March 31, 1987
ENDRIN
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
INTRODUCTION
The Health Advisory (HA) Program, sponsored by the Office of Drinking
Water (ODW), provides information on the health effects, analytical method-
ology and treatment technology that would be useful in dealing with the
contamination of drinking water. Health. Advisories describe nonregulatory
concentrations of drinking water contaminants at which adverse health effects
would not be anticipated to occur over specific exposure durations. Health
Advisories contain a margin of safety to protect sensitive members of the
population.
Health Advisories serve as informal technical guidance to assist Federal,
State and local officials responsible for protecting public health when
emergency spills or contamination situations occur. They are not to be
construed as legally enforceable Federal standards. The HAs are subject to
change as new information becomes available.
Health Advisories are developed for One-day, Ten-day, Longer-term
(approximately 7 years, or 10% of an individual's lifetime) and Lifetime
exposures based on data describing noncarcmogenic end points of toxicity.
Health Advisories do not quantitatively incorporate any potential carcinogenic
risk from such exposure. For those substances that are known or probable
human carcinogens, according to the Agency classification scheme (Group A or
B), Lifetime HAs are not recommended. The chemical concentration values for
Group A or B carcinogens are correlated with carcinogenic risk estimates by
employing a cancer potency (unit risk) value together with assumptions for
lifetime exposure and the consumption of drinking water. The cancer unit
risk is usually derived from the linear multistage model with 95% upper
confidence limits. This provides a low-dose estimate of cancer risk to
humans that is considered unlikely to pose a carcinogenic risk in excess
of the stated values. Excess cancer risk estimates may also be calculated
using the One-hit, Weibull, Logit or Probit models. There is no current
understanding of the biological mechanisms involved in cancer to suggest that
any one of these models is able to predict risk more accurately than another.
Because each model is based on differing assumptions, the estimates that are
derived can differ by several orders of magnitude.

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This Health Advisory (HA) is based on information presented in the
Office of Drinking Water's Health Effects Criteria Document (CD) for endrin
(U.S. EPA, 1985a). The HA and CD formats are similar for easy reference.
Individuals desiring further information on the toxicological data base or
rationale for risk characterization should consult the CD. The CD is available
for review at each EPA Regional Office of Drinking Water counterpart (e.g..
Water Supply Branch or Drinking Water Branch), or for a fee from the National
Technical Information Service, U.S. Department of Commerce, 5285 Port Royal
Rd., Springfield, VA 22161, PB # 86-117967/AS. The toll-free number is (800)
336-4700; in the Washington, D.C. area: (703) 487-4650.
GENERAL INFORMATION AND PROPERTIES
CAS No. 72-20-8
Structural Formula
H-C-H ICT-C
a
H
Synonyms
° 1,2,3,4,10,1O-Hexachloro-6,7-epoxy-1,4,4a,5,6,7,8,8a-octa-hydro-1,4-
endo, endo-5,8-dimethanonapthalene
Uses
° Organochlorine cyclodiene pesticide once widely used in the U.S.
° EPA cancelled the use of endrin for a number of uses and registration
for new uses of endrin was denied (Federal Register, 1979).
° Endrin is registered presently only for the control of cutworms,
grasshoppers and moles.
Properties (U.S. EPA, 1985a)
Chemical Formula
Molecular Weight
Physical State
Boiling Point
Melting Point
Density
Vapor Pressure
Water Solubility
Octanol/Water Partition
Coefficient
Taste Threshold
Odor Threshold
Conversion Factor
C12HbC160
380.93
solid
245°C
2.7 x 10~7 mm Hg (25°C)
0.24 mg/L (25°C)
2.18 x 10s

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Occurrence
° Endrin is considered to be a persistent compound. Endrin is bio-
degraded poorly. Once in the ground, endrin rapidly binds onto soils
and migrates slowly. Endrin has the potential for bi©accumulation
(U.S. EPA, 1983).
