Vol. 79 Monday, 

No. 202 October 20, 2014 

Part II 

Environmental Protection Agency 

40 CFR Part 141 

Announcement of Preliminary Regulatory Determinations for Contaminants 

on the Third Drinking Water Contaminant Candidate List; Proposed Rule 


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62716 Federal Register / Vol. 79, No. 202 / Monday, October 20, 2014 / Proposed Rules 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 141 

[EPA–HQ–OW–2012–0155; FRL–9917–87– 

OW] 

Announcement of Preliminary 

Regulatory Determinations for 

Contaminants on the Third Drinking 

Water Contaminant Candidate List 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Request for public comment. 

SUMMARY: The Safe Drinking Water Act 

(SDWA), as amended in 1996, requires 

the Environmental Protection Agency 

(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 (NPDWR) for an unregulated 

contaminant. These unregulated 

contaminants are chosen from the 

Contaminant Candidate List (CCL), 

which SDWA requires the agency to 

publish every five years. EPA published 

the third CCL (CCL 3) in the Federal 

Register on October 8, 2009. This notice 

presents the preliminary regulatory 

determinations and supporting rationale 

for 5 of the 116 contaminants listed on 

CCL 3. The agency is making 

preliminary determinations to regulate 

one contaminant (i.e., strontium) and to 

not regulate four contaminants (i.e., 1,3- 

dinitrobenzene, dimethoate, terbufos 

and terbufos sulfone). EPA seeks 

comment on these preliminary 

determinations. 

DATES: Comments must be received on 

or before December 19, 2014, 60 days 

after publication in the Federal 

Register. 

ADDRESSES: Submit your comments, 

identified by Docket ID No. EPA–HQ– 

OW–2012–0155, by one of the following 

methods: 

• www.regulations.gov: Follow the 

online instructions for submitting 

comments. 

• Mail: Water Docket, Environmental 

Protection Agency, Mailcode: [28221T], 

1200 Pennsylvania Ave. NW., 

Washington, DC 20460. 

• Hand Delivery: EPA Docket Center, 

[EPA/DC] EPA West, Room 3334, 1301 

Constitution Ave. NW., Washington, 

DC. Such deliveries are only accepted 

during the Docket’s normal hours of 

operation, and special arrangements 

should be made for deliveries of boxed 

information. 

Instructions: Direct your comments to 

Docket ID No. EPA–HQ–OW–2012– 

0155. EPA’s policy is that all comments 

received will be included in the public 

docket without change and may be 

made available online at 

www.regulations.gov, including any 

personal information provided, unless 

the comment includes information 

claimed to be Confidential Business 

Information (CBI) or other information 

whose disclosure is restricted by statute. 

Do not submit information that you 

consider to be CBI or otherwise 

protected through www.regulations.gov. 

The www.regulations.gov Web site is an 

‘‘anonymous access’’ system, which 

means EPA will not know your identity 

or contact information unless you 

provide it in the body of your comment. 

If you send an email comment directly 

to EPA without going through 

www.regulations.gov your email address 

will be automatically captured and 

included as part of the comment that is 

placed in the public docket and made 

available on the Internet. If you submit 

an electronic comment, EPA 

recommends that you include your 

name and other contact information in 

the body of your comment and with any 

disk or CD–ROM you submit. If EPA 

cannot read your comment due to 

technical difficulties and cannot contact 

you for clarification, EPA may not be 

able to consider your comment. 

Electronic files should avoid the use of 

special characters, any form of 

encryption, and be free of any defects or 

viruses. For additional information 

about EPA’s public docket visit the EPA 

Docket Center homepage at http://

www.epa.gov/epahome/dockets.htm. 

For additional instructions on 

submitting comments, go to Section I.B 

of the SUPPLEMENTARY INFORMATION

section of this document. 

Docket: All documents in the docket 

are listed in the www.regulations.gov 

index. Although listed in the index, 

some information is not publicly 

available, e.g., CBI or other information 

whose disclosure is restricted by statute. 

Certain other material, such as 

copyrighted material, will be publicly 

available only in hard copy. Publicly 

available docket materials are available 

either electronically in 

www.regulations.gov or in hard copy at 

the Water Docket, EPA/DC, EPA West, 

Room 3334, 1301 Constitution Ave. 

NW., Washington, DC. The Public 

Reading Room is open from 8:30 a.m. to 

4:30 p.m., Monday through Friday, 

excluding legal holidays. The telephone 

number for the Public Reading Room is 

(202) 566–1744, and the telephone 

number for the Water Docket is (202) 

566–2426. 

FOR FURTHER INFORMATION CONTACT: 

Zeno Bain, Standards and Risk 

Management Division, Office of Ground 

Water and Drinking Water, Office of 

Water (Mailcode 4607M), 

Environmental Protection Agency, 1200 

Pennsylvania Ave. NW., Washington, 

DC 20460; telephone number: (202) 

564–5970; email address: bain.zeno@

epa.gov. For general information, 

contact the Safe Drinking Water Hotline, 

telephone number: (800) 426–4791. The 

Safe Drinking Water Hotline is open 

Monday through Friday, excluding legal 

holidays, from 10 a.m. to 4 p.m. Eastern 

time. 

SUPPLEMENTARY INFORMATION: 

I. General Information 

A. Does this action apply to me? 

Neither these preliminary regulatory 

determinations nor the final regulatory 

determinations, when published, 

impose any requirements on anyone. 

Instead, this action notifies interested 

parties of EPA’s preliminary regulatory 

determinations for five unregulated 

contaminants for comment. 

B. Tips for Preparing Your Comments 

When submitting comments, 

remember to: 

• Identify the rulemaking by docket 

number and other identifying 

information (subject heading, Federal 

Register date and page number). 

• Explain why you agree or disagree 

and suggest alternatives. 

• Describe any assumptions and 

provide any technical information and/ 

or data that you used. 

• Provide specific examples to 

illustrate your concerns, and suggest 

alternatives. 

• Explain your views as clearly as 

possible. 

• Make sure to submit your 

comments by the comment period 

deadline identified. 

ABBREVIATIONS USED IN THIS

DOCUMENT

Abbreviation Meaning 

μg/L ................. Micrograms per liter. 

ADAF .............. Age Dependent Adjustment 

Factor. 

AM .................. Assessment Monitoring. 

AMWA ............. Association of Metropolitan 

Water Agencies. 

ATSDR ............ Agency For Toxic Substances And Disease 

Registry. 

AWWA ............ American Water Works Association. 

BATs ............... Best Available Technologies. 


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ABBREVIATIONS USED IN THIS

DOCUMENT—Continued 

Abbreviation Meaning 

BMD ................ Benchmark Dose. 

BMDL .............. Benchmark Dose (95% 

Lower Confidence 

Bound). 

BW .................. Body Weight. 

CARC .............. Cancer Assessment Peer 

Review Committee. 

CAS ................ Chemical Abstracts Service. 

CASRN ........... Chemical Abstract Service 

Registry Number. 

CBI .................. Confidential Business Information. 

CCL ................. Contaminant Candidate List. 

CCL 1 ............. First Contaminant Candidate List. 

CCL 2 ............. Second Contaminant Candidate List. 

CCL 3 ............. Third Contaminant Candidate List. 

CCR ................ Consumer Confidence Report. 

CFR ................ Code of Federal Regulations. 

ChE ................. Cholinesterase. 

CMR ................ Chemical Monitoring Reform. 

CSF ................. Cancer Slope Factor. 

CUSIUR .......... Chemical Update System/

Inventory Update Rule. 

cVOC .............. Carcinogenic Volatile Organic Compounds. 

CW .................. Concentration in Water. 

CWS ............... Community Water System. 

CWSS ............. Community Water System 

Survey. 

DBP ................ Disinfection Byproduct. 

DBP ICR ......... Disinfection Byproduct Information Collection Rule. 

DDE ................ 1,1-Dichloro-2,2-bis(pchlorophenyl)ethylene. 

DSMRT ........... Distribution System Maximum Residence Time. 

DWI ................. Drinking Water Intake. 

DWS ............... Drinking Water Strategy. 

EFSA .............. European Food Safety Authority. 

ELCD .............. Electrolytic Conductivity Detection. 

EPA ................. Environmental Protection 

Agency. 

EPCRA ........... Emergency Planning And 

Community Right-ToKnow Act. 

EPTC .............. S-Ethyl 

propylthiocarbamate. 

EPTDS ............ Entry Point to the Distribution System. 

ESA ................. Ethanesulfonic Acid. 

EWG ............... Environmental Working 

Group. 

F ...................... Fraction of a 70 year lifetime applicable to the age 

period. 

FFQ ................. Food Frequency Questionnaire. 

FIFRA ............. Federal Insecticide, Fungicide, And Rodenticide 

Act. 

FR ................... Federal Register. 

GAC ................ Granular Activated Carbon. 

ABBREVIATIONS USED IN THIS

DOCUMENT—Continued 

Abbreviation Meaning 

GAO ................ Government Accountability 

Office. 

GC .................. Gas Chromatography. 

GW .................. Ground Water. 

HA ................... Health Advisory. 

HRL ................. Health Reference Level. 

ICR .................. Information Collection Rule. 

IOC ................. Inorganic Compound. 

IREDs ............. Interim Eligibility Decisions. 

IRIS ................. Integrated Risk Information 

System. 

Kg ................... Kilogram. 

LOAEL ............ Lowest Observed Adverse 

Effect Level. 

MCLG ............. Maximum Contaminant 

Level Goal. 

MDL ................ Method Detection Limit. 

mg/L ................ Milligrams per liter. 

mg/kg/day ....... Milligrams per kilogram per 

day. 

MDBP ............. Microbial Disinfection Byproduct. 

MOA ................ Mode of Action. 

MRL ................ Minimum Reporting Limit. 

MS .................. Mass Spectrometry. 

MTBE .............. Methyl Tertiary Butyl Ether. 

NAS ................ National Academy of 

Sciences. 

NAWQA .......... National Water Quality Assessment. 

NCFAP ............ National Center for Food 

and Agricultural Policy. 

NCI .................. National Cancer Institute. 

NCOD ............. National Drinking Water 

Contaminant Occurrence 

Database. 

NDBA .............. N-Nitroso-di-n-butylamine. 

NDEA .............. N-Nitrosodiethylamine. 

NDMA ............. N-Nitrosodimethylamine. 

NDPA .............. N-Nitroso-di-n-propylamine. 

NDPhA ............ N-Nitrosodiphenylamine. 

NDWAC .......... National Drinking Water Advisory Council. 

NIRS ............... National Inorganics And 

Radionuclides Survey. 

NMEA ............. N-Nitrosomethylethylamine. 

NOAEL ............ No Observed Adverse Effect Level. 

NPDES ........... National Pollutant Discharge 

Elimination System. 

NPDWR .......... National Primary Drinking 

Water Regulation. 

NPYR .............. N-Nitrosopyrrolidine. 

NRC ................ National Research Council. 

NREC .............. National Reconnaissance of 

Emerging Contaminants. 

NTP ................. National Toxicology Program. 

OA ................... Oxanilic Acid. 

OPP ................ Office of Pesticides Program. 

OW .................. Office of Water. 

PCCL .............. Preliminary Contaminant 

Candidate List. 

PCE ................ Tetrachloroethylene. 

PDP ................ Pesticide Data Program. 

PFOA .............. Perfluorooctanoic Acid. 

PFOS .............. Perfluorooctanesulfonic 

Acid. 

PHA ................ Provisional Health Advisory. 

PID .................. Photoionization Detection. 

ABBREVIATIONS USED IN THIS

DOCUMENT—Continued 

Abbreviation Meaning 

PMP ................ Pesticide Monitoring Program. 

PWS ................ Public Water System. 

QA ................... Quality Assurance. 

RD 1 ............... Regulatory Determinations 

1. 

RD 2 ............... Regulatory Determinations 

2. 

RD 3 ............... Regulatory Determinations 

3. 

RED ................ Reregistration Eligibility Decision. 

RfD .................. Reference Dose. 

RL ................... Reporting Limit. 

RSC ................ Relative Source Contribution. 

SAP ................. Scientific Advisory Panel. 

SDWA ............. Safe Drinking Water Act. 

SEPW ............. U.S. Senate Committee on 

Environment and Public 

Works. 

SS ................... Screening Survey. 

SSCTs ............ Small System Compliance 

Technologies. 

STORET ......... Storage And Retrieval 

(STORET) Data System. 

SW .................. Surface Water. 

SY ................... Six Year Review. 

SY3 ................. Six Year Review 3. 

TCE ................. Trichloroethylene. 

TPTH .............. Triphenyltin Hydroxide. 

TRED .............. Tolerance Reassessment 

Progress And Risk Management Decision. 

TRI .................. Toxic Release Inventory. 

TT ................... Treatment Technique. 

UCM ................ Unregulated Contaminant 

Monitoring. 

UCMR 1 .......... First Unregulated Contaminant Monitoring Regulation. 

UCMR 2 .......... Second Unregulated Contaminant Monitoring Regulation. 

UCMR 3 .......... Third Unregulated Contaminant Monitoring Regulation. 

UF ................... Uncertainty Factor. 

USDA .............. United States Department of 

Agriculture. 

USGS .............. United States Geological 

Survey. 

VOC ................ Volatile Organic Compound. 

WHO ............... World Health Organization. 

Table of Contents 

I. General Information 

A. Does this action apply to me? 

B. Tips for Preparing Your Comments 

II. Purpose and Background 

A. What is the purpose of this action? 

B. Background on the CCL and Regulatory 

Determinations 

1. Statutory Requirements for CCL and 

Regulatory Determinations 

2. The First Contaminant Candidate List 

(CCL 1) and Regulatory Determinations 

(RD 1) 


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1The MCLG is the ‘‘maximum level of a 

contaminant in drinking water at which no known 

or anticipated adverse effect on the health of 

persons would occur, and which allows an 

adequate margin of safety. Maximum contaminant 

level goals are non-enforceable health goals.’’ (40 

CFR 141.2; 42 U.S.C. 300g–1) 

2An NPDWR is a legally enforceable standard 

that applies to public water systems. An NPDWR 

sets a legal limit (called a maximum contaminant 

level or MCL) or specifies a certain treatment 

technique (TT) for public water systems for a 

specific contaminant or group of contaminants. The 

MCL is the highest level of a contaminant that is 

allowed in drinking water and is set as close to the 

MCLG as feasible using the best available treatment 

technology and taking cost into consideration. 

3The statute authorizes a nine month extension 

of this promulgation date. 

4Consumer information about Acanthamoeba for 

people who wear contact lenses can be found at 

http://water.epa.gov/action/advisories/

acanthamoeba/index.cfm. 

5The health advisories for CCL 1 can be found 

at http://water.epa.gov/drink/standards/

hascience.cfm. 

6The health advisories for CCL 2 can be found 

at http://water.epa.gov/drink/standards/

hascience.cfm. 

3. The Second Contaminant Candidate List 

(CCL 2) and Regulatory Determinations 

(RD 2) 

4. The Third Contaminant Candidate List 

(CCL 3) and Regulatory Determinations 

(RD 3) 

5. The Drinking Water Strategy 

6. Outreach for RD 3 (Stakeholder Meeting 

and Expert Review) 

III. Approach and Overall Outcome for RD 3 

A. Summary of the Approach and Overall 

Outcome for RD 3 

1. Phase 1 (Data Availability Phase) 

2. Phase 2 (Data Evaluation Phase) 

3. Phase 3 (Regulatory Determination 

Assessment Phase) 

B. Supporting Documentation for EPA’s 

Preliminary Determinations 

C. Analyses Used To Support the 

Preliminary Regulatory Determinations 

1. Evaluation of Adverse Health Effects 

2. Evaluation of Contaminant Occurrence 

and Exposure 

IV. Contaminant-Specific Discussions for the 

RD 3 Preliminary Regulatory 

Determinations 

A. Summary of the Preliminary Regulatory 

Determination 

B. Contaminant Profiles 

1. Dimethoate 

2. 1,3-Dinitrobenzene 

3. Strontium 

4–5. Terbufos and Terbufos Sulfone 

V. What is the status of the agency’s 

evaluation of chlorate and the 

nitrosamines? 

VI. What about the remaining CCL 3 

contaminants? 

VII. EPA’s Next Steps 

VIII. References 

Appendix: HRL Derivation with AgeRelated Exposure Factors 

II. Purpose and Background 

This section briefly summarizes the 

purpose of this action, the statutory 

requirements, and previous activities 

related to the CCL and regulatory 

determinations. 

A. What is the purpose of this action? 

The purpose of this action is to 

present and request comment on EPA’s 

preliminary regulatory determinations 

for five unregulated contaminants. The 

five contaminants include: Dimethoate, 

1,3-dinitrobenzene, strontium, terbufos, 

and terbufos sulfone. The agency is 

making preliminary determinations to 

regulate one contaminant (strontium) 

and to not regulate the remaining four 

contaminants (dimethoate, 1,3- 

dinitrobenzene, terbufos, and terbufos 

sulfone). EPA seeks comment on these 

preliminary determinations. The agency 

is also presenting and requesting 

comment on the process used for this 

round of regulatory determinations (i.e., 

RD 3), the supporting information, and 

the rationale used to make these 

preliminary decisions. 

B. Background on the CCL and 

Regulatory Determinations 

1. Statutory Requirements for CCL 

and Regulatory Determinations. Section 

1412(b)(1)(B)(i) of the 1996 Safe 

Drinking Water Act Amendments 

(SDWA) requires EPA to publish the 

CCL every five years. The CCL is a list 

of contaminants which are not subject to 

any proposed or promulgated national 

primary drinking water regulations 

(NPDWRs), 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 whether to 

regulate at least five contaminants from 

the CCL every five years. For EPA to 

make a determination to regulate a 

contaminant, SDWA requires the 

Administrator to determine that: 

(a) The contaminant may have an 

adverse effect on the health of persons; 

(b) the contaminant is known to occur 

or there is substantial likelihood that the 

contaminant will occur in public water 

systems with a frequency and at levels 

of public health concern; and 

(c) in the sole judgment of the 

Administrator, regulation of such 

contaminant presents a meaningful 

opportunity for health risk reduction for 

persons served by public water systems. 

If EPA determines that these three 

statutory criteria are met and makes a 

final determination to regulate a 

contaminant, the agency has 24 months 

to publish a proposed Maximum 

Contaminant Level Goal 1 (MCLG) and 

NPDWR.2 After the proposal, the agency 

has 18 months to publish and 

promulgate a final MCLG and NPDWR 

(SDWA section 1412(b)(1)(E)).3

2. The First Contaminant Candidate 

List (CCL 1) and Regulatory 

Determinations (RD 1). EPA published 

the final CCL 1, which contained 60 

chemical and microbiological 

contaminants, in the Federal Register 

(FR) on March 2, 1998 (63 FR 10273; 

USEPA, 1998). The agency made and 

published the final regulatory 

determinations for 9 of the 60 CCL 1 

contaminants in the FR on July 18, 

2003. The agency determined that 

NPDWRs were not necessary for any of 

these nine contaminants: 

Acanthamoeba, aldrin, dieldrin, 

hexachlorobutadiene, manganese, 

metribuzin, naphthalene, sodium, and 

sulfate (68 FR 42898; USEPA, 2003a). 

The agency posted information about 

Acanthamoeba 4 on the EPA Web site 

and issued health advisories 5 for 

manganese, sodium, and sulfate. 

3. The Second Contaminant 

Candidate List (CCL 2) and Regulatory 

Determinations (RD 2). The agency 

published the final CCL 2 in the FR on 

February 24, 2005, (70 FR 9071; USEPA, 

2005a) and carried forward the 51 

remaining chemical and microbial 

contaminants listed on CCL 1. The 

agency made and published the final 

regulatory determinations for 11 of the 

51 CCL 2 contaminants in the FR on 

July 30, 2008. The agency determined 

that NPDWRs were not necessary for 

any of these 11 contaminants: boron, the 

dacthal mono- and di-acid degradates, 

1,1-dichloro-2,2-bis(pchlorophenyl)ethylene (DDE), 1,3- 

dichloropropene (Telone), 2,4- 

dinitrotoluene, 2,6-dinitrotoluene, sethyl propylthiocarbamate (EPTC), 

fonofos, terbacil, and 1,1,2,2- 

tetrachloroethane (73 FR 44251; USEPA, 

2008a). The agency issued new or 

updated health advisories 6 for boron, 

dacthal degradates, 2,4-dinitrotoluene, 

2,6-dinitrotoluene and 1,1,2,2- 

tetrachloroethane. 

4. The Third Contaminant Candidate 

List (CCL 3) and Regulatory 

Determinations (RD 3). The agency 

published the final CCL 3, which listed 

116 contaminants, in the FR on October 

8, 2009 (74 FR 51850; USEPA, 2009a). 

In developing CCL 3, EPA improved and 

built upon the process that was used for 

CCL 1 and CCL 2. The new CCL 3 

process was based on substantial expert 

input and recommendations from the 

National Academy of Science’s (NAS) 

National Research Council (NRC) and 

the National Drinking Water Advisory 

Council (NDWAC) as well as input from 

the public. Based on these consultations 

and input, EPA developed a multi-step 

process to select candidates for the final 


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7More information about the DWS can be found 

at water.epa.gov/lawsregs/rulesregs/sdwa/

dwstrategy/. 

8http://water.epa.gov/lawsregs/rulesregs/sdwa/

dwstrategy/. 

CCL 3, which included the following 

key steps: 

(a) Identification of a broad universe 

of ∼7,500 potential drinking water 

contaminants (the CCL 3 Universe); 

(b) screening the CCL 3 Universe to a 

preliminary CCL (PCCL) of ∼600 

contaminants based on the potential to 

occur in PWSs and the potential for 

public health concern; and 

(c) evaluation of the PCCL 

contaminants based on a more detailed 

review of the occurrence and health 

effects data to identify a final list of 116 

CCL 3 contaminants. 

The development of the CCL, 

regulatory determinations, and any 

subsequent rulemaking should be 

viewed as a progression where each 

process builds upon the previous 

process, including the collection of data 

and analyses conducted. The agency’s 

improvements in developing CCL 3 

provide an excellent foundation for RD 

3 by enhancing EPA’s ability to identify 

contaminants of concern for drinking 

water. 

While this notice focuses on the 

preliminary regulatory determinations 

for 5 of the 116 CCL 3 contaminants, it 

is important to note that the agency 

made and published a final 

determination to regulate one CCL 3 

contaminant, perchlorate, on February 

11, 2011 (76 FR 7762; USEPA, 2011a). 

Additional information about CCL 3 and 

the perchlorate final determination can 

be found in the October 8, 2009 (74 FR 

51850; USEPA, 2009a) and February 11, 

2011 (76 FR 7762; USEPA, 2011a) 

Federal Register notices, respectively. 

Sections III and IV in this notice provide 

more detailed information about the 

approach and outcome used for RD 3 

and the contaminant-specific regulatory 

determinations. 

5. The Drinking Water Strategy. In 

March 2010, EPA announced the 

agency’s new Drinking Water Strategy 

(DWS),7 which is aimed at finding ways 

to strengthen the protection of public 

health from contaminants in drinking 

water. The new vision is intended to 

streamline decision-making, expand 

protection under existing laws, and 

promote cost-effective new technologies 

to meet the needs of rural, urban, and 

other water-stressed communities. The 

four principles underlying the DWS are: 

(a) Address contaminants as groups 

rather than one at a time so that 

enhancement of drinking water 

protection can be achieved costeffectively. 

(b) Foster development of new 

drinking water technologies to address 

health risks posed by a broad array of 

contaminants. 

(c) Use the authority of multiple 

statutes to help protect drinking water. 

(d) Partner with States to develop 

shared access to all PWSs monitoring 

data. 

The first principle (i.e., addressing 

contaminants as groups) has a direct 

bearing on RD 3 and how to designate 

the contaminants for analysis, 

determination and subsequent 

regulation; that is, should they be 

considered individually or as a group. 

Although the agency has previously 

regulated contaminants as groups (e.g., 

total trihalomethanes, total haloacetic 

acids, gross alpha radionuclides, gross 

beta and photon emitters, etc.), all of the 

determinations for RD 1 and RD 2 were 

made on individual contaminants. As 

part of the DWS, the agency identified 

several factors to evaluate which 

contaminants might effectively be 

regulated as a group and considered 

these factors in evaluating contaminant 

groups for RD 3. All the factors do not 

have to be met, but the more factors that 

are met, the more suitable it may be to 

regulate the contaminants as a group. 

