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    Published under the joint sponsorship of
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    the International Labour Organisation,
    and the World Health Organization

    World Health Orgnization
    Geneva, 1986

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    toxicology. Other activities carried out by the IPCS include the
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     2.1. Identity
     2.2. Physical and chemical properties
     2.3. Analytical methods


     3.1. Man-made sources
     3.2. Uses


     4.1. Transport and distribution
     4.2. Biotransformation
     4.3. Abiotic degradation


     5.1. Environmental levels
          5.1.1. Water
          5.1.2. Soil
          5.1.3. Food and animal feed


     6.1. Absorption
     6.2. Distribution, storage, metabolic transformation,
          and excretion


     7.1. Aquatic organisms
     7.2. Terrestrial organisms
     7.3. Microorganisms
     7.4. Appraisal


     8.1. Single exposures
     8.2. Short-term exposures
          8.2.1. Oral
          8.2.2. Dermal
          8.2.3. Inhalation
     8.3. Long-term exposure
     8.4. Reproduction studies
     8.5. Mutagenicity
     8.6. Carcinogenicity
     8.7. Other studies



     10.1. Evaluation of the health risks for man
     10.2. Evaluation of environmental effects
     10.3. Conclusions and recommendations




Dr Z. Adamis, National Institute of Occupational Health,
   Budapest, Hungarya

Dr L. Albert, Environmental Pollution Programme, National
   Institute of Biological Resource Research, Xalapa, Mexico
    (Vice-Chairman) b

Dr Sakdiprayoon Deema, Ministry of Agriculture and
   Cooperatives, Bangkok, Thailandb

Dr R. Goulding, Chairman of the Scientific Sub-committee,
   UK Pesticides Safety Precautions Scheme, Ministry of
   Agriculture, Fisheries and Food, London, United Kingdom
    (Chairman) a

Dr Y. Hayashi, Pathology Division, National Institute of
   Hygienic Sciences, Tokyo, Japanb

Dr S.K. Kashyap, National Institute of Occupational Health
   (Indian Council of Medical Research), Meghaninager,
   Ahmedabad, Indiaa

Dr R. Kimbrough, Center for Environmental Health, Centers for
   Disease Control, Atlanta, Georgia, USA  (Rapporteur) b

Mr Y.T. Mosuro, Federal Ministry of Health, Food and Drug
   Administration and Laboratory Services, Oshodi, Nigeriab

Dr Y. Osman, Occupational Health Department, Ministry of
   Health, Khartoum, Sudanb

Dr L. Rosival, Centre of Hygiene, Research Institute of Preventive 
   Medicine, Bratislava, Czechoslovakia  (Chairman) b

Dr F.W. van der Kreek, Ministry of Welfare, Health, and
   Culture, Leidschendam, Netherlandsb

Dr D.C. Villeneuve, Environmental Contaminants Section,
   Environmental Health Centre, Tunney's Pasture, Ottawa,
   Ontario, Canada  (Rapporteur) a

Dr D. Wassermann, Department of Occupational Health, The
   Hebrew University, Haddassah Medical School, Jerusalem,
   Israel  (Vice-Chairman) a

Dr Xue Shou Zheng, School of Public Health, Shanghai Medical
   University, Shanghai, Chinab

a   Present at first Task Group meeting.
b   Present at second Task Group meeting.

 Representatives of Other Organizations

Dr A. Berlin, Health and Safety Directorate, Commission of the
   European Communities, Luxembourgb

Mrs M. Th. van der Venne, Health and Safety Directorate,
   Commission of the European Communities, Luxembourga


Dr C.J. Calo, European Chemical Industry Ecology and
   Toxicology Centre (ECETOC), Brussels, Belgiuma

Dr D.M. Whitacre, International Group of National Associations
   of Agrochemical Manufacturers (GIFAP), Brussels, Belgiuma

Dr A.A. van Kolfschoten, International Group of National Associations 
   of Agrochemical Manufacturers (GIFAP), Brussels, Belgiumb

Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood        
   Experimental Station, Huntingdon, United Kingdomb              
Dr M. Gilbert, International Register for Potentially Toxic       
   Chemicals, United Nations Environment Programme, Geneva,       
Ms B. Goelzer, Office of Occupational Health, World Health        
   Organization, Geneva, Switzerlanda                             
Dr Y. Hasegawa, Division of Environmental Health, Environmental 
   Hazards and Food Protection, World Health Organization, Geneva, 
Dr K.W. Jager, International Programme on Chemical Safety,        
   World Health Organization, Geneva, Switzerland  (Secretary)a,b 
Mr B. Labarthe, International Register for Potentially Toxic      
   Chemicals, United Nations Environment Programme, Geneva,       
Dr I.M. Lindquist, International Labour Organisation, Geneva,     
Dr A. Pelfrene, Insecticides Development and Safe Use Unit,       
   World Health Organization, Geneva, Switzerlandb                

Dr M. Vandekar, Pesticides Development and Safe Use Unit,
   World Health Organization, Geneva, Switzerlanda       

a   Present at first Task Group meeting.
b   Present at second Task Group meeting.

