FAO/PL:1968/M/9/1
WHO/FOOD ADD./69.35
1968 EVALUATIONS OF SOME PESTICIDE RESIDUES IN FOOD
THE MONOGRAPHS
Issued jointly by FAO and WHO
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 Geneva, 9-16 December,
1968.
FOOD AND AGRICULTURE ORGANIZATION OF THE UNITED NATIONS
WORLD HEALTH ORGANIZATION
Geneva, 1969
TOXAPHENE
IDENTITY
Chemical name
Chlorinated camphene containing 67-69 per cent chlorine.
Synonyms
3956, octachlorocamphene, Toxaphene(R) (Toxaphene is a common name
in some countries and a tradename in others).
Formula
The average empirical formula is C10H10Cl8
Other information on identity and properties
Chlorinated camphene (67-69 per cent chlorine) is a complex mixture
of polychloro bicyclic terpenses, with chlorinated camphenes
predominating. The source of terpene and the degree of chlorination
outside the 67-69 per cent range alter the insecticidal activity and
the mammalian toxicity. Toxaphene, which is a registered trademark in
most countries, is chlorinated camphene. Toxaphene is a complex
mixture. Ninety per cent pure camphene is chlorinated to between 67
and 69 per cent by weight which results in a general rearrangement of
camphene to form a large group of related compounds each with about
eight chlorines. The number of individual chemicals formed and their
structure is unknown. The investigations reviewed here have been
conducted on toxaphene.
EVALUATION FOR ACCEPTABLE DAILY INTAKE
Biochemical aspects
Toxaphene is absorbed through the skin and the intestinal tract, the
degree of absorption and its toxicity depending on the vehicle.
Studies on the tissue distribution and storage of toxaphene in the
body have demonstrated that the fat is the only organ of significant
storage and that the degree of storage is relatively low - one fourth
to one eighth of the feeding level for rats (Patterson and Lehman,
1953). Although most of the data on tissue distribution and storage
have been obtained by non-specific organochlorine determinations after
controlled exposures, more recent studies applying thin-layer
chromatography have confirmed the validity of the older data and of
the fact that the toxaphene present in tissues is unchanged (Dalton,
1966). After termination of exposure to toxaphene, elimination is
prompt and toxaphene residues in fat disappear rapidly (Lehman, 1952a;
Claborn, 1956).
Excretion of toxaphene in milk closely parallels the level of storage
in fat tissue. Cows fed 20, 60, 100 and 140 ppm toxaphene in the diet
excreted 0.37, 0.74, 1.15 and 1.88 ppm respectively in the milk (USDA,
1956).
As is the case with other chlorinated hydrocarbons, toxaphene induces
activity of liver microsomal enzymes. Feeding toxaphene for 13 weeks
to rats at dietary levels of 25 and 50 ppm produced marked induction
of N-demethylase, O-demethylase and EPN for detoxification enzymes.
Four weeks after termination of toxaphene feeding the enzyme activity
had returned almost to control level. Minimum induction occurred at 5
ppm feeding level of toxaphene, compared to a similar induction at 1
ppm with DDT (Kinoshita et al., 1966).
