Effects of urban coarse particles inhalation on oxidative and inflammatory parameters in the mouse lung and colon

Abstract

BackgroundAir pollution is a recognized aggravating factor for pulmonary diseases and has notably deleterious effects on asthma, bronchitis and pneumonia. Recent studies suggest that air pollution may also cause adverse effects in the gastrointestinal tract. Accumulating experimental evidence shows that immune responses in the pulmonary and intestinal mucosae are closely interrelated, and that gut-lung crosstalk controls pathophysiological processes such as responses to cigarette smoke and influenza virus infection. Our first aim was to collect urban coarse particulate matter (PM) and to characterize them for elemental content, gastric bioaccessibility, and oxidative potential; our second aim was to determine the short-term effects of urban coarse PM inhalation on pulmonary and colonic mucosae in mice, and to test the hypothesis that the well-known antioxidant N-acetyl-L-cysteine (NAC) reverses the effects of PM inhalation.ResultsThe collected PM had classical features of urban particles and possessed oxidative potential partly attributable to their metal fraction. Bioaccessibility study confirmed the high solubility of some metals at the gastric level. Male mice were exposed to urban coarse PM in a ventilated inhalation chamber for 15 days at a concentration relevant to episodic elevation peak of air pollution. Coarse PM inhalation induced systemic oxidative stress, recruited immune cells to the lung, and increased cytokine levels in the lung and colon. Concomitant oral administration of NAC reversed all the observed effects relative to the inhalation of coarse PM.ConclusionsCoarse PM-induced low-grade inflammation in the lung and colon is mediated by oxidative stress and deserves more investigation as potentiating factor for inflammatory diseases.Electronic supplementary materialThe online version of this article (10.1186/s12989-017-0227-z) contains supplementary material, which is available to authorized users.

Necroptosis Contributes to Urban Particulate Matter-Induced Airway Epithelial Injury

“…It is difficult to know what the main substance in the induction of the inflammatory response may be. We use PBS or saline as controls for PM treatment (PM is generally dispersed in sterile saline or PBS), similar to previous studies [4, 8, 46, 47]. It might be better to add an a-specific stimulus as a control which might enhance the robustness of our findings.…”

“…PM exposure has been shown to be a major risk factor for acute and chronic diseases including cardiovascular disease, liver fibrosis, various gastrointestinal diseases, and chronic respiratory disease, such as asthma and chronic obstructive pulmonary disease (COPD), along with lung cancer [4-8]. The sources of PM are complex and include transportation (e.g., vehicle exhaust), factory emissions (e.g., industries and coal-fired power plants), combustion (e.g., biomass and cigarette smoke) and agriculture (e.g., fertilizer and animal waste), and natural sources (e.g., volcanoes, forest fires and dust storms) [5].…”

Metalliferous Mine Dust: Human Health Impacts and the Potential Determinants of Disease in Mining Communities

“…the fluids covering the lung lining) will be subject to phagocytosis by the pulmonary alveolar macrophages. Complexation with biological components in the lung fluids can also influence dissolution rates [22], and once dissolved can negatively impact the immune system [36,100]. Different solubilities and dissolution rates in different body fluids [44,57], interactions of complex chemical mixtures [26•], and the role of enzymes, mucoproteins and surfactants are increasingly being investigated [19,65].…”

Sub-chronic inhalation of lead oxide nanoparticles revealed their broad distribution and tissue-specific subcellular localization in target organs

“…Occupational Safety and Health Administration’s (OSHA) set a Permissible Exposure Limit (PEL) for lead in workplace air of 50 μg/m 3 (8-h time weighted average) [ 16 ]. However, in urban areas and some megacities in India or China [ 17 , 18 ], concentrations of coarse particulate matter PM 10 (PM ≤ 10 μm; containing also metals from anthropogenic sources as Pb, Cd, Zn, Bi, Sb, Cu) can reach pollution peaks at >250 μg/m 3 [ 19 ]. Thus, mass concentration of nanoparticles applied to our experimental animals was approximately on the same level, which is inhaled by inhabitants of megacities during pollution peaks and also corresponding to the exposure of lead workers in industrial areas.…”