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Biological Risk Assessment
Published in Martha J. Boss, Dennis W. Day, Air Sampling and Industrial Hygiene Engineering, 2020
Inhalation of spores from fungus-like bacteria, called actinomycetes, and from molds can cause a lung disease called hypersensitivity pneumonitis. This condition is often associated with specific occupations. Hypersensitivity pneumonitis develops in people who live or work where an air-conditioning or a humidifying unit is contaminated with and emits these spores. The symptoms of hypersensitivity pneumonitis may resemble those of a bacterial or viral infection such as the flu. If hypersensitivity pneumonitis is allowed to progress, it can lead to serious heart and lung problems.
List of Chemical Substances
Published in T.S.S. Dikshith, and Safety, 2016
Beryllium and its salts are toxic and should be handled with the greatest of care. Beryllium and its compounds should not be tasted to verify its sweetish nature. Ingestion and breathing of beryllium is harmful. Acute exposures to high levels of beryllium cause mild inflammation of the nasal mucous membranes and pharynx, rhinitis and pharyngitis, tracheo-bronchitis, and pneumonitis. The symptoms of acute pneumonitis are cough, respiratory distress, substernal discomfort or pain, loss of appetite, weakness, tiredness, chest pain, and cyanosis.
A comprehensive summary of disease variants implicated in metal allergy
Published in Journal of Toxicology and Environmental Health, Part B, 2022
While the pathogenic effects of allergic asthma and rhinitis preferentially manifest in the upper airways and nasal region, hypersensitivity pneumonitis is an allergic response of the lungs that develops in the lower airways and lung interstitium (Moldoveanu et al. 2009). Hypersensitivity pneumonitis is less common than asthma and rhinitis, with an annual incidence of 1.28–1.94 cases per 100,000 individuals in the United States (Costabel et al. 2020; Fernández Pérez et al. 2018). In this disease, sensitization results in the development of antigen-specific CD4+ and CD8 + T-cells and Th1-polarized immune responsivity (Bogaert et al. 2009). Subsequent antigen exposures lead to an influx of effector T-cells to the lungs, alveolar macrophage activation, and lymphocytic inflammation of the alveoli and terminal bronchioles. Persistent alveolitis and granuloma formation might eventually lead to fibrosis and respiratory failure in subjects with hypersensitivity pneumonitis.