The action of small amounts of quartz and larger amounts of coal and graphite on the lungs of rats.

Experimental and field work on silicosis, while concentrating attention on the danger of exposure to the dust from hard rock, has produced a sense of false security in regard to the coal miner. Mavrogordato (1918) stated: " It may be regarded as established that all forms of dust enter the lungs and that some, such as coal, are relatively harmless, while others, such as flint, are deadly ". Bronchitis and emphysema were prevalent among old miners, but, as colliers were thought to be relatively immune to tuberculosis, it was assumed that inhalation of coal dust did not produce silicosis (Oliver, 1909; Collis, 1915; Haldane, 1931). Coal dust, as a result of experimental study, was not only claimed to be exempt from blame, but even came to be regarded as a beneficent agent capable of neutralizing the harmful effects of silica. Tattersall. (1926) reported cases of silicosis among hard ground workers in coal mines, and Jousset (1928) attributed to silicosis the most important place in the production of " black lung" of coal miners. He also found by analysis -that the silica content was 10 to 20 times more in the sclerosed lungs than in the normal ones. Policard and Devuns (1930), by a special microscopic technique, came to the conclusion that pulmonary anthracosis and fibrosis of the lungs of coal miners were merely two phases of the same process. Cummins (1927) advanced the hypothesis that silicosis; by causing interference with the lymph drainage of the lungs, led to the retention and accumulation of coal dust in the pulmonary tissues. Belt and King (1945) found in their experimental study that purest coal dust, whether anthracite or bituminous, had a low pathogenicity and caused only miniiimal fibrosis, but although results were not clear cut, there was some evidence that the pathogenicity increased with the increase of siliceous matter in the coal. Gough (1947) wrote: