Document NEjaMp7m7J1Bw48mQyeDDveQ8

V very ory ;h room 1 the-iob ations id with s Control or effectiveness, AN with ACToy as much as 97%. i not do. It cleanses ly against skin conaints, acids, printing its. It is non- irritatjrmal skin qualities. vent lost man hours, on claims, give your I CLEAN. all wash rooms and nomize and to speed X ( Improved Communication \ --HYQ1ENIC STANDARDS FOR DAILY INHALATION- I . ^cctwte | HENRY FIELD SMYTH. JR.. Ph.D. Mellon Institute and Union Carbide and Carbon Corporation Pittsburgh, Pennsylvania i Experience convinces us that we humans are unique in the universe. Because of Roger Bacon, whom today we call a scientist, could live a full life investigating the se t our ability to communicate, crets of nature, feeling no need 1 we may be well on the way toward emerging into a new and finding no opportunity to communicate his discoveries level of biological existence. and his conclusions to a living Each individual may eventu soul. He could bury his ally share completely' all past achievements in code, making and present experiences of the them difficult for posterity to species. Each may act in con unravel. We do not have such cert with his fellows toward people and such situations to common ideals and goals, still day. Each one of us benefits retaining his own individuali ty. Real progress in this di Henry F. Smylh, Jr. from the current division of labor, of experience, and of rection has been made during the past ten knowledge. Each one of ns is a unique thousand years through developments of specialist, depending upon a multitude of recording, duplicating and retrieval tech other unique specialists for the achievement niques. Despite brief back-sliding, there has of our aims, for our very existence. If noth furthermore been real spiritual progress, ing else motivates us, simple self-interest and an increase in the proportion of men should dictate that each one of us ought to of good will. The next ten thousand years make public all that he has learned, in order should bring substantial achievements in that his fellow specialists may use it to help communication upon higher levels, perhaps us all. even through inarticulate contact of mind with mind. There are hints that what some Communication have called the world mind may come into A year ago Sterner (1955) expressed the being before the present human species situation in more concrete terms. We evolves physically into whatever new species comprise persons separately trained in high its body is tending toward. ly specialized fields, led after training to However, until the world mind develops, cooperate in the common aim of providing we are forced to depend upon more prosaic means by which technological developments means of communication. Not so many gen in occupation may be utilized in a manner erations ago, a natural philosopher like compatible with complete health. He said, "We must provide a fluid and effective tO Presented at the Seventeenth Annual Meeting of the American Industrial Hyuiene Association, Philadelphia, means of communication between the chem- & April 25. 1956. ist, the engineer, the phvsicist, the toxicolo- tjfr a o to V 130 June, 1956 gist, the physician, and the other special The relatively new specialty of industrial ists brought into industrial hygiene. There toxicology has already contributed to the must result from this interchange of ideas equally new profession of industrial hy not only an appreciation of each team mem giene by means of communication. The toxi ber's contribution, but an ability actually to cologists are doing an acceptable job for bridge the gap between the disciplines, to those people who recognize their need for synthesize, from the offerings of each of the toxicological information and opinion. The fields, the solutions to the ever more com job could be done better, but it is at least ac plicated problems. Each member specialist ceptable. Success is by no means as great must not only contribute the information he in helping those people who do not recognize is most qualified to give, but also must en their need for help. Once more communica courage a sympathetic, intelligent, and mu tion cannot succeed unless the audience de tual understanding." sires to receive communication. In this matter of mutual understanding, we are very much like the inhabitants of Acceptable Concentrations Looking Glass Land. You remember that 'T'HE MOST important communication with- the White Queen told Alice, "Now here, you A in industrial hygiene, and between bur see, it takes all the running you can do, to profession and others, may be the collection keep in the same place. If you want to get of judgments upon acceptable concentra somewhere else, you must run at least twice tions of contaminants in working atmos as fast as that." With the entry of new pheres. During what may be called the age people into our profession and the recogni of chaos, every experienced industrial hy tion of new constituent specialties such as gienist had a few values uniquely his own, health physics and atmospheric pollution drawn from his own experience. For less control, each with .a tendency to keep to it familiar substances, he borrowed more or. self, are we running fast enough even to less judiciously from the values cherished stay in the same place? We all feel there by his professional colleagues. Some degree are too many conferences and too many com of unanimity was brought about when the mittees to leave us time to do our daily United States Public Health Service values, work. On the other hand, if we are to do our based on its long-time collective experience work as well as it can be done, we must be in in industrial hygiene, were published in a constant communication with related spe manual (USPHS 1943). Further unanimity cialists, because each one of us fully knows followed publication of the values collected only one facet of his own problems. and extended by Cook (1945). In 1947 the r\ Communication is not a simple process. It American Conference of Governmental In i'i.v\ requires an informed speaker or writer who dustrial Hygienists published its first list can express himself at the level of compre in the Industrial Hygiene Newsletter hension