Document 1Qdn2j9Qr70Vz0dbnmwYn4r4K

FILE NAME: No Safe Threshold (NST) DATE: 1956 June DOC#: NST007 DOCUMENT DESCRIPTION: Trade Journal Article - Improved CommunicationHygienic Standards for Daily Inhalation [Smyth Says No Justification for Exposure to Carcinogen] Industrial Hygiene 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! AMERICAN INDUSTRIAL HYQIENE ASSOCIATION Volume 17 JUNE, 1956 Number 2 I mproved Communication--Hygienic Standards for Daily I nhalation . . 129 Henry Field Smyth, Jr., Ph.D. A Direct Method for the Collection and Determination of Micro Amounts of Benzene or Toluene in Air ..................................................... 186 P. A. Maffett, T. F. Doherty, and J. L. Monkman Ground Level Contamination from Stack Ef f l u e n t s .................. ................ 189 P. B. Klevin, M. S. Weinstein and W. B. Harris Problems in Calibration of I ndustrial Hygiene I n st r u m e n t s...... .......... 193 Elgin D. Sallee and Robert H. Miller Air P ollution Methodology .........................................................; .........., .......... 197 W. C. L, Hemeon. T he Toxicity of the Vapors of Aroclor 1242 and Aroclor 1254 ............ 204 J. F. Treon, Ph.D., F. P. Cleveland, M.D., J. W. Cappel, and R. W. Atchley Radiation P rotection--I nsurance and I ndustrial Relations A spects . . 214 ' Charles R. Williams, Ph.D. Determination of Acetic ACid in Ai r .................................... .......................... 221 Franklin Miller, Richard Scherberger, Henry Broekmyre, and David W. Fassett, M.D. I ndustrial Hygiene Units in I ndustry ...................... .................................... 225 A Survey by the AIHA Development Committee <O3> QOO. Hygienic Guide Series ........ .................................................................................. 229 co CO P resident's Page ....................................................................................................... 236 CD Selected Titles and Abstracts........ i ................................................................. 237 CO Q_ News o f the Local Sections . . .......................... .................................. ^.......... 238 AIHA Officers, Directors a n d Committees ................................................... 240 Co > & A merican I ndustrial H ygiene A ssociation Quarterly, published by th e A m e ric a n I n d u s tria l H y g ie n e A s so ciatio n in M arch , J u n e , S ep tem b er, a n d D ecem ber. H oward N . Schulz, E d ito r; H erbert J . Weber, A dvisory CO E d ito r; L loyd E . Gordon, A sso ciate E d ito r; J ames A . Martin, A dvertising: E d ito r; P aul D. H alley, C ir E 1 <D cu latio n E d ito r; A . D . Cloud, P u b lish e r; Doris F lournoy, E d ito ria l A ss is ta n t. P u b lic a tio n a n d E d ito ria l O f _c fices, 605 N o rth M ich ig an A venue, C hicago 11, Illinois. S u b sc rip tio n $4.00 p e r y e a r in th e U n ite d S ta te s; $4.50 p e r y e a r in C anada; $5.00 p e r year. in o th e r co u n tries. S ingle copies, $1.50-- e x c e p t th e J u n e , 1956, issue w hich is $2.00. C o p y rig h t, 1956, th e A merican Industrial H ygiene Association. E n te re d a s second class m a t te r M ay 3, 1948, a t th e p o s t office a t Sheboygan, W isconsin, u n d e r th e A c t o f M arch 3, 1879. T h e A merican 1 I ndustrial H ygiene Association Quarterly reserv es th e r ig h t to e d it a ll a d v ertis em e n ts a n d to re fu s e a d v e rtis ing copy w hen it does no t m eet the high professional standards adopted by the Association. 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 Improved Communication --HYQIENIC STANDARDS FOR DAILY INHALATION- "DattaleC S - 7%e*HO>UtU ^.ectccie HENRY FIELD SM YTH, JR ., Ph.D. Mellon Institute and Union Carbide and Carbon Corporation Pittsburgh, Pennsylvania Experience 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, thre 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 M eeting of the A m erican I ndustrial H ygiene A ssociation, Philadelphia, A p ril 25, 1956. / y 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 year AGO 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- ! 1*1 : iii 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 'JpHE 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) of 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 hy.nmunication. The toxiari acceptable job for cognize their need for ition and opinion. The ter, but it is at least acby no means as great de who do not recognize Once more communicaunless the audience demunication. rations at communication with;iene, and between our :s, may be the collection i acceptable concentrants in working atmos,t may be called the age perienced 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 Ins published its first list il Hygiene Newsletter In the next two. years 3GIH 1949) revised lists :ulated to the members of hen (ACGIH 1950) pube in a scientific journal, ereafter 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 ances other than mineral ent list (ACGIH 1956) of tentative threshold limit ;hose which were first pro- Industrial Hygiene Quarterly 131 posed in Cook's list, some as definitely es Three other suggestions of the Commit tablished, others to be used cautiously until tee on Chemical Agents deserve reiteration verified by actual experience. and discussion. It was urged that the bases Not since Cook has anyone published a for the selection of each value should be summary of the data which serve as bases published, that the name should be changed for the selection of specific threshold limits. to hygienic standard, and that the particular The privately circulated documents which concept of permissible human response be give some of these data (ACGIH 1953b, hind each value should be clearly indicated. 1954b, 1955b) cannot be considered to be There is such a multitude of factors in publication, although they are freely avail volved in the protection of health in our able to any person. complex civilization that no one person or Threshold limits are, and must continue group of persons is competent to weigh to be the products of judgment, important them all with assurance. No oracular or ex' if true. Some few truly represent their defi cathedra statement on health deserves seri nition and are approximations of the maxi ous attention. Only when the facts upon mum concentrations which can be inhaled which a decision are based are furnished for continuously and repeatedly without injury general scrutiny jtnd evaluation can the de to health. These may possibly be fit para cision be considered even tentatively sound, meters for incorporation into codes and and only after there has been adequate op regulations. Many of the threshold limits portunity for criticism and modification can are well below concentrations which can in it be considered established. All toxicologi jure health. They represent current judg cal facts should be published, and all de ment as to concentrations to which, good cisions upon the facts should be accom practice dictates, men may be expected to panied by a summary of the reasoning subject themselves. These do not seem fit under which they were derived, before any parameters for regulations. In a particular one should be expected to act upon the de operation, if possible, it is desirable to cisions. Any publication of standards for, maintain concentrations below the bench maintenance of health ought to include ref mark by reasonable ventilation and precau erence to the underlying data. tion. It is always best to reduce exposure to The second suggestion referred to the chemicals to the lowest practical level. name by which the values are known. Sem antics is more than a sport for the'idle. No Previous Suggestions for Improvement matter how thoroughly a concept is origi Touring the Ninth Annual Congress on nally presented, it always becomes known Industrial Health, the writer was chair and referred to by a brief name, a catch man of the Committee on Chemical Agents word. Most persons who learn of the con (1949). The report of the 16-man commit cept hear the catch-word name, and do not tee devoted considerable attention to prais go back to the original presentation. The ing the development of threshold limits, and meaning they attach to the name comes 1 ttoionsucgoguelsdtibneg wmaaydse imn owrhe icuhsetfhuel.irSpinrceesetnhtaat fpraormticutlhaerirwoprrdesv.ioIutsmeaxypebrei,enbcuet iws iuthsuathlleyj report, two developments have taken place not, exactly what the originator of the idea along lines desired by the Committee. The intended. The more carefully one chooses: annual table of the Threshold Limits Com the name he assigns to a concept, the more: mittee of the American Conference of Gov likely are others to interpret the concept as] ernmental Industrial Hygienists is now pub he himself does. lished in the Archives of Industrial Health, The values now known as threshold limits] removing the earlier implication of quasi- are usually identified by phrases containing] I ` legal status arising from its appearance in the words allowable or permissible. Thes the Industrial Hygiene Newsletter of the two words have connotations of legal regU Division of Industrial Hygiene, ILS. Public lations. Such connotations cannot properlyj Health Service. In 1954, .the Committee on attach to the judgment of a voluntary pro Threshold Limits of that Association began fessional association. The identifying to supplement its table of accepted values phrases may also contain the words maxi with a list of tentative values. 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. 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 the degree of organoleptic response. The 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 be exposed for an eight-hour working day without injury to health." Careful study of the data which support the currently ac Committee's four concepts follow: a. Plus or minus: The maximal time- weighted average concentration which produces only minor injury, and that ih 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 demonstrable illness or other symptom of toxic effect in any workman during a lifetime of industrial exposure. i' & 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. In deed; 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 will be abbreviated M.A.C. Many will in terpret this abbreviation as maximum al- 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. Hygienic Standards for Daily Inhalation lotvable concentration, and nothing will have 'JpHE subject of hygienic standards for been gained by the`change from allowable to A daily inhalation should be re-examined, acceptable. the concepts represented by the values I conclude that the names maximum al should be restated in more realistic toxi lowable concentration and threshold limit cological terms, and more consistent and are misleading. They convey a wrong im more informative standards should be pre pression to those who are not already famili pared. Such a step will not undo any of the ar with the cpncepts behind the values. The accomplishments of the profession of in name suggested in 1949, hygienic standard, dustrial hygiene or of any organization. is not misleading. Standards of good prac Rather, it will supply informative standards tice are familiar to all of us in many fields. to supplement the accumulation of naked Looking toward the future provision of a numbers now accepted, some of which have I f.i vvaalruieetsy shofouhldygbieeniscelesctatendd,artods,bea ksneorwiens aosf noIttbiesencecrrtiatiincalyllyimrpe-eerxaatmivientehdaftotrhae dinehcaadlae. 11 i hygienic standards for daily inhalation. tion of substances during the working day The third suggestion is more far-reach shall not be allowed to result in any injury l l ing. The Committee on Chemical Agents. (1949) pointed out that there has been no simple or uniform relation between the ef to the physical well-being of workmen. It is furthermore imperative that inhalation shall not increase the probability of acci fects of a substance and the numerical value dents through the mental distress occa chosen for tabulation. The Committee con sioned by objectionable eye, nose or throat cluded that concentrations have been se irritation, transient though it may often be, fese ; lected on the basis of one of four concepts of nor through the impaired judgment and 8 the level best suited to hygienic control of delayed reaction time of light narcosis. It inhalation, the choice having been governed is desirable that inhalation shall result in by the nature of the toxic response and by no degree of discomfort whatsoever. On the 1956 f 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/table 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 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. fjf; f.ii ' HItelsSil m June, 1956 Acute toxicity. Some substances do not produce an injury progressing 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 fluorochloro 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 mg./cu.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 hydroquinone, 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 timeweighted 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 concentra 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. iiv y a Industrial Hygiene Quarterly rational experimental basis for defining a ards the decision should be clearly indicated concentration which will not sensitize a sus in the table. ceptible workman, or one to which no previ Three columns record personal judgments ously sensitized workman will respond. Con and estimates as to what responses may oc trol of exposure to allergenic substances cur in some workman inhaling continuously, 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 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 tected by a hygienic standard for daily in find no objectionable sensory effect, or even halation based upon irritation or systemic concentrations where no toxic symptoms will injury. Until it has been demonstrated that develop in any individual. a particular group includes no susceptible Next comes a column listing important workmen, no considerations can justify al injuries other than from inhalation of the lowing inhalation of any concentration substance itself, such as dangerous absorp which is avoidable. tion through the skin, chemical burns of eye Interpretations of Accepted Values and skin, frequent allergic dermatitis, pyrolysis to phosgene, and the like. The al VTO NEW values for standards are sug most universal defatting of the skin by sol gested at this time. The available data vents, and freezing of tissue by low boiling upon which the 238 values in the 1956 pro liquids, has not been entered. posed list (ACGIH 1956) appear to be based The last two columns give some indica have been studied. Table I is offered as an tion of the soundness of th value by de interpretation of these values, increasing scribing the supporting data, and by speci the information they convey. It presents fying the year in which it was first pro the familiar numbers, which give the engi posed or adopted. It is, of course, true that a C neer and the chemist an illusion of complete value proposed many years ago and recopied o understanding. It also presents, in the form in each succeeding year's list is not neces of abbreviations of self-evident meaning, sarily proven sound, but in general it is like .some description of actions which gives the ly to be better established than a more re biologically and medically trained a feeling cently adopted value. e of confidence. The table is obviously too com There may be objection that the table 2 plex for great popularity. Nevertheless, does not mention warning power nor at "<Od every class of information listed is required tempt to evaluate this property specifically. q_ by those who must apply the values. The The practical importance of warning power oo data relied upon for the interpretations and in preventing inhalation of an excess is CO CO some comments on their adequacy are sum much over-rated. Odor data are notoriously 5 marized after the table. unreliable. Estimates of tolerable working CD All substances in the proposed 1956 conditions with unacclimated subjects, CO Q- threshold limits table (ACGIH 1956), ex briefly exposed, have only limited usefulness 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 units of milligrams per cubic meter, the day. Early stages of narcosis reduce percep jD letter m precedes the number. When a ten tion of odor and irritation. Even with strong CO tative value was proposed the letter T fol irritants like ammonia and acrolein, physi e <D 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 column showing a personal judgment of the jured by a concentration which, all would most serious effect of inhalation of a con predict, cannot be inhaled voluntarily. centration somewhat higher than the thresh There is nothing in Table I which is not 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 .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 m 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 lawi 136 June, 1956 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 interpretax 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- 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 unacclimated 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 t io n s u se d in T a b l e I. acne-- chloracne from continued skin contact. acute-- acute toxicity, w ith little or no increase in severity from continued inhalation. all-- allergenic. D erm atitis and asthm a-like sen- sitization m ay result. ALL-- allergenic. D erm atitis and asthm a-like sen- sitizatio n a re likely. asp h y x ia---a s p h y x ia tio n a t v e ry h ig h co n ce n tratio n s. bur-- burn of the skin. BUR-- very severe burn of skin. cancer-- cancer reported in hum ans. chronic-- chronic toxicity, w ith increase in severity from continued inhalation. clin-- clinical exam ination o f workm en was cor- related w ith th eir exposure. cns-- ' central nervous system stim ulation, such as trem ors o r convulsions. cy-- cyanosis (blue skin) m ay be evident. CY-- cyanosis (blue skin) m ay be m arked. est-- estim ate from experience and analogy. eye-- eye irritatio n severe enough to require medical treatm ent. EYE-- eye burn m ay be severe. eye pig-- eye pigm entation w ithout injury. fume-*- fum e fever. head-- headache. This sym ptom has n o t been en- tered every tim e it m ay occur. hu-- hum an sensory data. HU-- hum an toxicological o r physiological data. ind-- in d u strial com plaints or observations, less quantitative than clinical exam inations. irr-- irrita tio n of eye, nose o r th ro a t in some. IR R -- irritatio n of eye, nose o r th ro a t m arked. lung?-- lung-- LUNG-- m-- med-- narcosis-- nar?-- nar-- NAR-- nau-- none-- odor-- ODOR-- pyr-- rad-- rp t-- sgl-- skp-- SKP-- T-- to x ?