Background: The mechanisms by which exposure to particulate matter might increase risk of cardiovascular morbidity and mortality are not fully known. However, few existing studies have investigated the potential role of particle radioactivity. Naturally occurring radionuclides attach to particulate matter and continue to release ionizing radiation after inhalation and deposition in the lungs. We hypothesize that exposure to particle radioactivity increases biomarkers of inflammation.
Methods: Our repeated-measures study included 752 men in the greater Boston area. We estimated regional particle radioactivity as a daily spatial average of gross beta concentrations from five monitors in the study area. We used linear mixed-effects regression models to estimate short- and medium-term associations between particle radioactivity and biomarkers of inflammation and endothelial dysfunction, with and without adjustment for additional particulate air pollutants.
Results: We observed associations between particle radioactivity on C-reactive protein (CRP), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1), but no associations with fibrinogen. An interquartile range width increase in mean 7-day particle radioactivity (1.2 × 10 Bq/m) was associated with a 4.9% increase in CRP (95% CI = 0.077, 9.9), a 2.8% increase in ICAM-1 (95% CI = 1.4, 4.2), and a 4.3% increase in VCAM-1 (95% CI = 2.5, 6.1). The main effects of particle radioactivity remained similar after adjustment in most cases. We also obtained similar effect estimates in a sensitivity analysis applying a robust causal model.
Conclusion: Regional particle radioactivity is positively associated with inflammatory biomarkers, indicating a potential pathway for radiation-induced cardiovascular effects.