FAO/PL:1967/M/11/1
WHO/Food Add./68.30
1967 EVALUATIONS OF SOME PESTICIDE RESIDUES IN FOOD
THE MONOGRAPHS
The content of this document is the result of the deliberations of the
Joint Meeting of the FAO Working Party of Experts and the WHO Expert
Committee on Pesticide Residues, which met in Rome, 4 - 11 December,
1967. (FAO/WHO, 1968)
FOOD AND AGRICULTURE ORGANIZATION OF THE UNITED NATIONS
WORLD HEALTH ORGANIZATION
Rome, 1968
DDT
This pesticide was evaluated by the 1966 Joint Meeting of the FAO
Working Party and the WHO Expert Committee on Pesticide Residues
(FAO/WHO, 1967). Since the previous publication the results of
additional experimental work have been reported. This new work and
some earlier studies comparing DDT with its metabolites, DDD and DDE,
are summarized and discussed in the following monograph addendum.
EVALUATION FOR ACCEPTABLE DAILY INTAKE
Biochemical aspects
Induction of hepatic microsomal enzyme activity was found to occur in
a dose-related manner at dietary levels of 1-50 ppm of DDT, but no
induction was found at 0.2 ppm. Maximal induction occurred within the
first three weeks, with fairly constant levels of increased activity
being maintained after that time for the duration (13 weeks) of the
study (Kinoshita et al, 1966).
Daily oral administration of 150 mg/kg body-weight of technical DDT in
the guinea-pig stimulated the formation of polar urinary cortisol
metabolites. Administration of recrystallized DDT did not induce such
an alteration of metabolism. (Balazs and Kupfer, 1966).
Studies on rats receiving 0, 1, 5, 10 and 50 ppm of DDT in their diet
for 4, 8 and 12 weeks, as well as 12 weeks followed by 4 weeks
withdrawal, showed storage in the body fat at all levels with the
possible exception of those receiving 1 ppm. Increased content of DDD
in the diet resulted in an increase in the degree of storage. With
continued ingestion of DDD its accumulation in the fat was progressive
over the 12 week period. DDD appeared to have similar storage pattern
in body fat to reported data on DDT, the major difference being that
DDD disappears more rapidly than DDT when dietary intake of it is
discontinued (Haag and Kampmeier, 1955).
In a comparative study of tissue storage of DDD and DDT, 5 dogs were
placed on 25 mg/kg/day DDD and 5 dogs ware placed on a similar amount
of DDT. Both substances were administered orally in a 10 per cent
solution of corn oil. Fat was found to be the major site of storage of
a similar degree for both substances. Skin and adrenal tissue had the
next highest content and small but measurable amounts were found in
other tissues. Analyses of tissues of pups, born to some dogs during
the course of the experiment showed that both DDD and DDT cross the
placental barrier (Finnegan et al, 1949).
Pure p,p'-DDD, technical DDD and various fractions isolated from the
technical compound were compared in adrenocorticolytic action by
peroral administration in normal dogs. As measured by peripheral
eosinophil response to ACTH administration, urinary
17-hydroxycorticoid excretion and general observation of well-being
and morbidity, no effect of pure p,p'-DDD at 80-200 mg/kg
body-weight/day for up to 60 days was seen, while the technical
product and fractions identified as containing o,p'-DDD were strongly
active. No histological change in the adrenals was found in the
animals fed pure p,p'-DDD, while the technical product produced marked
atrophy. Pure o,p'-DDD was found to produce massive necrosis and
atrophy of the adrenals at 4 mg/kg body-weight/day (Cueto et al,
1958).
In the rat, o,p'-DDD at 300 mg/kg/day orally or 100 mg/kg/day
sub-cutaneous for 3 days, and p,p'-DDD at 100-200 mg/kg/day orally for
3-30 days, have been found to shorten barbiturate sleeping times
markedly. This effect is associated with increased in vitro hepatic
metabolizing enzyme activity and proliferation of smooth endoplasmic
reticulum and is abolished by the administration of ethionine (Straw
et al, 1965; Azarnoff et al, 1966).
