This paper reports the follwing facts as revealed by a dust investigation of the working environment and by medical examinations of workers working in the same environment in two activated-carbon manufactories, in Kanagawa Prefecture, in 1962. (1) Concentrations of dust in air exceeded the maximum allowable concentration, ranging from 3 up to 96 mg/m³. Size of dust in air was distributed between 0.1μ (minimum) and 7.0μ (maximum). 92.4% of the dust was under 1μ. (2) Radiographical examination revealed that out of thirty six workers, who had been exposed to a considerable quantity of the dust more than one year, five were found to be in Category 1 and six were in Category 2, according to the International Classification of Radiograph on Pneumoconiosis. Smaller opacities shown under radiograph were all of the "punctiform" type. Generally speaking, the more the years of employment of the worker in dusty environments, the more was the number of cases of pneumoconiosis. (3) Authors supposed that pneumoconiosis could be caused by carbon dust from charcoal.

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Nitrocompouds as the ingredients of explosives have been incriminated for a number of toxic manifestations in factory employees. Besides nitroglycerol and nitroglycol which constitute the main explosive ingredient, cyclic nitrocompounds such as dinitrotoluene (DNT) are commonly in use. The recent technological development has enabled a cheap supply of xylene, and hence the sustitution of dinitroxylene (DNX) for DNT is being seriously considered. This study was undertaken to compare the toxicity of DNT with that of DNX in mice and rabbits. The LD₅₀ was determined under acute intoxication conditions and DNX was found to be less poisonous. Continuous administration of small doses to simulate chronic intoxication revealed a number of impairments in vital organs with either of the compounds, including anemia, methemoglobinemia, Heinz body formation and myelosuppresion. Blood chemistry and liver function studies demonstrated marked hepatotoxicity as demonstrated by increased GPT, retarded BSP clearance and decreased acetylating capacity of the excised and perfused liver. Acute intoxication gave rise to increases in NPN and urea N. Histological study showed myelosuppressive changes ranging from hypoplasia to aplasia, hemosiderosis, fatty metamorphosis of the liver, dilated sinusoids, and obliterating changes of lung arteries. Less marked were the changes of the heart muscle and too little morphological evidence was seen in the kidney to account for the increase of NPN. It was concluded that both DNT and DNX are highly poisonous if administered in large amounts to mice and rabbits, the latter being less toxic as far as the lethal dose is concerned. No demonstrable difference was noticed between the two in chronic intoxication when studied histologically, nor was there any difference elicited by blood chemistry and liver function study.

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