Document 3J0MwXxEVQrmOnjpnzyyoD1n3

FILE NAME: Union Carbide (UC) DATE: 1956 June DOC#: UC337 DOCUMENT DESCRIPTION: Journal Article - Improved Communication Hygienic Standards for Daily Inhalation - Donald E. Cummings Memorial Lecture The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. ft ft l i E ill ems. Its line :te--was deitry's toughsitators, dy esters. And actical solu more knowlist problems 1 it over to nent backed nswers. Call IR iet - ' ' 4 \ r .,, \'t}' F k i r ilte r c. 8, Kentucky Montreal, P. Q. Industrial Hygiene ASSOCIATION Quarterly VOLUME 17. NUMBER 2 JUNE, 1956 Plaintiffs ^ Exhibit /J 110681 ;HNEL, Consultant xperience in 3ALTH, AIR AND TION PROBLEMS Central Station >, New York Amaica 9-2438 \L HEALTH SAFETY SERVICE , Detroit, Michigan f 1-4812 ind ve., Royal Oak, Mich, a 2-9569 lARROLD, PH.D. Meek, M.D. SSOCIATES ngs for JLTANTS and .VICES in al H ygiene UARTERLY AM ERICAN INDUSTRIAL HYQIENE A SS O C IA T IO N Volume 17 JU N E, 1956 Number 2 I mproved Communication---Hygienic Standards for Daily I nhalation . . Henry Field Smyth, Jr., Ph.D. A D ir e c t M eth o d fo r t h e C o l le c t io n a n d D e t e r m in a t io n o f M icro Amounts of Benzene or T oluene in Air ...................................................... P. A. Maffett, T. F. Doherty, and J. L. Monkman G r o u n d L e v e l C o n t a m i n a t i o n f r o m S t a c k E f f l u e n t s ............................................... P. B. Klevin, M. S. Weinstein and W. B. Harris P r o b l e m s i n C a l ib r a t io n o f I n d u s t r i a l H y g i e n e I n s t r u m e n t s ....................... Elgin D. Sallee and Robert H. Miller A i r P o l l u t io n M e t h o d o l o g y .............................................................................................................. W. C. L. Hemeon. T h e T o x i c i t y o f t h e V a p o r s o f A r o c l o r 1242 a n d A r o c l o r 1254 ............. J. F. Treon, Ph.D., F. P. Cleveland, M.D., J. W. Cappel, and R. W. Atehley Radiation P rotection--I nsurance and I ndustrial Relations A spects . . Charles R. Williams, Ph.D. D e t e r m i n a t io n o f A c e t i c A c id i n A i r .................................................................................... Franklin Miller, Richard Seherberger, Henry Brockmyre, and David W. Fassett, M.D. I ndustrial H ygiene U nits in I ndustry ............................................................. A Survey by the AIHA Development Committee H y g ie n ic G u id e S e r ie s ........... '.................................................................................... President's Pa g e .......................................................................................................... S e l e c t e d T i t l e s a n d A b s t r a c t s ........... : .......................... .............................................................. N e w s o f t h e L o c a l S e c t i o n s .......................................................................................... ................ AIHA O f f i c e r s , D ir e c t o r s a n d C o m m i t t e e s ..................................................................... 129 186 189 193 197 204 214 221 225 229 236 237 238 240 American I ndustrial H ygiene A ssociation Quarterly, published by th e A m erican In d u s tria l H y g ien e A s sociation in M arch, J u n e, Septem ber, an d December. H oward N . Schulz, E d ito r; H errert J . W erer, Advisory j E d ito r; Lloyd E . Gordon, A ssociate E d ito r; J ames A . Martin, A dvertising E d ito r; P aul D. Halley, C ir * ' culatlcm Editor; A . D. Cloud, Publisher; DorIs F lournoy, E ditorial A ssistan t. 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The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law.' old easily to the e a r c a n a l, it is end valuable time sonnel. r from explosions, ghest attenuation, make FLENTS dis- ANCE COMPANIES erves to rS held ; 1927! r firm and employees, ENTS, without delay! iwn plant, es today. NEW YORK 17, N.Y f Improved Communication --HYQIENJC STANDARDS FOR DA/LY INHALAT/ON- *76e "Dettafat & . Tttetnaxicil ^e c tw te H EN RY FIELD SMYTH, JR., Ph.D. Mellon Institute and Union Carbide and Carbon Corporation Pittsburgh, Pennsylvania Ex p e r ie n c e convinces us that we humans are unique in the universe. Because of our 'ability to communicate, we may be well on the way toward emerging into a hew level of biological existence. Each individual may eventu ally share completely all past and present experiences of the species. Each may act in con cert with his fellows toward common ideals and goals, still retaining his own individuali ty. Real progress in this di Henry F. rection has been made during the past ten thousand years through developments of recording, duplicating and retrieval tech niques. Despite brief back-sliding, there has furthermore been real spiritual progress, and an increase in the proportion of men of good will. The next ten thousand years should, bring substantial achievements in communication upon higher levels, perhaps even through inarticulate contact of mind with mind. There are hints that what some have called the world mind may come into being before the present human species evolves physically into whatever new species its body is tending toward. However, until the world mind develops, we are forced to depend upon more prosaic means of communication. Not so many gen erations ago, a natural philosopher like Presented a t the Seventeenth A nnual Meeting of the American I ndustrial H ygiene Association, Philadelphia, A pril 25, 1966. , Roger Bacon, whom today we call a scientist, could live a full life investigating the-se crets of nature, feeling no need and finding no opportunity to communicate his discoveries and his conclusions to a living soul. He could bury his achievements in code, making them difficult for posterity to unravel. We do not have such people and such situations to day. Each one of us benefits Smyth, Jr. from the current division of labor, of experience, and of knowledge. Each one of us is a unique specialist, depending upon a multitude of other unique specialists for the achievement of our aims, for our very existence. If noth ing else motivates us, simple self-interest should dictate that each one of us ought to make public all that he has learned, in order that his fellow specialists may use it to help us all. Communication y e a r a g o Sterner (1955) expressed the situation in more concrete terms. We comprise persons separately trained in high ly specialized fields, led after training to cooperate in the common aim of providing means by which technological developments in occupation may be utilized in a manner compatible with complete health. He said, "We must provide a fluid and effective means of communication between the chem ist, the engineer, the physicist, the toxicolo- The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. I* " I ll1 n ISO . June-, 1956 gist, the physician, and the other special ists brought into industrial hygiene. There must result from this interchange of ideas not only an appreciation of each team mem ber's contribution, but an ability actually to bridge the gap between the disciplines, to synthesize, from the offerings of each of the fields, the solutions to the ever more com plicated problems. Each member specialist must not only contribute the information he is most qualified to give, but also must en courage a sympathetic, intelligent, and mu tual understanding." In this matter of mutual understanding, we are very much like the inhabitants of Looking Glass Land. You remember that the White Queen told Alice, "Now here, you see, it takes all the running you can do, to keep in the same place. If you want to get somewhere else, you must run at least twice as fast as that." With the entry of new people into our profession and the recogni tion of new constituent specialties such as health physics and atmospheric pollution control, each with a tendency to keep to it self, are we running fast enough even to stay in the same place? We all feel there are too many conferences and too many com mittees to leave us time to do our daily work. On the other hand, if we are to do our work as well as it can be done, we must be in constant communication with related spe cialists, because each one of us fully knows only one facet of his own problems. Communication is not a simple process. It requires an informed speaker or writer who can express himself at the level of compre hension of his audience. It requires an audi ence which wishes to receive communica tion. It must be carried on with words, those abstract symbols for reality, each of which has a different meaning to each in dividual, shaded by his entire past experi ence. Only a newly coined word is free from ambiguity, and it remains new for only a brief interval. Most important of all, suc cessful communication requires what is to ' day known as feed-back. By this, the speaker hears his audiences' impressions. He can correct and amplify his words until he thinks his audience truly perceives his mean ing. A leisurely conversation can be effective communication through feed-back; an arti cle in a journal is likely to be poor communi ' cation because feedback is inadequate. The relatively new specialty of industrial toxicology has already contributed to the equally new profession of industrial hy giene by means of communication. The toxi cologists are doing an acceptable job for those people who recognize their need for toxicological information and opinion. The job could be done better, but it is at least ac ceptable. Success is by no means as great in helping those people who do not recognize their need for help. Once more communica tion cannot succeed unless the audience de sires to receive communication. Acceptable Concentrations 'T'HE MOST important communication withA in industrial hygiene, and between our profession and others, may be the collection of judgments upon acceptable concentra tions of contaminants in working atmos pheres. During what may be called the age of chaos, every experienced industrial hy gienist had a few values uniquely his own, drawn from his own experience. For less familiar substances, he borrowed more or less judiciously from the values cherished by his professional colleagues. Some degree of unanimity was brought about when the United States Public Health Service values, based on its long-time collective experience in industrial hygiene, were published in a manual (USPHS 1943). Further unanimity followed publication of the values collected and extended by Cook (1945). In 1947 the American Conference of Governmental In dustrial Hygienists published its first list in the Industrial Hygiene Newsletter (ACGIH 1947). In the next two. years (ACGIH 1948, ACGIH 1949) revised lists were privately circulated to the members of the Association. Then (ACGIH 1950) pub lication took place in a scientific journal, and each year thereafter a revised list of threshold limit values has appeared in the scientific literature, and has been general ly accepted. The contributions of Cook (1945) in uni fying opinion, and in weighing threshold limit values then in use, judging new data and proposing a list of 129 values, are worthy of high regard. Among the 238 values for substances other than mineral dusts in the current list (ACGIH 1956) o f , established and tentative threshold limit values are 54 of those which were first pro- The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. June, 1956 specialty of industrial dy contributed to the ion of industrial by1 ' mmnication. The toxian acceptable job for cognize their need for vtion and opinion. The ter, but it is at least acby no means as great .le who do not recognize Once more eommunicaunless the audience demunication. rations at communication with;iene, and between our -s, may be the collection i acceptable concentra nts in working atmos.t may be called the age jerieneed industrial hy-alues uniquely his own, vn experience. For less he borrowed more or >m the values cherished colleagues. Some degree brought about when the ic Health Service values, ime collective experience me, were published in a 943). Further unanimity n of the values collected ook (1945). In 1947 the nee of Governmental In s published its first list il Hygiene Newsletter In the next two. years DGIH 1949) revised lists ulated to the members of hen (ACG1H 1950) pub e in a scientific journal, sreafter a revised list of dues has appeared in the e, and has been general- ns of Cook (1945) in uniid in weighing threshold in use, judging new data list of 129 values, are regard. Among the 238 inces other than mineral ent list (ACGIH 1956) of tentative threshold limit .hose which were first pro- Industrial Hygiene Quarterly 1S1 posed in Cook's list, some as definitely es tablished, others to be used cautiously until verified by actual experience. Not since Cook has anyone published a summary of the data which serve as bases for the selection of specific threshold limits. The privately circulated documents which give some of these data (ACGIH 1953b, 1954b, 1955b) cannot be considered to be publication, although they are freely avail able to any person. Threshold limits are, and must continue to be the products of judgment, important if true. Some few truly represent their defi nition and are approximations of the maxi mum concentrations which can be inhaled continuously and repeatedly without injury to health. These may possibly be fit para meters for incorporation into codes and regulations. Many of the threshold limits are well below concentrations which can in jure health. They represent current judg ment as to concentrations to which, good practice dictates, men may be expected to subject themselves. These do not seem fit parameters for regulations. In a particular operation, if possible, it is desirable to maintain concentrations below the bench mark by reasonable ventilation and precau tion. It is always best to reduce exposure to chemicals to the lowest practical level. Three other suggestions of the Commit tee on Chemical Agents deserve reiteration and discussion. It was urged that the bases for the selection of each value should be published, that the name should be changed to hygienic standard, and that the particular concept of permissible human response be hind each value should be clearly indicated. There is such a multitude of factors in volved in the protection of health in our complex civilization that no one person or group of persons is competent to weigh them all with assurance. No oracular or ex cathedra statement on health deserves seri ous attention. Only when the facts upon which a decision are based are furnished for general scrutiny .and evaluation can the de cision be considered even tentatively sound, and only after there has been adequate op portunity for criticism and modification can it be considered established. All toxicologi cal facts should be published, and all de cisions upon the facts should be accom panied by a summary of the reasoning under which they were derived, before any one should be expected to act upon the de cisions. Any publication of standards for maintenance of health ought to include ref erence to the underlying data. The second suggestion referred to the name by which the values are known. Sem antics is more than a sport for the idle. No Previous Suggestions tor Improvement matter how thoroughly a concept is origi Touring the Ninth Annual Congress on Industrial Health, the writer was chair man of the Committee on Chemical Agents (1949). The report of the 16-man commit tee devoted considerable attention to prais ing the development of threshold limits, and to suggesting ways in which their presenta tion could be made more useful. Since that report, two developments have taken place along lines desired by the Committee. The annual table of the Threshold Limits Com mittee of the American Conference of Gov ernmental Industrial Hygienists is now pub lished in the Archives of Industrial Health, removing the earlier implication of quasi legal status arising from its appearance in the Industrial Hygiene Newsletter of the Division of Industrial Hygiene, U.S. Public Health Service. In 1954,. the Committee on Threshold Limits of that Association began to supplement its table of accepted values with a list of tentative values. ' nally presented, it always becomes known | and referred to by a brief name, a catch word. Most persons who learn of the con cept hear the catch-word name, and do not go back to the original presentation. The meaning they attach to the name comes from their previous experience with the particular words. It may be, but is usually not, exactly what the originator of the idea intended. The more carefully one chooses the name he assigns to a concept, the morel likely are others to interpret the concept as, he himself does. _. i The values now known as threshold limits*, are usually identified by phrases containing! the words allowable or permissible. These two words have connotations of legal regu lations. Such connotations cannot properly attach to the judgment of a voluntary pro fessional association. The identifying phrases may also contain the words maxi mum, threshold and limit. These words all The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. 132 June, 1936 imply that below the concentration speci fied, human response is negligible, above the concentration it is dangerous. Actually, it is more than an implication. It is definitely stated. In the introduction to its 1956 list (ACGIH 1956) the Committee on Threshold Limits says, "Values are given . . . for the maximum average atmospheric concentra tions of contaminants to which workers may the degree of organoleptic response. The Committee's four concepts follow: ; a. Plus or minus: The maximal time- weighted average concentration which . produces only minor injury, and that in a very small proportion of exposed work men. < b. Safe: The maximal time-weighted average concentration which sound evi dence leads one to believe will cause no be exposed for an eight-hour working day without injury to health." Careful study of the data which support the currently ac cepted values suggests that no such de scription can be truthfully attached to most of them. Industrial hygienists recognize this. They are accustomed to emphasize that the values should be regarded simply as bench marks, guides to good practice. Indeedj the Threshold Limits Committee it self confusingly warns "Threshold limits . . . should not be regarded as fine lines be tween safe and dangerous concentrations." (ACGIH 1956) The term maximum acceptable concentra tion being used in revisions of standards by the American Standards Association Z-37 Committee is objectionable only because it demonstrable illness or other symptom of toxic effect in any workman during a lifetime of industrial exposure. c. Bench mark: A concentration based on the belief that any unnecessary ex posure is undesirable--a concentration lower than that of a or b, one as low as is consistent with practical engineering con trol. d. Comfort: A concentration lower than a or b, representing the maximum which in a short time is not objectionable to 9 out of 10 of a group of persons not accustomed to inhalation of the substance. Note well that these four concepts were judged to be those already used for the se lection of hygienic standards for daily in halation. All four were judged consistent with the goals of industrial hygiene. will be abbreviated M.A.C. Many will in terpret this abbreviation as maximum al lowable concentration, and nothing will have been gained by the change from allowable to acceptable. I conclude that the names maximum al lowable concentration and threshold limit are misleading. They convey a wrong im pression to those who are not already famili ar with the concepts behind the values. The name suggested in 1949, hygienic standard, is not misleading. Standards of good prac tice are familiar to all of us in many fields. Looking toward the future provision of a variety of hygienic standards, a series of values should be selected, to be known as hygienic standards for daily inhalation. The third suggestion is more far-reach ing. The Committee on Chemical Agents (1949) pointed out that there has been no simple or uniform relation between the ef fects of a substance and the numerical value chosen for tabulation. The Committee con cluded that concentrations have been se lected on the basis of one of four concepts of the level best suited to hygienic control of inhalation, the choice having been governed by the mature of the toxic response and by Hygienic Standards for Daily Inhalation . 'T 'h e s u b j e c t of hygienic standards for daily inhalation should be re-examined, the concepts represented by the values should be restated in more realistic toxi cological terms, and more consistent and more informative standards should be pre pared. Such a step will not undo any of the accomplishments of the profession of in dustrial hygiene or of any organization. Rather, it will supply informative standards to supplement the accumulation of naked numbers now accepted, some of which have not been critically re-examined for a decade. It is certainly imperative that the inhala tion of substances during the working day shall not be allowed to result in any injury to the physical well-being of workmen. It is furthermore imperative that inhalation shall not increase the probability of acci dents through the mental distress occa sioned by objectionable eye, nose or throat irritation, transient though it may often be, nor through the impaired judgment and delayed reaction time of light narcosis. It is desirable that inhalation shall result in no degree of discomfort whatsoever. On the n June, 1966 loleptic response, ncepts follow: , !: The maximal time- concentration which >r injury, and that in tion of exposed work- aximal time-weighted ion which sound evi- believe will cause no ;s or other symptom ry workman during a al exposure. \ concentration based any unnecessary exible--a concentration s or b, one as low as is 'tical engineering con- concentration lower ienting the maximum le is not objectionable group of persons not ition of the substance, e four concepts were Iready used for the setandards for daily in- 'ere judged consistent lustrial hygiene. r Daily Inhalation ygienic standards for hould be re-examined, ented by the values n more realistic toxi- more consistent and .ndards should be pre ill not undo any of the the profession of in- of any organization, informative standards ccumulation of naked d, some of which have examined for a decade, rative that the inhalairing the working day o result in any injury eing of workmen. It is tive that inhalation e probability of accimental distress oecade eye, nose or throat hough it may often be, paired judgment and ; of light narcosis. It ilation shall result in >rt whatsoever. On the Industrial Hygiene Quarterly , other hand, when it is impractical to avoid all discomfort, then such inhalation is cer tainly justified, provided there results no injury to workmen and no increase in the probability of accidents. . Tables of hygienic standards do not now carry indications of the nature and of the magnitude of the effects to be expected from inhalation of greater concentrations. It is only by a rather thorough study of the avail able data that one can decide whether or not a particular substance can safely be inhaled at a greater concentration. With most sub stances, it is quite practical to set two standards, one an inoffensive level, another a concentration which cannot safely be ex ceeded under any pressure of practicality. Administrative expediency may be served by a dable of numbers which constitute a part bf official regulations. Regulations need not be defended, they need not cite justifi cations. However, it is a minority of the pro fession of industrial hygiene who have regu latory responsibilities. Most of our colleagues act through obtaining voluntary cooperation with their judgments. They would be aided by a greater degree of explanation in a tabu lation of standards. They could then show that their recommendations are quite de fensible, that they ar not arbitrary de cisions having no regard for the realities of competitive industrial existence. A hygienic standard for daily inhalation should specify two concentrations, together with a description of the human response to be expected from inhalation of each. One concentration should be low enough so that no injurious effect can be expected in any workman, but it may have a detectable odor, it may cause a detectable eye, nose or throat irritation. The second concentration should produce somewhat more severe, but still re versible and non-progressive effects. From these two concentrations, one can at once see how strictly the standard should be ob served, the steepness of the dosage-response curve, the breadth of the plateau of-noninjurious concentrations. Despite the wide range in individual susceptibilities of work men, such values can be selected for most, if not all, substances. Adequate data for preparing this sort of standard consist of appropriate human ex perience, or repeated medical examinations -of workmen in atmospheres whose concen- tration has been frequently estimated. Sterner (1955) discussed this point in de tail. Experiments upon animals, verified by biochemical and physiological studies in humans, may demonstrate conclusively that a substance has an effect during one period of inhalation which does not progress dur ing oft-repeated inhalation. For such a sub stance, satisfactory data can be obtained from objective study and secretly recorded subjective effects of a group of humans in haling known concentrations for substan tially eight hours. Any lesser body of data should result in a hygienic standard being designated as tentative. Categories of Objectionable Action JUDGMENTS should be made to determine J which hygienic standards for daily in halation must be carefully observed, and which may be exceeded when it is im practical to observe them. These judgments will be most consistent if we first decide for each substance what objectionable action we are guarding against by the standard. Every toxicologist will realize that the ac tion at a low concentration which it is most important to guard against, may not be the same as the menace to life to be expected at a high concentration. In a tentative fashion, the writer has made these decisions for the 238 substances, exclusive of the mineral dusts, included in the 1956 tables of pro posed accepted and tentative standards (ACGIH 1956). The decisions can be divided into the following nine categories on the basis of the nature of human response. Chronic toxicity. The most dangerous ef fect of some substances is a progressive systemic injury, increasing in severity with continuing inhalation. Benzene, carbon di sulfide, carbon tetrachloride and lead are the most familiar examples. The lower stand ard for these substances should be a concen tration believed not to produce any effect in any workman, and no considerations of practicality are sufficient to justify inhala tion in excess of the standard. Close medical supervision is required for safe use of these substances. The standard for chronically toxic substances should refer to the timeweighted average concentration throughout a working day. Brief peaks of a few times the standard have no significance, save as they increase the average. g O s! JaQ> 05 E -cToO ">O_ 1er TO -Q TO %e **t2oo & ^ %& -2Q TO P O t <D O S3 TO E o "TOO aoo. ToTOO> Q. O To TO TO ETO If' m m m's m| I fill i l l % i$f Sgrtte-.lii*'pPSi Mi-ir li*!1 11r: s : f',i !j - -."W ^1 - 1. 'Y't.