820K88009 DRAFT
August, 1987
BAYGON (Propoxur)
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 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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II. GENERAL INFORMATION AND PROPERTIES
CAS No. 114-26-1
Structural Formula
2-( 1 -Me thylethoxy) -phenol methylcarbamate
Synonyms
0 Propoxur (proposed common name); Aprocarb; Blattenex; BAY 39007;
Bayer 39007; Pillargon; Propyon; Suncide; Tugon; QMS 33; Unden
(Meister, 1984).
Uses
0 A nonfood insecticide used on humans, animals and turf grass
(Meister, 1984).
Properties (ACGIH, 1984; Meister, 1984; and CHEMLAB, 1985)
Chemical Formula C
Molecular Weight 209.24
Physical State (at 258C) White to tan crystalline solid
Boiling Point
Melting Point 91 8C
Density (°C)
Vapor Pressure (120°C) 0.1 mmHg
Water Solubility (20°C) 2000 mg/L
Log Octanol/Water Partition 0.14
Coefficient
Taste Threshold
Odor Threshold
Conversion Factor
Occurrence
Baygon has been found in none of the 58 ground water samples analyzed
from 55 locations. No surface water samples were analyzed (STORET,
1987).
Environmental Fate
(Forthcoming from OPP)
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III. PHARMACOKINETICS
Absorption
0 Vandekar et al. (1971) administered a single oral dose of 1.5 mg/kg
of propoxur, 95% active ingredient (a.i.), to a 42-year-old male
volunteer. About 45% of the dose was recovered in urine within
24 hours as o-isopropoxyphenol. Since vomiting occurred 23 minutes
after ingestion, the authors assumed that much of the dose was expelled
by this route, so the percent actually absorbed could not be calculated.
0 Chemagro Corp. (no date) investigated the dermal absorption of 1^c-
labeled Baygon in human subjects. Baygon (4 ug/cm2, total dose less
than 1 mg) was applied to the forearm of the subjects(s) in four tests:
(1) application to the skin without preparation, (2) application
after stripping of the skin with an adhesive tape, (3) application
followed by occlusion and (4) application followed by induction of
sweating. The amounts excreted (route not specified, but presumably
in urine) after these treatments were 20, 51, 64 and 18%, respectively,
indicating that Baygon is well absorbed through the skin.
0 Krishna and Casida (1965) administered single oral doses of 14C-labeled
Baygon (50 mg/kg) to Sprague-Dawley rats. After 48 hours, about 4%
of the dose had been excreted in feces, and the remainder was detected
in urine (64 to 72%), expired air'(26%) or the body (4.2 to 7.9%).
This indicated that Baygon had been well absorbed (at least 96%) from
the gastrointestinal tract. Similar findings were reported by Foss
and Krechniak (1980).
Distribution
0 Foss and Krechniak (1980) investigated the fate of Baygon after oral
administration of 50 mg/kg to male albino rats. Analysis of tissues
indicated that Baygon levels were greatest in the kidneys, with
somewhat lower levels in the liver, blood and brain.
Metabolism
0 Dawson et al. (1964) administered single oral doses of 92.2 mg of
Baygon (purity not specified) to six male volunteers, and single oral
doses of 50 mg to three subjects. Urine samples were collected and
analyzed for metabolites. A material identified as 2-isopropoxyphenol
was observed in the urine of both groups. Similar results were
reported by Vandekar et al. (1971).
0 Foss and Krechniak (1980) investigated the metabolism of Baygon after
both oral and intravenous administration of 50 mg/kg to male albino
rats. Isopropoxyphenol was detected in tissues 10 minutes following
administration, and the highest concentrations were attained between
30 and 60 minutes after dosing. This metabolite prevailed in the
blood and liver, but in the kidney only unchanged Baygon could be
detected. Eight hours postdosing, only traces of Baygon and its
metabolites were detected in these tissues.
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* Everett and Gronberg (1971) studied the metabolism of Baygon in
Holtzman rats. Animals were dosed by gavage with Baygon (5 to 10
mg/kg) labeled with 1 4c Or ^H in the carbonyl or the isopropyl groups.
Pooled urine from eight rats (four/sex) dosed with 20 mg/kg/day of
unlabeled Baygon for 4 days was used to isolate sufficient quantities
of metabolites for identification of structure. Results indicated
that the major pathway of Baygon metabolism involved depropylation to
2-hydroxyphenol-N-methyl carbamate and hydrolysis of the carbamate to
isopropoxyphenol. Minor pathways involved ring hydroxylation at the
five- or six-position, secondary hydroxylation of the 2'-carbon of
the isopropoxy group and N-methyl hydroxylation. Metabolites that
contained the 6-hydroxy group formed N-conjugates, while those that
contained the 5-hydroxy group formed 0-glucuronides.
