```

[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]

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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.

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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 http://www.regulations.gov or in 
hard copy at the Water Docket, EPA/DC, EPA West, Room 3334, 1301 
Constitution Ave. NW, Washington, DC. The 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 http://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.
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    \1\ https://www.epa.gov/children/childhood-lifestages-relating-childrens-environmental-health.
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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.
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    \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
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                                                                      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.

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Albino Rats: Study No. 80030. Final rept. (Unpublished study 
received May 24, 1983 under 100-587; prepared by Hazleton Raltech, 
Inc., submitted by Ciba-Geigy Corp., Greensboro, NC; CDL: 250369-A; 
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Rev. February 20, 1985. USEPA, OTS, Washington, DC (as cited in 
ATSDR, 1992).
USEPA. 1986. Guidelines for Carcinogen Risk Assessment. EPA 630-R-
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USEPA. 1988. Chemical Assessment Summary Information for Octahydro- 
1,3,5,7-tetranitro-1,3,5,7-tetrazocine (HMX) on the Integrated Risk 
Information System (IRIS). National Center for Environmental 
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Information System. Carcinogenicity assessment verification date 
March 1, 1989. U.S. Environmental Protection Agency, Office of 
Research and Development, Washington, DC.
USEPA. 1990a. Integrated Risk Information System (IRIS) on 1,1-
Dichloroethane. Available on the internet at: https://cfpub.epa.gov/ncea/iris/iris_documents/documents/subst/0409_summary.pdf.

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USEPA. 1990b. Integrated Risk Information System (IRIS) on 
Metolachlor. Available on the internet at: https://cfpub.epa.gov/ncea/iris/iris_documents/documents/subst/0074_summary.pdf.
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Health Advisory: Munitions. Boca Raton FL: Lewis Publishers, pp 133-
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for Environmental Assessment. September 1, 1993. Available on the 
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20, 1995. Science Policy Council, Washington, DC. Available on the 
internet at: https://www.epa.gov/sites/production/files/2014-05/documents/1995_childrens_health_policy_statement.pdf; Cover memo at: 
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Carcinogenic Potential of Acetochlor (Fourth Evaluation). Final 
Report. Cancer Assessment Review Committee (CARC), Health Effects 
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03-001F. Available on the internet at: https://www.epa.gov/sites/production/files/2013-09/documents/cancer_guidelines_final_3-25-05.pdf.
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of Research and Development. 9-27-2006. Available on the internet 
at: https://hhpprtv.ornl.gov/issue_papers/Dichloroethane11.pdf.
USEPA. 2006b. Acetochlor Revised HED Chapter of the Tolerance 
Reassessment Eligibility Decision (TRED) Document, EPA-HQ-OPPTS, PC 
Code: 121601, DP Barcode: D292336. Available on the internet at: 
https://www.regulations.gov/document?D=EPA-HQ-OPP-2005-0227-0024.
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and Reregistration Eligibility Decision (RED) for Methyl Bromide's 
Commodity Uses. Office of Prevention, Pesticides and Toxic 
Substances. EPA 738-R-06-026. Available on the internet at: https://archive.epa.gov/pesticides/reregistration/web/pdf/methyl_bromide_tred.pdf.
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of Research and Development, U.S. Environmental Protection Agency, 
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modified November 9, 2007).
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Regulatory Determinations for the Second Drinking Water Contaminant 
Candidate List. EPA 815-R-08-012. June 2008.
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in Support of Summary Information on the Integrated Risk Information 
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for Contaminants on the Third Drinking Water Contaminant Candidate 
List. Federal Register 79 FR 62715, October 20, 2014.
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Health Risks to Children. October 11, 2018. Available on the 
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Swiss Chard; (2) Tolerance Translations from Table Beet Tops, Turnip 
Greens, and Radish Tops to Crop Group 2 (Leaves of Root and Tuber 
Vegetables), except Sugar Beets; (3) Tolerance Conversions (i) from 
Crop Subgroup 4B to Crop Subgroup 22B (Leaf Petiole Vegetable), (ii) 
from Crop Subgroup 5A to Crop Group 5-16 (Brassica, Head and Stem 
Vegetable) and (iii) from Crop Subgroup 5B to Crop Subgroup 4-16B 
(Brassica Leafy Greens); and (4) Tolerance Expansions of 
Representative Commodities to (i) Cottonseed Subgroup 20C, and (ii) 
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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]
BILLING CODE 6560-50-P
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