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A two-year rat feeding study in the Long Evans Strain showed
alachlor to be toxic at all doses tested (14.0, 42.0 or 126.0
mg/kg/day) (Monsanto, 1982). The principal toxic effects observed
were hepatoxicity and an ocular lesion, referred to as the uveal
degeneration syndrome (UDS). A second two-year feeding study using
the same strain of rat was conducted at 0.5, 2.5 or 15.0 mg/kg/day
(Stout et al., 1983a). Animals in the high dose group exhibited the
inital stage of UDS. The 2.5 mg/kg/day was judged to be the NOEL for
UDS.
In a three-generation rat study, alachlor showed a reproduction
NOEL level at 10.0 mg/kg/day and reproduction lowest-observed-effect-
level at 30.0 mg/kg/day (Schroeder et al./ 1981). In a teratology
study in the rat, alachlor was administered at dose levels of 50, 150
or 400 mg/kg/day. A maternal and fetotoxic NOEL was established at
150 mg/kg/day with no teratogenic potential indicated at the highest
dose tested, 400 mg/kg/day (Rodwell and Tacher, 1980).
Alachlor feeding studies in mice and rats have demonstrated
carcinogenic effects which include (1) lung tumors in mice and (2)
stomach, thyroid, and nasal turbinate tumors in rats. Alachlor
administered in the diet of mice for 18 months produced a
statistically significant increase in lung bronchioalveolar tumors in
female mice at the highest dose tested (260 mg/kg/day) (Daly et al.,
1981a). The increase of lung tumors in male mice was not significant.
Two chronic feeding studies were conducted in the Long-Evans strain of
rat. In the first study (Daly et al., 1981b), animals of both sexes
were 14, 42 or 126 mg/kg/day alachlor. Dose-related responses were
observed for tumors of the nasal turbinate in both sexes at the mid
and high doses. A statistically significant increase was also noted
in the incidence of stomach tumors in the high dose for both sexes.
Thyroid follicular tumors (adenomas plus carcinomas) increased in both
sexes at the high dose level with the increase being statistically
significant in males.
In the second two-year feeding study (Stout et al., 1983a), male
and female rats were exposed to 0.5, 2.5, and 15 mg/kg/day alachlor.
Incidences of nasal epithelial adenoma response was statistically
significant in both sexes. Data from an additional study which ran
concurrently with this study used a fourth treatment group, 126
mg/kg/day (Stout et al., 1983b). The design of this study was
different from the previous study (Stout et al., 1983a) because it
used a variety of dosing regimens and had the primary purpose of
investigating the nature and reversibility of the ocular lesions
(UDS). This study also used a chemical stabilizer different from that
used by Daly et al. (1981b). The results of Stout et al. (1983b)
indicate that the tumor response observed in Daly et al. (1981b)
cannot be explained by the presence of the stabilizer used in the test
material.
An increase was noted in the number of thyroid follicular cell
tumors in males, and in the number of nasal epithelial tumors in both
sexes (Stout et al., 1983b). A rare stomach tumor was also found in a
13
-------
male of the 2.5 mg/kg treatment and is considered biologically
significant since no stomach tumors were found in the control animals
in any of the cited chronic rat studies. No studies pertaining to the
effects of alachlor in humans were found in this review.
CRITERIA EVALUATION AND RECOMMENDATIONS
Aquatic
An Aquatic Life Criterion as defined by Stephan et al. (1985)
consists of two concentrations: the Criterion Maximum Concentration
(CMC) and the Criterim Continuous Concentration (CCC). The current
literature search has not yielded data on acute tests for eight
different genera, as required by the Guidelines to derive a CMC.
There is also insufficient information to calculate a CCC. A tenta-
tive acute value can be determined, however, even in the absence of a
complete data base. An estimate of the FAV was calculated using the
following equations from the Guidelines:
where:
Final Acute Value = eA
A = S( 0.05) + L
L = ( (In GMAV) - S( ( p)))/4)
((In GMAV)2) - (( if In GMAV)) 2/4)
S2 = (P) - (( ( P))2/4
P = cumulative probability as R/(N+1);
R = rank from "1" for the lowest to "N" for the highest GMAV
Genus Mean Acute Values (GMAVs) were obtained from the reviewed
literature (Table 1). Values used in calculating the FAV are
presented in Table 3.
