As part of the National Pesticide Survey, EPA collected samples
from approximately 1,300 community water systems and rural drinking
water wells between 1988 and 1990. The NPS included EPTC as an analyte
in the monitoring survey. EPTC was not detected using a minimum
reporting limit of 0.15 [mu]g/L (USEPA, 1990a).
    The Pesticides in Ground Water Database (USEPA, 1992b) indicates
that EPTC was found in 2 of 1,752 ground water wells that were sampled
in 10 States. Both contaminated wells were in Minnesota. The detected
concentrations ranged from 0.01 to 0.33 [mu]g/L. All of these positive
detections are less than the HRL of 175 [mu]g/L, as well as 87.5 [mu]g/
L (\1/2\ the HRL).
    The USGS NAWQA program included EPTC as an analyte in its 1992-2001
monitoring survey of ambient surface and ground waters across the
United States. EPA evaluated the results of the provisional data, which
are available on the Web (Martin et al., 2003; Kolpin and Martin,
2003). While the USGS detected EPTC in both surface and ground waters,
95 percent of the samples from the various land use settings were less
than or equal to 0.018 [mu]g/L. The estimated maximum surface water
concentration, 29.6 [mu]g/L (mixed land use settings), and the maximum
ground water concentration, 0.45 [mu]g/L (agricultural settings), are
both less than 175 [mu]g/L (the EPTC HRL).
    d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate EPTC with an NPDWR. Because EPTC does not
appear to occur at health levels of concern in PWSs, the Agency
believes that a national primary drinking water regulation does not
present a meaningful opportunity for health risk reduction. While EPTC
has been found in ambient waters, it was detected only at levels less
than the HRL (as well as \1/2\ the HRL) and it was not found in the
UCMR 1 survey of public water supplies.
9. Fonofos
    a. Background. Fonofos, an organophosphate, is a soil insecticide
used to control pests such as corn rootworms, cutworms, symphylans
(i.e., garden centipedes), and wireworms. Primarily used on corn crops,
fonofos was also used on other crops such as asparagus, beans, beets,
corn, onions, peppers, tomatoes, cole crops, sweet potatoes, peanuts,
peas, peppermint, plantains, sorghum, soybeans, spearmint,
strawberries, sugarcane, sugar beets, white (Irish) potatoes, and
tobacco (USEPA, 1999d).
    Fonofos was scheduled for a reregistration decision in 1999.
However, before the review was completed, the registrant requested
voluntary cancellation. The cancellation was announced in the Federal
Register on May 6, 1998 (63 FR 25033 (USEPA, 1998d)), with an effective
date of November 2, 1998, plus a one-year grace period to permit the
exhaustion of existing stocks (USEPA, 1999d).
    NCFAP data indicate that fonofos use declined significantly during
the 1990s (NCFAP, 2004). According to NCFAP,

approximately 3.2 million pounds of fonofos a.i. were applied annually
around 1992 and approximately 0.4 million pounds a.i. were applied
annually around 1997. The U.S. Geological Survey (USGS) estimates an
average of 2.7 million pounds a.i. were used annually around 1992
(Thelin and Gianessi, 2000).
    Fonofos is moderately persistent in soil and its persistence
depends on soil type, organic matter, rainfall, and sunlight. Since
fonofos adsorbs moderately well to soil, it is not readily leached or
transported to ground water but it can be transported to surface waters
in runoff. Fonofos is rapidly degraded by soil microorganisms
(Extoxnet, 1993). Fonofos tends to volatilize from wet soil and water
surfaces, but the process is slowed by adsorption to organic material
in soil, suspended solids, and sediment (HSDB, 2004d).
    b. Health Effects. Fonofos (like many organophosphates) is toxic to
humans and animals. Case reports and acute oral toxicity studies in
animals indicate that oral exposure to fonofos induces clinical signs
of toxicity that are typical of cholinesterase inhibitors. In humans,
accidental exposures produced symptoms of acute intoxication, nausea,
vomiting, salivation, sweating, muscle twitches, decreased blood
pressure and pulse rate, pinpoint pupils, profuse salivary and
bronchial secretions, cardiorespiratory arrest, and even death in 1
exposed individual (Hayes, 1982; Pena Gonzalez et al., 1996).
    In animals, clinical signs of exposure included tremors,
salivation, diarrhea, and labored breathing (USEPA, 1996c). Chronic
exposure studies also indicated that oral administration of fonofos
inhibits cholinesterase (Banerjee et al., 1968; Cockrell et al., 1966;
Hodge, 1995; Horner, 1993; Miller, 1987; Miller et al., 1979; Pavkov
and Taylor, 1988; Woodard et al., 1969). Cholinesterase inhibition is
one of the critical effects associated with the RfD, which was verified
by EPA (USEPA, 1991) at 0.002 mg/kg/day. EPA derived the RfD of 0.002
mg/kg/day using a NOAEL of 0.2 mg/kg/day (Hodge, 1995) and a 100-fold
uncertainty factor to account for inter- and intraspecies differences.
    Fonofos is classified as an unlikely human carcinogen (Group E)
because there is no evidence of carcinogenic potential in the available
long-term feeding studies in rats and mice (Banerjee et al., 1968;
Pavkov and Taylor, 1988; Sprague and Zwicker, 1987). In addition,
fonofos does not appear to be mutagenic (USEPA, 1996c).
    EPA evaluated whether health information is available regarding the
potential effects on children and other sensitive populations. In the
available developmental studies with rabbits (Sauerhoff, 1987) and mice
(Minor et al., 1982; Pulsford, 1991), no developmental effects were
observed at oral doses as high as 1.5 mg/kg/day in the rabbit (highest
dose tested) nor in mice at doses as high as 2.0 mg/kg/day (Minor et
al., 1982; Pulsford, 1991). However, in mice, effects were noted at
higher dose levels. These effects included an increase in the incidence
of variant sternebrae ossifications (at 6 mg/kg/day or greater) and a
slight dilation of the fourth brain ventricle in offspring (at 4 mg/kg/
day or greater). No developmental neurotoxicity study with fonofos is
available for further assessment of this endpoint. In a three-
generation reproduction study in rats (Woodard et al., 1968), no
treatment-related adverse effects were observed at the 2 dose levels
used in this study, 0.5 and 1.58 mg/kg/day.
    The Agency believes that the current RfD is adequately protective
of children. The current fonofos RfD of 0.002 mg/kg/day is 1000-fold
lower than the NOAEL observed in the Woodard et al. (1968)
developmental studies.
    Using the RfD of 0.002 mg/kg/day for fonofos and a 20 percent
screening relative source contribution, the Agency derived an HRL of
0.014 mg/L and rounded to 0.01 mg/L (or 10 [mu]g/L).
    c. Occurrence. EPA included fonofos as an analyte in the UCMR 1
List 2 Screening Survey. None of the 2,306 samples from the 295 PWSs
sampled (serving a population of 41 million) contained detects for
fonofos at the MRL of 0.5 [mu]g/L. Hence, these data indicate that no
occurrence and exposure is expected at levels greater than 5 [mu]g/L
(\1/2\ the HRL) and greater than 10 [mu]g/L (the HRL) (USEPA, 2006a and
2006b).
    The USGS NAWQA program included fonofos as an analyte in its 1992-
2001 monitoring survey of ambient surface and ground waters across the
United States. EPA evaluated the results of the provisional data, which
are available on the Web (Martin et al., 2003; Kolpin and Martin,
2003). While the USGS detected fonofos in both surface and ground
waters, 95 percent of the samples from the various land use settings
were less than 0.003 [mu]g/L (the reporting limit). The maximum surface
water concentration, 1.20 [mu]g/L (agricultural setting), and the
maximum ground water concentration, 0.009 [mu]g/L (agricultural
setting), are both less than 10 [mu]g/L and less than 5 [mu]g/L (the
fonofos HRL and \1/2\ the HRL).
    d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate fonofos with an NPDWR. Because fonofos
does not appear to occur at health levels of concern in PWSs, the
Agency believes that a national primary drinking water regulation does
not present a meaningful opportunity for health risk reduction. While
fonofos has been found in ambient waters, it was detected only at
levels less than the HRL (as well as \1/2\ the HRL) and it was not
found in UCMR 1 Screening Survey of public water supplies. Fonofos was
voluntarily cancelled in 1998 and the Agency expects any remaining
stocks and releases into the environment to decline. In addition, since
fonofos tends to bind strongly to soil, any releases to the environment
are not likely to contaminant source waters.
10. Terbacil
    a. Background. Terbacil, a synthetic organic compound, is a
selective herbicide used to control broadleaf weeds and grasses on
terrestrial food/feed crops (e.g., apples, mint, peppermint, spearmint,
and sugarcane), terrestrial food (e.g., asparagus, blackberry,
boysenberry, dewberry, loganberry, peach, raspberry, youngberry, and
strawberry), terrestrial feed (e.g., alfalfa, forage, and hay) and
forest trees (e.g., cottonwood) (USEPA, 1998e).
    In 1998, EPA estimated that agricultural usage of terbacil consumed
approximately 221,000 to 447,000 pounds of active ingredient annually
and non-agricultural usage consumed approximately 9,000 to 14,000
pounds. These estimates are based on data collected mostly between 1990
and 1995, and in some cases as early as 1987 (USEPA, 1998e). According
to NCFAP (2004), approximately 298,000 pounds of terbacil a.i. were
applied annually in agriculture around 1992 and approximately 342,000
pounds a.i. were applied around 1997.
    Terbacil is listed as a TRI chemical and data are reported from one
or more facilities in a single state, Texas, for the time period
covering 1995 to 1997. During this three-year period, all reported
releases were on-site releases to surface water that varied between
3,000 to 10,000 pounds annually (USEPA, 2006h).
    Terbacil is considered a persistent and potentially mobile
herbicide in terrestrial environments. Because of its low affinity to
soils, it can potentially leach into ground and/or surface waters
(USEPA, 1998e; Extoxnet, 1994).
    b. Health Effects. In acute and subchronic toxicity studies,
terbacil is practically non-toxic (Haskell Laboratories, 1965a and
1965b). Terbacil does not cause dermal sensitivity in

rabbits or guinea pigs and causes mild conjunctival eye irritation in
rabbits (Henry, 1986; Hood, 1966). In rats exposed subchronically to
dietary terbacil, effects were seen at a LOAEL of 25 mg/kg/day and
included increased absolute and relative liver weights, vacuolization,
and enlargement of liver cells (Wazeter et al.,1964; Haskell
Laboratories, 1965c).
    A primary target organ in rats following exposure to terbacil is
the liver. Chronic effects of dietary terbacil exposure in two-year
studies included increases in thyroid-to-body weight ratios, slight
increases in liver weights and elevated alkaline phosphatase levels in
beagle dogs, significant decreases in body weight in rats, increases in
serum cholesterol levels and increases in liver to body weight ratios
in rats (Wazeter et al.,1967a; Malek, 1993). In beagle dogs, effects
were seen at or above 6.25 mg/kg/day (NOAEL = 1.25 mg/kg/day). In rats,
effects (i.e., decreases in body weight, increases in liver weights and
cholesterol levels) were seen at higher levels (LOAELs = 56 mg/kg/day
for males and 83 mg/kg/day for females).
    Terbacil is not considered to be a developmental or reproductive
toxicant. In developmental studies, maternal effects were generally
seen prior to or at the same levels as developmental effects. Haskell
Laboratories (1980) reported maternal effects (i.e., decreased body
weight) and significant decreases in the number of live fetuses per
litter due to early fetal resorption at a LOAEL of 62.5 mg/kg/day in
rats. In rabbits administered terbacil via gavage, the maternal and
developmental LOAELs were equal (600 mg/kg/day). Maternal toxicity was
based on the death of the dams and developmental toxicity was based on
a decrease in live fetal weights (Solomon, 1984). No reproductive
effects were seen in a three-generation study where terbacil was
administered to male and female rats at dose levels of 2.5 and 12.5 mg/
kg/day (Wazeter et al., 1967b).
    Terbacil is not mutagenic. Terbacil was tested and found negative
in a chromosomal aberration study in rat bone marrow cells, found
negative in a gene mutation assay (with and without S9 activation), and
found negative for DNA synthesis when tested up to cytotoxic levels in
rats (Cortina, 1984; Haskell Laboratories,1984). Terbacil shows no
evidence of carcinogenicity and is unlikely to be carcinogenic to
humans (Group E) (USEPA, 1998e).
    The RfD of 0.013 mg/kg/day for terbacil (USEPA, 1998e) is
calculated from a two-year chronic study in beagle dogs. The LOAEL of
6.25 mg/kg/day was based on increased thyroid-to-body weight ratios,
slight increases in liver weights, and elevated alkaline phosphatase
levels with a NOAEL of 1.25 mg/kg/day. In deriving the RfD, the Agency
applied an uncertainty factor of 100 to account for interspecies and
intraspecies differences. Using the RfD of 0.013 mg/kg/day and applying
a 20 percent screening relative source contribution, the Agency derived
an HRL of 0.090 mg/L (or 90 g/L) for terbacil.
    EPA also evaluated whether health information is available
regarding the potential effects on children and other sensitive
populations. In the case of terbacil, the Agency determined that there
was no need to apply an FQPA factor to the RfD in order to protect
children (USEPA, 1998e). Other potentially sensitive subpopulations
have not been identified.
    c. Occurrence. EPA included terbacil as an analyte in UCMR 1. None
of the 3,866 PWSs sampled (serving a population of 226 million) had
detects for terbacil at the MRL of 2 g/L. Hence, these data indicate
that no occurrence and exposure is expected at levels greater than 45
g/L (\1/2\ the HRL) and greater than 90 [mu]g/L (the terbacil HRL)
(USEPA, 2006a and 2006b).
    EPA also evaluated several sources of supplemental information,
which included:
     The National Pesticide Survey,
     The Pesticides in Ground Water Database, and
     The provisional pesticide results from the 1992-2001 USGS
NAWQA survey of ambient surface and ground waters across the U.S.
    As part of the National Pesticide Survey, EPA collected samples
from approximately 1,300 community water systems and rural drinking
water wells between 1988 and 1990. The NPS included terbacil as an
analyte in the monitoring survey. Terbacil was not detected using a
minimum reporting limit of 1.7 [mu]g/L (USEPA, 1990a).
    The Pesticides in Ground Water Database (USEPA, 1992b) indicates
that terbacil was found in 6 of the 288 ground water wells tested for
this contaminant in 6 States. Terbacil was found in 1 ground water well
in Oregon (at a concentration of 8.9 [mu]g/L) and 5 ground water wells
in West Virginia (with concentrations ranging from 0.3 to 1.2 [mu]g/L).
All of the positive detections are less than the HRL of 90 [mu]g/L, as
well as 45 [mu]g/L (\1/2\ the HRL).
    The USGS NAWQA program included terbacil as an analyte in its 1992-
2001 monitoring survey of ambient surface and ground waters across the
United States. EPA evaluated the results of the provisional data, which
are available on the Web (Martin et al., 2003; Kolpin and Martin,
2003). While the USGS detected terbacil in both surface and ground
waters, 95 percent of the samples from the various land use settings
were less than 0.034 [mu]g/L (the USGS reporting limit). The maximum
surface water concentration, 0.54 [mu]g/L (agricultural setting), and
the maximum ground water concentration, 0.891 [mu]g/L (mixed land use
setting), are both less than 90 [mu]g/L and less than 45 [mu]g/L (the
terbacil HRL and \1/2\ the HRL).
    d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate terbacil with an NPDWR. Because terbacil
does not appear to occur at health levels of concern in PWSs, the
Agency believes that a national primary drinking water regulation does
not present a meaningful opportunity for health risk reduction.
Terbacil has been found in ambient waters but the levels were less than
the HRL (as well as \1/2\ the HRL). It was not found in the UCMR 1
survey of public water supplies.
11. 1,1,2,2-Tetrachloroethane
    a. Background. 1,1,2,2-Tetrachloroethane, a volatile organic
compound, is not known to occur naturally in the environment (IARC,
1979). Prior to the 1980s, 1,1,2,2-tetrachloroethane was synthesized
for use in the production of other chemicals, primarily chlorinated
ethylenes. 1,1,2,2-Tetrachloroethane was also once used as a solvent to
clean and degrease metals, in paint removers, varnishes, lacquers, and
photographic films, and for oil/fat extraction (Hawley, 1981).
Commercial production of 1,1,2,2-tetrachloroethane in the U.S. ceased
in the 1980s when other processes to generate chlorinated ethylenes
were discovered (ATSDR, 1996).
    Production of 1,1,2,2-tetrachloroethane in the U.S. was
approximately 440 million pounds in 1967 (Konietzko, 1984). Production
declined to an estimated 34 million pounds by 1974 (ATSDR, 1996).
Although U.S. commercial production ceased in the 1980s, 1,1,2,2-
tetrachloroethane is still generated as a byproduct and/or intermediate
in the production of other chemicals. TRI data indicate that
environmental releases have generally declined from a high of about
175,000 pounds in 1988 to a low of 3,500 pounds in 2003. Most releases
took the form of air emissions, though surface water discharges were
also documented nearly every year (USEPA, 2006i).

