Our study adds to the growing body of literature by investigating the relationship between pulmonary function and stroke in a large NHANES cohort. We observed a consistent inverse association between pulmonary function, as measured by spirometry-derived metrics such as FEV1, FVC, and PEF, and the risk of stroke, suggesting that preserved lung function may confer protective effects against stroke risk.
These findings are consistent with previous studies that have reported associations between lung function and cardiovascular events, including stroke [14, 15, 16]. Logitudinal studies found that a higher pulmonary function was associated with lower risk of new-onset stroke using data from the UK Biobank [11]. However, a two-sample Mendelian randomisation study confirmed that there was weak evidence that reduced lung function increased risk of ischaemic stroke [12]. Greater longitudinal declines in these spirometric measures are further associated with cardiovascular morbidity and mortality. Previous conclusions were mostly based on the patients with chronic obstructive pulmonary disease. Our study extended the association in general adults, affirming the significance of respiratory health in cardiovascular outcomes [17, 18]. Interestingly, we observed that the association between reduced pulmonary function and stroke was significantly stronger among participants aged 60 years and older. This age-dependent interaction may reflect cumulative vascular injury, reduced physiologic reserve, and heightened susceptibility to systemic inflammation and hypoxia in older adults. These findings suggest that pulmonary health maintenance may be particularly critical in mitigating stroke risk among the aging population. The inverse association between physical activity and stroke risk observed in our study is consistent with prior research. Physical activity improves vascular health through mechanisms such as lowering blood pressure, enhancing insulin sensitivity, and reducing inflammation. It also helps control key risk factors like obesity and dyslipidemia. Epidemiological studies, including the ARIC and Nurses’ Health Study, have similarly reported reduced stroke incidence with higher activity levels.
The mechanisms linking pulmonary function to stroke risk are complex and likely involve multiple pathways. Reduced pulmonary function cause reduced oxygen exchange and contribute to systemic inflammation [19], endothelial dysfunction [20], and impaired vascular homeostasis [21], all of which are implicated in the pathogenesis of atherosclerosis and cerebrovascular disease. Additionally, impaired lung function may lead to hypoxemia and neurovascular dysfunction [22, 23], thereby predisposing individuals to ischemic stroke. Finally, reduced pulmonary function may alter coagulation and platelet aggregation, increasing the risk of thromboembolic events, including stroke.
Our study builds on previous research by using a nationally representative cohort, which includes a broad range of demographic, clinical, and pulmonary function variables. However, several limitations should be considered when interpreting our findings. First, the cross-sectional design of NHANES precludes determination of temporal or causal relationships between pulmonary function and stroke risk. Stroke survivors may experience reduced physical activity, neuromuscular dysfunction, and an increased risk of aspiration pneumonia, all of which can impair respiratory mechanics and lung capacity. Second, stroke history was based on self-report, which may be affected by recall bias or misclassification. However, previous studies suggest that self-reported stroke in NHANES has reasonable validity. Third, despite extensive adjustment for confounders, residual confounding cannot be entirely excluded, such as a history of cerebrovascular disease and prior use of medications like hypoglycemic agents and statins. Forth, spirometry-derived metrics may not fully capture the complexity of respiratory physiology, and other measures of lung function, such as diffusion capacity and airway resistance, were not assessed in our study. Finally, we acknowledge that group size imbalance may still introduce residual confounding. We did not apply propensity score matching in the current analysis. Therefore, future studies with larger event numbers consider incorporating PSM as a complementary strategy will strengthen causal inference and improve the robustness of results.
These findings suggest that pulmonary function testing could serve as a useful adjunct in stroke risk assessment, especially among older adults. Although our findings suggest that lower pulmonary function is associated with higher stroke prevalence, our study does not evaluate whether pulmonary function measures add incremental predictive value beyond traditional risk scores such as the Framingham Stroke Risk Profile. Therefore, the clinical utility of incorporating pulmonary function testing into routine stroke risk assessment remains uncertain. Future studies should investigate whether pulmonary function improves risk prediction models and whether interventions aimed at preserving or improving lung function can reduce the burden of stroke.