° Endrin has been included in a number of national and regional surveys
of drinking water supplies. Endrin has not been detected in any of
the surveys. Endrin has been detected m a few surface waters. The
highest level reported was 0.008 ug/L.
° Endrin has been reported to occur at very low levels in food and air.
However, the available data are insufficient to evaluate exposures from
these routes or to determine if drinking water is a significant
source of exposure.
° Because endrin is no longer commercially used, future trends are
expected to be lower than current data indicate.
III. PHARMACOKINETICS
Absorption
° Rates of absorption by the oral, dermal and inhalational routes have
not been documented. Absorption has been demonstrated by the
detection of residue levels in animals and humans following exposure
(U.S. EPA, 1985a).
Distribution
° Endrin is distributed (fat, liver, brain, kidneys) and metabolized
rapidly in mammals. The time of sample collection is important
since endrin residues decline rapidly after cessation of exposure
(U.S. EPA, 1985a).
° Both wild and domestic birds, however, store endrin in various body
tissues, especially fat (Terriere et al., 1959; Reichel et al.,
1969).
"Metabolism
° The metabolic pathway for endrin in mammals is complex and species-
dependent. In all species, the unsubstituted methylene bridge (C12)
is attacked preferentially to form mostly anti- and lesser amounts of
syn-12-hydroxyendrin. The syn-isomer is oxidized quickly by micro-
somal mono-oxygenases to produce 12-ketoendrin, which is considered
to be the major toxicant. Glucuronide and sulfate conjugates of the
^nti-isomer are formed (Hutson, 1981; U.S. EPA, 1985a).
0 To a smaller extent, hydroxylation at the 3-position also occurs, and
the epoxide functional group probably is hydrated (U.S. EPA, 1985a).

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0 The rapid metabolism of endrin has been explained in terms of the steric
influence of the epoxide anion or C-12 hydroxylation in promoting
anti—C—12-hydroxylation. The bulky hexachlorinated fragment inhibits
attack at C-3 and C-4 (U.S. EPA, 1985a).
Excretion
° Endrin is eliminated rapidly in both humans and in animals. A half-
life of 1 to 2 days in blood serum was estimated for humans (U.S. EPA,
1985a).
° Anti-12-hydroxyendrin as the glucoronide has been detected in both the
feces and urine of endrin workers (Baldwin and Hutson, 1980), but
12-ketoendrin was not detected (Hutson, 1981). Analysis of D-glucunc
acid in urine is a useful test for endrin exposure (Vrij-Standhardt
et al., 1979).
° In rats, over 50 percent of endrin metabolites are eliminated in the
bile within 1 day as the glucuronides of anti-12-hydroxyendrin (Hutson
et al., 1975). In rabbits, the metabolites are conjugated with
sulfate and excreted in the urine (Bedford et al., 1975b). This
behavior is consistent with molecular weight thresholds for biliary
excretion, which are 325 *50 in the rat and 475 *50 in the rabbit
(Hirom et al., 1972).
IV. HEALTH EFFECTS
Humans
° Exposure to endrin may cause sudden convulsions which may occurr
from 30 minutes to 10 hours after exposure. Headache, dizziness,
sleepiness, weakness and loss of appetite may be present for 2 to 4
weeks following this exposure.
° A number of deaths have occurred from swallowing endrin. In less
severe cases of endrin poisoning, the complaints include headache,
dizziness, abdominal discomfort, nausea, vomiting, insomnia, agitation
and mental confusion (U.S. DHHS, 1978).
° Electroencephalograms (EEGs) show dysrrhythmic changes which frequently
precede convulsions; withdrawal from exposure usually results in a
normal electroencephalogram within 1 to 6 months (U.S. DHHS, 1978).
* Several incidents of endrin poisoning from contaminated flour have
been reported. In Wales, bread made from flour contaminated with
endrin during shipment in a railway car resulted in 59 poisoning
cases with no deaths in 1956 (Davies and Lewis, 1956). The bread
contained endrin at up to 150 mg/kg bread; the smallest dosage level
to elicit serious effects was calculated to be 0.2 mg/kg bw. Incidents
also have occurred in Doha, Qatar and Hofuf, Saudi Arabia (Weeks,
1967; Curley et al., 1970).

