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
LEAD ARSENATE (and CALCIUM ARSENATE)
IDENTITY
Chemical name
Calcium arsenate and lead arsenate.
Synonyms
(Lead salt) -diplumbic hydrogen arsenate, dilead arsenate, dilead
orthoarsenate, dibasic lead arsenate, acid lead arsenate, Gypsine.
Formulae
(Lead salt) -PbHAsO4
(Calcium salt) -3Ca3 (AsO4)2. Ca(OH)2
Relevant physical and chemical properties
Appearance: (lead salt) white powder
(calcium salt) white flocculent powder.
Solubility: (both salts) practically insoluble in water.
Stability: (lead salt) stable to light, air and water and not
decomposed by carbon dioxide; decomposed by alkalies,
including calcium hydroxide;
(calcium salt) soluble in dilute mineral acids;
commercial products are decomposed by carbon dioxide
yielding calcium carbonate and dicalcium hydrogen
arsenate, the latter being appreciably soluble in
water.
Composition of technical product: As commercially prepared, the lead
salt usually contains about 21 per cent As, the calcium sale about 26
per cent As.
EVALUATION FOR ACCEPTABLE DAILY INTAKE
Biochemical aspects
The total daily intake of lead varies according to the environment,
but it is generally agreed that the average person in a developed
country ingests up to 0.4 mg of lead per day (Patterson, 1965; Kehoe,
1966). Under normal circumstances the diet contributes 90 per cent of
man's total intake of lead. The element enters the food-chain through
many sources including aerial fall-out and the use of pesticides
containing lead in agriculture. Lead can appear in canned foods
because some of the metal is dissolved by food acids from the solder
of the can (Lewis, 1966). Lead is also inhaled from the atmosphere,
the most important source being the combustion of gasoline containing
lead tetraethyl (McCaldin, 1966). Tobacco smoke also constitutes an
inhalation source of lead (Patterson, 1965). Lead appears in drinking
water, where it arises largely from the lead pipes through which it
flows. The solubility of lead in water is increased by oxygen and
nitrates and is decreased by carbon dioxide and carbonates (Sollmann,
1957a).
Of the lead ingested from the food less than 10 per cent is absorbed
by the alimentary tract. It is excreted from the body largely in the
faeces and to a lesser extent in the urine (Lewis, 1966). Lead is a
cumulative poison, being stored in all tissues and organs and it is
transmitted to the foetus (Calvery et al., 1938; Castellino and Aloj,
1964). Evidence exists that children and pregnant women retain lead
more readily than others owing to the presence of rapidly developing
tissues with a high affinity for the metal (Anon., 1966).
Arsenic is used in many forms as pesticides, the most widely used
salts being lead and calcium arsenates.
The metabolic pathways for different arsenical compounds vary. The
level of arsenic deposited in the liver appears to reflect the
toxicity of the different compounds (Frost et al., 1955). Naturally
occurring organic arsenical compounds have been shown to accumulate to
a much lower extent than inorganic arsenic compounds (Coulson et al.,
1935). The arsenates are more toxic than the arsenites, which in turn
are more toxic than the organic arsenical compounds (Sollmann, 1957b).
Absorption of inorganic arsenical compounds occurs readily, to some
extent even from the intact skin. After oral administration excretion
is mainly in the faeces, in parental administration it is excreted
almost completely in the urine. A considerable proportion of ingested
arsenic is stored in all tissues (Sollmann, 1957b).
Acute toxicity
The oral fatal dose of arsenic trioxide in man is estimated to be
between 15 and 50 mg/kg body weight. The effects of arsenic may be
somewhat delayed; if the acute stage is survived, signs of hepatic and
renal damage are seen after one to three days, with skin rash later
on. Post-mortem appearances suggest haemorrhagic gastro-enteritis in
acute cases and necrotic or degenerative changes in liver, kidney and
bone marrow in delayed cases (Sollmann, 1957c).
