Captafol
| 1. NAME |
| 1.1 Substance |
| 1.2 Group |
| 1.3 Synonyms |
| 1.4 Identification numbers |
| 1.4.1 CAS number |
| 1.4.2 Other numbers |
| 1.5 Main brand names, main trade names |
| 1.6 Main manufacturers, main importers |
| 2. SUMMARY |
| 2.1 Main risks and target organs |
| 2.2 Summary of clinical effects |
| 2.3 Diagnosis |
| 2.4 First-aid measures and management principles |
| 3. PHYSICO-CHEMICAL PROPERTIES |
| 3.1 Origin of the substance |
| 3.2 Chemical structure |
| 3.3 Physical properties |
| 3.3.1 Colour |
| 3.3.2 State/form |
| 3.3.3 Description |
| 3.4 Hazardous characteristics |
| 4. USES |
| 4.1 Uses |
| 4.1.1 Uses |
| 4.1.2 Description |
| 4.2 High risk circumstance of poisoning |
| 4.3 Occupationally exposed populations |
| 5. ROUTES OF EXPOSURE |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Other |
| 6. KINETICS |
| 6.1 Absorption by route of exposure |
| 6.2 Distribution by route of exposure |
| 6.3 Biological half-life by route of exposure |
| 6.4 Metabolism |
| 6.5 Elimination by route of exposure |
| 7. TOXICOLOGY |
| 7.1 Mode of Action |
| 7.2 Toxicity |
| 7.2.1 Human data |
| 7.2.1.1 Adults |
| 7.2.1.2 Children |
| 7.2.2 Relevant animal data |
| 7.2.3 Relevant in vitro data |
| 7.2.4 Workplace standards |
| 7.2.5 Acceptable daily intake (ADI) |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS |
| 8.1 Material sampling plan |
| 8.1.1 Sampling and specimen collection |
| 8.1.1.1 Toxicological analyses |
| 8.1.1.2 Biomedical analyses |
| 8.1.1.3 Arterial blood gas analysis |
| 8.1.1.4 Haematological analyses |
| 8.1.1.5 Other (unspecified) analyses |
| 8.1.2 Storage of laboratory samples and specimens |
| 8.1.2.1 Toxicological analyses |
| 8.1.2.2 Biomedical analyses |
| 8.1.2.3 Arterial blood gas analysis |
| 8.1.2.4 Haematological analyses |
| 8.1.2.5 Other (unspecified) analyses |
| 8.1.3 Transport of laboratory samples and specimens |
| 8.1.3.1 Toxicological analyses |
| 8.1.3.2 Biomedical analyses |
| 8.1.3.3 Arterial blood gas analysis |
| 8.1.3.4 Haematological analyses |
| 8.1.3.5 Other (unspecified) analyses |
| 8.2 Toxicological Analyses and Their Interpretation |
| 8.2.1 Tests on toxic ingredient(s) of material |
| 8.2.1.1 Simple Qualitative Test(s) |
| 8.2.1.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.1.3 Simple Quantitative Method(s) |
| 8.2.1.4 Advanced Quantitative Method(s) |
| 8.2.2 Tests for biological specimens |
| 8.2.2.1 Simple Qualitative Test(s) |
| 8.2.2.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.2.3 Simple Quantitative Method(s) |
| 8.2.2.4 Advanced Quantitative Method(s) |
| 8.2.2.5 Other Dedicated Method(s) |
| 8.2.3 Interpretation of toxicological analyses |
| 8.3 Biomedical investigations and their interpretation |
| 8.3.1 Biochemical analysis |
| 8.3.1.1 Blood, plasma or serum |
| 8.3.1.2 Urine |
| 8.3.1.3 Other fluids |
| 8.3.2 Arterial blood gas analyses |
| 8.3.3 Haematological analyses |
| 8.3.4 Interpretation of biomedical investigations |
| 8.4 Other biomedical (diagnostic) investigations and their interpretation |
| 8.5 Overall Interpretation of all toxicological analyses and toxicological investigations |
| 8.6 References |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Systematic description of clinical effects |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurological |
| 9.4.3.1 Central Nervous System (CNS) |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 Others |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ears, nose, throat: local effects |
| 9.4.10 Haematological |
| 9.4.11 Immunological |
| 9.4.12 Metabolic |
| 9.4.12.1 Acid-base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Others |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks |
