INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
ENVIRONMENTAL HEALTH CRITERIA 42
TECNAZENE
This report contains the collective views of an international group of
experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization.
Published under the joint sponsorship of
the United Nations Environment Programme,
the International Labour Organisation,
and the World Health Organization
World Health Orgnization
Geneva, 1984
The International Programme on Chemical Safety (IPCS) is a
joint venture of the United Nations Environment Programme, the
International Labour Organisation, and the World Health
Organization. The main objective of the IPCS is to carry out and
disseminate evaluations of the effects of chemicals on human health
and the quality of the environment. Supporting activities include
the development of epidemiological, experimental laboratory, and
risk-assessment methods that could produce internationally
comparable results, and the development of manpower in the field of
toxicology. Other activities carried out by the IPCS include the
development of know-how for coping with chemical accidents,
coordination of laboratory testing and epidemiological studies, and
promotion of research on the mechanisms of the biological action of
chemicals.
ISBN 92 4 154182 2
The World Health Organization welcomes requests for permission
to reproduce or translate its publications, in part or in full.
Applications and enquiries should be addressed to the Office of
Publications, World Health Organization, Geneva, Switzerland, which
will be glad to provide the latest information on any changes made
to the text, plans for new editions, and reprints and translations
already available.
(c) World Health Organization 1984
Publications of the World Health Organization enjoy copyright
protection in accordance with the provisions of Protocol 2 of the
Universal Copyright Convention. All rights reserved.
The designations employed and the presentation of the material
in this publication do not imply the expression of any opinion
whatsoever on the part of the Secretariat of the World Health
Organization concerning the legal status of any country, territory,
city or area or of its authorities, or concerning the delimitation
of its frontiers or boundaries.
The mention of specific companies or of certain manufacturers'
products does not imply that they are endorsed or recommended by the
World Health Organization in preference to others of a similar
nature that are not mentioned. Errors and omissions excepted, the
names of proprietary products are distinguished by initial capital
letters.
CONTENTS
ENVIRONMENTAL HEALTH CRITERIA FOR TECNAZENE
1. SUMMARY AND RECOMMENDATIONS
1.1. Summary
1.1.1. Identity, analytical methods and
sources of exposure
1.1.2. Environmental concentrations and
exposures
1.1.3. Kinetics and metabolism
1.1.4. Studies on experimental animals
1.1.5. Effects on man
1.1.6. Effects on the environment
1.2. Recommendations
2. IDENTITY, PROPERTIES AND ANALYTICAL METHODS
2.1. Identity
2.2. Properties and analytical methods
2.2.1. Physical and chemical properties
2.2.2. Analytical methods
3. USES, ENVIRONMENTAL LEVELS AND EXPOSURES, TRANSPORT AND DISTRIBUTION
3.1. Uses
3.2. Environmental levels and exposures
3.2.1. Levels in food
3.2.2. General population exposure
3.3. Transport and distribution
4. KINETICS AND METABOLISM
5. STUDIES ON EXPERIMENTAL ANIMALS
5.1. Short-term exposures
5.1.1. Single exposure
5.1.2. Repeated exposure
5.2. Long-term exposure
5.3. Reproduction studies
5.4. Teratogenicity
5.5. Carcinogenicity
6. EFFECTS ON MAN
7. EFFECTS ON THE ENVIRONMENT
8. PREVIOUS EVALUATIONS OF TECNAZENE BY INTERNATIONAL BODIES
9. EVALUATIONS OF HEALTH RISKS FOR MAN AND EFFECTS ON THE ENVIRONMENT
9.1. Evaluation of health risk for man
9.2. Evaluation of overall environmental effects
9.3. Conclusions
REFERENCES
TASK GROUP MEETING ON ENVIRONMENTAL HEALTH CRITERIA FOR
ORGANOCHLORINE PESTICIDES OTHER THAN DDT (ENDOSULFAN,
QUINTOZENE, TECNAZENE, TETRADIFON)
Members
Dr E. Astolfi, Faculty of Medicine of Buenos Aires, Buenos
Aires, Argentina
Dr I. Desi, Department of Environmental Hygienic Toxicology,
National Institute of Hygiene, Budapest, Hungary
Dr R. Drew, Department of Clinical Pharmacology, Flinders
University of South Australia, Bedford Park, South
Australia
Dr S.K. Kashyap, National Institute of Occupational Health,
