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A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Michigan State University, Oregon State University, and University of California at Davis. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program.

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Lindane

Publication Date: 9/93

TRADE OR OTHER NAMES

Proprietary names for products containing BHC are Agrocide, Ambrocide, Benesan, Benexane, Borer-Tox, and Gamasan. Lindane may also be found in formulations with a host of fungicides and insecticides.

INTRODUCTION

Lindane is an organochlorine insecticide and fumigant which has been used on a wide range of soil-dwelling and plant-eating insects. Lindane is presently used primarily for seed treatment and in lotions, creams, and shampoos for the control of lice, and mites (scabies) in humans.

Benzene Hexachloride (BHC) is the 100% pure form of the product while lindane is slightly less pure (>99% pure). There are eight separate three dimensional forms (isomers) of BHC; the gamma configuration being one of those forms. As used in this profile lindane and BHC refer only to the gamma isomer of BHC.

Some formulations of lindane are classified as Restricted Use Pesticides (RUP). Restricted Use Pesticides may be purchased and used only by certified applicators. Most uses of lindane in agriculture and in the dairy industry have been cancelled by the EPA. Lindane is no longer manufactured in the United States.

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

Lindane is highly toxic and carries the signal word WARNING. It is a central nervous system stimulant with symptoms usually developing within one hour. Symptoms of acute exposure in humans can include mental and motor retardation, central nervous system excitation, clonic (intermittent) and tonic (continuous) convulsions, respiratory failure, pulmonary edema and dermatitis. Other symptoms in humans are more behavioral in nature such as loss of balance and somersaulting (7), grinding of the teeth, and hyperirritability. Lindane can be absorbed through the skin, through inhalation or through direct ingestion.

Most acute effects have been due to accidental or intentional ingestion, although inhalation occurred (especially among children) when it was used in vaporizers. Workers may be exposed to the product through absorption through the skin and through inhalation if handled incorrectly.

The oral LD50 for rats is 88-270 mg/kg, for mice 59-246 mg/kg, and for rabbits 60 mg/kg. The lowest oral dose which may be lethal for a child is estimated to be 180 mg/kg. Lotions (10%) applied for scabies have resulted in severe intoxication in some children and infants.

CHRONIC TOXICITY

Sixty male workers in a lindane producing factory had no signs of neurological impairment or perturbation after one to thirty years exposure. However another study of chronically exposed workers showed some mild differences in heart beat.

Small amounts of lindane fed to rabbits (1.5-12.0 mg/kg) for five to six weeks, and to rats (6.25-25 mg/kg) for 35 weeks suppressed their immune systems. This adversely affected the organisms' ability to fight off disease. In a two-year rat study, significant liver changes were attributed to the intake of moderately small amounts of lindane in the diets of the test animals (approximately 5 mg/kg/day).

Reproductive Effects

Female rats experienced a disturbance of their reproductive cycle and inhibited fertility with doses of 0.5 mg/kg for four months. Treatments of 0.05 mg/kg did not produce these effects. Lindane was found to be slightly estrogenic to female rats and also caused the seminiferous tubules in male rats to become atrophied at doses of 8 mg/kg/day over a ten day period (7). These tests suggest that the compound may have reproductive effects in human populations.

Teratogenic Effects

Beagles given 7.5 or 15 mg/kg from day five throughout gestation did not produce pups with any noticeable birth defects. Pregnant rats given small amounts of lindane in their food had offspring unaffected by the pesticide (3). Lindane, however, can be passed from the mother to the developing fetus (3). It appears that lindane will not cause developmental effects at low levels of exposure and causes reproductive effects at levels approaching the acute toxicity doses. These effects have not been observed in human populations.

Mutagenic Effects

A variety of tests on mice and on microbes have shown no mutagenicity in the cells tested (7). It has been shown to induce some changes in the chromosomes of cultured human lymphocytes during cell division at fairly low doses. It is unlikely that lindane would pose a mutagenic risk in humans at very low exposure levels.

Carcinogenic Effects

The carcinogenicity of lindane in experimental animals is low (or limited) as judged by the International Agency for Research on Cancer (1). Mice fed 100-500 mg/kg diets for 24 weeks showed no signs of tumors. Rats fed for a lifespan at 5-1,600 mg/kg diet with a mean age at death of 58 weeks, had no increase in tumor incidence.

One of the confounding factors in establishing a link between the insecticide and carcinogenicity is the presence of three different dimensional forms (isomers) of the compound BHC. Each form has a slightly different toxicity.

The International Agency for Research on Cancer has concluded that there is sufficient evidence to show that one of the lindane isomers is carcinogenic and limited evidence to establish the carcinogenicity of the beta and gamma isomers (10).

Fate in Humans and Animals

Of a single dose of 40 mg/kg to rats, 80% was excreted in urine and 20% in feces. Half of the administered lindane is excreted in three or four days. When administered for 18 days at 8 mg/kg, metabolites were found in blood, liver, kidneys, spleen, heart, and the brain. In humans, the mono, di, tri, and tetra-chlorophenolic metabolites are detected in urine with the trichlorophenols predominating. Residues disappear within three weeks after dosing ceases. Cows fed low doses in their daily ration for 35 days produced milk with residues from 0.002 to 0.015 ppm.

ECOLOGICAL EFFECTS

Lindane can be stored in the fat of mammals and birds. Birds of prey in the Netherlands contained up to 89 ppm in this tissue. Residues can also find their way into egg yolks at measurable concentrations for 32 days after dosing (5). Harbor seals from the German North Sea and racoons from North America were found to have lindane in their fat at concentrations ranging from 0.3 ppm to 1.0 ppm (8).