| 9.5 Other |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Life supportive procedures and symptomatic/specific treatment |
| 10.3 Decontamination |
| 10.4 Enhanced Elimination |
| 10.5 Antidote treatment |
| 10.5.1 Adults |
| 10.5.2 Children |
| 10.6 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 12. ADDITIONAL INFORMATION |
| 12.1 Specific preventive measures |
| 12.2 Other |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
CAPTAFOL
International Programme on Chemical Safety
Poisons Information Monograph 097
Chemical
1. NAME
1.1 Substance
Captafol
1.2 Group
Chloroalkyl thio fungicide
1.3 Synonyms
Difolatan;
N-(1,1,2,2-tetrachloroethylthio)cyclohex-4-ene-1,2-
dicarboximide (UPAC);
1.4 Identification numbers
1.4.1 CAS number
2425-06-1
1.4.2 Other numbers
formula: C10H9Cl4NO2S
RTECS NIOSH/GW4900000
1.5 Main brand names, main trade names
Alfloc 7020
Alfloc 7046
Captaspor
Captofol
CS 5623
Difosan
Haipen 50
Kenofol
Folcid
Nalco 7046
Ortho-5865 (First introduced by Chevron as Code no.)
Ortho Difolatan 80W
Ortho Difolatan 4 Flowable
Proxel EF
Sanspor
Sanseal
Sulfonimide
Sulfeimide
A number of formulations are commercially available which
include captafol together with other pesticides.
1.6 Main manufacturers, main importers
CHEVRON
SANDOZ
ICI Plant protection division
Atlas Interlates Ltd
Keno Gard VT AB
2. SUMMARY
2.1 Main risks and target organs
The acute oral toxicity is low. Skin, eyes and
respiratory tract are targets for local irritation and
sensitization. Animal studies have demonstrated a
carcinogenic potential.
2.2 Summary of clinical effects
Following ingestion of large quantities of captafol,
vomiting and diarrhoea may occur. Both allergic and contact
dermatitis have been reported. Respiratory sensitization and
conjunctivitis are also known to occur. Systemic disorders
including hypertension, and hepatic and renal disturbances,
usually paralleling the degree of dermatitis, have been
reported following captafol exposure.
2.3 Diagnosis
Wheezing due to bronchospasm, contact dermatitis and
vomiting and diarrhoea are the features of exposure to
captafol by inhalation, skin contact and ingestion
respectively. Chronic exposure can cause hypertension,
depression of liver function, dermatitis, conjunctivitis and
anaemia.
Although a sensitive assay is available for captafol, the
usefulness with respect to the clinical management of
exposures to captafol seems remote in view of its low
toxicity.
2.4 First-aid measures and management principles
In the event of exposure to captafol, contaminated
clothing and contact lenses should be removed to prevent
further absorption.In the case of skin contact, the affected
area should be washed carefully with soap and water. Wash
eyes for 10-15 minutes with clean running water. First aid
personnel should wear rubber or plastic gloves and avoid
contamination.
Ingestion of small amounts of captafol do not constitute a
significant risk, and may be managed by dilution with
water.
The management of large quantities of ingested captafol
should be primarily directed towards decontamination and
supportive care, as there is no specific antidote. The use
of Ipecac Syrup and activated charcoal are indicated in the
event of ingestion.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Captafol, a synthetic chloroalkyl thio fungicide, was
introduced by the Chevron Chemical Company in 1961 as Code
Number "Ortho-5865" under the trade name "Difolatan".
Captafol is formed by reacting the imide, produced by the
action of ammonia on tetrahydrophthalic anhydride, with
1,1,2,2-tetrachloroethyl sulfenyl chloride (Merck,
1983).
3.2 Chemical structure
The empirical formula for captafol is C10H9C14NO2S with
a molecular weight of 349.09.
3.3 Physical properties
3.3.1 Colour
3.3.2 State/form
3.3.3 Description
Melting point 160 to 161°C (slowly decomposes).
