&EPA
united states Summary oi
Environmental Protection J
Agency Nominations for the
Fourth Contaminant
Candidate List
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Office of Water (4607M)
EPA 815-R-15-001
January 2015
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EPA-OGWDW Summary of Nominations for the EPA 815-R-15-001
Fourth Contaminant Candidate List
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-l
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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EPA-OGWDW
Summary of Nominations for the
Fourth Contaminant Candidate List
EPA 815-R-15-001
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 Reregi strati on 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)(l) of the Safe Drinking Water Act (SOWA), 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/contaminant-
candidate-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)(l)(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)(l)(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-l)
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-HQ-
OW-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)(l));
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), alpha-
hexachlorocyclohexane 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
*alpha-hexachlorocyclohexane
manganese
*methyl tertiary butyl ether (MTBE)
*microcystin-LR
nonylphenol
*perfluorooctanoic acid (PFOA)
*permethrin
CASRN
319-84-6
7439-96-5
1634-04-4
101043-37-2
25154-52-3
335-67-1
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, Naegleriafowleri, 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 Naegleriafowleri
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 3Final. 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
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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 aldicarb-
induced 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,N-
dipropylthiocarbamate (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
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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
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.
68555-24-8
Alkylphenol mono-
to 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 pM for
octylphenol and 1 pM 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
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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 azinphos-
methyl 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~imethyl on apples (the most
frequently treated crop) at application rates equal to or higher than
those for peaches (1.0-1.5 Ib ai/A per application, 4.5 Ib ai/A per year
maximum on apples vs. 1.125 Ibs ai/A per application, 4.5 Ibs ai/A per
year maximum on peaches). Furthermore, the total amount of
azinphos-methyl used on apples (890,000 Ib active ingredient) is over
seven times the amount used on peaches (120,000 Ib). 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
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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
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.
25057-89-0
Bentazone
AWWA
None given
None given
None given
85-68-7
Benzyl butyl
phthalate
Natural Resources
Defense Council
Phthalates are endocrine disrupters 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 disrupter 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 (AGO), 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
A1-5
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
-------
EPA-OGWDW
Summary of Nominations for the
Fourth Contaminant Candidate List
EPA 815-R-15-001
CASRN
80-05-7
80-05-7
1689-84-5
63-25-2
Common Name
Bisphenol A
Bisphenol A
Bromoxynil
Carbaryl
Nominator
Anonymous 201
Natural Resources
Defense Council
AWWA
AWWA
Health Effects Information Provided with
Nomination
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.]
Weak endocrine disrupter - 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.
A number of recent studies have revealed that early life exposures to low-
doses 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.
None given
None given
Occurrence Information Provided
with Nomination
None given
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 3,41 0 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, 201 1 , 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.
None given
None given
Additional Information
Provided
with Nomination
None given
Bisphenol A -
(4,4'-(1-ethylethylidene)bisphenol
or 4,4'-lsopropylidenediphenol),
(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.
None given
None given
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EPA-OGWDW
Summary of Nominations for the
Fourth Contaminant Candidate List
EPA 815-R-15-001
CASRN
63-25-2
10045-97-3
1897-45-6
2821-88-2
Common Name
Carbaryl
Cesium 137
Chlorothalonil
Chlorpyrifos
Nominator
Natural Resources
Defense Council
Anonymous 197
AWWA
AWWA
Health Effects Information Provided with
Nomination
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.
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.
None given
None given
Occurrence Information Provided
with Nomination
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 non-
agricultural 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.
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.
None given
None given
Additional Information
Provided
with Nomination
None given
Monitoring existing conditions
leads to rate of change analysis
when done on a predictable time
frame.
None given
None given
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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.
