Document rem5MN6QZbxE4K9yB9DdX0jwE

ST085I5I2 THE JOURNAL OF PLAINTIFF'S EXHIBIT INDUSTRIAL HYGIENE AND TOXICOLOGY VOLUME 23 JANUARY, 1941--DECEMBER, 1941 PUBLISHED BY THE WILLIAMS & WILKINS COMPANY Baltimore, Md. ! ) ST085I5I3 CONTENTS OF VOLUME 13 JANUARY, 1941. NUMBER 1 Sou Facts and Reflections on the Problem or Poisoning bt Benzene and its Homologs. Emil Schwars and L. Teleky................................................................... 1-- Absorption, Distribution and Elimination or Benzene bt Bodt Tissues and Fluids or Dogs Exposed to Benzene Vapobs. H. H. Schrenk, W. P. Yant, S. J. Pearce, F. A. Patty and R. ft. Sayers.......................................................................... 20 The Control or Tuberculosis. III. Management or the Employe with Tubercu losis. Ada Chree Reid................................................................................................. 35 Acute Silicosis. Wm. D. McNally................................................................................... 45 Request ro* Information................................................................................................. 50 J Book Reviews...................................................................................................................... 52 ; FEBRUARY, 1941. NUMBER 2 The Pathology or Shielded Arc Welding. E. von Haam and J. J. Groom................ 55 Acute Oral Toxicity or Acetic, Chloracetic, Dichloracetic and Trichloracetic i Acids. Geoffrey Woodard, Stanley W. Lange, Kenneth W. Nelson and Herbert 0. ' Caloery............................................................................................................................. 78 -- * Measurement or Fusion Frequency or Fucker as a Test for Fatigue or the Central Nervous System. Observations on Laboratory Technicians and Office Workers. Ernst Simonson and Norbert Emer............................................. 83 , Book Reviews...................................................................................................................... 90 MARCH, 1941. NUMBER 3 Studies or Workers Exposed during the Production or Lead-Bearing Steel (Ledloy). A.G. Kammer............................................................................................ 93 Atmospheric Concentration or Lead Fume Associated with Forging, Welding, and Oxygen Cutting or Lead-Bearing Steel, based on Experimental Studies. James W. Halley............................................................................................................ 100 Effect or Short Rest Pauses in Standing and Sitting Position on the Efficiency or Muscular Work. Ernst Simonson and Norbert Emer........................................ 106 Carbon Tetrachloride as an Industrial Hazard. Report or Two Cases. Ernest M. Hammes, Jr............................................................................................................... 112 Severe Pneumoconiosis Caused by the Inhalation or Fuller's Earth. Wm. D. McNally and I. S. TrosUer............................................................................................ 118 BookReviewb...................................................................................................................... 127 APRIL, 1941. NUMBER 4 The Toxicology or Oxides or Nitrogen. I. Toxic Concentrations. Leroy W. La Totosky, E. L. MacQuiddy and J. Perry Tollman.................................................. 129 II. Physiological Effects and Symptomatology. E. L. MacQuiddy, Leroy W. La Totosky, J. Perry Tollman and Alisler I. Finlayson.................................................. 134 III. Gross and Histological Pathology. J. Perry Tollman, Ler-ry W. La Totosky, E. L. MacQuiddy and Stanley Schonberger................................................................... 141 A Modified Eyepiece Micrometer tor Use in Dust Counting. William B. Harris. 148 A Quantitative Microchemical-Colorimetric Determination or Carbon Di- bulfide in Air, Water and Biological Fluids. Ralph W. McKee....................... 151 iii iv JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY Note on ``Studies of the Lead Hazards in Certain Phases of Printing." Robert A.KeKoe......................................................................................................................... 160 Reply to Dr. Kehoe's Criticism. Elston L. Belknap................................................. 161 MAY, 1941. NUMBER 5 X-rat Diffraction--an Important Tool in Pneumoconiosis Research and a New Method of Tissue Analysis. Louis H. Berkelkamer.................................... 163 Silicosis in Soft Coal Miners. B. G. Clarke and C. E. Moffet.................................... 176 Fundamental Factors in the Design of Lateral Exhaust Hoods for Industrial Tanks. Leslie Silverman.............................................................................................. 187 An Automatic Carbon Disulfide Recorder. Ben E. White and W. R. Calvert......... 196 Chemical and Physiological Investigation of Electric Arc Welding. III. Coated Welding Rods. Carey P. McCord, Gordon C. Harrold and Stuart F. Meek. 200 JUNE, 1941. NUMBER 6 Recovery Following Exposure to Benzene (Benzol). Leonard J. Goldwater and Margaret H. Tewksbury................................................................................................. 217 Effects of the Inhalation of Benzene Vapor on the Red Blood Cells of Rabbits. Ellis J. Robinson and David R. Climenko.................................................................... 232 'Acute and Chronic Intoxications with Sodium Pentachlorophenate in Rabbits. T. H. MeGavack, L. J. Boyd, F. V. Piccione and R. Terranova................................... 239 A Portable Sampling Unit. Leslie Silverman and T. R. Thomas................................. 262 .Evaluation of the Lead Hazard: Urinary vs. Atmospheric Lead. Hervey B Elkins, John F. Ege, Jr., and Benjamin P. Ruotolo.................................................... 266 --The Single Dose Toxicity of Some Glycols and Derivatives. Henry F. Smyth, Jr., Jane Seaton and Louise Fischer................................................................................... 259 . .Inhalation of Filtered Carbon Arc Fumes and of Oxides of Nitrogen. J P Tollman, E. L. MacQuiddy and Stanley Schonberger.................................................. 269 SEPTEMBER, 1941. NUMBER 7 Observations on the Effect or Paint on the Kidneys with Particular Reference to the R6le or Turpentine. Earle M. Chapman.................................................. 277 The Etiology op Acne with Special Reference to Acne of Occupational Origin. A. Thelwell Jones............................................................................................................290 Renal Excretion of Industrial Chemicals. I. Urinary-Lead Concentration and Blood-Lead Clearance. Sherman S. Pinto, Hervey B. Elkins and John F. Ege, Jr............................................................................................................................ 313 .Ventilation in Arc Welding with Coated Electrodes. Bernard D Tebbens and Philip Drinker............................................................................................................... 322 ''"'Toxicity of Methyl, Ethyl andn-Butyl Methacrylate. Wilhelm Deichmann-- 343 OCTOBER, 1941. NUMBER 8 The Compensation of Occupational Diseases. L. Teleky......................................... 353 Industrial Manganese Poisonino. Robert H. Flinn, Paul A. Neal and William B. Fulton............................................................................................................................ 374 The Effects of CarbonDisulfide onthe Blood Corpuscles. H.Brieger................ 388 The Dropping Mercury Electrode for Lead Analysis. E. C. Barnes and H. W. Speicher......................................................................................................................... 397 The Chemical Changes of Methyl Bromide in the Animal Body in Relation to its Physiological Effects. D. D. Irish, E. M. Adams, H. C. Spencer and V. K. Rowe.................................................................................................................................408 Book Reviews........................................................................................................................412 i t i ii i< # * ST085I5I4 , , r 1 ' ', > l > 5 9 9 7 '0 3 12 3 >3 '4 !8 17 18 2 U.s 1 l-..\ I > V NOVEMBER, 1941. NUMBER 9 Experimental Chronic Cabbon Disulfide Poisoning in Dogs. A Clinical, Bio chemical and Pathological Studt. F. H. Lewey, B. J. Alpers, S. BeUet, D. L. Drabkin, W. E. Ehrieh, J. H. Frank, A. J. Creskoff, L. Joruu, R. McDonald, E. Montgomery and J. G. Reinhold.................................................................................. 415 A Studt of Hazards Involved in Sprat Painting with Gasoline as a Diluent. Jamet H. Sterner.......................................................................................................... 437 Investigations on the Possible Carcinogenic Effect of Anthracene and ChrTsene and Some of Their Compounds. II. The Effect of Subcutaneous Injec tion in Rats. Joseph A. Pollia.................................................................................449 A Micboprojection Screen. Charles R. Williams and Leslie Silverman...................... 462 Book Reviews.................................................................................................................... 454 DECEMBER, 1941. NUMBER 10 The Significance of Urinabt Mebcurt. I. Occupational Mercurt Exposure. II. Mercurt Absorption from Mercubt-Bearing Dental Fillings and Anti septics. Emani D. Storlass^ and Hervey B. Elkina................................................ 459 Phentl Mercuric Oleate. Ski* Irritant Properties. Carey P. McCord, Stuart F. Meek and Thomas A. Neal........................................................................................... 468 Toxicologt of 8elenium. VI. Effects of Subacute Exposure to Htdbooen Selenide. H. C. Dudley and John W. Miller................................................................. 470 Some Pharmacological Properties of the "Teboitol" Penetrants. Henry F. Smyth, Jr., Jane Seaton and Louise Fischer................................................................ 478 .Solubilitt of Carbon Disulfide Vapor in Bodt Fluids and Tissues. Ralph W McKee............................................................................................................................ 484 Book Reviews..................................................................................................................... 490 Index to Volume 23........................................................................................................... 493 ST085I 5 15 ST08515 I 6 N 1931 Alice Hamilton published have elapsed since Alice Hamilton's I a review of the literature on indus trial benzene poisoning up to De review. The classical picture of chronic ben cember 1930, and laid special emphasiszene intoxication as seen in industry on the deviations from the classical has been drawn by Santesson, Selling, picture of this form of intoxication and a host of observers and experi which were revealed in a number of the menters. Briefly stated it consists in published cases. She concluded: "If a loss of red blood corpuscles, resulting it is true that wide variations are found in profound anemia; a loss of the ele in the pathology of diseases of the ments and substances in the blood blood, which have been the subject of which are concerned in blood clotting, extensive study, it seems that one is resulting in hemorrhage; and a loss of justified in believing that further study white blood cells (especially the neutro- of chronic benzene poisoning will re philes) and of the substances in the veal a less one-sided picture than is at blood serum which are concerned in present accepted. The simple unvary defending the body against bacterial ing picture of this form of poisoning infection. On the basis of this descrip as it is found in the textbooks is cer tion a standard has been formed for tainly based on insufficient human the diagnosis of benzene poisoning in material." industry and practical rules for its pre It has seemed to us worthwhile to carry on this study of the atypical forms of benzene intoxication, covering the publications of the 10 years which vention have been laid down. Thus the well known "Final Report of the Committee of the National Safety Council on Benzol," May 1926, formu lates these rules: "Any worker who on Received for publication July 27, 1940. examination shows any of the following l 2 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY M. S3, no. 1 symptoms should be promptly ex cluded from benzene exposure.... (a) Hemorrhages. . . . (b) Decrease of more than the fol lowing amount from the em ployee's normal blood picture (normal conditions will be ob tained from previous examina tions of the individual em ployee). (1) White cells, decrease of 25%; but in no case should an employee with a white cell count of less than 5,000 be continued in benzene processes. (2) Red cells, decrease of 25%. (3) Hemoglobin below 70%. (Note: Reduction in white cells is the most important condition to be noted.)" These rules have been followed by many factories and physicians and they have proved to be very useful, as we know not only from publications but also from our own practical ex perience. The object of this study is to deter mine how far such diagnostic signs may be regarded as valid and sufficient. I. HEMATOLOGICAL CONSIDERATIONS Emil Schwarz The picture given by A. Hamilton (1931) does not need any completion. Her prophecy as to the result of fur ther studies in the field of hematology as a whole and especially of chronic benzene poisoning has been confirmed. Yet the belief that anemia from ben zene is an aplastic anemia with a cor responding blood picture still domi nates medical practice and deviation from this type is still regarded as out side the picture. The division of cases of chronic ben zene poisoning into typical and atypi cal classes is based on the preponderant majority of cases and not on the actual morbid process engendered by the poi son. Neither is our task accomplished by ranging the different appearances in the usual groups of blood pathology. One must trace the phenomena back to the primary processes which must be connected with the uniform cause. This fundamental problem is not re stricted to hematology. It touches pathology as a whole and even indus trial hygiene. The insight we may gain from this analysis will not only revise our estimation of the usual ben zene prophylaxis but perhaps raise a doubt in our assumption of the unity of the damaging agent. Increasing experience and new methods of investi gation are continually modifying our views in the field of hematology and tending to simplify them. The tend ency now is away from a strict classi fication of blood diseases on the basis of the particular blood element in volved (Ehrlich's aplastic anemia, Schultz' agranulocytosis, Frank's aleucia and panmyelophthisis, the symp tomatic leucopenias, the thrombopenic purpuras) toward a realization that regenerative activity sets to work in all these cases with greater or less success, and the resulting picture depends on the ratio of regenerative activity to the destructive effect of the injurious agent. The aplastic anemia of chronic ben zene poisoning has been established Jan. im ST085I 5 I 8 POISONING BY BENZENE AND ITS HOMOLOGS 3 again and again but the four signs of and accentuation of which may give aplasia, reduction of erythrocytes and the blood picture of myeloid reaction, leucocytes, a subnormal absolute count are consequences of an excess of regen of lymphocytes in more severe leuco- erative activity. Exaggerated im penia, and the absence of juvenile ele maturity with or without a raised ments in the blood are not represented leucocyte count turns the blood picture at the same time and to the same into that of leucemic or aleucemic degree. Variations, even in otherwise myelosis and myeloblastosis, and ben typical cases, were noted in the earliest zene anemia has afforded instances studies of benzene poisoning. A rela even of this reversion of aplasia into tive neutrophilia, instead of lympho its opposite. The problem of the rela cytosis, the appearance of more or less tion of increased functional regenera immature leucocytes, or of a rare nor tion to leucemic proliferation lies be moblast, a high color index, an increase yond the limits of this essay. of reticulocytes or a polychromato- Our enlarged and deepened experi philia, all point to regenerative ac ence permits full application of the tivity. All these seeming exceptions principles developed above for aplastic compel to the conclusion: The blood in anemia in general to the special ques typical cases of benzene poisoning is by tions of benzene poisoning. All the no means devoid of regenerative signs. varieties of hematologic appearance, Regenerative activity is not abolished all the fluctuations in its course are but combats constantly with more or to be explained by the conflict between less apparent effect the destructive the destructive action of the poison influence of the poison. and the compensating activities of the Deviations of a higher order are seen organism. There is no greater stimu in erythropoiesis, a temporary poly lus for regeneration than the products globulia, a marked macrocytosis or of decaying cells of the same kind. megalocytosis, more numerous normo Continuous destruction therefore auto blasts, the occurrence of megaloblasts. matically