Children and teenagers exposed to high levels of traffic pollution were found to show signs of premature aging, according to new study.
Researchers in California also found youngsters with asthma had higher levels of a pollutant caused by motor vehicle exhaust. Those with higher levels had a specific type of DNA damage called telomere shortening - the main cause of age-related break down of our cells.
Telomeres are vital to our health - they can be described as the caps at the end of each strand of DNA that protect our chromosomes, like the plastic tips at the end of shoelaces.
'Children may be especially vulnerable to the effects of telomeric DNA damage due to their physical development as well as developing immune system,' wrote Dr John Balmes from the University of California, Berkeley, and his colleagues who carried out the study published in the Journal of Occupational and Environmental Medicine.
We already know how harmful outdoor air pollution is - it is responsible for about 3.7 million deaths a year according to the World Health Organization.
Many previous studies have demonstrated that exposure is associated with heart and lung diseases - such as asthma, lung cancer, ischemic heart disease, and stroke. Despite this mounting evidence, the exact underlying mechanisms by which air pollutants cause this is not clear, the authors note. The new preliminary study suggests telomeres may be the key to understanding how pollution exposure leads to adverse health outcomes.
The study analyzed 14 children and adolescents living in Fresno, California - the second-most polluted city in the US.
The researchers assessed the relationship between an 'ubiquitous' motor vehicle exhaust air pollutant called polycyclic aromatic hydrocarbons (PAHs), and shortening of telomeres.
As the exposure to PAHs increased, telomere length decreased. Children and teenagers with asthma were exposed to higher PAH levels than those without asthma.
The relationship between PAH level and telomere shortening remained significant after adjustments for asthma and other factors (age, sex, and race/ethnicity) weer made.
Previous studies suggest that telomere length is linked to progression in chronic obstructive pulmonary disease (COPD).
It also suggests that children may have 'different telomere shortening regulation than adults' - which might make them more vulnerable to the damaging effects of air pollution.
The authors wrote, '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.
'Greater knowledge of the impact of air pollution at the molecular level is necessary to design effective interventions and policies.'
Telomeres are shortened as we age, but telomeres can also be shortened by stress, smoking, obesity, lack of exercise and a poor diet, previous research has shown.