of his audience. It requires an audi (ACGIH 1947). In the next two years ence which wishes to receive communica (ACGIH 1948, ACGIH 1949) revised lists tion. It must be carried on with words, were privately circulated to the members of those abstract symbols for reality, each of the Association. Then (ACGIH 1950) pub I! which has a different meaning to each in lication took place in a scientific journal, ; dividual, shaded by his entire past experi and each year thereafter a revised list of ence. Only a newly coined word is free from threshold limit values has appeared in the e i ambiguity, and it remains new for only a scientific literature, and has been general i : brief interval. Most important of all, suc ly accepted. cessful communication requires what is to The contributions of Cook (1945) in uni day known as feed-back. By this, the speaker fying opinion, and in weighing threshold hears his audiences' impressions. He can limit values then- in use, judging new data correct and amplify his words until he and proposing a list of 129 values, are thinks his audience truly perceives his mean worthy of high regard. Among the 238 ing. A leisurely conversation can be effective values for substances other than mineral communication through feed-back; an arti dusts in the current list (ACGIH 1956) of cle in a journal is likely to be poor communi established and tentative threshold limit cation because feedback is inadequate. values are 54 of those which were first pro- Induatrial Hygiene Qva * posed in Cook's list, sonil tablished, others to be uaj verified by actual experiW Not since Cook has an summary of the data wilt for the selection of specifs The privately circulated " give some of these data 1954b, 1955b) cannot be publication, although they able to any person. Threshold limits are, a. to be the products of juq if true. Some few truly re nition and are appro-rime mum concentrations whir continuously and repeated to health. These may pcmeters for incorporation regulations. Many of the are well below coneentrat. jure health. They rcprerment as to concentration practice dictates, men m. subject themselves. The.-s. parameters for regulatin'operation, if possible, it maintain concentrations mark by reasonable vent/' tion. It is always best to i chemicals to the lowest j: Previous Suggestions for li r^URiNG the Ninth An; Industrial Health, the man of the Committee or. (1949). The report of th tee devoted considerable mg the development of th to suggesting ways in wh tion could be made more report, two development: along lines desired by tl annual table of the Thre mittee of the American < ernmental Industrial Hyy lished in the Archives of removing the earlier im legal status arising fron the Industrial Hygiene Division of Industrial H Health Service. In 1954, Threshold Limits of thal to supplement its table with a list of tentative m June, 1956 of. industrial ontributed to the of industrial hynication. The toxitcceptable job for ize their need for and opinion. The >ut it is at least ac10 means as great 10 do not recognize ; more communica53 the audience de cation. is mmunication with, and between our ay be the collection :eptable concentrain working atmosy be called the age iced industrial hy3 uniquely his own, xperience. For less borrowed more or le values cherished agues. Some degree jht about when the salth Service values, :ollective experience ! e published in a rther unanimity tne values collected (1945).In 1947 the >f Governmental Inblished its first list fygiene Newsletter he next two years 1949) revised lists d to the members of (ACGIH 1950) puba scientific journal, ter a revised list of has appeared in the d has been general- Cook (1945) in uniweighing threshold ;e, judging new data of 129 values, are rd. Among the 238 other than mineral st (ACGIH 1956) of tive threshold limit which were first pro- I j > .. f S ., 1 ., .j - Industrial Hygiene Quarterly 1SI posed in Cook's list, some ns definitely es tablished, others to be used cautiously until verified by actual experience. Not since Cook has anyone published a summary of the data which serve as bases for the selection of specific threshold limits. The privately circulated documents which give some of these data (ACGIH 1953b, 1954b, 1955b) cannot be considered to be publication, although they are freely avail able to any person. Threshold limits are, and must continue to be the products of judgment, important if true. Some few truly represent their defi nition and are approximations of the maxi mum concentrations which can be inhaled continuously and repeatedly without injury to health. These may possibly be fit para meters for incorporation into codes and regulations. Many of the threshold limits are well below concentrations which can in jure health. They represent current judg ment as to concentrations to which, good practice dictates, men may be expected to subject themselves. These do not seem fit parameters for regulations. In a particular operation, if possible, it is desirable to maintain concentrations below the bench mark by reasonable ventilation and precau tion. It is always best to reduce exposure to chemicals to the lowest practical level. Previous Suggestions for Improvement TOURING the Ninth Annual Congress on Industrial Health, the writer was chair man of the Committee on Chemical Agents (1949). The report of the 16-man commit tee devoted considerable attention to pi'aising the development of threshold limits, and to suggesting wavs in which their presenta tion could be made more useful. Since that report, two developments have taken place along lines desired by the Committee. The annual table of the Threshold Limits Com mittee of the American Conference of Gov ernmental Industrial Hygienists is now pub lished in the Archives of Industrial Health, removing the earlier implication of quasilegal status arising from its appearance in the Industrial Hygiene Newsletter of the Division of Industrial Hygiene, U.S. Public Health Service. In 1954, the Committee on Threshold Limits of that Association began to supplement its table of accepted values with a list of tentative values. Three other suggestions of the Commit tee on Chemical Agents deserve reiteration and discussion. It