Occupational lung diseases in Australia
Authors: Ryan F Hoy and Fraser Brims
Published online: 13 November 2017
Occupational exposures are an important determinant of respiratory health
Summary
- Occupational exposures are an important determinant of respiratory health. International estimates note that about 15% of adult-onset asthma, 15% of chronic obstructive pulmonary disease and 10–30% of lung cancer may be attributable to hazardous occupational exposures. One-quarter of working asthmatics either have had their asthma caused by work or adversely affected by workplace conditions.
- Recently, cases of historical occupational lung diseases have been noted to occur with new exposures, such as cases of silicosis in workers fabricating kitchen benchtops from artificial stone products.
- Identification of an occupational cause of a lung disease can be difficult and requires maintaining a high index of suspicion. When an occupational lung disease is identified, this may facilitate a cure and help to protect coworkers.
- Currently, very little information is collected regarding actual cases of occupational lung diseases in Australia. Most assumptions about many occupational lung diseases are based on extrapolation from overseas data. This lack of information is a major impediment to development of targeted interventions and timely identification of new hazardous exposures.
- All employers, governments and health care providers in Australia have a responsibility to ensure that the highest possible standards are in place to protect workers’ respiratory health.
A typical Australian adult spends 25% of the entire week at work, and during that time his or her respiratory tract will be exposed to about 18 000 litres of air. This volume increases markedly if a job requires even light exertion with resultant increase in minute ventilation. The quality of air at work is a major determinant of respiratory health and any part of the respiratory tract from the nose to alveoli can be adversely affected.
Occupational exposures may cause lung disease or aggravate pre-existing conditions. Exposures can have immediate health effects (such as acute inhalation injury), some conditions develop over months or years of employment (such as sensitiser-induced occupational asthma) and some manifest decades later, even after the individual has left the workplace (such as mesothelioma). Some occupational lung diseases, such as coal workers’ pneumoconiosis and asbestos-related diseases, are well characterised, with a clear occupational cause and distinct radiological and pathology pattern. The lungs, however, have a limited array of responses to injury, therefore most occupational lung diseases will present with a non-specific disease pattern. The identification of an occupational cause in this situation can be challenging, not least because of the lag time from exposure to disease onset.
Enquiring about current and previous employment is an essential but frequently overlooked part of clinical assessment. A study from the United Kingdom noted that only one in seven family practitioners recorded an occupation for their asthmatic patients.1 Although challenging, identification of an occupational cause of lung disease may improve a patient’s outcome and, in some circumstances, could facilitate a cure. Identification of a sentinel case of lung disease caused by work should also trigger consideration of coworkers who may be at risk.
Apart from the Australian Mesothelioma Registry, there is minimal systematic collection of data regarding occupational lung diseases in Australia. Reported workers’ compensation data provides limited insight because these statistics underestimate the number of cases by at least a factor of ten for some conditions, fail to capture a sizeable proportion of the working population, and report some meaningless categories such as “other respiratory diseases due to substances”.2 Current knowledge in Australia is based largely on extrapolation from overseas data and local epidemiological research, rather than monitoring of actual cases. This lack of efficient access to data on the distribution of diseases by occupations and exposures severely impairs development of targeted preventive interventions.
The strategy for this narrative review was to search PubMed between 1985 and 2017, specialist society publications and the grey literature available on the internet for original research, review articles and meta-analyses relevant to occupational lung diseases in Australia.
Work-related asthma
Asthma is one of the most common medical conditions affecting the working population, and consideration of how occupational factors influence asthma is an integral part of asthma management. Occupational exposures can induce asthma (occupational asthma) or adversely affect the control of asthma (work-exacerbated asthma).3 Work-related asthma is an umbrella term for these conditions and affects one-quarter of adults with asthma4 (Box 1).
