Acetochlor.......................  EPA OPP HHRA, 2018.  ICI, Inc. 1988.....  increased salivation,             0.02             n/a  100.
                                                                              increased alanine
                                                                              aminotransferase
                                                                              (ALT), ornithine
                                                                              carbamyl transferase
                                                                              and triglyceride
                                                                              levels; decreased
                                                                              blood glucose; and
                                                                              histopathological
                                                                              changes in the
                                                                              kidneys, liver and
                                                                              testes of males, in
                                                                              beagle dogs.
Methyl Bromide (Bromomethane)....  EPA OPP HHRA, 2006.  Mertens, 1997......  decreased body weight,           0.022             n/a  100.
                                                                              decreased rate of
                                                                              body weight gain, and
                                                                              decreased food
                                                                              consumption in rats.
Metolachlor......................  EPA OPP HHRA, 2018.  Page, 1981.........  decreased pup body                0.26             n/a  300.
                                                                              weight in rats.
Nitrobenzene.....................  EPA IRIS, 2009.....  NTP, 1983..........  changes in absolute              0.002             n/a  10.
                                                                              and relative organ
                                                                              weights, splenic
                                                                              congestion, and
                                                                              increases in
                                                                              reticulocyte count
                                                                              and metHb
                                                                              concentration in rats.
RDX..............................  EPA IRIS, 2018.....  Crouse et al., 2006  convulsions in rats              0.004            0.08  30 (noncancer); 0.4
                                                         (noncancer); Lish    (noncancer); lung and                                   (cancer).
                                                         et al. 1984          liver tumors in mice
                                                         (cancer).            (cancer).
--------------------------------------------------------------------------------------------------------------------------------------------------------

                                                 Table 8--Occurrence Findings From Primary Data Sources
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                Population served                       Population served
                                                                          PWSs with at least    by PWSs with at   PWSs with at least    by PWSs with at
        RD 4  contaminant          HRL, [micro]g/L    Primary  database   1  detection > \1/  least 1  detection  1  detection > HRL   least 1 detection
                                                                                2\ HRL            > \1/2\ HRL                                > HRL
--------------------------------------------------------------------------------------------------------------------------------------------------------
PFOS............................  0.07.............  UCMR 3 AM..........  95/4,920 (1.93%)..  10,427,193/241 M    46/4,920 (0.93%)..  3,789,831/241 M
                                                                                (4.32%).                                (1.57%).
PFOA............................  0.07.............  UCMR 3 AM..........  53/4,920 (1.07%)..  3,652,995/241 M     13/4,920 (0.26%)..  490,480/241 M
                                                                                (1.51%).                                (0.20%).
1,1-Dichloroethane..............  1,000............  UCMR 3 AM..........  0/4,916 (0.00%)...  0/241 M (0.00%)...  0/4,916 (0.00%)...  0/241 M (0.00%).
Acetochlor......................  100..............  UCMR 1 AM..........  0/3,869 (0.00%)--   0/226 M (0.00%)--   0/3,869 (0.00%)--   0/226 M (0.00%)--
                                                                           UCMR 1.             UCMR 1.             UCMR 1.             UCMR 1.
                                                     UCMR 2 SS..........  0/1,198 (0.00%)--   0/157 M (0.00%)--   0/1,198 (0.00%)--   0/157 M (0.00%)--
                                                                           UCMR 2.             UCMR 2.             UCMR 2.             UCMR 2.
Methyl Bromide (Bromomethane)...  100..............  UCMR 3 AM..........  0/4,916 (0.00%)...  0/241 M (0.00%)...  0/4,916 (0.00%)...  0/241 M (0.00%).
Metolachlor.....................  300..............  UCMR 2 SS..........  0/1,198 (0.00%)...  0/157 M (0.00%)...  0/1,198 (0.00%)...  0/157 M (0.00%).
Nitrobenzene....................  10...............  UCMR 1 AM..........  2/3,861 (0.05%)...  255,358/226 M       2/3,861 (0.05%)...  255,358/226 M
                                                                                (0.11%).                                (0.11%).
RDX.............................  30, 0.4..........  UCMR 2 AM..........  0/4,139 (0.00%) >   0/229 M (0.00%) >   0/4,139 (0.00%) >   0/229 M (0.00%) >
                                                                           15 [micro]g/L.      15 [micro]g/L.      30 [micro]g/L.      30 [micro]g/L.

                                                                          3/4,139 (0.07%) >   96,033/229 M        3/4,139 (0.07%) >   96,033/229 M
                                                                           0.2 [micro]g/L.     (0.04%) > 0.2       0.4 [micro]g/L.     (0.04%) > 0.4
                                                                                [micro]g/L.                             [micro]g/L.
--------------------------------------------------------------------------------------------------------------------------------------------------------

B. Contaminant Profiles
---------------------------------------------------------------------------

    \20\ Using the CSF, the calculated concentration in drinking
water with one-in-a-million risk for an increase in testicular
tumors at levels greater than background is 0.0005 mg/L.
    The equivalent concentration derived from the RfD is lower than
the concentration of 0.0005 mg/L associated with a one-in-a-million
risk for testicular cancer indicating that a guideline derived from
the developmental endpoint will be protective for the cancer
endpoint. (USEPA, 2016g).
---------------------------------------------------------------------------

1. Perfluorooctane Sulfonate (PFOS) and Perfluorooctanoic Acid (PFOA)
a. Background
    PFAS are a group of synthetic chemicals that have been in use since
the 1940s. PFAS are found in a wide array of consumer and industrial
products. PFAS manufacturing and processing facilities, facilities
using PFAS in production of other products, airports, and military
installations have been associated with PFAS releases into the air,
soil, and water (USEPA, 2016e; USEPA, 2016f).
    PFOS and PFOA--two of the most widely-studied and longest-used
PFAS--are part of a subset of PFAS known as perfluorinated alkyl acids
(PFAA). These two compounds have been detected in up to 98% of serum
samples taken in biomonitoring studies that are representative of the
U.S. general population; however, since PFOA and PFOS have been
voluntarily phased out in the U.S., serum concentrations have been
declining (CDC, 2019). The National Health and Nutrition Examination
Survey (NHANES) data shows that 95th-percentile serum PFOS
concentrations have decreased from 75.7 [micro]g/L in the 1999-2000
cycle to 18.3 [micro]g/L in the 2015-2016 cycle (CDC, 2019; Jain, 2018;
Calafat et al., 2007; Calafat et al., 2019), a decrease of over 75
percent. In early 2000, the EPA worked with the 3M Company, which was
the only major manufacturer of PFOS in the United States at that time,
to support the company's voluntary phase-out and elimination of PFOS
production and use. Under the EPA's 2010/2015 PFOA Stewardship Program,
eight major chemical manufacturers and processors agreed to phase out
the use of PFOA and PFOA-related chemicals in their products and
emissions from their facilities. All companies met the PFOA Stewardship
Program goals by 2015. While companies participating in the PFOA
Stewardship program report that they no longer produce or use PFOA
domestically, PFOA may still be produced domestically or imported or
used by companies not participating in the PFOA Stewardship Program. In
addition, PFOA and PFOS can also be present in imported articles
(USEPA, 2017c). Due to the widespread use and persistence of PFAS in
the environment, most people have been exposed to PFAS, including PFOA
and PFOS (USEPA, 2016e; USEPA, 2016f).
    Production of PFOA and PFOS is subject to CDR reporting. Production
volumes of PFOA and PFOS were claimed by reporting companies as
confidential for the most recent reporting cycles. The last time
production (including import) of PFOA exceeded the CDR reporting
threshold was during the 2016 reporting cycles (which includes
production information from 2012-2015) and it was phased out by
companies participating in the 2010/2015 PFOA Stewardship Program in
2013. Similarly, PFOS was phased out by 3M in 2002 and the most
recently reported data for PFOS are from the 2002 reporting cycle
(which includes production information from 2001 only) (USEPA, 2019a).
Absence of recent reporting may indicate that production (including
import) of PFOA and PFOS has halted or has been below the CDR reporting
thresholds. Although PFOA and PFOS are not produced domestically or
imported by the companies participating in the 2010/2015 PFOA
Stewardship Program, PFOA and PFOS may still be produced domestically
or imported below the CDR reporting thresholds (i.e., 2,500 pounds) by
companies not participating in the PFOA Stewardship Program.
b. Statutory Criterion #1 (Adverse Health Effects)
    The EPA is preliminarily determining that PFOA and PFOS meet the
SDWA statutory criterion #1 for regulatory determinations: They may
have adverse effects on the health of persons. In 2016, the EPA
published health assessments (health effects support documents or
HESDs) for PFOA and PFOS based on the Agency's evaluation of the peer
reviewed science available at that time. This section presents a
summary of the adverse health effects discussed in the HESDs. For
specific details on the potential for adverse health effects and
approaches used to identify and evaluate information on hazard and
dose-response, please see USEPA (2016d), USEPA (2016e), USEPA (2016f),
and USEPA (2016g). The lifetime HA of 0.07 [micro]g/L is used as the
HRL for Regulatory Determination 4.
    Human epidemiology data report associations between PFOA exposure
and high cholesterol, increased liver enzymes, decreased vaccination
response, thyroid disorders, pregnancy-induced hypertension and
preeclampsia, and cancer (testicular and kidney). The associations for
most epidemiology endpoints are mixed. Although mean serum values are
presented in the human studies, actual estimates of PFOA exposure
(i.e., doses/duration) are not currently available. Thus, the serum
level at which the effects were first manifest and whether the serum
had achieved steady state at the point the effect occurred cannot be
determined. It is likely that some of the human exposures that
contribute to serum PFOA values come from PFOA derivatives or
precursors that break down metabolically to PFOA. These compounds could
originate from PFOA in diet and materials used in the home, which
creates potential for confounding. In addition, most of the subjects of
the epidemiology studies have many PFASs and/or other contaminants in
their blood. Although the study designs adjust for other potential
toxicants as confounding factors, their presence constitutes a level of
uncertainty that is usually absent in the animal studies. Taken
together, the weight of evidence for human studies supports the
conclusion that PFOA exposure is a human health hazard. At this time,
EPA concludes that the human studies are adequate for use qualitatively
in the identification hazard and are supportive of the findings in
laboratory animals.

    For PFOA, oral animal studies of short-term, subchronic, and
chronic duration are available in multiple species including monkeys,
rats and mice. These animal studies report developmental effects
(survival, body weight changes, reduced ossification, delays in eye
opening, altered puberty, and retarded mammary gland development),
liver toxicity (hypertrophy, necrosis, and effects on the metabolism
and deposition of dietary lipids), kidney toxicity (weight), immune
effects, and cancer (liver, testicular, and pancreatic) (USEPA, 2016e).
Overall, the animal toxicity studies available for PFOA demonstrate
that the developing fetus is particularly sensitive to PFOA-induced
toxicity. Human epidemiology data report associations between PFOA
exposure and high cholesterol, increased liver enzymes, decreased
vaccination response, thyroid disorders, pregnancy-induced hypertension
and preeclampsia, and cancer (testicular and kidney). Overall, the
developmental toxicity studies in animals available for PFOA
demonstrate that the developing rodent fetus and newborn rodent are
sensitive to PFOA-induced toxicity.
    PFOA is known to be transmitted to the fetus via cord blood and to
the newborn, infant, and child via breast milk (USEPA, 2016f). Under
the EPA's Guidelines for Carcinogen Risk Assessment (USEPA, 2005b),
there is ``suggestive evidence of carcinogenic potential'' for PFOA.
Similarly, the International Agency for Research on Cancer (IARC)
classifies PFOA as ``possibly carcinogenic to humans'' (IARC, 2019a;
IARC, 2019b).
    The EPA calculated several candidate RfDs for PFOA in the 2016 HESD
and selected the RfD of 0.00002 mg/kg/day based on reduced ossification
in proximal phalanges and accelerated puberty in male pups following
exposure during gestation and lactation in a developmental toxicity
study in mice (Lau et al., 2006) for the derivation of a lifetime HA.
The RfD for PFOA was calculated by applying uncertainty factors to
account for interspecies variability (3), intraspecies differences
(10), and use of a LOAEL (3). The Health Effects Support Document
(USEPA, 2016h) describes these uncertainties in Section 4.
Additionally, uncertainties and limitations (i.e., human
epidemiological data, immunological and mammary gland endpoints, and
exposure) are discussed in detail in Section 8 of the Health Advisory
(USEPA, 2016f) document. The lifetime HA of 0.07 [micro]g/L was
calculated using the 0.00002 mg/kg/day RfD for developmental effects, a
DWI to BW ratio for the 90th percentile \21\ for lactating women (0.054
L/kg/day) and a calculated 20% RSC (USEPA, 2016f). This RfD is
protective of effects other than those occurring during development
such as kidney and immune effects. Because of the potential for
increased susceptibility during the time period of pregnancy and
lactation observed in this study, the EPA used DWI and BW parameters
for lactating women in the calculation of a lifetime HA for this target
population during this potential critical time period. The EPA also
calculated a CSF of 0.07 (mg/kg/day)-\1\ based on testicular
tumors in rats. The resultant HA using this CSF is greater than the
lifetime HA based on noncancer effects, indicating that the HA derived
based on the developmental endpoint is protective for the cancer
endpoint (USEPA, 2016h).
---------------------------------------------------------------------------

    \21\ Consumers only estimate of combined direct and indirect
community water ingestion; see Table 3-81 in USEPA, 2011b.
---------------------------------------------------------------------------