Acute toxicity
LD50 mg/kg
Animal Route body-weight Vehicle Reference
Mouse Oral 112 Maize oil Negherbon, 1959
Rat Oral 60 Maize oil Lehman, 1948
Rat (M) Oral 90 Peanut oil Gaines, 1960
Rat Oral 120 Maize oil Shelanski, 1947
Rat i.v. 13 Peanut oil Gellhorn, 1947
Guinea-pig Oral 290 Maize oil Shelanski, 1947
Guinea-pig Oral 365 Kerosene Shelanski, 1947
Dog Oral 25 Maize oil Lackey, 1949
Dog i.v. 5-10 Peanut oil Gellhorn, 1947
Goat Oral 200 Xylene Radeleff and
Bushland, 1952
Sheep Oral 200 Xylene Radeleff and
Bushland, 1952
The signs of toxicity following acute exposure to toxaphene are the
result of diffuse stimulation of the cerebrospinal axis, and include
salivation, spasms of the back and leg muscles, nausea, vomiting,
hyper-excitability, tremors, shivering, clonic convulsions, then
tetanic contractions of all skeletal muscles. With lethal doses, the
convulsions often continue until death, which apparently is caused by
respiratory failure. There is very little effect on the heart rate or
blood pressure of the anaesthetized dog. Respiration is affected as a
result of the exertion from vomiting or convulsions. It is arrested
due to tetanic muscular contractions, then increased in both amplitude
and rate as the muscles relax. (McGee et al., 1952; Negherbon, 1959)
Short-term studies
Rat
Groups, each containing six male and six female rats, were fed 50 and
200 ppm toxaphene in the diet. One male and one female from each group
were sacrificed after two, four and six months. The rest were
sacrificed after nine months. There were no clinical signs of
toxicity, no change of food intake or body-weight gain and no increase
in liver weights of these rats. Only the liver, kidney and spleen of
each animal were examined histologically. There was no damage to the
kidney or spleen. Liver changes observed consisted of centrilobular
cell hypertrophy, peripheral migration of basophilic cytoplasmic
granulation and presence of liposphere inclusion bodies. Three of 12
rats fed 50 ppm showed slight changes as described above after being
fed toxaphene for six to nine months, and it was concluded that this
level produces possible borderline liver changes. Six of the 12 rats
fed 200 ppm showed liver changes (Ortega et al., 1957).
Dog
Toxaphene was administered in capsules at a daily dose of 4 mg/kg to
two dogs for 44 days and to two other dogs for 106 days. Occasional
manifestations of acute toxicity (CNS stimulation) occurred for a
short time after administration. There were no significant changes in
the body-weight, blood picture, or gross appearance of organs.
Histological examination of many organs revealed some damage to the
kidney (degeneration of the tubular epithelium) and to the liver
(generalized hydropic degenerative changes, but no destruction of the
cells). Liver glycogen levels were normal. (Lackey, 1949)
Toxaphene dissolved in maize oil was administered daily (five days per
week) to dogs in gelatin capsules. A dose of 25 mg/kg was fatal. Two
dogs were administered 10 mg/kg (equivalent to 400 ppm in the diet);
one dog died after 33 days, but the other lived and was sacrificed
after three-and-a-half years. Four dogs were administered 5 mg/kg; all
survived and were sacrificed after almost four years. No information
on the pathologic findings was reported (Lehman, 1952b).
Toxaphene was fed daily (six days per week) for two years to three
male and five female dogs approximately four months old. Toxaphene was
added to the diet at levels of 10 and 50 ppm of the total wet diet,
including their liquids, The dogs received a daily dose of 0.60-1.47
mg/kg and 3.12-6.56 mg/kg (equivalent to approximately 40 and 200 ppm
on a dry diet basis). Gross behaviour, body-weight, mortality,
peripheral circulating blood elements, gross pathology, organ to
body-weight ratios and histopathology were recorded (Treon et al.,
1952).
There were no effects on behaviour, body-weight, mortality or blood
elements, but there were increases in the liver weights, liver to
body-weight ratios and moderate liver degeneration at the higher level
(200 ppm). At the lower level (40 ppm) one of three dogs was reported
to have slight liver enlargement and slight granularity and
vacuolization of the cytoplasm. Re-examination of the sections of
these animals failed to confirm any difference from control animals.
All other tissues were normal at both feeding levels (Brock and
Calandra, 1964).
Groups each of 12 dogs (six male and six female) were fed toxaphene at
dietary levels of 5, 10 and 20 ppm along with control groups. Two male
and two female animals were sacrificed after six, 12 and 24 months.
None of the feeding levels produced any change revealed by organ
weights, gross or histological examination, or any of the clinical or
organ function tests at any time, (Industrial Bio-Test Laboratories,
Inc., 1965).
Monkey
Two adult, female monkeys were given toxaphene in their food six days
per week at a daily dose of 0.64 to 0.78 mg/kg for two years. A third
animal served as a control. There were no signs of intoxication and no
evidence of tissue or organ damage as evaluated by growth rate, ratios
of liver to body-weight, spleen to body-weight or by histological
examination of the tissues (Treon et al., 1952).
