[Federal Register: May 1, 2007 (Volume 72, Number 83)]
[Proposed Rules]
[Page 24015-24058]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr01my07-20]
[[Page 24015]]
-----------------------------------------------------------------------
Part III
Environmental Protection Agency
-----------------------------------------------------------------------
40 CFR Part 141
Drinking Water: Regulatory Determinations Regarding Contaminants on
the Second Drinking Water Contaminant Candidate List--Preliminary
Determinations; Proposed Rule
[[Page 24016]]
-----------------------------------------------------------------------
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.
-----------------------------------------------------------------------
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 (202) 566-1744, and the telephone number for the
EPA Docket Center is (202) 566-2426.
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 miller.wynne@epa.gov. For general information
contact the EPA Safe Drinking Water Hotline at (800) 426-4791 or e-
mail: hotline-sdwa@epa.gov.
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
[[Page 24017]]
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)
[[Page 24018]]
(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:
---------------------------------------------------------------------------
\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.
---------------------------------------------------------------------------
(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\
---------------------------------------------------------------------------
\3\ The statute authorizes a nine month extension of this
promulgation date.
---------------------------------------------------------------------------
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.
[[Page 24019]]
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
[[Page 24020]]
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.
---------------------------------------------------------------------------
\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).
---------------------------------------------------------------------------
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
[[Page 24021]]
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,
[[Page 24022]]
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
[[Page 24023]]
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
[[Page 24024]]
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
[[Page 24025]]
(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
[[Page 24026]]
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.
BILLING CODE 6560-50-P
[[Page 24027]]
[GRAPHIC] [TIFF OMITTED] TP01MY07.051
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,
[[Page 24028]]
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
[[Page 24029]]
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.
[[Page 24030]]
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).
---------------------------------------------------------------------------
\15\ 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane.
---------------------------------------------------------------------------
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.
---------------------------------------------------------------------------
\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.
---------------------------------------------------------------------------
[[Page 24031]]
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
[[Page 24032]]
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).
[[Page 24033]]
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
[[Page 24034]]
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.
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 EPTC as an analyte
in the monitoring survey. EPTC was not detected using a minimum
reporting limit of 0.15 [mu]g/L (USEPA, 1990a).
The Pesticides in Ground Water Database (USEPA, 1992b) indicates
that EPTC was found in 2 of 1,752 ground water wells that were sampled
in 10 States. Both contaminated wells were in Minnesota. The detected
concentrations ranged from 0.01 to 0.33 [mu]g/L. All of these positive
detections are less than the HRL of 175 [mu]g/L, as well as 87.5 [mu]g/
L (\1/2\ the HRL).
The USGS NAWQA program included EPTC 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). While the USGS detected EPTC in both surface and ground waters,
95 percent of the samples from the various land use settings were less
than or equal to 0.018 [mu]g/L. The estimated maximum surface water
concentration, 29.6 [mu]g/L (mixed land use settings), and the maximum
ground water concentration, 0.45 [mu]g/L (agricultural settings), are
both less than 175 [mu]g/L (the EPTC HRL).
d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate EPTC with an NPDWR. Because EPTC does not
appear to occur 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 EPTC
has been found in ambient waters, it was detected only at levels less
than the HRL (as well as \1/2\ the HRL) and it was not found in the
UCMR 1 survey of public water supplies.
9. Fonofos
a. Background. Fonofos, an organophosphate, is a soil insecticide
used to control pests such as corn rootworms, cutworms, symphylans
(i.e., garden centipedes), and wireworms. Primarily used on corn crops,
fonofos was also used on other crops such as asparagus, beans, beets,
corn, onions, peppers, tomatoes, cole crops, sweet potatoes, peanuts,
peas, peppermint, plantains, sorghum, soybeans, spearmint,
strawberries, sugarcane, sugar beets, white (Irish) potatoes, and
tobacco (USEPA, 1999d).
Fonofos was scheduled for a reregistration decision in 1999.
However, before the review was completed, the registrant requested
voluntary cancellation. The cancellation was announced in the Federal
Register on May 6, 1998 (63 FR 25033 (USEPA, 1998d)), with an effective
date of November 2, 1998, plus a one-year grace period to permit the
exhaustion of existing stocks (USEPA, 1999d).
NCFAP data indicate that fonofos use declined significantly during
the 1990s (NCFAP, 2004). According to NCFAP,
[[Page 24035]]
approximately 3.2 million pounds of fonofos a.i. were applied annually
around 1992 and approximately 0.4 million pounds a.i. were applied
annually around 1997. The U.S. Geological Survey (USGS) estimates an
average of 2.7 million pounds a.i. were used annually around 1992
(Thelin and Gianessi, 2000).
Fonofos is moderately persistent in soil and its persistence
depends on soil type, organic matter, rainfall, and sunlight. Since
fonofos adsorbs moderately well to soil, it is not readily leached or
transported to ground water but it can be transported to surface waters
in runoff. Fonofos is rapidly degraded by soil microorganisms
(Extoxnet, 1993). Fonofos tends to volatilize from wet soil and water
surfaces, but the process is slowed by adsorption to organic material
in soil, suspended solids, and sediment (HSDB, 2004d).
b. Health Effects. Fonofos (like many organophosphates) is toxic to
humans and animals. Case reports and acute oral toxicity studies in
animals indicate that oral exposure to fonofos induces clinical signs
of toxicity that are typical of cholinesterase inhibitors. In humans,
accidental exposures produced symptoms of acute intoxication, nausea,
vomiting, salivation, sweating, muscle twitches, decreased blood
pressure and pulse rate, pinpoint pupils, profuse salivary and
bronchial secretions, cardiorespiratory arrest, and even death in 1
exposed individual (Hayes, 1982; Pena Gonzalez et al., 1996).
In animals, clinical signs of exposure included tremors,
salivation, diarrhea, and labored breathing (USEPA, 1996c). Chronic
exposure studies also indicated that oral administration of fonofos
inhibits cholinesterase (Banerjee et al., 1968; Cockrell et al., 1966;
Hodge, 1995; Horner, 1993; Miller, 1987; Miller et al., 1979; Pavkov
and Taylor, 1988; Woodard et al., 1969). Cholinesterase inhibition is
one of the critical effects associated with the RfD, which was verified
by EPA (USEPA, 1991) at 0.002 mg/kg/day. EPA derived the RfD of 0.002
mg/kg/day using a NOAEL of 0.2 mg/kg/day (Hodge, 1995) and a 100-fold
uncertainty factor to account for inter- and intraspecies differences.
Fonofos is classified as an unlikely human carcinogen (Group E)
because there is no evidence of carcinogenic potential in the available
long-term feeding studies in rats and mice (Banerjee et al., 1968;
Pavkov and Taylor, 1988; Sprague and Zwicker, 1987). In addition,
fonofos does not appear to be mutagenic (USEPA, 1996c).
EPA evaluated whether health information is available regarding the
potential effects on children and other sensitive populations. In the
available developmental studies with rabbits (Sauerhoff, 1987) and mice
(Minor et al., 1982; Pulsford, 1991), no developmental effects were
observed at oral doses as high as 1.5 mg/kg/day in the rabbit (highest
dose tested) nor in mice at doses as high as 2.0 mg/kg/day (Minor et
al., 1982; Pulsford, 1991). However, in mice, effects were noted at
higher dose levels. These effects included an increase in the incidence
of variant sternebrae ossifications (at 6 mg/kg/day or greater) and a
slight dilation of the fourth brain ventricle in offspring (at 4 mg/kg/
day or greater). No developmental neurotoxicity study with fonofos is
available for further assessment of this endpoint. In a three-
generation reproduction study in rats (Woodard et al., 1968), no
treatment-related adverse effects were observed at the 2 dose levels
used in this study, 0.5 and 1.58 mg/kg/day.
The Agency believes that the current RfD is adequately protective
of children. The current fonofos RfD of 0.002 mg/kg/day is 1000-fold
lower than the NOAEL observed in the Woodard et al. (1968)
developmental studies.
Using the RfD of 0.002 mg/kg/day for fonofos and a 20 percent
screening relative source contribution, the Agency derived an HRL of
0.014 mg/L and rounded to 0.01 mg/L (or 10 [mu]g/L).
c. Occurrence. EPA included fonofos as an analyte in the UCMR 1
List 2 Screening Survey. None of the 2,306 samples from the 295 PWSs
sampled (serving a population of 41 million) contained detects for
fonofos at the MRL of 0.5 [mu]g/L. Hence, these data indicate that no
occurrence and exposure is expected at levels greater than 5 [mu]g/L
(\1/2\ the HRL) and greater than 10 [mu]g/L (the HRL) (USEPA, 2006a and
2006b).
The USGS NAWQA program included fonofos 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). While the USGS detected fonofos in both surface and ground
waters, 95 percent of the samples from the various land use settings
were less than 0.003 [mu]g/L (the reporting limit). The maximum surface
water concentration, 1.20 [mu]g/L (agricultural setting), and the
maximum ground water concentration, 0.009 [mu]g/L (agricultural
setting), are both less than 10 [mu]g/L and less than 5 [mu]g/L (the
fonofos HRL and \1/2\ the HRL).
d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate fonofos with an NPDWR. Because fonofos
does not appear to occur 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
fonofos has been found in ambient waters, it was detected only at
levels less than the HRL (as well as \1/2\ the HRL) and it was not
found in UCMR 1 Screening Survey of public water supplies. Fonofos was
voluntarily cancelled in 1998 and the Agency expects any remaining
stocks and releases into the environment to decline. In addition, since
fonofos tends to bind strongly to soil, any releases to the environment
are not likely to contaminant source waters.
10. Terbacil
a. Background. Terbacil, a synthetic organic compound, is a
selective herbicide used to control broadleaf weeds and grasses on
terrestrial food/feed crops (e.g., apples, mint, peppermint, spearmint,
and sugarcane), terrestrial food (e.g., asparagus, blackberry,
boysenberry, dewberry, loganberry, peach, raspberry, youngberry, and
strawberry), terrestrial feed (e.g., alfalfa, forage, and hay) and
forest trees (e.g., cottonwood) (USEPA, 1998e).
In 1998, EPA estimated that agricultural usage of terbacil consumed
approximately 221,000 to 447,000 pounds of active ingredient annually
and non-agricultural usage consumed approximately 9,000 to 14,000
pounds. These estimates are based on data collected mostly between 1990
and 1995, and in some cases as early as 1987 (USEPA, 1998e). According
to NCFAP (2004), approximately 298,000 pounds of terbacil a.i. were
applied annually in agriculture around 1992 and approximately 342,000
pounds a.i. were applied around 1997.
Terbacil is listed as a TRI chemical and data are reported from one
or more facilities in a single state, Texas, for the time period
covering 1995 to 1997. During this three-year period, all reported
releases were on-site releases to surface water that varied between
3,000 to 10,000 pounds annually (USEPA, 2006h).
Terbacil is considered a persistent and potentially mobile
herbicide in terrestrial environments. Because of its low affinity to
soils, it can potentially leach into ground and/or surface waters
(USEPA, 1998e; Extoxnet, 1994).
b. Health Effects. In acute and subchronic toxicity studies,
terbacil is practically non-toxic (Haskell Laboratories, 1965a and
1965b). Terbacil does not cause dermal sensitivity in
[[Page 24036]]
rabbits or guinea pigs and causes mild conjunctival eye irritation in
rabbits (Henry, 1986; Hood, 1966). In rats exposed subchronically to
dietary terbacil, effects were seen at a LOAEL of 25 mg/kg/day and
included increased absolute and relative liver weights, vacuolization,
and enlargement of liver cells (Wazeter et al.,1964; Haskell
Laboratories, 1965c).
A primary target organ in rats following exposure to terbacil is
the liver. Chronic effects of dietary terbacil exposure in two-year
studies included increases in thyroid-to-body weight ratios, slight
increases in liver weights and elevated alkaline phosphatase levels in
beagle dogs, significant decreases in body weight in rats, increases in
serum cholesterol levels and increases in liver to body weight ratios
in rats (Wazeter et al.,1967a; Malek, 1993). In beagle dogs, effects
were seen at or above 6.25 mg/kg/day (NOAEL = 1.25 mg/kg/day). In rats,
effects (i.e., decreases in body weight, increases in liver weights and
cholesterol levels) were seen at higher levels (LOAELs = 56 mg/kg/day
for males and 83 mg/kg/day for females).
Terbacil is not considered to be a developmental or reproductive
toxicant. In developmental studies, maternal effects were generally
seen prior to or at the same levels as developmental effects. Haskell
Laboratories (1980) reported maternal effects (i.e., decreased body
weight) and significant decreases in the number of live fetuses per
litter due to early fetal resorption at a LOAEL of 62.5 mg/kg/day in
rats. In rabbits administered terbacil via gavage, the maternal and
developmental LOAELs were equal (600 mg/kg/day). Maternal toxicity was
based on the death of the dams and developmental toxicity was based on
a decrease in live fetal weights (Solomon, 1984). No reproductive
effects were seen in a three-generation study where terbacil was
administered to male and female rats at dose levels of 2.5 and 12.5 mg/
kg/day (Wazeter et al., 1967b).
Terbacil is not mutagenic. Terbacil was tested and found negative
in a chromosomal aberration study in rat bone marrow cells, found
negative in a gene mutation assay (with and without S9 activation), and
found negative for DNA synthesis when tested up to cytotoxic levels in
rats (Cortina, 1984; Haskell Laboratories,1984). Terbacil shows no
evidence of carcinogenicity and is unlikely to be carcinogenic to
humans (Group E) (USEPA, 1998e).
The RfD of 0.013 mg/kg/day for terbacil (USEPA, 1998e) is
calculated from a two-year chronic study in beagle dogs. The LOAEL of
6.25 mg/kg/day was based on increased thyroid-to-body weight ratios,
slight increases in liver weights, and elevated alkaline phosphatase
levels with a NOAEL of 1.25 mg/kg/day. In deriving the RfD, the Agency
applied an uncertainty factor of 100 to account for interspecies and
intraspecies differences. Using the RfD of 0.013 mg/kg/day and applying
a 20 percent screening relative source contribution, the Agency derived
an HRL of 0.090 mg/L (or 90 g/L) for terbacil.
EPA also evaluated whether health information is available
regarding the potential effects on children and other sensitive
populations. In the case of terbacil, the Agency determined that there
was no need to apply an FQPA factor to the RfD in order to protect
children (USEPA, 1998e). Other potentially sensitive subpopulations
have not been identified.
c. Occurrence. EPA included terbacil as an analyte in UCMR 1. None
of the 3,866 PWSs sampled (serving a population of 226 million) had
detects for terbacil at the MRL of 2 g/L. Hence, these data indicate
that no occurrence and exposure is expected at levels greater than 45
g/L (\1/2\ the HRL) and greater than 90 [mu]g/L (the terbacil 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.
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 terbacil as an
analyte in the monitoring survey. Terbacil was not detected using a
minimum reporting limit of 1.7 [mu]g/L (USEPA, 1990a).
The Pesticides in Ground Water Database (USEPA, 1992b) indicates
that terbacil was found in 6 of the 288 ground water wells tested for
this contaminant in 6 States. Terbacil was found in 1 ground water well
in Oregon (at a concentration of 8.9 [mu]g/L) and 5 ground water wells
in West Virginia (with concentrations ranging from 0.3 to 1.2 [mu]g/L).
All of the positive detections are less than the HRL of 90 [mu]g/L, as
well as 45 [mu]g/L (\1/2\ the HRL).
The USGS NAWQA program included terbacil 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). While the USGS detected terbacil in both surface and ground
waters, 95 percent of the samples from the various land use settings
were less than 0.034 [mu]g/L (the USGS reporting limit). The maximum
surface water concentration, 0.54 [mu]g/L (agricultural setting), and
the maximum ground water concentration, 0.891 [mu]g/L (mixed land use
setting), are both less than 90 [mu]g/L and less than 45 [mu]g/L (the
terbacil HRL and \1/2\ the HRL).
d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate terbacil with an NPDWR. Because terbacil
does not appear to occur 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.
Terbacil has been found in ambient waters but the levels were less than
the HRL (as well as \1/2\ the HRL). It was not found in the UCMR 1
survey of public water supplies.
11. 1,1,2,2-Tetrachloroethane
a. Background. 1,1,2,2-Tetrachloroethane, a volatile organic
compound, is not known to occur naturally in the environment (IARC,
1979). Prior to the 1980s, 1,1,2,2-tetrachloroethane was synthesized
for use in the production of other chemicals, primarily chlorinated
ethylenes. 1,1,2,2-Tetrachloroethane was also once used as a solvent to
clean and degrease metals, in paint removers, varnishes, lacquers, and
photographic films, and for oil/fat extraction (Hawley, 1981).
Commercial production of 1,1,2,2-tetrachloroethane in the U.S. ceased
in the 1980s when other processes to generate chlorinated ethylenes
were discovered (ATSDR, 1996).
Production of 1,1,2,2-tetrachloroethane in the U.S. was
approximately 440 million pounds in 1967 (Konietzko, 1984). Production
declined to an estimated 34 million pounds by 1974 (ATSDR, 1996).
Although U.S. commercial production ceased in the 1980s, 1,1,2,2-
tetrachloroethane is still generated as a byproduct and/or intermediate
in the production of other chemicals. TRI data indicate that
environmental releases have generally declined from a high of about
175,000 pounds in 1988 to a low of 3,500 pounds in 2003. Most releases
took the form of air emissions, though surface water discharges were
also documented nearly every year (USEPA, 2006i).
[[Page 24037]]
Volatilization from water or soil surfaces to the atmosphere
appears to be the primary dissipation route for 1,1,2,2-
tetrachloroethane. In subsurface soils and ground water, 1,1,2,2-
tetrachloroethane is subject to biodegradation by soil organisms and/or
chemical hydrolysis by water (ATSDR, 1996).
b. Health Effects. Data on the toxicity of 1,1,2,2-
tetrachloroethane in humans are limited, consisting of one experimental
inhalation study, a few case reports of suicidal or accidental
ingestion, and dated occupational studies. In most cases, there was no
quantification of the exposure. Respiratory and mucosal effects, eye
irritation, nausea, vomiting, and dizziness were reported by human
volunteers exposed to 1,1,2,2-tetrachloroethane vapors under controlled
chamber conditions (Lehmann and Schmidt-Kehl, 1936). Effects from non-
lethal occupational exposures included gastric distress (i.e., pain,
nausea, vomiting), headache, loss of appetite, an enlarged liver, and
cirrhosis (Jeney et al., 1957; Lobo-Mendonca, 1963; Minot and Smith,
1921).
There have been a variety of animal studies in rats and mice using
both the inhalation and oral exposure routes. Recent studies by the
National Toxicology Program (NTP, 2004) provide a detailed evaluation
of the short-term and subchronic oral toxicity of 1,1,2,2-
tetrachloroethane and confirm many of the observations from earlier
studies. In rats and mice exposed orally, the liver appears to be the
primary target organ. The RfD (10 [mu]g/kg/day) for 1,1,2,2-
tetrachloroethane was derived from the BMDL for a 1 standard deviation
change in relative liver weight, a biomarker for liver toxicity. A
1,000-fold uncertainty factor was applied in the RfD determination.
A National Cancer Institute (1978) bioassay of 1,1,2,2-
tetrachloroethane found clear evidence of carcinogenicity in male and
female B6C3F1 mice based on a dose-related statistically significant
increase in liver tumors. There was equivocal evidence for
carcinogenicity in Osborn Mendel rats because of the occurrence of a
small number of rare-for-the species neoplastic and preneoplastic
lesions in the livers of the high dose animals. The Agency used the
slope factor of 8.5 x 10-2 for the tumors in female mice to
derive the HRL of 0.4 [mu]g/L for use in the analysis of the occurrence
data for 1,1,2,2-tetrachloroethane. Information on the reproductive
effects of 1,1,2,2-tetrachloroethane is limited. There is a single one-
generation inhalation study that does not follow a standard methodology
and examined a small number of rats (5 females and 7 males) exposed via
inhalation to 1 dose (13.3 mg/m\3\). There were no statistically
significant differences in the percentage of females having offspring,
number of pups per litter, average birth weight, sex ratio, or post
natal offspring mortality (Schmidt et al., 1972). Effects on sperm in
male rats were seen after oral (27 mg/kg/day; NTP, 2004) and inhalation
(13 mg/m\3\; Schmidt et al., 1972) exposures. Similar effects were seen
in mice but at higher doses. Fetal toxicity did not occur in the
absence of maternal toxicity.