Ahmedabad, India
Dr A.N. Mohammed, University of Calabar, Calabar, Nigeria
Dr O.E. Paynter, Office of Pesticide Programs, US
Environmental Protection Agency, Washington DC, USA
Dr W.O. Phoon, Department of Social Medicine and Public
Health, Faculty of Medicine, University of Singapore,
Outram Hill, Singapore (Chairman)
Dr D. Wassermann, Department of Occupational Health, The
Hebrew University, Hadassah Medical School, Jerusalem,
Israel
Representatives of Other Organizations
Dr H. Kaufmann, International Group of National Associations
of Agrochemical Manufacturers (GIFAP)
Dr V.E.F. Solman, International Union for Conservation of
Nature and Natural Resources (IUCN), Ottawa, Ontario,
Canada
Secretariat
Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood
Experimental Station, Abbots Ripton, Huntingdon, United
Kingdom (Temporary Adviser)
Dr M. Gilbert, International Register for Potentially Toxic
Chemicals, United Nations Environment Programme, Geneva,
Switzerland
Dr K.W. Jager, Division of Environmental Health, International
Programme on Chemical Safety, World Health Organization,
Geneva, Switzerland (Secretary)
Secretariat (contd.)
Dr D.C. Villeneuve, Health Protection Branch, Department of
National Health and Welfare, Tunney's Pasture, Ottawa,
Ontario, Canada (Temporary Adviser) (Rapporteur)
Mr J.D. Wilbourn, Unit of Carcinogen Identification and
Evaluation, International Agency for Research on Cancer,
Lyons, France
NOTE TO READERS OF THE CRITERIA DOCUMENTS
While every effort has been made to present information in
the criteria documents as accurately as possible without unduly
delaying their publication, mistakes might have occurred and are
likely to occur in the future. In the interest of all users of
the environmental health criteria documents, readers are kindly
requested to communicate any errors found to the Manager of the
International Programme on Chemical Safety, World Health
Organization, Geneva, Switzerland, in order that they may be
included in corrigenda, which will appear in subsequent volumes.
In addition, experts in any particular field dealt with in
the criteria documents are kindly requested to make available
to the WHO Secretariat any important published information
that may have inadvertently been omitted and which may change
the evaluation of health risks from exposure to the
environmental agent under examination, so that the information
may be considered in the event of updating and re-evaluation
of the conclusions contained in the criteria documents.
* * *
A detailed data profile and a legal file can be obtained from
the International Register of Potentially Toxic Chemicals, Palais
de Nations, 1211 Geneva 10, Switzerland (Telephone no. 988400-
985850).
ENVIRONMENTAL HEALTH CRITERIA FOR TECNAZENE
Following the recommendations of the United Nations
Conference on the Human Environment held in Stockholm in 1972,
and in response to a number of World Health Resolutions
(WHA23.60, WHA24.47, WHA25.58, WHA26.68), and the
recommendation of the Governing Council of the United Nations
Environment Programme, (UNEP/GC/10, 3 July 1973), a programme
on the integrated assessment of the health effects of
environmental pollution was initiated in 1973. The programme,
known as the WHO Environmental Health Criteria Programme, has
been implemented with the support of the Environment Fund of
the United Nations Environment Programme. In 1980, the
Environmental Health Criteria Programme was incorporated into
the International Programme on Chemical Safety (IPCS). The
result of the Environmental Health Criteria Programme is a
series of criteria documents.
A WHO Task Group on Environmental Health Criteria for
Organochlorine Pesticides other than DDT (Endosulfan,
Quintozene, Tecnazene, Tetradifon) was held at the Health
Protection Branch, Department of National Health and Welfare
Ottawa from 28 May - 1 June, 1984. The meeting was opened by
Dr E. Somers, Director-General, Environmental Health
Directorate, and Dr K.W. Jager welcomed the participants on
behalf of the three co-sponsoring organizations of the IPCS
(UNEP/ILO/WHO). The Task Group reviewed and revised the draft
criteria document and made an evaluation of the health risks
of exposure to tecnazene.
The drafts of this document were prepared by Dr D.C.
Villeneuve of Canada and Dr S. Dobson of the United Kingdom.
