(Ivanhoe Newswire) -- Children born in areas with high
traffic-related pollution may have a greater risk of developing asthma due
to genetic changes that occur in the womb, a new study found.
Researchers examined umbilical cord blood from New York City infants and
discovered evidence of a possible new biomarker associated with prenatal
exposure to polycyclic aromatic hydrocarbons (PAHs). PAHs are chemical
compounds that are created as byproducts of incomplete combustion from
carbon-containing fuels. There are typically high levels of PAHs in heavily
trafficked areas, and exposure to the chemicals have been linked to diseases
such as cancer and childhood asthma.
For the study, mothers-to-be wore backpack air monitors. At birth,
researchers analyzed umbilical cord white blood cell samples from 56
children for epigenetic alternations related to PAH exposure. Epigenetic
changes may disrupt the normal functioning of genes by affecting their
expression but do not cause structural change or mutations in the genes,
researchers said.
The researchers reported finding a significant association between changes
in ACSL3 methylation, a gene expressed in the lung, and maternal PAH
exposure. ACSL3 was also associated with a parental report of asthma
symptoms in children before the age of 5.
The researchers from the University of Cincinnati and Columbia University
said their findings provide a potential clue for predicting environmentally
related asthma in children, particularly those born to mothers who live in
high-traffic areas such as Northern Manhattan and the South Bronx.
"Our data support the concept that environmental exposures 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,"
senior author Shuk-mei Ho, Ph.D., was quoted as saying.
The study's authors said these findings could guide them to monitor changes
in the ACSL3 gene, which could help with early diagnosis of
pollution-related asthma.
SOURCE: PLoS ONE, Feb. 16, 2009