- - hi 13k . June, 1956 Acute toxicity. Some substances do not produce an injury progressing1 with re peated inhalation. Such systemic injury as they may cause takes place as the result of one excessive inhalation, or not at all: Familiar examples are carbon monoxide and hydrogen cyanide. The standards for acute ly toxic substances should be interpreted in the same light as those for chronically toxic substances. Narcosis. The most dangerous effect of some substances is narcosis, which becomes ' anesthesia in its extreme stage. At a rather low concentration they induce accidents by impairing judgment and delaying reaction time. Familiar examples are ethyl alcohol, ethyl ether and gasoline. The lower stand ard for a narcotic substance should be a concentration which produces no detectable effect upon judgment and reaction time af ter eight hours inhalation. It should refer to the average concentration existing during some appreciable period of time, the length of which can be estimated from absorption and elimination data. No considerations of practicality can justify exceeding the stand ard for a narcotic substance. Irritation. The most dangerous effect of some substances is irritation. Eye, nose and throat are irritated at a low concentration, the bronchi at a higher concentration, and fatal lung edema may be the result of inhal ing an extreme concentration. The alde hydes, halogens and acids are familiar ex amples. Highly odorous substances may also be considered in this category. The lower standard for an irritant substance should be a concentration which is detectable, but is not objectionably irritating to the majority of unhardened subjects who are exposed for a substantial part of a working day. The higher standard should be set at a concen tration which is well under one injuring bronchi or lungs, and which is justifiable when it is impractical to keep concentra tions at the lower standard. Standards for irritating substances should refer to concen trations existing for even a brief period during a work day. Asphyxiation. Some substances are inert in the body and can injure only by asphyxia at extremely high concentrations, exclud ing the oxygen of the atmosphere. Familiar examples are the fluoroehloro refrigerants. The lower standard for these asphyxiants should be a nominal bench mark of good en gineering practice, such as the 1000 ppm concentration now quoted. The inert nui sance dusts like iron oxide might well be placed in this same category, and the cur rently used bench mark of 15 mgVcu.m. seems an appropriate level. The standard should refer to the concentration existing during any brief period, but it should be recognized that higher concentrations are justified when it is impractical to keep below the standard. Fume fever. The most important effect of some substances is a transient influenza like condition known as fume fever. A familiar example is zinc oxide fume. The lower standard for a fume fever producer should be a concentration which will not produce that distressing but not menacing condition in any workman, and it should apply to an appreciable period, such as half an hour. No considerations of practicali ty can justify exceeding the standard for fume fever producing substances. Eye pigmentation. The most important effect of two substances, quinone and hy- droquinone, appears to be a slowly develop ing pigmentation of the sclera, which may reduce visual acuity, or even lead to blindness. The lower standard for these substances should be a concentration which produces no pigmentation after years of exposure, and it should refer to the time- weighted average concentration throughout the day. For a few days at a time, conditions of practicality should justify exceeding the standard. Cancer. One substance is reasonably well established as a cause of respiratory tract cancer. This is nickel carbonyl. It appears probable that the minimum cancerigenic ex posure will never be defined. At this time it is prudent to set the standard for a can cerigenic substance substantially at zero, as has already been done for nickel carbonyl, and no considerations can justify allowing the inhalation of any concentration which is avoidable. Allergy. Some substances are known to sensitize an appreciable proportion of ex posed workmen. They may produce distress ing and menacing asthma-like attacks when a sensitized person inhales a low concentrar tion. Examples are ethylene diamine and. the diisocyanates. At this time there is no; The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. June, 1956 Industrial Hygiene Quarterly 135 snch mark of good enlch as the 1000 ppm rational experimental basis for defining a ards the decision should be clearly indicated toted. The inert nui- concentration which will not sensitize a sus in the table. oxide might well be ceptible workman, or one to which no previ ously sensitized workman will respond. Con Three columns record personal judgments ategory, and the curark of 15 mg./eu.m. trol of exposure to allergenic substances and estimates as to what responses may oc cur in some workman inhaling continuously, level. The standard must rely heavily upon industrial medicine. all day, the threshold limit, twice, and ten After experience has allowed withdrawal times the limit. It will be obvious from these oncentration existing iod, but it should be ;r concentrations are of workmen susceptible to sensitization, the entries that the values may not always de remaining resistant individuals can be pro fine concentrations in which workmen will actical to keep below tected by a hygienic standard for daily in find no objectionable sensory effect, or even halation based upon irritation or systemic aost important effect injury. Until it has been demonstrated that concentrations where no toxic symptoms will develop in any individual. a transient influenza a particular group includes no susceptible Next comes a column listing important workmen, no considerations can justify al as fume fever. A inc oxide fume. The lowing inhalation of any concentration injuries other than from inhalation of the substance itself, such as dangerous absorp fume fever producer which is avoidable. tion through the skin, chemical burns of eye ation which will not 1- Interpretations of Accepted Values and skin, frequent allergic dermatitis, ng but not menacing kman, and it should pyrolysis to phosgene, and the like. The al n e w v a l u e s for standards are sug most universal defatting of the skin by sol I e period, such as half gested at this time. The available data vents, and freezing of tissue by low boiling upon which the 238 values in the 1956 pro ations of praeticaliing the standard for liquids, has not been entered. posed list (ACGIH 1956) appear to be based The last two columns give some indica substances. have been studied. Table I is offered as an tion of the soundness of th value by de interpretation of these values, increasing The most important ces, quinone and hy scribing the supporting data, and by speci the information they convey. It presents fying the year in which it was first pro ) be a slowly develop- the familiar numbers, which give the engi posed or adopted. It is, of course, true that a neer and the chemist an illusion of complete the sclera, which iity, or even lead to value proposed many years ago and recopied understanding. It also presents, in the form in each succeeding year's list is not neces standard for these . concentration which of abbreviations of self-evident meaning, some description of actions which gives the biologically and medically trained a feeling sarily proven sound, but in general it is like ly to be better established than a more re cently adopted value. ition after years of d refer to the time- of confidence. The table is obviously too com There may be objection that the table entration throughout 5at a time, conditions plex for great popularity. Nevertheless, does not mention warning power nor at every class of information listed is required tempt to evaluate this property specifically. 1 by those who must apply the values. The The practical importance of warning power justify exceeding the data relied upon for the interpretations and in preventing inhalation of an excess is ce is reasonably well some comments on their adequacy are sum much over-rated. Odor data are notoriously marized after the table. of respiratory tract carbonyl. It appears All substances in the proposed 1956 threshold limits table (ACGIH 1956), ex unreliable. Estimates of tolerable working conditions with unacclimated subjects, briefly exposed, have only limited usefulness num caneerigenic exfined. At this time it standard for a can- cept mineral dusts, appear in one alpha in predicting the responses of acclimated betical order. When a value is listed. in and usually hardened workmen, exposed all ibstantially a t zero, units of milligrams per cubic meter, the day. Early stages of narcosis reduce percep letter m precedes the number. When a ten e for nickel carbonyl, can justify allowing tion of odor and irritation. Even with strong tative value was proposed the letter T fol irritants like ammonia and acrolein, physi oncentration which is lows the number. cal circumstances, or a sense of duty, may Following the threshold limit values is a keep a man at his post to be seriously in anees are known to le proportion of ex column showing a personal judgment of the most serious effect of inhalation of a con centration somewhat higher than the thresh jured by a concentration which, all would predict, cannot be inhaled voluntarily. There is nothing in Table I which is not nay produce distressma-like attacks when old limit. These judgments allow one to easily accessible, if not already well known decide whether the value should refer to to a thousand experienced industrial hy ales a low concentra:hylene diamine and his time there is no .the time-weighted average concentration or gienists and toxicologists. Not one of these to peak concentrations* existing at any time but will object to some among the thousand during the day. In future tables of stand- personal judgments entered. However, the 136 . annual threshold limit tables are consulted by upwards of twenty thousand other per sons who do not have access to original sources and extensive experience. These peo ple rightly regard the threshold limits as a presentation of the best available judgment, and they may wrongly regard them as every thing they need to know about safe use of a substance. Despite specific disclaimers, printed with each year's table, these readers tend to regard each threshold limit as de fining the line between safety and injury. Table I is presented as a beginning in the extensive job of improving communica tion by developing a rational and informa tive series of hygienic standards for daily inhalation. Summary of Underlying Data 'J'HE data relied upon for the interpreta tions entered in Table I are summarized and .briefly commented upon in the pages which follow. It is believed that the most significant published information is in cluded, but no attempt has been made to list all pertinent articles. Certain hitherto un June, 1956 published observations are included when they appear to confirm or supplement ma terial in the literature. The term "most im portant effect" used with every substance, refers to the possible effect of inhalation of concentrations a few times the threshold limit, not necessarily to the possible effects at very high concentrations. Acetaldehyde. Cook (1945) quotes the 1911 report of Iwanoff that cats inhaling 280 ppm for seven hours were not noticeably affected. The unaeclimated subjects of Sil verman, Schulte and First (1946) found 25 ppm objectionable, 50 ppm irritating to the eyes, but even 200 ppm not irritating to the throat. Fairhall (1949, p. 199) describes the effects as irritation, narcosis, bronchitis, albuminuria, fatty liver and lung edema. He concludes that inhalation does not cause chronic poisoning, and that death is due to anesthesia when prompt, or to lung edema when delayed. Smyth (1937-55) found rats survive four hours inhalation of 8000 ppm but die from 16,000 ppm. The liquid causes severe corneal injury, irritates the skin and may sensitize some persons. M n e m o n ic a b b r e v ia tio n s u sed in T a b l e I. acne-- acute-- chioracne from continued skin contact, acute toxicity, wjth little or no increase in all-- severity from continued inhalation, allergenic. D erm atitis and asthm a-like sen ALL-- sitization may result. allergenic. D erm atitis and asthm a-like sen- aitization are likely. asphyxia- --asphyxiation a t very high concentrations, bur-- burn of the skin, BUR-- very severe burn of skin, cancer--- cancer reported In hum ans, chronic-- chronic toxicity, with Increase in severity clin-- from continued inhalation, clinical exam ination of workmen was cor related with their exposure, centra] nervous system stimulation, such as trem ors o r convulsions, cyanosis (blue skin) m ay be evident- cyanosis (blue skin) m ay be marked, estim ate from experience and analogy, EYE-- eye p ig fum e-- head-- eye irritation severe enough to require medical treatm ent, eye burn may be severe, eye pigm entation without injury, fume fever. headache. This symptom has no t been en tered every tim e it may occur, human sensory data. hum an toxicological o r physiological data, industrial com plaints o r observations, less quantitative than clinical examinations, irritation of eye, nose o r th ro a t in some, irritation of eye, nose o r th ro a t marked. minor irritation of bronchi (coughing) or lungs. definite irritation of bronchi o r lungs w ith injury of lungs possible, dangerous injury of lungs with little w arn ing. the quantity is expressed in milligram s med-- per cubic m eter (m g./cu.m .), n o t in ppm . medical uses yield some inform ation, narcosis-- narcosis, ranging from impaired coordina tion through dizziness, to anesthesia, nar-- NAR-- nau-- fain t narcosis, somewhat impaired reaction time and judgment, narcosis definite, sh o rt of dizziness, narcosis marked, dizziness to unconscious ness. nausea. This symptom has not been entered none-- odor-- ODOR-- pyr-- every time it may occur. no effects are expected. odor may be perceptible. odor marked. pyrolysis to lung injuring- halogen com pounds in a flame, o r on h o t metal, radiation injury is possible, repeated animal inhalation results, single animal inhalation results, skin penetration may cause symptoms, skin penetration of liquid is dangerous, tentatively proposed, toxic symptoms may arise very slowly, m inor toxic symptoms, m ajor toxic symptoms, visual acuity loss June, 1956 ations are included when lonfirm or supplement maature. The term "most imised with every substance, sible effect of inhalation of few times the threshold arily to the possible effects :entrations. Cook (1945) quotes the Iwanoff that cats inhaling n hours were not noticeably acclimated subjects of Siland First (1946) found 25 e, 50 ppm irritating to the 100 ppm not irritating to all (1949, p. 199) describes tation, narcosis, bronchitis, ;y liver and lung edema. He inhalation does not cause g, and that death is due to prompt, or to lung edema nyth (1937-55) found rats irs inhalation of 8000 ppm 100 ppm. The liquid causes jury, irritates the skin and ne persons. I. ation of bronchi (coughing) or tation of bronchi or lungs with ings possible. njury of lungs w ith little warn- ty is expressed in m illigram s leter (m g./cu.m .), not in ppm . is yield some in fo rm atio n , inging from impaired coordinah dizziness, to anesthesia, sis, somewhat im paired reaction ld g m en t. finite, sh o rt of dizziness, irked, dizziness to unconscious- s symptom has not been entered it may occur, ire expected. ie perceptible, i. o lung injuring halogen com i flame, o r on h o t metal, tjury is possible, imal inhalation results, al inhalation results. -ation may cause symptoms, ation of liquid is dangerous, proposed. toms may arise very slowly, symptoms, symptoms, y loss Industrial Hygiene Quarterly T able I. I n ter pr et a tio n of T h resh o ld L im it V a lu es P roposed for ' Exclusive of Mineral Dusts ______ (Mnemonic abbreviations explained at foot of table) Substance Threshold Lim it ppm or m g./cu.m ,. Most Im portant Effect of Inhalation Acetaldehyde Acetic acid Acetic anhydride Acetone Acrolein 200. 10. 5. 1000. 0.5 lung lung lung narcosis LUNG A cry lo n itrile A ldrin Ailyl alcohol Allyl chloride Ailyl propyl disulfide 20. acute m-0.25 chronic 6. EY E-lung 5. T lung 2. lung Predicted Effects of Daily eight-hour Inhalations At Threshold L im it IRR-odor irr-odor Additional A t Twice Threshold Lim it Additional A t Ten Times Threshold Lim it lung IR R -lung irr-odor irr-nar-odor irr none none irr none IRR odor none eye-IRR-lung NAR lung tox irr-tox eye-lung irr-odor irr IRR Im portant H azards Other Than from Inhalation a ll-E Y E bur-E Y E bur-E Y E bur-E Y E skp all-skp bur-E Y E pyr A m m ate A m m onia Amyl acetate Amyl alcohol Aniline A ntim ony ANTU A rsenic A rsine B ariu m (soluble) Benzene Benzyl chloride B ro m in e Butadiene Butanone (m ethyl ethyl ketone) Butyl acetate Butyl alcohol Butyl am ine Butyl CELLO SOLVE Butyl m ercaptan m-15. 100. 200. 100. 5. lung lung narcosis narcosis chronic m-0.5 chronic m-0.3 T chronic m-0.5 chronic 0.05 acute-lung m-0.5 35. 1. acute-lung chronic lung 1. 1000. lung narcosis 250. narcosis 200. narcosis 100. narcosis 5. lung 200. chronic 10. T lung none irr-odor irr-odor irr-odor none none none none none none tox? irr irr-odor none irr-odor irr-odor odor odor odor-tox ? ODOR IR R -nar IR R -nar cy none tox? IRR-lung NAR NAR CY-tox tox tox tox lung ?-tox tox odor tox nar-odor-TOX IR R -lung odor IR R -lung nar bur-eye EYE BUR-EYE IR R -n au IR R -n ar irr irr nar NAR IR R -N A R eye nar-tox irr-n ar-T O X eye-irr-lung ? BUR-EYE skp C adm ium oxide fume Calcium arsenate Carbon dioxide Carbon disulfide Carbon monoxide m-0.1 acute-lung m-0.1 T chronic 5000. asphyxia 20. chronic 100. acute none none none none none odor tox none nar nar-tox TOX Carbon tetrachloride 25. CELLO- SOLVE 200. CELLO- SOLVE acetate 100. chronic chronic chronic tox? odor odor tox nar-odor-TOX p y r nar-tox irr-nar-tox irr-tox IRR-nar-tox N ature of Interpretive D ata hu-sgl hu-ind-sgl sgl HU-ind hu-sgl rpt clin ind-sgl sgl ind est H U -ind-sgl hu-sgl hu-sgl rpt elin-rpt est clin-est ind-sgl est clin-rpt sgl ind-sgl hu-rpt hu-sgl hu-sgl clin ind-sgl rpt SKl ind-rpt est HU clin-rpt clin-HU clin-ind-rpt rpt rpt Prop I 19|' ii$ l f O >> CcO o 19{ "co 19j 19| 19 I 1945 194I i _CD 1 194 CO 1 <D 1943J 1943 1953 1946 1945 ; BSE5ST y ^ a 'J.i.1 INA }. , 7 ^ /; ,*;%':; - > ' " c V .S l ' ' - A0 '^ & 7 7 cj ^ 7 g ? S h ^ jja K ftjg '!'>*&.--'ttT-^CtC JL .'.WPt-- rjfc'afr' u3l ..'.'^S-=-lJ^ ---i--e--J^--^ - i - ' '- W --Vana^a^lraa ll'Ck2t' B B Sg& gife& ag^~3 <v: 'T zzzx ' *r a 9 >%T s 3 ?*g i "f 0s - ^g 62 2o s Qtr, :S s I 3 s r* ? a a a a .M Sj?29L3t ?L9. f f f | 3 S x0ks 0asr*fstr0 af0t*0sftr I f fAf3t oo iXt xM.xl {x) 333 3 3 0 0 0 0 n 2 no ro o o 3 ,, g-^g 8-f ? I s .3:003 ! i a* a 0 2 ^ 2 -1 3 2 * s g s &sr `35 9S.^S.^3 I : s H :l gSg* >: ca 2oo goo ex se.sorr g 2. asS-s. O O -9)fU3t 2o.2O. -C2l. f9t f9t ft *a3 ^ 3 3 p * a- & H ^ 0 9 9 0 9 ft ft o o 2 E gff z a *2 o9 #o oMr> oi - B# -M 2 S'S- ? ? 11 ? Jt>if>SH2 Z>P>3 cr 3 c* M hjrt> a>. t* *< a. 3|s ? wi s r i 3 ST 4 a- H a g. g* 3 ft * ? A * ^ ~ 3 '2- ec 3 33 _, o ,, g. S M 3 3 i Sg S2 3 ha '2"J3 P05*0 :' c to dd d <0 t o tO nO ntpfc9tOii to to to to to if* >t~ ifc iK 9 g l Oj W .o t <0 tO dtC >dU t#o* dt o M d fto* dto 0 d 3 Kj The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. June, 1956 im portant H azards ther Than from nhalation l-skp N ature of Interpretive Data clin . Proposed 1954 -skp est 1956 ne r-EYE r-EYE r r rp t hu-rpt rp t est-sg) rpt 1955 1948 1955 1943 1956 ne rp t 1946 ie rpt 1966 r est-med-sgl 1945 sgl clin r-skp rpt 1945 1956 1945 r-EYE clin est 'R -E E -K P est-sgl est. rpt hu-rpt hu-rpt sgl est-med est est rpt hu-sgl clin-rpt 1943 1954 1952 1947 1946 1945 1945 1945 1947 1954 1954 1956 1964 1955 ind-sgl 1947 rpt rpt sgl hu-sgl 1947 1945 1945 1945 sgl 1947 rpt 1945 Industrial Hygiene Quarterly T a b l e I-- Co ntinued Substance Threshold Lim it ppm ur m g./cu.m . D ich lo ro tetrafluoro- Most Im portant Effect of Inhalation Predicted Effects of Daily eight-hour Inhalations At Threshold Lim it A dd itio n al A t Twice Threshold Lim it A d d itio n al A t Ten Times Threshold Lim it Im portant Hazards Other Than from Inhalation N ature of Interpretive D ata m ethane Dieldrin Diethylamine Difluorodt- 1000. m-0.25 25. chronic asphyxia lung none none odor none none sye-irr none irr IRR-lung pyr sgl all-skp clin bur-EYE Sgl bromome- thane Diisobuty] ketone Diisocyano toluene D im ethyiani- line Dimethylsul- fate D in itro b en - 100. chronic none 50. narcosis 0.1 T A LL -lung irr-odor all 5. chronic none 1. acute-LU N G none none cy irr-nar-tox IR R -nar ALL CY-tox LUNG-TOX pyr rpt bu-rpt ind SKP sgl BUR-EYE-SKP sgl zene Dinitro-o- eresol D initrotoluene Dioxane EPN Ethyl acetate Ethyl acrylate Ethyl alcohol E thylam ine Ethyl benzene Ethyl bromide Ethyl chloride Ethylene ehlorhydrin Ethylene diam ine Ethylene dibro m id e Ethylene m-1. m-0.2 m-1.5 100. m-0.5 400. 25. 1000. 25. 200. 1000. 5. 10. 25. T chronic acute chronic chronic acute narcosis T lu n g narcosis lung narcosis none none tox? none none irr-odor odor irr-odor odor n a r ?-odor narcosis odor acute ALL-lung odor chronic-lung none tox tox? nar-odor nar irr nar eye-irr irr irr-odor tox? irr-tox irr-tox irr-N A R -to x tox IRR-NAR lung IRR-NAR IRR-lung NAR lung nar odor-tox irr-odor lung-tox skP skp skp bur-E Y E _____ pyr pyr est 5gl est hu-rpt est hu-sgl rpt HU 8gl hu-sg! sgl sgl SKP ind-sgl ALL-bur-EYE ind-rpt pyr rpt dichloride 100. Ethylene im in e 6. Ethylene oxide 100. Ethyl ether 400. Ethyl form ate 100. chronic a c u te -lu n g lung-nar cosis narcosis narcosis odor-tox? odor odor-nar irr-odor none nar-nau IRR TOX pyr lung-TOX bur-eye-S K P IRR-LUNG-NAR bur NAR ind-rpt hu-sgl hu-rpt HU-med Ethyl Sgl m ercaptan Ethyl silicate Ferbam Ferro vanadi um dust Fluoride dust Fluorine Fluoroacetates Fluorotri- ch lorom eth an e Formaldehyde Furfural Furfuryl 250. 100. m-15. m -I. m-2.6 0.1 m-0.1 1000. 5. 5 T lung acute-lung T lung lung chronic lung T acute asphyxia lung T lung ODOR odor none none tox ? none none none irr irr irr-tox irr eye-irr-lung IRR IRR none irr-tox irr-lung?-tox ? tox all BUR-EYE none odor none IRR-lung IRR-lung pyr all-E Y E a ll-E Y E sgl hu-rpt est rpt clin-rpt est sgl ind-sgl alcohol Gasoline 50. T narcosis odor irr-n ar IRR-NAR 500. narcosis odor irr-nar NAR rpt IS ll li i 193 19 i9; id 19^ 191 11991| 1943 19fj 1951 1945 IOS! 1951 19figj 1951 1945 1948 1956 The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyrigh June, 1956 t n N ature of Interpretive Year 1945 est 1956 1947 hu-sgl 1947 hu-sgl rpt hu ind-rpt hu-sgl ind-rpt 1947 195b 1956 1948 1948 1943 rpt hu-ind-rpt clin-sgl din ind clin hu-rpt 1955 1948 1943 1955 1948 1947 1945 ind-sgl din rpt rpt HU est-d in d in clin-rpt clin-sgl hu-rpt sgl est-sgl rpt rpt rpt rpt d in -rp t 1955 1943 1956 1954 ' 1945 1954 1945 1943 1954 1945 1954 1948 1955 1952 1956 1943 d n -rp t 1947 Industrial Hygiene Quarterly U1 * v- j j ' 1 . ,| t i i T able I --C ontinued Predicted Effects of Daily eight-hour Inhalations Substance L im it ppm or m g./cu.m . Most Im portant Effect of Inhalation Methyl CELLO- SOLVE acetate 25. chronic Methyl chloride 100. chronic Methyl chloroform 500. narcosis Methyl cyclo . hexane 500. M ethyl cyclo- hexanol 100. M ethyl cyclo* hexanone 100. M ethylene chloride 500. Methyl form ate 100. narcosis narcosis narcosis chronic narcosis Methyl isobutyl carbinol (m ethylam yl alcohol) Methyl m ercaptan M olybdenum (soluble) Molybdenum (insoluble) N ap h th a (coal tar) 25. 50. m-5. m-15. 200. narcosis T lung chronic chronic narcosis N aphtha (petroleum ) N ickel carbonyl Nicotine ` N itric acid p-N itro an ilin e 50. narcosis 0.001 cancer-lung m-0.5 T chronic 10. T lung 1. chronic N itro b en zen e N itroethane N itrogen dioxide N itroglycerine N itrom ethane 1. 100. 6. 0.6 100. chronic acute lung acute acute 2-N itro p ro pane N itro to lu en e Octane Ozone Parathion 60. 6. 500. 0.1 m-0-1 acute chronic narcosis lung acute At Threshold L im it Additional A t Twice Threshold Lim it none none odor odor irr-odor irr-odor none none odor-tox odor nar nar nar-tox odor irr-odor none irr-odor ODOR none irr-tox none none irr-nar?-odor odor none none irr none none none odor head none irr-nar none TRR irr-odor irr irr-odor nau-tox 7 none odor odor none fcox? irr-nar A dd itio n al A t Ten Times Threshold Lim it irr-nar-tox ens-nar NAR irr-N A R -toz IR R -N A R IR R -n ar nar nar IR R -nar eye-irr-Iung ? irr-tox NAR NAR none tox lung tox tox nar-tox LUNG tox nar-tox odor-tox tox NAR irr-lung tox P en taboran e 0.01 T acute none none Pentachloro- naphthalene m-0.5 chronic none tox? tox Pentachloro- phenol m-0.5 acute none irr-tox Pentane 1000. narcosis odor irr nar Pentanone (methyl pro- pyl ketone) . 200. narcosis irr-odor IRR nar Perchloroethylene Perchloro( methyl m ercaptan 200. narcosis 0.1 Tiling- odor none nar irr-N A R irr H azards Other Than from Inhalation N ature of Interpretive D ata Year Proposed est 1947 pyr rpt 1947 pyr rpt 1953 rpt 1947 rpt 1945 rpt 1945 pyr rpt 1945 sgl 1947 SKP BUR-EYE skp SKP SKP SKP SKP acne bur-skp pyr b u r-E Y E hu-sgl sgl rpt rpt est est ind-sgl est est est-ind est rpt ind-rpt din rpt clin-sgl est est rpt clin-est rpt rpt est hu hu-sgl m ed-rpt sgl 1954 1954 1955 1955 1945 1945 1954 1956 1956 1954 1947 1947 1945 1945 1947 1947 1943 1945 1964 1958 1956 1945 1947 1947 1947 1953 1954 The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. The materia! on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law,'' June, 1956 t .n N a tu re of Interpretive i ' D ata -SKP hu-rpt sgl H U -rpt rpt ind * Year 1 Proposed 1952 1954 1943 1947 1947 Sgl est sgl clin est-sgl 1947 1947 1945 1954 1945 est-hu rpt SKP sgl rpt rpt ind-med din est 1945 1947 1955 1945 1956 1954 1965 1956 clin-est ind sgl hu est hu-rpt clin-hu sgl H U -ind-sgl ind-sgl sgl est clin est 1947 1954 1947 1945 1956 1947 1943 1954 1948 1945 1954 1964 1947 1964 hu-rpt ind-sgl rpt rpt d in est 1955 1947 1956 1955 1943 1956 Industrial Hygiene Quarterly US T a b l e I -- C o n t in u e d Substance Lim it ppm or m g./cu.m. Most Im portant Effect of Inhalation Thirara Titanium dioxide Toluene o-Toluidine Trichloro- ethylene m-5. T chronic ra-15. 200. 6. lung narcosis chronic 200- narcosis Trichioronaphthalene T rifluorom onobromom ethane Trinitrotoluene T u rp en tin e U ran iu m (soluble) m-5. 1000. m-1.5 100. m-C.05 chronic narcosis chronic narcosis chronic U ran iu m (insoluble) V an ad iu m (V 2O5 d u st) V an ad iu m (V 2O5 fum e) Vinyl chloride W arfarin m-0.25 chronic m-0.5 lung m-0.1 lung 500. narcosis m- 0.5 T chronic Xylene Zinc oxide fum e Zirconium 200. ' m-15. m-5. narcosis fum e T lu n g - Predicted Effects of Daily eight-hour Inhalations . Im portant Additional Additional H azards At A t Twice A t Ten Times Other Than Threshold Threshold Threshold from Lim it L im it Lim it Inhalation none none nar-odor irr none cy irr-lung NAR CY-tox SKP nar-nau-odor irr-N A R pyr none tox acne none tox? irr-odor none none none none tox? IR R -n ar irr-nar irr-tox NAR-tox tox tox lung pyr skp rad ' rad none lung none nar pyr none tox irr-nar?-odor nar NAR fum e none fum e-irr lung lung N ature of Interpretive D ata est-sgl Proposed ' Year 1956 rpt 1954 elin-hu-rpt 1943 sgl 1945 ind-m ed-rpt 1948 rpt 1945 rpt clin-rpt hu-rpt rpt rpt rpt 1966 1943 1946 1953 - 1953 1964 rpt 1954 sgl 1947 est 1956 hu 1943 HU 1943 rpt 1956 The most important effect of acetaldehyde inhalation is irritation of upper respiratory tract, bronchi and even lung. The 200 ppm threshold limit can be interpreted from human sensory data. It is sufficiently low to prevent lung injury. Acetic acid. Sterner (1943) concludes 10 ppm is reasonably non-irritating on the basis of industrial experience. Patty (1948 9, p. 886) finds 1300 to 1200 ppm intoler able. Smyth (1937-55) found inhalation of 16,000 ppm by rats for four hours killed one of six. The liquid causes severe corneal injury. Vigliani and Zurlo (1955) report workers exposed seven to 12 years to con centrations of 60 ppm, with one hour daily at 100 to 260 ppm, had no injury except slight irritation of the respiratory tract, stomach and skin. They regard 20 to 30 ppm as without danger. . The only important effect of acetic acid inhalation is irritation, first evident in the eyes, then in the upper respiratory tract, bronchi and even lung. The 10 ppm thresh old limit can be interpreted from uncon trolled human sensory data. It is low enough to prevent lung injury. . Acetic anhydride. Hendex-son and Hag gard (1943, p. 130) mention eye, nose and throat irritation and suggest that bronchial and lung injury are likely. Fairhall (1949, p. 203) considers it a lacrimator and finds systemic effects unlikely. McLaughlin (1946) discusses serious corneal injury from the liquid in industry. Smyth (1937-55) found rats inhaling 1000 ppm for four hours survived, but 2000 ppm was fatal. The liquid causes skin burns. The only important effect of acetic an hydride inhalation is irritation, first evident in the eyes, then in the upper respiratory tract, bronchi and even lung. The 5 ppm threshold limit can be interpreted from an alogy with acetic acid. In view of rat mor tality from the two vapors, a lower value would be more consistent, although it is undoubtedly low enough to prevent lung in jury. Acetone. Nelson, Ege, Ross, Woodman and Silverman (1943) found slight -eye, lied from the collection of the National Library of Medicine by a third party and may be protected by U. nose and throat irritation with unacclimated Wilson (1944) in exposed workmen, found 1 subjects at 300 ppm, but 500 ppm was not evidence of skin penetration and effects ref-1 objectionable. Henderson and Haggard erable to liver injury. Smyth's (1937-55) | (1943, p. 196) conclude death is anesthetic, rats survived four hours at 500 ppm butg with no organic injury below a narcotic were killed at 1000 ppm. 1 level. Fairhall (1949, p. 205) concludes it The most important effect of acrylonitrile 8 causes narcosis, bronchial irritation and inhalation is acute poisoning, due to h y - | headache, but no chronic systemic effect. drolysis in the body to cyanide. The 20 ppm I Haggard, Greenburg and Turner (1944) threshold limit can be interpreted from re-1 found human narcosis like that from ethyl suits of repeated animal inhalation studies | alcohol. The highest concentration not caus and its relationship to the accepted 10 ppm | ing narcotic impairment of coordination threshold limit for hydrogen cyanide. It i s | and judgment is 2110 ppm, which results in low enough to prevent injury. 