    For PFOS, epidemiological studies have reported associations
between PFOS exposure and high serum cholesterol and reproductive and
developmental parameters. The strongest associations are related to
serum lipids with increased total serum cholesterol and high-density
lipoproteins (HDLs). As with PFOA, the associations for most
epidemiology endpoints are inconsistent. Although mean serum values are
presented in the human studies, actual estimates of PFOS exposure
(i.e., doses/duration) are not currently available. Thus, the serum
level at which the effects were first manifest and whether the serum
had achieved steady state at the point the effect occurred cannot be
determined (USEPA, 2016e) Human epidemiological studies suggest an
association between higher PFOS levels and decreases in female
fecundity and fertility, decreased birth weights in offspring and other
measures of postnatal growth (e.g., small for gestational age).
    Short-term and chronic exposure studies in animals demonstrate
increases in liver weight consistently. Co-occurring effects in these
studies include decreased cholesterol, hepatic steatosis, lower body
weight, and liver histopathology. One and two generation toxicity
studies also show decreased pup survival and body weights.
Additionally, developmental neurotoxicity studies show increased motor
activity and decreased habituation and increased escape latency in the
water maze test following in utero and lactational exposure to PFOS.
Gestational and lactational exposures were also associated with higher
serum glucose levels and evidence of insulin resistance in adult
offspring. Limited evidence suggests immunological effects in mice.
Short-term and subchronic duration studies are available in multiple
animal species including monkeys, rats and mice. These studies also
found increased serum glucose levels and insulin resistance in adult
animals exposed during development, developmental effects (decreased
body weight and survival), reproductive effects (impacts on mating
behavior), liver toxicity (increased liver weight co-occurring with
decreased serum cholesterol, hepatic steatosis), developmental
neurotoxicity (impaired spatial learning and memory), suppressed
immunological responses, and cancer (thyroid and liver). Increased
incidence of hepatocellular adenomas in the male (12% at the high dose)
and female rats (8% at the high dose) and combined adenomas/carcinomas
in the females (10% at the high dose) were observed, but they did not
display a clear dose-related response; Thyroid tumors (adenomas and
carcinomas) were seen in males receiving 0, 0.5, 2, 5, or 20 ppm and in
females receiving 5 or 20 ppm in their diet. The tumor (adenomas +
carcinomas) prevalence for males was consistent across dose groups. In
males the incidence of thyroid tumors was significantly elevated only
in the high-dose, recovery group males exposed for 52 weeks (10/39) but
not in the animals receiving the same dose at 105 weeks. There were
very few follicular cell adenomas/carcinomas in the females (5 total)
with no dose-response. The most frequent thyroid tumor type in the
females was C-cell adenomas, but the highest incidence was that for the
controls and there was a lack of dose response among the exposed
groups. C-cell adenomas were not observed in males (Thomford 2002;
Butenhoff et al. 2012). Overall, the animal toxicity studies available
for PFOS demonstrate that the developing fetus and newborn rodent are
sensitive to PFOS induced toxicity. PFOS is known to be transmitted to
the fetus via cord blood and to the newborn, infant, and child via
breast milk (USEPA, 2016f). Applying the EPA Guidelines for Carcinogen
Risk Assessment (USEPA, 2005b), there is suggestive evidence of
carcinogenic potential for PFOS. However, the weight of evidence for
humans is too limited to support a quantitative cancer assessment given
that there was no evidence for dose-response from which to derive a
slope factor for the tumor types identified in animals.

    The EPA calculated multiple candidate RfDs for PFOS in the HESD and
selected the RfD of 0.00002 mg/kg/day based on decreased neonatal rat
body weight from both the one- and two-generation studies by Luebker et
al. (2005a, 2005b) for the derivation of a lifetime HA. The RfD for
PFOS was calculated by applying uncertainty factors to account for
interspecies variability (3) and intraspecies differences (10). The
Health Effects Support Document (USEPA, 2016g) describes these
uncertainties in Section 4. Additionally, uncertainties and limitations
(i.e., human epidemiologic data, immunological and mammary gland
endpoints, and exposure) are discussed in detail in Section 8 of the
Health Advisory (USEPA, 2016e) document. The lifetime HA of 0.07
[micro]g/L was calculated using the 0.00002 mg/kg/day RfD for
developmental effects, a DWI to BW ratio for the 90th percentile \21\
for lactating women (0.054 L/kg/day) and a 20% RSC (USEPA, 2016e). The
lifetime HA of 0.07 [micro]g/L is used as the HRL for Regulatory
Determination 4.
    The RfDs for both PFOA and PFOS are both based on developmental
effects and are numerically identical. Thus, when both chemicals co-
occur at the same time and location, the EPA recommended a conservative
and health-protective approach of 0.07 [micro]g/L for the PFOA/PFOS
total combined concentration (USEPA, 2016e).
    The EPA has initiated a systematic literature review of peer-
reviewed scientific literature for PFOA and PFOS published since 2013
with the goal of identifying any new studies that may be relevant to
human health assessment. An annotated bibliography of identified
studies as well as the protocol used to identify the relevant
publications can be found in Appendix D of the Regulatory Determination
4 Support Document (USEPA, 2019a), available in the docket for this
document. Additional analyses of these new studies is needed to confirm
relevance, extract the data to assess the weight of evidence, and
identify critical studies in order to inform future decision making.
The EPA is seeking comment on any additional studies and information
that it should consider. Should the EPA make a final positive
regulatory determination for PFOA and PFOS, the Agency will undertake
the SDWA rulemaking process to establish a National Primary Drinking
Water Regulation for those contaminants. For that rulemaking effort, in
addition to using the best available science, the SDWA requires that
the Agency seek recommendations from the EPA Science Advisory Board,
and consider public comment on any proposed rule. Therefore, EPA
anticipates further scientific review of new science prior to
promulgation of any regulatory standard.
c. Statutory Criterion #2 (Occurrence at Frequency and Levels of Public
Health Concern)
    The EPA is preliminarily determining that PFOA and PFOS meet the
SDWA statutory criterion #2 for regulatory determinations: they occur
with a frequency and at levels of public health concern at PWSs based
on the EPA's evaluation of the available occurrence information. The
EPA is seeking public comment on whether the data described below
support such a determination and whether additional data or studies
exist which EPA should consider when finalizing a determination.
    EPA has made its preliminary determination based, in part, on the
UCMR 3 data (USEPA, 2019b). The EPA has determined in accordance with
SDWA 1412(b)(1)(B)(ii)(II) that the UCMR 3 data are the best available
occurrence information for the PFOA/PFOS regulatory determinations.
UCMR 3 monitoring occurred between 2013 and 2015and currently
represents the only nationally-representative finished water dataset
for PFOA and PFOS. Under UCMR 3, 36,972 samples from 4,920 PWSs were
analyzed for PFOA and PFOS. The MRL for PFOA was 0.02 [micro]g/L and
the MRL for PFOS was 0.04 [micro]g/L. A total of 1.37% of samples had
reported detections (greater than or equal to the MRL) of at least one
of the two compounds. To examine the occurrence of PFOS and PFOA in
aggregate, the EPA summed the concentrations detected in the same
sample to calculate a total PFOS/PFOA concentration.
    The EPA notes that when these two chemicals co-occur at the same
time and location in a drinking water source, a conservative and
health-protective approach that EPA recommends would be to compare the
sum of the concentrations (USEPA, 2016g; USEPA, 2016h). The Regulatory
Determination 4 Support Document presents a sample-level summary of the
results for the individual contaminants (USEPA, 2019a). Concentrations
of PFOS or PFOA below their respective MRLs were set equal to 0
[micro]g/L when calculating the total PFOS/PFOA concentration for the
sample. The maximum summed concentration of PFOA and PFOS was 7.22
[micro]g/L and the median summed value was 0.05 [micro]g/L. Summed PFOA
and PFOS concentrations exceeded the HRL (0.07 [micro]g/L) at a minimum
of 1.3% of PWSs (63 PWSs \22\). Since UCMR 3 monitoring occurred,
certain sites where elevated levels of PFOA and PFOS were detected may
have installed treatment for PFOA and PFOS, may have chosen to blend
water from multiple sources, or may have otherwise remediated known
sources of contamination. Those 63 PWSs serve a total population of
approximately 5.6 million people and are located in 25 states, tribes,
or U.S. territories (USEPA, 2019b). The HRLs for PFOA and PFOS are
based on the 2016 drinking water Health Advisories and reflect
concentrations of PFOA and PFOS in drinking water at which adverse
health effects are not anticipated to occur over a lifetime (USEPA,
2016e; USEPA, 2016f).
---------------------------------------------------------------------------

    \22\ Sum of PFOA + PFOS results rounded to 2 decimal places in
those cases where a laboratory reported more digits.
---------------------------------------------------------------------------

    Consistent with the Agency's commitment in the PFAS Action Plan
(USEPA, 2019d) to present information about additional sampling for
PFAS in water systems, the EPA has supplemented its UCMR data with data
collected by states who have made their data publicly available at this
time. In some cases, EPA obtained the data directly from the state's
public website while, in others, these data were provided to EPA.
Specifically, the EPA evaluated publicly available monitoring data that
permitted summed PFOA and PFOS analyses from the state websites of New
Hampshire, Colorado, and Michigan. Additional finished drinking water
monitoring data was provided to the EPA by the New Jersey Department of
Environmental Protection. These data are summarized in Table 9 below.
The EPA notes that some of these data are from targeted sampling
efforts and thus may not be representative of occurrence in the state.
The EPA also notes that states which chose to make their occurrence
data publicly available and the state that chose to provide its data to
the EPA may not necessarily represent occurrence in other states. The
Regulatory Determination 4 Support Document presents a detailed
discussion of additional information from states on occurrence of these
contaminants in drinking water systems (USEPA, 2019a). The EPA is also
aware that some of these states may have updated data available and
that additional states have or intend to conduct monitoring of finished
drinking water, such as Illinois, Pennsylvania, and Vermont. The EPA
will consider any data submitted in response to this proposal to inform
future regulatory decision making. The EPA is also aware of additional
locations with drinking

water impacts (including private wells) from contaminated sites. These
include sites near production facilities, active and former military
bases, and other point sources.\23\
---------------------------------------------------------------------------

    \23\ Examples include Chemours Washington Works Facility, West
Virginia (production facilities), Horsham Air National Guard
Station, Pennsylvania and former Wurtsmith Air Force Base, Michigan
(active and former military bases), and non-military firefighting
activities (other point sources).
    \24\ Some of these data in these tables are from targeted
sampling efforts and therefore, would be expected to have higher
detection rates than a random sample.
---------------------------------------------------------------------------

    For the following summed PFOA and PFOS analyses, monitoring data
sets from public water systems in New Hampshire and New Jersey
permitted combined analysis of PFOS and PFOA occurrence (i.e., with
paired PFOS and PFOA concentrations reported for each individual water
sample). In addition, Colorado and Michigan directly reported
monitoring results for combined PFOS and PFOA. All states data sets
summarized in Table 9 had at least one instance of summed PFOS and PFOA
concentrations greater than the HRL of 0.07 [micro]g/L. Additional
details can be found in the Regulatory Determination 4 Support Document
(USEPA, 2019a).

                                  Table 9--Combined PFOS and PFOA Occurrence: Summary of State Monitoring Results \24\
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                       Type of water
       State (reference)             Date range            tested               Notes on coverage           Summary of results          Survey type
--------------------------------------------------------------------------------------------------------------------------------------------------------
Colorado (CDPHE, 2018)           2013-2017.........  Surface Water      Data available from 28            The maximum summed      Targeted.
                                                      (Finished Water)   ``drinking water distribution     concentration of PFOA
                                                      and Drinking       zones'' (one or more per public   and PFOS was 0.3
                                                      Water              water system) in targeted         [micro]g/L and the
                                                      Distribution       sampling efforts at a known       median summed value
                                                      Samples.           contaminated aquifer region.      was 0.09 [micro]g/L.
                                                                         Data were collected by El Paso    Summed PFOA and PFOS
                                                                         County Public Health, local       concentrations
                                                                         water districts and utilities,    exceeded the EPA HRL
                                                                         and the Colorado Department of    (0.07 [micro]g/L) at
                                                                         Public Health and Environment     25% of distribution
                                                                         (CDPHE). Results represent data   zones (7 distribution
                                                                         collected in a targeted region.   zones).
                                                                         Detection limits ranged from
                                                                         0.002 [micro]g/L to 0.040
                                                                         [micro]g/L.
Michigan (Michigan EGLE, 2019)   2018-2019.........  Groundwater and    Data available from 1,119 public  The maximum summed      Statewide.
                                                      Surface Water--    community water systems,          concentration of PFOA
                                                      Raw and Finished   downloaded in October 2019.       and PFOS was 1.52
                                                      Water (Community   Results are from the Michigan     [micro]g/L and the
                                                      Water Supplies).   Department of Environment,        median summed value
                                                                         Great Lakes and Energy (EGLE)     was 0.004 [micro]g/L.
                                                                         statewide sampling efforts for    Summed PFOA and PFOS
                                                                         PFAS of drinking water from       concentrations
                                                                         community water supplies.         exceeded the EPA HRL
                                                                         Results are presented for the     (0.07 [micro]g/L) at
                                                                         sum of PFOA and PFOS              0.09% of PWSs (1 PWS).
                                                                         concentrations. Information on
                                                                         detection limits was not
                                                                         available.
New Hampshire (NHDES, 2017)      2013-2017.........  Groundwater and    Data available online from 295    The maximum summed      Targeted.
                                                      Surface Water.     PWSs providing results to NH,     concentration of PFOA
                                                                         including PWSs near               and PFOS was 0.242
                                                                         contaminated sites. Results       [micro]g/L and the
                                                                         represent all PFOA and PFOS       median summed value
                                                                         water quality data reported to    was 0.006 [micro]g/L.
                                                                         New Hampshire Department of       Summed PFOA and PFOS
                                                                         Environmental Services (NHDES)    concentrations
                                                                         through May 3, 2017. There is     exceeded the EPA HRL
                                                                         no discussion of                  (0.07 [micro]g/L) at
                                                                         representativeness. Detection     1.01% of PWSs (3
                                                                         limits ranged from 0.0005         PWSs).
                                                                         [micro]g/L to 0.04 [micro]g/L.
New Jersey (NJDEP, 2019)         2019..............  Groundwater and    Statewide sampling of finished    The maximum summed      Statewide.
                                                      Surface Water--    drinking water data between       concentration of PFOA
                                                      Finished Water.    January 1, 2019 and June 28,      and PFOS was 1.09
                                                                         2019. These represent the first   [micro]g/L and the
                                                                         two quarters of statewide         median summed value
                                                                         efforts to sample of finished     was 0.01 [micro]g/L.
                                                                         drinking water. Under this        Summed PFOA and PFOS
                                                                         sampling effort, 2,459 water      concentrations
                                                                         samples from 1,049 PWS were       exceeded the EPA HRL
                                                                         analyzed for PFOA and PFOS.       (0.07 [micro]g/L) at
                                                                         Detection limits ranged from      1.14% of PWSs (12
                                                                         0.0016 [hyphen] 0.0046 (doesn't   PWSs).
                                                                         specify for which PFAS
                                                                         compound).
--------------------------------------------------------------------------------------------------------------------------------------------------------