    Volatilization from water or soil surfaces to the atmosphere
appears to be the primary dissipation route for 1,1,2,2-
tetrachloroethane. In subsurface soils and ground water, 1,1,2,2-
tetrachloroethane is subject to biodegradation by soil organisms and/or
chemical hydrolysis by water (ATSDR, 1996).
    b. Health Effects. Data on the toxicity of 1,1,2,2-
tetrachloroethane in humans are limited, consisting of one experimental
inhalation study, a few case reports of suicidal or accidental
ingestion, and dated occupational studies. In most cases, there was no
quantification of the exposure. Respiratory and mucosal effects, eye
irritation, nausea, vomiting, and dizziness were reported by human
volunteers exposed to 1,1,2,2-tetrachloroethane vapors under controlled
chamber conditions (Lehmann and Schmidt-Kehl, 1936). Effects from non-
lethal occupational exposures included gastric distress (i.e., pain,
nausea, vomiting), headache, loss of appetite, an enlarged liver, and
cirrhosis (Jeney et al., 1957; Lobo-Mendonca, 1963; Minot and Smith,
1921).
    There have been a variety of animal studies in rats and mice using
both the inhalation and oral exposure routes. Recent studies by the
National Toxicology Program (NTP, 2004) provide a detailed evaluation
of the short-term and subchronic oral toxicity of 1,1,2,2-
tetrachloroethane and confirm many of the observations from earlier
studies. In rats and mice exposed orally, the liver appears to be the
primary target organ. The RfD (10 [mu]g/kg/day) for 1,1,2,2-
tetrachloroethane was derived from the BMDL for a 1 standard deviation
change in relative liver weight, a biomarker for liver toxicity. A
1,000-fold uncertainty factor was applied in the RfD determination.
    A National Cancer Institute (1978) bioassay of 1,1,2,2-
tetrachloroethane found clear evidence of carcinogenicity in male and
female B6C3F1 mice based on a dose-related statistically significant
increase in liver tumors. There was equivocal evidence for
carcinogenicity in Osborn Mendel rats because of the occurrence of a
small number of rare-for-the species neoplastic and preneoplastic
lesions in the livers of the high dose animals. The Agency used the
slope factor of 8.5 x 10-2 for the tumors in female mice to
derive the HRL of 0.4 [mu]g/L for use in the analysis of the occurrence
data for 1,1,2,2-tetrachloroethane. Information on the reproductive
effects of 1,1,2,2-tetrachloroethane is limited. There is a single one-
generation inhalation study that does not follow a standard methodology
and examined a small number of rats (5 females and 7 males) exposed via
inhalation to 1 dose (13.3 mg/m\3\). There were no statistically
significant differences in the percentage of females having offspring,
number of pups per litter, average birth weight, sex ratio, or post
natal offspring mortality (Schmidt et al., 1972). Effects on sperm in
male rats were seen after oral (27 mg/kg/day; NTP, 2004) and inhalation
(13 mg/m\3\; Schmidt et al., 1972) exposures. Similar effects were seen
in mice but at higher doses. Fetal toxicity did not occur in the
absence of maternal toxicity.
    Developmental range-finding studies conducted for NTP (1991a and b)
found that 1,1,2,2-tetrachloroethane was toxic to the dams and pups of
Sprague Dawley rats and CD-1 Swiss mice. Rats were more sensitive than
mice. The NOAEL in the rats for both maternal toxicity and associated
fetal toxicity was 34 mg/kg/day with a LOAEL of 98 mg/kg/day. In mice,
the NOAEL was 987 mg/kg/day and the LOAEL was 2,120 mg/kg/day.
    EPA also evaluated whether health information is available
regarding the potential effects on children and other sensitive
populations. Individuals with preexisting liver and kidney damage would
likely be sensitive to 1,1,2,2-tetrachloroethane exposure. Low intake
of antioxidant nutrients (e.g., Vitamin E, Vitamin C, and selenium)
could be a predisposing factor for liver damage. In addition,
individuals with a genetically low capacity to metabolize
dichloroacetic acid (the primary metabolite of 1,1,2,2-
tetrachloroethane) may be at greater risk than the general population
as a result of 1,1,2,2-tetrachloroethane exposure.
    c. Occurrence. EPA included 1,1,2,2-tetrachloroethane as an analyte
in the UCM Round 1 and UCM Round 2 surveys. EPA evaluated the UCM Round
1 Cross Section and the UCM Round 2 Cross Section data at levels
greater than 0.2 [mu]g/L (\1/2\ the HRL) and greater than 0.4 [mu]g/L
(the HRL) (USEPA, 2006a and 2006c). The MRLs for UCM Round 1 ranged
from 0.1 to 10 [mu]g/L and the MRLs for UCM Round 2 ranged from 0.1 to
2.5 [mu]g/L. Because some of the reporting limits exceeded the
thresholds of interest, the occurrence analyses may result in an
underestimate of systems affected. However, all the MRL values used for
UCM Round 1 and UCM Round 2 are within the 10-4 to the
10-6 cancer risk range.
    Analysis of UCM Round 1 Cross Section data indicates that
approximately 0.22 percent (or 44) of the 20,407 PWSs sampled had
detections of 1,1,2,2-tetrachloroethane at levels greater than 0.20
[mu]g/L (\1/2\ the HRL), affecting approximately 1.69 percent of the
population served (or 1.6 million of 95 million). The UCM Round 1 Cross
Section data indicate that approximately 0.20 percent (or 41) of the
20,407 PWSs sampled had detections of 1,1,2,2-tetrachloroethane at
levels greater than 0.4 [mu]g/L (the HRL), affecting approximately 1.63
percent of the population served (or 1.5 million of 95 million). The
99th percentile of all detects is 112 [mu]g/L and the maximum reported
value is 200 [mu]g/L.
    Analysis of the UCM Round 2 Cross Section data indicate that
approximately 0.07 percent (or 18) of the 24,800 PWSs sampled had
detections of 1,1,2,2-tetrachloroethane at levels greater than 0.2
[mu]g/L (\1/2\ the HRL), affecting approximately 0.51 percent of the
population served (or 362,000 of 71 million). The UCM Round 2 Cross
Section data indicate that approximately the same percentage and number
of the PWSs sampled (0.07 percent or 17 of the 24,800) had detections
of 1,1,2,2-tetrachloroethane at levels greater than 0.4 [mu]g/L (the
HRL), affecting approximately 0.08 percent of the population served (or
56,000 of 71 million). The 99th percentile of all detects is 2 [mu]g/L
and the maximum reported value is 2 [mu]g/L.
    EPA also evaluated several sources of supplemental information,
which included the USGS VOC National Synthesis Random Source Water
Survey and the Focused Source Water Survey. For the Random Source Water
Survey, the USGS collected samples from 954 source waters that supply
community water systems between 1999 and 2000. For the Focused Source
Water Survey, the USGS collected 451 samples from 134 source waters
that supply community water systems between 1999 and 2001. The USGS
included 1,1,2,2-tetrachloroethane as an analyte in both surveys and
did not detect it in any of the source water samples using a reporting
limit of 0.2 [mu]g/L (a level that is less than the 1,1,2,2-
tetrachloroethane HRL). In addition, USGS did not detect 1,1,2,2-
tetrachloroethane when using a detection level of 0.026 [mu]g/L (a
level that is over 10 times lower than the 1,1,2,2-tetrachloroethane
HRL) in the focused survey (Ivahnenko et al., 2001, Grady, 2003, Delzer
and Ivahnenko, 2003a).
    d. Preliminary Determination. The Agency has made a preliminary
determination not to regulate 1,1,2,2-tetrachloroethane with an NPDWR.
Because 1,1,2,2-tetrachloroethane appears to occur infrequently at
health levels of concern in PWSs, the Agency

believes that a national primary drinking water regulation does not
present a meaningful opportunity for health risk reduction. While
1,1,2,2-tetrachloroethane was detected in both the UCM Round 1 and the
UCM Round 2 surveys, the percentage of detections had decreased by the
time the UCM Round 2 survey was performed in the mid-1990's. In
addition, the USGS did not detect 1,1,2,2-tetrachloroethane in two
subsequent monitoring surveys of source waters that supply community
water systems using a reporting limit that is less than the 1,1,2,2-
tetrachloroethane HRL. The Agency believes that this decrease in
detections occurred because commercial production of 1,1,2,2-
tetrachloroethane ceased in the mid-1980's. Hence, the Agency does not
expect 1,1,2,2-tetrachloroethane to occur in many public water systems
today.
    EPA recognizes that 1,1,2,2-tetrachloroethane is listed as a likely
human carcinogen. For this reason, the Agency encourages those States
with public water systems that may have 1,1,2,2-tetrachloroethane above
the HRL to evaluate site-specific protective measures and to consider
whether State-level guidance (or some other type of action) is
appropriate. The Agency also plans to update the Health Advisory
document for 1,1,2,2-tetrachloroethane to provide more recent health
information. The updated Health Advisory will provide information to
any States with public water systems that may have 1,1,2,2-
tetrachloroethane at levels above the HRL.

V. What Is the Status of the Agency's Evaluation of Perchlorate?

    At this time, the Agency is not making a preliminary determination
as to whether a national primary drinking water regulation is needed
for perchlorate. However, the Agency has placed a high priority on
making a regulatory determination for perchlorate and will publish a
preliminary determination as soon as possible. EPA is not able to make
a preliminary determination at this time because, in order to evaluate
perchlorate against the three SDWA statutory criteria, the Agency
believes additional information may be needed to more fully
characterize perchlorate exposure and determine whether regulating
perchlorate in drinking water presents a meaningful opportunity for
health risk reduction. This is particularly true if the Agency uses
food exposure data to first calculate a relative source contribution
(RSC) and corresponding health reference level (HRL) below the drinking
water equivalent level (DWEL) \18\ in order to determine whether
regulating perchlorate would present a meaningful opportunity for
health risk reduction. However, the Agency is considering several other
approaches, discussed below, for making this statutory determination
and is requesting public comment on the strengths and limitations of
these approaches.
---------------------------------------------------------------------------

    \18\ DWEL = [(Reference Dose x Body Weight of 70 kg) / Drinking
Water Intake of 2 L per day].
---------------------------------------------------------------------------

    The following sections explain why EPA is not making a preliminary
regulatory determination for perchlorate at this time, and discusses
the information the Agency has collected to date (that may be relevant
to making a preliminary regulatory determination), the additional
information the Agency is soliciting in this action, and options for
additional analyses that the Agency may conduct to support a regulatory
determination. Sections V.A through V.D provide a summary of the
available and relevant information/data that the Agency has collected
and reviewed regarding the sources of perchlorate in the environment,
its potential health effects, and its occurrence in drinking water,
food, human urine, breast milk, and amniotic fluid. Section V.E
explains the Agency's basis for not making a preliminary regulatory
determination for perchlorate at this time and Section V.F. presents
the options the Agency is considering to better characterize
perchlorate exposure and the alternate approaches that EPA is
considering for making a preliminary regulatory determination. This
action provides an opportunity for the public to submit other relevant
data that may further characterize exposure to perchlorate through the
consumption of foods and/or through other pathways and to comment on
these alternate approaches. The Agency in particular seeks comment on
the use of urine biomonitoring data in estimating perchlorate exposure.
The Agency will consider any relevant information/data provided in
response to this action as the Agency determines whether to regulate
perchlorate with a national primary drinking water regulation and how
best to proceed to address perchlorate.

