Aldrin

Aldrin was synthesized in 1948 by Shell Chemical, named after the Nobel laureate Kurt Alder, and introduced as a highly effective soil insecticide against corn rootworm, wireworms, and other soil pests [1]. Along with dieldrin, endrin, and heptachlor, aldrin became part of what critics called the "dirty dozen" of persistent organochlorine pesticides — chemicals that were extraordinarily persistent in the environment and accumulated in the food chain. By the time the EPA banned aldrin in 1974 (for most uses; termite control continued until 1987), it had been applied to an estimated 10 million acres of US cropland annually [2]. Once in soil, aldrin is rapidly converted to its epoxide, dieldrin, which is more persistent and more toxic. Both compounds persist in soil for years to decades and accumulate in aquatic organisms and in the fat of animals that eat contaminated food [3].

For most Americans today, dietary fat is the primary aldrin/dieldrin exposure route — the compounds bioaccumulate in the fat of meat, dairy, and fish from areas with historical heavy use [1]. Contaminated soil at former agricultural sites continues to be a source in the Midwest, where aldrin was heavily applied on corn crops. Residents of homes built on former agricultural land in the Midwest may have soil exposure from aldrin/dieldrin residues [2]. Occupational exposure was highest for workers in aldrin and dieldrin manufacture (Shell's plant in Denver was a significant source), and for agricultural applicators. Legacy contamination at the former Shell Chemical plant in Denver contaminated surrounding soil and groundwater [3].

Aldrin is converted to dieldrin in the body and in the environment, so the health effects of both are closely linked [1]. Both are probable human carcinogens (IARC Group 2B), with the strongest animal evidence for liver tumors and supporting human epidemiological evidence for liver and pancreatic cancers. Aldrin/dieldrin suppress the immune system, disrupt sex hormone function (both androgenic and estrogenic effects are documented), and cause acute neurotoxicity — seizures — at high doses [2]. The Parkinson's disease link for dieldrin (shared with rotenone and paraquat) is increasingly supported by mechanistic and epidemiological evidence: dieldrin damages dopaminergic neurons and has been detected at higher concentrations in post-mortem brain tissue of Parkinson's patients compared to controls [3].

People in the Midwest with high consumption of locally produced meat, dairy, and fish from waterways in areas of historical aldrin use carry higher body burdens [1]. Residents near former aldrin/dieldrin manufacturing sites face soil and water contamination. Older Americans who worked as farmers or applicators during the peak use period (1950s–1970s) carry the highest lifetime exposures [2]. People with Parkinson's disease diagnoses and occupational pesticide histories should be aware of aldrin and dieldrin as potential contributing factors.

Reduce consumption of animal fats from conventionally raised livestock and locally caught freshwater fish from agricultural waterways as a general organochlorine exposure reduction strategy [1]. For property in the Midwest that may have been former agricultural land, soil testing for organochlorines (including aldrin, dieldrin, and DDT residues) is advisable before growing food gardens [2]. There is no specific antidote or chelation therapy for aldrin/dieldrin exposure; the primary strategy is minimizing ongoing dietary exposure to reduce body burden accumulation rate [3]. Former agricultural workers with aldrin exposure and Parkinson's symptoms should mention their pesticide history to their neurologist.