|
Acetochlor
CASRN 34256-82-1
Contents
0521
Acetochlor; CASRN 34256-82-1
Health assessment information on a chemical substance is included in IRIS only
after a comprehensive review of chronic toxicity data by U.S. EPA health
scientists from several Program Offices and the Office of Research and
Development. The summaries presented in Sections I and II represent a
consensus reached in the review process. Background information and
explanations of the methods used to derive the values given in IRIS are
provided in the Background Documents.
STATUS OF DATA FOR Acetochlor
File On-Line 09/01/1993
Category (section) Status Last Revised
----------------------------------------- -------- ------------
Oral RfD Assessment (I.A.) on-line 09/01/1993
Inhalation RfC Assessment (I.B.) no data
Carcinogenicity Assessment (II.) no data
_I. CHRONIC HEALTH HAZARD ASSESSMENTS FOR NONCARCINOGENIC EFFECTS
__I.A. REFERENCE DOSE FOR CHRONIC ORAL EXPOSURE (RfD)
Substance Name -- Acetochlor
CASRN -- 34256-82-1
Last Revised -- 09/01/1993
The oral Reference Dose (RfD) is based on the assumption that thresholds exist
for certain toxic effects such as cellular necrosis. It is expressed in units
of mg/kg-day. In general, the RfD is an estimate (with uncertainty spanning
perhaps an order of magnitude) of a daily exposure to the human population
(including sensitive subgroups) that is likely to be without an appreciable
risk of deleterious effects during a lifetime. Please refer to the Background
Document for an elaboration of these concepts. RfDs can also be derived for
the noncarcinogenic health effects of substances that are also carcinogens.
Therefore, it is essential to refer to other sources of information concerning
the carcinogenicity of this substance. If the U.S. EPA has evaluated this
substance for potential human carcinogenicity, a summary of that evaluation
will be contained in Section II of this file.
___I.A.1. ORAL RfD SUMMARY
Critical Effect Experimental Doses* UF MF RfD
-------------------- ----------------------- ----- --- ---------
Salivation, increased NOAEL: 2 mg/kg-day 100 1 2E-2
ALT and ornithine mg/kg-day
carbamyl transferase; LOAEL: 10 mg/kg-day
significant increases
in triglyceride and
decreased blood glucose
levels; histopathological
changes in kidneys and
testes of males
1-Year Dog Feeding Study
ICI, Inc., 1988a
*Conversion Factors and Assumptions: Actual dose tested
___I.A.2. PRINCIPAL AND SUPPORTING STUDIES (ORAL RfD)
ICI, Inc. 1988a. MRID No. 41565118; HED Doc No. 008478. Available from EPA.
Write to FOI, EPA, Washington, DC 20460.
Groups of 20-week old purebred beagles (5/sex/dose) were administered
acetochlor by gelatin capsule for 52 weeks at dose levels of 0, 2, 10, or 50
mg/kg-day. The capsules were administered orally once each day after feeding,
7 days a week. Control animals received empty capsules. All animals were
individually housed with temperature and humidity control to provide a uniform
environment. Each dog received 400 g of a dry pellet diet each morning before
treatment. The uneaten food was withdrawn and weighed the following morning.
Water was available ad libitum.
Systemic toxicity was evident at 10 and 50 mg/kg-day in both male and
female dogs. Symptoms included excessive salivation and abnormal shaking of
the head. At 50 mg/kg-day, significant increases in alanine aminotransferase
(ALT), gamma-glutamyl transpeptidase, and ornithine carbamyl transferase were
observed in male and female dogs over the course of treatment. At 10 mg/kg-
day, histopathological changes were observed only in the kidneys,
epididymides, and testes of males. Kidney changes consisted of interstitial
nephritis and chronic vasculitis. Hypospermia of the epididymides and
seminiferous tubule degeneration were reported at 10 mg/kg-day. Testicular
toxicity, evident at both 10 and 50 mg/kg-day, consisted of decreased relative
testes weight, atrophy, and degeneration of seminiferous tubules and
hypospermia. Renal toxicity was evident at 50 mg/kg-day after 24 weeks of
treatment as evidenced by increased water intake, urinary volume, and
significantly increased blood urea and creatinine values. This was
accompanied by renal histopathology consisting hyperplasia in the collecting
duct, transitional cell hyperplasia, cortical atrophy with fibrosis and
scarring accompanied by chronic vasculitis, interstitial nephritis, dilatation
of Bowman's space, and deposition of lipofuscin pigment in cortical tubules.