    In addition to the monitoring data available from public water
systems, North Carolina has made data from 17 private wells associated
with the Chemours facility in Fayetteville available (NCDEQ, 2018). The
maximum combined PFOS and PFOA concentration was 0.0319 [mu]g/L, while
the median was 0.004 [mu]g/L. Summed PFOS and PFOA concentrations did
not exceed the EPA HRL (0.07 [mu]g/L) at any of the sampling sites.
Note that the EPA does not regulate private drinking water wells but
may evaluate data from private wells where the data may be indicative
of contaminants in aquifers that are used as sources for public water
system wells.
    UCMR 3 data have also been used by researchers to evaluate co-
occurrence of PFAS in drinking water at PWSs. For example, Guelfo and
Adamson (2018) investigated PFAS data from UCMR 3 for occurrence and
co-contaminant mixtures, trends in PFAS detections relative to PWS
characteristics and potential release types, and temporal trends in
PFAS occurrence. The study identified that approximately 50% of samples
with PFAS detections contained [gteqt]2 PFASs, and 72% of detections
occurred in groundwater. Large PWSs (>10,000 customers) were 5.6 times
more likely than small PWSs (<=10,000 customers) to exhibit PFAS
detections; however, when detected, median total PFAS concentrations
were higher in small PWSs (0.12 [mu]g/L) than in large (0.053 [mu]g/L).
Hu et al. (2016) presented spatial analysis of PFAS concentrations
under UCMR 3 and found that the number of industrial sites

that manufacture or use these compounds, the number of military fire
training areas, and the number of wastewater treatment plants are all
significant predictors of PFAS detection frequencies and concentrations
in public water supplies. The authors found that for PFAS monitored
under UCMR 3, the detection frequency in drinking water sourced from
groundwater was more than twice that from surface water. Additionally,
PFOA and PFOS were more frequently detected in groundwater whereas UCMR
3 PFAS compounds with shorter chain lengths were detected more
frequently in surface waters. Hu et al. (2016) noted that this
observation could be due to the original mode of environmental release
(aerosol, application to soil, and aqueous discharge).
    The state data (as presented above and discussed in the Regulatory
Determination 4 Support Document), while some are from targeted
sampling efforts and therefore, would be expected to have higher
detection rates than a random sample, show occurrence in multiple
geographic locations consistent with what was observed during UCMR 3
monitoring. Additionally, some state monitoring efforts show detections
above the EPA Health Advisory in water systems that were not required
to conduct monitoring in the UCMR 3. EPA believes that these data
support the Agency's preliminary determination that PFOA and PFOS occur
with a frequency and at levels of public health concern in drinking
water systems across the United States. Additional details of the EPA
analyses of UCMR 3 monitoring data for PFAS can be found in the
Regulatory Determination 4 Support Document (USEPA, 2019a). The EPA
requests comment on whether there are additional occurrence data sets
that it can use to supplement the analyses already performed and inform
its determination, including more recent data from specific data sets
mentioned above.
d. Statutory Criterion #3 (Meaningful Opportunity)
    The EPA conducted extensive public outreach in the development of
the PFAS Action Plan, including gathering diverse perspectives through
the May 2018 National Leadership Summit, direct engagement with the
public in impacted communities in five states, engagement with tribal
partners, and roundtables conducted with community leaders near
impacted sites. In addition, the Agency reviewed approximately 120,000
comments in the public docket that was specifically established to
gather input for the Action Plan (USEPA, 2019d). Through these
engagements, the EPA heard significant concerns from the public on the
challenges these contaminants pose for communities nationwide and the
need for uniform, protective drinking water regulations across the
United States.
    Based on the significant public interest in the potential risks
posed by PFOA and PFOS, and the information currently available to the
EPA, the Administrator has made the preliminary determination that
regulation of PFOA and PFOS presents a meaningful opportunity for
health risk reduction for persons served by PWSs. In determining that
regulation of PFOA and PFOS presents a meaningful opportunity for
health risk reduction for sensitive populations, the EPA was
particularly mindful that PFOA and PFOS are known to be transmitted to
the fetus via cord blood and to the newborn, infant, and child via
breast milk (USEPA, 2016f).
    Data from recent state monitoring efforts validate the UCMR 3
monitoring results (USEPA, 2019b; NJ DEP, 2019). Sun et al. observed
similar temporal trends in their investigation in the Cape Fear
Watershed of North Carolina, where PFAS concentrations remained similar
between 2006 and 2013 (Sun et al., 2016). These observations suggest
that PFOA and PFOS can be persistent in the environment, lack
attenuation processes that would degrade these compounds over time and
may be subject to precursor transformations. The EPA believes PFOA and
PFOS occur at a frequency and at levels of public health concern. UCMR
3 indicates 1.3% of PWSs (63 PWSs) monitored reported combined PFOA/
PFOS above the HRL. These systems serve a total population of
approximately 5.6 million people. While this preliminary regulatory
determination is based, in part, on the UCMR occurrence data, it is
also based on additional factors discussed above.
    State data (as described above and discussed in the Regulatory
Determination 4 Support Document) support the UCMR results, and the
Agency's determination that PFOA and PFOS occur with a frequency and at
levels of public health concern in finished drinking water across the
United States, with some results substantially elevated above the EPA's
HAs. These data have also identified PFAS contamination in other
locations, such as in small, previously unmonitored systems, beyond
where the UCMR 3 required water systems to conduct monitoring. Due to
the anthropogenic nature of PFOA and PFOS and their persistence in the
environment, multiple localized areas of contamination across the
country may be a significant contributor to drinking water
contamination. The state data sets summarized in Table 9 had at least
one instance of summed PFOS and PFOA concentrations greater than the
HRL of 0.07 [micro]g/L. While many detections are marginally above the
EPA HA levels, there are many instances where localized samples
substantially exceed the HA levels, sometimes by 2-3 orders of
magnitude (i.e., a maximum summed concentration as high as 1.52 [mu]g/
L). The EPA believes there is significant public health risk reduction
potential in the localized areas with these significantly elevated
concentrations. To assess communities with the highest exposures, the
ATSDR has begun to perform PFAS exposure assessments in communities
near current or former military bases with elevated concentrations of
PFAS detected in drinking water (ATSDR, 2019a).
    Adverse effects observed following exposures to PFOA and PFOS are
the same or similar and include effects in humans on serum lipids,
birth weight, and serum antibodies. Some of the animal studies show
common effects on the liver, neonate development, and responses to
immunological challenges. Both compounds were also associated with
tumors in long-term animal studies (USEPA, 2016g; USEPA, 2016h). States
have taken action to reduce exposures (as further discussed below).
Some states have established regulatory or guidance levels in drinking
water for PFOA, PFOS, as well as other PFAS (ASDWA, 2019). Moving
forward with a national-level regulation for PFOA and PFOS may provide
additional national consistency and reduce regulatory uncertainty for
stakeholders across the country.
    PFOA and PFOS are resistant to environmental degradation processes
such as hydrolysis, photolysis, and biodegradation and are thus highly
persistent in the environment (USEPA, 2019a). In addition, biotic and
abiotic processes can degrade PFAS precursors to form PFAAs such as
PFOA and PFOS over time and thus are also important contributors to the
presence and persistence of these chemicals in the environment (ITRC,
2018). Additionally, PFOA and PFOS are expected to have a high
likelihood of partitioning to water based on their ionic nature at
typical environmental pH and their organic carbon partitioning
coefficients (Koc). PFOA has a high likelihood of
partitioning to water based on its water solubility while the water
solubility of PFOS anion indicates a moderate likelihood of
partitioning to water.

Therefore, PFOA and PFOS have high mobility and persistence in soil and
groundwater and are expected to form larger plumes than less mobile and
persistent contaminants in the same hydrogeological setting (ITRC,
2018). In addition, long-range atmospheric transport of PFOA and PFOS
through industrial releases (e.g., stack emissions) can accumulate to
measurable levels in soils and surface waters away from their point of
release (Young et al., 2007; Wallington et al., 2006; Dreyer et al.,
2010). Although some manufacturing companies agreed to phase out
production of PFOA and PFOS in the United States, other sources could
still exist such as fire training and emergency response sites,
industrial sites, landfills, and wastewater treatment plant biosolids
as well as imported in products (USEPA, 2017c; ITRC, 2018). Drinking
water analytical methods are available to measure PFOA, PFOS, and other
PFAS in drinking water. The EPA has published validated methodology for
detecting a total of 29 unique PFAS in drinking water including EPA
Method 537.1 (18 PFAS) (USEPA, 2018b) and EPA Method 533 (25 PFAS) (14
PFAS can be detected by both methods). Therefore, new information about
the occurrence of PFAS in drinking water will become available as the
Agency further evaluates regulatory action for these contaminants.
    Available treatment technologies for removing PFAS from drinking
water have been evaluated and reported in the literature (e.g.,
Dickenson and Higgins, 2016). The EPA's Drinking Water Treatability
Database (USEPA, 2019e) summarizes available technical literature on
the efficacy of treatment technologies for a range of priority drinking
water contaminants, including PFOA and PFOS. Conventional treatment
(comprised of the unit processes coagulation, flocculation,
clarification, and filtration) is not considered effective for the
removal of PFOA. Granular activated carbon (GAC), anion exchange
resins, reverse osmosis and nanofiltration are considered effective for
the removal of PFOA. However, there are limitations and uncertainties
pertaining to these removal processes for PFAS. For example, the
treatment efficacy of GAC and anion exchange resins is strongly
dependent upon the type of PFAS present and physio-chemical properties
of the solution matrix. When mixed PFAS are in the source water, short-
chain PFAS will break through the adsorber more quickly. When a system
makes treatment technology decisions, it is important to consider the
media reactivation and replacement frequency, the cost of reactivation
or disposal of spent media, and the potential for overshoot (i.e.,
higher concentrations of a contaminant in the effluent than the
influent, due to preferential adsorption of other contaminants) if a
treatment system is operated improperly (Crone et al., 2019; Speth,
2019). Reverse osmosis and nanofiltration are effective for removing a
wide range of PFAS. However, they have high capital and operations
costs (Crone et al., 2019; Speth, 2019). Additionally, membrane
fouling, corrosion control, and the disposal or treatment of
concentrate stream are issues that need to be addressed (Crone et al.,
2019; Speth, 2019). Additional literature and discussion on the
efficacy of these treatments can be found on the EPA's Drinking Water
Treatability Database (USEPA, 2019e).
    Considering the population exposed to PFOA and PFOS including
sensitive populations and lifestages, such as children, the potential
adverse human health impacts of these contaminants at low
concentrations, the environmental persistence, the persistence in the
human body, the availability of both methods to measure and treatment
technologies to remove these contaminants, and significant public
concerns regarding PFOA and PFOS contamination, the Agency proposes the
finding that regulation of PFOA and PFOS presents a meaningful
opportunity for health risk reduction for infants, children, and
adults, including pregnant and nursing women, served by PWS. While SDWA
specifies that the determination of whether PFOA and PFOS present ``a
meaningful opportunity for health risk reduction for persons served by
public water systems'' is made ``in the sole judgement of the
Administrator,'' the EPA seeks public comment on the information and
analyses described above.
e. Preliminary Regulatory Determination for PFOA and PFOS
    At this stage, the Agency is making a preliminary determination to
regulate PFOA and PFOS with an NPDWR after evaluating health,
occurrence, and other related information against the three SDWA
statutory criteria. The EPA has preliminarily determined that PFOA and
PFOS may have an adverse effect on human health; that PFOA and PFOS
occur in PWSs with a frequency and at levels of public health concern;
and that regulation of PFOA and PFOS presents a meaningful opportunity
for health risk reduction for persons served by PWSs. The Regulatory
Determination 4 Support Document (USEPA, 2019a) and the Occurrence Data
from the Third Unregulated Contaminant Monitoring Rule (UCMR 3) (USEPA,
2019b) present additional information and analyses supporting the
Agency's evaluation of PFOA and PFOS.
    The agency solicits comment on all aspects of this preliminary
regulatory determination. In particular, the EPA requests comment on
whether there are any additional data the agency should consider in
making its final regulatory determination and whether EPA has
appropriately considered the data.
f. Considerations for Additional PFAS
    As stated in the EPA's PFAS Action Plan (USEPA, 2019d): ``The
Agency recognizes that there is additional information that the EPA
should evaluate regarding PFAS other than PFOA and PFOS, including new
monitoring and occurrence data, recent health effects data, and
additional information to be solicited from the public, which will
inform the development of a national drinking water regulation for a
broader class of PFAS in the future.''
    The EPA is aware that many states, tribes, and local communities
face challenges from PFAS other than PFOA and PFOS. For example, in
addition to PFOA and PFOS, the EPA worked with states and public water
systems to characterize the occurrence of four additional PFAS
(perfluorononanoic acid (PFNA), perfluorohexanesulfonic acid (PFHxS),
perfluoroheptanoic acid (PFHpA), and PFBS)) in the nation's drinking
water served by public water systems under UCMR 3. The EPA found that
4.0% of PWSs reported results for which one or more of the six UCMR 3
PFAS were measured at or above their respective MRL. The 4.0% figure is
based on 198 PWSs reporting measurable PFAS results for one or more
sampling events from one or more of their sampling locations. Those 198
PWS serve an estimated total population of approximately 16 million.
    With the voluntary phase-out of PFOA and PFOS, manufacturers are
shifting to alternative PFAS compounds (e.g., hexafluoropropylene oxide
(HFPO) dimer acid and HFPO dimer acid ammonium salt (GenX chemicals),
and perfluorobutanesulfonic acid (PFBS)). There is less publicly
available information on the occurrence and health effects of these
replacements than for PFOA and PFOS and other members of the carboxylic
acid and sulfonate PFAS families (Brendel et al., 2018).
    The EPA plans to consider available human health toxicity and
occurrence