-- to x --TOX-- vis-- m inor irritation of bronchi (coughing) or lungs. definite irritatio n of bronchi or lungs w ith in ju ry of lungs possible. dangerous injury of lungs w ith little w arning. the qu an tity is expressed in m illigram s p er cubic m eter (m g./cu.m .), n o t in ppm . m edical uses yield some inform ation. narcosis, ranging from im paired eoordination through dizziness, to anesthesia. fa in t narcosis, som ew hat im paired reaction tim e and judgm ent. narcosis definite, sh o rt of dizziness. narcosis m arked, dizziness to unconsciousness. nausea. This sym ptom has not been entered every tim e it m ay occur. no effects are expected. odor m ay be perceptible. odor marked. pyrolysis to lung in ju rin g halogen compounds in a flame, o r on h o t m etal. radiation in ju ry is possible. repeated anim al inhalation results. single anim al inhalation results. skin penetration m ay cause symptoms. skin penetration of liquid is dangerous. tentatively proposed. toxic sym ptom s m ay arise very slowly. m inor toxic sym ptom s. m ajor toxic symptoms. v isual acu ity loss  K T ^vt 3^ife ^a aK a g fe s June, 1956 Industrial Hygiene Quarterly ations are included when onfirm or supplement maature. The term "most im- ' with every substance, effect of inhalation of times the threshold --ily to the possible effects (1945) quotes the that cats inhaling hours were not noticeably subjects of Sil- Table I. I nterpretation of Threshold Limit Values P roposed for 1956 Exclusive of Mineral Dusts (Mnemonic abbreviations explained at foot of table) Substance Threshold Lim it ppm or m g./cu.m . Acetaldehyde 200. Acetic acid 10. A cetic M ost Im portant Effect of Inhalation lung lung Predicted Effects of Daily eight-hour Inhalations At Threshold Lim it A dditional A t Twice Threshold Lim it A d d itio n al A t Ten Times Threshold Lim it IRR-odor irr-odor lung IR R -lu n g Im portant H azards O ther Than from Inhalation all-EY E bur-E Y E N ature of Interpretive D ata hu-sgl hu-ind-sgl VU P r i CO Q_ 19I First (1946) found 25 50 ppm irritating to the ppm not irritating to (1949, p. 199) describes , narcosis, bronchitis, liver and lung edema. He does not cause and that death is due to , or to lung edema dh (1937-55) found rats inhalation of 8000 ppm ppm. The liquid causes irritates the skin and persons. anhydride A cetone A cro lein A crylonitrile A ldrin Allyl alcohol Allyl chloride Allyl propyl disulde Anim ate A m m onia Amyl acetate Am yl alcohol A n ilin e. Antim ony ANTU A rsenic A rsine B ariu m 5. 1000. 0.5 lung narcosis LUNG 20. acute m-0.25 chi'onic 5. EY E-lung 5. T lung 2. lung m-15. 100. 200. 100. 5. lung lung narcosis narcosis elu*onic m-0.5 chronic m-0.3 T chronic m-0.5 chronic 0.05 acute-lung irr-odor irr-nar-odor irr . none none irr none irr none irr-odor irr-odor irr-odor none none none none none IR R odor none IR R IR R -n ar IR R -n ar cy tox? e y e-IR R -lu n g NAR lung tox irv-tox eye-lung irr-odor lung IR R -lu n g NAR NAR C Y -tox tox tox tox lung ?-tox bur-E Y E b ur-E Y E skp all-skp b ur-E Y E pyr bur-eye SKP sgl H U -ind hu-sgl rp t d in ind-sgl sgl ind H U -ind-sgl hu-sgl hu-sgl rpt clin-rpt est clin-est ind-sgl i M -T= 195 CO J O liti 191 191 191 19l 195j cc (soluble) m-0.5 acute-lung none tox est 191 of bronchi (coughing) or tation of bronchi or lungs w ith possible. * -- of lungs w ith little w arn- is expressed in m illigram s (m g./cu.m . ), not in ppm . yield some inform ation. from im paired coordina- dizziness, to anesthesia. , somewhat im paired reaction *' , s h o rt of dizziness. , dizziness to unconscious- sym ptom has no t been entered may occur, expected, perceptible. lung in ju rin g halogen cornflame, o r on h o t m etal, is possible, inhalation results, inhalation results. m ay cause sym ptom s, Benzene Benzyl chloride B rom ine B u tad ien e B utanone (m ethyl ethyl ketone) Butyl acetate Butyl alcohol Butyl am ine B u ty l CELLOSOLVE B u ty l m ercaptan C adm ium oxide fum e Calcium arsenate Carbon dioxide Carbon disulfide Carbon m onoxide 35. 1. 1. 1000. chronic lung lung narcosis 250. . narcosis 200. narcosis 100. n a rc o sis 5. lung 200. chronic 10. T lu n g m-0.1 acute-lung m-0.1 T chronic 5000. asphyxia 20. chronic 100. acute tox? irr irr-odor none irr-odor irr-odor odor odor odor-tox ? ODOR none none none none tox odor odor nar-odor-T O X IR R -lu n g IR R -lu n g nar IR R -nau IR R -n ar irr irr nar NAR IR R -N A R eye nar-tox irr-nar-TO X eye-irr-lung? none odor tox none nar nar-tox TOX EYE B U R -E Y E B U R -E Y E skp clin-rpt sgl ind-sgl hu-rpt hu-sgl hu-sgl clin ind-sgl rpt sgl ind-rpt est HU clin-rpt clin-H U 19? O 195 _0> o o 194 i m 1 9 ? _rz Bng .oCV-- 194 S Q- 195; j O 195) 8 CO I 5 1 CD 1946S S? 1 195 S 194 8 i CO P "5 194! 1 E 19431 19431 ation of liquid is dangerous, proposed. m ay arise very slowly, sy m ptom s, sy m ptom s, loss Carbon tetrachloride 25. chronic tox? CELLO- SOLVE 200. chronic odor CELLO- : 1 SOLVE tox nar-odor-TOX p y r nar-tox irr-nar-tox clin-ind-rpt rp t 1953 1945 acetate 100. chronic odor irr-tox IRR-nar-tox rp t 1945 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 138 June,, 1956 Substance Lim it ppm or m g./cu.m . M ost Im portant Effect of Inhalation C h lo rd an e C h lo rin ated cam phene (60% ) m-2.0 chronic m-0.5 T chronic C h lo rin ated diphenyl oxide C h lo rin e Chlorine tri- fluoride Chlorobenzene C hlorobrom o- m ethane m-0.5 1. chronic lung 0.1 lu n g 75. narcosis 400. T narcosis Chlorodiphenyl (42% Cl) C h lo ro d ip h en y l (54% Cl) Chloroform l-C hloro-l- nitropropane C h lo ro p icrin m-1. m-0.5 100. 20. 1. chronic T chronic chronic lung T lung C h lo ro p ren e Chromic acid, chrom ates as CrO CRAG herbicide Cresol . Cyanide as CN 25. m-0.1 m -15. 5. m -5. chronic irr chronic chronic acute Cyclohexane 400. Cyclohexanol 100. Cyclohexanone 100. Cyclohexene 400. Cyclopropane 400. narcosis narcosis narcosis narcosis narcosis 2,4-D DDT D ecaborane D icto n e alcohol D ib o ran e m-10. chronic m-1. T chronic 0.05 T acute 50. narcosis 0.1 cns-lung o-D ich lo ro benzene Dichlorodifluoromethane 1,1-DichIoroethane 1,2-Dichloroethylene D ichloroethyl ether 50. 1000. 100. 200. 15. chronic asphyxia chronic narcosis lung D ich lo ro m o n o fluorom ethane 1,1-D ich lo ro 1-nitroethane 1000. 10. asphyxia lung T a ble I-- C o n t in u e d Predicted Effects of Dailv eierht-hour Inhalations .At Threshold Lim it A dditio n al A t Twice Threshold Lim it A dditional A t Ten Times Threshold Lim it none none irr-tox none tox none odor none odor none tox? irr irr-tox nar tox IR R -Iu n g irr-lung nar tox none none odor-tox ? none tox? nar-tox tox? tox TOX none odor none irr nar-tox irr-lung-tox lung TOX none none odor none none irr-odor irr-odor none none none none none irr none odor-tox ? irr IR R none irr irr-tox? lung-tox nar-odor nar-tox nar-odor nar-odor tox irr-N A R-tox IRR-N A R IR R -n ar irr-N A R-tox irr-N A R none none irr-tox ? irr-tox odor odor IR R -n ar lung-tox? irr-tox nar none odor none none none odor irr-odor none nar-tox irr-n a r lung none none none irr none lung-tox Im portant H azards O ther Than from Inhalation all-skp N ature of Interpretive D ata clin H i f Year 1 Propose! 19541 all-skp acne bur-E Y E bur-E Y E pyr pyr acne acne pyr est rp t hu-rpt rp t est-sgl rpt rp t rp t est-m ed-sgl 1956 g 1 1955 1 1948 I 1955 i 1943 i 1956 I 19451 1 1956 1945 Sgl clin pyr-skp rp t 1945 1956 1945 bur-E Y E clin est B U R-EY E-SK P est-sgl est rp t hu-rpt hu-rpt sgl est-m ed est skp est rp t hu-sgl clin-rpt pyr ind-sgl 1943 1954 1952 1947 1945 1945 1945 1945 1947 1954 1954 1956 1954 1955 1947 pyr rp t 1947 pyr rp t 1945 pyr sgl 1945 skp hu-sgl 1945 pyr sgL 1947 rpt 1945 June, 1956 im portant H azards Than from nhalation skp N atu re of Interpretive D ata d in * Year Proposed 1954 skp 1956 -E Y E -E Y E rp t hu-rpt rp t est-sgl rp t 1955 1948 1955 1943 1956 rp t rp t est-m ed-sgl 1945 1956 1945 sgl din -skp rp t 1945 1956 1945 -E Y E din est -EY E-SKP est-sgl rp t hu-rpt hu-rpt sgl est-m ed est est rp t hu-sgl clin-rpt ind-sgl 1943 1954 1952 1947 1945 1945 1945 1945 1947 1954 1954 1956 1954 1955 1947 rp t rp t sgl hu-sgl 1947 1945 1945 1945 Sgl' 1947 rpt 1945 industrial Hygiene Quarterly T a b le I-- C o n t in u e d Substance Threshold Lim it ppm or m g./cu.ra. M ost Im portant Effect of Inhalation Predicted Effects of Daily eight-hour Inhalations At Threshold Lim it A d d itio n al A t Twice T h resh o ld Lim it A dditional A t Ten Times Threshold Lim it Im portant H azards O ther Than from Inhalation N ature of Interpretive D ata D ichlorotetrafluorom ethane Dieldrin Diethylam ine 1000. chronic asphyxia lung none none odor none none aye-irr none irr IR R -lu n g pyr 3gl all-skp d in b ur-E Y E sgl Diuorodibrom om ethane D iisobutyl ketone D iiso cy an o toluene D im ethylaniline D im ethylsulfate D in itro b en zene D in itro -o cresol D initro to lu en e D ioxane EPN Ethyl acetate Ethyl acrylate Ethyl alcohol Ethylam ine Ethyl benzene Ethyl bromide E thyl chloride E th y len e chlorhydrin Ethylene d iam ine Ethylene dibrom ide E th y len e dichloride Ethylene im ine Ethylene oxide Ethyl ether Ethyl form ate 100. 50. 0.1 5. 1. irt-1. m -0.2 m-1.5 100. m -0.5 400- 25. 1000. 25. 200. 200. 1000. 5. 10. 25. 100. 5. 100. 400. 100. chronic irr-odor T A LL-lung all chronic none acute-LUNG none T chronic none acute chronic chronic acute narcosis T lung narcosis lung narcosis lung , narcosis none tox? none none irr-odor odor irr-odor odor n a r ?-odor none odor acute none A LL-lung odor chronic-lung none chronic acute-lung lung-nar cosis narcosis narcosis odor-tox? odor odor-nar irr-odor none irr-nar-tox rp t IR R -n ar hu-rpt ALL ind cy C Y -tox SKP sgl L U N G -T O X BUR-EYE-SKP sgl tox tox ? nar-odor nar irr nar eye-irr irr irr-odor irr-tox irr-tox irr-N A R-tox tox IR R -N A R lung IR R -N A R IR R -lu n g NAR lung nar to x ? odor-tox irr eye irr-odor Iung-tox skp est skp skp bur-E Y E pyr pyr sgl est hu-rpt est hu-sgl rpt HU Sgl hu-sgl sgl sgl SKP ind-sgl ALL-bur-EYE ind-rpt pyr rpt nar-nau irr IR R irr-odor TOX pyr lung-T O X bur-eye-S K P IRR-LUNG-NAR bur NAR nar ind-rpt hu-sgl hu-rpt H U -m ed sgl if 4 'o 19: - o li 1 > If 2 1 -Q 1 -1 i l l <0 J ^ ll 2 iM 19J 1 ^ "o 19% m o 1 o I M o> _419i 1 o 19i 191 19 19# 19 Ethyl m ercaptan E thyl silicate Ferbam Ferro vanadi um dust Fluoride dust 250. 100, m-15. m rl. m -2.5 T lung acute-lung T lung lung chronic ODOR odor none none tox? irr-tox irr eye-irr-lung IR R IR R none all irr-tox ' sgl hu-rpt rp t c lin-H U Fluorine Fluoroacetates Fluorotri- chloroniethane F orm aldehyde Furfural 0.1 lu n g m-0.1 T acute 1000. asphyxia 5. lung 5. T lung none none none odor irr-lung?-tox ? tox , B U R -E Y E clin-rpt est sgl ind-sgl ind-sgl 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. uo June, 1956 Substance H eptane h etp Hexane Threshod Lim it ppm or m g./cu.m . M ost Im portant Effect of Inhalation 500. m-0.1 500. narcosis 'T a cu te narcosis T a b le I-- C o n t in u e d Predicted Effects of Daily eight-hour Inhalations At Threshold Lim it A dditional A t Twice Threshold Lim it A dditional A t T en Times Threshold Lim it odor none odor irr-nar irr NAR tox irr-nar-nau Im portant H azards O ther Than from Inhalation SKP N ature of Interpretive D ata hu est hu Y ear Proposed 1945 1956 1947 Hexanone (m ethyl butyl ketone) Hexone ( m ethyl isobutyl ketone) H ydrazine H ydrogen b rom ide Hydrogen chloride 100. narcosis odor 100. narcosis odor 1. lung none 5. lung irr 5. lung irr irr nar irr nar cns-irr-lung bur-eye IR R eye-lung bur-eye IR R eye-lung bur-eye hu-sgl hu-sgl rp t hu ind-rpt 1947 1947 1955 1955 1948 H ydrogen cyanide 10. acute odor TOX SKP hu-sgl 1948 H yd ro g en ' fluoride 3. c h ro n ic -lu n g i r r IR R eye-lung-tox B U R -E Y E ind-rpt 1943 Hydrogen peroxide, 90% 1. lung none irr-lung B U R -E Y E rp t 1955 H ydrogen selenide 0.05 c h ro n ic -lu n g n one lung-odor-tox hu-ind-rpt 1948 8 Hydrogen ! sulfide 20. lung irr-odor lung-tox clin-sgl 1943 H y d ro q u in o n e Iodine Iron oxide fum e Isophorone m-2. 0.1 m-15. 25. Isopropyla- m ine 5. eye pig lung fum e-lung chronic- narcosis lung none irr none irr-odor odor eye pig IR R vis eye-lung fum e-irr lung IR R -n ar-to x irr eye bur-eye BUR-EYE clin ind clin hu-rpt ind-sgl 1955 1948 1947 1945 1955 Lead Lead arsenate Lindane M agnesium oxide fum e M alathon m-0.15 chronic m-0.15 T chronic m-0.5 chronic m-15. m-15. fum e acute tox? none none none none tox none none TOX irr irr fum e-irr lung tox all-skp clin rp t rp t HU est-clin 1943 1956 1954 ' 1945 1954 M anganese M ercury M ercury, organic M esityl oxide M ethoxychlor m-6. m-0.1 m-0.01 50. m-15. chronic chronic chronic narcosis chronic Methyl acetate M ethyl acetylene M ethylal M ethyl acrylate Methyl alcohol 200. 1000. 1000. 10. 200. narcosis lung chronic T lung narcosis none none to x ? irr-odor none odor none odor none none none tox nar irr-tox irr odor irr odor odor tox TOX tox IR R -lu n g nar lung-nar lung-tox irr-n a r irr-nar-tox? SKP clin clin-rpt clin-sgl hu-rpt sgl est-sgl rpt rpt rp t rp t 1945 1943 1954 1945 1954 1948 J ! 1955 J 1952 J 1956 1 1943 J cns-odor irr-tox odor-tox? irr-nar-tox June, 1956 n N ature of Interpretive Y ear i D ata Proposed hu 1945 est 1956 hu 1947 hu-sgl 1947 hu-sgl rpt hu in d -rp t hu-sgl in d -rp t 1947 1955 1955 1948 1948 1943 rp t hu-ind-rpt clin-sgl d in ind d in hu-rpt 1955 1948 1943 1955 1948 1947 1945 ind-sgl d in rp t rp t HU est-clin clin clin-rpt clin-sgl hu-rpt sgl est-sgl rp t rp t rpt rpt clin-rpt 1955 1943 1956 1954 ' 1945 1954 1945 1943 1954 1945 1954 1948 1956 1952 1956 1943 1945 clin-rpt 1947 Industrial Hygiene Quarterly U1 T a ble I-- C o n t in u e d Substance Threshold Lim it ppm or m g./cu.m . M ost Im portant Effect of Inhalation > Predicted Effects of Daily eight-hour Inhalations At Threshold Lim it A d d itio n al A t Twice Threshold Lim it A d d itio n al A t Ten Times Threshold Lim it Im portant H azard s O ther Than from Inhalation N ature of Interpretive D ata Year Proposed M ethyl CELLO- SOLVE ' acetate 25. M ethyl chloride 100. M ethyl chloroform 500. chronic chronic narcosis odor odor-tox irr-nar-tox odor cns-nar pyr nar NAR pyr est 1947 rp t 1947 rp t 1953 M ethyl cyclo hexane 500. M ethyl cyclo- hexanol M ethyl cyclo odor irr-odor nar nar-tox irr-N A R-tox IR R -N A R rpt 1947 1? rpt 1945 I hexanone 100. M ethylene irr-odor IR R -nar rpt 1945 % chloride M ethyl form ate 500. ch ro n ic none none odor nar irr-odor nar rpt 1945 1 1 sgl 1947 & M ethyl isobu tyl carbinol . (methylamyl alcohbl) M ethyl 25. narcosis .none irr-odor IR R -nar hu-sgl 1954 m ercaptan M olybdenum 50. T lung ODOR eye-irr-lung sgl 1954 (soluble) M olybdenum m-5. chronic none irr-tox rpt' 1955 (insoluble) m-15. N aphtha chronic none none irr-tox rp t 1955 (coal tar) 200. narcosis irr-nar?-odor NAR est 1945 N aphtha , (p etroleum ) 500. narcosis odor N ickel irr-nar NAR est 1945 \ carbonyl 0.001 can cer-lu n g none , N ico tin e m-0.5 T chronic none | N itric acid 10. T lung irr ' p-N itroaniline 1. chronic none none IR R none tox lung tox SKP B U R -E Y E skp ind-sgl est est est-ind 1964 1956 1956 1954 I N itro b en zen e 1. chronic none tox SKP est 1947 J N itroethane 100. acute none irr-odor nar-tox rp t 1947 ; N itrogen dioxide 6. lung odor N itroglycerine 0.5 a c u te head ; N itro m eth a n e 100. a cu te none irr irr-odor LUNG tox nar-tox SKP in d -rp t clin rpt 1945 1946 1947 2-N itropro- pane N itrO to lu en e O ctane Ozone P a ra th io n 60. 5. 500. 0.1 m-0.1 acute chronic narcosis lung acute nau-tox 7 none odor odor none tox ? irr-n a r odor-tox tox NR irr-lung tox SKP SKP clin-sgl est est rpt cliii-est 1947 1943 1945 1954 1963 P e n ta b o ra n 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 P e n ta n o n e (m ethyl pro- p y l ketone) . 200. narcosis irr-odor IR R nar Perchloroethylene Perchloro, m ethyl m ercaptan 200. narcosis 0.1 T lung: odor none nar irr-N A R irr acne bur-skp pyr bur-EY E rp t rp t est hu hu-sgl m ed-rpt sgl 1956 1945 1947 1947 1947 1953 1964 The material on this page was copied from the collection of the National Library of Medicine by a third party a n Z a y t e ^ r o S e d b ^ June, 1956 Industrial Hygiene Quarterly US T a b le I--C o n t in u e d t .n N a tu re of t Interpretive Year i ' D ata Proposed Substance Threshold Lim it ppm or m g./cu.m . M ost Im portant Effect of Inhalation * Predicted Effects of Daily eight-hour Inhalations At Threshold Lim it A dditional A t Twice Threshold Lim it A dditional A t Ten Times Threshold Lim it Im portant H azards O ther Than from Inhalation N ature of Interpretive D ata Proposed Year -SKP h u -rp t sgl H U -rpt rpt ind sgl est 3gl clin est-sgl est-hu rpt SKP sgl rpt rpt ind-m ed clin est 1952 1954 1943 1947 1947 1947 1947 1945 1954 1945 1945 1947 1955 1945 1956 1954 1955 1956 Thiram T itan iu m dioxide Toluene o-Toluidine Trichloro- ethylene m-5. T chronic m-15. 200. 5. lung narcosis chronic 200. narcosis none none nar?-odor irr none cy nar-nau-odor irr-lung NAR C Y -to x irr-N A R SKP pyr est-sgl 1956 rpt 1954 clin-hu-rpt 1943 co sgl 1945 E ind-m ed-rpt 1948 T ric h lo ro - naphthalene m-5. T rifluorom on- chronic none tox acne rpt 1945 CO Q_ obrom o- m ethane 1000. narcosis none none irr-n a r pyr Trinitrotoluene m-1.5 chronic tox ? tox? irr-tox skp rpt clin-rpt 1955 1943 T u rp en tin e 100. narcosis irr-odor IR R -nar NAR-tox hu-rpt 1945 -Q U ranium CD (soluble) m-0.05 chronic none tox rad rpt 1953 CZ U ranium -O (insoluble) m-0.25 chronic none tox rad rp t - 1963 V an ad iu m . (V2O 5 .dust) m-0.5 lung none V an ad iu m lung rpt 1954 (V2O3 fum e) m-0.1 lung none lung rpt 1954 V inyl chloride 500. narcosis W arfarin m-0.5 T ch ronic none none nar pyr sgl 1947 tox est 1956 X y len e Zinc oxide fum e Zirconium 200. ' m -15. m-5. narcosis fum e T lung irr-nar?-odor nar NAR fum e none fum e-irr lung lung hu 1943 HU 1943 rp t . 