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.
Captafol is a "general use" pesticide with a toxicity classification of IV (relatively non-toxic). Check with specific regulations for local restrictions which may apply. Products containing captafol must bear the Signal Word "Warning" (3).
Formulation types include dusts, flowables, wettables, water dispersibles, and aqueous suspensions. Mixed formulations include (captafol +) triadimefon; ethirimol; folpet; halacrinate; propiconazole; and pyrazophos (1). Captafol is compatible with most plant-protection products, with the exception of alkaline preparations and formulating materials (1, 3).
Other studies indicated an acute oral LD50 for rats of 6,200 mg/kg (maize oil suspension) and 4,200 mg/kg (aqueous suspension) (1, 4). An acute oral LD50 for rats of 5,000-6,200 mg active ingredient/kg; and 2,500 mg wettable powder formulation (administered as an aqueous suspension)/kg were also reported (2, 3).
A study of captafol in rabbits indicated an acute percutaneous LD50 of >15,400 mg/kg; and it was noted that some people may develop an allergy to captafol (2).
Other feeding studies indicated captafol when fed to rats at 250 and 500 mg/kg body weight for 2 months did not induce pathological changes, though growth was inhibited at 1,500 mg/kg. Feeding at 500 mg/kg body weight for 2 years had no effect, whereas feeding to dogs at 300 mg/kg for 2 years caused changes in urine and blood profiles and liver insufficiency. No accumulation in animals was noted (1).
Another source found no ill-effect was observed in rats receiving 500 mg/kg diet; and in dogs receiving 10 mg/kg daily for 2 years (2).
Groups of two male and two female dogs were given daily doses of 0, 10, 30, 100 or 300 mg/kg body of captafol over a two year period. Increased absolute liver and kidney weights and liver and kidney to body weight ratios were seen in all animals at the 30, 100 and 300 mg/kg levels. Histopathology, blood chemistry, urine analysis and liver function tests revealed no adverse effects that could be attributed to the administration of captafol (9, 10).
There is a strong potential for reproductive effects in birds (7, 8).
Teratogenicity studies in rabbits indicated a teratogenic NOEL > 50 mg/kg/day; and a fetotoxic NOEL = 16.5 mg/kg/day; fetotoxic LEL = 50 mg/kg/day (increased minor skeletal abnormalities and resorptions); maternal NOEL = 16.5 mg/kg/day; maternal LEL = 50 mg/kg/day (deaths, decreased weight gain and food intake); levels tested 0, 5, 16.5 and 50 mg/kg/day (6).
In another study, when captafol was administered to two strains of rabbits at dosages ranging from 37.5 to 150 mg/kg/day from 6 through 16 weeks of gestation or to rats at different dosages of 100 and 500 mg/kg/day from 6 through 15 weeks, no evidence of teratogenicity was found (9, 12). Furthermore, captafol was not teratogenic when administered to rhesus monkeys at dosages of 6.25, 12.5 and 25 mg/kg/day during day 22 through 32 of gestation (9, 13).
Teratogenicity studies in hamsters indicated a fetotoxic NOEL = 300 mg/kg on days 7 or 8; and a teratogenic NOEL = 300 mg/kg on days 7 or 8 (6, 7, 8); the levels tested were 100, 200, 300, 400, 500, 600, 800, 1,000, 1,500 mg/kg/day (treated days 6-8, 6-10, 7 or 8) (6).
Captafol was given to male rats intraperitoneally at rates of 2.5, 5.0 and 10 mg/kg/day or orally at 50, 100 and 200 mg/kg/day for 5 days, then the animals were bred for the following 10 weeks in a dominant lethal test. Neither fertility nor mean total implants were affected. An oral dosage of 50 mg/kg/day was considered a no effect level (9, 15).
