Document 51mmbopzxVYN1b5LQ7gojJp8

$10852285 INDUSTRIAL TOXICOLOGY LAWRENCE T. FAIRHALL Scieniiet Director, Public Health Service, Federal Security Agency, Chief, Induetrial Hygiene Laboratory, Induetrial Hygiene Divieion. % BALTIMORE THE WILLIAMS & WILKINS COMPANY 1949 ST0852286 (f/S7 F/?/ Si Lab, COPTBIGHT 1949 Th* Williams & Wilkins Compant Made in the United States of America COMPOMO AXD PAINTED AT THE WAVERLY PRESS, INC. TO* Th Wnjji.ui A WiLxnn Compant Baltimore, Md., U. 8. A. ST0852281 J PREFACE This book has been written in response to many requests for information concerning the toxicity of new, as well as old, substances of industrial im portance. Its purpose is to serve as a bridge between the rapidly expanding field of toxicological investigation and the application of this knowledge of industrial poisons by the industrial hygienist. Many of the substances described are not poisons in the usual sense. Indeed, some are not toxic at all. These represent materials newly used in industry, however, and concerning which some doubt has existed. The industrial hygienist is occasionally compelled to search through may peri odicals and specialised books to acquaint himself with the current knowl edge concerning these substances. All too frequently the toxic effects of a substance are presented in case reports, which are often confusing and de tailed, and require careful study in order to define its toxicity. In the present manual this material has been surveyed and summarized with the object of relieving the industrial hygienist of much of this burden. Al though this has required the examination of the available literature regard ing each substance, only selected and pertinent bibliographical references are given, with such appraisal and interpretation as would serve to give the industrial hygienist an evaluation of toxicity without his having to digest a great mass of literature, or to seek out many obscure and difficultly obtain able publications. A short list of the more pertinent references is given at the end of each substance discussed. The references either relate directly to the subject matter, or are felt to be of general interest to the reader.. No attempt whatsoever was made to append a complete bibliography--to do so would only expand the book without adding significantly to its value. It will be apparent that whatever merit this book may possess is due to the vast fund of information which the many researchers in this field have contributed during the last two or three decades. The author's task has been to examine and compare these investigations and to assess them criti cally so that the gist of current thought is presented for the toxicological evaluation of a given substance. The form in which the material is presented was arrived at after much consideration. It is largely based upon the needs of the industrial hy gienist and is as brief as was felt consistent with his requirements. Some disparity of space will be found in that certain substances whose toxicity is well recognized are treated in more summary fashion, in comparison with those substances of obscure toxicity or substances which currently are of great importance, which are discussed in more detail. The purpose in presenting the characteristics of the various substances ST0852288 Vi PREFACE under consideration, is related to more than mere identification. The phys iological response to many substances depends to some extent upon their physical and chemical characteristics, such as volatility, solubility, solvent action, and stability. A knowledge of the outstanding characteristics of a substance is therefore often useful in defining a given occupational hazard. The chemical and physical constants are based upon the best information available for the pure substance and several may differ somewhat from those found in the usual tables. In all cases the most authentic values have been sought for these constants. They are of course particularly useful to the chemist in the examination of materials. Under the section on industrial uses, an attempt has been made to gather from governmental and other sources such material as would indicate the extent of production and use. In many cases this will give a rough idea of the extent to which exposure may occur in industry. Because of the diversity of the substances discussed, no attempt has been made to classify these substances in groups based upon either chemical re semblance or similarity of physiological response. Furthermore, it was felt that a simple alphabetical arrangement would facilitate reference. For further simplicity, the substances are broken down into two main groups--inorganic substances and the carbon compounds. It has not been the author's intention to give detailed analytical instruc tion with reference to the various substances described in the following pages. Under the heading of analysis, reference is made to standard methods or to recently proposed methods. In a number of cases where no present method of analysis is available, the writer has suggested possible procedures. The writer is most grateful for assistance from his colleagues in the In dustrial Hygiene Division of the United States Public Health Service. However, he assumes full responsibility for the material as presented. Despite every good intention and every earnest and painstaking effort, imperfections and errors may occur; readers will confer a favor by reporting them so that they may be corrected in a future edition. '* ST0852289 CONTENTS Preface................................................................................................................................. Introduction....................................................................................................................... 1 Past I INORGANIC SUBSTANCES flliiminnm............................. . Alundum.............................. Ammonia............................. Antimony............................. Arsenic.................................. Asbestos................................ Barium.................................. Beryllium.............................. Bismuth................................ Boron..................................... Bromine................................ Cadmium............................... Cerium.................................. Chlorine................................ Chromium............................. Cobalt.................................... Columbians........................... Fluorine................................ Gallium................................. Germanium............... ........... Glaaa fiber and mineral wool Hydrasoio add..................... Hydrogen ohloride................ Hydrogen fluoride................. Hydrogen nitrate.................. Hydrogen aulfate.................. Hydrogen aulfide................... Indium....... ............. ............. Iodine.................................... Iron....................................... T-untWnuTp........................... Lead...................................... Magnesium............................ Manganese............................. Mercury................................ Mica...................................... Molybdenum......................... Niokel................................... Nitrogen oxides..................... Omnium.................................. vii 15 17 19 21 25 29 32 34 38 40 43 44 49 51 53 56 60 61 64 68 70 72 75 77. 79 81 82 84 87 89 91 94 96 90 102 105 109 111 113 116 120 ST0852290 Viii CONTENTS Osone....................................................................................................................... 122 Palladium................................................................................................................. 125 Phoaphine................................................................................................................ 127 Phosphorus.............................................................................................................. 129 Platinum.................................................................................................................. 132 Plutonium................................................................................................................ 134 Portland cement..................................................................................................... 137 Badioactive substances.......................................................................................... 140 Bubidium and cesium............................................................................................ 142 Selenium.................................................................................................................. 144 Silica........................................................................................................................ 147 Silioones................................................................................................................... 151 Silver....................................................................................................................... 153 Btrontium................................................................................................................ 155 Sulfur....................................................................................................................... 157 Sulfur chlorides....................................................................................................... 159 Sulfur dioxide......................................................................................................... 181 Sulfur hexafluoride.................................................................................................. 163 Talc......................................................................................................................... 164 Tantalum................................................................................................................. 167 Tellurium................................................................................................................ 169 Thallium................................................................................................................. 171 Thorium................................................................................................................... 174 Tin........................................................................................................................... 176 Titanium................................................................................................................. 179 Tungsten................................................................................................................. 181 Uranium..................... 183 Vanadium................................................................................................................ 186 Zinc......................................................................................................................... 189 Zirconium................................................................................................................ 191 Past II CABBON COMPOUNDS Acetaldehyde.......................................................................................................... 197 Acetio acid.............................................................................................................. 200 Acetic anhydride.................................................................................................... 202 Acetone................................................................................................................... 204 Acridine.................................................................................................................. 206 Acrolein................................................................................................................... 208 Acrylonitrile............................................................................................................ 211 Allyl chloride and allyl bromide........................................................................... 213 Amyl acetate.......................................................................................................... 215 Amyl alcohol........................................................................................................... 217 Aniline..................................................................................................................... 220 Benzene................................................................................................................... 223 * Benzene hexachloride............................................................................................. 226 Benzoyl peroxide.................................................................................................... 229 Bromoform.............................................................................................................. 231 1,3-Butadiene.......................................................................................................... 232 2-Butanone............................................................................................................. 234 ST085229I *'r - CONTENTS ix 43utyl acetate......................................................................................................... 238 Butyl alcohol*............................................................................................................ 238 -Butyl methyl ketone............................................................................................. 241 iaoBatyl methyl ketone............................................................................................. 243 Carbon dioxide. ......................................................................................................... 244 Carbon disulfide........................................................................................................ 246 Carbon monoxide....................................................................................................... 248 Carbon tetrachloride................................................................................................. 250 Carbonyl ehloride (phoegene).................................................................................. 253 Chlorinated diphenyls and chloronapthaleaes....................................................... 255 Chlorinated mononitroparaffins.................... ........................................................ 257 Chlorobensene........................................................................................................... 250 2-Chloro-l, 3-butadiene (ohloroprene)..................................................................... 261 Chloroform................................................................................................................. 263 Chloronitrobensenes................................................................................................. 265 Chloropicrin..............................................................................>............................... 267 Creeols--creeylio acid................................................................................................ 270 Cyclohexane............................................................................................................... 272 Cyclohexanol............................................................................................................. 274 Cyclohexanone........................................................................................................... 276 Cyolohexene............................................................................................................... 278 Cyclopropane............................................................................................................. 280 Dibutyl phthalate..................................................................................................... 281 Diohlorobenzene........................................................................................................ 283 Diohlorodiphenyltrichloroethane (DDT)................................................................ 286 Dichloroethanes......................................................................................................... 288 Diohloroethylene....................................................................................................... 291 Diohloroethyl ether.................................................................................................. 293 Diohloromethane....................................................................................................... 295 2.4- Dichlorophenoxyacetic acid............................................................................ 297 1,2-Dichloropropane................................................................................................. 299 Diethylene glycol monoethyl ether and related aubstancea................................. 301 Diethyl ether............................................................................................................. 303 Di(2-ethylhexyl)phthalate........................................................................................ 305 Dimethylaniline......................................................................................................... 306 Dimethyl sulfate....................................................................................................... 308 Dinitrobenzene.......................................................................................................... 310 1.4- Dioxane............................................................................................................. 311 Diphenyl.................................................................................................................... 314 Ethyl acetate............................................................................................................. 316 Ethyl alcohol............................................................................................................. 318 Ethylbenzene............................................................................................................. 320 Ethyl bromide........................................................................................................... 322 Ethyl chloride........................................................................................................... 323 Ethylene chlorohydrin.............................................................................................. 325 Ethylene glycol......................................................................................................... 328 Ethylene glycol mono-n-butylether........................................................................ 331 Ethylene glycol monoethyl ether............................................................................ 332 Ethylene glycol monoethyl ether acetate...................................................... 7___ 334 Ethylene glycol monomethyl ether......................................................................... 336 ST 0852292 X CONTENTS Ethylene glycol monomethyl ether acetate.................................................. Ethylene imine........................................................................................................... 340 Ethylene oxide............................................................................................................ 341 Ethyl formate........................................................................................................... 343 Ethyl silicate........................................... ................................................................ 345 Fluorocarbons........................................................................................................... 346 Formaldehyde........................................................................................................... 348 Formic acid............................................................................................................... 351 Furfural..................................................................................................................... 353 Hydrocarbons, saturated--methane, ethane, propane, butane............................ 355 Hydrocarbons, saturated--pentane, hexane, heptane, octane.............................. 357 Hydrocarbons, unsaturated--acetylene.................................................................. 359 Hydrocarbons, unsaturated--ethylene, propylene,butylene, amylene, hexylene.. 361 Hydrogen cyanide..................................................................................................... 363 Isophorone................................................................................................................. 366 Ketene........................................................................................................................ 368 Meeityl oxide............................................................................................................ 369 Methanol................................................................................................................... 371 Methyl acetate................................................................................................. Methyl bromide.......................................................................................................... 378 Methyl chloride......................................................................................................... 378 Methylcydohexane.................................................................... ............................ 381 Methylcyolohexanol................................................................................................... 382 Methyloyclohexanone...........: ...................................................... ....................... 384 Methyl formate.......................................................................................................... 385 Methyl iodide............................................................................................................ 387 Methyl methacrylate................................................................................................ 388 Methyl n-propyl ketone (pentanone-2)................................................................... 391 Metol...................................................................................... Naphtha..................................................................................................................... 394 Naphthalene............................................................................................................... 395 Naphthylamine......................................................................................................... 397 Nitrobenzene............................................................................................................. 399 Nitro derivatives of aniline..................................................................................... 401 Nitroethane................................................................................................................ 403 Nitroglycerin.............................................................................................................. 405 Nitromethane............................................................................................................ 407 Nitropropane...............................................................................................................409 Oxalic acid................................................................................................................ 411 Pentachloroethane..................................................................................................... 411 Pentachlorophenol..................................................................................................... 414 Phenol......................................................................................................................... 416 Phenylenediamine...................................................................................................... 418 Phthalic anhydride................................................................................................... 421 Picric acid................................................................................................................... 422. Propyl acetates.......................................................................................................... 425 n-Propyl alcohol........................................................................................................ 427 woPropyl alcohol...................................................................................................... 428 MoPropyl benzene...................................................................................................... 430 woPropyl ether.......................................................................................................... 431 338 374 392 CONTENTS Pyridine........................................................ Qnimmii and hydroquinone...................... Styrene monomer....................................... Tetraobloroethane...................................... Tetraohloroethylene (perchloroethylene) Tetrenitromethane....................................... Toluene.......................................................... Toluidine........................................................ Triehloroethane............................................ Trichloroethylene......................................... Triorfhoereeyl phoephate.......................... Triethanolamine........................................... Trinitrotoluene (TNT)................................ Turpentine..................................................... Vinyl chloride............................................... Xylene............................................................ Xylidine.......................................................... Index................................................. ST 0852293 XI 473 i S S S S iS IS g g ST 085229U INTRODUCTION In an earlier period of our industrial development workmen were exposed to smoke, dust, fumes, and gases without regard to the possible injurious nature of many of these substances. Certain occupations, such as the n^ning of mercury, were formerly notorious in this respect. Furthermore, this condition was recognized in only very few instances and exposure to fumes or dusts of a deleterious type was generally recognized as a somewhat disagreeable and accepted condition of many occupations. The fact that soma workers in mines, mills, or factories sickened, were forced to leave their occupation, and later died, did not always bring with it the realization that the nature of their work was a factor. In some occupations where industrial disease was prevalent there were often individuals who had been immersed in such an environment most of their working life and yet re mained apparently strong and healthy. Such cases would be cited as indi cating the general harmlessness of their occupation and those who sickened were regarded as weaklings. Many industrial diseases, such as phos phorus poisoning, were undetected for years, or, as in the case of manganese poisoning, were undetected for generations. The scrutiny of occupation as a factor in disease, although emphasized long ago by Ramazzini, is a comparatively modem development. Industrial physicians only a genera tion ago were largely concerned with the more external factors of employ ment--hernia, lumbago, cataracts in the case of glass workers, deafness in boilermakers--or in incidental disease, such as ankylostomiasis among miners or tuberculosis among cotton spinners. The latter were, of course, related to poor sanitation and poor nutrition, respectively, and were by no means peculiar to the occupation of the worker. Knowledge, however, of the existence of occupational disease became more and more evident and, although locally confined at first, gradually spread. Thus, such terms as "grinder's rot", "phossy jaw", "painter's colic", "chrome itch", and "miner'B phthisic" gradually appeared in in dustry and in the literature. Within the past generation industrial physicians have been alerted to the danger of much of the smoke, dust, or gases to which workers were exposed, scientists have actively investigated the effects of many of these aerial contaminants on animal life, and engi neers have instituted control measures in industry to reduce the hazard of exposure. Poisoning familiarly occurs as the result of ingestion of toxic substances and this doubtless influenced much of the earlier industrial hygiene thought. As a result, stringent sanitary measures were advocated and adopted in certain industrial processes in order to prevent possible entrance of indus- l ST 0852295 2 INTBODUCTION trial poiaonB by mouth. These precautionary measures included such matters as a complete change of clothing on entering a shift, careful scrub bing of the hands and face before eating lunch, and a thorough washing and shower at the end of the work period. While excellent in themselves, these measures do not include the sanitation of breathing and instances of industrial poisoning have occurred where workers had observed strict cleanliness yet were exposed to dangerous concentrations of dust, fumes, or gases. Inhalation is now recognised as one of the most dangerous routes of entrance of industrial poisons. Gases, Fumes, and Dust While the greater part of industrial smoke consists largely of carbon and is relatively harmless, it frequently contains gases which are dangerous if continuously breathed or if breathed in high concentration and, in addition, it may contain noxious fumes or toxic dusts from certain processes. From the point of view of industrial hygiene a gas may be considered to be any aeriform or completely elastic fluid whioh does not become liquid or solid at ordinary temperatures. Fumes or vapors consist of material in the near-gaseous, or extremely fine particulate form which condense to liquids or solids at room temperature. Dusts, on the other hand, consist of larger particulate matter suspended in air. It must be realized that these definitions are not rigid and that they merely indicate somewhat roughly different stages of attenuation of matter. It is possible, for instance, to have mercury dust suspended in the air of a workroom, due to constant attrition of mercury spilled on the floor and carried into the air as extremely minute droplets following mechanical agitation. At the same time, mer cury fume may be present as the result of heating this substance and finally the vapor tension of mercury is such that true, gaseous mercury may also be present to a slight extent. It is important for the industrial hygienist to keep these distinctions in mind. The detection and estimation of mercury gas in air by means of the photoelectric mercury detector depends upon the absorption of ultra violet light of a wave length of 2537 A and the degree of absorption is a measure of the amount of gaseous mercury present. How ever, t.hia instrument would not indicate the total mercury present in an atmosphere where particulate mercury or dust from any of its compounds was also present. While dusts have been classified as particles or aggregates of particles of from 150 microns to one micron in diameter, fumes of from one micron to 0J2 micron in size, and smokes as particles less than 0.3 micron in diameter, size alone represents at best only a rough separation of these three classes. The mode of formation must also be considered. Thus, dusts ordinarily result from mechanical attrition and distribution, while fumes and smokes ST 0852296 INTRODUCTION pryuj and carried into the air usually as the result of chemical reaction ~ dispersion of a chemically active substance by release of pres- i;orby explosion. diqjerse systems, or aerosols, in which the dispersion medium is a i&Hi&Bec from other disperse systems in the great disparity that exists between the density and structure of the disperse phase and the dispersion lY^hmv The mere fact that two such disperse systems contain amicrojoopfo particle wmflnr in magnitude does not necessarily mean that the properties of the two systems are identical, although they may have many points of similarity. In the case of dust, a great deal of work is required in order to reduce a solid to fine dust, i.e., to overcome the forces of cohesion that originally held the particles together in addition to the work required in distributing the particles throughout the dispersing medium. Even though a certain degree of uniformity finally is attained by settling or other means, dispersed dust of the finest order of magnitude is less uniform in structure than aerosols produced by the cand^ uridon of vapor. These factors have scone weight in devising means of sampling and analysis of aerial contaminants. The evaluation of aerial contaminants is very frequently a matter of importance to the industrial hygienist and a knowledge of the properties of such disperse systems as those indicated above, as well as the properties of gases and vapors in relatively low concentrations, is of particular value with reference to the analytical detection and determination of the con stituent contaminants. The composition of the aerial contaminant to which workmen in a given ' plant are exposed is of course of paramount importance to the industrial hygienist. This is usually known, or information may be obtainable from the management. In some cases, however, an unknown or unsuspected factor may be present and careful investigation may be necessary before the culprit is revealed. Cases have occurred, for example, where arsenic, cadmium, or selenium existing as unsuspected impurities in the material being fabricated have caused illness and death. An unrecognized by product of manufacture may cause difficulty, or a change in the formula of basic material used in manufacture may bring about an unhygienic situa tion. The industrial hygienist is required not only to ferret out the occu pational disease hazard but also--very necessarily--to know its charac teristics, a proper method of sampling, and the most reliable method of analytical evaluation in terms of air content. His study includes the weighted or average exposure of employees at various stations and occupa tions. Furthermore, he is required to know something regarding the toxicity of the aerial contaminant in order to define the conditions under which employees are to be permitted to work in such an environment. ST 0852297 4 INTRODUCTION The toxic effects of many hazardous materials in industry are well known and it is comparatively easy to define safe working concentrations. There exist many substances in common use in industry, however, which are toxicologically not well defined. Unfortunately, toxicity cannot be evalu ated with the ease with which a chemical constant, such as a boiling point, melting point, or index of refraction, may be determined. Even with arduous investigation extending over many months, the toxicologist can at best give only a very general answer regarding the poisonous nature of a given substance. It would be of inestimable benefit of course, if one could--knowing the composition and molecular structure of such a sub stance--predict its physiological properties. Chemical Constitution and Physiological Response The possibility of relating chemical constitution and physiological ac tivity has long proved a fascinating field of speculation. The advantages of defining the toxicity of a substance from its constitution or structural formula are, as indicated above, obvious. Unfortunately, however, the matter is not simple. Certain relations exist, it is true, between structure and toxicity. For instance, ethyl and methyl alcohol, although differing in one important respect, are very similar in many of their other physio logical properties, and propyl, butyl, and amyl alcohols might be assumed to act similarly. These latter alcohols do, in fact, resemble the lower members but with a progressive increase in toxicity. An analogous in creasing toxicity might therefore be anticipated in the higher members of the alcohol series. This reasoning, however, is nullified by the changing physical properties of the higher members. In spite of a similar chemical structure, the higher alcohols become increasingly insoluble in body fluids and as a result there is an overall decreasing toxicity beyond a certain point. A similar increase in toxicity with an increasing number of carbon atoms is noted with sodium acetate, propionate, butyrate, and valerianate. Many other such relationships have been pointed out as more toxicological in formation has become available. The replacement of a hydrogen atom with chlorine in the saturated hy drocarbons results in an immediate change in toxicity; the entrance of such a halogen group in the organic sulfur compounds greatly intensifies the toxicity of the resulting compound. When one chlorine group is intro duced into ethyl sulfide, which is a weak poison, the resulting monochloroethyl sulfide, is found to be markedly toxic, while the introduction of a second chlorine atom results in dichlorodiethyl sulfide, or mustard gas, which is a very strong poison indeed. However, no such general rule can be applied in other cases. The successive replacement of hydrogens by chlorine in the methane molecule, which of itself is not toxic but merely it. INTBODTJCnON ST 08 52298 5 an asphyxiant, results in monochloromethane, CH*C1, dichloromethane, CHiCli, trichloromethane, CHCU, and tetrachloromethane, CCU, respec tively. These substances, however, do not follow a pattern of increasing toxicity. For instance, chloroform with its excellent narcotic properties, as well as the attendant possibilities of liver and heart damage, is less toxic in general than carbon tetrachloride on the one hand and much less toxic fhxi methyl chloride on the other hand. Yet dichloromethane, which occupies an intermediate position, is far less toxic than any of the other members of t-hia group. It does not follow therefore that there is any direct correlation between the number of chloro groups and the toxicity. The relatively inert and inoffensive hydroxyl group when introduced into an organic molecule frequently results in an increase in toxicity. Thus, methanol, CH*OH, has pronounced toxic properties compared with the parent substance and monohydroxybenzene, CH*OH, or phenol, has marked poisonous properties over and above those of benzene. Increas ing the number of hydroxyl groups may also increase the toxici+v of the aromatics. For example, the introduction of a second hydroxyl group in the benzene ring yields resorcinol, CH(OH)i, which is more toxic than phenol, while the introduction of a third group yields phloroglycinol which is the most toxic of the three. The entrance of an alkyl group into the molecule of a substance may also intensify its poisonous quality. Dimethyl resorcinol, C*H4(OCHj), is more toxic than resorcinol, CeH(OH)j. On the other hand, an alkyl group may diminish the toxic effect in other substances. Dichloromethyl arsine, As(CH)Clj, is very toxic, while the introduction of a second methyl group, as in dimethyl chloroarsine, As(CH)jCl, yields a substance of weaker toxicity. While the introduction of a chlorine