820K88115
August, 1987
DRAFT
METHYL PARATHION
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
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
(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 accuratel'' 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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II. GENERAL INFORMATION AND PROPERTIES
CAS No. 298-00-0
Structural Formula
-P(OCH,)2
0,0-Dimethyl-0-(4-nitrophenyl) phosphorothioic acid
Synonyms
0 Metron; Meptox; Metaphos; Dimethyl parathion; Nitrox; Azofos; Nitrox 80;
BAY 11405; Metacide; Folidol M; Azophos; Methyl-E 605; Dalf; Meticide;
Methylthiophos; Pencap M; Penncap M; Sinafid M-48; Wofotox; Vofatox;
Thiophenit; Wofatox (Meister, 1983).
Uses
0 A restricted-use pesticide for control of various insects of economic
importance; especially effective for boll weevil control (Meister, 1983),
Properties (Hawley, 1981; Meister, 1983; CHEMLAB, 1985; TDB, 1985)
Chemical Formula
Molecular Weight
Physical State (25°C)
Boiling Point
Melting Point
Density
Vapor Pressure (20°C)
Specific Gravity
Water Solubility (25°C)
Log Octanol/Water Partition
Coefficient
Taste Threshold
Odor Threshold
Conversion Factor
C8H1005NSP
263.23
White crystalline solid
35 to 36°C
0.97 x 10-5 mm Hg
55 to 60 mg/L
3.11 (calculated)
Occurrence
Methyl parathion has been found in 1,402 of 29,002 surface water
samples analyzed and in 25 of 2,878 ground water samples (STORET,
1987). Samples were collected at 3,676 surface water locations and
2,026 ground water locations, and methyl parathion was found in 22
states. The 85th percentile of all nonzero samples was 1.18 ug/L
in surface water and 1 ug/L in ground water sources. The maximum
concentration found was 13 ug/L in surface water and 1.6 ug/L in
ground water.
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Methyl Parathion August, 1987
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Environmental Fate
0 Methyl parathion (99% pure) at 10 ppm was added to sea water and
exposed to sunlight; some samples were also kept in the dark (controls).
After 6 days, 57% of the parent compound had degraded but the degradates
were not identified. Since only 27% of the parent compound had degraded
in the dark controls, this indicates that methyl parathion is subject
to photodegradation in sea water (U.S. EPA, 1981).
0 The degradation rate of two formulations (EC and MCAP) of methyl
parathion, applied at 0.04 ppm, was compared in a sediment/water
system. Degradates were not identified; however, the parent compound
had a half-life of 1 to 3 days in water. In the hydrosoil plus
sediment, methyl parathion applied as an emulsifiable concentrate
formulation had a half-life of 1 to 3 days, whereas for the micro-
encapsulated formulation, the half-life was 3 to 7 days (Agchem, 1983).
0 Methyl parathion was relatively immobile in 30-cm soil columns of sandy
loam, silty clay loam and silt loam soils leached with 15.7 inches of
water, with no parent compound found below 10 cm or in the column
leachate, which was the case for the column of sand (Pennwalt Corporation,
1977).
0 Methyl parathion (MCAP or EC formulation) at 5 Ib ai/A (active
ingredient/acre) was detected in runoff water from field plots irrigated
4 to 5 days posttreatment. Levels found in soil and turf plots ranged
from 0.13 to 21 ppm and 0.17 to 0.20 ppm, respectively (Pennwalt
Corporation, 1972).
0 A field dissipation study with methyl parathion (4 Ib/gal EC) at 3 Ib
ai/A, applied alone or in combinaton with Curacron, dissipated to
nondetectable levels (<0.05 ppm) within 30 days in silt loam and
loamy sand soils (Ciba-Geigy Corporation, 1978).
III. PHARMACOKINETICS
Absorption
0 Braeckman et al. (1983) administered a single oral dose of 35S-methyl
parathion (20 mg/kg) by stomach tube to four mongrel dogs. Peak
concentrations in plasma ranged from 0.13 to 0.96 ug/mL, with peak
levels occurring 2 to 9 hours after dosing. In two dogs given single
oral doses of 35s-methyl parathion (3 mg/kg) in this study, absorption
was estimated to be 77 and 79%, based on urinary excretion of label.
The authors concluded that methyl parathion was well absorbed from
the gastrointestinal tract.
0 Hollingworth et al. (1967) gave a single oral dose of 32P-labeled
methyl parathion by gavage (3 or 17 mg/kg, dissolved in olive oil) to
male Swiss mice. Recovery of label in the urine reached a maximum of
about 85%, most of this occurring within 18 hours of dosing. The
amount of label in the feces was low, never exceeding 10% of the
dose. This indicated that absorption was at least 90% complete.
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Methyl Parathion August, 1987
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Distribution
0 Ackermann and Engst (1970) administered methyl parathion to pregnant
albino rats and examined the dams and fetuses for the distribution
of the pesticide. The pregnant rats (weighing about 270 g each) were
given 3 mg (11.1 mg/kg) of methyl parathion orally on days 1 to 3 of
gestation and sacrificed 30 minutes after the last dose. Methyl
parathion was detected in the maternal liver (25 ng/g), placenta
(80 ng/g), and in fetal brain (35 ng/g), liver (40 ng/g) and back
musculature (60 ng/g).
Metabolism
0 Hollingworth et al. (1967) gave 32p_labeled methyl parathion by
gavage (3 or 17 mg/kg, dissolved in olive oil) to male Swiss mice.
About 85% of the label appeared in the urine within 72 hours. Urinary
metabolites identified -24 hours after the low dose were: dimethyl
phosphoric acid (53.1%); dimethyl phosphorothioic acid (14.9%);
desmethyl phosphate (14.1%); desmethyl phosphorothioate (11.7%);
phosphoric acid (2eO%); methyl phosphoric acid (1.7%); and phosphate
(0.6%). The radioactivity in the urine was fully accounted for by
hydrolysis products and P=0 activation products. No evidence was
found for reduction of the nitro group to an amine, oxidation of the
ring methyl group, or hydroxylation of the ring. A generally similar
pattern was observed at the high dose, except for a lower percentage
of dimethyl phosphoric acid (31.9%) and higher percentages of desmethyl
phosphate (23.1%) and desmethylphosphorothionate (18.8%). Based on
this, the authors proposed a metabolic scheme involving oxidative
desulfuration, oxidative cleavage of the phospho group from the ring
and hydrolysis of the phosphomethyl esters.