The efforts of all who helped in the preparation and
finalization of the document are gratefully acknowledged.
* * *
Partial financial support for the publication of this
criteria document was kindly provided by the United States
Department of Health and Human Services, through a contract
from the National Institute of Environmental Health Sciences,
Research Triangle Park, North Carolina, USA - a WHO
Collaborating Centre for Environmental Health Effects.
1. SUMMARY AND RECOMMENDATIONS
1.1. Summary
1.1.1. Identity, analytical methods and sources of exposure
Technical tecnazene (2,3,5,6-tetrachloronitrobenzene), is an
odourless, crystalline solid that is used in its formulated form as
a fungicide and as a sprout inhibitor on stored potatoes. Gas
chromatography with electron capture detection is the preferred
method for its determination.
Exposure of the general population is expected to be mainly
through residues in food. The residues reported are below the
FAO/WHO maximum residue levels.
No cases of accidental or occupational overexposure have been
reported.
1.1.2. Environmental concentrations and exposures
Tecnazene is rapidly lost from treated soil, probably mainly
through evaporation.
1.1.3. Kinetics and metabolism
Tecnazene is rapidly absorbed and metabolized in the rat and the
rabbit following oral administration. High single oral doses (3000
mg in rabbit) are predominantly passed unchanged in the faeces.
Several metabolities are presumed in urine, the most important being
the mercapturic acid conjugate.
1.1.4. Studies on experimental animals
Tecnazene is only slightly toxic according to the scale of Hodge
& Sterner (1956). The oral LD50 of tecnazene in the rat is 7500
mg/kg body weight. WHO (1984) has classified tecnazene in the
category of technical products unlikely to present an acute hazard
in normal use.
In long-term studies, no-observed-adverse-effect levels were:
rat: 750 mg/kg diet for 104 weeks, equivalent to 38 mg/kg
body weight per day;
mouse: 1500 mg/kg diet, equivalent to 200 mg/kg body weight
per day; and
dog: 15 mg/kg body weight per day (administered orally by
capsule for 2 years).
At higher dosages (4000 mg/kg in diets with rats and 240 mg/kg
body weight in dogs), growth inhibition occurs and in dogs, the
plasma alkaline phosphatase levels increase.
In the tests conducted so far, tecnazene did not affect
reproduction (rats), nor was it embryotoxic or teratogenic (rats
and mice). No information on mutagenicity and other related short-
term tests is available. Data available from a mouse and a rat
study do not indicate that tecnazene is a carcinogen.
1.1.5. Effects on man
Dermal sensitivity has been reported in agricultural workers.
1.1.6. Effects on the environment
A lack of effect on bacteria of the nitrogen cycle has been
reported, but no other relevant information has been found.
1.2. Recommendations
1. Monitoring studies on occupationally-exposed
workers, especially workers in greenhouses, are
required concerning both levels of exposure and
potential health effects.
2. More data should be made available on tecnazene
levels in greenhouse crops.
3. The dermal toxicity, skin sensitization, and eye
irritation capacity of tecnazene should be determined
in both experimental animals and in the occupational
setting.
4. The genotoxicity and cell transformation capacity
of tecnazene should be studied. If these studies
indicate a need for it, an adequate carcinogenicity
study should be done.
5. The level of hexachlorobenzene as an impurity in
tecnazene should be kept as low as possible.
2. IDENTITY, PROPERTIES AND ANALYTICAL METHODS
2.1. Identity
Molecular formula: C6HCl4NO2
CAS chemical name: 2,3,5,6-tetrachloronitrobenzene
Common trade names: Chipman 3,142, Folosan, Fusarex,
Fumite, Folosan DB905, TCNB
CAS registry Number: 117-18-0
Relative molecular mass: 260.88
2.2. Properties and Analytical Methods
2.2.1. Physical and chemical properties
Tecnazene is a colourless, odourless, crystalline solid with a
melting point of 99 °C. It is fairly volatile at room temperature.
It is readily soluble in carbon disulfide, benzene, chloroform,
ketones, and aromatic and chlorinated hydrocarbon compounds. It is
practically insoluble in water (0.44 mg/litre at 20 °C), and its
solubility in ethanol is 40 g/litre at 25 °C (Worthing, 1979).
