Announcement of Final Regulatory Determinations for Contaminants on the Fourth Drinking Water Contaminant Candidate List, 12272-12291 [2021-04184]
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Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations
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[FR Doc. 2021–04246 Filed 3–2–21; 8:45 am]
BILLING CODE 6560–50–P
ENVIRONMENTAL PROTECTION
AGENCY
40 CFR Part 141
[EPA–HQ–OW–2019–0583; FRL–10019–70–
OW]
RIN 2040–AF93
Announcement of Final Regulatory
Determinations for Contaminants on
the Fourth Drinking Water
Contaminant Candidate List
Environmental Protection
Agency (EPA).
ACTION: Regulatory determinations.
The U.S. Environmental
Protection Agency (EPA or Agency) is
announcing final regulatory
determinations for eight of the 109
contaminants listed on the Fourth
Contaminant Candidate List.
Specifically, the Agency is making final
determinations to regulate
perfluorooctanesulfonic acid (PFOS)
and perfluorooctanoic acid (PFOA) and
to not regulate 1,1-dichloroethane,
acetochlor, methyl bromide
(bromomethane), metolachlor,
nitrobenzene, and RDX. The Safe
Drinking Water Act (SDWA), as
amended in 1996, requires EPA to make
regulatory determinations every five
years on at least five unregulated
contaminants. A regulatory
determination is a decision about
whether or not to begin the process to
propose and promulgate a national
primary drinking water regulation for an
unregulated contaminant.
DATES: For purposes of judicial review,
the determinations not to regulate in
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*
this document are issued as of March 3,
2021.
FOR FURTHER INFORMATION CONTACT:
Richard Weisman, Standards and Risk
Management Division, Office of Ground
Water and Drinking Water, Office of
Water (Mail Code 4607M),
Environmental Protection Agency, 1200
Pennsylvania Ave. NW, Washington, DC
20460; telephone number: (202) 564–
2822; email address: weisman.richard@
epa.gov.
SUPPLEMENTARY INFORMATION:
I. General Information
AGENCY:
SUMMARY:
*
A. Does this action apply to me?
These final regulatory determinations
will not impose any requirements on
anyone. Instead, this action notifies
interested parties of EPA’s final
regulatory determinations for eight
unregulated contaminants and provides
a summary of the major comments
received on the March 10, 2020,
preliminary determinations (USEPA,
2020a).
B. How can I get copies of this document
and other related information?
Docket: EPA has established a docket
for this action under Docket ID No.
EPA–HQ–OW–2019–0583. Publicly
available docket materials are available
either electronically at https://
www.regulations.gov or in hard copy at
the Water Docket, EPA/DC, EPA West,
Room 3334, 1301 Constitution Ave. NW,
Washington, DC. The telephone number
for the Public Reading Room is (202)
566–1744, and the telephone number for
the Water Docket is (202) 566–2426.
Electronic Access: You may access
this Federal Register document
electronically from the Government
Printing Office under the ‘‘Federal
Register’’ listings at https://
www.gpo.gov/fdsys/browse/
collection.action?collectionCode=FR.
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EPA is approving only the
emissions inventory and
ment elements.
EPA is approving only the
emissions inventory and
ment elements.
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2014 base year
emissions state2014 base year
emissions state*
Table of Contents
I. General Information
A. Does this action apply to me?
B. How can I get copies of this document
and other related information?
II. Purpose and Background
A. What is the purpose of this action?
B. What are the statutory requirements for
the Contaminant Candidate List (CCL)
and regulatory determinations?
C. What contaminants did EPA consider
for regulation?
III. What process did EPA use to make the
regulatory determinations?
A. How EPA Identified and Evaluated
Contaminants for the Fourth Regulatory
Determination
B. Consideration of Public Comments
IV. EPA’s Findings on Specific Contaminants
A. PFOS and PFOA
1. Description
2. Agency Findings
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on PFOA
and PFOS and Agency Responses
3. Considerations for Additional PFAS
a. Summary of Public Comments on
Considerations for Additional PFAS and
Agency Responses
b. Summary of Public Comments on
Potential PFAS Monitoring Approaches
and Agency Responses
B. 1,1-Dichloroethane
1. Description
2. Agency Findings
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on 1,1Dichloroethane and Agency Responses
C. Acetochlor
1. Description
2. Agency Findings
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on
Acetochlor and Agency Responses
D. Methyl Bromide
1. Description
2. Agency Findings
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a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on
Methyl Bromide and Agency Responses
E. Metolachlor
1. Description
2. Agency Findings
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on
Metolachlor and Agency Responses
F. Nitrobenzene
1. Description
2. Agency Findings
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on
Nitrobenzene and Agency Responses
G. RDX
1. Description
2. Agency Findings
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on RDX
and Agency Responses
H. Strontium
I. 1,4-Dioxane
J. 1,2,3-Trichloropropane
V. Next Steps
VI. References
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II. Purpose and Background
A. What is the purpose of this action?
The purpose of this action is to
present a summary of EPA’s final
regulatory determinations for eight
contaminants listed on the Fourth
Contaminant Candidate List (CCL 4)
(USEPA, 2016a). The eight
contaminants are:
Perfluorooctanesulfonic acid (PFOS),
perfluorooctanoic acid (PFOA), 1,1dichloroethane, acetochlor, methyl
bromide (bromomethane), metolachlor,
nitrobenzene, and Royal Demolition
eXplosive (RDX). The Agency is making
final determinations to regulate two
contaminants (PFOS and PFOA) and to
not regulate the remaining six
contaminants (1,1-dichloroethane,
acetochlor, methyl bromide
(bromomethane), metolachlor,
nitrobenzene, and RDX). The Agency is
not making any determination at this
time on any other CCL contaminants,
including strontium, 1,4-dioxane, and
1,2,3-trichloropropane. This action
summarizes the statutory requirements
for targeting drinking water
contaminants for regulatory
determination, provides an overview of
the contaminants that the Agency
considered for regulation, and describes
the approach used to make the final
regulatory determinations. In addition,
this action summarizes the public
comments received on the Agency’s
preliminary determinations
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announcement and the Agency’s
responses to those comments.
B. What are the statutory requirements
for the Contaminant Candidate List
(CCL) and regulatory determinations?
Section 1412(b)(1)(B)(i) of SDWA
requires EPA to publish the CCL every
five years after public notice and an
opportunity to comment. The CCL is a
list of contaminants which are not
subject to any proposed or promulgated
National Primary Drinking Water
Regulations (NPDWRs) but are known or
anticipated to occur in public water
systems (PWSs) and may require
regulation under SDWA. SDWA section
1412(b)(1)(B)(ii) directs EPA to
determine, after public notice and an
opportunity to comment, whether to
regulate at least five contaminants from
the CCL every five years.
Under Section 1412(b)(1)(A) of
SDWA, EPA makes a determination to
regulate a contaminant in drinking
water if the Administrator determines
that:
(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 after considering public comment
on a preliminary determination, the
Agency makes a determination to
regulate a contaminant, EPA will
initiate the process to propose and
promulgate an NPDWR. In that case, the
statutory time frame provides for
Agency proposal of a regulation within
24 months and action on a final
regulation within 18 months of
proposal. When proposing and
promulgating drinking water
regulations, the Agency must conduct a
number of analyses.
C. What contaminants did EPA consider
for regulation?
On March 10, 2020, EPA published
preliminary regulatory determinations
for eight contaminants on the fourth
Contaminant Candidate List (CCL 4) (85
FR 14098) (USEPA, 2020a). The eight
contaminants are PFOS, PFOA, 1,1dichloroethane, acetochlor, methyl
bromide, metolachlor, nitrobenzene,
and RDX. The Agency is making final
regulatory determinations to regulate
two contaminants (i.e., PFOS and
PFOA) and to not regulate six
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contaminants (i.e., 1,1-dichloroethane,
acetochlor, methyl bromide,
metolachlor, nitrobenzene, and RDX).
Information on the eight contaminants
with regulatory determinations can be
found in the Final Regulatory
Determination 4 Support Document
(USEPA, 2021a). More information is
available in the Public Docket at
www.regulations.gov (Docket ID No.
EPA–HQ–OW–2019–0583) and also on
EPA’s Regulatory Determination 4
website at https://www.epa.gov/ccl/
regulatory-determination-4.
III. What process did EPA use to make
the regulatory determinations?
A. How EPA Identified and Evaluated
Contaminants for the Fourth Regulatory
Determination
This section summarizes the process
the Agency followed to identify and
evaluate contaminants for the Fourth
Regulatory Determination. For more
detailed information on the process and
the analyses performed, please refer to
the ‘‘Protocol for the Regulatory
Determination 4’’ found in Appendix E
of the Final Regulatory Determination 4
Support Document (USEPA, 2021a) and
the Federal Register publication for the
preliminary regulatory determinations
(USEPA, 2020a).
The CCL 4 identified 109
contaminants that are currently not
subject to any proposed or promulgated
national drinking water regulation, are
known or anticipated to occur in public
water systems, and may require
regulation under SDWA (USEPA,
2016a). Since some of the CCL 4
contaminants do not have adequate
health and/or occurrence data to
evaluate against the three statutory
criteria (see section II.B of this
document), as when EPA evaluated the
previous CCLs, the Agency used a threephase process to identify which of the
contaminants are candidates for
regulatory determinations. Priority was
given to identifying contaminants
known to occur or with substantial
likelihood to occur at frequencies and
levels of public health concern.
Because the regulatory determination
process includes consideration of
human health effects, the Agency’s
Policy on Evaluating Health Risks to
Children (USEPA, 1995a) reaffirmed by
Administrator Wheeler in a
memorandum dated October 11, 2018 to
Agency staff (USEPA, 2018a), applies to
this document. The policy requires EPA
to consistently and comprehensively
address children’s unique
vulnerabilities. We have explicitly
considered children’s health in the RD
4 process by reviewing all the available
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children’s exposure and health effects
information.
The three phases of the Fourth
Regulatory Determination process are
(1) the Data Availability Phase, (2) the
Data Evaluation Phase and (3) the
Regulatory Determination Assessment
Phase. The overall process is displayed
in Exhibit 1.
The purpose of the first phase, the
Data Availability Phase, is to screen out
contaminants that clearly do not have
sufficient data to support a regulatory
determination. The Agency applies
criteria to ensure that any contaminant
that potentially has sufficient data to
characterize the health effects and
known or likely occurrence in drinking
water will proceed to the Data
Evaluation Phase, the second phase of
the regulatory determination process.
From the 109 CCL 4 contaminants, the
Agency identified 25 CCL 4
contaminants to further evaluate in the
second phase. These are known as the
‘‘short list.’’
During the second phase, the Agency
evaluates the contaminants on the short
list in greater depth and detail to
identify those that have sufficient data
(or are expected to have sufficient data
within the timeframe allotted for the
second phase) for EPA to assess the
three statutory criteria. As part of the
second phase, the Agency specifically
focuses its efforts on identifying those
contaminants or contaminant groups
that are occurring or have substantial
likelihood to occur at levels and
frequencies of public health concern,
based on the best available peer
reviewed data. If, during the first or
second phase, the Agency finds that
sufficient data are not available or not
likely to be available to evaluate the
three statutory criteria, then the
contaminant is not considered a
candidate for making a regulatory
determination.
If sufficient data are available for a
contaminant to characterize the
potential health effects and known or
likely occurrence in drinking water, the
contaminant is evaluated against the
three statutory criteria in the Regulatory
Determination Assessment Phase,
which is the third phase of the process.
Of the 25 contaminants that were
evaluated under Phase 2, 10 were
designated for evaluation against the
three statutory criteria in Phase 3.
Of the 10 CCL4 contaminants that
were evaluated in Phase 3, the Agency
did not make preliminary regulatory
determinations for two contaminants
(1,4-dioxane and 1,2,3trichloropropane); see Section IV of this
document for discussion about these
contaminants. Additionally, in Section
IV of this document, EPA discusses
continuing with its previous 2016
decision to defer a final determination
for strontium (a CCL3 contaminant for
which the Agency made a preliminary
positive determination in the third
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Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations
regulatory determination (RD 3)) in
order to further consider additional
studies related to strontium exposure.
Of the eight remaining CCL 4
contaminants (PFOS, PFOA, 1,1dichloroethane, acetochlor, methyl
bromide, metolachlor, nitrobenzene,
and RDX) evaluated in Phase 3 against
the three statutory criteria, including an
evaluation of level and frequency of
occurrence in drinking water, the size of
the population exposed to
concentrations of health concern, and
information on sensitive populations
and lifestages 1 (e.g., pregnant women,
infants and children), the Agency made
preliminary regulatory determinations
to regulate PFOS and PFOA and to not
regulate the remaining six
contaminants. These preliminary
determinations, with their supporting
analyses and documentation, were
published in the Federal Register on
March 10, 2020, for public comment
(USEPA, 2020a). The public comment
period was initially intended to run
through May 11, 2020. In response to
stakeholder requests, on April 30, 2020,
EPA extended the comment period by
30 days to June 10, 2020.
B. Consideration of Public Comments
EPA received comments from
approximately 11,600 organizations and
individuals on the March 10, 2020,
Federal Register document including 12
states (California, Colorado,
Connecticut, Indiana, Massachusetts,
Michigan, Missouri, New Hampshire,
New Mexico, South Carolina, West
Virginia, and Wisconsin). Comments on
specific contaminants, and EPA’s
responses, are briefly summarized in the
sections below. The Agency prepared a
response-to-comments document for
this action (USEPA, 2021b) that is
available in the Public Docket at
www.regulations.gov under Docket ID
No. EPA–HQ–OW–2019–0583. The
response-to-comments document is
organized in a manner similar to this
document and generally contains more
detailed responses to the public
comments received than those found in
this document.
IV. EPA’s Findings on Specific
Contaminants
After considering the public
comments, EPA is making final
regulatory determinations to regulate
PFOS and PFOA and to not regulate 1,1dichloroethane, acetochlor, methyl
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bromide, metolachlor, nitrobenzene,
and RDX.
This document provides a brief
description of the Agency findings on
these contaminants. Details on the
background, health and occurrence
information, and analyses used to
evaluate and make final determinations
for these contaminants can be found in
the Final Regulatory Determination 4
Support Document (USEPA, 2021a) and
the Federal Register publication for the
preliminary regulatory determination
(USEPA, 2020a).
For each contaminant, the Agency
reviewed the available human and
toxicological data, derived a health
reference level (HRL),2 analyzed data on
occurrence in drinking water, and
estimated the population likely exposed
to concentrations of the contaminant at
levels of health concern in public water
systems. The Agency also considered
whether information was available on
sensitive populations. The Agency used
the findings to evaluate the
contaminants against the three SDWA
statutory criteria. Table 1 gives a
summary of the health and occurrence
information for the eight contaminants
with final determinations under RD 4.
TABLE 1—SUMMARY OF THE HEALTH AND OCCURRENCE INFORMATION AND THE FINAL DETERMINATIONS FOR THE EIGHT
CONTAMINANTS RECEIVING A FINAL DETERMINATION UNDER RD 4
Occurrence findings from primary data sources
Health reference
level (HRL), μg/L
Primary database
PWSs with at
least 1 detection
>1⁄2 HRL
Population served
by PWSs with at
least 1 detection
>1⁄2 HRL
PWSs with at
least 1 detection
>HRL
PFOS ....................
0.07 .....................
UCMR 3 AM ........
95/4,920 (1.93%)
46/4,920 (0.93%)
PFOA ....................
0.07 .....................
UCMR 3 AM ........
53/4,920 (1.07%)
1,1-Dichloroethane
Acetochlor .............
1,000 ...................
100 ......................
UCMR 3 AM ........
UCMR 1 AM ........
0/4,916 (0.00%) ...
0/3,869 (0.00%)—
UCMR 1.
UCMR 2 SS ........
0/1,198 (0.00%)—
UCMR 2.
Methyl Bromide
100 ......................
(Bromomethane).
Metolachlor ........... 300 ......................
Nitrobenzene ........ 10 ........................
UCMR 3 AM ........
0/4,916 (0.00%) ...
10,427,193/241 M
(4.32%).
3,652,995/241 M
(1.51%).
0/241 M (0.00%)
0/226 M
(0.00%)—
UCMR 1.
0/157 M
(0.00%)—
UCMR 2.
0/241 M (0.00%)
UCMR 2 SS ........
UCMR 1 AM ........
0/1,198 (0.00%) ...
2/3,861 (0.05%) ...
RDX ......................
UCMR 2 AM ........
..............................
0/4,139 (0.00%) ...
>15 μg/L ..............
3/4,139 (0.07%) ...
RD 4 contaminant
30 (noncancer) ....
0.4 (cancer) .........
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>0.2 μg/L .............
1 https://www.epa.gov/children/childhoodlifestages-relating-childrens-environmental-health.
2 An HRL is a health-based concentration against
which the Agency evaluates occurrence data when
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0/157 M (0.00%)
255,358/226 M
(0.11%).
0/229 M (0.00%)
>15 μg/L ..............
96,033/229 M
(0.04%).
>0.2 μg/L .............
13/4,920 (0.26%)
0/4,916 (0.00%) ...
0/3,869 (0.00%)—
UCMR 1.
0/1,198 (0.00%)—
UCMR 2.
0/4,916 (0.00%) ...
0/1,198 (0.00%) ...
2/3,861 (0.05%) ...
0/4,139 (0.00%) ...
>30 μg/L ..............
3/4,139 (0.07%) ...
>0.4 μg/L .............
making decisions about preliminary regulatory
determinations. An HRL is not a final determination
on establishing a protective level of a contaminant
in drinking water for a particular population; it is
derived prior to development of a complete health
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Population served
by PWSs with at
least 1 detection
>HRL
3,789,831/241 M
(1.57%).
490,480/241 M
(0.20%).
0/241 M (0.00%)
0/226 M
(0.00%)—
UCMR 1.
0/157 M
(0.00%)—
UCMR 2.
0/241 M (0.00%)
0/157 M (0.00%)
255,358/226 M
(0.11%).
0/229 M (0.00%)
>30 μg/L.
96,033/229 M
(0.04%).
>0.4 μg/L.
Final
determination
Regulate.
Regulate.
Do not regulate.
Do not regulate.
Do not regulate.
Do not regulate.
Do not regulate.
Do not regulate.
and exposure assessment and can be considered a
screening value. See Section E.5.1 of the Final
Regulatory Determination 4 Support Document for
information about how HRLs are derived (USEPA,
2021a).
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A. PFOS and PFOA
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1. Description
Per- and polyfluoroalkyl substances
(PFAS) are a class of synthetic
chemicals that have been manufactured
and in use since the 1940s (AAAS,
2020; USEPA, 2018b). PFAS are most
commonly used to make products
resistant to water, heat, and stains and
are consequently found in industrial
and consumer products like clothing,
food packaging, cookware, cosmetics,
carpeting, and fire-fighting foam (AAAS,
2020). PFAS manufacturing and
processing facilities, facilities using
PFAS in production of other products,
airports, and military installations have
been associated with PFAS releases into
the air, soil, and water (USEPA 2016b;
USEPA 2016c). People may potentially
be exposed to PFAS through the use of
certain consumer products, through
occupational exposure, and/or through
consuming contaminated food or
contaminated drinking water (Domingo
and Nadal, 2019; Fromme et al. 2009).
Perfluorooctane sulfonate (PFOS) and
perfluorooctanoic acid (PFOA) are part
of a subset of PFAS referred to as
perfluorinated alkyl acids (PFAA) and
are two of the most widely studied and
longest-used PFAS. Due to their
widespread use and persistence in the
environment, most people have been
exposed to PFAS, including PFOA and
PFOS (USEPA 2016b; USEPA 2016c).
PFOA and PFOS have been detected in
up to 98% of serum samples taken in
biomonitoring studies that are
representative of the U.S. general
population (CDC, 2019). Following the
voluntary phase-out of PFOA by eight
major chemical manufacturers and
processors in the United States under
EPA’s 2010/2015 PFOA Stewardship
Program and reduced manufacturing of
PFOS (last reported in 2002 under
Chemical Data Reporting), serum
concentrations have been declining. The
National Health and Nutrition
Examination Survey (NHANES) data
exhibited that 95th-percentile serum
PFOS concentrations have decreased
over 75%, from 75.7 mg/L in the 1999–
2000 cycle to 18.3 mg/L in the 2015–
2016 cycle (CDC, 2019; Jain, 2018;
Calafat et al., 2007; Calafat et al., 2019).
2. Agency Findings
The Agency is making a
determination to regulate PFOA and
PFOS with a NPDWR. EPA has
determined that PFOA and PFOS may
have adverse health effects; that PFOA
and PFOS occur in public water systems
with a frequency and at levels of public
health concern; and that, in the sole
judgment of the Administrator,
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regulation of PFOA and PFOS presents
a meaningful opportunity for health risk
reduction for persons served by public
water systems.
(a) Adverse Health Effects
The Agency finds that PFOA and
PFOS may have adverse effects on the
health of persons. In 2016, EPA
published health assessments (Health
Effects Support Documents or HESDs)
for PFOA and PFOS based on the
Agency’s evaluation of the peer
reviewed science available at that time.
The lifetime Health Advisory (HA) of
0.07 mg/L is used as the HRL for
Regulatory Determination 4 and reflect
concentrations of PFOA and PFOS in
drinking water at which adverse health
effects are not anticipated to occur over
a lifetime. Studies indicate that
exposure to PFOA and/or PFOS above
certain exposure levels may result in
adverse health effects, including
developmental effects to fetuses during
pregnancy or to breast-fed infants (e.g.,
low birth weight, accelerated puberty,
skeletal variations), cancer (e.g.,
testicular, kidney), liver effects (e.g.,
tissue damage), immune effects (e.g.,
antibody production and immunity),
and other effects (e.g., cholesterol
changes). Both PFOA and PFOS are
known to be transmitted to the fetus via
the placenta and to the newborn, infant,
and child via breast milk. Both
compounds were also associated with
tumors in long-term animal studies
(USEPA, 2016d; USEPA, 2016e; NTP,
2020). For specific details on the
potential for adverse health effects and
approaches used to identify and
evaluate information on hazard and
dose-response, please see (USEPA,
2016b; USEPA, 2016c; USEPA, 2016d;
USEPA, 2016e).
(b) Occurrence
EPA has determined that PFOA and
PFOS occur with a frequency and at
levels of public health concern at PWSs
based on the Agency’s evaluation of
available occurrence information. In
accordance with SDWA
1412(b)(1)(B)(ii)(II), EPA has determined
monitoring data from the third
Unregulated Contaminant Monitoring
Rule (UCMR 3) are the best available
occurrence information for PFOA and
PFOS regulatory determinations. UCMR
3 monitoring occurred between 2013
and 2015 and are currently the only
nationally representative finished water
dataset for PFOA and PFOS. Under
UCMR 3, 36,972 samples from 4,920
PWSs were analyzed for PFOA and
PFOS. The minimum reporting level
(MRL) for PFOA was 0.02 mg/L and the
MRL for PFOS was 0.04 mg/L. A total of
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1.37% of samples had reported
detections (greater than or equal to the
MRL) of at least one of the two
compounds. To examine the occurrence
of PFOS and PFOA in aggregate, EPA
summed the concentrations detected in
the same sample to calculate a total
PFOS/PFOA concentration. EPA notes
that the reference doses (RfDs) for both
PFOA and PFOS are based on similar
developmental effects and are
numerically identical; when these two
chemicals co-occur at the same time and
location in drinking water sources, EPA
has recommended considering the sum
of the concentrations (USEPA, 2016d;
USEPA, 2016e) and has done so for this
regulatory determination. The
maximum summed concentration of
PFOA and PFOS was 7.22 mg/L and the
median summed value was 0.05 mg/L.
Summed PFOA and PFOS
concentrations exceeded one-half the
HRL (0.035 mg/L) at a minimum of 2.4%
of PWSs (115 PWSs) and exceeded the
HRL (0.07 mg/L) at a minimum of 1.3%
of PWSs (63 PWSs 3). Since UCMR 3
monitoring occurred, certain sites where
elevated levels of PFOA and PFOS were
detected may have installed treatment
for PFOA and PFOS, may have chosen
to blend water from multiple sources, or
may have otherwise remediated known
sources of contamination. Those 63
PWSs serve a total population of
approximately 5.6 million people and
are located in 25 states, tribes, or U.S.
territories (USEPA, 2019a). Data from
more recent state monitoring (discussed
below) demonstrate occurrence in
multiple geographic locations consistent
with UCMR 3 monitoring and support
the Agency’s final determination that
PFOA and PFOS occur with a frequency
and at levels of public health concern in
finished drinking water across the
United States. The Final Regulatory
Determination 4 Support Document
presents a sample-level summary of the
results for PFOA and PFOS individually
and includes discussion on state
monitoring efforts as well as
uncertainties in occurrence data
(USEPA, 2021a).
Consistent with the Agency’s
commitment in the PFAS Action Plan
(the Agency’s first multi-media, multiprogram, national research,
management, and risk communication
plan to address a challenge like PFAS)
to present information about additional
sampling efforts for PFAS in water
systems, the Agency has supplemented
its Unregulated Contaminant
Monitoring Regulation (UCMR) data
3 Sum of PFOA + PFOS results rounded to 2
decimal places in those cases where a laboratory
reported more digits.
