• Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Reports of pulmonary fibrosis, emphysema, and, more recently, pulmonary alveolar proteinosis (PAP) in indium workers suggested that workplace exposure to indium compounds caused several different lung diseases. 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. Ten men (median age, 35 years) who produced, used, or reclaimed indium compounds were diagnosed with interstitial lung disease 4-13 years after first exposure (n = 7) or PAP 1-2 years after first exposure (n = 3). Common pulmonary histopathologic features in these patients included intraalveolar exudate typical of alveolar proteinosis (n = 9), cholesterol clefts and granulomas (n = 10), and fibrosis (n = 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 fibrosis and one also developed emphysematous changes. Epidemiologic investigations demonstrated the potential for exposure to respirable particles and an excess of lung abnormalities among coworkers. Occupational exposure to indium compounds was associated with PAP, cholesterol ester crystals and granulomas, pulmonary fibrosis, 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 fibrosis and emphysema, and, in some cases, premature death. Prospective studies are needed to better define the natural history and prognosis of this emerging lung disease and identify effective prevention strategies.
    Chest 12/2011; 141(6):1512-21. DOI:10.1378/chest.11-1880 · 7.48 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Clinical manifestations of interstitial lung diseases of occupational origin cover a wide spectrum and they are a moving target. They change their appearance in response to safety measures and new types of exposure. Recently recognized but long existing exposure requests new diagnostic approaches and safety measures. Thus, the incidence of well known disorders like asbestosis is reducing while newly identified exposure fields for beryllium lead to an increase of chronic beryllium disease which needs to be separated from chronic sarcoidosis, its perfect phenocopy. New techniques and new products cause new disorders like indium tin oxide-lung and flock worker’s lung disease which are hard to diagnose since pathognomonic features are missing. For timely diagnoses an intense cooperation of pulmonary and occupational specialists is mandatory. New hazardous techniques and materials like nanoparticles are introduced and widely used even with exposures of consumers without an in-depth knowledge of their toxicological features. These new developments request surveillance measures which still are in their infancy.
    Orphan Lung Diseases, 01/2015: pages 473-491; , ISBN: 978-1-4471-2400-9
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objectives: Although the serum granulocyte-macrophage colony stimulating factor autoantibody (GMAb) levels have been recognised as a diagnostic marker in primary pulmonary alveolar proteinosis (PAP), their role in PAP with occupational inhalational exposure (PAPo) remains unclear. Methods: Forty-five consecutive patients with PAP were enrolled. Each patient with PAP was assessed for baseline clinical characteristics, chest high-resolution CT (HRCT), serum GMAb and occupational exposure. Fifty healthy controls were included to define normal ranges for GMAb levels. Ninety-seven hospital controls with other respiratory diseases were included to establish prevalence of a history of occupational inhalation exposure. Results: According to the serum GMAb cut-off value of 2.39 μg/mL, 84.4% of the recruited patients with PAP had positive serum GMAb with a median level of 28.7 μg/mL, defined as autoimmune PAP, and the remaining 15.6% had negative serum GMAb with a median level of 0.16 μg/mL, defined as non-autoimmune PAP. Also, 34.2% of patients with autoimmune PAP had a history of occupational inhalational exposure, which was not significantly higher than that of hospital controls (34.2% vs 19.6%, p=0.072). Four patients with PAPo showed negative GMAb. Their arterial oxygen tension, pulmonary function parameters and chest HRCT features were significantly different when compared with patients with autoimmune PAP (p<0.05). These four non-autoimmune occupational lung disease cases culminated in 3 deaths and a lung transplant. Conclusions: A number of patients with PAP who may have occupational inhalational exposure and negative serum GMAb represent a high possibility of silicoproteinosis and very poor survival.
    Occupational and Environmental Medicine 07/2015; 72(7). DOI:10.1136/oemed-2014-102407 · 3.27 Impact Factor

Similar Publications