Occupational asthma has become the most prevalent occupational lung disease in developed countries At present, about 200 agents have been implicated in causing occupational asthma in the workplace These agents can be divided into two categories by their mechanism of action: immunological and nonimmunological Immunological causes can be further divided into those that induce asthma through an immunoglobulin E (IgE)-dependent mechanism, and those that induce asthma through a non-IgE-dependent mechanism In the latter category, specific IgE antibodies are found only in a small percentage of the patients with proven disease, even though the clinical picture is compatible with an allergic reaction The immunological mechanism(s) responsible for these agents has yet to be identified The best known example of nonimmunological asthma is Reactive Airways Dysfunction Syndrome (RADS) or irritant-induced asthma In this review, examples of types of agents causing occupational asthma are discussed and a compendium table of aetiological agents is given

https://erj.ersjournals.com/content/erj/7/2/346.full.pdf

Aetiological agents in occupational asthma

Five patients with respiratory disorders associated with hard metal exposure are described. In four patients electron microprobe analysis of bronchoalveolar lavage cells or lung tissue was used to show tungsten and other hard-metal components. Three patients had interstitial pneumonia and fibrosis with unusual multinucleate giant cells. Electron microscopy showed that the giant cells comprised both type II alveolar epithelial cells and alveolar macrophages. The multinucleate macrophages formed a distinctive feature of the bronchoalveolar lavage material but the multinucleate alveolar epithelial lining cells were evident only in lung tissue. The other two patients both suffered from work-related asthma, one of whom also had pulmonary opacities. Bronchial provocation tests in these patients supported the diagnosis of hard-metal-induced asthma and implicated cobalt as the agent responsible.

https://thorax.bmj.com/content/thoraxjnl/38/2/119.full.pdf

Interstitial lung disease and asthma in hard-metal workers: bronchoalveolar lavage, ultrastructural, and analytical findings and results of bronchial provocation tests.

Twelve persons working in the manufacture or grinding of tungsten carbide developed a progressive diffuse interstitial pneumonia, characterized clinically by nonproductive cough and by dys...

Diffuse interstitial lung disease in tungsten carbide workers.

Occupational Asthma from Cobalt Sensitivity in Workers Exposed to Hard Metal Dust

Background Worldwide, there is rigorous scientific activity concerning the further development of work safety regulations involving airway-sensitizing substances. Technical directives on hazardous substances are enforced in several countries and are being continuously updated. The European Union has established a code for several occupational substances, now labeled R 42 (‘‘may cause sensitization by inhalation’’). Methods We present an overview of the literature dealing with allergic occupational asthma. The literature was selected according to criteria of study design and diagnostic test methods. Approximately 300 publications were reviewed including both epidemiological studies and individual case reports. Results Airway sensitizers are systematically arranged and separately listed according to chemicals and their origin from animals, plants, and microorganisms. The clinical data as well as threshold limit values (TLV) and R 42 labeling of 250 airway-sensitizing substances are presented. Conclusions The most common sensitizing substances causing occupational asthma were dust of cereal flours, enzymes, natural rubber latex, laboratory animals as well as low molecular substances such as isocyanates and acid anhydrides. Am. J. Ind. Med. 38:164‐218, 2000. fl 2000 Wiley-Liss, Inc.

/pdf/occupational-airway-sensitizers-an-overview-on-the-23gch7qtp0.pdf

Howard C. Bruckner

Papers

Extrinsic asthma in a tungsten carbide worker.

Poisoning by parathion.