Long-term studies
Rat
Four groups each of 40 rats (20 males and 20 females) were fed 10,
100, 1000 and 1500 ppm toxaphene in the diet. Effects were determined
by gross observation, mortality, body-weight, blood tests, liver
weight, liver to body-weight ratio, gross autopsy and histological
examination of the tissues. After seven-and-a-half to 10 months of
feeding some of the rats fed 1500 ppm and a few of the rats fed 1000
ppm showed occasional convulsions. The body-weight gain of the rats
fed the highest feeding level (1500 ppm) for the first 20 weeks was
less than those of the controls, probably due to decreased food intake
because of the unpalatability of the diet. As the rats became
accustomed to the diet, their growth rate was essentially the same as
that of the controls. There were no significant effects on mortality
or the haematopoietic system. The liver weight and liver to
body-weight ratio was significantly increased only in the 1000 and
1500 ppm groups. Liver changes consisted of swelling and homogeneity
of the cytoplasm with a peripheral arrangement of the granules in the
cytoplasm of the centrilobular hepatic cells. These changes occurred
to a moderate degree in the 1500 ppm group and to a slight degree in
the 1000 ppm group (Treon et al., 1952).
Groups of rats were fed 25, 100 and 400 ppm in the diet. The only
organ which showed significant histological change was the liver and
occurred at the 100 ppm and 400 ppm levels. There were centrilobular
hepatic cell enlargement with increased oxyphilia, peripheral
margination of basophilic granules and a tendency to hyalinization of
the remainder of the cytoplasm. The effects at the various feeding
levels were summarized by Lehman as follows: 400 ppm was the lowest
level producing a gross effect of liver enlargement; 100 ppm the
highest level not producing gross effects; 100 ppm the lowest level
producing tissue damage; and 25 ppm the highest level not producing
tissue damage (Fitzhugh and Nelson, 1951; Lehman, 1952b).
Special studies
Reproduction
Rat. A three-generation, six-litter reproduction study was conducted
with toxaphene. Groups of weanling rats were fed 25 ppm and 100 ppm
for 79 days before mating. All animals were continued on their
respective dietary concentration of toxaphene during the mating,
gestation, weaning of two generations, or for a period of 36 to 39
weeks. Weanlings from the second litter were selected as parents for
the second generation and continued on their respective diets until
after weaning of 4 second litter. A third generation was selected in
the same manner. Complete gross and histological examination was
performed on all three parental generations after 36 weeks of
toxaphene administration. The only pathologic changes found were
slight alterations in the livers of the 100 ppm group similar to those
changes seen in long term studies. Reproductive performance, fertility
and lactation were normal. The progeny were viable, normal in size and
anatomical structure. Findings among all test animals, three parental
generations and six litters of progeny were comparable to control
animals for all parameters (Kennedy et al., 1968).
Pheasant. Pheasants were fed 100 or 300 ppm toxaphene in the diet.
In the 300 ppm group, egg-laying and hatchability were significantly
depressed, food consumption and weight gain were reduced. Both dose
levels caused a significantly greater total mortality of the young
pheasants than that of controls over the period from hatching to the
thirteenth day. Relative reproductive success was: for controls, 70
per cent; for the 100 ppm group, 62 per cent; and for the 300 ppm
group, 46 per cent (Genelly et al., 1956).
Observations in man
A nine-month-old girl was poisoned acutely by a dust containing 13.8
per cent toxaphene and 7.04 per cent DDT. Convulsions, respiratory
arrest and death followed. Cerebral oedema was found. Analysis of the
brain, liver and kidney indicated that toxaphene is stored to a
greater extent than DDT (Haun and Cueto, 1967).
Twenty-five human volunteers were exposed in a closed chamber to an
aerosol of toxaphene for 30 minutes a day for 10 consecutive days at
an average concentration of 500 mg/m3 of air. After three weeks,
they received the same exposure on three consecutive days. Based on an
assumed retention of 50 per cent of the inhaled toxaphene, each
individual received a dosage of 75 mg of toxaphene daily - or slightly
more than 1 mg/kg/day. Complete physical examinations, including
fluoroscopic, blood and urine tests, failed to reveal any toxic
manifestations (Shelanski, 1947).