Occupational asthma is a common, preventable occupational disease that is characterised by development of asthma specifically due to a workplace exposure. Recent international estimates attribute 15–20% of adult-onset asthma to workplace exposures.5 A cross-sectional survey of the general population in New South Wales identified 9.5% of prevalent cases of adult-onset asthma to be associated with occupational exposures.6 In Victoria and Tasmania, the Surveillance of Australian Workplace Based Respiratory Events program previously noted that occupational asthma was the most common occupational lung disease reported by respiratory and occupational physicians, and wood dust the most common cause.7 Occupational asthma tends to be more severe, associated with high medication usage, poorer asthma control, more rapid lung function decline and greater socio-economic impacts, than non-work-related asthma.8-10
Sensitiser-induced occupational asthma develops due to immune-mediated sensitisation to an occupational agent (sometimes referred to as an asthmagen). Once developed, even a very low level of exposure can induce asthma symptoms. Over 400 asthmagens have been reported; the most frequent agents include wheat flour, animal antigens and wood dust (online Appendix).11,12 A recent national survey of 4878 Australian workers noted that 47% of men and 40% of women are exposed to at least one asthmagen in the course of their work.13 Following development of occupational asthma, complete avoidance of the causative asthmagen is associated with the optimal outcome and sometimes resolution of asthma.14 However, if this requires a change of employment there may be major adverse socio-economic impacts for the worker, potentially including prolonged unemployment.8
Irritant-induced occupational asthma is a non-immunological condition that follows exposure of the airway to irritant substances, such as the alkaline concrete dust experienced by first responders to the World Trade Center disaster.15 Reactive airway dysfunction syndrome is a severe form of irritant-induced occupational asthma, first described in 1985.16 Criteria for irritant-induced occupational asthma are less restrictive than for reactive airway dysfunction syndrome and acknowledge that asthma may develop after one or more high level exposures and possibly also with chronic moderate or low level irritant exposure, such as may be experienced by professional cleaners.11,17
Work-exacerbated asthma describes asthma that is worsened but not caused by work.18,19 General population studies indicate that work-exacerbated asthma affects a large number of adults with asthma, with a median prevalence of 21.5% in this population.18 Work-exacerbated asthma may range from a single flare of asthma through to daily symptoms and severe exacerbations. The health and socio-economic outcomes for individuals with work-exacerbated asthma may be as poor as for those with occupational asthma.18 A broad range of workplace exposures can exacerbate asthma, including irritant chemicals, common environmental allergens (such as dust mites), worksite temperature, physical exertion and even emotional stress.18
Work-associated respiratory symptoms can be due to several other conditions that require consideration apart from asthma. In particular, there is growing recognition of vocal cord dysfunction as a condition that may mimic or be misdiagnosed as asthma, especially when associated with workplace irritant exposures.20,21
Chronic obstructive pulmonary disease
At a population level, it is estimated that 15% of chronic obstructive pulmonary disease (COPD) is attributable to occupational exposures.22 However, because of the very strong association between smoking and COPD, establishing occupational causation in an individual with a smoking history is very challenging. Conversely, when COPD occurs in a never-smoker, an occupational or environmental contribution should be explored. Many epidemiological studies examine the effect of any vapour, gas, dust or fume rather than particular occupational exposures.23 Some of the specific occupations that have been associated with the development of COPD include smelter workers, machine operators, cleaners, coalminers, cotton workers, construction workers and bus drivers.24-26
Obliterative bronchiolitis
Obliterative bronchiolitis is a rare cause of fixed obstructive lung disease. Obliterative bronchiolitis presents with breathlessness and cough and can easily be mistaken for COPD or asthma. In 2000, a cluster of obliterative bronchiolitis was identified in Missouri, United States. An in-depth multidisciplinary investigation identified that all patients worked at a microwave popcorn plant and were exposed to the volatile butter-flavouring ingredient diacetyl.27 The condition is now commonly known as popcorn workers’ lung. Subsequent elimination of diacetyl from the production of microwave popcorn is an excellent example of a primary prevention strategy. Volatile flavouring-associated obliterative bronchiolitis has been identified in association with production of other foods including biscuits, cereal, chocolate and coffee.28
Interstitial lung diseases
Occupational exposures are potentially controllable causes of interstitial lung disease and, in men, are a more frequent cause than adverse drug reactions and connective tissue diseases combined.29 Occupational interstitial lung diseases can be grouped into four (sometimes overlapping) categories: pneumoconiosis, hypersensitivity pneumonitis, granulomatous lung disease, and other interstitial disorders (Box 2).30 Identification of occupational factors associated with interstitial lung disease can be difficult given that most patients with the condition are diagnosed at over 60 years of age and are likely to have had many occupational exposures over the course of their working life.
