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New Study Investigates Pesticide Use, Autism Link
A recent publication in the journal Environmental Health Perspectives reported a possible connection between pesticide exposure and autism in central California. The study used multiple databases to both identify candidate exposures and analyze the relationship between the exposure and autism spectrum disorders, or ASD. These data sources include: 1) identification of ASD cases through the Department of Developmental Services database; 2) birth certificates which provided address at time of birth; 3) description of agricultural pesticide applications through the California Department of Pesticide Regulation; and 4) geographic information about the proximity of autism cases to pesticide applications using maps provided by the Department of Water Resources as well as other Geographic Information System software programs.

By linking these four databases, the researchers estimated when pregnant women were exposed to pesticides, which ones, and how much (based on timing during pregnancy, amount applied, and residential proximity to application location). Using this information, they then were able to stratify women into different exposure categories and compared rates of autism between those children whose mothers were exposed to the highest levels during a period of time surrounding conception, to those who were not exposed or exposed to lower levels.

The databases provided information on 465 cases of autism plus almost 7,000 matched controls, born between 1996-1998. Over 19 pesticide groups and 10 individual pesticides were examined, most of which produced no association with ASD. However, the researchers identified a significant association between autism and the highest exposure levels of two organochlorine pesticides called dicofol and endosulfan. Dicofol and endosulfan accounted for over 98% of the organochlorines applied during this time period. Of particular interest, the researchers were also able to identify a critical time window just prior to and after embryogenesis during which the association is statistically highest.

While the findings are interesting, the researchers caution that they should not be over-interpreted, saying: “we want to draw the reader's attention to the small numbers of subjects classified as ‘exposed' under our model that generated the largest magnitude of ASD risk” (n=29). The authors also stipulate that exposure to these pesticides was estimated based on residence at time of birth, which may be different than earlier during pregnancy, proximity to application but weather patterns may vary, and timing of application, and no individual levels were measured. Furthermore, these results do not demonstrate that organochlorine pesticide use is the cause of autism. These chemicals are not available for home use and the number of people exposed to these high levels is small. Use of these chemicals in agriculture has decreased during recent years and exposure is highly unlikely to be associated with the increase in children diagnosed with autism during this same time period.

However, regardless of the limitations of this study, the availability and utility of these datasets provide a unique and exciting opportunity to study environmental factors which may give us clues to the causes of autism. Without these important datasets and continued improvement of the quality of the data by the state of California, these sorts of projects would not be possible.

Further exploration is warranted, and special consideration with regards to organochlorine exposure should be given to women of reproductive age. The use of these datasets and the linking of information between different data sources represents an important technological advancement for identification of health risks from exposure to a variety of environmental toxicants in various areas of the United States and the world.

View a report of this study that aired on CNN.



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