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PHTHALIMIDE FUNGICIDES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) The phthalimide fungicides are derivatives of phthalic acid.

Specific Substances

    A) CAPTAN
    1) 1,2,3,6-Tetrahydro-n-(trichloromethylthio)phthalimide
    2) CAS 133-06-2
    FOLPET
    1) N-(trichloromethylthio)phthalimide
    2) CAS 133-07-3
    CAPTAFOL
    1) DIFOLATAN
    2) N-(Tetrachloroethylthio)tetrahydrophthalimide
    3) CAS 2425-06-1
    GENERAL TERM
    1) Fungicides (phthalimide)

Available Forms Sources

    A) FORMS
    1) CAPTAN: Wettable powder (500, 800, or 830 g active ingredient/kg); dustable powder (50 or 100 g/kg); powder for seed treatment (600 to 750 g/kg); water dispersible powder (contains dispersants); seed protectant (flowable concentrate 2.94 to 4 lb/gal) (HSDB, 1995).
    a) Technical grade is approximately 96% purity. Impurities are bis-(trichloromethyl)disulfide and tetrahydrophthalimide (HSDB, 1995).
    2) FOLPET: Wettable powder (500 or 750 g/kg); dustable powder; concentrated suspension; technical grade (90 to 95% pure). Impurities are unreacted phthalimide, water, calcium carbonate, and sulfur (HSDB, 1995).
    3) CAPTAFOL: 80% wettable powder; 39% flowable seed protectant; 7.5% dustable powder; soluble concentrate (480 g/L) (HSDB, 1995).
    4) The phthalimide fungicides are frequently mixed with other commonly used insecticides, such as diazinon, lindane or malathion, or with other fungicides such as maneb (HSDB, 1995).
    B) SOURCES
    1) CAPTAN: Is not known to be a natural product. It has been detected in ambient air, in drinking water, and in foods at ppb levels. The major source of intake is from the diet, especially fruits and vegetables, where allowable tolerances are as high as 100 ppm in the USA (HSDB, 1995).
    2) FOLPET: Has been measured in air and foods (HSDB, 1995).
    3) CAPTAFOL: Is not marketed in the USA, but is manufactured in India (HSDB, 1995).
    C) USES
    1) Captan, Folpet, and Captafol are widely used fungicides and seed protectants.
    a) CAPTAN: Used as a fungicide on fruits, berries, vegetables, and ornamentals, in oil-based paints, wallpaper paste, fabrics, and household articles. Also used as a preservative in cosmetics (HSDB, 1995).
    b) FOLPET: Used as fungicide for fruits, berries, vegetables, ornamentals, and turf in Western states; in paint and plastics; for treatment of internal and external surfaces of buildings (HSDB, 1995).
    c) CAPTAFOL: Used as fungicide on fruits, vegetables, field crops; as a seed treatment; to reduce wood rot in logs and wood products; and as a wound protectant for grafting and pruning wounds on trees (HSDB, 1995).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Phthalimide fungicides are commonly used to prevent fungus formation and as a food preservative.
    B) TOXICOLOGY: The major phthalimide fungicides include: captan, folpet, and captafol, which have a similar spectra of toxicity, consisting of irritant and allergic dermatitis, conjunctivitis, and respiratory sensitization. Because these agents are generally used in combination with other pesticides, it is difficult to correlate previous reports of human toxicity directly to the phthalimide agents.
    C) EPIDEMIOLOGY: This is a very uncommon cause of poisoning with only a handful of cases reported in the literature. Large overdoses produce mild to moderate symptoms with no confirmed fatalities reported in the literature.
    D) WITH POISONING/EXPOSURE
    1) All information about overdose is from a few case reports. Headache, nausea, vomiting, diarrhea, weakness, numbness of upper limbs, and substernal pain can be seen in very large ingestions with the most causing dermatitis, conjunctivitis and wheezing.
    0.2.20) REPRODUCTIVE
    A) The phthalimide fungicides contain the phthalimide moiety in common with phthalidomide, a known human teratogen. Captan has been teratogenic, fetotoxic, and/or embryotoxic in a variety of rodent species and caused stillbirths in dogs. Folpet was teratogenic in rabbits, chicks, and hamsters. Captafol has been embryo- or fetotoxic in experimental animals.
    B) Captan, folpet, and captafol have all induced testicular degeneration in laboratory animals.

