Chronic obstructive pulmonary disease (COPD) is a preventable disease characterized by airflow limitation that is usually progressive and not fully reversible. COPD is an important cause of morbidity and mortality worldwide and is especially prevalent among blue-collar workers. Even when it is not life-threatening, COPD often profoundly diminishes the affected individual's quality of life. Evidence shows that excessive decline in lung function is associated with premature functional impairment, disability, early retirement from work, and increased morbidity and mortality. Fortunately, severe consequences of COPD can be prevented through early recognition and effective interventions directed at controlling known risk factors. Current knowledge of the pathogenesis of COPD indicates that chronic inhalation of toxic particles and gases can lead to progressive tissue injury via a cascade of inflammatory processes in the lung. Tobacco smoking is recognized as the most important risk factor for COPD. Among blue-collar workers, however, occupational exposures contribute to an increased risk of the disease. In developed countries, an estimated 15% of all COPD is attributable to occupational exposure. In some occupations, the effect of occupational exposure can be as damaging as that of smoking. A study of autopsied U.S. coal miners found that the amount of emphysema associated with coal mine dust can be equivalent to that associated with tobacco smoking. Metal smelting is one of the oldest human activities, dating to prehistoric times. Mining and smelting, the two most prominent industries providing metals needed for the industrial development of the nineteenth and twentieth centuries, have contributed to the burden of occupational lung diseases. Smelting requires heat and carbon from such sources as coke, coal, and in some cases charcoal and woodchips to reduce mineral ores to smelted metals. Dust emitted into the workplace atmosphere during smelting is a risk factor for occupational lung diseases and therefore the exposure-response relationship needs to be established to identify safe exposure levels to prevent adverse health effects. Establishment of such an exposure-response relationship for lung function loss requires well-designed epidemiological studies with meticulous lung function measurements, individual workers' occupational history, and occupational exposure measurements. Given the potential for the healthy worker effect, cross-sectional studies can underestimate the effect of occupational exposure. Other limitations often encountered in studies of occupational exposure effects are small exposed population size, lack of access to the exposed population, and lack of occupational exposure measurements. In light of the previously described issues, the best approach to assess the exposure-response effect of occupational exposure involves longitudinal studies of lung function loss in large industry-wide cohorts of exposed workers with ongoing job-specific exposure measurements.