12272 Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 

EPA-APPROVED OHIO NONREGULATORY AND QUASI-REGULATORY PROVISIONS

Title 

Applicable 

geographical or 

non-attainment 

area 

State date EPA approval Comments 

*******

Summary of Criteria Pollutant Attainment Plans 

Ozone (8-Hour, 2015) ............. Cincinnati .......... 7/24/2020 3/3/2021, [INSERT Federal 

Register CITATION].

EPA is approving only the 2014 base year 

emissions inventory and emissions statement elements. 

Ozone (8-Hour, 2015) ............. Cleveland ......... 7/24/2020 3/3/2021, [INSERT Federal 

Register CITATION].

EPA is approving only the 2014 base year 

emissions inventory and emissions statement elements. 

* * * * * * * 

* * * * * 

[FR Doc. 2021–04246 Filed 3–2–21; 8:45 am] 

BILLING CODE 6560–50–P 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 141 

[EPA–HQ–OW–2019–0583; FRL–10019–70– 

OW] 

RIN 2040–AF93 

Announcement of Final Regulatory 

Determinations for Contaminants on 

the Fourth Drinking Water 

Contaminant Candidate List 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Regulatory determinations. 

SUMMARY: The U.S. Environmental 

Protection Agency (EPA or Agency) is 

announcing final regulatory 

determinations for eight of the 109 

contaminants listed on the Fourth 

Contaminant Candidate List. 

Specifically, the Agency is making final 

determinations to regulate 

perfluorooctanesulfonic acid (PFOS) 

and perfluorooctanoic acid (PFOA) and 

to not regulate 1,1-dichloroethane, 

acetochlor, methyl bromide 

(bromomethane), metolachlor, 

nitrobenzene, and RDX. The Safe 

Drinking Water Act (SDWA), as 

amended in 1996, requires EPA to make 

regulatory determinations every five 

years on at least five unregulated 

contaminants. A regulatory 

determination is a decision about 

whether or not to begin the process to 

propose and promulgate a national 

primary drinking water regulation for an 

unregulated contaminant. 

DATES: For purposes of judicial review, 

the determinations not to regulate in 

this document are issued as of March 3, 

2021. 

FOR FURTHER INFORMATION CONTACT: 

Richard Weisman, Standards and Risk 

Management Division, Office of Ground 

Water and Drinking Water, Office of 

Water (Mail Code 4607M), 

Environmental Protection Agency, 1200 

Pennsylvania Ave. NW, Washington, DC 

20460; telephone number: (202) 564– 

2822; email address: weisman.richard@

epa.gov. 

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 


jbell on DSKJLSW7X2PROD with RULES
Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 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 threephase process to identify which of the 

contaminants are candidates for 

regulatory determinations. Priority was 

given to identifying contaminants 

known to occur or with substantial 

likelihood to occur at frequencies and 

levels of public health concern. 

Because the regulatory determination 

process includes consideration of 

human health effects, the Agency’s 

Policy on Evaluating Health Risks to 

Children (USEPA, 1995a) reaffirmed by 

Administrator Wheeler in a 

memorandum dated October 11, 2018 to 

Agency staff (USEPA, 2018a), applies to 

this document. The policy requires EPA 

to consistently and comprehensively 

address children’s unique 

vulnerabilities. We have explicitly 

considered children’s health in the RD 

4 process by reviewing all the available 


jbell on DSKJLSW7X2PROD with RULES
12274 Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 

children’s exposure and health effects 

information. 

The three phases of the Fourth 

Regulatory Determination process are 

(1) the Data Availability Phase, (2) the 

Data Evaluation Phase and (3) the 

Regulatory Determination Assessment 

Phase. The overall process is displayed 

in Exhibit 1. 

The purpose of the first phase, the 

Data Availability Phase, is to screen out 

contaminants that clearly do not have 

sufficient data to support a regulatory 

determination. The Agency applies 

criteria to ensure that any contaminant 

that potentially has sufficient data to 

characterize the health effects and 

known or likely occurrence in drinking 

water will proceed to the Data 

Evaluation Phase, the second phase of 

the regulatory determination process. 

From the 109 CCL 4 contaminants, the 

Agency identified 25 CCL 4 

contaminants to further evaluate in the 

second phase. These are known as the 

‘‘short list.’’ 

During the second phase, the Agency 

evaluates the contaminants on the short 

list in greater depth and detail to 

identify those that have sufficient data 

(or are expected to have sufficient data 

within the timeframe allotted for the 

second phase) for EPA to assess the 

three statutory criteria. As part of the 

second phase, the Agency specifically 

focuses its efforts on identifying those 

contaminants or contaminant groups 

that are occurring or have substantial 

likelihood to occur at levels and 

frequencies of public health concern, 

based on the best available peer 

reviewed data. If, during the first or 

second phase, the Agency finds that 

sufficient data are not available or not 

likely to be available to evaluate the 

three statutory criteria, then the 

contaminant is not considered a 

candidate for making a regulatory 

determination. 

If sufficient data are available for a 

contaminant to characterize the 

potential health effects and known or 

likely occurrence in drinking water, the 

contaminant is evaluated against the 

three statutory criteria in the Regulatory 

Determination Assessment Phase, 

which is the third phase of the process. 

Of the 25 contaminants that were 

evaluated under Phase 2, 10 were 

designated for evaluation against the 

three statutory criteria in Phase 3. 

Of the 10 CCL4 contaminants that 

were evaluated in Phase 3, the Agency 

did not make preliminary regulatory 

determinations for two contaminants 

(1,4-dioxane and 1,2,3- 

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 


jbell on DSKJLSW7X2PROD with RULESER03MR21.101</GPH>
Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 12275 

1https://www.epa.gov/children/childhoodlifestages-relating-childrens-environmental-health. 

2An 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). 

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. 

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. 

TABLE 1—SUMMARY OF THE HEALTH AND OCCURRENCE INFORMATION AND THE FINAL DETERMINATIONS FOR THE EIGHT

CONTAMINANTS RECEIVING A FINAL DETERMINATION UNDER RD 4 

RD 4 contaminant Health reference 

level (HRL), μg/L 

Occurrence findings from primary data sources 

Final 

determination Primary database 

PWSs with at 

least 1 detection 

>1⁄2 HRL 

Population served 

by PWSs with at 

least 1 detection 

>1⁄2 HRL 

PWSs with at 

least 1 detection 

>HRL 

Population served 

by PWSs with at 

least 1 detection 

>HRL 

PFOS .................... 0.07 ..................... UCMR 3 AM ........ 95/4,920 (1.93%) 10,427,193/241 M 

(4.32%).

46/4,920 (0.93%) 3,789,831/241 M 

(1.57%).

Regulate. 

PFOA .................... 0.07 ..................... UCMR 3 AM ........ 53/4,920 (1.07%) 3,652,995/241 M 

(1.51%).

13/4,920 (0.26%) 490,480/241 M 

(0.20%).

Regulate. 

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%)— 

UCMR 1.

0/226 M 

(0.00%)— 

UCMR 1.

0/3,869 (0.00%)— 

UCMR 1.

0/226 M 

(0.00%)— 

UCMR 1.

Do not regulate. 

UCMR 2 SS ........ 0/1,198 (0.00%)— 

UCMR 2.

0/157 M 

(0.00%)— 

UCMR 2.

0/1,198 (0.00%)— 

UCMR 2.

0/157 M 

(0.00%)— 

UCMR 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 

(0.11%).

2/3,861 (0.05%) ... 255,358/226 M 

(0.11%).

Do not 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 μg/L .............. >15 μg/L .............. >30 μg/L .............. >30 μg/L.

3/4,139 (0.07%) ... 96,033/229 M 

(0.04%).

3/4,139 (0.07%) ... 96,033/229 M 

(0.04%).

>0.2 μg/L ............. >0.2 μg/L ............. >0.4 μg/L ............. >0.4 μg/L.


jbell on DSKJLSW7X2PROD with RULES
12276 Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 

3Sum of PFOA + PFOS results rounded to 2 

decimal places in those cases where a laboratory 

reported more digits. 

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 mg/L in the 1999– 

2000 cycle to 18.3 mg/L in the 2015– 

2016 cycle (CDC, 2019; Jain, 2018; 

Calafat et al., 2007; Calafat et al., 2019). 

2. Agency Findings 

The Agency is making a 

determination to regulate PFOA and 

PFOS with a NPDWR. EPA has 

determined that PFOA and PFOS may 

have adverse health effects; that PFOA 

and PFOS occur in public water systems 

with a frequency and at levels of public 

health concern; and that, in the sole 

judgment of the Administrator, 

regulation of PFOA and PFOS presents 

a meaningful opportunity for health risk 

reduction for persons served by public 

water systems. 

(a) Adverse Health Effects 

The Agency finds that PFOA and 

PFOS may have adverse effects on the 

health of persons. In 2016, EPA 

published health assessments (Health 

Effects Support Documents or HESDs) 

for PFOA and PFOS based on the 

Agency’s evaluation of the peer 

reviewed science available at that time. 

The lifetime Health Advisory (HA) of 

0.07 mg/L is used as the HRL for 

Regulatory Determination 4 and reflect 

concentrations of PFOA and PFOS in 

drinking water at which adverse health 

effects are not anticipated to occur over 

a lifetime. Studies indicate that 

exposure to PFOA and/or PFOS above 

certain exposure levels may result in 

adverse health effects, including 

developmental effects to fetuses during 

pregnancy or to breast-fed infants (e.g., 

low birth weight, accelerated puberty, 

skeletal variations), cancer (e.g., 

testicular, kidney), liver effects (e.g., 

tissue damage), immune effects (e.g., 

antibody production and immunity), 

and other effects (e.g., cholesterol 

changes). Both PFOA and PFOS are 

known to be transmitted to the fetus via 

the placenta and to the newborn, infant, 

and child via breast milk. Both 

compounds were also associated with 

tumors in long-term animal studies 

(USEPA, 2016d; USEPA, 2016e; NTP, 

2020). For specific details on the 

potential for adverse health effects and 

approaches used to identify and 

evaluate information on hazard and 

dose-response, please see (USEPA, 

2016b; USEPA, 2016c; USEPA, 2016d; 

USEPA, 2016e). 