Laboratory Monitoring

    A) No specific laboratory tests are necessary unless otherwise clinically indicated. General testing would be determined by the patient's overall clinical condition.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Patient with mild to moderate exposure are usually asymptomatic. Given the self-limiting and non-lethal effects of overdose, basic supportive care is all that is required. According to case reports, abnormal laboratory findings and symptoms abate with supportive care.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Patients with severe toxicity, through either dermal or oral exposure, usually have very mild to self-limiting symptoms such as headache, nausea, weakness, numbness of upper limbs, and substernal pain. Although some lab abnormalities such as leukocytosis and elevated CK have been reported, these are usually self-limiting. ECG T-wave inversions have been described but were not related to abnormal cardiac function.
    C) DECONTAMINATION
    1) PREHOSPITAL: No oral decontamination is indicated. DERMAL EXPOSURE: Wash exposed areas with soap and water. EYE EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature normal saline or water.
    2) HOSPITAL: No oral decontamination is indicated. DERMAL EXPOSURE: Wash exposed areas with soap and water. Lipophilic agents such as polyethylene glycol can also be used to decontaminate other lipophilic compounds. EYE EXPOSURE: Irrigate exposed eyes with copious amounts of room temperature normal saline or water.
    D) AIRWAY MANAGEMENTS
    1) There has never been a report of a patient needing an advanced airway due to exposure of this chemical. Consequently, airway compromise is not expected.
    E) ANTIDOTE
    1) None.
    F) ENHANCED ELIMINATION PROCEDURE
    1) There has never been a report of a patient needing enhanced elimination. Symptoms are self-limiting.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients can be managed at home. Any patient with significant symptoms, such as altered mental status, weakness, abdominal pain, headache, chest pain, numbness, or syncope should be evaluated at a healthcare facility.
    2) OBSERVATION CRITERIA: Patients with significant signs and symptoms, such as altered mental status, weakness, abdominal pain, headache, chest pain, numbness, or syncope should be evaluated at a healthcare facility and observed until their condition stabilizes or improves.
    3) ADMISSION CRITERIA: Patients rarely require admission due to this exposure. Reasons for admission might include significant electrolyte abnormalities or abnormalities that prevent them from accomplishing their activities of daily living (ADLs).
    4) CONSULT CRITERIA: If patients develop respiratory failure, hemodynamic instability, or any other symptoms not expected with this exposure, consult a toxicologist or regional poison center.
    H) PITFALLS
    1) Common errors for managing these patients include failing to look for other exposures, and not identifying other similar presenting medical conditions. Confusing phthalimide fungicides with phthalates; unlike the latter, phthalimide fungicides have not been shown to be endocrine disruptors.
    I) DIFFERENTIAL DIAGNOSIS
    1) Most patients are asymptomatic. Cases may be confused with other causes of dermatitis, nausea, headache, or chest discomfort.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Wash exposed areas with soap and water. Lipophilic agents such as polyethylene glycol can also be used to decontaminate other lipophilic compounds.

Range Of Toxicity

    A) TOXICITY: Human toxicity is not established. Phthalimide fungicides appear to be of a low order of acute toxicity by usual routes of exposure. CAPTAN: A 17-year-old girl developed headache, nausea, weakness, numbness of upper limbs, and substernal pain following the intentional ingestion of 7.5 g of Captan 50 WP.

Clinical Effects

Summary Of Exposure

    A) USES: Phthalimide fungicides are commonly used to prevent fungus formation and as a food preservative.
    B) TOXICOLOGY: The major phthalimide fungicides include: captan, folpet, and captafol, which have a similar spectra of toxicity, consisting of irritant and allergic dermatitis, conjunctivitis, and respiratory sensitization. Because these agents are generally used in combination with other pesticides, it is difficult to correlate previous reports of human toxicity directly to the phthalimide agents.
    C) EPIDEMIOLOGY: This is a very uncommon cause of poisoning with only a handful of cases reported in the literature. Large overdoses produce mild to moderate symptoms with no confirmed fatalities reported in the literature.
    D) WITH POISONING/EXPOSURE
    1) All information about overdose is from a few case reports. Headache, nausea, vomiting, diarrhea, weakness, numbness of upper limbs, and substernal pain can be seen in very large ingestions with the most causing dermatitis, conjunctivitis and wheezing.