group in aliphatic hydrocarbons increases the toxicity in general, this is not necessarily true in the case of the aromatic hydrocarbons. Thus, monochlorobenzene is less toxic than benzene itself and has been of no particular significance as an industrial poison. It appears to be a general rule that iso compounds are somewhat less toxic than normal compounds. woPropyl alcohol has a somewhat lower toxicity rating than normal propyl alcohol; isobutyl alcohol than normal butyl alcohol. A most interesting difference in toxicity has been found to exist in the benzene hexachlorides which have recently received attention as insecticides. In this case, the gamma derivative of 1,2,3,4,5,6 hexachlorocyclohexane, C*HCU, has been found to be especially lethal in action compared with the other four known isomers (1). Woodard and Hagan (2) found the gamma isomer to be as much as sixty times as toxic for certain warmblooded animals as other isomers of benzene hexachloride. In the -S T 0852293 6 INTRODUCTION case of many other optically isomeric substances, great differences may also be found in toadcities. For instance, 1-hyoscyamine is twice as active physiologically as dl-hyoscyamine (atropine) and moreover the laevo compound is twelve to twenty times as active as the dextro compound (3). Usually, but not invariably, the laevo compounds are more active than dextro compounds. Thus, Cushny found l-hyoscine to be sixteen to eighteen times as active as d-hyoecine and twice as active as dl-hyoscine. Similarly 1-adrenaline was twelve to fifteen times as active as d-adrenaline in its vasoconstrictor action and twice as active as dl-adrenaline. On the basis of rather indirect evidence, it is possible that the difference in physio logical behavior of suoh stereo-isomers is due to the ability of one or the other to combine with some protein or other constituent of the cell. How ever, sufficient quantitative data are not available to define clearly the mechanism of physiological activity and stereochemical configuration. The problem of relating chemical constitution and physiological action is even more confusing when it is recalled that substances of diverse chemical nature may produce similar physiological effects. The aliphatio narcotics, for example, include a large variety of structural type, such as hydrocar bons, alcohols, ethers, amines, and sulfones. According to Ing (4), these substances appear to achieve their effect by modifying the physico-chemical conditions of the cells due to certain physical properties shared by all classes of these compounds and not by the presence of certain pharmaco dynamic groups. It will be apparent therefore that while the temptation to rationalize regarding the prediction of tenacities may be great, the evaluation of toxicities of new substances is fraught with considerable uncertainty. Since no great rational scheme is available to aid, except rather sketchily, in deciding upon the toxicity of a given substance, it is inevitably necessary to carry out experimental work with animals. ExPKHIMKNTAIi TOXICOLOGY Experimental industrial toxicology does not differ widely from that of experimental pharmacology, since they both use the resources of chemistry, physics, physiology, and pathology to achieve their purpose. However, the pharmacologist is primarily interested in therapy rather than toxicity. Furthermore, he is interested in the effects of administration of a substance by mouth, or by intravenous or subcutaneous injection and rarely in the effects of inhalation, except in the case of inhalation anesthetics. The refinements of approach to certain physiological reactions adopted by the pharmacologist, however, often yield data of fundamental importance within a relatively short space of time. The toxicologist on the other hand may be compelled to follow an intricate procedure which is arduous and INTRODUCTION S T 0 8 5 2300 7 Nim* rf",ming m order to define a given physiological response. More over,' toxiodogioal studies frequently depend upon pathological changes following the administration of small amounts of such toxic materials as gases,1fumes, or dusts and these changes usually occur very slowly. ' i Toxicological investigations are in general based upon animal experi mentation for human experimentation is, of course, indefensible. It is true t*1** experiments provide only indirect evidence of the probable action of toxic substances on man, yet they are none-the-less of the greatest value. They not only afford information regarding upper toxic limits, but by long-eontinned study, reveal changes in lower concentrations which are of the greatest importance. In experimental work of this character, a con siderable amount of interpolation is necessary and evaluation of the experi mental results requires both acumen and careful judgment. Moreover, there are many poisons which produce completely different effects in differ ent species of animals. Mice and guinea pigs, for example, are more sensi tive to poisoning by trichloroethylene (acetylene trichloride) than cats, while rabbits are lees sensitive than cats. On the other hand, cats are more sensitive to lead poisoning than dogs and the latter more so than rats. Although such qualitative and quantitative differences may exist, never theless there can be no doubt that animal experiments are of value since they give an indication of the type of toxic action, as well as the relative toxicity of the substance under investigation. - The great advantage of animal experimentation is, first of all, the control of dosage and, secondly, the degree to which poisoning can be carried. This yields most useful information in tracing similar effects in humans accidentally poisoned and in warning against human exposure beyond a certain degree. Although the effects of exposure by inhalation are of paramount im portance, animal studies also usually include other forms of administration, such as ingestion, intravenous injection, intraperitoneal injection, and sub cutaneous injection. The latter form of administration is perhaps the least used as absorption is frequently slow and has less significance than the other forms. Intravenous injection provokes the most immediate response and is often useful in studying the immediate effects of substances upon the hemopoietic system. Intraperitoneal injection is one means of following the slow absorption of relatively insoluble substances, but is of particular value in studying the physiological response of various substances. For instance, when pure silica suspensions are intraperitoneally injected, a reaction occurs which is typical and fairly constant (5). Sayers and Miller found three types of reaction occurred with various dusts--absorptive, inert, and proliferative. The absorptive reaction occurs when fine dusts, guoh as calcite, limestone, gypsum, and cement, are injected. After suffi- ST. 08 52301 8 INTRODUCTION dent time, this material disappears from the peritoneal cavity without the formation of any scar tissue. In the case of the inert reaction, the dust re mains distributed about the peritoneum by the action of phagocytes, some times forming flat nodules, which do not tend to progress or form fibrous scar tissue. Soapstone, carborundum, and coal dusts exhibit this inert reaction. In the proliferative reaction, nodules form which continue to increase in size with the formation of fibrous or scar tissue. Quartz, chert, and flint dust produce this reaction. These three types of reaction corre spond very closely with the results obtained by the inhalation technique. While this method perhaps requires further exploration, it is useful in the approximate classification of dusts. The inhalation technique with reference to dusts, fumes, and gases is by far the most useful method used in experimental toxicology. In the case of gases, the various concentrations to which animals are exposed may be regulated with accuracy. Hence, the exposure may be clearly and accu rately defined. With fumes and dusts, the concentration of fume or dust in the air may be determined by exact chemical analysis. Whether or not the animals always breathe in the amount in the atmosphere may not be so accurately defined in many cases as animals, such as guinea pigs, tend to huddle together and jnay be able to filter out some of the dust or fume to which they are exposed. For the purpose of exposure, gas-tight or dust-tight exposure chambers of large size are usually used and animal cages may be placed directly in the exposure chamber. The gas may be introduced in known amounts and rapidly distributed throughout the exposure chamber by means of small fans. Substances which are sufficiently volatile, such as solvents, may be introduced in known amount into a constant current of air and the breath ing concentration may be accurately calculated. In addition, of course, samples of the exposure atmosphere may be taken in most cases and analyzed chemically. Fumes, such as metal fumes, may be generated by arcing between electrodes of the metal carrying 110 a.c. current and an appropriate re sistance. In order to prevent the formation of metallic oxide fume, it is usually necessary to generate this fume in an atmosphere of inert gas, such as nitrogen or helium, and "bleed" it into an incoming air current. Oxide fumes are readily formed by arcing in air or in an atmosphere of oxygen. Fumes of many organic substances may be formed by heating the material to the volatilization temperature in the incoming air stream. Dusts must be suspended in air in very finely divided form in order that they may remain in suspension as long as possible and so that the material is of sufficient degree of fineness to be carried deeply into the animals* lungs. An elutriating device is useful for this purpose (6), since it permits DJTEODtTCTION ST0852302 t flow of very finely divided dust of more or less uniform size. Ir f (tost exposures, it is difficult to control the amount of dust in th ^atmosphere and hence it is necessary to draw small samples from Hthne for analysis. Even though the dust concentration is accu;snown, the amount carried into the animals' lungs is questionable .invariable amount ia removed by the filtering action of the nose, part oi t2)t<du*t remaining in suspension is removed before the air enters deeply Into the lungs. The ciliated epithelium found throughout the extent of the air-passages and their prolongations constantly sweeps out air-borne parand only the very finest material penetrates to the lung alveoli. ^Description of the means of evaluating the effects of various industrial pqffPM will be found given in detail in the various publications referred to in the suooeeding text. It will be noted that a considerable latitude of experi mentation is necessary in order to study the effects of a given industrial poison. . Tha degree of exposure (that is, the total amount of substance to which an has been exposed for a given length of time) is, of course, only preliminary to the evaluation of the toxicity of the substance. The be havior of the animal must be observed for this is an index of the manner In which the poison acts. Some substances may cause death immediately or within a few minutes--for example, hydrogen cyanide, hydrogen sulfide, or carbon monoxide. Other substances may act as irritants with symptoms of pain, salivation, vomiting, and purging. Ammonia gas, cadmium oxide fume, and chloropicrin, respectively, produce these effects. Other sub stances affect the central nervous system and produce characteristic symp toms, such as narcosis, convulsions, and paralysis. The various symptoms, in general, serve at best only as a rough classifi cation of toxic substances. The effects of poisons are often subtle and a variety of symptoms may be displayed. In chronic poisoning, or in the case of a cumulative poison, anatomical changes may be produced in cer tain organs or tissues which are characteristic for the poison. Blood changes may occur with an increase or decrease in hemoglobin, in red or white cells, and often with characteristic morphological changes in either or both the erythrocytes and leukocytes. All these and many other effects must be studied with care in the evaluation of the toxicity of a substance. It will be apparent therefore that the term toxicity does not refer to a fixed quantity, such as, say, a constant of nature. On the contrary, it is a de scriptive term and is often more clearly understood when applied in relation to other analogous substances. When the toxicity of a substance is evalu ated in the broad sense described above, however, the industrial toxicologist is able to advise somewhat definitely the limitation of possible exposure of human beings to industrial poisons. ST 0852303 10 INTRODUCTION It should be clearly indicated that, while such procedures as those briefly indicated above serve to establish useful limits with regard to industrial poisons, the more fundamental aspects of toxicology involve far more exten sive and difficult physicochemical and physiological investigation. Vari ous physical factors such as surface activity, solubility, dispersibility, polarity, partition coefficient, particle size, and electrophoretic properties may require study. The mechanism whereby many substances produce toxic effects in is important and requires careful exploration. The fate of these substances in the body--the changes which organic compounds undergo and the metabolites formed--serves to indicate the means by which the body attempts to reduce their toxicity and thus protect itself against their poisonous effects. This is especially true of organic com pounds completely foreign to the body. In their passage through the ani mal organism these substances interact with the normal biochemical sys tems which they encounter. The enzymic systems which carry out the oxidations, reductions, hydrolyses, and syntheses in the body may be vari ously affected. The metabolic processes involved reflect an attempt to reduce or abolish the toxic action or damage to the organism. However, it is not true that the product or products formed are invariably less toxic than the parent substance. For example, Channon and his associates (7) found that 2,4,6-trinitrotoluene (a-TNT) is partly converted in the animal organism to 2,6-dinitro-4-hydroxylaminotoluene which is excreted as such in the urine. Furthermore, the biological reduction product of picric acid is picramic acid. In both these cases the end-products are more toxic than the original substances. Nevertheless in the case of many other poisons the toxic substance is converted to harmless metabolites and elimi nated. Fundamental investigation of the toxicity of a given substance therefore includes study of the course of the toxic agent through the body, its effects on various organs and tissues during its passage, and the changes produced in the substance by the detoxicating mechanism of the body as indicated by the metabolites formed. Rbfebznces 1. Slade, R.: The gamma isomer of hexachlorocyclohexane (gammexane). The Hurter Memorial Lecture, Soc. Chem. Ind., March 1945. 2. Woodard, G., and Hagan, E. C.: Toxicological studies on the isomers and mixtures of isomers of bensene hexachloride. Fed. Proo., Soc. Pharm. Exptl. Therap. 6: 386 (1947). 3. Cushny, A. R.: Biological Relations of Optically Isomeric Substances. Williams & Wilkins Co., Baltimore, 1926, p. 40. 4. Ing, H. R.: Chemical constitution and pharmacological action. Trans. Faraday Boc. 39: 373 (1943). ST0852304 INTBODUCnON 11 f3Xr.WS., a&nd S5ay"era, H. R.^: Phyaloloricsa- lp-.bnoR"n- "> . wy.7 W*iWnton, D. C., 1M0, p. r. U* 8' Pub< Hwlth 8emc. ?7. Cbtoanlmaenos, H(o.-JT.J, iM.Ti.ll)*., OB.ioTc.b,wann.dJW. illiam70* (1nM4t). . Mar tt*lbo.ll,m of 2:<;6-trinitro- ( W- Industrial Toxicology [ 29 ] ST 0852305 asbestos 13. Lewy, O. A.: A study of arsine poisoning. Quart. J. Ezper. Physiol. SI: 47 (1947). 13. Sandell, E. B.: Colorimetrio miorodetermination of arsenio after evolution as arsine. Ind. Eng. Cham., Anal. Ed. U: 82 (1942). 14. Mellan, I.: Organio Reagents in Inorganio Analysis. Blakiston Co., Philadel phia, 1941, p. 256. ASBESTOS Characteristics Asbestos, amianthus, earth flax, stone flax, mountain cork, is a charac teristically silky, fibrous mineral, the composition of which varies with its source. The form known as chiysotile is derived from serpentine and is a hydrous magnesium silicate containing from 12.5 to 14 per cent water of crystallization. About 95 per cent of commercial asbestos is chrysotile. Chrysotile has the silkiest and strongest fiber and can be spun. The fibers may be as long as six inches in length. Asbestos derived from amphibole occurs as a variety of minerals consisting of iron, calcium, and magnesium with little water of constitution. The latter type of asbestos consists of short fibers and is usually inferior to that derived from serpentine. Am phibole asbestos (anthophyllite) while not so suitable for spinning is more stable chemically than chrysotile and more resistant to acids and heat. Canada has been an important source for the chrysotile asbestos used largely in the United States. The Canadian asbestos industry is centered in the Thetford Mines area of the Province of Quebec. A new source for chyrsotile type asbestos is a large quarry on the eastern shoulder of Belvidere Mountain in Vermont which was opened in the summer of 1944. This deposit is of importance because it represents the only large source of long-fibered chiysotile so far found in the United States. Deposits of amphibole asbestos are mined in Georgia and North Carolina. Industrial Uses Asbestos is an important substance in industry and consumption in the United States for 1945 amounted to 377,875 short tons (1). Due to its fibrous nature, flexibility and heat resistant properties, it is used extensively for valve packings, gaskets, boiler lagging, and pipe covering in industrial plants and as friction material in the automotive industry. A considerable market exists in the building industry for asbestos-cement products, heat insulation, and fire-proofing. The utilization of asbestos for fibers for spinning in the manufacture of asbestos clothing for fire fighting is an im- ST 0852306 asbestos [ 30 ] Industrial Toxicology portant use for asbestos. The largest single outlet for asbestos in manu factured products in 1944 was for clutch facings, and next in quantity of output were brake linings. Asbestos roofing consumed the third largest amount of asbestos in that year. Industrial Injury The inhalation of asbestos dust produces a condition known as asbestosis. While certain other minerals of minor importance have been shown to pro duce lung fibrosis, asbestos is the only important silicate apart from talc and mica which does not contain free silica and yet produces pulmonary lung fibrotic changes leading to disability and death. Asbestosis occurs chiefly in industrial plants where asbestos is fabricated. The spinning and weaving of asbestos in combination with other textiles results in exposure of workmen to asbestos dust. The long continued inhalation of asbestos dust results in a form of pneumoconiosis. The primary effect of inhalation of asbestos dust is an interstitial pulmonary fibrosis. On an X-ray film the shadows cast by this type of fibrosis resemble ground glass in appearance and usually extend over the lower portions of the lung fields, frequently being heavier on the right side (2). Unlike silicosis, nodular fibrosis has not been detected in asbestos workers (3). A progressive dyspnea, vari able cough, substemal chest pains, decreased chest expansion, weakness, emaciation, clubbed finger tips, and curved fingernails are the chief symp toms of asbestosis, as in silicosis. A characteristic finding in asbestosis is that of asbestos bodies in the lungs and in the sputum (4). The so-called asbestos bodies are apparently formed only in the lungs and may be demon strated microscopically on sectioning lung tissue or in the sputum. The core of the body is an asbestos fiber which is surrounded by protein deposits. Unstained specimens are golden yellow or golden brown. They are not stained with ordinary histological stains but may be demonstrated by the Prussian blue staining procedure. The reaction to the fibrous needle in the tissue which becomes manifest in exudate cell infiltration is accompanied by numerous giant cells containing foreign particles and an increase of diffuse interstitial connective tissue and fibrosis. While the essential re action to asbestos particles is considered to be chemical by many investiga tors others consider the pathogenosis of the disease to be mechanical (5) in nature. When the lungs are examined by the naked eye after death, they are large and densely fibrotic. Often the lung is completely adherent to the chest wall and, in advanced cases, to the diaphragm with the formation of a thick and extremely dense layer of fibrous tissue. Four main complica tions and sequelae of pulmonary asbestosis are purulent bronchitis, bron chial pneumonia, pulmonary tuberculosis, and emphysema (6). Several cases of asbestosis have been reported which progressed to a fatal terraina- ST 0852327 INDEX [ 482 ] Industrial Toxicology Styrene monomer, 437 Sugar c&ne grub, 284 Sulfur, 157 . Sulfur diehloride,15, 202 Sulfur dioxide, 181 Sulfur hexafluoride, 163 Sulfurio acid, 82 Sulfurio ether, 308 Sulfur monoenloride, 150 Sulfur, pneumoconiosis from, 158 Sulfur trioxide, 161 Sulfur trioxide manufacture, 187 Sulfuryl chloride, 150 Sulfuryl oxychloride, 159 Superphosphate, 129 Sylveetrene, 463 Talc, 164, 286 Tannic acid, 51, 104, 183, 188 Tantalum, 167 Tantalum carbide, 168 Tantalum fluoride, 168 Tantalum oxide. 168 Tar camphor, 885 Teeth, mottled, 65 Teflon. 65 Tellurium, 169 Tellurium dioxide, 169 Tellurium hydride, 169 Terephthalic acid, 468 Tetrachloroethane, 439 1.1.1.2-Tetraohloroethane, 439, 440, 441 1.1.2.2-Tetrachloroethane. 439 i-Tetrachloroethane, 291, 439,453 Tetrachloroethane collodion, 440 Tetrachloroethylene, 413, 442 Tetrachloromethane, 5, 378 Tetraethylenepentamine, 63 Tetraethyl lead, 77, 98, 470 Tetraethylrhodamine, 24 Tetraethyl orfAo-silicate, 345 Tetrahydrobenzene, 278 . Tetrahydronaphthalene, 395 Tetrahydroxyquinone, 33 Tetralin, 395 Tetramethyldiaminobenzophenone, 807 Tetramethyldiaminotriphenylmethane, 104 Tetranitromethane, 444 Tetranitromethanates, 445 Tetryl, 307 Thallium, 171 Thallium oobaltinitrite, 173 Thallium iodide, 173 Thallium Bulfate, 172 Thermionic valves, 142 Thermite incendiary bombs, 32 Thermometry, high temperature, 68 precision, 125 Thetford mines, 29 ThiOcarbamid, 170 Thiocyanate excretion, 212 Thiodiethylamine, 340 Thiokol, 289, 452 Thionyl chloride, 169 Thiourea, 122 Thorite, 174 Thorium, 174 Thorium-alisarin lake method, 67 Thorium dioxide, 174 Thorium fluoride, 175 Thorium nitrate, 67 Thorium oxalate, 175 Throium-x, 175 Thoron, 140, 175, 176 Thorotrast, 135, 174, 175 Thylox process, 85 Tin. 178 Tinkal, 41 Tin tetrachloride, 178 Tin tetrahydride, 178 Tin tetramethyl, 178 Titanium, 179 . in human tissues, 180 Titanium carbide, 179,180 Titanium dioxide, 179 Titanium fluoride, 168 Titanium pigmentB, 180 Titanium tetrachloride, 180 Titan Yellow, 101 TNT, 459 exoretion of, 460, 461 Tobacco reaction, 255 Tobacco, thiocyanate excretion from, 212 ortAo-Tolidino, 52, 90 Tollen's reagent, 197, 353 Toluene, 187, 431, 448, 468 Toluene picrate, 447 Toluidine, ortho, meta, and para, 449 p-ToIuidine. 203 Toluidine blue, 450 Toluol, 448 m-Toluylene diamine, 207 ar-p-Tolyl-pyrrolidine, 433 Topaz, 64 Tourmaline, 64 Toxicity, 9 Tracer bullets, 32 Transuranium elements, 134 Tremolite, 165 Tribromomethane. 231 Tribromopkenol, 417, 418 Tributyl phosphate, 298 Triohloracetic acid.201 Trichlorobenzene, 229 Trichloroethane, 451 Trichloroethylene, 7, 265, 413, 453 Trichloroethylene poisoning, 454 Trichloromethane, 5, 263 Trichloromonofluoromethane, 347 Trichloronitromethane, 267 Triohlorotrifluoroethane, 347 Tricresol, 270 TriortAocreayl phosphate, 74, 282, 456 Tridymite, 149 Triethanolamine, 458 Industrial Toxicology [ 483 1 ST 0852328 INDEX Triethylene glycol, 828, 829 Triethjrlene glycol di(Methyl butyrate), Trifluoroethane, 840 8,0',/J'-Trihydroxytriethylamine, 4S8 Trimethylamine hydrochloride, 878 1,1, S-Tnmethyl-eyclohaxanone-6-sul- fonic acid-3, 860 3,5,5 - Trimethyl - 2 - cyclohexene - 1 - one, 860 Trimethylene, 880 Trimethylene bromide, 280 Trimethvlphenylammonium iodide, 388 TrinitroSensene, 395 2,4,0-Trinitro-l-ethylbenzene, 321 Trinitronaphthalene, 890 2.4,6-Trinitrophenol, 410, 488 Trinitrophenylmethylnitramine, 307 Trinitroetilbene, 400 Trinitrotoluene, 10, 895, 444, 459 Trioxymethylene, 295, 349 Tropfoel, 266 Trypaflavine, 207 Tryptophane, 210 Tuberouloeis. 1 Turnon, bladder, 398 Tungsten, 181 Tungsten carbides, 182 Turpentine, 468 Turpentine oil, 403 Vlnylbensene, 487 Vinyl chloride, 805, 451, 485 Vinyl cyanide, 811 Vinylidene chloride, 291 Vinylidine, 305 Vinylite, 400 Vinyl resins, 807, 404, 460 Vinyl resin solutions. 409 Vinyl trichloride, 451 Visooee, 211, 247 Vomiting gas, 268 Watch dial painting, 175 Weed killer. 20, 297 Welding rod coating, 179 Welsbach mantle, 50 Wire worms, 294 Witherite, 32 Wood aloohol, 871 Xanthate reaction, 427 Xanthogenate test, 241 Xenylamine, 314 X-rays, 140 Xylene, 407 5icrates of, 468 Cylenol, 400 Xylidene, 409 Xylol, 467 .< Uranium, 134,188 Uranium, hexafluoride, 05,184 Uranium isotopes, 184 Uranium tetrafluoride, 184 Uranyl salts, 184 Urobuinuria, 216 Uraol asthma, 420 Ursol D, 419 uoValerio acid, 243 Vanadio oxide. 180, 188 Vanadium, 186 in blood, 187 Vanadium pentoxide, 188, 421 Vanadium-sulfide, 188 Vanillin, 307, 408, 465 Vinegar, 200 Vinegar naphtha, 816 Vinyl acetals, 316 Vinyl acetate, 460 Vinyl acetylene, 261 Vinylamine, 840 Zapon lacquer, 219 Zine, 189 Zinc blende, 190 Zinc chloride fumes, 190 Zino chromate, 55 Zino diethyldithiocarbamate, 191 Zino hydroxide, 190 Zino naphthenate, 190 Zinc nitroprusside, 163 Zinc phosphide, 127 Zino sulfide, phosphorescent. 140 Zircon, 192 Zirconium, 191 Zirconium-alizarin method for fluorides, 80 Zirconium carbide, 192 Zirconium dihydride, 193 Zirconium dioxide, 192 Zirconium phosphate, 193 Zirconium silicate, 192 Zirconium triethyl phosphatei, 193 Zyklon, 363 ST 0852301 Industrial Tozia>k>?y [31] iSBMTOS tioa With heart failure and without evidence of infection or other complicat ing disease (7). Any appreciable decrease in the amount of asbestos dust will cause a decrease in the incidence and severity of asbestosis (8). It would appear that if the dust concentration in asbestos factories can be kept below five million particles per cubic foot, new cases of asbestosis would not arise (2). Analysis While the analysis of asbestos dust as an aerial contaminant is not of particular importance, its microscopy and above aQ the evaluation of the number of particles per cubic foot of air is of paramount importance. Air samples may be secured by the impinger method using 25-50 per cent al cohol as a collecting medium and dust counts made by the usual method. Microscopic examination of the dust reveals typical asbestos fibrous par ticles which may be accompanied also by cotton or other textile fibrous materials in samples taken from the air of weaving factories. The index of refraction being only slightly greater than that of Canada balsam, the relief is low. Other forms of asbestos than chrysotile have somewhat higher indices of refraction. Extinction is parallel except in the case of tremolite which has oblique extinction. The birefringence of chrysotile is moderate n, -- ru = 0.013. The maximum interference color is bright yellow of the first order. The air sampling of asbestos dust both by the impinger method and by'the electrostatic precipitator method is discussed in detail by Fehnel (9). Rbvsbznci. 1. Bowles, O., and Marsh, D. I.: Asbeetoa. Minerals Yearbook 1946. U. S. Bur. Mines, Washington, D. C., 1947, p. 1467. 2. Dreessen, W. C., Dall&Valle, J. M., Edwards, T. I., Miller, J. W., and Sayers, R. R.: A study of asbestosis in the asbestos textile industry. Pub. Health Bull No. 241, U. 8. Pub. Health Service, Washington D. C., 1938. 3. Sayers, R. R., and Dreessen, W. C.: Asbestosis. Am. J. Pub. Health t9: 205 (1939). 4. Lanxa, A. J.: Silicosis and Asbestosis. Oxford Univ. Press, New York, 1938. 5. Noro, L.: Histology of asbestosis. Aota pathol. miorobiol. acandinav., Kobenh. tS: 63.(1946). 6. Gloyne, 8. R., and Merewether, E. R. A.: Asbestos. Occupation and Health Supple. International Labour Office, Geneva, 1938. 7. Lanxa, A. J., and Goldberg, J. A.: Industrial Hygiene. Oxford Univ. Press, New York, 1939, p. 387. 8. Page, R. T., and Bloomfield, J. J.: A study of dust control methods in an asbestos fabricating plant. U. S. Pub. Health Service, Pub. Health Repts. St: 1713 (1937). 9. Fehnel, J. W.: Air sampling of asbestos dust: comparison of impinger and elec trostatic precipitator methods. Ind. Med. fi: Ind. Hyg. Scot. 1:6 (1940). [ti ST0852308 Industrial Toxicology [ 147 ] silica 3. McConnell, E. P.: Respiratory exoretion of selenium studied with the radio active isotope. J. Biol. Chem. US: 66 (1942). 4. Dudley, H. C.: Toxicology of selenium. I. A study of the distribution of sele nium in acute and chronic cases of selenium poisoning. II. The urinary exore tion of selenium. III. Determination of selenium in air-gas-dust mixtures. Am. J. Hyg. 83:109,181; 84: 237 (1936). .IV. Effects of exposure to hydrogen selenide, by H. C. Dudley, and J. W. Miller. V. Toxio and vesicant properties of selenium oxyohloride, by H. C. Dudley. U. S. Pub. Health Servic, Pub. Health Repts. St: 1217 (1937); S3: 94 (1938). Reprint Nos. 1856, 1901. VT. Effects of subacute exposure to hydrogen selenide, by H. C. Dudley and J. W. Miller. J. Ind. Hyg. Toxicol. 33:470 (1941). 6. Fitzhugh, Q. G., Nelson, A. A., and Bliss, C. I.: The chronic oral toxioity of selenium. J. Pharmacol. 80:289 (1944). 0. Dudley, H. C.: Selenium as a potential industrial hazard. U. S. Pub. Health Service, Pub. Health Repts. S3:281 (1938). Reprint No. 1910. 7. Clinton, M., Jr.: Selenium fume exposure. J. Ind. Hyg. Toxiool. 89: 226 (1947). 8. Buchan, R. F.: Industrial selenosis. Ooo. Med. 8:439 (1947). 9. Pringle, P.: Occupational dermatitis following exposure to inorganic selenium compounds. Brit. J. Dermatol. SI: 54 (1942). 10. Duvoir, M., Pollet, L., and Herrenschmidt,. J. L.: Occupational eczema due to selenium developing when work was resumed after a long interval. Bull. soc. franj. dermatol. syphillg. 44: 88 (1937). 11. Smith, M. I., Lillie, R. D., Stohlman, E. F., and Westfall, B. B.: Studies in chronio selenosis. Natl. Inst. Health Bull. No. 174. U. S. Pub. Health Serv ice, Washington, D. C., 1940. 12. Smith, M. I., Westfall, B. B., and Stohlman, E. F.: Studies on the fate of sele nium in the organism. U. S. Pub. Health Service, Pub. Health Repts. S3:1199 (1938). 13. Smith, M. I.: Chronio endemio selenium poisoning. A review. J. Am. Med. Assoc. 118:562 (1941). 14. Moxon, A. L.: Alkali disease or selenium poisoning. South Dakota Agri. Expt. Sta. Bull. (1937). 15. Challenger, F.: Biological methylation. Chem. Rev. 38: 315 (1945), (219 refer ences). 16. Moxon, A. L., and Rhiam, M.: Seleneum poisoning. Physiol. Revs. tS: 305 (1943), (195 references). 17. Painter, E. P.: The chemistry and toxicity of selenium compounds with special reference to the selenium problem. Chem. Rev. 88: 179 (1941). SILICA Silica (SiOj) or silicon dioxide, is the most abundant of all the minerals and rocks that form the earth's crust. It is characterized by its hardness and chemical resistance to reagents. It is slightly Boluble in alkalies but the finely particulate material is only very slightly soluble in water (1,2). ST 0852309 silica [ 148 ] Industrial Toxicology Silica fractures into very minute angular particles. In the crystalline form it occurs as quarts but two other forms are also known which are tridymite and cristobalite and each of these exists in a number of modifications. Sand, flint, and agate are familiar forms of silica and diatomaceous earth, which is occasionally found in nature in large deposits, is composed of the silicious skeletons of diatoms. In view of what is known about the disease called "silicosis", it is important to distinguish between silica in the free state, as SiOi, and silica in the combined state, such as the various silicates. The silicates are still considered innocuous when inhaled as dust with the exception of talc, mica, and the fibrous silicates which are known as asbestos (3). The percentage of free silica in the various dusts which have been analyzed in connection with health studies of workers in dusty trades has been shown to range from 64 per cent to a trace (4). Silicosis is a chronic disease caused by the inhalation of particulate matter containing free or uncombined silica. It is oharacterized anatomically by generalized fibrotio changes with miliary nodulation in the lungs. Clinical signs are shortness of breath, a lowered vital capacity, a lowered capacity for work, increased susceptibility to tuberculosis, and a characteristic X-ray appearance of the lungs. Silicosis is found to occur in such occupations as mining, the cutting of sandstone and granite, the coal industry, the smelting, refining, and grind ing of metals, the manufacture of certain abrasives, the pottery industry, and the processing of the various forms of free silica. The number of work ers exposed to dangerous amounts of silica dust has been estimated at more than one million (5). Because of the disabling nature of silicosis (6), the exter t to which ex posure occurs in industry and the number of workers involved, many sur veys have been made and these investigations have resulted in the setting up of efficient protective measures in working establishments. Dust control measures, taking into consideration the chemical composition of the dust and the size of the silica dust particles, as well as the concentration of the dust in the air, have been instituted. There is more or. less general agreement that it is desirable to avoid concentrations of more than five million particles per cubic foot of air in working places where the dust con tains a high percentage of free silica. Granite dust, which contains about 35 per cent free silica, when in concentrations of ten to twenty million particles per cubic foot has been found not to cause disabling silicosis in a working lifetime, while anthracite dust, containing less than 5 per cent free silica, has been found not to cause anthracosilicosis in concentrations of less than fifty million particles per cubic foot (3). Because air-borne dust may differ markedly from that of the source material from which it arises, it is common practice in appraising dust hazards to determine the ST08523I0 Industrial Toxicology [ 149 ] silica free silica content of samples. Furthermore, it been indicated that toxicity increases sharply with silica dust below 3 microns in size (7). Since particles too large to be significant in silicosis production often con* tain a much higher percentage of free silica than fine particles of significant size, Holden and his associates (8) describe a procedure to eliminate the oversize particles before analysis. The mechanism and pathology of silicosis have been very adequately described. It is well recognized that very fine particulate silica is carried to the air sac or alveolus which represents the terminal dilatation of the bronchioles in the lungs. The alveoli are in intimate contact with blood vessels through which the oxygen-carbon dioxide interchange phenomena of respiration occur and they are also in contact with lymphatics which are important for the removal of foreign or irritant material. This defense mechanism is motivated by the activity of phagocytic cells which carry off the minute silica particles to the lymph nodes. There an ineffective ac cumulation of this material occurs and fibrotic changes tal*1 place resulting in areas which constitute the silicotic lung marking revealed by the chest roentgenogram. Just why the phagocytic cell is affected by the silica-- whether, in fact, silica has a direct toxic action, or whether it initiates other effects--is still in the realm of speculation. Certain substances, such as aluminum, iron, and magnesium dusts, when used with quartz, as well as coal and cement dusts, have apparently been found to decrease the pulmonary changes associated with free Bilica alone. Outstanding in this respect is the work of Denny, Robson, and Irwin (9), who have shown that small quantities of metallic aluminum powder almost completely inhibit the solubility of silicious material. While this work represents an interesting and significant development in silicosis research, Heffeman (10) has recently pointed out that the surface activity of the silica particles is the important factor in the production of silicosis rather than solubility of the silicon dioxide. Recent investigation of the use of aluminum and alumina has been made by Policard (11), who confirms the view that the aluminum dust itself is innocuous and by King (12), who, in a critical discussion of the solubility of silica, reports that a mixture of one per cent of aluminum hydroxide with the quartz fractions lowered their solubility but did not prevent the formation of fibrosis in animals. The phase of silicosis therapy indicated above, however, is still in the stage of experimental investigation. Since free silica or quartz is the important factor in causing silicosis, the identification of this substance and its quantitative evaluation as a dust constituent are of prime consideration. The microscopic examination of Buch dusts yields especially valuable information. Of the six distinct silica minerals, quartz, chalcedony, and opal are the more common. Tridy- silica ST085231 I [ 150 ] Industrial Toxicology mite and cristobalite are more or less of volcanio origin and are also found as constituents of silica bricks, while lechatellierite is exceedingly rare. Quartz and chalcedony have refractive indices near that of Canada balsam and a birefringence of about 0.009. The other silica minerals have lower indices of refraction and weaker birefringence. The microscopic examina tion of such industrial dusts as are known to contain free silica can only be satisfactorily accomplished by the use of the petrographic microscope and a considerable amount of experience is necessary. Quantitative evaluation of the quartz content of a dust may be made microscopically by examining the dust and counting the dust particles in two different immersion media (13) having different indices of refraction. In one of these media all the particles are visible; in the other, having the same index of refraction as quartz, only the nonquartz particles are visible. The difference between these two estimations gives some approximation of the silica content of the dust. The method is not suitable for very fine particles and estimation based on particles of less than 10 microns in size is not good petrographic practice. Chemical methods for the estimation of free silica, such as the hydrofluosilicic acid method (14) and the fluoboric acid method (15), are tedious, time-consuming, and frequently yield information of no more quantitative value than less lengthy procedures. The X-ray diffraction method of dust analysis has become of increasing importance and is espe cially commendable from the point of view of speed, while it appears to yield results of as great accuracy as is obtainable by other methods of analysis. RsnaiNCBs 1. Titus, A. C.: Silica and silicate solubilities. J. Ind. Hyg. Toxicol. IP; 138 (1937). 2. Kitto, P. H., and Patterson, H. S.: The rate of solution of particles of quartz and certain silicates. J. Ind. Hyg. Toxicol. Af; 9 (1942). 