TRICHLORFON JMPR 1978
Explanation
Trichlorfon was evaluated in 1971 and 1975 (FA0/WHO, 1972b,
1976b). Further studies on the spontaneous conversion of
trichlorfon to dichlorvos in vitro and in vivo were considered
desirable. The temporary maximum residue limit for tomatoes was
increased from 0.1 to 0.2 mg/kg at the 1975 Meeting. The limited
additional data provided for consideration by the present Meeting
are evaluated in the following monograph addendum.
EVALUATION FOR ACCEPTABLE DAILY INTAKE
BIOCHEMICAL ASPECTS
In experiments with mice using 14C-labelled trichlorfon some
alkylation of nucleic acids was demonstrated. Based on the urinary
excretion of 14C-methyl guanine, the alkylation potency of
trichlorfon was about 4-10 times lower than that of DDVP (Dedek et
al, 1976). No quantitative data on the methylation of DNA in
tissues were reported. However, 24 hours after the administration,
14C-methylguanine was no longer detectable in liver nucleic acids.
TOXICOLOGICAL STUDIES
Special studies on mutagenicity
A dominant lethal test was performed in mice. Groups of male
mice of two different strains received a single i.p. injection of
1.6 m.mol/kg trichlorfon (405 mg/kg) or its metabolites (methyl-2,
2-dichloro-1-1-dihydroxy ethane-phosphonate) (390 kg/kg) and
dichloroacetaldehyde (170 mg/kg). The animals were noted. The
average number of living pups was lower in the treated groups then
in the controls. An increased pre-implantation loss was observed
only in one strain. No differentiation was made between early and
late foetal losses. Although the differences with regard to the
number of living pups were statistically significant within one
experiment they were within the range of variation seen in a
different control series (Fisher, et al, 1977).
Special studies on carcinogenicity
Three carcinogenicity studies were performed with groups of 30
AB/Jona mice of each sex. The animals were either treated with oral
doses of 0 and 30 mg/kg b.w., i.p. doses of 0 and 28.2 mg/kg b.w.
or were topically treated with 0 and 0.25 ml of a 1% solution
corresponding to 2.5 mg a.i. per animal. The doses were
administered twice a week for a period of 75 weeks (2-week
treatment interruption in the 46th and 47th week). After 80 weeks
the experiments were concluded.
The treatment caused reduction of the mean survival time and
body weight gain in the treated animals. The separate incidences of
benign and malign tumours respectively and the tumourspecies or
-localisation did not reveal any significant difference between
treated or control animals (Teichmann and Hauschild, 1978).
A summary of carcinogenicity study in mice which were
administered 100, 300 and 1000 ppm. Trichlorfon in the diet during
lifetime was available. Except for inhibition of cholinesterase no
other adverse effects and no increase of the incidences of tumours
was reported (Anonymous, 1978). In abstract form carcinogenicity
studies in mice and rats were reported showing an increased
incidence of tumours at dose levels of 0.03 - 30 mg/kg. Pertinent
information such as numbers of animals tested, duration of
treatment, route of administration, nature of and localisation of
tumours was not given (Petrouskaja and Knzmenko, 1978)
30 male and 35 female rats received oral doses of 22 mg/kg
b.w. or i.p. doses of 12 mg/kg b.w. twice a week for up to 90
weeks. The control groups consisted of 25 animals of each sex. The
study was terminated after 118 weeks.
The mean survival time was lower in test animals compared to
control animals, but, no intergroup differences between treatment
and control groups were evident with respect to incidences of
malign and benign tumours, tumour-species and -localisation
(Teichmann et al., 1978).
Groups of 23 male and 25 female hamsters were administered
intraperitoneally 20 mg trichlorfon 1 kg b.w. once weekly for 90
weeks, 22 males and 23 females served as control. The surviving
animals were killed at 100 weeks after initiation of the
experiment. Growth rate was lower in treated animals than in
controls. By week 80 the survival rate was 50% in treated animals
and 70% in male and 65% in female controls. The tumour incidence
was similar in all groups. 5 and 7 in treated males and females
versus 4 and 5 in the controls (Teichmann and Schmidit, 1978).
Special study on potentiation
The simultaneous oral administration of trichlorfon and
demeton-s-methyl to male rats in equitoxic doses resulted only in
additive toxicity (Flucke and Kimmerle, 1977).
