Traffic pollution may cause genetic changes in the womb that increase a child's risk of developing asthma, say researchers who studied umbilical cord blood from New York City children.
The researchers found evidence of a possible new biomarker-an epigenetic alteration in the gene ACSL3-associated with prenatal exposure to polycyclic aromatic hydrocarbons (PAH), which are created as byproducts of incomplete combustion of carbon-containing fuels such as gasoline.
Epigenetic changes can disrupt the normal functioning of genes by affecting their expression, but don't cause structural changes or mutations in the genes. PAH levels are high in heavy-traffic areas, and exposure to PAHS has been linked to such diseases as cancer and childhood asthma.
The findings, published in the journal PLOS One, offer a potential clue for predicting environmentally-related asthma in children, said the researchers from the University of Cincinnati and Columbia University Mailman School of Public Health in New York City.
"Our data support the concept that environmental exposure can interact with genes during key developmental periods to trigger disease onset later in life, and that tissues are being reprogrammed to become abnormal later," said the study's senior author, Shuk-mei Ho, PhD, professor and chair of University of Cincinnati's Department of Environmental Health.
If the findings are confirmed, changes in the ACSL3 gene could offer a new biomarker for early diagnosis of pollution-related asthma.
"Understanding early predictors of asthma is an important area of investigation because they represent potential clinical targets for intervention," said study co-author Rachel Miller, MD, director of the Asthma Project of the Columbia Center for Children's Environmental Health at Columbia University Medical Center in New York City.
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