TABLE 3. VALUES USED IN CALCULATION OF FINAL ACUTE VALUE
96-hr
Species LCSOs GMAV Rank P
Fathead minnow 5.0 5.0 2 0.33
(Pimephales promelas)
Rainbow trout 2.4,2.3 2.35 1 0.17
(Salmo gairdneri)
Bluegill 13.4,4.3 7.6 4 0.67
(Lepomis macrochirus)
Catfish 6.5 6.5 3 0.50
(Ictalurus punctatus)
Crayfish 19.5 19.5 5
14
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Substituting appropriate values into the equations gave an
estimate of the FAV of 1.52 ppm for alachlor. The estimated CMC (one-
half the FAV) is 0.76 ppm for alachlor.
This estimated CMC is limited by the lack of reported information
on test conditions and quality control measures employed in the
studies, as well as by the limited number of representative phyla
tested. However, the value of 0.76 ppm is supported by the study by
Call et al. (1984) which estimated a no-effect-level between 0.52 and
1.10 ppm. From this comparison, it appears that the CMC is
conservative and reasonable for the protection of aquatic life.
The CCC is equal to the lowest of the Final Chronic Value, the
Final Plant Value or the Final Residue Value.
Table 4 lists the data requirements needed to calculate these
values, as well as those for the CMC, as described by the EPA
guidelines (Stephan et al., 1985). Data are lacking for both acute
and chronic test results in several classes of organisms, including
planktonic crustaceans, insects, rotifers and/or annelids and
molluscs.
The only chronic data available are for freshwater fish (Call et
al., 1984), and no acute or chronic studies were located for any
invertebrate or insect species. Information was also lacking for
other phyla (other than Arthropoda or Chordata). Furthermore, none of
the studies reviewed noted any biomagnification of alachlor in the
aquatic food chain, although Call et al. (1984) noted a BCF of 6.0 in
the fathead minnow after 21-day exposure to alachlor. The lack of
these data precludes any further criteria calculations. One may
estimate a chronic protective value by assuming an acute-chronic ratio
of 10. The resultant advisory concentration would be 0.76mg/L/10 or
76 ug/L.
Health
Tolerances have been established (40 CFR 180.249) for alachlor and
its metabolites resulting from the use of the herbicide in or on raw
agricultural commodities. These tolerances range from 0.05 ppm to 3.0
ppm in vegetables and 0.02 ppm in animal meat-by-products and fat
(U.S. EPA, 1984).
No epidemiological studies of the effects of alachlor on human
health have been found which could contribute data useful to the
derivation of a criterion (Table 5).
Alachlor feeding studies have demonstrated oncogenic effects which
include: (1) lung tumors in mice and (2) stomach, thyroid and nasal
turbinate tumors in rats (U.S. EPA, 1984). The results of these
studies were presented in a U.S. EPA position document for alachlor
(U.S. EPA, 1984). Data were from unpublished studies submitted to EPA
for review. EPA has determined that the weight of evidence for these
experiments demonstrates that alachlor is oncogenic to laboratory
15
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animals and, in the absence of data on humans, believes it necessary
to treat alachlor as a probable human carcinogen. Therefore, since
the actual studies are unavailable for review, the following
recommendations are consistent with the data presented in the position
document .
EPA's Carcinogenic Assessment Group (CAG) is currently evaluating
alachlor for carcinogenic risk assessment. However, EPA's Office of
Pesticide Programs (OPP) has performed a risk characterization of the
nasal tumors of alachlor (U.S. EPA, 1984). The OPP assessment for
drinking water is summarized in the following table.
Table 1. Assessment of Drinking Water Risks for Alachlor
Exposure Level Upper Limit Estimate of
Lif etimeCancerRisk for:
10 Kg Child 60 Kg Adult
0.15 10-6 10-7 to 10-6
1.5 10-5 10-6 to 10-5
15.0 10-4 10-5 to 10-4
The Office of Water has traditionally used the 70 kg man as its
surrogate. In these risk calculations, we would not expect to see any
significant change in the degree of calculated risk because of the
difference in the reference man of 10 Kg.
