Drinking Water: Regulatory Determinations Regarding Contaminants on the Second Drinking Water Contaminant Candidate List-Preliminary Determinations

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Federal Register › Vol. 72 › 72 FR 24016

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ENVIRONMENTAL PROTECTION AGENCY 40 CFR Part 141 [EPA-HQ-OW-2007-0068 FRL-8301-3] RIN 2040-AE58 Drinking Water: Regulatory Determinations Regarding Contaminants on the Second Drinking Water Contaminant Candidate List—Preliminary Determinations AGENCY:

Environmental Protection Agency (EPA).

ACTION:

Notice.

SUMMARY:

The Safe Drinking Water Act (SDWA), as amended in 1996, requires the Environmental Protection Agency (EPA) to make regulatory determinations on at least five unregulated contaminants and decide whether to regulate these contaminants with a national primary drinking water regulation (NPDWR). SDWA requires that these determinations be made every five years. These unregulated contaminants are typically chosen from a list known as the Contaminant Candidate List (CCL), which SDWA requires the Agency to publish every five years. EPA published the second CCL (CCL 2) in the Federal Register on February 24, 2005 (70 FR 9071 (USEPA, 2005a)). This action presents the preliminary regulatory determinations for 11 of the 51 contaminants listed on CCL 2 and describes the supporting rationale for each. The preliminary determination is that an NPDWR is not appropriate for any of the 11 contaminants considered for regulatory determinations. The Agency seeks comment on these 11 preliminary determinations. While the Agency has not made a preliminary determination for perchlorate, this action provides an update on the Agency's evaluation of perchlorate. The Agency requests public comment on the information and the options that the Agency is considering in evaluating perchlorate and welcomes the submission of relevant, new information and/or data that may assist the Agency in its regulatory determination.

DATES:

Comments must be received on or before July 2, 2007.

ADDRESSES:

Submit your comments, identified by Docket ID No. EPA-HQ-OW-2007-0068, by one of the following methods:

• http://www.regulations.gov: Follow the online instructions for submitting comments

d welcomes the submission of relevant, new information and/or data that may assist the Agency in its regulatory determination.

DATES:

Comments must be received on or before July 2, 2007.

ADDRESSES:

Submit your comments, identified by Docket ID No. EPA-HQ-OW-2007-0068, by one of the following methods:

• http://www.regulations.gov: Follow the online instructions for submitting comments.

• Mail: Water Docket, Environmental Protection Agency, Mailcode: 2822T, 1200 Pennsylvania Ave., NW., Washington, DC 20460.

• Hand Delivery: Water Docket, EPA Docket Center (EPA/DC). Such deliveries are only accepted during the Docket's normal hours of operation, and special arrangements should be made for deliveries of boxed information.

Instructions: Direct your comments to Docket ID No. EPA-HQ-OW-2007-0068. EPA's policy is that all comments received will be included in the public docket without change and may be made available online at http://www.regulations.gov, including any personal information provided, unless the comment includes information claimed to be Confidential Business Information (CBI) or other information whose disclosure is restricted by statute. Do not submit information that you consider to be CBI or otherwise protected through http://www.regulations.gov. The http://www.regulations.gov Web site is an “anonymous access” system, which means EPA will not know your identity or contact information unless you provide it in the body of your comment. If you send an e-mail comment directly to EPA without going through http://www.regulations.gov your e-mail address will be automatically captured and included as part of the comment that is placed in the public docket and made available on the Internet. If you submit an electronic comment, EPA recommends that you include your name and other contact information in the body of your comment and with any disk or CD-ROM you submit

directly to EPA without going through http://www.regulations.gov your e-mail address will be automatically captured and included as part of the comment that is placed in the public docket and made available on the Internet. If you submit an electronic comment, EPA recommends that you include your name and other contact information in the body of your comment and with any disk or CD-ROM you submit. If EPA cannot read your comment due to technical difficulties and cannot contact you for clarification, EPA may not be able to consider your comment. Electronic files should avoid the use of special characters, any form of encryption, and be free of any defects or viruses. For additional instructions on submitting comments, go to Unit I.B of the SUPPLEMENTARY INFORMATION section of this document.

Docket: All documents in the docket are listed in the http://www.regulations.gov index. Although listed in the index, some information is not publicly available, e.g. , CBI or other information whose disclosure is restricted by statute. Certain other material, such as copyrighted material, will be publicly available only in hard copy. Publicly available docket materials are available either electronically in http://www.regulations.gov or in hard copy at the Water Docket, EPA/DC, EPA West, Room 3334, 1301 Constitution Ave., NW., Washington, DC. The Public Reading Room is open from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal holidays. The telephone number for the Public Reading Room is (202) 566-1744, and the telephone number for the EPA Docket Center is (202) 566-2426.

FOR FURTHER INFORMATION CONTACT:

Wynne Miller, Office of Ground Water and Drinking Water, Standards and Risk Management Division, at (202) 564-4887 or e-mail miller.wynne@epa.gov. For general information contact the EPA Safe Drinking Water Hotline at (800) 426-4791 or e-mail: hotline-sdwa@epa.gov.

SUPPLEMENTARY INFORMATION:

Abbreviations and Acronyms

ocket Center is (202) 566-2426.

FOR FURTHER INFORMATION CONTACT:

SUPPLEMENTARY INFORMATION:

Abbreviations and Acronyms

a. i.—active ingredient <—less than ≤—less than or equal to >—greater than ≥—greater than or equal to μ—microgram, one-millionth of a gram μg/g—micrograms per gram μg/kg—micrograms per kilogram μg/L—micrograms per liter ATSDR—Agency for Toxic Substances and Disease Registry AWWARF—American Water Works Association Research Foundation BMD—bench mark dose BMDL—bench mark dose level BW—body weight for an adult, assumed to be 70 kilograms (kg) CASRN—Chemical Abstract Services Registry Number CBI—confidential business information CDC—Centers for Disease Control and Prevention ChE—cholinesterase CCL—Contaminant Candidate List CCL 1—EPA's First Contaminant Candidate List CCL 2—EPA's Second Contaminant Candidate List CFR—Code of Federal Regulations CMR—Chemical Monitoring Reform CWS—community water system 1,3-DCP—1,3-dichloropropene DCPA—dimethyl tetrachloroterephthalate (dacthal) DDE—1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene DDT—1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane DNT—dinitrotoluene DW—dry weight DWEL—drinking water equivalent level DWI—drinking water intake, assumed to be 2 L/day EPA—United States Environmental Protection Agency EPCRA—Emergency Planning and Community Right-to-Know Act EPTC—s-ethyl dipropylthiocarbamate ESA—ethane sulfonic acid FDA—United States Food and Drug Administration FQPA—Food Quality Protection Act FR—Federal Register FW—fresh weight g—gram g/day—grams per day HRL—health reference level IOC—inorganic compound IRIS—Integrated Risk Information System kg—kilogram L—liter LD 50 —an estimate of a single dose that is expected to cause the death of 50 percent of the exposed animals; it is derived fr

ethane sulfonic acid FDA—United States Food and Drug Administration FQPA—Food Quality Protection Act FR—Federal Register FW—fresh weight g—gram g/day—grams per day HRL—health reference level IOC—inorganic compound IRIS—Integrated Risk Information System kg—kilogram L—liter LD 50 —an estimate of a single dose that is expected to cause the death of 50 percent of the exposed animals; it is derived from experimental data. LOAEL—lowest-observed-adverse-effect level MAC— mycobacterium avium intercellulare MCL—maximum contaminant level MCLG—maximum contaminant level goal mg—milligram, one-thousandth of a gram mg/kg—milligrams per kilogram body weight mg/kg/day—milligrams per kilogram body weight per day mg/L—milligrams per liter mg/m 3 —milligrams per cubic meter MRL—minimum or method reporting limit (depending on the study or suvey cited) MTBE—methyl tertiary butyl ether MTP—monomethyl-2,3,5,6-tetrachloroterephthalate N—number of samples NAS—National Academies of Sciences NAWQA—National Water Quality Assessment (USGS Program) NCEH—National Center for Environmental Health (CDC) NCFAP—National Center for Food and Agricultural Policy NCI—National Cancer Institute NCWS—non community water system ND—not detected (or non detect) NDWAC—National Drinking Water Advisory Council NHANES—National Health and Nutrition Examination Survey (CDC) NIRS—National Inorganic and Radionuclide Survey NIS—sodium iodide symporter NOEL—no-observed-effect-level NOAEL—no-observed-adverse-effect level NPS—National Pesticide Survey NQ—not quantifiable (or non quantifiable) NRC—National Research Council NPDWR—National Primary Drinking Water Regulation NTP—National Toxicology Program OA—oxanilic acid OW—Office of Water OPP—Office of Pesticide Programs PCR—Polymerase Chain Reaction PGWDB—pesticides in ground water data base PWS—public water system RED—Reregistration Eligibility Decision RfC—reference concentration RfD—reference dose RSC—relative source contribution SAB—Science Advisory Board SDWA—Safe Drinking Water Act SOC—synthetic organic compound S

tional Toxicology Program OA—oxanilic acid OW—Office of Water OPP—Office of Pesticide Programs PCR—Polymerase Chain Reaction PGWDB—pesticides in ground water data base PWS—public water system RED—Reregistration Eligibility Decision RfC—reference concentration RfD—reference dose RSC—relative source contribution SAB—Science Advisory Board SDWA—Safe Drinking Water Act SOC—synthetic organic compound SVOC—semi-volatile organic compound T3—triiodothyronine T4—thyroxine TDS—Total Diet Study (FDA) Tg-DNT—technical grade DNT TPA—2,3,5,6-tetrachchloroterephthalic acid TRI—Toxics Release Inventory TSH—thyroid stimulating hormone TT—treatment technique UCM—Unregulated Contaminant Monitoring UCMR 1—First Unregulated Contaminant Monitoring Regulation UF—uncertainty factor US—United States of America USDA—United States Department of Agriculture USGS—United States Geological Survey UST—underground storage tanks VOC—volatile organic compound I. General Information A. Does This Action Impose Any Requirements on My Public Water System? B. What Should I Consider as I Prepare My Comments for EPA? II. Purpose, Background and Summary of This Action A. What Is the Purpose of This Action? B. Background on the CCL and Regulatory Determinations C. Summary of the Approach Used To Identify and Evaluate Candidates for Regulatory Determination 2 D. What Are EPA's Preliminary Determinations and What Happens Next? E. Supporting Documentation for EPA's Preliminary Determinations III. What Analyses Did EPA Use To Support the Preliminary Regulatory Determinations? A. Evaluation of Adverse Health Effects B. Evaluation of Contaminant Occurrence and Exposure IV. Preliminary Regulatory Determinations A. Summary of the Preliminary Regulatory Determination B. Contaminant Profiles 1. Boron 2. and 3. Mono- and Di-Acid Degradates of Dimethyl Tetrachloroterephthalate (DCPA) 4. 1,1-Dichloro-2,2-bis( p -chlorophenyl) ethylene (DDE) 5. 1,3-Dichloropropene (1,3-DCP; Telone) 6. and 7. 2,4- and 2,6-Dinitrotoluenes (2,4- and 2,6-DNT) 8

inant Occurrence and Exposure IV. Preliminary Regulatory Determinations A. Summary of the Preliminary Regulatory Determination B. Contaminant Profiles 1. Boron 2. and 3. Mono- and Di-Acid Degradates of Dimethyl Tetrachloroterephthalate (DCPA) 4. 1,1-Dichloro-2,2-bis( p -chlorophenyl) ethylene (DDE) 5. 1,3-Dichloropropene (1,3-DCP; Telone) 6. and 7. 2,4- and 2,6-Dinitrotoluenes (2,4- and 2,6-DNT) 8. s-Ethyl dipropylthiocarbamate (EPTC) 9. Fonofos 10. Terbacil 11. 1,1,2,2-Tetrachloroethane V. What Is the Status of the Agency's Evaluation of Perchlorate? A. Sources of Perchlorate B. Health Effects C. Occurrence in Water, Food, and Humans. D. Occurrence Studies on Perchlorate in Human Urine, Breast Milk, and Amniotic Fluid E. Status of the Preliminary Regulatory Determination for Perchlorate F. What Are the Potential Options for Characterizing Perchlorate Exposure and Proceeding With the Preliminary Regulatory Determination for Perchlorate? G. Next Steps VI. What About the Remaining CCL 2 Contaminants? A. Metolachlor B. Methyl tertiary-butyl ether C. Microbial Contaminants VII. EPA's Next Steps VIII. References I. General Information

A. Does This Action Impose Any Requirements on My Public Water System?

None of these preliminary regulatory determinations or the final regulatory determinations, when published, will impose any requirements on anyone. Instead, this action notifies interested parties of the availability of EPA's preliminary regulatory determinations for 11 of the 51 contaminants listed on CCL 2 and seeks comment on these preliminary determinations. This action also provides an update on the Agency's review of perchlorate and methyl tertiary butyl ether (MTBE).

B. What Should I Consider as I Prepare My Comments for EPA?

You may find the following suggestions helpful for preparing your comments:

1. Explain your views as clearly as possible.

2. Describe any assumptions that you used.

3. Provide any technical information and/or data you used that support your views.

on the Agency's review of perchlorate and methyl tertiary butyl ether (MTBE).

B. What Should I Consider as I Prepare My Comments for EPA?

You may find the following suggestions helpful for preparing your comments:

1. Explain your views as clearly as possible.

2. Describe any assumptions that you used.

3. Provide any technical information and/or data you used that support your views.

4. If you estimate potential burden or costs, explain how you arrived at your estimate.

5. Provide specific examples to illustrate your concerns.

6. Offer alternatives.

7. Make sure to submit your comments by the comment period deadline.

8. To ensure proper receipt by EPA, identify the appropriate docket identification number in the subject line on the first page of your response. It would also be helpful if you provided the name, date, and Federal Register citation related to your comments.

II. Purpose, Background and Summary of This Action

This section briefly summarizes the purpose of this action, the statutory requirements, previous activities related to the Contaminant Candidate List and regulatory determinations, and the approach used and outcome of these preliminary regulatory determinations.

A. What Is the Purpose of This Action?

The Safe Drinking Water Act (SDWA), as amended in 1996, requires EPA to publish a list of currently unregulated contaminants that may pose risks for drinking water (referred to as the Contaminant Candidate List, or CCL) and to make determinations on whether to regulate at least five contaminants from the CCL with a national primary drinking water regulation (NPDWR)

The 11 regulatory determination contaminants candidates discussed in this action are boron, the dacthal mono- and di-acid degradates, 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE), 1,3-dichloropropene, 2,4-dinitrotoluene, 2,6-dinitrotoluene, s-ethyl propylthiocarbamate (EPTC), fonofos, terbacil, and 1,1,2,2-tetrachloroethane.

B. Background on the CCL and Regulatory Determinations

DWR)

B. Background on the CCL and Regulatory Determinations

1. Statutory Requirements for CCL and Regulatory Determinations. The specific statutory requirements for the CCL and regulatory determinations can be found in SDWA section 1412(b)(1). The 1996 SDWA Amendments require EPA to publish the CCL every five years. The CCL is a list of contaminants that are not subject to any proposed or promulgated NPDWRs, are known or anticipated to occur in public water systems (PWSs), and may require regulation under SDWA. The 1996 SDWA Amendments also direct EPA to determine whether to regulate at least five contaminants from the CCL every five years (within three and one-half years after publication of the final list). In making regulatory determinations, SDWA requires EPA to publish a Maximum Contaminant Level Goal 1 (MCLG) and promulgate an NPDWR 2 for a contaminant if the Administrator determines that:

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 nonenforceable health goals” (40 CFR 141.2).

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.

(a) The contaminant may have an adverse effect on the health of persons;

enforceable health goals” (40 CFR 141.2).

(a) The contaminant may have an adverse effect on the health of persons;

(b) the contaminant is known to occur or there is a substantial likelihood that the contaminant will occur in public water systems with a frequency and at levels of public health concern; and

(c) In the sole judgment of the Administrator, regulation of such contaminant presents a meaningful opportunity for health risk reduction for persons served by public water systems.

If EPA determines that all three of these statutory criteria are met and makes a final determination that a national primary drinking water regulation is needed, the Agency has 24 months to publish a proposed MCLG and NPDWR. After the proposal, the Agency has 18 months to publish and promulgate a final MCLG and NPDWR (SDWA section 1412(b)(1)(E)). 3

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

2. The First Contaminant Candidate List (CCL 1). Following the 1996 SDWA Amendments, EPA sought input from the National Drinking Water Advisory Council (NDWAC) on the process that should be used to identify contaminants for inclusion on the CCL. For chemical contaminants, the Agency developed screening and evaluation criteria based on recommendations from NDWAC. For microbiological contaminants, NDWAC recommended that the Agency seek external expertise to identify and select potential waterborne pathogens. As a result, the Agency convened a workshop of microbiologists and public health experts who developed criteria for screening and evaluation and subsequently developed an initial list of potential microbiological contaminants

recommendations from NDWAC. For microbiological contaminants, NDWAC recommended that the Agency seek external expertise to identify and select potential waterborne pathogens. As a result, the Agency convened a workshop of microbiologists and public health experts who developed criteria for screening and evaluation and subsequently developed an initial list of potential microbiological contaminants.