Pneumoconioses are diffuse non-malignant parenchymal lung diseases caused by occupational exposure to mineral dusts. The three most common forms are asbestosis, silicosis and coal workers’ pneumoconiosis. Although these conditions were more common before modern occupational health standards, they should not be considered as merely of historical interest. The re-identification of many cases of coal workers’ pneumoconiosis (black lung) in Queensland has recently been highlighted in this Journal.31
Mortality from silicosis in Australia has decreased substantially over the past 40 years;32 however, a recent cross-sectional survey noted that 6.4% of Australian workers are currently exposed to respirable crystalline silica at work, 3.3% at a high level.33 Artificial or engineered stone is a building material that has been available in Australia since the early 2000s and is used primarily for the fabrication of kitchen and bathroom benchtops. Cutting this product, especially if performed without water suppression, is associated with extremely high levels of respirable crystalline silica.34 The first case of complicated silicosis in an Australia worker was recently reported.35 In Israel, artificial stone has been available since the 1980s; a recent report noted 40 cases per year of artificial stone-associated silicosis and found that 4% of all lung transplants had been performed due to this disease between 1997 and 2012.36 There is an urgent need in the building industry to ensure that silica dust is maintained at a safe level and that at-risk workers are screened for silicosis.
Asbestos-related lung diseases
Australia has among the highest rates of asbestos-related lung disease in the world,37 which reflects the extent of asbestos mining, and the manufacturing and utilisation of asbestos-containing materials during the 20th century. It was only in 2004 that a complete ban on asbestos importation was enacted in Australia.38 The true prevalence of asbestos-related lung disease in the general Australian population is not known. Recent data from the Western Australian Asbestos Review Program39 show the presence of pleural plaques in 64% of patients, diffuse pleural thickening in 8%, and one-quarter having computed tomography (CT) evidence of asbestosis.40
Asbestos-related lung disease has a higher risk of development with increasing cumulative exposure and time since first exposure.37 Occupations where the risk of asbestos-related lung disease is substantial include mining, processing and transportation of raw asbestos.37 The principal industries that used asbestos included insulation and specialised cement production, ship-fitting and dockyard work, and railway carriage maintenance. Historically, construction tradesmen, heating engineers, boilermen, railwaymen and members of the Armed Services (particularly the Navy) were often exposed. Construction and demolition workers and asbestos removalists are some of the occupations that currently involve significant potential for exposure. A detailed asbestos exposure history should include possible exposures to asbestos dust on the work clothes of other members in the household (para-occupational exposure) and unpaid involvement in renovations to buildings that may have contained asbestos. The exposure history is important not only for an appropriate diagnosis but also for medico-legal reasons, as discussed further in relation to mesothelioma elsewhere in this issue of the MJA.41
Pleural plaques are the most common manifestation of asbestos exposure, although they do not cause physical impairment.42-46 Plaques usually become visible on radiology within the first 10 years of exposure and calcify over time, but do not subsequently progress in size or extent.47 There is no accepted, proven relationship between the presence of pleural plaques and risk of mesothelioma or lung cancer,37,41 and there is therefore no requirement for follow-up of individuals with pleural plaques.
Diffuse pleural thickening is extensive and progressive pleural fibrosis which involves both the visceral and parietal pleura. In contrast to pleural plaques, diffuse pleural thickening may markedly reduce lung volumes, resulting in exertional dyspnoea.44,46,48 The presence of chest wall pain in association with pleural thickening should raise the suspicion of pleural malignancy.