EPAs 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 EPAs 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
EPAs 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 Mid-
Continent 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. EPAs
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
84-74-2
1918-00-9
62-73-7
Common Name
Dibutyl phthalate
Dicamba
Dichlorvos
Nominator
Natural Resources
Defense Council
AWWA
Natural Resources
Defense Council
Health Effects Information Provided with
Nomination
Phthalates are endocrine disrupters 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 disrupter 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 (AGO), 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.]
None given
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
Occurrence Information Provided
with Nomination
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 201 2:
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
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
Additional Information
Provided
with Nomination
None given
None given
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
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.
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 disrupter 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 PRZM-
EXAMS 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 disrupters 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,
A1-10
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
-------
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
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 disrupter 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 (AGO), 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.
84-66-2
Diethyl phthalate
Natural Resources
Defense Council
Phthalates are endocrine disrupters 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 disrupter 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 (AGO), 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
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
was1000ug/L.
28553-12-0
Di-isononyl
phthalate
Natural Resources
Defense Council
Phthalates are endocrine disrupters 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 disrupter 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 (AGO), 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
A1-12
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-BranchedAlkyl
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/Existing-
None given
-------
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 disrupters 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 disrupter 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 (AGO), 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 disrupters 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 disrupter 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 (AGO), 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 disrupter,
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
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EPA-OGWDW
Summary of Nominations for the
Fourth Contaminant Candidate List
EPA 815-R-15-001
CASRN
2164-17-2
319-84-6
165800-03-3
330-55-2
Common Name
Fluometuron
Hexachlorocyclohe
xane (alpha
isomer)
Linezolid
Linuron
Nominator
AWWA
AWWA
Natural Resources
Defense Council
Natural Resources
Defense Council
Health Effects Information Provided with
Nomination
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 disrupter 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.
None given
None given
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.
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
Occurrence Information Provided
with Nomination
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 forthis population.
None given
None given
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.
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 (LOG) for groundwater quality. EPA
also expressed "moderate concerns" for drinking water supply systems
relying on surface water sources.
Additional Information
Provided
with Nomination
None given
None given
None given
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
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 EPAs 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 EPAs
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
A1-16
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,
-------
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
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.
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 etal, 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
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 EPAs 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 (Hoet 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 etal, 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
A1-19
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 microcystin-
LR 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 microcystin-
LR 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
-------
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
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,etal,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 pM for
octylphenol and 1 pM 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 pM for
octylphenol and 1 pM 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 pM for
octylphenol and 1 pM 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 pM for
octylphenol and 1 pM 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 serurrrdrinking 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.
A1-22
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
-------
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
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Occurrence Information Provided
with Nomination
Additional Information
Provided
with Nomination
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
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
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.
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 N J 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.
A1-24
Antibiotics are found in wast ewater 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
-------
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
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.
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 non-
food 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 disrupter
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
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Occurrence Information Provided
with Nomination
Additional Information
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with Nomination
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.
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 pg/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
A1-27
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
-------
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
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.
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
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.
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 Gl 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 UVdose
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
Naegleria fowleri
Toxoplasma
gondii
Toxoplasma
gondii
Vibrio choleras
Nominator
NJ Dept. of
Environmental
Protection
J. Jones
US Dept. of
Agriculture
Natural Resources
Defense Council
Health Effects Information Provided withNomination
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.
Ocular and congenital illness
Many outbreaks causing serious disease in humans detailed.
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.
Occurrence Information Provided with Nomination
Although in the US, there is a 14-year average of just 2 cases
of primary amoebic meningoencephalitis per year, 11 of 1 43
wells (8%), with an average water temperature of 29 oC were
found to contain Naegleria.
Waterborne Toxoplasma gondii has been implicated in other
countries and could contaminate drinking water that is not
filtered.
[See (de Moura et al., 2006) in Appendix 5]
As recently as April 201 1 , an outbreak of Vibrio cholerae 075
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.
Additional Information Provided with Nomination
Because 1 1 of 1 43 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).
