Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Arch Pathol Lab Med. 2010 Mar;134(3):462-80. doi: 10.5858/134.3.462.
Asbestosis is defined as diffuse pulmonary fibrosis caused by the inhalation of excessive amounts of asbestos fibers. Pathologically, both pulmonary fibrosis of a particular pattern and evidence of excess asbestos in the lungs must be present. Clinically, the disease usually progresses slowly, with a typical latent period of more than 20 years from first exposure to onset of symptoms.
IDIOPATHIC PULMONARY FIBROSIS: The pulmonary fibrosis of asbestosis is interstitial and has a basal subpleural distribution, similar to that seen in idiopathic pulmonary fibrosis, which is the principal differential diagnosis. However, there are differences between the 2 diseases apart from the presence or absence of asbestos. First, the interstitial fibrosis of asbestosis is accompanied by very little inflammation, which, although not marked, is better developed in idiopathic pulmonary fibrosis. Second, in keeping with the slow tempo of the disease, the fibroblastic foci that characterize idiopathic pulmonary fibrosis are infrequent in asbestosis. Third, asbestosis is almost always accompanied by mild fibrosis of the visceral pleura, a feature that is rare in idiopathic pulmonary fibrosis.
RESPIRATORY BRONCHIOLITIS: Asbestosis is believed to start in the region of the respiratory bronchiole and gradually extends outward to involve more and more of the lung acinus, until the separate foci of fibrosis link, resulting in the characteristically diffuse pattern of the disease. These early stages of the disease are diagnostically problematic because similar centriacinar fibrosis is often seen in cigarette smokers and is characteristic of mixed-dust pneumoconiosis. Fibrosis limited to the walls of the bronchioles does not represent asbestosis.
Histologic evidence of asbestos inhalation is provided by the identification of asbestos bodies either lying freely in the air spaces or embedded in the interstitial fibrosis. Asbestos bodies are distinguished from other ferruginous bodies by their thin, transparent core. Two or more asbestos bodies per square centimeter of a 5- mu m-thick lung section, in combination with interstitial fibrosis of the appropriate pattern, are indicative of asbestosis. Fewer asbestos bodies do not necessarily exclude a diagnosis of asbestosis, but evidence of excess asbestos would then require quantitative studies performed on lung digests.
Quantification of asbestos load may be performed on lung digests or bronchoalveolar lavage material, employing either light microscopy, scanning electron microscopy, or transmission electron microscopy. Whichever technique is employed, the results are only dependable if the laboratory is well practiced in the method chosen, frequently performs such analyses, and the results are compared with those obtained by the same laboratory applying the same technique to a control population.
石棉沉着病定义为吸入过量石棉纤维引起的弥漫性肺纤维化。病理学上,肺部必须既有特定模式的肺纤维化,又有过量石棉的证据。临床上,疾病通常进展缓慢,从首次暴露到症状出现的典型潜伏期超过 20 年。
特发性肺纤维化:石棉沉着病的肺纤维化为间质,呈基底胸膜下分布,与特发性肺纤维化相似,这是主要的鉴别诊断。然而,除了石棉的存在与否外,这两种疾病之间还有一些区别。首先,石棉沉着病的间质纤维化几乎没有炎症,尽管不明显,但在特发性肺纤维化中更为明显。其次,与疾病的缓慢节奏一致,特发性肺纤维化中特征性的成纤维细胞灶在石棉沉着病中很少见。第三,石棉沉着病几乎总是伴有轻微的内脏胸膜纤维化,这在特发性肺纤维化中很少见。
呼吸性细支气管炎:据信石棉沉着病始于呼吸细支气管区域,并逐渐向外扩展,累及越来越多的肺腺泡,直到纤维化的独立灶相连,从而导致疾病的特征性弥漫模式。由于在吸烟的人中经常看到类似的中心性细支气管炎纤维化,并且是混合尘肺的特征,因此疾病的这些早期阶段具有诊断上的问题。仅限于细支气管壁的纤维化不代表石棉沉着病。
通过识别游离存在于气腔或嵌入间质纤维化中的石棉体,可以提供石棉吸入的组织学证据。石棉体与其他含铁血黄素体的区别在于其薄而透明的核心。在 5μm 厚的肺切片的每平方厘米中发现两个或更多个石棉体,结合适当模式的间质纤维化,提示石棉沉着病。石棉体较少不一定排除石棉沉着病的诊断,但如果存在过量的石棉,则需要对肺消化物进行定量研究。
可以对肺消化物或支气管肺泡灌洗材料进行石棉负荷的量化,采用光学显微镜、扫描电子显微镜或透射电子显微镜。无论采用哪种技术,如果实验室在所选方法方面经验丰富,经常进行此类分析,并且将结果与同一实验室应用相同技术对对照人群的结果进行比较,则结果仅可靠。