August, 1987
DIELDRIN
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
DRAFT
I. 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 x
(approximately 7 years, or 10% of an individual's lifetime) and lifetime
exposures based on data describing noncarcinogenic 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 car differ by several orders of magnitude.
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Dieldrin
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II. GENERAL INFORMATION AND PROPERTIES
CAS No. 60-57-1
Structural Formula
Cl
Cl
Dieldrin; 3,4,5,6,9,9-hexachloro-1a,2,2a, 3,6,6a,7,7a-octahydro-
2, 7: 3,6-dimethanonaphth[2,3-b]oxirene (Windholz, 1983).
Synonyms
HEOD; Alvit; Quintox; Octalox (IPCS, 1987).
Uses
0 Formerly used for control of soil insects, public health insects,
termites and many other pests. These uses have been cancelled and
manufacture discontinued in the United States (Meister, 1983).
Properties (MAS, 1977; Weast and Astle, 1982; Windholz, 1983)
Chemical Formula
Molecular Weight
Physical State
Boiling Point
Melting Point
Density
Vapor pressure (20°C)
Water Solubility (25°C)
Log Octanol/water Partition
Coefficient
Taste Threshold
Odor Threshold (water)
Conversion Factor
C12H8C160
380.93
Crystals
175 to 176°C
*>•>
3.1 x 10~6 mm Hg
0.25 mg/L
0.04 mg/L
Occurrence
Dieldrin has been found in 9,809 of 52,453 surface water samples
analyzed and in 217 of 6,042 ground water samples (STORET, 1987).
Samples were collected at 8,831 surface water locations and 4,522
ground water locations, and Dieldrin was found in 48 states, Canada
and Puerto Rico. The 85th percentile of all nonzero samples was
0.01 ug/L in surface water and 0.10 ug/L in ground water sources.
The maximum concentration found was 301 ug/L in surface water and in
10.08 ug/L in ground water.
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Dieldrin August, 1987
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Environmental Fate
0 Dieldrin is stable and highly persistent in the environment.
0 Dieldrin has the longest half-life of the chlorinated hydrocarbons in
water 1-m deep (half-life - 723 days) (MacKay and Wolkoff, 1973).
III. PHARMACOKINETICS
Absorption
0 A single oral dose of dieldrin at 10 rag/kg body Weight (bw) administered
in corn oil to male Sprague-Dawley rats produced consistent concentrations
of dieldrin in plasma, muscle, brain, kidney and liver for periods up
to 48 hours suggesting slow absorption of the substance (Hayes, 1974).
Distribution
0 Rats given a single oral dose of dieldrin at 10 mg/kg showed concen-
trations of dieldrin in fat, muscle, liver, blood, brain and kidney.
The highest concentration of dieldrin was in fat. The lowest con-
centration was in the kidney (Hayes, 1974).
Metabolism
0 Both the CFE rat and CF1 mouse, following a single oral dose of
dieldrin (not less than 85% HEOD) at 3 and 10 mg/kg in olive oil,
respectively, metabolized dieldrin to 9-hydroxydieldrin, 6,7^trans-
dihydroaldrindiol and some unidentified metabolites. The rat, but
not the mouse, also metabolized dieldrin to pentachloroketone (Baldwin
and Robinson, 1972).
Excretion
0 Female rats infused with total doses of 8 to 16 mg 36ci-dieldrin/kg bw
excreted approximately 70% of the infused dose in the feces over a
period of 42 days, while only about 10% of the dose was recovered in
the urine. Excretion was markedly increased by restriction of the
diet indicating that the1 concentration of dieldrin in the blood
increased as fat was mobilized (Heath and Vandekar, 1964).
IV. HEALTH EFFECTS
Humans
Dieldrin has been reported to cause hypersensitivity and muscular
fasciculations that may be followed by convulsive seizures and
respective changes in the EEC pattern. Acute symptoms of intoxication
include hyperirritability, convulsions and/or coma sometimes accompanied
by nausea, vomiting and headache, while chronic intoxication may result
in fainting, muscle spasms, tremors and loss of weight. The lethal
dose for humans is estimated to be about 5 g (ACGIH, 1984).