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° No illnesses were noted when 1% endrin was applied at 544-634 kg/acre
as an emulsifiable concentrate for mouse control at a calculated
dermal dose of 0.28 mg/kg/day in combination with a calculated
respiratory exposure of 0.0011 mg/kg/day (Wolfe et al., 1963).
° Concentrations of endrin in the blood of 45 operators from an endrin
processing plant were determined at least once a year from 1964 to
1968 (Jager, 1970). The threshold level of endrin in the blood below
which no sign or symptoms of intoxication were seen was 0.050-0.100
ug/ml. The half-life of endrin in the blood, and thus in the body,
was estimated to be approximately 24 hours. Medical files and routine
medical examinations revealed no abnormalities other than those that
would be expected in any group of 233 long-term workers (4 to 13.3
years' exposure). Determinations of alkaline phosphatase, SGOT,
SGPT, LDH, total serum proteins and the spectra of serum proteins
did not show any changes that could be correlated with the level or
duration of exposure to these insecticides for these parameters. In
all cases of intoxication characterized by typical EEG changes, EEG
patterns returned to normal.
° Cases of fatal endrin poisoning have been reported from intentional
and accidental ingestion. Tewari and Sharma (1978) reported 11 fatal
poisonings; the time periods from administration of the pesticide
(route not known in seven cases) to death ranged from 1 to 6 months.
Endrin ingestion with milk or alcohol appeared to increase toxicity
as death occurred within an hour or two. Increased toxicity was
attributed by the authors to more rapid absorption through the GI
tract.
Animals
Short-term Exposure
° The acute oral LD^q of endrin given to mammals by gavage ranges from
2.3 mg/kg to 43.4 mg/kg (U.S. EPA, 1985a).
° Revzin (1968) reported an increase in the amplitude of the EEG and a
tendency toward spiking after 7 daily doses of endrin at 0.2 mg/kg in
rats. No effects were noted after 1 or 2 days' exposure at the same
dose level in monkeys.
° Speck and Maaske (1958) reported EEG changes and occasional convulsions
after 1 week of daily oral doses of 3.5 mg/kg bw in rats. No effects
were reported when the rats were dosed with 0.8 and 1.7 mg/kg bw.
° Bedford et al. (1975a) determined the acute oral LDjq values (based
on 10-day mortality) for three metabolites of endrin which have been
identified in mammals. Each metabolite was more toxic than the parent
pesticide. 12-Ketoendrin and syn-1 2-hydroxyendrin were about 5 times
more toxic in male rats, and anti-12-hydroxyendrin 2 times more toxic
than endrir itself in male rats. In females, 12-Ketoendrin was 5 times
and syn-12-hydroxyendrin 2 times more toxic than endrin.

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Long-term Exposure
° In an NCI (1979) study both mice and rats (fifty animals of each sex
constituted a treatment group of rats and mice) were exposed chronically
to endrin. The mice were administered a time-weighted-average (TWA)
concentration in the diet of 1.6 or 3.2 mg/kg/day, while the rats
received 3 or 6 ppm. Neither mortality nor body weights were affected
by either dose. According to the investigators, a variety of clinical
signs (alopecia, diarrhea, epistaris, rough hair coats, etc.) were
observed in the exposed rats. However, these findings and interpre-
tations were questioned by another reviewer (Reuber, 1979). These
have been explained in the support document (U.S. EPA, 1985a).
° Deichmann et al. (1970) administered endrin to rats at concentrations
of 2, 6 or 12 mg/kg/day in the diet for up to 37 months. There was
no significant effect on mean body weight or weight gain in endnn-
treated rats. Signs of toxicity observed during the course of the
experiment were limited to episodes of tremors and clonic convulsions
with "outcries". These signs were dose-related; however, no further
details were provided. Histologic changes in the livers of rats fed
endrin (2, 6 or 12 ppm) were similar to those receiving the control
diet with the exception of a moderate increase in the incidence of
centrilobular cloudy swelling. There was also an increase in cloudy
swelling of the renal tubular epithelium. Even though the authors
stated that the effects were not dose-related, the presence of centri-
lobular swellings and cloudy swellings of the renal tubular epithelium
are suspect.