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with data collected by states who have
made their data publicly available at
this time (USEPA, 2019b). A summary
of these occurrence data were presented
in the preliminary Regulatory
Determination 4 Federal Register
document. Subsequent to the
preliminary announcement, based on
comments and information received on
the proposed determination, the Agency
collected additional data from
additional states. The finished water
data available from fifteen states
collected since UCMR 3 monitoring
showed that there were at least 29 PWSs
where the summed concentrations of
PFOA and PFOS exceeded the EPA
HRL. The Agency notes that some of
these data are from targeted sampling
efforts and thus may not be
representative of levels found in all
PWSs within the state or represent
occurrence in other states. The state
data demonstrate occurrence in multiple
geographic locations and support EPA’s
finding that PFOA and PFOS occur with
a frequency and at levels of public
health concern in drinking water
systems across the United States. The
Final Regulatory Determination 4
Support Document presents a detailed
discussion of state PFOA and PFOS
occurrence information (USEPA, 2021a).
EPA acknowledges that there may be
other states with occurrence data
available and that additional states have
or intend to conduct monitoring of
finished drinking water. As such, EPA
will consider any new or additional
state data to inform the development of
the proposed NPDWR for PFOA and
PFOS.
(c) Meaningful Opportunity
Considering the population exposed
to PFOA and PFOS including sensitive
populations and lifestages, the potential
adverse human health impacts of these
contaminants, the environmental
persistence of these substances, the
persistence in the human body and
potential for bioaccumulation of these
substances, the availability of validated
methods to measure and treatment
technologies to remove PFOA and
PFOS, the detections that exceeded the
HRL and 1⁄2 the HRL, and significant
public concerns (particularly those
expressed in comments submitted by
state and local government agencies) on
the challenges that these contaminants
pose for communities nationwide, the
Agency has determined that regulation
of PFOA and PFOS presents a
meaningful opportunity for health risk
reduction for persons served by PWSs,
including sensitive populations such as
infants, children, and pregnant and
nursing women.
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PFOA and PFOS are both generated as
degradation products of other
perfluorinated compounds (e.g.,
fluorotelomer alcohols), and due to their
strong carbon-fluorine bonds, are
resistant to metabolic and
environmental degradation (USEPA,
2016b; USEPA, 2016c). Due to this
underlying chemical structure, PFOA
and PFOS are extremely persistent in
the environment, including resistance to
chemical, biological, and physical
degradation processes. While most U.S.
manufacturers have voluntarily phased
out production and manufacturing of
both PFOS and PFOA, their
environmental persistence and
formation as degradation products from
other compounds may still contribute to
their release in the environment. Upon
exposure to the human body, there is a
potential for bioaccumulation and
toxicity at environmentally relevant
concentrations as studies show it can
take years to leave the human body
(NIEHS, 2020; USEPA, 2016b; USEPA,
2016c).
Adverse effects observed following
exposures to PFOA and PFOS include
effects in humans on serum lipids, birth
weight, and serum antibodies. Some of
the animal studies show common effects
on the liver, neonate development, and
responses to immunological challenges.
Both compounds were also associated
with tumors in long-term animal studies
(USEPA, 2016d; USEPA, 2016e). In
determining that regulation of PFOA
and PFOS presents a meaningful
opportunity for health risk reduction for
sensitive populations, EPA noted that
both PFOA and PFOS are associated
with developmental toxicity in animals,
with reduced birth weight in humans,
and have been shown to be transmitted
to the fetus via the placenta and to the
newborn, infant, and child via breast
milk (USEPA, 2016b; USEPA, 2016c).
Drinking water analytical methods are
available to measure PFOA, PFOS, and
other PFAS in drinking water. EPA has
published validated drinking water
laboratory methods for detecting a total
of 29 unique PFAS in drinking water,
including EPA Method 537.1 (18 PFAS)
and EPA Method 533 (25 PFAS).
Available treatment technologies for
removing PFAS from drinking water
have been evaluated and reported in the
literature (e.g., Dickenson and Higgins,
2016). EPA’s Drinking Water
Treatability Database (USEPA, 2020b)
summarizes available technical
literature on the efficacy of treatment
technologies for a range of priority
drinking water contaminants, including
PFOA and PFOS. In summary,
conventional treatment (comprised of
the unit processes coagulation,
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flocculation, clarification, and filtration)
is not considered effective for the
removal of PFOA and PFOS. Granular
activated carbon (GAC), anion exchange
resins, reverse osmosis and
nanofiltration are considered effective
for the removal of PFOA and PFOS.
(d) Summary of Public Comments on
PFOA and PFOS and Agency Responses
EPA received many comments on the
Agency’s evaluation of the first statutory
criterion under section 1412(b)(1)(A) of
SDWA. Most commenters agreed with
EPA’s finding that PFOA and PFOS may
have adverse effects on the health of
persons. Most commenters also state
that there is ‘‘strong evidence’’ and
‘‘substantial scientific evidence’’ for
EPA’s finding of adverse health effects
of PFOA and PFOS. One commenter
disagreed with EPA’s evaluation of the
first statutory criterion, arguing that the
body of scientific evidence does not
show adverse effects from PFAS in
humans. EPA also received numerous
comments relating to the Agency’s 2016
Lifetime Health Advisory for PFOA and
PFOS, the corresponding HESD and the
HRL used to support the preliminary
regulatory determination. Numerous
commenters encouraged EPA to update
and ‘‘improve its health reference level’’
and ‘‘revise the PFOA and PFOS hazard
assessments’’ prior to making a final
regulatory determination.
EPA acknowledges commenters’
suggestions to consider and evaluate
newer studies; however, EPA disagrees
with recommendations to establish new
HRLs prior to a final regulatory
determination. Consistent with SDWA
section 1412(b)(3)(A)(i), EPA is using
the 2016 PFOA and PFOS Lifetime
Health Advisory as the basis in deriving
an HRL which the Agency has
concluded represent the best available
peer reviewed scientific assessment at
this time. Based upon the 2016 EPA
HESDs for PFOA and PFOS, and other
supporting studies cited in the record,
EPA finds that PFOA and PFOS may
have an adverse effect on the health of
persons. Consistent with commenters’
recommendations, EPA has initiated the
first steps of a systematic literature
review of peer-reviewed scientific
literature for PFOA and PFOS published
since 2013 with the goal of identifying
any new studies that may be relevant to
human health assessment. An annotated
bibliography of the identified relevant
studies as well as the protocol used to
identify the relevant publications can be
found in Appendix D of the Final
Regulatory Determination 4 Support
Document (USEPA, 2021a), available in
the docket for this document.
Additional analyses of these new
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studies is needed to confirm relevance,
extract the data to assess the weight of
evidence, and identify critical studies in
order to inform future decision making.
EPA also received comments on the
Agency’s evaluation of the second
statutory criterion under section
1412(b)(1)(A) of SDWA. Many
commenters supported EPA’s
preliminary determination that PFOA
and PFOS meet the second statutory
occurrence criterion under SDWA.
Several commenters stated that while
they are supportive of using UCMR 3
data as the basis of nationwide drinking
water occurrence for PFOA and PFOS,
solely relying on these monitoring data
may be an inaccurate reflection of PFOA
and PFOS exposure. The Agency also
received comments and information on
actions taken by a number of states to
monitor PFOA, PFOS, and other PFAS
in PWSs, particularly in locations that
were not previously required to conduct
UCMR monitoring. Some commenters
suggested that PFOA and PFOS UCMR
3 occurrence information used by EPA
in making the Preliminary
Determination for PFOA and PFOS is
not reflective of the actual occurrence of
PFOS and PFOS within public water
systems. These commenters stated that
UCMR 3 monitoring excludes small
public water systems and was
conducted with high minimum
reporting levels. Three commenters did
not support EPA’s preliminary
determination that PFOA and PFOS
meet the second statutory criterion
under SDWA. These commenters
expressed concern that the data EPA
relied upon are outdated, are skewed,
and overestimate current PFOA and
PFOS occurrence. These commenters
suggest that EPA should revise its
occurrence analysis with more recent
data prior to making a final
determination.
EPA disagrees with those commenters
who assert that UCMR 3 are not the best
available occurrence data. EPA also
disagrees that the UCMR 3 excludes
small water systems and disagrees that
the minimum reporting levels were too
high. The UCMR 3 assured a nationally
representative sample of 800 small
drinking water systems and established
minimum reporting levels based upon
laboratory performance data that are
lower than the HRLs for PFOA and
PFOS. The UCMR 3 data are the best
available information to assess the
frequency and level of occurrence of
PFOA and PFOS in the nation’s public
water systems. After considering the
public comments and additional
occurrence data provided by
commenters, EPA continues to find that
PFOA and PFOS meet the second
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statutory criterion for regulatory
determinations under Section
1412(b)(1)(A) of SDWA that ‘‘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.’’ Nonetheless,
EPA agrees with commenters who
recommend that the Agency consider
other existing available occurrence data
to inform its final regulatory
determination and PFOA and PFOS
rulemaking. As discussed previously,
the Final Regulatory Determination 4
Support Document presents a detailed
discussion of state PFOA and PFOS
occurrence information that were
analyzed and used to further support
the Agency’s finding that PFOA and
PFOS occur in public water systems
with a frequency and at levels of public
health concern (USEPA, 2021a).
EPA also received many comments on
the Agency’s evaluation of the third
statutory criterion under section
14121412(b)(1)(A) of SDWA. Many
commenters, including multiple state
regulators and organizations
representing states, agree with EPA’s
evaluation that regulation of PFOA and
PFOS presents a meaningful
opportunity for health risk reduction for
persons served by PWSs. These
commenters highlight the extensive
amount of work associated with
developing their own drinking water
standards for several PFAS compounds.
These commenters also noted the need
for a consistent national standard for
use in states where a state-specific
standard has not yet been developed.
Many commenters have also noted that
although some states have developed or
are in the process of developing their
own state-level PFAS drinking water
standards, regulatory standards
currently vary across states. These
commenters expressed concern that
absence of a national drinking water
standard has resulted in risk
communication challenges with the
public and disparities with PFAS
exposure. Some commenters noted there
are populations particularly sensitive or
vulnerable to the health effects of PFAS,
including newborns, infants and
children. One commenter did not
support EPA’s evaluation of the third
statutory criterion, noting that in their
opinion, the toxicity assessment for
PFOA and PFOS and existing
occurrence data do not suggest that
establishing drinking water standards
presents a meaningful opportunity for
health risk reduction.
EPA acknowledges commenter
concerns regarding sensitive and
vulnerable subpopulations and notes
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that the Agency has been particularly
mindful that PFOA and PFOS are
known to be transmitted to the fetus via
cord blood and to the newborn, infant
and child via breast milk. EPA agrees
with commenters that there is a need for
protective drinking water regulations
across the United States and that
moving forward with a national-level
regulation for PFOA and PFOS would
provide improved national consistency
in protecting public health and may
reduce regulatory uncertainty for
stakeholders across the country. The
Agency disagrees with the commenter’s
assertion that PFOA and PFOS health
and occurrence information are
insufficient to justify a drinking water
standard, and the Agency finds that
there is a meaningful opportunity for
health risk reduction potential based
upon consideration the population
exposed to PFOA and PFOS including
sensitive populations and lifestages,
such as newborns, infants and children.
3. Considerations for Additional PFAS
As EPA begins the process to
promulgate the NPDWR for PFOA and
PFOS, the Agency recognizes that there
is additional information to consider
regarding a broader range of PFAS,
including new monitoring and
occurrence data, and ongoing work
developing toxicity assessments by EPA,
other federal agencies, state
governments, international
organizations, industry groups, and
other stakeholders. While the Agency is
not making regulatory determinations
for additional PFAS at this time, the
Agency remains committed to filling
information gaps, including those
identified in the PFAS Action Plan, by
completing peer reviewed toxicity
assessments and collecting nationally
representative occurrence data for
additional PFAS to support future
regulatory determinations as part of the
UCMR monitoring program (see
discussion below).
EPA committed in the PFAS Action
Plan to characterize potential health
impacts and develop more drinking
water occurrence data for a broader set
of PFAS (USEPA, 2019b). EPA has
followed through on its commitments
and as a result expects to have peerreviewed health assessments and
national occurrence data for more PFAS
becoming available over the next few
years. EPA notes that although SDWA
does not require the Agency to complete
regulatory determinations for the
contaminants from the fifth CCL until
2026, because of the significant progress
related to developing new high-quality
PFAS information, combined with the
Agency’s commitment in the PFAS
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Action Plan to assist states and
communities with PFAS contaminated
drinking water, EPA will continue to
prioritize regulatory determinations of
additional PFAS in drinking water. The
Agency is committing to making
regulatory determinations in advance of
the next SDWA deadline for additional
PFAS for which the Agency has a peer
reviewed health assessment, has
nationally representative occurrence
data in finished drinking water, and has
sufficient information to determine
whether there is a meaningful
opportunity for health risk reduction for
persons served by public water systems.
EPA is currently developing
scientifically rigorous toxicity
assessments for seven PFAS chemicals.
The chemicals currently undergoing
assessment include PFBS, PFBA,
PFHxS, PFHxA, PFNA, PFDA, and
HFPO–DA (GenX chemicals), all of
which are currently scheduled to be
completed by 2023. These assessments
all include public comment periods,
independent scientific external peer
review, and a robust interagency review
process. Furthermore, these toxicity
assessments will provide critical health
information for PFAS with varying
chain lengths and functional groups.
When complete, these assessments will
summarize available scientific
information regarding the anticipated
human dose-response relationship for
these chemicals, which is a key
information need for informing a variety
of Agency decisions.
To inform EPA’s understanding of
PFAS occurrence in drinking water as
discussed in EPA’s PFAS Action Plan
(USEPA, 2019b), the Agency is also
leading efforts to gather additional
monitoring data for 29 PFAS
contaminants in finished drinking
water. EPA recently announced its
proposal for nationwide drinking water
monitoring for PFAS under the next
UCMR monitoring cycle (UCMR 5)
utilizing Methods 537.1 and 533 to
detect more PFAS chemicals and at
lower reporting limits than previously
possible.
EPA is also is generating new PFAS
toxicology data for a much larger set of
less-studied PFAS through new
approach methods (NAMs) 4 such as
high throughput screening,
computational toxicology tools, and
chemical informatics for chemical
prioritization, screening, and risk
assessment. EPA will continue research
4 New approach methods (NAMs) refer to any
technologies, methodologies, approaches, or
combinations thereof that can be used to provide
information on chemical hazard and potential
human exposure that can avoid or significantly
reduce the use of testing on animals.
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on methods for using these data to
support risk assessments using NAMs
such as read-across (i.e., an effort to
predict biological activity based on
similarity in chemical structure) and
transcriptomics (i.e., a measure of
changes in gene expression in response
to chemical exposure or other external
stressors), and to make inferences about
the toxicity of PFAS mixtures that
commonly occur in real world
exposures. This research can inform a
more complete understanding of PFAS
toxicity for the large set of PFAS
chemicals without conventional toxicity
data and can allow prioritization of
actions to potentially address groups of
PFAS. For additional information on the
NAMs for PFAS toxicity testing, please
visit: https://www.epa.gov/chemicalresearch/pfas-chemical-lists-and-tieredtesting-methods-descriptions. These
EPA actions, in addition to other
research, may provide useful
information for future EPA evaluations
of additional PFAS.
(a) Summary of Public Comments on
Considerations for Additional PFAS and
Agency Responses
EPA requested comment on potential
regulatory constructs the Agency may
consider for PFAS chemicals including
PFOA and PFOS. EPA specifically
requested input on a regulatory
approach to evaluate PFAS by different
grouping approaches.
EPA received multiple comments on
how the Agency could consider
additional PFAS for potential future
rulemaking. Many commenters support
a class-based approach for regulating
PFAS based on one or more
characteristics such as chain length,
functional group, treatment processes,
health effects, toxicity, common
analytical methods, and/or shared
occurrence with other contaminants
within a group. Additionally, many
commenters also urge EPA to make
additional regulatory determinations for
PFAS that have a proposed or final
drinking water standard in at least one
state; PFAS that have been measured in
water systems through monitoring
programs such as UCMR; and/or PFAS
for which EPA or the Agency for Toxic
Substances and Disease Registry
(ATSDR) has established a toxicity
value. Some commenters suggest that
EPA should make positive regulatory
determinations for PFHxS and PFNA as
well as in combination with PFOA,
PFOS, and other PFAS such as PFBS.
Many commenters recommend EPA
consider various grouping and treatment
technique approaches for PFAS beyond
PFOA and PFOS that may not have
sufficient health and occurrence data.
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Some of these commenters recommend
approaches that consider acute and
chronic health effects, long-term
compared to short-term exposures,
exposures during sensitive lifestages,
and type of water systems and
vulnerable populations such as
vulnerable workers. Many commenters
stated that the data may not be robust
enough for each PFAS and therefore
support a class-based approach for
regulating PFAS in drinking water. In
contrast, two commenters did not
support a class-based approach for
regulating PFAS. In summary, these
commenters suggest that regulation
without assessing each chemical’s
individual traits ‘‘would be contrary to
the intent of SDWA’’ and that the
Agency should address outstanding data
and knowledge gaps regarding PFAS of
concern prior to determining a
regulatory grouping approach.
With respect to comments received on
regulatory determinations for additional
PFAS compounds other than PFOA and
PFOS, EPA remains committed to filling
information gaps by completing peer
reviewed health assessments where
appropriate and collecting nationally
representative occurrence data. As
discussed above, in response to public
comments advocating timely regulation
of additional PFAS in drinking water,
where sufficient information is
available, EPA intends to make
regulatory determinations for additional
PFAS prior to the fifth Regulatory
Determination’s statutory deadline
(2026).
The Agency acknowledges many
commenters’ support for a class-based
approach for regulating PFAS and
appreciates commenter
recommendations regarding potential
regulatory constructs. EPA
acknowledges commenters’
recommendations to evaluate whether
PFAS can be regulated as groups, and
the Agency is developing the science
necessary to consider whether such
regulation is necessary and appropriate
for PFAS. Regarding commenters’
assertions that regulation without
assessing each chemical’s individual
traits ‘‘would be contrary to the intent
of SDWA,’’ the Agency notes that the
Safe Drinking Water Act establishes a
robust scientific and public
participation process that guide EPA’s
development of regulations for
unregulated contaminants that may
present a risk to public health.
Regulation by groups is a regulatory
strategy that is already used for certain
regulated contaminants like disinfection
byproducts, polychlorinated biphenyls,
and radionuclides. EPA will continue to
use best available science and available
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statutory authorities to guide Agency
decision making with respect to how the
Agency evaluates and potentially
regulates additional PFAS.
(b) Summary of Public Comments on
Potential PFAS Monitoring Approaches
and Agency Responses
As part of the proposed preliminary
regulatory determination for PFOA and
PFOS, EPA solicited comment on
potential monitoring approaches if the
Agency were to finalize a positive
regulatory determination for these
contaminants. EPA presented two
monitoring approaches in the Agency’s
preliminary Regulatory Determination
for CCL 4 contaminants. Under the
Standardized Monitoring Framework
(SMF) for synthetic organic chemicals,
monitoring schedules are based around
the detection levels of the regulated
contaminants, and state primacy
agencies can also issue waivers for
monitoring. The Agency also presented
an alternative monitoring approach to
allow state primacy agencies to require
monitoring at PWSs where information
indicates potential PFAS contamination,
such as proximity to facilities with
historical or on-going uses of PFAS.
Many commenters supported the
Agency’s goal of reducing potential
monitoring burden for PWSs without
compromising public health protection.
While there were differing views among
commenters regarding which
monitoring approach is best for PFAS,
many urged EPA to keep evaluating
different approaches as the Agency
promulgates the NPDWR for PFOA and
PFOS.
The Agency appreciates commenter
recommendations on monitoring
approaches. As the Agency promulgates
the regulatory standard for PFOA and
PFOS, EPA will continue to work to
establish monitoring requirements in
the rule that minimize burden while
ensuring public health protection.
B. 1,1-Dichloroethane
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1. Description
1,1-Dichloroethane is a halogenated
alkane. It is an industrial chemical and
is used as a solvent and a chemical
intermediate. 1,1-Dichloroethane is
expected to have moderate to high
persistence in water (USEPA, 2021a).
2. Agency Findings
The Agency is making a
determination not to regulate 1,1dichloroethane with an NPDWR. It does
not occur with a frequency and at levels
of public health concern. As a result, the
Agency finds that an NPDWR does not
present a meaningful opportunity for
health risk reduction.
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(a) Adverse Health Effects
The Agency finds that 1,1dichloroethane may have adverse effects
on the health of persons. Based on a 13week gavage study in rats (Muralidhara
et al., 2001), the kidney was identified
as a sensitive target for 1,1dichloroethane, and no-observedadverse-effect level (NOAEL) and
lowest-observed-adverse-effect level
(LOAEL) values of 1,000 and 2,000 mg/
kg/day, respectively, were identified
based on increased urinary enzyme
markers for renal damage and central
nervous system (CNS) depression
(USEPA, 2006a).
The only available reproductive or
developmental study with 1,1dichloroethane is an inhalation study
where pregnant rats were exposed on
days 6 through 15 of gestation (Schwetz
et al., 1974). No effects on the fetuses
were noted at 3,800 ppm. Delayed
ossification of the sternum without
accompanying malformations was
reported at a concentration of 6,000
ppm.
A cancer assessment for 1,1dichloroethane is available on IRIS
(USEPA, 1990a). That assessment
classifies the chemical, according to
EPA’s 1986 Guidelines for Carcinogenic
Risk Assessment (USEPA, 1986), as
Group C, a possible human carcinogen.
This classification is based on no
human data and limited evidence of
carcinogenicity in two animal species
(rats and mice), as shown by increased
incidences of hemangiosarcomas and
mammary gland adenocarcinomas in
female rats and hepatocellular
carcinomas and benign uterine polyps
in mice (NCI, 1978). The data were
considered inadequate to support
quantitative assessment. The close
structural relationship between 1,1dichloroethane and 1,2-dichloroethane,
which is classified as a B2 probable
human carcinogen and produces tumors
at many of the same sites where
marginal tumor increases were observed
for 1,1-dichloroethane, supports the
suggestion that the 1,1-isomer could
possibly be carcinogenic to humans.
Mixed results in initiation/promotion
studies and genotoxicity assays are
consistent with this classification. On
the other hand, the animals from the
1,1-dichloroethane National Cancer
Institute (NCI, 1978) study were housed
with animals being exposed to 1,2dichloroethane providing opportunities
for possible co-exposure impacting the
1,1-dichloroethane results. The
following groups of individuals may
have an increased risk from exposure to
1,1-dichloroethane (NIOSH, 1978;
ATSDR, 2015):
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• Those with chronic respiratory
disease,
• Those with liver diseases that
impact hepatic microsomal cytochrome
P–450 functions,
• Individuals with impaired renal
function and vulnerable to kidney
stones
• Individuals with skin disorders
vulnerable to irritation by solvents like
1,1-dichloroethane,
• Those who consume alcohol or use
pharmaceuticals (e.g., phenobarbital)
that alter the activity of cytochrome P–
450s.
A provisional chronic RfD was
derived from the 13-week gavage study
in rats based on a NOAEL of 1,000 mg/
kg/day administered for five days/week
and adjusted to 714.3 mg/kg/day for
continuous exposure (an increase in
urinary enzymes was the adverse impact
on the kidney). The chronic oral RfD of
0.2 mg/kg/day was derived by dividing
the normalized NOAEL of 714.3 mg/kg/
day in male Sprague-Dawley rats by a
combined UF of 3,000. The combined
UF includes factors of 10 for
interspecies extrapolation, 10 for
extrapolation from a subchronic study,
10 for human variability, and 3 for
database deficiencies (including lack of
reproductive and developmental
toxicity tests by the oral route). This
assessment noted several limitations in
the critical study and database as a
whole. Specifically, that the reporting of
the results in the critical study were
marginally adequate and that the
database lacks information on
reproductive and developmental and
nervous system toxicity.
EPA calculated an HRL for 1,1dichloroethane of 1,000 mg/L, based on
EPA oral RfD of 0.2 mg/kg/day, using
2.5 L/day drinking water ingestion, 80
kg body weight and a 20% relative
source contribution (RSC) factor.
(b) Occurrence
EPA has determined that 1,1dichloroethane does not occur with a
frequency and at levels of public health
concern at PWSs based on the Agency’s
evaluation of available occurrence
information. The primary occurrence
data for 1,1-dichloroethane are the
2013–2015 nationally representative
drinking water monitoring data
generated through EPA’s UCMR 3. 1,1Dichloroethane was not detected in any
of the 36,848 UCMR 3 samples collected
by 4,916 PWSs (serving ∼ 241 million
people) at levels greater than 1⁄2 the HRL
(500 mg/L) or the HRL (1,000 mg/L). 1,1Dichloroethane was detected in about
2.3% samples at or above the MRL (0.03
mg/L) (USEPA, 2019a; USEPA, 2021a).
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Other supplementary sources of
finished water occurrence data from
UCM Rounds 1 and 2 indicate that the
occurrence of 1,1-dichloroethane in
PWSs is likely to be low to non-existent
(USEPA, 2021a). 1,1-Dichloroethane
occurrence data for ambient water from
NAWQA and NWIS are consistent with
those for finished water (USEPA,
2021a).