In contrast to the rat, while hexobarbital sleeping time in the dog is
decreased, pentobarbital and secobarbital sleeping times are greatly
increased after feeding 200 mg/kg/day of p,p'-DDD (Azarnoff et al,
1966). In dogs given 200 mg/kg/day of technical DDD or recrystallized
p,p'-DDD or 50 mg/kg/day of technical residual liquor from the
recrystallization for 14 days, increased pentobarbital times were
found in all groups, most pronounced after two weeks' administration
and most profound in the animals given technical DDD; of five animals
in this group, one died immediately after the 40 mg/kg pentobarbital
test injection, and two others were sacrificed after 36 hours without
recovery. No gross or microscopic change in the hypothalamus was seen
in any group, and hepatic change was very slight or absent. No change
in the adrenals was seen in the group receiving p,p'-DDD, although the
other two showed typical atrophy. The rate of barbiturate clearance
from the blood was not affected by DDD administration (Nichols et al,
1958).
DDE inhibits the succinoxidase and cytochrome oxidase systems of rat
heart to a lesser degree than DDT (Johnson, 1951).
Acute Toxicity
LD50 mg/kg
Substance Animal Route body weight Reference
DDD Rat Oral 3400 ) Haag and Kampmeier, 1955
DDT Rat Oral 250 )
DDE Mouse Oral 700 von Oettingen and Sharpless (1946)
DDE Mouse Oral 1,000 Domenjoz (1946)
DDE Rat Oral 1,000 Smith, et al (1946)
Short-term studies
Rabbits - Five rabbits given daily doses of DDE at the rate of 50
mg/kg/day died after 11 to 18 days, whereas six other rabbits given
DDT at the same dosage died in 15 to 25 days. The rabbits on DDE
showed fewer clinal effects than those on DDT. On histological
examination of the tissues of the rabbits, as well as the tissues of
the rats on the acute studies, it was found that DDE produced less
injury to the liver than DDT, but slightly greater kidney damage. The
authors estimated that DDE was about 1/6 as toxic as DDT. (Smith et
al, 1946).
Dog - Dogs fed diets containing 100, 500 and 1,000 ppm DDD for 6
months to 2 years showed moderate atrophy of the adrenals at 1,000 ppm
and slight atrophy at the lower levels. The degree of atrophy did not
seem to become progressively greater after the first 6 months (Haag
and Kampmeier, 1955).
Dogs were fed different isomers of DDT, technical DDT, DDD and DDE at
80 mg/kg/day for up to 120 days. The isomers of DDT and technical DDT
killed the dogs in 37 to 55 days. DDD killed the dogs in 80 days,
whereas the dogs on DDE lived the entire period (Woodard et al, 1948).
Long-term studies
Mouse - BALB/c inbred mice were used in a five generation long-term
toxicity study on DDT. Fifteen bigamous families were used for
breeding in each generation. A total of 683 animals were selected from
the five generations in the treated group, and 406 in the control
group.
DDT was added at 2.8 - 3.0 ppm to the feed of the treated group. The
food contained a background contamination of 0.2 - 0.4 ppm of DDT.
Apart from the difference in the levels of DDT in the feed for the two
groups, the animals were kept under identical experimental conditions.
The pre-weaning mortality was very high in the F1 and F2 generations
in both treated and control groups, ranging between 50 and 60 per
cent; in the succeeding generations the mortality declined but
remained higher than that usually observed.
A total of 196 tumours (28.7 per cent) and, additionally, 85 cases of
leukaemia (12.4 per cent) were observed in the treated group. The
corresponding figures for the controls were : 13 (3.2 per cent) and 10
(2.4 per cent). The incidence of neoplasia was higher in the females
than in the males. No tumours were observed in the parental generation
of either group. Neoplasia first appeared in the F1 generation and a
marked difference in incidence between treated and control groups was
observed from the F2 generation onwards. This difference increased in
the later generations. The latent period of tumours is not clearly
stated, although there is some indication that tumours occurred late
in life; nor is it stated whether more than one tumour occurred in the
same animal. The most common neoplasm was leukaemia, followed by
reticulosarcoma and pulmonary adenocarcinoma. The incidence of
pulmonary adenoma, reported to be 5 per cent in the colony, and not
included in the percentages above, was not altered by the DDT
treatment.
The DDT content of adipose tissue in mice of the F3, F4 and F5
generations was 0.7 - 2 ppm in the controls and 5 -11 ppm in the
treated group. Only traces of DDE were found. (Kemény and Tarján,
1966; Tarján unpublished, 1967).
Rats - Groups of 7 male rats each were given diets containing 150,
300, 600, 900, 1,200, 1,800, 2,500, 5,000 and 10,000 ppm of DDD for
one year. All animals at 5,000 and 10,000 ppm died within 10 weeks.