Tecnazene is generally very stable; it can be dispersed by
pyrotechnic mixtures. It decomposes slowly in solution when
exposed to ultraviolet radiation. The technical grade material is
more than 99% pure and contains less than 1% of hexachlorobenzene.
2.2.2. Analytical methods
Polarographic, colorimetric, and gas chromatography combined
with a flame detector method are described in the literature, but
gas chromatography with an electron-capture detector is the
preferred method for the determination of tecnazene residues
(Dalziel & Duncan, 1974; FAO/WHO, 1979). The limit of detection
with this method is approximately 0.01 mg/kg with a recovery of
more than 90% (FAO/WHO, 1979).
3. USES, ENVIRONMENTAL LEVELS AND EXPOSURES, TRANSPORT AND
DISTRIBUTION
3.1. Uses
Tecnazene is used as a sprout inhibitor on stored potatoes and
as a fungicide. In the latter application it is mainly used as a
smoke generator formulation in greenhouses (Table 1).
Table 1. Usage data for tecnazene in selected countriesa
-------------------------------------------------------------------
Area Quantity Year Use
-------------------------------------------------------------------
Sweden 200 kg 1981 horticultural use against
fungi in greenhouses
United Kingdom 0.14 tonne 1975-79 fungicide and sprout sup-
per year pressant; used as a dust or
spray on potatoes in storage
USA unknown 1981 fungicide
-------------------------------------------------------------------
a From: IRPTC, personal communication, 1984.
3.2. Environmental Levels and Exposures
No data are available on levels in air and water, or on
occupational exposure levels.
3.2.1. Levels in food
Washing, peeling, and cooking potatoes reduced levels of
tecnazene (Dalziel & Duncan, 1974). Potatoes that had been treated
with 3% tecnazene at a rate of 4.5 g/kg were found to contain 3
mg/kg, after 4 - 5 months storage (FAO/WHO, 1979). Washing reduced
the levels of tecnazene to below 1 mg/kg, and peeling further
reduced the levels to below 0.1 mg/kg. Another 50% loss of
tecnazene occured when the peeled potatoes were boiled. Market
basket surveys in the USA of about 300 potato samples revealed that
14 samples had detectable residues of tecnazene (i.e., 0.001 mg/kg
or more). Trace levels (0.01 mg/kg or less) of tecnazene were
found in 15 out of 3500 samples of USA foodstuffs (FAO/WHO, 1979).
Analyses of vegetable products in Belgium and Sweden for tecnazene
revealed that most of the lettuce, chicory, mushrooms, carrots,
sweet peppers, corn, etc., had levels between 0.001 and 0.01 mg/kg
fresh weight (Valange, 1974; FAO/WHO, 1979).
The WHO/FAO (1979) has recommended temporary maximum residue
(tolerance) levels (MRL) for tecnazene (Table 2).
Table 2. Temporary maximum residue (tolerance) levels (MRL) for
tecnazene
-----------------------------------------------------------------
Commodity Temporary MRL (mg/kg)
-----------------------------------------------------------------
Lettuce 2
Potatoes (washed before analysis) 1
Chicory (witloot) 0.2
Other vegetables 0.1
Tomatoes 0.1
-----------------------------------------------------------------
3.2.2. General population exposure
Environmental exposure is probably low due to its limited use
outdoors.
3.3. Transport and Distribution
Tecnazene is rapidly lost from sandy soil, probably mainly
because of its volatility (FAO/WHO, 1979).
4. KINETICS AND METABOLISM
Rabbits receiving a single oral dose of 0.1 - 3.0 g/animal
eliminated 60 - 78% in the faeces within 3 days, while the urine
accounted for 35 - 38% (primarily as conjugated products). At 0.01
g/animal, 22 - 30% was recovered in the faeces (Bray et al., 1953).
Mercapturic acid conjugate was excreted at a rate of 11% within
48 h of the administration of 1 - 3 g of tecnazene to rabbits.
Other metabolites excreted included an ether glucuronide (12%),
2,3,5,6-tetrachloroaniline (10%), unconjugated 4-amine-2,3,5,6-
tetrachlorophenol (2%) and an etheral sulfate (1%) (Bray et al.,
1953; Betts et al., 1955). A suggested pathway for the
biotransformation of tecnazene in rabbits based on data obtained
from Betts et al. (1955) is shown in Fig. 1. Similar amounts of
mercapturic acid were excreted in the urine of rats dosed with
tecnazene (Barnes et al., 1959). Tecnazene administered orally to
pigeons was converted to mercapturic acid (Wit & Reenwangh, 1969).