was urged that the bases for the selection of each value should be published, that the name should'be changed to hygienic standard, and that the particular concept of permissible human response be hind each value should be clearly indicated. There is such a multitude of factors in volved in the protection of health in our complex civilization that no one person or group of persons is competent to weigh them all with assurance. No oracular or ex cathedra statement on health deserves seri ous attention. Only when the facts upon which a decision are based are furnished for general scrutiny and evaluation can the de cision be considered even tentatively sound, and only after there has been adequate op portunity for criticism and modification can it be considered established. All toxicologi cal facts should be published, and all de cisions upon the facts should be accom panied by a summary of the reasoning under which they were derived, before any one should be expected to act upon the de cisions. Any publication of standards for maintenance of health ought to include ref erence to the underlying data. The second suggestion referred to the name by which the values are known. Sem antics is more than a sport for the idle. No matter how thoroughly a concept is origi nally presented, it always becomes known and referred to by a brief name, a catch word. Most persons who learn of the con cept hear the catch-word name, and do not go back to the original presentation. The meaning they attach to the name comes from their previous experience with the particular words. It may be, but is usually not, exactly what the originator of the idea intended. The more carefully one chooses the name he assigns to a concept, the more likely are others to interpret the concept as he himself does. The values now known as threshold limits are usually identified by phrases containing the words allowable or permissible. These two words have connotations of legal regu lations. Such connotations cannot properly attach to the judgment of a voluntary pro fessional association. The identifying phrases may also contain the words maxi mum, threshold and limit. These words all 20 > CO 05 oo 132 June, 1956 Industrial Hygiene Qi imply that below the concentration speci fied, human response is negligible, above the concentration it is dangerous. Actually, it is more than an implication. It is definitely stated. In the introduction to its 1956 list (ACGIH 1956) the Committee on Threshold Limits says, "Values are given . . . for the maximum average atmospheric concentra tions of contaminants to which workers may be exposed for an eight-hour working day the degree of organoleptic response. The Committee's four concepts follow: a. Plus or minus: The maximal time- weighted average concentration which produces only minor injury, and that in a very small proportion of exposed work men. b. Safe: The maximal time-weighted average concentration which sound evi dence leads one to believe will cause no demonstrable illness or other symptom other hand, when it is? all discomfort, then aid tainly justified, provi<| injury to workmen anf probability of accident^ Tables of hygienic sf carry indications of t'f. magnitude of the effect? inhalation of greater ; only by a rather thorou: without injury to health." Careful study of of toxic effect in any workman during a able data that one can c the data which support the currently ac lifetime of industrial exposure. a particular substance cepted values suggests that no such de c. Bench mark: A concentration based at a greater concentra*. 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 CommiUee it self confusingly warns "Threshold limits . . . should not be regarded as fine lines be 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 6, representing the maximum which in a short time is not objectionable to 9 out of 10 of a group of persons not stances, it is quite j; standards, one an inoiTi. concentration which < ceeded under any press Administrative expet by a table of number' part of official regulati*' not be defended, they tween safe and dangerous concentrations." accustomed to inhalation of the substance. cations. However, it is ; (ACGIH 1956) Note well that these four concepts were fThe term maximum acceptable concentra judged to be those already used for the se fession of industrial h> latory responsibilities. ' tion being used in revisions of standards by lection of hygienic standards for daily in Ithe American Standards Association Z-37 halation. Ail four were judged consistent act through obtaining 1 with their judgments, Committee is objectionable only because it with the goals of industrial hygiene. by a greater degree of will be abbreviated M.A.C. Many will in terpret this abbreviation as maximum al Hygienic Standards for Daily Inhalation lation of standards. T that their recommend lowable concentration, and nothing will have 'T'he subject of hygienic standards for tbeen gained by the change from alloxcable to x daily inhalation should be re-examined, fensible, that they ai cisions having no rega acceptable. the concepts represented by the values competitive industrial I conclude that the names maximum al should be restated in more realistic toxi A hygienic standan lowable concentration and threshold limit cological terms, and more consistent and should specify two coj are misleading. They convey a wrong im more informative standards should be pre with a description of pression to those who are not already famili pared. Such a step will not undo any of the to be expected from iv ar with the concepts behind the values. The accomplishments of the profession of in concentration should I name suggested in 1949, hygienic standard, dustrial hygiene or of any organization. no injurious effect ca is not misleading. Standards of good prac Rather, it will supply informative standards workman, but it may i tice are familiar to all of us in many fields. to supplement the accumulation of naked it may cause a detccta Looking toward the future provision of a numbers now accepted, some of which have irritation. The second variety of hygienic standards, a series of not been critically re-examined for a decade. produce somewhat me values should be selected, to