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letter
. 2019 Dec 15;200(12):1558–1559. doi: 10.1164/rccm.201907-1288LE

Occupational Burden in Chronic Respiratory Disease: Call for Recognition, Training, and Data Capture

Cathryn T Lee 1,*, Mary E Strek 1
PMCID: PMC6909831  PMID: 31343258

To the Editor:

We read with great interest the recently published work entitled “The Occupational Burden of Nonmalignant Respiratory Diseases. An Official American Thoracic Society and European Respiratory Society Statement” (1). In this statement, Blanc and colleagues summarize the literature regarding the contribution of occupational exposures to a variety of chronic lung disorders. The authors pool previously published data to derive the population-attributable fraction (PAF) and estimate the contribution of meaningful exposures to individual pulmonary diseases. The proportion of patients with interstitial lung disease (ILD) and occupational exposures was of particular interest to us. In patients with idiopathic pulmonary fibrosis (IPF), the pooled PAF was highest for vapors, gas, dust, or fumes (at 26%), followed by metal dusts or fumes (8%), wood dusts (4%), and silica (3%). The PAF for work-related exposures was 19% for hypersensitivity pneumonitis (HP) and 30% for sarcoidosis. Although they were not addressed in the statement, inhalational exposures and environmental antigens have been known to stimulate the immune system and contribute to the development of autoimmune disease, most notably in rheumatoid arthritis from cigarette smoking and coal dust exposures, as well as systemic sclerosis from inhalation of silica particles (2, 3). At our tertiary referral center, systematic history taking has elicited inhalational exposures in the majority of patients with ILD, not only in those with IPF and HP but also in patients with connective tissue disease–related ILD and unclassifiable ILD (4).

Although occupational asthma has long been known to constitute a significant minority of all-comers with adult asthma, and workplace exposures are now recognized to cause chronic obstructive pulmonary disease, especially in nonsmokers, the environmental antigens that are usually believed to be causative in ILD, such as birds and mold, are often attributed to exposures in the home (5, 6). In contrast, the relatively high PAFs for occupational exposures in IPF and HP reported in this statement correlate with our own experience in our clinic, where we frequently see firefighters, construction workers, and metalworkers who have received multidisciplinary diagnoses of IPF or HP. A systematic review at our center showed that 45% of patients with IPF and 48% of patients with HP had a self-reported history of an exposure classified as occupational. Beyond the diagnoses mentioned in the consensus statement, 41% of the patients in that review had a connective tissue disease–related ILD and a history of potentially relevant work-related exposures. In addition, we see patients across all ILD diagnoses who are employed in workplaces that are not typically thought of as high risk, such as schools, hospitals, and hotels, which may be old, poorly maintained, or frequently remodeled, and thus are a potential source of dust and microbial antigen exposure.

The American Thoracic Society/European Respiratory Society statement is an important step toward increasing the pulmonary community’s understanding of the role of inhalational exposures in chronic nonmalignant lung diseases. It is likely that increased awareness will confirm our personal clinical observation that the occupational burden in diffuse parenchymal lung disease is greater than was previously recognized and may extend to patients with all types of ILD, including that associated with autoimmunity. The data support the routine assessment of exposures in a systematic and comprehensive fashion in patients with chronic lung disease and necessitate formal training in occupational medicine for all pulmonary fellows and additional education for current clinical practitioners. For the research community, the identification of inhalational exposures in the home and workplace provides insight into disease pathogenesis and suggests future investigations, but is dependent on the data being elicited and captured in multicenter studies and national registries. The goal of this training and research should be effective interventions to modify the disease course, with prevention of disease onset being the ultimate holy grail.

Footnotes

Originally Published in Press as DOI: 10.1164/rccm.201907-1288LE on July 25, 2019

Author disclosures are available with the text of this letter at www.atsjournals.org.

References

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