Heptachlor epoxide

The lARC has determined that there is sufficient evidence in experimental animals for the carcinogenicity of heptachlor and there is inadequate evidence of carcinogenicity in humans. Heptachlor is considered possibly carcinogenic to humans.  

Heptachlor was not mutagenic in bacterial assays, but it did cause gene mutations in rodent cells and unscheduled DNA synthesis in human fibroblasts.  

The 2003 ACGIH threshold limit value-time-weighted average (TLV-TWA) for heptachlor is 0.05mg/m with an A3-animal carcinogen designation and a notation for skin absorption. 

Registry (ATSDR) Toxicological Profile for Heptachlor/Heptachlor Epoxide. TP-92/11, 131pp. US Department of Health and Human Services, Public Health Service, 1993 

Wang HH, MacMahon B Mortality of workers employed in the manufacture of chlordane and heptachlor. J Occup Med 21 745-748, 1979 

Heptachlor induces tremors, convulsions, paralysis, and hypothermia in rats. Young calves fed with different doses (2.5, 5, or 10 mg/kg/day) of heptachlor formulation for 3 to 15 days showed muscle spasms in the head and neck region, convulsive seizures, elevated body temperatures, and engorged brain blood vessels. The photoisomer of heptachlor (photoheptachlor) and the major metabolite of heptachlor (heptachlor epoxide) are considered more toxic than the parent compound. 

Uses Heptachlor epoxide (HCE), also known as epoxyheptachlor, is a white crystalline solid. Heptachlor is converted to heptachlor epoxide and other degradation products in the environment. HCE degrades more slowly and, as a result, is more persistent than heptachlor. Both compounds adsorb strongly to sediments and are bioconcentrated in terrestrial and aquatic organisms biomagnification of both is significant.14 

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Report the concentration of heptachlor epoxide residue (in nanograms per gram) on the oranges. 

Heptachlor epoxide zero 0.0002 Liver damage risk of cancer Breakdown of hepatachlor... 

Musial CJ, Peach ME, Stiles DA. 1976. A simple procedure for the confirmation of residues of alpha-and beta-endosulfan, dieldrin, endrin, and heptachlor epoxide. Bull Environ Contam Toxicol 16 98-100. 

As mentioned earlier (Figure 5.5), aldrin and heptachlor are rapidly metabolized to their respective epoxides (i.e., dieldrin and heptachlor epoxide) by most vertebrate species. These two stable toxic compounds are the most important residues of the three insecticides found in terrestrial or aquatic food chains. In soils and sediments, aldrin and heptachlor are epoxidized relatively slowly and, in contrast to the situation in biota, may reach significant levels (note, however, the difference between aldrin and dieldrin half-lives in soil shown in Table 5.8). The important point is that, after entering the food chain, they are quickly converted to their epoxides, which become the dominant residues. 

In one example (Lawrence and Casida 1984, Abalis et al. 1985) rat brain microsacs were used to test the action of cyclodiene insecticides such as dieldrin and endrin on the GABA receptors contained therein. The influx of radiolabeled CL into the microsacs via the pore channel of the receptor was inhibited by these chemicals. A similar assay was developed using microsacs from cockroach nerve. Assays with this preparation showed again the inhibitory effect of a cyclodiene (this time heptachlor epoxide) on CL influx. Also, that microsacs from cyclodiene resistant cockroaches were insensitive to the inhibitory effect of picrotoxinin, which binds to the same site on the GABA receptor (Kadous et al. 1983). 

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