Churg A
Department of Laboratory Medicine, University Hospital, University of British Columbia, Vancouver, Canada.
Monogr Pathol. 1993(36):54-77.
Asbestos-related diseases continue to be sources of controversy for epidemiologist, clinician, and pathologist. Most investigators agree that the different fiber types behave differently in the lung, with chrysotile being rapidly removed, and amphibole persisting. These differences in biologic behavior probably account for the much greater disease potential of amphibole (amosite and crocidolite) compared with chrysotile asbestos, particularly in regard to mesothelioma induction in man. Asbestosis is defined as diffuse interstitial fibrosis of the lung caused by asbestos exposure, and this is the only condition to which the term asbestosis should be applied. The classical pathologic diagnostic criteria for asbestosis, namely the presence of diffuse interstitial fibrosis resembling usual interstitial pneumonia, and asbestos bodies visible in ordinary tissue sections, have proved to withstand the test of time. Cases without asbestos bodies visible in routine or iron-stained tissue sections almost never turn out to be asbestosis. It should be remembered that workers with asbestos exposure develop all of the interstitial lung diseases to which the remainder of the populace is subject; some of these conditions are treatable and should not be misdiagnosed as asbestosis, which is not treatable. There is strong epidemiologic and pathologic evidence that the only association of asbestos exposure and lung cancer is the association of asbestosis and lung cancer. Thus, a lung cancer should only be attributed to asbestos exposure when asbestosis is present on clinical or pathologic grounds. The histologic type and location of the tumor are irrelevant in this regard. Analytical electron microscopy indicates that chrysotile asbestos does induce mesothelioma in man, but that extremely high levels of retained fibers, levels as high as those seen in cases of asbestosis, are required for this event to occur. The weight of the evidence suggests that exposure of the general population to the very low levels of chrysotile that are found in some public building (levels not greatly different from ambient air) will never produce mesothelioma, asbestosis, or lung cancer because these diseases all appear to require quite high-level occupational chrysotile exposure. Even if one accepts the ideas (probably wrong) that any level of asbestos exposure carries a risk of cancer, and that mathematical extrapolation of risk from high-level occupational exposure to low-level building exposure is scientifically valid, the calculated risks are much smaller than real everyday risks such as driving to work. Thus, exposure to asbestos at environmental levels appears to produce no real dangers to health.
石棉相关疾病仍然是流行病学家、临床医生和病理学家争论的焦点。大多数研究人员一致认为,不同类型的纤维在肺部的行为不同,温石棉能迅速被清除,而闪石则会持续存在。这些生物学行为上的差异可能解释了与温石棉相比,闪石(铁石棉和青石棉)引发疾病的可能性要大得多,尤其是在诱发人类间皮瘤方面。石棉肺被定义为因接触石棉而导致的肺部弥漫性间质纤维化,这是唯一应使用石棉肺这一术语的病症。石棉肺的经典病理诊断标准,即存在类似寻常性间质性肺炎的弥漫性间质纤维化,以及在普通组织切片中可见石棉小体,已被证明经得起时间的考验。在常规或铁染色组织切片中未见石棉小体的病例几乎从未被证实为石棉肺。应当记住,接触石棉的工人会患上普通人群易患的所有间质性肺病;其中一些病症是可治疗的,不应误诊为无法治疗的石棉肺。有强有力的流行病学和病理学证据表明,石棉暴露与肺癌的唯一关联是石棉肺与肺癌的关联。因此,只有在临床或病理上存在石棉肺时,肺癌才应归因于石棉暴露。在这方面,肿瘤的组织学类型和位置无关紧要。分析电子显微镜表明,温石棉确实会诱发人类间皮瘤,但发生这种情况需要极高水平的留存纤维,其水平要与石棉肺病例中所见的水平一样高。证据的权重表明,一般人群接触某些公共建筑中发现的极低水平温石棉(其水平与环境空气水平相差不大)永远不会引发间皮瘤、石棉肺或肺癌,因为这些疾病似乎都需要相当高水平的职业性温石棉暴露。即使有人接受这样的观点(可能是错误的),即任何水平的石棉暴露都有患癌风险,并且从高水平职业暴露到低水平建筑暴露的风险数学外推在科学上是有效的,但计算出的风险比诸如开车上班等日常实际风险要小得多。因此,环境水平的石棉暴露似乎不会对健康造成实际危害。