0 Neal and DuBois (1965) investigated the in vitro detoxification of
methyl parathion and other phosphorothioates using liver microsomes
prepared from adult male Sprague-Dawley rats. Metabolism was found
to involve oxidative desulfuration followed by hydrolysis to yield
p-nitrophenol. Extracts from livers of adult male rats exhibited
higher metabolic activity than that of adult females (3.2 versus
1.9 units, where one unit equals 1 ug p-nitrophenol/50 mg liver
extract) (p
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Methyl Parathion August, 1987
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NADPH2. The amounts of phenol and oxygen analog formed were 3.8 and
3.7 uM in the rabbit liver extract and 2.5 and 5.4 uM in the rat
liver extract, respectively.
Excretion
Braeckman et al. (1983) administered individual doses of 3 mg/kg of
35s-methyl parathion to two mongrel dogs. In each dog, the agent was
given once intravenously and, 1 week later, once orally via stomach
tube. This dosing pattern was repeated once in one dog. Urine was
collected every 24 hours for 6 days after each'treatment. Urinary
excretion 6 days after oral dosing was 63% in the animal without
repeated dosing and 70% and 78% in the other. Urinary excretion
6 days after intravenous dosing was 80% in the animal without repeated
dosing and 95 to 96% in the other. Most of the label appeared in urine
within two days. Other excretory routes were not monitored.
Hollingworth et al. (1967) gave 32p-iabeled methyl parathion (3 or
17 mg/kg, dissolved in olive oil) by gavage to male Swiss mice.
Recovery of label in the urine reached a maximum of about 85%, most
of this occurring within 18 hours of dosing. The amount of label in
the feces was low, never exceeding 10% of the dose. This indicated
that absorption was at least 90% complete.
IV. HEALTH EFFECTS
Humans
Short-term Exposure
0 Nemec et al. (1968) monitored cholinesterase (ChE) levels in two
workers (entomologists) who examined plants in a cotton field after
it had been sprayed with an ultra-low-volume (nonaqueous) preparation
of methyl parathion (1.5 to 2 Ib/acre). The men entered a cotton
field to examine the plants on 3 different days over a 2-week period;
two of these occasions were within 2 hours after the ultra-low-volume
spraying, and the third occasion was 24 hours after a spraying.
After each field trip their arms were washed with acetone and the
adhering methyl parathion determined. It was found that contact with
the plants 2 hours after spraying resulted in 2 to 10 ng of methyl
parathion residue on the arms; exposure 24 hours after spraying
resulted in a residue on the arms of 0.16 to 0.35 mg. The amount of
pesticide absorbed was not estimated. No toxic symptoms were experienced
by either man, but measurement of red blood cell ChE activity immediately
after the third of these exposures showed a decrease in activity to
60 to 65% of preexposure levels. These values did not increase
significantly over the next 24 hours. It was concluded that workers
should not enter such a field until more than 24 hours, and preferably
48 hours, have elapsed after spraying with ultra-low-volume insecticide
sprays. Water emulsion sprays were not tested, but the authors
cautioned that it cannot be assumed that they are less hazardous than
the ultra-low-volume spray residues.
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0 Rider et al. (1969, 1970, 1971) studied the toxicity of technical
methyl parathion (purity not specified) in human volunteers. Each
phase of the study was done with different groups of seven male
subjects, five of whom were test subjects and two were vehicle
controls (Rider et al., 1969). Each study phase was divided into a
30-day pre-test period for establishing cholinesterase baselines, a
30-day test period when a specific dose of methyl parathion was
given, and a post-test period.
e Thirty-two different dosages were evaluated by Rider et al. (1969),
ranging from 1 to 19 mg/day. Early in the study, several of the
groups were given more than one dose level during a single phase.
The initial amount was 1.0 mg with an increase of 0.5 mg during each
succeeding test period up to 15.0 mg/day. At this point, the dose was
increased by 1.0 mg/day to a total dose of 19.0 mg/day. Pesticide in
corn oil was given orally in capsules, once per day for each test
period of 30 days. At no time during any of the studies were there
any significant changes in blood counts, urinalyses, or prothrombin
times, or was there any evidence of toxic side effects. Cholinesterase
activity of the plasma and red blood cells (RBCs) was measured twice
weekly prior to, during and after the dosing period. The authors
considered a mean depression of 20 to 25% or greater in ChE activity
below control levels to be indicative of the toxic threshold. At
11.0 mg/day, a depression of 15% in plasma ChE occurred, but doses up
to and including 19 mg/day did not produce any significant ChE
depression.
0 Rider et al. (1970) studied the effects of 22, 24 and 26 mg/day
technical methyl parathion. There were no effects observed at
22 mg/day. At 24 mg/day, plasma and RBC ChE depression was
produced in two subjects, the maximum decreases being 24 and 23% for
plasma, and 27 and 55% for RBC. The mean maximal decreases (in all
five subjects) were 17% for plasma and 22% for RBC. With 26 mg/day
RBC ChE depression was again produced in only two of the subjects,
with maximum decreases of 25 and 37%. The mean maximum decrease was
18%. Plasma cholinesterase was not significantly altered.
0 Rider et al. (1971) assessed the effects of 28 and 30 mg/day technical
methyl parathion. At 28 mg/day, a significant decrease in RBC ChE
was produced in three subjects (data not given), with a maximum mean
decrease of 19%. With a dose of 30 mVday, a mean maximum depression
of 37% occurred. Based on their criteria of 20 to 25% average
depression of ChE activity, the authors concluded that this was the
level of minimal incipient toxicity. Body weights of the test subjects
were not reported, but assuming an average body weight of 70 kg, a
dose of 22 mg/day corresponds to a No-Observed-Adverse-Effect-Level'
(NOAEL) of 0.31 mg/kg/day, and the 30 mg/day dose corresponds to 0.43
mg/kg/day. The NOAEL is considered to be 22 mg/day herein because of
the apparent sensitivity of, some individual subjects at higher doses
to have met the 20 to 25% criteria for ChE depression as an effect.