Comments
Long-term toxicity studies on toxaphene have been conducted in the rat
only, and several short-term studies in dogs and monkeys. Very little
difference in species susceptibility had been observed. No toxic
effect was observed at dietary levels of 25 ppm for the rat, 40 ppm
for the dog and 15 ppm for the monkey (only level studied). The toxic
manifestations of toxaphene at higher levels are primarily those of
liver enlargement and other hepatic alterations observed with most
chlorinated hydrocarbons. Microsomal stimulation has been measured and
demonstrated to be reversible. Toxaphene is stored in fat tissue at a
low level compared to most chlorinated hydrocarbons, and is more
rapidly eliminated after exposure is terminated. Reproduction is not
affected at the 100 ppm dietary level in the rat, but liver damage
occurs above 25 ppm.
Although adequate work has been done on the original compound of known
composition, the substance at present in agricultural use does not
necessarily conform to the specifications of the original material
tested biologically. Before an evaluation can be made, the identity of
the compounds presently in use must be established, and future
toxicological work must be related to them.
RESIDUES IN FOOD AND THEIR EVALUATION
Use pattern
Toxaphene is reported to be a widely used pesticide in many parts of
the world and particularly in the United States of America, both in
quantity used and in number of uses.
Pre-harvest treatments
Toxaphene is used in many countries for control of armyworms,
cutworms, earworms, budworms, thrips, beetles, weevils, grasshoppers
and many other insects. Crops treated include a wide variety of
agronomic, vegetable and fruit crops. Most treatments are foliar
applications except those for cutworms. Toxaphene is also used for
ectoparasite control on cattle, sheep and swine.
On crops the usual rates of application are 1.26 to 3.78 kg/ha.
Toxaphene is frequently applied in mixture with other insecticides
such as methyl parathion, parathion, DDT, naled and others.
Post-harvest treatment
Toxaphene is not used for post-harvest treatments.
Residues resulting from supervised trials
There have been many analyses made for toxaphene in treated crops.
Generally these show residues likely to occur with a specific
treatment or set of multiple treatments used in the production of that
crop. A compilation of published and unpublished data (Hercules, Inc.)
is held at FAO headquarters in Rome. Table I summarizes selective data
which indicate the levels of residues that result from usual
agricultural practice on representative types of crops. The residue
level is controlled by proper application restrictions such as
pre-harvest intervals, application prior to formation of edible parts
or application to crops where the harvested portion is protected from
the spray by pods, husks, outer leaves or other coverings.
Toxaphene residues resulting from a foliar application generally
exhibit a half-life of 5-10 days on growing crops. The half-life
varies with weathering conditions, plant or fruit type, and plant
growth rate, and for different formulations. Residues from wettable
powders or dusts are lost more rapidly than from emulsifiable
concentrates. Brett and Bowery (1951) show the declining rates of
toxaphene on three kinds of vegetables: snapbeans, tomatoes and
collards. On snapbeans, with no rain, a steady decline from 8.1 ppm to
1.5 ppm occurred in 12 days. Rain markedly hastened the disappearance
of residues in the other crops. Tomatoes with a small surface area in
comparison to total volume had a residue which declined from 4 ppm to
0.15 ppm in 12 days. In contrast, collards with a large surface area
in relation to total volume had a residue which decreased from 168 ppm
to 5.0 ppm in 12 days.
Nash and Woolson (1967) reported that when toxaphene was applied and
thoroughly mixed with soil, 45 per cent of the original application
remained after 14 years. This extreme persistence would not be
expected when toxaphene is used as a topical soil application for the
control of cutworms. Residue loss by volatilization and weathering
from a surface soil treatment would probably more closely resemble the
decline pattern on crops from foliar application. Because foliar
application is the major use of toxaphene, residues in the soil would
be primarily from this use.
In a soil monitoring study conducted in the Mississippi Delta by USDA
(1966) involving agricultural areas in which general use of toxaphene
had been made (but not known to have been used specifically on each
sample site), soil residues of 0.88 to 3.78 ppm were found. Muns et
al. (1970) found that residues of toxaphene in potatoes, table beets,
sugar beet roots and tops, and radishes grown in soil treated with
toxaphene were less than 0.4 ppm. There is no positive evidence to
indicate an excessive buildup in the soil from normal use or that
residues in the soil are absorbed by plants and concentrated to any
degree.