° Nelson et al. (1956) exposed adult Sprague-Dawley rats to endrin at
1, 5, 25, 50 and 100 mg/kg/day in the diet for 16 weeks. A dose-
dependent increase in alkaline phosphatase levels was observed, while
body weights in all exposed groups decreased in comparison with
controls after 16 weeks. All rats receiving 100 ppm endrin died
within the first two weeks of exposure. Rats exposed to 25, 50 or
100 ppm manifested convulsive spasms.
° Beagle dogs (4/group) were exposed to endrin at 1, 3 or 4 ppm in the
diet for 18.7 months. Body weight gains were depressed in the 4 ppm
but not in the 1 or 3 ppm groups. Kidney and heart weights were
significantly greater in the 3 ppm but not in the 1 ppm group. Based
upon increases in kidney and heart weights, the NOAEL for chronic
exposure of dogs is determined to be 0.045 mg/kg bw/day (Treon and
Cleveland, 1955).
° Rats (20 males and 20 females/group) were exposed to endrin at 1, 5,
25, 50 and 100 ppm in the diet for 2 years. The average length of
survival was decreased significantly in females exposed to 25 ppm or
greater and males exposed to 50 ppm or greater. Diffuse degeneration
o" the brain, liver, kidneys and adrenals was reported in animals
tnat died during exposure. Based upon liver weight change, the NOAEL
was determined to be 1 ppm (0.05 mg/kg/ bw assuming daily food intake
is 5% of body weight) (Treon and Cleveland, 1955).

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Reproductive Effects
° No information was found in the available literature on the repro-
ductive effects of endrin.
Developmental Effects
° Endrin administered by oral gavage to Golden Syrian hamsters on days
5 to 14 of gestation resulted in maternal lethality at doses of 1.5
mg/kg/day or greater. Fetal toxicity (including increased mortality,
reduced fetal weight and reduced skeletal ossification) resulted at
doses above 0.75 mg/kg/day (Chernoff et al., 1979).
° Golden Syrian hamsters were exposed to single oral doses of 5 mg/kg
(half the LD50) on days 7, 8 or 9 of gestation and sacrificed on day
14. A statistically significant increase in the incidence of fused
rib and cleft palate occurred. A marked and statistically significant
increase in fetal deaths was observed (Ottolenghi et al., 1974).
0 CD Rats were exposed to 0.075, 0.15 or 0.30 mg/kg/day by oral gavage
on days 7-15 of lactation (Gray et al., 1981). Pups from the 0.15
mg/kg and 0.30 mg/kg groups were 30 percent more active in terms of
locomotor activity than controls before weaning but not as adults.
Pup survival and growth were not affected. The dose of 0.075 mg/kg
appeared to have no effect on behavior.
0 Kavlock et al. (1981) reported that endrin was not teratogenic or
embryolethal in the CD rat when administered by gavage on days 7 to 20
of gestation. Doses of 0.075 mg/kg and 0.15 mg/kg had no effect on
maternal weight gain or on the fetus. Doses of 0.3 mg/kg and 0.45 mg/kg
caused a decrease in maternal weight with no effect on the fetus.
Mutagenicity
0 Endrin was not mutagenic in a Salmonella typhimurium reverse mutation
assay using strains TA1536, TA1537, TA1538, TA98 or TA100 or in
Escherichia coli WP2 her (Ames et al., 1975).
0 Endrin exposure of primary rat or hamster hepatocytes did not
result in increased unscheduled DNA synthesis (Probst et al., 1981;
Williams, 1980).
0 Adult Drosophilia were exposed to endrin by abdominal injection and
the Muller-5 test for recessive lethal mutation on the x-chromosome
was performed (Benes, 1969). No positive responses for endrin or
other chlorinated pesticides tested were reported.