A. Sources of Perchlorate

    Perchlorate (ClO4-) is an anion commonly
associated with the solid salts of ammonium, magnesium, potassium, and
sodium perchlorate. Perchlorate salts are highly soluble in water, and
because perchlorate sorbs poorly to mineral surfaces and organic
material, perchlorate can be mobile in surface and subsurface aqueous
environments. Although commonly known as a man-made chemical,
perchlorate also may be derived from natural processes.
    While perchlorate has a wide variety of industrial uses, it is
primarily used in the form of ammonium perchlorate as an oxidizer in
solid fuels used to power rockets, missiles, and fireworks.
Approximately 90 percent of perchlorate is manufactured for this
application (Wang et al., 2002). Perchlorate can also be present as an
ingredient or as an impurity in road flares, lubricating oils, matches,
aluminum refining, rubber manufacturing, paint and enamel
manufacturing, leather tanning, paper and pulp processing (as an
ingredient in bleaching powder), and as a dye mordant.
    Perchlorate can also occur naturally in the environment. Chile
possesses caliche ores rich in sodium nitrate (NaNO3), which
are also a natural source of perchlorate (Schilt, 1979 and Ericksen,
1983). These Chilean nitrate salts (saltpeter) have been mined and
refined to produce commercial fertilizers, which before 2001 accounted
for about 0.14 percent of U.S. fertilizer application (USEPA, 2001d).
The USEPA (2001d) conducted a broad survey of fertilizers and other raw
materials and found that all products surveyed were devoid of
perchlorate except for those known to contain or to be derived from
mined Chilean saltpeter.
    Perchlorate has also been found in other geologic materials. Orris
et al. (2003) measured perchlorate at levels exceeding 1,000 parts per
million (ppm or mg/kg) in several samples of natural minerals,
including potash ore from New Mexico and Saskatchewan (Canada), playa
crust from Bolivia, and hanksite from California.
    Texas Tech University Water Resources Center conducted a large-
scale sampling program to determine the source and distribution of
perchlorate in northwest Texas groundwater (Jackson et al., 2004;
Rajagopalan et al., 2006). Perchlorate was detected at concentrations
greater than 0.5 g/L in 46 percent of public wells and 47 percent of
private wells. Jackson et al. (2004) hypothesized that atmospheric
production and/or surface oxidative weathering is the source of the
perchlorate. In related research, Dasgupta et al. (2005) detected
perchlorate in many rain and snow samples and demonstrated that
perchlorate is formed by a variety of simulated atmospheric processes
suggesting that natural, atmospherically-

derived perchlorate exists in the environment. Barron et al. (2006)
developed a method for the rapid determination of perchlorate in
rainwater samples, with a detection limit between 70 and 80 ng/L. Of
the ten rainwater samples collected in Ireland in 2005, perchlorate was
detected in 4 samples at concentrations between 0.075 and 0.113 g/L,
and in 1 other sample at 2.8 g/L. Kang et al. (2006) conducted seven-
day experiments to determine if it was possible to produce perchlorate
by exposing various chlorine intermediates to UV radiation in the form
of high intensity UV lamps and/or ambient solar radiation. Perchlorate
formation was demonstrated in aqueous salt solutions with initial
concentrations of hypochlorite, chlorite, or chlorate between 100 and
10,000 mg/L.
    After a limited investigation, the Massachusetts Department of
Environmental Quality (MA DEP, 2005) found that perchlorate may be
present in sodium hypochlorite solutions used in water and wastewater
treatment plants, and that the level of occurrence depends upon storage
conditions and the initial purity of the stock solution (MA DEP, 2005).
According to MA DEP (2005), the Town of Tewksbury conducted a small
study to evaluate the impact of storage conditions (temperature and
light) on a new shipment of sodium hypochlorite stock solution.
Tewksbury found that the perchlorate concentration in the new stock
solution increased from 0.2 g/L to levels ranging from 995 to 6,750 g/L
depending on the storage conditions. Accounting for the large dilution
factor (e.g., 20,000 to 1 ratio) used in chlorination processes at
drinking water treatment plants, MA DEP (2005) concluded that ``absent
additional efforts to minimize breakdown of hypochlorite solutions, it
would appear that low levels of the perchlorate ion (0.2 to 0.4 g/L)
detected in a drinking water supply disinfected with sodium
hypochlorite solutions could be attributable to the chlorination
process.''
    It is not clear at this time what proportion of perchlorate found
in public water supplies or entering the food chain comes from these
various anthropogenic and natural sources. The significance of
different sources probably varies regionally. A study by Dasgupta et
al. (2006) analyzes the three principal sources of perchlorate and
their relative contributions to the food chain. These are its use as an
oxidizer including rocket propellants, Chilean nitrate used principally
as fertilizer, and that produced by natural atmospheric processes.

B. Health Effects

    Perchlorate can interfere with the normal functioning of the
thyroid gland by competitively inhibiting the transport of iodide into
the thyroid. Iodide is an important component of two thyroid hormones,
T4 and T3, and the transfer of iodide from the blood into the thyroid
is an essential step in the synthesis of these two hormones. Iodide
transport into the thyroid is mediated by a protein molecule known as
the sodium (Na+)--iodide (I-) symporter (NIS). NIS molecules bind
iodide with very high affinity, but they also bind other ions that have
a similar shape and electric charge, such as perchlorate. The binding
of these other ions to the NIS inhibits iodide transport into the
thyroid, which can result in intrathyroidal iodide deficiency and
consequently decreased synthesis of T4 and T3. There is compensation
for iodide deficiency, however, such that the body maintains the serum
concentrations of thyroid hormones within narrow limits through
feedback control mechanisms. This feedback includes increased secretion
of thyroid stimulating hormone (TSH) from the pituitary gland, which
has among its effects the increased production of T4 and T3 (USEPA,
2005e). Sustained changes in thyroid hormone and TSH secretion can
result in thyroid hypertrophy and hyperplasia (abnormal growth or
enlargement of the thyroid) (USEPA, 2005e).
    In January 2005, the National Research Council (NRC) of the
National Academies of Science (NAS) published ``Health Implications of
Perchlorate Ingestion,'' a review of the current state of the science
regarding potential adverse health effects of perchlorate exposure and
mode-of-action for perchlorate toxicity (NRC, 2005). Based on
recommendations of the NRC, EPA chose data from the Greer et al. (2002)
human clinical study as the basis for deriving a reference dose (RfD)
for perchlorate (USEPA, 2005e). Greer et al. (2002) report the results
of a well-controlled study that measured thyroid iodide uptake, hormone
levels, and urinary iodide excretion in a group of 24 healthy adults
administered perchlorate doses orally over a period of 14 days. Dose
levels ranged from 0.007 to 0.5 mg/kg/day in the different experimental
groups. No significant differences were seen in measured serum thyroid
hormone levels (T3, T4, total and free) in any dose group. The
statistical no observed effect level (NOEL) for perchlorate-induced
inhibition of thyroid iodide uptake was 0.007 mg/kg/day. Although the
NRC committee concluded that hypothyroidism is the first adverse effect
in the continuum of effects of perchlorate exposure, NRC recommended
that ``the most health-protective and scientifically valid approach''
was to base the perchlorate RfD on the inhibition of iodide uptake by
the thyroid (NRC, 2005). NRC concluded that iodide uptake inhibition,
although not adverse, is the key biochemical event in the continuum of
possible effects of perchlorate exposure and would precede any adverse
health effects of perchlorate exposure. The lowest dose (0.007 mg/kg/
day) administered in the Greer et al. (2002) study was considered a
NOEL (rather than a NOAEL) because iodide uptake inhibition is not an
adverse effect but a biochemical change (USEPA, 2005e). A summary of
the data considered and the NRC deliberations can be found in the NRC
report (2005) and the EPA Integrated Risk Information System (IRIS)
summary (USEPA, 2005e).
    The NRC recommended that EPA apply an intraspecies uncertainty
factor of 10 to the NOEL to account for differences in sensitivity
between the healthy adults in the Greer et al. (2002) study and the
most sensitive population, fetuses of pregnant women who might have
hypothyroidism or iodide deficiency. Because the fetus depends on an
adequate supply of maternal thyroid hormone for its central nervous
system development during the first trimester of pregnancy, iodide
uptake inhibition from low-level perchlorate exposure has been
identified as a concern in connection with increasing the risk of
neurodevelopmental impairment in fetuses of high-risk mothers (NRC,
2005). The NRC (2005) viewed the uncertainty factor of 10 as
conservative and health protective given that the point of departure is
based on a non-adverse effect (iodide uptake inhibition) that precedes
the adverse effect in a continuum of possible effects of perchlorate
exposure. NRC concluded that no uncertainty factor was needed for the
use of a less-than chronic study, for deficiencies in the database, or
for interspecies variability. To protect the most sensitive human
population from chronic perchlorate exposure, EPA derived an RfD of
0.0007 mg/kg/day with a ten-fold total uncertainty factor from the NOEL
of 0.007 mg/kg/day (USEPA, 2005e).
    Blount et al. (2006b) recently published a study examining the
relationship between urinary levels of perchlorate and serum levels of
TSH and total T4 in 2,299 men and women (ages 12 years and older), who
participated in CDC's 2001-2002

National Health and Nutrition Examination Survey (NHANES).\19\ Blount
et al. (2006b) evaluated perchlorate along with covariates known or
likely to be associated with T4 or TSH levels to assess the
relationship between perchlorate and these hormones, and the influence
of other factors on this relationship. These covariates included sex,
age, race/ethnicity, body mass index, serum albumin, serum cotinine (a
marker of tobacco smoke exposure), estimated total caloric intake,
pregnancy status, post-menopausal status, premenarche status, serum C-
reactive protein, hours fasting before sample collection, urinary
thiocyanate, urinary nitrate, and use of selected medications. The
study found that perchlorate was a significant predictor of thyroid
hormones in women, but not men. After finding evidence of gender
differences, the researchers focused on further analyzing the NHANES
data for the 1,111 women participants. They divided these 1,111 women
into two categories, higher-iodide and lower-iodide, using a cut point
of 100 [mu]g/L of urinary iodide based on the World Health Organization
(WHO) definition of sufficient iodide intake.\20\ Hypothyroid women
were excluded from the analysis. According to the study authors, about
36 percent of women living in the United States have urinary iodide
levels less than 100 [mu]g/L (Caldwell et al., 2005). For women with
urinary iodide levels less than 100 [mu]g/L, the study found that
urinary perchlorate is associated with a decrease in (a negative
predictor for) T4 levels and an increase in (a positive predictor for)
TSH levels. For women with urinary iodide levels greater than or equal
to 100 [mu]g/L, the researchers found that perchlorate is a significant
positive predictor of TSH but not a predictor of T4. The study found
that perchlorate was not a significant predictor of T4 or TSH in men.
The researchers state that perchlorate could be a surrogate for another
unrecognized determinant of thyroid function. Also, the study reports
that while large doses of perchlorate are known to decrease thyroid
function, this is the first time an association of decreased thyroid
function has been observed at these low levels of perchlorate exposure.
Of note is that the vast majority of the participants in this group had
urinary levels of perchlorate corresponding to estimated dose levels
that are below the RfD of 0.0007 mg/kg/day. The clinical significance
of the variations in T4/TSH levels, which were generally within normal
limits, has not been determined. The researchers noted several
limitations of the study (e.g., assumption that urinary perchlorate
correlates with perchlorate levels in the stroma and tissue and
preference for measurement of free T4 as opposed to total T4) and
recommended that these findings be confirmed in at least one more large
study focusing on women with low urine iodide levels. It is also not
known whether the association between perchlorate and thyroid hormone
levels is causal or mediated by some other correlate of both, although
the relationship between urine perchlorate and total TSH and T4 levels
persisted after statistical adjustments for some additional covariates
known to predict thyroid hormone levels (e.g., total kilocalorie
intake, estrogen use, and serum C-reactive protein levels). A planned
follow-up study will include additional measures of thyroid health and
function (e.g., TPO-antibodies, free T4). As EPA proceeds towards a
regulatory determination for perchlorate, the Agency will continue to
review any new findings/studies on perchlorate and their relationship
to thyroid function as they become available.
---------------------------------------------------------------------------

    \19\ While CDC researchers measured urinary perchlorate
concentration for 2,820 NHANES participants, TSH and total T4 serum
levels were only available for 2,299 of these participants.
    \20\ WHO notes that the prevalence of goiter begins to increase
in populations with a median iodide intake level below 100 [mu]g/L
(WHO, 1994).
---------------------------------------------------------------------------

