communities. For more detailed information on the NAWQA program design
and implementation, please refer to Leahy and Thompson (1994), Hamilton
et al. (2004), and NRC (2002).
    The NAWQA program has been designed in ten-year cycles to enable
national coverage that can be used for trends and causal assessments.
In the Cycle 1 monitoring period, which was conducted from 1991 through
2001, NAWQA collected data from over 6,400 surface water and 7,000
ground water sampling points. Cycle 2 monitoring covers the period from
2002 through 2012, with various design changes from Cycle 1 (see
Hamilton et al., 2004).
    EPA, with the cooperation of USGS, performed a summary analysis of
all Cycle 1 water monitoring data for the CCL 3 and Regulatory
Determination process. The surface water data consisted of stream
samples; all surface water data were included in the EPA summary
analysis. For ground water, all well data were used and data from
springs and drainage systems were excluded.

    For RD 3, EPA used and evaluated many USGS NAWQA reports to review
causal or spatial factors that USGS may have presented in their
interpretations. In particular, EPA evaluated many reports from the
Pesticide National Synthesis Programs (e.g., Gilliom et al., 2007) and
the VOC National Synthesis (e.g., Delzer and Ivahnenko, 2003). While
there is overlap in the data used in the USGS reports and the EPA
analysis, the USGS reports can provide unique observations related to
their synthesis of additional data.
    For RD 3, EPA also supplemented these data with information from
recent special USGS reports that also used additional data from other
programs, particularly reports that focused on contaminant occurrence
in source waters for PWSs, such as: Organic Compounds in Source Water
of Selected Community Water Systems (Hopple et al., 2009 and Kingsbury
et al., 2008), and Water Quality in Public-Supply Wells (Toccalino et
al., 2010).
(6) Storage and Retrieval (STORET) Data System
    EPA's STORET database contains raw biological, chemical, and
physical data from surface and ground water sampling conducted by
Federal, State and local agencies, Indian Tribes, volunteer groups,
academics, and others. A wide variety of data relating to water quality
from all 50 States as well as multiple territories and jurisdictions of
the United States are represented in this data system. These are
primarily ambient water data, but in some cases they include finished
drinking water data. STORET data have quality limitations. There are
few restrictions on submission of data based on analytical methods,
quality assurance (QA) practices, etc. For more general STORET data
information, please refer to: http://www.epa.gov/storet/index.html. EPA
reviewed STORET ground water data from wells and surface water data
from lakes, rivers/streams, and reservoirs.
c. Supplemental Production, Use and Release Data
    The agency reviews various sources of information to assess if
there are changes or trends in a contaminant's production, use, and
release that may affect its presence in the environment and potential
occurrence in drinking water. The cancellation of a pesticide or a
clear increase in production and use of a contaminant are trends that
can inform the regulatory determination process. A more detailed
discussion of the supplemental sources of information/data that EPA
evaluated and the occurrence data for each contaminant can be found in
the comprehensive regulatory determination support documents (USEPA,
2014a and 2014b). Several sources are described in more detail below.
(1) Chemical Update System/Inventory Update Rule (CUS IUR)
    The IUR regulation requires manufacturers and importers of certain
chemical substances, included on the Toxic Substances Control Act
(TSCA) Chemical Substance Inventory, to report site and manufacturing
information and the amount of chemicals produced or imported in amounts
of 25,000 pounds or more at a single site. Additional information on
domestic processing and use must be reported for chemicals produced or
imported in amounts of 300,000 pounds or more at a single site. Prior
to the 2003 TSCA Amendments (i.e., reporting from 2002 or earlier),
information was collected for only organic chemicals that were produced
or imported in amounts of 10,000 pounds or more, and was limited to
more basic manufacturing information such as production volume. Because
of changes in reporting rules, contaminants may have reports for some
years but not others (USEPA, 2010a).
(2) Toxic Release Inventory (TRI)
    EPA established the Toxics Release Inventory (TRI) in 1987 in
response to Section 313 of the Emergency Planning and Community Right-
to-Know Act (EPCRA). EPCRA Section 313 requires facilities to report to
both EPA and the States annual information on toxic chemical releases
from facilities that meet reporting criteria. The TRI database details
not only the types and quantities of toxic chemicals released to the
air, water, and land by facilities, but also provides information on
the quantities of chemicals sent to other facilities for further
management (USEPA, 2002c, 2003b). Currently, for most chemicals the
reporting thresholds are 25,000 pounds for manufacturing and processing
and 10,000 pounds for use. Both the number and type of facilities
required to report has increased over time.
    Although TRI can provide a general idea of release trends, it has
limitations because of the reporting changes over time. Finally, TRI
data are meant to reflect ``releases'' and should not be used to
estimate general public exposure to a chemical (USEPA, 2002c).
(3) Pesticide Usage Estimates
    For the regulatory determinations process, the agency reviews
various sources of information about pesticide usage. SDWA directs EPA
to consider pesticides in the CCL process. Pesticide use and
manufacturing information is considered confidential business
information and therefore, accurate measures of production and use are
not publically available. As a result, the agency reviews various
estimates of use as supplemental information in the deliberative
process.
    Occasionally, EPA presents estimations of annual U.S. usage of
individual pesticides in its pesticide reregistration documents (e.g.,
Reregistration Eligibility Decisions or (REDs), Interim Reregistration
Eligibility Decisions (IREDs), Tolerance Reassessment Progress and Risk
Management Decisions (TREDs)). EPA also periodically issues Pesticides
Industry Sales and Usage reports. The reports provide contemporary and
historical information on U.S. pesticide production, imports, exports,
usage, and sales, particularly with respect to dollar values and
quantities of active ingredient. The most recent report presents data
from the years 2000 and 2001 (USEPA, 2004).
    The National Center for Food and Agricultural Policy (NCFAP), a
private non-profit institution, has also produced national pesticide
use estimates based on USDA State-level statistics and surveys for
commercial agriculture usage patterns and State-level crop acreage. The
database contains estimates of pounds applied and acres treated in each
State for 220 active (pesticide) ingredients and 87 crops. The majority
of the chemicals monitored are herbicides, but the database also
follows significant numbers of fungicides and insecticides (NCFAP,
2000).
    The USGS produced usage estimates and maps for over 200 pesticides
used in United States crop production, providing spatial insight to the
regional use of many pesticides (USGS, 2007). These pesticide use
estimates were generated by the USGS through State-level estimates of
pesticide usage rates for individual crops that were compiled by the
CropLife Foundation and the Crop Protection Research Institute,
combined with county-level data on harvested crop acreage obtained from
the 2002 Census of Agriculture.

IV. Contaminant-Specific Discussions for the RD 3 Preliminary
Regulatory Determinations

A. Summary of the Preliminary Regulatory Determination

    Based on EPA's evaluation of the three SDWA criteria (discussed in
section II.B.1), the agency is making

preliminary determinations to regulate one contaminant and to not
regulate four contaminants. Table 7 summarizes the primary health and
occurrence information used to make these preliminary regulatory
determinations. Section IV.B of this notice provides a more detailed
summary of the information and the rationale used by the agency to
reach its preliminary decisions for these five contaminants.

                Table 7--Summary of the Health and Occurrence Information and the Preliminary Determinations for the Five Contaminants Considered for Regulatory Determinations 3
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                Occurrence findings from primary data sources
                                                                      ------------------------------------------------------------------------------------------------------
                                                            Health                                         Population served by                                                  Preliminary
               No.                   RD 3 contaminants     reference      Primary    PWSs with at least 1  PWSs with at least 1  PWSs with at least 1  Population served by     determination
                                                          level (HRL)    database      detection >=\1/2\     detection >=\1/2\      detection >=HRL    PWSs with at least 1
                                                                                HRL                   HRL                                   detection >=HRL
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
1................................  Dimethoate..........  15.4 [mu]g/L            UCMR0% (0 of 4138)......  0% (0 of 229M)......  0% (0 of 4138)......  0% (0 of 229M)......  Do not regulate.
2................................  1,3-Dinitrobenzene..  0.7 [mu]g/L             UCMR0% (0 of 4137)......  0% (0 of 229M)......  0% (0 of 4137)......  0% (0 of 229M)......  Do not regulate.
3................................  Strontium...........  1,500 [mu]g/         NIRS   14.3% (141 of 989)..  16.6% (246K of 1.5M)  7.0% (69 of 989)....  10.7% (158.5K of      Regulate.
                                                                   L                                                                                1.5M).
4................................  Terbufos............  0.35 [mu]g/L            UCMR0% (0 of 295).......  0% (0 of 41M).......  0% (0 of 295).......  0% (0 of 41M).......  Do not regulate.
5................................  Terbufos Sulfone....  0.35 [mu]g/L            UCMR0.02% (1 of 4138)...  0.01% (44.6K of       0.02% (1 of 4138)...  0.01% (44.6K of       Do not regulate.
                                                                                229M).                                      229M).
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------

B. Contaminant Profiles

    This section provides further information on the background,
health, and occurrence data that the agency uses to evaluate each of
the five candidate contaminants considered for regulatory
determinations. For each candidate, the agency evaluates the available
human and toxicological data, derives a health reference level, and
evaluates the potential and/or likely occurrence and exposed population
for the contaminant in public water systems. The agency also considers
whether information is available on sensitive populations. The agency
uses the findings from these evaluations to determine whether the three
SDWA statutory criteria are satisfied. The agency also prepares a
regulatory support document (USEPA, 2014b) that provides more details
on the background, health, and occurrence information/analyses used to
evaluate and make preliminary determinations for these five
contaminants.
1. Dimethoate
a. Background
    Dimethoate is an organophosphate pesticide, commonly used as an
insecticide on field crops (e.g., wheat, alfalfa, corn, and cotton),
orchard crops, vegetable crops, and in forestry. Synonyms for
dimethoate include dimethogen, dimeton, dimevur, and cygon (HSDB, 2009;
USEPA, 2007b). EPA has estimated that the total annual average domestic
use of dimethoate is approximately 1.8 million pounds (USEPA, 2007b).
EPA's most recent Pesticide Industry Sales and Usage reports indicate
that the amount of dimethoate active ingredient (a.i.) used in the
United States was between 1 and 2 million pounds in 1999 and 2001, and
less than 1 million pounds in 2005 and 2007 (USEPA, 2004: USEPA,
2011f). TRI data from the years 1997 to 2010 show that annual releases
to various sources range from tens of pounds to tens of thousands of
pounds, with the larger releases occurring only occasionally and in no
clear pattern (USEPA, 2012a). For example, reported on-site air
emissions were in the range of tens of pounds for 1997-2005 but
increased to the range of thousands of pounds in 2006-2010. The only
reported non-zero release by underground injection was in 2004 and was
over 28,000 pounds. Reported on-site releases to surface water and land
were low or non-existent in most years, but peaked suddenly at nearly
20,000 pounds in 1998 (land) and over 2,000 pounds in 2004 (surface
water). Dimethoate is considered highly mobile and relatively non-
persistent in the environment (USEPA, 2007b).
b. Statutory Criterion #1 (Adverse Health Effects)
    Dimethoate meets the SDWA statutory criterion #1 for regulatory
determinations; it may have an adverse effect on the health of persons.
Dimethoate belongs to a group of pesticides called organophosphates,
which share a common MOA. Organophosphates affect the proper function
of the nervous system by inhibiting cholinesterase (ChE), an important
enzyme involved in neurotransmission. Inhibition of ChE in the brain,
plasma, and red blood cells is the most sensitive endpoint described in
numerous studies with adult and juvenile animals, following oral,
dermal, or inhalation exposures of dimethoate or its primary toxic
metabolite omethoate (USEPA, 2007b). As discussed in the 2007 OPP
assessment, the U.S. EPA's Cancer Assessment Review Committee (CARC)
classified dimethoate as a Group C carcinogen (a possible human
carcinogen) in 1991, with concurrence from the FIFRA Scientific
Advisory Panel (SAP) on the agency's classification in 1992 (USEPA,
2007b).
    The 2007 OPP assessment established a chronic oral RfD for
dimethoate of 0.0022 mg/kg/day based on a 2-year feeding study in rats
with inhibition of brain ChE as the critical effect (USEPA, 2007b). The
RfD was derived using the BMD method and based on the lower 95%
confidence limit (BMDL) of 0.22 mg/kg/day, with application of a
composite UF of 100 (i.e., intraspecies and interspecies variability).
EPA calculated a non-cancer HRL of 15.4 [mu]g/L for dimethoate using
the RfD of 0.0022 mg/kg/day for a 70 kg adult ingesting 2 L of drinking
water per day and an RSC of 20%. The chronic RfD and subsequent HRL of
15.4 [mu]g/L for dimethoate are considered to be protective of any
potential cancer risk or acute ChE effects (USEPA, 1990a, 2007b). The
OPP RED (USEPA, 2007b) presents more detailed information