Acute Toxicity
Species Sex Route LC50 Reference
mg/m3
Rat M, F inhalation 533 Kimmerley 1975a
(4 hours)
Sheep
Treatments of sheep by bathing them in 0.025% trichlorfon
solution were well tolerated by the animals and only a slight
reduction of the cholinesterase activity in blood of about 20%
compared to normal values was observed. Pour-on application with 6%
trichlorfon solution at dose levels of 36 mg/kg b.w. and 60 mg/kg
b.w. caused inhibition of the blood cholinesterase activity of 30%
and 70%. These changes in the enzyme activity were not accompanied
by clinical symptoms of poisoning (Mieth et al., 1975).
Short Term Studies
Rat
Groups of 10 male and 10 female rats were exposed 6 hours a
day over a 3-week period (total of 15 exposures) to an atmosphere
containing trichlorfon at concentrations of 0, 12.7, 35:4 and 103.5
mg/m3. Exposures to concentrations of up to 35.4 mg/m3 were
tolerated without any symptoms, whereas rats exposed to 103.5
mg/m3 showed slightly affected health condition (no details
available). Body weight gain, parameters of haematological and
clinical chemistry examinations and urinalyses were not influenced
at any exposure levels.
Cholinesterase inhibition of 42, 31 and 22% was found in
plasma, erythrocytes and brain respectively in male animals at
103.5 mg/m3; female animals showed dose-dependent inhibition
values of 39, 26 and 26% at 35.4 mg/m3 and 48, 44 and 47% at 103.5
mg/m3 in plasma, erythrocyte and brain respectively. The only
significant alteration in relative organ weight was found in male
animals showing a dose related increase of the relative
spleen-weight of about 20 and 25% at the 35.4 and 103.5 mg/m3
exposure levels. No abnormal histological findings were observed in
any of the tissue microscopically examined (Kimmerle, 1975b)
COMMENTS
The Meeting evaluated data on mouse and rat carcinogenicity
studies, mutagenicity studies, and the results of studies on DNA
alkylation.
A mouse dominant lethal study could not be fully evaluated,
since the available data did not differentiate between early and
late foetal death.
Data on DNA alkylation indicated some activity with regard to
7-methyl guanine a reaction which has been postulated as indicative
of carcinogenic activity. However, the Meeting evaluated two rats,
three mice and one hamster long-term carcinogenicity studies and no
evidence of tumour induction was observed in any of these studies.
The Meeting therefore changed the temporary ADI to an ADI.
TOXICOLOGICAL EVALUATION
Level causing no toxicological effects
Rat: 50 ppm in the diet equivalent to 2.5 mg/kg bw
Dog: 50 ppm in the diet equivalent to 1.25 mg/kg bw
Estimate of acceptable daily intake for man
0 - 0.01 mg/kg bw
RESIDUES IN FOOD AND THEIR EVALUATION
USE PATTERN
In addition to the use patterns mentioned in previous
monographs, the use of trichlorfon for controlling lepidopterous
larvae, sawfly in apples and pears shortly before harvest (Anon.,
1978d) and the post-harvest use for controlling vinegar fly (Anon.,
1978a) have been reported.
RESIDUES RESULTING FROM SUPERVISED TRIALS
Residues resulting from post-harvest treatment of sultanas are
given in Table 1.
TABLE 1. Residues resulting from post-harvest treatment of sultanas
Dosage No. of Days after Residue, mg/kg
treatments last application
10 g/100 kg 1 15 0,15; 0,05; 0,1; 0,1
0,15; 0,1; 0.05; 0,05
2 9 0,25; 0,15; 0,15; 0,25; 0,1
0,15; 0,05; 0,1; 0,10
Results of supervised trials carried out on various plants as
foliar treatment are summarized in Tables 2 and 3 (Anon., 1978,c,d;
Nihon Tukushu, 1978).
FATE OF RESIDUES
In animals
Lactating cows were treated with different formulations of
trichlorfon at dose rates of 20-45 mg/kg. The trichlorfon residues
reached a maximum of 0.6-6 mg/kg in the blood depending on the
formulation during the first 12 hours. The residue in the milk is a
function of the trichlorfon concentration in the blood and the
equilibration in rapid (Table 4). The total residue detected contained
less than 5% of the metabolite dichlorvos in the blood and less than
2% in the milk.
