Kosarev V V
Gig Tr Prof Zabol. 1989(8):34-6.
The comment on the article by D. M. Zislin (Occupational Hygiene and Industrial Diseases, 1988, N 10) is presented. Proceeding from the author's own experience and literary data, the main statement of D. M. Zislin disputing the concept of dust pulmonary disease (DPD) in the modern occupational pulmonology, is analyzed. The common cause of pneumoconiosis and dust bronchitis has been identified as fibrogenic dust, allergic, carcinogenic and toxic characteristics of which can be only condition affecting the disease clinical character. The article shows that neither generality, nor the differences in the functional changes of external respiration can serve as a convincing argument for or against the existence of the concept of DPD. Modern histomorphologic studies give evidence that low-fibrogenic dusts practically simultaneously cause the onset of the pathologic process both in the interstitial tissue and in the bronchi, the outcome of the process being diffuse pneumosclerosis. The concept of DPD caused by low-fibrogenic dusts has been substantiated on the basis of common etiology and similar pathogenetic, clinical and functional manifestations.
本文对D. M. 齐斯林(《职业卫生与工业疾病》,1988年,第10期)的文章进行了评论。基于作者自身经验和文献资料,对D. M. 齐斯林质疑现代职业肺病学中尘肺病(DPD)概念的主要观点进行了分析。已确定尘肺病和尘性支气管炎的共同病因是致纤维化粉尘,其过敏、致癌和毒性特征可能只是影响疾病临床特征的条件。文章表明,外呼吸功能变化的普遍性或差异都不能作为支持或反对尘肺病概念存在的令人信服的论据。现代组织形态学研究表明,低致纤维化粉尘实际上同时在间质组织和支气管中引发病理过程,该过程的结果是弥漫性肺硬化。基于共同病因以及相似的发病机制、临床和功能表现,由低致纤维化粉尘引起的尘肺病概念得到了证实。