 Secretariat (contd.)                                                         

Dr T. Vermeire, National Institute for Public Health and
   Environmental Hygiene, Bilthoven, Netherlands  (Temporary
    Adviser) b                                              

Mr J.D. Wilbourn, International Agency for Research on Cancer,
   Lyons, Francea

a   Present at first Task Group meeting.
b   Present at second Task Group meeting.


    Every effort has been made to present information in the 
criteria documents as accurately as possible without unduly 
delaying their publication.  In the interest of all users of the 
environmental health criteria documents, readers are kindly 
requested to communicate any errors that may have occurred 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. 

                          *    *    *

    A detailed data profile and a legal file can be obtained from 
the International Register of Potentially Toxic Chemicals, Palais 
des Nations, 1211 Geneva 10, Switzerland (Telephone no. 988400 - 


    A WHO Task Group on Environmental Health Criteria for 
Organochlorine Pesticides other than DDT met in Geneva on 
28 November - 2 December, 1983.  Dr K.W. Jager opened the meeting 
on behalf of the Director-General. 
 The Task Group reviewed and revised the draft criteria
document.  The Task Group concluded that the data on kelevan
were too sparse to make an evaluation of the health risks for
man or the effects on the environment.  It recommended that
the draft should be recirculated to the IPCS and IRPTC focal
points with a request for further information.

    A second WHO Task Group was held in Geneva on 9 - 13
December, 1985 to review and revise an amended draft and to
make an evaluation of the risks of kelevan for human health
and the environment.

    The first drafts of the kelevan document were prepared by
DR D.C. VILLENEUVE of Canada and DR S. DOBSON of the United

    The present draft was prepared by the IPCS Secretariat,
updating the preliminary hazard assessment with new information 
received in more than 50 replies from Focal Points. 

    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.  The United Kingdom Department of Health and Social 
Security generously supported the costs of printing. 


    Technical kelevan is a brownish solid substance with a 
molecular formula of C17H12Cl10O4. 

    It is a chlordecone derivative and can be oxidized to 
chlordecone before determination by gas chromatography with 
electron capture detection. 

    Kelevan has been used in a number of countries as an 
insecticide, mainly for the control of the potato beetle and the 
banana root borer. 

    It is degraded quite rapidly by biotransformation and abiotic 
degradation to other caged structure products.  The half-life of 
kelevan in soil has been reported to be 5 - 12 weeks.  However, its 
major metabolite, chlordecone, persists in the soil for several 

    There is very little leaching of kelevan and its caged-
structure metabolites from the upper 10 cm of soil into lower 
layers and into drainage water.  Carrots, grown after an early 
potato crop that had been treated with 300 g kelevan/ha, contained 
up to 0.02 mg kelevan/kg and 0.04 mg chlordecone/kg; no residues 
(< 0.01 mg/kg) were found in the potatoes. 

    There are no data on levels of exposure to kelevan for the 
general population or in the work-place. 

    A few data are available on the environmental toxicity of
kelevan.  The toxic threshold level for rainbow trout is of the 
order of 0.1 mg/litre, and the oral LD50 for honey bees is > 1 
mg/bee.  Domestic hens dosed with 20 mg kelevan/bird per day for 8 
weeks did not show any adverse effects.  A soil level of 2500 mg 
kelevan/kg did not affect the microflora over a 30-month period.  
However, the available data are too few to make an informed 
assessment of kelevan's likely impact on the environment, 
especially on a long-term basis. 

    Kelevan is absorbed by experimental animals following 
ingestion, inhalation, and via the skin.  It accumulates in the 
liver, brain, and in adipose tissue.  It is metabolized to a 
certain extent to chlordecone, both compounds being mainly excreted 
with the bile into the faeces. 

