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Updated: Sep 24, 2025

Measuring Carbon Content in Airway Macrophages Exposed to Carbon-Containing Particulate Matters
Published on: July 12, 2024
Urban Air Pollution and Subclinical Atherosclerosis in Adolescents and Young Adults
Szu-Ying Chen1, Jing-Shiang Hwang2, Chang-Chuan Chan3
1Division of Occupational Medicine, E-Da Hospital, I-Shou University, Kaohsiung, Taiwan; Division of Surgical Intensive Care, Department of Critical Care Medicine, E-Da Hospital, I-Shou University, Kaohsiung, Taiwan; Department of Nursing, Fooyin University, Kaohsiung, Taiwan.
Purpose:
The contribution of air pollution to subclinical atherosclerosis in a young population remains limited. This study aimed to assess whether long-term exposure to urban air pollutants increases carotid intima-media thickness (CIMT) in adolescents and young adults.
Methods:
This study included 789 subjects between the ages of 12 and 30 years who lived in the Taipei metropolis from a cohort of young Taiwanese individuals. Residential addresses were geocoded, and annual average concentrations of particulate matter (PM) of different diameters, e.g., PM10, PM2.5-10, PM2.5, and nitrogen oxides (NOX), were assessed using land use regression models. The generalized least squares strategy with error term to consider the cluster effect of living addresses between individuals was used to examine the associations between urban air pollution and CIMTs.
Results:
After adjusting for potential confounders, we found that interquartile range increases in PM2.5 (8.2 μg/m3) and NOX (17.5 μg/m3) were associated with 0.46% (95% CI: 0.02-0.90) and 1.00% (95% CI: 0.10-1.91) higher CIMTs, respectively. Stratified analyses showed that the relationships between CIMT and PM2.5 and NOX were more evident in subjects who were 18 years or older, female, nonsmoking, nonhypertensive, and nonhyperglycemic than in their respective counterparts.
Discussion:
Long-term exposure to PM2.5 and NOX is associated with subclinical atherosclerosis in a young population. Age, sex, and health status may influence the vulnerability of air pollution-associated subclinical atherosclerosis.
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