None given
None given
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
77439-76-0
116-06-03
116-06-3
68555-24-8
26787-78-0
86-50-0
1405-89-6
25057-89-0
85-68-7
Contaminant Name
3-chloro-4-dichloromethyl-5-
hydroxy-2(5H)-furanone)
Aldicarb
Aldicarb
Alkylphenol mono- to tri-
oxylates
Amoxicillin
Azinphos-methyl
Bacitracin zinc
Bentazone
Benzyl butyl phthalate
Nominating Individual
Thomas W. Curtis
Thomas W. Curtis
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Thomas W. Curtis
Mae C. Wu & Jennifer
Sass
Organization Name
AWWA
AWWA
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
AWWA
Natural Resources
Defense Council
Abbreviated References
Cited in the Nomination
None given
None given
(Fioreetal., 1986)
(Grendon and Baum,
1994)
(Hajoui etal., 1992)
(Smuldersetal., 2003)
(Smuldersetal., 2004)
(USEPA, 1984)
(USEPA, 1988)
(USEPA, 2006)
(USEPA, 2006a)
(Gatidouetal., 2006)
(Ying etal. ,2002)
(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)
(Wallingaetal., 2006)
(Wallinga, 2005)
(Dabrowski etal., 2006)
(Loewy etal., 2003)
(Loewy etal., 2006)
(Rohlmanet al., 2005)
(Rothleinetal., 2006)
(Souza etal., 2004)
(Souzaet al., 2005)
(USEPA, 2001 a)
(USEPA, 2006a)
(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)
None given
(ATSDR)
(CDC, 2005)
(Gray etal., 2000)
(Gray etal., 2006)
(Main et al., 2006)
(Meeker etal., 2007)
(Stahlhutetal., 2007)
(USEPA)
A3-1
-------
EPA-OGWDW
Summary of Nominations for the
Fourth Contaminant Candidate List
EPA 815-R-15-001
CASRN
80-05-7
80-05-7
1689-84-5
63-25-2
63-25-2
10045-97-3
1897-45-6
2921-88-2
2921-88-2
84-74-2
1918-00-9
Contaminant Name
Bisphenol A
Bisphenol A
Bromoxynil
Carbaryl
Carbaryl
Cesium 137
Chlorothalonil
Chlorpyrifos
Chlorpyrifos
Dibutyl phthalate
Dicamba
Nominating Individual
Anonymous 201
Mae C. Wu & Jennifer
Sass
Thomas W. Curtis
Thomas W. Curtis
Mae C. Wu & Jennifer
Sass
Anonymous 197
Thomas W. Curtis
Thomas W. Curtis
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Thomas W. Curtis
Organization Name
None given
Natural Resources
Defense Council
AWWA
AWWA
Natural Resources
Defense Council
None given
AWWA
AWWA
Natural Resources
Defense Council
Natural Resources
Defense Council
AWWA
Abbreviated References
Cited in the Nomination
None given
(Adewaleetal.,2011a)
(Alonso-Magdalena et al.,
2006)
(Ayyanan et al., 201 1b)
(Calafatetal., 2008a)
(Carwile and Michels,
2011)
(ChemSec, 2012)
(Cousins et al., 2002)
(Durando et al., 2007)
(Frommeet al., 2002)
(Hoet al., 2006)
(Hunt et al., 2003)
(Melzeretal.,2012)
(Murray etal., 2007)
(National Institute of
Environmental Health
Sciences, 2008)
(Prins etal., 2011)
(Raloff, 2012)
(Sorianoet al., 2012)
(USEPA)
(vom Saal etal., 2007)
None given
None given
(Tarplee, 1999)
(Tarplee, 2001)
(USEPA, 2004a)
None given
None given