Carcinogenicity
0 The potential oral carcinogenic effect of endrin was evaluated in
Carworth Farm rats (Treon and Cleveland, 1955), Osborne-Mendel rats
(Deichmann et al., 1970; NCI, 1979), C57Bi/CJ mice (Witherup et al.,
1970), C3D2Fi/J mice (Witherup et al., 1970) and B6C3Fi mice (NCI,

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1979). The results were negative in all of these studies. Treon and
Cleveland (1955) also failed to note any increase in tumorigenesis in
dogs exposed to endrin up to 18.7 months at the maximum tolerated
dose. Details of various investigations have been given in the support
document (U.S. EPA, 1985a).
° The only positive carcinogenic effects of endrin were reported by
Reuber (1978, 1979). Reuber's criteria appear to differ from those
of other investigators (U.S. EPA, 1985a).
V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
Health Advisories (HAs) are generally determined for One-day, Ten-day,
Longer-term (approximately 7 years) and Lifetime exposures if adequate data
are available that identify a sensitive noncarcinogemc end point of toxicity.
The HAs for noncarcinogenic toxicants are derived using the following formula:
HA = (NOAEL or LOAEL) x (BW) = 	 mg/L (	 Ug/L)
(UF) x ( L/day)
where:
NOAEL or LOAEL =
BW =
UF =
L/day =
One-day Health Advisory
The study by Revzin (1968) is selected as the basis for the One-day HA.
In this study, Revzin reported alterations in the EEG of squirrel monkeys
after 7 daily doses of 0.2 mg/kg endrin. No effects were noted, however, at
this dose level for shorter exposures. Thus, 0.2 mg/kg can be considered a
NOAEL for a one-day exposure. If this study were considered suitable for the
development of a One-day HA, it would be derived as below. This study is
supported by Davis and Lewis (1959) and Hayes (1963).
One-day HA = (0.2 mg/kg/day) (10 kg) = 0.02 mg/L
(100) (1 L/day)
where:
0.2 mg/kg/day = NOAEL based on absence of EEG changes in squirrel
monkeys after one-day exposure.
No- or Lowest-Observed-Adverse-Effect-Level
in mg/kg bw/day.
assumed body weight of a child (10 kg) or
an adult (70 kg).
uncertainty factor (10, 100 or 1,000), in
accordance with NAS/ODW guidelines.
assumed daily water consumption of a child
(1 L/day) or an adult (2 L/day).

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10 kg = assumed body weight of a child.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal stady.
1 L/day = assumed daily water consumption of a child.
Based upon data from Davies and Lewis (1956) in which the human response
to ingestion of bread contaminated with 150 ppm endrin was reported, Hayes
(1963) estimated that the dosage necessary to produce a single convulsion in
man is about 0.25 mg/kg. If this estimate were considered suitable for the
development of a One-day HA, it would be derived thusly:
One-day HA = (0.25 mg/kg/day) (10 kg) = 0.025 mg/L
(100) (1 L/day)
where:
0.25 mg/kg/day - minimum-effect level for convulsions in humans.
10 kg = assumed body weight of a child.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for'use with a LOAEL from a human study.
1 L/day = Assumed daily water consumption of a child.
It is recommended that a concentration of 0.02 mg/L for a child be
accepted as the One-day HA for endrin. The derivations from the human data
are based upon rather severe effects and dosages are estimated rather than
actual measurements. The HAs based upon the Hayes (1963) estimates, however,
are only slightly greater than the ones developed using the Revzin (1968)
study and, thus, provides some support for the recommended values.
Ten-day Health Advisory
In the teratology studies by Kavlock et al. (1981) decreases in maternal
weights were reported for rats dosed orally for 14 consecutive days with 0.3
but not 0.15 mg/kg bw endrin. If this study were considered suitable for the
development of a Ten-day HA, it would be derived thusly:
Ten-day HA = (0.15 mg/kg/day) (10 kg) _ 0.015 mg/L
(100) (1 L/day)
where:
0.15 mg/kg/day = NOAEL for short-term effects in exposed animals.
