High prenatal BPA exposure may disrupt aromatase and raise odds of ASD in boys

A study by researchers in Australia, the United States, and Canada suggests that the chemical bisphenol A (BPA) may play a role in autism in males by disrupting aromatase, a hormone involved in fetal brain development.

In the study, Christos Symeonides and colleagues analyzed data collected on 1,074 children in the Barwon Infant Study. Of this group, 43 children had an autism diagnosis. The researchers also collected urine samples from 847 mothers late in pregnancy and measured their levels of BPA. In addition, they analyzed umbilical cord blood to determine which children had gene variants associated with low aromatase activity.

The researchers found that “higher pre-natal maternal BPA levels are associated with higher ASD symptoms at age two and diagnosis at age nine only in males with low aromatase genetic pathway activity scores.” (Their conclusions were limited to boys because the ASD group included too few girls with low aromatase levels.) Focusing specifically on boys with genes that reduce aromatase pathway activities, the researchers found that those whose mothers had high BPA levels in late pregnancy were 3.5 times more likely to have autism symptoms by two years of age, and six times more likely to have an ASD diagnosis, than those whose mothers had lower levels of BPA during pregnancy. Mouse experiments conducted by the researchers showed that prenatal BPA exposure suppresses aromatase, leading to anatomical, neurological, and behavioral changes in male mice that appear consistent with autism spectrum disorder.

The researchers conclude, “Overall, these findings add to the growing evidence base of adverse neurodevelopmental effects from bisphenol and other manufactured chemical exposure during pregnancy. The case is compelling and supports broader evidence on the need to further reduce BPA exposure, especially in pregnancy.”

Citations

“Male autism spectrum disorder is linked to brain aromatase disruption by prenatal BPA in multimodal investigations and 10HDA ameliorates the related mouse phenotype,” Christos Symeonides, Kristina Vacy, Sarah Thomson, Sam Tanner, Hui Kheng Chua, Shilpi Dixit, Toby Mansell, Martin O’Hely, Boris Novakovic, Julie B. Herbstman, Shuang Wang, Jia Guo, Jessalynn Chia, Nhi Thao Tran, Sang Eun Hwang, Kara Britt, Feng Chen, Tae Hwan Kim, Christopher A. Reid, Anthony El-Bitar, Gabriel B. Bernasochi, Lea M. Durham Delbridge, Vincent R. Harley, Yann W. Yap, Deborah Dewey, Chloe J. Love, David Burgner, Mimi L. K. Tang, Peter D. Sly, Richard Saffery, Jochen F. Mueller, Nicole Rinehart, Bruce Tonge, Peter Vuillermin, the BIS Investigator Group, Anne-Louise Ponsonby, and Wah Chin Boon, Nature Communications, August 2024 (free online). Address: Wah Chin Boon, [email protected].