Vapour pressure negligible at room temperature.
Solubility practically insoluble in water (1.4 mg/L)
slightly soluble most organic solvents.
Captafol is a white crystalline solid. The technical
trade is a light tan powder with a characteristic
odour. It is stable except under strongly alkaline
conditions. Commercially, captafol is available as
dusts, wettable powders and flowable
formulations.
3.4 Hazardous characteristics
Although captafol will not burn it is likely that under
fire conditions toxic decomposition products such as sulphur
oxides, phosgene, chlorine, nitrogen oxides will be produced,
and these may be harmful by inhalation and dermal
contamination.
Although the pure substance is practically insoluble in
water, the formulated product may pose an environmental risk
if released into an aquatic environment. The LC50(96-h) is
for:
rainbow trout 0.5 mg/L
goldfish 3.0 mg/L
bluegill 0.15 mg/L (Worthing, 1987)
Captafol applied at 50 and 100 ppm persisted in four soil
types up to 60 days (Venkatramesh, 1988). Persistent on
plant surfaces for 7-10 days.
Structurally captafol is chemically similar to captan, for
which alkaline treatment leads to the formation of nontoxic
degradation products and is considered to be an
environmentally acceptable disposal method (Dillon,
1981). Since captafol is also degraded by strong alkali, small
spillages and residues could be treated with alkali before
burial in an approved landfill area. Personnel involved in
captafol disposal should be provided with protective
equipment which should minimize dermal, ocular and
respiratory exposure. Empty containers should be thoroughly
drained before disposal.
4. USES
4.1 Uses
4.1.1 Uses
4.1.2 Description
Captafol is a protective non-systemic fungicide
widely used to control foliage and fruit diseases of
tomatoes, coffee berry disease, potato blight, tapping
panel disease of rubber and many other diseases. It
is also used in the lumber and timber industries to
reduce losses from wood rot fungi in logs and wood
products (Worthing, 1987).
4.2 High risk circumstance of poisoning
Accidental among adult farm or timber workers and
secondary exposure to their children.
4.3 Occupationally exposed populations
Workers involved in formulating and dispensing
pesticides.
Agricultural spray workers.
Crop harvesters during disease vector control periods.
Timber workers.
5. ROUTES OF EXPOSURE
5.1 Oral
Although no literature accounts were available at the
time of preparation of this monograph, the ingestion of
captafol either accidentally or intentionally is
possible.
5.2 Inhalation
Inhalation of captafol as spray mists or powders have
been reported in an occupational context. A TLV has been
established by ACGIH (see Section 7.2.4).
5.3 Dermal
Dermal absorption is appreciable but has not been
experimentally determined in humans. Studies in rabbits have
shown a high dermal LD50 (see Section 7.2.2).
5.4 Eye
No data available.
5.5 Parenteral
No data available.
5.6 Other
No date available
6. KINETICS
6.1 Absorption by route of exposure
No data available.
6.2 Distribution by route of exposure
No data available.
6.3 Biological half-life by route of exposure
No data available.
6.4 Metabolism
Animal feeding studies have shown that most of the
captafol is excreted unchanged, the major metabolite being
tetrahydrophthalimide (see Section 6.5).
6.5 Elimination by route of exposure
When rats, dogs, and monkeys were fed 14C-captafol,
almost 80% was excreted with 36 hours, mainly in the urine
and none via expired carbon dioxide. Most of the small amount
in the faeces was unmetabolized and probably unabsorbed. No
unchanged captafol was detected in the blood tissues or
urine.
The major single metabolite, tetrahydrophthalimide, was
detected in blood, faeces, and urine, but most of the
activity in the blood and urine was in the form of more
soluble metabolites. No captafol epoxide was detectable
(Hayes, 1982).
7. TOXICOLOGY
7.1 Mode of Action
No data available.
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
No data available.
7.2.1.2 Children
No data available.
7.2.2 Relevant animal data
Rat oral LD50 varies from 2500 to 6200 mg/kg,
depending on whether it is presented as an oil
solution or aqueous suspension.
Rabbit dermal LD50 is > 15400 mg/kg (80% wettable
powder).
