Summary of 

Nominations for the 

Fourth Contaminant 

Candidate List
Office of Water (4607M) 

EPA 815-R-15-001

January 2015 
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

Contents

1.0 Introduction ............................................................................................................................. 1

2.0 Requesting Nominations ......................................................................................................... 3

3.0 Nominated Contaminants ...................................................................................................... 4

3.1 Chemical Nominations ......................................................................................................... 4

3.1.1 Analysis of Nominated Chemical Contaminants ........................................................... 5

3.2 Microbial Nominations ......................................................................................................... 7

3.2.1 Analysis of Nominated Microbial Contaminants........................................................... 7

4.0 References ................................................................................................................................ 8

5.0 Appendices ........................................................................................................................... A-1

Appendix 1. Chemical Contaminants Nominated

Appendix 2. Microbial Contaminants Nominated

Appendix 3. References Provided with Chemical Nominations 

Appendix 4. References Provided with Microbial Nominations 

Appendix 5. Complete List of References Provided with CCL 4 Nominations 

Appendix 6. Outcome of Nominated Chemicals in the CCL 4 Process 

Appendix 7. Outcome of Nominated Microbes in the CCL 4 Process 

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Exhibits

Exhibit 1. Chemicals on the Final CCL 4 Included in Nominations .............................................. 7

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Acronyms and Abbreviations

ATSDR Agency for Toxic Substances and Disease Registry

AWWA American Water Works Association

CASRN Chemical Abstract Service Registry Number

CCL Contaminant Candidate List

CCL EPA’s First Contaminant Candidate List

CCL 2 EPA’s Second Contaminant Candidate List 

CCL 3 EPA’s Third Contaminant Candidate List 

CCL 4 EPA’s Fourth Contaminant Candidate List 

CDC Centers for Disease Control and Prevention 

CFR Code of Federal Regulations

EPA United States Environmental Protection Agency 

HA Health Advisories 

HPC Heterotrophic Plate Count 

MCL Maximum Contaminant Level

MCLG Maximum Contaminant Level Goal

MDEP Massachusetts Department of Environmental Protection

MDH Minnesota Department of Health

MTBE Methyl tertiary butyl ether

NJDEP New Jersey Department of Environmental Protection

NPDWR National Primary Drinking Water Regulations

NRDC National Resource Defense Council

OSHA Occupational Safety and Health Administration

PCCL Preliminary Contaminant Candidate List

PFOA Perfluorooctanoic acid

PWSs Public Water Systems

REDs Reregistration Eligibility Decision

SDWA Safe Drinking Water Act

TT Treatment Technique 

U.S. United States of America

USDA United States Department of Agriculture

USGS United States Geological Survey

WHO World Health Organization

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1.0 Introduction

Section 1412(b)(1) of the Safe Drinking Water Act (SDWA), as amended in 1996, requires EPA 

to publish the Contaminant Candidate List (CCL) every five years. The SDWA specifies that the 

list must include contaminants that 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 the SDWA. EPA uses this list of 

unregulated contaminants to help the agency identify priority contaminants for regulatory 

decision making and to prioritize research and data collection efforts. SDWA also requires the 

agency to consult with the scientific community, including the Science Advisory Board, and 

provide notice and opportunity for public comment prior to the publication of the Final CCL. In 

addition, SDWA directs the agency to consider the health effects and occurrence information for 

unregulated contaminants to identify those contaminants that present the greatest public health 

concern related to exposure from drinking water. 

EPA published the third CCL (CCL 3), which listed 116 contaminants on October 8, 2009 (74 

FR 51850 (USEPA, 2009a)). In developing the CCL 3, EPA implemented a multi-step process to 

select contaminants for the final CCL 3, which included the following key steps:

(1) The identification of a broad universe of potential drinking water contaminants (CCL 3 

Universe); 

(2) Screening the CCL 3 Universe to a Preliminary CCL (PCCL) using screening criteria 

based on the potential to occur in PWSs and the potential for public health concern; and 

(3) Evaluation of the PCCL contaminants based on a more detailed review of the occurrence 

and health effects data using a scoring and classification system to identify a final list of 

116 CCL 3 contaminants; and

(4) Incorporating public input and expert review in the CCL 3 process. 

Steps 1, 2 and 3 in the process are described in detail in the CCL 3 support documents: 

• Final CCL 3 Chemicals: Identifying the Universe (USEPA, 2009b);

• Final CCL 3 Chemicals: Screening to a PCCL (USEPA, 2009c);

• Final Contaminant Candidate List 3 Chemicals: Classification of the PCCL to the CCL

(USEPA, 2009d);

• Final CCL 3 Microbes: Identifying the Universe (USEPA, 2009e);

• Final CCL 3 Microbes: Screening to the PCCL (USEPA, 2009f); and

• Final CCL 3 Microbes: PCCL to CCL Process (USEPA, 2009g).

These documents can be found on the EPA web site at: http://www2.epa.gov/ccl/contaminantcandidate-list-3-ccl-3 or at http://www.regulations.gov (docket ID: EPA-HQ-OW-2007-1189). 

After a Final CCL is published, SDWA section 1412(b)(1)(B)(ii) as amended in 1996, requires 

EPA at five year intervals to make determinations of whether to regulate or not to regulate no 

fewer than five contaminants from the CCL in a process called regulatory determinations. This 

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is a separate process from the listing of contaminants on the CCL. The 1996 SDWA 

Amendments specify three criteria to determine whether a contaminant may require regulation: 

• the contaminant may have an adverse effect on the health of persons;

• the contaminant is known to occur or there is a substantial likelihood that the contaminant

will occur in PWSs with a frequency and at levels of public health concern; and

• in the sole judgment of the Administrator, regulation of such contaminant presents a

meaningful opportunity for health risk reduction for persons served by PWSs.

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 Goal1 (MCLG) and NPDWR2

. After the proposal, the agency has 18 months to publish 

and promulgate a final MCLG and NPDWR (SDWA section 1412(b)(1)(E))3. 

On February 11, 2011, as a separate action, the agency issued a positive regulatory determination 

for perchlorate, a chemical listed in CCL 1, CCL 2 and CCL 3 (76 FR 7762 (USEPA, 2011)). 

Recently, EPA has published preliminary regulatory determinations for five unregulated 

contaminants on the CCL 3 (79 FR 62716 (USEPA, 2014)). 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 four 

contaminants (dimethoate; 1,3-dinitrobenzene; terbufos; and terbufos sulfone). Therefore, the 

agency is removing perchlorate and these five contaminants from the Draft Fourth CCL (CCL 4), 

pending the result of the final regulatory determinations for CCL 3.

EPA conducted an abbreviated evaluation and selection process for the CCL 4. This abbreviated 

CCL 4 process includes a three pronged approach: (1) carrying forward CCL 3 contaminants 

(minus those with regulatory determinations), (2) seeking and evaluating nominations from the 

public for additional contaminants to consider and (3) evaluating any new data for those 

contaminants with previous negative regulatory determinations from CCL 1 or CCL 2 for 

potential inclusion on the CCL 4. 

As part of the process to develop the CCL 4, EPA published a Federal Register notice (77 FR

27057 (USEPA, 2012)) requesting that the public submit nominations for chemical and 

microbial contaminants to be considered for inclusion in the CCL 4. EPA also requested 

supporting information that has been made available since the development of the CCL 3 or 

existing information that was not considered in the development of the CCL 3, which shows that 

the nominated contaminant may have an adverse health effect on people and occurs or is likely to 

occur in public water systems. EPA reviewed the nominations and supporting information 

provided by nominators to determine if any new data were provided that had not been previously 

1 The MCLG is the "maximum level of a contaminant in drinking water at which no known or anticipated adverse 

effect on the health of persons would occur, and which allows an adequate margin of safety. Maximum contaminant 

level goals are non-enforceable health goals." (40 C.F.R. 141.2; 42 U.S.C. 300g-1) 2 An NPDWR is a legally enforceable standard that applies to public water systems. An NPDWR sets a legal limit 

(called a maximum contaminant level or MCL) or specifies a certain treatment technique (TT) for public water 

systems for a specific contaminant or group of contaminants. 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 analytical methods and taking cost into consideration. 3

 The statute authorizes a nine month extension of this promulgation date. 

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evaluated for CCL 3. The agency also collected additional data for the nominated contaminants, 

when it was available, from both CCL 3 data sources that had been updated and from new data 

sources that were not available at the time of CCL 3. A complete list of references provided by

nominators can be found in Appendices 3, 4 and 5 of this document. A more detailed description 

of the CCL data sources collected by EPA may be found in the support document Data Sources 

for the CCL 4 (USEPA, 2015a)). 

This document describes EPA’s request for contaminant nominations and summarizes the 

nominations received by EPA. In addition, it describes EPA’s analysis of the nominated 

contaminants and reports on their status in the Draft CCL 4. The specific contaminants 

nominated, the information provided by the nominators and the outcome of the nominated 

contaminants in the CCL 4 process are included in Appendices 1 through 7 of this document. 

More detailed information on the CCL 4 is available in the CCL 4 support documents found on 

the CCL 4 Web site at: http://www2.epa.gov/ccl/contaminant-candidate-list-4-ccl-4. The original 

nomination letters submitted via the docket and nominations submitted via the Web site can be 

found in the docket at http://www.regulations.gov (docket ID: EPA-HQ-OW-2012-0217). 

2.0 Requesting Nominations

The agency sought nominations for contaminants to be considered for possible inclusion in the 

CCL 4 by framing the SDWA requirements in a series of questions to document the anticipated 

or known occurrence in PWSs and the adverse health effects of potential contaminants. The 

agency requested that the public respond to those questions and provide the documentation and 

rationale for including a contaminant for consideration in the CCL 4 process. The questions 

posed to the public were: 

• What is the contaminant's name, Chemical Abstract Service Registry Number (CASRN),

and/or common synonym (if applicable)?

• What factors make this contaminant a priority for the CCL 4 process (e.g., widespread

occurrence; anticipated toxicity to humans; potentially harmful effects to susceptible

populations (e.g., children); potentially contaminated source water (surface or ground

water) and/or finished water; release to air, land and/or water; contaminant is

manufactured in large quantities with a potential to occur in source waters)?

• What are the new significant health effects and occurrence data that are available since

CCL 3 or existing information that was not considered in CCL 3, which you believe

supports the CCL requirement(s) that a contaminant may have an adverse effect on the

health of persons and is known or anticipated to occur in PWSs?

• Please provide complete citations, including author(s), title, journal and date. Contact

information for the primary investigator would also be helpful.

Nominations were received via the EPA Web site and via the EPA docket (docket ID: EPA-HQOW-2012-0217). The agency compiled the information from the nominations process to identify 

the contaminants nominated, the rationale for the nomination and to compare the supporting data 

submitted to information gathered by EPA. Where new information was of sufficient quality that 

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information was used in the analysis; EPA analyzed the nominated contaminants using the 

CCL 3 process, which is described briefly in Section 1, to select the Draft CCL 4. 

3.0 Nominated Contaminants

EPA received nominations for 59 unique contaminants for the CCL 4 submitted by 10 

organizations and individuals. These 59 nominations include 5 microbial and 54 chemical 

contaminants. Eight contaminants were nominated by more than one nominator. Aldicarb, 

bisphenol A, carbaryl, chlorpyrifos, Toxoplasma gondii, and microcystin LR were each 

nominated by two separate nominators. Manganese and perfluorooctanoic acid (PFOA) were 

nominated by three different nominators each. 

The agency did not require nominators to provide their name or an affiliated organization. Two 

nominators remained anonymous while providing documentation and rationale for the 

contaminants. Two other individuals identified themselves but did not provide an organization 

affiliation. 

The organizations that nominated contaminants were: 

• American Water Works Association (AWWA),

• Natural Resources Defense Council (NRDC),

• State of Massachusetts Department of Environmental Protection (MDEP),

• State of Minnesota Department of Health (MDH),

• State of New Jersey Department of Environmental Protection (NJDEP), and

• U.S. Department of Agriculture (USDA).

EPA received three general types of nominations: 

• specific individual chemicals,

• specific individual organisms, and

• groups of contaminants (Heterotrophic Plate Count (HPC) was considered as a group).

The AWWA also provided a letter with recommendations for the CCL 4 process. The full text of 

this letter can be found at http://www.regulations.gov (docket ID: EPA-HQ-OW-2012-0217). 

3.1 Chemical Nominations

There were a total of 54 unique chemical contaminant nominations for the CCL 4. The full list of 

chemical nominations and the supporting information provided by the nominators can be found 

in Appendix 1. The references provided by the nominators for chemical nominations can be 

found in Appendix 3. 

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3.1.1 Analysis of Nominated Chemical Contaminants

SDWA specifies that the CCL only includes those contaminants without any proposed or 

promulgated NPDWRs. There are two nominated contaminants covered under the existing 

NPDWR for beta photon emitters (strontium 90 and cesium 137) (40 CFR §141.66 (d)(1)); 

therefore, these will not be considered for CCL 4. Radon was also nominated but is not eligible

for CCL 4 since a proposed NPDWR has been developed (64 FR 59245, November 2, 1999 

(USEPA, 1999). Aldicarb was nominated but is not eligible for CCL 4 since it has an existing 

NPDWR (40 CFR §141.61(c)); (Note, in response to an administrative petition the agency issued 

an administrative stay of the effective date of the maximum contaminant levels (MCLs) for 

aldicarbs).

For the remaining 50 nominated chemicals, EPA reviewed the nominations and supporting 

information provided by nominators to determine if any new data were provided that had not 

been previously evaluated for CCL 3. In addition to the data provided by nominators, and the 

data EPA collected previously under CCL 3, EPA collected data for the nominated contaminants, 

when it was available, from both CCL 3 data sources that have been updated and from new data 

sources that were not available at the time of CCL 3. A list and description of these data sources 

can be found in the Data Sources For the CCL 4 (USEPA, 2015a) support document. If new data 

were available, EPA screened and scored the nominated contaminants using the same process as 

was used in CCL 3. Five of the nominated chemicals were on CCL 3 and were carried forward to 

the CCL 4 along with the other CCL 3 contaminants. The five chemicals are: perfluorooctanoic 

acid (PFOA), Microcystin-LR, methyl tertiary butyl ether (MTBE), alphahexachlorocyclohexane and permethrin. Microcystin-LR is included within the group of 

cyanotoxins in the Final CCL 3 and the Draft CCL 4.

Forty of the nominated chemicals were previously included in the CCL 3 Universe, and were 

carried forward to the CCL 4 Universe. In addition to these forty, EPA has added three 

nominated chemicals to the CCL 4 Universe (octylphenol ethoxylate, oxacillin and 

virginiamycin) based on health effects and/or occurrence data that is newly available since the

development of the CCL 3. Seven of the nominated chemicals did not have enough data in order 

to be added to the CCL 4 Universe. EPA screened all of the nominated chemicals in the CCL 4

Universe according to the screening criteria developed for CCL 3 and based on that evaluation, 

twenty of the nominated chemicals were included in the PCCL 4. Eighteen of those 20 chemicals 

were also included in the PCCL 3 and EPA added two new chemicals (manganese and 

nonylphenol) to the PCCL 4. The data used to screen the nominated chemicals from the CCL 4

Universe to the PCCL 4 can be found in the Screening Document for the Draft PCCL 4 

Nominated Contaminants (USEPA, 2015b). EPA further evaluated the nominated chemicals on 

the PCCL 4 based on the classification process developed in CCL 3 and determined that 

manganese and nonylphenol should be added to the Draft CCL 4 (in addition to the chemicals 

carried forward from the CCL 3 to the CCL 4) based on new health and/or occurrence 

information that warrants further evaluation. The data which was used to further evaluate the 

nominated contaminants from the PCCL 4 and to select those that were included in the Draft 

CCL 4 can be found in the Contaminant Information Sheets for the Draft PCCL 4 Nominated 

Contaminants (USEPA, 2015c). 

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Manganese is an element that naturally occurs in oxide forms and in combinations with other 

elements in many minerals. Small amounts, found in foods, are an essential nutrient for humans 

and animals. Manganese ores are used in a variety of applications in the US. Its principal use is 

in steel production to improve hardness, stiffness and strength (ATSDR, 2012). In 2003 and as 

part of the CCL 1 Regulatory Determination process, EPA made a negative regulatory 

determination for manganese based on the health and occurrence data available at that time. 

However, CCL 4 nominators cited more than 20 recent studies that indicate concern for 

neurological effects in children and infants exposed to excess manganese, which were not 

available at the time manganese was considered for Regulatory Determination 1 or CCL 3. In 

addition, new monitoring studies from USGS and drinking water monitoring information from 

several States support an earlier survey (i.e., the National Inorganics and Radionuclides Survey) 

that indicates manganese is known to occur in drinking water. EPA believes the new health 

effects information and additional occurrence data merit listing manganese in the Draft CCL 4.

Nonylphenol is used in the preparation of lubricating oil additives, resins, plasticizers and 

antioxidants for plastics and rubber. Additionally, sixty percent of nonylphenol is used in the 

production of nonylphenol ethoxylates, which are found in detergents and used in the treatment 

of textiles. Nonylphenol was previously considered for CCL 3. It was included in the CCL 3 

Universe, but was not included on the PCCL 3 or CCL 3. Updated health and occurrence data 

(since the development of the CCL 3) are now available for nonylphenol, and these data (as 

follows) were considered in evaluating nonylphenol for the Draft CCL 4. Nonylphenol and some 

of its degradation products have been found to have estrogenic activity in rats and mice (WHO, 

2004). Monitoring data are available from a USGS National Reconnaissance monitoring study of 

ambient water (Kolpin et al., 2002). EPA believes this updated health data and additional 

occurrence data show that nonylphenol is anticipated to occur in PWSs and has potential adverse 

health effects; therefore, it merits listing on the Draft CCL 4.

EPA considered adding dicofol to the Draft CCL 4; however, both recent manufacturers of the 

pesticide ceased all production as of May 17, 2011 and agreed to an EPA registration 

cancellation, which effectively prohibits all labeled uses of existing stocks after October 31, 

2016. Use of dicofol has declined significantly in recent years. The chemical properties of 

dicofol indicate that it is has low mobility in water because it is expected to adsorb to organic 

matter in soil and sediment and it has moderately low solubility in water. Therefore, EPA did 

not list dicofol on the Draft CCL 4 because it is not known or anticipated to occur in drinking 

water due to its low mobility. Additionally, the registration cancellation, which will prohibit use 

of existing stocks beyond October 2016, is expected to further lessen any potential occurrence in 

drinking water. 

Exhibit 1 shows the nominated chemicals that were included in the Draft CCL 4. In addition, 

Appendix 6 shows a list of the nominated chemicals and whether they were included in the CCL 

4 Universe, PCCL 4 or Draft CCL 4. 

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Exhibit 1. Nominated Chemicals Included in the Draft CCL 4

Contaminant Name CASRN

*alpha-hexachlorocyclohexane 319-84-6

manganese 7439-96-5

*methyl tertiary butyl ether (MTBE) 1634-04-4

*microcystin-LR 101043-37-2

nonylphenol 25154-52-3

*perfluorooctanoic acid (PFOA) 335-67-1

*permethrin 52645-53-1

*Indicates that this chemical was carried forward from CCL 3 to the Draft CCL 4

3.2 Microbial Nominations

Five unique microbial nominations were submitted by the public in response to EPA’s request 

for nominations for contaminants to be considered for possible inclusion in the Draft CCL 4 (77 

FR 27057). The following organisms or group of organisms were nominated: Heterotrophic Plate 

Count bacteria, Adenovirus, Naegleria fowleri, Toxoplasma gondii and Vibrio chloerae.

Toxoplasma gondii was nominated by two different nominators. Adenovirus and Naegleria 

fowleri were included in the Final CCL 3 and are being carried forward to the Draft CCL 4. 

Additional information on the nominated microbes and the information submitted by the 

nominators can be found in Appendix 2. 

3.2.1 Analysis of Nominated Microbial Contaminants

EPA reviewed the nominated microbial contaminants and the supporting information provided 

by nominators to determine if any new data were provided that had not been previously 

evaluated. The agency also collected additional data for the nominated microbial contaminants, 

when it was available, from both CCL 3 data sources that had been updated and from literature 

searches covering the time between CCL 3 and CCL 4 (2007– 2012). If new data were available, 

EPA screened and scored the microbial contaminants nominated for CCL 4 using the same 

process that was used for CCL 3. The new data did not change the CCL 3 scores or listing 

decisions for the nominated microbial contaminants. 

The group of HPC bacteria was nominated for the CCL 4; however, available epidemiological 

evidence shows no relationship between gastrointestinal illness and HPC bacteria in drinking 

water (Calderon, 1988; Calderon and Mood, 1991; Payment et al., 1997; WHO, 2003). Thus, 

EPA considers the potential health risk of HPC bacteria in drinking water as likely negligible and 

is not including HPC on the Draft CCL 4. In addition, HPC bacteria are addressed under the 

Surface Water Treatment Rule as a treatment technique (TT) where they can be monitored in lieu 

of a disinfectant residual.

Vibrio cholerae and Toxoplasma gondii will remain on the draft PCCL 4 and Naegleria fowleri

and Adenovirus will be carried forward to the Draft CCL 4, along with the other microbes 

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included on the Final CCL 3. A summary of the outcomes for the microbial contaminants for the 

CCL 3 and Draft CCL 4 can be found in Appendix 7. 

4.0 References 

Note: The following references apply to Sections 1.0, 2.0 and 3.0 above. References provided by 

CCL 4 nominators are listed in Appendix 5 below. 

Calderon, R.L. 1988. Bacteria Colonizing Point-of-Entry Granular Activated Carbon filters and 

their Relationship to Human Health. EPA CR-813978-01-0, US Environmental 

Protection Agency, Washington, DC. 

Calderon, R.L. and Mood, E.W. 1991. Bacteria Colonizing Point-of-Use Granular Activated 

Carbon Filters and their Relationship to Human Health. EPA CR 811904-01-0, US 

Environmental Protection Agency, Washington, DC. 

Kolpin, D. W., E. T. Furlong, M. T. Meyer, E. M. Thurman, S. D. Zaugg, L. B. Barber, and H. T. 

Buxton. 2002. Pharmaceuticals, Hormones, and Other Organic Wastewater Contaminants 

in U.S. Streams, 1999-2000: A National Reconnaissance. Environmental Science and 

Technology, v. 36, no. 6 

Payment, P., J. Siemiatycki, L. Richardson, G. Renaud, E. Franco, and M. Prevost. 1997. A 

prospective epidemiological study of gastrointestinal health effects due to the 

consumption of drinking water. Int. J. Environ. Health Res. (7): 5-31. 

USEPA, 1999. National Primary Drinking Water Regulations; Radon-222; Proposed Rule. 

Federal Register. Vol. 64, No. 211. p. 59245, November 2, 1999. 

USEPA. 2009a. Drinking Water Contaminant Candidate List 3--Final. Federal Register. Vol. 

747. No 194. p. 51850. October 8, 2009.

USEPA. 2009b. Final Contaminant Candidate List 3 Chemicals: Identifying the Universe. EPA

815-R09-006. August, 2009. 

USEPA. 2009c. Final Contaminant Candidate List 3 Chemicals: Screening to a PCCL. EPA 815-

R-09-007. August, 2009. 

USEPA. 2009d. Final Contaminant Candidate List 3 Chemicals: Classification of the PCCL to 

the CCL. EPA. 815-R-09-008. August, 2009. 

USEPA. 2009e. Final Contaminant Candidate List 3 Microbes: Identifying the Universe. EPA. 

815-R-09-004. August, 2009. 

USEPA. 2009f. Final Contaminant Candidate List 3 Microbes: Screening to the PCCL. EPA 

815-R-09-0005. August, 2009. 

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USEPA. 2009g. Final Contaminant Candidate List 3 Microbes: PCCL to CCL Process. EPA 

815-R-09-009. August, 2009. 

USEPA. 2011. Drinking Water: Regulatory Determination on Perchlorate. Federal Register. Vol. 

76, No. 29. p. 7762, February 11, 2011. 

USEPA. 2012. Request for Nominations of Drinking Water Contaminants for the Fourth 

Contaminant Candidate List. Federal Register. Vol. 77. No 89. p. 27057. May 8, 2012 

USEPA. 2014. Announcement of Preliminary Regulatory Determination for Contaminants on the 

Third Drinking Water Contaminant Candidate List. Federal Register. Vol. 79, No. 202, p. 

62716, October 20, 2014. 

