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Background: The potential effects of pulmonary dysfunction on cardiovascular diseases (CVD) are receiving attention. We aimed to investigate and quantify the cross-sectional and longitudinal associations between lung function and overall cardiovascular risk among Chinese general population.Methods: We studied 4019 participants from the Wuhan-Zhuhai cohort, with a follow-up of 3 years. A multivariable risk algorithm generated from the Framingham study was used to calculate individuals' overall cardiovascular risk i.e. 10-Year CVD Risk, which was further classified into 2 categories: low (< 10%) and high (≥10%) CVD risk. General linear model and logistic regression model were separately used to assess the associations of lung function with continuous and dichotomous 10-Year CVD Risk.Results: Cross-sectionally, each 5% decrease in FEV1/FVC was associated with a 0.47% increase in 10-Year CVD Risk (P < 0.001). The adjusted odds ratio (OR) (95% confidence interval [CI]) for the prevalence of high CVD risk (10-Year CVD Risk≥10%) was 1.12 (1.07, 1.17) corresponding to each 5% decrease in FEV1/FVC. The OR (95% CI) for high CVD risk in the lowest group of FEV1/FVC (< 70% i.e. chronic obstructive pulmonary disease [COPD]) was 2.37 (1.43, 3.91) when compared with the highest group. Longitudinally, the adjusted risk ratio (RR) (95% CI) for the incidence of high CVD risk was 1.14 (1.03, 1.25) with each 5% decrease in baseline FEV1/FVC. Compared with the highest group of FEV1/FVC, the RR (95% CI) for high CVD risk in the lowest group (COPD) was 4.06 (1.46, 11.26). Analyses of 10-Year CVD Risk with FVC or FEV1 showed similar trends and significant associations (all P < 0.05).Conclusion: Reduced lung function was cross-sectionally and longitudinally associated with increased cardiovascular risk in Chinese general population. [ABSTRACT FROM AUTHOR]

Background: Crystalline silica is considered as one of the most common and serious occupational hazards to workers' health. Although its association with lung cancer has been studied for many decades, the conclusion remains somewhat controversial. Our objectives are to review and summarize the epidemiological evidence on the relationship between occupational silica exposure and risk of lung cancer and to provide an update on this major occupational health concern.Methods: Eligible studies up to 29 April 2016 were identified. Pooled effect estimates were calculated according to the reported outcome and the study design. Cohort, case control and proportional mortality studies were examined separately. Studies reporting results according to silicotic status were grouped together and analyzed. Due to the significant amount of heterogeneity expected, random effects models were implemented. Subgroup and meta-regression analyses (both univariate and multivariate) were performed in an attempt to explain heterogeneity. Studies which had adequate exposure characterization were selected to find out whether there was an exposure-response relationship between silica and lung cancer.Results: The risk of lung cancer was found to be elevated in both silicotics and non-silicotics. The pooled standardized mortality ratio (SMR) was 2.32 with a 95 % confidence interval (95 % CI) of 1.91-2.81 and 1.78 (95 % CI 1.07-2.96) respectively. The pooled standardized incidence ratio (SIR) was 2.49 (95 % CI 1.87-3.33) and 1.18 (95 % CI 0.86-1.62) respectively. Subgroup analysis showed that workers in the mining industry had the highest risk of lung cancer with a pooled SMR of 1.48 (95 % CI 1.18-1.86) and the weakest association was seen in potteries with a pooled SMR of 1.14 (95 % CI 1.05-1.23). A positive exposure-response relation was found between cumulative silica exposure and risk of lung cancer.Conclusion: The results of our meta-analysis supported the carcinogenic role of silica on the lungs, which was more pronounced at higher levels of exposure, in the presence of silicosis and in the mining industry. Further research is needed to evaluate whether non-silicotics are truly at risk, whether a predisposing factor would explain this potential risk, and to determine the mechanism of carcinogenicity of silica in humans. [ABSTRACT FROM AUTHOR]