7.2.3 Relevant in vitro data
No data available.
7.2.4 Workplace standards
TLV 0.1 mg/m3 (ACGIH, 1986).
7.2.5 Acceptable daily intake (ADI)
A 14-day withholding period has been
recommended for fruit and vegetables that have been
treated with captafol (New Zealand Pesticide Board,
1983).
7.3 Carcinogenicity
In a dietary study of captafol fed to rats (250 to 5000
ppm) the incidence of tumours was not increased at any dosage
(Hayes, 1982).
Rats initially given a single dose (200 mg/kg) of
diethylinitrosamine i.p. were fed two weeks later with a diet
containing 3000 ppm of captafol for six weeks, and then
killed. Carcinogenic potential was scored by comparing the
number and area per cm2 of induced glutathione S-transferase
placental form positive foci in the liver with those of a
corresponding control group given diethylinitrosamine alone.
Captafol showed a significant increase in the value of
foci.
The authors of this study commented that this positive result
for captafol, which they had shown previously to induce liver
tumours in mice but not in rats (Ito et al., 1984), was
further evidence for the carcinogenic potential of captafol
(Ito et al., 1988).
7.4 Teratogenicity
Several teratology studies have been conducted with
captafol in many mammalian species, including non-human
primates. In most studies, where captafol was administered
throughout organogenesis, low to no teratogenic potential was
demonstrated. However, results of studies with rabbits were
contradictory. There have been two studies with no malformed
foetuses and one in which 9 of 75 foetuses were malformed.
Further investigation (371 foetuses) did not produce a single
increase in the number of abnormalities.
In a study with golden hamsters, effects of single
administration of captafol was compared with effects of
repeated administration throughout organogenesis. At the
highest single doses maternal mortality increased and some
abnormal foetuses were reduced. At the lowest single doses
and all multiple doses there were no indications of
teratogenic activity (Clayton & Clayton, 1981).
7.5 Mutagenicity
Many authors have evaluated the mutagenicity of captafol
and other related pesticides using the Salmonella/mammalian
microsome with strains containing both A-T and G-C base
pairs. The S9 mix decreased the mutagenic activity of
captafol. Mutagenic activity varied, depending upon the
strain tested (Barrueco & de la Pena, 1988).
In studies to test for the ability to induce chromosomal
mutations captafol was not mutagenic, except in a single
dominant lethal test which has been repeated by others
several times with negative findings. In other tests (i.e.,
sister chromatid exchange and testicular DNA synthesis)
captafol was negative (Clayton & Clayton, 1981).
7.6 Interactions
Captafol has strong sensitization reactions in
combination with daconil, kelthane, and bordeaux mixture
(Matsushita & Aoyama, 1980).
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
8.3.1.2 Urine
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
8.5 Overall Interpretation of all toxicological analyses and
toxicological investigations
Sample collection
Blood should be drawn in a heparinized tube and the red blood
cells and plasma separated by centrifuging and then frozen if
they must be kept for analysis.
Samples from gastric lavage washing should be frozen and
stored if subsequent analysis is desired. If the formulation
of captafol is available, it should also be stored for
possible subsequent analysis.
Biomedical analysis
Liver and renal function tests are indicated in the case of
large ingestion of captafol.
Toxicological analysis
Although a sensitive assay is available for captafol the
usefulness with respect to the clinical management of
exposures to captafol seems remote in view of its low
toxicity.
An HPLC analysis has been developed for determining technical
captafol and captafol in formulations. Captafol in ethyl
acetate can also be determined using GLC with detection
limits of 0.01 ppm (electron capture detector) and 0.03 ppm
(flame photometric detector). Recoveries were 78-95%
(Carlstrom, 1978).
Other investigations
No data available.
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
The acute oral toxicity is low (LD50 2500
mg/kg), probably due to rapid hydrolysis in the gut
(Gosselin et al., 1984). Since dogs that received
captafol 300 or 100 mg/kg/day suffered frequent
vomiting and diarrhoea (Hayes, 1982), it is not
unlikely that similar symptoms would occur in humans
following the ingestion of large quantities of
captafol.
9.1.2 Inhalation
Respiratory sensitization has been reported
(see Section 9.4.2).
