Occupational and Environmental Lung Disease

Workplace exposures contribute substantially to the burden of chronic lung disease in adults. Occupational lung diseases contributing to the greatest disease burden, mortality and disability globally include COPD (caused by particulate dusts, vapours, fumes and second-hand tobacco smoke), lung cancer and mesothelioma (commonly due to asbestos), work-related asthma, pneumoconioses (silicosis, coal worker's pneumoconiosis, asbestosis) and occupational infections (pulmonary tuberculosis in silica-exposed and healthcare workers, community-acquired pneumonia). Despite the decrease in per capita disease burden globally over the past two decades, this burden is not shared equitably across regions. It is influenced by rapid economic transition and population growth, unregulated economies, a burgeoning informal sector and inadequate exposure control, as well as poor access to the knowledge and resources to achieve good control of workplace respiratory hazards. Increased physician awareness, diligent disease investigation and regular reporting, as well as ongoing surveillance, will contribute to improved detection and management of occupational lung diseases.

Cite as: Jeebhay MF. The global perspective of occupational lung disease. In: Feary J, Suojalehto H, Cullinan P, eds. Occupational and Environmental Lung Disease (ERS Monograph). Sheffield, European Respiratory Society, 2020; pp. 1–18 [https://doi.org/10.1183/2312508X.10034019].

Sensitiser-induced occupational asthma (OA), like asthma in general, results from the complex interactions between environmental factors and individual susceptibility. Workplace agents causing OA include both high-molecular-weight proteins of animal or vegetal origin that act through a demonstrable IgE-mediated mechanism and low-molecular-weight chemicals for which the immunopathological mechanisms remain poorly elucidated. The diagnostic investigation of OA is based on a stepwise approach that includes a thorough clinical and occupational history, immunological testing, and the assessment of functional parameters and markers of airway inflammation in order to demonstrate the causal relationship between asthma and exposure to a specific workplace agent. Complete and definitive avoidance of exposure to the causative agent remains the optimal treatment, although the rate of full recovery is low, especially when the diagnosis is delayed and the asthma is more severe. The burden of OA is substantial, not only because of its long-term respiratory health consequences but also because of the socioeconomic impact for affected workers, employers and society.

Cite as: Vandenplas O, Lemière C. Sensitiser-induced occupational asthma. In: Feary J, Suojalehto H, Cullinan P, eds. Occupational and Environmental Lung Disease (ERS Monograph). Sheffield, European Respiratory Society, 2020; pp. 34–51 [https://doi.org/10.1183/2312508X.10034119].

Inhalation injuries can cause acute breathlessness within minutes of exposure or be delayed for days or occasionally weeks. Pathologies range from asphyxiation to acute mucosal injury to ulceration, asthma, pulmonary oedema and fibrosis of the airways or lung parenchyma. Some agents exert their toxicity by systemic effects. Exposures may be from natural disasters such as volcanic eruptions, from fires and industrial accidents, or from terrorist and warfare agents. This chapter classifies acute lung injury by the major site of damage, which is where emergency care should be directed, as the exact agent inhaled is often unknown in the acute situation. In addition, irritant-induced asthmas, both acute and chronic, are discussed.

Cite as: Burge S. Acute inhalation injury. In: Feary J, Suojalehto H, Cullinan P, eds. Occupational and Environmental Lung Disease (ERS Monograph). Sheffield, European Respiratory Society, 2020; pp. 70–85 [https://doi.org/10.1183/2312508X.10034319].

Occupational exposures are estimated to account for around one in five cases of hypersensitivity pneumonitis (HP), but making a link between work and disease can be challenging. All working-age patients with unexplained interstitial lung disease (ILD) should routinely be asked whether they have work-related symptoms and screened for exposures to common causes. Occupational HP frequently mimics other common respiratory conditions, particularly asthma, recurrent chest infections and idiopathic forms of ILD (particularly nonspecific interstitial pneumonia and IPF). In some cases, establishing a diagnosis is difficult, requiring careful evaluation of all available clinical data, ideally by an experienced multidisciplinary team. The key aims of management are early identification of the cause and, wherever possible, maintaining employment through workplace interventions that prevent further exposure. Clinical outcomes following cessation of exposure are highly variable but are generally much better for patients without established fibrosis. In addition to the management of the individual, it is also important to ensure that any other affected co-workers are identified as soon as possible and that control measures are reviewed to prevent further cases of disease.

Cite as: Barber CM, Barnes H. Occupational hypersensitivity pneumonitis. In: Feary J, Suojalehto H, Cullinan P, eds. Occupational and Environmental Lung Disease (ERS Monograph). Sheffield, European Respiratory Society, 2020; pp. 104–124 [https://doi.org/10.1183/2312508X.10034519].

Pleural disease resulting from asbestos exposure is a consequence of the physical characteristics of the fibres that determine their deposition and persistence in the subpleural alveoli resulting in both benign and malignant changes. The diameter of fibres permits them to enter the alveoli in the laminar flow of peripheral airways, but their long axis prevents their phagocytosis by macrophages that are responsible for clearance of the non-conducting airspaces of the lungs. The value of asbestos in industry is a result of its indestructability. The consequent persistence of asbestos fibres in the lung promotes ongoing inflammatory responses (pleural plaques, benign asbestos pleural effusion and diffuse pleural fibrosis) and neoplasia (malignant pleural mesothelioma).

Cite as: Musk AW, Hui J. Non-malignant pleural disease from asbestos and malignant pleural mesothelioma. In: Feary J, Suojalehto H, Cullinan P, eds. Occupational and Environmental Lung Disease (ERS Monograph). Sheffield, European Respiratory Society, 2020; pp. 141–149 [https://doi.org/10.1183/2312508X.10034719].