(b) Occurrence 

EPA has determined that PFOA and 

PFOS occur with a frequency and at 

levels of public health concern at PWSs 

based on the Agency’s evaluation of 

available occurrence information. In 

accordance with SDWA 

1412(b)(1)(B)(ii)(II), EPA has determined 

monitoring data from the third 

Unregulated Contaminant Monitoring 

Rule (UCMR 3) are the best available 

occurrence information for PFOA and 

PFOS regulatory determinations. UCMR 

3 monitoring occurred between 2013 

and 2015 and are currently the only 

nationally representative finished water 

dataset for PFOA and PFOS. Under 

UCMR 3, 36,972 samples from 4,920 

PWSs were analyzed for PFOA and 

PFOS. The minimum reporting level 

(MRL) for PFOA was 0.02 mg/L and the 

MRL for PFOS was 0.04 mg/L. A total of 

1.37% of samples had reported 

detections (greater than or equal to the 

MRL) of at least one of the two 

compounds. To examine the occurrence 

of PFOS and PFOA in aggregate, EPA 

summed the concentrations detected in 

the same sample to calculate a total 

PFOS/PFOA concentration. EPA notes 

that the reference doses (RfDs) for both 

PFOA and PFOS are based on similar 

developmental effects and are 

numerically identical; when these two 

chemicals co-occur at the same time and 

location in drinking water sources, EPA 

has recommended considering the sum 

of the concentrations (USEPA, 2016d; 

USEPA, 2016e) and has done so for this 

regulatory determination. The 

maximum summed concentration of 

PFOA and PFOS was 7.22 mg/L and the 

median summed value was 0.05 mg/L. 

Summed PFOA and PFOS 

concentrations exceeded one-half the 

HRL (0.035 mg/L) at a minimum of 2.4% 

of PWSs (115 PWSs) and exceeded the 

HRL (0.07 mg/L) at a minimum of 1.3% 

of PWSs (63 PWSs 3). Since UCMR 3 

monitoring occurred, certain sites where 

elevated levels of PFOA and PFOS were 

detected may have installed treatment 

for PFOA and PFOS, may have chosen 

to blend water from multiple sources, or 

may have otherwise remediated known 

sources of contamination. Those 63 

PWSs serve a total population of 

approximately 5.6 million people and 

are located in 25 states, tribes, or U.S. 

territories (USEPA, 2019a). Data from 

more recent state monitoring (discussed 

below) demonstrate occurrence in 

multiple geographic locations consistent 

with UCMR 3 monitoring and support 

the Agency’s final determination that 

PFOA and PFOS occur with a frequency 

and at levels of public health concern in 

finished drinking water across the 

United States. The Final Regulatory 

Determination 4 Support Document 

presents a sample-level summary of the 

results for PFOA and PFOS individually 

and includes discussion on state 

monitoring efforts as well as 

uncertainties in occurrence data 

(USEPA, 2021a). 

Consistent with the Agency’s 

commitment in the PFAS Action Plan 

(the Agency’s first multi-media, multiprogram, national research, 

management, and risk communication 

plan to address a challenge like PFAS) 

to present information about additional 

sampling efforts for PFAS in water 

systems, the Agency has supplemented 

its Unregulated Contaminant 

Monitoring Regulation (UCMR) data 


jbell on DSKJLSW7X2PROD with RULES
Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 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 


jbell on DSKJLSW7X2PROD with RULES
12278 Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 

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 peerreviewed health assessments and 

national occurrence data for more PFAS 

becoming available over the next few 

years. EPA notes that although SDWA 

does not require the Agency to complete 

regulatory determinations for the 

contaminants from the fifth CCL until 

2026, because of the significant progress 

related to developing new high-quality 

PFAS information, combined with the 

Agency’s commitment in the PFAS 


jbell on DSKJLSW7X2PROD with RULES
Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 12279 

4New 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. 

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/chemicalresearch/pfas-chemical-lists-and-tieredtesting-methods-descriptions. These 

EPA actions, in addition to other 

research, may provide useful 

information for future EPA evaluations 

of additional PFAS. 

(a) Summary of Public Comments on 

Considerations for Additional PFAS and 

Agency Responses 

EPA requested comment on potential 

regulatory constructs the Agency may 

consider for PFAS chemicals including 

PFOA and PFOS. EPA specifically 

requested input on a regulatory 

approach to evaluate PFAS by different 

grouping approaches. 

EPA received multiple comments on 

how the Agency could consider 

additional PFAS for potential future 

rulemaking. Many commenters support 

a class-based approach for regulating 

PFAS based on one or more 

characteristics such as chain length, 

functional group, treatment processes, 

health effects, toxicity, common 

analytical methods, and/or shared 

occurrence with other contaminants 

within a group. Additionally, many 

commenters also urge EPA to make 

additional regulatory determinations for 

PFAS that have a proposed or final 

drinking water standard in at least one 

state; PFAS that have been measured in 

water systems through monitoring 

programs such as UCMR; and/or PFAS 

for which EPA or the Agency for Toxic 

Substances and Disease Registry 

(ATSDR) has established a toxicity 

value. Some commenters suggest that 

EPA should make positive regulatory 

determinations for PFHxS and PFNA as 

well as in combination with PFOA, 

PFOS, and other PFAS such as PFBS. 

Many commenters recommend EPA 

consider various grouping and treatment 

technique approaches for PFAS beyond 

PFOA and PFOS that may not have 

sufficient health and occurrence data. 

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 


jbell on DSKJLSW7X2PROD with RULES
12280 Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 

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-observedadverse-effect level (NOAEL) and 

lowest-observed-adverse-effect level 

(LOAEL) values of 1,000 and 2,000 mg/ 

kg/day, respectively, were identified 

based on increased urinary enzyme 

markers for renal damage and central 

nervous system (CNS) depression 

(USEPA, 2006a). 

The only available reproductive or 

developmental study with 1,1- 

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 mg/L, based on 

EPA oral RfD of 0.2 mg/kg/day, using 

2.5 L/day drinking water ingestion, 80 

kg body weight and a 20% relative 

source contribution (RSC) factor. 

(b) Occurrence 

EPA has determined that 1,1- 

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 mg/L) or the HRL (1,000 mg/L). 1,1- 

Dichloroethane was detected in about 

2.3% samples at or above the MRL (0.03 

mg/L) (USEPA, 2019a; USEPA, 2021a). 


jbell on DSKJLSW7X2PROD with RULES
Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 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 mg/L) or the HRL 

(1,000 mg/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 mg/L 

based on the EPA OPP RfD for noncancer effects for acetochlor of 0.02 mg/ 

kg/day (USEPA, 2018c) using 2.5 L/day 

drinking water ingestion, 80 kg body 

weight, and a 20% RSC factor. 

(b) Occurrence 

EPA has determined that acetochlor 

does not occur with a frequency and at 

levels of public health concern at PWSs 

based on the Agency’s evaluation of 

available occurrence information. The 

primary occurrence data for acetochlor 

are from the first Unregulated 

Contaminant Monitoring Regulation 

(UCMR 1) assessment monitoring (AM) 

(2001–2003) and the second 

Unregulated Contaminant Monitoring 

Regulation (UCMR 2) screening survey 

(SS) (2008–2010). Acetochlor was not 

detected at levels greater than 1⁄2 the 

HRL (50 mg/L), the HRL (100 mg/L), or 

the MRL (2 mg/L) in any of the 33,778 

UCMR 1 assessment monitoring samples 

from 3,869 PWSs (USEPA, 2008; 

USEPA, 2021a) or in any of the 11,193 

UCMR 2 screening survey samples from 

1,198 PWSs (USEPA, 2015; USEPA, 

2021a). 

Findings from the available ambient 

water data for acetochlor are consistent 

with the results in finished water. 

Ambient water data in NAWQA show 

that acetochlor was detected in between 

13% and 23% of samples from between 

3% and 10% of sites. While maximum 

values in NAWQA Cycle 2 (2002–2012) 

and Cycle 3 (2013–2017) monitoring 

exceeded the HRL (215 mg/L in 2004 and 

137 mg/L in 2013) (only one sample in 

each of those two cycles exceeded the 

HRL), 90th percentile levels of 

acetochlor remained below 1 mg/L. More 

than 10,000 samples were collected in 

each cycle. Non-NAWQA NWIS data 

(1991–2016), which included limited 

finished water data in addition to the 

ambient water data, show no detected 

concentrations greater than the HRL 

(USEPA, 2021a). 

(c) Meaningful Opportunity 

The Agency has determined that 

regulation of acetochlor does not 

present a meaningful opportunity for 

health risk reduction for persons served 

by PWSs based on the estimated 

exposed populations, including 

sensitive populations. The estimated 

population exposed to acetochlor at 

levels of public health concern is 0% 

based on UCMR 1 finished water data 

gathered from 2001 to 2003 and UCMR 

2 finished water data gathered from 

2008 to 2010. As a result, the Agency 

finds that an NPDWR for acetochlor 

does not present a meaningful 

opportunity for health risk reduction. 

(d) Summary of Public Comments on 

Acetochlor and Agency Responses 

EPA received several comments on 

the Agency’s evaluation of acetochlor 

under section 1412(b)(1)(A) of SDWA, 

all of which were in support of its 

preliminary determination not to 

regulate acetochlor. EPA agrees with the 

comments that are in support of the 

negative regulatory determination. 


jbell on DSKJLSW7X2PROD with RULES
12282 Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 

D. Methyl Bromide 

1. Description 

Methyl bromide is a halogenated 

alkane and occurs as a gas. Methyl 

bromide has been used as a fumigant 

fungicide applied to soil before 

planting, to crops after harvest, to 

vehicles and buildings, and for other 

specialized purposes. Use of the 

chemical in the United States was 

phased out in 2005, except for specific 

critical use exemptions and quarantine 

and pre-shipment exemptions in 

accordance with the Montreal Protocol. 