5. STUDIES ON EXPERIMENTAL ANIMALS
5.1. Short-Term Exposures
5.1.1. Single exposure
The acute oral LD50 for tecnazene in the rat is 7500 mg/kg
body weight (Klimmer, 1971). The acute intraperitoneal LD50 in
the rat is 3500 mg/kg body weight (Wit et al., 1960).
5.1.2. Repeated exposure
Tecnazene at 0, 1344, or 13 440 mg/kg diet was fed to groups of
mice (12 mice per group) for 31 days. No adverse effects were
observed at the 1344 mg/kg level, but growth was inhibited at 13
440 mg/kg (Buttle & Dyer, 1950).
Groups of rats (5 males, 5 females per group) received
tecnazene at 0, 800, 4000, and 20 000 mg/kg diet for 10 weeks.
Death occurred at 20 000 mg/kg; growth was reduced at 4000 mg/kg.
There were no effects on growth or mortality rate at 800 mg/kg
(Buttle & Dyer, 1950). Tecnazene at 2000 mg/kg, fed to rats for 10
weeks, did not have any effects on the general health, blood
picture, autopsy findings, and histological pictures of the liver
and kidney. Increased liver and testes weights were observed in
the males (no other details reported) (Wit et al., 1960).
Groups of pigs (2 per group) were fed tecnazene at 0, 120, 800,
or 1200 mg/kg of potatoes for 26 weeks (1200 mg/kg, equivalent to
7.1 g tecnazene/pig per day or 50 mg/kg body weight). Reduced body
weight gains were observed in the first half of the study for the
animals in the highest-dose group. General health, and results of
haematological tests, and gross and microscopic examination of the
liver and kidney were not affected (Abrams et al., 1950).
5.2. Long-Term Exposure
In a 2-year study, groups of beagle dogs (2 males and 2 females
per group; controls - 1 male and 1 female) were treated orally (by
capsule) with 0, 3.75, 15, 60, or 240 mg tecnazene/kg body weight
per day, for 6 days a week. At the 240 mg level, all animals died
within the first year of the study, and microscopic changes were
observed in liver, kidney, and bone marrow. Growth was normal in
all animals at 60 mg/kg, and the clinical chemistry was normal at
15 mg/kg (Donikian et al., unpublished data, 1965).
5.3. Reproduction Studies
In a two-generation reproduction study, groups of rats (5 males
and 5 females per group) were fed tecnazene at 0, 200, 800, or 3200
mg/kg diet for 12 weeks, prior to mating. No effects on reproduction
were noted at any dose level. Maternal growth was slightly inhibited
at the 3200 mg/kg dose level during the 12 week feeding period in
each generation, and fatty infiltration of the liver was noted. No
effects were observed in the animals on the 800 mg/kg diet (Buttle,
unpublished data, 1974).
5.4. Teratogenicity
CD rats and C57B116 mice were administered doses of up to 200
mg tecnazene/kg body weight orally on gestation days 7 -18. Neither
embryotoxic nor teratogenic effects were observed (Courtney et al.,
1976). In the same study, CD-1 mice administered the same doses
orally on days 7 - 16, also did not show any effects.
5.5. Carcinogenicity
Groups of 65 male and 65 female rats were fed a diet containing
tecnazene (purity 99%) at doses of 0, 750, and 1500 mg/kg for 104
weeks. The feeding did not affect general appearance, behaviour,
mortality rates, or food consumption. In the second half of the
treatment period, a slight reduction in body weight was observed in
males in the 1500 mg/kg group. The macropathological findings and
non-neoplastic histological changes were those commonly found in
the strain used; thus they were not considered to be treatment-
related and did not show clear dose relationships. Thirty-nine
females of the control group, 48 females of the 750 mg/kg group,
and 50 females of the 1500 mg/kg group had benign or malignant
tumours of the mammary glands. Adenocarcinomas of the mammary
gland were found in 4 females of the control group, 5 in the 750
mg/kg group, and 8 in the 1500 mg/kg group. These differences are
of borderline statistical significance (Ben-Dyke et al.,
unpublished data, 1978a).