3. Meller, H. B.: Silicosis and Allied Disorders. Med. Ser. Bull. No. 1, Air Hygiene Foundation of Am., Pittsburgh, 1937. 4. Bloomfield, J. J., and DallaValle, J. M.: The determination and control of indus trial dust. Pub. Health Bull. No. 217,17. S. Pub. Health Service, Washington, D. C., 1935, p. 62. 5. Bloomfield, J. J., Trasko, V. M., Sayers, R. R., Page, R. T., and Peyton, M. F.: A preliminary survey of the industrial hygiene problem in.the United States. Pub. Health Bull. No. 259, U. S. Pub. Health Service, Washington, D. C., 1940. *6. Gardner, L. U., and Wright, G.: Disability in silicosis. Ind. Hyg. Foundation Am., Proc. Eighth Annual Meeting, Pittsburgh, 1943, p. 47. 7. Tebbens, B. D., Schulz, R. Z., and Drinker, P.: The potency of silica particles of different size. J. Ind. Hyg. Toxicol. S7:199 (1945). 8. Holden, F. R., Hemeon, W. C. L., and Hyatt, E. C.: Appraising exposures to silica dust. J. Ind. Hyg. Toxicol. 39: 265 (1947). 9. Denny, J. J., Robson, W. D., and Irwin, D. A.: The prevention of silioosis by metallic aluminum. Can. Med. Absoc. J. 37:1 (1937); Ind. Med. 8; 133 (1939). 10. Heffernan, P.: Aluminum dust for silicosis. Brit. Med. J. 1:928 (1946). ST0852312 Industrial Toxicology [ 151 ] silicones 11. Polioard,A.: New data on the uae of aluminum and of alumina in the prophylaxis and treatment of eilicoaia. Preaae m6d. 53; 006 (1046). 12. King, E. J.: Solubility theory of ailieoeia. Ooo. Med. 4:20 (1947). 13. Ro, H. L. and Sehl, F. W.: Determination of free silica. Ind. Eng. Chem., Anal. Ed. 7:80 (1936). 14. Knopf, A.: The quantitative determination of quarts ("free silica") in duata. U. S. Pub. Health Service, Pub. Health Repts. 45; 183 (1933). 16. Line, W. R., and Aradine, P. W.: Determination of quarts in the presence of silicates. Ind. Eng. Chem., Anal. Ed. 9: 00 (1937). 16. Hamlin, L. E.: Industrial dust--the pneumoconioses. Ind. Med. IS: 223 (1944). THE SILICONES Characteristics Silicon forms a large number of compounds which are analogous to thot : of carbon. The simplest of these is silane, SiH, which corresponds to methane. While these compounds have been known for some time, they were, however, of academic interest only and received no practical ap plication until about 1940 when the unique properties of the silicones caused them to assume considerable industrial importance. The silicones, R--SiO--R, correspond to the ketones but differ from the latter in most of their properties. The methyl silicones occur as oils, resins, and elastomers or rubber-like substances. The methyl silicone oils are soluble in benzene and the lighter hydrocarbons but are only partially soluble in alcohol. Many very complex alkyl and aryl silicones have been reported and studied within recent years. Some of these substances, such as methyl silicone oil, are characterized by their chemical inertness, low temperature coefficient of viscosity, wide liquid range, and low freezing point. Their high boiling points and heat stability are important properties for many industrial applications. Industrial Uses The uses of the silicones are as varied as their properties. Certain of the liquids are used as damping fluids for instruments and machinery. Other liquids find application as special lubricants for high temperature instruments, while others are used as high viscosity heat transfer liquids and as heavy diffusion pump oils. Minute amounts prevent foaming in fuel oils--an important problem in Diesel engines--and also the foaming of aqueous solutions. The relative insolubility of methyl silicone oil in petroleum oil may account for the success of this substance in suppressing foam. Silicone greases are used as hot valve lubricants, as insulating ST0852313 Industrial Toxicology [ 223 ] benzene 3. Clark, B. B., Van Loon, E. J., and Morrissey, R. W.: Acute experimental aniline intoxication. J. Ind. Hyg. Toxicol. MS: 1 (1043). 4. Hamblin, D. 0., and Mangelsdorff, A. F.: Methemoglobinemia and its measure ment. J. Ind. Hyg. Toxicol. SO: 623 (1938). 6. Lester, D., Greenberg, L. A., and Shukovaky, E.: Formation of methemoglobin. IV. Limited importance of methemoglobinemia in the toxicity of certain aniline derivatives. J. Pharmacol. 80: 78 (1944). 0. Bass, A. D., Frost, L. H., and Salter, W. T.: 2-AnilinoethanoI, an industrial hazard. Production of methemoglobinemia. J. Am. Med. Assoc. ItS: 761 (1943). 7. Rosenberg, P. A.: Biochemical changes in blood and urine in severe acute aniline poisoning. Farmakol. i Toksikol. 8: No. 4, 23 (1945). 8. Rehn, L.: Ueber Blasentumoren bei Fuchsinarbeitem. Arch. klin. Chir. SO: 588 (1895). 9. Hunter, D.: Industrial Toxicology. Clarendon Press, Oxford, 1944, p. 46. 10. Goldblatt, M. W.: Occupational cancer of the bladder. Brit. Med. Bull. 4-' 405 (1947). 11. Schwarts, L., Tulipan, L., and Peck, S. M.: Occupational Diseases of the Skin. Lea A Febiger, Philadelphia, 1947, p. 277.,. 12. Graubarth, J., Bloom, C. J., Coleman, F. C., and Solomon, H N.: Dye poisoning in the nursery. J. Am. Med. Assoc. 1S8: 1155 (1946). 13. Henderson, Y., and Haggard, H. W.: Noxious Gases. Reinhold Publ. Corp., New York, 1943, p. 228. 14. Elvove, E.: A method for the colorimetric estimation of small amounts of aniline. Ind. Eng. Chem. 9:953 (1917). 15. Anon.: Methods for detection of toxio gases in industry. Aniline. Leaflet No. 11, Dept. Sci. Ind. Research. H. M. Stationery Office, London, 1939. BENZENE Characteristics Benzene, benzol, CH, boiling point 80.094 C., melting point 5.51 C., density D 0.87895, and index of refraction n V-1-50124, is a colorless liquid with a characteristic odor. It is soluble in water only to the extent of 0.06 part per hundred at 20 C., but is miscible with organic solvents. Its flash point is from --12 C. to --10 C. and ignition may be caused by open flames or sparks from electrical appliances. The "light oil" from the fractional distillation of coal tar consists principally of the hydrocarbons-- benzene, toluene, xylene, and "solvent naphtha". On nitration, benzene yields both nitrobenzene with a boiling point of 209 C. and m-dinitrobenzene with a melting point of 90 C. On bromination, benzene yields bromobenzene, boiling point 157 C. and p-dibromobenzene, melting point 89 C. When heated with bromine plus iron catalyst, it yields mainly benzene [ 224 ] ST08523I4 Industrial Toxicology p-dibromobenzene. It forms a picrate of colorless needles, melting point 83.9 C. With CISOiH, it yields benzenesulfonyl chloride, melting point 14 C., boiling point 251 C., and diphenyl sulfone with a melting point of 128 C. It is slowly Bulfonated with boiling concentrated Bulfuric acid. Industrial Uses Domestic production of benzene has more than tripled during the past decade, chiefly due to the increased demand for the manufacture of phenol and for a motor fuel additive. The production of benzene amounted to 36,555,643 gallons for all purposes except motor fuel in 1940. Nearly three times as much (101,140,079 gallons) was produced for use as motor benzene alone in that year (1). During the war, however, the use of benzene for chemical purposes increased considerably, while its use for motor fuel dropped correspondingly. Thus in 1945, the total production of benzene for motor fuel amounted to 32,151,532 gallons, while the pro duction of benzene for all other purposes corresponded to 159,013,084 gallons (2). Apart from motor fuel, benzene is mostly used in manufac ture of rubber, chemicals, dyestuffs and intermediates, explosives, aniline, phenol, resorcinol, benzidine, picric acid, and miscellaneous organic prepara tions. It is used as a solvent for oils, fats, waxes, gums, natural and synthetic resins, cellulose esters and ethers, and a large variety of varnishes, airplane dopes, as well as in paint and varnish removers. Toxicity On inhalation in high concentration, benzene is narcotic in action pro ducing successively euphoria, hypermotility followed by sleepiness, and fatigue. The preliminary excitement is greater than with chloroform and as a general anesthetic, its action is more of a convulsive character. In concentrated form, it is especially toxic and may produce death. In dilute form, the vapors produce headache, vertigo, ataxia, twitchings, con vulsions, and coma. Chronic poisoning in industry is characterized by leukopenia and aplastic anemia.. Bowers has recently described a chronic case of benzene poisoning with fatal termination characterized by an in tractable anemia, leukopenia, and thrombocytopenia following long con tinued exposure to benzene. In this case, the bone marrow was grossly hyperplastic with extensive areas of extramedullary hemopoiesis (3). It should be emphasized that blood changes alone cannot be accepted as evidence of benzene intoxication in the absence of estimations of benzene as an atmospheric contaminant (4). Benzene is absorbed through the skin but clinically detectable benzene poisoning has not been found from this source (5). However, absorption from the skin is of far less importance than absorption from inhalation. A test for detecting active absorption ST08523I5 Industrial Toxicology [ 225 ] benzene of benzene may be made by determination of the ratio of the total urine sulfates to the inorganic sulfates (6). Since serious trouble may develop following exposure to benzene without any warning symptoms, the sig nificance of neglected disorders is often apparent when too late. Lambin (7) has indicated a procedure for the detection of benzene poisoning applica ble to large groups of individuals so exposed. The 1949 American Con ference of Governmental Industrial Hygienists has accepted 35 parts of benzene in air as a maximum allowable concentration in workrooms. Analysis Methods for the determination of minute amounts of benzene are at best, methods of approximation only. The chemical methods are colori metric in character and depend upon nitration and colorimetric evaluation of the reaction products. Various physical methods have been developed for the determination of benzene, such as the gas interferometer method and the combustible gas detector, and are useful when the air contaminant is solely benzene vapor. In contact with a nitrating mixture (equal parts of concentrated sulfuric acid and fuming nitric acid of d. 1.50) in the cold for 30 minutes, benzene is converted into a mixture of the ortho, meta, and para isomers of dinitrobenzene. The mixture contains about 95 per cent of the meta isomer. With aldehydes and ketones, the mixed dinitrobenzenes give a violet color in alkline solution. The meta isomer in par ticular gives a color with acetone. In low concentrations of benzene, the color develops within 30 minutes, is stable for three hours, and follows Beer's law. Schrenk and his associates (8) have adapted the nitration method to the determination of small amounts of benzene vapor as an air contaminant, using methyl ethyl ketone as reagent. A combined absorp tion nitration bubbler tube is used in which the benzene is converted to m-dinitrobenzene which is then estimated colorimetrically in saline solu tion with methyl ethyl ketone. Both Baernstein (9) and Dolin (10) have published methods for the determination of benzene in the presence of toluene and xylene, which depend upon oxidation of the nitro derivatives of the two latter substances. The oxidation products of the nitro deriva tives of toluene and xylene are colorless under the conditions described and therefore do not interfere with the benzene determination. BjerxEXNexs 1. U. 8. Tariff Commission: Synthetic organic chemioals, 1040. Rept. No. 148, 1941. 2. Anon.: United 8tates production of synthetic organio ohemicals. Chem. Eng. News U: 1556 (1946). 3. Bowers, V. H.: Reaction of human blood-forming tissues to chronic bensene ex posure. Brit. J. Ind. Med. 4; 87 (1947). benzene hexachloride [ 226 ] ST085231 6 Industrial Toxicology 4. Hunter, D., Milton, R., Perry, E. M. A., and Barrie, H. J.: Investigation for signs of benzene intoxication in workers using aeroplane dope and rubber sol vents. Brit. J. Ind. Med. 1:238 (1944). 5. Lehmann, E. B., and Fiury, F.: Toxicology and Hygiene of Industrial Solvents. Williams A Wilkins Co., Baltimore, 1943, p. 98. 8.Yant, W. P., Sohrenk, H. H., Sayers, R. R., Horvath, A. A., and Reinhart, W. A.: Urine sulfate determinations as a measure of benzene exposure. J. Ind. Hyg. Toxicol. 18:09 (1930). 7. Lambin, P.: Detection of poisoning due to benzene compounds. Arch, beiges m6d. sociale et hyg. 4:25 (March 1940). 8. Schrenk, H. H., Pearce, S. J., and Yant, W. P.: A microoolorimetric method for the determination of benzene. U. S. Bur. Mines, Rept. Investigations No. 8287,1935. 9. Baernstein, H. D.: Photometric determination of benzene, toluene and their nitro derivatives. Ind. Eng. Chem., Anal. Ed. 15:251 (1943). 10. Dolin, B. H.: Determination of benzene. Ind. Eng. Chem., Anal. Ed. 15: 242 (1943). Batchelor, J. J.: The relative toxicity of benzene and its higher homologues. Am. J. Hyg. 7:270 (1927). Division of Industrial Hygiene: Benzene (benzol): its toxicity and potential dangers. U. 8. Pub. Health Service, Pub. Health Repta. 68: 619 (1941). Re print No. 2248. Schrenk, H. H., Yant, W. P., Pearce, S. J., Patty, F. A., and Sayers, R. R.: Ab sorption, distribution and elimination of benzene by body tissues and fluids of dogs exposed to benzene vapor. J. Ind. Hyg. Toxicol. S3: 20 (1941). BENZENE HEXACHLORIDE (Gamma Hexachlorocyclohexane) Characteristics Benzene hexachloride, hexachlorocyclohexane, CH(Clj, one of the newer insecticides also known as "BHC" or "666", exists in five isomeric forms-- the alpha, beta, gamma, della, and epsilon. In the pure state, the isomers are well-defined colorless crystals, practically insoluble in water, soluble in organic solvents, and have a bitter taste and practically no odor. The melting points of the isomers are as follows: alpha, 157.5-158 C.; beta, 309 C.; gamma, 112.5 C.; della, 138-139 C.; and epsilon (1), 218.5219.3 C. At 40 C., the vapor pressure of these isomers are alpha, 0.06 millimeter of mercury; beta, 0.17 mm. Hg.; gamma, 0.15 mm. Hg.; and delta, 0.09 mm. Hg. The solubilities of the isomers of benzene hexachloride have been determined in each of forty-five organic solvents and the con- ST08523H INDEX Detailed discuuiona sbown by bold faoed page numbers Abrasives, 18 Acetaldehyde, 107, 288, 812, 818, 328 Acetaldehyde phenylhydraione, 107 Acetamide, 388 Acetanilide, 203, 222 Acetic acid, 200, 243, 360 Acetic acid, glacial, 200 Acetic acid, synthetic, 200 Acetic anhydride, 202, 368 Aoetio ether, 816 Acetoacetio acid, 204 Acetone, 204, 811. 860, 360, 868, 880, 428 Acetone cyanohydrin, 884, 880 Aoetone oxime. 204 Acetone phenylhydnuone, 204 Aceto-p-toluiaide. 203 4-AcetyIamino-l-uopropyl bensene, 430 Acetyl chloride, 200 Acetylene, 202, 205. 291, 816, 850 Acetylene dichloriae, 201 Acetylene tetrachloride, 489 Acetylene trichloride, 7 Acetyl:dee, 350 Acetylsalicylio acid, 203, 369 Acridine, 206 Acridine complexes, 208 Acridine Orange NO 207 Acridine Yellow, 207 Acriflavine, 207 Acrolein, 208, 368, 378 Acrylonitrile, 211, 364 Adipio acid, 275, 277 Adrenaline, 6 Aerosols, 3 Aeroeol insecticide bomb, 64 Agate, 148 Alcohol, 360 Alcohol, wood, 371 Alizarin, 100, 175, 181, 103 Alizarin red 8, 17 Alkyd resins, 404, 464 Allanite, 49 Allyl alcohol, 209 Allyl bromide, 21S Allyl chloride, 213 A nico alloy, 57 Aloxite, 17 Alpha rays, 140 Aluminon, 17 A uminum, 15 Alunrnum bronze, 15 Alumjnum ethoxide. 316 Aluminum phosphide, 128 Alundum, 17 Americ'um. 134 Am anthus, 29 Aminobenzne, 220 Am'nodimethylaniline, 86 Aminodimethyl bensene, 469 c-(2)-Am:nodiphenyl, 314 p-Aminodiphenyl, 314 1-Am:no-4-nydroxyanthraquinone, 87 para-Aminophenof, 392 Ammonia, 9, 19 Ammonia, synthetic, 20 Ammonium chloroplatinate, 133 Ammonium molybdate reagent, 28 Ammonium paratungstate, 182 Ammonium piorale, 423 Amphetamine, 406 Amphibole, 29 Amy! aoetate, 215 Amyl alcohol, 217 to-Amy! alcohol, 218, 219, 220 Amylene, 861 Amyl hydroxide, 217 Amyl nitrite, 365 Anesthetics, 362 Angles! te, 96 Aniline, 203, 220, 306, 398, 422, 436 Ani ine dyes, 222, 376 2-Anilinoethanol, 221 Ankylostomiasis, 1 Anode rays, 140 Anodizing, 54 Anthophyllite, 29 Anthracene, 206 Anthracosilicoeis, 148 Anti-fouling paints, 62 Anti-freeze, 372 Antimony, 21 Apatite, 64, 129 Arbutin, 436 Argyria, 153 Anstol, 89 Armor-piercing shells, 423 Arochlor, 255 Arsenic, 3, 25 Arsine, 360 Asbeetoe, 29 Asbestos bodies, 30 Asbestos dust, microscopy of, 81 sampling of, 31 Asbestosis, 30 Aspirin, 203 Asthma, occupational, 420 Atebrin, 207 Atropine, 6 Aurintricarboxylio acid, 17 Automobile radiators, 412 Aviation fuel, 430, 432, 468 Azobenzene hydrochloride, 314 472 ST08523I8 Industrial Toxicology [ 473 ] INDEX Aso dyes, 470 Asoimide, 75 Azophenol dyes, 418 Bacillus acetostkyUeum, 304 Bacillus clottridium aestobulylicum, 236 Bacillus macerant, 204. 239 Baddeleyite, 192 Bakelite, 463 BAL, 164,170 Barite, 32 Bar'um, 32 Barium carbonate, 32 Barium chloride, 32 Barium stearate, 32 Barium sulfate, 82 Barium sulfide, 83 Bauxite, 18 Belvidere Mountain, 29 Benzal chloride, 448 Bensaldehyde, 187,204,207,384,393,460, Benzene, 228, 314,417, 431, 488 Bensene hexachloride, 6, 226 Bensene monochloride, 269 Benzeneeulfonyl chloride, 224 Benzidine, 61, 62, 84, 104, 173, 183, 199, 222, 366, 446, 467 <x-Bnsil dioxime. 116 Benzofiavlne, 2Of Bensoio acid, 187, 820, 421, 430, 438 Bensol, 223 p-Bensoquinone, 436 Bensotrichloride, 307 Benxoyl peroxide, 229, 291 Benzyl aniline, 207 Bensylpyridine, 433 Beryllium, 34 Beryllium alloys, 34, 62 Beryllium nitrate, 174 Beryllium oxide, 34 Beryllium sulfate, 35 Beryllium zinc silicate, 34 Beta rays, 140 BHC, 228 Biotite, 109 Bismark brown, 420 Bismuth, 38 Bismuth hepatitis, 39 Bismuth hepta-dienecarboxylate, 39 Bismuth nephritis, 39 Bismuth trfoxide, 38 Bladder papillomata, 222 Blasting gelatine, 405 Blasting powder. 405 Blood cnanges, 9 Blood, vanadium in, 187 Bone oil, 433 Bone sarcoma, 136 Borax, 41 Borio acid, 40 Boron, 40 Boron carbide, 41 Boron fluoride etherate, 66 Boron phosphate catalyst, 202 Boron trifluoride, 41 Brass founder's ague, 190 Bread, furfural in, 364 Bromallylene, 214 Bromine, 42 Bromine burns, 44 Bromobenzene, 223,306 Bromoethane, 322 Bromoethylamine, 340 Bromofonn, 281 3-Bromo-l-propene. 214 Bromphenol blue, 44 Buna N, 211, 212, 233, 235, 267, 289, 299 Buna S, 211, 233, 438 Bush sickness, 57 Butadiene, 222, 864, 860 Butadiene manufacture, 168 Butane. 366 Butanol-1, 238 Butanol-2, 238 2-Butanone, 284 Butanone method f" xylene, 469 0-n-Butoxyethanol, sA n-Butyl acetate, 236, 243 Butyl alcohol, 5, 238 uoButyl alcohol, 5 n-Butyl bromide, 240 n-Butyl (J-bromoethyl ether, 331 Butylcarbinol, 218 uoButylcarbinol, 218 Butyl cellosolve, 221, 336 n-Butyl 0-chloroethyl ether, 331 Butylene, 361 uoButylene, 239 2,3-Buty ene glycol, 232 n-Butyl 0-hyuroxyethyl ether, 331 uoButyl methyl carbinol, 243 uoButyl methyl ketone, 243 n-Butyl methyl ketone, 241 n-Butyraldehyde, 240 uoButyrio acid, 243 Cable rash, 266 Cacotheline, 178 Cadion, 48 Cadmium, 3. 44, 189 Cadmium alloys, 45 Cadmium hydroxide, 45 Cadmium oxide, 9 Calcium phosphide, 127 Carbinol, 871 Carbitoi, 801, 336 Carbolic acid, 416 Carbomethene, 368 Carbon dichloride. 442 Carbon dioxide, 244 Carbon disulfide, 246 Carbon monoxide, 9, 123, 246, 364, 371, 411,463 polycythemia from, 249 Carbon tetrachloride, 260, 443, 467 ST08523I9 INDEX [ 474 ] Industrial Toxicology Carbonyl chlorido, 263, 454 Carbonyls, 248 Carboxide, 342 Carinoma, bladder, 398 Carnallite, 142 Caaale process, 20 Cataracts, 1,285 Catechol, 276 Cathode rays, 140 Celestite, 155 Cellosolve, 332, 335 Cellosolve acetate, 295,334,335,368,885, 404, 413, 440, 458 Cellulose aoetobutyrate, 404 Cellulose acetopropionate, 404 Cellulose formate, 369 Cerite, 49, 94 Cerium, 49 Cerium nitrate, 174 Cerium oxalate, 50 Cerium oxide, 50 Cerussite, 96 Cesium. 142 Chai sdony, 137 Chemical constitution and physiological action, 4 Chemical pneumonitis, beryllium, 35 Chemical pneumonitis, delayed, 86 Chemigum, 257 Chlor sons, 256 Chlorallylene, 313 Chloramine, 53 Chlorex, 293 Chlorinated diphenyls, 255 Chlorinated mononitroparaffins, 257 Chlorine, 61 Chloroanilines, 267 Chlorobenzene, 221. 259 2-Chloro-l, 3-butadiene, 261 l-Chloro-2-(5eto-chIoretboxy)ethane, 293 4-Chloro*l,2-dimercaptobenzene, 178 1- Chloro-2,4-dinitrobenzene, 266 Chloroethane, 323 " 2- Chloro-ethanol, 325 Chloroethyl alcohol, 325 Chloroethylene, 466 Chloroform, 205, 263, 378, 414, 443, 467 Chloronaphthalenes, 265 Chloronitrobenzene, 285 1-Chloro-l-nitroetbane, 258 1- Chloro-l-nitropropane, 258 2- Chloro-2-nitropropane, 258 Chloropentane, 217 Chloropicrin, 9, 253, 287, 376, 407 Chloroprene, 261 3- Chloropropene, 213 Chrome notes, 54 Chrome itch, 1 Chromite, 53, 54 Chromium, 63 Chromium carbide, 60 Chromium pi crate, 423 Chromium plating, 54 Chromotropio acid, 298 Chrysaniline, 207 Chipaotile, 29 birefringence of, 81 Cinchonine hydrochloride, 183 Citric acid, 849 Claude process, 20 Clay, 137 Clostridium acetobutylicum Weizmann, 236,239 Coal tar naphtha, 394 Cobalt, 66 Cobalt, allotropio forms, 56 Codeine sulfate, 146 Codling moth, 26, 286 Collidine, 434 Colonial spirits, 371 Columbian spirits, 371 Columbium, 60 Columbium carbide, 60 Columbium fuoride, 168 Columbium oxide, 168 Columbium potassium fluoride, 61 Contact acia, 82 v Contaminants, aerial; 8 Copper, 61 Copper acetylide, 289, 360 Copper fever, 63 Copper naphthenate, 62, 190 Corn borer, 286 Corundum, 17 Cosmetic preparations, 301, 302, 312 Cotton boll weevil, 227 Crane fly. 284 Cresol, 270, 382 Cresylie acid, 270 Cristobalite, 150 Cryolite, 64. 79 Cumene, 430, 431 Cupric acetoarsenite, 26 Cupric arsenite, 26 Curcumin, 101 Curium, 134 Cyanide antidote, 365 Cyanides, 378 Cyanogen chloride, 363 Cyclohexane. 272 Cyclohexanol, 274, 279, 383 Cyclohexanone, 276, 286, 884 Cyclohexanone oxime, 277 Cyclohexene, 278 Cyclohexene l,2*dithiocyanate, 279 Cyclohexyl bromide, 279 Cyclohexyl chloride, 275 Cyclopropane, 280 Cysteine, detoxicating action of, 68 2, 4-D, 297 DDT, 165, 227, 260, 286 Decahydronaphthalene, 395 Decalin, 396 Dental caries, 65 Dental erosion, 82, 83 ST0852320 Industrial Toxicology [ 475 ] INDEX Dertro a-pinene, 464 Diacetone, 205 Diaoetone alcohol, 870 2,4-Di-(acetylamino)-l-ethylbenzene, 320 p-Diaminobensaldehyde, 220 Diaminobensene, 418 Diaminophenol, 393 Diaznylphthalate, 230 Diatomaceous earth, 148, 405 Diatoms, 148, 387 Dibensalacetone, 204 Dibenzoyl peroxide, 229 p-Dibromobenzene, 223 1,2-Dibromooydohexane, 279 2,6-Dibromoindophenol, 418 Dibromomalonyl dibromide, 368 Dibutyl phthalate, 230, 281, 286, 421 Dibutyl sebacate, 282 Dicarboxylio acid. 411 Dichloracetio acid, 201 Diohloroacetyl chloride, 453 3:3'-Diohloroasoxybensene, 267 4:4'-Dichloroaaoxybenzene, 267 Diohlorobenaene, 283 ortAo-Diohlorobenzene, 260 para-Diohlorobenzene, 260 Diehlorodiethyl sulfide, 4, 253 Dichlorodifiuoromethane, 64, 251, 346, 847 Dichlorodiphenyltrichloroethane (DDT), 286 Diohloroethanes, 288 Dichloroethylene, 291, 359 Dichloroethyl ether, 293 /},0'-Diehloroethyl ether, 293 Diohloroethyl sulfide, 4 Diohloromethane, 5f 295, 378 Dichloromethyl arsine, 5 1.1-Diohloro-l-nitroethane, 258 2.4-Diohlorophenoxyaoetic acid, 297 1.2-Dichloropropane, 299 Dichlorotetrafluoroethane, 347 Diethanolamine, 458 Diethylaxnine, 247 Diethylcarbnol, 218 Diethyldithiocarbamate, copper, 247 1.4-Diethylene dioxide, 311 1,4-Diethylene ether, 311 Diethylene glycol, 328, 329, 335 Diethylene glycol monoethyl ether, 801, 328 Diethylene glycol monoethyl ether ci trate, 301 Diethylene glycol monoethyl ether laurate, 301 Diethylene glycol monoethyl ether phthalate, 301 Dietnylene glycol monoethyl ether ri- cinoleate, 301 Diethylene glycol monoethyl ether stearate, 301 Diethyl ether, 303 Di(2-ethylhexyl)phthalate, 282, 300, 422 Diethyl oxide, 803 Diethyl sulfate, 318 2.2- Difiuoropropane, 347 1.4- Dih^droxyanthraquinone-2-sulfonio 1.4- Dihydroxybenzene, 436 2.7- Dihydroxynaphthalene, 412 1.8- Dihydroxynaphthalene 3,6-disulfon- io acid, 298 Dihydroxyoctachlorodiphenyl, 315 Diiminoquinone, 420 Diketone, 369 2.3- Dimercaptopropanol (BAL), 154,170 Dimethylamine, 306 para-Dimethylaminobenialdehyde, 254 p-Dimethylaminobensalrhodamne, 154 p-Dimethylaminobenxylidine rhodanine, 126 p-Dimethylaminophenylasobensene&r- sonic acid, 193 Dimethylaniline, 269, 806, 388, 469 Dimethylbensene, 467 Dimethylohloroarsine, 5 Dimethylene imine, 340 Dimethylethylcarbinol, 218 Dimethyl gallium borohydride, 68 Dimethylglyoxime, 115^126, 162 Dimethyl nexine <nol, 889 Dimethylketone, 204 Dimethylphenylamine, 306 Dimethyl-p-phenylenediamine, 52, 90 Dimethyl phthalate, 286, 421 1.1- Dimethyl-l-propanol, 218 2.2- DimethylpropanoL 218 Dimethyl resorcinol, 5 Dimethyl sulfate^ 806, 332, 387 4,6-Dimtro-2-aminophenol, 424 Dinitrobenzene, 810, 400 m-Dinitrobenzene, 223, 225, 278 3.5- Dinitrobensoyl chloride, 304 Dinitrohydroxylaminotoluene, 10 Dinitrophenol, 393 2.4- Dimtrophenylhydrazine, 206, 278, 355 2.4-DinitrotoIuene, 447 Dioctyl phthalate, 305 Dioform, 291 1.4-Dioxane, 311, 335 Dioxane peroxide, 312 Dipentene, 463 Diphenyl, 814 Diphenylamine, 207, 254 Diphenylaminechloroarsine, 354 Diphenylcarbazide, 55 Diphenylcarbohydrazine, 255 Diphenylchlorarsine, 253 Diphenyloxide, 314 Diphenylsulfone. 224 Diphenylthiocarbaxone, 39, 48, 63, 98, 107, 154 Dipropylene glycol, 329 Diuopropyl ether, 431 a, a'-Dipyridyl, 93 ST 0852321 INDEX [ 476 ] Industrial Toxicology Disacryl, 209 Dithiaone, 89. 48, 83, 98, 107, 154 Dithymol di-iodide, 89 Dolomite, 100. 165 Dowioide O, 414 Dow metal, 100 Dowtherm A, 314 Drehaehmidt capillary, 119 Dry cleaning industry, 409 Dry ice, 245 D-Stoff, 808 Duprene, 261 Duralumin, 15 Dust, definition of, 2 Dusts, experimental exposure to, 9 reaction to, 7 Dynamite, 405 Earth flax, 29 Electrical odor, 122 Electron metal, 16 Elon, 892 Emery, 17 Ensootie marasmus, 57 Eoein, 44. 232 Essence d'orient, 440 Ethane, 555 Ethane-diacid, 411 Ethanoio acid, 200 Ethano , 818 Ethene, 861 Ether, 803 Ethide, 258 Ethoxyacetaldehyde, 832 2-Ethoxy-6,9-diaminoacridine, 207 Ethyl acetate, 816, 886, 426 Ethyl alcohol, 818, 362 Ethylamine, 840 Ethybensene, 820, 438 Dow pruoess of, 320 p-Ethyf bensene sulfonamide, 321 Ethyl bromide, 822 Ethyl chloride, 828, 418, 467 Ethylcydohexane, 438 Ethyl diethylene glycol, 801 Ethyl-3,5-dinitrooenzoate, 804 Ethylene, 326, 881, 466 Ethylene acetal, 312 Ethylene bromonydrin, 842 Ethylene chloride, 824, 451 Ethylene ohlorohydrin, 825, 328, 458 Ethylene cyanohydrin, 211 Ethylene dlchlonde, 288, 466 Ethylene glycol, 828, 832, 335, 349 Ethylene glycol mono-n-butyl ether, 831 Ethylene glycol monoethyl ether, 328, 832 Ethylene glycol monoethyl ether acetate, 884 Ethylene glycol monomethyl ether, 836 Ethylene glycol monomethyl ether ace tate, 838 Ethylene imine, 840 Ethylene oxide, 211. 832, 840, 841, 458 Ethylene tetrachloride, 442 Ethylene trichloride, 461, 453 Ethyl ether, 808 Ethyl formate, 848 n-Ethyl -8-hydroxy-tetrahydroquinoline hydrochloride. 28 Ethyhdene chloride, 824 Ethylidene diacetate. 202 Ethyl iodide, 318, 403 Ethyl polyglyool, 801 1-Ethyl-l -propanol, 218 Ethyl silicate, 845 Ethyl sulfide, 4 Ethyl sulfuric acid, 818 Fatigue resistance, metal, 34, 187 Fehling'a solution, 197, 354, 436 Ferrocnrome, 54 Ferron. 175 Ferrophosphorus. 129 Ferro-silioon, 127 Ferrous phosphide, 127 Fiberglas, 74 Fire damp, 356 Fire extinguishers, 876 Fischer-Tropsch process, 57 Flexol plasticizer DOP, 805 Flint, 148 Flour, bleaching of, 229, 230 Flour mills, fumigation. 864 Fluorescein, 124, 232, 283, 323, 422 Fluorescein reaction, 306 Fluorescent bead test, 185 Fluorescent lamps, 36 Fluorine, 64 Fluorine burns, 65 Fluorite, 64 Fluorocarbons, 346 Fluoroform, 347 Formaldehyde, 848, 354, 372 Formamide. 864 Formic acid. 343, 851, 372 Formic aldehyde, 848 Formio ether. 848 , Formylio acid, 851 Freon, 251, 286, 847 Fruit, ripening of, 362 Fuchsint basic, 44, 210 v-Fuchsin, 126 Fuel tablets, 198 Fulminate of mercury, 407 Fume, definition of, 2 generation of, 8 Furfural, 216, 858, 427, 429, 465 Furfural phenylhydrasone, 354 Furfuralaehyae, 863 a-Furil dioxime, 115 Furoic acid, 354 Furol, 363 Fused collars, 336 Fusil oil, 215, 217, 427 i Industrial Toxicology 0Alena, 06 Gallic Mid. 850 Gallium, 68 Gallium, borohydrides of, 68 Gallium hydroxide, 68 Gallium thermometer, 68 Gamma rays, 140 Gammexane, 227 Gases, definition of, 2 Gas mantles, 174 Gasolene, 304 Gasolene, easing head, 217 Gasolene, high octane, 70 Gelatine dynamite, 405 Gelignite, 406 Germanium, 70 excretion of. 71 oxides of, 70 Germanium hydride, 70 Germanium sulfide, 72 Germanium tetrachloride, 72 Glass fiber, 72 Glueuronio Mid, 883, 885 Glyoerol, 200, 328 Glyoerol triohlorohydrin, 214 Glyoeryl trinitrate, 406 Glycol, 812, 826 Glyptal, 421, 463 Golf greens, 284 Grain alcohol, 618 Grain oil. 217 Granite dust, 148 Grices reagent. 110 Grices test, 406 Grinder's rot. 1 GuaiMoldialdehyde test, 420 Gun cotton, 405 Qutieit test, 27 Gyspy moth, 28 Haber process, 20 Hafnium. 193 Hafnyl phosphate, 193 Hair dye, 420 Halowax, 255 HCN disco:ds, 363 Heavy naphtha, 394 Hematite, 91 Hematoxylin, 17 Hemoglobinuria, 201,331 Heptane, 857 Hexachlorobenzene, 227 HexMhlorocyclohexane, 228 Hexahydrobensol, 272 Hexahydrocreeol, 382 Hexahydromethylphenol, 882 Hexahydrophenol, 274 Hexahydrotoluene, 381 Hexalin, 274 Hexamethyl disiloxane, 152 Hexamethylene, 272 Hexamethylenetetramine, 170, 349 Hexane, 857 ST0852322 [ 477 ] INDEX Hexanone-2. 241 Hexone, 248 Hexylene, 861 Houseflies, 286 Hycar O. It.. 257 Hydraaine chloride, 170 Hydraaine hydrate, 75 Hydrasoio Mid, 76 Hydrocarbons, saturated paraffins, 355, 357 Hydrocarbons, unsaturated, acetylene, 859 Hydrocarbons, unsaturated--olefins, 361 Hydrochinone, 436 Hydrochloric acid, 77 Hydrochloric ether,323 Hydrocyanic acid, 868 absorption of, 363 preparation of, 363 Hydroforming. 447 Hydrogen aside, 75 Hydrogen chloride, 77 Hydrogen cyanide, 9, 868 Hydrogen fluoride, 79 Hydrogen nitrate, 81 Hydrogen phosphide, 127 Hydrogen selenlde, 145,146 Hydrogen sulfate, 82 Hydrogen sulfide, 9, 84, 860, 365 Hydroquinone, 892. 417, 485 Hydroxyacetie acid, 349 220 Hydroxybensene, 5, 416 p-Hydroxybiphenyl reagent, 199 0- HydroxyButyric Mid, 204 a-Hydroxy Mooutyrio Mid, 889 1- Hydroxy-2-ohloroethane, 825 Hydroxylamlnc, 162 Hydroxylamine hydrochloride. 277 4-Hydroxy-6-metnoxyuophthalalde- nyde test, 429 8-HydroxyqumoHne, 17, 39, 61, 69, 88, 95, 101, 104, 175. 191 Hydroxytoluene, 270 Hyoscine, 6 Hyosoyamine, 6 Hypophoephorous acid. 129 Hypovansrdic oxide. 186 Hypovanadoua oxide, 188 Igelite plastio, 466 Ilmenite, 179 Incendiary bombs, detection of, 145 Indigo, 22), 372, 421 Indium, 87 Indulene dyes, 423 Infra-red radiation, 142 Inhalation, experimental, 8 Insect repellent, 421 Iodine, 8s Iodine pentoxide method, 319 Iodobemene, 806 ST 0852 32 3 INDEX [ 478 ] Industrial Toxicology p-Iodobenzohydrazide, 277 Iodoform, 205, 318, 428 7-Iodo-8-hydroxyquinoIine-5-auI/onio acid (ferron), 178 Iodomethane, 387 Iron, 91 Iron, chilled, 169 Iron picrate, 423 Isoacstophorone, 366 Isophorone, 868 Isoprene rubber, 383 Jamaica ginger, 456 Jet.propelled airplanes, 60 Kelene, 323 Ketene, 203, 388 Ketoethylene, 388 Keto-hexamethylene, 376 /J-Ketopropane, 204 Kieselguhr, 405 L&evo a-pinene, 464 Lanthanum, 94 Lanthanum hydride, 94 Lead, 96 Lead aside, 75 Lead phthalate, 422 Lead picrate, 423 Lead poisoning. 97 Lead tetraethyl, 98 Lechatellierite, 160 Lepidolite, 109 Leptynol, 128 Lighter flints, 50, 94 Limonite, 91 Lithopone,33, 190 Lucidol, 229 Lucite, 389 Luminous paint, 140 Lutidine, 434 Magnalium, 15 Magnesium, 99 Magnesium perchlorate, 252 Magnesium phosphide, 127 Magnesium silicate, 164 Magnetite, 91 Malachite green, 307 Malarial control, 286 Maleic anhydride, 233 Malonic acid. 368 Manganese, 102 Manganese acetate, 197 Marcaaite, 91 Marsh gas, 356 Marsh test. 27 Mercurio chloride paper, 131 Mercuric sulfate, 197 Mercury, 2,105 Mercury-cadmium iodide paper, 128 Mercuiy detector, 2, 107 Meeityl oxide, 369 Mesothorium, 140, 174 Metaldehyde, 197 Metal fume fever, 190 Meta-styrene, 438 Methacrylate resins, 364 Methaerylio acid, 388 Methane, 355 Methanoic acid, 351 Methanol, 5, 364, 371, 374, 427 Methanol, synthetio, 372 Methemoglobinemia, 118, 221, 307, 402. 445 Methemoglobinuria, 221, 398 Methionine, 284 Methoxyacetaldehyde, 336 p-Methoxyphenyl-izo-thiocyanate, 398 Methyl acetate, 371, 374, 386, 426 Methyl alcohol, 371, 385 Methyiamine, 268 n-Methylaminophenol sulfate, 392, 393 Methylaniline, 308 Methyl anone, 364 Methyl benzene, 446 Methyl benzoate, 371 Methyl bromide, 376, 387 2- Methyl-l-butanol, 218, 219 3- Methyl-l-butanol, 218, 219 2-Methylbutanol-3, 218 2-Methyl-2-butanol, 218, 219 Methyl tzo-butenyl ketone, 369 Methyl isobutyl ketone, 367 1 -Methyl-3-carbohydrazidopyridinium S-toluenesulfonate, 277 yl cellosolve, 336 Methyl cellosolve acetate, 338 Methyl chloride, 378, 387 Methyl chloroform, 451 Methyleyclohexane, 381, 383 Metbylcyclohexanol, 882, 384 MethylcYclohexanone, 383, 384 4-Methy]-l,2-dimercaptobenzene, 178 Methylene blue, 51 Methylene chloride, 295 Methylene di-0-napnthol, 349 Methyl ethyl ketone, 234 Methyl formate, 364, 385 Methyl glycol acetate, 838 l-MsthyT-3-hydroxy-4-nitroeobenzene, 58 Methyl iodide, 371, 387 Methyl methacrylate, 230,383 Methyl nitrite, 447 4-Methyl-3-pentenone-2, 369 o-Methyl phenol, 270 2-Methyl propanol-1, 238 2-Methyl propanol-2, 238 Methylpropylcarbinol, 218 MethyUzopropylcarbinol, 218 Methyl n-propyl ketone, 311, 391 Methyl silicones, 151 Methyl sulfate, 393 9-Methyl-2,3,7-trihydroxy-6-fluorone,24 Methyl violet, 268, 307 Metol, 392 I I S T 0 8 52324 Industrial Toxicology [ 479 ) INDEX Mica. 109 Michier's ketone, 307 Mineral wool. 78 Aimer's phthisic, 1 Mischmetall, 50 Molybdenum, 111 Molybdenum chloride, 260 Molybdenum trioxide, 112 Monel metal, 64 Monobromoethane, 828 Monobromomethane, 876 cr-Monobromopropylene, 214 Monochlorobensene. 5. 259, 286, 417 Monoohloroethyl sulfide, 4 Monochloromethane, 5, 878 <t-MonochIoropropylene, 813 Monoethanolamlne, 468 Monofluorinated hydrocarbons, 346 Monofluorotriohloromethane, 347 Monohjrdroxybenseae, 6 Monomtrobensene, 310 Mononitroparafiiaa, ohlorinated, 857 Monosite, 60, 94, 174 Moth balls, 395 Moth proofing, 284 Motor fuel, 221 Mountain corkj29 Muriatio acid, 77 Muscovite, 109, 166 Mustard gas, 4, 362 Naphtha, 894 Naphtha, high flash, 894 Naphtha, wood, 371 Naphthalene, 187, 896, 397, 421 Naphthalene cataracts, 396 Naphthalene picrate, 395 Naphthalene-4-eulfonio acid-l-azo-5- ortto-hydroxyquinoline, 126 Naphthenic aoid, 190 a-Naphthol, 265, 397 0-Naphthol, 265, 349, 397 Naphthoquinoline, 48 l,2-Naphthoquinone-4-sulfonio acid, 403 Naphthylamine, 897 a-Naphthylamine, 119, 406 6-Naphthylamine, 222, 398 1,8-Naphthylenediamine sulfate, 146 Neoprene, 261, 273 Neoprene cement, 273 Neptunium, 134, 233, 258, 281 Nessler's reagent, 21, 365 Neutrons, 41, 136, 184 Nickel, 113 Nickel oarbonyl, 114 Nickel picrate, 423 Nicotine, 165, 434 Nicotinio acid, 434 Nigrosine, 423 Niobium, 60 Nitric acid, 81 Nitric acid pneumonia, 81 Nitrio oxide, 117 Nitroaniline, 401 m*Nitroaniline, 310, 811, 401 o-Nitroaniline, 311, 401 p-Nitroaniline, 272, 401 p-Nitroaniline red. 402 o-Nitroanisole, 26/ p-Nitroanisole. 287 c-NitrobensalaehydejJ^fi Nitrobenxene, 220, 223, 899 p-Nitrobenzene-azo-chromo-tropic acid, 42, 71 s-Nitrobensene diasonium chloride, 21 Nitrobruciquinone hydrate (cacothe- line), 178 Nitrocellulose, 216, 301, 316, 333, 367, 370, 374, 404, 458 solutions of, 282, 425 Nitrodiphenyl, 314 0- Nitrodiphenylamine, 311 Nitroethane, 403, 407 Nitroforxn. 867, 444 Nitrogen dioxide, 117 Nitrogen oxides, 116 Nitroglycerin, 405 5-Nitro-4-hydroxy-l,3-dimethyl benzene, 406 Nitromethane, 407 a-Nitronaphthalene, 397 e-Nitrophenylacetyl chloride, 427 Nitropropane, 409 1- Nitropropane, 407, 409 2- Nitropropane. 407, 409 -Nitrosocumetnylaniline, 307 Nitroeo-2-hydroxynaphthalene-3,6-disulfonate of sodium, 68 Nitroeo-6-naphthol, 58 a-Nitroso-fl-naphthol, 58 6-Nitroso-a-naphthol, 58 Nitroeophenylhydroxylamine, 93 Nitroeo-R-salt, 58 Nitrous oxide, 116 Nitroxylenes, 469 Nordhausen acid, 82 Novadelox, 230 Ootane, 357 Oil of ants, 353 Oil of bitter almonds, artificial, 399 Oil of mirbane, 399 Oleic acid, 354 Oleum, 82 Opal, 149 Orcinol , 355 Orthonitrosocresol, 58 Osmium, 120 Oxalic acid, 411 orlAo-Oxytoluene, 270 Ozone, 122 Painter's colic, 1 Paint remover. 295, 410 Palladium, 125, 133 Papillomatosis, bladder, 398 ST0852325 INDEX [ 480 ] Industrial Toxicology Paraformaldehyde, 349 Paraldehyde, 197 Paris green, 28 Pariaite, 94 Parroline, 434 Patronite, 187 Peach tree borer, 284 Pearls, artificial, 440 Pellagra, 434 Pentabromorosaniline, 877 Pentabromotoluene, 3ol Pentachloroethane, 413, 442 Pentachlorophenol, 414 Pentaerythntol, 349 Pentane, 867 Pentanoi, 218, 219 Pentanone-2. 391 Peracetie acid, 200 Perbensoio acid, 229 Perchlorethylene, 443 Peremesin, 60 Petroleum, 361. 428, 490, 447 Petroleum n&pntha, 894 Petroleum refining, 293, 878 Phenol, 6, 416 Phenoldisulfonie acid, 82, 119 Phenol-formaldehyde industry, 417 Phenolic resins, 271 Phenolphthalein, 417 Phenol red, 44 Phenylamine, 320 o-Phenylbenzamide, 314 Phenyltaooyanide, 222, 261, 264 Phenylenediamine, 418 m-Phenylenediamine, 199 o-Phenylenediamine, 811 p-Phenylenediamine, 402, 418 Phenylethane, 330 Phenylethylene, 487 Phenylhyarasine, 209, 269, 864 Phenylhydraiine hydrochloride, 360 Phenylmethane, 446 Phenylpyrasoline, 209 Phlogopite. 109 Phloroglucinol, 437 Phosgene, 263, 307, 369, 453 Phosphate rock, 129 Phosphine, 127, 130, 360 Phosphorous acid, 129 Phosphorus, 129 Phosphorus oxychloride, 131 Phosphorus pentaehloriae, 130 Phosphorus pentssulfide, 131 Phosphorus, red, 130 Phosphorus, tetra, trisulfide, 130 Phosphorus trichloride, 130, 213 Phosphorus tri-iodide, 387 Phosphorus trisulfide, 130 Phosphuretted hydrogen, 127 Phossy jawt 1 Photoelectno cells, 142 Phthalanil, 422 Phthalio acid, 396, 421, 468 uoPhthalic acid, 468 Phthalio acid esters. 422 Phthalio anhydride, 187,883,896,417,421 Physiological response and chemical con stitution, 4 Picooiine, 434 Pickling of metals, 27, 77 Picramic acid, 10, 424 Piorio acid, 416, 422 Picric acid in drinking water, 424 Picrolonio acid, 175 Pieryl ohloride, 424 Pimeiio acid, 276 Pimelic ketone, 276 Pinene. 463 Piperidine, 460 Platinum, 132 Platinum black, 132 Platinum sponge, 132,133 Plexiglas, 389 Plutonium, 134 Pneumoconiosis, 138, 177,188 Pneumonia, 139 -- Pneumonia, lobar, susceptibility to, 189 Pneumonitis, 145 Polycythemia, 50,. 57, 249 Polystyrene plastics, 438 Polytetrafluoroethylene, 65 Polyvinyl chloride, 466 Portland cement, 137 Potassium beryllium sulfate, 35 Potassium di-thio-oxalate, 115 Potassium nitromethane, 407 Potassium pierate, 423 Potassium tantalum fluoride, 61 Potato spirit, 217 Potstone, 165 Proflavine, 207 Propane. 866 Propanol-1, 427 Propanol-2, 428 2-Propanone, 204 Propene nitrile, 211 Propyl acetates, 426 Propyl alcohol, secondary, 428 tao-Propyl alcohol, 5, 204, 428 n-Propyf alcohol, 6, 427 wo-Propyl beniene, 430, 438 Propyl bromide, 430 tao-fVopyl oarbanilate, 429 iio-Propyl ohloride, 429 t*o-Propyl-3,6-dinitrobenxoate, 429 Propylene, 280, 861. 428 Propylene dichloriae, 299 Propylene glycol, 328, 329 wo-rropyl ether, 431 uo-Propylideneacetone, 389 tao-Propyl iodide, 301 n-Propyl iodide, 280 uo-Propyl-p-nitrobenayl phthalate, 429 Prostigmine bromide, 406 Prussian blue test, 365 Prussic acid, 383 ST0852326 Industrial Toxicology [ 481 ] INDEX Pyrethrin, 227 Pyrethrum, 186, 286 Pyridine, 170, 264, 831, 888, 414, 438 Pyridine ethiodide. 436 Pyridine methiodide, 486 Pyridine piorate, 436 Pyrite, 91 Pyroaoetio ether, 204 ..... Pyrocatechin, 41/ Pyrooateohol. 181 Pyrogallol, 61 Pyroligneous acid, 200 Pyrolusite, 103 Pyromucic aldehyde, 868 Pyrophorio alloy, 60 Pyrophyllite, 165, 166 Pyrrol, 146 ;uarta, 137.148 uinaorine nydroohloride, 207 uinaldinie acid, 191 uinalisarin, 17, 42, 69, 71, 88, 95, 10} uinol, 436 uinone, 486 Radioactive subetanoes, 140 Radioactivity, tolerance level, 136 Radio antimony, 23 Radio cobalt, 57 Radio elements, 140 Radium, 140 Radon, 140 Ramazsinj, 1 Rationite, 308 Refrigerants. 