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Background/aims: Ecological studies have shown that air pollution and prevalence of cigarette smoking are positively correlated. Evidence also suggests a synergistic effect of cigarette smoking and PM2.5 exposure (Environmental Particulate Matter ≤ 2.5 µm in diameter) on lung cancer risk. We aimed to evaluate the interaction between smoking prevalence and PM2.5 pollution in relation to lung cancer mortality and determine its underlying mechanisms in vitro., Methods: "MOVER" method was used to analyze the interaction between smoking prevalence and PM2.5 pollution in relation to lung cancer mortality. Cell autophagy and malignant behaviors induced by cigarette smoke extract (CSE) and PM2.5 exposure were examined in vitro. Gene expression was examined by qRT-PCR and western blot. RNA and protein interaction was determined using a RNA binding protein immunoprecipitation assay., Results: An increased risk for lung cancer death (RERI (the relative excess risk) =0.28) was observed with a synergistic interaction between cigarette smoking and PM2.5 pollution. Cell migration, invasion, EMT (epithelial-mesenchymal transition) and autophagy were elevated when lung cancer cells were treated with CSE and PM2.5 in combination. A lncRNA, named lung cancer progression-association transcript 1 (LCPAT1), was up-regulated after the treatment of CSE and PM2.5, and knocking down the lncRNA impaired the effect of CSE and PM2.5 on lung cancer cells. In addition, LCPAT1 was shown to bind to RCC2, and RCC2 mediated the effect of LCPAT1 on cell autophagy, migration, invasion and EMT in lung cancer., Conclusions: Our results suggest that combined exposure to CSE and PM2.5 induces LCPAT1 expression, which up-regulates autophagy, and promotes lung cancer progression via RCC2., (© 2018 The Author(s). Published by S. Karger AG, Basel.)

Objective: We investigated the association between respiratory health and particulate matter (PM) air pollution in elderly type 2 diabetes mellitus (T2DM) pre-, during, and post-the Chinese Lunar New Year (CLNY) holiday in Shanghai, China., Methods: We conducted repeated measurements of lung function and inflammation biomarker in a cohort consisted of 60 participants with T2DM., Results: Decreased PM2.5 exposure had an effect on respiratory health by increasing in forced expiratory flow in 1 second (FEV1) and forced vital capacity (FVC). Positive associations between PM exposure and exhaled nitric oxide (eNO) were observed., Conclusions: Our observations indicated that PM air pollution exposure would exert adverse effect on respiratory health in elderly T2DM population.

We aimed to investigate if short-term exposure to reduced particulate matter (PM) air pollution would affect respiratory function in healthy adults. We followed a cohort of 42 healthy participants from a community afflicted with severe PM air pollution to a substantially less polluted area for nine days. We measured daily airborne PM [with an aerodynamic diameter of less than 2.5 μm (PM 2.5 ) and 10 μm (PM 10 )] and PM 2.5 carbon component concentrations. Five repeated respiratory function measurements and fractional exhaled nitric oxide test were made for each participant. Associations between respiratory health and PM exposure were assessed using linear mixed models. Each 10 μg/m 3 decrease in same-day PM 2.5 was associated with small but consistent increase in the forced expiratory volume in 1 s (FEV 1 ) (9.00 mL) and forced vital capacity (14.35 mL). Our observations indicate that respiratory health benefits can be achieved even after a short-term reduction of exposure to PM. Our results provide strong evidence for more rigorous air pollution controls for the health benefit of populations.

Background: Evidence shows that individuals who are under long-term exposure to environmental PM 2.5 are at increased risk of lung cancer. Various laboratory experiments also suggest several mechanistic links between PM 2.5 exposure and lung carcinogenesis. However, a long non-coding RNA (lncRNA) mediated pathogenic change after PM 2.5 exposure and its potential roles in tumorigenesis and disease progression have not been reported., Methods: Cytotoxicity induced by PM 2.5 was assessed by using scanning electron microscopy and transmission electron microscopy. ROS generation, autophagy, and metastasis induced by PM 2.5 were detected by using comprehensive approaches. Expression of lncRNA-loc146880 and lc3b (autophagy marker) in A549 cells, lung tissue and serum were determined by RT-PCR and Western blotting., Results: PM 2.5 could be internalized into lung cancer cells, resulting in marked increases in ROS levels and autophagy. ROS may be responsible for increased expression of loc146880 which further up-regulates autophagy. Both loc146880 and autophagy could promote lung tumor cell migration, invasion and EMT. In addition, a positive correlation was observed between loc146880 expression and lc3b levels in tumor tissues and serum of lung cancer patients., Conclusion: Taken together, our data suggest that PM 2.5 exposure induces ROS, which activates loc146880 expression. The lncRNA, in turn, up-regulates autophagy and promotes the malignant behaviors of lung cancer cells., General Significance: The results show the toxicological effects of PM 2.5 in lung tumor progression and metastasis., (Copyright © 2016 Elsevier B.V. All rights reserved.)