Document aDer31vKe9o9xdw3LVXKG8mNa

Fikat Edition McGRAW-HILL BOOK COMPANY, Inc. NEW YORK AND LONDON 1936 V /J, C 3 ;i - i-. *5* >. . .*srr :( .*'*?**& ' " ---- * .*. I- ,*> f*-.' 'Pv--. ,, J*' -.* `' ' 1 pUlNTlFF'S exhibit -twsi CormioKT, 193G, bttbe McGraw-Hill Book Compaxt, lire. PRINTED IN THE UNITED STATES or AX ERICA AU right* reserved. Thit book, or parts thrrrtj, may not be reproduced tn any form irithout permission of the publishers. ! Table 4.--Number or Death* Expected prom Specified Caused and Number Which Actuai.lt Occurred amono Persons Engaged in Certain Occupatigns Exi-ohed to Silica Dubt1 ! Occupation ; Deaths from all causes Deaths from respiratory tuberculosis , i Actual F ported t Percentage actual uf et peeled Actual EcpacUd Percentage actual of expectad Metal-mine operatives (underground): Gold and eilrer minrn............................................. ,........................ Lead and line mines ........................................................................ Copper minee...................................................................................... Iron mints........................................................................................... Quarry operatirea................................................................................... Btooe rutleva: Granite and sandstone...................................................................... Marble and limestone......................................................................... Metal industries: , Grinders............................................................................................... Buffers and pollsbars........................................................................... Choppers (not ship)............................................................................. Core asters and sand-(solders........................................................ Iron and steel foundries: Molders. founders* and casters........................................................... Dnllers, flask makers, machine hands* miters, ate............................ 44 22 B3 33 37 29 12 4A fttl 31 32 i 202 43 #.77 6.03 22.63 12.12 22.45 17.47 10.55 28.63 (14.10 14.14 22 05 130.14 31.03 450 437 307 272 105 too 114 101 139 2A9 141 165 145 1.12 11 0.00 24 2.03 4 134 7 2.00 10 1.64 8 1.02 7 2.33 10 4.80 S 1.30 3 2.#2 24 13.38 7 3.03 804 1833 #13 280 203 070 294 210 147 013 103 17# 231 O Cr. co: 2 5- o *1 c: 5: 2 <5 *cu s: *u 5: * Ordinary department mortality experience of twelve life inauranee compaolee, 1915-1920 (159). CO plaintiff I EXHIBIT i 15Q%__ 32 JKDUSTKIAL DUST fully that, if lie lias silicosis, lie pot it in Cnnndu and Canada will take care of him. In the case of a first-stape silicotic without tubercular infection, there is no method, as yet, for determininp his lessened efficiency. The lung change, if any, caused by his dust inhalation is too small to measure. McCann and Hurtado (177) have estimated disability from lung fibroses of various origins but have not yet succeeded in developir-.z a method that is simple enough for routine use by compensation boards, insurance examiners, and the like. Their procedures involve various simple measurements of respiratory function but they have not established any methods of detecting fibrosis which are more sensitive than the present X-ray examination. Of course, industry' would welcome a diagnostic routine for detecting early harm from dust or, better, for forecasting harm. No such method is available and it seems fruitless to expect such help. The pneumoconioses are not diagnosed until harm "is demonstrable by' X-ray. Collis (42) has stressed the difference between the age group ings in pulmonary tuberculosis and in silicosis, with or without tubercular infection superimposed. Tuberculosis is most preva lent between the ages sixteen to twenty-four, while silicosis rarely becomes disabling until later in life. Inasmuch as a good many years of dust exposure are required before the average cm of silicosis (or asbestosis) becomes evident, it is obvious that ' is not likely to be acquired early' in life. However, there i.- an epidemiological side to the question which is of great imjxirtancc nnd it is that which Collis especially emphasized. The average healthy individual has acquired a fairly effective immunity or resistance to tuberculosis. His chest X-ray is likely to show one or more healed 6cars or fibrosed areas from tuberculosis. Such an individual, Cummings emphasizes (211), is a "better silicosis risk than the man who shows no evidence of past exposure to pulmonary tuberculosis. Consequently it is wise to select for dusty jobs men who are past the age of forty and not young men just taking up a trade. Asbestosis. The X-ray picture of the typical asbestotic chest is confusing to the layman. The effect is described as a diffuse fibrosis. Characteristic silicotic nodules are absent and even *'&**\K; vV- . J; |i. PLEAXIHNITBIFITF | m.% yWfif*c-r<:'7*~-K-a` S>~ '"- EFFECTS OF DUSTS AND FUMES UPON MAN 33 the expert roentgenologist withholds his diagnosis until the case history is complete. The pathology produced by asbestos is not like that of silicosis. The asbestos fibers group about the neck of an alveolus and shut it off, causing what is known as atelectasis. There is no definite migration or transportation of the dust particles to the lymph nodes and no formation of the fibrous nodules as shown in Fig. 13. As the atelectatic areas increase, the reduction in lung X \ \ ' : VTa-X*.V* . TV,**.-' * I-* ! - f. --*v - : :- ' j : ,J /H Fio. 15.