Long-term Exposure
0 No information was found in the available literature on the health
effects of methyl parathion in humans.
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Methyl Parathion August, 1987
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Animals
Short-term Exposure
0 Reported oral LD5Q values for methyl parathion include 14 and 24 rag/kg
in male and female Sherman rats, respectively (Gaines, 1969); 14.5 and
19.5 mg/kg in male and female CD-1 mice, respectively (Haley et al.,
1975); 30 mg/kg in male ddY mice (Isshiki et al., 1983); 18.0 and
8.9 mg/kg in male and female Sprague-Dawley rats, respectively (Sabol,
1985); and 9.2 mg/kg in rats of unreported strain (Galal et al., 1977).
0 Galal et al. (1977) determined the subchronic median lethal dose
(OLD5Q) of methyl parathion (purity not specified) in adult albino
rats. Groups of 10 animals received an initial daily oral dose (by
gavage) of 0.37 mg/kg (4% of the acute oral LD^Q). Every 4th day the
dose was increased by a factor of 1.5 (dose based on the
body weight of the animals as recorded at 4-day intervals). Treatment
was continued until death or termination at 36 days. Hematological
and blood chemistry analyses were performed initially and on the 21st
and 36th days of the study. Histopathological studies of the liver,
kidneys and heart were also carried out on the 21st and 36th days of
treatment. The C-LD5Q obtained was 13 mg/kg. The authors concluded
that the most predominant hazards of subchronic exposure to methyl
parathion were weight loss, hyperglycemia and macrocytic anemia, all
probably secondary to hepatic toxicity. Since an increasing dose
protocol was used, this study does not identify a NOAEL or a Lowest-
Observed-Adverse-Effect-Level (LOAEL).
0 Daly et al. (1979) administered methyl parathion (technical, 93.65%
active ingredient) to Charles River CD-1 mice for 4 weeks at levels
of 0, 25 or 50 ppm in the diet. Assuming that 1 ppm in the diet of
mice corresponds to 0.15 mg/kg/day (Lehman, 1959), this is equivalent
to doses of about 0, 3.75 or 7.5 mg/kg/day. Five animals of each sex
were used at each dose level. Mean body weights were lower (p <0.05)
than control for all treated animals throughout the test period. Mean
food consumption was lower (p <0.05) throughout for all test animals
except females at the 25-ppm level. Mortality, physical observations,
and gross postmortem examinations did not reveal any treatment-related
effects. Cholinesterase measurements were not performed. Based on
body weight gain, the LOAEL for this study was identified as 25 ppm
(3.75 mg/kg/day).
0 Tegeris and Underwood (1977) examined the effects of feeding methyl
parathion (94.32%.pure) to beagle dogs (4 to 6 months of age, weighing
5 to 10 kg) for 14 days. Two animals of each sex were given doses
of 0, 2.5, 5 or 10 mg/kg/day. All animals survived the 14-day test
period. Mean feed consumption and weight gain were significantly
(p <0.05) depressed for both sexes at the 5 and 10 mg/kg/day dose
levels. After the 3rd day, animals in the high-dose group began
vomiting after all meals. Vomiting was observed sporadically at the
lower dose levels, particularly during the 2nd week. The authors
attributed this to acetylcholinesterase inhibition, but no measure-
ments were reported. No other symptomatology was described. Based
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Methyl Parathion August, 1987
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on weight loss and vomiting, this study identified a LOAEL of
2.5 ing/kg/day in the dog.
0 Fan et al. (1978) investigated the immunosuppressive effects of methyl
parathion administered orally to Swiss (ICR) mice. The pesticide
(purity not specified) was fed in the diet at dose levels corresponding
to 0, 0.08, 0.7 or 3.0 mg/kg/day for 4 weeks. Active immunity was
induced by weekly injection of vaccine (acetone-killed Salmonella
typhimurium) during the period of diet treatment. Defense against
microbial infection was tested by intraperitoneal injection of a
single LD^g dose of active S_. typhimurium cells. Protection by
immunization was stated to be decreased in methyl parathion-treated
animals, but no dose-response data were provided. The authors stated
that pesticide treatment extending beyond 2 weeks was required to
obtain significant increases in mortality. Increased mortality was
associated with an increased number of viable bacteria in blood,
decreased total gamma-globulins and specific immunoglobins in serum,
and reduced splenic blast transformation in response to mitogens.
8 Shtenberg and Dzhunusova (1968) studied the effect of oral exposure to
methyl parathion (purity not specified) on immunity in albino rats
vaccinated with NIISI polyvaccine. Three tests (six animals each)
were conducted in which: (a) the vaccination was done after the
animals had been on a diet supplying 1.25 mg/kg/day metaphos (methyl
parathion) for 2 weeks; (b) the diet and vaccinations were initiated
simultaneously; and (c) the diet was initiated 2 weeks after vaccina~
tion. The titer of agglutins in immunized control rats was 1:1,200.
This titer was decreased in all exposed groups as follows: 1:46 in
series (a), 1:75 in series (b) and 1:33.3 in series (c). The authors
judged this to be clear evidence of inhibition of immunobiological
reactivity in the exposed animals. Changes in blood protein fractions
and in serum concentration of albumins were not statistically significant.
Based on immune suppression, a LOAEL of 1.25 mg/kg/day was identified.
Dermal/Ocular Effects
0 Gaines (1969) reported a dermal LD5Q of 67 mg/kg for methyl parathion
in male and female Sherman rats.
0 Galloway (1984a,b) studied the skin and eye irritation properties of
methvl parathion (technical; purity not specified) using albino New
Zealand White rabbits. In the skin irritation test, 0.5 mL undiluted
pesticide was applied and the treated area occluded for 4 hours.