Applying the criteria described in EPA's proposed guidelines for
assessment of carcinogenic risk (U.S. EPA, 1984b), alachlor may be
classified in Group B: Probable human carcinogen. This category is
for agents for which there is inadequate evidence from human studies
and sufficient evidence from animal studies.
The Office of Drinking Water has prepared a draft human health
advisory document for alachlor (U.S. EPA, 1985) which is presently
under review. The values given below are taken from the draft
document, and should not be taken as final. They will, however, give
an indication of health effects which may result from exposure to
alachlor for times shorter than a lifetime.
Health Advisories are based upon the identification of adverse
health effects associated with the most sensitive and meaningful non-
carcinogenic end-point of toxicity. The induction of this effect is
related to a particular exposure dose over a specified period of time,
most often determined from the results of an experimental animal
17
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TABLE 4. DATA REQUIREMENTS FOR CALCULATION OF AQUATIC
LIFE INTERIM CRITERIA ALACHLOR
Criterion Requirements Available
Aquatic Toxicity Data
Acute Test Results from tests on:
A salmonid (class Osteichthyes) YES
A warm water species YES
commercially or recreationally
important (class Osteichthyes)
Another family in the phylum YES
Chordata (fish, amphibian, etc.)
A planktonic crustacean NO
(cladoceran, copepod, etc.)
Benthic crustacean (ostracod, YES
isopod, scud, crayfish, etc.)
Insect (mayfly, dragonfly, NO
damselfly, stonefly-, mosquito,
etc.)
Phylum other than Arthropoda/ NO
Chordata (Rotifera, Annelida,
Mollusca)
Another family of insect NO
Acute-chronic ratios with species NO
from three different families:
One fish
One invertebrate
Acutely sensitive freshwater
animal species
Acceptable test results from a test with:
Freshwater algae
A vascular plant
Bioaccumulation factor with a
freshwater species (if a maximum
permissible tissue concentration
is available)
YES
NO
YES
Data Acceptability
YES
(controls, replicates)
YES
(controls, replicates)
NO
(questionable due to
light exposures)
Questionable
(96 hr test;
no QA specifications)
NO
(controls; replicates;
24-hr, not 96-hr; no
effect cone.)
YES
(controls, replicates)
17
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TABLE 5. DATA REQUIREMENTS FOR CALCULATION OF HUMAN
HEALTH INTERIM CRITERIA ALACHLOR
Criterion Requirements
Aquatic Toxicity
Available
Data
Data Acceptability
Non-Threshold: Carcinogen YES
Tumor incidence tests (Incidence of
tumor formation significantly more
than the control for as least one
dose level), or
Data set which can be used to YES
estimate of carcinogenic risk, or
Lifetime average exposure tests, YES
or
Human epidemiology studies
(if available, not required) NO
Threshold: Non-carcinogens NA
No observed adverse effect level
(at least 90-day), or YES
Lowest observed effect level YES
Lowest observed adverse effect YES
level
Acceptable Daily Intake:
Daily water consumption YES
Daily fish consumption YES
Bioconcentration factor NO
Non-fish dietary intake YES
Daily intake by inhalation NO
Threshold Limit Value: NO
(Based on 8-hour time-weighted
average concentrations in air)
Inhalation Studies: YES
Available pharmacokinetic data
Measurements of absorption efficiency
Comparative excretion data
NA = Not applicable
YES
(EPA Approved)
YES
(EPA Approved)
YES
(EPA Approved)
YES
(EPA Approved)
YES
(EPA Approved)
YES
(EPA Approved)
YES
(EPA assumption)
YES
(EPA assumption)
YES
(EPA assumption)
YES
(1-hr exposure LC
noQA specifications
18
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study. The advisories are designed for use where short term exposure
is expected. Traditional risk characterization methodology for
threshold toxicants is applied in HA development. The general formula
is as follows:
(NOAEL or LOAEL) (BW) = ug/L
(UF(s)) ( L/day)
Where:
NOAEL or LOAEL = No-Observed-Adverse-Effeet-Level
or
Lowest-Observed-Adverse-Effect-Level
(the exposure dose in mg/kg bw)
BW = assumed body weight of protected
individual in kg (10 or 70)
UF(s) = uncertainty factors, based upon quality
and nature of data
L/day = assumed daily water consumption (1 or 2)
in liters
One-day Health Advisory
No duration-specific data are available to derive a One-day Health
Advisory; therefore, it is recommended that the Ten-day Health
Advisory be applied for the One-day HA as well.