The first CCL process benefited from considerable input from the NDWAC, the scientific community, and the public through stakeholder meetings and the public comments received on the draft CCL published on October 6, 1997 (62 FR 52193 (USEPA, 1997a)). EPA published the final CCL, which contained 50 chemical and 10 microbiological contaminants, on March 2, 1998 (63 FR 10273 (USEPA, 1998a)). A more detailed discussion of how EPA developed CCL 1 can be found in the 1997 and the 1998 Federal Register notices (62 FR 52193 (USEPA, 1997a) and 63 FR 10273 (USEPA, 1998a)).

3. The Regulatory Determinations for CCL 1. EPA published its preliminary regulatory determinations for a subset of contaminants listed on CCL 1 on June 3, 2002 (67 FR 38222 (USEPA, 2002a)). The Agency published its final regulatory determinations on July 18, 2003 (68 FR 42898 (USEPA, 2003a)). EPA identified 9 contaminants from the 60 contaminants listed on CCL 1 that had sufficient data and information available to make regulatory determinations. The 9 contaminants were Acanthamoeba , aldrin, dieldrin, hexachlorobutadiene, manganese, metribuzin, naphthalene, sodium, and sulfate. The Agency determined that a national primary drinking water regulation was not necessary for any of these 9 contaminants. The Agency issued guidance on Acanthamoeba and health advisories for magnesium, sodium, and sulfate.

lation was not necessary for any of these 9 contaminants. The Agency issued guidance on Acanthamoeba and health advisories for magnesium, sodium, and sulfate.

The decision-making process that EPA used to make its regulatory determinations for CCL 1 was based on substantial expert input and recommendations from different groups including stakeholders, the National Research Council (NRC) and NDWAC. In June 2002, EPA consulted with the Science Advisory Board (SAB) Drinking Water Committee and requested its review and comment on whether the protocol EPA developed, based on the NDWAC recommendations, was consistently applied and appropriately documented. SAB provided verbal feedback regarding the use of the NRC and NDWAC recommendations in EPA's decision criteria for making its regulatory determinations. SAB recommended that the Agency provide a transparent and clear explanation of the process for making regulatory determinations. The Agency took SAB's recommendation into consideration and further explained the CCL 1 regulatory determination evaluation process in the July 18, 2003 (68 FR 42898 (USEPA, 2003a)) notice and in the supporting documentation.

EPA has used the same approach to develop the regulatory determinations discussed in this action. While this action includes a short description of the decision process used to make regulatory determinations (section II.C), a more detailed discussion can be found in the 2002 and the 2003 Federal Register notices (67 FR 38222 (USEPA, 2002a) and 68 FR 42898 (USEPA, 2003a)).

4. The Second Contaminant Candidate List (CCL 2). The Agency published its draft CCL 2 Federal Register notice on April 2, 2004 (69 FR 17406 (USEPA, 2004a)) and the final CCL 2 Federal Register notice on February 24, 2005 (70 FR 9071 (USEPA, 2005a)). The CCL 2 carried forward the 51 remaining chemical and microbial contaminants that were listed on CCL 1.

5. The Regulatory Determinations for CCL 2

. The Second Contaminant Candidate List (CCL 2). The Agency published its draft CCL 2 Federal Register notice on April 2, 2004 (69 FR 17406 (USEPA, 2004a)) and the final CCL 2 Federal Register notice on February 24, 2005 (70 FR 9071 (USEPA, 2005a)). The CCL 2 carried forward the 51 remaining chemical and microbial contaminants that were listed on CCL 1.

5. The Regulatory Determinations for CCL 2. This current action discusses EPA's preliminary determinations for 11 of the 51 contaminants listed on the CCL 2.

C. Summary of the Approach Used To Identify and Evaluate Candidates for Regulatory Determination 2

Figure 1 provides a brief overview of the process EPA used to identify which CCL 2 contaminants are candidates for regulatory determinations and the SDWA statutory criteria considered in making the regulatory determinations.

BILLING CODE 6560-50-P EP01MY07.050

BILLING CODE 6560-50-C In identifying which CCL 2 contaminants are candidates for regulatory determinations, the Agency considered whether sufficient information and/or data were available to characterize the potential health effects and the known/likely occurrence in and exposure from drinking water. With regards to sufficient health effects information/data, the Agency considered whether an Agency-approved health risk assessment 4 was available to identify any potential adverse health effect(s) and derive an estimated level at which adverse health effect(s) are likely to occur. With regards to sufficient occurrence information/data, the Agency considered whether information/data were available to

4 Health information used for the regulatory determinations process includes but is not limited to health assessments available from the Agency's Integrated Risk Information System (IRIS), the Agency's Office of Pesticide Programs (OPP) in a Reregistration Eligibility Decision (RED), the National Academy of Sciences (NAS), and/or the Agency for Toxic Substances and Disease Registry (ATSDR)

le to

If EPA chose a contaminant as a candidate for regulatory determination, the Agency used an approach similar to the first regulatory determination process to answer the three statutory criteria (listed in section II.B.1).

For the current regulatory determination process, the Agency considered the following in evaluating each of the three statutory criteria.

(1) First statutory criterion—Is the contaminant likely to cause an adverse effect on the health of persons? The Agency evaluated the best available, peer-reviewed assessments and studies to characterize the human health effects that may result from exposure to the contaminant when found in drinking water. Based on this characterization, the Agency estimated a health reference level (HRL) for each contaminant. Section III.A provides more detailed information about the approach used to evaluate and analyze the health information.

(2) Second statutory criterion—Is the contaminant known or likely to occur in public water systems at a frequency and level of concern? To evaluate known occurrence in PWSs, the Agency compiled, screened, and analyzed data from several occurrence data sets to develop representative occurrence estimates for public drinking water systems. EPA used the HRL estimates for each contaminant as a benchmark against which to conduct an initial evaluation or screening of the occurrence data. For each contaminant, EPA estimated the number of PWSs (and the population served by these PWSs) with detections greater than one-half the HRL (> 1/2 HRL) and greater than the HRL (> HRL)

sentative occurrence estimates for public drinking water systems. EPA used the HRL estimates for each contaminant as a benchmark against which to conduct an initial evaluation or screening of the occurrence data. For each contaminant, EPA estimated the number of PWSs (and the population served by these PWSs) with detections greater than one-half the HRL (> 1/2 HRL) and greater than the HRL (> HRL). To evaluate the likelihood of a contaminant to occur in drinking water, the Agency considered information on the use and release of a contaminant into the environment and supplemental information on occurrence in water ( e.g. , ambient water quality data, State ambient or finished water data, and/or special studies performed by other agencies, organizations and/or entities). Section III.B provides more details on the approach used to analyze the occurrence information/data.

(3) Third statutory criterion—In the sole judgment of the Administrator, does regulation of the contaminant present a meaningful opportunity for health risk reduction for persons served by public water systems? EPA evaluated the potential health effects and the results of the occurrence and exposure estimates (i.e., the population exposed and the sources of exposure) at the health level of concern to determine if regulation presents a meaningful opportunity for health risk reduction. EPA has made a preliminary determination regarding the meaningful opportunity for health risk reduction for 11 contaminants based upon the population exposed to these contaminants at levels of concern.

If the answers to all three statutory criteria are affirmative for a particular contaminant, then the Agency makes a determination that a national drinking water regulation is necessary and proceeds to develop an MCLG and a national primary drinking water regulation for that contaminant. It should be noted that this regulatory determination process is independent of the more detailed analyses needed to develop a national primary drinking water regulation

tive for a particular contaminant, then the Agency makes a determination that a national drinking water regulation is necessary and proceeds to develop an MCLG and a national primary drinking water regulation for that contaminant. It should be noted that this regulatory determination process is independent of the more detailed analyses needed to develop a national primary drinking water regulation. Thus, a decision to regulate is the beginning of the Agency regulatory development process, not the end.

If the answer to any of the three statutory criteria is negative, then the Agency makes a determination that a national drinking water regulation is not necessary for that contaminant.

D. What Are EPA's Preliminary Determinations and What Happens Next?

EPA has made preliminary determinations that no regulatory actions are appropriate for the 11 contaminants evaluated for this second round of regulatory determinations. EPA will make final determinations on these 11 contaminants after a 60-day comment period. EPA is making preliminary regulatory determinations only on those CCL 2 contaminants that have sufficient information to support such a determination at this time. The Agency continues to conduct research and/or to collect information on the remaining CCL 2 contaminants to fill identified data gaps. The Agency is not precluded from taking action when information becomes available and will not necessarily wait until the end of the next regulatory determination cycle before making other regulatory determinations.

E. Supporting Documentation for EPA's Preliminary Determinations

For this action, EPA prepared several support documents that are available for review and comment in the EPA Water Docket and at http://www.regulations.gov. These support documents include:

• A comprehensive regulatory support document entitled, “Regulatory Determinations Support Document for Selected Contaminants from the Second Drinking Water Contaminant Candidate List” (CCL 2) (USEPA, 2006a). This support document summarizes the information and data on the physical and chemical properties, uses and environmental release, environmental fate, potential health effects, occurrence and exposure estimates, the preliminary determination for each contaminant candidate, and the Agency's rationale for its determination. The technical health and occurrence support documents listed next served as the basis for the health information and the drinking water occurrence estimates summarized in this comprehensive regulatory support document.

• Technical health support documents. These documents address exposure from drinking water and other media, toxicokinetics, hazard identification, and dose-response assessment, and provide an overall characterization of the risk from drinking water for the contaminants considered for regulatory determination. These documents are listed in the reference section as “USEPA, 2006j” through “USEPA, 2006r.”

• Technical occurrence support documents (USEPA, 2006b and USEPA, 2006c). These documents include more detailed information about the sources of the data, how EPA assessed the data quality, completeness, and representativeness, and how the data were used to generate estimates of drinking water contaminant occurrence in support of these regulatory determinations. Section III.B.3 provides more information about the title and content of these technical support documents.

III

e documents include more detailed information about the sources of the data, how EPA assessed the data quality, completeness, and representativeness, and how the data were used to generate estimates of drinking water contaminant occurrence in support of these regulatory determinations. Section III.B.3 provides more information about the title and content of these technical support documents.

III. What Analyses Did EPA Use To Support the Preliminary Regulatory Determinations?

Sections III.A and B of this action outline the health effects and occurrence/exposure evaluation process EPA used to support these preliminary determinations.

A. Evaluation of Adverse Health Effects

Section 1412(b)(1)(A)(i) of SDWA requires EPA to determine whether each

There are two different approaches to the derivation of an HRL. One approach is used for chemicals that cause cancer and exhibit a linear response to dose and the other applies to noncarcinogens and carcinogens evaluated using a non-linear approach.

1. Use of Carcinogenicity Data for the Derivation of a Health Reference Level. For those contaminants considered to be likely or probable human carcinogens, EPA evaluated data on the mode of action of the chemical to determine the method of low dose extrapolation. When this analysis indicates that a linear low dose extrapolation is appropriate or when data on the mode of action are lacking, EPA uses a low dose linear extrapolation to calculate risk-specific doses. The risk-specific doses are the estimated oral exposures associated with lifetime excess risk levels that range from one cancer in ten thousand (10 −4 ) to one cancer in a million (10 −6 ). The risk-specific doses (expressed as mg/kg of body weight per day) are combined with adult body weight and drinking water consumption data to estimate drinking water concentrations corresponding to this risk range

risk-specific doses are the estimated oral exposures associated with lifetime excess risk levels that range from one cancer in ten thousand (10 −4 ) to one cancer in a million (10 −6 ). The risk-specific doses (expressed as mg/kg of body weight per day) are combined with adult body weight and drinking water consumption data to estimate drinking water concentrations corresponding to this risk range. EPA generally used the one-in-a-million (10 −6 ) cancer risk in the initial screening of the occurrence data for carcinogens evaluated using linear low dose extrapolation. Five of the eleven contaminants discussed in this action had data available to classify them as likely or probable human carcinogens. These five are also the only contaminants for which low dose linear extrapolations were performed. These five are p,p-dichlorodiphenyldichloroethylene (DDE), 1,3-dichloropropene (1,3-DCP or Telone), 2,4-dinitrotoluene, 2,6-dinitrotoluene, and 1,1,2,2-tetrachloroethane. The remaining 6 contaminants have not been identified as known, likely or probable carcinogens.

2. Use of Non-carcinogenic Health Effects Data for Derivation of an HRL. For those chemicals not considered to be carcinogenic to humans, EPA generally calculates a reference dose (RfD). A RfD is an estimate of a daily oral exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. It can be derived from either a “no-observed-adverse-effect level” (NOAEL), a “lowest-observed-adverse-effect level” (LOAEL), or a benchmark dose, with uncertainty factors applied to reflect limitations of the data used.

The Agency uses uncertainty factors (UFs) to address uncertainty resulting from incompleteness of the toxicological database. The individual UFs (usually applied as integers of 1, 3, or 10) are multiplied together and used to derive the RfD from experimental data. Individual UFs are intended to account for:

enchmark dose, with uncertainty factors applied to reflect limitations of the data used.

(1) The variation in sensitivity among the members of the human population ( i.e. , intraspecies variability);

(2) the uncertainty in extrapolating animal data to humans ( i.e. , interspecies variability);

(3) the uncertainty in extrapolating from data obtained in a study with less-than-lifetime exposure to lifetime exposure ( i.e. , extrapolating from subchronic to chronic exposure);

(4) the uncertainty in extrapolating from a LOAEL rather than from a NOAEL; and/or

(5) the uncertainty associated with an incomplete database.

For boron, the dacthal (DCPA) mono and di acid degradates, s-ethyl dipropylthiocarbamate (EPTC), fonofos and terbacil, EPA derived the HRLs using the RfD approach as follows:

HRL = [(RfD × BW)/DWI] × RSC Where: RfD = Reference Dose BW = Body Weight for an adult, assumed to be 70 kilograms (kg) DWI = Drinking Water Intake, assumed to be 2 L/day (90th percentile) RSC = Relative Source Contribution, or the level of exposure believed to result from drinking water when compared to other sources ( e.g. , food, ambient air). A 20 percent RSC is being used to estimate the HRL and screen the occurrence data because it is the lowest and most conservative RSC used in the derivation of an MCLG for drinking water. For each of the 6 aforementioned non-carcinogenic compounds for which the Agency has made a preliminary regulatory determination in this action, EPA used the RfD in conjunction with a 20 percent RSC to derive a conservative HRL estimate and perform an initial screening of the drinking water occurrence data

s the lowest and most conservative RSC used in the derivation of an MCLG for drinking water. For each of the 6 aforementioned non-carcinogenic compounds for which the Agency has made a preliminary regulatory determination in this action, EPA used the RfD in conjunction with a 20 percent RSC to derive a conservative HRL estimate and perform an initial screening of the drinking water occurrence data. Since the initial screening of the occurrence data at this conservative HRL value resulted in a preliminary negative determination for each of these 6 compounds, the Agency determined that it was not necessary to further evaluate the RSC in making the regulatory determination. As discussed in section IV.B.2 and 3, the HRL for the two dacthal degradates is based on the HRL value derived for the DCPA parent following the guidance provided by EPA's Office of Pesticide Programs.

3. Sources of Data/Information for Health Effects. EPA used the best available peer-reviewed data and analyses in evaluating adverse health effects. Peer-reviewed health-risk assessments were available for all chemicals considered for regulatory determinations from the Agency's Integrated Risk Information System (IRIS) Program 5 and/or the Office of Pesticide Programs (OPP) Reregistration Eligibility Decisions (RED). 6 Table 1 summarizes the sources of the health assessment data for each chemical under regulatory determination consideration. The Agency performed a literature search for studies published after the IRIS or OPP health-risk assessment was completed to determine if new information suggested a different outcome. The Agency collected and evaluated any peer-reviewed publications identified through the literature search for their impact on the RfD and/or cancer assessment. In cases where the recent data indicated that a change to the existing RfD or cancer assessment was needed, the updated OW assessment, as described in the health effects support document, was independently peer-reviewed

different outcome. The Agency collected and evaluated any peer-reviewed publications identified through the literature search for their impact on the RfD and/or cancer assessment. In cases where the recent data indicated that a change to the existing RfD or cancer assessment was needed, the updated OW assessment, as described in the health effects support document, was independently peer-reviewed. All quantitative cancer assessments conducted under the Guidelines for Carcinogen Risk Assessment (51 FR 33992 (USEPA, 1986)) were updated using the Guidelines for Carcinogen Risk Assessment (USEPA, 1999a) as directed in the November 2001 (66 FR 59593 (USEPA, 2001a)) Federal Register notice.