9.1.3 Skin exposure
Both allergic and contact dermatitis have been
reported (Hayes, 1982). Arimatsu (1970) reported that
farmers using captafol experienced numerous incidences
of skin irritation in a survey conducted between
1966-1969 in Kumamoto Prefecture (Japan). These
surveys revealed 442 cases (31.4%) of captafol-related
skin irritations in 1966, 572 cases (40.5%) in 1967,
442 cases (31.1%) in 1968, and 332 cases (24.6%) in
1969. Farmers affected with acute contact dermatitis
were engaged in spraying and other related operations.
Eruptions appeared as erythematous dermatitis of the
eyelids with local oedema,and eruptions were often of
the phototoxic type. Some affected individuals
suffered from photoallergic dermatitis. Most eruptions
disappeared about one week after exposure.
Similarly, Matsushita et al. (1979) have reported
rashes caused by captafol from other localities in
Japan. Twenty-three percent of 133 New Zealand timber
workers who were exposed to captafol, gave histories
suggestive of occupationally-induced dermatitis.
Although allergic dermatitis can occur, irritant
dermatitis is far more common (Stoke, 1979).
9.1.4 Eye contact
Conjunctivitis and periorbital oedema has been
reported following occupational exposure to captafol
(Hayes, 1982).
9.1.5 Parenteral exposure
No data available.
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
In a dietary study of captafol fed to rats (250
to 5000 ppm) liver and kidney abnormalities were
observed at 1500 ppm and above (Hayes, 1982).
9.2.2 Inhalation
Respiratory sensitization has been reported
(see Section 9.4.2).
9.2.3 Skin exposure
Both allergic and contact dermatitis have been
reported (Hayes, 1982). Patch tests to captafol were
positive in two laboratory chemists who had previously
worked with the chemical. In one case the chemist had
not handled captafol for several years but had
exhibited skin irritation towards the end of that
period. In the second case there was no previous
evidence of sensitivity but when contact had resumed
after an interval of several months the chemist
developed a rash on the neck and cheeks (Brown, 1984)
(see Section 11.1).
9.2.4 Eye contact
Conjunctivitis and periorbital oedema has been
reported following occupational exposure to captafol
(Hayes, 1982).
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
No human fatalities have been reported. The toxicity is
low.
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Hypertension has been reported to occur,
especially in individuals who exhibited marked oedema
following dermal exposure to captafol (Hayes, 1982).
9.4.2 Respiratory
9.4.2 Respiratory
Wheezing can occur after exposure (Royce et al,
1993). The sudden appearance of wheezing of a welder
was attributed to contact with bags of captafol in the
course of maintenance work for a company that
distributed captafol. Subsequent exposures lead to
re-occurrences. Patch tests were positive
(Groundwater, 1977).
9.4.3 Neurological
9.4.3.1 Central Nervous System (CNS)
No data available.
9.4.3.2 Peripheral nervous system
No data available.
9.4.3.3 Autonomic nervous system
No data available.
9.4.3.4 Skeletal and smooth muscle
No data available.
9.4.4 Gastrointestinal
Since dogs that received captafol 300 or 100
mg/kg/day suffered frequent vomiting and diarrhoea
(Hayes, 1982), it is not unlikely that similar
symptoms would occur in humans following the ingestion
of large quantities of captafol.
9.4.5 Hepatic
Depression of liver function usually
paralleling the degree of dermatitis has been reported
following captafol exposure (Hayes, 1982).
9.4.6 Urinary
9.4.6.1 Renal
Protein and urobilinogen in the
urine have been reported, usually paralleling
the degree of dermatitis following captafol
exposure (Hayes, 1982).
9.4.6.2 Others
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatological
Both allergic and contact dermatitis have been
reported (Hayes, 1982) (see Sections 9.1.3 and
9.2.3).
9.4.9 Eye, ears, nose, throat: local effects
Conjunctivitis and stomatitis have been
reported (Verhagen, 1974).
9.4.10 Haematological
Anaemia has been reported following captafol
exposure (Hayes, 1982).
9.4.11 Immunological
No data available.
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
No data available.