USEPA. 2015a. Data Sources for the CCL 4. EPA 815-R-15-004. January, 2015. 

USEPA. 2015b. Screening Document for the Draft PCCL 4 Nominated Contaminants. EPA 815-

R-15-002. January, 2015. 

USEPA. 2015c. Contaminant Information Sheets (CISs) for the Draft Fourth Preliminary 

Contaminant Candidate List (PCCL 4) Nominated Contaminants. EPA 815-R-15-003. 

January, 2015. 

WHO. 2003. Emerging Issues in Water and Infectious Disease Series: Heterotrophic Plate 

Counts and Drinking-water Safety. ed. J. Bartram, J. Cotruvo, M. Exner, C. Fricker, and 

A. Glasmacher. IWA Publishing, London, UK. p. 119 – 122. 

WHO. 2004. Integrated Risk Assessment: Nonylphenol Case Study. ed. D. Bontje, J. Hermens, 

T. Vermeire, and T. Damstra. 63 pp. December, 2004. Available on the Internet 

at:http://www.who.int/ipcs/methods/Nonylphenol.pdf. 

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5.0 Appendices

The appendices that follow provide tabulated summaries that present a list of the chemical and 

microbial contaminants nominated for consideration in CCL 4. Appendix 1 lists the chemical 

nominations, provides the chemical abstracts service registry number (CASRN) for each 

chemical contaminant, common name, nominating individual or organization, health effects 

information provided with the nomination, occurrence information provided with the nomination 

and additional information provided with the nomination. For the purpose of developing this 

appendix, EPA separated original text submitted with the nomination for each contaminant and 

placed it into the health effects information, occurrence information or additional information 

columns, as appropriate. EPA maintained the text submitted with each nomination verbatim; 

however, footnote numbers submitted in nominators’ letters have been removed for clarity. The 

footnotes generally refer to references or comments and can be found in the original letters 

located in the docket. 

Appendix 2 provides the same information for the microbial contaminants. 

Appendix 3 lists the references provided with chemical nominations including: CASRN, 

contaminant name, nominating organization or individual and references cited. The references 

cited in Appendix 3 are in an abbreviated citation format (e.g., Fiore et al., 1986). 

Appendix 4 lists the same information as Appendix 3; however, Appendix 4 covers microbial 

nominations. 

Appendix 5 includes the complete list of full references provided with CCL 4 nominations for 

both microbial and chemical nominations. The original nomination letters and the nominations 

submitted via the Web site can be found in the docket at http://www.regulations.gov (docket ID: 

EPA-HQ-OW-2012-0217). The original documents contain all tables referenced in Appendix 1 

and 2. 

Appendix 6 shows the outcome of the nominated chemicals in the CCL 4 process (i.e., whether 

the nominated chemical was included in the CCL 4 Universe, PCCL 4 or Draft CCL 4). It also 

denotes the status of the nominated chemicals in the CCL 3 process. An “X” denotes that a 

chemical was included in that stage of the process. Note that nominated contaminants with an 

NPDWR or proposed NPDWR were not eligible for CCL 4, as explained in Section 3.1.1 above. 

Appendix 7 shows the outcome of the nominated microbes in the CCL 4 process (i.e., whether 

the nominated microbe was included in the CCL 4 Universe, PCCL 4 or Draft CCL 4). It also 

denotes the status of the nominated microbe in the CCL 3 process. An “X” denotes that the 

microbe was included in that stage of the process. 

A1-1
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

Appendix 14. Chemical Contaminants Nominated

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

77439-76-0 3-chloro-4-

dichloromethyl-5-

hydroxy-2(5H)-

furanone)

AWWA None given None given None given

116-06-03 Aldicarb AWWA None given None given None given

116-06-3 Aldicarb Natural Resources 

Defense Council

Aldicarb is an N-methyl carbamate insecticide that causes reversible red blood 

cell and plasma cholinesterase inhibition. This pesticide is classified as 

Toxicity Category 1 because of its high toxicity through all routes of exposure 

(oral, dermal and inhalation). Symptoms of acute aldicarb exposure observed 

in animal studies include decreased motor activity, lacrimation, tremors, 

salivation, pinpoint pupils, and decreased grip strength. A rat study by 

EPA/ORD demonstrated that young animals are more susceptible to aldicarbinduced brain cholinesterase inhibition than adults. Although it is generally 

believed that acute high level exposure to aldicarb will not cause chronic 

health effects, one case study by Grendon et al. (1994) in Washington State 

documented long-term health problems in men and sheep resulting from a 

single poisoning incident. EPA has not assessed the risks of chronic exposure 

to aldicarb in its 2006 Revised Human Health Risk Assessment (HRA). The 

Agency reasoned that since cholinesterase inhibition due to aldicarb exposure 

is reversed in less than 24 hours, such an assessment is unnecessary and 

chronic exposure can be treated as a series of acute exposures. However, 

EPA mentioned in the Revised HRA that effects such as pale kidneys and 

hydroceles in the oviducts occurred in dams in a developmental study, 

symptoms that suggest chronic damage not seen in acute single-exposure 

cases. In addition, some studies suggest that chronic exposure to aldicarb 

may have longer-term effects on the immune and nervous systems. Fiore et al 

(2006) analyzed immune function in two groups of women, one exposed to 

aldicarb at environmental concentrations in groundwater at levels below 61 

ppb (23 subjects), and an unexposed group (27 subjects). No women in either 

group had known reasons for immune problems. The researchers found a 

significant association between aldicarb exposure and abnormalities in T-cell 

subset ratios. Hajoui et al. (1992) also found changes in the percentages of 

certain T-cell subsets after subchronic, but not chronic exposure.The results of 

a rat study by Smulders et al. (2003) suggest that exposure to carbamates 

such as aldicarb may also lead to chronic changes in the nervous system 

resulting from the inhibition of neuronal nicotinic acetylcholine receptors. A 

similar study of the carbamates fenoxycarb, carbaryl, and S-ethyl N,Ndipropylthiocarbamate (EPTC), which have the same mechanism of action, 

showed that increasing the pesticide dose or the length of exposure reduced 

the rate of reversal of acetylcholine receptor inhibition. Therefore, two 

mechanisms, cholinesterase inhibition and acetylcholine receptor inhibition 

may lead to chronic neurotoxicity from exposure to carbamate pesticides such 

EPA placed aldicarb under Special Review in 1984 due to concerns 

about groundwater contamination. Aldicarb degradation in 

groundwater is slow. This chemical is persistent and mobile in soil, and 

degrades in the environment to aldicarb sulfoxide and aldicarb sulfone, 

both of which are cholinesterase inhibitors. In 1991 EPA established 

MCLs of 0.003 ppb for aldicarb, 0.004 ppb for aldicarb sulfoxide and 

0.002 ppb for aldicarb sulfone, but these MCLs never went into effect. 

Instead, EPA issued a 7 ppb health advisory for each of the aldicarb 

species and for combined aldicarb residues. EPA based its drinking 

water risk assessment in the HRA on the highest aldicarb 

concentrations in groundwater found in eight regions where aldicarb

was used. The concentrations ranged from 0 to 24 ppb. The region 

with no aldicarb detections was removed from the analysis. Surface 

water concentrations, on the other hand, were derived from models for 

lack of sufficient monitoring data.

None given

4 For the purpose of developing this appendix, EPA separated original text submitted with the nomination for each contaminant and placed it into the health effects information, 

occurrence information or additional information columns, as appropriate. EPA maintained the text submitted with each nomination verbatim.

A1-2 
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank as aldicarb. This raises concerns about chronic low-level exposure such as 

may result from aldicarb contamination of drinking water.

Acute dietary exposure estimates from food alone exceeded the level of 

concern for children 1 to 2 years old (159% of the acute Population Adjusted 

Dose, or aPAD), and children 3 to 5 years old (129% aPAD), so that any 

additional exposures from drinking water would increase these risks of 

concern. The highest exposure from groundwater calculated for the regions 

where this pesticide was detected was 945% aPAD for the 95th percentile of 

the most exposed population sub-group. For the general U.S. population and 

other sub-groups, exposure ranged from 20% aPAD to 393% aPAD. It is clear 

from EPA’s own analysis that aldicarb is a water contaminant that poses 

health risks of concern at levels found in food and drinking water. Given that 

food exposure alone exceeds levels of concern for children, drinking water 

exposure creates an additional unacceptable risk. EPA must move to establish 

a protective MCL for aldicarb.

blank blank

68555-24-8 Alkylphenol monoto tri-oxylates Natural Resources 

Defense Council

Alkylphenols were first reported to be estrogenic in the 1930s. In 1991, 

publication of the effects of nonylphenol on cultured human breast cancer cells 

led to health concerns. Estrogenic effects have also been shown in the 

mouse. Estrogenic effects are present at tissue concentrations of 0.1 μM for 

octylphenol and 1 μM for nonylphenol. A recombinant yeast screen using the 

human estrogen receptor has shown similar results.

An estimated 450,000,000 pounds of alkylphenol polyethoxylates 

(APEs) are produced annually in the United States, and about half that 

amount is estimated to be released to wastewater. Alkylphenol 

polyethoxylates do not break down effectively in sewage treatment 

plants or in the environment. Instead they degrade to alkylphenols and 

alkylphenol ethoxylates, which persist for longer. Nonylphenol and its 

ethoxylates, and other alkylphenols, have been detected in 

wastewater and in waterways.

None given

26787-78-0 Amoxicillin Natural Resources 

Defense Council

Widespread exposure to antibiotics is contributing to the growth of bacterial 

resistance, and this problem is of grave concern. In the past several decades 

almost every bacteria that can cause infections in humans has developed 

resistance to at least one antibiotic, and some are resistant to multiple 

antibiotics. The Centers for Disease Control and Prevention (CDC) have 

identified antibiotic resistance as one of the most pressing public health 

problems to face our nation. Infections caused by bacteria with resistance to at 

least one antibiotic have been estimated to kill over 60,000 hospitalized 

patients each year.

Antibiotic resistance is caused by a number of factors including repeated and 

improper use of antibiotics in both humans and animals. Scientists also agree 

that exposure to low levels of antibiotics actually promotes bacterial resistance 

by exerting selective pressure for genes that promote resistance.

Beta-lactam antibiotics are a broad class of antibiotics which include penicillin 

derivatives, cephalosporins, monobactams, carbapenems and Beta-lactamase 

inhibitors. Methicillin, a form of penicillin, had been relied upon as an common 

effective treatment for Staphylococcus aureus infections but now many strains 

of S. aureus bacteria are resistant to methicillin (MRSA or methicillin-resistant 

Staphylococcus aureus.) Unfortunately, MRSA is resistant to much of the 

entire class of penicillin-like antibiotics called beta-lactams. Therefore, EPA 

must include penicillin, amoxicillin, oxacillin and methicillin on the CCL4.

Antibiotics are found in wastewater because the body does not 

completely metabolize all drugs, so both the metabolized and 

unmetabolized drug are excreted by humans into wastewater. For 

example,when amoxicillin is ingested, 60-75% of the antibiotic is 

excreted unchanged into the urine. This antibiotic, now in the 

environment, may encounter other bacteria and promote resistance. It 

is unknown how much of an impact current low levels of antibiotics in 

drinking water are having on the problem of bacterial resistance. 

However, the potential has been recognized for many years.

None given

A1-3 
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

86-50-0 Azinphos-methyl Natural Resources 

Defense Council

Azinphos-methyl (CAS # 86-50-0) is an organophosphate pesticide classified 

as toxicity category 1 for oral exposure. Exposure to azinphos-methyl causes 

plasma, red blood cell and brain cholinesterase inhibition, with symptoms 

including headache, nausea, vomiting, dizziness, anxiety, muscle tremors and 

weakness. Studies by Souza et al. (2004, 2005) found that azinphos-methyl 

affected human placental enzymatic activity, which may have adverse 

consequences for fetal development. Exposure to organophosphate pesticides 

(OPs) such as azinphos-methyl has been associated with lower performance 

on neurobehavioral tests in exposed adults. Children are more vulnerable than 

adults to the neurotoxic effects of OPs and may suffer developmental effects 

from low-level chronic exposures.

Azinphos-methyl has a high potential to pollute surface waters due to 

runoff and spray drift. Data on environmental concentrations of 

azinphos-methyl in the United States are limited, but studies in South 

Africa suggest that under certain conditions azinphos-methyl may also 

reach high concentrations (>40 ppb) in groundwater. 

EPA indicated in its drinking water assessment in the Interim 

Reregistration Eligibility Decision (IRED) document for azinphosmethyl that the estimated environmental concentration (EEC) of this 

pesticide in surface water is 16 ppb at typical application rates in 

peaches. This concentration is over three times the acute drinking 

water level of comparison (DWLOC) the agency calculated for infants 

less than a year old (5 ppb), and over twice the DWLOC for children 1-

6 years (6 ppb). The highest annual mean concentrations in surface 

water according to monitoring data and EPA models ranged from 0.27 

ppb to 7.2 ppb. The latter concentration exceeds the chronic DWLOC 

the agency calculated for infants less than a year old (7 ppb).

While EPA argued in the IRED that the phase-out of azinphos –methyl 

use on peaches will eliminate drinking water risks of concern, EPA is 

still allowing the use of azinphos¬methyl on apples (the most 

frequently treated crop) at application rates equal to or higher than 

those for peaches (1.0-1.5 lb ai/A per application, 4.5 lb ai/A per year 

maximum on apples vs. 1.125 lbs ai/A per application, 4.5 lbs ai/A per 

year maximum on peaches). Furthermore, the total amount of 

azinphos-methyl used on apples (890,000 lb active ingredient) is over 

seven times the amount used on peaches (120,000 lb). Therefore, the 

EPA assessment indicates that azinphos-methyl poses a risk to 

drinking water supplies. While EPA has issued a four-year limited 

registration for azinphos-methyl use on apples and seven other crops, 

the Agency has stated that these registrations may be extended, thus 

creating the need to regulate azinphos-methyl as a drinking water 

contaminant.

None given

1405-89-6 Bacitracin zinc Natural Resources 

Defense Council

Widespread exposure to antibiotics is contributing to the growth of bacterial 

resistance, and this problem is of grave concern. In the past several decades 

almost every bacteria that can cause infections in humans has developed 

resistance to at least one antibiotic, and some are resistant to multiple 

antibiotics. The Centers for Disease Control and Prevention (CDC) have 

identified antibiotic resistance as one of the most pressing public health 

problems to face our nation. Infections caused by bacteria with resistance to at 

least one antibiotic have been estimated to kill over 60,000 hospitalized 

patients each year.

Antibiotic resistance is caused by a number of factors including repeated and 

improper use of antibiotics in both humans and animals. Scientists also agree 

that exposure to low levels of antibiotics actually promotes bacterial resistance 

by exerting selective pressure for genes that promote resistance.

Antibiotics are found in wastewater because the body does not 

completely metabolize all drugs, so both the metabolized and 

unmetabolized drug are excreted by humans into wastewater. For 

example, when amoxicillin is ingested, 60-75% of the antibiotic is 

excreted unchanged into the urine. This antibiotic, now in the 

environment, may encounter other bacteria and promote resistance. It 

is unknown how much of an impact current low levels of antibiotics in 

drinking water are having on the problem of bacterial resistance. 

However, the potential has been recognized for many years. 

Large animal feeding operations generate a large amount of waste 

that can potentially contaminate groundwater and waterways 

contributing to antibiotic resistance and contamination of waterways 

with steroid hormones. As occurs in humans, some portion of the 

antibiotics administered to livestock will pass unchanged through their 

bodies and will be excreted in their waste. It has been estimated that 

None given

A1-4 
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank Massive quantities of antibiotics are used in agriculture both to treat infections 

and as food additives to promote growth and to compensate for conditions that 

contribute to infection. Animals raised in Concentrated Animal Feeding 

Operations (CAFOs) are at increased risk for infection due to close 

confinement and stress. In fact, it has been estimated that 70% of the 

antibiotics used in the U.S. are for animal husbandry. Improper use and 

overuse of antibiotics in livestock and poultry can cause resistance in strains 

of bacteria that can infect humans. Furthermore, half of the antibiotics used in 

livestock are in the same classes of drugs that are used in humans. As a 

result the U.S. Institute of Medicine (IOM) and the World Health Organization 

(WHO) both stated that the widespread use of antibiotics in agriculture is 

contributing to antibiotic resistance in humans.

between 25-75% of antibiotics are excreted unchanged in feces and 

can persist in the soil after land application. Manure is applied in large 

quantities as fertilizer in farm fields. In addition to potentially 

contaminating the food supply with antibiotic resistant bacteria, 

antibiotics in manure can persist in soil and promote the development 

of more antibiotic resistant bacteria. Animal waste and its associated 

contaminants can enter waterways through groundwater 

contamination, overflow of waste lagoons into surface water or by 

over-application of manure as fertilizer in farm fields. A recently 

published study found evidence of fecal contamination and increased 

levels of antibiotic resistant bacteria downstream of a swine 

concentrated feeding operation. Other studies have found antibiotic 

resistance in groundwater underlying a swine waste lagoon.

As such, antibiotics that are used both for human medical needs and 

in large-scale agriculture operations at low levels in animal feed to 

promote animal growth must be included on the CCL4 and must be 

regulated. These antibiotics include bacitracin zinc, spiramycin, tylosin, 

and virginiamycin. Notably, these antibiotics were all banned for 

agricultural use in the European Union in 1998.

blank

25057-89-0 Bentazone AWWA None given None given None given

85-68-7 Benzyl butyl 

phthalate 

Natural Resources 

Defense Council

Phthalates are endocrine disruptors that have been found to cause 

developmental and reproductive abnormalities in animal studies. Furthermore, 

studies have found an association between phthalate metabolite 

concentrations and obesity, insulin resistance and thyroid hormone levels in 

humans. Stahlhut et al.(2007) analyzed urinary concentrations of seven 

phthalate metabolites in 1,443 adult men and found a statistically significant 

positive association between concentrations of the metabolites MBzP, 

MEHHP, MEOHP and MEP and abdominal obesity. Concentrations of MBP, 

MBzP and MEP were positively and significantly associated with insulin 

resistance. In a different study, baby boys exposed to the phthalates, DMP, 

DEP or BBP, in their mother’s breast milk were found to have hormonal 

disturbances at 3 months of age. Studies have found that di-isononyl phthalate 

(DiNP) is an anti-androgenic endocrine disruptor with developmental and 

reproductive toxicity. Exposures in pregnant rats have been shown to 

adversely affect development of the male reproductive tract. Adverse effects 

include a cluster of outcomes that has been called “phthalate e syndrome” and 

includes underdeveloped or absent reproductive organs, retained nipples, 

cryptorchidism, decreased anogenital distance (AGD), hypospadias, and 

decreased or abnormal sperm. DINP does not bind to the androgen receptor 

and these effects are likely mediated through interference with testosterone 

synthesis.

Phthalates are ubiquitous in the U.S. population. Although significant exposure 

can occur due to consumer products, the contribution of drinking water to 

overall exposure deserves to be examined. The NHANES measured the 

concentrations of 12 phthalate metabolites in the urine of over 2,500 children 

Phthalates enter the environment as a result of releases from industrial 

facilities that manufacture or use these compounds, from waste 

disposal sites, through the use of phthalate-containing products by 

consumers and through discharge of municipal wastewaters 

containing phthalates. Phthalates have been found in numerous 

hazardous waste sites: diethyl phthalate (DEP) has been identified at 

348 sites, dibutyl phthalate (DBP) at 602 sites, dimethyl phthalate 

(DMP) at 167 sites, benzyl butyl phthalate (BzBP) at 413 sites, 

dicyclohexyl phthalate (DCHP) at one site, and di-n-octyl phthalate 

(DnOP) at 433 sites, among other phthalates.

Phthalates have been detected in environmental water samples across 

the United States, which raises concerns about drinking water as a 

route of exposure. The maximum concentrations found for some of 

these phthalates are particularly alarming. The following data were 

found in a search for stream water samples analyzed for phthalates in 

the EPA STORET database. Results are for the period January 2000 

through June 2012:

Benzyl butyl phthalate (BzBP) was present in 789 (19.3 %) out of 4077 

stream water samples analyzed for this chemical, with a maximum 

concentration of 1000 ug/L.

None given

A1-5 
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank and adults. The highest average concentration was 163 ug/g creatinine for 

MEP, a metabolite of the plasticizer diethyl phthalate (see Table 3). [See the 

CDC report cited below] The Centers for Disease Control and Prevention 

(CDC) did not report what percentage of samples had detectable 

concentrations of each of the metabolites, but nine of the metabolites were 

found in the urine of at least half of the individuals. [See Table 3. CDC report 

of phthalate concentrations in urine; NHANES 1999 – 2000 and 2001 - 2002 

located on page 27 of the NRDC Nomination Letter and Table 4 Frequency of 

detection of phthalate metabolites in human urine samples, United States 

located on pages 28 and 29 of the NRDC Nomination Letter.]

blank blank

80-05-7 Bisphenol A Anonymous 201 Weak endocrine disruptor - principal concern is for potential reproductive and 

developmental effects in early life stages. EPA has considered exposures to 

children from drinking water and from the use of BPA in consumer products. 

EPA also examined potential ecological impact from the presence of BPA in 

the environment.

None given None given

80-05-7 Bisphenol A Natural Resources 

Defense Council

A number of recent studies have revealed that early life exposures to lowdoses of BPA result in adverse effects later in life. The developing fetus is 

especially vulnerable. Although many of these studies were done in laboratory 

animals, the exposures occurred at concentrations currently found in the 

human population. Recent research finds low levels of BPA exposure causes 

harm in the mammary gland, prostate tissue, and brain. In rats, in utero 

exposure to BPA causes long-term effects on development of mammary 

tissue, causing preneoplastic lesions, increased susceptibility to cancer and 

increased sensitivity to a chemical known to cause breast cancer. Perinatal 

exposure to low levels of BPA causes precancerous prostate lesions (prostatic 

intraepithelial neoplasia) in rats. The effect appears to result from the failure in 

exposed animals of a gene to become hypermethylated as the rats age. 

Experiments with mice reveal that chronic adult exposure to BPA causes 

insulin resistance, a common problem in humans that can lead to Type II 

diabetes and heart disease. Recent human studies continue to find links 

between BPA and cardiovascular disease, obesity and metabolic changes 

affecting insulin levels, which could lead to diabetes. BPA has been shown to 

cause aneuploidy in mouse oocytes. Meiotic aneuploidy is the most common 

cause of miscarriage in women. In 2007, a group of 38 scientists issued a 

consensus statement expressing their concern that current levels of BPA 

exposure were contributing to the human health conditions of neurobehavioral 

problems, obesity, infertility and reproductive cancers. In addition, the U.S. 

National Toxicology Program has issued a draft report expressing “some 

concern” that BPA could cause neurobehavioral abnormalities, early onset 

puberty, and reproductive cancers, especially in fetuses, infants and children 

who are exposed.

BPA is produced at over one million pounds per year and is frequently 

found in the environment. BPA releases to the environment in the U.S. 

totaled 1.4 million pounds in 2006, including 3,410 pounds released 

directly to water and 108,805 pounds released to the air. 

BPA is a water contaminant. A study in Germany found BPA in surface 

water (0.0005 to 0.41 ug/L), in sewage effluents (0.018 to 0.702 ug/L), 

in sediments (0.01 to 0.19 mg/kg) and in sewage sludge (0.004 to 

1.363mg/kg dw). Cousins et al. (2002) reviewed previously published 

monitoring data for the United States and found a median reported 

water concentration of 0.5 ug/l (below the detection limit of the studies) 

and a 90th percentile of 4.4 ug/l. The same study also suggested a 

half-life for BPA of 4.5 days in surface water, indicating that BPA can 

be transported hundreds of kilometers in rivers before levels fall below 

detection limits.

In December, 2011, the International Chemical Secretariat in the E.U. 

reported that many drinking water pipes are being restored by relining 

them with epoxy resin that contains BPA, and that this BPA is leaching 

into the drinking water. Anecdotally, this practice seems to also be 

occurring in the U.S. This is another important source of exposure in 

the drinking water – and suggests that levels of BPA are even higher 

than articles suggest.

Bisphenol A -

(4,4'-(1-ethylethylidene)bisphenol 

or 4,4'-Isopropylidenediphenol), 

(CASRN 80-05-7), is a monomer 

used as the building block of 

polycarbonate plastics and other 

plastics including epoxy resins. 

