New research in America has drawn a link between exposure to specific toxic pollutants and accelerated epigenetic aging.
Epigenetic aging refers to the process of measuring biological age, (how old cells and tissues appear) as opposed to chronological age (the length of time someone has been alive).
An epigenetic age that is higher than the chronological age, suggests accelerated aging and may bring with it a higher risk of age-related diseases.
First author Dennis Khodasevich and corresponding author Andres Cardenas from Stanford University analysed data from 2,346 American adults between 50 to 84 years old who had taken part in the National Health and Nutrition Examination Survey (NHANES).
Because previous research into how the environment affects epigenetic aging has tended to focused on testing specific pollutants such as cigarette smoke, the researchers took a broader approach, using a an exposome-wide association study (ExWAS) which looks at a wide range of environmental exposures – like air quality, diet, stress, and toxins – simultaneously. This allowed the team to systematically search for links between these exposures and biological aging, making it easier to uncover new connections.
Participants in the study had their blood and urine samples tested for 64 different chemicals such as metals, pesticides, and industrial pollutants.
The team then looked at how these environmental exposures affected eight different epigenetic aging markers (indicators of how quickly a person’s body is aging based on changes in their DNA).
Following the tests, they reported that: ‘Our findings suggest that cadmium is among the strongest environmental chemicals influencing Epigenetic Age Acceleration in the general US population, with additional identified associations involving cotinine, lead, PCBs, and dioxins.’
Cadmium and cotinine are both present in tobacco smoke, although the team point out: ‘Beyond tobacco smoke, diet is a major source of cadmium exposure in the US, providing a pivotal intervention point. Taken together, these findings suggest that cadmium exposure and cotinine levels may be some of the strongest modifiable environmental influences on EAA in the general US population.’
They conclude that : ‘Reducing exposure to toxic substances like cadmium and lead—found in cigarettes, polluted air, and contaminated food—could help slow biological aging and improve long-term health. These insights highlight the need for stronger environmental health policies to protect individuals from premature aging and disease.’
The full research can be read here.