目的 探讨邻苯二甲酸二(2-乙基己基)酯(di-2-ethylhexyl phthalate,DEHP)染毒对GC-2 spd细胞半胱氨酰天冬氨酸酶(caspase)蛋白及mRNA表达的影响.方法 将体外培养的处于对数生长期的GC-2 spd细胞暴露于含终浓度为0(溶剂对照)、50、100、200 μmol/L DEHP的培养基中培养24 h.采用Real-time PCR法检测细胞caspase-3、caspase-8、caspase-9 mRNA的表达,采用Western blotting法检测细胞caspase-3蛋白酶原(procaspase-3)、procaspase-8 、procaspase-9的表达.结果 与溶剂对照组比较,100 μmol/L DEHP染毒组GC-2 spd细胞caspase-3 mRNA的表达水平和200 μmol/LDEHP染毒组GC-2 spd细胞caspase-8 mRNA的表达水平及50、200 μmol/L DEHP染毒组GC-2 spd细胞caspase-9mRNA的表达水平均较高,差异均有统计学意义(P＜0.05).与溶剂对照组比较,100、200 μmol/L DEHP染毒组GC-2 spd细胞proc aspase-3、 procaspase-8、 procaspase-9的表达水平均较低,差异均有统计学意义(P＜0.05);且随着DEHP染毒浓度的升高,GC-2 spd细胞procaspase-3、procaspase-8、procaspase-9的表达水平均呈下降趋势.结论 DEHP体外染毒可能通过启动caspase-8和caspase-9进而激活下游caspase-3级联反应,最终诱导生精细胞凋亡.

随着我国社会经济的进步,医疗卫生服务水平的提高,居民的健康观念、生活方式和行为习惯不断发生变化,居民疾病谱和死因谱也发生了显著变化,慢性病的发病率和死亡率呈逐年上升趋势[1,2],对居民的健康威胁日益凸显,成为重要的公共卫生问题[3].为了解武汉市居民慢性病防治知识的认知现状,为开展慢性病综合干预管理、制定慢性病防治策略和措施提供科学依据,在武汉市中心城区抽取18岁以上城市居民进行慢性病防治知识现状调查.