be known as It is certainly imperative that the inhala versibie and non-pros hygienic standards for daily inhalation. tion of substances during the working day these two concentrate The third suggestion is more far-reach shall not be allowed to result in any injury how strictly the atii ing. The Committee on Chemical Agents to the physical well-being of workmen. It is (1949) pointed out that there has been no furthermore imperative that inhalation i served, the steepness curve, the breadth o simple or uniform relation between the ef shall not increase the probability of acci injurious concentrati fects of a substance and the numerical value dents through the mental distress occa range in individual si chosen for tabulation. The Committee con sioned by objectionable eye, nose or throat men, such values can cluded that concentrations have been se irritation, transient though it may often be, not all, substances. lected on the basis of one of four concepts of nor through the impaired judgment and Adequate data for the level best suited to hygienic control of delayed reaction time of light narcosis. It standard consist of : inhalation, the choice having been governed is desirable that inhalation shall result in perience, or repeated by the nature of the toxic response and by no degree of discomfort whatsoever. On the of workmer^Oi ntmc m o o .'V o June, 1956 jsponse. The follow: maximal timentration which iry, and that in f exposed work- il time-weighted hich sound evir& will cause no other symptom irkman during a posure. icentration based unnecessary ex-a concentration one as low as is engineering con- ;entration lower ng the maximum not objectionable rp of persons not t of the substance, our concepts were dy used for the sedards for daily in- judged consistent rial hygiene. aily Inhalation epic standards for ie re-examined, a. by the values more realistic toxilore consistent and ards should be prenot undo any of the e profession of inf any organization. Normative standards umulation of naked some of which have amined for a decade, itive that the inhalaing the working day result in any injury ng of workmen. It is ve that inhalation probability of accilental distress occae eye, nose or throat ough it may often be, mired judgment and of light narcosis. It lation shall result in rt whatsoever. On the 4 Industrial Hygiene Quarterly 1SS 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 of 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 are 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 co. tration has been frequently estimated. Sterner (19S5) discussed this point in de tail. Experiments upon animals, verified by biochemical and physiological studies in humans, may demonstrate conclusively that a substance has an effect during one period of inhalation which does not progress dur ing oft-repeated inhalation. For such a sub stance, satisfactory data can be obtained from objective study and secretly recorded subjective effects of a group of humans in haling known concentrations for substan tially eight hours. Any lesser body of data should result in a hygienic standard being designated as tentative. Categories of Objectionable Action JUDGMENTS should be made to determine J which hygienic standards for daily in halation must be carefully observed, and which may be exceeded when it is im practical to observe them. These judgments will be most consistent if we first decide for each substance what objectionable action we are guarding against bj' 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 nt 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 1 >56 tables of pro posed accepted and tentative standards (ACGIH 195G). 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 .^..ncrease the average. * cP- JUL c=>\ ^t-_'-cJ YORK coRP* 'uT> Research tao '.<2 >' CO 4D oO o i 'V 1SU June, 1956 Industrial '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 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. f If: rational experimental baa concentration which will nj ceptible workman, or one t* ously sensitized uorkman t- trol of exposure to nlle must rely heavily upon inc 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 seems an appropriate level. The standard should refer to the concentration existing during any brief period, but it should be recognised that higher concentrations are justified when it is impractical to keep below After experience has allsuf workmen susceptible to, remaining resistant indivu tected by a hygienic stanf halation based upon irritf, some substances is narcosis, which becomes the standard. injury. Until it has been d anesthesia in its extreme stage. At a rather Fume fever. The most important effect a particular group inc]ud< low concentration they induce accidents by of some substances is a transient influenza impairing judgment and delaying reaction like condition known as fume fever. A workmen, no consideration lowing inhalation of an time. Familiar examples are ethyl aleohc', familiar example is zinc oxide fume. The which is avoidable. ethyl ether and gasoline. The lower stand lower standard for a fume fever producer ard for a narcotic substance should be a should be a concentration which will not I Interpretations of Accepted concentration which produces no detectable produce that distressing but not menacing 7\TO NEW VALUES for sta effect upon judgment and reaction time af condition in any workman, and it should ter eight houi-s inhalation. It should refer apply to an appreciable period, such as half gested at this time. T upon which the 238 values to the average concentration existing during an hour. No considerations of practicali posed list (AC-GIH 1956) a some appreciable period of time, the length ty can justify exceeding the standard for have been studied. Table 1 of which can be estimated from absorption fume fever producing substances. interpretation of these v and elimination data. No considerations of Eye pigmentation. The most important the information they con practicality can justify exceeding the stand effect of two substances, quinone and hy- the familiar numbers, whi ard for a narcotic substance. droquinone, appears to be a slowly develop neer and the chemist an ill Irritation. The