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PubMed1995

In vivo and in vitro effects of graded doses of the pesticide heptachlor on female sex steroid hormone production in rats.

Adult female Sprague-Dawley rats were injected with corn oil or 5 mg, 20 mg, 25 mg or 30 mg per kg body weight of heptachlor solution every other day for up to 18 days. The rats were killed at the end of the experimental period, and blood samples were assayed for progesterone and oestrogen by radioimmunoassay. Ovarian cells from the rats were isolated and incubated either on their own, or in the presence of LH or FSH, and production of progesterone and oestrogen determined. Control incubations consisted of cells from corn oil-treated rats. The latter were also incubated on their own or in the presence of LH or FSH. Heptachlor significantly suppressed blood progesterone and oestradiol levels (P < 0.05 to P < 0.001), the degree of suppression depending on the dose and the stage of the oestrous cycle in which samples were obtained. Production of oestradiol by ovarian cells from heptachlor-treated rats was lower than for corn oil-treated controls. Cells from rats treated with low doses of heptachlor (5 mg per kg body weight) showed an increased production of progesterone, while high doses (> 20 mg per kg body weight) suppressed production.

Animals↗
PubMed1998

The effect of heptachlor, a chlorinated hydrocarbon insecticide, on p53 tumor suppressor in human lymphocytes.

Previous studies have shown that heptachlor, a chlorinated hydrocarbon insecticide, is a liver tumor promoter in rats and mice and induces tumor promoting-like alterations in human myeloblastic leukemia cells. The nature of tumor promotion is multifaceted and has recently been shown to include suppression of programmed cell death (apoptosis) as a mechanism by which a tumor promoter can prolong cell viability. The ability of tumor promoters to suppress apoptosis prompted us to address the question of whether heptachlor is capable of effecting the expression of genes involved in lymphocyte apoptosis, in particular, the p53 tumor suppressor gene. Experiments with a CEM x 174 cell line, a hybrid of human T and B cells, revealed that heptachlor downregulated p53 gene expression at the post-transcriptional level without changing levels of mRNA in the cells. The heptachlor-induced reduction in the basal levels of expression of this gene was both in a concentration and time-dependent manner.

Apoptosis↗
PubMed1999

Effect of the chlorinated hydrocarbons heptachlor, chlordane, and toxaphene on retinoblastoma tumor suppressor in human lymphocytes.

Organochlorine use over the past 50 years has resulted in the contamination of soil, water, plant and animal species. This contamination has created a long-lasting environmental problem, as the members of the organochlorine class of pesticides are resistant to degradation and have been labeled as persistent bioaccumulators. Studies have shown certain organochlorines to be tumor promoters, liver toxicants and to induce immune cell dysfunction in rats and mice. Our laboratory has shown that the organochlorines heptachlor and chlordane affect leukocytic gene expression and differentiation. In this study, experiments with CEM x 174 cells, a hybrid of human T and B cells, were performed to investigate the effects of the tumor promoter heptachlor and its congeners chlordane and toxaphene on retinoblastoma (Rb) gene expression. The results indicated that heptachlor, chlordane or toxaphene, in the range of 10-50 microM, were able to reduce Rb protein levels in a concentration-dependent manner. In the case of heptachlor, the reduction could be seen as early as 12 h and was time-dependent. Analysis of Rb mRNA levels revealed no detectable difference over the same concentration range. These results suggest that members of the organochlorine class are able to downregulate Rb expression at the post-transcriptional level, an effect similar to that on p53 tumor suppressor previously reported by our laboratory.

Blotting, Western↗
PubMed1991

Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii.

