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    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, 1990

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    WHO Library Cataloguing in Publication Data


        (Environmental health criteria ; 97)

        1.Pyrethrins   I.Series

        ISBN 92 4 154297 7        (NLM Classification: WA 240)
        ISSN 0250-863X

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     1.1. Summary and evaluation
           1.1.1. Identity, physical and chemical properties, 
                  analytical methods
           1.1.2. Production and uses
           1.1.3. Human exposure 
           1.1.4. Environmental exposure and fate 
           1.1.5. Uptake, metabolism, and excretion 
           1.1.6. Effects on organisms in the environment 
           1.1.7. Effects on experimental animals and  in vitro test 
           1.1.8. Effects on human beings 
     1.2. Conclusions 
     1.3. Recommendations 


     2.1. Identity   
     2.2. Physical and chemical properties 
     2.3. Analytical methods  


     3.1. Industrial production  
     3.2. Use patterns 
     3.3. Residues in food 
     3.4. Levels in the environment 


     4.1. Transport and distribution between media 
     4.2. Abiotic degradation in air and water 
     4.3. Environmental fate 
     4.4. Bioaccumulation 


     5.1. Metabolism in experimental animals 
     5.2. Metabolism and fate in farm animals 
     5.3. Enzymatic systems for biotransformation 
     5.4. Metabolism in human beings 


     6.1. Aquatic organisms 
           6.1.1. Acute toxicity for fish 
           6.1.2. Acute toxicity for other aquatic organisms 
           6.1.3. Field studies and community effects 
           6.1.4. Appraisal  
     6.2. Terrestrial organisms 
           6.2.1. Plants 
           6.2.2. Soil microorganisms 
           6.2.3. Soil fauna 
          Soil arthropods 
           6.2.4. Beneficial insects 
          Foliar insects 
           6.2.5. Birds 
          Laboratory studies 
          Field studies on birds 


     7.1. Single exposures 
           7.1.1. Mouse 
           7.1.2. Rat 
           7.1.3. Rabbit 
           7.1.4. Dog 
     7.2. Irritation and sensitization  
           7.2.1. Skin irritation 
           7.2.2. Eye irritation 
           7.2.3. Sensitization 
     7.3. Short-term exposure 
           7.3.1. Rat 
           7.3.2. Dog 
     7.4. Long-term exposure and carcinogenicity  
           7.4.1. Mouse and rat 
           7.4.2. Dog 
     7.5. Mutagenicity 
           7.5.1. Microorganisms 
           7.5.2. Cultured cells 
           7.5.3. Mouse  
           7.5.4. Appraisal 
     7.6. Teratological and reproductive effects 
           7.6.1. Teratology 
           7.6.2. Reproduction studies  
     7.7. Neurotoxicity and behavioural effects 
     7.8. Miscellaneous effects   
     7.9. Potentiation 
     7.10. Mechanism of toxicity (mode of action) 
     7.11. Experimental studies on antidotes  


     8.1. General population-poisoning incidents 
     8.2. Occupational exposure  
           8.2.1. Acute toxicity-poisoning incidents 
           8.2.2. Effects of short- and long-term exposure 
     8.3. Clinical studies  








Dr V. Benes, Department of Toxicology & Reference Laboratory, 
   Institute of Hygiene and Epidemiology, Prague, Czechoslovakia

Dr A.J. Browning, Toxicology Evaluation Section, Department of 
   Community Services and Health, Woden, Australia

Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood 
   Experimental Station, Huntingdon, Cambridge, United Kingdom 

Dr K. Imaida, Section of Tumor Pathology, Division of Pathology, 
   National Institute of Hygienic Sciences, Tokyo, Japan

Dr P. Hurley, Office of Pesticide Programme, US Environmental 
   Protection Agency, Washington, DC, USA 

Dr S.K. Kashyap, National Institute of Occupational Health, 
   (I.C.M.R.) Ahmedabad, India  (Vice-Chairman)

Dr Yu. I. Kundiev, Research Institute of Labour, Hygiene and 
   Occupational Diseases, Kiev, USSR

Dr J.P. Leahey, ICI Agrochemicals, Jealotts Hill Research Station, 
   Bracknell, Berkshire, United Kingdom  (Rapporteur)

Dr M. Matsuo, Sumitomo Chemical Company Limited, Biochemistry & 
   Toxicology Laboratory, Osaka, Japan


Mr M. L'Hotellier, International Group of National Associations of 
   Manufacturers of Agrochemical Products (GIFAP) 

Dr N. Punja, International Group of National Associations of 
   Manufacturers of Agrochemical Products (GIFAP) 


Dr K.W. Jager, Division of Environmental Health, International 
   Programme on Chemical Safety, World Health Organization, Geneva, 
   Switzerland  (Secretary)

Dr R. Plestina, Division of Vector Biology and Control, World 
   Health Organization, Geneva, Switzerland

Dr J. Sekizawa, Division of Information on Chemical Safety, 
   National Institute of Hygienic Sciences, Tokyo, Japan  (Rapporteur)


    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. 7988400 - 

 NOTE:  The proprietary information contained in this document 
cannot replace documentation for registration purposes, because the 
latter has to be closely linked to the source, the manufacturing 
route, and the purity/impurities of the substance to be registered.  
The data should be used in accordance with para. 82-84 and 
recommendations para. 90 of the 2nd FAO Government Consultation 


    A WHO Task Group on Environmental Health Criteria for 
Tetramethrin, Cyhalothrin, and Deltamethrin met at the World Health 
Organization, Geneva, from 24 - 28 October 1988.  Dr M. Mercier, 
Manager of the IPCS, welcomed the participants on behalf of the 
three IPCS cooperating organizations (UNEP/ILO/WHO).  The Group 
reviewed and revised the draft Criteria Documents and Health and 
Safety Guides and made an evaluation of the risks for human health 
and the environment from exposure to tetramethrin, cyhalothrin, and 

    The first drafts of the documents on tetramethrin and 
deltamethrin were prepared by Dr J. MIYAMOTO and Dr M. MATSUO of 
Sumitomo Chemical Co. Limited.  Dr J. SEKISAURA of the National 
Institute of Hygienic Sciences, Tokyo, Japan, assisted in the 
finalization of the drafts.  The first draft of the document on 
cyhalothrin was prepared by the IPCS Secretariat based on material 
made available by ICI Agrochemicals, United Kingdom.  

    The second drafts were prepared by the IPCS Secretariat, 
incorporating comments received following circulation of the first 
drafts to the IPCS contact points for Environmental Health Criteria 

    Dr K. JAGER of the IPCS Central Unit was responsible for the 
scientific content of the deltamethrin document, and Mrs M.O. HEAD 
of Oxford, England, for the editing. 

    The fact that Sumitomo Chemical Company Limited, Japan, ICI 
Agrochemicals, United Kingdom, and Roussel Uclaf SA, France, made 
available to the IPCS and the Task Group their proprietary 
toxicological information on their products under discussion is 
gratefully acknowledged.  This allowed the Task Group to make their 
evaluation on a more complete data base. 

    The efforts of all who helped in the preparation and 
finalization of the documents is gratefully acknowledged. 

Synthetic pyrethroids-a profile 

    During investigations to modify the chemical structures of 
natural pyrethrins, a certain number of synthetic pyrethroids were 
produced with improved physical and chemical properties and greater 
biological activity.  Several of the earlier synthetic pyrethroids 
were successfully commercialized, mainly for the control of 
household insects.  Other more recent pyrethroids have been 
introduced as agricultural insecticides because of their excellent 
activity against a wide range of insect pests and their non-
persistence in the environment. 

    The pyrethroids constitute another group of insecticides in 
addition to organochlorine, organophosphorus, carbamate, and other 
compounds.  Pyrethroids commercially available so far include 
allethrin, resmethrin, d-phenothrin, and tetramethrin (for insects 
of public health importance), and cypermethrin, deltamethrin, 
fenvalerate, and permethrin (mainly for agricultural insects).  
Other pyrethroids are also available, including furamethrin, 
kadethrin, and tellallethrin (usually for household insects), 
fenpropathrin, tralomethrin, cyhalothrin, lambda-cyhalothrin, 
tefluthrin, cyfluthrin, flucythrinate, fluvalinate, and biphenate 
(for agricultural insects). 

    Toxicological evaluations of several synthetic pyrethroids have 
been performed by the FAO/WHO Joint Meeting on Pesticide Residues 
(JMPR).  The acceptable daily intake (ADI) has been estimated by 
the JMPR for cypermethrin, deltamethrin, fenvalerate, permethrin, 
d-phenothrin, cyfluthrin, cyhalothrin, and flucythrinate. 

    Chemically, synthetic pyrethroids are esters of specific acids 
(e.g., chrysanthemic acid, halo-substituted chrysanthemic acid, 
2-(4-chlorophenyl)-3-methylbutyric acid) and alcohols (e.g., 
allethrolone, 3-phenoxybenzyl alcohol).  For certain pyrethroids, 
the asymmetric centre(s) exist in the acid and/or alcohol moiety, 
and the commercial products sometimes consist of a mixture of both 
optical (1R/1S or  d/l) and geometric  (cis/trans) isomers.  However, 
most of the insecticidal activity of such products may reside in 
only one or two isomers.  Some of the products (e.g., d-phenothrin, 
deltamethrin) consist only of such active isomer(s). 

    Synthetic pyrethroids are neuropoisons acting on the axons in 
the peripheral and central nervous systems by interacting with 
sodium channels in mammals and/or insects.  A single dose produces 
toxic signs in mammals, such as tremors, hyperexcitability, 
salivation, choreo-athetosis, and paralysis.  The signs disappear 
fairly rapidly, and the animals recover, generally within a week.  
At near-lethal dose levels, synthetic pyrethroids cause transient 
changes in the nervous system, such as axonal swelling and/or 
breaks and myelin degeneration in the sciatic nerves.  They are not 
considered to cause delayed neurotoxicity of the kind induced by 
some organophosphorus compounds.  The mechanism of toxicity of 
synthetic pyrethroids, and their classification into two types, are 
discussed in Appendix I. 

    Some pyrethroids (e.g., deltamethrin, fenvalerate, 
flucythrinate, and cypermethrin) may cause a transient itching 
and/or burning sensation in exposed human skin. 

    Synthetic pyrethroids are generally metabolized in mammals 
through ester hydrolysis, oxidation, and conjugation, and there is 
no tendency to accumulate in tissues.  In the environment, 
synthetic pyrethroids are fairly rapidly degraded in soil and in 
plants.  Ester hydrolysis and oxidation at various sites on the 
molecule are the major degradation processes.  The pyrethroids are 
strongly adsorbed on soil and sediments, and are hardly eluted with 
water.  There is little tendency for bioaccumulation in organisms. 

    Because of low application rates and rapid degradation in the 
environment, residues in food are generally low. 

    Synthetic pyrethroids have been shown to be toxic for fish, 
aquatic arthropods, and honey-bees in laboratory tests.  But, in 
practical usage, no serious adverse effects have been noticed 
because of the low rates of application and lack of persistence in 
the environment.  The toxicity of synthetic pyrethroids in birds 
and domestic animals is low. 

    In addition to the evaluation documents of FAO/WHO, there are 
several good reviews and books on the chemistry, metabolism, 
mammalian toxicity, environmental effects, etc., of synthetic 
pyrethroids, including those by Elliot (1977), Miyamoto (1981), 
Miyamoto & Kearney (1983), and Leahey (1985). 


1.1  Summary and Evaluation

1.1.1  Identity, physical and chemical properties, analytical 

    Deltamethrin was synthesized in 1974, and first marketed in 
1977.  Chemically, it is the [1R,  cis; alphaS]-isomer of 8 
stereoisomeric esters of the dibromo analogue of chrysanthemic 
acid, 2,2-dimethyl-3-(2,2-dibromovinyl) cyclopropanecarboxylic acid 
(Br2CA) with alpha-cyano-3-phenoxybenzyl alcohol. 

    Technical grade deltamethrin is an odourless white powder with 
a melting point of 98 - 101 °C and contains more than 98% of the 
material.  The vapour pressure is 2.0 x 10-6 Pa at 25 °C and it is 
practically non-volatile.  It is insoluble in water, but soluble in 
organic solvents, such as acetone, cyclohexanone, and xylene.  It 
is stable to light, heat, and air, but unstable in alkaline media. 

    The determination of residues and analysis of environmental 
samples were carried out by solvent extraction with  n-hexane/ 
acetone, partitioning with  n-hexane/acetone/water, clean-up with a 
silica gel column chromatograph, and determination with a gas 
chromatograph equipped with an electron capture detector with a 
minimum detectable concentration of 0.01 mg/kg or less.  High- 
performance liquid chromatography with an UV-detector is used for 
product analysis. 

1.1.2  Production and uses

    The consumption of deltamethrin in the world was about 250 
tonnes in 1987.  It is mostly used on cotton (45% of the 
consumption) and on crops such as coffee, maize, cereals, fruit, 
vegetables, and hops, and on stored products.  Deltamethrin is also 
used in animal health, in vector control, and in public health.  It 
is formulated as an emulsifiable concentrate, ultra-low-volume 
concentrate, wettable powder, suspension concentrate, or dust 
powder, alone, or in combination with other pesticides. 

1.1.3  Human exposure

    Exposure of the general population to deltamethrin is mainly 
via dietary residues, but may also occur from its use in public 
health.  Residue levels in crops treated according to good 
agricultural practice are generally very low, except for those 
arising from post-harvest treatment.  Extensive data have been 
reviewed by FAO/WHO (see section 9). 

    Exposure of the general population is expected to be very low, 
but actual data in the form of total diet studies are lacking. 

1.1.4   Environmental exposure and fate

    When 14C-(acid, alcohol, or cyano labelling)-deltamethrin-[1R, 
 cis; alphaS] was exposed to sunlight as a thin film for 4 - 8 h, 
70% of it was transformed by  cis/trans-isomerization to give the 
[1R,  trans; alphaS] and [1S,  trans; alphaS] isomers, together with 
ester cleavage products, including Br2CA and alpha-cyano-3-
phenoxybenzyl alcohol. 

    Deltamethrin was degraded in cotton plants, under glasshouse 
conditions, with an initial half-life of 1.1 weeks, and the time 
needed for 90% loss was 4.6 weeks.  

    The major metabolites were free and conjugated Br2CA,  trans-
hydroxymethyl-Br2CA, and 3-(4-hydroxyphenoxy)benzoic acid formed by 
ester cleavage, oxidation, and conjugation.  

    Deltamethrin was incubated in sand and organic soil at 28 °C 
under laboratory conditions.  Approximately 52% and 74% of the 
applied deltamethrin was recovered from sand and organic soil, 
respectively, 8 weeks after treatment.  

    Deltamethrin is not mobile in the environment because of its 
strong adsorption on particles, its insolubility in water, and very 
low rates of application.  

    No data are available on actual levels in the environment, but 
with the current use pattern and under normal conditions of use, 
environmental exposure is expected to be very low.  Degradation to 
less toxic products is rapid. 

1.1.5  Uptake, metabolism, and excretion

    Deltamethrin is readily absorbed by the oral route, but less so 
dermally; the rate of absorption is strongly dependent on the 
carrier or solvent.  Absorbed deltamethrin is readily metabolized 
and excreted. 

    When rats were given 14C-(acid, alcohol, or cyano labelled)- 
deltamethrin orally at the rate of 0.64 - 1.60 mg/kg, the 
radiocarbon from the acid and alcohol moiety was almost completely 
eliminated within 2 - 4 days.  Tissue residue levels were generally 
very low, except in fat, where slightly higher residues occurred.  
However, the cyano portion was excreted more slowly, with total 
recovery of 79% in 8 days.  The major metabolic reactions were 
oxidation (at the  trans-methyl of the cyclopropane ring and at the 
2'-, 4'-, and 5-positions of the alcohol moiety), ester cleavage, 
and conversion of the cyano portion to thiocyanate.  The resultant 
carboxylic acids and phenols were conjugated with sulfuric acid, 
glycine, and glucuronic acid.  

    When mice were fed 14C-(acid, alcohol, or cyano labelled)- 
deltamethrin orally at rates of 1.7 - 4.4 mg/kg, the excretion of 
the radiocarbon was rapid and almost complete, except for the cyano 
portion.  The major metabolic reactions in mice were generally 
similar to those in rats. 

    In cows and poultry, degradation pathways are very close to 
those in rodents.  

1.1.6  Effects on organisms in the environment

    Deltamethrin is highly toxic for fish, the 96-h LC50 ranging 
between 0.4 and 2.0 µg/litre.  It is also highly toxic for aquatic 
invertebrates; the 48-h LC50 for  Daphnia is 5 µg/litre.  However, 
extensive field studies, in experimental ponds, and field use have 
shown that this high potential toxicity is not realized.  Some 
kills of aquatic invertebrates occur in the field, but these are 
usually compensated for rapidly. 

    The toxicity of deltamethrin for birds is very low with LD50 
values for a single oral dose exceeding 1000 mg/kg.  Under 
laboratory conditions, it is highly toxic for honey-bees with a 
contact LD50 of 0.051 µg/bee.  Field trials and actual usage have 
established that deltamethrin formulations have a repellent action, 
which means that, in practice, the hazard for bees is low. 

1.1.7  Effects on experimental animals and  in vitro test systems 

    In a non-aqueous vehicle, the acute oral toxicity of  
deltamethrin is high to moderate with LD50 values of 19 - 34 mg/kg 
(mouse) and 31 - 139 mg/kg (rat).  However, in a suspension in 
water, the toxicity is much less with LD50 values exceeding 
5000 mg/kg (rat).  Deltamethrin is a Type II pyrethroid; clinical 
signs of poisoning include tremor, salivation, and convulsion.  The 
onset of signs is rapid and they disappear within several days in 
survivors.  The electroencephalogram shows generalized spike and 
wave discharges prior to choreo-athetosis. 

    Single applications of technical deltamethrin did not produce 
any irritant effect on the intact and abraded skin of the rabbit.  
However, transient irritating effects were produced in the eye of 
the rabbit, with and without rinsing.  Deltamethrin was not a skin 
sensitizer in the guinea-pig. 

    When rats were dosed, by gavage, with deltamethrin levels of up 
to 10.0 mg/kg body weight per day for 13 weeks, hyperexcitability 
was observed at 6 weeks in males given the highest dose.  Body  
weight gain was lower in males given 2.5 and 10 mg/kg. 

    When beagle dogs were dosed orally with deltamethrin at levels 
of up to 10 mg/kg body weight per day for 13 weeks, there were 
various compound-related symptoms, such as vomiting, tremor, 
salivation, and depressed gag-, patellar-, and flexor reflexes.  In 
a 2-year feeding study on dogs, 1 mg/kg body weight per day was the 
no-observed-effect level (highest level tested). 

    When mice were fed deltamethrin at levels of up to 100 mg/kg 
diet for 24 months, tumour incidence was unaffected.  The no- 
observed-effect level for systemic toxicity was 100 mg/kg diet. 

    When rats were fed deltamethrin at levels of up to 50 mg/kg 
diet for 2 years, no compound-related tumours were observed.  The 
no-observed-effect level for systemic toxicity was 50 mg/kg diet. 

    Deltamethrin was not mutagenic in a variety of  in vivo and  in 
 vitro test systems, including:  DNA repair, gene mutation, 
chromosomal aberration, sister chromatid exchange, micronucleus 
formation, and dominant lethal tests. 

    Teratology studies were conducted on pregnant rats and mice in 
which deltamethrin was administered orally at levels of up to 
10 mg/kg body weight per day during the period of major 
organogenesis.  There were no teratogenic or reproductive effects, 
except for a dose-related decrease in mean fetal weight in the 
mouse study and slightly delayed ossification in the rat study. 

    Rabbits received deltamethrin at levels of up to 16 mg/kg body 
weight per day between days 6 and 19 of pregnancy.  A decreased 
average fetal weight was noted at the highest dose.  No teratogenic 
effects were observed in rabbits. 

    When rats were fed deltamethrin at levels of up to 50 mg/kg 
diet in a 3-generation, 2-litter reproduction study, no effects on 
reproduction were observed. 

    There are indications that potentiation of toxicity may occur 
when deltamethrin is combined with some organophosphorus compounds. 

1.1.8  Effects on human beings

    Deltamethrin can induce skin sensations in exposed workers.  
Several non-fatal cases of poisoning have been reported through 
occupational exposure resulting from neglect of safety precautions.  
Numbness, itching, tingling, and burning of the skin and vertigo 
are symptoms that are frequently reported.  Occasionally, a 
transient papular or blotchy erythema has been described.  Most of 
these symptoms are transient and disappear within 5 - 7 days.  No 
long-term adverse effects have been reported.  Three non-fatal 
cases of deltamethrin poisoning have been described following 
ingestion of several grams of the product. 

1.2  Conclusions

 General population:  The exposure of the general population to 
deltamethrin is expected to be very low and is not likely to 
present a hazard under recommended conditions of use. 

 Occupational exposure:  With good work practices, measures of 
hygiene, and safety precautions, deltamethrin is unlikely to 
present a hazard for those occupationally exposed. 

 Environment:  It is unlikely that deltamethrin or its degradation 
products will attain levels of adverse environmental significance 
with recommended rates of application.  Under laboratory 
conditions, deltamethrin is highly toxic for fish, aquatic 

arthropods, and honey-bees.  However, under field conditions, 
lasting adverse effects are not likely to occur under recommended 
conditions of use. 

1.3  Recommendations

    Although dietary levels are considered to be very low following 
recommended usage, confirmation of this through inclusion of 
deltamethrin in monitoring studies should be considered. 

    Deltamethrin has been used for many years and several cases of 
non-fatal poisoning and transient effects from occupational 
exposure have been reported.  Observations of human exposure should 
be maintained. 


2.1  Identity

Molecular formula:  C22H19Br2NO3
Chemical Structure

Chemical Structure

    Deltamethrin is the first pyrethroid composed of a single 
isomer of 8 stereoisomers selectively prepared by the 
esterification of [1R, 3R or  cis]-2,2-dimethyl-3-(2,2-dibromovinyl) 
cyclopropanecarboxylic acid with (alphaS)- or (+)-alpha-cyano-3-
phenoxybenzyl alcohol or by selective recrystallization of the 
racemic esters obtained by esterification of the (1R, 3R or  cis)-
acid with the racemic or [alphaR, alphaS, or alphaRS or ±]-alcohol 
(Elliott et al., 1974).  Thus, its stereospecific structure (4) is 
the ester of [1R, 3R or  cis]-acid with (alphaS)-alcohol. 

    The acid is a characteristic dibromo analogue of chrysanthemic 

2.2  Physical and Chemical Properties

    Technical grade deltamethrin contains more than 98% deltamethrin
(FAO/WHO, 1981).  It is stable to heat (6 months at 40 °C), light,
and air, but unstable in alkaline media (FAO/WHO, 1981; Meister et
al., 1983; Worthing & Walker, 1983).  Some physical and chemical
properties are listed in Table 1, and the chemical composition of
various stereoisomeric mixtures is shown in Table 2. 

Table 1.  Some physical and chemical properties of deltamethrin
Physical state            crystalline powder 
Colour                    colourless
Odour                     odourless
Density (20 °C)           0.5 g/cm3
Relative molecular mass   505.24
Melting point (°C)        98-101
Boiling point             decomposes above 300 °C
Water solubility (20 °C)  < 0.002 mg/litre (practically insoluble)
Solubility in organic     solublea
Vapour pressure (25 °C)   2.0 x 10-6 Pa
 n-Octanol-water           5.43
 partition coefficient 
 (Log Pow) 
a Acetone (500 g/litre), ethanol (15 g/litre), cyclohexanone (750 
  g/litre), dioxane (900 g/litre), xylene (250 g/litre), ethyl 

2.3  Analytical Methods

    Methods for the determination of deltamethrin residues and the 
analysis of environmental samples, and products are summarized in 
Table 3. 

    To analyse technical grade deltamethrin, a mixture of 
deltamethrin and diphenylamine (an internal standard) was injected 
in a high-performance liquid chromatograph equipped with a UV-
detector (Mourot et al., 1979). 

    The Joint FAO/WHO Codex Alimentarius Commission has published 
recommendations for methods for the determination of deltamethrin 
residues (FAO/WHO 1985b).  A further review of analytical methods 
for deltamethrin has been made by Vaysse et al. (1984). 

Table 2.  Chemical identity of deltamethrins of various stereoisomeric compositions
Common name           CA Index name (9CI)                        Stereoisomeric  Synonyms and trade names
CAS Registry No.                                                 compositionc    
NIOSH Accession No.a  Stereospecific nameb
Deltamethrin          Cyclopropanecarboxylic acid,               (4)             Decamethrin, Decis,
52918-63-5            3-(2,2-dibromovinyl)-2,2-dimethyl-,                        K-Othrine, NRDC 161,
GZ1233000a            alpha-cyano(3-phenoxyphenyl)methyl ester,                  WHO 1998, K-Obiol, Butox
                      [1R-[1 (S*), 3 R]]-,                                       Butoflin, Cislin, FMC 45498
                                                                                 RU 22974
                      (1R,  cis)-2,2-dimethyl-3-(2,2-di-

d- cis-Deltamethrin    same as deltamethrin                       -               Decamethrin, Decis
GZ1240000a            (S)-alpha-cyano-3-phenoxybenzyl
                      (d,  cis)-2,2-dimethyl-3-(2,2-di-
a Registry of Toxic Effects of Chemical Substances (RTECS) (1981-82 edition).
b (1R), d, (+) or (1S), 1, (-) in the acid part of deltamethrin signifies the same stereospecific conformation, 
c The number in the parenthesis identifies the structure shown in the figures of stereoisomers.

Table 3.  Analytical methods for deltamethrin
Sample         Extraction    Sample preparation                     Determination:         MDCb     % Recovery          Reference
               solvent       -----------------------------------                           (mg/kg)  (fortification
                             Partition     Clean up                 GLC or HPLC                     level in
                                           column      elution      condition; detector,            mg/kg)  
                                                                    carrier flow, column,
                                                                    temp, R.T.a
apple           n-hexane/     ext.sol.c/    silica gel  CH2Cl2       ECD-GC; N2;            0.01     105(0.1), 100(1.0)  1
               acetone       H2O                                    50 ml/min; 1 m 
               (1/1)                                                3% OV-7; 235 °C
pear                                                                                       0.01     125(0.1), 98(1.0)   
cabbage                                                                                    0.01     130(0.1), 118(1.0) 
potato                                                                                     0.01     126(0.1), 97(1.0) 
apple,         acetonitrile  petroleum     Florisil    ether/       EDC-GC; 1.2 m          0.005    85-100(0.02-0.1)    2 
peach,                       ether/H2O                  n-hexane     DC-200, OV-1 or 
grape,                                                 (1/4)        OV-101; 245 °C,  
tomato                                                              10-12 min
wheat          methanol       n-hexane      alumina                  HPLC; 235 nm;                   87(2.0)             3
grain                                                               30 cm; uBondapak;
                                                                    C 18; methanol/H2O
                                                                    (4/1); 2.5 ml/min
wheat                         n-hexane      Florisil    ether/       ECD-GC; N2;                     91                  4
                                                       petroleum    75 ml/min; 0.6 m 
                                                       ether (1/9)  5% SE-30; 215 °C
meat           ethyl ether/  acetonitrile  gel         diisopropyl  ECD-GLC; N2;           0.001    90-95% at 0.01      5
               petroleum                   permeation  ether        40 ml/min; 1.8 m
               ether                       column                   SE-30 1% on gas 
                                           (Styragel)               Chrom. PAW
milk           hexane        acetonitrile  Florisil +  benzene/     ECD-GLC; N2;           0.01     83-87% at 0.1       5
                                           cellulose/  hexane       40 ml/min; 1.8 m  
                                           charcoal    (1/1)        SE-30 1% on gas
                                                                    Chrom. PAW 

Table 3.  (contd.)
Sample         Extraction    Sample preparation                     Determination:           MDCb     % Recovery          Reference
               solvent       -----------------------------------                             (mg/kg)  (fortification
                             Partition     Clean up                 GLC or HPLC                       level in
                                           column      elution      condition; detector,              mg/kg)  
                                                                    carrier flow, column,
                                                                    temp, R.T.a
locust          n-hexane                    Florisil    ether/       ECD-GC; N2;                       92                  4
                                                       petroleum    75 ml/min; 0.6 m 5%
                                                       ether (1/9)  SE-30; 215 °C 
sea water      XAD-2         ext.sol.c/    alumina                  ECD-GC; N2;                                           6
               resin          n-hexane                               70 ml/min; 1.5 m 
               acetone                                              4% SE-30; 207 °C

water           n-hexane                    alumina                  ECD-GC; N2;                                           6
                                                                    70 ml/min; 1.5 m 
                                                                    4% SE-30; 207 °C 
water          petroleum                   Florisil    petroleum    ECD-GLC; 1 m OV          0.0001   97 at 0.010         8
               ether/                                  ether/       1-3% on Chromosorb
               diethyl-                                diethyl-     W.A.W. HMDS 60/80
               ether (1/1)                             ether   

soil           acetone,                    acid        hexane       ECD-GLC; 5.2%            0.001    > 91%               9
               acetone/                    alumina     ether        OV-210 with AR/CH4
               hexane (1/1)                            hexane 
               hexane                                  (5-10%)
               acetone,                    acid        hexane/      ECD-GLC; N2;             0.0001   > 91%               5
               acetone/                    alumina     ethyl ether  40 ml/min; 1.8 m 
               hexane (1/1)                            (90/10)      SE-30 1% on gas 
               hexane                                               Chrom. PAW
cotton          n-hexane                                             transesterification                                   7
foliage                                                             followed by ECD-GC; 
(dislodgeable                                                       31 ml/min; 0.45 m    
residue)                                                            5% SE-30; 120 °C
Table 3.  (contd.)
Sample         Extraction    Sample preparation                     Determination:           MDCb     % Recovery          Reference
               solvent       -----------------------------------                             (mg/kg)  (fortification
                             Partition     Clean up                 GLC or HPLC                       level in
                                           column      elution      condition; detector,              mg/kg)  
                                                                    carrier flow, column,
                                                                    temp, R.T.a

Technical                                                           HPLC, 230 nm; 15 cm                                   10
grade                                                               Lichrosorb Si-60; 
                                                                    ether (93/7); 80 ml/h; 
                                                                    7.6 min    

               isoctane/                                            HPLC - UV detector                                    5
               dioxane                                              254 nm (230 nm for
               (80/20)                                              conc. <0.5%) Silica-60; 
                                                                    100ml/h; isooctane/ 
                                                                    dioxane (95/5)   
a R.T.:  retention time;
b MDC: minimum detectable concentration;
c ext .sol.: extraction solvent.


