101. Organomercury compounds (FAO/PL:1967/M/11/1)

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

ORGANOMERCURY COMPOUNDS

These pesticides were evaluated under the heading "Phenylmercury
acetate (and other organomercury compounds)" by the 1966 Joint Meeting
of the FAO Working Party and the WHO Expert Committee on Pesticide
Residues (FAO/WHO, 1967a). Since the previous publication, the results
of additional experimental work have been reported. This new work is
summarized and discussed in the following monograph addendum.

IDENTITY

Chemical names

The following organomercury compounds additional to those in the
previous monograph are noted:

Methylmercury compounds: MeHgX

methylmercury acetate

methylmercury nitrile

methylmercury propionate

methylmercury sulphate

methylmercury p-chlorobenzoate

methylmercury pentachlorphenate

methylmercury oxinate

methylmercury 2,3-dihydroxyprophyl mercaptide

N-methylmercury 1,2,3,6-tetrahydro-3,6-endomethano-
3,4,5,6,7,7-hexachlorophthalimide

Ethylmercury compounds: EtHgX

ethylmercury silicate

ethylmercury oleate

ethylmercury stearate

ethylmercury hydroxide

ethylmercury pentachlorophenate

ethylmercury urea

ethylmercury acetone

ethylmercury 8-hydroxyquinolinate

Alkoxyarylmercury compounds RO(CH₂)MgX

methoxyethylmercury dicyandiamide

methoxyethylmercury benzoate

methoxyethylmercury lactate

ethoxymethylmercury silicate

ethoxythylmercury hydroxide

1-Carboxy-3-ethoxyethylmercury propanedicarboxylate-2,3
Chlorometroxypropylmethyl acetate

Arylmercury compounds: ArHgX

phenylmercury hydroxide

phenylmercury iodide

phenylmercury benzoate

phenylmercury lactate

phenylmercury oleate

phenylmercury propionate

phenylmercury naphthenate

phenylmercury pyrocatechinate

phenylmercury triethanolammonium lactate

phenylmercury formamide

diphenylmercury dodecenyl succinate

tolylmercury chloride

N-tolylmercury p-toluenesulphamilide

Other Organomercury Compounds

Ethyl phenethynyl mercury

Dichlorobromoethylmercury

Methyl bromide mercurimercaptide

Methoxacetyl mercurychloride

Cresol mercury naphthenate

EVALUATION FOR ACCEPTABLE DAILY INTAKES

Biochemical aspects

Groups of 15 rats were given drinking water containing 2µg/ml of
mercury as ²⁰³Hg-labelled methyl-, ethyl-, and propylmercury cyanide,
hydroxide and propanediolmercaptide, for 3 weeks. One-third of the
animals from each of the nine groups were killed at one, two and three
weeks for tissue analysis. Activity was examined in kidney, blood,
liver and brain, and concentrations were generally found to be
distributed in that order, the greatest concentrations always found in
the kidney. It was found that the tissue concentrations increased with
time. No special affinity of alkyl mercury for the brain was found:
the blood concentrations were generally 20 times brain levels, and the
author felt that most or all of the brain activity could be accounted
for on the basis of blood content. Relative tissue partitions were
constant with time for each alkyl mercury cation regardless of anion,
indicating marked stability of the alkyl-mercury bond (Ulfvarson,
1962).

In similar subcutaneous injection studies with methyl- and
phenylmercury hydroxide, methylmercury dicyandiamide,
methoxyethylmercury hydroxide and mercuric nitrate, lasting 18 days,
the body half-life of the methylmercury compounds was found to be
about 20 days and no steady-state was achieved during the time of the
experiment. In the case of the other three compounds, the half-life
was found to be about 10 days and steady states were achieved. The
renal concentration of the methylmercury compounds was relatively
quite low and the blood and muscle concentration high. The principal
route of excretion for all was via the faeces, even in the case of the
latter three compounds, which were highly concentrated in the kidneys
(Ulfvarson, 1962).

In dogs given intravenous injections of 30-60 mg/kg of methylmercury
thioacetamide, or of tracer doses labelled with ²⁰³Hg, the highest
brain concentrations were found in the calcarine fissure and
surrounding area; this was also the site of the greatest histological
change. The distribution was nearly equal in the gray and white
matter. In rats sacrificed 6-10 hours post-injection, the highest
subcellular concentrations were found in the mitochondria; but in
longer experiments, more equal distribution in these fractions was
seen, except that the major part of the mercury in the nuclear
fraction was accounted for by that carried in the erythrocytes
(Yoshino et al., 1966).