about the potential health effects for dimethoate.
c. Statutory Criterion #2 (Occurrence at Frequency and Levels of Public
Health Concern)
    Dimethoate does not meet the SDWA statutory criterion #2 for
regulatory determinations; it does not occur with a frequency and at
levels of public health concern in public water systems based on EPA's
evaluation of the following occurrence information.
    The primary data for dimethoate are recent (2008-2010) nationally-
representative drinking water monitoring data, generated through EPA's
UCMR 2. Dimethoate was not detected in any of the 32,013 UCMR 2 samples
collected by 4,138 PWSs (serving ~ 230 million people) at levels
greater than the \1/2\ HRL (7.7 [mu]g/L), the HRL (15.4 [mu]g/L), or
the MRL (0.7 [mu]g/L) (USEPA, 2014d).
    The State of California reported results from testing more than
20,000 finished drinking water samples from over 2,000 PWSs and
dimethoate was detected in two samples from two different PWSs. The
detected concentrations (1 [mu]g/L and 2 [mu]g/L) were less than the
\1/2\ HRL (7.7 [mu]g/L) and the HRL (15.4 [mu]g/L) (see USEPA, 2014b).
The USDA PDP monitored for dimethoate in finished water from 2001 to
2009 and had only two detections in 3,555 samples; both detected
concentrations were less than the \1/2\ HRL and the HRL (USDA, 2012).
The USGS PMP monitored for dimethoate in finished water in 1999 and had
no detections greater than \1/2\ the HRL or the HRL in any of the 221
samples (Blomquist et al., 2001).
    Dimethoate occurrence data for ambient water are consistent with
those for finished drinking water. The USGS PMP also monitored for
dimethoate in ambient water in 1999 and had no detections greater than
the \1/2\ HRL (7.7 [mu]g/L) or the HRL (15.4 [mu]g/L) in any of the 317
samples (Blomquist et al., 2001). Ambient water data from a two-phase
USGS study conducted between 2002 and 2005 by Hopple et al. (2009) and
Kingsbury et al. (2008) reported no detections in the 221 Phase 1
groundwater samples. Only two detections were reported from 146 Phase 1
surface water samples at nine PWSs. The highest concentration detected
was 0.009 [mu]g/L, which is less than the \1/2\ HRL and the HRL. In
Phase 2, there were no detections of dimethoate from 48 raw and
finished water groundwater samples (Hopple et al., 2009; Kingsbury et
al., 2008). Ambient water data in STORET included no measured results
above 0.44 [mu]g/L in 5,299 samples from 798 sites (USEPA, 2012b).
Ambient water data reported by the California Department of Pesticide
Regulation included no measured results above 2.4 [mu]g/L (USEPA,
2007b).
d. Statutory Criterion #3 (Meaningful Opportunity)
    EPA finds that dimethoate does not meet the SDWA statutory
criterion #3 for regulatory determinations; regulation of dimethoate
does not present a meaningful opportunity health risk reduction for
persons served by PWSs based on the estimated exposed population,
including sensitive populations. The estimated population exposed to
dimethoate at levels of public health concern is 0%; it was not found
to occur at levels above the HRL (or the \1/2\ HRL) in 4,138 PWSs and
32,013 samples from the UCMR 2 monitoring. In addition, other
supplementary sources of finished water and ambient water data indicate
that the occurrence of dimethoate in PWSs is likely to be low to non-
existent. As a result, the agency finds that an NPDWR for dimethoate
does not present a meaningful opportunity for health risk reduction.
    EPA also evaluated whether health information is available
regarding the potential health effects on children and other sensitive
populations. The database for dimethoate includes a 3-generation
reproductive study in mice, developmental (teratology) studies in rats
and rabbits, and a neurodevelopmental toxicity study (USEPA, 1990a,
2007b). The critical effect of ChE inhibition is a more sensitive
endpoint compared to the reproductive and developmental endpoints
(USEPA, 2007b); therefore no sensitive populations were identified or
characterized. The OPP RED (USEPA, 2007b) presents more detailed
information about the potential health effects and sensitive
populations for dimethoate.
e. Preliminary Regulatory Determination
    The agency is making a preliminary determination to not regulate
dimethoate with an NPDWR after evaluating health, occurrence, and other
related information against the three SDWA statutory criteria. While
data suggests that dimethoate may have an adverse effect on human
health, the occurrence data indicate that dimethoate is not occurring
or not likely to occur in PWSs with a frequency and at levels of public
health concern. Therefore, the agency finds that an NPDWR would not
present a meaningful opportunity to reduce health risk for persons
served by PWSs. The Regulatory Determinations 3 Support Document
(USEPA, 2014d) and the Occurrence Data from the Second Unregulated
Contaminant Monitoring Regulation (UCMR 2) (USEPA, 2014a) present
additional information and/or analyses supporting the agency's
evaluation of dimethoate.
2. 1,3-Dinitrobenzene
a. Background
    1,3-Dinitrobenzene is a nitro aromatic compound that is used as an
industrial chemical and formed as a by-product in the manufacture of
munitions as well as in the production of other substances (HSDB,
2009). There are no known natural sources of 1,3-dinitrobenzene. Annual
production and importation of 1,3-dinitrobenzene in the United States
was last reported by CUS-IUR in 1986 to be between 10-50 million pounds
(USEPA, 2010b). TRI data indicate 19,858 pounds were released to the
environment by industry in 2008 and 10,595 pounds in 2010 (USEPA,
2012a). 1,3-dinitrobenzene appears to be moderately persistent in
environmental media and moderately mobile in soil and water, though in
soils with high clay content it will be less mobile (USEPA, 2014b).
b. Statutory Criterion #1 (Adverse Health Effects)
    1,3-dinitrobenzene meets the SDWA statutory criterion #1 for
regulatory determinations; it may cause adverse effect on the health of
persons. 1,3-dinitrobenzene has demonstrated adverse health effects in
many rodent and occupational studies. Occupational studies indicate
that methemoglobinemia, hemolytic anemia, and cyanosis are seen in
workers who experience an acute reaction to 1,3-dinitrobenzene (Hajjar
et al., 1992). The EPA IRIS assessment (USEPA, 1990b) of the
carcinogenicity of 1,3-dinitrobenzene currently lists it as Group D
(not classifiable as to human carcinogenicity).
    The primary adverse biological effects from exposure to 1,3-
dinitrobenzene are on red blood cells, spleen, and testes. The RfD for
1,3-dinitrobenzene is 0.0001 mg/kg/day (Cody et al., 1981). The RfD was
derived from a NOAEL of 0.4 mg/kg/day in a subchronic oral study in
rats where increased spleen weight was identified as the critical
effect (Cody et al., 1981). A composite UF of 3,000 (intraspecies
variability, interspecies variability, subchronic to chronic duration,
and lack of chronic, developmental, and multigenerational reproductive
toxicity studies) was

