Part 2. Association of daily mortality with ambient air pollution, and effect modification by extremely high temperature in Wuhan, China.

Zhengmin Qian, Qingci He, Hung-Mo Lin, Lingli Kong, Dunjin Zhou, Shengwen Liang, Zhichao Zhu, Duanping Liao, Wenshan Liu, Christy M Bentley, Jijun Dan, Beiwei Wang, Niannian Yang, Shuangqing Xu, Jie Gong, Hongming Wei, Huilin Sun, Zudian Qin
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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.</p>","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 154","pages":"91-217"},"PeriodicalIF":0.0000,"publicationDate":"2010-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Research report (Health Effects Institute)","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

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.

第2部分。武汉地区日死亡率与环境空气污染的关系及极高温效应的改变
与美国和欧洲相比,亚洲发表的关于每日死亡率与环境空气污染之间关系的研究较少。本研究在中国武汉开展,旨在调查空气污染对死亡率的急性影响,重点关注颗粒物(PM*)。有三个主要目的:(1)检查所有自然原因导致的每日死亡率和每日原因特异性死亡率(心血管[CVD],中风,心脏[CARD],呼吸[RD],心肺[CP]和非心肺[non-CP]原因)与空气动力学直径的PM (10 PM (PM10),二氧化硫(SO2),二氧化氮(NO2)或臭氧(O3)的日平均浓度(微克/立方米)之间的关系;(2)研究极端高温对大气污染与全自然原因日死亡率和特定原因日死亡率之间关系的影响;(3)评估国际疾病分类(ICD)死亡率数据编码从修订版9 (ICD-9)到修订版10 (ICD-10)编码变化所造成的影响估计的不确定性。武汉因其极其炎热的夏季(7月的日平均气温为37.2摄氏度,最高日温度往往超过40摄氏度)而被称为中国的“烤箱城市”。大约450万居民居住在201平方公里的核心城区,那里的空气污染水平比大多数已发表文献研究的城市更高,范围更广。我们从武汉市环境监测中心(WEMC)运营的五个固定空气监测站获得了PM10、SO2和NO2浓度的日平均水平。O3数据来自两个站点,使用8小时平均值,从10:00到18:00。2000年7月1日至2004年6月30日期间,每日死亡率数据来自武汉市疾病预防控制中心。为了实现第一个目标,我们在控制天气、时间因素和其他重要协变量的同时,使用广义加性模型(GAMs)对四种污染物的日平均浓度对所有自然原因和特定原因死亡率的日计数进行对数回归。我们推导了0天、1天、2天、3天和4天滞后暴露水平的污染物影响估计,以及死亡事件发生前0天和1天滞后(滞后0-1天)和0天、1天、2天和3天滞后(滞后0-3天)的平均值。此外,我们使用个人水平的数据(例如,年龄和性别)在分层分析中对亚组进行分类。此外,我们还探讨了暴露-响应关系的非线性形状(“阈值”)。为了实现第二个目标,我们测试了一个假设,即极端高温会改变空气污染与每日死亡率之间的关系。我们制定了三个相应的天气指标:“极热”、“极冷”和“正常温度”。估算是根据主要影响和每种污染物和每种死亡原因的污染物-温度相互作用模型得出的。为了实现第三个目标,我们进行了额外的分析。我们检查了2002年icd -9编码死亡率数据与icd -10编码死亡率数据之间的一致性率和kappa统计。我们还比较了使用两种icd编码死亡率数据所产生的估计影响的大小。一般来说,滞后0-1天的污染物影响最大。因此,在本报告中,我们主要关注从滞后0-1模型中得到的结果。我们观察到PM10与死亡率之间的一致关联:滞后0-1天,PM10日浓度每增加10微克/立方米,与所有自然原因导致的死亡率增加产生统计学上显著的关联(0.43%;95%可信区间[CI], 0.24 ~ 0.62),心血管疾病(0.57%;95% CI, 0.31 ~ 0.84),卒中(0.57%;95% CI, 0.25 ~ 0.88), CARD (0.49%;95% CI, 0.04 ~ 0.94), RD (0.87%;95% CI, 0.34 ~ 1.41), CP (0.52%;95% CI, 0.27 ~ 0.77)和非cp (0.30%;95% CI, 0.05 ~ 0.54)。总的来说,这些影响在女性中强于男性,在老年人(>或= 65岁)中强于年轻人。对24.8至477.8微克/立方米暴露范围的敏感性测试结果也表明,假定每日死亡率与PM10之间存在线性关系是适当的。在气态污染物中,我们还观察到NO和SO2与死亡率的统计显著相关,并且这两种污染物的估计影响强于PM10的影响。在性别、年龄和线性关系方面,NO2和SO2的关联模式与PM10相似。O3与死亡率无关。 在极高温对空气污染与日死亡率关联的效应修正分析中,只有PM10与温度的交互作用具有统计学意义。具体来说,由于所有自然原因(P = 0.014)、心血管疾病(P = 0.007)和CP (P = 0.014)导致的死亡率,相互作用项具有统计学意义。在三个温度组中,PM10的最强影响主要发生在所有自然死亡率(2.20%;95% CI, 0.74 ~ 3.68), CVD (3.28%;95% CI, 1.24 ~ 5.37), CP (3.02%;95% CI, 1.03 - 5.04)。影响最弱的是常温日,中间是低温日。为了评估从icd -9编码的死亡率数据到icd -10编码的死亡率数据的变化所引起的效应估计的不确定性,我们比较了两组数据,发现高一致性率(> 99.3%)和kappa统计量接近1.0(> 0.98)。所有的效应估计都显示变化很小。所有统计上显著的估计效应水平保持不变。总之,当前研究的结果与之前大多数关于空气污染和死亡率的研究结果是一致的。使用ICD-9和ICD-10编码的死亡的死亡率效应之间的微小差异表明编码的变化对我们的研究的影响很小。很少有已发表的论文报告了极端高温和空气污染对死亡率的协同效应,需要进一步研究。确定高温、PM10和死亡率之间的因果关系需要进一步的毒理学和队列研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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