1 a blood level % that giving first alcoholic Aldrin. Princi and Spurbeck (1951) ex-g intoxication symptoms. Smyth's (1937-55) amined workers with one to three years ex-| rats survived four hours at 32,000 ppm, died posure to 1 to 2.6 mg./cu.m. aldrin and re-S from 64,000 ppm. Vigliani and Zurlo (1955) lated dusts, and found no clinical evidence! found chronic respiratory tract irritation of injury. McGee (1955), reviewing humanf and dizziness in workers inhaling 1000 ppm cases and animal data, finds aldrin and lin-g three hours a day. dane have similar actions. Acutely they in -| The most important effect of acetone in crease central nervous system irritability,! halation is narcosis. The 1000 ppm thresh leading to convulsions. Chronically they in-g old limit can be interpreted from human jure the liver, with effects also on kidney,g sensory and physiological data. It is not low lung and nervous system, and they sensitize! enough to prevent all narcotic symptoms. some skins. ACGIH (1954b) finds aldrin! Acrolein. Yant, Schrenk, Patty and Sayers twice as toxic to animals acutely as lindane,! (1930) found marked human eye, nose and and concludes half the threshold limit of thes throat irritation within five minutes at 1 latter is tentatively appropriate. I ppm. Patty (1948-9, p. 936) concludes 0.25 The. most important effect of aldrin m-g ppm is moderately irritating. Henderson halation is chronic poisoning centering ini and Haggard (1943, p. 138) conclude the. the liver. The 0.25 mg./cu.m. threshold lim-| main attack is_ on the upper respiratory it can be interpreted from the results off tract, but that a high concentration can examination of exposed workmen. I t is lows cause lung edema. They report 10 ppm to be enough to prevent injury. f lethal in a short time. Systemic effects are AUyl alcohol. McCord (1932) found some! not to be expected. Smyth (1937-55) found human irritation at 5 ppm. The review by four hours inhalation of 8 ppm kills one of von Oettingen (1943, p. 138) shows cats die Q . six rats and all die from 16 ppm. The liquid during 30 seven-hour inhalations of 50 ppm, 8 causes severe corneal injury and burns of with pulmonary edema, gastroenteritis, TCOO the skin. hematuria and nephritis. Smyth (1937-55) The only important effect of acrolein in found rats survive one hour at 500 ppm, CT> CO halation is irritation, first evident in the but die from 1000 ppm. The vapors irritate QCO eyes, then in the upper respiratory tract, eye and nose, but not sufficiently so to pre SZ bronchi and even lung. The 0.5 ppm thresh vent exposure to a concentration which C. O old limit can be interpreted from human temporarily blinded one man through de-8j CO sensory data. It is low enough to prevent layed corneal necrosis. Chronic toxicity is! cd lung edema. not to be expected, but skin penetration isg "as Acrylonitrile. Dudley, Sweeney and Miller dangerous, and skin contact causes burnsl CD (1942) found repeated inhalation of 153 when evaporation is prevented. 1 ppm injurious to animals, but believed the The most important effect of allyl alcohols ' effect not chronic toxicity. Dudley and Neal inhalation is irritation, manifest as dis-| (1942) concluded injury is due to formation abling corneal injury and pulmonary edema, of cyanide in the body. The 10 ppm hydrogen with non-progressive organic effects some cyanide threshold limit is equivalent to 20 what less important and narcosis over ppm acrylonitrile, if conversion is complete. shadowed. The 5 ppm threshold limit can be June, 1956 ' ed workmen, found tion and eifects refSmyth's (1937-55) rs at 500 ppm but feet of acrylonitrile soning, due to hyyanide. The 20 ppm iterpreted from re1 inhalation studies he accepted 10 ppm ogen cyanide. It is jury. jurbeck (1951) ex3 to three years exu.m. aldrin and re io clinical evidence , reviewing human tnds aldrin and lin s. Acutely they in system irritability, Ihronically they incts also on kidney, , and they sensitize 954b) finds aldrin acutely as lindane, reshold limit of the opriate. iffect of aldrin inming centering in u.m. threshold limom the results of workmen. It is low y(1932) found some sm. The review by 38) shows cats die alations of 50 ppm, i, gastroenteritis, Smyth (1937-55) hour at 500 ppm, ?he vapors irritate ficiently so to preicentration which man through deIhronic toxicity is kin penetration is tact causes burns ented. ect of allyl alcohol manifest as dispulmonary edema, anic effects someid narcosis, over s o l d limit can be , 1556 . Industrial Hygiene Quarterly interpreted from a report of human irrita tion and results of repeated animal inhala tion. It is probably low enough to prevent injury, but may be slightly irritating to some. Allyl chloride. Adams, Spencer and Irish (1940) found rats survive three hours in halation of 290 ppm, while eight hours killed all. Injury was chiefly in the lung, with some kidney effects. Narcosis was weak but mucous membrane irritation was prominent. The most important effect of allyl chloride inhalation is irritation of the upper respira tory tract, bronchi and lung. The 5 ppm ten tative threshold limit can be interpreted from single inhalations by animals and by analogy with chloroprene. It appears low enough to prevent injury. x Allyl propyl disulfide. Feiner, Burke and Baliff (1946) surveyed an onion dehydrat ing plant and found pronounced irritation of eye, nose and throat at 3.4 ppm onion oil calculated as this disulfide, with some irri tation at 2 ppm. Acclimitization was evi dent. The most important effect of allyl propyl disulfide inhalation is irritation of eye, upper respiratory tract and lung. The 2 ppm threshold limit can be interpreted from the results of complaints from exposed work men. It appears low enough to prevent in jury. Ammate. ACGIH (1954b) concludes the single dose LD50 for animals of 2000 mg./kg. justifies no more control on inhala tion than is required for a non-toxic nui sance dust. The most important effect of ammate dust inhalation is the low grade irritation of a substantially inert dust. The 15 mg./cu.m. threshold limit can be interpreted only by analogy. It appears low enough to prevent injury. Ammonia. Lehmann (1886) suggested 100 ppm is tolerable, and subsequent in dustrial experience has been favorable. Hen derson and Haggard (1943, p. 125) note incapacitating temporary blindness, and respiratory .arrest from a high concentra tion. They state 53 ppm is the least amount smelled, but Smyth (1937-55) found 1 ppm detected and identified by 10 subjects. They give 408 ppm as irritating to the throat, 698 ppm irritating to the eye, 2500 to 6500 ppm dangerous to life in 30 minutes. Fair hall (1949, p. 20) notes eye and upper respiratory tract irritation, salivation, bronchial irritation and lung edema, but no chronic systemic effect. Elkins (1950, p. 84) found 55 ppm not objectionable in industry but 125 ppm irritating. Silverman, Whittenberger and Muller (1949) found 500 ppm stimulated human respiration, irritated eye and throat, caused ' lacrimation. Smyth (1937-55) found rats survive four hours at 2000 ppm, die at 4000 ppm. Solutions irri tate the skin, erode mucous membrane and severely injure the cornea. Vigliani and Zurlo (1955) in workers inhaling 100 ppm, found irritation of the respiratory tract and conjunctiva. Even 20 ppm caused com plaints until workers became hardened. The most important effect of inhalation of ammonia gas is respiratory tract irritation, with lung edema or respiratory arrest the maximum injury. The 100 ppm threshold limit can be interpreted from human sen sory and physiological data. It is low enough to prevent injury. Amyl acetate. Patty, Yant and Schrenk (1936) found 2000 ppm does not injure guinea pigs in several hours, while a concen tration killing in 60 minutes can not be ob tained. Symptoms consisted of eye and nose irritation and narcosis. Nelson, Ege, Ross, Woodman and Silverman (1943) found slight throat irritation in unacclimated sub jects at 100 ppm, mild eye and nose sensa tion and severe throat irritation at 200 ppm. Smyth (.1937-55) with rats inhaling substantially saturated vapors found anes thesia in two hours and death in eight hours. Chronic toxicity is not to be expected. The most important effect of amyl acetate inhalation is narcosis. The 200 ppm thresh old limit can be interpreted from human sensory data and single inhalations by animals. It is low enough to prevent definite narcosis. Amyl alcohol (isoamyl alcohol.) Nelson, Ege, Ross, Woodman and Silverman (1943) found slight throat irritation in unac climated subjects at 100 ppm, and objection able eye, nose and throat irritation at higher concentrations. Haggard, Miller and Green berg (1945) found the toxicity 12 times that of ethyl alcohol for anesthetic death. No chronic systemic toxicity is to be ex pected. Smyth (1937-55) found rats not ns June, 1956 killed by eight hours at 2000 ppm, close to saturation. The most important effect of amyl al cohol inhalation is narcosis. The 100 ppm threshold limit can be interpreted' from human sensory data and analogy with butyl alcohol. It is low. enough to prevent signifi' cant narcosis, but not to prevent slight irri tation. Aniline. Henderson and Haggard (1943, p. 227) conclude 7 to 25 ppm gives slight symptoms in several hours, 100 to 160 ppm for one hour causes serious disturbance. Aniline is a chemical asphyxiant, causing methemoglobin cyanosis through its meta bolite, p-aminophenol. This can lead to anemia, but death from a single exposure is due to central nervous effects leading to respiratory paralysis. Skin penetration is more an industrial hazard than inhalation. Smyth (1937-55) found 340 ppm, substan tial saturation, did not kill rats in two hours but was fatal in four, with their hemoglobin 54% converted to methemoglobin. Oberst, Haekley and Comstock (1956) found re peated inhalation of 5 ppm caused methemo globinemia in rats but not any symptoms in dogs. They explained the difference in re sponse by the fact that rats breathe three times as much air per unit time as do dogs, hence absorbed more aniline. The most important effect of aniline in halation is acute poisoning, in which cyano sis is evident but not of major importance. The 5 ppm threshold limit can be inter preted from results of repeated animal in halations. It appears low enough to prevent injury. Antimony. Bradley and Fredrick (1941) administered various antimony compounds orally and intraperitoneally to rats. They concluded it is more toxic than lead, but is not stored. The most important effect was on the heart muscle, and they advised thatexposed workmen should be followed electrocardiographically. Dernehl, Nau and Sweets (1945) exposed guinea pigs to anti mony oxide of one micron diameter at 45 mg./cu.m., three hours a day for . several months. One-sixth died of pneumonitis with severe liver injury and white blood cell changes, but hearts remained normal. Eleetrocardigrams on the animals and on a few industrially exposed workmen were normal. Brieger, Senisch, Stasney and Piatnek (1945) in an industrial operation where antimdny trisulfide concentrations ranged from 0.58 to 5.5 mg./cu.m., found abnormali ties in blood pressure, electrocardiographic changes and two deaths from chronic throm bosis. The most important effects of inhalation of antimony dust are chronic poisoning marked by electrocardiographic changes, pneumonitis and liver injury. The 0.5 mg./cu.m. threshold limit can be interpreted from the results of repeated inhalations and examination of workmen. It appears low enough to prevent injury. ANTTJ (alphano/f>hthylthiourea). Mc- Closky and Smith (1945) found consider able species differences in acute oral toxici ty. The LD50 for rats, the most susceptible species, was about 0.03 gm./kg. Death was due to pleural efusion. Repeated doses caused liver injury. Fitzhugh and Nelson (1947) found rats are not affected by 50 ppm in their diet over a two-year period. Tolerance developed. The most important effect of ANTU in halation is chronic poisoning centering in the liver. The 0.3 mg./cu.m. tentative thresh- hold limit can be interpreted from the re sults of repeated oral doses to rats. It cor responds to a maximum daily absorption of three milligrams, about 0.05 mg./kg. This appears low enough to prevent injury. Arsenic. The earlier limit of 0.15 mg./eu.m. was based upon supposed quanti tative similarity to lead. Watrous and Me- Caughey (1945) found workers exposed to 0.007 to 0.60 mg./cu.m. showed no symp toms. Chronic arsenic poisoning causes ; varied symptoms (I.L.O., 1930, I, p. 161): . digestive disturbance, hyperemia, skin erup- ; tion, pigmentation, keratosis, epithelial ' cancer, polyneuritis, cirrhosis, confusion, delirium, irritation of eyes and respiratory ; tract. Arsenic is stored in the body, but n o t; to the extent of lead. ij The most important effect of inhalation of 1 arsenic compounds is chronic poisoning. The | 0.5 mg./eu.m. threshold limit can be in- s terpreted from the results of examinations 3 of exposed workmen. It appears low enough | to prevent injury. 1 Arsine. Henderson and Haggard (1943, p. 241) describe acute arsine poisoning as due to hemolysis of red blood cells with re sulting anemia and kidney damage, and lung June, 1.956, al operation where icentrations ranged m., found abnormalielectrocardiographic ' from chronic throm- effects of inhalation chronic poisoning liographic changes, : injury. The 0.5 it can be interpreted ated inhalations and en. It appears low ry. '.hylthiourea). Me15) found considerin acute oral toxicithe most susceptible gm./kg. Death was n. Repeated doses tzhugh and Nelson not affected by 50 a two-year period. effect of ANTU insoning centering in .m. tentative threshpreted from the re oses to rats. It cor- daily absorption of , 0.05 mg./kg. This revent injury, jr limit of 0.15 on supposed quanti l. Watrous and Mcworkers exposed to . showed no symp- poisoning causes 1930, I, p. 161) : /peremia, skin eruperatosis, epithelial irrhosis, confusion, yes and respiratory in the body, but not feet of inhalation of -onic poisoning. The 1 limit can be inlts of examinations appears low enough id Haggard 11943, arsine poisoning as blood cells with re;y damage, and lung ` , , ^rr'i^e*`<W,f\itriil Industrial Hygiene Quarterly edema. They state 250 ppm for 30 minutes mcaaptaobrl,eiroriftactaiunsgintog elyuen,gnoesdeeamnad. tFhrluorayt, aanndd tios mfastailn, aanfdew3 htoou1rs0. pNpamu c(a1n94c8a)usreepsoyrmtepd Zernik (1931, p. 538) conclude 170 ppm is an industrial episode showing the earlier dinatnogleerraobulsettoocmatasninineiognhet mhoinuurstea.nIdt m16apypbme l(i1m9i5t0,ofp.1 6p7p)mrewpaosrtetodo bhriigefhl,y aonnd aE.nlkoinns- inferred that the liquid causes severe fatal case at a level of about 0.5 ppm. corneal injury. The only important effect of benzyl chlor The most important effect of arsine in ide inhalation is irritation, first evident in halation is acute poisoning, largely lung the eyes, then in the upper respiratory tract, edema. The 0.05 ppm threshold limit can be bronchi and even lung. The 1 ppm threshold interpreted from the results of industrial limit can be interpreted from older human experience. It appears to be low enough to sensory data. It is undoubtedly low enough prevent injury. . Barium, (soluble compounds), kairhan to prevent lung injury. . (1949, p. 32) records the fatal dose of solu Bromine. Flury and Zernik (1931) quote Lehmann that 0.75 ppm in a workroom ble barium compounds as 0.8 to 0.9 grams caused no symptoms in six hours. Hender with gastro-intestinal disturbance the chiei son and Haggard (1943, p. 133) state bro symptom. He notes bronchial irritation mine acts as a respiratory irritant leading to from barium carbonate dust, and depilatory lung edema. They state 40 to 60 ppm is action of barium sulfide. dangerous on short inhalation, and 4 ppm The most important effect of inhalation allowable for 30 to 60 minutes. Elkins (1950, of soluble barium compounds is bronchial ir p. 87) found 1 ppm excessively irritating. ritation, with acute poisoning possible. The Severe burns of skin and cornea result from 0.5 mg./cu.m. threshold limit can be inter the liquid. Patty (1948-9, p. 554) concludes preted only by analogy with antimony. It ap 0.3 ppm is not objectionably irritating. _ pears low enough to prevent injury. The most important effect of inhalation Benzene. Winslow (1927) first proposed of bromine vapor is respiratory tract irrita a limit of 100 ppm, based on extensive ex tion, with lung edema the maximum effect. amination of exposed workmen and animal The 1 ppm threshold limit can be inter inhalation. He recognized that chronic preted from industrial experience. It ap poisoning would develop in some at this con pears low enough to prevent injury. centration, but believed it would progress Butadiene. Von Oettingen (1940) quotes slowly enough to be detected by periodic repeated animal exposures at 64,000 ppm medical examinations, and arrested by re which caused bronchial and lung irritation moval from exposure. Acute benzene poison ing is fatal anesthesia, and chronic poison and some hyperplasia of J hne ing is primarily injury to the bone marrow. fCoaurnpdenatnerim, Sahlsafnfeort, aWffeeiclteadndbySmreyptheat(e1d94i4n) Befefnecztesnecains ppraortgirceuslsartloyainfsaitdailououstbceocmaeusaeftietsr halation of 2300 ppm, while 6700 ppm all exposure ceases. Even brief inhalation smliignhotrly lirveetrardeeffdectgsr.owTtwho anhdumtahnesre fowuenrde obfe afathailg.hPnaottny-a(n1e9s4th8-e9ti,cp.co7n5c7e)ntsrtaattieosn tchaant psychomotor effects of early narcosis from 100 ppm has only a faint odor. Elkins (1950, 8000 ppm, equivalent to those from 200 p. 228) investigated a fatal case whose ppm toluene. The most important effect of butadiene 'exposure he was convinced had been only to vapor inhalation is narcosis. The 1000 ppm 40Ttohe80mpopsmt i.mportant effect of benzene i.n tshurletsshoolfd lriempeitatceadn baeniminatel rpirnehtaeldatfiroonm arned hthaelatbioonneismcahrrroowni.c Tpohieso3n5ingppcmenttherreinsgholind single human inhalation. It is low enough limit can be interpreted from extensive ex to prevent any degree of narcosis. Butanone (methyl, ethyl ketone). Patty. amination of exposed workmen, and was Schrenk and Yant (1935) found guinea pigs quantitatively defined by one fatal case. It tolerated 3000 ppm for several hours, and appears low enough to prevent the develop men found it irritating to nose and eyes. meBnetnozyf lircrhelvoerrisdieb.leTphoisisoisninag.potent lacri- Nelson, Ege, Ross, Woodman and Silverman  i ' : if: is $' ' i;i ' if 1 %I l i f e ; P I -t U8 June, 1956 (1943) found slight throat irritation in un acclimated subjects at 100 ppm, irritation of eyes at 200 ppm and objectionable irrita tion at 300 ppm. Elkins (1950, p. 118) found complaints of nausea at 500 ppm, irritation at 300 ppm, but no ill effects at 700 ppm. Smyth (1937-55) found rats survived two hours at 2000 ppm but 4000 ppm killed four of six. He found that an episode of indus trial eye injuries during inhalation of bu- tanone was caused by an unsaturated ketone impurity accidently present. The most important effect of butanone inhalation is narcosis. The 250 ppm thresh old limit can be interpreted from human sensory data. It appears low enough to pre vent definite narcosis. Butyl acetate. Sayers, Schrenk and Patty (1936) found guinea pigs are not affected by several hours inhalation of 3300 ppm. Nelson, Ege, Ross, Woodman and Silverman (1943) found throat irritation in unaccli mated subjects at 200 ppm, severe at 300 ppm. Henderson and Haggard (1943, p. 222) conclude the ester shows no chronic toxicity. Smyth (1937-55) found rats inhaling sub stantially saturated vapors are not killed in four hours, but died within an eight-hour inhalation period. . The most important effect of butyl acetate inhalation is narcosis. The 200 ppm thresh old limit can be interpreted from human sen sory response and single inhalations by animals. It is low enough to prevent defi nite narcosis. Butyl alcohol (n-butanol). Tabershaw, Fahy and Skinner (1944) reported eye in flammation in workmen above 50 ppm, but no systemic effects below 100 ppm. Sterner, Crouch, Broekmyre and Cusack (1949) fol lowed workmen for 10 years with butyl al cohol concentrations held to 100 ppm, and for a briefer period to 200 ppm. Neither ir ritation nor systemic effects were found at 100 ppm, but there was some eye irritation at 200 ppm. Smyth (1937-55) found rats are not killed in four hours at 8000 ppm. The most important effect of butyl al cohol inhalation is narcosis. The 100 ppm threshold, limit can be interpreted from an extensive study of workmen under condi tions of known peak exposure. No narcotic or irritative effects are to be anticipated. Butyl amine. Hanzlik (1923). reported central nervous stimulation, convulsions, then depression and narcotic death with pul monary edema. Smyth (1937-55) found rats survive four hours at 2000 ppm but die from 4000 ppm. Injury to skin and cornea from the liquid is severe. Unreported industrial experience suggests skin injury is the great est practical hazard. ACGIH (1955b) cites unpublished industrial experience that levels above 5 ppm tend to be irritating. The most important effect of butyl amine inhalation is respiratory tract irritation, with lung edema the maximum injury. The 5 ppm threshold limit can be interpreted from analogy with ethyl amine. It is prob ably low enough to prevent injury. Butyl CELLOSOLVE (2-butoxyethanol). Werner, Nawrocki, Mitchell, Miller and von Oettingen (1943) found 300 to 400 ppm, in repeated inhalation produced only small ef fects on rats, particularly on the blood pic ture. Werner, Mitchell, Miller and von Oet tingen (1943a, b) reporting on single in halations by rats and repeated by dogs, make it clear that the butyl ether produces somewhat greater blood cell changes than do the methyl or ethyl ethers. They also found hemoglobinuria, with lung, liver and kidney changes. Smyth (1937-55) found in rats fractional mortality from as little as 500 ppm inhaled eight hours, with hematuria a prominent symptom. The liquid penetrates the skin readily and is sufficiently toxic so that this is dangerous. The most important effect of butyl Ce l losolve inhalation is chronic poisoning, centering in the blood cells and kidney. The 200 ppm threshold limit can be interpreted from results of repeated animal inhalation studies. Based on reports from simultaneous studies of Ce l l o so l v e and butyl CELLOSOLVE it is obvious that the threshold limit for the latter should be lower than for the former if equal degrees of protection are to be at tained. Butyl mercaptan. Fieldner, et al. (1931) reports 733 ppm to be lethal to dogs in 30 . minutes, indicating 20 times the acute toxicity of ethyl mercaptan. Effects like those of hydrogen sulfide are to be expected. The most important effect of butyl mer captan is eye and respiratory tract irrita tion. The 10 ppm tentative threshold limit can be interpreted from the results of lim ited single inhalations by animals and an alogy with hydrogen sulfide. It appeal's low  D 'f? ':' Y ear: Mq b e 5 :'SM 1956 .1956. June, 1956 larcotic death with pulh (1937-55) found rats 2000 ppm but die from skin and cornea from Unreported industrial kin injury is the greatACGIH (1955b) cites il experience that levels be irritating, it effect of butyl amine atory tract irritation, maximum injury. The lit can be interpreted thyl amine. It is probu-event injury. VE (Z-butoxyethanol). titchell, Miller and von und 300 to 400 ppm, in iroduced only small efilarly on the blood picill, Miller and von Oeteporting on single innd repeated by dogs, ie butyl ether produces >od cell changes than do thers. They also found . lung, liver and kidney 37-55) found in rats from as little as 500 iurs, with hematuria a The liquid penetrates is sufficiently toxic so is. i t effect of butyl Celis chronic poisoning, i cells and kidney. The mit can be interpreted ated animal inhalation orts from simultaneous 3 and b u ty l Cellosolve threshold limit for the ir than for the former protection are to be at- Fieldner, et al. (1931) ie lethal to dogs in 30 20 times the acute ercaptan. Effects like fide are to be expected, it effect of butyl merispiratory tract irritantative threshold limit om the results of limi s by animals and an sulfide. It appears low Industrial Hygiene Quarterly ' enough to prevent injury and eye irritation. repeated exposure the effects may be neuro Cadmium oxide fume. Prodan (1932) on logical, not recognized by the victim. Hen the basis of animal experiment concluded derson and Haggard (1943, p. 223) state it is as toxic as lead. Spolyar, Keppler and that 480 to 1600 ppm is the maximum Porter (1944) reported on serious poison breathable for one hour without serious dis ing and fatalities from industrial exposure turbance. to the fume. Fairhall (1949, p. 45) con The most important effect of carbon di cludes inhalation causes bronchial irrita- sulfide inhalation is chronic poisoning with .tion and pneumonitis, while ingestion pro centra] nervous system effects. The 20 ppm duces gastro-intestinal disturbances. threshold limit can be interpreted from the The most important effect of inhalation results of repeated animal inhalations and of cadmium oxide fume is severe lung in examination of exposed workmen. It is low jury, with systemic poisoning less impor enough to prevent injury. tant. The 0.1 mg./cu.m. threshold limit can Carbon monoxide. Henderson, Haggard, not be interpreted quantitatively, but it Teague^ Prince and Wunderlich (1931) sug appears low enough to prevent injury. gested a limit of 100 ppm on the basis of Calcium Arsenate. ACGIH (1954b) bases extensive human experiment. Sayers, Yant, the tentative threshold limit upon a rat Levy and Fulton (1929) showed 200 ppm . oral LD60of 100 mg./kg., and blind litters in caused slight symptoms in humans. Sievers, rats fed 5 mg./kg. for 45 days. Edwards, Murray and Schrenk (1942) The most important effect of inhalation of found 70 ppm over a 13-year period had not calcium arsenate dust is chronic arsenic affected health. Carbon monoxide is a chemi poisoning, with bronchial irritation less cal asphyxiant, acting by combining with important. The 0.1 mg./cu.m. tentative hemoglobin. Henderson and Haggard (1943, threshold limit should be interpreted from p. 167) define its effects in terms of the ) the threshold limit for arsenic dusts. Since product of time and concentration, 100 ppm calcium arsenate is 20% arsenic, a thresh for three hours producing no effect; for six old limit of 2.5 mg./cu.m. would be consis hours, a just appreciable effect; for nine tent with the accepted limit for arsenic hours, headache and nausea; and for 15 dusts. hours, danger. One hour at 4000 ppm may Carbon dioxide. Flury and Zernik (1931) be fatal. Vigliani and Zurlo (1955) study ) quote Lehman-Hess to the effect that 5500 ing 100 workers found no injury to health ppm causes no noticeable symptoms in six at 100 ppm for eight hours every day. In hours. Aero Medical Association (1953, p. the United States chronic poisoning is not 52) considers the gas as weakly narcotic, considered a reality. 