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    World Health Orgnization
    Geneva, 1984

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     1.1. Summary
          1.1.1. Identity, properties and analytical methods
          1.1.2. Uses and sources of exposure; population at risk
          1.1.3. Environmental concentrations and exposures
          1.1.4. Kinetics and metabolism
          1.1.5. Studies on experimental animals
          1.1.6. Effects on man
     1.2. Recommendations


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


     3.1. Production and uses
     3.2. Transport and distribution
     3.3. Abiotic degradation
     3.4. Biodegradation


     4.1. Environmental levels
     4.2. General population exposure


     5.1. Absorption
     5.2. Distribution and storage
     5.3. Metabolism
     5.4. Excretion


     6.1. Single dose studies
     6.2. Short-term studies
          6.2.1. Oral exposure
          6.2.2. Dermal exposure
     6.3. Long-term and carcinogenicity studies
     6.4. Reproduction and teratogenicity studies
     6.5. Mutagenicity
     6.6. Other studies



     8.1. Aquatic organisms
     8.2. Terrestrial organisms
          8.2.1. Plants
          8.2.2. Insects
          8.2.3. Birds
     8.3. Microorganisms
     8.4. Bioaccumulation and biomagnification
     8.5. Population and community effects
     8.6. Effects on the abiotic environment
     8.7. Appraisal



     10.1. Mirex toxicity
     10.2. Exposure to mirex
     10.3. Evaluation of environmental impact
     10.4. Conclusions




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

Dr D.A. Akintonwa, Department of Biochemistry, Faculty of
   Medicine, University of Calabar, Calabar, Nigeriaa

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

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

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

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

 Representatives of Other Organizations

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

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

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

Dr M. Gilbert, International Register for Potentially Toxic 
   Chemicals, United Nations Environment Programme, Geneva, 
Mrs B. Goelzer, Division of Noncommunicable Diseases, Office
   of Occupational Health, World Health Organization, Geneva,

Dr Y. Hasegawa, Division of Environmental Health,         
   Environmental Hazards and Food Protection, World Health
   Organization, Geneva, Switzerland                      

a  Unable to attend.

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

Mr B. Labarthe, International Register for Potentially Toxic
   Chemicals, United Nations Environment Programme, Geneva,

Dr I.M. Lindquist, International Labour Organisation, Geneva,

Dr M. Vandekar, Division of Vector Biology and Control,
   Pesticides Development and Safe Use Unit, World Health
   Organization, Geneva, Switzerland

Mr J.D. Wilbourn, Unit of Carcinogen Identification and
   Evaluation, International Agency for Research on Cancer,
   Lyons, France


    While every effort has been made to present information in the 
criteria documents as accurately as possible without unduly 
delaying their publication, mistakes might have occurred and are 
likely to occur in the future.  In the interest of all users of the 
environmental health criteria documents, readers are kindly 
requested to communicate any errors found to the Manager of the 
International Programme on Chemical Safety, World Health 
Organization, Geneva, Switzerland, in order that they may be 
included in corrigenda, which will appear in subsequent volumes. 

    In addition, experts in any particular field dealt with in the 
criteria documents are kindly requested to make available to the 
WHO Secretariat any important published information that may have 
inadvertently been omitted and which may change the evaluation of 
health risks from exposure to the environmental agent under 
examination, so that the information may be considered in the event 
of updating and re-evaluation of the conclusions contained in the 
criteria documents. 

                         *     *     *

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


    Following the recommendations of the United Nations Conference 
on the Human Environment held in Stockholm in 1972, and in response 
to a number of World Health Assembly Resolutions (WHA23.60, 
WHA24.47, WHA25.58, WHA26.68), and the recommendation of the 
Governing Council of the United Nations Environment Programme, 
(UNEP/GC/10, 3 July 1973), a programme on the integrated assessment 
of the health effects of environmental pollution was initiated in 
1973.  The programme, known as the WHO Environmental Health 
Criteria Programme, has been implemented with the support of the 
Environment Fund of the United Nations Environment Programme.  In 
1980, the Environmental Health Criteria Programme was incorporated 
into the International Programme on Chemical Safety (IPCS).  The 
result of the Environmental Health Criteria Programme is a series 
of criteria documents. 

    A WHO Task Group on Environmental Health Criteria for 
Organochlorine pesticides other than DDT met in Geneva from 28 
November to 2 December 1983.  Dr K.W. Jager opened the meeting on 
behalf of the Director-General.  The Task Group reviewed and 
revised the draft criteria document and made an evaluation of the 
health risks of exposure to mirex. 

    The drafts of this document were prepared by Dr D.C. Villeneuve 
of Canada and Dr S. Dobson of the United Kingdom. 

    The efforts of all who helped in the preparation and 
finalization of the document are gratefully acknowledged. 

                               * * *

    Partial financial support for the publication of this criteria 
document was kindly provided by the United States Department of 
Health and Human Services, through a contract from the National 
Institute of Environmental Health Sciences, Research Triangle Park, 
North Carolina, USA - a WHO Collaborating Centre for Environmental 
Health Effects. 


1.1.  Summary

1.1.1.  Identity, properties and analytical methods

    Mirex (C10Cl12) is a white crystalline odourless solid; it is
an extremely stable substance.

    Gas chromatography with electron capture detection is the 
analytical method most commonly used for its determination. 

1.1.2.  Uses and sources of exposure

    Mirex is mainly used as a flame-retardant and as a stomach 
insecticide, mainly formulated into baits, for the control of ants, 
especially fire ants and harvester ants.  The USA appears to be the 
main country in which mirex was used for pest control, but this use 
was discontinued in 1978. 

    The same chemical substance is also used, under the name 
Dechlorane, as a fire retardant in plastics, rubbers, paints, etc.  
This application is not restricted to the USA. 

    A known source of exposure for the general population is food.  
However intake from this source is below the promulgated tolerance 

    No data are available on occupational exposures to mirex.

1.1.3.  Environmental concentrations and exposures

    Mirex is one of the most stable chemicals in use today. 
Biodegradation by microorganisms does not take place except, 
occasionally, under anaerobic conditions, and, even then, at a slow 

    Photodegradation under the influence of UV radiation is slow, 
photomirex (8-monohydromirex) being the major degradation product.  
The environmental half-life of mirex is of the order of many years, 
and its breakdown products are equally stable. 

    Because it is practically insoluble in water, sediments act as 
a sink for mirex that enters waterways. 

    Mirex bioaccumulates at all trophic levels and is biomagnified 
through food chains. 

    Long-term toxicity, with delayed onset of toxic effects and 
mortality is uniformly high.  Mirex is toxic for a range of aquatic 
organisms, with crustacea being particularly sensitive. 

    Thus, it appears that mirex presents a long-term environmental 

1.1.4.  Kinetics and metabolism

    Following oral ingestion, mirex is only partly absorbed into 
the body and the remainder - depending on the dose administered - 
is excreted unchanged in the faeces.  Mirex can also be absorbed 
following inhalation and via the skin. 

    It is a lipophilic compound and, as such, is stored in adipose 
tissue to a greater extent than in any other tissue.  Mirex is 
transferred across the placenta to the fetus and is excreted with 
the milk. 

    Mirex does not appear to be metabolized to any extent in any 
animal species investigated.  Its elimination from the body is 
slow.  Depending on the species tested, its half-life in the body 
is several months. 

1.1.5.  Studies on experimental animals

    Mirex is moderately toxic in single exposures.  In long-term 
studies, far lower daily dosages (1 mg/kg diet) have led to liver 
hypertrophy with morphological changes in the liver cells, and 
induction of mixed-function oxidases. 

    It is fetotoxic and teratogenic.

    Mirex is not generally active in short-term tests for genetic 

    Mirex is carcinogenic for both mice and rats.

1.1.6.  Effects on man

    No reports on accidental poisoning or occupational exposure and 
occupational health effects are available. 

1.2.  Recommendations

1.  Surveillance should be maintained over any future production,
    transport, and disposal of mirex and the nature and extent of
    both its agricultural and non-agricultural use.

2.  Levels of mirex in the environment should continue to be
    comprehensively monitored.


2.1.  Identity

Chemical Structure

Molecular formula:            C10C112

CAS chemical name:            1,1a,2,2,3,3a,4,5,5,5a,5b,6-dodeca-
                              cyclobuta[ cd]pentalene

Synonyms:                     dodecachloropentacyclo[]
                              2H-cyclo-buta[ cd]pentalene

Trade names:                  Dechlorane, Ferriamicide, GC 1283

CAS registry number:          2385-85-5

Relative molecular mass:      545.5

2.2.  Physical and Chemical Properties

    Mirex is a white crystalline, odourless solid with a melting 
point of 485 C.  It is soluble in several organic solvents 
including tetrahydrofuran (30%), carbon disulfide (18%), chloroform 
(17%), and benzene (12%), but is practically insoluble in water (US 
NRC, 1978).  It has a vapour pressure at 25 C of 3 x 10-7 mm 
(IARC, 1979).  Vapour pressures at other temperatures can be found 
in Matsumura (1975). 

    Mirex is considered to be extremely stable (US NRC, 1978).  It 
does not react with sulfuric, nitric, hydrochloric or other common 
acids and is unreactive with bases, chlorine or ozone.  Despite its 
stability, reductive dechlorination of mirex can be brought about 
by reaction with reduced iron porphyrin or more effectively by 
vitamin B12 (Schrauzer & Katz, 1978).  Slow partial decomposition 
will also result from ultraviolet (UV) irradiation in hydrocarbon 
solvents or from gamma rays (Lane, 1973; Baker & Applegate, 1974).  
Dechlorination by UV irradiation yields photomirex (8-monohydromirex) 
as a major product (Alley et al., 1974; Mehendale, 1977a) and this 
may represent the fate of most of the mirex in the environment 
(Mirex Advisory Committee, 1972a; Carlson et al., 1976). 

    Mirex is quite resistant to pyrolysis; decomposition begins 
at 525C (Kennedy et al., 1977), and 99 - 98% combustion is 
accomplished at 700C within 1 second (Wilkinson et al., 1978).  
Hexachlorobenzene is a major pyrolysis product with lesser amounts 
of carbon monoxide, carbon dioxide, hydrogen chloride, chlorine, 
carbon tetra-chloride, and phosgene given off as vapour. 

    According to US NRC (1978), technical grade preparations of 
mirex contain 95.19% mirex and 2.58% chlordecone; the rest of the 
composition was not specified.  The term "mirex" is also used to 
refer to a bait comprising corncob grits, soya bean oil, and mirex 
(IARC, 1979).  Insect bait formulations for aerial application 
containing 0.3 - 0.5% mirex and fire ant formulations containing 
0.075 - 0.3% mirex have also been used in the USA (IARC, 1979). 