Critical use exemptions have included 

strawberry cultivation and production 

of dry cured pork. Synonyms for methyl 

bromide include bromomethane, 

monobromomethane, curafume, MethO-Gas, and Brom-O-Sol. Methyl 

bromide is expected to have moderate 

persistence in water due to its 

susceptibility to hydrolysis (USEPA, 

2021a). 

2. Agency Findings 

The Agency is making a 

determination not to regulate methyl 

bromide with an NPDWR. Methyl 

bromide does not occur with a 

frequency and at levels of public health 

concern. As a result, the Agency finds 

that an NPDWR does not present a 

meaningful opportunity for health risk 

reduction. 

(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 


jbell on DSKJLSW7X2PROD with RULES
Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 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 exposuredependent increase in stomach cancer 

risk among 7,814 applicators of methyl 

bromide (Barry et al., 2012). In OPP’s 

Draft HHRA for Methyl Bromide, OPP 

reviews all the epidemiological studies 

for methyl bromide, including the Barry 

et al. (2012) Agricultural Health Study. 

OPP concludes that ‘‘based on the 

review of these studies, there is 

insufficient evidence to suggest a clear 

associative or causal relationship 

between exposure to methyl bromide 

and carcinogenic or non-carcinogenic 

health outcomes.’’ 

According to ATSDR (1992) and the 

EPA OPP assessment (USEPA, 2006c), 

no studies suggest that a specific 

subpopulation may be more susceptible 

to methyl bromide, though there is little 

information about susceptible lifestages 

or subpopulations when exposed via the 

oral route. Because the critical effects of 

decreased body weight, decreased rate 

of body weight gain, and decreased food 

consumption in this study are not 

specific to a sensitive subpopulation or 

life stage, the target population of the 

general adult population was selected in 

deriving the HRL for regulatory 

determination. EPA’s OPP assessment 

conducted additional exposure 

assessments for lifestages that may 

increase exposure to methyl bromide 

and concluded that no lifestages have 

expected exposure greater than 10% of 

the chronic population-adjusted dose 

(cPAD), including children. 

EPA calculated an HRL of 100 mg/L 

(rounded from 140.8 mg/L) based on an 

EPA OPP assessment cPAD of 0.022 mg/ 

kg/day and using 2.5 L/day drinking 

water ingestion, 80 kg body weight, and 

a 20% RSC factor (USEPA, 2006d; 

USEPA, 2011, Table 8–1 and 3–33). 

(b) Occurrence 

EPA has determined that methyl 

bromide does not occur with a 

frequency and at levels of public health 

concern at PWSs based on the Agency’s 

evaluation of available occurrence 

information. The primary data 

occurrence data for methyl bromide are 

the 2013–2015 nationally representative 

drinking water monitoring data 

generated through EPA’s UCMR 3. 

Methyl bromide was not detected in any 

of the 36,848 UCMR 3 samples collected 

by 4,916 PWSs (serving ∼ 241 million 

people) at levels greater than 1⁄2 the HRL 

(50 mg/L) or the HRL (100 mg/L). Methyl 

bromide was detected in about 0.3% 

samples at or above the MRL (0.2 mg/L) 

(USEPA, 2019a; USEPA, 2021a). 

Findings from the available ambient 

water data for methyl bromide are 

consistent with the results in finished 

water. Ambient water data in NAWQA 

show that methyl bromide was detected 

in fewer than 1% of samples from fewer 

than 2% of sites. No detections were 

greater than the HRL in any of the three 

cycles. The median concentration 

among detections were 0.5 mg/L and 0.8 

mg/L in Cycle 1 and Cycle 3, 

respectively. There were no detections 

in Cycle 2. The results of the NWIS 

analysis show that methyl bromide was 

detected in approximately 0.1% of 

samples at approximately 0.1% of sites. 

The median concentration among 

detections was 0.6 mg/L. 

(c) Meaningful Opportunity 

The Agency has determined that 

regulation of methyl bromide does not 

present a meaningful opportunity for 

health risk reduction for persons served 

by PWSs based on the estimated 

exposed populations, including 

sensitive populations. UCMR 3 findings 

indicate that the estimated population 

exposed to methyl bromide at levels of 

public health concern is 0%. As a result, 

the Agency finds that an NPDWR for 

methyl bromide does not present a 

meaningful opportunity for health risk 

reduction. 

(d) Summary of Public Comments on 

Methyl Bromide and Agency Responses 

EPA received several comments on 

the Agency’s evaluation of methyl 

bromide under section 1412(b)(1)(A) of 

SDWA, including several comments in 

support of its preliminary determination 

not to regulate methyl bromide. Three 

anonymous members of the public 

opposed the negative determination of 

methyl bromide because of their 

perceptions about its production and 

use. Specifically, commenters appear to 

be seeking to prohibit the production 

and use of methyl bromide. 

EPA agrees with the comments that 

are in support of the negative regulatory 

determination. Regarding comments 

that oppose the negative determination 

because of methyl bromide’s production 

and use; the production, importation, 

use, and disposal of specific chemicals 

are not regulated by SDWA and 

therefore are not relevant to this 

determination. As discussed above, 

methyl bromide was not found above 1⁄2

the HRL in drinking water in any UCMR 

3 samples. Furthermore, commenters 

did not provide any data or other 

information that suggested that their 

concerns had impacts on the occurrence 

of methyl bromide in drinking water or 

discuss any other methyl bromide issues 

that specifically related to drinkingwater. Hence, commenters concerns are 

not addressable by this decision not to 

regulate methyl bromide under SDWA. 

E. Metolachlor 

1. Description 

Metolachlor is a chloroacetanilide 

pesticide that is used as an herbicide for 

weed control. Initially registered in 

1976 for use on turf, metolachlor has 

more recently been used on corn, 

cotton, peanuts, pod crops, potatoes, 

safflower, sorghum, soybeans, stone 

fruits, tree nuts, non-bearing citrus, nonbearing grapes, cabbage, certain 

peppers, buffalograss, guymon 

bermudagrass for seed production, 

nurseries, hedgerows/fencerows, and 

landscape plantings. Synonyms for 

metolachlor include dual and bicep 

(USEPA, 2021a). Metolachlor is 

expected to have moderate to high 

persistence in water due to its 

biodegradation half-life (USEPA, 2021a). 

2. Agency Findings 

The Agency is making a 

determination not to regulate 

metolachlor with an NPDWR. 

Metolachlor does not occur with a 

frequency and at levels of public health 

concern. As a result, the Agency finds 

that an NPDWR does not present a 

meaningful opportunity for health risk 

reduction. 

(a) Adverse Health Effects 

The Agency finds that metolachlor 

may have adverse effects on the health 

of persons. The existing toxicological 

database includes studies evaluating 

both metolachlor and S-metolachlor. 

When combined with the toxicology 

database for metolachlor, the toxicology 

database for S-metolachlor is considered 

complete for risk assessment purposes 

(USEPA, 2018d). In subchronic 

(metolachlor and S-metolachlor) 

(USEPA, 1995b; USEPA, 2018d) and 

chronic (metolachlor) (Hazelette, 1989; 

Tisdel, 1983; Page, 1981; USEPA, 

2018d) toxicity studies in dogs and rats, 

decreased body weight was the most 

commonly observed effect. Chronic 

exposure to metolachlor in rats also 

resulted in increased liver weight and 

microscopic liver lesions in both sexes 

(USEPA, 2018d). No systemic toxicity 

was observed in rabbits when 

metolachlor was administered dermally, 

though dermal irritation was observed at 

lower doses (USEPA, 2018d). Portal of 

entry effects (e.g., hyperplasia of the 

squamous epithelium and mucous cell) 


jbell on DSKJLSW7X2PROD with RULES
12284 Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 

occurred in the nasal cavity at lower 

doses in a 28-day inhalation study in 

rats (USEPA, 2018d). Systemic toxicity 

effects were not observed in this study. 

Immunotoxicity effects were not 

observed in mice exposed to Smetolachlor (USEPA, 2018d). 

While some prenatal developmental 

studies in the rat and rabbit with both 

metolachlor and S-metolachlor revealed 

no evidence of a qualitative or 

quantitative susceptibility in fetal 

animals, decreased pup body weight 

was observed in a two-generation study 

(Page, 1981, USEPA, 2018d). Though 

there was no evidence of maternal 

toxicity, decreased pup body weight in 

the F1 and F2 litters was observed, 

indicating developmental toxicity (Page, 

1981; USEPA, 1990b). Therefore, 

sensitive lifestages to consider include 

infants, as well as pregnant women and 

their fetus, and lactating women. 

Although treatment with metolachlor 

did not result in an increase in 

treatment-related tumors in male rats or 

in mice (both sexes), metolachlor caused 

an increase in liver tumors in female 

rats (USEPA, 2018d). There was no 

evidence of mutagenic or cytogenetic 

effects in vivo or in vitro (USEPA, 

2018d). In 1994 (USEPA, 1995b), EPA 

classified metolachlor as a Group C 

possible human carcinogen, in 

accordance with the 1986 Guidelines for 

Carcinogen Risk Assessment (USEPA, 

1986). In 2017 (USEPA, 2018d), EPA reassessed the cancer classification for 

metolachlor in accordance with EPA’s 

final Guidelines for Carcinogen Risk 

Assessment (USEPA, 2005), and 

reclassified metolachlor/S-metolachlor 

as ‘‘Not Likely to be Carcinogenic to 

Humans’’ at doses that do not induce 

cellular proliferation in the liver. This 

classification was based on convincing 

evidence of a constitutive androstane 

receptor (CAR)-mediated mitogenic 

MOA for liver tumors in female rats that 

supports a nonlinear approach when 

deriving a guideline that is protective 

for the tumor endpoint (USEPA, 2018d). 