Significant neurological effects were also evident at 50 mg/kg-day and
consisted of abnormal head movements; stiffness and rigidity of the hindlimbs;
ataxia; tremor; depressed righting, hopping, and flexor reflexes; and
exaggerated tonic neck reflex. These neurologic symptoms were accompanied by
histopathological findings in the vermis cerebellum. Two males and 1 female
were killed between weeks 39-51 due to severe neurological effects.
Based upon the results of this study, the LEL for systemic toxicity is 10
mg/kg-day based on salivation, increased alanine aminotransferase and
ornithine carbamyl transferase accompanied by significant increases in
triglyceride levels, and decreased blood glucose levels, and histopathological
changes in the kidney and testes of males. The NOEL for systemic toxicity is
2 mg/kg-day.
___I.A.3. UNCERTAINTY AND MODIFYING FACTORS (ORAL RfD)
UF -- The uncertainty factor of 100 reflects 10 for interspecies extrapolation
and 10 for intraspecies variability.
MF -- None
___I.A.4. ADDITIONAL STUDIES / COMMENTS (ORAL RfD)
1) 1-Year Feeding - dog: Principal study -- see previous description; core
grade guideline (ICI, Inc., 1988a)
2) 1-Year Feeding - dog: Dietary levels tested: 0, 4, 12, and 40 mg/kg-day;
Purebred beagle dogs (6/sex/dose) were administered acetochlor by capsule for
12 months. Under the conditions of this study, the NOEL for systemic toxicity
is 12 mg/kg-day. The LEL for systemic effects is 40 mg/kg-day based on
decreased (p<0.05) body weight gains in males, decreased terminal body weights
in females, testicular atrophy (6/6) with accompanying decreased (p<0.05)
absolute and relative (to body weight) testicular weights, increased absolute
and relative adrenal weights in females, increased relative liver weights in
males and females, and increased SGOT and SGPT levels. Core grade minimum
(Monsanto Company, 1981)
3) 2-Year Feeding/Oncogenicity - rat: Dietary levels tested: 0, 40, 200, and
1000 ppm (0, 2, 10, and 50 mg/kg-day); Groups of Sprague-Dawley rats
(60/sex/dose with an interim sacrifice of 10/sex/dose) received from Charles
River Breeding Laboratory, Portage, MI were fed diets containing acetochlor
for 2 years. Body weight and body weight gain showed a decrease in high-dose
males from day 8 to the end of the study on (statistically significant from
days 455-678). High-dose females also had a slight, but not statistically
significant decrease in body weight and body weight gain. Statistically
significant increases in gamma glutamyl transpeptidase were observed in high-
dose males at 18 and 24 months (mid- and high-dose males at 1 year showed
slight increases as did mid-dose males at 2 years). Also, cholesterol levels
were increased (statistically significant) in high-dose males at 2 years (a
slight decrease was noted at 18 months) and total bilirubin was increased in
high-dose females at 2 years. Organ weights determined at the interim
sacrifice showed a slight increase in absolute and relative kidney weights in
high-dose males and a slight, dose-related increase in absolute and relative
liver weights in treated males. This continued to final sacrifice where
similar observations were noted including a statistically significant increase
in relative liver weight of high-dose males and an increase in absolute and
relative testicular weight (statistically significant) in high-dose males.
Females were not similarly affected. Based on the effects observed at the
high-dose, the LEL for systemic toxicity is 1000 ppm (50 mg/kg-day). The NOEL
for systemic toxicity is 200 ppm (10 mg/kg-day). Core grade minimum (Monsanto
Company, 1986a)
4) 2-Year Feeding/Oncogenicity - rat: Dietary Levels tested: 0, 18, 175, and
750 ppm (Male: 0, 0.67, 6.37, and 66.9 mg/kg-day; Female: 0, 0.88, 8.53, and
92.1 mg/kg-day); Groups of CD rats (50/sex/dose) received from Charles River
UK Ltd were administered acetochlor in the diet for 104 weeks. For 52 weeks,
an additional 10 males and females received doses of 18 and 175 ppm, and
another group of 20 males and females received doses of 0 and 1750 ppm. In
males and females, systemic toxicity in the form of reduced body weight gain,
decreased food efficiency, ophthalmologic abnormalities, elevated GGT and
cholesterol, and increased organ-to-body weight ratios were evident at 1750
ppm. No compound-related effects were noted at the low- and mid-dose. Based
on the effects observed at the high-dose, the LEL for systemic toxicity is
1750 ppm (Male: 66.9 mg/kg-day; Female: 92.1 mg/kg-day). The NOEL for
systemic toxicity is 175 ppm (Male: 6.37 mg/kg-day; Female: 8.53 mg/kg-day).