Toxaphene accumulates in fat of animals after ingestion or after
spraying or dipping for insect control. The research of Claborn and
associates (1960) established two important residue characteristics of
toxaphene: (1) with any given rate of subacute intake a certain
storage level is attained with no buildup above this level; and (2)
when the source of toxaphene is removed the residue is rapidly
reduced. The level of storage is lower and elimination more rapid than
with most other chlorinated hydrocarbons. As a rule storage level in
the fat of cattle and sheep will be one fourth to one half the level
in the food. Storage concentration in hogs is somewhat less than in
other livestock probably because of the greater fat content.
The work of Claborn et al. (1960) and Zweig et al. (1963) shows the
amount of residue that would occur in milk of cows fed toxaphene in
their diet. Both studies indicate that the ratio of toxaphene in the
milk to that in the feed is about 1:100. Uncontaminated milk was
produced in 14 days or less after feeding levels up to 10 ppm were
stopped. Spraying dairy cows for insect control causes residues in the
milk. For this reason dermal application of toxaphene is not permitted
on dairy animals.
Fate of residues
Toxaphene can be altered chemically by dechlorination or by
hydroxylation.
Non-specific organochlorine methods have been used to measure the
residues in supervised trials. The identity of the individual
components in the complex technical mixture is not known, nor has
isolation of the individual components which comprise the residue in
plants and animals been reported. Thin-layer, paper and gas
chromatography patterns can be used to identify the residue. Ives
(1967) by gas chromatography of toxaphene saw evidence of at least 25
different components.
Because of the complex nature of the parent chemical mixtures, it is
impossible to define the nature of the residue with any degree of
specificity.
Ihde and Taft (1954) have shown that insecticidal activity is
characteristic only of the parent material with chlorine content of
67-69 per cent. Slight alteration in the chlorine content either above
or below this level markedly decreases insecticidal activity. Carter
et al. (1950) extracted aged toxaphene residues from treated alfalfa
and compared the insecticidal activity of this residue with that of
standard toxaphene. They found very close agreement in insecticidal
activity of the alfalfa hay residue and the standard. They also
assayed the residue from beef fat and again found the insecticidal
TABLE I. TOXAPHENE RESIDUES RESULTING FROM SUPERVISED TRIALS
Rate of Pre-harvest* Residue
Crop application No. of interval at harvest Comments
(kg/ha) treatment (days) (ppm)
Vegetables
Lettuce 5.5 1-4 10 5.8-7.9 whole head
Kale 5.0 4 36 3.3-7.2
Cabbage 1.9-12 2-6 9-38 0.8-6.6 on outer leaves
Spinach 5.0 4 30 16.7-18.8
Celery 1.1-1.6 9 13 1.8 stalks washed
6.5 leaves
Cauliflower 3.8 1 8 1.1 (processed commercially
Broccoli 10 1 8 3.4 (and frozen before
(before analysis
Tomatoes 1.3-2.5 8-9 5-7 2.0-4.3
Greenbeans 7.5 1 7 1.3 unwashed
Lima beans 3.9 1 14 0.3 shelled beans
Carrots 25 2-4 0.9-3.3 soil applic. (1 yr)
Potatoes 0.95-2.5 6 21 0 detected
Field peas 2.5 3 4 1.8
Oil seeds
Cotton (seed) 3.9-5.0 15 6 3.6-5.2 lint bearing seed
Soybeans 3.8 3 60 0.5
Peanuts
(shelled) 25-50 1 0 detected soil treat.
Fruit
Oranges 5.7 2 7-70 0-10.9 skins
0-0.3 pulp
Bananas 3.8 1 1 0.3-1.3 whole fruit
Pineapple 2.8 2 84-96 1.3-2.7 whole fruit
TABLE I. (continued)
Rate of Pre-harvest* Residue
Crop application No. of interval at harvest Comments
(kg/ha) treatment (days) (ppm)
Cereal grains
Wheat 1.9-3.8 1 14-21 0.5-1.8
Barley 1.9-3.8 1 7-28 0.7-14.2
Oats 1.9-3.8 1 7 1.0-2.6
Rice 1.9-3.8 1 7-28 1.5-5.6 unfinished grain
Sorghum 2.5 1 28 2.5-3.1
Corn (maize) 2.5 1 12 0.08 kernels
Fat of meat animals
Beef 0.5% 12 28 5.0 12 weekly sprays
Swine 0.5% 2 28 0-0.6 2 sprays
Shelled nuts
Almonds 4.0 3 135 1.5
* Interval from last application if multiple applications were made.
activity from the beef fat residue to be equal to the standard
toxaphene.