BPA is found in a wide variety of 

everyday consumer products, 

such as the coating of food and 

drink packaging, dental sealants, 

baby bottles, water bottles, 

microwave ovenware and eating 

utensils. As these products age, 

the polycarbonate polymer 

breaks down, releasing the BPA 

monomer. 

1689-84-5 Bromoxynil AWWA None given None given None given

63-25-2 Carbaryl AWWA None given None given None given

A1-6 
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

63-25-2 Carbaryl Natural Resources 

Defense Council

Carbaryl (CAS # 63-25-2) is an N-methyl carbamate pesticide that acts as a 

neurotoxic acetylcholinesterase inhibitor and a “likely” carcinogen according to 

the Office of Pesticide Programs Cancer Assessment Review Committee. The 

systemic effects of carbaryl include headache, dizziness, weakness, shaking, 

nausea, stomach cramps, diarrhea, and sweating. Effects may also include 

loss of appetite, weakness, weight loss, and general malaise. Carbaryl is 

particularly toxic to the developing nervous system of fetuses, infants, and 

young children. Exposure to elevated levels of carbaryl may cause 

developmental neurotoxicity and “significant changes in some of the 

morphometric measurements of the brain”.

Given the limitations in the monitoring data that the Agency [EPA] has 

acknowledged, and the fact that the highest EEC estimated by EPA models 

was 55 times the acute DWLOC for children 1 to 2 years old, it is clear that 

carbaryl presents risks of concern from drinking water exposure and should be 

regulated as a drinking water contaminant by establishing an MCL.

Approximately 3.9 million pounds of carbaryl active ingredient are used 

annually in the U.S. When EPA issued its Revised Risk Assessment 

for carbaryl in 2003, its water assessment did not consider nonagricultural sources of carbaryl, which constitute a total of 40% of 

carbaryl use by weight, and which are the dominant sources of 

carbaryl pollution in surface water. Despite ignoring non-agricultural 

uses, the carbaryl health risk assessment in the Interim Reregistration 

Eligibility Decision (IRED) found that acute surface water risks 

presuming maximum label application rates exceeded the drinking 

water level of concern (DWLOC) for children and the general 

population when combined with estimated food exposures. U.S. 

Geological Survey National Water Quality Assessment (NAWQA) 

monitoring data presented in the carbaryl assessment demonstrated 

that streams draining urban areas had both higher concentrations of 

carbaryl and more frequent detections, when compared with streams 

draining agricultural or mixed land use areas. It is clear that 

contamination of water is predominantly from non-agriculture uses of 

carbaryl, and that by not considering these uses, the Agency 

dramatically underestimated the amount of carbaryl in drinking water 

(Estimated Environmental Concentration, or EEC), which is likely to be 

two-times higher than EPA estimates. Twenty-one percent of surface 

water samples in the NAWQA database contained detectable levels of 

carbaryl.EPA discussed in its IRED the limitations of existing 

monitoring data: "Carbaryl is fairly mobile, but is not likely to persist or 

accumulate in the environment. As such, it is difficult for monitoring 

studies to detect peak concentrations that can occur. EPA determined 

that currently available monitoring studies for carbaryl are limited in 

this regard, and did not use them to define peak values for 

carbaryl."As a result of these data limitations, EPA used models to 

estimate drinking water EECs for currently registered uses in the 

carbaryl IRED. The Agency reported that the acute drinking water 

EECs ranged from 23 to 410 ppb for acute exposure, and from 1.3 to 

23 ppb for chronic exposure, which exceeded the acute DWLOC for 

children 1-2 years old (7.4 ppb) and for the general population (200 

ppb). This is especially concerning, given that these calculations are 

likely to underestimate risk by excluding non-agricultural uses of 

carbaryl, which comprise 40% of total carbaryl used. Therefore, it is 

likely that actual EEC’s are even higher, possibly 40% higher, than 

what the Agency calculates. The high toxicity of carbaryl, coupled with 

the high exceedances of acceptable levels in drinking water, make this 

level of risk to infants and children unacceptably high.

None given

10045-97-3 Cesium 137 Anonymous 197 Cs-137 is prevalent in atmosphere due to melt down underway in Japan of 

four reactors with 40 years of spent fuel on site. Cs-137 interferes with 

endocrine function and fetal development.

There are 23 nuclear power plants of exact design to the fatal power 

plants in Japan, failure due to earthquakes near population centers 

and water sources.

Monitoring existing conditions 

leads to rate of change analysis 

when done on a predictable time 

frame.

1897-45-6 Chlorothalonil AWWA None given None given None given

2821-88-2 Chlorpyrifos AWWA None given None given None given

A1-7 
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

2921-88-2 Chlorpyrifos Natural Resources 

Defense Council

With chlorpyrifos and other developmental neurotoxic chemicals, risk to the 

fetus, infant, and child comes primarily from the timing of exposure. Even a 

very small dose, for even a short duration, during a developmental period of 

vulnerability will result in permanent neural dysfunction. There is no 

demonstrated reliable threshold of safety for this highly toxic chemical, as 

indicated in the IRED, where a no-effect level could not be determined for 

developmental neurotoxicity. However, there is demonstrated evidence of 

neuropathology and increased vulnerability of fetuses when exposed to 

chlorpyrifos. EPA has acknowledged this susceptibility in the chlorpyrifos 

Human Health Risk Assessment: In conclusion, the weight of the evidence 

raises concern for an increase in both the sensitivity and susceptibility of the 

fetus or young animal to adverse biochemical, morphological, or behavioral 

alterations from chlorpyrifos treatment during brain development. With respect 

to cholinesterase inhibition, an increase in sensitivity of the young compared 

to adults was seen all along the dose response curve, even at relatively low 

doses." 

Using the PRZM/EXAMS screening model, EPA estimated that 90-day 

average and peak chlorpyrifos concentrations were 6.7 and 40 ppb 

respectively. Meanwhile, acute DWLOCs for infants less than a year old, 

children 1-6 years and females 13 to 50 years ranged from 0.9 to 9 ppb. 

Chronic DWLOCs for these population groups ranged from 0.2 to 0.72 ppb. 

EPA’s modeling estimates therefore show that chlorpyrifos exposure in 

drinking water has the potential to expose vulnerable groups of the population 

to unacceptable levels of this chemical.

Chlorpyrifos (CAS # 2921-88-2) is an organophosphate pesticide used 

at approximately 21 to 24 million pounds active ingredient (a.i.) 

annually in the United States. Most chlorpyrifos is used in agriculture 

on crops such as corn and cotton, but other uses include golf courses, 

road medians, food processing plants, manufacturing plants, ship 

holds, railroad boxcars, and non-structural wood treatments. 

Chlorpyrifos is applied aerially, by chemigation, groundboom, hand 

wand, airblast sprayer, and other methods.

Although EPA said in the IRED that the drinking water risk is below the 

level of concern, the Agency noted that there have been cases of high 

levels of drinking water well contamination associated with localized 

applications of chlorpyrifos as a subterranean termiticide. This was 

addressed, EPA said, by eliminating all termiticidal uses. However, 

despite EPA’s assertions that only termiticidal use leads to water 

contamination problems, USGS and others have found contamination 

of ground and surface water with chlorpyrifos and its metabolites, and 

EPA’s own modeling shows that it is likely that in certain areas of 

heavy use, chlorpyrifos (and its metabolites) present significant water 

risks. There is no evidence that the water risks of chlorpyrifos and its 

metabolites are limited to termiticidal use.There is extensive evidence 

of the potential of chlorpyrifos to contaminate surface and 

groundwater. Combined USGS data for state, local, national, and 

multi-state studies that measured chlorpyrifos concentrations in 

surface water detected the pesticide at 7 of 108 (6%) sites sampled. 

Chlorpyrifos has medium runoff potential due to its relatively low water 

solubility, 2 mg/L. A chlorpyrifos flux as a percentage of use of 0.15 

has been measured in the Minnesota River. Chlorpyrifos is also used 

in non-agricultural settings and can drift or runoff directly into surface 

water bodies in areas of high population density.Data from the MidContinent Pesticide Study show that chlorpyrifos was present in the 

ground water in 4.2% of the wells sampled. Chlorpyrifos has been 

detected in 0.6% of wells sampled, according to the U.S. EPA's 

Pesticides in Ground Water Database. Long (1989) detected 

chlorpyrifos in the ground water of 30% of 56 sites examined beneath 

pesticide mixing and loading facilities in Illinois. The maximum 

concentration detected was 0.5 ppb.Water monitoring sample sites are 

not necessarily correlated with chlorpyrifos use sites, and in particular, 

may miss sites where multiple fields are treated with chlorpyrifos 

resulting in pooled runoff into a common water source. In fact, the 

IRED states, “it is not clear that they [monitoring data] represent the 

most vulnerable groundwater where chlorpyrifos is used most 

intensively” (IRED p.18). Monitoring of surface water is likely to be 

subject to the same problem. Levels of chlorpyrifos in pooled runoff 

sites are likely to be many times higher than single field sites. 

Similarly, data collection is not timed to correspond with worst-case 

scenarios, such as closely following chlorpyrifos applications, or 

following large storm runoff events, and thus most often misses these 

highly toxic environmental exposures.

None given

A1-8 
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

84-74-2 Dibutyl phthalate Natural Resources 

Defense Council

Phthalates are endocrine disruptors that have been found to cause 

developmental and reproductive abnormalities in animal studies.Furthermore, 

studies have found an association between phthalate metabolite 

concentrations and obesity, insulin resistance and thyroid hormone levels in 

humans. Stahlhut et al. (2007) analyzed urinary concentrations of seven 

phthalate metabolites in 1,443 adult men and found a statistically significant 

positive association between concentrations of the metabolites MBzP, 

MEHHP, MEOHP and MEP and abdominal obesity. Concentrations of MBP, 

MBzP and MEP were positively and significantly associated with insulin 

resistance. In a different study, baby boys exposed to the phthalates, DMP, 

DEP or BBP, in their mother’s breast milk were found to have hormonal 

disturbances at 3 months of age. Studies have found that di-isononyl phthalate 

(DiNP) is an anti-androgenic endocrine disruptor with developmental and 

reproductive toxicity. Exposures in pregnant rats have been shown to 

adversely affect development of the male reproductive tract. Adverse effects 

include a cluster of outcomes that has been called “phthalate e syndrome” and 

includes underdeveloped or absent reproductive organs, retained nipples, 

cryptorchidism, decreased anogenital distance (AGD), hypospadias, and 

decreased or abnormal sperm. DINP does not bind to the androgen receptor 

and these effects are likely mediated through interference with testosterone 

synthesis.

Phthalates are ubiquitous in the U.S. population. Although significant exposure 

can occur due to consumer products, the contribution of drinking water to 

overall exposure deserves to be examined. The NHANES measured the 

concentrations of 12 phthalate metabolites in the urine of over 2,500 children 

and adults. The highest average concentration was 163 ug/g creatinine for 

MEP, a metabolite of the plasticizer diethyl phthalate (see Table 3). [See the

CDC report cited below.] The Centers for Disease Control and Prevention 

(CDC) did not report what percentage of samples had detectable 

concentrations of each of the metabolites, but nine of the metabolites were 

found in the urine of at least half of the individuals. [See Table 3. CDC report 

of phthalate concentrations in urine; NHANES 1999 – 2000 and 2001 - 2002 

located on page 27 of the NRDC Nomination Letter and Table 4 Frequency of 

detection of phthalate metabolites in human urine samples, United States

located on pages 28 and 29 of the NRDC Nomination Letter.]

Phthalates enter the environment as a result of releases from industrial 

facilities that manufacture or use these compounds, from waste 

disposal sites, through the use of phthalate-containing products by 

consumers and through discharge of municipal wastewaters 

containing phthalates. Phthalates have been found in numerous 

hazardous waste sites: diethyl phthalate (DEP) has been identified at 

348 sites, dibutyl phthalate (DBP) at 602 sites, dimethyl phthalate 

(DMP) at 167 sites, benzyl butyl phthalate (BzBP) at 413 sites, 

dicyclohexyl phthalate (DCHP) at one site, and di-n-octyl phthalate 

(DnOP) at 433 sites, among other phthalates.

Phthalates have been detected in environmental water samples across 

the United States, which raises concerns about drinking water as a 

route of exposure. The maximum concentrations found for some of 

these phthalates are particularly alarming. The following data were 

found in a search for stream water samples analyzed for phthalates in 

the EPA STORET database. Results are for the period January 2000 

through June 2012:

Dibutyl phthalate (DBP) was found in 828 (19.9%) of the 4160 stream 

water samples for that period, with a maximum concentration of 2,760 

ug/L.

None given

1918-00-9 Dicamba AWWA None given None given None given

62-73-7 Dichlorvos Natural Resources 

Defense Council

Dichlorvos (CAS # 62-73-7), or DDVP, is an organophosphate insecticide 

widely used in agriculture. Like other organophosphates, dichlorvos is an 

acetylcholinesterase inhibitor. DDVP exposure may cause symptoms such as 

nausea, vomiting, dizziness, muscle spasms, and seizures. According to a 

2000 EPA Cancer Assessment review, there is suggestive evidence that 

dichlorvos may cause cancer. The National Toxicology Program has stated 

that there is “clear evidence” of carcinogenic activity of dichlorvos in a mice 

study. One study has linked dichlorvos exposure to leukemia in children under 

15. Another study has also found an association between dichlorvos exposure 

and leukemia in adult men. Furthermore, EPA has determined that “dichlorvos 

has been shown to be a direct acting mutagen by common in vitro bacterial 

Dichlorvos is soluble in water and may enter surface waters in runoff. 

However, no data on its occurrence in surface waters has been 

collected; there is also little data on dichlorvos in groundwater. Two 

other pesticides, naled and trichlorfon, degrade to dichlorvos in the 

environment and represent additional inputs of dichlorvos to water. 

However, monitoring data on these two pesticides is also very limited.

Given the lack of monitoring data, EPA used IR-PCA PRZM/EXAMS 

models to calculate estimated drinking water concentrations (EDWCs) 

of dichlorvos in surface water. The models produced estimates that 

were below the EPA level of concern. However; the complete lack of 

None given

A1-9 
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank genetic toxicity assays and in vitro mammalian test systems.” monitoring data raises questions about whether an exclusive reliance 

on modeling results is appropriate for a neurotoxic and potentially 

carcinogenic pesticide such as dichlorvos. EPA should collect data 

monitoring data for dichlorvos by requiring such data from the 

registrants or commissioning its own studies to better assess drinking 

water risks and set an MCL if necessary.

blank

115-32-2 Dicofol Natural Resources 

Defense Council

Animal studies have found that dicofol causes toxicity in the liver, adrenal 

glands, kidneys, thyroid, reproductive organs, heart and stomach. Liver and 

thyroid effects occurred at relatively low doses (100 ppm and 10 ppm, 

respectively). Dicofol is a possible human carcinogen. Dicofol has shown 

endocrine disruptor activity in vivo and in vitro. This chemical has been shown 

to interfere with blastocyst implantation in rats.

The first problem with the assessment is related to the way EPA calculated the 

Reference Dose (RfD). EPA is supposed to apply an additional safety factor of 

10x to the RfD calculation to protect infants and children, who may have 

increased susceptibility to health effects from chemical exposures compared 

to adults. The Agency reduced the FQPA safety factor of 10x to 3x based on 

the lack of increased pre-natal or post-natal susceptibility to dicofol in 

developmental toxicity studies. However, EPA stated that a developmental 

neurotoxicity study was necessary because dicofol produced neurotoxicity in

rats and such a study might identify an endpoint for dietary risk. Despite 

lacking such a study, EPA improperly reduced the safety factor to 3x. If the 

10x factor had been applied as mandated by the Food Quality Protection Act, 

a more protective acute RfD of 0.015 mg/kg day-1 would have been chosen 

instead of the 0.05 mg/kg day-1 dose EPA used in its assessment. Had EPA 

applied the 10x safety factor, dicofol exposure from food alone would have 

exceeded the acute RfD and the EPA level of concern for all population 

groups (see Table 1) [See Table 1. Comparison of acute dietary exposure 

values from food at the 99.9th percentile located on page 16 of the NRDC 

nomination letter]. This would have resulted in a DWLOC of zero (0), so that 

any drinking water exposure would have been of concern. The unwarranted 

reduction of the FQPA safety factor also affected the outcome of the chronic 

dietary exposure assessment. As shown in Table 2 [See Table 2. Chronic 

dietary food exposure and risk estimate from Dicofol (in food alone) located on 

page 17 of the NRDC nomination letter.], if the 10x factor had been applied, 

chronic exposures from food alone for infants and children 1 to 6 years old 

would have exceeded the level of concern. Therefore, any drinking water 

exposure would have been of concern as well. [See Table 2. Chronic dietary 

food exposure and risk estimate from Dicofol (in food alone) located on page 

17 of the NRDC nomination letter.]

Dicofol is an organochlorine pesticide used in agriculture, primarily on 

cotton and citrus crops. Approximately 860,000 pounds of active 

ingredient are used every year.EPA used its SCI-GROW model to 

estimate dicofol concentrations in groundwater and calculated a 90-

day average peak concentration of 0.069 ppb. An overall mean 

surface water concentration of 0.5 ppb was estimated with the PRZMEXAMS model. Both concentrations were below the Drinking Water 

Levels of Comparison (DWLOCs) for children and the general U.S. 

population for both acute and chronic exposure. However, there are 

some important shortcomings in EPA’s assessment of dicofol 

exposure and risk.

Another shortcoming in the EPA assessment is that the Agency relied 

on models to estimate environmental concentrations in surface and 

groundwater, but did not have a robust set of monitoring data. EPA 

should require the collection of surface and groundwater monitoring 

data in areas where dicofol is applied. The Agency should use these 

data to corroborate its exposure estimates and make a regulatory 

determination for dicofol under the SDWA.

None given

84-61-7 Dicyclohexyl 

phthalate

Natural Resources 

Defense Council

Phthalates are endocrine disruptors that have been found to cause 

developmental and reproductive abnormalities in animal studies. Furthermore, 

studies have found an association between phthalate metabolite 

concentrations and obesity, insulin resistance and thyroid hormone levels in 

humans. Stahlhut et al. (2007) analyzed urinary concentrations of seven 

phthalate metabolites in 1,443 adult men and found a statistically significant 

positive association between concentrations of the metabolites MBzP, 

MEHHP, MEOHP and MEP and abdominal obesity. Concentrations of MBP, 

Phthalates enter the environment as a result of releases from industrial 

facilities that manufacture or use these compounds, from waste 

disposal sites, through the use of phthalate-containing products by 

consumers and through discharge of municipal wastewaters 

containing phthalates. Phthalates have been found in numerous 

hazardous waste sites: diethyl phthalate (DEP) has been identified at 

348 sites, dibutyl phthalate (DBP) at 602 sites, dimethyl phthalate 

(DMP) at 167 sites, benzyl butyl phthalate (BzBP) at 413 sites, 

None given

A1-10
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank MBzP and MEP were positively and significantly associated with insulin 

resistance. In a different study, baby boys exposed to the phthalates, DMP, 

DEP or BBP, in their mother’s breast milk were found to have hormonal 

disturbances at 3 months of age. Studies have found that di-isononyl phthalate 

(DiNP) is an anti-androgenic endocrine disruptor with developmental and 

reproductive toxicity. Exposures in pregnant rats have been shown to 

adversely affect development of the male reproductive tract. Adverse effects 

include a cluster of outcomes that has been called “phthalate e syndrome” and 

includes underdeveloped or absent reproductive organs, retained nipples, 

cryptorchidism, decreased anogenital distance (AGD), hypospadias, and 

decreased or abnormal sperm. DINP does not bind to the androgen receptor 

and these effects are likely mediated through interference with testosterone 

synthesis. 

Phthalates are ubiquitous in the U.S. population. Although significant exposure 

can occur due to consumer products, the contribution of drinking water to 

overall exposure deserves to be examined. The NHANES measured the 

concentrations of 12 phthalate metabolites in the urine of over 2,500 children 

and adults. The highest average concentration was 163 ug/g creatinine for 

MEP, a metabolite of the plasticizer diethyl phthalate (see Table 3). [See the 

CDC report cited below.] The Centers for Disease Control and Prevention 

(CDC) did not report what percentage of samples had detectable 

concentrations of each of the metabolites, but nine of the metabolites were 

found in the urine of at least half of the individuals. [See Table 3. CDC report 

of phthalate concentrations in urine; NHANES 1999 – 2000 and 2001 - 2002 

located on page 27 of the NRDC Nomination Letter and Table 4 Frequency of 

detection of phthalate metabolites in human urine samples, United States 

located on pages 28 and 29 of the NRDC Nomination Letter.]

dicyclohexyl phthalate (DCHP) at one site, and di-n-octyl phthalate 

(DnOP) at 433 sites, among other phthalates.

Phthalates have been detected in environmental water samples across 

the United States, which raises concerns about drinking water as a 

route of exposure. The maximum concentrations found for some of 

these phthalates are particularly alarming.

blank

84-66-2 Diethyl phthalate Natural Resources 

Defense Council

Phthalates are endocrine disruptors that have been found to cause 

developmental and reproductive abnormalities in animal studies. Furthermore, 

studies have found an association between phthalate metabolite 

concentrations and obesity, insulin resistance and thyroid hormone levels in 

humans. Stahlhut et al. (2007) analyzed urinary concentrations of seven 

phthalate metabolites in 1,443 adult men and found a statistically significant 

positive association between concentrations of the metabolites MBzP, 

MEHHP, MEOHP and MEP and abdominal obesity. Concentrations of MBP, 

MBzP and MEP were positively and significantly associated with insulin 

resistance. In a different study, baby boys exposed to the phthalates, DMP, 

DEP or BBP, in their mother’s breast milk were found to have hormonal 

disturbances at 3 months of age. Studies have found that di-isononyl phthalate 

(DiNP) is an anti-androgenic endocrine disruptor with developmental and 

reproductive toxicity. Exposures in pregnant rats have been shown to 

adversely affect development of the male reproductive tract. Adverse effects 

include a cluster of outcomes that has been called “phthalate e syndrome” and 

includes underdeveloped or absent reproductive organs, retained nipples, 

cryptorchidism, decreased anogenital distance (AGD), hypospadias, and 

decreased or abnormal sperm. DINP does not bind to the androgen receptor 

Phthalates enter the environment as a result of releases from industrial 

facilities that manufacture or use these compounds, from waste 

disposal sites, through the use of phthalate-containing products by 

consumers and through discharge of municipal wastewaters 

containing phthalates. Phthalates have been found in numerous 

hazardous waste sites: diethyl phthalate (DEP) has been identified at 

348 sites, dibutyl phthalate (DBP) at 602 sites, dimethyl phthalate 

(DMP) at 167 sites, benzyl butyl phthalate (BzBP) at 413 sites, 

dicyclohexyl phthalate (DCHP) at one site, and di-n-octyl phthalate 

(DnOP) at 433 sites, among other phthalates.

Phthalates have been detected in environmental water samples across 

the United States, which raises concerns about drinking water as a 

route of exposure. The maximum concentrations found for some of 

these phthalates are particularly alarming. The following data were 

found in a search for stream water samples analyzed for phthalates in 

the EPA STORET database. Results are for the period January 2000 

through June 2012:

None given

A1-11
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank and these effects are likely mediated through interference with testosterone 

synthesis.

Phthalates are ubiquitous in the U.S. population. Although significant exposure 

can occur due to consumer products, the contribution of drinking water to 

overall exposure deserves to be examined. The NHANES measured the 

concentrations of 12 phthalate metabolites in the urine of over 2,500 children 

and adults. The highest average concentration was 163 ug/g creatinine for 

MEP, a metabolite of the plasticizer diethyl phthalate (see Table 3). [See the 

CDC report cited below.] The Centers for Disease Control and Prevention 

(CDC) did not report what percentage of samples had detectable 

concentrations of each of the metabolites, but nine of the metabolites were 

found in the urine of at least half of the individuals. [See Table 3. CDC report 

of phthalate concentrations in urine; NHANES 1999 – 2000 and 2001 - 2002 

located on page 27 of the NRDC Nomination Letter and Table 4 Frequency of 

detection of phthalate metabolites in human urine samples, United States 

located on pages 28 and 29 of the NRDC Nomination Letter.]

