We compared death certificates for asbestos-associated diseases (mesothelioma, lung cancer, asbestosis) in two asbestos workers' cohorts. One (insulation workers) had current or recent employment and a strong, continuing union support system which gave them much information about the effects of asbestos exposure. The second cohort, asbestos factory workers, had no such advantage. The factory had closed almost 30 years before, and its workers had dispersed into many areas of the state and nation. Accuracy of medical diagnosis was comparable in the two groups, but occupational listings were not. Three-quarters of the insulators' death certificates told of asbestos work, while virtually none of the factory workers' certificates provided such information, even for deaths of mesothelioma and asbestosis. The data indicate that disease categories, based on medical and pathological diagnoses, at least for asbestos-associated disease, tend to be accurate. Attempts to identify groups at risk by sorting occupational categories can give variable results, good for those with current exposures, much less satisfactory for those with long-past occupational exposures.
A cross-sectional medical examination of a copper smelter work force included determination of blood lead (Pb-B), zinc protoporphyrin (ZPP), blood cadmium (Cd-B), urinary cadmium (Cd-U), and urinary arsenic (As-U), since it was known that such metal impurities were present in the copper concentrate. A total of 776 copper smelter employees (680 active and 96 retirees and ex-employees) were examined. Another 144 men, never employed in the smelter, but who had worked in copper mines (and sometimes in gold mines) were also examined. Mean Pb-B, ZPP, Cd-B, and As-U were significantly higher in active copper smelter employees than in retirees or miners, indicating exposure and absorption in the copper smelter. Significant correlations between Pb-B and Cd-B, and Cd-U and As-U were present, confirming the common source of absorption. Although there was evidence for an increased lead absorption, this was very moderate, with practically no Pb-B levels in excess of 60 micrograms/dl. A marked effect of smoking on blood cadmium levels was present; nevertheless, for all smoking categories Cd-B levels were significantly higher in active employees, indicating the independent contribution of exposure to cadmium in the smelter. Cd-U did not exceed 10 micrograms/g creatinine, the generally accepted "critical" level for the kidney, but was higher than 2 micrograms/g creatinine, a level very rarely exceeded in the general population, in a sizable proportion of those examined. The highest Cd-U levels were found in retired copper smelter employees; age might have been a contributing factor, besides a longer duration of exposure in the smelter.
An investigation into the problem of the frequency and hazards of lung biopsy in asbestos workers was performed in two ways. The first study was into the frequency of lung biopsy among 2907 long term asbestos insulation workers in 1981-3 and the second was into the frequency of fatal complications of lung biopsy in 168 deaths from asbestosis among 2271 consecutive deaths of asbestos insulation workers 1967-76. Only 25 (0.9%) of the 2907 asbestos insulation workers reported having had either an open lung biopsy, a needle biopsy, or a transbronchial biopsy. Seven (24%) of these men suffered difficulties as a result of the biopsy. Lung biopsies had been performed on 14 of the 168 workers who died of asbestosis. Three (21%) of these 14 patients had died within 30 days of biopsy as a direct result of the procedure. In most cases there is no need for lung biopsy to establish a diagnosis of asbestosis; generally, it may be defined by history of exposure, clinical and radiological findings, and other well established non-invasive diagnostic procedures. Certainly, legal and compensation recommendation for biopsy should be considered with the possibility of death in mind. If biopsy is performed precautions should be taken, including adequate observation in hospital.
Cites: Dis Chest. 1966 Nov;50(5):504-85953790
Cites: Thorax. 1968 Sep;23(5):556-625680241
Cites: Chest. 1971 Jan;59(1):18-225099806
Cites: Johns Hopkins Med J. 1973 Feb;132(2):103-164684168
Cites: Am Rev Respir Dis. 1974 Jan;109(1):67-724809166
Cites: Clin Chest Med. 1983 Jan;4(1):3-146340926
Cites: Am Rev Respir Dis. 1976 Jul;114(1):187-227779552