These factors include whether the 

contaminants in the group: 

(a) Have a similar health endpoint, 

(b) can be measured by the same 

analytical methods, 

(c) can be treated using the same 

technology or treatment technique 

approach and/or 

(d) have been shown to occur 

individually (and possibly co-occur if 

data are available). 

EPA conducted extensive national 

outreach to solicit input from 

stakeholders on the DWS and how best 

to address groups of contaminants. 

Stakeholders generally agreed that while 

public health protection is of paramount 

importance, the grouping factors 

previously listed were some of the other 

important factors to consider in 

evaluating which contaminants would 

work best in a group regulation. Several 

CCL 3 contaminants (as well as non-CCL 

3 contaminants) belong to contaminant 

groups that underwent consideration for 

regulation during the RD 3 process. 

In February 2011,8 the agency decided 

to address carcinogenic volatile organic 

compounds (cVOCs) as a group in a 

separate and concurrent regulatory 

process (which the agency expects to 

release in late 2014). Some of the cVOCs 

being considered include unregulated 

cVOCs listed on CCL 3 (e.g., 1,2,3- 

trichloropropane). While the cVOC 

group is being evaluated in a separate 

regulatory process, the same factors 

used to group cVOCs (i.e., similar health 

endpoint, measured by the same 

analytical method, similar treatment 

technique approach, etc.) were used to 

evaluate groups of contaminants for RD 

3 as well (e.g., nitrosamines, 

chloroacetanilides, etc.). Although EPA 

evaluated the nitrosamines and 

chloroacetanilides groups as part of the 

RD 3 process, in the end, EPA decided 

not to make any preliminary 

determinations for these groups under 

RD 3. 

The SDWA requires EPA to review 

each existing NPDWR at least once 

every six years and revise them, if 

appropriate. The purpose of the review, 

called the Six Year Review (SY), is to 

identify those NPDWRs for which 

current health effects assessments, 

changes in technology, and/or other 

factors provide a health or technical 

basis to support a regulatory revision 

that will maintain or provide for greater 

protection of the health of persons. In 

contrast, the RD process is intended to 

address currently unregulated 

contaminants. The agency will review 

the existing Microbial Disinfection 

Byproduct (MDBP) regulations as part of 

the third Six Year Review (SY3). 

Because chlorate and nitrosamines are 

disinfection byproducts (DBPs) that can 

be introduced or formed in public water 

systems partly because of disinfection 

practices, the agency believes it is 

important to evaluate these unregulated 

DBPs in the context of the review of the 

existing DBP regulations. DBPs need to 

be evaluated collectively, because the 

potential exists that the chemical 

disinfection used to control a specific 

DBP could affect the concentrations of 

other DBPs. Therefore, the agency is not 

making a regulatory determination for 

chlorate and nitrosamines at this time. 

The agency expects to complete the 

review of these DBPs by the end of 

2015. 

6. Outreach for RD 3 (Stakeholder 

Meetings and Expert Review). 

EPA sought external advice and 

expert input for RD 3 by convening two 

public stakeholder meetings and 

conducting an Expert Review panel. On 

March 3, 2011, EPA held an 

Environmental Justice (EJ) Stakeholder 

meeting in Washington, DC to solicit 

input on RD 3 and environmental 

justice issues. Approximately 90 

stakeholders participated (either by 

phone or in person) including 

representatives of children’s advocacy 

groups, environmental organizations, 

community action groups, the drinking 

water industry, and State drinking water 

and public health programs. 

Stakeholders did not identify any EJ 


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9Subsequent to the June 2011 stakeholder 

meeting and before the October 2011 Expert 

Review, EPA identified two additional 

contaminants for the shortlist, bringing the total to 

34. In response to the Expert Review comments, an 

additional contaminant was added to the short list, 

bringing the final total to 35 CCL 3 contaminants. 

10The U.S. Senate Committee on Environment 

and Public Works full committee hearing, entitled 

‘‘Oversight Hearing on the Environmental 

Protection Agency’s Implementation of the Safe 

Drinking Water Act’s Unregulated Drinking Water 

Contaminants Program’’ can be found at (http://

www.epw.senate.gov/public/

index.cfm?FuseAction=Hearings.Hearing&Hearing_

ID=fc5a8756-802a-23ad-454a-b9eeb7bf1c36). 

11Under the statute, SDWA criterion 3 of Section 

1412(b)(1)(A) is solely the Administrator’s decision. 

issues specific to RD 3. On June 16, 

2011, EPA held another public 

Stakeholder Meeting in Washington, 

DC, to disseminate information on the 

progress of RD 3 and solicit input from 

stakeholders, the public, and other 

interested groups. Forty-six participants 

attended including representatives from 

States, environmental and public health 

organizations, drinking water systems, 

chemical manufacturers, local 

governments, and academia. EPA 

presented and discussed: (a) The 

approach used to narrow the 

contaminants listed on CCL 3 and 

identify potential candidates for RD 3 

(with a focus on those occurring at 

levels of health concern in drinking 

water) and (b) the background, health, 

and occurrence information for a ‘‘short 

list’’ of 32 9 contaminants being 

evaluated as potential RD 3 candidates. 

Stakeholders asked questions and 

provided comments about the approach 

as well as the health and occurrence 

information presented on several 

contaminants. One stakeholder 

provided additional health information 

on the chloroacetanilides and submitted 

a letter requesting that EPA regulate 

these compounds with an NPDWR 

(USEPA, 2011b). A summary of the June 

16, 2011, meeting is provided in the 

docket for this action (USEPA, 2011c). 

In May 2011, the Government 

Accountability Office (GAO) released a 

report entitled, ‘‘EPA Should Improve 

Implementation of Requirements on 

Whether to Regulate Additional 

Contaminants’’ (GAO, 2011). 

Specifically for regulatory 

determinations, GAO recommended that 

the agency develop criteria to identify 

contaminants of greatest public health 

concern and be more transparent, clear, 

and consistent by developing policies/

guidance to interpret the SDWA criteria 

and make determinations (i.e., include 

thresholds for positive findings, factors 

for determining adequacy of occurrence/ 

health data to make determinations, an 

approach for evaluating health effects 

on sensitive subpopulations, a process 

for presenting key information in 

documents, etc). In response to 

questions regarding the GAO report at a 

July 2011 U.S. Senate Committee on 

Environment and Public Works (SEPW) 

hearing,10 EPA committed to consulting 

with an independent panel of scientists 

on the RD 3 process to determine how 

SDWA criteria 1 and 2 are evaluated,11

how the best available science is used 

to make decisions, how the 

contaminants of greatest public health 

risk are assessed, and how vulnerable 

populations (especially children) are 

considered. EPA also committed to 

making the process used for regulatory 

determinations publicly available and to 

review the process every five years as 

EPA conducts the regulatory 

determination cycle. 

To implement the commitment, EPA 

convened a panel of experts in October 

2011 to provide an independent review 

of the approach used for RD 3, which 

EPA described in a draft of the 

document entitled, ‘‘Protocol for the 

Regulatory Determinations 3’’ (USEPA, 

2014a). The Expert Review panel 

included seven experts representing one 

or more of the following areas of 

expertise: health effects evaluation, 

drinking water occurrence/exposure 

information evaluation, State drinking 

water perspective, PWS perspective, 

and/or some familiarity with the RD 3 

process (including the Contaminant 

Candidate List). The review involved a 

three-week paper review of the October 

2011 Draft RD 3 Protocol document and 

an in-person meeting held in 

Washington DC, on October 26 and 27, 

2011. Panel members were encouraged 

to provide comments as individuals 

based upon their expertise and 

background, not as representatives of 

any respective organizational affiliation. 

The information and input provided by 

the expert reviewers assisted the agency 

in revising and clarifying the approach 

used for the RD 3 process. A summary 

of the October 26–27, 2011, meeting and 

the expert reviewers’ comments 

(USEPA, 2011d), as well as the protocol 

document (USEPA, 2014a), are provided 

in the docket for this action. 

III. Approach and Overall Outcome for 

RD 3 

This section describes (a) the 

approach EPA uses to identify and 

evaluate contaminants for the agency’s 

third round of Regulatory 

Determinations (RD 3) along with the 

overall outcome of applying this 

approach, (b) the supporting RD 3 

documentation, and (c) the technical 

analyses and sources of health and 

occurrence information. 

A. Summary of the Approach and 

Overall Outcome for RD 3 

The three phases of the RD 3 Process 

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

the Data Evaluation Phase, and (3) the 

Regulatory Determination Assessment 

Phase. Figure 1 provides a brief 

overview of the process EPA uses to 

identify which CCL 3 contaminants are 

candidates for regulatory determinations 

and the SDWA statutory criteria 

considered in making the regulatory 

determinations. For more detailed 

information on the three phases of the 

RD 3 process please refer to the 

‘‘Protocol for the Regulatory 

Determinations 3’’ (USEPA, 2014a). 


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12These may be assessments that are 

geographically distributed across the nation but not 

intended to be statistically representative of the 

nation. Examples include EPA’s Disinfection By 

Product Information Collection Request and various 

USGS water quality surveys. 

1. Phase 1 (Data Availability Phase) 

In Phase 1, the Data Availability 

Phase, the agency identifies 

contaminants that may have sufficient 

health and occurrence data to proceed 

to Phase 2 and be listed on a ‘‘short list’’ 

for further evaluation. With regard to 

sufficient health effects data used to 

identify potential adverse health 

effect(s), the agency considers whether a 

peer-reviewed health risk assessment is 

available or in process from one of the 

following sources: (a) The agency’s 

Integrated Risk Information System 

(IRIS); (b) the agency’s Office of Water 

(OW); (c) the agency’s Office of 

Pesticide Programs (OPP); (d) the 

National Academy of Sciences (NAS); 

(e) the Agency for Toxic Substances and 

Disease Registry (ATSDR); and/or (f) the 

World Health Organization (WHO). For 

a non-EPA health assessment (i.e., NAS, 

ATSDR, WHO) to be utilized for 

regulatory determinations, the health 

assessment must use comparable 

methods, standards, and guidelines to 

an EPA health assessment. If a health 

assessment is not available from one of 

these sources, then the contaminant is 

not considered for RD 3. 

In regard to sufficient occurrence 

data, the agency considers the 

availability of nationally representative 

finished water data and whether other 

finished water data are available that 

indicate known and/or likely 

occurrence in PWSs. Occurrence data 

from the following sources, 

administered or overseen by EPA, is 

considered nationally representative: (a) 

The Second Unregulated Contaminant 

Monitoring Regulation (UCMR 2); (b) 

the First Unregulated Contaminant 

Monitoring Regulation (UCMR 1) 

Assessment Monitoring; (c) the 

Unregulated Contaminant Monitoring 

(UCM) program; and/or (d) the National 

Inorganics and Radionuclides Survey 

(NIRS). 

If nationally representative data are 

not available, EPA identifies and 

evaluates other finished water data, 

which may include other national 

assessments as well as regional, State, 

and more localized finished water 

assessments. These other national 

finished water data include assessments 

that are geographically distributed 

across the nation but not intended to be 

statistically representative of the nation. 

These other finished water data include 

the following sources for consideration 

in the regulatory determination process: 

(a) Finished water assessments for 

Federal agencies (e.g., EPA and the 

United States Geological Survey 

(USGS)); 12 (b) state-level finished water 

monitoring data; (c) research performed 

by institutions and universities (e.g., 

scientific literature); and/or (d) other 

supplemental finished water monitoring 

surveys (e.g., Pesticide Monitoring 

Program (PMP), National 

Reconnaissance of Emerging 

Contaminants (NREC), and other 

targeted surveys or localized State/

Federal monitoring surveys). 

EPA prefers to have nationally 

representative data available when 

making regulatory determinations but 

may also use these other sources of 

finished water occurrence data to 

evaluate the contaminant and determine 

if there is ‘‘substantial likelihood that 

the contaminant will occur in PWSs 

with a frequency and at levels of public 

health concern.’’ If there is sufficient 

occurrence in these other finished water 

data sources, EPA uses this information 

to address the occurrence-related 

aspects of the statutory criteria when 

deciding to regulate a contaminant. 

However, it is difficult to determine that 

a contaminant is not occurring or not 

likely to occur based on these other 

sources of finished water data because 

the data are limited in scope and the 

contaminant could be occurring in other 

parts of the country that were not 

monitored. 

EPA also considers the availability of 

analytical methods for monitoring, and 

whether the contaminant is part of a 

contaminant group based on factors 

defined by the Drinking Water Strategy 


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13See section III.C for a discussion about how 

EPA derives an HRL. EPA developed the CCL 3 

HRLs using the most recent health data available 

during the CCL 3 process. EPA uses 1⁄2 CCL 3 HRL 

as a conservative value to identify contaminants 

with potential occurrence of concern during Phase 

1 of the RD process. The CCL 3 HRLs for the 116 

contaminants can be found at (http://water.epa.gov/ 

scitech/drinkingwater/dws/ccl/upload/Final-CCL-3- 

Contaminant-Information-Sheets.pdf). After 

updating, completing and peer-reviewing health 

assessments as necessary, the final HRL used for RD 

3 may be different than the CCL 3 HRL. 

(DWS) (see section II.B.5). After 

conducting the health and occurrence 

data availability assessments, the agency 

identifies those contaminants and 

contaminant groups that meet the 

following Phase 1 data availability 

criteria: 

(a) A peer-reviewed health assessment 

is available or in process, and 

(b) A widely available analytical 

method for monitoring is available, and 

(c) Either nationally representative 

finished water occurrence data are 

available, or other finished water 

occurrence data shows occurrence at 

levels >1⁄2 CCL 3 health reference level 

(HRL).13

If a contaminant meets these three 

criteria, it is placed on a ‘‘short list’’ and 

proceeds to Phase 2. EPA also evaluated 

whether the contaminant could be 

considered as part of a group using the 

DWS factors discussed earlier in section 

II.B.5. After evaluating the 116 CCL 3 

contaminants in Phase 1, the agency 

identified 35 CCL 3 contaminants and 

two non-CCL 3 contaminants (listed in 

Table 1) to evaluate further in Phase 2. 

The non-CCL 3 contaminants were 

included because they are part of a 

larger group (nitrosamines) that also 

includes a number of CCL 3 

contaminants. 

TABLE 1—CONTAMINANTS PROCEEDING FROM PHASE 1 TO PHASE 2 

1, 1, 1, 2-Tetrachloroethane 1 3 .............................................................................................................. Metolachlor oxanilic acid (OA).1 3

1, 2, 3-Trichloropropane 1 3 .................................................................................................................... Molinate.1

1, 3-Dinitrobenzene 1 ............................................................................................................................. Molybdenum.1

1, 4-Dioxane 2 ........................................................................................................................................ Nitrobenzene.1 3

Acephate 2 .............................................................................................................................................. N-Nitroso-di-n-butylamine (NDBA).135

Acetochlor 1 3 .......................................................................................................................................... N-Nitrosodiethylamine (NDEA).1 3

Acetochlor ethanesulfonic acid (ESA) 1 3 ............................................................................................... N-Nitrosodimethylamine (NDMA).1 3

Acetochlor oxanilic acid (OA) 1 3 ............................................................................................................ N-Nitroso-di-n-propylamine (NDPA).1 3

Alachlor ethanesulfonic acid (ESA) 1 3 ................................................................................................... N-Nitrosodiphenylamine (NDPhA).3

Alachlor oxanilic acid (OA) 1 3 ................................................................................................................ N-Nitrosomethylethylamine (NMEA).135

Chlorate 2 ............................................................................................................................................... N-Nitrosopyrrolidine (NPYR).1 3

Cobalt 1 ................................................................................................................................................... Perfluorooctanesulfonic acid (PFOS).2

Dimethoate 1 ........................................................................................................................................... Perfluorooctanoic acid (PFOA).2

Disulfoton 4 ............................................................................................................................................. RDX.1

Diuron 4 .................................................................................................................................................. Strontium.1

Methyl bromide (Bromomethane) 1 ........................................................................................................ Terbufos.2 3

Methyl tert-butyl ether 1 .......................................................................................................................... Terbufos sulfone.1 3

Metolachlor 1 3 ......................................................................................................................................... Vanadium.1

Metolachlor ethanesulfonic acid (ESA) 1 3 ..............................................................................................

1 Has nationally representative finished water data and available or in process health assessment. 

2 Has other finished water data (occurrence at levels >1⁄2 CCL 3 HRL) and available or in process health assessment. 3 Component of a contaminant group and will be further evaluated in Phase 2. 

4One exception to the criterion of having available nationally representative drinking water data applies to contaminants monitored in the 

UCMR 1 Screening Survey (SS). As noted in section 5, the UCMR 1 SS is a statistically defined, national sample of 300 PWSs. Because this 

survey only includes 300 systems, the agency identified and compiled additional supplemental data to compliment the UCMR 1 SS data for 

these contaminants that proceed to Phase 2 for further evaluation. 5A non-CCL 3 contaminant that is part of the nitrosamine group. 

The remaining 81 CCL 3 contaminants 

(listed in Table 2) did not meet either or 

both of the Phase 1 data availability 

criteria above and were not considered 

further for RD 3. 

TABLE 2—CONTAMINANTS NOT PROCEEDING FROM PHASE 1 TO PHASE 2 

Has nationally representative finished water data but no health assessment 

1,1-Dichloroethane ................................................................................................................................. Halon 1011 (Bromochloromethane). 

3-Hydroxycarbofuran .............................................................................................................................. n-Propylbenzene. 

Chloromethane (Methyl chloride) ........................................................................................................... sec-Butylbenzene. 

Germanium ............................................................................................................................................ Tellurium. 

Has available or in process health assessment and other finished drinking water data but no occurrence at levels >1⁄2 CCL 3 HRL 

1-Butanol ................................................................................................................................................ Formaldehyde. 

Acrolein .................................................................................................................................................. Methamidophos. 

alpha-Hexachlorocyclohexane ............................................................................................................... Oxydemeton-methyl. 

Bensulide ............................................................................................................................................... Oxyfluorfen. 

Benzyl chloride ....................................................................................................................................... Permethrin. 

Captan .................................................................................................................................................... Profenofos. 


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14HRLs are not final determinations about the 

level of a contaminant in drinking water that is 

necessary to protect any particular population and 

are derived prior to development of a complete 

exposure assessment. HRLs are risk derived 

concentrations against which to evaluate the 

occurrence data to determine if contaminants occur 

at levels of potential public health concern. 

TABLE 2—CONTAMINANTS NOT PROCEEDING FROM PHASE 1 TO PHASE 2—Continued 

Dicrotophos ............................................................................................................................................ Tebuconazole. 

Ethoprop ................................................................................................................................................. Tribufos. 

Ethylene glycol ....................................................................................................................................... Vinclozolin. 

Ethylene thiourea (Maneb) .................................................................................................................... Ziram. 

Fenamiphos ...........................................................................................................................................

Has other finished drinking water data but no health assessment 

17-alpha-Estradiol .................................................................................................................................. Estriol. 

Acetaldehyde ......................................................................................................................................... Estrone. 

Aniline .................................................................................................................................................... Ethinyl Estradiol (17-alpha-ethynyl estradiol). 

Butylated hydroxyanisole ....................................................................................................................... HCFC-22. 

Cyanotoxins (Anatoxin-a, Cylindrospermopsin, Microcystin-LR) ........................................................... Hexane. 

Equilenin ................................................................................................................................................ Mestranol. 

Equilin .................................................................................................................................................... Norethindrone (19-Norethisterone). 

Erythromycin .......................................................................................................................................... Naegleria fowleri.* 

Estradiol (17-beta-Estradiol) ..................................................................................................................

Does not have nationally representative or other finished water data 

1,3-Butadiene ......................................................................................................................................... Quinoline. 

2-Methoxyethanol ................................................................................................................................... Tebufenozide. 

2-Propen-1-ol ......................................................................................................................................... Thiodicarb. 

4,4′-Methylenedianiline .......................................................................................................................... Thiophanate-methyl. 

Acetamide .............................................................................................................................................. Toluene diisocyanate. 

Clethodim ............................................................................................................................................... Triethylamine. 

Cumene hydroperoxide .......................................................................................................................... Triphenyltin hydroxide (TPTH). 

Dimethipin .............................................................................................................................................. Urethane. 

Ethylene oxide ....................................................................................................................................... Campylobacter jejuni. 

Hydrazine ............................................................................................................................................... Escherichia coli (0157). 

Methanol ................................................................................................................................................ Helicobacter pylori. 

Nitroglycerin ........................................................................................................................................... Hepatitis A virus. 

N-Methyl-2-pyrrolidone ........................................................................................................................... Salmonella enteric. 

o-Toluidine ............................................................................................................................................. Shigella sonnei. 

Oxirane, methyl- .....................................................................................................................................

Does not have a widely available analytical method for occurrence monitoring 

Adenovirus ............................................................................................................................................. Legionella pneumophila. 

Caliciviruses ........................................................................................................................................... Mycobacterium avium. 

Enterovirus .............................................................................................................................................

Not within scope of this RD 3 since regulatory determination made in February 2011 

Perchlorate .............................................................................................................................................

* Does not have a widely available analytical method for occurrence monitoring. 

2. Phase 2 (Data Evaluation Phase) 

Contaminants that meet the minimum 

health and occurrence data availability 

requirements in Phase 1 are advanced to 

the Phase 2 evaluation. In addition to 

health and occurrence information data 

assessed in Phase 1, the agency collects 

additional health and occurrence data 

and more thoroughly evaluates this 

information to identify a list of 

contaminants that should proceed to 

Phase 3. The agency uses the following 

steps to develop this list: (a) Derive a 

draft HRL 14 (See section III.C) for each 

contaminant, (b) compare all occurrence 

data against the draft HRL (along with 

the analytical method minimum 

reporting limit (MRL)), (c) identify 

contaminants that occur at levels and 

frequencies of public health concern, 

and (d) identify contaminants that have 

no or low occurrence at levels of public 

health concern. 

Using the available health effects 

assessments, the agency derives a draft 

HRL and then evaluates this HRL value 

(along with the analytical method MRL), 

against the concentration values 

compiled for the nationally 

representative or other finished water 

occurrence information identified in 

Phase 1. The agency also gathers 

additional occurrence data and 

information on monitoring in ambient 

or source water (relative to the draft 

HRL and the analytical method MRL), 

production, use, release to the 

environment, and persistence and 

mobility. In Phase 2, the agency 

specifically focuses its efforts to identify 

those contaminants or contaminant 

groups that are occurring or have 

substantial likelihood to occur at levels 

and frequencies of public health 

concern. To identify such contaminants, 

the agency considers the following 

information: 

(a) How many samples (# and %) have 

detections > draft HRL and 1⁄2 draft HRL 

in the nationally representative and 

other finished water occurrence data? 

(b) How many systems (# and %) have 

detections > draft HRL and 1⁄2 draft HRL 

in the nationally representative and 

other finished water occurrence data? 

and 

(c) Is the contaminant associated with 

a contaminant group that is of public 


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15Carcinogenic Volatile Organic Compounds 

(including 1,2,3-trichloropropane) are being 

evaluated in a separate regulatory effort. 

16Note that the non-national data tend to be 

limited in scope and EPA does not use these data 

alone to support a determination that the 

contaminant is not or is not substantially likely to 

‘‘occur in PWSs with a frequency and at levels of 

public health concern,’’ which would therefore be 

a decision ‘‘not to regulate’’ (i.e., negative 

determination). 

health concern and is being considered 

as part of the DWS? 15

(d) Are there uncertainties or 

limitations with the data and/or 

analyses, such as the age of the dataset, 

limitation of the detection limit (i.e., 

MRL > draft HRL) and/or 

representativeness of the data (e.g., 

limited to a specific region) that may 

cause misestimation of occurrence in 

finished water at levels and frequency of 

public health concern? 

After identifying contaminants that 

are occurring at levels and frequencies 

of public health concern to proceed to 

Phase 3, the agency evaluates the 

remaining contaminants on the ‘‘short 

list’’ to determine which contaminants 

have no or low occurrence at levels of 

health concern that could also proceed 

to Phase 3 by considering the following 

factors: 

(a) Does the contaminant have 

nationally representative finished water 

data showing no or low # or % of 

detections > draft HRL? 16

(b) If a contaminant has other finished 

water data in addition to nationally 

representative finished water data, does 

it support no or low potential for 

occurrence in drinking water? 

(c) Does additional occurrence 

information of known quality support 

low or no occurrence or potential for 

occurrence in drinking water? For 

example, is the occurrence in ambient/ 

source water at levels below the draft 

HRL? Are releases to the environment or 

use/production decreasing over time? 