Liver lesions occurred in rats at levels of 900 and above. (Haag et
al, 1948). In another study, a dosage level of 100 ppm DDD produced
slight liver lesions in rats. The author estimated that DDD was 1/2 as
toxic as DDT. (Lehman, 1965).
Observations in man
It has been shown that the storage of DDT in man is directly
proportional to intake over a wide range of doses (0.04 to 35.0
mg/man/day), so that from the level in the fat the daily dose can be
estimated. Thus, it can be calculated that the highest average intake
of DDT of any human population yet observed is slightly less than 2
mg/man/day. From the data which have been reported, it is also
apparent that in the USA, where the levels of DDT and DDE in human fat
have been repeatedly investigated in the general population over a
number of years, no increase has been noted since 1955. (Hayes, 1966).
In 20 industrial workers heavily exposed to DDT for 11 -19 years, it
was estimated from the DDT content of the body fat and from urinary
DDA excretion that the average DDT intake was 17.5 - 18 mg/man/day. No
abnormalities attributable to DDT were found in these workers. (Laws
et al, unpublished).
In men having no industrial exposure to DDT, mean concentrations of
0.0058 ppm of p,p'-DDT, 0.0010 ppm of o,p'-DDT and 0.0114 ppm of
p,p'-DDE were found in the circulating blood, with 90 per cent, 45 per
cent and 87 per cent of the totals respectively in the serum. (Dale et
al, 1966).
A female patient with Cushing's syndrome was given 13.3 mg/kg/day of
DDD (isomer proportion not stated) orally in oil for 18 days, rested
for 39 days, given 34.6 mg/kg/day for 30 days, rested for 73 days,
given 63.1 mg/kg/day for 3 days, rested for 2 days, then given 15.8
mg/kg/day for 4 days. In all, a total of 127 g was administered over
168 days. No change wee seen in urinary 17-ketosteroids or
11-oxy-corticosteroids nor any other signs of improvement in her
adrenal hypertrophy. During the last two courses of treatment, marked
signs of intoxication were seen, i.e. somnolence, depression,
headache, vertigo and nausea and vomiting, remitting during the 2-day
rest period. Because of the failure of this treatment with DDD,
partial adrenalectomy was performed. The left adrenal was found to
have normal histological architecture and a DDD content of 50 ppm
(whole tissue). The DDD content of adipose tissue was 140 ppm.
(Sheehan et al, 1953).
Six males and twelve females with metastatic adrenocortical cancer
were given average courses of treatment of 8-40 g/day of o,p'-DDD for
4 - 8 weeks. All showed anorexia and nausea, regardless of the route
of administration, and many showed CNS depression without alteration
in the results of psychometric examinations. In 5 cases, EEG
examination showed indications of non-specific deterioration. No
clinical chemical evidence of hepatic, renal or myeloid damage was
found. Diminished urinary excretion of 17-ketosteroids and
17-hydroxycorticoids was reported in 14, and objective regression of
metastases in 7. Histological evidence of destruction and functional
impairment of the adrenal cortex was reported, but the incidence and
the number of glands examined microscopically was not given. Of orally
administered DDD, 30-40 per cent of the dose was absorbed and
subsequently concentrated principally in the fat-containing tissues.
About 25 per cent of the daily absorbed dose appeared in the urine as
metabolites, and a lesser and variable percentage in the faeces.
Concentrations of DDD in adipose tissue ranged from 460 to 8750 ppm
and adrenal concentrations from 114 to 987 ppm (Bergenstal et al,
1960; Moy, 1961).
One male and one female were given 1-10 g/day (the "usual maintenance
dose" was stated to be 1-1.5 g/day) of o,p'-DDD for total periods of
one and eight months respectively. CNS depression, nausea and vomiting
were seen in both, and the male experienced a severe cutaneous
reaction. Urinary 17-ketosteroids and 17-hydroxy-corticosteroids were
decreased and plasma 17-hydroxy-corticosteroids were slightly
decreased in the male. On histological examination of an adrenal gland
from the male, normal architecture was found. A complete autopsy was
performed on the female (death was due to myocardial infarction and
ventricular rupture), and no change suggestive of drug intoxication
was found in any organ. The adrenal cortex contained some areas of
focal necrosis believed attributable to the treatment. A third
patient, not reported in detail, was found to have no adrenal
histological changes following a similar regime (Wallace et al, 1961;
Weisenfeld and Goldner, 1962).
A female was treated with a total of 382 g of o,p'-DDD over 105 days.
