Pulmonary Inflammation and Cell Death in Mice After Acute Exposure to Air Particulate Matter From an Industrial Region of Buenos Aires

Abstract

Epidemiological studies have shown that air particulate matter (PM) can increase respiratory morbidity and mortality being the lungs the main target organ to PM body entrance. Even more, several in vivo and in vitro studies have shown that air PM has a wide toxicity spectra depending among other parameters, on its size, morphology, and chemical composition. The Reconquista River is the second most polluted river from Buenos Aires, and people living around its basin are constantly exposed to its contaminated water, soil and air. However, the air PM from the Reconquista River (RR-PMa) has not been characterized, and its biological impact on lung has yet not been assessed. Therefore, the present investigation was undertaken to study (1) RR-PMa morphochemical characteristic and (2) RR-PMa lung acute effects after intranasal instillation exposure through the analysis of three end points: oxidative stress, inflammation, and apoptosis. A single acute exposure of RR-PMa (1 mg/kg body weight) after 24 h caused significant (p < 0.05) enrichment in bronchoalveolar total cell number and polymorphonuclear (PNM) fraction, superoxide anion generation, production of pro-inflammatory cytokines TNF-α and IL-6, and induction of apoptosis. It was also observed that in lung homogenates, none of the antioxidant enzymes assayed showed differences between exposed RR-PMa and control mice. These data demonstrate that air PM from the Reconquista River induce lung oxidative stress, inflammation, and cell death therefore represents a potential hazard to human health.

MicroRNAs as Potential Biomarkers of Environmental Exposure to Polycyclic Aromatic Hydrocarbons and Their Link with Inflammation and Lung Cancer

“…PM acts as an important inducer of pro-inflammatory mediators [59,60]. It has been reported that VOCs induce an increase in cytokines and pro-inflammatory mediators in human bronchial epithelial cells (BEAS-2B) [10,61], a finding that correlates with an increase in inflammatory mediators (e.g., TNF-α, IL-6 and IL-8) in alveolar macrophages and type I pneumocytes in response to WSP [62].…”

Cardiac and mitochondrial dysfunction following acute pulmonary exposure to mountaintop removal mining particulate matter

“…Among the central roles for the mitochondrion are the production of ATP requisite for cardiac contraction and relaxation as well as its contribution to the signals initiating cellular apoptosis. In vivo and in vitro analyses have revealed an increase in apoptosis in numerous tissues following PM exposure (2, 16, 85, 86). Two pathways reported to activate the apoptotic cascade include the extrinsic pathway via caspase-8 and the intrinsic pathway involving the mitochondrion.…”

Indoor secondary organic aerosols formation from ozonolysis of monoterpene: An example of d-limonene with ammonia and potential impacts on pulmonary inflammations

“…Rohr et al (2002) suggested that the terpene/ozone reaction products may have moderate-lasting adverse effects on both the upper airways and pulmonary regions to human. In addition, more evidences showed that PM inhalation can perpetually damage pulmonary and cardiovascular systems (Astort et al, 2014;Bates et al, 2015;de Brito et al, 2014;Magnani et al, 2011); A wide variety of toxicities caused were also reported in vivo and in vitro studies, by means of inflammatory cytokines induction as exposure response to different PM components, (Ho et al, 2016;Leung et al, 2014;Michael et al, 2013;Seagrave et al, 2006).…”