(d) There are no critical information/ 

data gaps after evaluating the available 

health or occurrence data; and 

(e) The contaminant is not included 

or evaluated with a group of 

contaminants based on the factors 

defined by the DWS. 

After evaluating these factors and 

whether a contaminant appears to have 

sufficient data to evaluate the statutory 

criteria for regulatory determination, the 

agency determines if the contaminant 

should proceed to Phase 3. After 

evaluating the ‘‘short list’’ contaminants 

(listed in Table 1), the agency identified 

10 CCL 3 contaminants and 2 non-CCL 

3 contaminants (listed in Table 3) that 

were within one of the following Phase 

2 data evaluation categories to proceed 

to Phase 3: 

(a) A contaminant or part of a 

contaminant group occurring or likely to 

occur at levels and frequencies of public 

health concern, or 

(b) A contaminant not occurring or 

likely to occur at levels and frequencies 

of public health concern and no data 

gaps. 

TABLE 3—CONTAMINANTS PROCEEDING FROM PHASE 2 TO PHASE 3 

Chlorate 1 3 ................................................................................................................................................ N-Nitrosodiethylamine (NDEA).1

Dimethoate 2 ............................................................................................................................................ N-Nitrosomethylethylamine (NMEA).1 4

1,3-Dinitrobenzene 2 ................................................................................................................................. N-Nitrosopyrrolidine (NPYR).1

N-Nitroso-di-n-butylamine (NDBA) 1 4 ....................................................................................................... Strontium.1 3

N-Nitrosodimethylamine (NDMA) 1 ........................................................................................................... Terbufos.2

N-Nitroso-di-n-propylamine (NDPA) 1 ....................................................................................................... Terbufos Sulfone.2

1A contaminant or part of a contaminant group occurring or likely to occur at levels and frequencies of public health concern. 

2A contaminant not occurring or likely to occur at levels and frequencies of public health concern and no data gaps. 

3The UCMR 3 includes sampling at both the entry point to the distribution system (EPTDS) and distribution system maximum residence time 

(DSMRT) for this contaminant (77 FR 26071, May 2, 2012). For some contaminants, including disinfection byproducts and inorganics, occurrence 

values may differ between the EPTDS and the DSMRT due to dynamics within the distribution system such as contaminant degradation, formation, accumulation and release. 4A non-CCL 3 contaminant that is part of the nitrosamine group. 

Note that the agency does not have a 

threshold or a bright line for occurrence 

in drinking water that triggers whether 

a contaminant is of public health 

concern. There are a number of factors 

to consider in developing thresholds, 

some of which include the health 

effect(s), the potency of the 

contaminant, the level at which the 

contaminant is found in drinking water, 

how frequently the contaminant is 

found, the geographic distribution 

(national, regional, or local occurrence), 

other possible sources of exposure, and 

potential impacts on sensitive 

populations or lifestages, etc. Given the 

many possible combinations of factors 

and the constantly evolving science, 

EPA believes it is better to analyze each 

contaminant and characterize and 

present the best available information 

that helps identify whether the 

occurrence of a contaminant is of public 

health concern. In the end, the 

determination of whether there is a 

meaningful opportunity for health risk 

reduction by regulation of a 

contaminant in drinking water is a 

highly contaminant-specific one that 

takes into consideration a large number 

of factors. 

The remaining 25 CCL 3 contaminants 

(listed in Table 4) did not proceed to 

Phase 3 and were not considered for RD 

3 because of one or more of the 

following critical health, occurrence, 

and/or other data gaps: 

(a) An updated health assessment is 

needed, but was not completed by fall 

2011; 

(b) A health assessment is in process, 

but was not completed by fall 2011; 

(c) Critical health effects gap (e.g., 

lack of data to support quantification for 

the oral route of exposure); 

(d) Lacked nationally representative 

occurrence data; 

(e) Insufficient other finished water 

occurrence data to demonstrate 

occurrence at levels and frequencies of 

public health concern (although it may 

have some levels of public health 

concern); 

(f) Individual contaminants that were 

part of a group but lacked a widely 

available analytical method for 

occurrence monitoring; and 

(g) Critical occurrence data gap (e.g., 

inconsistent results and/or trends in 

occurrence data, significant uncertainty 

in occurrence analyses and/or data). 

Table 4 identifies the health, 

occurrence, and/or other data gaps that 

prevented the following 25 

contaminants from moving forward for 

RD 3. The agency continues to conduct 

research, collect information or find 

other avenues to fill the data and 

information gaps identified in Table 4. 


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TABLE 4—DATA AND RATIONALE SUMMARY OF THE 25 CONTAMINANTS NOT PROCEEDING TO PHASE 3 

No. Contaminant Health data 

available 

Occurrence 

data available Rationale 

1 ................... 1,4-Dioxane ............................. Yes ............... No 1 .............. Occurrence data gaps (no nationally representative finished 

water data or sufficient other finished water data). 

2 ................... Acephate .................................. Yes ............... No ................ Occurrence data gaps (no nationally representative finished 

water data or sufficient other finished water data). 

3 ................... Acetochlor ................................ No ................ Yes ............... Health data gap (no health assessment for the degradates) 

and no detections in nationally representative finished water 

data. 

4 ................... Acetochlor ethanesulfonic acid 

(ESA).

No ................ Yes ............... Health data gap (no health assessment for the ESA 

degradate) and no or low detections based on nationally 

representative finished water data. 

5 ................... Acetochlor oxanilic acid (OA) .. No ................ Yes ............... Health data gap (no health assessment for the OA degradate) 

and no or low detections based on nationally representative 

finished water data. 

6 ................... Alachlor ethanesulfonic acid 

(ESA).

No ................ Yes ............... Health data gap (no health assessment for the ESA 

degradate) and no or low detections based on nationally 

representative finished water data. 

7 ................... Alachlor oxanilic acid (OA) ...... No ................ Yes ............... Health data gap (no health assessment for the OA degradate) 

and no or low detections based on nationally representative 

finished water data. 

8 ................... Cobalt ...................................... No ................ Yes 2 ............. Health data gap (health assessment not updated by fall 2011) 

and no detections in nationally representative or other finished water data at levels of public health concern. 

9 ................... Disulfoton ................................. Yes ............... No ................ Occurrence data gap (no nationally representative finished 

water data and no detections in other finished water data). 

10 ................. Diuron ...................................... Yes ............... No ................ Occurrence data gap (no nationally representative finished 

water data and no detections in other finished water data). 

11 ................. Methyl Bromide ........................ No ................ Yes 1 ............. Health data gap (health assessment not updated by fall 2011). 

12 ................. Methyl tert-butyl ether .............. No ................ Yes ............... Health data gap (IRIS health assessment not completed by 

fall 2011) and no or low detections based on nationally representative finished water data. 

13 ................. Metolachlor .............................. No ................ Yes ............... Health data gap (no health assessment for degradates) and 

few detections in nationally representative finished water 

data. 

14 ................. Metolachlor ethanesulfonic 

acid (ESA).

No ................ Yes ............... Health data gap (no health assessment for ESA degradate) 

and no or low detections based on nationally representative 

finished water data. 

15 ................. Metolachlor oxanilic acid (OA) No ................ Yes ............... Health data gap (no health assessment for OA degradate) 

and no or low detections based on nationally representative 

finished water data. 

16 ................. Molinate ................................... No ................ Yes ............... Health data gap (OPP health assessment not completed by 

fall 2011 due to cancellation of molinate) and no detections 

in nationally representative or other finished water data at 

levels of public health concern. 

17 ................. Molybdenum ............................ No ................ Yes ............... Health data gap (health assessment not updated by fall 2011) 

and no detections in nationally representative or other finished water data at levels of public health concern. 

18 ................. N-Nitrosodiphenylamine 

(NDPhA).

Yes ............... No ................ Health data gap (health assessment not updated by fall 2011) 

and occurrence data gaps (no EPA approved analytical 

method for monitoring). 

19 ................. Perfluorooctanesulfonic acid 

(PFOS).

No ................ No 1 .............. Health data gap (health assessment not completed by fall 

2011) and occurrence data gaps (limited other finished 

water data available). 

20 ................. Perfluorooctanoic acid (PFOA) No ................ No 1 .............. Health data gap (health assessment not completed by fall 

2011) and occurrence data gaps (limited other finished 

water data available). 

21 ................. RDX ......................................... No ................ Yes ............... Health data gap (IRIS health assessment not updated by fall 

2011) and no detections in nationally representative or other 

finished water data at levels of public health concern. 

22 ................. Vanadium ................................. No ................ Yes 2 ............. Health data gap (health assessment not updated by fall 2011) 

and no to low detections in nationally representative finished water data at levels of public health concern. 

23 ................. 1,1,1,2-Tetrachloroethane ....... ...................... ...................... Will be evaluated and considered for the Carcinogenic Volatile 

Organic Compounds (cVOCs) group rule addressed in a 

separate process. 

24 ................. 1,2,3-Trichloropropane ............ ...................... (1) ................. Will be evaluated and considered for the Carcinogenic Volatile 

Organic Compounds (cVOCs) group rule addressed in a 

separate process. 


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17Note that the 1⁄2 HRL threshold is based on a 

recommendation from the NDWAC working 

grouping that provided recommendations on the 

first regulatory determinations effort. (USEPA, 

2000b) 

TABLE 4—DATA AND RATIONALE SUMMARY OF THE 25 CONTAMINANTS NOT PROCEEDING TO PHASE 3—Continued 

No. Contaminant Health data 

available 

Occurrence 

data available Rationale 

25 ................. Nitrobenzene ........................... ...................... ...................... Will be evaluated and considered for the Carcinogenic Volatile 

Organic Compounds (cVOCs) group rule addressed in a 

separate process. 

1The UCMR 3 includes sampling at the EPTDS for this contaminant (77 FR 26071, May 2, 2012). 

2The UCMR 3 includes sampling at both the EPTDS and DSMRT for this contaminant (77 FR 26071, May 2, 2012). For some contaminants, 

including disinfection byproducts and inorganics, occurrence values may differ between the EPTDS and the DSMRT due to dynamics within the 

distribution system such as contaminant degradation, formation, accumulation and release. 

3. Phase 3 (Regulatory Determination 

Assessment Phase) 

Phase 3, the Regulatory Determination 

Assessments Phase, involves a complete 

evaluation of the statutory criteria for 

each contaminant or group of 

contaminants that proceed from Phase 2 

and have sufficient information and 

data for making a regulatory 

determination. In this phase, the agency 

evaluates the following statutory 

criteria: 

(a) Statutory Criterion #1—The 

contaminant may have an adverse effect 

on the health of persons. To evaluate 

statutory criterion #1, EPA completes 

any health assessment that needs to be 

updated and externally peer-reviewed, 

and derives a final HRL. The derivation 

of the final HRL, further described in 

the section III.C.1, Evaluation of 

Adverse Health Effects, takes into 

account many of the key elements that 

are considered when evaluating 

criterion #1, which includes the mode 

of action, the critical health effect(s), the 

dose-response for critical health 

effect(s), impacts on sensitive 

populations(s) or lifestages, the RfD, 

and/or the cancer slope factor. HRLs are 

not final determinations about the level 

of a contaminant in drinking water that 

must not be exceeded to protect any 

particular population and are derived 

prior to the development of a complete 

exposure assessment. HRLs are risk 

derived concentrations against which to 

evaluate the occurrence data to 

determine if contaminants may occur at 

levels of potential public health 

concern. With this information, EPA 

determines whether the contaminant 

‘‘may have an adverse effect.’’ While 

CCL 3 contaminants are generally 

expected to meet statutory criterion #1 

because their adverse health effects 

were analyzed as part of the 

determination to list them on the CCL, 

the availability of a final HRL is derived 

as part of the first statutory criterion and 

is necessary to evaluate the second 

statutory criterion. 

(b) Statutory Criterion #2—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. EPA compares 

the occurrence data for each 

contaminant to the final peer-reviewed 

HRL to determine if the contaminant 

occurs at a frequency and levels of 

public health concern. The types of 

occurrence data used at this stage are 

described in section III.C.2, Evaluation 

of Contaminant Occurrence and 

Exposure. The agency considers the 

following factors when identifying 

contaminants or contaminant groups 

that are occurring at frequencies and 

levels of public health concern: 

• How many samples (# and %) have 

detections > final HRL in the nationally 

representative and other finished water 

occurrence data? 

• How many systems (# and %) have 

detections > final HRL in the nationally 

representative and other finished water 

occurrence data? 

• Is the contaminant associated with 

a contaminant group that is of public 

health concern and is being considered 

as part of the DWS? 

• Is the geographic distribution of the 

contaminant occurrence national, 

regional, or localized? 

• In addition to the number of 

systems, what type of systems does the 

contaminant occur in? Does the 

contaminant occur in large or small 

systems? Does the contaminant occur in 

surface or ground water systems? 

• Are there significant uncertainties 

or limitations with the data and/or 

analyses, such as the age of the dataset, 

limitation of the detection limit (i.e., 

MRL > final HRL) and/or 

representativeness of the data (e.g., 

limited in scope to a specific region)? 

Additional, less important factors that 

the agency considers when identifying 

contaminants or contaminant groups 

that are of public health concern also 

include: 

• How many samples (# and %) have 

detections >1⁄2 final HRL 17 in the 

nationally representative and other 

finished water occurrence data? 

• How many systems (# and %) have 

detections >1⁄2 final HRL in the 

nationally representative and other 

finished water occurrence data? 

• How many samples (# and %) have 

detections > final HRL and 1⁄2 final HRL 

in the ambient/source water occurrence 

data? 

• How many monitoring sites (# and 

%) have detections > final HRL and 1⁄2

final HRL in the ambient/source water 

occurrence data? 

• Are production and use trends for 

the contaminant increasing or 

decreasing? 

• How many pounds are discharged 

annually to surface water and/or 

released to the environment? 

• Do the environmental fate and 

transport parameters indicate that the 

contaminant would persist and/or be 

mobile in water? 

• Are there other uncertainties or 

limitations with the data and/or 

analyses for these additional factors that 

should be considered? 

• Is the contaminant introduced by 

water treatment processes (e.g., 

disinfection byproducts)? 

If a contaminant is known to occur or 

substantially likely to occur at a 

frequency and level of health concern in 

public water systems based on the 

factors listed above, then the agency 

answers ‘‘yes’’ to the second statutory 

criterion. 

(c) Statutory Criterion #3—In the sole 

judgment of the Administrator, 

regulation of the contaminant presents a 

meaningful opportunity for health risk 

reduction for persons served by public 

water systems. EPA evaluates the 

population exposed at the health level 

of concern along with several other 

factors to determine if regulation 

presents a meaningful opportunity for 

health risk reduction. EPA considers the 

following factors in evaluating statutory 

criterion #3: 

• Based on the occurrence 

information for statutory criterion #2 

(and the potential number of systems 

impacted), what is the national 

population exposed or served by 


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18 If appropriate and if available, the agency 

quantitatively takes into account exposure data 

applicable to sensitive populations or lifestages 

when deriving HRLs for regulatory determinations. 

When data is not available on sensitive populations, 

the derivation of the RfD typically includes an 

uncertainty factor to account for the weakness in 

the database. See section III.C.1. Sensitive 

populations are also qualitatively considered by 

providing national prevalence estimates for a 

particular sensitive population if available. 

19 If the agency decides to regulate a contaminant, 

SDWA requires that EPA issue a proposed 

regulation within two years of the final 

determination (with the possibility of a 9 month 

extension). As part of the proposal, the agency must 

list the best available technologies (BATs), small 

system compliance technologies (SSCTs), and 

approved analytical methods if it proposes an 

enforceable MCL. Alternatively, if EPA proposes a 

treatment technique (TT) instead of an MCL, the 

agency must identify the TT. EPA must also prepare 

a health risk reduction and cost analysis. This 

analysis includes an extensive evaluation of the 

treatment costs and monitoring costs at both system 

level and aggregated at the national level. To date, 

treatment information and approved analytical 

methods have not been a significant factor in 

regulatory determinations but are important 

considerations for regulation development. 

systems with levels ≥ HRL and 1⁄2 HRL 

(provide actual and estimated # and %)? 

• What is the nature of the health 

effect(s) identified in statutory criterion 

#1 and are there sensitive populations 

that may be impacted (either qualitative 

or quantitative 18)? 

• For non-carcinogens, are there other 

sources of exposure that should be 

considered (i.e., what is the relative 

source contribution)? 

• What is the geographic distribution 

of occurrence (e.g., local, regional, 

national)? 

• Are there any uncertainties and/or 

limitations in the health and occurrence 

information or analyses that should be 

considered? 

• What other factors or other pieces of 

information should be considered that 

may have direct bearing on any decision 

to regulate the contaminant (e.g., 

treatment, analytical methods,19 etc.)? 

After evaluating these factors, if the 

Administrator determines that there is a 

meaningful opportunity to reduce risk 

by regulating the contaminant in 

drinking water, then the agency answers 

‘‘yes’’ to the third statutory criterion. 

If the agency answers ‘‘yes’’ to all 

three statutory criteria in Phase 3 for a 

particular contaminant, then the agency 

makes a ‘‘positive’’ preliminary 

determination and requests public 

comment. 

If after the public comment period, 

the agency answers ‘‘yes’’ to all three 

statutory criteria, the agency then makes 

a ‘‘positive’’ final determination that 

regulation is necessary and proceeds to 

develop an MCLG and NPDWR. The 

agency has 24 months to publish a 

proposed MCLG and NPDWR and an 

additional 18 months to publish a final 

MCLG and promulgate a final NPDWR. 

It should be noted that this regulatory 

determination process is distinct from 

the more detailed analyses needed to 

develop a national primary drinking 

water regulation. Thus, a decision to 

regulate is the beginning of the agency’s 

regulatory development process, not the 

end. 

If a contaminant has sufficient 

information and the agency answers 

‘‘no’’ to any of the three statutory 

criteria, based on the available data, 

then the agency considers making a 

‘‘negative’’ determination that an 

NPDWR is not necessary for that 

contaminant at that time. The agency 

may decide to develop a Health 

Advisory (HA), which provides nonregulatory concentration values for 

drinking water contaminants at which 

adverse health effects are not 

anticipated to occur over specific 

exposure durations (one-day, ten-days, 

several years, and a lifetime). HAs serve 

as informal technical guidance to assist 

Federal, State, and local officials, and 

managers of public or community water 

systems (CWSs) in protecting public 

health when emergency spills or 

contamination situations occur. 

While a negative determination is 

considered a final agency action for this 

round of regulatory determinations, the 

contaminant is reconsidered for 

inclusion on the next CCL. If new health 

or occurrence information becomes 

available on contaminants with negative 

regulatory determinations, the agency 

considers whether the contaminant(s) 

should be listed on the next CCL and 

further evaluated in the next regulatory 

determinations process. 

Of the twelve contaminants that 

proceeded to Phase 3, the agency is not 

making preliminary regulatory 

determinations for seven contaminants 

at this time. The seven contaminants 

include chlorate and the six 

nitrosamines (i.e., NDBA, NDMA, 

NDPA, NDEA, NPYR, and NMEA). As 

discussed in section V, chlorate and the 

six nitrosamines are DBPs and the 

agency plans to consider these 

contaminants as part of the regulatory 

review of existing MDBP regulations. 

DBPs need to be evaluated collectively, 

because the potential exists that the 

control of one DBP could affect the 

concentrations of other DBPs or the 

necessary treatment. After evaluating 

the five remaining CCL 3 contaminants 

in Table 3 (i.e., dimethoate, 1,3- 

dinitrobenzene, strontium, terbufos, and 

terbufos sulfone) against the three 

SDWA criteria and considering the 

factors listed for each, the agency is 

making preliminary regulatory 

determinations for these five CCL 3 

contaminants. Table 5 provides a 

summary of the five contaminants 

evaluated for Phase 3 and the 

preliminary regulatory determination 

outcome. The agency seeks comment on 

the preliminary determination to 

regulate one contaminant (i.e., 

strontium) and to not regulate the 

remaining four contaminants (i.e., 

dimethoate, 1,3-dinitrobenzene, 

terbufos, and terbufos sulfone). Section 

IV.B of this notice provides a more 

detailed summary of the information 

and the rationale used by the agency to 

reach its preliminary decisions for these 

five contaminants. 

TABLE 5—CONTAMINANTS EVALUATED IN PHASE 3 AND THE REGULATORY DETERMINATION OUTCOME

No. RD 3 contaminants Preliminary determination outcome 

1 Dimethoate .................................................................................. Do not regulate. 

2 1,3-Dinitrobenzene ...................................................................... Do not regulate. 

3 Strontium ..................................................................................... Regulate. 

4 Terbufos ...................................................................................... Do not regulate. 

5 Terbufos Sulfone ......................................................................... Do not regulate. 


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B. Supporting Documentation for EPA’s 

Preliminary Determinations 

For this action, EPA prepared several 

support documents that are available for 

review and comment in the EPA Water 

Docket. These support documents 

include: 

• The comprehensive regulatory 

support document entitled, ‘‘Regulatory 

Determination 3 Support Document’’ 

(USEPA, 2014b), summarizes the 

information and data on the physical 

and chemical properties, uses and 

environmental release, environmental 

fate, potential health effects, occurrence 

and exposure estimates, the preliminary 

determinations, and the agency’s 

rationale for these determinations. 

• A separate health effects support 

document for strontium, entitled 

‘‘Health Effects Support Document for 

Strontium’’ (USEPA, 2014c), that 

addresses exposure from drinking water 

and other media, toxicokinetics, hazard 

identification, and dose-response 

assessment, and provides an overall 

characterization of the risk from 

drinking water containing strontium. 

For the contaminants with negative 

determinations, the agency refers the 

reader to the IRIS or OPP assessments 

for more detailed information regarding 

health effects (USEPA, 1990a, 1990b, 

2003c). These documents serve as the 

basis for the health information 

provided in the regulatory support 

documents. 

• A comprehensive technical 

occurrence support document for UCMR 

2 entitled, ‘‘Occurrence Data from the 

Second Unregulated Contaminant 

Monitoring Rule (UCMR 2)’’ (USEPA, 

2014d). This occurrence support 

document includes more detailed 

information about UCMR 2, how EPA 

assessed the data quality, completeness, 

and representativeness, and how the 

data were used to generate estimates of 

drinking water contaminant occurrence 

in support of these regulatory 

determinations. 

• A comprehensive protocol 

document, entitled ‘‘Protocol for the 

Regulatory Determination 3’’ (USEPA, 

2014a). This protocol document 

describes the approach implemented by 

the agency to evaluate 116 CCL 3 

contaminants in a three phase process 

and select the contaminants for 

preliminary determinations for RD 3. 

The protocol underwent expert review 

and the comments received were 

addressed by the agency. 

C. Analyses Used To Support the 

Preliminary Regulatory Determinations 

Sections III.C.1 and 2 of this action 

outline the health effects and 

occurrence/exposure evaluation process 

EPA used to support these preliminary 

determinations. 

1. Evaluation of Adverse Health Effects 

Section 1412(b)(1)(A)(i) of SDWA 

requires EPA to determine whether each 

candidate contaminant may have an 

adverse effect on public health. This 

section describes the overall process the 

agency uses to evaluate health effects, 

hazard and dose-response information, 

and the approach for deriving the health 

reference level (HRL) for the 

contaminants under consideration for 

regulatory determinations. HRLs are not 

final determinations about the level of a 

contaminant in drinking water that must 

not be exceeded to protect any 

particular population. HRLs are derived 

prior to the development of a complete 

exposure assessment. HRLs are risk 

derived concentrations against which to 

evaluate the occurrence data to 

determine if contaminants occur at 

levels of potential public health 

concern. More specific information 

about the potential for adverse health 

effects for each contaminant is 

presented in section IV.B of this action. 

In evaluating contaminants for 

regulatory determination, Section 1412 

(b)(1)(C) of SDWA also requires the 

agency to consider among other factors 

of public health concern, the effect of 

such contaminants upon subgroups that 

comprise a meaningful portion of the 

general population ‘‘such as infants, 

children, pregnant women, the elderly, 

individuals with a history of serious 

illness, or other subpopulations’’ that 

are identifiable as being at greater risk 

of adverse health effects compared to 

the general population. If appropriate 

and if available, the agency 

quantitatively takes into account data 

from sensitive populations and 

lifestages when deriving HRLs for 

regulatory determinations. 