2.3.  Analytical Methods

    Several analytical procedures, used for the determination 
of mirex, are summarized in Table 1.  Other methods used include 
gelpermeation chromatography, and gas chromatography using an 
electrolytic conductivity detector (IARC, 1979).  Mirex can be 
analysed in the presence of PCBs by using nitration procedures 
(Task Force on Mirex, 1977), perchlorination (Hallett et al., 
1976), or photodegradation (Lewis et al., 1976).  High pressure 
liquid chromatographic (HPLC) methods have also been used for the 
separation and quantitation of mirex and PCBs (Task Force on Mirex, 

a  Report to US Environmental Protection Agency

Table 1.  Methods for the determination of mirex
Sample type      Sampling method,                   Analytical  Limit of        Reference
or medium        Extraction/cleanupa                methoda     detection
general                                             GLC         0.2 pg          Hartman (1971)

air              trap on polyurethane foam,         GC/ECD      0.1 ng/m3       Lewis et al. (1977)
                 extract with hexane-ether, wash

 rural potable   extract with hexane, CC            GC/ECD      0.01 g/1itre   Sandhu et al. (1978)
 fresh & salt                                       GC/ECD      0.001 g/1itre  Markin et al. (1974b)

soil & sediment  extract with petroleum ether       GC/ECD      3-6 g/kg       Bevenue et al. (1975)
                 or acetone-petroleum ether, CC

fruit &          extract with acetonitrile or       GC/ECD,     -               Horwitz (1975)
vegetables       aq. acetonitrile, liquid/liquid    TLC, PC
                 partition, CC

fatty products   mix with florisil, extract with    GC/ECD      -               Bong (1975, 1977)
&  fish          acetonitrile, liquid/liquid
                 partition, CC

catfish          grind with anhyd. sodium sulfate,  GC/ECD      10 g/kg        Collins et al. (1973)
                 extract with hexane, CC

biological       grind with anhyd. sodium sulfate,  GC/ECD      1 g/kg         Collins et al. (1974)
material,        extract with hexane-isopropanol,
wildlife         wash with water, CC

wildlife         mix with florisil, extract with    GC/FID/ECD  -               Hallett et al. (1976)
                 5% water in acetonitrile, liquid/  /CD/GC/MS
                 liquid extraction, CC, chlorinate
a  GLC - gas-liquid chromatography.
   GC/ECD- gas chromatography/electron capture detection.
   CC- column chromatography.
   TLC- thin layer chromatography.
   PC- paper chromatography.
   FID- flame ionization detection.
   CD- conductivity detection.
   MS- mass spectrometry.


3.1.  Production and Uses

    Mirex was first synthesized in 1946 by Prins but was not used 
in pesticide formulations until 1955. 

    Mirex is made by the dimerization of hexachlorocyclopentadiene 
in the presence of aluminum chloride (IARC, 1979).  It is a stomach 
insecticide with little contact activity.  The insecticidal use of 
mirex has been largely focused on the control of the imported fire 
ant  Solenopsis saevissima richteri, in southeastern USA.  The 
imported fire ant was introduced into the USA at the beginning of 
this century and for the first twenty years confined itself to the 
area around the port of Mobile, Alabama.  However, a second wave of 
a closely related species  (Solenopsis invicta) appeared in the 
late 1920s and spread throughout the south of the USA.  Since then, 
the imported fire ant has infested some 76 million hectares in the 
southern USA (Gunby & Preston, 1979).  This pest can pose a 
nuisance as it can deliver a severe sting which often results in 
secondary infection.  In addition, the mounds produced by the ants 
make farming difficult and can cause damage to farm machinery.  To 
combat the problem, approximately 250 000 kg of mirex was applied 
to fields during 1962-75 (US NRC, 1978).  Most of the mirex was in 
the form of 4X mirex bait, which consists of 0.3% mirex in 14.7% 
soybean oil mixed with 85% corncob grits.  Preparations also came 
in 2X and 1X baits, which contained 0.15 and 0.1% mirex, 
respectively.  Application of the 4X bait was designed to give a 
coverage of 4.2 g mirex/ha and was delivered by aircraft, 
helicopter or tractor.  Another form of bait consists of 
microencapsulated mirex in soybean oil (Markin et al., 1975). 
Normal application rates are 750 mg active ingredient/kg for fire 
ant baits and 1500 mg/kg for harvester ant baits. 

    Other pests are also sensitive to mirex, including the western 
hamster ant, the yellow-jacket and the Texas leaf-cutting ant 
(Mirex Advisory Committee, 1972).a  Mirex bait has been applied to 
pineapple-growing areas in Hawaii to control mealy bug, under 
permit from US EPA since 1970 (Bevenue et al., 1975). 

    In 1971, the US EPA cancelled all federal regulations 
permitting the use of mirex pending release of an environmental 
impact study.  New regulations, issued by the US EPA in 1972, 
authorized the restricted use of mirex by permit only.  Allied 
Chemical Corporation, which at the time was the sole producer of 
bait formulations, sold the registration for mirex and the right to 
produce, for one dollar, to the Mississippi Department of 
Agriculture (Pesticide Chemical News, 1976).  During the same year, 
the US EPA ordered a phasing-out of the use of mirex for pest

a  Report to US Environmental Protection Agency

pest control and brought in a ban with exemptions on June 30, 1978.  
Mississippi has since been trying to gain approval for a new 
compound under the generic name Ferriamicide.  This bait contains 
long-chain alkyl amines and ferrous chloride in addition to mirex.  
With this composition, 80 - 90% of the mirex was claimed to degrade 
within 30 days, compared with the normal break-down time of 5 - 10 
years (Kaiser, 1978).  However, a Canadian study conducted in 1979 
(Villeneuve et al., 1979a) demonstrated that photomirex, a major 
break-down product of Ferriamicide, was considerably more toxic 
than mirex itself.  Hence, the US EPA has withheld permission for 
the Mississippi Pest Control Program, pending review of the 
Canadian study (Gunby & Preston, 1979).  The literature indicates 
that the USA may be the only country to have used mirex in pest 

    Mirex, under the name Dechlorane, is also used as a fire 
retardant in plastics, rubber, paint, paper, and electrical goods, 
and as a smoke-generating compound, when combined with zinc oxide 
and powered aluminum.  Statistics show that between 1959 and 1975, 
400 000 kg of mirex and 1 500 000 kg of Dechlorane were sold, of 
which 74% was used in the USA for non-agricultural purposes (US 
NRC, 1978).  Recently, non-agricultural mirex has been replaced in 
part by compounds such as Dechlorane plus, Dechlorane 4070, 510, 
602, 603, and 604, all of which have similiar fire retardent 
properties.  No recent consumption data for mirex in non-
agricultural applications could be obtained. 

    Unfortunately, complete information on the quantities of mirex 
produced in the USA and its fate is not available.  In fact, as 
much as half of the mirex used between 1962-73 cannot be accounted 
for (US NRC, 1978).  Little information is also available on world-
wide production and use, but patents for the use of mirex exist in 
several countries including Belgium, France, the Federal Republic 
of Germany, Japan, the Netherlands, and the United Kingdom (Task 
Force on Mirex, 1977). 

3.2.  Transport and Distribution

    (a)  Air

    There is no documentation concerning air-borne mirex 
contamination in the literature.  It is reasonable to assume, 
however, that facilities involved in the production of mirex and 
its by-products may have released significant levels of mirex dust 
into the atmosphere within and immediately surrounding the plants.  
The Task Force on Mirex (1977) suggested that aerial transport 
could possibly be involved in the contamination of non-target 
organisms in untreated areas. 

    (b)  Water

    As mentioned earlier, mirex has a very low solubility in water 
and if concentrations exceed 1 g/litre, mirex would be associated 
with the particulate matter in the water rather than with the water 
itself.  It has been demonstrated that mirex can be translocated to 
water bodies from adjacent agricultural land (Borthwick et al., 
1973; Spence & Markin, 1974; Tagatz et al., 1975). 

    (c)  Soil

    When mirex is used in pesticide formulations, it is generally 
in the form of a bait and, thus, not applied directly to the soil.  
After application of 0.04 g mirex bait/ha, mirex residues in the 
soil ranged from 0.1 - 10 g/kg (Mirex Advisory Committee, 1972).a  
Jones & Hodges (1974), found that only 6.6% of the mirex from bait 
leached into the top 1.5 cm of the soil in a test plot after 6 
months exposure to sun and rain.  This is supported by field 
studies such as the Residue Monitoring Program on Hawaii (Bevenue 
et al., 1975). 

    Sediments can act as sinks for the small amount of mirex that 
is leached and deposited via run-off.  Residue levels typically 
mimic soil levels, and are normally quite low.  However, in Lake 
Ontario, levels of mirex as high as 40 g/kg have been reported in 
sediments near the Oswego and Niagara areas.  These high levels 
have been attributed to the dumping of mirex in the rivers and not 
to soil run-off or leaching (Task Force on Mirex, 1977). 

    Very little information is available concerning the leaching of 
Dechlorane from landfill sites or disposal of flame retardant 
material, but this may also represent an important source of 

3.3.  Abiotic degradation

    Mirex is considered to be one of the most stable pesticides in 
use today (Baker & Applegate, 1974).  Several conditions under 
which reductive dechlorination of mirex will occur have been given 
in section 2 of this report.  The most significant factors involved 
in abiotic degradation in the environment are ultraviolet light and 
gamma irradiation. 

    Conversion of mirex to the 8-monohydro derivative (photomirex) 
was shown to occur when mirex was exposed to sunlight (Gibson et 
al., 1972).  Mirex has also been shown to undergo photolytic 
dechlorination in some organic solvents (Dilling & Dilling, 1967; 
Alley et al., 1973) and mallard duck eggs (Lane et al., 1976) when 
exposed to UV radiation.  The primary photodegradation product in 
these cases was photomirex with lesser amounts of 5,8 dihydromirex.

a  Report to US Environmental Protection Agency

Carlson et al. (1976) showed that from 16 to 19.5% of the total 
mirex-related residues from soil samples, recovered 12 years after 
treatment at 1.12 kg/ha, was photomirex.  Lesser amounts of 
chlordecone (3.1 - 6.3%), 10-monohydromirex, and 2 isomers of 
dihydromirex were also present.  When 4X mirex bait was exposed to 
intense UV radiation for 19.5 h, similar degradation patterns were 
found, the major degradation product being photomirex (19.9%), with 
lesser amounts of chlordecone (0.2%) and other derivatives (Carlson 
et al., 1976). 

    The half-life of mirex dispersed in water under intense UV 
radiation at 90 - 95C was 48.4 h (similar to DDT: 42.1 h); this 
was rather long compared with that of dieldrin (11.5 h) 
(Knoevenagel & Himmelreich, 1976). 

    Several photodegradation products that occur in the environment 
include 10-monohydromirex, 8-monohydromirex, 5,10-dihydromirex, 
chlordecone and 2,8-dihydromirex (Alley et al., 1973, 1974; Baker & 
Applegate, 1974; Ivie et al., 1974a; Carlson et al., 1976).  These 
compounds have been demonstrated to occur in the laboratory and 
under field conditions as a consequence of irradiation.  Levels in 
twelve-year-old experimental plots in Mississippi suggested that 
mirex had an environmental half-life of many years (Carlson et al., 
1976). As mentioned previously, an environmental half-life of 5 - 
10 years has been cited in other studies (Carlson et al., 1976; US 
NRC, 1978).  Data collected from a 5-year-old aircraft crash site 
in which a cargo of bait was dumped in a shallow pond, produced 
similar results (Andrade & Wheeler, 1974b).  The evidence to date 
suggests that slow partial photo-degradation is likely to be the 
ultimate fate of mirex in the environment. 

3.4.  Biodegradation

    Mirex is very resistant to microbiological degradation and is 
only slowly dechlorinated to a monohydro derivative by anaerobic 
microbial action in sewage sludge (Andrade et al., 1974a, 1975) and 
by enteric bacteria in monkeys (Stein et al., 1976).  There have 
been no reports of evidence of metabolic degradation by soil 
microorganisms (Jones & Hodges, 1974). 


