![]() Most studies on VOC have focused on tobacco smoke 9– 11 which represents a major source of human exposures. 8 In comparison with PM 2.5, data on VOCs tend to exhibit higher temporal and spatial variability. 7 The emphasis on PM 2.5 and cardiovascular disease (CVD) has been motivated largely by the availability of historical monitoring data, however in an urban setting, over 90% of pollutant mass consists of gases or vaporous compounds, such as volatile organic compounds (VOCs). 1 Exposure to fine particulate matter in the ambient air, defined as particle size < 2.5 μm in diameter (PM 2.5), is associated with an increased risk for hypertension, 2 myocardial infarction, 3 type 2 diabetes, 4, 5 stroke, 6 and cardiovascular mortality. The Global Burden of Disease (GBD) study estimates that in 2015, 4.2 million deaths could be attributed to ambient air pollutants, with an additional 2.8 million deaths due to household air pollution. Sex and race, hypertension, and diabetes significantly modified VOC associated CAC depletion.Įxposure to ambient air pollution has been widely recognized to be an important contributor to premature mortality and morbidity. We found a non-linear relationship for benzene, which showed an increase in CAC levels at low, but depletion at higher levels of exposure. ![]() Cumulative VOC risk score showed a strong negative association with CD45 dim/CD146 +/CD34 + cells, suggesting that total VOC exposure has a cumulative effect on pro-angiogenic cells. In analysis of non-smokers (n=375), multipollutant models showed a negative association with metabolites of ethylbenzene/styrene, benzene, and xylene with CD45 dim/CD146 +/CD34 + cells, independent of other VOC metabolite levels. The metabolite of acrylonitrile was negatively associated with CD45 dim/CD146 +/CD34 +/AC133 + cells and CD45 +/CD146 +/AC133 +, and the toluene metabolite with AC133 + cells. In single pollutant models, metabolites of ethylbenzene/styrene and xylene, were negatively associated with CAC levels in both the total sample, and in non-smokers. Associations between CAC and VOC metabolite levels were examined using generalized linear models in the total sample, and separately in non-smokers. Approach and Results In this cross-sectional study, we recruited 603 participants with low-to-high CVD risk and measured 15 subpopulations of CACs by flow cytometry and 16 urinary metabolites of 12 VOCs by LC/MS/MS.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |