Study shows dementia patients exposed to pollution had longer telomeres

A population-based study in Northern Sweden challenges assumptions about pollution and cellular aging, uncovering an unexpected signal of longer telomeres in patients with dementia that warrants further research.

Study: Associations between air pollution and relative leukocyte telomere length among northern Swedish adults based on findings from the Betula study. Image Credit: peterschreiber.media / Shutterstock

Associations between air pollution and subsequent risk of dementia are growing clinical concerns, but remain understudied. The biological underpinnings of these associations are especially unclear. In a recent study published in the journal Scientific Reports, researchers explored one hypothesized pathway involving telomeres (that shorten with age) by analyzing data from 473 older adults from Northern Sweden who had complete information on air pollution exposure, telomere length, and covariates.

Study findings did not reveal an overall association between exposure to air pollution and telomere length. However, study analyses highlight a slight, statistically nonsignificant trend suggesting that individuals who later developed dementia had longer telomeres, despite higher exposure to pollution, a counterintuitive finding that warrants further investigation.

Background

Telomeres are segments of DNA at the ends of our chromosomes that protect the underlying genetic material from degradation, external damage, and fusion. With each cell division, these telomeres naturally shorten, making telomeres a well-established hallmark of biological aging.

Recent research suggests that environmental factors (particularly pollutants) can accelerate this shortening process. Air pollution, a well-studied driver of systemic inflammation and oxidative stress, is hypothesized as a prime suspect. Evidence is mixed on whether long-term air-pollution exposure shortens telomeres, with some studies reporting no association or even longer telomeres.

Simultaneously, decades of research have now conclusively linked telomere length (shorter is worse) to a variety of age-related chronic diseases, including dementia. Dementia is an umbrella term for several neurological conditions characterized by significant cognitive decline and memory loss, substantially hampering patients’ daily lives.

In today’s rapidly aging society, identifying the mechanistic underpinnings of risk factors (such as air pollution) linked to age-associated chronic disease (like dementia) prevalence and risk could help delay symptom progression in the more than 57 million patients living with the condition, and the millions more likely to develop dementia in the near future. Unfortunately, mechanistic evidence for the association between air pollution and dementia remains limited, as previous studies have failed to explicitly test the relationship between these variables.

About the study

The present study leveraged data from the Betula project, a long-running, population-based cohort focused on aging and dementia in Northern Sweden. Researchers collated two different time waves (T1 and T2 out of the seven total waves of the Betula study) collected in five-year intervals between 1988 and 1995.

Data collections at each wave comprised health-related questionnaires, cognitive evaluations, and medical examinations (including blood collections). Notably, air-quality data for the locations of study participants were also available.

Blood samples were used for relative leukocyte telomere length (rLTL) measurements via quantitative polymerase chain reaction (qPCR). Air pollution exposure was assessed using a high-resolution dispersion model to estimate the annual mean concentrations of fine particulate matter (PM₂.₅) and black carbon (BC) at each participant’s home address in 1990, including source-specific estimates for vehicle exhaust and residential wood burning.

Analysis further included linear regression models to investigate the association between these pollution levels and telomere length, adjusting for age, gender, smoking status, lymphocyte proportion, and education. Subgroup analysis tested whether the relationship differed in the 74 participants who were later diagnosed with dementia.

Study findings

Linear regression analyses failed to demonstrate any significant associations between air pollution exposure (either PM₂.₅ or BC) and shorter telomeres. For total PM₂.₅ exposure, the beta coefficient (β, measure of relative leukocyte telomere length) was recorded at 0.01 (95% CI: -0.011, 0.024), indicating a negligible effect. Total BC was similarly negligible at 0.03 (95% CI: −0.046, 0.114).

However, subgroup analyses revealed a more complex, unexpected, and currently unexplained trend: a slight positive association between pollution exposure and telomere length.

While not statistically significant, these findings mean that among future dementia patients, those exposed to higher levels of air pollution tended to have longer, not shorter, telomeres. For example, this subgroup’s beta coefficient for total PM₂.₅ exposure was 0.03 (p-value = 0.12), and for total BC, it was 0.11 (p-value = 0.17). Effect-modification interaction terms were not significant.

Conclusions

This study, conducted in a low-pollution region of Northern Sweden, failed to validate the prevailing hypothesis that links air pollution to shorter telomere length (accelerated cellular aging) and, in turn, higher dementia risk. Instead, an unexpected and counterintuitive trend was observed in the dementia subgroup: higher air pollution exposure was linked to longer telomeres in participants who later developed dementia. These exploratory signals were imprecise and not statistically significant, necessitating further research to explain this observation.