Heent

    3.4.3) EYES
    A) CONJUNCTIVITIS has been reported in humans. Folpet is an irritant of the eyes and mucous membranes (HSDB, 1995).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CARDIOTOXICITY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 17-year-old girl developed headache, nausea, weakness, numbness of upper limbs, and substernal pain 3 hours after the suicidal ingestion of 7.5 g of Captan 50 WP (a suspension of Captan in a ratio of 50% mixed with water). Her vital signs were temperature 36.7 degrees C, pulse 110-120 beats/minute, and BP 120-140/60-90 mmHg. Laboratory results showed elevated WBC 11,200/mm(3), creatine kinase 309 Units/L (normal up to 43 Units/L), and aspartate aminotransferase 67 Units/L (normal up to 29 Units/L). ECG revealed inversion of T waves in the III and aVF leads and echocardiogram was normal with an ejection fraction of 67%. Following supportive care, she recovered without further sequelae (Chodorowski & Anand, 2003).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Inhalation of folpet dust or spray can cause respiratory tract irritation (HSDB, 1995).
    B) BRONCHOSPASM
    1) OCCUPATIONAL ASTHMA: Captafol can produce occupational asthma (HSDB, 1995) (Royce et al, 1993).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 17-year-old girl developed headache, nausea, weakness, numbness of upper limbs, and substernal pain 3 hours after the suicidal ingestion of 7.5 g of Captan 50 WP (a suspension of Captan in a ratio of 50% mixed with water). Her vital signs were temperature 36.7 degrees C, pulse 110-120 beats/minute, and BP 120-140/60-90 mmHg. Laboratory results showed elevated WBC 11,200/mm(3), creatine kinase 309 Units/L (normal up to 43 Units/L), and aspartate aminotransferase 67 Units/L (normal up to 29 Units/L). ECG revealed inversion of T waves in the III and aVF leads and echocardiogram was normal with an ejection fraction of 67%. Following supportive care, she recovered without further sequelae (Chodorowski & Anand, 2003).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTRITIS
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting with diarrhea may occur following ingestion of captan in large quantities (HSDB, 1995).
    b) CASE REPORT: A 17-year-old girl developed nausea 3 hours after the suicidal ingestion of 7.5 g of Captan 50 WP (a suspension of Captan in a ratio of 50% mixed with water) (Chodorowski & Anand, 2003).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) WITH POISONING/EXPOSURE
    a) Proteinuria, urobilinogen in the urine, and depression of liver function paralleled the degree of dermatitis from exposure to captafol (HSDB, 1995).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) The liver was the primary target for subchronic toxicity of captafol in mice (Tamano et al, 1993). Folpet was heptatotoxic in rats (Ashley et al, 1982).
    b) MICE: Cytoplasmic vacuolar degeneration was seen in the livers of mice given captafol at levels up to 1.25% in the diet for 12 weeks. The liver was the primary target for subchronic toxicity of captafol in mice (Tamano et al, 1993).
    c) RATS: Histopathological changes were seen in liver of rats given dietary levels of captafol up to 0.6% for 13 weeks. Changes in liver enzymes were also seen (Tamano et al, 1991).
    d) RATS: Folpet at intraperitoneal doses as low as 50 mg/kg altered levels of liver enzymes in rats (Ashley et al, 1982).

Genitourinary

    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CERVIX LESION
    a) RATS: Captan induced abnormalities of the uterus/cervix/vagina in pregnant rats given an oral dose of 2500 mg/kg on days 6 to 10 after conception (RTECS, 1995).
    2) RENAL FAILURE
    a) RATS: Captan induced chronic renal disease and severe testicular atrophy in rats when given in the diet (Reuber, 1989).
    b) RATS: Histopathological changes were seen in the kidneys of rats given dietary levels of captafol up to 0.6% for 13 weeks (Tamano et al, 1991).