Asbestosis is an interstitial lung disease that specifically refers to pulmonary fibrosis caused by inhalation of asbestos fibres. Asbestosis has the same pathological and radiological pattern as idiopathic pulmonary fibrosis. The presence of asbestos bodies or fibres on lung biopsy (although this is not usually required for diagnosis), or pleural plaques radiologically, is highly suggestive of asbestosis, but their absence does not exclude the diagnosis. Clinically, asbestosis is commonly associated with prolonged exposure, usually over 10–20 years; however, short, intense exposures can be sufficient.49
Exposure to asbestos is also associated with the development of malignant mesothelioma41) and lung cancer (discussed below).
The prevention of further asbestos exposure in the Australian population is a major public health issue that requires continuing public education and awareness of the ongoing presence of asbestos-containing material in homes and workplaces throughout the country.
Occupational lung cancer
While exposure to tobacco smoke remains by far the most significant risk factor associated with lung cancer, there are potentially preventable occupational exposures that increase the risk of developing the disease. The World Health Organization notes that every tenth lung cancer death is closely related to risk in the workplace.50 Extrapolating from Finnish data, researchers estimate that 29% of lung cancer cases in men and 5% in women may be attributable to occupational exposures in Australia.51
There are a large number of chemicals and products that are classified as carcinogens by the International Agency for Research on Cancer. This classification is of key importance; however, it does not inform clinicians or patients of causation at an individual level, only association at a population level. Further, the context of exposure (eg, enclosed space, ventilation, duration) and nature of the exposure–response relationship are extremely important. For instance, the combination of tobacco smoke and asbestos exposure raises the relative risk of lung cancer by more than an additive but less than a multiplicative amount.52,53 Similarly, in 2014, diesel exhaust emissions were classified as a carcinogen by the International Agency for Research on Cancer. However, the evidence for this relates mostly to exposure to diesel exhaust emissions in enclosed workspaces with poor ventilation and with an older generation of diesel engines, potentially limiting the applicability to current workplace exposures.54 Of concern is a recent Australia-wide survey that reported substantial current workplace exposures to diesel exhaust emissions in up to one in seven workers.55 A thorough occupational and environmental exposure history is required of all patients with lung cancer to provide an informed judgement regarding causation of their disease.
There has been considerable recent interest in Australia regarding the role of low-dose chest CT in screening for early lung cancer;56 however, this practice is currently not endorsed by the federal Department of Health.57 One of the key challenges is the appropriate identification of a high (enough) risk group. Box 3 presents occupations and exposures that may contribute to an increased risk of lung cancer, although current tobacco smoke exposure remains the most dominant single risk factor, with a 10- to 20-fold increased risk.58 At this time, there is therefore no role for population-based low-dose CT screening for lung cancer based on risk associated with occupational exposures.
Diagnosing and managing occupational lung diseases
Although seemingly self-apparent, it is essential to accurately diagnose the lung condition present before establishing the diagnosis of an occupational lung disease. Even a common condition such as asthma is frequently misdiagnosed because of a failure to perform appropriate investigations.59 Occupational factors should be considered in all patients with respiratory disease, but particular attention should be paid to new-onset disease in a working age person, when there is uncertainty regarding the cause of a disease, or if an individual has worked or is working in a high-risk industry.
The following screening questions may assist in identifying work-related factors and only take a few minutes to ask:
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What kind of work do you do? Please be as specific as possible and tell me exactly what you do at work.
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Do you think your breathing problems are related to your work?
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Do your symptoms get better when you are away from work, such as during weekends and holidays?
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Are you now or have you ever been exposed to fumes, gases or dusts?60
A follow-up full occupational history may be required (Box 4), with the aim of gaining detailed knowledge of the association between the condition and the individual’s work, exposure history, and risk reduction practices, such as provision of personal protective equipment. A comprehensive occupational history is time consuming and requires training and experience to be administered well.