This treatment resulted in dermal edema that persisted for 24 hours,
and in erythema that lasted for 6 days. After a total observation
period of 9 days, a score of 2.0 was derived, and technical methyl '
parathion was rated as a weak irritant. In the eye irritation test,
0.1 mL of the undiluted pesticide was applied to nine eyes. Three
were washed after exposure, and six were left unwashed. Conjunctival
irritation was observed starting at 1 hour and lasting up to 48 hours
postexposure. Maximum average irritation scores of 11 and 10.7 were
assigned for nonwashed and washed eyes, respectively, and technical
methyl parathion was considered a weak irritant.
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Methyl Parathion August, 1987
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0 Galloway (1985) used guinea pigs to examine the sensitizing potential
of methyl parathion (technical; purity not stated). Ten doses of
0.5 mL of a 10% solution (w/v in methanol) were applied to the clipped
intact skin of 10 male guinea pigs (albino Hartley strain) over a
36-day period. This corresponds to an average dose of 13.9 mg/kg/day.
Another group was treated with 2,4-dinitrochlorobenzene as a positive
control. No skin sensitization reaction was observed in methyl
parathion-treated animals.
0 Skinner and Kilgore (1982) studied the acute dermal toxicity of methyl
parathion in male Swiss-Webster mice, and simultaneously determined
ED50 values for cholinesterase and acetylcholinesterase inhibition.
Methyl parathion (analytical grade, 99% pure) was administered in
acetone solution to the hind feet of the mice; the animals were
muzzled to prevent oral ingestion through grooming. The derma'l LDsg
was 1,200 mg/kg. The ED50 was 950 mg/kg for cholinesterase inhibition
and 550 mg/kg for acetylcholinesterase inhibition.
Long-term Exposure
0 Daly and Rinehart (1980) conducted a 90-day feeding study of methyl
parathion (93.65% pure) using Charles River CD-1 mice. Groups of 15
mice of each sex were given diets containing the pesticide at levels
of 0, 10, 30 or 60 ppm. Assuming that 1 ppm in the diet of mice corre-
sponds to 0.15 mg/kg/day (Lehman, 1959), this is equivalent to doses
of about 0, 1.5, 4.5 or 9.0 mg/kg/day. All mice survived the test.
Mean body weights were significantly (p <0.05) depressed for both
sexes at 60 ppm throughout the study and for males during the first
5 weeks at 30 ppm. Animals of both sexes had a slight but not
significant (p >0.05) increase in the mean absolute and relative
brain weights at 60 ppm. There were dose-related decreases (p <0.05)
in the mean absolute and relative testes weights of all treated
males and in the ovary weights of the females at 30 and 60 ppm.
Gross and microscopic examination revealed no dose-related effects.
Histological examination revealed no findings in the brain, testes or
ovary to account for the observed changes in the weights of these
organs. Measurements on ChE were not performed. Based on decreased
testes weight, the LOAEL for this study was 10 ppm (1.5 mg/kg/day).
0 Tegeris and Underwood (1978) investigated the toxicity of methyl
parathion (94.32% active ingredient) in beagle dogs fed the pesticide
for 90 days at dose levels of 0, 0.3, 1.0 or 3.0 mg/kg/day. Four dogs
(4-months old, 4.5 to 8.0 kg) of both sexes were used at each dose
level. Soft stools were observed in all treatment groups throughout,
and there was also occasional spontaneous vomiting. There were no
persistent significant (p >0.05) effects on body weight gain, feed
intake, fasting blood sugar, BUN, SGPT, SGOT, hematological, or
urological indices. Organ weights were within normal limits, with
the exception of pituitary weights of females at 3.0 mg/kg, which
were significantly (p <0.05) higher than the control values. Gross
and microscopic examination revealed no compound-related abnormalities.
Plasma ChE was significantly (p <0.05) depressed in both sexes at 6
and 13 weeks at 3 mg/kg/day, and in the males only at 1.0 mg/kg/day
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Methyl Parathion August, 1987
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at 13 weeks; erythrocyte ChE was also significantly (p <0.05) depressed
in all animals at 6 and 13 weeks at 3 mg/kg/day, and in both sexes at
13 weeks at 1.0 mg/kg/day; brain ChE was significantly (p <0.05)
depressed in both sexes at 3.0 mg/kg/day. Based on ChE depression,
the NOAEL and LOAEL for this study were identified as 0.3 mg/kg/day
and 1.0 mg/kg/day, respectively.
0 Ahmed et al. (1981) conducted a 1-year feeding study in beagle dogs.
Methyl parathion (93.6% pure) was administered in the diet at ingested
dose levels of 0, 0.03, 0.1 or 0.3 mg/kg/day. Eight animals of each
sex were included at each dose level, with no overt signs of toxicity
noted at any dose. There were no treatment-related changes in food
consumption or body weight. Cholinesterase determinations in plasma,
red blood cells and brain revealed marginal variations, but the
changes were not consistent and were judged by the authors to be
unrelated to dosing. Organ weight determinations showed changes in
both males and females at 0.1 and 0.3 mg/kg/day, but the changes were
neither dose-related nor consistent. It was concluded that there was
no demonstrable toxicity of methyl parathion fed to the dogs at these
levels. The NOAEL for this study was 0.3 mg/kg/day.
0 NCI (1978) conducted a 2-year feeding study of methyl parathion
(purity not specified) in F344 rats (50/sex/dose) at dose levels of
0, 20 or 40 ppm in the diet. Assuming that 1 ppm in the diet of rats
corresponds to 0.05 mg/kg/day (Lehman, 1959), this is equivalent to
dose levels of about 0, 1 or 2 mg/kg/day. Cholinesterase levels were
not measured, but no remarkable clinical signs were noted, and no
significant (p <0.05) changes were observed in mortality, body weight,
gross pathology or histopathology. Based on this, a NOAEL of 40 ppm
(2 mg/kg/day) was identified in rats.