Background: Influenza H7N9 has become an endemic pathogen in China where circulating virus is found extensively in wild birds and domestic poultry. Two epidemic waves of Human H7N9 infections have taken place in Eastern and South Central China during the years of 2013 and 2014. In this study, we report on the first four human cases of influenza H7N9 in Shantou, Guangdong province, which occurred during the second H7N9 wave, and the subsequent analysis of the viral isolates.Methods: Viral genomes were subjected to multisegment amplification and sequenced in an Illumina MiSeq. Later, phylogenetic analyses of influenza H7N9 viruses were performed to establish the evolutionary context of the disease in humans.Results: The sequences of the isolates from Shantou have closer evolutionary proximity to the predominant Eastern H7N9 cluster (similar to A/Shanghai/1/2013 (H7N9)) than to the Southern H7N9 cluster (similar to A/Guangdong/1/2013 (H7N9)).Conclusions: Two distinct phylogenetic groups of influenza H7N9 circulate currently in China and cause infections in humans as a consequence of cross-species spillover from the avian disease. The Eastern cluster, which includes the four isolates from Shantou, presents a wide geographic distribution and overlaps with the more restricted area of circulation of the Southern cluster. Continued monitoring of the avian disease is of critical importance to better understand and predict the epidemiological behaviour of the human cases. [ABSTRACT FROM AUTHOR]

Background: Particulate air pollution has been recognized to be associated with a wide range of adverse health effects, including increased mortality, morbidity, exacerbation of respiratory conditions. However, earlier physiological or pathological changes or long-term bodies' reaction to air pollutants have not been studied in depth in China. The Wuhan-Zhuhai (WHZH) cohort study is designed to investigate the association between air pollutants exposure and physiological or pathological reactions on respiratory and cardiovascular system.Methods/design: The cohort is a community-based prospective study that includes 4812 individuals aged 18-80 years. The collections of data were conducted from April to May 2011 in Wuhan city and in May 2012 in Zhuhai city. At baseline, data on demographic and socioeconomic information, occupational history, family disease history, lifestyle, cooking mode, daily travel mode, physical activity and living condition have been collected by questionnaires. Participants underwent an extensive physical examination, including anthropometry, spirometry, electrocardiography, and measurements of blood pressure, heart rate, exhaled nitric oxide and carbon monoxide. Potential conditions in the lung, heart, liver, spleen, and skin were synchronously performed. In addition, samples of morning urine, fasting blood serum and plasma were collected during physical health examination. DNA were extracted and were stored at -80°C. Environment concentrations of particulate matter and chemicals were determined for 15 days in each of four seasons. Participants are followed for physiological or pathological changes or incidence of cardiopulmonary diseases every 3 years.Discussion: The results obtained in WHZH cohort study may increase a better understanding of the relationship between particulate air pollution and its components and possible health damages. And the potential mechanisms underlying the development of cardiopulmonary diseases has implications for the development of prevention and treatment strategies. [ABSTRACT FROM AUTHOR]

Background: The nucleotide excision repair (NER) protein, xeroderma pigmentosum C (XPC), participates in recognizing DNA lesions and initiating DNA repair in response to DNA damage. Because mutations in XPC cause a high risk of cancer in XP patients, we hypothesized that inherited sequence variations in XPC may alter DNA repair and thus susceptibility to cancer., Methods: In this hospital-based case-control study, we investigated five XPC tagging, common single nucleotide polymorphisms (tagging SNPs) in 1,010 patients with newly diagnosed lung cancer and 1,011 matched cancer free controls in a Chinese population., Results: In individual tagging SNP analysis, we found that rs3731055AG+AA variant genotypes were associated with a significantly decreased risk of lung adenocarcinoma [adjusted odds ratio (OR), 0.71; 95% confidence interval (CI), 0.56-0.90] but an increased risk of small cell carcinomas [adjusted OR, 1.79; 95% CI, 1.05-3.07]. Furthermore, we found that haplotype ACCCA was associated with a decreased risk of lung adenocarcinoma [OR, 0.78; 95% CI, 0.62-0.97] but an increased risk of small cell carcinomas [OR, 1.68; 95% CI, 1.04-2.71], which reflected the presence of rs3731055A allele in this haplotype. Further stratified analysis revealed that the protective effect of rs3731055AG+AA on risk of lung adenocarcinoma was more evident among young subjects (age < or= 60) and never smokers., Conclusion: These results suggest that inherited sequence variations in XPC may modulate risk of lung cancer, especially lung adenocarcinoma, in Chinese populations. However, these findings need to be verified in larger confirmatory studies with more comprehensively selected tagging SNPs.