5 IRIS is an electronic EPA database ( http://www.epa.gov/iris/index.html ) containing peer-reviewed information on human health effects that may result from exposure to various chemicals in the environment. These chemical files contain descriptive and quantitative information on hazard identification and dose response, RfDs for chronic noncarcinogenic health effects, as well as slope factors and unit risks for carcinogenic effects.

6 The OPP is required under the Federal Insecticide Fungicide and Rodenticide Act (FIFRA) to review all pesticides registered prior to 1984 and determine whether to reregister them for continued use. The results of the reregistration analysis are included in the REDs. Copies of the REDs are located at the following Web site: http://cfpub.epa.gov/oppref/rereg/status.cfm?show=rereg .

In March 2005, EPA updated and finalized the Cancer Guidelines and a Supplementary Children's Guidance,

The cancer assessment for 1,3-dichloropropene was done by OPP and IRIS (USEPA, 1998b and 2000a) under the Proposed Guidelines for Carcinogen Risk Assessment (61 FR 17960 (USEPA, 1996a))

the REDs are located at the following Web site: http://cfpub.epa.gov/oppref/rereg/status.cfm?show=rereg .

In March 2005, EPA updated and finalized the Cancer Guidelines and a Supplementary Children's Guidance,

The cancer assessment for 1,3-dichloropropene was done by OPP and IRIS (USEPA, 1998b and 2000a) under the Proposed Guidelines for Carcinogen Risk Assessment (61 FR 17960 (USEPA, 1996a)). The Administrator (USEPA, 2005d) has directed that current completed assessments can be considered to be scientifically sound based on the guidance used when the assessment was completed until a new assessment is performed by one of the responsible program offices.

Table 1.—Sources and Dates of EPA Health Risk Assessments Chemical IRIS Date OPP RED Date Boron X 2004 Dacthal and its mono- and di-acid degradates X 1994 X 1998 1,3-Dichloropropene X 2000 X 1998 DDE X 1988 2,4-Dinitrotoluene X 1990/1992 2,6-Dinitrotoluene * X 1990 EPTC X 1990 X 1999 Fonofos X 1991 ** X 1996 Terbacil X 1989 X 1998 1,1,2,2-Tetrachloroethane X 1986 * Applies to a mixture of 98 percent 2,4-dinitrotoluene and 2 percent 2,6-dinitrotoluene. ** Health Risk Assessment; RED not completed due to pesticide cancellation. As noted in section II.E, EPA has prepared several technical health effects support documents for the contaminants considered for this round of regulatory determinations. These documents address the exposure from drinking water and other media, toxicokinetics, hazard identification, and dose-response assessment, and provide an overall characterization of risk from drinking water.

B. Evaluation of Contaminant Occurrence and Exposure

EPA used data from several sources to evaluate occurrence and exposure for the 11 contaminants considered in these regulatory determinations

uments address the exposure from drinking water and other media, toxicokinetics, hazard identification, and dose-response assessment, and provide an overall characterization of risk from drinking water.

B. Evaluation of Contaminant Occurrence and Exposure

EPA used data from several sources to evaluate occurrence and exposure for the 11 contaminants considered in these regulatory determinations. The major or primary sources of the drinking water occurrence data used to support these determinations include the following sources:

• The first Unregulated Contaminant Monitoring Regulation (UCMR 1),

• The Unregulated Contaminant Monitoring (UCM) program, and

• The National Inorganic and Radionuclide Survey (NIRS).

In addition to these primary sources of occurrence data, the Agency also evaluated supplemental sources of occurrence information. Section III.B.1 of this action provides a brief summary of the primary sources of drinking water occurrence data and section III.B.2 provides brief summary descriptions of the supplemental sources of occurrence information and/or data. A summary of the occurrence data and the results or findings for each of the 11 contaminants considered for regulatory determination is presented in Section IV.B, the contaminant profiles section.

1. Primary Data Sources. As previously mentioned, the primary sources of the drinking water occurrence data used to support this action are the UCMR 1, the UCM program, and NIRS. The following sections provide a brief summary of the data sources and the approach used to estimate a given contaminant's occurrence. Table 2 lists the primary data sources the Agency used for each of the 11 contaminants considered for regulatory determinations

ntioned, the primary sources of the drinking water occurrence data used to support this action are the UCMR 1, the UCM program, and NIRS. The following sections provide a brief summary of the data sources and the approach used to estimate a given contaminant's occurrence. Table 2 lists the primary data sources the Agency used for each of the 11 contaminants considered for regulatory determinations.

Table 2.—Primary Sources of Drinking Water Occurrence Data Used in the Regulatory Determination Process Number Contaminant Primary data sources UCMR 1 List 1 assessment monitoring List 2 screening survey UCM Round 1 cross section Round 2 cross section NIRS 1 Boron 1 X 2 Dacthal mono- and 3 di-acid degradates X 4 DDE X 5 1,3-Dichloropropene 2 X X X 6 2,4-Dinitrotoluene X 7 2,6-Dinitrotoluene X 8 EPTC X 9 Fonofos X 10 Terbacil X 11 1,1,2,2-Tetrachloroethane X X 1 For boron, EPA also considered the results of a study funded by AWWARF (Frey et al. , 2004). 2 1,3-Dichloropropene was sampled as a UCM Round 1 and 2 analyte but due to sample degradation concerns the contaminant was re-analyzed using the samples provided by the small systems that participated in the UCMR 1 List 1 Assessment Monitoring. a. The Unregulated Contaminant Monitoring Regulation. In 1999, EPA developed the UCMR program in coordination with the CCL and the National Drinking Water Contaminant Occurrence Database (NCOD) to provide national occurrence information on unregulated contaminants (September 17, 1999, 64 FR 50556 (USEPA, 1999b); March 2, 2000, 65 FR 11372 (USEPA, 2000b); and January 11, 2001, 66 FR 2273 (USEPA, 2001b)). EPA used data from the UCMR 1 program to evaluate occurrence for 9 of the 11 contaminants considered for these regulatory determinations. These 9 contaminants include the dacthal mono- and di-acid degradates, DDE, 1,3-dichloropropene, 2,4-dinitrotoluene, 2,6-dinitrotoluene, EPTC, fonofos, and terbacil

9b); March 2, 2000, 65 FR 11372 (USEPA, 2000b); and January 11, 2001, 66 FR 2273 (USEPA, 2001b)). EPA used data from the UCMR 1 program to evaluate occurrence for 9 of the 11 contaminants considered for these regulatory determinations. These 9 contaminants include the dacthal mono- and di-acid degradates, DDE, 1,3-dichloropropene, 2,4-dinitrotoluene, 2,6-dinitrotoluene, EPTC, fonofos, and terbacil.

EPA designed the UCMR 1 data collection with three parts (or tiers) primarily based on the availability of analytical methods. Occurrence data for 8 of the 9 contaminants listed in the preceding paragraph are from the first tier of UCMR (also known as UCMR 1 List 1 Assessment Monitoring). Occurrence data for fonofos are from the second tier of UCMR 1 (also known as the UCMR 1 List 2 Screening Survey). EPA has not collected data as part of the third tier due to the lack of adequate analytical methods.

The UCMR 1 List 1 Assessment Monitoring was performed for a specified number of chemical contaminants for which analytical methods have been developed. EPA required all large 7 PWSs, plus a statistically representative national sample of 800 small 8 PWSs to conduct Assessment Monitoring. 9 Approximately one-third of the participating small systems were scheduled to monitor for these contaminants during each calendar year from 2001 through 2003. Large systems could conduct one year of monitoring anytime during the 2001-2003 UCMR 1 period. EPA specified a quarterly monitoring schedule for surface water systems and a twice-a-year, six-month interval monitoring schedule for ground water systems. The objective of the UCMR 1 sampling approach for small systems was to collect contaminant occurrence data from a statistically selected, nationally representative sample of small systems. The small system sample was stratified and population-weighted, and included some other sampling adjustments such as allocating a selection of at least 2 systems from each State

chedule for ground water systems. The objective of the UCMR 1 sampling approach for small systems was to collect contaminant occurrence data from a statistically selected, nationally representative sample of small systems. The small system sample was stratified and population-weighted, and included some other sampling adjustments such as allocating a selection of at least 2 systems from each State. With contaminant monitoring data from all large PWSs and a statistical, nationally representative sample of small PWSs, the UCMR 1 List 1 Assessment Monitoring program provides a contaminant occurrence data set suitable for national drinking water estimates.

7 Systems serving more than 10,000 people.

8 Systems serving 10,000 people or fewer.

9 Large and small systems that purchase 100% of their water supply were not required to participate in the UCMR 1 Assessment Monitoring or the UCMR 1 Screening Survey.

In total, 370,312 sample results have been collected under the UCMR 1 List 1 Assessment Monitoring program at approximately 3,083 large systems and 797 small systems. Approximately 33,600 samples were collected for each contaminant. The UCMR 1 List 1 Monitoring program included systems from all 50 States, the District of Columbia, 4 U.S. Territories, and Tribal lands in 5 EPA Regions. An additional 3,719 samples were collected for 1,3-DCP at all small systems that conducted UCMR 1 List 1 Assessment Monitoring.

In addition to the UCMR 1 List 1 Assessment Monitoring, EPA required monitoring for selected contaminants (including fonofos) for which analytical methods were developed but not widely used. Known as the UCMR 1 List 2 Screening Survey, EPA randomly selected 300 public water systems (120 large and 180 small systems) from the pool of systems required to conduct UCMR 1 List 1 Assessment Monitoring. In total, 29,765 sample results have been collected under the UCMR 1 List 2 Screening Survey from the participating large and small systems. Approximately 2,300 samples were collected for each contaminant

UCMR 1 List 2 Screening Survey, EPA randomly selected 300 public water systems (120 large and 180 small systems) from the pool of systems required to conduct UCMR 1 List 1 Assessment Monitoring. In total, 29,765 sample results have been collected under the UCMR 1 List 2 Screening Survey from the participating large and small systems. Approximately 2,300 samples were collected for each contaminant. The UCMR 1 List 2 Screening Survey included systems from 48 States, 2 U.S. Territories, and Tribal lands in 1 EPA Region. EPA used the occurrence data from this survey to evaluate fonofos.

EPA analyzed the UCMR 1 List 1 Assessment Monitoring and List 2 Screening Survey data to generate the following initial occurrence and exposure summary statistics:

• The total number of systems and the total population served by these systems,

• The number and percentage of systems with at least 1 observed detection that has a concentration greater than 1/2 the HRL and greater than the HRL (or in some cases greater than or equal to the minimum reporting limit or MRL), and

• The number of people and percentage of the population served by systems with at least one observed detection greater than 1/2 the HRL and greater than the HRL (or in some cases greater than or equal to the MRL). 10

10 EPA's support documents (USEPA, 2006a and 2006b) provide summary statistics for the median and 99th percentile concentrations of all analytical detections and detailed occurrence results based on UCMR data according to source water type (surface versus ground water), system size, and State.

The initial UCMR 1 summary occurrence statistics for dacthal mono- and di-acid degradates, DDE, 1,3-dichloropropene, 2,4-dinitrotoluene, 2,6-dinitrotoluene, EPTC, fonofos, and terbacil are presented in section IV.B of this action.

b. The Unregulated Contaminant Monitoring Program Rounds 1 and 2

d on UCMR data according to source water type (surface versus ground water), system size, and State.

b. The Unregulated Contaminant Monitoring Program Rounds 1 and 2. In 1987, EPA initiated the UCM program to fulfill a 1986 SDWA Amendment that required monitoring of specified unregulated contaminants to gather information on their occurrence in drinking water for future regulatory decision-making purposes. EPA used data from the UCM program to evaluate

EPA implemented the UCM program in two phases or rounds. The first round of UCM monitoring generally extended from 1988 to 1992 and is referred to as UCM Round 1 monitoring. The second round of UCM monitoring generally extended from 1993 to 1997 and is referred to as UCM Round 2 monitoring.

UCM Round 1 monitored for 34 volatile organic compounds (VOCs), including 1,3-dichloropropene and 1,1,2,2-tetrachloroethane (52 FR 25720 (USEPA, 1987)). UCM Round 2 monitored for 13 synthetic organic compounds (SOCs), sulfate and the same 34 VOCs from UCM Round 1 monitoring (57 FR 31776 (USEPA, 1992a)).

The UCM Round 1 database contains contaminant occurrence data from 38 States, Washington, DC, and the U.S. Virgin Islands. The UCM Round 2 database contains data from 34 States and several Tribes. Due to incomplete State data sets, national occurrence estimates based on raw (unedited) UCM Round 1 or Round 2 data could be skewed to low-occurrence or high-occurrence settings (e.g., some States only reported detections). To address potential biases in the data, 11 EPA developed national cross-sections from the UCM Round 1 and Round 2 State data using an approach similar to that used for EPA's 1999 Chemical Monitoring Reform (CMR), the first Six Year Review, and the first CCL Regulatory Determinations

2 data could be skewed to low-occurrence or high-occurrence settings (e.g., some States only reported detections). To address potential biases in the data, 11 EPA developed national cross-sections from the UCM Round 1 and Round 2 State data using an approach similar to that used for EPA's 1999 Chemical Monitoring Reform (CMR), the first Six Year Review, and the first CCL Regulatory Determinations. This national cross-section approach was developed to support occurrence analyses and was supported by scientific peer reviewers and stakeholders. This approach identified 24 of the original 38 States from the UCM Round 1 database and 20 of the original 34 States from the UCM Round 2 data base for the national cross-section.

11 The potential bias in the raw UCM data are due to lack of representativeness (since not all States provided UCM data) and incompleteness (since some States that provided data had incomplete data sets).

Because UCM Round 1 and Round 2 data represent different time periods and include occurrence data from different States, EPA developed separate national cross-sections for each data set. The UCM Round 1 national cross-section consists of data from 24 States, with approximately 3.3 million total analytical data points from approximately 22,000 unique PWSs. The UCM Round 2 national cross-section consists of data from 20 States, with approximately 3.7 million analytical data points from slightly more than 27,000 unique PWSs. The UCM Round 1 and 2 national cross-sections represent significantly large samples of national occurrence data. Within each cross-section, the actual number of systems and analytical records for each contaminant varies

ique PWSs. The UCM Round 2 national cross-section consists of data from 20 States, with approximately 3.7 million analytical data points from slightly more than 27,000 unique PWSs. The UCM Round 1 and 2 national cross-sections represent significantly large samples of national occurrence data. Within each cross-section, the actual number of systems and analytical records for each contaminant varies. The support document, “The Analysis of Occurrence Data from the Unregulated Contaminant Monitoring (UCM) Program and National Inorganics and Radionuclides Survey (NIRS) in Support of Regulatory Determinations for the Second Drinking Water Contaminant Candidate List” (USEPA, 2006c), provides a description of how the national cross-sections for the Round 1 and Round 2 data sets were developed.

EPA constructed the national cross-sections in a way that provides a balance and range of States with varying pollution potential indicators, a wide range of the geologic and hydrologic conditions, and a very large sample of monitoring data points. While EPA recognizes that some limitations exist, the Agency believes that the national cross-sections do provide a reasonable estimate of the overall distribution and the central tendency of contaminant occurrence across the United States.

EPA analyzed the UCM Round 1 and 2 National Cross-Section data to generate the following initial occurrence and exposure summary statistics:

• The total number of systems and the total population served by these systems,

• The number of people and percentage of the population served by systems with at least 1 observed detection that has a concentration greater than 1/2 the HRL and greater than the HRL (or in some cases greater than or equal to the MRL)

at least 1 observed detection that has a concentration greater than 1/2 the HRL and greater than the HRL (or in some cases greater than or equal to the MRL), and

12 EPA's support documents (USEPA, 2006a and 2006c) provide summary statistics for the median and 99th percentile concentrations of all analytical detections and detailed occurrence results based on the UCM Round 1 and 2 Nationals Cross-Sectons according to source water type (surface versus ground water), system size, and State.

The initial UCM summary occurrence statistics for 1,3-dichloropropene and 1,1,2,2-tetrachloroethane are presented in section IV.B of this action.

c. National Inorganic and Radionuclide Survey. In the mid-1980's, EPA conducted the NIRS to provide a statistically representative sample 13 of the national occurrence of inorganic contaminants in community water systems (CWSs) served by ground water. EPA used data from NIRS, as well as a supplemental survey, to evaluate occurrence for boron.

13 NIRS was designed to provide results that are statistically representative of natioal occurrence at CWSs using ground water sources and is stratified based on system size (population served by the system). Most of the NIRS data are from smaller systems (92 percent from systems serving 3,300 persons or fewer).

