Ambient Air Pollution Is Associated With HDL (High-Density Lipoprotein) Dysfunction in Healthy Adults

Abstract

Objective— We aimed to assess whether exposure to higher levels of ambient air pollution impairs HDL (high-density lipoprotein) function and to elucidate the underlying biological mechanisms potentially involved. Approach and Results— In the Beijing AIRCHD study (Air Pollution and Cardiovascular Dysfunction in Healthy Adults), 73 healthy adults (23.3±5.4 years) were followed-up with 4 repeated study visits in 2014 to 2016. During each visit, ambient air pollution concentrations, HDL function metrics, and parameters of inflammation and oxidative stress were measured. Average daily concentrations of ambient particulate matter in diameter <2.5 μm were 62.9 µg/m 3 (8.1–331.0 µg/m 3 ). We observed significant decreases in HDL cholesterol efflux capacity of 2.3% (95% CI, −4.3 to −0.3) to 5.0% (95% CI, −7.6 to −2.4) associated with interquartile range increases in moving average concentrations of particulate matter in diameter <2.5 μm and traffic-related air pollutants (black carbon, nitrogen dioxide, and carbon monoxide) 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 cholesterol and apoA-I (apolipoprotein A-I), as well as elevations in HDL oxidation index, oxidized LDL (low-density lipoprotein), malondialdehyde, and high-sensitivity C-reactive protein. Conclusions— Higher ambient air pollution concentrations were associated with impairments in HDL functionality, potentially because of systemic inflammation and oxidative stress. These novel findings further our understanding of the mechanisms whereby air pollutants promote cardiometabolic disorders.

Exposure to ambient fine particulate matter is associated with changes in fasting glucose and lipid profiles: a nationwide cohort study

“…For changes in TC and TG levels, no significant relationship with PM exposure was obtained after adjusting for covariates in this study. Previous studies have suggested that higher concentrations of ambient PM were correlated with lower concentrations and impaired functions of HDL-C, as well as poor health outcomes of TC and TG concentrations [22,[29][30][31]. However, their long-term effects could not be identified clearly and were inconsistent regarding the relationship between PM and lipid profiles, as most were conducted during short-term periods.…”

Effects of particulate matter on atherosclerosis: a link via high-density lipoprotein (HDL) functionality?

“…The current literature on PM-exposure and HDL functionality suggest that fine and ultrafine PM may impair functional properties of HDL via oxidative pathways [27,28,[30][31][32][33]. Accumulating evidence links particles to atherosclerosis, in particular those with a high amount of organic chemicals [3,6,31,36].…”

“…2). In some studies, PM exposure was found to be associated with reduced HDL-C levels as well as altered HDL functionality [28,32]. However, other studies report alteration in HDL functional properties without affecting the quantitative levels [31,33].…”

“…These were screened at the abstract level. All relevant epidemiological and human exposure studies as well as animal studies assessing the effects of particulate air pollution on HDL functionality were included, resulting in a total of two epidemiological [ 27 , 28 ], two clinical [ 29 , 30 ] and three animal studies [ 31 – 33 ]. Additional search strategies were also applied focusing on keywords (combinations of keywords): (“HDL” OR “high-density lipoprotein”) AND (“PM” OR “particulate matter” OR “air pollution” OR “inhalation exposure”).…”

“…A number of studies have found elevated PM exposure to be negatively correlated with the level of HDL-C [28,32,[37][38][39][40][41][42][43]. However, the literature is somewhat inconsistent on this issue, as some studies find exposure to PM associated with an increase in HDL-C [44][45][46], while others find no statistical Studies are shown in chronological order based on the year of publication association [47][48][49][50].…”