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A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Michigan State University, Oregon State University, and University of California at Davis. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program.

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Acephate

Publication Date: 9/95

TRADE OR OTHER NAMES

Acephate is found in a variety of commercial insecticides. Trade names for products containing acephate include Orthene, Asataf, Pillarthene, Kitron, Aimthane, Ortran, Ortho 12420, Ortril, Chrevron RE 12420, and Orthene 755 (8, 9).

REGULATORY STATUS

Acephate is considered a general use insecticide and is used on many crops inside and outside the U.S. (6). In Canada, maximum residue limits (MRL) have not been established under the Canadian Food and Drug Act and Regulations for acephate on any crop, and therefore only negligible residues (< 0.1 mg/kg) are permitted on any produce. MRLs have been established for acephate's transformation product, methamidophos, at 1.0 mg/kg for lettuce and peppers, and 0.5 mg/kg for tomatoes (10).

Products containing acephate must bear the signal word "Caution" on their label (3). Check with specific state regulations for local restrictions which may apply.

INTRODUCTION

Acephate is an organophosphate foliar spray insecticide of moderate persistence with residual systemic activity of about 10-15 days at the recommended use rate. It is used for control of a wide range of biting and sucking insects, especially aphids, including resistant species, in fruit, vegetables (e.g. potatoes and sugar beets), vine, and hop cultivation and in horticulture (e.g. on roses and chrysanthemums grown outdoors) (1). It also controls leaf miners, lepidopterous larvae, sawflies and thrips in the previously stated crops as well as turf, mint and forestry (6). It is considered non-phytotoxic on many crop plants (2). Although, a marginal leaf-burn has occurred on Red Delicious apples (6). Acephate and its primary metabolite, methamidophos, are toxic to Heliothis spp. that are considered resistant to other organophosphate insecticides (10).

Acephate emits toxic fumes of phosphorus, nitrogen, and sulfur oxides when heated to decomposition. Symptoms of exposure to acephate include a slight irritation of eyes and skin. Acephate comes in soluble powder, pressurized spray and granular formulations (2).

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

The amount of acephate that is lethal to one-half (50%) of experimental animals fed the material is referred to as its acute oral lethal dose fifty, or LD50. The acute oral toxicity of acephate to mammals is medium (LD50 = 500-5,000 mg/kg) to high (LD50 = 50-500 mg/kg), and acute toxicity from inhalation is medium (LC50 = 2-20 mg/l) (7). The acute dermal LD50 for rabbits is 2,000 mg/kg (11); no irritation or sensitization was observed in skin tests on guinea-pigs (2). The effect of 900 mg/kg on cholinesterase inhibition in rats was not as severe as parathion at 15 mg/kg. Atropine sulfate is an effective antidote (12).

The acute oral LD50 for technical grade acephate in female rats is 866 mg/kg; 945 mg/kg for male rats; 361 mg/kg for mice; 350 mg/kg for mallard ducks; 852 mg/kg for chickens; and 140 mg/kg for ringneck pheasants (2).

The oral LDLo (Lethal Dose Low - lowest dose of a substance other than LD50 introduced by any route other than inhalation, over any given period of time in one or more divided portions and reported to have caused death in humans or animals) for dogs is 681 mg/kg (8).

The lethal concentration fifty, or LC50, is that concentration of a chemical in air or water that kills half of the experimental animals exposed to it for a set period of time. The 96 hour LC50 for rainbow trout is >1,000 mg/l; 2,050 mg/l for bluegill fish; 1,725 mg/l for largemouth black bass; 2,230 mg/l for channel catfish; and 9550 mg/l for goldfish (2). The toxicity of acephate to rainbow trout increased with increasing temperature (14).

CHRONIC TOXICITY

In 2-year feeding trials, dogs exhibited depression of cholinesterase at 100 mg/kg diet (maximum dose level) of acephate but no other significant effects; rats showed depression of cholinesterase but no effect on weight gain or pathological effect at 30 mg/kg diet (2). Another feeding study noted that rats did not produce pathological changes over a 90-day period when fed up to 300 mg/kg body weight of acephate (1).