LD50 mg/kg
Compound Animal Route body-weight References
Calcium arsenate Rat Oral 20 Lehman, 1951
Lead arsenate Rat Oral 825 Voigt et al., 1948
Lead arsenate Rat Oral 100 Lehman, 1951
(continued)
LD50 mg/kg
Compound Animal Route body-weight References
Lead arsenate Rabbit Oral 125 Voigt et al., 1948
Lead arsenate Chicken Oral 450 Voigt et al., 1948
Short-term studies
Rat
Groups of albino rats were employed in paired-feeding studies using
500 g batches of feed containing 0 ppm and 215 ppm arsenic as calcium
arsenate or arsenic trioxide. Consumption of a 500 g batch of feed by
each rat required six to eight weeks. Greater arsenic absorption and
storage occurred in the animals which consumed the calcium arsenate,
the livers and kidneys retaining the heaviest concentrations. At the
conclusion of the study, the animals fed calcium arsenate had 41 per
cent larger livers and eight per cent smaller brains than the
controls on a dry weight basis (Morris and Wallace, 1938).
Dogs
A total of 20 dogs were fed diets containing either 13, 38 or 64 ppm
lead as the acetate, or 64 ppm lead as the arsenate. Fifteen animals
succumbed with severe symptoms of lead intoxication and the remaining
five were sacrificed having shown definite symptoms of poisoning at
approximately one year after the beginning of the experiment. The
shortest period of survival was 15 days, in which case the animal
received 2.56 mg of lead per kg of body-weight per day. Two animals
receiving the smallest amount of lead, namely 0.33 mg/kg, succumbed,
one after 140 days and the other after 167 days on the diet.
Differences in survival were explained partly by the ages of the
animals when placed on the experimental diets. Young animals were more
susceptible to lead intoxication than were older animals. The kidneys
of all the dogs showed tubular degeneration. Hyperaemia and oedema of
the brain were noted in all dogs which had convulsions. The bones of
many of the dogs were hard, brittle and thickened and the marrow
cavities of the long bones were narrowed. Compensatory formation of
marrow was noted in the skull. Lead deposits were noted in the bones
and stippled red cells were seen in the blood. The greatest amount of
lead storage was found in the bone, with smaller concentrations in the
kidneys, liver and brain. Lead was also found in the pups and milk of
lead-fed dams (Finner and Calvery, 1939; Calvery et al., 1938).
Long-term studies
Rat
In a study to determine whether the lead or the arsenic element was
principally responsible for the toxicity of lead arsenate, rats were
fed lead arsenate, lead carbonate and calcium arsenate for two years.
The lead and arsenic in the last two compounds were in amounts equal
to that in the lead arsenate. At the end of the two-year period each
rat that had received lead or calcium arsenate had consumed the
equivalent of approximately 1.7 g of elemental arsenic; for a rat that
eats an average of 15 g of food per day, this figure comprises a
dietary level of 155 ppm of arsenic. It was concluded from the
mortality rates that calcium arsenate was the most toxic. The
histopathological findings in the rats fed calcium arsenate differed
from the controls in showing excess haemosiderin in the spleen,
swollen cells and granular pigment in the renal convoluted tubules and
hyaline casts in the collecting tubules (Fairhall and Miller, 1941).
Observations in man
Liver and skin careers have been reported in vineyard workers exposed
to arsenates in West Germany (Roth, 1956, 1957a, 1957b, 1958) and an
unusual frequency of bronchial carcinoma was noted among vineyard
workers of the French region "Beaujolais" associated with signs of
chronic arsenical poisoning (Galy et al., 1963).
Comment
Lead is a non-essential element with toxic properties caused by
excessive cumulation. Although intake can not be avoided, it is
clearly desirable to reduce the bodyload to a level where equilibrium
between absorption and excretion can be maintained.
The total literature on toxicological studies with arsenical compounds
is voluminous and the available animal studies as well as human data
indicate that inorganic arsenic compounds are cumulative poisons. Much
controversy exists over the problem of whether or not inorganic
arsenicals possess carcinogenic potentials. Some of the
epidemiological studies raise possible suspicions of such activity,
but no real scientific proof has yet been forthcoming. Because of
these doubts and the inadequacy of the available long-term study in
rats, it is not possible to evaluate these compounds until unequivocal
evidence has been produced which will allow resolution of the problem.