1. Baker & Bottomley (1982); 2. Mestres et al. (1978a); 3. Noble et al. (1982); 4. Pansu et al. (1981); 5. Vaysse et al. (1984); 
6. Zitko et al. (1979); 7. Estesen et al. (1979); 8. Mestres et al. (1978b); 9. Hill (1982); 10. Mourot et al. (1979). 
3.1  Industrial Production

    Deltamethrin was first marketed in 1977.  Production volumes in 
recent years are shown in Table 4. 

Table 4.  Worldwide production of deltamethrin
Year  Production  Reference
1979  75          Wood Mackenzie (1980)
1980  100         Wood Mackenzie (1981)
1981  100         Wood Mackenzie (1982, 1983)
1982  115         Wood Mackenzie (1983)
1987  250         Information from Roussel Uclaf

3.2  Use Patterns

    After an initial period when the product was mainly used on 
cotton, several major crops were treated with deltamethrin from 
1980 to 1987.  Some 85% of the total production is used for crop 
protection.  Within this, 45% is used on cotton, 25%, on fruit and 
vegetable crops, 20% on cereals, corn, and soybean, and the 
remaining 10% on miscellaneous crops. 

    Deltamethrin is used to protect stored commodities (mainly 
cereals, grains, coffee beans, dry beans), in forestry, and in 
public health (e.g., Chagas disease control in South America, and 
malaria control in Central America and on the African continent).  
It is also used in animal facilities and against cattle 

    It is formulated as an emulsifable concentrate (25 - 100 
g/litre), an ultra-low-volume concentrate (1.5 - 30 g/litre), a 
wettable powder (25 - 50 g/kg), a flowable powder (7.5 - 50 
g/litre), or a dust powder (0.5 - 2.5 g/kg).  It is also used in 
combination with other pesticides and with piperonyl butoxide 
(unpublished information from Roussel Uclaf to the IPCS, 1988). 

3.3  Residues in Food

    Supervised trials have been carried out on a wide variety of 
crops and comprehensive summaries of analyses for residues in these 
trials can be found in the evaluation reports of the Joint FAO/WHO 
Meeting on Pesticide Residues (JMPR) (FAO/WHO 1981, 1982, 1983, 
1985a, 1986a, 1986b, 1988b).  A comprehensive list of maximum 
residue limits (MRLs) for a large number of commodities resulted 
from these evaluations (FAO/WHO, 1986c, 1988a,c) (see section 9). 

    Residues were determined in stored products, e.g., wheat, 
maize, and coffee.  The residue level in wheat grains treated with 
deltamethrin at the rate of 2 mg/kg was 1.08 mg/kg after storage 

for 9 months.  When the wheat was subjected to milling and baking, 
the residue levels in white bread were 0.11 mg/kg (Halls & Periam, 

    Mestres et. al. (1986) reviewed the changes in deltamethrin 
residues in edible crops resulting from processing and cooking and 
found that, depending on the commodity, pre- or post-harvest 
residues were reduced by 20 - 98% by processing, and especially by 

    When 0.27 g of 14C-(alcohol labelling)-deltamethrin was 
injected intrarumenally in a lactating Jersey cow, in solution in a 
sesame oil/alcohol mixture, only 0.4% of the compound was found in 
whole milk.  Peak residue levels of 0.045 and 0.92 mg/kg were found 
in whole milk and rendered butter fat, respectively, 1 day after 
administration.  Residues in omental fat and leg muscle were 0.088 
and 0.008 mg/kg, respectively, 2 days after treatment (Wellcome 
Foundation, 1979). 

3.4  Levels in the Environment

    No information is available.

4.1  Transport and Distribution Between Media

    Using three different soils (silty clay, silty clay loam, and 
loamy sand), Kaufman et al. (1981) found that deltamethrin was 
practically immobile in soil columns.  Approximately 96 - 97% of 
the 14C activity remained in the upper 0 - 2.5 cm layer of the 
columns with only 1.3 % in the 2.5 - 5.1 cm layer and no 14C in the 
leachate.  Soil thin layer chromatography (soil TLC) was also used 
to evaluate the mobility of deltamethrin.  According to the 
pesticide mobility classification system developed by Helling & 
Turner, deltamethrin is classified as a low-mobility to immobile 
compound in soils. 

    The immobility of deltamethrin in soil was also studied by 
Hascoet (1977) using a French Fontainebleau sand column leached 
with a very high volume of water (equivalent to 1030 mm of rain).  
In this experiment, approximately 97% of the applied 14C-
deltamethrin remained in the upper 0 - 2.5 cm layer and only 2% was 
found in the leachate.  The author concluded that deltamethrin was 
unlikely to leach in cultivated soil that had a higher organic 
matter content and/or higher clay contents than sand (organic 
matter 0.03%), which has especially good filtration and low 
adsorption properties. 

    The leaching of deltamethrin was also studied in three 
different German soils the organic contents of which ranged from 
0.8 to 2.6%.  The study was carried out using the commercial 
product Decis EC 25 at a rate equivalent to 1 litre/ha (i.e., 25 g 
deltamethrin/ha).  Each column was leached with 370 ml of water, 
which was equivalent to a rainfall of 200 mm for 2 days.  Under 
these conditions, the amount of active ingredient (a.i.) detected 
in seepage water was found to be less than 1 µg/ml, which was less 
than 2% of the original applied dose (Thier & Schmidt, 1976). 

    The mobility of the primary deltamethrin degradation products  
3-phenoxybenzoic acid (PBacid) and 3-phenoxybenzyl alcohol (PBalc) 
was also investigated by Kaufman et al. (1981) using soil TLC and 
soil columns.  PBacid was found to be relatively mobile, whereas 
PBalc was only slightly mobile.  2,2-Dimethyl-3-(2,2-dibromovinyl) 
cyclopropanecarboxylic acid (Br2CA) was not studied in this 
experiment, but Cl2CA, the chloride substituted analogue, was 
evaluated and also found to be relatively mobile.  However, these 
metabolites did not accumulate in the soil to any extent, since 
they were never in excess of 3% of the applied dose under the 
aerobic conditions reported by Kaufman & Kayser (1979a,b).  The 
very significant production of 14CO2 during the incubation period 
confirmed that they were further degraded. 

4.2  Abiotic Degradation in Air and Water

    Degradation pathways for deltamethrin are summarized in Fig. 1. 


    When 14C-deltamethrin-[1R, 3R; alphaS] (9) labelled at the 
cyano, benzylic, or dibromo-substituted carbon was exposed to 
sunlight as a thin film (40 µg/cm2) for 4 - 8 h, the  trans-[1R,
3S; alphaS] and -[1S, 3R; alphaS] isomers were formed.  They
accounted for approximately 70% of the applied radioactivity. 
Smaller amounts of ester cleavage products including the
2,2-dimethyl-3-(2,2-dibromovinyl) cyclopropanecarboxylic acid
(Br2CA) (18) and the cyanohydrin component, and 18% of
unidentified products were also formed (Fig. 1).  In a thick film (3
mg/cm2), small amounts of other products including
alpha-cyano-3-phenoxybenzyl 3,3-dimethylacrylate (13) and 3-phenoxy
2,2-dimethyl-3-(2,2- dibromovinyl)cyclopropan-1-yl-benzylcyanide
(14) (decarboxydeltamethrin) were also detected.  In contrast, the
predominant products in methanol were the  trans mixtures, which
amounted to approximately 35% of the applied radioactivity.  Under
UV radiation (peak output 290 - 320 nm), the photodegradation rate
of deltamethrin in alcohols decreased in the order of methanol, 
ethanol, and 2-propanol, as the solvent viscosity increased.  The 
relative photolysis rates in hexane and cyclohexane, with respective
relative viscosities of 0.33 and 1, were 1.5 and 1.  There was no
difference in the extent of the reaction on flushing the hexane with
O2 or N2, while the triplet quenchers piperilene and
1,3-cyclohexadiene reduced the reaction rate in hexane. 

    At 30 - 50% conversion, the  trans-[1R, 3S; alphaS] and -[1S, 
3R; alphaS] isomers were the major photoproducts in aqueous 
acetonitrile, whereas they were observed in only minor amounts in 
methanol and were absent in hexane.  The mono-debrominated esters 
(16) were the major ester products in methanol and hexane.  The 
 cis-acid (18) was always the major photoproduct from the acid 
moiety, with smaller amounts of the two isomeric debrominated acids 

    Major products from the alcohol moiety were 3-phenoxybenzoic 
acid (25) (PBacid) in aqueous acetonitrile, 3-phenoxybenzyl cyanide 
(15) in hexane, and methyl 3-phenoxybenzoate (22) in methanol.  
Photolysis of 3-phenoxybenzoyl cyanide (21) gave methyl 
3-phenoxybenzoate and the methyl ester of Br2CA (19) in methanol 
and PBacid in aqueous acetonitrile.  Thus, it appears that the 
photoproducts obtained originated from cyclopropane ring opening 
and various recombinations, scission of the ester oxygen-benzyl 
carbon bond, scission of the acyl-oxygen bond, and/or reductive 
debromination (Ruzo et al., 1976, 1977). 

    A photodegradation study with 14C-deltamethrin in aqueous 
solution showed that such a solution, at pH 5, is hydrolytically 
stable.  When exposed to simulated sunlight, degradation was 
induced.  The primary product observed was PBacid.  A half-life of 
47.7 days was calculated for the non-sensitized system, but this 
was reduced to 4.03 days when sensitized with 1% acetone.  
Practically no volatile degradation products were observed (Bowman 
& Carpenter, 1987). 

4.3  Environmental Fate

    The degradation and persistence of 14C-cyano- and 14C-phenoxy- 
deltamethrin was examined in a Dubbs fine sandy loam and a Memphis 
silt loam under aerobic laboratory conditions at 25 °C (Kaufman & 
Kayser 1979a); 14C-deltamethrin was applied at final concentrations 
equivalent to 0.02 and 0.2 kg/ha.  Deltamethrin degradation 
occurred rapidly in both soils with 62 - 77% and 52 - 60% of the 
14C-cyano- and 14C-phenoxy-labels, respectively, being evolved as 
14CO2 during the 128-day incubation period.  The half-life of 
deltamethrin varied from 11 to 19 days in the two soil types. 

    The effect of soil temperature on the degradation of 
deltamethrin was also examined in Dubbs fine sandy loam under 
laboratory conditions using 14C-cyano- and 14C-vinyl-labelled 
deltamethrin (Kaufman & Kayser 1979b).  Degradation and evolution 
of 14C-labelled forms of deltamethrin occurred most rapidly at 
25 °C and most slowly in soils incubated at 10 °C.  The half-life 
of deltamethrin was 46, 13, and 27 days in soils incubated at 10, 
25, and 40 °C, respectively. 

    The results of these two studies indicate that deltamethrin 
degradation occurs by two principal pathways (Fig. 2):  hydrolysis 
of the ester linkage to yield Br2CA (18) and 3-phenoxybenzoic acid; 
and hydrolysis of the cyano group to yield first the amide, and 
subsequently the carboxylic acid (DCOOH) analogues of deltamethrin.

Br2CA accumulated to a maximum of 5.7% of the original 14C in soil 
incubated at 40 °C, whereas DCOOH accumulated at 10 °C (to a 
maximum of 5.3%).  However, both products decreased in 
concentration by the end of the 64-day incubation period.  In the 
first experiment, DCOOH was also identified as the major 
degradation product to reach a maximum concentration of 6 - 9% of 
the original 14C.  But it ultimately dissipated to less than 2% at 
the end of the 128-day incubation period. 

    From the 14C-phenoxy label, 3-phenoxybenzoic acid (PBacid) was 
identified as the main degradation product resulting from 
hydrolysis of the ester bond.  This product was further degraded to 
yield both 3-(2-hydroxyphenoxy)-benzoic acid and 3-(4-hydroxyphenoxy) 
benzoic acid.  In this experiment, DCOOH was the only deltamethrin 
degradation product detected in excess of 3% of the original material 

    Although essentially no radiolabel was detected in the leachate 
from soil columns treated with 14C-deltamethrin, PBacid produced by 
degradation of deltamethrin was fairly mobile in the soil columns 
(Kaufman et al., 1981). 

    The degradation pathways are proposed in Fig. 2.


    The degradation of deltamethrin was also examined under 
anaerobic conditions using 14C-cyano-, 14C-phenoxy-, and 
14C-vinyl-labelled materials for the tests (Kaufman & Kayser, 
1980).  Under anaerobic conditions, 14CO2 evolution varied 
according to the 14C label position and the time of flooding.  
Generally, flooding reduced or initially inhibited the rate of 
14CO2 dissipation.  However, after one month, 14CO2 dissipation 
started again, which suggested the presence of a unique microbial 

flora.  It was also shown that all three carboxylic acids that 
accumulate initially in flooded soils are subsequently further 
degraded.  Some reduction of PBacid to 3-phenoxybenzyl alcohol 
(PBalc) was also observed in these flooded soils. 

    When deltamethrin was applied to a sandy clay loam soil at 
17.5 g/ha in an indoor incubation study and in two field 
experiments, the half-lives of deltamethrin were found to be 4.9 
and 6.9 weeks under indoor and field conditions, respectively 
(Hill, 1983).  This difference in the rate of decrease in the 
residue  was attributed to climatic effects. 

    This was further confirmed by Hill & Schaalje (1985) who 
pointed out a first-order dissipation, if degree-days above 0 °C 
rather than days was used as the independent variable, when 
deltamethrin was applied by pipette to soils.  When deltamethrin 
was boom-sprayed, a biphasic first-order plot was observed.  A two-
compartment model that predicts an initial fast loss of residue 
followed by a slower first-order degradation gave a good fit of the 

    Chapman & Harris (1981) examined the relative persistence of 
five pyrethroids, permethrin, cypermethrin, deltamethrin, 
fenpropathrin, and fenvalerate, in sand and organic soil at 28 °C, 
under laboratory conditions.  All of the insecticides (1 mg/kg) were
degraded more rapidly in natural soils than in sterilized soils,
suggesting the importance of microbial degradation.  The rate of
degradation under non-sterilized conditions decreased as follows: 
fenpropathrin > permethrin > cypermethrin > fenvalerate >
deltamethrin.  Amounts of approximately 52% and 74% of the 
deltamethrin applied were recovered from the sand and organic soil, 
respectively, 8 weeks after treatment. 

    It was pointed out by Chapman et al. (1981) that biological 
processes played a major role in the degradation of deltamethrin in 

    The degradation of deltamethrin was also investigated by Zhang 
et al. (1984) in an organic soil over a 180-day period.  The half- 
life of deltamethrin was found to be 72 days, indicating that 
deltamethrin is likely to be less susceptible to degradation in 
organic soils than in mineral soils.  Identification of metabolites 
present in the extractable phase confirmed the metabolic pathways 
previously reported by Kaufman.  Levels of bound 14C residues 
increased with the incubation period to reach 19% of the original 
14C after 180 days.  Most of these bound 14C residues were in the 
humic fraction.  Bacterial and actinomycete populations increased 
in the treated soil, but fungal populations remained relatively 
stable during the incubation period. 

    The degradation of deltamethrin was also studied in two German 
soils.  Half-lives for sandy soil and sandy loam soil were 35 and 
60 days, respectively (Thier & Schmidt, 1977). 

    All these studies demonstrate that deltamethrin is readily and 
quickly degraded in the soil.  The half-life of the compound 
depends on the nature of the soil as well as the temperature.  

Generally speaking, the half-life ranges from 11 to 72 days, under 
aerobic conditions.  Deltamethrin degradation is slower under 
anaerobic or sterile conditions, indicating that microorganisms and 
other biological processes play a very important role. 

    The metabolism of deltamethrin in cotton plants was studied 
using material 14C-labelled at the dibromovinyl, benzylic, and 
cyano carbons.  Under glasshouse conditions, the initial half-life 
of deltamethrin was 1.1 weeks and the time needed for 90% loss was 
4.6 weeks.  Conversion of deltamethrin to the  trans-isomer occurred 
via photochemical reactions and, after 6 weeks, the  trans/cis ratio 
was 0.44:1.  Deltamethrin degraded more rapidly under field 
conditions to give a higher proportion of  trans- to  cis-isomers and 
large amounts of unextractable products.  Trace amounts of three 
deltamethrin derivatives hydroxylated either at the 4'-position 
(10), or at the  trans-methyl relative to the carboxy group in the 
acid moiety (7), or at both sites (12) were detected with all three 
14C preparations (Fig. 1).  However, the major metabolites were 
free and conjugated Br2CA together with small quantities of the 
 trans-hydroxymethyl derivatives (20) of Br2CA and 3-(4-
hydroxyphenoxy) benzoic acid (26).  The above compounds were 
analogues of those formed from permethrin and cypermethrin in 
plants.  Several types of conjugated metabolites were isolated, but 
they were not fully characterized.  One type was cleaved readily 
with beta-glucosidase or hydrogen chloride to yield Br2CA and 
PBacid.  Two other types were resistant to beta-glucosidase, but 
cleaved readily with hydrogen chloride to yield Br2CA (from the 
dibromovinyl label) and 3-phenoxybenzoic acid, 3-phenoxybenzyl 
alcohol (from the alcohol label), and alpha-cyano-3-phenoxybenzyl 
alcohol (from the cyano and alcohol labels).  The metabolites of 
deltamethrin identified in plants were analogous to those in 
mammals, except for the conjugated products. 

    The metabolism of deltamethrin and its degradation products in 
cotton and bean leaf disks has also been studied.  Limited 
conversion (approximately 6%) of deltamethrin occurred to give 
Br2CA and 3-phenoxybenzyl alcohol (27) (PBalc) conjugates.  The 
ester cleavage products used as substrates underwent more extensive 
metabolism, and two to three types of glucosides were formed from 
Br2CA and four from PBalc.  3-Phenoxybenzaldehyde (24), 
administered directly or as the cyanohydrin (23), was reduced to 
PBalc, though part was oxidized to PBacid (Ruzo & Casida, 1979). 

4.4  Bioaccumulation

    Bioaccumulation studies with fish, have shown that pyrethroids 
have bioconcentration factors (BCFs) that are far lower than those 
predicted from the correlation between the Kow partition 
coefficient and BCF.  The low accumulation can be attributed to 
metabolism by the fish and to the reduced bioavailability to fish 
of deltamethrin bound by dissolved organic carbon and suspended 
colloids.  Metabolic kinetics were assessed by Cary (1978) in 
 Ictalurus punctatus maintained for 30 days in the water of a 
hydrosoil system, in which the soil was treated with a dose of 
125 g a.i./ha (10 times the normal agricultural dose) and then 
flooded after 31 days.  During the exposure period, none of the 

300 fish died or behaved abnormally despite a final deltamethrin 
concentration of 2.19 µg/litre, which is more than 3 times the 
acute 96-h LC50 of 0.63 µg/litre (Table 6).  During a third phase, 
fish were introduced into an uncontaminated liquid medium, 
continuously renewed, to monitor elimination of deltamethrin or its 
metabolites.  The main results are given in Table 5. 

Table 5.  Bioaccumulation factors after exposure of  Ictalurus 
 punctatus and depuration kineticsa
Organ            Value of bioconcentration  14C elimination (%)
                 factor (BCF)b during       after depuration of
                 exposure, 30 days          -------------------
                                            1 day  14 days
muscles          25                         <50    77
viscera          972                        67     86
carcasses        41                         >50    93
body as a whole  144                        >50    93
a From:  Cary (1978).
b BCF:  µg/kg concentration in fish/µg/litre concentration in 

    Muir et al. (1985) monitored the fate and uptake of 
14C-labelled deltamethrin in organisms in experimental ponds over 
306 days.  Initial concentrations of the pyrethroid ranged from 1.8 
to 2.5 µg/litre.  The deltamethrin rapidly became distributed in 
suspended solids, plants, sediment, and air with a half-life of 
2 - 4 h in the water.  Aquatic plants (the floating duckweed  Lemna 
sp. and a submerged/floating weed  (Potomageton berchtoldi) 
accumulated deltamethrin at concentrations of between 253 and 
1021 µg/kg, respectively, 24 h after treatment, but the compound 
had all disappeared within 14 days.  Fathead minnows,  Pimephales 
 promelas, showed bioconcentration factors of 248 - 907.  Although 
radioactivity remained in the fish throughout the experimental 
period, presumably in the fat, the levels fell steadily and no 
effects were seen on the fish. 

5.1  Metabolism in Experimental Animals

    Metabolic pathways of deltamethrin in mammals are summarized in 
Fig. 3. 


    After oral administration to male rats at 0.64 - 1.60 mg/kg, 
the acid and alcohol moieties of deltamethrin were almost 
completely eliminated from the body within 2 - 4 days (Ruzo et al., 
1978).  On the other hand, the cyano group was eliminated more 
slowly, the total recovery during 8 days being 79% of the 
radiocarbon dose (43% and 36% in the urine and faeces, 
respectively).  Tissue residues of deltamethrin labelled with 14C 
at the dibromovinyl carbon in the acid moiety and the benzylic 
carbon in the alcohol moiety were generally very low, whereas 
residue levels in the fat were somewhat higher (0.1 - 0.2 mg/kg).  
Residue levels of the radiocarbon derived from the cyano group were 
relatively high, especially in the skin and stomach.  Essentially, 
all the radiocarbon in the stomach was thiocyanate.  No noticeable 
14CO2 was evolved from any of the radioactive preparations, 
including the CN-labelled group, in contrast to the CN group from 
fenvalerate, which yielded 14CO2 in considerable amounts. 

    The major metabolic reactions of deltamethrin were oxidation 
(at the  trans methyl relative to carbonyl group of the acid moiety 
and at the 2'-, 4'-, and 5-positions of the alcohol moiety), 
cleavage of the ester linkage, and conversion of the cyano portion 
to thiocyanate and 2-iminothiazolidine-4-carboxylic acid (31) 
(ITCA) (see Fig. 3).  These carboxylic acid and phenol derivatives 
were conjugated with sulfuric acid, glycine, and/or glucuronic 

    The major faecal metabolites were unchanged deltamethrin (9), 
accounting for 13 - 21% of the dose, followed by 4'-OH- (10) and 
5-OH-deltamethrin (28), and a trace amount of 2'-OH-deltamethrin 
(29).  Intact deltamethrin and the 4'-OH-derivative appeared not 
only as the administered S-epimer, but also in parts as the 
R-epimer, probably due to artefactural racemization on exchange of 
the alpha-position hydrogen in methanol solution.  The metabolites 
from the acid moiety were mostly 3-(2,2-dibromovinyl)-2,2-
dimethylcyclopropanecarboxylic acid (18) (Br2CA) in free form 
(10% of the dose), glucuronide (51%) and glycine (trace level) 
conjugates, and OH-Br2CA (20) in free form and glucuronide 
conjugate (<1%). 

    The major metabolites of the aromatic portion of the alcohol 
moiety were 3-phenoxybenzoic acid (25) (PBacid) in free form (5%), 
and glucuronide (13%) and glycine (4%) conjugates and its 
4'-hydroxy derivative (26) (4'-OH-PBacid). 

    Sulfate of 4'-OH-PBacid accounted for about 50% of the dose, 
together with small amounts of free (4%) and glucuronide forms 
(2%).  The CN group was converted mainly to thiocyanate (30) and, 
in small amounts, to ITCA (31) (Ruzo et al., 1978).  The  trans-
isomer of deltamethrin was also rapidly metabolized and yielded 
almost the same metabolites as deltamethrin, though 5-OH-derivative 
was found in the  cis-isomer, but not in the  trans-isomer (Ruzo et 
al., 1978). 

    When a single oral dose of 14C-(acid-, alcohol-, or cyano- 
labelled) deltamethrin was administered to male mice at 1.7 - 4.4 
mg/kg, the acid moiety and the aromatic portion of the alcohol 
moiety were rapidly and almost completely excreted, whereas the CN 
group was excreted relatively slowly (Ruzo et al., 1979). 

    Gray & Rickard (1982) followed the distribution of 14C-acid-, 
14C-alcohol-, and 14C-cyano-labelled deltamethrin and selected 
metabolites in the liver, blood, cerebrum, cerebellum, and spinal 
cord after iv administration of a toxic, but non-lethal, dose 
(1.75 mg/kg) to rats.  Approximately 50% of the dose was cleared 
from the blood within 0.7 - 0.8 min, after which the rate of 
clearance decreased.  3-Phenoxybenzoic acid (PBacid) was isolated 
from the blood  in vivo, and was also the major metabolite when 
14C-alcohol-labelled deltamethrin was incubated with blood  in 
 vitro.  Deltamethrin levels in the liver peaked at 7 - 10 nmol/g at 
5 min and then decreased to 1 nmol/g by 30 min.  In contrast, peak 
central nervous system levels of deltamethrin were achieved within 
1 min (0.5 nmol/g), decreasing to 0.2 nmol/g at 15 min, and 

remaining stable until 60 min.  Peak levels of deltamethrin were 
not related to the severity of toxicity, though the levels of 
unextractable pentane radiolabel did appear to be correlated with 
signs of motor toxicity.  Experiments with brain homogenates from 
animals injected iv with deltamethrin failed to reproduce the 
pentane-unextractable radioactivity  in vitro and metabolism of the 
compound was not demonstrated. 

     The major metabolic pathways of deltamethrin in mice were 
similar to those in rats, though there were some differences.  These
included the presence of more unchanged deltamethrin in mouse faeces
than in rat faeces.  In mouse faeces, there were 4 monohydroxy ester
metabolites (2'-OH-, 4'-OH-, 5-OH-, and  trans-OH- deltamethrin
(11)) and one dihydroxy metabolite (12) (4'-OH- trans-
OH-deltamethrin) that were not found in mouse urine.  Major 
metabolites from the acid moiety in mice were Br2CA,
 trans-OH-Br2CA (20), and their glucuronide and sulfate
conjugates.  Among them,  trans-OH-Br2CA-sulfate was detected
only in mice, but not in rats.  Compared with rats, much larger
amounts of  trans-OH-Br2CA and its conjugates were formed in
mice.  A major metabolite of the alcohol moiety in mice was the
taurine conjugate of PBacid in the urine, which was not detected in
rats.  Generally, mice produced smaller amounts of phenolic
compounds compared with rats.  Also, 3-phenoxybenzaldehyde (24)
(PBald), 3-phenoxybenzyl alcohol (32) (PBalc), and its glucuronide,
and glucuronides of 3-(4- hydroxyphenoxy)benzyl alcohol (33)
(4'-OH-PBalc) and 5-hydroxy-3- phenoxybenzoic acid (34)
(5-OH-PBacid) were found in mice, but not in rats.  When mice were
given an ip dose of 14C-deltamethrin, with or without piperonyl
butoxide (PBO) and/or  S,S,S-tributyl- phosphorotrithioate (DEF),
the same metabolites were obtained as with oral administration. 
However, DEF decreased the hydrolytic products relative to the
controls, while PBO decreased the oxidation products (Ruzo et al.,

    The comparison between the excreted radioactivity of 
14C-deltamethrin in rats treated by the percutaneous route and iv 
(controls) showed that only 3.6% of the dosage applied on the skin 
was absorbed and excreted in 24 h with 1.1% excreted during the 
first 6 h.  Since the rat skin is more permeable than human skin, 
the uptake of deltamethrin through the human skin should be 
relatively weak (Pottier et al., 1982). 

5.2  Metabolism and Fate in Farm Animals

    In a metabolic study, 14C-deltamethrin was administered orally 
to lactating dairy cows at the rate of 10 mg/kg body weight per day 
for 3 consecutive days.  It was poorly absorbed and mainly 
eliminated in the faeces as unchanged deltamethrin.  Only 4 - 6% of 
the administered 14C was eliminated in the urine, and 0.42 - 1.62% 
was secreted in the milk.  The radiocarbon contents of various 
tissues were generally very low with the exception of those of the 
liver, kidney, and fat, which were higher (Akhtar et al. 1986).  
Deltamethrin degradation occurred by cleavage of the ester bond, as 
already reported in rats and mice (Ruzo et al. 1978, 1979).  The 
enzymes responsible for the ester bond cleavage were located in cow 

liver homogenate, mainly in the microsomal fraction, as seen in an 
 in vitro study (Akhtar, 1984).  Metabolites resulting from ester 
bond cleavage were further metabolized and/or conjugated, resulting 
in a large number of compounds excreted in the urine (see Fig. 3).  
In milk, the major identifiable radiolabelled compound was 

    In a feeding study by Akhtar et al. (1987), deltamethrin was 
administered twice daily to lactating dairy cows in portions of 
their daily feed at the rate of 2 or 10 mg/kg diet for 28 
consecutive days.  The level of 2 mg/kg diet was the residue level 
found in a recently treated pasture (Hill & Johnson, 1987), whereas 
10 mg/kg diet was five times this level.  Deltamethrin residues in 
the milk were dose-dependent and appeared to reach a plateau 
between 7 and 9 days after the start of treatment.  At the high 
deltamethrin intake of 10 mg/kg diet, the deltamethrin residue in 
milk was about 0.025 mg/litre.  Deltamethrin residues in tissues 
were measured 1, 4, and 9 days after the last dose.  At the 
10 mg/kg diet intake, very small amounts of deltamethrin residues 
were found in the liver (<0.005 mg/kg), kidney (<0.002 mg/kg), 
and muscle (0.002 - 0.014 mg/kg).  Residues in fat were about 
0.04 mg/kg and 0.2 mg/kg for the 2 and 10 mg/kg intake, 
respectively.  Depletion of deltamethrin residues in milk was very 
rapid (estimated half-life was about 1 day); while in fat (renal 
and subcutaneous) the half-life was 7 - 9 days.  Br2CA (3-(2,2- 
dibromovinyl)-2,2-dimethylcyclopropanecarboxylic acid) and PBacid 
(3-phenoxybenzoic acid) were the only metabolites detected in the 
milk and tissues of treated cows.  In all cases, they were found at 
trace levels of < 0.0235 mg/litre and < 0.034 mg/litre, 
respectively.  These two metabolites were also previously 
identified in rats and mice as the major degradation products of 
deltamethrin (Ruzo et al., 1978, 1979). 