raises proliferation and the Sometimes the picture of benzene ane increasing stimulus spreads beyond the mia approaches that of pernicious ane normal level of cell division, i.e., the mia, an extreme degree of blood forma myelocytes and the normoblasts, to the tion in response to the incessant call more primary stages, the myeloblasts for reproduction. In our opinion even and erythroblasts till it reaches the the maintenance of a normal count of mother-soil of all blood cells, the red cells in the presence of other signs reticulum. Either the stocks of new- of damage in the blood is better ex formed cells are time and again de plained by a stimulated compensating stroyed, in which case the result will regeneration than by an uninjured be a hypo- or aplastic bone marrow, erythropoiesis. The aberrations in or regeneration surpasses destruction leucopoiesis run in identical tracks. A and the result is a gradual transforma count of normal or higher level in ben tion of aplastic into hyperplastic bone zene anemia, an increased frequency of marrow. The heterotopic metaplastic less differentiated elements, a higher blood formation, especially in the degree of immaturity, the combination spleen clearly illustrates the intensity ST0851 5 I 9 4 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY M. S3, no. 1 and the spread of the stimulus. A thrombocyto-genesis and the early ap more complicated question, outside the pearance of hemorrhage makes it prob range of this study, is whether inten able that thrombopenia is the earliest sity and spread of the stimulus and precocious change, but technical diffi accelerated cell division furnish a suffi culties of thrombocyte counting and cient explanation for the findings in the wide differences in the accepted benzene poisoning, or if beyond that a normal limits (300,000-750,000) make checking of the capacity to maturation this sign ill-adapted for general use. must be admitted. The outbreak of In this regard the count of red and the disease a long time after cessation white cells has many advantages. The of exposure suggests a deeper and more limits adopted as critical anemia (see lasting shift in the biological disposi above) and leucopenia lie so far below tion of the cells. The transformation the normal standard that this sign suf into acute myelosis and, much more, fices to reveal a morbid state. How the occurrence of chronic myeloid or ever, according to our concept of the lymphatic leucemia in consequence of processes in benzene anemia it is im benzene exposme, support such a sug possible to be sure that all the indi gestion at least for some cases. Any viduals with a normal count are really how, this experience is an important unaffected by their exposure to ben contribution to any future theory of zene. In spite of the compensating leucemia. ' activity, a continued exposure might We must conclude therefore that mean a real damage. In Hunter's even in typical cases the tendency of table of the blood findings in 89 work blood forming tissues to maintain or to men exposed to benzene a quite re restore the stock is at work and that markable number show a leucocyte the atypical forms are those in which count between 10,000 and 17,000 with this tendency is not quite frustrated or no evident reasons for this striking is abnormally exaggerated. From this increase, and it would be a serious mis statement arise two questions of great take to allow further exposure in such importance for practical benzene pro cases. Leucopenia, therefore, is not a phylaxis. necessary sign of benzene poisoning. One concerns the value of the usual A relative lymphocytosis does not tell danger signals. A fully reliable sign us more than the absolute leucocyte must fulfill the logical demands of suf count, because in all leucopenias the ficiency and of invariability. It is granulocytes suffer more and earlier sufficient, when its presence positively than the lymphocytes and their drop reveals a pathological state, otherwise implies arithmetically a rise in the ratio a non-existing damage may be simu of lymphocytes. A very rarely en lated. Its presence in every case of countered relative neutrophilia belongs benzene poisoning is necessary, other among the compensatory reactions. wise a number of cases could escape Similar considerations apply to the identification. The inconstancy of red cells. It may happen that a strong other symptoms have resulted in a con effort at compensation veils the chronic centration of attention on the blood destruction. The paradox of initial changes. The high sensibility of polyglobulia reveals an excess of regen X I i 1 i > I i i Jan. im\ ST085I 520 POISONING BY BENZENE AND ITS HOMOLOGS 5 eration under the continuous stimulus, followed by exhaustion of erythropoiesis. It is clear that no absolute value is attributable to any of those signs and thehope that progressive study of ben zene poisoning will furnish such a sim ple sign is negatived by our increasing insight into the varying and interlock ing processes of this intoxication and the circumstances under which it occurs. A full hematological examina tion of all cases will certainly yield better results. But if it is impossible to ask such a routine procedure from the medical staff entrusted with the task, the method proposed by the National Safety Council Report men tioned above seems still the most prac tical, especially if by a periodic super vision (every fortnight or month) we are enabled to follow the blood changes in the workmen. The second question concerns the reasons for the variability in appear ance and in the outcome of the effects engendered by a seemingly uniform agent. Here the two factors of the injured subject and the active cause enter into consideration. Individual constitution and degree of sensitivity remain mere words so long as they are not determinable by observation. In any event, constitutional differences can never account for "epidemics" of benzene poisoning because there is no reason to assume a change in selection of the working force. Our attention, therefore, is directed to the variations in exposure and to the poisonous sub stance itself, a matter dealt with in the following paragraphs. II. STATISTICAL AND INDUSTRIAL HYGIENIC CONSIDERATIONS L. Txlxkt We have attempted in the following table to collect all the serious cases of chronic benzene poisoning published after the report by A. Hamilton as far as they were accessible to us. Natu rally we cannot claim completeness, but we believe that only a few cases have escaped us, such as cases from reports of factory inspectors in Euro pean countries, the details of which we could not obtain, and also some in re ports of Industrial Commissions of sev eral of the states in this country. A few of these reports which were at our disposal did not differentiate between damage caused by benzene and those caused by its derivatives. We have tried to avoid double counting of the came cases as far as possible. A large number of publications in the last decade report the results of peri odical examinations of benzene work ers; single serious cases induced exami nations of all other workers of a plant. Therefore we have now more reports about single or repeated examinations even of very slight cases than in pre vious years. We have included only serious cases in the table and we quali fied as "serious cases" only those with less than 3,250,000 erythrocytes. In one case the number of erythrocytes in a single examination was 3,200,000, but the counts before and after were mark edly higher, and therefore we con sidered the case not a "serious" one. That certainly is an arbitrary division; to be exact every case should be judged by its entire clinical picture, but if we did that the judgment would still be arbitrary and the limitation less clear. We call "typical" those cases which ST 0fi5 52 6 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY M. MS, no. 1 show: hemorrhage, decrease of red and picture is given, absolute and relative white blood corpuscles and, if afuli blood neutropenia and thrombocytopenia. TABLE 1 Ttmcal and Attpical Cams op Sxbious Benzene Poisoning Repobtzd, 1930-1938 e jl coxnrrBT iil ISM 1831 1832 1833 , 1 1834 1893 1833 1837 1833 1838 1890-39 England Typ... Atyp.. 1 (1) 1 (1) 3 (3) France* Typ... Atyp.. Germany 2 (1) 1 (1) 11 (9)b 3 (2) Typ... 1 (1) Atyp.. 2 (2) 1 (1) 2 7,(2) 7 (2) Austria* Typ... Atyp.. 12 (5) 4 Russia Typ... 1 1 Atyp. Italy Typ... 1 Atyp.. Belgium Typ. Atyp. Rumania Typ... Atyp.. Nether- lands Typ. Atyp.. U. S. Typ... 2 (1) 1 (I) 1 Atyp.. 1 (1) 1 (1) 1 (1) 4 (3)* 1 (1) 1 (1) 2 (1) 5 1 1 1 (D* 1 (1) 4 (2) 3 (3) 18 (4)* 1 12 8 (2) 2 (l) 8 9 (3) 6 (6) 0 43 (22) 4 (1) 28 (9) f 20 (5) 4 1 0 12 (4) 0 5 1 1 0 2 (1) 2 (1) 0 1 3 (3)d 9 (4) 2 (1) 23 (14) 2 (2) 1 2 (2) 6 (5) Total Typ... 4 (2) 3 (2) 16 (7) 2 20 (13) 18 (10) 11 (4) 31 (8) 8 (7) 29 (9) 3 (1) 141 (61) Atyp.. 3 (3) 1 (1) 5 (1) 1 1 (2) 3 2 (2) 15 (6) Numbers of fatalities are given in parentheses. * Regarding cases of Dimmel (Austria) and Sabrazfes (France). See text. b Of 8 fatal cases, no clinical picture is presented (Heim de Balsac and Agasse Lafont). * No full description given. 4 In one case no full description given. * Mignolet's 15 cases probably typical. ( A remarkable case of Kern's is omitted as it is not serious in our sense. Jan. mi] POISONING BY BENZENE AND ITS' 7 The cases of Diramel were especially difficult to classify. He published the histories of 66 cases observed among workers of a factory which was closed down after the first fatal cases. Ex amination of some of these workers was made some time after the factory was closed. Selecting from his table the cases which come under our classifica tion, we find 12 typical and 4 atypical cases. But Dimmel himself calls 15 cases serious in addition to 5 fatal cases, and his judgment is probably better than our classification for statis tical purposes. Among these 20 cases we could call 17 typical, 3 atypical. We include in the table all cases caused by benzene or by benzene mixed with other substances, if the benzene seemed to be the chief agent. In many cases the composition of the solvent was not clear. (We discuss later cases in which other compounds were em ployed.) But in all probability ben zene was inhaled too. In our compila tion of cases, we did not include those of Sabraz&s and his collaborators: three cases of leucemia. One man worked with lubricating oil; the other worked on the second floor of a factory on the first floor of which ben zene derivatives were employed. The only open connection between the floors was a staircase. The first man was a garage proprietor and mechanic. There is not the slightest possibility that these men were inj ured by benzene. We have arranged the cases accord ing to the year of death or of termina tion of observation, because often the onset of the illness is not made clear. Dates given are not those in which the material was published. Unfor tunately in some cases the date of ill ness is not given and must be approxi mated. Furthermore, some authors (Heim de Balsac and Agasse Lafont) tell us nothing specific about the clini cal picture, but if Mignolet's descrip tion is accepted, the cases may be considered typical, in our sense. But these deficiencies do not alter the gen eral picture gained from the table. Of more importance is the fact that perhaps a number of cases of poisoning have not been reported and that even more have gone unrecognized. One may assume this from the history of series of poisonings in certain factories. Such a series explains also the fre quency in one year (Dimmel, 1931; Heim de Balsac and Agasse Lafont, 1933; Mignolet, 1938). The number of cases is very high in France (47) and may be explained by the nature and organization of its in dustry. In this country the number (29) is relatively low, but is increasing. The totals, however are very high: in 10 years there have been 156 serious cases with 67 deaths, and one may expect that additional cases for 1939 will be published later. Concerning the proportion between typical and atypical cases we have 141 typical and 15 atypical cases between 1930-1939. That means 9.6% of atypical cases. If we consider different single coun tries, the numbers are mostly too small for statistical consideration, but it may be mentioned that the proportion be tween atypical and typical cases in France is 4:20, but in the United States 6:23. The number in single years is too small for statistical pur poses but we may note an apparent increase in the proportion of atypical cases compared with the typical, espe cially in the American list. In the last 5 years we find 5 atypical and 16 typi- ST085I 523 8 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [vol. tS, no. 1 cal, in the first 5 years only 1 atypical against 7 typical. It is not possible to draw definite conclusions from such small numbers, especially in view of the possibility of different opinions concerning what constitutes an atypi cal case. But it is, after all, probable that the atypical cases have increased in recent years and chiefly in the highly developed American industry. To what factors may this increase be attributed? Certainly not to ad vanced knowledge of hematology nor finer methods of examination. Changes in the constitution of workers or in their nutrition (vitamin C con tent) could change the clinical picture, but we have no reason to assume such changes in recent years. A different rate of absorption of the poison might possibly alter the clinical picture. Lignac and Emile-Weil believed that the cases of benzene leucemia they dis covered were to be explained on the ground of very slow absorption of the poison, the men having worked many years before the blood disease de veloped. But the job of one man was considered by his fellow workmen to be very dangerous. At present we have no proof of the different effect of very small doses as compared with larger. There may be a change in the injuri ous material, as a consequence of mix ing other solvents with benzene, espe cially its homologs. Changes in the Use of Benzene and Its Homologs The great confusion caused by the similarity of the words "benzene" and "benzine" has almost disappeared from the literature of today, but occa sionally it is still found, even in sci entific work. Besides the pure crystallixable ben zene (CH) used only in certain chemi cal productions, the following different sorts of benzene are used commercially. inrtnn Tomnre nun (C*Hf) (CHiCHj) (CcH(CHa)a Benzene 90. .. 84% 13% 3% Benzene 50... 43 46 11 Benzene 0 -- 15 75 10 In some countries (e.g. Germany) sol vent naphtha is called "solvent ben zene" and there is also a "heavy benzene," neither of which contains any benzene, only xylene and cumene. These proportions vary in practice and there may be impurities present, such as thiophene, paraffins, carbon disulfide. It is evident from these statements thatwhen the commercial nomenclature "benzene" is used it may signify a hydrocarbon containing only 15% ben zene or even no benzene at all. The use of the word benzene and its homo logs is still less accurate in workshops: Stocks, for instance, tells us, that a liquid which in the factory was called "xylene" was pure toluene. Brindeau reports that his patients inhaled vapors of "impure xylene," but the liquid was shown to contain 30% benzene and a considerable amount of carbon disul fide. It is often very difficult for the industrialist to know what he is using and this adds to uncertainty in some publications. The composition of cements, thinners, coatings and inks has changed decidedly in recent years. Rubber ce ment, which gave rise to the first pub lished cases of industrial benzene poi soning (Santesson's) was then prepared in the factory and only benzene was used. L. Greenburg described this ST085I 524 Jan. 194i] POISONING BY BENZENE AND ITS HOMOLOGS 9 procedure in 1926 and I saw it 10 years ago in some of the largest rubber fac tories in Germany. Later on rubber cement came into increasing use, espe cially in shoe manufacture, where it replaced nailing and sewing, but this cement is now produced in factories and sold to the users. Many different compositions of rubber cement are described in trade journals and the solvents used are benzene, gasoline (benzine) petroleum spirit, solvent naphtha and "non-inflammable" sol vents. So it is easy to see that the word "cement" does not disclose any thing about the constituents. As to the extent of the use of benzene in American industry at present, it is hard to get detailed information. The Report of the Committee of the Na tional Safety Council on Spray Coat ing, 1927, states that the use of ben zene in lacquers has been discontinued by practically every manufacturer be cause of its recognized danger to health. However, in the same report we find that H. F. Smyth reports that benzene vapors in the air of 6 plants contained an average of 375-1880 p.p.m. and that among 14 lacquers 9 contained benzene. Among Hunter's cases, described in 1939, there were some who had worked with lacquers. All this shows that benzene is still used in lacquers in this country. But there are reports from this and other coun tries showing that toluene, xylene and other solvents are being used in var nishes to an increasing extent. A new source of benzene poisoning is rotogravure printing ("heliogravure" in France, "Tiefdruckverfahren" in Ger many, "stampa a rotocalco" in Italy). It seems that at first harmless inks were used, but very soon benzene be came the solvent agent and was only gradually replaced by less poisonous solvents when ink manufacturers found less poisonous inks just as satis factory. Greenburg and his collabo rators tell us that in one plant for colored inks the solvents used con tained 70-75% benzene by volume, for black inks from 30-35%, for the thinners 60-80% benzene. In all plants "the benzene content of the thinners varied from 20-80% by volume. In addition, other volatile solvents were present, such as toluene, xylene, methyl-ethyl ketone, petroleum naph tha, ethyl, butyl and amyl acetate and butyl and amyl alcohol." Nothing is said in many publi cations about the quantity of these other solvents in the mixtures nor about the vapors of these solvents in the air. The vapors of benzene were measured, but that these other vapors may also be important will be shown later. Mixtures used in Ger man rotogravure printing, as given by Bachmann, may be quoted here: Plant 1: 41% Xylana, W% Benxina, 1% Banaana Plant 3: 50% Xylana, 50% Tolnana Plant 3: 50% Xylana, 40% Baniine Plant 4:15% Xylana, 80% Baniine, 5% Eater mixture# In summarizing we want to repeat: In contradistinction to former times we can no longer depend on the name of the job (as cementing, spreading, color mixing, rotogravure printing) to tell us whether the workers have been ex posed to vapors of benzene alone or in mixtures. We must take into con sideration also other solvents, espe cially toluene and xylene. The com position of the vapors necessarily differs from the composition of the sol vents, especially if there is a mixture ST085I 525 10 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [vol. tS, no. 1 of benzene and its homologs. The boiling point of pure benzene is 80C., of commercial toluene 109-111C.