Short-term studies

Chicken. Groups of 3-5 hens were fed 0 and approximately 3 and 4.5
ppm of mercury as methylmercury dicyandiamide on dressed grain for 1-2
months. Group average mercury consumptions were: 0, 2.8 and 3.5
mg/bird/week of mercury. No mercury-attributed difference in general
behaviour and egg production was seen between the groups, and gross
and microscopic pathology were comparable. Mercury levels in whole
eggs of the control birds averaged about 0.01 ppm while the mean in
both treated groups after one month was about 8 ppm. Residues in whole
eggs of the lower test level group rose to 11 ppm in the fifth and
sixth weeks and those in the higher level group rose to 12 ppm in the
seventh and eighth week. The first significant mercury residue was
detected 3 days after beginning the trial. Mercury residues in the
muscle of control hens ranged from 0.005 to 0.02 ppm, and in the test
groups from 1.5 to 8.7 ppm. Residues in control livers were from nil
to 0.1 ppm, and in test animals from 8.1 to 24.1 ppm (Smart & Lloyd,
1963).

Observations in man

A 16-month-old infant, apparently healthy-normal for his first 13
months, fed probably almost daily from the ninth month of age porridge
made from grain treated with methylmercury dicyandiamide, was found to
have signs of extensive central nervous system motor disturbance and
mental retardation, in addition to slight renal disease. The urine
contained about 30-100 µg/l of mercury. The EEG was essentially
unremarkable. Treatment with BAL was not effective. Of the other
members of the family, the father had undergone treatment for mercury
poisoning from the same source; and the mother, although showing 64
and 28 µg/1 of mercury in two urine samples taken, remained
asymptomatic, but gave birth to a baby girl who, although showing no
other signs of mercurialism and a urinary content of less than 3 µg/l,
later showed marked mental retardation and neuromotor deficit. The
authors also report four other cases of accidental methylmercury
dicyandiamide poisoning in children. None showed a urinary mercury
content greater than 3 µg/l; two showed initial acute cerebral signs,
excitement, dizziness, hallucinations and fever; and only one showed
any EEG change, a slight dysrhythmia (Engleson & Herner, 1952).

Eighty-nine cases of a severe neurological disorder from 1953 to 1965
in the small Minamata Bay area of south-western Japan were attributed
to ingestion of fish and shellfish from the bay, which has been
contaminated with mercury from the effluent of a vinyl chloride
manufacturing plant. The mercury was believed to be an alkylmercury
salt. Fish-eating birds and animals in the area were also affected. In
a few isolated instances, the person became ill after a definite
latent period of a few weeks after ingestion of shellfish from the
bay. Thirty-nine of the cases were fatal. No sex or age difference in
incidence was observed. Clinical findings included incoordination,
involuntary movements, upper motor neuron degeneration and often

severe emotional and intellectual impairment. It was felt that the
children were particularly liable to residual defects. Autopsies
showed that the pathological changes were mostly confined to the
central nervous system, with gross cerebral oedema and atrophy of the
paracalcarine cerebral cortex and the cerebellum. Nerve-cell
degeneration and gliosis was found in the granular layer of the
cerebellum and, to a lesser degree, in the basal ganglia,
hypothalamus, mid-brain and cerebral cortex (Kurland et al., 1960).

In the same geographic area, from 1955 to 1960, seventeen cases of
cerebral palsy have been observed in infants who had eaten no fish or
shellfish from the area, born of mothers with generally no
neurological disease. In two cases presented in detail, terminating
fatally at 2-1/2 years and 6-1/4 years, clinical findings included
spastic paralysis, upper motor neuron deficit, epilepsy and idiocy. At
autopsy, lesions very similar in type and distribution to those seen
in cases of "Minamata disease" were found. Although the disease had
been reported in the families of these two infants, one of the mothers
had remained asymptomatic and the other had only experienced
occasional numbness of the fingers (Matsumoto et al., 1965).

