Yumin Zhou

Biomass fuels are the probable risk factor for chronic obstructive pulmonary disease in rural South China

Background: There is increasing evidence for a possible association between chronic obstructive pulmonary disease (COPD) and the use of biomass fuels for cooking and heating in developing countries. Data on the prevalence of COPD and objective measurements of indoor pollution from biomass fuel have not been widely available from China. A study was undertaken to investigate the prevalence of COPD in two study communities in Guangdong province in China and to measure the association between COPD and indoor biomass fuel air pollution. Methods: A cluster disproportional random sampling survey was performed in populations aged over 40 years in urban (Liwang) and rural (Yunyan) areas in Guangdong, China. Spirometry was performed in all subjects and a post-bronchodilator ratio of the forced expiratory volume in 1 s to forced vital capacity of <0.70 was defined as COPD. Measurements of indoor and outdoor air pollutants were also performed in a random sample of households. Results: The overall prevalence of COPD in the two areas (Liwang and Yunyan) was 9.4%. The prevalence of COPD in both the whole population and a subpopulation of non-smoking women in rural Yunyan was significantly higher than in urban Liwang (12.0% vs 7.4%, and 7.2% vs 2.5%, respectively). The use of biomass fuel was higher in rural Yunyan than in urban Liwang (88.1% vs 0.7%). Univariate analysis showed a significant association between COPD and exposure to biomass fuel for cooking. Multivariate analysis showed a positive association between COPD and urban/rural area (surrogate for fuel type and local exhaust ventilation in kitchen) after adjustment for sex, age group, body mass index, education, occupational exposure, respiratory disease in family, smoking status, life quality and cough in childhood; similar results were found in non-smoking women. Pollutants measurements showed that concentrations of carbon monoxide, particulate matter with an aerodynamic diameter ⩽10 μm, sulphur dioxide and nitrogen dioxide in the kitchen during biomass fuel combustion were significantly higher than those during LPG combustion. Conclusions: Indoor pollutants from biomass fuels may be an important risk factor for COPD in rural South China.

Risk of COPD From Exposure to Biomass Smoke: A Metaanalysis

BACKGROUND Although many studies have suggested that biomass smoke is a risk factor for COPD, the relationship between the two has not been firmly established. In particular, the extent of the association between exposure of biomass smoke and COPD in different populations, as well as the relationship between biomass smoke and cigarette smoke, is not clear. To ascertain the relationship between biomass smoke and COPD, we performed a metaanalysis. METHODS We searched MEDLINE, EMBASE, and the Latin American and Caribbean Literature in Health Sciences Database and analyzed 15 epidemiologic (11 cross-sectional and four case-control) studies that met our criteria. Data were extracted and analyzed independently by two investigators using a standardized protocol. RESULTS Overall, people exposed to biomass smoke have an odds ratio (OR) of 2.44 (95% CI, 1.9-3.33) for developing COPD, relative to those not exposed to biomass smoke. Biomass smoke exposure was clearly identified as a risk factor for developing COPD in both women (OR, 2.73; 95% CI, 2.28-3.28) and men (OR, 4.30; 95% CI, 1.85-10.01), and in both the Asian population (OR, 2.31; 95% CI, 1.41-3.78) and the non-Asian population (OR, 2.56; 95% CI, 1.71-3.83). This risk factor has also been revealed in patients with chronic bronchitis (OR, 2.56; 95% CI, 1.77-3.70) and COPD (OR, 2.65; 95% CI, 1.75-4.03), and in cigarette smokers (OR, 4.39; 95% CI, 1.40-4.66) and non-cigarette smokers (OR, 2.55; 95% CI, 2.06-3.15). CONCLUSIONS Exposure to biomass smoke is a risk factor for COPD.

ORIGINAL RESEARCHCOPDRisk of COPD From Exposure to Biomass Smoke: A Metaanalysis

BACKGROUND Although many studies have suggested that biomass smoke is a risk factor for COPD, the relationship between the two has not been firmly established. In particular, the extent of the association between exposure of biomass smoke and COPD in different populations, as well as the relationship between biomass smoke and cigarette smoke, is not clear. To ascertain the relationship between biomass smoke and COPD, we performed a metaanalysis. METHODS We searched MEDLINE, EMBASE, and the Latin American and Caribbean Literature in Health Sciences Database and analyzed 15 epidemiologic (11 cross-sectional and four case-control) studies that met our criteria. Data were extracted and analyzed independently by two investigators using a standardized protocol. RESULTS Overall, people exposed to biomass smoke have an odds ratio (OR) of 2.44 (95% CI, 1.9-3.33) for developing COPD, relative to those not exposed to biomass smoke. Biomass smoke exposure was clearly identified as a risk factor for developing COPD in both women (OR, 2.73; 95% CI, 2.28-3.28) and men (OR, 4.30; 95% CI, 1.85-10.01), and in both the Asian population (OR, 2.31; 95% CI, 1.41-3.78) and the non-Asian population (OR, 2.56; 95% CI, 1.71-3.83). This risk factor has also been revealed in patients with chronic bronchitis (OR, 2.56; 95% CI, 1.77-3.70) and COPD (OR, 2.65; 95% CI, 1.75-4.03), and in cigarette smokers (OR, 4.39; 95% CI, 1.40-4.66) and non-cigarette smokers (OR, 2.55; 95% CI, 2.06-3.15). CONCLUSIONS Exposure to biomass smoke is a risk factor for COPD.