30,000 ppm increasing respiration by 90%, The most important effect of carbon mon increasing pulse and blood pressure, and oxide inhalation is chemical asphyxia, re decreasing acuity of hearing. Subjective ducing the oxygen carrying power of the symptoms arise above this level, 50,000 ppm blood. The 100 ppm threshold limit can be for 30 minutes giving the first signs of in interpreted from the results of extensive toxication, and 70,000 to 100,000 ppm caus human experiment and examination of ex ing unconsciousness in a few minutes. posed workman. It will prevent injury, but The most important effect of carbon di will allow a recognizable effect if inhaled oxide inhalation is asphyxia at very high for eight hours. concentrations. The 5000 ppm threshold Carbon tetrachloride. Elkins (1950, p. limit can be interpreted from the results of 229) on the basis of industrial experience, . extensive human experiments. It is low concluded the earlier figure of 100 ppm was enough to prevent noticeable effects. ^ too high and suggested 40 ppm. Adams, Carbon disulfide. Wiley, Hueper and von Spencer, Rowe, McCollister and Irish (1952) Oettingen (1936) found repeated inhalation in extensive animal studies, found some ef of 30 ppm has no significant effect on fect on the liver in some species at all con animals. Barthlmy (1930) found no in centrations above 5 ppm. Smyth (1937-55) juries to rayon workmen when concentra found rats survive eight hours at 3000 ppm, . tions were kept below 30 ppm. In single in but 8000 ppm is fatal. Human anesthesia, halations, it is markedly narcotic, and in or near anesthesia, is usually fatal from ISO kidney injury, while early narcosis occurs at a low concentration. Chrome toxicity is posures of the order of 5 mg./cu.m. showed! no clinical evidence of effect. Alvarez and! Hvman (1953) examined men m anotbei| chiefly marked by liver injury. ^ . The most important effect of carbon producing plant with up to five years e x | posure and found no effects, but conce" tra| tions were not measured. Ingle (1953)J shows that early reports of inhalation in | jury in animals were due to a volatilei u n | xtierience It is low enough to prevent ir t p ,r ta it 11 <to" reacted intermediate in the ear}y pf.od J and that 14 days continuous m halationos saturated air does not injure mice. AUtxil "S tS S Nawrocki, Mitchell, Killer <ren (1943) found rats repeatedly inhaling (1954b) bases its tentative threshold limil nn a rat oral IjDso of 590 8 The most important effect of chlordanl inhalation is chronic poisoning centenng if 300 to 400 ppm showed small but the liver. The 2 mg./cu.m. threshold lim j S . bleed "ell effects. W .m e,, M .tehdl can be interpreted from the results of ex Miller and von Oettmgen ^ ^ ^ v e l o p e d dogs inhaling BOO ppm repeatedly developed Onfall blood cell effects. Smytfc 1937-5^ L lirwi rats survive four hours at 2000 ppm, but half are killed by 4000 and all are killed ' e S hours at 4000 ppm, close to satura tion. Death is marked by severe kidney dam- aminations of exposed workmen. It is lo| enough to prevent injury. , $ Chlorinated camphene, 60% (toxaphenej T.ackev (1949) found an oral dose ox If mg./kg. caused convulsions in dogswlul| m g/kg. was fatal. A daily dose of 4 m g./k| for l06 days was not fatal, but at tames coj agThe most important effect of cbluisolve inhalation is chronic poisoning centering m vulsions were seen. Liver and k id n | changes resulted. ,,bw i! The most important effect of ehlorij the red blood cells. The 200 ppm threshold ated camphene is chronic poisoning centej limit can be interpreted from results of r ing in the liver. The 0.5 mg./cu.m. tentatif peated animal inhalation studies. Ita p p ^ to be low enough to prevent injury. There are no'data to judge the degree of eye and threshold limit can be interpreted fro tj results of single and repeated ral dos| and by analogy with the similar but le toxic DDT. It appears low enough to Pt VC^Chlorinated diphenyl oxide. After ext^ sive inhalation studies with rats, Drin f s m S c r e a s e in with eye and nose rrntatmn Rate surviv (close to saturation) tor iour S s t a t t i e e f X die after eight hours. (1949) concluded that 0.5 mg./cu.m. 1 permissible concentration which will L d to systemic injury. Liver injury is effect of chronic poisoning. Smyth (19 KWi si r e aUcid. tSoyds"te^micdi.n1j0ur'yT sohoSuldl otoilitoaw 55) found the material penetrates the sk| and repeated contact leads to chloracne. closely that of CELLOSOLTO. but respiratory The most important effect of chlonnaj tract irritation is somewhat greater. diohenvl oxide inhalation is chronic pois| " L most important effectef f f S centering in the liver. The 0 5>mg-/cu| acetate is chronic poisoning due to hydroly threshold limit can be mterpreted from | ^ to clbOSOhVE. The 100 ppm threshed results of repeated animal inhalations, it limit can be interpreted from analogy with low enough to prevent.mjury. at)| CELi.OSOLVE. It appears iow enoughtopre- Chlorine. Sklyanskaya and Rappap| vent injury. There are no data to judge xne (1935) found lung injuries and increased j S r e . T ,, ., and nose irritation it ataTM . cidence of pneumonia in guinea pigs . Chlordane. Frinci and Spurbcck O ) n e a S y Tnhahng 0.7 to 1.7 ppm. Fairhall quote animal data indicating effects are a950 p. 52) states it irritates eyes and principally neurological, with live* S a i d J y c.uee . ney injury and pulmonary irritation.'Th y T-liftlo+iATI nf *1000 J J __ vears with ex IT S T o l^JD 1956 Jwne, 1956 ' , ' 5 mg./cu.m. showed , ' effect. Alvarez and* ned men in another up to five years exffects, but concentra.ured. Ingle (1953) rts of inhalation in due to a volatile unn the early product, ;inuous inhalation of injure mice. ACGIH cative threshold limit >90 mg./kg. t effect of chlordane >oisoning centering in cu.m, threshold limit Dm the results of ex1 workmen. It is low jury. ne, 60% (toxaphene). I an oral dose of 10 sions in dogs while 15 laily dose of 4 mg./kg. atal, but at times con- Liver and kidney nt effect of chlorinonic poisoning center).5 mg./cu.m. tentative ; interpreted from the l repeated oral doses, , the similar but less rs low enough to pre- y l oxide. After exten es with rats, Drinker at 0.5 mg./cu.m. is a ation which will not ry. Liver injury is the soning. Smyth (1937al penetrates the skin, leads to chloracne. it effect of chlorinated ition is chronic poisoniver. The 0.5 mg./cu.m. e interpreted from the nimal inhalations. It is t injury. kaya and Rappaport juries and increased inia in guinea pigs re7 to 1.7 ppm. Fairhall s it irritates eyes and e fatal lung irritation. >pm is rapidly fatal, 40 Industrial Hygiene Quarterly to 60 ppm may lead to pneumonitis ana lung cphrologrroebsrsoivmeoemffeetchtasnoenislivnearrcanodsiskiwdniethy. nTohne ethdreomaat,ir3r0itaptipomn acnadus3e.5s pcpomugchainngb,e 1sm5 epllpemd. 400 ppm tentative threshold limit can be in Patty (1948-9, p. 547) concludes 1 to 2 ppm terpreted from the results of repeated in is tolerable, 3 to 6 ppm irritating. halations with animals. It appears low The most important effect of inhalation enough to prevent injury. Chlorodiphenyl (4-2% chlorine). After ex of chlorine gas is respiratory tract tensive inhalation studies with rats, Drink tion, with lung edema the maximum effect. er (1939) concluded that 10 mg./cu.m. of a The 1 ppm threshold limit can be interpreted sample 68% chlorine, but free from chlorin from repeated animal inhalation and human ated diphenyl benzene, would lead to no sensory data. I t is low enough to prevent systemic injury, but that the presence of injury. . Chlorine trifluoride. Horn and vyeii chlorinated diphenyl benzene reduced the (1955) found it an extremely active irri p(1er9m37is-5si5b)lefoluinmditthteo m0a.5termiagl.p/ceun.met.ratSems yththe tpapnmt., wRhaitlse raartes kainlldeddoigns i4n0hamliinngut5esppamt r9e6 skin, and repeated contact leads to chlor peatedly are severely injured. Pneumonia a(c1n9e5.6T) reroenp,oCrtleedveltahnadt, Cianphpaellataionnd Aotfchl8e.6y wficauslitnycirneaaslel.d Tahned tvhaeproerswainsjruersepitrhaetocroyrndeiaf. mg./cu.m. for 24 seven-hour periods did not Horn and W eir (1956) found repeated in affect four species of animals, and 1.9 halation of 1.17 ppm by rats and dogs in mg./cu.m. for 150 periods also was without jured only by increased incidence of pneu effect. The most important effect of chloro monia. The most important effect of inhalation diphenyl inhalation is chronic poisoning, of chlorine trifluoride gas is respiratory centering in the liver. The 1 mg./cu.m. threshold limit can be interpreted from the tract irritation, with lung edema the maxi results of repeated animal inhalations. It is mum effect. The 0.1 ppm threshold limit can be interpreted from repeated animal inhala low enough to prevent injury. tion. It appears low enough to prevent m- ClCevhelloarnodd,ipChaepnpyel,l a5nJdf%Atcchhlleoyrin(e1.95T6)reorne, jurCyh. lorobenzene. Fairhall (1949, p. 260) pmoorntetdh tpheartiordepoefat1e.d5 imnhga./lcauti.omn. ocvaeurseadsesvoemne- cboennczleundee,sbiutt ifsinsdosmneowheavtidmenocree otof xhicemthataon- minor liver injury in four species of rodents. The most important effect of inhalation of poetic effect. The most important effect of chloroben chlorodiphenyl (54% chlorine) is chronic zene inhalation is narcosis. The 75 ppm tmogx.i/cciuty.m.cetnentetraitnivge itnhrethsheolldivleirm. itThcean 0b.5e trhoruegshhoeldstilmimaitte.caBnybceoimntpearrpisroetnedwoitnhlyoathsear interpreted from the results of repeated in chlorinated hydrocarbons, it appears low halation by animals. It appears to be slight enough to prevent injury. ly below an injurious concentration, Chloroform. Fairhall (1949, p- 264) con Chlorobromomethane. Svirbely, Hignman, cludes it acts much like carbon tetrachlor Alford and von Oettingen (1947) found 3000 ide, and that anesthetic use has led to liver ppm to be the LC50 for mice in eight-hour injury, but regression is more likely than inhalations. Exposures of rats, rabbits and with carbon tetrachloride. A concentration dogs to 1000 ppm seven hours a day five of 4000 ppm causes slight symptoms after days a week for fourteen weeks were with several hours exposure. Patty (1948-9, p. out effect. Non-progressive liver injury was 793) concludes the least concentration found from single inhalations, but liver and smelled is 200 to 300 ppm.-Smyth (1937-55) kidney remained normal during the repeated found one of six rats die from four hours at inhalations. Comstock et al. (1952) found 4000 ppm, and all from 8000 ppm. light narcosis in rats and mice inhaling 3000 The most important effect of inhalation of ppm for 10 to 15 minutes, and about 30,000 chloroform is chronic poisoning centering in ppm was fatal within 15 minutes. Pulmo the liver. The 100 ppm threshold limit can naTryheedmeomsat iwmapsoprrteasnetnetffienctanoifminahlsaldaytiionng.of be interpreted from the results of single SIf 2Q. * JC^3D 5 to 1 E ft~ECO 6 >* Is *u "o t Q t v 11 11 I fr. o <as> =<1=5 1 8 o -go> ao. o 05 05 CO Q- r C * E t .55 | <L> t 1 V 0) x SI & \-- 152 June, 1956 animal inhalations and human sensory re sponse. It appears low enough to prevent injury, but in view of changes in ideas about carbon tetrachloride, new data are desirable. 1-Chloro-l-nitropropane. Machle, Scott, Treon, Heyroth and Kitzmiller (1945) ex posed animals for six hours to 400 ppm. Ef fects were chiefly irritation of eye, nose bronchi and lung, with some injury to liver, kidney and vascular system, and 25% died. Simultaneous repeated studies on 1,1-dichloro-l-nitroethane showed little cumula tive action. The most important effect of 1-chloro-lnitroethane is lung injury. The 20 ppm threshold limit can be interpreted from the results of single animal inhalations. It ap pears low enough to prevent injury. Chloropicrin. Fairhall (1949) concludes it is an irritant gas, producing bronchial and lung injury. He concludes 20 ppm produces lesions within one to two minutes and that 4 ppm will incapacitate a man. The most important effect of chloropicrin is respiratory tract irritation with lung in jury probable. The 1 ppm tentative thresh old limit can be interpreted from sum maries of studies of its use as a war gas. It appears low enough to prevent serious in jury. Ckloroprene (2-chlorobutadiene). Von Oettingen, Hueper, Deichmann-Gruebler and Wiley (1936) made repeated inhalation studies with animals. A concentration of 83 ppm caused some respiratory irritation, cen tral nervous system depression, and effects on liver, kidney and vascular system. Skin penetration was dangerous. The most important effect of chloroprene inhalation is chronic poisoning, centering in the liver. The 25 ppm threshold limit can be interpreted from the results of repeated animal inhalations. It appears low enough to prevent injury.Chromic acid. Bloomfield and Blum (1928) and Riley and Goldman (1937) dem onstrated in industrial surveys that per foration of the nasal septum and other up per respiratory tract effects of chromic acid mists are not found at a concentration of about 0.1 mg./cu.m. Other effects are not produced. Vigliani and Zurlo (1955) found ulcerated nasal septum, inflamed larynx, chronic bronchitis and two respiratory tract cancers among 150 workers exposed to 0.11 to 0.15 mg./cu.m. The most important effect of inhalation of chromic acid aerosol is upper respiratory tract irritation, leading to perforation of the nasal septum. The 0.1 mg./cu.m. thresh old limit can be interpreted from studies of exposed workmen. It is low enough to pre vent injury. CRAG herbicide. ACGIH (1954b) sug gests on the basis of a general low toxicity and a rat oral LD50 of 1500 mg./kg., that 10 mg./cu.m. is a fit limit. Smyth (1937-55) found death from a single oral dose due to respiratory paralysis with injuy to liver and kidney. Rats are not affected by 0.02% in their diet for two years, and 0.06% causes minor effects on liver and kidney. The most important effect of CRAG her bicide inhalation is chronic poisoning cen tering in the liver. The 15 mg./cu.m. thresh old limit can be interpreted from the results of single and repeated oral doses to animals. It appears low enough to prevent injury. Cresol. Fairhall (1949, p. 271) concludes effects and practical hazards are like those of phenol. Smyth (1937-55) found rats sur vive eight hours inhalation of vapors sub stantially saturated at room temperature; The liquid penetrates the skin to a danger ous extent, and causes severe skin and cor neal injury. The odor appears to be some what more intense than that of phenol. Although cresol vapors are odorous an . irritating, their major effect is chronic systemic poisoning. The 5 ppm threshol limit can be interpreted from analogy with phenol. It appears to be low enough to pre vent chronic poisoning. Cyanide as CN. To the extent that cya nide dusts dissolve, their toxicity is that o hydrogen cyanide, with some added local ir ritation due to hydrolysis on moist tissue Cyanide dust equivalent of the 10 pp threshold limit for hydrogen cyanide is 1' mg./cu.m. The 5 mg./cu.m. threshold limi is about half that for hydrogen cyanid) and hence is conservative. Cyclohexane. Treon, Crutchfield an Kitzmiller (1943) found minor liver akidney changes in animals repeatedly haling 786 ppm, none at 434 ppm. Fairh` (1949, p. 273) concludes acute poisoning; anesthesia and that repeated inhalati causes no hematopoetie changes. Pa' 15S June, 1956 Industrial Hygiene Quarterly kers exposed to 0.11 (1948-9, p. 769) reports 300 ppm has no dis aferdctionfincydculsotpriraolpaunsee. gTahseimnhoasltaitmiopnoirstannatrceof tinct odor or irritation. ' The most important effect of cyclohexane sis. The 400 ppm threshold limit can be in effect of inhalation is upper respiratory . inhalation is narcosis, with non-progressive terpreted from analogy with cyclopentane, organic effects. The 400 ppm threshold lim and by human surgical use. It is probably g to perforation of ' it can be interpreted from results of re low enough to prevent definite narcosis. ).l mg./cu.m. thresh- peated animal inhalation. It is low enough 2,4-D. Rowe and Hymas (1954) conclude eted from studies of , low enough to pre- ' to prevent definite narcosis. that it has a low degree of chronicity, and the acute LD50 values range from 300 to Cyclohexanol. Treon, Crutchfield and Kitz 1000 mg./kg. for various species. miller (1943) reported that repeated inhala The most important effect of 2,4-D inhala 1GIH (1954b) suggeneral low toxicity tion of 693 ppm caused minimal pathologi tion is chronic poisoning centering m the .500 mg./kg., that 10 cal changes in a monkey, and 145 ppm m liver. The 10 mg./cu.m. threshold limit can the livers and kidneys of rabbits. Nelson, be interpreted from the results of single and t. Smyth (1937-55) ingle oral dose due Ege, Ross, Woodman and Silverman (1943) repeated oral doses to animals. It appears 5 with injuy to liver found 100 ppm causes objectionable eye, low enough to prevent injury. nose and throat irritation in unacclimated DDT. Barnes (1953) finds no incidence of ot affected by 0.02% years, and 0.06% ' subjects. Smyth (1937-55) was unable to illness among workers using it throughout liver and kidney, kill rats by eight hours inhalation Oj. sub the world. Poisoning from accidental inges effect of CRAG her- stantially saturated vapors. The most important effect of cyclohexanol tion is marked by abdominal pain, vomit ronic poisoning cen15 mg./cu.m. thresh- inhalation is narcosis, with non-progressive ing dizziness and weakness. Long repeated organic 'effects less prominent. The 100 ppm doses of 25 to 50 mg./kg. are required to sted from the results threshold limit can be interpreted from re poison animals, although man is probably iral doses to animals. ;o prevent injury. sults of repeated animal inhalations and human sensory data. It is low enough to more sensitive. __ . , The most important effect of DDT inhala tion is chronic poisoning centering in the ;9, p. 271) concludes izards are like those . prevent significant narcosis or injury, but liver. The 1 mg./cu.m. tentative threshold -55) found rats sur- noCt tyoclporheevxeanntonirer.itaTtiroenon. , Crutchfield and limit can be interpreted from the results of ition of vapors sub Kitzmiller (1943) in animal experiments repeated oral doses to animals. It appears . room temperature. he skin to a danger- found only narcosis and irritation. Nelson low enough to prevent injury. Decaborane. Svirbely (1954a,b) found severe skin and cor- Ege, Ross, Woodman and Silverman (1943) the LC3o for mice inhaling vapors for four found 50 ppm caused objectionable eye, nose hours to be 25.7 ppm. Symptoms included appears to be somen that of phenol, and throat irritation in unacclimated sub central nervous excitability and corneal ars are odorous and jects. Smyth (1937-55) did not kill rats by opacity. Six-hour inhalations of 20 ppm by r effect is chronic four hours at 4000 ppm, but 8000 ppm rats, repeated 20 times, killed some with he 5 ppm threshold d from analogy with caused anesthetic death. The most important effect of cyclohexa none inhalation is narcosis. The 100 ppm fatty livers and central nervous excitability. Comstock and Oberts (1953) report that e low enough to pre- threshold limit can be interpreted from re the median detectable odor is 0.35 mg/cu.m. peated animal inhalations and human sen (0.07 ppm), described as foul or chocolate the extent that cyair toxicity is that of sory response. It is probably low enough to like. The most important effect of decaborane some added local ir- prevent definite narcosis. inhalation is acute toxicity involving the vsis on moist tissue. Cyclohexene. Fairhall (1949, p. 279) con central nervous system, with liver injury cludes that 9000 ppm causes mild narcosis in less important. The 0.05 ppm tentative ;nt of the 10 ppm irogen cyanide is 11 animals, while 13,500 to 15,000 ppm gives threshold limit can be interpreted from lim :u.m. threshold limit anesthetic death. This, indicates a toxicity ited animal inhalations. It appears to allow r hydrogen cyanide, greater than that of cyclohexane. The most important effect of cyclohexene an adequate margin of safety. ;ive. ' inhalation is nareosis. The 400 ppm thresh Diacetone alcohol. Von Oettingen v.1943, l, Crutchfield and nd minor liver and : old limit can be interpreted from results ot p 138) reports animals at 2100 ppm are restless, irritation and kidney effectsf are imals repeatedly in- single animal inhalations. It is low enough noted. He concludes it is twice as toxic as at 434 ppm. Fairhall to prevent definite narcosis. acetone. Silverman, Schulte and First Cyclopropane. Fairhall (1949, p. 280) re e s acute poisoning is repeated inhalation views reports of experience in surgical anes (1946) found 100 ppm irritating to eyes, nose and throat but not intolerable m un- tic changes. Patty . thesia and concludes there is no toxic haz- 154 June, 1956 acclimated subjects. Smyth (1937-55) found difluoromethane inhalation is asphyxia from 1500 ppm, approaching- saturation, did not extremely high concentrations. The 1000 kill rats in eight hours. ppm threshold limit can be interpreted from The most important effect of diacetone al the results of repeated animal inhalations. cohol inhalation is narcosis. The 50 ppm It represents good engineering control threshold limit can be interpreted from rather than a hazard limit. single animal inhalations and human re 1,1-Dickloroethane. Henderson and Hag sponse. It appears low enough to prevent gard (1943, p. 207) conclude it is similar to definite narcosis. carbon tetrachloride. Smyth (1937-55) Diborane. Rozendaal (1951) reported on found rats survive eight hours at 4000 ppm, five human injuries from inhalation of but are killed at 16,000 ppm, an acute toxici diborane and other boron hydrides. Dibor ty half that of carbon tetrachloride. In re-' ane produced symptoms like metal fume peated inhalations by rats and dogs, chron fever and severe central nervous system ir ic toxicity somewhat less than that of car ritation. Krachow (1953) reported that bon tetrachloride was likewise found. single inhalations of 50 ppm may be fatal to The most important effect of 1,1-diehlorrats, resulting in lung injury, while 6 ppm oethane inhalation is chronic poisoning repeatedly for three weeks causes lung centering in the liver. The 100 ppm. thresh damage, and 2 ppm causes some lung injury old limit can be interpreted from single and within four weeks. Kidney effects are also repeated animal inhalations. It may be low noted: He finds diborane about as injurious enough to prevent injury, but new data are as phosgene. Odor is evident at 2 to 4 ppm. desirable in view of current views on car The most important effects of diborane bon tetrachloride. inhalation are central nervous system irri -i/wMinrawywie. r airnall (.1949, p tation and lung injury. The 0.1 ppm thresh 292) concludes 39,000 to 50,000 ppm is lethal old limit can be interpreted from the effects to guinea pigs, and 18,000 ppm produces of repeated animal inhalation and clinical narcosis. Acute poisoning consists of narco studies on accidental human injuries. It is sis with central nervous system irritation. apparently low enough to prevent injury. No liver injury has been found. The vapors O-Dichlorobenzene. Cameron, Thomas, are irritating. Smyth (1937-55) found the Ashmore, Warren, Buchan, and Kenny- cis isomer did not kill nor anesthetize rats Hughes (1937) found 30 minutes inhalation in four hours at 8000 ppm, while 16,000 ppm of 390 ppm caused in animals, liver necro anesthetized in eight minutes and killed in sis and minor kidney injury. They concluded four hours. The trans isomer was twice as it is more toxic than chlorobenzene. Fairhall toxic and anesthetic. (1949, p. 284) points out its narcotic The most important effect of 1,2-dichlor- properties. Elkins (1950, p. 147) reports oethylene inhalation is narcosis. The 200 some irritation of eye and respiratory tract ppm threshold limit can be interpreted from from 100 ppm, without other effects. the results of single animal inhalations. It The most important effect of o-dichloro- is low enough to prevent definite narcosis. benzene inhalation is chronic poisoning cen Dichloroethyl ether. Schrenk, Patty and tering in the liver. The 50 ppm threshold Yant (1933) found 500 to 1000 ppm killed limit can be interpreted from the results of guinea pigs in 30 to 60 minutes with lung single animal inhalations and human sensory hemorx-hage and edema, while 35 ppm pro response data. It does not appear to allow duced slight irritation in several hours. This sufficient margin to prevent human in concentration can be smelled but is not im jury from continuous inhalation. mediately irritating to man, while 500 to Dichlorod/ifluoromethane. Sayers, Yant, 1000 ppm is lacrimating. Smyth (1937-55) Chornyak and Shoaf (1930) found animals found rats survive four hours at 125 ppm, exposed repeatedly to 200,000 ppm developed but are killed by 250 ppm. Skin penetration a generalized tremor and ataxic gait, but no is moderately dangerous. gross pathology. Fairhall (1949, p. 347) The most important effect of dichloroethyl. notes it has little, if any anesthetic or toxic action. ether inhalation is lung injury. The 15 ppm : threshold limit can be interpreted from the ? The most important effect of dichloro- results of single animal inhalations. I t : N otes : June, 1956 is asphyxia from .tions. The 1000 interpreted from imal inhalations, ineering control derson and Hagie it is similar to nyth (1937-55) mrs at 4000 ppm, i, an acute toxiciachloride. In reand dogs, chronhan that of carvise found, ct of 1,1-dichlorronic poisoning, 100 ppm threshfrom single and 3. It may be low >ut new data are it views on car- irhall (1949, p. 000 ppm is lethal 5 ppm produces insists of narco'stem irritation, und. The vapors 7-55) found the anesthetize rats vhile 16,000 ppm :es and killed in er was twice as t of 1,2-dichlor- rcosis. The 200 nterpreted from 1 inhalations. It inite narcosis, enk, Patty and 1000 ppm killed j i rutes with lung ile 35 ppm pro eral hours. This i but is not im i, while 500 to nyth (1937-55) irs at 125 ppm, kin penetration of dichloroethyl ry. The 15 ppm ireted from the inhalations: It Industrial Hygiene Quarterly seems to be low enough to prevent injury. Dichloromonofluoromethane. N u c k o 11 s (1933) showed it is little different from other fluorocarbons used as refrigerants. They are practically inert in the body. The most important effect of dichloro monofluoromethane inhalation is asphyxia from extremely high concentrations. The 1000 ppm threshold limit can be inter preted by analogy with other fluorocarbon refrigerants. It represents good engineering control rather than a hazard limit. 