The milk of each of ten cows contained less than 0.05 mg/kg of
trichlorfon residue 48 hours after a dermal pour-on application of
neguvon solution at a dose rate of 50 mg/kg (Juskiewicz, 1974).
Oral administration of 30 mg/kg trichlorfon resulted in a maximum
residue of 0.55 mg/kg in milk one hour after treatment. The level was
0.007 mg/kg after 24 hours. Small amounts of dichlorvos,
trichloroethanol and dimethyl phosphate were detected in the milk 3
hours after treatment but none was detectable after 9 hours (Nakahara,
1972).
Filatov et al., (1972) found that 0.32% of trichlorfon applied
dermally to cows was excreted with the milk in the first 24 hours. The
residues in the milk decreased rapidly after treatment trichlorfon;
1 h 1.7 mg/kg; 24 h 0.2 mg/kg; 36-96 h traces; dichlorvos 1 h 0.58
mg/kg; 3 h 0.29 mg/kg; 6-24 h traces.
The milk fat contained considerably lower residues than the whole
milk, indicating that trichlorfon is hydrophilic.
It should be pointed out that the evaluation of trichlorfon in
1971 contains a misinterpretation of the work of Arthur and Casida on
the metabolism of butonate in rats stating that "45% of the
administered dose was found in the fat." In fact the amount of
butonate and its metabolite trichlorfon was very low, but the ratio of
the compounds detected in the fat was as follows: butonate 17.9%,
trichlorfon 44.6%, hydrolysis product 37.5%. No measurement of
residues in the fat after direct treatment with trichlorfon was
mentioned in the papers available for evaluation.
Subcutaneous treatment of pigs with trichlorfon resulted in
somewhat lower residues in the meat and small intestine (ileum) than
in the blood. Dichlorvos was the only metabolite found in the blood
and ileum (Table 5; Dedek and Schwarz, 1969).
TABLE 2. Residues resulting from supervised trials.
Crop Country Year No. Rate Formulation
kg ai/ha 1-3 4-6 7-10 13-15 18-21 27-29
or as
specified
Cabbage(1) Japan 1975 6 2-5 EC 50% 0.14-0.05 0.08-0.03
Japan 8 0.23-0.07 0.05-0.03
Finland not 0.6 0.5 0.4 0.2
stated
Chinese(1) Japan 1972 3 2 EC 50% 0.13-0.04 0.09-0.02
cabbage
Japan 5 0.06 0.05
Japan 6 0.13 0.086
Citrus(1) Japan 1973 5 3 EC 50% <0.003
Eggplant(1) Japan 1972 5 1 EC 50% 0.02-0.03 0.01-<0.005 <0.005
8 0.02 0.007-<0.005 <0.005
Japanese(1) Japan 1975 3 0.063% EC 50% 0.57-0.53 0.36 0.3-0.25
kaki persimmon 18 l/tree
Japanese Japan 1971 2 EG 50% 2.76-0.22 0.26-0.09 0.07-0.02
radish leaf 5
root(1) 0.12-0.07 0.07-0.03 0.05-0.01
leaf 8 EC 50% 1.4-0.9 0.77-0.1 0.09-0.03
root(1) 0.12-0.008 0.04-0.03 0.04-0-01
Potatoe Japan 1976 6 2 EC 50% 0.03-0.02 0.02-<0.008
Black Finland 1.3 g/ not 2.6 0.2
currant(1) plant stated
TABLE 2. (Cont'd)
Crop Country Year No. Rate Formulation
kg ai/ha 1-3 4-6 7-10 13-15 18-21 27-29
or as
specified
Raspberry Finland 2 0.8 5.6
linean
0.5-0.6 not 0.7-2.9
g/plant stated
Red currant Finland 16 g/ not 25 12
plant stated
Strawberry Japan 1976 3 2 EC 50% 1.4 0.33
5 4.6 0.74
Strawberry Japan 3 3 EC 50% 2.12 0.46
5 3.31 1.06
1 1.6-2.4 0.02
Sugarbeet(1) Japan 1975 6 1.5 EC 50% 0.05-0.02 0.04-0.02
8 0.04-0.02 0.024-0.02
Finland 2 0.64 not 0.05
stated (48 days)
Watermelon(1) 1976 6 2 EC 50% 0.008
(1) These crops were analyzed for dichlorvos but none was detected (limit of detection 0.005 mg/kg). Low levels of dichlorvos were found
in strawberry (see Table 7).