The commercial milk supply on Oahu was contaminated by heptachlor epoxide for as long as 15 months during 1981-82 at levels possibly as high as 1.2 ug/g, fat basis. Following the contamination, several investigators attempted to evaluate potential adverse health outcomes, especially among infants and young children. However, results of the initial investigations are inconclusive due to lack of reliable measures of heptachlor exposure, use of non-random sampling techniques, and lack of definitive health outcomes attributable to heptachlor epoxide. The design of a current study to assess the body concentrations of heptachlor epoxide and related pesticides in Hawaii is presented. The study is designed (1) to relate these concentrations to prior exposure via the milk contamination, and (2) to assess the reliability of breast milk and serum pesticide concentrations as objective biological markers of body burden. No attempt is made to relate these data to health outcomes; instead, the findings may provide the foundation for future health studies or surveillance of environmental exposure to pesticides in Hawaii.

Animals↗
PubMed1988

An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor.

We studied a group of 45 dairy farm family members who had consumed undiluted raw milk products known to be contaminated with residues of the pesticide heptachlor at concentrations as high as 89.2 ppm (fat basis). We compared results of serum pesticide assays for these exposed persons with results for an unexposed group of 94 persons from the same geographic area and the results from the Second National Health and Nutrition Examination Survey. The exposed group had significantly higher mean levels of primary heptachlor metabolites--ie, heptachlor epoxide (0.84 +/- 1.0 vs 0.50 +/- 0.9 parts per billion) and oxychlordane (0.71 +/- 0.8 vs 0.49 +/- 1.1 parts per billion)--than the unexposed group. In the exposed group, 21.2% had elevated serum concentrations of these same metabolites; this rate was significantly greater than the rates in both the unexposed farm family members (heptachlor epoxide, 3.8%; oxychlordane, 6.3%) and the Second National Health and Nutrition Examination Survey sample (2.5% for both metabolites). However, we found no evidence of related acute and/or subacute hepatic effects in these exposed persons regardless of their serum concentrations of pesticide residues.

Adolescent↗
PubMed1981

Heptachlor epoxide in marine mammals.

The presence of heptachlor epoxide in harbour seals (Phoca vitulina) and white-beaked dolphins (Lagenorhynchus albirostris) has been confirmed by chemical derivatization and mass spectrometric analyses. An unknown compound at a retention time close to half of heptachlor epoxide interfered in the determination by electron capture detector-gas chromatography. On a WCOT CP-Sil 7 column programmed from 85 to 175 degree C two poorly separated peaks could be detected. Heptachlor epoxide contents up to 1.7 mg/kg (on a fat basis) were obtained, which were about 200 times lower than the PCB levels. The same ratio was also observed in fish from the same area.

Animals↗
PubMed1985

The effects of heptachlor and lindane on birds, Columbia Basin, Oregon and Washington, 1976-1981.

The effects of heptachlor seed treatments on birds in the vicinity of the Umatilla National Wildlife Refuge, Oregon and Washington, were investigated from 1978 to 1981. An egg was collected from each of 60 nests representing six species. Heptachlor epoxide (HE) residues were detected in 35 eggs and were particularly high (8-13 micrograms g-1) in a few eggs of the black-billed magpie, mallard, and ring-necked pheasant. These residues were within the range that induced reproductive problems in other species in the area. Diagnostically lethal residue levels (greater than or equal to 9 micrograms g-1) of HE were detected in the brains of nine birds (four species). Most of the avifauna in the area contained residues of HE and related compounds. Lindane, the replacement chemical for heptachlor, did not produce adverse effects in birds, and residues were not detected in either their eggs or brains.

Animals↗
PubMed1991

The effect of the insecticide heptachlor on ras proto-oncogene expression in human myeloblastic leukemia (ML-1) cells.

Expression of the ras proto-oncogene mRNA in human myeloblastic leukemia (ML-1) cells was analyzed as a function of cDNA amplification by polymerase chain reaction (PCR). By using a pair of oligonucleotides that flank exon-2 from opposite strands (5' and 3') of H-ras cDNA for PCR amplification, ML-1 cells were found to express a 112 bp segment of the ras transcript. A rapid decline in the expression of this transcript was seen in cells treated with heptachlor, a chlorinated hydrocarbon insecticide. Expression of the same ras segment was not affected by treatment of ML-1 with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Furthermore, addition of serum to quiescent, heptachlor-treated cultures of ML-1 cells inhibited the effect of heptachlor and restored the expression of the ras protooncogene mRNA.