466 Resorcinol, 5, 61, 284, 268, 350, 422 Resorufin, 62 Rhodamine B, 24 Rhodisonio acid, 33 Rivanol, 207 Rotenone, 165 Rubber cement, 432 Rubber, synthetic, 212, 370, 450, 452, 456 Rubidium, 142 distribution in tissues, 143 Rubidium, silico-tungstate, 143 Rutile, 179 Safetv glass, 316, 440, 466 8aftifume briquets, 363 8alicylic aldehyde, 220, 465 Salt sickness, 57 Sand, 148 Saran, 291 Sarcoma, osteogenic, 141 Scheele's Green, 26 Schiff's reagent, 44, 199, 373 Seekay, 255 Selenium, 3,144 Selenium, radioactive, 145 Selenium sulfide, 107 Serpentine, 29, 165 Sesame oil, 286 Shale, 137 # Shaver's disease, 18 Ships, fumigation of, 363, 364 Siderite, 91 Silane, 151 ___ Silica, 147. 345 ' '-- Silicic acid, 346 Silicone greases, 151 Silicone refcins, 152 Silicone rubber, 152 Silicones, 151 Silicosis, 148 Silver, 168 Silver acetylide, 359 8ilver fulminate, 154 Silver nitrate paper, 128, 131 Silver permanganate, 128 Soapstone, 164 Sodamide, 76 Sodium acetate, 201 Sodium alisarin sulfonate, 67 Sodium anilide, 220 Sodium arsanilate, 51 Sodium aside, 75, 158 Sodium benxenesuifonate-p-diazonium chloride, 399 Sodium chloride, electrolysis of, 52 Sodium diethydithiocarbamate, 63, 191 Sodium diphenylamine sulfonate, 82 Sodium fluoride, 64 Sodium formate, 371 Sodium formyl sulfonate, 269 Sodium nitrite, 365 Sodium nitromethane, 407 Sodium nitroprusside. 86, 206 Sodium pentachloropnenate, 415 Sodium rhodizonate, 156 Sodium tellurite, 170 Sodium tetraborate, 40 Sodium tungstate, 182, 188 Soil disinfestants, 227, 293, 294 Soil larvicide, 407 Solaesthin, 295 Solvay process, 245 Solvent naphtha, 223, 394 8phalerite, 190 Spine cells, 23 Spirit, wood, 871 Spotting fluids, 409 Spray painting, 55 Stannous phosphide, 127 Steatite, 164 Steel, stainless, 54, 114, 169, 179 8tellite steels, 66 Stibine, 22 Stoddard Solvent, 394 Stone flax, 29 Strontianite, 155 Strontium, 166 Strontium, radioactive, 136, 156 Strontium saccharate, 156 Styrene, 320, 487 Styrene dilhiocyanate, 438 ST G852284 RKCKiVED SEP 161949 Biuciiein. hes. Lept. BIOCHEMICAL research 3 > Ttw Dow Chemical Company H & ES Library 'X'. ST 0850476 CONTENTS OF VOLUME XII A. _________________ JANUARY, 1930. NUMBER 1 9MI MiNBHa' Nystagmus and Incapacity for Work: A Clinical Study Based on an Analysis of 512 Cases. J. W. Tudor Thomas, B.Sc., M.D., B.Ch., M.S., F.R.C.S., Assistant Ophthalmic Surgeon, Cardiff Royal Infirmary.......................................................................................... 1 r Improved Form of Burstein Apparatus for Determination of the Dust Coefficient of the Air. Dr. A. I. Buratein. From the nT^rmVA? Hygiene Section of the Odessa Institute for Industrial Pathol ogy and Hygiene.......................................................................................... 24 Odxfibd Design of Hay Dust Trap. Capt. P. S. Hay, A.M.I.E.E., V. A.M.I.Mech.E., Chief Engineer, Safety in Mines Research Board, London........................................................................................................... 28 FEBRUARY, 1930. NUMBER 2 r Experimental Study of Abnormalities Produced in the Organism by Electricity. Orthello R. Langworthy and William B. Kouwenhoven. From the Departments of Neurology and Electrical , ' Engineering, The Johns Hopkins University, Baltimore, Md.................. -New Kata-Thermometer for Hot Atmospheres and a Simplified 'Method for Computing. T. C. Angus, Leonard Hill, and H. E. Soper. From the National Institute for Medical-Research, Hamp stead, London............................................................................................... n Notices...................................................................................................... i"' MARCH, 1930. NUMBER 3 31 66 74 Control of the Silicosis Hazard in the Hard Rock Industries. I. '*I> A Laboratory Study of the Design of Dubt Control Systems ' for Use with Pneumatic Granite Cutting Tools. Theodore Hatch, Philip Drinker, and Sarah P. Choate. From the Department of Ven tilation and Illumination, Harvard School of Public Health, and the Department of Sanitary Engineering, Harvard Engineering School.. Comparative Action of 5 and 10 Per Cent. Carbon Dioxide Mixtures as Respiratory Stimulants in Carbon Monoxide Poi, ^ oning. Douglas P. Murphy, M.D., and Cecil K. Drinker, M.D. ; * ^rom the Department of Physiology, Harvard School of Public '*, Health, Boston, Mass................................................................................ -Quantitative Measurement of Human Efficiency under Fac tory Conditions. Osgood S. Lovekin, Department of Industrial i'i.. iii 75 92 ST0850U77 w THE JOURNAL OF INDUSTRIAL HYGIENE FAOl Research, Harvard Graduate School of Business Administration, Boston, Mass........................................................................................... 99 Boos Notices.................................................................................................. 121 Obituary. H. W. Armit, M.R.C.S., L.R.C.P............................................... 122 APRIL, 1930. NUMBER 4 The Silica Dust Hazard m the Granite Cutting Industry. L. R. Thompson, M.D., Surgeon, United States Public Health Service, and Rollo H. Britten, Associate Statistician, United States Public Health Service...................................................................................................... 123 A Rational Expression for Wet Kata Cooling Power. Walter S. Weeks, Professor of Mining, University of California........................... 148 The Quantitative Measurement of Human Efficiency under Fac tory Conditions (iConcluded). Osgood S. Lovekin, Department of Industrial Research, Harvard Graduate School of Business Adminis tration, Boston, Mass.............................................................................. 153 Book Notices........................................ 168 MAY, 1930. NUMBER 5 Occupational Cancers. Imre Heller, M.D., C.P.H.................................. 169 The Occurrence of Pulmonary Fibrosis and Other Pulmonary Af fections in Asbestos Workers. E. R. A. Merewether, M.D., H. M. Medical Inspector of Factories.................................................... 198 BookNotices................................................................................................ 222 JUNE, 1930. NUMBER 6 Personal Qualities in Accident Causation. E. G'. Chambers, M.A., Investigator for the Industrial Health Research Board, London......... 223 Total Heat Difference as a Measure of Wet Kata Cooling. Walter S. WeekB, Professor of Mining, University of California.....................233 The Infectivity of Silicotic Tuberculosis. Patrick HefFernan, M.D., Tuberculosis Officer, Derbyshire County Council.................................... 236 The Occurrence of Pulmonary Fibrosib and Other Pulmonary Af fections in Asbestos Workers (Concluded). E. R. A. Merewether, M.D., H. M. Medical Inspector of Factories......................................... 239 Book Notices................................................................................................. 258 SEPTEMBER, 1930. NUMBER 7 So-Called Cyanide Rash in Gold Mine Mill Workers. William H. Braddock, M.D., and George R. Tingle.............................. .................. 259 -Fatal Cabe of Poisoning by Ethylene Chlorhydrin. E. L. Middle-. ton, M.D., D.P.H., H.M. Medical Inspector of Factories.................... 265 Dust Inhalation and Iron Ore Mining. Edgar L. Collia, D.M., and Sir Kenneth W. Goadby, K.B.E..................................................... 266 .tion, 123 er S. 148 169 222 1 M.A., 223 Valter 233 M.D., 236 IY Afvether, 239 258 iam H. 259 vliddle265 I., and 266 CONTENTS ST0850U78 SjBW Methods of Heating Buildings. H. M. Vernon, M.D., Intigator for the Industrial Health Research Board, London.............. 281 I'JIotices..................................................................................................... 290 OCTOBER, 1930. NUMBER 8 mc Shock: Interpretation of Field Notes. Wills Maclachlan, $B.A.Sc., Toronto, Canada........................................................................... 291 Effect of Chemically Pure Carbon Monoxide, Illuminating jj&'GAB, and Automobile Exhaust Gas upon the Fragility of the Red Blood Cells. May R. Mayers, M.A., M.D., Bureau of InHdustrial Hygiene, New York State Department of Labor; Helen Rivkin, M.A., Assistant, Department of Biochemistry, College of Physicians id Surgeons; and Frances Krasnow, Ph.D., Instructor, Department ' Biochemistry, College of Physicians and Surgeons............................. 300 nation of Food Cooked or Stored in Contact with Nicksljmium-Iron Alloys. A. C. Titus, H. B. Elkins, H. G. Finn, j. T. Fairhall, and C. K. Drinker. From the Department of Physioljr, Harvard School of Public Health, Boston, Mass........................... 306 S)mb Plating and Anodic Oxidation....................................................... 314 Notices.................................................................................................. 316 ices............................................................................................................... 318 NOVEMBER, 1930. NUMBER 9 Hypertension in Industry. James N. Wychgel, M.D., LC.S. From the Surgical Department, American Steel and Wire ampany, Cleveland, Ohio.......................... '............................................ 319 Pathology of Different Types of Electric Shock on Mamma- Brains. L. Raymond Morrison, M.D., Arthur Weeks, and Stanley Cobb, M.D. From the Department of Neuropathology, rd Medical School, Boston, Mass................................................... 324 ^Incidence of Illness among Wage Earning Adults. Dean K. 3rundage....................................................................................................... 338 DECEMBER, 1930. NUMBER 10 Effects of Lead on the Vibion: A Case of Subhyaloid Hemor- Frank G. Pedley, M.D., Dr. P. H. From the Industrial | Clinic, Montreal General Hospital............................................................. 359 JPATHOLOGY OF DIFFERENT TYPES OF ELECTRIC SHOCK ON MaM- Lmalian Brains (Concluded). L. Raymond Morrison, M.D., Arthur fcVVeeks, and Stanley Cobb, M.D. From the Department of Neu ropathology, Harvard Medical School, Boston, Mass........................ 364 ^Incidence of Illness among Wage Earning Adults ([Concluded). " K. Brundage............................... 381 ST 0850479 THE OCCURRENCE OF PULMONARY FIBROSIS AND OTHER PULMONARY AFFECTIONS IN ASBESTOS WORKERS* E. R. A. Meriwether, M.D. H. M. Medical Inspector of Factories Introduction He was treated in the Charing Cross Hos pital for two months, and then returned to RIOR to the commencement of work. After a few months, however, he Pthia inquiry, in February, 1928, definite knowledge existed of became ill again, and was re-admitted to the Hospital in April, 1900, where he died. The only two deaths of asbestos workpeorsst-mortem examination confirmed the about whom there was expert opinion clinical diagnosis of extensive pulmonary fibrosis. There was no evidence of pulmo that the inhalation of asbestos dust nary tuberculosis, and examination of the ' had at least contributed to, if not sputum for B. tuberculosis was negative. caused, the fatal outcome. The first of these, in retrospeet the The second case was reported by Dr. most suggestive, only came to light W. E. Cooke in 1924, eighteen years some years after the occurrence, when later (2): full information was unobtainable. All that is known of this case, now referred to as "the Montague Murray Case," is contained in the evidence given by Dr. Montague Murray before The deceased, a woman, aged 33, who died in 1924, had worked in asbestos for 18 years, but intermittently for the last 5 years, owing to periods of ill-health. The post-mortem examination revealed, not the Departmental Committee on Com only extensive fibrosis of the lungs, but also pensation for Industrial Diseases in much change due to pulmonary tuberculosis. 1906 (1). From this source, we learn that: The patient, a male aged 33, came under the care of Dr. Montague Murray at the Charing Crow Hospital in the beginning of 1899. He had worked with asbestos for "some 14 years," 10 years as a cardroom Although Cooke (3) and Stuart McDonald (4) were conclusively of the opinion that in this case the lungs showed a progressive dust fibrosis, to gether with a chronic tuberculous in fection, the etiologic relationship be hand, and the remainder in some other room of the factory, "where there was much less dust." He volunteered that, of the 10 people working in the cardroom when he went into it, he was the only survivor, and that all the others had died somewhere about tween the inhalation of asbestos dust and fibrosis of the lungs would have been strengthened by the absence of a tuberculous infection. Cooke's case is, however, of out 30 years of age. There is no note as to the nature of his work, previous to that in the asbestos factory. standing importance, not only because of the discovery of "curious bodies" in the lungs--discussed later--but also, Eeceived for publication Feb. 17, 1930. and of more importance generally, be- 198 J. I. H. . M*y, IMG ST 0850480 PULMONARY FIBROSIS IN ASBESTOS WORKERS 199 cause its publication again directed attention to the possibility that inor ganic dusts containing little or no free silica may be productive of extensive pulmonary fibrosis. Of these dusts, the silicates form a very large class, of which asbestos is but one example. Many other members of the class, such as the feldspars, kaolin, French chalk, and pumice, are extensively used in industry. The importance, therefore, of<deIimiting the potentiali ties of the class as producers of pul monary fibrosis is clear. Cooke's case was the first to be generally reported in the medical press; the facts of the Montague Murray case, although contained in the evidence presented before the Departmental Committee in 1906, and published in 1907, were liable to be overlooked in the mass of important material on industrial diseases elicited by that Committee. Since Cooke's case, Dr. I. M. D. Grieve has made a careful study of a group of asbestos workers in his prac tice, and has courteously allowed access to his records. In February, 1928, Dr. MacGregor, Medical Officer of Health for Glasgow, drew my attention to an asbestos worker who was receiving treatment in one of the hospitals in that city. This case, the details of which have been reported by H. E. Seiler (5), pre sented, both clinically and radiologically, Bigns of a diffuse pulmonary fibrosis, with no evidence of a tubercu lous infection. On further investiga tion into the patient's industrial and medical history, no presumptive cause, other than the inhalation of asbestos dust, was found to account for the existence of the fibrosis. This case, at that time the third of which the Factory Department had knowledge, was, however, the first in which the four essential conditions, necessary to establish a relationship between the inhalation of asbestos dust and the development of fibrosis, could be demonstrated. These conditions are: 1. Work involving exposure to asbestos dust. 2. The existence, demonstrable clinically and radiologioally, of a definite pulmonary fibrosis. 3. The absence of previous or present in fections known to cause pulmonary fibrosis --t.g., tuberculosis, influenza, or pneu monia. 4. The u>ence of previous or present work involving exposure to other dusts, whioh might oause pulmonary fibrosis. These conditions being fulfilled, a relationship between the inhalation of asbestos dust and the development of the pulmonary fibrosis may be pre sumed. The importance of establishing whether the supervention of this dis ease in an asbestos worker was an exceptional occurrence, or evidence of a grave health risk in the industry, was now apparent, and steps were taken, forthwith, to obtain prima fade evi dence in proof, or disproof, of the exist ence of such a risk. A number of workers in asbestos were selected and examined clinically and radiographically. The findings invited further investigation through out the industry, with the result that a comprehensive inquiry involving the investigation of the different processes in relation to the evolution of dust, and the examination, both clinical and ra diologic, of workers, was undertaken during the year 1928, commencing Vol. 12 No. & ST 085048 200 THE JOURNAL OF INDUSTRIAL HYGIENE with the carding, spinning, and weav ing processes of the industry. In the meantime, in March, 1928, the death of an asbestos worker (one of Dr. Grieve'a cases) occurred in another part of the country, and, on post mortem examination, a condition of widespread fibrosis of the lungs, with out tuberculosis, was revealed. The microscopic examination also disclosed the presence of the curious bodies. In 1928, also, Dr. F. W. Simson (6) reported a fatal case of fibrosis of the lungs occurring in a native work ing in an asbestos mill in southern Rhodesia. In order that this brief survey of the events leading up to the present in quiry may be complete, it is necessary to review the investigation made in 1910 to 1911 by Dr. Collis and Miss Whitlock--the only previous inquiry into the subject. In May, 1910, the Registrar-Gen eral drew attention to a death which had been certified as "acute pulmonary phthisis in an asbestos worker," and to a statement (for which he was un able to vouch) that seven other deaths from phthisis had occurred in the same factory. Following this, extensive inquiries were made, a medical report on all the employees in the factory concerned was obtained, and Dr. Collis and Miss Whitlock investigated generally the various processes in the industry with respect to the evolution of dust, methods of ventilation, lost time due to sickness, etc. Also inquiries were made of the Canadian government as to the conditions in the asbestos quarries and mills in that Dominion, evidence of increased Bickness and mortality rates among the workers, and any methods of ventilation which had been found of especial value. The result of this investigation did not conclusively prove that asbestos possessed injurious properties, but it pointed to the probability that such was the case. It is interesting to con sider why it was that no conclusive proof one way or the other could be obtained, then, as to the injuriousnesa of asbestos dust. Some, if not all, of the factors which affected the position then are, in varying degree, continu ing factors, and have an important bearing on the present inquiry. Their operation, while providing a solution to this query, also affords an explana tion to another pertinent question: Why is it that this industry, founded in antiquity, has only recently excited attention, by reason of its raw material becoming suspected as a cause of indus trial disease? The answer appears to be that in the past it was not practicably possible to obtain proof of the injuriousness of asbestos dust, considering the limita tions imposed by the state of the indus try, and the point reached by research work into the relationship between dust inhalation and diseases of the lungs. The industry itself, not a large one today, was then (1910) consider ably smaller. Certainly it had begun to grow rapidly, but the number of workers who could have been employed for a period of time long enough to allow of the development of definite physical signs of pneumonokoniosis must have been quite small, and dis persed over the country. Precise knowledge of the morbid affections of the lungs produced by the inhalation of dusts was more fragmen- J.LH. iUy.lMO 1 t i. ST0850U82 PULMONARY FIBROSIS IN ASBESTOS WORKERS 201 tary than it is today. The position was clearly stated two years later in evidence placed before the Royal Com mission on Metalliferous Mines and Quarries. This Commission, when re porting in 1914 (7), stated "we do not know whether other dusts besides those containing free crystalline silica induce a pathological condition in the lungs, though the experiments of Professor Beattie in animals suggest that this may occur." It is only in the last year or two that research has produced some definite evidence as 'to the precise effects of some of these dusts on the lungs (8) (9) (10) (11) (12). In 1910, radiography of the lungs, in both its technical and its interpretative aspects, was still in its infancy and, so far from having attained its present status of being an indispensable aid to the diagnosis of the dust diseases of the lungs, was an unused ally. In addition, the existence of a meas ure of exhaust ventilation in the most dusty processes of the industry, incom plete as it was, had important results in modifying the onset, course, and duration of any pathologic lung condi tions resulting from the inhalation of the dust. This influence has been much more pronounced in the period intervening between 1912 and the present inquiry, and will be referred to again. Another factor which has tended and still tends to obscure the possible deleterious effects of the non-silica dusts, is the general use of the phthisis mortality rate as a comparative index of the degree of injuriousness of the dust encountered in the various dusty occupations. This rate, while of great value in separating dusty industries into two great groups--those which Bhow an excess mortality from phthisis, and those which do not--as well as being a comparative index of the in dustries belonging to the former group, not only is of little value as a means of classification in the latter group, but also tends to distract attention from it, and to result in the associated dusts be ing dismissed as more or less innocuous. Evolution of dust is only one factor, though an important one, which may cause variations in the phthisis mor tality rate in different industries. Wages, hours of work, aggregation of workers, amount of food, housing, and other social and environmental condi tions are, however, powerful influences in the same direction, and are not necessarily comparable as between the workers in any two industries. In thus reviewing some of the influ ences which have retarded recognition of the baneful effects of some dusts upon the lungs, the singular attributes of pulmonary fibrosis, the most impor tant of the diseases caused by the in halation of dust, must not be over looked. This disease, insidious in its onset, stealthily advances with but faint warnings of its progress; inexorably it cripples the essential tissues of the lungs, yet for a considerable period causes almost no inconvenience to the worker. As time goes on, however, the lung3 find more and more difficulty in re-aerating the blood; and breathing is quickened on slight exertion. Still the worker is able to remain at work, but is aware of his undue shortness of breath on extra effort. Usually, how ever, he ascribes it to causes other than the dust he is inhaling. As the disease progresses, if no acute illness has caused a fatal termination, Voi. 1a No. S ST 0850483 202 THE JOURNAL OF INDUSTRIAL HYGIENE a stage is reached when the lungs can asbestos dust has a totally different do little more than maintain life; and physicochemical constitutionfrom that the shortness of breath is extreme. of dusts containing much free silicaand Even in its terminal stages, the disease, causing silicosis. It was felt that deceitful to the last, may masquerade although much valuable guidance as chronic bronchitis, pulmonary tu could be obtained from the methods berculosis, bronchopneumonia, or the of investigation of silicious dusts, care like. had to be taken to keep an open mind, While more or less acute cases of so as not to be unconsciously biased fibrosis closely simulating miliary in the direction of assuming that the tuberculosis have occurred, even in this effects of the dust, if any, must be com country (13), they have all been asso parable in some degree to those of ciated with the inhalation of dense crystalline silica. concentrations of free silica dust, and are, fortunately, the exception rather than the rule. The difficulty of diagnosing pulmo Asbestos and the Asbestos Industry Asbestos nary fibrosis, especially in its early The term asbestos is a collective stages, or if complicated by tubercu name, of no definite mineralogic sig losis, has been stressed by a number of nificance, which has been applied to a authorities, and has, undoubtedly, con variety of silicate minerals, which differ tributed to impede the attainment of from one another in chemical compo precise knowledge of the extent to sition and physical properties, but which the various industrial dusts which resemble one another in their affect the lungs.. finely fibrous feature and flexibility Difficulties and obscurities still im (14). Their value depends on the pede, though to a less degree than in facility with which they are capable of the past, any investigation into the being split up into long and flexible effects of an industrial dust upon the fibers, which can be spun like cotton lungs of those exposed to it; but prior and woven into cloth; on their resist to the War, although there were certain ance to heat and acids; and on their Blight indications that asbestos, in insulating properties with respect to common with some other dusts, heat and electrioity. might produce permanent pathologic Varieties of asbestos possess these changes in the lungs, it was not possible qualities in differing degree. Com to obtain evidence sufficient to prove mercially, therefore, selection is made or disprove this hypothesis. by the manufacturer of that variety At the outset of the present inquiry and grade which is most suitable for into what, if any, pulmonary diseases the purpose in view, regard being paid workers exposed to the inhalation of to ordinary economic factors, such as asbestos dust are more prone to con the cost of the raw material, and the tract than the general population, it price which the finished article may be was considered essential to view the expected to command. problem afresh, and with complete Consignments of asbestos of the detachment, because of the fact that Bame general variety, but with differ- Hay, UK) S T 0 8 50484 PULMONARY FIBROSIS IN ASBESTOS WORKERS 203 ent countries of origin, are frequently mixed in the preliminary processes of manufacture. Thus Canadian chrysotile may be mixed with Russian, or Rhodesian chrysotile, and so on. Less frequently, totally different varieties, such as amosite add chrysotile, may be mixed. Practically speaking, all that goes under the name of asbestos, in com merce, is either fibrous serpentine or a fibrous mineral of the amphibole, or hornblende, group. The former is the most important commercially; but strictly, the mineralogists confine the bined water, and usually more cal cium, aluminium, and iron. Members of this group are resistant to acids, but are more difficult to spin, some being quite unsuitable for this purpose. The most important members of this group are crocidolite, amosite, and tremolite. Crocidolite and amosite are mainly silicates of iron, the former having a beautiful lavender-blue color, the latter being brownish-gray. Both are spun and the yarn is woven into cloth for various purposes, such as aoid filter ing, and for making into insulating TABLE 1.--COMPOSITION OF SERPENTINE AND AMPHIBOLE VARIETIES OF ASBESTOS IfUODRAL GROUP VARIETY SiOj PERCENTAGE OP AliO FeO FetOi Com MgO CaO NaiO KjO bined Water Serpentine Chrysotile 39-42.5 0-3.7 0.7-4.4 39-43 0-0.35 13.3-10.5 Amphibole [ Crocidolite 50.5-52.1 0-1 35.5-37.4 0-3 0.75 0.2-9 1.0-4.5 (horn- < Amosite 48-53 1.2-9.4 OVA) A'l'Al 0.7-0.4 0-2.5 . .. 2-3.8 blende) ( Tremolite 57.2 0.9 3.2 22.8 13.4 0.6 0.3 2.4 term asbestos to fibrous forms of horn blende. These two types are sharply distinguishable, chemically and mineralogically. Serpentine asbestos, or chrysotile, is a hydrated magnesium silicate, con taining practically no calcium, a high percentage of combined water, and a low percentage of iron. This variety is very suitable for spinning, but is attacked by acids. Nearly 80 per cent, of the world's production of asbestos is derived from Canada, and is of this variety; the remainder comes mainly from South Africa and Russia. The amphibole, or hornblende, vari eties contain less magnesium and com- mattresses, as well as for other pur poses. Both are produced extensively in South Africa, from which quarter all required commercially is obtained. Amosite, a comparatively recent dis covery, is found there in very large deposits; its use is steadily increasing, the initial difficulties associated with the manufacture of textiles from this variety having been overcome. Tremolite, found in various quarters of the world, has been mined in north ern Italy since the time of the Romans. Its chief use is in the manufacture of asbestos millboard and for filtering purposes. Table 1, compiled from various Vol. U No. S S T0850485 204 THE JOURNAL OF INDUSTRIAL HYGIENE eouroes, shows the main differences in reexported. Thus the consumption of the composition of these four varieties. asbestos in this country trebled within Only a very small proportion of the five years. world's production of asbestos, which is between 300,000 and 400,000 short tons per annum, is suitable for spin ning, and the most desirable grades of spinning fiber, consequently, command a high price--now over 100 a ton. The shortage of this grade has led to improvements in manufacturing proc esses which have enabled less expen sive grades of fiber to be utilized for spinning, some of which give rise to an increased amount of dust. About four-fifths of the world's pro duction of asbestos is fiber unsuitable for spinning, and this is used in the manufacture of asbestos millboard, tiles, sheeting, paper, and many other articles. It is the discovery of indus The Industry On considering the uses of asbestos one is astonished, not only at the wide range of articles manufactured from this mineral, in greater or lees propor tion, but also at the diversity of indus tries which nowadays find its use necessary, either in the form of the raw material, or as manufactured articles. Evidently, therefore, with the multi plicity of processes and dusts encoun tered in the ramifications of the indus try, discrimination would have to be exercised, and some limit set to the processes included in the inquiry. The processes selected may be divided, roughly, into trial uses for these very short fibers, 1. Processes involving the manipulation and the dust-like waste, which has been responsible for the phenomenal expan sion of the industry as a whole. The spinning and textile section has also shared, because of the extensive use of of asbestos, either pure, or admixed with a small proportion of cotton, or other vege table fiber. 2. Processes involving the manipulation of asbestos together with other dusty ma terials. the yarn and cloth in the manufacture 3. Processes involving the making up of of steam packings, insulating mat asbestos cloth into other articles. tresses, brake .linings for motor cars, Group 1 entails exposure to asbestos fireproof curtains, and the like. dust mainly, and to cotton, or other In 1880, three years after the dis vegetable dust, very slightly; group covery of the large Canadian deposits, 2 entails exposure to asbestos dust in the world production of asbestOB was very varying amounts, and also expos little over 500 short tons; by 1900 it ure to divers other dusts, Buch as brick had risen to about 35,000 short tons, dust, magnesia, kieselguhr, fossil meal, by 1920 to over 230,000 short tons, and and cement; in group 3 the exposure to by 1925 to over 330,000 short tons (15). asbestos dust--provided no other aa- The imports of asbestos (all grades) bestoB processes are being carried on into the United Kingdom rose from in the vicinity--is, in the majority of 18,591 tons in 1922 to 33,520 tons in cases, negligible. Processes belonging 1927 (16). The figures for 1927 refer to all three groups may be carried on in to Great Britain and northern Ireland the same factory, and workers may only. Of these quantities 8,844 tons transfer from one department to and 3,794 tons, respectively, were another (30). J. I. H. May, IttO ST08S0486 PULMONARY FIBROSIS IN ASBESTOS WORKERS 205 Investigation into the intricate ques the weaving of fabrics, which, them tion of the effects of mixed dusts, while selves are used for a multitude of pur possibly productive of some general poses, but, braided together, are made corollary, frould lose much of its value into ropes for use as steam packings in the absence of knowledge of the and other purposes. The interstices effects of the several component dusts, and center of the rope may be filled and moreover would introduce an in with other materials such as talc, oil, calculable variable into the final or graphite, depending on the precise results. For these reasons, and also use to which the rope is to be put. because the Montague Murray case, Asbestos mattresses, used for blan Cooke's, Grieve's, and Seiler's cases keting Bteam engines, and for other all occurred in processes included in insulating purposes, are made of asbes group 1, it was considered advisable tos cloth stuffed with asbestos fiber. to exclude, as far as possible, from the The stuffing material may be, however, inquiry all workers exposed to the in slag wool, magnesia (containing ap fluence of mixed dusts, and all those proximately 15 per cent, of asbestos not employed in processes included in fiber), or kieselguhr with a small per groups 1 and 3. centage of asbestos fiber. The man The processes inoluded, therefore, ufacture of mattresses filled with are the crushing, preparing, sieving, mixtures of asbestos fiber and other opening, mixing, carding, spinning, materials has not been included in this doubling, plaiting, braiding, and weav portion of the inquiry. ing of asbestos, together with the The shortness, slipperiness, and lack operations incidental thereto. Also of strength of the individual asbestos included is mattress making, where the fiber, as compared with cotton, flax, filling is asbestos, and the manufacture wool, silk, and other textile fibers, have of some insulating materials, where the been the cause of much technical diffi dust produced is asbestos. culty in manufacture. The efforts of The carding and spinning processes manufacturers to cope with these diffi have many points of resemblance to culties, together with those due to wide the corresponding processes in the variations in the physical properties of cotton industry, but with essential the raw material, are reflected in the modifications and restrictions caused methods employed by each. For these by the different physical characters of reasons, and because of the great num the asbestos fiber. These processes ber of patented and special products are aided by an admixture of cotton, manufactured, one finds considerable or other vegetable fiber, and usually differences in detail in the processes in from 2 to 10 per cent, by weight of use. cotton is added. More rarely, and for The majority of the processes men special purposes, long-fibered asbestos tioned result in the evolution of dust, is carded and spun with no admixture although by no means to the same of vegetable fiber, but usually asbestos extent. Differences in plant, quality yams contain a core of either cotton of asbestos used, methods of manufac or metal wire. ture, type of finished article, and extent Asbestos yarns are not only used for of application of exhaust ventilation, ST 08501*87 206 THE JOURNAL OF INDUSTRIAL HYGIENE all result in variations in the evolution of dust in similar processes in different factories. Variations in the evolution of dust in different processes being of outstanding importance, a series of samples of dust from the air of workrooms was col lected, by means of the Owens jet apparatus. Population at Risk.--A calculation of the total number of rrorkers employed in the processes already enumerated as TABLE 2.--DISTRIBUTION, ACCORD ING TO LENGTH OP EMPLOYMENT, OF (A) 775 WORKERS ENGAGED IN ASBESTOS PROCESSES AND (B) SELECTED SAMPLE OF 363 WORKERS (A) (B) TBS. XtfFLOYKD ig Be HPpak 6 pMa 0-4................................ 5-fl................................ 10-14.............................. 15-19.............................. 20 and over.................. 483 62.3 89 24.5 200 25.8 141 38.8 51 6.6 84 23.2 24 3.1 28 7.7 17 2.2 21 5.8 Total.......................... 