(c) Meaningful Opportunity
The Agency has determined that
regulation of 1,1-dichloroethane does
not present a meaningful opportunity
for health risk reduction for persons
served by PWSs based on the estimated
exposed populations, including
sensitive populations. UCMR 3 findings
indicate that the estimated population
exposed to 1,1-dichloroethane at levels
of public health concern is 0%, based
on lack of detections at levels greater
than 1⁄2 the HRL (500 mg/L) or the HRL
(1,000 mg/L). As a result, the Agency
finds that an NPDWR for 1,1dichloroethane does not present a
meaningful opportunity for health risk
reduction.
(d) Summary of Public Comments on
1,1-Dichloroethane and Agency
Responses
EPA received several comments on
the Agency’s evaluation of 1,1dichloroethane under section
1412(b)(1)(A) of SDWA, all of which
were in support of its preliminary
determination not to regulate 1,1dichloroethane. EPA agrees with the
comments that are in support of the
negative regulatory determination.
C. Acetochlor
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1. Description
Acetochlor is a chloroacetanilide
pesticide that is used as an herbicide for
pre-emergence control of weeds. It is
registered for use on corn crops (field
corn and popcorn) and has been
approved for use on cotton as a
rotational crop. Synonyms for
acetochlor include 2-chloro-2′-methyl-6ethyl-N-ethoxymethylacetanilide
(USEPA, 2021a). Acetochlor is expected
to have low to moderate persistence in
water due to its biodegradation half-life,
as well as susceptibility to photolysis
(USEPA, 2021a).
2. Agency Findings
The Agency is making a
determination not to regulate acetochlor
with an NPDWR. Acetochlor does not
occur with a frequency and at levels of
public health concern. As a result, the
Agency finds that an NPDWR does not
present a meaningful opportunity for
health risk reduction.
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(a) Adverse Health Effects
The Agency finds that acetochlor may
have adverse effects on the health of
persons. Subchronic and chronic oral
studies have demonstrated adverse
effects on the liver, thyroid (secondary
to the liver effects), nervous system,
kidney, lung, testes, and erythrocytes in
rats and mice (USEPA, 2006b; USEPA,
2018c). There was evidence of
carcinogenicity in studies conducted
with acetochlor in rats and mice and a
non-mutagenic mode of action was
demonstrated for nasal and thyroid
tumors in rats (USEPA, 2006b). Cancer
effects include nasal tumors and thyroid
tumors in rats, lung tumors and
histiocytic sarcomas in mice, and liver
tumors in both rats and mice (Ahmed
and Seely, 1983; Ahmed et al., 1983;
Amyes, 1989; Hardisty, 1997a; Hardisty,
1997b; Hardisty, 1997c; Naylor and
Ribelin, 1986; Ribelin, 1987; USEPA,
2004b; USEPA, 2006b; and Virgo and
Broadmeadow, 1988). No biologically
sensitive human subpopulations have
been identified for acetochlor.
Developmental and reproductive
toxicity studies do not indicate
increased susceptibility to acetochlor
exposure at early life stages in test
animals (USEPA, 2006b).
The study used to derive the oral RfD
is a 1-year oral chronic feeding study
conducted in beagle dogs. This study
describes a NOAEL of 2 mg/kg/day, and
a LOAEL of 10 mg/kg/day, based on the
critical effects of increased salivation;
increased levels of alanine
aminotransferase (ALT) and ornithine
carbamoyl transferase (OTC); increased
triglyceride levels; decreased blood
glucose levels; and alterations in the
histopathology of the testes, kidneys,
and liver of male beagle dogs (USEPA,
2018c; ICI, Inc., 1988). The UF applied
was 100 (10 for intraspecies variation
and 10 for interspecies extrapolation).
The EPA OPP RfD for acetochlor of 0.02
mg/kg/day, based on the NOAEL of 2
mg/kg/day from the 1-year oral chronic
feeding study in beagle dogs, is
expected to be protective of both
noncancer and cancer effects.
EPA calculated an HRL of 100 mg/L
based on the EPA OPP RfD for noncancer effects for acetochlor of 0.02 mg/
kg/day (USEPA, 2018c) using 2.5 L/day
drinking water ingestion, 80 kg body
weight, and a 20% RSC factor.
(b) Occurrence
EPA has determined that acetochlor
does not occur with a frequency and at
levels of public health concern at PWSs
based on the Agency’s evaluation of
available occurrence information. The
primary occurrence data for acetochlor
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are from the first Unregulated
Contaminant Monitoring Regulation
(UCMR 1) assessment monitoring (AM)
(2001–2003) and the second
Unregulated Contaminant Monitoring
Regulation (UCMR 2) screening survey
(SS) (2008–2010). Acetochlor was not
detected at levels greater than 1⁄2 the
HRL (50 mg/L), the HRL (100 mg/L), or
the MRL (2 mg/L) in any of the 33,778
UCMR 1 assessment monitoring samples
from 3,869 PWSs (USEPA, 2008;
USEPA, 2021a) or in any of the 11,193
UCMR 2 screening survey samples from
1,198 PWSs (USEPA, 2015; USEPA,
2021a).
Findings from the available ambient
water data for acetochlor are consistent
with the results in finished water.
Ambient water data in NAWQA show
that acetochlor was detected in between
13% and 23% of samples from between
3% and 10% of sites. While maximum
values in NAWQA Cycle 2 (2002–2012)
and Cycle 3 (2013–2017) monitoring
exceeded the HRL (215 mg/L in 2004 and
137 mg/L in 2013) (only one sample in
each of those two cycles exceeded the
HRL), 90th percentile levels of
acetochlor remained below 1 mg/L. More
than 10,000 samples were collected in
each cycle. Non-NAWQA NWIS data
(1991–2016), which included limited
finished water data in addition to the
ambient water data, show no detected
concentrations greater than the HRL
(USEPA, 2021a).
(c) Meaningful Opportunity
The Agency has determined that
regulation of acetochlor does not
present a meaningful opportunity for
health risk reduction for persons served
by PWSs based on the estimated
exposed populations, including
sensitive populations. The estimated
population exposed to acetochlor at
levels of public health concern is 0%
based on UCMR 1 finished water data
gathered from 2001 to 2003 and UCMR
2 finished water data gathered from
2008 to 2010. As a result, the Agency
finds that an NPDWR for acetochlor
does not present a meaningful
opportunity for health risk reduction.
(d) Summary of Public Comments on
Acetochlor and Agency Responses
EPA received several comments on
the Agency’s evaluation of acetochlor
under section 1412(b)(1)(A) of SDWA,
all of which were in support of its
preliminary determination not to
regulate acetochlor. EPA agrees with the
comments that are in support of the
negative regulatory determination.
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D. Methyl Bromide
1. Description
Methyl bromide is a halogenated
alkane and occurs as a gas. Methyl
bromide has been used as a fumigant
fungicide applied to soil before
planting, to crops after harvest, to
vehicles and buildings, and for other
specialized purposes. Use of the
chemical in the United States was
phased out in 2005, except for specific
critical use exemptions and quarantine
and pre-shipment exemptions in
accordance with the Montreal Protocol.
Critical use exemptions have included
strawberry cultivation and production
of dry cured pork. Synonyms for methyl
bromide include bromomethane,
monobromomethane, curafume, MethO-Gas, and Brom-O-Sol. Methyl
bromide is expected to have moderate
persistence in water due to its
susceptibility to hydrolysis (USEPA,
2021a).
2. Agency Findings
The Agency is making a
determination not to regulate methyl
bromide with an NPDWR. Methyl
bromide does not occur with a
frequency and at levels of public health
concern. As a result, the Agency finds
that an NPDWR does not present a
meaningful opportunity for health risk
reduction.
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(a) Adverse Health Effects
The Agency finds that methyl
bromide may have adverse effects on the
health of persons. The limited number
of studies investigating the oral toxicity
of methyl bromide indicate that the
route of administration influences the
toxic effects observed (USEPA, 2006c).
The forestomach of rats (forestomachs
are not present in humans) appears to be
the most sensitive target of methyl
bromide when it is administered orally
by gavage (ATSDR, 1992). Acute and
subchronic oral gavage studies in rats
identified stomach lesions (Kaneda et
al., 1998), hyperemia (excess blood)
(Danse et al., 1984), and ulceration
(Boorman et al., 1986; Danse et al.,
1984) of the forestomach. However,
forestomach effects were not observed
in rats and stomach effects were not
observed in dogs that were chronically
exposed to methyl bromide in the diet,
potentially because methyl bromide
degrades to other bromide compounds
in the food (Mertens, 1997). Decreases
in food consumption, body weight, and
body weight gain were noted in the
chronic rat study when methyl bromide
was administered in capsules (Mertens,
1997).
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In a subchronic (13-week) rat study
(Danse et al., 1984), a NOAEL of 1.4 mg/
kg/day (a time weighted average, 5⁄7
days, of the 2 mg/kg/day dose group)
was selected in the EPA IRIS assessment
based on severe hyperplasia of the
stratified squamous epithelium in the
forestomach, in the next highest dose
group of 7.1 mg/kg/day (USEPA, 1989).
In ATSDR’s Toxicological Profile
(ATSDR, 1992), a lower dose of 0.4 mg/
kg/day is selected as the NOAEL
because ‘‘mild focal hyperemia’’ was
observed at the 1.4 mg/kg/day dose
level. It is worth noting that authors of
this study reported neoplastic changes
in the forestomach. However, EPA and
others (USEPA, 1985; Schatzow, 1984)
re-evaluated the histological results,
concluding that the lesions were
hyperplasia and inflammation, not
neoplasms. ATSDR notes that
histological diagnosis of epithelial
carcinomas in the presence of marked
hyperplasia is difficult (Wester and
Kroes 1988; ATSDR 1992). Additionally,
the hyperplasia of the forestomach
observed after 13 weeks of exposure to
bromomethane regressed when
exposure ended (Boorman et al. 1986;
ATSDR 1992).
EPA selected an OPP Human Health
Risk Assessment from 2006 as the basis
for developing the HRL for methyl
bromide (USEPA, 2006c). As described
in the OPP document, the study was of
chronic duration (two years) with four
groups of male rats and four groups of
female rats treated orally via
encapsulated methyl bromide. In the
OPP assessment (USEPA, 2006c),
Mertens (1997) was identified as the
critical study and decreased body
weight, decreased rate of body weight
gain, and decreased food consumption
were the critical effects in rats orally
exposed to methyl bromide (USEPA,
2006c). The NOAEL was 2.2 mg/kg/day
and the LOAEL was 11.1 mg/kg/day.
The RfD derived in the 2006 OPP
Human Health Assessment is 0.022 mg/
kg/day, based on the point of departure
(POD) of 2.2 mg/kg/day (the NOAEL)
and a combined uncertainty factor (UF)
of 100 for interspecies variability (10)
and intraspecies variability (10). No
benchmark dose modeling was
performed.
Neurological effects reported after
inhalation exposures have not been
reported after oral exposures, indicating
that route of exposure may influence the
most sensitive adverse health endpoint
(USEPA, 1988).
Limited data are available regarding
the developmental or reproductive
toxicity of methyl bromide, especially
via the oral route of exposure. ATSDR
(1992) found no information on
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developmental effects in humans with
methyl bromide exposure. An oral
developmental toxicity study of methyl
bromide in rats (doses of 3, 10, or 30
mg/kg/day) and rabbits (doses of 1, 3, or
10 mg/kg/day) found that there were no
treatment-related adverse effects in
fetuses of the treated groups of either
species (Kaneda et al., 1998). ATSDR’s
1992 Toxicological Profile also did not
identify any LOAELs for rats or rabbits
in this study. In rats exposed to 30 mg/
kg/day, there was an increase in fetuses
having 25 presacral vertebrae; however,
ATSDR notes that there were no
significant differences in the number of
litters with this variation and the effect
was not exposure-related (ATSDR,
1992). No significant alterations in
resorptions or fetal deaths, number of
live fetuses, sex ratio, or fetal body
weights were observed in rats and no
alterations in the occurrence of external,
visceral, or skeletal malformations or
variations were observed in the rabbits.
Some inhalation studies reported no
effects on development or reproduction,
but other inhalation studies show
adverse developmental effects. For
example, Hardin et al. (1981) and Sikov
et al. (1980) conducted studies in rats
and rabbits and found no developmental
effects, even when maternal toxicity was
severe (ATSDR, 1992). However,
another inhalation study of rabbits
found increased incidence of
gallbladder agenesis, fused vertebrae,
and decreased fetal body weights in
offspring (Breslin et al., 1990).
Decreased pup weights were noted in a
multigeneration study in rats exposed to
30 ppm (Enloe et al., 1986).
Reproductive effects were noted in
intermediate-duration inhalation studies
in rats and mice (Eustis et al., 1988;
Kato et al., 1986), which indicated that
the testes may undergo degeneration
and atrophy at high exposure levels.
In the OPP HHRA for methyl bromide
(USEPA, 2006c), methyl bromide is
classified as ‘‘not likely to be
carcinogenic to humans’’. In 2007, EPA
published a PPRTV report which stated
that there is ‘‘inadequate information to
assess the carcinogenic potential’’ of
methyl bromide in humans (USEPA,
2007a). The PPRTV assessment agrees
with earlier National Toxicology
Program (NTP) conclusions that the
available data indicate that methyl
bromide can cause genotoxic and/or
mutagenic changes. The PPRTV
assessment states that the results in
studies by Vogel and Nivard (1994) and
Gansewendt et al. (1991) clearly
indicate methyl bromide is distributed
throughout the body and is capable of
methylating DNA in vivo. However, the
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PPRTV assessment also summarizes the
results of several studies in mice and
rats that have not demonstrated
evidence of methyl bromide-induced
carcinogenic changes (USEPA, 2007a;
NTP, 1992; Reuzel et al. 1987; ATSDR,
1992). In 2012, an epidemiology study
was published that concluded there was
a significant monotonic exposuredependent increase in stomach cancer
risk among 7,814 applicators of methyl
bromide (Barry et al., 2012). In OPP’s
Draft HHRA for Methyl Bromide, OPP
reviews all the epidemiological studies
for methyl bromide, including the Barry
et al. (2012) Agricultural Health Study.
OPP concludes that ‘‘based on the
review of these studies, there is
insufficient evidence to suggest a clear
associative or causal relationship
between exposure to methyl bromide
and carcinogenic or non-carcinogenic
health outcomes.’’
According to ATSDR (1992) and the
EPA OPP assessment (USEPA, 2006c),
no studies suggest that a specific
subpopulation may be more susceptible
to methyl bromide, though there is little
information about susceptible lifestages
or subpopulations when exposed via the
oral route. Because the critical effects of
decreased body weight, decreased rate
of body weight gain, and decreased food
consumption in this study are not
specific to a sensitive subpopulation or
life stage, the target population of the
general adult population was selected in
deriving the HRL for regulatory
determination. EPA’s OPP assessment
conducted additional exposure
assessments for lifestages that may
increase exposure to methyl bromide
and concluded that no lifestages have
expected exposure greater than 10% of
the chronic population-adjusted dose
(cPAD), including children.
EPA calculated an HRL of 100 mg/L
(rounded from 140.8 mg/L) based on an
EPA OPP assessment cPAD of 0.022 mg/
kg/day and using 2.5 L/day drinking
water ingestion, 80 kg body weight, and
a 20% RSC factor (USEPA, 2006d;
USEPA, 2011, Table 8–1 and 3–33).
(b) Occurrence
EPA has determined that methyl
bromide does not occur with a
frequency and at levels of public health
concern at PWSs based on the Agency’s
evaluation of available occurrence
information. The primary data
occurrence data for methyl bromide are
the 2013–2015 nationally representative
drinking water monitoring data
generated through EPA’s UCMR 3.
Methyl bromide was not detected in any
of the 36,848 UCMR 3 samples collected
by 4,916 PWSs (serving ∼ 241 million
people) at levels greater than 1⁄2 the HRL
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(50 mg/L) or the HRL (100 mg/L). Methyl
bromide was detected in about 0.3%
samples at or above the MRL (0.2 mg/L)
(USEPA, 2019a; USEPA, 2021a).
Findings from the available ambient
water data for methyl bromide are
consistent with the results in finished
water. Ambient water data in NAWQA
show that methyl bromide was detected
in fewer than 1% of samples from fewer
than 2% of sites. No detections were
greater than the HRL in any of the three
cycles. The median concentration
among detections were 0.5 mg/L and 0.8
mg/L in Cycle 1 and Cycle 3,
respectively. There were no detections
in Cycle 2. The results of the NWIS
analysis show that methyl bromide was
detected in approximately 0.1% of
samples at approximately 0.1% of sites.
The median concentration among
detections was 0.6 mg/L.
(c) Meaningful Opportunity
The Agency has determined that
regulation of methyl bromide does not
present a meaningful opportunity for
health risk reduction for persons served
by PWSs based on the estimated
exposed populations, including
sensitive populations. UCMR 3 findings
indicate that the estimated population
exposed to methyl bromide at levels of
public health concern is 0%. As a result,
the Agency finds that an NPDWR for
methyl bromide does not present a
meaningful opportunity for health risk
reduction.
(d) Summary of Public Comments on
Methyl Bromide and Agency Responses
EPA received several comments on
the Agency’s evaluation of methyl
bromide under section 1412(b)(1)(A) of
SDWA, including several comments in
support of its preliminary determination
not to regulate methyl bromide. Three
anonymous members of the public
opposed the negative determination of
methyl bromide because of their
perceptions about its production and
use. Specifically, commenters appear to
be seeking to prohibit the production
and use of methyl bromide.
EPA agrees with the comments that
are in support of the negative regulatory
determination. Regarding comments
that oppose the negative determination
because of methyl bromide’s production
and use; the production, importation,
use, and disposal of specific chemicals
are not regulated by SDWA and
therefore are not relevant to this
determination. As discussed above,
methyl bromide was not found above 1⁄2
the HRL in drinking water in any UCMR
3 samples. Furthermore, commenters
did not provide any data or other
information that suggested that their
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concerns had impacts on the occurrence
of methyl bromide in drinking water or
discuss any other methyl bromide issues
that specifically related to drinkingwater. Hence, commenters concerns are
not addressable by this decision not to
regulate methyl bromide under SDWA.
E. Metolachlor
1. Description
Metolachlor is a chloroacetanilide
pesticide that is used as an herbicide for
weed control. Initially registered in
1976 for use on turf, metolachlor has
more recently been used on corn,
cotton, peanuts, pod crops, potatoes,
safflower, sorghum, soybeans, stone
fruits, tree nuts, non-bearing citrus, nonbearing grapes, cabbage, certain
peppers, buffalograss, guymon
bermudagrass for seed production,
nurseries, hedgerows/fencerows, and
landscape plantings. Synonyms for
metolachlor include dual and bicep
(USEPA, 2021a). Metolachlor is
expected to have moderate to high
persistence in water due to its
biodegradation half-life (USEPA, 2021a).
2. Agency Findings
The Agency is making a
determination not to regulate
metolachlor with an NPDWR.
Metolachlor does not occur with a
frequency and at levels of public health
concern. As a result, the Agency finds
that an NPDWR does not present a
meaningful opportunity for health risk
reduction.
(a) Adverse Health Effects
The Agency finds that metolachlor
may have adverse effects on the health
of persons. The existing toxicological
database includes studies evaluating
both metolachlor and S-metolachlor.
When combined with the toxicology
database for metolachlor, the toxicology
database for S-metolachlor is considered
complete for risk assessment purposes
(USEPA, 2018d). In subchronic
(metolachlor and S-metolachlor)
(USEPA, 1995b; USEPA, 2018d) and
chronic (metolachlor) (Hazelette, 1989;
Tisdel, 1983; Page, 1981; USEPA,
2018d) toxicity studies in dogs and rats,
decreased body weight was the most
commonly observed effect. Chronic
exposure to metolachlor in rats also
resulted in increased liver weight and
microscopic liver lesions in both sexes
(USEPA, 2018d). No systemic toxicity
was observed in rabbits when
metolachlor was administered dermally,
though dermal irritation was observed at
lower doses (USEPA, 2018d). Portal of
entry effects (e.g., hyperplasia of the
squamous epithelium and mucous cell)
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occurred in the nasal cavity at lower
doses in a 28-day inhalation study in
rats (USEPA, 2018d). Systemic toxicity
effects were not observed in this study.
Immunotoxicity effects were not
observed in mice exposed to Smetolachlor (USEPA, 2018d).
While some prenatal developmental
studies in the rat and rabbit with both
metolachlor and S-metolachlor revealed
no evidence of a qualitative or
quantitative susceptibility in fetal
animals, decreased pup body weight
was observed in a two-generation study
(Page, 1981, USEPA, 2018d). Though
there was no evidence of maternal
toxicity, decreased pup body weight in
the F1 and F2 litters was observed,
indicating developmental toxicity (Page,
1981; USEPA, 1990b). Therefore,
sensitive lifestages to consider include
infants, as well as pregnant women and
their fetus, and lactating women.
Although treatment with metolachlor
did not result in an increase in
treatment-related tumors in male rats or
in mice (both sexes), metolachlor caused
an increase in liver tumors in female
rats (USEPA, 2018d). There was no
evidence of mutagenic or cytogenetic
effects in vivo or in vitro (USEPA,
2018d). In 1994 (USEPA, 1995b), EPA
classified metolachlor as a Group C
possible human carcinogen, in
accordance with the 1986 Guidelines for
Carcinogen Risk Assessment (USEPA,
1986). In 2017 (USEPA, 2018d), EPA reassessed the cancer classification for
metolachlor in accordance with EPA’s
final Guidelines for Carcinogen Risk
Assessment (USEPA, 2005), and
reclassified metolachlor/S-metolachlor
as ‘‘Not Likely to be Carcinogenic to
Humans’’ at doses that do not induce
cellular proliferation in the liver. This
classification was based on convincing
evidence of a constitutive androstane
receptor (CAR)-mediated mitogenic
MOA for liver tumors in female rats that
supports a nonlinear approach when
deriving a guideline that is protective
for the tumor endpoint (USEPA, 2018d).
A recent OPP HHRA identified a twogeneration reproduction study in rats as
the critical study (USEPA, 2018d). OPP
proposed an RfD for metolachlor of 0.26
mg/kg/day, derived from a NOAEL of 26
mg/kg/day for decreased pup body
weight in the F1 and F2 litters. A
combined UF of 100 was used based on
interspecies extrapolation (10),
intraspecies variation (10), and an FQPA
Safety Factor of 1. This RfD is
considered protective of carcinogenic
effects as well as effects observed in
chronic toxicity studies (USEPA,
2018d). The decreased F1 and F2 litter
pup body weights in the absence of
maternal toxicity were considered
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indicative of increased susceptibility to
the pups. Therefore, a rate of 0.15 L/kg/
day was selected from the Exposure
Factors Handbook (USEPA, 2011) to
represent the consumers-only estimate
of DWI based on the combined direct
and indirect community water ingestion
at the 90th percentile for bottle fed
infants. This estimate is more protective
than the estimate for pregnant women
(0.033 L/kg/day) or lactating women
(0.054 L/kg/day). DWI and BW
parameters are further outlined in the
Exposure Factors Handbook (USEPA,
2011).
EPA OW calculated an HRL for
metolachlor of 300 mg/L (rounded from
0.347 mg/L). The HRL was derived from
the oral RfD of 0.26 mg/kg/day for bottle
fed infants ingesting 0.15 L/kg/day
water, with the application of a 20%
RSC.
(b) Occurrence
EPA has determined that metolachlor
does not occur with a frequency and at
levels of public health concern at PWSs
based on the Agency’s evaluation of
available occurrence information. The
primary occurrence data for metolachlor
are from the UCMR 2 screening survey.
A total of 11,192 metolachlor samples
were collected from 1,198 systems. Of
these systems, three (0.25%) had
metolachlor detections (1 mg/L) and
none of the detections were greater than
1⁄2 the HRL (150 mg/L) or the HRL (300
mg/L) (USEPA, 2015; USEPA, 2021a).
Supplementary sources of finished
water occurrence data from UCM Round
2 indicate that the occurrence of
metolachlor in PWSs is likely to be low
to non-existent (USEPA, 2021a).
Metolachlor occurrence data for ambient
water from NAWQA and NWIS are
consistent with those for finished water
(USEPA, 2021a).
(c) Meaningful Opportunity
The Agency has determined that
regulation of metolachlor does not
present a meaningful opportunity for
health risk reduction for persons served
by PWSs based on the estimated
exposed populations, including
sensitive populations. UCMR 2 findings
indicate that the estimated population
exposed to metolachlor at levels of
public health concern is 0%. As a result,
the Agency finds that an NPDWR for
metolachlor does not present a
meaningful opportunity for health risk
reduction.
(d) Summary of Public Comments on
Metolachlor and Agency Responses
EPA received several comments on
the Agency’s evaluation of metolachlor
under section 1412(b)(1)(A) of SDWA,
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all of which were in support of its
preliminary determination not to
regulate metolachlor. EPA agrees with
the comments that are in support of the
negative regulatory determination.
F. Nitrobenzene
1. Description
Nitrobenzene is a synthetic aromatic
nitro compound and occurs as an oily,
flammable liquid. It is commonly used
as a chemical intermediate in the
production of aniline and drugs such as
acetaminophen. Nitrobenzene is also
used in the manufacturing of paints,
shoe polishes, floor polishes, metal
polishes, aniline dyes, and pesticides.
