Association between exposure to air pollution and blood lipids in the general population of Spain

Abstract

Background and AimsWe aimed to assess the associations of exposure to air pollutants and standard and advanced lipoprotein measures, in a nationwide sample representative of the adult population of Spain.MethodsWe included 4647 adults (>18 years), participants in the national, cross‐sectional, population‐based di@bet.es study, conducted in 2008–2010. Standard lipid measurements were analysed on an Architect C8000 Analyzer (Abbott Laboratories SA). Lipoprotein analysis was made by an advanced 1H‐NMR lipoprotein test (Liposcale®). Participants were assigned air pollution concentrations for particulate matter <10 μm (PM10), <2.5 μm (PM2.5) and nitrogen dioxide (NO2), corresponding to the health examination year, obtained by modelling combined with measurements taken at air quality stations (CHIMERE chemistry‐transport model).ResultsIn multivariate linear regression models, each IQR increase in PM10, PM2.5 and NO2 was associated with 3.3%, 3.3% and 3% lower levels of HDL‐c and 1.3%, 1.4% and 1.1% lower HDL particle (HDL‐p) concentrations (p < .001 for all associations). In multivariate logistic regression, there was a significant association between PM10, PM2.5 and NO2 concentrations and the odds of presenting low HDL‐c (<40 mg/dL), low HDL‐p (<p25) and higher LDL particle (LDL‐p) concentrations (≥p75). In subgroup analyses there were stronger associations between PM10 and NO2 and low HDL‐p in men (p for interaction .008 and .034), and between NO2 and low HDL‐p in individuals with obesity (p for interaction .015).ConclusionsOur study shows an association between the exposure to air pollutants and blood lipids in the general population of Spain, suggesting a link to atherosclerosis.

Relationship between exposure to fine particulate matter and cardiovascular risk factors and the modifying effect of socioeconomic status: a cross-sectional study in Beijing, China

“…A considerable amount of accumulating research suggested that long-term exposure to fine particulate matter (PM 2.5 ) is connected to an elevated likelihood of developing CVD ( 8 , 9 ). Based on biological plausibility, it is conceivable that prolonged exposure to air pollution, through the aforementioned mechanistic pathways, might induce undesirable alterations in CVD risk factors, encompassing blood lipid, glucose, and Hcy levels ( 10 , 11 ). Consequently, these modifications could serve as intermediaries connecting exposures to the overt manifestation of CVD ( 12 , 13 ).…”