applied to the NOAEL to obtain the RfD. EPA calculated a non-cancer HRL
of 0.7 [mu]g/L for 1,3-dinitrobenzene using the RfD of 0.0001 mg/kg/day
for a 70 kg adult ingesting 2 L of drinking water per day and an RSC of
20%.
    The current EPA oral RfD value is supported by a more recent 1,3-
dinitrobenzene assessment that was conducted by ATSDR, in which an oral
intermediate duration minimal risk level of 0.0005 mg/kg/day for
splenic hemosiderosis in male rats was established using a LOAEL of
0.54 mg/kg/day (Linder et al., 1986; dose adjusted for a 7-day/week
exposure) and a composite UF of 1,000 (intraspecies variability and
interspecies variability, LOAEL to NOAEL). Based on EPA assumptions and
a composite UF of 3,000 (intraspecies variability, interspecies
variability, LOAEL to NOAEL and subchronic to chronic duration) applied
to the LOAEL of 0.54 mg/kg/day, the resultant HRL value of 1 [mu]g/L
supports the HRL value of 0.7 [mu]g/L derived from the IRIS RfD (ATSDR,
1995). The IRIS assessment (USEPA, 1990b) presents more detailed
information about the potential health effects for 1,3-dinitrobenzene.
c. Statutory Criterion #2 (Occurrence at Frequency and Levels of Public
Health Concern)
    1,3-dinitrobenzene does not meet the SDWA statutory criterion #2
for regulatory determinations; it does not occur with a frequency and
at levels of public health concern in public water systems based on
EPA's evaluation of the following occurrence information.
    The primary data for 1,3-dinitrobenzene are recent (2008-2010)
nationally-representative drinking water monitoring data generated
through EPA's UCMR 2 (USEPA, 2014d). UCMR 2 is the only dataset with
finished water data for this contaminant. UCMR 2 collected 32,017
samples from 4,137 PWSs and 1,3-dinitrobenzene was not detected above
the MRL (0.8 [mu]g/L), which is only slightly higher than the HRL (0.7
[mu]g/L).
    Findings from the available ambient water data for 1,3-
dinitrobenzene are consistent with the results in finished water.
Ambient water data in STORET included no measured results above 0.33
[mu]g/L in 143 samples from 70 sites (USEPA, 2012b). It should be noted
that some occurrence above the HRL may have gone undetected since
reporting levels are not documented.
d. Statutory Criterion #3 (Meaningful Opportunity)
    EPA finds that 1,3-dinitrobenzene does not meet the SDWA statutory
criterion for regulatory determinations; regulation of 1,3-
dinitrobenzene does not present a meaningful opportunity for health
risk reduction for persons served by PWSs based on the estimated
exposed population, including sensitive populations. The estimated
population exposed to 1,3-dinitrobenzene at or above the MRL is 0%; it
was not found to occur in finished drinking water at levels > MRL (0.8
[mu]g/L), which is only slightly higher than the HRL (0.7 [mu]g/L), in
32,017 samples and 4,137 PWSs from the UCMR 2 monitoring. As a result,
the agency finds that an NPDWR for 1,3-dinitrobenzene does not present
a meaningful opportunity for health risk reduction.
    EPA also evaluated whether information is available regarding the
potential health effects on children and other sensitive populations.
Individuals with a genetic predisposition to methemoglobinemia
(estimated prevalence in the general population = 1% or 1 per 100) and/
or hemosiderosis, neonates, and those co-exposed to other hemolytic
agents, could be more sensitive to exposure to 1,3-dinitrobenzene
(ATSDR, 1995; Jaffe and Hultquist, 1989). Males having sperm production
complications could also have increased sensitivity to 1,3-
dinitrobenzene exposure (Hajjar et al., 1992). There is currently no
multigenerational animal study available for 1,3-dinitrobenzene, and no
data available from studies of 1,3-dinitrobenzene developmental
toxicity (Hajjar et al., 1992). However, the RfD incorporated a UF for
this database deficiency. The IRIS assessment (USEPA, 1990b) presents
more detailed information about the potential health effects and
sensitive populations for 1,3-dinitrobenzene.
e. Preliminary Regulatory Determination for 1,3-dinitrobenzene
    The agency is making a preliminary determination to not regulate
1,3-dinitrobenzene with an NPDWR after evaluating health, occurrence,
and other related information against the three SDWA statutory
criteria. While data suggest that 1,3-dinitrobenzene may have an
adverse effect on human health, the occurrence data indicate that 1,3-
dinitrobenzene is not occurring or not likely to occur in PWSs with a
frequency and at levels of public health concern. Therefore, the agency
has determined that an NPDWR for 1,3-dinitrobenzene would not present a
meaningful opportunity to reduce health risk for persons served by
PWSs. The Regulatory Determinations 3 Support Document (USEPA, 2014b)
and the Occurrence Data from the Second Unregulated Contaminant
Monitoring Regulation (UCMR 2) (USEPA, 2014d) present additional
information and analyses supporting the agency's evaluation of 1,3-
dinitrobenzene.
3. Strontium
a. Background
    Strontium is a naturally occurring element (atomic number 38) and a
member of the alkaline earth metals (ANL, 2007). There are several
radioactive strontium isotopes formed by nuclear fission of uranium or
plutonium. The best known is \90\Sr, a legacy from above ground testing
of the atomic bomb (half-life 29 years). Since drinking water
contamination by radioactive isotopes, including beta particle
emitters, is covered under the existing radionuclides rule, this FR
notice deals primarily with the stable \88\Sr isotope which represents
83% of total environmental strontium (ATSDR, 2004).
    Strontium mineral mining ceased in the United States in 1959. The
United States imports both strontium minerals for refining and refined
strontium containing compounds (USGS, 2009). Imports of strontium
minerals and compounds were approximately 31,000 to 38,500 metric tons
from 1994 to 2001 and have declined since 2001 (ATSDR, 2004; USGS,
2009). In the United States, total consumption of strontium minerals
and compounds was 16,700 metric tons of strontium content in 2004 and
approximately 7,750 metric tons in 2008 (USGS, 2009).
    Historically, the most important commercial use of strontium has
been in the faceplate glass of cathode-ray tube televisions to block x-
ray emissions (ATSDR, 2004). Conversely, flat panel televisions
incorporating LCD or Plasma displays are not capable of emitting x-
radiation; therefore, they do not require strontium (FDA, 2011). As
flat panel technology has become widespread in the United States in the
last decade, demand for strontium for this application has fallen
(USGS, 2009). In 2008, approximately 30% of commercial strontium
consumption was in pyrotechnics and signals (as strontium nitrate and
other compounds), 30% in ferrite ceramic magnets (as strontium
ferrite), 10% in master alloys (as strontium metal), 10% in pigments
and fillers (as strontium chromate), 10% in electrolytic production of
zinc (as strontium carbonate), and 10% in other applications such as
fluorescent lights (strontium phosphate), toothpaste (strontium
chloride), and medicines (strontium chloride and strontium peroxide).
The feed material for most

applications is strontium carbonate (ATSDR, 2004; HSDB, 2010; USGS,
2009). Strontium can exist in oxidation states 0 and +2; under normal
environmental conditions it is found in the +2 oxidation state in
various ionic or salt forms. Strontium is considered to have moderate
or moderate-to-low mobility in soils. The mobility of strontium in
water can increase with increased salt concentrations due to a decrease
in sorption to sediments (USEPA, 20104b). The Regulatory Determination
3 Support Document (USEPA, 2014b) for this notice presents more
detailed background information on strontium.
b. Statutory Criterion #1 (Adverse Health Effects)
    Strontium meets the SDWA statutory criterion #1 for regulatory
determinations; it may have an adverse effect on the health of persons.
The primary target of strontium exposure is the bone. The chemical
similarity of strontium to calcium allows it to exchange imperfectly
for calcium in a variety of biological processes; the most important of
these is the substitution of calcium in bone, affecting skeletal
development. Due to the MOA for strontium toxicity, strontium uptake
into bone is affected by the intake of nutrients related to bone
formation, such as calcium, phosphorous, and vitamin D (Clarke, 2008;
Grynpas and Marie, 1990; Marie et al., 1985). The decreased
calcification in bones results in increased width of the epiphyseal
cartilage, changes in the pattern of calcification, abnormally long
metaphyses, reduction in bone mineralization, and active osteoclasts in
young rats (Marie and Hott, 1986; Matsumoto, 1976; Neufeld and Boskey,
1994; Storey, 1961). Due to this effect on growing bones, infants,
children, and adolescents are of particular concern as a sensitive
population.
    A study based on decreased bone calcification rate in male weanling
rats (i.e., comparable to the sensitive time period in humans), which
administered strontium chloride in drinking water for nine weeks (Marie
et al., 1985), was identified by EPA as the critical study for RfD
determination. The RfD was established by using the BMD method and
based on the lower 95% confidence limit (BMDL) of 328 mg/kg/day for a
one standard deviation decrease in bone calcification compared to
control. Using a composite UF of 1000 (10 for intraspecies variability,
10 for interspecies variability, and 10 for database uncertainties) the
RfD for strontium is calculated to be 0.3 mg/kg/day. This RfD is
supported by additional studies reporting bone effects on weanling rats
at similar dose levels (Grynpas and Marie, 1990; Storey, 1961). EPA
calculated a non-cancer HRL of 1500 [micro]g/L for strontium using the
RfD of 0.3 mg/kg/day, a default RSC of 20% and age-specific exposure
factors (i.e., drinking water intake expressed as liters per kg of body
weight) for the sensitive population of birth through 18 years to
reflect the most active period of bone growth and development (see
section IV.B.10.d.3).
    EPA released an IRIS assessment for strontium in 1992 and developed
an RfD of 0.6 mg/kg/day based on the Storey, 1961 study. The IRIS
assessment was completed before the 1998 changes to the IRIS program
wherein the agency develops and peer reviews a detailed Toxicological
Review before posting an IRIS summary. The point of departure for the
1992 IRIS RfD of 0.6 mg/kg/day is a NOAEL of 190 mg Sr/kg-day with a
composite UF of 300 (10 for interspecies variability, 3 for
intraspecies variability, and 10 for database uncertainties). This
would yield an HRL of 3000 [micro]g/L, using the same age-specific
exposure adjustment factors described above. If the age-specific
exposure adjustment factors were not used, the HRL would be 2000
[micro]g/L based on the OW assessment, or 4000 [micro]g/L based on the
IRIS assessment. As noted in section III.C.1.c, EPA evaluates the
existing data and performs a literature search for studies published
after the available health assessment is completed to determine if new
information suggests a different outcome. In cases where the review
suggests that a change the existing RfD or cancer assessment is needed,
the EPA Office of Water prepares and independently peer-reviews an OW
Assessment of the data. In the case of strontium and because newer
information provided additional support for the 1985 Marie et al.
study, EPA chose to use the BMDL of 328 mg/kg/day from Marie et al.,
(over the 1961 Storey study) for the following reasons: (a) Marie et
al., (1985) reported the doses rather than estimated the doses; (b) the
study duration was longer (63 days for Marie as compared to 20 days for
Storey); (c) the monitoring of the bone effects for Marie et al.,
(1985) was more quantitative than the photomicrographs evaluated by
Storey (1961); (d) dosing was provided via drinking water, the medium
of interest (rather than a weakly soluble SrCO3 in the diet); (e) Marie
et al., (1985) reported the strain of rats and the age of the animals,
at the time that dosing was initiated and completed; (f) the data were
amenable to dose-response modeling to identify the BMD and BMDL; and
(g) the dietary calcium provided in the Storey study was three times
higher than that in the Marie study, making those rats less at risk due
to the calcium and strontium competition for uptake, as verified by a
comparison of serum data from the two studies. The OW assessment uses a
10x uncertainty factor for intraspecies variability, rather than the 3x
factor used in the 1992 IRIS assessment because it is not clear if the
window of vulnerability was adequately captured, since the weanling
rats were exposed only for 28-63 days, a period that did not include
exposure during gestation, lactation, and through young adulthood. EPA
requests comment on its revised RfD calculation and on its proposal to
use the OW assessment in lieu of the RfD from the 1992 IRIS assessment.
    There is inadequate information to assess the carcinogenic
potential of strontium due to the lack of adequate studies of chronic
duration. The Health Effects Support Document (USEPA, 2014c) for this
determination presents more detailed analysis of the health effects of
strontium.
c. Statutory Criterion #2 (Occurrence at Frequency and Levels of Public
Health Concern?)
    Strontium meets the SDWA statutory criterion #2 for regulatory
determinations; it does occur with a frequency and at levels of public
health concern in public water systems based on EPA's evaluation of the
following occurrence information.
    EPA used the National Inorganics and Radionuclides Survey (NIRS)
(USEPA, 2008b) as the primary data source to evaluate the occurrence of
strontium in PWSs. It provides contaminant occurrence data from 989
CWSs served by ground water sources. Each of these randomly selected
PWSs was sampled a single time between 1984 and 1986. Of the 989
systems in NIRS, 980 (99%) had detectable levels of strontium ranging
from 1.53 to 43,550 [micro]g/L. The mean concentration was 603
[micro]g/L. Approximately 7.0% (69 of 989) of the NIRS PWSs detected
strontium at a level greater than the HRL (1500 [micro]g/L) and 14.3%
(141 of 989) detected strontium at a level greater than \1/2\ HRL (750
[micro]g/L). Extrapolated by the total number of ground water CWSs
found nationally, this represents 2,798 and 5,718 groundwater CWSs that
could have strontium at a level greater than the HRL and the \1/2\ HRL,
respectively. These figures are summarized in Table 8 (USEPA, 2014b).

