Author, year and country | Design | Study population | Air pollutant | Exposure | Outcome | Results | Main findings |
---|---|---|---|---|---|---|---|
Mathew et al. 2018, United States [27] | Prospective follow-up study | Country: United States Age: 18–50 y (32.1 ± 9.6 y) Non-smoking adults without a history of CV disease or risk factors n = 50 (34 female subjects) | PM2.5 | Personal PM2.5 exposure for 24 h [12,2 ± 16,9 μg/m3] and ambient PM2.5 exposure for 7 days [9,1 ± 1,8 μg/m3]. | HDL-C level Serum cholesterol efflux capacity (CEC) HDL oxidation markers | Higher ambient PM2.5 exposures (per 10 mg/m3) were associated with reductions in CEC. Exposures were not associated with MPO-induced oxidation or other HDL-oxidation markers. Previous 24-h personal-level PM2.5 exposure did not impact outcomes. | Even low levels of PM2.5 exposure is linked to impaired HDL functionality (CEC). |
Li et al. 2019, China [28] | Prospective follow-up study | Country: China Age: 18–50 y (23.3 ± 5.4 y) Non-smoking adults without pre-existing CV disease or risk factors n = 73 (48 female subjects) | PM2.5 PNC5–50 PNC50–100 PNC100–560 BC | Average daily concentration of PM2.5were 62,9 μg/m3 (8,1–331,0 μg/m3), followed up with 4 study visits during a 14-month period. | HDL-C and apoA-I levels HDL cholesterol efflux capacity (CEC) HDL antioxidative activity measured as HDL oxidation index (HOI) Metrics of systemic inflammation and oxidative stress: ox-LDL, malondialdehyde (MDA), high sensitivity C-reactive protein (hs-CRP) | Significant decreases in CEC were associated with interquartile range increases in moving average concentrations of PM2.5 during the 1 to 7 days before each participant’s clinic visit. Higher ambient air pollutant levels were also associated with significant reductions in circulating HDL-C and apoA-I, as well as elevations in HOI, oxidized LDL, MDA, and hs-CRP. | Higher ambient air pollution exposure was associated with impairments in HDL functionality (CEC, HOI) and parameters of oxidative stress and inflammation. |