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Etiology

Review: Exposure to coal and gold-mining dust is associated with clinically important loss of lung function

ACP J Club. 1994 Mar-April;120:53. doi:10.7326/ACPJC-1994-120-2-053


Source Citation

Oxman AD, Muir DC, Shannon HS, et al. Occupational dust exposure and chronic obstructive pulmonary disease. A systematic overview of the evidence. Am Rev Respir Dis. 1993 Jul;148:38-48.


Abstract

Objective

To assess the association between occupational dust exposure and chronic obstructive pulmonary disease (COPD).

Data sources

Studies were identified using MEDLINE (January 1966 to July 1991), SCISEARCH, manual review of reference lists, and contact with 30 international experts.

Study selection

Studies were selected if the study population consisted of workers exposed to nonorganic occupational dust; exposure to occupational dust was measured quantitatively with industrial hygiene measurement of dust levels and the duration of exposure was recorded for each worker; the outcomes included COPD, lung function, emphysema, chronic bronchitis, or mortality; and the study design controlled for smoking and age and allowed for the calculation of a quantitative association between dust exposure and ≥ 1 of the outcomes of interest.

Data extraction

Data regarding the study populations, prognostic factors, and outcomes were extracted independently by 2 reviewers. Methodologic rigor was also assessed. Data were grouped by outcome and summarized in tabular form. Results were not combined across studies because of limitations of the available data.

Main results

13 reports met the inclusion criteria. These 13 reports were based on 4 cohorts of workers: 3 of coal miners in the United Kingdom, Germany, and the United States and 1 of gold miners in South Africa. All of the studies found a statistically significant association between loss of lung function and cumulative respirable dust exposure. Based on the results of the identified studies, it was estimated that of 1000 nonsmoking coal miners with a lifetime exposure of 122.5 gh (gram-hours)/m3 (equivalent to 35 y of work with a mean respirable dust level of 2 mg/m3), 80 miners (95% CI 34 to 137) would have a clinically important loss of lung function (> 20%) attributable to dust and 12 (CI 0 to 28) of these would have a loss of forced expiratory volume in 1 second (FEV1) > 35%. Among 1000 smoking miners with the same lifetime exposure, 66 (CI 49 to 84) would have a clinically important loss of lung function attributable to dust and 23 (CI 0 to 251) of these would have a loss of FEV1 > 35%. For nonsmoking gold miners with a maximum cumulative respirable dust exposure of 21.3 gh/m3 (< one fifth of a moderate exposure among coal miners), the relative odds ratio for > 20% loss of FEV1 attributable to dust exposure was 3 times as large when compared with coal miners (odds ratio 4.9 vs 1.5).

Conclusion

Exposure to coal and gold mining dust is associated with clinically important losses of lung function in smokers and nonsmokers.

Source of funding: Ontario Ministry of Health.

For article reprint: Dr. A.D. Oxman, Health Services Research Unit, National Institute of Public Health, Postboks 4404, Torshov N-0482, Oslo, Norway. FAX 011-47-22-042595.


Commentary

The study by Oxman and colleagues attempts to provide physicians with a response to the all-too-common statement, "I know I was a smoker, but it was all that dust at work that caused my lung problems." The authors exhaustively, and admirably, reviewed more than 2500 citations on the effects of occupational dust exposure using sophisticated epidemiologic and statistical tools. Unfortunately, only 13 reports met the criteria for inclusion, and these reports were based on only 4 cohorts of workers (3 of coal miners and 1 of gold miners). 8 reports came from a single cohort of coal miners. As a result, the most important conclusion from this review might be that we need more methodologically rigorous studies of different types of occupational dust exposure.

The title of the article is somewhat misleading in indicating an association between occupational dust exposure and COPD. The review does not adequately show this association, because it fails to clearly define COPD. In fact, the most common outcome measure cited was a decline in FEV1, an adequate measure for epidemiologic purposes but not for the diagnosis of individual patients. In addition, the results were based only on coal and gold miners and may not be generalizable to other types of occupational dust exposure.

Because of the paucity of available literature, the problem with the definition of COPD, and the uncertain generalizability of the 2 types of dust exposure, this article provides the internist with valuable but limited information on the association between certain types of occupational dust exposure and an increased risk for impairment of lung function. Based on the results of this study, the physician can probably respond to the patient (with a bit of poetic and professional license) by saying, "Dust, by itself, can cause some changes in lung function, but your smoking is at least as important a cause."

W. Michael Alberts, MD
University of South FloridaTampa, Florida, USA