Acid-Base

    3.11.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) URINE ABNORMAL
    a) RATS: Dose-dependent decrease in urinary pH was seen in rats fed captafol at dietary levels up to 0.6% for 13 weeks (Tamano et al, 1991).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Both irritant and allergic contact dermatitis have been reported from captan, folpet, and captafol (HSDB, 1995) (Thiboutot et al, 1990; Vilaplana & Romaguera, 1993; Stoke, 1979; Brown, 1984).
    a) CASE SERIES: 23% of timber workers exposed to captafol had histories of dermatitis; irritant contact dermatitis was far more common than allergic (Stoke, 1979).
    2) CASE REPORT: One case of urticaria has been reported with captan exposure. The patient reacted to both captan-treated plants and to the formulation (Croy, 1973).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) CASE REPORT: One case of dermal and respiratory sensitization to captan has been reported (HSDB, 1995).
    2) Captan, folpet, and captafol all were positive in patch testing in human subjects (Lisi et al, 1986; Thiboutot et al, 1990; Vilaplana & Romaguera, 1993; Brown, 1984). Of 46 thiophthalimides tested, these compounds most often evoked a reaction (Lisi et al, 1987).
    3) CASE REPORT: Multiple dermal sensitization to captan, folpet, and captafol (with maneb) was seen in one agricultural worker (Peluso et al, 1991).
    4) Captafol can produce photosensitization and occupational asthma (HSDB, 1995) (Royce et al, 1993).
    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IMMUNE SYSTEM DISORDER
    a) SUPPRESSION OF HUMORAL IMMUNITY: Captan suppressed red blood cell-antibody formation in sheep and lymphocyte stimulation by lipopolysaccharide in rats and mice given 0.3% in the diet (Lafarge-Frayssinet & Decloitre, 1982).
    2) ALLERGIC REACTION
    a) Captafol induced contact hypersensitivity in mice (Cushman & Street, 1991).

Reproductive

    3.20.1) SUMMARY
    A) The phthalimide fungicides contain the phthalimide moiety in common with phthalidomide, a known human teratogen. Captan has been teratogenic, fetotoxic, and/or embryotoxic in a variety of rodent species and caused stillbirths in dogs. Folpet was teratogenic in rabbits, chicks, and hamsters. Captafol has been embryo- or fetotoxic in experimental animals.
    B) Captan, folpet, and captafol have all induced testicular degeneration in laboratory animals.
    3.20.2) TERATOGENICITY
    A) FETOTOXICITY
    1) Captan, folpet, and captafol all share the ortho-dicarboximido moiety found in phthalidomide, a known human teratogen (Kennedy et al, 1968). Captan and folpet were teratogenic in multiple animal species, and captafol has been fetotoxic, but not teratogenic.
    B) ABORTION
    1) CAPTAN has been weakly linked with increased spontaneous abortions, prematurity, and congenital malformations in a large group of female floriculture workers and wives of male workers (Restrepo et al, 1990a).
    C) ANIMAL STUDIES
    1) CAPTAN has produced teratogenic effects in animal and bird studies:
    a) Captan is teratogenic in hamsters and chicks (Finkel, 1983). It produced defects of the nervous and skeletal systems when injected at doses of 3 to 20 mg/kg into chick eggs (Verrett et al, 1968). It produced a variety of defects in chicks injected with amounts up to 18 ppm before incubation (Martin et al, 1978).
    b) Craniofacial abnormalities were seen in fetal mice when Captan was given subcutaneously at 900 mg/kg on days 9-14 of gestation (RTECS, 1995). Microphthalmia was seen in fetal mice exposed to doses as high as 464 mg/kg/day (Anon, 1989). Captan was not teratogenic in mice by inhalation at 488 mg/h/m(3) on days 3 through 13, or by the SC or oral route at 100 mg/kg/day on days 6 through 15 of gestation (Courtney et al, 1978).
    c) Captan produced CNS abnormalities in hamsters receiving an oral dose of 300 mg/kg 8 days after conception (RTECS, 1995). A dose of 1000 mg/kg produced exencephaly, fused ribs, and short or curved tails in hamsters (HSDB, 1995). Fused ribs were increased at 400 mg/kg/day in hamsters, but were within normal background (HSDB, 1995). Increased fetal malformations and death were produced in hamsters at dietary doses as high as 2500 mg/kg/day (Robens, 1970; Kennedy et al, 1968).
    d) Captan was teratogenic in rabbits and produced cleft lip and deformed limbs (HSDB, 1995). Increased fetal deaths but no malformations were seen in offspring of rabbits fed doses as high as 150 mg/kg/day during gestation (Fabro et al, 1966; (Kennedy et al, 1968) Anon, 1989).
    e) Captan was not teratogenic in dogs given up to 60 ppm (HSDB, 1995). It was not teratogenic in dogs at dietary doses up to 60 mg/kg/day (Kennedy et al, 1975b).
    f) Captan did not produce any treatment-related effects in a one-generation dietary study in rats, at doses up to 25 mg/kg/day (HSDB, 1995; Chevron Chemical Co, 1982a). It was not teratogenic in rats fed doses up to 2000 mg/kg/day (Fabro et al, 1966; Kennedy et al, 1978; Anon, 1989).
    g) Captan was teratogenic in monkeys at doses higher than 25 mg/kg/day (IRIS , 1995) Stauffer Chemical Co, 1968). It was not teratogenic at oral doses up to 75 mg/kg/day on days 21 through 34 of gestation (Vondruska et al, 1971).
    2) FOLPET has produced mixed results in animal studies:
    a) Folpet was not teratogenic in mice exposed by inhalation to 830 mg/kg/m(3) on days 6 to 13 of gestation, or SC and oral doses of 100 mg/kg/day on days 6 to 15 (Courtney et al, 1978).
    b) Folpet induced incomplete ossification in rats at a dose of 360 mg/kg/day (Chevron Chemical Co, 1983). A dose of 500 mg/kg was not teratogenic in rats (Kennedy et al, 1968).
    c) Folpet was teratogenic in rabbits, inducing hydrocephalus and skull bone defects at a minimum dose of 20 mg/kg/day (Chevron Chemical Co, 1984). Delayed ossification, with no evidence of hydrocephalus or other skull defects, was seen in rabbits at 40 mg/kg/day (Chevron Chemical Co, 1985b); delayed ossification is not considered a structural malformation. A dose of 75 mg/kg was not teratogenic in rabbits (Kennedy et al, 1968).
    d) Folpet was teratogenic in chicks when injected at 12 mg/kg into eggs after 4 days of incubation (Verschueren, 1983; Martin et al, 1978).
    e) Folpet was teratogenic in hamsters (Robens, 1970).
    3) CAPTAFOL has been shown to produce fetotoxicity and embryotoxicity in animal studies:
    a) Captafol was fetotoxic in rabbits at a minimum dose of 50 mg/kg/day; it produced minor skeletal abnormalities and resorptions (Chevron Chemical Co, 1984). No adverse reproductive effects were seen in rabbits at doses up to 150 mg/kg/day (Kennedy et al, 1968).
    b) Captafol was fetotoxic in rats at doses of at least 200 mg/kg/day (Chevron Chemical Co, 1983a; (Kennedy et al, 1968).
    3.20.3) EFFECTS IN PREGNANCY
    A) EMBRYOTOXICITY
    1) Fetotoxicity and/or embryotoxicity including fetal death, increased resorptions, and stillbirths have been seen in mice, rats, hamsters, or rabbits given relatively high doses (RTECS, 1995).
    2) Embryonic or fetal death was seen in rats when MALES received captan at an oral dose of 500 mg/kg five days prior to mating (RTECS, 1995).
    3) Effects on extra-embryonic structures (placenta, etc) were seen in female mice given captan at 900 mg/kg on days 9-14 of pregnancy (RTECS, 1995).
    4) Captan was fetotoxic in monkeys fed 12.5 mg/kg/day for 84 days (HSDB, 1995).
    5) In a 3-generation dietary study in rats, litter weights were decreased at doses of 25, 100, 250, and 500 mg/kg/day. No teratogenicity was seen (HSDB, 1995; Chevron Chemical Co, 1982).
    6) Captan was more toxic in pregnant than in non-pregnant rats; it also caused increased resorption of embryos (Alnot et al, 1974).
    B) STILLBIRTH
    1) DOGS - Stillbirths were seen in dogs given captan at 1890 mg/kg on days 1-63 of pregnancy (RTECS, 1995).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS133-06-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Captan
    b) Carcinogen Rating: 3
    1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    B) IARC Carcinogenicity Ratings for CAS133-07-3 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    C) IARC Carcinogenicity Ratings for CAS2425-06-1 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Captafol
    b) Carcinogen Rating: 2A
    1) The agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) The National Academy of Sciences has estimated a lifetime risk of 474 cases of cancer per million people from captan exposure, based on treatment of 100 per cent of applicable crops and a 70-year exposure period (Nazario SL, 1989).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) CAPTAN -
    a) In one dietary study, captan was carcinogenic for inducing duodenal tumors in mice given 8,000 or 16,000 ppm in the diet for 80 weeks. It was not carcinogenic in rats given 2525 or 6050 ppm under the same conditions (HSDB , 1995; NCI, 1977).
    b) Captan was strongly carcinogenic in rats and mice when given in the diet. Increased neoplasms were seen at all sites, especially endocrine organs in male and female rats, adrenal and pituitary gland tumors, tumors of the reproductive system, and mammary gland and ovarian tumors in female rats. Mice developed duodenal tumors (Reuber, 1989).
    c) Captan induced renal tubular adenomas and carcinomas in rats fed 100 and 250 mg/kg/day (HSDB , 1995).
    2) FOLPET -
    a) Folpet induced carcinomas and adenomas of the duodenum in mice fed at 5000 or 12,000 ppm for 112 to 113 weeks, and 3800 and 7600 ppm for 104 weeks, respectively (HSDB , 1995); Chevron Chemical Co, 1982; (Nyska et al, 1989).
    1) Development of tumors appears to be correlated with presence of duodenal obstructions in mice (Nyska et al, 1990).
    b) Folpet was not carcinogenic by gavage in mice at a dose of 215 mg/kg from days 7 to 28, followed by 603 ppm in the diet for the remainder of the 17-month exposure period (HSDB , 1995).
    c) No adverse effects were seen in rats fed folpet for 17 months, or in dogs given doses up to 1500 mg/kg/day for 17 months (HSDB , 1995).
    d) Folpet was not carcinogenic in rats fed up to 10,000 mg/kg in the diet for 1.4 years (HSDB , 1995).
    3) CAPTAFOL -
    a) Captafol was carcinogenic in mice, inducing tumors of the GI tract, lymphatic system, and vascular system. It induced tumors of the heart, spleen, forestomach, small intestine, and liver in mice (Ito et al, 1984). It also induced tumors of the kidney, mammary gland, and liver in rats (HSDB , 1995; Quest et al, 1993).
    b) Captafol induced renal adenomas in male and hepatocellular carcinomas in female rats given levels up to 1500 ppm in the diet for 104 weeks, followed by 8 weeks without captafol (Tamano et al, 1990).

Genotoxicity

    A) Captan, folpet, and captafol are genotoxic in a variety of short-term test systems. Captan is an alkylating agent.
    1) DNA inhibition and repair, mutagenicity, chromosome aberrations, sister chromatid exchanges, sex chromosome loss and nondisjunction, and dominant lethal effects have been seen.
    B) One study evaluated the effects of spraying with captan on hematological parameters, urine mutagenicity (on three Salmonella typhimurium strains), and DNA damage in mononuclear leukocytes in 19 fruit growers during the 1998 (n = 12) and/or the 2000 (n=17) spraying seasons. No significant DNA damage in mononuclear leukocytes was observed in farmers following a one-day spraying period with captan. However, farmers with an inefficient protective clothing had an increase in urine mutagenicity as assessed by the TA 102 tester strain (Lebailly et al, 2003).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No specific laboratory tests are necessary unless otherwise clinically indicated. General testing would be determined by the patient's overall clinical condition.
    4.1.2) SERUM/BLOOD
    A) OTHER
    1) No specific laboratory tests are necessary unless otherwise clinically indicated. General testing would be determined by the patient's overall clinical condition.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients rarely require admission due to this exposure. Reasons for admission might include significant electrolyte abnormalities or abnormalities that prevent them from accomplishing their activities of daily living (ADLs).
    6.3.1.2) HOME CRITERIA/ORAL
    A) Asymptomatic patients can be managed at home. Any patient with significant symptoms, such as altered mental status, weakness, abdominal pain, headache, chest pain, numbness, or syncope should be evaluated at a healthcare facility.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) If patients develop respiratory failure, hemodynamic instability, or any other symptoms not expected with this exposure, consult a toxicologist or regional poison center.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with significant signs and symptoms, such as altered mental status, weakness, abdominal pain, headache, chest pain, numbness, or syncope should be evaluated at a healthcare facility and observed until their condition stabilizes or improves.