Core grade minimum (ICI, Inc., 1988b)
5) 2-Generation Reproduction - rat: Dietary levels tested: 0, 500, 1500, and
5000 ppm (Male: 0, 30.4, 74.1, and 324.5 mg/kg-day; Female: 0, 44.9, 130.1,
and 441.5 mg/kg-day); Groups of Charles River rats were fed diets containing
acetochlor over two generations. A slight decrease (about 20%) in litter size
was noted at the high-dose in all matings. The high-dose was also associated
with decreased pup body weight gain during lactation for both generations.
This effect was also noted in male F2b pups from the mid-dose group. Chronic
nephritis was increased in females of the F1 generation fed 5000 ppm; a slight
increase in prostatis in this level may have been related to treatment.
Apparent treatment-related increased thyroid weights were noted in low- and
mid-dose F1b male pups, in F2b male and female pups, and in mid- and high-dose
F1 dams. Liver weights (nonsignificant in males) and liver-to-body-weight
ratios were increased in mid- (not statistically significant) and high-dose F1
parents. Pituitary weights were decreased at all doses in F1 adult males
(absolute weights were decreased at low- and high-doses) and in low- and high-
dose F2b male pups but were increased in low-dose F1b female pups. Decreases
were observed for ovary weights for adult F1 females at all dose levels.
Based on the decreased body weight gain of F2b pups, the LEL for reproductive
toxicity is 1500 ppm (Male: 74.1 mg/kg-day; Female: 130.1 mg/kg-day). The
NOEL for reproductive toxicity is 500 ppm (Male: 30.4 mg/kg-day; Female: 44.9
mg/kg-day). Based on changes in absolute and relative organ weight (decreased
ovary weights in F1 females, decreased pituitary weights for F1 and F2 males,
and increased thyroid weights in F1 and F2b pups), the LEL for systemic
toxicity is 500 ppm (Male: 30.4 mg/kg-day; Female: 44.9 mg/kg-day), the lowest
dose tested. A NOEL for systemic toxicity was not established. Core grade
minimum (Monsanto Company, 1982)
6) 2-Generation Reproduction - rat: Dietary levels tested: 0, 18, 175, and
1750 ppm (0, 1.6, 21, and 160 mg/kg-day); Groups of Sprague-Dawley rats
(25/sex/dose) received from Charles River UK Ltd were administered
acetochlor in the diet over 2 generations. Systemic toxicity, as evidenced
by reductions in body weight accompanied by slight reductions in food
consumption and increases in relative organ weights, was observed in high-
dose parental males and females. Based on these effects, the LEL for
systemic toxicity is 1750 ppm (160 mg/kg-day). The NOEL for systemic
toxicity is 175 ppm (21 mg/kg-day). Reproductive performance and the rate
of physical development of offspring were not affected by the administration
of the test material in the diet. However, compound-related reductions in
body weight on lactational day 21 and total body weight gain during lactation
were observed in high-dose pups from both generations. Based on these
results, the LEL for reproductive toxicity is 1750 ppm (160 mg/kg-day). The
NOEL for reproductive toxicity is 175 ppm (21 mg/kg-day). Core grade minimum
(ICI Americas Inc., 1989a)
7) Developmental Toxicity - rat: Dose levels tested: 0, 50, 200, and 400
mg/kg-day; Groups of pregnant Charles River COBS CD rats (25/sex) were
administered acetochlor orally by gavage as a single daily dose on days 6
through 19 of gestation. Matting and/or staining of the anogenital region was
noted for rats in the high-dose group (13/25) and excessive salivation was
observed in 3 rats as a post-dose response on one occasion. A slight but not
dose-related increase in matting and/or staining of the anogenital region was
noted in the 50 and 200 mg/kg-day groups. A moderate decrease in mean
maternal body weight gain during the treatment period and in the adjusted mean
body weight gain on gestation day 20 was noted at 400 mg/kg-day when compared
to the control group. Based on the above effects, the maternal NOEL and LEL
are 200 and 400 mg/kg-day, respectively. A slight to moderate decrease in
mean fetal body weight, although not statistically significant, was noted at