10 kg = assumed body weight of a child.
100 = uncertainty fact.or, chosen in accordance with NAS/ODW
guidelines for vise with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.

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The study by Kavlock et al. (1981) is appropriate to calculate the
Ten-day HA. In this study behavioral effects in offspring o.f rats treated
for 14 consecutive days with 0.15 but not 0.075 mg/kg endrin were reported.
Using a NOAEL of 0.075 mg/kg/day, the Ten-day HA is calculated as follows:
Ten-day HA = (0.075 mg/kg/day) (10 kg) = 0.0075 mg/L
(100) (1 L/day)
where:
0.075 mg/kg/day = NOAEL based on absence of behavioral changes in
offspring of exposed rats.
10 kg = assumed body weight of a child.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.
Nelson et al. (1956) reported that body weights of rats exposed 13 weeks
to 5 ppm endrin but not 1 ppm in the diet decreased relative to controls. If
this study were considered suitable for the development of a Ten-day HA, it
would be derived thusly:
Ten-day HA = (0.05 mg/kg bw/day) (10 kg) = ,005 mg/L
(100) (1 L/day)
where:
0.05 mg/kg/day = NOAEL for body weight changes in rats based upon
1 ppm in the diet.
10 kg = assumed body weight of a child.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.
It is recommended that a concentration of 0.005 mg/L for a child, based
on Nelson et al. (1956), be accepted as the Ten-day HA for endrin. Depressed
body weight is considered to be an adequate indication of detrimental effect.
Behavioral effects in offspring of rats administered similar doses provide
additional support for this HA.
Longer-term Health Afl
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food intake, the daily dose for the 1 mg/kg/day group varied from 0.045-0.12
mg/kg bw.
The Longer-term HAs are calculated as follows:
For a child;
Longer-term HA = <0»045 mg/kg/day) (10 kg) = 0.0045 mg/L (4.5 ug/L)
(100) (1 L/day)
where:
0.045 mg/kg/day = NOAEL-based on absence of heart and kidney weight
changes in dogs.
10 kg = assumed body weight of a child.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
1	L/day = assumed daily water consumption of a child.
For an adult:
Longer-term HA = (0«045 mg/kg/day) (70 kg) = q.016 mg/L (16 ug/L)
(100) (2 L/day)
where:
0.045 mg/kg/day = NOAEL based on absence of heart and kidney weight
changes in dogs.
70 kg = assumed body weight of an adult.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
2	L/day = assumed daily water consumption of an adult.
Lifetime Health Advisory
The Lifetime HA represents that portion of an individual's total exposure
that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure. The Lifetime HA
is derived in a three step process. Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI). The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
the NOAEL (or LOAEL), identified from a chronic (or subchronic) study, divided
by an uncertainty factor(s). From the RfD, a Drink ng Water Equivalent Level
(DWEL) can be determined (Step 2). A DWEI? is a medium-specific (i.e., drinking
water) lifetime exposure level, assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health effects would not be expected to occur.
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The DWEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult. The Lifetime HA is determined in Step 3 by factoring in other sources
of exposure, the relative source contribution (RSC). The RSC from drinking
water is based on actual exposure data or, if data are not available, a
value of 20% is assumed for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals. If the contaminant is classifed as a
Group A or B carcinogen, according to the Agency's classification scheme of
carcinogenic potential (U.S. EPA, 1986), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.
The chronic study in dogs by Treon and Cleveland (1955) is also used to
calculate the Lifetime HA.
Using the NOAEL of 0.045 mg/kg/day, the Lifetime Health Advisory is
calculated as follows:
Step 1: Determination of the Reference Dose (RfD)
RfD = (0.045 mg/kg/day) = 0.000045 mg/kg/day
(100) (10)
where:
0.045 mg/kg/day = NOAEL based on absence of effects on heart and
kidney weight changes in dogs.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
10 = uncertainty factor, appropriate for question
regarding dietary intake (discrepancy between
published and unpublished studies).