most dangerous effect of ing pigmentation of the sclera, which understanding. It also pres some substances is irritation. Eye, nose and may reduce visual acuity, or even lead to of abbreviations of self-i throat are irritated at a low concentration, blindness. The lower standard for these some description of action: the bronchi at a higher concentration, and substances should be a concentration which biologically and medically fatal lung edema may be the result of inhal produces no pigmentation after years of of confidence. The tnble is < ing an extreme concentration. The alde exposure, and it should refer to the time- plex for great popularil hydes, halogens and acids are familiar ex weighted average concentration throughout every class of information amples. Highly odorous substances may also the day. For a few days at a time, conditions by those who must apply be considered in this category. The lower of practicality should justify exceeding the data relied upon for the in standard for an irritant substance should be standard. some comments on their a a concentration which is detectable, but is Cancer. One substance is reasonably well marized after the table. not objectionably irritating to the majority established as a cause of respiratory tract All substances in the of unhardened subjects who are exposed for cancer. This is nickel carbonyl. It appears threshold limits table (A a substantial part of a working day. The probable that the minimum cancerigenic ex cept mineral dusts, appe higher standard should be set at a concen posure will never be defined. At this time it betical order. When a v tration which is well under one injuring is prudent to set the standard for a can units of milligrams per bronchi or lungs, and which is justifiable cerigenic substance substantially at zero, letter t precedes the nuir fl when it is impractical to keep concentra as has already been done for nickel carbonyl, tions at the lower standard-. Standards for and no considerations can justify allowing tative value was proposed lows the number. irritating substances should refer to concen the inhalation of any concentration which is Following the threshold I:! trations existing for even a brief period avoidable. during a work day. Allergy. Some- substances are known to column showing a persona most serious effect of ini Asphyxiation. Some substances are inert sensitize an appreciable proportion of ex centration somewhat hfgh< in the body and can injure only by asphyxia posed workmen. They may produce distress old limit. These judgme at extremely high concentrations, exclud ing and menacing asthma-like attacks when jyMecide whether the vnlu< ing the oxygen of the atmosphere. Familiar a sensitized person inhales a low concentra ,<sjhe time-weighted averag examples are the fluoroehloro refrigerants. tion. Examples are ethylene diamine and /2o peak concentrations, ex The lower standard for these asphyxiants the di isocyanates. At this time there is no jj^luring the day. In futur oo t i,: o -4 X June, 1956 1 i .rk of good enas the 1000 ppm 2d. The inert nui- :ide might well be gory, and the cur.< of 15 mg./cu.m, avel. The standard centration existing I, but it should be concentrations are ictical to keep below st important effect transient influenzaas fume fever. A c oxide fume. The .tme fever producer ion which will not r but not menacing nan, and it should period, such as half tions of practicalig the standard for ubstances. he most important is, quinone and hybe a slowly developthe sclera, which ity, or even lead to standard for these '.entration which after years of l refer to the timemtration throughout at a time, conditions ustify exceeding the :e is reasonably well of respiratory tract carbonyl. It appears aum cancerigenic exfined. At this time it standard for a canibstantially at zero, e for nickel carbonyl, can justify allowing >ncentration which is ances are known to le proportion of exnay produce distressma-like attacks when ales a low concentra-hylene diamine and ;his time there is no I [ t A, j '< j i j J ( } j j I i | i , 1 1 j | 3 | | j i Industrial Hygiene Quarterly rational experimental basis for defining n concentration which will not sensitize a sus ceptible workman, or one to which no previ ously sensitized workman will respond. Con trol of exposure to allergenic substances must rely heavily upon industrial medicine. After experience has allowed withdrawal of workmen susceptible to sensitization, the remaining resistant individuals can be pro tected by a hygienic standard for daily in halation based upon irritation or systemic injury. Until it has been demonstrated that a particular group includes no susceptible workmen, no considerations can justify al lowing inhalation of any concentration which is avoidable. Interpretations of Accepted Values jvjo NEW VALUES for standards are sug gested at this time. The available data upon which the 238 values in the 105(5 pro posed list (ACGIH 1956) appear to be based have been studied. Table I is offered as an interpretation of these values, increasing the information they convey. It presents the familiar numbers, which give the engi neer and the chemist an illusion of complete understanding. It also presents, in the form of abbreviations of self-evident meaning, some description of actions which gives the biologically and medically trained a feeling of confidence. The table is obviously too com plex for great popularity. Nevertheless, every class of information listed is required by those who must apply the values. The data relied upon for the interpretations and some comments on their adequacy are sum marized after the table. All substances in the proposed 1956 threshold limits table (ACGIH 1956), ex cept mineral dusts, appear in one alpha betical order. When a value is listed in units of milligrams per cubic meter, the letter m precedes the number. When a ten tative value was proposed the letter T fol lows the number. Following the threshold limit values is a column showing a personal judgment of the most serious effect of inhalation of a con centration somewhat higher than the thresh old limit. These judgments allow one to decide whether the value should refer to the time-weighted average concentration