Lindane is very highly toxic to fish. The 96 hr LC50 ranges from 1.7 to 32 ppb for trout and salmon to 44 to 131 ppb for catfish, perch and goldfish. Water hardness did not seem to alter the toxicity to fish but temperature did. An increase in temperature from 2 degrees to 18 degrees C caused a 2.3-fold decrease in rainbow trout toxicity, but a 7 degree to 29 degrees C increase caused a 2.6-fold increase in bluegill toxicity. Chronic, sublethal exposures to lindane produced liver and kidney problems in fish. Most of the lindane in the fish was unmetabolized. In the snail (Physa) most of the lindane was found as the metabolite pentachloro-cyclohexene.

Birds are more tolerant of high doses of lindane than are mammals. Mallards have an LD50 of more than 5000 mg/kg. Pheasants, Japanese quail, and bobwhite quail have LC50 values of 561 ppm, 425 ppm and 882 ppm respectively. Thus lindane is only slightly toxic to these organisms. Egg shell thinning and reduced egg production has occurred in birds exposed to lindane.

Lindane is highly toxic to bees and to aquatic invertebrates. The compound is believed to cause birth defects in amphibians.

ENVIRONMENTAL FATE

On eight types of soil, it was found that lindane residues decreased by 40 to 80% per year. When sprayed on the surface, the half- life was 4-6 weeks with 90% gone in 30-40 weeks. When worked into the soil, the half-life was 15-20 weeks with 90% gone in two to three years. At the end of 15 years, 0.2% remained. The typical half-life for lindane was 400 days. Lindane can be washed off and into the soil, especially when humus content is low (5).

The pesticide has been found in a significant number of groundwater samples in New Jersey, California, Mississippi, South Carolina, and in Italy at very low concentrations (maximum concentration of 0.9 ppb in New Jersey) (8). Lindane is a contaminant in water in the Great Lakes at very low concentrations as well.

Lindane is very stable in both fresh and salt water environments. It will disappear from the water by secondary mechanisms such as adsorption on sediment, biological breakdown by microflora and fauna, and adsorption by fish through gills, skin and food (5). Storage in body fat is directly proportional to concentration in feed.

Plants pick up residues from not only direct application, but through water and vapor phases. While crops such as cauliflower and spinach had less than 0.1 ppm when grown in soil with residues of 0.1 to 0.5 ppm, carrots may accumulate high, persistent concentrations (5). Persistence is seen when plants are rich in lipid content. The half- life in lettuce was three to four days. The metabolism in plants is not well understood, but carrots were estimated to metabolize lindane at a rate of 43 to 47% after eight to ten weeks, based on the uptake by the plant.

Exposure Guidelines:

NOEL (rat): 0.33 mg/kg/day, based on multiple effects
Drinking Water: 4 ug/l (ppb) (EPA); 3 ug/l (ppb) (WHO)
HA: 0.0002 mg/l lifetime
TLV-TWA: 0.5 mg/m3
TLV STEL: 1.5 mg/m3
ADI: 0.008 mg/kg/day (WHO)
RfD: 0.0003 mg/kg/day (EPA)
LEL: 1.55 mg/kg/day

Physical Properties:

CAS #: 58-89-9
Chemical name: gamma-1,2,3,4,5,6-hexachlorocyclohexane
Chemical class/use: organochlorine insecticide
Solubility in water: 7 mg/l
Solubility in other solvents: >5 g/100g in acetone, benzene, ethanol and ethyl acetate
Melting Point: 112.5 degrees C
Vapor Pressure: 3.3 x 10 to the minus 5 power mm Hg
Partition Coefficient: 3.61-3.72 (log octanol/water)

BASIC MANUFACTURER

Drexel Chemical Company
PO Box 9306
2487 Pennsylvania St.
Memphis, Tn 38109
Telephone: 901/774-4370

Review by Basic Manufacturer:

Comments solicited: October, 1992
Comments received:

REFERENCES

  1. U.S. Department of Health and Human Services (1985). Fourth Annual report on Carcinogens, Summary 1985, Public Health Service, NTP 85-002
  2. Johnson, W.W. and M.T. Finley (1980). Handbook of Acute Toxicity of Chemicals to Fish and Aquatic Invertebrates. U.S. Department of Interior, Fish and Wildlife Service, Resource Publication 137.
  3. National Library of Medicine (1992). Hazardous Substances Databank. TOXNET, Medlars Management Section, Bethesda, MD.
  4. U. S. Environmental Protection Agency (1987). Health Advisory, Office of Drinking Water.
  5. Ulman, E. (1972). Lindane, Monograph of an Insecticide, Verlag K. Schillinger, Federal Republic of Germany.
  6. Menzie, Calvin M. (1980). Metabolism of Pesticides, Update III. U. S. Dept of the Interior, Fish and Wildlife Service, Special Scientific Report, Wildlife No. 232.
  7. Smith, Andrew G. (1991). Chlorinated Hydrocarbon Insecticides. in Handbook of Pesticide Toxicology, Volume 3, Classes of Pesticides. Wayland J. Hayes Jr. and Edward R. Laws, Jr. editors. Academic Press, Inc., NY.
  8. Howard, Philip H. (1991). Handbook of Environmental Fate and Exposure Data for Organic Chemicals. Volume III, Pesticides. Lewis Publishers, Chelsea, MI.
  9. Briggs, Shirley A. 1992. Basic Guide to Pesticides: Their characteristics and hazards. Hemisphere publishing Corp., Washington, DC.
  10. ACGIH. 1991. Documentation of the Threshold Limit Values and Biological Exposure Indices. American Conference of Governmental and Industrial Hygienists. Cincinnati, OH.