第3部分。估计泰国曼谷空气污染对死亡率的影响。

Nuntavarn Vichit-Vadakan, Nitaya Vajanapoom, Bart Ostro
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引用次数: 0

摘要

虽然在北美和西欧有充分的文献记录了颗粒物(PM*)对死亡率的影响,但对其在亚洲发展中国家的影响知之甚少。泰国曼谷现有的空气污染数据表明,空气中PM <或= 10 PM的空气动力学直径(PM10)浓度与北美和西欧大多数城市一样高或更高。与此同时,曼谷的人口结构、活动模式和人口的背景健康状况以及PM的化学成分都有所不同。因此,重要的是要确定在这个大都市区发生的PM10对死亡率的影响是否与西方城市相似。最近,由于完成了几项死亡率研究,并通过目前在曼谷每日测量PM10的监测人员的投入,曼谷死亡率数据的质量和完整性得到了提高。在本分析中,我们研究了1999年至2003年间PM10和几种气态污染物对日死亡率的影响。我们的研究结果表明,几种不同的死亡结果与PM10和几种气态污染物(包括二氧化氮(NO2)、一氧化氮(NO)和臭氧(O3))的水平有很强的相关性。根据美国环境保护署(EPA)和世界卫生组织(世卫组织)的审查,在许多情况下,影响估计高于西方工业化国家通常报告的每10微克/立方米约6% (Anderson等人,2004年)。例如,所有自然原因导致的死亡的超额风险(ER)为1.3%(95%置信区间[CI], 0.8至1.7),心血管和呼吸系统死亡率的超额风险(ER)分别为1.9% (95% CI, 0.8至3.0)和1.0% (95% CI, -0.4至2.4)。特别值得注意的是,对于这个大约有600万至1 000万人口的温暖热带城市来说,污染与寒冷天气及其相关的不利健康问题之间没有共变关系。PM10的多日平均值产生了更高的影响估计。我们对年龄和疾病特异性死亡率的分析表明,幼儿,特别是患有呼吸道疾病的婴儿、5岁以下患有下呼吸道感染(LRIs)的儿童和哮喘患者的er升高。年龄限制分析表明,所有自然原因导致的死亡率与PM10浓度之间的关联随着年龄的增长而增加,对75岁及以上人群的影响最大。然而,在所有其他年龄组中都观察到PM10浓度增加与死亡率之间的关联。除了少数例外,其他几种污染物——二氧化硫(SO2)、NO2、O3和NO——也观察到了相对相似的结果,它们与PM10高度相关。然而,在多污染物模型中,气态污染物的许多影响被减弱,而PM10的影响似乎最一致。此外,有一些证据表明,臭氧对某些健康结果有独立的影响。我们进行了大量的敏感性分析来检验我们的结果是否稳健。结果表明,我们的核心模型对于模型规格、样条模型、时间平滑函数的自由度(df)、温度滞后、自相关调整、流行病调整以及使用中心数据调整缺失值的选择通常具有鲁棒性(参见本卷末尾发现的共同协议中使用的中心方法的描述)。最后,大多数污染物的浓度-响应函数表现为线性。因此,我们的敏感性分析结果表明,污染对曼谷死亡率的影响是相当一致的。它们还支持将在北美和西欧进行的健康影响研究的结果外推到世界其他地区,包括亚洲的发展中国家。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Part 3. Estimating the effects of air pollution on mortality in Bangkok, Thailand.

While the effects of particulate matter (PM*) on mortality have been well documented in North America and Western Europe, considerably less is known about its effects in developing countries in Asia. Existing air pollution data in Bangkok, Thailand, indicate that airborne concentrations of PM < or = 10 pm in aerodynamic diameter (PM10) are as high or higher than those experienced in most cities in North America and Western Europe. At the same time, the demographics, activity patterns, and background health status of the population, as well as the chemical composition of PM, are different in Bangkok. It is important, therefore, to determine whether the effects of PM10 on mortality occurring in this large metropolitan area are similar to those in Western cities. The quality and completeness of Bangkok mortality data have been recently enhanced by the completion of a few mortality studies and through input from monitors currently measuring daily PM10 in Bangkok. In this analysis, we examined the effects of PM10 and several gaseous pollutants on daily mortality for the years 1999 through 2003. Our results suggest strong associations between several different mortality outcomes and levels of PM10 and several of the gaseous pollutants, including nitrogen dioxide (NO2), nitric oxide (NO), and ozone (O3). In many cases, the effect estimates were higher than the approximately 6% per 10 microg/m3 typically reported in Western industrialized nations-based on reviews by the U.S. Environmental Protection Agency (U.S. EPA) and the World Health Organization (WHO) (Anderson et al. 2004). For example, the excess risk (ER) for mortality due to all natural causes was 1.3% (95% confidence interval [CI], 0.8 to 1.7), with higher ERs for cardiovascular and respiratory mortality of 1.9% (95% CI, 0.8 to 3.0) and 1.0% (95% CI, -0.4 to 2.4), respectively. Of particular note, for this warm, tropical city of approximately 6 to 10 million people, is that there is no covariation between pollution and cold weather, with its associated adverse health problems. Multiday averages of PM10 generated even higher effect estimates. Our analysis of age- and disease-specific mortality indicated elevated ERs for young children, especially infants with respiratory illnesses, children less than 5 years of age with lower respiratory infections (LRIs), and people with asthma. Age-restricted analyses showed that the associations between mortality due to all natural causes and PM10 concentration increased with age, with the strongest effects among people aged 75 years and older. However, associations between increases in PM10 concentration and mortality were observed for all of the other age groups. With a few exceptions, relatively similar results were observed for several of the other pollutants-sulfur dioxide (SO2), NO2, O3, and NO, which were highly correlated with PM10. However, many of the effects from gaseous pollutants were attenuated in multipollutant models, while effects from PM10 appeared to be most consistent. In addition, there was some evidence of an independent effect of O3 for certain health outcomes. We conducted substantial sensitivity analyses to examine whether our results were robust. The results indicated that our core model was generally robust to the choice of model specification, spline model, degrees of freedom (df) of time-smoothing functions, lags for temperature, adjustment for autocorrelation, adjustment for epidemics, and adjustment for missing values using centered data (see the description of the centering method used in the Common Protocol found at the end of this volume). Finally, the concentration-response functions for most of the pollutants appear to be linear. Thus, our sensitivity analyses results suggest an impact of pollution on mortality in Bangkok that is fairly consistent. They also provide support for the extrapolation of results from health effects studies conducted in North America and Western Europe to other parts of the world, including developing countries in Asia.

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