Occupational asthma

Abstract

Work-related asthma is highly prevalent and represents a significant societal and financial burden worldwide. This State of the Art series article explores the epidemiology, clinical features, diagnosis and management of occupational asthma (OA), which comprises sensitiser-induced asthma and irritant-induced asthma (IIA). Sensitiser-induced OA is the development of asthma through sensitisation to a substance in the workplace. OA is largely underdiagnosed, and its clinical manifestations are non-specific, which makes its diagnosis challenging. Early and accurate diagnosis of OA through comprehensive testing is primordial to avoid unwarranted removal from exposure and to allow early management of confirmed cases. Despite optimal management, up to 70% of patients with OA will have persistent asthma several years after diagnosis. IIA classically refers to the development of de novo asthma acutely following an intense exposure to an irritant agent. However, some cases of IIA following multiple high-level exposures or a chronic low-dose exposure have been reported.

Progress in Occupational Asthma

“…Work-related asthma is the term used to define asthma worsened by the workplace and encompasses both occupational asthma (OA) and work-exacerbated asthma [3][4][5][6]. OA is de novo asthma induced by either sensitization to a specific substance or a chemical at work, which is termed sensitizer-induced OA (SI-OA) or by exposure to high concentrations of an inhaled irritant found in the workplace, which is termed irritant-induced OA (II-OA) [3][4][5]7]. Sensitizing agents that cause OA are classified into high-molecular weight (HMW) (glyco) proteins (>10 kD) from vegetable or animal origins and low-molecular-weight (LMW) agents (<1 kD) which include chemicals, metals and wood dust [8].…”

“…Sensitizing agents that cause OA are classified into high-molecular weight (HMW) (glyco) proteins (>10 kD) from vegetable or animal origins and low-molecular-weight (LMW) agents (<1 kD) which include chemicals, metals and wood dust [8]. If SI-OA has a latency period of exposure and sensitization before the symptoms begin, II-OA includes both an acute onset form, the "reactive airways dysfunction syndrome" (RADS) where asthma symptoms start 24 h after a single high level exposure to an inhaled irritant and delayed onset forms with latency where asthma develops insidiously over time after either an acute exposure (e.g., World Trade Center rescue workers) or after repeated lower level exposures (e.g., professional cleaners), also called "low-dose RADS" [3,7].Work-exacerbated asthma implies a preexisting or concurrent asthma that is worsened by exposure to non-specific stimuli at the work, but not caused by it [3,4].…”

“…The diagnosis of OA is difficult, requiring confirmation for the diagnosis of asthma, plus evidence that the asthma was caused by workplace conditions [7]. An accurate diagnosis of OA is a very important viewing of the significant health consequences for affected workers, but also the substantial socio-economic impact [3,5,7].…”

“…Asthma is a heterogeneous disease characterized by a chronic airway inflammation and defined by recurring episodes of wheezing, shortness of breath, chest tightness and coughing that vary over time and in intensity, associated with variable expiratory flow limitation [1]. Approximately 360 million people worldwide are affected and it is thought that up to 25% of adult-onset asthma is work-related [2,3].…”

The effectiveness of removal from exposure and reduction of exposure for managing occupational asthma: Summary of an updated Cochrane systematic review

“…Sensitizerinduced asthma is characterized by an immunologic-mediated sensitization to a workplace agent and can result from exposure to either high-molecular-weight (HMW) agents (e.g., animal or vegetable proteins) or low-molecular-weight (LMW) agents (e.g., diisocyanates, plicatic acid from western red cedar). 2 Irritant-induced OA has typically been characterized by onset shortly after high-level exposure to respiratory irritants (e.g., chlorine gases), 3 although it might also result from chronic low-to moderate-level irritant exposures. 4 Over 300 workplace agents are known to cause OA and can occur in a variety of occupations and industries.…”