1,1-Dichloro-l-nitroethane. Machle, Scott, Treon, Heyroth and Kitzmiller (1945) found 25 ppm did not kill animals in a total of 204 hours inhalation. The vapors irri tated eyes, nose, bronchi and lungs, with in jury to liver, kidney and vascular system. The most important effect of 1,1-dichloro1-nitroethane inhalation is lung injury. The 10 ppm threshold limit can be interpreted from the results of repeated animal inhala tions. It appears low enough to prevent injury. Dichlorotetrafluoroethane. N u c k o 11 s (1933) and Yant, Schrenk and Patty (1932) found only transient discomfort in animals exposed two hours to 25,000 ppm. No chron ic effects are to be expected from this physi ologically inert material. The most important effect of dichlorotetrafluorethane inhalation is asphyxia from very high concentrations. The 1000 ppm threshold limit can be interpreted from the results of single animal inhalations. It ap pears to be far below a possible injurious level. Dieldrin. The workers examined by Princi and Spurbeck (1951) after three years in dustrial exposure to several related insecti cides including dieldrin with concentrations of the order of 5 mg./cu.m., showed no evi dence of clinical effect. Treon and Cleveland (1955) found 25 ppm in the diet of rats for two years did not shorten their lives. Dogs are most sensitive, tolerating only 3 ppm. Chronic toxicity centered in the liver. In acute poisoning, central nervous system ir ritation is prominent. Dieldrin penetrates the skin. The most important effect of dieldrin in halation is chronic poisoning centering in the liver. The 0.25 mg./cu.m. threshold limit can be interpreted from the results of re peated oral doses to animals and results of examination of exposed workmen. It is low enough to prevent injury. Diethylamine. Brieger and Hodes (1951) exposed rabbits repeatedly to 50 ppm and found lung and corneal injury, but animals survived with some liver injury. Smyth (1937-55) found rats suffer fractional mor tality from four hours at 2000 and 4000 ppm, while 8000 is lethal to all. The liquid is extremely injurious to the cornea. The most important effect of diethylamine inhalation is respiratory tract irritation, with lung edema the maximum injury. The 25 ppm threshold limit can be interpreted from results of repeated animal inhalation. It appears low enough to prevent injury. Difluorodibrornomethane. ACGIH (1955b) quotes Chemical Corps Medical Laboratories Research Report No. 180, 1953. This shows six weeks daily inhalation of 2300 ppm kills some animals with lung injury, liver and central nervous system damage. The most important effects of difluorodibromomethane inhalation are chronic toxicity and respiratory tract irritation. The 100 ppm threshold limit can be interpreted from the results of single animal inhalations, in comparison with carbon tetrachloride, ethyl and methyl bromide. It appears low enough to prevent injury. Diisobutyl ketone. Silverman, Schulte and First (1946) found concentrations above 25 ppm give eye irritation in unacclimated sub jects. Carpenter, Pozzani and Weil (1953) found single eight-hour inhalations of 200 ppm killed some rats by anesthesia, re peated inhalation of 1650 ppm killed some and caused liver, kidney and lung injuries, while 125 ppm was without effect. Two humans found 50 ppm satisfactory for work during a three-hour period, but were un comfortable at 100 ppm. The most important effect of diisobutyl ketone inhalation is narcosis. The 50 ppm threshold limit can be interpreted from re peated animal inhalations and human sen sory response. It is low enough to prevent definite narcosis. BA-Diisocyanotoluene. Swenson, Holmquist and Lundgren (1955) quote French animal inhalations in which 1 to 2 gm./cu.m. (140 to 280 ppm) caused only respiratory tract irritation. They report three human industrial eases featuring upper respiratory tract irritation followed by sensitization >(U, E o # S I ^ o JD .LO_! to co: to o co JoD Eo -0a? Q- oo <D C(OO CL 156 June, 1956 and asthma-like attacks. Unpublished The most important effect of inhalation of American experience features sensitization. dimtrobenzene is chronic poisoning. The 1 The most important effect of 2,4-di- mg./cu.m. tentative threshold limit appears isocyanotoluene inhalation is respiratory to be based on the reasonable assumption tiact irritation, followed by sensitization. that dinitrobenzene is five times as toxic as The 0.1 ppm tentative threshold limit cannot nitrobenzene. be interpreted quantitatively. It is probably Dinitro-o-cresol. Baltimore (1943) re not low enough to prevent an attack in a sensitized person. ports a non-fatal case from inhalation of Dimethyl aniline (N-dimethyl aniline). 4Ir.7ishmg(1./9c4u8.m) .inSpaennimcearl, eRxopweeri,mAendtasm, sfouanndd cHluednedetrhsoant tahned aHlkayglgaarndili(n1e9s43a,rpe. l2e2s7s)tocxoinc 10 to 50 mg./kg. is a fatal dose for animals. than aniline, but von Oettingen (1941, p. It is a rapidly acting metabolic stimulant, 15) concludes dimethyl aniline has a greater increasing body temperature to the point of depressant effect than aniline. It forms heat stroke. Cataracts are produced in sus ceptible species, but chronicity is low. methemoglobin in the blood. He cites two The most important effect of dinitro-o- human poisonings with symptoms like ani line. cresol inhalation is acute poisoning, marked The most important effect of dimethyl by metabolic stimulation with rise of body aniline inhalation is poisoning like that temperature. The 0.2 mg./cu.m. threshold from aniline. The 5 ppm threshold limit can limit can be interpreted from the facts of one industrial accident. It appears low be interpreted by analogy with aniline. It enough to prevent injury. appears low enough to prevent injury. Dinitrotoluene. Von Oettingen (1941, p. Dimethyl sulfate. Flury and Zernik 110) concludes this is similar to trinitro (1931) report that 13 ppm severely poisoned toluene but less toxic when pure. The dust cats in 20 minutes. Patty (1948-9, p. 925) causes mucous membrane irritation. states it has only a faint odor and there is a The most important effect of dinitro considerable latent period before effects are toluene inhalation is chronic poisoning, evident. Fairhall (1949, p. 309) concludes it marked by central nervous system, liver is a powerful irritant upon inhalation, the and red blood cell changes. The 1.5 mg./cu.m. liquid causes severe skin burns and corneal threshold limit can be interpreted from an injury, and when swallowed, marked central alogy with trinitrotoluene. It does not ap nervous system effects such as convulsions pear low enough to prevent all injuries. and delirium result. Smyth (1937-55) Dioxane. Fairley, Linton and Ford-Moore found rats survive four hours inhalation of (1934) found liver and kidney injury in 15 ppm but die from 30 ppm. animals repeatedly inhaling 1000 ppm, and The most important effect of dimethyl from skin absorption. Silverman, Schulte sulfate inhalation is delayed irritation of and First (1946) found eye, nose and throat bronchi, and lung edema, not preceded by iiritation at 300 ppm in unacclimated sub promptly evident irritation of eye and upper jects. Patty (1948-9, p. 957) concludes there respiratory tract. Very high concentrations is only a faint odor at 200 ppm. Smyth may cause convulsions and delirium, then (1937-55) found rabbits particularly sus coma. The 1 ppm threshold limit can be in ceptible, repeated inhalation at 800 ppm terpreted from results of single animal in killing some with kidney injury within 30 halations. It appears to be low enough to days. protect against lung injury, but available The most important effect of dioxane in data do not indicate that it will prevent halation is chronic poisoning, centering in bronchial irritation. the liver and kidney. The 100 ppm thresh Dinitrobenzene. Fairhall (1949) con old limit can be interpreted from results of cludes the chief effect of dinitrobenzene is i epeated animal exposure studies. It ap the production of methemoglobin, leading pears to be low enough to prevent injury. to anoxia and anemia. Von Oettingen (1941) EPN. Hodge, Maynard etal (1954) found in a review of the literature finds chronic the acute oral LD50 for rats ranges from 7 liver injury and cites opinions that it is to 33 mg./kg., while 75 ppm in the diet is more toxic than nitrobenzene. without effect during two years. The ma- June, 1956 t effect of inhalation of ronic poisoning. T h e 'l . ;hreshold limit appears reasonable assumption s five times as toxic as Baltimore (1943) re se from inhalation of er, Rowe, Adams and lal experiments, found fatal dose for animals, g metabolic stimulant, erature to the point of s are produced in sus- hronicity is low. nt effect of dinitro-o- :ute poisoning, marked tion with rise of body i mg./cu.m. threshold ted from the facts of lent. It appears low ury. a Oettingen (1941, p. is similar to trinitro- when pure. The dust :ane irritation. .nt effect of dinitro s chronic poisoning, lervous system, liver . iges. The 1.5 mg./cu.m. : interpreted from an- uene. It does not ap- svent all injuries, inton and Ford-Moore md kidney injury in haling 1000 ppm, and l. Silverman, Schulte d eye, nose and throat in unacclimated sub . 957) concludes there at 200 ppm. Smyth . bits particularly sus- : lalation at 800 ppm s ney injury within 30 ; effect of dioxane in- - dsoning, centering in : The 100 ppm thresh- ? meted from results of I isure studies. It ap- | l to prevent injury. ; trd et al (1954) found \ r rats ranges from 7 i '5 ppm in the diet is \ two years. The ma- | Industrial Hygiene Quarterly 157 terial is a cholinesterase inhibitor, and symptoms of excess in animals are confined to excitability and tremors. It appears to be % to % as toxic as parathion. The most important effect of.EPN inhala tion is the reduction of blood cholinesterase. The 0.5 mg./cu.m. threshold limit can be interpreted from the results of single oral doses to animals and analogy with para thion. It appears low enough to prevent in jury. Ethyl acetate. The unacclimated subjects of Nelson, Ege, Ross, Woodman and Silver man (1943) found an objectionably strong odor at 200 ppm and eye, nose and throat irritation at 400 ppm. Henderson and Hag gard (1943, p. 222) conclude 10,000 to 20,000 ppm is dangerous for short ex posures. It is mildly narcotic but does not produce systemic effects. Smyth (1937-55) found rats inhaling 8000 ppm for four hours survive, but 16,000 ppm kills. The most important effect of ethyl acetate inhalation is narcosis. The 400 ppm thresh old limit can be interpreted by human sen sory data and results of single inhalations by animals. It apparently is low enough to prevent definite narcosis. Ethyl acrylate. Pozzani, Weil and Car penter (1949)' found 30 inhalations of 300 ppm injured lungs, liver and kidneys of rats and rabbits, while 70 ppm did not in jure rats. They found that 8 ppm is readily detectable by odor, and that the odor of 50 ppm is objectionable. Treon, Sigmon, Wright and Kitzmiller (1949) obtained closely similar results. The most important effect of ethyl acryl ate inhalation is respiratory tract irritation. The 25 ppm tentative threshold limit can be interpreted from repeated animal inhala tion results and limited human sensory data. It appears low enough to prevent injury. Ethyl alcohol. Henderson and Haggard (1943, p. 219) consider its vapors anesthetic but not toxic. Only under exceptional cir cumstances can inhalation cause slight in toxication. They estimate 1064 ppm for eight hours is not sufficient to produce the earliest stage of intoxication in man. Cook (1945) stated that industrial exposure at 1000 ppm has led only to a few complaints of eye irritation. Patty (1948-9, p. 851) con cludes 6000 to 9000 ppm is initially intoler ably irritating, but that acclimatization fol lows. Smyth (1937-55) found rats survive eight hours at 16,000 ppm but some are killed at 32,000 ppm. The most important effect of ethyl alco hol inhalation is narcosis. The 1000 ppm threshold limit can be interpreted from human physiological data. It is low enough to prevent significant narcosis, but some eye irritation will result. Ethyl amine. Brieger and Hodes (1951) exposed rabbits repeatedly to 50 ppm and found lung and corneal injury, with some ef fect on heart muscle. Smyth (1937-55) found four hours at 4000 to 8000 ppm kills some rats, and 16,000 ppm kills all. Respira tory tract irritation is prominent. The liquid is extremely injurious to the cornea. The most important effect of ethyl amine inhalation is respiratory tract irritation, with lung edema the maximum injury. The 25 ppm threshold limit can be interpreted from results of repeated animal inhalation. It appears low enough to prevent injury. Ethyl benzene. Yant, Schrenk, Waite and Patty (1930) found only slight irritation in guinea pigs breathing 1000 ppm for eight hours. Fatalities from higher levels showed lung edema. Humans found 1000 ppm was initially irritating to the eyes and 2000 ppm caused throat irritation, constriction in the chest and slight intoxication. Smyth (1937 55) found rats not killed by four hours at 2000 ppm, while 8000 ppm is fatal. There is general agreement that it does not exert the hematopoetic effects of benzene. The most important effect of ethyl ben zene inhalation is narcosis, with irritation of the entire respiratory tract contributing to injury. The 200 ppm threshold limit can be interpreted from results of single animal inhalations and limited human sensory re sponse. It is low enough to prevent injury. Ethyl bromide. Waite and Yant (1928) found lung edema a prominent effect of guinea pig inhalation. Sayers, Yant, Thomas and Berger (1929) found several hours in halation of 1700 ppm by animals was with out effect. Henderson and Haggard (1943, p. 207) note that vapors are not narcotic. The most important effect of ethyl bro mide inhalation is respiratory tract irrita tion. The 200 ppm threshold limit can be in terpreted from the results of single animal inhalations. It is probably low enough to pre vent injury. T3 ^h C>O> k -a <, o & TJ t & ?&O ? >> I 2 ! _5 _ f 1 <0 Q * <D ik *o5 Eo "cOr> oC L O to C?O <oD> CO CL co a> "co e b S 1 ( S S ` - ^ yT ' I " *-Th" *a 150,000 to MO 000 "d w, h " ,r" k a * t o J tion The'in y. . damage and sensitii<d terpretid f PPM th^eshoId limit can be I ^ imnnhaaiaStoionn aanndd h,rueSmUaltnS sefnsro6rPyeadteadta anIit S "S i JZuiy,eZbuft hprto0bhaZbleyVmnott - -to^ t ei olimn iInnatde i f of i d ^ T / - lmportant effect of ethyl chlor- sponse by persons already sensitized. f " lue mhajation is n arco^ tv** i / An Jt)1 C o f S p 'bromide. Rowe, Spencer, Mj ss:HSiFar:?P from 365 ppm for tum f y ^ thology LSSS i"SaSTM" Z h u V ' T * were affected and " d s " " Sy . and ^dneys was apparent T W ^ arnin& irritation Si cSontXtVe? eVi?TeofPten- ppm M ed o -Th, y f0Und one hour at 1120 tration is saf e fcJ dtvnClUde " concen- found fn Ho hngSworth and Adams (195| nested -\r ?P6CleSf animals tolerated j Mm M n f 25 ppm- but not " S Skindneery lnaJnddryceWnatSralinnleurnvgouasndsylsitvi t o pr,,,,,,nt Th, p e n e to a tS l sic n it JS painful m the eye, but can centrathm i6(?t iniUry' The odor of a c S . S S t o t " 1" 0" i0 < * f d i J 116 r?S.fc important effects of ethylei dibiomide inhalation are respiratory trai irritation and liver injury. The 25 nn S " T ,, be fs nrehati ?peated animal inhalations. ethyleney Tdich,elforuidgeh. toSpperenvceernt inRjouwr Adams, McCollister and Irish (1951) stud' nogeffePt 1 ed inhalatin b* * S , , 5ct fr.om 1Q0 ppm. Single dangero: c u X S ` iS S 1,," " 1, * w cceennttrraeli1n0enrSvlorursitasytesttehme, lwunhgileanddandgeeprroeusss tnl s*Sf Ti" *" TM s s f- Ti bheeyy^feeeelf cchhr^o0n"ic8 intoxiclaitvioern ainsd uknildiknee S S T t0lerated rePeated inhalations a ^ f f r r Pr e^ s r itw e*ra ccleonsterattoiocnosncsuefnftircaiteinotnstotoclaeursaetemd aornkceed Cnaoii rPeopzezaatmedlaynd+,,C.7arppenlteerr nUo9c5J4\) exposedf trloatns- itiraSctt aiAL dTamlst,atSinpSentc0ert,heRUowppee,r MrescpCioralltios:t and Irish (1952) simultaneously studyl time0" te+traChl0ride> found it at least fo ( S an m l ethylene dichloride. Elki: rfrroomM innddnus\t3ri7al1fe0xUpnodsucreosmtPola1i0n0tstoo1f5n0apupsi Patty (1948-9 p. 805) .finds little odor WOOPS . al,Sh* " d s * s s s g ??3 The most important effect of ethylen dichlonde inhalation is chronic poisoning oSlidd lHimmit?c/ amn bi,he einl ltVerepr-reTtheed 1fr0o0mpPthme trherseuslht repeated animal inhalations and humai o iL T o L & X lifS eE th lf' U 1Sl0W enoUiih t0 Prevent injury (1 9 4 H )tZ T me- SiIver and M cG ratl L f 1 ^ ai? eater, Smyth and Shaffer (1948) studied single inhalations in animals, m e LO50 for mice in a 10-minute exposure June, 1956 amage and sensitiza- eshold limit can be in- 1 ts of repeated animal ' m sensory data. It is jnt irritation and iij- not to eliminate re- eady sensitized. . e. Rowe, Spencer, Mc- th and Adams (1952) : animals tolerated re- 25 ppm, but not 50 vas in lung and liver, ntral nervous system liquid penetrates the l the eye, but causes The odor of a con s to life is definite at effects of ethylene are respiratory tract injury. The 25 ppm ; interpreted from the mimal inhalations. It gh to prevent injury. ie. Spencer, Rowe, id Irish (1951) study- , on by animals, found pm. Single dangerous e lung and depress the n, while dangerous reiure liver and kidney, toxication is unlikely 1 eated inhalations are ' s tolerated once. Con to cause marked narthe upper respiratory ir, Rowe, McCollister lultaneously studying found it at least four 'ene dichloride. Elkins complaints of nausea ires to 100 to 150 ppm. . ) finds little odor at md nose irritation at it effect of ethylene is chronic poisoning, The 100 ppm thresh- reted from the results halations and human rgh to prevent injury. Silver and McGrath Smyth and Shaffer nhalations in animals, a 10-minute exposure Industrial Hygiene Quarterly 159 is 2236 ppm, 500 ppm for one hour is fatal to rats and guinea pigs, 25 ppm kills some in eight hours, and 10 ppm kills none in eight hours. Symptoms and death are delayed, due to kidney tubujar injury, with lesser lung and liver injury. Humans can barely smell 2 ppm, while 100 ppm begins to irri tate eyes and nose. The liquid penetrates the skin, produces severe skin and corneal burns, and sensitizes the skin. The most important effect of ethylene imine inhalation is acute poisoning, center ing in the kidney, with lung injury of lesser importance. The 5 ppm threshold limit can be interpreted from results of single animal inhalation studies and limited human sen sory data. It is apparently low enough to prevent poisoning and upper respiratory tract irritation. Ethylene oxide. Waite, Patty and Yant (1930) in single animal inhalations found no symptoms from eight hours at 250 ppm. Greater concentrations caused eye and nose irritation, narcosis, bronchial and lung irri tation. Sensory response is only moderate at low concentrations, but eye and nose irrita tion are intolerable at high concentrations. Sexton and Henson (1950) have called at tention to spectacular human skin injuries with sensitization, which arise from contact with the liquid and its aqueous solutions. Smyth (1937-55) found rats survive four hours at 4000 ppm but are killed by 8000 ppm. Hollingsworth, Rowe, Oyen, McCollis ter and Spencer (1956) in animals repeated ly inhaling 204 ppm found lung irritation and some fatalities, with injury to liver, kidney, adrenal and testes. Rats and mice were not affected at 49 ppm, other species tolerated 113 ppm. Jacobson, Hackley and Feinsilver (1956) with dogs, rats and mice found some fatalities from repeated inhala tion of 400 ppm, but 100 ppm had little af fect. The most important effect of ethylene oxide inhalation is respiratory tract irrita tion leading to lung Injury, while injury to liver and kidney are less important. The 100 ppm threshold limit can be interpreted from results of repeated animal inhalation studies. It appears low enough to prevent injury. Ethyl ether. Henderson and Haggard (1943, p. 195) estimate the maximum human blood concentration from inhalation of 400 ppm is 0.018 gm./l., causing no in toxication, while 2000 ppm will give a blood level of 0.09 gm./l., corresponding to insta bility in some persons. They state 35,000 ppm anesthetizes in 30 minutes, and a higher concentration kills by respiratory paralysis. Experience in human anesthesia shows that pneumonitis may follow ether anesthesia, but other injuries are unlikely. Nelson, Ege, Ross, Woodman and Silverman (1943) found nasal irritation at 200 ppm with unac climated subjects, somewhat greater'at 300 ppm. The most important effect of ethyl ether inhalation is narcosis. The 400 ppm thresh old limit can be* interpreted from human physiological and sensory data. It is low enough to prevent definite narcosis. Ethyl formate. Flury and Zernik (1931) reported 330 ppm causes in man slight eye irritation and rapidly increasing nasal irri tation, while 10,000 ppm is anesthetic and fatal. Fairhall (1949, p. 344) notes its ef fects are irritation and narcosis, and that there is no chronic toxicity. Smyth (1937 55) found rats survive four hours inhala tion of 4000 ppm but die from 8000 ppm. The most important effect of ethyl for mate inhalation is narcosis. The 100 ppm threshold limit can be interpreted from scanty human sensory data and single animal inhalations. It appears to be low enough to prevent definite narcosis and irri tation. Ethyl mercaptan. Sayers, Fieldner, Yant, Leitch and Pearce (1930) report the odor detectable at one part per billion and dis agreeable at one part per fifteen million. They quote that its effects are like those of hydrogen sulfide, and by analogy with butyl mercaptan they conclude more than 733 ppm is required to kill in 30 minutes. Flury and Zernik (1931) quote 3000 ppm as harm less to dogs and 10,000 ppm causing hematologie and blood cell changes. The most important effect of ethyl mer captan is eye and respiratory tract irrita tion. The 250 ppm tentative threshold lim it can be interpreted from the results of single inhalation by animals. It appears low enough to prevent injury and eye irritation. Ethyl silicate. Smyth and Seaton (1940) found eight-hour inhalation of 550 ppm the least fatal exposure for guinea pigs. Death is due to' lung injury, with some kidney g co 1 g co 7rv X<--0 -o L 4C-- .2 Ko I. ~o <s> I l oo . o S* CO %l CO 5 <D o> f CQO_ 1 CO * sz fi c . Ic' o P Is sak (O Si, "" sz 1'. y- 1 r 8 f* 5. y:- ,. I II i!$.! !- fpi' F 13 |p- PfX' 1 f|i|l' ill!I * * m. | p 1 'I 160 June, 1956 damage. Humans found 85 ppm detectable equivalent to 1.5 to 2.3 mg./cu.m. soluble by odor; 250 ppm slightly irritating to eye fluoride dust. Higher concentrations pi'ovide and nose, and 3000 ppm extremely irritat respiratory tract irritation and effects on ing. Rowe, Spencer and Bass (1948) found liver and kidney, Largent (1952) found stor some kidney damage in rats repeatedly in age in the body occurs when as little as haling 125 ppm. Pozzani and Carpenter three milligrams per day fluoride in the (1951) exposed rodents repeatedly. Some form of sodium fluoride is ingested, rough died within 30 days at 440 ppm with injury ly equivalent to inhalation of 0.3 mg./cu.m. to lung, liver and kidney, but 88 ppm did soluble fluoride dust. not injure. The data suggest that repeated The most important effect of inhalation inhalation at a given concentration is no of fluoride dust is chronic poisoning, cen more injurious than a single inhalation. tering in the bones, with respiratory tract The most important effect of ethyl silicate irritation at high concentrations. The 2.5 inhalation is lung injury, with non-progres mg./cu.m. threshold limit can be interpreted sive kidney damage less important. The from results of examination of exposed 100 ppm threshold limit can be interpreted workmen and experimental studies of human from results of repeated animal inhalations fluoride retention. It is not low enough to and limited human sensory data. It can be prevent fluoride storage with resulting ef smelled, it is not irritating, and is low fects on the bones. enough to prevent lung or kidney injury. Fluorine. Machle and Evans (1940) ex Ferbam. Hodge, Maynard, Downs, Blan- amined workmen exposed intermittently to chet and Jones (1952) reported the oral as much as 10 ppm and found no clinical evi LD50 for rats to be over 17 gm./kg., with dence of damage, but there was some ac guinea pigs and rabbits more sensitive. Rats cumulation in bones and teeth. Stokinger tolerated 0.01% in their diet for 30 days (1949) found few toxic effects in dogs re without effect while 0.5% was required to peatedly exposed to 0.5 ppm. Greater con kill. Dogs were not injured by 25 mg./kg./ centrations injured lung and kidney. This is day for six months. The mechanism of in apparently below the level which leads to jury is not clear. _ bone abnormalities (Roholm 1937). The most important effect of inhalation The most important effect of inhalation of Ferbam appears to be the upper respira of fluorine gas is respiratory tract irrita tory tract irritation of a substantially inert tion, with lung edema the maximum effect. dust. The 15 mg./cu.m. tentative threshold Chronic effect on bone metabolism is also limit is in accord with this. important. The 0.1 ppm threshold limit can Ferro vanadium, dust. Roshchin (1952) be interpreted from results of animal in exposed rats two months to 1000 to 2000 halation and studies on exposed workmen. It mg./cu.m. and found no effect beyond some is low enough to prevent injury. lung irritation. The author suggests a Fluoroaeetates. Dieke and Richter (1946) threshold limit of 1 mg./cu.m. Vanadium report the median lethal oral dose to be 0.22 compounds irritate the upper respiratory mg./kg. for wild rats. The substance is tract, but Sjoberg (1951) found no chronic rapidly fatal through intervention in the general poisoning in workers exposed to tricarboxylic acid metabolic cycle. vanadium pentoxide dust, symptoms being The most important effect of fluoroaeetate confined to respiratory difficulties and skin inhalation is acute toxicity. The 0.1 allergies. mg./cu.m. tentative threshold limit .can be The most important effect of inhalation interpreted from acute oral toxicity data for of ferrovanadium dust is respiratory tract rats. It corresponds to a maximum human irritation. The 1 mg./cu.m. threshold lim intake of one milligram per day, apparently it can be interpreted from limited repeated well below a dangerous amount. animal inhalations and examination of ex Fluorotrichloromethane. Nuckolls (1933) posed workmen. It appears low enough to found in animals no more than occasional prevent injury. tremors and retching during two hours at Fluoride dust. Roholm (1937) found fluor 22,000 to 25,00Q ppm. No toxic effects are to osis of human bone, but no other effects, af be expected from this physiologically inert ter several years work in 2 to 3 ppm fluorine, material. i to ,1 is 8 Year: N o te g j l56 .. , June, 1956 ' Industrial Hygiene Quarterly mg./cu.m. soluble centrations provide ion and effects on (1952) found stor- when as little as ay fluoride in the is ingested, rough en of 0.3 mg./cu.m. The most important effect of flucrotrichloromethane inhalation is a minor degree of narcosis, and asphyxia from very high concentrations. The 1000 ppm threshold lim it can be interpreted from the results of single animal inhalations. It appears to be far below a possibly injurious level. Formaldehyde. Henderson and Haggard hours inhalation of 700 ppm killed 25% of a group of rats. The most important effect of furfuryl al cohol inhalation is narcosis. The 50 ppm ten tative threshold limit can be interpreted from results of single animal inhalations. It appears low enough to prevent injury. Gasoline. Sayers, Fieldner, Yant and ffect of inhalation nic poisoning, cenh respiratory tract mtrations. The 2.5 t can be interpreted nation of exposed ;al studies of human not low enough to with resulting ef- (1943, p. 128) conclude its action is chiefly . irritation of all tissues contacted, particular ly the respiratory tract, and that systemic effects are not important. Skin sensitization to solutions is frequent and respiratory tract sensitization to the gas is not unlikely. Elkins (1950, p. 231) reports irritation in workmen inhaling 5 to 6 ppm, and eye irri tation of unhardened persons at lower levels. Smyth (1937-55) found rats survive eight Thomas (1927) reported human dizziness at 700 ppm, and Drinker, Yaglou and War ren (1943) found human respiratory tract irritation and headache begin at 1000 ppm. Elkins (1950, p. 99) found industrially no sensory response to 660 to 800 ppm benzine, and dizziness at 2000 to 3000 ppm. He con cludes chronic effects do not occur when con centrations are too low to cause narcosis, but Hayhurst (1936) reported chronic Evans (1940) ex- :d intermittently to ound no clinical evi- here was some ac id teeth. Stokinger effects in dogs re- ppm. Greater con- and kidney. This is :vel which leads to mlm 1937). effect of inhalation ratory tract irrita- he maximum effect, metabolism is also threshold limit can suits of animal in- ixposed workmen. It t injury. and Richter (1946) oral dose to be 0.22 The substance is ntervention in the olic cycle. feet of fluoroaeetate toxicity. The 0.1 eshold limit can be ral toxicity data for a maximum human per day, apparently amount. ij* t le. Nuckolls (1933) } ore than occasional uring two hours at hours inhalation of 125 ppm but are killed by 250 ppm. The liquid causes severe corneal injury. The most important effect of formalde hyde inhalation is irritation, first evident in the eyes, then in the upper respiratory tract, bronchi and even lung. The 5 ppm threshold limit can be interpreted from uncontrolled human sensory data. It is sufficiently low to prevent lung injury. Furfural. Fairhall (1949, p. 354) quotes animal experiments in which inhalation of 280 ppm resulted only in slight mucous mem brane irritation, while 2800 ppm caused acute irritation, prostration and lung edema. ACGIH (1954b) quotes Korenman and Resnik, (Arch. Hyg., 104:344, 1931) to the effect that 2 to 14 ppm causes human head ache and eye irritation. Severe corneal in jury is to be expected from the fluid, and analogy with