Excretion
Dawson et al. (1964) reported that in humans given a single oral
doses of 92.2 mg Baygon (purity not specified), 38% of the dose was
excreted as phenols in urine over the next 24 hours; most was excreted
in the first 8 to 10 hours.
Krishna and Casida (1965) administered single oral doses of 50 mg/kg
of 14c-carbonyl-labeled Baygon to Sprague-Dawley rats. After 48
hours, recovery of label in excretory products was as follows: 64%
(males) and 72% (females)'in urine; 4% in feces (males and females);
and 26% in expired carbon dioxide (males and females). Residual
label in the body was 4.2% (males) and 7.9% (females). One-third of
the excreted dose was hydrolyzed, with most of the remainder being
intact.
Everett and Gronberg (1971) reported that 85% of orally administered
14c-carbonyl-labeled Baygon (5 to 8 mg/kg) was recovered from Holtzman
rats within 16 hours of dosing; 20 to 25% of the radioactivity appeared
in the expired air, and 60% of the radioactivity appeared in the
urine as conjugates. Also, Foss and Krechniak (1980) indicated that
85 to 95% of an oral dose (50 mg/kg) administered to male albino rats
was excreted in urine with a half-life of 0.18 to 0.26 hour.
IV. HEALTH EFFECTS
Humans
Short-term Exposure
0 Vandekar et al. (1971) studied the acute oral toxicity of Baygon in
human volunteers. A 42-year-old man ingested a single oral dose of
1.5 mg/kg of propoxur (Baygon) (95% a.i., recrystallized). Cholinergic
symptoms, including blurred vision, nausea, sweating, tachycardia and
vomiting, began about 15 to 20 minutes after exposure. Effects were
transient and disappeared within 2 hours. Cholinesterase (ChE)
activity (measured spectrophotometrically) in red blood cells decreased
to 27% of control values by 15 minutes after exposure, and returned
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to control levels by 2 hours. No effect was detected in plasma ChE
activity. In a second test, a single dose of 0.36 mg/kg caused
short-lasting stomach discomfort, blurred vision and moderate facial
redness and sweating. Red blood cell ChE activity fell to 57% of
control values within 10 minutes, then returned to control levels
within 3 hours.
0 Vandekar et al. (1971) administered five oral doses of 0.15 or 0.20
mg/kg to male volunteers at half-hour intervals (total dose of 0.75
or 1.0 mg/kg). In each subject, a symptomless depression of red
blood cell ChE was observed; the lowest level, about 60% of control
values, was reached between 1 and 2 hours following doses 3, 4 and 5.
After the final dose, red blood cell ChE activity rose to control
levels within about 2 hours. The authors noted that a dose of Baygon
was tolerated better if it was divided into portions and given over
time than if it was given as a single dose.
Long-term Exposure
0 Davies et al. (1967) described the effects of a large-scale spraying
operation in El Salvador in which Baygon (OMS-33, 100% a.i.) was
used. The trial was planned so that medical assistance would be
available, and appropriate clinical support could be provided to
those affected by the spraying. The total amount of OMS-33 sprayed
was 345 kg. Among the spraymen, exposure (expressed in person-days)
was 70.5; 19 experienced symptoms (26% incidence). In the general
population, the exposure was 3,340 person-days, and 35 experienced
symptoms (1% incidence). The primary symptoms were headache, vomiting
and nausea. In the spraymen, the symptoms occurred mostly in the
first days, with no visible symptoms after this time. In severe
cases, atropine was administered as antidote. It was concluded that
the acute toxicity symptoms were observed in a low incidence, and
they were, in general, mild, evanescent, reversible, responsive to
small doses of atropine, and tended to occur at the beginning of the
spray program.
0 Montazemi (1969) reported on the toxic effects of Baygon on the
population of 26 villages in Iran that were sprayed with Baygon at
the rate of 2 g/m2 daily for 18 days. Selected inhabitants from six
villages and sprayers were examined on days 2, 8 and 18 and after
the completion of the spraying. Depression of ChE activity was found
in the inhabitants and in the sprayers, but the sprayers generally
had more severe symptoms. Atropine or belladonna was adequate to
treat those exhibiting symptoms.
Animals
Short-term Exposure
0 The acute oral LD5Q value for technical Baygon (purity not spedified)
in male and female Sherman rats was reported to be 83 and 86 mg/kg,
respectively (Gaines, 1969). The oral LD5Q was reported to be 32 mg/kg
in mice and 40 mg/kg in guinea pigs (NIOSH, 1983).
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8 Farbenfabriken Bayer (1961) determined an oral LD5Q of 100 to 150 mg/kg
(purity not specified) in male albino rats. Severe muscle spasms
were observed, but no dose-response information was provided.