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Dieldrin August, 1987
Animals
Short-term Exposure
0 RTECS (1985) reported the acute oral LDs0 values of dieldrin in the
rat, mouse, dog, monkey, rabbit, pig, guinea pig and hamster as 38.3,
38, 65, 3, 45, 38, 49 and 60 mg/kg, respectively.
Dermal/Ocular Effects
0 Aldrin or Dieldrin (dry powder) applied to rabbit skin for 2 h/day,
5 days/week had no discernible effects (IPCS, 1987).
Long-term Exposure
0 Groups of Osborne-Mendel rats, 1 2/sex/level, were fed 0, 0.5, 2, 10,
50, 100 or 150 ppm dieldrin (recrystallized, 100% active ingredient)
in their diet for 2 years. These doses correspond to approximately
0, 0.025, 0.1, 0.5, 2.5, 5.0 or 7.5 mg/kg/day, respectively (Lehman,
1959). Survival was markedly decreased at levels of 50 ppm and
above. Liver-to-body weight ratios were significantly increased at
all treatment levels, with females showing the effect at 0.5 ppm and
males at 10 ppm and greater. Microscopic lesions were described as
being characteristic of chlorinated hydrocarbon exposure. These
changes were minimal at the 0.5 ppm level. Male rats, at the two
highest dose levels (100 and 150 ppm), developed hemorrhagic and/or
distended urinary bladders usually associated with considerable
nephritis (Fitzhugh et al., 1964). A Lowest-Observed-Adverse-Effect-
Level (LOAEL) of 0.025 mg/kg/day, the lowest dose tested, was identified
in this study.
0 Dogs, one/sex/dose level (two/sex at 0.5 mg/kg/day), fed dieldrin
(recrystallized, 100% active ingredient) at 0.2 to 10 mg/kg/day,
6 days/week for up to 25 months, showed toxic effects including weight
loss and convulsions at dosages of 0.5 mg/kg/day or more. Survival was
inversely proportional to dose level. No toxic effects, gross or
microscopic, were seen at a dose level of 0.2 mg/kg/day (Fitzhugh et
al., 1964).
0 Groups of Carworth Farm "E" strain rats, 2 5/ sex/dose level, were fed
dieldrin (>99% purity) in the diet at 0.0, 0.1, 1.0 or 10.0 ppm for
2 years. These doses correspond to approximately 0, 0.005, 0.05 or
0.5 mg/kg/day, respectively (Lehman, 1959). At 7 months, the 1-ppm
intake level was equivalent to approximately 0.05 and 0.06 mg/kg/day
for males and females, respectively. No effects on mortality, body
weight, food intake, hematology and blood or urine chemistries were
seen. At the 10-ppm level, all animals became irritable after 8 to
13 weeks of treatment and developed tremors and occasional convulsions.
Liver weight and liver-to-body weight ratios were significantly
increased in females receiving both 1.0 and 10 ppm. Pathological
findings described as organochlorine-insecticide changes of the liver
were found in one male and six females at the 10-ppm level. No
evidence of tumor igenesis was found (Walker et al., 1969).
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Dieldrin August, 1987
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0 Groups of beagle dogs (five/sex/dose) were treated daily by capsule
with dieldrin (>99% purity) at 0.0, 0.005 or 0.05 rag/kg in olive oil
for 2 years. No treatment-related effects were seen in general
health, behavior, body weight or urine chemistry. A significant
increase in plasma alkaline phosphate in both sexes and a significant
decrease in serum protein concentration in males receiving the high
dose were not associated with any clinical or pathological change.
Liver weight and liver-to-body weight ratios were significantly
increased in females receiving the high dose, 0.05 mg/kg/day, but no
gross or microscopic lesions were found. There was no evidence of
tumorigenic activity (Walker et al., 1969).
0 Dieldrin (>99% pure) was administered to CF1 mice of both sexes in
the diet for 128 weeks. Dosages were 1.25, 2.5, 5, 10 or 20 ppm
dieldrin. These doses are equivalent to 0.19, 0.38, 0.75, 1.5 or 3
mg/kg body weight (Lehman, 1959). At the 20-ppm dose level,-approximately
25% of the males and nearly 50% of the females died during the first
3 months of the experiment. Palpable intra-abdominal masses were
detected after 40, 75 or 100 weeks in the 10, 5 and 2.5-ppm-treated
groups, respectively. At 1.25 ppm, liver enlargement was not palpable
and morbidity was similar to that of controls. A No-Observed-Adverse-
Effect-Level (NOAEL) cannot be established because clinical chemistry
parameters were not determined (Walker et al., 1972).
