By Yervand Kondrahjian | Staff Writer
Heptachlor, a chlorinated dicyclopentadiene, was first registered in the United States in 1952 and was extensively used in soil and seed treatment to control insect pests that contaminated crops (corn, grains, citrus, and pineapple). They’re also used to control termites and household insects. Most of these uses were banned for causes such as carcinogenicity potential, toxicity to developing nervous system, environmental persistence, and bioaccumulation in the food chain. Hence, the US Environmental Protection Agency (USEPA) has classified heptachlor as a moderate oral toxicant (Category II) and as a probable human carcinogen (Group B2) with heptachlor epoxide.
Heptachlor is a pesticide and there are no known natural sources of heptachlor. The main exposure routes for heptachlor are via inhalation or skin penetration from extended exposure to dusts containing heptachlor, and indirectly by uptake of food that was contaminated through the crops they were collected from, or via the food-chain. Multiple studies showed that heptachlor can be found in all environmental compartments (air, water, soil and sediment), as well as vegetables, fish, reptiles and dairy milk.
The primary target for heptachlor is the nervous system. It acts as a noncompetitive antagonist of the Cl– channel of the GABAA receptor, by binding to the Cl– channel of the receptor and thereby blocking the actions of GABA. The liver is another target of heptachlor toxicity. In rats, heptachlor induced significant proliferation of quiescent hepatocytes by activation of protein kinase C and inhibition of the cytochrome c release into the cytosol. In humans, heptachlor decreases ras proto-oncogene expression in myeloblastic leukaemia cells. In cultured human lymphocytes, heptachlor down-regulated the tumor suppressor retinoblastoma protein and p53 gene expression. Moreover, heptachlor was found to block the cell cycle by preventing progression into S phase. Higher blood concentrations of heptachlor were found in breast cancer patients compared to controls, suggesting a correlation between heptachlor and breast cancer.
Regarding the genotoxicity of heptachlor, it has significantly increased unscheduled DNA synthesis in cultured human fibroblasts with metabolic activation by liver microsomes. It also inhibited gap junctional intercellular communication in cultured human breast epithelial cells with a loss of connexin Cx43 from the cell membranes.
At last, the ban of heptachlor use within the United States was a decent step, as misuse of heptachlor can cause severe environmental consequences, including toxic effects in humans and animals. Other countries should follow these steps and use other pesticides that have less environmental and biological damage than heptachlor.