0 Eben and Kimmerle (1973) studied the acute toxicity of Baygon in
SPF-Wistar rats. Single oral doses of propoxur (98.7% a.i.), diluted
with propylene glycol, were given by gavage to groups of three male
rats at levels of 15, 20, 40 or 60 mg/kg; female rats were given
doses of 10, 20, 40 or 60 mg/kg. Cholinesterase levels were measured
in plasma, erythrocytes and brain at 10, 20 and 180 minutes after
dosing. Maximum ChE depression was observed at 10 and 20 minutes in
the plasma and erythrocytes, and at 180 minutes in the brain. The
inhibition was dose-dependent and a no-effect level was not observed.
In plasma, ChE was inhibited from 19% (low dose) to 63% (high dose)
in males and from 0 to 32% in females. In erythrocytes, ChE was
inhibited from 27 (low dose) to 63% (high dose) in males and from 15
to 45% in females. Based on ChE inhibition, this study identified a
Lowest-Observed-Adverse-Effect-Level (LOAEL) of 10 mg/kg/day.
0 Farbenfabriken Bayer (1966) conducted a 9-week feeding study with
Bay 39007 (purity not specified) in male and female rats (Elberfeld FB),
Baygon was included in the diets of the male animals at dose levels
of 0, 1,000, 2,000, 4,000 or 8,000 ppm. Based on the assumption that
1 ppm in the diet of rats is equivalent to 0.05 mg/kg/day (Lehman,
1959), this corresponds to doses of 0, 50, 100, 200 or 400 mg/kg/day,
respectively. Females were given only one dose (4,000 ppm). The study
was begun when the animals (15/dose level) were 4 weeks of age and
weighed about 48 g. In males, food consumption and body weight were
depressed in a dose-dependent manner. At the 4,000 and 8,000-ppm
levels, the males were less lively and exhibited slightly shaggy
coats. Gross pathologic examinations of all animals were conducted.
Two males exposed to 4,000 ppm died during the study, one at 11 days
(evidence of myocarditis) and one at 23 days. Two males also died
at the 8,000-ppm level (at 23 and 25 days); one showed necrotic
inflammation of the mucosa of the small intestine. Females (exposed
to 4,000 ppm only) displayed decreased food consumption and reduced
weight gain similar to that seen in exposed males. One of 15 female
controls died at day 12 (death attributed to pneumonia), and two of
15 exposed females died, one at 7 days and one at 45 days (in this
rat there was suppuration of the cerebellar bottom). There were
apparently no measurements of ChE activity or other clinical tests
performed during this study. It was concluded by the authors that
the observed pathology could not be directly attributed to the presence
of Baygon in the diet. Based on gross observations, the No-Observed-
Adverse-Effect-Level (NOAEL) for male animals was identified as
2,000 ppm (100 mg/kg/day) and the LOAEL as 4,000 ppm (200 mg/kg/day).
In females, 4,000 ppm (200 mg/kg/day, the only dose tested) was a
toxic level.
0 Eben and Kimmerle (1973) exposed SPF-Wistar rats (four/sex/dose) by
gavage to doses of 3, 10 or 30 mg/kg/day of Baygon for 4 weeks. The
high-dose animals (30 mg/kg/day) displayed cholinergic symptoms.
Cholinesterase activity in plasma and red blood cells, measured 15
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minutes after dosing on days 3, 8, 14, 21 and 28, was generally
depressed in a dose-related manner at 10 and 30 mg/kg, but not at the
3-mg/kg dose. For example, on day 28, ChE activity in plasma was
reduced by 0, 21 or 27% in males and by 14, 27 or 41% in females. In
erythrocytes, ChE was inhibited by 9, 24 or 32% in males and by 11,
32 or 43% in females. No cumulative toxic effects were observed.
Based on ChE inhibition, the NOAEL for this study was 3 mg/kg/day,
and the LOAEL was 10 mg/kg/day.
Dermal/Ocular Effects
0 The acute dermal LD50 of technical Baygon (purity not specified) was
reported to be greater than 2,400 mg/kg for both male and female
Sherman rats (Gaines, 1969).
0 Crawford and Anderson (1971) indicated that 500 mg of technical
Baygon (purity not specified, dissolved in acetone) did not cause
any skin irritation within 72 hours of its application to the abraded
or unabraded skin of mature New Zealand White rabbits (six/group).
0 Heimann (1982) demonstrated that Baygon (98.8% pure) is not a skin
sensitizer when tested in guinea pigs.
0 Crawford and Anderson (1971) instilled 100 mg of technical Baygon
(purity not specified) in the left eye of six rabbits. Examination
at 48 and 72 hours revealed no evidence of ocular irritation or
corneal damage.
Long-term Exposure
0 Eben and Kimmerle (1973) fed propoxur (98.7% a.i.) to male rats in
the diet for 15 weeks. Doses were 0, 250, 750 or 2,000 ppm. Assuming
that 1 ppm in the diet is equivalent to 0.05 mg/kg/day (Lehman, 1959),
this corresponds to doses of about 0, 12.5, 37.5 or 100 mg/kg/day.
