James Craufurd Gregory, 19Th Century Scottish Physicians, and the Link between Occupation as a Coal Miner and Lung Disease

Abstract

By the mid-19th century about 200,000 miners were employed in a UK coal mining industry still growing with the advances of the Industrial Revolution. Coal miners were long known to suffer poor health but the link to inhaling dust in the mines had not been made. In 1813 George Pearson was the rst to suggest that darkening of lungs seen in normal individuals as they aged was caused by inhaled soot from burning oil, candles and coal, which were the common domestic sources of heat and light. In 1831 Dr James Craufurd Gregory rst described black pigmentation and disease in the lungs of a deceased coal miner and linked this to pulmonary accumulation of coal mine dust. Gregory hypothesised that the black material seen at autopsy in the collier's lungs was inhaled coal dust and this was con rmed by chemical analysis carried out by Professor Sir Robert Christison. Gregory suggested that coal dust was the cause of the disease and warned physicians in mining areas to be vigilant for the disease. This rst description of what came to be known as 'coal worker's pneumoconiosis' sparked a remarkable intellectual effort by physicians in Scotland, culminating in a large body of published work that led to the rst understandings of this disease and its link to coalblackened lungs. This paper sets out the history of the role of Scottish physicians in gaining this understanding of coal worker's pneumoconiosis. It describes Gregory's case and the lung -recently discovered in the pathology collection of the Surgeons' Hall Museums, Edinburgh, where it has lain unnoticed for over 180 years -on which Gregory based his landmark paper.

The recognition of lung disease in coal workers: The role of Gough–Wentworth whole lung sections

“…In fact, it turned out to be at odds with the observations he obtained later, regarding the impact of centrilobular emphysema on respiratory function in coal miners. 24 By 1968, 25 Gough was describing three kinds of centrilobular emphysema in his GWSs: (1) focal dust emphysema due to industrial dust-like coal; (2) soot emphysema caused by soot in atmospheric pollution in non-smokers of the general public; (3) Centrilobular Emphysema, due to bronchiolitis caused by exogenous agents such as smoking, infection, cadmium fumes, etc. With the benefit of hindsight, it is clear that Gough did not recognise the common feature of all three, namely the deposition of inhaled particles in the centrilobular region.…”

“…Lung disease in coal miners, known originally as miners’ phthisis or miners’ asthma, was first formally described in Edinburgh by Gregory in 1831, and its essential features were defined by the mid-nineteenth century. 1 However, in the late nineteenth and early twentieth century, before the advent of chest radiographs and based on the relatively good health of coal miners as opposed to urban dwellers and other miners, medical authorities judged the disease to have all but disappeared. Subsequently, some experts asserted that coal dust exposure was harmless, other than the effects of the quartz in it.…”

Black Lungs in the General Population: A New Look at An Old Dispute

“…17 With regard to the latter, Virchow had been sent preparations of coal miners' lungs by Swiss anatomist and histologist Rudolph Albert von Kolliker in the late 1850s, 18 who was at that time a guest of the anatomist, Dr John Goodsir and the surgeon Dr James Young Simpson, in Edinburgh. 17 By then, the midnineteenth century, Scottish physicians were advanced in their understanding of the role of the accumulated lung burden of coalmine dust in the development of disease in coalminer's lungs, 19 but Virchow remained unconvinced. In his paper on the pathology of coalminers' lungs in 1858, which described the preparations sent to him by von Kolliker and Goodsir, he wrongly concluded that it was 'extremely probable that we have here to do with pigmentary changes, resulting from extravasations of blood and the subsequent transformation of haematin, and not with an absorption and deposit of carbonaceous material inhaled into the lungs'.…”

“…In his paper on the pathology of coalminers' lungs in 1858, which described the preparations sent to him by von Kolliker and Goodsir, he wrongly concluded that it was 'extremely probable that we have here to do with pigmentary changes, resulting from extravasations of blood and the subsequent transformation of haematin, and not with an absorption and deposit of carbonaceous material inhaled into the lungs'. 18 It was not until particles of charcoal were incontrovertibly identified by German physician Ludwig Traube in human lung specimens in 1860, on the basis of their morphology, 19 that Virchow fi nally stated in 1866, 50 years after Pearson's paper, that: 'Traube's well-known case fi rst convinced me that large fragments of vegetable coal can reach the alveoli and collect there … The very characteristic shape of charcoal completely excluded any possibility of error and from that moment I was convinced that there is a true pulmonary anthracosis'. 12 The entity of environmental anthracosis was generally accepted by 1916, when Canadian pathologist Oskar Klotz could fi nally write: 'Admitting that but few individuals today can escape the accumulation of carbon particles in the respiratory system, it may be suggested that the condition should be looked upon as a normal process'.…”

The impact of coal mine dust characteristics on pathways to respiratory harm: investigating the pneumoconiotic potency of coals

“…These include the government, industry parties, and research institutes—predominantly from both Europe and the USA. Some of the major events from this timeline include the first pathological description of what we now know as coal workers’ pneumoconiosis (CWP) in 1831 (Donaldson et al, 2017 ) (Fig. 1 timepoint 1).…”