Satisfactory substitutes should be used wherever possible in an effort
to decrease the dietary intake of these elements.
RESIDUES IN FOOD AND THEIR EVALUATION
Use pattern
Calcium and lead arsenate were extensively used as stomach poisons for
insect control from 1900 to 1950. Since the advent of the new organic
insecticides the use of calcium and lead arsenate has declined.
However, there is still a substantial scale and pattern of use in
several countries, particularly of lead arsenate. Calcium arsenate,
due to its greater phytotoxicity, is used on crops less susceptible to
damage, e.g. cotton and potatoes. In evaluating residues, only lead
and arsenic are of toxicological significance.
Pre-harvest treatments
Calcium arsenate is applied to blueberries in eastern Canada and to
vegetables in Japan and is present in some proprietary slug control
formulations.
Lead arsenate is used in Canada, Japan, Britain, Israel, United States
of America and New Zealand for the control of insects such as apple
maggots, codling moth, plum curculio, fruit flies, leafrollers and
other chewing insects on fruit trees. It is also used to some extent
for the control of chewing insects on vegetables (cucumbers and
tomatoes in Japan) and ornamental crops.
In the production of apples, cherries, grapes, pears and plums, the
use of lead arsenate is economical and necessary, particularly on
apples grown for export to countries in which plant quarantine
regulations require freedom from certain important scheduled pests.
These requirements could not be met without the use of currently
recommended applications of lead arsenate (supplemented in some areas
with other insecticides). Lead arsenate is also used in integrated
control programmes to minimize the use of DDT.
Post-harvest treatments
None reported.
Other uses
Lead arsenate is also used for the control of earthworms and other
soil-inhabiting insects on golf greens and lawns, and on airport turf
adjoining runways to reduce bird hazard related to earthworm
abundance.
Residues resulting from supervised trials
Extensive residue data, mainly from the use of lead arsenate, were
collected for this review from several member countries of FAO and
WHO. These data, which have been deposited with FAO, are summarized
below.
Extensive data from Canada and New Zealand on residues of lead and
arsenic residues on apples range from less than 0.1 ppm to about 3 ppm
for arsenic and 6 ppm for lead, depending on many variables.
In the United Kingdom, field trials conducted for control of codling
moths have produced data on the weathering of lead arsenate residues
(Chiswell and Tew, 1965; Pocklington and Tatton, 1966; Tew et al.,
1961; Tew and Sillibourne, 1964). The ratio of lead to arsenic
remained close to the 3:1 ratio found in applied lead arsenate.
Applications using hand lances led to greater residues at harvest than
did reduced-volume machine applications.
The rate of application and pre-harvest interval are of major
importance on the amount of the final residue (Bishop et al., 1960).
There is a marked and rapid decrease in arsenic deposits on foliage
and fruit during the initial two to three weeks following the final
application (Bishop et al., 1958). On apples, early in the season
between "cover sprays" there is a loss in deposits on the apple
surface which amounts to 3.6 per cent daily, mostly due to increase
in size of apples. Later, the daily loss varies from 1.3 to 1.6 per
cent and closer to harvest less than one percent (Webster and
Marshall, 1934). A substantial portion of the residue is in the stem
and calyx end which is not normally eaten (Canada, 1964; Tatton, 1965;
Pocklington and Tatton, 1966; United Kingdom, 1964). When skin, stem
and calyx are removed rarely more than 30 per cent of the residue is
found in the edible pulp.
The residue on apples at harvest from as few as two late season
applications can, in the case of early varieties, be in excess of 2.0
ppm, but this is reduced after harvest (see below). Data for pears and
cherries are not as extensive but are similar to that for apples.
No residue data were available for plums. Japanese data indicate
residues no greater than 1.0 ppm arsenic and 1.0 ppm lead on grapes,
cucumbers and tomatoes (Japan, 1968).