1955 clin-est ind sgl hu est hu-rpt clin-hu sgl H U -in d -sg l ind-sgl sgl est clin est 1947 1954 1947 1945 1956 1947 1943 1954 1948 1945 1954 1954 1947 1954 hu-rpt ind-sgl rp t rp t clin est 1955 1947 1956 1955 1943 1956 The most important effect of acetaldehyde trolled human sensory data. It is low enough inhalation is irritation of upper respiratory to prevent lung injury. tract, bronchi and even lung. The 200 ppm Acetic anhydride. Henderson and Hag threshold limit can be interpreted from gard (1943, p. 130) mention eye, nose and gi human sensory data. It is sufficiently low throat irritation and suggest that bronchial to prevent lung injury. and lung injury are likely. Fairhall (1949, E Acetic acid. Sterner (1943) concludes 10 p. 203) considers it a lacrimator and finds p ppm is reasonably non-irritating on the systemic effects unlikely. McLaughlin "O basis of industrial experience. Patty (1948- (1946) discusses serious corneal injury from 92 Q. 9, p. 886) finds 800 to 1200 ppm intoler the liquid in industry. Smyth (1937-55) Oo 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, 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 C 5 CoD> CO K' O- CO I s co 1 76 stomach and skin. They regard 20 to 30 ppm alogy with acetic acid. In view of rat mor CEO as without danger. tality from the two vapors, a lower value CD . The only important effect of acetic acid would be more consistent, although it is sV--z inhalation is irritation, first evident in the undoubtedly low enough to prevent lung in eyes, thn in the upper respiratory tract, jury. bronchi and even lung. The 10 ppm thresh Acetone. Nelson, Ege, Ross, Woodman old limit can be interpreted from uncon and Silverman (1943) found slight 'eye, i Si- i- I I V June, 1956 nose any throat irritation with unacclimated subjects at 300 ppm, but 500 ppm was not objectionable. Henderson and Haggard (1943, p. 196) conclude death is anesthetic, with no organic injury below a narcotic level. Fairhall (1949, p. 205) concludes it causes narcosis, bronchial irritation and headache, but no chronic systemic effect. Haggard, Greenburg and Turner (1944) found human narcosis like that from ethyl alcohol. The highest concentration not caus ing narcotic impairment of coordination and judgment is 2110 ppm, which results in a blood level % that giving first alcoholic intoxication symptoms. Smyth's (1937-55) rats survived four hours at 32,000 ppm, died from 64,000 ppm. Yigliani and Zurlo (1955) found chronic respiratory tract irritation, and dizziness in workers inhaling 1000 ppm three hours a day. The most important effect of acetone in halation is narcosis. The 1000 ppm thresh old limit can be interpreted from human sensory and physiological data. It is not low enough to prevent all narcotic symptoms. Acrolein. Yant, Sehrenk, Patty and Sayers (1930) found marked human eye, nose and throat irritation within five minutes at 1 ppm. Patty (1948-9, p. 936) concludes 0.25 ppm is moderately irritating. Henderson and Haggard (1943, p. 138) conclude the, main attack is on the upper respiratory tract, but that a high concentration can cause lung edema. They report 10 ppm to be lethal in a short time. Systemic effects are not to be expected. Smyth (1937-55) found four hours inhalation of 8 ppm kills one of six rats and all die from 16 ppm. The liquid causes severe corneal injury and burns of the skin. The only important effect of acrolein in halation is irritation, first evident in the eyes, then in the upper respiratory tract, bronchi and even lung. The 0.5 ppm thresh old limit can be interpreted from human sensory data. It is low enough to prevent lung edema. Acrylonitrile. Dudley, Sweeney and Miller (1942) found repeated inhalation of 153 ppm injurious to animals, but believed the effect not chronic toxicity. Dudley and Neal (1942) concluded injury is due to formation of cyanide in the body. The 10 ppm hydrogen cyanide threshold limit is equivalent to 20 ppm acrylonitrile, if conversion is complete. Wilson (1944) in exposed workmen, found evidence of skin penetration and effects ref erable to liver injury. Smyth's (1937-55) rats survived four hours at 500 ppm but were killed at 1000 ppm. The most important effect of acrylonitrile inhalation is acute poisoning, due to hy drolysis in the body to cyanide. The 20 ppin threshold limit can be interpreted from re sults of repeated animal inhalation studies and its relationship to the accepted 10 ppm threshold limit for hydrogen cyanide. It is low enough to prevent injury. Aldrin. Princi and Spurbeck (1951) ex amined workers with one to three years ex posure to 1 to 2.6 mg./cu.m. aldrin and re lated dusts, and found no clinical evidence! of injury. McGee (1955), reviewing human cases and animal data, finds aldrin and lin dane have similar actions. Acutely they in-! crease central nervous system irritability, jj leading to convulsions. Chronically they in-] jure the liver, with effects also on kidney, lung and nervous system, and they sensitize] some skins. ACGIH (1954b) finds aldrin twice as toxic to animals acutely as lindane, and concludes half the threshold limit of the| latter is tentatively appropriate. The. most important effect of aldrin in-] halation is chronic poisoning centering in] the liver. The 0.25 mg./cu.m. threshold lim-j it can be interpreted from the results of examination of exposed workmen. It is low] enough to prevent injury. Allyl alcohol. McCord (1932) found som human irritation at 5 ppm. The review b; von Oettingen (1943, p. 138) shows cats dl during 30 seven-hour inhalations of 50 ppm,j with pulmonary edema, gastroenteritis; hematuria and nephritis. Smyth (1937-55) found rats survive one hour at 500 ppm, but die from 1000 ppm. The vapors irritate eye and nose, but not sufficiently so to pre vent exposure to a concentration which temporarily blinded one man through de layed corneal necrosis. Chronic toxicity is not to be expected, but skin penetration is dangerous, and skin contact causes burns when evaporation is prevented. The most important effect of allyl alcohol inhalation is irritation, manifest as dis abling corneal injury and pulmonary edema, with non-progressive organic effects some what less important and narcosis over shadowed. The 5 ppm threshold limit can be 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. 1956 Industrial Hygiene Quarterly interpreted from a report of human irrita ppm dangerous to life in 30 minutes. Fair- tion and results of repeated animal inhala hall (1949, p. 20) notes eye and upper tion. It is probably low enough ,to prevent respiratory tract irritation, salivation, injury, but may be slighfly irritating to bronchial irritation and lung edema, but no some. chronic systemic effect. Elkins (1950, p. 84) Allyl chloride. Adams, Spencer and Irish found 55 ppm not objectionable in industry (1940) found rats survive three hours in but 125 ppm irritating. Silverman, Whitten- halation of 290 ppm, while eight hours berger and Muller (1949) found 500 ppm killed all. Injury was chiefly in the lung, stimulated human respiration, irritated eye with some kidney effects. Narcosis was and throat, caused lacrimation. Smyth weak but mucous membrane irritation was (1937-55) found rats survive four hours at prominent. 2000 ppm, die at 4000 ppm. Solutions irri The most important effect of allyl chloride tate the skin, erode mucous membrane and 1 1C inhalation is irritation of the upper respira severely injure the cornea. Vigliani and tory tract, bronchi and lung. The 5 ppm ten Zurlo (1955) in workers inhaling 100 ppm, tative threshold limit can be interpreted found irritation of the respiratory tract from single inhalations by animals and by and conjunctiva. Even 20 ppm caused com analogy with chloroprene. It appears low plaints until workers became hardened. enough to prevent injury. ' The most important effeet of inhalation of Allyl propyl disulfide. Feiner, Burke and ammonia gas is respiratory tract irritation, Baliff (1946) surveyed an onion dehydrat with lung edema or respiratory arrest the ing plant and found pronounced irritation maximum injury. The 100 ppm threshold of eye,' nose and throat at 3.4 ppm onion oil limit can be interpreted from human sen calculated as this disulfide, with some irri sory and physiological data. It is low enough tation at 2 ppm. Acclimitization was evi to prevent injury. dent. Amyl acetate. Patty, Yant and Schrenk The most important effect of allyl propyl (1936) found 2000 ppm does not injure disulfide inhalation is irritation of eye, guinea pigs in several hours, while a concen upper respiratory tract and lung. The 2 ppm tration killing in 60 minutes can not be. ob threshold limit can be interpreted from the tained. Symptoms consisted of eye and nose results of complaints from exposed work irritation and narcosis. Nelson, Ege, Ross, men. It appears low enough to prevent in Woodman and Silverman (1943) found jury. slight throat irritation in unacclimated sub Ammate. ACGIH (1954b) concludes the jects at 100 ppm, mild eye and nose sensa single dose LD60 for animals of 2000 tion and severe throat irritation at 200 mg./kg. justifies no more control on inhala ppm. Smyth (1937-55) with rats inhaling tion than is required for a non-toxic nui substantially saturated vapors found anes sance dust. thesia in two hours and death in eight The most important effect of ammate dust hours. Chronic toxicity is not to be expected.' inhalation is the low grade irritation of a The most important effect of amyl acetate substantially inert dust. The 15 mg./cu.m. inhalation is narcosis. The 200 ppm thresh threshold limit can be interpreted only by old limit can be interpreted from human analogy. It appeal's low enough to prevent sensory data and single inhalations by injury. animals. It is low enough to prevent definite Ammonia. Lehmann (1886) suggested narcosis. 100 ppm is tolerable, and subsequent in Amyl alcohol (isoamyl alcohol.) Nelson, dustrial experience has been favorable. Hen Ege, Ross; Woodman and Silverman (1943) derson and Haggard (1943, p. 125) note found slight throat irritation in unac incapacitating temporary blindness, and climated subjects at 100 ppm, and objection respiratory arrest from a high concentra able eye, nose and throat irritation at higher tion. They state 53 ppm is the least amount concentrations. Haggard, Miller and Green smelled, but Smyth (1937-55) found 1 ppm berg (1945) found the toxicity 12 times detected and identified by 10 subjects. They that of ethyl alcohol for anesthetic death. give 408 ppm as irritating to the throat, No chronic systemic toxicity is to be ex 698 ppm irritating to the eye, 2500 to 6500 pected. Smyth (1937-55) found rats not U6 June, 1956 The material on this page was copied from the collection of the National Library of killed by eight hours at 2000 ppm, close to saturation. Th 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, Hackley 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. Electrocardigrams on the animals and on a few industrially exposed workmen were normal. Brieger, Senisch, Stasney and Piatnek (1945) in an industrial operation where antimony 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. AN TV (alphanayhthylthiourea). 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 i 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./cu.m. was based upon supposed quanti tative similarity to lead. Watrous and Mc- 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, i delirium, irritation of eyes and respiratory i tract. Arsenic is stored in the body, but not j to the extent of lead. s The most important effect of inhalation of j arsenic compounds is chronic poisoning. The j 0.5 mg./cu.m. threshold limit can be in- j terpreted from the results of examinations i of exposed workmen. It appears low enough ; to prevent injury. 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 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. Industrial Hygiene Quarterly edema. They state 250 ppm for 30 minutes is fatal, and 3 to 10 ppm can cause symp toms in a few hours. Nau (1948) reported an industrial episode showing the earlier limit of 1 ppm was too high, and Elkins (1950, p. 67) reported briefly on a.nonfatal case at a level of about 0.5 ppm. The most important effect of arsine in halation is acute poisoning, largely lung edema. The 0.05 ppm threshold limit can be interpreted from the results of industrial experience. It appears to be low enough to prevent injury. Barium (soluble compounds). Fairhall (1949, p. 32) records the fatal dose of solu ble barium compounds as 0.8 to 0.9 grams with gastro-intestinal disturbance the chief symptom. He notes bronchial irritation from barium carbonate dust, and depilatory action of barium sulfide. The most important effect of inhalation of soluble barium compounds is bronchial ir ritation, with acute poisoning possible. The 0.5 mg./cu.m. threshold limit can be inter preted only by analogy with antimony. It ap pears low enough to prevent injury. Benzene. Winslow (1927) first proposed a limit of 100 ppm, based on extensive ex amination of exposed workmen and animal inhalation. He recognized that chronic poisoning would develop in some at this con centration, but believed it would progress slowly enough to be detected by periodic medical examinations, and arrested by re moval from exposure. Acute benzene poison ing is fatal anesthesia, and chronic poison ing is primarily injury to the bone marrow. Benzene is particularly insidious because its effects can progress to a fatal outcome after all exposure ceases. Even brief inhalation of a high non-anesthetic concentration can be fatal. Patty (1948-9, p. 757) ,states that 100 ppm has only a faint odor. Elkins (1950, p. 228) investigated a fatal case whose `exposure he was convinced had been only to 40 to 80 ppm. The most important effect of benzene in halation is chronic poisoning centering in the bone marrow. The 35 ppm threshold limit can be interpreted from extensive ex amination of exposed workmen, and was quantitatively defined by one fatal case. It appears low enough to prevent the develop ment of irreversible poisoning. Benzyl chloride. This is a potent lacri- mator, irritating to eye, nose and throat, and capable of causing lung edema. Flury and Zernik (1931, p. 538) conclude 170 ppm is dangerous to cats in eight hours and 16 ppm intolerable to man in one minute. It may be inferred that the liquid causes severe corneal injury. The only important effect of benzyl chlor ide inhalation is irritation, first evident in the eyes, then in the upper respiratory tract, bronchi and even lung. The 1 ppm threshold limit can be interpreted from older human sensory data. It is undoubtedly low enough to prevent lung injury. Bromine. Flury and Zernik (1931) quote Lehmann that 0.75 ppm in a workroom caused no symptoms in six hours. Hender son and Haggard (1943, p. 133) state bro mine acts as a respiratory irritant leading to lung edema. They state 40 to 60 ppm is dangerous on short inhalation, and 4 ppm allowable for 30 to 60 minutes. Elkins (1950, p. 87) found 1 ppm excessively irritating. Severe burns of skin and cornea result from the liquid. Patty (1948-9, p. 554) concludes 0.3 ppm is not objectionably irritating. The most important effect of inhalation of bromine vapor is respiratory tract irrita tion, with lung edema the maximum effect. The 1 ppm threshold limit can be inter preted from industrial experience. It ap pears low enough to prevent injury. Butadiene. Von Oettingen (1940) quotes repeated animal exposures at 64,000 ppm which caused bronchial and lung irritation and some hyperplasia of bone marrow. Carpenter, Shaffer, Weil and Smyth (1944) found animals not affected by repeated in halation of 2300 ppm, while 6700 ppm slightly retarded growth and there were minor liver effects. Two humans found psychomotor effects of early narcosis from 8000 ppm, equivalent to those from 200 ppm toluene. . The most important effect of butadiene vapor inhalation is narcosis. The 1000 ppm threshold limit can be interpreted from re sults of repeated animal inhalation and single human inhalation. It is low enough to prevent any degree of narcosis. Butanone (methyl, ethyl ketone). Patty, Schrenk and Yant (1935) found guinea- pigs tolerated 3000 ppm for several hours, and men found it irritating to nose and eyes. Nelson, Ege, Boss, Woodman and Silverman 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: fr/V * U8 June, 1956 (1943) found slight throat irritation in un then depression and narcotic death with pul acclimated subjects at 100 ppm, irritation monary edema. Smyth (1937-55) found rats of eyes at 200 ppm and objectionable irrita survive four hours at 2000 ppm but die from tion at 300 ppm. Elkins (1950, p. 118) found 4000 ppm. Injury to skin and cornea from complaints of nausea at 500 ppm, irritation the liquid is severe. Unreported industrial at 300 ppm, but no ill effects at 700 ppm. experience suggests skin injury is the great Smyth (1937-55) found rats survived two est practical hazard. ACGIH (1955b) cites hours at 2000 ppm but 4000 ppm killed four unpublished industrial experience that levels of six. He found that an episode of indus above 5 ppm tend to be irritating. trial eye injuries during inhalation of bu- The most important effect of butyl amine tanone was caused by an unsaturated ketone inhalation is respiratory tract irritation, impurity accidently present. with lung edema the maximum injury. The The most important effect of butanone 5 ppm threshold limit can be interpreted inhalation is narcosis. The 250 ppm thresh from analogy with ethyl amine. It is prob old limit can be interpreted from human ably low enough to prevent injury. sensory data. It appears low enough to pre Butyl CELLOSOLVE (2-butoxyethanol). vent definite narcosis. Werner, Nawroeki, Mitchell, Miller and von Butyl acetate. Sayers, Schrenk and Patty Oettingen (1943) found 300 to 400 ppm, in (1936) found guinea pigs are not affected repeated inhalation produced only small ef by several hours inhalation of 3300 ppm. fects on rats, particularly on the blood pic Nelson, Ege, Ross, Woodman and Silverman ture. Werner, Mitchell, Miller and von Oet (1943) found throat irritation in unaccli tingen (1943a, b) reporting on single in mated subjects at 200 ppm, severe at 300 halations by rats and repeated by dogs, ppm. Henderson and Haggard (1943, p. 222) make it clear that the butyl ether produces conclude the ester shows no chronic toxicity. somewhat greater blood cell changes than do Smyth (1937-55) found rats inhaling sub the methyl or ethyl ethers. They also found \\\l isntafnotuiarllhyousrast,ubruatteddiedvawpoitrhsinaarne eniogtht-khiloluedr hchemanoggelso.biSnmuryiath, w(i1th93l7u-n5g5,) livfeorunadndinkidrnaetys inhalation period. fractional mortality from as little as 500 The most important effect of butyl acetate ppm inhaled eight hours, with hematuria a inhalation is narcosis. The 200 ppm thresh prominent symptom. The liquid penetrates old limit can be interpreted from human sen the skin readily and is sufficiently toxic so sory response and single inhalations by that this is dangerous. animals. It is low enough to prevent defi The most important effect of butyl CEL nite narcosis. LOSOLVE inhalation is chronic poisoning, Butyl alcohol (n-butanol). Tabershaw, centering in the blood cells and kidney. The Fahy and Skinner (1944) reported eye in 200 ppm threshold limit can be interpreted flammation in workmen above 50 ppm, but from results of repeated animal inhalation no systemic effects below 100 ppm. Sterner, studies. Based on reports from simultaneous Crouch, Brockmyre and Cusack (1949) fol studies of Cellosolve and butyl Cellosolve lowed workmen for 10 years with butyl al it is obvious that the threshold limit for the cohol concentrations held to 100 ppm, and latter should be lower than for the former for a briefer period to 200 ppm. Neither ir if equal degrees of protection are to be at ritation nor systemic effects were found at tained. 