information for other PFAS as they become available. The EPA is working
on hazard assessments for the following PFAS: GenX chemicals; PFBS;
PFNA; perfluorobutanoic acid (PFBA); perfluorodecanoic acid (PFDA);
perfluorohexanoic acid (PFHxA); and PFHxS.
    The following PFAS have literature available in the EPA's Health
and Environmental Research Online (HERO), which is a database of
scientific studies and other references used to develop the EPA's risk
assessments aimed at understanding the health and environmental effects
of pollutants and chemicals. While HERO uses a variety of reference
types, the majority are original research published in peer-reviewed
literature. For some PFAS, there are epidemiological and/or
experimental animal toxicity data available, which may be suitable to
inform the evaluation of potential human health effects. Other
references provide information on occurrence (both in humans and the
environment). Available references for the PFAS listed below can be
accessed at: https://hero.epa.gov/hero/index.cfm/litbrowser/public/#PFAS.

------------------------------------------------------------------------
        Chemical name                   Acronym               CAS No.
------------------------------------------------------------------------
Perfluorooctanoic acid.......  PFOA.....................        335-67-1
Perfluorooctanesulfonic acid.  PFOS.....................       1763-23-1
2H,2H,3H,3H-Perfluorooctanoic  5:3 acid.................     914637-49-3
 acid.
6:2/8:2 Fluorotelomer          6:2/8:2 diPAP............     943913-15-3
 phosphate diester.
Bis[2-(perfluorohexyl)ethyl]   6:2 diPAP................      57677-95-9
 phosphate.
Mono[2-(perfluorohexyl)ethyl]  6:2 monoPAP..............      57678-01-0
 phosphate.
Bis[2-(perfluorooctyl)ethyl]   8:2 diPAP................        678-41-1
 phosphate.
Mono[2-(perfluorooctyl)ethyl]  8:2 monoPAP..............      57678-03-2
 phosphate.
4,8-dioxa-3H-                  ADONA....................     919005-14-4
 perfluorononanoic acid.
6:2 Fluorotelomer alcohol....  FtOH 6:2.................        647-42-7
8:2 Fluorotelomer alcohol....  FtOH 8:2.................        678-39-7
6:2 Fluorotelomer sulfonic     FtS 6:2..................      27619-97-2
 acid.
8:2 Fluorotelomer sulfonic     FtS 8:2..................      39108-34-4
 acid.
HFPO dimer acid..............  GenX chemicals...........      13252-13-6
HFPO dimer acid ammonium salt  GenX chemicals...........      62037-80-3
2-(N-                          NEtFOSAA.................       2991-50-6
 Ethylperfluorooctanesulfonam
 ido) acetic acid.
2-(N-                          NMeFOSAA.................       2355-31-9
 Methylperfluorooctanesulfona
 mido) acetic acid.
Perfluorobutanoic acid.......  PFBA.....................        375-22-4
Perfluorobutanesulfonic acid.  PFBS.....................        375-73-5
Perfluorodecanoic acid.......  PFDA.....................        335-76-2
Perfluorododecanoic acid.....  PFDoA....................        307-55-1
Perfluorodecanesulfonic acid.  PFDS.....................        335-77-3
Perfluoroheptanoic acid......  PFHpA....................        375-85-9
Perfluoroheptanesulfonic acid  PFHpS....................        375-92-8
Perfluorohexanoic acid.......  PFHxA....................        307-24-4
Perfluorohexanesulfonic acid.  PFHxS....................        355-46-4
Perfluorononanoic acid.......  PFNA.....................        375-95-1
Perfluorononanesulfonic acid.  PFNS.....................      68259-12-1
Perfluorooctanesulfonamide...  PFOSA....................        754-91-6
Perfluoropentanoic acid......  PFPeA....................       2706-90-3
Perfluoropentanesulfonic acid  PFPeS....................       2706-91-4
Perfluorotetradecanoic acid..  PFTeDA...................        376-06-7
Perfluoroundecanoic acid.....  PFUnA....................       2058-94-8
------------------------------------------------------------------------

    The EPA continues to work towards filling information gaps for
human health, toxicity and occurrence including through collaborations
with federal, state, tribal, and other stakeholders. The EPA is
generating PFAS toxicology data through new approaches such as high
throughput screening, computational toxicology tools, and chemical
informatics for chemical prioritization, screening, and risk
assessment. This research can inform a more complete understanding of
PFAS toxicity for the large set of PFAS chemicals without conventional
toxicity data and allow prioritization of actions to potentially
address groups of PFAS. For additional information on the new approach
methods for PFAS toxicity testing, please visit: https://www.epa.gov/chemical-research/pfas-chemical-lists-and-tiered-testing-methods-descriptions. To further understand occurrence in drinking water and
discussed in the EPA's PFAS Action Plan (USEPA, 2019d), the EPA will
propose a nationwide drinking water monitoring for PFAS under the next
UCMR monitoring cycle (UCMR 5) utilizing newer methods available to
detect more PFAS chemicals and at lower MRLs than previous possible for
the earlier UCMR monitoring. These monitoring results will improve
understanding of the frequency and concentration of PFAS occurrence in
the finished U.S. drinking water.
    The EPA is also aware of ongoing toxicity work and guideline
development by other federal agencies, state governments, international
organizations, industry groups, and other stakeholders. For example,
the U.S. National Toxicology Program is conducting ongoing
toxicological studies for multiple PFAS compounds of varying length in
rats, including 28-day studies for 7 PFAS compounds (3 carboxylates and
4 sulfonates), and a 2-year chronic toxicity and carcinogenicity study
for PFOA that is currently undergoing peer-review. ATSDR developed a
draft toxicological profile that characterizes toxicologic and adverse
health effects information for PFOA, PFOS, and 10 other PFAS compounds
which include PFBA, PFHxA, PFHpA, PFNA, PFDA, PFUnA, PFDoA, PFBS,
PFHxS, and PFOSA (ATSDR, 2018). Some states, including California,
Michigan, Minnesota, New Hampshire, New Jersey, New York and Vermont,
are also developing health-based guidance or drinking water standards
for individual targeted PFAS or the sum for several targeted PFAS

(California OEHHA, 2019; Commonwealth of Massachusetts, 2019; MDH,
2019; Michigan Science Advisory Workgroup, 2019; NHDES, 2019; NJDOH,
2017; NYSDOH, 2018; VTDEC, 2019). PFAS that have been or are being
evaluated by at least one state include Hexafluoropropylene Oxide
(HFPO) Dimer Acid and its Ammonium Salt (GenX chemicals), PFBA, PFBS,
PFHpA, PFHxA, PFHxS, PFNA, PFOA, and PFOS. The EPA will evaluate all
available and reliable information to inform future decision making for
these PFAS contaminants. The EPA is also aware of PFAS monitoring
efforts by states and local communities to better understand PFAS
occurrence in drinking water, including both statewide drinking water
monitoring efforts and targeted sampling at locations that have
potentially been impacted by releases or locations where PFAS-
containing materials are known to have been used (Table 9). The EPA
will consider these other information sources to inform future
decisions for other PFAS.
g. Potential Regulatory Approaches
    Since PFOA and PFOS raise complicated issues and since the issuance
of any NPDWR imposes costs on the public, the EPA is taking advantage
of this document by exploring and seeking comment on potential
regulatory constructs and monitoring requirements the Agency may
consider for PFAS chemicals including PFOA and PFOS if it were to
finalize positive regulatory determinations. As noted above in the EPA
PFAS Action Plan (USEPA, 2019d), the EPA is seeking information from
the public to ``inform the development of national drinking water
regulation for a broader class of PFAS in the future''. The EPA is
seeking feedback on potential regulatory approaches to address PFAS to
support the potential development of a PFOA and PFOS regulation
(pending final regulatory determinations) or in future PFAS regulatory
actions. The EPA is exploring how to best use the available information
when developing potential regulatory approaches for PFAS. Three
potential regulatory approach options described below include (1)
evaluate each additional PFAS on an individual basis; (2) evaluate
additional PFAS by different grouping approaches; and (3) evaluate PFAS
based on drinking water treatment techniques.
Evaluate Each Additional PFAS on an Individual Basis
    This approach would focus on evaluating PFAS individually for
potential future regulatory actions using information completed prior
to a potential rule proposal. Examples of suitable information sources
the EPA could evaluate under future actions include current and
expected peer reviewed toxicity assessments, nationwide drinking water
monitoring data, state drinking water monitoring data, and monitoring
data from other Federal Agencies. This approach would be limited to
those individual PFAS for which sufficient health and occurrence
information is available or can be clearly and logically extrapolated.
The EPA is actively working to fill information gaps needed to support
this approach including developing toxicity assessments for PFBS, HFPO
dimer acid and HFPO dimer acid ammonium salt or GenX chemicals, PFBA,
PFHxA, PFNA, and PFHxS, and PFDA. The EPA plans to propose nationwide
drinking water monitoring for PFAS under the next UCMR monitoring cycle
(UCMR 5) utilizing newer methods available to measure more PFAS and at
lower minimum reporting levels than previous UCMR monitoring. The EPA
may also consider health assessments and occurrence data that are
currently being developed by other federal, state and international
agencies.
Evaluate Additional PFAS by Different Grouping Approaches
    Since the 1940s, over 4000 PFAS have been manufactured and used in
a variety of industries across the world (Guelfo et al., 2018; OECD
2019). Evaluations of the retrospective reporting requirements of the
TSCA Inventory Notification Rule indicates 602 PFAS are currently
commercially active in the United States. The EPA recognizes the
challenges associated with evaluating each PFAS that may impact
drinking water on an individual basis. The EPA has regulated
contaminants as a group in drinking water, including, for example,
disinfection byproducts (i.e., haloacetic acids and total
trihalomethanes).
    In their study of organohalogen flame retardants, the National
Academies of Sciences evaluated general approaches to forming chemical
classes at regulatory agencies and concluded that a ``science-based
class approach does not necessarily require one to evaluate a large
chemical group as a single entity for hazard assessment. That is, an
approach that divides a large group into smaller units (or subclasses)
to conduct the hazard assessment is still a class approach for purposes
of hazard or risk assessment'' (NASEM, 2019). An approach to exploring
PFAS by groups could, for example, include evaluating groups of PFAS to
account for similar physiochemical characteristics. The EPA's ORD and
the National Institute of Environmental Health Sciences' (NIEHS)
National Toxicology Program recently identified a subset of PFAS for
testing with the goals of supporting read-across within structure-based
subgroups and capturing the diversity of the broader PFAS class (Helman
et al., 2019; Patlewicz et al., 2019a, 2019b). The EPA is also
exploring new approaches such as high throughput and computational
approaches to explore different chemical categories of PFAS. The EPA
will continue research on methods for using these data to support risk
assessments using new approach methods such as read-across (i.e., an
effort to predict biological activity based on similarity in chemical
structure) and transcriptomics (i.e., a measure of changes in gene
expression in response to chemical exposure or other external
stressors), and to make inferences about the toxicity of PFAS mixtures
that commonly occur in real world exposures. Example classifications
that the EPA could consider in its group evaluation include common
adverse effects, chain length (e.g., long chain and short chain),
functional groups (e.g., sulfonates, acids), degradation products
(i.e., some PFAS degrade to shorter chain PFAS), co-occurrence, or
using a combination of physiochemical and fate characteristics (e.g.,
long chain perfluoroalkyl sulfonic acids).
Evaluate PFAS Based on Drinking Water Treatment Techniques
    SDWA 1412(b)(7)(A) authorizes the EPA to promulgate a treatment
technique rule rather than an MCL if the Agency determines it is not
economically or technologically feasible to ascertain the level of the
contaminant. The EPA continues to develop reliable analytical methods
to monitor for PFAS including evaluating methodologies to measure total
PFAS. However, the EPA does not anticipate that reliable and validated
methods that accurately and precisely capture all PFAS or total PFAS
(and not other fluorinated, non-PFAS compounds) will be available for a
number of years. Therefore, the Agency is considering whether a
treatment technique regulatory approach may be appropriate.
    The strength of the carbon-fluorine bond makes certain PFAS (such
as perfluoroalkyl acids) relatively stable compounds that are not
removed by conventional treatment such as coagulation/flocculation/
sedimentation. Technologies that have reported removal efficiencies of
greater than 90% for certain PFAS include granulated