There are two general approaches to 

the derivation of an HRL. One approach 

is used for chemicals that cause cancer 

and exhibit a linear response to dose 

and the other applies to noncarcinogens and carcinogens evaluated 

using a non-linear approach. The 

derivation of HRLs for carcinogens and 

non-carcinogens are described below. 

a. Derivation of an HRL for Carcinogens 

For those contaminants that are 

considered to be likely or probable 

human carcinogens by a mutagenic or 

unknown mode of action (MOA), the 

agency calculates a toxicity value that 

defines the relationship between dose 

and response (i.e., the cancer slope 

factor or CSF). 

(1) MOA: Unknown 

In cases where the data on the mode 

of action are lacking, EPA typically uses 

a default low dose linear extrapolation 

to calculate a CSF. The unit risk is the 

estimated upper-bound excess lifetime 

cancer risk from a continuous exposure 

to a chemical at a concentration of 0.001 

mg/L in drinking water. The exposure 

estimate assumes an adult body weight 

of 70 kg and the 90th percentile adult 

drinking water intake of 2 L/day. 

Unit Risk (mg/L)¥1 = CSF × [(DWI × 

CW)/BW] 

Where: 

CSF = Cancer Slope Factor (mg/kg/day)¥1

DWI = Drinking Water Intake for an adult, 

assumed to be 2 L/day (90th percentile) 

CW = Unit risk concentration in drinking 

water of 0.001 mg/L (1 mg/L) 

BW = Body Weight for an adult, assumed to 

be 70 kilograms (kg) 

The cancer HRL is the concentration of 

a contaminant in drinking water 

corresponding to an excess estimated 

lifetime cancer risk of one-in-a-million 

(1 × 10¥6), calculated as follows: 

HRL (mg/L) = Risk Level of 10¥6 ÷ Unit 

Risk (mg/L)¥1

As noted above, HRLs are not final 

determinations about the level of a 

contaminant in drinking water that must 

not be exceeded to protect any 

particular population. Rather, HRLs are 

risk derived concentrations against 

which to evaluate the occurrence data 

during the RD process to determine if 

contaminants occur at levels of potential 

public health concern. 

(2) MOA: Mutagenic 

If the chemical has a mutagenic mode 

of action, low dose linear extrapolation 

is used to calculate the CSF as described 

in the preceding paragraph. The U.S. 

EPA’s 2005 Guidelines for Carcinogen 

Risk Assessment (USEPA, 2005b) 

requires that the potential increased 

cancer risk due to early-life exposure be 

taken into account for chemicals with a 

mutagenic mode of action. When 

chemical-specific data to quantify the 

increased risk are lacking, Age 

Dependent Adjustment Factors (ADAFs) 

are applied to estimate age-adjusted unit 

risks. The age-adjusted unit risk is 

determined by using the sum of the unit 

risks for each of the three ADAF 

developmental groups (birth to <2 yrs; 

2 yrs to <16 yrs; 16 yrs to 70 yrs). The 

age-adjusted unit risks include a tenfold adjustment for early life (birth to <2 

yrs) exposures, a three-fold adjustment 

for childhood/adolescent (2 yrs to <16 

yrs) exposures, and no additional 

adjustment for exposures later in life (16 

yrs to 70 yrs), in conjunction with ageVerDate Sep<11>2014 16:52 Oct 17, 2014 Jkt 235001 PO 00000 Frm 00014 Fmt 4701 Sfmt 4702 E:\FR\FM\20OCP2.SGM 20OCP2

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20The drinking water intake values were derived 

from the data in the U.S. EPA’s Exposure Factors 

Handbook (USEPA, 2011e). The procedure used for 

the data normalization is described in the OW 

Policy paper for determining lifetime cancer risks 

involving early life exposures (USEPA, 2012c). 

21Because the critical health endpoint had doseresponse data associated with exposure during a 

specific period of sensitivity (i.e., sensitive 

population), EPA used age-specific drinking water 

intake to body weight ratio values (DWI/BWR) from 

the Exposure Factors Handbook (USEPA, 2011e) to 

derive the HRL for strontium. 

22 IRIS is an electronic EPA data base 

(www.epa.gov/iris/index.html) containing peerreviewed information on human health effects that 

may result from exposure to various chemicals in 

the environment. These chemical files contain 

descriptive and quantitative information on hazard 

identification and dose response, RfDs for chronic 

noncarcinogenic health effects, as well as slope 

factors and unit risks for carcinogenic effects. 

23The OPP is required under the Federal 

Insecticide Fungicide and Rodenticide Act (FIFRA) 

to periodically review the health effects data on all 

registered pesticides and reregister them for 

continued use. The results of the reregistration 

analysis are published in the Reregistration 

Eligibility Decision (RED) documents. Copies of the 

REDs are located at the following EPA Web site 

(http://www.epa.gov/oppsrrd1/reregistration/ 

status.htm). 

24ATSDR establishes oral minimal risk levels for 

non-neoplastic endpoints for acute (14 days or less), 

intermediate (15—364 days), and chronic (365 days 

or more) exposure durations. Minimal risk levels for 

oral chronic exposure are similar to EPA’s RfDs. 

However, ATSDR and EPA use different approaches 

when the database is limited to subchronic studies 

and no adequate chronic study is available. ATSDR 

derives an intermediate duration minimal risk level 

that protects against exposures up to 10% of a 

lifetime, and it does not incorporate an uncertainty 

factor to account for using a less-than-lifetime 

study. ATSDR does not perform quantitative cancer 

assessments or assign formal cancer classifications 

or descriptors. 

25WHO establishes a ‘‘guideline value’’, a 

drinking water concentration that uses different 

default assumptions than EPA for estimating water 

concentration from doses, including a 60 kg adult 

body weight, daily water consumption of 2 L/day, 

and a data derived or default RSC of 10%. WHO 

develops one guideline value that is based either on 

cancer or non cancer. 

specific drinking water intake values 

derived from the U.S. EPA’s 2011 

Exposure Factors Handbook (USEPA, 

2011e), and the fraction of a 70 year 

lifetime applicable to each age period. 

The increase in risk during early life 

results from active tissue growth 

resulting in limited time for repair of 

DNA replication errors. The ageadjusted unit risk is the upper-bound 

excess lifetime cancer risk estimated to 

result from continuous postnatal 

exposure to a chemical at a 

concentration of 0.001 mg/L in drinking 

water. 

Age-Adjusted Unit Risk (mg/L) ¥1 = 

è(CSF × ADAF × DWI/BWR × CW 

× F) 

Where: 

CSF = Cancer Slope Factor (mg/kg/day) ¥1

ADAF = The Age Dependent Adjustment 

Factor for the age group birth to twoyears (ADAF = 10), two years to sixteen 

years (ADAF = 3), and sixteen to seventy 

years (ADAF = 1) 

DWI/BWR = Drinking Water Intake Body 

Weight Ratio (DWI/BWR) expressed as 

liters per kg body weight for the agespecific group (90th percentile, 

consumers only) 20

CW = Unit risk concentration in drinking 

water of 0.001 mg/L (1 mg/L) 

F = The fraction of a 70 year lifetime 

applicable to the age period: 2/70 for 

birth to two years, 14/70 for two years to 

sixteen years and 54/70 for sixteen years 

to seventy years 

The cancer HRL is the concentration 

of a contaminant in drinking water 

corresponding to an excess estimated 

lifetime cancer risk of one-in-a-million 

(1 × 10¥6), calculated as follows: 

HRL (mg/L) = Risk Level of 10¥6 ÷ AgeAdjusted Unit Risk (mg/L) ¥1

The six nitrosamines discussed in 

section V had data available to classify 

them as known or likely human 

carcinogens with a mutagenic mode of 

action. Low-dose linear extrapolations 

and ADAFs were applied to all four of 

the CCL 3 nitrosamines: NDMA, NDPA, 

NDEA and NYPR, as well as the two 

non-CCL 3 nitrosamines, NMEA and 

NDBA. The five contaminants for which 

the agency is making preliminary 

regulatory determinations (dimethoate, 

1,3-dinitrobenzene, strontium, terbufos 

and terbufos sulfone) are noncarcinogens and were therefore 

evaluated using the RfD approach 

(discussed in the following section). 

b. Derivation of an HRL for NonCarcinogens 

EPA generally calculates a reference 

dose (RfD) for those chemicals 

considered to be non-carcinogenic or 

not likely to be carcinogenic to humans. 

An RfD is an estimate of a daily oral 

exposure to the human population 

(including sensitive populations or 

lifestages) that is likely to be without an 

appreciable risk of deleterious effects 

during a lifetime. The RfD can be 

derived from either a no-observedadverse-effect level (NOAEL), a lowestobserved-adverse-effect level (LOAEL), 

or the 95% lower confidence bound on 

a benchmark dose (BMD), known as a 

BMDL, with uncertainty factors applied 

to reflect limitations of the data used. In 

addition, if the critical health endpoint 

has high quality data associated with 

exposure for a specific developmental 

group or period of sensitivity, agespecific drinking water intake to body 

weight ratio values from the Exposure 

Factors Handbook (USEPA, 2011e) may 

be included in deriving an HRL from the 

RfD. 

The agency uses uncertainty factors 

(UFs) to address uncertainty resulting 

from incompleteness of the toxicological 

database (e.g., lacking sensitive 

population data). The individual UFs 

(usually applied as integers of one, 

three, or ten) are multiplied together 

and used to derive the RfD from 

experimental data. Individual UFs are 

intended to account for: 

(1) Variation in sensitivity among the 

members of the human population (i.e., 

intraspecies variability); 

(2) uncertainty in extrapolating 

animal data to humans (i.e., interspecies 

variability); 

(3) uncertainty in extrapolating from 

data obtained in a study with less-thanlifetime exposure to lifetime exposure 

(i.e., extrapolating from subchronic to 

chronic exposure); 

(4) uncertainty in extrapolating from 

an LOAEL rather than from an NOAEL; 

and/or 

(5) uncertainty associated with an 

incomplete database. 

For chlorate, dimethoate, 1,3- 

dinitrobenzene, strontium,21 terbufos, 

and terbufos sulfone, EPA derived the 

HRLs using the RfD approach as 

follows: 

HRL (mg/L) = [(RfD × BW)/DWI] × RSC 

Where: 

RfD = Reference Dose (mg/kg-day) 

BW = Body Weight for an adult, assumed to 

be 70 kilograms (kg); for a child, 

assumed to be 10 kg 

DWI = Drinking Water Intake for an adult, 

assumed to be 2 L/day (90th percentile); 

for child, assumed to be 1L/day (90th 

percentile) 

RSC = Relative Source Contribution, or the 

level of exposure believed to result from 

drinking water when compared to other 

sources (e.g., food, ambient air). In all 

cases, a 20% RSC is used for HRL 

derivation because (1) HRLs are 

developed prior to a complete exposure 

assessment and (2) 20% is the most 

conservative RSC used in the derivation 

of an MCLG for drinking water. 

c. Sources of Data/Information for 

Health Effects 

EPA uses the best available peerreviewed data and analyses in 

evaluating adverse health effects. Peerreviewed health-risk assessments are 

available for all chemicals considered 

for regulatory determinations from the 

agency’s Integrated Risk Information 

System (IRIS) Program, 22 the agency’s 

Office of Pesticide Programs (OPP),23

the National Academy of Sciences 

(NAS), the Agency for Toxic Substances 

and Disease Registry (ATSDR),24 and/or 

the World Health Organization 

(WHO).25 For a non-EPA health 


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26NIRS is designed to be statistically 

representative of groundwater systems and does not 

include surface water systems. 

assessment (i.e., NAS, ATSDR, WHO) to 

be considered for regulatory 

determinations, the health assessment 

must use comparable methods, 

standards, and guidelines to an EPA 

health assessment. Table 6 summarizes 

the sources of the health assessment 

data for each chemical under 

consideration for RD 3. 

The agency performs a literature 

search for studies published after the 

available health assessment is 

completed to determine if new 

information suggests a different 

outcome. The agency collects and 

evaluates any peer-reviewed 

publications identified through the 

literature search for their impact on the 

RfD and/or cancer assessment. In cases 

where the recent data indicate that a 

change to the existing RfD or cancer 

assessment is needed, the EPA Office of 

Water prepares and independently peerreviews an ‘‘OW Assessment’’ of the 

data. EPA updates all quantitative 

cancer assessments conducted under the 

Guidelines for Carcinogen Risk 

Assessment (USEPA, 1986) using the 

Guidelines for Carcinogen Risk 

Assessment (USEPA, 2005b), the 

Supplemental Guidance for Assessing 

Susceptibility from Early-life Exposures 

to Carcinogens (USEPA, 2005c), and the 

Exposure Factors Handbook (USEPA, 

2011e). These guidelines include 

considerations for contaminants with a 

mutagenic mode of action and potential 

risks due to early childhood exposure. 

TABLE 6—SOURCES AND DATES OF EPA HEALTH RISK ASSESSMENTS

Chemical IRIS 

(date) 

OPP RED 

(date) 

OW Assessment 

(date) 

Dimethoate ................................................................................................................. .............................. 2007 ..............................

1,3-Dinitrobenzene 1 .................................................................................................. 1988 .............................. ..............................

Strontium .................................................................................................................... 1992 .............................. 2012 

Terbufos ..................................................................................................................... .............................. 2006 ..............................

Terbufos Sulfone 2 ..................................................................................................... .............................. 2006 ..............................

1The agency also reviewed a non-EPA source (ATSDR, 1995) for 1,3-dinitrobenzene to corroborate the IRIS assessment. 

2The OPP RED for the parent compound (terbufos) was used. 

As noted in section III.B, EPA 

prepared a technical Health Effects 

Support Document for strontium 

(USEPA, 2014c). This document 

addresses the exposure from drinking 

water and other media, toxicokinetics, 

hazard identification, and dose-response 

assessment, and provides an overall 

characterization of risk from drinking 

water. For the contaminants with a 

preliminary negative determination (i.e., 

a decision not to regulate), refer to the 

EPA health risk assessments online from 

OPP or IRIS for additional health effect 

information. 

2. Evaluation of Contaminant 

Occurrence and Exposure 

EPA uses data from many sources to 

evaluate occurrence and exposure from 

drinking water contaminants. The 

following comprise the primary sources 

of finished drinking water occurrence 

data discussed in this Federal Register 

notice: 

• the Unregulated Contaminant 

Monitoring Regulation (UCMR 1 and 2), 

• the National Inorganic and 

Radionuclide Survey (NIRS), and 

• Disinfection Byproducts 

Information Collection Rule (DBP ICR). 

Several of the primary sources of 

finished water occurrence data are 

designed to be statistically 

representative of the nation. These data 

sources include UCMR 1, UCMR 2, and 

NIRS.26 The DBP ICR is geographically 

distributed across the country and 

national in scope but is not intended to 

be statistically representative of the 

nation. 

The agency also evaluates 

supplemental sources of information on 

occurrence in drinking water, 

occurrence in ambient and source water, 

and information on contaminant use 

and release to augment and compliment 

these primary sources of drinking water 

occurrence data. Section III.C.2.a. of this 

action provides a brief summary of the 

primary sources of finished water 

occurrence data, and sections III.C.2.b 

and II.C.2.c provide brief summary 

descriptions of some of the 

supplemental sources of occurrence 

information and/or data. These 

descriptions do not cover all the reports 

that EPA reviews and evaluates. For 

individual contaminants EPA reviews 

additional published reports and peerreviewed studies that may provide the 

results of monitoring efforts in limited 

geographic areas. A summary of the 

occurrence data and the results or 

findings for each of the contaminants 

considered for regulatory determination 

is presented in section IV.B, the 

contaminant profiles section, and the 

data are described in further detail in 

the support documents for the RD 3 

process (see USEPA, 2014a, b, c and d). 

a. Primary Sources of Finished Drinking 

Water Occurrence Data 

As previously mentioned, the primary 

national sources of the drinking water 

occurrence data discussed in this 

Federal Register notice are UCMR 1, 

UCMR 2, NIRS, and the DBP ICR. The 

following sections provide a brief 

summary of these data sources. Table 7 

in section IV lists the primary data 

source/finding used to evaluate each of 

the five contaminants considered for 

regulatory determinations. The 

contaminant-specific discussions in 

section IV provide more detailed 

information about the primary data 

source findings as well as any 

supplemental occurrence information. 

(1) The Unregulated Contaminant 

Monitoring Regulation (UCMR 1 and 

UCMR 2) 

The UCMR is currently EPA’s primary 

vehicle for collecting monitoring data 

on the occurrence of unregulated 

contaminants in PWSs. The UCMR is 

designed to collect nationally 

representative occurrence data and is 

developed in coordination with the CCL 

and Regulatory Determination process 

and the National Drinking Water 

Contaminant Occurrence Database 

(NCOD). The UCMR sampling is limited 

by statute to 30 contaminants during 

any five year cycle (SDWA section 

1445(a)(2)) and the PWSs and State 

primacy agencies are required to report 

the data to EPA. EPA published the list 

and requirements for the first 

Unregulated Contaminant Monitoring 

Regulation cycle (i.e., UCMR 1) in 

September 17, 1999 (64 FR 50556, 

September 17, 1999, USEPA, 1999; see 

also 65 FR 11372, March 2, 2000, 

USEPA, 2000a; and 66 FR 2273, January 

11, 2001, USEPA, 2001a), and the 

monitoring was conducted primarily 

during 2001–2003. UCMR 2 was 

published on January 4, 2007 (72 FR 

367; USEPA, 2007a), with monitoring 


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conducted during 2008–2010. (The 

complete analytical monitoring lists are 

available at: http://water.epa.gov/

lawsregs/rulesregs/sdwa/ucmr/.) 

The UCMR was designed as a threetiered approach for monitoring 

contaminants related to the availability 

of analytical methods and related 

analytical laboratory capacity. 

Assessment Monitoring (AM), the 

largest sampling tier, typically relies on 

analytical methods that are in common 

use in drinking water laboratories. The 

Screening Survey (SS), the second tier, 

uses newly developed analytical 

methods that may not be as commonly 

used in drinking water laboratories. The 

SS has involved a smaller number of 

PWSs because laboratory capacity is 

expected to be limited. The third tier, 

Pre-Screen Testing was designed to 

address contaminants with analytical 

methods that are in an early stage of 

development and the analyses would be 

limited to a few special laboratories. 

The expectation was that it would only 

involve the limited number of systems 

determined to be most vulnerable to the 

targeted contaminants. No Pre-Screen 

Testing was conducted during UCMR 1 

or UCMR 2. 

EPA designed the AM sampling frame 

to ensure that sample results would 

support a high level of confidence and 

a low margin of error (see USEPA, 1999 

and 2001b, for UCMR design details). 

AM is required for all large PWSs, those 

serving more than 10,000 people (i.e., a 

census of all large systems) and a 

national statistically representative 

sample of 800 small PWSs, those 

serving 10,000 or fewer people (for a 

total sample of approximately 4,000 

systems). PWSs that purchase 100% of 

their water were not required to 

participate. 

Each system conducts UCMR 

assessment monitoring for one year 

(during the three-year monitoring 

period). The rules require quarterly 

monitoring for surface water systems 

and twice-a-year, six-month interval 

monitoring for ground water systems. At 

least one sampling event must occur 

during a specified vulnerable period. 

Differing sampling points within the 

PWS may be specified for each 

contaminant related to the contaminants 

source(s). 

The objective of the UCMR sampling 

approach for small systems was to 

collect contaminant occurrence data 

from a statistically selected, nationally 

representative sample of small systems. 

The small system sample was stratified 

and population-weighted, and included 

some other sampling adjustments such 

as allocating a selection of at least two 

systems from each State for spatial 

coverage. The UCMR AM program 

includes systems from all 50 States, the 

District of Columbia, four U.S. 

Territories, and Tribal lands in five EPA 

Regions. With contaminant monitoring 

data from all large PWSs—a census of 

large systems—and a statistical, 

nationally representative sample of 

small PWSs, the UCMR AM program 

provides a robust dataset for evaluating 

national drinking water contaminant 

occurrence. 

UCMR 1 AM was conducted by 

approximately 3,090 large systems and 

797 small systems. Approximately 

33,800 samples were collected for each 

contaminant. In UCMR 2, sampling was 

conducted by over 3,300 large systems 

and 800 small systems, and resulted in 

over 32,000 sample results for each 

contaminant. 

As noted, in addition to AM, SS 

monitoring was required for 

contaminants. For UCMR 1, the SS was 

conducted at 300 PWSs (120 large and 

180 small systems) selected at random 

from the pool of systems required to 

conduct AM. Samples from the 300 

PWSs from throughout the nation 

provided approximately 2,300 analyses 

for each contaminant. While the 

statistical design of the SS is national in 

scope, the uncertainty in the results for 

contaminants that have low occurrence 

is relatively high. Therefore, EPA looked 

for additional data to supplement the SS 

data for regulatory determinations. 

For the UCMR 2 SS, EPA improved 

the design to include a census of all 

systems serving more than 100,000 

people (approximately 400 PWSs—but 

the largest portion of the national 

population served by PWSs) and a 

nationally representative, statistically 

selected sample of 320 PWSs serving 

between 10,001 and 100,000 people, 

and 480 small PWSs serving 10,000 or 

fewer people (72 FR 367, January 4, 

2007, USEPA, 2007a). With 

approximately 1,200 systems 

participating in the SS, sufficient data 

were generated to provide a confident 

national estimate of contaminant 

occurrence and population exposure. In 

UCMR 2, the 1,200 PWSs provided more 

than 11,000 to 18,000 analyses 

(depending on the sampling design for 

the different contaminants). 

As previously noted, the details of the 

occurrence data and the results or 

findings for each of the contaminants 

considered for regulatory determination 

is presented in Section IV.B, the 

contaminant profiles section, and is 

described in further detail in the 

support documents for the RD 3 process 

(USEPA, 2014a and 2014b). The 

national design, statistical sampling 

frame, any new analytical methods, and 

the data analysis approach for the 

UCMR program has been peer-reviewed 

at different stages of development (see, 

USEPA, 2001b, 2008c, 2014d, for 

example.) 

(2) National Inorganics and 

Radionuclides Survey (NIRS) 

EPA conducted the NIRS to provide a 

statistically representative sample of the 

national occurrence of 36 selected 

inorganic compounds (IOCs) and 

radionuclides in CWSs served by 

ground water. The sample was stratified 

by system size and 989 ground water 

CWSs were selected at random 

representing 49 States (all except 

Hawaii) as well as Puerto Rico. The 

survey focused on ground water 

systems, in part because IOCs tend to 

occur more frequently and at higher 

concentrations in ground water than in 

surface water. Each of the selected 

CWSs was sampled at a single time 

between 1984 and 1986. 

One limitation of the NIRS is a lack 

of occurrence data for surface water 

systems. EPA also reviews additional 

finished water data from State datasets 

and other sources, as well as data from 

ambient and source surface waters, to 

augment the NIRS data. Information 

about NIRS monitoring and data 

analysis is available in The Analysis of 

Occurrence Data from the Unregulated 

Contaminant Monitoring (UCM) 

Program and National Inorganics and 

Radionuclides Survey (NIRS) in Support 

of Regulatory Determinations for the 

Second Drinking Water Contaminant 

Candidate List (USEPA, 2008b). 

(3) Disinfection Byproducts Information 

Collection Rule (DBP ICR) 

The DBP ICR (61 FR 24353, May 14, 

1996 (USEPA, 1996)) required PWSs 

serving at least 100,000 people to 

monitor and collect data on DBPs from 

July 1997 to December 1998. The DBP 

ICR data were collected from 296 water 

systems that provided extensive 

information on the occurrence of DBPs 

and on water treatment methods. The 

DBP ICR data were collected as part of 

a national project to support 

development of national disinfection 

by-products and microbial drinking 

water standards. EPA used the data to 

identify national and regional patterns 

and overall water quality, not to reach 

system-by-system or treatment plant-bytreatment plant conclusions. Additional 

details on the data collection process for 

the DBP ICR, along with an independent 

analysis of the data, can be found in a 

report sponsored by the Microbial/

Disinfection Products Council (McGuire 

et al., 2002). 


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The DBP ICR provided a census of the 

largest systems that serve the largest 

proportion of the population served by 

PWSs at that time. It has previously 

been vetted for use in regulatory 

development, and EPA determined it 

can be used in the regulatory 

determination process. 

b. Supplemental Sources of Finished 

Drinking and Ambient Water 

Occurrence Data 

The agency evaluates several sources 

of supplemental information related to 

contaminant occurrence in finished 

water and ambient and source waters to 

augment the primary drinking water 

occurrence data. Some of these sources 

were part of other agency information 

gathering efforts or submitted to the 

agency in public comment or suggested 

by stakeholders during previous CCL 

and Regulatory Determination efforts. 

