DICLHORVOS

DICHLORVOS
This substance was considered by a previous Working Group in 1978 (IARC, 1979a).
Since that time, new data have become available, and these have been incorporated into the
monograph and taken into consideration in the present evaluation.
1. Exposure Data
1.1 Chemical and physical data
1.1.1 Synonyms, structural and molecular data
Chem. Abstr. Serv Reg. No.: 62-73-7
Replaced CAS Reg. Nos.: 8023-22-1; 8072-21-7; 8072-39-7; 8076-16-2; 11095-17-3;
11096-21-2; 11111-31-2; 11126-72-0; 12772-40-6; 55819-32-4; 62139-95-1; 62655-59-8;
95828-55-0; 116788-91-1
Chem. Abstr. Name: Phosphoric acid, 2,2-dichloroethenyl dimethyl ester
¡UPAC Systematic Name: 2,2-Dichlorovinyl dimethyl phosphate
Synonyms: 2,2-Dichloroethenol, dimethyl phosphate; dimethyl dichlorovinyl phosphate;
dimethyl 2,2-dichloroethenyl phosphate; dimethyl 2,2-dichlorovinyl phosphate;
O,O-dimethyl 2,2-dichlorovinyl phosphate; 2,2-dichloroethenyl dimethyl phosphate;
phosphoric acid, 2,2-dichlorovinyl dimethyl ester
o
Il
H3C - 0 - P - 0 - CH = CCI2
1
o
1
CH3
C4H7Cl204P MoL. wt: 221.0
1.1.2 Chemical and physical properties
From AMVAC Chemical Corp. (1986), otherwse specified
(a) Description: Clear, colourless to pale yellow, almost odourless liquid
(b) Boiling-point: 117°C at 10 mm Hg (1.33 kPa)
(c) Melting-point: .c -60°C (AMVAC Chemical Corp., 1990)
(d) Density: 1.422 at 25°C/4°C
(e) Spectroscopy data: Infrared (prism (7721); grating (4455 IP)) spectroscopy data have
been reported (Sadtler Research Laboratories, 1980).
- 267 -
268 IARC MONOGRAPHS VOLUME 53
if Solubility: Completely miscible with aromatic hydrocarbons, chlorinated hydro-

carbons, alcohols, ketones and esters; slightly soluble in water (approx. 1 %) and
glycerine (approx. 0.5%); insoluble in kerosene and aliphatic hydrocarbons
(g) Volatility: Vapour pressure, 0.012 mm Hg (1.6 x 10-3 kPa) at 20°C
(h) Stability: Hydrolysed by water and readily decomposed by strong acids and bases;
breaks down on standing in the presence of traces of moisture, with the formation of
acidic products that catalyse further decomposition; corrosive to black iron and
Id steel (WHO, 1989)
mi
(i) Octanollwater partition coeffcient (P): log P, 1.47 (WHO, 1989)

(j) Halftime in water: 301 min at pH 8; 462 min at pH 7; 2100 min at pH 6; 4620 min at
pH 5.4 (Latif et al., 1984)
(k) Conversion factor for airborne concentrations!: mg/m3 = 9.04 x ppm
1. 1.3 Trade names, technical products and impurities
Sorne examples of trade names are: Atgard; Bibesol; Brevinyl; Canogard; Chlorvnphos;
DDVP; Dedevap; Des; Dichlofos; Dichlorman; Dichlorovos; Divipan; ENT 20738;
Equigard; Equigel; Estrosel; Estrosol; Fecama; Fekama; Insectigas D; Mopari; Nefrafos;
Nerkol; Nogos; Novotox; Nuan; Nuvan; OKO; OMS 14; Panaplate; Phosvit; Prima U; SD
1750; Szklarniak; TAP 9VP; Task; Unifos; Unitox; Vapona; Vapona Insecticide; Vaponite;
Vinylofos; Vinylophos; Winylophos
WHO (1985, 1989) specifications for technical-grade dichlorvos for public health use
require a minimum purity of 97%; the value was previously 93% (WHO, 1967).
Dichlorvos is available in the USA as a technical-grade product with a minimal purity of
93 or 96% (MIVAC Chemical Corp., 1986, 1990). ln the past, 2-4% epichlorohydrin (see
IARC, 1987a) was added to stabilize the technical-grade product; other stabilizers may now
be used in sorne products, but improved technology and purity has largely eliminated the
need for them (WHO, 1989). Analysis of a sample of commercial-grade dichlorvos
(produced in about 1970) showed the following constituents (%): dichlorvos, 95-97; dipterex
(trichlorfon; O,O-dimethyl 2,2,2-trichloro-l-hydroxyethylphosphonate) (see IARC, 1983a,
1987b), 1.5-3; O,O-dimethyl 2-chlorovinyl phosphate, 0.4-0.7; O,O-dimethyl methyl-
phosphate, trace-O. 1; O,O,O-trimethyl phosphate, 0.3-0.8; and chloral (trichloro-
acetaldehyde), 0.1-0.5 (Santodonato et al., 1985).
ln the USA and Europe, registered formulations include dusts, granules, pellets/tablets,
impregnated resin strips, emulsifiable concentrates, soluble concentrates, wettable powders
and pressurized formulations (Royal Society of Chemistry, 1986; US Environmental
Protection Agency, 1987). ln the USSR, dichlorvos is formulated as emulsion concentra
tes,
pellets and aerosols (Izmerov, 1984). Dichlorvos is also formulated in combination with
dimethoate, dinocap, fenchlorphos, fenitrothion, iodofenphos, lindane (see IARC, 1987c),
malathion (see IARC, 1983b, 1987d), methoxychlor (see IARC, 1979b, 1987e), phosalone,
'Calculated from: mg/m3 = (molecular weight/24.45) X ppm, assuming standard temperature (25°C) and
pressure (760 mm Hg £101.3 kPaJ)
DICHLORVOS 269
piperonyl butoxide (see IARC, 1983c, 1987f), pirimiphos-methyl, propoxur, tetrasul,

pyrethrins and trichlorfon (Royal Society of Chemistry, 1986).
1.1.4 Analysis
Selected methods for the analysis of dichlorvos in various matrices are given in Table 1.
Dichlorvos residues can be determined by gas chromatography; the same method can be
used for product analysis. Alternative methods include infrared spectrometry and reaction
with excess iodine, with estimation by titration (WHO, 1989). Several other methods in
various media have been reviewed (Porter, 1964; Anon., 1972; Vevai, 1974; Worthing &
Walker, 1987; WHO, 1989).
Table 1. Methods for the analysis of dichlorvos
Sample matri Sample preparation Assay Limit of Reference

procedurea detection
Air Collect vapours on polyurethane GC/ECO Not reported US Environmental

foam; extract with 5% diethyl Protection Agency
ether in hexane (1988a)
Adsorb on XA-2; desorb with GC/FPD 0.2 Jlg/sample US National Insti-
toluene tute for Occupa-
tional Safety and
Health (1979)
Water Extract with dichloromethane; GC/NPO 2.5 Jlg/I US Environmental
isolate extract; dry; concentrate Protection Agency
with methyl tert-butyl ether (1988b)
Groundwater, Extract with dichloromethane; GC/MS 0.1 Jlg/I US Environmental
soil, wastes dry; concentrate; dean-up using Protection Agency
Florisil column or gel permea- (1986)
tion; exchange into hexane
Formulations Dissolve in chloroform; concen- IR Not reported Williams (1984)
trate using evaporation (baits &
emulsifiable concentrate forms)
Extract with sodium hydroxide; IR Not reported Williams (1984)
dry using anhydrous sodium
sulfate (spray solutions & sprays
in hydrocrbon solvents)
Fruits and Acidify with hydrochloric acid; GC/MCD 0.05 ppm (mg/kg) US Food and Drug
vegetables extract with hexane; dean-up on Administration
silicic acid column (1989a)
Animal tissues, Acidify with hydrochloric acid; GCrr or 0.01-0.02 ppm US Food and Drug
crops, milk extract with hexane; dean-up GC/ECOb (mg/l or mg/kg) Administration
with anhydrous sodium sulfate (milk & tissues) (1989a)
270 !ARC MONOGRAPHS VOLUME 53
Table 1 (contd)
Sample matri Sample preparation Assay Limit of Reference

