“Buying brains and experts”: British coal owners,regulatory capture and miners’ health, 1918 – 1946

This article examines British coal owners’ use of medical and scientific knowledge of occupational lung diseases in the mining industry to resist regulatory changes between 1918 and 1946. It explores the strategies deployed by coal owners in response to scientific and lay debates over the hazard to workers’ health presented by dust, and legislation to compensate miners for pneumoconiosis and silicosis contracted in the nation’s collieries. In particular, it investigates coal owner deployment of the views of notable scientists, especially the eminent physiologist John Scott Haldane (1860–1936), who insisted on the harmlessness of coal dust, in order to avoid costly compensation payments, as well as capital investment in ameliorative measures to reduce miners’ exposure to such hazards. In so doing, the article provides new insights by illustrating how coal owners influenced mining education programmes, deploying the arguments of Haldane and others, with direct implications for health and safety in British mines. This contributed to the mounting public health disaster wrought by coal dust on Britain’s mining communities. This process is viewed as part of the broader political activities of the coal owners – and their industry body, the Mining Association of Great Britain – in its attempts to influence the regulatory process in a period of dramatic change in the political economy of coal.     

青海藏獒尘肺的病理学观察

采用光镜和电镜技术对青海省果洛藏族自治州达日县的5例成年藏獒的肺、支气管淋巴结和纵隔淋巴结进行了病理学观察.结果表明,5例藏獒肺均有程度不等的尘肺病变,其中3例尘肺病变相对较重.表现为局灶型或弥漫型尘肺病变.局灶型尘灶与尘细胞结节呈星状、散状分布,多位于细支气管周围、肺泡隔和肺胸膜结缔组织中;弥漫型则尘灶与尘细胞弥漫性分布于大范围肺组织中,尘灶周围及尘细胞浸润局部有大量淋巴细胞浸润和结缔组织增生,局部肺泡隔因结缔组织增生而显著增宽,肺泡腔萎缩,肺组织结构破坏.细支气管周围常有慢性炎症,其下段管腔常可形成扩张和肺气肿区.同时,5例尘肺病例中均有程度不等的单核巨噬细胞性肺炎.5例支气管淋巴结和纵隔淋巴结均有严重的尘灶和尘细胞结节.3例出现灶性或较大范围纤维化.电镜观察发现,肺及淋巴结中尘细胞线粒体肿胀空泡化,内质网扩张,细胞中有大量尘粒聚集,尘粒聚集处细胞器破坏.尘细胞周围的肺泡上皮细胞也有程度不等的退行性变化.表明,青海藏獒尘肺为无机尘肺与有机尘肺组成的混合性尘肺,其发生与当地的环境密切相关.     

Silicosis: Diagnosis and Medicolegal Implications

Despite well‐publicized sources of occupational hazard, silicosis continues to threaten industrial workers in the United States. We performed a retrospective search of the University of Wisconsin electronic pathology database to retrieve autopsy cases of silicosis and collaborated with the Wisconsin Department of Health Services to obtain statewide epidemiologic data regarding silicosis morbidity/mortality since 2003. Three silicosis autopsy cases were retrieved: all were men with ≥ 30 years of occupational crystalline silica exposure and similar histologic features of collagenous pulmonary nodules with admixed refractile particles. Overall, our state exceeds the national rate of silicosis‐related hospitalizations and mortality, that is, 10.1 hospitalizations per million WI residents versus 1.2 nationally and 1.2 deaths per million WI residents versus 0.4 nationally. Surveillance is crucial to identify emerging occupational hazards and protect workers. A diagnosis of silicosis must be carefully considered at autopsy since it carries substantial implications for worker's compensation, compensatory losses, and employer liability.     

猪尘肺的病理组织学研究

对甘肃省河西地区102例猪的肺和支气管淋巴结进行了病理学研究。生前虽难以确定特征症状、但宰后可见一定的大体变化。组织上首次在国内发现了无机尘肺的病理改变。其病变可分为局灶型与弥漫型两型。前者呈星散状分布,多位于细支气管和肺泡隔局部,其特征是在粉尘灶或尘细胞积聚处有明显的结缔组织增生和淋巴细胞浸润。附近的肺结构也有一些形态改变。后者病变主要表现为弥漫性支气管周炎,几乎所有的支气管树都受到侵害。管周结缔组织增生和粉尘沉着。在严重病例,结缔组织可长入肺泡隔和小叶间。弥漫性生肺是局灶性尘肺的进一步发展,主要发生于浮尘含量很高的河西走廊西端的安西县。