activated carbon, powdered activated carbon, anion exchange resins,
nanofiltration and reverse osmosis (Crone et al., 2019; Dickenson and
Higgins, 2016; Ross et al., 2018; USEPA, 2019e). Each of these
technologies has benefits and limitations that need to be considered if
they are to be used when treating PFAS contaminated drinking water,
such as cost and operational feasibility (Speth, 2019). For example,
nanofiltration and reverse osmosis are highly effective at removing
PFAS but are more costly options and generate large waste streams that
may require additional treatment. Anion exchange is effective at
removing long-chain PFAS constituents but may be less effective at
removing short-chain PFAS. Granular activated carbon has the advantage
of being a less costly treatment technology and has the ability to be
regenerated, however other organic matter present in the influent water
may interact and compete for adsorption sites with PFAS, potentially
making treatment less effective. In addition, unintended consequences
of PFAS treatment also need consideration given regional differences in
source water quality and treatment strategies in the United States.
Additional discussion on benefits and limitations associated with
drinking water treatment technologies for PFAS can be found in the
Regulatory Determination Support Document (USEPA, 2019a).
    A treatment technique regulation would address multiple PFAS with
similar characteristics that may be removed by similar treatment
technologies including some for which validated drinking water methods
are currently available.
Monitoring Considerations
    Should an MCL be established for PFOA, PFOS, and/or other PFAS
chemicals pursuant to section 1412 of the SDWA, PWSs could be required
to monitor for these contaminants. The EPA may seek to minimize the
monitoring burden on water systems while assuring public health
protection. Minimizing the monitoring burden to the maximum extent
feasible and allowed by statute could reduce costs for drinking water
systems that have other important risk-reduction resource demands. The
EPA is considering alternative approaches for this monitoring that
reduce monitoring frequency for systems that are reliably and
consistently below the MCL or do not detect the contaminant. This
framework provides primacy agencies with the flexibility to issue
monitoring waivers, with the EPA's approval, which take into account
regional and state specific characteristics and concerns. The
Standardized Monitoring Framework for regulated synthetic organic
chemicals under 40 CFR 141.24(h) provides a framework for determining
compliance with a potential future MCL. Under this approach, monitoring
frequency would be dependent on whether the contaminant has been
detected above a certain ``trigger level'' and/or detected above an
MCL, and whether a waiver from monitoring has been granted by the
Primacy Agency.
    An alternative approach to the Standardized Monitoring Framework
could be to require monitoring at public water systems only when data
show the presence of PFAS in finished drinking water and those
designated by the Primacy Agency. Under this approach, monitoring would
be required for public water systems with PFAS monitoring data and/or
vulnerable systems designated by the state or Primacy Agency. For
example, monitoring could be required if a Primacy Agency is aware of
information indicating potential PFAS contamination of the public water
supply. Information that could be considered includes proximity to
facilities with historical or on-going use of fire-fighting foam and
proximity to facilities that use or manufacture PFAS.
2. 1,1-Dichloroethane
a. Background
    1,1-Dichloroethane is a halogenated alkane. It is an industrial
chemical and is used as a solvent and a chemical intermediate. Annual
production and importation of 1,1-dichloroethane in the United States
was last reported by IUR in 2006 to be between 500,000 and 1 million
pounds. The data show that production of 1,1-dichloroethane in the
United States has declined since reporting began in 1986. Under CDR,
there were no reports of 1,1-dichloroethane production in 2012, 2013,
2014, or 2015 (USEPA, 2019a).
    TRI data for 1,1-dichloroethane from the years 1994-2016 show that
an average of about 12,000 pounds per year of reported releases have
entered the environment from 2003 onward. The number of states with
releases of 1,1 dichloroethane has stayed steady at about five since
2004, while the number of states with surface water discharges has
averaged two since 1994; surface water discharges ranged from 0 to 235
pounds per year over the approximately 20-year period (USEPA, 2019a).
    1,1-Dichloroethane is expected to have a high likelihood of
partitioning to water based on its Koc and water solubility.
The octanol-water partitioning coefficient (log Kow)
indicates that 1,1-dichloroethane is expected to have a moderate
likelihood of partitioning to water, while the Henry's Law Constant
(KH) indicates that this compound is expected to have a low
likelihood of partitioning to water. 1,1-Dichloroethane is expected to
have moderate to high persistence in certain waters based on
biodegradation half-lives (USEPA, 2019a).
b. Statutory Criterion #1 (Adverse Health Effects)
    1,1-Dichloroethane may have an adverse effect on the health of
persons. Based on a 13-week gavage study in rats (Muralidhara et al.,
2001), the kidney was identified as a sensitive target for 1,1-
dichloroethane, and no-observed-adverse-effect level (NOAEL) and
lowest-observed-adverse-effect level (LOAEL) values of 1,000 and 2,000
mg/kg/day, respectively, were identified based on increased urinary
enzyme markers for renal damage and central nervous system (CNS)
depression (USEPA, 2006a).
    The only available reproductive or developmental study with 1,1-
dichloroethane is an inhalation study where pregnant rats were exposed
on days 6 through 15 of gestation (Schwetz et al., 1974). No effects on
the fetuses were noted at 3,800 ppm. Delayed ossification of the
sternum without accompanying malformations was reported at a
concentration of 6,000 ppm.
    A cancer assessment for 1,1-dichloroethane is available on IRIS
(USEPA, 1990a). That assessment classifies the chemical, according to
the EPA's 1986 Guidelines for Carcinogenic Risk Assessment (USEPA,
1986), as Group C, a possible human carcinogen. This classification is
based on no human data and limited evidence of carcinogenicity in two
animal species (rats and mice), as shown by increased incidences of
hemangiosarcomas and mammary gland adenocarcinomas in female rats and
hepatocellular carcinomas and benign uterine polyps in mice (NCI,
1978). The data were considered inadequate to support quantitative
assessment. The close structural relationship between 1,1-
dichloroethane and 1,2-dichloroethane, which is classified as a B2
probable human carcinogen and produces tumors at many of the same sites
where marginal tumor increases were observed for 1,1-dichloroethane,
supports the suggestion that the 1,1-isomer could possibly be
carcinogenic to humans. Mixed results in initiation/promotion studies
and genotoxicity assays are

consistent with this classification. On the other hand, the animals
from the 1,1-dichloroethane National Cancer Institute (NCI, 1978) study
were housed with animals being exposed to 1,2-dichloroethane providing
opportunities for possible co-exposure impacting the 1,1-dichloroethane
results. The following groups of individuals may have an increased risk
from exposure to 1,1-dichloroethane (NIOSH, 1978; ATSDR, 2015):

 Those with chronic respiratory disease
 Those with liver diseases that impact hepatic microsomal
cytochrome P-450 functions
 Individuals with impaired renal function and vulnerable to
kidney stones
 Individuals with skin disorders vulnerable to irritation by
solvents like 1,1- dichloroethane
 Those who consume alcohol or use pharmaceuticals (e.g.,
phenobarbital) that alter the activity of cytochrome P-450s
    A provisional chronic RfD was derived from the 13-week gavage study
in rats based on a NOAEL of 1,000 mg/kg/day administered for five days/
week and adjusted to 714.3 mg/kg/day for continuous exposure (an
increase in urinary enzymes was the adverse impact on the kidney). The
chronic oral RfD of 0.2 mg/kg/day was derived by dividing the
normalized NOAEL of 714.3 mg/kg/day in male Sprague-Dawley rats by a
combined UF of 3,000. The combined UF includes factors of 10 for
interspecies extrapolation, 10 for extrapolation from a subchronic
study, 10 for human variability, and 3 for database deficiencies
(including lack of reproductive and developmental toxicity tests by the
oral route). This assessment noted several limitations in the critical
study and database as a whole. Specifically, that the reporting of the
results in the critical study were marginally adequate and that the
database lacks information on reproductive and developmental and
nervous system toxicity.
    The EPA calculated an HRL for 1,1-dichloroethane of 1,000 [micro]g/
L, based on the EPA oral RfD of 0.2 mg/kg/day, using 2.5 L/day drinking
water ingestion, 80 kg body weight and a 20% RSC factor.
c. Statutory Criterion #2 (Occurrence at Frequency and Levels of Public
Health Concern)
    The EPA proposes to find that 1,1-dichloroethane does not occur
with a frequency and at levels of public health concern in public water
systems based on the EPA's evaluation of the following occurrence
information.
    The primary occurrence data for 1,1-dichloroethane are recent
(2013-2015) nationally-representative drinking water monitoring data
generated through the EPA's UCMR 3. Under UCMR 3, 36,848 samples were
collected from 4,916 PWSs and analyzed for 1,1-dichloroethane. The
contaminant was not detected in any of the samples at levels greater
than \1/2\ the HRL (500 [micro]g/L) or the HRL (1,000 [micro]g/L). 1,1-
Dichloroethane was detected in about 2.3% samples at or above the MRL
(0.03 [micro]g/L) (USEPA, 2019a; USEPA, 2019b).
    Occurrence data for 1,1-dichloroethane in finished drinking water
are also available from UCM Rounds 1 and 2 (1988-1992 and 1993-1997).
None of those samples exceeded \1/2\ the HRL or the HRL. In the Round 1
cross-section states, 1,1 dichloroethane was detected at 233 PWSs
(1.14% of PWSs). Detected concentrations ranged from 0.01 [micro]g/L to
500 [micro]g/L. In the Round 2 cross-section states, 1,1 dichloroethane
was detected at 184 PWSs (0.74% of PWSs). Detected concentrations
ranged from 0.00126 [micro]g/L to 159 [micro]g/L (USEPA, 2008c; USEPA,
2019a).
    Occurrence data for 1,1-dichloroethane in ambient water are
available from the NAWQA program. Those data show that 1,1-
dichloroethane was detected in between 2% and 4% of samples from
between 2% and 4% of sites. No detections were greater than the HRL.
The median concentrations based on detections were less than 0.06
[micro]g/L (WQP, 2018). Ambient water data for 1,1-dichloroethane
analysis are also available from the NWIS database. Those data show
that 1,1-dichloroethane was detected in approximately 5% of samples
(1,152 out of 24,560) and at approximately 5% of sites (620 out of
12,057). The median concentration of detections was 0.380 [micro]g/L
(USEPA, 2019a).
d. Statutory Criterion #3 (Meaningful Opportunity)
    1,1-Dichloroethane does not present a meaningful opportunity for
health risk reduction through regulation for persons served by PWSs
based on the estimated exposed population, including sensitive
populations. UCMR 3 findings indicate that the estimated population
exposed to 1,1-dichloroethane at levels of public health concern is 0%.
As a result, the Agency finds that an NPDWR for 1,1-dichloroethane does
not present a meaningful opportunity for health risk reduction.
e. Preliminary Regulatory Determination for 1,1-dichloroethane
    The Agency is making a preliminary determination to not regulate
1,1-dichloroethane with an NPDWR after evaluating health, occurrence,
and other related information against the three SDWA statutory
criteria. While data suggest that 1,1-dichloroethane may have an
adverse effect on human health, the occurrence data indicate that 1,1-
dichloroethane is not occurring or is 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 1,1-dichloroethane would not
present a meaningful opportunity to reduce health risk for persons
served by PWSs. The Regulatory Determination 4 Support Document (USEPA,
2019a) and the Occurrence Data from the Third Unregulated Contaminant
Monitoring Rule (UCMR 3) (USEPA, 2019b) present additional information
and analyses supporting the Agency's evaluation of 1,1-dichloroethane.
3. Acetochlor
a. Background
    Acetochlor is a chloroacetanilide pesticide that is used as an
herbicide for pre-emergence control of weeds. It was first registered
by the EPA in 1994. It is registered for use on corn crops (field corn
and popcorn); corn fields treated with acetochlor may later be rotated
to grain sorghum (milo), soybeans, wheat, and tobacco. In March of
2006, the EPA released a Report of the Food Quality Protection Act
(FQPA) Tolerance Reassessment Progress and Risk Management Decision
(TRED) for Acetochlor (USEPA, 2006b). In 2010, the EPA approved the use
of acetochlor on cotton as a rotational crop (USEPA, 2010a). Synonyms
for acetochlor include 2-chloro-2'-methyl-6-ethyl-N-
ethoxymethylacetanilide (USEPA, 2019a).
    According to the EPA Pesticide Industry Sales and Usage reports,
the amount of acetochlor active ingredient used in the United States
was between 31 and 36 million pounds in 1997; between 30 and 35 million
pounds in 1999, 2001 and 2003; between 26 and 31 million pounds in
2005; between 28 and 33 million pounds in 2007; between 23 and 33
million pounds in 2009; and between 28 and 38 million pounds in 2012
(USEPA, 2019a).
    USGS pesticide use data show that there has been an increase in the
annual usage of acetochlor, from about 32 million pounds per year in
2010 to over 45 million pounds in 2016. This increase can largely be
attributed to the