Ten-day Health Advisory
The Ten-day Health Advisory is derived from the teratogenicity
study in the rat reported by Rodwell and Taylor (1980). As noted
above, there was no teratogenicity produced but both maternal and
fetotoxicity were expressed at 400 mg/kg/day. The Office of
Pesticides Programs determined that the NOEL for this study was at 150
mg/kg/day (U.S. EPA, 1984). Alachlor was administered to the animals
on days 6 through 15 of gestation.
The Ten-day HA for the 10 kg child is calculated as follows:
(150 mg/kg/day) (10 kg) = 15 mg/L or 15,000 ug/L
(100) (1 L/day)
Where:
150 mg/kg = NOAEL (No-Observed-Adverse-Effect-Level)
10 kg = Assumed weight of protected individual
20
-------
100 = Uncertainty factor, appropriate for use with
a NOAEL from an animal study
1 L/day = Assumed volume of water ingested per day by
10 kg child
Longer-term Health Advisory
A Longer-term Health Advisory will not be determined for alachlor
because it has been shown to produce carcinogenicity in less than five
and one-half months in rats at the same rate as did the lifetime
exposure.
Life-time Health Advisory
See Longer-term HA.
Analysis
Determination of alachlor may be accomplished by a liquid-liquid
extraction gas chromatographic procedure (Method 102. U.S. EPA
1983). In this procedure, a 1-L water sample is spiked with an
internal standard and then extracted with methylene chloride. The
extract is concentrated to 5 mL and the methylene chloride solvent
is exchanged for a toluene/methanol mixture. Separation and
identification is by packed column gas chromatography using a
nitrogen selective detector. The method detection limit for
alachlor is approximately 0.2 ug/L. If the sample chromatogram
contains interfering peaks, the sample should also be analyzed
using a electron capture detector.
Treatment
Data are available on the removal of alachlor from potable water
using conventional treatment and absorption. The use of aeration
has also been considered.
Available data suggest that conventional water treatment is not
effective for removing alachlor from drinking water. Baker (1983)
monitored the concentration of alachlor in raw river and in
finished water after alum coagulation, flocculation, sedimentation
and filtration. The concentration range was <0.5 to 5.0 ug/L in
the influent and <0.2 to 2.0 ug/L in the effluent. The removal
rate was not consistent and generally less than 50%.
No actual data are available which demonstrate the removal of
alachlor using aeration. However, the estimated Henry's Law
Constant (1.94 x 10-4 atm x m3/mole) suggests that this pesticide
might be amenable to such treatment (ESE, 1984).
Limited data suggest that GAG (granular activated charcoal)
adsorption would have limited effectiveness for alachlor. In a
laboratory study (DeFilippi et al., 1980), a waste stream
21
-------
containing 11 mg/L alachlor was passed, at 1.1 gpm/ft2, through a
3/8 inch diameter, 11-inch column containing seven grams of (GAG).
After 2.6 liters had been passed through, an effluent
concentration of 0.22 mg/L broke through the column. It was
estimated that, for this effluent concentration, a usage rate of
21.7 lb/1,000 gal would be required.
Laboratory studies with rapid sand filters capped with 16.5 inches
of GAC (Filtrasorb 300) operated at a filtration rate of 1.2
gpm/ft2 with an empty bed contact time of nine minutes were
performed by Baker (1983). Reported alachlor concentrations
ranged form 0.7 to 5.0 mg/L in the raw river and 0.1 to 0.7 mg/L
in the finished water. However, powdered activated carbon in
conventional treatment (PAC dose not reported) resulted in an
average concentration reduction of only 43%.
22
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REFERENCES
Ahmed, F.E., A.S. Tegris, P.C. Underwood, et al. 1981. Alachlor: six
month study in the dog: Testing Facility's Report No. 7952; Sponsor's
Report No. PR-80-015. (Unpublished study including submitter summary,
received Dec. 1, 1981 under EPA Reg. No. 524-316; prepared by Pharma-
copathics Research Labs., Inc., submitted by Monsanto Co., Washington,
D.C., CDL: 246229-A and 246293. (as cited in U.S. EPA 1984).
