Associations of time-weighted individual exposure to ambient particulate matter with carotid atherosclerosis in Beijing, China

BACKGROUND: Time-location information (time spent on commuting, indoors and outdoors around residential and work places and physical activity) and infiltrated outdoor pollution was less considered estimating individual exposure to ambient air pollution. Studies investigating the association between individual exposure to particulate matter (PM) with aerodynamic diameter < 10 μm (PM(10)) and < 2.5 μm (PM(2.5)) and carotid atherosclerosis presented inconsistent results. Moreover, combined effect of pollutants on carotid atherosclerosis was not fully explored. We aimed to investigate the association between long-term individual time-weighted average exposure to PM(2.5) and PM(10) and the risk of carotid atherosclerosis, and further explore the overall effect of co-exposure to pollutants on carotid atherosclerosis. METHODS: The study population included 3069 participants derived from the Beijing Health Management Cohort (BHMC) study. Daily concentration of ambient air pollutants was estimated by land-use regression model at both residential and work addresses, and one- and two-year time-weighted average individual exposure was calculated by further considering personal activity pattern and infiltration of ambient air pollution indoors. We explored the association of PM(2.5) and PM(10) with carotid atherosclerosis and pooled the overall effect of co-exposure to ambient air pollutants by quantile g-computation. RESULTS: A significant association between time-weighted average exposure to PM(2.5) and PM(10) and carotid atherosclerosis was observed. Per interquartile range increase in two-year exposure to PM(2.5) (Hazard ratio (HR): 1.322, 95% confidence interval (CI): 1.219–1.434) and PM(10) (HR:1.213, 95% CI: 1.116–1.319) showed the strongest association with carotid atherosclerosis, respectively. Individuals in higher quartiles of pollutants were at higher risk for carotid atherosclerosis compared with those in the lowest quartile group. Concentration response functions documented the nearly linear and nonlinear relationship and interpreted the upward trends of the risk for carotid atherosclerosis with increasing level of pollutant concentrations. Moreover, effect estimates for the mixture of pollutants and carotid atherosclerosis were larger than any of the individual pollutants (HR (95% CI) was 1.510 (1.338–1.704) and 1.613 (1.428–1.822) per quartile increase for one-year and two-year time-weighted average exposure, respectively). CONCLUSIONS: Individual time-weighted average exposure to PM(2.5) and PM(10) was associated with carotid atherosclerosis. Co-exposure to ambient air pollution was also positively associated with carotid atherosclerosis. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12940-023-00995-8.