    It is moderately toxic according to the scale of Hodge & 
Sterner (1956) in single exposures (oral LD50 values for the rat 
range from 240 to 550 mg/kg body weight).  Symptoms of poisoning 
include apathy, tremors, CNS hypersensitivity, and tonic-clonic 
convulsions.  The no-observed-adverse-effect level in a 90-day oral 
study on rats was 5 mg/kg body weight.  At higher levels (300 mg/kg 
diet in females and 1000 mg/kg diet in both sexes), liver hypertrophy 
occurred.  In a 10-month oral study on rats, 0.28 mg/kg body weight 
per day was considered to be a threshold dose.  Oral exposure to 14 
mg/kg body weight per day for 4 months caused necrosis of the liver 
and kidneys in rats. 

    No abnormalities were found in reproduction studies on mice 
when low doses (5 mg/kg diet) were given from 30 days prior to 
mating to 90 days after mating.  Teratogenic effects have not been 
adequately evaluated. 

    Kelevan was not mutagenic in systems using microorganisms. 

    No carcinogenicity studies are available for kelevan, but there 
is sufficient evidence of carcinogenicity for chlordecone, a major 
metabolite, from studies on rats and mice. 

    No adverse health effects on human beings have been reported 
from exposure to kelevan. 

    In view of the sparsity of available data, it is quite 
impossible at this stage to arrive at an informed evaluation of 
keleven with regard to its danger for workers, the possible 
consumer hazards from food residues, or its impact on the 

    Therefore, since kelevan is converted to chlordecone in the 
mammalian body and in the environment, and the toxicity data 
available are similar to those on chlordecone, the evaluation of 
chlordecone should largely apply to kelevan, which, in practice, 
means that, unless kelevan is indispensable, it should not be used. 


2.1.  Identity

Chemical Structure

Molecular formula:         C17H12Cl10O4

CAS chemical name:         1,3,4-metheno-1 H-cyclobuta; cd pentalene-
                           2-pentanoic acid, 1,1a,3,3a,4,5,5a,5b,
                           oxo-ethyl ester

Trade names:               Despirol, Elevat, GC-9160, General
                           Chemicals 9160

CAS registry number:       4234-79-1

    Technical grade kelevan contains 94 - 98% pure kelevan, 0.1 - 
2% chlordecone, and 0.5 - 4.0% inorganic salts (Maier-Bode, 1976). 

2.2.  Physical and Chemical Properties

    The technical material is a brownish substance. 

    Some physical and chemical properties of kelevan are given
in Table 1.

2.3.  Analytical Methods

    Kelevan can be extracted from plant or animal tissues, or soils 
using methylene chloride, isopropanol, or acetone.  It can be 
oxidized by refluxing with chromium trioxide in glacial acetic acid 
to yield chlordecone.  The chlordecone is then determined by gas-
liquid chromatography (GLC) techniques (Westlake et al., 1970).  An 
analytical method using liquid chromatography/mass spectrometry has 
been described by Cairns et al. (1982). 

Table 1.  Some physical and chemical properties of kelevan
Physical state                       solid, powder

Colour                               white

Relative molecular mass              634.79

Melting point                        91 C

Vapour pressure (20 C)              < 0.0014 Pa (= < 10-2 mm Hg)

Solubility in water (20 C)          5.5 mg/litre
(readily soluble in most
organic solvents)

Decomposition                        > 170 C
From:  Maier-Bode (1976).


3.1.  Man-Made Sources

    Kelevan is a condensation product of chlordecone and ethyl 
levulinate (Gilbert et al., 1966). 

    The synthesis and insecticidal action of kelevan were reported 
by Gilbert et al. (1966).  Its synthesis has also been described by 
Heys et al. (1979).  The only information available in relation to 
the production of kelevan was reported by Cannon et al. (1978), who 
stated that approximately 99% of the production of chlordecone was 
exported to the Federal Republic of Germany, where it served as a 
raw material in the manufacture of another pesticide compound 

3.2.  Uses

    Reference has been made to the use of kelevan in central and 
southeastern Europe (Maier-Bode, 1976) and in South America (Cannon 
et al., 1978). 

    Kelevan has mainly been used in the control of the potato 
beetle  (Leptinotarsa decemlineata) on potatoes, the banana root 
borer on bananas, and  Tanymecus palliatus on beets and corn.  
Both dust and wettable-powder formulations have been used (Maier-
Bode, 1976). 