4.1.  Environmental Levels

    (a)  Air

    Atmospheric exposure to mirex could result from the air-borne 
dust from the production and processing of mirex or Dechlorane, 
combustion of either Dechlorane plastics or Dechlorane smoke 
compounds or volatilization of mirex used in bait formulations.  
The only information regarding any of the above occurrences is an 
estimate of potential volatilization of mirex based on the method 
of Gueckel et al. (1973). 

    (b)  Water

    Mirex has been found in one sample of ground water in the USA 
(Shackelford & Keith, 1976) and in water (0.0001 g/litre) (Alley 
et al., 1973) shortly after bait application.  Pond water in 
drainage areas is also known to contain high levels of mirex after 
treatment (0.2 and 0.53 g/litre) (Spence & Markin, 1974).  It has 
also been determined in rural drinking-water at levels of 0 - 437 
ng/litre (Sandhu et al., 1978).  However, mirex has not been found 
in tap water in studies with detection sensitivities as low as 5 
ng/litre (Smillie et al., 1977). 

    (c)  Food

    The US tolerances for residues of mirex in food products in 
1969 were: 0.1 mg/kg in all fat or meat of cattle, goats, horses, 
poultry and sheep, in milk fat, eggs, and fish; 0.01 mg/kg in all 
other raw agricultural commodities. 

    Mirex residues have been observed in beef fat in the south-
eastern USA and found to range between 0.001 mg/kg to 0.125 mg/kg 
with a mean of 0.026 mg/kg.  No mirex was found in areas where bait 
was not used (Ford et al., 1973). 

    Plants are also a potential source for mirex uptake.  Mirex 
residues of 0.01 - 1.71 mg/kg were found in soya beans, garden 
beans, sorghum, and wheat seedlings when grown on substrates 
containing 0.3 - 3.5 mg/kg mirex (de la Cruz & Rajanna, 1975).  
Based on these uptake data and the known soil concentrations of 
mirex, it has been calculated that plant tissues grown on 
contaminated soil could contain between 0.2 ng/kg and 2 g/kg mirex 
(US EPA, 1978). 

    (d)  Wildlife

    Residue levels in various non-target organisms were wide-
ranging and obviously dependent on the level of exposure and 
feeding habits.  Also, as expected in all organisms, the highest 
levels of mirex were found in adipose tissue.  Bird residue levels 
typically ranged from less than 1 mg/kg to 10 mg/kg.  Residue 
concentrations of 210 mg/kg have been reported by Hallett et al. 
(1976) in lipids extracted from homing gulls from Lake Ontario. 

    Vertebrates such as frogs, lizards, and shrews have been 
observed to contain mirex residue levels as high as 9 mg/kg (Wojcik 
et al., 1975), 5.46 mg/kg (Markin et al., 1974b), and 41.3 mg/kg 
(Mirex Advisory Committee, 1972),a respectively.  Again, typical 
residue levels are somewhat lower but generally range from 
approximately 1 to 10 mg/kg for the frog and lizard and 20 to 40 
mg/kg in the shrew.  It should be noted that these residue levels 
are maxima that are reached shortly after bait application and 
decrease over time.  But, small amounts of mirex have been observed 
in tissues up to 3 years after application (Madhukar & Matsumura, 

    In areas where mirex has been detected in sediments or in the 
water, residue levels in aquatic animals have ranged from non-
detectable to 0.97 mg/kg, with the majority of samples showing 
levels below 0.1 mg/kg.  Fish in Lake Ontario and the St. Lawrence 
river contained levels as high as  0.27 mg/kg (Suta, 1978).  For a 
more complete listing of US and Canadian residue data, see Baetcke 
et al. (1972), Borthwick et al. (1973, 1974), and US EPA (1978).  
World-wide data on mirex are lacking in the literature; however, 
mirex has been reported in Netherlands seals (Ten Noever de Brauw 
et al., 1973). 

4.2.  General Population Exposure

    It has been estimated by the US EPA that inhabitants in areas 
treated with mirex bait would inhale some 0.4 - 0.8 ng mirex per 
day (Suta, 1978). 

    Food probably represents the major source of mirex accumulation 
in the human body.  Within the food groups the largest intake of 
mirex would result from fish consumption, followed by wild game and 
then the commercial meats. 

    The average consumption of mirex via finfish would be 0.39 
g/day if the fish were from the St. Lawrence (US NRC, 1978).  
Mirex intake from Lake Ontario fish would on average be less than 
0.34 g/day.  In the southern states, based on a mean mirex 
level of 0.02 mg/kg in southern fish, the average person would 
consume 0.13 g of mirex per day.  No data were available for mirex 
consumption internationally. 

    Wild game represents the second most significant mirex source.
It has been estimated that in the USA approximately 9 million     
people will consume between 0.1 and 12 mg of mirex per person per 
day from wild game (US NRC, 1978).                                

a  Report to US Environmental Protection Agency

    (a)  Infants

    Mirex may be excreted in milk.  A survey of 1436 samples of 
human milk, collected in the USA, failed to show detectable levels 
of mirex (Suta, 1978).  However, in a Canadian survey, 3 out of 14 
human milk samples showed levels between 2 - 21.5 g/kg, on a fat 
basis (Mes et al., 1978). 

    (b)  Occupational exposure

    No data are available on occupational exposure to mirex.


5.1.  Absorption

    (a)  Inhalation

    Atallah & Dorough (1975) examined the transfer of mirex from 
cigarettes, through cigarette smoke, using 14C-mirex in rats.  Of 
the total residue inhaled, 47% was exhaled, the lung retaining 35%, 
the blood 11%, and heart 1%, 2 - 4 min after inhalation. 

    (b)  Gastrointestinal tract

    Approximately 55% of a single oral dose of 6 mg 14C-mirex/kg 
body weight, administered to rats, was excreted unchanged in the 
faeces within 48 h (Mehendale et al., 1972).  When a lower 
concentration of mirex was administered (0.2 mg/kg body weight), 
only 15% of the administered mirex was excreted in 48 h (Gibson et 
al., 1972).  Ivie et al. (1974b) dosed Japanese quail orally with 
1.2 mg 14C-mirex/kg body weight and found that only 12 - 25% of the 
dose was eliminated in the faeces after 1 week.  In another study, 
a female rhesus monkey was given 14C-mirex orally at 1 mg/kg body 
weight.  14C-mirex appeared in the plasma after 2 h and reached a 
peak after 5 h (Wiener et al., 1976). 

    (c)  Skin

    No studies on dermal uptake were found.

5.2.  Distribution and Storage

    (a)  Human studies

    The first discovery of mirex residues in human adipose tissue 
was reported by Kutz et al. (1974).  The levels found in 6 post-
mortem samples, all from patients who had resided in the south-
eastern states of the USA, ranged from 0.16 to 5.94 mg/kg.  More 
recently, the US EPA reported that 18% of 284 samples obtained from 
the southeast area general population contained mirex and that 
values ranged from trace amounts to 1.32 mg/kg (Suta, 1978).  Lloyd 
et al. (1974) analysed the blood of pregnant women in the Jackson 
and Mississippi delta areas for chlorinated pesticides including 
mirex.  Mirex was found in 106 of the 142 samples of this survey at 
a mean blood concentration of 0.5 mg/litre. 

    (b)  Animal studies

    Mirex is a lipophilic compound and as such is stored in the 
adipose tissue to a much greater extent than in any other tissue.  
Mehendale et al. (1972) showed that when rats were dosed with a 
single oral dose of mirex at 6 mg/kg body weight, the tissues and 
organs retained about 34% of the total dose, of which 28% was found 
in fat, 3.2% in muscle, 0.09% in the kidneys, and 1.8% in the 

    Ivie et al. (1974b) reported on the accumulation, distribution, 
and excretion of 14C-mirex fed to rats and quail for 16 months at 
levels of 0.3, 3, or 30 mg/kg diet.  The levels of mirex in the fat 
of rats and quail were about 120 to 185-fold greater than the 
dietary intake values, and no plateau was observed in the 
accumulation pattern.  As part of this study, rats and quail were 
given mirex-treated food for 6 months and then placed on a control 
diet for an additional 10 months.  Analyses of tissues indicated 
that the half-life of mirex in the quail was 20 - 30 days, whereas, 
in the rat, the residues had declined by only 40% after 10 months. 

    The distribution of mirex in female rhesus monkeys, dosed 
orally and intravenously at approximately 1 mg/kg body weight, was 
studied by Wiener et al. (1976).  Peak concentrations in the plasma 
were of the order of 1 mg/litre in the iv-treated animals and 
approximately 0.01 mg/litre, 400 days later.  At autopsy, all 
tissues examined contained mirex.  In a reproduction study on rats, 
mirex was transferred to the fetus across the placenta and was also 
excreted in the milk (Gaines & Kimbrough, 1970).  Rats fed mirex at 
25 mg/kg diet for 78 days excreted 11.3 mg/litre in milk, whereas 
fetuses removed by Caesarian section on the 19th day of gestation 
contained 0.23 mg/kg body weight. 

    Distribution studies have also been reported on the cow (Bond 
et al., 1975), goat (Smrek et al., 1977, 1978), mosquito fish (Ivie 
et al., 1974b), wild birds (Stickel et al., 1973), blue crab 
(Schoor, 1974), and winter flounder (Pritchard et al., 1973). 

5.3.  Metabolism

    Mirex does not appear to be metabolized to any significant 
extent in any animal species so far investigated (mice, rats, 
rabbits, monkeys) (Waters, 1976; Canada, Department of National 
Health and Welfare, 1977; IARC, 1979). 

5.4.  Excretion

    (a)  Animal studies

    Data from studies on rat (Gibson et al., 1972; Mehendale et 
al., 1972; Ivie et al., 1974b), monkey (Wiener et al., 1976), quail 
(Kendall et al., 1978), and goat (Smrek et al., 1977), exposed to 
mirex, showed fast tissue uptake and slow elimination.  Mehendale 
et al. (1972) estimated the half-life of mirex following oral 
administration to rats to be more than 100 days.  Pittman et al. 
(1976) used a mathematical model to predict an extremely long half-
life for mirex in rhesus monkeys with only a 2% decline in adipose 
tissue levels over a 10-year period.  However, after a 52-week 
recovery period, the mirex level in the adipose tissue of goats was 
one-third to one-quarter of the original value (Smrek et al., 
1978).  In a feeding study on rats, quail, and mosquito fish (Ivie 
et al., 1974b), a 40% decline in mirex levels in adipose tissue was 
found over a 10-month period, while the half-life of mirex was 20 - 
30 days in the adipose tissue of quails and 4 months in fish.  In 
rats, 12 - 25% of the dose was eliminated in the faeces after 1 
week (Ivie et al., 1974b). 


6.1.  Single Dose Studies

    Data indicating the acute oral, intraperitoneal, and dermal 
toxicity for mirex in various animals are shown in Table 2.  The 
acute toxic effects of mirex were characterized by muscle tremors, 
diarrhoea, and depression followed by death (Gaines & Kimbrough, 

Table 2.  Oral, intraperitoneal, and dermal LD50 values for mirex
Species  Sex    Exposure route     LD50     Reference
Rat      M      oral (corn oil)    740      Gaines (1969)
Rat      F      oral (corn oil)    600      Gaines (1969)
Rat      M & F  oral (peanut oil)  3000     Gaines (1969)
Rat      F      oral (corn oil)    365      Gaines & Kimbrough (1970)
Hamster  F      oral               125      Cabral et al. (1979)
Hamster  M      oral               250      Cabral et al. (1979)
Dog      M      oral (corn oil)    1000     Larson et al. (1979)
Rat      F      ip                 365      Kendall (1974)
Rabbit   -      dermal             800      Waters (1976)
Rat      M & F  dermal             2000     Gaines (1969)

    Several hepatic variables were studied, 2 days following a 
single oral dose of 100 mg mirex/kg body weight, in female rats.  
Microsomal cytochrome P-450 content, NADPH-cytochrome  c reductase 
(EC activity, and hepatic ascorbic acid concentration 
were found to be increased, and so was the microsomal protein 
concentration.  Relative liver weight was increased, as well as the 
activities of aminopyrine  N-demethylase and 4-nitroanisole- O-
demethylase (Chambers & Trevathan, 1983). 

