Ambient polycyclic aromatic hydrocarbons and cardiovascular disease in China.

Summary

Across 184 Chinese cities (2014–2017), each interquartile range increase in ambient PAHs was associated with higher daily hospitalizations for cardiovascular disease, ischemic heart disease, and ischemic stroke. Parallel mouse experiments confirmed PAH-induced cardiac injury with transcriptomic/proteomic signatures, providing mechanistic support for the epidemiologic associations.

Key Findings

• Each IQR increase in ambient PAHs (lag 0–7 days) associated with +5.18% cardiovascular hospitalizations.
• +5.72% for ischemic heart disease and +6.08% for ischemic stroke per IQR increase in PAHs.
• Associations persisted after adjusting for co-pollutants (e.g., particulate matter).
• Mouse PAH exposure induced cardiac injury with transcriptomic and proteomic pathway changes.

Clinical Implications

Clinicians should consider air pollution (including PAHs) as a cardiovascular risk modifier, counsel high-risk patients on exposure reduction, and support policies targeting combustion-derived pollutants.

Limitations

• City-level exposure metrics may introduce exposure misclassification and ecological bias.
• Residual confounding by unmeasured factors cannot be fully excluded; clinical outcomes were hospitalizations, not incident disease.

Future Directions

Personal-level exposure assessment, interventional policies targeting PAHs, and studies linking exposure reductions to cardiovascular outcomes are warranted.