C. Occurrence in Water, Food, and Humans

    1. Sources of Perchlorate. Section V.A. summarizes the potential
sources of perchlorate in the environment.
    2. Studies on Perchlorate Occurrence in Public Drinking Water
Systems and/or Drinking Water Sources. EPA included perchlorate as an
analyte in the 1999 Unregulated Contaminant Monitoring Regulation (UCMR
1) and collected drinking water occurrence data for perchlorate from
3,858 public water systems (PWSs) between 2001 and 2005. EPA analyzed
the available UCMR 1 data on perchlorate at concentrations greater than
or equal to 4 [mu]g/L, the minimum reporting limit (MRL) for EPA Method
314.0.\21\ The Agency found that approximately 4.1 percent (or 160) of
3,858 PWSs that sampled and reported under UCMR 1 had at least 1
analytical detection of perchlorate (in at least 1 entry/sampling
point) at levels greater than or equal to 4 [mu]g/L. These 160 systems
are located in 26 states and 2 territories. Of these 160 PWSs, 8 are
small systems (serving 10,000 or fewer people) and 152 are large
systems (serving more than 10,000 people). Approximately 1.9 percent
(or 637) of the 34,193 samples collected (by these 3,858 PWSs) had
positive detections of perchlorate at levels greater than or equal to 4
[mu]g/L. The maximum reported concentration of perchlorate was 420
[mu]g/L, which was found in a surface water sample from a PWS in Puerto
Rico. The average concentration of perchlorate for those samples with
positive detections for perchlorate was 9.85 [mu]g/L and the median
concentration was 6.40 [mu]g/L.
---------------------------------------------------------------------------

    \21\ EPA Method 314.0 was the analytical method approved and
used for UCMR 1 at the time of data collection.
---------------------------------------------------------------------------

    These 160 PWSs (with at least 1 analytical detection for
perchlorate at levels greater than or equal to 4 [mu]g/L) serve
approximately 7.5 percent (or 16.8 million) of the 225 million people
served by the 3,858 PWSs that sampled and reported results under UCMR
1. The 16.8 million population-served value represents the total number
of people served by the 160 PWSs with at least one detect. Not all
people served by these systems necessarily have perchlorate in their
drinking water. Some of these 160 public water systems have multiple
entry points to the distribution system and not all of the entry points
sampled had positive detections for perchlorate in the UCMR 1 survey.
An alternative approach to the system-level assessment of populations
served is to use an assessment at the entry (sampling) point level.\22\
EPA does not have population-served values for each entry point at the
system level. However, an assessment can be performed by assuming that
each entry (or sampling) point at a public water system serves an equal
proportion of the total population-served by the system. In other
words, for the alternative assessment, the population served by each
system is assumed to be equally distributed across all entry (or
sampling) points at each system. For example, if a system serves a
million people and has 5 entry points, it is assumed that each entry
point serves 200,000 people. Using this approach and counting only

the population served for the entry points with positive detections
(concentrations greater than or equal to 4 [mu]g/L), the total
population served by these entry points with perchlorate detections is
approximately 5 million. Section V.E provides the number of systems and
population-served estimates for other thresholds of interest.
---------------------------------------------------------------------------

    \22\ EPA acknowledges that uncertainties exist in the
population-served estimates for this alternative assessment since
the population for a system is assumed to be equally distributed
across the entry points for that system. Because the actual
population-served by an entry point is not known, this alternative
approach has an equal chance of underestimating or overestimating
the actual population-served by entry points with positive
detections for perchlorate. In addition, this approach could
underestimate the population served that is potentially exposed to
perchlorate and overestimate the level of exposure because it can
not incorporate the effects of mixing of water between different
entry points within the distribution system. This is because the
approach cannot account for the dilution that may occur when water
that has no detections of perchlorate is mixed within the
distribution system with water that has positive detections for
perchlorate.
---------------------------------------------------------------------------

    The California Department of Health Services (CA DHS) began
monitoring for perchlorate in 1997. In 1999, CA DHS began requiring
monitoring for perchlorate for drinking water sources that were
identified as vulnerable to perchlorate contamination under
California's own State monitoring program (i.e., Unregulated Chemicals
for which Monitoring is Required). About 60 percent (or 7,100) of all
drinking water sources in California (about 12,000) were monitored for
perchlorate under the State monitoring program. Between June 2001 and
June 2006, CA DHS (2006) reports that 284 (about 4%) of the
approximately 7,100 water sources that monitored had at least 2 or more
positive detections for perchlorate at concentrations greater than or
equal to 4 [mu]g/L (the reporting limit). These 284 sources supply
water for 77 drinking water systems (CA DHS, 2006) and represent active
and standby sources (and exclude inactive, destroyed, and abandoned
sources, and monitoring and agricultural wells) (CA DHS, 2006).
    In 2005, the State of Massachusetts's Department of Environment
Protection (MA DEP) reported monitoring results for 85 percent (379 of
450) of its community water systems and 86 percent (212 of 250) of its
non-transient, non-community water systems. MA DEP found that 9 (1.5%)
of the 591 public water systems detected perchlorate at levels greater
than or equal to 1 [mu]g/L (the reporting limit used for a modified
version of EPA Method 314.0). MA DEP found that the occurrence of
perchlorate for these water systems could be traced to the use of
blasting agents, military munitions, fireworks, and, to a lesser
degree, sodium hypochlorite disinfectant (MA DEP, 2005).
    3. Studies on Perchlorate Occurrence in Foods, Plants, Beverages,
and Dietary Supplements. The Food and Drug Administration (FDA), the
United States Department of Agriculture (USDA), and researchers from
academia and industry have studied perchlorate in foods. Some of these
studies are described briefly in this section, and also summarized in
Table 4. EPA has concluded that the sampling results described in this
section and Table 4 are too limited to characterize food-borne exposure
to perchlorate on a national scale. The sampling data are limited in
the types of foods sampled, sample sizes, geographic coverage, and/or
analytical method adequacy and many were targeted to foods or areas
known or likely to have elevated levels of perchlorate. Section V.F of
this action describes the limitations of the food sampling data and
also describes plans for including perchlorate as part of the FDA's
Total Diet Study. EPA requests that commenters provide the Agency with
any additional data that may further characterize the concentrations of
perchlorate in foods commercially available in the U.S. When providing
data to the Agency, please describe the specific locations where the
samples were collected, including geographic location, type of location
(e.g., grocery store, farmer's market, commercial field, home garden),
and the methodologies used to select, collect, prepare, and analyze the
samples. Please include available laboratory data reports as well as
all relevant quality assurance/quality control information.
BILLING CODE 6560-50-P
[GRAPHIC] [TIFF OMITTED] TP01MY07.052

[GRAPHIC] [TIFF OMITTED] TP01MY07.053

[GRAPHIC] [TIFF OMITTED] TP01MY07.054

BILLING CODE 6560-50-C
    a. FDA Targeted Sampling. The FDA released data on perchlorate in
milk, lettuce, and bottled water in November 2004. To analyze food
samples, FDA used ion chromatography (IC)-tandem mass spectrometry (MS/
MS), referred to as IC-MS/MS. The quantitation limits for perchlorate
in these analyses were 0.5 [mu]g/L for bottled water, 1 [mu]g/kg by
fresh weight (FW) for lettuce, and 3 [mu]g/L for dairy milk. The mean
concentration of perchlorate in 128 lettuce samples collected in 5
states (AZ, CA, FL, NJ, TX) was 10.3 [mu]g/kg FW (FDA, 2004), and
ranged from not quantifiable (NQ) to 129 [mu]g/kg FW. The mean
concentrations of perchlorate in several varieties of lettuce are
reported in Table 4. The mean concentration of perchlorate in 104 dairy
milk samples collected in 14 states (AZ, CA, GA, KS, LA, MD, MO, NJ,
NC, PA, SC, TX, VA, WA) was 5.76 [mu]g/L (FDA, 2004), with a range from
NQ to 11.3 [mu]g/L. FDA (2004) detected perchlorate in 2 of the 51
bottled water samples representing 34 distinct sources collected in 12
states (CA, CO, GA, MD, MN, MO, NC, NE, PA, SC, TX, WI) at levels of
0.56 [mu]g/L and 0.45 [mu]g/L.
    b. Other Published Studies. Sanchez (2004) and Sanchez et al.
(2005a) report the results of an analysis of agricultural products
sampled from the lower Colorado River region of Arizona and California,
the Imperial Valley of California, and the Coachella Valley of
California, where irrigation water is known or suspected to contain
perchlorate. The studies were partially supported by the U.S.
Department of

Agriculture--Agricultural Research Service (USDA-ARS). Samples of
iceberg, romaine, and leaf lettuce, carrots, onions, sweet corn,
squash, melons, tomatoes, peppers, broccoli, cauliflower, cabbage,
durum wheat, and alfalfa were analyzed for perchlorate using ion
chromatography (IC) as the primary analytical method. For these
analyses, the fresh-weight method reporting limit was not identified in
most cases, but was reported to range from 20 to 50 [mu]g/kg FW,
depending on the moisture content of the samples (Sanchez, 2004).
Sanchez et al. (2005a) report that the method reporting level for
iceberg lettuce was approximately 20 [mu]g/kg FW and for other types of
lettuce was 25-30 [mu]g/kg FW. Perchlorate in the irrigation water
ranged from 1.5 to 8.0 [mu]g/L over the period of the survey (Sanchez
et al., 2005a).
    Sanchez et al. (2005a) analyzed 44 samples of iceberg lettuce heads
that had been trimmed of frame and wrapper leaves, which are usually
removed before the lettuce is consumed. Perchlorate was quantified in 5
of the samples (ranging from 23 to 26 [mu]g/kg FW),\23\ perchlorate was
not detectable in 6 samples, and the results of the remaining samples
were less than the method reporting limit, which the authors defined as
``a detectable peak among duplicates and/or replicates but below a
level that can be quantitated.'' Perchlorate concentrations in 10
samples of romaine and green leaf lettuce ranged from less than the
method reporting limit to 81[mu]g/kg FW (Sanchez, 2004).
---------------------------------------------------------------------------

    \23\ Sanchez (2004) presents somewhat different results.
Specifically, of the 44 samples of ``edible head'' lettuce,
perchlorate was quantified in one of the samples (26 [mu]g/kg),
perchlorate was not detectable in 6 samples, and the remaining
sampling results were qualified as < MRL, which the author defined as
``represents a seemingly detectable peak but below a level that can
be quantitated.''
---------------------------------------------------------------------------

    As shown in Table 4, Sanchez (2004) also detected perchlorate in
samples of melons, tomatoes, and peppers, but at levels below the
method reporting limit. Perchlorate was not detected in carrots,
onions, sweet corn, squash, and durum wheat. Concentrations of
perchlorate in 10 samples of alfalfa ranged from 109 to 668 [mu]g/kg
FW. Six of the 10 alfalfa samples were sent to FDA for confirmatory
analysis by IC-MS/MS. The FDA results were generally lower than those
of the corresponding samples by Sanchez (2004), ranging from 121 to 382
[mu]g/kg FW.
    Sanchez et al. (2006) conducted studies to evaluate the uptake and
distribution of perchlorate in citrus trees and the occurrence of
perchlorate in lemons, grapefruit, and oranges grown in southern
California and southwestern Arizona. Five whole lemon trees irrigated
with Colorado River water were harvested for destructive sampling.
Sanchez et al. (2006) estimate that the irrigation water had an average
perchlorate concentration of 6 [mu]g/L. Most of the sample analysis was
conducted using IC-MS/MS, having an MRL of approximately 25 [mu]g/kg by
dry weight (DW). In samples of tree trunks, roots, and branches,
perchlorate was close to or below the MRL. Perchlorate was much higher
in the leaves than the fruit (peel and pulp), with mean concentrations
of 1,835 and 128 [mu]g/kg DW, respectively.
    Citrus samples were collected during 2004-2005 from the lower
Colorado River Valley, the University of Arizona Research Farm, the
Coachella Valley, and Los Angeles County. All analyses of fruit pulp
were conducted using IC-MS/MS with an approximate MRL of 2.5 [mu]g/kg
FW. For the 86 citrus samples collected, the perchlorate concentration
in the fruit pulp ranged from below detection to 37.6 [mu]g/kg FW. Mean
concentrations in lemons (33 samples), grapefruit (15 samples), and
oranges (28 samples) were 2.3, 3.3, and 7.4 [mu]g/kg FW, respectively.
    Sanchez et al. (2005b) surveyed perchlorate occurrence in lettuce
and other leafy vegetables produced outside the lower Colorado River
region. Samples were analyzed by IC, with a minimum reporting level of
approximately 20 to 40 [mu]g/kg FW, depending on the leafy vegetable
type. Results of some of the more heavily sampled food items are
presented in Table 4.
    While not shown in Table 4, Sanchez et al. (2005b) performed
additional analysis by partitioning the leafy vegetable samples by type
of culture. Perchlorate was detected in 70 of 268 samples of
conventionally-grown leafy vegetables and 72 of 170 samples of
organically-grown leafy vegetables. The range of perchlorate
concentrations was ND to 104 [mu]g/kg FW in conventional leafy
vegetables and ND to 628 [mu]g/kg FW in organic leafy vegetables.
Sanchez et al. (2005b) analyzed the results using regression analysis
and estimated that the median perchlorate concentration in organically-
grown samples was 2.2 times higher than in conventionally-grown
samples. The regression analysis also suggested that variation among
sampling locations was greater than variation among lettuce types.
    Researchers at Texas Tech University analyzed samples of dairy and
soy milk using IC and/or IC/MS analytical methods with detection limits
of 1 [mu]g/L or better (Kirk et al., 2005). In a study of perchlorate
in dairy milk, Kirk et al. (2005) found mean perchlorate levels of 2.0
[mu]g/L in 47 retail dairy milk samples from 11 states (AK, AZ, CA, FL,
HI, KS, ME, NH, NM, NY, PA), with a range from not detected (ND) to
11.0 [mu]g/L. A single sample of soy milk was analyzed and reported to
contain 0.7 [mu]g/L perchlorate (Kirk et al., 2005). An earlier study
by Kirk et al. (2003) found perchlorate ranging from 1.7 [mu]g/L to 6.4
[mu]g/L in 7 dairy milk samples purchased in a city in Texas.
    Jackson et al. (2005) conducted limited sampling of edible and
forage vegetation in 1 Texas county and in 1 Kansas home garden. In
Texas, wheat and alfalfa were sampled from commercial fields irrigated
with groundwater containing perchlorate from an unknown source, and a
cucumber was sampled from an irrigated home garden. In Kansas,
cantaloupe, cucumber, and tomatoes were sampled from an irrigated home
garden near a slurry explosives site. Researchers used IC for sample
analysis but did not report fresh-weight detection limits. Perchlorate
was detected in all 12 samples of winter wheat heads (whole, including
the chaff) at a mean concentration of 2,000 [mu]g/kg FW but perchlorate
was not detected in wheat endosperm (2 samples)\24\. The mean
perchlorate concentration in 3 samples of alfalfa was 2,900 [mu]g/kg
FW. A cucumber sample from a Texas home garden contained 40 [mu]g/kg FW
perchlorate; a sample of irrigation water from this garden contained
20.7 [mu]g/L perchlorate. In the Kansas home garden, the cucumber
sample contained 770 [mu]g/kg FW perchlorate, the cantaloupe sample
contained 1,600 [mu]g/kg FW perchlorate, and 2 samples of tomato
contained 42 and 220 [mu]g/kg FW perchlorate. The reported
concentration of perchlorate in irrigation water for the Kansas home
garden was 81 [mu]g/L. EPA notes that the perchlorate levels in
irrigation water samples associated with these two home gardens were
significantly higher than in the vast majority of surface and ground
water samples in the US.
---------------------------------------------------------------------------

    \24\ A wheat kernel (seed) has three major parts--the bran, the
germ, and the endosperm. The majority of the wheat kernel is the
endosperm, which is the portion of the kernel that is retained in
refined (white) wheat flours. Whole wheat flours contain endosperm,
wheat bran, and wheat germ in approximately the same proportions as
in the wheat kernel. Wheat flours do not contain the chaff (husk).
---------------------------------------------------------------------------

    Aribi et al. (2006) developed an analytical method for perchlorate
that uses ion chromatography with suppressed conductivity and
electrospray ionization tandem mass

spectrometry (IC-ESI-MS/MS). The method was used to measure perchlorate
in samples of various food products, including fresh/canned fruits and
vegetables, wine, beer, and other beverages. Most samples were
purchased in grocery and liquor stores in greater Toronto, Canada,
between January 2005 and February 2006. Produce samples originated from
many different parts of the world and all samples contained measurable
amounts of perchlorate. However, the survey was limited to only a few
samples of each food. Products from California, Chile, Costa Rica,
Guatemala, and Mexico had the highest levels of perchlorate. Products
from Canada and China had the lowest levels of perchlorate. The highest
detection was in cantaloupe from Guatemala (463.50 [mu]g/kg FW).
Analysis of raw asparagus (39.900 [mu]g/kg FW) and cooked asparagus
(24.345 [mu]g/kg FW) demonstrated that perchlorate can remain in food
processed at a high temperature. Perchlorate concentrations in 8
samples of produce from the U.S. ranged from 0.094 [mu]g/kg FW (for
blueberries) to 19.29 [mu]g/kg FW (for green grapes).
    Aribi et al. (2006) analyzed 77 samples of wine and 144 samples of
beer from many parts of the world. All samples contained measurable
amounts of perchlorate. The wine sample with the single highest
concentration of perchlorate, 50.250 [mu]g/L, was from Portugal.
Overall, wine samples from Chile contained the highest concentrations
of perchlorate, ranging from 5.358 to 38.88 [mu]g/L in 8 samples.
Twelve samples of wine from the U.S. contained perchlorate
concentrations ranging from 0.197 to 4.593 [mu]g/L. Results from
analysis of beer samples varied substantially among countries, with an
overall range from 0.005 [mu]g/L (Ireland) to 21.096 [mu]g/L (France).
Concentrations of perchlorate in 8 beer samples from the U.S. ranged
from 0.364 to 2.014 [mu]g/L.
    Snyder et al. (2006) measured perchlorate in dietary supplements
and flavor enhancing ingredients collected from various vendors in Las
Vegas, NV, and Seattle, WA. Analyses were performed using LC-MS/MS with
a limit of detection between 2 and 5 [mu]g/kg. Perchlorate was detected
in 20 of 31 analyzed supplements, with detectable concentrations
ranging from 10 to 2,420 [mu]g/kg. Based on manufacturers' recommended
intake of the supplements, the resulting daily oral doses of
perchlorate would range from 0.03 to 18 [mu]g/day. Twelve of the
supplements tested were prenatal or children's vitamins. The highest
level of perchlorate (2,420 [mu]g/kg or 0.018 mg/day at the recommended
daily dose) was found in a prenatal vitamin; in the remaining prenatal
and children's vitamins perchlorate did not exceed 28 [mu]g/kg. The
study noted that ``vitamin and mineral supplements are typically
formulated to include the Recommended Daily Allowance (RDA) of iodine,
a factor that would provide protection against any possible impacts of
microgram levels of perchlorate found in these supplements.''
Perchlorate was also detected at 740 [mu]g/kg in a sample of kelp
granules (a flavor enhancer), which equates to 2.2 [mu]g perchlorate
per serving.
    Martinelango et al. (2006a) measured perchlorate in seaweed, which
is often used as a source of iodide in food and nutritional
supplements. Martinelango et al. (2006a) collected samples of 11
different species of seaweed growing off the coast of northeastern
Maine. Perchlorate was detected in all species, with concentrations
ranging from 29 to 878 [mu]g/kg DW. The iodide content in the samples
was much higher, ranging from 16 to 3,134 mg/kg DW. Martinelango et al.
(2006a) found that samples of Laminaria species concentrated iodide
more selectively than perchlorate. Laminaria is a genus of large brown
seaweeds that are commonly used in kelp tablets. Martinelango et al.
(2006a) also analyzed 4 seaweed samples that had been washed with
deionized water and found that a single wash removed 38 to 73 percent
of the perchlorate and 34 to 44 percent of the iodide.

D. Occurrence Studies on Perchlorate in Human Urine, Breast Milk, and
Amniotic Fluid

    Recently researchers have used the results of the analysis of urine
samples to estimate human exposure to perchlorate. Ingested perchlorate
is not metabolized by humans and is excreted largely in the urine
(Merrill et al., 2005). The CDC's National Center for Environmental
Health (NCEH) developed a sensitive and selective analytical method to
analyze perchlorate in human urine (Valentin-Blasini et al., 2005). The
method uses ion chromatography coupled with electrospray ionization
tandem mass spectrometry (IC/MS/MS) and achieves an MRL of 0.025 [mu]g/
L in human urine. The authors report that the method is robust enough
to process first-morning-void urine samples, which are samples of the
first voiding of urine upon waking.
    Valentin-Blasini et al. (2005) analyzed urine samples from 61
healthy adult donors who lived in the area of Atlanta, Georgia. The
urine samples were provided anonymously, without associated donor
information. Perchlorate was detected in all of the urine samples, with
concentrations ranging from 0.66 to 21 [mu]g/L. The authors cited
dietary exposure as a potential source of perchlorate because
perchlorate was found only at low levels (0.1--0.2 [mu]g/L) in area tap
water samples (Valentin-Blasini et al., 2005).
    Valentin-Blasini et al. (2005) also analyzed the urine samples for
creatinine, which is a metabolic breakdown product in muscles that is
eliminated from the body in urine at a predictable rate. When adjusted
for urinary creatinine content, the reported range of perchlorate in
the samples is 1.0 to 35 [mu]g of perchlorate per gram of creatinine.
The median perchlorate concentration was 3.2 [mu]g/L (7.8 [mu]g/g
creatinine). The researchers stated that only 1 sample from the Atlanta
population contained perchlorate at a level slightly in excess of the
amount expected to be excreted by an individual exposed to perchlorate
at the reference dose of 0.0007 mg/kg/day (Valentin-Blasini et al.,
2005). Specifically, assuming that perchlorate is excreted uniformly in
urine throughout the day, a urinary excretion level of 34 [mu]g
perchlorate per gram creatinine would be associated with a daily
perchlorate intake of 0.0007 mg/kg/day, for a 70 kg male that excretes
creatinine at a typical rate of 1.44 grams per day (g/day). These
assumptions are imprecise for individual exposure assessment but allow
for spot urine perchlorate excretion to be related to the reference
dose for toxicological perspective. Estimating perchlorate exposure
from a single spot urine sample (as opposed to a sample collected
continuously over a period of time) is imprecise due to the episodic
nature of perchlorate exposure and the short half-life of perchlorate
in the human body. The precision of estimated individual perchlorate
exposure can be improved by more precise estimation of 24-hour
creatinine excretion based on sex, height, weight, and age as described
by Mage et al. (2004). In addition, imprecision stemming from the
episodic nature of perchlorate exposure can be reduced with increased
sampling.
    The analytical method developed by Valentin-Blasini et al. (2005)
was further used by Blount et al. (2006a) to evaluate urine samples
from 27 volunteers with differing dietary habits. Blount et al. (2006a)
collected first-morning-void urine specimens from volunteers living in
the Atlanta area. The study volunteers self-assessed their consumption
of milk, dairy products, and green/leafy vegetables within the 16 hours
before the sample was collected.

The samples were grouped into 2 categories (``one or fewer servings''
and ``three or more servings'') based on total consumption of these
selected foods. Total daily perchlorate exposure was calculated using a
bodyweight of 70 kg and a creatinine excretion rate of 1.44 g/day,
assuming that each first-morning void urine sample was representative
of that individual's daily perchlorate exposure. Each volunteer also
collected a drinking water sample from home and work. Blount et al.
(2006a) analyzed drinking water samples with the same method used for
urine analysis and estimated exposure from drinking water based on a
body weight of 70 kg and daily consumption of 2 liters of water per
day. The mean creatinine-adjusted urinary perchlorate level was 1.8
times higher for individuals who identified themselves as consuming
three or more servings of milk, dairy products, and/or green/leafy
vegetables (6.13 versus 3.45 [mu]g/g creatinine). There were no
significant differences in the perchlorate levels in the drinking water
samples of the 2 diet groups, which ranged from < 0.05 to 0.25 [mu]g/L
with a median of 0.10 [mu]g/L. Using a median drinking water level of
0.10 [mu]g/L, Blount et al. (2006a) estimated that the perchlorate dose
from drinking water was 0.003 [mu]g/kg/day. Compared to this drinking
water estimate, the total perchlorate dose estimate based on mean
urinary perchlorate excretion was 24 times higher (0.071 [mu]g/kg/day)
and 42 times higher (0.126 [mu]g/kg/day) for the low-consumption and
high-consumption diet groups, respectively. The overall range of
perchlorate found in urine was 0.94 to 17 [mu]g/g creatinine with a
median of 4.2 [mu]g/g creatinine.
    In the largest study of its kind, Blount et al. (2006c) measured
perchlorate in urine samples collected from a nationally representative
sample of 2,820 U.S. residents, ages 6 years and older, as part of the
2001-2002 NHANES. Blount et al. (2006c) detected perchlorate at
concentrations greater than 0.05 [mu]g/L in all 2,820 urine samples
tested, with a median concentration of 3.6 [mu]g/L (3.38 [mu]g/g
creatinine) and a 95th percentile of 14 [mu]g/L (12.7 [mu]g/g
creatinine). Only 0.7% of the study participants had an estimated
perchlorate dose in excess of 0.0007 mg/kg/day. Women of reproductive
age (15-44 years) had a median urinary perchlorate concentration of 2.9
[mu]g/L (2.97 [mu]g/g creatinine) and a 95th percentile of 13 [mu]g/L
(12.1 [mu]g/g creatinine). The demographic with the highest
concentration of urinary perchlorate was children (6-11 years), who had
a median urinary perchlorate concentration of 5.2 [mu]g/L (5.79 [mu]g/g
creatinine). Blount et al. (2006c) estimated a total daily perchlorate
dose for each adult and found a median dose of 0.066 [mu]g/kg/day
(about one tenth of the RfD) and a 95th percentile of 0.234 [mu]g/kg/
day (about one third of the RfD). Eleven adults (0.7%) had estimated
perchlorate exposure in excess of the RfD (0.7 [mu]g/kg/day). The
highest estimated exposure was 3.78 [mu]g/kg/day. Because of daily
variability in diet and perchlorate exposure, and the short residence
time of perchlorate in the body, these single sample measurements may
overestimate long-term average exposure for individuals at the upper
end of the distribution and may underestimate the long-term average
exposure for individuals at the lower end of the distribution. Daily
perchlorate dose is not presented for children and adolescents due to
the limited validation of formulas for these age groups (Blount et al.,
2006c).
    Valentin-Blasini et al. (2005) and T[eacute]llez et al. (2005)
analyzed urine samples of pregnant women in 3 cities in Chile and found
higher median levels of urinary perchlorate in cities with higher
concentrations of perchlorate in tap water. Based on an assessment of
drinking water intake, the researchers determined that, in all 3
cities, there was an additional source of perchlorate for the study
participants that may be explained by dietary (food) intake
(T[eacute]llez et al., 2005). This gap between estimated perchlorate
exposure and perchlorate intake from tap water consumption ranged from
21.7 [mu]g/day to 33.8 [mu]g/day in the 3 Chilean cities (T[eacute]llez
et al., 2005).
    Martinelango et al. (2006b) developed a method to measure
perchlorate in human urine with a limit of detection of 0.080 [mu]g/L,
and reported analytical results of 9 spot urine samples from male and
female volunteers. Perchlorate was present in all samples analyzed, at
concentrations ranging from 2.2 to 14.9 [mu]g/L, with a median value of
8.1 [mu]g/L.
    Other studies have investigated perchlorate in human breast milk.
Kirk et al. (2005) analyzed 36 breast milk samples from 18 states (CA,
CT, FL, GA, HI, MD, ME, MI, MO, NC, NE, NJ, NM, NY, TX, VA, WA, WV) and
found perchlorate concentrations in all samples ranging from 1.4 to
92.2 [mu]g/L in all samples, with a mean concentration of 10.5 [mu]g/L.
T[eacute]llez et al. (2005) report maternal parameters for participants
from the study in Chile. Breast milk samples indicated that a
significant amount of perchlorate leaves the body of the nursing mother
through breast milk, in addition to urine. However, the breast milk
perchlorate levels were highly variable and no significant correlations
could be established between breast milk perchlorate and either urine
perchlorate or breast milk iodide concentrations for the individuals
evaluated in these Chilean cities (T[eacute]llez et al., 2005). Kirk et
al. (2006) evaluated variations of iodide, thiocyanate and perchlorate
in human milk samples. These authors suggest that if the overall intake
of iodide is sufficient, it is unlikely that milk with an occasional
low iodide or high perchlorate content would pose a major risk to
infants. However, their limited data (evaluating only 10 women) show
that the milk of some women may not supply infants with adequate iodide
and they suggest that it may be important to base risk assessments for
perchlorate exposure on the iodide to perchlorate ratio or the ratio of
iodide to a ``selectively-weighted sum of iodide uptake inhibiting
agents.''
    Blount and Valentin-Blasini (2006) developed a sensitive and
selective method for quantifying iodide, perchlorate, thiocyanate, and
nitrate in human amniotic fluid. The analytical limit of detection for
perchlorate was calculated to be 0.020 [mu]g/L. Samples of amniotic
fluid at 15 to 20 weeks gestation were collected from 48 healthy women
in an Eastern U.S. city for analysis. Perchlorate was found in all
samples tested and exhibited a log-normal distribution. The perchlorate
concentrations ranged from 0.057 to 0.71 [mu]g/L with a median value of
0.18 [mu]g/L.

