Clinical Overview, Appendix A: Occupational Bronchiolitis
Small airways of less than 2 mm in diameter – both membranous and respiratory bronchioles – may be affected by workplace inhalational exposures. The pathogenesis of occupational bronchiolitis likely involves injury to the bronchiolar epithelium, followed by excessive proliferation of granulation tissue during the repair process. This leads to concentric narrowing (constrictive bronchiolitis) or obliteration (obliterative bronchiolitis) of the airway lumen. Acute, high-dose inhalational exposures to a number of toxic workplace agents — classically the oxides of nitrogen and sulfur — are associated with acute or sub-acute obliterative bronchiolitis, often with organizing pneumonia. More insidious onset of work-related bronchiolitis has been linked with exposure to diacetyl and other chemicals used in the manufacture of artificial flavorings. Workers producing microwave popcorn as well as flavor production and upstream flavor chemical manufacturing workers may be at risk [Centers for Disease Control and Prevention 2007]. Military personnel deployed to Iraq and Afghanistan may develop sub-acute bronchiolitis, though the causal agent or agents is uncertain [King et al. 2011]. Fiberglass boat builders working with styrene and other chemicals used in glass-reinforced plastics may develop rapidly progressive obliterative bronchiolitis [Cullinan et al 2013]. Diagnosis of occupational bronchiolitis requires a high index of suspicion, as clinical findings are often nonspecific. A work-related pattern of respiratory symptoms is generally lacking in the sub-acute and chronic forms. As with emphysema, accelerated decline in FEV1 may be seen, often with an elevated residual lung volume and normal diffusion capacity.