Assays for ChE activity in plasma, erythrocytes and brain showed no .
constancy of inhibition and no dependence on the administered dose.
No other details were given.
0 Root et al. (1963) studied the effect of Bayer 39007 added to the
diet of Sprague-Dawley rats for 16 weeks. The rats (12/sex/dose,
weighing 72 to 145 g at the start of the feeding trial) were fed Baygon
(technical, 95.1% pure) at dose levels of 0, 100, 200, 400 or 800 ppm.
Assuming that 1 ppm in the diet of rats is equivalent to 0.05 mg/kg/day
(Lehman, 1959), this corresponds to doses of 0, 5, 10, 20 or 40 mg/kg/day.
Biweekly measurements revealed no changes in growth or food consump-
tion. Cholinesterase was assayed in blood, brain and submaxillary
glands of five animals of each sex at each dose level, and no inhi-
bition was detected. Necropies were performed on five animals of
each sex at the termination of the study, and no significant pathology
was found. It was concluded that the NOAEL for the rats was greater
than 800 ppm (40 mg/kg/day, the highest dose tested).
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0 Suberg and Loeser (1984) conducted a chronic (106-week) feeding study
of Baygon (99.4% a.i.) in rats (Elberfeld strain) at dose levels of
0, 200, 1,000 or 5,000 ppm. Based on the assumption that 1 ppm in
the diet of rats is equivalent to 0.05 mg/kg/day (Lehman, 1959), this
corresponds to doses of about 0, 10, 50 or 250 mg/kg/day. There were
50 rats of each sex per dose level, plus an additional 10 of each sex
for interim autopsies at the end of the first year. At the 200-ppm
dose, there was no effect on food consumption or body weight, there
were no cholinergic signs, and clinical chemistry, gross pathology,
histopathology and organ weights showed no changes from control
values. At 1,000 ppm, retarded weight gain was observed in males
during the first 20 weeks. At 1,000 and 5,000 ppm, there were
significant hyperplasia of urinary bladder epithelium (described in
more detail in the Carcinogenicity section) and increased incidence
of neuropathy. At the 5,000-ppm dose, both weight gain and food
consumption were significantly retarded throughout the study; males
showed increased thromboplastin time, and females had consistently
lower mean plasma ChE activity than did controls or other test groups.
Both sexes showed some degree of splenic atrophy, but there were no
other significant changes in other organs. Based on body weight
gain, the NOAEL for this study was identified as 200 ppm (10 mg/kg/day),
and the LOAEL as 1,000 ppm (50 mg/kg/day).
0 Loser (1968a) conducted a 2-year feeding study of Baygon in male and
female SPF-Wistar rats. Starting at 1 month of age, the test material,
BAY 39007 (99.8% a.i., technical), was included in the diet at levels
of 0, 250, 750, 2,000 or 6,000 ppm. Based on the assumption that
1 ppm in the diet of rats is equivalent to 0.05 mg/kg/day (Lehman,
1959), this corresponds to doses of 0, 12.5, 37.5, 100 or 300 mg/kg/day.
The control group consisted of 50 animals of each sex, while test
groups contained 25 animals of each sex. Growth and behavior were
observed, liver function and ChE activity were tested, and blood and
urine were analyzed periodically. Necropsies on five animals of each
sex were conducted at the termination of the experiment. The major
adverse effects noted were low food consumption and low body weight
in all animals at the 6,000-ppm dose level, and low body weight in
the female (but not male) animals at the 2,000-ppm dose level.
Cholinesterase determinations on blood (measured at the high dose
only) revealed no changes; ChE activity was 9.8 and 9.9 units in
control males and females, respectively, compared with 9.9 and 10,0
in exposed males and females. The author indicated that the methodology
may have been too insensitive to detect small changes that may have
occurred. No spasms or other symptoms of ChE inhibition were observed.
No impairment of liver or kidney function was detected by clinical
tests, but necropsy revealed increased liver weight at all doses
greater than 250 ppm. Results of blood analysis were normal at all
dose levels except at 6,000 ppm. Apart from increased liver weights,
necropsy findings were unremarkable. Based on increased liver weights,
this study identified a NOAEL of 250 ppm (12.5 mg/kg/day) and a LOAEL
of 750 ppm (37.5 mg/kg/day).
