Accelerated aging can be captured in patterns of chemical modifications to parts of an individual’s DNA blueprint or genome. DNA-methylation is one such common modification that involves the chemical addition of a methyl group to DNA. Tracking DNA-methylation, which is one kind of epigenetic modification, across the genome, allows comparisons of a person’s chronological age (time since birth) and epigenetic age (the age suggested by the methylation patterns of their DNA).
Recently, an international team of researchers tested the effects of exposure of environmental pollutants on epigenetic age. The study targeted polycyclic aromatic hydrocarbons (PAHs) which have been associated with cardiovascular disease and cancer. PAHs result from the combustion of fossil fuels in vehicle exhausts and burning of organic matter in industrial and domestic settings. The effects of these pollutants were tested in three panels of Chinese populations: two urban groups and third group consisting of coke-oven workers. To accurately test exposure levels to PAHs and their effect on DNA-methylation, for all participants, PAHs were measured from urine samples and DNA-methylation patterns were analyzed from blood samples.
Results suggest a link between exposure levels of PAHs and increased methylation age acceleration. The group with the highest PAHs exposure levels, the coke-oven workers, had a difference between methylation-age and chronological age of 3.5 years; whereas in the control groups (urban populations) such difference was only 0.09 to 2.45 years. Further, the study finds a possible dose-response relationship between PAH exposure and increases in epigenetic age and aging rates. These findings highlight the negative effects of exposure to PAHs on epigenetic predictors for age-associated ailments and represent an important advancement in the study of environmental effects on human aging.