Fewer studies have been published on the association between daily mortality and ambient air pollution in Asia than in the United States and Europe. This study was undertaken in Wuhan, China, to investigate the acute effects of air pollution on mortality with an emphasis on particulate matter (PM*). There were three primary aims: (1) to examine the associations of daily mortality due to all natural causes and daily cause-specific mortality (cardiovascular [CVD], stroke, cardiac [CARD], respiratory [RD], cardiopulmonary [CP], and non-cardiopulmonary [non-CP] causes) with daily mean concentrations (microg/m3) of PM with an aerodynamic diameter--10 pm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), or ozone (O3); (2) to investigate the effect modification of extremely high temperature on the association between air pollution and daily mortality due to all natural causes and daily cause-specific mortality; and (3) to assess the uncertainty of effect estimates caused by the change in International Classification of Disease (ICD) coding of mortality data from Revision 9 (ICD-9) to Revision 10 (ICD-10) code. Wuhan is called an "oven city" in China because of its extremely hot summers (the average daily temperature in July is 37.2 degrees C and maximum daily temperature often exceeds 40 degrees C). Approximately 4.5 million residents live in the core city area of 201 km2, where air pollution levels are higher and ranges are wider than the levels in most cities studied in the published literature. We obtained daily mean levels of PM10, SO2, and NO2 concentrations from five fixed-site air monitoring stations operated by the Wuhan Environmental Monitoring Center (WEMC). O3 data were obtained from two stations, and 8-hour averages, from 10:00 to 18:00, were used. Daily mortality data were obtained from the Wuhan Centres for Disease Prevention and Control (WCDC) during the study period of July 1, 2000, to June 30, 2004. To achieve the first aim, we used a regression of the logarithm of daily counts of mortality due to all natural causes and cause-specific mortality on the daily mean concentrations of the four pollutants while controlling for weather, temporal factors, and other important covariates with generalized additive models (GAMs). We derived pollutant effect estimations for 0-day, 1-day, 2-day, 3-day, and 4-day lagged exposure levels, and the averages of 0-day and 1-day lags (lag 0-1 day) and of 0-day, 1-day, 2-day, and 3-day lags (lag 0-3 days) before the event of death. In addition, we used individual-level data (e.g., age and sex) to classify subgroups in stratified analyses. Furthermore, we explored the nonlinear shapes ("thresholds") of the exposure-response relations. To achieve the second aim, we tested the hypothesis that extremely high temperature modifies the associations between air pollution and daily mortality. We developed three corresponding weather indicators: "extremely hot," "extremely cold," and "normal temperatures." The estimates were obtained from the models for the main effects and for the pollutant-temperature interaction for each pollutant and each cause of mortality. To achieve the third aim, we conducted an additional analysis. We examined the concordance rates and kappa statistics between the ICD-9-coded mortality data and the ICD-10-coded mortality data for the year 2002. We also compared the magnitudes of the estimated effects resulting from the use of the two types of ICD-coded mortality data. In general, the largest pollutant effects were observed at lag 0-1 day. Therefore, for this report, we focused on the results obtained from the lag 0-1 models. We observed consistent associations between PM10 and mortality: every 10-microg/m3 increase in PM10 daily concentration at lag 0-1 day produced a statistically significant association with an increase in mortality due to all natural causes (0.43%; 95% confidence interval [CI], 0.24 to 0.62), CVD (0.57%; 95% CI, 0.31 to 0.84), stroke (0.57%; 95% CI, 0.25 to 0.88), CARD (0.49%; 95% CI, 0.04 to 0.94), RD (0.87%; 95% CI, 0.34 to 1.41), CP (0.52%; 95% CI, 0.27 to 0.77), and non-CP (0.30%; 95% CI, 0.05 to 0.54). In general, these effects were stronger in females than in males and were also stronger among the elderly (> or = 65 years) than among the young. The results of sensitivity testing over the range of exposures from 24.8 to 477.8 microg/m3 also suggest the appropriateness of assuming a linear relation between daily mortality and PM10. Among the gaseous pollutants, we also observed statistically significant associations of mortality with NO, and SO2, and that the estimated effects of these two pollutants were stronger than the PM10 effects. The patterns of NO2 and SO2 associations were similar to those of PM10 in terms of sex, age, and linearity. O3 was not associated with mortality. In the analysis of the effect modification of extremely high temperature on the association between air pollution and daily mortality, only the interaction of PM10 with temperature was statistically significant. Specifically, the interaction terms were statistically significant for mortality due to all natural (P = 0.014), CVD (P = 0.007), and CP (P = 0.014) causes. Across the three temperature groups, the strongest PM10 effects occurred mainly on days with extremely high temperatures for mortality due to all natural (2.20%; 95% CI, 0.74 to 3.68), CVD (3.28%; 95% CI, 1.24 to 5.37), and CP (3.02%; 95% CI, 1.03 to 5.04) causes. The weakest effects occurred at normal temperature days, with the effects on days with low temperatures in the middle. To assess the uncertainty of the effect estimates caused by the change from ICD-9-coded mortality data to ICD-10-coded mortality data, we compared the two sets of data and found high concordance rates (> 99.3%) and kappa statistics close to 1.0 (> 0.98). All effect estimates showed very little change. All statistically significant levels of the estimated effects remained unchanged. In conclusion, the findings for the aims from the current study are consistent with those in most previous studies of air pollution and mortality. The small differences between mortality effects for deaths coded using ICD-9 and ICD-10 show that the change in coding had a minimal impact on our study. Few published papers have reported synergistic effects of extremely high temperatures and air pollution on mortality, and further studies are needed. Establishing causal links between heat, PM10, and mortality will require further toxicologic and cohort studies.

In Asia, limited studies have been published on the association between daily mortality and gaseous pollutants of nitrogen dioxide (NO2), ozone (O3), and sulfur dioxide (SO2). Our previous studies in Wuhan, China, demonstrated long-term air pollution effects. However, no study has been conducted to determine mortality effects of air pollution in this region. This study was to determine the acute mortality effects of the gaseous pollutants in Wuhan, a city with 7.5 million permanent residents during the period from 2000 to 2004. There are approximately 4.5 million residents in Wuhan who live in the city's core area of 201 km2, where air pollution levels are highest, and pollution ranges are wider than the majority of the cities in the published literature. We used the generalized additive model to analyze pollution, mortality, and covariate data. We found consistent NO2 effects on mortality with the strongest effects on the same day. Every 10-microg/m3 increase in NO2 daily concentration on the same day was associated with an increase in nonaccidental (1.43%; 95% confidence interval [CI]: 0.87-1.99%), cardiovascular (1.65%; 95% CI: 0.87-2.45%), stroke (1.49%; 95% CI: 0.56-2.43%), cardiac (1.77%; 95% CI: 0.44-3.12%), respiratory (2.23%; 95% CI: 0.52-3.96%), and cardiopulmonary mortality (1.60%; 95% CI: 0.85-2.35%). These effects were stronger among the elderly than among the young. Formal examination of exposure-response curves suggests no-threshold linear relationships between daily mortality and NO2, where the NO2 concentrations ranged from 19.2 to 127.4 microg/m3. SO2 and O3 were not associated with daily mortality. The exposure-response relationships demonstrated heterogeneity, with some curves showing nonlinear relationships for SO2 and O3. We conclude that there is consistent evidence of acute effects of NO2 on mortality and suggest that a no-threshold linear relationship exists between NO2 and mortality.