    The fate of 14C-deltamethrin was examined in Leghorn hens 
(Akhtar et al., 1985).  When laying hens were administered 7.5 mg 
of 14C-labelled deltamethrin/hen per day orally for 3 consecutive 
days, about 83% and 90% of the administered 14C was eliminated 
during the first 24 h and 48 h after dosing, respectively.  Tissue 
residues were generally very low with the exception of those in the 
liver and kidney.  Very low levels of residues were found in eggs 
obtained within the first 24 h after dosing, but levels increased 
reaching a peak within 48 h of the last dose.  Residue levels were 
higher in the yolk (up to 0.6 mg/kg) than in the albumen (up to 
0.2 mg/kg), which is probably related to the lipid content of 
yolks.  Metabolites were the same as those found in rats and mice. 

    These studies showed that feeding domestic animals on 
deltamethrin-treated feed resulted in very low levels of residues 
(if any) in products of animal origin and is unlikely to present a 
hazard for the consumer. 

5.3  Enzymatic Systems for Biotransformation

    Deltamethrin (1 µg) was incubated at 37 °C for 30 min with each 
of the following mouse microsome preparations; a) tetraethyl 
pyrophosphate (TEPP)-treated microsomes (no esterase and oxidase 
activity); b) normal microsomes (esterase activity); c) TEPP-
treated microsomes plus NADPH (oxidase activity); and d) normal 
microsomes plus NADPH (esterase plus oxidase activity) (Shono et 
al., 1979).  Deltamethrin was more rapidly metabolized under the 
oxidase system than under the esterase system.  The major site of 
ring hydroxylation was the 4'-position and the secondary site was 
the 5-position.  The  trans methyl group was an important site of 
hydroxylation of the esters and  cis methyl oxidation was evident in 
the metabolites of the cleaved acid moiety.  The preferred sites of 
hydroxylation were as follows;  trans of dimethyl group, 
4'-position in the phenol group, and  cis of the dimethyl group, 
which was equal to the 5-position in the phenoxy group.  Cleavage 
of deltamethrin to cyanohydrin may result from both esterase and 
oxidase enzyme activities, since larger amounts of the cleaved 
products were evident in the oxidase system. 

    However, at a much higher (approximately 35-fold) concentration 
of deltamethrin than that in the above study, it was not detectably 
hydrolysed (Miyamoto, 1976; Soderlund & Casida, 1977). 

    Deltamethrin was hydrolysed by esterases in the blood, brain, 
kidney, and stomach of mice yielding PBald and PBacid (Ruzo et al., 

5.4  Metabolism in Human Beings

    Three young male human volunteers underwent a complete medical 
check-up one week prior to the morning of the study.  Each of them 
received a single dose of 3 mg of 14C-deltamethrin mixed in 1 g 
glucose and diluted first in 10 ml PEG 300 and again in 150 ml 
water.  Total radioactivity was 1.8 ± 09 mBq.  Samples of blood, 
urine, saliva, and faeces were taken at intervals over 5 days.  
Clinical and biological examinations were performed every 12 h 
during the trial and one week after its termination.  Radioactivity 
in the biological samples was measured with a liquid scintillation 
spectrometer.  The clinical and biological checks did not detect 
any abnormal findings.  There were no signs of side effects or 
intolerance reactions, either during or after the trial period.  
The maximum plasma radioactivity appeared between 1 and 2 h after 
administration of the product, and remained over the detection 
limit (0.2 KBq/litre) during the 48 h.  The apparent elimination 
half-life was between 10.0 and 11.5 h.  The radioactivity of blood 
cells, as well as the saliva, was extremely low.  Urinary excretion 
was 51 - 59% of the initial radioactivity; 90% of this 
radioactivity was excreted during the 24 h following absorption.  
The apparent half-life of urinary excretion was 10.0 - 13.5 h, 
which is consistent with the plasma data.  Faecal elimination at 
the end of the observation period represented 10 - 26% of the dose.  
The total faecal plus urine elimination was around 64 - 77% of the 
initial dose after 96 h (Papalexiou et al., 1984). 

6.1  Aquatic Organisms

6.1.1  Acute toxicity for fish

    Acute toxicity data for deltamethrin in fish have been 
summarized by L'Hotellier & Vincent (1986) (Table 6).  From this, 
it appears that deltamethrin is highly toxic for fish, though the 
toxicity varies with the formulation tested. 

Table 6.  Acute toxicity of deltamethrin tested as the technical or formulated product on 
fish; lethal concentrations all expressed as µg active ingredient (a.i.)/litre (96-h)
Species                Systema  LC50 (µg/litre)  Ref.  LC50 (µg/litre)   Ref.
(Common name)                   tested as        No.   tested as         No.
                                technical              formulated
                                product                productb
 Alburnus alburnus      S        0.69             4     82     (ULV)      4
 Brachydanio rerio      F,S      2.0              10    -
(Zebra fish)
 Cyprinodon macularius  S        -                      0.6c    (EC)      13
(Desert pupfish)
 Cyprinodon             S        -                      0.9     (EC)      19
(Sheepshead minnow)
 Cyrpinus carpio        F, S     1.84             4     0.65    (EC)      4
(Common carp)                   0.86             3     210.0   (ULV) 
 Gambusia affinis       F, S     -                      1.0c    (EC)      13
(Mosquito fish)
 Ictalurus nebulosus    F, S     1.2              7     2.3     (EC)      15
(Brown bullhead)
 Ictalurus punctatus    F, S     0.63             8     -
(Hannel catfish)
 Idus idus melanotus    S        -                      1.2     (EC)      16
(Golden orfe) 
 Lebistes reticulatus   F, S     -                      1.8     (EC)      17
 Lepomis gibbosus       F, S     0.58             5     0.87    (EC)      14
(Pumpkinseed sunfish)
 Lepomis machrochirus   F        1.2              6     -
(Bluegill sunfish)
 Osteochilus hasseltie  S        -                      1.2     (EC)      20
(Nilem carp) 
 Puntius gonionotuse    F,S      -                      0.87    (EC)      18
(Jawa carp)
 Rhodeus sericeus       S        1.12             4     140     (ULV)     4
 Salmo gairdneri        F, S     0.39             1     2.2     (EC)      12
(Rainbow trout)
 Salmo salar                     1.97             2     0.59    (EC)      2

Table 6.  (contd.)
Species                Systema  LC50 (µg/litre)  Ref.  LC50 (µg/litre)   Ref.
(Common name)                   tested as        No.   tested as         No.
                                technical              formulated      
                                product                productb
 Salmo trutta           F, S     -                      4.7c    (EC)      11
(Brown trout)
 Sarotherodon           F, S     3.5              9     2.0     (EC)      9
 Tilapia mossambicae    F, S     -                      0.8c    (EC)      13
a F: Flow system, S: Static condition.
b EC: 25 g a.i./litre; ULV: 1 g a.i./litre; values in a.i. equivalent obtained by 
c LC50 (48-h)
d Marine fish.
e River or pond fish from tropical areas (water temperature > 24 °C).


(1) Knauf & Horlein (1979); (2) Zitko et al. (1979); (3) Knauf & Schulze (1977a); 
(4) Gulyas & Csanyi (undated); (5) Waltersdorfer & Schulze (1976a); (6) Buccafusco et al. 
(1977a); (7) Knauf & Schulze (1977b); (8) Buccafusco et al. (1977b); (9) Adeney et al. 
(1980); (10) Lepailleur & Chambon (1984); (11) Lhoste et al. (1979); (12) Waltersdorfer & 
Schulze (1976c); (13) Mulla et al. (1978); (14) Waltersdorfer & Schulze (1976d); (15) Knauf 
& Schulze (1977b); (16) Waltersdorfer & Schulze (1976b); (17) Waltersdorfer & Schulze 
(1976a); (18) Santosa & Hadi (1980); (19) Heitmuller et al. (1978); (20) Santosa (1983)

    Zitko et al. (1979) established a 96-h lethal threshold for 
Atlantic salmon  (Salmo salar) of 1.97 µg/litre. 

6.1.2  Acute toxicity for other aquatic organisms

    Data on aquatic organisms other than fish are presented in 
Table 7 and are of the same order as those for fish, although the 
oyster  (Crassostrea virginica) is somewhat more tolerant and the 
Northern lobster  (Homarus americanus) (96-h lethal threshold 
0.0014 µg/litre) is far more sensitive (Zitko et al., 1979). 

    Mohsen & Mulla (1981) exposed aquatic insect larvae to 
deltamethrin (as a 2.5% emulsifiable concentrate) for 1 h under 
flow-through conditions, and calculated the LC50 after a 24-h 
holding period.  For the target species blackfly  (Simulium 
 virgatum) an LC50 of 0.9 µg/litre was calculated.  Non-target 
species tested, mayfly  (Baetis parvus) and caddisfly  (Hydropsyche  
 californica), were found to be more susceptible, with LC50 values 
of 0.4 µg/litre. 

    Varanka, (1987) investigated the effects of deltamethrin on 
three species of freshwater mussels.  Results presented in Table 8 
show that the mussels are very insensitive to the pyrethroid. 

Table 7.  Acute toxicity of deltamethrin tested as technical or 
formulated product on other aquatic organisms-lethal concentrations 
expressed as µg active ingredient (a.i.)/litre (96-h)a 
Species                LC50 (µg/litre)      LC50 (µg/litre)
                       tested as technical  tested as formulated
                       product              productb
 Crassostrea virginica  -                    12.0 
(Eastern oyster)
 Daphnia magna          5c                   -
(Water flea)
 Gammarus pulex         -                    0.03c
 Penaeus duorarum       -                    0.35
(Pink shrimp)
 Uca pugilatorulosus    -                    1.1
(Fiddler crab)
 Bufo bufo (larvae)     -                    0.93
(Common toad)
a Adapted from:  L'Hotellier & Vincent (1986).
b EC: 25 g a.i./litre; ULV: 1 g a.i./litre; values in a.i. 
  equivalent obtained by calculation.
c LC50 (48-h).

Table 8.  Acute toxicitya of deltamethrin formulationb in 
freshwater mussels, under static conditions at 21 - 23 °Cc
Species           24-h  48-h   72-h   96-h   7-day
 Anodonta cygnea   nd    nd     ~24.6  12.0   7.6

 Anodonta anatina  nd    nd     nd     ~23.4  10.3

 Unio pictorum     nd    ~31.8  9.7    7.0    6.0
a LC50 µg active ingredient (a.i.)/litre): values in a.i. 
  equivalent obtained by calculation.
b ULV 0.12%.
c From:  Varanka (1987).  

6.1.3  Field studies and community effects

    Two experimental pond studies have been performed.  Tooby et 
al. (1981) reported that application of deltamethrin to static 
water at 10 g a.i./ha did not have any lethal effects on two fish 
species  (Canassius auratus, Rutilus rutilus) or on molluscs.  
Aquatic insects and crustaceans present were killed.  Rawn et al. 
(1985) applied deltamethrin at a similar rate and also reported 
that no fish were killed.  The half-life of deltamethrin in the 
pond was 2 - 4 h for water and 2 - 14 days for bottom sediment. 

    Neto et al. (1983) sprayed-flooded fields in Brazil, at 
intervals of 2 days, with rates of deltamethrin progressively 
increased at 5, 10, 12, and 13 g a.i./ha.  The expected 
concentrations in water from these applications were between 3 and 
7 µg/litre.  No mortality was recorded in fish placed in the 
sprayed area in experimental cages.  Slight "agitation" was 
reported after exposure to the highest dose. 

    Impact assessments on the use of deltamethrin on paddy fields 
have been made in the field in various countries throughout the 
world.  The maximum normal usage rate of the compound was 6.5 g 
a.i./ha.  In these studies, fish ( Tilapia spp.,  Cyprinus carpio, 
 Gambusia spp.) tolerated deltamethrin up to 18.75 g a.i./ha without 
any adverse effects.  The compound is known to be toxic for aquatic 
organisms and is not recommended for use over water under any but 
exceptional circumstances.  However, it has been used to control 
vectors of major human diseases, i.e., mosquitos and blackfly 
( Elossina spp.), where benefit outweighed potential risk.  In these 
cases, extensive field evaluations of the environmental impact have 
been made.  While there have not been any instances of fish kills 
from these applications, there are reports of large numbers of 
deaths of aquatic invertebrates.  The populations usually recovered 
rapidly and all studies have shown numbers back to normal before 
the compound was applied again in the following season.  It is 
suggested that relatively resistant parts of the population soon 
recolonize the area; immigration also occurs (Takken et al., 1978; 
Smies et al., 1980; Baldry et al., 1981; Everts et al., 1983). 

6.1.4   Appraisal

    Notwithstanding its high toxicity for fish and crustacea, the 
results of many studies, as well as the wide use of deltamethrin 
for several years, have confirmed that its normal use does not 
cause significant mortality in fish populations.  This difference 
is due to its strong adsorption on soil and its rapid breakdown, 
decreasing its bioavailability under field conditions. 

6.2  Terrestrial Organisms

6.2.1  Plants

    Hargreaves & Cooper (1979) sprayed glasshouse-grown tomato 
seedlings with 50 mg deltamethrin/litre (2.5% emulsifiable 
concentrate) 3 weeks after emergence and again 7 days later.  Three 
days after the second application, plants were examined for damage.  
No damage was found and, at this rate of use, deltamethrin was not 

6.2.2  Soil microorganisms

    In a study by Tu (1980) on the effects of 5 pyrethroids on 
microbial populations and their activity in soil, 0.5 mg 
deltamethrin/kg incorporated into sandy loams (residues under 
normal use conditions would be of the order of < 0.001 mg/kg) 
produced only a few transient effects.  No effects were noted on 

the nitrifying microorganisms and their capacity to produce nitrate 
and there were no inhibitory effects on deshydrogenase or urease 
activity.  Deltamethrin induced an increase in oxygen consumption 
because of an increase in microbial respiration (probably linked 
with the microbial degradation of deltamethrin).  It also 
stimulated the growth of soil fungi and inhibited the development 
of bacteria.  Four weeks after treatment, deltamethrin-treated soil 
recovered completely and microorganism activity was equal to that 
in untreated soil. 

6.2.3  Soil fauna  Earthworms

    When deltamethrin at 12.5 g a.i./ha (high agricultural dose) 
was incorporated into the soil to a depth of 1 cm, there were no 
toxic effects on earthworms  (Lumbricus terrestris) during an 
observation period of 28 days (Bouche & Fayolle, 1979).  However, 
significant toxic effects on earthworms were observed at levels of 
60 - 125 g a.i./ha (5 - 10 times the highest rates applied in 

    In another study with  Eisenia foetida andrei, deltamethrin 
incorporated in artificial soil at concentrations of 1.7 mg/kg and 
10 mg/kg did not produce any lethal effects (Chambon & Lepailleur, 
1984).  Slugs

    Lettuce leaves treated with 4 times normal dosage rates, were 
fed to slugs ( Agrolimax sp.).  Leaves were quickly consumed but no 
toxic effects (mortality or activity) were observed (Ricou, 1978).  Soil arthropods

    Under laboratory conditions, deltamethrin, applied topically 
and by immersion, was very toxic for the carabid beetle 
 Pterostichus melanarius (Illiger).  Under natural conditions in the 
field, deltamethrin applied at normal dose rates was not toxic for 
these organisms (Dunning et al., 1981). 

    Everts et al. (1985) monitored the effects, on non-target 
organisms, of various compounds when used for the control of tsetse
fly in the Ivory Coast in Africa.  Deltamethrin was the most
effective compound against the tsetse and also killed non-target
musca flies.  After deltamethrin spraying, Orthoptera and 
Proctotrupoidea were also significantly decreased while Nematocera
increased in number.  The results of this study suggest that ground
spraying of the pyrethroid had greater effects on terrestrial
arthropods than aerial applications. 

    Concurrent laboratory and field studies were conducted on the 
effects of deltamethrin on beneficial predatory spiders in a polder 
area of the Netherlands (Everts et al., 1988).  During two growing 
seasons, 2800 samples were taken over an area of 17 different 

fields.  The authors found that effects on spiders were eliminated 
when it rained soon after application, since the effect of the 
pyrethroid appeared to be indirect, causing the dehydration of 
spiders.  This different response under dry and damp conditions was 
confirmed in the laboratory.  However, reduction of spider numbers 
in the field was much greater than predicted from laboratory tests 
and recovery was more rapid in laboratory populations than in field 
populations.  The uptake and effects of deltamethrin were greater 
through exposure to residues than through contact or oral exposure.  
There was a positive correlation between temperature and the 
toxicity of deltamethrin for spiders in the field.  This contrasted 
with reports of a negative correlation for target insects reported 
in the literature.  Laboratory studies showed that the negative 
temperature effect only occurred when spiders could not drink.  It 
appeared that qualitative prediction from laboratory to field was 
possible but that quantitative prediction was not. 

6.2.4  Beneficial insects  Honey-bees

    Single applications of deltamethrin are highly toxic for honey- 
bees  (Apis mellifera).  Stevenson et al (1978) found a contact LD50 
of 0.051 µg/bee and an oral LD50 of 0.079 µg/bee. 

    Arzone & Vidano (1978) did not find any difference in mortality 
between controls and bees fed on sugar solutions containing 0.2 µg 
deltamethrin/litre.  Increased mortality was recorded at all higher 
exposures reaching 100% within 1 h at a concentration of 12.5 

    In the field, direct treatment of caged bees caused a high 
mortality rate with doses of from 11.2 g/ha upwards (Atkins et al., 
1976).  Rape flowers were treated at a rate of 0.75 g a.i./100 
litre and 1.5 g a.i./100 litre with an emulsifiable concentrate 
formulation, 25 g/litre; control plots were treated with water.  
Cages (3 x 2 x 2 m) containing a small hive (2 frames + open brood) 
were put over the treated flowers once the spray had dried.  The 
mortality of the bees was then assessed over 7 days.  The average 
mortalities were not significantly higher in the treated plots than 
in water-sprayed control plots (Louveaux et al., 1977). 

    However, Bocquet et al. (1980, 1983) demonstrated, after 3 
years of field experiments, that deltamethrin under field 
conditions was innocuous at doses up to 12.5 g/ha.  They also noted 
a repellant effect by the formulating materials, which lasted for 
2 - 3 h.  Further studies have been reported by Florelli et al. 
(1987a,b).  Foliar insects

    Deltamethrin was 70 times more toxic to the tobacco budworm 
 (Heliothis virescens) than to its predator, green lacewing 

 (Chrysopa carnea), but it was only 1.25 times more toxic to the 
tobacco budworm than to its parasite  (Campoletis sonorensis) (Plapp 
& Bull, 1978). 

    In an apple orchard, where deltamethrin was applied at 
12.5 mg/kg, no predatory mites  (Typhlodromus pyri) were found 
during 10 weeks of observation, but spider mites  (Paponychus ulmi) 
were not affected.  The elimination of the predatory mite led to a 
marked increase in spider mite populations, later in the same 
season (Aliniazee & Cranham, 1980). 

    The impact of deltamethrin used against the English grain aphid 
 (Sitobion avenae) was studied in 1983, 1984, and 1985 in the Paris 
basin.  This study was carried out on wheat with pitfall traps, 
yellow water traps, suction sampling (D-vac), and sampling of ears.  
Effects were noted on:   S. avenae, phytophagous Diptera  (Opimyza 
 florum, Phytomyza nigra, and  Oscinella frit), Homoptera  (Zyginidia 
 scutellaris, Metopolophium dirhodum), Thysanoptera  (Limothrips 
 cerealium, Acolothrips intermedius), predatory Diptera (Empididae, 
Dolichopodidae), and on spiders (Erigonidae, Lycosidae, 
Linyphiidae, Theridiidae).  The detritiphagous insects (Sciaridae, 
Chironomidae), the Carabidae and Staphylinidae and most 
microhymenoptera showed little or no difference after treatment.  
During the 3 years, no differences were observed from year to year 
as a result of field treatment, populations appearing homogeneous 
at the beginning of each trial (Fischer & Chambon, 1987). 

    A large-scale field trial was carried out in 1984 in southern 
England to investigate the side-effects of deltamethrin on non- 
target arthropods in winter wheat.  The insecticides were applied 
in June and two methods, suction sampling (D-vac) and quadrats, 
were used to sample the arthropods for up to 75 days after 
treatment.  During the post-treatment period, the numbers of 
Carabidae and Staphylinidae adults found in D-vac samples were 
reduced by 22% and 20%, respectively, compared with the controls 
(Vickerman et al., 1987a). 

    In the same field trial, arthropods were sampled with a D-vac 
for 11 weeks.  Total numbers were similar in the control and 
deltamethrin-treated plots.  The numbers of Empididae were reduced 
by deltamethrin, but Dolichopodidae were more numerous in treated 
than in control plots.  The numbers of  Aphidius spp. were higher in 
the deltamethrin-treated plots than in the control plots.  The 
numbers of Coccinellidae larvae were reduced (Vickerman et al., 

6.2.5   Birds  Laboratory studies

    Data on the acute toxicity of deltamethrin for birds are given 
in Table 9. 

Table 9.  Acute toxicity of deltamethrin for birds
Species               Sex     Application  LD50 (mg/kg)  Reference
Red partridge         male &  oral         >3000         Grolleau & Griban, 
 (Alectonis tufa)      female                             1976b
Grey partridge        male &  oral         >1800         Grolleau & Griban, 
 (Perdix perdix)       female                             1976b
Chicken                       oral         >1000         Grandadam, 1976
 (Gallus domestica)       
Hen                   adult   oral         >2500         Ross et al., 1978
Mallard duck          oral                 >4640         Beavers & Fink, 
 (Anas platyrhynchos)                                     1977a
Game duck             oral                 >4000         Grolleau & Griban, 

    The toxicity of deltamethrin for birds is very low.  Both 
technical grade and commercially formulated deltamethrin 
administered in feed at 100 mg/kg diet was not palatable to 
Japanese quail  (Coturnix coturnix japonica), with strong individual 
variations.  Unpalatability diminished after repeated exposure and 
even became reversed in the case of the purified deltamethrin, 
which attracted quail already suffering from toxic effects (David, 

    Groups of 39 female Japanese quail  (Coturnix coturnix japonica)
were given daily doses of 0, 0.2, or 1 mg technical deltamethrin 
per animal, by gavage, over 34 days.  No significant effects were 
observed on reproduction (De Lavaur et al., 1985).   Field studies on birds

    The low toxicity of deltamethrin for birds, indicated by 
laboratory studies, has been confirmed in the field.  In studies on 
the ecological consequences of the use of the compound to control 
tsetse fly (Takken et al., 1978) and blackfly (Smies et al., 1980) 
in West Africa, populations of various species of insectivorous, 
granivorous, and piscivorous birds were examined before and after 
spraying.  There were no indications of any effects on either 
numbers or species diversity. 

7.1  Single Exposures

    Tables 10 and 11 show the results of acute toxicity studies on 
various animal species.  From these tables, it is clear that the 
vehicle has a great influence on the LD50, probably by influencing
absorption.  Powder formulations and aqueous suspensions are 
significantly less toxic than formulations in oils or organic
solvents (Pham Huu Chanh et al., 1984). 

    The acute oral toxicity of deltamethrin for rats produced such 
symptoms as:  staining of the fur, excessive grooming, salivation, 
diarrhoea, drowsiness, weakness, dyspnoea, piloerection, ptosis, 
difficulty in walking, general motor incoordination, hypotonia, 
choreoathetosis, clonic seizures, and death  (Glomot, 1979; Glomot 
et al., 1979, 1981a; Kavlock et al., 1979; Ray & Cremer, 1979; Pham 
Huu Chanh et al., 1984).  Electroencephalogram (EEG) records showed 
generalized spike discharges prior to choreoathetosis  (Ray & 
Cremer, 1979; Ray, 1980). 

    Mice presented far fewer symptoms than rats after oral dosing 
at comparable levels, diarrhoea being the only reportable 
observation (Glomot et al., 1980a).  

    Rats were injected intraperitoneally with 14C-labelled
deltamethrin at the threshold doses required to produce the motor
symptoms of toxicity of tremor and choreoathetosis.  Blood and brain
samples were analysed for their total radiolabel content, and were
also extracted with ethyl acetate to determine the levels of
extractable parent deltamethrin and 3-phenoxybenzyl-derived acid and
the residual radiolabel after this extraction.  There was a clear
correlation between onset of symptoms and blood and brain levels of
deltamethrin.  It was found that certain threshold levels of parent
deltamethrin in the blood and brain were required for symptoms
development, and that the symptoms persisted for as long as this
threshold was maintained (Rickard & Brodie, 1985). 

7.1.1  Mouse

    Mice intravenously injected with deltamethrin showed intense 
tremors, convulsions, and ataxia, immediately after administration.  
Tachycardia and respiratory defects were also observed at higher 
dosages.  Surviving animals appeared normal after 4 - 5 h.  
Immediately after intraperitoneal injection, jumping movements, 
slight convulsions and prostration, ptosis, tail hypertonicity, and 
cyanosis were observed.  These toxic signs disappeared after 72 h 
in surviving animals. 

    Animals administered deltamethrin by gavage showed muscular 
stiffening and convulsions, 1 h after dosing.  After 24 h, 
hypermotility, stereotype movements of the head, tachycardia, 
hypertonicity of the tail, and a few convulsions were observed.  
Behaviour and appearance were normal again after 48 h (Glomot & 
Chevalier, 1976a,c). 

Table 10.  Acute toxicity of technical grade deltamethrin
Species  Sex              Route             Vehicle               LD50 (mg/kg     Reference
                                                                  body weight) 
Rat      male             oral              sesame oil            128             Glomot & Chevalier (1976a)
         female                                                   139 
         male                               PEG 200               67 
         female                                                   86 

Rat      male adult                         peanut oil            52              Kavlock et al. (1979)
         female adult                                             31 
         female weanling                                          50  

Rat      male adult                         peanut oil            53              Gaines & Linder (1986)
         female adult                                             30
         female weanling                                          48

Rat      male + female                      aqueous suspension    > 5000          Audegond et al. (1981)
                                            with carboxy-         (no mortality) 

Rat                       dermal            -                     700             Panshina & Sasinovich (1983)
Rat      male                               methylcellulose (1%)  > 2940          Kynoch et al. (1979)
Rat      female adult                       xylene                > 800           Kavlock et al. (1979)
Rat      male + female    inhalation (6 h)  dust                  600 mg/m3       Coombs & Clark (1978)
Rat      male adult       (2 h)             DMSO 10% aerosol      940 mg/m3       Kavlock et al. (1979)
         female adult                                             > 785 mg/m3     

Rat      male + female    (1 h)             micronized powder     > 4620 mg/m3    Jackson & Hardy (1986)

Rat                       intraperitoneal   -                     58.8            Panshina & Sasinovich (1983)

Rat      male             intraperitoneal   sesame oil            209             Glomot & Chevalier (1976b)
         female                                                   186
         male                               PEG 200               24              Glomot & Chevalier (1976b)
         female                                                   25 

Table 10.  (contd.)
Species  Sex              Route             Vehicle               LD50 (mg/kg     Reference
                                                                  body weight) 
Rat      male            intravenous        PEG 200               3.3             Glomot & Chevalier, (1976c)
         female                                                   3.3 
Rat      female adult                       acetone               4               Kavlock et al. (1979)
         female weanling                                          1.8 

Mouse    male             oral              sesame oil            33              Glomot & Chevalier (1976a)
         female                                                   34 
         male                               PEG 200               21              Glomot & Chevalier (1976a)
         female                                                   19 

Mouse                     intraperitoneal   -                     33              Panshina & Sasinovich (1983)

Mouse    male             intraperitoneal   sesame oil            171             Glomot & Chevalier (1976b)
         female                                                   166

Mouse    male                               PEG 200               18              Glomot & Chevalier (1976b)
         female                                                   12  
Mouse    male                               PEG 200               4.1             Glomot & Chevalier (1976c)
         female                                                   4.0 

Mouse    male                               glycerol formal       5               Glomot & Chevalier (1976c)
         female                                                   5.8 

Dog      male + female    oral              in capsules           >300            Glomot et al. (1977)
                                                                  no mortality

Dog      male + female                      PEG 200               2               Glomot & Chevalier (1976c)

Rabbit   male             dermal            PEG 400               > 2000          Clair (1977)
         female                                                   > 2000

Table 11.  Acute toxicity of some formulations
Species  Sex           Route             Formulation                    LD50 (mg/kg     Reference
                                                                        body weight)
Rat      male, female  oral              2.5% flowable formulation      22 000          Glomot et al. (1979)

Rat      male, female  oral              2.5% wettable powder           >15 000         Glomot (1979)

Mouse    male, female  oral              2.5% wettable powder           >15 000         Glomot et al. (1980a)

Dog      male, female  oral              2.5% wettable powder           >10 000         Glomot et al. (1980b)

Rat      male, female  oral              2.5% emulsifiable concentrate  535             Coquet (1977)

Rat      male, female  oral              10 g/litre ULV                 >6 470          Coquet (1977)
Rat      male, female  inhalation (4 h)  aerosol-2.5% wettable powder   >2 800 mg/m3    Clark et al. (1980)
7.1.2  Rats

    Rats intravenously injected with deltamethrin showed muscular 
contractions, piloerection, respiratory defects, convulsions, and 
paresis of the hind quarters, immediately following treatment.  
Surviving animals showed normal behaviour after 48 h.  Immediately 
after intraperitoneal injection, tremor, convulsions, prostration, 
and cyanosis were observed.  These toxic signs disappeared after 
48 h in surviving animals.  Animals administered deltamethrin by 
gavage showed motor incoordination, convulsions, respiratory 
defects, and hypomotility, shortly after dosing.  Normal behaviour 
was observed after 3 days (Glomot & Chevalier, 1976c). 