The NIRS database includes 36 radionuclides and inorganic compounds (IOCs), including boron. The NIRS provides contaminant occurrence data from 989 ground water CWSs covering 49 States (all except Hawaii) and does not include surface water systems. The survey focused on ground water systems, in part because IOCs tend to occur more frequently and at higher concentrations in ground water than in surface water

atabase includes 36 radionuclides and inorganic compounds (IOCs), including boron. The NIRS provides contaminant occurrence data from 989 ground water CWSs covering 49 States (all except Hawaii) and does not include surface water systems. The survey focused on ground water systems, in part because IOCs tend to occur more frequently and at higher concentrations in ground water than in surface water. Each of the 989 randomly selected CWSs was sampled at a single time between 1984 and 1986.

EPA analyzed the NIRS data to generate the following occurrence and exposure summary statistics for boron:

• The total number of systems and the total population served by these systems,

• The number and the percentage of systems with at least 1 detection that has a concentration greater than 1/2 the HRL and greater than the HRL,

• The number of people and percentage of the population served by systems with at least 1 observed detection that has a concentration greater than 1/2 the HRL and greater than the HRL. 14

14 EPA's support documents (USEPA, 2006a and 2006c) provide the number and percentage of systems with detections, the 99th percentile concentration of all samples, the 99th percentile concentration of samples with detections, and the median concentration of samples with detections.

Similar to the treatment of the UCM cross-section data, the actual values for the NIRS analyses of boron are reported in section IV.B. Because the NIRS data were collected in a randomly designed sample survey, these summary statistics are representative of national occurrence in ground water CWSs.

One limitation of the NIRS is a lack of occurrence data for surface water systems. To provide perspective on the occurrence of boron in surface water systems relative to ground water systems, EPA reviewed and took into consideration a recent boron occurrence survey funded by American Water Works Association Research Foundation (AWWARF) (Frey et al. , 2004)

tional occurrence in ground water CWSs.

d. Presentation of Occurrence Data and Analytical Approach. As noted previously, the occurrence values and summary statistics presented in this action are the actual data from the UCMR 1, UCM, and NIRS data sets. These occurrence values represent direct counts of the number and percent of systems, and population served by systems, with at least 1 analytical detection above some specified concentration threshold. EPA considered this to be the most straightforward and accurate way to present these data for the regulatory determination process.

While both UCMR 1 and UCM data could support more involved statistical modeling to characterize occurrence based on mean (rather than peak) concentrations, EPA chose not to perform this step for the regulatory determinations proposed in this action. EPA believes that presenting the actual results of the occurrence monitoring is straight-forward and the use of an analysis based on peak concentrations provides conservative estimates of occurrence and potential exposure from drinking water. Given that the preliminary determinations for the 11 contaminants discussed in this action are negative, it is not necessary to go beyond the conservative (peak concentration) approach used for this analysis.

negative, it is not necessary to go beyond the conservative (peak concentration) approach used for this analysis.

2. Supplemental Data. The Agency evaluated several sources of supplemental occurrence information to augment the primary drinking water occurrence data, to evaluate the likelihood of contaminant occurrence, and/or to more fully characterize a contaminant's presence in the environment. Sections II.B.2.a through II.B.2.f provide brief descriptions of the main supplemental information/data sources cited in this action. Summarized occurrence findings from these supplemental sources are presented in Section IV.B, the contaminant profiles section. While the following descriptions cover the more commonly referenced supplemental sources of information/data, they do not include every study and survey cited in the contaminant discussions. A more detailed discussion of the supplemental sources of information/data that EPA evaluated for each contaminant can be found in the comprehensive regulatory determination support document (USEPA, 2006a).

a. USGS NAWQA Information/Data. The United States Geological Survey (USGS) collects long-term and nationally consistent data describing water quality in ground water and surface water. In 1991, USGS implemented the National Water-Quality Assessment (NAWQA) Program for 10-year cyclical data collection and data analyses. During the first cycle (1991-2001), the NAWQA program monitored 51 major watersheds and aquifers (study units), which supply more than 60% of the nation's drinking water and water used for agriculture and industry in the U.S. (Hamilton et al. , 2004). NAWQA has collected data from over 6,400 surface water and 7,000 ground water sampling points. USGS National Synthesis teams prepare comprehensive analyses of data on topics of particular concern. EPA evaluated information/data from the following USGS National Synthesis reports/projects:

the nation's drinking water and water used for agriculture and industry in the U.S. (Hamilton et al. , 2004). NAWQA has collected data from over 6,400 surface water and 7,000 ground water sampling points. USGS National Synthesis teams prepare comprehensive analyses of data on topics of particular concern. EPA evaluated information/data from the following USGS National Synthesis reports/projects:

(1) The NAWQA Pesticide National Synthesis Project. In 2003, USGS posted the preliminary results from the first cycle of monitoring for pesticides in streams and ground water. USGS considers these results to be provisional. The results and the data can be accessed at http://ca.water.usgs.gov/pnsp/. Data are presented separately for surface water and ground water, as well as bed sediments and biota. In each case, results are subdivided by land use category. Land use categories include agricultural, urban, mixed (deeper aquifers of regional extent in the case of ground water), and undeveloped. In this action, the NAWQA pesticide data for surface water are referenced as Martin et al. (2003) and the ground water data are referenced as Kolpin and Martin (2003).

(2) The National Survey of MTBE and Other VOCs in Community Drinking Water Sources (part of the VOC National Synthesis Project). In 2003, USGS published the survey findings for MTBE, other ether gasoline oxygenates, and other volatile organic compounds (VOCs) in source water used by CWSs in the United States. The survey was funded by AWWARF and performed by USGS in collaboration with the Metropolitan Water District of Southern California and the Oregon Health and Science University. USGS performed the survey in two independent stages designed to provide representative sampling of all CWSs in the United States (Random Source-Water Survey) and to improve understanding of the temporal variability of MTBE and other compounds in selected water sources (Focused Source-Water Survey). Participating water utilities provided samples that were analyzed for 66 VOCs

nd Science University. USGS performed the survey in two independent stages designed to provide representative sampling of all CWSs in the United States (Random Source-Water Survey) and to improve understanding of the temporal variability of MTBE and other compounds in selected water sources (Focused Source-Water Survey). Participating water utilities provided samples that were analyzed for 66 VOCs. The random survey design selected 954 CWSs to be nationally representative of surface and ground waters sources used by CWSs. The focused survey studied source waters from 134 CWSs suspected or known to contain MTBE. The reports/results and data sets from the survey can be accessed at http://sd.water.usgs.gov/nawqa/vocns/nat_survey.html . The random survey results can be found in the USGS Water Resources Investigations Report 02-4079, referenced as Grady (2003). The focused survey results can be found in the USGS Water Resources Investigations Report 02-4084, referenced as Delzer and Ivahnenko (2003a).

b. USGS National Highway Runoff Data and Methodology Synthesis. In addition to the NAWQA project, USGS has prepared additional surveys of national contaminant occurrence. For the National Highway Runoff Data and Methodology Synthesis, USGS conducted a review of 44 studies of semi-volatile organic compounds (SVOCs) and VOCs in runoff conducted since 1970. The USGS Synthesis sought to evaluate data quality parameters for comparison between and among these studies, including documentation of sampling protocols and methods, limits of reporting and detection, and protocols of quality-control and quality-assurance. The complete USGS report is Open-File Report 98-409 and is referenced as Lopes and Dionne (1998).

c. Toxics Release Inventory. EPA established the Toxics Release Inventory (TRI) in 1987 in response to section 313 of the Emergency Planning and Community Right-to-Know Act (EPCRA)

pling protocols and methods, limits of reporting and detection, and protocols of quality-control and quality-assurance. The complete USGS report is Open-File Report 98-409 and is referenced as Lopes and Dionne (1998).

c. Toxics Release Inventory. EPA established the Toxics Release Inventory (TRI) in 1987 in response to section 313 of the Emergency Planning and Community Right-to-Know Act (EPCRA). EPCRA section 313 requires facilities to report to both EPA and the States annual information on toxic chemical releases from facilities that meet reporting criteria. EPCRA section 313 also requires EPA to make this information available to the public through a computer database. This database is accessible through TRI Explorer, which can be accessed at http://www.epa.gov/triexplorer . In 1990 Congress passed the Pollution Prevention Act, which required that additional data on waste management and source reduction activities be reported under TRI. The TRI database details not only the types and quantities of toxic chemicals released to the air, water, and land by facilities, but also provides information on the quantities of chemicals sent to other facilities for further management (USEPA, 2002b and 2003b).

Facilities are required to report releases and other waste management activities related to TRI chemicals if they manufacture, process, or otherwise use more than established threshold quantities of these chemicals. Currently

d. Pesticides in Ground Water Database. The Pesticides in Ground Water Database (PGWDB) is a compilation of data from ground water studies conducted by Federal, State, and local governments, the pesticide industry, and other institutions between 1971 and 1991 (USEPA, 1992b). Data from 68,824 wells in 45 states are included. The vast majority of the wells (65,865) were drinking water wells. Monitoring was conducted for 258 pesticides and 45 degradates. Not all studies tested for every compound.

e. The National Pesticide Survey

udies conducted by Federal, State, and local governments, the pesticide industry, and other institutions between 1971 and 1991 (USEPA, 1992b). Data from 68,824 wells in 45 states are included. The vast majority of the wells (65,865) were drinking water wells. Monitoring was conducted for 258 pesticides and 45 degradates. Not all studies tested for every compound.

e. The National Pesticide Survey. In 1990, EPA completed a national survey of pesticides in drinking water wells. The purpose of the National Pesticide Survey (NPS) was to determine the national occurrence frequencies and concentrations of select pesticides in the nation's drinking water wells, and to improve EPA's understanding of how pesticide occurrence in ground water correlates with patterns of pesticide usage and ground water vulnerability. The survey included approximately 1,300 CWS wells and rural domestic wells. Sampling was conducted between 1988 and 1990. Wells were sampled for 101 pesticides, 25 pesticide degradates, and nitrate. The survey targeted areas representing a variety of pesticide usage levels and ground water vulnerability. The survey was designed to provide a statistically reliable estimate of pesticide occurrence in the nation's drinking water wells (USEPA, 1990a).

f. The AWWARF Boron Study. The American Water Works Research Foundation funded a survey to evaluate the occurrence of boron (as well as hexavalent chromium) in drinking water sources (Frey et al. , 2004). The AWWARF study recruited 189 PWSs representing 407 source waters in 41 states. Of the 407 source water sample kits distributed in 2003, approximately 342 were returned. Of these 342 samples, 341 were analyzed for boron. Approximately 67 percent (or 228) represented ground water sources and 33 percent (or 113) represented surface water sources. The results of the AWWARF survey for boron are presented in section IV.B of this action.

3. Supporting Documentation for Occurrence

Of the 407 source water sample kits distributed in 2003, approximately 342 were returned. Of these 342 samples, 341 were analyzed for boron. Approximately 67 percent (or 228) represented ground water sources and 33 percent (or 113) represented surface water sources. The results of the AWWARF survey for boron are presented in section IV.B of this action.

3. Supporting Documentation for Occurrence. As mentioned in section II.E, EPA prepared several technical occurrence documents to support this action. These technical occurrence documents include the following:

• “The Analysis of Occurrence Data from the Unregulated Contaminant Monitoring (UCM) Program and National Inorganics and Radionuclides Survey (NIRS) in Support of Regulatory Determinations for the Second Drinking Water Contaminant Candidate List” (USEPA, 2006c), which this action refers to as the “UCM and NIRS Occurrence Report.”

• “The Analysis of Occurrence Data from the First Unregulated Contaminant Monitoring Regulation (UCMR 1) in Support of Regulatory Determinations for the Second Drinking Water Contaminant Candidate List” (USEPA, 2006b), which this action refers to as the “UCMR 1 Occurrence Report.”

The “UCM and NIRS Occurrence Report” provides more detailed information about the UCM and the NIRS data, how EPA assessed the data quality, completeness, and representativeness, and how the data were used to generate estimates of contaminant occurrence. The “UCMR 1 Occurrence Report” provides more detailed information about the UCMR 1 data, how EPA assessed the data quality, completeness, representativeness, and how the data were used to generate estimates of contaminant occurrence

and the NIRS data, how EPA assessed the data quality, completeness, and representativeness, and how the data were used to generate estimates of contaminant occurrence. The “UCMR 1 Occurrence Report” provides more detailed information about the UCMR 1 data, how EPA assessed the data quality, completeness, representativeness, and how the data were used to generate estimates of contaminant occurrence.

The comprehensive regulatory support document (USEPA, 2006a) provides a summary of the results from the drinking water occurrence analyses discussed in the aforementioned technical support documents, as well as information on production and use, environmental releases, and/or occurrence in ambient water, potential health effects, the Agency's preliminary determination, and the rationale for the determination.

IV. Preliminary Regulatory Determinations

A. Summary of the Preliminary Regulatory Determination

The Agency has made a preliminary determination that each of the 11 contaminants listed in Table 3 do not meet all three of the SDWA criteria (discussed in section II.C) and thus do not warrant regulation with an NPDWR. Table 3 also summarizes the primary information used to make these regulatory determinations. Section IV.B of this action provides a more detailed summary of the information and the rationale used by the Agency to reach its preliminary decisions. The Agency solicits public comment on the preliminary determinations for these 11 contaminants.

BILLING CODE 6560-50-P EP01MY07.051

BILLING CODE 6560-50-C B. Contaminant Profiles

This section provides further details on the background, health, and occurrence information that the Agency used to evaluate each of the 11 candidate contaminants considered for regulatory determination. For each candidate, the Agency evaluated the available human and toxicological data, derived a health reference level, and evaluated the potential and/or likely occurrence and exposed population for the contaminant in public water systems

he background, health, and occurrence information that the Agency used to evaluate each of the 11 candidate contaminants considered for regulatory determination. For each candidate, the Agency evaluated the available human and toxicological data, derived a health reference level, and evaluated the potential and/or likely occurrence and exposed population for the contaminant in public water systems. The Agency used the findings from these evaluations to determine whether the three SDWA statutory requirements were satisfied.

As discussed in section II.E, the Agency has also prepared a regulatory support document (USEPA, 2006a) that provides more details on the background, health, and occurrence information/analyses used to evaluate and make preliminary determinations for these 11 candidates.

1. Boron

a. Background. Boron, a metalloid, tends to occur in nature in the form of borates (e.g., boric acid, borax, boron oxide). Man-made releases are typically in the form of borates or boron halides (e.g., boron trichloride, boron trifluoride). Boron compounds are used in the production of glass, ceramics, soaps, fire retardants, pesticides, cosmetics, photographic materials, and high energy fuels (USGS, 2004; ATSDR, 1992).

Natural processes such as the weathering of rocks, volcanic activity, and geothermal steam contribute to the release of boron in the environment. Releases to the environment from human activities occur through the production, use, and disposal of boron-containing compounds (e.g., industrial emissions, fertilizer and herbicide runoff, hazardous waste deposits, and municipal sewage) (HSDB, 2004a; ATSDR, 1992).

posits, and municipal sewage) (HSDB, 2004a; ATSDR, 1992).

Although quantitative data are not available on the man-made releases of most borates in the United States, two boron halide compounds, boron trichloride and boron trifluoride, are listed as Toxics Release Inventory (TRI) chemicals. TRI data for boron trichloride and boron trifluoride are reported for the years 1995 to 2003 (USEPA, 2006d). The TRI data show boron trichloride releases from facilities in 6 States and indicate that air emissions account for all of the total releases of boron trichloride (on- and off-site), which generally fluctuated in the range of hundreds of pounds per year during the period of record. The TRI data show boron trifluoride releases from facilities in 14 States and indicate that air emissions also account for nearly all of the boron trifluoride releases, which ranged in the tens of thousands of pounds annually.

b. Health Effects. The Institute of Medicine (IOM, 2001) of the National Academies categorizes boron as a possible trace mineral nutrient for humans. Boron is essential for plant growth and deficiency studies in animals and humans have provided some evidence that low intakes of boron affects cellular function and the activity of other nutrients. It may interact with Vitamin D and calcium homeostasis, influence estrogen metabolism, and play a role in cognitive function (IOM, 2001). Iyengar et al. (1988) reported an average dietary intake of 1.5 mg/day for male adults based on the Food and Drug Administration (FDA) Total Diet Study (TDS).

). Iyengar et al. (1988) reported an average dietary intake of 1.5 mg/day for male adults based on the Food and Drug Administration (FDA) Total Diet Study (TDS).

Some human oral data are available from cases where boron was ingested as a medical treatment. When the amount ingested was less than 3.68 mg/kg, subjects were asymptomatic, while doses of 20 and 25 mg/kg resulted in nausea and vomiting. Case reports and surveys of accidental poisonings indicate that the lethal doses of boron range from 15 to 20 grams (approximately 200 to 300 mg/kg) for adults, 5 to 6 grams (approximately 70 to 85 mg/kg) for children, and 2 to 3 grams (approximately 30 to 45 mg/kg) for infants (USEPA, 2004b).