Reproductive Effects
0 Coulston et al. (1980) studied the reproductive effects of dieldrin
in Long Evans rats. Pregnant rats were administered 0 or 4 mg/kg bw
dieldrin by gavage daily from day 15 of gestation through 21 days
postpartum. The treated group did not differ from the control group
when examined for fecundity, number of stillbirths, perinatal mortality
and total litter weights.
Developmental Effects
0 Pregnant Syrian golden hamsters given. 30 mg/kg bw dieldrin (_>99% pure)
in corn oil on days 7, 8 or 9 of gestation manifested an embryo-
cidal and teratogenic response as evidenced by a statistically
significant increase in fetal deaths, a decrease in live fetal weight
and an increased incidence of webbed foot, cleft palate and open eye
(Ottolenghi et al., 1974). Similar anomalies were observed in
CD^i mice administered 15 mg/kg bw dieldrin on day 9 of gestation, but
no effect was seen on fetal survival or weight.
0 Dieldrin (87% pure) was not found to be teratogenic in the CD rats and
CD-1 mice administered doses of 1.5, 3.0 or 6.0 mg/kg/day by gastric
intubation on days 7 through 16 of gestation. Fetal toxicity, as
indicated by a significant decrease in numbers of caudal ossification
centers at the 6.0-mg/kg/day dose level and a significant increase
in the number of supernumerary ribs in one study group at both the
3.0- and 6.0-mg/kg/day dose level, was reported in the experiments in
mice. Maternal toxicity in the high-dose rats was.indicated by a 41%
mortality and a significant decrease in weight gain; similarly, mice
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Dieldrin August, 1987
receiving 6.0 rag/kg/day showed a significant decrease in maternal
weight gain. A significant increase in liver-to-body weight
ratio in one group of maternal mice was reported at both 3.0 and 6.0
mg/k9/day (Chernoff et al., 1975).
Mutaqenicity
0 Dieldrin was not mutagenic in the Salmonella/microsome test with and
without S-9 mix (McCann et al., 1975).
0 Dieldrin significantly decreased the mitotic index and increased
chromosome abnormalities in STS mice bone marrow cells in an in vivo
study. Similar observations were made in human WI-38 embryonic lung
cells in an in vitro test that also gave evidence of cytotoxicity, as
indicated by degree of cell degeneration (Majumdar et al., 1976).
Carcinogenieity
8 A dose-related increase in the incidence of hepatocellular carcinomas
was observed in B6C3Fj mice, with the incidence in the high-dose
males being significantly higher when compared to pooled controls
(NCI, 1978). Mice were given dieldrin (technical grade, >85% purity)
in the diet at concentrations of 2.5 or 5 ppm for 80 weeks. These
doses correspond to approximately 0.375 or 0.75 mg/kg/day, respectively
(Lehman, 1959).
0 Osborne-Mendel rats treated with dieldrin at Time-Weighted Average (TWAf
doses of 29 or 65 ppm in the diet (approximately 1.45 or 3.25 mg/kg/day,
respectively, based on Lehman, 1959) for 80 weeks, did not elicit
treatment-related tumors (NCI, 1978).
• Diets containing 0.1, 1.0 or 10 ppm dieldrin (>99% purity), when
given to mice of both sexes for 132 weeks, were associated with an
increased incidence of liver tumors at all dose levels tested (Walker
et al., 1972). These doses are equivalent to approximately 0.015,
0.15 or 1.5 mg/kg/day, respectively (Lehman, 1959).
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 noncarcinogenic end point of toxicity.
The HAs for noncarcinogenic toxicants are derived using the following formula:
HA - (NOAEL or LOAEL) x (BW) = __ /L ( /L)
(UF) x ( L/day)
where:
NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect-Level
in mg/kg bw/day.
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Dieldrin August, 1987
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BW - assumed body weight of a child (10-kg) or
an adult (70 kg).
UF « uncertainty factor (10, 100 or 1,000), in
accordance with NAS/ODW guidelines.
