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PubMedDate not supplied

Heptachlor, heptachlor epoxide, and other chlordane compounds in Finnish plywood workers.

Residue levels of heptachlor, heptachlor epoxide, and other chlordane compounds were determined in sera from 74 Finnish plywood workers and 52 controls. Concentrations of heptachlor epoxide in plywood workers varied from below the detection limit of 0.1 ng/g to 19.2 ng/g serum (conversion factor for SI units = 975 [1 ng/g = 0.98 microgram/l]); the mean and standard deviation were 3.2 and 3.9 ng/g, respectively. Heptachlor expoxide values in controls varied from below the detection limit to 1.2 ng/g serum. The exposure time, i.e., number of years spent working with sizings that contained heptachlor, correlated with the residue levels of heptachlor epoxide that were measured in serum samples taken from employees at two companies (p = .03). The most common chlordane compound (contaminant of heptachlor) found in the sera of plywood workers was trans-nonachlor; also found were high concentrations of heptachlor epoxide. Headache, dizziness, and eye irritation were not related to serum levels of heptachlor or chlordane compounds.

Adolescent↗
PubMedDate not supplied

Carcinogenicity of heptachlor and heptachlor epoxide.

Heptachlor and its metabolite heptachlor epoxide are unequivocally carcinogenic in rats and mice. The chemicals induced carcinomas of the liver, which were highly significant. There were neoplasms at other sites in rats. Neoplasms at all sites, as well as malignant tumors, were increased in heptachlor-treated male rats. There were similar increases in benign and malignant neoplasms of endocrine organs, particularly in female rats. Neoplasms of the thyroid and pituitary were increased in male rats and neoplasms of the reproductive system, including the ovary and uterus, in female rats given heptachlor. Mice also developed hepatic vein thrombosis and thrombosis of the atria of the heart. Nephritis, myocarditis, encephalitis, hepatitis, polyarteritis and atrophy of the testes were observed in rats.

Animals↗
PubMed1977

Dominant lethal studies with technical chlordane, HCS-3260, and heptachlor: heptachlor epoxide.

Male albino mice in groups of eight were each given single doses, either by gavage or by intraperitoneal injection, of either technical chlordane (50 or 100 mg/kg), HCS-3260 (50 or 100 mg/kg), or heptachlor:heptachlor epoxide (25:75) (7.5 or 15 mg/kg). The males were subsequently mated with three untreated females for six consecutive weeks. No dominant lethal changes among females that had mated with the treated males were produced.

Animals↗
PubMed1977

Confirming heptachlor and heptachlor epoxide in food samples by gas-liquid chromatography of their photoderivates.

The food sample extract is cleaned up on a Florisil column and the 6% ethyl ether in petroleum ether cluate is subjected to repeated concentrations, using a micro-Snyder column, to expel volatile materials that absorb ultraviolet (UV) light. The sample and standard solutions of heptachlor and heptachlor epoxide are placed in quartz cells and exposed to UV radiation in the dark. Characteristic photoderivatives of the respective pesticides which form in the sample extract are identified and measured by comparison with those formed in the irradiated standard solutions, using electron capture gas-liquid chromatography. Recoveries of the 2 pesticides from 13 products, fortified at levels from 0.01 to 0.3 ppm and determined after derivatization, ranged from 67 to 110%.

Chromatography, Gas↗
PubMed1990

Ecological toxicology and human health effects of heptachlor.

The chlorinated cyclodiene heptachlor was registered in 1952 as an agricultural and domestic insecticide. By early 1984, registration for all purposes, except subterranean termite control and for limited use in the control of fire ants, had been cancelled. This restriction of use arose primarily from concerns over the environmental persistance and bioaccumulation potential of the organochlorine pesticides. Currently, sale of heptachlor has been voluntarily suspended over questions about its carcinogenic potential, and the absence of safe and effective application methods. As a persistent organochlorine pesticide, heptachlor residues are detected in all components of the environment. In historical use, heptachlor was directly applied to terrestrial systems, while air and water were secondarily contaminated via volatilization and land run-off, respectively. Within each environmental compartment, heptachlor undergoes a variety of metabolic and abiotic transformations. In vivo studies indicate that heptachlor epoxide is the predominant metabolite, formed as a product of the mixed-function oxidase system, while 1-hydroxychlordene is the major soil metabolite. For quantification, heptachlor and its metabolites are extracted from air, soil and sediment, water, or biological materials using various organic solvents and analyzed by gas chromatography or thin-layer chromatography. Residue reports comprise most of the literature concerning the effects of heptachlor on the biota. In many such reports, toxic effects cannot be conclusively attributed to heptachlor exposure. Toxicity to organisms seems more dependent on acute exposure, while the chronic effects of low level exposure to heptachlor are poorly defined. Maximal terrestrial residues coincide with temporal and spatial proximity to application; peak residues in aquatic systems on the other hand, correlate to periods of maximum run-off. The lipophilic nature of both heptachlor and heptachlor epoxide results in the potential for significant bioaccumulation in all lipid-type compartments in the environment. The toxic effects of heptachlor are not specific for any one organ system. The liver and the central nervous system are most significantly affected by heptachlor, although effects can also be seen in the reproductive, hematopoietic, immune, and renal systems. An important consideration is the relation of relevant environmental exposure levels to toxicity. The concentrations necessary to elicit results in laboratory experiments do not translate directly to the same results upon environmental exposure, nor do experimental laboratory animal models absolutely equate with native-state organisms or with humans.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1976

Heptachlor: uptake, depuration, retention, and metabolism by spot, Leiostomus xanthurus.

