Table 1 Epidemiological studies on PM exposure and HDL functionality

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)

PM_2.5

Personal PM_2.5 exposure for 24 h [12,2 ± 16,9 μg/m³] and ambient PM_2.5 exposure for 7 days [9,1 ± 1,8 μg/m³].

HDL-C level

Serum cholesterol efflux capacity (CEC)

HDL oxidation markers

Higher ambient PM_2.5 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 PM_2.5 exposure did not impact outcomes.

Even low levels of PM_2.5 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)

PM_2.5

PNC_5–50

PNC_50–100

PNC_100–560

BC

Average daily concentration of PM_2.5were 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 PM_2.5 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.