    In an inhalation study (whole body exposure for 6 h), 
hyperactivity, grooming, and irritation were observed during 
exposure.  The animals were hypersensitive to touch and noise and 
showed uncoordinated movements.  Gross pathological investigation 
showed a gas-filled stomach and small intestine, and massive 
haemorrhage and degeneration in the lung (Coombs & Clark, 1978). 

    Rats were exposed (whole body exposure) for 4 h to an aerosol 
concentration of deltamethrin equal to 2.8 g/m3, the highest 
attainable airborne concentration of a 2.5% wettable powder 
formulation.  Approximately 80% of the total aerosol had a mean 
aerodynamic diameter of less than 5.5 µm.  Dyspnoea and gasping 
were observed in exposed rats.  Relative lung weights and 
macroscopic pathology were normal.  There was no mortality (Clark 
et al., 1980). 

7.1.3  Rabbit

    Rabbits (10 males and 10 females) were treated with 2 g 
deltamethrin in 2 ml PEG 400 per kg body weight on 80 cm2 of 
occluded shaved skin for 24 h.  The animals were observed for 14 
days.  Two animals showed obvious erythema.  No body weight changes 
or abnormal behaviour were observed.  On histological observation 
of the liver, kidneys, and skin, small changes were observed, but 
these were common for this strain of rabbit and not related to 
treatment (Clair, 1977). 

7.1.4  Dog

    Dogs given oral doses of 100 mg deltamethrin/kg body weight or 
more showed transient hyperexcitability, akinesia, vomiting, and 
stiffness of the hind legs (Glomot et al., 1977). 

    Dogs orally dosed with 10.0 mg deltamethrin/kg body weight did
not display any clinical signs related to treatment (Glomot et al.,

7.2  Irritation and Sensitization

7.2.1  Skin irritation

    Male albino rabbits (12 per group) weighing 2.5 - 3.5 kg were 
administered 0.5 g deltamethrin on either shaved intact or abraded 
skin.  The occlusive patch was fixed on the skin for 23 h.  

Technical deltamethrin (98% purity) did not produce any irritant 
effects (Coquet, 1976a). 

    Male albino rabbits (6) weighing 2.5 - 2.9 kg were administered 
0.5 ml of formulated deltamethrin (25 g/litre flowable suspension 
concentrate) to both shaved intact and abraded skin.  The Primary 
Irritation Index after 24 h exposure of occluded sites was 1.2, 
i.e., slightly irritating (Glomot et al., 1981b).  

    An evaluation similar to the one described above was carried out
for a 2.5% wettable powder concentrate deltamethrin formulation. 
Rabbits had a Primary Irritation Index of 2.41, i.e., moderately
irritating.  Moderate erythema continued for 72 h, while the oedema
generally diminished, with the exception of scarified skin sites
(Glomot et al., 1981c). 

    The skin irritation potentials of Decis emulsifiable 
concentrate 2.5% and Decis Flowable 2.5% were studied on rabbits 
and guinea-pigs with 0.05, 0.10, 0.5, 1, and 2.5% deltamethrin.  
The threshold irritative levels were 0.05% for Decis emulsifiable 
concentrate and 2.5% for Decis Flowable.  The intensity of 
irritation depended on the relative content of organic solvents and 
emulsifiers in the trade products.  The water-soluble concentrate 
of Decis 2.5% caused negligible risk of contact irritative 
dermatitis  (Bainova & Kaloyanova, 1985).  

7.2.2  Eye irritation

    Deltamethrin (0.1 g/animal) was administered into the 
conjunctival sac of the eyes of 6 male albino rabbits, weighing 
2.5 kg, with or without rinsing 60 seconds after instillation.  
Deltamethrin produced transient irritating effects, both with and 
without rinsing (Coquet, 1976b). 

    Male albino rats (9) weighing between 2 and 3 kg were 
administered 0.1 ml of formulated deltamethrin (25 g/litre flowable 
suspension concentrate) in the conjunctival sac.  Six of the 
treated eyes remained unwashed, while the remaining three were 
rinsed with lukewarm water 20 - 30 seconds after instillation.  
There was only transient clouding of the cornea in 2 animals 1 h 
after dosing (1 washed, 1 unwashed), which cleared by day 2.  Low 
grade conjunctival irritation was noted among all animals 
initially, which disappeared following day 2 of observations 
(Glomot et al., 1981d). 

    A 2.5% deltamethrin formulation diluted 1/10 in distilled water 
(0.1 ml per rabbit) elicited a similar pattern of initial transient 
corneal clouding in 3 out of 9 rabbits examined, which cleared by 
day 4.  The undiluted formulation (100 mg) administered in the 
conjunctival sac of rabbits produced increased involvement of the 
conjunctiva, iris, and cornea in all animals, generally moderate in 
severity, with low grade corneal opacity persisting in 2 rabbits 
until day 7 (1 washed, 1 unwashed) (Glomot et al., 1981e). 

7.2.3  Sensitization

    Deltamethrin (0.5 g/animal) was applied topically to the skin 
of albino guinea-pigs (10 male and female) 3 times per week, with a 
2-day interval for 3 weeks, and once at the start of the fourth 
week.  The preparation was covered with an occlusive patch for 
48 h.  On days 1 and 10, the guinea-pigs received an intradermal 
injection of 0.1 ml of Freund's adjuvant.  The animals were 
challenged 12 days after the last application with 0.5 g 
deltamethrin.  No sensitization was found (Guillot & Guilaine, 

7.3  Short-Term Exposure

7.3.1  Rat

    Male and female weanling Sprague-Dawley rats (20 of each sex 
per group) were dosed (by gavage) with 0, 0.1, 1, 2.5, or 10 mg 
deltamethrin in PEG 200/kg body weight per day for 13 weeks.  No 
treatment-related effects were observed on food and water 
consumption, mortality, urinalysis, and haematology.  Neurological 
examinations and ophthalmoscopy did not reveal any abnormalities.  
At the highest dose level, a slight hyperexcitibility was observed 
among some rats in week 6.  Lower body weight gain was noted in 
males at 2.5 and 10 mg/kg.  No clear treatment-related effects were 
noted in the results of laboratory investigations or on the weights 
of the organs.  Gross and microscopic examination of a variety of 
tissues and organs did not show any treatment-related findings.  
Following the 13-week dosage period, 5 males and 5 females per 
group were allowed to recover for 4 weeks.  No evidence of 
hyperexcitability was observed among the rats; body weight gain was 
slightly higher in the treated groups than in the controls.  The 
no-observed-effect level was 1 mg/kg body weight (Hunter et al., 

    Four groups of CD rats (8 of each sex per group) were exposed to
aerosolized deltamethrin (technical grade powder) for 6 h per day, 5
days a week, for 2 weeks, and for 4 days during a third week.  Mean
aerosol concentrations were 3, 9.6, and 56.3 mg a.i./m3  with
about 87% of respirable particles (diameter lower than 5.5 µm).  No
rats died as a result of exposure.  Signs of irritation (agitated
grooming and ptyalism due to the powder were noted in all groups
during exposure, with more pronounced toxic signs (ataxia and
walking with arched backs) in the group receiving the highest dose
tested.  Male rats also showed a reduced body weight (-5%) in all
groups.  An elevation of the serum sodium ion content was noted at
the two highest doses.  No increased incidence of any particular
lesion was observed in the high-dose group compared with the control
group.  Irritation and weight loss were only slight at 3 mg/m3 and
this can be considered as a no-effect level (Coombs et al., 1978). 

7.3.2  Dog

    Male and female beagle dogs (3 - 5/sex per group), 25 weeks of 
age, received a daily oral dose of 0, 0.1, 1, 2.5, or 10 mg 
deltamethrin/kg body weight in PEG 200 in gelatin capsules over 13 
weeks.  All treated groups showed reduced body weight gain, but 
this was not dose-related.  Liquid faeces were associated with all 
groups of treated dogs throughout the dosing period.  Dilatation of 
the pupils was seen in dogs receiving 2.5 and 10 mg/kg per day.  
The sign was first seen 4 - 7 h after dosing and persisted 
throughout the day.  The incidence of vomiting increased dose- 
dependently in all treated groups, except the group receiving 
0.1 mg/kg.  In the highest dose group, unsteadiness, body tremors, 
and jerking movements were seen, particularly in males, in weeks 2, 
3, and 4.  Excessive salivation was seen initially and diminished 
during the dosing period.  After 5 and 12 weeks, depression of the 
gag reflex was noted in a proportion of animals in all treated 
groups.  However, this was not considered to be of toxicological 
significance.  Exaggeration or depression of the patellar reflex 
was observed in some animals in all treated groups after 5 and 12 
weeks, mainly at 1, 2.5, or 10 mg/kg per day.  Some animals in all 
treated groups showed depression of the flexor reflex.  Dose levels 
of 2.5 and 10 mg deltamethrin/kg per day caused modification of the 
EEG pattern in some animals, 12 weeks following administration.  
Histopathological evaluations of tissues and organs, including the 
nervous system and muscle tissue, did not reveal any abnormalities 
that could be related to the administration of the compound.  
During recovery, the gag reflex continued to be depressed, whereas 
exaggeration of the patellar reflex was still seen in some dogs 
that had previously received 1 mg/kg per day (Chesterman et al., 

7.4  Long-Term Exposure and Carcinogenicity 

7.4.1  Mouse and rat

    Male and female Charles River CD-1 mice (80 of each sex per 
group) were fed dietary levels of deltamethrin of 0, 1, 5, 25, or 
100 mg/kg, daily, for 24 months.  There were no clear effects 
related to the administration of deltamethrin on general behaviour, 
mortality, body weight, and food consumption.  Blood chemistry, 
haematology, and urine analysis parameters were normal after 12, 18,
and 24 months (at the times of interim and terminal sacrifice).  
Microscopic examination of tissues did not reveal any lesions 
indicative of a compound-related effect.  The tumour incidence was 
unaffected by deltamethrin administration.  The no-observed-effect 
level was 100 mg/kg diet (Goldenthal et al., 1980a). 

    Deltamethrin was administered, by gavage, to C57BL/6 mice at 4 
dose levels (0, 1, 4, and 8 mg/kg body weight) and to BDVI rats at 
3 dose levels (0, 3, and 6 mg/kg body weight) on 5 days a week for 
104 weeks.  After completion of the treatment, the animals were 
observed until 120 weeks of age, when all survivors were killed.  
The treatment had a slight effect on body growth and survival 
rates, especially in the groups of mice and rats treated with the 

highest dose.  In C57BL/6 mice, various types of tumours were 
observed in all treated groups.  An increased incidence of 
lymphomas was observed in mice receiving deltamethrin at levels of 
1 and 4 mg/kg body weight, but not in the group treated with 
8 mg/kg body weight.  No significant difference in the incidences 
of lung adenomas, liver-cell tumours, or other tumours was observed 
in treated groups compared with controls.  In BDVI rats, an 
increased incidence of pituitary, thyroid, and mammary tumours was 
noted; however, no clear dose-response relationship was shown 
(Cabral et al., 1986).  The details of this study were not 
available for evaluation. 

    Male and female Charles River CD rats (90 of each sex per 
group) were fed with 0, 2, 20, or 50 mg deltamethrin/kg diet for 
2 years.  A second control group (60 of each sex) was also used.  
Interim sacrifices (10 of each sex per group excluding control 
group 2) were made after 6, 12, and 18 months.  No changes in 
general behaviour and appearance were observed in relation to 
treatment.  Survival rate was similar for control and treated rats 
(50 - 67%).  Rats in the 50 mg/kg group gained slightly less weight 
than control rats, whereas the food consumption was essentially the 
same.  Ophthalmoscopic findings were generally similar for control 
and treated rats.  No haematological and biochemical parameters 
were changed in a biologically significant way in relation to 
treatment at any time, except for a decrease in SGPT (serum 
glutamic pyruvic transaminase) activity at 6 months in the mid- and 
high-dose groups.  Organ weights were not affected.  The 
macroscopic and microscopic findings were common for the species 
and the strain, except for a slightly increased incidence of axonal 
degeneration in sciatic, tibial, and/or plantar nerves in the 20 
and 50 mg/kg groups at 18 months, but not at termination.  Thus, 
this was not considered to be indicative of a compound-related 
effect.  The incidence of benign testicular tumours (interstitial 
cell adenomas) at terminal sacrifice in this study was:  control 
group 1, 0/37; control group 2, 4/35; low-dose group 1/38; mid-dose 
group 1/30; high-dose group 6/38.  The incidence seen in the high-
dose group was considered to be spontaneous, because it was not 
significantly higher than in the second control group or in 
historical control groups (Goldenthal et al., 1980b; Richter & 
Goldenthal, 1983). 

7.4.2  Dog

    Deltamethrin dissolved in maize oil was administered in the diet
to 64 beagle dogs (8 of each sex per group) at levels of 0, 1, 10,
and 40 mg/kg for 24 months.  This corresponds to 0, 0.025, 0.25, and
1 mg/kg body weight, respectively.  Individual body weights and food
consumption values were determined weekly.  Ophthalmoscopic,
haematological, biochemical, and urinalysis examinations were
conducted during the pre-test period and at 6, 12, 18, and 24 months
of the study.  Neurological examinations were conducted at
approximately 1 year and before termination.  No signs of overt
toxicity were observed in any of the dogs.  Body weight and food

consumption values were similar for control and treated dogs.  No
compound-related effects were observed during the ophthalmoscopic 
and physical examinations.  Although there were some random 
statistically significant differences between the control and 
other dose groups in the haematological and biochemical tests, 
physiologically significant changes were not observed at any 
interval in the study.  Two treated and two control animals died 
during the study.  No compound-related gross or microscopic changes 
were observed in the surviving dogs that were sacrificed and 
necropsied.  Inflammatory, degenerative, and proliferative changes 
described were spontaneous in nature, or related to the estrous 
phase of the menstrual cycle, and unrelated to compound 
administration.  On the basis of this study, it has been concluded 
that the no-observed-effect level is 40 mg/kg diet (equivalent to 
1 mg/kg body weight per day) (IRDC, 1980). 

7.5  Mutagenicity

7.5.1  Microorganisms

    DNA repair tests in  Escherichia coli were conducted at dose 
levels of 1250, 2500, or 5000 µg deltamethrin/ml.  Deltamethrin was 
dissolved in dimethyl sulfoxide (DMSO) and 0.1 ml of the solution 
was spread on a plate.  Growth inhibition was compared between DNA 
repair deficient mutants (p3478 and CM611) and wild types (W3110 
and WP2).  Partial precipitation of deltamethrin from the solution 
occurred when it came into contact with the aqueous bacterial 
growth medium.  Deltamethrin did not have any damaging effects on 
DNA (Peyre et al., 1980). 

    Deltamethrin was examined for its mutagenic potential in the 
Ames test with 5 strains of  Salmonella typhimurium (TA 1535, TA 
1537, TA 1538, TA 98, and TA100) at doses of 2, 10, 50, 200, 500, 
1000, or 5000 µg/plate, with and without S-9 mix (metabolic enzyme 
system).  It was dissolved in DMSO and precipitated out of solution 
at concentrations of 200 µg/plate or more.  Deltamethrin did not 
have any effect on the mutation rate in any of the strains at any 
of the concentrations tested (Peyre et al., 1980). 

    A similar Ames test was carried out at 0.2, 2, 20, 200, or 
400 µg deltamethrin/plate with microsome enzymes.  The compounds 
did not influence the number of revertants of the 5 strains (same 
as above) of  S. typhimurium.  Again, deltamethrin was dissolved in 
DMSO and precipitated out of solution at 200 µg/plate or more 
(Fouillet, 1976). 

    Kavlock et al. (1979) found deltamethrin not to be mutagenic in 
2 assays with  S. typhimurium at doses of 0 - 1000 µg/plate in DMSO, 
with or without metabolic activation.  They also obtained negative 
results with  E. coli at 10 - 1000 µg/plate as well as with 
 Saccharomyces cerevisiae at concentrations of 1 - 5%, in both cases 
with and without metabolic activation.  Deltamethrin was found not 
to be mutagenic in  S. typhimurium strains TA100 and TA98, in the 
presence or absence of a rat liver activation system, using the 
plate incorporation assay and fluctuation tests.  The compound, 
dissolved in DMSO, precipitated out of solution at 600 µg/plate 
(Pluijmen et al., 1984). 

7.5.2  Cultured cells

    Deltamethrin, dissolved in a mixture of cremaphor oil and 
ethanol (1:1), was applied to a culture of Chinese hamster ovary 
cells (CHO) at levels of 0.04, 0.2, 1.0, or 5.0 mmol/litre, with or 
without metabolic activation, and examined for chromosomal 
aberrations and sister chromatid exchanges (SCE).  Because of the 
cytotoxic effect of cremaphor oil when combined with S-9 mix or 
deltamethrin, no cells would grow in the control dish with 
activation, or in the 5 mmol/litre deltamethrin dishes, either with 
or without metabolic activation.  A high incidence of chromosomal 
aberrations and SCEs was observed in the dishes containing 1 mmol 
deltamethrin/litre, with activation.  However, the absence of 
control values (both with and without activation) because of a 
broken test tube, made the interpretation equivocal.  A second 
study was conducted in which deltamethrin was dissolved in DMSO and 
applied to the cells at levels of 0.001, 0.01, 0.1, or 0.2 
mmol/litre, with or without metabolic activation.  In this study, 
deltamethrin did not produce any cytotoxic effects and did not 
induce either chromosomal aberrations or SCEs in CHO cells.  
However, no positive controls were tested and only single plates 
were prepared per dose level (Sobels et al., 1978). 

    Deltamethrin was found not to be mutagenic in V79 Chinese 
hamster cells, in the presence or absence of hepatocytes.  It is 
not known which solvent was used (Pluijmen et al., 1984). 
7.5.3  Mouse

    An  in vivo cytogenetic test was conducted on mice (3 males and 
3 females per group).  Mice were treated orally with deltamethrin 
in sesame oil for 2 consecutive days at 5 or 10 mg/kg body weight.  
The incidence of chromosomal aberrations in bone marrow cells or 
micronuclei in the polychromatic erythrocytes of treated groups 
was, however, comparable to that of the control groups.  No 
positive controls were tested (Sobels et al., 1978). 

    Deltamethrin was applied orally, once, at 15 mg/kg body weight 
to Swiss mice.  A time-related effect on the chromosomes in bone 
marrow cells was observed by killing 2 animals every 3 h during 
24 h.  The report stated that the incidences of chromated 
aberrations were low and that there were no consistent time-related 
trends in the distribution of the aberrations.  However, the time- 
related trend of aberrations was not reported.  Again, no positive 
controls were tested (Sobels et al., 1978). 

    A dominant-lethal assay with deltamethrin was performed.  
Groups of 9 - 13 male mice were dosed orally at 3 mg/kg body weight 
in sesame oil for 7 days or at a single dose of 6 or 15 mg/kg body 
weight in sesame oil, and mated with 6 - 18 non-treated females.  
There were no effects on the rates of pre- and post-implantation 
losses, while the positive control, triethylene triphosphoramide 
(10 mg/kg body weight), reduced pregnancies in the second and third 
weeks after treatment and increased embryonal losses (Vannier & 
Glomot, 1977). 

    Deltamethrin in olive oil was administered orally to female 
Swiss mice at single or repeated (5 times at daily intervals) doses 
of 1.36, 3.4, or 6.8 mg/kg per day.  Bone marrow smears were 
prepared 6, 24, or 48 h after treatment.  No mutagenic activity was 
observed with deltamethrin, whereas the positive control, 
cyclophosphamide, induced a positive response (Polàkovà & Vargovà, 

    In a micronucleus test, a single dose of deltamethrin in corn 
oil was administered orally at 16 mg/kg body weight to Swiss CD-1 
mice (5 of each sex per group).  No mutagenic activity was observed 
with deltamethrin, whereas the positive controls, 
triethylenemelamine and dimethylbenzanthracene, both induced 
positive responses (Vannier & Fournex, 1983). 

7.5.4  Appraisal

    Deltamethrin is not mutagenic or clastogenic in a variety of  in 
 vitro and  in vivo test systems. 

7.6  Teratological and Reproductive Effects 

7.6.1  Teratology  Mouse 

    Deltamethrin was dissolved in corn oil and administered by 
gastric intubation at doses of 0, 3.0, 6.0, or 12.0 mg/kg body 
weight on days 7 - 16 of gestation to groups of CD-1 mice.  Mice 
were sacrificed on day 18 of gestation.  There was a dose-related 
( P <0.001) reduction in maternal weight gain during pregnancy and 
high-dose females gained 58% less weight than the controls.  There 
was no dose-related mortality but dams in the high- and mid-dose 
groups became convulsive after dosing.  Treatment did not affect 
the number of implantation sites, fetal mortality, fetal weights, 
or the number of sternal and caudal ossification centres. 

    A significant ( P <0.01) dose-related increase in the 
occurrence of supernumerary ribs was observed.  No other dose-
related skeletal or visceral anomalies were observed (Kavlock et 
al., 1979). 

    Pregnant female Swiss CD-1 SPF mice (24 per group) were given 
deltamethrin dissolved in sesame oil by oral intubation at dose- 
levels of 0, 0.1, 1, or 10 mg/kg body weight per day on days 
6 - 17 of pregnancy.  The animals were necropsied on day 18 of 
pregnancy.  The numbers of implantation sites, fetal losses, and 
viable fetuses were not affected by treatment.  There was a dose-
related decrease in mean fetal weight.  Apart from delayed 
ossification at all dose levels, skeletal examination revealed no 
abnormalities.  A teratogenic effect was not observed (Glomot & 
Vannier, 1977). 

    In a complementary teratology study, pregnant female Swiss CD-1 
mice were given deltamethrin dissolved in sesame oil by oral 
intubation at 0, 0.1, 1, or 10 mg/kg body weight per day from day 6 
to day 17 of gestation.  Females were either sacrificed on day 18 
of gestation or allowed to litter for subsequent examination of 
pups on days 1 or 21 of lactation.  The compound caused a moderate 
and transient retardation of development of the fetus at the 1 and 
10 mg/kg body weight dose rate, but these effects were not observed 
on days 1 or 21 post-partum.  There were no teratogenic effects 
related to treatment (Vannier & Glomot, 1982).  Rat 

    Pregnant female Sprague-Dawley rats (24 per group) received 0, 
0.1, 1, or 10 mg deltamethrin/kg body weight per day by oral 
intubation on days 6 - 18 of pregnancy.  Apart from 12 females in 
the control and 10 mg/kg groups, which were allowed to deliver, the 
dams were sacrificed and examined on day 21.  There were no effects 
on reproduction or on the teratogenic parameters examined, except 
for slightly delayed ossification at the highest dose level (Glomot 
& Vannier, 1977). 

    Deltamethrin was dissolved in corn oil and administered by 
gastric intubation at doses of 0, 1.25, 2.5, or 5.0 mg/kg body 
weight on days 7 - 20 of gestation.  Rats were sacrificed on day 21 
of gestation.  There was a dose-related reduction ( P <0.01) in 
maternal weight gain during pregnancy, and dams in the high-dose 
group gained only 80% of the control value.  Treatment did not 
affect the number of implantation sites, fetal mortality, fetal 
weight, or the number of sternal and caudal ossification centres 
(Kavlock et al., 1979).  Rabbit 

    Groups of 15 pregnant New Zealand White rabbits received 
deltamethrin dissolved in sesame oil at levels of 0, 1, 4, or 
16 mg/kg body weight per day during days 6 - 19 of pregnancy.  
Examination was carried out on day 28 of gestation.  The mean fetal 
loss was not dose-related.  The mean fetal weight in the highest-
dose group was decreased.  Some malformations (hydrocephaly, 
exencephaly, and thoracogastroschisis) were observed in 2 fetuses 
of animals at the highest dose level.  In a supplementary study, 
pregnant rabbits were similarly dosed with 16 mg/kg body weight per 
day; one fetus with spina bifida and shortened tail was detected 
among 69 apparently normal fetuses.  Malformations were within the 
normal limits of the strain used and were not considered to be 
related to the treatment, despite the occurrence at the highest 
dose level only (Glomot & Vannier, 1977, 1978). 

7.6.2  Reproduction studies

    Groups of 10 male and 20 female Charles River rats were fed 
deltamethrin in the diet at 0, 2, 20, or 50 mg/kg and mated to 
begin a 3-generation, 2-litter (first generation, 3 litter) 
standard reproduction study.  Parental body weights and food 

consumption were recorded during the study.  After weaning of the 
second litter, the surviving parent rats were sacrificed and 
necropsied.  Five male and 5 female pups of the F3b generation were 
necropsied.  No changes relevant to treatment were observed in 
general behaviour or survival of parent rats or pups.  The body 
weight of F0 males of the 50 mg/kg group was decreased from week 11 
onwards.  There were some slight decreases in mean food consumption 
of F1 male parent rats in the 50 mg/kg group.  The basic 
reproduction indices (fertility, gestation, lactation, viability, 
and litter size) were not affected by the treatment.  However, the 
mean pup weight in some litters, especially in the 50 mg/kg group, 
was slightly decreased in comparison to the controls on day 21 of 
lactation.  Gross external examination did not reveal any 
abnormalities.  No gross or microscopic lesions of treatment-
related significance or significant effects on the organ weights of 
the F3b generation were observed (Wrenn et al., 1980). 

    Deltamethrin was dissolved in corn oil and administered by 
gastric intubation at doses of 0, 2.5, or 5.0 mg/kg body weight to 
Sprague-Dawley rats from day 7 of gestation to day 15 of lactation.  
The dams were allowed to litter and rear their young:  litters were 
reduced at birth to 4 males and 4 females per litter.  The pups 
were weighed weekly and examined for the development of eye-
opening, startle reflex, and air-righting.  The litters were weaned 
on day 22 post-partum and the males discarded.   Weekly weighing of 
the females continued and at 6 weeks of age they were tested in a 
circular open-field.  There were no effects on parturition, litter 
size, or pup viability.  Weights at birth were similar for all 
groups, but a dose-related depression in growth was observed during 
the pre-weaning period.  This early diminution in pre-weaning 
weight appeared to have little effect on the morphological and 
behavioural parameters measured (Kavlock et al., 1979). 
7.7  Neurotoxicity and Behavioural Effects

    Adult hens (10 per group) were gavaged with a single dose of 0, 
500, 1250, or 5000 mg deltamethrin/kg body weight suspended in corn 
oil or 0 or 100 mg/kg body weight dissolved in sesame oil.  During 
21 days, observations were made on mortality, health, neurotoxic 
signs, and body weight.  Deltamethrin did not induce any clinical, 
macroscopic, or histological signs of delayed neurotoxicity (Ross 
et al., 1978). 

    Groups of 5 male and 5 female Wistar rats were administered 
25 mg deltamethrin/kg body weight in 10 mg corn oil/kg on 2 
consecutive days.  Controls received 10 mg corn oil/kg body weight.  
A tilting plane test was performed every second day from day 4 to 
day 16 of the study.  Two male rats died at 25 mg/kg.  No effect 
was found on the slip-angle (Davies et al., 1983). 

    The effects of deltamethrin were studied in a rat performance 
test that arranged for milk delivery after every fortieth lever 
press.  Deltamethrin (1 - 8 mg/kg body weight, given orally, 2 h 
before the test) produced both dose-related increases in pause 
duration and decreases in response rate.  Deltamethrin was also 

studied using a conditional flavour-aversion test.  Deltamethrin- 
treated, trained rats displayed an aversion to saccharin that was 
greatest at 2 mg/kg (Macphail, 1981). 

    The neurological effects of the 4 synthetic pyrethroids, 
resmethrin, permethrin, cypermethrin, and deltamethrin, have been 
investigated in the rat to establish whether there is a correlation 
between the clinical-functional status of the animal and peripheral 
nerve damage, as measured biochemically (Rose & Dewar, 1983).  
Neuromuscular dysfunction was assessed by means of the inclined 
plane test and peripheral nerve damage by reference to 
beta-glucuronidase and beta-galactosidase activity increases in 
nerve tissue homogenates from treated and control animals.  A 
transient functional impairment was found in animals treated with 
any one of the 4 pyrethroids tested and in all cases this was 
greatest at the end of the 7-day dosing regimen (deltamethrin doses 
of 5 - 20 mg/kg per day in arachis oil).  Significant increases in 
beta-glucuronidase and beta-galactosidase activities were found 
3 - 4 weeks after the start of dosing, in the distal portion of the 
sciatic/posterior tibial nerves from permethrin-, cypermethrin-, 
and deltamethrin-treated animals, but no changes were found in 
resmethrin-treated animals.  It is concluded, therefore, that there 
is no direct correlation between the time-course of the 
neuromuscular dysfunction and the neurobiochemical changes.  This 
suggests that these pyrethroids have at least two distinct actions-
a short-term pharmacological effect at near-lethal dose levels and 
a more long-term neurotoxic effect that results in sparse axonal 
nerve damage. 

    To better characterize the behavioural toxicity of pyrethroid 
insecticides, comparisons were made of the effects of cismethrin 
and deltamethrin exposure on motor activity and the acoustic 
startle response in male Long-Evans rats (Crofton & Reiter, 1984).  
Acute dose-effect, acute time-course, and 30-day repeated-exposure 
determinations of 1-h motor activity were made using figure-eight 
mazes.  The acoustic startle response was measured to a 13-kHz, 
120-dB(A), 40-millisecond tone at each of 3 background white noise 
levels (50, 65, and 80 dB).  Deltamethrin (0, 2, 4, 6, or 8 mg/kg 
body weight) or cismethrin (0, 6, 12, 18, or 24 mg/kg) were 
administered orally in 0.2 ml/kg corn oil.  Cismethrin and 
deltamethrin produced similar dose-dependent decreases in motor 
activity.  The time course of onset and recovery for this decreased 
activity was rapid (1 - 4 h).  No cumulative effects on motor 
activity of a 30-day exposure to 2 mg deltamethrin/kg per day or 
6 mg cismethrin/kg per day were found.  The effects of cismethrin 
and deltamethrin on the acoustic startle response were dissimilar:  
deltamethrin produced a dose-dependent decrease in amplitude and an 
increase in latency, and cismethrin produced an increase in 
amplitude and no change in latency.  The differential effects of 
cismethrin (Type I pyrethroids) and deltamethrin (Type II 
pyrethroids) on the acoustic startle response may be related to the 
contrasting effects previously shown with neurophysiological and/or 
neurochemical techniques (see Appendix I). 