The primary adverse effects seen in animals after chronic exposure to low doses of boron generally involve the testes and developing fetus. Chronic effects of dietary boron exposure in two-year studies included testicular atrophy and spermatogenic arrest in dogs, decreased food consumption,

In developmental studies with rats, mice, and rabbits, oral exposure to boric acid resulted in decreased pregnancy rate, increased prenatal mortality, decreased fetal weights, and increased malformations in fetuses and pups. However, these reproductive effects were associated with maternal toxicity including changes in maternal organ weights, body weights, weight gain, and increased renal tubular dilation and/or regeneration (Price et al. , 1990, 1994, 1996; Heindel et al. , 1992, 1994; Field et al. , 1989). Reproductive effects in males were noted in the subchronic and chronic studies described in the preceding paragraphs.

The EPA RfD for boron is 0.2 mg/kg/day (USEPA, 2004c) based on developmental effects in rats from two studies (Price et al. , 1996; Heindel et al. , 1992). The RfD was derived using the benchmark dose (BMD) method (bench mark dose level or BMDL from Allen et al. , 1996). EPA calculated the HRL of 1.4 mg/L or 1,400 μg/L for boron using the RfD of 0.2 mg/kg-day and a 20 percent screening relative source contribution

oron is 0.2 mg/kg/day (USEPA, 2004c) based on developmental effects in rats from two studies (Price et al. , 1996; Heindel et al. , 1992). The RfD was derived using the benchmark dose (BMD) method (bench mark dose level or BMDL from Allen et al. , 1996). EPA calculated the HRL of 1.4 mg/L or 1,400 μg/L for boron using the RfD of 0.2 mg/kg-day and a 20 percent screening relative source contribution.

EPA also evaluated whether health information is available regarding the potential effects on children and other sensitive populations. Studies in rats, mice, and rabbits identify the developing fetus as potentially sensitive to boron. Price et al. (1996) identified a LOAEL of 13.3 mg/kg-day and an NOAEL of 9.6 mg/kg-day in the developing fetus, based on decreased fetal body weight in rats. Accordingly, boron at concentrations greater than the HRL might have an effect on prenatal development. Individuals with severely impaired kidney function might also be sensitive to boron exposure since the kidney is the most important route for excretion.

c. Occurrence Analyses. The National Inorganics and Radionuclides Survey (NIRS) included boron as an analyte. Using data from NIRS, EPA performed an initial evaluation of occurrence and exposure at levels greater than 700 μg/L ( 1/2 the HRL) and greater than 1,400 μg/L (the HRL for boron). The NIRS data indicate that approximately 4.3 percent (or 43) of the 989 ground water PWSs sampled had detections of boron at levels greater than 700 μg/L, affecting approximately 2.9 percent of the population served (or 42,700 people from 1.48 million). Approximately 1.7 percent (or 17) of 989 ground water PWSs sampled had detections of boron at levels greater than 1,400 μg/L, affecting approximately 0.4 percent of the population served (6,400 people from 1.48 million) (USEPA, 2006a and 2006c).

Because NIRS did not contain data for surface water systems, the Agency evaluated the results of a survey funded by the American Water Works Association Research Foundation (Frey et al

) of 989 ground water PWSs sampled had detections of boron at levels greater than 1,400 μg/L, affecting approximately 0.4 percent of the population served (6,400 people from 1.48 million) (USEPA, 2006a and 2006c).

Because NIRS did not contain data for surface water systems, the Agency evaluated the results of a survey funded by the American Water Works Association Research Foundation (Frey et al. , 2004) to gain a better understanding of the potential occurrence of boron in surface water systems. The AWWARF study recruited 189 PWSs representing 407 source waters that covered 41 states. Of these 407 PWS source water samples, 342 were returned and 341 were analyzed for boron. Of these 341 samples, approximately 67 percent (or 228) represented ground water sources and 33 percent (or 113) represented surface water sources. None of the 113 surface water sources exceeded the boron HRL of 1,400 μg/L and the maximum concentration observed in surface water was 345 μg/L. Extrapolation of the data indicates that 95 percent of the ground water detections had boron levels less than 1,054 μg/L; the maximum observed concentration in ground water was approximately 3,300 μg/L. Seven of the 228 ground water sources (from 5 systems) had boron concentrations greater than 1,400 μg/L (Seidel, 2006).

d. Preliminary Determination. The Agency has made a preliminary determination not to regulate boron with an NPDWR. While boron was found at levels greater than the HRL (and 1/2 the HRL) in several of the ground water systems surveyed by NIRS, it was not found at levels greater than the HRL (or 1/2 the HRL) in the surface waters sources evaluated in the AWWARF study. Taking this surface water information into account, the Agency believes that the overall national occurrence and exposure from both surface and ground water systems together is likely to be lower than the values observed for the NIRS ground water data

tems surveyed by NIRS, it was not found at levels greater than the HRL (or 1/2 the HRL) in the surface waters sources evaluated in the AWWARF study. Taking this surface water information into account, the Agency believes that the overall national occurrence and exposure from both surface and ground water systems together is likely to be lower than the values observed for the NIRS ground water data. Because boron is not likely to occur at levels of concern when considering both surface and ground waters systems, the Agency believes that a national primary drinking water regulation does not present a meaningful opportunity for health risk reduction.

The Agency encourages those States with public water systems that have boron at concentrations above the HRL to evaluate site-specific protective measures and to consider whether State-level guidance (or some other type of action) is appropriate. The Agency also plans to update the Health Advisory for boron to provide more recent health information. The updated Health Advisory will provide information to any States with public water systems that may have boron above the HRL.

2 and 3. Mono- and Di-Acid Degradates of Dimethyl Tetrachloroterephthalate (DCPA)

a. Background. Dimethyl tetrachloroterephthalate (DCPA), a synthetic organic compound (SOC) marketed under the trade name “Dacthal,” is a pre-emergent herbicide historically used to control weeds in ornamental turf and plants, strawberries, seeded and transplanted vegetables, cotton, and field beans. As of 1990, more than 80 percent of its use was for turf, including golf courses and home lawns (USEPA, 1990b). On July 27, 2005, in response to concerns about groundwater contamination (especially for one of the DCPA degradates), the Agency published a Federal Register notice announcing that the registrant for Dacthal had voluntarily terminated a number of uses for products containing DCPA (70 FR 43408; USEPA, 2005f). The only uses retained were those for use on sweet potatoes, eggplant, kale and turnips

. On July 27, 2005, in response to concerns about groundwater contamination (especially for one of the DCPA degradates), the Agency published a Federal Register notice announcing that the registrant for Dacthal had voluntarily terminated a number of uses for products containing DCPA (70 FR 43408; USEPA, 2005f). The only uses retained were those for use on sweet potatoes, eggplant, kale and turnips.

DCPA is not especially mobile or persistent in the environment. Biodegradation and volatilization are the primary dissipation routes. Degradation of DCPA forms two breakdown products, the mono-acid degradate (or monomethyl tetrachloroterephthalate or MTP) and the di-acid degradate (tetrachloroterephthalic acid or TPA). The di-acid, which is the major degradate, is unusually mobile and persistent in the field, with a potential to leach into water (USEPA, 1998c).

Several studies and reports provide estimates of the amount of DCPA used during the 1990s in the United States. The Agency estimated that 1.6 million pounds of DCPA active ingredient a.i. were used annually in the early 1990s (USEPA, 1998c). USGS estimated that approximately 998 thousand pounds of DCPA a.i. were used annually circa 1992 (Thelin and Gianessi, 2000). The National Center for Food and Agricultural Policy (NCFAP, 2004) estimates that approximately 1.7 million

b. Health Effects. Currently, no subchronic or chronic studies are available to assess the toxicological effects of MTP (the mono-acid degradate) and 3 studies in rats (30 and 90-day feeding studies and a one-generation reproductive study) are available for TPA (the di-acid degradate). The effects of exposure were mild (weight loss and diarrhea) and occurred at doses greater than or equal to 2,000 mg/kg/day. No reproductive effects were observed.

The present toxicity database for MTP and TPA is not sufficient to derive RfDs for these two chemicals

dies in rats (30 and 90-day feeding studies and a one-generation reproductive study) are available for TPA (the di-acid degradate). The effects of exposure were mild (weight loss and diarrhea) and occurred at doses greater than or equal to 2,000 mg/kg/day. No reproductive effects were observed.

The present toxicity database for MTP and TPA is not sufficient to derive RfDs for these two chemicals. However, since the available data indicate that neither MTP nor TPA are more toxic than their parent compound, DCPA, the Agency suggests that the RfD for the DCPA parent would be protective against exposure from these two DCPA metabolites (USEPA, 1998c). Both compounds are formed in the body from the DCPA parent and therefore, the toxicity of these degradates is reflected in the toxicity of the parent. The RfD for DCPA is 0.01 mg/kg/day based on a chronic rat study (ISK Biotech Corporation, 1993) with a NOAEL of 1.0 mg/kg/day and an uncertainty factor of 100 for rat to human extrapolation and intra-species variability.

No carcinogenicity studies have been performed using either TPA or MTP. Based on the cancer data for the parent and lack of mutagenicity for TPA and DCPA, the Agency (USEPA, 2004d) concludes that TPA is unlikely to pose a cancer risk. Klopman et al. (1996) evaluated the carcinogenic potential of TPA based on its chemical and biological properties, as well as by a variety of computational tools, and determined that it did not present any substantial carcinogenic risk. There was suggestive evidence that DCPA could be carcinogenic based on an increased incidence of thyroid and liver tumors in rats. The presence of hexachlorobenzene and dioxin as impurities in the material tested could have contributed to the cancer risk.

Using the DCPA RfD of 0.01 mg/kg/day (USEPA, 1994) and a 20 percent screening relative source contribution, the Agency calculated an HRL of 0.07 mg/L or 70 μg/L for DCPA and used this HRL for TPA and MTP

based on an increased incidence of thyroid and liver tumors in rats. The presence of hexachlorobenzene and dioxin as impurities in the material tested could have contributed to the cancer risk.

EPA also evaluated whether health information is available regarding the potential effects on children and other sensitive populations. There are no data that identify a particular sensitive population for DCPA exposure. Results of a single developmental study indicate that exposure to pregnant dams with doses less than or equal to 2,500 mg/kg/day of TPA via gavage did not have an adverse effect on the fetus. EPA did not identify any data that suggest gender-related differences in toxicity or sensitivity in the elderly.

c. Occurrence. EPA included the DCPA mono- and di-acid degradates (MTP and TPA) as analytes in the UCMR 1. The analysis results reported for UCMR 1 are the sum of both the mono- and di-acid degradates. EPA converted the analysis result for the degradates to the parent DCPA equivalent and performed an initial evaluation of occurrence and exposure at levels greater than 35 μg/L ( 1/2 the HRL) and greater than 70 μg/L (the HRL). As previously discussed, EPA used the HRL derived for the DCPA parent because it includes the toxicity for the mono- and di-acid degradates. While the UCMR 1 data indicate that the DCPA degradates were the most commonly reported analytes in the monitoring survey (detected at an MRL of 1 μg/L in 772 samples from 175 of the 3,868 PWSs sampled), very few systems exceeded the health level of concern. PWSs with detections were found in 24 States and 1 Territory

PA parent because it includes the toxicity for the mono- and di-acid degradates. While the UCMR 1 data indicate that the DCPA degradates were the most commonly reported analytes in the monitoring survey (detected at an MRL of 1 μg/L in 772 samples from 175 of the 3,868 PWSs sampled), very few systems exceeded the health level of concern. PWSs with detections were found in 24 States and 1 Territory. The UCMR 1 data indicate that approximately 0.05 percent (or 2) of the 3,868 PWSs sampled had a detection of the DCPA degradates at levels greater than 35 μg/L, affecting approximately 0.33 percent of the population served (or 739,000 people from 225 million). Approximately 0.03 percent (or 1) of the 3,868 PWSs sampled have a detection of the DCPA degradates at levels greater than 70 μg/L, affecting less than 0.01 percent of the population served (or 500 people from 225 million) (USEPA, 2006a and 2006b).

EPA also evaluated several sources of supplemental occurrence information for the DCPA parent, the mono-acid degradate and/or the di-acid degradate. These supplemental sources include:

• The National Pesticide Survey (NPS),

• The provisional pesticide results from the 1992-2001 USGS NAWQA survey of ambient surface and ground waters across the U.S., and

• Studies performed by the DCPA or dacthal registrant.

As part of the National Pesticide Survey, EPA collected samples from approximately 1,300 community water systems and rural drinking water wells between 1988 and 1990. The NPS included monitoring for the DCPA parent and the di-acid degradate. The DCPA parent was not detected in any wells (using a detection limit of 0.06 μg/L). While the di-acid degradate was detected in 49 of 1,347 wells (using a detection limit of 0.1 μg/L), the maximum reported concentration of 7.2 μg/L did not exceed the HRL of 70 μg/L (USEPA, 1990a).

The USGS NAWQA program included the DCPA parent and the mono-acid degradate as analytes in its 1992-2001 monitoring survey of ambient surface and ground waters across the United States

oth of its degradates. The average reported values, which are the sum of the parent and its degradates, were 50.36 μg/L in New York and 12.75 μg/L in California. Neither average value exceeded the HRL of 70 μg/L (USEPA, 1998c).

d. Preliminary Determination. The Agency has made a preliminary determination not to regulate the DCPA mono-acid degradate and/or the DCPA di-acid degradate with an NPDWR. Because these degradates appear to occur infrequently at health levels of concern in PWSs, the Agency believes that a national primary drinking water regulation does not present a meaningful opportunity for health risk reduction. While the Agency recognizes that these degradates have been detected in the PWSs monitored under the UCMR 1, only 1 PWS had a detect above the HRL.

The Agency encourages those States with public water systems that have detects for these degradates to evaluate site-specific protective measures and to consider whether State-level guidance (or some other type of action) is appropriate. The Agency also plans to update the Health Advisory for the DCPA parent to include the mono and di acid degradates, as well as any recent health information related to these compounds. The updated Health Advisory will provide information to any States with public water systems that may have DCPA degradates at levels above the HRL.

4. 1,1-Dichloro-2,2-bis( p -chlorophenyl) ethylene (DDE)

a. Background. DDE is a primary metabolite of DDT, 15 a pesticide once used to protect crops and eliminate disease-carrying insects in the U.S. until it was banned in 1973. DDE itself has no commercial use and is only found in the environment as a result of contamination and/or breakdown of DDT. While DDE tends to adsorb strongly to surface soil and is fairly insoluble in water, it may enter surface waters from runoff that contains soil particles contaminated with DDE. In both soil and water, DDE is subject to photodegradation, biodegradation, and volatilization (ATSDR, 2002)

f has no commercial use and is only found in the environment as a result of contamination and/or breakdown of DDT. While DDE tends to adsorb strongly to surface soil and is fairly insoluble in water, it may enter surface waters from runoff that contains soil particles contaminated with DDE. In both soil and water, DDE is subject to photodegradation, biodegradation, and volatilization (ATSDR, 2002).

15 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane.

b. Health Effects. DDE is not produced as a commercial product. This has limited the numbers of conventional studies that have been performed to assess toxicological properties. Limited data on DDE, mostly from a National Cancer Institute (NCI) bioassay, suggest that the liver is the primary target organ in mammalian species. However, the NCI study did not evaluate a full array of noncancer endpoints. There is an RfD of 0.0005 mg/kg/day for the parent pesticide DDT based on a NOAEL of 0.05 mg/kg/day from a dietary subchronic study (USEPA, 1996b). In this study, liver lesions were identified at a LOAEL of 0.25 mg/kg/day. Data on DDT identify effects on the nervous and hormonal systems as adverse effects that might also be seen with DDE because it is one of DDT's primary metabolites. The limited data for DDE suggest that any effects on the nervous system are less severe than those seen with DDT. Endocrine effects from DDE are discussed in this section.

Based on animal studies DDE is likely to be carcinogenic to humans. This classification is based on increases in the incidence of liver tumors, including carcinomas, in two strains of mice and in hamsters after dietary exposure to DDE. Some epidemiological studies suggest a possible association of the levels of DDE in serum with breast cancer. However, other studies with similar methodologies do not show any association. DDE was mutagenic in mouse lymphoma L5178Y and Chinese hamster V79 cells but negative in the Ames assay

f liver tumors, including carcinomas, in two strains of mice and in hamsters after dietary exposure to DDE. Some epidemiological studies suggest a possible association of the levels of DDE in serum with breast cancer. However, other studies with similar methodologies do not show any association. DDE was mutagenic in mouse lymphoma L5178Y and Chinese hamster V79 cells but negative in the Ames assay. In the 1988 IRIS, EPA calculated an oral slope factor of 0.34 (mg/kg/day) −1 for DDE (USEPA, 1988a). For this regulatory determination, EPA calculated an oral slope factor from the same data set (from the 1988 IRIS) using the EPA 1999 Cancer Guidelines (USEPA, 1999a). The revised slope factor is 1.67 x 10 −1 (mg/kg/day) −1 resulting in a one-in-a-million cancer-risk (HRL) of 0.2 μg/L.