These supplemental data are useful to 

evaluate the likelihood of contaminant 

occurrence in drinking water and/or to 

more fully characterize a contaminant’s 

presence in the environment and 

potentially in source water, and to 

evaluate any possible trends or spatial 

patterns that may need further review. 

The descriptions that follow do not 

cover all the reports that EPA used. For 

individual contaminants EPA reviewed 

additional published reports and peerreviewed studies that may have 

provided the results of monitoring 

efforts in limited geographic areas. A 

more detailed discussion of the 

supplemental sources of information/

data that EPA evaluated and the 

occurrence data for each contaminant 

can be found in the comprehensive 

regulatory determination support 

documents (USEPA, 2014a and 2014b). 

(1) Individual States’ Data 

To support the second Six-Year 

Review of regulated contaminants (see 

USEPA, 2009b), EPA issued an ICR to 

collect compliance monitoring data 

from PWSs for the time period covering 

1998–2005. After issuing the ICR, EPA 

received monitoring data from 45 States 

plus Region 8 and Region 9 Tribes. Six 

States and Region 9 Tribes also 

provided monitoring data for 

unregulated contaminants along with 

their compliance monitoring data. EPA 

further collected additional unregulated 

contaminant data from two additional 

States that provide monitoring data 

through their Web sites. EPA reviews 

these datasets during the RD 3 process. 

These datasets vary from State to State 

in the contaminants included, the 

number of samples, and the 

completeness of monitoring. They are 

reviewed and used to augment the 

national data and assess if they provide 

supportive observations or any unique 

occurrence results that might warrant 

further review. 

(2) Community Water System Survey 

(CWSS) 

EPA periodically conducts the CWSS 

to collect data on the financial and 

operating characteristics from a 

nationally representative sample of 

CWSs. As part of the CWSS, all systems 

serving more than 500,000 people 

receive the survey. In the 2000 and 2006 

CWSS, these very large systems were 

asked questions about the occurrence 

and concentration of unregulated 

contaminants in their raw and finished 

water. The 2000 CWSS (USEPA, 2002a, 

2002b) requested data from 83 very large 

CWSs and the 2006 CWSS (USEPA, 

2009c, 2009d) requested data from 94 

very large CWSs. Not all systems 

answered every question or provided 

complete information on the 

unregulated contaminants. Because 

reported results are incomplete, they are 

illustrative, not representative, and are 

only used as supplemental information. 

(3) United States Department of 

Agriculture (USDA) Pesticide Data 

Program (PDP) 

Since 1991, the USDA PDP has 

gathered data on pesticide residues in 

food. In 2001 the program expanded to 

include sampling of pesticide residues 

in treated drinking water, and in 2004 

some sampling of raw water was 

incorporated as well (USDA, 2004). The 

CWSs selected for sampling tend to be 

small and medium-sized water surface 

water systems (serving under 50,000 

people) located in regions of heavy 

agriculture. The sampling frame is 

designed to monitor in regions of 

interest for at least two years to reflect 

the seasonal and climatic variability 

during growing seasons. PDP works 

with EPA and the American Water 

Works Association (AWWA) to identify 

specific water treatment facilities where 

monitoring data are collected. The 

number of sites and samples have varied 

among different sampling periods. EPA 

reviewed the PDP data on the 

occurrence of select contaminants in 

untreated and treated water (USDA, 

2004). 

(4) United States Geological Survey 

(USGS) Pilot Monitoring Program (PMP) 

In 1999, USGS and EPA conducted 

the PMP to provide information on 

pesticide concentrations in small 

drinking water supply reservoirs in 

areas with high pesticide use (Blomquist 

et al., 2001). The study was undertaken, 

in part, to test and refine the sampling 

approach for pesticides in such 

reservoirs and related drinking water 

sources. Sampling sites represent a 

variety of geographic regions, as well as 

different cropping patterns. Twelve 

water supply reservoirs considered 

vulnerable to pesticide contamination 

were included in the study. Samples 

were collected quarterly throughout the 

year and at weekly or biweekly intervals 

following the primary pesticideapplication periods. Water samples 

were collected from the raw water 

intake and from the finished drinking 

water prior to entering the distribution 

system. At some sites, samples were 

also collected at the reservoir outflow. 

(5) United States Geological Survey 

(USGS) National Water Quality 

Assessment (NAWQA) 

The USGS instituted the National 

Water Quality Assessment (NAWQA) 

program in 1991 to examine ambient 

water quality status and trends in the 

United States. The NAWQA program is 

designed to apply nationally consistent 

methods to provide a consistent basis 

for comparisons over time nationally 

and among significant watersheds and 

aquifers across the country. These 

occurrence assessments serve to 

facilitate interpretation of natural and 

anthropogenic factors affecting national 

water quality. The NAWQA program 

monitors the occurrence of chemicals 

such as pesticides, nutrients, VOCs, 

trace elements, and radionuclides, and 

the condition of aquatic habitats and 

fish, insects, and algal communities. For 

more detailed information on the 

NAWQA program design and 

implementation, please refer to Leahy 

and Thompson (1994), Hamilton et al. 

(2004), and NRC (2002). 

The NAWQA program has been 

designed in ten-year cycles to enable 

national coverage that can be used for 

trends and causal assessments. In the 

Cycle 1 monitoring period, which was 

conducted from 1991 through 2001, 

NAWQA collected data from over 6,400 

surface water and 7,000 ground water 

sampling points. Cycle 2 monitoring 

covers the period from 2002 through 

2012, with various design changes from 

Cycle 1 (see Hamilton et al., 2004). 

EPA, with the cooperation of USGS, 

performed a summary analysis of all 

Cycle 1 water monitoring data for the 

CCL 3 and Regulatory Determination 

process. The surface water data 

consisted of stream samples; all surface 

water data were included in the EPA 

summary analysis. For ground water, all 

well data were used and data from 

springs and drainage systems were 

excluded. 


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For RD 3, EPA used and evaluated 

many USGS NAWQA reports to review 

causal or spatial factors that USGS may 

have presented in their interpretations. 

In particular, EPA evaluated many 

reports from the Pesticide National 

Synthesis Programs (e.g., Gilliom et al., 

2007) and the VOC National Synthesis 

(e.g., Delzer and Ivahnenko, 2003). 

While there is overlap in the data used 

in the USGS reports and the EPA 

analysis, the USGS reports can provide 

unique observations related to their 

synthesis of additional data. 

For RD 3, EPA also supplemented 

these data with information from recent 

special USGS reports that also used 

additional data from other programs, 

particularly reports that focused on 

contaminant occurrence in source 

waters for PWSs, such as: Organic 

Compounds in Source Water of Selected 

Community Water Systems (Hopple et 

al., 2009 and Kingsbury et al., 2008), 

and Water Quality in Public-Supply 

Wells (Toccalino et al., 2010). 

(6) Storage and Retrieval (STORET) Data 

System 

EPA’s STORET database contains raw 

biological, chemical, and physical data 

from surface and ground water sampling 

conducted by Federal, State and local 

agencies, Indian Tribes, volunteer 

groups, academics, and others. A wide 

variety of data relating to water quality 

from all 50 States as well as multiple 

territories and jurisdictions of the 

United States are represented in this 

data system. These are primarily 

ambient water data, but in some cases 

they include finished drinking water 

data. STORET data have quality 

limitations. There are few restrictions 

on submission of data based on 

analytical methods, quality assurance 

(QA) practices, etc. For more general 

STORET data information, please refer 

to: http://www.epa.gov/storet/

index.html. EPA reviewed STORET 

ground water data from wells and 

surface water data from lakes, rivers/

streams, and reservoirs. 

c. Supplemental Production, Use and 

Release Data 

The agency reviews various sources of 

information to assess if there are 

changes or trends in a contaminant’s 

production, use, and release that may 

affect its presence in the environment 

and potential occurrence in drinking 

water. The cancellation of a pesticide or 

a clear increase in production and use 

of a contaminant are trends that can 

inform the regulatory determination 

process. A more detailed discussion of 

the supplemental sources of 

information/data that EPA evaluated 

and the occurrence data for each 

contaminant can be found in the 

comprehensive regulatory 

determination support documents 

(USEPA, 2014a and 2014b). Several 

sources are described in more detail 

below. 

(1) Chemical Update System/Inventory 

Update Rule (CUS IUR) 

The IUR regulation requires 

manufacturers and importers of certain 

chemical substances, included on the 

Toxic Substances Control Act (TSCA) 

Chemical Substance Inventory, to report 

site and manufacturing information and 

the amount of chemicals produced or 

imported in amounts of 25,000 pounds 

or more at a single site. Additional 

information on domestic processing and 

use must be reported for chemicals 

produced or imported in amounts of 

300,000 pounds or more at a single site. 

Prior to the 2003 TSCA Amendments 

(i.e., reporting from 2002 or earlier), 

information was collected for only 

organic chemicals that were produced 

or imported in amounts of 10,000 

pounds or more, and was limited to 

more basic manufacturing information 

such as production volume. Because of 

changes in reporting rules, 

contaminants may have reports for some 

years but not others (USEPA, 2010a). 

(2) Toxic Release Inventory (TRI) 

EPA established the Toxics Release 

Inventory (TRI) in 1987 in response to 

Section 313 of the Emergency Planning 

and Community Right-to-Know Act 

(EPCRA). EPCRA Section 313 requires 

facilities to report to both EPA and the 

States annual information on toxic 

chemical releases from facilities that 

meet reporting criteria. The TRI 

database details not only the types and 

quantities of toxic chemicals released to 

the air, water, and land by facilities, but 

also provides information on the 

quantities of chemicals sent to other 

facilities for further management 

(USEPA, 2002c, 2003b). Currently, for 

most chemicals the reporting thresholds 

are 25,000 pounds for manufacturing 

and processing and 10,000 pounds for 

use. Both the number and type of 

facilities required to report has 

increased over time. 

Although TRI can provide a general 

idea of release trends, it has limitations 

because of the reporting changes over 

time. Finally, TRI data are meant to 

reflect ‘‘releases’’ and should not be 

used to estimate general public 

exposure to a chemical (USEPA, 2002c). 

(3) Pesticide Usage Estimates 

For the regulatory determinations 

process, the agency reviews various 

sources of information about pesticide 

usage. SDWA directs EPA to consider 

pesticides in the CCL process. Pesticide 

use and manufacturing information is 

considered confidential business 

information and therefore, accurate 

measures of production and use are not 

publically available. As a result, the 

agency reviews various estimates of use 

as supplemental information in the 

deliberative process. 

Occasionally, EPA presents 

estimations of annual U.S. usage of 

individual pesticides in its pesticide 

reregistration documents (e.g., 

Reregistration Eligibility Decisions or 

(REDs), Interim Reregistration Eligibility 

Decisions (IREDs), Tolerance 

Reassessment Progress and Risk 

Management Decisions (TREDs)). EPA 

also periodically issues Pesticides 

Industry Sales and Usage reports. The 

reports provide contemporary and 

historical information on U.S. pesticide 

production, imports, exports, usage, and 

sales, particularly with respect to dollar 

values and quantities of active 

ingredient. The most recent report 

presents data from the years 2000 and 

2001 (USEPA, 2004). 

The National Center for Food and 

Agricultural Policy (NCFAP), a private 

non-profit institution, has also produced 

national pesticide use estimates based 

on USDA State-level statistics and 

surveys for commercial agriculture 

usage patterns and State-level crop 

acreage. The database contains estimates 

of pounds applied and acres treated in 

each State for 220 active (pesticide) 

ingredients and 87 crops. The majority 

of the chemicals monitored are 

herbicides, but the database also follows 

significant numbers of fungicides and 

insecticides (NCFAP, 2000). 

The USGS produced usage estimates 

and maps for over 200 pesticides used 

in United States crop production, 

providing spatial insight to the regional 

use of many pesticides (USGS, 2007). 

These pesticide use estimates were 

generated by the USGS through Statelevel estimates of pesticide usage rates 

for individual crops that were compiled 

by the CropLife Foundation and the 

Crop Protection Research Institute, 

combined with county-level data on 

harvested crop acreage obtained from 

the 2002 Census of Agriculture. 

IV. Contaminant-Specific Discussions 

for the RD 3 Preliminary Regulatory 

Determinations 

A. Summary of the Preliminary 

Regulatory Determination 

Based on EPA’s evaluation of the 

three SDWA criteria (discussed in 

section II.B.1), the agency is making 


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preliminary determinations to regulate 

one contaminant and to not regulate 

four contaminants. Table 7 summarizes 

the primary health and occurrence 

information used to make these 

preliminary regulatory determinations. 

Section IV.B of this notice provides a 

more detailed summary of the 

information and the rationale used by 

the agency to reach its preliminary 

decisions for these five contaminants. 

TABLE 7—SUMMARY OF THE HEALTH AND OCCURRENCE INFORMATION AND THE PRELIMINARY DETERMINATIONS FOR THE

FIVE CONTAMINANTS CONSIDERED FOR REGULATORY DETERMINATIONS 3 

No. RD 3 

contaminants 

Health 

reference 

level 

(HRL) 

Occurrence findings from primary data sources 

Preliminary 

Primary determination 

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 

1 ................. Dimethoate .... 15.4 μg/L UCMR 2 0% (0 of 

4138).

0% (0 of 

229M).

0% (0 of 

4138).

0% (0 of 

229M).

Do not regulate. 

2 ................. 1,3- 

Dinitrobenzene.

0.7 μg/L UCMR 2 0% (0 of 

4137).

0% (0 of 

229M).

0% (0 of 

4137).

0% (0 of 

229M).

Do not regulate. 

3 ................. Strontium ....... 1,500 μg/L NIRS 14.3% (141 of 

989).

16.6% (246K 

of 1.5M).

7.0% (69 of 

989).

10.7% 

(158.5K of 

1.5M).

Regulate. 

4 ................. Terbufos ........ 0.35 μg/L UCMR 1 0% (0 of 295) 0% (0 of 41M) 0% (0 of 295) 0% (0 of 41M) Do not regulate. 

5 ................. Terbufos 

Sulfone.

0.35 μg/L UCMR 2 0.02% (1 of 

4138).

0.01% (44.6K 

of 229M).

0.02% (1 of 

4138).

0.01% (44.6K 

of 229M).

Do not regulate. 

B. Contaminant Profiles 

This section provides further 

information on the background, health, 

and occurrence data that the agency 

uses to evaluate each of the five 

candidate contaminants considered for 

regulatory determinations. For each 

candidate, the agency evaluates the 

available human and toxicological data, 

derives a health reference level, and 

evaluates the potential and/or likely 

occurrence and exposed population for 

the contaminant in public water 

systems. The agency also considers 

whether information is available on 

sensitive populations. The agency uses 

the findings from these evaluations to 

determine whether the three SDWA 

statutory criteria are satisfied. The 

agency also prepares a regulatory 

support document (USEPA, 2014b) that 

provides more details on the 

background, health, and occurrence 

information/analyses used to evaluate 

and make preliminary determinations 

for these five contaminants. 

1. Dimethoate 

a. Background 

Dimethoate is an organophosphate 

pesticide, commonly used as an 

insecticide on field crops (e.g., wheat, 

alfalfa, corn, and cotton), orchard crops, 

vegetable crops, and in forestry. 

Synonyms for dimethoate include 

dimethogen, dimeton, dimevur, and 

cygon (HSDB, 2009; USEPA, 2007b). 

EPA has estimated that the total annual 

average domestic use of dimethoate is 

approximately 1.8 million pounds 

(USEPA, 2007b). EPA’s most recent 

Pesticide Industry Sales and Usage 

reports indicate that the amount of 

dimethoate active ingredient (a.i.) used 

in the United States was between 1 and 

2 million pounds in 1999 and 2001, and 

less than 1 million pounds in 2005 and 

2007 (USEPA, 2004: USEPA, 2011f). TRI 

data from the years 1997 to 2010 show 

that annual releases to various sources 

range from tens of pounds to tens of 

thousands of pounds, with the larger 

releases occurring only occasionally and 

in no clear pattern (USEPA, 2012a). For 

example, reported on-site air emissions 

were in the range of tens of pounds for 

1997–2005 but increased to the range of 

thousands of pounds in 2006–2010. The 

only reported non-zero release by 

underground injection was in 2004 and 

was over 28,000 pounds. Reported onsite releases to surface water and land 

were low or non-existent in most years, 

but peaked suddenly at nearly 20,000 

pounds in 1998 (land) and over 2,000 

pounds in 2004 (surface water). 

Dimethoate is considered highly mobile 

and relatively non-persistent in the 

environment (USEPA, 2007b). 

b. Statutory Criterion #1 (Adverse 

Health Effects) 

Dimethoate meets the SDWA statutory 

criterion #1 for regulatory 

determinations; it may have an adverse 

effect on the health of persons. 

Dimethoate belongs to a group of 

pesticides called organophosphates, 

which share a common MOA. 

Organophosphates affect the proper 

function of the nervous system by 

inhibiting cholinesterase (ChE), an 

important enzyme involved in 

neurotransmission. Inhibition of ChE in 

the brain, plasma, and red blood cells is 

the most sensitive endpoint described in 

numerous studies with adult and 

juvenile animals, following oral, dermal, 

or inhalation exposures of dimethoate or 

its primary toxic metabolite omethoate 

(USEPA, 2007b). As discussed in the 

2007 OPP assessment, the U.S. EPA’s 

Cancer Assessment Review Committee 

(CARC) classified dimethoate as a Group 

C carcinogen (a possible human 

carcinogen) in 1991, with concurrence 

from the FIFRA Scientific Advisory 

Panel (SAP) on the agency’s 

classification in 1992 (USEPA, 2007b). 

The 2007 OPP assessment established 

a chronic oral RfD for dimethoate of 

0.0022 mg/kg/day based on a 2-year 

feeding study in rats with inhibition of 

brain ChE as the critical effect (USEPA, 

2007b). The RfD was derived using the 

BMD method and based on the lower 

95% confidence limit (BMDL) of 0.22 

mg/kg/day, with application of a 

composite UF of 100 (i.e., intraspecies 

and interspecies variability). EPA 

calculated a non-cancer HRL of 15.4 mg/ 

L for dimethoate using the RfD of 0.0022 

mg/kg/day for a 70 kg adult ingesting 2 

L of drinking water per day and an RSC 

of 20%. The chronic RfD and 

subsequent HRL of 15.4 mg/L for 

dimethoate are considered to be 

protective of any potential cancer risk or 

acute ChE effects (USEPA, 1990a, 

2007b). The OPP RED (USEPA, 2007b) 

presents more detailed information 


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about the potential health effects for 

dimethoate. 

c. Statutory Criterion #2 (Occurrence at 

Frequency and Levels of Public Health 

Concern) 

Dimethoate does not meet the SDWA 

statutory criterion #2 for regulatory 

determinations; it does not occur with a 

frequency and at levels of public health 

concern in public water systems based 

on EPA’s evaluation of the following 

occurrence information. 

The primary data for dimethoate are 

recent (2008–2010) nationallyrepresentative drinking water 

monitoring data, generated through 

EPA’s UCMR 2. Dimethoate was not 

detected in any of the 32,013 UCMR 2 

samples collected by 4,138 PWSs 

(serving ∼ 230 million people) at levels 

greater than the 1⁄2 HRL (7.7 mg/L), the 

HRL (15.4 mg/L), or the MRL (0.7 mg/L) 

(USEPA, 2014d). 

The State of California reported 

results from testing more than 20,000 

finished drinking water samples from 

over 2,000 PWSs and dimethoate was 

detected in two samples from two 

different PWSs. The detected 

concentrations (1 mg/L and 2 mg/L) were 

less than the 1⁄2 HRL (7.7 mg/L) and the 

HRL (15.4 mg/L) (see USEPA, 2014b). 

The USDA PDP monitored for 

dimethoate in finished water from 2001 

to 2009 and had only two detections in 

3,555 samples; both detected 

concentrations were less than the 1⁄2

HRL and the HRL (USDA, 2012). The 

USGS PMP monitored for dimethoate in 

finished water in 1999 and had no 

detections greater than 1⁄2 the HRL or 

the HRL in any of the 221 samples 

(Blomquist et al., 2001). 

Dimethoate occurrence data for 

ambient water are consistent with those 

for finished drinking water. The USGS 

PMP also monitored for dimethoate in 

ambient water in 1999 and had no 

detections greater than the 1⁄2 HRL (7.7 

mg/L) or the HRL (15.4 mg/L) in any of 

the 317 samples (Blomquist et al., 2001). 

Ambient water data from a two-phase 

USGS study conducted between 2002 

and 2005 by Hopple et al. (2009) and 

Kingsbury et al. (2008) reported no 

detections in the 221 Phase 1 

groundwater samples. Only two 

detections were reported from 146 

Phase 1 surface water samples at nine 

PWSs. The highest concentration 

detected was 0.009 mg/L, which is less 

than the 1⁄2 HRL and the HRL. In Phase 

2, there were no detections of 

dimethoate from 48 raw and finished 

water groundwater samples (Hopple et 

al., 2009; Kingsbury et al., 2008). 

Ambient water data in STORET 

included no measured results above 

0.44 mg/L in 5,299 samples from 798 

sites (USEPA, 2012b). Ambient water 

data reported by the California 

Department of Pesticide Regulation 

included no measured results above 2.4 

mg/L (USEPA, 2007b). 

d. Statutory Criterion #3 (Meaningful 

Opportunity) 

EPA finds that dimethoate does not 

meet the SDWA statutory criterion #3 

for regulatory determinations; regulation 

of dimethoate does not present a 

meaningful opportunity health risk 

reduction for persons served by PWSs 

based on the estimated exposed 

population, including sensitive 

populations. The estimated population 

exposed to dimethoate at levels of 

public health concern is 0%; it was not 

found to occur at levels above the HRL 

(or the 1⁄2 HRL) in 4,138 PWSs and 

32,013 samples from the UCMR 2 

monitoring. In addition, other 

supplementary sources of finished water 

and ambient water data indicate that the 

occurrence of dimethoate in PWSs is 

likely to be low to non-existent. As a 

result, the agency finds that an NPDWR 

for dimethoate does not present a 

meaningful opportunity for health risk 

reduction. 

EPA also evaluated whether health 

information is available regarding the 

potential health effects on children and 

other sensitive populations. The 

database for dimethoate includes a 3- 

generation reproductive study in mice, 

developmental (teratology) studies in 

rats and rabbits, and a 

neurodevelopmental toxicity study 

(USEPA, 1990a, 2007b). The critical 

effect of ChE inhibition is a more 

sensitive endpoint compared to the 

reproductive and developmental 

endpoints (USEPA, 2007b); therefore no 

sensitive populations were identified or 

characterized. The OPP RED (USEPA, 

2007b) presents more detailed 

information about the potential health 

effects and sensitive populations for 

dimethoate. 

e. Preliminary Regulatory Determination 

The agency is making a preliminary 

determination to not regulate 

dimethoate with an NPDWR after 

evaluating health, occurrence, and other 

related information against the three 

SDWA statutory criteria. While data 

suggests that dimethoate may have an 

adverse effect on human health, the 

occurrence data indicate that 

dimethoate is not occurring or not likely 

to occur in PWSs with a frequency and 

at levels of public health concern. 

Therefore, the agency finds that an 

NPDWR would not present a 

meaningful opportunity to reduce 

health risk for persons served by PWSs. 

The Regulatory Determinations 3 

Support Document (USEPA, 2014d) and 

the Occurrence Data from the Second 

Unregulated Contaminant Monitoring 

Regulation (UCMR 2) (USEPA, 2014a) 

present additional information and/or 

analyses supporting the agency’s 

evaluation of dimethoate. 

2. 1,3-Dinitrobenzene 

a. Background 

1,3-Dinitrobenzene is a nitro aromatic 

compound that is used as an industrial 

chemical and formed as a by-product in 

the manufacture of munitions as well as 

in the production of other substances 

(HSDB, 2009). There are no known 

natural sources of 1,3-dinitrobenzene. 

Annual production and importation of 

1,3-dinitrobenzene in the United States 

was last reported by CUS–IUR in 1986 

to be between 10–50 million pounds 

(USEPA, 2010b). TRI data indicate 

19,858 pounds were released to the 

environment by industry in 2008 and 

10,595 pounds in 2010 (USEPA, 2012a). 