775 100.0 363 100.0 included in this inquiry, but excluding those engaged in processes included in group 3 in which the exposure to as bestos dust is negligible, gives a figure of approximately 1,600; if we could add to this the number of workers engaged in handling pure asbestos fiber only, in the preliminary stages of the processes included in group 2, we should obtain the total population at risk from the effects of asbestos dust it self. Unfortunately, this latter figure is unobtainable; but a rough estimate, and most probably an overestimate, is 600. Thus, about 2,200 appears to be the total population at risk in this country, for the purposes of this in quiry. This figure, however, does not include the large number of workers engaged in the processes in group 2 which involved exposure to the influ ence of mixed dusts, of which asbestos is but one, and commonly not more than 20 per cent, of the mixture. This estimate of the population at risk, although it may be excessive, is useful, since it enables us to judge of the adequacy of the sample of workers examined, and to apply more correctly the incidence rates of any pulmonary affections disclosed by the examination of the sample (30). The sample examined (after eleven cases are excluded of fibrosis and prefibrotic conditions due to causes other than the inhalation of asbestos dust) numbered 363, representing 16.5 per cent, of the population at risk, esti mated as above. The manner of selection of the sample must be referred to, since just interpretation of the results depends upon a due apprecia tion of the relationship of the sample to the whole population at risk. The principle of selecting primarily those longest employed was adopted; but regard was also paid to the other end of the scale, so as to obtain infor mation as to the length of exposure to dust necessary before effects are mani fested, and also as to the particular process in which the worker was engaged. It was felt that, in this way, the maximum information would be obtained in the shortest time. Table 2 Bhows the distribution, according to length of employment (not .necessarily in one factory), of j. i. H. Kay. 1K0 , ST0850488 PULMONARY FIBROSIS IN ASBESTOS WORKERS 207 775 workers engaged in the processes a center which is equipped with the under review, and of the sample of 363 necessary X-ray plant, and where the workers, distributed in the same way. services of a consultant versed in the The enormous preponderance numeri science of radiography of the lungs are cally of workers employed under five available. Furthermore, it must not years in these processes is striking, as be overlooked that such examinations is also the very low percentage of are voluntary, and not, as in South workers employed ten years or longer. Africa, compulsory. Moreover, re Comparison of the two parts of the peated and protracted examinations table shows that the effect of this only result in the exhaustion of all method of selection is that the number concerned, and much depends on the examined in each succeeding five-year willing co-operation of employers and employment group is a progressively employees, since the only incentive is greater proportion of the total number a desire to further the common welfare. which could have been examined in Radiography, therefore, has a differ each particular group. With a soli ent function in these inquiries, than tary exception, all those examined were when it is applied to individual cases at work on the day of examination. for compensation or other legal pur Not only the value, but the neces poses. uhis function is not that of sity, of radiographic examinations of replacing careful clinical examinations, the chest in investigations into the as has been recently foreshadowed (18, effects of dust upon the lungs, has been p. 40), but primarily that of 'being emphasized repeatedly by Watkins- an indispensable aid in diagnosis, Pitchford, and reaffirmed by the especially of doubtful cases, in the Departmental Committee on Compen determination of complicating lesions, sation for Silicosis (17). A high in measuring the extent and progress standard of radiography is essential; of the disease, in locating the point at as Watkins-Pitchford phrases it, the which the earliest radiographic signs radiograms must be "technically satis appear, and finally as a check upon factory.'' Indifferent films are useless, the human factor presented by the since it is the fine detail of the lung examiner himself. which is being studied. The examinations (except one) were In a general inquiry, such as this, carried out at each factory, in a room which involves the examination of set apart for the purpose, suitably workers in factories, large and small, warmed, and with the necessary scattered over the country, it is not appointments. On occasions the noise practicable, nor is it necessary, con of traffic or from the adjoining factory sidering the special purposes of the was a hindrance, but in one way or inquiry, for radiograms to be taken of another these difficulties were over all the workers examined. The dislo come or minimized. cation of work in a factory, caused by All the selected workers were exam the absence of a number of hands for ined by the writer. At three factories, this purpose, cannot be viewed with however, a number of workers were unconcern, especially when, as is not examined jointly with Dr. E. L. Middle- infrequent, the factory is remote from ton. His far-reaching experience of the Vol. lj No. fi ST 0850489 208 THE JOURNAL OF INDUSTRIAL HYGIENE pathologic changes in the lungs, pro duced by the inhalation of various dusts, was of great value, and his assistance was much appreciated. Every effort was made to complete the clinical examination of the workers before the onset of winter introduced difficulties due to ephemeral bronchitis, colds, and influenza, which would tend to obscure the main issues. Thus the clinical, and two-thirds of the radiographic examinations were completed by the middle of November, 1928, prior to the commencement of the influenza epidemic early in 1929. Clinical Examination Percussion The inhalation of asbestos dust originates changes in the lungs, which may be looked upon as a measure of the efforts of the living tissues to repel, or incarcerate, the irritant particles of dust. These changes modify the per cussion note. It is true that the note elicited may be similar on both sides, but the note is not normal. It is thinner and higher pitched than nor mal, and there is a sense of resistance imparted to the plexor Anger. In other words there is a diffuse, but slight, impairment of resonance. This alteration in the percussion note, however, is more difficult to recognize because it is bilateral, and extends over a wide area; consequently the aid of contrast percussion is denied. It is best elicited by rapidly, and very lightly, percussing the back of the chest from apex to base on each side. It will be found that the extreme apexes remain clear, but below the apexes the impairment is general. It increases over the root areas; below these, it diminishes in intensity, but still persists. In other words, we And tacked on to the paravertebral dulness an area, above and below, of impaired resonance, which is much more exten sive than that usually associated with old inactive hilar tuberculosis. Impairment of the percussion note was found to be constantly more marked in the right side; in fact, at first it was thought that in the earliest degrees of fibroBis it was confined to that side, but later, and more extended observations lead to the conclusion that the earliest detectable cases are bilateral, although the signs on the left side are tenuous. This change is so constant that it has been adopted as the moBt reliable single clinical sign presented by this type of pplmonary fibrosis, and no case has been classified as fibrotic in its ab sence. Considering the frequency with which signs indicating what may be termed "enlarged roots'' were found in asbestos workera, it may be that para vertebral dulness is one of the earliest signs produced by the inhalation of asbestos dust, indicating' congestive changes in the root areas and a choking of the lymphatics with dust. Reflex impairment of note, due to irritation of the lung tissue by dust, is, however, an attractive explanation. It does not follow1 of course, that workers present ing these signs will ever develop a defi nite asbestos fibrosis. Clearly, the physical signs presented by any case of diffuse pulmonary fibro sis not only may be modified by changes produced by some intercurrent lung disease, but, ab initio, will vary according to the state of the lungs be fore the onset of the fibrosis. ThuB, J. I. H. Mar, M30 ST0850490 PULMONARY FIBROSIS IN ASBESTOS WORKERS 209 the fibrosis may be implanted upon a perfectly normal chest, in which case the problem of diagnosis is straight forward. In other cases, however, preexisting root changes, so common in an industrial community, may be pres ent, or the lungs may be already the seat of emphysema and chronic bron chitis, or of definite old tuberculous lesions, or there may be a massive pleural thickening, the result of an old pleural effusion. All these examples have been noted in the present investi gation, and others will readily oome to mind. ' Although in most of these cases the dust fibrosis, if moderate in degree, can be confidently diagnosed, especially with the aid of radiography, it must be admitted that the problem becomes very difficult when the dust fibrosis is comparatively Blight, and the changes produced by other conditions are pro nounced and diffuse. Three types of these cases have caused most difficulty among those examined; fortunately, numerically they were few. The first of these is where the dustfibrosis has been implanted upon lungs already emphysematous. It seems that, at any rate in the case of the asbestos fibrosis, until the fibrotic changes get the upper hand, clinical diagnosis of the fibrosis in these cases is impossible. Nevertheless, although the problem of the diagnosis of a fibrosis implanted upon an emphy sematous cheat has caused some diffi culty in this inquiry, it seems likely that it can arise only under exceptional circumstances. The second type of case which has been a source of difficulty in clinical diagnosis is that in which there are extensive bilateral fibrotic changes due to healed tuberculosis. That there is an extensive fibrosis is clear enough, and that most of it is not due to asbes tos is strongly suggested when examin ation of the lower portions of the lungs shows that they are comparatively slightly affected. Further help in these cases, of course, may be obtained from the history and symptoms. The third type, also rare, is that in which changes following an old massive pleural effusion on one side so obsoure the physical signs of any dust fibrosis as to render that side useless clinically for diagnostic purposes. If the side affected by the pleurisy happens to be the right, the radiographic picture is also curtailed by the normal partial obscuration of the left lung base by the ' heart shadow. These three types were, with the possible exception of the first, uncom mon, and are mentioned merely to call to mind some of the ways in which an asbestos fibrosis may be masked, in greater or less degree, by changes due to other disease. Only passing reference need be made to the other physical signs found in the asbestos fibrosis, since they do not differ materially from those presented by silicosis. Chest expansion is dimin ished and may be reduced to one-half inch or even less in advanced cases. Retraction of the apexes is common, and sometimes shows a peculiar feature differentiating it from that found in fibroid phthisis. Instead of the im mobile and sunken apexes Been in the latter disease, the apexes are seen to descend during inspiration, and to rise again during expiration. This seems to indicate the anchoring of normal apexes by fibrous tissue in the lower portions of the lungs. Some confir- V0L12 No, t ST085049 I 210 THE JOURNAL OF INDUSTRIAL HYGIENE roation of this was obtained radiologically. Auscultation In the majority of the cases of fibrosis, the respiratory murmur is weakened, much or little, generally, more on the right side, and often still more at the base; the expiratory sound is weaker than the inspiratory, and often becomes less and less audible as one approaches the bases. Transitional phases between this and harshened breath sounds and pro longed expiration are not uncommon, even' in the same chest. The latter may be noticeable in the upper por tions of the lungs, but progressively diminish toward the bases. Other combinations were also noted, how ever. The dry character of this type of fibrosis during most of its course is rather striking. Scattered fine r&les and clicks in the root areas, axillae, and bases were not infrequent; slight edema of the lower halves of the lungs was noted in one of the more advanced cases; but in a number, no adventitious sounds at all were heard. Pleural crepitations, and rarely a slight pleural rub, were noted--these attacks seem to cause little pain--and in one case a little fluid at the right base. No doubt this variability in the sounds heard on auscultation reflects underlying changes, temporary or permanent, in the lung, and is depend ent, inter alia, on the extent of the fibrosis with its associated pleural thickening--changes due to past dis ease, catarrh, or other intercurrent affection, and to the degree of compen satory emphysema present. Symptoms The symptoms exhibited by these cases of fibrosis, as might be expected, closely resemble those of silicosis. The distribution of the main symp toms, and of one sign, cyanosis, which is included with' the symptoms for con venience, is given in Table 3. A few cases have been excluded on the grounds that one or other of the symp toms complained of might be assigned to causes other than the fibrosis, such TABLE 3.--DISTRIBUTION OF FOUR COMMON SYMPTOMS, AND OF CYANOSIS, AMONG CASES OF FIBROSIS STHFTOM CASKS IN l WHICH SYMPTOM WAS PRESENT m 6z No. Per Cent. Cough............................ Oy*nn*is............................. Dvinaa*. .>........... . 'Expectoration.................. Pain.............................. 01 03 91 01 04 54 50.3 52 65.0 47 51.0 31 34.1 10 10.0 1 Excluding those in which the presence of the symptom is referred to other causes. as a complaint o&shortness of breath in a case with a past history of mild thyroid intoxication, or of dyspnea associated with obesity. Between 50 and 60 per cent, of the cases complained of cough, dr of short ness of breath on slight exertion, or showed some degree of cyanosis, whereas only about one-third com plained of expectoration, and onetenth of pain, or discomfort, in the chest. Also, while 14.6 per cent, of the cases had no complaints and showed no cyanosis, and only 3.4 per J. I. H. May, TOO ST 0850U92 PULMONARY FIBROSIS IN ASBESTOS WORKERS 211 cent, presented all four complaints and were cyanosed, 60.6 per cent, presented two, three, or four of the five items. Clearly, none of the four complaints, or the presence of cyanosis, can be an infallible indication of the existence of fibrosis; but the presence of two of them, shortness of breath on slight exertion, and cyanosis in some degree, in an asbestos worker, is highly sugges tive, in the absence of other evident cause. Nevertheless an advanced degree of fibrosis may be present, and little com plaint made. Symptoms, unless dis tressing, are so often a function of the introepectiveness of the patient. Slight degrees of fibrosis, too, give rise to no symptoms, in the absence of an intercurrent bronchitis, since the remaining sound lung tissue is still amply sufficient for all purposes. Cough was the most fSequent symp tom, and was of two types. For a few weeks after commencing work in a dusty process, asbestos workers often find the dust irritating, and cough while in the dusty atmosphere; this lasts for a few weeks, and then usually disappears. The writer has noticed thiB effect on himself, but only while in a very heavy cloud of asbestos dust. The dust seems to be only slightly irritant in this way. One or two men who had previously worked in cotton card rooms, or blow rooms, and were affected by that duBt, stated that they were unaffected by asbestos dust. Certainly asbestos dust does not cause asthmatic attacks like those seen in cotton card room workers. One man, who migrated from a cotton card room ("hard waste") nine years ago to an asbestos card room, on account of the irritating effect of the dust, does not find asbestos dust irritating, but to this day cannot work with a cotton scutcher (as he occasionally does) with out precipitating a coughing attack within an hour or two. Although he suffers from winter cough and some shortness of breath, he stated that his health has been much better since the change. Asbestos dust, therefore, has only very mild powers as a reflex irritant of the upper respiratory tract, and is, in this respect, comparable to free silica. This is an unfortunate attribute, since it leads to the assumption that the dust is more or less innocuous. The second type of cough is more intimately associated with the develop ment of fibrosis, and occurs, or perhaps is noticed, after a varying number of years'work. Usually it is present only in the morning on getting up, when after rather a sharp attack of coughing, a little viscid sputum "like an oyster" is brought up. A similar bout may occur at night after ceasing work; at times it is sufficiently sharp to cause retching. It is generally rather worse in winter, and may be noticed only then. Although it closely resembles smokers' cough, its features are pre cisely the same in nonsmokers. Persons giving a history of cough dating from an attack of pneumonia or other illness in childhood, almost in variably state that the cough has not become worse since working with asbestos. One worker succinctly de scribed the cough as "first in the throat; later catches the chest." Generally, this cough causes very little inconvenience and may pass un noticed until the development of some other symptom directs attention to the general state of health. Thus, out of Vol. 11 No. t ST0850493 212 THE JOURNAL OF INDUSTRIAL HYGIENE sixty-six cases of fibrosis, in thirty- and in the remainder of the cases, three (60 per cent.) the cough was good. stated to have preceded the onset of shortness of breath, in twelve (18.2 per Radiography cent.) to have developed contempo Radiograms of the chest were ob raneously, and in twenty-one (31.8 per tained of 133 workers, or 35.5 per cent, cent.) was either not noticed until after of the number examined clinically. the onset of shortness of breath, or, Of these, over 100 were taken by Dr. although the latter was complained E. W. Twining of Manchester, and of, cough was not admitted. Dr. N. Tattersall of Leeds, and the Complaints suoh as "colds go to the remainder (except one) by Dr. F. L. chest," and "frequent colds on the Henderson of Glasgow. To all three, chest," were not uncommon. Com I am much indebted. Dr. Twining plaint of spitting of blood was excep and Dr. Tattersall have devoted many tional; and in all cases in which this hours to the joint study with the writer complaint was mentioned, the exciting of the radiograms, and have drawn cause was, primarily, some disease freely on their wide experience of radi other than the fibrosis--e.g., in one, it ography of the chest in furthering the was due to pulmonary tuberculosis; purpose of the investigation. in another, it occurred only during a Dr. R. S. Paterson of Manchester, prolonged attack of pleurisy; and in a too, added his experience to a final third, the hemorrhage was gastric in review of the films, and Dr. E. Barclay, origin. Cyanosis, a valuable sign now of Cambridge, lent his assistance when present, rarely amounts to more in interpreting some difficult films; than a duskiness, or slight blueness, of to both, grateful acknowledgment is the lips; it contrasts, however, with the made. general pallor of the face with which The standard of radiography was it is often associated in these cases. very high; indeed, a high standard is Cyanosis in some degree was noted in indispensable, if it is desired to trace 56 per cent, of the cases. It may be the cause of such a fine and diffuse absent even when there is a consider fibrosis as that produced by asbes able degree of fibrosis, or it may come tos. and go. The films are superficially, but only Pain in the chest is rarely com superficially, comparable to silicosis. plained of, and then it is usually de In the earliest negatives studied with scribed as "tightness of the chest," Dr. Tattersall, a characteristic slight "soreness," or "aching." It was noted obscuration of the lung fields, a general in 10.6 per cent, of the cases. lack of translucency, was noted. This Well-marked clubbing of the fingers appearance, for want of a better term, was noted in a few cases. The general was denominated as "veiling." Dr. nutrition is hardly affected, except in Burton Wood has independently noted the latest stages. Only ten (10.5 per (19) and confirmed this, referring to it cent.) were noted as being thin. In as the "ground glass appearance." one, the nutrition was very poor; in Dr. Tattersall also drew attention to twenty-one (22.1 per cent.), fair; the more or less rounded "whorls" of i.ia Har.lttO ST 0850494 PULMONARY FIBROSIS IN ASBESTOS WORKERS 213 varying size seen in the striation in the mid-rones in some of the films. There was general agreement as to the fine and delicate nature of the characteristic mottling. Dr. Twining (in a personal communication dated Aug. 2, 1929)--while lamenting that there has been, as yet, neither time nor opportunity to study the changes from every aspect, and therefore his present views may be modified on considera tion of all the evidence--states: In general my opinion is that the earli est stages are not characteristic radio* logically, but that the stage of fine dusty stippling is almost certain to be eventually provable as an early asbestos lesion. We saw it constantly in a large series of films, and after a little experience it is quite easy to detect it. Some of the other cases showed a few grouped lesions, like rosettes or leopard markings, each component being about the sise of a primary lobule. These are similar to lesions sometimes seen in tuberculosis. In the asbestos cases I regard them as being groups of primary lobules making up a lobule, the walla of which are infiltrated. They certainly seem to correspond in size with the macroscopic lesions seen in the pathological specimen. The advanced cases show heavy basal and mid-field mottlings, common in pneumonoconioeis, with a tendency to avoid the apices. On the whole the lesions are distinctly less dense than those of silicosis, and are less easy to group into well-defined stages, but I think we can recognise: 1. A very doubtful stage of increased linear striations. 2. Fairly definite fine dusty stippled appearance. 3. Coarser mottling with increased linear striations. 4. Gross lesions with pleural ohanges and displacements due to the pull of the fibros ing lesions. The few tuberouloua lesions we have come across have been easily distinguishable. The radiographic appearances in the earlier stages are most marked on the right side at the base or in the central rone. This corresponds with the clin ical findings. This preference for the right side has been noted also in silioosis, by the South African ob servers. The cases showing radiographic signs of a dust fibrosis have been classified in three broad groups. This grouping, although unscientific, is convenient practically, considering the main purpose of thiB investigation. Indeed more precise classification based on the particular radiographic changes noted might well be mislead ing at the present time. Much combined clinical, radiologic, and pathologic Btudy is required into the whole subject of these fine types of dust fibrosis, which have been noted in workers exposed not only to silicate dusts other than asbestos, but also to other inorganic dusts containing no silica, before it will be possible to classify the radiologic changes as has been done so successfully by the South African workers in respect to silicotic fibrosis. The hypothesis that, because asbes tos dust produces a pulmonary fibrosis with consequent deviations from the normal in the lung skiagram, the de gree and potentialities of this fibrosis can be assessed by comparison of its radiologic picture with those of stand ard silicotic films, is untenable. At least two general types of pul monary fibrosis caused by inorganic dusts can be recognized. A third, representing the purely peribronchial variety of fibrosis, might be added; or it may be that all duBt fibrosis will be found to approximate more or less closely one or the other of these two Vol. U No.{ ST 0850495 214 THE JOURNAL OF INDUSTRIAL HYGIENE types. These types are (1) that pro duced by combined silica dust, an example of which is seen in asbestos fibrosis, and (2) that produced by free silica dust, represented by silicotic fibrosis. These two types, while resembling one another in clinical signs and symp toms, differ materially both in the nature of the lesion produced in the lung, and in the character of the asso ciated radiographic picture. Thus, attempts to weigh, consciously or unconsciously, asbestos fibrosis, or any dust fibrosis other than Bilicosis, by means of the standard radiographic changes found in silicosis, is unsound and is likely to lead to a misconception of the potentialities of the dust in ques tion. Badham (8) gives an example of this source of error in reporting the unex pectedly early death of a man affected with a fine fibrosis caused by an orthoclase basalt containing no free silica. Referring to some of the radiologic differences between the fine fibrosis of dusts other than silica and the nodular fibrosis of quartz dust (i.e., true sili cosis), he states: Moreover, the coarse fibrosis of silica gave clear interspaces of normal lung, while the fine fibrosis presented a uniform granular mottling leading to the conclusion which is probably erroneous that the actual develop ment of fibrous tissue was greater in a nodular fibrosis as silicosis than in a general ised fine fibrosis caused by silicates. To me it appears that the mechanical damage to the lung is greater in a fine fibrosis than in a coarse fibrosis when both are well developed. The evidence obtained in the present inquiry amply confirms this general statement. On studying the development of asbestos fibrosis as displayed in a series of radiograms, and especially in the few available taken a year or more before a fatal termination, one cannot help asking the question, "What is there here which could have this effect?" The answer is that the damage to the lung is much greater than it appears to be when judged by the silicotio stand ard. Asbestos fibrosis is much more diffuse; it spins its fine web, as it were, crisscross throughout the lung, enveloping and eventually strangling the ultimate lobular structure, rather than depositing itself in numerous more or less isolated foci, as in silicosis. Thus, at any rate in the less advanced stages, the radiologic picture of the lesions does not impress the eye, uncon sciously viewing it from the standpoint of silicosis. The radiographic picture may show soft and fairly coarse nodulation, but it is never bo impressive as the nodulation in a silicotic film. Paradoxically, the distinctive fea ture, both clinically and radiologically, of the asbestos fibrosis is its uniformity. The modesty of the symptoms; the unobtrusive, but diffuse, impairment of the percussion note; the homo geneous stippling of the skiagram; all are fragments of an entity, unmistak able when assembled, but enigmatic when divorced. Only two references to the radiographic appearances of the chest in asbestos workers have been traced: one in a report by Pancoast and Pendergrass (10), and the other in an article by Burton Wood (19). Pancoast and Pendergrass together with Miller and Landis examined "17 asbestos workers, 2 of whom showed J.I.H. May, mo ST0850496 PULMONARY FIBROSIS IN ASBESTOS WORKERS 215 first stage changes and the other and by the time the stage is reached 15 definite second stage appearances. when the features discussed above are, Of the men longest at work, one after in varying degree, positive, and the seventeen years' occupation Bhowed radiologic picture is recognizable, the very definite diffuse, 'soft' spots fibrosis is not in its inception, nor even throughout both lungs, and another in its earliest stages, but is developed showed about the same appearance and fairly widespread. after fourteen years' occupation. We must, therefore, recognise an Very slight nodular shadows were earlier state when the fibrosis is present found in one man after only two years' in slight degree, and also when there is occupation. Most of these second evidence of choking of the lymphatics, stage cases Bhowed also well-marked and of a measure of pulmonary catarrh. first stage appearances still present, This Btage may be referred to conven indicating a persistence of free drainage iently as the prefibrotic stage. hilumward. In all instances the nodu The indications of this stage are lar shadows were characteristically indefinite, and some, at any rate, not 'soft' and varied considerably in size.1' specific. If, however, they can be Their first stage appears to correspond determined nd applied with only a with stage 1, and their second stage moderate degree of accuracy, informa with stages 2 and 3 mentioned above. tion of practical value will be available. It appears from the context that Efforts have been made, therefore, to these observers regard asbestos fibrosis distinguish workers in this stage. as being really a silicosis due to admix The following tabulation shows that ture of free silica derived from the twenty-one workers out of 363 exam original rock--a view difficult to sub ined (5.8 per cent.) were so classified: stantiate. Burton Wood (19) in a series of fif teen skiagrams of asbestos workers notes: "The most noticeable feature of skiagrams of workers exposed longest Clinical Examination* (36!): No. Fibrosis......... .................. 95 Prefibrotic conditions....... 21 Radiologic Examinations Per Cent. 26.2 5.8 to asbestos duBt is the presence of shadows suggesting a diffuse fibrosis affecting chiefly the lower two-thirds of the lungs. The fine quality of the shadows is worthy of note. Some of (US): Fibrosis............................... 52 Suggestive changes not definitely diffuse fi brosis............................... 22 39.1 16.5 the cases exhibit a 'ground glass' Many of these cases present a slight appearance, though on close inspection diffuse impairment of percussion note fine mottling is evident. . . . when --perhaps better described as a Blightly more definite mottling is present it increased sense of resistance felt on lacks the coarse quality described in percussion, mostly of the right lung, the skiagrams of chests showing pneu at least as contrasted with the left, moconiosis, e.g. South African gold and associated with some weakening miners............... " of the respiratory murmur. Prob Clearly, the maturation of asbestos ably this early stage could be detected fibrosis is spread over a period of years, radiographically, but only by means of Voi. No. 5 S T 0850U97 216 THE JOURNAL OF INDUSTRIAL HYGIENE comparison with a radiogram taken prior to commencing work with asbes tos. By such means the earliest stages of silicosis have been worked out by the South African observers. There, the radiograms taken at peri odic six-monthly medical examinations can always be compared with initial radiograms taken before the employees are permitted to work underground. group is dismissed from any further consideration. A general summary of the findings in the 374 workers who were examined clinically, classified under the most im portant lesion, is presented in Table 4. Illustrative Cases The salient points of a few oases are set out below to illustrate clinical and TABLE 4.-GENERAL SUMMARY OF FINDINGS CLASSIFIED UNDER THE MOST IMPORTANT LESION ' CABX8 or riBBOSIS PRB- TIBROT1C CONDI TIONS FTTLMOHAXT TUBERCU LOSIS ig 1g foc 3S H_ a5 egg OTHXB 4u *a i! PULMONARY LX8IONB Q ft S mSI n g 3 m3 3H 6z Due to Asbestos Due to Other Causes Due to Asbestoe Due to Other Causes W ith Evidence of a Dust Fibrosis Other Active Lesions Pleurisy* O ther Lesions 1 3I8 a 0D02 1* " 0 3 030 A Ml t. 9 rJSS.S O | Ih 3 is ft M 5| i p a l 1 ft 3 a 3 0ft ft 1 * 0-4................ 92 0 3 5 0 0 0 0 5-9................ 142 36 1 12 0 1 1 4 10-14.............. 89 27 5 3 0 3 0 3 15-19.............. 30 15 I 1 1 0 0 1 20 and over-- 21 17 0 0 0 1 0 0 13 3 5 0 0 7 1 0 1 62 3 6 2 2 72 0 3 2 0 88 2 110 7 1 010 1 Total........... 374 95 10 21 1 5 1 8 21 13 10 6 3 180 Percentage... 100 25.4 2.7 5.6 0.3 1.3 0.3 2.1 5.6 3.5 2.7 1.6 0.8 48.1 1 One case of thickened pleura due to old gunshot wound. 1 One caBe of emphysema due to gassing. In other cases included in this group, other features. Five radiograms are diffuse weakening of the respiratory reproduced to illustrate the radiologic murmur was noted, with fine sticky appearances of some of the cases. r&les in the root areas. At present no There are insuperable difficulties, stress can be laid upon this group. however, in reproducing the finer The clinical changes are so slightly changes depicted in the original nega marked that until comparative radio tives. grams are available it would be unsafe Cabs 1.--This worker, a female, aged 24, to draw any deductions. For the pur haB been employed in asbestos for ten and poses of this inquiry, therefore, thisi. one-half years--as a card tenter one year, i. I. H. Kit, 1M0 S TO 8 50498 PULMONARY FIBROSIS IN ASBESTOS WORKERS 217 and as a doubler nine and one-half years. Her family and personal medical history contain nothing of note. She has no com plaints and feels quite well. Her nutrition is good. She is pale, but shows no cyanosis. Chest.--She has a chest expansion of 1J inches. No impairment of the percussion note is detected. The breath sounds in the right lung are weaker, generally, than those in the left. Expiration is prolonged at the right root; no added sounds are heard. A skiagram showed some very slight and doubtful changes in the direction of in creased striation. Cask 2.--This man, aged 24, has been employed in asbestos for five years, carding and mixing. Previously he worked for four years in the cotton trade, yarn weighing. His family and personal medical history contain nothing of note. He has had a slight morning cough and expectoration for a year. His nutrition is good. His color is fresh, and there is no cyanosis. Chest.--There is some impairment of the percussion cote over the middle third of the right lung, behind, and slightly at the right base. The breath sounds are harsh, and expiration is prolonged in the upper half of the right lung, behind; expiration is also prolonged over the left upper lobe, behind. The respiratory murmur is weakened at the right base, and the breath sounds are of a "whiffing" character. There are no added sounds. A skiagram showed enlargement of the right root, and slight haziness and striation in the central zones in both lungs, suggesting early fibrosis. Case 3.--This man, aged 32, has been employed in asbestos for six years in the card room, and as a Btripper and grinder. Previously he was employed in a cotton card room for nine years. He had army service for five years, but was not gassed. He gives a family history of asthma; otherwise there is nothing of note in his family or personal medical history. He has no complaints and feels quite well. His musculature is very good. His color is pale, but he Bhows no cyanosis. Chest.--There is slight impairment of the percussion note generally, particularly at the right base. The respiratory murmur is a little weakened generally. No added sounds are detected. A skiagram showed old tuberculosis of the lung roots and gen eral increased striation, especially in the lower half of the right lung, suggesting early fibrosis. Case 4.--This worker, a male, aged 23, has been employed in asbestos for nine years, mostly mattress making. His family and personal medical history contain noth ing of note. He complains of occasional pain in both sides of the chest, and perhaps a little undue shortness of breath on exer- Fia. 1.--Case 4: Moderate fibrosis. Un due degree of striation and fine mottling in central zones of both lungs; calcified glands in roots, with rather coarse striation in upper lobes; ? interlobar pleurisy on right side, between the lower and middle lobes; emphysema at bases. tion. His color is normal. His muscula ture and nutrition are good. Chest.--There is no retraction of the apexes, but there is a slight flattening below the right clavicle. The percussion note is slightly impaired generally, behind, partic ularly on the right side. The breath sounds are weak, generally, and expiration is pro longed. No added sounds are detected. The skiagram (Fig. 1) Bhows an undue degree of striation and fine mottling in the central zones of both lungs; calcified glands in the roots, with rather coarse striation in Vol. 12 No. 5 ST 0850499 218 THE JOURNAL OF INDUSTRIAL HYGIENE the upper lobes; ? interlobar pleurisy on the right side, between the lower and middle lobes; and emphysema at the bases. The case was diagnosed as moderate fibrosis. Case 5.--This woman, aged 40, has been employed for eleven years in asbestos, for most of the period mattress making. Pre viously she was employed in a laundry. She has recently been ill for three months with pleurisy (no history of tapping); other wise her family and personal medical history moderate fibrosis, most marked toward the bases. Cass 6.--This worker, a female, aged 31, has been employed in asbestos for seven years, opening, and has been exposed to much dust. Her previous employment was non-dusty. Her family and personal history disclose nothing of note. She com plains of having had a cough for five years, and of shortness of breath on hurrying. She is thin and undernourished, and pale. Fio. 2.--Case 0: Moderate, but fully developed, fibrosis. Enlargea glands in both roots; diffuse fine mottling in both lungs, especially the right. Fio. 3.--Case 7: General fibrosis, mostly linear, but with little mottling of right lung. Old puerile tuberculous scars at apexes. are negative. She complains of having had a winter cough for three or four years, and of shortness of breath on exertion Bince her attack of pleurisy. Her nutrition is good; her weight is stationary. She has normal color, and no cyanosis. Chest.--There is some general impairment of the percussion note over both lungs, be hind, more noticeable at the bases. The respiratory murmur is weakened generally. Persistent crepitations and medium rflles are noted low down in the right axilla. A skiagram showed diffuse fine striation and fine nodular mottling, with light opacity at the bases. The case was diagnosed as Dust is present on her hair and in her nostrils. Chest.--She has a chest expansion of onefourth inch. There is slight general impair ment of the percussion note, definite at the apexes and the bases. The breath sounds are weak; expiration is slightly prolonged. No added sounds are heard. Her heart is not enlarged, and no murmurs are detected. The skiagram (Fig. 2) shows a number of enlarged glandB in both roots, and a diffuse fine mottling in both lungs, especially the right. This is a case of moderate, but fully developed, fibrosis. Case 7.--This woman, aged 48, has been J.LE My. 1>30 ST 0850500 PULMONARY FIBROSIS IN ASBESTOS WORKERS 219 employed in asbestos for thirty-two years-- about three years on cards, and the re mainder as a spinner. She has done no other factory work. Her family medical history discloses nothing of note. She haB a personal history of nephritis seven or eight years ago, causing three months' illness. Her complaints are: shortness of breath on hills, and winter cough for about six years. Her nutrition is fair. She is rather pale. Chest.--She has a chest expansion of onehalf inch. No retraction of the apexes is noted. There is general slight impairment of the percussion note, behind. Breath sounds are harsh and expiration is pro longed. No added sounds are heard. No gross enlargement of the heart is noted, but the second sound is found to be accentuated over the aortic area. The skiagram (Fig. 3) shows a general fibrosis, mostly linear, but with a little mottling of the right lung. There are also very old puerile tuberculous scars at the apexes. The case was diag nosed as general fibrosis. This case should be compared with Case 6. In Case 6 there was a heavy exposure to dust extending oyer a few years; in the pres ent case there was exposure to a very much less concentration of dust, except possibly in the firBt three years, but extending over many years. Cask 8.--This worker, a male, aged 62, has been employed in asbestos for twenty years as a weaver. He was previously a cotton and silk weaver. His family and personal medical history show nothing of note, except that he was regarded as a deli cate child. His complaints are: shortness of breath on exertion, and on going upstairs, for three years; morning cough and a little expectoration for the last three winters. He is thin and pale, with some cyanosis. Chest.--Chest expansion is 1 inch; there is retraction of the apexes. The percussion note is impaired over both upper lobeB, in front, and over the upper two-thirds of the right lung, behind. Expiration is pro longed at the bases. Pleural rub and incon stant riles are noted at the left base, and a few riles at the right base. A skiagram showed a definite diffuse fibrosis with nodulation. This is a case of fibrosis in the early advanced Btage. Case 9.--This man, aged 41, has been employed for twenty years in asbestos in many capacities. There is nothing of note in his family history. He gives a history of pneumonia a number of years ago. His complaints are: a little shortness of breath on exertion for the last two or three years; otherwise none. His nutrition is fair only. His color is fresh, but there is slight cyano sis of the lips, at times. Chest.--The skin is poorly elastic; there is some retraction of the apexes. There is an impaired, rather "boxy," note on percus sion, generally, especially over the upper half of the left lung, and over the upper twothirds of the right lung, behind, and in front. Respiratory murmur is generally weak. Expiration is slightly prolonged, but diminishing toward the bases. Pleural crepitations are noted low down in the right axilla. A skiagram showed a definite fine diffuse fibrosis. Neither lung lights up very well, and throughout both there is a very fine diffuse reticulation and mottling-- moderate, but fully developed, fibrosis. The fine diffuse character of the radiologic appearances is particularly noticeable here. Case 10.