There are some indications that DDE has an adverse impact on the immune system (Banerjee et al. , 1996). Oral exposures to 22 mg/kg/day for 6 weeks suppressed serum immunoglobin levels and antibody titers. Inhibition of leucocytes and macrophage migration were observed at the cellular level. Considerable evidence exists that DDE can act as an endocrine disruptor since it binds to the estrogen and androgen receptors. DDE has a stronger affinity for the androgen receptor than for the estrogen receptor. It competes with testicular hormones for the androgen receptor leading to receptor-related changes in gene expression (Kelce et al. , 1995).

EPA evaluated whether health information is available regarding the potential effects on children and other sensitive populations. Children and adolescents may be sensitive populations for exposure to DDE due to its endocrine disruption properties. Some data suggest that DDE can delay puberty in males (ATSDR, 2002).

s may be sensitive populations for exposure to DDE due to its endocrine disruption properties. Some data suggest that DDE can delay puberty in males (ATSDR, 2002).

c. Occurrence. EPA included DDE as an analyte in the UCMR 1. Because the HRL for DDE (0.2 μg/L) is lower than the minimum reporting limit (MRL) used for monitoring (0.8 μg/L), EPA used the MRL value to evaluate occurrence and exposure. The MRL is within the 10 −4 to the 10 −6 cancer risk range for DDE. In evaluating the UCMR 1 data, EPA found that approximately 0.03 percent (or 1) of the 3,867 PWSs sampled had a detection of DDE at the MRL of 0.8 μg/L, affecting approximately 0.01 percent of the population served (or 18,000 people from 226 million) (USEPA, 2006a and 2006b).

The USGS NAWQA program included DDE as an analyte in its 1992-2001 monitoring survey of ambient surface and ground waters across the United States. EPA evaluated the results of the provisional data, which are available on the Web (Martin et al. , 2003; Kolpin and Martin, 2003), as a supplemental source of occurrence information. While the USGS detected DDE in both surface and ground waters, 95 percent of the samples from the various land use settings were less than 0.006 μg/L (the USGS reporting limit). The maximum surface water concentration, 0.062 μg/L (agricultural setting), and the maximum ground water concentration, 0.008 μg/L (agricultural setting), are both less than 0.2 μg/L (the DDE HRL).

d. Preliminary Determination. The Agency has made a preliminary determination not to regulate DDE with an NPDWR. Because DDE appears to occur infrequently at levels of concern in PWSs, the Agency believes that a national primary drinking water regulation does not present a meaningful opportunity for health risk reduction. DDE was detected in only one of the PWSs monitored under the UCMR 1 at a level greater than the MRL (0.8 μg/L), a concentration that is within the 10 −4 to the 10 −6 cancer risk range

PDWR. Because DDE appears to occur infrequently at levels of concern in PWSs, the Agency believes that a national primary drinking water regulation does not present a meaningful opportunity for health risk reduction. DDE was detected in only one of the PWSs monitored under the UCMR 1 at a level greater than the MRL (0.8 μg/L), a concentration that is within the 10 −4 to the 10 −6 cancer risk range. In addition, ambient water data from the USGS indicate that the maximum concentrations detected in surface and ground water were less than the HRL of 0.2 μg/L.

EPA recognizes that DDE is listed as a probable human carcinogen. For this reason, the Agency encourages those States with public water systems that might have DDE above the HRL to evaluate site-specific protective measures and to consider whether State-level guidance (or some other type of action) is appropriate.

5. 1,3-Dichloropropene (1,3-DCP; Telone)

a. Background. 1,3-Dichloropropene (1,3-DCP), a synthetic volatile organic compound, is used as a pre-plant soil fumigant to control nematodes and other pests in soils to be planted with all types of food and feed crops. 1,3-DCP is typically injected 12″ to 18″ beneath the soil surface and can only be used by certified handlers (USEPA, 1998b). To mitigate risks to drinking water, 1999 labeling requirements restrict the use of 1,3-DCP:

• In areas with shallow ground water and vulnerable soils in certain northern tier States (ND, SD, WI, MN, NY, ME, NH, VT, MA, UT, and MT);

• In fields within 100 feet of a drinking water well; and

• In areas overlying karst 16 geology.

16 Karst is a type of typography that is formed by the dissolution and collapse of soluble rocks (typically limestone and dolomite)

ict the use of 1,3-DCP:

• In areas with shallow ground water and vulnerable soils in certain northern tier States (ND, SD, WI, MN, NY, ME, NH, VT, MA, UT, and MT);

• In fields within 100 feet of a drinking water well; and

• In areas overlying karst 16 geology.

16 Karst is a type of typography that is formed by the dissolution and collapse of soluble rocks (typically limestone and dolomite). According to the Karst Waters Institute, as excerpted by USGS (2006), common geological characteristics of karst regions that influence human use of its land and water resources include ground subsidence,

Estimates of national annual use during the 1990s vary widely, from approximately 23 to 40 million pounds of active ingredient a.i. Based on information from a 1991 data call-in and other sources, EPA estimates that approximately 23 million pounds of 1,3-DCP a.i. were used annually from 1990 to 1995 (USEPA, 1998b). NCFAP (2004) estimates that approximately 40 million pounds a.i. were used in 1992 and approximately 35 million pounds a.i. were used in 1997.

1,3-Dichloropropene is listed as a TRI chemical and releases are reported from facilities in 17 States over a time period covering 1988 to 2003 (although not all States had facilities reporting releases every year) (USEPA, 2006e). Air emissions appear to account for most of the on-site (and total) releases and generally declined between 1988 and 2003. A sharp decrease in air emissions is evident between 1995 and 1996. Surface water discharges are minor compared to air emissions and no obvious trend is evident between 1988 and 2003. Reported underground injection, releases to land, and off-site releases are generally insignificant.

b. Health Effects

ount for most of the on-site (and total) releases and generally declined between 1988 and 2003. A sharp decrease in air emissions is evident between 1995 and 1996. Surface water discharges are minor compared to air emissions and no obvious trend is evident between 1988 and 2003. Reported underground injection, releases to land, and off-site releases are generally insignificant.

b. Health Effects. Chronic and subchronic exposures to 1,3-DCP at doses of 12.5 mg/kg/day and above in animal dietary studies indicate that 1,3-DCP is toxic to organs involved in metabolism (liver), excretion of conjugated metabolites (e.g., urinary bladder and the kidney) and organs along the portals of entry (e.g., forestomach for oral administration; mucous membrane of the nasal passage and lungs for inhalation exposure). Exposure to 1,3-DCP has not been shown to cause reproductive or developmental effects. Neither reproductive nor developmental toxicity were observed in a two-generation reproductive study in rats or in developmental studies in rats and rabbits at maternal inhalation concentrations up to 376 mg/m 3 (USEPA, 2000a). Even concentrations that produced parental toxicity did not produce reproductive or developmental effects (USEPA, 2000a).

An RfD of 0.03 mg/kg/day for 1,3-DCP (USEPA, 2000a) has been established using a benchmark dose (BMD) analysis based on a two-year chronic bioassay (Stott et al. , 1995) in which chronic irritation (forestomach hyperplasia) and significant body weight reduction were the critical and co-critical effects, respectively. A reference concentration (RfC) of 0.02 mg/m 3 was derived from a two-year bioassay (Lomax et al. , 1989), which observed histopathology in the nasal epithelium.

Under the proposed cancer risk assessment guidelines, the weight of evidence for evaluation of 1,3-DCP's ability to cause cancer suggest that it is likely to be carcinogenic to humans (USEPA, 2000a)

nd co-critical effects, respectively. A reference concentration (RfC) of 0.02 mg/m 3 was derived from a two-year bioassay (Lomax et al. , 1989), which observed histopathology in the nasal epithelium.

Under the proposed cancer risk assessment guidelines, the weight of evidence for evaluation of 1,3-DCP's ability to cause cancer suggest that it is likely to be carcinogenic to humans (USEPA, 2000a). This characterization is supported by tumor observations in chronic animal bioassays for both inhalation and oral routes of exposure.

The oral cancer slope factors calculated from chronic dietary, gavage and inhalation data ranged from 5 × 10 − 2 to 1 × 10 − 1 (mg/kg/day) − 1 . Due to uncertainties in the delivered doses in some studies, EPA (IRIS) recommended using the oral slope factor of 1 × 10 − 1 (mg/kg/day) − 1 from an NTP (1985) study. Using this oral slope factor, EPA calculated an HRL of 0.4 μg/L at the 10 − 6 cancer risk level.

EPA also evaluated whether health information is available regarding the potential effects on children and other sensitive populations. No human or animal studies are available that have examined the effect of 1,3-DCP exposure on juvenile subjects. Therefore, its effects on children are unknown. Developmental studies in rats and rabbits show no evidence of developmental effects and therefore it is unlikely that 1,3-DCP causes developmental toxicity.

c. Occurrence. EPA included 1,3-DCP as an analyte in the UCM Round 1 and UCM Round 2 surveys. The MRLs for UCM Round 1 ranged from 0.02 to 10 μg/L and the MRLs for UCM Round 2 ranged from 0.08 to 1 μg/L. EPA also analyzed for 1,3-DCP using the samples from the small systems that were included in the UCMR 1 survey. The MRL used for the UCMR 1 survey was 0.5 μg/L. Because some of these reporting limits exceeded the thresholds of interest, the occurrence analyses may result in an underestimate of systems affected (USEPA, 2006a, 2006b and 2006c)

and the MRLs for UCM Round 2 ranged from 0.08 to 1 μg/L. EPA also analyzed for 1,3-DCP using the samples from the small systems that were included in the UCMR 1 survey. The MRL used for the UCMR 1 survey was 0.5 μg/L. Because some of these reporting limits exceeded the thresholds of interest, the occurrence analyses may result in an underestimate of systems affected (USEPA, 2006a, 2006b and 2006c). However, the MRL values used for UCM Round 1 and UCM Round 2 as well as UCMR 1 are within the 10 − 4 to the 10 − 6 cancer risk range.

The UCM Round 1 Cross Section data indicate that approximately 0.16 percent (or 15) of the 9,164 PWSs sampled had detections of 1,3-DCP at levels greater than 0.2 μg/L ( 1/2 the HRL), affecting approximately 0.86 percent of the population served (or 438,000 of 51 million). The UCM Round 1 Cross Section data also indicate the same values when the data are analyzed using 0.4 μg/L (the HRL). That is, 0.16 percent (or 15) of 9,164 PWSs sampled had detections greater than 0.4 μg/L (the HRL), affecting approximately 0.86 percent of the population served (or 438,000 of 51 million people). The 99th percentile of all detections is 2 μg/L and the maximum reported value is 2 μg/L.

The UCM Round 2 Cross Section data indicate that approximately 0.30 percent (or 50) of the 16,787 PWSs sampled had detections of 1,3-DCP at levels greater than 0.2 μg/L ( 1/2 the HRL), affecting approximately 0.42 percent of the population served (or 193,000 of 46 million). The UCM Round 2 Cross Section data indicate that approximately 0.23 percent (or 38) of the 16,787 PWSs sampled had detections of 1,3-DCP at levels greater than 0.4 μg/L (the HRL), affecting approximately 0.33 percent of the population served (or 152,000 of 46 million). The 99th percentile of all detections is 39 μg/L and the maximum reported value is 39 μg/L

tion served (or 193,000 of 46 million). The UCM Round 2 Cross Section data indicate that approximately 0.23 percent (or 38) of the 16,787 PWSs sampled had detections of 1,3-DCP at levels greater than 0.4 μg/L (the HRL), affecting approximately 0.33 percent of the population served (or 152,000 of 46 million). The 99th percentile of all detections is 39 μg/L and the maximum reported value is 39 μg/L.

Because the sample preservative used may have resulted in potential underestimates of occurrence for the UCM Rounds 1 and 2 data, EPA subsequently analyzed for 1,3-DCP using the samples provided by 796 of the small systems included in the recent UCMR 1 survey. None of the 3,719 samples from these 796 small systems (serving a population of 2.8 million) had detects of 1,3-DCP at levels greater than 0.5 μg/L (the minimum reporting limit used for the analysis of 1,3-DCP and a level that is slightly higher than the HRL).

EPA also evaluated several sources of supplemental information, which included:

• The National Pesticide Survey,

• The Pesticides in Ground Water Database,

• A well water survey submitted by the registrant of Telone (1,3-DCP),

• The USGS VOC National Synthesis Random Source Water Survey, and

• The USGS VOC National Synthesis Focused Source Water Survey.

As part of the National Pesticide Survey, EPA collected samples from approximately 1,300 community water systems and rural drinking water wells between 1988 and 1990. The NPS included cis and trans 1,3-DCP as analytes in the monitoring survey. Neither compound was detected in the survey using a minimum reporting limit of 0.010 μg/L (USEPA, 1990a).

The Pesticides in Ground Water Database (USEPA, 1992b) indicates that 1,3-DCP was found in 6 of 21,270 ground water wells sampled in 7 States. The 6 wells with positive detections for 1,3-DCP included 3 wells in California (at concentrations ranging from 0.890 to 31.0 μg/L), 2 wells in Florida (at concentrations of 0.279 to 7.83 μg/L), and 1 well in Montana (at concentrations of 18 to 140 μg/L)

In 1998, the registrant for Telone (1,3-DCP) submitted a private well water study to the Agency. The well water survey covered 5 regions where Telone was used intensively and evaluated 518 wells (~5,800 samples) for the presence of 1,3-DCP. Of the 518 wells, 65 had detectable levels of 1,3-DCP and/or its metabolites at levels greater than 0.015 μg/L (the detection limit for 1,3-DCP was 0.015 μg/L and the metabolites were 0.023 μg/L). None of the wells exceeded 0.2 μg/L (a level half the EPA-derived HRL for 1,3-DCP) (USEPA, 2004e and 2004f).

For the Random Source Water Survey, the USGS collected samples from 954 source waters that supply community water systems between 1999 and 2000. For the Focused Source Water Survey, the USGS collected 451 samples from 134 source waters that supply community water systems between 1999 and 2001. The USGS included 1,3-DCP as an analyte in both surveys. The USGS did not detect 1,3-DCP in any of the source water samples from the Random Source Water Survey using a reporting limit of 0.2 μg/L (a level that is one-half the HRL for 1,3-DCP). In addition, the USGS did not detect 1,3-DCP in any of the source water samples in the Focused Source Water Survey using a detection limit of 0.024 μg/L for cis-1,3-dichloropropene and 0.026 μg/L for trans-1,3-dichloropropene (levels that are about 16 times lower than the HRL for 1,3-DCP) (Ivahnenko et al. , 2001; Grady, 2003; Delzer and Ivahnenko, 2003a).

d. Preliminary Determination. The Agency has made a preliminary determination not to regulate 1,3-DCP with an NPDWR

les in the Focused Source Water Survey using a detection limit of 0.024 μg/L for cis-1,3-dichloropropene and 0.026 μg/L for trans-1,3-dichloropropene (levels that are about 16 times lower than the HRL for 1,3-DCP) (Ivahnenko et al. , 2001; Grady, 2003; Delzer and Ivahnenko, 2003a).

d. Preliminary Determination. The Agency has made a preliminary determination not to regulate 1,3-DCP with an NPDWR. Because 1,3-DCP appears to occur infrequently at health levels of concern in PWSs, the Agency believes that a national primary drinking water regulation does not present a meaningful opportunity for health risk reduction. While 1,3-DCP was detected in the UCM Round 1 (late 1980s) and the UCM Round 2 (mid 1990s) surveys, it was not detected in a subsequent evaluation of 796 small systems from the UCMR 1 survey. In addition, the USGS did not detect 1,3-DCP in two occurrence studies performed between 1999 and 2001 using monitoring levels that were lower than the HRL. EPA believes the 1999 pesticide labeling requirements, which are intended to mitigate risks to drinking water, may be one reason for the lack of occurrence of 1,3-DCP at levels of concern in subsequent monitoring surveys.

EPA recognizes that 1,3-dichloropropene is listed as a probable human carcinogen. For this reason, the Agency encourages those States with public water systems that may have 1,3-dichloropropene above the HRL to evaluate site-specific protective measures and to consider whether State-level (or some other type of action) is appropriate. The Agency also plans to update the Health Advisory document for 1,3-DCP to provide more recent health information. The updated Health Advisory will provide information to any States with public water systems that may have 1,3-DCP above the HRL.