A recent OPP HHRA identified a twogeneration reproduction study in rats as 

the critical study (USEPA, 2018d). OPP 

proposed an RfD for metolachlor of 0.26 

mg/kg/day, derived from a NOAEL of 26 

mg/kg/day for decreased pup body 

weight in the F1 and F2 litters. A 

combined UF of 100 was used based on 

interspecies extrapolation (10), 

intraspecies variation (10), and an FQPA 

Safety Factor of 1. This RfD is 

considered protective of carcinogenic 

effects as well as effects observed in 

chronic toxicity studies (USEPA, 

2018d). The decreased F1 and F2 litter 

pup body weights in the absence of 

maternal toxicity were considered 

indicative of increased susceptibility to 

the pups. Therefore, a rate of 0.15 L/kg/ 

day was selected from the Exposure 

Factors Handbook (USEPA, 2011) to 

represent the consumers-only estimate 

of DWI based on the combined direct 

and indirect community water ingestion 

at the 90th percentile for bottle fed 

infants. This estimate is more protective 

than the estimate for pregnant women 

(0.033 L/kg/day) or lactating women 

(0.054 L/kg/day). DWI and BW 

parameters are further outlined in the 

Exposure Factors Handbook (USEPA, 

2011). 

EPA OW calculated an HRL for 

metolachlor of 300 mg/L (rounded from 

0.347 mg/L). The HRL was derived from 

the oral RfD of 0.26 mg/kg/day for bottle 

fed infants ingesting 0.15 L/kg/day 

water, with the application of a 20% 

RSC. 

(b) Occurrence 

EPA has determined that metolachlor 

does not occur with a frequency and at 

levels of public health concern at PWSs 

based on the Agency’s evaluation of 

available occurrence information. The 

primary occurrence data for metolachlor 

are from the UCMR 2 screening survey. 

A total of 11,192 metolachlor samples 

were collected from 1,198 systems. Of 

these systems, three (0.25%) had 

metolachlor detections (1 mg/L) and 

none of the detections were greater than 

1⁄2 the HRL (150 mg/L) or the HRL (300 

mg/L) (USEPA, 2015; USEPA, 2021a). 

Supplementary sources of finished 

water occurrence data from UCM Round 

2 indicate that the occurrence of 

metolachlor in PWSs is likely to be low 

to non-existent (USEPA, 2021a). 

Metolachlor occurrence data for ambient 

water from NAWQA and NWIS are 

consistent with those for finished water 

(USEPA, 2021a). 

(c) Meaningful Opportunity 

The Agency has determined that 

regulation of metolachlor does not 

present a meaningful opportunity for 

health risk reduction for persons served 

by PWSs based on the estimated 

exposed populations, including 

sensitive populations. UCMR 2 findings 

indicate that the estimated population 

exposed to metolachlor at levels of 

public health concern is 0%. As a result, 

the Agency finds that an NPDWR for 

metolachlor does not present a 

meaningful opportunity for health risk 

reduction. 

(d) Summary of Public Comments on 

Metolachlor and Agency Responses 

EPA received several comments on 

the Agency’s evaluation of metolachlor 

under section 1412(b)(1)(A) of SDWA, 

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 


jbell on DSKJLSW7X2PROD with RULES
Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 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 malespecific reproductive toxicant (USEPA, 

2009). 

Under the Guidelines for Carcinogen 

Risk Assessment (USEPA, 2005), 

nitrobenzene is classified as ‘‘likely to 

be carcinogenic to humans’’ by any 

route of exposure (USEPA, 2009). A 

two-year inhalation cancer bioassay in 

rats and mice (Cattley et al., 1994; CIIT, 

1993) reported an increase in several 

tumor types in both species. However, 

the lack of available data, including a 

physiologically based biokinetic or 

model that might predict the impact of 

the intestinal metabolism on serum 

levels of nitrobenzene and its 

metabolites following oral exposures, 

precluded EPA’s IRIS program from 

deriving an oral CSF (USEPA, 2009). 

Additionally, a metabolite of 

nitrobenzene, aniline, is classified as a 

probable human carcinogen (B2) 

(USEPA, 1988). 

Nitrobenzene has been shown to be 

non-genotoxic in most studies and was 

classified as, at most, weakly genotoxic 

in the 2009 USEPA IRIS assessment 

(ATSDR, 1990; USEPA, 2009). 

Of the available animal studies with 

oral exposure to nitrobenzene, the 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 

mg/L (rounded from 12.8 mg/L), based on 

the RfD of 0.002 mg/kg/day, using 2.5 L/ 

day drinking water ingestion, 80 kg 

body weight, and a 20% RSC factor. 

(b) Occurrence 

EPA has determined that 

nitrobenzene does not occur with a 

frequency and at levels of public health 

concern at PWSs based on the Agency’s 

evaluation of available occurrence 

information. The primary occurrence 

data for nitrobenzene are nationally 

representative finished water 

monitoring data generated through 

EPA’s UCMR 1 a.m. (2001–2003). UCMR 

1 collected 33,576 finished water 

samples from 3,861 PWSs (serving ∼226 

million people) for nitrobenzene and it 

was detected in only a small number of 

those samples (0.01%) above the HRL 

(10 mg/L), which is the same as the MRL 

(10 mg/L). 

Findings from the available ambient 

water data for nitrobenzene are 

consistent with the results in finished 

water. Ambient water data in NAWQA 

show that nitrobenzene was not 

detected in any of the samples collected 

under any of the three monitoring 

cycles, while NWIS data show that 

nitrobenzene was detected in 

approximately 1% of samples. 

(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’ doseresponse in the Lish et al. (1984) study. 

The POD for the slope factor was the 

BMDL10 allometrically scaled to a HED 


jbell on DSKJLSW7X2PROD with RULES
12286 Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 

yielding a slope factor of 0.08 per mg/ 

kg/day. 

In mice fed doses of 0 to 35 mg/kg/ 

day for 24 months in the Lish et al. 

(1984) study, there were dosedependent increases in adenomas or 

carcinomas of the lungs and liver in 

males and females (USEPA, 2018e). The 

formulation used contained 3 to 10% 

HMX, another munition ingredient. EPA 

assessed the toxicity of HMX (USEPA, 

1988). No chronic-duration studies were 

available to evaluate the carcinogenicity 

of HMX (USEPA, 1988). HMX is 

classified as Group D, or not classifiable 

as to human carcinogenicity (USEPA, 

1992; USEPA, 1988). In the Levine et al. 

(1983) RDX dietary exposure study with 

Fischer 344 rats, a statistically 

significant increase in the incidence of 

hepatocellular carcinomas was observed 

in males but not in females (USEPA, 

2018e). Although evidence of 

carcinogenicity included dosedependent increases in two 

experimental animal species, two sexes, 

and two systems (liver and lungs), 

evidence supporting carcinogenicity in 

addition to the B6C3F1 mouse study 

was not robust; this factor contributed to 

the suggestive evidence of carcinogenic 

potential classification. EPA considered 

both the Lish et al. (1984) and Levine et 

al. (1983) studies to be suitable for doseresponse analysis because they were 

well conducted, using similar study 

designs with large numbers of animals 

at multiple dose levels (USEPA, 2018e). 

EPA (2018e) concluded that insufficient 

information was available to evaluate 

male reproductive toxicity from 

experimental animals exposed to RDX. 

In addition, EPA (2018e) concluded that 

inadequate information was available to 

assess developmental effects from 

experimental animals exposed to RDX. 

EPA selected the 2018 EPA IRIS 

assessment to derive two HRLs for RDX: 

The RfD-derived HRL (based on Crouse 

et al., 2006) and the oral cancer slope 

factor-derived HRL (based on Lish et al., 

1984). EPA has generally derived HRLs 

for ‘‘possible’’ or Group C carcinogens 

using the RfD approach in past 

Regulatory Determinations. However, 

for RDX, EPA decided to show both an 

RfD-derived and oral-cancer-slopefactor-derived HRL since the mode of 

action for liver tumors is unknown and 

the 1 × 10¥6 cancer risk level provides 

a more health protective HRL to 

evaluate the occurrence information. 

The RfD-derived HRL for RDX was 

calculated using the RfD of 0.004 mg/kg/ 

day based on a subchronic study in F– 

344 rats by Crouse et al. (2006) with 

convulsions as the critical effect 

(USEPA, 2018e). The point of departure 

for the RfD calculation was a human 

equivalent BMDL0.05 of 1.3 mg/kg/day. 

The HED was derived using a 

pharmacokinetic model based on 

arterial blood concentrations in the rats 

as the dose metric. A 300-fold 

uncertainty factor (3 for extrapolation 

from animals to humans, 10 for 

interindividual differences in human 

susceptibility, and 10 for uncertainty in 

the database) was applied in 

determination of the RfD. EPA 

calculated a RfD-derived HRL of 30 mg/ 

L (rounded from 25.6 mg/L), for the 

noncancer effects of RDX based on the 

RfD of 0.004 mg/kg/day, using 2.5 L/day 

drinking water ingestion, 80 kg body 

weight, and a 20% RSC factor. 

The oral-cancer-slope-factor-derived 

HRL for RDX was also based on values 

presented in the 2018 EPA IRIS 

assessment. The slope factor is derived 

from the dose-response for lung and 

liver tumors in the Lish et al. (1984) 

study, with elimination of the data for 

the high dose group due to high 

mortality. The point of departure for the 

slope factor of 0.08 (mg/kg/day)-1 was 

the BMDL10 which was allometrically 

scaled to a HED. EPA calculated an oral 

cancer slope factor-derived HRL of 0.4 

mg/L for RDX based on the cancer slope 

factor of 0.08 (mg/kg/day)-1, using 2.5 

L/day drinking water ingestion, 80 kg 

body weight, and a 1 in a million cancer 

risk level. 

