Peters A, Döring A, Wichmann H E, Koenig W
GSF-National Research Centre for Environment and Health, Institute of Epidemiology, Neuherberg, Oberschleissheim, Germany.
Lancet. 1997 May 31;349(9065):1582-7. doi: 10.1016/S0140-6736(97)01211-7.
Air pollution episodes have been consistently associated with increased mortality, and most strikingly with mortality due to cardiovascular disease. One hypothesis to explain this association is that inflammation of the peripheral airways caused by pollution might increase blood coagulability. We have tested this hypothesis in a cross-sectional study by comparing measurements of plasma viscosity during a severe episode of air pollution during 1985 with those made on less polluted days.
Plasma viscosity was measured as part of the MONICA Augsburg survey during the winter of 1984-85 in 3256 randomly selected men and women aged 25-64 years. Daily mean concentrations of air pollutants and meteorological variables were measured in Augsburg as part of the automated Bavarian air-quality network. We compared measurements of plasma viscosity made in 324 people who attended for screening during the pollution episode and in 2932 people screened during the remainder of the survey period.
In January, 1985, high concentrations of sulphur dioxide (mean 200 micrograms/m3) and total suspended particles (mean 98 micrograms/m3) were recorded during a 13-day period in Augsburg. In men, the odds ratio for plasma viscosity above the 95th percentile of the distribution (1.38 mPa s) was 3.6 (95% CI 1.6-8.1) comparing measurements during the air pollution episode with non-episode measurements after adjustment for cardiovascular risk factors and meteorological variables. The corresponding odds ratio for women (95th percentile of plasma viscosity 1.37 mPa s) was 2.3 (1.0-5.3). High concentrations of carbon monoxide were also associated with increased plasma viscosity in women.
During the 1985 air pollution episode, an increased risk of extreme values of plasma viscosity was observed in both men and women. Altered blood rheology due to inflammatory processes in the lung that induce an acute-phase reaction might therefore be part of the pathological mechanisms linking air pollution to mortality.
空气污染事件一直与死亡率增加相关,最显著的是与心血管疾病导致的死亡率相关。解释这种关联的一种假说是,污染引起的外周气道炎症可能会增加血液凝固性。我们在一项横断面研究中对这一假说进行了检验,比较了1985年一次严重空气污染事件期间的血浆粘度测量值与污染较轻日子的测量值。
作为1984 - 1985年冬季奥格斯堡莫妮卡(MONICA)调查的一部分,对3256名年龄在25 - 64岁之间随机选取的男性和女性测量了血浆粘度。作为巴伐利亚空气质量自动监测网络的一部分,在奥格斯堡测量了空气污染物的日平均浓度和气象变量。我们比较了在污染事件期间前来筛查的324人和在调查剩余期间筛查的2932人的血浆粘度测量值。
1985年1月,奥格斯堡在为期13天的时间段内记录到高浓度的二氧化硫(平均200微克/立方米)和总悬浮颗粒物(平均98微克/立方米)。在男性中,在对心血管危险因素和气象变量进行调整后,将空气污染事件期间的测量值与非事件期间的测量值进行比较,血浆粘度高于分布第95百分位数(1.38毫帕秒)的比值比为3.6(95%可信区间1.6 - 8.1)。女性血浆粘度第95百分位数为1.37毫帕秒,相应的比值比为2.3(1.0 - 5.3)。高浓度一氧化碳也与女性血浆粘度增加有关。
在1985年空气污染事件期间,男性和女性血浆粘度出现极值的风险均增加。因此,肺部炎症过程引起的血液流变学改变导致急性期反应,这可能是将空气污染与死亡率联系起来的病理机制的一部分。