9.4.12.2 Fluid and electrolyte disturbances
No data available.
9.4.12.3 Others
No data available.
9.4.13 Allergic reactions
Both allergic and contact dermatitis have been
reported (Hayes, 1982) (see Sections 9.1.3 and
9.2.3).
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks
Pregnancy - No data available.
Breast feeding - No data available.
Enzyme deficiencies - Depression of cholinesterase
activity has been reported (Hayes, 1982).
9.5 Other
No data available.
9.6 Summary
10. MANAGEMENT
10.1 General principles
The management of captafol poisoning should be
primarily directed towards decontamination and supportive
care, as there is no specific antidote. Ipecac Syrup or
gastric lavage and subsequent activated charcoal and a
cathartic are indicated in the event of ingestion.
10.2 Life supportive procedures and symptomatic/specific treatment
Following large ingestion of captafol, there are no
specific procedures recommended other than the basic
techniques for maintaining airways, breathing and
circulation.
10.3 Decontamination
Wash contaminated skin with soap and water.
Flush contaminated eyes (remove contact lenses if worn) with
copious amounts of fresh water for 10-15 minutes).
Ingestion of small amounts (less than 10 mg/kg bodyweight)
occurring less than one hour before treatment are probably
best managed by simpe dilution with water.
Ingestion of large amounts (more than 10 mg/kg bodyweight)
occurring less than one hour before treatment, are probably
best treated by:
* Syrup of Ipecac, followed by 1-2 glasses of water
Adults and children over 12 years: 30 ml Children
under 12 years: 15 ml.
* Activated charcoal in water Adults and children over
12 years: 50 g in 250 ml water Children under 12
years: 30 g in 100 ml water.
* Ingestion occurring more than one hour before
treatment are probably best treated only by activated
charcoal (30-50 g).
Because manifestations of toxicity may occasionally occur in
peculiarly predisposed individuals, maintain contact with
victim for at least 72 hours so that unsuspected adverse
effects can be treated promptly (Morgan, 1982).
10.4 Enhanced Elimination
No specific elimination procedures have been
established.
10.5 Antidote treatment
10.5.1 Adults
There is no specific antidote for captafol.
10.5.2 Children
There is no specific antidote for captafol.
10.6 Management discussion
There is an absence of clinical data in the human
overdose situation. Research into the allergic response
mechanism is required.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Case 1. Adult male, research chemist, occupational
exposure contact sensitivity.
A 37-year-old male research chemist who, after several years
away from contact with captafol, once again became interested
in research on certain aspects. He had, in his first period
of work with the substance, noticed towards the end that
occasional contact resulted in skin irritation and a mild
rash on the hands with irritation of the periorbital and
nasal skin. Before embarking on a further series of
experiments, it was decided that his apparent sensitivity
should be investigated. He was asthmatic but had not
experienced any exacerbation with captafol. Prick testing
confirmed his atopic status. Patch testing to captafol was
positive. Further occupational exposure to captafol was
avoided (Brown, 1984).
Case 2. A 34-year-old chemical manufacturing worker had new
onset of work-related asthma after several years of exposure
to captafol. On specific bronchial challenge testing, he
demonstrated a marked and persistent fall in FEV1. Cessation
of exposure resulted in improved symptoms and pulmonary
function. The delay in symptoms after several years of
work-place exposure and the dual reaction demonstrated on
specific bronchial challenge testing suggest sensitization to
some component of technical grade captafol, but an IgE
response was not detected (Royce et al, 1993).
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
It is essential that persons intending to use captafol
are provided with adequate health precautions and other
safety instructions prior to usage. This information should
be provided by the manufacturer in the form of either an
information leaflet or on a label attached to the captafol
container.
Protective clothing is important. Captafol may cause dermal
irritation and sensitization. The risk of this is greatest in
hot weather when the user is sweating. Protective measures
may include wearing a long-sleeved shirt, long trousers or
overalls, and a hat of some sort. Respiratory protection
should be considered. The label should give these details.
