tg-DNT had significant increases in
relative liver and spleen weights (Price et al., 1985). DNT toxicity
may be different in children, compared to adults, since it undergoes
bioactivation in the liver and by the intestinal microflora (ATSDR,
1998). Newborns may be more sensitive to DNT-related methemoglobinemia
because an enzyme that protects against increased levels of
methemoglobin is inactive for a short duration immediately after birth
(Gruener 1976; ATSDR, 1998). However, there are no experimental data on
differences in children's responses to 2,4-/2,6-DNT.
    c. Occurrence. EPA included both 2,4- and 2,6-DNT as analytes in
the UCMR 1. Because the HRL for both 2,4- and 2,6-DNT (0.05 [mu]g/L) is
lower than the minimum reporting limit used for monitoring (MRL of 2
[mu]g/L), EPA used the MRL to evaluate occurrence and exposure. The MRL
is within the 10-\4\ to the 10-\6\ cancer risk
range for either 2,4- or 2,6-DNT. In evaluating the UCMR 1 data, EPA
found that 1 of the 3,866 PWSs sampled (or 0.03 percent) detected 2,4-
DNT at the MRL of 2 [mu]g/L, affecting 0.02 percent of the population
served (or 38,000 people from 226 million). None of the 3,866 PWSs
sampled (serving 226 million) detected 2,6-DNT at the MRL of 2 [mu]g/L
(USEPA, 2006a and 2006b).
    EPA also evaluated the results of a USGS review of 3 highway and
urban runoff studies (Lopes and Dionne, 1998). These studies showed no
detects for either 2,4- or 2,6-DNT using a reporting limit of 5 [mu]g/L
(a value within the 10-\4\ to 10-\6\ risk range).
    d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate 2,4- or 2,6-DNT with an NPDWR. Because
2,4- and 2,6-DNT appear to occur infrequently at levels of concern in
PWSs, the Agency believes that a national primary drinking water
regulation does not present a meaningful opportunity for health risk
reduction. 2,4-DNT was detected only once at a minimum reporting level
that is within the 10-\4\ to the 10-\6\ cancer
risk range, while 2,6-DNT was not detected at this same level in any of
the PWSs monitored under the UCMR 1.
    EPA recognizes that 2,4- and 2,6-DNT are listed as probable human
carcinogens. For this reason, the Agency encourages those States with
public water systems that may have either 2,4- or 2,6-DNT above the HRL
to evaluate site-specific protective measures and to consider whether
State-level guidance (or some other type of action) is appropriate. The
Agency's original Health Advisories for 2,4- and 2,6-DNT were developed
for military installations. Because the Agency recognizes that 2,4- and
2,6-DNT may still be found at some military sites, the Agency has
updated the Health Advisories to reflect recent health effects
publications. The Health Advisories are available for review in the
docket. The updated Health Advisories will provide information to any
States with public water systems that may have either 2,4- or 2,6-DNT
above the HRL.
8. s-Ethyl dipropylthiocarbamate (EPTC)
    a. Background. EPTC, a synthetic organic compound, is a
thiocarbamate herbicide used to control weed growth during the pre-
emergence and early post-emergence stages of weed germination. First
registered for use in 1958, EPTC is used across the U.S. in the
agricultural production of a number of crops, most notably corn,
potatoes, dried beans, alfalfa, and snap beans. EPTC is also used
residentially on shade trees, annual and perennial ornamentals, and
evergreens (USEPA, 1999c).
    Estimates of EPTC usage in the United States suggest a decline from
approximately 17 to 21 million pounds active ingredient in 1987 to
approximately 7 to 9 million pounds active ingredient in 1999. TRI data
from 1995 to 2003 indicate that most on-site industrial releases of
EPTC tend to be releases to air and underground injections. Surface
water discharges are

minimal in comparison (USEPA, 2006g). Total releases for 2003 were
2,183 lbs.