0 NCI (1978) conducted a chronic (105-week) feeding study in B6C3Fi
mice (50/sex/dose). Animals were initially fed methyl parathion
(94.6% pure) at dose levels of 62.5 or 125 ppm. Assuming that 1 ppm
in the diet of mice corresponds to 0.15 mg/kg/day (Lehman, 1959),
this is equivalent to doses of about 9.4 or 18.8 mg/kg/day. Because
of severely depressed body weight gain in males, their doses were
reduced at 37 weeks to 20 or 50 ppm, and the time-weighted averages
were calculated to be 35 or 77 ppm. This corresponds to doses of
about 5.2 or 11.5 mg/kg/day, respectively. Females were fed at the
original levels throughout. Mortality was significantly (p <0.05)
increased only in female mice at 125 ppm. Body weights were lower
(p <0.05) for both sexes throughout the test period and decreases
were dose-related. No gross or histopathologic changes were noted,
and ChE activity was not measured. Based on body weight, this study
identified a LOAEL of 35 ppm (5.2 mg/kg/day) in male mice.
0 Daly et al. (1984) conducted a chronic feeding study of methyl
parathion (93.65% active ingredient) in Sprague-Dawley (CD) rats
(60/sex/dose) at dose levels of 0, 0.5, 5 or 50 ppm in the diet.
Using food intake/body weight data given in the study report, these
levels approximate doses of about 0, 0.025, 0.25 or 2.5 mg/kg/day.
At 24 months, five animals of each sex were sacrificed for qualitative
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Methyl Parathion August, 1987
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and quantitative tests for neurotoxicity. Ophthalmoscopic examinations
were conducted on females at 3, 12 and 24 months and terminally.
Hematology, urinalysis and clinical chemistry analyses were performed
at 6, 12, 18 and 24 months. Mean body weights were reduced (p <0.05)
throughout the study for both sexes at 50 ppm. At this dose level,
food consumption was elevated (p <0.05) for males during weeks 2
to 13, but reduced for females for most of the study. Hemoglobin,
hematocrit and RBC count were significantly (p <0.05) reduced for
females at 50 ppm at 6, 12, 18 and 24 months. For males at 5 and
50 ppm at 24 months, hematocrit and RBC count were significantly
(p <0.05) reduced and hemoglobin was reduced, but not significantly
(p >0.05). At 50 ppm, plasma and erythrocyte ChE were significantly
(p <0.05) depressed for both sexes during the test, and brain ChE was
significantly (p <0.05) decreased at termination. Slight decreases
in ChE activity were also observed in animals at 5 ppm, but these
changes were not statistically significant (p >0.05). For males, the
absolute weight and the ratio to brain weight of the testes, kidneys
and the liver were reduced by 10 to 16% (not significant, p >0.05) in
both the 5- and 50-ppm groups, while for females absolute and organ/body
weights for the brain and heart (also heart/brain weight) were found
to be elevated significantly (p <0.05) at the same dose levels. Overt
signs of cholinergic toxicity (such as alopecia, abnormal gait and
tremors) were observed in the 50-ppm animals and in one female at
5 ppm. At 24 months, 15 females were observed to have retinal degen-
eration. There was also a dose-related occurrence of retinal posterior
subcapsular cataracts, possibly related or secondary to the retinal
degeneration, since 5 of the 10 cataracts occurred in rats with retinal
atrophy. The incidence of retinal atrophy was 20/55 at 50 ppm, 1/60 at
5 ppm, 3/60 at 0.5 ppm and 3/59 in the control group. Examination of
the sciatic nerve and other nervous tissue from five rats per sex
killed at week 106 gave evidence of peripheral neuropathy (abnormal
fibers, myelin corrugation, myelin ovoids) in both sexes at 50 ppm
(p <0.05). Too few fibers were examined at the lower doses to perform
statistical analyses, but the authors stated that nerves from both
sexes in low- and mid-dose groups could not be distinguished qualita-
tively from controls. Slightly greater severity of nerve changes
found in two males was not clearly related to treatment. No other
lesions were observed that appeared to be related to ingestion of
methyl parathion. Based on hematology, body weight, organ weights,
clinical chemistry, retinal degeneration and cholinergic signs, a
NOAEL of 0.5 ppm (0.025 mg/kg/day) was identified in this study,
Reproductive Effects
0 Lobdel and Johnston (1964) conducted a three-generation study in
Charles River rats. Each parental dose group included 10 males and
20 females. The investigators incorporated methyl parathion (99% pure)
in the diet of males and females at dpse levels of 0, 10 or 30 ppm,
except for reduction of each dose by 50% during the initial 3 weeks
of treatment, to produce dose equivalents of 0, 1.0 and 3.0 mg/kg/day,
respectively. There was no pattern with respect to stillbirths,
although the 30-ppm groups had a higher total number of stillborn.
Survival was reduced in weanlings of the Fia, Flb and F2a groups at
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Methyl Parathion August, 1987
30 ppm, and in weanlings of the f^a 9roup at 10 ppm. At 30 ppm,
there was also a reduction in fertility of the ?2b dams at the second
mating; the first mating resulted in 100% of the animals having
litters, while at the second mating, only 41% had litters. Animals
exposed to 10 ppm methyl parathion did not demonstrate significant
deviations from the controls. A NOAEL of 10 ppm (t.O mg/kg/day) was
identified in this study.
0 Daly and Hogan (1982) conducted a two-generation study of methyl
parathion (93.65% pure) toxicity in Sprague-Dawley rats. Each parental
dose group consisted of 15 males and 30 females. The compound was
added to the diet at levels of 0, 0.5, 5.0 or 25 ppm. Using compound
intake data from the study report, equivalent dose levels are about
0, 0.05, 0.5 or 2.5 mg/kg/day. Feeding of the diet was initiated
14 weeks prior to the first mating and then continued for the remainder
of the study. Reduced body weight (p <0.05) was observed in FQ and
PI dams at the 25-ppm dose level. A slight decrease in body weight
was noted in F^a and F2a pups in the 25-ppm group, but this was not
significant (p >0.05). Overall, the authors concluded that there was
no significant (p >0.05) effect attributable to methyl parathion in
the diet. Based on maternal weight gain, the NOAEL for this study
was 5.0 ppm (0.5 mg/kg/day).
