Toxin Exposure in Late Pregnancy and Early Life Can Increase Autism Risk

Utilising evidence found in baby teeth, researchers from The Senator Frank R. Lautenberg Environmental Health Sciences Laboratory and The Seaver Autism Center for Research and Treatment at Mount Sinai determined that differences in the uptake of multiple toxic and primary factors over the second and third trimesters and early postnatal periods are related to the hazard of developing autism spectrum issues (ASD), according to a study published June 1 within the journal Nature Communications.

The relevant developmental windows for the determined discrepancies were varied for each element, suggesting that systemic dysregulation of environmental pollution and dietary factors may serve an essential role in ASD. In addition to opting for specific environmental factors that affect risk, the study also pinpointed developmental time periods when elemental dysregulation poses the biggest risk for autism later in life.

According to the U.S. Centers for Disease Control and Prevention, ASD occurs in 1 of every 68 children in the USA. The exact reasons are unknown, but earlier research suggests that both environmental and genetic reasons are possibly involved. At the same time that the genetic factor has been intensively studied, exact environmental factors and the levels of life when such exposures could have the largest impact on autism risk are poorly understood. Earlier research suggests that fetal and early childhood exposure to toxic metals and deficiencies of nutrients are linked with a few adverse developmental outcomes, together with intellectual incapacity and language, attentional, and behavioral problems.

According to Manish Arora, PhD, BDS, MPH, Director of Exposure Biology at the Senator Frank Lautenberg Environmental Health Sciences Laboratory at Mount Sinai and Vice Chair and Associate Professor in the Department of Environmental Medicine and Public Health at the Icahn School of Medicine at Mount Sinai, We found significant divergences in metal uptake between ASD-affected children and their healthy siblings, but only during discrete developmental periods. Specifically, the siblings with ASD had higher uptake of the neurotoxin lead, and reduced uptake of the essential elements manganese and zinc, during late pregnancy and the first few months after birth, as evidenced through analysis of their baby teeth. Furthermore, metal levels at three months after birth were shown to be predictive of the severity of ASD eight to ten years later in life.

ASD and toxic exposure

To investigate the consequences that the timing, amount, and subsequent absorption of toxic and nutrients have on ASD, Mount Sinai researchers used validated tooth-matrix biomarkers to study baby teeth collected from pairs of identical and non-identical twins, of which at least one had a prognosis of ASD. They also analyzed teeth from pairs of normally developing twins that served as the control. In the course of fetal and childhood progress, a new tooth layer is formed every week or so, leaving an “imprint” of the micro chemical composition from each exact layer, which provides a chronological record of exposure. The group at Lautenberg Laboratory used lasers to reconstruct these prior exposures alongside incremental markings, just like utilizing growth rings on a tree to examine the tree’s historical past.

According to Abraham Reichenberg, PhD, Professor of Psychiatry and Environmental Medicine and Public Health at the Icahn School of Medicine at Mount Sinai, Our data shows a potential pathway for interplay between genes and the environment. Our findings emphasize the importance of a collaborative effort between geneticists and environmental researchers for future investigations into the relationship between metal exposure and ASD to help us uncover the root causes of autism, and support the development of effective interventions and therapies.