    Responses received from 49 countries throughout the world 
indicated that kelevan had never been registered for use or used in 
33 of them.  In Spain, registration expired in 1975. In the Federal 
Republic of Germany, the use of kelevan has been forbidden since 
1982.  In Hungary and the USSR, kelevan is still registered, but is 
no longer used (personal communications to the IPCS and IRPTC, 


4.1.  Transport and Distribution

    Kelevan (determined as chlordecone) was shown in laboratory 
studies to have a half-life in soil of 6 - 12 weeks under dark 
conditions, and 5 - 10 weeks in diffused daylight (unpublished data 
summarized by Maier-Bode, 1976).  Analysis of soil samples in 
various regions of Europe, where kelevan has been used to control 
the potato beetle, confirmed this relatively rapid degradation 
(unpublished data summarized by Maier-Bode, 1976).  Soil treatment 
was carried out using 14C-kelevan at 1.5 kg/ha and, though initial 
residues in the soil were approximately 2 mg/kg, potatoes grown in 
the soil contained residues of < 0.001 mg/kg, after peeling 
(Klein, 1972). 

    Kelevan residues resulting from use in the field were predicted 
on the basis of the volatilization, mineralization, and conversion 
rates obtained from laboratory tests.  Field residues of the parent 
compound kelevan actually found in the field test were far lower 
than calculated (Scheunert et al., 1983). 

    14C-Kelevan was applied to a "potato field model ecosystem".  
The system was left to grow and ripen for 77 days.  Approximately 
95% of the applied radioactivity was recovered:  50.9% in soil, 
42.4% in, and on, the potato plant, 1.6% in the air, and less than 
0.001% in drainage water.  Of approximately 50.9% contained in 
soil, 38% was between 0 and 5 cm deep, 12.9% between 5 and 10 cm, 
0.01% between 10 and 15 cm, and less than 0.001% between 15 and 20 
cm deep.  Of the total of recovered radioactivity, 24.4% was 
unchanged kelevan, 40.5% kelvanic acid, 7.4% chlordecone, and 22.6% 
different non-identified kelevan metabolites.  Neither intact 
kelevan nor its metabolites could be identified in potato fields 
containing less than 0.03% of the initial radioactivity, or in 
drainage water (Figge & Rehm, 1977; Figge, 1978). 

    When 5.4 mg of 14C-kelevan was sprayed on potato leaves, 6.9% 
of the radioactivity was recovered from the plant, 26.3% from the 
soil, 0.9% in drainage water, and 65.9% was lost to the air over 11 
weeks.  Much of the kelevan had been converted to kelevanic acid 
including 68% of material recovered from soil and 65% of material 
from the plant (Sandrock et al., 1974). 

4.2.  Biotransformation

    Benigni et al. (1979) showed that kelevan was converted into 
chlordecone in  Nicotinea alata cell cultures and also in field 
tests on potatoes and beets, and that the amount converted was 
proportional to the length of treatment (see also Carere & Morpurgo, 

    In a laboratory study on 2 soil types, between 61 and 64% of 
applied kelevan was degraded by microorganisms and physical and 
chemical processes to kelevanic acid, in 4.5 months.  In a second 
study, under both laboratory and field conditions, one-third of 
applied kelevan was degraded by microorganisms to chlordecone and 
other unidentified products, over 30 months (Figge et al., 1983). 

4.3.  Abiotic degradation

    Parlar et al. (1972) and Begum et al. (1973) studied the 
decomposition of kelevan in the solid state or dissolved in 
acetone, methanol, or  n-hexane under the influence of ultra-
violet radiation (UVR).  Several dechlorination products were 
isolated, but the main degradation product was chlordecone.  In 
the gaseous phase, both mirex and chlordecone were formed. 

    Several photolysis products of kelevan have been described by 
Wilson & Zehr (1978).  These mainly concern modifications in the 
side chain. 

    Kelevan slowly hydrolyses in water forming products such as 
kelevanic acid and the carboxylic ester without the side chain, 
which are more readily soluble in water (Sandrock et al., 1974). 


    No data are available concerning the concentrations of kelevan 
in air, water, or food. 

5.1.  Environmental Levels

5.1.1.  Water

    In laboratory experiments designed to ascertain runoff 
characteristics of kelevan from soil, no traces of kelevan were 
found in the runoff water (unpublished data summarized by Maier-
Bode, 1976). 

5.1.2.  Soil

    Sandrock et al. (1974) studied the metabolism of 14C-kelevan in 
potatoes and soil, 11 weeks and again one year after application on 
leaves.  Kelevanic acid (the principal metabolite), unmetabolized 
kelevan, chlordecone, and chlordecone acetic acid were identified 
in the soil, 11 weeks after application.  Over 90% of the quantity 
applied was metabolized during the first crop growth period; the 
metabolites were products in which the side chain was shortened or 
eliminated, without apparent changes in the carbon skeleton.  
Chlordecone acetic acid was identified as the principal metabolite 
in the soil after 1 year. 