( of xylene 138-142.3<>C., of commercial xylene, 135-145C. The vapor pres sure at 40C. is for benzene 181.1, for toluene 59.1, for xylene 19.48-23.7. Therefore, the content of benzene vapors in the air is larger than its pro portion in the mixture. The Effects of Toluene and Xylene Animal experiments on the effects of the higher homologs of benzene, toluene and xylene have been carried out for many years. The earlier ex periments are reviewed by Batchelor in his part of the "Final Report on Benzol." Batchelor himself tested them on animals and found that tolu-. ene and xylene have a more powerful narcotic effect than benzene. At au topsy the majority of the animals which inhaled toluene "presented microscopically a definite hyperplasia of the bone marrow, of the Malpighian corpuscles of the spleen and of the germinal centers of the lymph nodes." In xylene poisoning he found that "microscopically slight hyperplasia of the bone marrow was present." Selma Meyer in 1928, upon my sug gestion, examined the blood of a num ber of men who had worked for the month preceding with a mixture of xylene, toluene and benzene in the proportions of 5:4:1. The single posi tive finding was a slight lymphocytosis (35-40%) with an increase in large lymphocytes. Ferguson, Harvey and Hamilton reported (1933) the first fatal case, caused by a solvent contain ing toluene (about 45%), but no ben zene. The man began work in 1919, fell ill in March, 1932 and showed hemorrhagic spots on his tongue, later bleeding from the gums and subcu taneous hemorrhages: blood nmot oBaallda Wblta Hb blood oalla Polymoipbomielsar Aug. 15 Oct. 4 Nov. 11 Dec. 23 mil lion* 4.00 75 2200 2.60 82 1000 23.0% (449). Poly- chromasia 3.80 72 2400 6.8% (127). Red cells irregular, some macro cytes. Polychromasia 2.21 50 1200 5-5% (67). Polychromaaia. 10 nucleated red cells. Platelets numerous The man developed gastroenteritis and pneumonia and died December 24. The autopsy showed the bone marrow of the femur shaft in a state of aplasia, although it was really a red marrow. The lymph nodes demonstrated a pro nounced proliferation of the reticular cells, absence of germinal centers and an apparent fibrosis. The authors, reviewing the literature and the history of this and their own animal experiments, conclude that benzene is a more powerful poison be cause it is more volatile than toluene and can therefore reach higher concen trations in the air, but because of this greater volatility benzene "is elimi nated more quickly and its effects are less lasting than those produced by toluene." G. de Oliveira reports a fatal case attributed to xylene. A man who had inhaled xylene vapors for a long time died and the autopsy showed changes ST085 I 526 Jan. 1H1] POISONING BY BENZENE AND ITS HOMOLOGS 11 of an apltustic anemia, serious damage to the bone marrow and also atrophy of the lymphoid tissue of the spleen and lymph nodes. The following two fatal cases, pub lished by S. Hirsch, should be men tioned also: These two men worked in a rotogravure printing shop. Analyses of the inks made several months later showed that the "ink" contained about 16% xylene, a thinner with 29% of a mixture of benzene and toluene and 64% xylene; another substance used alternatively had 3% benzene and toluene and nearly 87% xylene." Both men died of aplastic anemia, sep sis and endocarditis. The femur of one man showed a red bone marrow, of the other, a fatty marrow. Examina tion of the co-workers (performed a long time later) showed in nearly half less than 5 million erythrocytes, but no changes in the number or character of the leucocytes. The author thinks that xylene was the cause of death. I am not sure of it, because analyses of the material and examination of the other workers was performed a long time after the two fatal cases occurred and such accidents are usually followed by a prompt change in the material used. Even if we add these two cases the number of deaths caused by xylene or toluene is very small in proportion to the widespread use of these substances in recent years. But that disturbances of health less serious in character may be caused by these solvents is made clear by a large number of studies of workers in plants which use mixtures containingbenzene in small percentages and its homologs, or these homologs only, such as plants for rotogravure printing and for every kind of varnish ing, spray coating etc. Most of these publications are by German authors. Those which refer to plants using ho mologs only are the most important. Adler-Herzmark and A. Selinger published reports on workers using benzene or its homologs. I will dis cuss only the latter. Among those using toluene a moderate degree of anemia was found, no count being below million; also anisocytosis and poikilocytosis; and a relative lympho cytosis with an absolute leucopenia of low grade. In another investigation users of xylene or toluene showed an absolute neutropenia and alterations in the erythrocytes. In 11 women using a solvent with 15% to 17% toluene, threeshowed granulocytopenia (1850 to 2800) with lymphocytosis. Stocks was the first to report injury to workers in rotogravure printing (1929). In these shops pure toluene was used. The workers complained of irritation of the conjunctivae, head ache, vertigo, sleeplessness, anorexia, palpitation and stomach troubles. Among 10 who complained of illness, seven had a relative lymphocytosis between 30% and 46%, in a count of 7300 to 8800 leucocytes. A. Brandt examined two rotogra vure printing shops, one using as sol vent no benzene but 25% toluene, 70% xylene and 5% cumene; the other a mixture of 75% toluene, 10% xylene and 15% benzene. In both shops there were many complaints of head ache and stomach trouble and in both the blood pictures showed changes in the erythrocytes and a leucopenia (down to 2800) with marked neutro penia (down to 45%). The blood changes were more pronounced in the first shop than in the second where 12 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [vol. tS, no. 1 benzene was used but where the ven tilation was better. Litzner and Edlach report the results of an investiga tion of 7 workers who used "pure toluene." Here again the number of erythrocytes was slightly diminished but there was no anisocytosia or poikilocytosis. In three the neutrophiles were less than 55% of the white count. H. Gerbis examined the workers of 7 rotogravure printing shops. He gives us exact statements about the material used in five of them and from the results of the examinations (which are not always very clear) we quote as follows: := ft 9o gp LTinocra Ovr Ovflr *8% 60% A plant using beniene 166 77 73 3 mostly (46.8%) (48.8%) (1.36%) Two plants using xylene, toluene and 10% beniene in the solvent 81 It 66 (14.83%) 68% 8 .3% Two plants using pro* ponderantly pure xylene 67 6 40 11 (7.8%) (60%) (16.6%) Therefore we may conclude that benzene damages chiefly white blood cells as a whole, but its homologs, espe cially xylene, damage the granulocytes more than benzene does. Brachmann reports on an examina tion of 4 rotogravure printing shops using the material given above. In the first, using 3% benzene in the ink, no injury to the leucocytes was found, but two workers complained of nose bleed. Brachmann believes that the effect of chronic xylene and toluene action is a real damage to the neutro philic granulocytes. But he also often found anisocytosis and poikilocytosis. There were complaints of nervousness, headaches, insomnia, irritability and vertigo. Lind (1938) examined 230 spray coating workers, who were exposed principally to xylene and toluene, but also to other solvents, such as acetates, alcohols and esters. In some cases benzene too seemed to be present in small amounts. He writes: "The symptoms which characterize the health picture of spray coaters are ner vous ones." Leucopenia was present in a few workers (20); in 33 there was an absolute neutropenia. More often there was an absolute lymphocytosis (61 over 3000,103 from 2500 to 3000). As no distinction is made between the men working with different materials this publication is not very useful for our purpose, which is to make evident the effect of xylene and toluene as far as it iB possible. There are other pub lications about rotogravure printing, but they are of no help to us because the injurious substances are not ex actly described. For instance, Nelken writes about the intoxicating effects of "xylene (respectively toluene and ben zene)." Kahle's subjects were ex posed to the "effect of benzene and its homologs xylene and toluene," and later, he says, to the effect of "xylene and toluene." The nervous symp toms: headache, vertigo, insomnia, chronic fatigue, are in the foreground, besides vasomotor lability. In the cases of Castrovilli, the rotogravure printers worked with "xilolo," actually a mixture of benzene, toluene and xylene. We have to conclude that from the standpoint of industrial hygiene, xy lene and toluene (the published mate rial is not extensive enough nor de- ST085 I 528 Jpn. 19411 POISONING BY BENZENE AND ITS HOMOLOGS 13 tailed enough to allow us to treat these two substances separately) are far less dangerous than benzene. In spite of their abundant use, the number of fatal cases is very small (two positive cases, one caused by xylene, one by toluene, and two other probable cases in the literature). In the other reported cases the alterations of the blood pic ture are far less serious than those caused by benzene. We cannot de cide, however, whether the less damag ing effect is owing to the lessened evaporation or to the lesser toxicity of the same amount of vapor. There is no doubt that certain differences exist between these two substances and ben zene in their qualitative effects on the blood picture. They often produce alterations of erythrocytes (poikilocytosis, anisocytosis), they do not in fluence all the leucocytes to the same extent as does benzene, but they have a greater injurious effect on neutrophiles. Therefore, we ask ourselves whether or not deviations from the typical blood picture in cases of sup posed benzene poisoning (at least slighter deviations) should be traced back to the combined action of these substances. But we must also remem ber that the effect of two toxic sub stances may not necessarily be the sum of their effects, but may give an en tirely new clinical picture. One clinical effect is much more characteristic of these two homologs than of benzene itself: the effect on the nervous system. In rotogravure printing and spray coating the follow ing complaints stand in the fore ground: headache, confusion, vertigo, fatigue, insomnia and stomach trouble. This action on the nervous system is confirmed by animal experiments showing that the anesthetic effect of the toluene and xylene is greater than that of benzene. These symptoms are the result more of a slight acute poison ing, newly acquired every working day, while the blood changes are the conse quence of chronic poisoning. At all events, the effect of toluene and xylene, although rarely causing death, must be taken seriously into consideration from the clinical and the hygienic standpoint, even if benzene too is present in the liquid or solvent used. The "Final Report" quoted above, decided that the "allowable limit" of benzene in the air should be set at 100 p.p.m. Later observers (Bowditch and Elkins) urge a lower figure, 75 p.p.m., and Hunter declares "that the only really safe concentra tion of benzene is zero." The reason for this change of opinion may be that earlier examinations, made with less exact methods, caught benzene and its homologs together, the amount of the latter being small at that time. But today the vapors of benzene alone are captured and the vapors of the homologs, although today they form a greater part of the contamination of the air, are neglected. Other Admixtures in Solvents In their effect on the blood produc ing organs there are some other sub stances to be considered in modern sol vents of rubber, in cements, in inks, coatings and thinners. There are re ports about blood changes caused by benzine, but some of them concerning human beings seem to be not very reliable. Schustrow and Salistowskaja in describing their animal experiments refer also to a publication by myself and another by Briicken as examples of ST085 I 529 14 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY M. t3, no. 1 blood changes in man caused by ben- amounts of evaporating benzine, at sine, but both of us wrote under the tacks of fainting. One case suffered title "benzene poisoning" about work from serious polyneuritis, but not one ers of the same factory. Duvoir, Pollet showed any blood changes. Still there and Arnoldson present a case of poly remain, as we saw above, 4 cases of neuritis, especially of the lower extrem blood changes attributed to benzine, ities showing also serious blood changes: at least two of them reported by a I. 5 million erythrocytes, 9500 white very critical observer. This is a very blood cells with 81% neutrophiles. small number when one considers the The autopsy showed fatty marrow. widespread use of benzine. It would This woman had worked many years seem that there must have been some with benzine. I discussed this re exceptional circumstances in these markable case in a French journal (La cases, perhaps the unsuspected pres Medicine du Travail, 1938). Adler- ence of other harmful substances. Herzmark reports on two workers, Solvents often contain other com who, in the production of adhesive pounds, such as butyl alcohol, which, plaster, used 35 1. of benzine daily, according to H. F. Smyth, produces a containing 3.3 vol. % of aromatic com decrease of red cells with a relative pounds. They had pharyngitis, accel and absolute lymphocytosis; methyl eration of the pulse and tremor. One alcohol, "a true hematoxic" according of them had 6.2 million erythrocytes to Tyson and Schoenberg; butyl ace with anisocytosis and poikilocytosis, tate, etc. The use of mixtures has II, 700 leucocytes with 52.4% neutro increased in recent years, replacing philes. The other worker showed 4.2 the use of benzene alone. The effect million erythrocytes with anisocytosis, on the blood when two or more sub 74% hemoglobin, 5390 leucocytes. stances act simultaneously may be to Engelhardt discusses some Russian produce a different clinical picture publications, reporting blood changes and such a possibility should always in benzine workers. The most re be considered when a given case pre markable effects in Russian workers in sents deviations from the "typical rubber and other factories will prob picture" of benzene poisoning. The ably never be cleared up entirely, but coincidence of an increasing use of the cause seems to be the composition mixed solvents in American industry of Russian benzine (different from and of increasingly frequent occur American) which contains cyclic- rence of atypical cases of benzene hydrocarbons, and carbon bisulfide in poisoning in American literature point varying amounts. to this conclusion. Only clinical Gran describes the case of a man studies combined with exact chemical who as a consequence of chronic ben examination of every substance used zine poisoning had 1.58 million eryth and every vapor contaminating the rocytes, 28% hemoglobin, poikilo air (not benzene only) will suffice to cytosis, anisocytosis, 11,840 leucocytes clear up this problem. with 81% neutrophiles, 11% lympho cytes, 6% eosinophiles. The man re Industrial Hygiene covered. I myself have observed It is clear that the harmful effects among people working with large of toluene and xylene are far less ST 08 51530 Jan. 1841} (POISONING BY BENZENE AND ITS HOMOLOGS 15 serious than the effects of benzene, and therefore it is desirable to replace benzene by its homologB, or better, by still less harmful substances. Lind tells us that in Danish fac tories the use of benzene in varnishes and lacquers was greatly decreased in response to the wishes of the public. German factories producing inks for rotogravure printing have taken pains