other aldehydes suggests that skin and respiratory sensitization may be found. The most important effect of furfural in halation seems to be irritation, first evident in the eyes, then in the upper respiratory tract, bronchi and even lung. The 5 ppm ten tative threshold limit can be interpreted from uncontrolled human sensory data. It is sufficiently low to prevent lung injury. Furfuryl alcohol. Fine and Wills (1950) found that death from furfuryl alcohol is due to the respiratory paralysis of anes- poisoning consisting of central nervous sys tem effects and blood cell changes after many years of exposure. This article does not seem to be generally accepted. Henderson and Haggard (1943, p. 192) consider nausea and incoordination the significant effects, with anesthetic death at 20,000 to 30,000 ppm. Aromatic hydrocarbons in gasoline from cracking operations may much reduce safety. The most impoi'tant effect of gasoline in halation is narcosis. The threshold limit of 500 ppm can be interpreted from human sen sory data, both experimental and indus trially observed. It is low enough to prevent definite narcosis. Heptane. Patty and Yant (1929) reported slight human dizziness from 1000 ppm. The paraffin hydrocarbons are anesthetic agents and irritate mucous membrane, but they do not cause systemic toxicity. The most important effect of heptane in halation is narcosis. The 500 ppm thresh old limit can be interpreted from limited human sensory data and by analogy with the better studied gasoline. It is probably low enough to prevent definite narcosis. HETP (hexaethyltetraphosphate). This material is substantially identical in quanti tative and qualitative effect with the cholin esterase inhibitor TEPP. Apparently no data specifically upon inhalation have been published. o toxic effects are to >hysiologically inert 162 June, 1956 cc . ' \% * 1 ft! R i ll appears to be consistent with that value. Hexane. Nelson, Ege, Ross, Woodman and Silverman (1943) with unacclimated subjects found no irritation at 500 ppm. Drinker, Yaglou and Warren (1943) found human nausea, headache, eye and throat ir ritation at 1400 to 1500 ppm. The paraffin hydrocarbons anesthetize and irritate mu cous membrane, but do not cause systemic toxicity. . The most important effect of hexane in halation is narcosis. The 500 ppm thresh . old limit can be interpreted from human sensory data. It is low enough to prevent definite narcosis. Hexanone (methyl butyl ketone). Simple ketones are irritant and narcotic, but not chronically toxic. Schrenk, Yant and Patty (1936) found guinea pigs tolerate 1000 ppm with slight or no symptoms for several hours, a concentration with a strong odor, moderately irritating to human eyes and nose. Death from higher levels is anesthetic respiratory paralysis. Specht, Miller, Valaer and Sayers (1940) found it more depressant than acetone, butanone or pentanone. Smyth (1937-55) found rats survive four hours at 4000 ppm, but die at 8000 ppm. The most important effect of hexanone in halation is narcosis. The 100 ppm threshold limit can be interpreted from the results of single animal inhalations and limited human response data. It is low enough to prevent definite narcosis. Hexone (methyl isobutyl ketone). Simple ketones are irritant and narcotic, but not chronically toxic. Specht (1938) and Specht, Miller, Valaer and Sayers (1940) found guinea pigs are not injured by several hours at 1000 ppm, but men find eye and nose irritation. Smyth (1937-55) found rats sur vive four hours at 2000 ppm, but die from 4000 ppm. Silverman, Schulte and First (1946) found the odor objectionable at 200 ppm, eye irritation evident, but no nose and throat irritation with unacclimated subjects. The most important effect of hexone in halation is narcosis. The 100 ppm threshold limit can be interpreted from results of single animal inhalations and human sen sory response. I t is low enough to prevent definite narcosis. Hydrazine. Comstock, Lawson, Greene and Oberst (1954) found in animals dam age to lung and liver, tremors and convul- sions, irritation of eye, nose and throat. Most of the animals repeatedly inhaling 20 ppm died by 30th day. During six month's inhalation of 5 ppm, only minor changes in the lungs of rats and dogs were found. The most important effect of inhalation of hydrazine is respiratory tract irritation. The 1 ppm threshold limit can be interpreted from results of repeated animal inhalation. It is probably low enough to prevent injury. Hydrogen Bromide. ACGIH (1955b) quotes unpublished human response data from the Connecticut Bureau of Industrial Hygiene. Odor was evident at 2 ppm, nose and throat irritation began to be evident at 3 ppm, and eye irritation was not evident at 6 ppm. The most important effect of hydrogen bromide inhalation is respiratory tract ir ritation, with lung edema the maximum ef fect. The 5 ppm tentative threshold limit can be interpreted from analogy with hydrogen chloride and human sensory response. It is probably low enough to prevent injury. . Hydrogen chloride. Machle, Kitzmiller, Scott and Treon (1942) found animals not affected by repeated inhalation of 34 ppm. Henderson and Haggard (1943, p. 126) con sider it an irritant without systemic effect. They state 1000 to 2000 ppm is dangerous to life through lung edema in a short time. Elkins (1950, p. 79) finds 10 ppm highly irri tating to humans although immunity seems to develop; 5 ppm immediately irritating; apd even lower levels can erode the teeth. The most important effect of hydrogen chloride inhalation is respiratory tract irri tation, with lung edema the maximum ef fect. The 5 ppm threshold limit can be in terpreted from repeated animal inhalation and human sensory data. It is low enough to prevent injury. . Hydrogen cyanide. Flury and Zernik (1931) give 19 to 36 ppm as tolerable for six hours without symptoms. Henderson and Haggard (1943, p. 173) conclude injury is chemical asphyxia, and chronic toxicity is not to be expected. They state 3000 ppm is rapidly fatal, 100 to 240 ppm dangerous in 30 to 60 minutes, and 20 to 40 ppm gives slight symptoms in several hours. This is one of the few gashs which can penetrate the skin in dangerous amounts. Patty (1948-9, p. 633) finds the odor barely detectable at 0.9 ppm, and recognizable at 2 to 5 ppm. ill June, 1956 eye, nose and thro'at. 5 repeatedly inhaling 20 lay. During six month's , only minor changes in id dogs were found, nt effect of inhalation of ratory tract irritation, limit can be interpreted ;ated animal inhalation, tough to prevent injury. ide. ACGIH (1955b) human response data ' it Bureau of Industrial evident at 2 ppm, nose i began to be evident at ition was not evident at ant effect of hydrogen is respiratory tract ir- dema the maximum ef- itive threshold limit can analogy with hydrogen sensory response. It is to prevent injury. e. Machle, Kitzmiller, 42) found animals not . inhalation of 34 ppm. ard (1943, p. 126) con- vithout systemic effect. 000 ppm is dangerous edema in a short time, inds 10 ppm highly irri- hough immunity seems mmediately irritating; can erode the teeth. , > nt effect of hydrogen respiratory tract irri- ema the maximum ef- :shold limit can be in- tted animal inhalation ita. It is low enough to . Flury and Zernik >pmas tolerable for six toms. Henderson and (3) conclude injury is nd chronic toxicity is hey state 3000 ppm is 240 ppm dangerous in - d 20 to 40 ppm gives mral hours. This is one ich can penetrate the , lounts. Patty (1948-9, 1 r barely detectable at 1 able at 2 to 5 ppm. 1 Industrial Hygiene Quarterly The most important effect of hydrogen The most important effect of hydrogen | cyanide inhalation is acute poisoning, a selenide is acute poisoning, largely lung | chemical asphyxia. The 10 ppm threshold edema at high concentration, and chronic i limit can be interpreted from results of poisoning centering in the liver. The 0.05 I older single animal inhalation data and ppm threshold limit can be interpreted | some human sensory data. It is low enough from the results of single animal inhalations | to prevent injury. and industrial accidents. It appears low f Hydrogen fluoride. Stokinger (1949) enough to prevent injury | found 30 ppm is highly toxic to animals, Hydrogen sulfide. Henderson and Hag- fj causing pulmonary damage, kidney and gard (1943, p. 140, 243) state hydrogen I testis changes and increases in bone fluoride. sulfide may cause very rapid death from | Animals tolerated 7 ppm with only mild res respiratory paralysis, or delayed death from [ piratory tract irritation in repeated expo lung injury. It is not cumulative. Low con sure. Elkins (1950, p. 73) reports nosebleeds centrations irritate the cornea. A concentra- ? at 0.4 to 0.7 ppm. Patty (1948-9, p. 543) tion fatal in 30 minutes is 600 ppm, while t; finds 0.026 mg./l. (22 ppm) is slowly irri 70 to 150 ppm causs slight symptoms in | tating and at 0.1 mg./l. (120 ppm) the skin several hours. Barthlmy (1939) found no ?i smarts. The liquid causes severe slowly heal injury among viscose workers during 10 J; ing skin injuries, and destroys the cornea. years, with control at about 20 ppm. Elkins All soluble fluorides interfere with calcium (1950, p. 232) found eye irritation in indus- | metabolism and an excess produces bone and try at 10 ppm and some complaints even at | tooth abnormalities. 5 ppm. Patty (1948-9, p. 590) concludes 0.3 | The most important effect of hydrogen ppm can be smelled, 3 to 5 ppm is offensive. f fluoride inhalation is respiratory tract ir The most important effect of hydrogen | ritation, with lung edema the maximum ef sulfide inhalation is acute toxicity, marked j fect. Chronic effect on bone metabolism is by respiratory paralysis or lung edema. The | also important. The 3 ppm threshold limit 20 ppm threshold limit can be interpreted J can be interpreted from results of repeated from the results of examination of exposed g animal inhalation and human sensory data. workmen. It is low enough to prevent in- g It is low enough to prevent injury jury. ' | Hydrogen peroxide, 90%. Oberst, Com Hydroquinone. Sterner, Oglesby and I stock and Hackley (1954) found rats sur Anderson (1947) reported on several years | vive eight hours at 250 to 300 ppm without industrial experience with men exposed to | symptoms, but irritation and areas of edema quinone vapor and hydroquinone dust. No & are found in the lungs. Dogs survived six systemic effects could be found, but high t months at 7 ppm without injury, although concentrations caused transient eye irrita- | the skin was thickened and the lungs irri tion, and after several years, a pigmentation f tated. The liquid is extremely destructive of cornea and conjunctiva was apparent, due ; to skin and cornea. to local action on the exposed tissue. Loss of | The most important effect of hydrogen vision has followed pigmentation in some f peroxide aerosol inhalation is respiratory cases, according to Oglesby (1956). It is > tract irritation, with lung edema the maxi uncertain whether the vapor or the dust was f mum effect. The 1 ppm threshold limit can responsible. Hydroquinone dust ranged | be interpreted from results of repeated from 0.12 to 13 mg./cu.m. After comparing f animal inhalation. It is low enough to pre exposure with concentration, the authors i! vent injury. conclude hydroquinone dust should be kept % Hydrogen selenide. Dudley and Miller below 2 to 3 mg./cu.m. i (1941) found animals are killed in eight The most important effect of hydro- i hours at 0.3 to 1.2 ppm, with lung irritation quinone inhalation is transient eye irrita and changes in liver and spleen. Eye and tion and a slowly developing pigmentation nose irritation made 1.5 ppm intolerable to in the eye. Visual disability can result. The man, but 0.3 ppm is not irritating and per 2 mg./cu.m. threshold limit can be inter ception of its odor is soon lost. Buchan preted from the results of examination of (1947) reported industrial cases due to less exposed workmen. It appears low enough to than 0.2 ppm, with liver injury. prevent effect. The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. 1U /1*?e' , ii en.^efson and Haggard (1943, p. 133) state it is a respiratory tract irri tant with more effect on the lungs than chlorine and bromine. They quote an 1889 thesis by Matt to the effect that 0.1 ppm does not disturb workers. Fairhall (1949, p. 90) Points out that excessive absorption can disturb the metabolism through effect on the thyroid. The most important effect of iodine vapor inhalation is respiratory tract irritation, with lung edema the maximum injury. The 0.1 ppm threshold limit can be interpreted from analogy with chlorine. It appears low enough to prevent injury. Iron oxide fume. Fairhall (1949, p 92) reviews several articles. Inhalation of iron oxide dust for 5 to 10 years can lead to a benign pneumoconiosis, siderosis, revealed by x-ray but not injurious. U.S. Department of Labor (1941) in studies of welders, con cluded iron oxide fume below 30 mg./cu.m. was without effect, while in excess of this level a chronic bronchitis may result. The most important effect of inhalation ol iron oxide fume is bronchitis or metal fume fever. The 15 mg./cu.m. threshold limit can be interpreted by analogy with zinc oxide fume. It is low enough to prevent injury. ti!e ln!lal,ation is resPiratory tract irrita tion, with lung edema the maximum injury The 5 ppm threshold limit can be inter-' pieted from analogy with ethyl amines. It is probably low enough to prevent injury snH TU Russei1' Jones' Bloomfield, Britten nd Thompson (1933) after a survey of a f raf e, ,bf tt(:ry Plant, proposed that the threshold limit be reduced from 0.5 to 0.15 mg./cu.m. At this level disabling lead poisoning does not occur, and mild poison ing is rare. The most important effect of lead dust innaiation is chronic poisoning. The 0.15 mg./cu.m. threshold limit can be interpreted from the results of examinations of ex posed workmen. It is low enough to prevent disabling poisoning, but not to prevent some nula cases. Lead arsenate. Fairhall and Miller (1941) and Fairhall, Miller and Weaver (1943) lound the arsenate in lead arsenate de creases lead absorption or increases lead excretion, and reduces lead storage. The most important effect of inhalation ,nVeT t / o ? ate ,S chronie arsenic poisonng. lh e 0 15 mg./cu.m. tentative threshold limit can be interpreted from the results f biochemical studies on animals. It ap- riiT o!10/ 0716! Smyth> Seaton and Fischer (1942) found no effect upon animals from repeated inhalation of 25 ppm, while 50 ppm caused some lung and kidney injury. Single inhalation of 4600 ppm (saturation) for mght hours injured the lung but did not FFiWrst f(1t 9o4L6)f JfoCuilLndSiolvdeorrmoabnj>ecStciohnualtbeleanadt 10 ppm and eye, nose and throat irritation at 25 ppm with unacclimated subjects. 1he most important effects of isophorone inhalation are lung and kidney injury. The 25 ppm threshold limit' can be interpreted from the results of repeated animal inhala tion and human sensory data. It seems low enough to prevent injury. Sherlirm.iTt forr ilead?, swelheiclteedanaloagnyalowgiythwaitrhseme would yield a much higher figure A.M.A. (1951) in a summary, states lindane m large doses acts as a cen- tial nervous system stimulant, leading to hyperirritability, convulsions and death. Animals exposed several months to saturated vapors were not affected, but 10,000 m g / TM Tfr ne hour Hilled one of two llikshheed3 f1q9C51IrHepoarJt 5b4yb)J. qFu.oTterseoann etunapl.ubA year of repeated inhalation of 0.7 mg /cu m caused minimal pathology in animals. An unpublished 1952 thesis by Spear is quoted to the effect that 655 days at 0.19 mg./cu.m. Carpenter and Weil (1951) reported that rats survive four hours inhalation of 4000 ppm, but die from 8000 ppm This is half the acute toxicity AACLCPTrlfHr n(1o9H55'b)5)cit. , feo uunndpubfolirshbedtyinl daumstirniael. experience that levels above 5 ppm tend to be irritating. The most important effect of isopropyla- rats UrS 3 day dld n0t resu!t in Pathology in The most important effect of lindane in halation is chronic poisoning centering in the liver. The 0.5 mg./cu.m. threshold ifmit can be interpreted from the results of re peated animal inhalations. It appears low enough to prevent injury. Magnesium oxide fume. Drinker, Thom son and Finn (1927) reported that expert- June, 1956 ipiratory tract irritathe maximum injury 1 limit can be interivith ethyl amines- It rh to prevent injury; 5, Bloomfield, Britten after a survey of a ;, proposed that the uced from 0.5 to 0.15 level disabling lead :ur, and mild poison- t effect of lead dust poisoning. The 0.15 nit can be interpreted examinations of exow enough to prevent it not to prevent some tall and Miller C1941) and Weaver (1943) n lead arsenate de ni or increases lead ! lead storage. , effect of inhalation ronic arsenic poisonl. tentative threshold ;ed from the results on animals. It apcted by analogy with ile analogy with ar ch higher figure. 951) in a summary, doses acts as a centimulant, leading to /ulsions and death. .1months to saturated ed, but 10,000 mg./ur killed one of two ) quotes an unpubJ. F. Treon et al. A tion of 0.7 mg./eu.m. logy in animals. An s by Spear is quoted ays at 0.19 mg./cu.m. result in pathology in effect of lindane inisoning centering in cu.m, threshold limit m the results of reons. It appears low ry. me. Drinker, Thomeported that experi- . ' . . > . : 1 Industrial Hygiene Quarterly 165 mental fume fever in man results from ex gums. Ashe, Largent, Dutra, Hubbard and cessive inhalation, but does not occur below Blackstone (1953) in repeated inhalations a concentration of 15 mg./cu.m. This con by animals, found no effects at 0.1 mg./cu.- dition is transient fever with chills, muscu m., but damage to kidney and brain at 0.86 lar pain, nausea and vomiting. An im mg./cu.m. r munity is apparently build up. The most important effect of inhalation of The most important effect of inhalation mercury is chronic poisoning. The 0.1 of magnesium oxide fume is transient metal mg./cu.m. threshold limit can be interpreted fume fever. The 15 mg./cu.m. threshold from the results of repeated animal inhala limit can be interpreted from the results of tion and examination of exposed workmen. extensive human experiment. It is low Mercury (organic compounds). Ahlmark enough to prevent injury. ' (1948) on the basis of Swedish industrial Malathon. Johnson, Fletcher, Nolan and experience suggests a limit of 0.01 mg./cu.m. Cassaday (1952) reviewed toxicity data and Lundgren and Swensson (1949) consider conclude malathon is about one-hundredth concentrations fluctuate so widely that an as toxic to mammals as parathion. Tousey alysis does not detect important peaks, and (1954) reviews data and confirms that its that an M.A.C. cannot be defined. Organo ?' toxicity is considerably lower than that of mercurials produce effects like mercury, but many other cholinesterase inhibitors. Cul they have the added hazard of ready pene ver, Caplan and Batchelor (1955) found a tration of the skin. Trakhtenberg, (ab group of entomologists with maximum ex stracted from the Russian in Chemical Ab posure, about five hours at a peak of 56 stracts 44:10162g, 1950) reported mice die mg./cu.m.- and an average of about 3.3 mg./ at 10 to 30 mg./cu.m. within three to five cu.m. This had no effect on blood cholin hours and concludes 0.01 mg./cu.m. should esterase. not be tolerated for repeated human expo The most important effect of malathon in sures. ' halation is the reduction of blood cholin The most important effect of inhalation of esterase. The 15 mg./cu.m. threshold limit organo mercurials is chronic mercury poi can be interpreted from the results of oral soning. The 0.01 mg./cu.m. threshold limit doses to animals and limited examinations can be interpreted from the results of indus of exposed workmen. It appears low enough trial experience and single animal inhala %s* to prevent injury. tions. It is probably low enough to prevent Manganese. Flinn, Neal and Fulton injury. (1951) describe poisoning as an effect upon Mesityl oxide. Smyth, Seaton and Fischer ij the basal brain ganglia, leading to disability (1942) found no effect upon animals from 5k from weakness in the legs, spastic gait, stolid repeated inhalation of 50 ppm, while higher mask-like expression and emotional disturb concentrations killed by anesthesia, with ances, but not ordinarily shortening life. In minor lung, kidney and liver injuries. In an ore-crushing plant, they found no symp single inhalations, 100 ppm did not injure in tloesmssanind tmheeny ceoxnpcolsueddedtoco3n0cemntgra./tciou.nms . caonr ealilg,hatnhdoiunrso,ne50h0okuirll1e3d,0s0o0mpepamnd(s2a,5tu00raktiiollne)d % be effectively limited to 6 mg./cu.m. was fatal by anesthesia. Little cumulative The most important effect of inhalation action was revealed. Silverman, Schulte and of manganese dust is chronic poisoning. The First (1946) found some eye irritation at 6 mg./cu.m. threshold limit can be inter 25 ppm, and at 50 ppm nose irritation and a preted from the resuLts of examination of persistent unpleasant taste in unacclimated exposed workmen. It is low enough to pre subjects. vent injury. The most important effect of mesityl Mercury. Neal et al. (1941) in a study of oxide inhalation is narcosis. The 50 ppm the felt hat industry, found the incidence threshold limit can be interpreted from the of mercurialism proportional to atmospheric results of repeated animal inhalations and concentrations, with no cases found below human sensory response. It is low enough 0.1 mg./cu.m. Chronic symptoms consist of to prevent definite narcosis. psychic disturbances, timidity, tremors, Methoxychlor. Haag, Finnegan, Larson, pallor, salivation and tenderness of the Riese and Dreyfuss (1950) found methoxy- The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. June, 1956 166 chlor acts similarly to DDT in animals, and is less toxic by inhalation. Hodge, Maynard and Blanchet (1952) found no effect on rats in two years at 0.020% in the diet and no mortality or histological changes at 0.16%. Little accumulates in body fat. The most important effect of methoxy- chlor inhalation is chronic poisoning cen tering in the liver. The 15 mg./cu.m. thresh old limit can be interpreted from the results of repeated oral doses to animals. It appears low enough to prevent injury. Methyl acetate. Fairhall (1949, p. 375) notes irritation of eye and respiratory tract, narcosis less prominent than from higher acetates, but fatal dose close to anesthetic dose, and symptoms persistent after appre ciable narcosis. Death is due to anesthesia, but lung injury also occurs. Smyth (1937 55) found rats survive four-hour inhalations of 16,000 ppm, but die from 32,000 ppm. The most important effect of methyl ace tate inhalation is narcosis. The 200 ppm threshold limit can be interpreted by an alogy with ethyl acetate, allowing a margin for greater irritation and for the slow metabolism of methyl alcohol. It apparently is low enough to prevent narcotic symptoms. Methyl Acetylene. ACGIH (1955b) cites Horn, Chemical Corps Medical Laboratories Contract Report #35, 1954. For six months dogs and rats inhaled 28,700 ppm repeatedly. A few died. There was lung irritation and some central nervous system excitation. The most important effect of methyl acet ylene inhalation is lung injury. The 1000 ppm threshold limit can be interpreted from results of repeated animal inhalations. It is low enough to prevent injury. Methyl acrylate. Treon, Sigmon, Wright and Kitzmiller (1949) exposed animals re peatedly to vapor. They found that 130 seven-hour inhalations of 81 ppm had no ef fect upon four species, except some loss in weight. Higher concentrations caused re spiratory tract irritation and some narcosis. The most important effect of methyl acryl ate inhalation is respiratory tract irritation. The 10 ppm tentative threshold limit can be interpreted from repeated animal inhala tions. It appears to be low enough to pre vent injury. Methylal (dimethoxymethane). Weaver, Hough, Highman and Fairhall (1951) found . that high concentrations produce fatty changes in liver, kidney and heart of ani mals, with lung irritation. The threshold for chronic effects is 11,300 ppm. The most important effect of methylal in halation is chronic poisoning, centering in liver and kidneys, with narcosis and lung injury less important. The 1000 ppm thresh old limit can be interpreted from results of repeated animal inhalation studies. It ap pears low enough to prevent injury, but there are no data to judge the degree of ir ritation and narcosis it allows. Methyl alcohol. Sayers, Yant, Schrenk, Chornyak, Pearce, Patty and Linn (1942) found no effect on dogs from repeated inhal ation of 450 to 500 ppm. Henderson and Haggard (1943, p. 218) stress slow elimina tion, leading to progressive rise in blood level from daily inhalation. At 200 ppm 0.87 grams can be absorbed by a human in eight hours, but only part of this can be elimi nated before the next day. Methanol is pri marily a narcotic agent, but it may injure retina and optic nerve, leading to cloudy vision or blindness. There is some irrita tion of mucous membranes. Elkins (1950, p. I l l ) found industrial exposures ranging from 100 to 1700 ppm with no evidence of poisoning. Smyth (1937-55) found rats sur vive eight-hour inhalations of 32,000 ppm, and only a fraction are killed by 64,000 ppm. The most important effect of methyl al cohol inhalation is narcosis, with injury to retina and optic nerve likely only from quite excessive inhalation. The 200 ppm threshold limit can be interpreted from results of re peated animal inhalations. It will not cause significant narcosis, but continuous inhala tion will cause a daily rise in the degree of early narcosis, due to slow elimination. Methyl bromide. Irish, Adams, Spencer and Rowe (1940) found no effect from re peated inhalation at 17 ppm, and 34 ppm in jured only rabbits. Watrous (1942) found mild symptoms in one-third of 90 workers in concentrations generally under 35 ppm. In gram (1951) found injuries where workers were exposed to 100 to 1000 ppm. After': improvements reduced exposure to about. 20 ppm, injuries ceased. Fairhall (1949,- p. 376) notes it is a respiratory tract irri tant, a liver injurant, and a central nervoussystem poison leading to delirium, convul-. sions and even mania. It is rapidly metab olized and eliminated. 