Correct diagnosis of an occupational lung disease is very important because of the potential socio-economic impacts of the diagnosis for the worker and employer. Very few biomarkers are available to support a diagnosis, so there is a high reliance on clinical judgement, supporting physiological evidence and an understanding of occupational exposures. Guidelines produced by expert committees and occupational lung disease textbooks provide overviews of diagnostic strategies for certain conditions. A diagnosis should be established as early as possible and before a recommendation is made for a worker to significantly alter his or her duties or leave the workplace. Referral to an occupational or respiratory physician may be required.
Medical management of occupational lung diseases is generally the same as for non-occupational forms of the condition; however, there are many complex aspects to patient care. All physicians should understand the workers’ compensation system in their region and their role in this system. The current system can be confusing and frustrating for doctors and patients. Regulators also need to ensure that the compensation system stays up to date through recognition of new and emerging occupational exposures and lung diseases.
Conclusion
The identification of occupationally caused lung disease requires health care providers to maintain a high index of suspicion regarding the problem. Like enquiring about tobacco use, consideration of occupational factors should be a routine component of all health assessments. Identification of an occupational cause of lung disease will significantly influence patient management and has implications for coworkers who may also be at risk of the same disease.
Occupational exposures contribute significantly to the burden of respiratory disease. However, much remains unknown regarding the occupational lung diseases which are occurring in Australia. Current data sources, such as workers’ compensation statistics, provide little insight into the problem and are insufficient to target prevention activities. There is a pressing need to gather systematic data on the causes, prevalence, incidence and impact of occupational lung diseases, such as through a national occupational disease registry. Increasing knowledge, including monitoring trends of disease and rapidly identifying emerging issues, will improve management for patients who have developed lung disease because of their work, and will hopefully lead to effective preventive strategies.
Box 1 – Relationship of asthma to the workplace

Reproduced with permission from the Royal Australian College of General Practitioners from Hoy RF, Abramson MJ, Sim MR. Work related asthma - diagnosis and management. Aust Fam Physician 2010; 39: 39-42. Available at https://www.racgp.org.au/download/documents/AFP/2010/Jan-Feb/201001hoy.pdf. * Groups are not mutually exclusive.
Box 2 – Selected occupational interstitial lung diseases, causes and example occupations
|
Agent |
Example occupations |
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|
|
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|
Pneumoconiosis |
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|
Asbestos |
Asbestos waste handler, carpenter, construction worker, electrician, mechanic, miner, railway worker, shipyard worker |
||||||||||||||
|
Coalmine dust |
Coalminer |
||||||||||||||
|
Silica |
Benchtop fabricator, ceramics worker, miner, quarry worker, stonemason, sandblaster, tunneller |
||||||||||||||
|
Talc |
Talc miner and miller |
||||||||||||||
|
Kaolin |
Ceramics manufacturer |
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|
Hypersensitivity pneumonitis |
|||||||||||||||
|
Bacteria |
Compost worker, farmer, machinist, mushroom worker, swimming pool/spa worker |
||||||||||||||
|
Fungi |
Cheese worker, mushroom worker, tobacco grower, woodworker |
||||||||||||||
|
Animal proteins |
Bird breeder, laboratory worker, textile worker |
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|
Low molecular weight chemicals |
Dental technician, painter, plastic industry, polyurethane foam worker, yacht manufacturer |
||||||||||||||
|
Granulomatous lung disease |
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|
Beryllium |
Aerospace industry worker, electronics worker, electronics/computer parts recycler |
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|
Cobalt |
Diamond polisher, grinder operator, industrial tool sharpener |
||||||||||||||
|
Aluminium |
Aircraft industry worker, chemist, metal recycler |
||||||||||||||
|
Other interstitial disorders |
|||||||||||||||
|
Indium tin oxide |
Manufacture and recycling liquid crystal displays |
||||||||||||||
|
Acramin (organising pneumonia) |
Textile worker |
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|
Nylon flock |
Textile worker |
||||||||||||||
|
Mineral oils (lipoid pneumonia) |
Mill operator, painter |
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|
|
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|
References: Litow et al;30 Newman Taylor A, Cullinan P, Blanc P, Pickering A, editors. Parkes’ occupational lung disorders. 4th ed. Boca Raton: Boca Raton, 2016; Hendrick DJ, Burge PS, Beckett WS, Churg A, editors. Occupational disorders of the lungs: recognition, management and prevention. London: WB Saunders, 2002. |
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Box 3 – Relative risks of lung cancer in different occupational exposures and occupations58

PAH = polyaromatic hydrocarbons. * Indicates a dose–response relationship and synergistic effect of concurrent tobacco exposure.