Some anorexia was noted. Urinary excretion of 17-ketosteroids was
diminished. No alterations in the results of clinical chemical tests
for liver function were seen although a needle biopsy of the liver
showed marked fatty change. Adrenal tissue was not examined. (Gayer,
1962).
Five patients with adrenal adenoma or hyperplasia and eight without
adrenal function, maintained on exogenous cortisol, were given 4-9
g/day of o,p'-DDD orally for 3-42 days. Urinary
17-hydroxy-corticosteroids were reduced in both cases; however, plasma
17-hydroxy-corticosteroid levels and cortisol secretion rates were not
affected, a result that was interpreted as indicating that the drug
had no effect on adrenal function. From the further finding that the
proportion of cortisol excreted as tetrahydrocortisol and
tetrahydrocortisone was markedly diminished and the proportion
excreted as 6-hydroxy-cortisol was increased; the conclusion was drawn
that the effect of DDD on steroid excretion in the human is
accomplished by alteration of the extra-adrenal (presumably hepatic)
metabolism of cortisol. No change was seen in any of several clinical
chemical parameters of hepatic function. Adrenal tissue was not
examined in this study (Bledsoe et al, 1964).
Comments
Since the last evaluation further details on the long-term toxicity of
DDT in multigeneration experiments in mice have become available
indicating a higher incidence of neoplastic disorders in the DDT
group. Though these studies are not yet complete, the results raise
questions which cannot be dismissed. Taking into account the
difficulties of extrapolating these findings to man, an alteration in
the ADI for DDT was not considered justified pending the assessment of
the significance of these findings.
The animal data, with the exception of that for the DDD on dogs, show
that both DDD and DDE are less toxic than DDT. Large doses of DDD have
been used for therapeutic treatment of adrenal disorders in man. It
was concluded that the relatively small residues of DDD associated
with residues of DDT on agricultural products would cause no
deleterious effect on the adrenal glands of humans.
It was decided to treat mixtures of DDT and its metabolites, like DDT
and establish the same ADI for the mixture or of each separately.
TOXICOLOGICAL EVALUATION
Estimate of acceptable daily intake for man
0 - 0.01 mg/kg body weight for DDT, DDD or DDE or any combination
of the three.
Further work required
This will depend on the outcome of further re-evaluation of
carcinogenicity of this chemical in the light of the new data. If
further experiments were necessary the meeting urged that those should
be given a high priority.
EVALUATION FOR TOLERANCES
USE PATTERN
Pre-harvest treatments
DDT is used to a minor extent as a soil treatment, primarily for the
control of cutworms which attack vegetable crops. It is suggested for
use in many countries on a wide variety of food crops. It is suggested
for the control of about 20 different insects which attack cane
fruits, about 50 different insects which attack vegetables, 50
different insects which attack tree fruits, as well as for control of
insects of nut trees and other food crops. The usual rate of
application is about 2 to 4 lb. of the active chemical per acre;
however, some treatments may go as high as 12 lb. per acre.
RESIDUES RESULTING FROM SUPERVISED TRIALS
Although there have been many analyses made for DDT in agricultural
products, many of then were not made on controlled experiments
designed explicitly to ascertain the fate of the residue following
application. A summary of numerous data, which is too long to
reproduce here and which contains the related bibliography, is held at
the FAO headquarters in Rome. Table 1 has been prepared from this
summary. It contains estimates of the average high residues likely to
result from the practical use of DDT to control insects which attack
the different food commodities or that in animal products from animals
exposed to "unavoidable" or very limited feed residues.
TABLE 1
Residues of DDT resulting from good agricultural practice
Crop Type Preharvest Usage Resulting
period days lbs/A residue ppm
Tree fruits
Apples and quinces 30 12 7
(42 if more than
3 applications)
Peers " 12 7
Apricots and 30
nectarines (42 if more than 12 7
1 application)
Cherries 30 8 3.5
Peaches 30 8 7
Plums 30 8 3.5
Citrus
All citrus fruits 30 4 3.5
TABLE 1 (cont'd)
Residues of DDT resulting from good agricultural practice
Crop Type Preharvest Usage Resulting
period days lbs/A residue ppm
Tropical Fruits
Avocados 30 12 3.5
Guavas Soil application only 1
Mangoes 30 12 7
Papayas 30 8 3.5
Pineapples 90 3 1
Cranberries
and small fruits
Blackberries )
Boysenberries ) Do not apply after 2 1
Loganberries ) fruit forms
Raspberries )
Blueberries 21 2 7
Cranberries 35 6 7
Grapes 40 1.5 7
lbs/100 gal.
