Goldberg M S, Bailar J C, Burnett R T, Brook J R, Tamblyn R, Bonvalot Y, Ernst P, Flegel K M, Singh R K, Valois M F
Epidemiology and Biostatistics Unit, Research Centre on Human Health, INRS-IAF, University of Quebec, 531 Boulevard de Prairies, Laval, Quebec, Canada H7V 1B7.
Res Rep Health Eff Inst. 2000 Oct(97):7-113; discussion 115-20.
This study was undertaken in order to shed light on which groups of the general population may be susceptible to the effects of ambient particles. The objectives of the study were (1) to determine whether concentrations of particles in the ambient air of Montreal, Quebec, were associated with daily all-cause and cause-specific mortality in the period 1984 to 1993, and (2) to determine whether groups of the population had higher than average risks of death from exposure to particles. From the network of fixed-site air pollution monitors in Montreal we obtained daily mean levels of various measures of particles, gaseous pollutants, and weather variables measured at Dorval International Airport. We also used measurements of sulfate from an acid rain monitoring station 150 km southeast of the city (Sutton, Quebec). We estimated associations for particulate matter (PM) with an aerodynamic diameter of 10 microns or smaller (PM10), or 2.5 microns or smaller (PM2.5), total suspended particles (TSP), coefficient of haze (COH), an extinction coefficient, and sulfate. Because substantial data for fine particles were missing, we developed a regression model to predict PM2.5 and to predict sulfate from PM2.5. In the main body of the report, we present results for COH, predicted PM2.5, and sulfate. Detailed results for all pollutants are included in Appendices H through O, which are available on request from Health Effects Institute and from the HEI web site at www.healtheffects.org. To address the first objective, we made use of the underlying causes of death among all 140,939 residents of Montreal who died between 1984 and 1993. We regressed the logarithm of daily counts of cause-specific mortality on the daily mean levels for a variety of measures of particles, accounting for seasonal and subseasonal fluctuations in the mortality time series, overdispersion, and weather factors. To address the second objective, we developed algorithms to define conditions that subjects had prior to death, with the focus on cardiopulmonary diseases. These algorithms were based on information retained on the databases of the universal Quebec Health Insurance Plan (QHIP). The databases include records of all procedures (e.g., type of surgery), physician visits, and consultations carried out by all physicians in Quebec. For persons > or = 65 years and for all recipients of social assistance the prescription database contains records of all pharmaceuticals dispensed (type of medication, dose, quantity). For each group of conditions defined, we used the same statistical model that was used in the analyses of all nonaccidental causes of death. In the analyses of cause-specific mortality, we found evidence of associations for all nonaccidental causes of death and specific causes of death--cancer, coronary artery disease, respiratory diseases, and diabetes--that were consistent across most metrics of ambient air particle concentrations, evaluated