400 mg/kg-day. Mean fetal body weight values at 50 and 200 mg/kg-day were
comparable to controls. Based on the decrease in mean fetal body weight, the
NOEL and LEL for developmental toxicity are 200 and 400 mg/kg-day,
respectively. Core grade minimum (Monsanto Company, 1980a)
8) Developmental Toxicity - rat: Dose levels tested: 0, 40, 150, and 600
mg/kg-day; Animals were apparently received "timed pregnant" from Charles
River Breeding Laboratories, Portage, MI. According to the information
provided, the females were mated with males of the same strain and shipped
in 2 batches (Group A and B) mated one day apart. "The day of mating, as
judged by the appearance of sperm in the vaginal smear or by the presence
of a vaginal plug, was considered as Day 0 of gestation." Rats (Group A:
15/dose; Group B: 10/dose) were orally administered acetochlor on gestation
days 6 through 15, inclusive. The LEL for maternal toxicity is 600
mg/kg-day based on animals sacrificed moribund, clinical observations,
decreased body weight gain during the dosing period and the entire
gestation period and corrected body weight gain for gestation day 6 through
20. The NOEL for maternal toxicity is 150 mg/kg-day. The LEL for
developmental toxicity is 600 mg/kg-day based on increased resorptions per
dam, postimplantation loss, and decreased mean fetal weight. The NOEL for
developmental toxicity is 150 mg/kg-day. Core grade minimum (ICI Americas
Inc., 1989b)
9) Developmental Toxicity - rabbit: Dose levels tested: 0, 15, 50, and 190
mg/kg-day; Groups of pregnant New Zealand White rabbits (20/dose) received
from Hazleton-Dutchland, Inc., Denver, PA. were administered acetochlor via
gastric intubation in 0.5 ml/kg of corn oil on gestation days 7 through 19.
No mortality or spontaneous abortions were observed in any of the groups.
There was a statistically significant mean body weight loss during the
dosing period (days 7 through 19 of gestation) in the high-dose group.
From days 19-29, the mean body weight gain for this group was greater than
the control, low- and mid-dose groups. There were no apparent group
differences regarding any other parameter. Based on body weight loss, the
NOEL and LEL for maternal toxicity are 50 and 190 mg/kg-day, respectively.
There were no apparent compound-related differences regarding any
developmental toxicity parameters in any dose group. Therefore, the NOEL
for developmental toxicity is equal to or greater than 190 mg/kg-day. Core
grade minimum (Monsanto Company, 1986b)
10) Developmental Toxicity - rabbit: Dose levels tested: 0, 30, 100, and 300
mg/kg-day; Groups (16/dose) of time-mated New Zealand White rabbits
received from Interfauna UK Ltd were administered acetochlor by gavage on
gestation days 6 through 18, inclusive. Based on the data provided, no
significant effects on either the maternal animal or the fetus were noted
at the dose levels tested. Therefore the NOEL for maternal and
developmental toxicity is equal to or greater than 300 mg/kg-day. Core
grade minimum (ICI Americas Inc., 1989c)
Other Data Reviewed:
1) 2-Year Feeding/Oncogenicity - mouse: Dietary levels tested: 0, 500, 1500,
5000 ppm (0, 75, 225, and 750 mg/kg-day); Groups of Swiss albino CD-1 mice
(50/sex/dose with an 12-month interim sacrifice of 10/sex/dose) were fed
'diets containing acetochlor for 2 years. Dose-related changes included: 1)
increased mortality in both high-dose males and females; 2) decreased mean
body weights in both high-dose males and females; 3) decreased red blood cell
count, hematocrit, and hemoglobin in high-dose females at terminal sacrifice;
4) increased white blood cell count in high-dose males at terminal sacrifice;
5) increased platelet count in mid- and high-dose females at terminal
sacrifice; 6) increased mean liver weight and liver-to-body-weight ratios at
study termination in all dose groups of males and in high-dose females as
well, as increased liver-to-body-weight ratios in all dosed males and females
at 12 months; increased absolute and relative kidney weights in all dose
groups of males at termination; and increased absolute and relative adrenal
