Updated: Nov 15, 2020
Exposures at work may explain the illness of more than one in ten adults with asthma, COPD, pulmonary fibrosis or pneumonia.
It is an old and well-known knowledge that certain lung diseases, such as silicosis and asbestosis, are caused by occupational exposure to stone dust (quartz dust) and asbestos. In recent years, we have gained increased knowledge that various forms of occupational exposure significantly increase the risk of other lung diseases, such as chronic obstructive pulmonary disease (COPD), pulmonary fibrosis and lobular pneumonia.
A group of occupational, pulmonary, and allergy practitioners from the United States, South Africa, Kazakhstan, Italy, Switzerland, the United Kingdom, France, Denmark, and Sweden, on behalf of the European Respiratory Society (ERS) and the American Thoracic Society (ATS), produced a literature review on the quantitative the importance of workplace exposures for the occurrence of non-malignant lung disease .
The document, which is an official position of the two companies, was published in June 2019 in one of the internationally leading lung medical journals . The document concludes that a significant proportion of chronic non-malignant lung diseases have their origin in workplace exposures.
The document's conclusions are based on calculations of the disease burden in a population (population attributable fraction (PAF)). The underlying assumption in such calculations is that there is a relationship between a certain occupational exposure and an increased risk of a particular disease, such as inorganic dust and COPD. This knowledge comes from studies of relative risks based on well-conducted population studies. From these studies it is possible to calculate the etiological fraction (EF), the disease burden, for the exposed group. For this, the formula EF = (relative risk - 1) / relative risk) is used. To then calculate the disease burden in the entire population of a certain exposure, the etiological fraction is multiplied by the exposure prevalence among the cases from the current population study: PAF = [(relative risk - 1) / relative risk] × case exposure rate] . The burden of illness is usually stated as a percentage, ie the percentage of morbidity that can be attributed to the occupational exposure in question.
It is well-established knowledge that occupational exposure is important for the onset of asthma, and this compilation confirms previous knowledge that about 15 percent (95 percent confidence interval [95KI] 9-22 percent) of all incidental cases of adult asthma are related to occupational exposure. A profession with increased risk is bakers exposed to flour dust. Other risk churches are plastic workers and spray painters that can be exposed to diisocyanates. Nail sculptors are a newly arrived professional group that usually have high exposure to acrylates and thus an increased asthma risk. Chemical process workers and rescue personnel may have an increased asthma risk following exposure to irritating gases such as chlorine gas, ammonia or fire smoke.
Tobacco smoking is the dominant risk factor for COPD. Several compilations of knowledge have led to the conclusion that occupational exposure plays a crucial role in the onset of the disease in 15–20 percent of cases. A previous document from the American Thoracic Society 2010 concluded that, after tobacco smoking, occupational exposure and alpha-1 antitrypsin deficiency, the factors that had the greatest evidence were to increase the risk of COPD . The same document describes that biomass burning is an important risk factor for COPD in a global perspective . The occupational exposure that is associated with an increased risk of COPD applies to a fairly wide group of inorganic dust, gas and smoke. The fact that occupational exposure is an important factor for the occurrence of COPD is confirmed in the current overview, which concludes that a considerable proportion, 14% (95KI 10-18%) of all cases with COPD can be attributed to occupational exposure . A significant proportion of COPD occurs in people who have never been smokers [3, 4]. In these, the importance of other risk factors increases, such as occupational exposure. The overview states that about 31 percent (95KI 18–43 percent) of COPD in non-smokers can be attributed to occupational exposure.
Chronic bronchitis is a symptom diagnosis that is defined by a history of long-term mucosa and can occur with or without COPD, even in people who have never been smokers. The overview states that 13 percent (95KI 6–21 percent) of cases of chronic bronchitis can be attributed to occupational exposure to gas, dust and smoke.