Diethyl phthalate (DEP) was detected in 840 (20.1%) of the 4174 

stream water samples analyzed. The maximum concentration found 

was 1000 ug/L.

blank

28553-12-0 Di-isononyl 

phthalate 

Natural Resources 

Defense Council

Phthalates are endocrine disruptors that have been found to cause 

developmental and reproductive abnormalities in animal studies. Furthermore, 

studies have found an association between phthalate metabolite 

concentrations and obesity, insulin resistance and thyroid hormone levels in 

humans. Stahlhut et al. (2007) analyzed urinary concentrations of seven 

phthalate metabolites in 1,443 adult men and found a statistically significant 

positive association between concentrations of the metabolites MBzP, 

MEHHP, MEOHP and MEP and abdominal obesity. Concentrations of MBP, 

MBzP and MEP were positively and significantly associated with insulin 

resistance. In a different study, baby boys exposed to the phthalates, DMP, 

DEP or BBP, in their mother’s breast milk were found to have hormonal 

disturbances at 3 months of age. Studies have found that di-isononyl phthalate 

(DiNP) is an anti-androgenic endocrine disruptor with developmental and 

reproductive toxicity. Exposures in pregnant rats have been shown to 

adversely affect development of the male reproductive tract. Adverse effects 

include a cluster of outcomes that has been called “phthalate e syndrome” and 

includes underdeveloped or absent reproductive organs, retained nipples, 

cryptorchidism, decreased anogenital distance (AGD), hypospadias, and 

decreased or abnormal sperm. DINP does not bind to the androgen receptor 

and these effects are likely mediated through interference with testosterone 

synthesis. 

Phthalates are ubiquitous in the U.S. population. Although significant exposure 

can occur due to consumer products, the contribution of drinking water to 

overall exposure deserves to be examined. The NHANES measured the 

concentrations of 12 phthalate metabolites in the urine of over 2,500 children 

and adults. The highest average concentration was 163 ug/g creatinine for 

MEP, a metabolite of the plasticizer diethyl phthalate (see Table 3). [See the

CDC report cited below.] The Centers for Disease Control and Prevention 

Phthalates enter the environment as a result of releases from industrial 

facilities that manufacture or use these compounds, from waste 

disposal sites, through the use of phthalate-containing products by 

consumers and through discharge of municipal wastewaters 

containing phthalates. Phthalates have been found in numerous 

hazardous waste sites: diethyl phthalate (DEP) has been identified at 

348 sites, dibutyl phthalate (DBP) at 602 sites, dimethyl phthalate 

(DMP) at 167 sites, benzyl butyl phthalate (BzBP) at 413 sites, 

dicyclohexyl phthalate (DCHP) at one site, and di-n-octyl phthalate 

(DnOP) at 433 sites, among other phthalates.

Phthalates have been detected in environmental water samples across 

the United States, which raises concerns about drinking water as a 

route of exposure. The maximum concentrations found for some of 

these phthalates are particularly alarming. The following data were 

found in a search for stream water samples analyzed for phthalates in 

the EPA STORET database. Results are for the period January 2000 

through June 2012:

Di-isononyl phthalate (DiNP) – No data available. [The Institute for 

Health and Consumer Protection (IHCP) of the European Chemicals 

Bureau estimated a half life in surface water for DINP of 50 days. 

According to the IHCP, 7 percent of the DINP in the influent in sewage 

treatment plants will be released in the effluent. See European 

Commission Joint Research Centre, Institute for Health and Consumer 

Protection, 1,2-Benzenedicarboxylic acid, Di-C8-10-Branched Alkyl 

Esters, C9-Rich and Di-“Isononyl” Phthalate (DINP), CAS Nos: 68515-

48-0 and 28553-12-0, EINECS Nos: 271-090-9 and 249-079-5, 

Summary Risk Assessment Report, 2003. 

http://ecb.jrc.it/DOCUMENTS/ExistingNone given

A1-12
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

(CDC) did not report what percentage of samples had detectable 

concentrations of each of the metabolites, but nine of the metabolites were 

found in the urine of at least half of the individuals. [See Table 3. CDC report 

of phthalate concentrations in urine; NHANES 1999 – 2000 and 2001 - 2002 

located on page 27 of the NRDC Nomination Letter and Table 4 Frequency of 

detection of phthalate metabolites in human urine samples, United States 

located on pages 28 and 29 of the NRDC Nomination Letter.]

Chemicals/RISK_ASSESSMENT/SUMMARY/dinpsum046.pdf. Given 

the widespread use and high production volumes of DINP, these 

releases could pose risks for water quality.]

131-11-3 Dimethyl phthalate Natural Resources 

Defense Council

Phthalates are endocrine disruptors that have been found to cause 

developmental and reproductive abnormalities in animal studies. Furthermore, 

studies have found an association between phthalate metabolite 

concentrations and obesity, insulin resistance and thyroid hormone levels in 

humans. Stahlhut et al. (2007) analyzed urinary concentrations of seven 

phthalate metabolites in 1,443 adult men and found a statistically significant 

positive association between concentrations of the metabolites MBzP, 

MEHHP, MEOHP and MEP and abdominal obesity. Concentrations of MBP, 

MBzP and MEP were positively and significantly associated with insulin 

resistance. In a different study, baby boys exposed to the phthalates, DMP, 

DEP or BBP, in their mother’s breast milk were found to have hormonal 

disturbances at 3 months of age. Studies have found that di-isononyl phthalate 

(DiNP) is an anti-androgenic endocrine disruptor with developmental and 

reproductive toxicity. Exposures in pregnant rats have been shown to 

adversely affect development of the male reproductive tract. Adverse effects 

include a cluster of outcomes that has been called “phthalate e syndrome” and 

includes underdeveloped or absent reproductive organs, retained nipples, 

cryptorchidism, decreased anogenital distance (AGD), hypospadias, and 

decreased or abnormal sperm. DINP does not bind to the androgen receptor 

and these effects are likely mediated through interference with testosterone 

synthesis.

Phthalates are ubiquitous in the U.S. population. Although significant exposure 

can occur due to consumer products, the contribution of drinking water to 

overall exposure deserves to be examined. The NHANES measured the 

concentrations of 12 phthalate metabolites in the urine of over 2,500 children 

and adults. The highest average concentration was 163 ug/g creatinine for 

MEP, a metabolite of the plasticizer diethyl phthalate (see Table 3). [See the

CDC report cited below.] The Centers for Disease Control and Prevention 

(CDC) did not report what percentage of samples had detectable 

concentrations of each of the metabolites, but nine of the metabolites were 

found in the urine of at least half of the individuals. [See Table 3. CDC report 

of phthalate concentrations in urine; NHANES 1999 – 2000 and 2001 - 2002 

located on page 27 of the NRDC Nomination Letter and Table 4 Frequency of 

detection of phthalate metabolites in human urine samples, United States 

located on pages 28 and 29 of the NRDC Nomination Letter.]

Phthalates enter the environment as a result of releases from industrial 

facilities that manufacture or use these compounds, from waste 

disposal sites, through the use of phthalate-containing products by 

consumers and through discharge of municipal wastewaters 

containing phthalates. Phthalates have been found in numerous 

hazardous waste sites: diethyl phthalate (DEP) has been identified at 

348 sites, dibutyl phthalate (DBP) at 602 sites, dimethyl phthalate 

(DMP) at 167 sites, benzyl butyl phthalate (BzBP) at 413 sites, 

dicyclohexyl phthalate (DCHP) at one site, and di-n-octyl phthalate 

(DnOP) at 433 sites, among other phthalates.

Phthalates have been detected in environmental water samples across 

the United States, which raises concerns about drinking water as a 

route of exposure. The maximum concentrations found for some of 

these phthalates are particularly alarming. The following data were 

found in a search for stream water samples analyzed for phthalates in 

the EPA STORET database. Results are for the period January 2000 

through June 2012:

Dimethyl phthalate (DMP) was present in 587 (15.9%) of 3687 stream 

water samples, with a maximum of 2,500 ug/L.

None given

A1-13
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

117-84-0 Di-n-octyl phthalate Natural Resources 

Defense Council

Phthalates are endocrine disruptors that have been found to cause 

developmental and reproductive abnormalities in animal studies. Furthermore, 

studies have found an association between phthalate metabolite 

concentrations and obesity, insulin resistance and thyroid hormone levels in 

humans. Stahlhut et al. (2007) analyzed urinary concentrations of seven 

phthalate metabolites in 1,443 adult men and found a statistically significant 

positive association between concentrations of the metabolites MBzP, 

MEHHP, MEOHP and MEP and abdominal obesity. Concentrations of MBP, 

MBzP and MEP were positively and significantly associated with insulin 

resistance. In a different study, baby boys exposed to the phthalates, DMP, 

DEP or BBP, in their mother’s breast milk were found to have hormonal 

disturbances at 3 months of age. Studies have found that di-isononyl phthalate 

(DiNP) is an anti-androgenic endocrine disruptor with developmental and 

reproductive toxicity. Exposures in pregnant rats have been shown to 

adversely affect development of the male reproductive tract. Adverse effects 

include a cluster of outcomes that has been called “phthalate e syndrome” and 

includes underdeveloped or absent reproductive organs, retained nipples, 

cryptorchidism, decreased anogenital distance (AGD), hypospadias, and 

decreased or abnormal sperm. DINP does not bind to the androgen receptor 

and these effects are likely mediated through interference with testosterone 

synthesis. 

Phthalates are ubiquitous in the U.S. population. Although significant exposure 

can occur due to consumer products, the contribution of drinking water to 

overall exposure deserves to be examined. The NHANES measured the 

concentrations of 12 phthalate metabolites in the urine of over 2,500 children 

and adults. The highest average concentration was 163 ug/g creatinine for 

MEP, a metabolite of the plasticizer diethyl phthalate (see Table 3). [See the

CDC report cited below.] The Centers for Disease Control and Prevention 

(CDC) did not report what percentage of samples had detectable 

concentrations of each of the metabolites, but nine of the metabolites were 

found in the urine of at least half of the individuals. [See Table 3. CDC report 

of phthalate concentrations in urine; NHANES 1999 – 2000 and 2001 - 2002 

located on page 27 of the NRDC Nomination Letter and Table 4 Frequency of 

detection of phthalate metabolites in human urine samples, United States

located on pages 28 and 29 of the NRDC Nomination Letter.]

Phthalates enter the environment as a result of releases from 

industrial facilities that manufacture or use these compounds, from 

waste disposal sites, through the use of phthalate-containing products 

by consumers and through discharge of municipal wastewaters 

containing phthalates. Phthalates have been found in numerous 

hazardous waste sites: diethyl phthalate (DEP) has been identified at 

348 sites, dibutyl phthalate (DBP) at 602 sites, dimethyl phthalate 

(DMP) at 167 sites, benzyl butyl phthalate (BzBP) at 413 sites, 

dicyclohexyl phthalate (DCHP) at one site, and di-n-octyl phthalate 

(DnOP) at 433 sites, among other phthalates. 

Phthalates have been detected in environmental water samples across 

the United States, which raises concerns about drinking water as a 

route of exposure. The maximum concentrations found for some of 

these phthalates are particularly alarming. The following data were 

found in a search for stream water samples analyzed for phthalates in 

the EPA STORET database. Results are for the period January 2000 

through June 2012: 

Di-n-octyl phthalate (DnOP) was found in 129 out of 2469 stream 

water samples, with a maximum concentration of 20 ug/L.

None given

115-29-7 Endosulfan Natural Resources 

Defense Council

Endosulfan is an organochlorine insecticide and acaricide. Technical grade 

endosulfan is made of both alpha and beta stereoisomers whose toxicity is 

manifested through blockage of inhibitory GABA (gamma amino butyric acid) 

gated chloride channels, resulting in over-stimulation of the central nervous 

system. Endosulfan is a recognized neurotoxin and endocrine disruptor, 

making even extremely low-dose exposures of very great concern, especially 

to vulnerable populations such as children and fetuses.

Endosulfan is similar in its acute oral toxicity to the related insecticides aldrin 

and dieldrin, except that it is slightly more toxic than these substances in 

female laboratory animals. Inhalation of endosulfan dust by humans has been 

In 2010, EPA’s pesticide office announced that it was cancelling all 

uses of endosulfan in the U.S. However, because endosulfan is 

persistent, past uses of this pesticide continue to contaminate our 

water. According to the EFED risk assessment for the RED on 

endosulfan, monitoring data show widespread contamination of 

surface water. EPA modeled surface water contamination and 

calculated acute estimated environmental concentrations ranging from 

4.49 ppb to 23.86 ppb. Chronic EECs ranged from 0.53 ppb to 1.5 

ppb. The acute and chronic EEC for endosulfan in groundwater was 

0.012 ppb. EPA concluded in the RED that “residues of endosulfan in 

drinking water are of concern” for acute exposure for infants less than 

None given

A1-14
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank associated with slight nausea, confusion, excitement, flushing, and dry mouth. 

Nine employees who had been working with 50-percent water-wettable 

endosulfan powder for only a few days had convulsions. 

Endosulfan is a significant endocrine disruptor and reproductive toxicant. This 

pesticide increases the rate of testosterone breakdown and excretion. In 

immature rats, endosulfan causes significant dose-related decreases in sperm 

counts, and causes sperm deformities at low exposure levels. In fish, 

endosulfan elevates levels of thyroxine and suppresses levels of 

triiodothyronine, probably by inhibiting the conversion of thyroxine to T3. The 

developing brain is potentially most severely affected by this pesticide via 

altered levels of critical neurotransmitters such as dopamine, noradrenaline 

and serotonin; the altered neurotransmitter levels are associated with deficits 

in learning and memory.

one year old and for children 1-6 years old. EPA determined that 

exposure from food alone created risks of concern for children 1 to 6 

years old and set a DWLOC of zero ppb for this population.

blank

2164-17-2 Fluometuron AWWA None given None given None given

319-84-6 Hexachlorocyclohe

xane (alpha 

isomer)

AWWA None given None given None given

165800-03-3 Linezolid Natural Resources 

Defense Council

Widespread exposure to antibiotics is contributing to the growth of bacterial 

resistance, and this problem is of grave concern. In the past several decades 

almost every bacteria that can cause infections in humans has developed 

resistance to at least one antibiotic, and some are resistant to multiple 

antibiotics. The Centers for Disease Control and Prevention (CDC) have 

identified antibiotic resistance as one of the most pressing public health 

problems to face our nation. Infections caused by bacteria with resistance to at 

least one antibiotic have been estimated to kill over 60,000 hospitalized 

patients each year.

Antibiotic resistance is caused by a number of factors including repeated and 

improper use of antibiotics in both humans and animals. Scientists also agree 

that exposure to low levels of antibiotics actually promotes bacterial resistance 

by exerting selective pressure for genes that promote resistance.

Linezolid resistance in Staphylococcus aureus was reported in 2003. 

Community-acquired MRSA (CA-MRSA) has now emerged as an epidemic 

that is responsible for rapidly progressive, fatal diseases including necrotizing 

pneumonia, severe sepsis and necrotizing fasciitis. Outbreaks of CA-MRSA 

infections have been reported in correctional facilities, among athletic teams, 

among military recruits, in newborn nurseries, and among active homosexual 

men. Therefore, linezolid must be included on the CCL4.

Antibiotics are found in wastewater because the body does not 

completely metabolize all drugs, so both the metabolized and 

unmetabolized drug are excreted by humans into wastewater. For 

example, when amoxicillin is ingested, 60-75% of the antibiotic is 

excreted unchanged into the urine. This antibiotic, now in the 

environment, may encounter other bacteria and promote resistance. It 

is unknown how much of an impact current low levels of antibiotics in 

drinking water are having on the problem of bacterial resistance. 

However, the potential has been recognized for many years.

None given

330-55-2 Linuron Natural Resources 

Defense Council

Linuron (CAS # 330-55-2) is an urea-based herbicide used primarily on 

soybeans (79 percent of usage). It has been shown to cause non-malignant 

testicular and liver tumors in animals. Investigation of the testicular tumors 

revealed that this herbicide acts by blocking the function of male androgens. In 

animals, at relatively low doses, linuron is a recognized anti-androgen. This 

chemical has been shown in laboratory studies to decrease male sex organ 

weights, cause testicular atrophy, delay puberty, and increase estrogen levels 

About 400,000 pounds of linuron are used in U.S. agriculture each 

year. This herbicide persists for 1-5 months in soil, and has been 

shown to run off of fields into surface and groundwater supplies. EPA 

concluded in its Reregistration Eligibility Decision (RED) that linuron 

exceeded the Levels of Concern (LOC) for groundwater quality. EPA 

also expressed “moderate concerns” for drinking water supply systems 

relying on surface water sources.

Since linuron is not regulated 

under the Safe Drinking Water 

Act (SDWA), water supply 

systems are not required to 

sample or analyze for it. This is a 

particular problem because EPA 

admits that drinking water 

A1-15
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank in males.

Casting further doubt on EPA’s estimates of the risks of linuron in drinking 

water sources is the fact that the model used for surface water assessment 

was not tested against any data whatsoever. The exposure estimates (18 ppb) 

for infants and children exceed EPA’s chronic DWLOC (6 ppb) by three-fold. 

This result is of particular concern in light of the serious flaws in the drinking 

water risk assessment that conspire to underestimate the actual risk. EPA 

admits that “residues of linuron and its metabolites in drinking water may 

represent a chronic human health risk...”

Several factors in EPA’s drinking water exposure assessment raise 

concerns about groundwater contamination. In the groundwater 

portion of the assessment, data were present for only four states: 

Georgia, Missouri, Virginia, and Wisconsin. In Georgia linuron was 

found in groundwater in concentrations up to 5 ppb. EPA later cast 

doubt on the reliability of the data and removed it from consideration in 

the final RED, basing its decision on new information received from the 

State of Georgia.

Valid groundwater detections in Missouri (up to 1.9 ppb), Virginia (up 

to 1.31 ppb in 4 of 8 wells) and Wisconsin (up to 2.7 ppb) may 

seriously underestimate linuron levels throughout the country because 

these three states are not among the 16-20 states where linuron is 

most heavily used. The sixteen states listed on page 3 of EPA’s 

Overview of Linuron Risk Assessment appear to account for well over 

80% of linuron use in the United States, so the complete absence of 

any data on groundwater in any of these states is a critical data gap. 

The USGS has also reported on areas where linuron is most heavily 

used on a per-acre basis. The USGS maps indicate that Indiana, Ohio, 

Michigan, Delaware, and Maryland are heavy use states. These states 

are not among the ones from which groundwater data are available. 

Strangely, only one of these (Michigan) is listed by EPA as among 

heavy use states.

treatment is unlikely to remove 

linuron and its degradates. The 

Agency must move rapidly to 

collect more data on linuron in 

water and must make a high 

priority of regulating linuron 

under the SDWA. 

121-75-5 Malathion AWWA None given None given None given

7439-96-5 Manganese Massachusetts 

Department of 

Environmental 

Protection

There has been an accumulating body of work since US EPA's last review of 

manganese suggesting an association between drinking water exposures in 

school age children and a variety of subtle neurological effects (see selected 

references in Appendix B).

Effects in one of the more recent studies have been seen at manganese water 

concentrations below the current US EPA lifetime Health Advisory (HA) value, 

suggesting that the validity of that research finding be critically examined and 

that possibly the basis for the current HA be revisited.

The effect — exposure duration relationship deserves attention in view of the 

fact that some children may have altered neurological function after exposures 

to manganese in water at concentrations greater than the lifetime HA level but 

after less than lifetime durations of exposure. New federal guidance could 

contribute towards providing protective guidance for sensitive subgroups for 

less than lifetime exposures.

Identifying protective toxicity values for ingestion of manganese is particularly 

challenging because it is an essential element and there appears to be 

differential bioavailability of manganese between water and food stuffs.

Present drinking water guidance (applicable to the entire population except for 

infants) is based upon a safe, no effect level of manganese derived from adult 

dietary intake studies. The recent studies with children suggest that they 

Occurrence: From sampling across Massachusetts, we have 

manganese in groundwaters serving as sources of drinking water for 

public and private water supplies at concentrations above current 

health-based guidance concentrations (see Appendix A for examples);

We see a clear need for national 

level drinking water guidance for 

manganese which reflects 

emerging science. There is 

currently no clear, up-to-date, 

national uniform message about 

the health risks from ingestion of 

manganese in drinking water, 

resulting in states having to 

handle manganese issues 

individually. Our experience has 

been that manganese in drinking 

water is not perceived as a 

potential health issue, but rather 

purely an aesthetic one. We 

believe this to not be the case 

and strongly support the 

inclusion of manganese on the 

CCL4 list. Doing so would raise 

the prominence of this issue. 

Given the complexity of 

manganese's toxicity (exposure 

route and chemical form specific, 

essentiality versus toxicity, 

A1-16
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank should be evaluated as a susceptible subgroup of the population and that 

toxicity should be factored into setting manganese drinking water exposure 

limits, possibly along with considerations of essentiality.

While infants have been singled out as of special concern by US EPA in its 

existing HA, we are especially concerned about bottle-fed infants due to their 

apparently low nutritional requirement for Mn in early life, their immature 

homeostatic mechanism for controlling Mn absorption and excretion, and 

potentially high levels of Mn in infant formulas.

blank differential life stage, 

susceptibility, emerging science 

not currently reflected in US EPA 

guidance), we believe that an 

examination of manganese 

toxicity for drinking water is in 

order. 

The current US EPA HA gives no 

guidance to the states in terms of 

what advice they should offer to 

regulated entities or private well 

owners, or what regulatory 

stance they should take with 

exceedances of HA levels, 

leaving states to craft their own 

positions on this issue. National 

leadership with a national 

primary drinking water standard 

would provide some uniformity in 

how manganese health risks are 

communicated and dealt with.

7439-96-5 Manganese Minnesota 

Department of 

Health

Since US EPA’s last review of manganese, a body of research has 

accumulated suggesting an association between drinking water exposures in 

school age children and a variety of subtle neurological effects (see 

manganese references in Appendix B).

In two recent epidemiology studies, effects have been seen at manganese 

water concentrations below the current US EPA lifetime HA value, suggesting 

that the basis for the current HA should be revisited (Bouchard et al., 2011, 

Khan et al., 2011).

The relationship between exposure duration and health effects deserves 

attention in light of the fact that some children have exhibited altered 

neurological function after exposures to manganese in water at concentrations 

greater than the lifetime HA level but after less than lifetime durations. New 

federal guidance could contribute towards providing protective guidance for 

sensitive subgroups for less than lifetime exposures.

Identifying protective toxicity values for ingestion of manganese is particularly 

challenging because it is an essential element and there appears to be 

differential bioavailability of manganese between water and foodstuffs. 

Present drinking water guidance (applicable to the entire population except for 

infants) is based upon a safe, no effect level of manganese derived from adult 

dietary intake studies. The recent studies with children suggest that they 

should be evaluated as a susceptible subgroup of the population. 

Manganese is commonly detected in groundwater in the United States 

at concentrations greater than the lifetime Health Advisory (HA) value 

of 300 ug/L. Twelve percent of 4,976 groundwater samples taken 

throughout the United States by the US Geological Survey from 1992 

– 2003 exceeded the HA for manganese (Ayotte, Gronberg, &

Apodaca, 2011). 

Manganese is found in groundwater throughout Minnesota, including 

groundwater that serves as source of drinking water for public and 

private water supplies, at concentrations above current health-based 

guidance concentrations (See Appendix A - Minnesota Department of 

Health nomination letter).

Appendix A. Occurrence Information for Manganese in Groundwater in 

Minnesota

Over 4000 groundwater well samples were collected from throughout 

Minnesota and analyzed for manganese. Almost two-thirds (61%) of 

wells which might serve as water sources for public supplies or private 

residences had manganese concentrations greater than the 

Secondary Maximum Contaminant Level of 0.050 mg/L. Twenty-one 

percent had concentrations greater than the lifetime health advisory 

value (See Table 1- Minnesota Department of Health nomination 

letter).

We are nominating manganese 

for CCL4 because it is frequently 

detected in public and private 

wells, and there is some recent 

evidence of health effects at 

concentrations below the current 

EPA health advisory value. Also, 

we have concerns about 

manganese exposures among 

sensitive populations such as 

infants and children, and for less 

than lifetime exposure durations.

The current US EPA HA gives no 

guidance to the states in terms of 

what advice they should offer to 

regulated entities or private well 

owners, or what regulatory 

stance they should take when of 

HA levels are exceeded, leaving 

states to craft their own positions 

on this issue. National leadership 

with a national primary drinking 

water standard would provide 

some uniformity in how 

A1-17
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank While infants have been singled out as a special concern by US EPA in its 

existing HA, we are especially concerned about bottle-fed infants due to their 

apparently low nutritional requirement for Mn in early life, their naturally high 

blood Mn concentrations at birth, their immature homeostatic mechanism for 

controlling Mn absorption and excretion, and potentially high levels of Mn in 

infant formulas.

manganese health risks are 

communicated and dealt with.