7.8  Miscellaneous Effects 

    Analgesic effects of deltamethrin for thermic (hot plate test, 
60 °C) and mechanical stimuli were investigated in mice and rats, 
respectively.  Deltamethrin prolonged the response-time to these 
tests.  Although this action was not significant at 500 mg 
deltamethrin/kg body weight given orally, the reaction time was 
increased at 1000 and 1500 mg/kg given orally in aqueous suspension 
with 10% gum arabic (Chanh et al., 1981). 

    In rats, treatment with deltamethrin increased mean arterial 
pressure and aortic output (Forshaw & Bradbury, 1983).  The 
cardiovascular effects of deltamethrin were due to both increased 
catecholamine release in peripheral vascular beds, and to a direct 
positive inotropic effect on the heart.  

    Krasnjih & Pavlova (1985) demonstrated induction of microsomal 
oxygenases in rats 20 h after a single administration of 1/2 LD50.  
Daily administration of 1/10th LD50 for 2 months reduced 
acetylcholinesterase activity in the serum, erythrocytes, liver, 
and cerebrum.  It also led to some changes in the aspartate 
aminotransferase activity and the urea and protein contents of 

    When rats were dosed orally with a single dose of 1/2 LD50 or 3 
daily doses of 1/5 LD50 deltamethrin, the activities of transferrin 
and ceruloplasmin in plasma, 20 h after dosing, were unchanged.  
After the single dose, microsomal monooxygenase activity was 
increased by 87%, and after the 3 doses, it was increased by 290% 
(Kagan et al., 1986).  

7.9  Potentiation

    Deltamethrin was hydrolysed  in vitro by esterases in blood, 
brain, kidney, liver, and stomach preparations of mice.  
Pretreatment of mice with the oxidase inhibitor, piperonyl butoxide 
(PBO), or the esterase inhibitor,  S,S,S-tributylphosphorotrithioate 
(DEF), delayed metabolism of intraperitoneally administered 
deltamethrin.  PBO or DEF made mice more sensitive to deltamethrin 
(Ruzo et al., 1979). 

    Plasma esterases, in addition to hepatic esterases, play a role 
in the metabolism of deltamethrin in mammals and cause its rapid 
detoxification by the oral route.  In a potentiation study, a range 
of esterase inhibitors, consisting mainly of organophosphorus 
insecticides, was given to male rats in oral doses that inhibited 
50% of the plasma cholinesterase.  After 15 min, or 2 or 24 h, an 
oral LD50 dose of deltamethrin EC formulation was given, which 
showed potentiation with azinphos ethyl, omethoate, and dichlorvos.  
It appears that users must handle deltamethrin in these 
combinations very carefully because of their high toxicity.  
Acephate, monocrotophos, phosphamidon, parathion methyl, and the 2 
controls did not act as potentiators (Audegond et al., 1988). 

7.10  Mechanism of Toxicity (Mode of Action)

    Deltamethrin is classified as a Type II pyrethroid.  For the 
mode of action of pyrethroids in general see Appendix I. 

    The lowest concentration of deltamethrin to have an effect in 
crayfish stretch receptor neurones on sodium channels was 10-12 
mol/litre, but the response of the preparation to gamma- 
aminobutyric acid (GABA) appeared to be unaffected by concentrations
of deltamethrin up to 10-7 mol/litre.  Although 10-6  mol/litre
deltamethrin had a slight effect on the GABA response of the dactyl
abductor muscle, it appears that the majority of the effects of
cyano-pyrethroids in invertebrates could be accounted for solely by
their action on sodium channels (Chalmers et al., 1987). 

    Pyrethroid-induced motor symptoms, i.e., deltamethrin-induced 
writhing and cismethrin-induced tremor, were studied, using a 
number of pharmacological agents, in intact conscious rats and 
spinal rats.  The results suggest that pyrethroid-induced motor 
symptoms, i.e., writhing and tremor, are mediated via a spinal site 
of action, probably involving interneurones.  Deltamethrin-induced 
"non-motor" symptoms, i.e., increase in brain blood flow and blood 
glucose may result from a supraspinal component of deltamethrin 
activity.  In contrast, the cardiovascular effects of deltamethrin 
are mediated via a peripheral site of action (Bradbury et al., 

    Tissue culture experiments have shown that the dorsal root 
ganglion is more sensitive to deltamethrin than the spinal cord or 
peripheral nerve fibres.  The morphological alterations observed in 
the neuronal bodies of the ganglia may reflect some perturbation of 
the ionic equilibrium (Na+ and Ca+) (Souyri, 1985). 

    The results of several other, sometimes very detailed and 
specialized, studies on the mode of action of deltamethrin have 
been reported.  Because these results do not basically influence 
the present evaluation of deltamethrin, they are not reviewed in 
detail.  The interested reader is referred to the following 
publications and a review by Bidet et al. (1988):  Aldridge et al. 
(1978), Duclohier & Georgescauld (1979), Gray et al. (1980), 
Jacques et al. (1980), Miller & Adams (1980), Gammon et al. (1981), 
Pichon  (1981), Brodie & Aldridge (1982), Dyball (1982), Parkin & 
LeQuesne (1982), Ray (1982), Staatz et al. (1982), Brodie (1983), 
Takahashi & LeQuesne (1983), Berlin et al. (1984), Prasada Rao et 
al. (1984), Bloomquist & Soderlund (1985), Brodie (1985), Brodie & 
Opacka (1985), Bloomquist et al. (1986), Chinn & Narahashi (1986), 
Doherty et al. (1986), Forshaw & Ray (1986), Staatz-Benson & Hosko 
(1986), Brooks & Clark (1987), Forshaw et al. (1987), Leibowitz et 
al. (1987), Lummis et al. (1987), Stein et al. (1987). 

7.11  Experimental Studies on Antidotes

    Treatments capable of counteracting acute deltamethrin 
poisoning have been investigated in experimental animals.  Ray & 
Cremer (1979) have proposed atropine, Gammon et al. (1982), 
phenobarbital and diazepam, and Bradbury et al. (1981, 1983), 

    In order to find a therapeutically usable antagonist, 
pharmacological screening was carried out by Dumont (1978), Dumont 
& Chifflot (1978), and Dumont & Laurent (1979).  The outcome was 
that barbiturates are therapeutically active, but that the most 
efficient product is ethyl carbamate.  Cotonat et al. (1987) and 
Fournier (1988) have confirmed that ethyl carbamate is an effective 
treatment for severe deltamethrin poisoning.  However, a serious 
drawback is its antimitotic activity.  Leclercq et al. (1986) began 
by evaluating the activity of common anticonvulsants, such as 
diazepam and clomethiazole.  These products exhibited satisfactory 
activity in rats and dogs (Thiebault et al., 1985, 1988). 

    Phenoprobamate and mephenesin carbamate have been shown to be 
effective in the experimental treatment of deltamethrin poisoning 
(Cotonat et al., 1987; Leclercq et al., 1986).  A summary of the 
results of the antidote studies can be found in Bleys et al. 
(1986).  Clinical trials based on these studies will be undertaken 
(unpublished information given to the IPCS by Roussel Uclaf). 

    The therapeutic effects of methocarbamol have also been shown 
by Hiromori et al. (1986).  However, the mechanism underlying this 
activity is not clear as the actual anticonvulsant activity is 

    It appears that for the time being barbiturates, and especially 
diazepam, offer the safest symptomatic treatment in case of 
deltamethrin poisoning.  Advice on treatment for deltamethrin 
poisoning is given in the IPCS  Deltamethrin health and safety guide 
(WHO, 1989). 

8.1  General Population-Poisoning Incidents

    A few cases of attempted suicides with deltamethrin 
formulations (mainly EC), all non-fatal, have been reported in 
anti-poison centres.  Two typical cases are described below. 

    The first poisoning case in a 13-year-old girl who ingested 
voluntarily 200 ml of a 2.5% EC formulation, (5 grams of 
deltamethrin) was described by Rousselin (1983).  After an unknown 
time, she lost consciousness and developed generalized muscle 
cramps, myosis, and tachycardia.  Treatment in hospital was as 
follows:  gastric lavage, PAM 0.5 mg; atropine 2 mg; sodium 
nitrite, 3% sodium thiosulfate; and, lastly, high doses of 
diazepam.  She completely recovered in 48 h. 

    A second poisoning case, concerning another attempted suicide 
by a 23-year-old man, was reported by Foulhoux (1988).  After oral 
absorption of 70 cc of a 2.5% EC formulation (1.75 g pure 
deltamethrin), there were no neurological signs in this patient.  
Digestive and hepatic signs occurred, probably due to absorption of 
the solvent, since determination of xylene in plasma was positive.  
The patient was treated with haemodialysis, phenobarbital, 
lidocaine, and provoked alkaline diuresis.  Recovery followed 
within 48 h. 

8.2  Occupational Exposure

8.2.1  Acute toxicity-poisoning incidents

    Rousselin (1983) described a case of poisoning in an 
agricultural worker as a result of skin contamination with a liquid 
containing 5 g deltamethrin/litre.  He developed paraesthesia in 
the legs, mouth, and tongue, and diarrhoea.  Following washing of 
the skin and administration of antihistamines, he still had 
tingling sensations in his toes after 24 h, but was fully recovered 
after 48 h. 

    Outbreaks of acute deltamethrin and fenvalerate poisoning 
occurred in cotton growers in China in 1982 - 84.  The farmers 
handled the pyrethroid insecticides without taking any precautions.  
Skin sensations occurred in more than 90% of the exposed workers.  
After repeated spraying in the cotton fields, the mild cases 
presented severe headaches, dizziness, fatigue, nausea, and 
anorexia, with transient changes in the EEG.  A severe case 
developed muscular fasciculation, repetitive discharges in the EMG, 
and frequent convulsions, which were treated with diazepam and 
phenobarbital.  However, in follow-up studies, all workers were 
found to have made complete recovery, and the prognosis of acute 
pyrethroid poisoning was found to be good (He, 1987; Tong Ying, 

    More recently He et al. (1989) reviewed 573 cases of acute 
pyrethroid poisoning reported in the Chinese medical literature 
during 1983 - 88.  Among these there were 325 cases of acute 
deltamethrin poisoning:  158 occupational, due to inappropriate 
handling, and 167 accidental, mostly due to ingestion.  Two 
patients died of convulsions.  All others recovered with 
symptomatic and supportive treatment within 1 - 6 days.  Clinical 
manifestations are well reviewed (He, 1987). 

8.2.2  Effects of short- and long-term exposure

    Among plant workers dermally exposed to technical deltamethrin 
or its formulations, cutaneous and mucuous manifestations were 
observed.  Initial lesions were tenacious and painful pruritus, 
especially observed after exposure to hot water or perspiration, 
followed by a blotchy local burning sensation with blotchy erythema 
for about 2 days.  Thereafter, slight and regular desquamation, 
restricted to the contaminated area, occurred.  Cutaneous signs 
were sometimes accompanied by itching of the face (mainly around 
the mouth) and/or rhinorrhoea or lachrymation (Husson, 1978). 

    Apart from the above-mentioned effects, no long-term or 
persistent effect, or allergic diseases were reported in 70 
workers, who had been exposed from 1977 - 87 in a deltamethrin-
manufacturing and -formulating plant in France (unpublished 
Roussel Uclaf information supplied to the IPCS, 1988). 

    A field study was carried out in the United Kingdom with three 
unprotected operators and one operator wearing hood, gloves, and 
respirator, all of whom were involved in orchard spraying with 
deltamethrin according to normal field practice.  The exposure time 
was 3.5 h.  No changes were found in blood cell counts, total 
protein, urea, alkaline phosphates, gamma-GT and SGOT in blood.  
Little deltamethrin was found in the respirator pad and no residues 
were found in the urine.  There was no decrease in nerve conduction 
velocity, but a slight tendency to the opposite reaction.  None of 
the operators experienced facial sensations (Hewson & Burgess, 1981). 

    Four operators were evaluated by the same authors during normal 
field applications of deltamethrin lasting one day.  Three of the 
operators did not wear any protection on their heads or hands, 
while one wore hood, gloves, and a respirator.  Motor and sensory 
nerve conduction velocities were determined as well as 
haematological and biochemical parameters and urinalysis.  No 
changes were observed in the blood parameters measured and no 
residues were found in the urine samples.  Furthermore, nerve 
conduction velocity did not decrease.  Residues were primarily 
confined to gloves and legs.  None of the operators experienced 
facial sensations (Hewson & Burgess, 1981). 

    Persons exposed to deltamethrin for 7 - 8 years in production 
and formulation were subjected to clinical and haematological 
examinations.  Evaluations were conducted at several plants.  There 
were no measurable effects other than transient irritation of 

cutaneous and mucous membranes, which was without sequelae.  
Adequate precautionary measures, such as the wearing of gloves and 
face masks, provided protection from exposure (Foulhoux, 1981). 

    A medical survey of agricultural workers involved in the use 
and application of EC and WP formulations of deltamethrin in 
Yugoslavia revealed no untoward symptoms of exposure, other than 
itching and burning of the face, and nasal hypersecretion.  Medical 
examinations included chest X-ray, ECG, liver function tests, 
neurological examinations (eye tonometry, Goldman perimetry, dark 
adaptation ability), kidney function tests, and whole blood and 
plasma cholinesterase activity.  No adverse effects were noted.  
The need for the proper use of masks and gloves, as well as good 
personal hygiene (e.g., washing), was emphasized (Plestina, 1981). 

    Five healthy volunteers, 16 - 40 years of age, were exposed to 
deltamethrin during 5 days of spraying in a cotton field in India 
in 1981.  A sixth volunteer was engaged in mixing and loading the 
emulsion during the same period.  Spraymen were exposed for 7 h 
daily.  No one complained about any symptoms.  No clinical 
abnormalities were detected, particularly with respect to 
neurological examination (muscle power, coordination, tremors, 
reflexes, and both light and deep sensations).  No cardiovascular, 
respiratory, or abdominal abnormalities were detected, and no skin, 
mucous membrane, or eye lesions were observed during, and after 
cessation of, exposure (Trivedi, 1981). 

    A health survey was carried out among spraymen exposed to 2.5% 
deltamethrin emulsifiable concentrate in cotton fields in China.  
The subjects were exposed to deltamethrin at concentrations of 
0.022 - 24.070 µg/m3 in the air of the respiratory zone and 
0.013 - 0.347 µg/cm2 of skin contact.  One half of the 44 sprayers 
complained of itching and burning sensations on their faces.  A few 
miliary red papules also appeared on the face of one of them, but 
no signs of acute deltamethrin poisoning were noticed during 
physical examination.  There were no significant differences in the 
sodium, potassium, and urea contents of the serum, the sodium, 
potassium, ATPase, and serotonin contents of whole blood, and the 
levels of 3-methyl-4-hydroxymandelic acid and 5-hydroxy-
indoleacetic acid in the urine between the subjects examined and 
the controls.  Deltamethrin in the urine of spraymen was below the 
detection limit of 0.10 µg/litre (Wang et al., 1988). 

    Mestres et al. (1985) measured the dermal and inhalation 
exposure of mixer/applicators who applied deltamethrin to vegetable 
crops in greenhouses in southern France and of workers who picked 
fruit from treated trees in the same area.  This appeared to be 
less than 0.0065% of the toxic dose per hour with a mask and 
0.0017%, without a mask. 

    In a department producing an aerosol of the domestic Bulgarian 
insecticide "Dekazol" containing 0.02, 0.04, or 0.08% deltamethrin, 
severe subjective complaints of sensory irritation were found 
because of the high levels of contamination of the workplace air 
with deltamethrin and also dermal contamination.  Skin irritation 

with conjunctivitis and irritation of the respiratory system were 
discovered in all 25 workers.  Two of them had contact urticaria.  
Patch testing with 0.03% deltamethrin showed a positive reaction in 
5 out of 23 workers tested (Bainova et al., 1986). 

8.3  Clinical Studies

    Three formulations of deltamethrin in petroleum solvent were 
patch tested on 37 human volunteers (double blind trial against 
solvent control).  A dose of 20 µl of a 1% suspension in water, of 
a 25 g/litre emulsifiable concentrate was put on the facial skin of 
each volunteer, with a randomized distribution of control and 
active dilution.  The duration of the irritation was short (from 
some minutes to 1 h) and the severity was described as slight by 
most of the volunteers.  No skin damage was reported (Foulhoux et 
al., 1981). 


    The Joint FAO/WHO Meeting on Pesticide Residues (JMPR) 
discussed and evaluated deltamethrin at its meetings in 1980, 1981, 
1982, 1984, 1985, 1986, 1987, and 1988 (FAO/WHO, 1981, 1982, 1983, 
1985a, 1986a, 1986b, 1988a,b,c).  In 1982, an acceptable daily 
intake (ADI) of 0 - 0.01 mg/kg body weight was established. 

    The following Maximum Residue Limits (MRLs), in mg/kg, resulted 
from these evaluations: 

tea                                    10.0

hops dry, wheat bran unprocesseda      5.0

coffee beans (post-harvest)            2.0

wheat wholemeal,a cereal grains,a      1.0
(ph) lentil (dry),a beans (dry),a 
field pea (dry)a

straw and fodder (dry) of cereal       0.5
grains, legume animal feeds (dry 
weight), leafy vegetables

brassica leafy vegetables,a edible     0.2
peel of fruiting vegetablesa

bulb vegetables, edible peel of        0.1
assorted fruits, legume vegetables, 
oilseeds, pome fruits, wheat floura

artichokes, bananas, clementines,      0.05
coco beans, grapes, kiwi fruit, 
oranges (sweet, sour), stone 

legume oilseeds, melons,               0.01
mushrooms, pineapples, root and 
tuber vegetables, milksa 

    WHO has classified deltamethrin as a moderately hazardous 
technical product in normal use (WHO, 1988).  A Data Sheet on 
deltamethrin (No. 50) has been issued (WHO/FAO, 1984). 

a Not yet confirmed by Codex Alimentarius Commission (FAO/WHO, 
  1986c, and 1988c).
ADENEY, R.J., GRZYWACZ, D., & MATTHIESSEN P.  (1980)  The acute 
toxicities of pyrethrin analogues to  Sarotherodon mossambicus 
(Peters), Centre for Overseas Pest Research, 6 pp. (Unpublished 
proprietary data submitted to WHO by Roussel Uclaf). 

AKHTAR, M.H.  (1984)  Metabolism of deltamethrin by cow and chicken 
liver enzyme preparations. J. agric. food Chem., 32: 258-262. 

AKHTAR, M.H., HAMILTON, R.M.G., & TRENHOLM, H.L.  (1985)  
Metabolism, distribution and excretion of deltamethrin by leghorn 
hens. J. agric. food Chem., 33: 610-617. 

AKHTAR, M.H., MARTIN, K.E., & TRENHOLM, H.L.  (1986)  Fate of 
14C-deltamethrin in lactating dairy cows. J. agric. food Chem., 
34: 753-758. 

AKHTAR, M.H., DANIS, C., TRENHOLM, H.L., & MARTIN, K.E.  (1987)  
Residues in milk and tissues of lactating dairy cows fed 
deltamethrin for 28 consecutive days.  J. agric. food Chem., 

C.  (1978)  The effect of DDT and the pyrethroids cismethrin and 
decamethrin on the acetyl choline and cyclic nucleotide content of 
rat brain.  Biochem. Pharmacol., 27: 1703-1706. 

ALINIAZEE, M.T. & CRANHAM, J.E.  (1980)  Effects of four synthetic 
pyrethroids on a predatory mite,  Typhlodroums pyri, and its prey, 
 Panonychus ulmi, on apples in southeast England. Environ. Entomol., 
9: 436-439. 

ARZONE, A. & VIDANO, C.  (1978)  [Azione sull'ape di etiofencaus, 
decamethrin e ciexatin.] Apic. mod., 69: 157-162, (in Italian). 

ATKINS, E.L., KELLUM D., & NEUMAN, K.J.  (1976)  Effect of 
pesticides on apiculture project No. 1449:  The annual report, 
University of California Riverside, pp. 536-567. 

L'HOTELLIER, M., & STEPNIEWSKI, J.P.  (1988)  Potentialisation de 
la toxicité de la deltaméthrine par les insecticides 
organophosphorés (Unpublished proprietary data submitted to WHO by 
Roussel Uclaf). 

AUDEGOND L., COLLAS E., & GLOMOT R.  (1981)  RU 22974 
(deltamethrin) single administration study by oral route in the rat 
(the compound is given as a suspension) (Unpublished report RU-
81239/A, submitted to WHO by Roussel Uclaf). 

BAINOVA, A. & KALOYANOVA, F.  (1985)  [Study of allergenic and 
irritating effect of synthetic pyrethroids on skin.]  Hig. Zdrav., 
28(2): 19-21 (in Bulgarian). 

Specific skin irritation after contact with specific pyrethroids.  
6th Congress of Bulgarian Dermatologists, Varna, 2-5 October, 1986, 
(Abstract No. 74)  (in Bulgarian). 

BAKER, P.G. & BOTTOMLEY, P.  (1982)  Determination of residues of 
synthetic pyrethroids in fruit and vegetables by gas-liquid and 
high-performance liquid chromatography. Analyst, 107: 206-212. 

LAVEISSIERE, C.  (1981)  The experimental application of 
insecticides from a helicopter for the control of riverine 
populations of  Glossina tachinoides in West Africa. Part VIII: The 
effects of two spray applications of OMS-570 (endosulfan) and of 
OMS 1998 (decamethrin) on  G. tachinoides and non-target organisms 
in Upper Volta. Trop. Pest Manage., 27(1): 83-110. 

BEAVERS, J.B. & FINK, R.  (1977a)  Actue oral LD50 Mallard duck 
technical DECIS final report, (Unpublished report WI77.06.06/A, 
submitted to WHO by Roussel Uclaf). Wildlife International. 

BERLIN, J.R., AKERA, T., BRODY, T.M., & MATSUMURA, F.  (1984)  The 
inotropic effects of a synthetic pyrethroid decamethrin on isolated 
guinea pig atrial muscle.  Eur. J. Pharmacol., 98: 313-322. 

(1988) Mechanisms responsible for the toxicity of deltamethrin and 
other pyrethroids.  (Unpublished document, submitted to WHO by 
Roussel Uclaf). 

BLEYS, M., COTONAT, J., FOULHOUX, P.  (1986)  Lettre à l'éditeur, 
J. Toxicol. clin. exp., 6(3): 211-212. 

BLOOMQUIST, J.R., SODERLUND, D.M.  (1985)  Neurotoxic insecticides 
inhibit GABA-dependent chloride uptake by mouse brain vesicles. 
Biochem. biophys. Res. Commun., 133(1): 37-43. 

Inhibition of gamma-aminobutyric acid-stimulated chloride flux in 
mouse brain vesicles by polychlorocycloalkane and pyrethroid 
insecticides. Neurotoxicology, 7(3): 11-20. 

BOCQUET, J.C., PASTRE, P., ROA, L., & BAUMEISTER, R.  (1980)  Etude 
de l'action de la deltaméthrine sur  Apis mellifera en conditions de 
plein-champ. Phytiatr. Phytopharm., 29: 83-92.      

BOCQUET, J.C., PASTRE, P., & BAUMEISTER, R.  (1983)  Bilan de cinq 
années d'études de l'effet de la deltaméthrine sur abeilles en 
conditions naturelles.  6ème Congrès International du Colza, Paris, 
mai 1983. 

BOUCHE, M.B. & FAYOLLE, L.  (1979)  Tests carried out with Procida 
compound Decis EC 2.5 on earthworms lethal effect in relation with 
time  (Unpublished proprietary report No. INRA-VT-79.05.22/78.10.
10/A, submitted to WHO by Roussel Uclaf). 

BOWMAN, H. & CARPENTER, M.  (1987)  Determination of 
photodegradation of 14C-deltamethrin in aqueous solution 
(Unpublished proprietary report ABC LABS 35491, submitted to WHO by 
Roussel Uclaf). 

BRADBURY, J.E., GRAY, A.J., & FORSHAW, P.  (1981)  Protection 
against pyrethroid toxicity in rats with mephenesin.  Toxicol. 
appl. Pharmacol., 60: 382. 

BRADBURY, J.E., FORSHAW, P.J., GRAY, A.J., & RAY, D.E.  (1983)  The 
action of mephenesin and other agents on the effects produced by 
two neurotoxic pyrethroids in the intact and spinal rat.  
Neuropharmacology, 22(7): 907-914. 

BRODIE, M.E.  (1983)  Correlations between cerebellar cyclic GMP 
and motor effects induced by deltamethrin: independence of olivo-
cerebellar tract.  Neurotoxicology, 4(4): 1-11. 

BRODIE, M.E.  (1985)  Deltamethrin infusion into different sites in 
the neuraxis of freely moving rats.  Neurobehav. Toxicol. Teratol., 
7(1): 51-55. 

BRODIE, M.E. & ALDRIDGE, W.N.  (1982)  Elevated cerebellar cyclic 
GMP levels during the deltamethrin-induced motor syndrome. 
Neurobehav. Toxicol. Teratol., 4: 109-113. 

BRODIE, M.E. & OPACKA, J.  (1985)  Dissociation between circling 
behaviour and striatal dopamine activity following unilateral 
deltamethrin administration to rats.  Naunyn-Schmiedeberg's Arch. 
Pharmacol., 331:  341-346. 

BROOKS, M.W. & CLARK, J.M.  (1987)  Enhancement of norepinephrine 
release from rat brain synaptosomes by alpha cyano pyrethroids.  
Pestic. Biochem. Physiol., 28: 127-139. 

BUCCAFUSCO, R.J., ELLS, S.J., & CARY, G.A.  (1977a)  Acute toxicity 
of NRDC 161 to bluegill  (Lepomis macrochirus) under dynamic test 
conditions, E.G. & G. Bionomics Aquatic Toxicology Laboratory, 12 pp.  
(Unpublished proprietary data submitted to WHO by Roussel Uclaf).

BUCCAFUSCO R.J., ELLS, S.J., & CARY, G.A.  (1977b)  Acute toxicity 
of NRDC 161 (Decamethrine) to Channel Catfish  (Ictalurus 
 punctatus), E.G. & G. Bionomics Aquatic Toxicology Laboratory, 
7 pp. (Unpublished proprietary data supplied to WHO by Roussel 

CABRAL, J.R.P., GALENDO, D., LAVAL, M., & LYANDRUT, N.  (1986)  
Carcinogenicity study of the pesticide deltamethrin in mice and 
rats.  Summary Report in Poster Session at IUPAC Meeting, Ottawa, 
August 1986. 

CARY, G.A.  (1978)  Kinetics of 14C-NRDC-161 in a model aquatic 
ecosystem, E.G. & G. Bionomics Aquatic Toxicology Laboratory.  
(Unpublished proprietary report BW-78-2-075, submitted to WHO by 
Roussel Uclaf). 

CHALMERS, A.E., MILLER, T.A, & OLSEN, R.W.  (1987)  Deltamethrin:  
a neurophysiological study of the sites of action.  Pestic. 
Biochem. Physiol., 27: 36-41. 

CHAMBON, A. & LEPAILLEUR, H.  (1984)  Etude de l'effet toxique de 
la deltamethrine (produit technique > 98%) et de la formulation CE 
25 g/l Decis vis-à-vis de l'espece de vers  (Eisenia fetida andrei)  
(Unpublished proprietary report IRCHA-84.30.07/F, submitted to WHO 
by Roussel Uclaf). 

ZIADE, F., & SAMAHA, F.  (1981)  Analgesic effects of decamethrin, 
Surg. Transplant., 9: 503-504. 

CHAPMAN, R.A. & HARRIS, C.R.  (1981)  Persistence of four 
pyrethroid insecticides in a mineral and organic soil. J. environ. 
Sci. Health, B16: 605-615. 

CHAPMAN, R.A., TU, C.M., HARRIS, C.R., & COLE, C.  (1981)  
Persistence of five pyrethroid insecticides in sterile and natural, 
mineral and organic soil. Bull. Environ. Contam. Toxicol, 26: 

PRENTICE, D.E.  (1977)  RU 22974.  Oral toxicity study in Beagle 
dogs, Huntingdon, Huntingdon Research Centre, (Unpublished report 
RSL 253/7751/A3, submitted to WHO by Roussel Uclaf). 

CHINN, K. & NARAHASHI, T. (1986)  Stabilization of sodium channel 
states by deltamethrin in mouse neuroblastoma cells.  J. Physiol., 
380: 191-207. 

CLAIR, M.  (1977)  RU 22974 DECIS.  Acute toxicity in the rabbit by 
percutaneous administration.  Joinville-le-Pont, Institut Français 
de Recherches et Essais Biologique (Unpublished report IFREB-R 
770257.1/A, submitted to WHO by Roussel Uclaf). 

CLARK, G.C., JACKSON, G.C., & ALEXANDER, D.J. (1980)  Acute 
inhalation toxicity in rats, 4-hour exposure (Decis PM 2.5 
percent), Huntingdon Research Centre, (Unpublished report RSL 
437/80568, submitted to WHO by Roussel Uclaf). 

COOMBS, D.W. & CLARK, G.C. (1978) RU 22974: Acute inhalation 
toxicity in rats.  6 Hour LC50. Huntingdon, Huntingdon Research 
Centre, (Unpublished report RSL 310/78453/A, submitted to WHO by 
Roussel Uclaf). 

COOMBS, D.W., CLARK, G.C., STREET, A.E., & GIBSON, W.A. (1978)  RU 
22974 inhalation toxicity study in rats 14 x 6 hour exposures over 
a period of 3 weeks (Unpublished proprietary report 
RSL/318/78638/A, submitted to WHO by Roussel Uclaf). 