EPA’s (USEPA, 2018e) derivation of 

an oral slope factor for cancer is in 

accordance with the Guidelines for 

Carcinogen Risk Assessment (USEPA, 

2005) while RDX is classified as having 

‘‘suggestive evidence of carcinogenic 

potential.’’ Specifically, the guidelines 

state ‘‘when the evidence includes a 

well-conducted study, quantitative 

analyses may be useful for some 

purposes, for example, providing a 

sense of the magnitude and uncertainty 

of potential risks, ranking potential 

hazards, or setting research priorities’’ 

(USEPA, 2005). The EPA IRIS 

assessment concluded that the database 

for RDX contains well-conducted 

carcinogenicity studies (Lish et al., 

1984; Levine et al., 1983) suitable for 

dose response and that the quantitative 

analysis may be useful for providing a 

sense of the magnitude and uncertainty 

of potential carcinogenic risk (USEPA, 

2018e). Therefore, EPA felt it was 

important to evaluate the occurrence 

information against both the RfDderived HRL and the oral cancer slope 

factor-derived HRL. 

(b) Occurrence 

EPA has determined that RDX does 

not occur with a frequency and at levels 

of public health concern at PWSs based 

on the Agency’s evaluation of available 

occurrence information. The primary 

data for RDX are nationally 

representative drinking water 

monitoring data generated through 

EPA’s UCMR 2 AM (2008–2010). UCMR 

2 collected 32,150 finished water 

samples from 4,139 PWSs (serving ∼229 

million people) for RDX and it was 

detected in only a small number of 

those samples (0.01%) at or above the 

MRL. The detections occurred in three 

large surface water systems; the 

maximum detected concentration of 

RDX was 1.1 mg/L. The MRL is 1 mg/L, 

which is about 2.5 times higher than the 

oral cancer slope factor-derived HRL 

(0.4 mg/L). The RfD-derived HRL (30 mg/ 

L) is 30 times higher than the MRL and 

75 times higher than the cancer slope 

factor-derived HRL. 

Findings from the available ambient 

water data for RDX in ambient water, 

available from NWIS, show that RDX 

was detected in approximately 46% of 

samples and at approximately 29% of 

sites; RDX data are not available from 

the NAWQA program. 

(c) Meaningful Opportunity 

The Agency has determined that 

regulation of RDX does not present a 

meaningful opportunity for health risk 

reduction for persons served by PWSs 

based on the estimated exposed 

populations, including sensitive 

populations. UCMR 2 findings indicate 

that the estimated population exposed 

to RDX at or above the MRL is 0.04%. 

There were no detections greater than 

the non-cancer HRL (30 mg/L) or the 

one-half the non-cancer HRL (15 mg/L). 

Because the MRL of 1 mg/L is higher 

than the cancer HRL of 0.4 mg/L, the 

population exposed relative to the 

cancer HRL and 1⁄2 the cancer HRL is 

not presented here. As a result, the 

Agency finds that an NPDWR for RDX 

does not present a meaningful 

opportunity for health risk reduction. 

Based on the small number of samples 

measured at or marginally above the 

MRL, EPA does not believe that there 

would be enough occurrence in the 

narrow range between the HRL and the 

MRL to change the meaningful 

opportunity determination. 

(d) Summary of Public Comments on 

RDX and Agency Responses 

EPA received several comments on 

the Agency’s evaluation of RDX under 

section 1412(b)(1)(A) of SDWA, all of 

which were in support of its 

preliminary determination not to 

regulate RDX. EPA agrees with the 

comments that are in support of the 

negative regulatory determination. 


jbell on DSKJLSW7X2PROD with RULES
Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 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 mg/L) is more 

than 75 times the HRL (0.0004 mg/L) for 

1,2,3-trichloropropane. This 

discrepancy allows for a broad range of 

potential contaminant concentrations 

that could be in exceedance of the HRL 

but below the MRL. EPA did not make 

a preliminary determination for 1,2,3- 

trichloropropane due to these analytical 

method-based limitations. The Agency 

noted that it needs additional lowerlevel occurrence information prior to 

making a preliminary regulatory 

determination for 1,2,3- 

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. 


jbell on DSKJLSW7X2PROD with RULES
12288 Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 

V. Next Steps 

As required by SDWA, EPA will 

initiate the process to propose a NPDWR 

for PFOA and PFOS within 24 months 

of the publication of this document in 

the Federal Register. For this 

rulemaking effort, in addition to using 

the best available science, the Agency 

will seek recommendations from the 

EPA Science Advisory Board and 

consider public comment on the 

proposed rule. Therefore, EPA 

anticipates further scientific review of 

new science and an opportunity for 

additional public input prior to the 

promulgation of the regulatory standard 

for PFOA and PFOS. Additionally, the 

Agency will continue to collect and 

review additional state and other 

occurrence information during the 

development of the proposed NPDWR 

for PFOA and PFOS. The Agency will 

not be taking any further regulatory 

action under SDWA for the six negative 

determinations at this time. 

VI. References 

American Association for the Advancement 

of Science (AAAS). 2020. Per- and 

Polyfluoroalkyl Substances (PFAS) in 

Drinking Water. Available on the 

internet at: https://www.aaas.org/ 

programs/epi-center/pfas. 

Ahmed, F.E. and J.C. Seely. 1983. Acetochlor: 

Chronic Feeding Toxicity and 

Oncogenicity Study in the Rat. 

Pharmacopathics Research Laboratories, 

Inc., Laurel, MD. Study No. PR–80–006. 

May 20, 1983. Unpublished report (as 

cited in USEPA, 2006b). 

Ahmed, F.E., A.S. Tegeris, and J.C. Seely. 

1983. MON 097: 24-Month Oncogenicity 

Study in the Mouse. Pharmacopathics 

Research Laboratories, Inc., Laurel, MD. 

Report No. PR–80–007. May 4, 1983. 

Unpublished report (as cited in USEPA, 

2006b) 

Agency for Toxic Substances and Disease 

Registry (ATSDR). 1990. Toxicological 

Profile for Nitrobenzene. U.S. 

Department of Health and Human 

Services, Public Health Service. 

Available on the internet at: https://

www.atsdr.cdc.gov/toxprofiles/ 

tp.asp?id=532&tid=95. 

ATSDR. 1992. Toxicological Profile for 

Bromomethane. U.S. Department of 

Health and Human Services, Public 

Health Service. 

ATSDR. 2012. Toxicological Profile for RDX. 

U.S. Department of Health and Human 

Services, Public Health Service. 

Available on the internet at: https://

www.atsdr.cdc.gov/ToxProfiles/ 

tp.asp?id=412&tid=72. 

ATSDR. 2015. Toxicological Profile for 1,1- 

Dichloroethane. U.S. Department of 

Health and Human Services, Public 

Health Service. Available on the internet 

at: https://www.atsdr.cdc.gov/ 

ToxProfiles/tp133.pdf. 

Barry, K.H., S. Koutros, J. Lupin, H.B. Coble, 

F. Barone-Adesi, L.E. Beane Freeman, 

D.P. Sandler, J.A. Hoppin, X. Ma, T. 

Zheng, and M.C.R. Alavanja. 2012. 

Methyl bromide exposure and cancer 

risk in the Agricultural Health Study. 

Cancer Causes Control 23:807–818. 

Bond, J.A., J.P. Chism, D.E. Rickert, et al. 

1981. Induction of hepatic and testicular 

lesions in Fischer 344 rats by single oral 

doses of nitrobenzene. Fundam Appl 

Toxicol 1:389–394 (as cited in USEPA, 

2009). 

Boorman, G.A., H.L. Hong, C.W. Jameson, et 

al. 1986. Regression of methyl bromide 

induced forestomach lesions in the rat. 

Toxicol Appl Pharmacol 86:131–139. 

Breslin, W.J., C.L. Zublotny, G.J. Bradley, et 

al. 1990. Methyl bromide inhalation 

teratology study in New Zealand white 

rabbits with cover letter and attachment 

(declassified). Dow Chemical Company. 

Submitted to the U.S. Environmental 

Protection Agency under TSCA Section 

8E. OTS0522340–3 (as cited in ATSDR, 

1992). 

Calafat, A.M., L-Y Wong, Z. Kuklenyik, J.A. 

Reidy, and L.L. Needham. 2007. 

Polyfluoroalkyl Chemicals in the U.S. 

Population: Data from the National 

Health and Nutrition Examination 

Survey (NHANES) 2003–2004 and 

Comparisons with NHANES 1999–2000. 

Environ Health Perspect 115(11):1596– 

1602. 

Calafat, A.M., K. Kato, K. Hubbard, et al. 

2019. Legacy and alternative per and 

polyfluoroalkyl substances in the U.S. 

general population: Paired serum-urine 

data from the 2013–2014 National Health 

and Nutrition Examination Survey, 

Environment International 131:105048. 

Cattley, R.C., J.I. Everitt, E.A. Gross, et al. 

1994. Carcinogenicity and toxicity of 

inhaled nitrobenzene in B6C3F1 mice 

and F344 and CD rats. Fundam Appl 

Toxicol 22:328–340 (as cited in USEPA, 

2009). 

Centers for Disease Control and Prevention 

(CDC). 2019. Fourth National Report on 

Human Exposure to Environmental 

Chemicals, Updated Tables, January 

2019, Volume 1. Department of Health 

and Human Services, Centers for Disease 

Control and Prevention. Available on the 

internet at: https://www.cdc.gov/ 

exposurereport/pdf/FourthReport_

UpdatedTables_Volume1_Jan2019- 

508.pdf. 

