Black lung.

The quantitative relationship between exposure to respirable coal mine dust and mortality from nonmalignant respiratory diseases was investigated in a study of 8,878 working male coal miners who were medically examined from 1969 to 1971 and followed to 1979. Exposure-related mortality was evaluated using Cox proportional hazards modeling for underlying or contributing causes of death and modified lifetable methods for underlying causes. For pneumoconiosis mortality, the lifetable analyses showed increasing standardized mortality ratios (SMRs) with increasing cumulative exposure category. Significant exposure-response relationships for mortality from pneumoconiosis (p < 0.001) and from chronic bronchitis or emphysema (p < 0.05) were observed in the proportional hazards models after controlling for age and smoking. No exposure-related increases in lung cancer or stomach cancer were observed. Pneumoconiosis mortality was found to vary significantly by the rank of coal dust to which miners were exposed. Miners exposed at or below the current U.S. coal dust standard of 2 mg/m3 over a working lifetime, based on these analyses, have an elevated risk of dying from pneumoconiosis or from chronic bronchitis or emphysema.

Coal Mining↗

PubMed1995

Evaluation of serum type III procollagen peptide as an exposure marker in retired coal workers.

Serum type III procollagen peptide (PIIIP), a degradation product of the type III collagen precursor, has been put forward as an exposure marker for mineral dust. We evaluated PIIIP levels as a marker of exposure to and effects of coal dust in retired coal miners (n = 104). To this end: (a) the individual cumulative dust exposure was calculated from job-exposure matrices, and (b) in addition to routine chest radiography (CR) of all miners according to the criteria of the International Labour Organisation (ILO), a subgroup (n = 46) was screened by high-resolution computed tomography (HRCT). Profusion score (CR and HRCT) tended to increase with cumulative dust exposure, even in the absence of CR evidence for pneumoconiosis (i.e. CR < or = 0/1, n = 35). In contrast to our previous findings in active miners, PIIIP levels were not increased in miners as compared with non-dust-exposed controls (n = 29), and no differences were observed between miners without (ILO = 0/0) and miners with coal workers' pneumoconiosis (CWP; ILO > or = 0/1). No trend in PIIIP versus pneumoconiosis stage was present, either by CR or by the more sensitive HRCT score. PIIIP was also unrelated to any lung function parameter (FEV1, FVC, impedance, diffusion capacity). Age, medication, medical history and smoking habits had no significant effect on PIIIP levels. In the miners with CWP (i.e. ILO > 0/0, n = 28) a significant negative correlation was present between PIIIP values and (log) cumulative dust exposure. This decrease in serum PIIIP levels with increasing cumulative exposure may be due to chronic adaptive changes in type III collagen deposition and/or breakdown. Other relations between exposure and PIIIP were not observed. In conclusion, the present findings do not support the use of serum type III procollagen peptide as a marker of exposure to and (early) interstitial or respiratory effects of coal dust.

Coal Mining↗