Box 4 – Key elements of an occupational history
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|
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|
Employment
|
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|
|
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|
Reproduced with permission from Taiwo OA, Mobo BH Jr, Cantley L. Recognizing occupational illnesses and injuries. Am Fam Physician 2010; 82: 169-174. |
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Competing interests
No relevant disclosures.
References
- Walters GI, McGrath EE, Ayres JG. Audit of the recording of occupational asthma in primary care. Occup Med (Lond) 2012; 62: 570-573.
- Australian Safety and Compensation Council. Occupational respiratory diseases in Australia. Canberra: Commonwealth of Australia, 2006. https://www.safeworkaustralia.gov.au/doc/occupational-respiratory-diseases-australia-0 (accessed June 2017).
- Tarlo SM, Balmes J, Balkissoon R, et al. Diagnosis and management of work-related asthma: American College of Chest Physicians Consensus Statement. Chest 2008; 134(3 Suppl): 1S-41S.
- Sama SR, Milton DK, Hunt PR, et al. Case-by-case assessment of adult-onset asthma attributable to occupational exposures among members of a health maintenance organization. J Occup Environ Med 2006; 48: 400-407.
- Toren K, Blanc PD. Asthma caused by occupational exposures is common - a systematic analysis of estimates of the population-attributable fraction. BMC Pulm Med 2009; 9: 7.
- Johnson A, Toelle BG, Yates D, et al. Occupational asthma in New South Wales (NSW): a population-based study. Occup Med (Lond) 2006; 56: 258-262.
- Elder D, Abramson M, Fish D, et al. Surveillance of Australian workplace Based Respiratory Events (SABRE): notifications for the first 3.5 years and validation of occupational asthma cases. Occup Med (Lond) 2004; 54: 395-399.
- Vandenplas O. Socioeconomic impact of work-related asthma. Expert Rev Pharmacoecon Outcomes Res 2008; 8: 395-400.
- Anees W, Moore VC, Burge PS. FEV1 decline in occupational asthma. Thorax 2006; 61: 751-755.
- Malo JL, Tarlo SM, Sastre J, et al. An official American Thoracic Society Workshop Report: presentations and discussion of the fifth Jack Pepys Workshop on Asthma in the Workplace. Comparisons between asthma in the workplace and non-work-related asthma. Ann Am Thorac Soc 2015; 12: S99-S110.
- Tarlo SM, Lemiere C. Occupational asthma. N Engl J Med 2014; 370: 640-649.
- Hoy RF, Burgess JA, Benke G, et al. Occupational exposures and the development of new-onset asthma: a population-based cohort study from the ages of 13 to 44 years. J Occup Environ Med 2013; 55: 235-239.
- Fritschi L, Crewe J, Darcey E, et al. The estimated prevalence of exposure to asthmagens in the Australian workforce, 2014. BMC Pulm Med 2016; 16: 48.
- Vandenplas O, Dressel H, Nowak D, et al. What is the optimal management option for occupational asthma? Eur Respir Rev 2012; 21: 97-104.
- Landrigan PJ, Lioy PJ, Thurston G, et al. Health and environmental consequences of the world trade center disaster. Environ Health Perspect 2004; 112: 731-739.
- Brooks SM. Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures. Chest 1985; 88: 376.