to exclude benzene, and Gerbis tells us that in these plants benzine is used to a great extent now. The German government had made ex periments (Koldenhofe) in substitut ing benzene in cements for waterproof material; for usual purposes replace ment by benzine is possible, but for some specific purposes a small amount of benzene is still needed. Royal decrees in Belgium from 1936 to 1938 forbade the use of benzene containing cements in the manufacture or repair of waterproof clothing, and the use of varnishes in mirror manu facture, of inks, thinners or detergents in rotogravure, which contain more than 1% of aromatic compounds. Evidently the substitution of ben zene by other solvents is possible. To make it possible for the customer to buy innocuous material if he wishes to do so, to enable inspectors to carry out the regulations of the government, the material brought on the market containing dangerous substances must be recognizable as such by proper labeling. That is an old demand of industrial hygienists. Belgium has such a law (January 23, 1937), Germany is introducing it. The Mas sachusetts Benzene Labeling law (Chapter 149, General Laws, Acts of 1933 and 1935) prescribes exactly how every receptacle with material containing benzene must be marked. However these ideas may be exe cuted in a country or state, restriction of the use of benzene is necessary; but as long as its use is continued, medical supervision is essential, with complete blood examination every month at least. This recommendation was made in the often quoted National Safety Council report. When toluene or xylene are used, it would be suf ficient to make such an examination every 4 months, or even every 6 months. In some States the Labor Department has the right to order such periodical medical examinations, for instance in New York, according to the Labor Law 28,2. The French government prescribed a periodic med ical examination of workers exposed continually to benzene vapor (decree of Oct. 29, 1939). Summary Analysis of blood formation in benzene poisoning shows that the balance of destructive and regenerat ing processes determines the resulting blood picture and the state of the blood forming organs. A review of all the cases of poisoning that have been published in the last 10 years shows a large number of serious cases. There are 156 cases with 67 fatalities, besides a large number of slight in toxications. The number of cases in this country is increasing markedly. Toluene and xylene are more widely used today than in earlier years, often mixed with benzene, while for merly the latter was used alone. These homologs have, as industrial poisons, a greater effect on the nerv ous system than benzene but they may also injure the blood-forming tissues and cause death, although very rarely. Changes in the blood differ STp05 I 53 I 16 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY M. tS, no. t to some degree from those caused by benzene. There are also other substances present in mixed solvents, such as benzine, butyl alcohol and acetate, methyl alcohol, some of which may have an influence on the blood-forming organs, at least under certain circumstances. As the combined effect of several harmful substances is not always the same as the sum of the individual ef fects but may result in an entirely new clinical picture, an atypical case of benzene poisoning should be viewed as possibly caused by a mixture of different toxic solvents. This is in dicated by the fact that atypical cases seem more frequent in recent years, and especially in this country where the use of mixed solvents has greatly increased. To clarify the effect of these mix tures on blood formation, we need exact determinations of all the air contaminating substances, not only benzene. The restriction of the use of benzene, its replacement by less dangerous (preferably quite innocu ous) solvents, is imperative in any work where evaporation into the air breathed by the workers occurs. As long as benzene is used, medical supervision is indispensable and ac curate blood examinations must be made each month at least, while where toluene and xylene are used, an exami nation every 4 to 6 months is sufficient. BIBLIOGRAPHY Adlxb-Hkbziiarx, J.: Berafserkr&nkungen in den Berichten "Die Amtst&tigkeit der daterreichiachen Gewerbe-Inspecto rate in dem Jahren 1930-1936." -------- : Periodiaehe TJnterauchungen von Wiener Arbeitem, die mit benzol-, toluol-u. xylolh&ltigen Materialien beach&ftigt aind. Arch. f. Gewerbepath., 4,486-489 (1933). -------- , ANn Selinoer, A.: Unterauchungen von Wiener Arbeitern, die mit benzol-, toluol- u. xylolhftltigem Materialien beschfiftigt aind. Ibid., 1, 763-790 (1930). Anatabtasic, T., and Vasilitr, C. T.: Intoxicatiuni professionals cu benzol. Rev. de igiena aoc., 6, 418-421 (1935) Bucharest. Anderson, D. H.: Benzol poisoning with hyperplasia of the bone marrow. Am. J. Path., 10, 101-111 (1934). Bowditch, M., and Elkins, H. B.: Chronic exposure to benzene (benzol). I. The industrial aspects. This Jour., tl, 321-330 (1939). Brachiiann, J.: Gesundheitssch&digungen in Tiefdruckbetrieben. Arch. f. Hyg., 118, 328-353 (1937). Brandt, A.: ZurVergiftungdurchLBsungsmittel in Tiefdruclcereien. Arch. f. Gewerbepath., 3, 527-534 (1932). Brindeau: Deux cas d'an6mie pernicieuse gravidiques par intoxication bensolique. Ann. d'hyg. pub., 9, 99-102 (1931); Ann. de med. leg., 11, 95-99 (1931). Cain, A., Cattan, R., and Hebte, 8.: Action du splenectomie dans deux cas mortals d'intoxication benzolique. Bull, et m&n. 8oc. md. d. h6p. de Paris, 84, 530-537 (1938). Cathala, J., Polgebt, M., and Gbbnxt, P.: Scorbut chez un sujet sounds 5 une intoxication benzolique professionnelle. Ibid., St, 1648-1661 (1936). Dieckhoff, J.: Ein Fall von chronischer Benzolvergiftung durch Verscblucken. Arch. f. Gewerbepath., J, 549-554 (1932). Diumxl, H.: Zur Klinik der chronischen Benzolvergiftung. Ibid., 4, 414-464 (1933). Dovoin, M.: La prevention des hemo- pathies benzoliques. Sang, It, 520-628 (1938). ST085I532 Jan. lHH POISONING BY BENZENE AND ITS HOMOLOGS 17 DtTVOIH, M., POLLET, L., AND AbNOLDSO"N, M.: La polyneurite beminique existe-telleT Bull, et m6m. Soo. m6d. d. h6p. de Paris, 84, 359-369 (1038). Emilx-Weil, P.: La leueemie poet-benzolique. Ibid., 48, 103-108 (1032). -------- : Lea hematopathies benzoliques. Paris m6d., 89, 112-110 (1033). -------- , Pebles, 8., Ascbunast, A.: Etude sur le bensolisme latent. Sang, It, 151-170 (1038). Enoelhabdt, W. E.: Vergleichende Tierversuohe liber die Blutwirkung von Bensin und Bensol. Arch. f. Gewerbepath., Jt, 470-614 (1031). -------- : Vergleichende Tierversuche fiber die Blutwirkung von Toluol und Xylol. Arcb. f. Hyg., 114,210 (1035). --------, and Estleb, W.: Versuche fiber die akut narkotische Wirkung aliphatischer und aromatischer Kohlenwasserstoffe. I. Die Wirkung einmaliger Einatmung verschiedener Konsentrationen Ben zine, Benzol, Toluol, Xylol auf Kaninchen und Katzen. Ibid., 114, 240-280 (1035). Ebf, L. A., and Rhoads, C. P.: The hema tological effects of benzene (benzol) poisoning. This Joub., tl, 421-435 (1030). Estleb, W.: Versuche fiber die akut nar kotische Wirkung aliphatischer und aromatischer Kohlenwasserstoffe. II. Die Wirkung wiederholter Einatmungen verschiedener Konzentrationen von Benzin, Benzol, Toluol und Xylol auf weisse Mftuse. Arch. f. Hyg., 114, 281271 (1035). Falconeb, E. H.: An instance of lymphatic leukemia following benzol poisoning. Am. J. Med. Sci., 188, 353 (1033). Fellinoeb, K.: Zur Diagnose und Pathologie des Frfihstadiums der chronisch gewerblichen Benzolschftden. Arch. f. Gewerbepath., 8, 88-96 (1939). Febquson, T., Habvet, W. F., and Hamil ton, T. D.: An enquiry into the rela tive toxicity of benzene and toluene. J. Hyg., S3, 547-575 (1933). Fbiemann: Zur Diagnose der chronischen Benzolvergiftung. Arch. f. Gewerbe path., 7, 278-283 (1937). Gall, E. A.: Benzene poisoning with bizarre extra-medullary hematopoiesis. Arob. of Path., tS, 315-828 (1038). Gebbis, H.: Geaundheitsgefahren ties Tiefdruckverfahrens. Arbeitsschutz, 279282 (1035). Glibebt, D.: Nombreux cas de benzenisme en Belgique. M6d. du travail, 8, 8189 (1936). Gounelle, H., and Dumas, G.: Manifesta tions prolongtes de I'intoxication benzoliques. Persistence de troubles morbides dix-huit mois plus tard. Sang, 9, 204-206 (1035). Ghan, B.: Di un caso di benzinismo professionale con prevalente sindrome anemica. Gazz. d. osp., S4, 643-648 (1933). Gbeenbubq, L.: Benzol poisoning as an industrial hazard. Pub.'Health Repts., 41, 1357-1375; 1410-1431; 1516-1539 (1926). -------- , Matzbs, M. R., Goldwateb, L., and Smith, A. R.: Benzene (bensol) poisoning in the rotogravure printing industry in New York City. This Joub., tl, 305-420 (1939). Hamilton, A.: Industrial poisons in the United States. Macmillan Company, New York, 1925. -------- : Benzene (benzol) poisoning. Arch. Path., 11, 434-454; 601-637 (1931). Hathubst, E. R., and Neiswandeb, B. E.: A case of chronic benzene poisoning. J. A. M. A., 96, 269-270 (1931). Heim de Balsac, F., and Aqasse Laeont, E.: Intoxications mortelles ou de gravity variable, en s6rie, par I'emploi d'un adhesif solubilise par le benzine. Indications prophylatiques. Bull. Acad, de m6d. Paris, 110, 31-35 (1933). Hibsch, 8.: Ueber chronische Xylolvergiftung, insbesondere fiber die Einwirkung des Xylols auf Herz und Geffisse. Verhandl. Dtsch. Gesellsch. f. inn. Med., 483-493 (1932). Holstein, E.: Benzolerkrankungen bei Gummiklebern. Med. Welt, //, 391- 393 (1937). Hunteb, F. T.: Chronic exposure to ben zene (benzol). II. The clinical effects. This Joub., tl, 331-354 (1939). ST085I 533 18 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [vol. tS, no. 1 Kahlx, 8.: Untersuohungen an Tiefdruckern Leipsiger Firmen. Arch. f. Hyg., ltl, 67-88 (1938). Knur, B.: Isolierte Thrombopenie duroh chronische Benzolvergiftung. MUnch. mad. Wchnachr., to, 1062-1063 (1938). Koldehope: Verwendung von Bentol in Gummilfisungen. Arbeitssohutz, 86-82 (1939). Kobvin, E.: Ueber das Auftreten von Epilepaie bei chroniscber Benzol-Vergiftung. Dtsoh. mod. Wchnschr., SO, 816-818 (1933). Lamt, M., and Bernard: Un cas d'intoxi- cation par le benzol. J. de m6d. Paris, to, 916-916 (1935). -------- , Kissel, P., and Pixrquin, L.: La myelotoxicose benzolique. Sang, IS, 467-488 (1939). Lxdxbkb, E.: Chronische Benzolvergiftung unter Morbus Gaucher&hnlichem Bilde? Arch. f. Gewerbepath., S, 535-548 (1932). Lignac, G. O. E.: Die Benzolleuk&emie bei Menscheh und weiasen M&usen. Klin. Wchnachr., It, 109-118 (1933). Limprice: Das Gesetz fiber geaundheitssch&dliche oder feuergef&hrliche Arbeitsstoffe. Arbeitsschutz, 161-164 (1939). Lind, G.: Ueber die Bedeutung von Blut- ver&nderungen bei Spritzlakierern. Arch. f. Gewerbepath., P, 141-166 (1939). Litzneb, St., and Edlich, W.: Ueber Toluol-Sch&digungen bei der Herstel- IungvonTiefdruekfarben. Med. Klin., t8, 1741 (1932). McCobd, C. P-, Cox, N., and O'Botlb, C.: Benzol poisoning. A new investiga tion on the toxicity of benzene and benzene impurities. Indust. Health Conservancy Laboratories, Cincinnati, Ohio, 1932. Malloby, T. B., Gall, E. A., and Bricklbt, W. J.: Chronic exposure to benzene (benzol). III. The pathologic results. This Jour., tl, 355-377 (1939). Mabchal, G., Maubxl, G., and Pobgb, J.: Syndrome agranulocytaire accompagne de necrose du maxillaire superior par intoxication benzolique professionnelle. Sang, 11, 430-436 (1937). MAssachu8*tt8 Gxnzbal Hospital Cash Rxcobds. N. E. J. Med., tlS, 182-185 (1935). Matthxs, H. G.: Beitr&ge sur Aetiologie und Verlauf der Panmyelophthise. Dtsch. Arch. f. klin. Med., 180, 68-87 (1937). Mbrklxn, P., and Ibrabl, L.: Intoxication par le benzol. Sang, 6, 700-708 (1934). -------- , Gbbt, L., and Ibbabl, L.: fitude clinique et anatomique d'un cas d'aleucie vraie. Absence des globules blancs dans le sang. Presse med., 4t, 1553-1557 (1934). Mxtkb, A.: Chronische Benzolvergiftung und Vitamin C. Ztschr. f. Vitaminforsch., 8, 83-88 (1937). Mbtbb, S.: Changes in the blood as reflect ing industrial damages. This Jour., 10, 29-55 (1928). Mionolbt, F.: Lea hemopathies du benzol. Sang, IS, 268-281 (1939). Mitnik, P., and Gbnkin, S.: Zur Klinik der chronischen Benzolvergiftung. Arch. f. Gewerbepath., t, 457-478 (1931). National Sajtbtt Council: Final Report of Committee on benzol. Chemical and Rubber Section. Chicago, 1926. -------- : Final Report of Committee Spray Coating. Chicago, 1927. Nxlkbn, L.: Untersuchungen fiber XylolSch&digungen in Berliner Tiefdruckbetrieben. Zbl. f. Gewerbehyg., 18, 182-184 (1931). Oliveira, G.: Ueber eine chronische Xylol- vergiftung. Verhandl. Dtsch. Natur- forsch. u. Aerzte, p. 180 (1936.) Pabst, W.: Gewerbliche Benzolvergiftung. Samml. v. Vergiftungsfftllen, 8, 11-12 (1937). Panchbbi, G., and Pogoi, J.: IIbenzolismo fra gli opaerai di calziaturifici usanti determinati mostici. Med. del lavoro, *7, 9-16 (1936). Penati, F., and Vigliani, E. C.: Sul problema delle mielopatie aplastiche, pseudoaplastiche e leucemiche da ben- zolo. Rasa. med. app. lavoro ind., 9, 346-361 (1938). Perrin, M., Kissel, P., and PiinquiN, L.: Leucose aigue benzolique. Paris md., 107, 633-538 (1938). ST085153U Jan. 1941] POISONING BY BENZENE AND ITS HOMOLOGS 19 Pmjiij L.: Benzolismo professionale. Med. del lavoro, 87, 65-77 (1836). Poltobp, D. 8.: Benzol poisoning. Cal. & West. Med., 36, 361-366 (1931). RBZNIXOZT, P., and Fullerton, R.: The aetion of benzol on granulocytes. Folia Hematol., 60, 454-459 (1933). Roch, M.: Diagnostic d'une an6mie grave compliquG de syndrome hdmogenique et d'hypogranulocytose. Presse m6d., 47, 495-496 (1939). Rosenblatt: Neurasthenic, hervorgerufen durch Einatmung von XyloldAmfen. Aerztl. Sacherst&nd.-Ztg., 8, 197-201 (1902). 8ABBAsi, J., and Bidbatj, J.: Leucemie myeloid chronique chez un graisseur de machines. Gaz.hebdomad.desci.med. Bordeaux, 68, 339-342 (1937). -------- , Bideau, J., and Glauneb, P.: Leucemie myeloid benzolique chez un ouvrier travaillant dans une miroiterie. Ibid., 68, 676-681 (1937). -------- , Bideau, J., and Glauneb, P.: Nouveau cas de leucemie benzolique. Ibid., 68, 726-731 (1937). Schilling, V.: Zwei FBlle von XylolBenzol Aleukie bei Kupfer-Tiefdruckern. Med. Welt, 8, 1143-1145 (1934). Schneider, H.: Zur Klinik und Therapie der chronischen gewerblichen BenzolVergiftung. Ibid., 88, 1112-1114 (1930). 8chubtbow and Saubtowskaja : Daa Blut bei der Benzin-Intoxication. Arch. f. klin. Med., 160, 271-276 (1926). Smtth, H. F., Jb.: The determination of small amounts of benzene vapors in air. This Jotjb., 11, 338-348 (1929). Smith, H. F., and Smtth, H. F., Jr.: In halation experiments with certain lacquer solvents. This Joub., 10, 261-271 (1928). Stasskns, A. P.: Benzols, benzines et pro tection du travail. Ind. chim. Beige, 8, 383-394, 429-438, 489-501 (1937); 9, 3-24 (1938). Stock!, A.: Akute Xylol- und Toluolvergiftung beim Tiefdruckverfahren. Zbl. f. Gewerbehyg., 8, 355-359 (1929). Stodmxistkb, R.: Ueber die klinische Beurteilung von Knochenmark- und Blutbildern. Dtsch. Arch. f. klin. Med., 188, 459-466 (1938). Tara, S.: Enqudte sur le benzlnisme larv6 chez les ouvriers d'une region industrielle de la grande banlieue de Paris. Sang, 11, 529-534 (1937). Thompson, W. P., Richtdb, M. N., and Edsall, K. S.: An analysis of so-called aplastic anemia. Am. J. Med. Sci., 187, 77-88 (16*4). Ttson, H. H., and Schoenbbbo, M. J.: Changes in the blood and aqueous humor in methyl alcohol inhalation. Arch, of Ophthal., 44, 275-280 (1915). Tzanck, A., Dreytuss, A., and Jais, M.: H6mopathie postbenzolique et leucoblastose medullaire. Sang, 11, 550-556 (1937). Undrxtz, E.: Un cas d'intoxication professionnelle par les vapours de benzine, collophane et huile de lin. Progres m6d., 569-570 (1938). Viguani, E. C., and Giannini: La prevenzione medics dell intosaicazione chronica da benzolo con particulare riguardo alia determinazione dei solfato orinare. Rass. med. App. lavoro in dust., 8, 376 (1937). Zolezzi, G. G.: Richerche in vivo sulla citologia del midello osseo nella intossicazione professionale da benzolo. Med. del lavoro, 88, 202-216 (1937). ST0851 535 BOOK REVIEWS Studio bull' asbestosi nelle manitatTUBE DI AMIANTO. (STUDT or ASBESTOSIS IN THE MANUVAOTUBB OF ASBESTOS.) By Enrico C. Vigliani. Paper. Pp. 74. Ente nas. di Propaganda per la Prev. deg. Infortuni, Turin, 1040 (40 1.) The author surveys briefly the literature and gives a good description of processes in asbestos textile work, especially in 4 facto ries. After some chemical examination of different kinds of asbestos, the results of dust counts made by thermal precipitator and konimeter are quoted. 40% of the particles are under 1 m', dust counts ranged from 110-5300 per cc., being highest in the early stages of the work; in the carding room the count was 300-3300, in the spinning room 80-420, and in the weaving room, 100-2600. In three plants each worker was examined and in the fourth, only those who had worked more than 6 yrs.; altogether 439 persons were included. 350 were x-rayed, 200 of them twice. Most of the workers were women. Among the 160 persons work ing more than 6 yrs., 60% had ooughs, 35% were dyspneic, 27% had slight dulness at the bases of the lungs, and 39% had crep itant rales. The corresponding figures for the 72 persons suffering asbestosis were 82%, 65%, 61% and 70%. Of all the work ers, 9.6% had asbestosis warts, 66% of those who worked more than 6 yrs. had fibrosis, and in the preparation process, 10 of 11. The frequency of asbestosis in creases with the average concentration of inhaled dust. It is remarkable that there was no case of tuberculosis among the workers and no case of pulmonary cancer, although there was one case of malignant lympho-granuloma of the mediastinum. This carefully prepared publication is. accompanied by a large number of valuable illustrations, first of the manufacturing processes, then of the dust, and finally of the roentgenograms of 49 cases of asbestosis in different stages.