TABLE 3. Residues resulting from supervised trials.
Application Residues (mg/kg)1 at intervals (days) after application
Crop Country Year No. Rate, Formulation
kg ai/ha 0/1 2 3 4-5 7-8 9-10
Apple, Netherland 1976 1 1.2 WP 80% 0.8
winston (0.6-0.9)
Apple, Netherland 1976 1 1.2 WP 80% 1.4
golden (0.-1-1.9)
Brussels Netherland 1970 3 1.2 WP 80% 0.26 0.26 0.1
sprouts (0.15-0.4) (0.15-0.4) (0.08-0.13)
1970 4 1.2 WP 80% 0.29 0.1 0.05
(0.08-0.9) (0.08-0.1) (0.03-0.05)
Carrot Hungary 1976 1 0.8 WP 50% 0.5 0.1 0.02 0.01 0.012
Green Hungary 1976 1 1.0 WP 50% 0.13 0.06 0.05 0.03 0.02 0.02
pepper (14-16 days)
Kale Netherland 1976 1 1.0 WP 80% 0.26
(0.12-0.33)
Kohlrabi Netherland 1976 1 1.0 WP 80% 0.02
(0.01-0.02)
Parsley Hungary 1976 1 0.8 WP 50% 0.2 0.02 0.01 0.012
Red cabbage Netherland 1976 1 1.0 WP 80% 0.05
(0.03-0.05)
Savoy Netherland 1976 1 1.0 WP 50% 0.2
cabbage (0.12-0.36)
TABLE 3. (Cont'd)
Application Residues (mg/kg)1 at intervals (days) after application
Crop Country Year No. Rate, Formulation
kg ai/ha 0/1 2 3 4-5 7-8 9-10
Spinach Netherland 1976 1 1.0 WP 80% 4.0
(3.4-5.3)
1976 1 1.0 WP 80% 3.2
(2.1-6.2)
1 Average of 3 or 4 samples
2 Average of 7 samples
TABLE 4. Residues in the blood and milk of cows treated with trichlorfon.
Treatment Dosage, Sample Residue (mg/kg(at intervals (h) after treatment
mg ai/kg bw
2 4 6 8 10 24
Intramuscular, 25 blood 4-6 2-4 1-2 - - -
50% in polyethylene
glycol milk 2.4 1.3 0.7 0.5 0.25 0.1
Pour-on, 2% 20 blood 2 0.5 0.3 0.2 0.1 0.05
in mineral oil milk 1.2 0.5 0.3 0.2 0.1 0.05
Pour-on, 2% 20 blood 0.3 0.5 0.55 0.6 0.6 0.3
in vegetable
oil milk 0.2 0.3 0.35 0.35 0.2 0.1
Sheep were treated with an aerosol formulation of trichlorfon at
49/m3 and kept in a closed pen for 3 hours. The animals were
slaughtered 1, 3, 5, 7 and 10 days after the treatment (Nepoklonov and
Bukstynor). The residues of trichlorfon and dichlorvos was determined
by TLC. The results are summarized in Table 6.
In plants
Strawberries, sugar beets and radishes were treated with
trichlorfon and analysed for both trichlorfon and dichlorvos (limit of
detection 0.005 mg/kg). Dichlorvos was detected in strawberries but
only in the leaves of radishes and sugar beets. The dichlorvos residue
was 20-30 times lower than that of trichlorfon and disappeared at a
rate similar to the parent compound (Table 7).
RESIDUES IN FOOD MOVING IN COMMERCE
The residues found in samples taken from the yield at harvest in
Hungary and known to have been treated are summarized in Table 8. 90%
of the samples contained residues below 0.02 mg/kg.
In routine market surveys in Australia, low residues of
trichlorfon (< 0.1 mg/kg) were found in 9% of the samples analysed
during a 12-month period in 1977-78 (Anon., 1978a). No trichlorfon
residues were detected in 66 total diet samples in England in 1966-67
(Abbott et al., 1970).
NATIONAL MRLs REPORTED TO THE MEETING
The following new or amended MRLs have been reported to the Meeting.
METHODS OF ANALYSIS
A well established multi-residue method (based on acetone
extraction and partition of the diluted extract with methylene
chloride) can be recommended for regulatory purposes
(Methodensammulung zur Rückstandsanalytik, 1976).