    A dust or a suspension of 150 g kelevan aia/ha was applied
to 3 different soils in Slovakia.  Three months after application, 
approximately 30% of the kelevan was recovered as chlordecone.  
Kelevan residues in potatoes grown in all three soil types ranged 
from 0.001 - 0.004 mg/kg, whereas chlordecone was present in 
traces only (Madaric & Sackmauerova, 1974). 

5.1.3.  Food and animal feed
    When 14C-kelevan was applied to potato plants, neither the 
compound nor any of its caged structure products were detectable in 
the potato tubers (unpublished data summarized by Maier-Bode, 
1976).  Furthermore, detectable residues (> 0.01 mg/kg) were not 
found in other crops growing in the same field including winter 
wheat, winter rye, summer barley, and silo corn, even though the 
field had been treated with 150 g kelevan/ha, the year before.  
Carrots that had been planted in a field treated earlier in the 
season with 150 and 300 g kelevan/ha, showed residues of 0.02 and 
0.04 mg kelevan/kg.  Rape, planted in a field treated with 250 and 
150 g kelevan/ha, showed residues in seed of 0.07 mg/kg at harvest 
(unpublished data summarized by Maier-Bode, 1976).  Field studies 
using 14C-kelevan showed that total residues, both in soil and 
potatoes, mainly comprised hydrophilic metabolites including more 
a   ai = active ingredient.

than 80% kelevanic acid.  Chordecone was also identified, but it 
was uncertain whether it was an impurity or a metabolite (Klein, 

    Kelevan applied at 0.3 kg/ha increased the potato yield. At 0.6 
kg/ha, its residues could be detected in the soil and the potato 
roots during the vegetative period (Krasnykh, 1980). 

    Alfalfa, contaminated by spray-drift from the aerial spraying 
of potatoes with kelevan, contained 4.8 mg kelevan/kg, directly 
after spraying, 1.1 mg/kg, 3 days later, and 0.1 mg/kg, after 5 - 7 
days.  Fourteen days after spraying, kelevan could no longer be 
detected (Jonas, 1983). 

    Residues of up to 0.02 and 0.04 mg/kg, respectively, of kelevan 
and chlordecone were found in carrots planted after a crop of early 
potatoes treated with the recommended application rate of 300 g 
kelevan/ha.  No residues were found in the potatoes (< 0.01 
mg/kg).  Residues were also found in the leaves and roots of 
sugarbeets and in the seed and straw of summer and winter rape (up 
to 0.06 mg/kg) (Maier-Bode, 1976). 

    Two groups of two, 200-kg steers were fed 0.05 or 0.1 mg 
kelevan/kg feed for 6 weeks.  No kelevan was detected in muscle, 
kidneys, heart, or body fat, 2 and 4 weeks, respectively, after 
this feeding period.  The liver, however, contained 0.02 - 0.1 mg 
kelevan/kg.  Biopsies during the feeding period showed concentrations 
of up to 1.6 mg kelevan/kg in body fat (Jonas, 1983). 


6.1.  Absorption

    Kelevan can enter the body orally and by inhalation.  It is 
also absorbed through the skin, as shown by acute and short-term 
dermal toxicity studies on rabbits (section 8.1, 8.2) (Maier-Bode, 

6.2.  Distribution, Storage, Metabolic Transformation, and 

    Several unpublished studies have been summarized by Maier-Bode 
(1976).  Male rats were administered 14C-kelevan intra-gastrically 
at 4.75 mg/kg body weight.  As little as 3 h after administration, 
14C activity was found in all tissues examined, but primarily in 
the liver.  The resulting pattern of accumulation was similar to 
that of chlordecone in that it was greater in the heart, brain, 
liver, etc. than in adipose tissue.  The levels of kelevan in mg/kg 
were as follows:  serum 1.4, liver 20.9, heart 2.7, kidney 3.5, 
brain 1.1, fat 0.84, muscle 0.87.  After 14 days, levels in all 
tissues were below 0.1 mg/kg, except for the liver, which contained 
1.8 mg/kg.  The liver still contained 0.3 mg/kg, 110 days later.  
The data also indicated that kelevan is excreted through the liver 
with the bile into the faeces and is not excreted to any great 
extent in the urine.  It appears primarily as unchanged kelevan and 
also as chlordecone (Maier-Bode, 1976). 