--This man, aged 46, has been employed for twenty-five years in asbestos, during nine years of which he was not ex posed to dust. For eleven years of the remainder he was employed in the card room, and mattress making. His family and personal medical history disclose noth ing of note. His complaints are: shortness of breath on exertion for three months; cough after a few hours' work in dust during the last two or three years, with little or no expectoration; and pain in the left side of the chest for the last three months. His nutrition is good. He is pale, with slight duskiness of the lips. Chest.--There is some retraction of the apexes. The percussion note generally is impaired, and of a "boxy" character. Breath sounds are harsh and expiration is prolonged over the right upper lobe; else where the respiratory murmur is a little weakened and expiration is not materially prolonged. No added sounds are heard. The heart is normal. The skiagram (Fig. 4) shows diffuse striation and fine speckled mottling throughout both lungs--fibrosis, fully developed. Case 11.--This worker, a male, aged 40, Vol. is No. J S T085050I 220 THE JOURNAL OF INDUSTRIAL HYGIENE has been employed for twenty-two years in asbestos--during the first eleven years on cards and as a weaver, during which he was exposed to a considerable concentration of dust. During the remainder of the time he was employed on a non-dusty process, but was exposed to a less concentration of dust derived from other processes. His family and personal medical history give nothing of note. His complaints are: shortness of breath on climbing stairs for the last five years; slight morning cough and expectora- Fio. 4.--Case 10: Fully developed fibro sis. Diffuse striation and fine speckled mottling throughout both lungs. tion for about the same time; and slight aching of the chest in front, below the left clavicle. His nutrition is good. There is slight cyanosis of the face. Cheat.--Chest expansion is 1 inch; there is retraction of the apexes. There is im pairment of the percussion note generally, most evident over the whole of the right lung, behind, and over the right upper lobe in front. The note is "boxy" over the remainder of the chest. The breath sounds are slightly weakened generally, except at the right apex, but there is no gross change. Expiration is prolonged generally. Fine crepitations are heard in both axillae, and over the right upper lobe, in front. The heart is normal. Sputum is mucoid, but is negative for Bacillus tuberculosis. Club bing of the fingers has been noted for about two years. A skiagram showed an exten sive diffuse fibrosis--fibrosis in a fairly advanced stage. Cass 12.--This worker, a male, aged 60, has been employed in asbestos for twentysix years in the card room. Previously he was a sawyer's laborer. There is nothing of note in his family and personal medical history. He complains of slight shortness of breath on exertion of recent years, and of winter cough for the last three or four years; expeotoration is stated to be nil. His musculature and nutrition are fair. There is slight cyanosis of the face. Chest.--He has a cheat expansion of threefourths inch. The percussion note is im paired generally, especially over the left upper lobe in front. The respiratory mur mur is weakened over the whole of the chest except the left upper lobe, where there are whistling breath sounds, and medium riles. The heart is normal. A skiagram showed very extensive changes throughout the chest of a coarse type without fine stippling. The roots showed a choked appearance. There was heavy mottling at the base. One old tuberculosis focus was noted at the left base, and some calcified glands in the left hilum. The diagnosis was fibrosis in the advanced stage. Cask 13.--This man, aged 66, has been employed in asbestos for twenty-one years as a weaver. For about sixteen years pre viously he was a cotton and silk weaver. His father died of "chest trouble" at the age of 45; his sister died aged 15 of pulmonary tuberculosis. He has only been away sick a week or two in twenty-one years, and has never had any serious illness. His com plaints are: undue shortness of breath on exertion during the last two years; cough for the last two or three winters.. Expector ation is creamy, and occurs a fair amount of times. He has lost weight, and is thin. He is pale, but with some cyanosis of the face, and with a malar flush. Cheat.--Chest expansion is 1J inches; there is retraction of both apexes. Dulness is detected on percussion over the upper two-thirds of the right lung and over the left J. L H. May, 1B30 S T 0850502 PULMONARY FIBROSIS IN ASBESTOS WORKERS 221 upper lobe, behind, and over both upper lobes in front. Breath sounds are rather weak, with prolonged expiration. Scat tered variable rhonchi and riles are heard over the right lung, behind, over the left upper lobe in front, and over the left root. The skiagram showed a definite diffuse fibrosis plus tuberculosis. Sputum was negative (one examination). The diagnosis was dust fibrosis in the advanced stage, with tuberculosis, probably active. Caa* 14.--This worker, a male, aged 36, commenced work in an asbestos plant in 1910, but was employed on other work until January, 1914. During the next five years, until early in 1919, about three years and nine months were spent in army serv ice, for nine months of which he was a pris oner of war, but he had two short periods of work in asbestos--eleven months in the weaving, and six months in the mattress, departments. From early in 1919 to No vember, 1927, he worked in asbestos proc esses, but for only six years and ten months in a dusty one (mattress making). He then ceased work. He was referred to a tubercu losis dispensary on Oct. 19, 1927, when he gave a history of bronchitis in 1916 and 1917 during the War, and of never being very well since; complaining of dyspnea, pain in the right side, and a slight cough of only about six months' duration, with a small amount of grayish sputum. Dr. N. Tattersall states that at that time: "Dyspnoea was very marked, even on talking, and there was definite cyanosis. He had marked hollowing and respiratory retraction at both apiceB, especially the right; Iobb of note over most of the right lung and the upper half of the left; bronchial breath sounds at both apices; fairly numer ous crepitations, mostly on the right side, and a pleural rub at the right base. He had a Bystolio bruit at the apex and pleuro pericardial friction. "I examined him a number of times, the laBt occasion being April 20, 1928. In that time he had lost 9 pounds, felt very weak, and the dyspnoea was increasing. The signs remained much the same, though occa sionally, if he got a cold, the moist sounds were more numerous, especially at the bases. Seven sputum examinations were negative, and up to the time I last saw him the sputum had remained small in amount, and its appearance did not suggest tubercle. "My diagnosis from the beginning was one of pulmonary asbestosis with possibly added tubercle. "I took two X-rays of him, neither of which showed appearances suggestive of tubercle, everything pointing to a very extreme degree of fibrosis." He died on Oct. 13, 1928. No postmortem examination was obtained. Fia. 5.--Case 14: Massive fibrosis, with pleural thickening, retracted apexes, and pneumothorax on left side with incomplete collapse of lung. It will be noted that the length of expo sure to asbestos dust is unlikely to have been more than about ten years and two months, and of this time he was employed only about eight and one-half years in a dusty process. War service, of course, may have reduced his resistance. The skiagram (Fig. 5) shows a massive fibrosis with pleural thickening, retracted apexes, and pneumo thorax on the left side with incomplete col lapse of the lung. No doubt fibrosis of the type pro duced by asbestos dust can of itself lead to complete disablement, and Vol. 12 No. 5 ST 0850503 222 THE JOURNAL OF INDUSTRIAL HYGIENE finally to a fatal termination, even in the absence of a superadded tubercu lous infection. The primary effect of the fibrosis would appear to be that of causing defective aeration of the blood, result ing in an added strain on the heart. For many years, and even with an advanced degree of fibrosis this may be of little inconvenience, provided physical exertion is limited, and acute illnesses are avoided. Ultimately, however, the margin of safety, already diminished, is lost and the circulation slowly fails, with the usual signs of edema of the lungs. More often, however, an attack of bronchopneu monia, influenza, or other acute infec tion adds too much to the strain, im pairs the cardiac musculature, and results in a fatal termination. (To be concluded) BOOK REVIEWS Bleivmujiftunq. By Prof. Dr. Paul Schmidt, Director dea Hygienischen In stitute der Univerait&t Halle a. d. S.; Priv.-Doz. Dr. Adolf Setter, Oberaaaiatent am Hvgieniacnen Inatitut Halle a. d. S.; und Priv.-Doz. Dr. Stillfried Liitner, Asaiatent an der Mediziniachen Klinik Halle a. d. S. Paper. Pp. 79 with index, illustrations, and bibliogra phy. Berlin and Vienna: Urban k Schwarzenberg, 1930. This monograph is divided into a short introductory or general section and a special section. The first part is devoted principally to a discussion of the outstanding diagnostic symp toms of lead poisoning and of the work done by Dr. Schmidt and his collabora tors in the microchemical determina tion of lead in blood, urine, and feces. The second part discusses in detail the usual sources of lead poisoning; the absorption, distribution, and excretion of lead; the pathology and clinical find ings associated with lead poisoning; and, finally, the diagnosis, prophylaxis, and therapeutic treatment of lead poi soning. Dr. Schmidt's monograph is particu larly apposite. It brings the literature of the subject down to the present date and represents the mature thought of an investigator who has long made this field particularly his own. The discus sion of the diagnostic features of lead poisoning is especially clear and to the point. In this connection it is of in terest to note that emphasis is placed on the importance of the determina tion of lead in the blood. No attempt is made to discuss the details of technic. The monograph presents instead a critical review of the more recent experimental work relat ing to lead poisoning and will, in con sequence, doubtless have a wide ap peal to all investigators in this field. The bibliography, which contains 298 references to the recent work and brings the literature of the subject down to 1930, is particularly valuable. "Bleivergiftung" may well be recom mended as a valuable addition to the library of students of public health.-- L. T. Fairhall. J.LH. Uay, IMO . ST 0850504 THE JOURNAL OF INDUSTRIAL HYGIENE Volume XII JUNE, 1930 Number 6 PERSONAL QUALITIES IN ACCIDENT CAUSATION* E. G. Chambers, M.A. Investigator for the Industrial Health Research Hoard, London HE main purpose of this article or by avoiding one. If we can find out Tis to give some account of the practical and theoretical diffi why some people react in the one way and some in the other, we shall have culties encountered in a research ilnetaorned a good deal about the nature the personal qualities involved in of the reactions of mind to its environ accident causation. This problem is ment. exceedingly important and is, in a About the practical importance of sense, one of the main problems of this problem to industry there can be psychology since its solution demands little doubt. The cost of accidents is. a stringent research into mental inte enormous not only in actual money gration. The occurrence of an acci but also in loss of time and efficiency. dent, as I shall show later, is not neces It is difficult to gauge the full extent of sarily fortuitous but is often the result this latter loss, but the financial cost of of the complicated interaction of vari accidents, as represented by the annual ous psychologic and physiologic func expenditure in insurance premiums, tions; and a research which has as its runs into hundreds of thousands of object the disentanglement of such pounds. This insurance, of course, complex mental situations (using men only covers cases where compensation tal in its widest sense) is bound to has to be paid, and compensated acci throw light on the nature of mental dents are actually only 1 or 2 per cent, life as a whole. The accident situa of the total number of industrial tion is one in which everybody finds accidents. himself sooner or later, and to which he An accident is commonly regarded reacts either by incurring an accident as being due to chance: that is, as an * Received for publication March 26, event the causes of which are external to the sufferer and not affected in any 223 THE JOURNAL OF INDUSTR^A^yS^NE 224 way by the nature of the sufferer him workers are actually sustained by only self. If this were so, one person would 25 per cent, of the workers; therefore, be just as likely to sustain an accident by weeding out a quarter of the work as would another in circumstances of ers a very considerable reduction in equal risk; and if records were taken accident incidence would be effected. for a large enough group of workers All the accident records which have over a sufficient period of equal expo yet been examined yield the J-shaped sure to risk, it would be found that the distribution curve, and all agree with accidents sustained during that period the theory that the individuals in the were equally distributed among the groups concerned differ in their prone people concerned. In 1919 Green ness to accidents. Newbold (3) has wood and Woods (1) showed that the shown that the frequency distribution curve of the frequency distribution of curve for foreign bodies in the eye--a accidents is not a straight line or a particular type of acoident--is like normal, saddleback curve, but is a wise J-shaped, so that even in this curve shaped rather like the letter J. apparently unlikely instance the This was confirmed by Newbold (3) theory of differing personal proneness in 1926. Broadly interpreted, this is confirmed. fact means that some people have more and Borne fewer accidents than can be Types of Accidents accounted for by the operation of Accidents may be divided roughly chance alone--a fact of great impor into three categories. First there are tance from a psychologic standpoint those which are purely accidental in since it definitely postulates the exist the popular sense of the word; in the ence of a liability to have accidents second class are accidents which which is more or less constant for each depend on the instrumentality of person but varies from one person to other people and not on the sufferer another. In other words, accidents himself; and third there are the acci are due not solely to chance but also to dents which depend directly on one's some personal quality which we may individual proneness. The first of call accident proneness. This fact these divisions comprises what insur alone gives a prima fade warrant for a ance policies call "Acts of God," study of individual psychologic dif which consist essentially in such ferences; it was the basis of the subse injuries to the person as are the inevi quent practical work done by the table results of nonhuman environmen Industrial Health Research Board1 tal changes. The Becond class of acci on the causation of accidents. dents is similar to the first from the Another fact of practical importance point of view of the sufferer. Again which may be deduced from the J- environmental change results in inevi shaped distribution curve of accidents table injury to him, but in this case'the is that approximately 70 per cent, of change is produced by human agency. the accidents sustained by a group of Finally, there is the class which em 1 Throughout the text the Board ia re ferred to uniformly under its new name; in the bibliography the name used is that given on the cover of the report. braces accidents that are the result of environmental changes either pro duced by the sufferer himself or of such j. I. H. June, 1M0 PERSONAL QUALITIES IN ACCIDE! 225 a nature as to be avoidable by certain The foregoing remarks suggest a reactions on his part. definition for the accidents which are The point of this classification is that due to personal proneness. Such an the first and second categories are accident may be defined as a physical marked by the inevitability of the injury due to a faulty reaction on the accident: the sufferer cannot escape part of the sufferer to some environ the accident whether the causes are mental change. The causes of this human or nonhuman--he may be faulty reaction lie in the sufferer him struck by lightning or he may be shot self, and it is the attempt to discover by a careless sportsman. Any acci the nature of these causes which con dents which are directly avoidable stitutes the research which Mr. Eric properly fall into the third category, Farmer and I are making in this field and it is only accidents in this class (4) (5). which can be regarded as due to per sonal proneness. As. yet there is no Difficulties in Practical evidence to show what proportion of Research accidents fall into each of these classes, but the universality of the J-shaped distribution curve shows definitely that the majority of industrial acci dents belong to the third category: that is, that they are due to personal proneness. There is, of course, a certain amount of overlap between these classes. For example, the activ ity of an accident-prone worker may produce an accident which is sustained not by himself but by another worker near him. Really such an accident should count as a third-category acci dent to the first worker; actually in the records it would figure as a secondcategory accident to the worker who sustained it. It will be seen at the outset that any research into accident causation is handicapped by uncertainty as to the type of accidents sustained by any group of workers. It is also obvious that no investigation can lead to changes in practice which would completely eliminate accidents, since accidents in the firet and second cate gories are not due to personal differ So far, for the sake of convenience in argument, accident proneno<K has been alluded to as a personal quality, but it is by no means necessarily the case that such proneness is a single quality. A study of the nature of accidents themselves suggests, on the contrary, that this proneness is complex in nature and the resultant of a number of psychologic and physiologic functions. For example, speed of movement, muscular control, and general intelli gence, all seem to play a part in the avoidance of such accidents as cut or crushed fingers and burns. Further, there is nothing to indicate that these functions are combined in certain definite proportions to produce a new, integral function which we have called accident proneness; rather it would seem that in some cases one function predominates, and in other cases another. Hence, proneness may be regarded as a group of co-operating functions and not as a definite unitary function, and this in its turn forms a further handicap to practical research ences. in this field. Not only the type of Vol. 1J No. 6 226 THE JOURNAL OF INDUSTRY accident may vary, but also the causes distinguish between redressings of the of the same type of accident may vary. same wound and further accidents. Another difficulty arises imme Apart from this there is rarely any diately we begin to consider the meas guarantee that all accidents are re urement of accident proneness, for it ported to the surgical stations. Some is evident that proneness and number factories have first aid boxes in the of accidents sustained are not synony workshops. Unless there is very strict mous. We cannot say that a person supervision and a high standard of with a high degree of accident prone reporting, workers are likely to ban ness will have many accidents and that dage small cuts and the like for them another person with a low degree of selves without troubling to report proneness will have few accidents. them, unless, as frequently happens, Such a statement would leave entirely they are compelled to report with a out of account all accidents falling septic wound a few days later. Fur into the first two categories and also thermore, considerable difficulty is inequalities of exposure to risk. All often experienced in getting details we can definitely say is that in a group regarding the length of time that of people equally exposed to risk but of workers have been exposed to risk. varying accident proneness, those with Short time and holidays, as a rule, the greater proneness to accidents will affect all the members of a homoge tend to sustain a larger number of acci neous group equally; but records of lost dents than those with a lesser prone time through sickness and the dates ness. Of course, the longer the period when workers are taken on and dis over which accidents are recorded, the charged are quite often not available. nearer does the actual accident rate The discovery of the age and experi approximate a true measure of acci ence of the workers is sometimes a dent proneness; therefore, the acci matter of considerable trouble; and dent rate of the whole working life finally, even if all accidents have been would be the closest measure of acci reported, it is not always an easy dent proneness that is possible. matter to find out exactly how many Some of the practical difficulties workers have had no accidents at all. connected with the collection of acci Many of these difficulties can be dent records may be mentioned here. obviated, however, by a careful choice These records are not always kept in a of the groups of workers to be exam way which makes analysis easy. This ined, and statistical analysis has shown is to be expected since the records are that some of the other difficulties are usually kept to serve practical pur unimportant. For example, major poses and not as a basis for statistical and minor accidents have been found inquiry. In most cases a bare state to correlate fairly highly in some cases ment of the occurrence of an accident (though this is a point which needs to a particular person on a particular confirmation), so that if a record of date is all that is recorded. The na either alone is available it will serve ture of the accident is sometimes given, as an indication of the varying accident but its gravity is rarely recorded. proneness of the workers. Moreover it is sometimes difficult to At this point the foregoing remarks J. I. H. Juna. 1W0 S T 0850508 PERSONAL QUALITIES IN ACCIDENT CAUSATION 227 may be summarized into a statement attempt to elucidate this problem. of our position at the beginning of a Psychologic tests may be grouped practical research into the nature of under the two heads of general and accident proneness. We have, as the specific. Now it has not yet been sole criterion of our success in discover shown that there is a specific test ing the functions involved in prone or tests for accident proneness. The ness, a set of accident records which sustaining of an accident may be may have been inaccurately kept, due to so many different causes which will include an unknown per that it is impossible to devise an centage of accidents not due to per analogous test for accidents in general sonal proneness, and which will have in the same way that a test may be an unknown correlation with accident devised for proficiency in a particular proneness itself. We have then to repetitive task. In other words, al devise a series of psychologic tests, the though the individual has a certain ability to perform which must be re proneness to accidents, it may be that lated as closely as possible to accident he has no special ability for their incidence. When this has been done, avoidance. Hence, until the existence if we succeed in finding a test for every of a specific factor or factors in acci psychologic and physiologio function dent proneness has been established, that plays a part in accident prone we can only apply tests of a general ness, and if further we combine these nature. These tests may be for func test scores, each correctly weighted, tions at any mental level from pure to form a single combined score which reflex to ideation; and if we consider shall have the closest possible rela the nature of the various types of tionship to accident proneness, even accidents which occur, we shall find then we can never hope to get any no reason for Hamming that the func thing approaching perfect correlation tions involved in accident proneness between the combined score and ac all lie at some definite mental level. cident incidence. The reasons for Rather, the reverse is true. In some this have already been pointed out: cases the accident may be due to fail The accidents recorded do not them ure or slowness in making the simplest selves correlate perfectly with prone muscular reaction, in some to poorness ness, the records include an un of neuromuscular coordination of a known proportion of accidents of the more complex type, and in others to inevitable type, and the functions sheer lack of intelligence. Hence it is tested probably are not involved to necessary to use a number of tests the same degree in the individual's which together cover as large a mental reactions to different accident situa field as possible. tions. The ideal battery of tests would Relationship between Tests, Ac cident Incidence, and Industrial Proficiency include one for each function involved in accident proneness. The actual relation of each test to accident inci dence could then be found and all the We now come to a consideration of tests weighted together in their correct the actual tests to be applied in an proportions to yield a single score (.EL 1M VoL u No. 9 ST0850509 228 THE JOURNAL OF INDUSTRIAL HYGIENE which would have the highest possible dent proneness if by so doing he gets correlation with accident incidence. less efficient workers. This suggests a Theoretically, as we have already seen, further aspect of the research into the correlation between this ideal accident proneness--namely: What is group of testa and accident proneness the connection between accident inci would still fall short of unity to a dence and industrial proficiency? To degree which we have no means of answer this question it is necessary to measuring. For practical purposes it discover the relation between the tests is of course desirable to limit the used for accident proneness and such actual number of tests used to as few records of industrial proficiency as as possible. Such tests should not are available. Theoretically it would correlate with one another, since high seem likely that there is a fairly high intercorrelation in this case would connection between a high accident mean unnecessary overlapping. proneness and a low standard of It should perhaps be said here that efficiency, for the accident situation the foregoing depends on the assump is also a situation occurring in the tion that all the functions involved in performance of an industrial task and accident proneness are directly meas a reaction to this' situation which re urable. However, there is no reason sults in an accident cannot at the same to assume that psychologic functions time yield an efficient performance of which cannot be measured at our that task. However, the question can present stage of knowledge do not also by no means be fully answered in this play their part in accident causation. way since the number of accidents Temperamental differences may be sustained by even the most highly cited as an example of such nonmeaaur- accident-prone worker is very small able functions. Here we have yet an in comparison with the number of other factor militating against success tasks he performs unscathed. The in measuring accident proneness, since only way to solve this problem satis we have no means of scoring non- factorily is to see if the tests which measurable functions and combining correlate with aocident rate also cor such scores with those of functions relate with industrial proficiency. which are directly measurable. In face of all the difficulties which So far only the attempt to measure beset an investigation of this sort, it is accident proneness with the practical evident that the greatest care in object of reducing industrial accident technic and accuracy in analysis must incidence has been discussed. The be exercised if the results are to have avoidance of a large accident rate is, any real meaning and value. It is not, however, only one of the problems aris as a rule, possible in the biologic ing in industry. One of the most im sciences to keep all factors constant portant of the other problems is how except the one we desire to measure. to obtain the maximum efficiency from Therefore, it is necessary to examine the workers, and it will be seen at once the results obtained from several dif that, as a matter of practical politics, ferent angles in order to make Bure no employer can be expected to choose that we are actually measuring what operatives with a low degree of acci we set out to measure. To apply j. i. H. Jum.1930 ST0850510 PERSONAL QUALITIES IN ACCIDENT CAUSATION 229 ^ certain testa to a group of workers and correlate the scores obtained with the accident records of the subjects is by no means sufficient to yield a reli able answer to the problem. High correlation coefficients may in isolated instances arise quite by chance, and even if they are not Bpurious they may be due to a relation quite different from that which they appear to measure on first sight. This can be guarded against only by repeating the same tests on as many different groups of subjects as possible and by subjecting all the results obtained to statistical analysis by such methods as that of partial correlation. Correlation coef ficients which consistently repeat themselves in a number of different groups may be regarded as fairly reliable, and even if low in actual numerical value are probably definite indications of real relationships. It is necessary to examine the data with the utmost care at each stage in the investigatkm. The frequency distri butions of the scores made in the tests, the intercorrelations of the tests them selves, the relationship between the tests and such variables as the age and experience of the workers, and the time of day at which the tests were per formed--all these points have to be carefully examined for each group tested, and their influence, if any, on the final results eliminated before we can decide what meaning to attach to the results obtained. An investigation of the nature de scribed above, made over a large enough field, is of value quite apart from the practical solution of the immediate problem that it may afford. It will add new facts to the body of scientific knowledge and may definitely advance psychologic theory. As was said at the beginning of this article, such a research involves a thorough investigation into the interconnection of various mental functions; and pro vided the work is of sufficient scope, light will be thrown not only on the nature of these functions themselves but also on their relationships with one another and their relative importance in different psychologic situations. Our attitude toward the study of accident proneness is pragmatic: We are concerned with finding tests which will correlate with accident incidence, no matter what they actually measure. However, it is useful from the point of view of theory to name tests even though we cannot define the functions which they measure. Hence a set of intercorrelating tests which bear a definite relation to what is commonly called intelligence may conveniently be called intelligence tests. Similarly another set of tests may be called aesthetokinetic tests and be said to measure aesthetokinesis.* Such names, of course, throw no direct light on the nature of intelligence and aesthetokinesis, but the nomenclature is useful for purposes of reference and comparison. For example, if we make the statement that both intelligence and aesthetokinesis play a part in engineering ability, what we actually mean is that there is some factor in volved in both engineering proficiency and the ability to do well in certain 'Three sensorimotor tests which were found to intercorrelate were called aestheto kinetic tests because their successful per formance required accurate and rapid co ordinated reaction to perceptual stimuli, although the form or perceptual setting of the tests differed considerably. They therefore form a special group of Bensonmotor tests, distinguishable from sensori motor tests in general (4) (5). Voi. ia No. s ST08505I I 230 THE JOURNAL OF INDUSTRIAL HYGIENE tests which we call intelligence and ords; consequently direct comparison aeethetokinetic tests. This is a defi between the relations of the tests nite advance in psychologio theory; to accident incidence and to indus for, without knowing in the least what trial proficiency was not possible. the function we have called aestheto- This comparison could, however, be kinesis really is, we can definitely say made indirectly. that it is a function which is measured It was found that a group of sensori by a certain set of sensorimotor tests motor tests, those designated as and that it plays a part in engineering aesthetokinetic tests, correlated with proficiency and in the avoidance of accident incidence, and that when their accidents. The relative importance scores were weighted together with the of the part it plays in the two cases entrance examination scores of the may be determined by 'correlation. subjects, a final correlation coefficient This article would not be complete of 0.406 with the accident rate was without a brief account of the practical obtained. The correlation coefficient work which has already been done in between the entrance examination this field. In the course of several alone and accidents was 0.294. years Mr. Farmer and I have given In the course of analyzing (these thirteen different tests to a large num results an interesting fact was revealed. ber of groups of workers, totaling over It was found that where the accident 1,800 subjects in all. Full details of records extended over several years, the early part of this investigation the relation between aesthetokinesis have already been published by the and proneness to accidents became Industrial Health Research Board (4) more marked as the period of exposure (5), and I shall just indicate here, in a to risk increased. Thus, while the few words, the scope of the experiment coefficient of the correlation between and the chief facts elicited. aesthetokinesis and accidents for only Tests were given designed to meas one year was 0.099, it increased in size ure intelligence--expressed through when the accidents were recorded for both a linguistic and a mechanical periods of two and three years, and medium--sensorimotor ability of vari became 0.444 when the period of ous degrees of complexity, physiologic exposure was four years.' It is evident characteristics such as physical that the longer the period over which strength and muscular control, and accident records are taken, the nearer nervous stability. The subjects, who does the actual number of accidents were for the most part engineering sustained come to being a true measure apprentices, were carefully chosen so of accident proneness. AIbo, if a test that as many as possible of the factors really measures accident pronaness, Buch as age, experience, and exposure it is obvious that the better the measure to risk were kept constant. These of proneness, the higher will be the subjects fell into two groups, those correlation between the test scores and who had suitable accident records proneness. Hence it follows that the and those who had suitable records of relation between the test scores and industrial proficiency. Unfortunately, accident incidence should become no group possessed both sets of rec more marked as the period of exposure J. I. H. June, 1930 ST08505 I 2 PERSONAL QUALITIES IN ACCIDENT CAUSATION 231 increases. Since this condition is sat show that the maximum coefficient of isfied in the case of the aesthetokinetio correlation that could possibly be tests, within the limits of the data obtained falls short of unity by available in this experiment, we have an unknown, but probably consider yet more evidence from a different able, amount. standpoint to show that the aestheto- Summarizing these results it will be kinetic tests really do measure a factor seen that tests have been found which, in accident proneness. when combined with the entrance On examining the relation between examination of apprentices to a the tests and industrial proficiency, skilled trade, correlate more highly it was found that three groups of tests with accident proneness than does the correlated significantly with profi entrance examination alone. Also, ciency. First, there was the group of the same tests combined with the aesthetokinetic tests; second, a group entrance examination correlate more of intercorrelating intelligence tests; highly with industrial proficiency than and third, a dynamometer test for does the entrance examination alone. physical strength. Since these three Therefore, if the entrance examination groups of tests did not correlate with of these eng. eering apprentices were one another, we were able, by taking a supplemented with certain of the single score for each group, to obtain psychologic tests, the candidates se three nonintercorrelating measures of lected would on the whole be more pro industrial proficiency. When these ficient and less liable to have accidents were weighted together with the en than those selected by the present trance examination scores of the sub methods. The experiments are still in jects, a final coefficient of 0.472 with progress, and in the course of time proficiency was yielded, the entrance it will be possible to publish a more examination alone giving a coefficient extensive report in which the results of 0.388 with proficiency. of new tests for other psychologic Representative tests from each of functions, as well as the results of these three groups had been given to applying the same tests to further four groups of subjects with suitable groups of subjects, will be given. accident records. For these subjects, the tests were weighted into a Bingle Conclusion score, using the same weights as in In conclusion I should like to empha the case of the correlation with indus size the fact that although the study of trial proficiency; and the correlation accident causation is full of difficulties, coefficient between this new weighted as we have seen in the foregoing survey score and accidents was 0.446, which of the problem, yet certain definite should be compared with the coeffi advances have been made. That cient of 0.294 between the entrance individuals differ in their proneness to examination alone and accidents. accidents has been established beyond These correlation coefficients, though dispute, and it has further been shown statistically significant, are in no that certain measurable psychologic case very large; but a number of functions play a definite part in this reasons have already been given to proneness. Moreover, imperfections in Vol u No. 8 ST08505I 3 THE JOURNAL OF INDUSTRIAL HYGIENE the accident records militate against success in establishing the existence of a relation between any tests and acci dent incidence, so that any correla tion that is found is not due to faulty data.