Acephate has a negligible chronic toxicity to fish (14).

Reproductive Effects

Acephate is considered a fetotoxin (can poison the fetus) and there is some evidence of hormonal effects (7).

Teratogenic Effects

No effects were observed in 2-year feeding trials on dogs (2).

Mutagenic Effects

No effects were observed in 2-year feeding trials on dogs (2).

Carcinogenic Effects

No effects were observed in 2-year feeding trials in dogs (2).

Organ Toxicity

Exposure effects of acephate in humans can include: cardiac responses (bradycardia/tachycardia, heart block), central nervous system impairment, eye problems (miosis/mydriasis, loss of accommodation, ocular pain, sensation of retrobulbar pressure, tearing, dark or blurred vision, conjunctiva hyperemia, cataracts), gastrointestinal problems (abdominal cramps, heart burn, hyperperistalsis), respiratory effects (apnea, dyspnea, hypopnea, atelectasis, bronchoconstriction, bronchopharyngeal secretion, chest tightness, productive cough, rales/ronchi, wheezing, pulmonary edema, laryngeal spasms, rhinorrhea, oronasal frothing) and death due to respiratory failure (15).

Fate in Humans and Animals

Exposure to acephate can result in alkyl phophates in urine (15).

ECOLOGICAL EFFECTS

Effects on Birds

Acephate is considered moderately toxic to upland game birds. The LD50 for acephate in mallard ducks is 350 mg/kg; 140 mg/kg in pheasants; > 5,000 ppm for the mallard and 1,280 ppm for the bobwhite quail (3). Acephate may affect behavior and breeding success (7).

Effects on Aquatic Organisms

The compound is considered relatively non-toxic to fish with an LC50 for goldfish of 9,550 mg/l and rainbow trout >1,000 mg/l over 96 hours (1). Another study noted that the LC50 was >1,000 ppm for both the rainbow trout and the bluegill (3).

Acephate did not increase "coughing" (interruption of normal ventilating cycle, with a more rapid expansion and contraction of the buccal and opercular cavities, which serves the purpose of clearing the gills of accumulated debris) frequency of rainbow trout (14).

In laboratory studies, the cholinesterase activity in the erythrocytes, gills, and serum of rainbow trout was reduced within 3 hours of exposure to acephate. With methamidophos, the extent of brain and liver AChE inhibition in carp was proportional to the insecticide concentration and exposure time. Smaller fish started dying when the AChE inhibition was 40 to 50%, but very large fingerlings survived an inhibition of more than 80% (14).

In field studies, however, subsequent to aerial spraying of acephate to control spruce budworm, no significant depression of brain AChE activity of brook trout and salmon in streams near the target area occurred; but, there was a significant depression of brain AChE activity in suckers, which returned to normal by the eighth day (14).

Effects on Other Animals (Nontarget species)

Acephate is considered toxic to bees (1). The LC50 for bees is 1.2 ug/bee (3).

In studies examining the residual toxicity of insecticides on beneficial species in citrus, it was found that acephate had the longest residual activity toward Aphytis melinus, DeBach, and that mortality with dimethoate treatment occurred for a shorter period of time than with acephate treatment. This same study showed that residues of acephate caused greater mortalities over a longer period of time to A. melinus than other materials tested (13).

In some cases, there is no effect on fecundity of the beneficial, but survival of the offspring is affected. For example, fecundity of Diaeretiella rapae was not reduced by treatment of Myzus persicae host mummies with acephate, but acephate significantly affected survival for the first day after emergence (13).

In studies of insecticides commonly used in cotton, acephate was shown to be very toxic to adult Microplitis croceipes parasitoids, and caused 100% mortality at the lowest recommended field rates (13).