Chemical Industry Institute of Toxicology 

(CIIT). 1993. Initial submission: A 

chronic inhalation toxicity study of 

nitrobenzene in B6C3F1 mice, Fischer 

344 rats and Sprague-Dawley (CD) rats. 

Chemical Industry Institute of 

Toxicology. Research Triangle Park, NC. 

EPA Document No. FYI–OTS–0794– 

0970; NTIS No. OTS0000970 (as cited in 

USEPA, 2009). 

Crouse, L.C.B., M.W. Michie, M. Major, M.S. 

Johnson, R.B. Lee, and H.I. Paulus. 2006. 

Subchronic oral toxicity of RDX in rats. 

(Toxicology Study No. 85–XC–5131–03). 

Aberdeen Proving Ground, MD: U.S. 

Army Center for Health Promotion and 

Preventive Medicine. 

Danse, L.H., F.L. van Velsen, and C.A. Van 

Der Heljden. 1984. Methylbromide: 

Carcinogenic effects in the rat 

forestomach. Toxicol Appl Pharmacol 

72:262–271 (as cited in ATSDR, 1992). 

Dickenson, E.R.V. and C. Higgins. 2016. 

Treatment Mitigation Strategies for Polyand Perfluoroalkyl Substances. Web 

Report #4322. Water Research 

Foundation. Denver, CO. 

Domingo, J.L., and M. Nadal. 2019. Human 

exposure to per- and polyfluoroalkyl 

substances (PFAS) through drinking 

water: A review of the recent scientific 

literature. Environmental Research 177: 

108648. 

Enloe, P.V., C.M. Salamon, and S.V. Becker. 

1986. Two-generation reproduction 

study via inhalation in albino rats using 

methyl bromide. American Biogenics 

Corp. Submitted to the U.S. 

Environmental Protection Agency under 

TSCA Section 8d. OTS0515364. EPA 

Doc. ID 86–870000926 (as cited in 

ATSDR, 1992). 

Eustis, S.L., S.B. Haber, R.T. Drew, et al. 

1988. Toxicology and pathology of 

methyl bromide in F344 rats and B6C3F1 

mice following repeated inhalation 

exposure. Fundam Appl Toxicol 11:594– 

610 (as cited in ATSDR, 1992). 

Fromme H, Tittlemier SA, Volkel W, 

Wilhelm M, Twardella D. 2009. 

Perfluorinated Compounds—Exposure 

Assessment for the General Population 

in Western Countries. International 

Journal of Hygiene and Environmental 

Health 212: 239–270, doi: 10.1016/ 

j.ijheh.2008.04.007. 

Gansewendt, B., U. Foest, D. Xu et al. 1991. 

Formation of DNA adducts in F–344 rats 

after oral administration or inhalation of 

[14C] methyl bromide. Food Chem. 

Toxicol 29:557–563. 

Hardin, B.D., G.P. Bond, M.R. Sikov, et al. 

1981. Testing of selected workplace 

chemicals for teratogenic potential. 

Scand J Work Environ Health 7:66–75 (as 

cited in ATSDR, 1992). 

Hardisty, J.F. 1997a. Pathology Working 

Group Peer Review of Histiocytic 

Sarcoma in Female Mice from Two LongTerm Studies with Acetochlor. 

Experimental Pathology Laboratories, 

Inc., Research Triangle Park, NC. 

Laboratory Project ID CTL/C/3196, 

February 11, 1997. Unpublished report 

(as cited in USEPA, 2006b). 

Hardisty, J.F. 1997b. Pathology Working 

Group Peer Review of Hepatocellular 

Neoplasms in the Liver of Rats and Mice 

from Five Long-Term Studies with 

Acetochlor. Experimental Pathology 

Laboratories, Inc., Research Triangle 

Park, NC. Laboratory Project ID CTL/C/ 

3197, February 11, 1997. Unpublished 

report (as cited in USEPA, 2006b). 

Hardisty, J.F. 1997c. Pathology Working 

Group Peer Review of Neoplastic Lesions 

in the Lung of Male and Female Mice 

from Two Long-Term Studies with 

Acetochlor. Experimental Pathology 

Laboratories, Inc., Research Triangle 

Park, NC. Laboratory Project ID CTL/C/ 

3198, February 11, 1997. Unpublished 

report (as cited in USEPA, 2006b). 

Hazelette, J. 1989. Metolachlor Technical: 

Chronic Toxicity Study in Dogs: Study 


jbell on DSKJLSW7X2PROD with RULES
Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 12289 

No. 862253. Unpublished study prepared 

by Ciba-Geigy Corp. 758 p. MRID: 

4098070 (as cited in USEPA, 2018d). 

Health Canada. 2018. 1,4-Dioxane in 

Drinking Water—Guideline Technical 

Document for Public Consultation. 

Available on the internet at: https://

www.canada.ca/content/dam/hc-sc/ 

documents/programs/consultation-1-4- 

dioxane-drinking-water/pub-eng.pdf. 

ICI, Inc. 1988. MRID No. 41565118; HED Doc 

No. 008478. (or Broadmeadow, A. 1988). 

SC–5676: Toxicity Study by Oral 

(Capsule) Administration to Beagle Dogs 

for 52 Weeks. Life Science Research, 

Ltd., Suffolk, England. Study No.: LSR 

Report 88/SUC018/0136; December 2, 

1988 (as cited in USEPA, 1993). 

Jain, R.B. 2018. Time trends over 2003–2014 

in the concentrations of selected 

perfluoroalkyl substance among U.S. 

adults aged ≥20 years: Interpretational 

issues. Science of the Total Environment 

645:946–957. 

Kaneda, M., H. Hojo, S. Teramoto, et al. 1998. 

Oral teratogenicity studies of methyl 

bromide in rats and rabbits. Food Chem 

Toxicol. 36(5):421–427. 

Kato, N., S. Morinobu, and S. Ishizu. 1986. 

Subacute inhalation experiment for 

methyl bromide in rats. Ind Health 

24(2):87–103 (as cited in ATSDR, 1992). 

Kawashima, K, M. Usami, K. Sakemi, et al. 

1995. Studies on the establishment of 

appropriate spermatogenic endpoints for 

male fertility disturbance in rodent 

induced by drugs and chemicals. I. 

Nitrobenzene. J Toxicol Sci 20:15–22 (as 

cited in USEPA, 2009). 

Koida, M, T. Nakagawa, K. Irimura, et al. 

1995. Effects on the sperm and testis of 

rats treated with nitrobenzene: Age and 

administration period differences. 

Teratology 52:39B (as cited in USEPA, 

2009). 

Levine, B.S., P.M. Lish, E.M. Furedi, V.S. 

Rac, and J.M. Sagartz. 1983. 

Determination of the chronic mammalian 

toxicological effects of RDX (twentyfourmonth, chronic toxicity/ 

carcinogenicity study of hexahydro1,3,5-trinitro-1,3,5-triazine (RDX) in the 

Fischer 344 rat): Final report—phase V. 

Chicago, IL: IIT Research Institute. (As 

cited in ATSDR, 2012; USEPA, 2018e; 

USEPA, 1992.) 

Lish, P.M., B.S. Levine, E.M. Furedi, J.M. 

Sagartz, and V.S. Rac. 1984. 

Determination of the chronic mammalian 

toxicological effects of RDX: Twentyfour-month, chronic toxicity/ 

carcinogenicity study of hexahydro1,3,5-trinitro-1,3,5-triazine (RDX) in the 

B6C3F1 hybrid mouse (Volumes 1–3). 

(ADA181766. DAMD17–79–C–9161). 

Fort Detrick. (As cited in ATSDR, 2012; 

USEPA, 2018e; USEPA, 1992.) 

Matsuura, I., N. Hoshino, Y. Wako, et al. 

1995. Sperm parameter studies on three 

testicular toxicants in rats. Teratology 

52:39B (as cited in USEPA, 2009). 

Mertens, J.J.W.M. 1997. A 24-month chronic 

dietary study of methyl bromide in rats. 

WIL Research Laboratories, Inc., 1407 

George Road, Ashland, OH 44805–9281, 

Laboratory Study No. WIL–49014, 

December 9, 1997, MRID 44462501. 

Unpublished. 

Muralidhara, S., R. Ramanathan, S.M. Mehta, 

L.H. Lash, D. Acosta, and J.V. Bruckner. 

2001. Acute, subacute, and subchronic 

oral toxicity studies of 1,1- 

dichloroethane in rats: Application to 

risk evaluation. Toxicol. Sci. 64:135–145. 

Naylor, M.W. and W.E. Ribelin. 1986. 

Chronic Feeding Study of MON 097 in 

Albino Rats. Monsanto Environmental 

Health Laboratory, St. Louis, MO. 

Laboratory Project ID EHL–83107 (Report 

No. MSL–6119). September 25, 1986. 

Unpublished report (as cited in USEPA, 

2006b). 

National Cancer Institute (NCI). 1978. 

Bioassay of 1,1-Dichloroethane for 

Possible Carcinogenicity. Bethesda, MD: 

National Cancer Institute. NCI 

Carcinogenesis Technical Report Series 

No. 66 (NCI–CG–TR–66). DHEW 

Publication No. (NIH) 78–1316. 

Available on the internet at: http://

ntp.niehs.nih.gov/ntp/htdocs/LT_rpts/ 

tr066.pdf. 

National Institute of Environmental Health 

Services (NIEHS). 2020. Perfluoroalkyl 

and Polyfluoroalkyl Substances (PFAS). 

Available on the internet at: https://

www.niehs.nih.gov/health/topics/agents/ 

pfc/index.cfm. 

National Institute for Occupational Safety 

and Health (NIOSH). 1978. Occupational 

health guidelines for 1,1-dichloroethane. 

Occupational health guidelines for 

chemical hazards. Washington, DC: US 

Department of Labor, National Institute 

for Occupational Safety and Health, 1–4. 

National Toxicology Program (NTP). 1983. 