None given
(Barbasand Resek, 1996)
(Becker etal., 1989)
(Burkart and Kolpin, 1993)
(Goss, 1992)
(Larson, etal., 1997)
(Long, 1989)
(Makris et al., 1998)
(USEPA, 2000a)
(USEPA, 2002)
(USEPA, 2002a)
(ATSDR)
(CDC, 2005)
(Gray etal., 2000)
(Gray etal., 2006)
(IHCP, 2003)
(Main et al., 2006)
(Meeker etal., 2007)
(Stahlhutetal., 2007)
(USEPA)
None given
A3-2
-------
EPA-OGWDW
Summary of Nominations for the
Fourth Contaminant Candidate List
EPA 815-R-15-001
CASRN
62-73-7
115-32-2
84-61-7
84-66-2
28553-12-0
131-11-3
117-84-0
Contaminant Name
Dichlorvos
Dicofol
Dicyclohexyl phthalate
Diethyl phthalate
Di-isononyl phthalate
Dimethyl phthalate
Di-n-octyl phthalate
Nominating Individual
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Organization Name
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Abbreviated References
Cited in the Nomination
(Brown et al., 1990)
(Leissand Savitz, 1995)
(National Toxicology
Program, 1989)
(USEPA, 2000b)
(USEPA, 2000c)
(USEPA, 2006b)
(Hoekstra et al. 2005)
(Ishiharaetal., 2003)
(Jadaramkunti and Kaliwal,
2001)
(Thibaut and Porte, 2004)
(USEPA, 1998)
(ATSDR)
(CDC, 2005)
(Grayetal., 2000)
(Grayetal., 2006)
(Main et al., 2006)
(Meeker etal., 2007)
(Stahlhutetal., 2007)
(ATSDR)
(CDC, 2005)
(Grayetal., 2000)
(Grayetal., 2006)
(Main et al., 2006)
(Meeker etal., 2007)
(Stahlhutetal., 2007)
(USEPA)
(ATSDR)
(CDC, 2005)
(Grayetal., 2000)
(Grayetal., 2006)
(IHCP, 2003)
(Main et al., 2006)
(Meeker etal., 2007)
(Stahlhut et al., 2007)
(USEPA)
(ATSDR)
(CDC, 2005)
(Grayetal., 2000)
(Grayetal., 2006)
(Main et al., 2006)
(Meeker etal., 2007)
(Stahlhutetal., 2007)
(USEPA)
(ATSDR)
(CDC, 2005)
(Grayetal., 2000)
(Grayetal., 2006)
(Main et al., 2006)
(Meeker etal., 2007)
(Stahlhutetal., 2007)
(USEPA)
A3-3
-------
EPA-OGWDW
Summary of Nominations for the
Fourth Contaminant Candidate List
EPA 815-R-15-001
CASRN
115-29-7
2164-17-2
319-84-6
165800-03-3
330-55-2
121-75-5
Contaminant Name
Endosulfan
Fluometuron
Hexachlorocyclohexane
(alpha isomer)
Linezolid
Linuron
Malathion
Nominating Individual
Mae C. Wu & Jennifer
Sass
Thomas W. Curtis
Thomas W. Curtis
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Thomas W. Curtis
Organization Name
Natural Resources
Defense Council
AWWA
AWWA
Natural Resources
Defense Council
Natural Resources
Defense Council
AWWA
Abbreviated References
Cited in the Nomination
(Association of American
Pesticide Control Officials,
Inc, 1969)
(Lakshmana and Raju,
1994)
(OSHA, 1989)
(Sinhaetal., 1991)
(Sinhaetal., 1997)
(State of California:
Department of Industrial
Relations)
(USEPA, 2002b)
(Willey and Kron, 2001)
(Wilson and LeBlanc,
1998)
None given
None given
(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)
(Cook, 1993)
(EXTOXNET, 1996)
(Grayetal., 1999)
(USEPA, 1995)
(USEPA, 2002c)
