Institute of Occupational Medicine and Industrial Hygiene, College of Public Health, National Taiwan University, Taipei, Taiwan.
Sci Total Environ. 2010 Mar 15;408(8):1818-23. doi: 10.1016/j.scitotenv.2010.01.044. Epub 2010 Feb 16.
In this study, the relationship between cardiovascular mortality and traffic-related air pollutants (NO(2), CO, PM(10), and six volatile organic compounds (VOCs), propane, iso-butane, propylene, benzene, meta-, para-, and ortho-xylenes) was investigated. The concentrations of NO(2), PM(10) and CO from 1993 to 2006 were measured at a fixed-site air monitoring station, and VOC data from 2003 to 2006 were obtained from a photochemical assessment monitoring site in an urban area in central Taiwan. Outcome variables were data on mortality due to cardiovascular diseases (ICD-9-CM 410-411, 414, 430-437) from 1993 to 2006. Cardiovascular mortality averaged 1.5 cases, ranging between 0 and 9 cases per day. Daily air pollution levels ranged from 0.5 to 80.5ppb for NO(2) and from 0.1 to 3.8ppm for CO. From the subset of data from 2003 to 2006, daily average values ranged from 0.6 to 17.5ppb for propane, 0.3 to 6.7ppb for iso-butane, 0.3 to 6.7ppb for propylene, 0.2 to 3.8ppb for benzene, 0.3 to 26.0ppb for m,p-xylene, and 0.02 to 7.6ppb for o-xylene. Poisson generalized additive model was used to estimate the effects of elevated air pollutant levels on daily mortality, adjusting for meteorological conditions and temporal trends. Single-pollutant model showed that cardiovascular mortality was significantly associated with NO(2) lagged 2 days, and with propane, iso-butane, and benzene lagged 0 day. The relative risk for an interquartile range increase in air pollutant levels was 1.053 for NO(2), 1.064 for propane, 1.055 for iso-butane, and 1.055 for benzene. In conclusion, daily cardiovascular mortality showed association with data on acute exposure to traffic air pollutants in Taichung, which is an important factor to consider in studying cardiovascular mortality in urban environments.
在这项研究中,调查了心血管死亡率与交通相关的空气污染物(二氧化氮(NO2)、一氧化碳(CO)、PM10 和六种挥发性有机化合物(VOCs)、丙烷、异丁烷、丙烯、苯、间-、对-和邻-二甲苯)之间的关系。1993 年至 2006 年,在一个固定的空气监测站测量了二氧化氮(NO2)、PM10 和 CO 的浓度,2003 年至 2006 年,从台湾中部一个城市的光化评估监测站获得了 VOC 数据。结果变量是 1993 年至 2006 年因心血管疾病(ICD-9-CM 410-411、414、430-437)导致的死亡率数据。心血管死亡率平均为 1.5 例,每天介于 0 至 9 例之间。空气污染水平从二氧化氮(NO2)的 0.5 至 80.5ppb 到一氧化碳(CO)的 0.1 至 3.8ppm 不等。在 2003 年至 2006 年的数据子集中,丙烷的日平均值从 0.6 至 17.5ppb,异丁烷的日平均值从 0.3 至 6.7ppb,丙烯的日平均值从 0.3 至 6.7ppb,苯的日平均值从 0.2 至 3.8ppb,间二甲苯的日平均值从 0.3 至 26.0ppb,邻二甲苯的日平均值从 0.02 至 7.6ppb。使用泊松广义加性模型来估计升高的空气污染物水平对每日死亡率的影响,同时调整气象条件和时间趋势。单污染物模型表明,心血管死亡率与二氧化氮(NO2)滞后 2 天,以及丙烷、异丁烷和苯滞后 0 天呈显著相关。空气污染物水平每增加一个四分位距的相对风险为 1.053 倍的二氧化氮(NO2)、1.064 倍的丙烷、1.055 倍的异丁烷和 1.055 倍的苯。总之,台中急性交通空气污染物暴露数据与每日心血管死亡率有关,这是研究城市环境中心血管死亡率时需要考虑的一个重要因素。