A new study by a team led by Assistant Professor Ami Zota of the Milken Institute School of Public Health Department of Environmental and Occupational Health (EOH) looks at how higher exposure to persistent organic pollutants (POPs) impacts a biomarker that governs how aging is regulated at the cellular level. The research, published in Environmental Health Perspectives, suggests that uptake of pollutants including dioxins, furans, and some polychlorinated biphenyls (PCBs) can lead to significantly longer telomeres, bits of DNA at the ends of chromosomes that are associated with cardiovascular disease, diabetes and other diseases of old age, including cancer.
PCBs and dioxins are “legacy” pollutants that are ubiquitous in the environment. Most people are exposed to low levels through food, particularly fatty foods of animal origin. Zota is an expert on the human impacts of exposure to POPs, and she currently has a K99/R00 Career Development Award from the National Institute of Environmental Health Sciences (NIEHS) to develop frameworks for examining the effects of endocrine-disrupting chemicals and psychosocial stressors on pregnancy outcomes. Her coauthors for the new work include EOH Research Associate Susanna Mitro and Linda Birnbaum, the director of the NIEHS.
Zota’s research interests include identifying how environmental hazards may interact with social disadvantage and psychosocial stressors to exacerbate health disparities. “Telomere length may be a promising biomarker for measuring the body’s response to cumulative stress from environmental and psychosocial hazards,” she says. Her previous research has linked elevated exposure to the metal cadmium with telomere changes.
In this study, Zota and her colleagues looked at blood samples taken from more than 4,250 adults who in 2001 and 2002 participated in the National Health and Nutrition Examination Survey (NHANES), a nationally representative health survey of the U.S. population. The researchers obtained purified DNA from leukocyte blood cells and then used a genetic technique known as polymerase chain reaction to measure the telomeres, the caps on the tips of chromosomes that help protect the genetic code.
The researchers correlated this telomere data with measurements of the concentrations of dioxins, furans and dioxin-like PCBs in the samples. They divided the participants up into fourths based on the concentrations of these compounds found in their bloodstream. After adjusting for potential confounding variables, such as chronological age, they found that people in the most exposed group had telomeres that were significantly longer than those in the least exposed group.
The relationship between telomere length and cancer is complicated, but many cancers linked to dioxin and dioxin-like PCB exposures in multiple epidemiological studies have been associated with longer telomere length. Animal research suggests that dioxins may bind to a widely studied receptor known as the aryl hydrocarbon receptor (AhR) and induce enzyme activity which elongates the telomeres. The role of telomere biology and dioxins in causing cancers warrants further research in both experimental and observational studies, Zota says.
In addition to Zota, Birnbaum and Mitro, Belinda L. Needham of the University of Michigan, Ann Arbor, served as a collaborator on the study, Cross-Sectional Associations between Exposure to Persistent Organic Pollutants and Leukocyte Telomere Length among U.S. Adults in NHANES, 2001-2002. Their work was funded by the National Institutes of Health.