Coal mine dust lung diseases (CMDLDs) are entirely preventable, yet they continue to occur and are on the rise in some countries. While most physicians think of coal worker's pneumoconiosis as the sole manifestation of coal mine dust exposure, it is now well known that respirable coal mine dust causes a broad spectrum of respiratory diseases, including obstructive lung diseases such as chronic bronchitis and emphysema, as well as pulmonary fibrosis. In order to make an accurate diagnosis and determine the risk of disease progression, physicians must obtain a detailed occupational and exposure history from coal mine workers who present with lung disease. CMDLD is incurable and difficult to treat. Therefore, the greatest focus should be placed on primary prevention by limiting coal mine dust exposure, followed by secondary prevention through periodic medical surveillance with chest imaging and physiological screening.

Cite as: Go LH, Cohen RA. Coal mine dust lung disease. In: Feary J, Suojalehto H, Cullinan P, eds. Occupational and Environmental Lung Disease (ERS Monograph). Sheffield, European Respiratory Society, 2020; pp. 176–189 [https://doi.org/10.1183/2312508X.10034919].

Inhaled cotton dust remains an important workplace hazard globally and is associated with the risks of byssinosis and accelerated lung function decline. The former is typified by chest tightness that is worse on the first working day and improves as the week progresses, while the latter may lead to airways obstruction. Traditional industrial activities such as waste disposal and relatively newer activities such as the handling of pre-combustion biomass fuels have both been associated with lung problems. Mill fever, Pontiac fever (probably predominantly caused by a noninfectious response to Legionella pneumophilia and possibly endotoxin) and organic dust toxic syndrome are a set of similar systemic responses to microbiological agents inhaled at work. Exposures to metal and polymer fume produce similar preventable systemic responses, normally associated with fever, although the mechanisms are yet to be fully elucidated. Organising pneumonia is an unusual condition that has been linked to various occupational jobs including textile sprayers and biocide users. Thus, bioaerosols, metals and polymers are associated with a variety of potentially preventable short- and longer-latency respiratory illnesses.

Cite as: Fishwick D. Cotton, other bioaerosols, inhalation fevers and occupational organising pneumonia. In: Feary J, Suojalehto H, Cullinan P, eds. Occupational and Environmental Lung Disease (ERS Monograph). Sheffield, European Respiratory Society, 2020; pp. 211–226 [https://doi.org/10.1183/2312508X.10035119].

Welding exposes the welder and potentially others in the workplace to particulate metal fume and secondary pollutant gases such as NO_x, CO and ozone. There is agreement that welding increases the risk of chronic productive cough, pneumonia and lung cancer, and may cause occupational asthma. There has been a long-standing debate about whether welding causes an accelerated decline in lung function, but recent research and systematic reviews suggest that this is not the case; rather, the long-term effect of welding at high concentrations of fume exposure is a form of pulmonary fibrosis, possibly an occupational respiratory bronchiolitis leading to desquamative interstitial pneumonia. There is a synergistic effect of smoking and welding on nonmalignant respiratory disease, in particular accelerated lung function decline, and therefore welders should be strongly encouraged not to smoke.

Cite as: Cosgrove MP. Interstitial lung disease in welders. In: Feary J, Suojalehto H, Cullinan P, eds. Occupational and Environmental Lung Disease (ERS Monograph). Sheffield, European Respiratory Society, 2020; pp. 238–251 [https://doi.org/10.1183/2312508X.10035319].

Diving is usually associated with immersion but can include exposure to elevated pressure in a dry environment. The density of compressed gas increases the work of breathing and the elimination of CO₂ limits exercise capacity. Respiratory epithelium is often exposed to toxic partial pressures of O₂. Immersion redistributes blood and increases the risk of pulmonary oedema, even in apparently healthy individuals. Symptoms in different diving disorders are often very similar, so the equipment used and the circumstances in which a problem occurs frequently contribute significantly towards making a confident diagnosis. A diver can also suffer from a non-diving illness, which should always be included in the differential diagnosis. The most important aspects of respiratory fitness to dive depend on adequate gas flow and exchange to support all reasonably foreseeable physical activity, plus free movement of gas around the respiratory tract to avoid distortion and, in particular, over-distension and rupture of structures which, if damaged, lead to incapacitation or death.

Cite as: Glover M. Diving. In: Feary J, Suojalehto H, Cullinan P, eds. Occupational and Environmental Lung Disease (ERS Monograph). Sheffield, European Respiratory Society, 2020; pp. 266–282 [https://doi.org/10.1183/2312508X.10035519].

Air pollution levels continue to be high worldwide, vary greatly within and between countries, and contribute to a substantial burden of disease. There is convincing evidence that long-term exposure to air pollution adversely affects numerous health outcomes. This chapter presents the recent and growing epidemiological evidence for its effect on respiratory health, focusing on asthma and lung function. Further research should prioritise the pollutant mixtures most detrimental to health and identify the most appropriate health protection measures. Respiratory health is also influenced by outdoor pollen and mould exposures, which are not commonly monitored or regulated by standards. Climate change and interactions with air pollutants influence the growing pattern of outdoor allergens, affecting allergic and asthmatic symptom onset, duration and severity. These changes occur gradually but can result in acute outbreaks of disease, such as thunderstorm-related asthma. While waiting for the implementation of effective controls, there are some limited actions individuals can take to reduce their exposure to air pollution and outdoor allergens.

Cite as: Fuertes E, Brauer M. The outdoor environment. In: Feary J, Suojalehto H, Cullinan P, eds. Occupational and Environmental Lung Disease (ERS Monograph). Sheffield, European Respiratory Society, 2020; pp. 301–316 [https://doi.org/10.1183/2312508X.10035719].