Tecnazene (purity 99%) was administered continuously in the
diet to 65 male and 65 female mice in each dose group at levels of
0, 750, and 1500 mg/kg for 80 weeks. The only dose-related
distribution of neoplasms observed was pulmonary adenoma in the
male animals of the 1500 mg/kg group (8 animals showed this lesion,
compared with 4 in the control group) (Ben-Dyke et al., unpublished
data, 1978b).
6. EFFECTS ON MAN
Occupational dermal sensitivity has been reported in
agricultural workers (Lupuknova, 1965).
7. EFFECTS ON THE ENVIRONMENT
Tecnazene has no effect on the bacteria involved in the nitrogen
cycle. At 100 mg/kg in a fine sandy loam, no effects were found on
the respiration of microorganisms on nitrification (Caseley &
Broadbent, 1968).
No other relevant information on the environmental toxicity of
tecnazene was found.
8. PREVIOUS EVALUATIONS OF TECNAZENE BY INTERNATIONAL BODIES
The Joint Meeting on Pesticide Residues (JMPR) reviewed
residues and toxicity data on tecnazene in 1974, 1978, 1981, and
1983 (FAO/WHO, 1975, 1979, 1982, 1984). Although further
toxicological information is still required on tecnazene, the
meeting concluded that the no-observed-adverse-effect levels for
the rat, mouse, and dog were 750 mg/kg in the diet, 1500 mg/kg in
the diet, and 15 mg/kg body weight (by capsule), respectively, and
estimated the acceptable daily intake (ADI) for man to be 0 - 0.01
mg/kg body weight.
WHO, in its "Guidelines to the Use of the WHO Recommended
Classification of Pesticides by Hazard" (WHO, 1984), classified
tecnazene in the list of technical products unlikely to present an
acute hazard in normal use.
9. EVALUATION OF HEALTH RISKS FOR MAN AND EFFECTS ON THE
ENVIRONMENT
9.1. Evaluation of Health Risks for Man
Tecnazene toxicity
Tecnazene is only slightly toxic according to the scale of
Hodge & Sterner (1956). The oral LD50 in the rat was 7500 mg/kg
body weight. WHO (1978) classified tecnazene in the category of
technical products unlikely to present an acute hazard in normal
use.
Tecnazene is rapidly absorbed and metabolized in animals after
oral administration, and with higher doses, an increasing amount is
passed unchanged in the faeces.
In long-term studies the no-observed-adverse-effect levels are:
rat: 750 mg/kg diet, equivalent to 38 mg/kg body
weight per day;
mouse: 1500 mg/kg diet, equivalent to 200 mg/kg body
weight per day; and
dog: 15 mg/kg body weight per day (administered
orally by capsule).
At higher dosage levels tested, growth inhibition occurs and in
the dog there are increases in plasma alkaline phosphatase levels.
Tecnazene was neither embryotoxic nor teratogenic in the
studies reported. There is no information on mutagenicity or other
related short-term tests. Based on the results of an oral feeding
study on the mouse and the rat, there are no indications of
carcinogenicity.
The only observation in man has been dermal sensitivity.
Exposure to tecnazene
Exposure of the general population is expected to be mainly via
residues in food. The residue data available are below the FAO/WHO
maximum residue limits.
No data are available on tecnazene levels in air and water and
on the levels of occupational exposure.
No cases of human overexposure have been reported.
Hazard assessment
The experimental animal data available indicate that tecnazene
(purity greater than 99%) has a low degree of toxicity, even in
long-term studies. An acceptable daily intake has been estimated
at 0.01 mg/kg body weight.
In the absence of human exposure data, other than residues in
food, a factual hazard assessment of present total exposure cannot
be made.
The data available on tecnazene would indicate a low degree of
concern in relation to human health effects.
9.2. Evaluation of Overall Environmental Effects
In the absence of information on levels in the environment and
effects on the environment, such an evaluation cannot be made.
9.3. Conclusions
1. The general population does not seem to be at
risk from exposure to tecnazene.
2. With the exception of one report on dermal
sensitization in agricultural workers, tecnazene does
not seem to be a problem occupationally.
3. With the exception of information on the
bacteria involved in the nitrogen cycle there are no
available data on other environmental effects. Since
the use of this chemical is mainly confined to
greenhouses there is little concern for risk to the
general environment.