Bostian, A.L., D.P. Schmitt and K.R. Barker. 1984. In vitro hatch
and survival of Heterodera glycines as affected by alachlor and
phenamiphos. J. Nemat. 16(1) :22-26.
Call, D.J., L.T. Brooke, R.J. Kent, S.H. Poirier, M.L. Knuth, P.J.
Shubat, and E.J. Slick. 1984. Toxicity, uptake, and elimination of
the herbicides alachlor and dinoseb in freshwater fish. J. Environ.
Qual. 13(3):493-498.
Daly, I.W., G.K. Hagan, R. Plutnick, et al 1981a. An eighteen month
chronic feeding study of alachlor in mice: Project No. 77-1064.
Final Report. Unpublished study received July 1, 1981 under EPA Reg.
No. 524-285, prepared by Bio/Dynamics, Inc., submitted by Monsanto
Co., Washington, D.C., CDL: 070168-A, 070169 (as cited in U.S. EPA
1984) .
Daly, I.W., J.B. McCandless, H. Jonassen, et al. 1981b. A chronic
feeding study of alachlor in rats, Project No. 77-2065. Final Report.
Unpublished Study received Jan. 5, 1982 under EPA Reg. No. 524-285,
prepared by Bio/Dynamics, Inc., submitted by Monsanto Co., Washington,
D.C., CDL: 070586-A, 070587, 8, 9 & 90 (as cited in U.S. EPA 1984).
Federal Register, November 28, 1980. Guidelines and methodology used
in preparation of health effect assessment chapters of the consent
decree water quality criteria documents. Vol. 45:79347, 79353, 79374.
Georgian, I. Moraru, T. Draghicescu, I. Dinu, and G. Ghizelea. 1983.
Cytogenetic effects of alachlor and mancozeb. Mutat. Res. 116:341-348.
Hartley, D., and H. Kidd. 1983. The Agrochemicals Handbook. Royal
Society of Chemistry.
Hawxby, K., B. Tubea, J. Ownby and E. Easier.- 1977 Effects of
various classes of herbicides on four species of algae. Pestic.
Biochem. Physiol. 7(3):203-209.
Hudson, R.H., R.K. Tucker, and M.A. Haegele. 1982. Handbook of
toxicity of pesticides to wildlife, 2nd ed. U.S. Fish and Wildlife
Service, Patuxent Wildlife Research Center, Laurel, Maryland, 20708.
Johnson, W.W., and M.T. Finley. 1980. Handbook of acute toxicity of
chemicals to fish and aquatic invertebrates. U.S. Dept. of the
Interior; Fish and Wildlife Resource Publ. No. 137. U.S. Govt.
Printing Office, Washington, D.C.
23
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McEwen, F.L. and G.K. Stephenson. 1979. The use and significance of
pesticides in the environment. John Wiley and Sons, New York, N.Y.
141.
Metcalf, R. L., G. K. Sangha, I. P. Kapoor, 1971. Environ. Sci.
Technol. 5,709 (as cited in Yu et al., 1975)
Monsanto Co. 1978. Acute oral-rat, acute dermal-rabbit. Submitted by
Bio/Dynamics, Inc., PD-77-433 on June 28, 1978. Unpublished study
received 1978; CDL: 241273 (as cited in U.S. EPA 1984).
Monsanto Co. 1981. Acute inhalation LD50 rat. Submitted by
Bio/Dynamics, Inc., PD-81-183 on Dec. 3, 1981. Unpublished study
received 1981; CDL: 248053. (as cited in U.S. EPA 1984).
Monsanto Co. 1982. Environmental fate of microencapsulated alachlor:
Vol. I and II. Unpublished study received May 26, 1982 under EPA Reg.
No. 524-344, prepared by Monsanto Agricultural Products Co., submitted
by Monsanto Co., Washington, D.C., CDL: 07084.
Rodwell, D.E., and E.J. Tacher. 1980. Technology study in rats:
IRDC No. 401-058, IR-79-020. Unpublished study including submitter
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