Occupational hypersensitivity pneumonitis: an EAACI position paper

Abstract

The aim of this document was to provide a critical review of the current knowledge on hypersensitivity pneumonitis caused by the occupational environment and to propose practical guidance for the diagnosis and management of this condition. Occupational hypersensitivity pneumonitis (OHP) is an immunologic lung disease resulting from lymphocytic and frequently granulomatous inflammation of the peripheral airways, alveoli, and surrounding interstitial tissue which develops as the result of a non-IgE-mediated allergic reaction to a variety of organic materials or low molecular weight agents that are present in the workplace. The offending agents can be classified into six broad categories that include bacteria, fungi, animal proteins, plant proteins, low molecular weight chemicals, and metals. The diagnosis of OHP requires a multidisciplinary approach and relies on a combination of diagnostic tests to ascertain the work relatedness of the disease. Both the clinical and the occupational history are keys to the diagnosis and often will lead to the initial suspicion. Diagnostic criteria adapted to OHP are proposed. The cornerstone of treatment is early removal from exposure to the eliciting antigen, although the disease may show an adverse outcome even after avoidance of exposure to the causal agent.

Epidemiology of occupational hypersensitivity pneumonitis; reports from the SWORD scheme in the UK from 1996 to 2015

“…Although it is not possible to establish the reasons for this increase from the SWORD data, possible explanations include the increased use of water-soluble MWF, an increased number of cases found during outbreak investigations17 18 and an increased awareness among reporting clinicians. This temporal change in proportionate causation from the agricultural to metalworking sectors has not been noted in other European reporting schemes 12 13. The majority of reported cases of MWF-HP have occurred in workers manufacturing components for cars and airplanes, as time-limited clusters of disease 17.…”

“…International comparisons are inherently difficult,8 and the reasons for this difference are not apparent from our study. It is clear however that the UK estimate of the incidence of OHP is within the 0.4–2.7 per million workers range that has been estimated by other reporting schemes from Australia,9 Catalonia,10 the Czech Republic,12 France and Germany 13. A higher estimate of 12.2 per million workers comes from the Finnish National Register,11 which may relate to the design of reporting schemes in different countries.…”

Biological and chemical hazards in water-mix metalworking fluids and mists

“…It is a result of immunologically mediated inflammation of the lung parenchyma i.e., alveoli and surrounding interstitial tissues (Lacasse, Girard and Cromier, 2012;Quirce et al, 2016). The inflammation is the result of a non-IgE mediated response to complex antigens (Ag) which are not easily broken down in the body (i.e., they bio-persist) (Quirce et al, 2016).…”

“…It is a result of immunologically mediated inflammation of the lung parenchyma i.e., alveoli and surrounding interstitial tissues (Lacasse, Girard and Cromier, 2012;Quirce et al, 2016). The inflammation is the result of a non-IgE mediated response to complex antigens (Ag) which are not easily broken down in the body (i.e., they bio-persist) (Quirce et al, 2016). These Ag's are typically 1 -5 µm in diameter (e.g., bacterial and fungal spores) and their continued presence in the lung leads to an immunological sensitisation response (Lacasse, Girard and Cormier 2012;Baur, Fischer and Budnik, 2015).…”

“…Ag's recognised in the development of HP include bacteria, mould, yeast, proteins, and fungal spores (Quirce et al, 2016). Additionally, some chemicals such as isocyanates, dyes and inks can act as haptens (chemicals which react with proteins in the body converting them to antigens) to induce the disease progression (Cochrane et al, 2015).…”