L/day » assumed daily water consumption of a child
(1 L/day) or an adult (2 L/day).
One-day Health Advisory
No data were found in the available literature that was suitable for
determination of a One-day HA value for dieldrin. It is, therefore, recommended
that the modified DWEL for a 10-kg child (0.0005 mg/L, calculated below) be
used as a conservative estimate for the One-day HA value.
Ten-day Health Advisory
No data were found in the available literature that was suitable for
determination of a Ten-day HA value for dieldrin. It is, therefore, recommended
that the modified DWEL for a 10-kg child (0.0005 mg/L, calculated below) be
used as a conservative estimate for the Ten-day HA value.
Longer-term Health Advisory
\
No data were found in the available literature that was suitable for
determination of a Longer-term HA value for dieldrin. It is, therefore,
recommended that the modified DWEL for a 10-kg child (0.0005 mg/L,
calculated below) be used as a conservative estimate for the Longer-term HA
value.
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 Drinking Water Equivalent Level
(DWEL) can be determined (Step 2). A DWEL 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.
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 classified as a
Group A or B carcinogen, according to the Agency's classification scheme of
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Dieldrin
August, 1987
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carcinogenic potential (U.S. EPA, 1986), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.
The study of Walker et al. (1969), in which rats were fed dieldrin in
the diet at 0.0, 0.1, 1 or 1 0 ppm for 2 years (approximately 0, 0.005, 0.05
or -0.5 mg/kg/day based on Lehman, 1959), has been selected as the basis for
calculating the DWEL. In this study, liver weight and liver-to-body weight
ratios were significantly increased in females receiving 1 and 10 ppm, while
pathological changes consistent with exposure to organochlorides were evident
at the 10-ppm level. This study established a NOAEL of 0.1 ppm (equivalent
to 0.005 mg/kg/day).
Using a NOAEL of 0.005 mg/kg/day, the Lifetime HA is calculated as
follows:
Step 1: Determination of the Reference Dose (RfD)
RFD • . = 0.00005 mg/kg/day
0.005 mg/kg/day
100
where:
0.005 mg/kg/day » NOAEL, based on the absence of hepatic effects in
rats fed dieldrin in the d^et.
1 00 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
Step 2: Determination of the Drinking Water Equivalent (DWEL)
DWEL = . a 0. 001 75 mg/L (1.75 ug/L)
(0.00005 mg/kg/day) (70 kg)
2 L/day
where:
0.00005 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 Health Advisory
Dieldrin may be classified in Group B2: probable human carcinogen. A
Lifetime HA is not recommended for dieldrin.
The estimated excess cancer risk associated with lifetime exposure to
drinking water containing dieldrin at 1.75 ug/L is approximately 8.05 x 10-4.
This estimate represents the .upper 95% confidence limit from extrapolations
prepared by EPA's Carcinogen Assessment Group (U.S. EPA, 1987) using the
linearized multistage model. The actual risk is unlikely to exceed this
value, but there is considerable uncertainty as to the accuracy of risks
calculated by this methodology.
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Dieldrin August, 1987
Evaluation of Carcinogenic Potential
4 Applying the criteria described in EPA's proposed guidelines for
assessment of carcinogenic risk. (U.S. EPA, 1986), dieldrin may be
classified in Group B2: probable human carcinogen.
0 Evidence has been presented in several carcinogenicity studies showing
that dieldrin is carcinogenic to mice. Thirteen data sets from these
studies are adequate for quantitative risk estimation. Utilizing the
linearized multistage model, the U.S. EPA performed potency estimates
for each of these data sets. The geometric mean of the potency
estimates, Q1 * = 16 (mg/kg/day)~1, was estimated as the potency for the
general population (U.S. EPA, 1987).
0 Using this Qi* value and assuming that a 70-kg human adult consumes
2 liters of water a day over a 70-year lifespan, the linearized
multistage model estimates that concentrations of 0.219, 0.0219 and
0.00219 ug dieldrin per liter may result in excess cancer risk of
10-4, 10-5 and 10~6, respectively.