Developmental range-finding studies conducted for NTP (1991a and b)
found that 1,1,2,2-tetrachloroethane was toxic to the dams and pups of
Sprague Dawley rats and CD-1 Swiss mice. Rats were more sensitive than
mice. The NOAEL in the rats for both maternal toxicity and associated
fetal toxicity was 34 mg/kg/day with a LOAEL of 98 mg/kg/day. In mice,
the NOAEL was 987 mg/kg/day and the LOAEL was 2,120 mg/kg/day.
EPA also evaluated whether health information is available
regarding the potential effects on children and other sensitive
populations. Individuals with preexisting liver and kidney damage would
likely be sensitive to 1,1,2,2-tetrachloroethane exposure. Low intake
of antioxidant nutrients (e.g., Vitamin E, Vitamin C, and selenium)
could be a predisposing factor for liver damage. In addition,
individuals with a genetically low capacity to metabolize
dichloroacetic acid (the primary metabolite of 1,1,2,2-
tetrachloroethane) may be at greater risk than the general population
as a result of 1,1,2,2-tetrachloroethane exposure.
c. Occurrence. EPA included 1,1,2,2-tetrachloroethane as an analyte
in the UCM Round 1 and UCM Round 2 surveys. EPA evaluated the UCM Round
1 Cross Section and the UCM Round 2 Cross Section data at levels
greater than 0.2 [mu]g/L (\1/2\ the HRL) and greater than 0.4 [mu]g/L
(the HRL) (USEPA, 2006a and 2006c). The MRLs for UCM Round 1 ranged
from 0.1 to 10 [mu]g/L and the MRLs for UCM Round 2 ranged from 0.1 to
2.5 [mu]g/L. Because some of the reporting limits exceeded the
thresholds of interest, the occurrence analyses may result in an
underestimate of systems affected. However, all the MRL values used for
UCM Round 1 and UCM Round 2 are within the 10-4 to the
10-6 cancer risk range.
Analysis of UCM Round 1 Cross Section data indicates that
approximately 0.22 percent (or 44) of the 20,407 PWSs sampled had
detections of 1,1,2,2-tetrachloroethane at levels greater than 0.20
[mu]g/L (\1/2\ the HRL), affecting approximately 1.69 percent of the
population served (or 1.6 million of 95 million). The UCM Round 1 Cross
Section data indicate that approximately 0.20 percent (or 41) of the
20,407 PWSs sampled had detections of 1,1,2,2-tetrachloroethane at
levels greater than 0.4 [mu]g/L (the HRL), affecting approximately 1.63
percent of the population served (or 1.5 million of 95 million). The
99th percentile of all detects is 112 [mu]g/L and the maximum reported
value is 200 [mu]g/L.
Analysis of the UCM Round 2 Cross Section data indicate that
approximately 0.07 percent (or 18) of the 24,800 PWSs sampled had
detections of 1,1,2,2-tetrachloroethane at levels greater than 0.2
[mu]g/L (\1/2\ the HRL), affecting approximately 0.51 percent of the
population served (or 362,000 of 71 million). The UCM Round 2 Cross
Section data indicate that approximately the same percentage and number
of the PWSs sampled (0.07 percent or 17 of the 24,800) had detections
of 1,1,2,2-tetrachloroethane at levels greater than 0.4 [mu]g/L (the
HRL), affecting approximately 0.08 percent of the population served (or
56,000 of 71 million). The 99th percentile of all detects is 2 [mu]g/L
and the maximum reported value is 2 [mu]g/L.
EPA also evaluated several sources of supplemental information,
which included the USGS VOC National Synthesis Random Source Water
Survey and the Focused Source Water Survey. 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 1,1,2,2-tetrachloroethane as an analyte in both surveys and
did not detect it in any of the source water samples using a reporting
limit of 0.2 [mu]g/L (a level that is less than the 1,1,2,2-
tetrachloroethane HRL). In addition, USGS did not detect 1,1,2,2-
tetrachloroethane when using a detection level of 0.026 [mu]g/L (a
level that is over 10 times lower than the 1,1,2,2-tetrachloroethane
HRL) in the focused survey (Ivahnenko et al., 2001, Grady, 2003, Delzer
and Ivahnenko, 2003a).
d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate 1,1,2,2-tetrachloroethane with an NPDWR.
Because 1,1,2,2-tetrachloroethane appears to occur infrequently at
health levels of concern in PWSs, the Agency
[[Page 24038]]
believes that a national primary drinking water regulation does not
present a meaningful opportunity for health risk reduction. While
1,1,2,2-tetrachloroethane was detected in both the UCM Round 1 and the
UCM Round 2 surveys, the percentage of detections had decreased by the
time the UCM Round 2 survey was performed in the mid-1990's. In
addition, the USGS did not detect 1,1,2,2-tetrachloroethane in two
subsequent monitoring surveys of source waters that supply community
water systems using a reporting limit that is less than the 1,1,2,2-
tetrachloroethane HRL. The Agency believes that this decrease in
detections occurred because commercial production of 1,1,2,2-
tetrachloroethane ceased in the mid-1980's. Hence, the Agency does not
expect 1,1,2,2-tetrachloroethane to occur in many public water systems
today.
EPA recognizes that 1,1,2,2-tetrachloroethane is listed as a likely
human carcinogen. For this reason, the Agency encourages those States
with public water systems that may have 1,1,2,2-tetrachloroethane 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
document for 1,1,2,2-tetrachloroethane to provide more recent health
information. The updated Health Advisory will provide information to
any States with public water systems that may have 1,1,2,2-
tetrachloroethane at levels above the HRL.
V. What Is the Status of the Agency's Evaluation of Perchlorate?
At this time, the Agency is not making a preliminary determination
as to whether a national primary drinking water regulation is needed
for perchlorate. However, the Agency has placed a high priority on
making a regulatory determination for perchlorate and will publish a
preliminary determination as soon as possible. EPA is not able to make
a preliminary determination at this time because, in order to evaluate
perchlorate against the three SDWA statutory criteria, the Agency
believes additional information may be needed to more fully
characterize perchlorate exposure and determine whether regulating
perchlorate in drinking water presents a meaningful opportunity for
health risk reduction. This is particularly true if the Agency uses
food exposure data to first calculate a relative source contribution
(RSC) and corresponding health reference level (HRL) below the drinking
water equivalent level (DWEL) \18\ in order to determine whether
regulating perchlorate would present a meaningful opportunity for
health risk reduction. However, the Agency is considering several other
approaches, discussed below, for making this statutory determination
and is requesting public comment on the strengths and limitations of
these approaches.
---------------------------------------------------------------------------
\18\ DWEL = [(Reference Dose x Body Weight of 70 kg) / Drinking
Water Intake of 2 L per day].
---------------------------------------------------------------------------
The following sections explain why EPA is not making a preliminary
regulatory determination for perchlorate at this time, and discusses
the information the Agency has collected to date (that may be relevant
to making a preliminary regulatory determination), the additional
information the Agency is soliciting in this action, and options for
additional analyses that the Agency may conduct to support a regulatory
determination. Sections V.A through V.D provide a summary of the
available and relevant information/data that the Agency has collected
and reviewed regarding the sources of perchlorate in the environment,
its potential health effects, and its occurrence in drinking water,
food, human urine, breast milk, and amniotic fluid. Section V.E
explains the Agency's basis for not making a preliminary regulatory
determination for perchlorate at this time and Section V.F. presents
the options the Agency is considering to better characterize
perchlorate exposure and the alternate approaches that EPA is
considering for making a preliminary regulatory determination. This
action provides an opportunity for the public to submit other relevant
data that may further characterize exposure to perchlorate through the
consumption of foods and/or through other pathways and to comment on
these alternate approaches. The Agency in particular seeks comment on
the use of urine biomonitoring data in estimating perchlorate exposure.
The Agency will consider any relevant information/data provided in
response to this action as the Agency determines whether to regulate
perchlorate with a national primary drinking water regulation and how
best to proceed to address perchlorate.
A. Sources of Perchlorate
Perchlorate (ClO4-) is an anion commonly
associated with the solid salts of ammonium, magnesium, potassium, and
sodium perchlorate. Perchlorate salts are highly soluble in water, and
because perchlorate sorbs poorly to mineral surfaces and organic
material, perchlorate can be mobile in surface and subsurface aqueous
environments. Although commonly known as a man-made chemical,
perchlorate also may be derived from natural processes.
While perchlorate has a wide variety of industrial uses, it is
primarily used in the form of ammonium perchlorate as an oxidizer in
solid fuels used to power rockets, missiles, and fireworks.
Approximately 90 percent of perchlorate is manufactured for this
application (Wang et al., 2002). Perchlorate can also be present as an
ingredient or as an impurity in road flares, lubricating oils, matches,
aluminum refining, rubber manufacturing, paint and enamel
manufacturing, leather tanning, paper and pulp processing (as an
ingredient in bleaching powder), and as a dye mordant.
Perchlorate can also occur naturally in the environment. Chile
possesses caliche ores rich in sodium nitrate (NaNO3), which
are also a natural source of perchlorate (Schilt, 1979 and Ericksen,
1983). These Chilean nitrate salts (saltpeter) have been mined and
refined to produce commercial fertilizers, which before 2001 accounted
for about 0.14 percent of U.S. fertilizer application (USEPA, 2001d).
The USEPA (2001d) conducted a broad survey of fertilizers and other raw
materials and found that all products surveyed were devoid of
perchlorate except for those known to contain or to be derived from
mined Chilean saltpeter.
Perchlorate has also been found in other geologic materials. Orris
et al. (2003) measured perchlorate at levels exceeding 1,000 parts per
million (ppm or mg/kg) in several samples of natural minerals,
including potash ore from New Mexico and Saskatchewan (Canada), playa
crust from Bolivia, and hanksite from California.
Texas Tech University Water Resources Center conducted a large-
scale sampling program to determine the source and distribution of
perchlorate in northwest Texas groundwater (Jackson et al., 2004;
Rajagopalan et al., 2006). Perchlorate was detected at concentrations
greater than 0.5 g/L in 46 percent of public wells and 47 percent of
private wells. Jackson et al. (2004) hypothesized that atmospheric
production and/or surface oxidative weathering is the source of the
perchlorate. In related research, Dasgupta et al. (2005) detected
perchlorate in many rain and snow samples and demonstrated that
perchlorate is formed by a variety of simulated atmospheric processes
suggesting that natural, atmospherically-
[[Page 24039]]
derived perchlorate exists in the environment. Barron et al. (2006)
developed a method for the rapid determination of perchlorate in
rainwater samples, with a detection limit between 70 and 80 ng/L. Of
the ten rainwater samples collected in Ireland in 2005, perchlorate was
detected in 4 samples at concentrations between 0.075 and 0.113 g/L,
and in 1 other sample at 2.8 g/L. Kang et al. (2006) conducted seven-
day experiments to determine if it was possible to produce perchlorate
by exposing various chlorine intermediates to UV radiation in the form
of high intensity UV lamps and/or ambient solar radiation. Perchlorate
formation was demonstrated in aqueous salt solutions with initial
concentrations of hypochlorite, chlorite, or chlorate between 100 and
10,000 mg/L.
After a limited investigation, the Massachusetts Department of
Environmental Quality (MA DEP, 2005) found that perchlorate may be
present in sodium hypochlorite solutions used in water and wastewater
treatment plants, and that the level of occurrence depends upon storage
conditions and the initial purity of the stock solution (MA DEP, 2005).
According to MA DEP (2005), the Town of Tewksbury conducted a small
study to evaluate the impact of storage conditions (temperature and
light) on a new shipment of sodium hypochlorite stock solution.
Tewksbury found that the perchlorate concentration in the new stock
solution increased from 0.2 g/L to levels ranging from 995 to 6,750 g/L
depending on the storage conditions. Accounting for the large dilution
factor (e.g., 20,000 to 1 ratio) used in chlorination processes at
drinking water treatment plants, MA DEP (2005) concluded that ``absent
additional efforts to minimize breakdown of hypochlorite solutions, it
would appear that low levels of the perchlorate ion (0.2 to 0.4 g/L)
detected in a drinking water supply disinfected with sodium
hypochlorite solutions could be attributable to the chlorination
process.''
It is not clear at this time what proportion of perchlorate found
in public water supplies or entering the food chain comes from these
various anthropogenic and natural sources. The significance of
different sources probably varies regionally. A study by Dasgupta et
al. (2006) analyzes the three principal sources of perchlorate and
their relative contributions to the food chain. These are its use as an
oxidizer including rocket propellants, Chilean nitrate used principally
as fertilizer, and that produced by natural atmospheric processes.
B. Health Effects
Perchlorate can interfere with the normal functioning of the
thyroid gland by competitively inhibiting the transport of iodide into
the thyroid. Iodide is an important component of two thyroid hormones,
T4 and T3, and the transfer of iodide from the blood into the thyroid
is an essential step in the synthesis of these two hormones. Iodide
transport into the thyroid is mediated by a protein molecule known as
the sodium (Na+)--iodide (I-) symporter (NIS). NIS molecules bind
iodide with very high affinity, but they also bind other ions that have
a similar shape and electric charge, such as perchlorate. The binding
of these other ions to the NIS inhibits iodide transport into the
thyroid, which can result in intrathyroidal iodide deficiency and
consequently decreased synthesis of T4 and T3. There is compensation
for iodide deficiency, however, such that the body maintains the serum
concentrations of thyroid hormones within narrow limits through
feedback control mechanisms. This feedback includes increased secretion
of thyroid stimulating hormone (TSH) from the pituitary gland, which
has among its effects the increased production of T4 and T3 (USEPA,
2005e). Sustained changes in thyroid hormone and TSH secretion can
result in thyroid hypertrophy and hyperplasia (abnormal growth or
enlargement of the thyroid) (USEPA, 2005e).
In January 2005, the National Research Council (NRC) of the
National Academies of Science (NAS) published ``Health Implications of
Perchlorate Ingestion,'' a review of the current state of the science
regarding potential adverse health effects of perchlorate exposure and
mode-of-action for perchlorate toxicity (NRC, 2005). Based on
recommendations of the NRC, EPA chose data from the Greer et al. (2002)
human clinical study as the basis for deriving a reference dose (RfD)
for perchlorate (USEPA, 2005e). Greer et al. (2002) report the results
of a well-controlled study that measured thyroid iodide uptake, hormone
levels, and urinary iodide excretion in a group of 24 healthy adults
administered perchlorate doses orally over a period of 14 days. Dose
levels ranged from 0.007 to 0.5 mg/kg/day in the different experimental
groups. No significant differences were seen in measured serum thyroid
hormone levels (T3, T4, total and free) in any dose group. The
statistical no observed effect level (NOEL) for perchlorate-induced
inhibition of thyroid iodide uptake was 0.007 mg/kg/day. Although the
NRC committee concluded that hypothyroidism is the first adverse effect
in the continuum of effects of perchlorate exposure, NRC recommended
that ``the most health-protective and scientifically valid approach''
was to base the perchlorate RfD on the inhibition of iodide uptake by
the thyroid (NRC, 2005). NRC concluded that iodide uptake inhibition,
although not adverse, is the key biochemical event in the continuum of
possible effects of perchlorate exposure and would precede any adverse
health effects of perchlorate exposure. The lowest dose (0.007 mg/kg/
day) administered in the Greer et al. (2002) study was considered a
NOEL (rather than a NOAEL) because iodide uptake inhibition is not an
adverse effect but a biochemical change (USEPA, 2005e). A summary of
the data considered and the NRC deliberations can be found in the NRC
report (2005) and the EPA Integrated Risk Information System (IRIS)
summary (USEPA, 2005e).
The NRC recommended that EPA apply an intraspecies uncertainty
factor of 10 to the NOEL to account for differences in sensitivity
between the healthy adults in the Greer et al. (2002) study and the
most sensitive population, fetuses of pregnant women who might have
hypothyroidism or iodide deficiency. Because the fetus depends on an
adequate supply of maternal thyroid hormone for its central nervous
system development during the first trimester of pregnancy, iodide
uptake inhibition from low-level perchlorate exposure has been
identified as a concern in connection with increasing the risk of
neurodevelopmental impairment in fetuses of high-risk mothers (NRC,
2005). The NRC (2005) viewed the uncertainty factor of 10 as
conservative and health protective given that the point of departure is
based on a non-adverse effect (iodide uptake inhibition) that precedes
the adverse effect in a continuum of possible effects of perchlorate
exposure. NRC concluded that no uncertainty factor was needed for the
use of a less-than chronic study, for deficiencies in the database, or
for interspecies variability. To protect the most sensitive human
population from chronic perchlorate exposure, EPA derived an RfD of
0.0007 mg/kg/day with a ten-fold total uncertainty factor from the NOEL
of 0.007 mg/kg/day (USEPA, 2005e).
Blount et al. (2006b) recently published a study examining the
relationship between urinary levels of perchlorate and serum levels of
TSH and total T4 in 2,299 men and women (ages 12 years and older), who
participated in CDC's 2001-2002
[[Page 24040]]
National Health and Nutrition Examination Survey (NHANES).\19\ Blount
et al. (2006b) evaluated perchlorate along with covariates known or
likely to be associated with T4 or TSH levels to assess the
relationship between perchlorate and these hormones, and the influence
of other factors on this relationship. These covariates included sex,
age, race/ethnicity, body mass index, serum albumin, serum cotinine (a
marker of tobacco smoke exposure), estimated total caloric intake,
pregnancy status, post-menopausal status, premenarche status, serum C-
reactive protein, hours fasting before sample collection, urinary
thiocyanate, urinary nitrate, and use of selected medications. The
study found that perchlorate was a significant predictor of thyroid
hormones in women, but not men. After finding evidence of gender
differences, the researchers focused on further analyzing the NHANES
data for the 1,111 women participants. They divided these 1,111 women
into two categories, higher-iodide and lower-iodide, using a cut point
of 100 [mu]g/L of urinary iodide based on the World Health Organization
(WHO) definition of sufficient iodide intake.\20\ Hypothyroid women
were excluded from the analysis. According to the study authors, about
36 percent of women living in the United States have urinary iodide
levels less than 100 [mu]g/L (Caldwell et al., 2005). For women with
urinary iodide levels less than 100 [mu]g/L, the study found that
urinary perchlorate is associated with a decrease in (a negative
predictor for) T4 levels and an increase in (a positive predictor for)
TSH levels. For women with urinary iodide levels greater than or equal
to 100 [mu]g/L, the researchers found that perchlorate is a significant
positive predictor of TSH but not a predictor of T4. The study found
that perchlorate was not a significant predictor of T4 or TSH in men.
The researchers state that perchlorate could be a surrogate for another
unrecognized determinant of thyroid function. Also, the study reports
that while large doses of perchlorate are known to decrease thyroid
function, this is the first time an association of decreased thyroid
function has been observed at these low levels of perchlorate exposure.
Of note is that the vast majority of the participants in this group had
urinary levels of perchlorate corresponding to estimated dose levels
that are below the RfD of 0.0007 mg/kg/day. The clinical significance
of the variations in T4/TSH levels, which were generally within normal
limits, has not been determined. The researchers noted several
limitations of the study (e.g., assumption that urinary perchlorate
correlates with perchlorate levels in the stroma and tissue and
preference for measurement of free T4 as opposed to total T4) and
recommended that these findings be confirmed in at least one more large
study focusing on women with low urine iodide levels. It is also not
known whether the association between perchlorate and thyroid hormone
levels is causal or mediated by some other correlate of both, although
the relationship between urine perchlorate and total TSH and T4 levels
persisted after statistical adjustments for some additional covariates
known to predict thyroid hormone levels (e.g., total kilocalorie
intake, estrogen use, and serum C-reactive protein levels). A planned
follow-up study will include additional measures of thyroid health and
function (e.g., TPO-antibodies, free T4). As EPA proceeds towards a
regulatory determination for perchlorate, the Agency will continue to
review any new findings/studies on perchlorate and their relationship
to thyroid function as they become available.
---------------------------------------------------------------------------
\19\ While CDC researchers measured urinary perchlorate
concentration for 2,820 NHANES participants, TSH and total T4 serum
levels were only available for 2,299 of these participants.
\20\ WHO notes that the prevalence of goiter begins to increase
in populations with a median iodide intake level below 100 [mu]g/L
(WHO, 1994).
---------------------------------------------------------------------------
C. Occurrence in Water, Food, and Humans
1. Sources of Perchlorate. Section V.A. summarizes the potential
sources of perchlorate in the environment.