100 ppm, but there was some eye irritation Butyl mercaptan. Fieldner, et al. (1931) at 200 ppm. Smyth (1937-55) found rats reports 733 ppm to be lethal to dogs in 30 are not killed in four hours at 8000 ppm. minutes, indicating 20 times the acute The most important effect of butyl al toxicity of ethyl mercaptan. Effects like cohol inhalation is narcosis. The 100 ppm those of hydrogen sulfide are to be expected. threshold, limit can be interpreted from an The most important effect of butyl mer extensive study of workmen under condi captan is eye and respiratory tract irrita tions of known peak exposure. No narcotic tion. The 10 ppm tentative threshold limit or irritative effects are to be anticipated. can be interpreted from the results of lim Butyl amine. Hanzlik (1923) reported ited single inhalations by animals and an central nervous stimulation, convulsions, alogy with hydrogen sulfide. It appears low lr {! :! Dt : Year: Notes.: 1956 1956 lied from the collection of the National Library of Medicine by a third party and may be protected by U .S. Copyright law. Industrial Hygiene Quarterly U9 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 central 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 LD50 of 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 acC>Oo for 30 minutes giving the first signs of in interpreted from the results of extensive Q_ toxication, and 70,000 to 100,000 ppm caus human experiment and examination of ex CD 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 1-- enough to prevent noticeable effects. too high and suggested 40 ppm. Adams, Carbon disulfide. Wiley, Hueper and von Spencer, Rowe, Mcollister and Irish (1952) Oettingn (1936) found repeated inhalation in extensive animal studies, found some ef of 30 ppm has no significant effect on fect on th 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 conentra- 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 kidney injury, while early narcosis occurs at a low concentration. Chronic toxicity is chiefly marked by liver injury. The most important effect of carbon tetra chloride inhalation is chronic toxicity cen tering in the liver. The 25 ppm threshold limit can be interpreted from the results of repeated animal inhalations and industrial experience. It is low enough to prevent ir reversible injury, but perhaps it will allow minor injury. . Cellosolve (2-ethoxyethanol). Werner, Nawrocki, Mitchell, Miller and von Oettingen (1943) found rats repeatedly inhaling 300 to 400 ppm showed small but measur able blood cell effects. Werner, Mitchell, Miller and von Oettingen (1943b) found dogs inhaling 800 ppm repeatedly developed small blood cell effects. Smyth (1937-55) found rats survive four hours at 2000 ppm, but half are killed by 4000 and all are killed by eight hours at 4000 ppm, close to satura tion. Death is marked by severe kidney dam age. The most important effect of cellosolve inhalation is chronic poisoning centering in the red blood cells. The 200 ppm threshold limit can be interpreted from results of re peated animal inhalation studies. It appears to be low enough to prevent injury. There are no data to judge the degree of eye and nose irritation it allows. Cellosolve acetate (2-ethoxyethyl ace tate). Smyth (1937-55) found in dogs after 120 seven-hour inhalations of 600 ppm, only a small increase in bromosulfalein retention, with eye and nose irritation. Eats survive 1500 ppm (close to saturation) for four hours, but two of six die after eight hours. It is easily hydrolyzed to cellosolve and acetic acid. Systemic injury should follow closely that of cellosolve, but respiratory tract irritation is somewhat greater. The most important effect of cellosolve acetate is chronic poisoning due to hydroly sis to cellosolve. The 100 ppm threshold limit can be interpreted from analogy with cellosolve. It appears low enough to pre vent injury. There are no data to judge the degree of eye and nose irritation it allows. Chlokdane. Princi and Spurbeck (1951) quote animal data indicating effects are principally neurological, with liver and kid ney injury and pulmonary irritation. They found workers for three years with ex- posures of the order of 5 mg./cu.m. showedg no clinical evidence of effect. Alvarez andf Hyman (1953) examined men in another! producing plant with up to five years ex-f posure and found no effects, but concentra-| tions were not measured. Ingle (1953)1 shows that early reports of inhalation in i jury in animals were due to a volatile uni reacted intermediate in the early product! and that 14 days continuous inhalation of saturated air does not injure mice. ACGIlf (1954b) bases its tentative threshold limil on a rat oral LD50 of 590 mg./kg. I The most important effect of chlordani inhalation is chronic poisoning centering if the liver. The 2 mg./cu.m. threshold limil can be interpreted from the results of ex aminations of exposed workmen. It is lo| enough to prevent injury. Chlorinated camphene, 60% (toxaphenej Lackey (1949) found an oral dose of mg./kg. caused convulsions in dogs while mg./kg. was fatal. A daily dose of 4 mg./k| for 106 days was not fatal, but at times col vulsions were seen. Liver and kidnJ changes resulted. J The most important effect of ehlorif ated camphene is chronic poisoning centel ing in the liver. The 0.5 mg./cu.m. tentatif threshold limit can be interpreted from t l results of single and repeated oral dos^* and by analogy with the similar but le toxic DDT- It appears low enough to pi vent injury. Chlorinated diphenyl oxide. After exte sive inhalation studies with rats, Drini (1949) concluded that 0.5 mg./cu.m. is| permissible concentration which will lead to systemic injury. Liver injury is effect of chronic poisoning. Smyth (191 55) found the material penetrates the si and repeated contact leads to chioracne. The most important effect of chlorinal diphenyl oxide inhalation is chronic poise ing centering in the liver. The 0.5 mg./cu| threshold limit can be interpreted from results of repeated animal inhalations. It low enough to prevent injury. Chlorine. Sklyanskaya and Rappapl (1935) found lung injuries and increased { cidence of pneumonia in guinea pigs peatedly inhaling 0.7 to 1.7 ppm. Fairhall (1950, p. 52) states it irritates eyes and nose, and may cause fatal lung irritation. Inhalation of 1000 ppm is rapidly fatal, 40 1956 JWie, 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, sinuous inhalation of injure mice. ACGIH native 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 i interpreted from the i repeated oral doses, i the similar but less cs low enough to pre- yl 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 (1937- i al penetrates the skin, ) leads to chloracne. i it effect of chlorinated = ition is chronic poison- ) iver. The 0.5 mg./cu.m. f e interpreted from the | nimal inhalations. It is . \ t injury. ! ;kaya and Rappaport | juries and increased in- 3 ia in guinea pigs re- ; 7 to 1.7 ppm. Fairhall | 3 it irritates eyes and j e fatal lung irritation. | ipm is rapidly fatal, 40 | Industrial Hygiene Quarterly to 60 ppm may lead to pneumonitis and lung edema, 30 ppm causs coughing, 15 ppm throat irritation and 3.5 ppm can be smelled. Patty (1948-9, p. 547) concludes 1 to 2 ppm is tolerable, 3 to 6 ppm irritating. The most important effect of inhalation of chlorine gas is respiratory tract irrita tion, with lung edema the maximum effect. The 1 ppm threshold limit can be interpreted from repeated animal inhalation and human sensory data. It is low enough to prevent injury. Chlorine trifluoride. Horn and Weir (1955) found it an extremely active irri tant. Rats are killed in 40 minutes at 96 ppm, while rats and dogs inhaling 5 ppm re peatedly are severely injured. Pneumonia was increased and there was respiratory dif ficulty in all. The vapors injure the cornea. Horn and Weir (1956) found repeated in halation of 1.17 ppm by rats and dogs in jured only by increased incidence of pneu monia. The most important effect of inhalation of chlorine trifluoride gas is respiratory tract irritation, with lung edema the maxi mum effect. The 0.1 ppm threshold limit can be interpreted from repeated animal inhala tion. It appears low enough to prevent in jury. Chlorobenzene. Fairhall (1949, p. 260) concludes it is somewhat more toxic than benzene, but finds no evidence of hematopoetic effect. The most important effect of chloroben zene inhalation is narcosis. The 75 ppm threshold lim it can be interpreted only as a rough estimate. By comparison with other chlorinated hydrocarbons, it appears low enough to prevent injury. Chlorobromomethane. Svirbely, Highman, Alford and von Oettingen (1947) found 300,0 ppm to be the LC50 for mice in eight-hour inhalations. Exposures of rats, rabbits and dogs to 1000 ppm seven hours a day five days a week for fourteen weeks were with out effect. Non-progressive liver injury was found from single inhalations, but liver and kidney remained normal during the repeated inhalations, Comstock et al. (1952) found light narcosis in rats and mice inhaling 3000 ppm for 10 to 15 minutes, and about 30,000 ppm was fatal within 15 minutes. Pulmo nary edema was present in animals dying. The most important effect of inhalation of chlorobromomethane is narcosis with non progressive effects on liver and kidney. The 400 ppm tentative threshold limit can be in terpreted from the results of repeated in halations with animals. It appears low enough to prevent injury. Chlorodiphenyl (42% chlorine), After ex tensive inhalation studies with rats, Drink er (1939) concluded that 10 mg./cu.m. of a sample 68% chlorine, but free from chlorin ated diphenyl benzene, would lead to no systemic injury, but that the presence of chlorinated diphenyl benzene reduced the permissible limit to 0.5 mg./cu.m. Smyth (1937-55) found the material penetrates the skin, and repeated contact leads to chlor acne. Treon, Cleveland, Cappel and Atchley (1956) reported that inhalation of 8.6 mg./cu.m. for 24 seven-hour periods did not affect four species of animals, and 1.9 mg./cu.m. for 150 periods also was without effect. The most important effect of chloro diphenyl inhalation is chronic poisoning, centering in the liver. The 1 mg./cu.m. threshold limit can be interpreted from the results of repeated animal inhalations. It is low enough to prevent injury. Chlorodiphenyl, 54% chlorine. Treon, Cleveland, Cappel and Atchley (1956) re ported that repeated inhalation over a sevenmonth period of 1.5 mg./cu.m. Caused some minor liver injury in four species of rodents. The most important effect of inhalation of chlorodiphenyl (54% chlorine) is chronic toxicity centering in the liver. The 0.5 mg./cu.m. tentative threshold limit can be interpreted from the results of repeated in halation by animals. It appears to be slight ly below an injurious concentration, Chloroform. Fairhall (1949, p. 264) con cludes, it acts much like carbon tetrachlor ide, and that anesthetic use has led to liver injury, but regression is more likely than with carbon tetrachloride. A concentration of 4000 ppm causes slight symptoms after several hours exposure. Patty (1948-9, p. 793) concludes the least concentration smelled is 200 to 300 ppm.-Smyth (1937-55) found one of six rats die from four hours at 4000 ppm, and all from 8000 ppm. The most important effect of inhalation of chloroform is chronic poisoning centering in the liver. The 100 ppm threshold limit can be interpreted from the results of single a z> I C3~ CD I -0 I I E IE & CD I CD I ^ f >> i _Q CD c o o >> CD _Q CD c O z03 <D o *o CD Q_ O CO CD 5 C0D5 CD Q- O Is Jd *cb CD _fZ ft 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 ill HI it ? J llfv 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-nitrppropane. 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-l- nitroethane 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. Chloroprene (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-f 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 and! irritating, their major effect is chronicj systemic poisoning. The 5 ppm threshold limit can be interpreted from analogy with! phenol. It appears to be low enough to pre;j vent chronic poisoning. Cyanide as CN. To the extent that cyai nide dusts dissolve, their toxicity is that of hydrogen cyanide, with some added local iil ritation due to hydrolysis on moist tissue] Cyanide dust equivalent of the 10 ppp| threshold limit for hydrogen cyanide is mg./cu.m. The 5 mg./cu.m. threshold limlj is about, half that for hydrogen cyanid| and hence is conservative. Cyclohexane. Treon, Crutchfield aiijj Kitzmiller (1943) found minor liver a |f kidney changes in animals repeatedly | haling 786 ppm, none at 434 ppm. Fairh| (1949, p. 273) concludes acute poisoning! anesthesia and that repeated inhalatiff causes no hematopoetic changes. Pat] in m i' 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 Industrial Hygiene Quarterly 15S (1948-9, p. 769) reports 300 ppm has no dis ard in industrial use. The most important ef tinct odor or irritation. fect of cyclopropane gas inhalation is narco The most important effect of cyclohexane sis. The 400 ppm threshold limit can be in 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 it can be interpreted from results of re low enough to prevent definite narcosis. peated animal inhalation. It is low enough 2,4-D. Rowe and Hymas (1954) conclude to prevent definite narcosis. that it has a low degree of chronicity, and Cyclohexanol. Treon, Crutchfield and Kitz- the acute LDg0 values range from 300 to miller (1943) reported that repeated inhala 1000 mg./kg. for various species. tion of 693 ppm caused minimal pathologi The most important effect of 2,4-D inhala cal changes in a monkey, and 145 ppm in tion is chronic poisoning centering in the the livers and kidneys of rabbits. Nelson, liver. The 10 mg./cu.m. threshold limit can Ege, Ross, Woodman and Silverman (1943) be interpreted from the results of single and found 100 ppm causes objectionable eye, repeated oral doses to animals. It appears nose and throat irritation in unacclimated low enough to prevent injury. subjects. Smyth (1937-55) was unable to DDT. Barnes (1953) finds no incidence of kill rats by eight hours inhalation of sub illness among workers using it throughout stantially saturated vapors. the world. Poisoning from accidental inges The most important effect of cyclohexanol tion is marked by abdominal pain, vomit 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 threshold limit can be interpreted from re poison animals, although man is probably sults of repeated animal inhalations and more sensitive. human sensory data. It is low enough to The most important effect of DDT inhala prevent significant narcosis or injury, but tion is chronic poisoning centering in the not to prevent irritation. liver. The 1 mg./cu.m. tentative threshold Cyclohexanone. Treon, Crutchfield and limit can be interpreted from the results of Kitzmiller (1943) in animal experiments repeated oral doses to animals. It appears found only narcosis and irritation. Nelson, low enough to prevent injury. Ege, Ross, Woodman and Silverman (1943) Decaborane. Svirbely (1954a,b) found found 50 ppm caused objectionable eye, nose the LCgo for mice inhaling vapors for four and throat irritation in unacclimated sub hours to be 25.7 ppm. Symptoms included jects. Smyth (1937-55) did not kill rats by central nervous excitability and corneal four hours at 4000 ppm, but 8000 ppm opacity. Six-hour inhalations of 20 ppm by caused anesthetic death. rats, repeated 20 times, killed some with The most important effect of cyclohexa fatty livers and central nervous excitability. none inhalation is narcosis. The 100 ppm Comstock and Oberts (1953) report that 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 sory response. It is probably low enough to like. prevent definite narcosis. The most important effect of decaborane Cyclohex'ene. Fairhall (1949, p. 279) con inhalation is acute toxicity involving the cludes that 9000 ppm causes mild narcosis in central nervous system, with liver injury animals, while 13,500 to 15,000 ppm gives less important. The 0.05 ppm tentative anesthetic death. This, indicates a toxicity threshold limit can be interpreted from lim greater than that of cyclohexane. ited animal inhalations. It appears to allow The most important effect of cyclohexene an adequate margin of safety. inhalation is narcosis. The 400 ppm thresh Diacetone alcohol. Von Oettingen (1943, old limit can be interpreted from results of p. 138) reports animals at 2100 ppm are single animal inhalations. It is low enough restless, irritation and kidney effects^ are to prevent definite narcosis. noted. He concludes it is twice as toxic as Cyclopropane. Fairhall (1949, p. 280) re acetone. Silverman; Schulte and First views reports of experience in surgical anes (1946) found 100 ppm irritating to eyes, '~1I thesia and concludes there is no toxic haz nose and throat but not intolerable in un- |hJ % Pi;s i 1. d,'ll IS#' ' 15 i June, 1956 acclimated subjects. Smyth (1937-55) found 1500 ppm, approaching' saturation, did not kill rats in eight hours. The most important effect of diacetone al cohol inhalation is narcosis. The 50 ppm threshold limit can be interpreted from single animal inhalations and human re sponse. It appears low enough to prevent definite narcosis. Diborane. Rozendaal (1951) reported on five human injuries from inhalation of diborane and other boron hydrides. Dibor ane produced symptoms like metal fume fever and severe central nervous system ir ritation. Krachow (1953) reported that single inhalations of 50 ppm may be fatal to rats, resulting in lung injury, while 6 ppm repeatedly for three weeks causes lung damage, and 2 ppm causes some lung injury within four weeks. Kidney effects are also noted; He finds diborane about as injurious as phosgene. Odor is evident at 2 to 4 ppm. The most important effects of diborane inhalation are central nervous system irri tation and lung injury. The 0.1 ppm thresh old limit can be interpreted from the effects of repeated animal inhalation and clinical studies on accidental human injuries. It is apparently low enough to prevent injury. O-Dichlorobenzene. Cameron, Thomas, Ashmore, Warren, Buchan, and KennyHughes (1937) found 30 minutes inhalation of 390 ppm caused in animals, liver necro sis and minor kidney injury. They concluded it is more toxic than chlorobenzene. Fair-hall (1949, p. 284) points out its narcotic properties. Elkins (1950, p. 147) reports some irritation of eye and respiratory tract from 100 ppm, without other effects. The most important effect of o-dichlorobenzene inhalation is chronic poisoning cen tering in the liver. The 50 ppm threshold limit can be interpreted from the results of single animal inhalations and human sensory response data. It does not appear to allow sufficient margin to prevent human in jury from continuous inhalation. Dichlorodifluoromethane. Sayers, Yant, Chornyak and Shoaf (1930) found animals exposed repeatedly to 200,000 ppm developed a generalized tremor and ataxic gait, but no gross pathology. Fairhall (1949, p. 347) notes it has little, if any anesthetic or toxic action. The most important effect of dichloro- difluoromethane inhalation is asphyxia from extremely high concentrations. The 1000 ppm threshold limit can be interpreted from the results of repeated animal inhalations. It represents good engineering control rather than a hazard limit. 1.1- Dichloroethane. Henderson and Hag gard (1943, p. 207) conclude it is similar to carbon tetrachloride. Smyth (1937-55) found rats survive eight hours at 4000 ppm, but are killed at 16,000 ppm, an acute toxici ty half that of carbon tetrachloride. In re peated inhalations by rats and dogs, chron ic toxicity somewhat less than that of car bon tetrachloride was likewise found. The most important effect of 1,1-diehloroethane inhalation is chronic poisoning, centering in the liver. The 100 ppm thresh old limit can be interpreted from single and repeated animal inhalations. It may be low enough to prevent injury, but new data are desirable in view of current views on car bon tetrachloride. 1.2- Dichloroethylene. Fairhall (1949, p. 292) concludes 39,000 to 50,000 ppm is lethal to guinea pigs, and 18,000 ppm produces narcosis. Acute poisoning consists of narco sis with central nervous system irritation. No liver injury has been found. The vapors are irritating. Smyth (1937-55) found the cis isomer did not kill nor anesthetize rats in four hours at 8000 ppm, while 16,000 ppm anesthetized in eight minutes and killed in four hours. The trans isomer was twice as toxic and anesthetic. The most important effect of 1,2-dichloroethylene inhalation is narcosis. The 200 ppm threshold limit can be interpreted from the results of single animal inhalations. It is low enough to prevent definite narcosis. Dichloroethyl ether. Schrenk, Patty and Yant (1933) found 500 to 1000 ppm killed guinea pigs in 30 to 60 minutes with lung hemorrhage and edema, while 35 ppm pro duced slight irritation in several hours. This concentration can be smelled but is not im mediately irritating to man, while 500 to 1000 ppm is lacrimating. Smyth (1937-55) found rats survive four hours at 125 ppm, but are killed by 250 ppm. Skin penetration , is moderately dangerous. The most important effect of dichloroethyl ether inhalation is lung injury. The 15 ppm-i threshold limit can be interpreted from the; resuits of single animal inhalations. It 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. Industrial Hygiene Quarterly 155 seems to be low enough to prevent injury. Dichloromonofluoromethane. N u c k o l l 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 dichloromonofluoromethane 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 l l 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. Difluorodibromomethane. 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 difluoro dibromomethane 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. 