Mud from Minamata Bay showed mercury residues ranging from 19 to 59
ppm and 2010 ppm in the town effluent channel. Oysters from the middle
of the bay contained 38-69 ppm of mercury and mercury residues in
samples of shellfish from three different areas showed residues
ranging from 27 to 102 ppm. Shellfish from the bay were found to be
toxic to laboratory animals, producing weight loss, neurological
damage, convulsions, coma and death. Day-old chicks were affected 8-10
days after beginning diets containing the seafood, whereas signs
developed in cats only after 5-8 weeks. Total ingestion of only 20-80
mg of mercury per animal from this source sufficed to produce
intoxication in cats. Abnormal quantities of mercury were found in
Minamata cats dying of the disease up to 62,36,19 and 70 ppm in liver,
kidney, brain and hair, respectively, vs.4, 0.8, 0.1 and 3 ppm in
the same tissues of "control" cats from the same area.

Mercury residue ranges in eight patients who died within three months
of development of the disease were: liver, 35-71 ppm; kidney, 29-144
ppm; and brain, 5-21 ppm (Kurland et al., 1960)

Comments

In view of the toxicity of organo-mercurial compounds, as well as the
fact that mercury is present in nature at various levels, it is very
important to know more about the overall intake of mercury from the
environmental background, as well as its health hazards.

It will also be helpful to know the nature of the mercurial compounds
appearing in food.

TOXICOLOGICAL EVALUATION

It is not possible to establish an acceptable daily intake on the
basis of available information. Any use of mercury compounds that
increases the level of mercury in food should be strongly discouraged.

Further work required

Information on the background level of mercury in the environment in
different parts of the world as well as epidemiological observation in
regions where the background level is known.

EVALUATION FOR TOLERANCES

This section draws particularly upon the paper on Organomercury
Compounds prepared for the Codex Committee on Pesticide Residues by
the UK Delegation to the Committee with assistance from the Swedish
delegation (CCPR, 1967a) which at its meetings in the Hague 18-22
September 1967 was referred by the Codex Committee to the Joint
Meeting for a toxicological evaluation of the maximum residues therein
suggested. These residues relate to crops or food stuffs treated with
organomercury compounds in accordance with good agricultural practice
and are:

rice 0.3 ppm (provisional)

apples, tomatoes 0.1 ppm

eggs, meat + 0.1 ppm

potatoes 0.05 ppm

wheat, barley 0.03 ppm

+ except liver and kidney

The Codex Committee (CCPR, 1967b) also commented that a permissible
residue for organomercury, as distinct from inorganic mercury [or
total mercury] could not be put forward on information then available;
and added that the maximum level of mercury in sea water fish appeared
from the limited evidence available to be 0.1 ppm although in a
mercury-contaminated environment fish tended to accumulate mercury and
very high residue levels could occur in these circumstances.

USE PATTERN

Pre-harvest treatments

Table I gives supplementary details of the rates of application of
organomercurials for pre-harvest and seed treatments, and is taken
from the Codex Committee paper, having been obtained by that Committee
by means of a questionnaire to FAO Member Governments thought to be
using significant quantities of mercury in agriculture.

Table I Rate of Application of Organomercurials

Crop/Seed Country Rate of each application Stage of
g mercury/kg g mercury/ha application

wheat Australia 0.1 - 6.0 seed
barley 1.6 - 2.5
oats
sorghum Israel 0.01
millet Belgium 2
Sweden 0.02 - 0.04
Korea 0.4
Germany 0.04 - 0.06
U.S.A. 0.01 - 0.2
Bulgaria 0.02
Norway 1 - 2
Morocco 0.01 - 0.02
Hungary 0.5
Portugal 0.03
Austria 0.04
Spain 0.03 - 0.05
Denmark 0.01 - 0.1
N.Zealand 0.01 - 0.03
U.K. 0.01 - 0.03

rice Korea 0.4 seed
10 - 20 up to tillering
U.S.A. seed
India 60 up to tillering

flax U.S.A 0.02 - 0.3 seed

cotton Australia 0.08 seed
Israel 0.2
U.A.R. 5
U.S.A. 0.03 - 0.3 seed
11 soil treatment in furrow

Table I (cont'd)

Crop/Seed Country Rate of each application Stage of
g mercury/kg g mercury/ha application

potatoes Australia 0.1 - 0.2 seed tubers
U.K. 20 foliar spray

hops Australia 0.1 - 0.2 setts

apples Sweden paint early spring
Australia 40 - 280 up to early fruit growth
Germany 100 pre-blossom
U.S.A. 60 - 400 delayed dormant to petal fall
N. Zealand 50 - 250 up to 8 weeks before harvest
U.K. 15 - 90 up to 6 weeks before harvest
Denmark 15

pears Australia 250 - 800 dormant
45 - 250 bud burst to petal fall
U.S.A 80 to petal fall

tomatoes U.K. not more than
40 mg mercury/
1000 cu ft
glasshouse on growing fruit

vine Australia 1.3 kg dormant

sugar Israel 0.14 seed
beet Germany 0.12
Austria 0.12
Sweden 0.05

beans/corn U.S.A 0.3 - 0.7 seed
peas/peanuts

Table I (cont'd)