--L. Teleky. Public health administration in thb unitbd states. By Wilton O. SmiUit. 2d edition. Cloth. Pp. xiv + 563. Mac millan Co., New York, 1940 (53.76). This is a second edition of a book origi nally reviewed 4 years ago in this Journal (Vol. 18, p. 89). The original edition has been enlarged by about 100 pages, brought up to date and materially strengthened. It gives a thoughtful and well balanced view of the field and should be valuable to the industrial hygienist who desires to understand the general public health background of the community in which he works.--C.-E. A. Winslow. Statistical calculation tor bnqinnbbs. By E. O. Chambers. Cloth. Pp. viii + 110. Cambridge University Press, London, 1940. (7 s. 6 d.) The non-mathematioal student or re search worker often experiences difficulty with the calculations involved in even the commoner statistical methods, and he will welcome the appearance of this little book. It is not in any way intended as a textbook on the theory of statistics, and only con tains enough theory to enable the reader to understand and apply the methods de scribed. Its one purpose is to explain 'as simply as possible how the calculations should be performed. Mathematical abil ity on the part of the reader is not assumed; all the calculations described involve the use of arithmetic only. A worked example of each method given is provided, and exer cises with answers are a useful feature. The author has addressed the book chiefly to students of psychology and the other biological sciences, but it should be of great use to any who have to employ elementary statistical methods and many research workers will find it a useful desk book.--T. Bedford. 90 ST0851536 A CHEMICAL AND PHYSIOLOGICAL INVESTIGATION OF ELECTRl ARC WELDING* III. Coated Welding Rods Carey P. McCord,f Gordon C. HarroldJ and Stuart F. Meek$ REVIOUS papers (1, 2) in this of various gases and fumes on animallj P series have cited literature sources and the general pur over a period of weeks were determined under controlled conditions; during the pose of these investigations. Elecetrnictire tinie these substances were arc welding with bare washed rods was quantitatively measured. In addi dealt with in one article (1) showing tion some new features of work were the influences which are common to all provided including blood counts, electric arc welding with metallic methemoglobin determination, x-ray electrodes, while medical situations examination and intraperitoneal in have been emphasized in the second jection. publication (2). The present paper is devoted to Chemical and Physical Data results from similar experimental in The same equipment and method; vestigations in which a widely used of sampling employed in the investiga* coated electrode has been studied. tion on bare rods were used in the Here the general factors encountered present study. The methods of anal in the simpler case of bare rods are ysis were the same when identical, modified, and in addition the prob substances were estimated (1). ability of harmful actions from new Comparisons between the amount chemical agents in rod coatings arise. of "nitrous gases," ozone, CO, Cl For this reason a rod containing only a and iron and manganese fumes found few toxic chemicals in the coating was with bare rods are therefore on an desired. The rod coating chosen was equivalent basis in the two investiga more complex in chemical nature than tions. Approximations were made of we preferred but practical industrial the amounts of silica and Ti02--the considerations dictated its selection. major new components found in the The investigative approach to the coated rods. All exposures in this problems of a coated rod was identical experiment were produced by 44 v. to that for bare rods in that the effects and 300-350 amp. across the arc. * Received for publication February 10, 1941. To be read before the American Indus trial Hygiene Association, May 7, 1941, Pittsburgh, Pa. t The Industrial Health Conservancy Laboratories, Detroit, Michigan. $ Chrysler Industrial Hygiene Labora tories, Chrysler Corporation, Detroit, Michigan. A. Analyses of Electrode, Coating and Fumes The analyses of the rod coating in this investigation is shown in table 1. The analysis of the coating was checked by several observers using 200 ay, iW1 ST0851 537 ELECTRIC ARC WELDING. Ill 201 ious standard colorimetric and vimetric methods. The only dis agreement was in the amount of osphorus which was found only in Taking this into considera'on, the total constituents established uld be reduced by 0.4% to 98.6%, j*in place of the 99.0% reported. However, on the basis of the analyt ical data for airborne dust and fume TABLE 1 yalybis or Rod Coating and Aib-Bokne Fuiu | Aia-aom rtma reported on so that changes in the gaseous and fumous concentrations can be attributed to the effects of the coating on the arc and the added factors resulting from chemicals in the coating itself. B. Gases The quantities of gases evolved by the welding process using coated rods varied greatly from the amounts found TABLE 2 Oxygen and Cabbon Monoxide Concentrations SAMTUHO TOCS oxraasr CO, Mature, organic vola tile matter................ ab,........................... m........................... UdO*......................... %% 1.70 16 min.................. 8:58 20.6 0.22 8.40 Immediately........ 9:13 20.7 0.21 5.40 16 min................... 12:58 21.0 0.20 5.00 Immediately........ 1:13 20.9 0.00 (PO), (PtO.- *0.85%).................. TeiOj..................... 79.00 P' Total........................ 99.5 - Net MgO - 5.9%--used 0.5% MgO With 0.55% POi. "i . in the exposure chamber as shown in table 1, such minor discrepancies as reported in the coating analyses are probably negligible. The components which appeared in the coating are diminished in the fume, presumably because of their inclusion in the slag, and the added iron from the core. The rod itself was found to contain .6% Fe, 0.4% Mn and negligible ounts of other substances as P and (less than 0.05% each). This is pproximately the 6ame composition the bare washed rod previously TABLE 3 Ozone Concentrations, in P.P.M., S.T.P. Of. FBOK ABC 4 at. rmox i*c CBNTBB OF CHAUBBB 2.07 0.72 1.10 0.28 0.36 0.16 when welding with bare rods. The percentages of oxygen were normal (table 2) with no value less than 20% Ojj no excessive COj was found. No CO was detected though small amounts of organic matter were pres ent in the coating. The ozone concentrations (table 3) were less than those found when weld ing with bare rods at 44 v, and 300350 amp. This diminution was most marked close to the arc; while the concentrations near the animals were less than previously noted, they were ST0851538 202 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [vol. tS. no. s of about the same order. It was assumed that the coating on the rod resulted in a shield which protects the 0* from the ultraviolet light, or that the 0* is kept from contact with the available energy across the arc. The decreased amounts present as the distance from the arc increased are mmilar to the decreases noted in the experiments with bare rods except for the variations in quantity. No High TABLE 4 Animal Exposures NOi FmOi tin xroctm TIKI p.p.m. mg/ cu.m. mg/ cu.m. hr. min. 1* 21 446.0 16.5 12 16 2t 31 605.3 21.2 61 20 Low 1* 13 176.0 5.0 12 16 2t 21 292.3 10.1 61 20 Inter- 1* 12 270.0 9.5 21 28 mediate 2t 22 439.4 15.25 107 20 Average 1* 14 290.5 10.1 40t 2t 24 444.1 15.45 2301 * 8:30 a.m. to 9:30 a.m. 19:30 a.m. to 2:30 p.m. J Total. chlorine or chlorides were found at any time in the exposure chamber. "Nitrous Gases." Samples for "ni trous gases" were all taken at the armports as conditions at that point were previously shown (1) to be repre sentative. Table 4 provides a sum mary of conditions which existed during this experiment showing aver age concentrations of 24 p.p.m. of "nitrous gases" always computed as NOj for the 5 hour period and less than 20 p.p.m. of NOj for the first hour of exposure. Comparing this with the average concentrations from bare rod experiments using 44 v. and 300-350 amp. and all conditions the same, shows that this is about one-third the average concentration of 72 p.p.m. for the 5 horn: period and the low for the 8:30 to 9:30 period is also about, one-third of the "nitrous produced. Similarly we have made comparisons between the ratios of nitrites and nitrates in the cases of bare and coated rods (table 5). The ratios show about 4 times the quantity of "nitrous gases" when tested for all nitrates. Three methods were used for the determination of nitrites. The sulfanilic acid method was used in pre vious experiments but neither the brucine method (3) nor the modified phenoldisulfonic method. The phenoldisulfonic acid method employed the same procedure as for total nitrates, except that no oxidizing medium was introduced to convert lower valence products to the higher form. The results should afford some indication of the nitrates present and, by differ ence after oxidation, give a measure of the nitrites. It is believed that sufficient additional evidence is avail able to draw more positive conclusions regarding the composition of the mixture. In our previous work we indicated that NO was probably present near the arc up to 40% but that not more than 12 to 17% of the mixture the animals breathed could be ascribed to this gas. We also showed the increased time factor leading to greater oxidation of the NO and consequent decrease of this gas. It is believed that the pres ent results confirm these findings. rod -350 une,i thg P-m. ' for bout see*'] song and and vtios { of aU the BUlprethe 9 fied aolthe itea was | ;nce rhe ion fer(ure hat ailons the ted the lan ials ;as. me of of es- ST0851539 ELECTRIC ARC WELDING. Ill 203 we accept the usual statement that It the time of formation, neglecting jfoineroufl factors previously men- fr- TABLE 5 | j analtsis or NOi as Nitratxs and Kt1 Nitrites All concentrations in p.p.m. NO*, S. T. P. 5r tub nt jnyaopnro cnni W" NALTXSD A1 BATXO Ni puvw1 irmura trate (> (b)t <0)t m min, after 11.88 2.97 4.58 2.6 f0:60 welding 8.9 2.22 4.12 2.2 14.86 2.96 3.67 4.0 \ Average........ 11.88 2.97 2.69 4.12 2.9 10 min. after 19.38 2.98 5.53 3.5 10:23 welding 19.36 2.97 3.67 6.2 26.79 2.97 6.97 4.5 Average........ 21.84 2.98 2.97 6.05 4.3 '4: min., after 22.53 9.01 6.60 - 10:47 welding 19.47 7.48 6.48 26.95 5.98 6.46 I Average........ 22.98 9.01 6.73 6.48 Iqunediately 31.83 3.03 7.10 Bhe: after 11:13 27.39 welding 21.27 6.08 7.30 7.58 6.56 3.6 3.0 4.1 3.5 4.5 3.7 3.2 Average........ 26.83 3.03 6.83 6.98 3.8 During 11:3a 18.06 3.00 3.79 4.6 welding i'\ 18.17 15.09 3.02 4.20 4.3 4.62 3.72 4.1 A Average........ 17.11 3.00 3.77 3.88 4.4 * Sulfanilic acid and a-naphthylamine. t Brucine. t Phenoldisulfonic acid less hydrogen peroxide. tioned, the diazo reaction multiplied by 2 gives the combined NO* in the form of HNO* and HNO*, we find that the theoretical volume of NO gas varies from 40% of the total imme diately after welding and within 2 feet of the arc to about 25% 16 min utes after. At from 7 to 8 feet from the arc the amounts of NO calculated on the above assumption are from 15% immediately after welding to 10%, 16 minutes after welding. The values obtained while welding indicate that the largest amount of NO a short distance from the arc is 50% and that under the conditions of our experi ments the largest amount of NO breathed by the animals was less than. 20%. While these results obtained TABLE 6 NO* Concentrations in P.P.M., 8.T.P. si s m * < 8oi i< s 3 si M 8 shi 8 iti 8 ift 8 M Immediately after welding............ 17 28 28 33 33 29 27 4 min. after welding............ 26 33 33 34 40 30 29 10 min. after welding............ 18 28 31 24 31 25 25 16 min. after welding............ 7 15 14 15 11 16 20 During welding... 13 30 26 28 20 20 27 under the assumptions mentioned are somewhat higher than those indicated in our former experiments, it must be recalled that these assumptions have been previously criticized by us as leading to errors of various magni tudes. Furthermore these represent maximum quantities which were pres ent for only a short time in the welding cycle. The amounts of unreacted NO the animals breathed over the whole experiment with coated rods was more nearly 12% of the total gas concentration reported as NO*. The actual amount of unreacted NO may well be smaller than we have stated ST0851540 204 JOURNAL OF INDUSTRIAL HYOIENE AND TOXICOLOGY [sol. 33, no. J as we have shown that the factors to be used when converting the diazo reaction representing HNO} to a true value of total NO} are quite variable, ranging from 1.7 to 5 or 6. We have merely attempted to set the top limits to the amounts of unreacted NO that could reasonably be expected in our experiments. The determination of totqi NO} gas appears to be the most regular factor and this is of aid in determining welding exposures (ta ble 6). exists when rods with differing coat ings are employed in the welding process (4). The increased values of manganese are probably due to the Mn content of the coating. This explanation is also tenable in regard to the increased amounts of FetOi but in addition changed physical and chemical conditions immediately about the arc may be significant. As in the case of the bare rod no correlation is evident in the instance of the coated rod between the re- TABLE 7 FeiOi and Mn Concentrations Mgm per cu. meter of air 8:80 A.M. :* a.m. 10:80 A.U. 11:80 A.K. 13:80 r.u. 1:80 pj. 3:80 i 1 s a * S 1 a * 1 1 Immediately after welding........................ 4 min. after welding....... 10 min. after welding___ 16 min. after welding___ During welding.............. 450 17 442 16 262 8 00 2 285 10 615 20 535 19 262 9 232 7 450 16 555 21 585 20 365 12 270 8 525 17 592 21 565 20 330 13 307 10 480 18 615 22 635 21 330 13 262 8 487 17 615 23 620 21 330 12 322 10 450 17 682 650 292 307 577 C. Metallic Fumes The amount of iron fume obtained from the chamber air (table 7) ranged from 90 to 682 mg./cu.m. and 2 to 23 mg./cu. m. for the manganese. These quantities for both substances are considerably higher than in the case of bare rods--about twice as much Fe20* and ten times as much Mn were found. The average amount of manganese in the form Mn was about 16 mg./cu. m. with above 20 mg./cu. m. present for a considerable period of time. These results indi cate that metallic fumes are consider ably increased when coated rods are burned, even though some variation spective values of "nitrous gases" and metallic fumes (table 4). In addition there is such considerable variation from one type of rod to another that no exact conclusions can be reached. When toxic agents are found, other than the gases usually associated with metallic arc welding, such as the manganese as reported for this rod, additional determinations other than NOj must be made if true exposure conditions are to be evaluated. Table 1 includes the presence of SiO} and TiOt in appreciable quanti ties. Corresponding tests were made for the values of these substances in ST085154 I ELECTRIC ARC WELDING. Ill 205 chamber fumes. In both in aces standard laboratory methods applied (5, 6). Only traces of oium were found in the samples air collected to determine the exBynires of animals to various fumes. The only explanations are that th4 methods for titanium were not sensi|ve to the small quantities present, fed the fact that the impinger method Ed not collect the small size particles 0.5 n) which comprised the larger J^rt of the sample. This explanation probably also true for the MgO cjind the CaO. The air borne samples Collected with the electric precipitator for fumes alone gave the check results ihown in table 1. We have reason to believe that most of the titanium 'is found in the welding slag. Silica was found in quantities rang ing from 19.6 mg./cu. m. to 97.5 mg./cu. m. The average value during tiie course of the experiment for 92 samples taken at various times in the welding cycle was 61 mg./cu. m. of air, calculated as SiOi. The exact form in which silicon appears either in the rod coating or in the chamber fumes has not been investigated. Further examinations were carried out for fluorides (7) and lead (8) but both of these substances were absent. Animal Exposure Results Rabbits and albino rats of both sexes were selected from our labora tory stock. A few purchased rabbits were distributed equally between con trol and exposed groups. There was little age variation; all rats, for Sample, were within 20 days of the same age. 24 rats were used in each of the exposed and control groups. 