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Coal Workers' Pneumoconiosis: an Australian Perspective

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Coal Workers' Pneumoconiosis: an Australian Perspective Clinical focus Coal workers’ pneumoconiosis: an Australian perspective neumoconiosis” refers to a group of fibrotic Summary lung diseases caused by the retention of dust “ ’ Coal workers’ pneumoconiosis (CWP) is an in the lung. Coal workers pneumoconiosis P untreatable but preventable lung disease arising “ ” (CWP), also known as black lung , is an irreversible from chronic inhalation of coal dust. interstitial lung disease resulting from chronic inhalation Recent reports of CWP in Queensland, along with 1 fi of coal dust. CWP has a long history, with the rst case international data, suggest that there is a resurgence 2 being reported in 1831. Workers exposed to coal dust are in pneumoconiosis. 1 at risk of a range of chronic lung diseases including CWP, The prevalence of CWP varies considerably between 1 3 silicosis, mixed dust pneumoconiosis, chronic obstruc- countries. In Australia, there is no mandatory tive pulmonary disease4 and chronic bronchitis.4 In cases reporting system and no national data on the prevalence of CWP. Graeme R Zosky of heavy dust exposure, CWP may develop into pro- 5 PhD, MBiostat1 gressive massive fibrosis (PMF), which can be fatal. In The symptoms and manifestations of CWP vary 6 depending on the composition of the inhaled dust, Ryan F Hoy 2013, CWP resulted in 25 000 deaths globally. Most cases MB BS, FRACP, MOccEnvHlth2 of CWP occur in the setting of poor occupational hygiene duration of exposure, stage of disease and host- and dust control.7 related factors. CWP may develop into progressive Elizabeth J Silverstone massive fibrosis (PMF), which can be fatal. MB BS, FRANZCR3 Recent reports of CWP in Australia — six confirmed cases Radiological assessment should be performed Fraser J Brims were reported by nominated medical advisers in the according to evidence-based standards using the MB ChB, MD, FRACP4,5 Queensland coal industry between May 2015 and ILO (International Labour Office) International Susan Miles February 20168 — are highly concerning and point to a Classification of Radiographs of Pneumoconioses. BMed, FRACP6,7 potential decline in exposure control in Australian mines As preventing exposure to coal dust prevents CWP, it Anthony R Johnson or a failure of the screening process, or both. If true, this is is important to implement and enforce appropriate MB BS, MOHS, FRACP8 particularly disappointing given the historical success of standards limiting exposure. In Australia, these Peter G Gibson Australian systems, such as the Joint Coal Board (formed standards currently vary between states and are not MB BS, FRACP6 in keeping with international understanding of the in 19469), in reducing the burden of lung disease in the levels of coal dust that cause disease. Deborah H Yates coal industry through comprehensive screening pro- MB BChir, MD, FRACP9 Longitudinal screening programs are crucial for grams and oversight of dust exposure control. Given the monitoring the health of coal workers to identify 1 School of Medicine, potential resurgence of CWP, it is important that we un- individuals with early-stage disease and prevent University of Tasmania, derstand the potential determinants of disease preven- Hobart, TAS. progression from mild disease to PMF. 2 Allergy, Immunology and tion. Here, we consider CWP in the Australian context but We recommend: Respiratory Medicine, do not discuss the other lung diseases attributable to coal < Alfred Hospital, standardisation of coal dust exposure limits, with Melbourne, VIC. dust exposure. harmonisation to international regulations; 3 Department of < implementation of a national screening program Medical Imaging, St Vincent’s Hospital, for at-risk workers, with use of standardised Sydney, NSW. Epidemiology of coal workers’ questionnaires, imaging and lung function testing; 4 Department of pneumoconiosis < development of appropriate training materials to Respiratory Medicine, Sir Charles Gairdner Hospital, assist general practitioners in identifying Perth, WA. There is a strong relationship between inhaled dust dose pneumoconiosis; and 5 School of 10 < a system of mandatory reporting of CWP to a Population Health, and the risk of developing CWP. Airborne respirable University of dust in coal mines consists of a number of dusts that are centralised occupational lung disease register. Western Australia, Perth, WA. potentially dangerous to the lung. It originates from 6 Department of Respiratory within the coal seam or from adjacent fractured rock and and Sleep Medicine, is caused by coal cutting and other operations such as roof John Hunter Hospital, Newcastle, NSW. bolting. The proportion of different dusts affects the type 7 Faculty of Medicine and and severity of lung disease that may develop. reader technique may explain the some of the increase in Public Health, CWP, the concomitant increase in PMF suggests that this University of Newcastle, In 1990 and 2013, 29 000 and 25 000 deaths, respectively, Newcastle, NSW. is a true increase in disease prevalence. In the 2010 ex- 8 Thoracic Medicine, were