7439-96-5 Manganese NJ Department of 

Environmental 

Protection

Manganese in drinking water is of current interest to a number of states. State 

and EPA FSTRAC members have formed a partner group to evaluate recent 

health effects information relevant to drinking water exposure to manganese. 

The current EPA Health Advisory for manganese is based on the assumption 

that manganese exposure from drinking water is much lower than from the 

diet, and is not based on health effects. This manganese Health Advisory is 

several-fold higher than the secondary standard for manganese that is based 

on aesthetic effects. However, manganese occurs in NJ and other states in 

both public water supplies and private wells at levels which result in much 

higher exposures than those assumed by EPA in their comparison to dietary 

exposures. Also, several recent studies suggest that manganese by the oral 

route may cause neurodevelopmental effects. There is a need for an updated 

health assessment for manganese in drinking water based on current health 

effects data. This health assessment could be used for an updated Health 

Advisory or as the basis for a proposed MCLG. 

None given None given

61-32-5 Methicillin Natural Resources 

Defense Council

Widespread exposure to antibiotics is contributing to the growth of bacterial 

resistance, and this problem is of grave concern. In the past several decades 

almost every bacteria that can cause infections in humans has developed 

resistance to at least one antibiotic, and some are resistant to multiple 

antibiotics. The Centers for Disease Control and Prevention (CDC) have 

identified antibiotic resistance as one of the most pressing public health 

problems to face our nation. Infections caused by bacteria with resistance to at 

least one antibiotic have been estimated to kill over 60,000 hospitalized 

patients each year.

Antibiotic resistance is caused by a number of factors including repeated and 

improper use of antibiotics in both humans and animals. Scientists also agree 

that exposure to low levels of antibiotics actually promotes bacterial resistance 

by exerting selective pressure for genes that promote resistance.

Beta-lactam antibiotics are a broad class of antibiotics which include penicillin 

derivatives, cephalosporins, monobactams, carbapenems and Beta-lactamase 

inhibitors. Methicillin, a form of penicillin, had been relied upon as an common 

effective treatment for Staphylococcus aureus infections but now many strains 

of S. aureus bacteria are resistant to methicillin (MRSA or methicillin-resistant 

Staphylococcus aureus.) Unfortunately, MRSA is resistant to much of the 

entire class of penicillin-like antibiotics called beta-lactams. Therefore, EPA 

must include penicillin, amoxicillin, oxacillin and methicillin on the CCL4.

Antibiotics are found in wastewater because the body does not 

completely metabolize all drugs, so both the metabolized and 

unmetabolized drug are excreted by humans into wastewater. For 

example, when amoxicillin is ingested, 60-75% of the antibiotic is 

excreted unchanged into the urine. This antibiotic, now in the 

environment, may encounter other bacteria and promote resistance. It 

is unknown how much of an impact current low levels of antibiotics in 

drinking water are having on the problem of bacterial resistance. 

However, the potential has been recognized for many years. 

None given

298-00-0 Methyl parathion AWWA None given None given None given

A1-18
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

1634-04-4 Methyl tertiary butyl 

ether

NJ Department of 

Environmental 

Protection

A recent chronic cancer bioassay of MTBE by the drinking water exposure 

route in rats (Dodd et al., 2011) should be considered by USEPA. Previously, 

a chronic inhalation study in mice and rats (an exposure route that is not as 

relevant to drinking water exposure, Bird et al., 1997) and an oral gavage 

study in rats from the Ramazzini Institute in Italy, which USEPA has decided 

not to consider this study because of issues related to the pathology 

evaluations (http://www.epa.gov/iris/ramazzini.htm) were the only studies 

available as the basis for the assessment of the carcinogenic potential of 

MTBE in drinking water. The recent Dodd et al. (2011) study suggests that 

MTBE in drinking water may cause brain tumors in rats and should be 

considered by EPA. 

None given None given

101043-37-2 Microcystin-LR Minnesota 

Department of 

Health

Liver toxicity has long been identified as the most sensitive toxicological 

endpoint for microcystin-LR. As part of the CCL3 process, EPA derived a draft 

RfD of 0.000003 mg/kg-d based on hepatotoxicity, using an estimated NOAEL 

of 3 ug/kg-d in mice from ingestion of water containing 20 ug/L microcystin-LR 

(Ueno et al., 1999). However, a more recent study reports male reproductive 

effects in mice exposed to lower doses of microcystin-LR in drinking water. 

(Chen et al., 2011). Significant decreases in testosterone and sperm motility 

and count were observed at doses as low as approximately 0.64 ug/kg-d. 

(This dose is estimated based on ingestion of water containing 3 ug/L 

microcystin-LR.) In addition to the Chen et al. study, there are a limited 

number of intraperitoneal injection studies in mice, rats and rabbits and in vitro 

studies in Sertoli cells which reported male reproductive effects on sperm, 

testes and Sertoli cells (Li, Y., J. Sheng, et al., 2008; Liu, Y., P. Xie, et al., 

2010; Wang, X., F. Ying, et al.,2012). A recent oral study reported altered 

reproductive function and disruption in spermatogenesis in medaka fish 

(Trinchet, I., C. Djediat, et al., 2011) Because the Chen et al. study identifies a 

new toxicological endpoint at a dose level nearly five-fold lower than that used 

in EPA’s draft RfD, and some supporting data also indicate potential 

reproductive toxicity, we believe microcystin-LR is worthy of consideration for 

updated guidance at the federal level.Because of the episodic nature of 

microcystin "outbreaks" in surface water (see Occurrence section), we believe 

that short-term exposures and effects should be given special consideration 

for this chemical.

Microcystin –LR is largely a surface water contaminant, and is 

commonly detected in lakes in temperate climates (Ohio 

Environmental Protection Agency, 2012; Boyer et al., 2005; Graham et 

al., 2004). Surface water is used as a drinking water source in many 

locations in the United States. Contamination of a surface water body 

with microcystin-LR is likely to be episodic in nature, exhibiting both 

seasonal variation (Billam et al., 2006) and aquatic concentrations that 

are highly sensitive to total phosphorus, total nitrogen, and other 

chemical parameters (Graham et al., 2004). Therefore, we believe that 

short-term exposures and effects should be given special 

consideration for this chemical. The use of “recycled” wastewater for 

drinking water is increasingly being viewed as a water supply 

management option in some areas of the United States (City of San 

Diego, 2012; Barringer, 2012). Wastewater, including treated 

wastewater, provides nutrients that can promote the growth of 

cyanobacteria in surface water (Ho et al., 2010). This indicates a 

potential future route of microcystin exposure via drinking water.

None given

101043-37-2 Microcystin-LR Minnesota 

Department of 

Health

Liver toxicity has long been identified as the most sensitive toxicological 

endpoint for microcystin-LR. As part of the CCL3 process, EPA derived a draft 

RfD of 0.000003 mg/kg-d based on hepatotoxicity, using an estimated NOAEL 

of 3 ug/kg-d in mice from ingestion of water containing 20 ug/L microcystin-LR 

(Ueno et al., 1999).

However, a more recent study reports male reproductive effects in mice 

exposed to lower doses of microcystin-LR in drinking water. (Chen et al., 

2011). Significant decreases in testosterone and sperm motility and count 

were observed at doses as low as approximately 0.64 ug/kg-d. (This dose is 

estimated based on ingestion of water containing 3 ug/L microcystin-LR.)

In addition to the Chen et al. study, there are a limited number of 

intraperitoneal injection studies in mice, rats and rabbits and in vitro studies in 

Microcystin –LR is largely a surface water contaminant, and is 

commonly detected in lakes in temperate climates (Ohio 

Environmental Protection Agency, 2012; Boyer et al., 2005; Graham et 

al., 2004). Surface water is used as a drinking water source in many 

locations in the United States.

Contamination of a surface water body with microcystin-LR is likely to 

be episodic in nature, exhibiting both seasonal variation (Billam et al., 

2006) and aquatic concentrations that are highly sensitive to total 

phosphorus, total nitrogen, and other chemical parameters (Graham et 

al., 2004). Therefore, we believe that short-term exposures and effects 

should be given special consideration for this chemical.

The use of “recycled” wastewater for drinking water is increasingly 

We are nominating microcystinLR for CCL4 because its oral 

RfD, while already low, may need 

to be revised downward in light of 

new toxicological data. Also, 

there is some concern that the 

human exposure to microcystinLR in drinking water may 

increase due to more favorable 

conditions for algal growth in 

lakes and reservoirs (i.e., 

nutrients, temperature, 

wastewater releases), and new 

A1-19
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank Sertoli cells which reported male reproductive effects on sperm, testes and 

Sertoli cells (Li, Y., J. Sheng, et al., 2008; Liu, Y., P. Xie, et al., 2010; Wang, 

X., F. Ying, et al.,2012). A recent oral study reported altered reproductive 

function and disruption in spermatogenesis in medaka fish (Trinchet, I., C. 

Djediat, et al., 2011)

Because the Chen et al. study identifies a new toxicological endpoint at a dose 

level nearly five-fold lower than that used in EPA’s draft RfD, and some 

supporting data also indicate potential reproductive toxicity, we believe 

microcystin-LR is worthy of consideration for updated guidance at the federal 

level.

being viewed as a water supply management option in some areas of 

the United States (City of San Diego, 2012; Barringer, 2012). 

Wastewater, including treated wastewater, provides nutrients that can 

promote the growth of cyanobacteria in surface water (Ho et al., 2010). 

This indicates a potential future route of microcystin exposure via 

drinking water.

efforts to recycle wastewater into 

drinking water. 

25154-52-3 Nonylphenol Natural Resources 

Defense Council

Alkylphenols were first reported to be estrogenic in the 1930s. In 1991, 

publication of the effects of nonylphenol on cultured human breast cancer cells 

led to health concerns. Estrogenic effects have also been shown in the 

mouse. Estrogenic effects are present at tissue concentrations of 0.1 μM for 

octylphenol and 1 μM for nonylphenol. A recombinant yeast screen using the 

human estrogen receptor has shown similar results.

An estimated 450,000,000 pounds of alkylphenol polyethoxylates 

(APEs) are produced annually in the United States, and about half that 

amount is estimated to be released to wastewater. 

Alkylphenol polyethoxylates do not break down effectively in sewage 

treatment plants or in the environment. Instead they degrade to 

alkylphenols and alkylphenol ethoxylates, which persist for longer. 

Nonylphenol and its ethoxylates, and other alkylphenols, have been 

detected in wastewater and in waterways.

None given

9016-45-9 Nonylphenol 

ethoxylate 

Natural Resources 

Defense Council

Alkylphenols were first reported to be estrogenic in the 1930s. In 1991, 

publication of the effects of nonylphenol on cultured human breast cancer cells 

led to health concerns. Estrogenic effects have also been shown in the 

mouse. Estrogenic effects are present at tissue concentrations of 0.1 μM for 

octylphenol and 1 μM for nonylphenol. A recombinant yeast screen using the 

human estrogen receptor has shown similar results. 

An estimated 450,000,000 pounds of alkylphenol polyethoxylates 

(APEs) are produced annually in the United States, and about half that 

amount is estimated to be released to wastewater. 

Alkylphenol polyethoxylates do not break down effectively in sewage 

treatment plants or in the environment. Instead they degrade to 

alkylphenols and alkylphenol ethoxylates, which persist for longer. 

Nonylphenol and its ethoxylates, and other alkylphenols, have been 

detected in wastewater and in waterways.

None given

27193-28-8 Octylphenol Natural Resources 

Defense Council

Alkylphenols were first reported to be estrogenic in the 1930s. In 1991, 

publication of the effects of nonylphenol on cultured human breast cancer cells 

led to health concerns. Estrogenic effects have also been shown in the 

mouse. Estrogenic effects are present at tissue concentrations of 0.1 μM for 

octylphenol and 1 μM for nonylphenol. A recombinant yeast screen using the 

human estrogen receptor has shown similar results.

An estimated 450,000,000 pounds of alkylphenol polyethoxylates 

(APEs) are produced annually in the United States, and about half that 

amount is estimated to be released to wastewater. 

Alkylphenol polyethoxylates do not break down effectively in sewage 

treatment plants or in the environment. Instead they degrade to 

alkylphenols and alkylphenol ethoxylates, which persist for longer. 

Nonylphenol and its ethoxylates, and other alkylphenols, have been 

detected in wastewater and in waterways.

None given

9036-19-5 Octylphenol 

ethoxylate 

Natural Resources 

Defense Council

Alkylphenols were first reported to be estrogenic in the 1930s. In 1991, 

publication of the effects of nonylphenol on cultured human breast cancer cells 

led to health concerns. Estrogenic effects have also been shown in the 

mouse. Estrogenic effects are present at tissue concentrations of 0.1 μM for 

octylphenol and 1 μM for nonylphenol. A recombinant yeast screen using the 

human estrogen receptor has shown similar results.

An estimated 450,000,000 pounds of alkylphenol polyethoxylates 

(APEs) are produced annually in the United States, and about half that 

amount is estimated to be released to wastewater. 

Alkylphenol polyethoxylates do not break down effectively in sewage 

treatment plants or in the environment. Instead they degrade to 

alkylphenols and alkylphenol ethoxylates, which persist for longer. 

Nonylphenol and its ethoxylates, and other alkylphenols, have been 

detected in wastewater and in waterways.

None given

A1-20
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

66-79-5 Oxacillin Natural Resources 

Defense Council

Widespread exposure to antibiotics is contributing to the growth of bacterial

resistance, and this problem is of grave concern. In the past several decades 

almost every bacteria that can cause infections in humans has developed 

resistance to at least one antibiotic, and some are resistant to multiple 

antibiotics. The Centers for Disease Control and Prevention (CDC) have 

identified antibiotic resistance as one of the most pressing public health 

problems to face our nation. Infections caused by bacteria with resistance to at 

least one antibiotic have been estimated to kill over 60,000 hospitalized 

patients each year. 

Antibiotic resistance is caused by a number of factors including repeated and 

improper use of antibiotics in both humans and animals. Scientists also agree 

that exposure to low levels of antibiotics actually promotes bacterial resistance 

by exerting selective pressure for genes that promote resistance.

Beta-lactam antibiotics are a broad class of antibiotics which include penicillin 

derivatives, cephalosporins, monobactams, carbapenems and Beta-lactamase 

inhibitors. Methicillin, a form of penicillin, had been relied upon as an common 

effective treatment for Staphylococcus aureus infections but now many strains 

of S. aureus bacteria are resistant to methicillin (MRSA or methicillin-resistant 

Staphylococcus aureus.) Unfortunately, MRSA is resistant to much of the 

entire class of penicillin-like antibiotics called beta-lactams. Therefore, EPA 

must include penicillin, amoxicillin, oxacillin and methicillin on the CCL4.

Antibiotics are found in wastewater because the body does not 

completely metabolize all drugs, so both the metabolized and 

unmetabolized drug are excreted by humans into wastewater. For 

example, when amoxicillin is ingested, 60-75% of the antibiotic is 

excreted unchanged into the urine. This antibiotic, now in the

environment, may encounter other bacteria and promote resistance. It 

is unknown how much of an impact current low levels of antibiotics in 

drinking water are having on the problem of bacterial resistance. 

However, the potential has been recognized for many years.

None given

multiple CAS 

#s

Penicillin Natural Resources 

Defense Council

Widespread exposure to antibiotics is contributing to the growth of bacterial 

resistance, and this problem is of grave concern. In the past several decades 

almost every bacteria that can cause infections in humans has developed 

resistance to at least one antibiotic, and some are resistant to multiple 

antibiotics. The Centers for Disease Control and Prevention (CDC) have 

identified antibiotic resistance as one of the most pressing public health 

problems to face our nation. Infections caused by bacteria with resistance to at 

least one antibiotic have been estimated to kill over 60,000 hospitalized 

patients each year.

Antibiotic resistance is caused by a number of factors including repeated and 

improper use of antibiotics in both humans and animals. Scientists also agree 

that exposure to low levels of antibiotics actually promotes bacterial resistance 

by exerting selective pressure for genes that promote resistance.

Beta-lactam antibiotics are a broad class of antibiotics which include penicillin 

derivatives, cephalosporins, monobactams, carbapenems and Beta-lactamase 

inhibitors. Methicillin, a form of penicillin, had been relied upon as an common 

effective treatment for Staphylococcus aureus infections but now many strains 

of S. aureus bacteria are resistant to methicillin (MRSA or methicillin-resistant 

Staphylococcus aureus.) Unfortunately, MRSA is resistant to much of the 

entire class of penicillin-like antibiotics called beta-lactams. Therefore, EPA 

must include penicillin, amoxicillin, oxacillin and methicillin on the CCL4.

Antibiotics are found in wastewater because the body does not 

completely metabolize all drugs, so both the metabolized and 

unmetabolized drug are excreted by humans into wastewater. For 

example, when amoxicillin is ingested, 60-75% of the antibiotic is 

excreted unchanged into the urine. This antibiotic, now in the 

environment, may encounter other bacteria and promote resistance. It 

is unknown how much of an impact current low levels of antibiotics in 

drinking water are having on the problem of bacterial resistance. 

However, the potential has been recognized for many years.

None given

A1-21
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

335-67-1 Perfluorooctanoic 

acid

Eileen Murphy http://www.c8sciencepanel.org/publications.html 

The C8 Panel has been reporting detrimental effects at relatively low exposure 

levels, particularly in children.

In areas where monitoring for PFOA (and other perfluorinated 

chemicals) occurs, it is detected at some level. Where there are known 

sources, levels are higher. However, PFOA is often detected in areas 

with no obvious source. 

None given

335-67-1 Perfluorooctanoic 

Acid

Natural Resources 

Defense Council

None given None given None given

335671 Perfluorooctanoic 

Acid

NJ Department of 

Environmental 

Protection

Post et al. (2012) summarizes many recent toxicology and epidemiology 

studies relevant to the assessment of potential health effects of PFOA in 

drinking water. The studies cited in Post et al. (2012) should be considered by 

USEPA. Two additional very recent publications showing associations of 

PFOA exposure and kidney and testicular cancer in communities with drinking 

water exposure (C8 Science Panel, 2012), and with hypertension and 

elevated homocysteine (a marker for risk of heart disease; Min et al., 2012) in 

the general population should also be considered by USEPA. While the C8 

Science Panel (2012) report is not a peer-reviewed publication, several 

publications on the cancer incidence study are cited as “in press” in the report; 

these publications are expected to be available in the near future and should 

be considered by USEPA.

The following information is a summary of information discussed in 

Post et al. (2012, citation below): Unlike most other commonly 

detected organic drinking water contaminants, PFOA and other 

perfluorinated chemicals do not degrade in the environment and 

persist indefinitely. PFOA and other perfluorinated compounds are 

highly water soluble, unlike most other persistent organic pollutants 

(e.g. PCBs, dioxins, chlordane) which bind preferentially to soil and 

sediments and are not highly water soluble. For this reason, drinking 

water is a major exposure route, while drinking water is not a major 

exposure route for these other persistent organic pollutants (e.g. 

PCBs, dioxins, chlordane). PFOA bioaccumulates from drinking water 

to serum with a serum:drinking water ratio of about 100:1 after ongoing 

exposure, and exposure to even relatively low drinking water 

concentrations substantially increases total exposure in humans. 

PFOA persists in humans with a serum half-life of several years. 

Exposure to PFOA in drinking water by breast-fed and formula-fed 

infants, a potentially susceptible subpopulation for PFOA's 

developmental effects, is higher than in adults using the same drinking 

water source.

The review by Post et al. (2012) summarizes many recent studies of 

the environmental fate and transport, sources, and occurrence of 

PFOA in source waters (groundwater and surface water) and drinking 

water. These studies should be considered by USEPA.

None given

52645-53-1 Permethrin AWWA None given None given None given

732-11-6 Phosmet Natural Resources 

Defense Council

Phosmet is a neurotoxicant that causes red blood cell, plasma, serum and 

brain cholinesterase inhibition. It also shows mutagenic activity. Phosmet 

interferes with human placental enzymatic activity, which may affect fetal 

development. EPA has stated in its Interim Reregistration Eligibility Decision 

(IRED) for phosmet that there is “suggestive evidence of carcinogenicity” 

based on increased incidence of liver adenomas and carcinomas in male 

mice, and of mammary gland tumors in females. 

The EPA IRED used modeling estimates to assess phosmet exposure through 

drinking water due to the limited amount of monitoring data available. 

Estimated environmental concentrations ranged from 0.4 to 140 ppb. While 

EPA concluded that drinking water exposure through surface and groundwater 

was not of concern, there are several flaws in the EPA analysis that 

undermine that conclusion, as explained below. The IRED drinking water 

assessment should not be relied upon to decide whether to regulate phosmet 

under the SDWA.

Phosmet is an organophosphate pesticide used primarily on apples, 

peaches, walnuts, almonds and pears. Approximately 1.25 million 

pounds of active ingredient are applied every year.Phosmet is mobile 

in runoff and has the potential to contaminate drinking water sources. 

EPA has done a drinking water risk assessment for phosmet as part of 

the pesticide reregistration process. 

None given

A1-22
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank EPA determines whether the drinking water risks of a pesticide are of concern 

as part of its dietary risk assessment for that chemical. For drinking water risk 

to remain below the Agency’s level of concern, the sum of food and drinking 

water exposures must be less than the Population Adjusted Dose (PAD). [The 

PAD is a term that expresses the dietary risk of a chemical, and reflects the 

Reference Dose, either acute or chronic, that has been adjusted to account for 

the FQPA safety factor (i.e., RfD/FQPA safety factor)]. A risk estimate that is 

less than 100% of the acute or chronic PAD does not exceed the Agency’s 

risk concern.)The IRED risk summary for phosmet indicates that dietary risk, 

acute and chronic, is below the Agency’s level of concern. However, the 

Agency had initially determined that acute dietary exposures were of great 

concern for infants and children, with up to 2000% of the acute Reference 

Dose (aRfD) consumed.. Such an exceedance in exposure from food alone 

means that any additional exposure from drinking water would create 

additional unacceptable risks.

The assessment of food exposure was subsequently revised using a newly 

submitted acute neurotoxicity study by the registrant, reviewed by the Agency 

in February 1999, and by the hazard identification assessment review 

committee (HIARC) in July, 1999. This new acute neurotoxicity study in rats 

was used to raise the No Observable Adverse Effects Level (NOAEL) to 4.5 

mg/kg/day, from the 1.1 value that had been used, based on a chronic toxicity 

study in rats. The result was a four-fold change, which also resulted in an 

increase in the PAD. The HIARC executive summary of the study states that 

“no effects of treatment were seen in the 3.0 or 4.5 mg/kg group”, which is in 

agreement with the registrants conclusions. However, the study DER finds 

some critical problems with this study:

-“Extremely high variability was noted in the data from the motor activity 

testing, raising questions about the sensitivity of the procedures used in this 

study. For example, an increase in subsession activity approaching 300% 

above control levels was not found to be statistically significantly different from 

controls.”

 -“There was also some large variability in some of the blood cholinesterase 

measurements (especially for the red blood cells), such that decreases of 25% 

were not statistically significant. Again, it is possible that true differences 

caused by exposure to phosmet might be obscured by the high variability of 

the measure.” In fact, the DER states that “the smallest statistically significant 

change detected in blood measures was 40% (DER p. 10)

-“no information is available regarding the dose response curves for 

cholinesterase inhibition or behavioral effects. This is especially relevant since 

similar levels of inhibition (60-75%) were seen in brain and red blood cell 

cholinesterase at the high dose, with brain inhibition persisting throughout the 

study.”

NRDC suggests that this study is not sufficient to establish a NOAEL, since 

the variability in cholinesterase inhibition was so great that the study design 

did not provide any statistical power to detect treatment effects. Therefore, the 

increase in the PAD that made it possible for food and drinking water

blank blank

A1-23
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank exposures to remain below the level of concern was not scientifically 

supported.Notwithstanding EPA’s previous determination that phosmet in 

drinking water does not pose risks of concern (which, as noted above, was 

based on a flawed study), phosmet should be regulated as a water 

contaminant under the SDWA and an MCL should be established.

blank blank

57-83-0 Progesterone Natural Resources 

Defense Council

While each of these compounds [See Table 5 Concentrations of reproductive 

hormones in U.S. streams (USGS, 2002) located on page 29 of the NRDC 

letter] is generally found at low concentrations, the potential effects on human 

health of mixtures of these compounds are unknown. Based on the individual 

effects of these chemicals, possible risks include defects of the reproductive 

system in individuals exposed during critical stages of development (e.g. 

testosterone). 