Strawberries Do not apply after 4 1
fruit forms
Melons 5 12 7
Leafy vegetables
Celery 3 - 4 weeks 1.2 1
Collards 21 2.5 3.5
Endive Do not apply after 2 1
seedling stage
Kale 21 2.5 3.5
Leaf lettuce Do not apply after 2.5 1
seedling stage
TABLE 1 (cont'd)
Residues of DDT resulting from good agricultural practice
Crop Type Preharvest Usage Resulting
period days lbs/A residue ppm
Mustard greens 21 2.5 3.5
Spinach 21 2.5 3.5
Swiss chard 21 2.5 3.5
Turnip, parsnip, etc. 21 2.5 3.5
tops
Brassica crops
Broccoli Do not apply after 4 1
edible parts form
Brussels sprouts Do not apply after 4 1
edible parts form
Cabbage 14 1.2 7
(if wrapper leaves
are stripped)
Cauliflower Do not apply after 1.2 1
edible parts form
Kohlrabi Do not apply after 4 1
edible parts form
Root Vegetables
Beets 1.5 1
Carrots 1.5 1
Dry onions 1.5 1
Parsnips 1.5 1
Radishes 1.5 1
Rutabagas 1.5 1
Turnips 1.5 1
TABLE 1 (cont'd)
Residues of DDT resulting from good agricultural practice
Crop Type Preharvest Usage Resulting
period days lbs/A residue ppm
Legumes and
other vegetables
Artichokes Do not apply after 2.5 1
edible parts form
Asparagus Do not apply during 3 1
cutting season
Beans 7 2 3.5
Cucumbers 10 (soil only)
Pumpkins and Squash 2 (soil only)
OR
Cucumber 5 4 2
Pumpkins and Squash 5 2 2
Eggplant 5 (wash or brush) 2 7
Lettuce (Head) 7 (if outer leaves 2.5 7
are removed)
Mushrooms Spray houses before 1
mushrooms are present
Okra 7 1.2 1
Pepper 5 3 7
Peas Do not apply after 1.2 3.5
pods form
RESIDUES IN FOOD AT TIME OF CONSUMPTION
A number of samples from total diet studies have been analyzed in the
United States. Although a high proportion have had detectable amounts
of DDT, DDE and DDD, the average values are very low (Mills, 1963;
Williams, 1964; Cummings, 1965). The highest values were found in the
meat and meat products portion of the diet. In a two-year summary
(Duggan, Barry and Johnson, 1967) the average values for all samples
of meat and meat products was 0.30 ppm DDT, 0.25 ppm DDE, and 0.14 ppm
TDE. However, when the total diet values were calculated to daily
intake values (Duggan and Dawson, 1967), the value 0.0005 mg/kg/day
was found, which is much below the WHO ADI value of 0.01 mg/kg/day.
FATE OF RESIDUES
In storage and processing
DDT is stable under most of the conditions which prevail when it is a
residue on stored food products. Therefore, residues in food products
will not normally diminish greatly from most food products during
shipping and storage. It is especially stable in a fatty medium.
Recent studies reported by Lamb et al (1967) show that during short
storage periods for tomatoes (6 days at 55°F), green beans (16 days at
45°F), spinach (15 days at refrigerator temperature), and potatoes (40
days at 45°F), the residues of DDT did not diminish nor did isomeric
composition of the residue change.
On the other hand, washing and processing produced a marked reduction
in residues. Surface residues of DDT applied as a wettable powder were
easily removed, especially from tomatoes. A high proportion was
removed from green beans and spinach. For instance, a cold water wash
of green beans removed about half of the o,p'-DDT, about 75 percent of
the p,p'-DDT, and better than 40 percent of the p,p'-DDE. DDT and
related compounds present on potatoes can be almost completely removed
by removal of the skins, but cannot be removed to any significant
extent by washing without peeling or by cooking when skins are not
removed.
Data are also presented which show a very significant conversion of
DDT to DDD during certain heat processing. The extent to which DDT is
converted to DDD depends on the time and temperature of processing.
After processing green beans for 12 minutes at 250°F, DDT and DDD were
found in the canned product, but after processing spinach for 50
minutes at 252°F only DDD and DDE could be found. The DDD and DDE
found in these products account for less than half of the DDT. (Lamb,
et al, 1967 and Farrow, et al, 1966).
NATIONAL TOLERANCES
Additional information on national tolerances will be found in the
Report of the Second Session of the Codex Committee on Pesticide
Residues (FAO/WHO, 1967b).