E. Status of the Preliminary Regulatory Determination for Perchlorate

    As stated earlier, the Agency is not making a preliminary
regulatory determination for perchlorate in this notice. The Agency
believes that additional information is needed on the sources of human
exposure if it decides to base its determination regarding health risk
reduction potential on a health reference level (HRL) derived from the
RfD and the relative source contribution (RSC) for drinking water.
Under this approach, the Agency would use the RfD and RSC to estimate
an HRL and then use this HRL as a benchmark against which to conduct an
evaluation of the occurrence data. In conducting such an assessment for
the 6 non-carcinogens discussed previously in this action, EPA used a
20 percent RSC, which is the lowest and most conservative RSC used to
estimate an HRL. Since the initial screening of the occurrence data
against the HRL resulted in a preliminary negative determination, the
Agency found that it

was not necessary to further evaluate the RSC for these contaminants.
In the case of perchlorate, the Agency is not at the point of being
able to make either a negative or a positive determination using this
approach because it is not yet clear what an appropriate RSC for
perchlorate is. If EPA were to use a default RSC of 20% for
perchlorate, the resulting HRL would be 5 [mu]g/L. Approximately 3.16%
of the 3,858 PWSs in the UCMR1 data set had at least one detect of
perchlorate greater than or equal to 5 [mu]g/L. Given this level of
occurrence at the default-derived HRL, the Agency believes a better
informed RSC and HRL would be needed to use this approach to determine
whether regulation of perchlorate in drinking water presents a
meaningful opportunity for health risk reduction.
    Table 5 shows the number of systems and population served that
would exceed the HRL under various RSC scenarios and the sensitivity of
this estimate to relatively small changes in the estimated RSC. For
example, increasing the RSC from 20 to 30 percent would lower the
estimated number of systems impacted by about a third and the estimated
population served by about half. Hence, the choice of an appropriate
RSC and resulting HRL could impact EPA's determination of whether
regulation of perchlorate represents a meaningful opportunity for
health risk reduction if it uses this approach.
    EPA recognizes that system-level population estimates shown in
Table 5 may be conservative because some systems have multiple entry
points to the distribution system and not all entry points had a
positive detection for perchlorate in the UCMR 1 survey. Hence, to
derive a less conservative population estimate (last column in Table
5), EPA assumed that the population for each system is equally
distributed over all of the entry (or sampling) points and estimated a
population-served value based on entry points that had at least 1
analytical detection for perchlorate at levels greater than each of the
HRL thresholds.

                            Table 5.--UCMR 1 Occurrence and Population Estimates for Perchlorate at Various HRL Thresholds a
--------------------------------------------------------------------------------------------------------------------------------------------------------
                                                                                Population
                                                                                Population      estimate for
                                                                                PWS entry or sample     served by PWSs  entry or sample
                                         Estimated HRL thresholds     PWSs with at least 1     points with at least 1   with at least 1   points having
        RSC scenarios (percent)            based on various RSC     detection > threshold of  detection > threshold of    detection >       at least 1
                                              scenarios \b\                 interest                 interest \c\         threshold of     detection >
                                                                                interest \d\     threshold of
                                                                                interest \e\
--------------------------------------------------------------------------------------------------------------------------------------------------------
20....................................  5 [mu]g/L................  3.16% (122 of 3,858).....  1.88% (281 of 14,984)...          14.6 M            4.0 M
30....................................  7 [mu]g/L................  2.13% (82 of 3,858)......  1.14% (171 of 14,984)...           7.2 M            2.2 M
40....................................  10 [mu]g/L...............  1.35% (52 of 3,858)......  0.65% (97 of 14,984)....           5.0 M            1.5 M
50....................................  12 [mu]g/L...............  1.09% (42 of 3,858)......  0.42% (63 of 14,984)....           3.6 M            1.2 M
60....................................  15 [mu]g/L...............  0.80% (31 of 3,858)......  0.29% (44 of 14,984)....           2.0 M            0.9 M
70....................................  17 [mu]g/L...............  0.70% (27 of 3,858)......  0.24% (36 of 14,984)....           1.9 M            0.8 M
80....................................  20 [mu]g/L...............  0.49% (19 of 3,858)......  0.16% (24 of 14,984)....           1.5 M            0.7 M
100...................................  25 [mu]g/L...............  0.36% (14 of 3,858)......  0.12% (18 of 14,984)....           1.0 M            0.4 M
--------------------------------------------------------------------------------------------------------------------------------------------------------
Footnotes:
\a\ These data represent summary statistics for the 3,858 public water systems that have sampled for perchlorate as a part of the UCMR 1 survey.
\b\ HRL threshold = [(RfD of 0.0007 mg/kg/day x 70 kg BW for pregnant female) / (2 L DWI)] x the RSC scenario. Each HRL threshold value is converted
  from mg/L to [mu]g/L units and then rounded to the nearest whole number.
\c\ The entry/sample-point-level population served estimate is based on the system entry/sample points that had at least 1analytical detection for
  perchlorate greater than the HRL threshold of interest. The UCMR 1 small system survey was designed to be representative of the nation's small
  systems, not necessarily to be representative of small system entry points.
\d\ The system-level population served estimate is based on the systems that had at least 1analytical detection for perchlorate greater than the HRL
  threshold of interest.
\e\ Because the population served by each entry/sample point is not known, EPA assumed that the total population served by a particular system is
  equally distributed across all entry/sample points. To derive the entry/sample point-level population estimate, EPA summed the population values for
  the entry/sample points that had at least 1 analytical detection greater than the threshold of interest.

    Table 5 also includes information on the effects of using an RSC of
100% (that is, using an HRL set at the DWEL of 24.5 [mu]g/L, rounded to
a whole number). Crawford-Brown et al. (2006), in an estimate of risk
variability from perchlorate exposure through community water systems,
noted that the subjects in the original 2002 Greer et al., study (on
which the RfD of .0007 mg/L was based) presumably had other sources of
perchlorate exposure outside of the study and suggested that it may be
appropriate to view their results as reflecting the effects of
incremental exposure to perchlorate above the background levels already
in food and water rather than the effects of total exposure, as is
implicitly assumed when the HRL is derived using an RSC to account for
other sources of exposure. Use of an RSC to derive the HRL is clearly
appropriate when the RfD or cancer slope factor is derived from animal
studies with carefully controlled exposure. Crawford-Brown et al.
suggest, however, that an RSC is not necessary for perchlorate because
there is no reason to assume that the background exposure of the study
subjects was different than that of the general population. EPA notes
that the sample size in the Greer study was small and EPA is not aware
of data on their background exposure to perchlorate or how
representative it may be. EPA requests comment on whether information
is available on the background exposure of subjects in the Greer study
and whether it should consider the background exposure of these
subjects in determining an HRL for perchlorate.
    While several States have recommended guidelines or public health
goals for perchlorate, EPA recognizes that at least 1 state,
Massachusetts,\25\ has already promulgated a final drinking water
standard for perchlorate, that other States may set drinking water
standards in the future, and that these standards

could impact national occurrence estimates once these standards are
fully implemented.
---------------------------------------------------------------------------

    \25\ Massachusetts promulgated a final drinking water standard
of 2 [mu]g/L for perchlorate on July 28, 2006. For more information
about the final standard, see http://www.mass.gov/dep/public/press/pchl0706.htm
 (MA DEP, 2006).

---------------------------------------------------------------------------

F. What Are the Potential Options for Characterizing Perchlorate
Exposure and Proceeding With the Preliminary Regulatory Determination
for Perchlorate?

    While the Agency recognizes that food and other pathways may be
important sources of perchlorate exposure, the Agency believes the
currently available food data (summarized in section V.C.3) are
inadequate to develop a better informed RSC (and HRL). First, some of
the existing data are limited in their sample numbers, geographic
coverage, and analytical method adequacy. Second, the current studies
provide little or no data for several food groups (e.g., meat, poultry,
fish, eggs, root and tuber vegetables, brassica vegetables, bulb
vegetables, tree fruits, legumes, and cereal grains) that account for
about half of the diet (by mass) for females of reproductive age (mid-
teens to mid-forties).
    This section presents and requests comment on data EPA might use to
estimate an RSC based on food-borne exposure as well as on several
other options that the Agency is considering to better characterize
perchlorate exposure and assist the Agency in making its regulatory
determination for perchlorate. These options could serve as a
supplement or an alternative to developing an HRL based on a better
informed RSC derived from food concentration and consumption data. The
Agency specifically seeks comment on the use of urine biomonitoring
data in estimating perchlorate exposure. If the Agency decides to use
any of the approaches discussed in V.F.2, EPA will need to determine
what statistics (e.g., mean, median, percentile, etc.) are most
appropriate for consideration in a regulatory determination. The Agency
will also conduct a peer review, as appropriate, of any new methodology
it decides to use.
    The Agency also invites the public to submit relevant data that may
further characterize exposure to perchlorate through consumption of
foods and/or through other pathways. The Agency will consider any new,
relevant information/data provided in response to this action as the
Agency determines whether to regulate perchlorate with a national
primary drinking water regulation.
    1. Use of Food Concentration and Consumption Data to Estimate an
RSC. In the past, the Agency has relied on dietary exposure information
from the FDA Total Diet Study (TDS) to determine the RSC allowed for
drinking water and to set health goals (i.e., Maximum Contaminant Level
Goals) for several inorganic compounds (e.g., antimony, cadmium,
chromium, and selenium). Under the TDS, foods are sampled at retail
outlets, prepared as they would be consumed, and analyzed for a variety
of analytes (e.g., nutrients, pesticides, industrial chemicals).
Approximately 280 foods, covering a broad spectrum of the diet, are
currently sampled in each sampling event. Sampling events (known as
``market baskets'') occur about 4 times per year, with each event being
confined to 1 of the 4 regions of the country. The dietary intake of
the analyzed compounds can be calculated for the U.S. population by
multiplying the concentrations found in TDS foods by the consumption
amounts for each food. FDA compiles food consumption amounts for the
total U.S. population by gender and by age group.\26\
---------------------------------------------------------------------------

    \26\ Information about FDA's TDS design, food list, analytes,
and analytical results can be found at http://www.cfsan.fda.gov/~comm/tds-toc.html.
 (FDA, 2006)

---------------------------------------------------------------------------

    FDA is including perchlorate as an analyte in the 2006 TDS. EPA
believes that a comprehensive dietary intake estimate for perchlorate
will be useful in evaluating dietary exposure relative to drinking
water. When sufficient quantitative exposure data are available (such
as the data published by FDA in conjunction with the TDS), EPA can use
the procedure used previously for several regulated inorganic compounds
(i.e., chromium and selenium) to calculate the relative source
contribution for perchlorate. In these cases where dietary intake
values were available, EPA subtracted the dietary intake value from the
Drinking Water Equivalent Level DWEL and used the remainder as the
allowance for water. This procedure assures that total exposure does
not exceed the RfD.
    The Agency invites the public to submit relevant data that may
further characterize exposure to perchlorate through consumption of
foods and/or through other pathways. This information may help the
Agency in the evaluation of currently available food data and the 2006
TDS.
    2. Use of Urinary Biomonitoring Data to Evaluate Exposure to
Perchlorate. Researchers at CDC's National Center for Environmental
Health (NCEH) have conducted a large national study of total
perchlorate exposure through analysis of urine samples collected for
NHANES 2001-2002 (Blount et al., 2006b and 2006c). The use of urinary
perchlorate excretion to estimate perchlorate exposure has been
demonstrated in Valentin-Blasini et al. (2005), Tollez et al. (2005),
and Blount et al. (2006c). While this would be the first time the
Agency has used biomonitoring data to assist EPA in making a
preliminary regulatory determination for a CCL contaminant, the Agency
believes that estimating perchlorate exposure among large populations
using urinary perchlorate excretion data may be appropriate for the
following reasons:
     Perchlorate is not metabolized in the body and is excreted
unchanged primarily via the renal pathway (Merrill et al., 2005),
     Perchlorate does not bioaccumulate, that is, it is
excreted essentially completely (Merrill et al., 2005),
     Perchlorate has a short half-life in the human body
(approximately 8 hours), simplifying the estimation of daily exposure
(Greer et al., 2002), and
     A methodology exists that allows estimation of daily
perchlorate intake from all sources (e.g., water, food) using standard
creatinine adjustment factors to account for variations in urine
concentration (Mage et al., 2004).
    The Agency could use the 2001-2002 NHANES urine data in several
ways as described in the following paragraphs. The Agency welcomes
comment from the public on these approaches, as well as suggestions for
other analyses that may inform the preliminary regulatory determination
for perchlorate.
    One potential approach is to use the 2001-2002 NHANES urine data to
directly determine whether regulation of perchlorate in drinking water
presents a meaningful opportunity for health risk reduction. More
specifically, we could use the urine data (as in Blount et al., 2006b
and c) to evaluate whether total exposure from food and water is likely
to result in an appreciable risk of adverse health effects for the U.S.
population. If the Agency concluded that total exposure, as estimated
from the urine data, does not pose an appreciable risk, even at the
upper end of the exposure distribution, then it would follow logically
that reducing this exposure by regulating drinking water would not
present a meaningful opportunity for health risk reduction. As
summarized above, Blount et al. (2006c) estimated a median total daily
perchlorate dose for adults of 0.066 [mu]g/kg/day (about one tenth of
the RfD) and a 95th percentile dose of 0.234 [mu]g/kg/day (about one
third of the RfD). Only eleven adults (0.7%) had an estimated dose in
excess of the RfD (0.7 [mu]g/kg/day). EPA requests comment on whether
or not these data provide an adequate basis to support a regulatory