or to peak concentrations, existing at any time during the day. In future tables of stand ards the decision should be clearly Indicated in the table. Three columns record personal judgments and estimates as to what responses may oc cur in some workman inhaling continuously, all day, the threshold limit, twice, and ten times the limit. It will be obvious from these entries that the values may not always de fine concentrations in which workmen will find no objectionable sensory effect, or even concentrations where no toxic symptoms will develop in any individual. Next comes a column listing important injuries other than from inhalation of the substance itself, such as dangerous absorp tion through the skin, chemical burns of eye and skin, frequent allergic dermatitis, pyrolj'sis to phosgene, and the like. The al most universal defatting of the skin by sol vents, and freezing of tissue by low boiling liquids, has not been entered. The last two columns give some indica tion of the soundness of the value by de scribing the supporting data, and by speci fying the year in which it was first pro posed or adopted. It is, of course, true that a value proposed many years ago and recopied in each succeeding year's list is not neces sarily proven sound, but in general it is like- 13' to be better established than a more re cently adopted value. There may be objection that the table does not mention warning power nor at tempt to evaluate this property specifically. The practical importance of warning power in preventing inhalation of an excess is much over-rated. Odor data are notoriousl}' unreliable. Estimates of tolerable working conditions with unacclimated subjects, briefly exposed, have only limited usefulness in predicting the responses of acclimated and usually hardened workmen, exposed all day. Early stages of narcosis reduce percep tion of odor and irritation. Even with strong irritants like ammonia and acrolein, physi cal circumstances, or a sense of duty, may keep a man at his post to be seriously in jured by a concentration which, all would predict, cannot be inhaled voluntarily. There is nothing in Table I which is not easily accessible, if not already well known to a thousand experienced industrial hygienists and toxicologists. Not one of these^k but will object to some among the thousand^ personal judgments entered. However, th<^} o o OaD n 4/ - - '-tt - M June, 1956 Industrial Hygiene Qvai%f annual threshold limit tables are consulted published observations are included when by upwards of twenty thousand other per they appear to confirm or supplement ma sons who do not have access to original terial in the literature. The term "most im I , -i Intermeta^ sources and extensive experience. These peo portant effect" used with every substance, ple rightly regard the threshold limits as a refers to the possible effect of inhalation of (Mm* presentation of the best available judgment, concentrations a few times the threshold and they may wrongly regard them as every limit, not necessarily to the possible effects Threshold gt thing they need to know about safe use of a at very high concentrations. Limit Moat' substance. Despite specific disclaimers, Acetaldehyde. Cook (1945) quotes the printed with each year's table, these readers 1911 report of Iwanoff that cats inhaling h Subatanc* PPro Importc r Effort y wg./ew.m, Jnhalattf. tend to regard each threshold limit ns de 280 ppm for seven hours were not noticeably fining the line between safety and injury. affected. The unacclimated subjects of Sil Acetaldehyde 200. Jun* Acetic acid 10. Ionit Acetic Table I is presented as a beginning in verman, Schulte and First (1946) found 25 the extensive job of improving communica ppm objectionable, 50 ppm irritating to the tion by developing a rational and informa eyes, but even 200 ppm not irritating to ar.hj-Jri.Je Acetone Acrolein 10050*. nluanrgco*!* .5 LUNG tive series of hygienic standards for daily the throat. Fairhall (1949, p. 199) describes inhalation. the effects as irritation, narcosis, bronchitis, Acrylonitrile AJdnn A flyl alcohol 2C. :tctuc n\-0.2$ chronic 5. EYE-Urn albuminuria, fatty liver and lung edema. He Ally! chloride 5. T lung Summary of Underlying Data 'T'HE data relied upon for the interpretax tions entered in Table I are summarized and briefly commented upon in the pages 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 Ally] propyl disulfide Ammate Ammonia Amyl acetate 2. m-15. 100. 200. Jung lung narcosis which follow. It is believed that the most survive four hours inhalation of 8000 ppm ) significant published information is in but die from 16,000 ppm. The liquid causes Amyl alcohol Ail:ne 100. S. narcoxL chronic it cluded, but no attempt has been made to list severe cornea! injury, irritates the skin and jt all pertinent articles. Certain hitherto un may sensitize some persons. Antimony ANTU Arsenic Arsine ni-o.S m-0.3 T chronic m-0,5 chronic 0.05 Barium Mnemonic abbreviations used in Table I. acne-- chloracne from continued akin contact. acute-- acute toxicity, with little or no increase in severity from continued inhalation. all-- allergenic. Dermatitis and asthma-like sen- sitization may result. ALL-- allergenic. Dermatitis and asthma-like sen- sitization are likely. asphyxia---asphyxiation at very high concentrations. lung?-- lung-- LUNG-- m-- minor irritation of bronchi (coughing) or hingft. definite irritation of bronchi or lungs with injury of lungs possible. dangerous injury of lungs with little warn- ing. the auantity ts expressed in milligrams per cubic meter (mg./cu.m.), not in ppm. (soluble) Benzene Benzyl chloride Bromine Butadiene Rutanbne ' (methyl ethyl ketone) m-0.5 55, 1. 1. 1000. acute-lu: lung 2B0. narcfwjN bur-- bum of the skin. met!-- medical uses yield some information. 1 BUR-- very seven? burn ot skin. cancer-- cancer reported in humans. narcosis-- narcosis, ranging from impaired coordinalion through dizziness, to anesthesia. chronic-- chronic toxicity, with increase itt severity nnrT-- (hint narcosis, somewhat impaired reaction from continued inhalation. time and judgment. din-- clinical examination of workmen was cor- nar-- narcosis definite, short of dizziness. related with their exposure. NAR-- narcosis marked, dizziness to unconscious' Butyl acetate Butyl alcohol Butyl amine Butyl CELLOSOLVE Butyl 200. !