APPRAISAL
The new data available for evaluation support the conclusions of
the previous Meetings and indicate that the concentration of
trichlorfon in various organs after direct application to animals
largely depends on the treatment procedure and the formulation used.
The residue level in organs and tissues reached its maximum within 12
hours of dosing in cows and pigs. Only low residues were detectable
after 24 hours. The fat of milk contains much lower residue than the
whole milk since trichlorfon is hydrophilic. Trichlorfon was detected
in organs and tissues of sheep 7 days after aerosol treatment.
TABLE 5. Residues of trichlorfon and its metabolite dichlorvos in pigs after subcutaneous treatment (25 mg/kg).
Sample Residue (mg/kg) at intervals (h) after treatment
0.5 1 1.5 2 3 4 6 12 24
trichlorfon
Blood 9-10 5-6 4-5 3-4 1-2 0.2 -
Meat 6 5 3-4 2-3 1 0.1 <0.01
Ilium 5-6 5-6 3 1.5 1 - -
dichlorvos
Blood 0.5-1 0.3-0.5 <0.05
Ilium 0.3-0.5 0.2-0.4 <0.1
TABLE 6. Residues of trichlorfon and dichlorvos in organs and tissues of sheep treated with trichlorfon aerosol.
Sample Residue (mg/kg) at intervals (days) after treatment
1 3 5 7 10
Trichlorfon Dichlorvos Trichlorfon Dichlorvos Trichlorfon Dichlorvos Trichlorfon Dichlorvos Trichlorfon Dichlorvos
Muscle 2.3 0 0.8 0 0.6 0 Trace 0 0 0
Heart 1.7 0 0.3 0 0.3 0
Liver 1.7 0 1.4 0 1.1 0.8 0.6
Spleen 2 0 0.8 0 0.3 1 Trace 0 0 0
Lung 1.7 0 0.3 0 Trace 0
Kidney 2.3 0 0.5 0.8 0.6 1.2 0.3
Brain 1.4 0 0.3 0 0.3 0 -
Milk 0.8 0 0.6 0 0.4 0 -
TABLE 7. Trichlorfon and dichlorvos residues in crops treated with trichlorfon.
Crop Dosage No. of Days after Residue, mg/kg
kg a.i./ha treatments last application Trichlorfon Dichlorvos
Strawberry 2-3 3 13-14 2.1-1.4 0.08
20-21 0.46-0.33 <0.005
5 6-7 4.6-3.3 0.23-0.1
13-14 1.1-0.74 0.04-0.02
Sugar beet 1.5 6 6-7 0.24-0.06 0.02-0.01
13-14 0.07-0.02 <0.01
8 6-7 0.29-0.05 0.06-0.02
13-14 0.08-0.02 0.02-0.003
Radish (leaf) 1.5-2 8 1 1.4-0.22 0.006
5 0.77-0.1 <0.004
10 0.09-0.03 <0.004
TABLE 8. Residues of trichlorfon in samples taken from fields at or about harvest.
(Hungary; MRL = 1 mg/kg)
Crop No. of No. of samples and their mean residues in the ranges
samples mg/kg shown *
0.5 - 1 0.02 - 0.5 0.02
No. Mean No. Mean No.
Apple 184 1 0.54 9 0.14 174
Apricot 40 2 0.69 4 0.21 34
Bean 18 1 0.52 0 0. 17
Cabbage 83 0 0.0 23 0.10 60
Carrot 37 0 0.0 1 0.04 36
Cauliflower 36 2 0.60 5 0.19 29
Cherry 106 1 1.0 8 0.15 97
Cucumber 21 0 0.0 0 0.0 21
Grape 118 0 0.0 7 0.18 111
Kale 40 3 0.71 6 0.15 31
Kohlrabi 33 1 0.6 7 0.16 25
Lettuce 9 1 0.78 1 0.12 7
Paprika 53 0 0.0 3 0.06 50
Parsley 20 0 0.0 1 0.02 19
Peach 67 1 0.58 6 0.15 60
Pear 54 0 0.0 4 0.18 50
Plum 42 1 0.8 1 0.08 40
Potatoe 212 1 0.95 17 0.14 194
Radish 18 0 0.0 1 0.07 17
TABLE 8. (Cont'd.)