procedurea detection
Animal tissues, Extract into hexane; dean-up on GC/FPD 0.002 ppm (mg/l US Food and Drug
crops, eggs, silicic acid column with dichloro- milk) Administration
milk methane:hexane (3:2) eluant
(1989b)
aAbbreviations: GC/ECD, gas chromatography/electron capture detection; GC/FPD, gas chromatography/
flame photometrie detection; GC/MS, gas chromatography/mass spectrometiy; GC/NPD, gas chromatogra-
phy/nitrogen-phosphorus detection; GC/MCD, gas chromatography/microculometric detection; GCfI,
gas chromatography/thermionic detection; IR, infrared spectrophotometiy
bUsed if interfering organophosphorus or organochlorine pesticides are present
1.2 Production and use
1.2.1 Production
Dichlorvos was first synthesized in the late 1940s (Tinker, 1972). It has been
commercially manufactured and used throughout the world since 1961 (WHO, 1989). It was
first found as a highly insecticidal impurity of trichlorfon (chlorophos) in 1955; trichlorfon is
rapidly converted to dichlorvos at above pH 6 (Eto, 1974). Dichlorvos is manufactured by the
dehydrochlorination of trichlorfon in aqueous alkali at 40-50 °C or by the reaction between
chloral and trimethyl phosphite (WHO, 1989).
Dichlorvos is produced currently in Argentina, Brazil, Germany, India, Israel, Japan, the
Republic of Korea, Mexico, the Netherlands, Spain, Sweden, Switzerland and the USA
(Meister, 1990). The present worldwide production of dichlorvos is about 4000 tonnes per
year (WHO, 1989). Worldwide production figures for 1984 were as follows (tonnes): eastern
Europe, 220; western Europe, 300; Latin America, 400; south-east Asia, 500; USA, 500;
Japan, 1100; Middle East, India and Pakistan, 1200 (WHO, 1989).
1.2.2 Use
Dichlorvos is a contact and stomach insecticide with fumigant and penetrant action. It is
used as granules or impregnated resin to control internaI and external parasites (especially
fleas and ticks) in livestock and as aerosols or liquid sprays or as impregnated cellulose,
ceramic or resin strips to control insects in houses, buildings and outdoor areas (especially
fles and mosquitos). It is also used to protect certain crops (and other plants) from insects in
the field and in storage. Dichlorvos is not generally applied directly to soil, but it is added to
water to control parasites in the case of intensive fish farming (WHO, 1989). It is used as an
antihelminthic by incorporation in animal feeds (Worthing & Walker, 1987).
Worldwide, it is estimated that 60% is used in plant protection, 30% for public health
and vector control and 10% to protect stored products (WHO, 1989).
ln the USA, in 1971, 16 tonnes of dichlorvos were used on crops (mainly tobacco) and
1100 tonnes were used on livestock and livestock buildings; in 1976, 50 tonnes were used on
crops and 390 on livestock. ln 1975, 80% of the dichlorvos produced in the USA was
formulated into polyvnyl chloride resin strips containing 20% byweight of dichlorvos, which
were used primarily in households. These strips were first marketed in 1967 to control flies
DICHLORVOS 271
and mosquitoes in the home; they were introduced earlier in dairy and poultry operations.
FIea collars containing dichlorvos, for dogs and cats, have also been commercially marketed
(Santodonato et al., 1985).
ln the USA in 1980, the yearly agricultural usage of dichlorvos (active ingredient) was
estimated as follows (tonnes): dairy cattle, 340; beef cattle, 30; hogs, 6; poultry, 2; and other
livestock, 14; about 50 tonnes were used for treatment of tobacco. Overall, 680-1200 tonnes
of dichlorvos were used for agricultural uses, 450 tonnes for public health and about 450
tonnes for household use (US Environmental Protection Agency, 1980). Less than 450
tonnes of dichlorvos (active ingredient) are believed to have been used in the USA in 1989.
ln Finland, about 1500 kg (active ingredient) of dichlorvos were sold in 1988
(Agrochemical Producers' Association of Finland, 1989).
1.3 Occurrence
1.3.1 Air
Dichlorvos is degraded rapidly in air, the rate depending on humidity. The method of
application is an important factor in determining its concentration in air (Gillett et al.,
1972a).
Examples of indoor air concentrations resulting from household and public health use
are shown in Table 2 (WHO, 1989).
The highest exposure recorded in a vaporizer production plant and its packaging rooms
was 3 mg/m3, with an average value of 0.7 mg/m3 (Menz et aL., 1974). The mean concen-
tration of dichlorvos in air did not exceed 0.5 ppb (0.005 mg/m3) in the office and insecticide
storage rooms of commercial pest control buildings and 0.1 ppb (0.001 mg/m3) in vehicles
(Wright & Leidy, 1980).
Dichlorvos was sprayed at 8 ml active ingredientllOO m3 in a unit used for mushroom
cultures, and kept cIosed for 24 h. The air concentration decreased from 3.3 to 0.006 mg/m3
in 24 h. The unit was also treated with paper strips drenched in 50% dichlorvos formulations
(40 ml/l00 m3), which gave air concentrations of 0.38 and 0.024 mg/m3 at 3 and 24 h,
respectively (Grübner, 1972).
Following weekly 6-h applications, the maximum concentrations of dichlorvos observed
in a large warehouse ranged from 2.4 to 7 mg/m3. The amount of dichlorvos dispensed per
application was 25-59 mg/m3, which resulted in average air concentrations after eight
applications of 4 mg/m3 (Gilenwater et al., 1971).
The work place concentration resulting from hot spraying of dichlorvos in six
greenhouses at 0.4 ml/m3 was 7-24 mg/m3 (average, 16 mg/m3) (Wagner & Hoyer, 1975).
Spraying of 12 glass and plastic greenhouses gave concentrations between 0.7 and 2.7 mg/m3
(average, 1.3 mg/m3). Field application by spraying resulted in air concentrations of
0.01-0.26 mg/m3 (average, 0.08 mg/m3) (as reported by WHO, 1989). The air concentration
of dichlorvos in greenhouses immediately after spraying with 0.2-0.3% dichlorvos solutions
was 1.2 mg/m3, which decreased to 0.01 mg/m3 within 24 h. Disturbing the plants resulted in
an increase of 10-26% in the dichlorvos concentration in air (Zotov et aL., 1977).
ln a study designed to test the aeration period needed for safe reentry into a room
following dichlorvos treatment with a pressurized home-fogger, the air levels after 30 min
N
Table 2. Indoor air concentrations of dichlorvos following various applications a
tj
Location Application Doseb Temperature RHC Ventilation Time after Concentration
C) (%) application (mg/m3)
Food shops Resin strips 1 strip/30 m 3 Normal First week 0.03
4 weeks 0.02
10 weeks 0.01
Houses Resin strips 1 strip/30 m3 18-35 20-60 Normal First week 0.06-0.17
2-3 weeks 0.01
Hospital wards Resin strips 1 strip/30 m 3 20-27 35-70 Varied Several days
20-30 days
0.10-0.28
0.02
-
Hospital wards Strips of paper 0.2 ml ai/m3 - - 2h 3 days 0.06
drenched in 50% 0.2 ml ai/m3 17 - 2h 66 h 0.1-0.3
~
dichlorvos solution 0.2 ml ai/m3 17 - 2h 90 h 0.3 ~
hanging in rooms for 0.8 ml ai/m3 30 High 2h 3h 3.7
0
Z
24-36 h 46 h 0.6 0
Houses 0.5% solution 225 or 1200 ml 26 47-60 None 0 0.4
0
according to typical 8h 0.2 ~
""
pest control practice 24 h -: 0.1
Bathroom 0.5% solution wall
::
CJ
25 ml 26 60 None 0 1.1
(sealed) spray 4h 0.3 ~
24 h -: 0.1
0
Living room Spray cans 2.3 mg ai/m3 20- 22 30 min 0 0.24 8
(experimental) 1h 0 0.13 ~
tT
Fogging 240 mg ai/m3 20-22 None 1h 37 VI
w
None 24 h 5.5
1h 1h 2.5
120 h 1h -:0.2
Apartmentsd 0.5% solution 190 mg ai/m 3 26 82 - 0-2 h 0.5
2-24 h 0.2
lleviewed by WHO (1989)

bai, active ingredient
CRH, relative humidity
dprom Gold et al. (1984)
-, not stated
DICHLORVOS 273
were below the industrial workplace permissible exposure level of 1 mg/m3. Without
ventilation, 18 h were required to reach an acceptable IeveI. Because of concern for the
health of infants and elderly persons, the acceptable level for homes was established at 1/40
of the permissible exposure leveI. Rooms treated with this tye of applicator and ventilated
after treatment were considered safe for reentry after 10 h (as reported by WHO, 1989).
Monitoring of mushroom-growing houses in the USA gave air concentrations of
0.1 mg/m3; swabs of exposed surfaces revealed maximal residues of 0.026 l1g/cm2 (as
reported by WHO, 1989).
ln houses treated for pest control with 230-330 g dichlorvos as an aerosol and 40-50 g as
emulsion spray, the mean dichlorvos residue on surfaces was 0.24 l1g/cm2 at the end of day 1
and decreased to 0.06 l1g/cm2 by day 5 (Das et al., (1983).
1.3.2 Uiter
ln water, dichlorvos is hydrolysed into dimethyl phosphoric acid and dichloroacetic acid
(WHO, 1989).
1.3.3 Soi!
Dichlorvos vaporized in a mushroom house to give 0.2-0.4 mg/m3 degraded rapidly in

the moist loam soiL, with only 37% remaining after 3 days. The am ou nt of free
dichloroacetaldehyde at that time was 4% (Hussey & Hughes, 1964).
Dichlorvos is degraded by microorganisms. Bacillus cereus utilizes it as a single carbon
source. ln soil columns perfused with an aqueous solution containing dichlorvos at 1 kg/litre,
30% of the loss of the compound was attributed to microbial action (Lamoreaux & Newland,
1978). Species of Pseudomonas derived from sewage converted dichlorvos to dichloro-
ethanol, dichloroacetic acid and ethyl dichloroacetate (Lieberman & Alexander, 1983).
Fungi, such as Trichoderma viride, also degrade dichlorvos into water-soluble metabolites
(Matsumura & Boush, 1968).
1.3.4 Plants
Dichlorvos is rapidly lost from leaf surfaces by volatilization and hydrolysis, with a
half-time of only a few hours. A small amount penetrates the waxy layers of plant tissues,
where it may persist for longer (FAO/WHO, 1971).
ln California, the estimated safe level of dislodgeable foliar dichlorvos from turf is
0.06l1g/cm2 (WHO, 1989). Studies by Goh et aL. (1986a,b) found that dislodgeable foliar
dichlorvos residues decreased rapidly after 2-6 h and were not detectable after 24-48 h.
1.3.5 Food
Data on residues in food commodities resulting from pre- and post-harvest treatment
and from use on animaIs were summarized by FAO/WHO (1967, 1968, 1971, 1975).
ln Canada, of262 bovine and porcine fat samples analysed between 1973 and 1981, only
one was contaminated with dichlorvos (Frank et al., 1983). ln a national surveilence
programme in Canada, 1984-85 to 1988-89, no residue was found in 898 samples of fruit,
vegetables, meat or wine (Government of Canada, 1990).
Normally, dichlorvos residues present in food are destroyed by washing and cooking.
Abbott et aL. (1970) confirmed the absence of residues in a total-diet study in the United
274 IAC MONOGRAHS VOLUME 53
Kingdom, 1966-67, finding no dichlorvos in 462 samples. A total-diet study carried out In the
USA from 1975 to 1976 gave similar results (Johnson et al., 1981).
Food, meals and unwrapped ready-to-eat foodstuffs exposed to dichlorvos from resin
strips had mean residue levels of -c 0.05 mg/kg (range, c( 0.01-0.1 mg/kg) (Elgar et al.,
1972a,b) and -c 0.02 mg/kg (Collins & deVries, 1973). No residue of dichloroacetaldehyde
(-c 0.03 mg/kg) was detected in the ready-to-eat foodstuffs (Elgar et al., 1972b). Food and
beverages exposed to air concentrations of 0.04-0.58 mg/m3 for 30 min contained dichlorvos
residues of 0.005-0.5 mg/kg, except for margarine which had up to 1.7 mg/kg (Dale et aL.,
1973).
1.3.6 Occupational exposure
Mixed dermal and inhalation exposures were assessed for 13 professional pesticide
applicators after a day's work spraying dichlorvos preparations. Absorbent pads recorded
average exposures of 0.08 l1g/cm2 on the back and 0.04 l1g/cm2 on the chest. Levels found in
respirator filters were 1.1 l1g/cm2, in contrast to surface residues of 0.04-0.5 l1g/cm2
measured at various sites around the treated houses. Although the men wore protective
equipment, sorne absorption of dichlorvos occurred, as shown by the recovery of 0.32-1.4 l1g
dimethylphosphate from their urine (Das et al., 1983).
1.4 Regulations and guidelines
The FAO/WHO Joint Meeting on Pesticide Residues evaluated dichlorvos at its
meetings in 1965, 1966, 1967, 1969, 1970, 1974 and 1977 (FAO/WHO, 1965, 1967, 1968,
1970, 1971, 1975, 1978). ln 1966, the Meeting established an acceptable daily intake for
humans of 0.004 mg/kg bw (FAO/WHO, 1967).
Maximum residue levels have been established by the Codex Alimentarius Commission
for dichlorvos in or on the following agricultural commodities (in mg/kg): fruit (e.g., apples,
peaches, pears, strawberries), 0.1; mushrooms and vegetables (except lettuce), 0.5; head
lettuce, 1; cereal grains, coffee beans, dried lentils, dried soya beans and peanuts, 2; and
cacao beans, 5. As such residues decline rapidly during storage and shipment, these limits are
based on residues likely to be found at harvest (Codex Committee on Pesticide Residues,
1990).
Maxmum residue limits have also been established by the Codex Alimentarius
Commission for dichlorvos in or on the following animal commodities (in mg/kg): milk, 0.02;
eggs, goat meat, meat of cattle, pigs, sheep and poultry, 0.05, based on residues likely to be
found at slaughter (Codex Committee on Pesticide Residues, 1990).
ln the USSR, dichlorvos residues are not allowed in fishing are
as; however, a level of
0.1 mg/l was established for other surface waters (Izmerov, 1984).
National and regional pesticide residue limits for dichlorvos in foods are presented in
Table 3.
DICHLORVOS 275
Table 3. National and regional pesticide residue limits for dichlorvos in foosa
Country or Residue limit Commodities
region (mg/kg)
Argentina 2 Stored cereals in general