(USGS, 1992)
None given
A3-4
-------
EPA-OGWDW
Summary of Nominations for the
Fourth Contaminant Candidate List
EPA 815-R-15-001
CASRN
7439-96-5
Contaminant Name
Manganese
Nominating Individual
Michael S. Hutcheson
Organization Name
Massachusetts
Department of
Environmental
Protection
Abbreviated References
Cited in the Nomination
(Ayotte, etal., 2001)
(Bouchard et al., 2007)
(Bouchard et al., 2011)
(Boyes, 2010)
(Brown and Foos, 2009)
(Glaus etal. ,2010)
(Deveau, 2010)
(Dorman and Wong, 2006)
(Eriksonetal., 2007)
(Fordahlet al., 2012)
(Golub et al., 2005)
(Kern etal., 2010)
(Khan etal., 2011)
(Khan etal., 201 2)
(Kim et al., 2009)
(Ljung etal., 2009)
(Ljung, 2007)
(Menezes-Filho et al.,
2009)
(Moreno et al., 2009)
(Parvez et al., 2011)
(Riojas-Rodriguez et al.,
2010)
(Roelsetal.,2012)
(Santamaria and Sulsky,
2010)
(Santamaria, 2008)
(USEPA, 1979)
(USEPA, 2004b)
(Wasserman et al., 2006)
(Wasserman et al., 2011)
(Yoon etal., 2011)
(Yoon et al., 2009)
A3-5
-------
EPA-OGWDW
Summary of Nominations for the
Fourth Contaminant Candidate List
EPA 815-R-15-001
CASRN
7439-96-5
7439-96-5
61-32-5
298-00-0
1634-04-4
Contaminant Name
Manganese
Manganese
Methicillin
methyl parathion
Methyl tertiary butyl ether
Nominating Individual
James Kelly
Gloria B. Post
Mae C. Wu & Jennifer
Sass
Thomas W. Curtis
Gloria B. Post
Organization Name
Minnesota
Department of Health
NJ Department of
Environmental
Protection
Natural Resources
Defense Council
AWWA
NJ Department of
Environmental
Protection
Abbreviated References
Cited in the Nomination
(Anoka County, 2004)
(Ayotte, etal., 2001)
(Bouchard et al., 2007)
(Bouchard et al., 2011)
(Boyes, 2010)
(Brown and Foos, 2009)
(Glaus etal. ,2010)
(County Geologic Atlas)
(Deveau, 2010)
(Dorman and Wong, 2006)
(Erikson etal. ,2007)
(Fong, etal., 1998)
(Fordahlet al., 2012)
(Golub et al., 2005)
(GWMAP)
(Kern etal., 2010)
(Khan etal., 2011)
(Khan etal., 201 2)
(Kim et al., 2009)
(Lively etal., 1992)
(Ljungetal., 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)
(Yoonetal., 2011)
(Yoon et al., 2009)
(Bouchard et al., 2011)
(Khan etal., 2011)
(Wasserman et al., 201 1)
(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)
None given
(Bird etal., 1997)
(Doddetal., 2011)
(Ramazzini Institute Study)
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Summary of Nominations for the
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EPA 815-R-15-001
CASRN
101043-37-2
101043-37-2
25154-52-3
9016-45-9
27193-28-8
9036-19-5
66-79-5
multiple CAS #s
Contaminant Name
Microcystin-LR
Microcystin-LR
Nonylphenol
Nonylphenol ethoxylate
Octylphenol
Octylphenol ethoxylate
Oxacillin
Penicillin
Nominating Individual
Christopher Greene
James Kelly
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Organization Name
Minnesota