use of acetochlor on crops other than corn (USEPA, 2019a).
    If released to soil, acetochlor is expected to have moderate to
high mobility (HSDB, 2012). Acetochlor is expected to have a high
likelihood of partitioning to water based on its KH. The
values for Koc indicate that acetochlor is expected to have
a moderate to high likelihood of partitioning to water. The water
solubility indicates that acetochlor is expected to have a moderate
likelihood of partitioning to water. Acetochlor is expected to have low
to moderate persistence based on aerobic and anaerobic biodegradation/
biotransformation half-lives (USEPA, 2019a).
b. Statutory Criterion #1 (Adverse Health Effects)
    Acetochlor may have an adverse effect on the health of persons.
Subchronic and chronic oral studies have demonstrated adverse effects
on the liver, thyroid (secondary to the liver effects), nervous system,
kidney, lung, testes, and erythrocytes in rats and mice (USEPA, 2006c;
USEPA, 2018c). There was evidence of carcinogenicity in studies
conducted with acetochlor in rats and mice and a non-mutagenic mode of
action was demonstrated for nasal and thyroid tumors in rats (USEPA,
2006c). Cancer effects include nasal tumors and thyroid tumors in rats,
lung tumors and histocytic sarcomas in mice, and liver tumors in both
rats and mice (Ahmed and Seely, 1983; Ahmed et al., 1983; Amyes, 1989;
Hardisty, 1997a; Hardisty, 1997b; Hardisty, 1997c; Naylor and Ribelin,
1986; Ribelin, 1987; USEPA, 2004b; USEPA, 2006c; and Virgo and
Broadmeadow, 1988). No biologically sensitive human subpopulations have
been identified for acetochlor. Developmental and reproductive toxicity
studies do not indicate increased susceptibility to acetochlor exposure
at early life stages in test animals (USEPA, 2006c).
    The study used to derive the oral RfD is a 1-year oral chronic
feeding study conducted in beagle dogs. This study describes a NOAEL of
2 mg/kg/day, and a LOAEL of 10 mg/kg/day, based on the critical effects
of increased salivation; increased levels of alanine aminotransferase
(ALT) and ornithine carbamoyl transferase (OTC); increased triglyceride
levels; decreased blood glucose levels; and alterations in the
histopathology of the testes, kidneys, and liver of male beagle dogs
(USEPA, 2018c; ICI, Inc., 1988). The UF applied was 100 (10 for
intraspecies variation and 10 for interspecies extrapolation). The EPA
OPP RfD for acetochlor of 0.02 mg/kg/day, based on the NOAEL of 2 mg/
kg/day from the 1-year oral chronic feeding study in beagle dogs, is
expected to be protective of both noncancer and cancer effects.
    The EPA calculated an HRL of 100 [micro]g/L based on the EPA OPP
RfD for non-cancer effects for acetochlor of 0.02 mg/kg/day (USEPA,
2018c) using 2.5 L/day drinking water ingestion, 80 kg body weight, and
a 20% RSC factor.
c. Statutory Criterion #2 (Occurrence at Frequency and Levels of Public
Health Concern)
    The EPA proposes to find that acetochlor does not occur with a
frequency and at levels of public health concern in public water
systems based on the EPA's evaluation of the following occurrence
information.
    The primary data for acetochlor are from the UCMR 1 a.m. (2001-
2003) and UCMR 2 SS (2008-2010). Acetochlor was not detected at or
above the MRL of 2 [micro]g/L or above the HRL of 100 [micro]g/L in any
of the 33,778 UCMR 1 a.m. samples (USEPA, 2008b; USEPA, 2019a) or in
any of the 11,193 UCMR 2 SS samples (USEPA, 2015a; USEPA, 2019a).
    To ascertain the impact of increased usage of acetochlor since the
end of UCMR 2, the EPA assessed ambient water and limited finished
water data collected after 2010. Sources of such data include the NAWQA
program and the NWIS database. Three cycles of NAWQA data show that
acetochlor was detected in between 13% and 23% of samples from between
3% and 10% of sites. While maximum values in NAWQA Cycle 2 (2002-2012)
and Cycle 3 (2013-2017) monitoring exceeded the HRL (215 [micro]g/L in
2004 and 137 [micro]g/L in 2013) (only one sample in each of those two
cycles exceeded the HRL), 90th percentile levels of acetochlor remained
below 1 [micro]g/L. More than 10,000 samples were collected in each
cycle. Non-NAWQA NWIS data (1991-2016), which included limited finished
water data in addition to the ambient water data, show no detected
concentrations greater than the HRL (USEPA, 2019a).
d. Statutory Criterion #3 (Meaningful Opportunity)
    Acetochlor 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 acetochlor at levels of public health concern is
0% based on UCMR 1 finished water data gathered from 2001 to 2003 and
UCMR 2 finished water data gathered from 2008 to 2010. As a result, the
Agency finds that an NPDWR for acetochlor does not present a meaningful
opportunity for health risk reduction.
e. Preliminary Regulatory Determination for Acetochlor
    The Agency is making a preliminary determination to not regulate
acetochlor with an NPDWR after evaluating health, occurrence, and other
related information against the three SDWA statutory criteria. While
data suggest that acetochlor may have an adverse effect on human
health, the occurrence data indicate that acetochlor is not occurring
or not likely to occur in PWSs with a frequency and at levels of public
health concern. The EPA also noted that the use of acetochlor has
increased since the nationally representative data collection from
finished water under UCMR 2 (i.e., 2008-2010). A review of ambient and
limited finished water monitoring data collected since 2010 in NAWQA
and NWIS show no 90th percentile values exceeding 1 [micro]g/L.
    Therefore, the Agency has determined that an NPDWR for acetochlor
would not present a meaningful opportunity to reduce health risk for
persons served by PWSs. The Regulatory Determination 4 Support Document
(USEPA, 2019a), The Analysis of Occurrence Data from the First
Unregulated Contaminant Monitoring Regulation (UCMR 1) in Support of
Regulatory Determinations for the Second Drinking Water Contaminant
Candidate List (USEPA, 2008b), and the Occurrence Data from the Second
Unregulated Contaminant Monitoring Regulation (UCMR 2) (USEPA, 2015a)
present additional information and analyses supporting the Agency's
evaluation of acetochlor.
4. Methyl Bromide (Bromomethane)
a. Background
    Methyl bromide is a halogenated alkane and occurs as a gas. Methyl
bromide has been used as a fumigant fungicide, applied to soil before
planting, to crops after harvest, to vehicles and buildings, and for
other specialized purposes.
    Methyl bromide is an ozone-depleting chemical regulated under the
Montreal Protocol. Use of the chemical in the United States was phased
out in 2005, except for specific critical use exemptions and quarantine
and pre-shipment exemptions. Critical use exemptions have included
strawberry cultivation and production of dry cured pork. Additional
information on the methyl bromide phase-out and exemptions in the
United States can be found on the EPA's website: https://

www.epa.gov/ods-phaseout/methyl-bromide.
    In August of 2006, the EPA released a TRED for methyl bromide and a
RED for commodity uses (USEPA, 2006d). A RED for soil fumigant uses was
released in July 2008, and amended in May 2009 (USEPA, 2009e). In 2011,
the EPA issued a cancellation order for certain soil-related uses of
methyl bromide, but this order did not affect its use as a post-harvest
fumigant (76 FR 29238; USEPA, 2011d). Synonyms for methyl bromide
include bromomethane, monobromomethane, curafume, Meth-O-Gas, and Brom-
O-Sol (HSDB, 2019).
    A report by the United Nations Environment Programme (UNEP, 2018)
indicates that critical use exemptions in the United States under the
Montreal Protocol declined steadily from 9,553 metric tons of methyl
bromide in 2005 to 235 metric tons in 2016 and stood at 0 in 2017 and
2018. A total 50 metric tons were ``on hand'' in the United States at
the end of 2016 (UNEP, 2018). Exempted quarantine and pre-shipment uses
continue. Production data for methyl bromide are available from the
EPA's IUR and CDR programs, and industrial release data are available
from the EPA's TRI database, as described below.
    The most recent quantities of methyl bromide produced and imported
(in 2013, 2014, and 2015, as reported in CDR) are classified as CBI.
The last publicly available data for production of methyl bromide are
from 2006, under IUR, when production was in the range of 10 to <50
million pounds (USEPA, 2019a).
    TRI data from 1988 to 2016 show a general long-term declining trend
in industrial releases of methyl bromide, from over one million pounds
per year in the 1990s to under 500,000 pounds most years since 2010.
Air emissions have tended to dominate releases, with the exception of
2015, when an anomalous large quantity (350,000 pounds) was reported
released by underground injection from a single facility. In 2016,
facilities in 11 states reported releases of any kind and facilities in
two states reported on-site surface water discharges (USEPA, 2019a).
    According to the EPA's Pesticide Industry Sales and Usage reports,
the amount of methyl bromide active ingredient used in the United
States was between 38 and 45 million pounds in 1997; between 28 and 33
million pounds in 1999; between 20 and 25 million pounds in 2001;
between 13 and 17 million pounds in 2003; between 12 and 16 million
pounds in 2005; between 11 and 15 million pounds in 2007; between 5 and
9 million pounds in 2009; and between 2 and 6 million pounds in 2012
(USEPA, 2019a).
    USGS pesticide use data show that there has been a decrease of
methyl bromide use through 2016 down to about 2 million pounds from a
high of about 78 million pounds in 1995 (USGS, 2018).
    If released to dry or moist soil, methyl bromide is expected to be
volatile (HSDB, 2019); its KH indicates that methyl bromide
is expected to have a low likelihood of partitioning to water from air.
Methyl bromide is expected to have a high likelihood of partitioning to
water based on its Koc and water solubility. The log
Kow indicates that methyl bromide is expected to have a
moderate likelihood of partitioning to water. Methyl bromide is
predicted to have low persistence in soil based on experiments under
simulated conditions in reaction with aniline. Measured hydrolysis
half-lives indicate moderate persistence in water (USEPA, 2019a).
b. Statutory Criterion #1 (Adverse Health Effects)
    Methyl bromide may have an adverse effect on the health of persons.
The limited number of studies investigating the oral toxicity of methyl
bromide indicate that the route of administration influences the toxic
effects observed (USEPA, 2006e). The forestomach of rats (forestomachs
are not present in humans) appears to be the most sensitive target of
methyl bromide when it is administered orally by gavage (ATSDR, 1992a).
Acute and subchronic oral gavage studies in rats identified stomach
lesions (Kaneda et al., 1998), hyperemia (excess blood) (Danse et al.,
1984), and ulceration (Boorman et al., 1986; Danse et al., 1984) of the
forestomach. However, forestomach effects were not observed in rats and
stomach effects were not observed in dogs that were chronically exposed
to methyl bromide in the diet, potentially because methyl bromide
degrades to other bromide compounds in the food (Mertens, 1997).
Decreases in food consumption, body weight, and body weight gain were
noted in the chronic rat study when methyl bromide was administered in
capsules (Mertens, 1997).
    In a subchronic (13-week) rat study (Danse et al., 1984), a NOAEL
of 1.4 mg/kg/day (a time weighted average, \5/7\ days, of the 2 mg/kg/
day dose group) was selected in the EPA IRIS assessment based on severe
hyperplasia of the stratified squamous epithelium in the forestomach,
in the next highest dose group of 7.1 mg/kg/day (USEPA, 1989a). In
ATSDR's Toxicological Profile (ATSDR, 1992a), a lower dose of 0.4 mg/
kg/day is selected as the NOAEL because ``mild focal hyperemia'' was
observed at the 1.4 mg/kg/day dose level. It is worth noting that
authors of this study reported neoplastic changes in the forestomach.
However, the EPA and others (USEPA, 1985; Schatzow, 1984) re-evaluated
the histological results, concluding that the lesions were hyperplasia
and inflammation, not neoplasms. ATSDR notes that histological
diagnosis of epithelial carcinomas in the presence of marked
hyperplasia is difficult (Wester and Kroes 1988; ATSDR 1992a).
Additionally, the hyperplasia of the forestomach observed after 13
weeks of exposure to bromomethane regressed when exposure ended
(Boorman et al. 1986; ATSDR 1992a).
    The EPA selected an OPP Human Health Risk Assessment from 2006 as
the basis for developing the HRL for methyl bromide (USEPA, 2006e). As
described in the OPP document, the study was of chronic duration (two
years) with four groups of male rats and four groups of female rats
treated orally via encapsulated methyl bromide. In the OPP assessment
(USEPA, 2006e), Mertens (1997) was identified as the critical study and
decreased body weight, decreased rate of body weight gain, and
decreased food consumption were the critical effects in rats orally
exposed to methyl bromide (USEPA, 2006e). The NOAEL was 2.2 mg/kg/day
and the LOAEL was 11.1 mg/kg/day. The RfD derived in the 2006 OPP Human
Health Assessment is 0.022 mg/kg/day, based on the point of departure
(POD) of 2.2 mg/kg/day (the NOAEL) and a combined uncertainty factor
(UF) of 100 for interspecies variability (10) and intraspecies
variability (10). No benchmark dose modeling was performed.
    Neurological effects reported after inhalation exposures have not
been reported after oral exposures, indicating that route of exposure
may influence the most sensitive adverse health endpoint (USEPA, 1988).
    Limited data are available regarding the developmental or
reproductive toxicity of methyl bromide, especially via the oral route
of exposure. ATSDR (1992a) found no information on developmental
effects in humans with methyl bromide exposure. An oral developmental
toxicity study of methyl bromide in rats (doses of 3, 10, or 30 mg/kg/
day) and rabbits (doses of 1, 3, or 10 mg/kg/day) found that there were
no treatment-related adverse effects in fetuses of the treated groups
of either species (Kaneda et al., 1998). ATSDR's 1992 Toxicological
Profile also did not