Australia 5 Cocoa beans
2 Cereal grains, coffee beans (green), lentils, nuts, peanuts, soya beans
1 Lettuce
0.5 Mushrooms, tomatoes, vegetables (except lettuce)
0.1 AlI foods for which no other maximum residue limit is specified (e.g.,
bread, cakes, cooked meats), fruit
0.05 Eggs, meat, poultry
0.02 Whole milk
Austria 2.0 Cereals
0.1 Other foods of vegetable origin
0.05 Eggs (without shell), meat, milk
Belgium 5 Cocoa beans
2 Coffee beans, grains, leguminous vegetables (dried)
0.5 Flour
0.1 Fruit, vegetables
0.05 Animal fats, fowl, game, hare, meat, meat products, poultry
0.02 Milk and dairy products
o (O.02)b Other foodstuffs of animal and vegetable origin
B razil 5.0 Cocoa
2.0 Barley, maize, coffee, cottonseed, peanuts, rice, rye, soya beans, wheat
1.0 Lettuce, ornamental plants, tobacco
0.5 Chick peas, eggs (without shell), field beans, onions, potatoes, vegetables
(except lettuce)
0.1 Apples, bran, Brazil nuts, cakes, citrus fruits, flour, mushrooms, piñon
seed, strawberries, watermelon
0.05 Meat and meat products, poultry
0.02 Milk
Canada 2.0 Non-perishable packaged foos of high fat content (:: 6%)
0.5 Non-perishable packaged foods of low fat content (-c 6%)
0.25 Tomatoes
Negligible Beef and dairy catte (meat and milk), foods exposed in food storage
areas, homes and restaurants to dichlorvos generated from 20% resin
strips
Chile 2.0 Lentils, raw cereals
1.0 Lettuce
0.5 Cereal products, garden vegetables (except lettuce)
0.1 Fruits
0.05 Eggs, carcasses, poultry
0.02 Whole milk
China 0.2 Vegetables
0.1 Grain
None Vegetable oils
Table 3 (contd)

region (mg/kg)
Czechoslovakia 2.0 Imported lentils, peanuts, raw cereals, soya beans, unroasted coffee
1.0 Imported head lettuce
0.5 Imported min products, mushrooms, tomatoes
0.2 Dried medicinal herbs (for preservation)
0.1 Foodstuffs in general (for preservation), fruits, vegetables
0.1 Imported fruits, various foodstuffs
0.02 Imported eggs (without shell), milk
Denmark 2 Cereals
1 Leafy vegetables
0.5 Mushrooms
0.1 Berries and sman fruits, citrus fruits, other fruits, pome and stone fruits
European 2.0 Barley, buckwheat, grain sorghum, maize, millet, oats, other cereals,
Community paddy rice, rye, triticale, wheat
0.1 Other products
Finland 1.0 Cereal grains
0.2 Flour
0.1 Fruit, vegetables
France 2 Wheat
0.1 Fruits, vegetables
Germany 2.0 Cereals
0.5 Cereal products
0.1 Other foods of plant origin
Hungary 2.0 Barley grain, maize, oat grain, rice (brown, polished), rye, sorghum,
triticale, wheat grain
1.0 Greenhouse lettuce, lettuce
0.5 Beetroot, Brussels' sprouts, cabbage, carrots, caulifower, celery, celery
leaf, garlic, green beans, greenhouse cucumber, greenhouse green papri-
ka, greenhouse tomatoes, horseradish, kohlrabi, mushrooms, paprika,
peas, parsley, parsley root, radishes, red onion, savoy, sorrel, spinach
Apples, apricots, cherries, grapes, greengages, peaches, pears, plums,
0.2 quince, sour cherries, wine grapes
India 1.0 Food grains
0.25 Miled food grains
0.15 Vegetables
0.1 Fruit
Ireland 1.0 Lettuce
0.5 Mushrooms, other vegetables
0.1 Other products
DICHLORVOS 277
Table 3 (contd)

rcgion (mg/kg)
Israel 5.0 Cocoa beans
2.0 Coffee beans, raw cereals (e.g., barlcy, maize, oats, nec, sorghum,
wheat), lentils, pcanuts, soya bcans
1.0 Lettuce
0.5 Miled prOOucts from raw grain, mushrooms, vegetables (except lettuce),
tomatocs
0.1 Fruit (e.g., applcs, peachcs, pcars, strawbcrrics), miscellancous food
items not otherwise specificd that were trcated with dichlorvos in ware-
houses, shops, ctc. (e.g., bread, cakes, chcese, cooked meat)
0.05 Eggs (without shell), meat of catte, goats, sheep, pigs and poultry
0.02 Milk
Italy 2.0 Cereals in bulk
0.5 Milled products (from treated cereals)
0.1 Fruits, garden vcgetables, sugar bcets
Japan O.3c Strawberries
0.1 Asparagus, celery, eggplants, garden radishes, gardcn radish leavcs,
grapes, Japanese pcars, Spanish paprika, spinach, stone lceks
O.ic Fruit (except strawberries); ricc, oats and other minor cercals; potatoes,
tea, vegctables
Kenya 5.0 Cocoa beans
2.0 Coffee beans, lentils, peanuts, raw grain (e.g., barley, maize, oats, rice,
rye, sorghum, wheat), soya beans
1.0 Lettuce
0.5 Fresh vegetables (exeept lcttuce), milled prOOucts from raw grain, mush-
0.1 rooms, tomatoes
0.05 Fresh fruit (e.g., apples, pcaches, pears, strawberries), miscellaneous
0.02 food items not otherwise specified
Eggs (without shell), meat of catte, goats, pigs, poultry and shecp
Milk (whole)
Nethcrlands 5 Cocoa beans
2 Buckwheat cereal, coffee bcans, peanuts, poo vegetables, pulscs
0.5 Whole meal flom
0.1 Fruit, other vegetables
0.05 Eggs, meat, poultry meat
0.02d Milk
o (0.02)e Other crops and foodstuffs
New Zealand 2.0 Cereals, fruit, vegetables
Peru 5.0 Cocoa beans
2.0 Coffee beans, grain cereals, grain lentils, grain soya, peanuts
1.0 Lettuce
0.5 Edible mushrooms, tomatoes, vegetables (except lettuce)
0.3 Cereal products (ground, for human consumption)
0.1 Bread, cakes, cheese, cooked meat, fruits (except citrus)
0.05 Eggs (without shell), meat of cattle, goats, hogs, poultry, sheep
0.02 Whole milk
Romania 0.05 Eggs (without shell), meat
0.02 Whole milk
278 lAC MONOGRAPHS VOLUME 53
Table 3 (contd)

region (mg/kg)
Singapore 0.5 Fruit, grains, vegetables

South Africa 0.1 Bananas, beans, cherres, cruciferae, grapes, lettuce, tomatoes, wheat
0.05 Carcass meat (on the rendered or extracted carcass fat), eggs (without
shen)
0.02 Milk (on a fat basis)
Spain 2.0 Cereal grains
0.1 Other plant products
Sweden 2.0 Cereals
Oost Flakes and flour made from cereals, hulled grain
O.l! Fruit (fresh and dried, fresh and deep-frozen berres), vegetables (green
and root)
0.1 Butter, cheese
0.05 Raw meat, eggs
0.02 Milk
Switzerland 2.0 Cereals, cocoa beans
0.3 Cereal products, vegetables (canned, fresh, frozen)
0.1 Citrus fruit, fruit, other foodstuffs
0.01 Milk
Taiwan 0.5 Fruit, vegetables, leafy vegetables with large wrapper leaves, leafy vege-
tables with small leaves, melon, mushrooms, peas, snap beans
0.1 Root vegetables
United 2 Barley, maize, oats, other cereals, paddy rice, rye, wheat
Kingdom 1 Lettuce
0.5 Beans, Brussels' sprouts, cabbage, carrots, caulifower, celery, cucum-
bers, leeks, lettuce, mushrooms, onions, peas, potatoes, swedes, toma-
toes, turnips
0.1 Apples, bananas, blackcurrants, citrus, grapes, nectarines, peaches,
pears, plums, raspberres, strawberries
0.05 Eggs (birds' eggs in shen (other than eggs for hatching) and whole egg
products and egg yolk products (whether fresh, dried or otherwise
prepared)), meat, fat and preparations of meat, milk
0.02 Milk (fresh raw cows' milk and fresh whole-cream cows' milk expressed
as whole milk)
USAg 2.0 Raw agricutural commodities (nonperishable, packaged or bagged, con-
taining more than 6% fat (post-harvest))
1.0 Lettuceh
0.5 Cucumbersh, dried figs, mushroomsh and tomatoes (pre- and post-
harvest)h; radishes, raw agricultural commodities (nonperishable, bulk
stored regardless of fat content (post-harvest)); raw agricultural commo-
dities (nonperishable, packaged or bagged, containing 6% fat or less
(post-harvest))
0.1 Figs
0.1 (negligible) Edible tissue of swine
0.05 (negligible) Eggs and poultry (fat, meat, and meat by-products)
0.02 (negligible) Cattle, goats, horses, sheep (fat, meat and meat by-products), milk
DICHLORVOS 279
Table 3 (contd)

reglOn (mg/kg)
USSR 0.3 Bran, grain

0.05 Apples, grapes
Not permitted Flour, grouts
Yugoslavia 2.0 Cereals
0.3 Processed cereals, vegetables
0.1 Other foostuffs
Ilrom Health and Welfare Canada (199)

bResidues should not be present; the value in parentheses indicates the lower limit for residue determina-
tion according to the standard method of analysis, this limit having been used to reach the no-residue con-
clusion.
CStandard for withholding registration of agricultural chemicals
dA pesticide may be used on an eating or drinking ware or raw mate
rial without a demonstrable residu,e
remaining; the value listed is considered the highest concentration at which this requirement is deemed to
have been met.
eResidues shaH be absent; the value in parentheses is the highest concentration at which this requirement
is still deemed to have been met.
Jif analysis shows that two or more of certain substances are present in the same sample, in addition to the
limit which applies for each substance, a maximum level of 1.0 mg/kg applies to the sum of the residues of
these substances.
8From US Environmental Protection Agency (1989a,b)
hResidues expressed as naled
Occupational exposure limits and guidelines for dichlorvos in sorne countries and
regions are given in Table 4.
Table 4. Occupational exposure lImIts and guidelines for

dichlorvosa
Country or region Year Concentrationb Interpretation C
(mg/m3)
Austria 1987 1 1WA
Belgium 1987 1 1WA
China 1987 0.3 1WA
Denmark 1987 1 1WA
Finland 1987 1 1WA
3 STEL
Germany 1989 1 1WA
Hungary 1987 0.2 1WA
0.2 STEL
India 1987 1 1WA
3 STEL
Indonesia 1987 1 1WA
Mexico 1987 1.5 1WA
Netherlands 1987 1 1WA
Table 4 (contd)
Country or region Year Concentrationb InterpretationC