Department of Health
Minnesota
Department of Health
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Abbreviated References
Cited in the Nomination
(Barringer, 2012)
(Billam et al., 2006)
(Boyeretal.,2005)
(Chen etal., 2011)
(City of San Diego, 2012)
(Graham et al., 2004)
(Ho L, etal., 2010)
(Li etal., 2008)
(Liu etal. ,2010)
(Ohio EPA, 2012)
(Trinchetetal., 2011)
(Uenoetal., 1999)
(Wang etal., 201 2)
(Boyeretal.,2005)
(Chen etal., 2011)
(City of San Diego, 2012)
(Graham etal., 2004)
(Ho L, etal., 2010)
(Li etal., 2008)
(Liu etal., 2010)
(Ohio EPA, 2012)
(Trinchetetal., 2011)
(Uenoetal., 1999)
(Wang etal., 201 2)
(Gatidouetal., 2006)
(Ying etal. ,2002)
(Gatidou et al., 2006)
(Ying etal. ,2002)
(Gatidouetal., 2006)
(Ying etal. ,2002)
(Gatidou et al., 2006)
(Ying etal. ,2002)
(CDC, 2012)
(Chee-Sanford etal.,
2001)
(Gilchrist etal., 2007)
(Health Care Without
Harm, 2005)
(Mellon et al., 2000)
(Sapkotaetal., 2007a)
(USA Today, 2000)
(Wallinga et al., 2006)
(Wallinga, 2005)
(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 etal., 2006)
(Wallinga, 2005)
A3-7
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EPA-OGWDW
Summary of Nominations for the
Fourth Contaminant Candidate List
EPA 815-R-15-001
CASRN
68141-02-6
52645-53-1
732-11-6
multiple CAS #s
57-83-0
10043-92-2
8025-81-8
121831-99-0
58-22-0
52-68-6
101-20-2
Contaminant Name
Perfluoro octanoic acid
Permethrin
Phosmet
PhthalatesS
Progesterone
Radon
Spiramycin
Strontium 90
Testosterone
Trichlorfon
Triclocarban
Nominating Individual
Eileen Murphy
Thomas W. Curtis
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Gloria B. Post
Mae C. Wu & Jennifer
Sass
Anonymous 197
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Organization Name
None given
AWWA
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
NJ Department of
Environmental
Protection
Natural Resources
Defense Council
None given
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Abbreviated References
Cited in the Nomination
(C8 Science Panel, 2012)
(Postetal., 2009)
None given
(C8 Science Panel, 2012)
(Minetal., 2012)
(Postetal. ,2012)
None given
(Cappon, 1998)
(Hasegawaet al., 1993)
(Raffaele, 1999)
(Raffaele, 2002)
(Souza et al., 2005)
(Swartz, 1999)
(Taylor, 1999)
(USEPA, 2001 b)
(Vlckovaetal., 1993)
(Adibietal.,2003)
(Blount et al., 2000)
(Meeker etal., 2007)
(Silva et al., 2007)
(Stahlhut RW, et al., 2007)
(Wolff etal., 2007)
(Hotchkissetal., 2007)
(Kolpin et al., 2002)
(New Jersey Drinking
Water Quality Institute,
2009)
(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)
None given
(Hotchkissetal., 2007)
(Kolpin et al., 2002)
(USEPA, 1997)
(USEPA, 1997)
(Chen et al., 2008)
(Halden and Paull, 2004)
(Halden and Paull, 2005)
(Heidler etal. ,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.