--Asbontooia IkkIi'cs in iputum. (After Eltman |76); courier]/ J. Jnd. Ht/g.) \ area causes serious dyspnea or labored breathing. Lanza (158) suggests that the enlarged hearts noted frequently in his cases of second-stage asbestosis may be the result of the increased work of the heart resulting from this condition; it takes more work to pump blood through the atelectatic than through the normal lung. In silicosis it seems TT be a general rule thnt, after a certain point, the victim's condition grows worse even if his dust exposure has ceased. But Wood and Gloyne (25S) Btatc that they have BeeD patients with asbestosis "whose condition appears to have T_-/ -~r" ym , , fr , --------- ' K ~- ^ - `'T. > . ;. V. - , . ,m . ,t .1 <r> . ,,TZ '- i V ' r a exhibit [| IS&zOil, 34 ISDl'STKIAl. DUST 1 remained stationary shire stopping woik in the factory/imi they advise definitely that the nshestotie individual he removed from his dusty job. Mcrewcthcr (1S3) und Lanza are less certain on this point. Asbestosis Bodies. In the lungs of patients who died after prolonged exposure to asbestos dust and in the Bputum of men with considerable asbestos-dust exposure are found wlmt first were called curious bodies and later asbcslosis bodies (Fig. 15) (75). \Vhile so:.- what similar bodies occur in the lungs of coal workers and even of normal persons, it is ndmitted that asbestosis bodies in sputum are characteristic of asbestosis. Stewart (223) gives considerable diagnostic weight to their presence. Pneumoconiosis in Animals. Silicosis has been produced experimentally by quartz dusting guinea pigs, rabbits, mice, cats, and domestic fowl, thus emphasizing the specificity of quartz dust to biological tissue. In like manner asbestosis has been produced in experimental animals. The Equidae, such as horses and mules, apparently are not susceptible to ordinary pulmonary tuberculosis but there is no reason to believe they have any special immunity or resistance to silicosis. The normal silica content of horses' or mules' lungs is not known but it would seem wholly reasonable to use the lungs of animals which have worked 5 to 15 years underground in mines as physiological dust samples. A brief report on *his subject was published by Haynes (121) but data such as one m-.-ds are singularly lacking. TOXIC DUSTS Poisoning from inhaling toxic dusts is much more likely than poisoning from swallowing them. Dusts thnt reach the lungs may pass directly into the blood stream, thence to the heart, and immediately be pumped all over the body. Distribution to all the body tissue is thus brought about rapidly and effec tively. But dust taken in with the food goes to the stomach and the major part passes out in the feces. Some is picked up by the portal blood circulation and moves on to the liver. That portion which causes poisoning must first pass through the liver, which is an effective filter and detoxifier; only then can it enter the general circulation. . EFFECTS OF DUSTS AND FUMES UPON MAN 35 The practical significance of this physiological distinction between the two ports of entry of dust is considerable. Hamilton (103) states, A great deal of money has been wasted by well-meaning employers who sought to protect lead furnacemen or oxide roasters or white lead grinders against poisoning, by providing baths and lunchrooms and clean overalls and mouth washes and such, instead of preventing the escape of lead into the air the men were obliged to breathe, and unfor' tunately this has sometimes been done under a physician's advice. It must never be forgotten that the great majority of industrial poisons enter the body with the inspired air and that while a workman eats only three times a day he breathes sixteen times a minute during the eight or ten hours of his working day. Goadby (SS) found that cats dusted with lead acquired lead poisoning more easily than did a control animal which was fed over ten times the total lead dosage for the dusted animals. Drinker and Sluiw 51) showed how efficiently the liver removed foreign dust part: s injected into the blood stream. Minot (188) emphasized tT.e much greater danger of lead poisoning from inhaled than from swallowed dusts. Blumgart (24) showed that the absorption of lead directly in the nasal passages wa^; rapid and might be "of a magnitude far in excess of the minimal dose by mouth." * All this experimental evidence confirms the view so often expressed by the late Sir Thomas Lcgge (162), but which is only now beginning to be accepted, namely, that there is far more danger of being poisoned by inhaling toxic dusts than by ingesting them in food or drink. _. Metal-fume Fever. Of interest in connection with the breath ing of dusts is metal-fume fever, a transient noncumulative malady that results from breathing rather heavy concentrations of metal fumes like zinc oxide, copper oxide, magnesium oxide, "lead, probably lead oxide (227), and manganese dioxide. About 2 to 8 hr. after a heavy exposure to the well-dispersed metallic or metallic-oxide fumes, the victim experiences chills followed by fever like that of malaria or the protein reaction following a typhoid inoculation. The patient's fever may reach uncomfortable heights (we have recorded 104F.) and the next day he feels debilitated but gcnerully cun go to work. With 3G INDUSTRIAL DUST the fever goes nn in creased white-blood-erll count or'jeur like that experienced in any infection. Hy tlie next morning the fever has abated but the leucocytosis persists (Fig. 16). Then the victim is fairly immune; generally he can take another inhalation without experiencing a second attack (70). In indus try' it is a commonplace that attacks on successive days are unlikely. The cause of this peculiar malady is probably the absorption of protein material which results from the action of the inhaled Pic, 1G.--A typical attack of motaJ-fumc fever, thawing inrrenae in leururyi* count, body temperature, and drop in vital capacity. Note that fever aboiea before the white count rrturna to normal, (After Sturgis ft of.; courtrsy J. Jnd. Hvq.) I fume particles upon the tissue of the respiratory passages. In our own experiments we found that the chilis and fever were acquired far more easily if one took a few deep breaths at a rate of say five breaths per minute than at the normal rate of twelve to fifteen breaths per minute. Slow, deep breathing insures penetration into the alveolar spaces. Electric or acetylene welding in a confined spare may generate metal-fume concentrations in excess of those used by Lehmann or Drinker in studying metal-fume fever. At present there are no data on the effects of breathing dense concentrations for .613 Industrial dust. Hygienic silence, seasurenient and control Tinker, Philip and Patch, Theodore Dust