A leucopoietic-arterial axis underlying the link between ambient air pollution and cardiovascular disease in humans

Abstract

Aims Air pollution [i.e. particulate matter with diameter <2.5 μm (PM2.5)] is a risk factor for major adverse cardiovascular events (MACE). While PM2.5 promotes leucopoiesis and atherosclerotic inflammation in experimental models, it is unknown whether this occurs in humans. We tested in humans (a) whether PM2.5 associates with higher leucopoietic tissue activity and arterial inflammation (ArtI), (ii) whether these associations persist after accounting for the effects of potential confounders including socioeconomics, traffic noise, and risk factors, and (iii) whether these tissue effects mediate the association between air pollution and MACE. Methods and results Individuals (N = 503) without cardiovascular disease (CVD) or active malignancy underwent 18 F-fluorodeoxyglucose positron emission tomography/computed tomography. Major adverse cardiovascular event was adjudicated over 5 years of follow-up. Leucopoietic tissue activity (in bone marrow and spleen) as well as ArtI were measured. Annual PM2.5 levels were assessed at each individual’s home address. At baseline, higher PM2.5 associated with increased leucopoietic activity [standardized (95% CI): 0.129 (0.042, 0.215), P = 0.004] as well as ArtI [0.088 (0.006, 0.171), P = 0.036] after adjusting for CVD risk factors. Over a median 4.1 years, 40 individuals experienced MACE. PM2.5 exposure associated with MACE [Cox HR (95% CI): 1.404 (1.135, 1.737), P = 0.002], remaining significant after adjustment for CVD risk factors and other potential confounders. Mediation analysis demonstrated that increased leucopoietic activity and ArtI serially mediate the link between PM2.5 exposure and MACE. Conclusions Higher air pollution exposure associates with heightened leucopoietic activity and ArtI and independently predicts MACE through a biological pathway that includes higher leucopoietic activity and ArtI in series.

Particulate Air Pollution and Osteoporosis: A Systematic Review

“…Four studies 83 , 84 , 86 , 87 adopted the WHO definition of osteopenia and/or osteoporosis to classify the subjects. 57 , 58 , 60 , 61 Besides, Alvær et al 81 defined subjects with Z-score ≤ −1 as having low BMD, which does not comply with the existing recommendation. Adjusted regression coefficient (β), 81 , 82 , 85 , 86 , 93 , 94 odd ratio (OR), 81 , 82 , 84 , 87 mean differences, 86 , 88 or Pearson correlation coefficient (r) 83 were used in these studies to demonstrate the association between PM and bone mass.…”

Extracellular vesicles enclosed‐miR‐421 suppresses air pollution (PM2.5)‐induced cardiac dysfunction via ACE2 signalling

“…To date, multiple causes are considered be associated with high dose or long‐term exposure to PM 2.5 ‐induced cardiac injury such as oxidative stress (Gangwar et al., 2020 ; Wang et al., 2018 ) and inflammation (Abohashem et al., 2021 ). Prolonged exposure to particulate pollution is identified to cause endothelial and systematic inflammation (Pope et al., 2016 ) and epigenetic changes (Madrigano et al., 2011 ), which may contribute to cardiac injury.…”

Accelerated Aging and Age-Related Diseases (CVD and Neurological) Due to Air Pollution and Traffic Noise Exposure

“…Exposure studies in animals revealed that in the setting of atherosclerosis, plaque development was accelerated [104,105]. Body scans by positron emission tomography in men revealed that particulate matter induces coronary inflammation, which was associated with higher cardiovascular risk [106]. In further human studies, platelet hyperreactivity and thrombus formation were observed [107,108].…”