The role of air pollution in myocardial remodeling

Abstract

BackgroundExcessive air pollution in urban environments can impact morbidity and mortality. The authors evaluated the role of particulate matter2.5 (PM2.5) in structural, geometric, and functional remodeling in hearts, using an experimental model of myocardial infarction.Methods and findingsSeventy-five rats were divided into 5 groups: control (CG), CG exposed to PM2.5 pollution (CGP), myocardial infarcted group (MI), infarcted group immediately exposed to pollution (IGP-I), and infarcted group previously exposed to pollution and kept exposed after infarction (IGP-II). Greater deposition of interstitial collagen occurred in the left ventricle in CGP, MI, IGP-I, and IGP-II groups compared with that in controls (p = 0.002 CG vs CGP and p<0.0001 CG vs MI, IGP-I, and IGP-II). In the right ventricle, greater collagen deposition existed in CGP, MI, IGP-I, and IGP-II compared with that in CG (p<0.021 CG vs CGP and p<0.0001 CG vs MI, IGP-I, and IGP-II). At the end of the study, CG had a higher mean shortening fraction than the other groups had (p≤0.03). Left ventricular systolic diameter was lower in CG than in infarcted groups (p≤0.003). The infarcted groups had greater expression of TGF-β (p≤0.04). PM2.5 increased the expression of TGF-β in the IGP-II compared with the MI group (p = 0.004). The TNF-α gene was overexpressed in the IGP-II compared with the CGP group (p = 0.012). INF-γ gene expression was greater in IGP-II (p≤0.01). Oxidative stress analysis showed a higher glutathione concentration in CGP (p = 0.03), MI (p = 0.014), and IGP-I (p = 0.008) compared with that in CG.ConclusionsPM2.5 stimulates the deposition of fibrosis in the myocardium of healthy hearts, but not in infarcted hearts. PM2.5 modulates the inflammatory response, which was greater in the IGP-II group. It also modulates oxidative stress in healthy hearts but not in infarcted hearts.

Changes in gene expression in chronic allergy mouse model exposed to natural environmental PM2.5-rich ambient air pollution

“…A recent study has suggested that particulates act as adjuvants and promote long-lasting allergic inflammation in the airways 7 . Studies investigating the potential mechanisms underlying the adverse effects of exposure to PM2.5 have suggested that these include inflammation, oxidative stress, and apoptosis response 8 . Although some studies have investigated the effect of natural exposure to PM2.5 on the health of traffic policeman or employees at trucking terminals 9 , 10 , the precise mechanism/s linking the effects of PM2.5 pollution in real-life settings on human health have not yet been elucidated.…”

Biomass Fuel Use and Cardiac Function in Nepali Women

“…The observed trend of increased left ventricular and atrial volumes may be a result of direct adverse cardiac remodeling and fibrosis stimulated by HAP. Studies in rats have previously documented the role of fine particulate matter (PM 2.5 ) in stimulating cardiac fibrosis [14,34].…”

“…Prior studies evaluating masked hypertension have shown an 8-20% prevalence in the general population and up to 50% prevalence in treated hypertensive patients, although the Nepali population has not been specifically studied [9,27]. It is also possible that prior studies have found an association with hypertension and HAP because such studies relied on field evaluations [5,14,16]. Transient blood pressure effects similar to "white coat" hypertension may have been attenuated in our study given that study participants had to travel to Pokhara for evaluation.…”

Effects of Environmental PM_2.5 on Adult SD Rat Lung Transcriptional Profile

“…Several studies have suggested that the alternation of gene expression played a major role in the activation of pathways induced by toxicant exposure [20][21][22][23][24]. Recent studies indicated that PM 2.5 could enter cells via pinocytosis, and could alter the gene expression of lung epithelial and myocardial cells.…”

“…Recent studies indicated that PM 2.5 could enter cells via pinocytosis, and could alter the gene expression of lung epithelial and myocardial cells. These alterations then inhibited cell apoptosis, induced cell proliferation and promoted angiogenesis, which are considered as indicators of tumor genesis [21,25]. Meanwhile, the chronic obstructive pulmonary disease (COPD) progress could also be accelerated, and even the mortality was increased by the short term PM 2.5 exposure [26].…”