- Hence the results that have already been obtained must not be dis counted by the fact that the data are imperfect; on the contrary, it may be said that if the data were free from error, the relation- shown to exist be tween aesthetokinesis and accident proneness would be seen to be still closer than now appears. Stress has been laid upon the ex treme care and accuracy necessary to produce reliable results in an investiga tion of the sort described in this article. This, of course, only applies to the actual investigation itself. Once rela tions between certain psychologic func tions and accident proneness have been definitely established, the tests measuring these functions may be used as a practical basis for selection, with the effect of lowering accident rate and increasing industrial proficiency. The results presented in the fore going are most encouraging and sug gest that further research along similar lines may show what other functions are involved in accident proneness and may yield results that will be of great practical value. BIBLIOGRAPHY Study of the Human Factor in the Causation of Accidents. Ibid., Rep. No. 34,1920. 4. Farmer, E., and Chambers, E. G.: A Psychological Study of Individual Dif ferences in Accident Rates. Ibid., Rep. No. 38,1920. 0. Farmer, E., and Chambers, E. G.: A Study of Personal Qualities in Accident ProneneBS and Proficiency. Indust. Health Res. Board, Rep. No. 65, 1929. ST08505II* TOTAL HEAT DIFFERENCE AS A MEASURE OF WET KATA COOLING* Walter S. Weeks Profeator of Mining, University of California N 1922, 0. W. Armspach and Mar C - Film coefficient of conduction from I garet Ingels (1) proposed as the measure of wet kata cooling rate, water to air. T1 - Wet bulb temperature of air. e, -- Vapor pressure of water at temper at a given velocity, the difference be ature T, in inches of mercury. tween the total heat content of air e1 -- Vapor pressure of water at wet saturated at the average temperature of the kata-thermometer and the total bulb temperature, in inches of mercury. heat content of air saturated at the wet bulb temperature. This idea re ceived little attention from other inves tigators until lately, when a number of correlations have been attempted with varying success. If total heat differ ence can be made the basis for calculat ing cooling rate, it should be possible W. H. Carrier (3) has sho^i: that the total heat above 0F. in 1 pound of air can be calculated from the formula H - C, T` + JJ W1 H - Total heat in British thermal units per pound of dry air. C,, *= Specific heat of air at constant pressure (0.24 British thermal to develop a formula involving total heat difference which can be shown to give the same results as the rational formula published in a recent issue of This Journal (2). unit per pound). T1 = Wet bulb temperature, in degrees Fahrenheit. L1 " Latent heat at wet bulb tempera ture (British thermal units per pound). The rational formula for the rate of cooling of a warm body at constant temperature, and covered with a film of moisture, was shown to be W* =* Weight of vapor in pounds asso ciated with 1 pound of dry air, assuming saturated condition, at the wet bulb temperature. n (Tk - T.) R (T. - TO + Consider 1 mol of dry air saturated C[(T. - T<) + 91 (e. - e`)I with moisture. If the barometric n -> Combined coefficient of conduc tion and radiation into the water film, from the body. Tk =* Temperature of body, in degrees pressure is P and the pressure of the vapor is e, the pressure of the air is P -- e. With every mol of air there will Fahrenheit. Tw " Temperature of surface of water film, in degrees Fahrenheit. T, - Temperature of surrounding ob jects. be associated -------- mols of vapor, P--e and with every pound of air there will be associated R Coefficient of radiation. Received for publication April 28, 1930. c 18 e ------- X ---- -- 0.621 -------lbs. of vapor P - e 28.98 P-e v Voi la No. < ST08505.15 234 THE JOURNAL OF INDUSTRIAL HYGIENE where 18 and 28.98 are the molecular weights of water and air. Total heat may then be expressed for a given wet bulb temperature LV H = C, Tl + 0.621 ------- -r " 6* Consider now a warm body at con stant temperature covered with a film of moisture. The difference between the total heat of air saturated at the temperature of the water surface and the total heat of air saturated at the wet bulb temperature is expression with the last term of the ra tional formula, we see that the rational formula could be written n(Tk-T) -R(T,-TJ+^(H.-H0 where H, and H' are the total heats at the temperature of the water and at the wet bulb temperature, computed by the approximate method. Accordingly the cooling effect of the air can be computed either by the ex pression C [<T. - T>) + 91 (e. - e1)] CP(T. - T`) +0.621 or by the expression In the temperature range from 60 to 95 the latent heat may be considered constant at the average value of 1,048 British thermal units.1 Since the va por pressures are small compared with the barometric pressure, they may be neglected in the denominators with out great error, and the total heat difference may be written Cp (T. - TO + 0.6211 (e. - e1) 4.16 C (H,, - H>) If actual values, not approximate values for total heat are used, the ex pression should be 3.94 C (H,, - H1) This factor was determined empirically by UBing values of total heat and vapor pressure from the psychrometric chart of Dr. E. Vernon Hill (4). The fol lowing are some values from the chart: If the barometric pressure is 29.92 inches and L is 1,048, the expression becomes 0.24 (T, - TO + 21.8 (e. - e0 Take 0.24 outside of the bracket, and we have 0.24 [(T. - TO + 91 (e. - e01 This is the total heat difference, the total heats being computed by neg lecting the vapor pressures in the expression P -- e. Comparing this 1 From the Steam Tables of Marks and Davis. Wei Bulb Temperature `F. 95 80 70 60 Total Heat B.t.u./lb. 61.01 42.64 33.51 26.18 Vapor Preeeure in. Hg 1.645 1.022 0.732 0.617 For example, assume that the tem perature of the water is 95 and the wet bulb temperature 70. The cool ing effect of the air, by the rational expression, is, then C [(95 - 70) + 91 (1.645 - 0.732)1 - 108.08 C By the total heat expression, it is 3.94 C (61.01 - 33.51) - 108.35 C J. I. H. Junt. 1030 ST085051 6 TOTAL HEAT OF AIR ADD WET KATA COOLING BATE 235 The agreement, when any wet bulb difference between the total heat of temperature in the range from 60 to air saturated at the temperature as 90 is used, is within 2 per cent. sumed by the surface of the water film The heat balance equation expres and the total heat of air saturated at sing the heat loss in a given environ the wet bulb temperature. ment is as follows, when the total heat The total heat of air saturated at difference is used. the temperature of the body is in no way involved. n (T* - T.) - R (T. - TJ + 3.94C OH. - H>) The rate of cooling of the warm body Summary in a given environment cannot be ex pressed as a function of total heat dif The effect of air at constant veloc ference, because total heat difference ity on the rate of cooling of a warm has to do only with the effect of the body at constant temperature and air, while the total rate of cooling is covered with a film of moisture can be influenced by radiation exchange with expressed closely as a function of the surrounding objects. BIBLIOGRAPHY 1. AaifSFACH, O. W., AND INOBL8, M.: Temperature, Humidity and Air Mo tion Effects in Ventilation. Tr. Am. Soc. Heating and Ventil. Eng., 1922, tS, 103. 2. Want, W.8.: A Rational Expression for Wet Kata Cooling Power. ThisJoub., 1930, It, 148. 3. Carbibr, W. H.: Rational Psychrometrie Formulae. Their Relation to the Problems of Meteorology and'of Air Conditioning. Tr. Am. Soc. Mech. Eng., 1911, S3, 1005. 4. Paychrometric and Comfort Chart. Chi cago, E. Vernon Hill Co. Vol. No. ST08505n THE INFECnVITY OF SILICOTIC TOBEBCDLOSIS* Patbics Hsffxbnan, M.D. Tuberculorit Officer, Derbythire County Council R. COLLI8, in "The Statisti D cal Characteristics of Dust Phthisis," published in This by Dr. Collis would not emerge from an investigation of the health of the families of the few cases of silicotic Journal in November, 1926, refetrurebde,rculosis which I had under my at the end of his paper, to "one last care in the gritstone - districts of statistical peculiarity . . . . , the Derbyshire, despite the smallness of certitude of which rests upon rather their numbers. With that object in insecure data . . . m., the sup view, the following investigation was posed low infectivity of silicotic tuber made in the winter months of 1927 to culosis. He then set forth the evidence 1928. upon which this belief was based. It Up to 1927 I had met with twentywill, I think, be generally agreed that four cases of silicosis with pulmonary the evidence is mainly inferential in tuberculosis, mainly among the Derby character, and that more positive data shire gritstone masons.1 In every case are needed before the fact can be re the diagnosis had been verified by the garded as established. presence of tubercle bacilli in the spu The examination and observation of tum, and the majority of the cases "contacts" to cases of tuberculosis is had already ended fatally. Although now one of the statutory duties of British Tuberculosis Medical Officers. Accurate data regarding the infectiv ity of tuberculosis should, in time, emerge as a result of their labors. As far as silicotic tuberculosis is con cerned, a special opportunity for the number of cases was small, I thought that it might be worth while to investigate the condition of the wid ows, wives, and children of these men, and to compare it with the condition of the widows, wives, and children of a similar number of men with non- settling a very interesting problem silicotic open tuberculosis, from the awaits the Tuberculosis Officers who same district and of the same age at work in areas where industrial silicosis the time when tuberculosis was first prevails. diagnosed. Although the examination of con tacts was not so prominent a part of the work of a Tuberculosis Officer in 1926 as it is today, it seemed worth endeavoring to see whether some fig ures bearing on the matter referred to * Received for publication Feb. 6, 1930. 1 The distribution of these cases accord ing to occupation was as follows: Gritstone bench hand...................... 13 Gritstone scappler..........................- 4 Gritstone quarryman....................... 3 Potter................................................ 2 Silica and ganiater briclcmalcer....... 1 Cutlery grinder................................ 1 236 J.LH. June, 1930 ST08505I 8 INJECTIVITY OF SILICOTIC TUBERCULOSIS 237 I found, however, that in the dis trict under investigation married men over 45 years of age rarely developed tuberculosis except they were silicotic; consequently I had to go a little fur ther afield and to include some cases from outside the gritstone area in order to make up the necessary twenty-four controls. Finally, when I had col lected the controls, I found that their ages averaged 52.5 years as against 48.5 years in the silicotic group. The results worked out as follows: Tuber- Tubereuloti* culosia with without Sili- Sili cont com Cases: Total no....................... 24 24 Average age on diag nosis.......................... 48.5 52.5 Wives and Widows: Total no....................... 19 20 No. developing tuber culosis....................... 0 1 Percentage developing tuberculosis............. 0 5 Children Born: Total no........................ 91 68 No. developing tuber culosis....................... 13 8 Percentage develop ing tuberculosis....... 14.3 11.8 Children under 14 on Date of Fathers' Diagnosis: Total no....................... 23 9 No. developing tuber culosis....................... 11 3 Percentage developing tuberculosis............ 48 33.3 The general rate of incidence of con jugal tuberculosis has been the cause of much controversy, but is, I think, now generally accepted as averaging about 5.6 per cent, of noninfected per sons who marry infected persons; and the investigations of the Tuberculosis Officers of Lancashire have given us monumental figures of the percentage of children of tuberculous fathers who develop the disease--figures which show a higher incidence of the disease than in the cases of the forty-eight fathers detailed above. As far as the meager figures which I collected can be relied on, they show that for approxi mately the same age group, the Bilicotic fathers were slightly more in fectious to their children than the non-silicotic. And further, the figures suggest that the apparent low infeotivity of silicotic tuberculosis is attrib utable to the late age at which the tuberculosis develops. The British workman, in the silica industries as in others, marries young. By the time he has reached 48 years of age, most of his children have grown up and passed the most dangerous period of susceptibility to tuberculous infec tion. In the exceptional cases in which young children were found in the households of the silicotic fathers, the tuberculosis incidence rate was very high. The total absence of conjugal in fection among the wives and widows of the silicotic cases is on all fours with the oft-quoted observation of George Bauer--better known as Georgius Agricola--who wrote, in 1557, that women could be found in the min ing communities of the Carpathian mountains, who had been widowed six times over by miners' phthisis. The work of this German on miners' phthisis, published nearly 400 years ago, suggests to us that we might pay a little more attention today to Ger man work on silica and its biochemis try, if for no other reason than be cause its priority is so unassailable. The figure of 5.6 per cent, men- Vol. 1J No. a ST0850519 238 THE JOURNAL OF INDUSTRIAL HYGIENE tioned for conjugal tuberculosis is an "average" figure, and therefore sub ject to the usual fallacies of averages. There is, for example, little doubt that the incidence rate among young mar ried couples is higher than 5.6 per cent., and that in middle age it is lower. There are many other factors to be considered, as well as the ages of the infectious and the noninfected spouse. Child bearing, lactation, housing, nutrition, educational and social condition, all have their influ ence. But when, eventually, all the factors which determine the incidence of conjugal tuberculosis come to be included in one comprehensive equa tion, we must not be surprised to find that the variable for "silicosis" has dropped out. Meanwhile, facts are needed. It is in the power of the Tuberculosis Offi cers working in silicotic areas to pile up these facts, little by little, from the families of silicotic patients who come under their observation. J.LH. Jua*. 1910 S T 0 8 50520 THE OCCURRENCE OF PULMONARY FIBROSIS AND OTHER PULMONARY AFFECTIONS IN ASBESTOS WORKERS (Concluded) E. R. A. Merewether, M.D. H. M. Medical Inspector of Factories Morbid Anatomy Professor M. J. Stewart of Leeds has kindly supplied me with a detailed description (dated March 28, 1929) of postmortem appearances of several cases. From this account the follow ing points are extracted: The totally fibrosed areas of lung show grayish-black mottling, owing to immobili zation of carbon. This tissue is excessively dense and completely airless; but there is no evidence of calcification. Other por tions of lung show varying grades of the same process, and even the least affected parts are definitely tougher than normal. In none of the cases was there any evidence of an active tuberculous lesion. The gross morbid anatomy of this lesion, as seen in persons who have been at work for many years in the dusty atmosphere of an asbestos factory, consists in a widespread pulmonary fibrosis affecting especially the basal region of both lungs. There are ex tensive, densely fibrous adhesions through out the pleural sacs, which may, indeed, be come completely obliterated. In particular, the bases of the lungs are firmly adherent to the diaphragm, and between these two structures there is often a thick, homo geneous layer of fibrous tissue, similar in appearance and consistence to yellow fibrocartilage. As a result of these two proc esses--pulmonary fibrosis and pleural sac obliteration--bronchiectasis develops in the midst of the more grossly diseased tissue and may go on to the formation of multiple abscesses with Bmooth walls. The distribution of the fibrosis, apart from the extensive basal lesions., is rather irregular, the peripheral, subpleural regions of the lungs being more affected than the oentral areas. In one case in which the pa tient had been away from work for four years (following nineteen years in the mill), the areas of dense fibrosis were extraordinarily sharply circumscribed. The nodular char acter of the legion which is so striking a feature of silicosis in its earlier stages is not met with in this disease. Histology The essential lesion is a chronic interstitial fibrosis of the lung. In the earlier stages, there is fibroblastic proliferation in the alveolar walls, which become increasingly thickened in consequence; and there is catarrhal desquamation of the alveolar epithe lium. At this stage of the diseasepeculiar golden-yellow "asbestosis bodies" are found in varying, usually con siderable numbers, both in the alveolar spaces and in the thickness of their walls. Detached portions of bodies may often be seen engulfed by alveolar phagocytes, or a large unbroken body may be partially surrounded by these cells. In the more advanced stages of the disease, the fibrosis of the lung is complete. Alveoli can no longer be made out; but the asbestosis bodies still remain embedded in the fibrous tissue. Varying quantities of carbon are also present, chiefly in little masses as though it had been contained with in phagocytes. Chronic bronchitic Vol. u No. s 239 'ji ST085052 I 240 THE JOURNAL OF INDUSTRIAL HYGIENE changes are present and all grades of bronchiectasis may be seen, in cases of long standing, from simply bronchial and bronchiolar dilatation, with walls still more or less intact, to large spaces filled with pus in which the original bronchial walls have become converted more or less completely into fibrous and granulation tissue. Many of the smaller arteries Bhow obliterative end arteritis. Reversionary metamorphosis of alveolar epithelium iB frequent, and such alveoli are often filled with albuminous fluid, in which clumps of "bodies" may be found. Asbestos Dust in the Lungs Dr. W. E. Cooke has supplied (under date of June 25, 1929) details of his researches on asbestos dust in the lungs, and on the constitution of the curious bodies, which have been freely used in the following notes:-- Sections of lung and the results of digestion of the lung with trypsin show an enormous amount of fine black granular dust, much of which is carbonaceous. In addition, there are two striking features. The first is the almost complete absence of the fine translucent spicules of fiber which make up a great proportion of asbestos dust in factories. The second feature is the presence of large fragments vary ing in length from 10 to 360 microns. They are found in fibrotic and necrotic areas, singly and in groups. The particles are so large--masses of them are seen in Borne sections--that they must have occluded small bronchi and resulted in fibrosis of the surrounding area. Comparing these large particles in the lung with those found in asbestos dust, close resemblance in sizes, shapes, and colors is apparent. There are the same black, blue, brown, and trans lucent fragments. In fact it is easy to take such a single particle from the lung and immediately find its brother in a slide made from the dust. Curious Bodies In addition to the fine granular dust and larger fragments of asbestos, sec tions of the lungs show curious bodies. They are found in alveoli, bronchioles, fibrous and necrotic areas, and in phagocytes in sections of both lungs. If a portion of lung is teased and extracted with water, or digested with trypsin, or, as Professor Stewart pointed out (1928), if a smear is made from the cut surface of the fresh lung, these bodies are seen in myriads. The larger bodies measure from 20 to 100 microns or more in length, and are of a golden-brown color. They may have single clubbed ends or may appear as elongated dumb-bells; some are filamentous, while others suggest a series of disks. Single coccal and spore-like forms, and aggregations of these, and strepto coccal forms are not uncommon; the color varies in the smaller types from a very pale yellow to a yellowish-brown. The bodies do not stain with any of the aniline dyes, but in chrysotile workers, they give the Prussian blue reaction for iron in varying degrees of intensity. These curious bodies have been found in every autopsy in pulmonary asbestosis. It would be unprofitable to retrace all the steps which led down many by-lanes during the course .of the work, but I will mention a few per tinent details of interest. Professor Stewart suggested to me J. I. H. June. 1S30 ST0S50522 PULMONARY FIBROSIS IN ASBESTOS WORKERS 241 that a better method than simple the large black, blue, and brown par extraction of the lungs with water or ticles and what appear to be pieces of saline would be to digest portions with quartz. Relatively few fine spicules trypsin. During this process it was are found; but curious bodies of all found that if the specific gravity was descriptions tun present in enormous kept at about 1,070, the black dust numbers. and larger fragments of asbestos, as All these facts lead us to imagine well as the partially digested lung the bodies to consist of a central tissue, sank to the bottom of the tube. nucleus of asbestos spicules, upon By decanting the apparently clear which colloidal aggregate of blood supernatant liquid, and by centrifugal- proteins plus, possibly, soluble frac izing, neutralizing, and washing the tions of asbestos and, in the case of deposit, the curious bodies could be chrysotile workers, an iron salt have obtained in a pure state. This was been adsorbed and molded by currents done, and sufficient material for X- in the bronchi and the alveoli. ray examination was obtained. The The method of formation would bodies were attached to a hair with appear to be as follows: The fine gum and subjected to a seven-hour spicules of asbestos cause, by mechan exposure by Professor Bragg's method. ical action on the bronchioles and If the bodies were mineral, the X-ray alveoli, either minute extravasations film would have shown a definite of whole blood, or serous exudates translatable atomic pattern. The which envelop them. Solution of any films, however, did not do so, and we soluble fraction of asbestos takes were then able to exclude the sugges plaoe. The total amount of asbestos tion that the bodies were altered that is soluble must be extremely asbestos fiber. The result definitely small, as is proved by the X-ray pointed to the greater proportion of pattern of the curious bodies, but in their composition being of nonmineral the case of chryBOtile workers some origin. solution is suggested by the free iron The bulk of the curious bodies is soluble in strong acids and alkalies, and if the solution is observed under dark ground illumination, their bases are seen as extremely fine spicules some of which by transmitted light would probably be invisible. Under a dis secting microscope it is possible par tially to fracture the larger bodies and to show a central fine core. The greater portion of asbestos dust consists of Blender translucent fibers. In sections and extracts of the lungs there is a remarkable paucity of these fine spicules. The end-results of diges reaction. We must remember, how ever, that the Prussian blue reaction may be due to the iron of the hemo globin. Any surface in contact with a colloidal solution may act as an adsorbent, and in the present case the fine spicules must be considered to do so. Interaction between the soluble fraction of chrysotile and plasma proteins takes place, syneresis occurs, and, with the loss of water, the adsorp tion is rendered irreversible. The adsorbent is permanently ensheathed with stable colloidal aggregates which tion show the fine granular dust and become molded into the familiar ST0850523 242 THE JOURNAL OF INDUSTRIAL HYGIENE' Bhapes by alveolar and bronchial cur rents. Support for this idea is found in the fact that micro-organisms adsorb col loidal material in the presence of blood serum and colloidal asbestos. Staphy lococci so treated appear as large round yellowish-brown disks; in the process their property of staining with aniline dyes is loBt. The organisms coalesce and form masses; and I think it probable that Borne of the cocc&l and spore forms are similar organisms. Finally, are the curious bodies diagnostic of pulmonary asbestosis? Asbestos is unique among minerals in being fibrous; and its dust, generated during manufacturing processes, is also unique. As can be imagined from the formation of the curious bodies, there is no reason why, given any silicosiB, a fine spicule of mineral should not have colloidal matter deposited around it and become molded into a curious body. But as no other min eral dust is fibrous, this occurrence must be so rare as to be negligible from a diagnostic point of view. The con ditions which, apparently, must obtain for the formation of curious bodies are the presence' of plasma proteins and fine spicules soluble only with diffi culty. These conditions are ideally found in asbestos workers; for this reason I believe that curious bodies, if found in any numbers, are pathog nomonic of pulmonary asbeBtosis.-- W. E. Cooke and also Roodhouse Gloyne (20) have independently dem onstrated the presence of a mineral core, evidently derived from asbestos fibers, in the curious bodies. The bodies have been found (Stewart and Haddow (21)) in the intrathoracic lymphatic glands; in material obtained by lung puncture during life, first sug gested by S. A. Henry; in the sputa; and in smear preparations from the cut surface of the lung. In smear preparations they can be readily demonstrated. The importance of these findings lies in the fact that the bodies have never been found, as yet, in any other human affection. That similar bodies may be found to occur in the lungs of workers exposed to other dusts, is quite possible, although they have not been found in silicosis, nor were they present, according to Simson (6), in the fibrosed lungs of a hematite miner. They appear within a comparatively short period of time after exposure to asbestos dust; at the moment, their presence in the sputa, in the absence of clinical or radiologic evidence of pul monary fibrosis, cannot be taken as in dicating anything more than previous inhalation of asbestos dust. The pres ence of the bodies, however, in the sputa of persons with signs of a diffuse fibrosis, or their presence in numbers on postmortem examination of a fibrosed lung, has evident implications. Professor Stewart, who is continuing his work on this subject, has devised the following method of examining sputum for asbestosis bodies: Half an ounce or bo of sputum is added to an equal quantity of undiluted antiformin. This is gently agitated until the sputum is completely dissolved, after which it is diluted with 2 or 3 ounces of water and allowed to stand in a large test tube for three or four hourB. The bulk of the super natant fluid having then been decanted, the remainder is centrifuged at a moderate speed for ten to fifteen minutes. The whole of the supernatant fluid is now poured off, and the deposit transferred to an albumin- mng daed rung . I. H. >. 1U0 ST 0850524 PULMONARY FIBROSIS IN ASBESTOS WORKERS 243 ized alide, by mean* of either a platinum loop or a pipette. After thorough drying on a hot plate and final fixation over a bunsen burner, the film ia very gently washed in water, dried, and mounted in Canada bal sam. After a little experience the aabestoeis bodies are readily picked up with the low power, and their true nature is then con firmed with the {-inch or oil immersion lena. As a rule they are present in very small num bers, perhaps only one or two in a whole film. In the case of some of the older workers, however, numerous bodies, up to one or two per field in certain portions of the film, have been found. It is obviously neoessary to cleanse thoroughly all glass ware, eto., used in making these examina tions; otherwise there is a risk of contami nation of subsequent specimens. The films can be treated with hydro chloric acid and ferrooyanide of potash to demonstrate the Prussian blue reaotion given by the bodies. Asbestosib an Occupational Hazard Out of a total of 374 workers exam ined, 105, or 28.1 per cent., were found to be affected with fibrosis of the lungs, in greater or less degree. But when these figures are corrected by the exclu sion of cases in which previous work in dusty occupations (e.g., quarrying, coal mining) may have been the prime, or a contributory, factor in the develop ment of the fibrosis, ninety-five, or 26.2 per cent., of 363 workers were found to be affected with pulmonary fibrosis due to the inhalation of asbestos dust, and a further twenty-one, or 5.8 per cent., showed precursive signs of this disease. This percentage may well be com pared with the corresponding figures found by Middleton (22) in his exami nation of metal grinderB (46.9 per cent.) and by Sutherland and Bryson (23) (24) in their examinations of potters (39.9 per cent.) and of sandstone workers (58.1 per cent.). The precise significance of the lower figure found in this inquiry is not easy to determine. At first sight it seems to indicate that asbestos dust is less potent as a cause of pulmonary fibrosis than are the dusts containing free silica. Other factors, however--such as the measure of exhaust ventilation, or other means of reducing the concen tration of dust, in the several indus tries; differences in the average length of employment of the comparable groups in the samples examined in the respective inquiries; and the relative numbers employed in the more dusty and the less dusty processes--will affect the crude incidence rates ex pressed by these percentages. From comparison of the amounts of dust evolved--determined visually and by means of dust counts--in dusty asbestos processes, uncontrolled by local exhaust ventilation, with obvi ously defective exhaust ventilation, and with comparatively good exhaust ventilation, there can be no doubt that this preventive measure, which has been applied in some degree for more than seventeen years, has been a posi tive factor in minimizing the produc tion of fibrosis--probably in the direc tion of lengthening the period before the fibrosis becomes fully developed. Consideration given to the distribu tion of the workers examined both according to length of employment, and according to age, together with the incidence rates of fibrosis in each case, indicates the outstanding importance of length of employment (and hence length of exposure to dust), and the negligible effects of age, on the produc tion of fibrosis. Thus age groups 30 to Vol. II No. t ST 0850525 244 THE JOURNAL OF INDUSTRIAL HYGIENE 39 and 50 to 59 have incidence rates of 30 per cent, and 37.9 per cent., respec tively--not a wide difference, since the groups include workers in various processes exposed to different concen trations of dust. Moreover, the aver age length of employment in these two groups, excluding the cases of fibrosis, fibrosis in age group 20 to 29, has been shortened by increased susceptibility at ages under 20. As, however, the average age of this group of oases of fibrosis is 26.7 years, and also because the establishment of fibrosis does not necessitate immediate retirement from work, this is largely discounted. TABLE 5.--DISTRIBUTION OP WORKERS EXAMINED WHO HAD BEEN EMPLOYED FOR FIVE YEARS OR OVER, TOGETHER WITH CASES OF FIBROSIS, ACCORDING TO PROCESS IN WHICH WORKER WAS LONGEST EMPLOYED PHOCXS8 HO. EX AMINED casks or riBHosia AVXRAOK LKNOTOLpr BMPL0TK2NT IN TBS. No. Per Cent, of Group Group Less Cases of Fibrosis Cases of Fibrosis 1. Crushing, opening, disintegrating, and mixing............ 2. Carding.................................... 3. Spinning, twisting^ doubling, plaiting, etc......................... 4. Mattress making.................... 5. Weaving and associated proc- eases...................................... a. Cloth weaving................... 28 b. Band weaving.................... 21 c. Cloth and band and un- classified weavers............ 14 d. Warpers, beamers, loom tuners, charge hands, and others associated with weaving.................. 25 0. Miscellaneous processes and remaining unclassified workers................................. 21 9 39 16 42.9 41.0 8.9 10.9 9.1 13.2 87 12 13.8 10.1 18.7 15 7 46.7 7.3 13.0 88 40 45.5 10.0 12.7 21 75.0 9.5 14.1 4 19.0 10.9 13.5 4 28.6 7.2 9.5 11 44.0 11.2 10.3 24 11 45.8 8.8 13.8 Total.......................................... 274 95 34.7 9.6 13.5 is also similar, but considerably less than the average length for all the cases of fibrosis (13.5 years). No special susceptibility to the development of fibrosis is shown by young persons, unless it is considered that the figure of 8.7 years, the average length of employment of the cases of The effects of length of employ ment are such that after five years' exposure, the incidence rate of fibrosis mounts rapidly, and after ten years increases almost in geometric progres sion. Table* 5 Bhows the distribution of 274 workers examined, and of those with fibrosis, according to the process ST 0850526 PULMONARY FIBROSIS IN ASBESTOS WORKERS 245 in which they were longest employed. This was a compromise necessitated by the common customs in the indus try of having several different processes going on in the same room, and of workers transferring from one process to another. Since the intention was to obtain some measure of the relative incidence of fibrosis in workers in the various processes enumerated, and since no case of fibrosis clearly due to asbestos dust was found among eightynine workers examined, who had been employed for less than five years, in clusion of this group of workers would only have introduced a varying source of error. The processes differ, some very materially, in the amount of dust which they cause, and consequently in the amount inhaled by the operators (30). The outstanding point brought out by Table 5 is the relatively low incidence rate of fibrosis in "spinners" (group 3), as compared with each of the other groups. They are corrobo rated by counts of the dust particles in samples of air, a number of which have been taken and are discussed under Dust Risk. There is also some indication in these figures that not only are "spinners" less likely to develop fibrosis, but when they do, it takes longer to develop. Study of the radiograms suggests that in such cases (t'.e., in the less dusty processes) the resulting fibrosis is, for a considerable period, much more linear in its radiologic features, and showB less mottling. The history and clinical features in these cases, and the com parative dust counts, all contribute to the view that with comparatively low concentrations of dust, the resulting fibrosis is longer in developing and remains longer in the milder, and radiologically linear stage. This view is evidently of consider able practical importance since it sug gests that in such cases, the rate of accumulation of dust in the lung has not greatly exceeded the rate of elim ination, the changes still being centered in the main lymphatic system. If this hypothesis is accurate, it should follow that in order to prevent the full development of the disease, among asbestos workers, within an average working lifetime, it is neces sary to reduce the concentration of dust in the air of the workrooms to a figure somewhat below that pertaining to spinning at the present time. Fortunately, also, the spinning group is the largest individual group in this section of the industry--e.g., out of over 400 workers employed by one firm, this group accounts for more than one-third. Although all workers examined who have been included aa spinners have been engaged in spinning, or in simi lar processes for convenience termed "spinning," for a longer time than on any other process, only a few have been employed solely on spinning, and in workrooms where no other, and more dusty processes, were being carried on. These two factors, prior work in more dusty processes and present work in proximity to more dusty proc esses--especially the latter--have had, it is believed, some effect in raising the incidence rate of fibrosis for this group. Dust Risk In an effort to obtain additional data on the influence of concentration of dust in workrooms, a number of sam ples of air were taken and the dust con- voi. n No. oT 0850527 246 THE JOURNAL OF INDUSTRIAL HYGIENE TABLE 6.--SUMMARY OF DETERMINATION OF DUST CONTENT OF ATMOSPHERE OF WORKROOMS AND OTHER PLACES SAMPLE NO. PROCESS AND SOUBCD OP SAMPLE LOCAL MHAU81 VSNTILA TIONTO PROCSSS OR NOT OTHER PBOCrssxs IN SAME BOOM NO. Of PAR TICLES PER C.C. PERCENT AGE 2)t AND UNDER PERCENT AGE 7.5fl AND UNDER 1. 1/2 2. 1/5 3. 1/3 4. 1/7 5. 1/6 6. 1/8 7. 1/1 8. 2/11 9. 2/1 10. 2/14 11. 2/10 12. 2/8 13. 2/7 14. 2/9 15. 3/1 16. 3/4 17. 3/3 18. 3/5 19. 3/2 20. 4/1 21. 4/1 22. 4/3 23. 4/4 24. 4/5 25. 4/5& 28. 4/6 27. 4/7 28. 4/9 29. 4/10 30. 4/11 31. 4/12 32. 4/13 33. 5/1 34. 6/2 35. 6/3 36. 6/9 37. 6/6 Carding; passageway between cards Spinning Cloth weaving, dry Opening Sieving; shoveling fiber on to sieve Plaiting Office Offioe Cloth weaving Spinning Mattress making; filling Mattress making; beating, damp Mattress making; beating, dry Mattress making; after filling 2 mattresses Band weaving, wet Opening Carding; between cards Carding; feeding card Office Mattress making; filling Mattress making; filling basket Emptying settling chamber Same Insulating sections; leveling fiber Carding; side of dirty card Carding; end of clean card Carding; feeding card Cloth weaving, very Blightly damp Cloth weaving, damp Braiding Spinning Office Band weaving, dry Cloth weaving, dry Band weaving, dry Opening Carding; feeding card Yes No No Yes No No ,., . . No No Yes Yes Yes Yes No Yes Yes Yes No No No No No Yes Yes Yes No No No No No Yes Yes Yes Yes Yes 2,139 Yea 1,456 Yes 1,756 Yes 2,384 Yes 2,829 No .,. Yes Yes No No . 1,687 901 1,480 1,788 1,073 985 970 No 1,629 No 1,204 No 808 No 2,313 Yes 1,528 Yes 1,321 1,049 Yes 1,858 Yes 1,390 Yes 3,401 Yes 4,711 Yes 1,838 No 1,402 No 1,092 No 1,689 Yes 3,033 Yes 758 Yes 506 Yes 954 689 Yes 2,202 No 885 No 701 Yes 643 Yes 662 81.3 .95.1 95.9 84.1 80.9 83.0 100.0 96.7 93.7 97.6 99.0 98.8 98.7 88.9 96.2 92.5 85.9 99.0 100.0 100.0 98.6 100.0 98.1 95.8 86.9 96.6 96.6 99.4 96.6 77.7 82.5 82.9 96.3 60.1 -- .... .* .... 100.0 96.6 97.4 96.4 100.0 90.1 < .... -- ,,,, .... .... - J. I. H. PULMONARY FIBROSIS IN ASBESTOi 247 TABLE 8.--Continued SAMPLE NO. PROCESS AND SOURCE OP SAMPLE LOCAL OTHER BXHAOBT PROC VXNTILA- ESSES TION TO IN SAME PROCESS ROOM OR NOT NO. OF PAR TICLES PER C.C. PERCENT- PERCENT 'AGE AGE 2(1 AND 7.5(1 AND UNDER UNDER 38. 6/4 39. 6/5 40. 6/7 41. 6/8 42. 7/2 43. 7/1 44. 7/3 46. 7/4 46. 7/5 47. 7/6 48. 7/7 49. 8/2 50. 8/3 51. 