- Tarlo SM. Irritant-induced asthma in the workplace. Curr Allergy Asthma Rep 2014; 14: 406.
- Henneberger PK, Redlich CA, Callahan DB, et al. An official American Thoracic Society statement: work-exacerbated asthma. Am J Respir Crit Care Med 2011; 184: 368-378.
- Fishwick D. Work aggravated asthma; a review of the recent evidence. Br Med Bull 2014; 110: 77-88.
- Hoy R. Work-related laryngeal syndromes. Curr Opin Allergy Clin Immunol 2012; 12: 95-101.
- Hoy RF, Ribeiro M, Anderson J, et al. Work-associated irritable larynx syndrome. Occup Med (Lond) 2010; 60: 546-551.
- Blanc PD, Toren K. Occupation in chronic obstructive pulmonary disease and chronic bronchitis: an update. Int J Tuberc Lung Dis 2007; 11: 251-257.
- Ryu JY, Sunwoo YE, Lee SY, et al. Chronic obstructive pulmonary disease (COPD) and vapors, gases, dusts, or fumes (VGDF): a meta-analysis. COPD 2015; 12: 374-380.
- Kraim-Leleu M, Lesage FX, Drame M, et al. Occupational risk factors for COPD: a case-control study. PLoS One 2016; 11: e0158719.
- Bang KM. Chronic obstructive pulmonary disease in nonsmokers by occupation and exposure: a brief review. Curr Opin Pulm Med 2015; 21: 149-154.
- De Matteis S, Jarvis D, Hutchings S, et al. Occupations associated with COPD risk in the large population-based UK Biobank cohort study. Occup Environ Med 2016; 73: 378-384.
- Kreiss K, Gomaa A, Kullman G, et al. Clinical bronchiolitis obliterans in workers at a microwave-popcorn plant. N Engl J Med 2002; 347: 330-338.
- Holden VK, Hines SE. Update on flavoring-induced lung disease. Curr Opin Pulm Med 2016; 22: 158-164.
- Coultas DB, Zumwalt RE, Black WC, et al. The epidemiology of interstitial lung diseases. Am J Respir Crit Care Med 1994; 150: 967-972.
- Litow FK, Petsonk EL, Bohnker BK, et al. Occupational interstitial lung diseases. J Occup Environ Med 2015; 57: 1250-1254.
- Zosky GR, Hoy RF, Silverstone EJ, et al. Coal workers’ pneumoconiosis: an Australian perspective. Med J Aust 2016; 204: 414-418.
- Smith DR, Leggat PA. 24 years of pneumoconiosis mortality surveillance in Australia. J Occup Health 2006; 48: 309-313.
- Si S, Carey RN, Reid A, et al. The Australian Work Exposures Study: prevalence of occupational exposure to respirable crystalline silica. Ann Occup Hyg 2016; 60: 631-637.
- Cooper JH, Johnson DL, Phillips ML. Respirable silica dust suppression during artificial stone countertop cutting. Ann Occup Hyg 2015; 59: 122-126.
- Matar E, Frankel A, Blake LKM, et al. Complicated silicosis resulting from occupational exposure to engineered stone products. Med J Aust 2017; 206: 385-386.
- Pushnoy L. Outbreak of silicosis in Israel. EU-Israel Workshop on issues associated with silica and artificial stone. 28 Jan 2015; Bilbao, Spain. https://osha.europa.eu/en/tools-and-publications/seminars/eu-israel-workshop-on-issues-associated-with-silica-and-artificial-stone (accessed June 2017).
- Musk AW, de Klerk NH, Brims FJH. Asbestos-related non-malignant pleural disease and mesothelioma. In: Newman Taylor A, Cullinan P, Blanc P, Pickering A, editors. Parkes’ occupational lung disorders. 4th ed. Boca Raton: CRC Press, 2016: 171-187.
- Safe Work Australia. Asbestos. https://www.safeworkaustralia.gov.au/asbestos (accessed Aug 2017).
- Brims FJ, Murray CP, de Klerk N, et al. Ultra-low-dose chest computer tomography screening of an asbestos-exposed population in Western Australia. Am J Respir Crit Care Med 2015; 191: 113-116.
- Murray CP, Wong PM, Teh J, et al. Ultra low dose CT screen-detected non-malignant incidental findings in the Western Australian Asbestos Review Program. Respirology 2016; 21: 1419-1424.
- Musk AW, de Klerk N, Brims F. Mesothelioma in Australia: a review. Med J Aust 2017; 207: 449-452.
- Hillerdal G, Lindgren A. Pleural plaques: correlation of autopsy findings to radiographic findings and occupational history. Eur J Respir Dis 1980; 61: 315-319.
- Paris C, Thierry S, Brochard P, et al. Pleural plaques and asbestosis: dose- and time-response relationships based on HRCT data. Eur Respir J 2009; 34: 72-79.
- Weill D, Dhillon G, Freyder L, et al. Lung function, radiological changes and exposure: analysis of ATSDR data from Libby, MT, USA. Eur Respir J 2011; 38: 376-383.
- Broderick A, Fuortes LJ, Merchant JA, et al. Pleural determinants of restrictive lung function and respiratory symptoms in an asbestos-exposed population. Chest 1992; 101: 684-691.
- Clin B, Paris C, Ameille J, et al. Do asbestos-related pleural plaques on HRCT scans cause restrictive impairment in the absence of pulmonary fibrosis? Thorax 2011; 66: 985-991.
- de Klerk NH, Cookson WOC, Musk AW, et al. Natural-history of pleural thickening after exposure to crocidolite. Br J Ind Med 1989; 46: 461-467.
- Cotes JE, King B. Relationship of lung function to radiographic reading (ILO) in patients with asbestos related lung disease. Thorax 1988; 43: 777-783.
- American Thoracic Society. Diagnosis and initial management of nonmalignant diseases related to asbestos. Am J Respir Crit Care Med 2004; 170: 691-715.
- World Health Organization. Environmental and occupational cancers. Fact sheet no. 350, March 2011. Geneva: WHO, 2011.
- Fritschi L, Driscoll T. Cancer due to occupation in Australia. Aust N Z J Public Health 2006; 30: 213-219.
- Markowitz SB, Levin SM, Miller A, et al. Asbestos, asbestosis, smoking, and lung cancer. New findings from the North American insulator cohort. Am J Respir Crit Care Med 2013; 188: 90-96.
- de Klerk NH, Musk B, Armstrong B, et al. Crocidolite, radiographic asbestosis and subsequent lung cancer. Br J Ind Med 1991; 48: 412-417.
- IARC Working Group on the Evaluation of Carcinogenic Risk to Humans. Diesel and gasoline engine exhausts and some nitroarenes. IARC Monogr Eval Carcinog Risks Hum 2014; 105: 9-699.
- Peters S, Carey RN, Driscoll TR, et al. The Australian Work Exposures Study: prevalence of occupational exposure to diesel engine exhaust. Ann Occup Hyg 2015; 59: 600-608.
- Brims F, McWilliams A, Fong K. Lung cancer screening in Australia: progress or procrastination? Med J Aust 2016; 204: 4-5.
- Australian Government Department of Health Standing Committee on Screening. Position statement: lung cancer screening using low-dose computed tomography. 2015. http://www.cancerscreening.gov.au/internet/screening/publishing.nsf/Content/lung-cancer-screening (accessed July 2017).
- Cancer Australia. Risk factors for lung cancer: an overview of the evidence. Sydney: Cancer Australia, 2014. https://canceraustralia.gov.au/publications-and-resources/cancer-australia-publications/risk-factors-lung-cancer-overview-evidence (accessed Aug 2017).
- Heffler E, Pizzimenti S, Guida G, et al. Prevalence of over-/misdiagnosis of asthma in patients referred to an allergy clinic. J Asthma 2015; 52: 931-934.
- Newman LS. Occupational illness. N Engl J Med 1995; 333: 1128-1134.
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