Telomere length and prevalent chronic lung disease in adults aged 50+ in the 2008 HRS
In 4,994 adults aged 50+ in the 2008 Health and Retirement Study, longer telomeres were associated with lower odds of prevalent self-reported chronic lung disease, but the association was no longer significant after excluding those exposed to parental smoking in childhood. [1]
Automatic summary · not editorially reviewed
The key findings
The study included 4,994 participants aged 50 or older from the 2008 Health and Retirement Study wave with telomere measurements; chronic lung disease was self-reported physician diagnosis excluding asthma. [1]
Each interquartile range increase in telomere length was associated with 14.3% lower odds of prevalent pulmonary disease (adjusted OR 0.857, 95% CI 0.774–0.945). [1]
After excluding participants exposed to parental smoking in childhood, the association was no longer statistically significant (OR 0.901, 95% CI 0.736–1.091). [1]
The source at a glance
- Study type / format
- Cross-sectional analysis of survey data (abstract)
- Population / context
- 4,994 adults aged 50 or older in the 2008 Health and Retirement Study wave with telomere measurements.
- Summary based on
- Study abstract
- Original publication
- September 30, 2026
Telomeres and lung disease in 4,994 HRS adults
The abstract notes that telomere shortening is a hallmark of aging and age-related diseases, but evidence linking it to lung diseases is limited. The study included 4,994 participants aged 50 or older from the 2008 Health and Retirement Study wave who had telomere measurements. Chronic lung disease was defined by self-report of a physician diagnosis in 2008, covering conditions such as chronic bronchitis or emphysema and excluding asthma. The authors used multivariable logistic regression to examine the association between telomere length and the odds of prevalent chronic lung disease.
Supporting source [1]
Longer telomeres linked to lower odds in full sample
Each interquartile range increase in telomere length was associated with 14.3% lower odds of prevalent pulmonary disease (adjusted odds ratio 0.857, 95% confidence interval 0.774–0.945, P = 0.002). Participants in the longest telomere quartile had 38.0% lower odds than those in the shortest quartile. The authors describe this as an association, not a cause. They suggest telomere shortening may be biologically related to pulmonary disease processes via cellular senescence and chronic inflammation, and call for longitudinal studies to clarify timing.
Supporting source [1]
Association weakened after excluding childhood parental smoking
After excluding participants exposed to parental smoking during childhood, the association was attenuated and no longer statistically significant (odds ratio 0.901, 95% confidence interval 0.736–1.091, P = 0.297). The authors state that the full-sample association should therefore not be interpreted as independent of early-life tobacco exposure. This is an abstract only; the full text was not reviewed. The design is cross-sectional, so it cannot establish whether telomere length preceded or followed lung disease.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The design is cross-sectional, so temporality between telomere length and lung disease cannot be established. Lung disease was self-reported. The association was not independent of childhood parental smoking exposure.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Dai Y, Cai H, Su W, Wang S, Yang M, Chuai X. · europepmc.org · September 30, 2026