Positive benefits of theophylline in a randomized, double-blind, parallel-group, placebo-controlled study of low-dose, slow-release theophylline in the treatment of COPD for 1 year.

Objective and background:  Increasing evidence suggests that low‐dose theophylline has anti‐inflammatory benefits and is safe in the treatment of COPD. This study aims to evaluate the efficacy and safety of low‐dose, slow‐release oral theophylline administered over a 1‐year period in patients with COPD.

COPD in Chinese nonsmokers

Little is known about chronic obstructive pulmonary disease (COPD) in Chinese nonsmokers. The present study aimed to investigate the profiles of COPD among nonsmokers based on the Chinese Epidemiological Survey of COPD (CESCOPD). In the CESCOPD, 20,245 subjects aged 40 yrs or older were interviewed with questionnaires and spirometry tests. Subjects with a post-bronchodilator forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) ratio of <0.70 were identified as having COPD. Data of 12,471 nonsmokers and 1,024 smoking COPD patients were analysed in the current study. The overall prevalence of COPD among nonsmokers was 5.2% (95% confidence interval 4.8–5.6). Being male, of advanced age, lower body mass index (BMI) and lower educational level, having exposure to environmental tobacco smoke, coal and/or biomass smoke, poor ventilation in the kitchen, a family history of respiratory disease and recurrent childhood cough were all independently associated with a higher risk of having COPD among nonsmokers. Nonsmokers with respiratory symptoms without airflow limitation showed a somewhat different pattern of risk factors. Nonsmokers with COPD were less likely to present with chronic productive coughs and lower BMI, while more likely to have received a physician diagnosis of asthma and respiratory diseases in childhood, than smokers with COPD. Chronic obstructive pulmonary disease is prevalent among Chinese nonsmokers, and nonsmoking chronic obstructive pulmonary disease may have different profiles from smoking chronic obstructive pulmonary disease.

Community based integrated intervention for prevention and management of chronic obstructive pulmonary disease (COPD) in Guangdong, China: cluster randomised controlled trial.

Objective To evaluate the effects of a community based integrated intervention for early prevention and management of chronic obstructive pulmonary disease (COPD) in China. Design Cluster randomised controlled trial. Setting Eight healthcare units in two communities. Participants Of 1062 people aged 40-89, 872 (101 with COPD and 771 without COPD) who fulfilled the inclusion and exclusion criteria were allocated to the intervention or the usual care programmes. Intervention Participants randomly assigned to integrated intervention (systematic health education, intensive and individualised intervention, treatment, and rehabilitation) or usual care. Main outcome measures Annual rate of decline in forced expiratory rate in one second (FEV1) before use of bronchodilator. Results Annual rate of decline in FEV1 was significantly lower in the intervention community than the control community, with an adjusted difference of 19 ml/year (95% confidence interval 3 to 36) and 0.9% (0.1% to 1.8%) of predicted values (all P<0.05), as well as a lower annual rate of decline in FEV1/FVC (forced vital capacity) ratio (adjusted difference 0.6% (0.1% to 1.2%) P=0.029). There were also higher rates of smoking cessation (21% v 8%, P<0.004) and lower cumulative death rates from all causes (1% v 3%, P<0.009) in the intervention community than in the control community during the four year follow-up. Improvements in knowledge of COPD and smoking hazards, outdoor air quality, environmental tobacco smoke, and working conditions were also achieved (all P<0.05). The difference in cumulative incidence rate of COPD (both around 4%) and cumulative death rate from COPD (2% v 11%) did not reach significance between the two communities. Conclusions A community based integrated intervention can have a significant impact on the prevention and management of COPD, mainly reflected in the annual rate of decline in FEV1. Trial registration Chinese Clinical Trials Registration (ChiCTR-TRC-00000532).

Functional Polymorphisms of CHRNA3 Predict Risks of Chronic Obstructive Pulmonary Disease and Lung Cancer in Chinese