0 Loser (1968b) conducted a 2-year study of Baygon toxicity in beagle
dogs. The product, BAY 39007 (technical, 99.8% pure), was included in
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the diet at levels of 0, 100, 250, 750 or 2,000 ppm. Assuming that
1 ppm in the diet of dogs is equivalent to 0.025 mg/kg/day (Lehman,
1959), this corresponds to doses of about 0, 2.5, 6.25, 18.7 or
50 mg/kg/day. The study was begun when the dogs (four/sex/dose) were
4 to 5 months old. Observations on the animals included weight and
food consumption at periodic intervals, ChE determinations in blood
at 16 weeks, clinical evaluations of blood and urine, and tests for
liver and kidney function. Necropsies were performed on animals that
died during the study and at termination of the study. The appearance,
behavior, and food consumption of dogs at the 100, 250 or 750 ppm
levels were comparable to those of the controls. At the 2,000-ppm
level, dogs of both sexes appeared to be weak and sick. One of the
males and all four females at this dose died before completion of the
study. During the first 6 months, dogs at this dose level exhibited
quivering and spasms, particularly in the abdominal region, and food
consumption was less than for the controls (especially in females);
as expected, the dogs showed statistically significant depression
in weight gain compared with the controls. Males, but not females,
showed lower weights than did controls at the 750-ppm dose level, but
the decrease was not statistically significant. Clinical analyses
did not reveal any aberrations in the blood or any changes in liver
or kidney function. However, increased liver weights were observed
at necropsy, and serum electrophoresis performed at the time of
sacrifice revealed decreased levels of some serum proteins, inter-
preted by the author as reflecting impaired protein synthesis.
Cholinesterase determinations in whole blood at 16 weeks did not
reveal any significant inhibition of activity. In males, ChE inhibi-
tion at 100, 250, 750 and 2,000 ppm was 0, 11, 1 and 13%, respectively,
and in females ChE inhibition was 0, 10, 7 and 0%, respectively. The
author indicated that the assay method may have been too insensitive
to detect small changes that may have occurred. Emaciation was the
principal finding in dogs that died during the study; one female had
abnormal liver parenchyma. The NOAEL for this study was 250 ppm
(6.25 mg/kg/day), and the LOAEL (based on increased liver weight,
decreased body weight and altered blood proteins) was 750 ppm (18.7
mg/kg/day).
Bomhard and Loeser (1981) conducted a 2-year feeding study of propoxur
(99.5% a.i.) in SPF CFI/W71 mice at dose levels of 0, 700, 2,000 or
6,000 ppm. Assuming that 1 ppm in the diet of mice is equivalent to
0.15 mg/kg/day (Lehman, 1959), this corresponds to doses of about 0,
105, 300 or 900 mg/kg/day. Mice were 5 to 6 weeks of age, weighing
22 to 25 g at the beginning of the study; each group consisted of 50
animals of each sex, plus an additional 10/sex/group included for
interim autopsy at 1 year. Body weight gain was slightly depressed
in male mice at the 6,000-ppm level. Apart from this observation,
all aspects of behavior, appearance, food intake, weight and mortality
were comparable to control values. Clinical chemistry and blood
studies, including glucose and cholesterol levels, were within the
normal range for all groups, and there were no significant gross
pathological or histopathological findings that could be attributed
to the ingestion of Baygon. It was concluded that the male mice
tolerated the pesticide at levels up to and including 2,000 ppm,
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while the female mice tolerated doses up to and including 6,000 ppm
without adverse effects. Based on these conclusions, the NOAEL for
this study was 2,000 ppm (300 mg/kg/day), and the LOAEL (based on
depressed weight gain in males) was 6,000 ppm (900 mg/kg/day).
Reproductive Effects
0 No multigeneration studies of the effects of Baygon on reproductive
function of animals were found in the available literature.
0 In a developmental toxicity study in rabbits, Schlueter and Lorke
(1981) observed no adverse effects on several reproductive end points.
This study is described below.
Developmental Effects
0 Schlueter and Lorke (1981) studied the effect of propoxur (99.6% a.i.)
on Himalayan CHBBsHM rabbits during gestation. Propoxur was admini-
stered by gavage (in 0.5% cremophor) to 15 animals/dose at 0, 1, 3
or 10 mg/kg. No adverse effects were observed in the dams, and no
changes were detected in implantation index, mean placental weight,
resorption index or litter size. Embryos were examined for visceral
and skeletal defects grossly, then were stained with Alizarin, and
transverse sections were prepared using the Wilson technique. No
adverse fetal effects were found at any dose level with respect to
mean fetal weight, the percent of stunting, the percent of slight
skeletal deviations, or the malformation index. These results indicate
that the NOAEL for maternal toxicity, teratogenicity and fetotoxicity
is greater than 10 mg/kg/day (the highest dose tested).
0 Lorke (1971) fed Baygon (technical, 98.4% a.i., 0.82% isopropoxyphenol)
in the diet to female FB-30 rats on days 1 to 20 of gestation, at
levels of 0, 1,000, 3,000 or 10,000 ppm (10/dose). Assuming that
1 ppm in the diet of rats is equivalent to 0.05 mg/kg/day, (Lehman,
1959), this corresponds to doses of about 50, 150 or 500 mg/kg/day.
The rats were 2.5 to 3.5 months of age, weighing 200 to 250 g at the
time of the experiment. Cesarean sections were performed on day 20.