(mg/m3)
Romania 1987 0.5 TWA

1.5 STEL
Switzerland 1987 1 TWA
Thiwan 1987 1 TWA
United Kingdom 1987 1 TWA
3 STEL
URSS 1987 0.2 TWA
USA
ACGIH 0.9 Guideline
OSHA 1 TWA
Venezuela 1987 1 TWA
3 Ceiling
Yugoslavia 1987 0.1 TWA
OFrom Izmerov (1984); Cook (1987); American Conference of Govern-
mental Industrial Hygienists (ACGIH) (1989); Deutsche Forschungs-
gemeinschaft (1989); US Occupational Safetyand Health Administration
(OSHA) (1989)
b AlI values given are with skin notation
CT A, time-weighted average; STEL, short-term exposure limit
2. Studies of eancer in Humans
2.1 Case reports
ln a case series, four children with aplastic anaemia and one with acute lymphoblastic
leukaemia were reported by their parents to have been exposed at home to dichlorvos and
propoxur (Reeves et al., 1981).
2.2 Case-control studies
ln a case-control study of leukaemia in the USA (Brown et aL., 1990), described in detail
in the monograph on occupational exposure in spraying and application of insecticides
(p. 68), significant excesses of leukaemia were noted among farmers who reported use of
dichlorvos on animaIs (odds ratio, 2.0; 95% confidence interval (Ci), 1.2-3.5). Risks were
greater among those who had first used dichlorvos 20 or more years before diagnosis of
leukaemia (odds ratio, 2.4; 95% Ci, 1.1-5.4). The risks were greatest among farmers who
used dichlorvos on animaIs on 10 or more days per year (odds ratio, 3.8; 95 % Ci, 1.0-14.8).
The risk for leukaemia in this study was also associated with use of other agricultural
pesticides, including crotoxyhos, famphur, pyrethrins, methoxychlor, nicotine and DDi:
and It was not possible to evaluate exposure to dichlorvos in the absence of these other
pesticides.
DICHLORVOS 281
3. Studies of eancer in Experimental Animais

The Working Group was aware of a study by Horn et aL. (1987), which was of short
duration and not considered informative for an evaluation.
3.1 Oral administration
3.1.1 Mouse
Groups of 50 male and 50 female B6C3Fi hybrid mice, five to seven weeks of age, were
fed technical-grade dichlorvos (minimum purity, 94%) in the diet at initial doses of 1000 and
2000 mg/kg. After two weeks, the doses were reduced to 300 and 600 mg/kg of diet,
respectively, due to severe toxicity, and treated animaIs were maintained at these dietary
levels for 78 weeks followed by 12- 14 weeks on dichlorvos-free diets, after which time (92-94
weeks) the animais were kiled and necropsied. The measured time-weighted average doses
were 318 and 635 mg/kg of diet, respectively. Groups of 10 male and 10 female mice that
served as matched controls were maintained on dichlorvos-free diets for 92 weeks; further
control data were obtained from pooled control animaIs (100 males and 80 females). ln
females, 13/50 low-dose animaIs died before week 90; survival to 90 weeks was greater th an
84% in aIl other groups. Average weights of high-dose males and females were generally
an those of the low-dose and control groups, but the differences did not exceed 10%.
lower th
The only findings of note were two squamous-cell carcinomas of the oesophagus (in one
low-dose male and one high-dose female), one papilloma of the oesophagus (in a high-dose
female) and three cases of focal hyperplasia of the oesophageal epithelium (in three
low-dose males) (US National Cancer Institute, 1977). (The Working Group noted the short
duration of treatment.j
Groups of 50 male and 50 female B6C3Fi mice, eight weeks of age, were administered 0,
10 or 20 (males) and 0, 20 or 40 mg/kg bw (females) dichlorvos (99% pure) in corn oil by
gavage per day on five days per week for 103 weeks. Survival was not affected by treatment.
The incidence of squamous-cell papillomas of the forestomach was increased in males and
females. A significant dose-response trend for the incidence of squamous-cell papilomas
was seen in males (1/50 control, 1/50 low-dose, 5/50 high-dose; p = 0.032) and in females
(5/49 control, 6/49 low-dose, 18/50 high-dose; p = 0.002). ln females, the incidence in the
high-dose group was significantly greater than that in controls (p = 0.004). Two of 50
high-dose females also had squamous-cell carcinomas (US National Toxicology Pro gram,
1989).
3.1.2 Rat
Groups of 50 male and 50 female Osborne-Mendel rats, five to seven weeks of age, were
fed diets containing 150 or 1000 mg/kg of di et technical-grade dichlorvos (minimum purity,
94%); due to severe toxicity, the high-dose was reduced to 300 mg/kg of di et after three
weeks. Both groups were treated for 80 weeks and were maintained for a further 30 weeks on
a dichlorvos-free diet. Time-weighted average doses were 150 and 326 mg/kg of diet,
respectively. Groups of 10 males and 10 females served as matched controls and groups of 60
animaIs of each sex as pooled con troIs. Weight gain was consistently lower in high-dose
groups than in low-dose and control groups. No significant difference in survval was
observed between treated and control groups at 105 weeks. The incidence of malignant
fibrous histiocyomas in male rats showed a statistically significant trend (pooled control,
2/58; low-dose, 4/48; high-dose, 8/50;p = 0.018); a histiocyoma occurred in 1/10 matched
male controls (US National Cancer Institute, 1977). (The Working Group noted the short
duration of treatment).
Technical-grade dichlorvos (97% purity) was administered by gavage in water to 70 male
and 70 female rats (inbred strain BD IX/Bln), six to eight weeks of age, at a dose of 0.1 mg per
animal twce a week; or to 99 male and 99 female rats at a dose of 0.1 mg per animal three
times a week for 60 weeks. Groups of 59 male and 60 female rats served as vehicle controls.
AnimaIs were kiled 111 weeks after the beginning of treatment. There was no difference in
median survval times between treated and control animaIs. Forestomach papillomas were
observed in two males and in one female that received 0.3 mg dichlorvos. One male and one
female rat receiving 0.3 mg had two and five papillomas of the urinary bladder, respectively
(Horn et aL., 1988). (The Working Group noted the short duration of exposure.)
Groups of 50 male and 50 female Fischer 344/N rats, seven weeks of age, were
administered 0, 4 or 8 mg/kg bw dichlorvos (99% pure) per day in corn oil by gavage on five
days per week for 103 weeks. Survival was 31/50 control, 25/50 low-dose and 24/50 high-dose
males and 31/50 control, 26/50 low-dose and 24/50 high-dose females; body weight gain was
not affected by administration of dichlorvos. The incidence of acinar-cell adenomas of the
pancreas was increased in treated males (16/50 control, 25/49 low-dose and 30/50 high-dose;
p -: 0.001 for trend). Further examination of horizontal sections of aIl pancreases revealed
increases of reduced statistical significance (25/50,30/50 and 33/50; (p for trend = -: 0.05)).
There were also more male rats with multiple adenomas in the treated groups th
an among
con troIs (2/50, 7/49 and 13/50). Mononuclear-cell leukaemia occurred with a significant
dose-response trend in male rats (p = 0.0 Il), and the incidence in each of the treated groups
was significantly greater than that in controls (11/50 control, 20/50 low-dose and 21/50
high-dose males). ln females, fibroadenomas and adenomas of the mammary gland occurred
with a significant dose-response trend (p = 0.028), and the incidence in both treated groups
was significantly greater than that in controls (9/50 control, 19/50 low-dose and 17/50
high-dose females). Two female rats in the control group and two in the low-dose group had
carcinomas of the mammary gland (US National Toxicology Program, 1989).
3.2 Inhalation and/or intratracheal administration
Rat: Groups of 50 male and 50 female Carworth Farm E strain rats, five weeks of age,
were exposed continuously to atmospheres containing 0 (control), 0.05, 0.5 or 5 mg/m3
technical-grade dichlorvos (purity, :; 97%) for 104 weeks. The mean values for the entire
test period were 0.05, 0.48 and 4.7 mg/m3 (range :i 20%). AlI treated groups showed
decreased weight gain compared with controls, especially in the high-dose group. The
numbers of males survving at 99-102 weeks were 11/50 control, 21/50 low-dose, 15/50
mid-dose and 32/50 high-dose; survval in females at 104 weeks was 22/47 control, 27/47
low-dose, 26/47 mid-dose and 34/47 high-dose. Complete necropsy and histopathologywere
performed on 20-32% of males and 22-38% of females, reducing the effective numbers of
animaIs per group to between 10 and 18. No significant Increase in tumour incidence could
DICHLORVOS 283
be attributed to treatment (Blair et al., 1976). (The Working Group noted the small numbers
of animaIs submitted for complete necropsy.l
Studies of cancer in ex¡erimental animaIs are summarized in Table 5.
4. Other Relevant Data