2,i-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 cases featuring upper respiratory tract irritation followed by sensitization A1ll!' Hw 1!! |filT& 156 June, 1956 and asthma-like attacks. Unpublished American experience features sensitization. The most important effect of 2,4-diisocyanotoluene inhalation is respiratorytract irritation, followed by sensitization. The 0.1 ppm tentative threshold limit cannot be interpreted quantitatively. It is probably not low enough to prevent an attack in a sensitized person. Dimethyl aniline (N-dimethyl aniline). Henderson and Haggard (1943, p. 227) con clude that the alkyl anilines are less toxic than aniline, but von Oettingen (1941, p. 15) concludes dimethyl aniline has a greater depressant effect than aniline. It forms methemoglobin in the blood. He cites two human poisonings with symptoms like ani line. The most important effect of dimethyl aniline inhalation is poisoning like that from aniline. The 5 ppm threshold limit can be interpreted by analogy with aniline. It appears low enough to prevent injury. Dimethyl sulfate. Flury and Zernik (1931) report that 13 ppm severely poisoned cats in 20 minutes. Patty (1948-9, p. 925) states it has only a faint odor and there is a considerable latent period before effects are evident. Fairhall (1949, p. 309) concludes it is a powerful irritant upon inhalation, the liquid causes severe skin burns and corneal injury, and when swallowed, marked central nervous system effects such as convulsions and delirium result. Smyth (1937-55) found rats survive four hours inhalation of 15 ppm but die from 30 ppm. The most important effect of dimethyl sulfate inhalation is delayed irritation of bronchi, and lung edema, not preceded by promptly evident irritation of eye and upper respiratory tract. Very high concentrations may cause convulsions and delirium, then coma. The 1 ppm threshold limit can be in terpreted from results of single animal in halations. It appears to be low enough to protect against lung injury, but available data do not indicate that it will prevent bronchial irritation. Dinitrobenzene. Fairhall (1949) con cludes the chief effect of dinitrobenzene is the production of methemoglobin, leading to anoxia and anemia. Yon Oettingen (1941) in a review of the literature finds chronic liver injury and cites opinions that it is more toxic than nitrobenzene. The most important effect of inhalation of dinitrobenzene is chronic poisoning. The 1 mg./cu.m, tentative threshold limit appears to be based on the reasonable assumption that dinitrobenzene is five times as toxic as nitrobenzene. Dinitro-o-cresol. Baltimore (1943) re ports a non-fatal case from inhalation of 4.7 mg./cu.m. Spencer, Rowe, Adams and Irish (1948) in animal experiments, found 10 to 50 mg./kg. is a fatal dose for animals. It is a rapidly acting metabolic stimulant, increasing body temperature to the point of heat stroke. Cataracts are produced in sus ceptible species, but chronicity is low. The most important effect of dinitro-ocresol inhalation is acute poisoning, marked by metabolic stimulation with rise of body temperature. The 0.2 mg./cu.m. threshold limit can be interpreted from the facts of one industrial accident. It appears low enough to prevent injury. Dinitrotoluene. Von Oettingen (1941, p. 110) concludes this is similar to trinitro toluene but less toxic when pure. The dust causes mucous membrane irritation. The most important effect of dinitro toluene inhalation is chronic poisoning, marked by central nervous system, liver and red blood cell changes. The 1.5 mg./cu.m. threshold limit can be interpreted from an-, alogy with trinitrotoluene. It does not ap- j pear low enough to prevent all injuries. Dioxane. Fairley, Linton and Ford-Moore ) (1934) found liver and kidney injury in animals repeatedly inhaling 1000 ppm, andj from skin absorption. Silverman, Schulte 1 and First (1946) found eye, nose and throat] irritation at 300 ppm in unacclimated sub jects. Patty (1948-9, p. 957) concludes there! is only a faint odor at 200 ppm. Smyth! (1937-55) found rabbits particularly sus-1 ceptible, repeated inhalation at 800 ppm| killing some with kidney injury within 30 j days. The most important effect of dioxane in-1 halation is chronic poisoning, centering inf the liver and kidney. The 100 ppm thresh-1 old limit can be interpreted from results off repeated animal exposure studies. It ap pears to be low enough to prevent injury. EPN. Hodge, Maynard et al (1954) found! the acute oral LDg0 for rats ranges from 7 j to 33 mg./kg., while 75 ppm in the diet is without effect during two years. The ma- 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 " lection of the National Library of Medicine b , a third parly and may be protected by U .S. Copyright law. Industrial Hygiene Quarterly 157 terial is a cholinesterase inhibitor, and lows. Smyth (1937-55) found rats survive ' symptoms of excess in animals are confined eight hours at 16,000 ppm but some are to excitability and tremors. It appears to killed at 32,000 ppm. be % to % as toxic as parathion. The most important effect of ethyl alco The most important effect of. EPN inhala hol inhalation is narcosis. The 1000 ppm tion is the reduction of blood cholinesterase. threshold limit can be interpreted from The 0.5 mg./cu.m. threshold limit can be human physiological data. It is low enough interpreted from the results of single oral to prevent significant narcosis, but some eye doses to animals and analogy with para irritation will result. thion. It appears low enough to prevent in Ethyl amine. Brieger and Hodes (1951) jury. exposed rabbits repeatedly to 50 ppm and Ethyl acetate. The unacclimated subjects found lung and corneal injury, with some ef of Nelson, Ege, Ross, Woodman and Silver- fect on heart muscle. Smyth (1937-55) ! man (1943) found an objectionably strong found four hours at 4000 to 8000 ppm kills 1 odor at 200 ppm and eye, nose and throat some rats, and 16,000 ppm kills all. Respira irritation at 400 ppm. Henderson and Hag tory tract irritation is prominent. The liquid gard (1943, p. 222) conclude 10,000 to is extremely injurious to the cornea. 20,000 ppm is dangerous for short ex The most important effect of ethyl amine posures. It is mildly narcotic but does not inhalation is respiratory tract irritation, produce systemic effects. Smyth (1937-55) with lung edema the maximum injury. The found rats inhaling 8000 ppm for four hours 25 ppm threshold limit can be interpreted survive, but 16,000 ppm kills. from results of repeated animal inhalation. The most important effect of ethyl acetate It appears low enough to prevent injury. inhalation is narcosis. The 400 ppm thresh Ethyl benzene. Yant, Schrenk, Waite and old limit can be interpreted by human sen Patty (1930) found only slight irritation in sory data add results of single inhalations guinea pigs breathing 1000 ppm for eight by animals. It apparently is low enough to hours. Fatalities from higher levels showed prevent definite narcosis. lung edema. Humans found 1000 ppm was Ethyl acrylate. Pozzani, Weil and Car initially irritating to the eyes and 2000 ppm penter (1949) found 30 inhalations of 300 caused throat irritation, constriction in the ppm injured lungs, liver and kidneys of chest and slight intoxication. Smyth (1937- rats and rabbits, while 70 ppm did not in 55) found rats not killed by four hours at : jure rats. They found that 8 ppm is readily 2000 ppm, while 8000 ppm is fatal. There 56 detectable by odor, and that the odor of 50 is general agreement that it does not exert ppm is objectionable. Treon, Sigmon, Wright the hematopoetic effects of benzene. and Kitzmiller (1949) obtained closely The most important effect of ethyl ben similar results. zene inhalation is narcosis, with irritation % The most important effect of ethyl acryl of the entire respiratory tract contributing 1 ate inhalation is respiratory tract irritation. to injury. The 200 ppm threshold limit can % The 25 ppm tentative threshold limit can be be interpreted from results of single animal i interpreted from repeated animal inhala inhalations and limited human sensory re tion results and limited human sensory data. sponse. It is low enough to prevent injury. i It appears low enough to prevent injury. Ethyl bromide. Waite and Yant (1928) Ethyl alcohol. Henderson and Haggard found lung edema a prominent effect of (1943, p. 219) consider its vapors anesthetic guinea pig inhalation. Sayers, Yant, Thomas but not toxic. Only under exceptional cir and Berger (1929) found several hours in cumstances can inhalation cause slight in halation of 1700 ppm by animals was with toxication. They estimate 1064 ppm for out effect. Henderson and Haggard (1943, p. eight hours is not sufficient to produce the 207) note that vapors are not narcotic. earliest stage of intoxication in man. Cook The most important effect of ethyl bro (1945) stated that industrial exposure at mide inhalation is respiratory tract irrita 'a 1000 ppm has led only to a few complaints of tion. The 200 ppm threshold limit can be in eye irritation. Patty (1948-9, p. 851) con terpreted from the results of single animal cludes 6000 to 9000 ppm is initially intoler inhalations. It is probably low enough to pre ably irritating, but that acclimatization fol- vent injury. 158 Ethyl chloride. Sayers, Yant, Thomas and Berger (1929) found with animals that 150.000 to 300,000 ppm is rapidly fatal, death being due to anesthesia, that 40,000 ppm does not kill in 270 minutes, 20,000 ppm causes only moderate unsteadiness, and 10.000 ppm is without effect. The most important effect of ethyl chlor ide inhalation is narcosis. The 1000 ppm threshold limit can be interpreted from the results of single animal inhalations. It is low enough to prevent significant narcosis. Ethylene chlorhydrin. Dierker and Brown (1944) reported one fatality with estimated exposure of 305 ppm for two hours. Animal experiment produced kidney pathology from 365 ppm for two hours. Goldblatt (1944) and Goldblatt and Chiesman (1944) report 11 cases, two of them fatal. Nervous system, cardiovascular system and kidneys were affected, and no warning irritation was apparent. They found one hour at 1120 ppm killed animals, with evidence of poten tial chronic effect. They conclude no concen tration is safe for daily exposure. Smyth and Carpenter (1945) point out very rapid skin penetration of the liquid, the absence of warning skin irritation and the failure of rubber gloves to protect. The most important effect of ethylene chlorhydrin inhalation is acute poisoning, centering in the kidney. The 5 ppm thresh old limit can be interpreted from the re sults of single animal inhalations. It appears low enough to prevent injury. Ethylene diamine. Dernehl (1951) re lated industrial experience showing this is a sensitizer upon contact and inhalation. Pozzani and Carpenter (1954) exposed rats repeatedly to the vapors. All died within 20 days at 484 ppm, with loss of hair, injury to the kidney and lesser effects on liver and lung. There was no effect except loss of hair at 132 ppm, and none whatever at 59 ppm. Very brief human exposures found 100 ppm inoffensive, tingling of skin and nose at 200 ppm and intolerable sensory response at 400 ppm. Smyth (1937-55) found eight hours at 2000 ppm did not kill rats while 4000 ppm was fatal. Death was due chiefly to kidney injury, with some injury to lung. The liquid irritates the skin and severely in jures the cornea. The most important effects of ethylene diamine inhalation are respiratory tract June, l(1m ocl 1 irritation, kidney damage and sensitii w tion. The 10 ppm threshold limit can be il terpreted from results of repeated aning inhalation and human sensory data. It 111 low enough to prevent irritation and it 8 jury, but probably not to eliminate n 2 sponse by persons already sensitized. Ethylene dibromide. Rowe, Spencer, Mj Collister, Hollingsworth and Adams (195: CO found four species of animals tolerated rj "cOr peated inhalation of 25 ppm, but not CO ppm. Major injury was in lung and liv with kidney and central nervous syst CO CL less prominent. The liquid penetrates tl *C skin. It is painful in the eye, but causj only transient injury. The odor of a co| centration dangerous to life is definig ^ and sickening. 1 The most important effects of ethylel dibromide inhalation are respiratory tra| ; irritation and liver injury. The 25 pp| o threshold limit can be interpreted from tl results of repeated animal inhalations, is probably low enough to prevent injur] Ethylene dichloride. Spencer, Ro Adams, McCollister and Irish (1951) stud; ing repeated inhalation by animals, fou: no effect from 100 ppm. Single dangero inhalations irritate the lung and depress t! central nervous system, while dangerous r< peated inhalations injure liver and kidne; They feel chronic intoxication is unlike! because tolerated repeated inhalations a: close to concentrations tolerated once. Co: centrations sufficient to cause marked na: cbsis are irritating to the upper respirato: Eg tract. Adams, Spencer, Rowe, McCollist' -V5 32 and Irish (1952) simultaneously studying CL carbon tetrachloride, found it at least fo' 8 tfi times as toxic as ethylene dichloride. Elki: C3 (1950, p. 137) found complaints of nausej CoD> from industrial exposures to 100 to 150 pp: 03 Patty (1948-9, p. 805) finds little odor CL CO 100 ppm, slight eye and nose irritation 1000 ppm. The most important effect of ethylen] dichloride inhalation is chronic poisonin; centering in the liver. The 100 ppm thres! CD oolfdrleimpeiat tceadn abneiminatel ripnrheateladtifornosmatnhde hreusmualt:] X<DI response. It is low enough to prevent injur; Ethylene imine. Silver and McGrat! (1948) and Carpenter, Smyth and Shaffer (1948) studied single inhalations in animals. The LC50 for mice in a 10-minute exposure Industrial Hygiene Quarterly 159 is 2236 ppm, 500 ppm for one hour is fatal of 400 ppm is 0.018 gm./l., causing no in to rats and guinea pigs, 25 ppm kills some in toxication, while 2000 ppm will give a blood eight hours, and 10 ppm kills none in eight level of 0.09 gm./L, corresponding to insta hours. Symptoms and death are delayed, bility in some persons. They state 35,000 "O due to kidney tubular injury, with lesser ppm anesthetizes in 30 minutes, and a higher a> o lung and liver injury. Humans, can barely concentration kills by respiratory paralysis. a> smell 2 ppm, while 100 ppm begins to irri Experience in human anesthesia shows that 7 o Q_ tate eyes and nose.. The liquid penetrates the pneumonitis may follow ether anesthesia, CD skin, produces severe skin and corneal but other injuries are unlikely. Nelson, Ege, -a J >> burns, and sensitizes the skin. Ross, Woodman and Silverman (1943) I E The most important effect of ethylene found nasal irritation at 200 ppm with unaeimine inhalation is acute poisoning, center climated subjects, somewhat greater'at 300 1%4 "ccOa ing in the kidney, with lung injury of lesser ppm. importance. The 5 ppm threshold limit can The most important effect of ethyl ether be interpreted from results of single animal inhalation is narcosis. The 400 ppm thresh inhalation studies and limited human sen old limit can be- interpreted from human sory data. It is apparently low enough to physiological and sensory data. It is low u -Q prevent poisoning and upper respiratory enough to prevent definite narcosis. & CD tract irritation. Ethyl formate. Flury and Zernik (1931) i- *o Ethylene oxide. Waite, Patty and Yant reported 330 ppm causes in man slight eye T3 (1930) in single animal inhalations found irritation and rapidly increasing nasal irri - CD s no symptoms from eight hours at 250 ppm. tation, while 10,000 ppm is anesthetic and JV O Greater concentrations caused eye and nose fatal. Fairhall (1949, p. 344) notes its ef k-. CuO- irritation, narcosis, bronchial and lung irri fects are irritation and narcosis, and that p JCt tation. Sensory response is only moderate at there is no chronic toxicity. Smyth (1937- _i low concentrations, but eye and nose irrita 55) found rats survive four hours inhala $St 15 cr tion are intolerable at high concentrations. tion of 4000 ppm but die from 8000 ppm. no f. -CO Sexton and Henson (1950) have called at The most important effect of ethyl for 't-,1 tention to spectacular human skin injuries mate inhalation is narcosis. The 100 ppm & CD with sensitization, which arise from contact threshold limit can be interpreted from O with the liquid and its aqueous solutions. scanty human sensory data and single fc p I Smyth (1937-55) found rats survive four animal inhalations. It appears to be low 1 o hours at 4000 ppm but are killed by 8000 enough to prevent definite narcosis and irri CD ppm. Hollingsworth, Rowe, Oyen, McCollis- tation. ~n o > ter and Spencer (1956) in animals repeated Ethyl mercaptan. Sayers, Fieldner, Yant, 1 i -- ly inhaling 204 ppm found lung irritation Leith and Pearce (1930) report the odor F and some fatalities, with injury to liver, detectable at one part per billion and dis o fc kidney, adrenal and testes. Rats and mice agreeable at one part per fifteen million. 1 a 1 CD were not affected at 49. ppm, other species They quote that its effects are like those of 8 Qo_ tolerated 113 ppm. Jacobson, Hackley and hydrogen sulfide, and by analogy with butyl y- O Feinsilver (1956) with dogs, rats and mice mercaptan they conclude more than 733 CO f- CO found some fatalities from repeated inhala ppm is required to kill in 30 minutes. Flury 5 i <D tion of 400 ppm, but 100 ppm had little af fect. The most important effect of ethylene and Zernik (1931) quote 3000 ppm as harm less to dogs and 10,000 ppm causing hema tologic and blood cell changes. i T> CO Cl 1 CO r- oxide inhalation is respiratory tract irrita The most important effect of ethyl mer c -2k tion leading to lung injury, while injury captan is eye and respiratory tract irrita j?3 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. 