1,3-dinitrobenzene appears to be 

moderately persistent in environmental 

media and moderately mobile in soil 

and water, though in soils with high 

clay content it will be less mobile 

(USEPA, 2014b). 

b. Statutory Criterion #1 (Adverse 

Health Effects) 

1,3-dinitrobenzene meets the SDWA 

statutory criterion #1 for regulatory 

determinations; it may cause adverse 

effect on the health of persons. 1,3- 

dinitrobenzene has demonstrated 

adverse health effects in many rodent 

and occupational studies. Occupational 

studies indicate that 

methemoglobinemia, hemolytic anemia, 

and cyanosis are seen in workers who 

experience an acute reaction to 1,3- 

dinitrobenzene (Hajjar et al., 1992). The 

EPA IRIS assessment (USEPA, 1990b) of 

the carcinogenicity of 1,3- 

dinitrobenzene currently lists it as 

Group D (not classifiable as to human 

carcinogenicity). 

The primary adverse biological effects 

from exposure to 1,3-dinitrobenzene are 

on red blood cells, spleen, and testes. 

The RfD for 1,3-dinitrobenzene is 0.0001 

mg/kg/day (Cody et al., 1981). The RfD 

was derived from a NOAEL of 0.4 mg/ 

kg/day in a subchronic oral study in rats 

where increased spleen weight was 

identified as the critical effect (Cody et 

al., 1981). A composite UF of 3,000 

(intraspecies variability, interspecies 

variability, subchronic to chronic 

duration, and lack of chronic, 

developmental, and multigenerational 

reproductive toxicity studies) was 


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applied to the NOAEL to obtain the RfD. 

EPA calculated a non-cancer HRL of 0.7 

mg/L for 1,3-dinitrobenzene using the 

RfD of 0.0001 mg/kg/day for a 70 kg 

adult ingesting 2 L of drinking water per 

day and an RSC of 20%. 

The current EPA oral RfD value is 

supported by a more recent 1,3- 

dinitrobenzene assessment that was 

conducted by ATSDR, in which an oral 

intermediate duration minimal risk 

level of 0.0005 mg/kg/day for splenic 

hemosiderosis in male rats was 

established using a LOAEL of 0.54 mg/ 

kg/day (Linder et al., 1986; dose 

adjusted for a 7-day/week exposure) and 

a composite UF of 1,000 (intraspecies 

variability and interspecies variability, 

LOAEL to NOAEL). Based on EPA 

assumptions and a composite UF of 

3,000 (intraspecies variability, 

interspecies variability, LOAEL to 

NOAEL and subchronic to chronic 

duration) applied to the LOAEL of 0.54 

mg/kg/day, the resultant HRL value of 1 

mg/L supports the HRL value of 0.7 mg/ 

L derived from the IRIS RfD (ATSDR, 

1995). The IRIS assessment (USEPA, 

1990b) presents more detailed 

information about the potential health 

effects for 1,3-dinitrobenzene. 

c. Statutory Criterion #2 (Occurrence at 

Frequency and Levels of Public Health 

Concern) 

1,3-dinitrobenzene does not meet the 

SDWA statutory criterion #2 for 

regulatory determinations; it does not 

occur with a frequency and at levels of 

public health concern in public water 

systems based on EPA’s evaluation of 

the following occurrence information. 

The primary data for 1,3- 

dinitrobenzene are recent (2008–2010) 

nationally-representative drinking water 

monitoring data generated through 

EPA’s UCMR 2 (USEPA, 2014d). UCMR 

2 is the only dataset with finished water 

data for this contaminant. UCMR 2 

collected 32,017 samples from 4,137 

PWSs and 1,3-dinitrobenzene was not 

detected above the MRL (0.8 mg/L), 

which is only slightly higher than the 

HRL (0.7 mg/L). 

Findings from the available ambient 

water data for 1,3-dinitrobenzene are 

consistent with the results in finished 

water. Ambient water data in STORET 

included no measured results above 

0.33 mg/L in 143 samples from 70 sites 

(USEPA, 2012b). It should be noted that 

some occurrence above the HRL may 

have gone undetected since reporting 

levels are not documented. 

d. Statutory Criterion #3 (Meaningful 

Opportunity) 

EPA finds that 1,3-dinitrobenzene 

does not meet the SDWA statutory 

criterion for regulatory determinations; 

regulation of 1,3-dinitrobenzene does 

not present a meaningful opportunity 

for health risk reduction for persons 

served by PWSs based on the estimated 

exposed population, including sensitive 

populations. The estimated population 

exposed to 1,3-dinitrobenzene at or 

above the MRL is 0%; it was not found 

to occur in finished drinking water at 

levels > MRL (0.8 mg/L), which is only 

slightly higher than the HRL (0.7 mg/L), 

in 32,017 samples and 4,137 PWSs from 

the UCMR 2 monitoring. As a result, the 

agency finds that an NPDWR for 1,3- 

dinitrobenzene does not present a 

meaningful opportunity for health risk 

reduction. 

EPA also evaluated whether 

information is available regarding the 

potential health effects on children and 

other sensitive populations. Individuals 

with a genetic predisposition to 

methemoglobinemia (estimated 

prevalence in the general population = 

1% or 1 per 100) and/or hemosiderosis, 

neonates, and those co-exposed to other 

hemolytic agents, could be more 

sensitive to exposure to 1,3- 

dinitrobenzene (ATSDR, 1995; Jaffe and 

Hultquist, 1989). Males having sperm 

production complications could also 

have increased sensitivity to 1,3- 

dinitrobenzene exposure (Hajjar et al., 

1992). There is currently no 

multigenerational animal study 

available for 1,3-dinitrobenzene, and no 

data available from studies of 1,3- 

dinitrobenzene developmental toxicity 

(Hajjar et al., 1992). However, the RfD 

incorporated a UF for this database 

deficiency. The IRIS assessment 

(USEPA, 1990b) presents more detailed 

information about the potential health 

effects and sensitive populations for 1,3- 

dinitrobenzene. 

e. Preliminary Regulatory Determination 

for 1,3-dinitrobenzene 

The agency is making a preliminary 

determination to not regulate 1,3- 

dinitrobenzene with an NPDWR after 

evaluating health, occurrence, and other 

related information against the three 

SDWA statutory criteria. While data 

suggest that 1,3-dinitrobenzene may 

have an adverse effect on human health, 

the occurrence data indicate that 1,3- 

dinitrobenzene is not occurring or not 

likely to occur in PWSs with a 

frequency and at levels of public health 

concern. Therefore, the agency has 

determined that an NPDWR for 1,3- 

dinitrobenzene would not present a 

meaningful opportunity to reduce 

health risk for persons served by PWSs. 

The Regulatory Determinations 3 

Support Document (USEPA, 2014b) and 

the Occurrence Data from the Second 

Unregulated Contaminant Monitoring 

Regulation (UCMR 2) (USEPA, 2014d) 

present additional information and 

analyses supporting the agency’s 

evaluation of 1,3-dinitrobenzene. 

3. Strontium 

a. Background 

Strontium is a naturally occurring 

element (atomic number 38) and a 

member of the alkaline earth metals 

(ANL, 2007). There are several 

radioactive strontium isotopes formed 

by nuclear fission of uranium or 

plutonium. The best known is 90Sr, a 

legacy from above ground testing of the 

atomic bomb (half-life 29 years). Since 

drinking water contamination by 

radioactive isotopes, including beta 

particle emitters, is covered under the 

existing radionuclides rule, this FR 

notice deals primarily with the stable 

88Sr isotope which represents 83% of 

total environmental strontium (ATSDR, 

2004). 

Strontium mineral mining ceased in 

the United States in 1959. The United 

States imports both strontium minerals 

for refining and refined strontium 

containing compounds (USGS, 2009). 

Imports of strontium minerals and 

compounds were approximately 31,000 

to 38,500 metric tons from 1994 to 2001 

and have declined since 2001 (ATSDR, 

2004; USGS, 2009). In the United States, 

total consumption of strontium minerals 

and compounds was 16,700 metric tons 

of strontium content in 2004 and 

approximately 7,750 metric tons in 2008 

(USGS, 2009). 

Historically, the most important 

commercial use of strontium has been in 

the faceplate glass of cathode-ray tube 

televisions to block x-ray emissions 

(ATSDR, 2004). Conversely, flat panel 

televisions incorporating LCD or Plasma 

displays are not capable of emitting xradiation; therefore, they do not require 

strontium (FDA, 2011). As flat panel 

technology has become widespread in 

the United States in the last decade, 

demand for strontium for this 

application has fallen (USGS, 2009). In 

2008, approximately 30% of commercial 

strontium consumption was in 

pyrotechnics and signals (as strontium 

nitrate and other compounds), 30% in 

ferrite ceramic magnets (as strontium 

ferrite), 10% in master alloys (as 

strontium metal), 10% in pigments and 

fillers (as strontium chromate), 10% in 

electrolytic production of zinc (as 

strontium carbonate), and 10% in other 

applications such as fluorescent lights 

(strontium phosphate), toothpaste 

(strontium chloride), and medicines 

(strontium chloride and strontium 

peroxide). The feed material for most 


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applications is strontium carbonate 

(ATSDR, 2004; HSDB, 2010; USGS, 

2009). Strontium can exist in oxidation 

states 0 and +2; under normal 

environmental conditions it is found in 

the +2 oxidation state in various ionic 

or salt forms. Strontium is considered to 

have moderate or moderate-to-low 

mobility in soils. The mobility of 

strontium in water can increase with 

increased salt concentrations due to a 

decrease in sorption to sediments 

(USEPA, 20104b). The Regulatory 

Determination 3 Support Document 

(USEPA, 2014b) for this notice presents 

more detailed background information 

on strontium. 

b. Statutory Criterion #1 (Adverse 

Health Effects) 

Strontium meets the SDWA statutory 

criterion #1 for regulatory 

determinations; it may have an adverse 

effect on the health of persons. The 

primary target of strontium exposure is 

the bone. The chemical similarity of 

strontium to calcium allows it to 

exchange imperfectly for calcium in a 

variety of biological processes; the most 

important of these is the substitution of 

calcium in bone, affecting skeletal 

development. Due to the MOA for 

strontium toxicity, strontium uptake 

into bone is affected by the intake of 

nutrients related to bone formation, 

such as calcium, phosphorous, and 

vitamin D (Clarke, 2008; Grynpas and 

Marie, 1990; Marie et al., 1985). The 

decreased calcification in bones results 

in increased width of the epiphyseal 

cartilage, changes in the pattern of 

calcification, abnormally long 

metaphyses, reduction in bone 

mineralization, and active osteoclasts in 

young rats (Marie and Hott, 1986; 

Matsumoto, 1976; Neufeld and Boskey, 

1994; Storey, 1961). Due to this effect on 

growing bones, infants, children, and 

adolescents are of particular concern as 

a sensitive population. 

A study based on decreased bone 

calcification rate in male weanling rats 

(i.e., comparable to the sensitive time 

period in humans), which administered 

strontium chloride in drinking water for 

nine weeks (Marie et al., 1985), was 

identified by EPA as the critical study 

for RfD determination. The RfD was 

established by using the BMD method 

and based on the lower 95% confidence 

limit (BMDL) of 328 mg/kg/day for a one 

standard deviation decrease in bone 

calcification compared to control. Using 

a composite UF of 1000 (10 for 

intraspecies variability, 10 for 

interspecies variability, and 10 for 

database uncertainties) the RfD for 

strontium is calculated to be 0.3 mg/kg/ 

day. This RfD is supported by additional 

studies reporting bone effects on 

weanling rats at similar dose levels 

(Grynpas and Marie, 1990; Storey, 

1961). EPA calculated a non-cancer HRL 

of 1500 mg/L for strontium using the RfD 

of 0.3 mg/kg/day, a default RSC of 20% 

and age-specific exposure factors (i.e., 

drinking water intake expressed as liters 

per kg of body weight) for the sensitive 

population of birth through 18 years to 

reflect the most active period of bone 

growth and development (see section 

IV.B.10.d.3). 

EPA released an IRIS assessment for 

strontium in 1992 and developed an RfD 

of 0.6 mg/kg/day based on the Storey, 

1961 study. The IRIS assessment was 

completed before the 1998 changes to 

the IRIS program wherein the agency 

develops and peer reviews a detailed 

Toxicological Review before posting an 

IRIS summary. The point of departure 

for the 1992 IRIS RfD of 0.6 mg/kg/day 

is a NOAEL of 190 mg Sr/kg-day with 

a composite UF of 300 (10 for 

interspecies variability, 3 for 

intraspecies variability, and 10 for 

database uncertainties). This would 

yield an HRL of 3000 mg/L, using the 

same age-specific exposure adjustment 

factors described above. If the agespecific exposure adjustment factors 

were not used, the HRL would be 2000 

mg/L based on the OW assessment, or 

4000 mg/L based on the IRIS assessment. 

As noted in section III.C.1.c, EPA 

evaluates the existing data and performs 

a literature search for studies published 

after the available health assessment is 

completed to determine if new 

information suggests a different 

outcome. In cases where the review 

suggests that a change the existing RfD 

or cancer assessment is needed, the EPA 

Office of Water prepares and 

independently peer-reviews an OW 

Assessment of the data. In the case of 

strontium and because newer 

information provided additional 

support for the 1985 Marie et al. study, 

EPA chose to use the BMDL of 328 mg/ 

kg/day from Marie et al., (over the 1961 

Storey study) for the following reasons: 

(a) Marie et al., (1985) reported the 

doses rather than estimated the doses; 

(b) the study duration was longer (63 

days for Marie as compared to 20 days 

for Storey); (c) the monitoring of the 

bone effects for Marie et al., (1985) was 

more quantitative than the 

photomicrographs evaluated by Storey 

(1961); (d) dosing was provided via 

drinking water, the medium of interest 

(rather than a weakly soluble SrCO3 in 

the diet); (e) Marie et al., (1985) reported 

the strain of rats and the age of the 

animals, at the time that dosing was 

initiated and completed; (f) the data 

were amenable to dose-response 

modeling to identify the BMD and 

BMDL; and (g) the dietary calcium 

provided in the Storey study was three 

times higher than that in the Marie 

study, making those rats less at risk due 

to the calcium and strontium 

competition for uptake, as verified by a 

comparison of serum data from the two 

studies. The OW assessment uses a 10x 

uncertainty factor for intraspecies 

variability, rather than the 3x factor 

used in the 1992 IRIS assessment 

because it is not clear if the window of 

vulnerability was adequately captured, 

since the weanling rats were exposed 

only for 28–63 days, a period that did 

not include exposure during gestation, 

lactation, and through young adulthood. 

EPA requests comment on its revised 

RfD calculation and on its proposal to 

use the OW assessment in lieu of the 

RfD from the 1992 IRIS assessment. 

There is inadequate information to 

assess the carcinogenic potential of 

strontium due to the lack of adequate 

studies of chronic duration. The Health 

Effects Support Document (USEPA, 

2014c) for this determination presents 

more detailed analysis of the health 

effects of strontium. 

c. Statutory Criterion #2 (Occurrence at 

Frequency and Levels of Public Health 

Concern?) 

Strontium meets the SDWA statutory 

criterion #2 for regulatory 

determinations; it does occur with a 

frequency and at levels of public health 

concern in public water systems based 

on EPA’s evaluation of the following 

occurrence information. 

EPA used the National Inorganics and 

Radionuclides Survey (NIRS) (USEPA, 

2008b) as the primary data source to 

evaluate the occurrence of strontium in 

PWSs. It provides contaminant 

occurrence data from 989 CWSs served 

by ground water sources. Each of these 

randomly selected PWSs was sampled a 

single time between 1984 and 1986. Of 

the 989 systems in NIRS, 980 (99%) had 

detectable levels of strontium ranging 

from 1.53 to 43,550 mg/L. The mean 

concentration was 603 mg/L. 

Approximately 7.0% (69 of 989) of the 

NIRS PWSs detected strontium at a level 

greater than the HRL (1500 mg/L) and 

14.3% (141 of 989) detected strontium 

at a level greater than 1⁄2 HRL (750 mg/ 

L). Extrapolated by the total number of 

ground water CWSs found nationally, 

this represents 2,798 and 5,718 

groundwater CWSs that could have 

strontium at a level greater than the HRL 

and the 1⁄2 HRL, respectively. These 

figures are summarized in Table 8 

(USEPA, 2014b). 


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TABLE 8—ESTIMATES OF POPULATION EXPOSED TO STRONTIUM, OBSERVED AND EXTRAPOLATED FROM NIRS 

Threshold 

National Inorganics and Radionuclides Survey 

(NIRS) 

Extrapolation of NIRS data to groundwater 

systems nationwide 

Systems Population Systems Population 

Systems with Detectable Concentrations ........ 99.1% 

(980 of 989) 

99.9% 

(1.481M of 1.482M) 

99.1% 

(39.7K of 40.1K) 

99.9% 

(93.0M of 93.1M) 

Systems detecting strontium above one half 

the HRL (>750 μg/L) .................................... 14.3% 

(141 of 989) 

16.6% 

(246K of 1.5M) 

14.3% 

(5.7K of 40.1K) 

16.6% 

(15.4M of 93.1M) 

Systems detecting strontium above the HRL 

(>1500 μg/L) ................................................. 7.0% 

(69 of 989) 

10.7% 

(159K of 1.5M) 

7.0% 

(2.8K of 40.1K) 

10.7% 

(10.0M of 93.1M) 

As a point of reference to the earlier 

IRIS assessment, if EPA used the HRL 

derived from this assessment of 3000 

mg/L, 30/989 systems (3%) would have 

finished water samples that exceed the 

HRL using the NIRS data, compared to 

69/989 (7%) using the HRL of 1500 mg/ 

L derived from the more recent OW 

assessment. 

Finished water data, analyzed 

between 1998 and 2005, from Ohio and 

Illinois are also consistent with the 

NIRS data. The State of Illinois reported 

results from testing 21 drinking water 

samples from 19 PWSs and strontium 

was detected in all 21 samples (100%) 

from all 19 systems (100%). 

Approximately 23.8% (5 of 21) of 

samples from five systems (26.3%) had 

strontium at levels greater than the 1⁄2

HRL (750 mg/L) and approximately 

23.8% (5 of 21) of samples from five 

systems (26.3%) had strontium at levels 

greater than the HRL (1500 mg/L) 

(USEPA, 2012b). The State of Ohio 

reported results from testing 77 samples 

from 32 PWSs and strontium was 

detected in 75 samples (97.4%) from 30 

different systems (93.8%). 

Approximately 27.3% (21 of 77) of 

samples from 10 systems (31.3%) had 

strontium at levels greater than the 1⁄2

HRL and approximately 23.4% (18 of 

77) of samples from seven systems 

(21.9%) had strontium at levels greater 

than the HRL (USEPA, 2014b). 

Although there are limited surface 

water data available for strontium, the 

available data are consistent and 

demonstrate high occurrence in surface 

waters. Ambient water data for 

strontium are also consistent with high 

occurrence in finished water, which is 

expected since it is a naturally occurring 

element. The NAWQA Quality of Public 

Supply Wells (Toccalino et al., 2010) 

study collected water samples from 

source (untreated) groundwater public 

supply wells in 41 states. Each well was 

sampled once from 1993–2007 and 

100% of samples (503 of 503) had a 

strontium detection. Of the detections, 

25.1% (126 of 503) were above the 1⁄2

HRL (750 mg/L) and 12.1% (61 of 503) 

were above the HRL (1500 mg/L). 

Additional occurrence information on 

strontium can be found in the 

Regulatory Determinations 3 Support 

Document (USEPA, 2014b). 

d. Statutory Criterion #3 (Meaningful 

Opportunity?) 

EPA makes a preliminary finding that 

strontium meets the SDWA statutory 

criterion #3 for regulatory 

determinations; regulation of strontium 

in drinking water presents a meaningful 

opportunity for health risk reduction 

based on the estimated exposed 

population, potential impacts on 

sensitive populations and estimated 

exposure from other sources (e.g., food). 

1. National Population Exposed: In 

the NIRS dataset 989 ground water 

systems were sampled serving a 

population of 1.48 million. The NIRS 

data indicates that the population 

exposed to strontium at a level greater 

than the HRL (1500 mg/L) is 158,557 

(11%) and the 1⁄2 HRL (750 mg/L) is 

245,870 (17%) (USEPA, 2012b). EPA 

also performed national extrapolations 

generated by multiplying the NIRS 

findings of system/population 

percentages and the national system/

population inventory numbers for PWSs 

developed from EPA’s Safe Drinking 

Water Information System, the CWSS, 

and UCMR. Out of the 93.1 million 

people served by 40,106 ground water 

CWSs in the nation, the national 

extrapolation indicates that 10.0 million 

may be exposed to concentrations 

greater than the HRL (1500 ug/L) and 

15.4 million may be exposed to 

concentrations greater than the 1⁄2 HRL 

(750 ug/L). The system and population 

estimates are summarized in Table 8. 

Strontium occurs naturally and is 

abundant in the environment. Its 

occurrence in water at concentrations 

>HRL may be a reflection of the geologic 

and geochemical setting of the source 

waters for PWSs. The NIRS drinking 

water data showed that strontium was 

detected in one or more systems 

sampled in all 48 continuous states, 

Alaska and Puerto Rico (Hawaii was not 

included in NIRS). The occurrence data 

(e.g., NIRS) show that PWSs with 

strontium at concentrations greater than 

the HRL and the 1⁄2 HRL occur in 26 

states and 34 states, respectively 

(USEPA, 2014b). 

2. Exposure from media other than 

water: EPA has determined that there is 

a meaningful opportunity to regulate 

strontium in drinking water to reduce 

the public’s overall exposure after 

evaluating the available exposure data 

from media other than water. Although 

strontium is known to occur in food, air, 

and soil, data on levels in those media 

are limited as are estimates of intake 

from those sources. Therefore, EPA used 

the default 20% RSC to calculate the 

HRL. This section provides a summary 

of the available exposure data. 

An FDA Total Diet Study by 

Pennington and Jones (1987) collected 

234 individual foods in 1984 from three 

cities in one region of the country and 

indicated dietary intakes of 493 mg/day 

for young children (6 to 11 months), 928 

to 1,388 mg/day for 14 to 16 year old 

adolescents, and 979–1,489 mg/day for 

adults. The FDA Total Diet Study foods 

are prepared with distilled water and do 

not reflect any contributions from the 

cooking water during preparation of 

foods that absorb water such as rice and 

pasta. Thus, the strontium in many 

foods will be impacted by the strontium 

levels in the local water supply. Using 

the mean of the detected water 

concentrations from the NIRS dataset 

(603 mg/L), the estimated water intake 

for young children (90th percentile 

water intake of 1L/day) is 603 mg/day 

and 1,206 mg/day for adults (90th 

percentile water intake of 2L/day). The 

estimated strontium intakes from air 

and soil are very low compared with 

those from food and drinking water. The 

estimated air exposure for children is 

0.1 mg/day and for adults is 0.3 mg/day 

(Dzubay and Stevens, 1975). The 

estimated exposure from soil is 24 mg/ 

day for children and 12 mg/day for 


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adults (Shacklette and Boerngen, 1984). 

No data were identified on consumer 

products, such as toothpaste that 

contain strontium as an ingredient or 

impurity. 

3. Sensitive populations: Children are 

expected to be a sensitive population, 

since they are actively growing and 

strontium can substitute for calcium in 

growing bone. This means that changes 

in bone structure and homeostasis may 

have more severe and/or a long-term 

impact than similar changes in adults. 

These effects would be expected to have 

the greatest impact during periods of 

rapid growth in the developing fetus, 

during childhood and adolescence, 

particularly if their calcium intake is 

insufficient (Abrams et al., 2000; Lee et 

al., 1996; Matkovic et al., 2005; Storey, 

1961). The estimated populations of 

pregnant women (and thus fetuses) and 

of children (<17 years old) are 6 and 75 

million, respectively (O’Day et al., 

1998). The RfD was based on changes in 

bone growth in weanling rats (i.e., the 

sensitive population). As a result, the 

data do not include the risk during 

prenatal development and lactation so 

these factors were considered when 

selecting the UFs used to derive the RfD. 

Age-specific exposure factors (USEPA, 

2012c) were also used to reflect the 

sensitive population (birth through 18 

years) in derivation of the HRL. 

Exposures from drinking water at or 

below the HRL (1500 mg/L) are expected 

to be protective of the sensitive 

population, assuming that 80% of 

exposure comes from other sources such 

as air, soil and food. 

