Banned Pesticide Increases Risk for Alzheimer’s Disease

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Elevated blood levels of dichlorodiphenyltrichloroethylene (DDE), a metabolite of the banned pesticide dichlorodiphenyltrichloroethane (DDT), may increase risk for the development of Alzheimer’s disease in those who are genetically at higher risk of cognitive decline, according to a study published January 27 in JAMA Neurology.

Researchers from the Rutgers-Robert Wood Johnson Medical School, University of Texas-Southwestern, and Emory University Alzheimer’s Disease Research Center conducted a study investigating the association between serum levels of DDE and the onset of Alzheimer’s and whether the presence of the apolipoprotein E4 (ApoE4)—a genetic risk factor for Alzheimer’s—makes the association stronger.

According to the authors, DDT was used in the United States in the 1940s to protect crops from insect infestations and humans from insect-borne illnesses, until the pesticide was banned in 1972 by the Environmental Protection Agency for being hazardous to the environment and human health.

Although exposure to DDT and its derivatives has significantly decreased among U.S. citizens over the past three decades, the toxic pesticide was found in 75 percent to 80 percent of blood samples collected in a study conducted by the Centers for Disease Control and Prevention—indicating that the long-lasting toxin remains an environmental threat to public health.

In the current study, researchers analyzed blood samples of 86 subjects with Alzheimer’s disease and 79 controls to assess the impact of elevated DDE serum levels on the development of Alzheimer’s disease. The subjects’ blood was also genotyped for the ApoE4 allele. Cognitive function of each participant was evaluated by the Mini-Mental State Examination.

The results showed that DDE serum levels were nearly four times higher in individuals with AD than in controls. The highest blood levels of DDE was associated with low scores on cognitive function tests, as well as the presence of the ApoE4 genotype. In addition, the researchers found that DDE increased the levels of amyloid precursor protein, after exposing human neuronal cells to DDE in vitro.

“This is one of the first studies identifying a strong environmental risk factor for Alzheimer’s disease,” commented coauthor Allan Levey, M.D., Ph.D., director of the Alzheimer’s Disease Research Center at Emory University School of Medicine. “The magnitude of the effect is strikingly large—it is comparable in size to the most common genetic risk factor for late-onset Alzheimer’s.”

Though the United States has banned the usage of DDT, other countries still use the toxin to combat malaria—which in turn affects the U.S. population.

“We are still being exposed to these chemicals in the United States, both because we get food products from other countries and because DDE persists in the environment for a long time,” commented coauthor Dwight German, Ph.D., a professor of psychiatry at UT Southwestern.

The authors said that more studies are under way that seek to directly link DDT exposure to Alzheimer’s. They noted that identifying people who have elevated levels of the long-lasting toxin and carry an ApoE4 allele may lead to early identification of some cases of Alzheimer’s.

The study was funded by the National Institutes of Health. ■