This nationwide prospective cohort study (China Kadoorie Biobank, n=512,701 adults aged 30–79) examined whether exhaled carbon monoxide (CO) levels — both from smoking and non-smoking sources — are associated with incident Parkinson disease (PD) risk over ~12 years of follow-up (2004–2019).
Regular smoking was associated with lower PD risk (adjusted HR 0.70; 95% CI 0.62–0.79). Among never-smokers, higher exhaled CO showed a dose-dependent inverse association with PD: HRs ranged from 0.85 (2.0–<3.0 ppm) to 0.62 (3.0–<5.0 ppm) to 0.65 (≥11.5 ppm) vs. reference <2.0 ppm (P for trend <.001), with no corresponding signal for smoking-related diseases or other neurodegenerative diseases.
- Observational design cannot establish causality; residual confounding (e.g., unaccounted CO sources such as solid fuel use) is possible despite adjustments. - PD ascertainment relied on linkage to death/disease registries and health insurance — clinical underdiagnosis in rural China could bias case counts. - Exhaled CO was measured only at baseline (single time point), limiting assessment of cumulative or changing exposure.
CO itself — not just other tobacco constituents — may drive smoking's inverse association with PD, supporting the biological plausibility of ongoing CO-based clinical trials for PD. Clinicians should be aware that this does not endorse smoking, given its well-confirmed harms for lung cancer, heart disease, and stroke.
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