Document jmv5nNrQnv7OQvXQGvo6KrN7R

-6- VJhile the type of pulmonary lesion depends on the particular dust inhaled, the underlying pathological principle is the same in all forms of the disease, namely, an ultimate fibrosis and replacement of the elastic lung tissue by a hard unyielding fi brous tissue. All occupations that expose men to large amounts of dust may give rise to pneumoconiosis but not necessarily to silicosis. It is now generally agreed that in order to produoe the latter, (silicosis) inhaled silica dust must reach the lungs in a chemically uncombined condition, in very fine particles not more than ten mi crons (10/25,000 inch) in diameter and in sufficient amount and over a sufficiently long period of time. In relatively recent literature it appears that the proponents of the idea that only "free silica" is harmful are beginning to have some doubts and to have the thought that possibly some silicates may under some conditions be harm ful. Generally speaking, the necessary length of exposure to produce silicosis is in direct proportion to the 6ize of the dust particles and inverse proportion to the dust concentration and the amount of free silica in the dust. Silicosis is char acterized anatomically by a generalized fibrosis of the lungs and clinically by short ness of breath, decreased chest expansion and a progressively lessened capacity for work which is out of proportion to the objective physioal findings. The effect of ex posure to dust suoh as silica is cumulative, the rapidity of development of the dis ease depending upon the time and amount of inhalation. Silioosis may develop to the point of causing symptoms only after several years exposure to silicious dust, but it may be progressive in some cases even after exposure has ceased and may cause symp- . toms or beoome disabling long after the workman has left the environment that caused the condition. Some may improve or at least remain stationary in the absence of in fection. Watkins-Pitchford ( J, Ind. Eyg. 9,109 - 1927) tells of Welsh miners who passed the physioal examination for enlistment in the British Army, fought through the World War, then came back to England, and died of silioosis. Unfortunately, it is not stated whether these persons died from silicosis complicated with tuberculosis. Brit ton and Bead (J.Am.Med.Assoc, 96, 1926 - 1931) give more detailed descriptions of similar latent oases in the United States. Silicosis in General - It is generally agreed that silicosis may be defined as "A chronic disease due to the breathing of air containing silica (Si02), characterized anatomically by generalized fibrotic ohanges and miliary nodules in both lungs, and clinically by shortness of breath, decreased chest expansion, lessened capacity for work, ab sence of fever, increased susceptibility to tuberculosis (some of all of which may be present), and by characteristic roentgenolo gical findings." In other words, silioosis is a disease of the lungs in which the normal lung tissue is replaoed by 6car tissue due to breathing air containing silica dust. Un fortunately there is no known cure for silioosis - but SILICOSIS and nearly all other forms of dust diseases CAB BE PREVENTED. Beoognizing the wide interest and even hysteria among apprehensive employers against whom claims had been filed by alarmed workers, and the necessity of thought ful consideration of the silicosis problem^ the Secretary of Labor on April 14, 1936 called the First National Silioosis Conference attended by more than 300 persons representing workers, employers. State and Federal Agencies, Insurance companies, and other interested groups. Fbur Committees were organized to study specific phases of the silicosis problem; and assemble the essential facts about 6ilicosis in a series of reports; also to present specific suggestions for silioosis prevention and straighten out other difficulties that silicosis has created. Reports made by these Committees were formally adopted at a second conference held February 2nd and 3rd 1937 in Washington, from which we quote: EM001495