Crop/Seed Country Rate of each application Stage of
g mercury/kg g mercury/ha application

cherries/peaches U.S.A 20 - 40 up to petal fall
apricots/almonds 120 - 600 before buds swell to
petal fall

turf Australia 450g-10kg

Other uses

Widmark (1967) has indicated a number of other uses of organomercurial
compounds which, whilst not agricultural in character, may have a
bearing on the general situation of organomercury residues in food.
These were reviewed at the 1967 Commission meetings arranged by IUPAC
Pesticides Section and are summarized below:

(i) Metallic mercury finds a variety of technical uses; during
manufacture or especially in the disposal of worn or used products
such as electrical relays, an unknown quantity of metallic mercury is
introduced into the environment.

(ii) Soluble inorganic salts of mercury are also used industrially on
a reduced scale and thus some mercury will be introduced into sewage.

(iii) In chemical industries electrodes of mercury are in use and
vapours of mercury will accompany the waste gases through chimneys
into the air. In Sweden it has been estimated that in 1964 the
chlorine industry added approximately five tons of mercury into the
air and another five tons to the water; this can be compared with 3.5
tons of phenyl mercury as waste from the pulp industry (+ 0.5 tons
from the burning of newspaper) and 4.5 tons of methyl mercury as seed
dressing. (The use of alkyl and phenyl mercury is now banned in
Sweden).

(iv) Since most minerals, fuels and soils contain trace amounts of
mercury, heating of these materials on a large scale will serve as a
source for the contamination of mercury in nature.

(v) The same might be true for extraction processes, e.g. flotation of
ore using reagents of complex forming properties.

(vi) Non-mercury containing pollutants with complex forming properties
may be able to convert mercurial minerals into a biologically
receptable form.

Regarding the widespread natural occurrence of traces of mercury,
Widmark (1967) quotes atmospheric levels as approximately 20 nanograms
per cubic metre and rainwater levels as about 200 nanograms per litre.

Other aspects of mercury occurrence

(i) In commenting on the geochemistry of mercury as applied to
prospecting, Warren et al. (1966) say that British Columbia contains
extensive mercury-bearing metallogenetic areas, but soils may be
considered normal where they contain less than 0.05 ppm mercury. In
the vicinity of the gold, molybdenum, and base metal deposits they
have examined, soils may be expected to carry from 0.05 to 0.25 ppm
reaching, in a few instances, as much as 2 ppm mercury. Varying
amounts of humic material and clay in soil fractions modify the
ability of a soil to accumulate mercury. Around mercury deposits there

are usually from 1 to 10 ppm mercury in soils and in some cases much
more. Different organs, and different species of plants vary widely in
their ability to concentrate mercury. In medium and low ranges, plant
sampling offers some advantages over soil sampling. If the calculated
ash contents of vegetation runs more than 10 ppm mercury, there
probably in mineralization in the vicinity. (In subsequent
correspondence Professor Warren has said that he does not know the
form in which mercury is present in vegetation. The above remarks
presumably relate to mercury in the inorganic form).

(ii) The following is extracted from the Tenth Report of the Joint
FAO/WHO Expert Committee on Food Additives (FAO/WHO,p 1967b).

Mercury occurs naturally in minute amounts in foods and beverages and
as a contaminant from its uses as fungicides and in industry. Mercury
is a particular cumulative-poison and not known to serve any essential
function in man or animals. However, there is evidence that
contamination of the environment with mercury is increasing.

Average intakes of mercury from the diet were estimated some years ago
to range from 0.00083 to 0.00033 mg/kg body-weight/day, with little
accumulation at these levels of intake. Modern studies of the
distribution of mercury in human foods and beverages and in human
tissues in different environments and at different ages are urgently
required.