Lead arsenate is quite stable and readily accumulates in soils either
as a result of use in specific soil treatments or foliar application
(Bishop and Chisholm, 1962; MacPhee et al., 1960). Crops grown in such
soils will contain residues of arsenic (MacPhee et al., 1960). Arsenic
can build up in soils to a level where it can reduce the yield of some
sensitive crops such as peas and beans (Bishop and Chisholm, 1962;
Chisholm et al., 1955; MacPhee et al., 1960). However, lead
accumulation has not presented any problem to date as the result of
agricultural use (Chisholm and Bishop, 1967).
Calcium arsenate residues in soil after use on cotton have been
included in the USDA monitoring programme. In one report, the average
arsenic content of cultivated fields ranged from 2.8 to 12.8 ppm,
while in uncultivated areas the range was 1.2 to 5.9 ppm NRC, 1966).
Fate of residues
In storage and processing
Substantial reductions of both arsenic and lead residues result from
mechanic removal during sorting, grading, movement on belts and
brushing operations in most commercial packing operations. Residues
followed through from practical rates of application to apples to
sampling this fruit after packaging for export and transported
indicated that in most instances the residues were reduced by a factor
of 50 per cent or more (Canada, 1964).
There is an increasing tendency to wash and wax apples prior to
export, procedures which further reduce residues. Most consumers wash
and wipe apples and pears if the peel is consumed. In many countries,
the peel is removed before consumption. After processing, apple
products contain small amounts of arsenic, ranging from 0 to 0.27 ppm.
with an average of 0.11 ppm. Apple pomace, used as cattle food, can
contain substantial amounts of residue. When made from whole fruit,
these levels can go as high as 16 ppm, and if skins and cores only are
used, as high as 16 ppm.
Evidence of residues in food in commerce or at consumption
The Public Analysts' reports for 1963, 1964 and 1965 (Hamence, 1965a
and 1965b; Rymer and Hamence, 1967) indicated that about one per cent
or less of the two to three hundred samples of fruit or apples
examined in the United Kingdom failed to meet the statutory limits for
arsenic and lead. In Canada various crops which may be treated with
arsenates, such as apples and blueberries, have been examined over the
last 10 years. In over 500 commercial samples of apples, less than one
per cent contained more than 1 ppm arsenic. Blueberries presented no
problem.
Methods of residue analysis
The AOAC (1965) method for arsenic can serve as a referee method.
Various modifications of the Gutzeit Test were used in earlier work
for the determination of arsenic residues. While a fair degree of
reliance can be placed on data obtained through this method,
especially if the analysts were experienced in its use, the newer
methods (AOAC, 1965) have been demonstrated to be superior (Hoffman
and Morse, 1961; Hoffman and Gordon, 1963).
There is still a requirement for a simple method of analysis to
distinguish between the trivalent and pentavalent forms of arsenic.
The dithiazone extraction methods of analysis for lead are not
satisfactory. A co-precipitation technique with strontium sulfate
(Flann and Bartlett, 1968) and atomic absorption methods are presently
being considered by AOAC.
National tolerances
There are wide differences in the approach various countries take to
regulating the amounts of arsenic or lead allowed to remain in food or
in ingredients used in food manufacture and preservation. Most
countries rely on a general clause in their pure food law which
prohibits harmful or poisonous substances in foods. In addition, some
countries also have extensive lists of legally permitted amounts which
may be present in food. In addition, some countries (e.g. United
States of America) have recently established tolerances for arsenic in
meat, edible byproducts and eggs to accommodate the use of arsenic
compounds in animal feed. A comprehensive survey of the regulations
pertaining to products ranging from fish, cocoa, fruits, vegetables,
chemicals used in food manufacture, beer, wine, etc., has been
deposited with FAO and WHO. Some countries list the tolerances for
arsenic as "arsenious oxide", As2O3, while others express the
tolerance in terms of As only. Lead is expressed only as Pb. Some
examples appear in the following table. In addition, some countries
(e.g. Britain) have a general clause covering foods other than those
specifically scheduled which limit their arsenic content to 1 ppm and
the lead content to 2 ppm.