The toxic effects of strontium result 

from strontium ions substituting for 

calcium ions, therefore calcium 

deficiency would be expected to result 

in increased risk among sensitive 

populations. In this respect, it is 

important to note that recent NHANES 

data indicate that about 50% of females, 

nine years and older, fail to receive 

adequate calcium from diet and 

supplements on a daily basis (IOM, 

2010). Groups with higher risks of 

becoming calcium deficient include: 

Adolescent girls, postmenopausal 

women, amenorrheic women, female 

athletes, vegans, and individuals with 

lactose intolerance or cow’s milk 

allergies (IOM, 2010; NIH, 2011a). 

The major route of elimination of 

strontium is via the kidneys, therefore 

individuals with impaired renal 

function are another sensitive 

population. This population may 

potentially have impaired strontium 

clearance, as has been shown in renal 

failure patients. There are 

approximately 20 million people (10%) 

above the age of 20 with chronic kidney 

disease (CDC, 2010) and 548,000 people 

with kidney end-stage renal disease 

(USRDS, 2010), who may be at an 

increased risk. People with disorders 

affecting the normal equilibrium 

between the breakdown of old bone and 

the formation of new bone (such as 

Paget’s disease) might also be sensitive 

to strontium exposure (D’Haese et al., 

1999, 2000; Schrooten et al., 1998, 2003; 

Tothill et al., 1983). According to the 

National Institute of Arthritis and 

Musculoskeletal and Skin Diseases, 

there are approximately 1 million 

people (1.2 people per 100 men and 

women age 45 to 74) diagnosed with 

Paget’s disease of the bone (NIH, 2011b). 

The Health Effects Support Document 

(USEPA, 2014c) for strontium presents 

more detailed information about the 

potential health effects and sensitive 

populations. Because the RfD includes 

an uncertainty factor of 10 for 

intraspecies variability, the RfD is also 

expected to be protective of these 

sensitive populations. 

d. Preliminary Regulatory 

Determination 

At this time, the agency is making a 

preliminary determination to regulate 

strontium with an NPDWR after 

evaluating the available health, 

occurrence, and other related 

information against the three SDWA 

statutory criteria. Specifically, it is 

EPA’s preliminary determination that 

(a) strontium may have an adverse effect 

on the health of persons, (b) it is known 

to occur or there is substantial 

likelihood that strontium will occur in 

public water systems with a frequency 

and at levels of public health concern, 

(c) regulation of strontium with an 

NPDWR presents a meaningful 

opportunity to reduce health risks for 

persons served by PWSs. 

It is important to note that the agency 

included strontium in UCMR 3. As of 

January 2014, a preliminary analysis 

(USEPA, 2014e) of the first nine months 

of the UCMR 3 monitoring data indicate 

that 4.9% (70 of 1,423) of systems, 3.8% 

(175 of 4,547) of entry points, and 3.9% 

(274 of 7,061) of samples have detects 

of strontium at levels greater than the 

HRL of 1500 mg/L. While EPA believes 

the occurrence data from NIRS (in 

concert with the supplemental 

information discussed earlier) are 

sufficient to make the regulatory 

determination, the agency believes the 

additional monitoring results from 

UCMR 3 will assist EPA in making the 

final regulatory determination for 

strontium and in developing the 

proposed NPDWR. As noted in section 

III.A.3, this regulatory determination 

process is distinct from the more 

detailed analyses needed to develop a 

national primary drinking water 

regulation. To inform the agency, the 

EPA plans to conduct more extensive 

field testing of treatment technologies to 

assess the effectiveness of strontium 

removal in PWSs prior to promulgating 

a national primary drinking water 

regulation. Thus a decision to regulate 

is the beginning of the agency’s 

regulatory development process, not the 

end. As the agency collects additional 

information about drinking water and 

other sources of exposure (and performs 

more detailed analyses), this 

information will inform the agency’s 

opinion as to whether strontium should 

be regulated. The agency asks the public 

to submit any data or information that 

may be useful in evaluating drinking 

water and other sources of exposure 

(e.g., food, food prepared in drinking 

water, air, soil, etc.). 

4 and 5. Terbufos and Terbufos Sulfone 

a. Background 

Terbufos is a phosphorodithioate 

pesticide (i.e., an organophosphate) 

used as an insecticide-nematicide to 

control a variety of insect pests, 

primarily used on corn and sugar beets 

(USEPA, 2006c). Terbufos sulfone is a 

degradate of terbufos. EPA’s most recent 

Pesticide Industry Sales and Usage 

report states that between 5 and 7 

million pounds of terbufos active 

ingredient were used in 1999 and 

between 3 and 5 million pounds of 

active ingredient were used in 2001 

(USEPA, 2004). There are no industrial 

release data available for terbufos from 

TRI. As a pesticide degradate, terbufos 

sulfone is neither produced nor used 

commercially. Total toxic residues of 

terbufos and degradates are highly 

mobile and persistent in the 

environment, with terbufos sulfone 

being more mobile and substantially 

more persistent than terbufos (USEPA, 

2006c). 

b. Statutory Criterion #1 (Adverse 

Health Effects?) 

Terbufos and its degradate, terbufos 

sulfone, meet the SDWA statutory 

criterion #1 for regulatory 

determinations; they may cause an 

adverse effect on the health of persons. 

Terbufos and terbufos sulfone belong to 

a group of pesticides called 

organophosphates, which share a 

common mechanism of toxicity. 

Organophosphates affect the proper 

function of the nervous system by 

inhibiting ChE, an essential enzyme in 

neurotransmission. There has been no 

evidence that terbufos is carcinogenic in 

animal studies (Rapp, 1974; Silverman 


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et al., 1986) and it is classified as a class 

D carcinogen (inadequate evidence of 

carcinogenicity) (USEPA, 1988). 

Overall, health effects information for 

the terbufos sulfone degradate is 

lacking; there are no long-term studies 

or cancer classification for terbufos 

sulfone. 

The 2006 OPP RED assessment 

(USEPA, 2006c) established an oral RfD 

for terbufos of 0.00005 mg/kg/day, 

derived from the NOAEL of 0.005 mg/ 

kg/day for ChE inhibition in the 28-day 

and 1-year dog studies by Shellenberger 

(1984) and Shellenberger and Billups 

(1986). A composite UF of 100 

(interspecies and intraspecies 

variability) was applied to the NOAEL 

to obtain the RfD. EPA calculated a noncancer HRL of 0.35 mg/L for terbufos 

using the RfD of 0.00005 mg/kg/day for 

a 70 kg adult ingesting 2 L of drinking 

water per day and an RSC of 20%. The 

agency has not developed an RfD for 

terbufos sulfone because subchronic and 

chronic studies are not available. 

However, Bailey (1988) conducted a 14- 

day study of both terbufos and its 

sulfone degradate in dogs. The NOAEL 

based on ChE activity for terbufos 

sulfone was greater than the LOAEL of 

2.5 mg/kg/day for the same endpoint 

following 14-day dosing with the parent 

compound terbufos. This suggests that 

the terbufos sulfone degradate is less 

toxic than its parent, and that the use of 

the terbufos HRL of 0.35 mg/L for the 

degradate, terbufos sulfone, is 

acceptable. The OPP RED (USEPA, 

2006c) presents more detailed 

information about the health effects for 

terbufos and terbufos sulfone. 

c. Statutory Criterion #2 (Occurrence at 

frequency and levels of public health 

concern?) 

Terbufos and terbufos sulfone do not 

meet the SDWA statutory criterion #2 

for regulatory determinations; they do 

not occur with a frequency and at levels 

of public health concern in public water 

systems based on EPA’s evaluation of 

the following occurrence information. 

The primary data for terbufos sulfone 

are nationally-representative finished 

water monitoring data generated 

through EPA’s UCMR 2 (2008–2010) 

(USEPA, 2014d). UCMR 2 collected 

32,012 finished water samples from 

4,138 PWSs (serving ∼ 230 million 

people) and terbufos sulfone was 

detected in only one sample, at a 

concentration of 0.42 mg/L. The MRL 

was 0.4 mg/L, which is slightly higher 

than the HRL (0.35 mg/L) (USEPA, 

2012d). The primary data for terbufos 

are from the UCMR 1 screening survey 

(2001–2003) (USEPA, 2008c). The 

UCMR 1 screening survey collected 

2,301 finished water samples from 295 

PWSs. Terbufos was not detected at 

levels at or above the MRL (0.5 mg/L), 

which is slightly higher than the HRL 

(0.35 mg/L) (USEPA, 2008c). Finished 

water data for terbufos and terbufos 

sulfone from California, Iowa, USDA, 

and USGS are also consistent with the 

UCMR 1 and UCMR 2 data. The State 

of California reported no detections of 

terbufos in 191 samples from 23 PWSs 

(see USEPA, 2014b). The State of Iowa 

reported no detections of terbufos 

sulfone from 13 wells (see USEPA, 

2014b). The USDA PDP monitored for 

terbufos (2,597 samples) and terbufos 

sulfone (2,923 samples) in finished 

water from 2001 to 2009 and reported 

no detections at or above method 

reporting levels ranging from 0.005 mg/ 

L to 0.1 mg/L (USDA, 2012: USEPA, 

2014b). The USGS PMP monitored for 

terbufos in finished water in 1999 and 

reported no detections, at or above their 

method reporting level of 0.013 mg/L 

(Blomquist et al., 2001). 

Terbufos and (very limited) terbufos 

sulfone occurrence data for ambient 

water from EPA, STORET, and several 

USGS programs or studies are consistent 

with those for finished water. The USGS 

NAWQA Program (1992–2001) reported 

no groundwater detections above the 1⁄2

HRL (0.175 mg/L) or the HRL (0.35 mg/ 

L) for terbufos in 20,960 samples at 

7,118 sites. NAWQA reported surface 

water detections for terbufos in 28 of 

14,480 samples (0.19%) at 20 of 1,907 

sites (1.05%). Of the 28 surface water 

detections for terbufos, only four 

samples (0.03%) at four sites (0.21%) 

were above the 1⁄2 HRL and only one 

sample (0.01%) at one site (0.05%) was 

above the HRL (Gilliom et al., 2007). 

The NAWQA Carbonate Aquifer Study 

(1993–2005; Lindsey et al., 2008) and 

the NAWQA Domestic Well Water 

Quality Study (1991–2004; DeSimone, 

2009) reported no detections for 

terbufos above the 1⁄2 HRL or the HRL 

in 1,027 and 2,539 samples, 

respectively. The NAWQA National 

Synthesis Program (1992–2001) reported 

no groundwater detections for terbufos 

above the 1⁄2 HRL or the HRL and one 

surface water detection (0.56 mg/L), from 

agricultural sites, above the HRL 

(Gilliom et al., 2007). 

Ambient water data from a two phase 

USGS study conducted between 2002 

and 2005 by Hopple et al. (2009) and 

Kingsbury et al. (2008) reported no 

terbufos detections in the 221 Phase 1 

groundwater samples nor the 146 Phase 

1 surface water samples. In Phase 2, 

there were no detections of terbufos 

from 48 raw and 48 finished 

groundwater samples. Ambient water 

data from a USGS study conducted 

between 1993 and 2007 by Toccalino et 

al. (2010) reported no terbufos 

detections in 898 groundwater samples. 

Terbufos ambient data reported in 

EPA’s OPP RED for Terbufos (USEPA, 

2006c) document included 20 

detections in 4,563 groundwater 

samples from 13 States. The detections 

ranged from 0.01 to 20 mg/L, a range that 

extends both above and below the 1⁄2

HRL (0.175 mg/L) and the HRL (0.35 mg/ 

L). The USGS PMP monitored for 

terbufos in ambient water in 1999 and 

reported no detections (Blomquist et al., 

2001). 

Terbufos ambient data are reported in 

STORET from 17 States (USEPA, 

2012b). No groundwater detections were 

reported in 699 samples at 441 sites. 

STORET reported surface water 

detections in 457 of 5,826 samples 

(7.84%) at 138 of 625 sites (22.1%). Of 

the 457 surface water detections, only 

23 samples (0.39%) at 14 sites (2.24%) 

were above the 1⁄2 HRL and only two 

samples (0.03%) at two sites (0.32%) 

were above the HRL. 

d. Statutory Criterion #3 (Meaningful 

Opportunity?) 

Terbufos and terbufos sulfone do not 

meet the SDWA statutory criterion #3 

for regulatory determinations; regulation 

of terbufos and terbufos sulfone do not 

present a meaningful opportunity for 

health risk reduction based on the 

estimated population exposed, 

including sensitive populations. The 

estimated population exposed to 

terbufos at or above the MRL is 0%; the 

compound was not found to occur in 

finished water at levels greater than or 

equal to the MRL (0.4 mg/L), which is 

slightly higher than the HRL (0.35 mg/L), 

in 2,301 samples from 295 PWSs in 

UCMR 1 (USEPA, 2008c). The estimated 

population exposed to terbufos sulfone 

at a level of public health concern 

(based on the HRL for terbufos) is 

44,600 (0.02% of the population served 

by PWSs); there was only one detection 

greater than the HRL in 4,138 PWSs (1 

of 32,012 samples in UCMR 2) (USEPA, 

2014d). As a result, the agency finds 

that an NPDWR does not present a 

meaningful opportunity for health risk 

reduction. 

EPA also evaluated whether health 

information is available regarding the 

potential health effects on children and 

other sensitive populations. 

Developmental studies with terbufos in 

rats and rabbits did not find any 

developmental effects (USEPA, 2003c). 

There are no data on reproductive and 

developmental effects for terbufos 

sulfone. No sensitive populations were 

identified or characterized. The OPP 

RED (USEPA, 2006c) presents more 


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detailed information about the potential 

health effects and sensitive populations 

for terbufos and terbufos sulfone. 

e. Preliminary Regulatory Determination 

The agency is making preliminary 

determinations to not regulate terbufos 

and terbufos sulfone with NPDWRs after 

evaluating health, occurrence, and other 

related information against the three 

SDWA statutory criteria. While the data 

suggests that terbufos and terbufos 

sulfone may have adverse effects on 

human health, the occurrence data 

indicate there is no substantial 

likelihood that terbufos or terbufos 

sulfone will occur in PWSs with a 

frequency and at levels of public health 

concern. Therefore, the agency finds 

that NPDWRs for terbufos and terbufos 

sulfone would not present meaningful 

opportunities to reduce health risk for 

persons served by PWSs. The 

Regulatory Determinations 3 Support 

Document (USEPA, 2014b) presents 

additional information and/or analyses 

supporting the agency’s evaluation of 

terbufos and terbufos sulfone. 

V. What is the Status of the Agency’s 

Evaluation of Chlorate and 

Nitrosamines? 

The agency will review the existing 

MDBP regulations as part of the SY3. 

Because chlorate and nitrosamines are 

DBPs that can be introduced or formed 

in public water systems partly because 

of disinfection practices, the agency 

believes it is important to evaluate these 

unregulated DBPs in the context of the 

review of the existing DBP regulations. 

DBPs need to be evaluated collectively, 

because the potential exists that the 

chemical disinfection used to control a 

specific DBP could affect the 

concentrations of other DBPs. Therefore, 

the agency is not making a regulatory 

determination for chlorate and 

nitrosamines at this time. The agency 

expects to complete the review of these 

DBPs by the end of 2015. 

A. Chlorate 

The following sections provide the 

background, health and occurrence 

information/data that the agency has 

collected to date for chlorate. If the 

public has any additional health and 

occurrence information that may be 

useful as the agency evaluates chlorate 

in the context of the existing MDBP 

rules, please provide this information to 

the docket. 

1. Background 

The chlorate anion (ClO3

¥) forms a 

variety of salts (e.g., sodium chlorate, 

calcium chlorate, potassium chlorate, 

and magnesium chlorate) collectively 

known as chlorates, which are powerful 

oxidizers. Chlorate compounds 

(especially sodium chlorate) are used as 

herbicides and to generate chlorine 

dioxide (ClO2) as a bleaching agent 

(USEPA, 2006a). Disinfection practices 

are the most important source of 

chlorate in drinking water; this includes 

formation as a DBP from use of chlorine 

dioxide and its presence in hypochlorite 

disinfectants as an impurity (USEPA, 

2006a). 

Chlorate can be formed during 

decomposition of hypochlorite (ClO¥) 

solutions, which are used as a 

disinfectant and/or oxidant in water 

treatment. Hypochlorite solutions that 

are more aged are generally less 

effective and require higher doses to 

achieve the treatment (disinfection) 

objectives, which can result in more 

chlorate to be introduced into the 

chlorinated water. In addition to being 

a DBP (along with chlorite) formed from 

the use of chlorine dioxide as a 

disinfectant, chlorate ion may also be 

present as an impurity in the chlorine 

dioxide (Gates et al., 2009; USEPA, 

2006a). Chlorate can also form by the 

reaction of chlorite with free chlorine 

applied as a residual disinfectant in the 

distribution system (Gallagher et al., 

1994). In addition, chlorite can be 

oxidized by a strong oxidant (such as 

ozone) to produce chlorate in the water 

(von Gunten, 2003). Chlorate salts 

readily dissolve in water and are highly 

mobile because of the absence. In the 

absence of redox reactions, the chlorate 

ion would be expected to partition 

predominantly into water and to be 

highly mobile in water. However, under 

most environmental conditions chlorate 

is subject to redox reactions, which are 

expected to reduce the concentration of 

chlorate in the water column (USEPA, 

2006a). 

2. Health Effects Information 

Acute ingestion of high levels of 

sodium chlorate has resulted in acute 

kidney failure and hemolysis among 

other effects based on numerous case 

reports of individuals accidently 

ingesting high levels of chlorate 

compounds (USEPA, 2006b; WHO, 

2005). A population-based case-control 

study of chlorate as a DBP at 

concentrations >200 mg/L identified 

significantly increased odds ratios for 

obstructive urinary defects, cleft palate, 

and spina bifida (Righi et al., 2012). The 

median chlorate exposure for the study 

population was 280 mg/L. In a casecontrol study of the same population in 

Italy, Aggazzotti et al. (2004) found no 

association between preterm births and 

exposure to chlorate. 

The animal studies provide clear and 

consistent evidence that subchronic and 

chronic exposure to chlorate results in 

effects on blood and thyroid. 

Subchronic studies in rats have reported 

decreased hemoglobin, hematocrit, and 

red blood cell (RBC) counts (AbdelRahman et al., 1984; Barrett, 1987; 

McCauley et al., 1995) and thyroid 

colloid depletion, follicular cell 

hypertrophy and hyperplasia (Hooth et 

al., 2001). 

A chronic study based on increased 

thyroid gland follicular cell hypertrophy 

in male rats (NTP, 2005a) was identified 

as the critical study for establishing an 

RfD of 0.03 mg/kg/day (USEPA, 2006b). 

The RfD was derived by using the BMD 

method and based on the lower 95% 

confidence limit (BMDL) of 28 mg/L as 

sodium chlorate (22 mg/L as chlorate), 

corresponding to 0.9 mg/kg/day 

(USEPA, 2006b), with a composite UF of 

30 for intraspecies (i.e., sensitive 

populations) and interspecies variability 

(i.e., thyroid hormone differences 

between humans and rats). EPA 

calculated a non-cancer HRL of 210 mg/ 

L for chlorate using the RfD of 0.03 mg/ 

kg/day for a 70 kg adult ingesting 2 L 

of drinking water per day and an RSC 

of 20%. 

A cancer risk assessment was not 

conducted for chlorate because sodium 

chlorate is classified as not likely to be 

carcinogenic to humans at doses that do 

not alter thyroid hormone homeostasis 

under the USEPA (2005b) Cancer 

Guidelines. The RfD is protective 

against acute alterations in thyroid 

homeostasis and therefore considered to 

also be protective of tumorigenicity as 

well as other chronic and subchronic 

adverse health effects discussed in the 

literature (Hooth et al., 2001; Khan et 

al., 2005; NTP, 2005a). 

EPA also evaluated whether health 

information is available regarding 

sensitive populations. According to the 

OPP RED, there was no pre- or postnatal 

sensitivity or susceptibility observed in 

the submitted developmental studies in 

rats and rabbits or the 2-generation 

reproduction study in rats. However, 

there is a concern for developing 

offspring because of the effects of 

inorganic chlorate on thyroid function 

in rats (USEPA, 2006a). Chlorate is one 

of a number or inorganic ions that may 

interfere with iodine uptake by the 

thyroid, but chlorate is not highly 

potent in this respect (Van Sande et al., 

2003). 

Chlorate may also cause hemolysis, 

thus persons with low red blood cell 

counts such as those with anemia may 

be particularly sensitive to sodium 

chlorate. Data from the 1994 National 

Health Interview Survey (O’Day et al., 


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1998) indicate that there were about 5 

million people in the U.S. who suffered 

from some form of anemia. About 3 to 

5% of the population may have an 

inherited glucose-6-phosphate 

dehydrogenase (G6PD) deficiency, with 

males more sensitive than females 

(Luzzatto and Mehta, 1989), and about 

1% may have a form of hereditary 

methemoglobinemia (Jaffe and 

Hultquist, 1989). Each one of these 

conditions is a contributor to low red 

blood cell counts within the population. 

Individuals co-exposed to other ions 

that decrease iodine uptake by the 

thyroid or have low RBC counts may be 

more sensitive to chlorate exposure. 

3. Occurrence Data and Information 

a. Drinking Water 

The 1997–1998 DBP ICR is currently 

the best available data source for 

characterizing the national occurrence 

baseline for chlorate. The DBP ICR, 

which included monitoring data for 296 

water systems serving 100,000 people or 

more (representing a total population of 

130 million), required water systems 

that use hypochlorite solutions or 

chlorine dioxide for disinfection to 

monitor for chlorate (USEPA, 1996). 

Subsequently, 82 water systems serving 

approximately 40 million people 

monitored and reported chlorate 

occurrence under the DBP ICR (using an 

MRL of 20 mg/L). Table 9 presents the 

number and percentage of samples and 

systems (along with the population 

served) that measured chlorate at levels 

exceeding the specified threshold 

concentrations (i.e., HRL and 1⁄2 HRL). 

These samples were associated with 

41.5% (34 of 82) of the ICR systems 

using hypochlorite solutions or chlorine 

dioxide for disinfection and 11.5% (34 

of 296) of all of the ICR systems. EPA 

assumes there was no occurrence of 

chlorate among the ICR systems that 

were not required to monitor for it, 

since they use disinfection techniques 

not expected to produce chlorate. 

Approximately 51.1% (878 of 1,719) of 

ICR samples from the finished water or 

distribution system of the systems 

required to monitor had chlorate at 

levels greater than the 1⁄2 HRL (105 mg/ 

L) and 19.3% (332 of 1,719) had 

chlorate at levels greater than the HRL 

(210 mg/L). The samples greater than the 1⁄2 HRL were associated with 73.2% (60 

of 82) of the ICR systems using 

hypochlorite solutions or chlorine 

dioxide for disinfection and 20.3% (60 

of 296) of all ICR systems (including 

those that were not required to monitor 

for chlorate). The samples greater than 

the HRL were associated with 41.5% (34 

of 82) of the ICR systems using 

hypochlorite solutions or chlorine 

dioxide for disinfection and 11.5% (34 

of 296) of all ICR systems (including 

those that were not required to monitor 

for chlorate) (McGuire et al., 2002). 

Since the DBP ICR was completed in 

1998, these data likely underestimate 

current (2012) chlorate occurrence 

among the systems serving 100,000 

people or more for the following two 

reasons: (1) Some of these systems may 

have changed the disinfectant type from 

chlorine gas to chlorine dioxide for 

compliance with the existing Stage 1 or 

Stage 2 DBP rules; and/or (2) some 

systems may have switched from 

chlorine gas to hypochlorite solution 

due to a security concern (i.e., a concern 

of safety of transportation and storage 

for chlorine gas). Disinfection surveys 

conducted by the AWWA Disinfection 

Systems Committee in 1998 and 2007 

have confirmed that chlorine dioxide 

and hypochlorite use has increased 

(AWWA Disinfection Systems 

Committee, 2008a, 2008b; Connell et al., 

2000a, 2000b). 