Nitrobenzene is expected to have a
moderate to high likelihood of
partitioning to water and moderate
persistence in water (USEPA, 2021a).
2. Agency Findings
The Agency is making a
determination not to regulate
nitrobenzene with an NPDWR.
Nitrobenzene does not occur with a
frequency and at levels of public health
concern. As a result, the Agency finds
that an NPDWR does not present a
meaningful opportunity for health risk
reduction.
(a) Adverse Health Effects
The Agency finds that nitrobenzene
may have adverse effects on the health
of persons. NTP (1983) conducted a 90day oral gavage study of nitrobenzene in
F344 rats and B6C3F1 mice. The rats
were more sensitive to the effects of
nitrobenzene exposure than the mice,
and changes in absolute and relative
organ weights, hematologic parameters,
splenic congestion, and histopathologic
lesions in the spleen, testis, and brain
were reported. Based on statistically
significant changes in absolute and
relative organ weights, splenic
congestion, and increases in reticulocyte
count and methemoglobin (metHb)
concentration, a LOAEL of 9.38 mg/kg/
day was identified for the subchronic
oral effects of nitrobenzene in F344
male rats (USEPA, 2009). This was the
lowest dose studied, so a NOAEL was
not identified. The mice were treated
with higher doses and were generally
more resistant to nitrobenzene toxicity,
the toxic endpoints were similar in both
species.
The testis, epididymis, and
seminiferous tubules of the male
reproductive system are targets of
nitrobenzene toxicity in rodents. In
male rats (F344/N and CD) and mice
(B6C3F1), nitrobenzene exposure via the
oral and inhalation routes results in
histopathologic lesions of the testis and
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seminiferous tubules, testicular atrophy,
a large decrease in sperm count, and a
reduction of sperm motility and/or
viability, which contribute to a loss of
fertility (NTP, 1983; Bond et al., 1981;
Koida et al., 1995; Matsuura et al., 1995;
Kawashima et al., 1995). These data
suggest that nitrobenzene is a malespecific reproductive toxicant (USEPA,
2009).
Under the Guidelines for Carcinogen
Risk Assessment (USEPA, 2005),
nitrobenzene is classified as ‘‘likely to
be carcinogenic to humans’’ by any
route of exposure (USEPA, 2009). A
two-year inhalation cancer bioassay in
rats and mice (Cattley et al., 1994; CIIT,
1993) reported an increase in several
tumor types in both species. However,
the lack of available data, including a
physiologically based biokinetic or
model that might predict the impact of
the intestinal metabolism on serum
levels of nitrobenzene and its
metabolites following oral exposures,
precluded EPA’s IRIS program from
deriving an oral CSF (USEPA, 2009).
Additionally, a metabolite of
nitrobenzene, aniline, is classified as a
probable human carcinogen (B2)
(USEPA, 1988).
Nitrobenzene has been shown to be
non-genotoxic in most studies and was
classified as, at most, weakly genotoxic
in the 2009 USEPA IRIS assessment
(ATSDR, 1990; USEPA, 2009).
Of the available animal studies with
oral exposure to nitrobenzene, the 90day gavage study conducted by NTP
(1983) is the most relevant study for
deriving an RfD for nitrobenzene. This
study used the longest exposure
duration and multiple dose levels.
Benchmark dose software (BMDS)
(version 1.4.1c; USEPA, 2007b) was
applied to estimate candidate PODs for
deriving an RfD for nitrobenzene. Data
for splenic congestion and increases in
reticulocyte count and metHb
concentration were modeled. The POD
derived from the male rat increased
metHb data with a benchmark response
(BMR) of 1 standard deviation (SD) was
selected as the basis of the RfD (see
USEPA, 2009 for additional detail).
Therefore, the benchmark dose level
(BMDL) used as the POD is a BMDL1SD
of 1.8 mg/kg/day.
In deriving the RfD, EPA’s IRIS
program applied a composite UF of
1,000 to account for interspecies
extrapolation (10), intraspecies variation
(10), subchronic-to-chronic study
extrapolation (3), and database
deficiency (3) (USEPA, 2009). Thus, the
RfD calculated in the 2009 IRIS
assessment is 0.002 mg/kg/day. The
overall confidence in the RfD was
medium because the critical effect is
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supported by the overall database and is
thought to be protective of reproductive
and immunological effects observed at
higher doses; however, there are no
chronic or multigenerational
reproductive/developmental oral
studies available for nitrobenzene.
Because the critical effect in this study
(increased metHb in the adult rat) is not
specific to a sensitive subpopulation or
lifestage, the general adult population
was selected in deriving the HRL for
regulatory determination.
EPA calculated an HRL for the
noncancer effects of nitrobenzene of 10
mg/L (rounded from 12.8 mg/L), based on
the RfD of 0.002 mg/kg/day, using 2.5 L/
day drinking water ingestion, 80 kg
body weight, and a 20% RSC factor.
all of which were in support of its
preliminary determination not to
regulate nitrobenzene. EPA agrees with
the comments that are in support of the
negative regulatory determination.
(b) Occurrence
EPA has determined that
nitrobenzene does not occur with a
frequency and at levels of public health
concern at PWSs based on the Agency’s
evaluation of available occurrence
information. The primary occurrence
data for nitrobenzene are nationally
representative finished water
monitoring data generated through
EPA’s UCMR 1 a.m. (2001–2003). UCMR
1 collected 33,576 finished water
samples from 3,861 PWSs (serving ∼226
million people) for nitrobenzene and it
was detected in only a small number of
those samples (0.01%) above the HRL
(10 mg/L), which is the same as the MRL
(10 mg/L).
Findings from the available ambient
water data for nitrobenzene are
consistent with the results in finished
water. Ambient water data in NAWQA
show that nitrobenzene was not
detected in any of the samples collected
under any of the three monitoring
cycles, while NWIS data show that
nitrobenzene was detected in
approximately 1% of samples.
2. Agency Findings
(c) Meaningful Opportunity
The Agency has determined that
regulation of nitrobenzene does not
present a meaningful opportunity for
health risk reduction for persons served
by PWSs based on the estimated
exposed populations, including
sensitive populations. UCMR 1 data
indicate that the estimated population
exposed to nitrobenzene above the HRL
is 0.1%. The Agency finds that an
NPDWR for nitrobenzene does not
present a meaningful opportunity for
health risk reduction.
(d) Summary of Public Comments on
Nitrobenzene and Agency Responses
EPA received several comments on
the Agency’s evaluation of nitrobenzene
under section 1412(b)(1)(A) of SDWA,
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G. RDX
1. Description
RDX is a nitrated triazine and is an
explosive. The name RDX is an
abbreviation of ‘‘Royal Demolition
eXplosive.’’ The formal chemical name
is hexahydro-1,3,5-trinitro-1,3,5triazine. RDX is expected to have a
moderate to high likelihood of
partitioning to water and low to
moderate persistence in water (USEPA,
2021a).
The Agency is making a
determination not to regulate RDX with
an NPDWR. RDX does not occur with a
frequency and at levels of public health
concern. As a result, the Agency finds
that an NPDWR does not present a
meaningful opportunity for health risk
reduction.
(a) Adverse Health Effects
The Agency finds that RDX may have
adverse effects on the health of persons.
Available health effects assessments
include an IRIS toxicological review
(USEPA, 2018e), and older assessments
including an ATSDR toxicological
profile (ATSDR, 2012) and an OW
assessment published in the 1992
Drinking Water Health Advisory:
Munitions (USEPA, 1992). The EPA
IRIS assessment (2018e) presents an RfD
of 0.004 mg/kg/day based on
convulsions as the critical effect
observed in a subchronic study in F–344
rats by Crouse et al. (2006). The POD for
the derivation was a BMDL0.05 of 1.3
mg/kg/day derived using a
pharmacokinetic model that identified
the human equivalent dose (HED) based
on arterial blood concentrations in the
rats as the dose metric. A 300-fold UF
(3 for extrapolation from animals to
humans, 10 for interindividual
differences in human susceptibility, and
10 for uncertainty in the database) was
applied in determination of the RfD.
Additionally, the EPA IRIS
assessment (USEPA, 2018e) classified
data from the Lish et al. (1984) chronic
study in B6C3F1 as providing suggestive
evidence of carcinogenic potential
following EPA (USEPA, 2005)
guidelines. The slope factor was derived
from the lung and liver tumors’ doseresponse in the Lish et al. (1984) study.
The POD for the slope factor was the
BMDL10 allometrically scaled to a HED
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yielding a slope factor of 0.08 per mg/
kg/day.
In mice fed doses of 0 to 35 mg/kg/
day for 24 months in the Lish et al.
(1984) study, there were dosedependent increases in adenomas or
carcinomas of the lungs and liver in
males and females (USEPA, 2018e). The
formulation used contained 3 to 10%
HMX, another munition ingredient. EPA
assessed the toxicity of HMX (USEPA,
1988). No chronic-duration studies were
available to evaluate the carcinogenicity
of HMX (USEPA, 1988). HMX is
classified as Group D, or not classifiable
as to human carcinogenicity (USEPA,
1992; USEPA, 1988). In the Levine et al.
(1983) RDX dietary exposure study with
Fischer 344 rats, a statistically
significant increase in the incidence of
hepatocellular carcinomas was observed
in males but not in females (USEPA,
2018e). Although evidence of
carcinogenicity included dosedependent increases in two
experimental animal species, two sexes,
and two systems (liver and lungs),
evidence supporting carcinogenicity in
addition to the B6C3F1 mouse study
was not robust; this factor contributed to
the suggestive evidence of carcinogenic
potential classification. EPA considered
both the Lish et al. (1984) and Levine et
al. (1983) studies to be suitable for doseresponse analysis because they were
well conducted, using similar study
designs with large numbers of animals
at multiple dose levels (USEPA, 2018e).
EPA (2018e) concluded that insufficient
information was available to evaluate
male reproductive toxicity from
experimental animals exposed to RDX.
In addition, EPA (2018e) concluded that
inadequate information was available to
assess developmental effects from
experimental animals exposed to RDX.
EPA selected the 2018 EPA IRIS
assessment to derive two HRLs for RDX:
The RfD-derived HRL (based on Crouse
et al., 2006) and the oral cancer slope
factor-derived HRL (based on Lish et al.,
1984). EPA has generally derived HRLs
for ‘‘possible’’ or Group C carcinogens
using the RfD approach in past
Regulatory Determinations. However,
for RDX, EPA decided to show both an
RfD-derived and oral-cancer-slopefactor-derived HRL since the mode of
action for liver tumors is unknown and
the 1 × 10¥6 cancer risk level provides
a more health protective HRL to
evaluate the occurrence information.
The RfD-derived HRL for RDX was
calculated using the RfD of 0.004 mg/kg/
day based on a subchronic study in F–
344 rats by Crouse et al. (2006) with
convulsions as the critical effect
(USEPA, 2018e). The point of departure
for the RfD calculation was a human
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equivalent BMDL0.05 of 1.3 mg/kg/day.
The HED was derived using a
pharmacokinetic model based on
arterial blood concentrations in the rats
as the dose metric. A 300-fold
uncertainty factor (3 for extrapolation
from animals to humans, 10 for
interindividual differences in human
susceptibility, and 10 for uncertainty in
the database) was applied in
determination of the RfD. EPA
calculated a RfD-derived HRL of 30 mg/
L (rounded from 25.6 mg/L), for the
noncancer effects of RDX based on the
RfD of 0.004 mg/kg/day, using 2.5 L/day
drinking water ingestion, 80 kg body
weight, and a 20% RSC factor.
The oral-cancer-slope-factor-derived
HRL for RDX was also based on values
presented in the 2018 EPA IRIS
assessment. The slope factor is derived
from the dose-response for lung and
liver tumors in the Lish et al. (1984)
study, with elimination of the data for
the high dose group due to high
mortality. The point of departure for the
slope factor of 0.08 (mg/kg/day)-1 was
the BMDL10 which was allometrically
scaled to a HED. EPA calculated an oral
cancer slope factor-derived HRL of 0.4
mg/L for RDX based on the cancer slope
factor of 0.08 (mg/kg/day)-1, using 2.5
L/day drinking water ingestion, 80 kg
body weight, and a 1 in a million cancer
risk level.
EPA’s (USEPA, 2018e) derivation of
an oral slope factor for cancer is in
accordance with the Guidelines for
Carcinogen Risk Assessment (USEPA,
2005) while RDX is classified as having
‘‘suggestive evidence of carcinogenic
potential.’’ Specifically, the guidelines
state ‘‘when the evidence includes a
well-conducted study, quantitative
analyses may be useful for some
purposes, for example, providing a
sense of the magnitude and uncertainty
of potential risks, ranking potential
hazards, or setting research priorities’’
(USEPA, 2005). The EPA IRIS
assessment concluded that the database
for RDX contains well-conducted
carcinogenicity studies (Lish et al.,
1984; Levine et al., 1983) suitable for
dose response and that the quantitative
analysis may be useful for providing a
sense of the magnitude and uncertainty
of potential carcinogenic risk (USEPA,
2018e). Therefore, EPA felt it was
important to evaluate the occurrence
information against both the RfDderived HRL and the oral cancer slope
factor-derived HRL.
(b) Occurrence
EPA has determined that RDX does
not occur with a frequency and at levels
of public health concern at PWSs based
on the Agency’s evaluation of available
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occurrence information. The primary
data for RDX are nationally
representative drinking water
monitoring data generated through
EPA’s UCMR 2 AM (2008–2010). UCMR
2 collected 32,150 finished water
samples from 4,139 PWSs (serving ∼229
million people) for RDX and it was
detected in only a small number of
those samples (0.01%) at or above the
MRL. The detections occurred in three
large surface water systems; the
maximum detected concentration of
RDX was 1.1 mg/L. The MRL is 1 mg/L,
which is about 2.5 times higher than the
oral cancer slope factor-derived HRL
(0.4 mg/L). The RfD-derived HRL (30 mg/
L) is 30 times higher than the MRL and
75 times higher than the cancer slope
factor-derived HRL.
Findings from the available ambient
water data for RDX in ambient water,
available from NWIS, show that RDX
was detected in approximately 46% of
samples and at approximately 29% of
sites; RDX data are not available from
the NAWQA program.
(c) Meaningful Opportunity
The Agency has determined that
regulation of RDX does not present a
meaningful opportunity for health risk
reduction for persons served by PWSs
based on the estimated exposed
populations, including sensitive
populations. UCMR 2 findings indicate
that the estimated population exposed
to RDX at or above the MRL is 0.04%.
There were no detections greater than
the non-cancer HRL (30 mg/L) or the
one-half the non-cancer HRL (15 mg/L).
Because the MRL of 1 mg/L is higher
than the cancer HRL of 0.4 mg/L, the
population exposed relative to the
cancer HRL and 1⁄2 the cancer HRL is
not presented here. As a result, the
Agency finds that an NPDWR for RDX
does not present a meaningful
opportunity for health risk reduction.
Based on the small number of samples
measured at or marginally above the
MRL, EPA does not believe that there
would be enough occurrence in the
narrow range between the HRL and the
MRL to change the meaningful
opportunity determination.
(d) Summary of Public Comments on
RDX and Agency Responses
EPA received several comments on
the Agency’s evaluation of RDX under
section 1412(b)(1)(A) of SDWA, all of
which were in support of its
preliminary determination not to
regulate RDX. EPA agrees with the
comments that are in support of the
negative regulatory determination.
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Summary of Public Comments on
Strontium, 1,4-Dioxane, and 1,2,3Trichloropropane, and the Agency’s
Responses
H. Strontium
Strontium is an alkaline earth metal.
On October 20, 2014 the Agency
published its preliminary regulatory
determination to regulate strontium and
requested public comment on the
determination and supporting technical
information (USEPA, 2014). Informed
by the public comments received, rather
than making a final determination for
strontium in 2016, EPA delayed the
final determination to consider
additional data, and to decide whether
there is a meaningful opportunity for
health risk reduction by regulating
strontium in drinking water (USEPA,
2016f). Specifically, the publication on
the delayed final determination
mentioned that EPA would evaluate
additional studies on strontium
exposure and health studies related to
strontium exposure. Since 2016, EPA
has worked to identify and evaluate
published studies on health effects
associated with strontium exposure,
sources of exposure to strontium, and
treatment technologies to remove
strontium from drinking water. In its
March 10, 2020 document (USEPA,
2020a), EPA clarified that it is
continuing with its previous 2016
decision (USEPA, 2016f) to delay a final
determination for strontium in order to
further consider additional studies
related to strontium exposure.
The Agency received several
comments in support of a continued
evaluation of strontium and not making
a final determination for strontium in
this action. One commenter requested
that EPA complete its evaluation of
strontium in a more timely manner. EPA
agrees with the comments that are in
support of the continued evaluation
prior to making a final regulatory
determination for strontium. Regarding
making a regulatory determination for
strontium in this rulemaking, EPA notes
that there continues to be a need for
additional information and analyses
before a regulatory determination can be
made for strontium. While EPA
determined in 2014 that strontium may
have adverse effects on the health of
persons including children, the Agency
continues to consider additional data,
consult existing assessments (such as
Health Canada’s Drinking Water
Guideline from 2018), and evaluate
whether there is a meaningful
opportunity for health risk reduction by
regulating strontium in drinking water.
Additionally, EPA understands that
strontium may co-occur with beneficial
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calcium in some drinking water systems
and treatment technologies that remove
strontium may also remove calcium.
The Agency is evaluating the
effectiveness of treatment technologies
under different water conditions,
including calcium concentrations. EPA
intends to make a determination after
these data needs have been resolved as
part of its regulatory determination
process.
I. 1,4-Dioxane
1,4-Dioxane is used as a solvent in
cellulose formulations, resins, oils,
waxes, and other organic substances;
also used in wood pulping, textile
processing, degreasing; in lacquers,
paints, varnishes, and stains; and in
paint and varnish removers.
While the health effects data suggest
that 1,4-dioxane may have an adverse
effect on human health and the
occurrence data indicate that 1,4dioxane is occurring in finished
drinking water above the current HRL in
some systems, EPA has not made a
preliminary determination for 1,4dioxane, as the Agency has not
determined whether 1,4-dioxane occurs
in public water systems with a
frequency and at levels of public health
concern and whether there is a
meaningful opportunity for public
health risk reduction by establishing an
NPDWR for 1,4-dioxane (USEPA,
2020a). The Final Regulatory
Determination 4 Support Document
(USEPA, 2021a) and the Occurrence
Data from the Third Unregulated
Contaminant Monitoring Rule (UCMR 3)
(USEPA, 2019a) present additional
information and analyses supporting the
Agency’s evaluation of 1,4-dioxane.
The Agency received several
comments in support of a continued
evaluation and not making a 1,4dioxane determination at this time. One
commenter provided information
summarizing their belief that 1,4
dioxane has a non-linear mode of
action. Another commenter requested
that EPA complete its evaluation of 1,4dioxane in a more-timely manner. EPA
agrees with the comments that are in
support of the continued evaluation.
Regarding making a regulatory
determination for 1,4-dioxane today,
EPA notes that there is a need for
additional information and analyses
before a regulatory determination can be
made for 1,4-dioxane. Based on UCMR
3 data, EPA derived a national estimate
of less than two baseline cancer cases
per year attributable to 1,4-dioxane in
drinking water (USEPA, 2021a).
However, while the number of baseline
cancer cases is relatively low, other
adverse health effects following
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exposure to 1,4-dioxane may also
contribute to potential risk to public
health, and these analyses under SDWA
have not yet been completed. The
Agency recently completed its new
TSCA risk evaluation for 1,4-dioxane by
the Office of Chemical Safety and
Pollution Prevention (OCSPP) (USEPA,
2020c) and intends to consider it and
the Canadian guideline technical
document, once finalized, (Health
Canada, 2018) and other relevant new
science relevant to drinking water
contamination prior to making a
regulatory determination. This
evaluation may provide clarity as to
whether a new HRL is appropriate for
evaluating the occurrence of 1,4-dioxane
and whether there is a meaningful
opportunity for an NPDWR to reduce
public health risk.
J. 1,2,3-Trichloropropane
1,2,3-Trichloropropane is a man-made
chemical used as an industrial solvent,
cleaning and degreasing agent, and
synthesis intermediate.
While the UCMR 3 data indicated
1,2,3-trichloropropane occurrence was
relatively low at concentrations above
the MRL, the MRL (0.03 mg/L) is more
than 75 times the HRL (0.0004 mg/L) for
1,2,3-trichloropropane. This
discrepancy allows for a broad range of
potential contaminant concentrations
that could be in exceedance of the HRL
but below the MRL. EPA did not make
a preliminary determination for 1,2,3trichloropropane due to these analytical
method-based limitations. The Agency
noted that it needs additional lowerlevel occurrence information prior to
making a preliminary regulatory
determination for 1,2,3trichloropropane. The Final Regulatory
Determination 4 Support Document
(USEPA, 2021a) and the Occurrence
Data from the Third Unregulated
Contaminant Monitoring Rule (UCMR 3)
(USEPA, 2019a) present additional
information and analyses supporting the
Agency’s evaluation of 1,2,3trichloropropane.
The Agency received several
comments in support of a continued
evaluation and not making a 1,2,3trichloropropane determination at this
time. In addition, EPA notes that several
comments requested that EPA find
solutions to the analytical method
limitations and collect additional
monitoring data with an MRL adequate
to support decision-making. EPA agrees
with the comments that are in support
of the continued evaluation. EPA also
agrees that further evaluation of 1,2,3tricholoropropane is warranted when
new methods or other tools are available
to do so.
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V. Next Steps
As required by SDWA, EPA will
initiate the process to propose a NPDWR
for PFOA and PFOS within 24 months
of the publication of this document in
the Federal Register. For this
rulemaking effort, in addition to using
the best available science, the Agency
will seek recommendations from the
EPA Science Advisory Board and
consider public comment on the
proposed rule. Therefore, EPA
anticipates further scientific review of
new science and an opportunity for
additional public input prior to the
promulgation of the regulatory standard
for PFOA and PFOS. Additionally, the
Agency will continue to collect and
review additional state and other
occurrence information during the
development of the proposed NPDWR
for PFOA and PFOS. The Agency will
not be taking any further regulatory
action under SDWA for the six negative
determinations at this time.
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VI. References
American Association for the Advancement
of Science (AAAS). 2020. Per- and
Polyfluoroalkyl Substances (PFAS) in
Drinking Water. Available on the
internet at: https://www.aaas.org/
programs/epi-center/pfas.
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Hexahydro-1,3,5-trinitro-1,3,5-triazine
(RDX). EPA 635–R–18–211Fa. Available
on the internet at: https://cfpub.epa.gov/
ncea/iris/iris_documents/documents/
toxreviews/0313tr.pdf.
USEPA. 2019a. Occurrence Data from the
Third Unregulated Contaminant
Monitoring Rule (UCMR 3). EPA 815–R–
19–007.
USEPA. 2019b. EPA’s Per- and
Polyfluoroalkyl Substances Action Plan.
EPA 823–R–18–004.
USEPA. 2020a. Announcement of
Preliminary Regulatory Determinations
for Contaminants on the Fourth Drinking
Water Contaminant Candidate List.
Federal Register 85 FR 14098, March 10,
2020.
E:\FR\FM\03MRR1.SGM
03MRR1
Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations
USEPA. 2020b. Drinking Water Treatability
Database. https://iaspub.epa.gov/tdb/
pages/general/home.do. Last updated
March 2020.
USEPA. 2020c. Final Risk Evaluations for
1,4-Dioxane. EPA Document # EPA–740–
R1–8007. December 2020. https://
www.epa.gov/assessing-and-managingchemicals-under-tsca/final-riskevaluation-14-dioxane#riskevaluation.
USEPA. 2021a. Final Regulatory
Determination 4 Support Document.
EPA 815–R–21–001.
USEPA. 2021b. Responses to Public
Comments on Preliminary Regulatory
Determinations for Contaminants on the
Fourth Drinking Water Contaminant
Candidate List. EPA 815–R–21–002.
Virgo, D.M. and A. Broadmeadow. 1988. SC–
5676: Combined Oncogenicity and
Toxicity Study in Dietary Administration
to CD Rats for 104 Weeks. Life Science
Research Ltd., Suffolk, England. Study
No. 88/SUC017/0348. March 18, 1988.
Unpublished report (as cited in USEPA,
2006b).
Vogel, E.W. and M.J.M. Nivard. 1994. The
subtlety of alkylating agents in reactions
with biological macromolecules. Mutat.
Res. 305: 13–32 (as cited in USEPA,
2007a).
Wester, P.W. and R. Kroes, 1988.
Forestomach carcinogens: pathology and
relevance to man. Toxicologic Pathology
16(2): 165–71 (as cited in ATSDR, 1992).
Signing Statement
This document of the Environmental
Protection Agency was signed on
January 15, 2021, by Andrew Wheeler,
Administrator, pursuant to the statutory
requirements of the Safe Drinking Water
Act, Section 1412(b). That document
with the original signature and date is
maintained by EPA. For administrative
purposes only, and in compliance with
requirements of the Office of the Federal
Register, the undersigned EPA Official
re-signs the document for publication,
as an official document of the
Environmental Protection Agency. This
administrative process in no way alters
the legal effect of this document upon
publication in the Federal Register.