Developmental Effects
0 Gupta et al. (1985) dosed pregnant Wistar-Furth rats (10 to 12 weeks
of age) with methyl parathion (purity not specified) on days 6 to 20
of gestation. Two doses were used: 1.0 mg/kg (fed in peanut butter)
or 1.5 mg/kg (administered by gavage in peanut oil). The low dose
produced no effects on maternal weight gain, caused no visible signs
of cholinergic toxicity and did not result in increased fetal resorp-
tions. The high dose caused a slight but significant (p <0.05)
reduction in maternal weight gain (11% in exposed versus 16% in
controls, by day 15) and an increase in late resorptions (25% versus
0%). The high dose also resulted in cholinergic signs (muscle fasicu-
lation and tremors) in some dams. Acetylcholesterase (AChE) activity,
choline acetyltransferase (CAT) activity, and quinuclidinyl benzilate
(QNB) binding to muscarinic receptors were determined in several
brain regions of fetuses at 1, 7, 14, 21 and 28 days postnatal age,
and in maternal brain at day 19 of gestation. Exposure to 1.5 mg/kg
reduced (p <0.05) the AChE and increased CAT activity in all fetal
brain regions at each developmental period and in the maternal brain.
Exposure to 1.0 mg/kg caused a significant (p <0.05) but smaller and
less persistent reduction of AChE activity in offspring, but no change
in brain CAT activity. Both doses reduced QNB binding in maternal
frontal cortex (p <0.05), but did not alter the postnatal pattern of
binding in fetuses. In parallel studies, effects on behavior (cage
emergence, accommodated locomotor activity, operant behavior) were
observed to be impaired in rats exposed prenatally to 1.0 mg/kg, but
not to the 1.5-mg/kg dose. No morphological changes were observed in
hippocampus or cerebellum. It was concluded that subchronic prenatal
exposure to methyl parathion altered postnatal development of
cholinergic neurons and caused subtle alterations in selected
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Methyl Parathion August, 1987
-13-
behaviors of the offspring. The fetotoxic LOAEL for this study was
1.0 rag/kg.
0 Gupta et al. (1984) administered oral doses of 1.0 or 1.5 mg/kg/day
of methyl parathion (purity not specified) to female Wistar-Furth rats
on days 6 through 15 or on days 6 through 19 of gestation. Protein
synthesis in brain and other tissues was measured on day 15 or day 19
by subcutaneous injection of radioactive valine. The specific activity
of this valine in the free amino acid pool and protein-bound pool
(measured 0.5, 1.0 and 2.0 hours after injection) was significantly
(p <0.05) reduced in various regions of the maternal brain and in
maternal viscera, placenta and whole embryos (day 15), and in fetal
brain and viscera (day 19). The inhibitory effect of methyl parathion
on protein synthesis was dose dependent, greater on day 19 than on
day 15 of gestation and more pronounced in fetal than in maternal
tissues. With respect to protein synthesis in both maternal and
fetal tissues, the LOAEL of this study was 1.0 mg/kg.
Mutagenicity
0 Van Bao et al. (1974) examined the lymphocytes from 31 patients exposed
to various organophosphate pesticides for indications of chromosome
aberrations. Five of the examined patients had been exposed to methyl
parathion. Blood samples were taken 3 to 6 days after exposure and
again at 30 and 180 days. A temporary, but significant (p <0.05)
increase was found in the frequency of chromatid breaks and stable
chromosome-type aberrations in acutely intoxicated persons. Two of
the methyl parathion-exposed persons were in this category, having
taken large doses orally in suicide attempts. The authors concluded
that the results of this study strongly suggest that the organic
phosphoric acid esters exert direct mutagenic effects on chromosomes.
0 Shigaeva and Savitskaya (1981) reported that metophos (methyl para-
thion) induced visible morphological mutations and biochemical mutations
in Pseudomonas aeruginosa at concentrations between 100 and 1,000 ug/mL,
and significantly (p <0.05) increased the reversion rate in Salmonella
typhimurium at concentrations between 5 and 500 ug/mL.
0 Grover and Malhi (1985) examined the induction of micronuclei in bone
marrow cells of Wistar male rats that had been injected with methyl
parathion at doses between one-third and one-twelfth of the LD5Q.
The increase in micronuclei formation led the authors to conclude
that methyl parathion has high mutagenic potential.
0 Mohn (1973) concluded that methyl parathion was a probable mutagen,
based on the ability to induce 5-methyltryptophan resistance in
Escherichia coli. Similar results were obtained using the streptomycin-
resistant system of j:. coli and the trp-conversion system of Saccharo-
myces cerevisiae.
0 Rashid and Mumma (1984) found methyl parathion to be mutagenic to S.
typhimurium strain TA100 after activation with rat liver microsomal
and cytosolic enzymes.
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Methyl Parathion August, 1987
-14-
0 Chen et al. (1981) investigated sister-chromatid exchanges (SCE) and
cell-cycle delay in Chinese hamster cells (line V79) and two human
cell lines (Burkitt lymphoma B35M and normal human lymphoid cell
Jeff), and found methyl parathion to be the most active pesticide
of eight tested with respect to its induction potential.
8 Riccio et al. (1981) found methyl parathion to be negative in two
yeast assay systems (diploid strains D3 and D7 of Saccharomyces
cerevisiae), based on mitotic recombination (in D3), and mitotic
crossing over, mitotic gene conversion, and reverse mutation (in D7)»
Carcinogenici ty
0 NCI (1978) conducted chronic (105-week) feeding studies of methyl
parathion in F344 rats and B6C3F1 mice (50/sex/dose). Rats were fed
methyl parathion (94.6% pure) at dose levels of 0, 20 or 40 ppm
(equivalent to doses of 0, 1 or 2 mg/kg/day). Mice were initially
fed dose levels of 62.5 or 125 ppm, but because of severely depressed
body weight gain in males, their doses were reduced at 37 weeks to
20 or 50 ppm, respectively. Time-weighted averages for males were
calculated to be 35 or 77 ppm (about 5.2 or 11.5 mg/kg/day). Females
received the original dose level throughout. Based on gross and
histological examinations, no tumors were observed to occur at an
incidence significantly higher than that of the control value in either
the mice or rats. The authors concluded that methyl parathion was
not carcinogenic in either species under the conditions of the test.