2. Studies on Perchlorate Occurrence in Public Drinking Water
Systems and/or Drinking Water Sources. EPA included perchlorate as an
analyte in the 1999 Unregulated Contaminant Monitoring Regulation (UCMR
1) and collected drinking water occurrence data for perchlorate from
3,858 public water systems (PWSs) between 2001 and 2005. EPA analyzed
the available UCMR 1 data on perchlorate at concentrations greater than
or equal to 4 [mu]g/L, the minimum reporting limit (MRL) for EPA Method
314.0.\21\ The Agency found that approximately 4.1 percent (or 160) of
3,858 PWSs that sampled and reported under UCMR 1 had at least 1
analytical detection of perchlorate (in at least 1 entry/sampling
point) at levels greater than or equal to 4 [mu]g/L. These 160 systems
are located in 26 states and 2 territories. Of these 160 PWSs, 8 are
small systems (serving 10,000 or fewer people) and 152 are large
systems (serving more than 10,000 people). Approximately 1.9 percent
(or 637) of the 34,193 samples collected (by these 3,858 PWSs) had
positive detections of perchlorate at levels greater than or equal to 4
[mu]g/L. The maximum reported concentration of perchlorate was 420
[mu]g/L, which was found in a surface water sample from a PWS in Puerto
Rico. The average concentration of perchlorate for those samples with
positive detections for perchlorate was 9.85 [mu]g/L and the median
concentration was 6.40 [mu]g/L.
---------------------------------------------------------------------------
\21\ EPA Method 314.0 was the analytical method approved and
used for UCMR 1 at the time of data collection.
---------------------------------------------------------------------------
These 160 PWSs (with at least 1 analytical detection for
perchlorate at levels greater than or equal to 4 [mu]g/L) serve
approximately 7.5 percent (or 16.8 million) of the 225 million people
served by the 3,858 PWSs that sampled and reported results under UCMR
1. The 16.8 million population-served value represents the total number
of people served by the 160 PWSs with at least one detect. Not all
people served by these systems necessarily have perchlorate in their
drinking water. Some of these 160 public water systems have multiple
entry points to the distribution system and not all of the entry points
sampled had positive detections for perchlorate in the UCMR 1 survey.
An alternative approach to the system-level assessment of populations
served is to use an assessment at the entry (sampling) point level.\22\
EPA does not have population-served values for each entry point at the
system level. However, an assessment can be performed by assuming that
each entry (or sampling) point at a public water system serves an equal
proportion of the total population-served by the system. In other
words, for the alternative assessment, the population served by each
system is assumed to be equally distributed across all entry (or
sampling) points at each system. For example, if a system serves a
million people and has 5 entry points, it is assumed that each entry
point serves 200,000 people. Using this approach and counting only
[[Page 24041]]
the population served for the entry points with positive detections
(concentrations greater than or equal to 4 [mu]g/L), the total
population served by these entry points with perchlorate detections is
approximately 5 million. Section V.E provides the number of systems and
population-served estimates for other thresholds of interest.
---------------------------------------------------------------------------
\22\ EPA acknowledges that uncertainties exist in the
population-served estimates for this alternative assessment since
the population for a system is assumed to be equally distributed
across the entry points for that system. Because the actual
population-served by an entry point is not known, this alternative
approach has an equal chance of underestimating or overestimating
the actual population-served by entry points with positive
detections for perchlorate. In addition, this approach could
underestimate the population served that is potentially exposed to
perchlorate and overestimate the level of exposure because it can
not incorporate the effects of mixing of water between different
entry points within the distribution system. This is because the
approach cannot account for the dilution that may occur when water
that has no detections of perchlorate is mixed within the
distribution system with water that has positive detections for
perchlorate.
---------------------------------------------------------------------------
The California Department of Health Services (CA DHS) began
monitoring for perchlorate in 1997. In 1999, CA DHS began requiring
monitoring for perchlorate for drinking water sources that were
identified as vulnerable to perchlorate contamination under
California's own State monitoring program (i.e., Unregulated Chemicals
for which Monitoring is Required). About 60 percent (or 7,100) of all
drinking water sources in California (about 12,000) were monitored for
perchlorate under the State monitoring program. Between June 2001 and
June 2006, CA DHS (2006) reports that 284 (about 4%) of the
approximately 7,100 water sources that monitored had at least 2 or more
positive detections for perchlorate at concentrations greater than or
equal to 4 [mu]g/L (the reporting limit). These 284 sources supply
water for 77 drinking water systems (CA DHS, 2006) and represent active
and standby sources (and exclude inactive, destroyed, and abandoned
sources, and monitoring and agricultural wells) (CA DHS, 2006).
In 2005, the State of Massachusetts's Department of Environment
Protection (MA DEP) reported monitoring results for 85 percent (379 of
450) of its community water systems and 86 percent (212 of 250) of its
non-transient, non-community water systems. MA DEP found that 9 (1.5%)
of the 591 public water systems detected perchlorate at levels greater
than or equal to 1 [mu]g/L (the reporting limit used for a modified
version of EPA Method 314.0). MA DEP found that the occurrence of
perchlorate for these water systems could be traced to the use of
blasting agents, military munitions, fireworks, and, to a lesser
degree, sodium hypochlorite disinfectant (MA DEP, 2005).
3. Studies on Perchlorate Occurrence in Foods, Plants, Beverages,
and Dietary Supplements. The Food and Drug Administration (FDA), the
United States Department of Agriculture (USDA), and researchers from
academia and industry have studied perchlorate in foods. Some of these
studies are described briefly in this section, and also summarized in
Table 4. EPA has concluded that the sampling results described in this
section and Table 4 are too limited to characterize food-borne exposure
to perchlorate on a national scale. The sampling data are limited in
the types of foods sampled, sample sizes, geographic coverage, and/or
analytical method adequacy and many were targeted to foods or areas
known or likely to have elevated levels of perchlorate. Section V.F of
this action describes the limitations of the food sampling data and
also describes plans for including perchlorate as part of the FDA's
Total Diet Study. EPA requests that commenters provide the Agency with
any additional data that may further characterize the concentrations of
perchlorate in foods commercially available in the U.S. When providing
data to the Agency, please describe the specific locations where the
samples were collected, including geographic location, type of location
(e.g., grocery store, farmer's market, commercial field, home garden),
and the methodologies used to select, collect, prepare, and analyze the
samples. Please include available laboratory data reports as well as
all relevant quality assurance/quality control information.
BILLING CODE 6560-50-P
[GRAPHIC] [TIFF OMITTED] TP01MY07.052
[[Page 24042]]
[GRAPHIC] [TIFF OMITTED] TP01MY07.053
[GRAPHIC] [TIFF OMITTED] TP01MY07.054
BILLING CODE 6560-50-C
a. FDA Targeted Sampling. The FDA released data on perchlorate in
milk, lettuce, and bottled water in November 2004. To analyze food
samples, FDA used ion chromatography (IC)-tandem mass spectrometry (MS/
MS), referred to as IC-MS/MS. The quantitation limits for perchlorate
in these analyses were 0.5 [mu]g/L for bottled water, 1 [mu]g/kg by
fresh weight (FW) for lettuce, and 3 [mu]g/L for dairy milk. The mean
concentration of perchlorate in 128 lettuce samples collected in 5
states (AZ, CA, FL, NJ, TX) was 10.3 [mu]g/kg FW (FDA, 2004), and
ranged from not quantifiable (NQ) to 129 [mu]g/kg FW. The mean
concentrations of perchlorate in several varieties of lettuce are
reported in Table 4. The mean concentration of perchlorate in 104 dairy
milk samples collected in 14 states (AZ, CA, GA, KS, LA, MD, MO, NJ,
NC, PA, SC, TX, VA, WA) was 5.76 [mu]g/L (FDA, 2004), with a range from
NQ to 11.3 [mu]g/L. FDA (2004) detected perchlorate in 2 of the 51
bottled water samples representing 34 distinct sources collected in 12
states (CA, CO, GA, MD, MN, MO, NC, NE, PA, SC, TX, WI) at levels of
0.56 [mu]g/L and 0.45 [mu]g/L.
b. Other Published Studies. Sanchez (2004) and Sanchez et al.
(2005a) report the results of an analysis of agricultural products
sampled from the lower Colorado River region of Arizona and California,
the Imperial Valley of California, and the Coachella Valley of
California, where irrigation water is known or suspected to contain
perchlorate. The studies were partially supported by the U.S.
Department of
[[Page 24043]]
Agriculture--Agricultural Research Service (USDA-ARS). Samples of
iceberg, romaine, and leaf lettuce, carrots, onions, sweet corn,
squash, melons, tomatoes, peppers, broccoli, cauliflower, cabbage,
durum wheat, and alfalfa were analyzed for perchlorate using ion
chromatography (IC) as the primary analytical method. For these
analyses, the fresh-weight method reporting limit was not identified in
most cases, but was reported to range from 20 to 50 [mu]g/kg FW,
depending on the moisture content of the samples (Sanchez, 2004).
Sanchez et al. (2005a) report that the method reporting level for
iceberg lettuce was approximately 20 [mu]g/kg FW and for other types of
lettuce was 25-30 [mu]g/kg FW. Perchlorate in the irrigation water
ranged from 1.5 to 8.0 [mu]g/L over the period of the survey (Sanchez
et al., 2005a).
Sanchez et al. (2005a) analyzed 44 samples of iceberg lettuce heads
that had been trimmed of frame and wrapper leaves, which are usually
removed before the lettuce is consumed. Perchlorate was quantified in 5
of the samples (ranging from 23 to 26 [mu]g/kg FW),\23\ perchlorate was
not detectable in 6 samples, and the results of the remaining samples
were less than the method reporting limit, which the authors defined as
``a detectable peak among duplicates and/or replicates but below a
level that can be quantitated.'' Perchlorate concentrations in 10
samples of romaine and green leaf lettuce ranged from less than the
method reporting limit to 81[mu]g/kg FW (Sanchez, 2004).
---------------------------------------------------------------------------
\23\ Sanchez (2004) presents somewhat different results.
Specifically, of the 44 samples of ``edible head'' lettuce,
perchlorate was quantified in one of the samples (26 [mu]g/kg),
perchlorate was not detectable in 6 samples, and the remaining
sampling results were qualified as < MRL, which the author defined as
``represents a seemingly detectable peak but below a level that can
be quantitated.''
---------------------------------------------------------------------------
As shown in Table 4, Sanchez (2004) also detected perchlorate in
samples of melons, tomatoes, and peppers, but at levels below the
method reporting limit. Perchlorate was not detected in carrots,
onions, sweet corn, squash, and durum wheat. Concentrations of
perchlorate in 10 samples of alfalfa ranged from 109 to 668 [mu]g/kg
FW. Six of the 10 alfalfa samples were sent to FDA for confirmatory
analysis by IC-MS/MS. The FDA results were generally lower than those
of the corresponding samples by Sanchez (2004), ranging from 121 to 382
[mu]g/kg FW.
Sanchez et al. (2006) conducted studies to evaluate the uptake and
distribution of perchlorate in citrus trees and the occurrence of
perchlorate in lemons, grapefruit, and oranges grown in southern
California and southwestern Arizona. Five whole lemon trees irrigated
with Colorado River water were harvested for destructive sampling.
Sanchez et al. (2006) estimate that the irrigation water had an average
perchlorate concentration of 6 [mu]g/L. Most of the sample analysis was
conducted using IC-MS/MS, having an MRL of approximately 25 [mu]g/kg by
dry weight (DW). In samples of tree trunks, roots, and branches,
perchlorate was close to or below the MRL. Perchlorate was much higher
in the leaves than the fruit (peel and pulp), with mean concentrations
of 1,835 and 128 [mu]g/kg DW, respectively.
Citrus samples were collected during 2004-2005 from the lower
Colorado River Valley, the University of Arizona Research Farm, the
Coachella Valley, and Los Angeles County. All analyses of fruit pulp
were conducted using IC-MS/MS with an approximate MRL of 2.5 [mu]g/kg
FW. For the 86 citrus samples collected, the perchlorate concentration
in the fruit pulp ranged from below detection to 37.6 [mu]g/kg FW. Mean
concentrations in lemons (33 samples), grapefruit (15 samples), and
oranges (28 samples) were 2.3, 3.3, and 7.4 [mu]g/kg FW, respectively.
Sanchez et al. (2005b) surveyed perchlorate occurrence in lettuce
and other leafy vegetables produced outside the lower Colorado River
region. Samples were analyzed by IC, with a minimum reporting level of
approximately 20 to 40 [mu]g/kg FW, depending on the leafy vegetable
type. Results of some of the more heavily sampled food items are
presented in Table 4.
While not shown in Table 4, Sanchez et al. (2005b) performed
additional analysis by partitioning the leafy vegetable samples by type
of culture. Perchlorate was detected in 70 of 268 samples of
conventionally-grown leafy vegetables and 72 of 170 samples of
organically-grown leafy vegetables. The range of perchlorate
concentrations was ND to 104 [mu]g/kg FW in conventional leafy
vegetables and ND to 628 [mu]g/kg FW in organic leafy vegetables.
Sanchez et al. (2005b) analyzed the results using regression analysis
and estimated that the median perchlorate concentration in organically-
grown samples was 2.2 times higher than in conventionally-grown
samples. The regression analysis also suggested that variation among
sampling locations was greater than variation among lettuce types.
Researchers at Texas Tech University analyzed samples of dairy and
soy milk using IC and/or IC/MS analytical methods with detection limits
of 1 [mu]g/L or better (Kirk et al., 2005). In a study of perchlorate
in dairy milk, Kirk et al. (2005) found mean perchlorate levels of 2.0
[mu]g/L in 47 retail dairy milk samples from 11 states (AK, AZ, CA, FL,
HI, KS, ME, NH, NM, NY, PA), with a range from not detected (ND) to
11.0 [mu]g/L. A single sample of soy milk was analyzed and reported to
contain 0.7 [mu]g/L perchlorate (Kirk et al., 2005). An earlier study
by Kirk et al. (2003) found perchlorate ranging from 1.7 [mu]g/L to 6.4
[mu]g/L in 7 dairy milk samples purchased in a city in Texas.
Jackson et al. (2005) conducted limited sampling of edible and
forage vegetation in 1 Texas county and in 1 Kansas home garden. In
Texas, wheat and alfalfa were sampled from commercial fields irrigated
with groundwater containing perchlorate from an unknown source, and a
cucumber was sampled from an irrigated home garden. In Kansas,
cantaloupe, cucumber, and tomatoes were sampled from an irrigated home
garden near a slurry explosives site. Researchers used IC for sample
analysis but did not report fresh-weight detection limits. Perchlorate
was detected in all 12 samples of winter wheat heads (whole, including
the chaff) at a mean concentration of 2,000 [mu]g/kg FW but perchlorate
was not detected in wheat endosperm (2 samples)\24\. The mean
perchlorate concentration in 3 samples of alfalfa was 2,900 [mu]g/kg
FW. A cucumber sample from a Texas home garden contained 40 [mu]g/kg FW
perchlorate; a sample of irrigation water from this garden contained
20.7 [mu]g/L perchlorate. In the Kansas home garden, the cucumber
sample contained 770 [mu]g/kg FW perchlorate, the cantaloupe sample
contained 1,600 [mu]g/kg FW perchlorate, and 2 samples of tomato
contained 42 and 220 [mu]g/kg FW perchlorate. The reported
concentration of perchlorate in irrigation water for the Kansas home
garden was 81 [mu]g/L. EPA notes that the perchlorate levels in
irrigation water samples associated with these two home gardens were
significantly higher than in the vast majority of surface and ground
water samples in the US.
---------------------------------------------------------------------------
\24\ A wheat kernel (seed) has three major parts--the bran, the
germ, and the endosperm. The majority of the wheat kernel is the
endosperm, which is the portion of the kernel that is retained in
refined (white) wheat flours. Whole wheat flours contain endosperm,
wheat bran, and wheat germ in approximately the same proportions as
in the wheat kernel. Wheat flours do not contain the chaff (husk).
---------------------------------------------------------------------------
Aribi et al. (2006) developed an analytical method for perchlorate
that uses ion chromatography with suppressed conductivity and
electrospray ionization tandem mass
[[Page 24044]]
spectrometry (IC-ESI-MS/MS). The method was used to measure perchlorate
in samples of various food products, including fresh/canned fruits and
vegetables, wine, beer, and other beverages. Most samples were
purchased in grocery and liquor stores in greater Toronto, Canada,
between January 2005 and February 2006. Produce samples originated from
many different parts of the world and all samples contained measurable
amounts of perchlorate. However, the survey was limited to only a few
samples of each food. Products from California, Chile, Costa Rica,
Guatemala, and Mexico had the highest levels of perchlorate. Products
from Canada and China had the lowest levels of perchlorate. The highest
detection was in cantaloupe from Guatemala (463.50 [mu]g/kg FW).
Analysis of raw asparagus (39.900 [mu]g/kg FW) and cooked asparagus
(24.345 [mu]g/kg FW) demonstrated that perchlorate can remain in food
processed at a high temperature. Perchlorate concentrations in 8
samples of produce from the U.S. ranged from 0.094 [mu]g/kg FW (for
blueberries) to 19.29 [mu]g/kg FW (for green grapes).
Aribi et al. (2006) analyzed 77 samples of wine and 144 samples of
beer from many parts of the world. All samples contained measurable
amounts of perchlorate. The wine sample with the single highest
concentration of perchlorate, 50.250 [mu]g/L, was from Portugal.
Overall, wine samples from Chile contained the highest concentrations
of perchlorate, ranging from 5.358 to 38.88 [mu]g/L in 8 samples.
Twelve samples of wine from the U.S. contained perchlorate
concentrations ranging from 0.197 to 4.593 [mu]g/L. Results from
analysis of beer samples varied substantially among countries, with an
overall range from 0.005 [mu]g/L (Ireland) to 21.096 [mu]g/L (France).
Concentrations of perchlorate in 8 beer samples from the U.S. ranged
from 0.364 to 2.014 [mu]g/L.
Snyder et al. (2006) measured perchlorate in dietary supplements
and flavor enhancing ingredients collected from various vendors in Las
Vegas, NV, and Seattle, WA. Analyses were performed using LC-MS/MS with
a limit of detection between 2 and 5 [mu]g/kg. Perchlorate was detected
in 20 of 31 analyzed supplements, with detectable concentrations
ranging from 10 to 2,420 [mu]g/kg. Based on manufacturers' recommended
intake of the supplements, the resulting daily oral doses of
perchlorate would range from 0.03 to 18 [mu]g/day. Twelve of the
supplements tested were prenatal or children's vitamins. The highest
level of perchlorate (2,420 [mu]g/kg or 0.018 mg/day at the recommended
daily dose) was found in a prenatal vitamin; in the remaining prenatal
and children's vitamins perchlorate did not exceed 28 [mu]g/kg. The
study noted that ``vitamin and mineral supplements are typically
formulated to include the Recommended Daily Allowance (RDA) of iodine,
a factor that would provide protection against any possible impacts of
microgram levels of perchlorate found in these supplements.''
Perchlorate was also detected at 740 [mu]g/kg in a sample of kelp
granules (a flavor enhancer), which equates to 2.2 [mu]g perchlorate
per serving.
Martinelango et al. (2006a) measured perchlorate in seaweed, which
is often used as a source of iodide in food and nutritional
supplements. Martinelango et al. (2006a) collected samples of 11
different species of seaweed growing off the coast of northeastern
Maine. Perchlorate was detected in all species, with concentrations
ranging from 29 to 878 [mu]g/kg DW. The iodide content in the samples
was much higher, ranging from 16 to 3,134 mg/kg DW. Martinelango et al.
(2006a) found that samples of Laminaria species concentrated iodide
more selectively than perchlorate. Laminaria is a genus of large brown
seaweeds that are commonly used in kelp tablets. Martinelango et al.
(2006a) also analyzed 4 seaweed samples that had been washed with
deionized water and found that a single wash removed 38 to 73 percent
of the perchlorate and 34 to 44 percent of the iodide.
D. Occurrence Studies on Perchlorate in Human Urine, Breast Milk, and
Amniotic Fluid
Recently researchers have used the results of the analysis of urine
samples to estimate human exposure to perchlorate. Ingested perchlorate
is not metabolized by humans and is excreted largely in the urine
(Merrill et al., 2005). The CDC's National Center for Environmental
Health (NCEH) developed a sensitive and selective analytical method to
analyze perchlorate in human urine (Valentin-Blasini et al., 2005). The
method uses ion chromatography coupled with electrospray ionization
tandem mass spectrometry (IC/MS/MS) and achieves an MRL of 0.025 [mu]g/
L in human urine. The authors report that the method is robust enough
to process first-morning-void urine samples, which are samples of the
first voiding of urine upon waking.
Valentin-Blasini et al. (2005) analyzed urine samples from 61
healthy adult donors who lived in the area of Atlanta, Georgia. The
urine samples were provided anonymously, without associated donor
information. Perchlorate was detected in all of the urine samples, with
concentrations ranging from 0.66 to 21 [mu]g/L. The authors cited
dietary exposure as a potential source of perchlorate because
perchlorate was found only at low levels (0.1--0.2 [mu]g/L) in area tap
water samples (Valentin-Blasini et al., 2005).