Jane Nishida,
Acting Administrator.
[FR Doc. 2021–04184 Filed 3–2–21; 8:45 am]
jbell on DSKJLSW7X2PROD with RULES
BILLING CODE 6560–50–P
VerDate Sep<11>2014
16:13 Mar 02, 2021
Jkt 253001
DEPARTMENT OF COMMERCE
National Oceanic and Atmospheric
Administration
50 CFR Part 635
[Docket No. 180117042–8884–02; RTID
0648–XA714]
Atlantic Highly Migratory Species;
Atlantic Bluefin Tuna Fisheries
National Marine Fisheries
Service (NMFS), National Oceanic and
Atmospheric Administration (NOAA),
Commerce.
ACTION: Temporary rule; closure of the
General category January fishery for
2021.
AGENCY:
NMFS closes the Atlantic
bluefin tuna (BFT) General category
fishery for the January subquota period.
The intent of this closure is to prevent
overharvest of the adjusted January
subquota.
SUMMARY:
Effective 11:30 p.m., local time,
February 27, 2021, through May 31,
2021.
DATES:
FOR FURTHER INFORMATION CONTACT:
Sarah McLaughlin, sarah.mclaughlin@
noaa.gov, 978–281–9260, Nicholas
Velseboer, nicholas.velseboer@
noaa.gov, 978–675–2168, or Larry Redd,
Jr., larry.redd@noaa.gov, 301–427–8503.
SUPPLEMENTARY INFORMATION:
Regulations implemented under the
authority of the Atlantic Tunas
Convention Act (ATCA; 16 U.S.C. 971 et
seq.) and the Magnuson-Stevens Fishery
Conservation and Management Act
(Magnuson-Stevens Act; 16 U.S.C. 1801
et seq.) governing the harvest of BFT by
persons and vessels subject to U.S.
jurisdiction are found at 50 CFR part
635. Section 635.27 subdivides the U.S.
BFT quota recommended by the
International Commission for the
Conservation of Atlantic Tunas (ICCAT)
among the various domestic fishing
categories, per the allocations
established in the 2006 Consolidated
Atlantic Highly Migratory Species
Fishery Management Plan (2006
Consolidated HMS FMP) (71 FR 58058,
October 2, 2006) and amendments, and
in accordance with implementing
regulations.
Under § 635.28(a)(1), NMFS files a
closure notice with the Office of the
Federal Register for publication when a
BFT quota (or subquota) is reached or is
projected to be reached. Retaining,
possessing, or landing BFT under that
quota category is prohibited on and after
the effective date and time of a closure
notice for that category, for the
remainder of the fishing year, until the
PO 00000
Frm 00035
Fmt 4700
Sfmt 4700
12291
opening of the subsequent quota period
or until such date as specified.
The base quota for the General
category is 555.7 mt. See § 635.27(a).
Each of the General category time
periods (January, June through August,
September, October through November,
and December) is allocated a subquota
or portion of the annual General
category quota. Although it is called the
‘‘January’’ subquota, the regulations
allow the General category fishery under
this quota to continue until the
subquota is reached or March 31,
whichever comes first. The baseline
subquotas for each time period are as
follows: 29.5 mt for January; 277.9 mt
for June through August; 147.3 mt for
September; 72.2 mt for October through
November; and 28.9 mt for December.
Any unused General category quota
rolls forward from one time period to
the next and is available for use in
subsequent time periods within the
fishing year. Effective January 1, 2021,
NMFS transferred 19.5 mt of the 28.9mt General category quota allocated for
the December 2021 period to the
January 2021 period, resulting in an
adjusted subquota of 49 mt for the
January period and a subquota of 9.4 mt
for the December 2021 period (85 FR
83832, December 23, 2020). Effective
February 8, 2021, NMFS transferred an
additional 26 mt from the Reserve
category to the General category, in the
same notice as NMFS made the annual
reallocation of Purse Seine category
quota to the Reserve category, resulting
in an adjusted subquota of 75 mt for the
General category 2021 January subquota
period and 168 mt for the Reserve
category (86 FR 8717, February 9, 2021).
Closure of the January 2021 General
Category Fishery
Based on the best available General
category BFT Landings information (i.e.,
57.7 mt landed as of February 25, 2021),
as well as average catch rates and
anticipated fishing conditions, NMFS
projects that the adjusted General
category January 2021 subquota of 75 mt
will be reached shortly, and that the
General category fishery should be
closed. Therefore, retaining, possessing,
or landing large medium or giant BFT
by persons aboard vessels permitted in
the Atlantic Tunas General category and
the Atlantic HMS Charter/Headboat
category (while fishing commercially)
must cease at 11:30 p.m. local time on
February 27, 2021. The General category
will reopen automatically on June 1,
2021, for the June through August 2021
subquota period. This action applies to
those vessels permitted in the General
category, as well as to those HMS
Charter/Headboat permitted vessels
E:\FR\FM\03MRR1.SGM
03MRR1
Agencies
[Federal Register Volume 86, Number 40 (Wednesday, March 3, 2021)]
[Rules and Regulations]
[Pages 12272-12291]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2021-04184]
-----------------------------------------------------------------------
ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 141
[EPA-HQ-OW-2019-0583; FRL-10019-70-OW]
RIN 2040-AF93
Announcement of Final Regulatory Determinations for Contaminants
on the Fourth Drinking Water Contaminant Candidate List
AGENCY: Environmental Protection Agency (EPA).
ACTION: Regulatory determinations.
-----------------------------------------------------------------------
SUMMARY: The U.S. Environmental Protection Agency (EPA or Agency) is
announcing final regulatory determinations for eight of the 109
contaminants listed on the Fourth Contaminant Candidate List.
Specifically, the Agency is making final determinations to regulate
perfluorooctanesulfonic acid (PFOS) and perfluorooctanoic acid (PFOA)
and to not regulate 1,1-dichloroethane, acetochlor, methyl bromide
(bromomethane), metolachlor, nitrobenzene, and RDX. The Safe Drinking
Water Act (SDWA), as amended in 1996, requires EPA to make regulatory
determinations every five years on at least five unregulated
contaminants. A regulatory determination is a decision about whether or
not to begin the process to propose and promulgate a national primary
drinking water regulation for an unregulated contaminant.
DATES: For purposes of judicial review, the determinations not to
regulate in this document are issued as of March 3, 2021.
FOR FURTHER INFORMATION CONTACT: Richard Weisman, Standards and Risk
Management Division, Office of Ground Water and Drinking Water, Office
of Water (Mail Code 4607M), Environmental Protection Agency, 1200
Pennsylvania Ave. NW, Washington, DC 20460; telephone number: (202)
564-2822; email address: [email protected].
SUPPLEMENTARY INFORMATION:
I. General Information
A. Does this action apply to me?
These final regulatory determinations will not impose any
requirements on anyone. Instead, this action notifies interested
parties of EPA's final regulatory determinations for eight unregulated
contaminants and provides a summary of the major comments received on
the March 10, 2020, preliminary determinations (USEPA, 2020a).
B. How can I get copies of this document and other related information?
Docket: EPA has established a docket for this action under Docket
ID No. EPA-HQ-OW-2019-0583. Publicly available docket materials are
available either electronically at https://www.regulations.gov or in
hard copy at the Water Docket, EPA/DC, EPA West, Room 3334, 1301
Constitution Ave. NW, Washington, DC. The telephone number for the
Public Reading Room is (202) 566-1744, and the telephone number for the
Water Docket is (202) 566-2426.
Electronic Access: You may access this Federal Register document
electronically from the Government Printing Office under the ``Federal
Register'' listings at https://www.gpo.gov/fdsys/browse/collection.action?collectionCode=FR.
Table of Contents
I. General Information
A. Does this action apply to me?
B. How can I get copies of this document and other related
information?
II. Purpose and Background
A. What is the purpose of this action?
B. What are the statutory requirements for the Contaminant
Candidate List (CCL) and regulatory determinations?
C. What contaminants did EPA consider for regulation?
III. What process did EPA use to make the regulatory determinations?
A. How EPA Identified and Evaluated Contaminants for the Fourth
Regulatory Determination
B. Consideration of Public Comments
IV. EPA's Findings on Specific Contaminants
A. PFOS and PFOA
1. Description
2. Agency Findings
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on PFOA and PFOS and Agency
Responses
3. Considerations for Additional PFAS
a. Summary of Public Comments on Considerations for Additional
PFAS and Agency Responses
b. Summary of Public Comments on Potential PFAS Monitoring
Approaches and Agency Responses
B. 1,1-Dichloroethane
1. Description
2. Agency Findings
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on 1,1-Dichloroethane and Agency
Responses
C. Acetochlor
1. Description
2. Agency Findings
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on Acetochlor and Agency Responses
D. Methyl Bromide
1. Description
2. Agency Findings
[[Page 12273]]
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on Methyl Bromide and Agency
Responses
E. Metolachlor
1. Description
2. Agency Findings
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on Metolachlor and Agency
Responses
F. Nitrobenzene
1. Description
2. Agency Findings
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on Nitrobenzene and Agency
Responses
G. RDX
1. Description
2. Agency Findings
a. Adverse Health Effects
b. Occurrence
c. Meaningful Opportunity
d. Summary of Public Comments on RDX and Agency Responses
H. Strontium
I. 1,4-Dioxane
J. 1,2,3-Trichloropropane
V. Next Steps
VI. References
II. Purpose and Background
A. What is the purpose of this action?
The purpose of this action is to present a summary of EPA's final
regulatory determinations for eight contaminants listed on the Fourth
Contaminant Candidate List (CCL 4) (USEPA, 2016a). The eight
contaminants are: Perfluorooctanesulfonic acid (PFOS),
perfluorooctanoic acid (PFOA), 1,1-dichloroethane, acetochlor, methyl
bromide (bromomethane), metolachlor, nitrobenzene, and Royal Demolition
eXplosive (RDX). The Agency is making final determinations to regulate
two contaminants (PFOS and PFOA) and to not regulate the remaining six
contaminants (1,1-dichloroethane, acetochlor, methyl bromide
(bromomethane), metolachlor, nitrobenzene, and RDX). The Agency is not
making any determination at this time on any other CCL contaminants,
including strontium, 1,4-dioxane, and 1,2,3-trichloropropane. This
action summarizes the statutory requirements for targeting drinking
water contaminants for regulatory determination, provides an overview
of the contaminants that the Agency considered for regulation, and
describes the approach used to make the final regulatory
determinations. In addition, this action summarizes the public comments
received on the Agency's preliminary determinations announcement and
the Agency's responses to those comments.
B. What are the statutory requirements for the Contaminant Candidate
List (CCL) and regulatory determinations?
Section 1412(b)(1)(B)(i) of SDWA requires EPA to publish the CCL
every five years after public notice and an opportunity to comment. The
CCL is a list of contaminants which are not subject to any proposed or
promulgated National Primary Drinking Water Regulations (NPDWRs) but
are known or anticipated to occur in public water systems (PWSs) and
may require regulation under SDWA. SDWA section 1412(b)(1)(B)(ii)
directs EPA to determine, after public notice and an opportunity to
comment, whether to regulate at least five contaminants from the CCL
every five years.
Under Section 1412(b)(1)(A) of SDWA, EPA makes a determination to
regulate a contaminant in drinking water if the Administrator
determines that:
(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 after considering public comment on a preliminary determination,
the Agency makes a determination to regulate a contaminant, EPA will
initiate the process to propose and promulgate an NPDWR. In that case,
the statutory time frame provides for Agency proposal of a regulation
within 24 months and action on a final regulation within 18 months of
proposal. When proposing and promulgating drinking water regulations,
the Agency must conduct a number of analyses.
C. What contaminants did EPA consider for regulation?
On March 10, 2020, EPA published preliminary regulatory
determinations for eight contaminants on the fourth Contaminant
Candidate List (CCL 4) (85 FR 14098) (USEPA, 2020a). The eight
contaminants are PFOS, PFOA, 1,1-dichloroethane, acetochlor, methyl
bromide, metolachlor, nitrobenzene, and RDX. The Agency is making final
regulatory determinations to regulate two contaminants (i.e., PFOS and
PFOA) and to not regulate six contaminants (i.e., 1,1-dichloroethane,
acetochlor, methyl bromide, metolachlor, nitrobenzene, and RDX).
Information on the eight contaminants with regulatory
determinations can be found in the Final Regulatory Determination 4
Support Document (USEPA, 2021a). More information is available in the
Public Docket at www.regulations.gov (Docket ID No. EPA-HQ-OW-2019-
0583) and also on EPA's Regulatory Determination 4 website at https://www.epa.gov/ccl/regulatory-determination-4.
III. What process did EPA use to make the regulatory determinations?
A. How EPA Identified and Evaluated Contaminants for the Fourth
Regulatory Determination
This section summarizes the process the Agency followed to identify
and evaluate contaminants for the Fourth Regulatory Determination. For
more detailed information on the process and the analyses performed,
please refer to the ``Protocol for the Regulatory Determination 4''
found in Appendix E of the Final Regulatory Determination 4 Support
Document (USEPA, 2021a) and the Federal Register publication for the
preliminary regulatory determinations (USEPA, 2020a).
The CCL 4 identified 109 contaminants that are currently not
subject to any proposed or promulgated national drinking water
regulation, are known or anticipated to occur in public water systems,
and may require regulation under SDWA (USEPA, 2016a). Since some of the
CCL 4 contaminants do not have adequate health and/or occurrence data
to evaluate against the three statutory criteria (see section II.B of
this document), as when EPA evaluated the previous CCLs, the Agency
used a three-phase process to identify which of the contaminants are
candidates for regulatory determinations. Priority was given to
identifying contaminants known to occur or with substantial likelihood
to occur at frequencies and levels of public health concern.
Because the regulatory determination process includes consideration
of human health effects, the Agency's Policy on Evaluating Health Risks
to Children (USEPA, 1995a) reaffirmed by Administrator Wheeler in a
memorandum dated October 11, 2018 to Agency staff (USEPA, 2018a),
applies to this document. The policy requires EPA to consistently and
comprehensively address children's unique vulnerabilities. We have
explicitly considered children's health in the RD 4 process by
reviewing all the available
[[Page 12274]]
children's exposure and health effects information.
The three phases of the Fourth Regulatory Determination process are
(1) the Data Availability Phase, (2) the Data Evaluation Phase and (3)
the Regulatory Determination Assessment Phase. The overall process is
displayed in Exhibit 1.
[GRAPHIC] [TIFF OMITTED] TR03MR21.101
The purpose of the first phase, the Data Availability Phase, is to
screen out contaminants that clearly do not have sufficient data to
support a regulatory determination. The Agency applies criteria to
ensure that any contaminant that potentially has sufficient data to
characterize the health effects and known or likely occurrence in
drinking water will proceed to the Data Evaluation Phase, the second
phase of the regulatory determination process. From the 109 CCL 4
contaminants, the Agency identified 25 CCL 4 contaminants to further
evaluate in the second phase. These are known as the ``short list.''
During the second phase, the Agency evaluates the contaminants on
the short list in greater depth and detail to identify those that have
sufficient data (or are expected to have sufficient data within the
timeframe allotted for the second phase) for EPA to assess the three
statutory criteria. As part of the second phase, the Agency
specifically focuses its efforts on identifying those contaminants or
contaminant groups that are occurring or have substantial likelihood to
occur at levels and frequencies of public health concern, based on the
best available peer reviewed data. If, during the first or second
phase, the Agency finds that sufficient data are not available or not
likely to be available to evaluate the three statutory criteria, then
the contaminant is not considered a candidate for making a regulatory
determination.
If sufficient data are available for a contaminant to characterize
the potential health effects and known or likely occurrence in drinking
water, the contaminant is evaluated against the three statutory
criteria in the Regulatory Determination Assessment Phase, which is the
third phase of the process. Of the 25 contaminants that were evaluated
under Phase 2, 10 were designated for evaluation against the three
statutory criteria in Phase 3.
Of the 10 CCL4 contaminants that were evaluated in Phase 3, the
Agency did not make preliminary regulatory determinations for two
contaminants (1,4-dioxane and 1,2,3-trichloropropane); see Section IV
of this document for discussion about these contaminants. Additionally,
in Section IV of this document, EPA discusses continuing with its
previous 2016 decision to defer a final determination for strontium (a
CCL3 contaminant for which the Agency made a preliminary positive
determination in the third
[[Page 12275]]
regulatory determination (RD 3)) in order to further consider
additional studies related to strontium exposure.
Of the eight remaining CCL 4 contaminants (PFOS, PFOA, 1,1-
dichloroethane, acetochlor, methyl bromide, metolachlor, nitrobenzene,
and RDX) evaluated in Phase 3 against the three statutory criteria,
including an evaluation of level and frequency of occurrence in
drinking water, the size of the population exposed to concentrations of
health concern, and information on sensitive populations and lifestages
\1\ (e.g., pregnant women, infants and children), the Agency made
preliminary regulatory determinations to regulate PFOS and PFOA and to
not regulate the remaining six contaminants. These preliminary
determinations, with their supporting analyses and documentation, were
published in the Federal Register on March 10, 2020, for public comment
(USEPA, 2020a). The public comment period was initially intended to run
through May 11, 2020. In response to stakeholder requests, on April 30,
2020, EPA extended the comment period by 30 days to June 10, 2020.
---------------------------------------------------------------------------
\1\ https://www.epa.gov/children/childhood-lifestages-relating-childrens-environmental-health.
---------------------------------------------------------------------------
B. Consideration of Public Comments
EPA received comments from approximately 11,600 organizations and
individuals on the March 10, 2020, Federal Register document including
12 states (California, Colorado, Connecticut, Indiana, Massachusetts,
Michigan, Missouri, New Hampshire, New Mexico, South Carolina, West
Virginia, and Wisconsin). Comments on specific contaminants, and EPA's
responses, are briefly summarized in the sections below. The Agency
prepared a response-to-comments document for this action (USEPA, 2021b)
that is available in the Public Docket at www.regulations.gov under
Docket ID No. EPA-HQ-OW-2019-0583. The response-to-comments document is
organized in a manner similar to this document and generally contains
more detailed responses to the public comments received than those
found in this document.
IV. EPA's Findings on Specific Contaminants
After considering the public comments, EPA is making final
regulatory determinations to regulate PFOS and PFOA and to not regulate
1,1-dichloroethane, acetochlor, methyl bromide, metolachlor,
nitrobenzene, and RDX.
This document provides a brief description of the Agency findings
on these contaminants. Details on the background, health and occurrence
information, and analyses used to evaluate and make final
determinations for these contaminants can be found in the Final
Regulatory Determination 4 Support Document (USEPA, 2021a) and the
Federal Register publication for the preliminary regulatory
determination (USEPA, 2020a).
For each contaminant, the Agency reviewed the available human and
toxicological data, derived a health reference level (HRL),\2\ analyzed
data on occurrence in drinking water, and estimated the population
likely exposed to concentrations of the contaminant at levels of health
concern in public water systems. The Agency also considered whether
information was available on sensitive populations. The Agency used the
findings to evaluate the contaminants against the three SDWA statutory
criteria. Table 1 gives a summary of the health and occurrence
information for the eight contaminants with final determinations under
RD 4.
---------------------------------------------------------------------------
\2\ An HRL is a health-based concentration against which the
Agency evaluates occurrence data when making decisions about
preliminary regulatory determinations. An HRL is not a final
determination on establishing a protective level of a contaminant in
drinking water for a particular population; it is derived prior to
development of a complete health and exposure assessment and can be
considered a screening value. See Section E.5.1 of the Final
Regulatory Determination 4 Support Document for information about
how HRLs are derived (USEPA, 2021a).
Table 1--Summary of the Health and Occurrence Information and the Final Determinations for the Eight Contaminants Receiving a Final Determination Under
RD 4
--------------------------------------------------------------------------------------------------------------------------------------------------------
Occurrence findings from primary data sources
----------------------------------------------------------------------------------------
Health reference Population
RD 4 contaminant level (HRL), PWSs with at served by PWSs PWSs with at Population Final
[mu]g/L Primary database least 1 with at least 1 least 1 served by PWSs determination
detection >\1/ detection >\1/ detection >HRL with at least 1
2\ HRL 2\ HRL detection >HRL
--------------------------------------------------------------------------------------------------------------------------------------------------------
PFOS......................... 0.07............ UCMR 3 AM....... 95/4,920 (1.93%) 10,427,193/241 M 46/4,920 3,789,831/241 M Regulate.
(4.32%). (0.93%). (1.57%).
PFOA......................... 0.07............ UCMR 3 AM....... 53/4,920 (1.07%) 3,652,995/241 M 13/4,920 490,480/241 M Regulate.
(1.51%). (0.26%). (0.20%).
1,1-Dichloroethane........... 1,000........... UCMR 3 AM....... 0/4,916 (0.00%). 0/241 M (0.00%). 0/4,916 (0.00%) 0/241 M (0.00%) Do not
regulate.
Acetochlor................... 100............. UCMR 1 AM....... 0/3,869 (0.00%)-- 0/226 M (0.00%)-- 0/3,869 0/226 M Do not
UCMR 1. UCMR 1. (0.00%)--UCMR (0.00%)--UCMR regulate.
1. 1.
UCMR 2 SS....... 0/1,198 (0.00%)-- 0/157 M (0.00%)-- 0/1,198 0/157 M
UCMR 2. UCMR 2. (0.00%)--UCMR (0.00%)--UCMR
2. 2.
Methyl Bromide (Bromomethane) 100............. UCMR 3 AM....... 0/4,916 (0.00%). 0/241 M (0.00%). 0/4,916 (0.00%) 0/241 M (0.00%) Do not
regulate.
Metolachlor.................. 300............. UCMR 2 SS....... 0/1,198 (0.00%). 0/157 M (0.00%). 0/1,198 (0.00%) 0/157 M (0.00%) Do not
regulate.
Nitrobenzene................. 10.............. UCMR 1 AM....... 2/3,861 (0.05%). 255,358/226 M 2/3,861 (0.05%) 255,358/226 M Do not
(0.11%). (0.11%). regulate.
RDX.......................... 30 (noncancer).. UCMR 2 AM....... 0/4,139 (0.00%). 0/229 M (0.00%). 0/4,139 (0.00%) 0/229 M (0.00%) Do not
regulate.
0.4 (cancer).... ................ >15 [mu]g/L..... >15 [mu]g/L..... >30 [mu]g/L.... >30 [mu]g/L....
3/4,139 (0.07%). 96,033/229 M 3/4,139 (0.07%) 96,033/229 M
(0.04%). (0.04%).
>0.2 [mu]g/L.... >0.2 [mu]g/L.... >0.4 [mu]g/L... >0.4 [mu]g/L...
--------------------------------------------------------------------------------------------------------------------------------------------------------
[[Page 12276]]
A. PFOS and PFOA
1. Description
Per- and polyfluoroalkyl substances (PFAS) are a class of synthetic
chemicals that have been manufactured and in use since the 1940s (AAAS,
2020; USEPA, 2018b). PFAS are most commonly used to make products
resistant to water, heat, and stains and are consequently found in
industrial and consumer products like clothing, food packaging,
cookware, cosmetics, carpeting, and fire-fighting foam (AAAS, 2020).
PFAS manufacturing and processing facilities, facilities using PFAS in
production of other products, airports, and military installations have
been associated with PFAS releases into the air, soil, and water (USEPA
2016b; USEPA 2016c). People may potentially be exposed to PFAS through
the use of certain consumer products, through occupational exposure,
and/or through consuming contaminated food or contaminated drinking
water (Domingo and Nadal, 2019; Fromme et al. 2009).
Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA)
are part of a subset of PFAS referred to as perfluorinated alkyl acids
(PFAA) and are two of the most widely studied and longest-used PFAS.
Due to their widespread use and persistence in the environment, most
people have been exposed to PFAS, including PFOA and PFOS (USEPA 2016b;
USEPA 2016c). PFOA and PFOS have been detected in up to 98% of serum
samples taken in biomonitoring studies that are representative of the
U.S. general population (CDC, 2019). Following the voluntary phase-out
of PFOA by eight major chemical manufacturers and processors in the
United States under EPA's 2010/2015 PFOA Stewardship Program and
reduced manufacturing of PFOS (last reported in 2002 under Chemical
Data Reporting), serum concentrations have been declining. The National
Health and Nutrition Examination Survey (NHANES) data exhibited that
95th-percentile serum PFOS concentrations have decreased over 75%, from
75.7 [mu]g/L in the 1999-2000 cycle to 18.3 [mu]g/L in the 2015-2016
cycle (CDC, 2019; Jain, 2018; Calafat et al., 2007; Calafat et al.,
2019).
2. Agency Findings
The Agency is making a determination to regulate PFOA and PFOS with
a NPDWR. EPA has determined that PFOA and PFOS may have adverse health
effects; that PFOA and PFOS occur in public water systems with a
frequency and at levels of public health concern; and that, in the sole
judgment of the Administrator, regulation of PFOA and PFOS presents a
meaningful opportunity for health risk reduction for persons served by
public water systems.