The toxicity of dichlorvos has been reviewed (FAO/WHO, 1965, 1967, 1968, 1971;
Anon., 1974; FAO/WHO, 1978; WHO, 1989).
4.1 Absorption, distribution, metabolism and excretion
4.1.1 Humans
Dichlorvos is rapidly hydrolysed in human blood (half-time, 7-11 min), and no
unchanged dichlorvos was found (detection limit, 0.1 j.g/g) in blood samples taken 1 min
after cessation of inhalation by two male volunteers exposed to 0.25 mg/m3 for 10 h or to
0.7 mg/m3 for 20 h (Blair et al., 1975).
A human volunteer who ingested 5 mg p4C-vinyll-dichlorvos excreted radiolabel at a
rate similar to that seen after comparable oral dosing of rats, mice and hamsters, except that
the output of l4COZ was somewhat greater. The urinary metabolites were tentatively
identified as demethyldichlorvos, urea and hippuric acid (Hutson & Hoadley, 1972a).
More recently, it was established that dimethylphosphate is a metabolite in the urine of
workers occupationally exposed to dichlorvos (Das et al., 1983).
4.1.2 Experimental systems
The metabolism and disposition of dichlorvos have been reviewed (Wright et al., 1979).
Metabolic disposition studies using radiolabelled dichlorvos have been reported in rats,
mice, hamsters, pigs and humans. Labelling at different sites (e.g., 14C-methyl, 14C-vinyl,
36CI-chlorovinyl, 3zp-phosphate) has enabled specifie pathways to be traced (Hutson et al.,
1971; Hutson & Hoadley, 1972a,b; Page et al., 1972; Potter et al" 1973; Blair et al., 1975).
Furthermore, metabolic disposition has been determined after both inhalation exposure and
oral administration (including slow-release polyvnyl chloride-pelleted dose forms).
There are two main metabolic pathways for dichlorvos: (1) ester hydrolysis of the
PO-vinyl group to yield dimethylphosphate and dichloroacetaldehyde and (2) oxidative
O-demethylation to demethyldichlorvos and formaldehyde. An alternative pathway for
O-demethylation involves conjugation with glutathione (Dicowsky & Morello, 1971; Hutson
et al., 1971; Hutson & Hoadley, 1972a,b; Page et al., 1972; Potter et al" 1973; Blair et al.,
1975). Hydrolysis of the O-demethylated metabolite yields methylphosphate and, eventually,
phosphoric acid and methanol (WHO, 1989). Radiolabel from p4C-methyl)- and
(14C-vinyl)-dichlorvos is ultimately incorporated into COz (e.g., 39% of an oral dose of
p4C-vinyl)-dichlorvos over four days in rats) and enters the 1 and 2-carbon metabolic pools,
resulting in the labelling of amino acids, proteins and purines. This labelling may confound
the interpretation of studies of tissue disposition and urinary excretion if the chemical
specificity and source of the radiolabel are not determined.
Patterns of urinary metabolites indicate that metabolic clearance varies very little by
species or route. The hydrolysis pathway generally predominates over the O-demethylation
pathway, although the latter is more prominent in mice.
~
Table 5. Studies of cancer in experimental animaIs
Reference Species/strain Sex Dose Exprimental parameter/ Graup Statistical Comment
schedule observation conclusion
0 1 2 3
US National Cancer Mouse M 1 n diet for 80 Dose (mglg of diet)a 0 0 318 635
Institute (1977) B63F¡ weeks Oesophageal carcinoma
1/50
F ln diet for 80 Dose (mglg of diet) 0 0 318 635 No significant
weeks
US National Mouse M
Oesophageal carcinoma
Oesophageal papilloma
1/50
1/50
increase in
tumours -~
Toxicology Program
Gavage, 5 Dose (mg/g bw) 0 10 20 -
B6C3F¡ days/week for
(1989) 103 weeks
Forestomach papilloma 1/50 1/50 5/50 p = 0.032 trend fi
F ~
Gavage, 5
days/week for
Dose (mglg bw)
Forestomach papilloma
0 20 4D 0
0Z
5/49 6/49 18/50 p = 0.002 trend
103 weeks Forestomach carcinoma 0/49 0/49 2/50
US National Cancer
Institute (1977)
Rat Osborne-
Mendel
M ln diet for 80
wecks
Dose (rnglg of diet)" 0 0 150 326 0
Malignant fibraus histiocytomas 1/10 2/58 4/48 8/50 p = 0.018 trend
F ln diet for 80 Dose (mglg of diet) 0 0 150 326 No significant ~
weeks
increase in ::
C/
tumours
Horn et al. (1988) Rat M Gavage, 2 or Dose (mg/animal) per week ~
BDIX/Bln 3 per week for Forestomach papillomas
0
0110
0.1 X 2
0/1
0.1 X 3
2/26 NS Number of
0
60 weeks Urinary bladder papillornas 0/55 0/65 1/95 NS animaIs with B
F Gavage 2 or 3 Dose (mg/animal) per week
papilIomas
~
per week for 60 Forestomach papillomas
0 0.1 X 2 0.1 X 3 tr
0/22 0/20 1/38 NS Number of VI
weeks Urinary bladder papillomas 0/6 0/7 1/10 NS animais with
v.
papillomas
US National Rat Fischer M Gavage, 5 Dose (mglg bw) 0 4 8
Toxicology Program 344/N days/weeks for Pancreatic acinar-cell adenomas 25/50 30/50 33/50 p -c 0.05 trend
(1989) 103 weeks Mononuclear-cll leukaemia ll50 20/50 21/50 p = 0.011 trend
F Gavage, 5 Dose (mglg bw) 0 4 8
days/weeks for Pancreatic acinar-cell adenomas 2/50 3/50 6/50 NS
103 weeks Mammary fibraadenomas/adenomas 9/50 19/50 17/50 P = 0.028 trend
"araups: 0, matched contraIs; 1, poled contraIs
DICHLORVOS 285
Hydrolytic metabolism of dichlorvos to dimethylphosphate and dichloroacetaldehyde,

which in turn is rapidly reduced to dichloroethanol and conjugated with glucuronic acid, is so
rapid that the half-time for the reaction in vivo has not been determined with any accuracy. ln
vitro, the half-time for blood-catalysed hydrolysis ranges from 2 min in rabbits to 30 min in
rats. ln human blood, the half-time is approximately 10 min, and the Km for the reaction has
been estimated to be approximately 3 llM. For this reason, unchanged dichlorvos is detected
in blood only at relatively high dose rates (Blair et al., 1975).
4.2 lloxic effects
4.2.1 Humans
The adverse effects of dichlorvos in humans have been reviewed (Cavagna & Vigliani,
1970; Gilett et al., 1972a,b; Hayes, 1982). Depression of plasma cholinesterase is the most
sensitive indicator of exposure to dichlorvos but is not necessarily an indicator of toxicity. At
higher dose levels, red blood cell cholinesterase may also be affected.
Dichlorvos was administered in the form of slow-release polyvnyl resin formulation
pellets as single doses (1-32 mg/kg bw) to 107 men and as repeated dosesO-32 mg/kg bwper
day for 2-7 days; 1-16 mg/kg bw per day for up to three weeks) to 38 men. Maximal plasma
cholinesterase depression occurred at approximately 6 mg/kg bw (single dose) and 1 mg/kg
bw per day (repeated dose over three weeks). The single-dose threshold for plasma
cholinesterase depression was approximately 1-3 mg/kg bw. Redblood cell cholinesterase
activity was depressed at doses approximately four-.fold higher. While the incidence of
transient gastrointestinal and central nervous system-related subjective effects which
accompanied the cholinesterase depression was relatively low at the lowest dose rates, they
were sufficiently adverse to cause subjects given repeated doses of 8-32 mg/kg bw per day to
withdraw from the study (Slomka & Hine, 1981).
Airborne levels of dichlorvos which cause slight to moderate cholinesterase depression
have been reported to be 0.7 mg/m3 average over one year in factory workers producing
dichlorvos vaporizers (Menz et al., 1974) and 0.1 mg/m3 for 24 h per day in children and
adults hospitalized for various periods in wards provided with dichlorvos-impregnated
plastic strips. Plasma (but not red blood cell) cholinesterase levels were slightly depressed in
Il hospitalized babies exposed to air levels of over 0.1 mg/m3 for 24 h per day, but children of
2-7 years were not affected at the same exposure level for 16 h per day (Cavagna et aL., 1969).
As reported in an abstract, neither plasma nor red blood cell cholinesterase depression was
found in 22 newborn babies when the average air levels of dichlorvos were reported to be up
to 0.159 mg/m3 (Vigliani, 1971).
Lethal exposures to dichlorvos have been reported in connection with accidental
splashing of a concentrated formulation, coupled with failure to wash the material off
(Hayes, 1982). A case of systemic poisoning resulted from an accident in which dichlorvos
spray leaked down a man's back (Bisby & Simpson, 1975). Another accidental incident of
skin contact resulted in symptomatic effects followed by the development of a persistent
contact dermatitis (Mathias, 1983).
28 IARC MONOGRAHS VOLUME 53
The toxicology of dichlorvos in experimental animaIs has been reviewed (Attfield &
Webster, 1966; Gilett et al., 1972a,b; Anon., 1974; Wright et al., 1979).
Dichlorvos is acutely neurotoxic by virtue of its ability to inhibit brain cholinesterase.
The acute oral LDso in rats was cited as 56-80 (Durham et al., 1957) and 25-30 mg/kg bw
(Ben-Dyke et al., 1970) and that in mice as 140-275 mg/kg bw(Anon., 1974; Holmstedt al.,
et
1978). The oral LDso of dichlorvos in young pigs was 157 mg/kg bw; no death occurred in
animais administered up to 100 mg/kg of a polyvnyl chloride formulation of dichlorvos
(Stanton et al., 1979). The large range cited for the dermal LDso (75-900 mg/kg bw) in rats
suggests that skin absorption is vehicle-dependent (Jones et al., 1968).
Exposures after which cholinesterase depression was the only discernible toxic effect
include two-year inhalation exposure of rats to 0.5-5 mg/m3 (Blair et al., 1976), 90-day
feeding of 0.4-70 mg/kg bw per day to rats (effects observed at 3.5 mg/kg per day and above;
Durham et al., 1957), administration for 30 days of 1- 16 mg/kg bw per day in polyvnyl
chloride pellets to pigs (Stanton et al., 1979) and administration for 10-21 days of
10-80 mg/kg bw per day in polyvnyl chloride pellets to rhesus monkeys (Hass et al., 1972).
Dichlorvos has been ascribed only a slight risk of causing delayed neuropathy, because
doses that inhibit neuropathy target esterase and result in ataxia in hens exceed the LDso by
several fold; protection with atropine is required if the test is to be completed (Johnson,
1978; Caroldi & Lotti, 1981; Johnson, 1981).
Both humoral immune response and cell-mediated immunity were inhibited in rabbits
treated orally with dichlorvos for five days a week for up to five to six weeks at high dose rates
(0.31-2.5 mg/kg bw: 2.5-20% of the LDso; Dési et al., 1978, 1980). Immunosuppression was
also observed in mice given 120 mg/kg bw orally, but the authors commented that this
phenomenon, seen with other organophosphonates and the cholinomimetic compound,
arecoline, may be secondary to a profound cholinergic stimulation (Casale et al., 1983).
The diurnal rhythm of the pituitary/adrenal axis was altered in rats given 2 ppm (mg/l)
dichlorvos in the drinking-water for two weeks (approximate intake, 0.3 mg/kg bw per day),
causing changes in plasma adrenocorticotrophic hormone levels and adrenal cholesterol
ester concentrations. While adrenocorticotrophic hormone secretion is believed to be
acetylcholine-sensitive, there was no detectable change in cholinesterase activity (Civen et
al., 1980).
Reactions with macromolecules: Dichlorvos is a phosphorylating and alkylating agent
(Wright et al., 1979). 4-Nitrobenzylpyridine is alkylated by dichlorvos (half-time, 28 min)
more slowly th an methyl methanesulfonate (half-time, 9.6 min). Metabolites of dichlorvos
did not react with 4-nitrobenzylpyridine in this system (Bedford & Robinson, 1972). The
relative reactivity of dichlorvos toward 4-nitrobenzyIpyridine and acetylcholinesterase was
greatly in favour of esterase phosphorylation (WHO, 1989), indicating that dichlorvos-
associated methylatión' of DNA purines may not be as important in vivo as the esterase
phosphorylation reaction (Wright et aL., 1979; Wooder et aL., 1977).
There may appear to be some conflict between this conclusion and the detection of
radiolabelled N-7-methylated guanine in mouse urine following administration of
(14C-methyl)- or (3H-methyl)-dichlorvos (24-90 ¡.Ci intraperitoneally or an estimated
DICHLORVOS 287
8.5-11 J.Ci by inhalation) (Wennerberg & Löfroth, 1974). Since, however, methylated
purines occur naturally in urine and p4C-methyl)-dichlorvos metabolites enter the 1- and
2-carbon metabolic pool, it has been suggested that the mechanism of methylation may be
indirect (Wooder & Wright, 1981). No N-7-guanine methylation was found in the DNA of
lung, liver, heart, brain, testes or spleen of 20 rats exposed to p4C-methyI)-dichlorvos by
inhalation at 0.064 J.g/l for 12 h (estimated total dose, 6 J.g; specifie activity, 113 J.Ci/mmol;
resulting in. a DNA detection limit of 0.000001 % of the dose) (Wooder et al., 1977).
Segerbäck and Ehrenberg (1981) also concluded that the likelihood of DNA
methylation after dosing with dichlorvos in vivo is extremely smalL. Their estimate of the
amount of DNA methylation in mice after intraperitoneal dosing with 1.9 J.mol/kg bw
(0.42 mg/kg) is of the order of 8 x 10-13 mol methyl per gram of DNA.
4.3 Reproductive and developmental efTects
4.3.1 Humans
No data were available to the Working Group.
Female Sherman rats were treated intraperitoneally with dichlorvos at 15 mg/kg bw in
peanut oil on day 11 of gestation. No difference was noted in weight gain, number offetuses
per litter, number of resorptions per pregnant rat or weight of the fetuses or placentae on day
20 of gestation. Three omphalocoeles occurred among 41 offspring in the treated group, but
no malformation was noted among controls (Kimbrough & Gaines, 1968).
No adverse developmental effect was observed in CF-1 mice administered the maximal
tolerated dose by gavage on days 6-15 of gestation or in New Zealand rabbits administered
60 and 5 mg/kg bw per day on days 6-18 of gestation or by inhalation at 4 mg/m3 for 7 h per
day (Schwetz et al., 1979).
Pregnant rabbits were treated (route not given) with dichlorvos at a dose of 6 mg/kg bw
per day for the last 10 days of gestation. Light-microscopic examination of the brains of six
pups from treated and six from untreated dams sacrificed at birth revealed no alteration in
brain morphology; electron microscopie examination suggested 'immaturity' or delay in
brain development in the treated animaIs. Synaptic junctions quantified in the motor cortex
using electron microscopy were considered to be immature (Dambska et aL., 1979). (The
Working Group noted the lack of adequate con troIs and the poor description of the study. i
Carworth E rats and Dutch rabbits were exposed to dichlorvos in air at concentrations of
up to 6.25 mg/m3 and 4 mg/m3, respectively, for 23 h per day on seven days per week from the
day of mating until the end of gestation. These treatments produced a dose-dependent
decrease in plasma, red cell and brain cholinesterase activity in both species but had no effect
on the number of pregnancies, the number of resorptions, the number of fetal deaths, litter
size or fetal weight in rats or rabbits (Thorpe et al., 1972).
ln pregnant sows fed a polyvnyl chloride formulation of dichlorvos at doses of 5 or
25 mg/kg bw per day for the last 30 days of gestation, no alteration in reproductive
performance was observed. Plasma and red cell cholinesterase activities and, at the high
dose, myometrial acetylcholinesterase activity were decreased in the sows; the rhomb-
encephalic acetylcholinesterase level was increased in fetuses (Stan
ton et aL., i 979).
A series of early studies reported in abstracts also examined reproductive and

