Living in polluted cities found to cause DNA damage that leads to shortened life spans

Excessive exposure to traffic-related air pollution was found to induce DNA damage in both children and adolescents, according to a small study published in the Journal of Occupational and Environmental Medicine. As part of the study, a team of researchers at the University of California, Berkeley examined 14 children and adolescents living in Fresno, Calif. Fresno was touted as the second most polluted city in the state.

The research team also examined the correlation between polycyclic aromatic hydrocarbons (PAHs) and telomere shortening. According to the scientists, PAHs are ubiquitous air pollutants produced by motor vehicle exhaust. On the other hand, telomere shortening was defined as a DNA damage closely associated with the onset of aging. The study showed increased exposure to PAHs coincided with marked reductions in telomere length. The research team also noted that children and teens with asthma had higher PAH exposure compared with their healthier counterparts. According to the researchers, excessive exposure to air pollution may exacerbate asthma, which in turn may lead to telomere shortening. The research team also noted that the inverse association between increased PAH exposure and shorter telomere length remained constant when other factors — such as age, sex, and race — were taken into account.

“The relationship between PAH exposure and telomere length we observed in this study of adolescents is consistent with studies in healthy adults that have shown telomere shortening with increasing air pollution levels…Previous studies have reported a dose–response relationship between PAH exposure and biomarkers of oxidative stress. Although preliminary pilot data, our results are consistent with the hypothesis that exposure to ambient PAHs (largely generated during combustion of diesel and gasoline fuels in Fresno) leads to oxidative stress, which in turn causes telomere shortening…Our pilot study results suggest that telomere shortening in children may be associated with exposure to traffic-related air pollution. Greater knowledge of the impact of air pollution at the molecular level is necessary to design effective interventions and policies. Our preliminary data will inform the design of a larger study to examine the hypothesis generated from these results,” the researchers wrote.

Studies confirm that air pollution exposure spurs DNA damage

The latest research is only one of the many studies confirming the link between air pollution exposure and DNA damage.

For instance, a study published in 2015 revealed that even short-term exposure to diesel exhaust fumes may significantly affect the DNA structure. To carry out the study, a team of researchers from the University of British Columbia and Vancouver Coastal Health in Canada put participants in a small room with diluted and aged exhaust fumes. The air quality in the room was comparable to those of a Beijing highway or a busy B.C. port.

The research team found that just two hours of exposure to polluted air affected the chemical coating attached in human DNA, which in turn prompted a methylation process that can inhibit a gene from producing protein. The researchers cautioned that while a two-hour exposure may not adversely affect a person’s health, the results provide an overview of how long-term exposure could be detrimental to the body. (Related: Brain smog: Traffic pollution reduces children’s ability to learn in school.)

Another study published in PLOS ONE revealed that traffic-related air pollutants such as PAHs and particulate matter cause significant damage in human DNA. As part of the research, the scientists analyzed spot urine and blood samples from 91 traffic conductors and 53 indoor office workers. The study revealed that traffic conductors had higher levels of air pollution markers than those who worked in the office. The research team also found that the occurrence of DNA strand breaks were more prevalent among traffic conductors compared with the office workers.

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