Step 2: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL = (0.000045 mg/kg/day) (70 kg) = 0.0016 mg/L (1.6 ug/L)
(2 L/day)
where:
0.000045 mg/kg/day = RfD.
70 kg = assumed body weight of an adult.
2 L/day = assumed daily water consumption of an adult.
Step 3: Determination of the Lifetime Hi-alth Advisory
Lifetime HA = 0.0016 mg/L x 0.20 = 0.00032 mg/L (0.32 ug/L)
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where:
0.0016 mg/L = DWEL.
0.20 = assumed relative source contribution from water.
Evaluation of Carcinogenic Potential
° Assessment of the evidence for carcinogenicity of endrin in either
humans or animals suggests that no potential exists. As a result, a
quantitative risk estimate for cancer induction was not derived.
° IARC has not evaluated the carcinogenic potential of endrin.
° Applying the criteria in the guideline for assessment of carcinogenic
risk (U.S. EPA, 1986), endrin is classified in Group E: No evidence
of carcinogenicity in at least two adequate animal tests or in both
epidemiologic and animal studies.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
° The U.S. EPA (1975) has set an interim standard for endrin in finished
drinking water of 0.0002 mg/L or 0.2 ug/L.
° The U.S. EPA (1980) proposed an ambient water criterion for endrin of
0.001 mg/L or 1 ug/L.
° The World Health Organization (FAO/WHO, 1973) established as a guide-
line a maximum intake of 2 ug/kg/day.
VII. ANALYTICAL METHODS
0 Determination of endrin is by a liquid-liquid extraction gas chromato-
graphic procedure (U.S. EPA, 1978; Standard Methods, 1985). Specifi-
cally, the procedure involves the use of 15% methylene chloride in
hexane for sample extraction, followed by drying with anhydrous sodium
sulfate, concentration of the extract and identification by gas
chromatography. Detection and measurement is accomplished by electron
capture, microcoulometric or electrolytic conductivity gas chromato-
graphy. Identification may be corroborated through the use of two
unlike columns or by gas chromatography-mass spectroscopy (GC-MS).
The method sensitivity is 0.001 to 0.010 ug/L for single component
pesticides and 0.050 to 1.0 ug/L for multiple component pesticides
when analyzing a 1-liter sample with the electron capture detector.
VIII. TREATMENT TECHNOLOGIES
° Treatment technologies which are capable of removing endrin from
drinking water include adsorption by activated carbon, both granular
and powdered (GAC and PAC, respectively), air strippirg, reverse
osmosis (RO) and coagulation/filtration.
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° Dobbs and Cohen (1980) developed adsorption isotherms for a number
x of organics, including enarin. Based upon the isotherm data, they
reported that activated carbon exhibited absorptive capacities of
106 mg, 17 mg and 2.7 mg of endrin at initial endrin concentrations
of 100 ug/L, 10 ug/L and 1 ug/L, respectively.
° One study was undertaken to evaluate a number of water treatment
processes by PAC for pesticide removal (U.S. EPA, 1985b). PAC was
examined by conducting test runs with initial concentrations (1 to
10 ug/L) of pesticide in distilled and river water. The distilled
water was spiked with the required concentration of endrin, PAC was
added and mixed with the water. The river water was used in a pilot
plant where it was mixed with PAC. Based upon the reported results,
PAC treatment appears to be an effective technology for the removal
of endrin.
° A RO pilot plant in Miami, Florida, was evaluated for the removal of
certain organic chemicals, including endrin. The RO unit showed 90+%
removal of endrin from an initial concentration of 1 ug/L.
° A study pilot plant was used to test the effectiveness of conventional
treatment in removing endrin. In this study, the treatment scheme
consisted of the addition of alum, flocculation, sedimentation and
sand filtration. The results indicated that alum coagulation removed
about 35% of the endrin, no matter what the initial concentration was.
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Endrin
March 31, 1987
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