Long-term exposure to air pollution and the blood lipid levels of healthy young men.

Background: There is insufficient evidence of an association between long-term exposure to air pollution and changes in blood lipid levels, and assessments may be influenced by residual confounding factors, such as socioeconomic status.

Objectives: To investigate the associations between long-term exposure to air pollution and blood lipid profiles while controlling for the risk of residual confounding factors.

Methods: We conducted a study involving conscripted Korean soldiers to assess the associations between air pollution and blood lipid levels. The soldiers, who were randomly distributed among military units throughout the country, led homogenous lives and were subjected to health checkups 8-12 months post-enlistment. We analyzed data pertaining to those who enlisted and underwent health checkups in 2019 (n = 12,778) using linear mixed models. Additionally, we evaluated quantile-specific associations using quantile regression models. We also assessed interactions based on body mass index (BMI) at the time of enlistment (≥25.0 vs. < 25.0 kg/m).

Results: The linear mixed models revealed that a 10-µg/m increase in fine particulate matter ≤ 2.5 μm (PM) decreased high-density lipoprotein cholesterol (HDL-C) levels by -0.66% (95% confidence interval [CI]: -1.21, -0.10), and a 10-ppb increase in nitrogen dioxide (NO) increased total cholesterol (TC) levels by 1.04% (95% CI: 0.24, 1.84). In the quantile regression models, associations were also found at specific deciles. PM exposure contributed to higher TC, NO resulted in higher triglycerides and lower HDL-C, and ozone (O) led to lower HDL-C. The association between O and TC differed according to BMI (p-value for interaction = 0.03); among those with a BMI ≥ 25.0 kg/m, a 10-ppb increase in O increased TC by 1.09% (95% CI: 0.20, 1.09).

Discussion: These results shed new light on the importance of controlling air pollution, which can contribute to abnormal blood lipid levels, an independent risk factor for cardiovascular disease.