6.2.  Short-Term Studies

6.2.1.  Oral exposure

    The toxic effects of mirex in short-term studies are generally 
characterized by a decrease in body weight, hepatomegaly, 
induction of mixed-function oxidases, morphological changes in 
liver cells, and sometimes death. 

    Decreased body weight gain was observed in female rats fed a 
total of 365 mg/kg body weight over a 12-day period (Kendall, 
1974), and in male rats dosed orally for 14 days at 10 mg/kg 
(Villeneuve et al., 1977).  In a 13-week feeding study, decreased 
body weight gain was observed in female rats at a dietary level of 
1280 mg/kg and in male rats at 320 and 1280 mg/kg (Larson et al., 
1979).  Reduced body weight gain was also observed when beagle dogs 
were fed mirex at 100 mg/kg diet for 13 weeks (Larson et al., 

    Liver hypertrophy was observed in: male rats dosed by gavage 
with 1.0 and 10 mg mirex/kg body weight, in corn oil, for 14 days 
(Villeneuve et al., 1977); male and female rats dosed from 5 - 50 
mg/kg body weight for 5 days (Mehendale et al., 1973); male and 
female rats dosed orally once, with 50 mg mirex/kg body weight and 
then observed for 28 days (Robinson & Yarbrough, 1968); and in male 
rats dosed ip with 50 mg/kg body weight for 5 days (Kaminsky et 
al., 1978).  Female rats fed 20, 30, or 40 mg mirex/kg and male 
rats fed 40 or 50 mg mirex/kg for 28 days exhibited liver 
enlargement (Abston & Yarbrough, 1976). 

    In another study, rats (sex not specified) fed 100 mg mirex/kg 
diet for 4 weeks, exhibited liver hypertrophy (Davison et al., 
1976), whereas in a study carried out over 166 days, liver 
hypertrophy was observed at 25 mg/kg diet for both sexes (Gaines & 
Kimbrough, 1970).  When mirex was fed for 13 weeks to male and 
female rats, liver hypertrophy was observed at levels of 80 mg/kg 
and higher in males and at 320 mg/kg in females (Larson et al., 
1979).  Liver enlargement was also observed in female rabbits fed 
20 mg mirex/kg diet for 8 weeks (Warren et al., 1978), in dogs fed 
100 mg/kg for 13 weeks (Larson et al., 1979), and in male mice fed 
30 mg/kg for 12 weeks (Pitz et al., 1979). 

    Induction of mixed-function oxidase (EC enzymes was 
shown for the male rat, when mirex was administered:  by gavage at 
levels as low as 1.0 mg/kg body weight per day, for 14 days 
(Villeneuve et al., 1977); at 5 mg/kg per day ip for 5 days 
(Kaminsky et al., 1978); at 5 mg/kg diet (0.5 mg/kg per day) for 13 
weeks (Villeneuve et al., 1979b); and at 1 mg/kg diet for 14 days 
(Iverson, 1976).  Mirex has also been shown to induce microsomal 
enzyme activity in rabbits when administered at 20 mg/kg diet for 8 
weeks (Warren et al., 1978) in neonatal mice, suckled on mothers 
exposed to 10 mg mirex/kg diet (Fabacher & Hodgson, 1976), but not 
in chickens or quail exposed to 160 or 80 mg mirex/kg diet for 16 
and 12 weeks, respectively (Davison et al., 1976).  In a study 
designed to investigate the type of enzyme induction, mirex was 
found to induce a pattern similar to phenobarbital, DDT, chlordane, 
and chlordecone (Madhukar & Matsumura, 1979). 

    Morphological changes observed in the liver of mirex-treated 
rats consisted of hepatocyte enlargement, depletion of glycogen and 
lipid accumulation (Kendall, 1974, 1979), and some cell necrosis 
(Kendall, 1974; Davison et al., 1976).  Ultrastructural changes 
included altered architecture of the rough endoplasmic reticulum 
(RER), dilated RER cisternae, an increase in the number of free 
ribosomes, and proliferation of the smooth endoplasmic reticulum 
(Gaines & Kimbrough, 1970; Kendall, 1979).  The lowest level 
reported to cause histological changes was 1.0 mg/kg diet, and was 
observed in male rats during a 166-day study (Gaines & Kimbrough, 
1970) and a 90-day study (Villeneuve et al., 1979c). 

    Other important effects observed in several studies were the 
mirex-induced impairment of hepatobiliary function (Mehendale, 
1976, 1977a, 1979; Mehendale et al., 1979), and bile stasis (Gaines 
& Kimbrough, 1970). 

6.2.2.  Dermal exposure

    In a short-term dermal study (Larson et al., 1979), rabbits 
were exposed to 3.33 or 6.7 g of mirex bait/kg body weight for 6 - 
7 h each day, 5 days a week, for 9 weeks.  There were no gross or 
histopathological changes resulting from treatment in any of the 

6.3.  Long-Term and Carcinogenicity Studies

    The long-term and carcinogenic effects of mirex are summarized 
in Table 3.  Some of these studies have been discussed extensively 
by IARC (1979).  The data indicate that mirex is carcinogenic for 
rats and mice (IARC, 1979). 

6.4.  Reproduction and Teratogenicity Studies

    Ware & Good (1967) carried out a study on mice and found that 
administration of 5 mg mirex/kg diet for 30 days, prior to mating, 
resulted in a reduced litter size.  In a more recent study, Wolfe 
et al. (1979) found a cessation in reproduction in mice fed 17.8 
mg/kg diet for 3 months and decreased reproduction in the group fed 
1.8 mg/kg.  Gaines & Kimbrough (1970) fed diets containing 25 mg 
mirex/kg to rats and found reduced litter size, reduced viability 
of the neonates, and cataract formation in surviving neonates.  In 
addition, the results of a cross-fostering study indicated that the 
formation of cataracts was due to exposure through the milk.  
Females fed mirex at 5 mg/kg produced normal litters. 

    Pregnant rats were given 6 mg mirex/kg body weight per day in 
an oily solution, by gavage, on days 8 1/2 - 15 1/2 of pregnancy.  
The majority of the moderate to severely oedematous fetuses had 
abnormal ECGs and were either dead or dying on the morning before 
parturition was expected (Grabowski & Payne, 1983). 

Table 3.  Summary of long-term and carcinogenicity studies with mirex
Species   Duration Doses used                    Effects                             Reference
Mouse     up to    1 - 90 mg/kg diet             increased liver weights at 5 mg/kg  Byard et al. (1975)
          70                                     & higher, mixed function oxidase
          weeks                                  activity increased at 1 mg/kg after
                                                 70 weeks; total liver DNA & total
                                                 liver protein & mitochondrial
                                                 respiration increased at 1 mg/kg,
                                                 after 70 weeks

Rat       up to    5 and 30 mg/kg diet           no effects on liver weight;         Fulfs et al. (1977)
          36                                     proliferation of SER observed
          months                                 after 12 monthsat both dose levels

Mouse (2  70       dosed orally with 10 mg       increased incidence of hepatomas    Innes et al. (1969)
strains)  weeks    mirex/kg from day 7-28 after  in both strains
                   birth, then placed on a diet
                   containing 26 mg mirex/kg
                   until 70 weeks of age

Mouse     78       mice received 1 single sub-   increased incidence of reticulum-   US NTIS (1968)
          weeks    cutaneous injection of 1000   cell sarcomas
                   mg mirex/kg body weight
                   in gelatine on their 28th
                   day of life

Table 3.  (contd.)
Species   Duration Doses used                    Effects                             Reference
Mouse     up to    1, 5, 15, and 30 mg/kg        increased liver weights at 1 mg/kg  Fulfs et al. (1977)
          18       diet                          in female mice, 5 mg/kg and higher
          months                                 in male mice; histological changes
                                                 at 5 mg/kg and higher; prolifera-
                                                 tion of SER observed ultrastructur-
                                                 ally at 1 mg/kg and above

Monkey    up to    0.25 and 1.0 mg/kg body       no effect on liver weights, liver   Fulfs et al. (1977)
          26       weight orally 6 days per      histology, or liver ultrastructure
          months   week (equivalent to 5 and
                   20 mg/kg in diet)

Rat       18       50 or 100 mg/kg diet          dose-related effect on survival     Ulland et al. (1977)
          months   exposure, + 6 months on       noted; increased incidence of        
                   control diet                  neoplastic nodules observed in
                                                 high-dose male rats; of 17 rats
                                                 from all groups, 6 animals including
                                                 4 high-dose males had liver-cell
                                                 carcinomas; no metastases were
    In reproduction studies on birds, dietary administration of 
mirex did not reduce egg production or embryo survival in chickens 
(Davison & Cox, 1974), mallards, or bobwhite quail (Heath & Spann, 

    The teratogenic potential of mirex was studied in rats given 
daily oral doses of 0, 1.5, 3.0, 6.0, or 12.5 mg/kg body weight on 
days 6 - 15 of gestation (Khera et al., 1976).  The 12.5 mg/kg 
dosage caused maternal toxic effects, decreased fetal survival, 
reduced fetal weight, and an increased incidence of visceral 
anomalies in the fetus.  Maternal effects and increased incidence 
of visceral anomalies in the fetus were observed at 6.0 mg/kg body 
weight.  The lower doses did not induce any adverse effects. 

    Mirex administered to pregnant rats at 7 mg/kg body weight per 
day during days 7 - 16 of gestation, and also post-partum, induced 
oedema, undescended testes, and reduced weight in offspring 
(Chernoff et al., 1976).  Mirex-induced cataract formation was 
observed in mice in the same study. 

6.5.  Mutagenicity

    Mirex was negative in a dominant lethal test on rats, in which 
doses of 1.5 - 6.0 mg/kg body weight per day were used (Khera et 
al., 1976).  Mirex was found to be negative when tested by the 
standard Ames bacterial assay including a liver microsomal 
activation mixture (Hallett et al., 1978). 

6.6.  Other Studies

    Adult male rats were fed diets containing mirex at 1.78 and 
17.8 mg/kg for several weeks and were tested on a variety of 
behavioural tasks.  No differences in behaviour were seen between 
control and treated animals (Thorne et al., 1978).  In a study in 
which male rats were fed diets containing mirex at levels up to 80 
mg/kg diet for 8 weeks, mirex was found to cause hyporeactivity 
with attenuated startle response, increased emergence time, and 
decreased ambulation (Reiter et al., 1977).  The results of other 
studies also indicated that mirex might influence behaviour 
(Peeler, 1976; Reiter et al., 1977; Dietz & McMillan, 1978). 

