28028
Time Windows of Exposure to Neonicotinoids in Parents of Autistic Children
Neonicotinoids were first synthesized in the 1980s and introduced into agricultural use and into pet products in the 1990s. Imidacloprid was the first neonicotinoid in widespread use. All are designed to target nicotinic acetylcholine receptors (nAChRs) and these are ubiquitous in humans as well as in insects. While differences between insect and mammalian receptors make them less acutely toxic to humans, effects of preconception and gestational exposures have been suspected. In particular, preconception exposures are understudied, even while the role of de novo (thus predominantly preconception) mutations in association with neurodevelopmental disorders has become increasingly apparent.
Our study nests within a larger study which asks parents of autistic children to answer questionnaires regarding geospatial exposure, health, occupational history, medication use, autism features and severity of their children.
Objectives:
Within our study population, we wanted to compare various time windows of in-home neonicotinoid exposure to each other. The five time windows studied are the three months prior to conception, the three trimesters of pregnancy and the three months postpartum.
Methods:
For broad outreach, we used social media to let parents know of the study. We invited birth mothers of autistic children to answer a questionnaire. Inclusion criteria were a diagnosis of ASD, child’s birth in the year 2000 or later and valid consent. The questions regarding neonicotinoid exposure included imidacloprid-containing pet products for flea control. We felt mothers were likely to recall whether they were pet owners during pregnancy, and whether their pet received a flea product through application to the fur. We also asked about indoor pest control and home garden use. Lists of product names were supplied. Responses of “do not recall” or none were always options.
To analyze specific time window specificity of exposure, analysis was first restricted to those who reported exposure to a product in a single time window. We also analyzed exposures among the 32 possible patterns of multiple exposure. Importantly, here we are comparing time windows of exposure, with other time windows of exposure – not exposures of populations with and without autism.
Results:
The questionnaire was completed by 2212 mothers. For imidacloprid containing pet products, 670 (30.3%) recorded specific information regarding timing of exposure, of whom 242 recorded exposure in a single time window. Of these, 143 recorded exposure in only the pre-conception time window, 30 in the first trimester, 24 in the second trimester, 5 in the third trimester and 40 in the postnatal 90-day period. Importantly, this trend was also observed for other neonicotinoid home and garden exposures (p < 0.001).
Conclusions:
Our results show highest responses to exposures in the 90-day pre-conception time window. As parents are likely to share the same environment at the time of conception, paternal environmental exposures within this time period may be especially important since de novo mutations in autism are more frequently of paternal origin. Spermatogenesis takes place entirely within this time window. We believe neonicotinoids should be studied for their effects on gamete development in both sexes.