(a) Adverse Health Effects
The Agency finds that PFOA and PFOS may have adverse effects on the
health of persons. In 2016, EPA published health assessments (Health
Effects Support Documents or HESDs) for PFOA and PFOS based on the
Agency's evaluation of the peer reviewed science available at that
time. The lifetime Health Advisory (HA) of 0.07 [mu]g/L is used as the
HRL for Regulatory Determination 4 and reflect concentrations of PFOA
and PFOS in drinking water at which adverse health effects are not
anticipated to occur over a lifetime. Studies indicate that exposure to
PFOA and/or PFOS above certain exposure levels may result in adverse
health effects, including developmental effects to fetuses during
pregnancy or to breast-fed infants (e.g., low birth weight, accelerated
puberty, skeletal variations), cancer (e.g., testicular, kidney), liver
effects (e.g., tissue damage), immune effects (e.g., antibody
production and immunity), and other effects (e.g., cholesterol
changes). Both PFOA and PFOS are known to be transmitted to the fetus
via the placenta and to the newborn, infant, and child via breast milk.
Both compounds were also associated with tumors in long-term animal
studies (USEPA, 2016d; USEPA, 2016e; NTP, 2020). For specific details
on the potential for adverse health effects and approaches used to
identify and evaluate information on hazard and dose-response, please
see (USEPA, 2016b; USEPA, 2016c; USEPA, 2016d; USEPA, 2016e).
(b) Occurrence
EPA has determined that PFOA and PFOS occur with a frequency and at
levels of public health concern at PWSs based on the Agency's
evaluation of available occurrence information. In accordance with SDWA
1412(b)(1)(B)(ii)(II), EPA has determined monitoring data from the
third Unregulated Contaminant Monitoring Rule (UCMR 3) are the best
available occurrence information for PFOA and PFOS regulatory
determinations. UCMR 3 monitoring occurred between 2013 and 2015 and
are currently the only nationally representative finished water dataset
for PFOA and PFOS. Under UCMR 3, 36,972 samples from 4,920 PWSs were
analyzed for PFOA and PFOS. The minimum reporting level (MRL) for PFOA
was 0.02 [mu]g/L and the MRL for PFOS was 0.04 [mu]g/L. A total of
1.37% of samples had reported detections (greater than or equal to the
MRL) of at least one of the two compounds. To examine the occurrence of
PFOS and PFOA in aggregate, EPA summed the concentrations detected in
the same sample to calculate a total PFOS/PFOA concentration. EPA notes
that the reference doses (RfDs) for both PFOA and PFOS are based on
similar developmental effects and are numerically identical; when these
two chemicals co-occur at the same time and location in drinking water
sources, EPA has recommended considering the sum of the concentrations
(USEPA, 2016d; USEPA, 2016e) and has done so for this regulatory
determination. The maximum summed concentration of PFOA and PFOS was
7.22 [mu]g/L and the median summed value was 0.05 [mu]g/L. Summed PFOA
and PFOS concentrations exceeded one-half the HRL (0.035 [mu]g/L) at a
minimum of 2.4% of PWSs (115 PWSs) and exceeded the HRL (0.07 [mu]g/L)
at a minimum of 1.3% of PWSs (63 PWSs \3\). Since UCMR 3 monitoring
occurred, certain sites where elevated levels of PFOA and PFOS were
detected may have installed treatment for PFOA and PFOS, may have
chosen to blend water from multiple sources, or may have otherwise
remediated known sources of contamination. Those 63 PWSs serve a total
population of approximately 5.6 million people and are located in 25
states, tribes, or U.S. territories (USEPA, 2019a). Data from more
recent state monitoring (discussed below) demonstrate occurrence in
multiple geographic locations consistent with UCMR 3 monitoring and
support the Agency's final determination that PFOA and PFOS occur with
a frequency and at levels of public health concern in finished drinking
water across the United States. The Final Regulatory Determination 4
Support Document presents a sample-level summary of the results for
PFOA and PFOS individually and includes discussion on state monitoring
efforts as well as uncertainties in occurrence data (USEPA, 2021a).
---------------------------------------------------------------------------
\3\ Sum of PFOA + PFOS results rounded to 2 decimal places in
those cases where a laboratory reported more digits.
---------------------------------------------------------------------------
Consistent with the Agency's commitment in the PFAS Action Plan
(the Agency's first multi-media, multi-program, national research,
management, and risk communication plan to address a challenge like
PFAS) to present information about additional sampling efforts for PFAS
in water systems, the Agency has supplemented its Unregulated
Contaminant Monitoring Regulation (UCMR) data
[[Page 12277]]
with data collected by states who have made their data publicly
available at this time (USEPA, 2019b). A summary of these occurrence
data were presented in the preliminary Regulatory Determination 4
Federal Register document. Subsequent to the preliminary announcement,
based on comments and information received on the proposed
determination, the Agency collected additional data from additional
states. The finished water data available from fifteen states collected
since UCMR 3 monitoring showed that there were at least 29 PWSs where
the summed concentrations of PFOA and PFOS exceeded the EPA HRL. The
Agency notes that some of these data are from targeted sampling efforts
and thus may not be representative of levels found in all PWSs within
the state or represent occurrence in other states. The state data
demonstrate occurrence in multiple geographic locations and support
EPA's finding that PFOA and PFOS occur with a frequency and at levels
of public health concern in drinking water systems across the United
States. The Final Regulatory Determination 4 Support Document presents
a detailed discussion of state PFOA and PFOS occurrence information
(USEPA, 2021a). EPA acknowledges that there may be other states with
occurrence data available and that additional states have or intend to
conduct monitoring of finished drinking water. As such, EPA will
consider any new or additional state data to inform the development of
the proposed NPDWR for PFOA and PFOS.
(c) Meaningful Opportunity
Considering the population exposed to PFOA and PFOS including
sensitive populations and lifestages, the potential adverse human
health impacts of these contaminants, the environmental persistence of
these substances, the persistence in the human body and potential for
bioaccumulation of these substances, the availability of validated
methods to measure and treatment technologies to remove PFOA and PFOS,
the detections that exceeded the HRL and \1/2\ the HRL, and significant
public concerns (particularly those expressed in comments submitted by
state and local government agencies) on the challenges that these
contaminants pose for communities nationwide, the Agency has determined
that regulation of PFOA and PFOS presents a meaningful opportunity for
health risk reduction for persons served by PWSs, including sensitive
populations such as infants, children, and pregnant and nursing women.
PFOA and PFOS are both generated as degradation products of other
perfluorinated compounds (e.g., fluorotelomer alcohols), and due to
their strong carbon-fluorine bonds, are resistant to metabolic and
environmental degradation (USEPA, 2016b; USEPA, 2016c). Due to this
underlying chemical structure, PFOA and PFOS are extremely persistent
in the environment, including resistance to chemical, biological, and
physical degradation processes. While most U.S. manufacturers have
voluntarily phased out production and manufacturing of both PFOS and
PFOA, their environmental persistence and formation as degradation
products from other compounds may still contribute to their release in
the environment. Upon exposure to the human body, there is a potential
for bioaccumulation and toxicity at environmentally relevant
concentrations as studies show it can take years to leave the human
body (NIEHS, 2020; USEPA, 2016b; USEPA, 2016c).
Adverse effects observed following exposures to PFOA and PFOS
include effects in humans on serum lipids, birth weight, and serum
antibodies. Some of the animal studies show common effects on the
liver, neonate development, and responses to immunological challenges.
Both compounds were also associated with tumors in long-term animal
studies (USEPA, 2016d; USEPA, 2016e). In determining that regulation of
PFOA and PFOS presents a meaningful opportunity for health risk
reduction for sensitive populations, EPA noted that both PFOA and PFOS
are associated with developmental toxicity in animals, with reduced
birth weight in humans, and have been shown to be transmitted to the
fetus via the placenta and to the newborn, infant, and child via breast
milk (USEPA, 2016b; USEPA, 2016c).
Drinking water analytical methods are available to measure PFOA,
PFOS, and other PFAS in drinking water. EPA has published validated
drinking water laboratory methods for detecting a total of 29 unique
PFAS in drinking water, including EPA Method 537.1 (18 PFAS) and EPA
Method 533 (25 PFAS).
Available treatment technologies for removing PFAS from drinking
water have been evaluated and reported in the literature (e.g.,
Dickenson and Higgins, 2016). EPA's Drinking Water Treatability
Database (USEPA, 2020b) summarizes available technical literature on
the efficacy of treatment technologies for a range of priority drinking
water contaminants, including PFOA and PFOS. In summary, conventional
treatment (comprised of the unit processes coagulation, flocculation,
clarification, and filtration) is not considered effective for the
removal of PFOA and PFOS. Granular activated carbon (GAC), anion
exchange resins, reverse osmosis and nanofiltration are considered
effective for the removal of PFOA and PFOS.
(d) Summary of Public Comments on PFOA and PFOS and Agency Responses
EPA received many comments on the Agency's evaluation of the first
statutory criterion under section 1412(b)(1)(A) of SDWA. Most
commenters agreed with EPA's finding that PFOA and PFOS may have
adverse effects on the health of persons. Most commenters also state
that there is ``strong evidence'' and ``substantial scientific
evidence'' for EPA's finding of adverse health effects of PFOA and
PFOS. One commenter disagreed with EPA's evaluation of the first
statutory criterion, arguing that the body of scientific evidence does
not show adverse effects from PFAS in humans. EPA also received
numerous comments relating to the Agency's 2016 Lifetime Health
Advisory for PFOA and PFOS, the corresponding HESD and the HRL used to
support the preliminary regulatory determination. Numerous commenters
encouraged EPA to update and ``improve its health reference level'' and
``revise the PFOA and PFOS hazard assessments'' prior to making a final
regulatory determination.
EPA acknowledges commenters' suggestions to consider and evaluate
newer studies; however, EPA disagrees with recommendations to establish
new HRLs prior to a final regulatory determination. Consistent with
SDWA section 1412(b)(3)(A)(i), EPA is using the 2016 PFOA and PFOS
Lifetime Health Advisory as the basis in deriving an HRL which the
Agency has concluded represent the best available peer reviewed
scientific assessment at this time. Based upon the 2016 EPA HESDs for
PFOA and PFOS, and other supporting studies cited in the record, EPA
finds that PFOA and PFOS may have an adverse effect on the health of
persons. Consistent with commenters' recommendations, EPA has initiated
the first steps of a systematic literature review of peer-reviewed
scientific literature for PFOA and PFOS published since 2013 with the
goal of identifying any new studies that may be relevant to human
health assessment. An annotated bibliography of the identified relevant
studies as well as the protocol used to identify the relevant
publications can be found in Appendix D of the Final Regulatory
Determination 4 Support Document (USEPA, 2021a), available in the
docket for this document. Additional analyses of these new
[[Page 12278]]
studies is needed to confirm relevance, extract the data to assess the
weight of evidence, and identify critical studies in order to inform
future decision making.
EPA also received comments on the Agency's evaluation of the second
statutory criterion under section 1412(b)(1)(A) of SDWA. Many
commenters supported EPA's preliminary determination that PFOA and PFOS
meet the second statutory occurrence criterion under SDWA. Several
commenters stated that while they are supportive of using UCMR 3 data
as the basis of nationwide drinking water occurrence for PFOA and PFOS,
solely relying on these monitoring data may be an inaccurate reflection
of PFOA and PFOS exposure. The Agency also received comments and
information on actions taken by a number of states to monitor PFOA,
PFOS, and other PFAS in PWSs, particularly in locations that were not
previously required to conduct UCMR monitoring. Some commenters
suggested that PFOA and PFOS UCMR 3 occurrence information used by EPA
in making the Preliminary Determination for PFOA and PFOS is not
reflective of the actual occurrence of PFOS and PFOS within public
water systems. These commenters stated that UCMR 3 monitoring excludes
small public water systems and was conducted with high minimum
reporting levels. Three commenters did not support EPA's preliminary
determination that PFOA and PFOS meet the second statutory criterion
under SDWA. These commenters expressed concern that the data EPA relied
upon are outdated, are skewed, and overestimate current PFOA and PFOS
occurrence. These commenters suggest that EPA should revise its
occurrence analysis with more recent data prior to making a final
determination.
EPA disagrees with those commenters who assert that UCMR 3 are not
the best available occurrence data. EPA also disagrees that the UCMR 3
excludes small water systems and disagrees that the minimum reporting
levels were too high. The UCMR 3 assured a nationally representative
sample of 800 small drinking water systems and established minimum
reporting levels based upon laboratory performance data that are lower
than the HRLs for PFOA and PFOS. The UCMR 3 data are the best available
information to assess the frequency and level of occurrence of PFOA and
PFOS in the nation's public water systems. After considering the public
comments and additional occurrence data provided by commenters, EPA
continues to find that PFOA and PFOS meet the second statutory
criterion for regulatory determinations under Section 1412(b)(1)(A) of
SDWA that ``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.'' Nonetheless, EPA
agrees with commenters who recommend that the Agency consider other
existing available occurrence data to inform its final regulatory
determination and PFOA and PFOS rulemaking. As discussed previously,
the Final Regulatory Determination 4 Support Document presents a
detailed discussion of state PFOA and PFOS occurrence information that
were analyzed and used to further support the Agency's finding that
PFOA and PFOS occur in public water systems with a frequency and at
levels of public health concern (USEPA, 2021a).
EPA also received many comments on the Agency's evaluation of the
third statutory criterion under section 14121412(b)(1)(A) of SDWA. Many
commenters, including multiple state regulators and organizations
representing states, agree with EPA's evaluation that regulation of
PFOA and PFOS presents a meaningful opportunity for health risk
reduction for persons served by PWSs. These commenters highlight the
extensive amount of work associated with developing their own drinking
water standards for several PFAS compounds. These commenters also noted
the need for a consistent national standard for use in states where a
state-specific standard has not yet been developed. Many commenters
have also noted that although some states have developed or are in the
process of developing their own state-level PFAS drinking water
standards, regulatory standards currently vary across states. These
commenters expressed concern that absence of a national drinking water
standard has resulted in risk communication challenges with the public
and disparities with PFAS exposure. Some commenters noted there are
populations particularly sensitive or vulnerable to the health effects
of PFAS, including newborns, infants and children. One commenter did
not support EPA's evaluation of the third statutory criterion, noting
that in their opinion, the toxicity assessment for PFOA and PFOS and
existing occurrence data do not suggest that establishing drinking
water standards presents a meaningful opportunity for health risk
reduction.
EPA acknowledges commenter concerns regarding sensitive and
vulnerable subpopulations and notes that the Agency has been
particularly mindful that PFOA and PFOS are known to be transmitted to
the fetus via cord blood and to the newborn, infant and child via
breast milk. EPA agrees with commenters that there is a need for
protective drinking water regulations across the United States and that
moving forward with a national-level regulation for PFOA and PFOS would
provide improved national consistency in protecting public health and
may reduce regulatory uncertainty for stakeholders across the country.
The Agency disagrees with the commenter's assertion that PFOA and PFOS
health and occurrence information are insufficient to justify a
drinking water standard, and the Agency finds that there is a
meaningful opportunity for health risk reduction potential based upon
consideration the population exposed to PFOA and PFOS including
sensitive populations and lifestages, such as newborns, infants and
children.
3. Considerations for Additional PFAS
As EPA begins the process to promulgate the NPDWR for PFOA and
PFOS, the Agency recognizes that there is additional information to
consider regarding a broader range of PFAS, including new monitoring
and occurrence data, and ongoing work developing toxicity assessments
by EPA, other federal agencies, state governments, international
organizations, industry groups, and other stakeholders. While the
Agency is not making regulatory determinations for additional PFAS at
this time, the Agency remains committed to filling information gaps,
including those identified in the PFAS Action Plan, by completing peer
reviewed toxicity assessments and collecting nationally representative
occurrence data for additional PFAS to support future regulatory
determinations as part of the UCMR monitoring program (see discussion
below).
EPA committed in the PFAS Action Plan to characterize potential
health impacts and develop more drinking water occurrence data for a
broader set of PFAS (USEPA, 2019b). EPA has followed through on its
commitments and as a result expects to have peer-reviewed health
assessments and national occurrence data for more PFAS becoming
available over the next few years. EPA notes that although SDWA does
not require the Agency to complete regulatory determinations for the
contaminants from the fifth CCL until 2026, because of the significant
progress related to developing new high-quality PFAS information,
combined with the Agency's commitment in the PFAS
[[Page 12279]]
Action Plan to assist states and communities with PFAS contaminated
drinking water, EPA will continue to prioritize regulatory
determinations of additional PFAS in drinking water. The Agency is
committing to making regulatory determinations in advance of the next
SDWA deadline for additional PFAS for which the Agency has a peer
reviewed health assessment, has nationally representative occurrence
data in finished drinking water, and has sufficient information to
determine whether there is a meaningful opportunity for health risk
reduction for persons served by public water systems.
EPA is currently developing scientifically rigorous toxicity
assessments for seven PFAS chemicals. The chemicals currently
undergoing assessment include PFBS, PFBA, PFHxS, PFHxA, PFNA, PFDA, and
HFPO-DA (GenX chemicals), all of which are currently scheduled to be
completed by 2023. These assessments all include public comment
periods, independent scientific external peer review, and a robust
interagency review process. Furthermore, these toxicity assessments
will provide critical health information for PFAS with varying chain
lengths and functional groups. When complete, these assessments will
summarize available scientific information regarding the anticipated
human dose-response relationship for these chemicals, which is a key
information need for informing a variety of Agency decisions.
To inform EPA's understanding of PFAS occurrence in drinking water
as discussed in EPA's PFAS Action Plan (USEPA, 2019b), the Agency is
also leading efforts to gather additional monitoring data for 29 PFAS
contaminants in finished drinking water. EPA recently announced its
proposal for nationwide drinking water monitoring for PFAS under the
next UCMR monitoring cycle (UCMR 5) utilizing Methods 537.1 and 533 to
detect more PFAS chemicals and at lower reporting limits than
previously possible.
EPA is also is generating new PFAS toxicology data for a much
larger set of less-studied PFAS through new approach methods (NAMs) \4\
such as high throughput screening, computational toxicology tools, and
chemical informatics for chemical prioritization, screening, and risk
assessment. EPA will continue research on methods for using these data
to support risk assessments using NAMs such as read-across (i.e., an
effort to predict biological activity based on similarity in chemical
structure) and transcriptomics (i.e., a measure of changes in gene
expression in response to chemical exposure or other external
stressors), and to make inferences about the toxicity of PFAS mixtures
that commonly occur in real world exposures. This research can inform a
more complete understanding of PFAS toxicity for the large set of PFAS
chemicals without conventional toxicity data and can allow
prioritization of actions to potentially address groups of PFAS. For
additional information on the NAMs for PFAS toxicity testing, please
visit: https://www.epa.gov/chemical-research/pfas-chemical-lists-and-tiered-testing-methods-descriptions. These EPA actions, in addition to
other research, may provide useful information for future EPA
evaluations of additional PFAS.
---------------------------------------------------------------------------
\4\ New approach methods (NAMs) refer to any technologies,
methodologies, approaches, or combinations thereof that can be used
to provide information on chemical hazard and potential human
exposure that can avoid or significantly reduce the use of testing
on animals.
---------------------------------------------------------------------------
(a) Summary of Public Comments on Considerations for Additional PFAS
and Agency Responses
EPA requested comment on potential regulatory constructs the Agency
may consider for PFAS chemicals including PFOA and PFOS. EPA
specifically requested input on a regulatory approach to evaluate PFAS
by different grouping approaches.
EPA received multiple comments on how the Agency could consider
additional PFAS for potential future rulemaking. Many commenters
support a class-based approach for regulating PFAS based on one or more
characteristics such as chain length, functional group, treatment
processes, health effects, toxicity, common analytical methods, and/or
shared occurrence with other contaminants within a group. Additionally,
many commenters also urge EPA to make additional regulatory
determinations for PFAS that have a proposed or final drinking water
standard in at least one state; PFAS that have been measured in water
systems through monitoring programs such as UCMR; and/or PFAS for which
EPA or the Agency for Toxic Substances and Disease Registry (ATSDR) has
established a toxicity value. Some commenters suggest that EPA should
make positive regulatory determinations for PFHxS and PFNA as well as
in combination with PFOA, PFOS, and other PFAS such as PFBS. Many
commenters recommend EPA consider various grouping and treatment
technique approaches for PFAS beyond PFOA and PFOS that may not have
sufficient health and occurrence data. Some of these commenters
recommend approaches that consider acute and chronic health effects,
long-term compared to short-term exposures, exposures during sensitive
lifestages, and type of water systems and vulnerable populations such
as vulnerable workers. Many commenters stated that the data may not be
robust enough for each PFAS and therefore support a class-based
approach for regulating PFAS in drinking water. In contrast, two
commenters did not support a class-based approach for regulating PFAS.
In summary, these commenters suggest that regulation without assessing
each chemical's individual traits ``would be contrary to the intent of
SDWA'' and that the Agency should address outstanding data and
knowledge gaps regarding PFAS of concern prior to determining a
regulatory grouping approach.
With respect to comments received on regulatory determinations for
additional PFAS compounds other than PFOA and PFOS, EPA remains
committed to filling information gaps by completing peer reviewed
health assessments where appropriate and collecting nationally
representative occurrence data. As discussed above, in response to
public comments advocating timely regulation of additional PFAS in
drinking water, where sufficient information is available, EPA intends
to make regulatory determinations for additional PFAS prior to the
fifth Regulatory Determination's statutory deadline (2026).
The Agency acknowledges many commenters' support for a class-based
approach for regulating PFAS and appreciates commenter recommendations
regarding potential regulatory constructs. EPA acknowledges commenters'
recommendations to evaluate whether PFAS can be regulated as groups,
and the Agency is developing the science necessary to consider whether
such regulation is necessary and appropriate for PFAS. Regarding
commenters' assertions that regulation without assessing each
chemical's individual traits ``would be contrary to the intent of
SDWA,'' the Agency notes that the Safe Drinking Water Act establishes a
robust scientific and public participation process that guide EPA's
development of regulations for unregulated contaminants that may
present a risk to public health. Regulation by groups is a regulatory
strategy that is already used for certain regulated contaminants like
disinfection byproducts, polychlorinated biphenyls, and radionuclides.
EPA will continue to use best available science and available
[[Page 12280]]
statutory authorities to guide Agency decision making with respect to
how the Agency evaluates and potentially regulates additional PFAS.
(b) Summary of Public Comments on Potential PFAS Monitoring Approaches
and Agency Responses
As part of the proposed preliminary regulatory determination for
PFOA and PFOS, EPA solicited comment on potential monitoring approaches
if the Agency were to finalize a positive regulatory determination for
these contaminants. EPA presented two monitoring approaches in the
Agency's preliminary Regulatory Determination for CCL 4 contaminants.
Under the Standardized Monitoring Framework (SMF) for synthetic organic
chemicals, monitoring schedules are based around the detection levels
of the regulated contaminants, and state primacy agencies can also
issue waivers for monitoring. The Agency also presented an alternative
monitoring approach to allow state primacy agencies to require
monitoring at PWSs where information indicates potential PFAS
contamination, such as proximity to facilities with historical or on-
going uses of PFAS.
Many commenters supported the Agency's goal of reducing potential
monitoring burden for PWSs without compromising public health
protection. While there were differing views among commenters regarding
which monitoring approach is best for PFAS, many urged EPA to keep
evaluating different approaches as the Agency promulgates the NPDWR for
PFOA and PFOS.
The Agency appreciates commenter recommendations on monitoring
approaches. As the Agency promulgates the regulatory standard for PFOA
and PFOS, EPA will continue to work to establish monitoring
requirements in the rule that minimize burden while ensuring public
health protection.
B. 1,1-Dichloroethane
1. Description
1,1-Dichloroethane is a halogenated alkane. It is an industrial
chemical and is used as a solvent and a chemical intermediate. 1,1-
Dichloroethane is expected to have moderate to high persistence in
water (USEPA, 2021a).
2. Agency Findings
The Agency is making a determination not to regulate 1,1-
dichloroethane with an NPDWR. It does not occur with a frequency and at
levels of public health concern. As a result, the Agency finds that an
NPDWR does not present a meaningful opportunity for health risk
reduction.
(a) Adverse Health Effects
The Agency finds that 1,1-dichloroethane may have adverse effects
on the health of persons. Based on a 13-week gavage study in rats
(Muralidhara et al., 2001), the kidney was identified as a sensitive
target for 1,1-dichloroethane, and no-observed-adverse-effect level
(NOAEL) and lowest-observed-adverse-effect level (LOAEL) values of
1,000 and 2,000 mg/kg/day, respectively, were identified based on
increased urinary enzyme markers for renal damage and central nervous
system (CNS) depression (USEPA, 2006a).
The only available reproductive or developmental study with 1,1-
dichloroethane is an inhalation study where pregnant rats were exposed
on days 6 through 15 of gestation (Schwetz et al., 1974). No effects on
the fetuses were noted at 3,800 ppm. Delayed ossification of the
sternum without accompanying malformations was reported at a
concentration of 6,000 ppm.