Monitoring

    A) No specific laboratory tests are necessary unless otherwise clinically indicated. General testing would be determined by the patient's overall clinical condition.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ORAL EXPOSURE
    1) No oral decontamination is indicated.
    B) DERMAL EXPOSURE
    1) Wash exposed areas with soap and water. Lipophilic agents such as polyethylene glycol can also be used to decontaminate other lipophilic compounds.
    C) EYE EXPOSURE
    1) Irrigate exposed eyes with copious amounts of room temperature normal saline or water.
    6.5.2) PREVENTION OF ABSORPTION
    A) No oral decontamination is indicated.
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Patient with mild to moderate exposure are usually asymptomatic. Given the self-limiting and non-lethal effects of overdose, basic supportive care is all that is required. According to case reports, abnormal laboratory findings and symptoms abate with supportive care.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Patients with severe toxicity, through either dermal or oral exposure, usually have very mild to self-limiting symptoms such as headache, nausea, weakness, numbness of upper limbs, and substernal pain. Although some lab abnormalities such as leukocytosis and elevated CK have been reported, these are usually self-limiting. ECG T-wave inversions have been described but were not related to abnormal cardiac function.
    B) MONITORING OF PATIENT
    1) No specific laboratory tests are necessary unless otherwise clinically indicated. General testing would be determined by the patient's overall clinical condition.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

    A) HEMODIALYSIS
    1) There has never been a report of a patient needing enhanced elimination. Symptoms are self-limiting.

Abstracts

Case Reports

    A) PEDIATRIC
    1) A 17-year-old girl developed headache, nausea, weakness, numbness of upper limbs, and substernal pain 3 hours after the suicidal ingestion of 7.5 g of Captan 50 WP (a suspension of Captan in a ratio of 50% mixed with water). Her vital signs were temperature 36.7 degrees C, pulse 110-120 beats/minute, and BP 120-140/60-90 mmHg. Laboratory results showed elevated WBC 11,200/mm(3), creatine kinase 309 Units/L (normal up to 43 Units/L), and aspartate aminotransferase 67 Units/L (normal up to 29 Units/L). ECG revealed inversion of T waves in the III and aVF leads and echocardiogram was normal with an ejection fraction of 67%. Following supportive care, she recovered without further sequelae (Chodorowski & Anand, 2003).

Range Of Toxicity

Summary

    A) TOXICITY: Human toxicity is not established. Phthalimide fungicides appear to be of a low order of acute toxicity by usual routes of exposure. CAPTAN: A 17-year-old girl developed headache, nausea, weakness, numbness of upper limbs, and substernal pain following the intentional ingestion of 7.5 g of Captan 50 WP.

Minimum Lethal Exposure

    A) Captan and phthalan were less toxic than their parent compound, perchlormethylmercaptan, when given in single oral doses or in 10 oral doses at 5% or 10% of the LD50 dose (pp 75-78).

