LDI Senior Fellow Jamaji Nwanaji-Enwerem was the first to show that exposure to airborne fine particles may accelerate DNA methylation-based biological aging. Faster biological aging is linked to a higher risk of chronic disease and earlier death.

His subsequent study found that people with health insurance showed fewer signs of biological aging, as measured by two specific aging biomarkers, than those without coverage.

Building on these two results, Nwanaji-Enwerem and colleagues found that among people exposed to similar levels of lead, those with health insurance showed fewer changes associated with biological aging than those without insurance. The link between health insurance and reduced biological aging suggests that the access to health care that insurance affords might be another way to protect people from the effects of some environmental hazards.

Nwanaji-Enwerem is optimistic, yet cautious about interpreting these findings. “Overall, the study provides early evidence that health insurance may offer some protection in the face of harmful environmental exposures,” he said. “It should be viewed as a starting point rather than a definitive conclusion, and it highlights the need for future longitudinal work that can clarify mechanisms and better define clinical relevance.”

We asked Nwanaji-Enwerem more about biological aging, his research, and the policy implications of his latest results.

How can non-scientists think about biological measures of aging compared to chronological age?

Nwanaji-Enwerem: Chronological age is just a clock that measures the amount of time that has passed since your birth. It is useful because the risk of many health conditions increases as we get older, so it gives us a general sense of risk. At the same time, it is a blunt instrument. Two people who are both 60 years old may have very different levels of health and disease risks.

Biological measures of aging, such as DNA methylation-based biomarkers (epigenetic age), provide a more individualized picture. Instead of only tracking time, they capture signals related to our genetics, environmental exposures, lifestyle, stress, and other experiences. Because of this, they can provide a closer reflection of how well or how poorly our bodies are aging.

Why are biological measures of aging important to improving population health?

Nwanaji-Enwerem: In 2022, I wrote a commentary outlining scenarios that demonstrate why biological age can be so valuable. One clear example involves colon cancer screening. Current guidelines recommend that people at average risk begin screening at age 45. However, individuals who have higher risk factors, such as a first-degree relative with colon cancer or a personal history of inflammatory bowel disease, are advised to begin earlier, sometimes at age 40 or even sooner. This is because their underlying biology places them on a different risk trajectory.

Biological aging measures can further refine this approach. Instead of grouping large numbers of people into a single average risk category based only on chronological age, biological age could help us identify who needs earlier screening and why. In this way, biological age can support prevention and early detection strategies that are better tailored to each person’s true health risks rather than the number of years they have lived.

What motivated you to explore the link between health insurance and epigenetic aging?

Nwanaji-Enwerem: I led the first study to show that physical environmental exposures can influence epigenetic aging. That finding raised an important question: If something as common as air pollution can shift biological aging, what other exposures across a person’s life course might have similar effects?

My motivation has also been influenced by my clinical practice. As a board-certified emergency medicine physician, I regularly see how much variation there is in aging and disease risk among people with the same chronological age.

At its core, the motivation has always been the same. I want to understand why some individuals age faster than others, how exposures shape that process, and how we can eventually use this information to improve health outcomes at both the individual and population level.

How did you choose the dataset and biomarkers for this research on biological aging?

Nwanaji-Enwerem: We chose this study design because the National Health and Nutrition Examination Survey, or NHANES, offers a unique combination of strengths. Although it is cross-sectional, it is nationally representative and contains detailed information on lifestyle factors, clinical history, environmental exposures, and biological markers. NHANES also includes epigenetic aging measures. This allowed us to study health insurance, 64 environmental exposures, and biological aging within the same population, something that is very difficult to do in most datasets.

We chose the biomarkers GrimAge2 and DunedinPoAm because our earlier work pointed us there. In 2025, I led an analysis in which we examined the relationship between having health insurance and epigenetic aging. We looked at several biological aging markers, but the clearest and most consistent findings were with GrimAge2 and DunedinPoAm. GrimAge2 captures mortality risk, and DunedinPoAm captures the pace of biological aging across multiple organ systems. Since these two markers gave us the strongest and most robust results, they became the logical choice for examining more complex questions.

What is your most important finding about the link between health insurance and epigenetic aging?

Nwanaji-Enwerem: While the relationships between cotinine, lead, and PCB180 exposure and epigenetic aging were reduced among insured participants compared to those without insurance, our most important finding was that having health insurance appeared to weaken the association between higher blood lead levels and greater epigenetic aging. In other words, insurance seemed to lessen some of the biological aging burden linked with harmful lead exposures. We believe that health insurance may act as a protective factor, possibly by improving access to exposure monitoring, preventive care, or earlier treatment. While health insurance cannot replace environmental regulation or removal of harmful exposures, it may offer a complementary and more immediate tool to help reduce harm for people who are already exposed.

At the same time, there are important limitations. First, this is an association study, so we cannot infer causation. The cross-sectional nature of NHANES means that exposure levels, insurance status, and epigenetic aging are measured at a single time point, which limits our ability to determine directionality. Second, although the patterns we observed were consistent, the magnitude of the model estimates was small. This means that even though the findings are statistically meaningful, their practical significance should be interpreted with care.

What can policymakers take away from these results?

Nwanaji-Enwerem: The results point toward several policy-relevant themes.

• First, the findings reinforce the importance of expanding access to meaningful health insurance coverage. We already know that insurance improves access to primary care, preventive services, and chronic disease management. If insurance also provides even a modest buffer against the biological aging impacts of harmful environmental exposures, that is an added reason to continue strengthening coverage, particularly for communities with higher exposure burdens.
• Second, the study highlights the need for creativity in how we think about environmental protection. Removing harmful exposures from the environment remains the gold standard and should always be the priority. But we also know that regulatory and policy processes often move slowly because of scientific review, economic pressures, and political considerations. While those long-term solutions are pursued, people are still living with exposures that affect their health today.
• Finally, the idea that health insurance might offer a near-term, complementary form of protection suggests pursuing layered strategies that combine structural environmental policy with tools that can be implemented immediately.

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The study, “The Environmental Chemical Exposome and Health Insurance: Examining Associations and Effect Modification of Epigenetic Aging in a Representative Sample of United States Adults” was published in Exposome on November 24, 2025. Authors include Jamaji C. Nwanaji-Enwerem, Dennis Khodasevich, Nicole Gladish, Hanyang Shen, Anne K. Bozack, Saher Daredia, Belinda L. Needham, David H. Rehkopf, and Andres Cardenas.

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