developmental effects. No effect on reproduction or development was seen in more than
6000 offspring of male and female rats treated for three generations with dichlorvos in feed
at doses of up to 500 ppm (mg/kg) (Witherup et al., 1971). ln rabbits treated orally with a
polyvnyl chloride formulation of dichlorvos, maternaI toxicity was seen at 34 mg/kg; no
alteration was observed in reproductive or developmental parameters at doses not
associated with maternaI toxicity (Vogin et aL., 1971). No effect on reproduction or
development was seen over two generations in male and female swine treated for 37 months
at doses in the feed of up to 500 ppm (mg/kg) (Collins et al., 1971).
4.4 Genetic and related effects (see also Table 6 and Appendices 1 and 2)
4.4.1 Humans
No data were available to the Working Group.
The genetic activity of dichlorvos has been reviewed (Ramel et al., 1980).
ln bacteria, dichlorvos bound covalently to DNA, RNA and protein and caused DNA
damage and point mutations. Bacterial mutagenicity was reduced in the presence of liver
preparations. Dichlorvos induced gene conversion, mutation and aneuploidy in yeast and
fungi, and mutation, chromosomal aberrations and micronucleus formation in plants. ln
Drosophila melanogaster, chromosomal aberrations but not sex-linked recessive lethal
mutation were induced. Autosomal lethal and polygenic viability mutations were induced in
D. melanogaster by treatment over multiple generations. (The Working Group considered
that these tests are not weIl validated.) ln mammalian cells in vitro, dichlorvos caused DN A
strand breaks, mutation, sister chromatid exchange, chromosomal aberrations and cell
transformation. ln human cells in vitro, it induced unscheduled DNA synthesis but neither
chromosomal aberrations nor sister chromatid exchange.
No significant response was observed in vivo in any of the mammalian tests used for the
induction of unscheduled DNA synthesis, sister chromatid exchange, micronucleus
formation, chromosomal aberrations or dominant lethal mutation.
5. Summary of Data Reported and Evaluation
5.1 Exposure data
Dichlorvos has been used widely as an insecticide since 1961 to control internaI and
external parasites in livestock and domestic animaIs, to control insects in houses, and in crop
protection.
Dichlorvos has been formulated for use as dusts, granules, pellets/tablets, impregnated
resin strips and concentra tes.
Household and public health uses represent the main sources of human exposure to
dichlorvos. Exposure may also occur during its production and application.
Table 6. Genetic and related etTects of dichlorvos
Test system Resulta Doseb Reference