Valentin-Blasini et al. (2005) also analyzed the urine samples for
creatinine, which is a metabolic breakdown product in muscles that is
eliminated from the body in urine at a predictable rate. When adjusted
for urinary creatinine content, the reported range of perchlorate in
the samples is 1.0 to 35 [mu]g of perchlorate per gram of creatinine.
The median perchlorate concentration was 3.2 [mu]g/L (7.8 [mu]g/g
creatinine). The researchers stated that only 1 sample from the Atlanta
population contained perchlorate at a level slightly in excess of the
amount expected to be excreted by an individual exposed to perchlorate
at the reference dose of 0.0007 mg/kg/day (Valentin-Blasini et al.,
2005). Specifically, assuming that perchlorate is excreted uniformly in
urine throughout the day, a urinary excretion level of 34 [mu]g
perchlorate per gram creatinine would be associated with a daily
perchlorate intake of 0.0007 mg/kg/day, for a 70 kg male that excretes
creatinine at a typical rate of 1.44 grams per day (g/day). These
assumptions are imprecise for individual exposure assessment but allow
for spot urine perchlorate excretion to be related to the reference
dose for toxicological perspective. Estimating perchlorate exposure
from a single spot urine sample (as opposed to a sample collected
continuously over a period of time) is imprecise due to the episodic
nature of perchlorate exposure and the short half-life of perchlorate
in the human body. The precision of estimated individual perchlorate
exposure can be improved by more precise estimation of 24-hour
creatinine excretion based on sex, height, weight, and age as described
by Mage et al. (2004). In addition, imprecision stemming from the
episodic nature of perchlorate exposure can be reduced with increased
sampling.
The analytical method developed by Valentin-Blasini et al. (2005)
was further used by Blount et al. (2006a) to evaluate urine samples
from 27 volunteers with differing dietary habits. Blount et al. (2006a)
collected first-morning-void urine specimens from volunteers living in
the Atlanta area. The study volunteers self-assessed their consumption
of milk, dairy products, and green/leafy vegetables within the 16 hours
before the sample was collected.
[[Page 24045]]
The samples were grouped into 2 categories (``one or fewer servings''
and ``three or more servings'') based on total consumption of these
selected foods. Total daily perchlorate exposure was calculated using a
bodyweight of 70 kg and a creatinine excretion rate of 1.44 g/day,
assuming that each first-morning void urine sample was representative
of that individual's daily perchlorate exposure. Each volunteer also
collected a drinking water sample from home and work. Blount et al.
(2006a) analyzed drinking water samples with the same method used for
urine analysis and estimated exposure from drinking water based on a
body weight of 70 kg and daily consumption of 2 liters of water per
day. The mean creatinine-adjusted urinary perchlorate level was 1.8
times higher for individuals who identified themselves as consuming
three or more servings of milk, dairy products, and/or green/leafy
vegetables (6.13 versus 3.45 [mu]g/g creatinine). There were no
significant differences in the perchlorate levels in the drinking water
samples of the 2 diet groups, which ranged from < 0.05 to 0.25 [mu]g/L
with a median of 0.10 [mu]g/L. Using a median drinking water level of
0.10 [mu]g/L, Blount et al. (2006a) estimated that the perchlorate dose
from drinking water was 0.003 [mu]g/kg/day. Compared to this drinking
water estimate, the total perchlorate dose estimate based on mean
urinary perchlorate excretion was 24 times higher (0.071 [mu]g/kg/day)
and 42 times higher (0.126 [mu]g/kg/day) for the low-consumption and
high-consumption diet groups, respectively. The overall range of
perchlorate found in urine was 0.94 to 17 [mu]g/g creatinine with a
median of 4.2 [mu]g/g creatinine.
In the largest study of its kind, Blount et al. (2006c) measured
perchlorate in urine samples collected from a nationally representative
sample of 2,820 U.S. residents, ages 6 years and older, as part of the
2001-2002 NHANES. Blount et al. (2006c) detected perchlorate at
concentrations greater than 0.05 [mu]g/L in all 2,820 urine samples
tested, with a median concentration of 3.6 [mu]g/L (3.38 [mu]g/g
creatinine) and a 95th percentile of 14 [mu]g/L (12.7 [mu]g/g
creatinine). Only 0.7% of the study participants had an estimated
perchlorate dose in excess of 0.0007 mg/kg/day. Women of reproductive
age (15-44 years) had a median urinary perchlorate concentration of 2.9
[mu]g/L (2.97 [mu]g/g creatinine) and a 95th percentile of 13 [mu]g/L
(12.1 [mu]g/g creatinine). The demographic with the highest
concentration of urinary perchlorate was children (6-11 years), who had
a median urinary perchlorate concentration of 5.2 [mu]g/L (5.79 [mu]g/g
creatinine). Blount et al. (2006c) estimated a total daily perchlorate
dose for each adult and found a median dose of 0.066 [mu]g/kg/day
(about one tenth of the RfD) and a 95th percentile of 0.234 [mu]g/kg/
day (about one third of the RfD). Eleven adults (0.7%) had estimated
perchlorate exposure in excess of the RfD (0.7 [mu]g/kg/day). The
highest estimated exposure was 3.78 [mu]g/kg/day. Because of daily
variability in diet and perchlorate exposure, and the short residence
time of perchlorate in the body, these single sample measurements may
overestimate long-term average exposure for individuals at the upper
end of the distribution and may underestimate the long-term average
exposure for individuals at the lower end of the distribution. Daily
perchlorate dose is not presented for children and adolescents due to
the limited validation of formulas for these age groups (Blount et al.,
2006c).
Valentin-Blasini et al. (2005) and T[eacute]llez et al. (2005)
analyzed urine samples of pregnant women in 3 cities in Chile and found
higher median levels of urinary perchlorate in cities with higher
concentrations of perchlorate in tap water. Based on an assessment of
drinking water intake, the researchers determined that, in all 3
cities, there was an additional source of perchlorate for the study
participants that may be explained by dietary (food) intake
(T[eacute]llez et al., 2005). This gap between estimated perchlorate
exposure and perchlorate intake from tap water consumption ranged from
21.7 [mu]g/day to 33.8 [mu]g/day in the 3 Chilean cities (T[eacute]llez
et al., 2005).
Martinelango et al. (2006b) developed a method to measure
perchlorate in human urine with a limit of detection of 0.080 [mu]g/L,
and reported analytical results of 9 spot urine samples from male and
female volunteers. Perchlorate was present in all samples analyzed, at
concentrations ranging from 2.2 to 14.9 [mu]g/L, with a median value of
8.1 [mu]g/L.
Other studies have investigated perchlorate in human breast milk.
Kirk et al. (2005) analyzed 36 breast milk samples from 18 states (CA,
CT, FL, GA, HI, MD, ME, MI, MO, NC, NE, NJ, NM, NY, TX, VA, WA, WV) and
found perchlorate concentrations in all samples ranging from 1.4 to
92.2 [mu]g/L in all samples, with a mean concentration of 10.5 [mu]g/L.
T[eacute]llez et al. (2005) report maternal parameters for participants
from the study in Chile. Breast milk samples indicated that a
significant amount of perchlorate leaves the body of the nursing mother
through breast milk, in addition to urine. However, the breast milk
perchlorate levels were highly variable and no significant correlations
could be established between breast milk perchlorate and either urine
perchlorate or breast milk iodide concentrations for the individuals
evaluated in these Chilean cities (T[eacute]llez et al., 2005). Kirk et
al. (2006) evaluated variations of iodide, thiocyanate and perchlorate
in human milk samples. These authors suggest that if the overall intake
of iodide is sufficient, it is unlikely that milk with an occasional
low iodide or high perchlorate content would pose a major risk to
infants. However, their limited data (evaluating only 10 women) show
that the milk of some women may not supply infants with adequate iodide
and they suggest that it may be important to base risk assessments for
perchlorate exposure on the iodide to perchlorate ratio or the ratio of
iodide to a ``selectively-weighted sum of iodide uptake inhibiting
agents.''
Blount and Valentin-Blasini (2006) developed a sensitive and
selective method for quantifying iodide, perchlorate, thiocyanate, and
nitrate in human amniotic fluid. The analytical limit of detection for
perchlorate was calculated to be 0.020 [mu]g/L. Samples of amniotic
fluid at 15 to 20 weeks gestation were collected from 48 healthy women
in an Eastern U.S. city for analysis. Perchlorate was found in all
samples tested and exhibited a log-normal distribution. The perchlorate
concentrations ranged from 0.057 to 0.71 [mu]g/L with a median value of
0.18 [mu]g/L.
E. Status of the Preliminary Regulatory Determination for Perchlorate
As stated earlier, the Agency is not making a preliminary
regulatory determination for perchlorate in this notice. The Agency
believes that additional information is needed on the sources of human
exposure if it decides to base its determination regarding health risk
reduction potential on a health reference level (HRL) derived from the
RfD and the relative source contribution (RSC) for drinking water.
Under this approach, the Agency would use the RfD and RSC to estimate
an HRL and then use this HRL as a benchmark against which to conduct an
evaluation of the occurrence data. In conducting such an assessment for
the 6 non-carcinogens discussed previously in this action, EPA used a
20 percent RSC, which is the lowest and most conservative RSC used to
estimate an HRL. Since the initial screening of the occurrence data
against the HRL resulted in a preliminary negative determination, the
Agency found that it
[[Page 24046]]
was not necessary to further evaluate the RSC for these contaminants.
In the case of perchlorate, the Agency is not at the point of being
able to make either a negative or a positive determination using this
approach because it is not yet clear what an appropriate RSC for
perchlorate is. If EPA were to use a default RSC of 20% for
perchlorate, the resulting HRL would be 5 [mu]g/L. Approximately 3.16%
of the 3,858 PWSs in the UCMR1 data set had at least one detect of
perchlorate greater than or equal to 5 [mu]g/L. Given this level of
occurrence at the default-derived HRL, the Agency believes a better
informed RSC and HRL would be needed to use this approach to determine
whether regulation of perchlorate in drinking water presents a
meaningful opportunity for health risk reduction.
Table 5 shows the number of systems and population served that
would exceed the HRL under various RSC scenarios and the sensitivity of
this estimate to relatively small changes in the estimated RSC. For
example, increasing the RSC from 20 to 30 percent would lower the
estimated number of systems impacted by about a third and the estimated
population served by about half. Hence, the choice of an appropriate
RSC and resulting HRL could impact EPA's determination of whether
regulation of perchlorate represents a meaningful opportunity for
health risk reduction if it uses this approach.
EPA recognizes that system-level population estimates shown in
Table 5 may be conservative because some systems have multiple entry
points to the distribution system and not all entry points had a
positive detection for perchlorate in the UCMR 1 survey. Hence, to
derive a less conservative population estimate (last column in Table
5), EPA assumed that the population for each system is equally
distributed over all of the entry (or sampling) points and estimated a
population-served value based on entry points that had at least 1
analytical detection for perchlorate at levels greater than each of the
HRL thresholds.
Table 5.--UCMR 1 Occurrence and Population Estimates for Perchlorate at Various HRL Thresholds a
--------------------------------------------------------------------------------------------------------------------------------------------------------
Population
Population estimate for
PWS entry or sample served by PWSs entry or sample
Estimated HRL thresholds PWSs with at least 1 points with at least 1 with at least 1 points having
RSC scenarios (percent) based on various RSC detection > threshold of detection > threshold of detection > at least 1
scenarios \b\ interest interest \c\ threshold of detection >
interest \d\ threshold of
interest \e\
--------------------------------------------------------------------------------------------------------------------------------------------------------
20.................................... 5 [mu]g/L................ 3.16% (122 of 3,858)..... 1.88% (281 of 14,984)... 14.6 M 4.0 M
30.................................... 7 [mu]g/L................ 2.13% (82 of 3,858)...... 1.14% (171 of 14,984)... 7.2 M 2.2 M
40.................................... 10 [mu]g/L............... 1.35% (52 of 3,858)...... 0.65% (97 of 14,984).... 5.0 M 1.5 M
50.................................... 12 [mu]g/L............... 1.09% (42 of 3,858)...... 0.42% (63 of 14,984).... 3.6 M 1.2 M
60.................................... 15 [mu]g/L............... 0.80% (31 of 3,858)...... 0.29% (44 of 14,984).... 2.0 M 0.9 M
70.................................... 17 [mu]g/L............... 0.70% (27 of 3,858)...... 0.24% (36 of 14,984).... 1.9 M 0.8 M
80.................................... 20 [mu]g/L............... 0.49% (19 of 3,858)...... 0.16% (24 of 14,984).... 1.5 M 0.7 M
100................................... 25 [mu]g/L............... 0.36% (14 of 3,858)...... 0.12% (18 of 14,984).... 1.0 M 0.4 M
--------------------------------------------------------------------------------------------------------------------------------------------------------
Footnotes:
\a\ These data represent summary statistics for the 3,858 public water systems that have sampled for perchlorate as a part of the UCMR 1 survey.
\b\ HRL threshold = [(RfD of 0.0007 mg/kg/day x 70 kg BW for pregnant female) / (2 L DWI)] x the RSC scenario. Each HRL threshold value is converted
from mg/L to [mu]g/L units and then rounded to the nearest whole number.
\c\ The entry/sample-point-level population served estimate is based on the system entry/sample points that had at least 1analytical detection for
perchlorate greater than the HRL threshold of interest. The UCMR 1 small system survey was designed to be representative of the nation's small
systems, not necessarily to be representative of small system entry points.
\d\ The system-level population served estimate is based on the systems that had at least 1analytical detection for perchlorate greater than the HRL
threshold of interest.
\e\ Because the population served by each entry/sample point is not known, EPA assumed that the total population served by a particular system is
equally distributed across all entry/sample points. To derive the entry/sample point-level population estimate, EPA summed the population values for
the entry/sample points that had at least 1 analytical detection greater than the threshold of interest.
Table 5 also includes information on the effects of using an RSC of
100% (that is, using an HRL set at the DWEL of 24.5 [mu]g/L, rounded to
a whole number). Crawford-Brown et al. (2006), in an estimate of risk
variability from perchlorate exposure through community water systems,
noted that the subjects in the original 2002 Greer et al., study (on
which the RfD of .0007 mg/L was based) presumably had other sources of
perchlorate exposure outside of the study and suggested that it may be
appropriate to view their results as reflecting the effects of
incremental exposure to perchlorate above the background levels already
in food and water rather than the effects of total exposure, as is
implicitly assumed when the HRL is derived using an RSC to account for
other sources of exposure. Use of an RSC to derive the HRL is clearly
appropriate when the RfD or cancer slope factor is derived from animal
studies with carefully controlled exposure. Crawford-Brown et al.
suggest, however, that an RSC is not necessary for perchlorate because
there is no reason to assume that the background exposure of the study
subjects was different than that of the general population. EPA notes
that the sample size in the Greer study was small and EPA is not aware
of data on their background exposure to perchlorate or how
representative it may be. EPA requests comment on whether information
is available on the background exposure of subjects in the Greer study
and whether it should consider the background exposure of these
subjects in determining an HRL for perchlorate.
While several States have recommended guidelines or public health
goals for perchlorate, EPA recognizes that at least 1 state,
Massachusetts,\25\ has already promulgated a final drinking water
standard for perchlorate, that other States may set drinking water
standards in the future, and that these standards
[[Page 24047]]
could impact national occurrence estimates once these standards are
fully implemented.
---------------------------------------------------------------------------
\25\ Massachusetts promulgated a final drinking water standard
of 2 [mu]g/L for perchlorate on July 28, 2006. For more information
about the final standard, see http://www.mass.gov/dep/public/press/pchl0706.htm
(MA DEP, 2006).
---------------------------------------------------------------------------
F. What Are the Potential Options for Characterizing Perchlorate
Exposure and Proceeding With the Preliminary Regulatory Determination
for Perchlorate?
While the Agency recognizes that food and other pathways may be
important sources of perchlorate exposure, the Agency believes the
currently available food data (summarized in section V.C.3) are
inadequate to develop a better informed RSC (and HRL). First, some of
the existing data are limited in their sample numbers, geographic
coverage, and analytical method adequacy. Second, the current studies
provide little or no data for several food groups (e.g., meat, poultry,
fish, eggs, root and tuber vegetables, brassica vegetables, bulb
vegetables, tree fruits, legumes, and cereal grains) that account for
about half of the diet (by mass) for females of reproductive age (mid-
teens to mid-forties).
This section presents and requests comment on data EPA might use to
estimate an RSC based on food-borne exposure as well as on several
other options that the Agency is considering to better characterize
perchlorate exposure and assist the Agency in making its regulatory
determination for perchlorate. These options could serve as a
supplement or an alternative to developing an HRL based on a better
informed RSC derived from food concentration and consumption data. The
Agency specifically seeks comment on the use of urine biomonitoring
data in estimating perchlorate exposure. If the Agency decides to use
any of the approaches discussed in V.F.2, EPA will need to determine
what statistics (e.g., mean, median, percentile, etc.) are most
appropriate for consideration in a regulatory determination. The Agency
will also conduct a peer review, as appropriate, of any new methodology
it decides to use.
The Agency also invites the public to submit relevant data that may
further characterize exposure to perchlorate through consumption of
foods and/or through other pathways. The Agency will consider any new,
relevant information/data provided in response to this action as the
Agency determines whether to regulate perchlorate with a national
primary drinking water regulation.
1. Use of Food Concentration and Consumption Data to Estimate an
RSC. In the past, the Agency has relied on dietary exposure information
from the FDA Total Diet Study (TDS) to determine the RSC allowed for
drinking water and to set health goals (i.e., Maximum Contaminant Level
Goals) for several inorganic compounds (e.g., antimony, cadmium,
chromium, and selenium). Under the TDS, foods are sampled at retail
outlets, prepared as they would be consumed, and analyzed for a variety
of analytes (e.g., nutrients, pesticides, industrial chemicals).
Approximately 280 foods, covering a broad spectrum of the diet, are
currently sampled in each sampling event. Sampling events (known as
``market baskets'') occur about 4 times per year, with each event being
confined to 1 of the 4 regions of the country. The dietary intake of
the analyzed compounds can be calculated for the U.S. population by
multiplying the concentrations found in TDS foods by the consumption
amounts for each food. FDA compiles food consumption amounts for the
total U.S. population by gender and by age group.\26\
---------------------------------------------------------------------------
\26\ Information about FDA's TDS design, food list, analytes,
and analytical results can be found at http://www.cfsan.fda.gov/~comm/tds-toc.html.
(FDA, 2006)
---------------------------------------------------------------------------
FDA is including perchlorate as an analyte in the 2006 TDS. EPA
believes that a comprehensive dietary intake estimate for perchlorate
will be useful in evaluating dietary exposure relative to drinking
water. When sufficient quantitative exposure data are available (such
as the data published by FDA in conjunction with the TDS), EPA can use
the procedure used previously for several regulated inorganic compounds
(i.e., chromium and selenium) to calculate the relative source
contribution for perchlorate. In these cases where dietary intake
values were available, EPA subtracted the dietary intake value from the
Drinking Water Equivalent Level DWEL and used the remainder as the
allowance for water. This procedure assures that total exposure does
not exceed the RfD.
The Agency invites the public to submit relevant data that may
further characterize exposure to perchlorate through consumption of
foods and/or through other pathways. This information may help the
Agency in the evaluation of currently available food data and the 2006
TDS.
2. Use of Urinary Biomonitoring Data to Evaluate Exposure to
Perchlorate. Researchers at CDC's National Center for Environmental
Health (NCEH) have conducted a large national study of total
perchlorate exposure through analysis of urine samples collected for
NHANES 2001-2002 (Blount et al., 2006b and 2006c). The use of urinary
perchlorate excretion to estimate perchlorate exposure has been
demonstrated in Valentin-Blasini et al. (2005), Tollez et al. (2005),
and Blount et al. (2006c). While this would be the first time the
Agency has used biomonitoring data to assist EPA in making a
preliminary regulatory determination for a CCL contaminant, the Agency
believes that estimating perchlorate exposure among large populations
using urinary perchlorate excretion data may be appropriate for the
following reasons:
Perchlorate is not metabolized in the body and is excreted
unchanged primarily via the renal pathway (Merrill et al., 2005),
Perchlorate does not bioaccumulate, that is, it is
excreted essentially completely (Merrill et al., 2005),
Perchlorate has a short half-life in the human body
(approximately 8 hours), simplifying the estimation of daily exposure
(Greer et al., 2002), and
A methodology exists that allows estimation of daily
perchlorate intake from all sources (e.g., water, food) using standard
creatinine adjustment factors to account for variations in urine
concentration (Mage et al., 2004).