16 rabbits were exposed and the same number maintained as controls. Roentgen ray films were made of all animals at the beginning and end of this experiment. All animals were weighed weekly and subjected to the same diet, care and laboratory environ ment. Complete blood studies were made every 7 to 14 days of a represent ative portion of control and exposed animals. Animals were exposed for 6 hours daily, 5 days per week for a total of 46 days during an elapsed time of 65 days. The exposure chamber temperature was taken at the beginning of each day of exposure, after 2, 4, and 6 hours. Relative humidity was measured less regularly, but in all there were 149 such determinations. The temperature averaged 85.3F at the start of exposure. After 2 and 4 hours' operation of the chamber the temperature averages were respec tively 90.0F and 92.6F, while the average temperature at the close of the exposure day was 92.6F. For these same periods the exposure chamber temperatures exceeded those of the laboratory as follows: 6.9, 8.3, 9.7 and 9.5F. Relative humidity values averaged 56% with 18 out of 149 below 50% and 6 above 70%. Ice was necessary in the chamber for cooling purposes since previous ex perience revealed that temperatures only slightly in excess of the maximum here reported were responsible for some animal deaths. All experimental rabbits survived; one control died. 2 exposed rabbits lost an average of 5.5 ounces while 14 gained an average of 10.2 ounces; the average weight change was a gain of 9.6 ounces. The surviving control rabbits exhibited an average ST 08515U2 '206 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY M. , w ** " weight gain of 12.9 ounces; two lost weight for an average of 3.4 ounces each while 13 gained an average of 14.3 ounces each. 3 exposed rats died, one after the first day of exposure, and the autopsy revealed no gross pathology. Another died after 22 days of exposure. The autopsy disclosed marked siderosis and multiple minute lung abscesses. The third died after 26 days but was not autopsied. The control rats all survived and gained weight for the duration of the experiment with an average of 32 gm. each. The exposed rats gained only an average of 2.9 gm., with 11 losing an average of 8.5 and 12 gaining an average of 13.5 gm. 1 rabbit and 2 rats were sacrificed for necropsy 3 days after exposure ceased and siderosis was found in all, but no significant gross pathology. 1 exposed rabbit died 5 weeks after exposure terminated and at autopsy presented siderosis and lobar pneu monitis. 10 exposed rabbits and 13 exposed rats were necropsied 6 weeks after exposure ended and gross ex amination revealed only siderosis; 1 rat presented multiple lung abscesses, and 3 revealed various degrees of atelectasis. 4 rabbits and 6 rats from the exposed groups, now in apparent full health, are maintained for any late pathologic developments. 7 weeks following the end of the experiment, 5 rabbit" and 6 rat con trols were sacrificed. Among these control rabbits no gross pathology was found. While the same was true of 3 rat controls, two revealed multiple lung abscesses and one showed atelectasis. Adequate tissues from representative animals have been pre served for microscopic inquiry. Roentgen Examinations The roentgenograms made before' and after this experiment revealed no ! significant abnormalities. The fihaj j of rats included the entire animjji yyhile those of rabbits included the head, neck and thorax. The lung' fields were available for study in all instances, as well as teeth and sufficient ' bony structures to detect likely metal] bolic changes due to the action of] metals to the extent that such changes] might occur in adult animals and be" demonstrable radiographically. In, three instances animals were rejected.1 for the purpose of this experiment; because of radiographic appearances! which suggested lung abscesses.' These aniirutlH were autopsied but no' evidence of lung abscesses was found.; Therefore, it is believed that in terpretive errors are conservative/ No roentgen findings from long-ex posed animals have demonstrated any action of welding products. Intraperitoneal Injections 4 groups of 6 rats each were used, for peritoneal injections. 1 control group received physiological saline. Each of the three remaining groups were given injections of one of the following: (a) free silica; (b) ferric oxide; and (c) welding fume particulate matter collected by an electric pre cipitator. Suspensions of these dusts were prepared and injected according to established procedure (9, 10);" albino rats (11) were substituted for?j guinea pigs. Approximately 8 weeks after the,j intraperitoneal injections, these ani-< mals were sacrificed. The animals, j injected with physiological saline pr*. ST0851543 v, 1941} ELECTRIC ARC WELDING. Ill 207 ted no abnormalities. Those inwith ferric oxide and welding dust exhibited inert reactions, group that received the silica ion all presented character- proliferative reactions. .Thus, the particulate matter com- "welding fume," which upon was found to contain about of substance calculated as SiOt, not produce the peritoneal pro`erative reaction characteristic of icant amount of free silica. igration of Iron Pigment in Lung Parenchyn a Previously it has been shown in lental animals that, after exto "welding fume" ceases, iron pigment deposited in lung i migrated through the lymphatics the tracheobronchial nodes (12). ler has reviewed the mechanism ovided for the removal of pigment cm the air spaces of the lung and portation of this material to the cbronchial nodes. The periphatic and lymphoid tissue aculations of pigment particles are Mated to be responsible for the roscopic appearance of the lungs, the extent that the gross appearce of pigmentation is due to lymph oid tissue deposits and provided ade quate lymph drainage exists, the gross pigmentation will decrease gradually ofter exposure ceases. We have been terested in ascertaining how comfete this process is. Accordingly, animals from previous exposures been saved. From a group of having 25 days of exposure to ding fumes, 2 rats were autopsied days after the last exposure, 1 bit after 104 days, 2 rats and 2 rabbits after 232 days, 2 rats and 1 rabbit after 1 year. Out of another group of animals having had 20 days' exposure, autopsies were performed on 1 rat 83 days after exposure, 4 rats and 5 rabbits 94 days after exposure, 1 rat and 1 rabbit after 232 days, and 1 rat and 1 rabbit after 336 days. From examinations of this series of animals, it was found that in all instances tracheobronchial lymph nodes were pigment-laden but the distribution of pigment in lung tissue was much less dense and no longer lobular in outline. In some instances (animals examined 232 days to 1 year after exposure ceased) there were as few as 30 foci of pigmentation grossly visible in a single section of lung tissue. Complete elimination of gross iron pigment from welding fumes from the lungs of laboratory animals appears to be a reasonable expectancy. Blood Studies Complete cytologic studies and hemoglobin determinations were made on a representative number of exposed and control animals before, during and after the period of exposure. The cytology included the basophilic aggregation test and enumeration of erythrocytes and leucocytes. Differ ential leucocytic counts in all instances consisted of percentage determinations of polymorphonuclear neutrophils (seg mented and non-segmented forms counted separately), small and large lymphocytes, monocytes, eosinophils and basophils. Hemoglobin values were obtained by an acid hematin method using Newcomer's standard disc in a B. & L. Duboscq color imeter. The results of this work (111 complete blood counts including ST085154 U 208 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [.of. , w.j hemoglobin determinations) reveal no significant changes in the formed elements of the blood. While there are some variations in hemoglobin these are not sufficient to warrant conclusions. This, as regards ani mals exposed to "nitrous gases" is in keeping with Lehmann's find,ings (14). Methemoglobin "Nitrous gases" have long been known to produce methemoglobin indirectly through the formation of nitrite compounds. This fact prompted a series of determinations for methemoglobin in exposed laboratory animals and practiced welders. Fur ther impetus to this step came from Lehmann's observation (14) of "a considerable amount of methemo globin" in one animal among a total of 20 animals used in his experi ments. For test purposes we adapted a modified spectroscopic method, using the Pulfrich-Zeiss photometer, for this analysis. The narrow absorption band at 630 n is selected for use be cause the difference in transmittance between hemoglobin and methemo globin is greatest at this point and the quantitative absorption of hemo globin is small. The absorption band at 410 fi is not useful and that at 500 /x not as effective as the band at 630 n. The general procedure involves hemolizing the unknown blood by diluting a 0.1 ml. sample to 10 ml. with dilute ammonium hydroxide (1 ml. of concentrated NH4OH per liter). Determine the transmittance of this hemolized blood at 630 n and employ a similarly hemolized sample of "nor mal" (100% Hb) blood as reference. Consult the calibration curve and read direct the percentage concentra,. tion of methemoglobin in the un known blood. With the filters obtainable for use in the Pulfrich-Zeiss Photometer, the 630 n band has a width of about 30 # which is somewhat large but ap parently satisfactory in practice, though it would be preferable to use an instrument having a slit gratiz and band width of 5 fi. To compen sate for some of the errors involved we devised separate calibration curves for both male and female rats and rabbits. These calibration curves were obtained by preparing several hemolized blood solutions which were artificially adjusted to suitable known methemoglobin concentrations. The transmittance of each one was de termined against a reference and the. data plotted on semi-logarithmic paper. Details of Calibration Defibrinate "normal" (100%) blood of known hemoglobin concentration. Divide the sample into 2 parts and dilute one of these to 10 times its original volume with dilute ammonium hydroxide (1 ml. of concentrated NH4OH per liter). Add to this di luted portion 3 drops of a freshly, prepared 10% solution of potassium ferricyanide; this transforms all the hemoglobin to methemoglobin. Mix and make up to 100 times the volume of the original blood with the dilute ammonia to form solution (a). Dilute the remaining portion of the defibrinated blood to 100 times its original volume with the same dilute ammonia to form solution (b). Prepare solutions (al), (a2), (a3) ST085 1545 tyfay, lWl ELECTRIC ARC WELDING. Ill 209 rj,y diluting (a) with distilled water to oncentrations of 70, 50 and 30%. Prepare solutions (bl), (b2), (b3) Pby diluting (b) with distilled water to concentrations of 70, 50 and 30%. Operating at 630 fi and 13 mm. solution depth, determine the trans mittance of (a) with (b) as reference; ;y{al) with (bl) as reference, etc. Form the calibration graph by plotting the determined transmittance Thus, if the artificial methemoglobin solution is, say, representative of 80% methemoglobin blood, it is 20% de ficient in hemoglobin and consequently an 80% hemoglobin reference is nec essary in its examination. Experimental Results Blood samples from 10 male and 11 female rats that had been exposed to welding fumes and gases in the TABLE 8 Mbthbuoglobin Psscxntaozs in Animals (Standard hemoglobin for male and female rabbits, 84.1%. For male and female rats, 94.6% and 92.2% respectively.) Mn nroiiD DATS A>TB IXPOCCU CIAIID 45 (Babbit* H F 41 Rata If F Babbitt If F 4 Bat* If F 14 Rabbit* HF 11 Rat* MF 8.6 4.5 21.7 15.4 2.5 0.6 2.7 0.6 0.5 0.1 4.3 3.1 2.0 0.9 17.5 8.0 3.1 1.3 1.5 2.7 5.5 0.2 3.5 2.1 4.8 2.1 10.4 12.0 3.5 0.7 2.5 0.6 1.7 0.1 1.9 2.5 1.3 5.5 14.7 5.5 1.5 0.5 4.2 0.3 0.3 0.1 2.5 2.4 1.0 3.5 11.5 9.5 3.5 0.3 3.8 0.6 0.0 0.4 1.5 1.5 3.2 1.3 16.0 17.3 0.1 4.2 4.2 0.2 3.3 3.5 16.3 18.5 1.0 0.0 2.5 0.1 2.4 3.3 2.5 10.4 18.0 0.1 0.7 2.3 0.6 3.6 2.7 2.1 13.0 4.5 0.9 3.1 4.5 0.5 3.5 3.0 18.7 5.5 0.8 2.3 0.2 0.1 3.6 2.4 12.6 3.1 1.9 Average 2.7 2.9 15.0 11.2 2.8 0.61 2.6 2.0 1.5 0.2 3.0 2.5 values of the "a" solutions against the corresponding known methemoglobin contents of 100, 70, 50 and 30%. The resulting series of solutions are equivalent to like concentrations of hemolized blood of the same methemoglobin content except that they do not contain the corresponding hemoglobin or cloudiness. It is neces sary then to select as reference a hemolized "normal" blood similarly deficient in hemoglobin and cloudiness. coated rod experiments were taken at the end of the forty-third exposure day. The standard normal hemo globin for a male and 2 female rats as well as the methemoglobin concen trations for these animals are shown in table 8. Methemoglobin concen trations ranging from 21.7 to 4.5% were found, with an average of 15% for the males and 11.2% for the females. 4 days after exposure had ceased the methemoglobin concen- ST085I 5U6 210 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [vol. SS, no. s trations had dropped to a 2.6% average for the males and 2.0% for the females. This methemoglobin concentration was about the same 11 days after exposure had ceased. 16 controls showed a methemoglobin con centration average of 0.98%. This value of approximately 1% can be methemoglobin or error in the method. Assuming that this represents in herent errors, the rats 11 days after exposure would still have between 1 and 2% methemoglobin present according to the data presented. The appearance of high values of 4.2% TABLE 9 Methrmoqlobin ik Maub Rats Rod Wbldino) (Bars 1 DATS bbtobb 1 DAT S DAT AFTBB COKBXBOfUBB xroauBB BXFOBUBB BSBoroma TBOLB CBABBD % *% 0.5 2.4 2.0 3.8 0.6 3.0 0.0 2.1 0.0 1.0 0.4 0.0 % %% 2.3 0.0 0.5 2.4 0.0 0.0 3.5 0.0 1.5 3.1 0.0 1.8 3.6 0.1 3.1 0.2 Average 0.6 2.6 3.0 0.05 0.95 and 3.5% among the male rat controls and one value of 3.5% for one female rat control indicate a small amount of methemoglobin formed from unknown causes with some 1 to 2% of these values ascribable to error. These high values for methemoglobin were in such marked contrast to the majority of the rat controls that the above explanation seems necessary. 6 male and 10 female rabbits ex posed for 45 days gave much lower methemoglobin percentages, the aver age for the males being 2.7% and the females 2.9% at the end of the ex posure period. 6 days after exposure to welding fumes and gases ceased the males showed 2.8% and the. females 0.6% methemoglobin. 14 days after exposure ceased the males' methemoglobin percentage dropped to 1.5% and that of the females to 0.2%. The animals used as controls furnished a general average of 0.6%. The data show that the rats' blood contained high percentages of methemoglobin after exposure to welding fumes and that this methe moglobin largely disappeared within 4 days. The rabbits' blood did not show a large amount of methemo globin and the small amount found was largely dissipated withip 1 week. Since the animals in this experiment were exposed to somewhat less than 24 p.p.m. NOj and the animals in the bare rod experiments were subjected to about 70 p.p.m. NO*, a 3-day exposure experiment duplicating the bare rod experiments was arranged. The average exposure was 70 p.p.m. As seen in table 9 the amount of methemoglobin increased gradually until the experiment stopped. 3 days after exposure ceased the methemo globin dropped back to a negligible percentage. On the basis of these experiments it appears that significant percentages of methemoglobin are created in the blood of exposed labora tory rats whenever there are con siderable concentrations of "nitrous gases'' and that this methemoglobin readily appears within a few hours of exposure. These observations possibly are of some importance since the rabbit is known to be resistant to methemoglobin formation. Inasmuch as our animals previously ELECTRIC ARC WELDING. Ill 211 ;rted on had been subjected to at 70 p.p.m. of nitrous fumes atively for 25 and 20 exposure , methemoglobin determinations made on those animals that had saved. These determinations re- no methemoglobin in the blood any of the animals. It will be ited that none of our values were as i as those reported by MacQuiddy, concentrations in the areas where these men worked did not exceed 13.3 p.p.m. in any case. A typical set of data is shown in table 10. On the basis of the material pre sented it is believed that the determin ation of methemoglobin in workers exposed to "nitrous gases" will present some evidence of exposure to welding fumes. In the absence of other causes NO. *0. 2. ,3 4 '5 '6 7 8 p.p.m. 5.4 2.9 3.9 2,9 5.2 7.6 2.0 10.3 TABLE 10 Welder's Exposure EEMilTI Plant. A By welder's face (#1) 1 ft. from arc By welder's face (#2) 1 ft. from arc By welder's face (#3) 1 ft. from arc 6 ft. from floor 3 ft. from floor laramcooumx % 2.3 #1 welder 2.3 %2 welder 2.6 #3 welder 2.5 Relief welder for the above Plant B 1 4.6 By welder's face in direct path of fumes; 4 ft. from floor. 2 10.6 Approx. 10' above arc in direct path of fumes; 5 ft. from floor. 3 Trace By welder's face; exhaust (canopy type) system appears to remove major part of smoke and fumes; 5 ft. from floor. 4 7.6 Approx. 14' above arc; by welder's face in direct path of fumes; no exhaust; 5 ft. from floor. 5 9.1 Welding at rear right comer inside of body; face high in path of smoke and fumes; 3 ft. from floor. 