weights in all groups of males and in high-dose females at study termination;
and 7) increased interstitial nephritis in high-dose males and females. Based
on increased liver and kidney weights, the LEL for systemic toxicity is 500
ppm (75 mg/kg-day), the lowest dose tested. The NOEL for systemic toxicity
was not established. Core grade minimum (Monsanto Company, 1983a)
2) 78-Week Feeding/Oncogenicity - mouse: Dietary levels tested: 0, 10, 100,
and 1000 ppm (Male: 0, 1.1, 11, and 116 mg/kg-day; Female: 0, 1.4, 13, and
135 mg/kg-day); Groups of CD-1 mice (50/sex/dose with an 52-week interim
sacrifice of 10/sex/dose) received from Charles River (UK) Ltd., Kent,
England, were administered acetochlor in the diet for 78 weeks. In males,
a dose-related increase in absolute and relative (to body weight) kidney
weight was observed and accompanied by significant but not dose-dependent
increases in renal tubular basophilia at all dietary levels. Similar
effects were observed in the older CD-1 mouse study (Monsanto Co., 1983a)
but were inconsistent and not dose-dependent. OPP considers the renal
tubular basophilia observed at all dose levels to be most likely the result
of normal aging. In females, the only compound-related finding was a
significant increase in anterior polar vacuoles in the lens of the eye at
the high-dose level. Based on these results, the NOEL and LEL for systemic
toxicity in females are 100 and 1000 ppm (13 and 135 mg/kg-day),
respectively. Core grade minimum (ICI Americas Inc., 1989d)
3) 2-Year Feeding/Oncogenicity - rat: Dietary levels tested: 0, 500, 1500,
and 5000 ppm (Male: 0, 22, 69, and 250 mg/kg-day; Female: 0, 30, 93, and
343 mg/kg-day); Groups of Sprague-Dawley rats (60/sex/dose with an 12-month
interim sacrifice of 10/sex/dose) received from Charles River Breeding
Laboratories, Wilmington, MA were fed diets containing acetochlor for 2
years. There was increased mortality in high-dose females. There was a
significant (p<0.05) dose-related decrease in mean body weights in males
and females of the mid- and high-dose groups, and a significant (p<0.05)
decrease in food consumption in high-dose males and females. A decrease in
the mean body weight of low-dose males also reached a significant (p<0.05)
level at the end of the study (weeks 103-115). Histopathologic examination
of the tissues indicated increased incidences of polyarteritis of the
testis and arteries of high-dose males and liver necrosis and alveolar
histiocytosis in high-dose females (p<0.05). Based on body weight,
the LEL for systemic toxicity is 500 ppm (22 mg/kg-day), the lowest dose
tested. A NOEL for systemic toxicity was not established. Core grade
minimum (Monsanto Company, 1983b)
4) 119-Day Feeding - dog: Dietary levels tested: 0, 25, 25/50/1975,
50/100/150/200 mg/kg-day; Groups of beagle dogs (6/sex/dose) were
administered acetochlor in capsules at various dose levels for 119 days.
The dosages of acetochlor were as follows: (a) control animals received a
sham capsule for the duration of the study; (b) the low-dose group received
25 mg/kg-day for the duration of the study; (c) the mid-dose group received
25 mg/kg-day during the 1st week, 50 mg/kg-day during the 2nd week, and 75
mg/kg-day for the remainder of the study; and (d) the high-dose group
received 50 mg/kg-day during the 1st, 100 mg/kg-day during the 2nd, 150
mg/kg-day during the 3rd week, and 200 mg/kg-day for the remainder of the
study. Capsules were given once daily, approximately 1 hour after feed was
withdrawn. Under the conditions of this study, administration of
acetochlor produced severe toxic effects at the high-dose (death or
morbidity, decreased body weight, abnormal urinalysis, and
histopathological findings), moderate toxic effects at the mid-dose (death
or morbidity and histopathological findings), and mild toxic effects at the
low-dose (abnormally elevated SGPT and increased liver-to-body-weight
ratio). Therefore, the LEL for systemic toxicity is 25 mg/kg-day, the
lowest dose tested. A NOEL for systemic toxicity was not established.