                               Table 8--Estimates of Population Exposed to Strontium, Observed and Extrapolated From NIRS
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                              National Inorganics and Radionuclides Survey    Extrapolation of NIRS data to groundwater
                                                                                (NIRS)                                  systems nationwide
                          Threshold                          -------------------------------------------------------------------------------------------
                                                                     Systems               Population              Systems               Population
--------------------------------------------------------------------------------------------------------------------------------------------------------
Systems with Detectable Concentrations......................                 99.1%                  99.9%                  99.1%                  99.9%
                                                                      (980 of 989)     (1.481M of 1.482M)       (39.7K of 40.1K)       (93.0M of 93.1M)
Systems detecting strontium above one half the HRL (>750                     14.3%                  16.6%                  14.3%                  16.6%
 [micro]g/L)................................................          (141 of 989)         (246K of 1.5M)        (5.7K of 40.1K)       (15.4M of 93.1M)
Systems detecting strontium above the HRL (>1500 [micro]g/L)                  7.0%                  10.7%                   7.0%                  10.7%
                                                                       (69 of 989)         (159K of 1.5M)        (2.8K of 40.1K)       (10.0M of 93.1M)
--------------------------------------------------------------------------------------------------------------------------------------------------------

    As a point of reference to the earlier IRIS assessment, if EPA used
the HRL derived from this assessment of 3000 [micro]g/L, 30/989 systems
(3%) would have finished water samples that exceed the HRL using the
NIRS data, compared to 69/989 (7%) using the HRL of 1500 [micro]g/L
derived from the more recent OW assessment.
    Finished water data, analyzed between 1998 and 2005, from Ohio and
Illinois are also consistent with the NIRS data. The State of Illinois
reported results from testing 21 drinking water samples from 19 PWSs
and strontium was detected in all 21 samples (100%) from all 19 systems
(100%). Approximately 23.8% (5 of 21) of samples from five systems
(26.3%) had strontium at levels greater than the \1/2\ HRL (750
[micro]g/L) and approximately 23.8% (5 of 21) of samples from five
systems (26.3%) had strontium at levels greater than the HRL (1500
[micro]g/L) (USEPA, 2012b). The State of Ohio reported results from
testing 77 samples from 32 PWSs and strontium was detected in 75
samples (97.4%) from 30 different systems (93.8%). Approximately 27.3%
(21 of 77) of samples from 10 systems (31.3%) had strontium at levels
greater than the \1/2\ HRL and approximately 23.4% (18 of 77) of
samples from seven systems (21.9%) had strontium at levels greater than
the HRL (USEPA, 2014b).
    Although there are limited surface water data available for
strontium, the available data are consistent and demonstrate high
occurrence in surface waters. Ambient water data for strontium are also
consistent with high occurrence in finished water, which is expected
since it is a naturally occurring element. The NAWQA Quality of Public
Supply Wells (Toccalino et al., 2010) study collected water samples
from source (untreated) groundwater public supply wells in 41 states.
Each well was sampled once from 1993-2007 and 100% of samples (503 of
503) had a strontium detection. Of the detections, 25.1% (126 of 503)
were above the \1/2\ HRL (750 [micro]g/L) and 12.1% (61 of 503) were
above the HRL (1500 [micro]g/L). Additional occurrence information on
strontium can be found in the Regulatory Determinations 3 Support
Document (USEPA, 2014b).
d. Statutory Criterion #3 (Meaningful Opportunity?)
    EPA makes a preliminary finding that strontium meets the SDWA
statutory criterion #3 for regulatory determinations; regulation of
strontium in drinking water presents a meaningful opportunity for
health risk reduction based on the estimated exposed population,
potential impacts on sensitive populations and estimated exposure from
other sources (e.g., food).
    1. National Population Exposed: In the NIRS dataset 989 ground
water systems were sampled serving a population of 1.48 million. The
NIRS data indicates that the population exposed to strontium at a level
greater than the HRL (1500 [micro]g/L) is 158,557 (11%) and the \1/2\
HRL (750 [micro]g/L) is 245,870 (17%) (USEPA, 2012b). EPA also
performed national extrapolations generated by multiplying the NIRS
findings of system/population percentages and the national system/
population inventory numbers for PWSs developed from EPA's Safe
Drinking Water Information System, the CWSS, and UCMR. Out of the 93.1
million people served by 40,106 ground water CWSs in the nation, the
national extrapolation indicates that 10.0 million may be exposed to
concentrations greater than the HRL (1500 ug/L) and 15.4 million may be
exposed to concentrations greater than the \1/2\ HRL (750 ug/L). The
system and population estimates are summarized in Table 8.
    Strontium occurs naturally and is abundant in the environment. Its
occurrence in water at concentrations >HRL may be a reflection of the
geologic and geochemical setting of the source waters for PWSs. The
NIRS drinking water data showed that strontium was detected in one or
more systems sampled in all 48 continuous states, Alaska and Puerto
Rico (Hawaii was not included in NIRS). The occurrence data (e.g.,
NIRS) show that PWSs with strontium at concentrations greater than the
HRL and the \1/2\ HRL occur in 26 states and 34 states, respectively
(USEPA, 2014b).
    2. Exposure from media other than water: EPA has determined that
there is a meaningful opportunity to regulate strontium in drinking
water to reduce the public's overall exposure after evaluating the
available exposure data from media other than water. Although strontium
is known to occur in food, air, and soil, data on levels in those media
are limited as are estimates of intake from those sources. Therefore,
EPA used the default 20% RSC to calculate the HRL. This section
provides a summary of the available exposure data.
    An FDA Total Diet Study by Pennington and Jones (1987) collected
234 individual foods in 1984 from three cities in one region of the
country and indicated dietary intakes of 493 [micro]g/day for young
children (6 to 11 months), 928 to 1,388 [micro]g/day for 14 to 16 year
old adolescents, and 979-1,489 [micro]g/day for adults. The FDA Total
Diet Study foods are prepared with distilled water and do not reflect
any contributions from the cooking water during preparation of foods
that absorb water such as rice and pasta. Thus, the strontium in many
foods will be impacted by the strontium levels in the local water
supply. Using the mean of the detected water concentrations from the
NIRS dataset (603 [micro]g/L), the estimated water intake for young
children (90th percentile water intake of 1L/day) is 603 [micro]g/day
and 1,206 [micro]g/day for adults (90th percentile water intake of 2L/
day). The estimated strontium intakes from air and soil are very low
compared with those from food and drinking water. The estimated air
exposure for children is 0.1 [micro]g/day and for adults is 0.3
[micro]g/day (Dzubay and Stevens, 1975). The estimated exposure from
soil is 24 [micro]g/day for children and 12 [micro]g/day for

adults (Shacklette and Boerngen, 1984). No data were identified on
consumer products, such as toothpaste that contain strontium as an
ingredient or impurity.
    3. Sensitive populations: Children are expected to be a sensitive
population, since they are actively growing and strontium can
substitute for calcium in growing bone. This means that changes in bone
structure and homeostasis may have more severe and/or a long-term
impact than similar changes in adults. These effects would be expected
to have the greatest impact during periods of rapid growth in the
developing fetus, during childhood and adolescence, particularly if
their calcium intake is insufficient (Abrams et al., 2000; Lee et al.,
1996; Matkovic et al., 2005; Storey, 1961). The estimated populations
of pregnant women (and thus fetuses) and of children (<17 years old)
are 6 and 75 million, respectively (O'Day et al., 1998). The RfD was
based on changes in bone growth in weanling rats (i.e., the sensitive
population). As a result, the data do not include the risk during
prenatal development and lactation so these factors were considered
when selecting the UFs used to derive the RfD. Age-specific exposure
factors (USEPA, 2012c) were also used to reflect the sensitive
population (birth through 18 years) in derivation of the HRL. Exposures
from drinking water at or below the HRL (1500 [micro]g/L) are expected
to be protective of the sensitive population, assuming that 80% of
exposure comes from other sources such as air, soil and food.
    The toxic effects of strontium result from strontium ions
substituting for calcium ions, therefore calcium deficiency would be
expected to result in increased risk among sensitive populations. In
this respect, it is important to note that recent NHANES data indicate
that about 50% of females, nine years and older, fail to receive
adequate calcium from diet and supplements on a daily basis (IOM,
2010). Groups with higher risks of becoming calcium deficient include:
Adolescent girls, postmenopausal women, amenorrheic women, female
athletes, vegans, and individuals with lactose intolerance or cow's
milk allergies (IOM, 2010; NIH, 2011a).
    The major route of elimination of strontium is via the kidneys,
therefore individuals with impaired renal function are another
sensitive population. This population may potentially have impaired
strontium clearance, as has been shown in renal failure patients. There
are approximately 20 million people (10%) above the age of 20 with
chronic kidney disease (CDC, 2010) and 548,000 people with kidney end-
stage renal disease (USRDS, 2010), who may be at an increased risk.
People with disorders affecting the normal equilibrium between the
breakdown of old bone and the formation of new bone (such as Paget's
disease) might also be sensitive to strontium exposure (D'Haese et al.,
1999, 2000; Schrooten et al., 1998, 2003; Tothill et al., 1983).
According to the National Institute of Arthritis and Musculoskeletal
and Skin Diseases, there are approximately 1 million people (1.2 people
per 100 men and women age 45 to 74) diagnosed with Paget's disease of
the bone (NIH, 2011b). The Health Effects Support Document (USEPA,
2014c) for strontium presents more detailed information about the
potential health effects and sensitive populations. Because the RfD
includes an uncertainty factor of 10 for intraspecies variability, the
RfD is also expected to be protective of these sensitive populations.
d. Preliminary Regulatory Determination
    At this time, the agency is making a preliminary determination to
regulate strontium with an NPDWR after evaluating the available health,
occurrence, and other related information against the three SDWA
statutory criteria. Specifically, it is EPA's preliminary determination
that (a) strontium may have an adverse effect on the health of persons,
(b) it is known to occur or there is substantial likelihood that
strontium will occur in public water systems with a frequency and at
levels of public health concern, (c) regulation of strontium with an
NPDWR presents a meaningful opportunity to reduce health risks for
persons served by PWSs.
    It is important to note that the agency included strontium in UCMR
3. As of January 2014, a preliminary analysis (USEPA, 2014e) of the
first nine months of the UCMR 3 monitoring data indicate that 4.9% (70
of 1,423) of systems, 3.8% (175 of 4,547) of entry points, and 3.9%
(274 of 7,061) of samples have detects of strontium at levels greater
than the HRL of 1500 [micro]g/L. While EPA believes the occurrence data
from NIRS (in concert with the supplemental information discussed
earlier) are sufficient to make the regulatory determination, the
agency believes the additional monitoring results from UCMR 3 will
assist EPA in making the final regulatory determination for strontium
and in developing the proposed NPDWR. As noted in section III.A.3, this
regulatory determination process is distinct from the more detailed
analyses needed to develop a national primary drinking water
regulation. To inform the agency, the EPA plans to conduct more
extensive field testing of treatment technologies to assess the
effectiveness of strontium removal in PWSs prior to promulgating a
national primary drinking water regulation. Thus a decision to regulate
is the beginning of the agency's regulatory development process, not
the end. As the agency collects additional information about drinking
water and other sources of exposure (and performs more detailed
analyses), this information will inform the agency's opinion as to
whether strontium should be regulated. The agency asks the public to
submit any data or information that may be useful in evaluating
drinking water and other sources of exposure (e.g., food, food prepared
in drinking water, air, soil, etc.).
4 and 5. Terbufos and Terbufos Sulfone
a. Background
    Terbufos is a phosphorodithioate pesticide (i.e., an
organophosphate) used as an insecticide-nematicide to control a variety
of insect pests, primarily used on corn and sugar beets (USEPA, 2006c).
Terbufos sulfone is a degradate of terbufos. EPA's most recent
Pesticide Industry Sales and Usage report states that between 5 and 7
million pounds of terbufos active ingredient were used in 1999 and
between 3 and 5 million pounds of active ingredient were used in 2001
(USEPA, 2004). There are no industrial release data available for
terbufos from TRI. As a pesticide degradate, terbufos sulfone is
neither produced nor used commercially. Total toxic residues of
terbufos and degradates are highly mobile and persistent in the
environment, with terbufos sulfone being more mobile and substantially
more persistent than terbufos (USEPA, 2006c).
b. Statutory Criterion #1 (Adverse Health Effects?)
    Terbufos and its degradate, terbufos sulfone, meet the SDWA
statutory criterion #1 for regulatory determinations; they may cause an
adverse effect on the health of persons. Terbufos and terbufos sulfone
belong to a group of pesticides called organophosphates, which share a
common mechanism of toxicity. Organophosphates affect the proper
function of the nervous system by inhibiting ChE, an essential enzyme
in neurotransmission. There has been no evidence that terbufos is
carcinogenic in animal studies (Rapp, 1974; Silverman

