A newly published research paper in Aging (Aging-US) on February 11, 2025, Volume 17, Issue 2, is titled “Exposome-wide association study of environmental chemical exposures and epigenetic ageing in the national health and nutrition examination survey.” The study’s lead author, Dennis Khodasevich, and corresponding author, Andres Cardenas, both affiliated with Stanford University, collaborated with peers from various U.S. institutions to investigate the impact of environmental chemical exposure on ageing. Their research utilised data from the National Health and Nutrition Examination Survey (NHANES) and identified significant connections between exposure to harmful chemicals such as cadmium, lead, and cotinine and accelerated biological ageing. This acceleration is pivotal as it heightens the risk of developing age-related diseases.
Their analysis encompassed data from 2,346 U.S. adults aged between 50 and 84, all participants in a national health survey. The research involved testing participants’ blood and urine samples for 64 different chemicals, including metals, pesticides, and industrial pollutants. The primary aim was to determine how these chemical exposures influence various epigenetic ageing markers. These markers, known as biological clocks, gauge an individual’s rate of ageing at the DNA level.
Dennis Khodasevich elaborated on their methodology: “We harnessed data from the National Health and Nutrition Examination Survey 1999-2000 and 2001-2002 cycles to examine exposome-wide associations between environmental exposures and epigenetic ageing.” The results showed that exposure to cadmium, prevalently found in cigarette smoke and certain foods, was strongly linked to signs of accelerated ageing in individuals with elevated blood levels of the metal. Similarly, cotinine, a metabolite of nicotine and an indicator of tobacco exposure, and lead, commonly found in old paints and contaminated water, were also associated with quicker ageing.
Interestingly, the research also uncovered that certain pollutants, such as PCB118 (polychlorinated biphenyl) and HpCDD (dioxin), appeared to be linked to slower biological ageing. The implications of these findings are ambiguous, as slower ageing might not necessarily confer benefits, considering past studies have associated it with potential health risks.
This study stands out due to its extensive scope, contrasting with earlier studies that focused narrowly on a few chemicals and smaller participant groups. The findings are significant, suggesting that everyday exposure to toxic substances can expedite cellular ageing, thereby escalating the risk of age-related conditions such as heart disease, cancer, and cognitive decline.
In conclusion, the insights from this research underscore the urgent need for robust environmental health policies that aim to reduce exposure to harmful substances like cadmium and lead, commonly found in cigarettes, polluted air, and contaminated food sources. Such policies could decelerate biological ageing and enhance long-term health, highlighting the critical link between environmental quality and public health. This study deepens our understanding of how pollutants impact ageing and reinforces the importance of safeguarding environmental quality to prevent premature ageing and associated chronic diseases.
More information: Dennis Khodasevich et al, Exposome-wide association study of environmental chemical exposures and epigenetic aging in the national health and nutrition examination survey, Aging-US. DOI: 10.18632/aging.206201
Journal information: Aging-US Provided by Impact Journals LLC