Core grade minimum (Monsanto Company, 1980b)
5) 90-Day Feeding - dog: Dietary levels tested: 0, 2, 10, and 60 mg/kg-day;
Groups of beagle dogs (4/sex/dose) were administered acetochlor by gelatin
capsule for 13 weeks. At 60 mg/kg-day, systemic toxicity was evident in
both male and female dogs and consisted of diarrhea and mucous in the
feces, significant decreases in body weight gain in males (32%) and females
(40%); a significant decrease in hemoglobin, hematocrit, and RBC values in
females; a significant increase in alanine aminotransferase in both sexes
(51-59%); a decrease in blood glucose; and a significant increase in the
liver-body-weight ratio for both sexes. No treatment-related effects were
noted at the low- and mid-dose levels. Based on the effects observed at
the high-dose, the LEL for systemic toxicity is 60 mg/kg-day. The NOEL for
systemic toxicity is 10 mg/kg-day. Core grade supplementary (ICI Americas
Inc., 1986)
6) 3-Month Feeding - rat: Dietary levels tested: 0, 800, 2000, and 6000 ppm
(0, 40, 100, and 300 mg/kg-day); Groups of Sprague-Dawley rats
(30/sex/dose) were fed diets containing acetochlor for 3 months. A
statistically and biologically meaningful decrease in the food consumption
and body weight was observed in mid- and high-dose males and females.
The differences in these parameters between the control and low-dose group
were statistically significant (3-8% decreases), but were not considered to
be as biologically meaningful in either sex. Therefore, based on decreased
food consumption and body weight, the NOEL and LEL for systemic toxicity
are 800 and 2000 ppm (40 and 100 mg/kg-day), respectively. Core grade
minimum (Monsanto Company, 1980c)
7) 13-Week Feeding - rat: Dietary levels tested: 0, 20, 200, and 2000 ppm
(Male: 0, 1.6, 16.1, and 161.1 mg/kg-day; Female: 0, 1.9, 18.7, and 191.9
mg/kg-day); Groups of Sprague-Dawley CD rats (10/sex/dose) received from
Charles River UK Ltd were administered acetochlor in the diet for 13 weeks.
Systemic toxicity was observed at 2000 ppm. These effects, although
somewhat marginal, included hematological effects in both male and female
rats; increased organ-to-body weight ratios for the liver, kidney, and
brain; decreased plasma acetyl- and butyrylcholinesterase activity;
decreased brain acetylcholinesterase activity (males only); and increased
plasma urea and cholesterol. No significant effects related to test
article administration were observed at other doses. Based on the effects
observed at the high-dose, the LEL for systemic toxicity is 2000 ppm (Male:
161.1 mg/kg-day; Female: 191.9 mg/kg-day). The NOEL for systemic toxicity
is 200 ppm (Male: 16.1 mg/kg-day; Female: 18.7 mg/kg-day). Core grade
supplementary (ICI Central Toxicology Lab., 1986)
Data Gap(s): None
___I.A.5. CONFIDENCE IN THE ORAL RfD
Study -- High
Data Base -- High
RfD -- High
The principal study is of good quality and is given a high confidence
rating. Additional studies are of adequate quality and supportive of the
critical study. Therefore, the data base is given a high confidence rating.
High confidence in the RfD follows.
___I.A.6. EPA DOCUMENTATION AND REVIEW OF THE ORAL RfD
Source Document -- This assessment is not presented in any existing U.S. EPA
document.
Other EPA Documentation -- None
Agency Work Group Review -- 03/27/1991, 03/24/1992
Verification Date -- 03/24/1992
___I.A.7. EPA CONTACTS (ORAL RfD)
Please contact the Risk Information Hotline for all questions concerning this
assessment or IRIS, in general, at (513)569-7254 (phone), (513)569-7159 (FAX)
or RIH.IRIS@EPAMAIL.EPA.GOV (internet address).
__I.B. REFERENCE CONCENTRATION FOR CHRONIC INHALATION EXPOSURE (RfC)
Substance Name -- Acetochlor
CASRN -- 34256-82-1
Not available at this time.
_II. CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
Substance Name -- Acetochlor
CASRN -- 34256-82-1
Not available at this time.
_VI. BIBLIOGRAPHY
Substance Name -- Acetochlor
CASRN -- 34256-82-1
Last Revised -- 09/01/1993
__VI.A. ORAL RfD REFERENCES
ICI Americas Inc. 1986. MRID No. 41565116; HED Doc. 008478. Available from
EPA. Write to FOI, EPA, Washington, DC 20460.
