In agricultural and other environments, inhalation of airborne microorganisms is linked to respiratory disease development. Bacterial endotoxins, peptidoglycans, and fungi are potential causative agents, but relative microbial characterization and inflammatory comparisons amongst agricultural dusts are not well described. The aim of this study was to determine the distribution of microbial endotoxin, 3-hydroxy fatty acids (3-OHFA), muramic acid, and ergosterol and evaluate inflammatory responses in human monocytes and bronchial epithelial cells with various dust samples. Settled surface dust from 5 environments was obtained: swine facility, dairy barn, grain elevator, domestic home (no pets) and domestic home with dog. Endotoxin concentration was determined by recombinant Factor C (rFC). 3-OHFA, muramic acid and ergosterol were measured using gas chromatography-mass spectrometry. Dust-induced inflammatory cytokine secretion in human monocytes and bronchial epithelial cells was evaluated. Endotoxin-independent dust-induced inflammatory responses were evaluated. Endotoxin and 3-OHFA levels were highest in agricultural dusts. Muramic acid, endotoxin, 3-OHFA and ergosterol were detected in dusts samples. Muramic acid was highest in animal farming dusts. Ergosterol was most significant in grain elevator dust. Agricultural dusts induced monocyte TNFα, IL-6, IL-8 and epithelial cell IL-6 and IL-8 secretion. Monocyte and epithelial IL-6 and IL-8 secretion was not dependent on endotoxin. House dust(s)-induced monocyte TNFα, IL-6, IL-8 secretion. Swine facility dust generally produced elevated responses compared to other dusts. Agricultural dusts are complex with significant microbial component contribution. Large animal farming dust(s)-induced inflammation is not entirely dependent on endotoxin. Addition of muramic acid to endotoxin in large animal farming environment monitoring is warranted.

Indium is a relatively rare element that has had limited use for decades as a metal, in alloys, and for electronics applications. During the past 15 years, global demand for indium has increased several-fold, driven by the novel use of indium-tin oxide (ITO) thin fi lms in the production of fl at-panel displays (such as liquid crystal displays [LCDs]), touch screens, and other electronic devices. 1,2 ITO is a sintered ceramic material typically consisting of 90% indium oxide (In 2 O 3 ) and 10% tin oxide (SnO 2 ). Exposures to indium metal and indium compounds (including indium hydroxide [In(OH) 3 ], indium oxide, and ITO) may occur during ITO production, ITO use for the creation of thin fi lms, and reclamation. The bulk of the ITO industry is located in Japan, with some activity in the United States, China, Taiwan, and South Korea. 3 As of May 2010, 10 clinical cases of lung disease in indium workers from three countries (Japan, United States, and China) had been reported. 2 Seven cases were described as interstitial lung disease (ILD) characterized by pulmonary fi brosis with or without emphysema. Three cases were described as pulmonary alveolar proteinosis (PAP). Individually, these 10 case reports left unclear why some workers developed ILD and others developed PAP, and the relationship, if any, between these distinct pulmonary disease processes.Background: Reports of pulmonary fi brosis, emphysema, and, more recently, pulmonary alveolar proteinosis (PAP) in indium workers suggested that workplace exposure to indium compounds caused several different lung diseases. Methods: To better understand the pathogenesis and natural history of indium lung disease, a detailed, systematic, multidisciplinary analysis of clinical, histopathologic, radiologic, and epidemiologic data for all reported cases and workplaces was undertaken. Results: Ten men (median age, 35 years) who produced, used, or reclaimed indium compounds were diagnosed with interstitial lung disease 4-13 years after fi rst exposure (n 5 7) or PAP 1-2 years after fi rst exposure (n 5 3). Common pulmonary histopathologic features in these patients included intraalveolar exudate typical of alveolar proteinosis (n 5 9), cholesterol clefts and granulomas (n 5 10), and fi brosis (n 5 9). Two patients with interstitial lung disease had pneumothoraces. Lung disease progressed following cessation of exposure in most patients and was fatal in two. Radiographic data revealed that two patients with PAP subsequently developed fi brosis and one also developed emphysematous changes. Epidemiologic investigations demonstrated the potential for exposure to respirable particles and an excess of lung abnormalities among coworkers. Conclusions: Occupational exposure to indium compounds was associated with PAP, cholesterol ester crystals and granulomas, pulmonary fi brosis, emphysema, and pneumothoraces. The available evidence suggests exposure to indium compounds causes a novel lung disease that may begin with PAP and progress to include fi brosis and emphysema, and, in som...

Background Healthcare workers have an elevated prevalence of asthma and related symptoms associated with the use of cleaning/disinfecting products. The objective of this study was to identify and characterize cleaning/disinfecting tasks and products used among hospital occupations. Methods Workers from 14 occupations at five hospitals were monitored for 216 shifts, and work tasks and products used were recorded at five-minute intervals. The major chemical constituents of each product were identified from safety data sheets. Results Cleaning and disinfecting tasks were performed with a high frequency at least once per shift in many occupations. Medical equipment preparers, housekeepers, floor strippers/waxers, and endoscopy technicians spent on average 108–177 min/shift performing cleaning/disinfecting tasks. Many occupations used products containing amines and quaternary ammonium compounds for > 100 min/shift. Conclusions This analysis demonstrates that many occupations besides housekeeping incur exposures to cleaning/disinfecting products, albeit for different durations and using products containing different chemicals.