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EPA 815-R-15-001
CASRN
3380-34-5
1401-69-0
1404-90-6
11006-76-1
Contaminant Name
Triclosan
Tylosin
Vancomycin
Virginiamycin
Nominating Individual
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Mae C. Wu & Jennifer
Sass
Organization Name
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Natural Resources
Defense Council
Abbreviated References
Cited in the Nomination
(Boydetal.,2003)
(Boydetal.,2004)
(Calafatetal.,2008b)
(Dayan, 2007)
(Fair etal., 2009)
(Greyshock and Vikesland,
2006)
(Hovanderetal.,2002)
(Jacobs etal., 2005)
(Kolpin, etal., 2002)
(Latch et al., 2005)
(Loraine and Pettigrove,
2006)
(Veldhoen etal., 2006)
(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)
(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 etal., 2006)
(Wallinga, 2005)
(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 etal., 2006)
(Wallinga, 2005)
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EPA 815-R-15-001
Appendix 4. References Provided with Microbial Nominations
Contaminant Name
Adenovirus
HPC Heterotrophic Plate Count
Bacteria
Naegleria fowleri
Toxoplasma gondii
Toxoplasma gondii
Vibrio cholerae
Nominating Individual
Thomas B. Atherholt
Thomas B. Atherholt
Thomas B. Atherholt
J. Jones
Jitender P.Dubey
Mae C. Wu & Jennifer Sass
Organization Name
NJ Department of
Environmental Protection
NJ Department of
Environmental Protection
NJ Department of
Environmental Protection
None given
U.S. Department of Agriculture
Natural Resources Defense
Council
Abbreviated References Cited
in the Nomination
(Atkinson, 2012)
(Borchart et al., 2008)
(Gibbons etal., 2010)
(Jiang, 2006)
(Katayamaetal., 2008)
(Langley, 2005)
(Post etal., 2011)
(Rodriguez et al., 2008)
(USEPA, 2006)
(USEPA, 2011)
(Atherholt etal., 2003)
(But scher etal., 2011)
(Francy et al., 2000)
(Francyetal., 2004)
(Goeppert et al., 2011)
(Blair etal., 2008)
(Post etal., 2011)
None given
(de Moura et al., 2006)
(Jones etal., 2010)
(Natural Resources Defense
Council, 2010)
(Onifade etal., 2011)
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EPA-OGWDW Summary of Nominations for the EPA 815-R-15-001
Fourth Contaminant Candidate List
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.
Adewale HB, Todd KL, Mickens JA, Patisaul HB. (2011) The impact of neonatal bisphenol-a
exposure on sexually dimorphic hypothalamic nuclei in the female rat. NeuroToxicology
32(l):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 Waterworks 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.nvtimes.com/2012/02/10/science/earth/despite-yuck-factor-treated-
wastewater-used-for-drinking.html? r= 1 &pagewanted=all.
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Fourth Contaminant Candidate List
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 Microcystin-
LR in two lakes in western Texas, USA. Environ Toxicol Chem 25(2):349-355.
Bird etal. (1997).
Blair B, Sarkar P, Bright KR, et al. (2008) Naegleria fowled 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
athttp://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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Fourth Contaminant Candidate List
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(l):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(l):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/l 11214_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 disrupter? Endocrinology 149(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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Fourth Contaminant Candidate List
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, Mackayl 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.!776. [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(l):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(l):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 3 6(6): 1429-143 8.
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(l-2):94-l 18.
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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
Technol40(8):2615-2622.
GWMAP (MinGWMAP. Minnesota Pollution Control Agency, Minesota Ground Water
Monitoring and Assessment Program). Ambient groundwater samples collected from
1989-2001. Minnesota Pollution Control Agency.
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.
Hasegawa R, Cabral R, Hoshiya T, et al. (1993) Carcinogenic potential of some pesticides in a
medium-term multi-organ bioassay in rats. Int J Cancer 54(3):489-493. (Erratum in: Int J
Cancer 55(3):528.
Health Care Without Harm. (2005) Antibiotic Resistance and Agricultural Overuse of
Antibiotics, 2005. Available
at http://www.noharm.org/details.cfm?ID=938&tvpe=document.
Healthcare Without Harm. (2005) Antibiotic Resistance and Agricultural Overuse of Antibiotics.
Available at http://www.noharm.org/us/food/issue.
Health Care Without Harm (2005) Antibiotic Resistance and Agricultural Overuse of
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.