et al., 1986) and it is classified as a class D carcinogen (inadequate
evidence of carcinogenicity) (USEPA, 1988). Overall, health effects
information for the terbufos sulfone degradate is lacking; there are no
long-term studies or cancer classification for terbufos sulfone.
    The 2006 OPP RED assessment (USEPA, 2006c) established an oral RfD
for terbufos of 0.00005 mg/kg/day, derived from the NOAEL of 0.005 mg/
kg/day for ChE inhibition in the 28-day and 1-year dog studies by
Shellenberger (1984) and Shellenberger and Billups (1986). A composite
UF of 100 (interspecies and intraspecies variability) was applied to
the NOAEL to obtain the RfD. EPA calculated a non-cancer HRL of 0.35
[micro]g/L for terbufos using the RfD of 0.00005 mg/kg/day for a 70 kg
adult ingesting 2 L of drinking water per day and an RSC of 20%. The
agency has not developed an RfD for terbufos sulfone because subchronic
and chronic studies are not available. However, Bailey (1988) conducted
a 14-day study of both terbufos and its sulfone degradate in dogs. The
NOAEL based on ChE activity for terbufos sulfone was greater than the
LOAEL of 2.5 mg/kg/day for the same endpoint following 14-day dosing
with the parent compound terbufos. This suggests that the terbufos
sulfone degradate is less toxic than its parent, and that the use of
the terbufos HRL of 0.35 [micro]g/L for the degradate, terbufos
sulfone, is acceptable. The OPP RED (USEPA, 2006c) presents more
detailed information about the health effects for terbufos and terbufos
sulfone.
c. Statutory Criterion #2 (Occurrence at frequency and levels of public
health concern?)
    Terbufos and terbufos sulfone do not meet the SDWA statutory
criterion #2 for regulatory determinations; they do not occur with a
frequency and at levels of public health concern in public water
systems based on EPA's evaluation of the following occurrence
information.
    The primary data for terbufos sulfone are nationally-representative
finished water monitoring data generated through EPA's UCMR 2 (2008-
2010) (USEPA, 2014d). UCMR 2 collected 32,012 finished water samples
from 4,138 PWSs (serving ~ 230 million people) and terbufos sulfone was
detected in only one sample, at a concentration of 0.42 [micro]g/L. The
MRL was 0.4 [micro]g/L, which is slightly higher than the HRL (0.35
[micro]g/L) (USEPA, 2012d). The primary data for terbufos are from the
UCMR 1 screening survey (2001-2003) (USEPA, 2008c). The UCMR 1
screening survey collected 2,301 finished water samples from 295 PWSs.
Terbufos was not detected at levels at or above the MRL (0.5 [micro]g/
L), which is slightly higher than the HRL (0.35 [micro]g/L) (USEPA,
2008c). Finished water data for terbufos and terbufos sulfone from
California, Iowa, USDA, and USGS are also consistent with the UCMR 1
and UCMR 2 data. The State of California reported no detections of
terbufos in 191 samples from 23 PWSs (see USEPA, 2014b). The State of
Iowa reported no detections of terbufos sulfone from 13 wells (see
USEPA, 2014b). The USDA PDP monitored for terbufos (2,597 samples) and
terbufos sulfone (2,923 samples) in finished water from 2001 to 2009
and reported no detections at or above method reporting levels ranging
from 0.005 [micro]g/L to 0.1 [micro]g/L (USDA, 2012: USEPA, 2014b). The
USGS PMP monitored for terbufos in finished water in 1999 and reported
no detections, at or above their method reporting level of 0.013
[micro]g/L (Blomquist et al., 2001).
    Terbufos and (very limited) terbufos sulfone occurrence data for
ambient water from EPA, STORET, and several USGS programs or studies
are consistent with those for finished water. The USGS NAWQA Program
(1992-2001) reported no groundwater detections above the \1/2\ HRL
(0.175 [micro]g/L) or the HRL (0.35 [micro]g/L) for terbufos in 20,960
samples at 7,118 sites. NAWQA reported surface water detections for
terbufos in 28 of 14,480 samples (0.19%) at 20 of 1,907 sites (1.05%).
Of the 28 surface water detections for terbufos, only four samples
(0.03%) at four sites (0.21%) were above the \1/2\ HRL and only one
sample (0.01%) at one site (0.05%) was above the HRL (Gilliom et al.,
2007). The NAWQA Carbonate Aquifer Study (1993-2005; Lindsey et al.,
2008) and the NAWQA Domestic Well Water Quality Study (1991-2004;
DeSimone, 2009) reported no detections for terbufos above the \1/2\ HRL
or the HRL in 1,027 and 2,539 samples, respectively. The NAWQA National
Synthesis Program (1992-2001) reported no groundwater detections for
terbufos above the \1/2\ HRL or the HRL and one surface water detection
(0.56 [micro]g/L), from agricultural sites, above the HRL (Gilliom et
al., 2007).
    Ambient water data from a two phase USGS study conducted between
2002 and 2005 by Hopple et al. (2009) and Kingsbury et al. (2008)
reported no terbufos detections in the 221 Phase 1 groundwater samples
nor the 146 Phase 1 surface water samples. In Phase 2, there were no
detections of terbufos from 48 raw and 48 finished groundwater samples.
Ambient water data from a USGS study conducted between 1993 and 2007 by
Toccalino et al. (2010) reported no terbufos detections in 898
groundwater samples.
    Terbufos ambient data reported in EPA's OPP RED for Terbufos
(USEPA, 2006c) document included 20 detections in 4,563 groundwater
samples from 13 States. The detections ranged from 0.01 to 20 [micro]g/
L, a range that extends both above and below the \1/2\ HRL (0.175
[micro]g/L) and the HRL (0.35 [micro]g/L). The USGS PMP monitored for
terbufos in ambient water in 1999 and reported no detections (Blomquist
et al., 2001).
    Terbufos ambient data are reported in STORET from 17 States (USEPA,
2012b). No groundwater detections were reported in 699 samples at 441
sites. STORET reported surface water detections in 457 of 5,826 samples
(7.84%) at 138 of 625 sites (22.1%). Of the 457 surface water
detections, only 23 samples (0.39%) at 14 sites (2.24%) were above the
\1/2\ HRL and only two samples (0.03%) at two sites (0.32%) were above
the HRL.
d. Statutory Criterion #3 (Meaningful Opportunity?)
    Terbufos and terbufos sulfone do not meet the SDWA statutory
criterion #3 for regulatory determinations; regulation of terbufos and
terbufos sulfone do not present a meaningful opportunity for health
risk reduction based on the estimated population exposed, including
sensitive populations. The estimated population exposed to terbufos at
or above the MRL is 0%; the compound was not found to occur in finished
water at levels greater than or equal to the MRL (0.4 [mu]g/L), which
is slightly higher than the HRL (0.35 [mu]g/L), in 2,301 samples from
295 PWSs in UCMR 1 (USEPA, 2008c). The estimated population exposed to
terbufos sulfone at a level of public health concern (based on the HRL
for terbufos) is 44,600 (0.02% of the population served by PWSs); there
was only one detection greater than the HRL in 4,138 PWSs (1 of 32,012
samples in UCMR 2) (USEPA, 2014d). As a result, the agency finds that
an NPDWR does not present a meaningful opportunity for health risk
reduction.
    EPA also evaluated whether health information is available
regarding the potential health effects on children and other sensitive
populations. Developmental studies with terbufos in rats and rabbits
did not find any developmental effects (USEPA, 2003c). There are no
data on reproductive and developmental effects for terbufos sulfone. No
sensitive populations were identified or characterized. The OPP RED
(USEPA, 2006c) presents more

detailed information about the potential health effects and sensitive
populations for terbufos and terbufos sulfone.
e. Preliminary Regulatory Determination
    The agency is making preliminary determinations to not regulate
terbufos and terbufos sulfone with NPDWRs after evaluating health,
occurrence, and other related information against the three SDWA
statutory criteria. While the data suggests that terbufos and terbufos
sulfone may have adverse effects on human health, the occurrence data
indicate there is no substantial likelihood that terbufos or terbufos
sulfone will occur in PWSs with a frequency and at levels of public
health concern. Therefore, the agency finds that NPDWRs for terbufos
and terbufos sulfone would not present meaningful opportunities to
reduce health risk for persons served by PWSs. The Regulatory
Determinations 3 Support Document (USEPA, 2014b) presents additional
information and/or analyses supporting the agency's evaluation of
terbufos and terbufos sulfone.

V. What is the Status of the Agency's Evaluation of Chlorate and
Nitrosamines?

    The agency will review the existing MDBP regulations as part of the
SY3. Because chlorate and nitrosamines are DBPs that can be introduced
or formed in public water systems partly because of disinfection
practices, the agency believes it is important to evaluate these
unregulated DBPs in the context of the review of the existing DBP
regulations. DBPs need to be evaluated collectively, because the
potential exists that the chemical disinfection used to control a
specific DBP could affect the concentrations of other DBPs. Therefore,
the agency is not making a regulatory determination for chlorate and
nitrosamines at this time. The agency expects to complete the review of
these DBPs by the end of 2015.