RECOMMENDATIONS FOR TOLERANCES AND PRACTICAL RESIDUE LIMITS
Appraisal
Calcium and lead arsenate are not used in combination, but they can be
considered together for the purposes of recommending tolerances since
only residues of arsenic and lead have to be considered. Although
these two compounds were used extensively in the past, their
modern-day use is restricted to specific pest control problems which
cannot be satisfactorily controlled with the modern organic
insecticides. While calcium arsenate is still extensively used on
cotton and potatoes with minor risks of residues resulting in human
food, lead arsenate is now used mostly in the production of apples,
with some small scale use on pears, cherries, grapes and plums and a
limited number of vegetables. Its use is particularly important in the
commercial production of apples in some regions in meeting
requirements prior to phytosanitary certification for apple maggot
control and in integrated control programmes for apple insects. It is
most economical and practical to use and where its use is permitted,
there is a much lower scale of use of DDT and other organochlorine
insecticides.
Although residues of both lead and arsenic are persistent, data are
available which indicate that approximately 50 per cent of these
residues are removed during the commercial handling and packing of
apples and further losses occur during the processing of apples to
such products as apple sauce. Under conditions of good agricultural
practice residues at harvest on apples average about 2 ppm. Most of
this residue is on the surface, with rarely more than 30 per cent in
SOME EXAMPLES OF CURRENT LIMITS (PPM) FOR ARSENIC AND LEAD IN FOOD
United
Canada New Zealand Britain* France** States Japan
Food of
America
As Pb As Pb As Pb As Pb As Pb As Pb
Apples, pears 2 7 1.1 nil 1 3 1.0 combined 2.7 5.0
7.0
Grapes 2 7 1.0 combined
7.0 0.76 1.0
Fresh vegetables 1 2 1.0 combined
7.0 0.76 1.0
Fruit and fruit 1.0 nil
products, canned
Marine and fresh canned canned
water animal 5 10 nil nil 5
products
Dried vegetables 2
(dry onions) 5 1.0
Fruit juices 0.1-0.2 0.2-0.5 0.1-0.5 0.2-2.0 0.2-0.3
0.5 muscle
Meat and/or meat 1 meat
products (not all liver 2 nil nil canned 1.0 1-2 by-products
included) only 5.0 0.5 eggs
Tea 1 10 5.0
Cocoa
(fat free, dry) 5
(continued)
SOME EXAMPLES OF CURRENT LIMITS (PPM) FOR ARSENIC AND LEAD IN FOOD
United
Canada New Zealand Britain* France** States Japan
Food of
America
As Pb As Pb As Pb As Pb As Pb As Pb
Wine 0.2 0.5 0.2 1.0 0.2
Ale, beer, stout 0.2 0.5 0.15 2 0.2-0.5 0.2
* When not scheduled limit is 1 ppm As and 2 ppm Pb.
** Suggested levels, 1950.
the edible pulp. However, after packaging this fruit for export, less
than one per cent of 500 commercial lots of samples contained
residues over 1 ppm, the average being between 0.2 and 0.5 ppm.
Total environmental and food monitoring surveys in North America and
information from other sources indicate that less than one per cent
of the arsenic and less than 10 per cent of lead ingested daily
results from the agricultural use of lead arsenate. The balance of the
load results from the use of arsenicals and lead for other purposes or
the presence of these elements in the environment. Thus, the amount of
arsenic in the total diet is not likely to be greater than 0.1 ppm or
a maximum of about 0.2 mg per day, while the total daily intake of
lead from all sources in food has been estimated at 0.2 to 0.4 mg per
day in the United States of America and 0.4 to 0.6 mg per day in a
major western European country. The former levels include the residues
resulting from currently approved agricultural uses of calcium and
lead arsenate in the United States of America, Canada, New Zealand and
other countries.
The attention of Member governments, however, should be drawn to this
situation so that they may take appropriate steps to reduce the intake
of lead and arsenic from other sources, should they so desire, bearing
in mind that the agricultural use of these compounds combined is
contributing much less than 15 per cent of the total lead currently
being ingested by man. In this connexion, it should be pointed out
that in several countries residues of arsenic and lead, resulting from
incidental contamination in the production of several foods, e.g.
grapes (i.e. residues in wine) have already been approved as "food
additives".
Recommendations
Since no acceptable daily intake has been recommended for either
arsenic or lead, no recommendation for tolerances can be made at this
time.