168 June, 1956 nent. The 100 ppm threshold limit can be in terpreted from results of repeated animal inhalation. It is low enough to prevent sig nificant narcosis, and probably to prevent minor effects on liver and kidneys. Methyl cyclohexanone. Treon, Crutchfield and Kitzmiller (1943) found no effect on rabbits from 300 hours at 182 ppm, slight eye irritation at 514 ppm, while 1822 ppm caused some narcosis and eye irritation. The most important effect of methyl cyclohexanone inhalation is narcosis. The 100 ppm threshold limit can be interpreted from results of repeated animal inhalations. It appears low enough to prevent definite narcosis. Methylene chloride. Heppel, Neal, Perrin, Orr and Porterfield (1944) found repeated inhalation of 10,000 ppm caused moderate narcosis in animals, some deaths from lung edema and liver damage. A concentration of 5000 ppm for six months had no effect upon four species, but reduced the voluntary activity of rats, indicative of a very early stage of narcosis not usually detected in animals. Fairhall (1949, p. 296) mentions a human fatality after accidental anesthesia. The most important effect of inhalation of methylene chloride is chronic poisoning cen tering in the liver. The 500 ppm threshold limit can be interpreted from the results of repeated animal inhalations. It is low enough to prevent injury. Methyl formate. Sehrenk, Yant, Chornyak and Patty (1936) found guinea pigs toler ate 1500 to 2000 ppm for several hours with out disturbance, and 5000 ppm for one hour. Symptoms of higher concentrations were nose and eye irritation, lung irritation, nar cosis and anesthetic death. The most important effect of methyl for mate inhalation is narcosis. The 100 ppm threshold limit can be interpreted from re sults of single inhalations by animals. It appears to be low enough to prevent definite narcosis. Methyl isobutyl carbinol (methyl amyl alcohol). Silverman, Schulte and First (1946) at 50 ppm found eye irritation in unacclimated subjects, although the odor was not objectionable. Experience with other alcohols indicates systemic effects are not to be expected. Smyth (1937-55) found rats inhaling 1000 ppm for eight hours are not killed, but 2000 ppm is fatal. The most important effect of methyl isobutyl carbinol inhalation is narcosis. The 25 ppm threshold limit can be interpreted from human sensory data. It is low enough to prevent significant narcosis and irrita tion. Methyl mercaptan. ACGIH (1954b) quotes de Rikowski who in 1893 found methyl mercaptan similar to but somewhat less toxic than hydrogen sulfide. The most important effect of methyl mer captan is eye and respiratory tract irrita tion. The 50 ppm tentative threshold limit can be interpreted by analogy with hydro gen sulfide. It appears low enough to prevent injury and eye irritation. Molybdenum. Fairhall, Dunn, Sharpless and Pritchard (1945) in animal experi ments, found some bronchial and alveolar irritation, with fatty changes in liver and kidneys. Animals survived repeated expo sure one hour daily to 53 mg./cu.m. molyb- dic oxide fume and only one of a group was killed by 286 mg./cu.m. molybdenite dust. The Industrial Hygiene Digest (16:1083, 1952) abstracts Mogilevskaya to the effect that histopathologieal changes in rat heart, liver and kidney are found after repeated inhalation of 3 to 10 mg./cu.m. molybdenum oxide aerosol. The most important effect of inhalation of molybdenum compounds is chronic poison ing, centering in liver and kidney. The threshold limits of 5 mg./cu.m. for soluble and 15 mg./cu.m. for insoluble molybdenum compounds can be interpreted from the re sults of repeated animal inhalations. They appear low enough to prevent injury, but slight toxic effects may result from soluble compounds. Naphtha (coal tar). A mixture of toluene and xylene chiefly. The predominantly nar cotic effects of these closely similar ma terials are additive and a mixture is no more injurious than the sum of its components. Cook (1945) points out that if a sample has a low boiling point, an appreciable content of benzene is to be suspected, and working concentrations should be reduced according ly. Year: Notes : 1956 of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. June, 1956 ect of methyl s narcosis. The be interpreted : is low enough ' isis and irrita- GIH (1954b) in 1893 found >but somewhat Ide. of methyl mer ry tract irritathreshold limit gy with hydroough to prevent 'unn, Sharpless animal experial and alveolar ;es in liver and repeated expoig./cujn. molybof a group was jlybdenite dust, igest (16:1083, ya to the effect ;es in rat heart, after repeated ,m. molybdenum of inhalation of chronic poisonid kidney. The u.m. for soluble ble molybdenum ;ed from the reihalations. They ;ent injury, but ult from soluble xture of toluene dominantly narely similar ma xture is no more its components, t if a sample has ireciable content ed, and working duced according- of toluene and effect of coal tar free from benation of the resnt. The 200 ppm Industrial Hygiene Quarterly threshold limit can be interpreted by an alogy with those of toluene and xylene. It is lungs in high concentration. It also erodes the teeth. He suggests a threshold limit ol low enough to prevent injury. Naphtha (petroleum). A mixture of par affin hydrocarbons of somewhat highe molecular weight than gasoline. The discus sion under gasoline appl13Nickel carbonyl. Fairhall (1949, p. 114) quotes Armit to the effect that this PTMduces a deposit of finely divided nickel in the res piratory tract, leading to irritation and lung edema. Hueper (1950) summarizes the The most important effect of inhalation of nitric acid is upper respiratory tract irritation. The 10 ppm tentative threshold limit appears to be based upon undocu mented analogy with other add gases. p-Nitroaniline. Fairhall (1949, p. 402) concludes p-nitroaniline is more toxic than aniline, causing headache, nausea and cyano sis. This is based on British industrial ex inferences that it produces cancer ongi- P The most important effect of p-nitro- nating in the nasal sinuses. Kincaid, Strong aniline inhalation is acute poisoning. The 1 andSunderman (1953) found 30 mmutes at ppm threshold limit is apparently an esti 10 ppm killed mice, 270 ppm killed cats, and mate based on analogy with aniline. It ap they suggest toxicity may be related to body pears low enough to prevent injury. weight, with man surviving high concentra Nitrobenzene. Henderson and Haggard tions. They found lung edema and severe (1943, p. 227) note that injury by skin ab liver injury, but conclude it is not cumul - sorption is more frequent than by inhala tive and that a tolerance develops. Sunder- tion The compound is an anesthetic, pro man and' Kincaid (1954) report on 36 ducing methemoglobin and reducing blood human cases, two fatal. The fatalities weie pressure. Acute toxicity is marked by head delayed, due to lung edema. ache, narcosis, cyanosis, and death from The immediate effect of nickel carbony respiratory paralysis. Chronic absorption vapor inhalation is lung irritation and de results in anemia, cyanosis, muscular weak layed edema. Cancer originating in the ness, bladder irritation. The maximum con nasal sinuses has been reported from long centration which gives no serious dis time exposure. The 0.001 ppm threshold lim turbance in one hour is 200 ppm, and 40 to it is apparently an approximation of zero, 80 ppm cause symptoms in several hours. designed to prevent cancer. I t is low enough The most important effect of nitrobenzene to prevent all possibility of immediate ef inhalation is chronic poisoning, marked by fect, but there are no data to judge its ef reduced blood pressure and cyanosis. The l fectiveness in preventing cancer ppm threshold limit can be interpreted from Nicotine. Wilson and De Eds (1936) 1 results of single animal inhalation. It ap diets containing nicotine to growing rats pears low enough to prevent injury. for a 60-day period. Rats did not suivive Nitroethane. Machle, Scott and Treon on 0.05% nicotine. Rats were not affected (1940) found guinea pigs inhaling 500 bv 0 006% nicotine, equivalent to 4 mg./Kg. for a total of 140 hours are not injured, but body weight per day. A greater concentra some die from 1000 ppm. Eye and nose ir tion reduced growth, due largely but not en ritation, narcosis, central nervous system tirely to reduced food intake. Lehman irritation and lung edema are produced. (1949) estimates the fatal human dose to be Toxic symptoms are evident before narco- 60 milligrams. ' ,,. . The most important effect of nicotine in The most important effect of nitroethane halation is ill-defined chronic Poisnmg. inhalation is acute poisoning accompanied The 0 5 mg./cu.m. tentative threshold limit by narcosis and irritation. The 100 ppm can be interpreted from repeated feeding threshold limit can be interpreted from re ! - studies on rats. It corresponds to a maxi sults of animal inhalation. It appears low mum human intake of five milligrams per day, apparently well below an injurious enough to prevent injury. Nitrogen dioxide. Henderson and Hag level. Nitric acid. Fairhall (1949, p. 81) con cludes it is an upper respiratory tract ir ritant, injuring the bronchi and even the gard (1943, p- 137) state that 62 ppm causes immediate throat irritation, 300 ppm coughing and 100 to 150 ppm is danger- ;! Eg -Go> Q- 8 <n C5O o>CD CO O. co 170 June, 1956 ous for 30 to 60 minutes. Pairhall (1949, p. 117) finds the vapor irritates the entire res piratory tract, leading to delayed lung edema. There is some reduction in blood pressure, causing headache. Gray, McNamee and Goldberg (1952) found respiratory tract inflammation in rats, inhaling 9 ppm for a total of 48 hours in 10 days. Patty (1948-9, p. 610) reports 5 ppm is evident by odor, 10 to 20 ppm is irritating to eyes and nose. Vigliani and Zurlo (1955) in workers exposed several years to 30 to 35 ppm found no symptoms. They regard a threshold limit of 15 ppm satisfactory when ozone is absent. The most important effect of nitrogen dioxide inhalation is respiratory tract irri tation, with delayed lung edema probable. The 5 ppm threshold limit can be inter preted from results of repeated animal in halation and human sensory data. It ap pears low enough to prevent injury. Nitroglycerine. Cook (1945) quotes U. S. Public Health Service experience of no systemic effects from 10 ppm, but with as little as 0.5 ppm causing severe headache upon return to work after a week-end. Fairhall (1949, p. 405) notes headache from lowered blood pressure, excitement, dizzi ness, fainting, cyanosis, death from res piratory paralysis. Acclimatization is prom inent, skin penetration is a major hazard. Elkins (1950, p. 160) found some headaches at 0.04 ppm. The most important effect of nitroglycer ine inhalation is acute poisoning, marked by reduced blood pressure. The 0.5 ppm thresh old limit can be interpreted from studies on exposed workmen. It is sufficiently low to prevent injury, but not to prevent headache. Nitromethane. Machle, Scott and Treon (1940) found animals not affected by 500 ppm for a total of 140 hours, but 1000 ppm was fatal. The vapors are eye and respira tory irritants and mildly narcotic. Central nervous system irritation and lung edema result. Toxic symptoms are evident before narcosis. The most important effect of nitromethane inhalation is acute poisoning, accompanied by narcosis and irritation. The 100 ppm threshold limit can be interpreted from re sults of repeated animal inhalation. It ap pears low enough to prevent injury. 2-Nitropropane. The animal work of Machle, Scott and Treon (1940) concluded that in the nitro paraffins toxicity increases with molecular weight. Thus, 2-nitropropane should be more toxic than nitroethane. Skin ner (1947) found workmen in concentra tions of 10 to 30 ppm were not affected, but 20 to 45 ppm caused anorexia, nausea, vom iting and diarrhea. The most important effect of 2-nitropro pane inhalation is acute poisoning accom panied by narcosis and irritation. The 50 ppm threshold limit can be interpreted from results of repeated animal inhalation and industrial experience. It is probably low enough to prevent injury, but not to pre vent disturbing symptoms. Nitrotoluene. Von Oettingen (1941) re viewed the literature and could find no clear distinction between the toxicities of nitro toluene and nitrobenzene. The most important effect of nitrotoluene inhalation is chronic poisoning, marked by reduced blood pressure and cyanosis. The 5 ppm threshold limit appeal's to be an esti mate without quantitative support. It is June, 1956 i (1940) concluded s toxicity increases ' hus, 2-nitropropane i nitroethane. Skinmen in concentra- ' re not affected, but rexia, nausea, vom- ffect of 2-nitropropoisoning accomirritation. The 50 ie interpreted from sal inhalation and t is probably low y, but not to pre is. tingen (1941) recould find no clear toxicities of nitro- 'ect of nitrotoluene soning, marked by nd cyanosis. The 5 :ars to be an esti ve support. It is tifference between luene is sufficient n threshold limits. Wished data spefound, but analogy ; is close. feet of octane in500 ppm threshold only by analogy ae. It is probably definite narcosis. , p. 122) quotes reported work to .lation of 0.1 ppm meumonia, higher > lung edema. He ritation with fatal a, but no systemic itement that 0.015 my higher concen- ffect of ozone in.ct irritation, with m effect. The 0.1 i interpreted from ed animal inhala- data. It appears injury. it effect of this s a reduction of Industrial Hygiene Quarterly that enzyme activity in the blood.. Brown and Bush (1950) in tests on industrial workers found inhalation of 0.1 to 0.8 mg./ cu.m, causes definite reduction in blood cho linesterase activity. Vigliani and Zurlo (1955) on the basis of cholinesterase reduc tion conclude that a threshold limit of- 0.07 to 0.12 mg./cu.m. is satisfactory. , The most important effect of parathion inhalation is the reduction of blood cholin esterase. The 0.1 mg./cu.m. threshold limit can be interpreted from the results of exam ination of exposed workmen. It is not cer tain that it is low enough to prevent meas urable reduction of blood cholinesterase, but it is low enough to prevent injury. Pentaborane. Svirbely (1954a,b) found the LCsfl for mice inhaling vapors for two hours to be 10.9 ppm. Symptoms were cen tral nervous excitability and corneal opacity. Six-hour inhalations of 3.3 ppm by rats killed all within four repetitions. Comstock and Oberst (1953) report that the median detectable odor is 2.5 mg./cu.m. (0.5 ppm), described as garlic or slightly sweet. , The most important effect of pentaborane inhalation is acute toxicity involving the central nervous system. The 0.01 ppm tenta tive threshold limit can be interpreted from limited repeated inhalations by animals. It appears to be a conservative estimate. Pentachlornaphthalene. After extensive inhalation studies with rats, Drinker (1939) concluded that injury is exclusively in the liver and that the permissible limit for repeated inhalation is 0.5 mg./cu.m. The solid material or its oil solutions penetrates the skin, and repeated contact leads to chloracne. The most important effect of pentachlor naphthalene inhalation is chronic poison ing centering in the liver. The 0.5 mg./cu.m. threshold limit can be interpreted from the results of repeated animal inhalations. I t is low enough to prevent injury. Pentaehlorophenol. Kehoe, DeichmannGruebler and Kitzmiller (1939) found no evidence of chronic poisoning in rabbits, and the smallest lethal intravenous dose was 22 mg./kg. It penetrates the skin readily. In ternal injury is primarily to the vascular system with heart failure. The most important effect of pentaehlor ophenol inhalation is acute poisoning center ing in the circulatory system. The 0.5 mg./ cu.m, threshold limit can be interpreted from the results of repeated doses to ani mals. It appears low enough to prevent in jury. Pentane. Patty and Yant (1929) found no effect on humans from 10 minutes inhala tion of 5000 ppm. Fairhall (1949, p. 358) concludes that only narcosis and irritation are produced. The most important effect of pentane in halation is narcosis. The 1000 ppm thresh old limit can be interpreted from limited human sensory data and analogy with the better studied gasoline. It is probably low enough to prevent definite narcosis. Pentanone (methyl propyl ketone). Yant, Patty and Schrenk (1936) found 30,000 to 50,000 ppm killed guinea pigs in 30 to 60 minutes; 1500 ppm caused slight or no symptoms in several hours and was strongly odorous and irritating to human eye and nose. Death was anesthetic. Smyth (1937 55) found four hours at 2000 ppm killed part of a group of rats. The most important effect of pentanone inhalation is narcosis. The 200 ppm thresh old limit can be interpreted from the results of single animal inhalation and limited human response data. It is low enough to prevent definite narcosis. Perchloroethylene. Carpenter (1937) found rats inhaling 230 ppm for 150 days showed slight non-progressive liver and kidney effects, while 70 ppm had no effect. Humans perceived the odor at 50 ppm, slight eye irritation at 500 ppm, light narcosis at 1000 ppm, nausea at 5000 ppm. Rowe, Mc- Collister, Spencer, Adams and Irish (1952) found repeated inhalation of 400 ppm does not affect rats, rabbits and monkeys, while 100 ppm does not affect guinea pigs. Hu mans found no symptoms at 100 ppm, mini mum narcosis at 200 ppm, eye and nose irri tation at 600 ppm, painful irritation at 1000 ppm. The most important effect of perchloro ethylene inhalation is narcosis. The 200 ppm threshold limit can be interpreted from the results of repeated animal inhalations and human response. It appears low enough to prevent significant narcosis. : . Perchloromethyl mercaptan. ACGIH (1954b) cites Flury and Zernik (1931) to the effect that after 15 minutes inhalation of  ! .* I. T ,'-5 I il ill p >. 13-5, f V '4 |f e 3 -i f c : * B f'P! 4 .*' 9 IV- 4H. t e i : '# ; if, ]: I ^ 172 June, 1956 45 ppm, mice and cats die within two days. The most important effect of perchlor- omethyl mercaptan inhalation is eye and respiratory tract irritation. The 0.1 ppm tentative threshold limit can be interpreted on the basis of limited single inhalations by animals. It appears to be low enough to pre vent injury. Phenol. Deichmann, Kitzmiller and Witherup (1944) found guinea pigs are severely injured by 20 days inhalation of 25 to 50 ppm, rabbits suffer lung injury in 63 days, but rats are not affected. They con clude human injury from repeated inhala tion is marked by digestive disturbance, nervous disorders, skin eruption and liver and kidney damage. The liquid penetrates the skin to a dangerous extent, and causes severe skin and corneal injury. Patty (1948 9, p. 1034) reports that 5 ppm can be recog nized by odor. Smyth (1937-55) found rats survive eight hours inhalation of vapors saturated at room temperature. Although phenol vapors are odorous and irritating, their major effect is chronic sys temic poisoning. The 5 ppm threshold limit can be interpreted from results of repeated inhalations by animals. It appears to be low enough to prevent chronic toxic effects. Phenylhydrazine. Yon Oettingen (1941, p. 158) concludes death from a large dose is due to respiratory paralysis. There is hemo lytic anemia, formation of methemoglobin, injury to the liver and heart muscle. Skin penetration is rapid and dermal sensitiza tion takes place. The fatal oral dose for rats is of the order of 0.04 gm./kg. The most important effect of phenyl hydrazine inhalation is chronic poisoning, centering in the red blood cells.' The 5 ppm threshold limit can be interpreted from analogy with aniline. Quantitative data are not available to judge the effectiveness of the limit. . Phosgene. Fieldner, Katz and Kinne (1921) cite the Chemical Warfare Service as authority for a 1 ppm allowable concen tration for prolonged exposure, based on human tests. Henderson and Haggard (1943, p. 137) consider phosgene a lung injurant producing delayed edema. They say 3.1 ppm is immediately irritating to throat, 4 ppm to eyes, 4.9 ppm causes cough ing, 5.6 ppm detectable by odor and 50 ppm rapidly fatal. The most important effect of phosgene in halation is respiratory tract irritation with delayed lung edema probable. The 1 ppm threshold limit can be interpreted from re sults of human studies. It is low enough to prevent injury. Phosphine. Henderson and Haggard (1943, p. 243) report 1000 to 2000 ppm fatal in 30 minutes, 100 to 200 ppm the maximum for one hour without serious disturbance. Fairhall (1949, p. 127) quotes Mller to the effect that animals die from two four-hour inhalations of 20 ppm, or 7 of 10 ppm, but two months at 5 ppm did not injure. Acute poisoning is rapidly fatal with convulsions, paralysis and coma. Chronic poisoning is marked by anemia and nervous disturb ances. Patty (1948-9, p. 576) concludes there is only a faint odor at 1 ppm. The most important effect of phosphine! inhalation is chronic poisoning. The 0.05 ppm threshold limit can be interpreted from the results of repeated animal inhalation It appears low enough to prevent injury. Phosphorous (yellow). Fairhall (1949, p.j 131) summarizes the literature. The effects; of chronic poisoning are upon bone meta-j bolism. They may be noticed first as painful] swollen gums, or as spontaneous fractures! of the long bones. They develop into peri-] ostitis and necrosis of the lower jaw, with] secondary infection. In single exposures on< milligram per kilogram is usually fatal. The most important effect of phosphorou inhalation is chronic poisoning, centering i: the bones. The 0.1 mg./cu.m. threshold limi cannot be interpreted in quantitative terms.] Phosphorous pentachloride. Hendersoi and Haggard (1943, p. 134) conclude thii material is an irritant to'nose, throat an lungs through hydrolysis to hydrogen chlor ide. Skin burns from the solid are likel; Mice are killed in 10 minutes by 120 ppm. The most important effect of phosphorou, pentachloride inhalation is respiratory trac] irritation, with lung edema possible. Th! 1 mg./cu.m. threshold limit is apparent) an estimate without quantitative support. appears low enough to prevent injury. Phosphorous pentasulfide. Fairhall (1949) p. 131) quotes Barillet to the effect tha' phosphorous pentasulfide is somewhat lesi hazardous than phosphorous pentachloride] The most important effect of phosphorous] pentasulfide inhalation is respiratory trad The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected bv l J s nnrwnnht i Year: N o tes: 1956 1956 June, 1956 it effect of phosgene in- ry tract irritation with ' probable. The 1 ppm le interpreted from re es. It is low enough to erson and Haggard 1000 to 2000 ppm fatal 200 ppm the maximum it serious disturbance. 7) quotes Mller to the . ie from two four-hour n, or 7 of 10 ppm, but l did not injure. Acute fatal with convulsions, Chronic poisoning is and nervous disturb- -9, p. 576) concludes odor at 1 ppm. nt effect of phosphine : poisoning. The 0.05 an be interpreted from ted animal inhalation, h to prevent injury. tu). Fairhall (1949, p. literature. The effects i are upon bone meta- noticed first as painful spontaneous fractures hey develop into peri- f the lower jaw, with , n single exposures one m is usually fatal, t effect of phosphorous poisoning, centering in t ./cu.m, threshold limit in quantitative terms. achloride. Henderson ; p. 134) conclude this " it to nose, throat and . . 'sis to hydrogen chlor- ; i the solid are likely. > ninutes by 120 ppm. , . effect of phosphorous on is respiratory tract : edema possible. The . I limit is apparently ] uantitative support. It ' 0 prevent injury. ' ulfide. Fairhall (1949, i let to the effect that i fide is somewhat less \ . horous pentachloride. ,J' effect of phosphorous . :1 1 is respiratory tract / Industrial Hygiene Quarterly 173 irritation. The 1 mg./cu.m. threshold limit is apparently an estimate without quantita tive support. It appears low enough to pre vent injury. Phosphorous trichloride. Henderson and Haggard (1943, p. 134) consider it an irri tant and lung injurant. They cite 600 ppm as rapidly fatal, and 2 to 4 ppm as the maxi mum for 30 to 60 minutes without serious disturbance. Cook (1945) quotes Butjog as finding 0.7 ppm causes only slight irritation in animals. The most important effect of phosphorous trichloride inhalation is respiratory tract ir ritation, with lung edema the maximum ef fect. The 0.5 ppm threshold limit can be interpreted from limited animal inhalation data. It appears low enough to prevent in jury. Picric acid. Fairhall (1949, p. 423) de scribes systemic poisoning as gastro enteritis, hemorrhagic nephritis and hepa titis. Sunderman, Weidman and Batson (1945) studied workers handling ammoni um picrate in atmospheres from 0.0088 to 0.1942 mg./cu.m. They found little res piratory tract irritation, no systemic ef fects but considerable dermatitis. The most important effect of picric acid inhalation is chronic poisoning. The 0.1 mg./cu.m. threshold limit can be interpreted from observations on exposed workmen. It is low enough to prevent systemic injury but not respiratory tract irritation and sen sitization. Propyl acetate. Fairhall (1949, p. 426) concludes it is more irritating than ethyl acetate, more narcotic than ethyl or methyl acetates, but less lethal. Some respiratory tract irritation and liver injury are found. Death is due to anesthesia, but even deep narcosis may leave no after effects. Smyth (1937-55) found four hours inhalation of 32,000 ppm kills four of six rats. The most important effect of propyl ace tate inhalation is narcosis. The 200 ppm threshold limit can be interpreted by an alogy with ethyl acetate, not by data. It appears to be low enough to prevent definite narcosis. Propyl alcohol, iso. Nelson, Ege, Boss, Woodman and Silverman (1943) found 400 ppm causes mild irritation of eye, nose and throat, and 800 ppm is no more severe in un acclimated subjects. Fairhall (1949, p. 429) concludes it is similar to ethyl alcohol with no delayed effects, but twice as toxic. Smyth (1937-55) found rats survive four hours at 12,000 ppm, but half are killed in eight hours. The most important effect of isopropyl alcohol inhalation is narcosis. The 400 ppm threshold limit can be interpreted from human sensory data and analogy with ethyl alcohol. It is low enough to prevent signifi cant narcosis, but some irritation will result. Propylene dichloride. Heppel, Neal, High- man and Porterfield (1946) found repeated inhalation of 1000 ppm by animalsdkilled the first animal in seven days with severe liver effects. They conclude it is more toxic than ethylene dichloride but less so than carbon tetrachloride. The. most important effect of propylene dichloride inhalation is chronic poisoning centering in the liver. The 75 ppm thresh old limit can be interpreted from the results of repeated animal inhalations. It appears low enough to prevent injury. Propylene imine. Carpenter, Smyth and Shaffer (1948) found rats and guinea pigs killed by four hours at 500 ppm, and not by 30 minutes. This is about %th the acute toxicity of ethylene imine in simultaneous work. The most important effect of propylene imine vapor inhalation is acute poisoning, centering in th kidney, with lung injury of lesser importance. The 25 ppm threshold limit can be interpreted from results of scanty single animal inhalation studies and analogy with ethylene imine. It is apparent ly low enough to prevent injury. Propyl ether (isopropyl ether). Machie, Scott and Treon (1939) found incomplete anesthesia in animals at 30,000 ppm, light narcosis at 10,000 ppm, and no effect in re peated exposures at 1000 ppm. They con clude it is 1.5 to 2 times as active as ethyl ether and less so than gasoline. The most important effect of isopropyl ether inhalation is narcosis. The 500 ppm threshold limit can be interpreted from re sults of repeated animal inhalation. In com parison with data on ethyl ether it does not seeih low enough to prevent definite narcosis. Pyrethrum. There is little published on the toxicity of pyrethrum but many years of wide use as an insecticide indicates a low to I4 T3 5? 0C3 i $ fl 8. ti -g F cn .Q CD , W CD f 2 i CD CO I i <D & 5: 5i O c ji o o ! a > io o a> JZ ? 2E . XJ io Q. w, O O I tn CO V- 3 5 Q> o> CO k Q. f eCO ;* r- c il o 75 s $ CO i 5 - <x> JT &V1 } - 1I1;< >(-{ Al! % k 'S i il il . !!'- I1 ' r*p e?v.rr Kj! ;f JBi* fli ;-m f |v . P: 1W pU; psi ifeliS! `Si m t m .... . P ^ :# 3 l| -, _r* ` . 8. K ' Uf ii M- |-y 1 fj-lf.i r'.