The U.S. Geological Survey (USGS) conducted a study of 139 

streams in 30 states that found widespread presence of estrogenic 

compounds, ovulation inhibitors and other reproductive hormones in 

surface water near urbanized and agricultural areas (see Table 5).

[See Table 5 Concentrations of reproductive hormones in U.S. 

streams (USGS, 2002) located on page 29 of the NRDC letter]

Wastewater treatment plants, the likely sources of most of these 

chemicals, do not treat sewage for these pollutants. Furthermore, 

drinking water treatment plants do not generally test or treat water for 

these contaminants, so the frequency of occurrence of these 

chemicals in treated drinking water and the degree of human exposure 

are not known. Additional monitoring of water sources and drinking 

water are necessary to determine the full extent of the contamination, 

to assess risks to human health, and to determine acceptable levels of 

exposure and appropriate regulatory action.

EPA properly included many of these reproductive hormones on 

CCL3, although it has not made a final regulatory determination on any 

of them. However, considering that progesterone and testosterone 

also occur at similar concentrations and similar frequency as some of 

the hormones that were include, they should also be added to the 

CCL4.

None given

10043-92-2 Radon NJ Department of 

Environmental 

Protection

Radon is a known human carcinogen. In New Jersey and other states where 

radon is prevalent in groundwater, the cancer risk from radon in drinking water 

is higher than for most other drinking water contaminants that are regulated 

based on their carcinogenicity. For example, the average level in NJ public 

water supplies is 921 pCi/L, and the lifetime cancer risk at this level (from 

inhalation plus ingestion) is 7 x 10-4. 

Radon occurs widely in drinking water using groundwater sources in 

New Jersey and some other states. In New Jersey, the concentration 

of radon ranged from nondetectable levels to 41,000 pCi/L with an 

average concentration of 921 pCi/L in public water supplies, and from 

50 pCi/L to 170,000 pCi/L with an average concentration of 5,040 

pCi/L in private wells.

None given

8025-81-8 Spiramycin Natural Resources 

Defense Council

Widespread exposure to antibiotics is contributing to the growth of bacterial 

resistance, and this problem is of grave concern. In the past several decades 

almost every bacteria that can cause infections in humans has developed 

resistance to at least one antibiotic, and some are resistant to multiple 

antibiotics. The Centers for Disease Control and Prevention (CDC) have 

identified antibiotic resistance as one of the most pressing public health 

problems to face our nation. Infections caused by bacteria with resistance to at 

least one antibiotic have been estimated to kill over 60,000 hospitalized 

patients each year. 

Antibiotic resistance is caused by a number of factors including repeated and 

improper use of antibiotics in both humans and animals. Scientists also agree 

that exposure to low levels of antibiotics actually promotes bacterial resistance 

by exerting selective pressure for genes that promote resistance.

Antibiotics are found in wastewater because the body does not 

completely metabolize all drugs, so both the metabolized and 

unmetabolized drug are excreted by humans into wastewater. For 

example, when amoxicillin is ingested, 60-75% of the antibiotic is 

excreted unchanged into the urine. This antibiotic, now in the 

environment, may encounter other bacteria and promote resistance. It 

is unknown how much of an impact current low levels of antibiotics in 

drinking water are having on the problem of bacterial resistance. 

However, the potential has been recognized for many years. 

Large animal feeding operations generate a large amount of waste 

that can potentially contaminate groundwater and waterways 

contributing to antibiotic resistance and contamination of waterways 

with steroid hormones. As occurs in humans, some portion of the 

None given

A1-24
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank Massive quantities of antibiotics are used in agriculture both to treat infections 

and as food additives to promote growth and to compensate for conditions that 

contribute to infection. Animals raised in Concentrated Animal Feeding 

Operations (CAFOs) are at increased risk for infection due to close 

confinement and stress. In fact, it has been estimated that 70% of the 

antibiotics used in the U.S. are for animal husbandry. Improper use and 

overuse of antibiotics in livestock and poultry can cause resistance in strains 

of bacteria that can infect humans. Furthermore, half of the antibiotics used in 

livestock are in the same classes of drugs that are used in humans. As a 

result the U.S. Institute of Medicine (IOM) and the World Health Organization 

(WHO) both stated that the widespread use of antibiotics in agriculture is 

contributing to antibiotic resistance in humans.

antibiotics administered to livestock will pass unchanged through their 

bodies and will be excreted in their waste. It has been estimated that 

between 25-75% of antibiotics are excreted unchanged in feces and 

can persist in the soil after land application. Manure is applied in large 

quantities as fertilizer in farm fields. In addition to potentially 

contaminating the food supply with antibiotic resistant bacteria, 

antibiotics in manure can persist in soil and promote the development 

of more antibiotic resistant bacteria. Animal waste and its associated 

contaminants can enter waterways through groundwater 

contamination, overflow of waste lagoons into surface water or by 

over-application of manure as fertilizer in farm fields. A recently 

published study found evidence of fecal contamination and increased 

levels of antibiotic resistant bacteria downstream of a swine 

concentrated feeding operation. Other studies have found antibiotic 

resistance in groundwater underlying a swine waste lagoon.

As such, antibiotics that are used both for human medical needs and 

in large-scale agriculture operations at low levels in animal feed to 

promote animal growth must be included on the CCL4 and must be 

regulated. These antibiotics include bacitracin zinc, spiramycin, tylosin, 

and virginiamycin. Notably, these antibiotics were all banned for 

agricultural use in the European Union in 1998.

blank

121831-99-0 Strontium 90 Anonymous 197 Public Health goals recommend a reasonable standard of 0.35 pCi/L based 

upon carcinogenic potency of 5.59 x 10E-11 pCi/L for Sr-90 in drinking water.

There are 23 nuclear power plants of exact design to the fatal power 

plants in Japan, failure due to earthquakes near population centers 

and water sources.

Monitoring existing conditions 

leads to rate of change analysis 

when done on a predictable time 

frame.

58-22-0 Testosterone Natural Resources 

Defense Council

While each of these compounds (see Table 5) [See Table 5 Concentrations of 

reproductive hormones in U.S. streams (USGS, 2002) located on page 29 of 

the NRDC letter] is generally found at low concentrations, the potential effects 

on human health of mixtures of these compounds are unknown. Based on the 

individual effects of these chemicals, possible risks include defects of the 

reproductive system in individuals exposed during critical stages of 

development (e.g. testosterone).

The U.S. Geological Survey (USGS) conducted a study of 139 

streams in 30 states that found widespread presence of estrogenic 

compounds, ovulation inhibitors and other reproductive hormones in 

surface water near urbanized and agricultural areas (see Table 5). 

[See Table 5 Concentrations of reproductive hormones in U.S. 

streams (USGS, 2002) located on page 29 of the NRDC letter]

Wastewater treatment plants, the likely sources of most of these 

chemicals, do not treat sewage for these pollutants. Furthermore, 

drinking water treatment plants do not generally test or treat water for 

these contaminants, so the frequency of occurrence of these 

chemicals in treated drinking water and the degree of human exposure 

are not known. Additional monitoring of water sources and drinking 

water are necessary to determine the full extent of the contamination, 

to assess risks to human health, and to determine acceptable levels of 

exposure and appropriate regulatory action.

EPA properly included many of these reproductive hormones on 

CCL3, although it has not made a final regulatory determination on any

of them. However, considering that progesterone and testosterone 

also occur at similar concentrations and similar frequency as some of 

the hormones that were include, they should also be added to the 

CCL4.

None given

A1-25
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

52-68-6 Trichlorfon Natural Resources 

Defense Council

Like the other organphosphates, trichlorfon is a neurotoxicant and 

cholinesterase inhibitor. Trichlorfon exposure is associated with kidney, lung 

and gastrointestinal abnormalities in animal studies. Anemia has also been 

reported, as well as benign pheochromocytomas. A statistically significant 

increase in mononuclear cell leukemia was also observed. Incidences of 

alveolar/bronchiolar adenomas, renal tubular adenomas and 

alveolar/bronchiolar carcinomas, while not statistically significant, occurred 

with frequencies “well outside of the historical control range for all three tumor 

types.” While EPA decided to classify trichlorfon in Group E for carcinogenicity 

arguing that the statistically significant increases in tumors in the studies were 

seen in the lower but not the higher doses, we argue that the evidence 

remains suggestive given that separate studies found significant increases in 

the same types of tumors.

In the studies analyzed by EPA during the reregistration process, trichlorfon 

also showed developmental toxicity in animals (decreased fetal body weight, 

delayed or reduced ossification) and mutagenic activity in an in vitro 

cytogenetic study in mammalian cells.

Trichlorfon is an organophosphate insecticide with agricultural nonfood and feed crop uses (e.g. agricultural non-cultivated areas, 

ornamental trees, etc.), as well as indoor and outdoor residential use. 

Usage volume data for these registered uses is not available.

Trichlorfon is highly mobile in soil, but EPA did not assess its 

groundwater contamination potential during the reregistration process 

for lack of appropriate data. Trichlorfon can enter surface waters in 

ground spray and runoff. Well samples from Georgia in the EPA 

Pesticides in Ground Water Database showed trichlorfon detections in 

12 of 179 wells with concentration up to 10 ppb. EPA did not consider 

these samples useful, citing analytical uncertainties.

Trichlorfon has a half-life in soil of 1 to 27 days, depending on soil 

type, which increases its potential to contaminate surface waters. 

However, the trichlorfon RED does not address drinking water risks. 

Despite the cancellation of feed and food crop uses, trichlorfon still has 

registered agricultural and residential outdoor uses that pose a risk of 

surface and possibly groundwater contamination. The scarcity of 

monitoring data on environmental concentrations should not lead to an 

assumption of negligible risk. The known toxicity of trichlorfon, its 

mobility and extended half-life in soil all make it a likely water 

contaminant in high use areas. EPA should require the collection of 

monitoring data for these areas to enable the Agency to assess water 

contamination risks and make a regulatory decision concerning 

trichlorfon.

None given

101-20-2 Triclocarban Natural Resources 

Defense Council

Triclocarban is a possible endocrine disruptor

An animal study indicates that triclocarban exposure enhanced the effects of 

testosterone both in vitro and in vivo in male rats.

Triclocarban (Urea, N-(4-chlorophenyl)-N'-(3,4-dichlorophenyl) 3,4,4'-

Trichlorocarbanilide), an antimicrobial pesticide also known as TCC, 

has been widely detected in effluent from wastewater treatment plants 

(WWTPs) in the United States. TCC has also been frequently detected 

in environmental water samples. 

The half-life of TCC in sediment is 540 days. One study predicted the 

magnitude and frequency of TCC contamination nationwide based on 

experimental and modeling data to be 1150 ng/L and 60%, 

respectively; much higher than previously recognized by EPA (240 

ng/L, 30%). Another study in the Greater Baltimore area found an 

average TCC level of 6.75 ug/L in wastewater samples, while river 

water samples had concentrations of up to 5.6 ug/L. These 

concentrations are higher than the Predicted Environmental 

Concentrations (PEC) calculated by the TCC Consortium in a report 

submitted to EPA in 2003 as part of the High Production Volume 

Chemical program, which estimated PECs from 0.0013 to 0.050 jtg/L. 

The actual measurements from the Greater Baltimore area study also 

exceed the TCC Consortium’s Predicted No Effect Concentration of 

0.146 ~g/L. 

None given

A1-26
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank A study of a 684 million liter per day typical activated sludge WWTP 

found a concentration of 6.1 ± 2.0 ug/L in the influent and 0.17 ± 0.03 

ug/L in the effluent. Approximately 127 ± 6 g/d exited the plant in the 

effluent, a clear indication that conventional wastewater treatment may 

leave considerable levels of TCC in the water. Because of this, TCC 

concentrations tend to be higher downstream of WWTPs. The most 

important sources of triclocarban to the aquatic environment were 

estimated to be activated sludge treatment plants (contributing 39-

67%), followed by trickling filters (31- 54%), combined sewer overflows 

(2-7%) and sanitary sewer overflows (<0.2%).

Given these data, triclocarban should be added to the CCL4.

blank

3380-34-5 Triclosan Natural Resources 

Defense Council

The chemical structure of triclosan is similar to other endocrine disrupting 

compounds and potential breakdown products of triclosan include dioxins.

Recently, low levels of triclosan were found to interfere with the 

metamorphosis of frogs. Exposure to as little as 0.15 μg/L triclosan caused an 

earlier metamorphosis than normal, with effects on the tadpole brain and tail. 

Triclosan activates the human pregnane X receptor (hPXR), which is involved 

in the enzymatic metabolism of steroids and xenobiotics.

Triclosan (5-chloro-2-(2,4-dichlorophenoxy)-phenol), is a broad 

spectrum antimicrobial pesticide that is widely used in personal care 

products such as soaps, toothpastes, cosmetics, skin creams and 

deodorants; kitchen accessories such as cutting boards and utensils; 

and in textiles such as sportswear, shoes and carpets. Approximately 

three quarters of Americans between the ages of six to over 65 have 

triclosan in their urine. Triclosan has even been detected in human 

blood plasma and breast milk. 

Triclosan is produced at over one million pounds per year. Triclosan is 

one of the most frequently detected chemicals in streams across the 

U.S. Wild Atlantic bottlenose dolphins have been found with triclosan 

in their bodies. Triclosan has been found in wastewater treatment 

effluent and drinking water sources. Triclosan was detected in 

Louisiana sewage treatment plant effluent at 10-21 ng/l. Boyd (2004) 

reported triclosan concentrations of ND – 29 ng/l in two stormwater 

canals in New Orleans. Triclosan has also been detected in raw and 

finished drinking water samples from Southern California.

None given

1401-69-0 Tylosin Natural Resources 

Defense Council

Widespread exposure to antibiotics is contributing to the growth of bacterial 

resistance, and this problem is of grave concern. In the past several decades 

almost every bacteria that can cause infections in humans has developed 

resistance to at least one antibiotic, and some are resistant to multiple 

antibiotics. The Centers for Disease Control and Prevention (CDC) have 

identified antibiotic resistance as one of the most pressing public health 

problems to face our nation. Infections caused by bacteria with resistance to at 

least one antibiotic have been estimated to kill over 60,000 hospitalized 

patients each year. 

Antibiotic resistance is caused by a number of factors including repeated and 

improper use of antibiotics in both humans and animals. Scientists also agree 

that exposure to low levels of antibiotics actually promotes bacterial resistance 

by exerting selective pressure for genes that promote resistance.

Massive quantities of antibiotics are used in agriculture both to treat infections 

and as food additives to promote growth and to compensate for conditions that 

contribute to infection. Animals raised in Concentrated Animal Feeding 

Antibiotics are found in wastewater because the body does not 

completely metabolize all drugs, so both the metabolized and 

unmetabolized drug are excreted by humans into wastewater. For 

example, when amoxicillin is ingested, 60-75% of the antibiotic is 

excreted unchanged into the urine. This antibiotic, now in the 

environment, may encounter other bacteria and promote resistance. It 

is unknown how much of an impact current low levels of antibiotics in 

drinking water are having on the problem of bacterial resistance. 

However, the potential has been recognized for many years. 

Large animal feeding operations generate a large amount of waste 

that can potentially contaminate groundwater and waterways 

contributing to antibiotic resistance and contamination of waterways 

with steroid hormones As occurs in humans, some portion of the 

antibiotics administered to livestock will pass unchanged through their 

bodies and will be excreted in their waste. It has been estimated that 

between 25-75% of antibiotics are excreted unchanged in feces and 

can persist in the soil after land application. Manure is applied in large 

None given

A1-27
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank Operations (CAFOs) are at increased risk for infection due to close 

confinement and stress. In fact, it has been estimated that 70% of the 

antibiotics used in the U.S. are for animal husbandry. Improper use and 

overuse of antibiotics in livestock and poultry can cause resistance in strains 

of bacteria that can infect humans. Furthermore, half of the antibiotics used in 

livestock are in the same classes of drugs that are used in humans. As a 

result the U.S. Institute of Medicine (IOM) and the World Health Organization 

(WHO) both stated that the widespread use of antibiotics in agriculture is 

contributing to antibiotic resistance in humans. [Quotes from the Healthcare 

Without Harm factsheet. Antibiotic Resistance and Agricultural Overuse of 

Antibiotics. 2005. http://www.noharm.org/us/food/issue

U.S. Institute of Medicine/National Academy of Science: “Clearly, a decrease 

in antimicrobial use in human medicine alone will have little effect on the 

current [antibiotic-resistant] situation. Substantial efforts must be made to 

decrease inappropriate overuse in animals and agriculture as well.”

World Health Organization: “There is clear evidence of the human health 

consequences due to resistant organisms resulting from non-human usage of 

antimicrobials. These consequences include infections that would not have 

otherwise occurred, increased frequency of treatment failures (in some cases 

death) and increased severity of infections.”]

quantities as fertilizer in farm fields. In addition to potentially 

contaminating the food supply with antibiotic resistant bacteria, 

antibiotics in manure can persist in soil and promote the development 

of more antibiotic resistant bacteria. Animal waste and its associated 

contaminants can enter waterways through groundwater 

contamination, overflow of waste lagoons into surface water or by 

over-application of manure as fertilizer in farm fields. A recently 

published study found evidence of fecal contamination and increased 

levels of antibiotic resistant bacteria downstream of a swine 

concentrated feeding operation. Other studies have found antibiotic 

resistance in groundwater underlying a swine waste lagoon.

As such, antibiotics that are used both for human medical needs and 

in large-scale agriculture operations at low levels in animal feed to 

promote animal growth must be included on the CCL4 and must be 

regulated. These antibiotics include bacitracin zinc, spiramycin, tylosin, 

and virginiamycin. Notably, these antibiotics were all banned for 

agricultural use in the European Union in 1998.

blank

1404-90-6 Vancomycin Natural Resources 

Defense Council

Widespread exposure to antibiotics is contributing to the growth of bacterial 

resistance, and this problem is of grave concern. In the past several decades 

almost every bacteria that can cause infections in humans has developed 

resistance to at least one antibiotic, and some are resistant to multiple 

antibiotics. The Centers for Disease Control and Prevention (CDC) have 

identified antibiotic resistance as one of the most pressing public health 

problems to face our nation. Infections caused by bacteria with resistance to at 

least one antibiotic have been estimated to kill over 60,000 hospitalized 

patients each year.

Antibiotic resistance is caused by a number of factors including repeated and 

improper use of antibiotics in both humans and animals. Scientists also agree 

that exposure to low levels of antibiotics actually promotes bacterial resistance 

by exerting selective pressure for genes that promote resistance.

Beta-lactam antibiotics are a broad class of antibiotics which include penicillin 

derivatives, cephalosporins, monobactams, carbapenems and Beta-lactamase 

inhibitors. Methicillin, a form of penicillin, had been relied upon as an common 

effective treatment for Staphylococcus aureus infections but now many strains 

of S. aureus bacteria are resistant to methicillin (MRSA or methicillin-resistant 

Staphylococcus aureus.) Unfortunately, MRSA is resistant to much of the 

entire class of penicillin-like antibiotics called beta-lactams. Therefore, EPA 

must include penicillin, amoxicillin, oxacillin and methicillin on the CCL4.

Infections among hospital patients (nosocomial infections) from enterococci 

bacteria are very common. Such infections that result in human disease can 

Antibiotics are found in wastewater because the body does not 

completely metabolize all drugs, so both the metabolized and 

unmetabolized drug are excreted by humans into wastewater. For 

example, when amoxicillin is ingested, 60-75% of the antibiotic is 

excreted unchanged into the urine. This antibiotic, now in the 

environment, may encounter other bacteria and promote resistance. It 

is unknown how much of an impact current low levels of antibiotics in 

drinking water are having on the problem of bacterial resistance. 

However, the potential has been recognized for many years. 

None given

A1-28
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

CASRN Common Name Nominator Health Effects Information Provided with

Nomination

Occurrence Information Provided

with Nomination

Additional Information 

Provided

with Nomination

blank blank blank be fatal, particularly those caused by strains of vancomycin-resistant 

enterococci (VRE). During 2004, VRE caused about one of every three 

infections in hospital intensive-care units, according to the Centers CDC. As of 

2007, the U.S. had reported seven cases of vancomycin-resistant 

Staphylococcus aureus (VRSA) infection. Therefore, vancomycin must be 

included on the CCL3.

blank blank

11006-76-1 Virginiamycin Natural Resources 

Defense Council

Widespread exposure to antibiotics is contributing to the growth of bacterial 

resistance, and this problem is of grave concern. In the past several decades 

almost every bacteria that can cause infections in humans has developed 

resistance to at least one antibiotic, and some are resistant to multiple 

antibiotics. The Centers for Disease Control and Prevention (CDC) have 

identified antibiotic resistance as one of the most pressing public health 

problems to face our nation. Infections caused by bacteria with resistance to at 

least one antibiotic have been estimated to kill over 60,000 hospitalized 

patients each year.

Antibiotic resistance is caused by a number of factors including repeated and 

improper use of antibiotics in both humans and animals. Scientists also agree 

that exposure to low levels of antibiotics actually promotes bacterial resistance 

by exerting selective pressure for genes that promote resistance.

Massive quantities of antibiotics are used in agriculture both to treat infections 

and as food additives to promote growth and to compensate for conditions that 

contribute to infection. Animals raised in Concentrated Animal Feeding 

Operations (CAFOs) are at increased risk for infection due to close 

confinement and stress. In fact, it has been estimated that 70% of the 

antibiotics used in the U.S. are for animal husbandry. Improper use and 

overuse of antibiotics in livestock and poultry can cause resistance in strains 

of bacteria that can infect humans. Furthermore, half of the antibiotics used in 

livestock are in the same classes of drugs that are used in humans. As a 

result the U.S. Institute of Medicine (IOM) and the World Health Organization 

(WHO) both stated that the widespread use of antibiotics in agriculture is 

contributing to antibiotic resistance in humans. [Quotes from the Healthcare 

Without Harm factsheet. Antibiotic Resistance and Agricultural Overuse of 

Antibiotics. 2005. http://www.noharm.org/us/food/issue

U.S. Institute of Medicine/National Academy of Science: “Clearly, a decrease 

in antimicrobial use in human medicine alone will have little effect on the 

current [antibiotic-resistant] situation. Substantial efforts must be made to 

decrease inappropriate overuse in animals and agriculture as well.”

World Health Organization: “There is clear evidence of the human health 

consequences due to resistant organisms resulting from non-human usage of 

antimicrobials. These consequences include infections that would not have 

otherwise occurred, increased frequency of treatment failures (in some cases 

death) and increased severity of infections.”]

Antibiotics are found in wastewater because the body does not 

completely metabolize all drugs, so both the metabolized and 

unmetabolized drug are excreted by humans into wastewater. For 

example, when amoxicillin is ingested, 60-75% of the antibiotic is 

excreted unchanged into the urine. This antibiotic, now in the 

environment, may encounter other bacteria and promote resistance. It 

is unknown how much of an impact current low levels of antibiotics in 

drinking water are having on the problem of bacterial resistance. 

However, the potential has been recognized for many years. 

Large animal feeding operations generate a large amount of waste 

that can potentially contaminate groundwater and waterways 

contributing to antibiotic resistance and contamination of waterways 

with steroid hormones. As occurs in humans, some portion of the 

antibiotics administered to livestock will pass unchanged through their 

bodies and will be excreted in their waste. It has been estimated that 

between 25-75% of antibiotics are excreted unchanged in feces and 

can persist in the soil after land application. Manure is applied in large 

quantities as fertilizer in farm fields. In addition to potentially 

contaminating the food supply with antibiotic resistant bacteria, 

antibiotics in manure can persist in soil and promote the development 

of more antibiotic resistant bacteria. Animal waste and its associated 

contaminants can enter waterways through groundwater 

contamination, overflow of waste lagoons into surface water or by 

over-application of manure as fertilizer in farm fields. A recently 

published study found evidence of fecal contamination and increased 

levels of antibiotic resistant bacteria downstream of a swine 

concentrated feeding operation. Other studies have found antibiotic 

resistance in groundwater underlying a swine waste lagoon.