0 The linearized multistage model is only one method of estimating
carcinogenic risk. From the data contained in U.S. EPA (1987), it
was determined that five of the thirteen data sets were suitable for
determining slope estimates for the probit, logit, Weibull and gamma-
multihit models. Using the geometric mean of these slope estimates
(13 for multistage, 5 for other models) at their upper 95% confidence
limits, the following comparisons of unit risk (i.e., a 70-kg man
consuming 2 liters of water per day containing 1 ug/L of dieldrin over
a lifetime) can be made: multistage, 4.78 x 10-4. probit, 7.7 x 10"12;
logit, 5.09 x 10~6; Weibull, 1.13 x 10-4; multihit, 5.68 x 10-4. Each
model is based on different assumptions. No current understanding of
the biological mechanisms of carcinogenesis is able to predict which
of these models is more accurate than another.
0 While recognized as statistically alternative approaches, the range
of risks described by using any of these modelling approaches has
little biological significance unless data can be used to support
the selection of one model over another. In the interest of consistency
of approach and in providing an upper bound on the potential cancer
risk, the Agency has recommended use of the linearized multistage
approach.
0 IARC (1982) concluded that there is limited evidence that dieldrin is
carcinogenic in laboratory animals.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 ACGIH (1984) has established a short-term exposure limit (STEL) of
0.75 mg/m3 and an 8-hour Threshold Limit Value (TLV)-TWA exposure
0.25 mg/m3 for dieldrin.
0 U.S. EPA (1980) has recommended ambient water quality criteria of
0.71 ng/L for dieldrin. it is based on a carcinogenic potency factor
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Dieldrin August, 1987
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(q. *) of 30.37 (ngA9/day)~1 derived from the incidence of hepato-
cellular carcinoma in a mouse feeding study conducted by Walker et
al. (1972).
0 Residue tolerances ranging from 0.02 to 0.1 ppm have been established
for dieldrin in or on agricultural commodities (U.S. EPA, 1985).
0 WHO (1982) established guidance of 0.03 ug dieldrin/L in drinking water.
VII. ANALYTICAL METHODS
0 Determination of dieldrin is by a liquid-liquid extraction gas
chromatographic (GC) procedure (U.S. EPA, 1984a). In this procedure,
a 1-liter sample is extracted with methylene chloride using a separatory
funnel. The methylene chloride extract is dried and exchanged to
hexane during concentration to a volume of 10 mL or less. The extract
is separated by GC, and the components are then measured with an
electron-capture detector. Identification may be corroborated through
the use of two unlike columns or by gas chromatography-mass
spectroscopy (GC-MS). A GC-MS procedure is available (U.S. EPA,
1984b) that allows for the qualitative and quantitative confirmation
of results obtained by the GC procedure.
VIII. TREATMENT TECHNOLOGIES
0 Available data indicate that reverse osmosis (RO), granular-activated
carbon (GAC) adsorption, ozonation and conventional treatment will
remove dieldrin from water. The percent removal efficiency ranges
from 50 to 99+%.
0 Laboratory studies indicate that RO is a promising treatment method
for dieldrin-contaminated waters. Chian et al. (1975) reported 99+%
removal efficiency for two types of membranes operating at 600 psig and
a flux rate of 8 to 12 gal/ft2/day» Membrane adsorption, however, is
a major concern and must be considered, since breakthrough of dieldrin
would probably occur once the adsorption potential of the membrane
was exhausted.
0 GAC is effective for dieldrin removal. Pirbazari and Weber (1983)
reported 99+% dieldrin removal efficiency of a GAC column operating
at an empty bed contact time (EBCT) of 15 minutes and a hydraulic
loading of 1.4 gal/ft2/minf for the entire test period (approximately
7.5 months).
0 Pirbazari and Weber (1983) determined adsorption isotherms using GAC
on dieldrin in water solutions. Resin adsorption was also found to
remove dieldrin from water. The Preundlich values determined by
The authors indicate that the tested resins are not quite as effective
as GAC in the removal of dieldrin from water.
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Dieldrin August, 1987
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Ozonation treatment appears to be an effective dieldrin removal
method. Treatment with 36 mg/L ozone (03) removed 50% of dieldrin
while 11 mg/L 03 removed only 15% of dieldrin (Robeck et al., 1965).
Conventional water-treatment techniques using alum coagulation,
sedimentation and filtration proved to be 55% effective in removing
dieldrin from contaminated potable water supplies (Robeck et al.,
1965). Lime- and soda-ash softening with ferric chloride as a coagulant
did not improve upon the removal efficiency achieved with alum alone.