Maximum Tolerated Exposure

    A) SUMMARY
    1) There is little acute toxicity with these agents, except (possibly) with parenteral exposure (Fishbein, 1977) (NAS, 1977).
    B) CAPTAN
    1) CASE REPORT: A 17-year-old girl developed headache, nausea, weakness, numbness of upper limbs, and substernal pain 3 hours after an intentional ingestion of 7.5 g of Captan 50 WP (a suspension of Captan in a ratio of 50% mixed with water). Her vital signs were temperature 36.7 degrees C, pulse 110 to 120/minute, and BP 120-140/60-90 mmHg. Laboratory results showed elevated WBC 11,200/mm(3), creatine kinase 309 Units/L (normal up to 43 Units/L), and aspartate aminotransferase 67 Units/L (normal up to 29 Units/L). ECG revealed inversion of T waves in the III and aVF leads and echocardiogram was normal with an ejection fraction of 67%. Following supportive care, she recovered without further sequelae (Chodorowski & Anand, 2003).
    C) ANIMAL DATA
    1) The no-effect level for rats in 2-year feeding trials was 1000 mg/kg in the diet (HSDB, 1995).

Workplace Standards

    A) ACGIH TLV Values for CAS133-06-2 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Captan
    a) TLV:
    1) TLV-TWA: 5 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: I, SEN
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    b) I: Inhalable fraction; see Appendix C, paragraph A (of TLV booklet).
    c) SEN: The designation SEN refers to the potential for an agent to produce sensitization, as confirmed by human or animal data. The notation does not imply that this is the critical effect or that this is the sole basis for the TLV. Although, for those TLVs that are based on sensitization, the TLV is meant to protect workers from induction of this effect, but cannot protect workers who have already become sensitized. The notation should be used to assist in identifying sensitization hazards and reducing respiratory, dermal, and conjunctival exposures to sensitizing agents in the workplace. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): Skin irr
    d) Molecular Weight: 300.6
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) ACGIH TLV Values for CAS133-07-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    C) ACGIH TLV Values for CAS2425-06-1 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Captafol
    a) TLV:
    1) TLV-TWA: 0.1 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: Skin
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): Skin irr
    d) Molecular Weight: 349.06
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    D) NIOSH REL and IDLH Values for CAS133-06-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Captan
    2) REL:
    a) TWA: 5 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix A
    3) IDLH: Not Listed

    E) NIOSH REL and IDLH Values for CAS133-07-3 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    F) NIOSH REL and IDLH Values for CAS2425-06-1 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Captafol
    2) REL:
    a) TWA: 0.1 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    e) Skin Designation: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s): See Appendix A
    3) IDLH: Not Listed

    G) Carcinogenicity Ratings for CAS133-06-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Captan
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Captan
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 3 ; Listed as: Captan
    a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Captan
    a) Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    H) Carcinogenicity Ratings for CAS133-07-3 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: Folpet
    a) B2 : Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals.
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    I) Carcinogenicity Ratings for CAS2425-06-1 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Captafol
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 2A ; Listed as: Captafol
    a) 2A : The agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Captafol
    a) Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    J) OSHA PEL Values for CAS133-06-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    K) OSHA PEL Values for CAS133-07-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    L) OSHA PEL Values for CAS2425-06-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Pharmacology Toxicology

Toxicologic Mechanism

    A) CAPTAN -
    1) Captan inhibited RNA polymerase in bovine hepatocytes; inhibition was prevented by dithiothreitol (Vinocour & Lewis, 1985). Captan also inhibited cytochrome P450 from rat liver microsomes; reduced glutathione prevented inhibition (Dalvi & Ashley, 1979). These results imply that captan reacts with sulfhydryl groups.
    2) Captan is an alkylating agent (HSDB, 1995; ACGIH, 1991; (Bridges et al, 1972).
    B) FOLPET -
    1) Folpet, in chronic studies, has produced reduced hemoglobin, leukopenia, reduced prothrombin time, and reduced hippuric acid excretion in experimental animals (Fishbein, 1977).
    2) Folpet reacts with thiols, such as cysteine and glutathione (HSDB, 1995).
    C) CAPTAFOL -
    1) Captafol has caused contact dermatitis and conjunctivitis, perhaps through a hypersensitivity mechanism (Peoples, 1978).
    2) Captafol was more potent than either captan or folpet in inhibiting cytochrome P450 in rat liver after intraperitoneal injection (Dalvi & Mutinga, 1990).

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