    Studies have been conducted to evaluate the influence of mirex 
on antibody-mediated immunity in the chicken (Glick, 1974).  A 
level of 500 mg mirex/kg diet for up to 5 weeks of age depressed 
the levels of immunoglobulin M and G but did not affect antibody 
production.  The same observations were made in a subsequent study 
(Rao & Glick, 1977) where chickens were fed diets containing mirex 
at 100 mg/kg for 40 days from hatching. 

    Pregnant mare serum (PMS)-induced ovulation was significantly 
inhibited in immature rats by a single administration of 0.4 - 50 
mg of mirex per animal (Fuller & Draper, 1975).  This suppression 
of PMS-induced ovulation was thought to be due to an action on the 
central nervous system, inhibiting the release of luteinizing 
hormone rather than to a direct effect on the ovary. 

    The effects of mirex on Ehrlich ascites tumour cells have been 
assessed using certain  in vivo and  in vitro measurements (Walker et
al., 1977).  Mirex retarded the development of this tumour  in vivo  
and inhibited the synthesis of RNA purines. 

    Food deprivation has been shown to enhance the inducing 
properties of mirex on the mixed function oxidases (Villeneuve et 
al., 1977). 

    Both the acute toxicity data (Table 2) and some short-term 
exposure effects (Larson et al., 1979) seem to suggest that the 
female is more sensitive to mirex than the male, but no study has 
addressed this question specifically. 

    Several publications include reports on the toxicological 
properties of the mirex breakdown products  photomirex (8-mono-
hydromirex) and 2,8-dihydromirex.  The results of short-term 
studies indicate that photomirex can induce: liver enlargement, 
mixed-function oxidases, histological changes in the liver, 
thyroid, and testes, and even death (Villeneuve et al., 1979b,c; 
Sundaram et al., 1980).  The histological changes induced by 
photomirex (the most sensitive of the variables mentioned) 
generally occurred at levels approximately one order of magnitude 
lower than those observed with mirex.  Dihydromirex also causes 
morphological changes in the liver and thyroid but generally at the 
same dosage levels as mirex (Chu et al., 1980a).  Photomirex is not 
teratogenic in the rabbit, but does cause reproductive impairment 
in the rat including cataract formation in the pups (Villeneuve et 
al., 1979a; Chu et al., 1981).  Photomirex has a very long half-
life in primates and only 10% of the administered dose was 
eliminated over a one-year period (Chu et al., 1982). 

    Ultrastructural changes in the thyroid follicular cells of 
male rats persisted for at least 18 months following cessation of a 
28-day exposure to 0.05 - 50 mg photomirex/kg diet or 50 mg mirex/kg 
diet.  The morphological changes consisted of increased follicular 
cell heights and a numerical increase in secondary lysosomes.  In 
the 50 mg mirex/kg group, columnar thyroid follicular cells were 
engorged with deformed lysosomal bodies (Singh et al., 1982). 


    No reports of poisoning incidents or levels of occupational 
exposure are available. 


8.1.  Aquatic Organisms

    Information on the toxicity of mirex is available for a wide 
range of aquatic organisms. 

    Data on mirex toxicity for a variety of algae are given in 
Table 4.  A more comprehensive table, listing different conditions 
and exposure times is available on request from the IRPTC, Geneva.  
Results of disc assay tests of estuarine bacterial growth 
inhibition were inconsistent from batch to batch of technical grade 
mirex, with some batches producing little or no growth inhibition 
in the bacterial isolates while others showed marked inhibition 
(Brown et al., 1975).  Although purified mirex was not toxic, UV-
irradiated mirex was bacteriologically toxic.  The only appreciable 
microbial activity affected by mirex at concentrations below 100 
mg/litre was the inhibition of primary production.  This is 
unlikely to be a significant effect in the field, since most 
phytoplankton are in the aqueous phase, whereas mirex tends to 
become associated with the sediments.  Mirex degradation products 
with substitution at the 5 and/or 10 positions were highly toxic 
for bacterial cultures and, as these compounds are more polar than 
mirex, they may be more soluble in water and therefore pose a 
greater environmental threat for aquatic bacteria. 

    Exposure of phytoplankton to mirex at 1 mg/litre for 4 h 
reduced productivity by 28 - 46% (Butler, 1963).  The ciliate 
protozoan  Tetrahymena pyriformis exhibited reduced growth rate 
when exposed to 0.9 g mirex/litre during the exponential growth 
phase (Cooley et al., 1972).  Exposure of pure cultures of the 
green marine algae  Chlamydomonas sp. to 1 mg mirex/litre for 168 h 
reduced net photosynthesis by 55% and respiration by 28.4% (de la 
Cruz & Naqvi, 1973).  Population growth and oxygen evolution in 
marine unicellular algae were not affected by exposure to 0.2 g 
mirex/litre (highest concentration of mirex obtainable in seawater) 
when tested under various conditions of salinity and nutrient 
concentration (Hollister et al., 1975).  Exposure to 10.2 g/litre 
(maximum concentration of mirex obtainable in synthetic seawater) 
did not adversely affect photosynthesis and the chemical 
composition of green and red marine algae (Sikka et al., 1976).  
Mirex at a concentration of 100 g/litre in a culture medium of a 
freshwater algae,  Chlorella pyrenoidosa, depressed population 
growth by 8% in 92 h and 19% in 164 h (Kritcher et al., 1975). 

    Mirex is highly toxic for crustacea; data are summarized in 
Table 5.  Delayed mortality appears to be characteristic of mirex 
poisoning in crustacea.  Freshwater crayfish, particularly third 
instars, were extremely sensitive to mirex, through direct and 
indirect exposure under laboratory conditions (Ludke et al., 1971).  
Although authors have suggested that crayfish would not be exposed 
to sufficient mirex under field conditions to cause population 
decline (Muncy & Oliver, 1963; Markin et al., 1972), three 
applications of mirex bait at 1.4 kg/ha, about 90 days apart, 
reduced the number of red crayfish eventually harvested (Hyde, 

1973).  Estuarine crustaceans exposed to mirex under laboratory 
conditions become irritated, lose equilibrium, move randomly, 
become paralysed and may die (Bell et al., 1978).  The onset 
and severity of such symptoms depend on the level of exposure, 
water temperature (Tagatz et al., 1975) and salinity (Leffler, 
1975), and the age and size of animal under test (Lowe et al., 
1971).  Juvenile and larval stages are most sensitive.  Exposure 
to 0.01 - 10 g mirex/litre medium did not have any appreciable 
effect on day-to-day survival in 2 replicate series of larval 
blue crabs, for 5 days after hatching.  Delayed mortality then 
occurred with 1 and 10 mg being acutely toxic and 0.01 and 0.1 
being sublethal (Bookhout & Costlow, 1976).  McKenzie (1970) 
found that the toxicity of mirex bait for crabs was temperature 
dependent; no mortality occurred in treated crabs held at 10C 
but survival time decreased as the water temperature increased 
from 20 to 27C. 

    At subacute internal levels of mirex (0.19 - 0.03 mg/kg body   
weight), caused by the ingestion of 0.14 g mirex bait, crabs 
held in water of intermediate salinity (6.8 - 20.4o/oo) showed 
an elevated metabolic rate, inhibition of limb autotomization, 
thin carapaces, and abnormal behaviour.  A sub-acute level of 
0.01 g/litre medium lengthened the duration of the developmental 
stagesin mud crabs but had no effect on stone crab development 
(Bookhout et al., 1972).  In a simulated field application of 
mirex fire ant bait, the bait was applied at 1.4 kg/ha on a sandy 
slope with a pool of flowing seawater (29C; salinity 27o/oo) at 
the other end of a tank.  After 2 treatments, one week apart, 73% 
of fiddler crabs became paralysed or died within 2 weeks of the 
applications (Lowe et al., 1971).                                               

    Oxygen consumption of the pond snail,  Physa gyrina was         
increased by exposure to low concentrations of mirex (0.008 - 
0.07 mg/litre) for 3 days but decreased by 44% by exposure to 
1 mg/litre mirex (de la Cruz & Naqvi, 1973).  Exposure to very 
low concentrations of mirex (initial concentration 0.062, final        
concentration of 0.016 mg/litre) for 30 days was sufficient to     
decrease the feeding and burrowing activities of adult lugworms,   
 Arenicola cristata, even 45 days after termination of the 
exposure (Schoor & Newman, 1976).                                           

    Some toxicity data for fish are given in Table 6.  Young  
juveniles are more sensitive to mirex than adults (Lee et al.,

Table 4.  Toxicity of mirex for algae
Organism                   End point                   Parameter    Concentration Reference
Alga                       decrease in productivity    4-h EC28-46  1000          Butler (1963)


  Uva lactuca               no effect at maximum        EC0          10.2          Sikka et al. (1976)
  Enteromorpha linza        solubility in water
  Rhodymenia pseudopalmata

Marine algae:

  Chlorococcum sp.          no effect on population     168-h EC0    0.2           Hollister et al.
  Dunaliella tertiolecta    growth or oxygen evolution                             (1975)
  Chlamydomonas sp.
  Porphiridium cruentum
  Thallasiosira pseudonana
  Nitzschia sp.

Table 5.  Toxicity of mirex for crustacea
Organism               Size    Flow/    pH   Temp  Hard-   Salin- Parameter     Concen-  Reference
                               stat          (C)  ness    ity                  tration          
                                                   (mg/)   (o/oo)               (g/
                                                   ltr)                         litre)
Crayfish, juvenile     0.6 cm  aerated  7.8        28             48-h LC65     0.1      Ludke et al.      
 (Procambarus hayi)             stat                                                      (1971)

Blue crab, larva               stat          25            30     20-day 98%    1        Bookhout & 
 (Callinectes sapidus)                                             survival to            Costlow (1976)
                               stat          25            30     20-day 0.5%   1        Bookhout & 
                                                                  survival to            Costlow (1976)
                                                                  1st crab
                               stat          25            30     20-day 56%    0.01     Bookhout & 
                                                                  survival to            Costlow (1976)
                               stat          25            30     20-day 41.5%  0.01     Bookhout & 
                                                                  survival to            Costlow (1976)
                                                                  1st crab

Blue crab, juvenile            flow                               96-h exposure 100      Lowe et al.       
 (Callinectes sapidus)          400 l/h                            100% died              (1970)
                                                                  within 18 days

Pink shrimp, juvenile  51-76   flow          14            29     3-week LC11   0.1      Lowe et al.       
 (Penaeus duorarum)     mm      400 l/h                                                   (1971)

Glass shrimp                   stat          23-25                120-h LC50    190      Naqvi & de la 
 (Palaemonetes                                                                            Cruz (1973b)

Amphipod                       stat          23-25                600-h LC54    1        Naqvi & de la 
 (Hyallela azteca)                                                                        Cruz (1973b)

    Bluegills and goldfish were exposed to mirex either through a 
single application of a formulation to holding ponds or by mirex-
treated diet (Van Valin et al., 1968).  No mortality occurred in 
bluegills, but growth was slow in fish fed 5 mg/kg diet.  A dose-
related mortality rate and pathological changes were observed in 
goldfish exposed to 0.1 and 1 mg/litre.  Goldfish that died at 
these concentrations were emaciated, lacked slime layers, had 
roughened skin with many protruding scales, and exhibited 
oedematous gill changes.  Survivors suffered microbial infection 
(the severity of which was related to treatment level), distended 
gall bladders, and granulomatous kidney lesions by day 224.  In 
another study, treatment of ponds with mirex reduced the survival 
of 4 species of fish to 43.3%, compared with 71.6% survival in 
controls, 10 months after the application, but spawning was not 
affected (Bookhout & Costlow, 1975).  Mosquito fish and bluegills 
exposed to 1 mg mirex/litre leached from fire ant bait exhibited 
differences in oxygen consumption compared with controls during the 
7-week exposure, but whether the differences were significant was 
not stated (de la Cruz & Naqvi, 1973).  Mirex affects fish 
behaviour.  Temperature selection was altered in sailfin molly 
exposed to mirex at 1 mg/litre (Degrove cited in Task Force Report 
on Mirex, 1977).  The activity rhythm of diamond killifish was 
affected by exposure to mirex (Tolman & Livingston cited in Canada, 
Department of National Health and Welfare, 1977). 