REFERENCES
Anon. (1966) More leads on lead. Brit. industr. biol. Res. Assoc.,
Info. Bull., 5 (9): 565-569
AOAC. (1965) Official methods of analysis, 10th ed., 24.045-24.056
Bishop, R. F., Chisholm, D. and Patterson, N. A. (1958) Arsenical
residues on the fruit and foliage of apple trees. Ninety-fifth Annual
Report of Nova Scotia Fruit Growers' Association, 81-85
Bishop, R. F., Chisholm, D. and Patterson, N. A. (1960) Arsenical
spray deposits on the fruit and foliage of apple trees. Ninety-sixth
Annual Report of Nova Scotia Fruit Growers' Association, 65-72
Bishop, R. F. and Chisholm, D. (1962) Arsenic accumulation in
Annapolis Valley orchard soils. Can. J. Soil Sci., 42: 77-80
Calvery, H. O., Lang, E. P. and Morris, H. J. (1938) The chronic
effects on dogs of feeding diets containing lead acetate, lead
arsenate and arsenic trioxide in varying concentrations. J. Pharmacol.
exp. Ther., 64: 364-387
Canada. (1964) Report of survey of arsenic residues on apples.
Submitted by Canada Department of Agriculture, Canada Food and Drug
Directorate
Castellino, N. and Aloj, D. (1964) Kinetics of the distribution and
excretion of lead in the rat. Brit. J. industr. Med., 21: 308-314
Chisholm, D., MacPhee, A. W. and MacEachern, C. R. (1955) Effects of
repeated applications of pesticides to soil. Can. J. Agric. Sci.,
35: 433-439
Chisholm, D. and Bishop, R. F. (1967) Lead accumulation in Nova Scotia
orchard soils. Phytoprotection, 482: 78-81
Chiswell, J. R. and Tew, R. P. (1965) Field trials with lead arsenate
for the control of the codling moth, Cydia pomonella (L.) on apples.
J. Hort. Sci., 40: 21-30
Coulson, E. J., Remington, R. E. and Lynch, K. M. (1935) Metabolism in
the rat of the naturally occurring arsenic of shrimp as compared with
arsenic trioxide. J. Nutr., 10: 254-270
Fairhall, L. T. and Miller, J. W. (1941) A study of the relative
toxicity of the molecular components of lead arsenate. Publ. Hlth
Rep., 56: 1610-1625
Finner, L. L. and Calvery, H. O. (1939) Pathologic changes in rats and
dogs fed diets containing lead and arsenic compounds. Arch. Path.,
27: 433-443
Flann, B. C. and Bartlett, J. C. (1968) Isolation and concentration of
traces of lead with strontium sulfate. J.A.O.A.C., 51: 719-724
Frost, D. V., Overby, L. R. and Spruth, H. C. (1955) Studies with
arsenilic acid and related compounds. J. Agr. Food Chem., 3: 235-243
Galy, P., Touraine, R., Brune, J., Gallois, P., Roudier, P.,
Loire, R., Lheureux, P. and Weisendanger, T. (1963) Les cancers
broncho-pulmonaires de l'intoxication arsenicale chronique chez les
viticulteurs du Beaujolais. Lyon Méd., 735-744
Hamence, J. H. (1965a) Annual Report on foods examined by public
analysts for pesticide residues during 1963. J. Assn. Publ. Anal.,
3: 17-20
Hamence, J. H. (1965b) Annual Report on foods examined by public
analysts for pesticide residues during 1964. J. Assn. Publ. Anal.,
3: 130-132
Hoffman, I. and Morse, P. M. (1961) Evaluation of several arsenic
residue methods. J.A.O.A.C., 44: 179-182
Hoffman, I. and Gordon, A. D. (1963) Arsenic in foods: Collaborative
comparison of the arsine-molybdenum blue and the silver
diethyldithiocarbamate methods. J.A.O.A.C., 46: 245-249
Japan. (1968) Residues of lead and arsenic in various crops grown in
Japan. Codex Contact Point
Kehoe, R. A. (1966) Summary: Risk of exposure and absorption of lead
in Symposium on Environmental Lead Contamination. U.S. Publ. Hlth
Service Publ. No. 1440 pages 155-157
Lehman, A. J. (1951) Chemicals in foods: A report of the Association
of Food and Drug Officials on Current Developments. Part II.