Male mice were given a single intraperitoneal injection of captafol (1.5 and 3.0 mg/kg) and a dominant lethal test was carried out. There was no increase in early embryonic death among conceptuses of females mated to treated males. A similar result was obtained in rats after the males were dosed orally for 14 days at rates of 125 or 250 mg/kg/day. Indicator microorganisms isolated from the peritoneal cavity of treated male rats showed no increase in reversion rate. Thus, captafol was not mutagenic at the dosages tested in any of these systems (9, 16).
Captafol was studied for mutagenic activities in a microbial system. The effect on the mutagenic activity of captafol of adding S-9 mix or L-cysteine to the system was investigated. The mutagenicity of captafol observed in Escherichia coli WP2 her and Ta 1535 disappeared after addition of S-9 or L-cysteine (9, 17).
A two-year mouse study (Chevron Chemical Company, 1981) showed both compound and dose-related oncogenic lesions at the middle and high dose groups. These lesions included lymphosarcomas, myeloproliferative disease, harderian gland hyperplasia, benign harderian gland adenomas, and hemangiosarcomas. This compound also produced dose-related non- oncogenic lesions at all dose levels. There was a significant increase in mortality in the middle and high dose mice, frequently accompanied by neoplastic lesions (7). Oncogenic lesions were observed at 1,000 ppm and 3,000 ppm but not at 300 ppm (8).
In another 2-year rat feeding study (Hazelton Laboratories, 1983) a dose- related increased incidence of fibroadenomas of the mammary gland and an increased incidence of neoplastic nodules in the liver on females occurred. Not all the animals at the middle and low doses were subjected to histopathological examination so that the numbers may not be representative (7).
US EPA has determined that captafol has oncogenic potential (potential to cause cancer) (7).
No parent captafol was detected in ruminant tissues or in milk. Several metabolites were identified in animal tissue (8).
In a 21-day study it was found that the lethal dose of captafol for leghorn chicks was >10,000 mg/kg body weight and was > 10,500 mg/kg body weight for pigeons (9).
Another study found the LC50 (96 hour) for rainbow trout to be 0.5 mg/l; 3.0 mg/l for goldfish; and 0.15 mg/l for bluegill (1, 2, 3).
The aquatic crustacean Daphnia magna has a 96-hr LC50 = 3.34 ppm. Captafol is considered moderately to very highly toxic to freshwater invertebrates (7, 8).
Field exposure studies with eight volunteers exposed to the spray drifts of captafol for three consecutive days at the rate of six hours per day did not show any abnormalities which could be attributed to the effects of this fungicide (9).
Captafol is considered non-toxic to bees (1).
Degradation and metabolism in plants and animals is through hydrolytic cleavage to tetrahydrophthalimide (THPI) and dichloroacetic acid. THPI is degraded to tetrahydrophthalimidic acid and further to phthalic acid and ammonia (1).
Captafol and/or its metabolites and degradates are absorbed by roots and shoots of plants. Captafol is also translocated in plant tissue as a result of seed treatment, soil treatment and foliar application (7, 8).
Grapes, apples and citrus have been injured from phytotoxicity under certain weather conditions. Roses have shown injury at high rates of application (4).
|TLV-TWA:||0.1 mg/m3 OSHA (5)|
|CAS No.:||2425-06-1 (1)|
|Chemical name:||cis-N-(I, 1,2,2,-Tetrachloroethylthio)-4-cyclohexene-I,2-dicarboximide|
|Chemical Class/Use:||Carboximide/Foliar protectant fungicide (4)|
|Solubility in water:||1.4 mg/L at 20 degrees C (1, 2)|
|Solubility in other solvents (all in g/100 ml):||isopropanol 1.3, benzene 2.5, toluene 1.7, xylene 10.0, acetone 4.3, methyl ethyl ketone 4.4, dimethyl sulphoxide 17.0 (1)|
|Melting point:||160-162 degrees C; 320-323 degrees F (5, 7)|
|Decomposition temperature:||slowly decomposes at its melting point (2)|
|Vapor pressure:||less than 1.3 x 10 to the minus 9 mbar at 20 degrees C (1)|