8.2.  Terrestrial Organisms

8.2.1.  Plants

    Little work has been done on the effects of mirex on 
terrestrial plants.  In one study (Rajanna & de la Cruz, 1975), the 
phytotoxic effects of recrystallized technical mirex on 6 crops 
were investigated.  Reduction in germination and emergence occurred 
as the concentration of mirex increased.  In germination studies, 
where germination blotters were soaked in solutions of mirex, the 
percentage of germination occurring over 21 days was significantly 
reduced by 0.15 mg/litre in tall fescue, alisike clover, and 
alfalfa; by 0.3 mg/litre in crimson clover and johnson grass; and 
by 0.7 mg/litre in annual rye grass.  Similar doses caused a 
reduction in percent emergence, when mirex was applied to the sandy 
substrate in which the seeds were grown.  In a duplicate study, 
emerged seedlings were harvested 2 weeks after planting, for dry 
weight determinations.  Significant reductions in growth rate 
occurred at 0.15 mg/litre in crimson clover, johnson grass and 
annual rye grass; at 0.3 mg/litre in fescue and alfalfa; and at 0.7 
mg/litre in alisike clover.  Visual examination of seedlings 
revealed poor development.  Other studies have demonstrated uptake, 
accumulation (de la Cruz & Rajanna, 1975), and translocation 
(Mehendale et al., 1972) of mirex in plants, but there was no 
evidence of metabolic transformation. 

Table 6.  Toxicity of mirex for fish
Species                Flow/  Temp  Para-  Concentration   Effect                      Reference
                       stat   (C)  meter  (g/litre)                                 
Goldfish               stat   2-28         1000            death 24 days after ex-     Van Valin et al.
 (Carassius auratus)                                        posure 75-100%, granul-     (1968)
                                                           omatous lesions of kidney
                                                           224 days after exposure

Mullet                 flow         96-h   10-10 000       adult (260-380 mm), old     Lee et al. (1975)
 (Mugil cephalus)       15.61                               juv. (70-150 mm); no
                       1/h                                 deaths; mortality rate in
                                                           young juv. (20-43 mm);
                                                           6.4% (0.01 mg/litre), 26.9%
                                                           (0.1 mg/litre), 32.1%
                                                           (1 mg/litre), 90% (10

Bluegill                            LC0    1.3-1000        no effect on reproduction,  Van Valin et al.
 (Lepomis macrochirus)                                      body weight, size;          (1968)
                                                           population decreased
Sheepshead minnow      flow   19.1         0.53            some gill changes           Tagatz et al.
 (Cyprinodon                   29.8                                                     (1975)
 variegatus) a,d

Pinfish, juvenile      flow         5-     20 mg/kg        no effect                   Lowe et al. (1971)
 (Lagodon rhomboides)b               month  diet

Channel catfish        stat                1.4 kg/ha       survival decreased by       Hyde et al. (1974)
 (Ictalurus punctatus)c                     3 applications  39.5% compared with
a  Exposed to leachate from fire ant bait.
b  Technical grade, 98% mirex.
c  Three applications of mirex bait 0.3% technical.
d  Four 28-day seasonal exposures.

8.2.2.  Insects

    Mirex is moderately toxic for bees and should not be applied 
directly to bees in the field or in the colonies; the authors quote 
an LD50 of 7.15 mg/bee (Atkins et al., 1975).  In adult field 
crickets, a lethal dose of 25 mg per animal produced characteristic 
symptoms of a latent period of at least 72 h followed by hyper-
activity, ataxia, convulsions, and paralysis (MacFarlane et al., 
1975).  The primary action of mirex was suggested to be on synaptic 
transmission; mirex exposure results in prolonged synaptic after  
discharge and enhanced spontaneous transmission.  Houseflies 
respond slowly to mirex (Plapp, 1973).  Exposure of 11 strains to 1 
mg mirex residues per jar of flies resulted in a 50% knock-down in 
2 - 4 days exposure and 90% knock-down in 3 - 5 days.  Exposure to 
100 mg/kg diet produced 50% knock-down in 4.5 - 7 days and 90% in 5 
- 10 days.  With lower concentrations, knock-down time increased 
and differences in response between strains became greater. 

8.2.3.  Birds

    Mirex is not very toxic for birds (Table 7).  It is of low 
short-term toxicity for wild birds; dietary doses of 2250, 750, and 
250 mg/kg diet killed 50% of juvenile male grackles in 5, 14, and 
38 days, respectively.  Death occurred sooner in colder weather, 
presumably because food consumption increased (Stickel et al., 

Table 7.  Toxicity of mirex for birds
Species        Route   Age        Sex  Parameter    Concen-    Reference
Mallard        oral                    acute LD50   2400a      Waters (1976)

Mallard        oral    10 day          8-day LD50b  > 5000     Hill et al. (1975)

Mallard        oral    3-4 month  M    acute LD50c  2400a      Tucker & Crabtree (1970)

Japanese       oral                    acute LD50   10 000     Waters (1976)

Japanese       oral    14 day          8-day LD50b  > 5000     Heath et al. (1972)

Bobwhite       oral    14 day          8-day LD50b  2511       Heath et al. (1972)

Pheasant       oral                    acute LD50   1400-1600  Waters (1976)

Ring-necked    oral    14 day          8-day LD50b  1540       Heath et al. (1972)

Grackle        oral    juv        M    12-day LD50  750        Stickel et al. (1973)

Cowbird        oral    adult      M    12-day LD50  750        Stickel et al. (1973)

Redwinged      oral    adult      F    11-day LD50  750        Stickel et al. (1973)

Starling       oral    juv        F    9-day LD50   750        Stickel et al. (1973)
a  mg/kg body weight, otherwise mg/kg diet.
b  Fed mirex for 5 days, untreated diet for 3 days, mortality estimated on day 8.
c  Single dose, mortality estimated 14 day post treatment.
    Most toxicological studies on birds have monitored the effects 
of mirex on reproductive variables.  Under field conditions, no 
significantly adverse effects on reproduction were observed when 
bobwhite quail were kept on plots treated with 11.2 (the regular 
field-rate use), 112, or 1120 kg/ha (Baker, 1963).  In laboratory 
studies, feeding bobwhite quail with 40 mg mirex/kg, and mallard 
with 1 or 10 mg/kg in their diet, did not have any effects on egg 
production, shell strength or thickness, embryonation and embryo 
survival, or hatching and survival of chicks up to 14 days of age 
(Heath & Spann, 1973).  Exposure of white leghorn hens to 5, 10, 
20, 80, and 160 mg mirex/kg diet, and of Japanese quail to 5, 40, 
and 80 mg/kg, for 12 weeks did not affect egg production, egg 
weight, shell calcium content, shell thickness, shell weight, or 
the proportion of broken or soft-shelled eggs (Davison & Cox, 1974; 
Davison et al., 1975).  Laying hens tolerated up to 200 mg mirex/kg 
diet without adverse effects on hatchability or chick growth and 
survival, but there were some eggshell abnormalities (Waters, 
1976).  Twelve weeks of daily exposure to mirex at 300 or 600 mg/kg 
in the feed produced weight loss in hens.  Exposure to 600 mg/kg 
also caused a significant decrease in egg hatchability and chick 
survival (Naber & Ware, 1965).  Exposure of third-generation 
progeny of wild mallards to a diet treated with mirex at 100 mg/kg 
for 25 weeks caused a significant reduction in duckling survival 
(Hyde et al., 1973b).  The percentage of ducklings surviving up to 
2 weeks after hatching was 72.6 in the 100 mg/kg group compared 
with 93.8 and 95.7 in the 1 mg/kg and control groups, respectively.  
There appeared to be a deleterious association between residue 
concentration in the egg and subsequent duckling survival.  When 
0.1 mg mirex/kg diet was fed to laying white leghorn hens in 
combination with similar low levels of dieldrin, DDT, and 
heptachlor, there were no synergistic effects on reproductive 
variables (Driver et al., 1976). 

    In studies on the biochemical effects of mirex on birds, 
dietary levels of 5 - 80 mg/kg, fed to quail, and 5 -160 mg/kg fed 
to chickens, for 12 weeks, did not affect liver weight, aniline 
hydroxylase and aminopyrine- N-demethylase activities of hepatic 
microsomes, or cytochrome P-450 concentrations in hepatic 
microsomes (Davison & Cox, 1974).  Chickens fed 10 or more mg 
mirex/kg diet showed structural changes in their livers; 500 mg/kg 
fed to newly hatched chickens up to 5 weeks of age significantly 
depressed levels of IgG and IgM but did not influence antibody 
production (Glick, 1974). 

8.3.  Microorganisms

    Estuarine microorganisms are not affected by concentrations of 
mirex that are likely to be found in the estuarine environment.  
The only variable affected by mirex at concentrations below 100 
mg/litre is primary productivity (Brown et al., 1975).  However, 
mirex is rapidly associated with sediments and the highest 
concentrations recorded in Lake Ontario were around 40 g/litre 
(Canada, Department of National Health and Welfare, 1977).  The 
degradation products of mirex, e.g., kepone and photomirex, are 
more toxic than the parent compound (Brown et al., 1975). 

    Total populations of soil fungi and bacteria were not affected 
by exposure to 20 g technical mirex/kg soil for 7 days, but 
concentrations of 10 and 20 g/kg did reduce the actinomycete 
population in 1 out of 3 soils treated (Jones & Hodges, 1974). 

8.4.  Bioaccumulation and Biomagnification

    Mirex is highly cumulative; bioaccumulation data are summarized 
in Table 8.  The amount taken up varies with species, and is also 
related to the concentration and duration of exposure (de la Cruz & 
Naqvi, 1973).  Kobylinski & Livingston (1975) studied the uptake of 
mirex from contaminated sediment by the Hogchoker (a freshwater 
flatfish) under both static and constant flow conditions.  Mirex 
was added to sand at concentrations of 1430, 470, and 140 g/kg, 
and this was covered by 14 litres of water.  Uptake by Hogchoker 
tissues was dose-dependent, with accumulation increasing over time 
without reaching an equilibrium.  Fish absorbed mirex from both the 
water and sediments.  In the flowing system, appreciable amounts of 
mirex were lost from the environment. 

    Wojcik et al. (1975) measured mirex residues in a variety 
of non-target organisms and suggested that biomagnification had 
occurred.  This had presumably followed ingestion of animals 
containing lower residues.  Residues tended to be higher in 
insectivorous species that ate targeted insects.  In fish, residues 
tended to be higher in predators than in omnivores (Collins et al., 
1974).  It has been shown that mirex can be moved through a simple 
2-level food chain by feeding crab on shrimp that had been poisoned 
by mirex (Lowe et al., 1971).  During mirex treatment of coastal 
areas for fire ant control and for a year afterwards, residues were 
less than 10 mg/litre in water and were 0 - 0.07 mg/kg in sediment 
(Borthwick et al., 1973).  However, in organisms up the food chain, 
concentrations increased significantly; birds contained 0 - 0.17 
mg/kg and mammals 0 - 4.4 mg/kg. 