RECOMMENDATIONS FOR TOLERANCES AND PRACTICAL RESIDUE LIMITS
Considering the additional data summarized above, the Joint Meeting
withdraws the previously published Recommendations for Tolerances on
pages 63 and 64 of the 1966 monographs (FAO/WHO, 1967a) and
substitutes the following therefor :
Temporary tolerances
When DDT is utilized in accordance with good agricultural practice to
protect food products, when necessary, against insect infestation, the
treated product may have residues as high as those shown below :
Fruits
Apples, pears, peaches, apricots 7
Cherries, plums, citrus, tropical fruits 3.5
Small fruits (except strawberries) 7
Strawberries 1
Vegetables
Leafy and brassica 7
Root vegetables 1
Other 7
Meat, fish, poultry 7 (in fat)
By no means will all samples of these products contain this amount of
residue; in fact, only a relatively small, yet unknown, portion of
each product in these categories is likely to be treated. Also, an
extensive study on the effect of washing and other preparation of food
processing (Lamb, et al, 1967) shows a significant amount of reduction
in incurred residues. (Data reviewed above).
Other data which gives support to the above factors is that in the
United States "total diet" samples DDT and metabolites DDD and DDE are
found at very low levels (data reviewed above).
The Joint Meeting is convinced that under the conditions of practical
use, the above residues on products which need to be protected will
not produce a total diet which will contain an amount of DDT and
metabolic analogues in excess of the ADI for DDT.
Because further work is required for the Evaluation for Acceptable
Daily Intake, the meeting recommends that temporary tolerances be
adopted for a period ending December 31, 1970, for the residue values
for the products shown above. The temporary tolerances apply to DDT
and its related compounds DDD and DDE.
Practical residue limits :
Milk 0.005 ppm
Milk products 0.2 ppm (fat basis)
Recommendations for practical residue limits are made because the
widespread use and stability of DDT have resulted in small residues
being ubiquitous. Small residues have been found to be present in most
dairy products. This is considered to be undesirable but is also
unavoidable at the present time. Since this residue is generally not
present from direct application to the animals or their feed, no
tolerance recommendation is made. However, to assist regulatory
officials in identifying those samples which have residues much in
excess of the unavoidable level, a practical residue limit of 0.20
ppm DDT is suggested.
Residues of DDT in animal products are invariably associated with
varying amounts of the DDT metabolites DDE and DDD. In many instances
the residues of either of these or the sum of the two exceeds the
residue of DDT. As shown in the paragraph on fate of residues during
processing, DDD and DDE may be found in processed food by conversion
by the processing.
FURTHER WORK
Further work desirable
Further data on the possible disappearance of residues during washing,
cooking and other preparation of food products for consumption.
REFERENCES PERTINENT TO EVALUATION FOR ACCEPTABLE DAILY INTAKES
Azarnoff, D.L., Grady, H.J. and Svoboda, D.J. (1966) Biochem.
Pharmacol., 15, 1985
Balazs, T. and Kupfer, D. (1966) Toxicol. appl. Pharmacol., 9, 40
Bergenstal, D.M., Herts, R., Lipsett, M.B. and Moy, R.H. (1960) Ann.
intern. Med. 53, 672.
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Dale, W.E., Curley, A. and Cueto, C. jr. (1966) Life Sci., 5, 47
Domenjoz, R., Arch. int. Pharmacodyn. 73, 128
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Geyer, G. (1962) Acta Endocrinol., 40, 332
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REFERENCES PERTINENT TO EVALUATION FOR TOLERANCES
Cummings, J.G. (1965) Pesticide residues in total diet samples.
J. Assoc. Offic. Agr. Chem. 48 : 1177-1180.
Duggan, R.E., Barry, H.C. and Johnson, L.Y. (1967) Residues in food
and feed. Pesticide residues in total diet samples, II. Pesticides
Monitoring Journal 1 (2) 2 - 12.
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See Also:
Toxicological Abbreviations
Ddt (ICSC)
DDT (JECFA Evaluation)
DDT (PIM 127)
DDT (FAO Meeting Report PL/1965/10/1)
DDT (FAO/PL:CP/15)
DDT (FAO/PL:1968/M/9/1)
DDT (FAO/PL:1969/M/17/1)
DDT (Pesticide residues in food: 1979 evaluations)
DDT (Pesticide residues in food: 1980 evaluations)
DDT (Pesticide residues in food: 1984 evaluations)
DDT (JMPR Evaluations 2000 Part II Toxicological)