6 and 7. 2,4- and 2,6-Dinitrotoluenes (2,4- and 2,6-DNT)

a. Background. 2,4- and 2,6-dinitrotoluene (DNT), semi-volatile organic compounds, are two of 6 isomers of dinitrotoluene

ate the Health Advisory document for 1,3-DCP to provide more recent health information. The updated Health Advisory will provide information to any States with public water systems that may have 1,3-DCP above the HRL.

6 and 7. 2,4- and 2,6-Dinitrotoluenes (2,4- and 2,6-DNT)

a. Background. 2,4- and 2,6-dinitrotoluene (DNT), semi-volatile organic compounds, are two of 6 isomers of dinitrotoluene. Dinitrotoluenes are used in the production of polyurethane foams, automobile air bags, dyes, ammunition, and explosives, including trinitrotoluene or TNT (HSDB, 2004b and 2004c; ATSDR, 1998). Neither 2,4-nor 2,6-DNT occur naturally. They are generally produced as individual isomers or as a mixture called technical grade DNT (tg-DNT). Technical grade DNT primarily contains a mixture of 2,4-DNT and 2,6-DNT with the remainder consisting of the other isomers and minor contaminants such as TNT and mononitrotoluenes (HSDB, 2004b).

No recent quantitative estimates of DNT production or use are available. The Hazardous Substances Data Bank (HSDB, 2004b) cites a 1980 EPA Ambient Water Quality Criteria Document that places combined 2,4- and 2,6-DNT production at 272,610,000 pounds in 1975.

Both 2,4-DNT and 2,6-DNT are listed as TRI chemicals. TRI data for 2,4-DNT are reported from facilities in 21 States over a time period covering 1988 to 2003. Total releases nationally in 2003 were 14,899 lbs. Releases of all kinds (off-site releases and on-site air, surface, underground injection, and land releases) declined in the early 1990s, and then peaked again around 1999-2001. On-site air emissions and surface water releases of 2,4-DNT were generally the most consistent (least fluctuating) types of releases, with surface water releases generally declining over the period on record (USEPA, 2006f).

2,4-DNT were generally the most consistent (least fluctuating) types of releases, with surface water releases generally declining over the period on record (USEPA, 2006f).

TRI data for 2,6-DNT are reported from facilities in 10 States over a time period covering 1988 to 2003 (with no more than 9 States having reporting facilities in any one year). Total reported releases for 2003 were 10,937 lbs. Trends for 2,6-DNT are similar to those for 2,4-DNT. The TRI data for 2,6-DNT show a trend of declining releases in the late 1980s and early 1990s, and a subsequent peak around 1999-2001. On-site air emissions and surface water discharges are the most consistent types of release for 2,6-DNT and surface water discharges exhibit a declining trend (USEPA, 2006f).

In addition, TRI lists mixed DNT isomer releases as a separate category over the same time period (1990-2003). TRI releases of mixed isomers were reported from facilities in 9 States, with no more than 7 States having reporting facilities in any one year. Total releases in 2003 were 13,790 lbs. Underground injections made up the bulk of on-site releases during the 1990s, but diminished thereafter. Air emissions remained relatively constant. Surface water discharges and releases to land were generally insignificant but peaked in 2003. Off-site releases varied widely. Total releases peaked in 1993 and 1997, and generally diminished in recent years (USEPA, 2006f).

b. Health Effects. In experimental animal studies, 2,4- and 2,6-DNT appear to be acutely toxic at moderate to high levels (LD 50 's 17 ranging from 180 to 1,954 mg/kg) when administered orally. In subacute studies (4 weeks) conducted by Lee et al. (1978), dogs, rats, and mice were fed 2,4-DNT and studied for toxic effects. A NOAEL of 5 mg/kg/day was established; decreased body weight gain and food consumption, neurotoxic signs, and lesions in the brain, kidneys, and testes occurred at 25 mg/kg/day (the highest dose tested)

's 17 ranging from 180 to 1,954 mg/kg) when administered orally. In subacute studies (4 weeks) conducted by Lee et al. (1978), dogs, rats, and mice were fed 2,4-DNT and studied for toxic effects. A NOAEL of 5 mg/kg/day was established; decreased body weight gain and food consumption, neurotoxic signs, and lesions in the brain, kidneys, and testes occurred at 25 mg/kg/day (the highest dose tested).

17 LD 50 = An estimate of a single dose that is expected to cause the death of 50% of the exposed animals. It is derived from experimental data.

Subchronic studies in mice, rats, and dogs that administered 2,4- and 2,6-DNT in the diet produced similar effects in all species. All species exposed to 2,4-DNT exhibited methemoglobinemia, anemia, bile duct hyperplasia sometimes accompanied by hepatic degeneration, and depressed spermatogenesis. Neurotoxicity and renal degeneration occurred in dogs at a dose level of 20 mg/kg/day of 2,6-DNT (Lee et al. , 1976). At a dose level of 25 mg/kg/day of 2,4-DNT, male and female dogs developed impaired muscle movement and paralysis, methemoglobinemia, aspermatogenesis, hemosiderosis of the spleen and liver, cloudy swelling of the kidneys, and lesions of the brain (Ellis et al. , 1985).

2,4-DNT has been shown to cause reproductive effects in rats, mice, and dogs (Ellis et al. , 1979; Lee et al. , 1985; Hong et al. , 1985; Ellis et al. , 1985). Ellis et al. (1979) observed effects in rats following dietary exposure after a dose of 35 mg/kg/day but not 5 mg/kg/day over 3 generations. Male mice fed 2,4-DNT for 13 weeks exhibited testicular degeneration and atrophy and decreased spermatogenesis at 95 mg/kg/day (Hong et al. , 1985). In another reproductive study, dogs exhibited mild to severe testicular degeneration and reduced spermatogenesis (Ellis et al. , 1985) when administered 2,4-DNT in capsules at 25 mg/kg/day

a dose of 35 mg/kg/day but not 5 mg/kg/day over 3 generations. Male mice fed 2,4-DNT for 13 weeks exhibited testicular degeneration and atrophy and decreased spermatogenesis at 95 mg/kg/day (Hong et al. , 1985). In another reproductive study, dogs exhibited mild to severe testicular degeneration and reduced spermatogenesis (Ellis et al. , 1985) when administered 2,4-DNT in capsules at 25 mg/kg/day. There are currently no studies of the reproductive or developmental toxicity of 2,6-DNT although a subchronic study in dogs identified atrophy of spermatogenic cells in males suggesting a one- or two-generation study as a data need for 2,6-DNT.

Some studies evaluated the effects of DNT in the form of a technical mixture (tg-DNT). In a study by Price et al. (1985), the teratogenic potential of tg-DNT (containing approximately 76 percent 2,4-DNT and 19 percent 2,6-DNT) was investigated in rats. The study was conducted in two phases to evaluate the possible teratogenicity of DNT as well as DNT effects on postnatal development. For the first phase, rats were administered 0, 14, 35, 37.5, 75, 100, or 150 mg/kg/day of DNT in corn oil by gavage. In the postnatal phase, rats were administered 14, 35, 37.5, 75, or 100 mg/kg/day of DNT in corn oil by gavage. The NOAEL and LOAEL for developmental toxicity were 14 and 35 mg/kg/day, respectively, based on significant increases in relative liver and spleen weight in the fetuses of dams administered DNT at levels of 35 mg/kg/day or greater. No teratogenic toxicity was seen in the study rats.

In chronic exposures, oral dietary administration of 2,4-DNT to dogs primarily affected the nervous system, erythrocytes, and biliary tract (Ellis et al. , 1979, 1985). Based on neurotoxicity, hematologic changes, and effects on the bile ducts in dogs, the LOAEL was determined to be 1.5 mg/kg/day and the NOAEL was 0.2 mg/kg/day. EPA established an RfD of 0.002 mg/kg/day for 2,4-DNT (USEPA, 1992c) based on this study

s, oral dietary administration of 2,4-DNT to dogs primarily affected the nervous system, erythrocytes, and biliary tract (Ellis et al. , 1979, 1985). Based on neurotoxicity, hematologic changes, and effects on the bile ducts in dogs, the LOAEL was determined to be 1.5 mg/kg/day and the NOAEL was 0.2 mg/kg/day. EPA established an RfD of 0.002 mg/kg/day for 2,4-DNT (USEPA, 1992c) based on this study. An uncertainty factor of 100, to account for interspecies and intraspecies variability, was applied to derive the RfD.

EPA established an RfD of 0.001 mg/kg/day for 2,6-DNT (USEPA, 1992c). This RfD was also based on neurotoxicity, Heinz body formation, biliary tract hyperplasia, liver and kidney histopathology, and death in beagle dogs that were fed gelatin capsules containing 2,6-DNT daily for up to 13 weeks (Lee et al. , 1976). The NOAEL for this study was 4 mg/kg/day, and an uncertainty factor of 3,000 (100 for inter- and intra-species variability, 10 for the use of a subchronic study, 3 to account for the limited database) was applied to derive the RfD.

DNT is likely to be carcinogenic to humans (classified as a B2 carcinogen; USEPA, 1990c). This is based on significant increases in hepatocellular carcinoma and mammary gland tumors in female rats fed DNT (98 percent 2,4-DNT with 2 percent 2,6-DNT) in the diet in a two-year study (Ellis et al. , 1979). The tumor incidence in the female rats was used to establish a slope factor of 6.67 × 10 −1 according to the 1999 EPA guidelines. Concentrations of 5 μg/L, 0.5 μg/L, and 0.05 μg/L are associated with carcinogenic risks of 10 −4 , 10 −5 , and 10 −6 respectively. There were no studies found in the literature that evaluated the effects of 2,4- or 2,6-DNT on children. There is evidence that the pups and fetuses from dams administered tg-DNT had significant increases in relative liver and spleen weights (Price et al. , 1985)

nes. Concentrations of 5 μg/L, 0.5 μg/L, and 0.05 μg/L are associated with carcinogenic risks of 10 −4 , 10 −5 , and 10 −6 respectively. There were no studies found in the literature that evaluated the effects of 2,4- or 2,6-DNT on children. There is evidence that the pups and fetuses from dams administered tg-DNT had significant increases in relative liver and spleen weights (Price et al. , 1985). DNT toxicity may be different in children, compared to adults, since it undergoes bioactivation in the liver and by the intestinal microflora (ATSDR, 1998). Newborns may be more sensitive to DNT-related methemoglobinemia because an enzyme that protects against increased levels of methemoglobin is inactive for a short duration immediately after birth (Gruener 1976; ATSDR, 1998). However, there are no experimental data on differences in children's responses to 2,4-/2,6-DNT.

c. Occurrence. EPA included both 2,4- and 2,6-DNT as analytes in the UCMR 1. Because the HRL for both 2,4- and 2,6-DNT (0.05 μg/L) is lower than the minimum reporting limit used for monitoring (MRL of 2 μg/L), EPA used the MRL to evaluate occurrence and exposure. The MRL is within the 10 − 4 to the 10 − 6 cancer risk range for either 2,4- or 2,6-DNT. In evaluating the UCMR 1 data, EPA found that 1 of the 3,866 PWSs sampled (or 0.03 percent) detected 2,4-DNT at the MRL of 2 μg/L, affecting 0.02 percent of the population served (or 38,000 people from 226 million). None of the 3,866 PWSs sampled (serving 226 million) detected 2,6-DNT at the MRL of 2 μg/L (USEPA, 2006a and 2006b).

EPA also evaluated the results of a USGS review of 3 highway and urban runoff studies (Lopes and Dionne, 1998). These studies showed no detects for either 2,4- or 2,6-DNT using a reporting limit of 5 μg/L (a value within the 10 − 4 to 10 − 6 risk range).

d. Preliminary Determination. The Agency has made a preliminary determination not to regulate 2,4- or 2,6-DNT with an NPDWR

2006a and 2006b).

d. Preliminary Determination. The Agency has made a preliminary determination not to regulate 2,4- or 2,6-DNT with an NPDWR. Because 2,4- and 2,6-DNT appear to occur infrequently at levels of concern in PWSs, the Agency believes that a national primary drinking water regulation does not present a meaningful opportunity for health risk reduction. 2,4-DNT was detected only once at a minimum reporting level that is within the 10 − 4 to the 10 − 6 cancer risk range, while 2,6-DNT was not detected at this same level in any of the PWSs monitored under the UCMR 1.

EPA recognizes that 2,4- and 2,6-DNT are listed as probable human carcinogens. For this reason, the Agency encourages those States with public water systems that may have either 2,4- or 2,6-DNT above the HRL to evaluate site-specific protective measures and to consider whether State-level guidance (or some other type of action) is appropriate. The Agency's original Health Advisories for 2,4- and 2,6-DNT were developed for military installations. Because the Agency recognizes that 2,4- and 2,6-DNT may still be found at some military sites, the Agency has updated the Health Advisories to reflect recent health effects publications. The Health Advisories are available for review in the docket. The updated Health Advisories will provide information to any States with public water systems that may have either 2,4- or 2,6-DNT above the HRL.

8. s-Ethyl dipropylthiocarbamate (EPTC)

vide information to any States with public water systems that may have either 2,4- or 2,6-DNT above the HRL.

8. s-Ethyl dipropylthiocarbamate (EPTC)

a. Background. EPTC, a synthetic organic compound, is a thiocarbamate herbicide used to control weed growth during the pre-emergence and early post-emergence stages of weed germination. First registered for use in 1958, EPTC is used across the U.S. in the agricultural production of a number of crops, most notably corn, potatoes, dried beans, alfalfa, and snap beans. EPTC is also used residentially on shade trees, annual and perennial ornamentals, and evergreens (USEPA, 1999c).

Estimates of EPTC usage in the United States suggest a decline from approximately 17 to 21 million pounds active ingredient in 1987 to approximately 7 to 9 million pounds active ingredient in 1999. TRI data from 1995 to 2003 indicate that most on-site industrial releases of EPTC tend to be releases to air and underground injections. Surface water discharges are

Environmental fate data indicate that EPTC would not be persistent under most environmental conditions. Volatilization into the atmosphere and degradation by soil organisms appear to be the primary dissipation routes. EPTC has a low affinity for binding to the soil so the potential to leach to ground water does exist. If EPTC reaches ground water, volatilization is less likely to occur (USEPA, 1999c).

b. Health Effects. In acute animal toxicity studies, EPTC was shown to be moderately toxic via oral and dermal routes and highly toxic via inhalation exposures. EPTC is a reversible cholinesterase (ChE) inhibitor. Similar to other thiocarbamates, it does not produce a consistent ChE inhibition profile. There was no consistent pattern observed in any of the toxicity studies with regard to species, duration of treatment, or the type of ChE enzyme measured. Typically, studies showed inhibition of plasma ChE with dose-related decreases in red blood cell and brain ChE activity

ble cholinesterase (ChE) inhibitor. Similar to other thiocarbamates, it does not produce a consistent ChE inhibition profile. There was no consistent pattern observed in any of the toxicity studies with regard to species, duration of treatment, or the type of ChE enzyme measured. Typically, studies showed inhibition of plasma ChE with dose-related decreases in red blood cell and brain ChE activity. Some studies have shown that brain ChE activity was inhibited without any effect on either plasma or erythrocyte ChE activities. Other studies illustrated erythrocyte ChE inhibition with no effect on either plasma or brain ChE (USEPA, 1999c). In a primary eye irritation study in rabbits, technical grade EPTC was shown to be slightly irritating (USEPA, 1999c).

In subchronic and chronic studies performed in both rats and dogs, there was a dose-related increase in the incidence and severity of cardiomyopathy, a disorder of the heart muscle (Mackenzie, 1986; USEPA, 1999c). An increase in the incidence and severity of degenerative effects (neuronal and/or necrotic degeneration) in both the central and peripheral nervous system was observed in rats and dogs following exposure to EPTC (USEPA, 1999c).

EPA derived an RfD of 0.025 mg/kg/day for EPTC (USEPA, 1990d; USEPA, 1999c). This value was calculated using a NOAEL of 2.5 mg/kg/day from a study by Mackenzie (1986). An uncertainty factor of 100 was applied for inter- and intraspecies differences. The critical effect associated with the RfD is cardiomyopathy (disease of the heart muscle). In the reregistration of EPTC, the application of a ten-fold Food Quality Protection Act (FQPA) factor was recommended in order to be protective against residential exposures of infants and children. The Agency derived the HRL for EPTC using the RfD of 0.025 mg/kg/day and a 20 percent relative source contribution. The HRL is calculated to be 0.175 mg/L or 175 μg/L

hy (disease of the heart muscle). In the reregistration of EPTC, the application of a ten-fold Food Quality Protection Act (FQPA) factor was recommended in order to be protective against residential exposures of infants and children. The Agency derived the HRL for EPTC using the RfD of 0.025 mg/kg/day and a 20 percent relative source contribution. The HRL is calculated to be 0.175 mg/L or 175 μg/L.