    These studies indicate that chlordecone is a metabolite of 
kelevan in the rat and suggest that kelevanic acid is an 

    In another study, a single oral dose of 4.75 mg 14C-kelevan/kg 
body weight, in carboxymethylcellulose, was given to 60 male rats 
by gavage (Maier-Bode, 1976).  A considerable portion of the 14C was 
excreted through the liver with the bile into the intestine.  Eight 
and 16 weeks later 14C could still be detected in organs and tissues. 

    In a study on rats administered a single oral dose of 1.52 mg 
14C-kelevan/kg body weight, it was possible to identify14C-
chlordecone (as a transformation product partly as chlordecone-
arginine) by thin-layer chromatography in the faeces and urine of 
the rats (Maier-Bode 1976). 

    Daily doses of a kelevan suspension in water were given to 15 
male and 15 female rats by gavage.  The total dose in the course of 
8 weeks was 10 mg kelevan/kg body weight (Maier-Bode, 1976).  Three 
male and 3 female animals were killed and the tissues analysed, 1, 
2, 4, 8, and 10 weeks after the first application.  The liver, 
brain, and body fat were analysed for kelevan and chlordecone.  The 
concentrations of kelevan and chlordecone, separately and combined, 
were approximately constant.  The conclusion of the author was that 
there was no accumulation of kelevan or its metabolite chlordecone.  
The faeces collected from the surviving rats during the entire 10-
week test period contained an average of 2.25 mg kelevan/kg and 
0.84 mg chlordecone/kg.  Neither kelevan nor chlordecone was found 
(< 0.02 mg/litre) in the urine of the animals. 

    On the basis of the studies, the Task Group concluded that 
chlordecone is a metabolite of kelevan, but that the extent of this 
transformation is not known.  It has to be taken into account that 
chlordecone is also an impurity of kelevan. 

    The amounts of kelevan and chlordecone in the liver, brain, and 
body fat are almost equal.  Because of the short duration of the 
study, nothing can be said of the half-life of kelevan and 
chlordecone, but on the basis of the 2-week depletion period, it 
appears that both half-lives are long. 


7.1.  Aquatic Organisms

    Studies on the toxicity of kelevan (LC50) for juvenile fish 
(rainbow trout) are reported in Table 2; no studies on other 
aquatic organisms are available.  Two separate studies indicate a 
toxic threshold for rainbow trout of 0.1 mg/litre.  Symptoms of 
sublethal poisoning include disturbed swimming coordination (Maier-
Bode 1976). 

7.2.  Terrestrial Organisms

    Under laboratory conditions, the toxicity for bees of kelevan, 
at concentrations used in agriculture, was low (Tomaszewska, 1981).  
The LD50 of Despirol (wettable powder 50% kelevan) for honey bees 
was > 1 mg/bee (the maximum level tested) after testing orally, by 
inhalation, by prolonged contact, or by spraying.  The toxicity of 
kelevan was lower for beneficial insects than for target species 
(Maier-Bode, 1976). 

    Soil microarthropods (Collembola and Acarina) showed no change 
in absolute or relative, species to species, population numbers 
within 75 days of a single spraying of a potato crop at a rate of 
300 g/ha (Hrlec & Ostrec, 1981). 

    Five pheasants and 3 domestic doves dosed with kelevan as 
Despirol at 10 g/kg diet for 10 days did not show any effects 
during the dosing period or during the 10-day period following 
dosing.  The amount of insecticide ingested averaged 101 mg/kg per 
day for pheasants and 250 mg/kg per day for doves (Maier-Bode, 
1976).  When large numbers of laying domestic hens were dosed at up 
to 20 mg/bird per day, for 8 weeks, no effects were observed on 
laying activity; histological examination of tissues at the end of 
the study did not reveal any differences between treated and 
control birds (Maier-Bode, 1976). 

7.3.  Microorganisms

    A laboratory study on microorganisms in two types of soil 
treated with between 500 and 2500 mg 14C-kelevan/kg showed that, 
whilst the organisms degraded kelevan, the insecticide caused no 
change in either total or relative numbers of microorganisms.  The 
organisms were neither selected nor decimated by kelevan or its 
degradation products over a 30-month period (Figge et al., 1983). 

Table 2.  Toxicity of kelevan for fisha
Species             Life stage   Length   Water hardness   Temperature   Exposure time   LC50
                                 (cm)     (dH01)b          (C)          (h)             (mg/litre)
Rainbow trout       juvenile     7 - 9c   11               10            24              > 2
 (Salmo gairdnerii)

Rainbow trout       juvenile     7 - 9c   11               10            72              1.0

Rainbow trout       juvenile     6 - 10   1                14            96              1.5
Rainbow trout       juvenile     6 - 10   9                14            96              2.2
a   From: Maier-Bode (1976).
b   1 degree of hardness (dH0) corresponds to 10.0 mg Ca0/litre water.
c   For the studies on 7 - 9 cm trout, pH 6; pH not stated for other tests.