Report on the subchronic toxicity via 

gavage of nitrobenzene (C60082) in 

Fischer 344 rats and B6C3F1 mice 

[unpublished]. National Toxicology 

Program, prepared by the EG&G Mason 

Research Institute, Worcester, MA, for 

the National Toxicology Program, 

National Institute of Environmental 

Health Services, Public Health Service, 

U.S. Department of Health and Human 

Services, Research Triangle Park, NC; 

MRI–NTP 08–83–19 (as cited in USEPA, 

2009). 

NTP. 1992. Toxicology and carcinogenesis 

studies of methyl bromide (CAS NO. 74– 

83–9) in B6C3F1 mice (inhalation 

studies). U.S. Department of Health and 

Human Services. Public Health Service. 

National Institutes of Health. 

NTP. 2020. Technical report on the 

toxicology and carcinogenesis studies of 

perfluorooctanoic acid (CASRN 335–67– 

1) administered in feed to Sprague 

Dawley (Hsd: Sprague Dawley® SD®) 

rats. U.S. Department of Health and 

Human Services. Public Health Service. 

National Institutes of Health. 

Page, J.G. 1981. Two-Generation 

Reproduction Study in Albino Rats with 

Metolachlor Technical. Toxigenics, 

Decatur, IL. Study Number 450–0272, 

August 31, 1981. Unpublished. MRID: 

00080897 (cited as ‘‘Smith et al. 1981’’ 

in USEPA 1995b, cited as ‘‘Ciba-Geigy 

1981’’ in USEPA 1990b, cited as ‘‘Page 

1981’’ in USEPA 2018d). 

Reuzel, P.G., C.F. Kuper, H.C. Dreef-Van Der 

Meulen, et al. 1987. Initial submission: 

Chronic (29-month) inhalation toxicity 

and carcinogenicity study of methyl 

bromide in rats with cover letter dated 

081092. DuPont Chem Co. Submitted to 

the U.S. EPA under TSCA Section ECP. 

OTS0546338. EPA Doc. 88–920008788 

(as cited in ATSDR, 1992). 

Ribelin, W.E. 1987. Histopathology Findings 

in Noses of Rats Administered MON 097 

in a Lifetime Feeding Study. Tegeris 

Laboratories, Laurel, MD and Monsanto 

Environmental Health Laboratory, St. 

Louis, MO. Laboratory Project No. ML– 

86–44/EHL 86027. November 4, 1987. 

Unpublished report (as cited in USEPA, 

2006b). 

Schatzow, S. 1984. Memorandum to D. Clay, 

November 9, 1984. FXI–OTS–1184–0327. 

Supplement, Sequence D (as cited in 

USEPA, 2007a). 

Schwetz, B.A., B.K. Leong, and P.J. Gehring. 

1974. Embryo- and fetotoxicity of 

inhaled carbon tetrachloride, 1,1- 

dichloroethane, and methyl ethyl ketone 

in rats. Toxicol Appl Pharmacol. 28: 

452–464 (as cited in CalEPA, 2003). 

Sikov M.R., W.C. Cannon, and D.B. Carr. 

1980. Teratologic Assessment of 

Butylene Oxide, Styrene Oxide and 

Methyl Bromide. Cincinnati, OH: 

National Institute for Occupational 

Safety and Health. PBSl168510 (as cited 

in ATSDR, 1992). 

Tisdel, M., T. Jackson, P. MacWilliams, et al. 

1983. Two-year Chronic Oral Toxicity 

and Oncogenicity Study with 

Metolachlor in 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; 

250370; 250371; 250372; 250373; 

250374; 250375) (cited as MRID 

00129377 in USEPA, 2018d). 

United States Environmental Protection 

Agency (USEPA). 1985. Chemical 

Hazard Information Profile. Draft Report. 

Methyl Bromide. Rev. February 20, 1985. 

USEPA, OTS, Washington, DC (as cited 

in ATSDR, 1992). 

USEPA. 1986. Guidelines for Carcinogen Risk 

Assessment. EPA 630–R–00–004. 

USEPA. 1988. Chemical Assessment 

Summary Information for Octahydro1,3,5,7-tetranitro-1,3,5,7-tetrazocine 

(HMX) on the Integrated Risk 

Information System (IRIS). National 

Center for Environmental Assessment, 

Washington, DC. Available on the 

internet at: https://cfpub.epa.gov/ncea/ 

iris2/chemicalLanding.cfm?substance_

nmbr=311. 

USEPA. 1989. Bromomethane (CASRN 74– 

83–9). Integrated Risk 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. 


jbell on DSKJLSW7X2PROD with RULES
12290 Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 

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. 

USEPA. 1992. Health Advisory for 

Hexahydro-1,3,5-trinitro-1,3,5-triazine 

(RDX). In Roberts, WC and WR Hartley 

eds. Drinking Water Health Advisory: 

Munitions. Boca Raton FL: Lewis 

Publishers, pp 133–180. 

USEPA. 1993. Integrated Risk Information 

System (IRIS) Chemical Assessment 

Summary. Acetochlor; CASRN 34256– 

82–1. National Center for Environmental 

Assessment. September 1, 1993. 

Available on the internet at: https://

cfpub.epa.gov/ncea/iris/iris_documents/ 

documents/subst/0521_summary.pdf. 

USEPA. 1995a. Policy on Evaluating Health 

Risks to Children. October 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: https://www.epa.gov/sites/ 

production/files/2014-05/documents/ 

health_policy_cover_memo.pdf. 

USEPA. 1995b. Reregistration Eligibility 

Decision (RED)—Metolachlor. EPA 738– 

R–95–006. Office of Prevention, 

Pesticides and Toxic Substances. 

Available on the internet at: https://

www3.epa.gov/pesticides/chem_search/ 

reg_actions/reregistration/red_PC108801_1-Dec-94.pdf. 

USEPA. 2004b. Cancer Assessment 

Document. Evaluation of the 

Carcinogenic Potential of Acetochlor 

(Fourth Evaluation). Final Report. Cancer 

Assessment Review Committee (CARC), 

Health Effects Division Office of 

Pesticide Programs. EPA–HQ–OPP– 

2005–0227–0016. Available on the 

internet at: https://archive.epa.gov/ 

pesticides/chemicalsearch/chemical/ 

foia/web/pdf/121601/121601-2004-08- 

31a.pdf. 

USEPA. 2005. Guidelines for Carcinogen Risk 

Assessment. EPA–630–P–03–001F. 

Available on the internet at: https://

www.epa.gov/sites/production/files/ 

2013-09/documents/cancer_guidelines_

final_3-25-05.pdf. 

USEPA. 2006a. Provisional Peer Reviewed 

Toxicity Values for 1,1-Dichloroethane 

(CASRN 75–34–3). Superfund Health 

Risk Technical Support Center, National 

Center for Environmental Assessment, 

Office 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. 

USEPA. 2006c. Methyl Bromide: Phase 5 

Health Effects Division (HED) Human 

Health Risk Assessment for Commodity 

Uses. PC Code 053201, DP Barcode 

D304623. Office of Prevention, Pesticides 

and Toxic Substances. 

USEPA. 2006d. Report of Food Quality 

Protection Act (FQPA) Tolerance 

Reassessment and Risk Management 

Decision (TRED) for Methyl Bromide, 

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. 

USEPA. 2007a. Provisional Peer Reviewed 

Toxicity Values for Bromomethane 

(CASRN 74–83–9). Superfund Health 

Risk Technical Support Center, National 

Center for Environmental Assessment, 

Office of Research and Development, 

U.S. Environmental Protection Agency, 

Cincinnati, OH. https://hhpprtv.ornl.gov/ 

issue_papers/Bromomethane.pdf. 

USEPA. 2007b. Benchmark dose software 

(BMDS) version 1.4.1c (last modified 

November 9, 2007). 

USEPA. 2008. The Analysis of Occurrence 

Data from the First Unregulated 

Contaminant Monitoring Regulation 

(UCMR 1) in Support of Regulatory 

Determinations for the Second Drinking 

Water Contaminant Candidate List. EPA 

815–R–08–012. June 2008. 

USEPA. 2009. Toxicological Review of 

Nitrobenzene (CAS No. 98–95–3) in 

Support of Summary Information on the 

Integrated Risk Information System 

(IRIS). National Center for 

Environmental Assessment, Washington, 

DC. EPA 635–R–08–004F. 

USEPA. 2011. Exposure Factors Handbook 

2011 Edition (Final Report). EPA 600–R– 

09–052F. 

USEPA. 2014. Announcement of Preliminary 

Regulatory Determinations for 

Contaminants on the Third Drinking 

Water Contaminant Candidate List. 

Federal Register 79 FR 62715, October 

20, 2014. 

USEPA. 2015. Occurrence Data from the 

Second Unregulated Contaminant 

Monitoring Regulation (UCMR 2). EPA 

815–R15–013. December 2015. 

USEPA. 2016a. Drinking Water Contaminant 

Candidate List 4—Final. Federal 

Register 81 FR 81099, November 17, 

2016. 

USEPA. 2016b. Drinking Water Health 

Advisory for Perfluorooctane Sulfonate 

(PFOS). EPA 822–R–16–004. Available 

on the internet at: https://www.epa.gov/ 

sites/production/files/2016-05/ 

documents/pfos_health_advisory_final_

508.pdf. 

USEPA. 2016c. Drinking Water Health 

Advisory for Perfluorooctanoic Acid 

(PFOA). EPA 822–R–16–005. Available 

on the internet at: https://www.epa.gov/ 

sites/production/files/2016-05/ 

documents/pfoa_health_advisory_final_

508.pdf. 

USEPA. 2016d. Health Effects Support 

Document for Perfluorooctane Sulfonate 

(PFOS). EPA 822–R–16–002. Office of 

Water. Available on the internet at: 

https://www.epa.gov/sites/production/ 

files/2016-05/documents/pfos_hesd_

final_508.pdf. 