6 0.0 Outdoors in open. Tollman, LaTowsky and Bayliss (13) in experiments with carbon arc burning where larger concentrations of "nitrous gases" were involved. Methemoglobin in Welders Determinations of methemoglobin in a number of welders showed no values over 3% with the majority averaging 2.5%. The "nitrous gas" of methemoglobin formation the pres ence of any considerable quantity of this substance in an arc welder would suggest exposure. The same probably is true for gas welders. Comment From the foregoing results of animal exposures it may be agreed that formation of methemoglobin and ST085I 5U8 t 212 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [vol. S3, no. S weight loss are the two significant findings. These two possibly are re lated but the extent of any relation ship is not known. Apart from methemoglobinemia, other exposure results should be con sidered in connection with animal weight changes. Roentgenographic examination of animals, chemical anal ysis - of welding fume particulate matter, and intraperitoneal injection of this material all lead to the con clusion that the welding fumes contain too low a concentration of free silica to produce significant lung changes, or any concomitant growth disturbance. Presumably the weight loss is not caused by iron fume because earlier experiments provided exposures of significant amount of iron without comparable weight losses. No sig nificant weight losses occurred among animals of earlier work on exposure to 3 times the concentration of NO* reported here. Through this procedure of exclusion there remain only titanium and man ganese to be considered in connection with growth retardation. In fact the limited observations made by us as to weight changes may not be associated with any particular substance related to arc welding. Of the two substances, titanium has little repute as a danger ous substance. Conversely manganese is a known toxic material with pro tean actions including that of pro moting metabolic dysfunction. At this time, without any other proof, the disposition is to regard manganese as that welding material conclusively requiring further investigation. It is tacitly accepted that the methemoglobinemia herein described results from "nitrous gases" and in percentages as low as 13. This may appear to be at variance with earlier statements that 70 p.p.m. NO* rep resents tolerable atmospheric condi tions for prolonged periods. At present no literature discloses any harmful influence from methemoglobin when the percentage is of the order presented from our human and animal subjects. The work of Lehmann and Hasegawa (14) from which stems most of the threshold standards widely ac cepted in this country and Europe, furnishes positive evidences only from quantities near to 70 p.p.m. and not from 39 p.p.m. as so often quoted. Certain anomalous interpretations of Lehmann's results cause us to cite direct statements in translation from an investigation carried out in part as long ago as 1907. At the same time mention will be made of other pub lications of the same general period not in keeping with the interpretations of Lehmann's studies. The traditionally accepted "39 p.p.m." derives from a sentence in Lehmann's conclusions (not based on any published protocol data) stating that 0.1 mg. nitrous and nitric acid may be tolerated by many men for several hours and that 0.3 to 0.4 mg. always figured as total nitric acid appears to be directly dangerous. These authors state also that the danger point rises rapidly when doses of 0.6 to 1 mg. are given. It is not clear that these figures from nitrous and nitric acid may be associated directly with "nitrous gases" since the lowest concentrations of such gases investigated with animals (with nega tive results) was 0.19 mg. when calculated as total nitric acid. IQ no. 4] ST085I5U9 layi mn ELECTRIC ARC WELDING. Ill 213 of p.p.m. of NO* this is the [equivalent of 74 p.p.m. The lowest r exposure in the three times that 'Hasegawa subjected himself to "ni trous gases" was 62 p.p^m. with 'negative or trivial consequences. A number of their individual experi ments now are cited: In animal experiment 1, 1 cat and 1 rabbit showed "no noteworthy symptoms" during the experiment or ' .after 3 hours and no findings noted at ' autopsy. The concentration during this experiment was 0.19 mg. calcu lated as HNO* or 74 p.p.m. The next lowest concentration was in experi ment 3 where 0.28 mg. calculated as HNO* or about 108 p.p.m. NO* was the exposure for 1 cat and no reaction or after-effects were noted at the autopsy 7 hours after the experiment started. Also in experiment 4, 1 rabbit showed no clear symptoms either during the experiment or at autopsy after being exposed to 0.42 mg. HNO* (163 p.p.m. NO*) for 3 hours. The same results were found when another rabbit was exposed to 0.52 mg. HNO* (200 p.p.m. NO*) for Ij hours. Their first conclusive re sults were obtained in experiments 6, 7 and 8 when a total of 3 cats were subjected to 0.56, 0.58 and 0.6 mg. HNO* respectively for 4J, 5$ and 7$ hours. However they again record no symptoms in experiments 9 and 10 when a rabbit and a cat were exposed for 1 and 1 hour, 50 minutes respectively, each to 0.74 mg. HNO* (287 p.p.m. NO*). No effects were clearly shown in regard to rabbits after 2 hours and 5 minutes when ex posed to 9.66 mg.--a matter of several thousand p.p.m. of NO*. In Hasegawa's experiments on him self scant effects were noted from 62 p.p.m. though he reported irritation to the throat and thirst; no more actual difficulty reported after 60 minutes at from 75 to 100 p.p.m. and lesser concentrations for the next hour. Coughing, irritation of nose and throat, headache, vomiting, etc. were reported but no after-effects following a night of rest after exposure to 158 p.p.m. However, Ronzani (15) who also did some animal work at about the same time found that 50 p.p.m. was without effect for the length of the experiment, 1 month. Ronzani found minimal effects in from 7 to 18 days with 100 p.p.m. Yant (16) on the basis of a critical appraisal of the literature notes that there does not appear to be a logical correlation of response from increasing concentrations. Thus if 105 p.p.m. can be breathed for 6 hours without noticeable symptoms (17) and 105 to 210 p.p.m. is endurable for 30-60 minutes, why is 117-154 p.p.m. (14) hazardous even for a short exposure and 240-275 quickly fatal even for short exposures? Yant also points out that two publications (14, 18) quote 240-775 p.p.m. as quickly fatal even for short exposure while another notes (17) 240-275 p.p.m. for the same condition. A further item of confusion appears in the German publication of Flury and Zemik (17) who credit the 39 p.p.m. figure to Henderson and Hag gard (19) while the latter in their English work only ascribe that figure to Flury and Zernik's compatriots Lehmann and Hasegawa. Hess (17) could find no symptoms after 6 hours' human exposure to 105 p.p.m. Simi- ST085 I 550 214 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY [uoZ. S3, no. 5 laxly the U. S. Bureau of Miues often is quoted as the source of the much bandied "39 p.p.m." in its Technical Paper No. 248 (18). Actually this publication merely includes figures from the original Lehmann and Hasegawa paper as one item in a general table. It should also be noted that Leh mann denies the chronic form of "nitrous gas" poisoning and this is important in removing apprehension concerning the cumulative effect of low concentrations of "nitrous gases." Careful reading of some of these early publications indicates that these authors provided exposures of approxi mately 70 p.p.m. without injurious effects. Our work, instead of denying the accuracy of this preceding work, seems to confirm it. Summary This publication furnishes results on animals exposed to gases and fumes from arc welding with one coated electrode, in a 1000 cu. ft. experi mental chamber. For 6 hours daily (5 days weekly) welding at one-half hour intervals (12 minute duration) was performed at 44 v. and 300-350 amp. To the gaseous and fumous welding products animals (rabbits and albino rats) were exposed 6 hours daily for 46 exposure days in a total of 65 days. In addition to products created by the bare electrode, were the new items, silica and titanium. No results sug gest any injury from either of these agents. Contrary to findings from bare rods, growth rate disturbances were encountered, chiefly in rats for which the cause is unknown. Substantial quantities of methemoglobin were found in the blood of rats. , In our previous animal work, no determinations were made for methemoglobin. Casual repetition of bare rod experiments established prompt methemoglobinemia in rats on the first day of exposure. A limited ' number of production welders were examined at a time when the NOs concentration in the work place was only 13 p.p.m. Methemoglobinemia was established. It is possible that, in the absence of other sources of methemoglobin, the presence of this entity in the blood of welders may indicate exposure to nitrous gases. The quantity of nitrous gases pro duced by uniform electric power in case of the one coated rod investigated is distinctly less than in the case of bare rods at the same power. . Metallic fume in the gassing cham ber is substantially increased when coated rods are employed. This is notably true of manganese fume in the coated rod used. As in the case of bare rod experi ments in which high quantities of nitrous gases were evolved, no evi dence whatever accrued relative to pulmonary edema, severe respiratory tract inflammation or similar findings, traditionally associated with nitrous gas action. We wish to acknowledge the as sistance of Dr. Neal of the In dustrial Health Conservancy Labora tories and F. Macaulay, L. Gordon, T. Markell, G. Collins, E. Plaxton and R. Murphy of the Chrysler Industrial Hygiene Laboratories. Jfai/, 1941] ELECTRIC ARC WELDING. Ill 215 $**$* BIBLIOGRAPHY 1. Habrold, G. C., Mill, S. F., AND McCord, C. P.: A chemical and physiological investigation of electric arc welding. I. Bare, washed weld ing rods. Thxs J., 99, 347 (1940). 2. Meek, S. F., McCord, C. P., and HarroIjD, G. C.: Electric arc welding. The effects of welding gases and fume. J. A. M. A. (in press). 8. Snell, F. D., and Snell, C. T.: Color imetric methods of analysis. Vol. 1. Nitrates by bruoine. 2nd ed. D. Van Nostrand Co., Inc., New York, 1936 (p. 636). 4. Txbbrns, B. D.: Personal communica tion. 6. Willard, H. H.: Elementary quantita tive analysis. 2nd ed. D. Van Nostrand Company, Inc., New York, 1936 (pp. 329-331, 347). 6. Thornton, W. M., Jr.: Titanium. Chemical Catalog Co., New York, 1927 (p. 90). 7. Warren, A. G., Giminghorn, C. T., and Page, H. J.: The chemistry of basic slag. J. Agr. Sci., IB, 516 (1926). 8. Habrold, G. C., Meek, S. F., and Holden, F. R.: A practical method for the rapid determination of lead when found in the atmosphere. This J., 18, 724 (1936). 9. Miller, J. W., and Saters, R. R.: The physiological response of the peri toneal tissue to dusts introduced as foreign bodies. Pub. Health Repts., 49, 80-89 (1934). 10. McCord, C. P., Fleming, R. L., Ainslee, H., and Johnston, J.: The measurement of the harmfulness of dusts for humans through the agency of animal reactions. Surg. Gyn. it Obst., 88,129-137 (1936). 11. McCord, C. P., Frederick, W. G., and Stole, 8.: The toxicity of silicon. J. Lab. & Clin. Med., 98, 278 (1937). 12. Gardner, L. U.: The pathology and roentgenographic manifestations of pneumoconiosis. J. A. M. A., 114, 635-646 (1940). 13. MacQuiddt, E. L., Tollman, J. P., La Towbkt, L. W., and Batlisb, M.: The biological effects of inhalation of carbon arc fumes. This J., 90, 297 (1938). 14. Lehmann, K. B., and Hasegawa: Studien fiber die Wirkung teehnisch und hygienisch wichtiger Gase und D&mpfe auf den Menschen. XXXI. Die nitrosen Gase: Stickoxyd, Stiokstoffdioxyd, jaltpetrige S&ure, Saltpeters&ure. Arch. f. Hyg., 77, 323 (1912-13). 16. Ronzani, E.: Ueber den Einfluss der Einatmungen reizender Gase der Industrien auf die Verteidigungskr&fte des Organismus gegenfiber den infektiven Krankheiten. Ibid., 87, 287-368 (1908). 16. Yant, W. P.: Personal communication. 17. Flurt, F., and Zernik, F.: Sch&dliche Gase. J. Springer, Berlin, 1931 (pp. 158-165). 18. Fieldner, A. C., Katz, S. H., and Kinnet, S. P.: Gas masks for gases met in fighting fires. Bur. Mines Tech. Paper no. 248, 1921 (p. 61). 19. Henderson, Y., and Haggard, H. W.: Noxious gases. Chemical Catalog Co., New York, 1927 (p. 136). ST0851552 Not. 1W\ BOOK REVIEWS 467 in these days, the movements of industries to unusual places may likewise bring them unaccustomed diagnostic questions to an* gwer.--E- L. Middleton. INDUSTRIAL HYGIENE AMO OCCUPATIONAL diseases. Course outline and digest or LEOIUBES GIVEN IN COOPERATION WITH the national conservation bureau. Paper. Mimeoyraphed. Center for Safety Ed., Die. Qen. Ed., New York Unieereity, New York, 1941. This volume presents material of a course in industrial hygiene in 16 lectures given by various specialists: Dr. Greenburg gave the lecture on industrial dust, Dr. Lanza that on industrial health and prevention of oc cupational diseases, Dr. Patty on protective equipment, Mr. Stratton on air sampling and analyses, Dr. Schwarts on occupational dermatitis, Mr. Ficklen on toxic gases, etc. Each lecturer has given his story in a straightforward, well-condensed manner so that the collection makes an excellent primer for newcomers to the field. Besides the references given with each paper, there is a general bibliography for the whole field. The volume might profitably be given to industrial nurses and plant foremen as well as to student or practising physicians un familiar with industrial hygiene problems. --Helen Lawton. Cancer and occupation in Denmark 1936-1939. By Johannee Clemmeeen. Translation by Robert Prater. Paper. Pp. 76. NYT Nordisk Forlag-Amold Busck, Copenhagen, 1941. This study is based on the official records of the Danish National Health Service, which are known to be well kept. It was supported by the Danish Anti-Cancer League, which had 150,000 members. As the population of Denmark about 3) Bullions, approximately 1 person in 23 is a member of the Anti-Cancer League. First come discussions of earlier Danish cancer .statistics, the character of the Danish death certificates and the regional distribution of cancer in Denmark. The yearly deaths from cancer during 1935-1939 were 140 per 100,000 of population. Then follow the classification of male "bread winners" in Denmark according to occupation, with tables and analytic diagrams of the canoer mortality of the different occupation and age groups, general as well as according to sites. The outstanding result of the work "is the low mortality from canoer in agricul ture and the high mortality from that cause in industry, in the age group 46-64," whioh, as the author puts it, "very strongly sug gests that also in Denmark [as in certain other countries] occupation has a bearing on the development of the malignant growths." The significance of these results with respect to prevention of cancer is em phasized and the need of comprehensive statistical studies of canoer, morbidity as well as mortality, in relation to occupation is urged. The normal conditions in Den mark would be especially favorable for the establishment of such a center. "At a first glance it may perhaps seem that this will be a very expensive way of proceeding, but in practice it will be a far shorter way to knowledge about human canoer than the untold costly experiments on animals that are going on the world over, while we neglect the registration of the great, un happy experiment which nature itself is carrying out on our fellow man."-- J. A. M. A. Theory of oocufational therapy fob students and nurses. By Norah A. Haworth and E. Mary MacDonald. Cloth. Pp. 129. Williams & Wilkins Co., Balti more, 1941 ($2.00). This small volume will be a useful guide for persons interested in rehabilitation of ill or injured workmen. The title is mislead ing since there is little of theory in the book, but the practice of occupational therapy is considered in some detail and with a great many practical illustrations. Special kinds of work are suggested for various conditions (mental, cardiac, orthopedic, etc.) as well as work most suitable for men and for women. An appendix supplies illustrations of tools, looms and other equipment neces sary in an occupational therapy depart ment.--Helen Lawton. ST085I 553 VOLUME 13. INDEX TO TEXT AND BOOK REVIEWS (Asterisk denotes book review) Acetic acids, ohloracetic, diohloraoetio Carbon disulfide, poisoning in dogs, clin and trichloracetic, acute oral tox ical, biochemical ana pathological icity of (Woodard et al.)............... 78 study (Lewey and others).............. 415 Acne, occupational, etiology of acne quantitative microchemical-colori (Jones)...................................... :... 290 metric determination of, in air, Adaau, B. M., see Irish, D. D. water, biological fluids (McKee).. 151 Alpers, B. J., see Lewey, F. H. recorder, automatic (White, Calvert) 196 (Amor, A. J.: An x-ray atlas of silicosis. 466 Anthracene and chrysene, carcinogenic effect of, effeot of subcutaneous in- [. jection in rats (Pollia).................... 449 I Asbestosls in manufacture of asbestos, vapors, solubility of m body fluids and tissues (McKee).........23:484,1941. Carbon tetrachloride as industrial haz ard, two cases (Hammes, Jr.)-- 112 Chambers. E. G.: Statistical calcu j study of (Vigliani)........................... 90 lation for beginners..............,........ 90 Chapman, B. M.: Observations on the [Barnes, B. C., and Spelcher, H. W.: The effect of paint on the Iddqeys with particular reference to the role of !' dropping mercuryelectrode for turpentine....................................... 277 ! lead analysis.................................... 397 Clarke, B. G., and Moffet, C. B.: Silico Belknap, B. L.: Reply to. Dr. Kehoe's sis in soft coal miners.......... ......... 176 criticism........................................... 161 Chloracetic acid, acute oral toxicity of CBelief, S., see Lewey, F. H. Benzene, absorption, distribution and (Woodard et al.)............................. 78 Chrysene, carcinogenic effect' of an elimination of bv body tissues and fluids of exposed dogs (Schrenk et : al)................................................... and homologs, facts and reflections on pprroobblem of poisoning by (Schwarz, Teleky). recovery following exposure to (Goldwater, Tewksbury).......................... vapor, effects of inhalation of on red blood cells of rabbits (Robinson, Climenko)..................................... Berkelhamer, L. H.: X-ray diffraction, an important tool in pneumoconio sis research and a new method of thracene and, effect of subcutane 20 ous injection in rats (PolHa)........ 