<>0. y 2P-0. narco*;* Jung ens-- central nervous system stimulation, such ns tremon or convulsion*. nau-- ness. nnusro. This symptom has not been entered 10. T lung cy-- CY-- eat-- eye-- cyanosis (blue skin) may be evident Cyanosis (blue skin) may be marked. estimate from experience and analogy. eye irritation severe enough to require none-- odor-- ODOR-- every time it may oceur. no ejects are expected. odor may be perceptible. odor marked. oxide fume Calcium arsenate m-0.1 m-0.1 aentedu medical treatment. pyr-- pyrolysis to lung injuring halogen com- Carbon (' EYE-- eye burn may be severe. eye pig-- eye pigmentation without injury. fume-- fume fever. rad-- rpt-- pounds in a flame, ot1 on hot metal. radiation injury is possible. repeated animal inhalation results. head-- headache. This symptom has not been en- sgl-- single animal inhalation reauKa. tered every time it may occur. skp-- skin penetration may cause symptoms. hu-- human sensory data. SKP-- skin penetration of liquid is dangerous. HU-- human toxicological or physiological data. T-- tentatively proposed. ind-- industrial complaints or observations, less tox -- toxic symptoms may arise very slowly. quantitative than clinical examinations. tox-- minor toxic symptoms. irr-- irritation of eye. nose or throat in some. TOX-- major toxie symptoms. THR-- irritation of eye, nose or throat marked. via--* visual acuity loss dioxide Carbon disulfide Carbon monoxide 5000. 20. 100. Carbon tetrachloride V\# CELLOyh solve Px^CELLO- W SOLVE Ul acetate 25. 200. 100. asphyx chronic acute ehroaitf chrpnii ehroni O O a Q jest. i June, 1956 . .aded when upplement ma.erm "most imery substance, >f inhalation of the threshold possible effects sO) quotes the t cats inhaling e not noticeably subjects of SiJ.1946) found 25 irritating to the ot irritating to ). 199) describes cosis, bronchitis, . lung edema. He does not cause ; death is due to r to lung edema 7-55) found rats ion of 8000 ppm .'he liquid causes ates the skin and T * '* (couching1) or k or lungs with gs with little warn- ssed in milligrams u.m.), not in ppm. e information. impaired coordinato anesthesia, it impaired reaction of dizziness, ness to unconscious* has not been entered ur. 1. >le. wring halogen com* on hot met&L isible. tion results, in results. cause symptoms, luid is dangerous. arise very alowiy. Industrial Hygiene Quarteiiy 137 Table I. Interpretation of Threshold Limit Values Proposed for 1956 Exclusive of Mineral Ousts (Mnemonic abbreviations explained at foot of table) Substance Threshold Limit ppm or mg./cu.rr. Most Important Effect of Inhalation Acetaldehyde Acetic acid Acetic anhydride Acetone Acrolein 200. 10. 5. 1000. 0.5 lung lung lung narcosis LUNG Acrylonitrile Aldrin Ally! alcohol Allyl chloride Ally! propyl disulfide 20. acute m-0.25 chronic 6. EYE-lung 5. T lung 2. lung Ammftte Ammonia Amyl acetate Amyl alcohol Aniline m-15. 100. 200. 100. 5. lung lung narcosis narcosis chronic Predicted Effects of Daily eight-hour Inhalations At Threshold Limit Additional At Twice Threshold Limit Additional At Ten Times Threshold Limit IRR-odor irr-odor lung IRR-lung irr-odor irr-nar-odor irr none none irr none IRR odor none eyc-IRR-lung NAR lung tox irr-tox cye-Jung irr-odor irr none irr-odor irr-odor irr-odor none IRR IRR-nar IRR-nar cy lung IRR-lung NAR NAR CY-tux Important Hazards Other Than from Inhalation I1-EYE bur-EYE Nature of Interpretive Data hu-sgl hu-ind-sgl Year Proposed 1945 1945 bur-EYE bur-EYE sJcp all-skp bur-EYE pyr sgl HU-ind hu-sgl rpt clin ind-sgl sgl 1947 1953 1945 1943 1954 1054 1956 bur-eye SKP ind est HU-ind-sgi hu-sgl hu-sgl rpt 1954 1954 1943 1945 1945 1943 Antimony ANTU Arsenic Arsine Barium (soluble) m-0.5 chronic m-0.3 T chronic m-0.5 chronic 0.05 acute-lung none none none none m-0.5 acute-lung none none tox? tox tox tox lung?-tox tox clin-rpt est clin-*t ind-sgl est 2 94* 1956 1948 1947 1943 Benzene Benzyl chloride Bromine Butadiene Butanhne (methyl ethyl ketone) Butyl acetate Rutyl alcohol Butyl amine Butyl CELLOSOLVE Duty) mercaptan 35. 1. 1. 1000. chronic lung lung narcosis 250. 200. 100. 5. narcosis narcosis narcosis lung 200. chronic 10. T lung tox? irr irr-odor none irr-odor irr-odor odor odor odor-tox ? ODOR tox odor odor nar-odor-TOX IRR-lung IRR-lung nar EYE BUR-EYE IRR-nau IRR-nar irr irr nar NAR IRR-NAR eye nar-tox irr-nar-TOXcye-irr-lung? HUR-EYE skp e!in-rpt sgl ind-sgl hurpt hu-sgl hu-sgl clin ind-sgl rpt sgl 1949 1954 1945 1947 194* 1945 ipsn 1955 1945 1954 Cadmium oxide fume Calcium arsenate Carbon diox'ide Carbon disulAde Carbon monoxide m-0.1 acute-lung m-0-1 T chronic $000. asphyxia 20. chronic 100. acute none none none none none odor tox none nar nar-tox TOX ind-rpt wt HU clin-rpt rlln-HU 1943 1956 1943 1943 1943 Carbon tetrachloride CELLOSOLVE CELLOSOLVE acetate 25. 200. 100. chronic chronic chronic toxT odor odor tox nar-tox nar-odor-TOX irr-nar-toX pyr irr-tox IRR-nsr-tox clin-ind-rpt 1953 Srpt 1945 ctonrpt 1945 o o h* o m 3? 190 June, 1956 Substance Threshold Limit ppm or mg./cu.m. Most Important Effect of Inhalation Chlordane Chlorinated camphene (60%) m-2.0 chronic m-0.5 T chronic Chlorinated diphenyl oxide Chlorine Chlorine tri- fluoride Chlorobentene Chlorobromo- methane .m-0.5 1 chronic lung 0.1 75, lung narcosis 400. T narcosis Chlorodi* phenyl (42% Cl) m-l. Chlorodiphenyl <54% Cl) m0.5 Chloroform 100. l-Ch)oro-l- nitrop ro- pane Chloropicrin .20. 1 chronic T chronic chronic lung T lung Table I--Continued Predicted Effects of Dally eight-hour Inhalations At Threshold Limit Additional At Twice Threshold Limit Additional At Ten Times Threshold Limit none none irr-tox none tox none odor none odor none tox? irr irr-tox nar tox lUR-htng irr-lung nnr tox none none odor-tox ? none tox? nar-tox tox? tox TOX none odor irr-lung-tox irr lung Chloroprene Chromic acid. chromates as CrOj CRAG herbicide *eso) yanide as CN 25. n-0.1 m-15. 5. m-5. chronic irr chronic chronic acute none none none odor none nar-tox TOX irr none irr IRR irr-tox? lung-tox tox Cyclohexane CycJohexanol Cyclohexanone Cyclohexene Cyclopropane 400. 100. 100. 400. 