A. Chlorate

    The following sections provide the background, health and
occurrence information/data that the agency has collected to date for
chlorate. If the public has any additional health and occurrence
information that may be useful as the agency evaluates chlorate in the
context of the existing MDBP rules, please provide this information to
the docket.
1. Background
    The chlorate anion (ClO3-) forms a variety of
salts (e.g., sodium chlorate, calcium chlorate, potassium chlorate, and
magnesium chlorate) collectively known as chlorates, which are powerful
oxidizers. Chlorate compounds (especially sodium chlorate) are used as
herbicides and to generate chlorine dioxide (ClO2) as a
bleaching agent (USEPA, 2006a). Disinfection practices are the most
important source of chlorate in drinking water; this includes formation
as a DBP from use of chlorine dioxide and its presence in hypochlorite
disinfectants as an impurity (USEPA, 2006a).
    Chlorate can be formed during decomposition of hypochlorite
(ClO-) solutions, which are used as a disinfectant and/or
oxidant in water treatment. Hypochlorite solutions that are more aged
are generally less effective and require higher doses to achieve the
treatment (disinfection) objectives, which can result in more chlorate
to be introduced into the chlorinated water. In addition to being a DBP
(along with chlorite) formed from the use of chlorine dioxide as a
disinfectant, chlorate ion may also be present as an impurity in the
chlorine dioxide (Gates et al., 2009; USEPA, 2006a). Chlorate can also
form by the reaction of chlorite with free chlorine applied as a
residual disinfectant in the distribution system (Gallagher et al.,
1994). In addition, chlorite can be oxidized by a strong oxidant (such
as ozone) to produce chlorate in the water (von Gunten, 2003). Chlorate
salts readily dissolve in water and are highly mobile because of the
absence. In the absence of redox reactions, the chlorate ion would be
expected to partition predominantly into water and to be highly mobile
in water. However, under most environmental conditions chlorate is
subject to redox reactions, which are expected to reduce the
concentration of chlorate in the water column (USEPA, 2006a).
2. Health Effects Information
    Acute ingestion of high levels of sodium chlorate has resulted in
acute kidney failure and hemolysis among other effects based on
numerous case reports of individuals accidently ingesting high levels
of chlorate compounds (USEPA, 2006b; WHO, 2005). A population-based
case-control study of chlorate as a DBP at concentrations >200 [mu]g/L
identified significantly increased odds ratios for obstructive urinary
defects, cleft palate, and spina bifida (Righi et al., 2012). The
median chlorate exposure for the study population was 280 [mu]g/L. In a
case-control study of the same population in Italy, Aggazzotti et al.
(2004) found no association between preterm births and exposure to
chlorate.
    The animal studies provide clear and consistent evidence that
subchronic and chronic exposure to chlorate results in effects on blood
and thyroid. Subchronic studies in rats have reported decreased
hemoglobin, hematocrit, and red blood cell (RBC) counts (Abdel-Rahman
et al., 1984; Barrett, 1987; McCauley et al., 1995) and thyroid colloid
depletion, follicular cell hypertrophy and hyperplasia (Hooth et al.,
2001).
    A chronic study based on increased thyroid gland follicular cell
hypertrophy in male rats (NTP, 2005a) was identified as the critical
study for establishing an RfD of 0.03 mg/kg/day (USEPA, 2006b). The RfD
was derived by using the BMD method and based on the lower 95%
confidence limit (BMDL) of 28 mg/L as sodium chlorate (22 mg/L as
chlorate), corresponding to 0.9 mg/kg/day (USEPA, 2006b), with a
composite UF of 30 for intraspecies (i.e., sensitive populations) and
interspecies variability (i.e., thyroid hormone differences between
humans and rats). EPA calculated a non-cancer HRL of 210 [mu]g/L for
chlorate using the RfD of 0.03 mg/kg/day for a 70 kg adult ingesting 2
L of drinking water per day and an RSC of 20%.
    A cancer risk assessment was not conducted for chlorate because
sodium chlorate is classified as not likely to be carcinogenic to
humans at doses that do not alter thyroid hormone homeostasis under the
USEPA (2005b) Cancer Guidelines. The RfD is protective against acute
alterations in thyroid homeostasis and therefore considered to also be
protective of tumorigenicity as well as other chronic and subchronic
adverse health effects discussed in the literature (Hooth et al., 2001;
Khan et al., 2005; NTP, 2005a).
    EPA also evaluated whether health information is available
regarding sensitive populations. According to the OPP RED, there was no
pre- or postnatal sensitivity or susceptibility observed in the
submitted developmental studies in rats and rabbits or the 2-generation
reproduction study in rats. However, there is a concern for developing
offspring because of the effects of inorganic chlorate on thyroid
function in rats (USEPA, 2006a). Chlorate is one of a number or
inorganic ions that may interfere with iodine uptake by the thyroid,
but chlorate is not highly potent in this respect (Van Sande et al.,
2003).
    Chlorate may also cause hemolysis, thus persons with low red blood
cell counts such as those with anemia may be particularly sensitive to
sodium chlorate. Data from the 1994 National Health Interview Survey
(O'Day et al.,

1998) indicate that there were about 5 million people in the U.S. who
suffered from some form of anemia. About 3 to 5% of the population may
have an inherited glucose-6-phosphate dehydrogenase (G6PD) deficiency,
with males more sensitive than females (Luzzatto and Mehta, 1989), and
about 1% may have a form of hereditary methemoglobinemia (Jaffe and
Hultquist, 1989). Each one of these conditions is a contributor to low
red blood cell counts within the population. Individuals co-exposed to
other ions that decrease iodine uptake by the thyroid or have low RBC
counts may be more sensitive to chlorate exposure.
3. Occurrence Data and Information
a. Drinking Water
    The 1997-1998 DBP ICR is currently the best available data source
for characterizing the national occurrence baseline for chlorate. The
DBP ICR, which included monitoring data for 296 water systems serving
100,000 people or more (representing a total population of 130
million), required water systems that use hypochlorite solutions or
chlorine dioxide for disinfection to monitor for chlorate (USEPA,
1996). Subsequently, 82 water systems serving approximately 40 million
people monitored and reported chlorate occurrence under the DBP ICR
(using an MRL of 20 [mu]g/L). Table 9 presents the number and
percentage of samples and systems (along with the population served)
that measured chlorate at levels exceeding the specified threshold
concentrations (i.e., HRL and \1/2\ HRL). These samples were associated
with 41.5% (34 of 82) of the ICR systems using hypochlorite solutions
or chlorine dioxide for disinfection and 11.5% (34 of 296) of all of
the ICR systems. EPA assumes there was no occurrence of chlorate among
the ICR systems that were not required to monitor for it, since they
use disinfection techniques not expected to produce chlorate.
Approximately 51.1% (878 of 1,719) of ICR samples from the finished
water or distribution system of the systems required to monitor had
chlorate at levels greater than the \1/2\ HRL (105 [mu]g/L) and 19.3%
(332 of 1,719) had chlorate at levels greater than the HRL (210 [mu]g/
L). The samples greater than the \1/2\ HRL were associated with 73.2%
(60 of 82) of the ICR systems using hypochlorite solutions or chlorine
dioxide for disinfection and 20.3% (60 of 296) of all ICR systems
(including those that were not required to monitor for chlorate). The
samples greater than the HRL were associated with 41.5% (34 of 82) of
the ICR systems using hypochlorite solutions or chlorine dioxide for
disinfection and 11.5% (34 of 296) of all ICR systems (including those
that were not required to monitor for chlorate) (McGuire et al., 2002).
    Since the DBP ICR was completed in 1998, these data likely
underestimate current (2012) chlorate occurrence among the systems
serving 100,000 people or more for the following two reasons: (1) Some
of these systems may have changed the disinfectant type from chlorine
gas to chlorine dioxide for compliance with the existing Stage 1 or
Stage 2 DBP rules; and/or (2) some systems may have switched from
chlorine gas to hypochlorite solution due to a security concern (i.e.,
a concern of safety of transportation and storage for chlorine gas).
Disinfection surveys conducted by the AWWA Disinfection Systems
Committee in 1998 and 2007 have confirmed that chlorine dioxide and
hypochlorite use has increased (AWWA Disinfection Systems Committee,
2008a, 2008b; Connell et al., 2000a, 2000b).

                                            Table 9--Summary of Chlorate Monitoring Results Under the DBP ICR
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                              Of DBP ICR PWSs that monitored for chlorate,   Of all DBP ICR PWSs, PWSs with at least one
                                                              samples and PWSs with at least one detection       detection > threshold and estimated
                                                                              > threshold *                             population served **
                                                             -------------------------------------------------------------------------------------------
                     Chlorate threshold                                                                      Number (percentage)
                                                               Number (percentage)    Number (percentage)    of DBP ICR PWSs with   Population served by
                                                                of DBP ICR samples    of DBP ICR PWSs with       at least one       DBP ICR PWSs with at
                                                                 with detection >         at least one      detection > threshold  least one detection >
                                                                    threshold        detection > threshold           \*\               threshold \**\
--------------------------------------------------------------------------------------------------------------------------------------------------------
HRL (210 [mu]g/L)...........................................          332 of 1,719               34 of 82              34 of 296    11.8 of 130 million
                                                                           (19.3%)                (41.5%)                (11.5%)                 (9.1%)
\1/2\ HRL (105 [mu]g/L).....................................          878 of 1,719               60 of 82              60 of 296    31.7 of 130 million
                                                                           (51.1%)                (73.2%)                (20.3%)                (24.4%)
--------------------------------------------------------------------------------------------------------------------------------------------------------
\*\ 82 PWSs that used hypochlorite or chlorine dioxide were required to monitor for chlorate during the DBP ICR monitoring period, based on their
  potential to form chlorate. Number and percentage of samples and PWSs are based on those 82 PWSs that monitored for chlorate.
\**\ The number and percentage of PWSs and population served > threshold is based on all 296 systems. EPA assumes that the 214 systems not required to
  monitor do not have chlorate concentrations above the thresholds.

    Finished water data for chlorate from California collected between
2001 and 2007 show lower occurrence compared to the DBP ICR. The State
of California reported results from testing more than 1,200 drinking
water samples from 45 PWSs and chlorate was detected in 945 samples
(78.4%) from 24 different systems (53.3%) (Ranalli, B., 2013).
Approximately 41.6% (501 of 1,205) of samples from 17 systems (37.8%)
had chlorate at levels greater than the \1/2\ HRL (105 [mu]g/L) and
approximately 12.4% (149 of 1,205) of samples from 10 systems (22.2%)
had chlorate at levels greater than the HRL (210 [mu]g/L) (Ranalli, B.,
2013).
    It is important to note that the agency included chlorate in the
UCMR 3, which is currently in process. UCMR 3 will provide a national
dataset of chlorate occurrence in drinking water and will update the
occurrence data provided by the DBP ICR.
    Ambient water data for chlorate are limited, but chlorate could be
present in areas where it is used as an herbicide or discharged from
paper plants where it is used as a bleaching agent. Since chlorate is a
DBP, higher concentrations are expected in finished water than in
ambient water.
b. Exposure from media other than water
    There is very little quantitative information available on the
occurrence of chlorate in food, air, and soil or other products
resulting in residential exposures. Without reliable estimates of
intakes, it is not possible to estimate the contribution of drinking
water to total exposure. However, based on modeling results, the agency
estimated that the chlorate intake from food (as a result of sodium
chlorate use as a pesticide) for the overall population is
approximately 3 [mu]g/kg-day, with somewhat higher intakes for children
under five years old

of approximately 5 to 8 [mu]g/kg-day (USEPA, 2006a). Additional food
exposure from use of sanitizing solutions in food preparation plants
(e.g., equipment and contact surfaces) and processing (e.g., bleaching
agent) may also be a source of exposure (21 CFR section 178.1010).
Intake for adults from dietary supplements containing chlorate may
range from 0.001 to 0.29 [mu]g/kg-day.