identify any LOAELs for rats or rabbits in this study. In rats exposed
to 30 mg/kg/day, there was an increase in fetuses having 25 presacral
vertebrae; however, ATSDR notes that there were no significant
differences in the number of litters with this variation and the effect
was not exposure-related (ATSDR, 1992a). No significant alterations in
resorptions or fetal deaths, number of live fetuses, sex ratio, or
fetal body weights were observed in rats and no alterations in the
occurrence of external, visceral, or skeletal malformations or
variations were observed in the rabbits. Some inhalation studies
reported no effects on development or reproduction, but other
inhalation studies show adverse developmental effects. For example,
Hardin et al. (1981) and Sikov et al. (1980) conducted studies in rats
and rabbits and found no developmental effects, even when maternal
toxicity was severe (ATSDR, 1992a). However, another inhalation study
of rabbits found increased incidence of gallbladder agenesis, fused
vertebrae, and decreased fetal body weights in offspring (Breslin et
al., 1990). Decreased pup weights were noted in a multigeneration study
in rats exposed to 30 ppm (Enloe et al., 1986). Reproductive effects
were noted in intermediate-duration inhalation studies in rats and mice
(Eustis et al., 1988; Kato et al., 1986), which indicated that the
testes may undergo degeneration and atrophy at high exposure levels.
    In the OPP HHRA for methyl bromide (USEPA, 2006e), methyl bromide
is classified as ``not likely to be carcinogenic to humans''. In 2007,
the EPA published a PPRTV report which stated that there is
``inadequate information to assess the carcinogenic potential'' of
methyl bromide in humans (USEPA, 2007b). The PPRTV assessment agrees
with earlier National Toxicology Program (NTP) conclusions that the
available data indicate that methyl bromide can cause genotoxic and/or
mutagenic changes. The PPRTV assessment states that the results in
studies by Vogel and Nivard (1994) and Gansewendt et al. (1991) clearly
indicate methyl bromide is distributed throughout the body and is
capable of methylating DNA in vivo. However, the PPRTV assessment also
summarizes the results of several studies in mice and rats that have
not demonstrated evidence of methyl bromide-induced carcinogenic
changes (USEPA, 2007b; NTP, 1992; Reuzel et al. 1987; ATSDR, 1992a). In
2012, an epidemiology study was published that concluded there was a
significant monotonic exposure-dependent increase in stomach cancer
risk among 7,814 applicators of methyl bromide (Barry et al., 2012). In
OPP's Draft HHRA for Methyl Bromide, OPP reviews all the
epidemiological studies for methyl bromide, including the Barry et al.
(2012) Agricultural Health Study. OPP concludes that ``based on the
review of these studies, there is insufficient evidence to suggest a
clear associative or causal relationship between exposure to methyl
bromide and carcinogenic or non-carcinogenic health outcomes.''
    According to ATSDR (1992a) and the EPA OPP assessment (USEPA,
2006e), no studies suggest that a specific subpopulation may be more
susceptible to methyl bromide, though there is little information about
susceptible lifestages or subpopulations when exposed via the oral
route. Because the critical effects of decreased body weight, decreased
rate of body weight gain, and decreased food consumption in this study
are not specific to a sensitive subpopulation or life stage, the target
population of the general adult population was selected in deriving the
HRL for regulatory determination. EPA's OPP assessment conducted
additional exposure assessments for lifestages that may increase
exposure to methyl bromide and concluded that no lifestages have
expected exposure greater than 10% of the chronic population-adjusted
dose (cPAD), including children.
    The EPA calculated an HRL of 100 [micro]g/L (rounded from 140.8
[micro]g/L) based on an EPA OPP assessment cPAD of 0.022 mg/kg/day and
using 2.5 L/day drinking water ingestion, 80 kg body weight, and a 20%
RSC factor (USEPA, 2006d; USEPA, 2011b, Table 8-1 and 3-33).
c. Statutory Criterion #2 (Occurrence at Frequency and Levels of Public
Health Concern)
    The EPA proposes to find that methyl bromide does not occur with a
frequency and at levels of public health concern in PWSs based on the
EPA's evaluation of the following occurrence information.
    The primary data for methyl bromide are from the UCMR 3 a.m., which
was collected from January 2013 to December 2015. A total of 36,848
samples for methyl bromide were collected from 4,916 systems. Of these
systems, 49 (1.0% of systems) reported at least one detection at or
above the MRL of 0.2 [micro]g/L. A total of 0.31% of samples had
concentrations greater than or equal to the MRL (0.2 [micro]g/L).
Reported methyl bromide concentrations range from 0.2 [micro]g/L to 6.9
[micro]g/L. There was no occurrence above the \1/2\ HRL or HRL
thresholds.
    In all three NAWQA cycles, methyl bromide was detected in fewer
than 1% of samples from fewer than 2% of sites. No detections were
greater than the HRL in any of the three cycles. The median
concentration among detections were 0.5 [micro]g/L and 0.8 [micro]g/L
in Cycle 1 and Cycle 3, respectively. There were no detections in Cycle
2. The results of the non-NAWQA NWIS analysis show that methyl bromide
was detected in approximately 0.1% of samples at approximately 0.1% of
sites. The median concentration among detections was 0.6 [micro]g/L.
d. Statutory Criterion #3 (Meaningful Opportunity)
    Methyl bromide does not present a meaningful opportunity for health
risk reduction for persons served by PWSs based on the estimated
exposed population, including sensitive populations. UCMR 3 findings
indicate that the estimated population exposed to methyl bromide at
levels of public health concern is 0%. As a result, the Agency finds
that an NPDWR for methyl bromide does not present a meaningful
opportunity for health risk reduction.
e. Preliminary Regulatory Determination for Methyl Bromide
    The Agency is making a preliminary determination to not regulate
methyl bromide with an NPDWR after evaluating health, occurrence, and
other related information against the three SDWA statutory criteria.
While data suggest that methyl bromide may have an adverse effect on
human health, the occurrence data indicate that methyl bromide is not
occurring or not likely to occur in PWSs with a frequency and at levels
of public health concern. Furthermore, in accordance with U.S.
obligations under the Montreal Protocol, production and importation of
methyl bromide has steadily declined since 2005.
    Therefore, the Agency has determined that an NPDWR for methyl
bromide would not present a meaningful opportunity to reduce health
risk for persons served by PWSs. The Regulatory Determination 4 Support
Document (USEPA, 2019a) and the Occurrence Data from the Third
Unregulated Contaminant Monitoring Rule (UCMR 3) (USEPA, 2019b) present
additional information and analyses supporting the Agency's evaluation
of methyl bromide.
5. Metolachlor
a. Background
    Metolachlor is a chloroacetanilide pesticide that is used as an
herbicide for weed control. Initially registered in

1976 for use on turf, metolachlor has more recently been used on corn,
cotton, peanuts, pod crops, potatoes, safflower, sorghum, soybeans,
stone fruits, tree nuts, non-bearing citrus, non-bearing grapes,
cabbage, certain peppers, buffalograss, guymon bermudagrass for seed
production, nurseries, hedgerows/fencerows, and landscape plantings. In
April of 1995, the EPA released a RED for metolachlor (USEPA, 1995b)
and a TRED was released in June of 2002 (USEPA, 2002c). In 2012, the
EPA reinstated tolerances for metolachlor on popcorn to rectify an
omission of these tolerances in previous documentation (USEPA, 2012b).
The metolachlor molecule can exist in right- and left-handed versions
(enantiomers), labeled ``R-'' and ``S-''. (The chemical terms are
dextrorotatory and levorotatory: the factor refers to the direction the
compound in solution rotates polarized light.) The ``S-'' version is
more potent as a pesticide. When manufacturers found a way of producing
metolachlor that was predominantly the ``S-'' enantiomer in the late
1990s, they began marketing that as ``S-metolachlor,'' while the
racemic (roughly evenly balanced) mixture continues to be sold as
``metolachlor'' (Hartzler, 2004). Metolachlor and S-metolachlor are
under registration review (USEPA, 2014b). Synonyms for metolachlor
include dual and bicep (USEPA, 2019a).
    Based on private market usage data, the EPA estimated that
approximately 9 million pounds of metolachlor active ingredient and 28
million pounds of S-metolachlor active ingredient were applied annually
between 1998 and 2012, both mostly on corn (USEPA, 2014b).
    According to the EPA's Pesticide Industry Sales and Usage reports,
the amount of metolachlor active ingredient (the racemic mixture) used
in the United States was between 45 and 50 million pounds in 1987;
between 63 and 69 million pounds in 1997; between 26 and 30 million
pounds in 1999; between 15 and 22 million pounds in 2001; between 1 and
5 million pounds on 2009; and between 4 and 8 million pounds in 2012.
Furthermore, the amount of S-metolachlor active ingredient used was
between 16 and 19 million pounds in 1999; between 20 and 24 million
pounds in 2001; between 28 and 33 million pounds in 2003; between 27
and 32 million pounds in 2005; between 30 and 35 million pounds in
2007; between 24 and 34 million pounds in 2009; and between 34 and 44
million pounds in 2012 (USEPA, 2019a).
    USGS pesticide use data show that there has been a mild increase in
metolachlor (racemic mixture) with a greater change in the amount of S-
metolachlor relative to metolachlor. Between 2010 and 2016, the
increase in metolachlor usage is about 3 million pounds, or about 30%,
and for S-metolachlor the increase is about 25 million pounds, or about
75% (USEPA, 2019a).
    If released to soil, metolachlor is expected to have moderate to
high mobility. The EPA's RED document indicates that substantial
leaching and/or runoff of metolachlor from soil is expected to occur
(USEPA, 1995b). Metolachlor is expected to have a high likelihood of
partitioning to water based on its KH, while its log
Kow and water solubility indicate that metolachlor is
expected to have a moderate likelihood of partitioning to water. The
literature provides a wide range of values for Koc (USEPA,
2019a provides additional information). Metolachlor is expected to have
moderate to high persistence in soil and water under aerobic conditions
based on aerobic biodegradation half-lives and high persistence in soil
and water under anaerobic conditions based on anaerobic biodegradation
half-lives (USEPA, 2019a).
b. Statutory Criterion #1 (Adverse Health Effects)
    Metolachlor may have an adverse effect on the health of persons.
The existing toxicological database includes studies evaluating both
metolachlor and S-metolachlor. When combined with the toxicology
database for metolachlor, the toxicology database for S-metolachlor is
considered complete for risk assessment purposes (USEPA, 2018d). In
subchronic (metolachlor and S-metolachlor) (USEPA, 1995b; USEPA, 2018d)
and chronic (metolachlor) (Hazelette, 1989; Tisdel, 1983; Page, 1981;
USEPA, 2018d) toxicity studies in dogs and rats, decreased body weight
was the most commonly observed effect. Chronic exposure to metolachlor
in rats also resulted in increased liver weight and microscopic liver
lesions in both sexes (USEPA, 2018d). No systemic toxicity was observed
in rabbits when metolachlor was administered dermally, though dermal
irritation was observed at lower doses (USEPA, 2018d). Portal of entry
effects (e.g., hyperplasia of the squamous epithelium and mucous cell)
occurred in the nasal cavity at lower doses in a 28-day inhalation
study in rats (USEPA, 2018d). Systemic toxicity effects were not
observed in this study. Immunotoxicity effects were not observed in
mice exposed to S-metolachlor (USEPA, 2018d).
    While some prenatal developmental studies in the rat and rabbit
with both metolachlor and S-metolachlor revealed no evidence of a
qualitative or quantitative susceptibility in fetal animals, decreased
pup body weight was observed in a two-generation study (Page, 1981,
USEPA, 2018d). Though there was no evidence of maternal toxicity,
decreased pup body weight in the F1 and F2 litters was observed,
indicating developmental toxicity (Page, 1981; USEPA, 1990b).
Therefore, sensitive lifestages to consider include infants, as well as
pregnant women and their fetus, and lactating women.
    Although treatment with metolachlor did not result in an increase
in treatment-related tumors in male rats or in mice (both sexes),
metolachlor caused an increase in liver tumors in female rats (USEPA,
2018d). There was no evidence of mutagenic or cytogenetic effects in
vivo or in vitro (USEPA, 2018d). In 1994 (USEPA, 1995b), the EPA
classified metolachlor as a Group C possible human carcinogen, in
accordance with the 1986 Guidelines for Carcinogen Risk Assessment
(USEPA, 1986). In 2017 (USEPA, 2018d), the EPA re-assessed the cancer
classification for metolachlor in accordance with the EPA's final
Guidelines for Carcinogen Risk Assessment (USEPA, 2005b), and
reclassified metolachlor/S-metolachlor as ``Not Likely to be
Carcinogenic to Humans'' at doses that do not induce cellular
proliferation in the liver. This classification was based on convincing
evidence of a constitutive androstane receptor (CAR)-mediated mitogenic
MOA for liver tumors in female rats that supports a nonlinear approach
when deriving a guideline that is protective for the tumor endpoint
(USEPA, 2018d).
    A recent OPP HHRA identified a two-generation reproduction study in
rats as the critical study (USEPA, 2018d). OPP proposed an RfD for
metolachlor of 0.26 mg/kg/day, derived from a NOAEL of 26 mg/kg/day for
decreased pup body weight in the F1 and F2 litters. A combined UF of
100 was used based on interspecies extrapolation (10), intraspecies
variation (10), and an FQPA Safety Factor of 1.\24\ This RfD is

considered protective of carcinogenic effects as well as effects
observed in chronic toxicity studies (USEPA, 2018d). The decreased F1
and F2 litter pup body weights in the absence of maternal toxicity were
considered indicative of increased susceptibility to the pups.
Therefore, a rate of 0.15 L/kg/day was selected from the Exposure
Factors Handbook (USEPA, 2011b) to represent the consumers-only
estimate of DWI based on the combined direct and indirect community
water ingestion at the 90th percentile for bottle fed infants. This
estimate is more protective than the estimate for pregnant women (0.033
L/kg/day) or lactating women (0.054 L/kg/day). DWI and BW parameters
are further outlined in the Exposure Factors Handbook (USEPA, 2011b).
---------------------------------------------------------------------------