External and internal examinations on fetuses were performed, and
fetuses were subjected to skeletal staining. At the 3,000- and
10,000-ppm dose levels, average fetal weights were significantly
lower than control values, but ether fetal measurements were in the
control range. No terata were observed at a higher incidence than in
the control group. Data on fetal ossification were not adequately
described for an adequate evaluation. Although this study appears to
reflect a NOAEL of 1,000 ppm (50 mg/kg/day) based on fetotoxic effects,
information obtained from this study is limited due to the small
number of animals tested and an apparent dose-related decrease in
maternal weight gain and fetal weight at the lowest dose tested
(although these effects were not statistically significant).
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Mutagenicity
0 DeLorenzo et al. (1978) evaluated the mutagenic properties of Baygon
and other carbamate pesticides by use of the Salmonella mutagenicity
test of Ames. In assays using five strains of Salmonella typhimurium,
no mutagenic activity was obtained with Baygon (with microsomal
activation).
0 Moriya et al. (1983) tested Baygon in five strains of £. typhimurium
and one strain of Escherichia coli using the Ames technique (without
metabolic activation) and observed no evidence of mutagenic activity.
0 Blevins et al. (1977) used five mutants of _S. typhimurium LT2 to
examine the mutagenic properties of Baygon and other methyl carbamates
and their nitroso derivatives. No mutagenic activity was observed
with Baygon in this experiment using the Ames technique.
Carcinogenicity
0 Suberg and Loeser (1984) conducted a chronic (106-week) feeding study
of Baygon (99.4% a.i.) in rats (Elberfeld strain) at dose levels of
0, 200, 1,000 or 5,000 ppm. Assuming that 1 ppm in the diet of rats
is equivalent to 0.05 mg/kg/day (Lehman, 1959), this corresponds to
doses of about 0, 10, 50 or 250 mg/kg/day. The study utilized 50
rats/sex/dose, plus an additional 10 of each sex included for interim
necropsies at the end of the first year. At 5,000 ppm there was
significant hyperplasia of the urinary bladder epithelium was noted.
The incidence at this dose level after 2 years was 44/49 in males and
48/48 in females, as compared with 1/49 and 0/49 in control males and
females, respectively. At 1,000 ppm, there was a smaller increased
incidence (10/50 and 5/49 in males and females), respectively. No
significant effect occurred at 200 ppm (1/50 and 0/49, males and
females, respectively). Bladder papillomas were observed in both
males (26/57) and females (28/48) at the highest dose after 2 years.
In addition, at the 5,000-ppm level, carcinoma of the bladder was
found in 8/57 males and 5/48 females, and carcinoma of the uterus was
seen in 8/49 females, as compared with 3/49 for the control group.
At the mid-dose level (1,000 ppm) only papillomas were noted in one
male. The tumors of significance in this study are the uncommon
bladder tumors (carcinoma and papillomas) with high incidences at the
high dose level. The combined tumor incidences were 34/57 males and
33/48 females at 5,000 ppm; 1/59 males and 0/48 females at 1,000 ppm.
and none in the 200-ppm or control groups.
0 Bomhard and Loeser (1981) conducted a 2-year feeding study of propoxur
(99.5% a.i.) in SPF CFI/W71 mice at dose levels of 0, 700, 2,000 or
6,000 ppm. Assuming that 1 ppm in the diet is equivalent to 0.15
mg/kg/day (Lehman, 1959), this corresponds to doses of about 0, 105,
300 or 900 mg/kg/day. Mice were 5 to 6 weeks of age, weighing 22 to
25 g at the beginning of the study; each group consisted of 50 animals
of each sex, plus an additional 10/sex/group included for interim
necropsy at 1 year. Gross and histological examination of tissues
revealed no evidence of increased tumor frequency.
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Baygon August, 1987
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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 ( /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).
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
The study by Vandekar et al. (1971) has been selected to serve as the
basis for determination of the One-day HA for Baygon. In this study, human
volunteers who ingested single oral doses of 0.36 or 1.5 mg/kg displayed
transient cholinergic signs accompanied by marked (43 and 75%, respectively)
inhibition of red blood cell ChE (measured 10 to 15 minutes after exposure).