COQUET, B.  (1976a)  RU 22974.  Test to determine primary cutaneous 
irritation in the rabbit. Joinville-le-Pont, Institut Francais de 
Recherches et Essais Biologiques (Unpublished report IFREB-R 
761157/A, submitted to WHO by Roussel Uclaf). 

COQUET, B.  (1976b)  RU 22974.  Test to evaluate ocular irritation 
in the rabbit, Joinville-le-Pont, Institut Français de Recherches 
et Essais Biologiques (Unpublished report IFREB- R 761158/A, 
submitted to WHO by Roussel Uclaf). 

COQUET, B.  (1977)  RU 22974. Decis formulations - Determination of 
the LD50 in the rat by oral administration, Joinville-le-Pont, 
Institut Français de Recherches et Essais Biologiques (Unpublished 
report 770257-A, submitted to WHO by Roussel Uclaf). 

COTONAT, J., BLEYS, M., & FOULHOUX, P.  (1987)  Effets antagonistes 
du phenprobamate et du carbamate de mephenesine sur l'intoxication 
à la deltaméthrine.  J. Toxicol. clin. exp., 7: 5-19. 

CROFTON, K.M. & REITER, L.W.  (1984)  Effects of two pyrethroid 
insecticides on motor activity and the acoustic startle response in 
the rat.  Toxicol. appl. Pharmacol., 75: 318-328

DAVID, D.  (1981)  Laboratory evaluation of repellent properties 
against birds of the synthetic pyrethroid decamethrin. Poult. Sci., 
60: 1149-1151. 

DAVIES, J.E., MUNT, P.L., & GOOR, J.L.  (1983)  RU 22974.  
Investigation of possible neurological effects using the tilting 
plane test.  Huntingdon, Huntingdon Research Centre (Unpublished 
proprietary report RSL603/83232/A, submitted to WHO by Roussel 

DE LAVAUR, E., LE SECH, J., & GROLLEAU, G.  (1985)  Accumulation et 
élimination de la deltaméthrine chez la caille japonaise. Ann. 
Fals. Exp. Chim., 835: 73-78. 

DOHERTY, J.D., LAUTER, C.J., & SALEM, N., Jr  (1986)  Synaptic 
effects of the synthetic pyrethroid resmethrin in rat brain  in 
 vitro.  Comp. Biochem. Physiol., C84(2): 373-9. 

DUCLOHIER, H. & GEORGESCAULD, D.  (1979)  The effects of the 
insecticide decamethrin on action potential and voltage-clamp 
currents of myxicola giant axon.  Comp. Biochem. Physiol., C62(2):  

DUMONT, C. & CHIFFLOT, L.  (1978)  Recherche d'un antidote contre 
les effets toxiques aigus  (Unpublished report RU-AE-72, submitted 
to WHO by Roussel Uclaf). 

DUMONT, C. & LAURENT, J.  (1979)  Recherche d'antagonistes des 
effets neurotoxiques aigus du RU 22 974  (Unpublished report RU-AG-
35, submitted to WHO by Roussel Uclaf). 

DUNNING, R.A., COOPER, J.M., WARDMAN, J.M., & WINDER, G.  (1981)  
Susceptibility of the carabid  Pterostichus melanarius (Illiger) to 
aphicide sprays applied to the sugar-beet crop. (Unpublished 
proprietary report  UK-SOIL-F.81/A, submitted to WHO by Roussel 

DYBALL, R.E.J.  (1982)  Inhibition by decamethrin and resmethrin of 
hormone release from the isolated rat neurohypophysis - a model 
mammalian neurosecretory system.  Pestic. Biochem. Physiol., 17: 

ELLIOTT, M.  (1977)  Synthetic pyrethroids, Washington, DC, 
American Chemical Society, p. 229 (ACS Symposium Series 42). 

D.A.  (1974)  Synthetic insecticide with a new order of activity. 
Nature, 248: 710-711. 

ESTESEN, B.J., BUCH, N.A., & WARE, G.W.  (1979) Dislodgeable 
insecticide residue on cotton foliage; permethrin, curacron, 
fenvalerate, sulprofos, decis and endosulfan. Bull. environ. 
Contam. Toxicol., 22: 245-248. 

EVANS, M.H.  (1976)  End-plate potentials in frog muscle exposed to 
a synthetic pyrethroid.  Pestic. Biochem. Physiol., 6: 547-550. 

(1983)  Side effects of experimental pyrethroid applications for 
the control of tsetse flies in a riverine forest habitat in Africa.  
Arch. environ. Contam. Toxicol., 12: 91-97. 

R., & KOEMAN. J.H. (1985) Effects on man-target terrestrial 
arthropods of synthetic pyrethroids asked for the control of the 
Tsetse Fly ( Glossina spp.) in settlement areas of the Southern 
Ivory Coast, Africa. Arch. environ. Contam. Toxicol., 14: 647-650. 

FAO  (1982)  Second Government Consultation on International 
Harmonization of Pesticide Registration Requirements, Rome, 11-15 
October, 1982, Rome, Food and Agriculture Organization of the 
United Nations. 

FAO/WHO  (1981)  1980 Evaluations of some pesticide residues in 
food, Rome, Food and Agriculture Organization of the United Nations 
(FAO Plant Production and Protection Paper No. 26 Sup). 

FAO/WHO  (1982)  198l Evaluations of some pesticide residues in 
food, Rome, Food and Agriculture Organization of the United Nations 
(FAO Plant Production and Protection Paper No. 42). 

FAO/WHO  (1983)  1982 Evaluations of some pesticide residues in 
food, Rome, Food and Agriculture Organization of the United Nations 
(FAO Plant Production and Protection Paper No. 49). 

FAO/WHO  (1985a)  1984 Evaluations of some pesticide residues in 
food, Rome, Food and Agriculture Organization of the United Nations 
(FAO Plant Production and Protection Paper No. 67). 

FAO/WHO  (1985b)  Guide to Codex recommendations concerning 
pesticide residues.  Part 8.  Recommendations for methods of 
analysis of pesticide residues, 3rd ed., Rome, Food and Agriculture 
Organization of the United Nations, Codex Committee on Pesticide 

FAO/WHO  (1986a)  1985 Evaluations of some pesticide residues in 
food. Part I  - Residues, Rome, Food and Agriculture Organization 
of the United Nations (FAO Plant Production and Protection Paper 
No. 72/1). 

FAO/WHO  (1986b)  1986 Evaluations of some pesticide residues in 
food. Part I  - Residues, Rome, Food and Agriculture Organization 
of the United Nations (FAO Plant Production and Protection Paper 
No. 78). 

FAO/WHO  (1986c)  Codex maximum limits for pesticide residues, 2nd 
ed., Rome, Food and Agriculture Organization of the United Nations, 
Codex Alimentarius Commission, CAC XIII. 

FAO/WHO, (1988a)  1987 Evaluations of some pesticide residues in 
food. Part I  - Residues, Rome, Food and Agriculture Organization 
of the United Nations (FAO Plant Production and Protection Paper 
No. 86/1). 

FAO/WHO, (1988b)  1988 Evaluations of some pesticide residues in 
food. Part 1  - residues, Rome, Food and Agriculture Organization 
of the United Nations. (FAO Plant Production and Protection Paper 

FAO/WHO, (1988c) Supplement 1 to Codex maximum limits for pesticide 
residues, Rome, Food and Agriculture Organization of the United 

FISCHER, L. & CHAMBON, J.P.  (1987)  Faunistical inventory of 
cereal arthropods after flowering and incidence of insecticide 
treatments with deltamethrin, dimethoate and phosalone on the 
apigeal fauna. Meded. Fac. Landbouwwet. Rijksuniv. Gent, 52(2a): 

FLANNIGAN, S.A. & TUCKER, S.B.  (1985)  Variation in cutaneous 
sensation between synthetic pyrethroid insecticides.  Contact 
Dermatitis, 13: 140-147. 

FLORELLI, F., GARNIER, P., & ROA, L.  (1987a)  Bilan de 8 années 
d'expérimentation sur la selectivite du Decis vis à vis des 
abeilles - La défense des végétaux, 243: 8 

Incidence sur les abeilles, les ruches et leur production, de 
traitements aériens du colza avec la deltaméthrine - Annales ANPP - 
Conférence Internationale sur les Ravageurs en Agriculture, Paris, 
1-3 décembre 1987, 189-203. 

FORSHAW, P.J. & BRADBURY, J.E.  (1983)  Pharmacological effects of 
pyrethroids on the cardiovascular system of the rat.  Eur. J. 
Pharmacol., 91: 207-213. 

FORSHAW, P.J. & RAY, D.E.  (1986)  The effects of two pyrethroids, 
cismethrin and deltamethrin, on skeletal muscle and the trigeminal 
reflex system in the rat.  Pestic. Biochem. Physiol., 25: 143-151. 

FORSHAW, P.J., LISTER, T., & RAV, D.E.  (1987)  The effects of two 
types of pyrethroid on rat skeletal muscle.  Eur. J. Pharmacol., 
134(1): 89-96. 

FOUILLET, X.  (1976)  RU 22974  Mutagenicity study of various 
preparations.   Salmonella microsome test, Institut Français de 
Recherches et Essais Biologiques (Unpublished report no. IFREB-R 
761153/A, submitted to WHO by Roussel Uclaf). 

FOULHOUX, P.  (1981)  Medical observations of personnel working on 
synthesis or formulation of deltamethrin (Unpublished report  RU-
81.18.06/A, submitted to WHO by Roussel Uclaf). 

FOULHOUX, P.  (1988)  Assessment of potential adverse effects of 
deltamethrin on man, Département Central de Toxicovigilance Roussel 
Uclaf, 16 pp. (Unpublished report submitted to WHO by Roussel 

SUTTET  (1981)  Cutaneous irritation patch test on human volunteers 
with Decis EC25, Decis flowable 25, Decis + mineral oil 25 
(Unpublished report RU-81.03.02/DM/A, submitted to WHO by Roussel 

FOURNIER, P.E.  (1988)  Etude de l'activité antidote du carbamate 
d'éthyl dans l'intoxication aiguë par la deltaméthrine chez le rat, 
Paris, Unité de Pharmacologie Clinique, Hospital Fernand Widal 
(Unpublished report submitted to WHO by Roussel Uclaf). 

GAINES, T.B. & LINDER, R.E.  (1986)  Acute toxicity of pesticides 
in adult and weanling rats, Fundam. appl. Toxicol., 7: 299-308. 

GAMMON, D.W. & CASIDA, J.E.  (1983)  Pyrethroids of the most potent 
class antagonize GABA action at the crayfish neuromuscular 
junction.  Neurosci. Lett., 40: 163-168.  

GAMMON, D.W., BROWN, M.A., & CASIDA, J.E.  (1981)  Two classes of 
pyrethroid action in the cockroach. Pestic. Biochem. Physiol., 15: 

GAMMON, D.W., LAWRENCE, L.J., & CASIDA, J.E.  (1982)  Pyrethroid 
toxicology:  Protective effects of diazepam and phenobarbital in 
the mouse and the cockroach.  Toxicol. appl. Pharmacol., 66: 

GLICKMAN, A.H. & CASIDA, J.E.  (1982)  Species and structural 
variations affecting pyrethroid neurotoxicity.  Neurobehav. 
Toxicol. Teratol., 4(6): 793-799. 

GLOMOT, R.  (1979)  Acute toxicity study by oral route in the rat  
(Proprietary report RU-79803-54/A2, submitted to WHO by Roussel 

GLOMOT, R. & CHEVALIER, B.  (1976a)  RU 22974.  Acute toxicity 
study mouse and rat by oral route  (Unpublished report TOX 76810/A, 
submitted to WHO by Roussel Uclaf). 

GLOMOT, R. & CHEVALIER, B.  (1976b)  RU 22974.  Acute toxicity 
study mouse and rat by intraperitoneal route  (Unpublished report 
TOX 76811/A, submitted to WHO by Roussel Uclaf). 

GLOMOT, R. & CHEVALIER, B.  (1976c)  RU 22974.  Acute toxicity 
study mouse and rat by intravenous route  (Unpublished report TOX 
76812/A, submitted to WHO by Roussel Uclaf). 

GLOMOT, R. & VANNIER, B.  (1977)  RU 22974.  Teratological study in 
mouse, rat and rabbit  (Unpublished report TOX 76534-76536/2/A, 
submitted to WHO by Roussel Uclaf). 

GLOMOT, R. & VANNIER, B.  (1978)  RU 22974. Teratological study in 
rabbit.  Complementary information  (Unpublished report TOX 76534-
76536/A3, submitted to WHO by Roussel Uclaf). 

GLOMOT, R., AUDEGOND, L., & COLLAS, E.  (1979)  Acute oral toxicity 
study in the rat (Decis 25 G/L Mixofluid)  (Proprietary report  RU 
79824/A, submitted to WHO by Roussel Uclaf). 

GLOMOT, R., AUDEGOND, L., &  COLLAS, E.  (1980a)  Single 
administration by oral route in the mouse (Decis Wettable Powder, 
2.5%)  (Proprietary report RU-80817/A, submitted to WHO by Roussel 

GLOMOT, R., AUDEGOND, L., & COLLAS, E.  (1980b)  Single 
administration study by oral route in the dog (Decis Wettable 
Powder, 2.5%)  (Proprietary report RU 80194/A, submitted to WHO by 
Roussel Uclaf). 

GLOMOT, R., AUDEGOND, L., & COLLAS, E.  (1981a)  Single 
administration study by oral route in the rat  (Proprietary report 
RU-81239/A, submitted WHO by Roussel Uclaf). 

GLOMOT, R., AUDEGOND, L., & COLLAS, E.  (1981b)  Primary dermal 
irritation study in the rabbit.  Deltamethrin 25 G/L Mixofluid  
(Proprietary report RU-79193/A, submitted to WHO by Roussel Uclaf). 

GLOMOT, R., AUDEGOND, L., & COLLAS, E.  (1981c)  Primary dermal 
irritation study in the rabbit (Deltamethrin wettable powder, 2.5%)  
(Proprietary report RU-80200/A, submitted to WHO by Roussel Uclaf). 

GLOMOT, R., AUDEGOND, L., & COLLAS, E.  (1981d)  Primary eye 
irritation study in the rabbit (Deltamethrin in 25 G/L Mixofluid)  
(Proprietary report RU-79192/A, submitted to WHO by Roussel Uclaf). 

GLOMOT, R., AUDEGOND, L., & COLLAS., E.  (1981e)  Primary eye 
irritation study in the rabbit (Decis Wettable Powder, 2.5%)  
(Proprietary report RU-79192/A, submitted WHO by Roussel Uclaf). 

22974.  Acute toxicity study by oral route in male and female 
Beagle dogs  (Unpublished report TOX 77804/JL-5, submitted to WHO 
by Roussel Uclaf). 

ARCEO, R.J., & KAHN, A., III (1980a)  RU 22974. Two year toxicity 
and carcinogenicity study in mice, Mattawan, Michigan, 
International Research and Development Corporation (Unpublished 
report IRDC 406-001/A-4, submitted to WHO by Roussel Uclaf). 

SPICER, E.J.F., ARCEO, R.J., & KAHN, A., III (1980b)  RU 22974.  
Two year oral toxicity and carcinogenicity study in rats, 
Mattawan, Michigan, International Research and Development 
Corporation (Unpublished report IRDC 406-002/A.4, submitted to WHO 
by Roussel Uclaf). 

GRANDADAM, A.  (1976)  Test to determine the toxicity in the 
chicken by oral route  (Unpublished report RU76.05.05/A, submitted 
to WHO by Roussel Uclaf). 

GRAY, A.J. & RICKARD, J.  (1982)  The toxicokinetics of 
deltamethrin in rats after intravenous administration of a toxic 
dose.  Pestic. Biochem. Physiol.., 18: 205-215. 

GRAY, A.J., CONNORS, T.A., & RICKARD, J.  (1980)  Mechanism of 
mammalian toxicity of the pyrethroids. In: Littaner, U.Z. et al., 
ed. Neurotransmitters  and their receptors, New York, John Wiley 
and Sons, pp. 565-568. 

GROLLEAU G. & GRIBAN, J.  (1976a)  Toxicity of deltamethrin or 
DECIS in single ingestion in game duck  Anas platyrhnchos L., 
JoyenJossas, France, Institut National de la Recherche Agronomique 
(Unpublished report INRA-76.21 12/A, submitted to WHO by Roussel 

GROLLEAU, G. & GRIBAN, J.  (1976b)  Toxicity of deltamethrin or 
DECIS by single ingestion in grey partridge,  Perdix Perdix L. and 
red partridge,  Alectotis rufa L., JoyenJossas, France, Institut 
National de la Recherche Agronomique (Unpublished report INRA76.28 
09/A, submitted to WHO by Roussel Uclaf). 

GUILLOT, J.P. & GUILAINE, J.  (1977)  RU 22974.  Decaméthrine.  
Decis technical Roussel Uclaf.  Sensitization test in the guinea 
pig.  Joinville-le-Pont, Institut Français de Recherches et Essais 
Biologique (Unpublished report no. IFREB-R 709241/A, submitted to 
WHO by Roussel Uclaf). 

GULYAS P. & CSANYI B.  (undated)  Acute fish toxicological 
investigation of diverse insecticides, Hungary, Scientific Research 
Centre of Economy of Water Supplies, 21 pp. (Unpublished 
proprietary data supplied to WHO by Roussel Uclaf). 

HALLS, G.R.H. & PERIAM, A.W.  (1980)  The fate of residues of NRDC 
161 on wheat during storage and after milling and baking - Report 
after 9 months storage, November 1980, Wellcome Research 
Laboratories Report  (Unpublished report HEFH 80-4, submitted to 
WHO by Roussel Uclaf). 

HARGREAVES, J.R. & COOPER, L.P.  (1979)  Phytotoxicity tests with 
pyrethroid insecticides on glasshouse grown tomato seedlings.  
Queensland J. Agric. anim. Sci., 36: 151-154. 

HASCOET, M.  (1977)  Laboratory leaching soil study with 
decamethrin (RU 22974), Versailles, Institut National de la 
Recherche Agronomique  (Unpublished proprietary report INRA-
77.20.09/A, submitted to WHO by Roussel Uclaf). 

HE, F.  (1987)  Occupational neurotoxicology:  Current problems and 
trends. Paper presented at the XXII International Congress on 
Occupational Health, Sydney, 27 September-2 October, 1987. 

HE, F., WANG, S., LIU, L., CHEN, S., ZHANG, Z., & SUN, J. (1989) 
Clinical manifestations and diagnosis of acute pyrethroid 
poisoning.  Arch. Toxicol., 63: 54-58. 

HEHEITMULLER, T., SHUBA, P.J., & PARRISH, R.  (1978)  Acute 
toxicity of Decis to sheepshead minnows  (Cyprinodon variegatus), 
E.G. & G. Bionomics Marine Laboratory, 7 pp. (Unpublished 
proprietary report BR-78-12219, supplied to WHO by Roussel Uclaf). 

HEWSON, R.T. & BURGESS, J.E.  (1981)  An operator study with 
deltamethrin including measurements of nerve conduction times 
(Unpublished proprietary report GB-NT-11.81A, submitted to WHO by 
Roussel Uclaf). 

HILL, B.D.  (1982)  Determination of Deltamethrin residues in 
soils, Alberta, Agriculture Canada Research Station, 7 pp 
(Unpublished proprietary report CAN-82.12.10/A, submitted to WHO by 
Roussel Uclaf). 

HILL, B.D.  (1983)  Persistence of deltamethrin in a Lethbridge 
sandy clay loam. J. environ. Sci. Health, B18(6): 691-703. 

HILL, B.D. & JOHNSON, D.L.  (1987)  Persistence of deltamethrin and 
its isomers on pasture forage and litter.  J. agric. Food Chem., 
35: 373-378. 

HILL, B.D. & SCHAALJE, G.B.  (1985)  A two-compartment model for 
the dissipation of deltamethrin on soil. J. agric. food Chem., 33: 

KIYAMOTO, J.  (1986)  Therapeutic effects of methocarbamol on acute 
intoxication by pyrethroids in rats.  J. pestic. Sci., 11: 9-14. 

PRENTICE, D.E.  (1977)  RU 22974.  Assessment of toxicity to rats 
by oral administration for 13 weeks (followed by a 4-week 
withdrawal period)  (Unpublished report RSL-254/76938/A3, submitted 
to WHO by Roussel Uclaf). 

HUSSON, J.M.  (1978)  Medical observations made on people working 
on the manufacture and formulation of the pyrethroid insecticide 
decamethrin  (Unpublished report RU 78.25.08/A, submitted to WHO by 
Roussel Uclaf). 

IRDC  (1980)  Two year chronic dog feeding study, Matawan, 
Michigan, International Research and Development Corporation 
(Unpublished proprietary report IRDC-406-004/AI, submitted to WHO 
by Roussel Uclaf). 

JACKSON, G. & HARDY, C.  (1986)  RU 22974. Acute inhalation 
toxicity in rats 1-hour exposure (Unpublished report RSL-DTM-
851457/A, submitted to WHO by Roussel Uclaf). 

M.  (1980)  Interaction of pyrethroids with the sodium channel in 
mammalian neuronal cells in culture. Biochem. Biophys. Acta, 600: 

Biochemical effects of toxic action of synthetic pyrethroids.  Gig. 
i Sanit., 1: 7-9. 

KAUFMAN, D.D. & KAYSER, A.J.  (1979a)  Degradation of 14C-phenoxy- 
and 14C-cyano-decamethrin in soil (Unpublished proprietary report 
USDA-I-23.04.79/A2, submitted to WHO by Roussel Uclaf). 

KAUFMAN, D.D. & KAYSER, A.J.  (1979b)  The effect of soil 
temperature on the degradation of 14C-cyano-decamethrin in soil 
(Unpublished proprietary report USDA-II-24.04.79/A2, submitted to 
WHO by Roussel Uclaf). 

KAUFMAN, D.D. & KAYSER, A.J.  (1980)  Degradation of 14C-cyano-, 
14C-phenoxy-, and 14C-vinyl-decamethrin in flooded soil 
(Unpublished proprietary report USDA-III-12.05.80/A, submitted to 
WHO by Roussel Uclaf).  

KAUFMAN, D.D., RUSSEL, B.A., HELLING, C.S., & KAYSER, A.J.  (1981)  
Movement of cypermethrin, decamethrin, permethrin and their 
degradation products in soil. J. agric. food Chem., 29: 239-245. 

CARVER, B., DILLEY, J., & SIMMON, V.  (1979)  Toxicity studies with 
decamethrin, a synthetic pyrethroid insecticide. J. environ. 
Pathol. Toxicol., 2: 751-765. 

KNAUF, W. & HORLEIN, G.  (1979  The acute toxicity of decamethrine 
to the Rainbow trout  Salmo gairdneri, Richardson, Frankfurt, 
Hoechst AG, 19 pp (Unpublished proprietary report 19/79, submitted 
to WHO by Roussel Uclaf). 

KNAUF, W. & SCHULZE, E.F.  (1977a)  Effect of decamethrine on 
 Cyprinus carpio, Frankfurt, Hoechst AG, 9 pp (Unpublished 
proprietary report 15/77, submitted to WHO by Roussel Uclaf). 

KNAUF, W. & SCHULZE, E.F.  (1977b)  The effect of decamethrin 
6E0660 on Catfish  (Ictalurus nebulosus) in a static test, 
Frankfurt, Hoechst Ag, 18 pp (Unpublished proprietary report 
32/79, submitted to WHO by Roussel Uclaf). 

KRASNJIH, A. & PAVLOVA, L.  (1985)  Harmful effects of 
deltamethrin. In: Levina, E., ed. Harmful substances in industry, 
Moscow, Khimija Publishing House, p. 154. 

KYNOCH, S.R., LLOYD, G.K., & ANDREWS, C.D.  (1979)  Acute 
percutaneous toxicity to rats of decamethrin, Huntingdon, 
Huntingdon Research Centre (Unpublished report RSL-1009 8/D, 
submitted to WHO by Roussel Uclaf). 

LAWRENCE, L.J. & CASIDA, J.E.  (1982)  Pyrethroid toxicology: Mouse 
intracerebral structure-toxicity relationship. Pestic. Biochem. 
Physiol., 18: 9-14. 

LAWRENCE, L.J. & CASIDA, J.E.  (1983)  Stereospecific action of 
pyrethroid insecticides on the gamma-aminobutyric acid receptor-
ionophore complex.  Science, 221: 1399-1401.

LAWRENCE, L.J., GEE, K.W., & YAMAMURA, H.I.  (1985)  Interactions 
of pyrethroid insecticides with chloride ionophore-associated 
binding sites.  Neurotoxicology, 6: 87-98. 

LEAHEY, J.P.  (1985)  The pyrethroid insecticide, London, Taylor & 
Francis Ltd., p. 440. 

LECLERCQ, M., COTONAT, J., & FOULHOUX, P.  (1986)  Recherche d'un 
antagoniste à l'intoxication par la deltaméthrine.  J. Toxicol. 
clin. exp., 6, 83-85. 

LEIBOWITZ, M.D., SCHWARZ, J.R., HOLAN, G., & HILLE, B.  (1987)  
Electrophysiological comparison of insecticide and alkaloid 
agonists of Na channels.  J. gen. Physiol., 90(1): 75-93. 

LEPAILLEUR, H. & CHAMBON, A.  (1984)  Etude de la toxicité létale 
du produit technique deltaméthrine vis à vis du poisson-zebré, 5 pp 
(Unpublished proprietary dated report IRCHA B.7827, submitted to 
WHO by Roussel Uclaf). 

LHOSTE, J., FRANCOIS, Y., & RUPAUD, Y.  (1979)  Ichtyotoxicité de 
la decaméthrine vis à vis de  Salmo trutta L. (poisson téléostéen) 
en fonction de l'age et des conditions expérimentales - Congrès sur 
la lutte contre les insectes en milieu tropical, Marseilles - March 
13-16 1979, pp. 885-902. 

L'HOTELLIER, M. & VINCENT, P.  (1986)  Assessment of the impact of 
deltamethrin on aquatic species.  In British Crop Protection 
Conference - Pests and Disease:  1109-1116. 

LOUVEAUX, J., MISSONNIER, J., & MESQUIDA, J.  (1977)  Tests de 
toxicité sur abeille domestique avec le Decis CE (Unpublished 
proprietary report submitted to WHO by Roussel Uclaf). 

LUMMIS, S.C., CHOW, S.C., HOLAN, G., & JOHNSTON, G.A.  (1987)  
Gamma-aminobutyric acid receptor ionophore complexes: differential 
effects of deltamethrin, dichlorodiphenyltrichloroethane, and some 
novel insecticides in a rat brain membrane preparation.  J. 
Neurochem., 48(3): 689-94. 

LUND, A.E. & NARAHASHI, T.  (1983)  Kinetics of sodium channel 
modification as the basis for the variation in the nerve membrane 
effects of pyrethroids and DDT analogs.  Pestic. Biochem. Physiol., 
20: 203-216. 

MACPHAIL, R.C.  (1981)  Behavioral effects of a synthetic 
insecticide  (decamethrin). Fed. Proc. Fed. Am. Soc. Exp. Biol., 
40: 678. 

(1983) Farm  chemicals handbook. Section C. Pesticide dictionary, 
Willoughby, Ohio, Meister Publishing Co. 

Dosage des résidues de decaméthrine dans les produits végétaux. 
Trav. Soc. Pharm. Montpellier, 38: 183-192. 

MESTRES R., CHEVALLIER C., & ESPINOZA, C.  (1978b)  Analytical 
method for decamethrine residue analysis, Montpellier, Faculte de 
Pharmacie, 2 pp. (Proprietary report FP-78.08.07/A, dated 7/8/1978 
submitted to WHO by Roussel Uclaf). 

(1985)  Survey of exposure to pesticides in greenhouses. Bull. 
environ. Contam. Toxicol., 35: 750-756. 

MESTRES, R., ESPINOZA, C., & CHEVALLIER, C.  (1986)  Effets sur les 
résidus de deltaméthrine de la transformation des produits 
agricoles en vue de leur consommation. Med. Nutr., XXII (3): 

MILLER, T.A. & ADAMS, M.E.  (1980)  Neural and behavioral 
correlates of pyrethroid and DDT-type poisoning in the housefly, 
 Musca domestica. Pestic. Biochem. Physiol., 13: 137-147. 

MIYAMOTO, J.  (1976)  Degradation, metabolism and toxicity of 
synthetic pyrethroids. Environ. Health Perspect., 14: 15-28. 

MIYAMOTO, J.  (1981)  The chemistry, metabolism and residue 
analysis of synthetic pyrethroids.  Pure appl. Chem., 53: 1967-2022. 

MIYAMOTO, J. & KEARNEY, P.C.  (1983)  Pesticide chemistry - Human 
welfare and the environment. Proceedings of the Fifth International 
Congress of Pesticide Chemistry, Kyoto, Japan, 29 August - 4 
September, 1982, Oxford, Pergamon Press, Vol. 1-4. 

MOHSEN, Z.H. & MULLA, M.S.  (1981)  Toxicity of blackfly larvicidal 
formulations to some aquatic insects in the laboratory. Bull. 
environ. Contam. Toxicol., 26: 696-703. 

MOUROT, D., DELEPINE, B., BOISSEAU, J., & GAYOT, G.  (1979)  High-
performance liquid chromatography of decamethrin. J. Chromatogr., 
173: 412-414. 

MUIR, D.C.G., RAWN, G.P., & GRIFT, N.P., (1985)  Fate of the 
pyrethroid insecticide deltamethrin in small ponds: A mass balance 
study. J. agric. food Chem., 33: 603-609. 

Toxicity of mosquito larvicidal pyrethroids to four species of 
freshwater fishes. Environ. Entomol.., 7(3): 428-430. 

NETO, P.X.R., RODRIGUES, I.C.F., & FILHO, A.M  (1983)  Etude sur 
les effets secondaires de la deltaméthrine sur l'ichtyofaune de la 
region du projet "Rio Formoso" (Unpublished report submitted to WHO 
by Roussel Uclaf). 