Crop No. of No. of samples and their mean residues in the ranges
samples mg/kg shown *
0.5 - 1 0.02 - 0.5 0.02
No. Mean No. Mean No.
Red currant 16 0 0.0 2 0.09 14
Sour cherry 51 0 0.0 13 0.17 38
Spinach 15 0 0.0 0 0.0 15
Strawberry 93 4 0.72 2 0.03 87
Tomatoe 53 0 0.0 1 0.05 52
* No residues above 1 mg/kg were found.
TABLE 9. National MRLs reported to the Meeting
Country Commodity MRL, mg/kg
Australia Dried fruits 2
Bananas, peaches 0.2
Brussels sprouts
Caluiflower, kale
Sweetcorn, celery
Beetroot
Raw cereals 0.1
Vegetables (except those above) 0.1
Milk, sugarbeet 0.05
Sugar cane 0.05*
TABLE 9. (Cont'd.)
Country Commodity MRL, mg/kg
the Netherlands
Established Fruit 0.5
Vegetables 0.5
Under Consideration
Raw cereals 0.2
Sugar beet 0.05
Peanut (shelled) 0.1
Milk and milk products 0.05
Meal and meal products 0.1
Other food commodities 0.05*
Sweden Fruit and vegetables 0.5
* At or about the limit of determination.
After treating strawberries, sugar beets and radishes with
trichlorfon, residues of dichlorvos were detected In strawberries but
only in the leaves of radishes and sugar beets. The level of
dichlorvos was 20-30 times lower than that of trichlorfon.
RECOMMENDATIONS
With the establishment of an ADI, the previously recommended
temporary MRLs are converted to MRLs.
In the light of new use patterns and residue data from supervised
trials on various commodities some previous recommendations are
amended and additional MRLs are recommended.
Commodity MRL, mg/kg Pre-harvest (pre-slaughter)
intervals on which
recommendations are based
(days)
Amended recommendations
Apple 2 10
Strawberries 1 21
Cabbage 0.5 10
Additional recommendations
Grapes 0.5 14
Meat of sheep 0.1 7
Radishes 0.1 10
Parsley 0.05 10
Carrots 0.05 10
Eggplants 0.05 14
FURTHER WORK OR INFORMATION
Desirable
1. Submission of full reports of carcinogenicity studies available
to the Meeting in summary form only and therefore not considered.
2. Further studies on the spontaneous conversion of trichlorfon to
dichlorvos in vitro and in vivo and of the possible intermediates
involved.
3. An adequate dominant lethal study in mice.
4. Residue data from recent supervised trials or from selected
surveys on commodities on which trichlorfon is known to be used, where
there is evidence of good agricultural practice.
REFERENCES
Abbott, D.C., Crips, S., Tarrant, K.R., Tatton, J.O'G. Pesticide
(1970) residues in the total diet in England and Wales,
1966-1967. Pestic. Sci. 1; 10-13.
Arthur, B.M., Casida, J.E. Biological activity of several
(1958) O-O-dialkyl alpha-acyloxyethyl phosphonates J.
Agr. Food Chem. 6; 360-365.
Anonymous Unpublished summary from the Institue of Comparative and
(1978) Human Toxicology, Albany (USA) submitted by Bayer.
Anonymous Information on trichlorfon from Australia.
(1978a)
Anonymous Information on trichlorfon from Finland.
(1978b)
Anonymous Information on trichlorfon from the Netherlands
(1978c)
Anonymous Information on trichlorfon from Sweden.
(1978d)
Dedek, W., Koch, H., Uhlenhut, G., Bröse, F. Zur Kenntnis der
(1969) Umsetzung von 3H-trichlorphon zu DDVP,
Zeitschrift f. Naturforschung, Serie B. 24
663-664.
Dedek, W., Schwarz, H. Zur Rückstandsbildung von
(1970) 32p-markierten/Organophosphorinsktiziden bei
landwirschaftlichen Nutztieren/Archir
experimentelle Veterinaermedizin 24 719-726.
Dedek, W., Lobs, K.H., Fischer, G.W. and Schmidt, R. Alkylation
(1976 of guanine in Mice in vivo by Organophosphorus
Insecticides. I. Trichlorphone and Butonate. Pest.
Biochem, Physiol. 6, 101-110.