Total doses of 0.75 or 1.0 mg/kg administered in five equal portions over 2
hours did not cause clinical signs, but inhibited red blood cell ChE by about
40%, A NOAEL was not identified; 0.36 mg/kg is taken as the LOAEL for bolus
exposure, and 0.45 mg/kg (three-fifths of a 0.75-mg/kg/day total dose,
administered in the first 3/5 doses) is the LOAEL when exposure to this
dose is spread over several hours. It should be noted that both values are
considerably lower than the NOAEL values for Baygon identified in subchronic
and chronic feeding studies in animals, especially rodents. Possible reasons
for this disparity are that humans may be more sensitive to this chemical
than animals are; furthermore, single oral doses probably produce higher peak
inhibitions than if the same total dose is ingested over a longer period of
time. It is also likely that measurement of ChE activity 10 to 15 minutes
after exposure (as in the case of human studies) detects peak inhibition,
while sampling later reveals smaller effects (due to the reversible nature of
ChE inhibition with carbamates). Since a child's exposure is more likely to
occur in a manner similar to Vandekar's test, where doses were administered
in five equal portions over time, the LOAEL of 0.45 mg/kg (three-fifths of a
0.75 mg/kg total dose) is used for the calculation below:
The One-day HA for a 10-kg child is calculated as follows:
One-day HA = (0-45 mg/kg/day) (10 kg) = 0>045 /L (4Q /L)
(100) (1 L/day)
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Baygon August, 1987
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where:
0.45 mg/kg/day = LOAEL, based on an inhibition of 40% in red blood cell
ChE activity in humans as determined 10 minutes after
oral exposure to three-fifths of a 0.75-mg/kg dose,
each fifth given at half-hour intervals, and based on
the fact that complete recovery of the ChE activity
occurred within 2 hours after administration of the
last fifth of the total dose.
1 0 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.
Ten-day Health Advisory
In addition to human studies by Vandekar et al. (1971) discussed above,
two studies were considered for determination of the Ten-day HA. In a tera-
tology study in rabbits by Schlueter and Lorke (1981), the NOAEL appeared to
be higher than 10 mg/kg/day, the highest dose tested. In a teratology study
in rats by Lorke (1971), the dietary administration of Baygon to animals
during gestation was designed to assess both maternal and fetal effects.
While sufficient data were obtained to derive a NOAEL of 50 mg/kg/day and
a LOAEL of 150 mg/kg/day in rats, it is important to note that a dosage of
50 mg/kg/day was sufficient to kill all female animals in a chronic study in
dogs by Loser (1968b); all deaths occurred before the end of the 2-year study
period. Because humans appear to be more sensitive to Baygon than animals,
the human study by Vandekar et al. (1971), used in the determination of the
One-day HA value, is also the most suitable study for calculation of the Ten-day
HA. The two LOAELs identified in this study, 0.36 mg/kg (bolus exposure) and
0.45 mg/kg/day (exposure to three-fifths of a 0.75-mg/kg total dose spread
out over the day) can be approximated to 0.40 mg/kg; this value is used below
for calculation of the Ten-day HA.
The Ten-day HA for a 10-kg child is calculated as follows:
Ten-day HA = (0.40 mg/kg/day) (10 kg) = 0>040 /L (40 /L)
(100) (1 L/day)
where:
0.40 mg/kg/day = LOAEL, based on mild cholinergic signs and 40%
inhibition of red blood cell ChE in humans 10 minutes
after a single oral dose.
10 kg = assumed body weight of a child.
100 = uncertainty factor, chosen in accordance NAS/ODW
guidelines for use with a LOAEL from a human study.
1 L/day = assumed daily water consumption of a child.
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Baygon f August, 1987
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Longer-tenn Health Advisory
No suitable information was found in the available literature for the
determination of the Longer-term HA value for Baygon. It is, therefore,
recommended that the modified Drinking Water Equivalent Level (DWEL) of
40 ug/L for a 10-kg child be used as a conservative estimate for a Longer-term
exposure. The DWEL of 100 ug/L, calculated below, should be used for the
Longer-term value for a 70-kg 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. 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 dogs by Loser (1968b) and the human study
by Vandekar et al. (1971) have been considered for determination of the
Lifetime HA. In the 2-year dog study by Loser (1968b), the chronic NOAEL was
identified as 6.25 mg/kg/day and the LOAEL as 18.7 mg/kg/day. The dog NOAEL
value is supported by the data of Loser (1968a) and of Suberg and Loeser
(1984), which identified NOAEL values of 12.5 and 10 mg/kg/day, respectively,
in chronic studies in rats. However, t^e dog appears to be far more sensitive
at the higher doses than are rodents; all female dogs and some of the males
in the high-dose group, 50 mg/kg/day, died before the end of the study
period, while mild systemic toxicity was noted at this dose level in rats.
Cholinesterase determinations were not performed in the dog study for use in
comparison with human data. Due to the reversible nature of ChE inhibition
by carbamates, a large difference is noted between the dosages that can cause
biologically significant levels of ChE inhibition and the dosages that can
produce cholinergic symptoms of toxicity (including death). Hence, in the
absence of ChE data in the dog study, and because of the sensitivity of this
end point in the determination of the toxicity of this chemical, the study by
Vandekar et al. (1971) in humans has been selected to serve as the basis for
the Lifetime HA for Baygon. This study was discussed in the previous sections
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Baygon August, 1987
-15-
on the One-day and Ten-day HAs. The 2-year mouse study by Bomhard and Loeser
(1981) was not considered, since the data suggest that the mouse is even less
sensitive than the rat.