Ho L, et al. (2010) Investigations into the biodegradation of microcystin-LR in wastewaters. J
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A5-6
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EPA-OGWDW Summary of Nominations for the EPA 815-R-15-001
Fourth Contaminant Candidate List
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Fourth Contaminant Candidate List
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EPA-OGWDW Summary of Nominations for the EPA 815-R-15-001
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EPA-OGWDW Summary of Nominations for the EPA 815-R-15-001
Fourth Contaminant Candidate List
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EPA-OGWDW Summary of Nominations for the EPA 815-R-15-001
Fourth Contaminant Candidate List
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Fourth Contaminant Candidate List
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EPA 815-R-15-001
Appendix 6: Outcome of Nominated Chemicals in the CCL 4 Process
CASRN
54
77439-
76-0
319-84-6
116-06-3
68555-
24-8
26787-
78-0
86-50-0
1405-89-
6
25057-
89-0
85-68-7
80-05-7
1689-84-
5
63-25-2
10045-
97-3
1897-45-
6
2921-88-
2
84-74-2
1918-00-
9
62-73-7
115-32-2
84-61-7
84-66-2
28553-
12-0
131-11-3
117-84-0
115-29-7
2164-17-
2
165800-
03-3
330-55-2
Common Name -
Registry Name
54
3-chloro-4-
dichloromethyl-5-
hydroxy-2(5H)-
furanone
alpha-
Hexachlorocyclohexan
e
Aldicarb
Alkylphenol mono- to
tri-oxylates
Amoxicillin
Azinphos-methyl
Bacitracin zinc
Bentazone
Benzyl butyl phthalate
Bisphenol A
Bromoxynil
Carbaryl
Cesium 137
Chlorothalonil
Chlorpyrifos
Dibutyl phthalate
Dicamba
Dichlorvos
Dicofol
Dicyclohexyl phthalate
Diethyl phthalate
Di-isononyl phthalate
Dimethyl phthalate
Di-n-octyl phthalate
Endosulfan
Fluometuron
Linezolid
Linuron
NPDWR
or
Proposed
NPDWR
4
X
X
CCL 3
Universe
40
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
CCL 4
Universe
43
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
PCCL3
18
X
X
X
X
X
X
X
X
X
X
X
X
PCCL4
20
X
X
X
X
X
X
X
X
X
X
X
X
Final
CCL 3
5
X
Draft
CCL 4
7
X
A6-1
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EPA-OGWDW
Summary of Nominations for the
Fourth Contaminant Candidate List
EPA 815-R-15-001
CASRN
121-75-5
7439-96-
5
61-32-5
298-00-0
1634-04-
4
101043-
37-2
25154-
52-3
9016-45-
9
27193-
28-8
9036-19-
5
66-79-5
(multiple
CASRNs
)
335-67-1
52645-
53-1
732-11-6
57-83-0
10043-
92-2
8025-81-
8
121831-
99-0
58-22-0
52-68-6
101-20-2
3380-34-
5
1401-69-
0
1404-90-
6
11006-
76-1
Common Name -
Registry Name
Malathion
Manganese
Methicillin
Methyl parathion
Methyl tertiary butyl
ether (MTBE)
Microcystin-LR
Nonylphenol
Nonylphenol ethoxylate
Octylphenol
Octylphenol ethoxylate
Oxacillin
Penicillin
Perfluorooctanoic acid
(PFOA)
Permethrin
Phosmet
Progesterone
Radon
Spiramycin
Strontium 90
Testosterone
Trichlorfon
Triclocarban
Triclosan
Tylosin
Vancomycin
Virginiamycin
NPDWR
or
Proposed
NPDWR
X
X
CCL3
Universe
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
CCL4
Universe
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
PCCL3
X
X
X
X
X
X
PCCL4
X
X
X
X
X
X
X
X
Final
CCL3
X
X
X
X
Draft
CCL4
X
X
X
X
X
X
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
Adenovirus
Naegleria fowleri
Toxoplasma gondii
Vibrio cholerae
Heterotrophic plate
count (HPC)
CCL 3
Universe
X
X
X
X
CCL 4
Universe
X
X
X
X
PCCL3
X
X
X
X
PCCL4
X
X
X
X
Final
CCL 3
X
X
Draft
CCL 4
X
X
A7-1
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