Clothing worn during spraying should be washed daily after
use. Contaminated clothing should be washed separately from
the general wash to avoid cross-contamination. When working
with liquids, there is often a danger of a splash in the
eyes. This may damage the eyes. Simple goggles or a face
shield will protect against this. Eye protection is most
important if wearing contact lenses because captafol may get
in behind the lenses. They must be removed before the eyes
are washed, and in the time this takes, serious damage can
occur.
Greater precautions are necessary when mixing the
concentrated material than when spraying. Measurements should
be accurate and spillages should be cleaned up promptly. Mix
the chemical carefully using a stick or paddle. Ensure there
is minimal skin exposure by the use of gloves. if any
concentrate is spilled on the skin, wash it off as soon as
possible.
The hazards of spraying increase dramatically on windy days
as there is an increased risk of inhaling spray drift or
contaminating the skin. Also, the risk of drift on to other
properties or crops is increased.
Always wash hands before eating, drinking or smoking. After
spraying, shower and change clothing.
By preference, captafol should be stored in a locked shed,
safely out of reach of children and animals. Captafol should
also be kept away from work areas and separate from other
stored materials such as animal foods. Always leave captafol
in its original containers, or if it must be transferred to
another container ensure that this is one not normally used
for food or drink. This secondary container should be
well-labelled and of a variety that is not likely to
leak.
Empty containers must be disposed of carefully so as to
ensure that rivers, streams, and other water sources are not
polluted, and that unsuspecting people or animals are not
exposed to residues of concentrate. Crushing or burning,
followed by burial, is generally the best method. Workers
involved in harvesting crops must adhere carefully to
re-entry standards which have been set in order to prevent
toxicity from captafol.
First Aid Sheet
Poisoning from captafol may occur after it is absorbed
following:
- ingestion
- contact with the skin
- contact with the eyes
- inhalation.
Signs and symptoms
- Ingestion may cause vomiting and diarrhoea.
- Skin contact and inhalation may result in local
irritation and also sensitization.
- Eye contact may produce conjunctivitis.
Decontamination
- It is important that captafol is removed as quickly as
possible. Contaminated clothing and contact lenses
should be removed. Avoid contact of captafol with skin
and eyes; first-aid personnel should wear rubber or
plastic gloves and avoid contamination.
Treatment - general
- Never give fluids or induce vomiting if the patient is
unconscious or fitting.
- The patient must be watched constantly.
- It is important to keep the airways open and to
prevent inhaling the vomit if nausea and vomiting is a
problem.
- Give artificial respiration if the patient is not
breathing.
Treatment - ingestion
- Give 1-2 cups of cold water. Vomiting may be induced
if advised by medical personnel. Obtain medical
attention.
Treatment - skin
- Remove all contaminated clothing immediately.
- Wash affected area carefully with soap and rinse with
copious amounts of water. Obtain medical
attention.
Treatment - eyes
- Make sure any contact lenses are removed.
- Flush with water for 10-15 minutes. Obtain medical
attention.
Treatment - inhalation
- Remove the patient from the area of exposure.
- Be careful to avoid any contact with captafol.
- Protect skin and eyes. Give oxygen if available.
Obtain medical attention.
12.2 Other
No data available.
13. REFERENCES
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Barrueco C & de la Pena E (1988) Mutagenic evaluation of the
pesticides captan, folpet, captafol, cichlofluanid and related
compounds with the mutants TA102 and TA104 of Salmonella
typhimurium. Mutagenesis, 3(6): 467-480.
Brown R (1984) Contact sensitivity to difolatan (captafol) Contact
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Carlstrom AA (1978) Captafol. Anal. Methods Pestic. Plant Growth
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588.
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Stoke, JCJ (1979) Captafol dermatitis in the timber industry.
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Venkatramesh M & Agnihothrudu V (1988) Persistence of captafol in
soils with and without amendments and its effects on soil
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES),
COMPLETE ADDRESS(ES)
Authors: Dr Wayne A. Temple
National Poisons and Hazardous
Chemical Information Centre
Dr Nerida A. Smith
Department of Pharmacy
University of Otago Medical School
P.O. Box 913
Dunedin
New Zealand
Date: 16 October 1989
Peer Review: London, United Kingdom, March 1990.
Strasbourg, France, April 1990
Update: Dr R. Fernando
Date: June 1993