The Agency used long-term studies in mice and rats and short-term studies of mutagenicity to evaluate the potential for carcinogenicity (USEPA, 1990d). Based on these data and using EPA's 1999 Guidelines for Carcinogen Risk Assessment, EPTC is not likely to be carcinogenic to humans (USEPA, 1999a).

EPA also evaluated whether health information is available regarding the potential effects on children and other sensitive populations. Data do not suggest increased pre- or post-natal sensitivity of children and infants to EPTC exposure. In animal studies, adverse developmental effects (i.e., decreased fetal body weight and decreased litter size) were only seen at doses that were toxic to the mother (USEPA, 1999c). Results from both developmental and reproductive studies indicate that there are only minimal adverse effects. The behavior patterns of children that lead to heightened opportunities for exposure in the indoor environment and the need for a developmental neurotoxicity study lead OPP to recommend the application of a ten-fold FQPA factor for EPTC. However, EPA did not apply this factor in the screening analysis because it does not apply to programs other than the pesticide registrations.

c. Occurrence. EPA included EPTC as an analyte in the UCMR 1. None of the 3,866 PWSs sampled (serving a population of 226 million) had detects of EPTC at the MRL of 1 μg/L. Hence, these data indicate that no occurrence and exposure is expected at levels greater than 87.5 μg/L ( 1/2 the HRL) and greater than 175 μg/L (the HRL) (USEPA, 2006a and 2006b)

grams other than the pesticide registrations.

EPA also evaluated several sources of supplemental information, which included:

• The National Pesticide Survey,

• The Pesticides in Ground Water Database, and

• The provisional pesticide results from the 1992-2001 USGS NAWQA survey of ambient surface and ground waters across the U.S.

The Pesticides in Ground Water Database (USEPA, 1992b) indicates that EPTC was found in 2 of 1,752 ground water wells that were sampled in 10 States. Both contaminated wells were in Minnesota. The detected concentrations ranged from 0.01 to 0.33 μg/L. All of these positive detections are less than the HRL of 175 μg/L, as well as 87.5 μg/L ( 1/2 the HRL).

The USGS NAWQA program included EPTC as an analyte in its 1992-2001 monitoring survey of ambient surface and ground waters across the United States. EPA evaluated the results of the provisional data, which are available on the Web (Martin et al. , 2003; Kolpin and Martin, 2003). While the USGS detected EPTC in both surface and ground waters, 95 percent of the samples from the various land use settings were less than or equal to 0.018 μg/L. The estimated maximum surface water concentration, 29.6 μg/L (mixed land use settings), and the maximum ground water concentration, 0.45 μg/L (agricultural settings), are both less than 175 μg/L (the EPTC HRL).

in and Martin, 2003). While the USGS detected EPTC in both surface and ground waters, 95 percent of the samples from the various land use settings were less than or equal to 0.018 μg/L. The estimated maximum surface water concentration, 29.6 μg/L (mixed land use settings), and the maximum ground water concentration, 0.45 μg/L (agricultural settings), are both less than 175 μg/L (the EPTC HRL).

d. Preliminary Determination. The Agency has made a preliminary determination not to regulate EPTC with an NPDWR. Because EPTC does not appear to occur at health levels of concern in PWSs, the Agency believes that a national primary drinking water regulation does not present a meaningful opportunity for health risk reduction. While EPTC has been found in ambient waters, it was detected only at levels less than the HRL (as well as 1/2 the HRL) and it was not found in the UCMR 1 survey of public water supplies.

9. Fonofos

a. Background. Fonofos, an organophosphate, is a soil insecticide used to control pests such as corn rootworms, cutworms, symphylans (i.e., garden centipedes), and wireworms. Primarily used on corn crops, fonofos was also used on other crops such as asparagus, beans, beets, corn, onions, peppers, tomatoes, cole crops, sweet potatoes, peanuts, peas, peppermint, plantains, sorghum, soybeans, spearmint, strawberries, sugarcane, sugar beets, white (Irish) potatoes, and tobacco (USEPA, 1999d).

Fonofos was scheduled for a reregistration decision in 1999. However, before the review was completed, the registrant requested voluntary cancellation. The cancellation was announced in the Federal Register on May 6, 1998 (63 FR 25033 (USEPA, 1998d)), with an effective date of November 2, 1998, plus a one-year grace period to permit the exhaustion of existing stocks (USEPA, 1999d).

NCFAP data indicate that fonofos use declined significantly during the 1990s (NCFAP, 2004)

the review was completed, the registrant requested voluntary cancellation. The cancellation was announced in the Federal Register on May 6, 1998 (63 FR 25033 (USEPA, 1998d)), with an effective date of November 2, 1998, plus a one-year grace period to permit the exhaustion of existing stocks (USEPA, 1999d).

NCFAP data indicate that fonofos use declined significantly during the 1990s (NCFAP, 2004). According to NCFAP,

Fonofos is moderately persistent in soil and its persistence depends on soil type, organic matter, rainfall, and sunlight. Since fonofos adsorbs moderately well to soil, it is not readily leached or transported to ground water but it can be transported to surface waters in runoff. Fonofos is rapidly degraded by soil microorganisms (Extoxnet, 1993). Fonofos tends to volatilize from wet soil and water surfaces, but the process is slowed by adsorption to organic material in soil, suspended solids, and sediment (HSDB, 2004d).

b. Health Effects. Fonofos (like many organophosphates) is toxic to humans and animals. Case reports and acute oral toxicity studies in animals indicate that oral exposure to fonofos induces clinical signs of toxicity that are typical of cholinesterase inhibitors. In humans, accidental exposures produced symptoms of acute intoxication, nausea, vomiting, salivation, sweating, muscle twitches, decreased blood pressure and pulse rate, pinpoint pupils, profuse salivary and bronchial secretions, cardiorespiratory arrest, and even death in 1 exposed individual (Hayes, 1982; Pena Gonzalez et al. , 1996).

zalez et al. , 1996).

In animals, clinical signs of exposure included tremors, salivation, diarrhea, and labored breathing (USEPA, 1996c). Chronic exposure studies also indicated that oral administration of fonofos inhibits cholinesterase (Banerjee et al. , 1968; Cockrell et al. , 1966; Hodge, 1995; Horner, 1993; Miller, 1987; Miller et al. , 1979; Pavkov and Taylor, 1988; Woodard et al. , 1969). Cholinesterase inhibition is one of the critical effects associated with the RfD, which was verified by EPA (USEPA, 1991) at 0.002 mg/kg/day. EPA derived the RfD of 0.002 mg/kg/day using a NOAEL of 0.2 mg/kg/day (Hodge, 1995) and a 100-fold uncertainty factor to account for inter- and intraspecies differences.

Fonofos is classified as an unlikely human carcinogen (Group E) because there is no evidence of carcinogenic potential in the available long-term feeding studies in rats and mice (Banerjee et al. , 1968; Pavkov and Taylor, 1988; Sprague and Zwicker, 1987). In addition, fonofos does not appear to be mutagenic (USEPA, 1996c).

EPA evaluated whether health information is available regarding the potential effects on children and other sensitive populations. In the available developmental studies with rabbits (Sauerhoff, 1987) and mice (Minor et al. , 1982; Pulsford, 1991), no developmental effects were observed at oral doses as high as 1.5 mg/kg/day in the rabbit (highest dose tested) nor in mice at doses as high as 2.0 mg/kg/day (Minor et al. , 1982; Pulsford, 1991). However, in mice, effects were noted at higher dose levels. These effects included an increase in the incidence of variant sternebrae ossifications (at 6 mg/kg/day or greater) and a slight dilation of the fourth brain ventricle in offspring (at 4 mg/kg/day or greater). No developmental neurotoxicity study with fonofos is available for further assessment of this endpoint. In a three-generation reproduction study in rats (Woodard et al

at higher dose levels. These effects included an increase in the incidence of variant sternebrae ossifications (at 6 mg/kg/day or greater) and a slight dilation of the fourth brain ventricle in offspring (at 4 mg/kg/day or greater). No developmental neurotoxicity study with fonofos is available for further assessment of this endpoint. In a three-generation reproduction study in rats (Woodard et al. , 1968), no treatment-related adverse effects were observed at the 2 dose levels used in this study, 0.5 and 1.58 mg/kg/day.

The Agency believes that the current RfD is adequately protective of children. The current fonofos RfD of 0.002 mg/kg/day is 1000-fold lower than the NOAEL observed in the Woodard et al. (1968) developmental studies.

Using the RfD of 0.002 mg/kg/day for fonofos and a 20 percent screening relative source contribution, the Agency derived an HRL of 0.014 mg/L and rounded to 0.01 mg/L (or 10 μg/L).

c. Occurrence. EPA included fonofos as an analyte in the UCMR 1 List 2 Screening Survey. None of the 2,306 samples from the 295 PWSs sampled (serving a population of 41 million) contained detects for fonofos at the MRL of 0.5 μg/L. Hence, these data indicate that no occurrence and exposure is expected at levels greater than 5 μg/L ( 1/2 the HRL) and greater than 10 μg/L (the HRL) (USEPA, 2006a and 2006b).

The USGS NAWQA program included fonofos as an analyte in its 1992-2001 monitoring survey of ambient surface and ground waters across the United States. EPA evaluated the results of the provisional data, which are available on the Web (Martin et al. , 2003; Kolpin and Martin, 2003). While the USGS detected fonofos in both surface and ground waters, 95 percent of the samples from the various land use settings were less than 0.003 μg/L (the reporting limit). The maximum surface water concentration, 1.20 μg/L (agricultural setting), and the maximum ground water concentration, 0.009 μg/L (agricultural setting), are both less than 10 μg/L and less than 5 μg/L (the fonofos HRL and 1/2 the HRL).

tected fonofos in both surface and ground waters, 95 percent of the samples from the various land use settings were less than 0.003 μg/L (the reporting limit). The maximum surface water concentration, 1.20 μg/L (agricultural setting), and the maximum ground water concentration, 0.009 μg/L (agricultural setting), are both less than 10 μg/L and less than 5 μg/L (the fonofos HRL and 1/2 the HRL).

d. Preliminary Determination. The Agency has made a preliminary determination not to regulate fonofos with an NPDWR. Because fonofos does not appear to occur at health levels of concern in PWSs, the Agency believes that a national primary drinking water regulation does not present a meaningful opportunity for health risk reduction. While fonofos has been found in ambient waters, it was detected only at levels less than the HRL (as well as 1/2 the HRL) and it was not found in UCMR 1 Screening Survey of public water supplies. Fonofos was voluntarily cancelled in 1998 and the Agency expects any remaining stocks and releases into the environment to decline. In addition, since fonofos tends to bind strongly to soil, any releases to the environment are not likely to contaminant source waters.

10. Terbacil

a. Background. Terbacil, a synthetic organic compound, is a selective herbicide used to control broadleaf weeds and grasses on terrestrial food/feed crops (e.g., apples, mint, peppermint, spearmint, and sugarcane), terrestrial food (e.g., asparagus, blackberry, boysenberry, dewberry, loganberry, peach, raspberry, youngberry, and strawberry), terrestrial feed (e.g., alfalfa, forage, and hay) and forest trees (e.g., cottonwood) (USEPA, 1998e).

, and hay) and forest trees (e.g., cottonwood) (USEPA, 1998e).

In 1998, EPA estimated that agricultural usage of terbacil consumed approximately 221,000 to 447,000 pounds of active ingredient annually and non-agricultural usage consumed approximately 9,000 to 14,000 pounds. These estimates are based on data collected mostly between 1990 and 1995, and in some cases as early as 1987 (USEPA, 1998e). According to NCFAP (2004), approximately 298,000 pounds of terbacil a.i. were applied annually in agriculture around 1992 and approximately 342,000 pounds a.i. were applied around 1997.

Terbacil is listed as a TRI chemical and data are reported from one or more facilities in a single state, Texas, for the time period covering 1995 to 1997. During this three-year period, all reported releases were on-site releases to surface water that varied between 3,000 to 10,000 pounds annually (USEPA, 2006h).

Terbacil is considered a persistent and potentially mobile herbicide in terrestrial environments. Because of its low affinity to soils, it can potentially leach into ground and/or surface waters (USEPA, 1998e; Extoxnet, 1994).

b. Health Effects. In acute and subchronic toxicity studies, terbacil is practically non-toxic (Haskell Laboratories, 1965a and 1965b). Terbacil does not cause dermal sensitivity in et al. ,1964; Haskell Laboratories, 1965c).

A primary target organ in rats following exposure to terbacil is the liver. Chronic effects of dietary terbacil exposure in two-year studies included increases in thyroid-to-body weight ratios, slight increases in liver weights and elevated alkaline phosphatase levels in beagle dogs, significant decreases in body weight in rats, increases in serum cholesterol levels and increases in liver to body weight ratios in rats (Wazeter et al. ,1967a; Malek, 1993). In beagle dogs, effects were seen at or above 6.25 mg/kg/day (NOAEL = 1.25 mg/kg/day). In rats, effects ( i.e

d-to-body weight ratios, slight increases in liver weights and elevated alkaline phosphatase levels in beagle dogs, significant decreases in body weight in rats, increases in serum cholesterol levels and increases in liver to body weight ratios in rats (Wazeter et al. ,1967a; Malek, 1993). In beagle dogs, effects were seen at or above 6.25 mg/kg/day (NOAEL = 1.25 mg/kg/day). In rats, effects ( i.e. , decreases in body weight, increases in liver weights and cholesterol levels) were seen at higher levels (LOAELs = 56 mg/kg/day for males and 83 mg/kg/day for females).

Terbacil is not considered to be a developmental or reproductive toxicant. In developmental studies, maternal effects were generally seen prior to or at the same levels as developmental effects. Haskell Laboratories (1980) reported maternal effects ( i.e. , decreased body weight) and significant decreases in the number of live fetuses per litter due to early fetal resorption at a LOAEL of 62.5 mg/kg/day in rats. In rabbits administered terbacil via gavage, the maternal and developmental LOAELs were equal (600 mg/kg/day). Maternal toxicity was based on the death of the dams and developmental toxicity was based on a decrease in live fetal weights (Solomon, 1984). No reproductive effects were seen in a three-generation study where terbacil was administered to male and female rats at dose levels of 2.5 and 12.5 mg/kg/day (Wazeter et al. , 1967b).

Terbacil is not mutagenic. Terbacil was tested and found negative in a chromosomal aberration study in rat bone marrow cells, found negative in a gene mutation assay (with and without S9 activation), and found negative for DNA synthesis when tested up to cytotoxic levels in rats (Cortina, 1984; Haskell Laboratories,1984). Terbacil shows no evidence of carcinogenicity and is unlikely to be carcinogenic to humans (Group E) (USEPA, 1998e).

The RfD of 0.013 mg/kg/day for terbacil (USEPA, 1998e) is calculated from a two-year chronic study in beagle dogs

ion assay (with and without S9 activation), and found negative for DNA synthesis when tested up to cytotoxic levels in rats (Cortina, 1984; Haskell Laboratories,1984). Terbacil shows no evidence of carcinogenicity and is unlikely to be carcinogenic to humans (Group E) (USEPA, 1998e).

The RfD of 0.013 mg/kg/day for terbacil (USEPA, 1998e) is calculated from a two-year chronic study in beagle dogs. The LOAEL of 6.25 mg/kg/day was based on increased thyroid-to-body weight ratios, slight increases in liver weights, and elevated alkaline phosphatase levels with a NOAEL of 1.25 mg/kg/day. In deriving the RfD, the Agency applied an uncertainty factor of 100 to account for interspecies and intraspecies differences. Using the RfD of 0.013 mg/kg/day and applying a 20 percent screening relative source contribution, the Agency derived an HRL of 0.090 mg/L (or 90 g/L) for terbacil.

EPA also evaluated whether health information is available regarding the potential effects on children and other sensitive populations. In the case of terbacil, the Agency determined that there was no need to apply an FQPA factor to the RfD in order to protect children (USEPA, 1998e). Other potentially sensitive subpopulations have not been identified.

c. Occurrence. EPA included terbacil as an analyte in UCMR 1. None of the 3,866 PWSs sampled (serving a population of 226 million) had detects for terbacil at the MRL of 2 g/L. Hence, these data indicate that no occurrence and exposure is expected at levels greater than 45 g/L ( 1/2 the HRL) and greater than 90 μg/L (the terbacil HRL) (USEPA, 2006a and 2006b).

EPA also evaluated several sources of supplemental information, which included:

• The National Pesticide Survey,

• The Pesticides in Ground Water Database, and

• The provisional pesticide results from the 1992-2001 USGS NAWQA survey of ambient surface and ground waters across the U.S

ls greater than 45 g/L ( 1/2 the HRL) and greater than 90 μg/L (the terbacil HRL) (USEPA, 2006a and 2006b).

EPA also evaluated several sources of supplemental information, which included:

• The National Pesti

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