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) 'S JD & CO fc <1> sz. 1 h- ft Ethyl ether. Henderson and Haggard found eight-hour inhalation of 550 ppm the (1943, p. 195) estimate the maximum least fatal exposure for guinea pigs. Death human blood concentration from inhalation is due to' lung injury, with some kidney i I f ! I'-'1 I! 1. Siii !I5!8 ai K 160 June, 1956 damage. Humans found 85 ppm detectable by odor,' 250 ppm slightly irritating to eye and nose, and 3000 ppm extremely irritat ing. Rowe, Spencer and Bass (1948) found some kidney damage in rats repeatedly in haling 125 ppm. Pozzani and Carpenter (1951) exposed rodents repeatedly. Some died within 30 days at 440 ppm with injury to lung, liver and kidney, but 88 ppm did not injure. The data suggest that repeated inhalation at a given concentration is no more injurious than a single inhalation. The most important effect of ethyl silicate inhalation is lung injury, with non-progres sive kidney damage less important. The 100 ppm threshold limit can be interpreted from results of repeated animal inhalations and limited human sensory data. It can be smelled, it is not irritating, and is low enough to prevent lung or kidney injury. Ferbam. Hodge, Maynard, Downs, Blanchet and Jones (1952) reported the oral LD50 for rats to be over 17 gm./kg., with guinea pigs and rabbits more sensitive. Rats tolerated 0.01% in their diet for 30 days without effect while 0.5% was required to kill. Dogs were not injured by 25 mg./kg./ day for six months. The mechanism of in jury is not clear. The most important effect of inhalation of Ferbam appears to be the upper respira tory tract irritation of a substantially inert dust. The 15 mg./cu.m. tentative threshold limit is in accord with this. Ferro vanadium dust. Roshchin (1952) exposed rats two months to 1000 to 2000 mg./cu.m. and found no effect beyond some lung irritation. The author suggests a threshold limit of 1 mg./cu.m. Vanadium compounds irritate the upper respii'atory tract, but Sjoberg (1951) found no chronic general poisoning in workers exposed to vanadium pentoxide dust, symptoms being confined to respiratory difficulties and skin allergies. The most important effect of inhalation of ferrovanadium dust is respiratory tract irritation. The 1 mg./cu.m. threshold lim it can be interpreted from limited repeated animal inhalations and examination of ex posed workmen. It appears low enough to prevent injury. Fluoride dust. Roholm (1937) found fluor osis of human bone, but no other effects, af ter several years work in 2 to 3 ppm fluorine, equivalent to 1.5 to 2.3 mg./cu.m. soluble fluoride dust. Higher concentrations provide respiratory tract irritation and effects on liver and kidney. Largent (1952) found stor age in the body occurs when as little as three milligrams per day fluoride in the form of sodium fluoride is ingested, rough ly equivalent to inhalation of 0.3 mg./cu.m. soluble fluoride dust. The most important effect of inhalation of fluoride dust is chronic poisoning, cen tering in the bones, with respiratory tract irritation at high concentrations. The 2.5 mg./cu.m. threshold limit can be interpreted from results of examination of exposed workmen and experimental studies of human fluoride retention. It is not low enough to prevent fluoride storage with resulting ef fects on the bones. Fluorine. Machle and Evans (1940) ex amined workmen exposed intermittently to as much as 10 ppm and found no clinical evi dence of damage, but there was some ac cumulation in bones and teeth. Stokinger (1949) found few toxic effects in dogs re peatedly exposed to 0.5 ppm. Greater con centrations injured lung and kidney. This is apparently below the level which leads to bone abnormalities (Roholm 1937). The most important effect of inhalation of fluorine gas is respiratory tract irrita tion, with lung edema the maximum effect. Chronic effect on bone metabolism is also important. The 0.1 ppm threshold limit can be interpreted from results of animal in halation and studies on exposed workmen. It is low enough to prevent injury. Fluoroacetates. Dieke and Richter (1946) report the median lethal oral dose to be 0.22 mg./kg. for wild rats. The substance is rapidly fatal through intervention in the tricarboxylic acid metabolic cycle. The most important effect of fluoroacetate inhalation is acute toxicity. The 0.1 mg./cu.m. tentative threshold limit .can be interpreted from acute oral toxicity data for rats. It corresponds to a maximum human intake of one milligram per day, apparently well below a dangerous amount. Fluorotrichlorornethane. Nuckolls (1933) found in animals no more than occasional tremors and retching during two hours at 22,000 to 25,00Q ppm. No toxic effects are to be expected from this physiologically inert material. Year: Notes : 1956 Industrial Hygiene Quarterly The most important effect of flucrotri- hours inhalation of 700 ppm killed 25% of chloromethane inhalation is a minor degree a group of rats. of narcosis, and asphyxia from very high The most important effect of furfuryl al concentrations. The 1000 ppm threshold lim cohol inhalation is narcosis. The 50 ppm ten it can be interpreted from the results of tative threshold limit can be interpreted single animal inhalations. It appears to be from results of single animal inhalations. It far blow a possibly injurious level. appears low enough to prevent injury. CO Formaldehyde. Henderson and Haggard Gasoline. Sayers, Fieldner, Yant and (1943, p. 128) conclude its action is chiefly Thomas (1927) reported human dizziness TD . irritation of all tissues contacted, particular at 700 ppm, and Drinker, Yaglou and War ly the respiratory tract, and that systemic ren (1943) found human respiratory tract effects are not important. Skin sensitization irritation and headache begin at 1000 ppm. to solutions is frequent and respiratory Elkins (1950, p. 99) found industrially no tract sensitization to the gas is not unlikely. sensory response to 660 to 800 ppm benzine, Elkins (1950, p. 231) reports irritation in and dizziness at 2000 to 3000 ppm. He con _Q workmen inhaling 5 to 6 ppm, and eye irri cludes chronic effects do not occur when con CCD tation of unhardened persons at lower levels. centrations are too low to cause narcosis, o Smyth (1937-55) found rats survive eight but Hayhurst (1936) reported chronic <D hours inhalation of 125 ppm but are killed poisoning consisting of central nervous sys by 250 ppm. The liquid causes severe corneal tem effects and blood cell changes after injury. many years of exposure. This article does CO The rnost important effect of formalde not seem to be generally accepted. Henderson x5 hyde inhalation is irritation, first evident in and Haggard (1943, p. 192) consider nausea the eyes, then in the upper respiratory tract, and incoordination the significant effects, bronchi and even lung. The 5 ppm threshold With anesthetic death at 20,000 to 30,000 CO Z limit can be interpreted from uncontrolled ppm. Aromatic hydrocarbons in gasoline G3 human sensory data. It is sufficiently low from cracking operations may much reduce to prevent lung injury. safety. Furfural. Fairhall (1949, p. 354) quotes The most important effect of gasoline in animal experiments in which inhalation of halation is narcosis. The threshold limit of _OG3 280 ppm resulted only in slight mucous mem 500 ppm can be interpreted from human sen "oo brane irritation, while 2800 ppm caused sory data, both experimental and indus 03 acute irritation, prostration and lung edema. trially observed. It is low enough to prevent ACGIH (1954b) quotesKorenmanandR.es- definite narcosis. g nik, {Arch. Hyg., 104:344, 1931) to the Heptane. Patty and Yant (1929) reported effect that 2 to 14 ppm causes human head slight human dizziness from 1000 ppm. The ~Go3 ache and eye irritation. Severe corneal in paraffin hydrocarbons are anesthetic agents 'OOo_ jury is to be expected from the fluid, and and irritate mucous membrane, but they do <F> analogy with other aldehydes suggests that not cause systemic toxicity. CO skin and respiratory sensitization may be The most important effect of heptane in 0033 found. halation is narcosis. The 500 ppm thresh CO Q_ The most important effect of furfural in old limit can be interpreted from limited halation seems to be irritation, first evident human sensory data and by analogy with the C in the eyes, then in the -upper respiratory better studied gasoline. It is probably low o tract, bronchi and even lung. The 5 ppm ten enough to prevent definite narcosis. tative threshold limit can be interpreted HETP (hexaethyltetraphosphate). This CD CO from uncontrolled human sensory data. It material is substantially identical in quanti is sufficiently low to prevent lung injury. tative and qualitative effect with the cholin 03 Furfuryl alcohol. Fine and Wills (1950) esterase inhibitor TEPP. Apparently no found that death from furfuryl alcohol is data specifically upon inhalation have been due to the respiratory paralysis of anes published. thesia, and that short of death, its effects are The most Important effect of HETP is reversible. ACGIH (1955b) quotes Chemi reduction of blood cholinesterase. The 0.1 cal Corps Medical Laboratories Research mg./cu.m. tentative threshold limit can be Report No. 139, 1942, to the effect that eight interpreted by analogy with parthion. It 162 June, 1956 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. It 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; and 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 gas'es 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. J- a u v , x /, .no 1956 '1956 Industrial Hygiene Quarterly 163 6 . a The most important effect of hydrogen The most important effect of hydrogen & ccyhaemniidceal inashpahlaytxioian. Tisheac1u0tepppmoistohnriensgh,olda esedleemniadeatishigahcutceonpcoenistornaitniogn, , laanrgdelcyhrlounnigc ti$p oUQ_. limit can be interpreted from results of poisoning centering in the liver. The 0.05 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 Hydrogen fluoride. Stokinger (1949) enough to prevent injury found 30 ppm is highly toxic to animals, Hydrogen sulfide. Henderson and Hag causing pulmonary damage, kidney and gard (1943, p. 140, 243) state hydrogen 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 finds 0.026 rtig./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 O smarts. The liquid causes severe slowly heal injury among viscose workers during 10 3 2 ing skin injuries, and destroys the cornea. years, with control at about 20 ppm. Elkins & -Q All soluble fluorides interfere with calcium (1950, p. 232) found eye irritation in indus I "J 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. fluoride inhalation is respiratory tract ir- The most important effect of hydrogen W <D 1 ritation, with lung edema the maximum ef- sulfide inhalation is acute toxicity, marked $ K o > feet. 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 can be interpreted from results of repeated from the results of examination of exposed o<D animal inhalation and human sensory data. workmen. It is low enough to prevent in It is low enough to prevent injury jury. Hydrogen peroxide, 90%. Oberst, Corn- Hydroquinone. Sterner, Oglesby and stock and Hackley (1954) found rats sur Anderson (1947) reported on several years o vive eight hours at 250 to 300 ppm without industrial experience with men exposed to "O CD A 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 COOL 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 tated. The liquid is extremely destructive of cornea and conjunctiva was apparent, due Qo>> CD to skin and cornea. to local action on the exposed tissue. Loss of CL The most important effect of hydrogen vision has followed pigmentation in some peroxide aerosol inhalation is respiratory cases, according to Oglesby (1956). It is C o tract irritation, with- lung edema the maxi uncertain whether the vapor or the dust was mum effect. The 1 ppm threshold limit can responsible. Hydroquinone dust ranged a) be interpreted from results of repeated from 0.12 to 13 mg./cu.m. After comparing "cb animal inhalation. It is low enough to pre exposure with concentration, the authors CD vent injury. conclude hydroquinone dust should be kept Hydrogen selenide. Dudley and Miller below 2 to 3 mg./cu.m. (1941) found animals are killed in eight The most important effect of hydro 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 eases due to less exposed workmen. It appears low enough to than 0.2 ppm, with liver injury. prevent effect. it \ if 1i I I- 1p li! a J 16U June, 1956 Iodine. Henderson 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 d,ust 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 of 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. Isophorone. 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 eight hours injured the lung but did not anesthetize or kill. Silverman, Schulte and First (1946) found odor objectionable at 10 ppm and eye, nose and throat irritation at 25 ppm with unacclimated subjects. The 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. Isopropylamine. Smyth, 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 Smyth (1937-55) found for butyl amine. ACGIH (1955b) cite unpublished industrial experience that levels above 5 ppm tend to be irritating. The most important effect of isopropyla- mine inhalation is respiratory tract irrita tion, with lung edema the maximum injury. The 5 ppm threshold limit can be inter preted from analogy with ethyl amines. It is probably low enough to prevent injury. Lead. Russell, Jones, Bloomfield, Britten and Thompson (1933) after a survey of a storage battery 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 inhalation 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 mild cases. Lead arsenate. Fairhall and Miller (1941) and Fairhall, Miller and Weaver (1943) found the arsenate in lead arsenate de creases lead absorption or increases lead excretion, and reduces lead storage. The most important effect of inhalation of lead arsenate is chronic arsenic poison ing. The 0.15 mg./cu.m. tentative threshold limit can be interpreted from the results of biochemical studies on animals. It ap pears to have been selected by analogy with the limit for lead, while analogy with ar senic would yield a much higher figure. Lindane. A.M.A. (1951) in a summary, states lindane in large doses acts as a cen tral nervous system stimulant, leading to hyperirritability, convulsions and death. Animals exposed several months to saturated vapors were not affected, but 10,000 mg./cu.m. dust for one hour killed one of two mice. ACGIH (1954b) quotes an unpub lished 1951 report by J. F. Treon et al. A 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. 24 hours a day did not result in pathology in rats. The most important effect of lindane in halation is chronic poisoning centering in the liver. The 0.5 mg./cu.m. threshold limit 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 experi- 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. industrial Hygiene Quarterly 165 mental fuifte 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. 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 mtal mg./cu.m. threshold limit can be interpreted fume fevr. 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 Malaihon. 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 te group p'f 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 $ 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 the basal brain ganglia, leading to disability (1942) found no effect upon animals from 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 toms in men exposed to 30 mg./cu.m. or eight hours, 500 killed some and 2,500 killed less and they concluded concentrations can all, and in one hour 13,000 ppm (saturation) 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 Sr! 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 eases found below 0.1 mg./cu.m. Chronic symptoms consist of psychic disturbances, timidity, tremors, pallor, salivation and tenderness of the human sensory response. It is low enough to prevent definite narcosis. Methoxychlor. Haag, Finnegan, Larson, Riese and Dreyfuss (1950) found methoxy- sfo ibA a J `gjftVTy'.1 V.tlV' 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 ii ! fl Rj H Ili I 166 June, 1956 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 (193755) 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 31 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. Afters improvements reduced exposure to about. 20 ppm, injuries ceased. Fairhall ( 1949, : p. 376) notes it is a respiratory tract irri-i| tant, a liver injurant, and a central nervous^ system poison leading to delirium, convul-i sions and even mania. It is rapidly metab|| olized and eliminated. Year: Notes: 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. Copyright law. Industrial Hygiene Quarterly 167 The most important effect of methyl species has no effect, but 500 ppm causes ? bromide inhalation is chronic poisoning, central nervous system effects. Complete re- centering in the central nervous system and covery from injury is slow. Fairhall (1949, liver. The 20 ppm threshold limit can be in- p. 379) concludes it acts chiefly by narco- terpreted from the results of repeated ani- sis, but liver, kidney and bone marrow in- mal inhalations and examination of exposed juries are found. workmen. It appears to be rather precisely The most important effect of methyl set at the maximum concentration humans chloride inhalation is central nervous sys- tolerate without effect. tern injury, with less important chronic . Methyl CELLOSOLVE (methoxyethanol). poisoning. The 100 ppm threshold limit can Donley (1936) and Parsons and Parsons be interpreted from the results of repeated (1938) reported toxic encephalopathy with animal inhalations. It is low enough to pre- granuiopenic anemia from industrial ex- vent injury. posure to a mixed solvent containing methyl Methyl chloroform. Adams, Spencer, CELLOSOLVE. Greenberg, Mayers, Goldwater, Rowe and Irish (1950) found in repeated Burke and Moskowitz (1938) estimated con- exposures that 650 ppm retarded guinea pig centrations in the establishment some time growth, and 3000 ppm caused slight liver after the cases developed, and found 25 ppm effects. Three other species were less sensi- of the glycol ether. Werner, Mitchell, Miller tive. Rats were mildly narcosed in one hour and von Oettingen (1943, a,b) in experi- at 5000 ppm. The level tolerated in repeated ments on dogs did not confirm the degree of inhalation was close to that tolerated in a toxicity suggested by the human cases. The single exposure. They concluded it is close blood cell effects were obtained from re- to methylene chloride in toxicity and less peated inhalation of 500 ppm, but no en- toxic than trichloroethylene, cephalopathy was found. Fairhall (1949, p. The most important effect of methyl : 336) concludes the vapors are somewhat ir- chloroform inhalation is narcosis. The 500 ritating, and produce narcosis and kidney ppm threshold limit can be interpreted from changes. Smyth (1937-55) found rats sur- the results of repeated animal inhalation, vive four hours at 2000 ppm, but die from It is low enough to prevent definite narcosis, eight hours. / Methyl cyclohexane. Treon, Crutchfield The most important effect of methyl and Kitzmiller (1943) found no effect on cellosolve inhalation is chronic poisoning, rabbits exposed 300 hours to 1162 ppm, centering in the brain and red blood cells, slight kidney and liver changes from 90 The 25 ppm threshold limit can be inter- hours at 2886 ppm and fractional mortality, ? preted from atmospheric analyses of doubt- eye and entire respiratory tract irritation ful validity after human industrial injuries, and narcosis at 7308 ppm. Patty (1948-9, and from the results of repeated animal in- p. 770) concludes the odor is weak at 500- halations. It appears lower than is required 800 ppm. 1 to prevent injuries. The most important effect of methyl- Methyl CELLOSOLVE acetate (2-meth- cyclohexane inhalation is narcosis, with non- oxyethyl acetate.) This ester hydrolyzes in progressive organic changes. The 500 ppm , the body to methyl CELLOSOLVE and acetic threshold limit can be interpreted from re acid, and its vapors are somewhat more irri- suits of repeated animal inhalation. It is tating than those of the former. low enough to prevent definite narcosis. The most important effect of methyl Methyl cyclohexanol. Treon, Crutchfield cellosolve acetate inhalation is. chronic and Kitzmiller (1943) found 300 hours at poisoning due to hydrolysis to methyl CEL- 121 ppm causes slight liver and kidney losolve. The 25. ppm threshold limit can be changes in rabbits, and 300 hours at 503 . interpreted from analogy with methyl cel- ppm causes eye irritation with some nar- losolve. It is low enough to prevent injury, cosis, but does not kill. Patty (1948-9, p. Methyl chloride. Sayers, Yant, Thomas 881) concludes that odor and irritation are 168 June, 1956 nent. The 100 ppm thi'eshold 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 cycloheodanone. 