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Few prior cohort studies exist in developing countries examining the association of ambient particulate matter (PM) with mortality. We examined the association of particulate air pollution with mortality in a prospective cohort study of 71,431 middle-aged Chinese men. Baseline data were obtained during 1990-1991. The follow-up evaluation was completed in January, 2006. Annual average PM exposure between 1990 and 2005, including TSP and PM10, were estimated by linking fixed-site monitoring data with residential communities. We found significant associations between PM10 and mortality from cardiopulmonary diseases; each 10 μg/m(3) PM10 was associated with a 1.6% (95%CI: 0.7%, 2.6%), 1.8% (95%CI: 0.8%, 2.9%) and 1.7% (95%CI: 0.3%, 3.2%) increased risk of total, cardiovascular and respiratory mortality, respectively. For TSP, we observed significant associations only for cardiovascular morality. These data contribute to the scientific literature on long-term effects of particulate air pollution for high exposure settings typical in developing countries., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Background: Exposure to airborne fine particulate matter (PM2.5) has been reported to be harmful to the human kidney. However, whether the activation of oxidative stress and cell apoptosis plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of cytotoxicity after PM2.5 exposure in human proximal tubule epithelial cells (HK-2 cells). Results: PM2.5 exposure resulted in a significant decrease in cell viability, with an increase in LDH release and the early kidney damage marker kidney injury molecule-1 (KIM-1) expression in a dose-dependent manner and time-dependent manner. PM2.5 exposure induced reactive oxygen species (ROS) generation and markedly elevated apoptosis in HK-2 cells. In addition, PM2.5 exposure resulted in the activation of antioxidant pathway, as evidenced by the increased expressions of Nrf2, HO-1 and NQO1 and decreased expression of Keap1. Moreover, PM2.5 exposure also induced the activation of apoptotic pathway, as evidenced by the increased expressions of pro-apoptotic proteins Bax, caspase-3 and caspase-8 and decreased expression of antiapoptotic protein Bcl-2. Conclusions: Our results demonstrated that both antioxidant pathway and apoptotic pathway played critical roles in the damage mediated by PM2.5 in HK-2 cells. This study would give us a strategy to prevent the impairment of renal function by PM2.5 induced through repression of oxidative stress and apoptosis. [ABSTRACT FROM AUTHOR]

Ambient fine particulate matter (PM 2.5) pollution poses a great threat on global health. Previous studies have reported that PM 2.5 regulates circulating fibrinogen and IL-6 levels in the development of cardiovascular and respiratory disease. However, the correlation between PM 2.5 exposure and both biomarkers remains inconsistent. We searched related articles through PubMed, Web of Science and ScienceDirect. Random effects model was used to obtain a pooled estimate effect of both biomarkers as PM 2.5 concentration increased by every 10 μg/m3. Meta-regression analysis, sensitivity analysis and publication bias test were conducted to evaluate the heterogeneity, stability and reliability of this meta-analysis. A total of 22 articles were included. Each 10 μg/m3 increase in PM 2.5 concentration was significantly correlated with a 1.76% increase in circulating fibrinogen level (95% CI: 0.38%–3.14%, P = 0.013) and a 4.66% increase in IL-6 level (95% CI: 1.14%–8.18%, P = 0.010). Subgroup analysis revealed that high-level PM 2.5 exposure had a more significant association with circulating IL-6 level (11.67%, 95% CI: 0.66%–22.69%, P = 0.038) than low-level exposure, but this association was not observed in fibrinogen (2.50%, 95% CI: −0.78%–5.77%, P = 0.135). Sensitivity analysis and publication bias test confirmed the stability of the results. Circulating fibrinogen and IL-6 significantly increased with exposure to PM 2.5 , may serve as promising biomarkers for PM 2.5 -related adverse effects. • Association of PM 2.5 exposure with circulating fibrinogen and IL-6 levels was evaluated. • A 1.76% increase in fibrinogen level and 4.66% in IL-6 were observed with per 10 μg/m3 increase in PM 2.5 exposure. • High-level exposure to PM 2.5 has a stronger effect on circulating IL-6 than low-level exposure. • Circulating fibrinogen and IL-6 may serve as promising biomarkers for PM 2.5 -related adverse effects. [ABSTRACT FROM AUTHOR]

Abstract: The air quality in China's cities has improved in recent years, but its impact on public health has rarely been investigated. This study was aimed at estimating the potential effects of air quality on life expectancy between 2003 and 2010 in China. We collected annual average concentrations of particulate matter less than 10 microns in aerodynamic diameter (PM10) in 113 key cities, covering all provinces in China, along with the national average age-specific mortality from 2003 to 2010. We constructed a cause-eliminated life table after excluding premature deaths attributable to PM10. The annual average PM10 levels in these cities decreased from 125.3 μg m−3 in 2003 to 88.3 μg m−3 in 2010. As the result, life expectancy loss due to PM10 decreased from 2.13 years in 2003 to 1.30 years in 2010. The estimated life expectancy increase due to PM10 mitigation accounted for 34% of the total increase in life expectancy in the same period. Our results suggested that air quality might have contributed substantially to life expectancy in China. [Copyright &y& Elsevier]