0 Daly et al. (1984) fed Sprague-Dawley rats (60/sex/dose) methyl
parathion (93.65%) in the diet for 2 years. Doses tested were 0,
0.5, 5 or 50 ppm, estimated as equivalent to doses of 0, 0.025, 0.25
or 2.5 mg/kg/day. There were no significant (p >0.05) increases in
neoplastic lesions between treated and control groups.
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) , mg/L { ug/L)
(UF) x ( L/day)
where:
NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect-Level
in mg/kg bw/day.
BW = assumed body weight of a child (10 kg) or
an adult (70 kg).
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Methyl Parathion August, 1987
-15-
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 located in the available literature that were suitable for
deriving a One-day HA value. It is recommended that the Ten-day HA value for
the 10-kg child (0.31 mg/L calculated below) be used at this time as a
conservative estimate of the One-day HA value.
Ten-day Health Advisory
The studies by Rider (1969, 1970, 1971) have been selected to serve as
the basis for calculation of the Ten-day HA for methyl parathion. In these
studies, human volunteers ingested methyl parathion for 30 days at doses
ranging from 1 to 30 mg/day. The most sensitive indicator of effects was
inhibition of plasma ChE. No effects in any subject were observed at a dose
of 22 mg/day (about 0.31 mg/kg/day with assumed 70-kg body weight), and this
was identified as the NOAEL. Doses of 24 mg/day inhibited ChE activity in
plasma and red blood cells in two of five subjects, maximum decreases being
23 and 24% in plasma and 27 and 55% in red blood cells. Higher doses (26 to
30 mg/day) caused greater inhibition. On this basis, 24 mg/day (0.34 mg/kg/day)
was identified as the LOAEL. Short-term toxicity or teratogenicity studies
in animals identified LOAEL values of 1.0 to 2.5 mg/kg/day (Gupta et al.,
1984, 1985; Shtenberg and Dzhunusova, 1968; Tegeris and Underwood, 1977), but
did not identify a NOAEL value.
Using a NOAEL of 0.31 mg/kg/day, the Ten-day HA for a 10-kg child is
calculated as follows:
Ten-day HA = (0-31 mg/kg/day) (10 kg) = 0.31 mg/L (310.0 ug/L)
(10) (1 L/day)
where:
0.31 mg/kg/day = NOAEL, based on absence of toxic effects or inhibition
of ChE in humans exposed orally for 30 days.
10 kg = assumed body weight of a child.
10 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from a study in humans.
1 L/day = assumed daily water consumption of a child.
Longer-term Health Advisory
The 90-day feeding study in dogs by Tegeris and Underwood (1978) has
been selected to serve as the basis for calculation of the Longer-term HA
for methyl parathion. In this study, a NOAEL of 0.3 mg/kg/day was identified.
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Methyl Parathion August, 1987
-16-
based on absence of effects on body weight, food consumption, clinical chem-
istry, hematology, urinalysis, organ weights, gross pathology, histopathology
and ChE activity. Itie LOAEL, based on ChE inhibition, was 1.0 mg/kg/day.
These values are supported by the results of Ahmed et al. (1981), who
identified a NOAEL of 0.3 mg/kg/day in a 1-year feeding study in dogs, and
by the study of Daly and Rinehart (1980), which identified a LOAEL of
1.5 mg/kg/day (based on decreased testes weight) in a 90-day feeding study in
mice.
Using a NOAEL, of 0.3 mg/kg/day, the Longer-term HA for a 10-kg child is
calculated as follows:
Longer-term HA = (0.3 mg/kg/day) (10 kg) = 0.03 mg/L (30 ug/L)
(100) (1 L/day)
where:
0.3 mg/kg/day = NOAEL, based on absence of effects on body weight,
food consumption, clinical chemistry, hematology,
urinalysis, organ weights, gross pathology, histo-
pathology and ChE activity in dogs fed methyl parathion
for 90 days.
10 kg = assumed body weight of a child. ^
100 = uncertainty factor, chosen in accordance with NAS/OCW
guidelines for use with a NOAEL from an animal study.
1 L/day » assumed daily water consumption of a child.
Using a NOAEL of 0.3 mg/kg/day, the Longer-term HA for a 70-kg adult is
calculated as follows:
Longer-term HA = (0.3 mg/kg/day) (70 kg) , 0.i0 mg/L (100 ug/L)
(100) (2 L/day)
where:
0.3 mg/kg/day = NOAEL, based on absence of effects on body weight,
food consumption, clinical chemistry, hematology,
urinalysis, organ weights, gross pathology, histo-
pathology and ChE activity in dogs fed methyl parathion
for 90 days.
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 by an adult.
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Methyl Parathion , August, 1987
-17-
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
carcinogenic potential (U.S. EPA, 1986a), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.
The 2-year feeding study in rats by Daly et al. (1984) has been selected
to serve as the basis for calculation of the Lifetime HA for methyl parathion.
In this study, a NOAEL of 0.025 mg/kg/day was identified, based on the absence
of effects on body weight, organ weights, hematology, clinical chemistry, retinal
degeneration and cholinergic signs. A LOAEL of 0.25 mg/kg/day was identified,
based on decreased hemoglobin, red blood cell counts, and hematocrit (males),
changes in organ-to-body weight ratios (males and females) and one case of
visible cholinergic signs. There was increased retinal degeneration at
2.5 mg/kg/day, but this was not greater than control at 0.25 or 0.025 mg/kg/day.