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. Schrenk, 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. molybdic 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 histopathological 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 lyBeing composed chiefly of toluene and xylene, the most important effect of coal tar naphtha inhalation, when free from ben zene, is narcosis with irritation of the res piratory tract less important. The 200 ppm Year: ...Notes: 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. Copyright law! Industrial Hygiene Quarterly threshold limit can be interpreted by an lungs in high concentration. It also erodes , alogy with those of toluene and xylene. It is the teeth. He suggests a threshold limit of low enough to prevent injury. 10 ppm. Naphtha (petroleum). A mixture of par The most important effect of inhalation affin hydrocarbons of somewhat higher of nitric acid is upper respiratory tract molecular weight than gasoline. The discus irritation. The 10 ppm tentative threshold sion under gasoline applies. limit appears to be based upon undocu Nickel carbonyl. Fairhall (1949, p. 114) mented analogy with other acid gases. quotes Armit to the effect that this produces p-Nitroaniline. Fairhall (1949, p. 402) a deposit of finely divided nickel in the res concludes p-nitroaniline is more toxic than piratory tract, leading to irritation and aniline, causing headache, nausea and cyano lung edema. Hueper (1950) summarizes the sis. This is based on British industrial ex inferences that it produces cancer, origi perience. nating in the nasal sinuses. Kincaid, Strong The most important effect of p-nitro and Sunderman (1953) found 30 minutes at aniline inhalation is acute poisoning. The 1 10 ppm killed mice, 270 ppm killed cats, and ppm threshold limit is apparently an esti they suggest toxicity may be related to body mate based on analogy with aniline. It ap weight, with man surviving high concentra pears low enough to prevent injury. tions. They -found lung edema and severe Nitrobenzene. Henderson and Haggard liver injury; but conclude it is not cumula (1943, p. 227) note that injury by skin ab tive and that a tolerance develops. Sunder sorption is more frequent than by inhala man and Kincaid (1954) report on 36 tion. The compound is an anesthetic, pro human cases, two fatal. The fatalities were ducing methemoglobin and reducing blood delayed, due to lung edema. pressure. Acute toxicity is marked by head The immediate effect of nickel carbonyl ache, narcosis, cyanosis, and death from vapor inhalation is lung irritation and de respiratory paralysis. Chronic absorption layed edema. Cancer originating in the results in anemia, cyanosis, muscular weak nasal sinuses has been reported from long ness, bladder irritation. The maximum con time exposure. The 0.001 ppm threshold lim centration which gives no serious dis it is apparently an approximation of zero, turbance in one hour is 200 ppm, and 40 to designed to prevent cancer. It is low enough 80 ppm cause symptoms in several hours. to prevent all possibility of immediate ef The most important effect of nitrobenzene fect, but there are no data to judge its ef inhalation is chronic poisoning, marked by fectiveness in preventing cancer. reduced blood pressure and cyanosis. The 1 Nicotine. Wilson and De Eds (1936) fed ppm threshold limit can be interpreted from diets containing nicotine to growing rats results of single animal inhalation. It ap for a 60-day period. Rats did not survive pears low enough to prevent injury. on 0.05% nicotine. Rats were not affected Nitroethane. Machle, Scott and Treon by 0.006% nicotine, equivalent to 4 mg./kg. (1940) found guinea pigs inhaling 500 ppm body weight per day. A greater concentra for a total of 140 hours are not injured, but tion reduced growth, due largely but not en some die from 1000 ppm. Eye and nose ir tirely to reduced food intake. Lehman ritation, narcosis, central nervous system (1949) estimates the fatal human dose to be irritation and lung edema are produced. 60 milligrams. Toxic symptoms are evident before narco The most important effect of nicotine in sis. halation is ill-defined chronic poisoning. The most important effect of nitroethane The 0.5 mg./cu.m. tentative threshold limit inhalation is acute poisoning accompanied can be interpreted from repeated feeding by narcosis and irritation. The 100 ppm studies on rats. It corresponds to a maxi threshold limit can be interpreted from re mum human intake of five milligrams per sults of animal inhalation. It appears low day, apparently well below an injurious enough to prevent injury. level. Nitrogen dioxide. Henderson and Hag Nitric acid. Fairhall (1949, p. 81) con gard (1943, p. 137) state that 62 ppm cludes it is an upper respiratory tract ir causes immediate throat irritation, 300 ritant, injuring the bronchi and even the ppm coughing and 100 to 150 ppm is danger-  h& I III i p ip h |j ife 1 " . 51Jf - y i iiifc in ii m i: 3BWB1 170 June, 1956 ous for 30 to 60 minutes. Fairhall (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-Nitro'prop` ane. 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. Yon Oettingen (1941) re viewed the literature and could find no clear distinction between the toxicities of nitrotoluene and nitrobenzene. The most important effect of nitrotoluene inhalation is chronic poisoning, marked by reduced blood pressure and cyanosis. The 5 ppm threshold limit appears to be an esti mate without quantitative support. It is doubtful whether the difference between nitrobenzene and nitrotoluene is sufficient to justify the difference in threshold limits. Octane. No useful published data spe cifically upon octane were found, but analogy with heptane and gasoline is close. The most important effect of octane in halation is narcosis. The 500 ppm threshold limit can be interpreted only by analogy with pentane and gasoline. It is probably low enough to prevent definite narcosis. Ozone. Fairhall (1949, p. 122) quotes McDonnell's incompletely reported work to the effect that daily inhalation of 0.1 ppm killed guinea pigs with pneumonia, higher concentrations leading to lung edema. He : notes respiratory tract irritation with fatal pneumonitis or lung edema, but no systemic ; poisoning. He quotes a statement that 0.015 ' ppm can be smelled, and any higher concen tration is irritating. The most important effect of ozone in-g halation is respiratory tract irritation, with:| lung edema the maximum effect. The 0.11 ppm threshold limit can be interpreted from| results of limited repeated animal inhala-| tions and human sensory data. It appearsj low enough to prevent injury. Paratkin. The earliest effect of this! cholinesterase inhibitor is a reduction oil fi T ITTI f I f ll iT f fllT ! f 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 LC50 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. It is low enough to prevent injury. Pentachlorophenol. 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 pentachlor 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 (193755) 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, McCollister, 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. ACGIII (1954b) cites Flury and Zernik (1931) to the effect that after 15 minutes inhalation of Si "O Ift o I$ <o 1 &- H CD s8i J CD -co CO CD Q- $& CD < ; <C1> *o $ i CD 2 |I! o >% CD j5 mcH P 1 7c5 o it 1 To S .CgD IO 'M co 131j J"o5D Mo STy-i -*C--D &E o 1 i CD Q. | Oo ?5 CCOD 11jtc; 5 CD 172 ' June, 1956 45 ppm, mice and cats die within two days. The most important effect of phosgene in The most important effect of perchlor- halation is respiratory tract irritation with omethyl mercaptan inhalation is eye and delayed lung edema probable. The 1 ppm respiratory tract irritation. The 0.1 ppm threshold limit can be interpreted from re tentative threshold limit can be interpreted sults of human studies. It is low enough to on the basis of limited single inhalations by prevent injury. animals. It appears to be low enough to pre Phosphine. Henderson and Haggard vent injury. (1943, p. 243) report 1000 to 2000 ppm fatal Phenol. Deichmann, Kitzmiller and in 30 minutes, 100 to 200 ppm the maximum Witherup (1944) found guinea pigs are for one hour without serious disturbance. severely injured by 20 days inhalation of 25 Fairhall (1949, p. 127) quotes Mller to the to 50 ppm, rabbits suffer lung injury in 63 effect that animals die from two four-hour days, but rats are not affected. They con inhalations of 20 ppm, or 7 of 10 ppm, but clude human injury from repeated inhala two months at 5 ppm did not injure. Acute tion is marked by digestive disturbance, poisoning is rapidly fatal with convulsions, nervous disorders, skin eruption and liver paralysis and coma. Chronic poisoning .o <D and kidney damage. The liquid penetrates marked by anemia and nervous disturb' co. tsheveesrkeisnkitno aanddacnogrnereoaul sinejuxtreyn. tP, aatntdy c(1a9u4se8s- tahnecrees. isPoantltyy a (f1a9in48t-9o,dorp.at5716p)pmc.oncludes (U 9, p. 1034) reports that 5 ppm can be recog The most important effect of phosphine nized by odor. Smyth (1937-55) found rats inhalation is chronic poisoning. The 0.05 survive eight hours inhalation of vapors ppm threshold limit can be interpreted from CO _Q saturated at room temperature. the results of repeated animal inhalation Although phenol vapors are odorous and It appears low enough to prevent injury irritating, their major effect is chronic sys Phosphorous (yellow). Fairhall (1949, p temic poisoning. The 5 ppm threshold limit 131) summarizes the literature. The effects can be interpreted from results of repeated of chronic poisoning are upon bone meta CD SZ inhalations by animals. It appears to be low bolism. They may be noticed first as painful enough to prevent chronic toxic effects. swollen gums, or as spontaneous fractures Phenylhydrazine. Von Oettingen (1941, p. 158) concludes death from a large dose is of the long bones. They develop into peri ostitis and necrosis of the lower jaw, with _o03 due to respiratory paralysis. There is hemo secondary infection. In single exposures one o lytic anemia, formation of methemoglobin, milligram per kilogram is usually fatal. Cr--D injury to the liver and heart muscle. Skin The most important effect of phosphorous penetration is rapid and dermal sensitiza inhalation is chronic poisoning, centering in 2 tion takes place. The fatal oral dose for the bones. The 0.1 mg./cu.m. threshold limil "oO rats is of the order of 0.04 gm./kg. cannot be interpreted in quantitative terms The most important effect of phenyl Phosphorous pentachloride. Hendersor ooo_ hydrazine inhalation is chronic poisoning, and Haggard (1943, p. 134) conclude thii co 5 centering in the red blood cells. The 5 material is an irritant to'nose, throat am CD ppm threshold limit can be interpreted from lungs through hydrolysis to hydrogen chlor 05 CO analogy with aniline. Quantitative data are ide. Skin burns from the solid are likely Q . not available to judge the effectiveness of Mice are killed in 10 minutes by 120 ppm. the limit. The most important effect of phosphoroui CO Phosgene. Fieldner, Katz and Kinne pentachloride inhalation is respiratory tracj (1921) cite the Chemical Warfare Service irritation, with lung edema possible. Th as authority for a 1 ppm allowable concen 1 mg./cu.m. threshold limit is apparentl; tration for prolonged exposure, based on an estimate without quantitative support. I human tests. Henderson and Haggard appears low enough to prevent injury. (1943, p. 137) consider phosgene a lung Phosphorous pentasulfide. Fairhall (1941 injurant producing delayed edema. They p. 131) quotes Barillet to the effect tha say 3.1 ppm is immediately irritating to phosphorous pentasulfide is somewhat les throat, 4 ppm to eyes, 4.9 ppm causes cough ing, 5.6 ppm detectable by odor and 50 ppm rapidly fatal. Year: Notes : iy 56 1956 The m a te ria ls this pagewas'copied from the collection of the National Library of Medicine by a third party and may be protected by U .S. Copyright law! Industrial Hygiene Quarterly irritation. The 1 mg./cu.m. threshold limit concludes it is similar to ethyl alcohol with is apparently an estimate without quantita no delayed effects, but twice as toxic. Smyth I tive support. It appears low enough to pre (1937-55) found rats survive four hours at vent injury. 12,000 ppm, but half are killed in eight Phosphorous trichloride. Henderson and hours. Haggard (1943, p. 134) consider it an irri The most important effect of isopropyl tant and lung injurant. They cite 600 ppm alcohol inhalation is narcosis. The 400 ppm as rapidly fatal, and 2 to 4 ppm as the maxi threshold limit can be interpreted from mum for 30 to 60 minutes without serious human sensory data and analogy with ethyl disturbance. Cook (194.5) quotes Butjog as alcohol. It is low enough to prevent signifi finding 0.7 ppm causes only slight irritation cant narcosis, but some irritation will result. in animals. Propylene dichloride. Heppel, Neal, High- The most important effect of phosphorous man and Porterfield (1946) found repeated trichloride inhalation is respiratory tract ir inhalation of 1000 ppm by animalsfkilled the ritation, with lung edema the maximum ef first animal in seven days with severe liver fect. The 0.5 ppm threshold limit can be effects. They conclude it is more toxic than interpreted from limited animal inhalation ethylene dichloride but less so than carbon data. It appears low enough to prevent in tetrachloride. jury. The most important effect of propylene Picric acid. Fairhall (1949, p. 423) de dichloride inhalation is chronic poisoning scribes systemic poisoning as gastro centering in the liver. The 75 ppm thresh enteritis, hemorrhagic nephritis and hepa old limit can be interpreted from the results titis. Sunderman, Weidman and Batson of repeated animal inhalations. It appears (1945) studied workers handling ammoni low enough to prevent injury. I um picrate in atmospheres from 0.0088 to Propylene imine. Carpenter, Smyth and 0.1942 mg./cu.m. They found little res Shaffer (1948) found rats and guinea pigs I7* piratory tract irritation, no systemic ef killed by four hours at 500 ppm, and not by : $ fects but considerable dermatitis. 30 minutes. This is about V8th the acute The most important effect of picric acid toxicity of ethylene imine in simultaneous fl inhalation is chronic poisoning. The 0.1 work. mg./cu.m. threshold limit can be interpreted The most important effect of propylene from observations on exposed workmen. It imine vapor inhalation is acute poisoning, is low enough to prevent systemic injury centering in the kidney, with lung injury of but not respiratory tract irritation and sen lesser importance. The 25 ppm threshold s sitization. limit can be interpreted from results of f} Propyl acetate. Fairhall (1949, p. 426) scanty single animal inhalation studies and concludes it is more irritating than ethyl analogy with ethylene imine. It is apparent acetate, more narcotic than ethyl or methyl ly low enough to prevent injury. acetates,: but less lethal. Some respiratory Propyl ether (isopropyl ether). Machle, tract irritation and liver injury are found. Scott and Treon (1939) found incomplete Death is due to anesthesia, but even deep anesthesia in animals at 30,000 ppm, light narcosis may leave no after effects. Smyth narcosis at 10,000 ppm, and no effect in re (1937-55) found four hours inhalation of peated exposures at 1000 ppm. They con 32,000 ppm kills four of six rats. clude it is 1.5 to 2 times as active as ethyl The most important effect of propyl ace ether and less so than gasoline. tate inhalation is narcosis. The 200 ppm The most important effect of isopropyl threshold limit can be interpreted by an ether inhalation is narcosis. The 500 ppm alogy with ethyl acetate, not by data. It threshold limit can be interpreted from re appears to be low enough to prevent definite sults of repeated animal inhalation. In com narcosis. parison with data on ethyl ether it does Propyl alcohol, iso. Nelson, Ege, Ross, not seeih low enough to prevent definite Woodman,and Silverman (1943) found 400 narcosis. ppm causes mild irritation of eye, nose and Pyrethrum. There is little published on throat, and 800 ppm is no more severe in un the toxicity of pyrethrum but many years acclimated subjects, Fairhall (1949, p. 429) of wide use as an insecticide indicates a low , s. - am-.1:'M-t il-'-p' j t l I I I m June, 1956 degree of hazard, except for some slight skin sensitizing property. Carpenter, Weil, Pozzani and Smyth (1950) found the rat oral LD50 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. Rats 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) reported 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 ujpper respira tory tract. The 5 mg./cu.m. tentative thresh old limit can be interpreted by analogy with pyrethrum. It appears 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-1 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 toj ulceration. Patty (1949, p. 561) on the basis! of experience with caustic mists from 1 to| 40 mg./cu.m., concludes a concentration off 2 mg./cu.m. is noticeably but not excessivelyj irritating. The most important effect of sodium hy| droxide mist or dust inhalation is uppef respiratory tract irritation, leading to ull| ceration. The 2 mg./cu.m. threshold limit 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. Year : Notes : 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. Copyright law. Industrial Hygiene Quarterly can be interpreted from observations upon tating the eye and causing coughing, 8 to 12 exposed workmen. It appears low enough to ppm irritating the throat, and 3 to 5 ppm prevent injury. detectable by odor. Elkins (1950, p. 81) Stibine. Webster (1946) finds stibine a finds slight human irritation at 2 ppm and - lung injurant and powerful hemolytic agent, objectionable irritation at 10 to 30 ppm. injuring liver and kidney as well. Some The most important effect of sulfur diox animals die after one hour inhalation of 40 ide inhalation is respiratory tract irrita ppm. Its action resembles, that of the better tion, with lung edema or respiratory arrest understood arsine. the maximum effect. The 10 ppm threshold The most important effect of stibine in limit can be interpreted from human sensory halation is acute poisoning, largely lung data and examination of exposed work edema. The 0.1 ppm threshold limit can be men. It is low enough to prevent injury. interpreted by analogy with arsine. It ap Sidfur hexafluoride. Lester and Green pears low enough to prevent injury. berg (1950) found that it is a physiological Stoddard Solvent. Nelson, Ege, Ross, ly inert gas, rats inhaling 800,000 ppm in Woodman and Silverman (1943) found 400 oxygen for 16 to 24 hours were not affected. ppm produced no marked effects on unac The most important effect of sulfur hexa climated subjects. This solvent is toxi- fluoride inhalation is asphyxia from very cologieally identical with gasoline and re high concentrations. The 1000 ppm thresh marks under that material apply. old limit can be interpreted from the re Strychnine. McNally (1937) reports that sults of prolonged animal inhalations. It is a human death has resulted from swallow so far below any possible injurious level ing 30 milligrams. It is a convulsive poison. that it represents good engineering control, The most important effect of strychnine rather than a hazard limit. inhalation is acute poisoning. The 0.15 Sulfuric acid. Fairhall (1949, p. 83) mg./cu.m, tentative threshold limit can be considers it an upper respiratory tract ir interpreted from the known human fatal ritant with lung injury possible. It is cor dose. It corresponds to a maximum intake of rosive to the skin and eyes, and erodes the 1.5 milligrams in a working day, apparently teeth. Amdur, Silverman and Drinker low enough to prevent injury. (1952) with normal human subjects, found Styrene monomer. Spencer, Irish, Adams changes in respiration at a concentration as and Rowe (1942) found immediate animal low as 0.35 mg./cu.m., and pronounced de death was anesthetic, delayed death was due crease in minute volume at 5 mg./cu.m. to lung injury. Blood cells were not affected. Elkins (1950, p. 82) considers concentra Repeated inhalation of 650 ppm had no tions above 1 ppm (4 mg./cu.m.) are irri effect on animals. Humans found 1300 ppm tating. Sterner (1943) considered 5 mg./ extremely irritating to eye and nose, and cu.m, as tolerable. 