NOBLE, R.M., HAMILTON, D.J., & OSBORNE, W.J.  (1982)  Stability of 
pyrethroids on wheat in storage. Pestic. Sci., 13: 246-252. 

PANSHINA T.N. & SASINOVICH, L.M.  (1983)  Toxicology of synthetic 
pyrethroids.  Khim. sel'sk. khoz., 12: 51-53. 

PANSU, M., DHOUIBI, M.H., & PINTA, M.  (1981)  Determination of 
traces of biopermethrine and decamethrine pyrethrinoids in 
biological substrates by gas chromatography. Analysis, 9: 55-59. 

PAPALEXIOU, Ph., BITAR, N., & STOCKIS, A.  (1984)  Absorption of 
radiocarbon labelled deltamethrin given orally in healthy 
volunteers, Charleroi, Belgium, Institut de Pharmacologie et 
d'Investigations Biomédicales (Unpublished proprietary report 
50/22, submitted to WHO by Roussel Uclaf). 

PARKIN, P.J. & LEQUESNE, P.M.  (1982)  Effects of a synthetic 
pyrethroid deltamethrin on excitability changes following a nerve 
impulse. J. Neurol. Neurosurg. Psychiatry., 45: 337-342. 

PEYRE, M., CHANTOT, J.F., GLOMOT, R., & PENASSE, L.  (1980)  
Detection of a mutagenic potency of decamethrin (RU 22974), in 
bacterial tests (Unpublished report RU/TOX/80-2101/A, submitted to 
WHO by Roussel Uclaf). 

HAVERBEKE, G., CHEAV, S.L.  (1984)  Toxicological studies of 
deltamethrin.  Int. J. Tissue React., 6(2): 127-33. 

PICHON, Y.  (1981)  Pharmacological characterization of ionic 
channels in unmyelinated axons. J. Physiol., 17(9): 1119-1128. 

PLAPP, F.W., Jr & BULL, D.L.  (1978)  Toxicity and selectivity of 
some insecticides to Chrysopa carnea, a predator of the tobacco 
budworm. Environ. Entomol., 7: 431-434. 

PLESTINA, R.  (1981)  An evaluation of the use of deltamethrin in 
public health  (Unpublished report ZAG. KOT. 81/A, submitted to WHO 
by Roussel Uclaf). 

HAUTEFEUILLE, A., & BARTSCH, H.  (1984)  Lack of mutagenicity of 
synthetic pyrethroids in  Salmonella typhimurium strains and in V79 
Chinese hamster cells. Mutat. Res., 137: 7-15. 

POLAKOVA, H. & VARGOVA, M.  (1983)  Evaluation of the mutagenic 
effects of decamethrin: cytogenetic analysis of bone marrow. Mutat. 
Res., 120: 167-171. 

POTTIER J., CHATELET, P., & JOUQUEY, S.  (1982)  Resorption 
percutanée de la deltaméthrine - Etude d'un modèle animal, 10 pp. 
(Unpublished proprietary report AN.34, submitted to WHO by Roussel 

PRASADA RAO, K.S., CHETTY, C.S., & DESAIAH, D.  (1984)   In vitro 
effects of pyrethroids on rat brain and liver ATPase activities.  J 
Toxicol. environ. Health, 14(2-3): 257-65. 

RAWN, G.P., MUIR, D.O.G., & GRIFT, P.G.  (1985)  Fate of the 
pyrethroid insecticide deltamethrin in small ponds, a mass balance 
study. J. agr. food Chem., 33: 603-609. 

RAY, D.E.  (1980)  An EEG investigation of decamethrin-induced 
choreathetosis in the rat. Exp. Brain Res., 38: 221-227. 

RAY, D.E.  (1982)  Changes in brain blood flow associated with 
deltamethrin-induced choreoathetosis in the rat.  Exp. Brain Res., 
45: 269-276. 

RAY, D.E. & CREMER, J.E.  (1979)  The action of decamethrin (a 
synthetic pyrethroid) on the rat. Pestic. Biochem. Physiol., 10: 

RICHTER, W.R. & GOLDENTHAL, E.I.  (1983)  Two-year oral toxicity 
and carcinogenicity study in rats.  Amendment to the final report. 
Matawan, Michinga, International Research and Development 
Corporation  (Unpublished proprietary report IRDC 406.002/A5, 
submitted to WHO by Roussel Uclaf). 

RICKARD, J. & BRODIE, M.E.  (1985)  Correlation of blood and brain 
levels of the neurotoxic pyrethroid deltamethrin with the onset of 
symptoms in rats.  Pestic. Biochem. Physiol., 23: 143-156. 

RICOU  (1978)  Assessment of side effects of S 276-B (Decis EC 
25 g/l) towards grey slugs  (Agriolimax spp.) (Unpublished 
proprietary report INRA-LIM.78.10/A, submitted to WHO by Roussel 

ROSE, G.P. & DEWAR, A.J.  (1983)  Intoxication with four synthetic 
pyrethroids fail to show any correlation between neuromuscular 
dysfunction and neurobiochemical abnormalities in rats.  Arch. 
Toxicol., 53: 297-316. 

L., & GIBSON, W.A.  (1978)  RU 22974. (Decamethrine) LD50 
determination and assessment of neurotoxicity in the domestic hen, 
Huntingdon, Huntingdon Research Centre (Unpublished report RSL 293-
NT/7830/A, submitted to WHO by Roussel Uclaf). 

ROUSSELIN, X.  (1983)  Toxicité des dérivés du pyrèthre, Paris, 
Faculté de Médecine Lariboisiere-Saint-Louis (Thèse de l'Université 
Paris VII). 

RUIGT, G.S.F. & VAN DEN BERCKEN, J.  (1986)  Action of pyrethroids 
on a nerve-muscle preparation of the clawed frog,  Xenopus laevis.  
Pestic. Biochem.  Physiol., 25: 176-187. 

RUZO, L.O. & CASIDA, J.E.  (1979)  Degradation of decamethrin on 
cotton plants. J. agric. food Chem., 27: 572-575. 

RUZO, L.O., HOLMSTEAD, R.L., & CASIDA, J.E.  (1976)  Solution 
photochemistry of the potent pyrethroid insecticide alpha-cyano-3-
phenoxy-benzyl  cis-2,2-dimethyl-3-(2,2-dibromovinyl)
cyclopropanecarboxylate. Tetrahedron Lett., 3045-3048. 

RUZO, L.O., HOLMSTEAD, R.L., & CASIDA, J.E.  (1977)  Pyrethroid 
photochemistry: decamethrin. J. agric. food Chem., 25: 1385-1394. 

RUZO, L.O., UNAI, T., & CASIDA, J.E.  (1978) Decamethrin metabolism 
in rats. J. agric. food Chem., 26: 918-925. 

RUZO, L.O., ENGEL, J.L., & CASIDA, J.E.  (1979)  Decamethrin 
metabolites from oxidative, hydrolytic and conjugative reactions in 
mice. J. agric. food Chem., 27: 725-731. 

SANTOSA, K.  (1983)  Toxicity of Decis 2.5 EC (Decamethrin) to 
fish, Jakarta, Department of Agriculture Research and Development 
Inland Fisheries Institute, 4 pp. (Unpublished proprietary data 
submitted to WHO by Roussel Uclaf). 

SANTOSA, K. & HADI, H.  (1980)  Trial results pesticide lethal 
toxicity to fish, Department of Agriculture Research and 
Development Inland Fisheries Institute, Jakarta, Indonesia - 
Report no. 174/UI/80 dated 5 December 1980, 3 pp. (Unpublished 
proprietary data submitted to WHO by Roussel Uclaf). 

(1980)  Environmental aspects of field trials with pyrethroids to 
eradicate tsetse fly in Nigeria.  Ecotoxicol. environ. Saf., 4: 

SOBELS, F.H., TATES, A.D., & VANNIER, B.  (1978)  Cytogenetic study 
with RU 22974.  Detection of a mutagenic potency in mammalian 
cells, Leiden, The Netherlands, State University of Leiden 
(Unpublished report ULN-782211/A, submitted to WHO by Roussel 

SODERLUND, D.M. & CASIDA, J.E.  (1977) Effects of pyrethroid 
structure on rates of hydrolysis and oxidation by mouse liver 
microsomal enzymes. Pestic. Biochem. Physiol., 7: 391-401. 

SOUYRI, F.  (1985)  Autoradiographic studies of (3H)-deltamethrin 
binding with nerve tissue cultures.  Pestic. Sci., 6(6): 701-703. 

STAATZ, C.G., BLOOM, A.S., & LECH, J.J.  (1982)  Effects of 
pyrethroids on [3H]-kainic acid binding to mouse forebrain 
membranes. Toxicol. appl. Pharmacol., 64: 566-569. 

STAATZ-BENSON, C.G. & HOSKO, M.J.  (1986)  Interaction of 
pyrethroids with mammalian spinal neurons.  Pestic. Biochem. 
Physiol., 25: 19-30. 

STEIN, E.A., WASHBURN, M., WALCZAK, C., & BLOOM, A.S.  (1987)  
Effects of pyrethroid insecticides on operant responding maintained 
by food.  Neurotoxicol. Teratol., 9(1): 27-31. 

STEVENSON, J.H., NEEDHAM, P.H., & WALKER, J.  (1978)  Poisoning of 
honey bee by pesticides: investigations of the changing pattern in 
Britain over 20 years. Rothamsted Exp. Stn Rep., Part 2: 55-72. 

TAKAHASHI, M. & LEQUESNE, P.  ((1982)  The effects of the 
pyrethroids deltamethrin and cismethrin on nerve excitability in 
rats.  J. Neurol. Neurosurg. Psychiatry, 45: 1005-1011. 

TAKKEN, W., BALK, F., JANSEN, R.C., & KOEMAN, J.H.  (1978)  The 
experimental application of insecticides from a helicopter for the 
control of riverine populations of  Glossina tachinoides in West 
Africa.  VI. Observations on side effects. P.A.N.S., 24: 455-466. 

THIEBAULT, J.J., BOST, J., & FOULHOUX, P.  (1985)  Intoxication 
expérimentale par la deltaméthrine chez le chien et son traitement.  
Toxicol. vét. Collect. Méd. lég. Toxicol. méd., 131, 47-62. 

(in press)  Intravenous deltamethrin intoxication of dogs.  
Therapeutic attempts. Veterinary and Human Toxicology. 

THIER, W. & SCHMIDT, D.  (1976)  Laboratory leaching studies of 
Decis EC 25 in three different German soils (Unpublished 
proprietary report RL-77.25.05/A, submitted to WHO by Roussel 

THIER, W. & SCHMIDT, D.  (1977)  The behaviour of the pesticide in 
the soil: Decamethrin, (Unpublished proprietary report A09232, 
submitted to WHO by Roussel Uclaf) (in German). 

TONG YING  (1988)  Clinical manifestations of 211 cases intoxicated 
by deltamethrin and fenvalerate (Unpublished report submitted to 
WHO by Roussel Uclaf). 

R.T. (1981)  A pond study to investigate the effects on fish and 
aquatic invertebrates of deltamethrin applied directly onto water, 
Fisheries Laboratory, Ministry of Agriculture, Fisheries and Food 
(Unpublished report AEP-81.30.09A, submitted to WHO by Roussel 

TRIVEDI, K.  (1981)  Spray worker exposure and health survey during 
decamethrin (decis) spray in the field, Sevagram, India, Mahatma 
Gandhi Institute of Medical Sciences (Unpublished information 
submitted to WHO by Roussel Uclaf). 

TU, C.M.  (1980)  Influence of five pyrethroid insecticides on 
microbial populations and activities in soil.  Microb. Ecol., 5: 

VAN DEN BERCKEN, J.  (l977)  The action of allethrin on the 
peripheral nervous system of the frog.  Pestic. Sci., 8: 692-699. 

VAN DEN BERCKEN, J. & VIJVERBERG, H.P.M.  (1980)  Voltage clamp 
studies on the effects of allethrin and DDT on the sodium channels 
in frog myelinated nerve membrane. In: Insect neurobiology and 
pesticide action (Neutox 79), London, Society of Chemical Industry, 
Vol. 2, pp. 79-85. 

(1973)  DDT-like action of allethrin in the sensory nervous system 
of  Xenopus laevis.  Eur. J. Pharmacol., 21: 95-106. 

Effect of insecticides on the sensory nervous system.  In:  
Narahashi, T., ed. Neurotoxicology of insecticides and pheromones, 
New York, London, Plenum Press, pp. 183-210. 

VANNIER, B. & FOURNEX, R.  (1983)  Deltamethrin detection of a 
mutagenic potency/micronucleus test in the mouse (Proprietary 
unpublished report RU-83607/A, submitted to WHO by Roussel Uclaf). 

VANNIER, B. & GLOMOT, R.  (1977)  RU 22974.  Mutagenic study.  
Dominant lethal assay in the male mouse (Unpublished report TOX 
76533/DB9/A, submitted to WHO by Roussel Uclaf). 

VANNIER, B. & GLOMOT, R.  (1982)  RU 22974 complementary 
teratological study in the mouse (Unpublished report RU-82506-12/A, 
submitted to WHO by Roussel Uclaf). 

VARANKA, I.  (1987)  Effect of mosquito killer insecticides on 
freshwater mussels. Comp. Biochem. Physiol. C. Comp. Pharmacol., 
86: 157-162. 

Decis, in Zweig analytical methods for pesticides and plant growth 
regulators.  Vol XIII, 3: 53-68, New York, Academic Press. 

VERSCHOYLE, R.D. & ALDRIDGE, W.N.  (1980)  Structure-activity 
relationship of some pyrethroids in rats. Arch. Toxicol., 45: 

EDWARDS, J.  (1987a)  The effects of pirimicarb, dimethoate and 
deltamethrin on carabidae and staphylinidae in winter wheat. Meded. 
Fac. Landbouwwet. Rijksuniv. Gent, 52(2a): 

EDWARDS, J.  (1987b)  The effects of pirimicarb, dimethoate and 
deltamethrin on non-target arthropods in winter wheat. 
International Conference on Pests in Agriculture, Paris, 1-3 
December 1987, Annales ANPP, pp. 67-74. 

VIJVERBERG, H.P.M., VAN DEN BECKEN, J.  (1982)  Action of 
pyrethroid insecticides on the vertebrate nervous system.  
Neuropathol. appl. Neurobiol., 8: 421-440. 

VIJVERBERG, H.P.M. & VAN DEN BERCKEN, J.  (1979)  Frequency 
dependent effects of the pyrethroid insecticide decamethrin in frog 
myelinated nerve fibres.  Eur. J. Pharmacol., 58: 501-504. 

Structure-related effects of pyrethroid insecticides on the 
lateral-line sense organ and on peripheral nerves of the clawed 
frog,  Xenopus laevis.  Pestic. Biochem. Physiol., 18: 315-324. 

(1982b)  Similar mode of action of pyrethroids and DDT on sodium 
channel gating in myelinated nerves.  Nature, (Lond.) 295: 601-603. 

DEN BERCKEN, J.  (1983)  Temperature and structure-dependent 
interaction of pyrethroids with the sodium channels in frog node of 
Ranvier.  Biochim.  Biophys. Acta, 728: 73-82. 

WALTERSDORFER & SCHULZE E.F.  (1976a)  Decis 2.5. Effect on 
 Lebistes reticulatus, Francfort, Hoechst Ag, 8 pp. (Unpublished 
proprietary report 42/76, submitted to WHO by Roussel Uclaf). 

WALTERSDORFER & SCHULZE E.F.  (1976b)  Decis 2.5. Effect on  Idus 
 melanotus, Frankfurt, Hoechst AG, 5 pp (Unpublished proprietary 
report 33/76, submitted to WHO by Roussel Uclaf). 

WALTERSDORFER & SCHULZE E.F.  (1976c)  Decis 2.5. Effect on  Salmo 
 gairdneri (rainbow trout), Frankfurt, Hoechst AG, 7 pp (Unpublished 
proprietary report 35/76, submitted to WHO by Roussel Uclaf). 

WALTERSDORFER & SCHULZE E.F.  (1976d)  Decamethrine effect on 
 Lepomis gibbosus (Bluegill sunfish), Frankfurt, Hoechst AG, 6 pp. 
(Unpublished proprietary report 16/77, submitted to WHO by Roussel 

WANG, S., ZHENG, Q., YU, L., XU, B., & LIX., Y.  (1988)  Health 
survey among farmers exposed to deltamethrin in the cotton fields.  
Ecotoxicol. environ. Saf., 15: 1-6. 

WELLCOME FOUNDATION  (1979)  Residues in cow's milk resulting from 
intrarumenal, and later, dermal administration of 14C-labelled 
decamethrin (Unpublished report submitted to WHO by Roussel Uclaf). 

WHO  (1979)  Safe use of pesticides.  Third Report of the WHO 
Expert Committee on Vector Biology and Control, Geneva, World 
Health Organization, pp. 18-23.  (WHO Technical Report Series, 
No. 634). 

WHO  (1988)  The WHO recommended classification of pesticides by 
hazard and guidelines to classification 1988-1989, Geneva, World 
Health Organization (Unpublished document WHO/VBC/88.953). 

WHO  (1989)  Health and Safety Guide No. 30: Deltamethrin, Geneva, 
World Health Organization. 

WHO  (1984) Data sheet on pesticides, No. 50: Deltamethrin, Geneva, 
World Health Organization, 9 pp (Unpublished document 

WOOD MACKENZIE  (1980)  Agrochem. Monit., 9: 12. 

WOOD MACKENZIE  (1981)  Agrochem. Monit., 15: 12. 

WOOD MACKENZIE  (1982)  Agrochem. Monit., 21: 13. 

WOOD MACKENZIE  (1983)  Agrochem. Monit., 27: 3-12. 

WORTHING, C.R. & WALKER, S.B.  (1983)  Pesticide manual, 7th ed., 
Croydon, British Crop Protection Council, p. 161.

WOUTERS, W. & VAN DEN BERCKEN, J. (1978) Action of pyrethroids. 
Gen. Pharmacol., 9: 387-398. 

RAJASEKARAN, D.  (1980)  Three-generation reproduction study in 
rats, Matawan, Michigan, International Research and Development 
Corporation (Unpublished report IDC-406 003/A4. submitted to WHO by 
Roussel Uclaf). 

ZHANG, L.Z., KHAN, S.U., AKHTAR, M.H., & IVARSON, K.C.  (1984)  
Persistence, degradation, and distribution of Deltamethrin in an 
organic soil under laboratory conditions, J. agric. food Chem., 32: 

ZITKO, V., MCLEESE, D.W., METCALFE, C.D., & CARSON, W.G.  (1979)  
Toxicity of permethrin, decamethrin, and related pyrethroids to 
salmon and lobster. Bull. environ. Contam. Toxicol., 21: 338-343. 


    On the basis of electrophysiological studies with peripheral 
nerve preparations of frogs  (Xenopus laevis; Rana temporaria; and 
 Rana esculenta), it is possible to distinguish between 2 classes of 
pyrethroid insecticides: (Type I and Type II).  A similar 
distinction between these 2 classes of pyrethroids has been made on 
the basis of the symptoms of toxicity in mammals and insects (Van 
den Bercken et al., 1979; WHO, 1979; Verschoyle & Aldridge, 1980; 
Glickman & Casida, 1982; Lawrence & Casida, 1982).  The same 
distinction was found in studies on cockroaches (Gammon et al., 

    Based on the binding assay on the gamma-aminobutyric acid 
(GABA) receptor-ionophore complex, synthetic pyrethroids can also 
be classified into two types:  the alpha-cyano-3-phenoxybenzyl 
pyrethroids and the non-cyano pyrethroids (Gammon et al., 1982; 
Gammon & Casida, 1983; Lawrence & Casida, 1983; Lawrence et al., 

    Pyrethroids that do not contain an alpha-cyano group 
(allethrin, d-phenothrin, permethrin, tetramethrin, cismethrin, and 
bioresmethrin) (Type I: T-syndrome) 

    The pyrethroids that do not contain an alpha-cyano group give 
rise to pronounced repetitive activity in sense organs and in 
sensory nerve fibres (Van den Bercken et al., 1973).  At room 
temperature, this repetitive activity usually consists of trains of 
3 - 10 impulses and occasionally up to 25 impulses.  Train duration 
is between 10 and 5 milliseconds. 

    These compounds also induce pronounced repetitive firing of the 
presynaptic motor nerve terminal in the neuromuscular junction (Van 
den Bercken, 1977).  There was no significant effect of the 
insecticide on neurotransmitter release or on the sensitivity of 
the subsynaptic membrane, nor on the muscle fibre membrane.  
Presynaptic repetitive firing was also observed in the sympathetic 
ganglion treated with these pyrethroids. 

    In the lateral-line sense organ and in the motor nerve 
terminal, but not in the cutaneous touch receptor or in sensory 
nerve fibres, the pyrethroid-induced repetitive activity increases 
dramatically as the temperature is lowered, and a decrease of 5 °C 
in temperature may cause a more than 3-fold increase in the number 
of repetitive impulses per train.  This effect is easily reversed 
by raising the temperature.  The origin of this "negative 
temperature coefficient" is not clear (Vijverberg et al., 1983). 

    Synthetic pyrethroids act directly on the axon through 
interference with the sodium channel gating mechanism that 
underlies the generation and conduction of each nerve impulse.  The 
transitional state of the sodium channel is controlled by 2 
separately acting gating mechanisms, referred to as the activation 
gate and the inactivation gate.  Since pyrethroids only appear to 
affect the sodium current during depolarization, the rapid opening  

of the activation gate and the slow closing of the inactivation 
gate proceed normally.  However, once the sodium channel is open, 
the activation gate is restrained in the open position by the 
pyrethroid molecule.  While all pyrethroids have essentially the 
same basic mechanism of action, however, the rate of relaxation 
differs substantially for the various pyrethroids (Flannigan & 
Tucker, 1985). 

    In the isolated node of Ranvier, allethrin causes prolongation 
of the transient increase in sodium permeability of the nerve 
membrane during excitation (Van den Bercken & Vijverberg, 1980).  
Evidence so far available indicates that allethrin selectively 
slows down the closing of the activation gate of a fraction of the 
sodium channels that open during depolarization of the membrane.  
The time constant of closing of the activation gate in the 
allethrin-affected channels is about 100 milliseconds compared with 
less than 100 microseconds in the normal sodium channel, i.e., it 
is slowed down by a factor of more than 100.  This results in a 
marked prolongation of the sodium current across the nerve membrane 
during excitation, and this prolonged sodium current is directly 
responsible for the repetitive activity induced by allethrin 
(Vijverberg et al., 1983). 

    The effects of cismethrin on synaptic transmission in the frog 
neuromuscular junction, as reported by Evans (1976), are almost 
identical to those of allethrin, i.e., presynaptic repetitive 
firing, and no significant effects on transmitter release or on the 
subsynaptic membrane. 

    Interestingly, the action of these pyrethroids closely 
resembles that of the insecticide DDT in the peripheral nervous 
system of the frog.  DDT also causes pronounced repetitive activity 
in sense organs, in sensory nerve fibres, and in motor nerve 
terminals, due to a prolongation of the transient increase in 
sodium permeability of the nerve membrane during excitation.  
Recently was demonstrated that allethrin and DDT have essentially 
the same effect on sodium channels in frog myelinated nerve 
membrane.  Both compounds slow down the rate of closing of a 
fraction of the sodium channels that open on depolarization of the 
membrane (Van den Bercken et al., 1973, 1979; Vijverberg et al., 

    In the electrophysiological experiments using giant axons of 
crayfish, the type I pyrethroids and DDT analogues retain sodium 
channels in a modified open state only intermittantly, cause large 
depolarizing afterpotentials, and evoke repetitive firing with 
minimal effect on the resting potential (Lund & Narahashi, 1983). 

    These results strongly suggest that permethrin and cismethrin, 
like allethrin, primarily affect the sodium channels in the nerve 
membrane and cause a prolongation of the transient increase in 
sodium permeability of the membrane during excitation. 

    The effects of pyrethroids on end-plate and muscle action 
potentials were studied in the pectoralis nerve-muscle preparation 
of the clawed frog  (Xenopus laevis).  Type I pyrethroids 
(allethrin, cismethrin, bioresmethrin, and 1R,  cis-phenothrin) 
caused moderate presynaptic repetitive activity, resulting in the 
occurrence of multiple end-plate potentials (Ruigt & Van den 
Bercken, 1986). 

    Pyrethroids with an alpha-cyano group on the 3-phenoxybenzyl 
alcohol (deltamethrin, cypermethrin, fenvalerate, and fenpropanate) 
(Type II: CS-syndrome) 

    The pyrethroids with an alpha-cyano group cause an intense 
repetitive activity in the lateral line organ in the form of long-
lasting trains of impulses (Vijverberg et al., 1982a).  Such a 
train may last for up to 1 min and contains thousands of impulses.  
The duration of the trains and the number of impulses per train 
increase markedly on lowering the temperature.  Cypermethrin does 
not cause repetitive activity in myelinated nerve fibres.  Instead, 
this pyrethroid causes a frequency-dependent depression of the 
nervous impulse, brought about by a progressive depolarization of 
the nerve membrane as a result of the summation of depolarizing 
after-potentials during train stimulation (Vijverberg & Van den 
Bercken, 1979; Vijverberg et al., 1983). 

    In the isolated node of Ranvier, cypermethrin, like allethrin, 
specifically affects the sodium channels of the nerve membrane and 
causes a long-lasting prolongation of the transient increase in 
sodium permeability during excitation, presumably by slowing down 
the closing of the activation gate of the sodium channel 
(Vijverberg & Van den Bercken, 1979; Vijverberg et al., 1983).  The 
time constant of closing of the activation gate in the 
cypermethrin-affected channels is prolonged to more than 100 
milliseconds.  Apparently, the amplitude of the prolonged sodium 
current after cypermethrin is too small to induce repetitive 
activity in nerve fibres, but is sufficient to cause the long-
lasting repetitive firing in the lateral-line sense organ. 

    These results suggest that alpha-cyano pyrethroids primarily 
affect the sodium channels in the nerve membrane and cause a long-
lasting prolongation of the transient increase in sodium 
permeability of the membrane during excitation. 

    In the electrophysiological experiments using giant axons of 
cray-fish, the Type II pyrethroids retain sodium channels in a 
modified continuous open state persistently, depolarize the 
membrane, and block the action potential without causing repetitive 
firing (Lund & Narahashi, 1983). 

    Diazepam, which facilitates GABA reaction, delayed the onset of 
action of deltamethrin and fenvalerate, but not permethrin and 
allethrin, in both the mouse and cockroach.  Possible mechanisms of 
the Type II pyrethroid syndrome include action at the GABA receptor 
complex or a closely linked class of neuroreceptor (Gammon et al., 

    The Type II syndrome of intracerebrally administered pyrethroids
closely approximates that of the convulsant picrotoxin (PTX). 
Deltamethrin inhibits the binding of [3H]-dihydropicrotoxin to rat
brain synaptic membranes, whereas the non-toxic R epimer of
deltamethrin is inactive.  These findings suggest a possible
relation between the Type II pyrethroid action and the GABA receptor
complex.  The stereospecific correlation  between  the  toxicity of 
Type II  pyrethroids  and  their potency to inhibit the [35S]-TBPS
binding was established using a radioligand, 
[35S]- t-butyl-bicyclophosphorothionate [35S]-TBPS.  Studies
with 37 pyrethroids revealed an absolute correlation, without any
false positive or negative, between mouse intracerebral toxicity and
in vitro inhibition:  all toxic cyano compounds including 
deltamethrin, 1R, cis-cypermethrin, 1R, trans-cypermethrin, and
[2S, alpha S]-fenvalerate were inhibitors, but their non-toxic 
stereoisomers were not; non-cyano pyrethroids were much less potent 
or were inactive (Lawrence & Casida, 1983). 

    In the [35S]-TBPS and [3H]-Ro 5-4864 (a convulsant benzo-
diazepine radioligand) binding assay, the inhibitory potencies of 
pyrethroids were closely related to their mammalian toxicities.  
The most toxic pyrethroids of Type II were the most potent 
inhibitors of [3H]-Ro 5-4864 specific binding to rat brain 
membranes.  The [3H]-dihydropicrotoxin and [35S]-TBPS binding 
studies with pyrethroids strongly indicated that Type II effects of 
pyrethroids are mediated, at least in part, through an interaction 
with a GABA-regulated chloride ionophore-associated binding site.  
Moreover, studies with [3H]-Ro 5-4864 support this hypothesis and, 
in addition, indicate that the pyrethroid-binding site may be very 
closely related to the convulsant benzodiazepine site of action 
(Lawrence et al., 1985). 

    The Type II pyrethroids (deltamethrin, 1R,  cis-cypermethrin and 
[2S, alphaS]-fenvalerate) increased the input resistance of 
crayfish claw opener muscle fibres bathed in GABA.  In contrast, 
two non-insecticidal stereoisomers and Type I pyrethroids 
(permethrin, resmethrin, allethrin) were inactive.  Therefore, 
cyanophenoxybenzyl pyrethroids appear to act on the GABA receptor-
ionophore complex (Gammon & Casida, 1983). 

    The effects of pyrethroids on end-plate and muscle action 
potentials were studied in the pectoralis nerve-muscle preparation 
of the clawed frog  (Xenopus laevis).  Type II pyrethroids 
(cypermethrin and deltamethrin) induced trains of repetitive muscle 
action potentials without presynaptic repetitive activity.  
However, an intermediate group of pyrethroids (1R-permethrin, 
cyphenothrin, and fenvalerate) caused both types of effect.  Thus, 
in muscle or nerve membrane the pyrethroid induced repetitive 
activities due to a prolongation of the sodium current.  But no 
clear distinction was observed between non-cyano and alpha-cyano 
pyrethroids (Ruigt & Van den Bercken, 1986). 


