Gordon T, Nadziejko C, Chen L C, Schlesinger R
Department of Environmental Medicine, New York University School of Medicine, Tuxedo, USA.
Res Rep Health Eff Inst. 2000 Apr(93):5-34; discussion 35-42.
Considerable controversy surrounds the biological plausibility of adverse effects from exposure to ambient particulate matter (PM)*, chiefly because these adverse effects have been observed at particle mass concentrations below those that have been shown to produce effects in healthy animals and human volunteers in the laboratory. To address this research gap, we examined the potential for concentrated ambient PM to produce pulmonary and cardiovascular changes in compromise rodent models. Normal healthy and monocrotaline-treated rats received single or multiple exposures to concentrated ambient PM, and their responses were tested using functional, cellular, biochemical, and histological endpoints. Analyses determined that no changes in pulmonary function or structure occurred after exposure to concentrated ambient PM. Cardiac arrhythmias did not increase after PM exposure in normal or monocrotaline-treated rats. Increased atrial conduction time, accompanied by a decrease in the duration of the T wave portion of the electrocardiogram (ECG) waveform, was observed in PM-exposed monocrotaline-treated rats in one experiment. In addition, on several but not all exposure days, small yet statistically significant increases in heart rate and peripheral blood cell differential counts were observed in normal and monocrotaline-treated rats within 6 hours after exposure to concentrated ambient PM. The observed changes in cardiovascular parameters in rats returned to control values by 24 hours after exposure. In a hamster cardiomyopathy model, no adverse cardiac or pulmonary changes were detected after exposure to concentrated ambient PM. Thus, these studies found that cardiopulmonary effects could be produced in rats, but not in hamsters with cardiomyopathy, exposed to concentrated ambient PM. None of the changes occurred on every exposure day and none appeared to be life threatening. Thus, the cardiac changes may reflect changes in homeostasis that could affect individuals who are critically ill, and these findings do not resolve the biological plausibility of adverse health effects associated with ambient PM in epidemiologic studies.
暴露于环境颗粒物（PM）*是否会产生不良反应，这一问题在生物学合理性方面存在相当大的争议，主要原因是在实验室中，当颗粒物质量浓度低于已证明会对健康动物和人类志愿者产生影响的浓度时，就已经观察到了这些不良反应。为了填补这一研究空白，我们研究了浓缩环境PM对处于健康受损状态的啮齿动物模型产生肺部和心血管变化的可能性。正常健康和用野百合碱处理过的大鼠接受了单次或多次浓缩环境PM暴露，并使用功能、细胞、生化和组织学指标来测试它们的反应。分析确定，暴露于浓缩环境PM后，肺功能或结构没有发生变化。正常或用野百合碱处理过的大鼠在暴露于PM后，心律失常并未增加。在一项实验中，暴露于PM的用野百合碱处理过的大鼠出现了心房传导时间增加，同时心电图（ECG）波形的T波部分持续时间缩短。此外，在几个（但并非所有）暴露日，正常和用野百合碱处理过的大鼠在暴露于浓缩环境PM后6小时内，心率和外周血细胞分类计数出现了虽小但具有统计学意义的增加。大鼠心血管参数的观察到的变化在暴露后24小时恢复到对照值。在仓鼠心肌病模型中，暴露于浓缩环境PM后未检测到心脏或肺部的不良反应。因此，这些研究发现，暴露于浓缩环境PM的大鼠会产生心肺效应，但患有心肌病的仓鼠则不会。并非每次暴露日都会出现这些变化，而且似乎没有一个变化会危及生命。因此，心脏变化可能反映了内环境稳态的变化，这可能会影响重症患者，而这些发现并未解决流行病学研究中与环境PM相关的不良健康影响的生物学合理性问题。