determination for perchlorate. EPA also requests comment on the
relevance, if any, to a regulatory determination for perchlorate, of
the Blount et al (2006b) study, which showed an association between T4/
TSH levels in women and urinary perchlorate concentrations at levels
below the RfD (see Section V.B).
    EPA could also use the 2001-2002 NHANES urine data to qualitatively
evaluate the importance of the water contribution to overall exposure.
For this approach, the Agency could merge data from the 2001-2002
NHANES and UCMR 1 and compare the total perchlorate exposure values
(based on the urine data) for the population of individuals whose
drinking water contains perchlorate at various concentration levels,
ranging from non-detect to the upper end of the occurrence
distribution. The intent of this analysis would be to permit the Agency
to determine whether total perchlorate exposure (as measured in urine)
is meaningfully correlated with concentrations in local public drinking
water supplies, though EPA would only use these results qualitatively
because it is not possible to match up individual urine samples with
individual drinking water exposures. However, the results could be
useful in determining at least qualitatively the potential significance
of drinking water exposure for total exposure. If there were not a
significant correlation between public water system perchlorate
occurrence and individual exposure as measured through biomonitoring,
this might suggest that there is not a meaningful opportunity for
health risk reduction through regulation of drinking water.
    The Agency could also potentially use the 2001-2002 NHANES urine
data to derive an RSC to use for drinking water. This could potentially
be done in several different ways as follows.
    a. Use of Urinary Biomonitoring Total Exposure Value to Estimate an
RSC. One possible approach to estimating an RSC for water would be to
use the urine data to estimate total perchlorate exposure, then
subtract this exposure value from the reference dose and allow the
remainder as the exposure limit for water. The allowed remainder
divided by the RfD would be the RSC for drinking water. This approach
would yield a conservative RSC value because the exposure used to
represent food would actually correspond to both food and drinking
water exposure, whereas, if it were possible to estimate the exposure
from food alone, the relative amount allowed for water would be larger
(resulting in a higher RSC and higher health reference value). As
discussed in Section V.D, Blount et al. (2006c) estimated a total daily
perchlorate dose for adults from urine data and found a median dose of
0.066 [mu]g/kg/day (about one tenth of the RfD) and a 95th percentile
of 0.234 [mu]g/kg/day (about one third of the RfD). If EPA were to use
the estimated 95th percentile total dose from the Blount study as if it
represented the exposure from food alone, this would suggest a residual
screening-level RSC of about 70% allocated to water. One possible
limitation of this approach is that the Blount study estimates exposure
for adults only. Therefore, an RSC developed based upon this data would
not necessarily be representative of children. EPA requests comment on
using this approach as the basis for deriving a screening-level RSC.
    b. Use of the Urine Data and UCMR 1 to Deduce Exposure from Other
Sources and Derive the RSC. Alternately, for those NHANES survey
subjects served by public drinking water systems with positive
detections for perchlorate (based on UCMR 1), EPA could estimate the
expected perchlorate dose contributed by drinking water (using
individual water consumption data from the NHANES survey combined with
UCMR 1 data for the area in which they live) and subtract it from the
total perchlorate dose (based on urinary perchlorate excretion data) to
calculate the amount contributed by food. Subtraction of this
calculated food contribution from the RfD would yield the amount
allowed for drinking water, which could be divided by the RfD to
calculate an RSC. One limitation of this methodology would be the
assumption that subjects in the NHANES study are uniformly consuming
drinking water that contains perchlorate at the concentration indicated
in the UCMR 1 data for their area.
    c. Use of Urinary Biomonitoring Data from Exclusive Bottled Water
Drinkers to Estimate an RSC. The 2001-2002 NHANES data includes urinary
perchlorate data for populations who exclusively drink bottled water.
As noted in section V.C.3.a, FDA (2004) tested 51 samples of bottled
water from 34 distinct sources in 12 states and detected perchlorate in
2 samples (at levels of 0.56 [mu]g/L and 0.45 [mu]g/L). These levels
are well below the MRL for the UCMR 1 data and would not contribute
significant amounts of perchlorate relative to the RfD. If the
population of exclusive bottled water drinkers is sufficiently
representative of the U.S. population, these data potentially could be
used to estimate the contribution of perchlorate exposure coming from
food and allow the Agency to estimate an RSC for drinking water. The
RSC value could be derived by subtracting the estimated perchlorate
exposure for exclusive bottled water drinkers from the RfD of 0.0007
mg/kg/day, using the remainder as the allowance for drinking water. One
limitation of this methodology is that the perchlorate concentration of
the bottled water used by this NHANES population is not known. Hence,
we would have to assume that the bottled water concentration data
collected by FDA (2004) is representative of the perchlorate
concentration in the bottled water used by the NHANES exclusive bottled
water population. Another limitation of this approach is that it would
not subtract out the fraction of the drinking water intake that comes
from water used for cooking purposes (since bottled water is probably
not used by most subjects in cooking and household food preparation).
It would thus produce a conservative (health protective) estimate of
the RSC as it would overestimate the fraction of total exposure coming
from food.

G. Next Steps

    After the Agency evaluates and thoroughly reviews public comments
and any new information/data on perchlorate obtained following this
notice, and performs the necessary analyses, the Agency intends to move
expeditiously to publish a preliminary regulatory determination for
perchlorate. Depending on how quickly the Agency is able to complete
the necessary analyses and determine the best approach for making this
determination, EPA may be able to publish the preliminary determination
in time to include a final determination for perchlorate as part of the
final CCL 2 regulatory determination, which is due by July, 2008. If
not, the Agency will publish its final determination for perchlorate as
soon thereafter as possible. EPA does not intend to wait until the CCL
3 regulatory determination cycle to complete its determination for
perchlorate.

VI. What About the Remaining CCL 2 Contaminants?

    As previously stated, EPA is only making regulatory determinations
on CCL 2 contaminants that have sufficient information to support a
regulatory determination at this time. Section V discusses the status
of EPA's review of perchlorate. For the 30 remaining chemicals and the
9 microbial pathogens, the Agency lacks adequate information in the
areas of health effects or occurrence or both.
    The Agency continues to conduct research and/or to collect
information

on the remaining CCL 2 contaminants to fill identified data gaps.
Stakeholders may be concerned that regulatory determinations for such
contaminants should not necessarily wait until the end of the next
regulatory determination cycle. In this regard, it is important to
recognize that the Agency is not precluded from conducting research,
monitoring, developing guidance or health advisories, and/or making a
determination prior to the end of the next cycle. In addition, the
Agency is not precluded from regulating a contaminant at any time when
it is necessary to address an urgent threat to public health, including
any contaminant not listed on the CCL.
    Because the focus of this action is to announce and solicit public
comment on the Agency's preliminary determinations for 11 of the 51 CCL
2 contaminants, this action primarily provides information on these 11
contaminants. The Agency recognizes that the public may have a
particular interest in metolachlor, methyl tertiary butyl ether (MTBE),
and the microbial contaminants. Therefore, this action includes some
additional information for these contaminants in the following sections
and requests public comment on any further data, information and/or
analyses that the Agency should be aware of.

A. Metolachlor

    1. Background. Metolachlor is a broad spectrum herbicide used for
general weed control in many agricultural food and feed crops
(primarily corn, soybeans and sorghum), on lawns and turf, ornamental
plants, trees, shrubs and vines, rights of way, fencerows and
hedgerows, and in forestry. Metolachlor appears to be moderately
persistent to persistent and depending on the type of soil, can be
highly mobile. Degradation of metolachlor in the environment is
dependent on microbially-mediated and abiotic processes. Metolachlor
has at least 5 major degradates. Two of the more common degradates are
metolachlor ethane sulfonic acid (ESA) and metolachlor oxanilic acid
(OA).
    2. Health. The Agency established an RfD for metolachlor of 0.1 mg/
kg/day based on an NOAEL of 9.7 mg/kg/day and a UF of 100 (USEPA,
1995). The Agency derived the NOAEL from a one-year chronic feeding
study in beagle dogs where the critical effect was decreased body
weight gain. Metolachlor shows some evidence of causing developmental
toxicity effects in rats but none in rabbits. The doses associated with
the developmental effect in rats are greater than the NOAEL and
therefore the NOAEL would be protective against developmental toxicity.
    Metolachlor has been evaluated for carcinogenic activity in both
rats and mice. No treatment-related cancer effects were observed in 2
studies using mice. In studies using rats, metolachlor caused a
significant increase in liver nodules and carcinomas in high dose
females. Negative results from mutagenicity studies suggest that tumors
may result from a nonmutagenic mode of action. In 1991, a peer review
committee recommended that metolachlor be classified as a possible
human carcinogen based on increases in liver tumors in the female rat.
However, a peer review conducted in July 1994 recommended that the
evidence for cancer was suggestive and should not be quantified. This
recommendation was supported by negative mutagenicity data and recent
metabolism data indicating that the formation of the metabolite
presumed to be the ultimate carcinogen is very low (USEPA, 1995).
    3. Occurrence. EPA included metolachlor as an analyte in the UCM
Round 2 survey. EPA evaluated the UCM Round 2 Cross Section data and
found that metolachlor was detected at or above the reporting limit of
0.1 [mu]g/L in 0.83% of the 12,953 systems that sampled for metolachlor
(USEPA, 2006a).
    The USGS NAWQA program included metolachlor as an analyte in its
1992-2001 monitoring survey of ambient surface and ground waters across
the United States. EPA evaluated the results of the provisional data,
which are available on the Web at http://ca.water.usgs.gov/pnsp/

(Martin et al., 2003; Kolpin and Martin, 2003). While the USGS detected
metolachlor in both surface and ground waters, 95 percent of the
samples from the various land use settings were less than 1.38 [mu]g/L.
The maximum surface water concentration is 77.6 [mu]g/L (agricultural
setting) and the maximum estimated ground water concentration is 32.8
[mu]g/L (agricultural setting).
    4. Consideration of the ESA and OA degradates. While EPA has health
and occurrence information for metolachlor itself, the Agency believes
it is prudent to also consider the occurrence and exposure of the ESA
and OA degradates as well. At this time, there is no finished water
occurrence and exposure information for these 2 degradates from a
nationally representative sample of PWSs. However, a few small-scale
studies indicate that the ESA and the OA degradates may be occurring at
greater frequencies and at higher concentrations than the metolachlor
parent (Phillips et al., 1999a and 1999b; Rheineck and Postle, 2000).
In order to gather more information about the occurrence of the ESA and
OA degradates in finished water (along with the metolachlor parent),
the Agency has added these degradates and their parent to the second
unregulated contaminant monitoring regulation (UCMR 2; 70 FR 49093;
USEPA, 2005g). While EPA awaits the results of the UCMR 2 survey, the
Agency is planning to update the health advisory for metolachlor to
include the ESA and OA degradates. The Agency requests comment from the
public as to whether updating the health advisory to include these
degradates will be useful for States and public water utilities.
    In addition, the Agency requests answers to the following questions
and any available data:
     Are States collecting data on the co-occurrence of
metolachlor and its degradates in source waters on a state-wide basis?
In drinking water on a state-wide basis?
     If available, are States willing to provide data on the
co-occurrence of metolachlor and its ESA and OA degradates in community
and public water systems? What analytical method and reporting limit
were used to gather these data?
     Do States have any information on the number of PWSs
impacted by metolachlor and/or its degradates?
     Have States seen an increase or decrease in the number of
PWSs impacted by metolachlor and/or its degradates?
     How many systems have taken wells or sources offline due
to impacts from metolachlor and/or its degradates?