attributed to CWP globally, compared with 55 000 plosion that killed 29 miners in West Virginia, post mor- Liverpool Hospital, and 46 000 for silicosis.6 In the United States, there has Sydney, NSW. tem examination showed pathological changes consistent been a resurgence of CWP. While there was a decrease in 9 Department of with CWP in 17 of 24 victims; 16 of these workers had Thoracic Medicine, the prevalence of CWP in coal miners in the US from the started working after modern dust limits were applied.12 St Vincent’s Hospital, Sydney, NSW. 1970s to 1990s (from 6.5% to 2.1%), prevalence then increased from the 1990s to the 2000s (to 3.2%).11 This was The recent increase in CWP is concerning and has been deborahy88@ hotmail.com accompanied by a substantial increase in the prevalence attributed to several potential causes: changes in the of coal mine workers with PMF (1990s, 0.14%; 2000s, physicochemical characteristics of the dust, reduction in doi: 10.5694/mja16.00357 0.31%).11 While improvements in the quality of x-rays and dust suppression activities, and increased workload (ie, 414 MJA 204 (11) j 20 June 2016 Clinical focus increased exposure).11 CWP is still an important occupa- gas trapping and impaired diffusion capacity.22 Restric- tional lung disease, even in developed countries, and any tive deficits may also occur as a result of fibrosis,3 and late reduction in vigilance regarding inhaled coal dust is likely complications include pulmonary hypertension,23 cor to result in a significant increase in morbidity and pulmonale24 and death. The symptoms of CWP are non- mortality. specific and identical to those of lung disease from other causes. Chronic bronchitis and emphysema are also well The prevalence of CWP varies considerably by country. documented to occur with coal dust exposure,25 further In the United Kingdom, the incidence of CWP declined complicating diagnosis. dramatically between 2004 and 2008 and has remained relatively stable since; it is unclear how these data reflect Pure carbon, the main constituent of coal, is largely inert. CWP prevalence in coal workers.13 In some countries, the However, the physicochemical properties of processed prevalence of CWP in coal workers remains high, such as coal are complex and include organic and inorganic China (6.02%) and India (3.03%).14,15 In Australia, there contaminants with known pro-inflammatory and carci- are very few data regarding the true prevalence of CWP nogenic properties, such as silica, iron, cadmium, lead, in coal workers, although long-term data from Coal Ser- kaolin, pyrite and polycyclic aromatic hydrocarbons.1,26 vices (which replaced the Joint Coal Board) suggest that The nature and extent of these, along with the physical there have been no new cases of CWP in New South Wales properties of the carbon particles, have a significant since the 1980s.16 It is difficult to access information about “As the only impact on the risk of developing pneumoconiosis.27 cases due to a lack of mandatory reporting in Australia. cause of CWP Crystalline free silica, the commonest contaminant, independently causes silicosis28 and is often found in high One retrospective study of pneumoconiosis mortality in is coal dust, quantities in dust associated with coal mining.29 Thus, Australia found that, of the more than 1000 deaths prevention is CWP and silicosis have significant overlap. attributed to pneumoconiosis between 1979 and 2002, only 6% were classified as CWP, with the number of fa- straightforward CWP results from the aberrant repair processes that occur 17 talities decreasing steadily over time. Data from the — preventing when prolonged exposure leads to the activation of pro- fl fi 30 National Occupational Health and Safety Commission, exposure to in ammatory and pro- brotic pathways in the lung. based on potentially unreliable workers compensation Coal dust stimulates pathways that lead to fibrosis due statistics, suggest that between 2001 and 2003 there were coal dust to the cytotoxic effects of the particles31 and the release of 750 new cases of pneumoconiosis (including CWP, prevents pro-inflammatory and pro-fibrotic mediators by cells asbestosis and silicosis), with 92 deaths in 2003.18 Mor- 30 disease” responding to the particles. Central to this is the capacity tality from pneumoconiosis in this period of < 1 per of coal particles to produce abundant reactive oxygen 100 000 population is in stark contrast to the 1950s rate of species32 and induce oxidative stress.33 3.9 per 100 000.18 Again, it is difficult to determine the current prevalence of CWP among coal workers based The manifestations of CWP can vary greatly between individuals, depending on the composition of the dust on these data, and it is likely that CWP incidence is 34 underestimated. One study comparing the prevalence of and duration of exposure, as well as host-related factors. CWP in the US and NSW suggested that CWP was almost Accumulation of dust occurs initially in the walls of the absent in Australian coal workers (prevalence < 0.5%).19 respiratory bronchioles, the adventitia of the blood This is despite documented higher levels of dust in vessels and the bronchoalveolar canals.
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