ICI Americas Inc. 1989a. MRID No. 41565120; HED Doc. No. 008478. Available
from EPA. Write to FOI, EPA, Washington, DC 20460.
ICI Americas Inc. 1989b. MRID No. 41592005; HED Doc. 008478. Available from
EPA. Write to FOI, EPA, Washington, DC 20460.
ICI Americas Inc. 1989c. MRID No. 41592006; HED Doc. 008478. Available from
EPA. Write to FOI, EPA, Washington, DC 20460.
ICI Americas Inc. 1989d. MRID No. 41565119; HED Doc. 008478. Available from
EPA. Write to FOI, EPA, Washington, DC 20460.
ICI Central Toxicology Laboratory. 1986. MRID No. 41565115; HED Doc No.
008478. Available from EPA. Write to FOI, EPA, Washington, DC 20460.
ICI, Inc. 1988a. MRID No. 41565118; HED Doc No. 008478. Available from EPA.
Write to FOI, EPA, Washington, DC 20460.
ICI, Inc. 1988b. MRID No. 41592004; HED Doc No. 008478. Available from EPA.
Write to FOI, EPA, Washington, DC 20460.
Monsanto Company. 1980a. MRID No. 00050929; HED Doc No. 0005865. Available
from EPA. Write to FOI, EPA, Washington, DC 20460.
Monsanto Company. 1980b. MRID No. 00050928; HED Doc No. 005865. Available
from EPA. Write to FOI, EPA, Washington, DC 20460.
Monsanto Company. 1980c. MRID No. 00050933; HED Doc No. 005865. Available
from EPA. Write to FOI, EPA, Washington, DC 20460.
Monsanto Company. 1981. MRID No. 00116631, 00164944; HED Doc No. 004586,
005943. Available from EPA. Write to FOI, EPA, Washington, DC 20460.
Monsanto Company. 1982. MRID No. 00131391; HED Doc No. 004586, 005353.
Available from EPA. Write to FOI, EPA, Washington, DC 20460.
Monsanto Company. 1983a. MRID No. 00131089; HED Doc No. 004586. Available
from EPA. Write to FOI, EPA, Washington, DC 20460.
Monsanto Company. 1983b. MRID No. 00131088, 40484801; HED Doc No. 004586,
006764. Available from EPA. Write to FOI, EPA, Washington, DC 20460.
Monsanto Company. 1986a. MRID No. 40077601; HED Doc No. 006571, 007002.
Available from EPA. Write to FOI, EPA, Washington, DC 20460.
Monsanto Company. 1986b. MRID No. 40134101; HED Doc No. 005968. Available
from EPA. Write to FOI, EPA, Washington, DC 20460.
__VI.B. INHALATION RfD REFERENCES
None
__VI.C. CARCINOGENICITY ASSESSMENT REFERENCES
None
_VII. REVISION HISTORY
Substance Name -- Acetochlor
CASRN -- 34256-82-1
-------- -------- --------------------------------------------------------
Date Section Description
-------- -------- --------------------------------------------------------
08/01/1991 I.A. Oral RfD now under review
08/01/1991 II. Carcinogenicity assessment now under review
09/01/1993 I.A. Oral RfD on-line
09/01/1993 VI.A. Oral RfD references on-line
VIII. SYNONYMS
Substance Name -- Acetochlor
CASRN -- 34256-82-1
Last Revised -- 09/01/1993
2-CHLORO-N-(ETHOXYMETHYL)-6'-ETHYLACET-O-TOLUIDIDE
2-CHLORO-N-(ETHOXYMETHYL)-6'-ETHYL-O-ACETOTOLUIDIDE
2-CHLORO-N-(ETHOXYMETHYL)-N-(2-ETHYL-6-METHYLPHENYL)ACETAMIDE
34256-82-1
ACETAMIDE, 2-CHLORO-N-(ETHOXYMETHYL)-N-(2-ETHYL-6-METHYLPHENYL)-
ACETOCHLOR
ACETOCHLORE
AZETOCHLOR
CASWELL NO. 003B
EPA PESTICIDE CHEMICAL CODE 121601
MG 02
MON 097
NEVIREX
O-ACETOTOLUIDIDE, 2-CHLORO-N-(ETHOXYMETHYL)-6'-ETHYL-
Last updated: 5 May 1998
URL: http://www.epa.gov/iris/SUBST/0521.HTM
|