Table 8.  Bioaccumulation of mirex
Organism                  Organ    BCF      Concentration      Exposure  Conditions   Reference
                                            (mg/litre)         period    
Turtle grass              leaf     0        0.1                10 days   exposed      US EPA (1972)
 (Thalassia testudinum)    rhizome  0.36                                  through

 Ulva lactuca              WB       350-     10.2                                      Sikka et al. (1976)
 Enteromorpha linza                 1100                        
 Rhodymenia pseudopalmata
4 Species of unicellular  WB       3200-    0.2                7 days    stat         Hollister et al.
algae                              7300                                               (1975)

Blue crab, 5-day larva    WB       1100     0.1                3 weeks   stata        Bookhout & Costlow
 (Callinectes sapidus)                                                                 (1975)

Blue crab, 15-day larva   WB       3000     0.01                         stata        Bookhout & Costlow
 (Callinectes sapidus)                                                                 (1975)

Blue crab, megalopa       WB       2000     0.01                         stata        Bookhout & Costlow
 (Callinectes sapidus)                                                                 (1975)

Pink shrimp, larva        WB       2600     0.1                3 weeks                Lowe et al. (1971)
 (Penaeus duorarum)        liver    24 000   0.1                3 weeks

Amphipod                  WB       2530     1                  28 days   stat         de la Cruz & Naqvi
 (Hyalla azteca)                                                                       (1973)

Fathead minnow            WB       51 400   0.37               56 days   flow         Huckins et al.

Chicken, adult male       fat      138      7.2 mg/kg diet     26 weeks               Medley et al.
                          fat      103      7 g/kg diet       20 weeks               (1974)
                          fat      69       0.71 mg/kg diet    20 weeks

Mallard                   egg      2.4-2.8  1 and 10mg/kg diet 25 weeks               Hyde et al. (1973b)
Mallard, adult female     wings    3.6-5.5  1 and 10mg/kg diet 25 weeks
                          liver    1.5-3.8                     25 weeks
                          fat      30                          25 weeks
a  Static culture bowl method with a change to fresh medium and chemical each day.
WB - Whole body.
BCF - Bioconcentration factor: concentration in tissue/concentration in medium.
    In birds, mirex may accumulate to high levels.  This is 
particularly so in insectivorous birds where mirex levels of 1 - 10 
mg/kg tissue have been reported (Mirex Advisory Committee, 1972).a  
Mirex residues transferred to eggs persist in juveniles.  For 
example, in snowy egrets, eggs contained 13 mg/kg, nestlings 3 - 5 
mg/kg, and parents, 0.64 mg/kg, after an application of mirex baits 
in the  area  (Mirex Advisory Committee, 1972).a  Where point 
discharges of mirex have taken place, accumulation of residues in 
birds' eggs is indicative of widespread distribution of mirex in 
the local environment. 

    According to Naqvi & de la Cruz (1973a), habitat appeared to 
affect bioaccumulation, the highest residues being found in ponds 
(0.37 mg/litre), creeks (0.31 mg/litre), grassland (0.28 mg/kg), 
lakes (0.27 mg/litre), and estuaries (0.20 mg/litre).  Within 
ecosystems, there appeared to be a hierarchy of accumulation.  In 
an aquatic ecosystem, the following residue levels were found; 
annelids (0.63 mg/kg), crustaceans (0.44 mg/kg), insects (0.29 
mg/kg), fish (0.26 mg/kg), and molluscs (0.15 mg/kg). 

8.5.  Population and Community Effects

    Mirex residues in aquatic ecosystems do not appear to be 
directly toxic to algae and phytoplankton at environmentally 
realistic concentrations.  However, mirex can be concentrated by 
various species of phytoplankton, which can thus serve as passive 
agents of transfer of mirex up the food chain.  In addition, 
adsorption on organic material in sediments results in a high 
toxicant input to detritus feeders (Leffler, 1975). 
Bioconcentration in aquatic species (Table 8) is a very common 
problem.  Transportation of mirex in a food chain was demonstrated 
when grass shrimp, which had been poisoned by being individually 
fed one particle of mirex bait, were fed to juvenile blue crab.  
These crabs then died from mirex poisoning within 14 days of eating 
1 - 4 shrimps (Lowe et al., 1971).  As expected, predatory animals 
contain higher residues than omnivores or herbivores (Collins et 
al., 1974). 

    Sensitivity of larval and juvenile crustaceans to mirex is very 
significant because their survival success determines the fate of 
entire populations (Bookhout & Costlow, 1976).  However, no massive 
die-offs or declines in population have been reported for crustacea 
(Markin et al., 1972).  Dose-dependent secondary effects observed 
may be particularly important at low concentrations.  In fish, 
bacterial infection and growth inhibition are secondary effects of 
mirex poisoning (Van Valin et al., 1968), but there have been no 
detailed field surveys of the effects of mirex on fish populations 
(Task Force on Mirex, 1977).  Of importance to the aquatic 
community is the depressive effect of mirex on lugworm activity, 
which will delay trapping of pollutants in sediments (Schoor & 
Newman, 1976). 

a  Report to US Environmental Protection Agency

    There is evidence of accumulation of mirex in aquatic and 
terrestrial food chains to harmful levels.  After 6 applications of 
mirex bait at 1.4 kg/ha, high mirex levels were found in some 
species; turtle fat contained 24.8 mg mirex/kg, kingfishers, 1.9 
mg/kg, coyote fat, 6 mg/kg, oppossum fat, 9.5 mg/kg, and racoon 
fat, 73.9 mg/kg (Hyde et al., 1973a). 

    In a model ecosystem with a terrestrial-aquatic interface, 
sorgum seedlings were treated with mirex at 1.1 kg/ha (Metcalf et 
al., 1973).  Caterpillars fed on sorgum seedlings and their faeces 
contaminated the water which contained algae, snails,  Daphnia,  
mosquito larvae, and fish.  After 33 days, the ecological 
magnification value was 219 for fish and 1165 for snails. 

    An area of early old-field treated with mirex showed less 
vegetation biomass and lower species diversity than an untreated 
old-field ecosystem (Cassita & Kricher, 1973).  Most terrestrial 
invertebrates in the USA contained less than 0.1 mg mirex/kg 
residues, but some species, particularly scavengers (that eat bait 
directly) and predators, contained as much as 30 mg/kg.  Mirex can 
cause temporary population decline in insects.  A 0.3% granular 
formulation of mirex applied at 0.20 kg/ha (recommended rate for 
the control of fire ant) caused a significant reduction in carabid, 
staphylid, and cricket numbers, though spider numbers were 
unaffected (Reagan et al., 1972).  It was noted that application of 
twice this recommended rate did not eliminate fire ants.  Mirex 
applied as corncob bait and sprayed at 4.2 -42 kg/ha in a mixed 
hardwood forest caused a decline in centipede numbers but not in 
numbers of spiders, millipedes, beetles, and scorpions (Lee, 1974).  
Leaf decomposition was significantly accelerated.  As would be 
expected, control measures against fire ants cause destruction of 
general ant fauna (Markin et al., 1974a).  However, a decline in an 
insect population is not permanent (Mirex Advisory Committee, 
1972;a Lee, 1974).  There was no effect of mirex treatment on 
population size in 18 insect species in the year following 
application to one ecosystem (Wojcik et al., 1975). 

    Most mammals living in areas treated with mirex contain mirex 
residues.  These reach a maximum 1 - 3 months after application and 
decline significantly during the next 12 months (Wojcik et al., 
1975).  No toxic effects of mirex on wildlife have been recorded in 
Canada (Canada, Department of National Health and Welfare, 1977). 

    Very low mirex levels in falcon eggs collected in eastern and 
northern Canada in 1975 indicated that there was no apparent 
indigenous problem with mirex contamination, since falcons are near 
the top of the food pyramid in these terrestrial ecosystems (Task 
Force on Mirex, 1977). 

a  Report to US Environmental Protection Agency

8.6.  Effects on the Abiotic Environment

    Levels in sediment samples collected from Lake Ontario 
indicated that mirex continues to accumulate in harbour and 
offshore sediments, although decreasing amounts are being deposited 
in more recent lake sediments (Scrudato & del Prete, 1982).  Mirex-
contaminated sediments are accumulating in deeper water (100 m) of 
the lake at about 2.2 - 7.0 mm/year.  It was suggested that it might 
be 200 - 600 years before mirex-contaminated sediments were covered 
by 'clean' sediments (Halfon, 1981).  In addition, natural and 
anthropogenic mixing of contaminated sediments would provide a 
continuing source of mirex for lake organisms. 

8.7.  Appraisal

    Mirex is one of the most environmentally stable of the 
organochlorine insecticides.  There are 2 clearly established 
routes of contamination of the environment, the first from the 
manufacture and industrial use of mirex and the second from its 
agricultural use in control programmes for fire ants.  Mirex 
bioaccumulates at all trophic levels and biomagnifies in food 
chains.  It degrades slowly and its breakdown products are as toxic 
and stable as the parent compound.  Mirex is strongly adsorbed on 
sediments and only poorly soluble in water.  These characteristics 
combine with biotic factors, such as inhibition of activity of 
burrowing detritus feeders, to guarantee environmental accumulation 
of mirex and to slow down its removal from sediment and the 
covering of contaminated sediment layers with clean material. 

    A major pathway of mirex movement is from sediments or water 
into scavengers or herbivores.  These are eaten by predatory 
invertebrates that are themselves ultimately eaten by vertebrates.  
This is the classic food-chain concentration of a contaminant.  
Biomagnification in the food chain is further encouraged by the 
delayed mortality typical of mirex poisoning.  Because of its 
delayed effects, mirex shows a wide range of acute toxicity in 
different species.  Chronic toxicity is a better indicator of the 
true toxicity of mirex and is uniformly high.  This delayed effect 
appears to result from its high rate of uptake and slow rates of 
metabolism and excretion. 

    Effects on organisms combined with its persistence suggest that 
mirex presents a long-term hazard for the environment.  Mirex 
induces pervasive chronic physiological and biochemical disorders 
in various vertebrates.  Aquatic crustaceans show extreme 
sensitivity to the compound, and game birds and fish feeding close 
to manufacturing plants accumulate enough mirex to constitute a 
health hazard.  Some birds feed in contaminated areas and then 
migrate to other areas, resulting in the unpredictable dispersal of 

    Although general environmental levels of mirex are low, it is 
widespread.  The broadcast use of mirex in agriculture poses the 
greatest threat in increasing this contamination. 


    IARC (1979) evaluated the carcinogenic hazard resulting from 
exposure to mirex and concluded that "there is sufficient evidence 
for its carcinogenicity to mice and rats.  In the absence of 
adequate data in humans, it is reasonable, for practical purposes, 
to regard mirex as if it presented a carcinogenic risk to humans". 

    No acceptable daily intake (ADI) for mirex has been advised by 

    Over recent years, official registrations for a number of uses 
of mirex have been withdrawn in several countries for various 
reasons.  Details can be obtained from IRPTC. 

    Regulatory standards established by national bodies in 12 
different countries (Argentina, Brazil, Czechoslovakia, the Federal 
Republic of Germany, India, Japan, Kenya, Mexico, Sweden, the 
United Kingdom, the USA, and the USSR) and the EEC can be obtained 
from the IRPTC (International Register of Potentially Toxic 
Chemicals) Legal File (IRPTC, 1983). 


