Short term Pm2.5 exposure caused a robust lung inflammation, vascular remodeling, and exacerbated transition from left ventricular failure to right ventricular hypertrophy

Abstract

Heart failure (HF) is the single largest cause for increased hospitalization after fine particulate matter (PM2.5) exposure. Patients with left HF often progress to right ventricular (RV) failure even with optimal medical care. An increase of PM2.5 of 10 μg per cubic meter was associated with a 76% increase in the risk of death from cardiovascular disease in 4 years' period. However, the role and mechanism of PM2.5 in HF progression are not known. Here we investigated the role of PM2.5 exposure in mice with existing HF mice produced by transverse aortic constriction (TAC). TAC-induced HF caused lung inflammation, vascular remodeling and RV hypertrophy. We found increased PM2.5 profoundly exacerbated lung oxidative stress in mice with existing left HF. To our surprise, PM2.5 exposure had no effect on LV hypertrophy and function, but profoundly exacerbated lung inflammation, vascular remodeling, and RV hypertrophy in mice with existing left HF. These striking findings demonstrate that PM2.5 and/or air pollution is a critical factor for overall HF progression by regulating lung oxidative stress, inflammation and remodeling as well as RV hypertrophy. Improving air quality may save HF patients from a dismal fate.

Ophiopogonin D attenuates PM2.5‑induced inflammation via suppressing the AMPK/NF‑κB pathway in mouse pulmonary epithelial cells

“…For example, He et al (9) have established that PM2.5 can cause inflammatory effects in MLE-12 cells, which are derived from a female mouse. In addition, multiple studies in male mice have reported that PM2.5 can activate inflammation and lead to lung injury (23)(24)(25). Altogether, these findings suggest that sex differences do not affect the outcome of PM2.5 exposure; therefore, the MLE-12 cell line was selected to perform this research.…”

Down-regulation of Fine Dusts-induced Airway Inflammation by the PDZ motif peptide of ZO-1

“…Ambient air pollution in both urban and suburban areas was estimated to cause 4.2 million premature deaths worldwide per year in 2016; this mortality is due to exposure to airborne particulates 2.5 µm or less in diameter (PM2.5), which cause respiratory and cardiovascular disease, and cancers [20]. Many epidemiological reports have linked exposure to air pollution and increased morbidity and mortality associated with cardiovascular and respiratory diseases, such as chronic obstructive pulmonary disease (COPD) and asthma [3,4,47]. Interestingly, although PM has been known to be a critical risk factor for COPD, evidence supporting the relationship between the incidence of COPD and PM2.5 is currently very limited and insufficient.…”

Assessment on the lung injury of mice posed by airborne PM2.5 collected from developing area in China and associated molecular mechanisms: from histopathology to integrated transcriptome analysis

“…Yuan et al (2020) found that C57BL/6 mice whole-body exposed to PM 2.5 (59.77 µg/m 3 ) sampled from Beijing, China exhibited severe lung injury and brosis [11]. They also demonstrated that treatment with local PM 2.5 polluted air at Beijing, China would strikingly induce lung oxidative stress and injury in mice for 3 weeks and 6 months, respectively [15,16]. Zhou et al (2019) exposed C57BL/6 mice to PM 2.5 collected from Shijiazhuang, China, and found that signi cant increase in circulating white blood cells and in ammation in lungs of mice from exposure groups [17].…”