Silicosis and asbestosis are pulmonary fibrosis where it is believed that the etiology is clear: quartz dust and asbestos. The remaining group has various designations - essential pulmonary fibrosis, cryptogenic pulmonary fibrosis or idiopathic pulmonary fibrosis - suggesting that the cause is unknown. However, there are many studies, including from Sweden, which have shown that occupational exposure to tree dust, metals and microorganisms increases the risk of so-called idiopathic pulmonary fibrosis. This is not particularly noteworthy, and the current compilation shows that 26 percent (95KI 10–41 percent) of all idiopathic pulmonary fibrosis can be attributed to occupational exposure.
Several studies, both epidemiological studies and case studies, have shown that exposure to dust, especially metal smoke / welding smoke, increases the risk of pneumonia, especially lobar pneumonia [5, 6]. The epidemiological studies have shown that exposure to metal fumes / welding fumes results in an approximately four to five times increased risk of lobar pneumonia. This means that the etiological fraction in an exposed group, such as welders, is over 50 percent. In the current document, seven cohorts with exposure to metal smoke or welding smoke were reported. The average etiologic fraction in these cohorts regarding exposure to metal smoke / welding smoke and pneumonia was 53 percent. This is not a measure of the burden of disease in the population but of the burden of disease in an exposed group. This means that infectious pneumonia, especially lobular pneumonia, should be perceived as an occupational lung disease among people of working age with exposure to metal smoke / welding smoke. One proposed mechanism is that ionized iron found in welding fumes and on the surface of inorganic dust particles reduces the ability of alveolar macrophages to fight bacteria. There is also evidence from population studies that the broader outcome of infectious pneumonia (community-acquired pneumonia) is related to occupational exposure, and the document states that 10 percent (95KI of 3 to 45 percent) of all pneumonia in the adult population can be attributed to occupational exposure.
Allergic alveolite has well-known causes such as contact with birds or exposure to mold and various microorganisms. The disease is easily confused with other febrile conditions, and the diagnostic challenge is to consider the disease at all when you have a patient at the hospital with recurrent fever and lung infiltration. The current document estimates that about 19 percent (95KI 12-28 percent) can be attributed to workplace exposure.
This disease is usually not associated with exposures at work. However, there are studies showing a relationship between occupational exposure to metals, bioaerosols and organic dust and sarcoidosis disease. In the current document, it is estimated, based on seven studies, that about 30 percent (95KI 17-45 percent) of the sarcoidosis disease can be attributed to occupational exposure, which is a surprisingly high figure.
Occupational exposures must be noted
The current compilation shows that the importance of occupational exposures must be taken into account in the management of patients with chronic lung diseases. The medical profession, both in primary care and in hospital-based care, must to a greater extent demand professional exposures that cause a number of common lung diseases. Of course, this is most relevant for patients of working age, but also high in the age of for example lung fibrosis and COPD. This means that a complete professional history of these patients must be recorded, as the exposure may be many years back in time.
A patient with suspected lung disease caused by occupational exposure may also be a signal that there may be more cases in the workplace.
For the patient in question, it is important that exposure is stopped or minimised, as this can affect prognosis and treatment. For example, ongoing occupational exposure may increase the risk of exacerbations of both asthma and COPD. Therefore, contact with occupational health care and / or occupational and environmental medical clinics is important in these investigations. These bodies can investigate and contribute to actions in the workplace.
The significance of occupational exposures has not been sufficiently noted in the latest version of the National Board of Health and Welfare's "National guidelines for care for asthma and COPD" . This is a shortcoming that should lead to a supplement. Future guidelines for other chronic lung diseases, such as pulmonary fibrosis, should also include the importance of occupational exposure.
As a patient investigating physician, it is important to consider at all whether a patient with lung disease may have an occupational disease. Begin by asking what the patient is working on or has worked with before in life.
+Potential bindings or conflicts: The author was one of the participants in the international constellation who worked out the document in question.
Article written by Kjell Torén, senior professor, chief physician, occupational and environmental medicine, Sahlgrenska University Hospital; occupational and environmental medicine, Department of Community Medicine and Public Health, Department of Medicine, University of Gothenburg
1. Blanc PD, Annesi-Maesano I, Balmes JR, et al. The occupational burden of nonmalignant respiratory diseases. An official American Thoracic Society and European Respiratory Society Statement. Am J Respir Crit Care Med. 2019; 199 (11): 1312-34.
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