LED/HID
Without With
exogenous exogenous
metabolic metabolic
sytem system
PRB, Prophage induction + + 60.0000 Houk & DeMarini (1987)
ECB, Escherichia coli WP2, DNA strand breaks + 0 2000.0000 Green et al. (1974)
ECB, Escherichia coli WP67, DNA strand breaks + 0 500.0000 Green et al. (1974)
ECB, Escherichia coli ColE1 plasmid, DNA strand breaks + 0 1000.0000 Griffin & Hil (1978)
ECO, Escherichia coli pol A, differential toxicity (spot test) + 0 13.~~ Rosenkranz (1973)
ECO, Escherichia coli pol A, differential toxicity (liquid) + 0 1400.~~ Rosenkranz (1973)
BSD, Bacillus subtils fec, differential toxicity + 0 200.~~ Shirasu et al. (1976) 0..
BSD, Bacillus subtils fec, differential toxicity + 0 0.000 Kawachi et al. (1980) ()
BRD, Bacteria (other), differential toxicity (+ ) 0 5~~.000 Adler et al. (1976) ~
BRD, Bacteria (other), differential toxicity + 0 2.~~ Braun et al. (1982) 0t"
SAO, Salmonella typhimurium TA100, reverse mutation + + 300.0000 Byeon et al. (1976)
SAO, Salmonella typhimurium TA1oo, reverse mutation + + 275.~~ Löfroth (1978) 0C/~
SAO, Salmonella typhimurium TA1oo, reverse mutation + + 0.~~ Kawachi et al. (1980)
SAO, Salmonella typhimurium TA1oo, reverse mutation + 0 0.~~ Ishidate et al. (1981)
SAO, Salmonella typhimurium TA1oo, reverse mutation + (+ ) 1.0000 Braun et al. (1982)
SAO, Salmonella typhimurium TA1oo, reverse mutation + + 375.~~ Moriya et al. (1983)
SAO, Salmonella typhimurium TA1oo, reverse mutation (+ ) + 250.~~ Breau et al. (1985)
SAO, Salmonella typhimurium TA1oo, reverse mutation + - 250.~~ Choi et al. (1985)
SAO, Salmonella typhimurium TA1oo, reverse mutation + + 167.~~ Zeiger et al. (1988)
SAO, Salmonella typhimurium TA1oo, reverse mutation + + 500.~~ US National Toxicology
Program (1989)
SA2, Salmonella typhimurium TA102, reverse mutation - - 0.000 Choi et al. (1985)
SA3, Salmonella typhimurium TA1530, reverse mutation + 0 0.~~ Hanna & Dyer (1975)
SAS, Salmonella typhimurium TA1535, reverse mutation + 0 0.~~ Hanna & Dyer (1975)
SAS, Salmonella typhimurium TA1535, reverse mutation (+ ) (+ ) 1500.~~ Byeon et al. (1976)
SAS, Salmonella typhimurium TA1535, reverse mutation + 0 2500.000 Shirasu et al. (1976)
SAS, Salmonella typhimurium TA1535, reverse mutation + 0 1500.0000 Carere et al. (1978)
- - N
00
SAS, Salmonella typhimurium TA1535, reverse mutation 2500.0000 Moriya et al. (1978) v:
Table 6 (contd) N
8
Test system Resulta Dosé Reference
LED/HID
Withou t With
exogenous exogenous
metabolic metabolic
sytem system
SAS, Salmonella typhimurium TAlS3S, reverse mutation + 0 0.~~ Choi et al. (198S)
-
SA7, Salmonella typhimurium TAlS37, reverse mutation
SA7, Salmonella typhimurium TAlS37, reverse mutation -
0
0
0.~~
2S00.oo
Hanna & Dyer (197S)
Shirasu et al. (1976)
-~
SA7, Salmonella typhimurium TA1537, reverse mutation - 0 2800.~~ Carere et al. (1978)
SA7, Salmonella typhimurium TAlS37, reverse mutation - - f3
2500.~~ Moriya et al. (1983)
SA8, Salmonella typhimurium TAlS38, reverse mutation - 0.~~ ~
SA8, Salmonella typhimurium TA1538, reverse mutation -
0 Hanna & Dyer (197S) 0
SA8, Salmonella typhimurium TA1538, reverse mutation -
0
-
2500.~~ Shirasu et al. (1976)
0Z
SA8, Salmonella typhimurium TAlS38, reverse mutation -
ISOO.OO Byeon et al. (1976) 0
0 2800.~~ Carere et al. (1978)
SA8, Salmonella typhimurium TA1538, reverse mutation - - 2500.~~ Moriya et al. (1983) ~
SA8, Salmonella typhimurium TA1538, reverse mutation - - 0.~~ Choi et al. (1985) ::
CI
SA9, Salmonella typhimurium TA98, reverse mutation - - 1500.~~ Byeon et al. (1976)
SA9,Salmonella typhimurium TA98, reverse mutation - - 0.~~ Kawachi et al. (1980) â
SA9, Salmonella typhimurium TA98, reverse mutation - - 2500.~~
- -
Moriya et al. (1983) 5
SA9, Salmonella typhimurium TA98, reverse mutation
0.~~ Breau et al. (1985) ~
SA9, Salmonella typhimurium TA98, reverse mutation - - 0.~~ Choi et al. (1985) tT
SA9, Salmonella typhimurium TA98, reverse mutation - - \J
w
500.~~ Zeiger et al. (1988)
SA9, Salmonella typhimurium TA98, reverse mutation - - SOO.OO US National Toxicology
Program (1989)
SAS, Salmonella typhimurium 64-320, reverse mutation + 0 SOO.OO Voogd et al. (1972)
SAS, Salmonella typhimurium C117, reverse mutation (+ ) 0 6630.~~ Dyer & Hanna (1973)
SAS, Salmonella typhimurium C1l7, reverse mutation - 0 0.~~ Hanna & Dyer (1975)
SAS, Salmonella typhimurium G46, reverse mutation - 0 0.~~ Hanna & Dyer (1975)
SAS, Salmonella typhimurium TA1536, reverse mutation - 0 2500.~~ Shirasu et al. (1976)
SAS, Salmonella typhimurium TAlS36, reverse mutation - 0 2800.~~ Carere et al. (1978)
ECF, Escherichia coli B, forward mutation + 0 1100.~~ Wild (1973)
ECK, Eschelichia coli K12, forward or reverse mutation + 0 14S.00 Mohn (1973)
ECW, Escherichia coli WP2 uvrAj reverse mutation + 0 200.~~ Bridges et al. (1973)
~..
ir ir ~ir ~
ir .. ..
DICHLORVOS 291
~ -~
~~-~~
i.~ ~i.~~~
~~
ir ir
- - -~ -r- -~-~
~~ir~~~~-~~~~~~~~
~~~~i.~i.~i.~i.
~~- -
~~~ ~"
~~~~~~C~C~C '-~N
(l~-
~~ 00.. ~(l~~~-~~~~(!~(l~(l~(l-~~~
. ~T" '- .00 .. '--- £--. .?-" ~.. ~OO . ,-'f ~"-"\ ~
Cl~~~~~~~~~~ ~~ ~~~~~~~~~~~~~~~~~~
u(l
i:
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~~~~~
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i.
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i: ;; Oû i: Oû i: ;; (l ce Oû ';;i: 8 Oû Oû i: 00 i: Oû i: 00 i: Oû'r" 00 i: 'i: 'C ...
ce ce 'C (l 'i: ce ce ì: ... 'i: 0 ;0 0 'i: ce'i: ce'i: ce'i: ce'c 0 0 (l - - ..
¡: ~ Z ~ Cl ~ ~ Z d ~ ~ ~ .. ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ Cl æ æ u
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.Q tS ~ê ~ Š~~~~ ~~§§ ~ ~§§å § §§~ ~ §§§§ ê §
00 § ó § 0 0 ir ~ ir ~ ~ § § 0 § 0 § 0 § 0 0 ~ ~ § ~ ~ §
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"'''''.......;.;.;...;S ",;:;:SSS sssS (l'5§§ § ~
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:: :: :: (l (l (l (!~ (l~ (l
S;S;S;;;;;~;;~;;;;;; (l ~(l.~:! ~ ~~ ~~ ~~ ~~ ~~ ::~::~00
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i:.. ~~~~
N N N~.-~ ..i.~...... ~~
"0 ~ ~1 ir;: li~ ir ir \C \0 00 ;; ~._.~ ~'~'~'ë:'ë:
.~ .~
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~(.(. 88888888(.(.8(.888888(. (.~(.(. (. g
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.~ .~-S~ ~ 0..(..~~(..~~-S
.~.~.~
.~-S ~ 0- - - -~~...~
.~~~.~~~.~~:s.~ ~:s..~-S
0- .~
.~ ~~-S
0-(.
.~ ~ ~ 'c
.~.~(..~~~~ ~
cs c~f
~ ..
~ f~ ..~f ..
oi:
'-~ s ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ lU ~ ~ ~ ~ ~ ~ .~ -S -S -S -S
\C ..'"(l ~~ ~ ~~~~~~~~~~ ~~~~~~~~~ ~~~~ ~ ~
~ ~ ~-S-S-S-S-S-S-S-S ~ ~-S-S-S-S-S-S-S-S ~ ~~ ~ ~ ~ ~
- ~ ~~~ uuNNNNNNNN~~ NNÑNNNÑN~~~ÓÓÓ
u uuu u u ~uu u U ~
QJ
.J ..
~
'"
~
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P- P- P- P- P- P- P- P- P- P- P- P- ~ P- P- P- ~ P- P- P- P- ~ ~ ~ ~ ~ ~ ~
Table 6 (contd) ~
N
Test system Resulta Dosé Reference
LED/HID
Without With
exogenous exogenous
metabolic metabolic
sytem system
ANG, Aspergillus nidulans, genetic crossing-over + ,0 2800.~~ Morpurgo et al. (1977)
SZF, Schizosaccharomyces pombe, forward mutation + (+ ) 330.~~ Gilot-Delhalle et al.
..
ANR, Aspergillus nidulans, reverse mutation + 0 1400.0000
(1983) ~
Morpurgo et al. (1977)
ANN, Aspergillus nidulans, aneuploidy + 0 80.~~ Morpurgo et al. (1979) ~
HSM, Hordeum species, mutation - 0 166.~~ Bhan & Kaul (1975) ~
HSM, Hordeum species, mutation + 150.~~ 0
0Z
0 Panda & Sharma (1979)
HSM, Hordeum species, mutation + 0 500.~~ Singh et al. (1980)
HSM, Hordeum species, mutation + 0 0.~~ Sharma et al. (1983)
0
TSM, Tradescantia paludosa, mutation - 0 0.~~ Schairer et al. (1978)
TSI, Tradescantia paludosa, micronuclei ~
+ 0 0.~~ Ma et al. (1984) ::
ACC, Allum cepa, chromosomal aberrations + en
0 50.000 Rao et al. (1987)
HSC, Hordeum species, chromosomal aberrations + 55.~~
HSC, Hordeum species, chromosomal aberrations
HSC, Hordeum species, chromosomal aberrations
+
0
0 100.~~
Bhan & Kaul (1975)
Panda & Sharma (1979) rCd
+ 0 0.~~ Sharma et al. (1983) ~
VFC, Vicia taba, chromosomal aberrations + 0 125.~~ Amer & Ali (1986) t'
PLC, Capsicum annuum, chromosomal aberrations + 0 500.0000 Devadas et al. (1986)
Vi
w
DMG, Drosophila melanogaster, crossing-over/recombination - 0 350.~~ Jayasuriya & Ratnayake
(1973)
DMX, Drosophila melanogaster, sex-linked recessive lethal - 0 350.0000 Jayasuriya & Ratnayake
mutations
(1973)
DMX, Drosophila melanogaster, sex-lInked recessive lethal - 0 0.0900 Kramers & Knaap (1978)
mutations
DMX, Drosophila melanogaster, sex-linked recessive lethal - 0 0.0700 Sobels & Todd (1979)
mutations
*, Drosophila melanogaster, polygenic viability mutations + 0 4.0000 Marcos et al. (1989)
*, Drosophila melanogaster, autosomal recessive lethal + 0 0.7500 Hanna & Dyer (1975)
mutations
Table 6 (contd)

LED/HID
Without With
exogenous exogenous
metabolic metabolic
sytem system
DMC, Drosophila melanogaster, chromosomal aberrations + 0 1. ~~ Gupta & Singh (1974)

DIA, DNA strand breaks, Chinese hamster V-79-4 cells in vitro (+ ) 0 200.~~ Green et al. (1974)
G90, Gene mutation, Chine se hamster V79 lung cells - 0 1100.~~ Aquilina et al. (1984)
(ouabain)
G5l Gene mutation, mouse lymphoma L5178Y cells in vitro. + 0 25.~~ US National Toxicology
tk locus Program (1989)
sic, Sister chromatid exchange, Chinese hamster cens in vitro + 0 20.~~ Tezuka et al. (1980) 0
sic, Sister chromatid exchange, Chinese hamster cells in vitro + 0 7. ()
""
Nishio & Uyeki (1981) ()
22.~~ ::
0r
sic, Sister chromatid exchange, Chinese hamster cells in vitro + 0 Shirasu et al. (1984)
sic, Sister chromatid exchange, Chinese hamster cens in vitro + + 25.~~ US National Toxicology
Program (1989)
SIR, Sister chromatid exchange, rat cens in vitro + 10.000 Lin et al. (1988) ~
CIC, Chromosomal aberrations, Chinese hamster cells in vitro -
0
0 1 (). ~~ Sasaki et al. (1980)
0C/
CIC, Chromosomal aberrations, Chinese hamster cells in vitro + 0 110.~~ Tezuka et al. (1980)
CIC, Chromosomal aberrations, Chinese hamster cens in vitro + 0 130.0000 Ishidate et al. (1981)
CIR, Chromosomal aberrations, rat cens in vitro + 0 80.~~ Lin et al. (1988)
TCS, Cell transformation, Syrian hamster embryo cells in vitro + 0 0.0000 Tu et al. (1986)
TCL, Cell transformation, rat tracheal epithelial cells in vitro + 0 40.0000 Lin et al. (1988)