    Environmental fate data indicate that EPTC would not be persistent
under most environmental conditions. Volatilization into the atmosphere
and degradation by soil organisms appear to be the primary dissipation
routes. EPTC has a low affinity for binding to the soil so the
potential to leach to ground water does exist. If EPTC reaches ground
water, volatilization is less likely to occur (USEPA, 1999c).
    b. Health Effects. In acute animal toxicity studies, EPTC was shown
to be moderately toxic via oral and dermal routes and highly toxic via
inhalation exposures. EPTC is a reversible cholinesterase (ChE)
inhibitor. Similar to other thiocarbamates, it does not produce a
consistent ChE inhibition profile. There was no consistent pattern
observed in any of the toxicity studies with regard to species,
duration of treatment, or the type of ChE enzyme measured. Typically,
studies showed inhibition of plasma ChE with dose-related decreases in
red blood cell and brain ChE activity. Some studies have shown that
brain ChE activity was inhibited without any effect on either plasma or
erythrocyte ChE activities. Other studies illustrated erythrocyte ChE
inhibition with no effect on either plasma or brain ChE (USEPA, 1999c).
In a primary eye irritation study in rabbits, technical grade EPTC was
shown to be slightly irritating (USEPA, 1999c).
    In subchronic and chronic studies performed in both rats and dogs,
there was a dose-related increase in the incidence and severity of
cardiomyopathy, a disorder of the heart muscle (Mackenzie, 1986; USEPA,
1999c). An increase in the incidence and severity of degenerative
effects (neuronal and/or necrotic degeneration) in both the central and
peripheral nervous system was observed in rats and dogs following
exposure to EPTC (USEPA, 1999c).
    EPA derived an RfD of 0.025 mg/kg/day for EPTC (USEPA, 1990d;
USEPA, 1999c). This value was calculated using a NOAEL of 2.5 mg/kg/day
from a study by Mackenzie (1986). An uncertainty factor of 100 was
applied for inter- and intraspecies differences. The critical effect
associated with the RfD is cardiomyopathy (disease of the heart
muscle). In the reregistration of EPTC, the application of a ten-fold
Food Quality Protection Act (FQPA) factor was recommended in order to
be protective against residential exposures of infants and children.
The Agency derived the HRL for EPTC using the RfD of 0.025 mg/kg/day
and a 20 percent relative source contribution. The HRL is calculated to
be 0.175 mg/L or 175 [mu]g/L.
    The Agency used long-term studies in mice and rats and short-term
studies of mutagenicity to evaluate the potential for carcinogenicity
(USEPA, 1990d). Based on these data and using EPA's 1999 Guidelines for
Carcinogen Risk Assessment, EPTC is not likely to be carcinogenic to
humans (USEPA, 1999a).
    EPA also evaluated whether health information is available
regarding the potential effects on children and other sensitive
populations. Data do not suggest increased pre- or post-natal
sensitivity of children and infants to EPTC exposure. In animal
studies, adverse developmental effects (i.e., decreased fetal body
weight and decreased litter size) were only seen at doses that were
toxic to the mother (USEPA, 1999c). Results from both developmental and
reproductive studies indicate that there are only minimal adverse
effects. The behavior patterns of children that lead to heightened
opportunities for exposure in the indoor environment and the need for a
developmental neurotoxicity study lead OPP to recommend the application
of a ten-fold FQPA factor for EPTC. However, EPA did not apply this
factor in the screening analysis because it does not apply to programs
other than the pesticide registrations.
    c. Occurrence. EPA included EPTC as an analyte in the UCMR 1. None
of the 3,866 PWSs sampled (serving a population of 226 million) had
detects of EPTC at the MRL of 1 [mu]g/L. Hence, these data indicate
that no occurrence and exposure is expected at levels greater than 87.5
[mu]g/L (\1/2\ the HRL) and greater than 175 [mu]g/L (the HRL) (USEPA,
2006a and 2006b).
    EPA also evaluated several sources of supplemental information,
which included:
     The National Pesticide Survey,
     The Pesticides in Ground Water Database, and
     The provisional pesticide results from the 1992-2001 USGS
NAWQA survey of ambient surface and ground waters across the U.S.