Jerrett Michael, Burnett Richard T, Pope C Arden, Ito Kazuhiko, Thurston George, Krewski Daniel, Shi Yuanli, Calle Eugenia, Thun Michael
Division of Environmental Health Sciences, School of Public Health, University of California, 710 University Hall, Berkeley, CA 94720, USA.
N Engl J Med. 2009 Mar 12;360(11):1085-95. doi: 10.1056/NEJMoa0803894.
Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution-related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes.
Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are < or = 2.5 microm in aerodynamic diameter [PM(2.5)]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models.
In single-pollutant models, increased concentrations of either PM(2.5) or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM(2.5) was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used.
In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM(2.5) was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration.
尽管许多研究已将对流层臭氧升高与不良健康结局联系起来,但长期暴露于臭氧对与空气污染相关的死亡率的影响仍不确定。我们研究了臭氧暴露对心肺原因导致的死亡风险,特别是对呼吸道原因导致的死亡风险的潜在影响。
美国癌症协会癌症预防研究II队列研究的数据与美国96个大都市统计区的空气污染数据相关联。对448,850名受试者的数据进行了分析,在18年的随访期内有118,777人死亡。1977年至2000年4月1日至9月30日的每日最大臭氧浓度数据。1999年和2000年获得了细颗粒物(空气动力学直径≤2.5微米的颗粒物[PM(2.5)])浓度数据。使用标准和多水平Cox回归模型评估臭氧浓度与死亡风险之间的关联。
在单污染物模型中,PM(2.5)或臭氧浓度升高均与心肺原因导致的死亡风险增加显著相关。在双污染物模型中,PM(2.5)与心血管原因导致的死亡风险相关,而臭氧与呼吸道原因导致的死亡风险相关。臭氧浓度每增加10 ppb,呼吸道原因导致的死亡估计相对风险为1.040(95%置信区间,1.010至1.067)。臭氧与呼吸道原因导致的死亡风险之间的关联对混杂因素的调整和所用统计模型的类型不敏感。
在这项大型研究中,当考虑PM(2.5)浓度时,我们未能检测到臭氧对心血管原因导致的死亡风险的影响。然而,我们确实证明了随着臭氧浓度增加,呼吸道原因导致的死亡风险显著增加。