ENVIRONMENTAL FATE

Breakdown of Chemical in Soil and Groundwater

Acephate dissipates rapidly with half-lives of <3 and 6 days in aerobic and anaerobic soils, respectively. The major metabolite was CO2 in both soil types. TLC and soil column studies indicate acephate is mobile in most soils but that aged residues (excluding acephate and its degradate methamidophos) are immobile in sandy loam soil. Most of the applied acephate and degradate methamidophos degrade to immobile compounds in 20 days (4). Methamidophos and carbon dioxide were identified as the major soil metabolites (9).

Breakdown of Chemical in Surface Water

No information was currently available.

Breakdown of Chemical in Vegetation

Acephate is quickly absorbed, translocated, and transformed in pine seedlings and cotton plants. The chemical was metabolized via cleavage of the amide bond to form methamidophos and an unknown, but insecticidally active compound, which were identified in the roots, stems, and leaves. Methamidophos was also found in cotton leaves following a single application of acephate. Four additional degradation products were formed - two of which were tentatively identified as O, S- dimethyphosphorothioate and S-methyl acetylphosphoramidothioate. The amount of methamidophos and the four products represented about 9% and 5% of the applied amount, respectively (9).

In studies on tobacco leaves, citrus fruit, greenhouse tomatoes, and celery and lettuce, half-life disappearance of residues ranged from 1 to 15 days, depending on the crop species and the part of the plant analyzed. This same study showed residues of both acephate and methamidophos on carrots and potatoes even though no direct spraying of the underground portion of these crops occurred. Carrots contained much higher residues (up to 5.2 mg/kg) than potatoes (up to 3.6 mg/kg). In contrast to carrots, potatoes and the fruit bearing vegetables studied, the amount of rainfall occurring was directly proportional to the disappearance of both acephate and methamidophos residues on lettuce and celery. The level of residues on the eight crops studied on day 3 after application generally reflected the weight to volume ratios of the crops except where translocation appeared to give higher residues than would be expected. In carrots, potatoes, peppers and tomatoes, residues on day 7 were higher than on day 3 and day 14, thus suggesting absorption and translocation from foliage to root, tuber or fruit. Methamidophos was identified in the eight crops studied, at high levels on peppers, but at very low levels on lettuce and celery (10).

Acephate is rapidly absorbed into the leaf tissue of cotton plants when applied foliarly, with nearly 40% of the applied acephate present in the internal extract and 25% remaining on the leaf surface 24 hours after application. The unrecovered acephate probably was translocated from the leaves or bound in unextractable form in the leaf tissue. The low vapor pressure of acephate indicates that loss due to volatilization would be negligible. Translocation of acephate into the fruiting body of the cotton plant following foliar application is not sufficient to be toxic to cotton insect pests. Little to no degradation of acephate to methamidophos occurred on the leaf surface. Methamidophos was more persistent in plant tissue than acephate (i.e. acephate was degrading to methamidophos faster than methamidophos was degrading to another compound) (11).

PHYSICAL PROPERTIES AND GUIDELINES

Exposure Guidelines:

ADI: Until 1987, the temporary acceptable daily intake (ADI) for man was 0.005 mg/kg (2)
H-t1/2: at 40 degrees C and pH 9: 60 hours, at 40 degrees C and pH 3: 710 hours (9)
KH: 5.2 x 10 to the minus 13 atm x m3/mol at 20-24 degrees C (9)

Physical Properties:

Appearance: Colorless to white solid (9)
CAS No.: 30560-19-1 (5)
RTECS (Registry of Toxic Effects of Chemical Substances Number): TB4760000 (8, 9)
Chemical name: O, S-dimethyl acetylphos-phoramidothioate (IUPAC) (1, 3), O, S-dimethyl acetic phosphoramidothioate, (7) N-[methoxy (methylthio)phosphinoyl] acetamide (2, 9)
Chemical Class/Use: organophosphate/systemic insecticide (3)
Specific gravity: 1.35 (5)
Specific density: 1.35 at 20 - 24 degrees C (2, 9)
Solubility in water: readily soluble in water (79 g/100 ml at 20 degrees C) (1). 650 g/l at 20 degrees C (2)
Solubility in other solvents: In acetone 15.1, ethyl acetate 3.5, benzene 1.6, hexane 0.01 (all in g/100 ml at 20 degrees C) (1) ethanol < 50 g/l at 20 degrees C (2, 9)
Melting point: 93 degrees C (198-199 degrees F) (1, 5), technical grade acephate (purity 80 - 90%) is 82 - 89 degrees C (2), 72 - 80 degrees C (12), 64 - 68 degrees C for impure (9)
Molecular weight: 183.18 (8)
Molecular Formula: C4H10NO3P5 (8)
Boiling point: decomposes on distillation (1)
Decomposition temperature: at 40 degrees C, 50% decomposition occurs in 60 hours at pH 9 and in 710 hours at pH 3 (1)
Flashpoint: low volatility, but some of the minor degradation products are volatile (12)
Vapor pressure: 2.3 x 10 to the minus 6 mbar at 24 degrees C (1), 0.226 mPa (24 degrees C) (2), 1.7 x 10 to the minus 6 mmHg at 24 degrees C (9)
log Koc: 0.48 (9)
log Kow: -1.87 (9)

BASIC MANUFACTURER

Valent USA
1333 North California Blvd.
Suite 600
P. O. Box 8025
Walnut Creek, CA 94596-8025
Telephone: 510-256-2700
Emergency: 800-457-2022

Review by Basic Manufacturer:

Comments solicited: March, 1994
Comments received:

REFERENCES

  1. The Agrochemicals Handbook. 1983. The Royal Society of Chemistry, The University, Nottingham, England.
  2. Worthing, C. R. (ed.) 1987. The Pesticide Manual: A World Compendium. Eighth edition. Published by The British Crop Protection Council.
  3. Farm Chemicals Handbook. 1994. Meister Publishing Co. Willoughby, OH.
  4. Thomson, W. T. 1989. Agricultural Chemicals. Book 1: Insecticides. Thomson Publications, Fresno, CA.
  5. OHS Database. Occupational Health Services, Inc. 1993 (August) MSDS for Acephate. OHS Inc., Secaucus, NJ.
  6. Thomson, W. T. Agricultural Chemicals. Book 1: Insecticides. 1992. Thomson Publications, Fresno, CA.
  7. Briggs, S. A. 1992. Basic Guide to Pesticides: Their Characteristics and Hazards. Hemisphere Publishing Corp. Washington, Philadelphia, London.
  8. Fairchild, E. J. (ed.) PhD. Agricultural Chemicals and Pesticides: A Subfile fo the Registry of Toxic Effects of Chemical Substances. 1977. Published by U.S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control, National Institute for Occupational Safety and Health.
  9. Montgomery, J. H. (ed.). Agrochemicals Desk Reference. 1993. Environmental Data. Published by Lewis Publishers, Chelsea, MI.
  10. Frank, R., G. Ritcy, H.E. Braun and F.L. McEwen. 1984. Disappearance of Acephate Residue from Beans, Carrots, Celery, Lettuce, Peppers, Potatoes, Strawberries and Tomatoes. J. Econ. Ent. 77:5 1110- 1115.
  11. Bouchard, D. C. and T. L. Lavy. 1982. Fate of Acephate in the Cotton Plant. J. Econ. Ent. 75:5 921-923.
  12. Spencer, E. Y. 1981. Guide to the Chemicals Used in Crop Protection. 7th edition. Publication 1093. Research Branch. Agriculture Canada.
  13. Elzen, G. W. 1989. Sublethal Effects of Pesticides on Beneficial Parasitoids. In: Pesticides and Non-target Invertebrates. Ed. by Paul C. Jepson. Intercept Ltd. Dorset, England. pp 129-150.
  14. Morty, A. S. 1986. Toxicity of Pesticides to Fish. Volume II. CRC Press. Boca Raton, FL.
  15. Hallenbeck, W. H. and K. M. Cunningham-Burns. 1985. Pesticides and Human Health. Springer-Verlag. New York, Berlin, Heidelberg and Tokyo.