Prenatal Plastic Exposure Linked to Autism in Boys

Researchers at Florey have discovered evidence that moms who were pregnant when their autistic boys were born had greater concentrations of the plastic chemical bisphenol A (BPA). The theory that there may be a connection between autism and prenatal plastic exposure is supported by research headed by Florey scientists Dr. Wah Chin Boon and Professor Anne-Louise Ponsonby that was published in Nature Communications.

According to Professor Ponsonby, the researchers examined two sizable birth cohorts: the American Columbia Center for Children’s Health and Environment and the Australian Barwon Infant Study (BIS).

“Exposure to plastic chemicals during pregnancy has already been shown in some studies to be associated with subsequent autism in offspring,” Professor Ponsonby said.

“Our work is important because it demonstrates one of the biological mechanisms potentially involved. BPA can disrupt hormone controlled male fetal brain development in several ways, including silencing a key enzyme, aromatase, that controls neurohormones and is especially important in fetal male brain development. This appears to be part of the autism puzzle.”

According to Professor Ponsonby, the study looked at kids with reduced amounts of the enzyme aromatase, which in the brain changes testosterone into neuroestrogen.

In boys who were in the top fifth of those susceptible to the endocrine-disrupting effects of BPA, the correlation between the chemical’s presence and autism was especially clear. In other words, people had reduced aromatase levels. Boys in that group, according to the study, whose mothers had greater urine BPA levels in the latter stages of their pregnancies were:

• At age two, there is a 3.5-fold increased risk of developing autism symptoms.
• Six times as likely as children whose mothers had lower levels of BPA during pregnancy to receive a validated autism diagnosis by the time they turned 11 years old.
• Mechanistic data showed that elevated BPA levels were linked to a general epigenetic (gene switching) inhibition of the aromatase enzyme in both birth cohorts.

In laboratory work, Dr. Boon studied the impact of prenatal BPA on mice.

“We found that BPA suppresses the aromatase enzyme and is associated with anatomical, neurological and behavioral changes in the male mice that may be consistent with autism spectrum disorder,” Dr. Boon said.

“This is the first time a biological pathway has been identified that might help explain the connection between autism and BPA,” she said.

According to Professor Ponsonby, people can hardly avoid BPA, comparable bisphenols, and other plastic compounds that have endocrine-disrupting effects since they are so widely used.

“We all ingest plastic chemicals in many ways—through ingesting plastic food and drink packaging, inhaling home renovation fumes, and through the skin from sources such as cosmetics. There are so many ways these chemicals enter our bodies, so, it’s not surprising that BPA was present in a large proportion of the women’s urine samples we studied. It’s important for us to understand how these plastics affect our health,” Professor Ponsonby said.

Public safety officials are now using these data to revise safety recommendations on exposure to produced chemicals, especially plastic compounds, during pregnancy and the early stages of life.

The group also searched for strategies to lessen BPA’s harmful effects on the aromatase system.

Dr. Boon also mentioned that more research may be worthwhile on a fatty acid type known as 10-hydroxy-2-decenoic acid that was studied in mice.

“10-hydroxy-2-decenoic acid shows early indications of potential in activating opposing biological pathways to improve autism-like characteristics when administered to animals that have been prenatally exposed to BPA. It warrants further studies to see whether this potential treatment could be realized in humans.”

For more information: Male autism spectrum disorder is linked to brain aromatase disruption by prenatal BPA in multimodal investigations and 10HDA ameliorates the related mouse phenotype, Nature Communications, DOI: 10.1038/s41467-024-48897-8