Actins↗
PubMed1995

Effects of graded doses of the pesticide heptachlor on body weight, mating success, oestrous cycle, gestation length and litter size in laboratory rats.

Adult female Sprague-Dawley rats were injected with 5 or 20 mg/kg body weight heptachlor solution every other day for up to 18 days. They were weighed every day and the stage of oestrus determined by vaginal smears. One experimental group was mated and pregnancy characteristics studied. Heptachlor affected body weights, cycle patterns, length of gestation period and litter sizes in a dose-related manner. At a dose of 20 mg/kg body weight, heptachlor caused a significant decrease in average body weight (P < 0.01), disrupted and/or prolonged oestrous cycles, decreased mating success (P < 0.001), slightly increased gestation length (P < 0.05) and decreased litter size (P < 0.01).

Animals↗
PubMed1984

Dieldrin, heptachlor, and chlordane residues in soybeans in Illinois 1974, 1980.

The Illinois soybean crop was monitored in 1974 and 1980 for dieldrin, heptachlor, and chlordane residues resulting from the use of these compounds for corn soil insect control in the years before extensive soybean cultivation. Residue levels were compared with past published amounts. Dieldrin residue levels in soybeans declined between 1974 and 1980. Heptachlor and heptachlor epoxide levels remained level between 1974 and 1980. Chlorinated hydrocarbon residues were lower in the southern third of Illinois than for the remainder of the state.

Chlordan↗
PubMed1984

Promotion of mouse liver neoplasms by the organochlorine pesticides chlordane and heptachlor in comparison to dichlorodiphenyltrichloroethane.

The organochlorine pesticides chlordane and heptachlor were demonstrated to be liver neoplasm promoters in mice. Male B6C3F1 mice exposed to diethylnitrosamine (DEN) for 14 weeks followed by 25 weeks on control diet developed a 40% incidence of liver neoplasms whereas those given chlordane or heptachlor afterwards had approximately an 80% incidence of liver neoplasms, as did mice given DDT, a positive reference compound. Mice exposed to DEN also developed neoplasms of the forestomach and lung, but the incidences of these were not increased by chlordane, heptachlor or any other exposure. None of the chemicals given alone for the last 25 weeks of the study increased the incidence of liver neoplasms and none given before DEN produced a syncarcinogenic effect.

2-Acetylaminofluorene↗
PubMedDate not supplied

Modulation by the insecticides heptachlor and chlordane of the cell-mediated immune proliferative responses of rhesus monkeys.

Peripheral blood mononuclear cells (PBMC) were isolated from heparinized blood samples from twelve young, healthy male rhesus monkeys. Triplicate cultures were made in RPMI 1640 with 10% heat-inactivated homologous plasma with or without the test mitogens (phytohemagglutinin, concanavalin A and pokeweed mitogen). Under a defined assay condition, although a different monkey responded to a different degree (3 to 4-fold difference in stimulation index) to a specific mitogen, the proliferative responses of all monkeys were affected significantly by the addition of the chlorinated hydrocarbon heptachlor or chlordane to the test cultures. The insecticides, at 10-40 microM, may also act as mitogens for the unstimulated monkey PBMC or stimulate the release of IL-2 from a mitogen-stimulated culture. At 80 microM, both heptachlor and chlordane completely suppressed the proliferation and IL-2 release of the monkey lymphocytes. These studies suggest immunomodulatory effects of the insecticides heptachlor and chlordane.

Animals↗
PubMed1987

[Contamination of game in Schleswig-Holstein. 2. Residues of dieldrin, heptachlor epoxide and other cyclodiene insecticides in the liver fat of hares (Lepus europaeus L.)].

