Children and teenagers exposed to high levels of traffic-related air pollution may be at an increased risk of a specific DNA damage called telomere shortening, a new study warns.
Young people with asthma also have evidence of telomere shortening, a type of DNA damage typically associated with ageing, researchers said.
“Our results suggest that telomere length may have potential for use as a biomarker of DNA damage due to environmental exposures and/or chronic inflammation,” said John R Balmes of University of California, Berkeley, in the US.
The study included 14 children and adolescents living in Fresno, California — the second-most polluted city in the US.
Researchers assessed the relationship between polycyclic aromatic hydrocarbons (PAHs), a “ubiquitous” air pollutant caused by motor vehicle exhaust and shortening of telomeres.
As the exposure to PAHs increased, telomere length decreased in linear fashion. Children and teens with asthma were exposed to higher PAH level than those without asthma.
The relationship between PAH level and telomere shortening remained significant after adjustment for asthma and other factors (age, sex, and race/ethnicity) related to telomere length.
The study, published in the Journal of Occupational and Environmental Medicine, adds to previous evidence that air pollution causes oxidative stress, which can damage lipids, proteins and DNA.
Research has suggested that children may have different telomere shortening regulation than adults, which might make them more vulnerable to the damaging effects of air pollution.
“Greater knowledge of the impact of air pollution at the molecular level is necessary to design effective interventions and policies,” Balmes said.
With further research, telomeres could provide a new biomarker to reflect the cellular-level effects of exposure to air pollution, researchers said.
Telomeres might also provide new insights into the understanding how pollution exposure leads to adverse health outcomes, they said.
Source: The Tribune