RESIDUES RESULTING FROM SUPERVISED TRIALS

Pre-harvest treatments

Residues in the case of cereals sown from dressed seed are
insignificant: wheat normally dressed has been found to contain 0.01
ppm Hg whilst barley contained 0.008 - 0.012 ppm whether dressed or
not. Furutani and Osajima (1965) found 0.2 ppm for undusted rice and
twice that level after treatment. Tomizawa (1966) found similar levels
for untreated polished rice but 0.1 to 1.0 after field treatment with
phenylmercury acetate.

Smart and Hill (1967) have examined samples of rice imported into
Britain and concluded that, in contrast to the position in Japan the
mercury levels found were often negligible (mean 0.001 ppm) though an
occasional sample might contain as much an 0.015 ppm Hg. Stone et al.
(1957) have shown that phenylmercuric sprays applied to apples under
commercial conditions do not give rise to residues in excess of 0.05
ppm Hg when application is discontinued at closed calyx. Nardin (1965)
found an average of 0.02 ppm Hg on treated apples over two seasons.
Smart (1961) found residues well below 0.1 ppm five weeks or more
after the last of eight commercial mercury applications. Limited data
for treated pears gives 0.04 ppm (untreated), and 0.14 to 0.26 ppm
two to four months after treatment.

RESIDUES IN FOOD MOVING IN COMMERCE

Westoo et al (1965) have examined eggs on the Swedish retail market
and elsewhere: the mean value for Swedish eggs (79 samples) was
0.029 ppm whilst elsewhere in Europe the mean value was less than
0.010 ppm. Westoo (1966a) has also examined chicken (0.005 - 0.023
ppm) and other meets from Denmark and Sweden: levels in Danish pork
and beef were 0.003 - 0.005 (liver 0.009) ppm, and in Swedish pork
and beef up to ten times higher. Mean values for fish in Sweden ranged
from 0.031 to 1.30 ppm (25 samples of perch) with individual fish
containing up to 5 ppm (Westoo, 1966b). The 1967 Codex paper (CCPR,
1967a) suggested that, based on limited evidence, the maximum "normal"
level in sea fish was 0.1 ppm.

FATE OF RESIDUES

General considerations

At meetings in August 1967 the IUPAC Commission on Terminal Pesticide
Residues (IUPAC, 1967) recognised that recent work had shown that
inorganic mercury can be transformed into methylmercury compounds in
nature; this is a further complication in an already complex residue
situation. Westoo (1966b) has examined gas and thin-layer
chromatographic methods for the determination of methylmercury
compounds in fish from Baltic and Swedish waters, with results varying
from 0.07 to 4.45 ppm. Widmark (1967) concluded that contamination by
mercury in nature seemed to be due to a complex series of factors of
which organomercury pesticides was only one factor. A full scientific
understanding of the complex is desirable and calls for the fullest
cooperation of scientists in a variety of disciplines.

METHODS OF RESIDUE ANALYSIS

These have been further reviewed by Widmark (1967). Only limited
progress in the development of analytical residue methods specifically
for alkyl, alkoxy and arylmercurials was reported. Of particular
promise are methods based on chromatography as described by Westoo,
(1966b), together with methods making use of ion exchanges
electrophoresis and gel filtration.

NATIONAL TOLERANCES

Existing tolerances (all of which refer to residue measured as Hg
without distinction between the forms in which the metal may actually
be present in the food) are as follows:-

Established

USA - zero on fruits and vegetables

Brazil - 0.05 ppm

Australia - 0.1 in S. Australia and Victoria, 0.01 ppm in
Western Australia

N. Zealand - zero, except fruit and vegetables (0.05 ppm)

Benelux - 0.03 ppm

Germany - zero (where derived from pesticide treatment)

Guidance only (maximum acceptable levels)

Denmark - 0.05 ppm

Sweden - 0.05 ppm except for fish (1.0) and drinking water

RECOMMENDATIONS FOR TOLERANCES

Since no acceptable daily intake level or temporary acceptable daily
intake level can be given for mercury or for organomercurial
compounds, it is not possible to recommend tolerances or temporary
tolerances. Small natural concentrations of mercury appear to be
widespread but the levels vary from area to area; it is also
difficult, therefore, to suggest a practical residue limit for
mercury. By way of guidance, however, practical residue limits of from
0.02 ppm to 0.05 ppm mercury, according to local conditions, are
suggested. Of the present uses of organomercurials reviewed, only
those relating to the use on apples before and up to petal fall and to
the treatment of cereal and other seeds do not appear to produce
residues of mercury in the harvested crop significantly in excess of
the natural background level of mercury. Surplus, waste or other seed
which has been treated with organomercurial compounds should not be
fed to poultry.