A cancer assessment for 1,1-dichloroethane is available on IRIS
(USEPA, 1990a). That assessment classifies the chemical, according to
EPA's 1986 Guidelines for Carcinogenic Risk Assessment (USEPA, 1986),
as Group C, a possible human carcinogen. This classification is based
on no human data and limited evidence of carcinogenicity in two animal
species (rats and mice), as shown by increased incidences of
hemangiosarcomas and mammary gland adenocarcinomas in female rats and
hepatocellular carcinomas and benign uterine polyps in mice (NCI,
1978). The data were considered inadequate to support quantitative
assessment. The close structural relationship between 1,1-
dichloroethane and 1,2-dichloroethane, which is classified as a B2
probable human carcinogen and produces tumors at many of the same sites
where marginal tumor increases were observed for 1,1-dichloroethane,
supports the suggestion that the 1,1-isomer could possibly be
carcinogenic to humans. Mixed results in initiation/promotion studies
and genotoxicity assays are consistent with this classification. On the
other hand, the animals from the 1,1-dichloroethane National Cancer
Institute (NCI, 1978) study were housed with animals being exposed to
1,2-dichloroethane providing opportunities for possible co-exposure
impacting the 1,1-dichloroethane results. The following groups of
individuals may have an increased risk from exposure to 1,1-
dichloroethane (NIOSH, 1978; ATSDR, 2015):
Those with chronic respiratory disease,
Those with liver diseases that impact hepatic microsomal
cytochrome P-450 functions,
Individuals with impaired renal function and vulnerable to
kidney stones
Individuals with skin disorders vulnerable to irritation
by solvents like 1,1-dichloroethane,
Those who consume alcohol or use pharmaceuticals (e.g.,
phenobarbital) that alter the activity of cytochrome P-450s.
A provisional chronic RfD was derived from the 13-week gavage study
in rats based on a NOAEL of 1,000 mg/kg/day administered for five days/
week and adjusted to 714.3 mg/kg/day for continuous exposure (an
increase in urinary enzymes was the adverse impact on the kidney). The
chronic oral RfD of 0.2 mg/kg/day was derived by dividing the
normalized NOAEL of 714.3 mg/kg/day in male Sprague-Dawley rats by a
combined UF of 3,000. The combined UF includes factors of 10 for
interspecies extrapolation, 10 for extrapolation from a subchronic
study, 10 for human variability, and 3 for database deficiencies
(including lack of reproductive and developmental toxicity tests by the
oral route). This assessment noted several limitations in the critical
study and database as a whole. Specifically, that the reporting of the
results in the critical study were marginally adequate and that the
database lacks information on reproductive and developmental and
nervous system toxicity.
EPA calculated an HRL for 1,1-dichloroethane of 1,000 [mu]g/L,
based on EPA oral RfD of 0.2 mg/kg/day, using 2.5 L/day drinking water
ingestion, 80 kg body weight and a 20% relative source contribution
(RSC) factor.
(b) Occurrence
EPA has determined that 1,1-dichloroethane does not occur with a
frequency and at levels of public health concern at PWSs based on the
Agency's evaluation of available occurrence information. The primary
occurrence data for 1,1-dichloroethane are the 2013-2015 nationally
representative drinking water monitoring data generated through EPA's
UCMR 3. 1,1-Dichloroethane was not detected in any of the 36,848 UCMR 3
samples collected by 4,916 PWSs (serving ~ 241 million people) at
levels greater than \1/2\ the HRL (500 [mu]g/L) or the HRL (1,000
[mu]g/L). 1,1-Dichloroethane was detected in about 2.3% samples at or
above the MRL (0.03 [mu]g/L) (USEPA, 2019a; USEPA, 2021a).
[[Page 12281]]
Other supplementary sources of finished water occurrence data from
UCM Rounds 1 and 2 indicate that the occurrence of 1,1-dichloroethane
in PWSs is likely to be low to non-existent (USEPA, 2021a). 1,1-
Dichloroethane occurrence data for ambient water from NAWQA and NWIS
are consistent with those for finished water (USEPA, 2021a).
(c) Meaningful Opportunity
The Agency has determined that regulation of 1,1-dichloroethane
does not present a meaningful opportunity for health risk reduction for
persons served by PWSs based on the estimated exposed populations,
including sensitive populations. UCMR 3 findings indicate that the
estimated population exposed to 1,1-dichloroethane at levels of public
health concern is 0%, based on lack of detections at levels greater
than \1/2\ the HRL (500 [mu]g/L) or the HRL (1,000 [mu]g/L). As a
result, the Agency finds that an NPDWR for 1,1-dichloroethane does not
present a meaningful opportunity for health risk reduction.
(d) Summary of Public Comments on 1,1-Dichloroethane and Agency
Responses
EPA received several comments on the Agency's evaluation of 1,1-
dichloroethane under section 1412(b)(1)(A) of SDWA, all of which were
in support of its preliminary determination not to regulate 1,1-
dichloroethane. EPA agrees with the comments that are in support of the
negative regulatory determination.
C. Acetochlor
1. Description
Acetochlor is a chloroacetanilide pesticide that is used as an
herbicide for pre-emergence control of weeds. It is registered for use
on corn crops (field corn and popcorn) and has been approved for use on
cotton as a rotational crop. Synonyms for acetochlor include 2-chloro-
2'-methyl-6-ethyl-N-ethoxymethylacetanilide (USEPA, 2021a). Acetochlor
is expected to have low to moderate persistence in water due to its
biodegradation half-life, as well as susceptibility to photolysis
(USEPA, 2021a).
2. Agency Findings
The Agency is making a determination not to regulate acetochlor
with an NPDWR. Acetochlor does not occur with a frequency and at levels
of public health concern. As a result, the Agency finds that an NPDWR
does not present a meaningful opportunity for health risk reduction.
(a) Adverse Health Effects
The Agency finds that acetochlor may have adverse effects on the
health of persons. Subchronic and chronic oral studies have
demonstrated adverse effects on the liver, thyroid (secondary to the
liver effects), nervous system, kidney, lung, testes, and erythrocytes
in rats and mice (USEPA, 2006b; USEPA, 2018c). There was evidence of
carcinogenicity in studies conducted with acetochlor in rats and mice
and a non-mutagenic mode of action was demonstrated for nasal and
thyroid tumors in rats (USEPA, 2006b). Cancer effects include nasal
tumors and thyroid tumors in rats, lung tumors and histiocytic sarcomas
in mice, and liver tumors in both rats and mice (Ahmed and Seely, 1983;
Ahmed et al., 1983; Amyes, 1989; Hardisty, 1997a; Hardisty, 1997b;
Hardisty, 1997c; Naylor and Ribelin, 1986; Ribelin, 1987; USEPA, 2004b;
USEPA, 2006b; and Virgo and Broadmeadow, 1988). No biologically
sensitive human subpopulations have been identified for acetochlor.
Developmental and reproductive toxicity studies do not indicate
increased susceptibility to acetochlor exposure at early life stages in
test animals (USEPA, 2006b).
The study used to derive the oral RfD is a 1-year oral chronic
feeding study conducted in beagle dogs. This study describes a NOAEL of
2 mg/kg/day, and a LOAEL of 10 mg/kg/day, based on the critical effects
of increased salivation; increased levels of alanine aminotransferase
(ALT) and ornithine carbamoyl transferase (OTC); increased triglyceride
levels; decreased blood glucose levels; and alterations in the
histopathology of the testes, kidneys, and liver of male beagle dogs
(USEPA, 2018c; ICI, Inc., 1988). The UF applied was 100 (10 for
intraspecies variation and 10 for interspecies extrapolation). The EPA
OPP RfD for acetochlor of 0.02 mg/kg/day, based on the NOAEL of 2 mg/
kg/day from the 1-year oral chronic feeding study in beagle dogs, is
expected to be protective of both noncancer and cancer effects.
EPA calculated an HRL of 100 [mu]g/L based on the EPA OPP RfD for
non-cancer effects for acetochlor of 0.02 mg/kg/day (USEPA, 2018c)
using 2.5 L/day drinking water ingestion, 80 kg body weight, and a 20%
RSC factor.
(b) Occurrence
EPA has determined that acetochlor does not occur with a frequency
and at levels of public health concern at PWSs based on the Agency's
evaluation of available occurrence information. The primary occurrence
data for acetochlor are from the first Unregulated Contaminant
Monitoring Regulation (UCMR 1) assessment monitoring (AM) (2001-2003)
and the second Unregulated Contaminant Monitoring Regulation (UCMR 2)
screening survey (SS) (2008-2010). Acetochlor was not detected at
levels greater than \1/2\ the HRL (50 [mu]g/L), the HRL (100 [mu]g/L),
or the MRL (2 [mu]g/L) in any of the 33,778 UCMR 1 assessment
monitoring samples from 3,869 PWSs (USEPA, 2008; USEPA, 2021a) or in
any of the 11,193 UCMR 2 screening survey samples from 1,198 PWSs
(USEPA, 2015; USEPA, 2021a).
Findings from the available ambient water data for acetochlor are
consistent with the results in finished water. Ambient water data in
NAWQA show that acetochlor was detected in between 13% and 23% of
samples from between 3% and 10% of sites. While maximum values in NAWQA
Cycle 2 (2002-2012) and Cycle 3 (2013-2017) monitoring exceeded the HRL
(215 [mu]g/L in 2004 and 137 [mu]g/L in 2013) (only one sample in each
of those two cycles exceeded the HRL), 90th percentile levels of
acetochlor remained below 1 [mu]g/L. More than 10,000 samples were
collected in each cycle. Non-NAWQA NWIS data (1991-2016), which
included limited finished water data in addition to the ambient water
data, show no detected concentrations greater than the HRL (USEPA,
2021a).
(c) Meaningful Opportunity
The Agency has determined that regulation of acetochlor does not
present a meaningful opportunity for health risk reduction for persons
served by PWSs based on the estimated exposed populations, including
sensitive populations. The estimated population exposed to acetochlor
at levels of public health concern is 0% based on UCMR 1 finished water
data gathered from 2001 to 2003 and UCMR 2 finished water data gathered
from 2008 to 2010. As a result, the Agency finds that an NPDWR for
acetochlor does not present a meaningful opportunity for health risk
reduction.
(d) Summary of Public Comments on Acetochlor and Agency Responses
EPA received several comments on the Agency's evaluation of
acetochlor under section 1412(b)(1)(A) of SDWA, all of which were in
support of its preliminary determination not to regulate acetochlor.
EPA agrees with the comments that are in support of the negative
regulatory determination.
[[Page 12282]]
D. Methyl Bromide
1. Description
Methyl bromide is a halogenated alkane and occurs as a gas. Methyl
bromide has been used as a fumigant fungicide applied to soil before
planting, to crops after harvest, to vehicles and buildings, and for
other specialized purposes. Use of the chemical in the United States
was phased out in 2005, except for specific critical use exemptions and
quarantine and pre-shipment exemptions in accordance with the Montreal
Protocol. Critical use exemptions have included strawberry cultivation
and production of dry cured pork. Synonyms for methyl bromide include
bromomethane, monobromomethane, curafume, Meth-O-Gas, and Brom-O-Sol.
Methyl bromide is expected to have moderate persistence in water due to
its susceptibility to hydrolysis (USEPA, 2021a).
2. Agency Findings
The Agency is making a determination not to regulate methyl bromide
with an NPDWR. Methyl bromide does not occur with a frequency and at
levels of public health concern. As a result, the Agency finds that an
NPDWR does not present a meaningful opportunity for health risk
reduction.
(a) Adverse Health Effects
The Agency finds that methyl bromide may have adverse effects on
the health of persons. The limited number of studies investigating the
oral toxicity of methyl bromide indicate that the route of
administration influences the toxic effects observed (USEPA, 2006c).
The forestomach of rats (forestomachs are not present in humans)
appears to be the most sensitive target of methyl bromide when it is
administered orally by gavage (ATSDR, 1992). Acute and subchronic oral
gavage studies in rats identified stomach lesions (Kaneda et al.,
1998), hyperemia (excess blood) (Danse et al., 1984), and ulceration
(Boorman et al., 1986; Danse et al., 1984) of the forestomach. However,
forestomach effects were not observed in rats and stomach effects were
not observed in dogs that were chronically exposed to methyl bromide in
the diet, potentially because methyl bromide degrades to other bromide
compounds in the food (Mertens, 1997). Decreases in food consumption,
body weight, and body weight gain were noted in the chronic rat study
when methyl bromide was administered in capsules (Mertens, 1997).
In a subchronic (13-week) rat study (Danse et al., 1984), a NOAEL
of 1.4 mg/kg/day (a time weighted average, \5/7\ days, of the 2 mg/kg/
day dose group) was selected in the EPA IRIS assessment based on severe
hyperplasia of the stratified squamous epithelium in the forestomach,
in the next highest dose group of 7.1 mg/kg/day (USEPA, 1989). In
ATSDR's Toxicological Profile (ATSDR, 1992), a lower dose of 0.4 mg/kg/
day is selected as the NOAEL because ``mild focal hyperemia'' was
observed at the 1.4 mg/kg/day dose level. It is worth noting that
authors of this study reported neoplastic changes in the forestomach.
However, EPA and others (USEPA, 1985; Schatzow, 1984) re-evaluated the
histological results, concluding that the lesions were hyperplasia and
inflammation, not neoplasms. ATSDR notes that histological diagnosis of
epithelial carcinomas in the presence of marked hyperplasia is
difficult (Wester and Kroes 1988; ATSDR 1992). Additionally, the
hyperplasia of the forestomach observed after 13 weeks of exposure to
bromomethane regressed when exposure ended (Boorman et al. 1986; ATSDR
1992).
EPA selected an OPP Human Health Risk Assessment from 2006 as the
basis for developing the HRL for methyl bromide (USEPA, 2006c). As
described in the OPP document, the study was of chronic duration (two
years) with four groups of male rats and four groups of female rats
treated orally via encapsulated methyl bromide. In the OPP assessment
(USEPA, 2006c), Mertens (1997) was identified as the critical study and
decreased body weight, decreased rate of body weight gain, and
decreased food consumption were the critical effects in rats orally
exposed to methyl bromide (USEPA, 2006c). The NOAEL was 2.2 mg/kg/day
and the LOAEL was 11.1 mg/kg/day. The RfD derived in the 2006 OPP Human
Health Assessment is 0.022 mg/kg/day, based on the point of departure
(POD) of 2.2 mg/kg/day (the NOAEL) and a combined uncertainty factor
(UF) of 100 for interspecies variability (10) and intraspecies
variability (10). No benchmark dose modeling was performed.
Neurological effects reported after inhalation exposures have not
been reported after oral exposures, indicating that route of exposure
may influence the most sensitive adverse health endpoint (USEPA, 1988).
Limited data are available regarding the developmental or
reproductive toxicity of methyl bromide, especially via the oral route
of exposure. ATSDR (1992) found no information on developmental effects
in humans with methyl bromide exposure. An oral developmental toxicity
study of methyl bromide in rats (doses of 3, 10, or 30 mg/kg/day) and
rabbits (doses of 1, 3, or 10 mg/kg/day) found that there were no
treatment-related adverse effects in fetuses of the treated groups of
either species (Kaneda et al., 1998). ATSDR's 1992 Toxicological
Profile also did not identify any LOAELs for rats or rabbits in this
study. In rats exposed to 30 mg/kg/day, there was an increase in
fetuses having 25 presacral vertebrae; however, ATSDR notes that there
were no significant differences in the number of litters with this
variation and the effect was not exposure-related (ATSDR, 1992). No
significant alterations in resorptions or fetal deaths, number of live
fetuses, sex ratio, or fetal body weights were observed in rats and no
alterations in the occurrence of external, visceral, or skeletal
malformations or variations were observed in the rabbits. Some
inhalation studies reported no effects on development or reproduction,
but other inhalation studies show adverse developmental effects. For
example, Hardin et al. (1981) and Sikov et al. (1980) conducted studies
in rats and rabbits and found no developmental effects, even when
maternal toxicity was severe (ATSDR, 1992). However, another inhalation
study of rabbits found increased incidence of gallbladder agenesis,
fused vertebrae, and decreased fetal body weights in offspring (Breslin
et al., 1990). Decreased pup weights were noted in a multigeneration
study in rats exposed to 30 ppm (Enloe et al., 1986). Reproductive
effects were noted in intermediate-duration inhalation studies in rats
and mice (Eustis et al., 1988; Kato et al., 1986), which indicated that
the testes may undergo degeneration and atrophy at high exposure
levels.
In the OPP HHRA for methyl bromide (USEPA, 2006c), methyl bromide
is classified as ``not likely to be carcinogenic to humans''. In 2007,
EPA published a PPRTV report which stated that there is ``inadequate
information to assess the carcinogenic potential'' of methyl bromide in
humans (USEPA, 2007a). The PPRTV assessment agrees with earlier
National Toxicology Program (NTP) conclusions that the available data
indicate that methyl bromide can cause genotoxic and/or mutagenic
changes. The PPRTV assessment states that the results in studies by
Vogel and Nivard (1994) and Gansewendt et al. (1991) clearly indicate
methyl bromide is distributed throughout the body and is capable of
methylating DNA in vivo. However, the
[[Page 12283]]
PPRTV assessment also summarizes the results of several studies in mice
and rats that have not demonstrated evidence of methyl bromide-induced
carcinogenic changes (USEPA, 2007a; NTP, 1992; Reuzel et al. 1987;
ATSDR, 1992). In 2012, an epidemiology study was published that
concluded there was a significant monotonic exposure-dependent increase
in stomach cancer risk among 7,814 applicators of methyl bromide (Barry
et al., 2012). In OPP's Draft HHRA for Methyl Bromide, OPP reviews all
the epidemiological studies for methyl bromide, including the Barry et
al. (2012) Agricultural Health Study. OPP concludes that ``based on the
review of these studies, there is insufficient evidence to suggest a
clear associative or causal relationship between exposure to methyl
bromide and carcinogenic or non-carcinogenic health outcomes.''
According to ATSDR (1992) and the EPA OPP assessment (USEPA,
2006c), no studies suggest that a specific subpopulation may be more
susceptible to methyl bromide, though there is little information about
susceptible lifestages or subpopulations when exposed via the oral
route. Because the critical effects of decreased body weight, decreased
rate of body weight gain, and decreased food consumption in this study
are not specific to a sensitive subpopulation or life stage, the target
population of the general adult population was selected in deriving the
HRL for regulatory determination. EPA's OPP assessment conducted
additional exposure assessments for lifestages that may increase
exposure to methyl bromide and concluded that no lifestages have
expected exposure greater than 10% of the chronic population-adjusted
dose (cPAD), including children.
EPA calculated an HRL of 100 [mu]g/L (rounded from 140.8 [mu]g/L)
based on an EPA OPP assessment cPAD of 0.022 mg/kg/day and using 2.5 L/
day drinking water ingestion, 80 kg body weight, and a 20% RSC factor
(USEPA, 2006d; USEPA, 2011, Table 8-1 and 3-33).
(b) Occurrence
EPA has determined that methyl bromide does not occur with a
frequency and at levels of public health concern at PWSs based on the
Agency's evaluation of available occurrence information. The primary
data occurrence data for methyl bromide are the 2013-2015 nationally
representative drinking water monitoring data generated through EPA's
UCMR 3. Methyl bromide was not detected in any of the 36,848 UCMR 3
samples collected by 4,916 PWSs (serving ~ 241 million people) at
levels greater than \1/2\ the HRL (50 [mu]g/L) or the HRL (100 [mu]g/
L). Methyl bromide was detected in about 0.3% samples at or above the
MRL (0.2 [mu]g/L) (USEPA, 2019a; USEPA, 2021a).
Findings from the available ambient water data for methyl bromide
are consistent with the results in finished water. Ambient water data
in NAWQA show that methyl bromide was detected in fewer than 1% of
samples from fewer than 2% of sites. No detections were greater than
the HRL in any of the three cycles. The median concentration among
detections were 0.5 [mu]g/L and 0.8 [mu]g/L in Cycle 1 and Cycle 3,
respectively. There were no detections in Cycle 2. The results of the
NWIS analysis show that methyl bromide was detected in approximately
0.1% of samples at approximately 0.1% of sites. The median
concentration among detections was 0.6 [mu]g/L.
(c) Meaningful Opportunity
The Agency has determined that regulation of methyl bromide does
not present a meaningful opportunity for health risk reduction for
persons served by PWSs based on the estimated exposed populations,
including sensitive populations. UCMR 3 findings indicate that the
estimated population exposed to methyl bromide at levels of public
health concern is 0%. As a result, the Agency finds that an NPDWR for
methyl bromide does not present a meaningful opportunity for health
risk reduction.
(d) Summary of Public Comments on Methyl Bromide and Agency Responses
EPA received several comments on the Agency's evaluation of methyl
bromide under section 1412(b)(1)(A) of SDWA, including several comments
in support of its preliminary determination not to regulate methyl
bromide. Three anonymous members of the public opposed the negative
determination of methyl bromide because of their perceptions about its
production and use. Specifically, commenters appear to be seeking to
prohibit the production and use of methyl bromide.
EPA agrees with the comments that are in support of the negative
regulatory determination. Regarding comments that oppose the negative
determination because of methyl bromide's production and use; the
production, importation, use, and disposal of specific chemicals are
not regulated by SDWA and therefore are not relevant to this
determination. As discussed above, methyl bromide was not found above
\1/2\ the HRL in drinking water in any UCMR 3 samples. Furthermore,
commenters did not provide any data or other information that suggested
that their concerns had impacts on the occurrence of methyl bromide in
drinking water or discuss any other methyl bromide issues that
specifically related to drinking-water. Hence, commenters concerns are
not addressable by this decision not to regulate methyl bromide under
SDWA.
E. Metolachlor
1. Description
Metolachlor is a chloroacetanilide pesticide that is used as an
herbicide for weed control. Initially registered in 1976 for use on
turf, metolachlor has more recently been used on corn, cotton, peanuts,
pod crops, potatoes, safflower, sorghum, soybeans, stone fruits, tree
nuts, non-bearing citrus, non-bearing grapes, cabbage, certain peppers,
buffalograss, guymon bermudagrass for seed production, nurseries,
hedgerows/fencerows, and landscape plantings. Synonyms for metolachlor
include dual and bicep (USEPA, 2021a). Metolachlor is expected to have
moderate to high persistence in water due to its biodegradation half-
life (USEPA, 2021a).
2. Agency Findings
The Agency is making a determination not to regulate metolachlor
with an NPDWR. Metolachlor does not occur with a frequency and at
levels of public health concern. As a result, the Agency finds that an
NPDWR does not present a meaningful opportunity for health risk
reduction.
(a) Adverse Health Effects
The Agency finds that metolachlor may have adverse effects on the
health of persons. The existing toxicological database includes studies
evaluating both metolachlor and S-metolachlor. When combined with the
toxicology database for metolachlor, the toxicology database for S-
metolachlor is considered complete for risk assessment purposes (USEPA,
2018d). In subchronic (metolachlor and S-metolachlor) (USEPA, 1995b;
USEPA, 2018d) and chronic (metolachlor) (Hazelette, 1989; Tisdel, 1983;
Page, 1981; USEPA, 2018d) toxicity studies in dogs and rats, decreased
body weight was the most commonly observed effect. Chronic exposure to
metolachlor in rats also resulted in increased liver weight and
microscopic liver lesions in both sexes (USEPA, 2018d). No systemic
toxicity was observed in rabbits when metolachlor was administered
dermally, though dermal irritation was observed at lower doses (USEPA,
2018d). Portal of entry effects (e.g., hyperplasia of the squamous
epithelium and mucous cell)
[[Page 12284]]
occurred in the nasal cavity at lower doses in a 28-day inhalation
study in rats (USEPA, 2018d). Systemic toxicity effects were not
observed in this study. Immunotoxicity effects were not observed in
mice exposed to S-metolachlor (USEPA, 2018d).
While some prenatal developmental studies in the rat and rabbit
with both metolachlor and S-metolachlor revealed no evidence of a
qualitative or quantitative susceptibility in fetal animals, decreased
pup body weight was observed in a two-generation study (Page, 1981,
USEPA, 2018d). Though there was no evidence of maternal toxicity,
decreased pup body weight in the F1 and F2 litters was observed,
indicating developmental toxicity (Page, 1981; USEPA, 1990b).
Therefore, sensitive lifestages to consider include infants, as well as
pregnant women and their fetus, and lactating women.
Although treatment with metolachlor did not result in an increase
in treatment-related tumors in male rats or in mice (both sexes),
metolachlor caused an increase in liver tumors in female rats (USEPA,
2018d). There was no evidence of mutagenic or cytogenetic effects in
vivo or in vitro (USEPA, 2018d). In 1994 (USEPA, 1995b), EPA classified
metolachlor as a Group C possible human carcinogen, in accordance with
the 1986 Guidelines for Carcinogen Risk Assessment (USEPA, 1986). In
2017 (USEPA, 2018d), EPA re-assessed the cancer classification for
metolachlor in accordance with EPA's final Guidelines for Carcinogen
Risk Assessment (USEPA, 2005), and reclassified metolachlor/S-
metolachlor as ``Not Likely to be Carcinogenic to Humans'' at doses
that do not induce cellular proliferation in the liver. This
classification was based on convincing evidence of a constitutive
androstane receptor (CAR)-mediated mitogenic MOA for liver tumors in
female rats that supports a nonlinear approach when deriving a
guideline that is protective for the tumor endpoint (USEPA, 2018d).