Increased levels of Dieldrin (0.01-2.94 mg/kg fat, median mean = 0.38 mg/kg fat) and cis-Heptachlor Epoxide (less than 0.01-1.38 mg/kg fat, mean = 0.20 mg/kg fat) were determined by GC/ECD in liver fat of 199 hares (Lepus europaeus L.) from Schleswig-Holstein, North Germany. This investigation was carried out within the scope of a game investigation program. The dependence of these residues on endogenous and exogenous factors are discussed. Oxychlordane and trans-Nonachlor, residues of Chlordane, were also analysed in liver fat by GC/MS. The application of the cyclodiene insecticides Aldrin/Dieldrin, Heptachlor and Chlordane has been prohibited in West Germany for several years; the residues indicate the high soil persistence of these substances.

Animals↗
PubMed2001

The effects of perinatal/juvenile heptachlor exposure on adult immune and reproductive system function in rats.

This study was performed to determine if developmental exposure of rats to heptachlor (H) during the last half of gestation through puberty adversely affects adult functioning of the immune and reproductive systems. Time-bred pregnant female Sprague-Dawley rats were dosed by gavage with H (0, 30, 300, or 3000 microg/kg/day) from gestation day (GD) 12 to postnatal day (PND) 7, followed by direct dosing of the pups with H through PND 42. Separate groups of rats were evaluated with a battery of immune function tests, while other groups of rats were evaluated for reproductive development and function. Additional groups of rats were euthanized at the end of the dosing period for histological analyses of major organ systems. Some dams and PND 7 pups were euthanized; milk, plasma, fat and/or tissues were assayed for H and heptachlor epoxide B (HEB), a major metabolite of H. The amount of H and HEB found in milk, blood, fat, and tissues was proportional to the dose of H administered. There were no effects on the number or survival of pups born to H-exposed dams nor to pups exposed postnatally. There were no effects on the number of treated dams delivering litters or on litter size, nor were there any effects on any of the reproductive end points examined in the F(0) or F(1) rats. There were no effects of H exposure on lymphoid organ weights, splenic natural killer (NK) cell activity, and splenic lymphoproliferative (LP) responses to mitogens and allogeneic cells in a mixed lymphocyte response (MLR) assay at 8 weeks of age. H exposure did not alter delayed or contact hypersensitivity at 10 or 17 weeks of age, respectively. However, the primary IgM antibody response to sheep red blood cells (SRBCs) was suppressed in a dose-dependent manner in males, but not females, at 8 weeks of age. The percentage of B lymphocytes (OX12(+)OX19(-)) in spleen was also reduced in the high-dose males. The anti-SRBC IgM response was reduced only in males exposed to 30 microg H/kg/day in a separate group of rats 21 weeks of age. In these same rats, at 26 weeks of age, the secondary IgG antibody response to SRBCs was suppressed in all of the H-exposed males, but not females. These data indicate that perinatal exposure of male rats to H results in suppression of the primary IgM and secondary IgG anti-SRBC responses. Suppression of these antibody responses persisted for up to 20 weeks after the last exposure to H, at a total exposure of approximately 1500 microg H/kg/rat.

Animals↗
PubMed1988

Residues in beef cattle accidentally exposed to commercial heptachlor.