400 ppm had an objectionable odor but little The most important effect of sulfuric acid irritation. Carpenter, Shaffer, Weil and inhalation is respiratory tract irritation, Smyth (1944) found irritation and early with lung edema possible. The 1 mg./cu.m. narcosis in humans at 800 ppm. threshold limit can be interpreted from U The most important effect of styrene human sensory and physiological data. It vapor inhalation is narcosis. The threshold is low enough to prevent injury. limit of 200 ppm can be interpreted from Sulfur monochloride. Henderson and results of repeated animal inhalations and Haggard (1943, p. 130) consider it an upper human sensory response. It is low enough to respiratory tract irritant through release prevent definite narcosis. of hydrochloric a,cid, but rarely a lung in Sulfur dioxide. Kehoe, Machle, Kitzmiller jurant. Mice die from one minute inhala and LeBlane (1932) studied many workmen tion of 150 ppm, cats from 15 minutes at 48 continuously exposed to sulfur dioxide and ppm. Fairhall (1949, p. 160) concludes found only upper respiratory tract chronic chronic systemic effects do not occur. Elkins irritation. Henderson and Haggard (1943, (1950, p. 81) found 2 to 9 ppm mildly irri p. 131) conclude it is an irritant without tating to humans. systemic effect. They give 400 to 500 ppm The most important effect of sulfur mono- as dangerous in a short time, 20 ppm irri chloride vapor inhalation is respiratory 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. 176 June, 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 be 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 pentafluoride 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 componds manifests little tendency to chronic effect. Yigliani 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 0.05 mg./cu.m. threshold limit c | interpreted only by analogy with parafl It appeal's low enough to prevent injug p-Tertiary butyl toluene. Hine ej (1954) in repeated animal inhalaj found narcosis, respiratory tract irritl liver and kidney changes, blood cell cm like those from benzene, and degenerl in spinal cord and brain. Rats are kill one hour by about 900 ppm, and sligli dence of effect was fpund in animal peatedly inhaling 25 ppm. Humans del ppm by odor, 80 ppm was unpleasant ritating and some giddiness was not| 160 ppm. I The most important effect of p-te| butyl toluene inhalation appears |( chronic toxicity, combining effect on! cells, central nervous system, liver anl ney. The 10 ppm threshold limit can | terpreted from results of repeated a| inhalations and human sensory data, jj pears to be low enough to prevent sign| toxic effect. | 1,1,2,2-Tetrachloroethane. Fairhall | p. 440) concludes this is the most chlorinated hydrocarbon, nine times a i as carbon tetrachloride. It is a narcotl produces liver damage, polyneuritic white blood cell changes. Elkins (19| 139) refers to an unpublished report! 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 poifj centering in the liver. The 5 ppm thr limit can be interpreted from industrf perience. It is uncertain whether it enough to prevent some degree of ir Tetrahydrofuran. Lehman and (1943, p. 269) report it a narcotic! tating mucous membrane and injuria! kidneys. In animals 3400 ppm fo r | hours daily for 20 days caused some n| membrane irritation and light naf with albuminuria, lung and kidney and lung irritation in one animal I ACGIH (1955b) quotes John A. Zappjj the effect that repeated inhalation ppm, then 400 ppm, slightly affect^ pulse pressure of dogs, but resulted __ histopat.hology. Hoffmann and Oett< (1954) in rabbits and cats found somena cosis and mucosal irritation after six hou w ater Year; v 1956 no. i _4 1956 . `J a-*- 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! Industrial Hygiene Quarterly 177 inhalation of 3400 ppm. There was no liver or kidney injury from inhalation of even 60,000 ppm. The most important effect of tetrahydrofuran inhalation is narcosis, with less im portant injury to liver and kidneys. The 200 ppm tentative threshold limit can be in terpreted from results of repeated animal inhalation studies. It appears low enough to prevent injury. Tetranitromethane. Sievers, Rushing, Gay and Monaco (1947) found in cats ir ritation of eyes, upper respiratory tract, lung edema, methemoglobinuria and injury to liver and kidney. Concentrations of 3.3 to 25.2 ppm were severely injurious, while 0.1 to 0.4 ppm caused only mild irritation in two exposures. Horn (1954) found in re peated inhalation of 6.35 ppm that some rats died from pneumonia. The effect on dogs was transient anorexia. The most important effect of tetrani tromethane inhalation is poisoning, accom panied by irritation. The 1 ppm threshold limit can be interpreted from results of re peated animal inhalation. It is low enough to prevent injury, but not to prevent all irri tation. Tetryl. Bergman (1952) summarizes ten years' experience in an ordnance plant with more than 1000 exposed workers and concen trations kept below 1.5 mg./cu.m. by con stant diligence. Skin sensitization was fre quent but no systemic poisoning was found. Hardy and Maloof (1950) report two fatal and eight non-fatal cases with liver injury the most prominent effect. There was upper respiratory tract irritation, very frequent skin sensitization and a few asthmatic sensi tizations. Concentrations were as high as 17.7 mg./cu.m. The most important effect of tetryl inhala tion is chronic poisoning like that of trini trotoluene, but the most frequent effect is sensitization. The 1.5 mg./cu.m. threshold limit can be interpreted from experience with exposed workmen. It is low enough to prevent injury but not sensitizations. Thallium. Fairhall (1949) reviewing the literature, concludes that thallium has a chronic toxicity greater than that of lead. Useful quantitative data on inhalation ap pear to be lacking. The most important effect of thallium in halation is chronic poisoning. The 0.15 mg./cu.m. tentative threshold limit appears to be based on a quantitative analogy with lead. Its propriety cannot be judged. Thiram. Meagre data have been found on this substance. Smyth (1937-55) found the rat oral LD50 to be 1.30 gm./kg. Rats sur vived four hours inhalation of a dense dust cloud, unmeasured but estimated to be at least 500 mg./cu.m., with no effect but some brief retardation of growth. ` The most important effect of inhalation of thiram appears to be an ill-defined chron ic toxicity. The 5 mg./cu.m. tentative thresh old limit cannot be interpreted from pub lished data found by the writer, but it ap pears to be reasonable. Titanium dioxide. Fairhall (1949, p. 180) concludes titanium dioxide is chemically inert and is not toxic. Lenzi (1936) found a pneumoconiosis in guinea pig lungs after prolonged inhalation of high concen trations. Inhaled titanium dioxide acts as an inert dust, with only a slight tendency to produce pneumoconiosis. The 15 mg./cu.m. threshold limit is an arbitrary figure uniformly ap plied to inert nuisance dusts. It appears low enough to prevent injury. Toluene. Von Oettingen, Neal and Dona hue (1942) in repeated exposure of animals, found no blood cell changes or other toxic effects at 800 ppm. Humans inhaling 200 ppm for an eight-hour period found the earliest signs of impaired coordination and lengthened reaction time, while the effects were more prominent and more prompt at 600 to 800 ppm. Fairhall (1949, p. 447) con cludes it is a narcotic with irritating proper ties, but manifests no chronic effects. Elkins (1950, p. 108) cites Greenburg's examina tion of over 100 workers in atmospheres of 100 to 1100 ppm without marked symptoms. Smyth (1937-55) found rats survive four hours at 4000 ppm, but die from 16,000 ppm. Commercial toluene may contain significant amounts of benzene and may be more toxic than these data indicate. The most important effect of toluene in halation is narcosis. The 200 ppm threshold limit can be interpreted from results of re peated animal inhalation, studies of human narcosis and examination of exposed work men. It appears to be low, enough to prevent all effects except the earliest signs of nar cosis. in a I i 8m! I:'fSi Ui aJ | i! si P r Ki rs iS3jiigd?J $ "i |l !i 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. ACGIH (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 trifluoro monobromomethane 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 Oettingen 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 un acclimated 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 i of soluble uranium dusts is chronic poisoning, centering in the kidney. The 0.05 j from the collection of the National Library of Medicine by a third party and may be protected by U.S. Copyright law. 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. Copyright law. Industrial Hygiene Quarterly mg./cu.m. threshold limit can be interpreted from the results of repeated animal inhala tions. It is low enough to prevent injury. Uranium (insoluble). Hodge, Stokinger, Neuman, Bale and Brandt (1949) show that on inhalation, the toxicological action. of uranium on the kidney is much more a haz ard than the alpha radiation hazard of the uranium stored in the bones. In repeated animal experiments, they find 0.20 to 0.25 mg./cu.m. allows reasonable margin of safe ty over the level producing kidney injury. The most important effect of inhalation of insoluble uranium dusts is chronic poison ing centering in the kidney. The 0.25 mg./cu.m. threshold limit cn be interpreted from the results of repeated animal inhala tions. It is low enough to prevent injury. Vanadium. Roshchin (1952) exposed rats to vanadium pentoxide fume of 0.3 to 0.5 mg./cu.m, for two hours every other day for three months, and to dust at 1 to 3 mg./cu.m. for one-hour daily for four months. They lost some weight and had bloody nasal secre tion. Some evidence of pulmonary edema was seen from the fume. Acutely 8 mg./cu.m. of the dust was injurious in one hour and 70 to 80 mg./cu.m. was lethal. The author suggests a threshold limit of 0.1 mg./cu.m. for fume and 0.5 mg./cu.m. for dust. The most important effect of inhalation of vanadium dusts is bronchial and lung injury. The threshold limits of 0.5 mg./cu.m. for dust and 0.1 mg./cu.m. for fume can be interpreted from the results of repeated animal inhalations. They appear low enough to prevent injury. Vinyl chloride. Patty, Yant and Waite (1930) found no serious disturbance in guinea pigs inhaling 5000 ppm for several hours. Higher concentrations produced only narcosis. In humans, 50,000 ppm is noticed as a slight odor and nose irritation, and dizziness is evident. The most important effect of vinyl chlor ide inhalation is narcosis. The 500 ppm threshold limit can be interpreted from the results of single animal inhalations and human response. It appears low enough to prevent significant narcosis. Warfarin: Saunders, Heisey, Goldstone and Bay (1955) found injection of 0.5 mg./'kg. for five days killed most of a small group of rats, while a single injection of 100 mg./kg. caused only 30% mortality. One human fatality arose from the consumption of a total of 750 mg. over a 15-day period. The most important effect of warfarin in halation is chronic poisoning centering in the blood coagulation mechanism. The 0.5 mg./cu.m. tentative threshold limit cannot be interpreted in quantitative terms. It in volves a maximum daily absorption of 5 mg., about one-tenth the amount which was fatal to one man. Xylene. Nelson, Ege, Ross, Woodman and Silverman (1943) found 200 ppm definitely irritating to eye, nose and throat. Fairhall (1949, p. 468) concludes the effects are like those of toluene, narcosis without damage to red blood cells. The most important effect of xylene in halation is narcosis. The 200 ppm thresh old limit can be interpreted from human sensory data. It is irritating to eye, nose and throat. There are no data to show whether or not significant narcosis occurs at this concentration, but since narcotic ac tivity is greater than that of toluene it is to be anticipated. Zinc oxide fume. Drinker, Thomson and Finn (1927b) reported that experimental fume fever from zinc oxide in man results from excessive inhalation, but does not oc cur below 15 mg./cu.m. In industry it was found that 14 mg./cu.m. caused no reaction after eight hours, and in the laboratory 45 mg./cu.m. was without effect in 20 minutes. This condition is a .transient fever with chills, muscular pains, nausea and vomitting. An immunity is apparently built up. The most important effect of zinc oxide fume inhalation is transient metal fume fever. The 15 mg./cu.m. threshold limit can be interpreted from the results of extensive human experiment and experience in indus try. It is low enough to prevent injury. Zirconium. ACGIH (1955b) quotes un published data from the University of Rochester A.E.C. Project. Four species of animals inhaled the following, all expressed in terms of contained zirconium: Zirconi um oxide, 1.5 micron dust, 75 mg./cu.m. for 30 days, 11 mg./cu.m. for 60 days, 3.5 mg./cu.m. for one year; zirconium tetra chloride, 0.6 micron dust, 6 mg./cu.m, for 60 days, 3.5 mg./cu.m.' for a year. Only the higher concentration of tetrachloride had any effect, presumably due to liberated hy drochloric acid. 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 B altim ore City H ealth D epartm ent (1943), Division of In d ustrial H ygiene: Baltim ore H ealth N ew s, 20: Sep tem ber, 1943. Ba r n e s, J . M. (1953): Toxic hazards of certain pesti cides to m an. W orld H ealth O rganization, Geneva. M onograph 16. B a r t h e le m y, H . L. (1939) : Ten years experience w ith results of repeated animal inhalations. It in d u strial hygiene in connection w ith th e m an u fa c tu re appears low enough to prevent injury. of viscose rayon. J. Ind. H yg. & Tox., 21:141-151. Df B er g m a n , B. B. (1952) : T etryl toxicity. A rch. Ind. H yg. i & Occup. Med., 5:10-20. D Bibliography B loomfield, J . 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(1952) : Mono- If! a A ero M ed ical A sso ciatio n (1953), C om m ittee on A via tion Toxicology: A viation Toxicology, B lakiston, New Y ork. chloromonobromomethane; inhalation toxicity, patholo gy an d sym ptom atology in ra ts and mice. Chemical C orps M edical L a b o ra to ries, R ese arch R e p o rt N o. 113. A h l m a r k , A . (1 9 4 8 ): P o iso n in g by m e th y l m e rc u ry com C o m st o c k , C. C., a n d Ob e r s t , F . W . (1 9 5 3 ): T h e m edian pounds. B rit. J . In d . Med., 5:117-119. detectable concentration of diborane, pentaborane and A lva r ez, W . C., and H y m a n , S . (1953) : A bsence of toxic decaborane by odor fo r m an. Chem ical C orps Medical m anifestations in w orkers exposed to chlordane. Arch. L aboratories, R esearch R ep o rt N o. 206. Ind. H yg. & Occup. Med., 8:480-483. C o m s t o c k , C. C.; L a w s o n , L . H.,* G r e e n e , E . A ., a n d AMA (1951) Council on Pharm acy and Chem istry: Toxic Oberst, F . W . (1954): Inhalation toxicity of hy effects of technical benzene hexachloride and its p rin drazine vapor. Arch. Ind. H yg. & Occup. M ed., 10:476- cipal isom ers. J.A .M .A ., 147:571-574. 490. A m dur, M. O.j S il v e r m a n , L ., a n d Dr in k e r , P . (1952): C ook, W . A . (1945) : M axim um allow able concentrations Inhalation of sulfuric acid m ist by hum an subjects. of in d u strial atm ospheric contam inants. In d . Med., A rch . Ind. H yg. & O ccup. Med., 6:305-313. 14:936-946. A s h e , W . F .; L a r g e n t , E . J .; D u t r a , F . R .; H ubbard , D. C u lv er , D.; C a p l a n , P ., a n d B a t c h e lo r , G. S. (1956): M., a n d B l a c k s t o n e , M. (1 9 5 3 ): B ehavior o f m ercu ry Studies of hum an exposure during aerosol application of in the anim al organism following inhalation. Arch. Ind. m alathion and chlorthion. A M A A rch. Ind. Health, H yg. & Occup. Med., 7:19-43. 13:37-50. Tear : Notes xy56 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. Copyright law. Industrial Hygiene Quarterly D e ic h m a n n , W . B.; K it z m ill e r , K . V ., an d W ith er u p , F l in n , R. H .; N e a l , P. A., and F u lto n , W . B. (1941): S. (1944): Phenol studies V II. Chronic phenol poison In d u stria l m anganese poisoning. J . Ind. H yg . fo Tox., ing, w ith special reference to th e effects upon ex 23:374-387. perim ental anim als of th e inhalation of phenol vapor. F lu r y, F., and Z er n ik , F . (1931) : Schdliche Gase und A m . J. Clin. P ath., 14:273-277. Dam pfe. J. Springer, Berlin. De r n e h l , C. U .; N a u , C. A., an d S w e e t s, H . H . (1945): G oldblatt, M. W . (1944) : Toxic effects of ethylene A nim al studies on the toxicity of inhaled antim ony tr i chlorhydrin. II--E x perim ental. B rit. J. Ind. Med., oxide, J . In d . H yg. & Tax., 27:256-262. 1:213-223. De r n e h l , C.*U, (1951): C linical experiences w ith expo Goldblatt, M. W ., and C h ie s m a n , W . E . (1944) : Toxic sures to ethylene am ines. Ind. Med. & Surg., 20:541-546. effects of ethylene chlorhydrin. I-- Clinical. B rit. J. Die k e , S. H ., and R ich ter , C. P . (1946): C om parative Ind. Med., 1:207-213. assays of rodenticides on w ild N orw ay ra ts . U .S . Public G r a y , E . L eB., M a c N a m e e , J . K., and G oldberg, S. B. H ealth Service, Pub. H ealth R p ts., 61:672-679. (1952) : T oxicity o f NO2 vapors a t very low levels. D ier k er , H ., and B ro w n , P . G. (1944): Study of a fa ta l A rc h . In d . H y g . & O ccup. M ed., 6 :20-21. case of ethylene chlorhydrin poisoning. J . Ind. H yg. & . T o x., 26:277-279. D o n ley, D. E. (1936) : Toxic encephalopathy an d volatile solvents in industry. J . Ind. H yg. & Tox., 18:571-577. D r in k e r , C. K . (1 9 3 9 ): F u r th e r o b serv atio n s on th e po s sible system ic toxicity of certain of th e chlorinated hy drocarbons. J . Ind. H yg. & Tox., 21:155-159. Dr in k e r , P .; T h o m so n , R. M., a n d F in n , J . L . (1927) : M etal fum e fever. III. T he effects of inhaling m agnesi um oxide fum e. J. Ind. H yg., 9:187-192. D r in k e r , P .; T h o m s o n , R . M ., a n d F i n n , J . L . (1927b}s: Green berg, L. A., and L est er , D. (1950): T he toxicity of sulfurpentafluoride. Arch. Ind. H yg. & Occup. Med2:350-352. G r een b er g , L.; M a y e r s , M. R .; G o ld w ater , L. J .; B u r k e , W. J., and M o sko w itz, S. (1938): H ealth hazards in th e m anufacture of fused collars. I-- E xposure to ethyl ene glycol m onomethyl ether. J. Ind. H yg. & Tox., 20:134-147. H aag, H . B.,* F innegan, J . k . ; L arson, P . S.; R iese, W ., and Dreyfuss, M. L. (1950): C om parative chronic toxicities fo r warm-blooded anim als, of 2,2-bis-(p-chloro- M etal fum e fever. IV . 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P u b lic H e alth Service, P ub. 9:61-74. H ealth R p ts., 51:392-399. Reprints Available 1 R epein ts of the preceding Cummings Memorial Lecture may be obtained from george d. clayton, Executive Secretary, AMERICAN INDUSTRIAL HYGIENE ASSOCIATION, 14125 Prvost, De- troit 2Y, Michigan, at $1.50 each. The price of this issue of the AIHA QUARTERLY is $2.00.