The Agency could use the 2001-2002 NHANES urine data in several
ways as described in the following paragraphs. The Agency welcomes
comment from the public on these approaches, as well as suggestions for
other analyses that may inform the preliminary regulatory determination
for perchlorate.
One potential approach is to use the 2001-2002 NHANES urine data to
directly determine whether regulation of perchlorate in drinking water
presents a meaningful opportunity for health risk reduction. More
specifically, we could use the urine data (as in Blount et al., 2006b
and c) to evaluate whether total exposure from food and water is likely
to result in an appreciable risk of adverse health effects for the U.S.
population. If the Agency concluded that total exposure, as estimated
from the urine data, does not pose an appreciable risk, even at the
upper end of the exposure distribution, then it would follow logically
that reducing this exposure by regulating drinking water would not
present a meaningful opportunity for health risk reduction. As
summarized above, Blount et al. (2006c) estimated a median total daily
perchlorate dose for adults of 0.066 [mu]g/kg/day (about one tenth of
the RfD) and a 95th percentile dose of 0.234 [mu]g/kg/day (about one
third of the RfD). Only eleven adults (0.7%) had an estimated dose in
excess of the RfD (0.7 [mu]g/kg/day). EPA requests comment on whether
or not these data provide an adequate basis to support a regulatory
[[Page 24048]]
determination for perchlorate. EPA also requests comment on the
relevance, if any, to a regulatory determination for perchlorate, of
the Blount et al (2006b) study, which showed an association between T4/
TSH levels in women and urinary perchlorate concentrations at levels
below the RfD (see Section V.B).
EPA could also use the 2001-2002 NHANES urine data to qualitatively
evaluate the importance of the water contribution to overall exposure.
For this approach, the Agency could merge data from the 2001-2002
NHANES and UCMR 1 and compare the total perchlorate exposure values
(based on the urine data) for the population of individuals whose
drinking water contains perchlorate at various concentration levels,
ranging from non-detect to the upper end of the occurrence
distribution. The intent of this analysis would be to permit the Agency
to determine whether total perchlorate exposure (as measured in urine)
is meaningfully correlated with concentrations in local public drinking
water supplies, though EPA would only use these results qualitatively
because it is not possible to match up individual urine samples with
individual drinking water exposures. However, the results could be
useful in determining at least qualitatively the potential significance
of drinking water exposure for total exposure. If there were not a
significant correlation between public water system perchlorate
occurrence and individual exposure as measured through biomonitoring,
this might suggest that there is not a meaningful opportunity for
health risk reduction through regulation of drinking water.
The Agency could also potentially use the 2001-2002 NHANES urine
data to derive an RSC to use for drinking water. This could potentially
be done in several different ways as follows.
a. Use of Urinary Biomonitoring Total Exposure Value to Estimate an
RSC. One possible approach to estimating an RSC for water would be to
use the urine data to estimate total perchlorate exposure, then
subtract this exposure value from the reference dose and allow the
remainder as the exposure limit for water. The allowed remainder
divided by the RfD would be the RSC for drinking water. This approach
would yield a conservative RSC value because the exposure used to
represent food would actually correspond to both food and drinking
water exposure, whereas, if it were possible to estimate the exposure
from food alone, the relative amount allowed for water would be larger
(resulting in a higher RSC and higher health reference value). As
discussed in Section V.D, Blount et al. (2006c) estimated a total daily
perchlorate dose for adults from urine data and found a median dose of
0.066 [mu]g/kg/day (about one tenth of the RfD) and a 95th percentile
of 0.234 [mu]g/kg/day (about one third of the RfD). If EPA were to use
the estimated 95th percentile total dose from the Blount study as if it
represented the exposure from food alone, this would suggest a residual
screening-level RSC of about 70% allocated to water. One possible
limitation of this approach is that the Blount study estimates exposure
for adults only. Therefore, an RSC developed based upon this data would
not necessarily be representative of children. EPA requests comment on
using this approach as the basis for deriving a screening-level RSC.
b. Use of the Urine Data and UCMR 1 to Deduce Exposure from Other
Sources and Derive the RSC. Alternately, for those NHANES survey
subjects served by public drinking water systems with positive
detections for perchlorate (based on UCMR 1), EPA could estimate the
expected perchlorate dose contributed by drinking water (using
individual water consumption data from the NHANES survey combined with
UCMR 1 data for the area in which they live) and subtract it from the
total perchlorate dose (based on urinary perchlorate excretion data) to
calculate the amount contributed by food. Subtraction of this
calculated food contribution from the RfD would yield the amount
allowed for drinking water, which could be divided by the RfD to
calculate an RSC. One limitation of this methodology would be the
assumption that subjects in the NHANES study are uniformly consuming
drinking water that contains perchlorate at the concentration indicated
in the UCMR 1 data for their area.
c. Use of Urinary Biomonitoring Data from Exclusive Bottled Water
Drinkers to Estimate an RSC. The 2001-2002 NHANES data includes urinary
perchlorate data for populations who exclusively drink bottled water.
As noted in section V.C.3.a, FDA (2004) tested 51 samples of bottled
water from 34 distinct sources in 12 states and detected perchlorate in
2 samples (at levels of 0.56 [mu]g/L and 0.45 [mu]g/L). These levels
are well below the MRL for the UCMR 1 data and would not contribute
significant amounts of perchlorate relative to the RfD. If the
population of exclusive bottled water drinkers is sufficiently
representative of the U.S. population, these data potentially could be
used to estimate the contribution of perchlorate exposure coming from
food and allow the Agency to estimate an RSC for drinking water. The
RSC value could be derived by subtracting the estimated perchlorate
exposure for exclusive bottled water drinkers from the RfD of 0.0007
mg/kg/day, using the remainder as the allowance for drinking water. One
limitation of this methodology is that the perchlorate concentration of
the bottled water used by this NHANES population is not known. Hence,
we would have to assume that the bottled water concentration data
collected by FDA (2004) is representative of the perchlorate
concentration in the bottled water used by the NHANES exclusive bottled
water population. Another limitation of this approach is that it would
not subtract out the fraction of the drinking water intake that comes
from water used for cooking purposes (since bottled water is probably
not used by most subjects in cooking and household food preparation).
It would thus produce a conservative (health protective) estimate of
the RSC as it would overestimate the fraction of total exposure coming
from food.
G. Next Steps
After the Agency evaluates and thoroughly reviews public comments
and any new information/data on perchlorate obtained following this
notice, and performs the necessary analyses, the Agency intends to move
expeditiously to publish a preliminary regulatory determination for
perchlorate. Depending on how quickly the Agency is able to complete
the necessary analyses and determine the best approach for making this
determination, EPA may be able to publish the preliminary determination
in time to include a final determination for perchlorate as part of the
final CCL 2 regulatory determination, which is due by July, 2008. If
not, the Agency will publish its final determination for perchlorate as
soon thereafter as possible. EPA does not intend to wait until the CCL
3 regulatory determination cycle to complete its determination for
perchlorate.
VI. What About the Remaining CCL 2 Contaminants?
As previously stated, EPA is only making regulatory determinations
on CCL 2 contaminants that have sufficient information to support a
regulatory determination at this time. Section V discusses the status
of EPA's review of perchlorate. For the 30 remaining chemicals and the
9 microbial pathogens, the Agency lacks adequate information in the
areas of health effects or occurrence or both.
The Agency continues to conduct research and/or to collect
information
[[Page 24049]]
on the remaining CCL 2 contaminants to fill identified data gaps.
Stakeholders may be concerned that regulatory determinations for such
contaminants should not necessarily wait until the end of the next
regulatory determination cycle. In this regard, it is important to
recognize that the Agency is not precluded from conducting research,
monitoring, developing guidance or health advisories, and/or making a
determination prior to the end of the next cycle. In addition, the
Agency is not precluded from regulating a contaminant at any time when
it is necessary to address an urgent threat to public health, including
any contaminant not listed on the CCL.
Because the focus of this action is to announce and solicit public
comment on the Agency's preliminary determinations for 11 of the 51 CCL
2 contaminants, this action primarily provides information on these 11
contaminants. The Agency recognizes that the public may have a
particular interest in metolachlor, methyl tertiary butyl ether (MTBE),
and the microbial contaminants. Therefore, this action includes some
additional information for these contaminants in the following sections
and requests public comment on any further data, information and/or
analyses that the Agency should be aware of.
A. Metolachlor
1. Background. Metolachlor is a broad spectrum herbicide used for
general weed control in many agricultural food and feed crops
(primarily corn, soybeans and sorghum), on lawns and turf, ornamental
plants, trees, shrubs and vines, rights of way, fencerows and
hedgerows, and in forestry. Metolachlor appears to be moderately
persistent to persistent and depending on the type of soil, can be
highly mobile. Degradation of metolachlor in the environment is
dependent on microbially-mediated and abiotic processes. Metolachlor
has at least 5 major degradates. Two of the more common degradates are
metolachlor ethane sulfonic acid (ESA) and metolachlor oxanilic acid
(OA).
2. Health. The Agency established an RfD for metolachlor of 0.1 mg/
kg/day based on an NOAEL of 9.7 mg/kg/day and a UF of 100 (USEPA,
1995). The Agency derived the NOAEL from a one-year chronic feeding
study in beagle dogs where the critical effect was decreased body
weight gain. Metolachlor shows some evidence of causing developmental
toxicity effects in rats but none in rabbits. The doses associated with
the developmental effect in rats are greater than the NOAEL and
therefore the NOAEL would be protective against developmental toxicity.
Metolachlor has been evaluated for carcinogenic activity in both
rats and mice. No treatment-related cancer effects were observed in 2
studies using mice. In studies using rats, metolachlor caused a
significant increase in liver nodules and carcinomas in high dose
females. Negative results from mutagenicity studies suggest that tumors
may result from a nonmutagenic mode of action. In 1991, a peer review
committee recommended that metolachlor be classified as a possible
human carcinogen based on increases in liver tumors in the female rat.
However, a peer review conducted in July 1994 recommended that the
evidence for cancer was suggestive and should not be quantified. This
recommendation was supported by negative mutagenicity data and recent
metabolism data indicating that the formation of the metabolite
presumed to be the ultimate carcinogen is very low (USEPA, 1995).
3. Occurrence. EPA included metolachlor as an analyte in the UCM
Round 2 survey. EPA evaluated the UCM Round 2 Cross Section data and
found that metolachlor was detected at or above the reporting limit of
0.1 [mu]g/L in 0.83% of the 12,953 systems that sampled for metolachlor
(USEPA, 2006a).
The USGS NAWQA program included metolachlor 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 at http://ca.water.usgs.gov/pnsp/
(Martin et al., 2003; Kolpin and Martin, 2003). While the USGS detected
metolachlor in both surface and ground waters, 95 percent of the
samples from the various land use settings were less than 1.38 [mu]g/L.
The maximum surface water concentration is 77.6 [mu]g/L (agricultural
setting) and the maximum estimated ground water concentration is 32.8
[mu]g/L (agricultural setting).
4. Consideration of the ESA and OA degradates. While EPA has health
and occurrence information for metolachlor itself, the Agency believes
it is prudent to also consider the occurrence and exposure of the ESA
and OA degradates as well. At this time, there is no finished water
occurrence and exposure information for these 2 degradates from a
nationally representative sample of PWSs. However, a few small-scale
studies indicate that the ESA and the OA degradates may be occurring at
greater frequencies and at higher concentrations than the metolachlor
parent (Phillips et al., 1999a and 1999b; Rheineck and Postle, 2000).
In order to gather more information about the occurrence of the ESA and
OA degradates in finished water (along with the metolachlor parent),
the Agency has added these degradates and their parent to the second
unregulated contaminant monitoring regulation (UCMR 2; 70 FR 49093;
USEPA, 2005g). While EPA awaits the results of the UCMR 2 survey, the
Agency is planning to update the health advisory for metolachlor to
include the ESA and OA degradates. The Agency requests comment from the
public as to whether updating the health advisory to include these
degradates will be useful for States and public water utilities.
In addition, the Agency requests answers to the following questions
and any available data:
Are States collecting data on the co-occurrence of
metolachlor and its degradates in source waters on a state-wide basis?
In drinking water on a state-wide basis?
If available, are States willing to provide data on the
co-occurrence of metolachlor and its ESA and OA degradates in community
and public water systems? What analytical method and reporting limit
were used to gather these data?
Do States have any information on the number of PWSs
impacted by metolachlor and/or its degradates?
Have States seen an increase or decrease in the number of
PWSs impacted by metolachlor and/or its degradates?
How many systems have taken wells or sources offline due
to impacts from metolachlor and/or its degradates?
B. Methyl tertiary-butyl ether
1. Background
Methyl tertiary-butyl ether (MTBE) is a volatile organic compound
synthesized for use as a gasoline additive. First used as an octane
enhancer to improve engine performance, MTBE is also used to reduce
emissions that form carbon monoxide and ozone. Leaking underground
storage tanks, gasoline distribution facilities, and even recreational
boating can release MTBE into the environment.
In 1997, EPA issued a drinking water advisory of 20 to 40 [mu]g/L
based on taste and odor (USEPA, 1997b). EPA is currently revising its
health risk assessment for MTBE, and thus, will not be making a
regulatory determination for MTBE as part of this action. The IRIS
Chemical Assessment Tracking System http://cfpub.epa.gov/iristrac/index.cfm
has the most up-to-date information on
[[Page 24050]]
the status of the MTBF health risk assessment and interested members of
the public should check that Web site to find out the latest schedule.
The Agency collected data on MTBE occurrence as part of the UCMR 1
survey. In addition, EPA evaluated several sources of supplemental
occurrence information described in the supporting documentation for
this action entitled ``Regulatory Determinations Support Document for
Selected Contaminants from the Second Drinking Water Contaminant
Candidate List (CCL 2)'' (USEPA, 2006a). Section VI.B.2 provides a
summary of some of the data and information on MTBE occurrence
collected to date.
2. Occurrence Information
a. UCMR 1. EPA collected sampling results for MTBE from over 98.9
percent (3,068 of 3,100) of the large PWSs and over 99.5 percent (796
of 800) of the small systems required to sample under UCMR 1. Based on
these data, 19 public water systems (0.49 percent of the 3,864 sampled)
in 14 states (CA, CT, GA, IL, MA, MO, NH, NJ, NM, NY, PA, SD, TN, and
WV) reported MTBE occurrence in drinking water. These 19 systems
reported MTBE in 26 samples at the minimum reporting level of 5 [mu]g/L
or above, representing approximately 0.33 percent (or 754 thousand of
226 million) of the population served by the public water systems that
sampled for MTBE. (USEPA, 2006a)
Of the PWSs reporting detections at or above 5 [mu]g/L (the MRL),
15 were ground water systems and 4 were surface water systems. One
small ground water system (49 [mu]g/L) and 3 large ground water PWSs
(48 [mu]g/L, 36 [mu]g/L, and 33.2 [mu]g/L) reported MTBE at levels
greater than 20 [mu]g/L (the lower end of the taste and odor
threshold). One large surface water system (33 [mu]g/L) reported MTBE
at levels greater than 20 [mu]g/L. The remaining 14 systems had detects
between 5 [mu]g/L and 20 [mu]g/L (USEPA, 2006a).
b. USGS studies/surveys/reviews. In 2003, the USGS reported results
of national source water sampling (previously introduced in section
III.B.2.a.(2)). USGS sampling included a random study of a
representative sample of untreated source waters (known as the ``Random
Survey'') and a study of source waters from areas known or suspected of
having MTBE (known as the ``Focused Survey''). In the Random Survey,
USGS found that none of the source waters exceeded 20 [mu]g/L, and the
three highest concentration sources ranged from 6 [mu]g/L to 19.5
[mu]g/L (Grady, 2003). Of the areas known or suspected of having MTBE
in the Focused Survey, USGS found that 5 percent (e.g., ground waters
for 7 of the 134 systems) had concentrations greater than 20 [mu]g/L
(Delzer and Ivahnenko, 2003a).
USGS also reviewed the literature for national, regional, and State
MTBE information (Delzer and Ivahnenko, 2003b), including 13 state-wide
assessments. This information is summarized in Table 6. USGS noted that
because study objectives varied, information varied in terms of
reporting levels, sampling frequencies, and sources (e.g., ambient
water, public and homeowner wells, treated drinking water).
Previously, USGS (Grady and Casey, 2001) studied MTBE occurrence in
the drinking water of 12 States (New England and the Mid-Atlantic). The
study found less than 1 percent of the CWSs had drinking water samples
at or above 20 [mu]g/L, while 7.8 percent of the CWSs had MTBE at 1
[mu]g/L or higher.
BILLING CODE 6560-50-P
[GRAPHIC] [TIFF OMITTED] TP01MY07.055
BILLING CODE 6560-50-C
c. New England Interstate Water Pollution Control Commission
(NEIWPCC). In 2003, the NEIWPCC surveyed the States under a grant from
EPA's Office of Underground Storage Tanks (UST). Twenty-six States
estimated that they had public wells that were contaminated by MTBE at
some level, and of those, 5 States (ME,
[[Page 24051]]
NH, NJ, DE, and MD) estimated having detectable levels of MTBE in at
least 100 public water supply wells. Thirteen States did not know the
answer, 8 States did not respond, and 3 States reported that no PWS
wells were impacted. The survey established no reporting level to
define ``contamination.'' Only 3 States documented the basis for their
estimates (projected from several studies, raw and treated water
analyses, and a survey of funded petroleum spill projects) (NEIWPCC,
2003).
d. California Department of Health Services. In 2000, California
developed a drinking water standard of 13 [mu]g/L for MTBE (CA DHS,
2000). According to California's annual compliance reports, there were
no violations of the 13 [mu]g/L standard by public water systems in
2002 and 2003, and 2 violations at 2 public water systems (serving
almost 14,000 people) in 2004 (CA DHS, 2002; CA DHS, 2003; CA DHS,
2004).
e. Other Sources of Data. In April 2005, the Environmental Working
Group (EWG, 2005) released a report, Like Oil and Water, on their Web
page. In response to Freedom of Information Act requests, 29 State
agencies submitted data to EWG. EPA informally evaluated the data
posted by EWG to determine if this information might be useful in
projecting state-wide occurrence. While EPA found the report
interesting, the data as reported on the Web lacked some of the
information needed to assess the representativeness and the quality of
the data. For example, States submitted different time periods of
monitoring data (e.g., Alaska submitted 7 months of data for 1 system
during the 2000 timeframe and Illinois submitted data that spanned 1990
to 2002). States did not report monitoring results for every system.
Also, the data do not indicate if the samples came from source water or
finished water, from ground water or surface water, the analytical
method used for analysis nor the reporting level, the frequency of the
sampling (e.g., annual, quarterly), number of samples from each water
system, number of non-detects, etc.
3. Request for Additional MTBE Occurrence Information
As discussed earlier, EPA is not making a regulatory determination
for MTBE; however, EPA is presenting this information because of
ongoing interest in MTBE. And as noted earlier, additional information
is presented in the regulatory support document for this action (i.e.,
USEPA, 2006a). While the Agency waits for the final health risk
assessment, EPA will continue to collect and evaluate occurrence
information. The Agency requests any data, information, or analyses
that may be available on the following topics:
Are there additional occurrence data for MTBE in community
and non-community public water systems on a state-wide or more local
basis? As noted in the previous section, the State data submitted to
EWG lack some elements needed to assess the quality of the data, as
required in EPA's guidance for information quality guidelines (USEPA,
2003c), and project state-wide occurrence.
What analytical method and reporting limit were used to
gather these data?
Has there been an increase or decrease in the number of
impacted PWSs? Over what time frame?
For those PWSs whose water supplies have been impacted,
has there been an increase or a decrease in the concentration of MTBE?
How many systems have taken wells or sources offline,
consolidated with other PWSs, or added customers due to impacts from
MTBE?
What treatments are being used in the field? What range of
treatment effectiveness is being achieved?
Is the listing of State bans for MTBE shown in Table 7
complete? Have state-wide bans decreased MTBE contamination in drinking
water?
Table 7.--State Actions Banning MTBE (State-wide)
[Adapted from USEPA, 2004g and McCarthy and Tiemann, 2005]
------------------------------------------------------------------------
State Effective date Extent of MTBE ban
------------------------------------------------------------------------
Arizona..................... January 1, 2005..... 0.3% max volume in
gasoline.
California.................. December 31, 2003... complete ban in
gasoline.
Colorado.................... April 30, 2002...... complete ban in
gasoline.
Connecticut................. January 1, 2004..... complete ban in
gasoline.
Illinois.................... July 24, 2004....... 0.5% max volume in
gasoline.
Indiana..................... July 24, 2004....... 0.5% max volume in
gasoline.
