Dataset Information

The Role of Ambient Particle Radioactivity in Inflammation and Endothelial Function in an Elderly Cohort.

ABSTRACT:

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.

SUBMITTER: Blomberg AJ

PROVIDER: S-EPMC7269805 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundDecay products of radioactive materials may attach to ambient fine particles and form radioactive aerosol. Internal ionizing radiation source from inhaled radioactive aerosol may contribute to the fine particulate matter (PM2.5)-inflammation pathway. However, few studies in humans have examined the associations.ObjectivesTo examine the associations between particle radioactivity and biomarkers of oxidative stress and inflammation among participants from the Framingham Offspring and Third Generation cohorts.MethodsWe included 3996 participants who were not current smokers and lived within 50 km from our central air pollution monitoring station. We estimated regional mean gross beta radioactivity from monitors in the northeastern U.S. as a surrogate for ambient radioactive particles, and calculated the 1- to 28-day moving averages. We used linear regression models for fibrinogen, tumor necrosis factor α, interleukin-6, and myeloperoxidase which were measured once, and linear mixed effect models for 8-epi-prostaglandin F2α, C-reactive protein, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), P-selectin, and tumor necrosis factor receptor-2 that were measured up to twice, adjusting for demographics, individual- and area-level socioeconomic positions, time, meteorology, and PM2.5. We also examined whether the associations differed by median age, sex, diabetes status, PM2.5 levels, and black carbon levels.ResultsThe mean age was 54 years and 54% were women. An interquartile range (3 × 10-3 pCi/m3) higher beta radioactivity level at the 7-day moving average was associated with 5.09% (95% CI: 0.92, 9.43), 2.65% (1.10, 4.22), and 4.71% (95% CI: 3.01, 6.44) higher levels of interleukin-6, MCP-1, and P-selectin, but with 7.01% (95% CI: -11.64, -2.15) and 2.70% (95% CI: -3.97, -1.42) lower levels of 8-epi-prostaglandin F2α and ICAM-1, respectively.ConclusionsRegional mean particle radioactivity was positively associated with interleukin-6, MCP-1, and P-selectin, but negatively with ICAM-1 and 8-epi-prostaglandin F2α among our study participants.