Article Text
Abstract
Occupational exposure is an important risk factor for chronic obstructive pulmonary disease (COPD), and silica dust is one of the most important occupational respiratory toxins. Epidemiological and pathological studies suggest that silica dust exposure can lead to COPD, even in the absence of radiological signs of silicosis, and that the association between cumulative silica dust exposure and airflow obstruction is independent of silicosis. Recent clinicopathological and experimental studies have contributed further towards explaining the potential mechanism through which silica can cause pathological changes that may lead to the development of COPD. In this paper we review the epidemiological and pathological evidence relevant to the development of COPD in silica dust exposed workers within the context of recent findings. The evidence surveyed suggests that chronic levels of silica dust that do not cause disabling silicosis may cause the development of chronic bronchitis, emphysema, and/or small airways disease that can lead to airflow obstruction, even in the absence of radiological silicosis.
- crystalline silica dust
- chronic obstructive pulmonary disease
- airflow obstruction
- emphysema
- chronic bronchitis
- small airways disease
- α1-AT
- α1 protease inhibitor
- BHR, bronchial hyperresponsiveness
- COPD, chronic obstructive pulmonary disease
- CT, computed tomography
- DLCO, carbon monoxide diffusion in the lung
- ES, emphysema score
- FEF, forced expiratory flow
- FEV1, forced expiratory volume in one second
- FVC, forced vital capacity
- MDAD, mineral dust airways disease
- MMEF, maximal mid-expiratory flow
- NMRD, non-malignant respiratory disease
- TB, tuberculosis
- VC, vital capacity