B. Methyl tertiary-butyl ether

1. Background
    Methyl tertiary-butyl ether (MTBE) is a volatile organic compound
synthesized for use as a gasoline additive. First used as an octane
enhancer to improve engine performance, MTBE is also used to reduce
emissions that form carbon monoxide and ozone. Leaking underground
storage tanks, gasoline distribution facilities, and even recreational
boating can release MTBE into the environment.
    In 1997, EPA issued a drinking water advisory of 20 to 40 [mu]g/L
based on taste and odor (USEPA, 1997b). EPA is currently revising its
health risk assessment for MTBE, and thus, will not be making a
regulatory determination for MTBE as part of this action. The IRIS
Chemical Assessment Tracking System http://cfpub.epa.gov/iristrac/index.cfm
 has the most up-to-date information on

the status of the MTBF health risk assessment and interested members of
the public should check that Web site to find out the latest schedule.
    The Agency collected data on MTBE occurrence as part of the UCMR 1
survey. In addition, EPA evaluated several sources of supplemental
occurrence information described in the supporting documentation for
this action entitled ``Regulatory Determinations Support Document for
Selected Contaminants from the Second Drinking Water Contaminant
Candidate List (CCL 2)'' (USEPA, 2006a). Section VI.B.2 provides a
summary of some of the data and information on MTBE occurrence
collected to date.
2. Occurrence Information
    a. UCMR 1. EPA collected sampling results for MTBE from over 98.9
percent (3,068 of 3,100) of the large PWSs and over 99.5 percent (796
of 800) of the small systems required to sample under UCMR 1. Based on
these data, 19 public water systems (0.49 percent of the 3,864 sampled)
in 14 states (CA, CT, GA, IL, MA, MO, NH, NJ, NM, NY, PA, SD, TN, and
WV) reported MTBE occurrence in drinking water. These 19 systems
reported MTBE in 26 samples at the minimum reporting level of 5 [mu]g/L
or above, representing approximately 0.33 percent (or 754 thousand of
226 million) of the population served by the public water systems that
sampled for MTBE. (USEPA, 2006a)
    Of the PWSs reporting detections at or above 5 [mu]g/L (the MRL),
15 were ground water systems and 4 were surface water systems. One
small ground water system (49 [mu]g/L) and 3 large ground water PWSs
(48 [mu]g/L, 36 [mu]g/L, and 33.2 [mu]g/L) reported MTBE at levels
greater than 20 [mu]g/L (the lower end of the taste and odor
threshold). One large surface water system (33 [mu]g/L) reported MTBE
at levels greater than 20 [mu]g/L. The remaining 14 systems had detects
between 5 [mu]g/L and 20 [mu]g/L (USEPA, 2006a).
    b. USGS studies/surveys/reviews. In 2003, the USGS reported results
of national source water sampling (previously introduced in section
III.B.2.a.(2)). USGS sampling included a random study of a
representative sample of untreated source waters (known as the ``Random
Survey'') and a study of source waters from areas known or suspected of
having MTBE (known as the ``Focused Survey''). In the Random Survey,
USGS found that none of the source waters exceeded 20 [mu]g/L, and the
three highest concentration sources ranged from 6 [mu]g/L to 19.5
[mu]g/L (Grady, 2003). Of the areas known or suspected of having MTBE
in the Focused Survey, USGS found that 5 percent (e.g., ground waters
for 7 of the 134 systems) had concentrations greater than 20 [mu]g/L
(Delzer and Ivahnenko, 2003a).
    USGS also reviewed the literature for national, regional, and State
MTBE information (Delzer and Ivahnenko, 2003b), including 13 state-wide
assessments. This information is summarized in Table 6. USGS noted that
because study objectives varied, information varied in terms of
reporting levels, sampling frequencies, and sources (e.g., ambient
water, public and homeowner wells, treated drinking water).
    Previously, USGS (Grady and Casey, 2001) studied MTBE occurrence in
the drinking water of 12 States (New England and the Mid-Atlantic). The
study found less than 1 percent of the CWSs had drinking water samples
at or above 20 [mu]g/L, while 7.8 percent of the CWSs had MTBE at 1
[mu]g/L or higher.
BILLING CODE 6560-50-P
[GRAPHIC] [TIFF OMITTED] TP01MY07.055

BILLING CODE 6560-50-C
    c. New England Interstate Water Pollution Control Commission
(NEIWPCC). In 2003, the NEIWPCC surveyed the States under a grant from
EPA's Office of Underground Storage Tanks (UST). Twenty-six States
estimated that they had public wells that were contaminated by MTBE at
some level, and of those, 5 States (ME,

NH, NJ, DE, and MD) estimated having detectable levels of MTBE in at
least 100 public water supply wells. Thirteen States did not know the
answer, 8 States did not respond, and 3 States reported that no PWS
wells were impacted. The survey established no reporting level to
define ``contamination.'' Only 3 States documented the basis for their
estimates (projected from several studies, raw and treated water
analyses, and a survey of funded petroleum spill projects) (NEIWPCC,
2003).
    d. California Department of Health Services. In 2000, California
developed a drinking water standard of 13 [mu]g/L for MTBE (CA DHS,
2000). According to California's annual compliance reports, there were
no violations of the 13 [mu]g/L standard by public water systems in
2002 and 2003, and 2 violations at 2 public water systems (serving
almost 14,000 people) in 2004 (CA DHS, 2002; CA DHS, 2003; CA DHS,
2004).
    e. Other Sources of Data. In April 2005, the Environmental Working
Group (EWG, 2005) released a report, Like Oil and Water, on their Web
page. In response to Freedom of Information Act requests, 29 State
agencies submitted data to EWG. EPA informally evaluated the data
posted by EWG to determine if this information might be useful in
projecting state-wide occurrence. While EPA found the report
interesting, the data as reported on the Web lacked some of the
information needed to assess the representativeness and the quality of
the data. For example, States submitted different time periods of
monitoring data (e.g., Alaska submitted 7 months of data for 1 system
during the 2000 timeframe and Illinois submitted data that spanned 1990
to 2002). States did not report monitoring results for every system.
Also, the data do not indicate if the samples came from source water or
finished water, from ground water or surface water, the analytical
method used for analysis nor the reporting level, the frequency of the
sampling (e.g., annual, quarterly), number of samples from each water
system, number of non-detects, etc.
3. Request for Additional MTBE Occurrence Information
    As discussed earlier, EPA is not making a regulatory determination
for MTBE; however, EPA is presenting this information because of
ongoing interest in MTBE. And as noted earlier, additional information
is presented in the regulatory support document for this action (i.e.,
USEPA, 2006a). While the Agency waits for the final health risk
assessment, EPA will continue to collect and evaluate occurrence
information. The Agency requests any data, information, or analyses
that may be available on the following topics:
     Are there additional occurrence data for MTBE in community
and non-community public water systems on a state-wide or more local
basis? As noted in the previous section, the State data submitted to
EWG lack some elements needed to assess the quality of the data, as
required in EPA's guidance for information quality guidelines (USEPA,
2003c), and project state-wide occurrence.
     What analytical method and reporting limit were used to
gather these data?
     Has there been an increase or decrease in the number of
impacted PWSs? Over what time frame?
     For those PWSs whose water supplies have been impacted,
has there been an increase or a decrease in the concentration of MTBE?
     How many systems have taken wells or sources offline,
consolidated with other PWSs, or added customers due to impacts from
MTBE?
     What treatments are being used in the field? What range of
treatment effectiveness is being achieved?
     Is the listing of State bans for MTBE shown in Table 7
complete? Have state-wide bans decreased MTBE contamination in drinking
water?

            Table 7.--State Actions Banning MTBE (State-wide)
       [Adapted from USEPA, 2004g and McCarthy and Tiemann, 2005]
------------------------------------------------------------------------
            State                Effective date      Extent of MTBE ban
------------------------------------------------------------------------
Arizona.....................  January 1, 2005.....  0.3% max volume in
                                                     gasoline.
California..................  December 31, 2003...  complete ban in
                                                     gasoline.
Colorado....................  April 30, 2002......  complete ban in
                                                     gasoline.
Connecticut.................  January 1, 2004.....  complete ban in
                                                     gasoline.
Illinois....................  July 24, 2004.......  0.5% max volume in
                                                     gasoline.
Indiana.....................  July 24, 2004.......  0.5% max volume in
                                                     gasoline.
Iowa........................  July 1, 2000........  0.5% max volume in
                                                     gasoline.
Kansas......................  July 1, 2004........  0.5% max volume in
                                                     gasoline.
Kentucky....................  January 1, 2006.....  0.5% max volume in
                                                     gasoline.
Maine.......................  January 1, 2007.....  0.5% max volume in
                                                     gasoline.
Michigan....................  June 1, 2003........  complete ban in
                                                     gasoline.
Minnesota...................  July 2, 2005........  complete ban in
                                                     gasoline.
                                                     (following partial
                                                     ban in 2000).
Missouri....................  July 1, 2005........  0.5% max volume in
                                                     gasoline.
Montana.....................  January 1, 2006.....  no more than trace
                                                     amounts in
                                                     gasoline.
Nebraska....................  July 13, 2000.......  1% max volume in
                                                     gasoline.
New Hampshire...............  January 1, 2007.....  0.5% max volume in
                                                     gasoline.
New Jersey..................  January 1, 2009.....  0.5% max volume in
                                                     gasoline.
New York....................  January 1, 2004.....  complete ban in
                                                     gasoline.
North Carolina..............  January 1, 2008.....  0.5% max volume in
                                                     gasoline.
Ohio........................  July 1, 2005........  0.5% max volume in
                                                     gasoline.
Rhode Island................  June 1, 2007........  0.5% max volume in
                                                     gasoline.
South Dakota................  July 1, 2001........  0.5% max volume in
                                                     gasoline.
Vermont.....................  January 1, 2007.....  0.5% max volume in
                                                     gasoline.
Washington..................  January 1, 2004.....  0.6% max volume in
                                                     gasoline.
Wisconsin...................  August 1, 2004......  0.5% max volume in
                                                     gasoline.
------------------------------------------------------------------------

C. Microbial Contaminants

    1. Evaluation of Microbial Contaminants for Regulatory
Determination. The 9 microbial contaminants listed on CCL 2 include:
     Four virus groups--Caliciviruses, Echoviruses,
Coxsackieviruses, and Adenoviruses
     Four bacteria/bacterial groups-Aeromonas hydrophila;
Helicobacter pylori; Mycobacterium avium intercellulare (or MAC); and
Cyanobacteria (called blue-green algae\27\), fresh water algae, and the
associated toxins
---------------------------------------------------------------------------

    \27\ Cyanobacteria are called blue-green algae even though they
are technically bacteria.
---------------------------------------------------------------------------

     One group of protozoa--Microsporidia (Enterocytozoon
bieneusi and Septata intestinalis, now renamed Encephalitozoon
intestinalis).
    In addition to considering if the Agency had sufficient information
to address the three statutory criteria listed in section II.B.1 (i.e.,
adverse health effects, known/likely occurrence, and meaningful
opportunity for health risk reduction), the Agency also considered
whether sufficient information was available to determine whether
current treatment requirements adequately controlled for any of the 9
microbial contaminants. After consideration of these factors, the
Agency determined that none of the 9 microbial contaminants have
sufficient information at this time to address the three statutory
criteria to make a regulatory determination. Table 8 identifies the
specific areas for which information is insufficient.

                            Table 8.--Information Gaps for the Microbial Contaminants
----------------------------------------------------------------------------------------------------------------
            Health effects                    Treatment           Analytical  methods           Occurrence
----------------------------------------------------------------------------------------------------------------
Microsporidia........................  Aeromonas..............  Aeromonas..............  Aeromonas.
Some Cyanotoxins.....................  MAC....................  MAC....................  MAC.
                                       Adenoviruses...........  Helicobacter...........  Helicobacter.
                                       Caliciviruses..........  Microsporidia..........  Adenoviruses.
                                       Coxsackieviruses.......  Some Cyanotoxins.......  Caliciviruses.
                                       Echoviruses............  .......................  Coxsackieviruses.
                                       Microsporidia..........  .......................  Echoviruses.
                                       Some Cyanotoxins.......  .......................  Microsporidia.
                                       Helicobacter...........  .......................  Some Cyanotoxins.
----------------------------------------------------------------------------------------------------------------

    2. Research and Other Ongoing Activities. EPA has supported an
active research program to fill the information gaps on the CCL 2
microorganisms. While several examples of the ongoing research
activities are listed below, further information on these and other
projects can be found on EPA's Drinking Water Research Information
Network (DRINK). DRINK is a publicly-accessible, Web-based system that
tracks over 1,000 ongoing research projects and can be accessed at:
http://www.epa.gov/safewater/drink/intro.html.

    a. Virus. For the CCL virus groups (or surrogates), the Agency has
initiated treatment studies that simulate realistic conditions where
viruses may be protected in aggregates. EPA also plans to conduct virus
removal/inactivation studies in drinking water treatment plants and/or
pilot plants. In order to assess the effectiveness of treatment and to
perform monitoring studies, methods development for viruses is also in
progress.
    b. Bacteria. For Aeromonas spp., EPA recently completed a one-year
UCMR 1 survey of 293 public water systems. The Agency is currently
attempting to characterize and distinguish pathogenic from non-
pathogenic strains, as well as develop methods to detect Aeromonas
virulence factors. For H. pylori, the Agency is in the process of
developing a culture method and method for its identification. For MAC,
preliminary drinking water surveys have been conducted using a culture
method followed by genetic detection. EPA is also conducting further
research into methods development and the characterization of virulence
factors for this organism.
    EPA has funded projects to evaluate the effect of disinfectants on
cyanotoxins, and on the removal of algal cells and cyanotoxins in a
pilot scale treatment plant. EPA is developing analytical methods for
potential use for future monitoring and has available analytical
chemistry standards for the toxins of most concern in the United
States--microcystin, cylindrospermopsin, and anatoxin-a. EPA has
conducted several small-scale preliminary occurrence surveys for
cyanotoxins using a screening method followed by confirmation by
instrumental analysis. A number of health effects studies are also in
progress on several high priority cyanotoxins. These include behavioral
studies in mice, acute and subacute effects in neonatal mice, and
biomarkers of human exposure. Risk assessments are being conducted at
EPA on the cyanotoxins to determine reference doses where possible. The
Agency has organized and participated in several workshops on
cyanotoxins to assess the state-of-the-science.
    As an interim measure to assist public water utilities, the Agency
is planning to develop an information sheet that discusses pertinent
information on cyanobacteria and some of its key toxins. The document
will discuss the state of the knowledge on the prevention and treatment
of cyanobacteria and its toxins, as well as the available information
on the potential health effects of some of the toxins. EPA requests
comment from the public as to whether such a document would be useful
for public water utilities.
    c. Protozoa. EPA has several ongoing projects to evaluate the
susceptibility of microsporidia to chlorine and chloramine
disinfectants. EPA has sponsored methods-related projects for
microsporidia, which have included the use of fluorescent gene probes,
real-time PCR, concentration methods, and immunomagnetic separation.
Ongoing monitoring at EPA has revealed that microsporidia are present
in ground water. EPA has funded work to determine exposure to