Iowa........................ July 1, 2000........ 0.5% max volume in
gasoline.
Kansas...................... July 1, 2004........ 0.5% max volume in
gasoline.
Kentucky.................... January 1, 2006..... 0.5% max volume in
gasoline.
Maine....................... January 1, 2007..... 0.5% max volume in
gasoline.
Michigan.................... June 1, 2003........ complete ban in
gasoline.
Minnesota................... July 2, 2005........ complete ban in
gasoline.
(following partial
ban in 2000).
Missouri.................... July 1, 2005........ 0.5% max volume in
gasoline.
Montana..................... January 1, 2006..... no more than trace
amounts in
gasoline.
Nebraska.................... July 13, 2000....... 1% max volume in
gasoline.
New Hampshire............... January 1, 2007..... 0.5% max volume in
gasoline.
New Jersey.................. January 1, 2009..... 0.5% max volume in
gasoline.
New York.................... January 1, 2004..... complete ban in
gasoline.
North Carolina.............. January 1, 2008..... 0.5% max volume in
gasoline.
Ohio........................ July 1, 2005........ 0.5% max volume in
gasoline.
Rhode Island................ June 1, 2007........ 0.5% max volume in
gasoline.
South Dakota................ July 1, 2001........ 0.5% max volume in
gasoline.
Vermont..................... January 1, 2007..... 0.5% max volume in
gasoline.
Washington.................. January 1, 2004..... 0.6% max volume in
gasoline.
Wisconsin................... August 1, 2004...... 0.5% max volume in
gasoline.
------------------------------------------------------------------------
[[Page 24052]]
C. Microbial Contaminants
1. Evaluation of Microbial Contaminants for Regulatory
Determination. The 9 microbial contaminants listed on CCL 2 include:
Four virus groups--Caliciviruses, Echoviruses,
Coxsackieviruses, and Adenoviruses
Four bacteria/bacterial groups-Aeromonas hydrophila;
Helicobacter pylori; Mycobacterium avium intercellulare (or MAC); and
Cyanobacteria (called blue-green algae\27\), fresh water algae, and the
associated toxins
---------------------------------------------------------------------------
\27\ Cyanobacteria are called blue-green algae even though they
are technically bacteria.
---------------------------------------------------------------------------
One group of protozoa--Microsporidia (Enterocytozoon
bieneusi and Septata intestinalis, now renamed Encephalitozoon
intestinalis).
In addition to considering if the Agency had sufficient information
to address the three statutory criteria listed in section II.B.1 (i.e.,
adverse health effects, known/likely occurrence, and meaningful
opportunity for health risk reduction), the Agency also considered
whether sufficient information was available to determine whether
current treatment requirements adequately controlled for any of the 9
microbial contaminants. After consideration of these factors, the
Agency determined that none of the 9 microbial contaminants have
sufficient information at this time to address the three statutory
criteria to make a regulatory determination. Table 8 identifies the
specific areas for which information is insufficient.
Table 8.--Information Gaps for the Microbial Contaminants
----------------------------------------------------------------------------------------------------------------
Health effects Treatment Analytical methods Occurrence
----------------------------------------------------------------------------------------------------------------
Microsporidia........................ Aeromonas.............. Aeromonas.............. Aeromonas.
Some Cyanotoxins..................... MAC.................... MAC.................... MAC.
Adenoviruses........... Helicobacter........... Helicobacter.
Caliciviruses.......... Microsporidia.......... Adenoviruses.
Coxsackieviruses....... Some Cyanotoxins....... Caliciviruses.
Echoviruses............ ....................... Coxsackieviruses.
Microsporidia.......... ....................... Echoviruses.
Some Cyanotoxins....... ....................... Microsporidia.
Helicobacter........... ....................... Some Cyanotoxins.
----------------------------------------------------------------------------------------------------------------
2. Research and Other Ongoing Activities. EPA has supported an
active research program to fill the information gaps on the CCL 2
microorganisms. While several examples of the ongoing research
activities are listed below, further information on these and other
projects can be found on EPA's Drinking Water Research Information
Network (DRINK). DRINK is a publicly-accessible, Web-based system that
tracks over 1,000 ongoing research projects and can be accessed at:
http://www.epa.gov/safewater/drink/intro.html.
a. Virus. For the CCL virus groups (or surrogates), the Agency has
initiated treatment studies that simulate realistic conditions where
viruses may be protected in aggregates. EPA also plans to conduct virus
removal/inactivation studies in drinking water treatment plants and/or
pilot plants. In order to assess the effectiveness of treatment and to
perform monitoring studies, methods development for viruses is also in
progress.
b. Bacteria. For Aeromonas spp., EPA recently completed a one-year
UCMR 1 survey of 293 public water systems. The Agency is currently
attempting to characterize and distinguish pathogenic from non-
pathogenic strains, as well as develop methods to detect Aeromonas
virulence factors. For H. pylori, the Agency is in the process of
developing a culture method and method for its identification. For MAC,
preliminary drinking water surveys have been conducted using a culture
method followed by genetic detection. EPA is also conducting further
research into methods development and the characterization of virulence
factors for this organism.
EPA has funded projects to evaluate the effect of disinfectants on
cyanotoxins, and on the removal of algal cells and cyanotoxins in a
pilot scale treatment plant. EPA is developing analytical methods for
potential use for future monitoring and has available analytical
chemistry standards for the toxins of most concern in the United
States--microcystin, cylindrospermopsin, and anatoxin-a. EPA has
conducted several small-scale preliminary occurrence surveys for
cyanotoxins using a screening method followed by confirmation by
instrumental analysis. A number of health effects studies are also in
progress on several high priority cyanotoxins. These include behavioral
studies in mice, acute and subacute effects in neonatal mice, and
biomarkers of human exposure. Risk assessments are being conducted at
EPA on the cyanotoxins to determine reference doses where possible. The
Agency has organized and participated in several workshops on
cyanotoxins to assess the state-of-the-science.
As an interim measure to assist public water utilities, the Agency
is planning to develop an information sheet that discusses pertinent
information on cyanobacteria and some of its key toxins. The document
will discuss the state of the knowledge on the prevention and treatment
of cyanobacteria and its toxins, as well as the available information
on the potential health effects of some of the toxins. EPA requests
comment from the public as to whether such a document would be useful
for public water utilities.
c. Protozoa. EPA has several ongoing projects to evaluate the
susceptibility of microsporidia to chlorine and chloramine
disinfectants. EPA has sponsored methods-related projects for
microsporidia, which have included the use of fluorescent gene probes,
real-time PCR, concentration methods, and immunomagnetic separation.
Ongoing monitoring at EPA has revealed that microsporidia are present
in ground water. EPA has funded work to determine exposure to
microsporidia, and to determine strains (animal and human) of
Enterocytozoon bieneusi found in water. EPA also held a workshop in
2003 on microsporidia to assess the state-of-the-science.
VII. EPA's Next Steps
EPA intends to respond to the public comments it receives on the 11
[[Page 24053]]
preliminary determinations and subsequently issue its final regulatory
determinations. Although the preliminary determinations for all 11
contaminants are not to regulate, if after consideration of public
comments, the Agency determines that a national primary drinking water
regulation is warranted for any of these 11 contaminants, the
regulation would then need to be formally proposed within 24 months of
the determination and promulgated 18 months following the proposal.\28\
---------------------------------------------------------------------------
\28\ The statute authorizes a nine-month extension of this
promulgation date.
---------------------------------------------------------------------------
VIII. References
Agency for Toxic Substances and Disease Registry (ATSDR). 1992.
Toxicological Profile for Boron. Atlanta, GA: Agency for Toxic
Substances and Disease Registry, Public Health Service, U.S.
Department of Health and Human Services. Available on the Internet
at: http://www.atsdr.cdc.gov/toxprofiles/tp26.html.
ATSDR. 1996. Toxicological Profile for 1,1,2,2-
Tetrachloroethane. Available on the Internet at: http://www.atsdr.cdc.gov/toxprofiles/tp93.html
.
ATSDR. 1998. Toxicological Profile for 2,4- and 2,6-
Dinitrotoluene. Available on the Internet at: http://www.atsdr.cdc.gov/toxprofiles/tp109.html
.
ATSDR. 2002. Toxicological Profile DDT, DDE, and DDD. Available
on the Internet at: http://www.atsdr.cdc.gov/toxprofiles/tp35.html.
Allen, B.C., P.L. Strong, C.J. Price, S.A. Hubbard, and G.P.
Datson. 1996. Benchmark Dose Analysis of Developmental Toxicity in
Rats Exposed to Boric Acid. Fundamental and Applied Toxicology. Vol.
32. pp. 194-204. (As cited in USEPA, 2004b)
Aribi, H., Y.J.C. Le Blanc, S. Antonsen, T. Sakuma. 2006.
Analysis of Perchlorate in Foods and Beverages by Ion Chromatography
Couple with Tandem Mass Spectrometry (IC-ESI-MS/MS). Analytica
Chimica Acta. Vol. 567, No. 1. pp. 39-47.
Banerjee, B.M., D. Howard, and M.W. Woodard. 1968. Dyfonate (N-
2790) safety evaluation by dietary administration to rats for 105
weeks. (As cited in USEPA, 1988b)
Banerjee, B.D., A. Ray, and S.T. Pasha. 1996. A Comparative
Evaluation of Immunotoxicity of DDT and its Metabolites in Rats.
Indian Journal of Experimental Biology. Vol. 34. pp. 517-522. (As
cited in ATSDR, 2002)
Barron, L., P.N. Nesterenko, and B. Paull. 2006. Rapid On-line
Preconcentration and Suppressed Micro-bore Ion Chromatography of
Part per Trillion Levels of Perchlorate in Rainwater Samples.
Analytica Chimica Acta. Vol. 567, No. 1. pp. 127-134.
Blount, B.C., L. Valent[iacute]n-Blasini, D.L. Ashley. 2006a.
Assessing Human Exposure to Perchlorate Using Biomonitoring. Journal
of ASTM International. Vol. 3, No. 7. pp. 1-6.
Blount, B.C., J.L. Pirkle, J.D. Osterloh, L. Valent[iacute]n-
Blasini, and K.L. Caldwell. 2006b. Urinary Perchlorate and Thyroid
Hormone Levels in Adolescent and Adult Men and Women Living in the
United States. Environmental Health Perspectives. Vol. 114, No. 12.
pp. 1865-1871.
Blount, B.C., L. Valent[iacute]n-Blasini, J.D. Osterloh, J.P.
Mauldin, and J.L. Pirkle. 2006c. Perchlorate Exposure of the U.S.
Population, 2001-2002. Journal of Exposure Science and Environmental
Epidemiology. Advance online publication 18 October 2006. Available
on the Internet at: http://www.nature.com/jes/journal/vaop/ncurrent/pdf/7500535a.pdf
.
Blount, B.C., L. Valent[iacute]n-Blasini. 2006. Analysis of
Perchlorate, Thiocyanate, Nitrate and Iodide in Human Amniotic Fluid
using Ion Chromatography and Electrospray Tandem Mass Spectrometry.
Analytica Chimica Acta. Vol. 567, No. 1. pp. 87-93.
CA DHS. 2000. California Department of Health Services. Final
Statement of Reasons Primary MCL for MTBE. Title 22, California Code
of Regulations. Available on the Internet at: http://www.dhs.ca.gov/ps/ddwem/chemicals/mtbe/4-17-00MTBESOR.PDF
.
CA DHS. 2002. California Department of Health Services. Annual
Compliance Report for Public Water Systems, Calendar Year 2002.
Available on the Internet at: http://www.dhs.ca.gov/ps/ddwem/publications/2002annualcompliancereport-final.pdf
.
CA DHS. 2003. California Department of Health Services. Annual
Compliance Report for Public Water Systems, Calendar Year 2003.
Available on the Internet at: http://www.dhs.ca.gov/ps/ddwem/publications/2003ARCFinal.pdf
.
CA DHS. 2004. California Department of Health Services. Annual
Compliance Report for Public Water Systems, Calendar Year 2004.
Available on the Internet at: http://www.dhs.ca.gov/ps/ddwem/publications/AnnualComplianceReport2004.pdf
.
CA DHS. 2006. California Department of Health Services.
``Perchlorate in California Drinking Water: Monitoring Update.''
Available on the Internet at: http://www.dhs.ca.gov/ps/ddwem/chemicals/perchl/monitoringupdate.htm.
Updated June 2, 2006.
Caldwell K.L., Jones R., and Hollowell J.G. 2005. Urinary iodine
concentration: United States National Health And Nutrition
Examination Survey 2001-2002. Thyroid. Vol. 15, pp. 692-699.
Cockrell, K.O., M.W. Woodard, and G. Woodard. 1966. N-2790
Safety Evaluation by Repeated Oral Administration to Dogs for 14
Weeks and to Rats for 13 Weeks. (As cited in USEPA, 1988b)
Cortina, T. 1984. In vivo Bone Marrow Chromosome Study in Rats:
H14,673. Final Report: Project No. 201-695. (As cited in
USEPA, 1998e)
Crawford-Brown, D., B. Raucher and M. Harrod, 2006. Intersubject
Variability of Risk from Perchlorate in Community Water Supplies.
Environmental Health Perspectives. 114(7): 975-79.
Dasgupta, P.K., P.K. Martinelango, W.A. Jackson, T.A. Anderson,
K. Tian, R.W. Tock, and S. Rajagopalan. 2005. The Origin of
Naturally Occurring Perchlorate: The Role of Atmospheric Processes.
Environmental Science and Technology. Vol. 39, No. 6. pp. 1569-1575.
Dasgupta, P.K., J.V. Dyke, A.B.Kirk, and A.W. Jackson. 2006.
Perchlorate in the United States. Analysis of Relative Source
Contributions to the Food Chain. Environmental Science and
Technology. 40(21):6608-6614.
Delzer, G.C. and T. Ivahnenko. 2003a. Occurrence and Temporal
Variability of Methyl tert-Butyl Ether (MTBE) and Other Volatile
Organic Compounds in Select Sources of Drinking Water: Results of
the Focused Survey. U.S. Geological Survey Water-Resources
Investigations Report 02-4084, 65 p. Available on the Internet at:
http://sd.water.usgs.gov/nawqa/pubs/wrir/wrir02_4084.pdf.
Delzer, G.C. and T. Ivahnenko. 2003b. A Review of Literature for
Methyl tert-Butyl Ether (MTBE) in Sources of Drinking Water in the
United States. U.S. Geological Survey Open-File Report 01-322, 16 p.
Available on the Internet at: http://sd.water.usgs.gov/nawqa/pubs/ofr/ofr01_322.pdf
.
Ellis, H.V., J.H. Hagensen, J.R. Hodgson, et al. 1979. Mammalian
Toxicity of Munitions Compounds. Phase BI: Effects of Lifetime
Exposure. Part I: 2,4-Dinitrotoluene. Final Report No. 7. (As cited
in USEPA, 1992c)
Ellis, H.V., C.B. Hong, C.C. Lee, J.C. Dacre, and J.P. Glennon.
1985. Subchronic and Chronic Toxicity Studies of 2,4-Dinitrotoluene.
Part I: Beagle Dog. Journal of the American College of Toxicology.
Vol. 4. pp. 233-242. (As cited in USEPA, 1992c)
Ericksen, G.E. The Chilean nitrate deposits. American Scientist,
1983, 71, 366-374, and references cited therein, as cited in USEPA,
2001c.
EWG. 2005. Environmental Working Group. Like Oil and Water.
http://www.ewg.org/reports/oilandwater.
Extoxnet. 1993. ``Extension Toxicology Network Pesticide
Information Profiles-Fonofos.'' Available on the Internet at: http://pmep.cce.cornell.edu/profiles/extoxnet/dienochlor_glyphosate/fonofos_ext.html.
Accessed March 10, 2006.
Extoxnet. 1994. ``Extension Toxicology Network Pesticide
Information Profiles-Terbacil.'' Available on the Internet at:
http://pmep.cce.cornell.edu/profiles/Extoxnet/pyrethrins-ziram/terbacil-ext.html.
Accessed March 10, 2006.
Food and Drug Administration (FDA). 2004. ``Exploratory Data on
Perchlorate in Food.'' FDA Center for Food Safety and Applied
Nutrition, Office of Plant & Dairy Foods. November 2004. Available
on the Internet at: http://www.cfsan.fda.gov/dms/clo4data.html
Food and Drug Administration (FDA). 2006. Center for Food Safety
and Applied Nutrition, Office of Plant & Dairy Foods. Total Diet
Study. Available on the Internet at: http://www.cfsan.fda.gov/comm/tds-toc.html
.
Field, E.A., C.J. Price, M.C. Marr, C.B. Myers, R.E. Morrissey,
and B.A. Schwetz. 1989. Final Report on the Developmental Toxicity
of Boric Acid (CAS No. 10043-35-3) in CD-1-Swiss Mice. NTP Final
Report No. 89-250. (As cited in USEPA, 2004b)
Frey, M.M., C. Seidel, M. Edwards, J. Parks, and L. McNeill.
2004. Occurrence Survey for Boron and Hexavalent Chromium. AwwaRF
Report 91044F.
Grady, S.J. 2003. A National Survey of Methyl tert-Butyl Ether
and Other Volatile
[[Page 24054]]
Organic Compounds in Drinking-Water Sources: Results of the Random
Survey. U.S. Geological Survey Water-Resources Investigations Report
02-4079, 85 p. Available on the Internet at: http://sd.water.usgs.gov/nawqa/pubs/wrir/wrir02_4079.pdf
.
Grady, S.J. and G.D. Casey. 2001. Occurrence and Distribution of
Methyl tert-Butyl Ether and Other Volatile Organic Compounds in
Drinking Water in the Northeast and Mid-Atlantic Regions of the
United States, 1993-98. U.S. Geological Survey Water-Resources
Investigations Report 00-4228, 123 p. Available on the Internet at:
http://sd.water.usgs.gov/nawqa/pubs/wrir/wrir00.4228.pdf.
Greer, M.A., G. Goodman, R.C. Pleuss, and S.E. Greer. 2002.
Health Effect Assessment for Environmental Perchlorate
Contamination: The Dose Response for Inhibition of Thyroidal
Radioiodide Uptake in Humans. Environmental Health Perspectives.
Vol. 110. pp. 927-937.
Gruener, N. 1976. Ontogenetic Development of NADH-dependent
Methemoglobin Reductase in Erythrocytes of Man and Rat. Journal of
Toxicology and Environmental Health. Vol. 1. pp. 787-791. (As cited
in ATSDR, 1998)
Hamilton, P.A., T.L. Miller, and D.N. Myers. 2004. Water Quality
in the Nation's Streams and Aquifers: Overview of Selected Findings,
1991-2001. USGS Circular 1265. Available on the Internet at: http://water.usgs.gov/pubs/circ/2004/1265/pdf/circular1265.pdf
Haskell Laboratories. 1965a. 14-Day Rat Feeding Study.
(Unpublished study, as cited in USEPA, 1998e)
Haskell Laboratories. 1965b. 3-Week Rabbit Dermal Toxicity
Study. (Unpublished study, as cited in USEPA, 1998e)
Haskell Laboratories. 1965c. Rat 90-day feeding study in Rats.
(Unpublished study, as cited in USEPA, 1998e)
Haskell Laboratories. 1980. Rat Oral Teratology with Terbacil.
(Unpublished study, as cited in USEPA, 1998e)
Haskell Laboratories. 1984. CHO (HGPRT) Gene Mutation Assay with
Terbacil. (Unpublished study, as cited in USEPA, 1998e)
Hawley, G.G. 1981. Condensed Chemical Dictionary. 10th ed. New
York, NY: Van Nostrand Reinhold Co. (As cited in ATSDR, 1996)
Hayes, W.J. 1982. Pesticides Studied in Man. Baltimore, MD:
Williams and Wilkins. p. 413. (As cited in USEPA, 1988b)
Hazardous Substances Database (HSDB). 2004a. ``TOXNET:
Toxicology Data Network--Boron.'' Available on the Internet at:
http://toxnet.nlm.nih.gov/cgi-bin/sis/search. [Search for boron.]
Accessed November 1, 2004.
HSDB. 2004b. ``TOXNET: Toxicology Data Network--2,4-
Dinitrotoluene.'' Available on the Internet at:-http://toxnet.nlm.nih.gov/cgi-bin/sis/search.
[Search for 2,4-
dinitrotoluene.] Accessed November 1, 2004.
HSDB. 2004c. ``TOXNET: Toxicology Data Network--2,6-
Dinitrotoluene.'' Available on the Internet at: http://toxnet.nlm.nih.gov/cgi-bin/sis/search.
[Search for 2,6-
dinitrotoluene.] Accessed November 1, 2004.