Klein and Link (1967) reported field weathering of toxaphene on kale
for a 28-day period. One foliar application was made at a rate of 2.52
kg/ha using a water suspension of a 40 per cent wettable powder.
Electron capture and microcoulometric gas chromatography and the
colorimetric method of Graupner and Dunn (1960) were used for the
analyses. An initial residue of 155 ppm was reduced to essentially
zero in 28 days. At the seventh day only about 8 per cent of the
initial residue was present. Its composition remained fairly constant
although some of the more volatile fractions were lost as evidenced by
GLC. However, at 14 days with only about 1 per cent of the pesticide
remaining, its composition had altered. Even at low levels the
remaining components appeared to be organic chlorine compounds.
Evidence of residues in food in commerce or at consumption
The United States Food and Drug Administration has conducted residue
studies in foods and total diet samples since 1962. Duggan (1967,
1968b) shows the frequency and magnitude of pesticides in different
classes of foods and in individual diet samples.
Toxaphene was not among the 15 pesticide chemicals most frequently
found in the 888 total diet composites examined from 1964 to 1967.
When toxaphene is found in total diet composites, it is usually in
either the leafy vegetable or garden fruit composite. For the period
June 1964 to April 1967 toxaphene was found in 1.4 per cent of the
leafy vegetable composites at an average level of 0.005 ppm and in 2.7
per cent of the garden fruit composites at an average level of
<0.001 ppm.
From 1963 to 1966, 26 326 domestic raw agricultural samples (not
including animal tissues) were found to contain pesticide residues.
Toxaphene was present in 754 of these samples and ranked tenth in
incidence among the 11 pesticides which contributed 95 per cent of
all residues found during that period. Toxaphene ranks third in
incidence in animal tissues.
Table II shows the percentage of domestic samples from 1964 to 1967
which contained toxaphene and the average level found for various raw
agricultural products.
TABLE II
Raw agricultural product Indicence Average
per cent. ppm
Leaf and stem vegetables 6.4 0.18
Vine and ear vegetables 1.4 0.01
Root vegetables 1.1 <0.005
TABLE II (continued)
Raw agricultural product Indicence Average
per cent. ppm
Small fruit 1.0 <0.005
Beans 0.9 <0.005
Large fruit 0.3 <0.005
Cereal grains 0.3 <0.005
Nuts 0.3 <0.005
Eggs 0.2 <0.005
Animal food grains 0.1 <0.005
Among the domestic samples of canned and frozen products examined from
1964 to 1967 toxaphene ranked sixth in incidence with 5.0 per cent of
the samples containing residues at an average level of 0.45 ppm, the
highest average level found among the 17 most frequently encountered
pesticide residues.
Duggan (1968a) showed that toxaphene was frequently found in oil seed
products. Table III gives the per cent of samples containing
toxaphene and the average level found in 1544 samples analysed from
1964 to 1966.
TABLE III
Raw product Crude oil Meal Refined oil
Soybeans 8.0* 4.1 - 4.3
(0.004)** (0.024) (<0.001)
Peanuts 1.7 2.8 - -
(0.006) (0.008)
Cottonseed 30.4 1.3 1.1 12.2
(0.023) (0.010) (0.003) (0.140)
* Incidence in per cent.
** Average residue found (ppm).
Methods of residue analysis
In the past, several total chloride methods have been used for residue
studies. These methods are accurate for known residues. Where mixtures
with other organic chlorine insecticides were encountered such as DDT,
a specific method for that compound was employed and the toxaphene was
determined by difference. The toxaphene was then identified by
thin-layer or paper chromatography. While these methods are accurate,
they are somewhat difficult to use in surveillance work.