as the 3-day mean of particle concentrations measured on the day of death (lag 0) and on each of the two days before death (lag 1, lag 2). Associations for all cardiovascular diseases combined were found only with sulfate. As well, we generally found increased daily mortality for persons 65 years of age and over. The results for all nonaccidental causes of death are similar to findings from other studies; the mean percent increase in mortality for a 100 micrograms/m3 increase in daily TSP at lag 0 was 6.7%. In the analyses of the groups defined from the QHIP data, there was little evidence of associations with air pollutants among persons who before death were classified as having acute or chronic upper respiratory diseases, airways diseases, hypertension, acute coronary artery diseases, and cerebrovascular diseases. On the other hand, we found consistent increases across most types of ambient particles for persons who had cancer, acute lower respiratory diseases, any form of cardiovascular disease, chronic coronary artery diseases, and congestive heart failure. As well, we found an association for individuals who did not have any cardiovascular disease, lower respiratory diseases, and cancer. This latter group consisted of persons who had no interactions with the health care system one year before death (12%) and individuals with a wide variety of potentially fatal diseases (52%), including neurological conditions (12%), diabetes (8%), cardiac dysrhythmias (8%), dementia (6%), organic psychotic disorders (6%), and anemias (4%). As statistical power was reduced in the analyses presented above, differences between groups (e.g., < 65 and > or = 65 year age groups) were not usually statistically significant. The association with diabetes has not been reported previously, and this needs to be replicated in other studies. (ABSTRACT TRUNCATED)
开展这项研究是为了弄清楚普通人群中的哪些群体可能易受环境颗粒物影响。该研究的目的是:(1)确定1984年至1993年期间魁北克省蒙特利尔市环境空气中颗粒物浓度是否与每日全因死亡率和特定病因死亡率相关;(2)确定人群中是否有因接触颗粒物而死亡风险高于平均水平的群体。我们从蒙特利尔市的固定站点空气污染监测网络中获取了在多瓦尔国际机场测量的颗粒物、气态污染物和气象变量的各种测量指标的每日平均水平。我们还使用了位于该市东南150公里处(魁北克省萨顿)的酸雨监测站的硫酸盐测量数据。我们估计了空气动力学直径为10微米或更小(PM10)、2.5微米或更小(PM2.5)的颗粒物、总悬浮颗粒物(TSP)、霾系数(COH)、消光系数和硫酸盐之间的关联。由于细颗粒物的大量数据缺失,我们开发了一个回归模型来预测PM2.5并从PM2.5预测硫酸盐。在报告主体中,我们展示了COH、预测的PM2.5和硫酸盐的结果。所有污染物的详细结果包含在附录H至O中,可应要求从健康影响研究所及该研究所网站(www.healtheffects.org)获取。为实现第一个目标,我们利用了1984年至1993年间蒙特利尔市所有140939名死亡居民的潜在死因。我们将特定病因死亡率的每日计数的对数与各种颗粒物测量指标的每日平均水平进行回归分析,同时考虑了死亡率时间序列中的季节性和亚季节性波动、过度离散以及气象因素。为实现第二个目标,我们开发了算法来定义受试者死亡前的状况,重点关注心肺疾病。这些算法基于魁北克省全民健康保险计划(QHIP)数据库中留存的信息。该数据库包含所有程序(如手术类型)、医生诊疗以及魁北克省所有医生进行的会诊记录。对于年龄大于或等于65岁的人群以及所有社会救助接受者,处方数据库包含所有配发药品的记录(药物类型、剂量、数量)。对于定义的每组状况,我们使用了与分析所有非意外死因时相同的统计模型。在特定病因死亡率分析中,我们发现所有非意外死因以及特定死因——癌症、冠状动脉疾病、呼吸系统疾病和糖尿病——存在关联的证据,这些关联在环境空气颗粒物浓度的大多数指标中是一致的,以死亡当天(滞后0)以及死亡前两日(滞后1、滞后2)测量的颗粒物浓度的3天均值来评估。所有心血管疾病合并后的关联仅在与硫酸盐之间发现。此外,我们总体上发现65岁及以上人群的每日死亡率增加。所有非意外死因的结果与其他研究的发现相似;滞后0时每日TSP每增加100微克/立方米,死亡率平均增加百分比为6.7%。在根据QHIP数据定义的群体分析中,几乎没有证据表明在死亡前被归类为患有急性或慢性上呼吸道疾病、气道疾病、高血压、急性冠状动脉疾病和脑血管疾病的人群与空气污染物之间存在关联。另一方面,我们发现对于患有癌症、急性下呼吸道疾病、任何形式的心血管疾病、慢性冠状动脉疾病和充血性心力衰竭的人群,在大多数类型的环境颗粒物中死亡率持续增加。此外,我们发现对于没有任何心血管疾病、下呼吸道疾病和癌症的个体也存在关联。后一组人群包括在死亡前一年未与医疗保健系统有过接触的人(12%)以及患有各种潜在致命疾病的个体(52%),包括神经系统疾病(12%)、糖尿病(8%)、心律失常(8%)、痴呆(6%)、器质性精神障碍(6%)和贫血(4%)。由于上述分析中的统计功效降低,各群体之间(如年龄小于65岁和大于或等于65岁的年龄组)的差异通常无统计学意义。与糖尿病的关联此前未被报道,这需要在其他研究中进行重复验证。(摘要截选)