-ys m June, 1956 degree of hazard, except for some slight skin sensitizing property. Carpenter, Weil, Pozzani and Smyth (1950) found the rat oral LDS0 of two samples to be 0.82 and 1.87 gm./kg. Inhalation studies were made with an insecticidal aerosol containing 10% pyrethrum and 90% peanut oil and a Freon propellant. Eats inhaled a concentration of 6000 mg./cu.m. pyrethrum with 10 times as much peanut oil for 30 minutes, and only moderate lung congestion resulted. Rats and dogs inhaled a concentration of 16 mg./cu.m. pyrethrum with 10 times as much peanut oil for 40 thirty-minute periods dur ing 31 calendar days, without injuries greater than those in peanut oil controls. Lehman (1949) estimates the fatal human dose to be 100 grams. The most important effect of pyrethrum inhalation is irritation of the upper respira tory tract. The 2 mg./cu.m. tentative thresh old limit can be interpreted from limited repeated animal inhalation data. It appears low enough to prevent injury. Pyridine. Pollock, Finkelman and Arieff (1943) using pyridine for human therapy, found no toxic symptoms after daily doses of 0.31 to 1.54 ml., but 1.85 to 2.46 ml. was toxic, with one death of liver and kidney injury. Fairhall (1949, p. 434) considers small repeated doses affect the bone marrow, increasing the platelet count. Elkins (1950, p. 167) quotes a Czech report of mild central nervous symptoms at 6 to 12 ppm. The most important effect of pyridine in halation is chronic poisoning, centering in liver, kidney and bone marrow. The 10 ppm threshold limit can be interpreted from limited human symptom data. Mild symp toms may be found. Quinone. Sterner, Oglesby and Anderson (1947) imported on several years industrial experience with men exposed to quinone va por and hydroquinone dust. No systemic ef fects could be found, but high concentration caused transient eye irritation, and after several years a pigmentation of cornea and conjunctiva was apparent, due to local ac tion on the exposed tissue. Loss of vision has followed pigmentation in some cases, ac cording to Oglesby (1956). It is uncertain whether the vapor or the dust was responsi ble. Concentrations from 0.01 to 3.2 ppm quinone were found in the plant. The odor of quinone is perceptible at about 0.1 ppm, definite at about 0.15 ppm, irritating at 0.5 ppm and markedly irritating at 3 ppm. After comparing exposure with concentra tion, the authors conclude quinone vapor should be kept below 0.1 ppm. The most important effect of quinone in halation is transient eye irritation and a slowly developing pigmentation in the eye. The 0.1 ppm threshold limit can be inter preted from the results of examination of exposed workmen. It appears low enough to prevent effect. . Rotenone. On the basis of the literature and his own work, Lehman (1949) esti mates the fatal human dose to be 200 grams by mouth. The most important effect of rotenone in halation is irritation of the upper respira tory tract. The 5 mg./cu.m. tentative thresh old limit can be interpreted by analogy with pyrethrum. It appeal's low enough to pre vent injury. Selenium compounds (as Se). Fairhall (1949, p. 145) summarizes experimental studies which stress oral doses of selenium dioxide and inhalation of hydrogen selenide. Even at 3 ppm dioxide in the diet rats are injured, while 10 ppm kills within eight weeks. Dudley and Miller (1941) found ani mals killed in eight hours at 0.3 to 1.2 ppm hydrogen selenide, primarily due to lung in jury, with changes in liver and spleen. Buchan (1947). reports industrial cases due to less than 0.2 ppm (0.65 mg./cu.m.) hy drogen selenide, with symptoms largely referable to the liver. The most important effect of inhalation of selenium-bearing dusts is chronic poison ing, centering in the liver. The 0.1 mg./cu.m. threshold limit can be interpreted from the results of repeated feeding to animals and ' by analogy with hydrogen selenide. This is probably low enough to prevent injury. Sodium hydroxide. Elkins (1950, p. 84) states inhalation of mists result in upper ; respiratory tract irritation leading to.j ulceration. Patty (1949, p. 561) on the basis| of experience with caustic mists from 1 toj 40 mg./cu.m., concludes a concentration of| 2 mg./cu.m. is noticeably but not excessively! irritating. The most important effect of sodium hy|| droxide mist or dust inhalation is uppei; respiratory tract irritation, leading to ulg ceration. The 2 mg./cu.m. threshold limit The materia! on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright i a w H Year: N otes: 1956 , . June, 1956 rritating at 0.5 ing at 3 ppm. with coneentraquinone -vapor n. ; of quinone inrritation and a tion in the eye. ,t can be inter examination of irs low enough f the literature in (1949) estito be 200 grams ; of rotenone in s upper respira.entative threshby analogy with enough to pre s Se). Fairhall es experimental oses of selenium drogen selenide. he diet rats are Is within eight L941) found anit 0.3 to 1.2 ppm y due to lung in ver and spleen, ustrial cases due mg./cu.m.) hymptoms largely c of inhalation of chronic poison"he 0.1 mg./cu.m. preted from the ; to animals and selenide. This is event injury, is (1950, p. 84) result in upper ion leading to 561) on the basis mists from 1 to concentration of it not excessively ct of sodium hyalation is upper a, leading to ul . threshold limit Industrial Hygiene Quarterly can be interpreted from observations upon exposed workmen. It appears low enough to prevent injury. Stibine. Webster (1946) finds stibine a lung injurant and powerful hemolytic agent, injuring liver and kidney as well. Some animals die after one hour inhalation of 40 ppm. Its action resembles that of the better understood arsine. The most important effect of stibine in halation is acute poisoning, largely lung edema. The 0.1 ppm threshold limit can be interpreted by analogy with arsine. It ap pears low enough to prevent injury. Stoddard Solvent. Nelson, Ege, Ross, Woodman and Silverman (1943) found 400 ppm produced no marked effects on unae- climated subjects. This solvent is toxi cologically identical with gasoline and re marks under that material apply. Strychnine. McNally (1937) reports that a human death has resulted from swallow ing 30 milligrams. It is a convulsive poison. The most important effect of strychnine inhalation is acute poisoning. The 0.15 mg./cu.m. tentative threshold limit can be interpreted from the known human fatal dose. It corresponds to a maximum intake of 1.5 milligrams in a working day, apparently low enough to prevent injury. Styrene monomer. Spencer, Irish, Adams and Rowe (1942) found immediate animal death was anesthetic, delayed death was due to lung injury. Blood cells were not affected. Repeated inhalation of 650 ppm had no effect on animals. Humans found 1300 ppm extremely irritating to eye and nose, and 400 ppm had an objectionable odor but little irritation. Carpenter, Shaffer, Weil and Smyth (1944) found irritation and early narcosis in humans at 800 ppm. The most important effect of styrene vapor inhalation is narcosis. The threshold limit of 200 ppm can be interpreted from results of repeated animal inhalations and human sensory response. It is low enough to prevent definite narcosis. Sulfur dioxide. Kehoe, Maehle, Kitzmiller and LeBlanc (1932) studied many workmen continuously exposed to sulfur dioxide and found only upper respiratory tract chronic irritation. Henderson and Haggard (1943, p. 131) conclude it is an irritant without systemic effect. They give 400 to 500 ppm as dangerous in a short time, 20 ppm irri tating the eye and causing coughing, 8 to 12 ppm irritating the throat, and 3 to 5 ppm detectable by odor. Elkins (1950, p. 81) finds slight human irritation at 2 ppm and objectionable irritation at 10 to 30 ppm. The most important effect of sulfur diox ide inhalation is respiratory tract irrita tion, with lung edema or respiratory arrest the maximum effect. The 10 ppm threshold limit can be interpreted from human sensory data and examination of exposed work men. It is low enough to prevent injury. Sulfur hexafluoride. Lester and Green berg (1950) found that it is a physiological ly inert gas, rats inhaling 800,000 ppm in oxygen for 16 to 24 hours were not affected. The most important effect of sulfur`hexa fluoride inhalation is asphyxia from very high concentrations. The 1000 ppm thresh old limit can be interpreted from the re sults of prolonged animal inhalations. It is so far below any possible injurious level that it represents good engineering control, rather than a hazard limit. Sulfuric acid. Fairhall (1949, p. 83) considers it an upper respiratory tract ir ritant with lung injury possible. It is cor rosive to the skin and eyes, and erodes the teeth. Amdur, Silverman and Drinker (1952) with normal human subjects, found changes in respiration at a concentration as low as 0.35 mg./cu.m., and pronounced de crease in minute volume at 5 mg./cu.m. Elkins (1950, p. 82) considers concentra tions above 1 ppm (4 mg./cu.m.) are irri tating. Sterner (1943) considered 5 mg./ cu.m, as tolerable. The most important effect of sulfuric acid inhalation is respiratory tract irritation, with lung edema possible. The 1 mg./cu.m. threshold limit can be interpreted from human sensory and physiological data. It is low enough to prevent injury. Sulfur monochloride. Henderson and Haggard (1943, p. 130) consider it an upper respiratory tract irritant through release of hydrochloric acid, but rarely a lung in jurant. Mice die from one minute inhala tion of 150 ppm, cats from 15 minutes at 48 ppm. Fairhall (1949, p. 160) concludes chronic systemic effects do not occur. Elkins (1950, p. 81) found 2 to 9 ppm mildly irri tating to humans. . The most important effect of sulfur mono chloride vapor inhalation is respiratory tract irritation. The 1 ppm threshold limit can be interpreted from results of single animal inhalations and human sensory data. It is low enough to prevent injury. Sulfur pentafluoride. Greenberg and Les ter (1950) found this to he a lung injur ant. Rat lungs were severely injured by one hour, at 10 ppm, less severely injured at 1 ppm and. not affected at 0.1 ppm. Sixteen hours at 1 ppm was lethal, due to lung in jury, while 18 hours at 0.5 ppm injured lungs but did not kill. The most important effect of sulfur penta fluoride vapor inhalation is lung injury. The 0.025 ppm threshold limit can be interpreted from results of repeated animal inhalation. It is probably low enough to prevent injury. TEDP. This cholinesterase inhibitor is about half as toxic in single doses to animals as parathion, and the class of cholinesterase inhibiting compounds manifests little ten dency to chronic effect. The most important effect of TEDP in halation is the reduction of blood cholin esterase. The 0.2 mg./cu.m. threshold limit can be interpreted only by analogy with parathion. It appears low enough to prevent injury. Tellurium. Steinberg, Massari, Miner and Rink (1942) examined workmen exposed to tellurium fume ranging from 0,01 to 0.1 mg./cu.m., with a peak of 0.74 mg./cu.m. in one sample. The symptoms found were garlic odor of breath and sweat, dryness of mouth, metallic taste and somnolence. No signs of poisoning were found. Excessive absorption would have been shown by gas tro-intestinal disturbances, reduction in red blood cells, diminished reflexes, and tremor. The most important effect of inhalation of tellurium-containing dusts is chronic poison ing centering in the liver. The 0.1 mg./cu.m. threshold limit can be interpreted from the results of examination of exposed workmen. It appears low enough to prevent injury. TEPP. This cholinesterase inhibitor is about twice as toxic in single doses to ani mals as parathion, and the class of cholin esterase inhibiting compounds manifests little tendency to chronic effect. Vigliani and Zurlo (1955) on the basis of cholinesterase reduction in workmen, consider 0.0007 mg./cu,m. a satisfactory threshold limit. The most important effect of tepp inhala tion is the reduction of blood cholinesterase. The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. .. I The 0.05 mg./cu.m. threshold limit caj interpreted only by analogy with p a ra | It appears low enough to prevent injur p-Tertiary butyl toluene. Hie (1954) in repeated animal inhalaf found narcosis, respiratory tract irrit liver and kidney changes, blood cell ch like those from benzene, and degener in spinal cord and brain. Rats are kill one hour by about 900 ppm, and sligh dence of effect was fpund in animal peatedly inhaling 25 ppm. Humans de ppm by odor, 80 ppm was unpleasanif ritating and some giddiness was not* 160 ppm. I, The most important effect of p-te| butyl toluene inhalation appears' |i chronic toxicity, combining effect o n | cells, central nervous system, liver an | ney. The 10 ppm threshold limit can 1 terpreted from results of repeated if inhalations and human sensory data. | pears to be low enough to prevent signil toxic effect. | 1,1,2,2-Tetrachloroethane. Fairhall 1 p. 440) concludes this is the most! chlorinated hydrocarbon, nine times a s as carbon tetrachloride. It is a narcot| produces liver damage, polyneuritis; white blood cell changes. Elkins (19J 139) refers to an unpublished reporta ness from a concentration below 10| Smyth (1937-55) found rats survive hours at 500 ppm but are killed by 100 The most important effect of 1,1,2,2| chloroethane inhalation is chronic poia centering in the liver. The 5 ppm th if limit can be interpreted from industry perience. It is uncertain whether it | enough to prevent some degree of in| Tetrahydrofuran. Lehman and | (1943, p. 269) report it a narcotic! tating mucous membrane and injuri kidneys. In animals 3400 ppm f r | hours daily for 20 days caused some n | membrane irritation and light nag with albuminuria, lung and kidney and lung irritation in one animal! ACGIH (1955b) quotes John A. Zapp| the effect that repeated inhalation ppm, then 400 ppm, slightly affect^, pulse pressure of dogs, but resulted'!-- histopathology. Hoffmann and Oett< (1954) in rabbits and cats found some'na cosis and mucosal irritation after six hou The material on this page was copied from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. Jte.- Y ear; N qtgg no. i -4 'S-L 1956 1956 m June, 1956 Industrial Hygiene Quarterly 1 177 hreshold limit can be' lalogy with parathion. i to prevent injury, toluene. Hine et al. animal inhalations, atory tract irritation, ges, blood cell changes ne, and degenerations ain. Rats are killed in 0 ppm, and slight evifound in animals reppm. Humans detect 5 1 was unpleasantly ir- ddiness was noted at inhalation of 3400 ppm. There was no liver mg./cu.m. tentative threshold limit appears or kidney injury from inhalation of even to be based on a quantitative analogy with s) 60,000 ppm. lead. Its propriety cannot be judged. V) The most important effect of tetrahydro Thiram. Meagre data have been found on furan inhalation is narcosis, with less im this substance. Smyth (1937-55) found the portant injury to liver and kidneys. The 200 rat oral LD50 to be 1.30 gm./kg. Rats sur ppm tentative threshold limit can be in vived four hours inhalation of a dense dust terpreted from results of repeated animal cloud, unmeasured but estimated to be at 3 inhalation studies. It appears low enough least 500 mg./cu.m., with no effect but some to prevent injury. brief retardation of growth. S* Tetranitromethane. Sievers, Rushing, The most important effect of inhalation Gay and Monaco (1947) found in cats ir of thiram appears to be an ill-defined chron ritation of eyes, upper respiratory tract, ic toxicity. The 5 mg./cu.m. tentative thresh lung edema, methemoglobinuria and injury old limit cannot be interpreted from pub to liver and kidney. Concentrations of 3.3 lished data found by the writer, but it ap it effect of p-tertiary ition appears to be bining effect on blood system, liver and kid- ;shold limit can be in ts of repeated animal ,n sensory data. It ap l to prevent significant to 25.2 ppm were severely injurious, while pears to be reasonable. 0.1 to 0.4 ppm caused only mild irritation in Titanium dioxide. Fairhall (1949, p. 180) two exposures. Horn (1954) found in re concludes titanium dioxide is chemically peated inhalation of 6.35 ppm that some inert and is not toxic. Lenzi (1936) found rats died from pneumonia. The effect on a pneumoconiosis in guinea pig lungs dogs was transient anorexia. after prolonged inhalation of high concen The most important effect of tetrani trations. *1 tromethane inhalation is poisoning, accom Inhaled titanium dioxide acts as an inert 3, panied by irritation. The 1 ppm threshold dust, with only a slight tendency to produce I thane. Fairhall (1949, lis is the most toxic ion, nine times as toxic le. It is a narcotic and ige, polyneuritis and lges. Elkins (1950, p. jublished report of ill- ration below 10 ppm. md rats survive four are killed by 1000 ppm. t effect of 1,1,2,2-tetra- >n is chronic poisoning . The 5 ppm threshold ,ed from industrial ex- ;ain whether it is low me degree of injury. Lehman and Flury rt it a narcotic, irri- > rane and injuring the 3400 ppm for eight /s caused some mucous !. and light narcosis, ng and kidney injury I< in one animal each, es John A. Zapp, Jr. to ited inhalation of 200 . slightly affected the gs, but resulted in no ffmann and Oettell i cats found some nar- itation after six hours limit can be interpreted from results of re pneumoconiosis. The 15 mg./cu.m. threshold peated animal inhalation. I t is low enough limit is an arbitrary figure uniformly ap to prevent injury, but not to prevent all irri plied to inert nuisance dusts. It appears low tation. enough to prevent injury. Tetryl. Bergman (1952) summarizes ten Toluene. Von Oettingen, Neal and Dona years' experience in an ordnance plant with hue (1942) in repeated exposure of animals, more than 1000 exposed workers and concen found no blood cell changes or other toxic trations kept below 1.5 mg./cu.m. by con effects at 800 ppm. Humans inhaling 200 stant diligence. Skin sensitization was fre ppm for an eight-hour period found the quent but no systemic poisoning was found. earliest signs of impaired coordination and Hardy and Maloof (1950) report two fatal lengthened reaction time, while the effects rk and eight non-fatal cases with liver injury were more prominent and more prompt at the most prominent effect. There was upper 600 to 800 ppm. Fairhall (1949, p. 447) con respiratory tract irritation, very frequent cludes it is a narcotic with irritating proper skin sensitization and a few asthmatic sensi ties, but manifests no chronic effects. Elkins tizations. Concentrations were as high as (1950, p. 108) cites Greenburg's examina 17.7 mg./cu.m. tion of over 100 workers in atmospheres of The most important effect of tetryl inhala 100 to 1100 ppm without marked symptoms. tion is chronic poisoning like that of trini Smyth (1937-55) found rats survive four trotoluene, but the most frequent effect is hours at 4000 ppm, but die from 16,000 ppm. sensitization. The 1.5 mg./cu.m. threshold Commercial toluene may contain significant limit can be interpreted from experience amounts of benzene and may be more toxic with exposed workmen. It is low enough than these data indicate. to prevent injury but not sensitizations. The most important effect of toluene in Thallium. Fairhall (1949) reviewing the halation is narcosis. The 200 ppm threshold literature, concludes that thallium has a limit can be interpreted from results of re chronic toxicity greater than that of lead. peated animal inhalation, studies of human Useful quantitative data on inhalation ap narcosis and examination of exposed work pear to be lacking. men. It appears to be low. enough to prevent The most important effect of thallium in all effects except the earliest signs of nar halation is chronic poisoning. The 0.15 cosis. 178 June, 1956 O-Toluidine. Henderson and Haggard (1943, p. 228) quote slight symptoms after several hours at 6 to 23 ppm, and for aniline they give 7 to 53 ppm. Fairhall (1949, p. 450) find symptoms are like those from aniline.. Smyth (1937-55) found rats not killed by eight hours inhalation of sub stantially saturated vapors. The most important effect of o-toluidine inhalation is poisoning like that from ani line. The 5 ppm threshold limit can be in terpreted by analogy with aniline. It ap pears low enough to prevent injury. Trichloroethylene, Morse and Goldberg (1943) found headache, nausea and dizzi ness common in industrial exposures well under the 200 ppm figure proposed by USPHS (1943) on the basis of European opinion. Adams, Spencer, Rowe, McCollister and Irish (1951) found no adverse effects from repeated inhalation by monkeys at 400 ppm, in rats and rabbits at 200 ppm, or in guinea pigs at 100 ppm. Single massive exposures kill by anesthesia. Even 3000 ppm inhaled repeatedly causes no more than very minor organic changes in the liver. They found almost identical effects from single and repeated inhalation of a single concen tration, and concluded the effects are chiefly those of narcosis. Voluntary habituation has been found in industry. The most important effect of trichloro ethylene inhalation is narcosis. The 200 ppm threshold limit can be interpreted from the results of repeated animal inhalations and observations in industry. It is not low enough to prevent significant narcosis. Trichloronaphthalene. After extensive in halation studies with rats, Drinker (1939) concluded injury is exclusively in the liver and that the permissible limit for repeated inhalation is 5 mg./cu.m. The solid material or its oil solution penetrates the skin and repeated contact leads to chloracne. The most important effect of trichloro naphthalene inhalation is chronic poisoning centering in the liver. The 5 mg./cu.m. threshold limit can be interpreted from the results of repeated animal inhalations. It is low enough to prevent injury. Trifluoromonobromomethane. A CGIH (1955b) quotes Chemical Corps Medical Laboratories Research Report No. 180, 1953. This shows that the material is narcotic at high concentrations, but that 23,000 ppm for 18 weeks had no toxic or lung injuring ef fects on dogs or rats. The most important effects of trifluoromonobromomethane inhalation are narcosis and respiratory tract irritation. The 1000 ppm threshold limit can be interpreted from the results of repeated animal inhalations. It appears low enough to prevent injury. Trinitrotoluene. Von Oettingn et al (1944) in experiments on dogs found only tracheal irritation and some effects on red blood cells from daily intratracheal insuf flation of 50 mg./kg. This daily dosage by mouth did not kill in three months but re sulted in definite central nervous system, liver and blood cell effects. The material penetrates the skin. Eddy (1944) reports fatal aplastic anemia in three humans at concentrations of 1 to 3.5 mg./cu.m. The most important effect of trinitrotolu ene inhalation is chronic poisoning marked by central nervous system, liver and red blood cell changes. The 1.5 mg./cu.m. thresh old limit can be interpreted from a report of industrial fatality. It is probably not low enough to prevent all injuries. Turpentine. Smyth and Smyth (1928) found that repeated inhalation of 750 ppm did not injure animals. Nelson, Ege, Ross, Woodman and Silverman (1943) with unacelimated subjects found nose and throat irritation at 75 ppm, while 175 ppm was judged intolerable. Fairhall (1949, p. 464) notes irritation, narcosis, and kidney injury. The most important effect of turpentine inhalation is narcosis, but irritation of the respiratory tract is more frequently en countered. The 100 ppm threshold limit can be interpreted from results of repeated ani mal inhalations and human sensory data. It is low enough to prevent injury. Uranium (soluble). Uranium is a radio logical hazard through emission of alpha particles, and a toxicological hazard prima rily through injury to kidney tubules. Hodge, Stokinger and Neuman (1949) show that on inhalation, the toxicological hazard is much greater than the radiological haz ard. In repeated animal experiments, they find that 0.5 mg./cu.m. allows a reasonable, margin of safety over the level producing kidney injury. The most important effect of inhalation - of soluble uranium dusts is chronic poison- : ing, centering in the kidney. The 0.05 1956 June, 1956 ' lung injuring ef fects of trifluoro- , ition are narcosis itation. The 1000 ; interpreted from nimal inhalations, prevent injury. ' Oettingen et al i dogs found only ime effects on red tratracheal insuf,s daily dosage by ee months but re1 nervous system, cts. The material ly (1944) reports three humans at i mg./cu.m. ect of trinitrotolupoisoning marked em, liver and red 5mg./cu.m. thresh ed from a report of probably not low jries. nd Smyth (1928) ilation of 750 ppm Nelson, Ege, Ross, l (1943) with un id nose and throat hile 175 ppm was iall (1949, p. 464) and kidney injury, fleet of turpentine at irritation of the are frequently enthreshold limit can Its of repeated anitan sensory data. It injury. ranium is a radio emission of alpha gical hazard prima,o kidney tubules, euman (1949) show toxicological hazard ae radiological haz1 experiments, they allows a reasonable the level producing effect of inhalation 5 is chronic poison- kidney. The 0.05 Industrial Hygiene Quarterly mg./cu.m. threshold limit can be interpreted human fatality arose from the consumption from the results of repeated animal inhala of a total of 750 mg. over a 15-day period. tions. It is low enough to prevent injury- The most important effect of warfarin in Uranium (insoluble). Hodge, Stokinger, halation is chronic poisoning centering in Neuman, Bale and Brandt (1949) show that the blood coagulation mechanism. The 0.5 on inhalation, the toxicological action of mg./cu.m. tentative threshold limit cannot uranium on the kidney is much more a haz be interpreted in quantitative terms. It in ard than the alpha radiation hazard of the volves a maximum daily absorption of 5 uranium stored in the bones. In repeated mg., about one-tenth the amount which was animal experiments, they find 0.20 to 0.25 fatal to one man. mg./cu.m. allows reasonable margin of safe Xylene. Nelson, Ege, Ross, Woodman and ty over the level producing kidney injury. Silverman (1943) found 200 ppm definitely The most important effect of inhalation of irritating to eye, nose and throat. Fairhall insoluble uranium dusts is chronic poison (1949, p. 468) concludes the effects are like ing centering in .the kidney. The 0.25 those of toluene, narcosis without damage to mg./cu.m. threshold limit can be interpreted red blood cells. from the results of repeated animal inhala The most important effect of xylene in tions. It is low enough to prevent injury. halation is narcosis. The 200 ppm thresh Vanadium. Roshchin (1952) exposed rats old limit can be interpreted from human to vanadium pentoxide fume of 0.3 to 0.5 sensory data. It is irritating to eye, nose mg./cu.m, for two hours every other day for and throat. There are no data to show three months, and to dust at 1 to 3 mg./cu.m. whether or not significant narcosis occurs for one-hour daily for four months. They at this concentration, but since narcotic ac lost some weight and had bloody nasal secre tivity is greater than that of toluene it is tion. Some evidence of pulmonary edema to be anticipated. was seen from the fume. Acutely 8 mg./cu.m. Zinc oxide fume. Drinker, Thomson and of the dust was injurious in one hour and Finn (1927b) reported that experimental 70 to 80 mg./cu.m. was lethal. The author fume fever from zinc oxide in man results suggests a threshold limit of 0.1 mg./cu.m. from excessive inhalation, but does not oc for fume and 0.5 mg./cu.m. for dust. cur below 15 mg./cu.m. In industry it was The most important effect of inhalation found that 14 mg./cu.m. caused no reaction of vanadium dusts is bronchial and lung after eight hours, and in the laboratory 45 injury. The threshold limits of 0.5 mg./cu.m. mg./cu.m. was without effect in 20 minutes. for dust and 0.1 mg./cu.m. for fume can be This condition is a transient fever with interpreted from the results of repeated chills, muscular pains, nausea and vomitting. animal inhalations. They appear low enough An immunity is apparently built up. to prevent injury. The most important effect of zinc oxide Vinyl chloride. Patty, Yant and Waite fume inhalation is transient metal fume (1930) found no serious disturbance in fever. The 15 mg./cu.m. threshold limit can guinea pigs inhaling 5000 ppm for several be interpreted from the results of extensive hours. Higher concentrations produced only human experiment and experience in indus narcosis. In humans, 50,000 ppm is noticed try. It is low enough to prevent injury. as a slight odor and nose irritation, and Zirconium. ACGIH (1955b) quotes un dizziness is evident. published data from the University of The most important effect of vinyl chlor Rochester A.E.C. Project. Four species of ide inhalation is narcosis. The 500 ppm animals inhaled the following, all expressed threshold limit can be interpreted from the in terms of contained zirconium: Zirconi results of single animal inhalations and um oxide, 1.5 micron dust, 75 mg./cu.m. for human response. I t appears low enough to 30 days, 11 mg./cu.m. for 60 days, 3.5 prevent significant narcosis. mg./cu.m. for one year; zirconium tetra Warfarin: Saunders, Heisey, Goldstone chloride, 0.6 micron dust, 6 mg./cu.m. for and Bay (1955) found injection of 0.5 6h0igdhaeyr s,co3.n5cemngtr./actuio.mn .'offorteatryaecahrl.orOidnely hthade mg./kg. for five days killed most of a small group of rats, while a single injection of any effect, presumably due to liberated hy 100 mg./kg. caused only 30% mortality. One drochloric acid. I lf 1 Ilfi'P I ll->fs?J'fIvk:::'Ht! 'i 180 June, 1956 The effect of zirconium dust inhalation is that of an inert nuisance dust when insolu ble, and possibly bronchial and lung irrita tion when soluble. The 5 mg./cu.m. tentative threshold limit can be interpreted from the results of repeated animal inhalations. It appears low enough to prevent injury. Bibliography ACGIH (1947): 1947 M.A.C. values. Ind. H yg. N ew sletter, 7 :15-16, A ugust. ACGIH (1948): Threshold lim it values adopted a t April, 1948 m eeting (p riv ately circu lated). ACGIH (1949) : Threshold lim it values adopted a t A pril 1949 m eeting (privately circu lated ). ACGIH (1950): Threshold lim it values. Arch. Ind. Hyg. & Occup. Med., 2:98-100. ACGIH (1951): Threshold lim it values fo r 1951. A rch. Ind. H yg. & Occup. Med., 4:398-400. ACGIH (1952): Threshold lim it values fo r 1952. A rch. Ind. H yg. & Occup. Med., 0:178-180. ACGIH (1953): Threshold lim it values fo r 1953. A rch. Ind. H yg. & Occup. Med., 8:296-298. 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