USEPA. 2016e. Health Effects Support 

Document for Perfluorooctanoic Acid 

(PFOA). Office of Water. EPA 822–R–16– 

003. Available on the internet at: https:// 

www.epa.gov/sites/production/files/ 

2016-05/documents/pfoa_hesd_final_

508.pdf. 

USEPA. 2016f. Announcement of Final 

Regulatory Determinations for 

Contaminants on the Third Drinking 

Water Contaminant Candidate List. 

Federal Register 81 FR 13, January 4, 

2016. 

USEPA. 2018a. Reaffirmation of EPA’s 1995 

Policy on Evaluating Health Risks to 

Children. October 11, 2018. Available on 

the internet at: https://www.epa.gov/ 

sites/production/files/2018-10/ 

documents/childrens_health_policy_

reaffirmation_memo.10.11.18.pdf. 

USEPA. 2018b. Basic Information on PFAS. 

Available on the internet at: https://

www.epa.gov/pfas/basic-informationpfas. 

USEPA. 2018c. Acetochlor Human Health 

Risk Assessment for Proposed New Use 

on Alfalfa and Related Animal 

Commodities. Office of Chemical Safety 

and Pollution Prevention. April 4, 2018. 

Available on the internet at: https://

beta.regulations.gov/docket/EPA-HQOPP-2017-0235/document. 

USEPA. 2018d. S-Metolachlor: Human 

Health Risk Assessment for (1) 

Establishment of Tolerances for New 

Uses on Chicory, Stevia and 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) Stalk and Stem Vegetable 

Subgroup 22A, except Kohlrabi. Human 

Health Risk Assessment. EPA–HQ–OPP– 

2017–0465. September. 

USEPA. 2018e. Integrated Risk Information 

System (IRIS). Toxicological Review of 

Hexahydro-1,3,5-trinitro-1,3,5-triazine 

(RDX). EPA 635–R–18–211Fa. Available 

on the internet at: https://cfpub.epa.gov/ 

ncea/iris/iris_documents/documents/ 

toxreviews/0313tr.pdf. 

USEPA. 2019a. Occurrence Data from the 

Third Unregulated Contaminant 

Monitoring Rule (UCMR 3). EPA 815–R– 

19–007. 

USEPA. 2019b. EPA’s Per- and 

Polyfluoroalkyl Substances Action Plan. 

EPA 823–R–18–004. 

USEPA. 2020a. Announcement of 

Preliminary Regulatory Determinations 

for Contaminants on the Fourth Drinking 

Water Contaminant Candidate List. 

Federal Register 85 FR 14098, March 10, 

2020. 


jbell on DSKJLSW7X2PROD with RULES
Federal Register / Vol. 86, No. 40 / Wednesday, March 3, 2021 / Rules and Regulations 12291 

USEPA. 2020b. Drinking Water Treatability 

Database. https://iaspub.epa.gov/tdb/ 

pages/general/home.do. Last updated 

March 2020. 

USEPA. 2020c. Final Risk Evaluations for 

1,4-Dioxane. EPA Document # EPA–740– 

R1–8007. December 2020. https://

www.epa.gov/assessing-and-managingchemicals-under-tsca/final-riskevaluation-14-dioxane#riskevaluation. 

USEPA. 2021a. Final Regulatory 

Determination 4 Support Document. 

EPA 815–R–21–001. 

USEPA. 2021b. Responses to Public 

Comments on Preliminary Regulatory 

Determinations for Contaminants on the 

Fourth Drinking Water Contaminant 

Candidate List. EPA 815–R–21–002. 

Virgo, D.M. and A. Broadmeadow. 1988. SC– 

5676: Combined Oncogenicity and 

Toxicity Study in Dietary Administration 

to CD Rats for 104 Weeks. Life Science 

Research Ltd., Suffolk, England. Study 

No. 88/SUC017/0348. March 18, 1988. 

Unpublished report (as cited in USEPA, 

2006b). 

Vogel, E.W. and M.J.M. Nivard. 1994. The 

subtlety of alkylating agents in reactions 

with biological macromolecules. Mutat. 

Res. 305: 13–32 (as cited in USEPA, 

2007a). 

Wester, P.W. and R. Kroes, 1988. 

Forestomach carcinogens: pathology and 

relevance to man. Toxicologic Pathology 

16(2): 165–71 (as cited in ATSDR, 1992). 

Signing Statement 

This document of the Environmental 

Protection Agency was signed on 

January 15, 2021, by Andrew Wheeler, 

Administrator, pursuant to the statutory 

requirements of the Safe Drinking Water 

Act, Section 1412(b). That document 

with the original signature and date is 

maintained by EPA. For administrative 

purposes only, and in compliance with 

requirements of the Office of the Federal 

Register, the undersigned EPA Official 

re-signs the document for publication, 

as an official document of the 

Environmental Protection Agency. This 

administrative process in no way alters 

the legal effect of this document upon 

publication in the Federal Register. 

Jane Nishida, 

Acting Administrator. 

[FR Doc. 2021–04184 Filed 3–2–21; 8:45 am] 

BILLING CODE 6560–50–P 

DEPARTMENT OF COMMERCE 

National Oceanic and Atmospheric 

Administration 

50 CFR Part 635 

[Docket No. 180117042–8884–02; RTID 

0648–XA714] 

Atlantic Highly Migratory Species; 

Atlantic Bluefin Tuna Fisheries 

AGENCY: National Marine Fisheries 

Service (NMFS), National Oceanic and 

Atmospheric Administration (NOAA), 

Commerce. 

ACTION: Temporary rule; closure of the 

General category January fishery for 

2021. 

SUMMARY: NMFS closes the Atlantic 

bluefin tuna (BFT) General category 

fishery for the January subquota period. 

The intent of this closure is to prevent 

overharvest of the adjusted January 

subquota. 

DATES: Effective 11:30 p.m., local time, 

February 27, 2021, through May 31, 

2021. 

FOR FURTHER INFORMATION CONTACT: 

Sarah McLaughlin, sarah.mclaughlin@

noaa.gov, 978–281–9260, Nicholas 

Velseboer, nicholas.velseboer@

noaa.gov, 978–675–2168, or Larry Redd, 

Jr., larry.redd@noaa.gov, 301–427–8503. 

SUPPLEMENTARY INFORMATION: 

Regulations implemented under the 

authority of the Atlantic Tunas 

Convention Act (ATCA; 16 U.S.C. 971 et 

seq.) and the Magnuson-Stevens Fishery 

Conservation and Management Act 

(Magnuson-Stevens Act; 16 U.S.C. 1801 

et seq.) governing the harvest of BFT by 

persons and vessels subject to U.S. 

jurisdiction are found at 50 CFR part 

635. Section 635.27 subdivides the U.S. 

BFT quota recommended by the 

International Commission for the 

Conservation of Atlantic Tunas (ICCAT) 

among the various domestic fishing 

categories, per the allocations 

established in the 2006 Consolidated 

Atlantic Highly Migratory Species 

Fishery Management Plan (2006 

Consolidated HMS FMP) (71 FR 58058, 

October 2, 2006) and amendments, and 

in accordance with implementing 

regulations. 

Under § 635.28(a)(1), NMFS files a 

closure notice with the Office of the 

Federal Register for publication when a 

BFT quota (or subquota) is reached or is 

projected to be reached. Retaining, 

possessing, or landing BFT under that 

quota category is prohibited on and after 

the effective date and time of a closure 

notice for that category, for the 

remainder of the fishing year, until the 

opening of the subsequent quota period 

or until such date as specified. 

The base quota for the General 

category is 555.7 mt. See § 635.27(a). 

Each of the General category time 

periods (January, June through August, 

September, October through November, 

and December) is allocated a subquota 

or portion of the annual General 

category quota. Although it is called the 

‘‘January’’ subquota, the regulations 

allow the General category fishery under 

this quota to continue until the 

subquota is reached or March 31, 

whichever comes first. The baseline 

subquotas for each time period are as 

follows: 29.5 mt for January; 277.9 mt 

for June through August; 147.3 mt for 

September; 72.2 mt for October through 

November; and 28.9 mt for December. 

Any unused General category quota 

rolls forward from one time period to 

the next and is available for use in 

subsequent time periods within the 

fishing year. Effective January 1, 2021, 

NMFS transferred 19.5 mt of the 28.9- 

mt General category quota allocated for 

the December 2021 period to the 

January 2021 period, resulting in an 

adjusted subquota of 49 mt for the 

January period and a subquota of 9.4 mt 

for the December 2021 period (85 FR 

83832, December 23, 2020). Effective 

February 8, 2021, NMFS transferred an 

additional 26 mt from the Reserve 

category to the General category, in the 

same notice as NMFS made the annual 

reallocation of Purse Seine category 

quota to the Reserve category, resulting 

in an adjusted subquota of 75 mt for the 

General category 2021 January subquota 

period and 168 mt for the Reserve 

category (86 FR 8717, February 9, 2021). 

Closure of the January 2021 General 

Category Fishery 

Based on the best available General 

category BFT Landings information (i.e., 

57.7 mt landed as of February 25, 2021), 

as well as average catch rates and 

anticipated fishing conditions, NMFS 

projects that the adjusted General 

category January 2021 subquota of 75 mt 

will be reached shortly, and that the 

General category fishery should be 

closed. Therefore, retaining, possessing, 

or landing large medium or giant BFT 

by persons aboard vessels permitted in 

the Atlantic Tunas General category and 

the Atlantic HMS Charter/Headboat 

category (while fishing commercially) 

must cease at 11:30 p.m. local time on 

February 27, 2021. The General category 

will reopen automatically on June 1, 

2021, for the June through August 2021 

subquota period. This action applies to 

those vessels permitted in the General 

category, as well as to those HMS 

Charter/Headboat permitted vessels 


jbell on DSKJLSW7X2PROD with RULES