As such, antibiotics that are used both for human medical needs and 

in large-scale agriculture operations at low levels in animal feed to 

promote animal growth must be included on the CCL4 and must be 

regulated. These antibiotics include bacitracin zinc, spiramycin, tylosin, 

and virginiamycin. Notably, these antibiotics were all banned for 

agricultural use in the European Union in 1998.

None given

A1-29
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

Appendix 2. Microbial Contaminants Nominated

Common Name Nominator Health Effects Information Provided withNomination Occurrence Information Provided with Nomination Additional Information Provided with Nomination

Adenovirus NJ Dept. of 

Environmental 

Protection

Adenoviruses (Ads) are a common cause of childhood gastroenteritis. 

Persons with weakened immune systems are most susceptible to 

infection, with high rates of severe illness and mortality. As with many 

other pathogens, infants are most susceptible among persons with normal 

immune system function (Post et al, 2011).

Some serotypes are shed in feces but cause respiratory (e.g., Ads 1 

through 7) or eye disease (e.g., Ads 3, 7, and 14). These types can also 

spread via aerosol, direct contact, or sexual routes (Jiang, 2006; Langley, 

2005). Ads 12, 18, and 31 may cause diarrhea on occasion, but infection 

usually results in apparent illness in infants. Other serotypes are 

associated with GI illness but have not been proven to cause illness. 

However, there is probably sufficient evidence that Ad 40 and Ad 41 are 

waterborne pathogens that can cause diarrhea in infants. Recent 

evidence has also shown a possible connection between infection with 

Adenovirus 36 and obesity in humans, including a potential waterborne 

route of exposure (Atkinson, 2012). Ads can be shed in the feces for 

months to years following infection.

Although data from Borchardt (2008) show low concentrations 

of adenovirus in drinking water and a lack of association 

between the presence of adenoviruses and enteric disease. 

And although the waterborne transmission route for 

adenoviruse-based disease has not been definitively proven, 

Borchardt (2008) and others (e.g., Katayama et al, 2008; 

Rodriguez et al, 2008) have shown that adenoviruses are 

among the most common virus groups detected in water.

What is the correlation, or co-occurrence, of adenovirus and 

other viruses in the Borchardt (2008) and other studies? The 

EPA may wish to also consider monitoring for adenoviruses, 

not as pathogens themselves, but as a potential “viral 

indicator” of the presence of other pathogenic human enteric 

viruses (HEV). However, if adenoviruses are monitored, the 

NanoCeram filter may not be appropriate for this group of 

viruses (Gibbons et al, 2010; as cited in the proposed 

UCMR3 [USEPA, 2011]). 

Also, with regard to the Ground Water Rule (GWR)(USEPA, 

2006), because adenoviruses are the most UV-resistant 

group of microbes, and because the GWR UV dose 

requirements are based on inactivating adenoviruses, the 

EPA may wish to generate additional data on the presence of 

adenoviruses in GW. Such data could be generated in 

conjunction with epidemiological studies similar to those of 

Borchardt (2008) but in other locations in the US.

If such studies confirmed the findings of Borchardt (2008), 

who observed a lack of association of gastrointestinal illness 

with adenovirus concentrations, then perhaps the GWR UV 

dose requirements could be reduced. Reduced UV dose 

requirements would result in substantial cost savings for 

many public water systems.

Heterotrophic 

Plate Count 

Bacteria

NJ Dept. of 

Environmental 

Protection

None provided There is evidence that HPC counts in a well significantly above 

average for all sources could serve as a trigger for fecal 

indicator monitoring in ground water, but the data was limited 

and a definitive conclusion could not be drawn (Atherholt et al, 

2003). Other investigators have shown that HPC may be a 

useful GW indicator (Butscher et al, 2011, Goeppert and 

Goldscheider, 2011). HPC testing is also very useful for QC 

purposes including negative control counts and for the ease of 

determining quantifiable and reproducible (similar) counts in 

replicates of field samples.

The proposed UCMR3 stated that aerobic spores would be 

monitored. It is not clear why aerobic spores would be 

monitored as pathogen indicators. Anaerobic spores (e.g., 

spores of Clostridia) are a more fecal-specific indicator than 

are aerobic spores (presumably from soil-borne Bacillus 

spp.), but it has been shown that anaerobic spores are poor 

indicators of fecal contamination compared to other 

indicators such as coliform or enterococcus bacteria (Francy 

et al, 2000 & 2004; Atherholt et al, 2003; Butscher et al, 

2011). 

If aerobic spores are to be employed, not as a fecal indicator, 

but as an indicator of surface water influence, we suggest 

monitoring for heterotrophic plate count (HPC) bacteria 

instead.

A2-1
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001 

Common Name Nominator Health Effects Information Provided withNomination Occurrence Information Provided with Nomination Additional Information Provided with Nomination

Naegleria fowleri NJ Dept. of 

Environmental 

Protection

The disease, primary amoebic meningoencephalitis, is fatal following 

exposure of susceptible individuals with death occurring within 72 hours 

after symptoms (similar to viral and bacterial meningitis) first appear.

Although in the US, there is a 14-year average of just 2 cases 

of primary amoebic meningoencephalitis per year, 11 of 143 

wells (8%), with an average water temperature of 29 oC were 

found to contain Naegleria.

Because 11 of 143 wells (8%), with an average water 

temperature of 29°C were found to contain Naegleria (Blair et 

al, 2008), the EPA may wish to consider conducting a 

summer monitoring survey of “warm water” wells in the US 

(with a suitable control group of “cold water” wells).

Toxoplasma 

gondii

J. Jones Ocular and congenital illness Waterborne Toxoplasma gondii has been implicated in other 

countries and could contaminate drinking water that is not 

filtered.

None given

Toxoplasma 

gondii

US Dept. of 

Agriculture

Many outbreaks causing serious disease in humans detailed. [See (de Moura et al., 2006) in Appendix 5] None given 

Vibrio cholerae Natural Resources 

Defense Council

This bacterium is known to cause outbreaks of cholera, an acute diarrheal 

illness caused by intestinal infection with the bacterium Vibrio cholerae, 

with serious and occasionally fatal human consequences.

As recently as April 2011, an outbreak of Vibrio cholerae O75 

was reported in Florida. Ten cases were identified in the 

outbreak. Their occurrence is likely to expand as climate 

change continues, which makes it appropriate to include this 

pathogen in the CCL4.

None given

A2-2
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

Appendix 3. References Provided with Chemical Nominations

CASRN Contaminant Name Nominating Individual Organization Name Abbreviated References 

Cited in the Nomination

77439-76-0 3-chloro-4-dichloromethyl-5-

hydroxy-2(5H)-furanone) Thomas W. Curtis AWWA None given

116-06-03 Aldicarb Thomas W. Curtis AWWA None given

116-06-3 Aldicarb Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Fiore et al., 1986)

(Grendon and Baum, 

1994)

(Hajoui et al., 1992)

(Smulders et al., 2003)

(Smulders et al., 2004)

(USEPA, 1984)

(USEPA, 1988)

(USEPA, 2006)

(USEPA, 2006a)

68555-24-8 Alkylphenol mono- to trioxylates 

Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Gatidou et al., 2006)

(Ying et al., 2002)

26787-78-0 Amoxicillin Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(CDC, 2012)

(Chee-Sanford et al., 

2001)

(Gilchrist et al., 2007)

(Health Care Without 

Harm, 2005)

(Mellon et al., 2000)

(Sapkota et al., 2007a)

(USA Today, 2000)

(Wallinga et al., 2006)

(Wallinga, 2005)

86-50-0 Azinphos-methyl Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Dabrowski et al., 2006)

(Loewy et al., 2003)

(Loewy et al., 2006)

(Rohlman et al., 2005)

(Rothlein et al., 2006)

(Souza et al., 2004)

(Souza et al., 2005)

(USEPA, 2001a)

(USEPA, 2006a)

1405-89-6 Bacitracin zinc Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(CDC, 2012)

(Chee-Sanford et al., 

2001)

(Gilchrist et al., 2007)

(Health Care Without 

Harm, 2005)

(Mellon et al., 2000)

(Sapkota et al., 2007a)

(USA Today, 2000)

(Wallinga et al., 2006)

(Wallinga, 2005)

25057-89-0 Bentazone Thomas W. Curtis AWWA None given

85-68-7 Benzyl butyl phthalate Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(ATSDR)

(CDC, 2005)

(Gray et al., 2000)

(Gray et al., 2006)

(Main et al., 2006)

(Meeker et al., 2007)

(Stahlhut et al., 2007)

(USEPA)

A3-1
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

CASRN Contaminant Name Nominating Individual Organization Name Abbreviated References 

Cited in the Nomination

80-05-7 Bisphenol A Anonymous 201 None given None given

80-05-7 Bisphenol A Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Adewale et al., 2011a)

(Alonso-Magdalena et al., 

2006)

(Ayyanan et al., 2011b)

(Calafat et al., 2008a)

(Carwile and Michels, 

2011)

(ChemSec, 2012)

(Cousins et al., 2002)

(Durando et al., 2007)

(Fromme et al., 2002)

(Hoet al., 2006)

(Hunt et al., 2003)

(Melzer et al., 2012)

(Murray et al., 2007)

(National Institute of 

Environmental Health 

Sciences, 2008)

(Prins et al., 2011)

(Raloff, 2012)

(Sorianoet al., 2012)

(USEPA)

(vom Saal et al., 2007)

1689-84-5 Bromoxynil Thomas W. Curtis AWWA None given

63-25-2 Carbaryl Thomas W. Curtis AWWA None given

63-25-2 Carbaryl Mae C. Wu & Jennifer

Sass

Natural Resources 

Defense Council

(Tarplee, 1999)

(Tarplee, 2001)

(USEPA, 2004a)

10045-97-3 Cesium 137 Anonymous 197 None given None given

1897-45-6 Chlorothalonil Thomas W. Curtis AWWA None given

2921-88-2 Chlorpyrifos Thomas W. Curtis AWWA None given

2921-88-2 Chlorpyrifos Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Barbas and Resek, 1996)

(Becker et al., 1989)

(Burkart and Kolpin, 1993)

(Goss, 1992)

(Larson, et al., 1997)

(Long, 1989)

(Makris et al., 1998)

(USEPA, 2000a)

(USEPA, 2002)

(USEPA, 2002a)

84-74-2 Dibutyl phthalate Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(ATSDR)

(CDC, 2005)

(Gray et al., 2000)

(Gray et al., 2006)

(IHCP, 2003)

(Main et al., 2006)

(Meeker et al., 2007)

(Stahlhut et al., 2007)

(USEPA)

1918-00-9 Dicamba Thomas W. Curtis AWWA None given

A3-2
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

CASRN Contaminant Name Nominating Individual Organization Name Abbreviated References 

Cited in the Nomination

62-73-7 Dichlorvos Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Brown et al., 1990)

(Leissand Savitz, 1995)

(National Toxicology 

Program, 1989)

(USEPA, 2000b)

(USEPA, 2000c)

(USEPA, 2006b)

115-32-2 Dicofol Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Hoekstra et al. 2005)

(Ishihara et al., 2003)

(Jadaramkunti and Kaliwal,

2001)

(Thibaut and Porte, 2004)

(USEPA, 1998)

84-61-7 Dicyclohexyl phthalate Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(ATSDR)

(CDC, 2005)

(Gray et al., 2000)

(Gray et al., 2006)

(Main et al., 2006)

(Meeker et al., 2007)

(Stahlhut et al., 2007)

84-66-2 Diethyl phthalate Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(ATSDR)

(CDC, 2005)

(Gray et al., 2000)

(Gray et al., 2006)

(Main et al., 2006)

(Meeker et al., 2007)

(Stahlhut et al., 2007)

(USEPA)

28553-12-0 Di-isononyl phthalate Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(ATSDR)

(CDC, 2005)

(Gray et al., 2000)

(Gray et al., 2006)

(IHCP, 2003)

(Main et al., 2006)

(Meeker et al., 2007)

(Stahlhut et al., 2007)

(USEPA)

131-11-3 Dimethyl phthalate Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(ATSDR)

(CDC, 2005)

(Gray et al., 2000)

(Gray et al., 2006)

(Main et al., 2006)

(Meeker et al., 2007)

(Stahlhut et al., 2007)

(USEPA)

117-84-0 Di-n-octyl phthalate Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(ATSDR)

(CDC, 2005)

(Gray et al., 2000)

(Gray et al., 2006)

(Main et al., 2006)

(Meeker et al., 2007)

(Stahlhut et al., 2007)

(USEPA)

A3-3
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

CASRN Contaminant Name Nominating Individual Organization Name Abbreviated References 

Cited in the Nomination

115-29-7 Endosulfan Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Association of American 

Pesticide Control Officials, 

Inc, 1969)

(Lakshmana and Raju, 

1994) 

(OSHA, 1989)

(Sinha et al., 1991)

(Sinha et al., 1997)

(State of California: 

Department of Industrial 

Relations)

(USEPA, 2002b)

(Willey and Kron, 2001)

(Wilson and LeBlanc, 

1998)

2164-17-2 Fluometuron Thomas W. Curtis AWWA None given

319-84-6 Hexachlorocyclohexane 

(alpha isomer) Thomas W. Curtis AWWA None given

165800-03-3 Linezolid Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(CDC, 2012)

(Chee-Sanford et al., 

2001)

(Gilchrist et al., 2007)

(Health Care Without 

Harm, 2005)

(Mellon et al., 2000)

(Sapkota et al., 2007a)

(USA Today, 2000)

(Wallinga et al., 2006)

(Wallinga, 2005)

330-55-2 Linuron Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Cook, 1993)

(EXTOXNET, 1996)

(Gray et al., 1999)

(USEPA, 1995)

(USEPA, 2002c)

(USGS, 1992)

121-75-5 Malathion Thomas W. Curtis AWWA None given

A3-4
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

CASRN Contaminant Name Nominating Individual Organization Name Abbreviated References 

Cited in the Nomination

7439-96-5 Manganese Michael S. Hutcheson

Massachusetts 

Department of 

Environmental 

Protection

(Ayotte, et al., 2001)

(Bouchard et al., 2007)

(Bouchard et al., 2011)

(Boyes, 2010)

(Brown and Foos, 2009)

(Claus et al., 2010)

(Deveau, 2010)

(Dorman and Wong, 2006)

(Erikson et al., 2007)

(Fordahlet al., 2012)

(Golub et al., 2005)

(Kern et al., 2010)

(Khan et al., 2011)

(Khan et al., 2012)

(Kim et al., 2009)

(Ljung et al., 2009)

(Ljung, 2007)

(Menezes-Filho et al., 

2009)

(Moreno et al., 2009)

(Parvez et al., 2011)

(Riojas-Rodriguez et al., 

2010)

(Roels et al., 2012)

(Santamaria and Sulsky, 

2010)

(Santamaria, 2008)

(USEPA, 1979)

(USEPA, 2004b)

(Wasserman et al., 2006)

(Wasserman et al., 2011)

(Yoon et al., 2011) 

(Yoon et al., 2009)

A3-5
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

CASRN Contaminant Name Nominating Individual Organization Name Abbreviated References 

Cited in the Nomination

7439-96-5 Manganese James Kelly Minnesota 

Department of Health

(Anoka County, 2004)

(Ayotte, et al., 2001)

(Bouchard et al., 2007)

(Bouchard et al., 2011)

(Boyes, 2010)

(Brown and Foos, 2009)

(Claus et al., 2010)

(County Geologic Atlas)

(Deveau, 2010)

(Dorman and Wong, 2006)

(Erikson et al., 2007)

(Fong, et al., 1998)

(Fordahlet al., 2012)

(Golub et al., 2005)

(GWMAP)

(Kern et al., 2010)

(Khan et al., 2011)

(Khan et al., 2012)

(Kim et al., 2009)

(Lively et al., 1992)

(Ljung et al., 2009)

(Ljung, 2007)

(MARS data set)

(Menezes-Filho et al., 

2009)

(Minesota, 2011)

(Moreno et al., 2009)

(Parvez et al., 2011)

(Riojas-Rodriguez et al., 

2010)

(Santamaria and Sulsky, 

2010)

(Santamaria, 2008)

(Smith and Nemetz, 1995)

(State of Minnesota)

(USEPA, 1979)

(USEPA, 2004)

(Wall and Regan, 1994)

(Wasserman et al., 2006)

(Wasserman et al., 2011)

(Yoon et al., 2011)

(Yoon et al., 2009)

7439-96-5 Manganese Gloria B. Post

NJ Department of 

Environmental 

Protection

(Bouchard et al., 2011)

(Khan et al., 2011)

(Wasserman et al., 2011)

61-32-5 Methicillin Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(CDC, 2012)

(Chee-Sanford et al., 

2001)

(Gilchrist et al., 2007)

(Health Care Without 

Harm, 2005)

(Mellon et al., 2000)

(Sapkota et al., 2007a)

(USA Today, 2000)

(Wallinga et al., 2006)

(Wallinga, 2005)

298-00-0 methyl parathion Thomas W. Curtis AWWA None given

1634-04-4 Methyl tertiary butyl ether Gloria B. Post

NJ Department of 

Environmental 

Protection

(Bird et al., 1997)

(Dodd et al., 2011)

(Ramazzini Institute Study)

A3-6
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

CASRN Contaminant Name Nominating Individual Organization Name Abbreviated References 

Cited in the Nomination

101043-37-2 Microcystin-LR Christopher Greene Minnesota 

Department of Health

(Barringer, 2012)

(Billam et al., 2006)

(Boyer et al., 2005)

(Chen et al., 2011)

(City of San Diego, 2012)

(Graham et al., 2004)

(Ho L, et al., 2010)

(Li et al., 2008)

(Liu et al., 2010)

(Ohio EPA, 2012)

(Trinchet et al., 2011)

(Ueno et al., 1999)

(Wang et al., 2012)

101043-37-2 Microcystin-LR James Kelly Minnesota 

Department of Health

(Boyer et al., 2005)

(Chen et al., 2011)

(City of San Diego, 2012)

(Graham et al., 2004)

(Ho L, et al., 2010)

(Li et al., 2008)

(Liu et al., 2010)

(Ohio EPA, 2012)

(Trinchet et al., 2011)

(Ueno et al., 1999)

(Wang et al., 2012)

25154-52-3 Nonylphenol Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Gatidou et al., 2006)

(Ying et al., 2002)

9016-45-9 Nonylphenol ethoxylate Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Gatidou et al., 2006)

(Ying et al., 2002)

27193-28-8 Octylphenol Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Gatidou et al., 2006)

(Ying et al., 2002)

9036-19-5 Octylphenol ethoxylate Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Gatidou et al., 2006)

(Ying et al., 2002)

66-79-5 Oxacillin Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(CDC, 2012)

(Chee-Sanford et al., 

2001)

(Gilchrist et al., 2007)

(Health Care Without 

Harm, 2005)

(Mellon et al., 2000)

(Sapkota et al., 2007a)

(USA Today, 2000)

(Wallinga et al., 2006)

(Wallinga, 2005)

multiple CAS #s Penicillin Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(CDC, 2012)

(Chee-Sanford et al., 

2001)

(Gilchrist et al., 2007)

(Health Care Without 

Harm, 2005)

(Mellon et al., 2000)

(Sapkota et al., 2007a)

(USA Today, 2000)

(Wallinga et al., 2006)

(Wallinga, 2005)

A3-7
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

CASRN Contaminant Name Nominating Individual Organization Name Abbreviated References 

Cited in the Nomination

68141-02-6 Perfluoro octanoic acid Eileen Murphy None given

(C8 Science Panel, 2012)

(Post et al., 2009)

None given

(C8 Science Panel, 2012)

(Min et al., 2012)

(Post et al., 2012)

52645-53-1 Permethrin Thomas W. Curtis AWWA None given

732-11-6 Phosmet Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Cappon, 1998)

(Hasegawa et al., 1993)

(Raffaele, 1999)

(Raffaele, 2002)

(Souza et al., 2005)

(Swartz, 1999)

(Taylor, 1999)

(USEPA, 2001b)

(Vlckova et al., 1993)

multiple CAS #s Phthalates5 Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Adibiet al., 2003)

(Blount et al., 2000)

(Meeker et al., 2007)

(Silva et al., 2007)

(Stahlhut RW, et al., 2007)

(Wolff et al., 2007)

57-83-0 Progesterone Mae C. Wu & Jennifer 

Sass

Natural Resources

Defense Council

(Hotchkiss et al., 2007)

(Kolpin et al., 2002)

10043-92-2 Radon Gloria B. Post

NJ Department of 

Environmental 

Protection

(New Jersey Drinking 

Water Quality Institute, 

2009)

8025-81-8 Spiramycin Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(CDC, 2012)

(Chee-Sanford et al., 

2001)

(Gilchrist et al., 2007)

(Health Care Without 

Harm, 2005)

(Mellon et al., 2000)

(Sapkota et al., 2007a)

(USA Today, 2000)

(Wallinga et al., 2006)

(Wallinga, 2005)

121831-99-0 Strontium 90 Anonymous 197 None given None given

58-22-0 Testosterone Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Hotchkiss et al., 2007)

(Kolpin et al., 2002)

52-68-6 Trichlorfon Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(USEPA, 1997)

(USEPA, 1997)

101-20-2 Triclocarban Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Chen et al., 2008)

(Halden and Paull, 2004)

(Halden and Paull, 2005)

(Heidler et al., 2006)

(Sapkota et al., 2007b)

(TCC Consortium, 2002)

5 The Natural Resources Defense Council nomination letter contained several references that were included in a 

general discussion of phthalates. The references included in this general discussion are included under this listing. See 

the individual phthalates listings above for specific references.

A3-8
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

CASRN Contaminant Name Nominating Individual Organization Name Abbreviated References 

Cited in the Nomination

3380-34-5 Triclosan Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(Boyd et al., 2003)

(Boyd et al., 2004)

(Calafat et al., 2008b)

(Dayan, 2007)

(Fair et al., 2009)

(Greyshock and Vikesland, 

2006)

(Hovander et al., 2002)

(Jacobs et al., 2005)

(Kolpin, et al., 2002)

(Latch et al., 2005)

(Loraine and Pettigrove, 

2006)

(Veldhoen et al., 2006)

1401-69-0 Tylosin Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(CDC, 2012)

(Chee-Sanford et al., 

2001)

(Gilchrist et al., 2007)

(Health Care Without 

Harm, 2005)

(Mellon et al., 2000)

(Sapkota et al., 2007a)

(USA Today, 2000)

(Wallinga et al., 2006)

(Wallinga, 2005)

1404-90-6 Vancomycin Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(CDC, 2012)

(Chee-Sanford et al., 

2001)

(Gilchrist et al., 2007)

(Health Care Without 

Harm, 2005)

(Mellon et al., 2000)

(Sapkota et al., 2007a)

(USA Today, 2000)

(Wallinga et al., 2006)

(Wallinga, 2005)

11006-76-1 Virginiamycin Mae C. Wu & Jennifer 

Sass

Natural Resources 

Defense Council

(CDC, 2012)

(Chee-Sanford et al., 

2001)

(Gilchrist et al., 2007)

(Health Care Without 

Harm, 2005)

(Mellon et al., 2000)

(Sapkota et al., 2007a)

(USA Today, 2000)

(Wallinga et al., 2006)

(Wallinga, 2005)

A3-9
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

Appendix 4. References Provided with Microbial Nominations

Contaminant Name Nominating Individual Organization Name Abbreviated References Cited 

in the Nomination

Adenovirus Thomas B. Atherholt NJ Department of 

Environmental Protection

(Atkinson, 2012)

(Borchart et al., 2008)

(Gibbons et al., 2010) 

(Jiang, 2006)

(Katayama et al., 2008)

(Langley, 2005)

(Post et al., 2011)

(Rodriguez et al., 2008)

(USEPA, 2006)

(USEPA, 2011)

HPC Heterotrophic Plate Count 

Bacteria Thomas B. Atherholt NJ Department of Environmental Protection

(Atherholt et al., 2003)

(Butscher et al., 2011)

(Francy et al., 2000)

(Francy et al., 2004)

(Goeppert et al., 2011)

Naegleria fowleri Thomas B. Atherholt NJ Department of 

Environmental Protection

(Blair et al., 2008)

(Post et al., 2011)

Toxoplasma gondii J. Jones None given None given

Toxoplasma gondii Jitender P.Dubey U.S. Department of Agriculture (de Moura et al., 2006)

(Jones et al., 2010)

Vibrio cholerae Mae C. Wu & Jennifer Sass Natural Resources Defense 

Council

(Natural Resources Defense 

Council, 2010)

(Onifade et al., 2011)

A4-1
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

Appendix 5. Complete List of References Provided with CCL 4 

Nominations 

Note: References are cited as they were received from the nominating individual or organization. 