    \24\ The EPA notes that for pesticide registrations under FIFRA,
EPA's Office of Pesticides derives acute or chronic population
adjusted doses (PADs) using an FQPA Safety Factor mandated by the
FQPA taking into consideration potential pre and/or postnatal
toxicity and completeness of the data with respect to exposure and
toxicity to infants and children. In the majority of instances, the
PAD and the RfD are the same. It is only in those few instances when
the FQPA Safety Factor is attributed to residual uncertainty with
regard to exposure or pre/postnatal toxicity that the RfD and PAD
differ. More recently, FQPA Safety Factors can account for
uncertainties in the overall completeness of the toxicity database,
extrapolation from subchronic to a chronic study duration, and LOAEL
to NOAEL extrapolation.
---------------------------------------------------------------------------

    The EPA OW calculated an HRL for metolachlor of 300 [micro]g/L
(rounded from 0.347 mg/L). The HRL was derived from the oral RfD of
0.26 mg/kg/day for bottle fed infants ingesting 0.15 L/kg/day water,
with the application of a 20% RSC.
c. Statutory Criterion #2 (Occurrence at Frequency and Levels of Public
Health Concern)
    The EPA proposes to find that metolachlor does not occur with a
frequency and at levels of public health concern in public water
systems based on the EPA's evaluation of the following occurrence
information.
    The primary data for metolachlor are from the UCMR 2 SS. A total of
11,192 metolachlor samples were collected from 1,198 systems. Of these
systems, three (0.25%) had metolachlor detections and none of the
detections were greater than \1/2\ the HRL or the HRL of 300 [micro]g/L
(USEPA, 2015a; USEPA, 2019a).
    Nationally representative finished water occurrence data for
metolachlor are also available from the UCM Round 2 data set. In the
Round 2 cross-section states, metolachlor was detected at 108 PWSs
(0.83% of PWSs). Detected concentrations ranged from 0.01 [micro]g/L to
13.8 [micro]g/L. There were no exceedances of \1/2\ the HRL or the HRL
of 300 [micro]g/L (USEPA, 2008c; USEPA, 2019a).
    To ascertain the impact of increased usage of metolachlor since the
end of UCMR 2, the EPA assessed ambient water and limited finished
water data collected after 2010. Sources of such data include the NAWQA
program and the NWIS database. The EPA found no values in the NAWQA
data set that exceeded the HRL. The highest value in the NWIS data set
(376 [micro]g/L) exceeded the HRL, but the 99th percentile value (13.3
[micro]g/L) did not exceed the HRL\25\ (USEPA, 2019a).
---------------------------------------------------------------------------

    \25\ Approximately 99.9% of the metolachlor samples in NWIS are
from ambient water. The highest finished water value in the NWIS
data set is 0.24 [micro]g/L, which is much lower than the HRL.
---------------------------------------------------------------------------

d. Statutory Criterion #3 (Meaningful Opportunity)
    Metolachlor does not present a meaningful opportunity for health
risk reduction for persons served by PWSs based on the estimated
exposed population, including sensitive populations. UCMR 2 findings
indicate that the estimated population exposed to metolachlor at levels
of public health concern is 0%. As a result, the Agency finds that an
NPDWR for metolachlor does not present a meaningful opportunity for
health risk reduction.
e. Preliminary Regulatory Determination for Metolachlor
    The Agency is making a preliminary determination to not regulate
metolachlor with an NPDWR after evaluating health, occurrence, and
other related information against the three SDWA statutory criteria.
While data suggest that metolachlor may have an adverse effect on human
health, the occurrence data indicate that metolachlor is not occurring
or not likely to occur in PWSs with a frequency and at levels of public
health concern. The EPA will continue to evaluate metolachlor as new
finished water data become available.
    Therefore, the Agency has determined that an NPDWR for metolachlor
would not present a meaningful opportunity to reduce health risk for
persons served by PWSs. The Regulatory Determination 4 Support Document
(USEPA, 2019a) and the Occurrence Data from the Second Unregulated
Contaminant Monitoring Regulation (UCMR 2) (USEPA, 2015a) present
additional information and analyses supporting the Agency's evaluation
of metolachlor.
6. Nitrobenzene
a. Background
    Nitrobenzene is a synthetic aromatic nitro compound and occurs as
an oily, flammable liquid. It is commonly used as a chemical
intermediate in the production of aniline and drugs such as
acetaminophen. Nitrobenzene is also used in the manufacturing of
paints, shoe polishes, floor polishes, metal polishes, aniline dyes,
and pesticides (USEPA, 2019a).
    IUR data indicate that production of nitrobenzene in the United
States increased between 1986 and 1990 and stood at over 1 billion
pounds per year from 1990 to 2006. Data from the EPA's CDR program
indicate that production of nitrobenzene was in the range of 1-5
billion pounds per year in 2012, 2013, 2014, and 2015 (USEPA, 2019a).
    TRI data for nitrobenzene show that total releases were in the
range of hundreds of thousands of pounds per year from 1988 through
2016. Underground injection dominated total reported releases,
fluctuating between approximately 191,000 pounds (in 2003) and over
860,000 pounds (in 1992). On-site air emissions were in the range of
tens of thousands of pounds annually. Since 1999, surface water
discharges of nitrobenzene have not exceeded 500 pounds per year
(USEPA, 2019a).
    Nitrobenzene is expected to have a high likelihood of partitioning
to water based on its water solubility. Multiple values for
Koc indicate that nitrobenzene is expected to have a
moderate to high likelihood of partitioning to water, while the log
Kow and KH indicate that nitrobenzene is expected
to have a moderate likelihood of partitioning to water. Nitrobenzene is
expected to have moderate persistence in water based on its aerobic
biodegradation half-life (USEPA, 2019a).
b. Statutory Criterion #1 (Adverse Health Effects)
    Nitrobenzene may have an adverse effect on the health of persons.
NTP (1983) conducted a 90-day oral gavage study of nitrobenzene in F344
rats and B6C3F1 mice. The rats were more sensitive to the effects of
nitrobenzene exposure than the mice, and changes in absolute and
relative organ weights, hematologic parameters, splenic congestion, and
histopathologic lesions in the spleen, testis, and brain were reported.
Based on statistically significant changes in absolute and relative
organ weights, splenic congestion, and increases in reticulocyte count
and methemoglobin (metHb) concentration, a LOAEL of 9.38 mg/kg/day was
identified for the subchronic oral effects of nitrobenzene in F344 male
rats (USEPA, 2009f). This was the lowest dose studied, so a NOAEL was
not identified. The mice were treated with higher doses and were
generally more resistant to nitrobenzene toxicity, the toxic endpoints
were similar in both species.
    The testis, epididymis, and seminiferous tubules of the male
reproductive system are targets of nitrobenzene toxicity in rodents. In
male rats (F344/N and CD) and mice

(B6C3F1), nitrobenzene exposure via the oral and inhalation routes
results in histopathologic lesions of the testis and seminiferous
tubules, testicular atrophy, a large decrease in sperm count, and a
reduction of sperm motility and/or viability, which contribute to a
loss of fertility (NTP, 1983; Bond et al., 1981; Koida et al., 1995;
Matsuura et al., 1995; Kawashima et al., 1995). These data suggest that
nitrobenzene is a male-specific reproductive toxicant (USEPA, 2009f).
    Under the Guidelines for Carcinogen Risk Assessment (USEPA, 2005b),
nitrobenzene is classified as ``likely to be carcinogenic to humans''
by any route of exposure (USEPA, 2009f). A two-year inhalation cancer
bioassay in rats and mice (Cattley et al., 1994; CIIT, 1993) reported
an increase in several tumor types in both species. However, the lack
of available data, including a physiologically based biokinetic or
model that might predict the impact of the intestinal metabolism on
serum levels of nitrobenzene and its metabolites following oral
exposures, precluded the EPA's IRIS program from deriving an oral CSF
(USEPA, 2009f). Additionally, a metabolite of nitrobenzene, aniline, is
classified as a probable human carcinogen (B2) (USEPA, 1988).
    Nitrobenzene has been shown to be non-genotoxic in most studies and
was classified as, at most, weakly genotoxic in the 2009 USEPA IRIS
assessment (ATSDR, 1990; USEPA, 2009f).
    Of the available animal studies with oral exposure to nitrobenzene,
the 90-day gavage study conducted by NTP (1983) is the most relevant
study for deriving an RfD for nitrobenzene. This study used the longest
exposure duration and multiple dose levels. Benchmark dose software
(BMDS) (version 1.4.1c; USEPA, 2007c) was applied to estimate candidate
PODs for deriving an RfD for nitrobenzene. Data for splenic congestion
and increases in reticulocyte count and metHb concentration were
modeled. The POD derived from the male rat increased metHb data with a
benchmark response (BMR) of 1 standard deviation (SD) was selected as
the basis of the RfD (see USEPA, 2009f for additional detail).
Therefore, the benchmark dose level (BMDL) used as the POD is a
BMDL1SD of 1.8 mg/kg/day.
    In deriving the RfD, the EPA's IRIS program applied a composite UF
of 1,000 to account for interspecies extrapolation (10), intraspecies
variation (10), subchronic-to-chronic study extrapolation (3), and
database deficiency (3) (USEPA, 2009f). Thus, the RfD calculated in the
2009 IRIS assessment is 0.002 mg/kg/day. The overall confidence in the
RfD was medium because the critical effect is supported by the overall
database and is thought to be protective of reproductive and
immunological effects observed at higher doses; however, there are no
chronic or multigenerational reproductive/developmental oral studies
available for nitrobenzene. Because the critical effect in this study
(increased metHb in the adult rat) is not specific to a sensitive
subpopulation or lifestage, the general adult population was selected
in deriving the HRL for regulatory determination.
    The EPA calculated an HRL for the noncancer effects of nitrobenzene
of 10 [micro]g/L (rounded from 12.8 [micro]g/L), based on the RfD of
0.002 mg/kg/day, using 2.5 L/day drinking water ingestion, 80 kg body
weight, and a 20% RSC factor.
c. Statutory Criterion #2 (Occurrence at Frequency and Levels of Public
Health Concern)
    The EPA proposes to find that nitrobenzene does not occur with a
frequency and at levels of public health concern in public water
systems based on the EPA's evaluation of the following occurrence
information.
    The primary data for nitrobenzene are nationally-representative
drinking water monitoring data generated through the EPA's UCMR 1
(USEPA, 2008b), collected from 2001 to 2003. UCMR 1 is the only dataset
with nationally-representative finished water data for this
contaminant. The EPA does not anticipate nitrobenzene occurrence
meaningfully changing from the UCMR 1 monitoring period given that
reported releases to surface water have generally decreased over time
and detections of nitrobenzene in ambient waters and Six-Year Review
monitoring data are at low levels. UCMR 1 collected 33,576 nitrobenzene
samples from 3,861 PWSs. The contaminant was detected in only a small
number of those samples (0.01%) above the HRL (10 [micro]g/L), which is
the same as the MRL (10 [micro]g/L). The detections occurred in two
large water systems (one surface water, the other groundwater); the
maximum detected concentration of nitrobenzene was 100 [micro]g/L.
    Occurrence data for nitrobenzene in ambient water from the NAWQA
program show that nitrobenzene was not detected in any of the samples
collected under any of the three monitoring cycles. Non-NAWQA NWIS data
show that nitrobenzene was detected in approximately 1% of samples (60
out of 7,265) and at approximately 1% of sites (25 out of 2,747). The
median concentration among detections was 83.0 [micro]g/L.
d. Statutory Criterion #3 (Meaningful Opportunity)
    Nitrobenzene does not present a meaningful opportunity for health
risk reduction for persons served by PWSs based on the estimated
exposed population. UCMR 1 data indicate that the estimated population
exposed to nitrobenzene above the HRL is 0.1%. As a result, the Agency
finds that an NPDWR for nitrobenzene does not present a meaningful
opportunity for health risk reduction.
e. Preliminary Regulatory Determination for Nitrobenzene
    The Agency is making a determination to not regulate nitrobenzene
with an NPDWR after evaluating health, occurrence, and other related
information against the three SDWA statutory criteria. While data
suggest that nitrobenzene may have an adverse effect on human health,
the occurrence data indicate that nitrobenzene is not occurring or not
likely to occur in PWSs with a frequency and at levels of public health
concern, and regulation of such contaminant does not present a
meaningful opportunity for health risk reduction for persons served by
PWSs. Therefore, the Agency has determined that an NPDWR for
nitrobenzene would not present a meaningful opportunity to reduce
health risk for persons served by PWSs. The Regulatory Determination 4
Support Document (USEPA, 2019a) and the Occurrence Data from the First
Unregulated Contaminant Monitoring Regulation (UCMR 1) (USEPA, 2008b)
present additional information and analyses supporting the Agency's
evaluation of nitrobenzene.
7. RDX
a. Background
    RDX is a nitrated triazine and is an explosive. The name RDX is an
abbreviation of ``Royal Demolition eXplosive.'' The formal chemical
name is hexahydro-1,3,5-trinitro-1,3,5-triazine (USEPA, 2019a). Annual
production and importation of RDX in the United States was last
reported by the EPA's CDR program in 2015 to be in the range of 1-10
million pounds. It appears to have held steady in that range from 2002
onward (USEPA, 2019a).
    Studies have shown that this compound is mobile in soil and
therefore likely to leach into groundwater (ATSDR, 2012a). RDX is
expected to have a high likelihood of partitioning to water based on
its log Kow and KH. Multiple values for
Koc

indicate that RDX is expected to have a moderate to high likelihood of
partitioning to water, while its water solubility indicates that RDX is
expected to have a moderate likelihood of partitioning to water. RDX is
expected to have low to moderate persistence based on modeled
biodegradation rates (USEPA, 2019a).
b. Statutory Criterion #1 (Adverse Health Effects)