The purpose of this review of the last ten years' publications was to show our present knowledge about welding-fume effects on the respiratory system. Welding generates particles and gases which are characteristic for the method used and the material welded. Various investigations to determine if respiratory system diseases occur more often in welders than in others not exposed have yielded diverging results. One explanation of this may be that the exposure of welders in the various studies may not be directly comparable and the majority of authors did not take into consideration the impact of other conditions of the working environment. This review represents all known respiratory symptoms, like siderosis, chronic bronchitis, fibrosis of lung, asthma, lung cancer and diseases of the upper respiratory tract, which can occur in welders. Furthermore are given the legal base for declaration of these diseases as an occupational disease and the fitness rules for welders in GDR.
The acute effects of a single subcutaneous (sc) administration of methyl bromide (MB) on electroencephalographic (EEG) activity and on sleep-wakefulness and its circadian rhythms were investigated in rats with indwelling electrodes for EEG, electromyographic (EMG) and electrooculographic (EOG) recordings. The LD50 of MB was found to be 135 mg/kg for the sc administration. Slowing of the EEG frequency in the wakefulness (W) stage and spike-wave activity appeared at a dose of 135 mg MB/kg. These abnormal EEG activities did not occur at lower dose levels. Administration of MB at doses of 45, 15 and 5 mg/kg produced dose-related changes in amounts of W, non-REM sleep (NREMS) and REM sleep (REMS) and in their circadian rhythms. Logarithmic concentrations of bromine in blood and brain decreased linearly after the MB administrations, and the half-life of bromine in blood and brain was approximately 8.7 and 4.3 days, respectively. Pretreatment with glutathione effectively lessened the detrimental effects of MB on sleep-wakefulness and its circadian rhythms and increased the LD50.
While both nickel (II) oxide and nickel (III) oxide affect the human body, nickel (III) oxide may be more toxic since it could act as an oxidizing agent. Hence, it is necessary to perform differential determinations of nickel (II) oxide and nickel (III) oxide in airborne particulate substances. Such determinations have not been performed because nickel (III) ions are unstable in aqueous solutions. Nickel (III) oxide was found to release molecular oxygen with sufficient reproduci-bility when it was dissolved in 1 N hydrochloric acid solution by stirring for 20 minutes. The released and dissolved oxygen in the solution was then determined by sampled-dc polarography. The diffusion current was proportional to the amount of nickel (III) oxide applied. However, slight deviation from the linear relationship between the current and amount of sample was observed. This might be caused by the coexistence of the polarographic maximum current and the reduction of oxygen by chloride ions. A third-order polynomial was fitted to the data ob-tained with the standard samples by the least squares method ; it was used as the calibration curve for the determination of testing samples. Using the present method, nickel (III) oxide in the range from 5 mg to 50 mg in the mixure with nickel (II) oxide was determined with an error of only a few percent. Nickel (III) oxide of about 1 mg was determined with an error of about 10%.
Repeated inhalation exposures of rats to 900 ppm and 2700 ppm of toluene vapor produced a dose-related increase in drinking behavior and daily water intake with an increase in both the vapor concentration and number of the repeated exposures. A dose-related increase in plasma osmolality and plasma sodium concentration with a concomitant decrease in plasma protein concentration was found in the rats sacrificed 4 hours after cessation of the repeated exposures for 3 weeks to 900 ppm and 2700 ppm of toluene vapor. More positive water balance, increased urine volume, lowered urine osmolality without a significant increase in urinary sodium and potassium excretions occurred on Day 1 following repeated exposures to toluene vapor for 3 weeks. The present blood and urine data indicated that the polydipsia induced by repeated exposure to toluene vapor was related to the increase in both plasma sodium concentration and plasma osmolality.
Synthetic resin active carbon beads were applied to adsorption sampling of arsine in the air, and the accompanying analytical procedures including desorption of arsenic from the adsorbent and graphite furnace atomic absorption spectrophotometry to determine desorbed arsenic were studied. Results showed that active carbon produced from synthetic thermosetting resin beads was not contaminated with arsenic, an advantage over coconut-shell active carbon. The sampling tube, which was 4 mm in inside diameter and packed with 150 mg of the resin active carbon, was able to adsorb arsine at 0.5 ppm in 51 of dry air only with negligible breakthrough. The same tube previously humidified had a lower adsorption capacity: 0.5 ppm in 41 air. The adsorbed arsine on the resin active carbon was desorbed to 80%-94% with 2 ml or 10 ml of 0.01 M HNO3 solution with or without 10% ethyl alcohol under heat treatment at 75°C for 1 h. Arsenic desorbed into nitric acid solution was determined by atomic absorption spectrophotometry with pyrocoated graphite furnace and electrodeless discharge lamp, and the lower determination limit of arsenic in the final solution was 5 ng/ml (n =6, CV =0.12).