HSDB. 2004d. ``TOXNET: Toxicology Data Network--Fonofos.''
Available on the Internet at: http://toxnet.nlm.nih.gov/cgi-bin/sis/search.
[Search for fonofos.] Accessed November 1, 2004.
Heindel, J.J., C.J. Price, E.A. Field, M.C. Marr, C.B. Myers,
R.E. Morrissey, and B.A. Schwetz. 1992. Developmental Toxicity of
Boric Acid in Mice and Rats. Fundamental and Applied Toxicology.
Vol. 18. pp. 266-277. (As cited in USEPA, 2004b)
Heindel, J.J., C.J. Price, and B.A. Schwetz. 1994. The
Developmental Toxicity of Boric Acid in Mice, Rats and Rabbits.
Environmental Health Perspectives Supplements. Vol. 102, No. S7. pp.
107-112. (As cited in USEPA, 2004b)
Henry, J. 1986. Skin Sensitization Test of Terbacil (IND-732-53)
in Guinea Pigs for EPA Pesticide Registration. Revised. Report No.
600-85: MR No. 4581-277. (As cited in USEPA, 1998e)
Hodge, M. 1995. Fonofos: 1-Year Oral Toxicity Study in Dogs.
Report Number CTL/P/4499, Study Number PDO944. Zeneca Central
Toxicology Lab. (As cited in USEPA, 1996c)
Hong, C.B., H.V. Ellis, C.C. Lee, H. Sprinz, J.C. Dacre, and
J.P. Glennon. 1985. Subchronic and Chronic Toxicity Studies of 2,4-
Dinitrotoluene. Part III. CD-1 Mice. Journal of the American College
of Toxicology. Vol. 4, No. 4. pp. 257-269. (As cited in ATSDR, 1998)
Hood, D. 1966. 15-exposure Skin Absorption Studies with 3-Tert-
Butyl-5-Chloro-6-Methyluracil. Report No. 33-66. (As cited in USEPA,
1998e)
Horner, J. 1993. Fonofos: Subchronic Neurotoxicity Study in
Rats. Lab Project Number: CTL/P/3879, PRO889. Zeneca Central
Toxicology Lab. (As cited in USEPA, 1996c)
International Agency for Research on Cancer (IARC). 1979.
1,1,2,2-Tetrachloroethane. IACR Monographs on the Evaluation of the
Carcinogenic Risk of Chemicals to Humans: Some Halogenated
Hydrocarbons. Vol. 20. pp. 477-489. (As cited in ATSDR, 1996)
Institute of Medicine (IOM). 2001. ``Boron.'' Chapter in Dietary
Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron,
Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel,
Silicon, Vanadium and Zinc. Washington, DC: National Academy Press.
pp. 510-521.
ISK Biotech Corporation. 1993. MRID No. 42731001, 42998401 HED
No. 010513. (Unpublished study, as cited in USEPA, 1994)
Ivahnenko, T., S.J. Grady, and G.C. Delzer. 2001. Design of a
National Survey of Methyl tert-Butyl Ether and Other Volatile
Organic Compounds in Drinking-Water Sources. U.S. Geological Survey
Open-File Report 01-271, 42 p. Available on the Internet at: http://sd.water.usgs.gov/nawqa/pubs/ofr/ofr01_271.pdf
.
Iyengar, G.V., W.B. Clarke, R.G. Downing, and J.T. Tanner. 1988.
Lithium in Biological and Dietary Materials. Chapter in Proceedings
of the 5th International Workshop on Trace Element Analytical
Chemistry in Medicine and Biology. Vol. 5. pp. 267-269. (As cited in
USEPA, 2004c)
Jackson, W.A., P. Joseph, P. Laxman, K. Tan, P.N. Smith, L. Yu,
and T.A. Anderson. 2005. Perchlorate Accumulation in Forage and
Edible Vegetation. Journal of Agricultural and Food Chemistry. Vol.
53, No. 2. pp. 369-373.
Jackson W.A., K. Rainwater, T. Anderson, T. Lehman, R. Tock, S.
Rajagopalan, and M. Ridley, 2004. Distribution and Potential Sources
of Perchlorate in the High Plains Region of Texas. Texas Tech
University Water Resources Center.
Jeney, E., F. Bartha, L. Kondor, and S. Szendrei. 1957.
Prevention of Industrial Tetrachloroethane Intoxication--Part III.
Egeszsegtudomany. Vol. 1. pp. 155-164. (As cited in USEPA, 1989)
Kang, N., T.A. Anderson, and W.A. Jackson. 2006. Photochemical
Formation of Perchlorate from Aqueous Oxychlorine Anions. Analytica
Chimica Acta. Vol. 567, No. 1. pp. 48-56.
Kelce, W.R., C.R. Stone, S.C. Laws, L.E. Gray, J.A. Kemppainen
and E.M. Wilson. 1995. Persistent DDT Metabolite p,p'-DDE is a
Potent Androgen Receptor Antagonist. Nature. Vol. 375. pp. 581-585.
(As cited in ATSDR, 2002)
Kirk, A.B., E.E. Smith, K. Tian, T.A. Anderson, and P.K.
Dasgupta. 2003. Perchlorate in Milk. Environmental Science and
Technology. Vol. 37, No. 21. pp. 4979-4981.
Kirk, A.B., P.K. Martinelango, K. Tian, A. Dutta, E.E. Smith,
and P.K. Dasgupta. 2005. Perchlorate and Iodide in Dairy and Breast
Milk. Environmental Science and Technology. Vol. 39, No. 7. pp.
2011-2017.
Kirk, A.B., J.V. Dyke, C.F. Martin, and P.K. Dasgupta. 2006.
Temporal Patterns in Perchlorate, Thiocyanate and Iodide Excretion
in Human Milk. Environmental Health Perspectives Online. November
2006. In press.
Klopman, G., D. Fercu, and H.S. Rosenkranz. 1996. The
Carcinogenic Potential of Dacthal and its Metabolites. Environmental
Toxicology and Chemistry. Vol. 15, No. 2. pp. 80-84.
Kolpin, D.W. and J.D. Martin. 2003. ``Pesticides in Ground
Water: Summary Statistics; Preliminary Results from Cycle I of the
National Water Quality Assessment Program (NAWQA), 1992-2001.''
Available on the Internet at: http://ca.water.usgs.gov/pnsp/pestgw/Pest-GW_2001_Text.html.
Accessed August 24, 2004.
Konietzko, H. 1984. Chlorinated Ethanes: Sources, Distribution,
Environmental Impact, and Health Effects. Hazard Assessment of
Chemicals Current Developments. Vol. 3. pp. 401-448. (As cited in
ATSDR, 1996)
Lee, C.C., J.V. Dilley, J.R. Hodgson, D.O. Helton, W.J. Wiegand,
D.N. Roberts, B.S. Andersen, B.N. Halfpap, L.D. Kurtz, and N. West.
1975. Mammalian Toxicity of Munition Compounds: Phase I. Acute Oral
Toxicity, Primary Skin and Eye Irritation, Dermal Sensitization, and
Disposition and Metabolism. (Unpublished study, as cited in ATSDR,
1998)
Lee C.C., H.V. Ellis III, J.J. Kowalski, J.R. Hodgsen, R.D.
Short, J.C. Bhandari, T.W. Reddig, and J.L. Minor. 1976. Mammalian
Toxicity of Munitions Compounds. Phase II: Effects of Multiple
Doses. Part III: 2,6-
[[Page 24055]]
Dinitrotoluene. (Unpublished study, as cited in USEPA, 1992c)
Lee, C.C., H.V. Ellis III, J.J. Kowalski, J.R. Hodgson, and S.W.
Hwang. 1978. Mammalian Toxicity of Munitions Compounds. Phase II:
Effects of Multiple Doses. Part II: 2,4-Dinitrotoluene. (Unpublished
study, as cited in ATSDR, 1998)
Lee, C.C., C.B. Hong, H.V. Ellis III, J.C. Dacre, and J.P.
Glennon. 1985. Subchronic and Chronic Toxicity Studies of 2,4-
Dinitrotoluene. Part II. CD Rats. Journal of the American College of
Toxicology. Vol. 4. pp. 243-256. (As cited in ATSDR, 1998)
Lehman, K.B. and L. Schmidt-Kehl. 1936. Study of the 13 Most
Important Chlorohydrocarbons from the Standpoint of Industrial
Hygienics. Archiv Fuer Hygiene und Bakteriologie. Vol. 116. pp. 132-
268. (As cited in ATSDR, 1996 and USEPA, 1989)
Lobo-Mendonca, R. 1963. Tetrachloroethane--A Survey. British
Journal of Industrial Medicine. Vol. 20. pp. 51-56. (As cited in
ATSDR, 1996 and USEPA, 1989)
Lomax, L.G., W.T. Stott, K.A. Johnson, L.L. Calhoun, B.L. Yano,
and J.F. Quast. 1989. The Chronic Toxicity and Oncogenicity of
Inhaled Technical Grade 1,3-Dichloropropene in Rats and Mice.
Fundamental and Applied Toxicology. Vol. 12. pp. 418-431. (As cited
in USEPA, 2000a)
Lopes, T.J. and S.G. Dionne. 1998. A Review of Semivolatile and
Volatile Organic Compounds in Highway Runoff and Urban Stormwater.
U.S. Geological Survey Open-File Report 98-409, 67 p. Available on
the Internet at: http://sd.water.usgs.gov/nawqa/pubs/ofr/ofr98-409.pdf
.
Mackenzie, K. 1986. Two-generation Reproduction Study with EPTC
in Rats: Report: Study No. 6100-108. Unpublished study prepared by
Hazleton Laboratories America, Inc. 1192 p. (As cited in USEPA,
1999c)
Mage, D.T., R. Allen, G. Gondy, W. Smith, D.B. Barr, and L.L.
Needham. 2004. Estimating Pesticide Dose from Urinary Pesticide
Concentration Data by Creatinine Correction in the Third National
Health and Nutrition Examination Survey (NHANES-III). Journal of
Exposure Analysis and Environmental Epidemiology. Vol. 14. pp. 457-
465.
Massachusetts Department of Environmental Protection (MA DEP).
2005. The Occurrence and Sources of Perchlorate in Massachusetts.
Draft Report. Available on the Internet at: http://www.mass.gov/dep/cleanup/sites/percsour.pdf
.
Massachusetts Department of Environmental Protection (MA DEP).
2006. Press Release. Massachusetts' First-In-The-Nation Perchlorate
Standards Take Effect Today Drinking Water, Cleanup Standards of 2
ppb Are Set to Protect Public Health. July 28, 2006.
Available on the Internet at: http://www.mass.gov/dep/public/press/pchl0706.htm
.
Malek, D. 1993. Combined Chronic Toxicity/Oncogenicity Study
with DPX-D732-66 (Terbacil) Two Year Feeding Study in Rats. Lab
Project Number: 9027-001: 453-93: 18260. (As cited in USEPA, 1998e)
Martin, J.D., C.G. Crawford, and S.J. Larson. 2003. ``Pesticides
in Streams: Summary Statistics; Preliminary Results from Cycle I of
the National Water Quality Assessment Program (NAWQA), 1992-2001.''
Available on the Internet at: http://ca.water.usgs.gov/pnsp/pestsw/Pest-SW_2001_Text.html.
Accessed August 24, 2004.
Martinelango, P.K., K. Tian, and P.K. Dasgupta. 2006a.
Perchlorate in Seawater: Bioconcentration of Iodide and Perchlorate
by Various Seaweed Species. Analytica Chimica Acta. Vol. 567, No. 1.
pp. 100-107.
Martinelango, P.K., G. G[uuml]m[uuml]s, and P.K. Dasgupta.
2006b. Matrix Interference Free Determination of Perchlorate in
Urine by Ion Association-Ion Chromatography-Mass Spectrometry.
Analytica Chimica Acta. Vol. 567, No. 1. pp. 79-86.
McCarthy, J.E. and M. Tiemann. 2005. MTBE in Gasoline: Clean Air
and Drinking Water Issues. CRS Report for Congress. Updated August
17, 2005. Available on the Internet at: http://www.cnie.org/nle/crsreports/05aug/RL32787.pdf
.
Merrill, E.A., R.A. Clewell, P.J. Robinson, A.M. Jarabek, J.M.
Gearhart, T.R. Sterner, and J.W. Fisher. 2005. PBPK Model for
Radioactive Iodide and Perchlorate Kinetics and Perchlorate-Induced
Inhibition of Iodide Uptake in Humans. Toxicological Sciences. Vol.
83. pp. 25-43.
Miller, J.L., L. Sandvik, G.L. Sprague, A.A. Bickford, and T.R.
Castles. 1979. Evaluation of Delayed Neurotoxic Potential of
Chronically Administered Dyfonate in Adult Hens. Abstract presented
in Toxicology and Applied Pharmacology. 48(Part 2):A197.
Miller, J. 1987. Neurotoxicity of 90-day Oral Administration of
Technical Dyfonate to Adult Hens. T-6237: Final Report. Stauffer
Chemical Co. pp. 59. (As cited in USEPA, 1996c)
Minor, J., J. Downs, G. Zwicker, et al. 1982. A Teratology Study
in CD-1 Mice with Dyfonate Technical. T-10192. Final Report.
Stauffer Chemical Co. (As cited in USEPA, 1988b)
Minot, G.R. and L.W. Smith. 1921. The Blood in Tetrachlorethane
Poisoning. Archives of Internal Medicine. Vol. 28. pp. 687-702. (As
cited in ATSDR, 1996)
National Center for Food and Agricultural Policy (NCFAP). 2004.
National Pesticide Use Database. [Searches for 1,3-DCP and FONOFOS].
Available on the Internet at: http://www.ncfap.org/database/national/default.asp.
Accessed August 24, 2004.
National Cancer Institute (NCI). 1978. Bioassay of 1,1,2,2-
Tetrachloroethane for Possible Carcinogenicity. NCI-CG-TR-27. (As
cited in ATSDR, 1996)
National Toxicology Program (NTP). 1985. Toxicology and
Carcinogenesis Studies of Telone II (Technical Grade 1,3-
Dichloropropene Containing 1% Epichlorohydrin as a Stabilizer) in
F344/N Rats and B6C3F1 Mice (Gavage Studies). (As cited in USEPA,
2000a)
National Research Council (NRC). 2005. Health Implications of
Perchlorate Ingestion. National Academies Press, Board on
Environmental Studies and Toxicology. January 2005. 276 p.
NEIWPCC. 2003. The Compiled Results of the Survey of State
Experiences with MtBE and Other Oxygenate Contamination at LUST
Sites (March-April 2003): A Project of the New England Interstate
Water Pollution Control Commission (NEIWPCC). Available on the
Internet at: http://www.neiwpcc.org/PDF_Docs/2003mtbecom.pdf.
NTP. 1991a. Range Finding Studies: Developmental Toxicity--
1,1,2,2-Tetrachloroethane When Administered via Feed in CD Sprague-
Dawley Rats. NTP-91-RF/DT-017.
NTP. 1991b. Range Finding Studies: Developmental Toxicity--
1,1,2,2-Tetrachloroethane (Repeat) When Administered via Feed in
Swiss CD-1 Mice. NTP-91-RF/DT-020.
NTP. 2004. NTP Technical Report on the Toxicity Studies of
1,1,2,2-Tetrachloroethane Administered in Microcapsules in Feed to
F-344/N Rats and B6C3F1 Mice. NIH Publication No. 04-4414.
Orris, G.J., G.J. Harvey, D.T. Tsui, and J.E. Eldrige. 2003.
Preliminary Analyses for Perchlorate in Selected Natural Materials
and their Derivative Products. USGS Open-File Report 03-314.
Pavkov, K. and D. Taylor. 1988. Rat Chronic Toxicity and
Oncogenicity Study with Dyfonate. Laboratory Project ID T-11997.
(Unpublished study, as cited in USEPA, 1996c)
Pena Gonzalez, P., J. Perez-Rendon Gonzalez, E. Dominguez
Alberdi, M. Gomez Labat, and J. Bajo Arenas. 1996. Epidemic Outbreak
of Acute Food Poisoning Caused by Pesticides [Article in Spanish].
Atencion Primaria. Vol. 17, No. 7. pp. 467-70.
Phillips, P.J., G.R. Wall, E.M. Thurman, D.A. Eckhardt, and J.
Vanhoesen. 1999a. Metolachlor and Its Metabolites in Tile Drain and
Stream Runoff in the Canajoharie Creek Watershed. Environmental
Science and Technology. 33(20):3531-3537.
Phillips, P.J., D.A. Eckhardt, S.A. Terracciano, and L.
Rosenmann. 1999b. Pesticides and their Metabolites in Wells of
Suffolk County, New York, 1998. U.S. Geological Survey Water-
Resources Investigations Report 99-4095, 12p. Available on the
Internet at: http://ny.water.usgs.gov/projects/nypesticides/reports/WRI99-4095.pdf
.
Price, C.J., R.W. Tyl, T.A. Marks., L.L. Paschke, T.A. Ledoux
and J.R. Reel. 1985. Teratologic Evaluation of Dinitrotoluene in the
Fischer 344 Rat. Fundamental and Applied Toxicology. Vol. 5. pp.
948-961. (As cited in USEPA, 1992c)
Price, C.J., E.A. Field, M.C. Marr, C.B. Myers, R.E. Morrissey,
and B.A. Schwetz. 1990. Developmental Toxicity of Boric Acid (CAS
No. 10043-35-3) in Sprague Dawley Rats. NTP Report No. 90-105. (As
cited in USEPA, 2004b)
Price, C.J., M.C. Marr, and C.B. Myers. 1994. Determination of
the No-Observable-Adverse-Effect Level (NOAEL) for Developmental
Toxicity in Sprague-Dawley (CD) Rats Exposed to Boric Acid in Feed
on Gestational Days 0 to 20, and Evaluation of Postnatal Recovery
through Postnatal Day 21. Final Report. (As cited in USEPA, 2004b)
Price, C.J., P.L. Strong, M.C. Marr, C.B. Myers, and F.J.
Murray. 1996. Developmental Toxicity NOAEL and Postnatal Recovery in
Rats Fed Boric Acid During Gestation. Fundamental and Applied
Toxicology. Vol. 32. pp. 179-193. (As cited in USEPA, 2004b)
[[Page 24056]]
Pulsford, A. 1991. First Amendment to a Teratology Study in CD-1
Mice with Dyfonate Technical (MRID No. 118423), Lab Project No. T-
10l92, T-10192C. MRID No. 42057601. (Unpublished study as cited in
USEPA, 1996c)
Rajagopalan, S., T.A. Anderson, L. Fahlquist, K.A. Rainwater, M.
Ridley, and W.A. Jackson. 2006. Widespread Presence of Naturally
Occurring Perchlorate in High Plains of Texas and New Mexico.
Environmental Science and Technology. Vol. 40. pp. 3156-3162.
Rheineck, B. and J. Postle. 2000. Chloroacetanilide Herbicide
Metabolites in Wisconsin Groundwater. Wisconsin Department of
Agriculture, Trade, and Consumer Protection. Available on the
Internet at: http://datcp.state.wi.us/arm/agriculture/land-water/water-quality/pdf/metabrpt.pdf
.
Sanchez, C.A. 2004. Perchlorate Residues on Agricultural Produce
Irrigated by Water from the Colorado River. Report Submitted to the
USDA-ARS under a Cooperative Agreement.
Sanchez, C.A., R.I Krieger, N. Khandaker, R.C. Moore, K.C.
Holts, and L.L. Neidel. 2005a. Accumulation and Perchlorate Exposure
Potential of Lettuce Produced in the Lower Colorado River Region.
Journal of Agricultural and Food Chemistry. Vol. 53. pp. 5479-5486.
Sanchez C.A., K.S. Crump, R.I. Krieger, N.R. Khandaker, and J.P.
Gibbs. 2005b. Perchlorate and Nitrate in Leafy Vegetables of North
America. Environmental Science and Technology. Vol. 39, No. 24, pp
9391-9397.
Sanchez C.A., R.I. Krieger, N.R. Khandaker, L. Valentin-Blasini,
and B.C. Blount. 2006. Potential Perchlorate Exposure from Citrus
sp. Irrigated with Contaminated Water. Analytica Chimica Acta. Vol.
567, No. 1. pp. 33-38.
Sauerhoff, M. 1987. A Teratology Study in Rabbits with Dyfonate
Technical. T-l2630: Volume 1: Final Report: Laboratory Project ID:
WIL 27027. (As cited in USEPA, 1996c)
Schilt, A.A. Perchloric Acid and Perchlorates. GFS Chemicals,
Inc.: Columbus, OH, 1979, p. 35, and references therein, as cited in
USEPA, 2001c.