    In summary, the results strongly suggest that the primary 
target site of pyrethroid insecticides in the vertebrate nervous 
system is the sodium channel in the nerve membrane.  Pyrethroids 
without an alpha-cyano group (allethrin, d-phenothrin, permethrin, 
and cismethrin) cause a moderate prolongation of the transient 
increase in sodium permeability of the nerve membrane during 
excitation.  This results in relatively short trains of repetitive 
nerve impulses in sense organs, sensory (afferent) nerve fibres, 
and, in effect, nerve terminals.  On the other hand, the alpha-
cyano pyrethroids cause a long-lasting prolongation of the 
transient increase in sodium permeability of the nerve membrane 
during excitation.  This results in long-lasting trains of 
repetitive impulses in sense organs and a frequency-dependent 
depression of the nerve impulse in nerve fibres.  The difference in 
effects between permethrin and cypermethrin, which have identical 
molecular structures except for the presence of an alpha-cyano 
group on the phenoxybenzyl alcohol, indicates that it is this 
alpha-cyano group that is responsible for the long-lasting 
prolongation of the sodium permeability. 

    Since the mechanisms responsible for nerve impulse generation 
and conduction are basically the same throughout the entire nervous 
system, pyrethroids may also induce repetitive activity in various 
parts of the brain.  The difference in symptoms of poisoning by 
alpha-cyano pyrethroids, compared with the classical pyrethroids, 
is not necessarily due to an exclusive central site of action.  

    It may be related to the long-lasting repetitive activity in 
sense organs and possibly in other parts of the nervous system, 
which, in a more advance state of poisoning, may be accompanied by 
a frequency-dependent depression of the nervous impulse. 

    Pyrethroids also cause pronounced repetitive activity and a 
prolongation of the transient increase in sodium permeability of 
the nerve membrane in insects and other invertebrates.  Available 
information indicates that the sodium channel in the nerve membrane 
is also the most important target site of pyrethroids in the 
invertebrate nervous system (Wouters & Van den Bercken, 1978; WHO, 

    Because of the universal character of the processes underlying 
nerve excitability, the action of pyrethroids should not be 
considered restricted to particular animal species, or to a certain 
region of the nervous system.  Although it has been established 
that sense organs and nerve endings are the most vulnerable to the 
action of pyrethroids, the ultimate lesion that causes death will 
depend on the animal species, environmental conditions, and on the 
chemical structure and physical characteristics of the pyrethroid 
molecule (Vijverberg & Van den Bercken, 1982). 


1.1  Résumé et évaluation

1.1.1  Identité, propriétés physiques et chimiques, méthodes 

    La deltaméthrine a été synthétisée en 1974 et commercialisée 
pour la première fois en 1977.  Sur le plan chimique, c'est un 
ester de l'analogue dibromé de l'acide chrysanthémique (acide 
diméthyl-2,2(dimbromo-2,2 vinyl)-3 cyclopropanecarboxylique) 
(Br2CA) et de l'alcol alpha-cyano-phénoxy-3 benzylique; plus 
précisément, c'est l'isomère [1R, cis;alpha S] parmi les huit 
stéréoisomères que compte cet ester. 

    La deltaméthrine de qualité technique se présente sous la forme 
d'une poudre blanche inodore dont le point de fusion est de 98 - 
101 °C et qui contient plus de 98% de deltaméthrine.  Sa tension de
vapeur est de 2,0 x 10-6 Pa à 25 °C; autrement dit, elle n'est
pratiquement pas volatile.  Insoluble dans l'eau, elle est en 
revanche soluble dans des solvants organiques tels que l'acétone, la
cyclohexanone et le xylène.  Elle est stable à la lumière, à la 
chaleur et à l'air, mais instable en milieu alcalin. 

    Pour doser les résidus et analyser des échantillons prélevés 
dans l'environnement, on procède à une extraction par solvant au 
moyen d'un mélange  n-hexane/acétone, à un partage entre le 
 n-hexane, l'acétone et l'eau, suivi d'une purification par 
chromatographie sur colonne de gel de silice, le dosage final 
s'effectuant par chromatographie en phase gazeuse avec détection 
par capture d'électrons.  La concentration minimale décelable par 
cette méthode est de 0,01 mg/kg, voire moins.  L'analyse des 
produits s'effectue par chromatographie en phase liquide à haute 
performance avec détecteur UV. 

1.1.2  Production et usage

    En 1987, la consommation mondiale de deltaméthrine était 
d'environ 250 tonnes.  On l'utilise essentiellement pour traiter le 
coton (45% de la consommation) ainsi que pour les cultures telles 
que le café, le maïs, les céréales, les fruits, les légumes, le 
houblon et les produits stockés.  On l'utilise aussi pour l'hygiène 
des animaux, la lutte contre les vecteurs ainsi qu'à des fins de 
santé publique.  On l'applique soit seule, soit associée à d'autres 
pesticides en formulations telles que concentrés émulsionnables, 
concentrés pour pulvérisation à très bas volume, poudres 
mouillables, concentrés pour suspension, poudres pour poudrage, etc.

1.1.3  Exposition humaine

    L'exposition de la population dans son ensemble provient 
principalement de la présence de résidus alimentaires mais peut 
également résulter de son utilisation en santé publique.  Sur les 
récoltes correctement traitées, le taux de résidus est généralement 

très faible sauf lorsque le traitement a eu lieu après la récolte.  
La FAO et l'OMS ont passé en revue de nombreuses données sur ces 

    L'exposition de la population dans son ensemble est vrai- 
semblablement très faible, mais on manque de données effectives 
découlant d'études sur la ration alimentaire totale. 

1.1.4  Exposition et destinée dans l'environnement

    En exposant à la lumière solaire une fine pellicule de 
deltaméthrine [1R,  cis; alpha S] marquée au C14 au niveau de la 
fonction acide, de la fonction alcool ou du groupe cyano, pendant 4 
à 8 heures, on a constaté que 70 % du produit était transformé en 
isomères [1R,  trans alpha S] et [1S,  trans alpha S] par 
isomérisation  cis/trans, accompagnés des produits de clivage de 
l'ester, en particulier l'acide diméthyl-2,2(dibromovinyl-2,2)-3 
cyclo-propane-carboxylique et l'alcool alpha-cyano-phénoxy-3 

    La deltaméthrine présente sur des plants de coton en serre se 
dégrade avec une demi-vie initiale de 1,1 semaine, le taux de 
dégradation étant de 90 % au bout de 4,5 semaines. 

    Les principaux métabolites consistent en Br2CA libre et 
conjugué, en  trans-hydroxyméthyl-Br2CA et en acide (hydroxy-4 
phénoxy)-3 benzoïque résultant du clivage de l'ester, d'une 
oxydation et d'une conjugaison. 

    Après avoir fait incuber de deltaméthrine dans du sable et du 
terreau à 28 °C dans les conditions du laboratoire, on en a 
récupéré respectivement 52 % et 74 %, huit semaines après ce 

    La deltaméthrine ne se déplace pas dans l'environnement du fait 
qu'elle est fortement adsorbée sur les particules, qu'elle est 
insoluble dans l'eau et qu'elle est appliquée à très faibles doses. 

    On ne dispose pas de données sur les concentrations effectives 
dans l'environnement, mais compte tenu des modalités actuelles 
d'utilisation et pour peu que l'insecticide soit utilisé 
normalement, l'exposition environnementale devrait être très 
faible.  La deltaméthrine se dégrade rapidement en produits moins 

1.1.5   Absorption, métabolisme et excrétion

    Administrée par voie orale, la deltraméthrine est facilement 
absorbée; l'absorption est moindre par la voie percutanée encore 
que sa vitesse dépende fortement du véhicule ou du solvant utilisé.  
Une fois absorbée, la deltaméthrine est rapidement métabolisée et 

    On a administré à des rats par voie orale, à raison de 0,64 à 
1,60 mg/kg, de la deltaméthrine marquée au carbone-14 au niveau des 
fonctions acide, alcool et nitrile; le radiocarbone provenant de 
la fraction acide et de la fraction alcoolique a été complètement 
éliminé en l'espace de 2 à 4 jours.  Les taux de résidus 
tissulaires étaient généralement faibles sauf dans les graisses où 
ils étaient un peu plus élevés.  Cependant, le reste nitrile a été 
excrété plus lentement, le taux global de récupération étant de 
79 % en huit jours.  Les principales réactions métaboliques étaient 
l'oxydation (au niveau du méthyl- trans, du cycle cyclopropane et 
des positions 2', 4' et 5' du reste alcoolique), le clivage de 
l'ester et la conversion du nitrile en thiocyanate.  Les acides 
carboxyliques et les phénols résultants étaient conjugués à l'acide 
sulfurique, à la glycine et à l'acide glucuronique. 

    Après avoir administré par voie orale à des souris de la 
deltaméthrine marquée au 14C au niveau des fonctions acide, alcool 
et nitrile à raison de 1,7 et 4,4 mg/kg, on a constaté que 
l'excrétion du radiocarbone s'effectuait rapidement sauf dans le 
cas du reste nitrile.  Les principales réactions métaboliques 
étaient en général analogues chez les souris et chez les rats. 

    Chez les vaches et la volaille, les voies de dégradation sont 
tout à fait analogues à celles des rongeurs. 

1.1.6  Effets sur les êtres vivants dans leur milieu naturel

    La deltaméthrine est extrêmement toxique pour les poissons, la 
CL50 à 96 heures allant de 0,4 à 2,0 µg/litre.  Elle est également 
très toxique pour les invertébrés aquatiques;  pour la daphnie, la 
CL50 à 48 heures est de 5 µg/litre.  Toutefois des études 
approfondies sur des étangs expérimentaux ainsi que les résultats 
de l'utilisation en plein champ ont montré que cette forte toxicité 
potentielle était inopérante.  On a observé sur le terrain une 
certaine mortalité parmi les invertébrés aquatiques mais les 
populations se reconstituent généralement assez vite. 

    pour les oiseaux, la toxicité de la deltaméthrine est très 
faible, les valeurs de la DL50 pour une dose unique par voie orale 
étant supérieure à 1000 mg/kg.  Au laboratoire, la deltaméthrine 
est très toxique pour les abeilles, avec une DL50 de contact de 
0,051 µg/abeille.  Les essais en situation réelle et l'expérience 
acquise dans l'utilisation effective du produit ont montré que les 
formulations de deltaméthrine exerçaient une action répulsive, ce 
qui signifie qu'en pratique le danger pour les abeilles est très 

1.1.7  Effets sur les animaux d'expérience et systemes d'epreuve 
 in vitro

    Dans un véhicule non aqueux, la deltaméthrine présente une 
toxicité aiguë par voie orale forte à modérée avec des DL50 de 19 à 
34mg/kg chez la souris et de 39 à 139 mg/kg chez le rat.  
Toutefois, en suspension dans l'eau, la toxicité est bien moidre, 
les valeurs de la DL50 dépassant 5000 mg/kg chez le rat.  La 
deltaméthrine est un pyréthroide du Type II.  Les signes cliniques 

d'intoxication consistent en tremblements, salivation et  
convulsions.  L'intoxication est rapide et chez les survivants, les 
signes disparaissent en quelques jours.  L'électro-encéphalogramme 
présente des décharges pointes-ondes généralisées qui précèdent 
la choréo-athétose. 

    Une seule application de deltaméthrine technique n'a pas 
produit d'effets irritants sur la peau intacte ou abrasée du lapin.  
Toutefois elle a produit de effets irritants passagers au niveau de 
l'oeil avec ou sans rinçage.  La deltaméthrine n'a pas d'effet 
sensibilisateur cutané chez le cobaye. 

    En administrant à des rats par gavage de la deltaméthrine à des 
doses quotidiennes allant jusqu'à 10 mg/kg de poids corporel 
pendant 13 semaines, on a provoqué chez ces animaux une  
hyperexcitabilité qui se manifestait au bout de six semaines chez 
les mâles recevant la dose la plus forte.  Aux doses de 2,5 et 
10 mg/kg, le gain de poids a été plus faible chez les mâles. 

    Chez des chiens beagle qui avaient reçu par voie orale de la 
deltaméthrine en doses quotidiennes allant jusqu'à 10 mg/kg de 
poids corporel pendant 13 semaines, on a observé divers symptômes 
liés à cette substance, tels que des vomissements, des 
tremblements, de la salivation et un affaiblissement du réflexe 
pharyngé, du réflexe rotulien et du réflexe de flexion.  Lors d'une 
étude d'alimentation de deux ans sur des chiens, on a constaté que 
la dose sans effet observable se situait à 1 mg/kg de poids 
corporel par jour (dose la plus forte expérimentée). 

    L'administration de deltraméthrine à des souris à des doses 
atteingnant 100 mg/kg de nourriture pendant 24 mois n'a pas modifié 
l'incidence des tumeurs.  La dose sans effet observé relative à la 
toxicité générale était de 100 mg/kg de nourriture. 

    Chez des rats à qui l'on avait administré de la deltaméthrine 
en doses allant jusqu'à 50 mg/kg de nourriture pendant deux ans, on 
n'a observé aucune tumeur attribuable à cette substance.  La dose 
sans effet observé relative à la toxicité générale était de 5 mg/kg 
de nourriture. 

    La deltaméthrine ne s'est pas révélée mutagène dans divers 
systèmes d'épreuve  in vivo et  in vitro; notamment la réparation de 
l'ADN, la mutation génique, les aberrations chromosomiques, 
l'échange entre chromatides-soeurs, la formation de micronoyaux et 
la létalité dominante. 

    Des études de tératogénicité ont été effectuées chez des rates 
et des souris gravides à qui l'on administrait par voie orale des 
doses quotidiennes de deltaméthrine allant jusqu'à 1000 mg/kg  
pendant la phase principale de l'organogénèse.  On n'a constaté 
aucun effet tératogène ni altération de la fonction de reproduction 
chez ces rates et ces souris, si ce n'est une réduction, liée à la 
dose, dans le poids moyen des foetus chez les souris et un léger 
retard d'ossification chez les rats. 

    Des lapines gravides ont reçu au sixième et dix-neuvième jours 
de leur grossesse des doses quotidiennes de deltaméthrine allant 
jusqu'à 16 mg/kg.  A la dose la plus forte, on a noté une réduction 
du poids moyen des foetus.  Aucun effet tératogène n'a été observé 
chez les lapins. 

    Après administration de deltaméthrine à des rats à des doses 
allant jusqu'à 5 mg/kg de nourriture, dans le but d'effectuer une 
étude de reproduction sur trois générations et deux portées, on a 
constaté l'absence totale de tout effet. 

    Il existe certains indices selon lesquels l'association de 
delta- méthrine à certains composés organophosphorés pourrai 
conduire à une potentialisation de la toxicité de ces produits. 

1.1.8  Effets sur l'homme

    La deltaméthrine peut provoquer certaines sensations cutanées 
chez des travailleurs exposés.  Plusieurs cas d'intoxication 
professionnelle non mortelle ont été signalés qui étaient dus à 
l'inobservation des mesures de sécurité.  Un engourdissement, un 
prurit, des fourmillements et une sensation de brûlure de la peau 
ainsi que des vertiges sont des symptômes fréquemment signalés.  On 
a décrit occasionnellement un érythème papulaire ou une couperose à 
caractère passager.  La plupart de ces symptômes sont passagers et 
disparaissent en cinq à sept jours.  Aucun effet indésirable à long 
terme n'a été signalé.  On a décrit trois cas d'empoisonnement non 
mortel par la deltamétrine à la suite de l'ingestion de plusieurs 
grammes de ce produit. 

1.2  Conclusions

 Population générale:  l'exposition de la population générale à la 
deltaméthrine est vraisemblablement très faible et ce produit, 
lorsqu'il est utilisé conformément aux recommandations, ne présente 
probablement aucun risque. 

 Exposition professionnelle:  moyennant de bonnes méthodes de 
travail et l'application de mesures d'hygiène et de sécurité, la 
deltaméthrine ne devrait pas présenter de danger pour les personnes 
qui y sont exposées de par leur profession. 

 Environnement:  Utilisée aux doses recommandées, il est improbable 
que la deltaméthrine ou ses produits de dégradation s'accumulent au 
point d'avoir des effets nocifs sur l'environnement.  Au 
laboratoire, la deltaméthrine est très toxique pour les poissons, 
les arthropodes aquatiques et les abeilles.  Toutefois, sur le 
terrain, il est peu probable que le produit ait des effets nocifs 
s'il est utilisé conformément aux recommandations. 

1.3  Recommandations

    Bien que les teneurs dans les aliments soient très faibles 
lorsque la deltaméthrine est utilisée conformément aux 
recommandations, il est souhaitable de s'en assurer en soumettant 
la deltaméthrine à une surveillance. 

    La deltaméthrine est utilisée depuis de nombreuses années et 
l'on signale un certain nombre de cas d'intoxications non mortelles 
ainsi que des effets passagers par suite d'exposition 
professionnelle.  Il est souhaitable que l'exposition humaine 
continue d'être surveillée. 


1.1  Resumen y evaluación

1.1.1  Identidad, propiedades fíisicas y químicas, métodos de

    La deltametrina fue sintetizada en 1974 y se comercializó por 
primera vez en 1977.  Químicamente, es el isómero [1R, cis; S] de 8
ésteres estereoisoméricos del análogo dibromo del ácido 
crisantémico, ácido 2,2-dimetil-3-(2,2-dibromovinil) ciclopro- 
panocarboxílico (Br2CA) con alcohol alpha-ciano-3-fenoxibencílico.

    La deltametrina de calidad técnica es un polvo blanco inodoro 
con un punto de fusión de 98 - 101 °C y contiene más del 98% del 
material.  La presión del vapor es 2,0 x 10-6 Pa a 25 °C y es 
prácticamente no volátil.  Es insoluble en agua, pero soluble en 
disolventes orgánicos como la acetona, la ciclohexanona y el 
xileno.  Es estable a la luz, el calor y el aire, pero inestable en 
medios alcalinos. 

    La determinación de la presencia de residuos y el análisis de 
muestras ambientales se efectuaron por extracción con los 
disolventes  n-hexano/acetona, partición con  n-hexano/acetona/agua, 
absorción con un cromatógrafo de columna de gel de sílice y 
determinación con un cromatógrafo de fase gaseosa equipado con un 
detector de captura de electrones con una concentración mínima 
detectable de 0,01 mg/kg o menos.  Para el análisis de productos se 
utiliza la cromatografía de fase líquida de alto rendimiento con un 
detector de rayos UV. 

1.1.2  Producción y empleo

    El consumo mundial de deltametrina era de 250 toneladas 
aproximadamente en 1987.  La deltametrina se utiliza sobre todo en 
el algodón (45% del consumo), en cultivos como el café, el maíz, 
los cereales, la fruta, las hortalizas y el lúpulo, y en productos 
almacenados.  Se emplea también en higiene animal, en la lucha 
contra los vectores y en salud pública.  Se fabrica como solución 
concentrada emulsionable, solución concentrada de pequeñísimo 
volumen, polvo humectable, solución concentrada en suspensión y 
polvo para utilización en seco, sola o en combinación con otros 

1.1.3  Exposición humana

    La exposición de la población en general a la deltametrina 
procede principalmente de residuos en la dieta, pero puede resultar 
también de su empleo en salud pública.  En los cultivos tratados de 
acuerdo con buenas prácticas agrícolas, las concentraciones 
residuales son por lo general muy bajas, excepto en caso de 
tratamiento después de la recolección.  La FAO y la OMS han 
examinado abundantes datos al respecto. 

    Se cree que la exposición de la población en general es muy 
baja, pero no se dispone de datos en forma de estudios de dietas 

1.1.4  Exposición ambiental y evolución

    Cuando la deltametrina-[1R, cis; alpha S] marcada con 
C14-(compuesto irradiado ácido, alcohol o ciano) se expuso a la 
luz del sol en forma de una película fina durante 4 a 8 horas, el 
70% se transformó por isomerización- cis/trans produciendo los 
isómeros [1R, trans; alpha S] y [1S, trans; alpha S], junto con 
productos de la escisión de los ésteres, entre ellos Br2CA y 
alcohol alpha-ciano-3-fenoxibencílico. 

    La deltametrina se degradó en las plantas de algodón, en 
condiciones de invernadero, con una vida media inicial de 1,1 
semanas, y el tiempo necesario para una pérdida del 90% fue de 4,6 

    Los principales metabolitos fueron Br2CA libre y combinado, 
 trans-hidroximetil-Br2CA y ácido 3-(4-hidroxifenoxi)benzoico, 
formados por la escisión, la oxidación y la combinación de los 

    La deltametrina se incubó en arena y mantillo orgánico a 28 °C 
en condiciones de laboratorio.  Ocho semanas después del 
tratamiento, se recuperó de la arena y del mantillo orgánico 
alrededor del 52% y el 74%, respectivamente, de la deltametrina 

    La deltametrina no es móvil en el medio debido a su fuerte 
adsorción en las partículas, su insolubilidad en el agua y sus 
tasas muy bajas de aplicación. 

    No se dispone de datos sobre las concentraciones existentes en 
el medio pero, dadas las modalidades actuales de uso y en 
condiciones normales, es de esperar que la exposición ambiental sea 
muy baja.  Se degrada rápidamente, convirtiéndose en productos 
menos tóxicos. 

1.1.5  Ingestion, metabolismo y excreción

    La deltametrina se absorbe fácilmente por vía oral y con menor 
facilidad por la piel, pero la tasa de absorción depende 
considerablemente del portador o disolvente.  La deltametrina 
absorbida se metaboliza y se excreta fácilmente. 

    En la administración por vía oral a ratas de deltametrina 
marcada con C14-(compuesto irradiado ácido, alcohol o ciano), a 
tasas de 0,64 - 1,60 mg/kg, el radiocarbono de las partes ácido y 
alcohol se eliminó casi por completo en 2 - 4 días.  Las 
concentraciones residuales en los tejidos fueron por lo general muy 
bajas, excepto en la grasa, en donde fueron ligeramente más altas.  
Sin embargo, la parte ciano se excretó más lentamente, con una 
recuperación total del 79% en 8 días.  Las principales reacciones 

metabólicas fueron oxidación (en el  trans-metilo del anillo de 
ciclopropano y en las posiciones 2'-, 4'-, y 5 de la parte 
alcohol), escisión de ésteres y conversión de la parte ciano en 
tiocianato.  Los ácidos carboxílicos y fenoles resultantes se 
combinaron con ácido sulfúrico, glicocola y ácido glucurónico. 

    Cuando se administró a ratones C14-(compuesto irradiado ácido, 
alcohol o ciano)-deltametrina por vía oral, a tasas de 1,7 - 4,4 
mg/kg, la excreción del radiocarbono fue rápida y casi total, 
excepto en la parte ciano.  Las principales reacciones metabólicas 
observadas en los ratones fueron en general semejantes a las 
observadas en las ratas. 

    En el ganado vacuno y las aves de corral, las vías de 
degradación son muy similares a las observadas en los roedores. 

1.1.6  Efectos en los organismos presentes en el medio

    La deltametrina es muy tóxica para los peces, ya que la CL50 en 
96 horas oscila entre 0,4 y 2,0 µg/litro.  Es también muy tóxica 
para los invertebrados acuáticos:  la CL50 en 48 horas para  Daphnia 
es de 5 µg/litro.  Sin embargo, extensos estudios realizados en 
estanques experimentales y el empleo sobre el terreno han 
demostrado que esa elevada toxicidad potencial no llega a 
concretarse.  En la práctica hay algunas muertes de invertebrados 
acuáticos que, por lo general, se compensan con rapidez. 

    La toxicidad de la deltametrina en las aves es muy baja, con 
valores de la DL50 superiores a 1000 mg/kg cuando se administra una 
sola dosis por vía oral.  En condiciones de laboratorio, la 
deltametrina es muy tóxica para las abejas, con una DL50 por 
contacto de 0,051 µg/abeja.  Los ensayos sobre el terreno y el 
empleo no experimental han demostrado que los preparados de 
deltametrina tienen una acción repelente, lo cual quiere decir que, 
en la práctica, el riesgo para las abejas es escaso. 

1.1.7  Efectos en animales experimentales y en sistemas de pruebas 
 in vitro

    En un vehículo no acuoso, la toxicidad de la deltametrina 
administrada por vía oral en forma aguda va de alta a moderada, con 
DL50 de 19 a 34 mg/kg (ratones) y de 31 a 139 mg/kg (ratas).  Sin 
embargo, cuando la deltametrina está en suspensión en agua, su 
toxicidad es mucho menor con DL50 superiores a 5000 mg/kg (ratas).  
La deltametrina es un piretroide de tipo II; los signos clínicos 
comprenden temblor, salivación y convulsiones.  La intoxicación se 
presenta rápidamente y, en los supervivientes, los signos 
desaparecen en unos días.  El electroencefalograma muestra 
descargas generalizadas en picos y ondas, seguidas de 

    Aplicaciones únicas de deltametrina técnica no tuvieron ningún 
efecto irritante en la piel, intacta o con abrasiones, de conejos.  
Sin embargo, se observaron efectos irritantes transitorios en los 
ojos de conejos, con y sin lavado.  La deltametrina no actuó como 
sensibilizante dérmico en cobayas. 

    En ratas a las que se administró deltametrina con sonda, en 
dosis de hasta 10,0 mg/kg de peso corporal diarios durante 13 
semanas, a las 6 semanas se observó hiperexcitabilidad en los 
machos que habían recibido la dosis más alta.  El aumento del peso 
corporal en los machos fue menor con dosis de 2,5 y 10 mg/kg. 

    En perros de la raza beagle a los que se administró por vía 
oral deltametrina en dosis de hasta 10 mg/kg de peso corporal 
diarios durante 13 semanas, se observaron varios síntomas 
relacionados con el compuesto, como vómitos, temblor, salivación y 
reflejos faríngeo, patelar y flexor deprimidos.  En un estudio de 
alimentación en perros, de dos años de duración, la dosis 
desprovista de efectos fue de 1 mg/kg de peso corporal diario 
(dosis más alta estudiada). 

    En ratones a los que se administró deltametrina en dosis de 
hasta 100 mg/kg de alimentos durante 24 meses, no resultó afectada 
la incidencia de tumores.  En cuanto a la toxicidad general, la 
dosis desprovista de efectos fue de 100 mg/kg de alimentos. 

    En ratas a las que se administró deltametrina a niveles de 
hasta 50 mg/kg de alimentos durante dos años, no se observaron 
tumores relacionados con el compuesto.  La concentración 
desprovista de efectos de la toxicidad general fue de 50 mg/kg de 

    No se observaron efectos mutagénicos de la deltametrina en una 
multitud de sistemas de pruebas  in vivo e  in vitro, incluidos:  
reparación del ADN, mutación génica, aberración cromosómica, 
intercambio de cromátidas hermanas, formación de micronúcleos y 
genes letales dominantes. 

    Se realizaron estudios teratológicos con ratas y ratonas 
preñadas, administrando deltametrina por vía oral en dosis de hasta 
10 mg/kg diarias durante el periodo de mayor organogénesis.  No se 
observaron efectos teratogénicos ni reproductivos en las ratas ni 
en las ratonas, excepto una disminución, relacionada con la dosis, 
del peso fetal medio en el estudio con ratonas y una osificación 
ligeramente retrasada en el estudio con ratas. 

    Se administró a conejas deltametrina en dosis de hasta 16 mg/kg 
diarios entre los días 6 y 19 del embarazo.  Con la dosis más alta, 
se registró una disminución del peso fetal medio.  No se observaron 
efectos teratogénicos. 

    Se administró a ratas deltametrina en dosis de hasta 50 mg/kg 
de alimentos en un estudio sobre reproducción con tres generaciones 
y dos camadas, sin que se observaran efectos sobre la reproducción. 

    Hay indicios de que la toxicidad puede potenciarse cuando la 
deltametrina se combina con algunos compuestos organofosforados. 

1.1.8  Efectos en los seres humanos

    La deltametrina puede provocar sensaciones cutáneas en los 
trabajadores expuestos.  Se han notificado varios casos de 
intoxicación no mortal debidos a exposición ocupacional por no 
respetar las precauciones de seguridad.  Son síntomas 
frecuentemente mencionados adormecimiento, picor, hormigueo y 
quemazón de la piel, y vértigo.  En ocasiones se ha descrito un 
eritema papular o maculoso.  La mayor parte de esos síntomas son 
temporales y desaparecen en 5 ó 7 días.  No se han comunicado 
efectos negativos a largo plazo.  Se han descrito tres casos no 
mortales de intoxicación por deltametrina tras la ingestión de 
varios gramos del producto. 

1.2  Conclusiones

 Población en general:  No es probable que la exposición de la 
población en general a la deltametrina, que se cree muy baja, 
represente un riesgo en las condiciones de empleo recomendadas. 

 Exposición ocupacional:  Si se aplican buenas prácticas laborales, 
medidas de higiene y precauciones de seguridad, no es probable que 
la deltametrina represente un riesgo para las personas 
ocupacionalmente expuestas a ella. 

 Medio ambiente:  Es improbable que la deltametrina o los productos 
de su degradación alcancen niveles que puedan tener efectos 
negativos en el medio con las tasas de aplicación recomendadas.  En 
condiciones de laboratorio, la deltametrina es muy tóxica para los 
peces, los artrópodos acuáticos y las abejas.  No obstante, en la 
práctica, no es probable que haya efectos perjudiciales duraderos 
con las condiciones de empleo recomendadas. 

1.3  Recomendaciones

    Aunque se cree que con el uso recomendado las concentraciones 
en la dieta son muy bajas, debe considerarse la conveniencia de 
confirmarlo incluyendo la deltametrina en estudios de vigilancia. 

    La deltametrina se utiliza desde hace muchos años y se han 
notificado varios casos de intoxicación no mortal y efectos 
transitorios debidos a exposición ocupacional.  Debe mantenerse la 
observación de la exposición humana. 


    See Also:
       Toxicological Abbreviations
       Deltamethrin (HSG 30, 1989)
       Deltamethrin (ICSC)
       DELTAMETHRIN (JECFA Evaluation)
       Deltamethrin (Pesticide residues in food: 1980 evaluations)
       Deltamethrin (Pesticide residues in food: 1981 evaluations)
       Deltamethrin (Pesticide residues in food: 1982 evaluations)
       Deltamethrin (Pesticide residues in food: 1984 evaluations)
       Deltamethrin (JMPR Evaluations 2000 Part II Toxicological)
       Deltamethrin (UKPID)
       Deltamethrin (IARC Summary & Evaluation, Volume 53, 1991)