TABLE 9—SUMMARY OF CHLORATE MONITORING RESULTS UNDER THE DBP ICR 

Chlorate threshold 

Of DBP ICR PWSs that monitored for chlorate, 

samples and PWSs with at least one detection 

> threshold * 

Of all DBP ICR PWSs, PWSs with at least 

one detection > threshold and estimated population served ** 

Number (percentage) 

of DBP ICR samples 

with detection > 

threshold 

Number (percentage) 

of DBP ICR PWSs 

with at least one detection > threshold 

Number (percentage) 

of DBP ICR PWSs 

with at least one detection > threshold *

Population served by 

DBP ICR PWSs with 

at least one detection 

> threshold **

HRL (210 μg/L) ................................................ 332 of 1,719 

(19.3%) 

34 of 82 

(41.5%) 

34 of 296 

(11.5%) 

11.8 of 130 million 

(9.1%) 1⁄2 HRL (105 μg/L) ........................................... 878 of 1,719 

(51.1%) 

60 of 82 

(73.2%) 

60 of 296 

(20.3%) 

31.7 of 130 million 

(24.4%) 

* 82 PWSs that used hypochlorite or chlorine dioxide were required to monitor for chlorate during the DBP ICR monitoring period, based on 

their potential to form chlorate. Number and percentage of samples and PWSs are based on those 82 PWSs that monitored for chlorate. **The number and percentage of PWSs and population served > threshold is based on all 296 systems. EPA assumes that the 214 systems 

not required to monitor do not have chlorate concentrations above the thresholds. 

Finished water data for chlorate from 

California collected between 2001 and 

2007 show lower occurrence compared 

to the DBP ICR. The State of California 

reported results from testing more than 

1,200 drinking water samples from 45 

PWSs and chlorate was detected in 945 

samples (78.4%) from 24 different 

systems (53.3%) (Ranalli, B., 2013). 

Approximately 41.6% (501 of 1,205) of 

samples from 17 systems (37.8%) had 

chlorate at levels greater than the 1⁄2

HRL (105 mg/L) and approximately 

12.4% (149 of 1,205) of samples from 10 

systems (22.2%) had chlorate at levels 

greater than the HRL (210 mg/L) (Ranalli, 

B., 2013). 

It is important to note that the agency 

included chlorate in the UCMR 3, which 

is currently in process. UCMR 3 will 

provide a national dataset of chlorate 

occurrence in drinking water and will 

update the occurrence data provided by 

the DBP ICR. 

Ambient water data for chlorate are 

limited, but chlorate could be present in 

areas where it is used as an herbicide or 

discharged from paper plants where it is 

used as a bleaching agent. Since 

chlorate is a DBP, higher concentrations 

are expected in finished water than in 

ambient water. 

b. Exposure from media other than 

water 

There is very little quantitative 

information available on the occurrence 

of chlorate in food, air, and soil or other 

products resulting in residential 

exposures. Without reliable estimates of 

intakes, it is not possible to estimate the 

contribution of drinking water to total 

exposure. However, based on modeling 

results, the agency estimated that the 

chlorate intake from food (as a result of 

sodium chlorate use as a pesticide) for 

the overall population is approximately 

3 mg/kg-day, with somewhat higher 

intakes for children under five years old 


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of approximately 5 to 8 mg/kg-day 

(USEPA, 2006a). Additional food 

exposure from use of sanitizing 

solutions in food preparation plants 

(e.g., equipment and contact surfaces) 

and processing (e.g., bleaching agent) 

may also be a source of exposure (21 

CFR section 178.1010). Intake for adults 

from dietary supplements containing 

chlorate may range from 0.001 to 0.29 

mg/kg-day. 

B. Nitrosamines Group (6 Nitrosamines) 

The following sections provide the 

background, health and occurrence 

information/data that the agency has 

collected to date for nitrosamines. If you 

have any additional health and 

occurrence information that may be 

useful as the agency evaluates 

nitrosamines in the context of the 

regulatory review of existing MDBP 

rules, please provide this information to 

the docket. 

1. Background 

Nitrosamines are a class of nitrogencontaining organic compounds that 

share a common nitrosamino functional 

group (HSDB, 2010). EPA included five 

nitrosamine compounds on the CCL 3: 

N-nitrosodimethylamine (NDMA), Nnitrosodiethylamine (NDEA), Nnitrosodi-n-propylamine (NDPA), Nnitrosopyrrolidine (NPYR), and Nnitrosodiphenylamine (NDPhA). EPA 

monitored six nitrosamines under 

UCMR 2 using EPA Analytical Method 

521, four of which are CCL 3 

compounds (i.e., NDMA, NDEA, NDPA, 

NPYR), and two non-CCL 3 

nitrosamines [i.e., Nnitrosomethylethylamine (NMEA) and 

N-nitrosodi-n-butylamine (NDBA)]. The 

fifth CCL 3 nitrosamine compound, 

NDPhA, was not monitored under 

UCMR 2 due to lack of a reliable 

analytical method. Although other 

nitrosamines (e.g., N-nitrosomorpholine, 

N-nitrosopiperidine) have been 

identified in finished water (Mitch et 

al., 2009), they were also not included 

in UCMR 2 for similar analytical 

reasons. The nitrosamines from the 

UCMR 2 thus comprise the list of six 

nitrosamines that moved forward to the 

data evaluation phase of regulatory 

determination and are the focus of the 

information that follows below. 

All six nitrosamines may be produced 

in small quantities for research 

purposes, but only one (NDEA) is 

currently produced commercially in the 

United States. NDEA is used as an 

additive in gasoline and in lubricants, as 

an antioxidant, and as a stabilizer in 

plastics, though no data are available 

about quantities used (HSDB, 2010). 

NDMA was once used in the production 

of rocket fuel, as a solvent, and as a 

rubber accelerator. It was also used or 

proposed for use as an antioxidant, an 

additive for lubricants, and a softener 

for copolymers (ATSDR, 1989). There 

are no production data on any of the 

nitrosamine compounds from EPA’s 

Inventory Update Reporting (IUR) 

program. 

NDMA can be formed as an 

unintended byproduct of manufacturing 

processes that involve the use of nitrite 

or nitrate and amines, including 

tanneries, fish processing plants, 

foundries, and pesticide, dye, rubber or 

tire manufacturing plants (ATSDR, 

1989). Nitrosamines have been found in 

tobacco products, cured meats, ham, 

bacon, beer, whiskey, fish, cheese, 

soybean oil, toiletries, household 

cleaners, pesticides, rubber baby bottle 

nipples and pacifiers (ATSDR, 1989; 

Drabik-Markiewicz et al., 2009; Fine et 

al., 1977; NTP, 2011; Pe ́rez et al., 2008; 

Yurchenko and Mo ̈lder, 2007). 

NDMA is commonly present in 

municipal sewage sludge (ATSDR, 

1989). NPYR has also been detected in 

municipal sewage sludge (HSDB, 2010). 

ATSDR (1989) cites several studies 

indicating that nitrosamine formation in 

sewage sludge appears to be the result 

of biological and chemical 

transformation of alkylamines in the 

presence of nitrite. In addition, 

nitrosamines may form in air, soil, 

water, sewage, food, animal systems and 

other media where precursors (e.g., 

amines and nitrite) are present (HSDB, 

2010). NDMA can be produced 

endogenously in humans from the 

interaction of nitrates and nitrites with 

amines in the stomach (Mirvish 1975, 

1992; Tricker et al., 1994). 

As described in the following 

occurrence section, nitrosamines in 

finished water are commonly 

considered as DBPs because most of the 

literature indicates that the main source 

of nitrosamines in finished water is 

associated with water treatment, 

particularly from disinfection with 

chloramines. NDMA is the predominant 

species of nitrosamines found in 

finished water; other nitrosamines are 

detected less frequently. Based on their 

physical and chemical properties, the 

nitrosamines appear to be moderately to 

very mobile in the environment (the 

exception being NDBA, which is of low 

mobility). The nitrosamines are subject 

to a variety of removal mechanisms 

when present in soil and water, 

including volatilization (particularly 

NDMA), photodegradation, and 

microbial degradation, although the 

rates and extent of biodegradation are 

highly variable (HSDB, 2010). 

2. Health Effects Information 

As the more thoroughly studied 

nitrosamine compared to the other 

nitrosamine compounds, NDMA 

provides epidemiological case-control 

and other evidence that human 

nitrosamine exposure is associated with 

an increased risk of several types of 

cancer, including cancer of the stomach, 

esophagus, oral cavity, and pharynx (La 

Vecchia et al., 1995; Larsson et al., 2006; 

Loh et al., 2011; Straif et al., 2000). In 

accordance with the most recent 

Guidelines for Carcinogen Risk 

Assessment (USEPA, 2005b), EPA has 

categorized the six nitrosamine 

compounds as likely to be carcinogenic 

to humans based on sufficient evidence 

of carcinogenicity in animal studies 

with multiple tumor types 

(predominately liver and esophageal) in 

multiple animal species (e.g., rats, mice, 

and hamsters) (Clapp et al., 1968, 1971; 

Druckrey et al., 1967; Lijinsky, 1987a, 

1987b; Peto et al., 1991a, 1991b). All of 

the six nitrosamines have been 

determined to cause cancer through a 

mutagenic MOA because of DNA adduct 

formation leading to errors in DNA 

replication, altered cell proliferation 

and ultimately tumors (Diaz Gomez et 

al., 1986; Goto et al., 1999; Jarabek et al., 

2009; Souliotis et al., 1998). The 

mutagenic MOA is supported by 

positive findings from mutagenicity and 

genotoxicity in vitro and in vivo studies 

(Gollapudi et al., 1998; Kushida et al., 

2000; Martelli et al., 1988, Robbiano et 

al., 1996, Tinwell et al., 1994). 

With a mutagenic MOA, Age 

Dependent Adjustment Factors (ADAFs) 

are used to account for the potential 

increased cancer risk due to early-life 

exposure for infants and children 

(USEPA, 2005c). The age-adjusted unit 

risk is determined by summing up each 

of the time-weighted unit risks for the 

three ADAF developmental groups. The 

age-adjusted unit risks include a tenfold adjustment for birth to <2 years, a 

three-fold adjustment for 2 years to <16 

years, and no additional adjustment for 

exposures later in life, in conjunction 

with age-specific drinking water intake 

values (USEPA. 2012c), and the fraction 

of a 70-year lifetime applicable to each 

age period. The main cancer risk values 

used to derive the HRLs are further 

explained in section III.C.1 and are also 

summarized for nitrosamines in Table 

10 below. 


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TABLE 10—EPA DERIVED RISK VALUES AND HRLS FOR THE SIX INDIVIDUAL NITROSAMINES

Nitrosamines Studies for establishing a slope factor 

Cancer slope 

factor 

(mg/kg/day)¥1

1Age-adjusted 

unit risk 

(μg/L)¥1

2 HRL 

(μg/L) 

3 HRL 

(ng/L) 

NDBA .......................... Liver and esophageal tumors in rats (Druckrey et 

al., 1967).

0.4 3.0 × 10¥5 3 × 10¥2 30 

NDEA .......................... Liver and esophageal tumors in rats (Peto et al., 

1991a,b).

30 2.3 × 10¥3 4 × 10¥4 0.4 

NDMA ......................... Liver tumors in rats (Peto et al., 1991a,b) .............. 21 1.6 × 10¥3 6 × 10¥4 0.6 

NDPA .......................... Liver and esophageal tumors in rats (Druckrey et 

al., 1967).

2 1.5 × 10¥4 7 × 10¥3 7 

NMEA ......................... Liver tumors in rats (Druckrey et al., 1967) ............ 4 3.0 × 10¥4 3 × 10¥3 3 

NPYR .......................... Liver tumors in rats (Peto et al., 1984) ................... 7 5.3 × 10¥4 2 × 10¥3 2 

1Based on the recommendations of the U.S EPA’s 2005 Supplemental Guidance for Assessing Susceptibility from Early-Life Exposure to Carcinogens, the Unit Risk applicable to exposures beginning in early-life was adjusted with ADAFs and age-specific drinking water intakes resulting 

in a lifetime value of unit risk for exposure to 1 μg/L of a contaminant. The calculation for Age-Adjusted Unit Risk = è(CSF × ADAF × DWI/BWR 

× CW × F). The risk calculations for each individual nitrosamine can be found in the HESDs. 2The cancer HRL is determined by dividing the population risk level, one-in a million (10¥6), by the age-adjusted unit risk. 3The nitrosamine HRL values are converted to ng/L units by multiplying the μg/L values by 1000. 

As shown in table 10, the available 

data indicate a range of cancer risk 

values for the individual nitrosamines. 

Moreover, when multiple nitrosamines 

from this group are present in finished 

water together, their individual cancer 

risks are additive (Berger et al., 1987). 

EPA also evaluated whether health 

information is available regarding 

sensitive populations. The fetus, 

newborns, and infants may be 

potentially sensitive to the carcinogenic 

effects of nitrosamines due to the 

mutagenic MOA and evidence of 

transplacental carcinogenicity (Althoff 

et al., 1977; Donovan and Smith, 2008). 

Studies have found that younger rats 

were more susceptible to the 

development of liver tumors compared 

to rats exposed later in life to 

nitrosamines (Gray et al., 1991; Peto et 

al., 1984; Vesselinovitch et al., 1984). 

EPA’s Supplemental Guidance for 

Assessing Susceptibility from Early-Life 

Exposure to Carcinogens (USEPA, 

2005c) indicates that potential increased 

cancer risk due to early-life exposure 

should be taken into account for such 

compounds when there is the potential 

for greater susceptibility for structural 

changes to DNA leading to tumors when 

the exposures occur in infancy or 

childhood. Thus, the Supplemental 

Guidance (USEPA, 2005c) recommends 

using CSF estimates from chronic 

studies with ADAFs when chemicalspecific data that quantify the potential 

increased risk are lacking. All of the 

HRLs are based on lifetime exposure 

and include application of ADAFs, 

which adjust for the increased risk from 

early life exposure (see section III.C.1). 

In addition, habitual consumers of 

alcoholic beverages may be more 

susceptible to carcinogenic effects of 

nitrosamines because alcohol increases 

the metabolism of nitrosamines via a 

metabolic pathway that leads to the 

formation of mutagenic DNA adducts. 

Co-exposure to ethanol has been shown 

to exacerbate the cancer effects of 

nitrosamines in animal studies 

(Anderson et al., 1993; Kamataki et al., 

2002; McCoy et al., 1986). There are 

approximately five million people in the 

U.S. who suffer from alcoholism (O’Day 

et al., 1998) that may have an increased 

risk if co-exposed to nitrosamines 

(Amelizad et al., 1989; Verna et al., 

1996). 

3. Occurrence Data and Information 

The data collected under UCMR 2 

(USEPA, 2014d) are currently the best 

available data for characterizing the 

national occurrence baselines for the six 

nitrosamines. Under UCMR 2, PWSs 

were required to collect a sample at 

each entry point to the distribution 

system as well as at the maximum 

residence time locations within the 

distribution system associated with each 

entry point, and to report the 

disinfectant type in use at these 

locations at the time that the samples 

were being taken. The agency was 

unable to measure at the HRL for some 

of the nitrosamines. Therefore, Table 11 

presents all of the monitoring results for 

each of the six nitrosamines relative to 

the MRLs. 

TABLE 11—SUMMARY OF UCMR 2 MONITORING RESULTS FOR SIX NITROSAMINES

Nitrosamines considered under RD 3 MRL Percentages (number) of 

samples with detection 

Percentages (number) of 

UCMR 2 PWSs with at 

least one detection 

Percentages (number) of 

actual UCMR 2 population served with at 

least one detection* 

Nitrosamine Group ................................................................................ 2 to 7 ng/L 10.6% 

(1,907 of 18,053) 

28.6% 

(343 of 1,198) 

46.43% 

(73 of 157 million) 

NDBA .................................................................................................... 4 ng/L 0.05% 

(9 of 18,043) 

0.4% 

(5 of 1,198) 

1.07% 

(1.7 of 157 million) 

NDEA .................................................................................................... 5 ng/L 0.3% 

(46 of 18,038) 

2.2% 

(26 of 1,198) 

7.14% 

(11.2 of 157 million) 

NDMA .................................................................................................... 2 ng/L 10.2% 

(1,841 of 18,040) 

27.0% 

(324 of 1,198) 

41.54% 

(65.3 of 157 million) 

NDPA .................................................................................................... 7 ng/L 0% 

(0 of 18,049) 

0% 

(0 of 1,198) 

0% 

(0 of 157 million) 

NMEA .................................................................................................... 3 ng/L 0.02% 

(3 of 18,043) 

0.3 

(3 of 1,198) 

0.003% 

(0.004 of 157 million) 

NPYR .................................................................................................... 2 ng/L 0.2% 

(41 of 18,043) 

1.8% 

(21 of 1,198) 

4.73% 

(7.4 of 157 million) 

* The population-served values have been adjusted to include both the population served directly by a system and also the estimated attributable proportion of the 

population served by other systems that purchase water from the system. These adjustments are described in the UCMR 2 support document. 


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Finished water data for the 

nitrosamines from California (Ranalli, 

B., 2013) are consistent with the UCMR 

2 data. The State of California reported 

NDMA detections in 23.8% (24 of 101) 

of PWSs and NDEA detections in 7.1% 

(1 of 14) of PWSs. There were no NPYR, 

NDPA, NMEA, or NDBA detections 

reported. Reporting levels are not 

known. For California data on NDMA 

and NDEA, the minimum reported 

detections were 1 ng/L and 30 ng/L, 

respectively. NDBA, NDPA, NMEA, and 

NPYR had no detections and thus no 

minimum reported value in the dataset 

(Ranalli, B., 2013). While ambient water 

data for the nitrosamines are limited, 

because they are DBPs, it is expected 

that in general there would be higher 

concentrations in finished water than in 

ambient water. 

V. What about the remaining CCL 3 

contaminants? 

For the remaining CCL 3 

contaminants, the agency lacked 

adequate health and/or occurrence 

information needed to address the three 

SDWA statutory criteria to make a 

regulatory determination. Table 2 and 

Table 4 of this notice provide 

information about the data or 

information gap(s) that prevented the 

contaminant from moving forward for 

this regulatory determination effort. The 

agency continues to conduct research, 

collect information or find other 

avenues to fill the data and information 

gaps identified in Table 2 and 4. One 

mechanism the agency plans to 

continue to use to fill occurrence gaps 

for several of these contaminants is the 

UCMR. 

VI. EPA’s Next Steps 

EPA intends to carefully evaluate and 

respond to the public comments 

received on the five preliminary 

determinations and issue its final 

regulatory determinations in 2015. If the 

agency makes a final determination to 

regulate any of the contaminants, EPA 

will begin the process to propose an 

NPDWR within 24 months and 

promulgate a final NPDWR within 18 

months following the proposal. 

VII. References 

Abdel-Rahman, M.S., D. Couri, and R.J. Bull. 

1984. Toxicity of chlorine dioxide in 

drinking water. Journal of the American 

College of Toxicology 3(4):277–284. 

Abrams, S. A., K. C. Copeland, S. K. Gunn, 

et al. 2000. Calcium absorption, bone mass 

accumulation, and kinetics increase during 

early pubertal development in girls. 

Journal of Clinical Endocrinology & 

Metabolism 85(5):1805–1809. 

Agency for Toxic Substances and Disease 

Registry (ATSDR). 1989. Toxicological 

Profile for N-Nitrosodimethylamine. U.S. 

Department of Health and Human Services, 

Public Health Service. Available on the 

internet at: http://www.atsdr.cdc.gov/

substances/toxsubstance.asp?toxid=173. 

Accessed July 22, 2009. 

ATSDR. 1995. Toxicological Profile for 1,3- 

Dinitrobenzene and 1,3,5-Trinitrobenzene. 

U.S Department of Health and Human 

Services, Public Health Service. Available 

on the Internet at: http://www.

atsdr.cdc.gov/toxprofiles/tp.asp?id=842&

tid=164. Accessed July 22, 2009. 

ATSDR. 2004. Toxicological Profile for 

Strontium. U.S. Department of Health and 

Human Services, Public Health Service. 

Available on the Internet at: http://www.

atsdr.cdc.gov/toxprofiles/index.asp. 

Accessed July 22, 2009. 

Aggazzotti G., E. Righi, G. Fantuzzi, et al. 

2004. Chlorination by-products (CBPs) in 

drinking water and adverse pregnancy 

outcomes in Italy. J. Water Health. 

2(4):233–47 (as cited in U.S. EPA, 2006c). 

Althoff, J., P. Pour, C. Grandjean, et al. 1977. 

Transplacental effects of nitrosamines in 

Syrian hamsters. Z. Krebsforsch Klin. O. 

90:79–86. 

Amelizad, S., K.E. Appel, M. Schoepke, et al. 

1989. Enhanced demethylation and 

denitrosation of N-nitrosodimethylamine 

by human liver microsomes from 

alcoholics. Cancer Lett. 46(1):43–9. 

Anderson, L.M., J.P. Carter, C.L. Driver et al. 

1993. Enhancement of tumorigenesis by Nnitrosodiethylamine, N-nitrosopyrrolidine 

and N6-(methylnitroso)-adenosine by 

ethanol. Cancer Lett, 68: 61–66. 

AWWA Disinfection Systems Committee. 

2008a. Committee Report: Disinfection 

Survey, Part 1-Recent changes, current 

practices, and water quality. Journal 

AWWA 100(10):76–90. 

AWWA Disinfection Systems Committee. 

2008b. Committee Report: Disinfection 

Survey, Part 2-Alternatives, experiences, 

and future plans. Journal AWWA 

100(11):110–124. 

Argonne National Laboratory (ANL). 2007. 

Radiological and Chemical Fact Sheets to 

Support Health Risk Analyses for 

Contaminated Areas. Environmental 

Science Division. Available on the Internet 

at: http://www.gfxtechnology.com/Argonne

RadFacts.pdf. 

Bailey, D.E. 1988. 14-Day oral toxicity study 

in the dog with AC 92 100 and its 

metabolites, CL 94 301 and CL94320. 

Unpublished report on HLA Study No. 

362–190 (BASF RDI No. TE–420–007) from 

Hazleton Laboratories America, Inc., 

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Appendix: HRL Derivation With AgeRelated Exposure Factors 

DERIVATION OF THE HEALTH REFERENCE LEVEL (HRL) FOR STRONTIUM USING AGE-SPECIFIC EXPOSURE FACTORS

Age range DWI/BWR 

(L/kg/day) 

Age-specific fractions of 

a 19-year exposure 

duration 

Time-weighted 

DWI/BWR 

(L/kg/day) 

Birth to <1 month ......................................................................... 0.235 0.004 0.001 

1 to <3 months ............................................................................. 0.228 0.009 0.002 

3 to <6 months ............................................................................. 0.148 0.013 0.002 

6 to <12 months ........................................................................... 0.112 0.026 0.003 

1 to <2 years ................................................................................ 0.056 0.053 0.003 

2 to <3 years ................................................................................ 0.052 0.053 0.003 

3 to <6 years ................................................................................ 0.043 0.158 0.007 

6 to <11 years .............................................................................. 0.035 0.263 0.009 

11 to <16 years ............................................................................ 0.026 0.263 0.007 

16 to <18 years ............................................................................ 0.023 0.105 0.002 

18 to <21 years # ......................................................................... 0.026 0.053 0.001 

Summation of the Time-Weighted DWI/BWRs = ............................................................................................................ 0.040 L/kg/day * 

Reference Dose = .............................................................................................................................................................. 0.3 mg/kg/day 

RSC = .................................................................................................................................................................................. 20% 

+HRL = (0.3 mg/kg/day ∞ 0.040 L/kg/day) μ .20 = ........................................................................................................ 1.500 mg/L 

Final child specific HRL: ................................................................................................................................................... 1500 μg/L 

* Rounded; # includes 18th year; DWI/BWR = drinking water intake to body weight ratio; HRL= health reference level; RSC = relative source 

contribution. + HRL = (RfD/è(DWI/BWR × F)) × RSC. 


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62750 Federal Register / Vol. 79, No. 202 / Monday, October 20, 2014 / Proposed Rules 

The age-specific data on drinking 

water intakes in units of L/kg/day from 

birth through age 3 are from Table 3–19 

in the EPA Exposures Factors Handbook 

(USEPA, 2011e) and from Table 3–38 for 

ages 3 to <19 . The exposure duration 

adjustment was calculated by dividing 

the age-specific fraction of a 19 year 

exposure by the total exposure in 

months or years as appropriate (e.g., 

birth to <1 month = (1/12)/19 years = 

0.00439; 6 to <11 years = 5/19 years = 

0.26316). The time-weighted DWI/BWR 

values are the product of the agespecific DWI/BWR multiplied by the 

age-specific fraction of a 19 year 

exposure. The time-weighted DWI/

BWRs are summed to obtain the 

normalized value. 

[FR Doc. 2014–24582 Filed 10–17–14; 8:45 am] 

BILLING CODE 6560–50–P 


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