FURTHER WORK

Further work required

Further work on the development on sensitive methods of analysis
specifically for alkyl, alkoxy and arylmercurials is still required in
order to study the occurrence of these forms of mercury in foodstuffs
from different sources. Further work on the possible natural
conversion of inorganic mercury to organically bound mercury is also
required.

The Codex Committee on Pesticide Residues (CCPR, 1967b) also
considered the need for additional information on background levels of
mercury in foods from a range of environments and on the nature,
amounts and fate of mercury compounds in industrial effluents and the
resultant levels of mercury likely to occur in fish, including
shellfish. The Joint FAO/WHO Expert Committee on Food Additives
(FAO/WHO 1967b) has also expressed the view that modern studies of the
distribution of mercury in human food and beverages (and in human

tissue) in different environments is urgently needed and has concluded
that until the results of such studies are available it is not
possible to set meaningful maximum permissible limits in dietary
intakes for this element.

REFERENCES PERTINENT TO EVALUATION FOR ACCEPTABLE DAILY INTAKES

Engleson, G. & Herner, T. (1952) Acts Ped., 41, 289

Kurland, L.T., Paro, S.N. & Siedler, H. (1960) Wld Neurol, 1, 370

Matsumoto, H., Koya, G. & Takeuchi, T. (1965) J. Neuropathol.
exper. Neurol., 24, 563

Smart, N.A. & Loyd, M.K. (1963) J. Sci. Food Agric., 14, 734

Ulfvarson, U. Int. Arch. Gewerbepathol. Gewerbepharmakol., 19, 12

Yoshino, Y., Mozai, T. & Nakao, K. J. Neurochem., 13, 397

REFERENCES PERTINENT TO EVALUATION FOR TOLERANCES

CCPR. (1967a) Organomercury compounds. Paper prepared by the United
Kingdom Delegation assisted by the Delegation of Sweden for
presentation to the Second Session of the Codex Committee on Pesticide
Residues. The Hague, The Netherlands. CCPR 67.13

CCPR. (1967b) Report of the Second Session of the Codex Committee on
Pesticide Residues. SF 10/115

FAO/WHO. (1967a) Evaluation of some pesticide residues in food. FAO,
PL:CP/15:WHOFood Add./67.32

FAO/WHO. (1967b) Specifications for the identity and purity of food
additives and their toxicological evaluation: some emulsifiers and
stabilizers and certain other substances. (Tenth Report of the Joint
FAO/WHO Expert Committee on Food Additives.) FAO Nutrition Mtg. Rept.
43;WHO Tech. Rept. 373.

Furutani, S., Osajima, Y. (1965) Residual components from agricultural
chemicals in food. Kyusho Daigaku Nogakubu Gakugei Zasshi 21: 363-369;
22: 45-48

IUPAC. (1967) Proceedings of the Commission on Pesticide Residue
Analysis. IUPAC Pesticides Section, Vienna.

Nardin, H.F., (1965) An investigation of spray residues in apples and
pears. N.S. Wales Dept. Agr. Chem. Bull. S.36

Smart, N.A. (1961) Arylmercury spray residue in apples. Plant Pathol.
10: 150-160

Smart, N.A., Hill, A.R.C. (1967) Supplement to CCPR, 1967a

Stone, H.M., P.J. Clark, Jacks, H. (1967) Mercury content of apples.
N. Zealand J.Sci. Technol. 38: 843-848

Tomizawa, C. (1966) Behaviour of mercury in rice plants treated with
organomercury Hg-203 fungicides. Shokuhin Eiseigakn Zasshi 7 : 26

Warren, H.V., Delavault, R.E., Barakso, J. (1966) Some observations on
the geochemistry of mercury as applied to prospecting. Econ. Geog.
61 : 1010-1028.

Westoo, G., Sjostrand, B., Westermark, T. (1965) (Mercury in hens
eggs). Var Foda 17 : 1

Westoo, G. (1966a) (Mercury in chicken and other meat). Var Foda 18 :
85-88

Westoo, G. (1966b) Methylmercury compounds in fish: identification and
determination. Acta Chem. Scand. 20 : 2131-2137.

Widmark, G. (1967) Proceedings of the Commission on Pesticide Residue
Analysis. IUPAC Pesticides Section. Appendix XIV.

    See Also:
       Toxicological Abbreviations