Lipid levels during prenatal brain development may be linked to autism, according to a recent study.

Researchers from York University in Canada found that  abnormal levels of lipid molecules in the brain can affect the interaction between two key neural pathways in early prenatal brain development can trigger autism.

They also found that environmental causes such as exposure to chemicals in some cosmetics and common over-the-counter medication can also affect lipid levels.

"We have found that the abnormal level of a lipid molecule called Prostaglandin E2 in the brain can affect the function of Wnt proteins," researcher Dorota Crawford, member of the York Autism Alliance Research Group, said in a statement. "It is important because they can change the course of early embryonic development."

For the study, researchers used real-time imaging microscopy to determine that higher levels of Prostaglandin E2 can change Wnt-dependent behavior of neural stem cells by increasing cell migration and proliferation. This could affect how the brain is organized and wired.

Autism is a disorder of neural development characterized by impaired social interaction and communication difficulties.  It is four times more prevalent in boys than in girls and the incidence continues to rise. The U.S. Center for Disease Control and Prevention data from 2010 estimates that 1 in 68 children now has autism.

"The statistics are alarming. It's 30 percent higher than the previous estimate of 1 in 88 children, up from only two years earlier. Perhaps we can no longer attribute this rise in autism incidence to better diagnostic tools or awareness of autism," Crawford said.

She added that it is even more apparent from the recent literature that the environment might have a greater impact on vulnerable genes, particularly in pregnancy.

"Our study provides some molecular evidence that the environment likely disrupts certain events occurring in early brain development and contributes to autism," Crawford said.

The findings were recently published in the journal Cell Communication and Signaling.