Oxidation with chlorine and potassium permanganate is ineffective in
degrading dieldrin (Robeck et al., 1965).
Treatment technologies for the removal of dieldrin from water are
available and have been reported to be effective. However, selection
of individual or combinations of technologies to attempt dieldrin
removal from water must be based on a case-by-case technical evaluation,
and an assessment of the economics involved.
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Dieldrin August, 1987
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IX. REFERENCES
ACGIH. 1984. American Conference of Governmental Industrial Hygienists.
Documentation of the threshold limit values for substances in workroom
air. 3rd ed. Cincinnati, OH: ACGIH. p. 139.
Baldwin, M.K. and J. Robinson. 1972. A comparison of the metabolism of
HEOD (Dieldrin) in CF1 mouse with that in the CFE rat. Food Cosinet.
Toxicol. 10:333-351.
Chernoff, N., R.J. Kavlock, J.R. Kathrein, J.M. Dunn and J.K. Haseman.
1975. Prenatal effects of dieldrin and photodieldrin in mice and rats.
Toxicol. Appl. Pharmacol. 31:302-308.
Chian, E.S., W.N. Bruce and H.H.P. Fang. 1975. Removal of pesticides by
reverse osmosis. Environ. Sci. Technol. 9(1):52-59.
Coulston, F., R. Abraham and R. Mankes. 1980. Reproductive study in female
rats given dieldrin, alcohol or aspirin orally. Albany, NY: Albany
Medical College of Union University. Institute of Comparative and
Human Toxicology. Cited in IPCS, 1987.
Fitzhugh, O.G., A.A. Nelson and M.L. Quaife. 1964. Chronic oral toxicity of
aldrin and dieldrin in rats and dogs. Food Cosmet. Toxicol. 2:551-562.
Hayes, W.J., Jr. 1974. Distribution of dieldrin following a single oral
dose. Toxicol. Appl. Pharmacol. 28:485-492.
Heath, D.F. and H. Vandekar. 1964. Toxicity and metabolism of dieldrin in
rats. Br. J. Ind. Med. 21:269-279.
IARC. 1982. International Agency for Research on Cancer. IARC monographs
on the evaluation of the carcinogenic risk of chemicals to humans.
Chemicals, industry process and industries associated with cancer in
humans. IARC Monographs Vols. 1-29, Supplement 4. Geneva: World Health
Organization.
IPCS. 1987. International Programme on Chemical Safety. Environmental Health
Criteria for Aldrin and Dieldrin. United Nations Environment Programme.
International Labour Organization. Geneva: World Health Organization.
Lehman, A. 1959. Appraisal of the safety of chemicals in foods, drugs and
cosmetics. Association of Food and Drug Officials of the United States.
MacKay, D. and A.W. Wolkoff. 1973. Rate of evaporation of low-solubility
contaminants from water bodies to atmosphere. Environ. Sci. Technol.
7:611.
Majumdar, s.K., H.A. Kopelman and M.J. Schnitman. 1976. Dieldrin-induced
chromosome damage in mouse bone marrow and Wi-38 human lung cells.
J. Hered. 67:303-307.
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Dieldrin August, 1987
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McCann, J., E. Choi, E. Yamasaki and B.N. Ames. 1975. Detection of carcinogens
as mutagens in the Salmonella/microsome test: Assay of 300 chemicals.
Proc. Natl. Acad. Sci. 72(12):5135-5139.
Meister, R., ed. 1983. Farm chemicals handbook. Willoughby, OH: Meister
Publishing Company.
NAS. 1977. National Academy of Sciences. Drinking water and health.
Vol. 1. Washington, DC: National Academy Press, pp. 556-571.
NCI. 1978. National Cancer Institute. Bioassay of aldrin and dieldrin for
possible carcinogenicity. Technical Report Series No. 21.
Ottolenghi, A.D., J.K. Haseman and F. Suggs. 1974. Teratogenic effects of
aldrin, dieldrin, and endrin in hamsters and mice. Teratology.' 9:11-16.
Pirbazari, M. and H.J. Weber. 1983. Removal of dieldrin from water by
activated carbon. J. Environ. Eng. 110(3):656-669.
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