Commentary on “COPD Causation and Workplace Exposures: An Assessment of Agreement Among Expert Clinical Raters”

Over the past two decades, evidence has mounted linking occupational exposures to risk for COPD (1–3). Multiple studies and epidemiologic data from nearly 30 countries show a population attributable fraction (PAF) of 15-20% for workplace exposures in chronic obstructive lung disease (4–8), with an even higher PAF in non-smokers. Specific workplace exposures that have been definitively linked to COPD include coal mine dust, respirable silica, agricultural dusts (cotton, grain and wood dust), metal fumes (particularly cadmium and vanadium), certain flavoring chemicals and second hand smoke.

Clinicians, including pulmonary and occupational medicine practitioners, have been slow to incorporate these scientific findings into their worldviews, particularly in the context of patient care. There are two main reasons for this reluctance: smoking is well-recognized as the primary cause of COPD, and obtaining an individual's smoking history is a relatively straightforward component of the basic medical history; in contrast, it is substantially harder to make the clinical case for an occupational etiology.

Many clinicians remain frustrated in their often futile efforts to cure smoking patients of this profound addiction. In supporting a patient's long, hard slog to successful smoking cessation, there may be less time and energy directed towards other factors that contribute to obstructive lung disease. Moreover, few physicians have the skills or take the time to obtain a detailed occupational and environmental history –the foundation of exposure assessment in the clinical setting.

Even if this information is obtained, establishing the link between exposure and causation can be problematic. Many patients with COPD have multiple risk factors, with a combination of smoking and complex workplace exposures that makes attribution difficult. And in cases where there is a reasonable probability of work-related COPD, the diagnosis has daunting implications. Physicians must counsel such patients to explore their legal rights and benefits. Paperwork must be completed providing a reasoned medical opinion, often requiring review of additional records and reports. Lawyers and bureaucracies are usually involved. Patients may lose their jobs or face financial strain and, in the United States, medical indigency with job change or unemployment. Communication with employers to recommend changes in work practices or with government agencies charged with enforcing workplace regulations is time-consuming and beyond the comfort level of most physicians. Is it any wonder that few clinicians embrace the challenge of diagnosing work-related COPD?

In this issue of “COPD: Journal of Chronic Obstructive Pulmonary Disease”, a group of physicians with expertise in either COPD or occupational lung disease (OLD) were recruited to rate the relative contributions of smoking and occupational exposure in 15 COPD case scenarios. Smoking was consistently identified as the strongest contributor to COPD causation except in cases with light smoking and high occupational exposure. Surprisingly, COPD experts assigned higher work-related attribution, averaging a 9.4% greater proportion of occupational causation per case compared to OLD experts. Not surprisingly, the OLD experts were more likely than their COPD counterparts to recommend changes at the workplace, such as use of respiratory protection, improved ventilation, and alternative work practices to reduce exposures, rather than simply recommending that affected patients leave their jobs. The overall weighting of 20 pack-years of smoking compared to 20 years of high occupational exposures was remarkably similar.

The study experts also assessed rates of decline in FEV1 in the COPD cases over time. While excessive decline in FEV1 is unlikely to be helpful in causal attribution of COPD, understanding what constitutes a critical decline is important for patient care. The physician attentive to excessive longitudinal declines in FEV1 may be more likely to ask questions about workplace exposure, and take steps to assure that potentially causal exposures are mitigated.

As this study suggests, recognizing COPD from occupational causes creates critical opportunities for patient care directed at prevention of disease progression. At minimum, clinicians should be aware of high-risk occupational exposures and dusty trades and prepared to take a targeted history to elicit such risks in their patients with COPD. Though smoking remains central in COPD causation, the contribution of occupational exposures at the individual level must not be ignored.