Recently, several genome-wide association studies (GWAS) have identified many susceptible single nucleotide polymorphisms (SNPs) for chronic obstructive pulmonary disease (COPD) and lung cancer which are two closely related diseases. Among those SNPs, some of them are shared by both the diseases, reflecting there is possible genetic similarity between the diseases. Here we tested the hypothesis that whether those shared SNPs are common predictor for risks or prognosis of COPD and lung cancer. Two SNPs (rs6495309 and rs1051730) located in nicotinic acetylcholine receptor alpha 3 (CHRNA3) gene were genotyped in 1511 patients with COPD, 1559 lung cancer cases and 1677 controls in southern and eastern Chinese populations. We found that the rs6495309CC and rs6495309CT/CC variant genotypes were associated with increased risks of COPD (OR = 1.32, 95% C.I. = 1.14–1.54) and lung cancer (OR = 1.57; 95% CI = 1.31–1.87), respectively. The rs6495309CC genotype contributed to more rapid decline of annual Forced expiratory volume in one second (FEV1) in both COPD cases and controls (P<0.05), and it was associated with advanced stages of COPD (P = 0.033); the rs6495309CT/CC genotypes conferred a poor survival for lung cancer (HR = 1.41, 95%CI = 1.13–1.75). The luciferase assays further showed that nicotine and other tobacco chemicals had diverse effects on the luciferase activity of the rs6495309C or T alleles. However, none of these effects were found for another SNP, rs1051730G>A. The data show a statistical association and suggest biological plausibility that the rs6495309T>C polymorphism contributed to increased risks and poor prognosis of both COPD and lung cancer.

Chronic obstructive pulmonary disease in the absence of chronic bronchitis in China.

Background and objective:  COPD has a variable natural history and not all individuals follow the same course. The aim of this study was to assess the prevalence of COPD in the absence of chronic bronchitis (CB) based on a population survey in China, and to identify the determinants of CB in patients with COPD.

Association between exposure to ambient particulate matter and chronic obstructive pulmonary disease: results from a cross-sectional study in China.

Objective The association between exposure to ambient particles with a median aerodynamic diameter less than 10/2.5 µm (particulate matter, PM10/2.5) and COPD remains unclear. Our study objective was to examine the association between ambient PM10/2.5 concentrations and lung functions in adults. Methods A cross-sectional study was conducted in southern China. Seven clusters were randomly selected from four cities across Guangdong province. Residents aged ≥20 years in the participating clusters were randomly recruited; all eligible participants were examined with a standardised questionnaire and spirometry. COPD was defined as a post-bronchodilator FEV1/FVC less than 70%. Atmosphere PM sampling was conducted across the clusters along with our survey. Results Of the subjects initially recruited, 84.4% (n=5993) were included for analysis. COPD prevalence and atmosphere PM concentration varied significantly among the seven clusters. COPD prevalence was significantly associated with elevated PM concentration levels: adjusted OR 2.416 (95% CI 1.417 to 4.118) for >35 and ≤75 µg/m3 and 2.530 (1.280 to 5.001) for >75 µg/m3 compared with the level of ≤35 µg/m3 for PM2.5; adjusted OR 2.442 (95% CI 1.449 to 4.117) for >50 and ≤150 µg/m3 compared with the level of ≤50 µg/m3 for PM1. A 10 µg/m3 increase in PM2.5 concentrations was associated with a 26 mL (95% CI −43 to −9) decrease in FEV1, a 28 mL (−49 to −8) decrease in FVC and a 0.09% decrease (−0.170 to −0.010) in FEV1/FVC ratio. The associations of COPD with PM10 were consistent with PM2.5 but slightly weaker. Conclusions Exposure to higher PM concentrations was strongly associated with increased COPD prevalence and declined respiratory function. Trial registration number ChiCTR-OO-14004264; Post-results.

Development and systematic oxidative stress of a rat model of chronic bronchitis and emphysema induced by biomass smoke

ABSTRACT Background: Epidemiological research and meta-analyses of published data have shown that biomass smoke (BS) is a risk factor for chronic obstructive pulmonary disease (COPD). However, the link between BS and COPD lacks experimental confirmation. Objectives: To verify whether BS can induce pathologic changes and systemic oxidative stress, which may be relevant to the development of emphysema and chronic bronchitis in rats. Methods: Rats were exposed to BS, cigarette smoke (CS), or clean air (sham) for 14 weeks. During the exposure, the O2, SO2, and CO levels were monitored. Pathological changes in the lungs, systemic oxidative stress, and inflammation biomarkers, together with GSTM1 and GSTP1 mRNA expression in the lung were measured. The glutamate–cysteine ligase catalytic subunit (GCLC) protein expression in the lung was measured using immunohistochemistry and western blotting. Results: The O2, CO, and SO2 levels were 20.31 ± 0.03%, 981.72 ± 64.76, and 2.59 ± 0.26 mg/m3 for the BS group, respectively, while their levels in the CS group were 20.28 ± 0.15%, 745.56 ± 30.83, and 12.64 ± 0.591 mg/m3 respectively. As with the rats exposed to CS, the BS rats showed an increased number of inflammatory cells in the bronchoalveolar lavage fluid, an increased pulmonary mean linear intercept and a decreased pulmonary mean alveolar number. Characteristics of chronic bronchitis and peribronchial fibrosis were also found in the BS-exposed rat lungs. Reduced body weight, systemic oxidative stress, and increased GCLC protein expression in the lungs were observed in the rats exposed to BS and CS. Conclusions: BS can cause emphysema and chronic bronchitis similar to that caused by CS, which is accompanied by systemic oxidative stress and inflammation.