The estuarine fish, spot (Leiostomus xanthurus), was exposed to 0.27, 0.52, 1.01, 1.99, and 3.87 mug/liter technical grade heptachlor (65% heptachlor, 22% trans-chlordane, 2% cis-chlordane, 2% nonachlor, and 9% unidentified compounds) for 24 days in a flowthrough bioassay, followed by 28 days in heptachlor-free seawater. Concentrations of heptachlor, heptachlor epoxide, and trans- and cis-chlordane in edible tissues were monitored at day 3 and weekly thereafter throughout the bioassay and at the end of the postexposure period. All four chemicals were accumulated by spot. Maximum concentrations of heptachlor were observed on day 3; maximum concentrations of the other three compounds were observed on day 17. The average bioconcentration factors for heptachlor and trans-chlordane were 3,600 and 4,600, respectively. Only 10% or less of the maximum concentrations of heptachlor, heptachlor epoxide, and trans-chlordane accumulated during the exposure period remained after 28 days in pesticide-free seawater; an average of 35% of the cis-chlordane remained. Relative total amounts of heptachlor and cis-chlordane changed during the exposure and post-exposure periods. Nearly all of the heptachlor was eliminated or metabolized to its epoxide. Cis-chlordane, which averaged 4-7% of the total residues (chlordanes and heptachlors) in edible tissues during the exposure, increased to 18-23% of the total residues by the end of the postexposure period.

Animals↗
PubMed1976

Heptachlor: toxicity to and uptake by several estuarine organisms.

Technical-grade heptachlor (65% heptachlor, 22% trans-chlordane, 2% cis-chlordane, and 2% nonachlor) was tested in 96-hr bioassays to determine its toxicity to estuarine animals. The test organisms and the 96-hr LC50 or EC50s based on measured concentrations in water) are as follows: American oyster (Crassostrea virginica), 1.5 mug/liter; pink shrimp (Penaeus duorarum), 0.11 mug/liter; grass shrimp (Palaemonetes vulgaris), 1.06 mug/liter; sheepshead minnow (Cyprinodon variegatus), 3.68 mug/liter; pinfish (Lagodon rhomboides), 3.77 mug/liter; and spot (Leiostomus xanthurus), 0.85 mug/liter. Analytical-grade heptachlor (99.8% heptachlor) and heptachlor epoxide (99%) were also studied. The analytical-grade heptachlor 96-hr LC50 for pink shrimp and spot was 0.03 mug/liter and 0.86 mug/liter, respectively, while that for pink shrimp exposed to heptachlor epoxide was 0.04 mug/liter. Heptachlor was accumulated and some metabolized to its epoxide by all animals tested. Fish and oysters accumulated heptachlor in their tissues 2,800-21,300 times the measured concentration in water; shrimp, only 200-700 times.

Animals↗
PubMed1986

Residues in cattle grazed on land contaminated with heptachlor.

Heptachlor epoxide residues exceeding the maximum residue limit of 0.2 mg/kg have been found in fat of cattle grazed on land previously treated with heptachlor prior to planting potatoes or maize. To determine the residues accumulated in cattle exposed to contaminated land and the rate of decline on removal from the contamination, steers were grazed on a former potato paddock which had been treated the 2 previous years with heptachlor at 1.1 kg/ha. Soil residues in the paddock varied from a total of 0.42 mg/kg heptachlor and its epoxide at the beginning of the trial to 0.31 mg/kg after 16 months. Residues in the soil decreased only slightly down to a depth of 300 mm. Pasture residues were less than 0.02 mg/kg (wet basis). Heptachlor epoxide residues in the body fat of the steers increased during 19 months of exposure and reached a maximum of 0.72 mg/kg. In 4 steers removed after 14 weeks exposure, the heptachlor epoxide concentrations continued to increase from a mean of 0.24 mg/kg to a mean of 0.34 mg/kg after a further 4 weeks. Concentrations then fell progressively with a half life of 11 weeks in the body fat. There was an apparent relationship between pasture length and body fat residue, with residues increasing as pasture length decreased. The results of the experiments preclude the option of grazing cattle on pasture grown on soil treated with heptachlor for any extended period of time. It is possible that if short pastures and soft soil are avoided, and if cattle are not exposed to contaminated land for any more than 1 week in each month, then residues would remain below the maximum residue limit of 0.2mg/kg heptachlor.

Adipose Tissue↗
PubMed1990

Effect of heptachlor on hepatic mitochondrial oxidative phosphorylation in rat.

In a study of the hepatotoxicity of heptachlor (1,4,5,6,7,8,8-heptachlor 3a, 4,7,7 a-tetrahydro-4,7-methanoindene), a major compound of chlordane, the effect of heptachlor on the respiratory activity (oxidative phosphorylation and electron transport) of rat liver mitochondria was investigated. Heptachlor at a final concentration of 50 microM with succinate as substrate decreased the respiratory control index (RCI) due to a marked inhibition of state 3 respiration and a slight inhibition of state 4 respiration. One hundred microM heptachlor with succinate as substrate suppressed the states 3 and 4 respiration almost completely. On the other hand, heptachlor at a final concentration ranging from 50 to 100 microM with beta-hydroxybutylate (beta-HB) slightly decreased the RCI and decreased the RCI hardly at all with ascorbate plus N,N,N',N', -tetramethylphenylene diamine (TMPD) as substrate. Heptachlor at a concentration of 50 microM in the presence of succinate also decreased the ADP/O ratio of mitochondria. The mode of inhibition of succinate oxidation by heptachlor apparently is a noncompetitive inhibition, as shown by Lineweaver-Burk plot.

Animals↗