Workplace inhalational hazards remain common worldwide, even though they are ameliorable. Previous American Thoracic Society documents have assessed the contribution of workplace exposures to asthma and chronic obstructive pulmonary disease on a population level, but not to other chronic respiratory diseases. The goal of this document is to report an in-depth literature review and data synthesis of the occupational contribution to the burden of the major nonmalignant respiratory diseases, including airway diseases; interstitial fibrosis; hypersensitivity pneumonitis; other noninfectious granulomatous lung diseases, including sarcoidosis; and selected respiratory infections. Methods: Relevant literature was identified for each respiratory condition. The occupational population attributable fraction (PAF) was estimated for those conditions for which there were sufficient population-based studies to allow pooled estimates. For the other conditions, the occupational burden of disease was estimated on the basis of attribution in case series, incidence rate ratios, or attributable fraction within an exposed group. Results: Workplace exposures contribute substantially to the burden of multiple chronic respiratory diseases, including asthma (PAF, 16%); chronic obstructive pulmonary disease (PAF, 14%); chronic bronchitis (PAF, 13%); idiopathic pulmonary fibrosis (PAF, 26%); hypersensitivity pneumonitis (occupational burden, 19%); other granulomatous diseases, including sarcoidosis (occupational burden, 30%); pulmonary alveolar proteinosis (occupational burden, 29%); tuberculosis (occupational burden, 2.3% in silica-exposed workers and 1% in healthcare workers); and community-acquired pneumonia in working-age adults (PAF, 10%). Conclusions: Workplace exposures contribute to the burden of disease across a range of nonmalignant lung conditions in adults (in addition to the 100% burden for the classic occupational pneumoconioses). This burden has important clinical, research, and policy implications. There is a pressing need to improve clinical recognition and public health awareness of the contribution of occupational factors across a range of nonmalignant respiratory diseases.

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...

For chronic hepatitis C that is nonresponsive to prior interferon monotherapy, combination therapy is more effective than re-treatment with interferon alone. Response rates remain less than 20% even in the most responsive subgroups, demonstrating a need for better therapeutic options.

Two cases of pulmonary alveolar proteinosis, including one death, occurred in workers at a facility producing indium-tin oxide (ITO), a compound used in recent years to make flat panel displays. Both workers were exposed to airborne ITO dust and had indium in lung tissue specimens. One worker was tested for autoantibodies to granulocytemacrophage-colonystimulating factor (GM-CSF) and found to have an elevated level. These cases suggest that inhalational exposure to ITO causes pulmonary alveolar proteinosis, which may occur via an autoimmune mechanism.

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Background Hospital staff expressed health concerns after a surface disinfectant product containing hydrogen peroxide, peracetic acid, and acetic acid was introduced. We sought to determine if this product posed a health hazard. Methods An interviewer-administered questionnaire on work and health characteristics was completed by 163 current staff. Symptoms that improved away from work were considered work-related. Forty-nine air samples were taken for hydrogen peroxide, peracetic acid, and acetic acid. Prevalence ratios (PRs) were calculated using Poisson regression, and standardized morbidity ratios (SMRs) were calculated using nationally representative data. Results Product users reported higher prevalence of work-related wheeze and watery eyes than non-users (P < .05). Workers in the department with the highest air measurements had significantly higher prevalence of watery eyes (PR, 2.88; 95% confidence interval [CI], 1.18–7.05) than those in departments with lower air measurements, and they also had a >3-fold excess of current asthma (SMR, 3.47; 95% CI, 1.48–8.13) compared with the U.S. population. Conclusions This disinfectant product was associated with mucous membrane and respiratory health effects. Risks of mucous membrane irritation and asthma in health care workers should be considered in development of disinfection protocols to protect patients from hospital-acquired infections. Identification of optimal protocols that reduce worker exposures while maintaining patient safety is needed.

A comprehensive preventive programme reduced beryllium sensitisation in new workers during the first years of employment, despite airborne beryllium levels for production workers that were similar to pre-programme levels.

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