7.4.  Appraisal

    The data on kelevan are few.  There is no information on its 
immediate metabolite, kelevanic acid.  Thus, it is difficult to 
come to firm conclusions about the environmental significance of 
kelevan.  However, there are considerable data on the metabolite, 
chlordecone.  This is known to be stable and persistent.  It 
bioaccumulates and is more toxic for aquatic organisms than 
kelevan.  Chlordecone has severe sublethal effects on birds (WHO, 
1984).  The interpretation of data for kelevan, therefore, needs to 
take into account the significance of chlordecone. 


8.1.  Single Exposures

    Data on the acute toxicity of kelevan are given in Table 3.  A 
similar pattern of response to acutely toxic doses of kelevan was 
seen in the three species and included apathy, tremor, hyper-
sensitivity, and tonic-clonic convulsions. 

Table 3.  Acute toxicity of kelevan
Animal  Sex    Route  Vehicle      LD50          Reference
                                   body weight)
Rat     M & F  oral   corn oil,    240 - 290     Maier-Bode (1976)
                      soybean oil

Rat            oral                255 - 325     Kenaga & Allison

Dog     M & F  oral   corn oil,    400 - 550     Maier-Bode (1976)
                      soybean oil

Dog            oral                400 - 500     Kenaga & Allison

Rabbit  M      dermal corn oil     251           Maier-Bode (1976)

Rabbit         dermal              188 - 314     Kenaga & Allison

8.2.  Short-Term Exposures

8.2.1.  Oral

    Male rats were administered kelevan by oral intubation at 29 
mg/kg body weight for 20 consecutive days (Medical College, 
Virginia, 1968).  No effects were observed on behaviour, organ 
weights, or in the histopathological examination of liver and 
kidneys.  In a 90-day study (Medical College, Virginia, 1968), male 
and female rats were fed kelevan incorporated in the diet at levels 
of 0, 10, 30, 100, 300, or 1000 mg/kg.  No animals died during the 
course of the study, but animals fed 1000 mg/kg showed a reduced 
weight gain.  No treatment-related abnormalities were seen in food 
consumption, haematology, urinalysis, or histopathology.  Dose-
related liver hypertrophy was observed in females at 300 mg/kg diet 
and in both sexes at 1000 mg/kg diet.  Thus, 100 mg kelevan/kg 
diet, equivalent to 5 mg/kg body weight per day, was a no-observed-
adverse-effect level in this study. 

    Albino rats were exposed to daily doses of 14 mg kelevan/kg 
body weight for 4 months, or, 2.8 or 0.28 mg/kg body weight for 10 
months.  Hyperaemia of internal organs and necrosis of the liver 
and kidneys were described, as well as lymphoid infiltration of 
interstitial tissue in the lung.  At 0.28 mg/kg, these changes were 
reversible, and the author regarded this dose as a threshold dose 
(Boreiko, 1980). 

8.2.2.  Dermal

    Male and female rabbits were administered 25 or 50 mg 
Despirol/kg body weight (12.5 or 25 mg kelevan/kg body weight), 5 
days per week, for 9 weeks.  The material was administered as an 
aqueous paste to the shaved skin of the animals.  There was no 
difference between the treatment groups and controls.  Only a 
slight erythema was observed at the highest dose of kelevan 
(Medical College, Virginia, 1968). 

    Kelevan, applied to the skin of rats, rabbits, and guinea-pigs, 
in either one dose of 2000 mg/kg or 20 doses of 100 mg/kg caused 
dystrophic changes in the liver and kidneys (Sasinovich et al., 

8.2.3.  Inhalation

    No adequately reported studies available. 

8.3.  Long-Term Exposure

    No studies available.

8.4.  Reproduction Studies

    Reproduction was investigated in 100 male and 100 female BALB/C 
mice fed kelevan in the diet at 5 mg/kg, from 30 days prior to 
mating to 90 days after mating, over several litters (Ware & Good, 
1967).  No effects of treatment were observed on mortality, number 
of females producing litters, pregnancy period, number of litters, 
litter size, and sex ratio. 