The changes in concentration of heptachlor epoxide (HCE) and oxychlordane (OCD) were studied in the tissues of beef cattle that had previously grazed pasture contaminated with commercial heptachlor. In 25 cows and heifers monitored over 488 days, the mean concentration of HCE decreased from 22.0 to 0.08 mg/kg and of OCD from 5.68 to 0.18 mg/kg. The respective half-lives were estimated to be 66 and 92 days. In a controlled feeding experiment, nine steers were subjected to one of three dietary regimes; a high plane of nutrition for 81 days then a low plane for 140 days; a moderate plane of nutrition for the total period; and a low plane of nutrition for 81 days then a high plane for 140 days. Approximately five months later similar treatments were applied for 101 and 94 days. The rate of decline of HCE and OCD was consistently greatest in animals on the high plane of nutrition and lowest in those on the low plane. Lactation did not appear to have a major effect on the rate of decline in the tissue concentrations of these compounds. No significant (P greater than 0.05) relationships were found between the concentrations of HCE or OCD in the subcutaneous fat and either milk or blood at any stage of the experiment. At slaughter, from 18 to 24 months after the commencement of the experiments, significant correlations (P less than 0.05) were found among concentrations of HCE and OCD in subcutaneous fat, renal fat and fat from the bone marrow.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1987

Leukemias and blood dyscrasias following exposure to chlordane and heptachlor.

We present 25 new cases of blood dyscrasia, including leukemias, production defects, and thrombocytopenic purpura, generally following home termite treatment with the chlorinated hydrocarbon pesticides chlordane and heptachlor (C/H). These newly reported cases are consistent with 34 previously published case reports associating blood dyscrasias with C/H exposure. Additionally, the newly reported leukemias are consistent with epidemiologic evidence of excess risk of leukemia and other cancers in C/H-exposed populations and with the carcinogenic action of C/H in animals. The importance of case reports in warning of the association of blood dyscrasias to C/H exposure is emphasized. Until the voluntary halt in production in July 1987, millions of homes in the United States were treated with chlordane and heptachlor for termites even though their agricultural uses were phased out in 1978, largely on the grounds of "imminent hazard" because of carcinogenicity. In view of the recognized myelotoxicity, carcinogenicity, and other chronic toxic effects of these pesticides, a national program for monitoring all homes treated is urgently needed to detect persistent contamination.

Anemia, Aplastic↗
PubMed1978

Effects of chlordane and heptachlor on the marine dinoflagellate, Exuviella baltica, Lohmann.

Chlordane and heptachlor at 50 microgram/1 reduced cell density, chlorophyll a per unit volume of culture, 14C uptake per cell and carbon fixation per unit of chlorophyll a in the marine dinoflagellate Exuviella baltica Lohmann. The concentration of chlorophyll a per cell was not reduced, however, by treatment with either compound. Chlordane was more toxic than heptachlor at this concentration, and caused the disintegration of many cells, thus affecting particle size distribution in the cultures. In nature, such an inhibition and shift in size class distribution could affect the availability of food for particle-feeding herbivores.

Chlordan↗
PubMed1991

Application of biological data in cancer risk estimations of chlordane and heptachlor.

Regulatory agencies traditionally use doses associated with ambient concentrations of contaminants in environmental media to estimate lifetime excess cancer risks. This approach is, however, limited by the errors inherent in making several default assumptions such as daily water and food intakes and organ absorption factors. A methodology was developed in this study to estimate daily human doses of chlordane and heptachlor from measured metabolites in adipose tissue. Human biomonitoring data, pharmacodynamic and pharmacokinetic parameters in humans and animals, and selected dose-response data from animal carcinogenicity studies were utilized in this procedure for cancer risk assessment in man. Conversion factors, based on body surface area, were used for animal-to-man extrapolation. Conservative estimates from the Global 82 linearized multistage mathematical model (95% upper confidence limit) associate a 1 x 10(-5) risk probability level to chlordane and heptachlor doses of 1.1 x 10(-4) and 4.0 x 10(-5) mg/kg-day, respectively, via all potential routes of exposure. The unit cancer risks associated with "internal" dose estimates from human adipose tissue concentrations were calculated and compared with U.S. Environmental Protection Agency (1986a, Carcinogenicity Assessment of Chlordane and Heptachlor/Heptachlor Epoxide, EPA-600/6-87-004) unit risks in air and water. The implications and uncertainties associated with the risk estimates were also discussed.

Animals↗