8/5 Carding; center of room Carding; grinding rollers Spinning Offioe Cloth weaving, dry Opening; shoveling fiber into box Opening Band weaving, wet Spinning Carding; between cards Office Cloth weaving, dry Band weaving, dry Carding Yes Yea No ... Yes Yes Yes No No Yes ... No No Yes Yes Yes Yes ... Yes Yes Yes Yes Yea Yes Yes Yes Yes 620 540 620 666 4,688 4,880 6,324 5,353 6,044 4,607 3,413 1,287 1, 1,195 88.6 78.2 67.2 94.9 93.7 94.9 tent was determined by means of Owens' jet apparatus. Here also the undetermined effect of dust from neighboring processes must be noted. Nevertheless some information of prac tical value was obtained. Reference to Table 6 shows that the counts ranged from 506 to 6,324 particles per cubic centijaeter in the air of workrooms, and from 668 to 3,413 per cubic centimeter in the air of offices associated with the factories. In some cases there was a smaller count in a workroom than in an office of the Bame factory; this was due either to there being much fewer smoke particles in the air of the workroom, or to adher ence of the smoke particles to the inorganic dust in the workroom. The character of the dust in the two cases is, however, entirely different. In the air of the office almost all the particles are black, or brownish, and amorphous, evidently smoke; in the air of the workroom, the majority of the particles are, just as clearly, crystalline particles of asbestos, to gether with, frequently, some cotton fibers and numbers of black and brown ish particles, some adherent to asbestos spicules and some free. Most of the latter are iron containing and are derived from the asbestos, and there are relatively few smoke particles. Iso lated golden-brown scales or plaques, also derived from the asbestos, are scattered about the field. The asbestos fiber first fragments longitudinally, and apparently this process can go on indefinitely, since there is no ultimate fiber comparable to a vegetable fiber such as cotton. The dust collected in the Owens appa ratus contains numbers of these very fine fibers--some about 0.5 micron in transverse diameter, many less--which have fragmented transversely. Thus spicules of very diverse length--up to Vol. 1J No. '> '005052S 248 THE JOURNAL OF INDUSTRIAL HYGIENE about 80 microns--but about 0.5 the dust content of the atmosphere-- micron broad, are found in numbers on such as that produced by shoveling the Bample, together with the black, asbestos fiber into a sack--can be brownish, and yellow particles already detected and estimated. This is of mentioned. The great majority of the great importance since short, but spicules are found broken down into repeated, exposure to massive concen particles of the order of 2 microns and trations of dust is agreed to be very less, many being about 0.5 micron and harmful. Counts Nos. 5, 22, 23, and more or less rounded. The proportion 43 in Table 6 are examples. Much of elongated to rounded particles Beems useful work can be done by means of to vary in the different processes; for serial dust counts in various dusty example, a greater proportion of elon processes in the same factory, and by gated particles is found in the air near comparison of the results. dry cloth weaving than near a spinning The counts set out in Table 6 are frame. Weaving damp reduces the derived from eight different factories, proportion of elongated particles. and it is a matter of interest to con This variety of microscopic spicules, sider whether counts from different particles, and frequently some cotton factories can be directly compared with fibers, found in the samples of dust col one another. Strictly they cannot, lected in the Owens apparatus, results since the content of smoke particles in a tendency to clumping on the cover varies in each group. The difficulty slip, making counting, especially of the might be obviated by counting only higher concentrations, a matter of the particles derived from asbestos. extreme difficulty. Occasionally, also, The method has been applied success part of the slot of the apparatus choked fully to counts of crystalline silica up with dust. The effect of the clump dusts; but it is not so easily applicable ing is to reduce the counts of all except to counts of asbestos dust, which con the low concentrations. tains numbers of black and brownish Furthermore, this apparatus is much iron containing particles, many of influenced by local air eddies and cur which are not quickly distinguishable rents. It takes a grab sample, which from smoke and tarry particles. is accurate enough as an indicator of To classify the processes accurately the local conditions at the moment of on the basis of amount of dust evolved, sampling, but does not give a picture it is necessary to take serial samples at of the average state of the atmosphere intervals corresponding to the details during a period of time, as does a and complexity of the processes. gravimetric apparatus. Moreover, With some straightforward processes, with high concentrations of dust, such as spinning, few samples will be accurate counting becomes impossible. necessary; but in others, such as mat The apparatus has, however, many tress making, mixing, grading and advantages, including those of con opening--especially with old-fashioned venience, quickness in operation, and plant--in which the evolution of dust direct examination of the nature of the rises and falls rapidly in a compara dust. By serial observations, too, tively short space of time, many more temporary and local large increases in observations are necessary throughout J. I. H. Juno, 1939 0850530 PULMONARY FIBROSIS IN ASBESTOS WORKERS 249 a shift, to determine the average con when asbestos tape weaving dry, and centration of dust. Repeated controls only once a day when weaving asbestos are also required. wet. Comparative data show that the Nextinorder comes mattress making, dustiest processes are opening (with without any precautions such as ex old-fashioned teasers), sieving (with haust ventilation, or damping floors, no local exhaust ventilation), and doth, and tables. Application of ex shoveling, or otherwise handling asbes haust ventilation and damping reduce tos fiber. The heaviest counts of all the count considerably, but it is be were found in this group, in filling sacks, lieved that the figures are too low, since by hand, with disintegrated fiber in a counts for some subsidiary processes settling chamber. The visual cloud of such as buttoning, sewing, and cutting dust was intense, and irritating enough out are not available. to provoke immediate coughing on the The figures for spinning, plaiting, part of the observer. The clumping of and braiding are believed to be rather the dust particles of the sample on the too high, owing to contamination of cover slip was very marked, with the dust from neighboring and more dusty result that the total dust count arrived processes, and further investigation is at was undoubtedly too low. With required here. counts of asbestos particles of this A number of the samples taken with order, however, the precise count is of the Owens apparatus were examined little practical importance, since the to determine the size of the particles, dust concentration is far beyond the and the percentages of particles 2 safe limit. microns and under, and 7.5 microns Next in order is cloth weaving, dry and under, were ascertained. The 2- and without the application of local micron standard was retained for exhaust. This is undoubtedly a dusty purposes of comparison, and because process, and although local exhaust of its accepted importance in silicosiB. reduces the count at the breathing level The 7.5-micron figure was also adopted of the weaver, much dust still escapes because of the pronounced acicular into the workroom. Further counts are character of much of the asbestos dust, necessary to estimate this. Weaving and because, representing the diameter doth wet, not merely damp, reduces of the human red blood corpuscle, it the dust count to a remarkable degree. is a standard easily distinguishable, The figure for band (*.., narrow) and may conceivably represent the weaving, wet, is not accurate since it limit size of particles which can be con was raised by dust from a neighboring veniently engulfed by phagocytic cells, dry cloth loom; still the improvement which are somewhat larger. Among due to wet methods is noticeable. One twenty counts from various processes asbestos weaver, who was formerly a (Table 6), in two, between 60 and 70 cotton weaver, and who has to wear per cent, of the particles were of sizes glasses, stated that whereas he used to 2 microns and under; in two, 70 to clean his glasses about three times a 80 per cent.; in ten, 80 to 90 per cent.; day when cotton weaving, he has to and in Bix, 90 per cent, and upward. dean them about five times a day When the counts were analyzed ac- Vol. No. 8 S`'Q8o9o3 ! 250 THE JOURNAL OF INDUSTRIAL HYGIENE cording to the 7.5-micron standard, all twenty Bhowed 90 per cent, or more of the particles to be of this sise or less. With regard to the effect on the lungs of different varieties of asbestos, no evidence was found to indicate that any one of its varieties is more potent in producing fibrosis than the others, other factors, such as concentration of dust, being equal. There is now no doubt, however, that both chrysotile and crocidolite \rill produce fibrosis; while the third, the comparatively newly discovered amosite, resembles crocidolite so closely in its chemical constitution, and in the characteristics of the dust, that there can be no reasonable doubt, also, with respect to it. Length of Duel Exposure No case of diffuse fibrosis clearly due to asbestos was discovered with under 5 years' employment. Three cases were found with 3, 3J, and 4$ years' work, respectively, who showed clinical signs of fibrosis. Definite confirmatory radiologic evidence was obtained in the first, definite but slighter radiologic changes in the sec ond, and indefinite suggestive changes in the third. The previous occupation in the first case was flax weaving for 18 years; in the second, coal hewing for 16 years; and in the third, work in an iron foundry for 1 year. All these occupations are dusty; and in the last two there may be some exposure to free silica. Also increased silica con tent has been found in the lungs, after incineration, of flax dressers. For these reasons, these three cases could not be certainly ascribed to asbestos dust, although it was, probably, at least a contributory factor. Among the oases of fibrosis found, thirty-six had been employed in asbestos for periods ranging from 5 to 10 years; two of these cases, one employed for 9 years and the other for 7 years, show that a considerable degree of fibrosis may occur with less than 10 years' exposure. F. W. Simson (6) examined the lungs of a guinea-pig which had been experi mentally dusted by Mavrogordato for two hours a day on each of fifty days between February and April, 1925, and which died from other causes in December, 1927. He states that his tologic sections showed a slight gen eralised fibrosis. This observer also examined portions of the lungs of two . native asbestos mill workers; one had been employed for twelve months and had died from a miliary tuberculosis, and the other, employed for two years, had apparently never recovered from an attack of lobar pneumonia a year before death. In commenting on the amount of fibrosis found, he states that "a com parison between the human cases and the experimental animal showed that the fibrosis was more rapid and exten sive in the human cases than in the experimental animal," and, again, that "the amount of fibrosis in two of the human cases .... was quite definite, and, if due to the presence of asbestos dust, the initial rate of pro duction was rapid when compared with present-day non-infective silicosis on the Rand." Experiments by Professor Beattie, in 1912, demonstrated that the lungs of guinea-pigs exposed to asbestos dust for forty-three and sixty-seven hours showed "definite cellular, proliferation, though not very extensive, and this is j. I. H. June, 1930 ST0850532 PULMONARY FIBROSIS IN ASBESTOS WORKERS 251 certainly & preliminary stage in the contributory factor. In six of the production of fibrosis." eight cases the diagnosis was verified These pathologic and experimental by postmortem examination; in the findings suggest that the inhalation of other two cases, confirmatory radio- asbestos dust rapidly causes some graphic evidence was obtained. changes in the lungs. But no evidence Information has recently been ob was obtained that asbestos dust can tained in regard to three other cases, produce an acute type of fibrosis com in which death occurred in 1929. The parable to that formerly noted in details of one have been published by South Africa after repeated exposure Wood and Page (25). Postmortem to massive concentration of free silica, examinations have been made in all a few cases of which have occurred three cases, and in all, the presence of recently in Great Britain, causing pulmonary asbestosis, without tuber death in from two to four years. culosis, was verified. In one case, the The amount of disablement pro pulmonary fibrosis was the primary duced by the development of pulmo cause of death; in one, information as nary fibrosis in these workers is surpris to the extent of the fibrosis has not yet ingly slight for a number of years, even been obtained; and in the third case, a more so than is generally the case in lobar pneumonia was superimposed on silicosis. The nature of the work, the fibrosis. however, in the majority of the proc It is not suggested that these few esses does not involve much physical fatalities, in which the cause of death exertion--in fact, in this respect it is has been verified by strict inquiry, are ``light work." The affected person any criterion of the true effect of may, and often does, continue at work the disease on the mortality rates of --with occasional intermissions, lat asbestos workers. Others are known terly, due to exacerbations of bron to have occurred in which the exist chitis--until the condition is advanced, ence of the asbestos fibrosis has been although he suffers increasing incon determined in life, but no postmortem venience from shortness of breath on examination has been possible. the slightest exertion. Usually these cases cease work a year Difficulties in Diagnosis or more before death, but sometimes a Many factors have contributed to terminal bronchopneumonia, or other impede both the recognition of indi acute infection, commences while they vidual cases of this disease, and the are still at work, and there is no long establishment of asbestos dust as the period of invalidism. determining cause. These factore are Fatalities consequent, partly on the nature of the disease, partly on the nature of the Particulars of eight deaths have dust, and partly on the industry itself, been collected, and are summarized in its rapid growth and internal condi Table 7. In six of these, advanced tions. Difficulties in diagnosing the pulmonary fibrosis was the primary disease, its points of resemblance, in cause of death. In the remaining two its latest stages, to fibroid tuberculosis, ca^es, pulmonary tuberculosis was a and the liability of those affected to be Vol. 12 No. s --1Arrangement of dates follows the American custom * Estimated. month, day of month, year. ST0850533 252 THE JOURNAL OF INDUSTRIAL HYGIENE ST 0850534 PULMONARY FIBROSIS IN ASBESTOS WORKERS 253 carried off by some intercurrent dis ease--which alone is noted onthe death certificate--are all of importance. A concrete example encountered during the inquiry will illustrate one of these points. J. C., Case No. 7 in Table 7, was known by his own doctor and bythe Chief Tuberculosis Officer of the town to be affected with advanced fibrosis of the lungs. Four or five months before his death it was thought that a change of air would be of advantage to him. Through the gen erosity of the firm with which he had been employed, he was transferred from the town to a farm in the country, where he died. The death certificate, given locally, stated that pulmonary tuberculosis was the cause of death. In another case chronic bronchitis was given as the cause of death. In the less advanced stages of the disease, the symptoms are so unob trusive that the worker rarely consults his doctor. In the later stages, bron chitis, or the supervention of acute bronchopneumonia, pulmonary tuber culosis, or other acute infection, all so much'more common, masks the under lying fibrosis; and the terminal condi tion is noted as the cause of death. In the second place, the silicate dusts --of which asbestos dust is one--repre senting silica in the combined form as opposed to free silica, have naturally been overshadowed by the silica dusts, since they do not produce the picture of silicosis and have not been shown to be associated with an increased mor tality from pulmonary tuberculosis. Moreover, although the asbestos in dustry has very rapidly expanded, it is still comparatively small, and scattered over the country. A large proportion of the workers have been employed in asbestos only for comparatively short periods, and of the processes considered so far, the less dusty spinning group is at the same time the largest. Thus only now the existence of a health risk in the industry is beginning to be recognised. Does Asbestos Dust Predis pose to Other Pulmonary Diseases? The important question as to whether asbestos workers show an in creased liability to other diseases of the lungs, such as pneumonia, pleurisy, and pulmonary tuberculosis--espec ially the latter--requires further in vestigation. A history of pleurisy was given by ten workers, in eight since commencing work in asbestos; in addition, one worker had a slight pleural effusion at the time of examination, and one showed signs of old pleurisy, but no history was obtainable. Of the two with attacks prior to work in asbestos, one had normal lungs, and the other showed signs of a bronchiectasis. Of the eight giving histories of pleurisy, three showed signs of fibrosis, four showed signs of the old pleurisy only (one being due to a gunshot wound during the War), and the eighth Bhowed signs of an old inactive tuber culous lesion of the right upper lobe. A history of pneumonia was ob tained in sixteen workers--in ten prior to commencing work in asbestos, and in six since. Of these eix, two showed signs of a thickened pleura only, one showed merely enlarged lung roots, two had diffuse fibrosis, and in one the lungs were normal. Of the remaining ten, one had a thickened pleura, two bronchiectasis, two diffuse fibrosis, one VoL 1J No. a ST0850535 254 THE JOURNAL OF INDUSTRIAL HYGIENE commencing fibrosis, and in four the and are of no importance unless it is lungs were normal. shown that the inhalation of asbestos With regard to evidence of bron dust is associated with pulmonary chitis, and bronchial and pulmonary tuberculosis to an increased degree, catarrh, fifty-eight of the 363 workers when such cases, as indicating a group (16 per cent.) showed signs offone or of workers with a latent infection, other of these conditions, all being would assume a greater significance. quite mild. Of these, thirty-one also No close association is apparent, how showed signs of diffuse fibrosis, repre ever, since only thirty-seven, or 9.9 senting 32.6 per cent, of the fibrotic per cent, of the 374 examined, showed group, and eight were in the prefibrotic evidence of this disease, excluding cases stage (38.1 per cent, of that group). of old inactive hilar tuberculosis, even The fact that the clinical examinations when those showing the minor changes were conducted during the warmer mentioned above are included. In months of the year, no doubt operated only four was there a family history of to reduce the incidence of these com pulmonary tuberculosis; and three out plaints. Under the circumstances, the of four active cases belonged to this preponderance among the cases of group. Thirty-three cases were inac fibrosis is the more noteworthy, as in tive, of which twenty-one presented no dicating persistent irritation resulting evidence of dust fibrosis, and twelve from the dust. . presented evidence. Of other diseases, eight gave his Out of the 374 persons examined, tories of rheumatic fever, and of these, fourteen, or 3.7 per cent., gave a two had definite valvular disease of the family history of tuberculosis. Evi heart. In addition, valvular disease of dence of active pulmonary tubercu the heart was noted in one worker, but losis was present in three; in two of no history of rheumatic fever was ob these three the source of infection tained. appears to have been a near relative. With regard to pulmonary tubercu Thus, no outstanding susceptibility losis, so definitely an added risk in sili to pulmonary tuberculosis was dis cosis, this disease group has been closed, either among asbestos workers drawn up to include all workers pre as a class, or among those with fibrosis, senting signs indicating a past or pres considering the frequency of old healed ent pulmonary tuberculous infection, apical lesions among the general but excluding cases of old inactive hilar population. tuberculosis. Under this heading are We have, however, by no means dis included not only workers with definite posed of the question. The superven clinical signs of active tuberculous tion of a tuberculous infection on a lung infections, or of old inactive lung already the subject of fibrosis pro lesions, equally definite, but also those duces an increase in symptoms, pre workers showing signs of old apical col viously unnoticed or disregarded, and lapse, usually attributed to a past causes the worker to seek his doctor's, tuberculous infection. advice. He is then appropriately Signs of the latter are not uncom advised to give up his dusty employ monly found in quite healthy persons, ment, migrates from the industry, and j. I. H. June. 1M0 38 it is sbestos ronary degree, group action, ic&nce. , howor 9.9 howed ^ cases ., even langes i. In ory of out ) this inaoed no welve ST 0850536 PULMONARY FIBROSIS IN ASBESTOS WORKERS 255 may or may not accept sanatorium produce a serious and even fatal degree treatment. Thus there tends to be a of pulmonary fibrosis. drift of such cases from the fibrosis 2. The type of fibrosis produced, producing industry. however, exhibits a number of diverg During the course of the inquiry, ences from that caused by the inhala information was obtained of a number tion of free Bilica dust, and the outcome of persons, previously employed in of these variations is not yet apparent. asbestos, who were either at home or in 3. The divergences noted so far are sanatoriumB, suffering from chest com exhibited in the radiologic picture, plaints. Where an examination of and on postmortem examination of workers is confined to those at work, a the affected lungs, both in the gross certain number of advanced cases of morbid anatomy and in microscopic fibrosis, and a certain number of cases sections. of pulmonary tuberculosis, with or 4. In the latter case the appearances without an asbestos fibrosis, in persons of the asbestos fibrosis seem to be who have either given up work, or who sufficiently distinctive not to permit are off work temporarily, will be of confusion between it and silicosis. missed. 5. The radiologic appearances of the It is necessary, therefore, to leave asbestos type jf fibrosis, even in the this question of increased susceptibility more developed stage, are more deli to pulmonary tuberculosis in abeyance, cate, softer, and more diffuse than the pending further investigation. silicotic fibrosis. . With respect to any increased suscep 6. It follows, therefore, that an tibilitytothe supervention ofotherlung opinion as to the degree and intensity diseases in workers with an asbestos of an asbestos fibrosis, based on a com fibrosis, the data obtained were insuffi parison of the radiologic changes with cient to lead to any conclusion, except those shown in standard silicosis filmB, as to bronchial catarrh. There are in will be an underestimate. dications, however, that when pneu 7. In the absence of a full medical monia or bronchopneumonia super and industrial history, possibilities of venes qn a fibrotic lung, the prognosis confusion of the two types of fibroBis is grave. will arise in the interpretation of radio grams. Abbestosis and Srucosis Contrasted 8. There is evidence that other in In view of the relationship between organic dusts, containing no free silica, the asbestos fibrosis and silicosis, since may be productive of this fine type of they are both varieties of fibrosis of fibrosis in varying degree. the lungs caused by the inhalation of dusts, it seems desirable to summarize Summary shortly the main points of similarity 1. There is a definite risk of the and dissimilarity between the two dis development of a diffuse pulmonary eases, so far as has been ascertained. fibrosis in persons exposed to the in 1. Inhalation of asbestos dust, under halation of asbestos dust. favorable conditions of concentration 2. This risk varies directly as the of dust and length of exposure, will length of employment (and hence Vol. 13 . No. S T 08 50537 256 THE JOURNAL OF INDUSTRIAL HYGIENE length of exposure to dust), and is tion of pulmonary tuberculosis asso unaffected by the age of the worker. ciated with the development of the 3. There is a considerable difference asbestos fibrosis. between the least dusty and the most dusty processes investigated, and there is a corresponding variation in the rela tive risk of the development of fibrosis in the workers in these processes. Much generous assistance has been re ceived from many sources during the course of this inquiry, and for this acknowledgment is gratefully tendered. In addition to those already referred to, 4. With continued exposure to high the writer is beholden especially to Dr. S. A. concentrations of dust, the disease may be fully developed in seven to nine years, and may cause death after about thirteen years' exposure, exceptionally in a shorter period. Henry, who did much to facilitate the inves tigation, particularly by his detailed reports on various relevant matters, and by much organization and liaison work; to many others of his colleagues in the different dis tricts, to a number of directors and officials 5. Fibrosis as it occurs in asbestos workers differs considerably from the disease as it occurs in workers exposed to free crystalline silica dust; it differs in tne radiologic picture, and also of various firms, foremen, and employees; to Dr. W. E. Cooke of Wigan and Professor M. J. Stewart of Leeds for pathologic mate rial and for much information as to the progress and results of their own researches into the gross anatomic and the histologio on postmortem examination of the features of the asbestos fibrosis, and the affected lungs. 6. The more dusty processes are constitution and location of the curious bodies; to Dr. MacGregor, Medical Officer of Health for Glasgow, for various clinical those involving the preparation and and radiologic facilities, and for his ever ill manipulation of the raw asbestos present readiness to lend the aid of his (other than crushing), dry cloth weav ing, and mattress making. 7. The less dusty processes are spin ning and similar processes, and proc esses, other than dry weaving, in Department, and especially to Dr. H. E. Seiler of his staff; to Dr. J. C. Robertson for the loan of a radiogram, together with detailed clinical notes df one patient and other valuable information; to Dr. W. H. Bateman for the loan of a radiogram, for volving the manipulation of the spun yam. 8. Further investigation is required to determine whether there is any in creased susceptibility to the superven some clinical histories, for obtaining and examining several specimens of sputum, and for other aid; and to Dr. J. Rennie, Chief Tuberculosis Officer at Sheffield, for a series of radiograms showing various stages of silicosis. BIBLIOGRAPHY 1. Departmental Committee on Compen sation for Industrial Diseases. Min utes of Evidence, Appendices and In dex, 1907. Cd. 3496, p. 127; Report, 1907. Cd. 3495, p. 14. 2. Coou, W. E.: Fibrosis of the Lungs Due to the Inhalation of Asbestos Dust. Brit. Med. Jour., 1924, l, 147. 3. Cooke, W. E.: Pulmonary Asbestosis. Ibid., 1927, t, 1024. 4. McDonald, S.: Histology of Pulmo nary Asbestosis. Ibid., p. 1025. 5. Seiler, H. E.: A Case of Pneumoconio sis. Result of the Inhalation of Asbestos Dust. Ibid., 1928, S, 982. 6. Simbon, F. W.: Pulmonary Asbestosis in South Africa. Ibid., 1928, 1, 685. 7. Royal Commission on Metalliferous Mines and Quarries. Second Report, 1914. Cd. 7478, p. 148. J. I. H. Jus*. MU MSO- the 10- ST0850538 PULMONARY FIBROSIS IN ASBESTOS WORKERS 257 .. 8. Badham, C.: Notea on & Fine Type of 21 Stiwart, M. J., and Haddow, A. C.: Fibroua Pneumonokonioais Produced Demonstration of the Peculiar Bodies by Silicates and Other Minerals. of Pulmonary Asbestosis ("Asbestosis Studies in Indust. Hyg. No. 13, Rep. Bodies") in Material Obtained by Dir.-Gen. Pub. Health, New South Lung Puncture and in the Sputum. Wales, for 1027, Section I.-E, Indust. Jour. Path, and Bact., 1929, St, 172. Hyg., p. 102. 8ydney, 1929. .22 Macxlin, E. L., and Middleton, E. L.: 9. Clam, W. I.: The Dust Hazard in the Report on the Grinding of Metals and Abrasive Industry: Second Study. Cleaning of Castings with Special Thjb Joint., 1929, 11, 92. 10. Pancoast, H. K., and Pendergrass, E. Reference to the Effects of Dust In halation upon the Workers. London, P.: Pneumoconiosis (Silicosis). A H. M. Stationery Office, 1923. Roentgenological 8tudy. New York, Paul B. Hoeber, Inc., 1926, p. 155. 11. Thompson, L. R., Bbundaox, D. K., Rossill, A. E., and Bloompiild, J. J.: The Health of Workers in Dusty Trades. I. Health of Workers in a Portland Cement Plant. U. S. Pub. Health Bull. No. 176, 1928. 12. Goadbt, K. W.: Fibrosis of the Lung in Iron Miners. Jour. Roy. Micr. Soc., 1925, p. 432. 13. Annual Report of the Chief Inspector of Factories and Workshops for 1928, p. 94. London, H. M. Stationery Office, 23. Sutherland, C. L., and Brtson, S.: Report on the Inoidenoe of Silicosis in the Pottery Industry. London, H. M. Stationery Office, 1926. 24. Sutherland, C. L., and Bryson, S.: Report on the Occurrence of Silicosis among Sandstone Workers. London, H. M. Stationery Office, 1929. 25. Wood, W. B., and Paoe, D. S.: A C\se of Pulmonary Asbestosis. Tubercle, 1929,10, 457. For the geologic and the manufacturing and industrial aspects of asbestos, tee: 1929. 26. Cibzxl, F.: Chrysotile-Asbestos, its 14. Penny, F. W.: In "Industrial and Occurrence, Exploitation, Milling, Manufacturing Chemistry" by G. and Uses. Seoond edition. Ottawa, Martin. 1917, Part 2, p. 281. Govt. Printing Bureau, 1910. 15. Compiled by Asbestos, a monthly trade journal published in Philadelphia, Pa. 16. Annual Statement of the Trade of the United Kingdom, for 1922 and 1927. London, H. M. Stationery Office. 17. Departmental Committee on Compen sation for Silicosis dealing with the Refractories Industries (Silicosis) Scheme 1919. First Report, 1924, p. 29. 18. Smith, A. R.: Silicosis among Rock Drillers, Blasters, and Excavators in New York City. This Jour., 1929, 11, 39. 27. Asbestos, its Sources, Extraction, Prep aration, Manufacture and Uses in Industry and Engineering. Berlin, Becker and Haag, 1928. 28 Thorpe, E.: A Dictionary of Applied Chemistry. London, Longmans, Green <fc Co., 1912. 29. Atbetios, a monthly trade journal pub lished in Philadelphia, Pa. For description of processes, and further discussion on the incidence rate of fibrosis, and effect of work in different processes and also preventive measures, see: 19. Wood, W. B.: Pulmonary Asbestosis. 30. Merewether, E. R. A., and Price, C. Tubercle, 1929, 10, 353. W.: Report on Effects of Asbestos 20. Gloynz, S. R.: The Presence of the Dust on the Lungs and Dust Suppres Asbestos Fibre in the Lesions of sion in the Asbestos Industry. Lon Asbestos Workers. Ibid., p. 404. don, H. M. Stationery Office, 1930. Vol. u No. i ST 0850539 SUBJECT INDEX TO VOLUME XII Thu is a subject index to all the reading matter in the Joubnal or Industrial Htanmi, and one should, therefore, look for the subject word, with the following exception: "Book Notioes" are indexed under this title on page 402. The name of the author follows the subjeot entry in parenthesis. For author index, see page 403. rsos Accidents. personal qualities in causa tion of (Chambers)......................... 223 Aib conditions, rational expression for wet kata cooling power (Weeks)... 148 conditions, total heat difference as measure of wet kata oooling (Weeks).............................................. 233 Anodic Oxidation................................. 314 Abmit, H. W., obituary........................ 122 Asbbstos workers, pulmonary fibrosis and other pulmonary affections in (Merewether)........................... 198, 239 Atmosfhxbx, see Air. Automobile exhaust gas, see Gas, auto mobile exhaust. Blood cells, red, effect of chemically pure carbon monoxide, illuminating gas, and automobile exhaust gas on fragility of (Mayers, Rivkin, and Krasnow)............................................300 pressure, nigh, arterial, in industry (Wychgel)........................................ 319 Bbain, nistopathology of electric shock on (Morrison, Weeks, and Cobb)........................................ 324, 364 TA.QM Dust inhalation and iron ore mining (Collis and Goadby)........................ 286 silica, hazard, in granite cutting in dustry (Thompson and Britten)___ 123 trap (Elay)......................................... ; 28 EmcrxNCT, quantitative measurement of, under factory conditions (Lovelrin)................................. 99, 153 Electbic shock, histopathology of, on brain (Morrison, Weeks, and Cobb)........................................ 324, 864 shock, interpretation of field notes (Maclachlan)......................................291 Elxctbicitt, abnormalities produced by (Langworthy and Kouwen- horen).............................................. 31 Ethtlenx Cblobhtdbin poisoning, fatal case of (Middleton)................ 265 Eras, effects of lead on vision .(Pedley)........................................... 859 miners' nystagmus and incapacity for work (Thomas)................................ 1 subhyaloid hemorrhage in lead poi soning (Pedley)................ 359 Canceb, occupational (Heller)........... 169 Cabbon Dioxide, 5 and 10 per cent, mixtures as respiratory stimulants in carbon monoxide poisoning (Murphy and Drinker)................... 92 Cabbon Monoxide, chemically pure. ' - effect of, on fragility of red blood cells (Mayers, Rivkin) and Krasnow)......................................... 300 ' poisoning, 6 and 10 per cent, carbon dioxide mixtures as respiratory stimulants in (Murphy and Drinker)............................................. 92 Chbome plating and anodic oxidation. 314 Chbomium, contamination of food cooked or stored in contact with ' nickel-chromium-iron alloys (Ti tus, Elkins, linn, Fairhall, and Drinker).............................................. 300 Ctanidb rash, so-called, in gold mine mill workers (Braddock and Tingle).............................................. 259 FooD cooked or stored in contact with nickel-chromium-iron alloys, con tamination of (Titus, Elkins, Finn, Fairhall, and Drinker)................... 306 Gas, automobile exhaust, effect of, on fragility of red'blood cells (Mayers, Rivkin, and Krasnow)......... ......... 300 illuminating, effect of, on fragility of red blood cells (Mayers, Rivkin, and Krasnow)................................... 300 Gold mine mill workers, so-called cyanide rash in (Braddock and Tingle)............................................. 259^ Granite cutting industry, silica duBt hazard in (Thompson and Britten). 123 cutting tools, dust control systems for (Hatch, Drinker, and Choate)...... 75 Hkatino, new methods of (Vernon).:. 281 Hemobrhaqb, subhyaloid, in lead poi soning (Pedley)............................... 359 Hypxbtenbion, see Blood pressure, high. bt coefficient, apparatus for deter mination of (Burstein)..................... control systems for granite cutting T tools (Hatch, Drinker, and Choate).............................................. *$ V 24 Illness, see Sickness. Intbbnational Medioal Congress for Industrial Accidents and Occupa 75 tional Diseases, sixth..................... 318 401 ST 0850541 AUTHOR INDEX TO VOLUME XII FAOB Angus, T. C., Hill. L., and Soper, H. E.: A New Kata-Thermometer for Hot Atmospheres and a Simplified Method for Computing....................... CO Braddock, W. Hand Tingle, O. R.: So-Called Cyanide Rash in Gold Mine Mill Workers...........................................269 V; Britten, R. H., tee Thompson, L. R. Brundage, D. K.: The Incidence of Illness among Wage Earning , Adults.......................................... 338.381 Burstein, A. I.: An Improved Form of Y Burstein Apparatus for Determina1 tion of the Dust Coefficient of the Air........................................................... 24 Chambers, E. G.: Personal Qualities in Accident Causation............................. 223 Choate, S. P.. tee Hatch, T. Cobb, 8., tee Morrison, L. R. ,'Collis, E. L., and Goadby, K. W.: Dust Inhalation and Iron Ore Mining....... 266 Maclachlan, W.: Electric - Shock: Interpretation of Field Notes............291 Mayers, M. R., Rivldn, H., and Krasnow, F.: The Effect of Chemically Pure Carbon Monoxide, Illuminating Gas, and Automobile Exhaust Gas upon the Fragility of the Red Blood Cells....................................................... 300 Merewether, E. R. A.: The Occurrence of Pulmonary Fibrosis and Other Pulmonary Affections in Asbestos Workers......................................... 198, 239 Middleton, E. L.: Fatal Case of Poison ing by Ethylene Chlorhydrin............ 266 Morrison, L. R., Weeks, A., and Cobb, S.: Hiatopathology of Different Types of Electric Shock on Mam malian Brains............................... 324, 364 Murphy. D. P., and Drinker, C. K.: The Comparative Action of 6 and 10 Per Cent. Carbon Dioxide Mixtures as Respiratory Stimulants in Carbon Monoxide Poisoning............................. 92 Drinker, C. K., tee Murphy, D. P. linker, C. K., tee Titus, A. C. ker, P., tee Hatch, T. s, H. B., tee Titus, A. C. rhall, L. T., tee Titus, A. C. H. G., tee Titus, A. C. Pedley, F. G.: The Meets of Lead on the Vision: A Case of Subhyaloid Hemorrhage........................................... 369 Rivkin, H., see Mayers, M. R. Soper, H. E., see Angus, T. C. iby, K. W., see Collis, E. L. atoh, T., Drinker. P.( and Choate. _! B. P.: Control of tne 8ilicosis Hazara 'in the Hard Rock Industries. I. A ^"Laboratory Study of the Design of Dust Control Systems for Use with ' Pneumatic Granite Cutting Tools___ 76 av, P. 8.: Modified Design of Hay Dust Trap............................................. 28 fernan, P.: The Infectivity of Silicotic Tuberculosis............................... 236 ier, I.: Occupational Cancers......... 169 i L, tee Angus, T. C. enhoven, W. B., see Langworthy, O. R. ow, F., tee Mayers, M. R. Thomas, J. W. T.: Miners' Nystagmus and Incapacity for Work: A Clinical Study Based on an Analysis of 512 Cases................................ _.................... 1 Thompson, L. R., and Britten, R. H.: The Silica Dust Hazard in the Granite Cutting Industry.................................. 123 Tingle, G. R., see Braddock, W. H. Titus, A. C.L Elkina, H. B., Finn, H. G., Fairhall. L. T., and Drinker, C. K.: Contamination of Food Cooked or Stored in Contact with NickelChromium-Iron Alloys........................ 306 Vernon, H. M.: Some New Methods of Heating Buildings............................... 281 orthy, 0. R., and Kouwenhoven. B.: An _ Experimental Study of ^normalities Produced in the Orby Electricity.......................... 31 O. S.: The Quantitative aasurement of Human Efficiency der Factory Conditions.......... 99, 153 Weeks, A., see Morrison, L. R. Weeks, W. S.: A Rational Expression for Wet Kata Cooling Power............. 148 Weeks, W. S.: Total Heat Difference as a Measure of Wet Kata Cooling....... 233 Wychgel, J. N.: Arterial Hypertension m Industry............................................ 319 *( 403 f.-.