B. Nitrosamines Group (6 Nitrosamines)

    The following sections provide the background, health and
occurrence information/data that the agency has collected to date for
nitrosamines. If you have any additional health and occurrence
information that may be useful as the agency evaluates nitrosamines in
the context of the regulatory review of existing MDBP rules, please
provide this information to the docket.
1. Background
    Nitrosamines are a class of nitrogen-containing organic compounds
that share a common nitrosamino functional group (HSDB, 2010). EPA
included five nitrosamine compounds on the CCL 3: N-
nitrosodimethylamine (NDMA), N-nitrosodiethylamine (NDEA), N-nitrosodi-
n-propylamine (NDPA), N-nitrosopyrrolidine (NPYR), and N-
nitrosodiphenylamine (NDPhA). EPA monitored six nitrosamines under UCMR
2 using EPA Analytical Method 521, four of which are CCL 3 compounds
(i.e., NDMA, NDEA, NDPA, NPYR), and two non-CCL 3 nitrosamines [i.e.,
N-nitrosomethylethylamine (NMEA) and N-nitrosodi-n-butylamine (NDBA)].
The fifth CCL 3 nitrosamine compound, NDPhA, was not monitored under
UCMR 2 due to lack of a reliable analytical method. Although other
nitrosamines (e.g., N-nitrosomorpholine, N-nitrosopiperidine) have been
identified in finished water (Mitch et al., 2009), they were also not
included in UCMR 2 for similar analytical reasons. The nitrosamines
from the UCMR 2 thus comprise the list of six nitrosamines that moved
forward to the data evaluation phase of regulatory determination and
are the focus of the information that follows below.
    All six nitrosamines may be produced in small quantities for
research purposes, but only one (NDEA) is currently produced
commercially in the United States. NDEA is used as an additive in
gasoline and in lubricants, as an antioxidant, and as a stabilizer in
plastics, though no data are available about quantities used (HSDB,
2010). NDMA was once used in the production of rocket fuel, as a
solvent, and as a rubber accelerator. It was also used or proposed for
use as an antioxidant, an additive for lubricants, and a softener for
copolymers (ATSDR, 1989). There are no production data on any of the
nitrosamine compounds from EPA's Inventory Update Reporting (IUR)
program.
    NDMA can be formed as an unintended byproduct of manufacturing
processes that involve the use of nitrite or nitrate and amines,
including tanneries, fish processing plants, foundries, and pesticide,
dye, rubber or tire manufacturing plants (ATSDR, 1989). Nitrosamines
have been found in tobacco products, cured meats, ham, bacon, beer,
whiskey, fish, cheese, soybean oil, toiletries, household cleaners,
pesticides, rubber baby bottle nipples and pacifiers (ATSDR, 1989;
Drabik-Markiewicz et al., 2009; Fine et al., 1977; NTP, 2011;
P[eacute]rez et al., 2008; Yurchenko and M[ouml]lder, 2007).
    NDMA is commonly present in municipal sewage sludge (ATSDR, 1989).
NPYR has also been detected in municipal sewage sludge (HSDB, 2010).
ATSDR (1989) cites several studies indicating that nitrosamine
formation in sewage sludge appears to be the result of biological and
chemical transformation of alkylamines in the presence of nitrite. In
addition, nitrosamines may form in air, soil, water, sewage, food,
animal systems and other media where precursors (e.g., amines and
nitrite) are present (HSDB, 2010). NDMA can be produced endogenously in
humans from the interaction of nitrates and nitrites with amines in the
stomach (Mirvish 1975, 1992; Tricker et al., 1994).
    As described in the following occurrence section, nitrosamines in
finished water are commonly considered as DBPs because most of the
literature indicates that the main source of nitrosamines in finished
water is associated with water treatment, particularly from
disinfection with chloramines. NDMA is the predominant species of
nitrosamines found in finished water; other nitrosamines are detected
less frequently. Based on their physical and chemical properties, the
nitrosamines appear to be moderately to very mobile in the environment
(the exception being NDBA, which is of low mobility). The nitrosamines
are subject to a variety of removal mechanisms when present in soil and
water, including volatilization (particularly NDMA), photodegradation,
and microbial degradation, although the rates and extent of
biodegradation are highly variable (HSDB, 2010).
2. Health Effects Information
    As the more thoroughly studied nitrosamine compared to the other
nitrosamine compounds, NDMA provides epidemiological case-control and
other evidence that human nitrosamine exposure is associated with an
increased risk of several types of cancer, including cancer of the
stomach, esophagus, oral cavity, and pharynx (La Vecchia et al., 1995;
Larsson et al., 2006; Loh et al., 2011; Straif et al., 2000). In
accordance with the most recent Guidelines for Carcinogen Risk
Assessment (USEPA, 2005b), EPA has categorized the six nitrosamine
compounds as likely to be carcinogenic to humans based on sufficient
evidence of carcinogenicity in animal studies with multiple tumor types
(predominately liver and esophageal) in multiple animal species (e.g.,
rats, mice, and hamsters) (Clapp et al., 1968, 1971; Druckrey et al.,
1967; Lijinsky, 1987a, 1987b; Peto et al., 1991a, 1991b). All of the
six nitrosamines have been determined to cause cancer through a
mutagenic MOA because of DNA adduct formation leading to errors in DNA
replication, altered cell proliferation and ultimately tumors (Diaz
Gomez et al., 1986; Goto et al., 1999; Jarabek et al., 2009; Souliotis
et al., 1998). The mutagenic MOA is supported by positive findings from
mutagenicity and genotoxicity in vitro and in vivo studies (Gollapudi
et al., 1998; Kushida et al., 2000; Martelli et al., 1988, Robbiano et
al., 1996, Tinwell et al., 1994).
    With a mutagenic MOA, Age Dependent Adjustment Factors (ADAFs) are
used to account for the potential increased cancer risk due to early-
life exposure for infants and children (USEPA, 2005c). The age-adjusted
unit risk is determined by summing up each of the time-weighted unit
risks for the three ADAF developmental groups. The age-adjusted unit
risks include a ten-fold adjustment for birth to <2 years, a three-fold
adjustment for 2 years to <16 years, and no additional adjustment for
exposures later in life, in conjunction with age-specific drinking
water intake values (USEPA. 2012c), and the fraction of a 70-year
lifetime applicable to each age period. The main cancer risk values
used to derive the HRLs are further explained in section III.C.1 and
are also summarized for nitrosamines in Table 10 below.

                 Table 10--EPA Derived Risk Values and HRLs for the Six Individual Nitrosamines
----------------------------------------------------------------------------------------------------------------
                                                                     \1\ Age-
                                   Studies for     Cancer slope    adjusted unit  \2\ HRL ([mu]g/
         Nitrosamines            establishing a   factor (mg/kg/  risk ([mu]g/L)-       L)        \3\ HRL (ng/L)
                                  slope factor        day)-1             1
----------------------------------------------------------------------------------------------------------------
NDBA..........................  Liver and                    0.4      3.0 x 10-5        3 x 10-2              30
                                 esophageal
                                 tumors in rats
                                 (Druckrey et
                                 al., 1967).
NDEA..........................  Liver and                     30      2.3 x 10-3        4 x 10-4             0.4
                                 esophageal
                                 tumors in rats
                                 (Peto et al.,
                                 1991a,b).
NDMA..........................  Liver tumors in               21      1.6 x 10-3        6 x 10-4             0.6
                                 rats (Peto et
                                 al., 1991a,b).
NDPA..........................  Liver and                      2      1.5 x 10-4        7 x 10-3               7
                                 esophageal
                                 tumors in rats
                                 (Druckrey et
                                 al., 1967).
NMEA..........................  Liver tumors in                4      3.0 x 10-4        3 x 10-3               3
                                 rats (Druckrey
                                 et al., 1967).
NPYR..........................  Liver tumors in                7      5.3 x 10-4        2 x 10-3               2
                                 rats (Peto et
                                 al., 1984).
----------------------------------------------------------------------------------------------------------------
\1\ Based on the recommendations of the U.S EPA's 2005 Supplemental Guidance for Assessing Susceptibility from
  Early-Life Exposure to Carcinogens, the Unit Risk applicable to exposures beginning in early-life was adjusted
  with ADAFs and age-specific drinking water intakes resulting in a lifetime value of unit risk for exposure to
  1 [mu]g/L of a contaminant. The calculation for Age-Adjusted Unit Risk = [sum](CSF x ADAF x DWI/BWR x CW x F).
  The risk calculations for each individual nitrosamine can be found in the HESDs.
\2\ The cancer HRL is determined by dividing the population risk level, one-in a million (10-6), by the age-
  adjusted unit risk.
\3\ The nitrosamine HRL values are converted to ng/L units by multiplying the [mu]g/L values by 1000.

    As shown in table 10, the available data indicate a range of cancer
risk values for the individual nitrosamines. Moreover, when multiple
nitrosamines from this group are present in finished water together,
their individual cancer risks are additive (Berger et al., 1987).
    EPA also evaluated whether health information is available
regarding sensitive populations. The fetus, newborns, and infants may
be potentially sensitive to the carcinogenic effects of nitrosamines
due to the mutagenic MOA and evidence of transplacental carcinogenicity
(Althoff et al., 1977; Donovan and Smith, 2008). Studies have found
that younger rats were more susceptible to the development of liver
tumors compared to rats exposed later in life to nitrosamines (Gray et
al., 1991; Peto et al., 1984; Vesselinovitch et al., 1984). EPA's
Supplemental Guidance for Assessing Susceptibility from Early-Life
Exposure to Carcinogens (USEPA, 2005c) indicates that potential
increased cancer risk due to early-life exposure should be taken into
account for such compounds when there is the potential for greater
susceptibility for structural changes to DNA leading to tumors when the
exposures occur in infancy or childhood. Thus, the Supplemental
Guidance (USEPA, 2005c) recommends using CSF estimates from chronic
studies with ADAFs when chemical-specific data that quantify the
potential increased risk are lacking. All of the HRLs are based on
lifetime exposure and include application of ADAFs, which adjust for
the increased risk from early life exposure (see section III.C.1).
    In addition, habitual consumers of alcoholic beverages may be more
susceptible to carcinogenic effects of nitrosamines because alcohol
increases the metabolism of nitrosamines via a metabolic pathway that
leads to the formation of mutagenic DNA adducts. Co-exposure to ethanol
has been shown to exacerbate the cancer effects of nitrosamines in
animal studies (Anderson et al., 1993; Kamataki et al., 2002; McCoy et
al., 1986). There are approximately five million people in the U.S. who
suffer from alcoholism (O'Day et al., 1998) that may have an increased
risk if co-exposed to nitrosamines (Amelizad et al., 1989; Verna et
al., 1996).
3. Occurrence Data and Information
    The data collected under UCMR 2 (USEPA, 2014d) are currently the
best available data for characterizing the national occurrence
baselines for the six nitrosamines. Under UCMR 2, PWSs were required to
collect a sample at each entry point to the distribution system as well
as at the maximum residence time locations within the distribution
system associated with each entry point, and to report the disinfectant
type in use at these locations at the time that the samples were being
taken. The agency was unable to measure at the HRL for some of the
nitrosamines. Therefore, Table 11 presents all of the monitoring
results for each of the six nitrosamines relative to the MRLs.

                                           Table 11--Summary of UCMR 2 Monitoring Results for Six Nitrosamines
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                Percentages (number) of
                                                                             Percentages (number) of   Percentages (number) of  actual UCMR 2 population
             Nitrosamines considered under RD 3                    MRL       samples with detection      UCMR 2 PWSs with at    served with at least one
                                                                                least one detection           detection*
--------------------------------------------------------------------------------------------------------------------------------------------------------
Nitrosamine Group...........................................  2 to 7 ng/L                     10.6%                     28.6%                    46.43%
                                                                                (1,907 of 18,053)            (343 of 1,198)       (73 of 157 million)
NDBA........................................................       4 ng/L                     0.05%                      0.4%                     1.07%
                                                                                (9 of 18,043)              (5 of 1,198)      (1.7 of 157 million)
NDEA........................................................       5 ng/L                      0.3%                      2.2%                     7.14%
                                                                                (46 of 18,038)             (26 of 1,198)     (11.2 of 157 million)
NDMA........................................................       2 ng/L                     10.2%                     27.0%                    41.54%
                                                                                (1,841 of 18,040)            (324 of 1,198)     (65.3 of 157 million)
NDPA........................................................       7 ng/L                        0%                        0%                        0%
                                                                                (0 of 18,049)              (0 of 1,198)        (0 of 157 million)
NMEA........................................................       3 ng/L                     0.02%                       0.3                    0.003%
                                                                                (3 of 18,043)              (3 of 1,198)    (0.004 of 157 million)
NPYR........................................................       2 ng/L                      0.2%                      1.8%                     4.73%
                                                                                (41 of 18,043)             (21 of 1,198)      (7.4 of 157 million)
--------------------------------------------------------------------------------------------------------------------------------------------------------
* The population-served values have been adjusted to include both the population served directly by a system and also the estimated attributable
  proportion of the population served by other systems that purchase water from the system. These adjustments are described in the UCMR 2 support
  document.

    Finished water data for the nitrosamines from California (Ranalli,
B., 2013) are consistent with the UCMR 2 data. The State of California
reported NDMA detections in 23.8% (24 of 101) of PWSs and NDEA
detections in 7.1% (1 of 14) of PWSs. There were no NPYR, NDPA, NMEA,
or NDBA detections reported. Reporting levels are not known. For
California data on NDMA and NDEA, the minimum reported detections were
1 ng/L and 30 ng/L, respectively. NDBA, NDPA, NMEA, and NPYR had no
detections and thus no minimum reported value in the dataset (Ranalli,
B., 2013). While ambient water data for the nitrosamines are limited,
because they are DBPs, it is expected that in general there would be
higher concentrations in finished water than in ambient water.

V. What about the remaining CCL 3 contaminants?

    For the remaining CCL 3 contaminants, the agency lacked adequate
health and/or occurrence information needed to address the three SDWA
statutory criteria to make a regulatory determination. Table 2 and
Table 4 of this notice provide information about the data or
information gap(s) that prevented the contaminant from moving forward
for this regulatory determination effort. The agency continues to
conduct research, collect information or find other avenues to fill the
data and information gaps identified in Table 2 and 4. One mechanism
the agency plans to continue to use to fill occurrence gaps for several
of these contaminants is the UCMR.

VI. EPA's Next Steps

    EPA intends to carefully evaluate and respond to the public
comments received on the five preliminary determinations and issue its
final regulatory determinations in 2015. If the agency makes a final
determination to regulate any of the contaminants, EPA will begin the
process to propose an NPDWR within 24 months and promulgate a final
NPDWR within 18 months following the proposal.

VII. References

Abdel-Rahman, M.S., D. Couri, and R.J. Bull. 1984. Toxicity of
chlorine dioxide in drinking water. Journal of the American College
of Toxicology 3(4):277-284.
Abrams, S. A., K. C. Copeland, S. K. Gunn, et al. 2000. Calcium
absorption, bone mass accumulation, and kinetics increase during
early pubertal development in girls. Journal of Clinical
Endocrinology & Metabolism 85(5):1805-1809.
Agency for Toxic Substances and Disease Registry (ATSDR). 1989.
Toxicological Profile for N-Nitrosodimethylamine. U.S. Department of
Health and Human Services, Public Health Service. Available on the
internet at: http://www.atsdr.cdc.gov/substances/toxsubstance.asp?toxid=173. Accessed July 22, 2009.
ATSDR. 1995. Toxicological Profile for 1,3-Dinitrobenzene and 1,3,5-
Trinitrobenzene. U.S Department of Health and Human Services, Public
Health Service. Available on the Internet at: http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=842&tid=164. Accessed July
22, 2009.
ATSDR. 2004. Toxicological Profile for Strontium. U.S. Department of
Health and Human Services, Public Health Service. Available on the
Internet at: http://www.atsdr.cdc.gov/toxprofiles/index.asp.
Accessed July 22, 2009.
Aggazzotti G., E. Righi, G. Fantuzzi, et al. 2004. Chlorination by-
products (CBPs) in drinking water and adverse pregnancy outcomes in
Italy. J. Water Health. 2(4):233-47 (as cited in U.S. EPA, 2006c).
Althoff, J., P. Pour, C. Grandjean, et al. 1977. Transplacental
effects of nitrosamines in Syrian hamsters. Z. Krebsforsch Klin. O.
90:79-86.
Amelizad, S., K.E. Appel, M. Schoepke, et al. 1989. Enhanced
demethylation and denitrosation of N-nitrosodimethylamine by human
liver microsomes from alcoholics. Cancer Lett. 46(1):43-9.
Anderson, L.M., J.P. Carter, C.L. Driver et al. 1993. Enhancement of
tumorigenesis by N-nitrosodiethylamine, N-nitrosopyrrolidine and N6-
(methylnitroso)-adenosine by ethanol. Cancer Lett, 68: 61-66.
AWWA Disinfection Systems Committee. 2008a. Committee Report:
Disinfection Survey, Part 1-Recent changes, current practices, and
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USEPA. 2000a. Unregulated Contaminant Monitoring Regulation for
Public Water Systems: Analytical Methods for Perchlorate and
Acetochlor; Announcement of Laboratory Approval and Performance
Testing (PT) Program for the Analysis of Perchlorate; Final Rule and
Proposed Rule. Federal Register. Vol. 65, No. 42, p. 11372. March 2,
2000.
USEPA. 2000b. National Drinking Water Advisory Council Minutes of
Meeting Held June 14, 2000. EPA 810-S-00-001. August 2000.
USEPA. 2001a. Unregulated Contaminant Monitoring Regulation for
Public Water Systems; Analytical Methods for List 2 Contaminants;
Clarifications to the Unregulated Contaminant Monitoring Regulation.
Federal Register. Vol. 66, No. 8, p. 2273. January 11, 2001.
USEPA. 2001b. Reference Guide for the Unregulated Contaminant
Monitoring Regulation. EPA 815-R-01-023. 65 pp. Office of Water.
October 2001. Available on the Internet at: http://www.epa.gov/ogwdw/ucmr/ucmr1/pdfs/guidance_ucmr1_ref_guide.pdf.
USEPA. 2002a. Community Water System Survey 2000. Volume I:
Overview. EPA 815-R-02-005A. December 2002. Available on the
Internet at: http://www.epa.gov/safewater/consumer/pdf/cwss_2000_volume_i.pdf.
USEPA. 2002b. Community Water System Survey 2000. Volume II:
Detailed Tables and Survey Methodology. EPA 815-R-02-005B. December
2002. Available on the Internet at: http://www.epa.gov/safewater/consumer/pdf/cwss_2000_volume_ii.pdf.
USEPA. 2002c. The Toxics Release Inventory (TRI) and Factors to
Consider When Using TRI Data. EPA 260-F-02-017. November 2002.
Available on the Internet at: http://www.epa.gov/tri/triprogram/FactorsToConPDF.pdf.
USEPA. 2003a. Announcement of Regulatory Determinations for Priority
Contaminants on the Drinking Water Contaminant Candidate List.
Federal Register. Vol. 68, No. 138, p. 42898. July 18, 2003.
USEPA. 2003b. How are the Toxics Release Inventory Data Used? EPA
260-R-002-004. May 2003. Available on the Internet at: http://www.epa.gov/tri/guide_docs/pdf/2003/2003_datausepaper.pdf.
USEPA. 2003c. Terbufos. First draft prepared by K.L. Hamernik from
the Office of Science Coordination and Policy Division. JMPR 333-
385. Available on the Internet at: http://whqlibdoc.who.int/publications/2004/924166519X_terbufos.pdf.
USEPA. 2004. Pesticide Industry Sales and Usage: 2000 and 2001
Market Estimates. Biological and Economic Analysis Division, Office
of Pesticide Programs. Available on the Internet at: http://www.epa.gov/opp00001/pestsales/.
USEPA. 2005a. Drinking Water Contaminant Candidate List 2; Final
Notice. Federal Register. Vol. 70, No. 36, p. 9071. February 24,
2005.
USEPA. 2005b. Guidelines for Carcinogen Risk Assessment. EPA 630-P-
03-001B. March 2005. Available on the Internet at: http://www.epa.gov/ttn/atw/cancer_guidelines_final_3-25-05.pdf.
USEPA. 2005c. Supplemental Guidance for Assessing Susceptibility to
Early-life Exposure to Carcinogens. EPA 630-R-03-003F. March 2005.
Available on the Internet at: http://www.epa.gov/ttn/atw/childrens_supplement_final.pdf.
USEPA. 2006a. Reregistration Eligibility Decision (RED) for
Inorganic Chlorates. EPA 738-R-06-014. Office of Prevention,
Pesticides and Toxic Substances. Available on the Internet at:
http://www.epa.gov/oppsrrd1/REDs/inorganicchlorates_red.pdf.
USEPA. 2006b. Revised Inorganic Chlorates. HED Chapter of the
Reregistration Eligibility Decision Document (RED). EPA-HQ-OPP-2005-
0507-0004. January 26, 2006. Available on the Internet at: http://www.regulations.gov/fdmspublic/component/main?main=DocketDetail&d=EPA-HQ-OPP-2005-0507.
USEPA. 2006c. Reregistration Eligibility Decision for Terbufos.
Office of Pesticide Programs. Available on the Internet at: http://www.epa.gov/pesticides/reregistration/REDs/terbufos_red.pdf.
USEPA. 2007a. Unregulated Contaminant Monitoring Regulation (UCMR)
for Public Water Systems Revisions; Final Rule. Federal Register.
Vol. 72, No. 2, p. 367. January 4, 2007.
USEPA. 2007b. Revised Interim Reregistration Decision for
Dimethoate. Available on the Internet at: http://www.epa.gov/pesticides/reregistration/REDs/dimethoate_ired_revised.pdf.
USEPA. 2008a. Drinking Water: Regulatory Determinations Regarding
Contaminants on the Second Drinking Water Contaminant Candidate
List. Federal Register. Vol. 73, No. 147, p. 44251. July 30, 2008.
USEPA. 2008b. 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. EPA 815-R-
08-014. June 2008.
USEPA. 2008c. The Analysis of Occurrence Data from the First
Unregulated Contaminant Monitoring Regulation (UCMR 1) in Support of
Regulatory Determinations for the Second Drinking Water Contaminant
Candidate List. EPA 815-R-08-012. June 2008.
USEPA. 2009a. Drinking Water Contaminant Candidate List 3--Final.
Federal Register. Vol. 74, No. 194, p. 51850. October 8, 2009.
USEPA. 2009b. The Analysis of Regulated Contaminant Occurrence Data
from Public Water Systems in Support of the Second Six-Year Review
of National Primary Drinking Water Regulations. EPA-815-B-09-006.
October 2009.
USEPA. 2009c. Community Water System Survey 2006. Volume I:
Overview. EPA 815-R-09-001. Available on the Internet at: http://water.epa.gov/infrastructure/drinkingwater/pws/upload/cwssreportvolumeI2006.pdf.
USEPA. 2009d. Community Water System Survey 2006. Volume II:
Detailed Tables and Survey Methodology. EPA 815-R-09-

002. Available on the Internet at: http://water.epa.gov/infrastructure/drinkingwater/pws/upload/cwssreportvolumeII2006.pdf.
USEPA. 2010a. Non-confidential Inventory Update Reporting (IUR).
Available on the Internet at: http://www.epa.gov/iur/index.html.
Accessed July 1, 2010.
USEPA. 2010b. Non-confidential IUR Production Volume Information.
Available on the Internet at: http://epa.gov/cdr/tools/data/2002-vol.html. Accessed July 1, 2010.
USEPA. 2011a. Drinking Water: Regulatory Determination on
Perchlorate. Federal Register. Vol. 76, No. 29, p. 7762. February
11, 2011.
USEPA. 2011b. Letter from Acetochlor Registration Partnership
requesting regulation of chloroacetanilides, June 16, 2011.
USEPA. 2011c. Summary of Comments and Discussion, Preliminary
Regulatory Determinations for the Third Contaminant Candidate List
Stakeholder Meeting, June 16, 2011.
USEPA. 2011d. Support for Regulatory Determination 3 Expert Reviews;