UHL, Unscheduled DNA synthesis, human lymphocytes in vitro + 0 5.~~ Perocco & Fini (1980)
UIH, Unscheduled DNA synthesis, EUE human cells in vitro + 0 14365.0000 Aquilina et al. (1984)
SHF, Sister chromatid exchange, human fibroblasts in vitro - 0 10. () Nicholas et al. (1978)
SHL, Sister chromatid exchange, human lymphoctes in vitro - 0 10.000 Nicholas et al. (1978)
CHL, Chromosomal aberrations, human lymphoctes in vitro - 0 40.0000 Dean (1972b)
HMM, Host-mediated assay, Salmonella typhimurium in mice - 0 25.00 Buselmaier et al. (1972)
HMM, Host-mediated assay, Salmonella typhimurium in mice - 0 8.~~ Voogd et al. (1972)
HMM, Host-mediated assay, Saccharomyces cerevisiae in mice - 0 100.~~ Dean et al. (1972)
UPR, Unscheduled DNA synthe sis, rat hepatocytes in vivo - 0 35.~~ Mirsalis et al. (1989)
SV A, Sister chromatid exchange, mouse lymphocytes in vivo - 0 25.~~ Kligerman t al. (1985) N
\0
V)
Table 6 (contd) N
\0
.t
LED/HID
Without With
exogenous exogenous
metabolic metabolic
sytem system
MV, Micronucleus test, mouse bone-marrow cens in vivo 0 0.0150 Paik & Lee (1977)
CBA, Chromosomal aberrations, mou se bone-marrow cens
in vivo
CBA Chromosomal aberrations, Chinese hamster bone marrow _
0 15.0000 (16-h inhaL.) Dean & Thorpe (1972a)
-
~
0 15.0000 Dean & Thorpe (1972a)
in vivo ~
CBA, Chromosomal aberrations, mouse bone-marrow cens 0 100.0000 a:
Kurinnyi (1975)
in vivo 0
CBA, Chromosomal aberrations, mouse bone-marrow cens 0 10.~~ Moutschen-Dahmen et
z
0
in vivo
CBA Chromosomal aberrations, mouse bone-marrow cens
al. (1981) 0
0 0.3300c Degraeve et al. (1984a)
in vivo
~
CBA, Chromosomal aberrations, Syrian hamster bone marrow ( + )
0 15.~~ Dzwonkowska & Hübner ::
cr
in vivo
CCC, Chromosomal aberrations, mouse spermatoctes in vivo (1986) ~
CCC, Chromosomal aberrations, mouse spermatoctes in vivo
0 0.3300c l)egraeve et al. (1984a) 0
0 10.0000 Degraeve et al. (1984b)
CGC, Chromosomal aberrations, mouse spermatogonia in vivo E
0 0.3300c Degraeve et al. (1984a) a:
CGC, Chromosomal aberrations, mouse spermatogonia in vivo tT
0 10.~~ Degraeve et al. (1984b)
DLM, Dominant lethal test, mice 0 53.0000 (16-h inhaL.)
VI
w
Dean & Thorpe (1972b)
DLM, Dominant lethal test, mice 0 16.500 Epstein et al. (1972)
DLM, Dominant lethal test, mice 0 50.0000 Dean & Blair (1976)
DLM, Dominant lethal test, mice 0 10.0000 Moutschen-Dahmen et
al. (1981)
DLM, Dominant lethal test, mice 0 0.3300c Degraeve et al. (1984a)
BID, Binding to caif thymus DNA in vitro + 0 2000.0000 Löfroth (1970)
BIO, Binding to DNA, Escherichia coli WP2 uvrA in vitro + 0 300.0000 Lawley et al. (1974)
BIO, Binding to DNA, HeLa cens in vitro + 0 215.~~ Lawley et al. (1974)
BID, Binding to DNA, Escherichia coli B in vitro + 0 155.~~ Wennerberg & Löfroth
BID, Binding to caif thymus DNA in vitro + (1974)
0 3.7500 Segerback (1981)
Table 6 (contd)

LED/HID
Without With
exogenous exogenous
metabolic metabolic
sytem system
u-
("
BIp, Binding to RNAIprotein, Escherichia coli WP2 uvrA in vitro + a 215.0000 Lawley et al. (1974) ~
Blp, Binding to RNAIprotein, HeLa cens in vitro +
BIp, Binding to RNA/protein, Escherichia coli B in vitro +
a
o
215.0000
155.0000
Lawley et al. (1974)
Wennerberg & Löfroth
ot'
(1974) ~
BVD, Binding to DNA rats in vivo a 0.0150 (12-h inhaL.) Wooder et al. (1977) oC/
BVD, Binding 10 DNA, mIce in vivo a 0.4000 Segerback (1981)
BVp, Binding to RNA/protein, rats in vivo o 0.0150 (12-h inhaL.) Wooder et al. (1977)
SPF, Sperm morphology, FI mice in vivo (+ ) o 12.0000 Wyrobeck & Bruce
(1975)
*Not displayed on profile

a+, positive; (+), weakly positive; -, negative; 0, not tested, ?, inconclusive (variable response in several experiments within an adequate study)
bln~vitro tests, Ilg/m1; in~vivo tests, mg/kg bw
CIn drinking-water
t5
Vl
5.2 Carcinogenicity in humans

One case-control study of leukaemia in the USA found an association with use of
dichlorvos on animaIs; there were few exposed subjects, and they had potential exposure to
many pesticides.
5.3 Carcinogenicity in experimental animais
Dichlorvos was tested for carcinogenicity by oral administration in two experiments in
mice and in three experiments in rats. A few rare oesophageal squamous-cell tumours were
found in mice treated with dichlorvos in the diet. A dose-related increase in the incidence of
squamous-cell tumours (mainly papillomas) was noted in the forestomachs of mice that
received dichlorvos in corn oil by gavage. ln rats that received dichlorvos in water by gavage,
a few squamous-cell papilomas of the forestomach were seen. ln rats that received
dichlorvos in corn oil by gavage, a dose-related increase in the incidence of mononuclear-cell
leukaemia and an increased incidence of pancreatic acinar-cell adenomas were observed in
males.
5.4 Other relevant data
A variety of studies in several species did not demonstrate developmental toxicity due to
dichlorvos.
ln vitro, dichlorvos phosphorylates esterases to a greater extent than it methylates
nucleophiles; the likelihood of DNA methylation in vivo is extremely smalL.
Immunosuppression has been noted after short-term administration of high doses of
dichlorvos which are associated with profound cholinergie hyperstimulation.
No data were available on the genetic and related effects of dichlorvos in humans.
Dichlorvos was not shown to have genetic activity in various assays in mammals in vivo. It
induced gene mutation and chromosomal damage in cultured mammalian cells "and in
insects, plants, fungi, yeast and bacteria.
5.5 Evaluation 1
There is inadequate evidence in humans for the carcinogenicity of dichlorvos.

There issuffcient evidence in experimental animais for the carcinogenicity of dichlorvos.
Overall evaluation
Dichlorvos is possibly carcinogenic to humans (Croup 2E).
6. References
Abbott, D.C., Crisp, S., Tarrant, K.R. & Tatton, l.O'G. (1970) Pesticide residues in the total diet in
England and WaIes, 1966-1967. III. Organophosphorus pesticide residues in the total diet. Pestic.
Sei., 1, 10-13
lFor definition of the italicized terms, see Preamble, pp. 26-28.

DICHLORVOS 297
Adler, B., Braun, R, Schöneich, J. & Böhme, H. (1976) Repair-defective mutants of Proteus mirabilis
as a prescreening system for the detection of potential carcinogens. Biol. Zbl., 95, 463-469
Agrochemical Producers' Association of Finland (1989) 1988 Finnish pesticide sales. AGROW, 97,
11-12
Amer, S.M. & Ali, E.M. (1986) Cyological effects of pesticides. XVII. Effect of the insecticide
dichlorvos on root-mitosis of Vicia faba. Cytologia, 51, 21-25
American Conference of Governmental Industrial Hygienists (1989) Threshold Limit Values and
Biological Expsure Indices for 1989-1990, Cincinnati, OH, p. 20
AMYAC Chemical Corp. (1986) Product Data Sheet: DDVP Technical, Los Angeles, CA
AMVAC Chemical Corp. (199) Material Safety Data Sheet: DDVP Technical Grade, Los Angeles, CA
Anon. (1972) Yapona~ insecticide. AnaL. Methods pestic. plant growth Regul., 6, 529-533
Anon. (1974) Studies on dichlorvos. Food Cosmet. Toxicol., 28, 765-772
Aquilina, G., Benigni, R, Bignami, M., Calcagnile, A, Dogliotti, E., Falcone, E. & Carere, A. (1984)
Genotoxic activity of dichlorvos, trichlorfon and dichloroacetaldehyde. Pestic. Sei, 15, 439-442
Attfield, J.G. & Webster, D.A. (1966) Dichlorvos. Chem. Ind., 12 February, pp. 272-278
Bedford, C.T. & Robinson, J. (1972) The alkylating properties of organophosphates. Xenobiotica, 2,
307-337
Ben-Dyke, R, Sanderson, D.M. & Noakes, D.N. (1970) Acute toxicity data for pésticides. World Rev.
Pest Control, 9, 119-127
Bhan, A.K. & Kaul, RL. (1975) Cytotoxic activity of dichlorvos in barley. Indian J exp. BioL., 13,
403-405
Bisby, J.A & Simpson, GoR. (1975) An unusual presentation of systemic organophosphate poisoning.
Med. J Aust., 2, 394-395
Blair, Do, Hoadley, E.C. & Hutson, D.H. (1975) The distribution of dichlorvos in the tissues of
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DICHLORVOS

if Solubility: Completely miscible with aromatic hydrocarbons, chlorinated hydro-

(i) Octanollwater partition coeffcient (P): log P, 1.47 (WHO, 1989)

piperonyl butoxide (see IARC, 1983c, 1987f), pirimiphos-methyl, propoxur, tetrasul,

Sample matri Sample preparation Assay Limit of Reference

Air Collect vapours on polyurethane GC/ECO Not reported US Environmental

Sample matri Sample preparation Assay Limit of Reference

1.2 Production and use

lleviewed by WHO (1989)

Dichlorvos vaporized in a mushroom house to give 0.2-0.4 mg/m3 degraded rapidly in

Argentina 2 Stored cereals in general

Country or Residue limit Commodities

Country or Residue limit Commodities

Country or Residue limit Commodities

Singapore 0.5 Fruit, grains, vegetables

Country or Residue limit Commodities

USSR 0.3 Bran, grain

Ilrom Health and Welfare Canada (199)

Table 4. Occupational exposure lImIts and guidelines for

Country or region Year Concentrationb InterpretationC

Romania 1987 0.5 TWA

2. Studies of eancer in Humans

2.1 Case reports

2.2 Case-control studies

3. Studies of eancer in Experimental Animais

3.2 Inhalation and/or intratracheal administration

4. Other Relevant Data

Hydrolytic metabolism of dichlorvos to dimethylphosphate and dichloroacetaldehyde,

4.2 lloxic effects

4.2.2 Experimental systems

A series of early studies reported in abstracts also examined reproductive and

4.4.2 Experimental systems

5. Summary of Data Reported and Evaluation

5.1 Exposure data

Test system Resulta Doseb Reference

Test system Resulta Doseb Reference

DMC, Drosophila melanogaster, chromosomal aberrations + 0 1. ~~ Gupta & Singh (1974)

Test system Resulta Doseb Reference

*Not displayed on profile

5.2 Carcinogenicity in humans

There is inadequate evidence in humans for the carcinogenicity of dichlorvos.

lFor definition of the italicized terms, see Preamble, pp. 26-28.

Tinker, J. (1972) The Vapona dossier. New Scí, 53,489-492

Environ. Mutagenesis, 8, 77-98

US Environmental Protection Agency (1980) Preliminary Quantitative Usage Analysis of DDVP,

US National Cancer Institute (1977) Bioassay of DichlOlvos for Possible Carcinogenicity

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