This LOAEL value (0.25 mg/kg/day) is lower than most other NOAEL or LOAEL
values reported in other reports. For example, NOAEL values of 0.3 to 3.0
mg/kg/day have been reported in chronic studies by Ahmed et al. (1981), NCI
(1978), Lobdell and Johnston (1964) and Daly and Hogan (1982).
Using a NOAEL of 0.025 mg/kg/day, the Lifetime HA for a 70-kg adult is
calculated as follows:
Step 1: Determination of the Reference Dose (RfD)
RfD = (0.025 mq/kg/day) = Q.00025 mg/kg/day
where:
0.025 mg/kg/day = NOAEL, based on absence of cholinergic signs or
other adverse effects in rats exposed to methyl ,
parathion in the diet for 2 years.
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Methyl Parathion t August, 1987
>
-18-
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal studyc
Step 2: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL = (0.00025 mg/kg/day) (70 kg) . 0.009 /L (9 /L)
(2 L/day)
where:
0.00025 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
Lifetime HA = (0.009 mg/L) (20%) = 0.002 mg/L (2 ug/L)
where:
0.009 mg/L = DWEL.
20% = relative source contribution from water.
Evaluation of Carcinogenic Potential
0 No evidence of carcinogenic activity was detected in either rats or
mice in a 105-week feeding study (NCI, 1978).
0 Statistically significant (p <0.05) increases in neoplasm frequency
were not found in a 2-year feeding study in rats (Daly et al., 1984).
0 The International Agency for Research on Cancer (IARC) has not
evaluated the carcinogenicity of methyl parathion.
° Applying the criteria described in EPA's guidelines for assessment of
carcinogenic risk (U.S. EPA, 1986a), methyl parathion may be classified
in Group D: not classified. This category is for substances with
inadequate animal evidence of carcinogenicity.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 NAS (1977) concluded that data were inadequate for calculation of an
ADI for methyl parathion. However, using data on parathion, NAS
calculated an ADI for both parathion and methyl parathion of 0.0043
n"3A9/day, using, a NOAEL of 0.043 mg/kg/day in humans (Rider et al.,
1969) and an uncertainty factor of 10 (NAS, 1977). From this ADI,
NAS calculated a chronic Suggested-No-Adverse—Response Level (SNARL)
of 0.03 mg/L, based on water consumption of 2 L/day by a 70-kg adult,
and assuming a 20% RSC.
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Methyl Parathion August, 1987
-19-
The U.S. EPA Office of Pesticide Program (EPA/OPP) previously calcu-
lated a provisional ADI (PADI) of 0.0015 mg/kg/day, based on a NOAEL
of 0.3 mg/kg/day. This is based on the 90-day dog study by Tegeris
and Underwood (1978) and a 200-fold uncertainty factor. This PADI
has been updated to use a value of 0.0025 mg/kg/day based on a NOAEL
of 0.0250 mg/kg/day in a 2-year rat chronic feeding study and a
100-fold uncertainty factor.
ACGIH (1984) has proposed a time-weighted average threshold limit
value of 0.2 mg/m3.
The National Institute for Occupational Safety and Health has recom-
mended a standard for methyl parathion in air of 0.2 mg/ra3 (TDB, 1985).
The U.S. EPA has established residue tolerances for parathion -and
methyl parathion in or on raw agricultural commodities that range
from 0.1 to 0.5 ppm (CFR, 1985). A tolerance is a derived value
based on residue levels, toxicity data, food consumption levels,
hazard evaluation and scientific judgment; it is the legal maximum
concentration of a pesticide in or on a raw agricultural commodity or
other human or animal food (Paynter et al., undated).
The World Health Organization established an ADI of 0.02 mg/kg/day
(Vettorazi and van den Hurk, 1985).
VII. ANALYTICAL METHODS
Analysis of methyl parathion is by a gas chromatographic (GC) method
applicable to the determination of certain nitrogen-phosphorus
containing pesticides in water samples (U.S. EPA, 1986b). In this
method, approximately 1 liter of sample is extracted with methylene
chloride. The extract is concentrated and the compounds are separate.3
using capillary column LGC. Measurement is made using a nitrogen-
phosphorus detector. The method detection limit has not been determined
for methyl parathion, but it is estimated that the detection limits
for analytes included in this method are in the range of 0.1 to 2 ug/L.
VIII. TREATMENT TECHNOLOGIES
Available data indicate that granular-activated carbon (GAC) and
reverse osmosis (RO) will effectively remove methyl parathion from
water.
Whittaker (1980) experimentally determined adsorption isotherms for
methyl parathion and methyl parathion diazinion bi-solute solutions.
As expected, the bi-solute solution showed a lesser overall carbon
capacity than that achieved by the application of pure solute solution.
Under laboratory conditions, GAC removed 99+%. of methyl parathion
(Whittaker et al., 1982).
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Methyl Parathion August, 1987
20
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CHEMLAB. 1985. The chemical information system. CIS, Inc., Bethesda, MD.
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methyl parathion 4E on soil. Compilation; unpublished study, including
AG-A Nos. 4635 I, II, II, and 5023.
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Daly, I., G. Hogan and J. Jackson.* 1984. A two-year chronic feeding study
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Daly, I.W., and W.E. Rinehart.* 1980. A three month feeding study of methyl
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Daly, I.W., W.E. Rinehart and M. Cicco.* 1979. A four week pilot study in
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Fan, A., J.C. Street and R.M. Nelson. 1978. Immunosuppression in mice
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Gabovich, R.D., and I.L. Kurennoy. 1974. Ozonation of water containing
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Gaines, T.B. 1969. Acute toxicity of pesticides. Toxicol. Appl. Pharmacol.
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\
Galloway, C.* 1985. Guinea pig skin sensitization: methyl parathion tech-
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Grover, I.S., and P.K. Malhi. 1985. Genotoxic effects of some organophos-
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Haley, T.J., J.H. Farmer, J.R. Harmon and K.L. Dooley. 1975. Estimation of
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Hollingworth, R.M., R.L. Metcalf and I.R. Fukuto. 1967. The selectivity of
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•Confidential Business Information submitted to the Office of Pesticide
Programs.
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