Pesticides. Ass. Food and Drug Office, Quart. Bull., 15 (4): 122-131
and Table I
Lewis, K. H. (1966) The diet as a source of lead pollution in
Symposium on Environmental Lead Contamination. U.S. Publ. Hlth
Service Publ. No. 1440 pp. 17-20
MacPhee, A. W., Chisholm, D. and MacEachern, C. R. (1960) The
persistence of certain pesticides in the soil and their effect on crop
yields. Can. J. Soil Sci., 40: 59-62
McCaldin, R. O. (1966) Estimation of sources of atmospheric lead and
measured atmospheric lead levels in Symposium on Environmental Lead
Contamination. U.S. Publ. Hlth Service Publ. No. 1440 pages 7-15
Morris, H. J. and Wallace, E. W. (1938) The storage of arsenic in rats
fed a diet containing calcium arsenate and arsenic trioxide.
J. Pharmacol. exp. Therap., 64: 411-419
NRC. (1966) Scientific aspects of pest control. Symposium National
Academy of Science, National Research Council, Washington, D.C.
Patterson, C. C. (1965) Contaminated and natural lead environments of
man. Arch. environm. Hlth, 11: 344-360
Pocklington, W. D. and Tatton, J. O'G. (1966) Pesticide residues in
foodstuffs in Great Britain. III. Arsenic and Lead Residues in
Imported Apples. J. Sci. Food Agric., 17: 570-572
Roth, F. (1956) Über die chronische Arsenvergiftung der Moselwinzer
unter besonderer Berücksichtigung des Arsenkrebses. Z. Krebsforsch.,
61: 287-319. Chem. Abstr., 51: 18450 h
Roth, F. (1957a) Arsenic liver tumours (translated title).
Z. Krebsforsch., 61: 468-503. Chem. Abstr., 52: 4836 c
Roth, F. (1957b) Über die Spätfolgen des chronischen Arsenismus der
Moselwinzer. Dtsch. med. Wschr., 82: 211-217. Chem. Abstr.,
51: 15796 c
Roth, F. (1958) Über den Bronchialkrebs arsengeschädigter Winzer.
Virchows Arch. path. Anat., 331: 119-137. Chem. Abstr.,
53: 10649 d
Rymer, T. E. and Hamence, J. H. (1967) Annual Report on food examined
by public analysts for pesticide residues during 1965. J. Assn. Publ.
Anal., 5: 24-26
Sollmann, T. (1957a) A Manual of Pharmacology, page 1342. W. B.
Saunders Co., Philadelphia
Sollmann, T. (1957b) A Manual of Pharmacology, page 1199. W. B.
Saunders Co., Philadelphia
Sollmann, T. (1957c) A Manual of Pharmacology, page 1203. W. B.
Saunders Co., Philadelphia
Tatton, J. O'G. (1965) Lead and arsenic in Canadian apples. Part I.
Scientific Sub-Committee on Poisonous Substances used in Agriculture
and Food Storage Report (unpublished)
Tew, R. P., Sillibourne, J. M. and Silva-Fernandes, A. M. (1961)
Pesticide residues on fruit. V. Harvest residues of codling moth
insecticides on apples. J. Sci. Food Agric., 12: 666-674
Tew, R. P. and Sillibourne, J. M. (1964) Pesticide residues on fruit.
VI. Lead and arsenic residues on apples. J. Sci. Food Agric.,
15: 678-683
Webster, R. L. and Marshall, J. (1934) Arsenic deposit and codling
moth control. State College of Washington Agricultural Experiment
Station Bull., 293: 5-31
Voigt, J. L., Edwards, L. D. and Johnson, C. H. (1948) Acute toxicity
of arsenate of lead in animals. J. Amer. pharm. Ass., sci. Ed.,
37: 122-123
See Also:
Toxicological Abbreviations
Lead arsenate (ICSC)
Lead arsenate (FAO Meeting Report PL/1965/10/1)