449 Clemmeaen, J.: Cancer and occupa tion in Denmark, 1935-1939 ............ 457 Cllmenko,D. R., see Robinson, E. J. Collier, H. E.: Outlines of mdqstrial 217 medical practice............................... 127 Compensation, workmen's, accidental injuries and medico-legal aspects 232 of (Kessler).......................... _.........412 workmen's, of occupational diseases (Teleky)........................................... 353 Creskoff, A. J., see Lewey, F. H. tissue analysis................................. 163 ' Boyd, L. J., see UcGavack, T. H. Boyd, M. F. : Preventive medicine___ 63 Brahdy, L., and Kahn, S.: Trauma and disease............................................... 454 Deichmann, W.: Toxicity of methyl, ethyl and n-butyl methacrylate... 343 Dlchloracetic acid, acute oral toxicity of (Woodard et al.)............................. 78 Diseases, occupational, industrial hy Brleger, H.: The effects of carbon di giene and, course outline and digest sulfide on the blood corpuscles___388 of lectures........................................ 457 of workers (Ramazzini)..................... 52 Calvert, W. R., see White, B. E. Calvery, H. O., see Woodard, G. Cancer and occupation in Denmark, 1935-1939 (Clemmeaen)................... 457 carcinogenic effect of anthracene and chrysene, effect of subcutaneous in jection in rats (Pollia)................... 449 Carbon arc fumes, filtered, and oxides of nitrogen, inhalation of (Toll man, MacQuiddy, 8chonberger)... 269 Carbon disulfide, effects of on blood trauma and (Brahdy, Kahn).........454 Drabkin, D. L., see Lewey, F. H. Drinker, P., see Tebbens, D. B. Dudley, H. C., and Miller, J. W.: Toxi cology of selenium. VI. Effects of subacute exposure to hydrogen selenide............................................. 470 Dust counting, microproiection screen (Williams, Silverman)..................... 452 counting, modified eyepiece microm eter for (Harris)............................... 148 sampling, portable unit (Silverman, corpuscles (Brieger)........................ 388 Thomas)........................................... 252 493 ST0851554 494 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY Ege, J. F., Jr., tee Elkins, H. B. ass Pinto, S. S. Bhrlch, W. E., tec Lower, F. H. Elkins, H. B., Ego, J. F.. Jr., and Roo tslo, B. P.: Evaluation of the lead hazard: urinary vs. atmospheric lead.................................................. 266 see Pinto, S. S. tee Storlazzi, E. D. Enzer, N., tee Simonson, B. Exhaust hoods, lateral, design of, for tanks, (Silverman).......................... 187 Fatigue, effect of rest pauses in atom and sitting position on efficiency o! muscular work (Simonson, Enzer) 106 of central nervous system, fusion fre quency of ffioker test for (Simon son, Enzer).......... ........................ Flnlayson, A. I., tee MacQuiddv, B. L. Fischer, L~.ee Smyth, H. F., Jr. Fllnn, R. H., Neal, P. A., ana Fulton, w. B.: Industrial manganese poi soning.. ........................................... 374 Frank, J. H., tee Lewey, F. H. Fuller's earth, severe pneumoconiosis caused by inhalation of (McNally, Trostler).......................................... 118 Fulton, W. B., tee Flinn, R. H. Fusion frequency of flicker test for fa tigue of central nervous system (Simonson, Enzer).......................... 83 Gas sampling, portable unit (Silverman, Thomas)................................. 262 Gasoline, as diluent, spray painting with, study of hazards involved (Sterner).......................................... 437 Gerontology, request for information.. 50 Glycols and derivatives, single dose toxicity of (Smyth, Jr., Seaton, Fischer)........................................... 259 Goldwater, L. J., and Tewksbury, M. H.: Recovery following exposure to benzene (benzol)........................ 217 *Gray, R. N.: Attorneys' textbook of medicine.......................................... 491 Groom, J. J., see von Haam, E. *Haldane, J. B. S.: Science and every day life............................................ 91 Halley, J. W.: Atmospheric concentra tion of lead fume associated with forging, welding and oxygen cutting of lead bearing steel, based on ex perimental studies.......................... 100 Hammes, E. M., Jr.: Carbon tetra chloride as an industrial hazard. .Report of two cases...................... 112 Hauls, W. B.: A modified eyepiece micrometer for use in dust counting 148 Harrold, G. C., see McCord, C. P. Haworth, N. A., and MacDonald, E. M.: Theory of occupational therapy for students and nurses............... 457 Hydrogen selenlde, effects of subacute exposure to (Dudley, Miller).......... 470 Hygiene, industrial, and occupational diseases, course outline and digest of lectures..........................................457 Injuries accidental, medico-legal as pects of wprkmen's compensation (Kessler).,.................................. 412 Irish, D. D., Adams, B. M., Spencer, H. C., and Rowe, v. K.: The chemical' changes of methyl bromide in the animal body in relation to its physiological effects..........................40g Jacobs, M. B.: The analytical chem istry of industrial poisons, hazards ana solvents...................................... 413 Jonas, L., tee Lewey, F. H. Jones, A. T.: The etiology of acne with special reference to acne of occu pational origin................ 260 Kahn, S., tee Brahdy. L. Kammer, A. G.: Studies of workers ex posed during the production of lead bearing steel (Ledloy)..................... 83 Kehoe, R. A.: Note on "Studies of the lead hazards in certain phases of printing"......................................... 169 Kessler, S. H.: Accidental injuries. The medico-legal aspects of work men's compensation and publio liability........................................... 412 Kidneys, effect of paint on, and role of turpentine (Chapman)................... 277 Lam S. W., tee Woodard, G. La irsky, L. W., MacOulddy, E. L., and Tollman, J. P.: The toxicology of oxides of nitrogen. I. Toxic concentrations................................ 129 tee MacQuiddv, E. L. see Tollman, J. P. Lead analysis, dropping mercury elec trode for (Barnes, Speicher)........ 397 bearing steel (Ledloy), studies of workers exposed during produc tion of (Kammer)........................... 93 concentration, urinary, and bloodlead clearance (Pinto, Elkins, Ege). 313 fume, atmospheric concentration of, associated with forging, welding and oxygen cutting of lead bearing steel (Halley).................................. 100 hazard, evaluation of. urinary vs. atmospheric lead (Elkins, Ege, Ruotolo).......................................... 256 hazards in printing, note on paper by Belknap (Kehoe)............................ 160 hazards in printing, reply to Dr. Kehoe's criticism (Belknap).......... 161 Leather manufacture, modern prac tice (Wilson)................................... 412 Ledloy, atmospheric cVoUnUcDeCnmtirifatUtiUoUnOs oVf lead fume asBsoociated with forigi'ng, welding and 0sxygen cutting oflead bearing steel (Halley)................... 100 lead bearing steel, study of workers exposed during production of (Kammer)........................................ 93 ST085I 555 INDEX TO TEXT AND BOOK REVIEWS 495 Lewey, F. H., Alpers, B. J., Bellet, S., Neal, P. A., tee Flinn, R. H. Drabkin, D. L., Bhrtch, W. B., Neal, T. A., tee McCord, C. P. Frank,T. H., Creskoff, A. J., Jonas, Nelson, SL. W., tee Woodard, G. L., McDonald, R., Montgomery, B., Nervous system, central, fatigue of, and Relnhold, J. G.: Experimental fusion frequenoy of flicker test for chronic odrbon disulfide poisoning (Simonson, Enser).......................... 83 in dogs. A clinical, biochemical Nitrogen, oxides, inhalation of filtered and pathological study................... 415 carbon arc fumes and (Tollman, MacQuiddy, Sohonberger).......... 289 'McCord, C. P., Harrold, G. C., and oxides of, toxicology (La Towsky et Meek, S. F.: Chemical and physio al.)......................................129, 134, 141 logical investigation of electrio arc welding. III. Coated welding rods.................................................. 200 Meek, S. F., and Neal, T. A.: Phenyl mercuric oleate, skin irritant prop* ertiea................. 466 , MacDonald, B. M., im Haworth, N. A. McDonald, sm Lewey.F. H. i McGavack, T. H., Boyd, L. J., Picdone. F. V., and Terranova, R.: Acute and chronic intoxications with sodium pentaohlorophenatein rabbits____239 McKee, R. W.: A quantitative micro chemical colorimetric determina- ton of carbon disulfide in air, water and biological fluids......................... 151 Solubility oi carbon disulfide vapor in body fluids and tissues 23:484,1941. McNsUv, W. D.: Acute silicosis............ 45 andTrostler, I. S: Severe pneumoco niosis caused by the inhalation of fuller's earth..................................... 118 MacQulddy, B. L., La Towsky, L. W., Tollman, J. P., and Finlayson, A. I.: Toxicology of oxides of nitrogen. II. Physiological effects and symp tomatology....................................... 134 tee La Towsky, L. W. tee Tollman, J. P. Maniranese poisoning, industrial (Flinn, Neal, Fulton)..................... 374 `Medicine, attorneys' textbook of (Gray}.............................................. 491 * `industrial, outline of practice (Col Paint, effect of on kidneys, and role of turpentine (Chapman).................... 277 Painting, spray, with gasoline as dilu ent, study of hazards involved (Sterner).......................................... 437 Patty, F. k., tee Schrenk, H. H. Pearce. S. J.. tee Schrenk, H. H. Pentachloropnenol, acute and chronic intoxications with sodium penta chlorophenate in rabbits (McGavack et al.)...................................... 239 Phenyl mercuric oleate, skin irritant properties (McCord, Meek, Neal). 466 Plccione, F. V., tee McGavack, T. H. Pinto, S. S., Blklns, H. B., and Ege, J. F., Jr.: Renal excretion of indus trial chemicals. I. Urinary-lead concentration and blood-lead clear ance................................................... 313 Pneumoconiosis, severe, caused by ful ler's earth (McNally, Trostler)___ 118 x-ray diffraction in research on, and method of tissue analysis (Berkelhamer)............................................. 163 `Poisons, industrial, and solvents, ana lytical chemistry of (Jacobs)......... 413 Pollia, J. A.: Investigations on the possible carcinogenic effect of an thracene and chrysene and some of their compounds. II. The effect of subcutaneous injection in rats___449 `Poverty and progress (Rowntree)........ 490 lier).................................................. 127 preventive (Boyd)............................ 53 `Ramazzlnl, Bemardinl: Diseases of Meek, S. F., tee McCord, C. P. workers.............................................. 52 Mercury electrode, dropping, for lead analysis (Barnes, Speicher)............ 397 urinary, in occupational exposure and from absorption from mercurybearing dental fillings and anti septics (Storlassi, Elkins).............. 459 Methacrylate, methyl, ethyl and n-butyl, toxicity of (Deichmann).. 343 Methyl bromide, chemical changes in body (Irish et al.).......................... 408 Micrometer, eyepiece, modified, for use in dust counting (Harris)............ 148 Microprojection screen (Williams, Sil verman)........................................... 452 Miller, J. w., tee Dudley, H. C. Miners, coal, soft, silicosis in (Clarke, Moffet)............................................. 176 Mo&et, C. ., see Clarke, B. G. Montgomery, B., tee Lewey, F. H. Reid, A. C.: The control of tuberculo sis. III. Management of the em ployee with tuberculosis................. 35 Relnhold, J. G., tee Lewey, F. H. Rest pauses, short, in standing and sit ting position, effect on efficiency of muscular work (Simonson, Enzer). 106 Robinson, E. J., and Climenko, D. R.: Effects of the inhalation of benzene vapor on the red blood cells of rab bits................................................... 232 Rowe, V. K., tee Irish, D. D. Rowntree, B. S.: Poverty and prog ress................................................... 490 Ruotolo, B. P., tee Blklns, H. B. Sayers, R. R., tee Schrenk, H. H. Schonberger, S., tee Tollman, J. P. Schrenk, H. H., Yant, W. P., Pearce, `Munitions workers, health and effi S. J., Patty, F. A., and Sayers, R. ciency of (Vernon)........................ 52 R.: Absorption, distribution and ST085I 556 490 JOURNAL OF INDUSTRIAL HYGIENE AND TOXICOLOGY elimination of benzene by body tissues and fluids of dogs exposed to benzene vapor................................. 20 Schwarz, B., and Teleky, L.: Some facts and reflections on the problem of poisoning by benzene and its homo logs................................................... 1 Science and everyday life (Haldane).. 91 Seaton, J., tee Smyth, H. F., Jr. Selenium, toxicology of. VI. Subacute exposure to hydrogen selenide (Dudley, Miller)............................. 470 Silicosis, acute (McNally)................... 45 in soft coal miners (Clarke, Moffet).. 176 x-ray atlas of (Amor)....................... 455 Silverman, L.: Fundamental factors in the design of lateral exhaust hoods for industrial tanks......................... 187 and Thomas, T. R.: A portable sampling unit.................................. 252 tee Williams, C. R. Simonson, B., and Enzer, N.: Effect of short rest pauses in standing and sitting position on the efficiency of muscular work................................. 106 and Enzer, N.: Measurement of fu sion frequency of flicker as a test for fatigue of the central nervous system, Observations on laboratory technicians and office workers........ 83 SUn diseases, etiology of acne (Jones). 290 irritant properties of phenyl mercuric oleate (McCord, Meek, Neal)......... 466 Smyth, H. F., Jr., Seaton, J., and Fischer, L.: Some pharmacological properties of the ''Tergitol" pene trants............................................... 478 Seaton, J., and Fischer, L.: The single dose toxicity of some glycols and derivatives....................................... 259 Sodium pentachlorophenate, acute and chronic intoxications with, in rab bits (McGavack et al.).................... 239 Solvents, industrial, and poisons, ana lytical chemistry of (Jacobs)......... 413 Spelcher, H. W., tee Barnes, E. C. Spencer, H. C., see Irish, D. D. Statistics for beginners (Chambers)... 90 Steel, lead bearing, atmospheric con centration of lead fume during forging, welding and oxygen cut ting of (Halley)............................... 100 lead-bearing, (Ledloy), studies of workers exposed during produc tion of (Kammer)........................... 93 Sterner, J. H.: A study of hazards in volved in spray painting with gaso line as a diluent.............................. 437 Storlazzl, E. D., and Elkins, H. B.: The significance of urinary mercury. I. Occupational mercury exposure. II. Mercury absorption from mer cury-bearing dental fillings and antiseptics....................................... 459 Tebbens, B. D., and Drinker, P.: Venti lation in arc welding with coated electrodes......................................... 322 Teleky, L.: The compensation of occu pational diseases............................. 353 tee Schwarz, B. Terranova, R., tee McGavack, T. H. Tewksbury, M. H., tee Goldwater, L. J. Therapy, occupational for students and nurses, theory of (Haworth, MacDonald)..................................... 457 Thomas, T. R., tee Silverman, L. Tollman, T. P., La Towaky, L. W., MacQulddy, E. L., and Schonberger, S.: The toxicology of oxides of nitrogen III. Gross and histological 141 MacQulddy, E. L., and Schonberger, S.: Inhalation 01 filtered carbon arc fumes and of oxides of nitrogen. 269 tee La Towsky, L. W. tee MacQuiday, E. L. Trauma and disease (Brahdy, Kahn).. 454 Trichloracetic add, acute oral toxicity of (Woodard)................................... 78 Trostler, I. S., tee McNally, W. D. Tuberculosis, control of, III. Man agement of tubercular employee (Reid)............................................... 35 Turpentine, effect of paint on kidneys and role of (Chapman)..................... 277 Ventilation, design of lateral exhaust hoods ror tanks (Silverman).......... 187 in arc welding with coated electrodes (Tebbens, Drinker)......................... 322 Vernon, H. M.: The health and effi ciency of munition workers............ 52 Vigilant, S. C.: Study of asbeatosis in the manufacture of asbestos......... 90 von Haam, E., and Groom, J. J.: The pathology of shielded arc welding.. 55 Welding, arc, shielded, pathology of (von Haam, Groom)....................... 55 arc. with coated electrodes, ventila tion in (Tebbens, Drinker)............. 322 electric arc, with coated welding rods, investigation of, Pt. 3 (McCord, Harrola, Meek)................................. 200 White, B. E., and Calvert, W. R.: An automatic carbon disulfide recorder 196 Williams, C. R., and Silverman, L.: A microprojection screen................... 452 Wilson. J. A.: Modern practice in leather manufacture....................... 412 Wood preservatives, phenyl mercuric oleate skin irritant properties (Mc Cord, Meek, Neal).......................... 466 Woodard, G., Lange, S. W., Nelson, K. W., and Calvery, H. C.: Acute oral toxicity of acetic, chloracetic, dichloracetic and trichloracetic acids................................................. , 78 Work, muscular, effect of rest pauses in standing and sitting position on efficiency of (Simonson, Enzer)---- 10 niosis research, method of tissue analysis (Berkelhamer).................. 163 Yant, W. P., tee Schrenk, H. H.