Using a human ChE LOAEL of 0.36 mg/kg/day, the Lifetime HA is calculated
as follows:
Step 1: Determination of the Reference Dose (RfD)
RfD = (0*36 mg/kg/day) = 0.004 mg/kg/day
(100)
where:
0.36 mg/kg/day = LOAEL, based on mild cholinergic signs and 43%
inhibition of red blood cell ChE in a human 10 minutes
after a single oral dose.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a LOAEL from a human study.
Step 2: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL = (0-004 mg/kg/day) (70 kg) = 0.140 mg/L (140 ug/L)
(2 L/day)
where:
0.004 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 = (0-140 mg/L) (20%) = Q.003 ng/L (3 ug/L)
(10)
where:
0.140 mg/L = DWEL.
20% = assumed relative source contribution from water.
10 = additional uncertainty factor in accordance with ODW
policy* to account for possible carcinogenicity.
*This policy is used only for group C oncogen. However, since there is a
•potential that this chemical may be a more potent oncogen, its oncogenic
potency (qi*) was calculated using the multistage model (U.S. EPA, 1987a).
The q1* was estimated to be 7.9 x 10~3 (mg/kg/day)~1; if the oncogenic risk .
level associated with the above determined Lifetime HA value is computed
using this q,*, the risk level would be 7 x 10~7 (7 in 10,000,000).
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Baygon August, 1987
-16-
Evaluation of Carcinogenic Potential
0 Suberg and Loeser (1984) detected an increased frequency of urinary
bladder epithelium hyperplasia, bladder papillomas and carcinomas, and
carcinoma of the uterus in rats fed Baygon (250 mg/kg/day) for 2
years.
0 Bomhard and Loeser (1981) did not detect an increased incidence of
tumors in mice fed Baygon at doses up to 90 mg/kg/day for 2 years.
e The International Agency for Research on Cancer (IARC) has not evalu-
ated the carcinogenic potential of Baygon.
0 Applying the criteria described in EPA's guidelines for assessment
of carcinogenic risk (U.S. EPA, 1986a), Baygon may be classified in
Group C: possible human carcinogen. This category is for substances
with limited evidence of carcinogenicity in animals in the absence of
human data. However, this classification group may be considered
preliminary at the present (U.S. EPA, 1987b) since the U.S. EPA
Office of Pesticide Programs (OPP) has classified this chemical in
Group 82: probable human carcinogen (U.S. EPA, 1987a). A resolution
will be reached between OPP and the Cancer Assessment Group (CAG) in
the near future.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 Residue tolerances have not been established for Baygon by the OPP.
• The American Conference of Governmental Industrial Hygienists (ACGIH,
1984) has proposed a threshold limit value of 0.5 mg/m3.
0 The World Health Organization (WHO) calculated an ADI of 0.02 mg/kg/day
for Baygon (Vettorazzi and Van den Hurk, 1985).
VII. ANALYTICAL METHODS
8 Analysis of Baygon is by a high-performance liquid chromatographic
(HPLC) procedure used for the determination of N-methyl carbamoyloximes
and N-methylcarbamates in water samples (U.S. EPA, 1986b). In this
method, the water sample is filtered and a 400-uL aliquot is injected
into a reverse-phase HPLC column. Separation of compounds is achieved
using gradient elution chromatography. After elution from the HPLC
column, the compounds are hydrolyzed with sodium hydroxide. The
methyl amine formed during hydrolysis is reacted with o-phthalaldehyde
(OPA) to form a fluorescent derivative that is detected with a
fluorescence detector. The method detection limit has not been
determined for Baygon, but it is estimated that the detection limits
for analytes included in this method are in the range of 0.5 to 3 ug/L.
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Baygon August, 1987
-17-
VIII. TREATMENT TECHNOLOGIES
0 Available data indicate granular activated carbon (GAC) adsorption
to be a possible Baygon removal technique.
0 Adsorption of Baygon on GAC proceeds in accordance with both Freundlich
and Langmuir isotherms (El-Dib et al., 1974; Whittaker et al., 1982).
0 One full-scale laboratory test was carried out on a commercially
available system (Dennis et al., 1983; Kobylinski et al., 1984).
Different levels of Baygon (20 mg/L, 60 mg/L and 100 mg/L) were added
to tap water. At a flow rate of 67.4 gpm, the column removed 99% of
the Baygon in 3.5, 8.5, and 21 hours, respectively, using only 45 Ib
of granular carbon.
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Baygon August, 1987
-18-
IX. REFERENCES
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-19-
Everett, L.J., and R.R. Gronberg.* 1971. The metabolic fate of Baygon
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Baygon August, 1987
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'Confidential Business Information submitted to the Office of Pesticide
Programs
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