REFERENCES
ABRAMS, T.J., SCORGIE, N.J., & WILLIS, G.A. (1950) Pig
feeding trials with 2,3,5,6-tetrachloronitrobenzene. Br. vet.
J., 106: 413-420.
BARNES, M.M., JAMES, S.P., & WOOD, P.B. (1959) The formation
of mercapturic acids. I. Formation of mercapturic acid and the
levels of glutathione in tissues. Biochem. J., 71: 680-690.
BETTS, J.J., JAMES, S.P., & THORPE, W.V. (1955) The
metabolism of pentachloronitrobenzene and 2,3,4,6-tetrachloro-
nitrobenzene and the formation of mercapturic acids in the
rabbit. Biochem. J., 61: 611-617.
BRAY, H.G., HYBS, Z., JAMES, S.P., & THORPE, W.V. (1953) The
metabolism of 2,3,5,6- and 2,3,4,5-tetrachloronitrobenzenes in
the rabbit and the reduction of aromatic nitro compounds in
the intestine. Biochem. J., 53: 266-273.
BUTTLE, G.A.H. & DYER, F.J. (1950) Experiments on the
toxicology of 2,3,5,6-tetrachloronitrobenzene. J. Pharm.
Pharmacol., 2: 371-375.
CASELEY, J.C. & BROADBENT, F.E. (1968) The effect of five
fungicides on soil respiration and some nitrogen
transformations in yolo fine sandy loam. Bull. environ.
Contam. Toxicol., 8: 58-64.
COURTNEY, K.D., COPELAND, M.F., & ROBBINS, A. (1976) The
effects of pentachloronitrobenzene, hexachlorobenzene and
related compounds on fetal development. Toxicol. appl.
Pharmacol., 35: 239-256.
DALZIEL, J. & DUNCAN, H.J. (1974) Studies on potato sprout
suppressants. I. Residual levels of tecnazene in lab-treated
and in commercial samples of potatoes. Potato Res., 17:
215-223.
FAO/WHO (1975) Tecnazene. In: 1974 Evaluations of some
pesticide residues in foods, Rome, Food and Agriculture
Organization of the United Nations, pp. 531-536.
FAO/WHO (1979) Tecnazene. In: 1978 Evaluations of some
pesticide residues in foods, Rome, Food and Agriculture
Organization of the United Nations, pp. 227-238.
FAO/WHO (1982) Tecnazene. In: 1981 Evaluations of some
pesticide residues in foods, Rome, Food and Agriculture
Organization of the United Nations, pp. 43-44.
FAO/WHO (1984) Tecnazene. In: 1983 Evaluations of some
pesticide residues in foods, Rome, Food and Agriculture
Organization of the United Nations, pp. 44-45.
HODGE, H.C. & STERNER, J.H. (1956) Combined tabulation of
toxicity classes. In: Spector, W.S., ed. Handbook of
toxicology, Philadelphia, W.B. Saunders Company, Vol. 1.
LUPUKNOVA, K.A. (1965) [Case of occupational toxicodermia
caused by 2,3,5,6-tetrachloronitrobenzene.] Gig. Tr. Prof.
Zabol., 9: 56-58 (in Russian).
VALANGE, B. (1974) Pesticide residues in fruits and
vegetables. Results of a survey performed in 1972.
Parasitica, 30: 13-21.
WHO (1984) The WHO recommended classification of pesticides
by hazard, Geneva, World health Organization (Unpublished
Report VBC/84.2).
WIT, S.L. & REENWANGH, P. (1969) Mercapturic acid formation
and enzyme catalyzed conjugations with glutathione in pigeons.
Biochem. Biophys. Acta, 177: 329-355.
WIT, S.L., VAN ESCH, G.J., & VAN GENDEREN, H. (1960)
Toxicity of some chloronitrobenzene compounds (trichloro-
dinitrobenzene, trichlorotrinitrobenzene, tetrachloro-
nitrobenzene, and pentachloronitrobenzene) to laboratory rats
and residues in food crops treated with these fungicides. In:
Proceedings of the 4th International Crop Protection, Hamburg,
1957, Braunschweig, Vol. 2, pp. 1665-1668.
WORTHING, C.R. (1979) The pesticide manual, 6th ed.,
Croydon, British Crop Protection Council, p. 496.