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exposure on sexually dimorphic hypothalamic nuclei in the female rat. NeuroToxicology 

32(1):38–49. 

Adibi JJ, Perera FP, Jedrychowski W, et al. (2003) Prenatal exposures to phthalates among 

women in New York City and Krakow, Poland. Environ Health Perspect 111(14):1719-

1722. 

Agency for Toxic Substances and Disease Registry (ATSDR). Hazardous substance release and 

health effects database (HazDat). Available at http://www.atsdr.cdc.gov/Hazdat.html. 

Alonso-Magdalena P, Morimoto S, Ripoll C, Fuentes E, Nadal A. (2006) The estrogenic effect 

of bisphenol A disrupts pancreatic beta-cell function in vivo and induces insulin 

resistance. Environ Health Perspect.114(1):106-112. 

Anoka County. (2004) Anoka County trace metals study. 

Association of American Pesticide Control Officials, Inc. (1969) As cited in ACGIH 1986/Ex. 1-

3, p. 230.) 

Atherholt T, Feerst E, Hovendon, B, et al. (2003) Evaluation of indicators of fecal contamination 

in groundwater. J Am Water Works Assoc 95(10):119-131. 

Atkinson RL. (2012) Virus-induced obesity in humans. Microbe 7(6):263-267. 

Ayotte J D, Gronberg JM, et al. (2001) Trace elements and radon in groundwater across the 

United States. U.S. Geological Survey Scientific Investigations Report 2011-5059: 115. 

Ayyanan A, Laribi O, Schuepbach-Mallepell S, et al. (2011) Perinatal exposure to bisphenol a 

increases adult mammary gland progesterone response and cell number. Mol Endocrinol 

25(11):1915–1923. 

Barbas JE, Resek EA. (1996) Pesticides in ground water: distribution, trends, and governing 

factors. Chelsea, MI: Ann Arbor Press, 588 p., at pp. 98-99, 167. 

Barringer F. (2012) As ‘yuck factor’ subsides, treated wastewater flows from taps. The New 

York Times. February 9, 2012. Available 

at http://www.nytimes.com/2012/02/10/science/earth/despite-yuck-factor-treatedwastewater-used-for-drinking.html?_r=1&pagewanted=all. 

A5-1
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

Becker RL, Herzfeld D, Ostlie KR, Stamm-Katovich EJ. (1989) Pesticides: Surface runoff. 

leaching, and exposure concerns. University of Minnesota, Minnesota Extension Service 

Publication AG-BU-3911, 32 p. 

Billam M, Tang L, Cai Q, et al. (2006) Seasonal variations in the concentration of MicrocystinLR in two lakes in western Texas, USA. Environ Toxicol Chem 25(2):349-355. 

Bird et al. (1997). 

Blair B, Sarkar P, Bright KR, et al. (2008) Naegleria fowleri in well water. Emerg Infect Dis 

14:1499-1501. 

Blount BC, Silva MJ, Caudill SP, et al. (2000) Levels of seven urinary phthalate metabolites in a 

human reference population. Environ Health Perspect 108(10):979-982. 

Borchart M. (2008) Wisconsin water and health trial for enteric risks (WAHTER Study). Part 1: 

Risk of illness from municipal groundwater consumption. in press. 

Bouchard M, Laforest F, et al. (2007) Hair manganese and hyperactive behaviors: pilot study of 

school-age children exposed through tap water. Environ Health Perspect 115(1):122- 127. 

Bouchard MF, Sauve S, et al. (2011) Intellectual impairment in school-age children exposed to 

manganese from drinking water. Environ Health Perspect 119:138-143. 

Boyd GR, Palmeri JM, Zhang S, Grimm DA. (2004) Pharmaceuticals and personal care products 

(PPCPs) and endocrine disrupting chemicals (EDCs) in stormwater canals and Bayou St. 

John in New Orleans, Louisiana, USA. Sci Total Environ 333(1-3):137-148. 

Boyd GR, Reemtsma H, Grimm DA, Mitra S. (2003) Pharmaceuticals and personal care 

products (PPCPs) in surface and treated waters of Louisiana, USA and Ontario, Canada. 

Sci Total Environ 311(1-3):135-149. 

Boyer et al. (2005) Cyanobacterial Toxins in New York and the Lower Great Lakes Ecosystems. 

In Monograph: International Symposium on Cyanobacterial Harmful Algal Blooms 

(ISOC-HAB). Monograph: International Symposium on Cyanobacterial Harmful Algal 

Blooms (ISOC-HAB). Available 

at http://www.epa.gov/cyano_habs_symposium/monograph/Ch07.pdf. 

Boyes WK. (2010) Essentiality, toxicity, and uncertainty in the risk assessment of manganese. J 

Toxicol Environ Health A 73(2):159-165. 

Brown LM, Blair A, Gibson R, et al. (1990) Pesticide exposures and other agricultural risk 

factors for leukemia among men in Iowa and Minnesota. Cancer Res 50(20):6585-6591. 

Brown MT, Foos B. (2009) Assessing children's exposures and risks to drinking water 

contaminants: a manganese case study. Hum Ecol Risk Assess 15(5):923-947. 

A5-2
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EPA 815-R-15-001

Burkart MR, Kolpin DW. (1993) Hydrologic and land-use factors associated with herbicides and 

nitrate in near-surface aquifers. J Environ Qual 22(4):646-656. 

Butscher C, Auckenthaler, Scheidler S, Huggenberger P. (2011) Validation of a numerical 

indicator of microbial contamination for karst springs. Groundwater 49(1):66-76. 

C8 Science Panel. (2012) Probable link evaluation of cancer. Web accessed. Available 

at http://www.c8sciencepanel.org/pdfs/Probable_Link_C8_Cancer_16April2012.pdf. 

C8 Science Panel. (2012). C8 Science Panel Web site. Web site accessed 2012. Available 

at http://www.c8sciencepanel.org/publications.html. 

Calafat AM, et al. (2008b) Urinary concentrations of triclosan in the U.S. pPopulation: 2003-

2004. Environ Health Perspect 116(3):303-307. 

Calafat AM, Ye X, Wong LY, et al. (2008a) Exposure of the U.S. population to bisphenol A and 

4-tertiary-octylphenol: 2003-2004. Environ Health Perspect 116(1):39-44. 

Cappon GD. (1998) Phosmet: Acute neurotoxicity study. GD Cappon, lead investigator; Gowan 

Co., Yuma, AZ, sponsor). MRID No. 44673301. WIL Research Labs, Ashland OH. Oct 

8, 1998. 

Carwile, Jenny L, Karin B, Michels KB. (2011) Urinary bisphenol A and obesity: NHANES 

2003–2006. Environ Res 111(6):825–830. 

CDC (Centers for Disease Control and Prevention (CDC). (2005) Third national report on human 

exposure to environmental chemicals. Atlanta (GA): CDC, 2005. 

CDC (Centers for Disease Control and Prevention (CDC). (2012) Campaign to prevent 

antimicrobial resistance in healthcare settings. Website accessed 2012. Available 

at http://www.cdc.gov/drugresistance/healthcare/problem.htm. 

Chee-Sanford, J.C., et al. (2001) Occurrence and diversity of tetracycline resistance genes in 

lagoons and groundwater underlying two swine production facilities. Appl Environ 

Microbiol 6(4):1494-1502. 

ChemSec. (2012) Bisphenol A in relining of water pipes. Available 

at http://chemsec.org/images/stories/2011/chemsec/111214_Bisphenol_A_in_relinig_of_

water_pipes_ChemSec.pdf. Accessed June 22, 2012. 

Chen J, Ahn KC, Gee NA, et al. (2008) Triclocarban enhances testosterone action: a new type of 

endocrine disruptor? Endocrinology149(3):1173-1179. 

Chen Y, Xu J, et al. (2011) Decline of sperm quality and testicular function in male mice during 

chronic low-dose exposure to microcystin-LR. Reprod Toxicol 31(4):551-557. 

City of San Diego. (2012) Water purification demonstration project. Website accessed June 20, 

2012. http://www.sandiego.gov/water/waterreuse/demo/index.shtml. Claus Henn B, 

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Ettinger AS, et al. (2010) Early postnatal blood manganese levels and children's 

neurodevelopment. Epidemiology 21(4):433-439. 

Cook JC, Mullin LS, Frame SR, Biegel LB. (1993) Investigation of a mechanism for Leydig cell 

tumorigenesis by linuron in rats. Toxicol Appl Pharmacol 119:195-204. 

County Geologic Atlas. County Geologic Atlas water quality data set. 

Cousins IT, Staples CA, Klecka GM, Mackay1 D. (2002) Multimedia assessment of the 

environmental fate of bisphenol A. Hum Ecol Risk Assess 8(5):1107-1135. 

Dabrowski JM, Bennett ER, Bollen A, Schulz R. (2006) Mitigation of azinphos-methyl in a 

vegetated stream: comparison of runoff- and spray-drift. Chemosphere 62(2):204-212. 

Dayan AD. (2007) Risk assessment of triclosan [Irgasan] in human breast milk. Food Chem 

Toxicol 45:125-129. 

de Moura L, Bahia-Oliveira LMG, Wada MY, et al. (2006) Waterborne toxoplasmosis, Brazil, 

from field to gene. Emerg Infect Dis 12:326-329. 

Deveau M. (2010) Contribution of drinking water to dietary requirements of essential metals. J 

Toxicol Environ Health A 73(2/3):235-241. 

Dodd D, Willson G, Parkinson H, Bermudez E. (2011) Two-year drinking water carcinogenicity 

study of methyl tertiary-butyl ether (MTBE) in Wistar rats. J Appl Toxicol 2011 Dec 7. 

doi:10.1002/jat.1776. [Epub ahead of print]. 

Dorman DC, Wong BA. (2006) Neurotoxicity of inhaled manganese: A reanalysis of human 

exposure arising from showering. Med Hypoth 66(1):199-200. 

Durando M, Kass L, Piva J, et al. (2007) Prenatal Bisphenol A exposure induces preneoplastic 

lesions in the mammary Gland in Wistar Rats. Environ Health Perspect 115(1):80-86. 

Erikson KM, Thompson K, et al. (2007) Manganese neurotoxicity: a focus on the neonate. 

Pharmacol Ther 113(2):369-377. 

EXTOXNET (Extension Toxicology Network) (EXTOXNET). (1996) Pesticide information 

profiles. June 1996. Available at http://extoxnet.orst.edu/pips/linuron.htm. 

Fair PA, Lee H, Adams J, et al. (2009) Occurrence of triclosan in plasma of wild Atlantic 

bottlenose dolphins (Tursiops truncatus) and in their environment. Environ Poll 

157:2248-2254. 

Fiore MC, Anderson HA, Hong R, et al. (1986) Chronic exposure to aldicarb-contaminated 

groundwater and human immune function. Environ Res 41(2):633-645. 

Fong, et al. (1998) USGS Water-Resources Investigation WRI 98-4248. 

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Fordahl S, Cooney P, et al. (2012) Waterborne manganese exposure alters plasma, brain, and 

liver metabolites accompanied by changes in stereotypic behaviors. Neurotoxicol Teratol 

34(1):27-36. 

Francy et al. (2000). 

Francy et al. (2004). 

Fromme H, Kuchler T, Otto T, et al. (2002) Occurrence of phthalates and bisphenol A and F in 

the environment. Water Res 36(6):1429-1438. 

Gatidou G, Thomaidis NS, Stasinakis AS, Lekkas TD. (2006) Simultaneous determination of the 

endocrine disrupting compounds nonylphenol, nonylphenol ethoxylates, triclosan and 

bisphenol A in wastewater and sewage sludge by gas chromatography-mass 

spectrometry. J Chromatogr A. 

Gibbons et al., (2010) via UCMR3 USEPA (2011). 

Gilchrist MJ, Greko C, Wallinga DB, et al. (2007) The potential role of concentrated animal 

feeding operations in infectious disease epidemics and antibiotic resistance. Environ 

Health Perspect 115(2):313-316. 

Goeppert N, Goldscheider, N. (2011) Transport and variability of fecal bacteria in carbonate 

conglomerate aquifers. Groundwater 49(1):77-84. 

Golub MS, Hogrefe CE, et al. (2005) Neurobehavioral evaluation of rhesus monkey infants fed 

cow's milk formula, soy formula, or soy formula with added manganese. Neurotoxicol 

Teratol 27(4):615-627. 

Goss DW. (1992) Screening procedure for soil and pesticides relative to potential water quality 

impacts. Weed Technol 6:701-408. 

Graham et al. (2004) Environmental factors influencing microcystin distribution and 

concentration in the Midwestern United States. Water Res 38(20):4395-4404. 

Gray LE Jr, Ostby J, Furr J, et al. (2000) Perinatal exposure to the phthalates DEHP, BBP, and 

DINP, but not DEP, DMP, or DOTP, alters sexual differentiation of the male rat. Toxicol 

Sci 58(2):350-365. 

Gray LE Jr, Wilson VS, Stoker T, et al. (2006) Adverse effects of environmental antiandrogens 

and androgens on reproductive development in mammals. Int J Androl 29(1):96-108. 

Gray LE Jr, Wolf C, Lambright C, et al. (1999) Administration of potentially antiandrogenic 

pesticides (procymidone, linuron, iprodione, chlozolinate, p,p'-DDE, and ketoconazole) 

and toxic substances (dibutyl- and diethylhexyl phthalate, PCB 169, and ethane 

dimethane sulphonate) during sexual differentiation produces diverse profiles of 

reproductive malformations in the male rat. Toxicol Ind Health 15(1-2):94-118. 

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Grendon J, Frost F, Baum L. (1994) Chronic health effects among sheep and humans surviving 

an aldicarb poisoning incident. Vet Hum Toxicol 36(3):218-223. 

Greyshock AE, Vikesland PJ. (2006) Triclosan reactivity in chloraminated waters. Environ Sci 

Technol 40(8):2615-2622. 

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Monitoring and Assessment Program). Ambient groundwater samples collected from 

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Hajoui O, Flipo D, Mansour S, et al. (1992) Immunotoxicity of subchronic versus chronic 

exposure to aldicarb in mice. Int J Immunopharmacol 14(7):1203-1211. 

Halden RU, Paull DH. (2004) Analysis of triclocarban in aquatic samples by liquid 

chromatography electrospray ionization mass spectrometry. Environ Sci Technol 

38(18):4849-4855. 

Halden RU, Paull DH. (2005) Co-occurrence of triclocarban and triclosan in U.S. water 

resources. Environ Sci Technol 15;39(6):1420-1426. 

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medium-term multi-organ bioassay in rats. Int J Cancer 54(3):489-493. (Erratum in: Int J 

Cancer 55(3):528. 

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Antibiotics, 2005. Available 

at http://www.noharm.org/details.cfm?ID=938&type=document. 

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Available at http://www.noharm.org/us/food/issue. 

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Antibiotics. What Health Care Food Systems Can Do. Health Care Without Harm, 

Arlington, VA. Available at http://www.diningatpenn.com/penn/env/poultry/poultry--

health_care_without_harm.pdf. 

Heidler J, Sapkota A, Halden RU. (2006) Partitioning, persistence, and accumulation in digested 

sludge of the topical antiseptic triclocarban during wastewater treatment. Environ Sci 

Technol 40(11):3634-3639. 

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Haz Mater 180(1-3):628-633. 

Ho SM, Tang WY, Belmonte de Frausto J, Prins GS. (2006) Developmental exposure to 

estradiol and bisphenol A increases susceptibility to prostate carcinogenesis and 

epigenetically regulates phosphodiesterase type 4 variant 4. Cancer Res 66(11):5624-

5632. 

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Hoekstra PF, Burnison BK, Garrison AW, et al. (2005) Estrogenic activity of dicofol with the 

human estrogen receptor: Isomer- and enantiomer-specific implications. Chemosphere 

64(1):174-177. Epub 2005 Dec 7. 

Hotchkiss AK, Lambright CS, Ostby JS, et al. (2007) Prenatal testosterone exposure permanently 

masculinizes anogenital distance, nipple development, and reproductive tract morphology 

in female Sprague-Dawley rats. Toxicol Sci 96(2):335-345. 

Hovander L, Malmberg T, Athanasiadou M, et al. (2002) Identification of hydroxylated PCB 

metabolites and other phenolic halogenated pollutants in human blood plasma. Arch 

Environ Contam Toxicol 42:105–117. 

Hunt PA, Koehler KE, Susiarjo M, et al. (2003) Bisphenol A exposure causes meiotic 

aneuploidy in the female mouse. Curr Biol 13(7):546-553. 

IHCP (Institute for Health and Consumer Protection (IHCP)., European Commission Joint 

Research Centre, Institute for Health and Consumer Protection. (2003) 1,2-

Benzenedicarboxylic acid,Di-C8-10-branched alkyl esters, C9-rich and di-“isononyl” 

phthalate (DINP), CAS Nos: 68515-48-0 and 28553-12-0, EINECS Nos: 271-090-9 and 

249-079-5, Summary risk assessment report. European Commission Joint Research 

Centre. Available at http://ecb.jrc.it/DOCUMENTS/ExistingChemicals/RISK_ASSESSMENT/SUMMARY/dinpsum046.pdf. 

Ishihara A, Sawatsubashi S, Yamauchi K. (2003) Endocrine disrupting chemicals: interference of 

thyroid hormone binding to transthyretins and to thyroid hormone receptors. Mol Cell 

Endocrinol 199(1-2):105-117. 

Jacobs MN, Nolan GT, Hood SR. (2005) Lignans, bacteriocides and organochlorine compounds 

activate the human pregnane X receptor (PXR). Toxicol Appl Pharmacol 209(2):123-133. 

Jadaramkunti UC, Kaliwal BB. (2001) Possible mechanisms for the anti-implantation action of 

dicofol in albino rats. J Basic Clin Physiol Pharmacol 12(3):217-226. 

Jiang SC. (2006) Human adenoviruses in water: occurrence and health implications: a critical 

review. Environ Sci Technol 40:7132–7140. 

Jones JL, Dubey, JP. (2010) Waterborne toxoplasmosis - recent developments. Parasitol 124:10-

25. 

Katayama H, Haramoto E, Oguma, K et al. (2008) One-year monthly quantitative survey of 

noroviruses, enteroviruses, and adenoviruses in wastewater collected from six plants in 

Japan. Water Res 42:1441-1448. 

Kern CH, Stanwood GD, et al. (2010) Preweaning manganese exposure causes hyperactivity, 

disinhibition, and spatial learning and memory deficits associated with altered dopamine 

receptor and transporter levels. Synapse 64(5): 363-378. 

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Khan K, Factor-Litvak P, et al. (2011) Manganese exposure from drinking water and children's 

classroom behavior in Bangladesh. Environ Health Perspect 119(10):1501-1506. 

Khan K, Wasserman Kim Y, Kim BN, et al. (2009) Co-exposure to environmental lead and 

manganese affects the intelligence of school-aged children. Neurotoxicology 30(4):564-

571. 

Kolpin DW, Furlong ET, Meyer MT, et al. (2002) Pharmaceuticals, hormones, and other organic 

wastewater contaminants in U.S. streams, 1999-2000: a national reconnaissance. Environ 

Sci Technol 6(6):1202-1211. 

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A5-8
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

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A5-9
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

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EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

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EPA 815-R-15-001

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EPA 815-R-15-001

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93

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EPA 815-R-15-001

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and neonatal manganese exposure in humans: describing manganese homeostasis during 

development. Toxicol Sci 122(2):297-316. 

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EPA 815-R-15-001

Appendix 6: Outcome of Nominated Chemicals in the CCL 4 Process

CASRN Common Name – 

Registry Name

NPDWR 

or 

Proposed 

NPDWR

CCL 3 

Universe

CCL 4 

Universe PCCL 3 PCCL 4 Final CCL 3

Draft 

CCL 4

54 54 4 40 43 18 20 5 7

77439-

76-0 

3-chloro-4-

dichloromethyl-5-

hydroxy-2(5H)-

furanone

blank X X blank blank blank blank

319-84-6 alphaHexachlorocyclohexan

e

blank X X X X X X 

116-06-3 Aldicarb X blank blank blank blank blank blank

68555-

24-8

Alkylphenol mono- to 

tri-oxylates blank blank blank blank blank blank blank

26787-

78-0

Amoxicillin blank blank blank blank blank blank blank

86-50-0 Azinphos-methyl blank X X X X blank blank

1405-89-

6

Bacitracin zinc blank blank blank blank blank blank blank

25057-

89-0

Bentazone blank X X X X blank blank

85-68-7 Benzyl butyl phthalate blank X X X X blank blank

80-05-7 Bisphenol A blank X X X X blank blank

1689-84-

5

Bromoxynil blank X X blank blank

63-25-2 Carbaryl blank X X X X blank blank

10045-

97-3 

Cesium 137 X blank blank blank blank blank blank

1897-45-

6

Chlorothalonil blank X X X X blank blank

2921-88-

2

Chlorpyrifos blank X X blank blank blank blank

84-74-2 Dibutyl phthalate blank X X blank blank blank blank

1918-00-

9

Dicamba blank X X blank blank blank blank

62-73-7 Dichlorvos blank X X X X blank blank

115-32-2 Dicofol blank X X X X blank blank

84-61-7 Dicyclohexyl phthalate blank X X blank blank blank blank

84-66-2 Diethyl phthalate blank X X blank blank blank blank

28553-

12-0

Di-isononyl phthalate blank X X blank blank blank blank

131-11-3 Dimethyl phthalate blank X X blank blank blank blank

117-84-0 Di-n-octyl phthalate blank X X blank blank blank blank

115-29-7 Endosulfan blank X X X X blank blank

2164-17-

2

Fluometuron blank X X X X blank blank

165800-

03-3

Linezolid blank blank blank blank blank blank blank

330-55-2 Linuron blank X X X X blank blank

A6-1
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

CASRN Common Name – 

Registry Name

NPDWR 

or 

Proposed 

NPDWR

CCL 3 

Universe

CCL 4 

Universe PCCL 3 PCCL 4 Final CCL 3

Draft 

CCL 4

121-75-5 Malathion blank X X X X blank blank

7439-96-

5

Manganese blank X X blank X blank X 

61-32-5 Methicillin blank blank blank blank blank

298-00-0 Methyl parathion blank X X blank blank blank blank

1634-04-

4

Methyl tertiary butyl 

ether (MTBE) blank X X X X X X 

101043-

37-2

Microcystin-LR blank X X X X X X 

25154-

52-3

Nonylphenol blank X X blank X X 

9016-45-

9

Nonylphenol ethoxylate blank X X blank blank blank blank

27193-

28-8

Octylphenol blank X X blank blank blank blank

9036-19-

5

Octylphenol ethoxylate blank X blank blank blank blank

66-79-5 Oxacillin blank X blank blank blank blank

(multiple 

CASRNs

)

Penicillin 

blank X X blank blank blank blank

335-67-1 Perfluorooctanoic acid 

(PFOA) blank X X X X X X 

52645-

53-1

Permethrin blank X X X X X X 

732-11-6 Phosmet blank X X X X

57-83-0 Progesterone blank X X blank blank blank blank

10043-

92-2

Radon X blank blank blank blank blank blank

8025-81-

8

Spiramycin blank nk blank blank blank blank blank blank

121831-

99-0

Strontium 90 X blank blank blank blank blank blank

58-22-0 Testosterone blank X X blank blank blank blank

52-68-6 Trichlorfon blank X X blank blank blank blank

101-20-2 Triclocarban blank X X blank blank blank blank

3380-34-

5

Triclosan blank X X blank blank blank blank

1401-69-

0

Tylosin blank X X blank blank blank blank

1404-90-

6

Vancomycin blank blank blank blank blank blank blank

11006-

76-1

Virginiamycin blank blank X blank blank blank blank

A6-2
EPA-OGWDW Summary of Nominations for the

Fourth Contaminant Candidate List

EPA 815-R-15-001

Appendix 7: Outcome of Nominated Microbes in the CCL 4 Process

Microbe CCL 3 

Universe

CCL 4 

Universe PCCL 3 PCCL 4 Final

CCL 3

Draft

CCL 4

Adenovirus x x x x x x 

Naegleria fowleri x x x x x x 

Toxoplasma gondii x x x x blank blank

Vibrio cholerae x x x x blank blank

Heterotrophic plate 

count (HPC)

blank blank blank blank blank blank

A7-1