    Thirty pregnant CD-1 mice were given the minimal toxic dose of 
kelevan of 125 mg/kg body weight in 0.5 ml corn oil, by gavage, 
from day 8 to day 12 of pregnancy.  Four animals died.  There were 
no significant maternal weight changes nor effects on litter size 
or pup weights (Chernoff & Kavlock, 1983). 

    It is known that chlordecone affects reproduction (WHO, 1984).  
The dose of 5 mg kelevan/kg per day may have been too low to elicit 
an effect on reproduction.  The dose of 125 mg/kg apparently caused 
sufficient toxicity in the dams to kill four of the animals.  The 
validity of both these studies, which were the only studies 
available for evaluation, is limited. 

8.5.  Mutagenicity

    Benigni et al. (1979) tested the mutagenic activity of kelevan 
and its metabolite chlordecone on  Aspergillus nidulans.  As pure 
compounds, both were negative (Carere & Morpurgo, 1981). 

    Kelevan and its degradation products did not show any mutagenic 
activity in the Ames test with  Salmonella typhimurium (Jaszczuk & 
Syrowatka, 1980). 

8.6.  Carcinogenicity

    No carcinogenicity studies are available for kelevan. However, 
there is sufficient evidence of the carcinogenicity of its 
metabolite chlordecone in animals (IARC, 1979; WHO, 1984) 

8.7.  Other Studies

    A single intragastric dose of 140 mg kelevan/kg body weight 
(approximately half the LD50), given to rats, decreased the rate 
of bile secretion on the first day.  From day 3 onwards, it 
increased again, but it had not reached the level of the controls 
on day 5 (Glukhova et al., 1978, 1979).  Kelevan sharply increased 
the levels of alanine aminotransferase and aspartate aminotransferase 
in blood serum and caused structural changes in the liver at this 
dose level. 


    No adverse health effects on human beings from exposure to
kelevan have been reported.


10.1.  Evaluation of the Health Risks for Man

    Kelevan, which is developed from chlordecone, is metabolized 
in the mammalian body and in the environment back to chlordecone.  
The acute toxicity of kelevan is similar to that of chlordecone, 
which may well be its active metabolite. 

    Data on kelevan are sparse; several reports have not been 
published and are not available for scrutiny and others lack 
sufficient detail or are inadequate.  No information exists on 
actual human exposure. 

    The acute toxicity of kelevan in test animals is moderate (oral 
LD50s ranging from 240 to 550 mg/kg body weight, according to the 
scale of Hodge & Sterner (1956)), and similar to that of chlordecone.  
However, the no-observed-adverse-effect level of 5 mg/kg body weight 
per day observed in a 90-day oral study on the rat and a threshold 
level of 0.28 mg/kg body weight per day observed in a 10-month oral 
rat study, are very similar to those obtained with chlordecone (WHO, 
1984).  The pathological findings of liver hypertrophy and necrosis 
of liver and kidneys are also similar. 

    Kelevan is not mutagenic in systems using microorganisms. 

    No carcinogenicity studies are available.  However, there
is sufficient evidence of the carcinogenicity of its metabolite 
chlordecone for mice and rats (IARC, 1979; WHO, 1984).

    No adverse effects on human health due to exposure to
kelevan have been reported.

10.2.  Evaluation of Environmental Effects

    There have not been any reports of adverse effects on the 
environment due to exposure to kelevan.  Available information 
suggests that the probability of deleterious effects on terrestrial 
organisms from kelevan is low.  Its metabolite, chlordecone, is 
toxic for birds and microorganisms, though there is no indication 
of this for the parent compound.  Aquatic data for kelevan are 
limited to one species and one life stage; it is moderately to 
highly toxic for juvenile rainbow trout.  It is possible, but 
improbable, that local concentrations of kelevan after recommended 
agricultural use could exceed the toxic threshold for trout fry.  
The compound gives concern with aquatic organisms because its 
degradation product is both more persistent and more toxic for fish 
than the parent compound. 

10.3.  Conclusions and Recommendations

    In view of the sparsity of available data, it is impossible to 
arrive at an informed evaluation of kelevan with regard to its 
danger for workers, the possible consumer hazards from food 
residues, or its impact on the environment.  Thus, as kelevan is 
converted to chlordecone in the mammalian body and in the 
environment, and as the available toxicity data are similar to 
those on chlordecone, the evaluation for chlordecone (WHO, 1984) 
should also largely apply to kelevan, unless further data to the 
contrary become available.  In practice, this means that, unless 
kelevan is indispensable, it should not be used. 


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    See Also:
       Toxicological Abbreviations
       Kelevan (HSG 2, 1987)