Schmidt P., S. Binnevies, R. Gohlke, and R. Roth. 1972. Subacute
Action of Low Concentration of Chlorinated Ethanes on Rats with and
without Additional Ethanol Treatment. I. Biochemical and
Toxicometrical Aspects, Especially Results in Subacute and Chronic
Toxicity Studies with 1,1,2,2-Tetrachloroethane. Internationales
Archiv Fur Arbeitsmedizin. Vol. 30. pp. 283-298.
Seidel, C. 2006. Email Communication to Brent Ranalli at The
Cadmus Group, Inc. [concerning boron data from an AWWARF-sponsored
study, with data in an attached spreadsheet]. Denver, CO: McGuire
Malcolm Pirnie; May 19, 2006.
Snyder, S.A., R.C. Pleus, B.J. Vanderford, and J.C. Holady.
2006. Perchlorate and Chlorate in Dietary Supplements and Flavor
Enhancing Ingredients. Analytica Chimica Acta. Vol. 567, No. 1. pp.
26-32.
Solomon, H. 1984. Embryo-Fetal Toxicity and Teratogenicity Study
of Terbacil by Gavage in the Rabbit. Medical Research Project No.
4512-001: Haskell Report No. 528-83. (As cited in USEPA, 1998e)
Sprague, G. and G. Zwicker. 1987. 18-Month Dietary Oncogenicity
Study with Dyfonate Technical in Mice. Final Report: T-11995. (As
cited in USEPA, 1996c)
Stott, W.T., K.A. Johnson, T.K. Jeffries, K.T. Haut, and S.N.
Shabrang. 1995. Telone II Soil Fumigant: Two-year Chronic Toxicity/
Oncogenicity Study in Fischer 344 Rats. Study M-003993-
031l. (As cited in USEPA, 2000a)
T[eacute]llez, R.T., P.M. Chac[oacute]n, C.R. Abraca, B.C.
Blount, C.B. Van Landingham, K.S. Crump, and J.P. Gibbs. 2005.
Chronic Environmental Exposure to Perchlorate Through Drinking Water
and Thyroid Function During Pregnancy and the Neonatal Period.
Thyroid. Vol. 15, No. 9. pp. 963-975.
Thelin, G.P. and L.P. Gianessi. 2000. Method for Estimating
Pesticide Use for County Areas of the Conterminous United States.
U.S. Geological Survey Open-File Report 00-250, 62 p. Available on
the Internet at: http://ca.water.usgs.gov/pnsp/rep/ofr00250/ofr00250.pdf
.
USEPA. 1986. EPA Guidelines for Carcinogen Risk Assessment.
Federal Register. Vol. 51, No. 185. p. 33992, September 24, 1986.
USEPA. 1987. Substitution of Contaminants and Priority List of
Additional Substances Which May Require Regulation Under the Safe
Drinking Water Act. Federal Register. Vol. 52, No. 130. p. 25720,
July 8, 1987.
USEPA. 1988a. ``Integrated Risk Information System (IRIS),
p,p''-Dichlorodiphenyldichloroethylene (DDE).'' August 1988.
Available on the Internet at: http://www.epa.gov/iris/subst/0328.htm.
Accessed February 2, 2005.
USEPA. 1988b. Fonofos Health Advisory. EPA Report 820-K-88-003.
August, 1988.
USEPA. 1989. 1,1,2,2-Tetrachloroethane Health Advisory. May,
1989.
USEPA. 1990a. National Pesticide Survey: Survey Analytes. EPA
Report 570-9-90-NPS2. Available on the Internet at: http://nepis.epa.gov/pubtitleOSWER.htm.
[Search for document number
570990NPS2.]
USEPA. 1990b. National Survey of Pesticides in Drinking Water
Wells. Phase I Report. EPA Report 570-9-90-015.
USEPA. 1990c. ``Integrated Risk Information System (IRIS), 2,4-/
2,6-Dinitrotoluene Mixture.'' September 1990. Available on the
Internet at: http://www.epa.gov/iris/subst/0397.htm. Accessed
December 16, 2004.
USEPA. 1990d. ``Integrated Risk Information System (IRIS), S-
Ethyl Dipropylthiocarbamate (EPTC).'' September 1990. Available on
the Internet at: http://www.epa.gov/iris/subst/0237.htm. Accessed
February 2, 2005.
USEPA. 1991. ``Integrated Risk Information System (IRIS),
Fonofos.'' March 1991. Available on the Internet at: http://www.epa.gov/iris/subst/0158.htm.
Accessed February 2, 2005.
USEPA. 1992a. National Primary Drinking Water Regulation--
Synthetic Organic Chemicals and Inorganic Chemicals; National
Primary Drinking Water Regulations Implementation. Federal Register.
Vol. 57, No. 138. p. 31776, July 17, 1992.
USEPA. 1992b. Pesticides in Ground Water Database: A Compilation
of Monitoring Studies, 1971-1991. National Summary. Office of
Prevention, Pesticides and Toxic Substances. EPA Report 734-12-92-
001. Available on the Internet at: http://nepis.epa.gov/pubtitleOPPTS.htm.
[Search for document number 7341292001.]
USEPA. 1992c. 2,4-& 2,6-Dinitrotoluene (DNT) Health Advisory.
EPA Report 820-R-92-002. April 1992.
USEPA. 1994. ``Integrated Risk Information System (IRIS),
Dacthal.'' August 1994. Available on the Internet at: http://www.epa.gov/iris/subst/0221.htm.
Accessed February 2, 2005.
USEPA. 1995. Reregistration Eligibility Decision (RED)--
Metolachlor. EPA Report 738-R-95-006. Washington, DC: USEPA Office
of Prevention, Pesticides and Toxic Substances. April 1995.
Available on the Internet at: http://www.epa.gov/oppsrrd1/REDs/0001.pdf
.
USEPA. 1996a. Proposed Guidelines for Carcinogen Risk
Assessment. Federal Register. Vol. 61, No. 79. p. 17960, April 23,
1996.
USEPA. 1996b. ``Integrated Risk Information System (IRIS), p,p'-
Dichlorodiphenyltrichloroethane (DDT).'' February 1996. Available on
the Internet at: http://www.epa.gov/iris/subst/0147.htm. Accessed
February 2, 2005.
USEPA. 1996c. Memorandum--041701. Fonofos (Dyfonate[supreg]).
Draft Toxicology Chapter for Reregistration Eligibility. Health
Effects Division. September 11, 1996.
USEPA. 1997a. Announcement of the Draft Drinking Water
Contaminant Candidate List; Notice. Federal Register. Vol. 62, No.
193. p. 52193, October 6, 1997.
USEPA. 1997b. Drinking Water Advisory: Consumer Acceptability
Advice and Health Effects Analysis on Methyl Tertiary-Butyl Ether
(MTBE). EPA Report 822-F-97-009. December 1997. Available on the
Internet at: http://www.epa.gov/waterscience/drinking/mtbefact.pdf.
USEPA. 1998a. Announcement of the Draft Drinking Water
Contaminant Candidate List; Notice. Federal Register. Vol. 63, No.
40. p. 10273, March 2, 1998.
USEPA. 1998b. Reregistration Eligibility Decision (RED)--1,3-
Dichloropropene. EPA Report 738-R-98-016. Washington, DC: Office of
Prevention, Pesticides and Toxic Substances. December 1998.
Available on the Internet at: http://www.epa.gov/oppsrrd1/REDs/0328red.pdf
.
USEPA. 1998c. Reregistration Eligibility Decision (RED)--DCPA.
EPA Report 738-R-98-005. Washington, DC: Office of Prevention,
Pesticides and Toxic Substances. November 1998. Available on the
Internet at: http://www.epa.gov/oppsrrd1/REDs/0270red.pdf.
USEPA. 1998d. Notice of Receipt of Requests to Voluntarily
Cancel Certain Pesticide Registrations. Federal Register. Vol. 63,
No. 87. p. 25033, May 6, 1998.
USEPA. 1998e. Reregistration Eligibility Decision (RED)--
Terbacil. EPA Report 738-R-97-011. Washington, DC: Office of
Prevention, Pesticides and Toxic Substances. January 1998. Available
on the Internet at: http://www.epa.gov/oppsrrd1/REDs/0039red.pdf.
[[Page 24057]]
USEPA. 1999a. Guidelines for Carcinogen Risk Assessment. NCEA-F-
0644, Review Draft. July 1999. Available on the Internet at: http://www.epa.gov/iris/cancer_gls.pdf
.
USEPA. 1999b. Revisions to the Unregulated Contaminant
Monitoring Regulation for Public Water Systems. Federal Register.
Vol. 64, No. 180. p. 50556, September 17, 1999.
USEPA. 1999c. Reregistration Eligibility Decision (RED)--EPTC.
EPA Report 738-R-99-006. Washington, DC: Office of Prevention,
Pesticides and Toxic Substances. December 1999. Available on the
Internet at: http://www.epa.gov/oppsrrd1/REDs/0064red.pdf.
USEPA. 1999d. Reregistration Eligibility Decision (RED) Facts--
O-Ethyl S-phenyl ethylphosphonodithiolate (Fonofos). EPA Report 738-
F-99-019. Washington, DC: Office of Prevention, Pesticides and Toxic
Substances. November 1999. Available on the Internet at: http://www.epa.gov/oppsrrd1/REDs/factsheets/0105fact.pdf
.
USEPA. 2000a. ``Integrated Risk Information Systems (IRIS), 1,3-
Dichloropropene.'' May 2000. Available on the Internet at: http://www.epa.gov/iris/subst/0224.htm.
Accessed February 2, 2005.
USEPA. 2000b. Unregulated Contaminant Monitoring Regulation for
Public Water Systems: Analytical Methods for Perchlorate and
Acetochlor; Announcement of Laboratory Approval and Performance
Testing (PT) Program for the Analysis of Perchlorate; Final Rule and
Proposed Rule. Federal Register. Vol. 65, No. 42. p. 11372, March 2,
2000.
USEPA. 2001a. Notice of Opportunity to Provide Additional
Information and Comment on Draft Revised Guidelines for Carcinogen
Risk Assessment (July 1999), Availability of Draft Revised
Guidelines, and Adoption of Draft Revised Guidelines as Interim
Guidance. Federal Register. Vol. 66, No. 230. p. 59593, November 29,
2001.
USEPA. 2001b. Unregulated Contaminant Monitoring Regulation for
Public Water Systems; Analytical Methods for List 2 Contaminants;
Clarifications to the Unregulated Contaminant Monitoring Regulation.
Federal Register. Vol. 66, No. 8. p. 2273, January 11, 2001.
USEPA. 2001c. Survey of Fertilizers and Related Materials for
Perchlorate (ClO4). EPA Report 600-R-01-049. Cincinnati,
OH: Office of Research and Development. July 2001.
USEPA. 2002a. Announcement of Preliminary Regulatory
Determinations for Priority Contaminants on the Drinking Water
Contaminant Candidate List. Federal Register. Vol. 67, No. 106. p.
38222, June 3, 2002.
USEPA. 2002b. The Toxics Release Inventory (TRI) and Factors to
Consider When Using TRI Data. EPA Report 260-F-02-017. November
2002. Available on the Internet at: http://www.epa.gov/triinter/2002_tri_brochure.pdf
.
USEPA. 2003a. Announcement of Regulatory Determinations for
Priority Contaminants on the Drinking Water Contaminant Candidate
List. Federal Register. Vol. 68, No. 138. p. 42898, July 18, 2003.
USEPA. 2003b. How are the Toxics Release Inventory Data Used?
EPA Report 260-R-002-004. May 2003. Available on the Internet at:
http://www.epa.gov/tri/guide_docs/2003_datausepaper.pdf.
USEPA. 2003c. A summary of general assessment factors for
evaluating the quality of scientific and technical information. EPA
100/B-03/001, June 2003. Available on the Web at: http://www.epa.gov/OSA/spc/pdfs/assess2.pdf
.
USEPA. 2004a. Drinking Water Contaminant Candidate List 2;
Notice. Federal Register. Vol. 69, No. 64. p. 17406, April 2, 2004.
USEPA. 2004b. Toxicological Review of Boron and Compounds. EPA
Report 635-04-052. June 2004. Available online at: http://www.epa.gov/iris/toxreviews/0410-tr.pdf
.
USEPA. 2004c. ``Integrated Risk Information System (IRIS), Boron
and Compounds.'' August 2004. Available on the Internet at: http://www.epa.gov/iris/subst/0410.htm.
Accessed February 2, 2005.
USEPA. 2004d. Memorandum--TPA (Tetrachloroterephthalic Acid)-
Metabolite of DCPA (Dacthal). Evaluation of Potential for
Carcinogenicity. Office of Prevention, Pesticide, and Toxic
Substances. May 25, 2004.
USEPA. 2004e. Memorandum--EFED Review of a Telone Well
Monitoring Study. Office of Prevention, Pesticide, and Toxic
Substances. March 10, 2004.
USEPA. 2004f. Email Communication between James Breithaupt and
Wynne Miller regarding the Memorandum--EFED Review of a Telone Well
Monitoring Study. September 8, 2004.
USEPA. 2004g. State Actions Banning MTBE (State-wide). EPA
Report 420-B-04-009. June 2004. Available on the Internet at: http://www.epa.gov/mtbe/420b04009.pdf
.
USEPA. 2005a. Notice--Drinking Water Contaminant Candidate List
2; Final Notice. Federal Register. Vol. 70, No. 36. p. 9071,
February 24, 2005.
USEPA. 2005b. Guidelines for Carcinogen Risk Assessment. EPA
Report 630-P-03-001B. March 2005. Available on the Internet at:
http://www.epa.gov/ttn/atw/cancer_guidelines_final_3-25-05.pdf.
USEPA. 2005c. Supplemental Guidance for Assessing Susceptibility
to Early-life Exposure to Carcinogens. EPA Report 630-R-03-003F.
March 2005. Available on the Internet at: http://www.epa.gov/ttn/atw/childrens_supplement_final.pdf
.
USEPA. 2005d. Application of New Cancer Guidelines. Memorandum
from Acting Administrator Stephen L. Johnson. March 29, 2005.
USEPA. 2005e. ``Integrated Risk Information System (IRIS),
Perchlorate and Perchlorate Salts.'' February 2005. Available on the
Internet at: http://www.epa.gov/iris/subst/1007.htm. Accessed
February 2, 2005.
USEPA. 2005f. Notice--DCPA; Order to Amend to Terminate Uses.
Federal Register. Vol. 70, No. 143. p. 43408, July 27, 2005.
USEPA. 2005g. Unregulated Contaminant Monitoring Regulation
(UCMR) for Public Water Systems Revisions. Proposed Rule. Federal
Register. Vol. 70, No. 161. p. 49093, August 22, 2005.
USEPA. 2006a. Regulatory Determinations Support Document for
Selected Contaminants from the Second Drinking Water Contaminant
Candidate List (CCL 2). EPA Report 815-D-06-007. Draft. December
2006.
USEPA. 2006b. 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. EPA Report 815-D-06-007. Draft. December 2006.
USEPA. 2006c. 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. EPA Report 815-D-06-009. Draft. December 2006.
USEPA. 2006d. ``TRI Explorer: Trends--Boron.'' Last modified
June 8, 2005. Available on the Internet at: http://www.epa.gov/triexplorer/trends.htm.
[Search for boron trichloride and boron
trifluoride.] Accessed February 8, 2006.
USEPA. 2006e. ``TRI Explorer: Trends--1,3-Dichloropropylene.''
Last modified June 8, 2005. Available on the internet at: http://www.epa.gov/triexplorer/trends.htm.
[Search for 1,3-
dichloropropylene.] Accessed February 8, 2006.
USEPA. 2006f. ``TRI Explorer: Trends--2,4-Dinitrotoluene and
2,6-Dinitrotoluene.'' Last modified June 8, 2005. Available on the
Internet at: http://www.epa.gov/triexplorer/trends.htm. [Search for
2,4-dinitrotoluene, 2,6-dinitrotoluene, and dinitrotoluene (mixed
isomers).] Accessed February 8, 2006.
USEPA. 2006g. ``TRI Explorer: Trends--EPTC.'' Last modified June
8, 2005. Available on the Internet at: http://www.epa.gov/triexplorer/trends.htm.
[Search for ethyl dipropylthiocarbamate.]
Accessed February 8, 2006.
USEPA. 2006h. ``TRI Explorer: Trends--Terbacil.'' Last modified
June 8, 2005. Available on the Internet at: http://www.epa.gov/triexplorer/trends.htm.
[Search for terbacil.] Accessed February 8,
2006.
USEPA. 2006i. ``TRI Explorer: Trends--1,1,2,2-
Tetrachloroethane.'' Last modified June 8, 2005. Available on the
Internet at: http://www.epa.gov/triexplorer/trends.htm. [Search for
1,1,2,2-tetrachloroethane.] Accessed February 8, 2006.
USEPA. 2006j. Health Effects Support Document for Boron. EPA
Report 822-R-06-005. December 2006.
USEPA. 2006k. Health Effects Support Document for Dacthal
Degradates: Tetrachloroterephthalic Acid (TPA) and Monomethyl
Tetrachloroterephthalic Acid (MTP). EPA Report 822-R-06-006.
December 2006.
USEPA. 2006l. Health Effects Support Document for 1,1-Dichloro-
2,2-bis(p-chlorophenyl)ethylene (DDE). EPA Report 822-R-06-0007.
December 2006.
USEPA. 2006m. Health Effects Support Document for S-Ethyl
dipropylthiocarbamate (EPTC). EPA Report 822-R-06-008. December
2006.
USEPA. 2006n. Health Effects Support Document for Fonofos. EPA
Report 822-R-06-009. December 2006.
USEPA. 2006o. Health Effects Support Document for Terbacil. EPA
Report 822-R-06-010. December 2006.
[[Page 24058]]
USEPA. 2006p. Health Effects Support Document for 1,3-
Dichloropropene. EPA Report 822-R-06-011. December 2006.
USEPA. 2006q. Health Effects Support Document for 1,1,2,2-
Tetrachloroethane. EPA Report 822-R-06-012. December 2006.
USEPA. 2006r. Health Advisory for 2,4- and 2,6-Dinitrotoluene.
EPA Report 822-R-06-017. December 2006.
USGS. 2004. ``Mineral Commodity Summaries, January 2004--
Boron.'' January 2004. Available on the Internet at: http://minerals.usgs.gov/minerals/pubs/commodity/boron/boronmcs04.pdf
.
USGS. 2006. ``Information Page on Karst Geology.'' Last modified
December 5, 2005. Available on the Internet at: http://water.usgs.gov/ogw/karst/.
Accessed February 20, 2006.
Valent[iacute]n-Blasini, L., J.P. Mauldin, D. Maple, and B.C.
Blount. 2005. Analysis of Perchlorate in Human Urine Using Ion
Chromatography and Electrospray Tandem Mass Spectrometry. Analytical
Chemistry. Vol. 77. pp. 2475-2481.
Wang, H., A. Eaton, and B. Narloch. 2002. National Assessment of
Perchlorate Contamination Occurrence. Denver: AWWA Research
Foundation and American Water Works Association.
Wazeter, F.X., R.H. Buller, and R.G. Geil. 1964. Ninety-day
Feeding Study in the Rat: IRDC No. 125-004. (Unpublished study, as
cited in USEPA, 1998e)
Wazeter, F.X., R.H. Buller, and R.G. Geil. 1967a. Two-year
Feeding Study in the Dog: IRDC No. 125-011. (Unpublished study, as
cited in USEPA, 1998e)
Wazeter, F.X., R.H. Buller, and R.G. Geil. 1967b. Three-
generation Reproduction Study in the Rat: IRDC No. 125-012.
(Unpublished study, as cited in USEPA, 1998e)
Woodard, M.W., C.L. Leigh, and G. Woodard. 1968. Dyfonate (N-
2790) Three-generation Reproduction Study in Rats. (Unpublished
study, as cited in USEPA, 1996c)
Woodard, M.W., J. Donoso, and J.P. Gray, et al. 1969. Dyfonate
(N-2790) Safety Evaluation by Dietary Administration to Dogs for 106
Weeks. (Unpublished study, as cited in USEPA, 1988b and USEPA,
1996c)
World Health Organization (WHO), 1994. Indicators for Assessing
Iodine Deficiency Disorders and Their Control through Salt
iodization. WHO/NUT/94.6.Geneva:World Health Organization(WHO)/
International Council for the Control of Iodine Deficiency Disorders
(Unpublished study, as cited in Blount et al., 2006b)
Dated: April 12, 2007.
Stephen L. Johnson,
Administrator.
[FR Doc. E7-7539 Filed 4-30-07; 8:45 am]
BILLING CODE 6560-50-P