A recent OPP HHRA identified a two-generation reproduction study in
rats as the critical study (USEPA, 2018d). OPP proposed an RfD for
metolachlor of 0.26 mg/kg/day, derived from a NOAEL of 26 mg/kg/day for
decreased pup body weight in the F1 and F2 litters. A combined UF of
100 was used based on interspecies extrapolation (10), intraspecies
variation (10), and an FQPA Safety Factor of 1. This RfD is considered
protective of carcinogenic effects as well as effects observed in
chronic toxicity studies (USEPA, 2018d). The decreased F1 and F2 litter
pup body weights in the absence of maternal toxicity were considered
indicative of increased susceptibility to the pups. Therefore, a rate
of 0.15 L/kg/day was selected from the Exposure Factors Handbook
(USEPA, 2011) to represent the consumers-only estimate of DWI based on
the combined direct and indirect community water ingestion at the 90th
percentile for bottle fed infants. This estimate is more protective
than the estimate for pregnant women (0.033 L/kg/day) or lactating
women (0.054 L/kg/day). DWI and BW parameters are further outlined in
the Exposure Factors Handbook (USEPA, 2011).
EPA OW calculated an HRL for metolachlor of 300 [mu]g/L (rounded
from 0.347 mg/L). The HRL was derived from the oral RfD of 0.26 mg/kg/
day for bottle fed infants ingesting 0.15 L/kg/day water, with the
application of a 20% RSC.
(b) Occurrence
EPA has determined that metolachlor does not occur with a frequency
and at levels of public health concern at PWSs based on the Agency's
evaluation of available occurrence information. The primary occurrence
data for metolachlor are from the UCMR 2 screening survey. A total of
11,192 metolachlor samples were collected from 1,198 systems. Of these
systems, three (0.25%) had metolachlor detections (1 [mu]g/L) and none
of the detections were greater than \1/2\ the HRL (150 [mu]g/L) or the
HRL (300 [mu]g/L) (USEPA, 2015; USEPA, 2021a).
Supplementary sources of finished water occurrence data from UCM
Round 2 indicate that the occurrence of metolachlor in PWSs is likely
to be low to non-existent (USEPA, 2021a). Metolachlor occurrence data
for ambient water from NAWQA and NWIS are consistent with those for
finished water (USEPA, 2021a).
(c) Meaningful Opportunity
The Agency has determined that regulation of metolachlor does not
present a meaningful opportunity for health risk reduction for persons
served by PWSs based on the estimated exposed populations, including
sensitive populations. UCMR 2 findings indicate that the estimated
population exposed to metolachlor at levels of public health concern is
0%. As a result, the Agency finds that an NPDWR for metolachlor does
not present a meaningful opportunity for health risk reduction.
(d) Summary of Public Comments on Metolachlor and Agency Responses
EPA received several comments on the Agency's evaluation of
metolachlor under section 1412(b)(1)(A) of SDWA, all of which were in
support of its preliminary determination not to regulate metolachlor.
EPA agrees with the comments that are in support of the negative
regulatory determination.
F. Nitrobenzene
1. Description
Nitrobenzene is a synthetic aromatic nitro compound and occurs as
an oily, flammable liquid. It is commonly used as a chemical
intermediate in the production of aniline and drugs such as
acetaminophen. Nitrobenzene is also used in the manufacturing of
paints, shoe polishes, floor polishes, metal polishes, aniline dyes,
and pesticides. Nitrobenzene is expected to have a moderate to high
likelihood of partitioning to water and moderate persistence in water
(USEPA, 2021a).
2. Agency Findings
The Agency is making a determination not to regulate nitrobenzene
with an NPDWR. Nitrobenzene does not occur with a frequency and at
levels of public health concern. As a result, the Agency finds that an
NPDWR does not present a meaningful opportunity for health risk
reduction.
(a) Adverse Health Effects
The Agency finds that nitrobenzene may have adverse effects on the
health of persons. NTP (1983) conducted a 90-day oral gavage study of
nitrobenzene in F344 rats and B6C3F1 mice. The rats were more sensitive
to the effects of nitrobenzene exposure than the mice, and changes in
absolute and relative organ weights, hematologic parameters, splenic
congestion, and histopathologic lesions in the spleen, testis, and
brain were reported. Based on statistically significant changes in
absolute and relative organ weights, splenic congestion, and increases
in reticulocyte count and methemoglobin (metHb) concentration, a LOAEL
of 9.38 mg/kg/day was identified for the subchronic oral effects of
nitrobenzene in F344 male rats (USEPA, 2009). This was the lowest dose
studied, so a NOAEL was not identified. The mice were treated with
higher doses and were generally more resistant to nitrobenzene
toxicity, the toxic endpoints were similar in both species.
The testis, epididymis, and seminiferous tubules of the male
reproductive system are targets of nitrobenzene toxicity in rodents. In
male rats (F344/N and CD) and mice (B6C3F1), nitrobenzene exposure via
the oral and inhalation routes results in histopathologic lesions of
the testis and
[[Page 12285]]
seminiferous tubules, testicular atrophy, a large decrease in sperm
count, and a reduction of sperm motility and/or viability, which
contribute to a loss of fertility (NTP, 1983; Bond et al., 1981; Koida
et al., 1995; Matsuura et al., 1995; Kawashima et al., 1995). These
data suggest that nitrobenzene is a male-specific reproductive toxicant
(USEPA, 2009).
Under the Guidelines for Carcinogen Risk Assessment (USEPA, 2005),
nitrobenzene is classified as ``likely to be carcinogenic to humans''
by any route of exposure (USEPA, 2009). A two-year inhalation cancer
bioassay in rats and mice (Cattley et al., 1994; CIIT, 1993) reported
an increase in several tumor types in both species. However, the lack
of available data, including a physiologically based biokinetic or
model that might predict the impact of the intestinal metabolism on
serum levels of nitrobenzene and its metabolites following oral
exposures, precluded EPA's IRIS program from deriving an oral CSF
(USEPA, 2009). Additionally, a metabolite of nitrobenzene, aniline, is
classified as a probable human carcinogen (B2) (USEPA, 1988).
Nitrobenzene has been shown to be non-genotoxic in most studies and
was classified as, at most, weakly genotoxic in the 2009 USEPA IRIS
assessment (ATSDR, 1990; USEPA, 2009).
Of the available animal studies with oral exposure to nitrobenzene,
the 90-day gavage study conducted by NTP (1983) is the most relevant
study for deriving an RfD for nitrobenzene. This study used the longest
exposure duration and multiple dose levels. Benchmark dose software
(BMDS) (version 1.4.1c; USEPA, 2007b) was applied to estimate candidate
PODs for deriving an RfD for nitrobenzene. Data for splenic congestion
and increases in reticulocyte count and metHb concentration were
modeled. The POD derived from the male rat increased metHb data with a
benchmark response (BMR) of 1 standard deviation (SD) was selected as
the basis of the RfD (see USEPA, 2009 for additional detail).
Therefore, the benchmark dose level (BMDL) used as the POD is a BMDL1SD
of 1.8 mg/kg/day.
In deriving the RfD, EPA's IRIS program applied a composite UF of
1,000 to account for interspecies extrapolation (10), intraspecies
variation (10), subchronic-to-chronic study extrapolation (3), and
database deficiency (3) (USEPA, 2009). Thus, the RfD calculated in the
2009 IRIS assessment is 0.002 mg/kg/day. The overall confidence in the
RfD was medium because the critical effect is supported by the overall
database and is thought to be protective of reproductive and
immunological effects observed at higher doses; however, there are no
chronic or multigenerational reproductive/developmental oral studies
available for nitrobenzene. Because the critical effect in this study
(increased metHb in the adult rat) is not specific to a sensitive
subpopulation or lifestage, the general adult population was selected
in deriving the HRL for regulatory determination.
EPA calculated an HRL for the noncancer effects of nitrobenzene of
10 [mu]g/L (rounded from 12.8 [mu]g/L), based on the RfD of 0.002 mg/
kg/day, using 2.5 L/day drinking water ingestion, 80 kg body weight,
and a 20% RSC factor.
(b) Occurrence
EPA has determined that nitrobenzene does not occur with a
frequency and at levels of public health concern at PWSs based on the
Agency's evaluation of available occurrence information. The primary
occurrence data for nitrobenzene are nationally representative finished
water monitoring data generated through EPA's UCMR 1 a.m. (2001-2003).
UCMR 1 collected 33,576 finished water samples from 3,861 PWSs (serving
~226 million people) for nitrobenzene and it was detected in only a
small number of those samples (0.01%) above the HRL (10 [mu]g/L), which
is the same as the MRL (10 [mu]g/L).
Findings from the available ambient water data for nitrobenzene are
consistent with the results in finished water. Ambient water data in
NAWQA show that nitrobenzene was not detected in any of the samples
collected under any of the three monitoring cycles, while NWIS data
show that nitrobenzene was detected in approximately 1% of samples.
(c) Meaningful Opportunity
The Agency has determined that regulation of nitrobenzene does not
present a meaningful opportunity for health risk reduction for persons
served by PWSs based on the estimated exposed populations, including
sensitive populations. UCMR 1 data indicate that the estimated
population exposed to nitrobenzene above the HRL is 0.1%. The Agency
finds that an NPDWR for nitrobenzene does not present a meaningful
opportunity for health risk reduction.
(d) Summary of Public Comments on Nitrobenzene and Agency Responses
EPA received several comments on the Agency's evaluation of
nitrobenzene under section 1412(b)(1)(A) of SDWA, all of which were in
support of its preliminary determination not to regulate nitrobenzene.
EPA agrees with the comments that are in support of the negative
regulatory determination.
G. RDX
1. Description
RDX is a nitrated triazine and is an explosive. The name RDX is an
abbreviation of ``Royal Demolition eXplosive.'' The formal chemical
name is hexahydro-1,3,5-trinitro-1,3,5-triazine. RDX is expected to
have a moderate to high likelihood of partitioning to water and low to
moderate persistence in water (USEPA, 2021a).
2. Agency Findings
The Agency is making a determination not to regulate RDX with an
NPDWR. RDX does not occur with a frequency and at levels of public
health concern. As a result, the Agency finds that an NPDWR does not
present a meaningful opportunity for health risk reduction.
(a) Adverse Health Effects
The Agency finds that RDX may have adverse effects on the health of
persons. Available health effects assessments include an IRIS
toxicological review (USEPA, 2018e), and older assessments including an
ATSDR toxicological profile (ATSDR, 2012) and an OW assessment
published in the 1992 Drinking Water Health Advisory: Munitions (USEPA,
1992). The EPA IRIS assessment (2018e) presents an RfD of 0.004 mg/kg/
day based on convulsions as the critical effect observed in a
subchronic study in F-344 rats by Crouse et al. (2006). The POD for the
derivation was a BMDL0.05 of 1.3 mg/kg/day derived using a
pharmacokinetic model that identified the human equivalent dose (HED)
based on arterial blood concentrations in the rats as the dose metric.
A 300-fold UF (3 for extrapolation from animals to humans, 10 for
interindividual differences in human susceptibility, and 10 for
uncertainty in the database) was applied in determination of the RfD.
Additionally, the EPA IRIS assessment (USEPA, 2018e) classified
data from the Lish et al. (1984) chronic study in B6C3F1 as providing
suggestive evidence of carcinogenic potential following EPA (USEPA,
2005) guidelines. The slope factor was derived from the lung and liver
tumors' dose-response in the Lish et al. (1984) study. The POD for the
slope factor was the BMDL10 allometrically scaled to a HED
[[Page 12286]]
yielding a slope factor of 0.08 per mg/kg/day.
In mice fed doses of 0 to 35 mg/kg/day for 24 months in the Lish et
al. (1984) study, there were dose-dependent increases in adenomas or
carcinomas of the lungs and liver in males and females (USEPA, 2018e).
The formulation used contained 3 to 10% HMX, another munition
ingredient. EPA assessed the toxicity of HMX (USEPA, 1988). No chronic-
duration studies were available to evaluate the carcinogenicity of HMX
(USEPA, 1988). HMX is classified as Group D, or not classifiable as to
human carcinogenicity (USEPA, 1992; USEPA, 1988). In the Levine et al.
(1983) RDX dietary exposure study with Fischer 344 rats, a
statistically significant increase in the incidence of hepatocellular
carcinomas was observed in males but not in females (USEPA, 2018e).
Although evidence of carcinogenicity included dose-dependent increases
in two experimental animal species, two sexes, and two systems (liver
and lungs), evidence supporting carcinogenicity in addition to the
B6C3F1 mouse study was not robust; this factor contributed to the
suggestive evidence of carcinogenic potential classification. EPA
considered both the Lish et al. (1984) and Levine et al. (1983) studies
to be suitable for dose-response analysis because they were well
conducted, using similar study designs with large numbers of animals at
multiple dose levels (USEPA, 2018e). EPA (2018e) concluded that
insufficient information was available to evaluate male reproductive
toxicity from experimental animals exposed to RDX. In addition, EPA
(2018e) concluded that inadequate information was available to assess
developmental effects from experimental animals exposed to RDX. EPA
selected the 2018 EPA IRIS assessment to derive two HRLs for RDX: The
RfD-derived HRL (based on Crouse et al., 2006) and the oral cancer
slope factor-derived HRL (based on Lish et al., 1984). EPA has
generally derived HRLs for ``possible'' or Group C carcinogens using
the RfD approach in past Regulatory Determinations. However, for RDX,
EPA decided to show both an RfD-derived and oral-cancer-slope-factor-
derived HRL since the mode of action for liver tumors is unknown and
the 1 x 10-6 cancer risk level provides a more health
protective HRL to evaluate the occurrence information.
The RfD-derived HRL for RDX was calculated using the RfD of 0.004
mg/kg/day based on a subchronic study in F-344 rats by Crouse et al.
(2006) with convulsions as the critical effect (USEPA, 2018e). The
point of departure for the RfD calculation was a human equivalent
BMDL0.05 of 1.3 mg/kg/day. The HED was derived using a
pharmacokinetic model based on arterial blood concentrations in the
rats as the dose metric. A 300-fold uncertainty factor (3 for
extrapolation from animals to humans, 10 for interindividual
differences in human susceptibility, and 10 for uncertainty in the
database) was applied in determination of the RfD. EPA calculated a
RfD-derived HRL of 30 [mu]g/L (rounded from 25.6 [mu]g/L), for the
noncancer effects of RDX based on the RfD of 0.004 mg/kg/day, using 2.5
L/day drinking water ingestion, 80 kg body weight, and a 20% RSC
factor.
The oral-cancer-slope-factor-derived HRL for RDX was also based on
values presented in the 2018 EPA IRIS assessment. The slope factor is
derived from the dose-response for lung and liver tumors in the Lish et
al. (1984) study, with elimination of the data for the high dose group
due to high mortality. The point of departure for the slope factor of
0.08 (mg/kg/day)-1 was the BMDL10 which was allometrically
scaled to a HED. EPA calculated an oral cancer slope factor-derived HRL
of 0.4 [mu]g/L for RDX based on the cancer slope factor of 0.08 (mg/kg/
day)-1, using 2.5 L/day drinking water ingestion, 80 kg body weight,
and a 1 in a million cancer risk level.
EPA's (USEPA, 2018e) derivation of an oral slope factor for cancer
is in accordance with the Guidelines for Carcinogen Risk Assessment
(USEPA, 2005) while RDX is classified as having ``suggestive evidence
of carcinogenic potential.'' Specifically, the guidelines state ``when
the evidence includes a well-conducted study, quantitative analyses may
be useful for some purposes, for example, providing a sense of the
magnitude and uncertainty of potential risks, ranking potential
hazards, or setting research priorities'' (USEPA, 2005). The EPA IRIS
assessment concluded that the database for RDX contains well-conducted
carcinogenicity studies (Lish et al., 1984; Levine et al., 1983)
suitable for dose response and that the quantitative analysis may be
useful for providing a sense of the magnitude and uncertainty of
potential carcinogenic risk (USEPA, 2018e). Therefore, EPA felt it was
important to evaluate the occurrence information against both the RfD-
derived HRL and the oral cancer slope factor-derived HRL.
(b) Occurrence
EPA has determined that RDX does not occur with a frequency and at
levels of public health concern at PWSs based on the Agency's
evaluation of available occurrence information. The primary data for
RDX are nationally representative drinking water monitoring data
generated through EPA's UCMR 2 AM (2008-2010). UCMR 2 collected 32,150
finished water samples from 4,139 PWSs (serving ~229 million people)
for RDX and it was detected in only a small number of those samples
(0.01%) at or above the MRL. The detections occurred in three large
surface water systems; the maximum detected concentration of RDX was
1.1 [mu]g/L. The MRL is 1 [mu]g/L, which is about 2.5 times higher than
the oral cancer slope factor-derived HRL (0.4 [mu]g/L). The RfD-derived
HRL (30 [mu]g/L) is 30 times higher than the MRL and 75 times higher
than the cancer slope factor-derived HRL.
Findings from the available ambient water data for RDX in ambient
water, available from NWIS, show that RDX was detected in approximately
46% of samples and at approximately 29% of sites; RDX data are not
available from the NAWQA program.
(c) Meaningful Opportunity
The Agency has determined that regulation of RDX does not present a
meaningful opportunity for health risk reduction for persons served by
PWSs based on the estimated exposed populations, including sensitive
populations. UCMR 2 findings indicate that the estimated population
exposed to RDX at or above the MRL is 0.04%. There were no detections
greater than the non-cancer HRL (30 [mu]g/L) or the one-half the non-
cancer HRL (15 [mu]g/L). Because the MRL of 1 [mu]g/L is higher than
the cancer HRL of 0.4 [mu]g/L, the population exposed relative to the
cancer HRL and \1/2\ the cancer HRL is not presented here. As a result,
the Agency finds that an NPDWR for RDX does not present a meaningful
opportunity for health risk reduction. Based on the small number of
samples measured at or marginally above the MRL, EPA does not believe
that there would be enough occurrence in the narrow range between the
HRL and the MRL to change the meaningful opportunity determination.
(d) Summary of Public Comments on RDX and Agency Responses
EPA received several comments on the Agency's evaluation of RDX
under section 1412(b)(1)(A) of SDWA, all of which were in support of
its preliminary determination not to regulate RDX. EPA agrees with the
comments that are in support of the negative regulatory determination.
[[Page 12287]]
Summary of Public Comments on Strontium, 1,4-Dioxane, and 1,2,3-
Trichloropropane, and the Agency's Responses
H. Strontium
Strontium is an alkaline earth metal. On October 20, 2014 the
Agency published its preliminary regulatory determination to regulate
strontium and requested public comment on the determination and
supporting technical information (USEPA, 2014). Informed by the public
comments received, rather than making a final determination for
strontium in 2016, EPA delayed the final determination to consider
additional data, and to decide whether there is a meaningful
opportunity for health risk reduction by regulating strontium in
drinking water (USEPA, 2016f). Specifically, the publication on the
delayed final determination mentioned that EPA would evaluate
additional studies on strontium exposure and health studies related to
strontium exposure. Since 2016, EPA has worked to identify and evaluate
published studies on health effects associated with strontium exposure,
sources of exposure to strontium, and treatment technologies to remove
strontium from drinking water. In its March 10, 2020 document (USEPA,
2020a), EPA clarified that it is continuing with its previous 2016
decision (USEPA, 2016f) to delay a final determination for strontium in
order to further consider additional studies related to strontium
exposure.
The Agency received several comments in support of a continued
evaluation of strontium and not making a final determination for
strontium in this action. One commenter requested that EPA complete its
evaluation of strontium in a more timely manner. EPA agrees with the
comments that are in support of the continued evaluation prior to
making a final regulatory determination for strontium. Regarding making
a regulatory determination for strontium in this rulemaking, EPA notes
that there continues to be a need for additional information and
analyses before a regulatory determination can be made for strontium.
While EPA determined in 2014 that strontium may have adverse effects on
the health of persons including children, the Agency continues to
consider additional data, consult existing assessments (such as Health
Canada's Drinking Water Guideline from 2018), and evaluate whether
there is a meaningful opportunity for health risk reduction by
regulating strontium in drinking water. Additionally, EPA understands
that strontium may co-occur with beneficial calcium in some drinking
water systems and treatment technologies that remove strontium may also
remove calcium. The Agency is evaluating the effectiveness of treatment
technologies under different water conditions, including calcium
concentrations. EPA intends to make a determination after these data
needs have been resolved as part of its regulatory determination
process.
I. 1,4-Dioxane
1,4-Dioxane is used as a solvent in cellulose formulations, resins,
oils, waxes, and other organic substances; also used in wood pulping,
textile processing, degreasing; in lacquers, paints, varnishes, and
stains; and in paint and varnish removers.
While the health effects data suggest that 1,4-dioxane may have an
adverse effect on human health and the occurrence data indicate that
1,4-dioxane is occurring in finished drinking water above the current
HRL in some systems, EPA has not made a preliminary determination for
1,4-dioxane, as the Agency has not determined whether 1,4-dioxane
occurs in public water systems with a frequency and at levels of public
health concern and whether there is a meaningful opportunity for public
health risk reduction by establishing an NPDWR for 1,4-dioxane (USEPA,
2020a). The Final Regulatory Determination 4 Support Document (USEPA,
2021a) and the Occurrence Data from the Third Unregulated Contaminant
Monitoring Rule (UCMR 3) (USEPA, 2019a) present additional information
and analyses supporting the Agency's evaluation of 1,4-dioxane.
The Agency received several comments in support of a continued
evaluation and not making a 1,4-dioxane determination at this time. One
commenter provided information summarizing their belief that 1,4
dioxane has a non-linear mode of action. Another commenter requested
that EPA complete its evaluation of 1,4-dioxane in a more-timely
manner. EPA agrees with the comments that are in support of the
continued evaluation. Regarding making a regulatory determination for
1,4-dioxane today, EPA notes that there is a need for additional
information and analyses before a regulatory determination can be made
for 1,4-dioxane. Based on UCMR 3 data, EPA derived a national estimate
of less than two baseline cancer cases per year attributable to 1,4-
dioxane in drinking water (USEPA, 2021a). However, while the number of
baseline cancer cases is relatively low, other adverse health effects
following exposure to 1,4-dioxane may also contribute to potential risk
to public health, and these analyses under SDWA have not yet been
completed. The Agency recently completed its new TSCA risk evaluation
for 1,4-dioxane by the Office of Chemical Safety and Pollution
Prevention (OCSPP) (USEPA, 2020c) and intends to consider it and the
Canadian guideline technical document, once finalized, (Health Canada,
2018) and other relevant new science relevant to drinking water
contamination prior to making a regulatory determination. This
evaluation may provide clarity as to whether a new HRL is appropriate
for evaluating the occurrence of 1,4-dioxane and whether there is a
meaningful opportunity for an NPDWR to reduce public health risk.
J. 1,2,3-Trichloropropane
1,2,3-Trichloropropane is a man-made chemical used as an industrial
solvent, cleaning and degreasing agent, and synthesis intermediate.
While the UCMR 3 data indicated 1,2,3-trichloropropane occurrence
was relatively low at concentrations above the MRL, the MRL (0.03
[mu]g/L) is more than 75 times the HRL (0.0004 [mu]g/L) for 1,2,3-
trichloropropane. This discrepancy allows for a broad range of
potential contaminant concentrations that could be in exceedance of the
HRL but below the MRL. EPA did not make a preliminary determination for
1,2,3-trichloropropane due to these analytical method-based
limitations. The Agency noted that it needs additional lower-level
occurrence information prior to making a preliminary regulatory
determination for 1,2,3-trichloropropane. The Final Regulatory
Determination 4 Support Document (USEPA, 2021a) and the Occurrence Data
from the Third Unregulated Contaminant Monitoring Rule (UCMR 3) (USEPA,
2019a) present additional information and analyses supporting the
Agency's evaluation of 1,2,3-trichloropropane.
The Agency received several comments in support of a continued
evaluation and not making a 1,2,3-trichloropropane determination at
this time. In addition, EPA notes that several comments requested that
EPA find solutions to the analytical method limitations and collect
additional monitoring data with an MRL adequate to support decision-
making. EPA agrees with the comments that are in support of the
continued evaluation. EPA also agrees that further evaluation of 1,2,3-
tricholoropropane is warranted when new methods or other tools are
available to do so.
[[Page 12288]]
V. Next Steps
As required by SDWA, EPA will initiate the process to propose a
NPDWR for PFOA and PFOS within 24 months of the publication of this
document in the Federal Register. For this rulemaking effort, in
addition to using the best available science, the Agency will seek
recommendations from the EPA Science Advisory Board and consider public
comment on the proposed rule. Therefore, EPA anticipates further
scientific review of new science and an opportunity for additional
public input prior to the promulgation of the regulatory standard for
PFOA and PFOS. Additionally, the Agency will continue to collect and
review additional state and other occurrence information during the
development of the proposed NPDWR for PFOA and PFOS. The Agency will
not be taking any further regulatory action under SDWA for the six
negative determinations at this time.
VI. References
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Signing Statement
This document of the Environmental Protection Agency was signed on
January 15, 2021, by Andrew Wheeler, Administrator, pursuant to the
statutory requirements of the Safe Drinking Water Act, Section 1412(b).
That document with the original signature and date is maintained by
EPA. For administrative purposes only, and in compliance with
requirements of the Office of the Federal Register, the undersigned EPA
Official re-signs the document for publication, as an official document
of the Environmental Protection Agency. This administrative process in
no way alters the legal effect of this document upon publication in the
Federal Register.
Jane Nishida,
Acting Administrator.
[FR Doc. 2021-04184 Filed 3-2-21; 8:45 am]
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