Abstract

The results of a cross-sectional survey of an occupational population (n = 706) exposed to hard metal dust revealed distribution of specific immunoglobulin E antibodies against cobalt-conjugated serum albumin (Co-HSA). This population was segregated with respect to smoking and dust-exposure doses. Standard deviations (0.08-0.13) of Co-HSA RAST were sufficiently small (< 7%) to warrant reproducibility. Confirming evidence for 8 workers who had mean + 3 standard deviations of Co-HSA RAST indices and who had been diagnosed with occupational asthma also provided better sensitivity (8/19) and specificity (687/687) of hard metal asthma, rather than metal-induced asthma. Cobalt exposure resulted in significant increases in Co-HSA RAST indices in males, whose mean index was 1.16 +/- 0.13 in nonexposed subjects and 1.37 +/- 0.13 in exposed subjects. There was no difference, however, in the females. This difference between males and females cannot be explained by differences in ages or dust-exposure doses. Furthermore, the specific RAST indices against Co-HSA displayed a strong correlation not only to the intensity of cobalt exposure (r = .488, p < .001), but to log(total exposure doses) (r = .578, p < .001). These results suggest that Co-HSA RAST might be useful as a biological marker for the allergic etiology of hard metal asthma. Nonexposed smokers had similar mean RAST indices: 1.18 +/- 0.12 IU/ml, compared with 1.15 +/- 0.16 IU/ml for nonexposed subjects who had never smoked. There was no correlation between Brinkman indices (i.e., number of cigarettes/d x y) and RAST indices in any of the male groups. Higher, but not significant, mean RAST indices were found for ex-smokers in both the nonexposed (1.18 +/- 0.14) and exposed subjects (1.26 +/- 0.12), compared with subjects who had never smoked. Serum immunoglobulin E levels in the ex-smokers declined with age after they quit smoking, irrespective of exposure status. In contrast, hard metal (cobalt) exposure elevated specific immunoglobulin E. The results of the study suggest that elimination of hard dust exposure is more important than cessation of smoking in the minimization of risk of bronchial asthma. Hard metal exposure may be a preventable risk factor for occupational asthma

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