A specific residue method is now available. A gas chromatographic
electron capture system has been applied to toxaphene residue analyses
(Eastman, 1968). Toxaphene residues are dehydrohalogenated with
potassium hydroxide and measured by gas chromatography. The clean-up
procedures and dehydrohalogenation remove all possible interfering
residues except chlordane.
National tolerances
Tolerance
Country Crop (ppm)
Canada* Oats, pineapple, wheat 3
Barley, grain sorghum, rice 5
Beans, blackeyed peas, broccoli,
Brussel sprouts, cabbage,
cauliflower, celery, citrus fruit,
egg-plant, fat of meat from cattle,
sheep, goats and hogs, kohlrabi,
lettuce, okra, onions, pears, peas,
strawberries, tomatoes 7
Germany Pears, strawberries, raspberries,
cherries, plums 0.4
Other plant products 0.04
Netherlands Fruit, vegetables, except potatoes 0.4
United States Soybeans 2
of America* Pineapples, bananas (0.3 ppm in pulp) 3
Wheat, barley, rye, rice, cottonseed,
stone and pome fruit, cane fruit,
corn, leafy, fleshy and fruit
vegetables, nuts, beans, peanuts, peas,
strawberries and fat of beef, sheep,
goats, swine and horses 7
* Tolerances are under review in Canada and the United States of America.
RECOMMENDATIONS FOR TOLERANCES AND PRACTICAL RESIDUE LIMITS
Appraisal
Because of the many questions related to this compound, outlined in
detail below, no recommendations can be made at this time.
Further work or information
Required (before an acceptable daily intake or tolerance can be
established)
1. Data relating to the uniformity of the technical product:
(a) variability in biological activity (e.g., LD50 variation in
mammals or in insects) from batch to batch;
(b) variability in the chemical composition as determined by gas
chromatography, thin-layer chromatography or other analytical
methods;
(c) variability in the starting product and in the final product from
different sources;
(d) criteria for control of the degree of chlorination.
2. Information on the chemical nature of terminal residues in
plants, animals, and their products, as determined by modern
analytical methods, including the possibility of formation of
photo-oxidation products.
3. Further residue data from supervised trials on a variety of
crops.
4. Residue data in:
(a) poultry, cattle, sheep and swine;
(b) unprocessed and processed vegetable oils;
(c) cereals, after processing into flour, bread, etc.
5. Development and comparative evaluation of methods of analysis for
regulatory purposes.
6. Complete toxicological studies based upon a standardized
technical product, the constituents of which have been
identified.
REFERENCES
Brett, C. H. and Bowery, T. C. (1951) Insecticide residues on
vegetables. J. Econ. Entomol., 51: 818-821
Brock, D. and Calandra, J. C. (1964) Re-evaluation of microscopic
sections from chronic oral toxaphene study. Industrial Bio-Test
Laboratories, Inc., unpublished report
Carter, R. H., Nelson, R. H. and Gersdorff, W. A. (1950) Organic
chlorine determination as a measure of insecticide residues in
agricultural products. Advances in Chem. Series, 1: 271-3
Claborn, H. V. (1956) Insecticide residues in meat and milk. United
States Department of Agriculture, ARS-33-25
Claborn, H. V., Radeleff, R. D. and Bushland, R. C. (1960) Pesticide
residues in meat and milk. United States Department of Agriculture,
ARS. 33-36
Dalton, C. J. Toxaphene residue in dog tissues. (1966) Two-year
feeding study, 1965. Hercules Research Center, unpublished report
Duggan, R. E. (1967) Pesticide residues in foods. Presented at the
Conference on Biological Effects of Pesticides on Mammalian Systems.
New York Academy of Science, New York, New York. 3 May 1967
Duggan, R. E. (1968a) Pesticide residues in vegetable oil seed, oils
and by-products. Pesticide Monitoring Journal, 1: 2-7
Duggan, R. E. (1968b) Pesticide residue levels in foods in the United
States from July 1, 1963 to June 30, 1967. Pesticide Monitoring
Journal, 2: 2-46
Eastman, G. E. (1968) Toxaphene determination by electron capture gas
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See Also:
Toxicological Abbreviations
Toxaphene (IARC Summary & Evaluation, Volume 79, 2001)