FAO/WHO 1975 evaluations of some pesticides residues in food.
(1977) IAG.P 1975/M/13.
FAO/WHO 1971 evaluations of some pesticides residues in food.
(1972)
Filatov, G.V., Sivokhin, P.A., Metelitsa, V.K. Trichlorfon
(1972) excretion in milk. Veterinariya Moscow/5 102.
Flucke W. and Kimmerle, G. Trichlorfon and Demeton-S-methyl,
(1977) Untersuchungen zur akuten Toxizität nach
gleichzeitiger Verabreichung beider Wirkstoffe.
Unpublished report from Bayer AG, No. 7066,
submitted by Bayer AG.
Juskiewicz, T., Kosmala, K., Zumdrit J. Trichlorfon residues in
(1974) milk following dermal application of neguvon
(Bayer) against hypodermo Bovis. Bull. vel. Inst.
Pulawy 18 93-96.
Kimmerle, G. Acute Inhalation toxicity study on rats. Unpublished
(1975a) report from Bayer AG. Unpublished report from
Bayer AG, No. 5581, submitted by Bayer AG.
Kimmerle, G. Subacute inhalation toxicity study on rats.
(1975b) Unpublished report from Bayer AG, No. 5582,
submitted by Bayer AG.
Mieth, K., Beier, D. and Losch, K. Untersuchen mit
(1975) Phosphorsäureesterpräparaten beim Rind, Schwein
und Schaf unter besonderer Berücksichtigung der
Cholinesteraseaktivität. 4. Mitteilung: Der
Einsatz von Phosphorsäurepräparaten und deren
Einfluss auf die Acetylcholinesteraseaktivität
beim Schaf. Arch. Exp. Veterinärmed. 29, 501-517.
Methodensammlung zur Rückstandsanalytik von Pflanzenschutzmitteln
Liefenung 1976 s-8 Verlag Chemie GmbH,
Weinheim/Bergstrasse F.R.G.
Nakahara, T. et al. Residues of trichlorfon and its metabolites in
(1972) fresh milk. BotyuKagaku 37 149-154/in
Japanese/English abstract was used only.
Nihon Tokushu, Noyaku Seizo, K.K. Analytical test results on
(1978) residues of trichlorfon.
Nepoklonov, A.A., Bukstynov, V.I. On terms of chlorophos release
from the sheep organizm in aerosol treatment UOK
619:615.777/779:61Y.484:541.12.213:636.32/38.
Petrouskaja, O.G. and Kuzmenko. N.M. Unpublished summary from the
(1978) All-Union Research Institute for Hygiene and
Toxicology, Kiev, USSR.
Teichmann, B. and Hauschild, F. Zur Prüfung von
(1978) O.O-Di-methyl(1-hydroxy-2,2,2-trichloräthyl)-phosp
onat (Trichlorphon) auf kanzerogene Wirkung in
Mäusen durch orale (ösophago-gastrale Sondung),
intraperitoneale und dermale Applikation. Arch.
Geschwulstforschung 48, 301-307.
Teichmann, B., Hauschild, F. and Eckelmann, A. Zur Prüfung von
(1978) O.O-Dimethyl(1-hydroxy-
2,2,2-trichloräthyl)-phosphonat (Trichlorphon) auf
kanzerogene Wirkung in Ratten durch orale
(ösophago-gastrale Sondung) und intraperitoneale
Applikation. Arch, Geschwulstforschung 48,
112-119.
Teichmann, B. and Schmidt, A. Zur Prüfung von
(1978) O,O-Dimethyl(1-hydroxy-2,2,2-trichloräthyl)
phosphonat (Trichlorphon) auf kanzerogene Wirkung
in syrischen Goldhamstern (Resocricetus anratus
Waterhouse) durce intraperitoneale Iniekton.
Arch. Geschmulstforschung 48, 718-721.
See Also:
Toxicological Abbreviations
Trichlorfon (EHC 132, 1992)
Trichlorfon (HSG 66, 1991)
Trichlorfon (JECFA Food Additives Series 51)
Trichlorfon (WHO Food Additives Series 45)
TRICHLORFON (JECFA Evaluation)
Trichlorfon (WHO Pesticide Residues Series 1)
Trichlorfon (WHO Pesticide Residues Series 5)
Trichlorfon (IARC Summary & Evaluation, Volume 30, 1983)