Mirex (EHC 44, 1984)

INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

ENVIRONMENTAL HEALTH CRITERIA 44

MIREX

This report contains the collective views of an international group of
experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization.

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the United Nations Environment Programme,
the International Labour Organisation,
and the World Health Organization

World Health Orgnization
Geneva, 1984

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CONTENTS

ENVIRONMENTAL HEALTH CRITERIA FOR MIREX

1. SUMMARY AND RECOMMENDATIONS

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. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND
ANALYTICAL METHODS

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

3. PRODUCTION, USES, TRANSPORT AND DISTRIBUTION

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

4. ENVIRONMENTAL LEVELS AND EXPOSURES

4.1. Environmental levels
4.2. General population exposure

5. KINETICS AND METABOLISM

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

6. EFFECTS ON EXPERIMENTAL ANIMALS

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

7. EFFECTS ON MAN

8. EFFECTS ON ORGANISMS IN THE ENVIRONMENT

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

9. PREVIOUS EVALUATIONS OF MIREX BY INTERNATIONAL BODIES

10. EVALUATION OF HEALTH RISKS FOR MAN AND EFFECTS
ON THE ENVIRONMENT

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

REFERENCES

TASK GROUP MEETING ON ENVIRONMENTAL HEALTH CRITERIA FOR
ORGANOCHLORINE PESTICIDES OTHER THAN DDT (CHLORDANE,
HEPTACHLOR, MIREX, CHLORDECONE, KELEVAN, CAMPHECHLOR)

Members

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

Dr D.A. Akintonwa, Department of Biochemistry, Faculty of
Medicine, University of Calabar, Calabar, Nigeria^a

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

Secretariat

Dr M. Gilbert, International Register for Potentially Toxic
Chemicals, United Nations Environment Programme, Geneva,
Switzerland

Mrs B. Goelzer, Division of Noncommunicable Diseases, Office
of Occupational Health, World Health Organization, Geneva,
Switzerland

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

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^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,
Switzerland

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

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

NOTE TO READERS OF THE CRITERIA DOCUMENTS

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

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

* * *

A detailed data profile and a legal file can be obtained from
the International Register of Potentially Toxic Chemicals, Palais
des Nations, 1211 Geneva 10, Switzerland (Telephone no. 988400 -
985850).

ENVIRONMENTAL HEALTH CRITERIA FOR MIREX

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. SUMMARY AND RECOMMENDATIONS

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
levels.

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
rate.

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
hazard.

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
activity.

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. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL METHODS

2.1. Identity

Molecular formula: C₁₀C1₁₂

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

Synonyms: dodecachloropentacyclo[5.2.1.0²⁶0³⁹0⁵⁸]
decanedodecachlorooctahydro-1,3,4-metheno-
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, 1972^a; Carlson et al., 1976).

Mirex is quite resistant to pyrolysis; decomposition begins
at 525°C (Kennedy et al., 1977), and 99 - 98% combustion is
accomplished at 700°C 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,
1977).

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^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/cleanup^a method^a 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

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

soil & sediment extract with petroleum ether GC/ECD 3-6 µg/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 µg/kg Collins et al. (1973)
extract with hexane, CC

biological grind with anhyd. sodium sulfate, GC/ECD 1 µg/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. PRODUCTION, USES, TRANSPORT AND DISTRIBUTION

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

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^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
control.

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 µg/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).

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 µg/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 µg/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
contamination.

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.

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^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 - 95°C 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. ENVIRONMENTAL LEVELS AND EXPOSURES

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 µg/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 µg/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).

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 µg/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,
1979).

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
µg/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 µg/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 µg 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 µg/kg, on a fat
basis (Mes et al., 1978).

(b) Occupational exposure

No data are available on occupational exposure to mirex.

5. KINETICS AND METABOLISM

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).

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
liver.

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. EFFECTS ON EXPERIMENTAL ANIMALS

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,
1970).

Table 2. Oral, intraperitoneal, and dermal LD₅₀ values for mirex
---------------------------------------------------------------------
Species Sex Exposure route LD₅₀ Reference
(mg/kg
body
weight)
---------------------------------------------------------------------
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 1.6.2.4) 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.,
1979).

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 1.14.14.1) 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
animals.

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
observed
---------------------------------------------------------------------------------------------------------
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,
1973).

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).

7. EFFECTS ON MAN

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

8. EFFECTS ON ORGANISMS IN THE ENVIRONMENT

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 µg 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 µg
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 µg/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 µg/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 µg 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 10°C
but survival time decreased as the water temperature increased
from 20 to 27°C.

At subacute internal levels of mirex (0.19 - 0.03 mg/kg body
weight), caused by the ingestion of 0.14 µg mirex bait, crabs
held in water of intermediate salinity (6.8 - 20.4^o/oo) showed
an elevated metabolic rate, inhibition of limb autotomization,
thin carapaces, and abnormal behaviour. A sub-acute level of
0.01 µg/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 (29°C; salinity 27^o/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.,
1975).

Table 4. Toxicity of mirex for algae
------------------------------------------------------------------------------------------------------
Organism End point Parameter Concentration Reference
(µg/litre)
------------------------------------------------------------------------------------------------------
Alga decrease in productivity 4-h EC_28-46 1000 Butler (1963)

Algae:

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) (µg/
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)
megalopa
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)
megalopa
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)
kadiakensis)

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 (µg/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
mg/litre)

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
control
---------------------------------------------------------------------------------------------------------
^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.,
1973).

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

Mallard oral 10 day 8-day LD₅₀^b > 5000 Hill et al. (1975)

Mallard oral 3-4 month M acute LD₅₀^c 2400^a Tucker & Crabtree (1970)

Japanese oral acute LD₅₀ 10 000 Waters (1976)
quail

Japanese oral 14 day 8-day LD₅₀^b > 5000 Heath et al. (1972)
quail

Bobwhite oral 14 day 8-day LD₅₀^b 2511 Heath et al. (1972)
quail

Pheasant oral acute LD₅₀ 1400-1600 Waters (1976)

Ring-necked oral 14 day 8-day LD₅₀^b 1540 Heath et al. (1972)
pheasant

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)
blackbird

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 µg/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 µg/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
rhizomes

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 stat^a Bookhout & Costlow
(Callinectes sapidus) (1975)

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

Blue crab, megalopa WB 2000 0.01 stat^a 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.
(1982)

Chicken, adult male fat 138 7.2 mg/kg diet 26 weeks Medley et al.
fat 103 7 µg/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
mirex.

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.

9. PREVIOUS EVALUATIONS OF MIREX BY INTERNATIONAL BODIES

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
FAO/WHO.

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. EVALUATION OF HEALTH RISKS FOR MAN AND EFFECTS ON THE ENVIRONMENT

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
months.

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
Group.

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
environment.

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.

REFERENCES

ABSTON, P.A. & YARBROUGH, J.D. (1976) The in vivo effect of
mirex on soluble hepatic enzymes in the rat. Pestic. Biochem.
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PITZ, E.P., ROURKE, D., ABRAHAM, R., & COULSTON, F. (1979)
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PRITCHARD, J.B., GUARINO, A.M., & KINTER, W.B. (1973)
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SCHOOR, W.P. & NEWMAN, S.M. (1976) The effect of mirex on
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SCHRAUZER, G.N. & KATZ, R.N. (1978) Reductive dechlorination
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    See Also:
       Toxicological Abbreviations
       Mirex (HSG 39, 1990)
       Mirex (IARC Summary & Evaluation, Volume 5, 1974)
       Mirex (IARC Summary & Evaluation, Volume 20, 1979)