Dusts produced in different working areas of a hard metal workshop in a machinery factory were analyzed by an energy despersive X-ray (EDX) micro-analyzer, X-ray diffractometer and atomic absorption spectrophotometer (AAS). Cobalt excretion in the urine of workers was also analyzed by AAS. The raw material used for hard metal production was a mixed powder of metal cobalt and tungsten carbide. Almost all of the powder particles were of respira-ble size. The dust produced in the grinding process was also a combination of metal cobalt and tungsten carbide. Its size, shape and chemical composition were very similar to the raw material powder. The airborne dust in the workshop was less than 3μm in diameter. The chemical nature of cobalt and tungsten and the ratio of the two metals in the airborne dust was similar to those of the grinding dust and the raw material powder. Thus, there was no essential difference in the physical and chemical nature of the dusts produced in different working areas. These results supported the idea that urinary cobalt excretion could be used as a biological indicator of hard metal dust expsure. Urinary cobalt excretion showed an association with environmental cobalt ex-posure even when the exposure level was below 0.05 mg/m3. Thus, urinary cobalt excretion is sensitive enough to be used as a biological indicator in a modern factory where hard metal dust exposure is well controlled.
Serum angiotensin converting enzyme (ACE) activity was measured in 107 male silicosis patients. In agreement with previous reports, the mean activity of ACE in silicosis patients was elevated (47.4 ± 14.2 U/ml; normal 30.5 ± 8.6). Among the various characteristics of the patient analyzed in this study, only the progression of radiographical profusion category showed a statistically significant association with the elevation of ACE, and severity of dyspnea was inversely associated with ACE. Previous studies on the relationship between ACE and severity of radiographical category have been conflicting and any difference found in our study are also marginal. No association was found between ACE and age of the patient, duration of exposure to dust, and smoking habits.
Abstract; Levels of biogenic amines and activities of monoamine oxidase and acetylcholine esterase were investigated in developing rat brain following acryla-mide (ACR) exposure. The ACR exposed rats showed a significant reduction in noradrenaline (NA), dopamine (DA) and 5-hydroxytryptamine (5-HT) contents at 4, 8 and 15 days of age whereas the adult animals exhibited no such changes. Exposure of rats to ACR resulted in decrease of NA levels in basal ganglia, pons medulla and mid brain regions and of DA in cerebellum, mid brain, pons medulla and hypothalamus in age groups (12, 15 and 21 days). The 15 and 21 days old treated rats also showed a marked reduction in 5-HT content in pons medulla, hypothalamus and cerebral cortex. Exposure to ACR of 2, 4, 8 and 15 days old rats resulted in an increase in monoamine oxidase activity and decrease in acetyl-choline esterase activity in brain. These results suggest that suckling and growing rats are more vulnerable to neurotoxic effects of ACR and such effects are not uniform in brain but are localized to certain brain regions which regulate motor activity and behaviour.