10.1.  Mirex Toxicity

    Mirex is moderately toxic in single-dose animal studies (oral 
LD50 values range from 365 - 3000 mg/kg body weight).  It can enter 
the body via inhalation, ingestion, and via the skin. 

    It is one of the most stable pesticides in use today.  It 
accumulates in adipose tissue and biomagnifies in food chains.  
Excretion is slow and elimination half-lives can extend over many 

    The most sensitive effects of repeated exposure in experimental 
animals are principally associated with the liver, and these have 
been observed with doses as low as 1.0 mg/kg diet (0.05 mg/kg body 
weight per day), the lowest dose tested. 

    At higher dose levels, it is fetotoxic (25 mg/kg in diet) and 
teratogenic (6.0 mg/kg per day). 

    Mirex was not generally active in short-term tests for genetic 
activity.  There is sufficient evidence of its carcinogenicity in 
mice and rats. 

    No data on effects on human beings were available to the Task 

10.2.  Exposure to Mirex

    In the general population, food probably represents the major 
source of intake of mirex, fish, wild game, and meat being the main 
sources.  Normally, such intake will be below established residue 
tolerances.  Mirex may occur in breast milk but levels are very low 
or below detection limits. 

    No data are available, regarding occupational exposure.

10.3.  Evaluation of Environmental Impact

    Mirex is one of the most stable of the organochlorine 
insecticides.  Although general environmental levels are low, it is 
widespread in the biotic and abiotic environment.  Mirex is both 
accumulated and biomagnified.  Mirex is strongly adsorbed on 
sediments and has a low water solubility. 

    The delayed onset of toxic effects and mortality is typical of 
mirex poisoning.  The long-term toxicity of mirex is uniformly 
high.  Mirex is toxic for a range of aquatic organisms, with 
crustacea being particularly sensitive.  Mirex induces pervasive 
long-term physiological and biological disorders in vertebrates. 

    Although no field data are available, the adverse effects of 
long-term exposure to low levels of mirex combined with its 
persistence suggest that the use of mirex presents a long-term 
environmental risk. 

10.4.  Conclusions

1.  No data on human health effects are available in connection
    with occupational exposure to mirex.  Based on the findings
    in mice and rats, this chemical should be considered, for
    practical purposes, as being potentially carcinogenic for
    human beings.

2.  For the same reason, reservations must remain about the
    safety of this chemical in food, despite the relatively low
    residues so far reported.

3.  Effects on the organisms studied, as well as its persistence,
    suggest that mirex presents a long-term hazard for the

4.  Taking into account these considerations, it is felt that
    the use of this chemical for both agricultural and
    non-agricultural applications should be discouraged, except
    where there is no adequate alternative.


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O'NEAL, J., MARKIN, G.P., & COLLINS, H.L.  (1974)  Effects of
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PEELER, D.F.  (1976)  Open field activity as a function of
pre-weaning or generational exposure to mirex.  J. Miss. Acad.
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PESTICIDE CHEMICAL NEWS  (1976)  June 9th, p. 8.

PITTMAN, K.A., WIENER, M., & TREBLE, D.H.  (1976)  Mirex
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 Metab. Dispos., 4: 288-295.

Alterations in hepatic microsomal proteins of mice
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21: 344-351.

PLAPP, F.W.  (1973)  Mirex: toxicity, tolerance and metabolism
in the house fly  Musca domestic  L.  Environ. Entomol., 2:

Distribution, metabolism and excretion of DDT and mirex by a
marine Teleost, the winter flounder.  Environ. Health
 Perspect., 4:45-54.

RAJANNA, B. & DE LA CRUZ, A.A.  (1975)  Mirex incorporation in
the environment. Phytotoxicity on germination, emergence and
early growth of seedlings.  Bull. environ. Contam. Toxicol.,
14: 77-82.

RAO, D.S.V.S. & GLICK, B.  (1977)  Pesticide effects on the
immune response and metabolic activity of chicken lymphocytes.
 Proc. Soc. Exp. Biol. Med., 154:27-29.

REAGAN, T.E., COBURN, G., & HENSLEY, S.D.  (1972)  Effects of
mirex on the arthropod fauna of a Louisiana sugar cane field.
 Environ. Entomol., 1: 588-591.

REITER, L.  (1977)  Behavioral toxicology: effects of early
postnatal exposure to neurotoxins on development of locomotor
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L.E., Jr  (1977)  Comparative behavioral toxicology of mirex
and kepone in the rat.  Toxicol. appl. Pharmacol., 41: 143.

ROBINSON, K.M. & YARBROUGH, J.D.  (1968)  Liver response to
oral administration of mirex in rats.  Pestic. Biochem.
 Physiol., 8: 65-72.

ROBINSON, K.M. & YARBROUGH, J.D.  (1978)  A study of liver
function in rats with mirex-induced enlarged livers.  Pestic.
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SANDHU, S.S., WARREN, W.J., & NELSON, P.  (1978)  Pesticidal
residue in rural potable water.  J. Am. Water Works Assoc., 70:

SAVAGE, E.P.  (1976)   National study to determine levels of
 chlorinated hydrocarbon insecticides in human milk: 1975-76,
Fort Collins, Colorado, Colorado State University,
Epidemiologic Studies Center (Report, Iss. EPA/540/9-78/005,
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SCHOOR, W.P.  (1974)  Accumulation of mirex in the adult blue
crab,  Callinectes sapidus. Bull. environ. Contam. Toxicol.,
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SCHOOR, W.P. & NEWMAN, S.M.  (1976)  The effect of mirex on
the burrowing activity of the lugworm  Arenicola cristala.
 Trans. Am. Fish. Soc., 105: 700-703.

SCHRAUZER, G.N. & KATZ, R.N.  (1978)  Reductive dechlorination
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SCRUDATO, R.J. & DEL PRETE, A.  (1982)  Lake Ontario sediment
- mirex relationships.  J. Great Lake Res., 8: 659-699.

SHACKELFORD, W.M. & KEITH, L.H.  (1976)   Frequency of organic
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SIKKA, H.C., BUTLER, G.L., & RICE, C.P.  (1976)   Effects,
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(1982)  Ultrastructure of the thyroid glands of rats fed
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 in drinking-water. Part II,  Ontario, Ministry of the
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(1977)  Pharmacokinetics of mirex in goats. 1. Effect on
reproduction and lactation.  J. agric. food Chem., 25: 945-947.

(1978)  Pharmacokinetics of mirex in goats. 2. Residue tissue
levels, transplacental passage during recovery.  J. agric. food
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SPENCE, J.H. & MARKIN, G.P.  (1974)  Mirex residues in the
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STEIN, V.B., PITTMAN, K.A., & KENNEDY, M.W.  (1976)
Characterization of a mirex metabolite from monkeys.  Bull.
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(1973)  Toxicity and persistance of mirex in birds. In:
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BECKING, G.C.  (1980)  Sub-chronic toxicity of photomirex in
the female rat - results of 28-day and 90-day feeding studies.
 Drug chem. Toxicol., 3: 105-134.

SUTA, B.E.  (1978)   Human population exposures to mirex and
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Seasonal effects of leached mirex on selected estuarine
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TASK FORCE ON MIREX  (1977)   Mirex in Canada,  Ottawa (Report
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(1973)  Mirex in seals.   Sci. total Environ., 2: 196-198.

THORNE, B.M., TAYLOR, E., & WALLACE, T.  (1978)  Mirex and
behavior in the Long-Evans rat.  Bull. environ. Contam.
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TUCKER, R.K. & CRABTREE, D.G.  (1970)   Handbook of toxicity of
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Interior, Fisheries and Wildlife Service, 131 pp (Resource
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CYPHER, R.L.  (1977)  A carcinogenicity assay of mirex in
Charles River rats.  J. Natl Cancer Inst., 58: 133-140.

US EPA  (1972)   Effects of pesticides in water - a report to
 the United States,  Washington DC, US Environmental Protection
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US EPA  (1978)   Kepone-mirex-hexachlorocyclopentadiene: an
 environmental assessment,  Washington DC, US Environmental
Protection Agency, pp. 36-50.

US NRC  (1978)   Kepone/mirex/hexachlorocyclopentadiene - an
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US NTIS  (1968)   Evaluation of chronic, teratogenic, and
 mutagenic activities of selected pesticides and industrial
 chemicals, Vol. 1. Carcinogenic study,  Washington DC, US
Department of Commerce.

VAN VALIN, C.C., ANDREWS, A.K., & ELLER, L.L.  (1968)  Some
effects of mirex on two warm-water fishes.  Trans. Am. Fish.
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REYNOLDS, L.M.  (1977)  Effects of food deprivation in rats
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 Contam. Toxicol., 18: 278-284.

NORSTROM, R.J., & CHU, I.  (1979a)  Photomirex: a
teratogenicity and tissue distribution study in the rabbit. 
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MARINO, I.A., VALLI, V.E., CHU, I., & BECKING, G.C.  (1979b)
Short-term toxicity of photomirex in the rat.  Toxicol. appl.
 Pharmacol., 47: 105-114.

L., & BECKING, G.C.  (1979c)  Ninety-day toxicity of
photomirex in the male rat.  Toxicology, 12: 235-250.

(1977)  Some effects of dieldrin and mirex on Ehrlich ascites
tumor cells  in vivo  and  in vitro. Arch. environ. Contam.
 Toxicol., 5: 333-341.

WARE, G.W. & GOOD, E.E.  (1967)  Effects of insecticides on
reproduction in the laboratory mouse. II. Mirex, telodrin and
DDT.  Toxicol. appl. Pharmacol., 10: 54-61.

Barbiturate-induced sleeping times, liver weights, and
reproduction of cottontail rabbits after mirex ingestion.
 Bull. environ. Contam. Toxicol., 19: 223-228.

WATERS, E.M.  (1976)   Mirex: an overview and abstracted
 literature collection, 1947-1976,  Oak Ridge, Oak Ridge
National Laboratory, Toxicology Information Response Center,
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WIENER, M., PITTMAN, K.A., & STEIN, V.  (1976)  Mirex
kinetics.  Drug Metab. Dispos., 4: 281-287.

KELSO, G.L, & HOPKINS, S.C.  (1978)  State of the art report
on pesticide disposal research. In: Kennedy, M.V., ed.
 Disposal and decontamination of pesticides. A Symposium at the
 174th Meeting of ACS, Chicago, August 29 - September 2, 1977,
pp. 73-79 (American Chemical Society Symposium Series 73).

MIDDELEM, C.H., & LOFGREN, C.S.  (1975)  Mirex residues in
non-target organisms after application of experimental baits
for fire ant control - South West Georgia 1971-1972.  Pestic.
 Monit. J., 9: 124-133.

(1979)  Lethal and reproductive effects of dietary mirex and
DDT on old-field mice,  Peromyscus polionotus. Bull. environ.
 Contam. Toxicol., 21: 397-402.

(1975)  The cumulation and disappearance of mirex residues.
III. In eggs and tissues of hens fed two concentrations of the
insecticide in their diet.  Bull. environ. Contam. Toxicol.,
14: 98-104.

    See Also:
       Toxicological Abbreviations
       Mirex (HSG 39, 1990)
       Mirex (IARC Summary & Evaluation, Volume 5, 1974)
       Mirex (IARC Summary & Evaluation, Volume 20, 1979)