Pesticide DDT Linked to Alzheimer's Disease
Credit: Artem Chernyshevych | Stock Xchng

Exposure to the pesticide DDT, which was banned in the United States in the 1970s but is still found in the environment, may increase the risk of Alzheimer's disease, a new study suggests.

People with Alzheimer's disease in the study had levels of a DDT byproduct, called DDE, in their blood that were nearly four times higher on average than the levels seen in people without Alzheimer's.

Among the people with the highest levels of DDE, those who carried a gene known to increase the risk for Alzheimer's disease scored lower on a test of mental abilities than those without the gene. This suggests that carriers of this gene may be more susceptible to the effects of DDE, the researchers said. [12 Hormone-Disrupting Chemicals & Their Health Effects]

Further, exposing brain cells in a dish to either DDT or DDE increased the production of a protein involved in the formation of amyloid plaques, the brain plaques that are hallmarks of Alzheimer's disease.

The results identify DDT exposure as an environmental risk factor for Alzheimer's disease, the researchers said.

If future studies confirm the findings, doctors may one day use patients' DDE levels along with their genes to identify those people at increased risk for Alzheimer's disease, the researchers said.

However, at this time, the findings are preliminary, and people who grew up around the time of DDT spraying should not worry about increased risk for Alzheimer's disease, said study researcher Jason Richardson, of the Department of Environmental and Occupational Medicine at the Rutgers Robert Wood Johnson Medical School. The findings need to be replicated in future studies, experts say.

DDT and Alzheimer's

DDT was widely used in the United States in the 1940s, '50s and '60s, both as a pesticide and a way to reduce the spread of malaria. It was banned in the United States in 1972 due to environmental concerns, but it is still used legally in other countries around the world, so imported products may have been exposed to DDT.

In the blood, DDT breaks down into DDE. Because DDE can last for a long time (20 years or longer), levels of DDE in the blood measured at one point can reasonably represent a person's lifetime of exposure to DDT, Richardson said.

In a previous study of 20 patients with Alzheimer's disease, Richardson and colleagues found that the patients had significantly higher levels of DDE in their blood compared to people without the disease.

In the new study, the researchers analyzed blood samples from 86 patients with Alzheimer's disease (including the original 20 patients), and 79 people without the disease. Researchers divided the participants into three groups based on their DDE levels.

The odds of having Alzheimer's disease were about four times greater for those in the group with the highest DDE levels, as compared with the group with the lowest DDE levels.

Levels of DDE in the blood also tended to match levels of DDE found in the brain, according to a postmortem analysis of the brains of 11 patients.

Future research

In an editorial accompanying the study, Dr. Steven T. DeKosky, of the University of Virginia School of Medicine, and Dr. Sam Gandy, of the Mount Sinai Alzheimer's Disease Research Center, point out that blood levels of DDE are much higher in parts of the world where DDT was phased out later, such as Spain and India. Yet, they write, "there are no data to suggest a cluster of higher [Alzheimer's disease] prevalence in those regions."

The new findings "should be noted, but for now, these conclusions should be considered as preliminary until there is independent confirmation in other populations," DeKosky and Gandy wrote.

Richardson said that if there were a single environmental factor that caused Alzheimer's disease, it would have likely been found by now. Instead, researchers need to study how the environment can interact with the genes of an individual, Richardson said.

"When you're talking about a complex disease like Alzheimer's, gene-environment interactions likely play a significant role," Richardson said.

The study and editorial are published in the Jan. 27 issue of the journal JAMA Neurology.

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