400. narcosis narcosis narcosis narcosis narcosis none irr-odor irr-odor none none nar-odor nar-tox nar-odor nar-odor irr-N AR-tox IRR-NAR lHR-nar irr-N AR-tox irr-NAR 2,4-D DDT Decaborane Diacetone alcohol Diborane m-10. chronic m-1. T chronic 0.05 T acute 50. 0.1 narcosis cns-lung none none none irr none none none odor irr-tox? irr-tox odor IRR-nar lung-tox? o-Dichlorobenzene Dichlorodifluoromethane l,l-Dichloro ethane 1,2-DichIoroethylene Dichloroethyl ether 50- 1000. 100. 200. 15. chronic odor-tox ? asphyxia chronic narcosis lung none odor none none irr-tox nar none none nar-tox odor irr-nar irr-odor lung Dichloromonoflttoromethane 1,1-Dicbloro1-nitro- ethane 1000. 10. asphyxia none lung none none irr none lung-tox Important Hazards Other Than from lnhalntlon nll-skp Nature of Interpretive Data clin Year Proposed 1954 all-slip est 1956 nerte bur-EYE bur-EYE pyr pyr rpt hu-rpt rpt cst-sgl rpt 1955 1948 1955 1943 1956 acne acne pyr rpt rpt est-Vncd-sgl 1945 1966 1945 pyr-skp Rgl clin rpt 1945 1956 1945 bur-EYE clin cst DUR-EYE-SKP est-sgl rst rpt hu-rpt hu-rpt sgl est-med cst skp cst rpt hti-sgl elin-rpt pyr ind-sgl 1943 1964 1952 1947 1945 1945 1945 1945 1947 1964 1954 1956 2954 1955 194T pyr rpt 1947 pyr rpt 1946 pyr sgl 1946 skp hu-*g) 1946 pyr sgl 1947 rpt 1946 Industrial Hygiene Quarterly. f Substance Threshold Limit ppm or mg./cu.m. U<Mt ImporUnt R/Tet of Inhalation 4, '*) DfchJorotetra- r fluoromethane 10PO. DirJdrin m-9.25 asphyxia Diethylnmlne 26. lung r, Dlfluorodi- bromomethane Djisooutyl 2 00. chronic ketone Dijsocyano toluene Dimethylanl- line Dimethybul- fate ro. (0.1 5. chronic . I. acute-LUNG f- Dinitroben- t rene Dinitro-o- m-l. T chronic cresol m-ft.2 tMnitrotohiene m-1.5 Dioxane 100. KPN m-O.S acute Ethyl acetate Ethyl acrylnte Ethyl alcohol Ethy famine Ethyl benzene 400. 25. 1000. 25. 240. narcosis nn remix Ethyl bromide Ethyl chloride Ethylene chlorhydrin Ethylene diamine Ethylene oibromide 200. 101*0. 5. 50. 25. chror,ii*-lunn Ethylene dichloride Ethylene iminc Kihylc.-.c oxide 100. 5. 100. Ethyl ether 400. Ethyl formate 1*0. chronic 6n:fe-h.ng lung.nar- cords narcosis narcosis Ethyl mercaptan 200. Ethyl silicate 100. Ferbam m-15. Ferro vanadi- um dust nul. Fluoride dust m-2.5 ri.intf T!un* chronic N> CD Fluorine FluoroneeUitos Fluorotri- chioromethane Formaldehyde Furfural Furfuryl alcohol Gasoline <U m-0.l Jong 1000. 5. 5. asphyxia lung T lung -- 50. T narcosis 500. narcosis $> oO K BFG36772 k June , 1956 ant d* Nature of Interpretive Year ion Data Proposed clin 1954 cst 1D56 E hu-rpt E rpt est-sgl rpt 1956 1948 1955 1943 1966 rpt rpt cst-'med-sgl 1945 1965 1945 clin > rpt E clin est ;KP rat-sgl est hu-rpt hu-rpt sgl est-med est rpt hu-sgl clin-rpt ind-sgl 1945 1956 1945 1943 1954 1952 1947 1946 1945 1945 1945 1947 1964 1954 1956 1954 1955 1947 rpt rpt sgl hu-sgl 1947 1945 1946 1946 sgl rpt 1947 1946 f \ < 1 Industrial Hygiene Quarterly 139 Table I--Continued Predicted E(Tecta of Daily eight-hour Inhalations Substance Limit ppm or mg./cu.m. Most Important EfTcct or* Inhalation At Threshold Limit Additional At Twice Th res hold Limit Additional At Ten Times Threshold Limit Dichlorotetrafiuoromethane Dicldrin Dicttiylaminc 1000. m-0.25 25. chronic asphyxia lung none none odor none none ?ye-lrr none irr IRR-lung DtHuorodibromomethane Diisobutyl ketone Diisocyano toluene Dimethylaniline Dimethylsulfate 100. chronic none 50. narcosis irr-odor 0.1 T ALL-lung all 5. chronic none 1. ncute-LUNG none none cy irr-nnr-tox IRR-nar ALL CY-tox LUNG-TOX Hazards Other Than from Inhalation Nature of Interpretive Data pyr nll-skp bu r-F.YE *gl clin -gi pyr rpt hu-rpt ind SKP sgl miR-EYF.-RKr sgl Dinitrobonr.ene Dinitro-oc resol Dinitrotolucne DioxAne EPN m-l. T chronic m-0.2 m-l.5 100. m-0.5 acute chronic chronic acute none none tox? none none Ethyl nectate Ethyl ncryiate Ethyl alcohol Ethylamine Ethyl benzene 400. 25. 1000. 25. 200. narcosis Thing narcosis lung narco* is irr-odor odor irr-odor odor nar?-odor Ethyl bromide Ethyl chloride Ethylene chlorhydrin Ethylene Unmine Ethylene dibromide 200. 1000. 5. 10. 25. lung narcosis none odor acute none ALL-lung odor chronic-lung none Ethylene dichloride Ethylene imine Ethylene oxide 100. 5. 100. Ethyl ether 400. Ethyl formate 100. chronic odor-toxT acute-lung lung-narcosis narcosis narcosis odor odor-nar irr-odor none tox tox 7 nnr-odor nnr irr nar eye-irr irr irr-odor irr-tox irr-tox irr-NAR-tox tox IRR-NAR Jung IRR-NAR IRR-lung NAR lung nar tox 7 udor-tox irr eye irr-odor lung-tox skp est skp skp bur-EYE pyr pyr gl est hu-rpt est hu-sgl rpt HU Sgl hu-sg| Sgl gl SKP ind-sgl ALL-bur-EYE iml-rpt pyr rpt nnr-nau TOX pyr lung-TOX bur-eye-SKP irr 1RR-LUNG-NAR bur IRR NAR irr-odor nar lnd*rpt hu-sgl hu-rpt HU-med *l Ethyl mereaptan Ethyl silicate Ferbam Ferro vanAdi- um dust Fluoride dust 250. 100. m-15. m-l. m-2.5 T lung acute-lung T lung lung chronic Fluorine Fluoroacetates Fluorotri- chloromethane Formaldehyde Furfural 0.1 m-0.1 1000. 5. 6. lung T acute asphyxia lung T lung ODOR odor none none tox 7 none . none none irr irr irr-tox irr cye-irr-lung IRR IRR none irr-tox irr-lungT-tox? tox alt BUR-EYE none mlor none IRR-lung IRR-lung pyr all-EYE all-EYS sgl hu-rpt est rpt clin.HU clin-rpt est sgl ind-sgl ind-sgl Furfuryl alcohol Gasoline 50. T narcosis 500. narcosis odor odor irr-nsr irr-nar IRR-NAR NAR rpt hu-ind Year Proposed 1947 1964 I0S2 1956 1954 1956 1948 ** 1945 1956 1949 1943 1947 1964 1945 195$ 1945 1962 1946 1947 1947 1947 1965 1953 1953 1935 1945 1947 1947 1954 19451956 1954 1047 1963 1956 1946 1946 1954 1965 1945 * i A , >3 V fO two cyi O h* ts> no June, 195$ Substance Heptane HETP Hexane Threshold Limit ppm or mg./cu.m. Most Important Effect of Inhalation 500. narcosis m-0.1 T acute 500. narcosis Table I--Continued Predicted Effect* of Daily eight-hour Inhalations At Threshold Limit Additional At Twice Threshold Limit Additional At Ten Times Threshold Limit odor none odor irr-nar irr NAR tox irr-nar-nau Kexanone (methyl butyl ketone) Hoxone (methyl isobutyl ketone) Hydrazine Hydrogen bromide Hydrogen chloride 100. narcosis odor 100. 1. 5. 5. narcosis lung lung lung odor none irr irr irr nar irr IRR IRR mtr cns-irr-lung eye-lung eyc-lung Hydrogen cyanide Hydrogen fluoride Hydrogen peroxide S09& Hydrosen selenide Hydrogen sulfide 30. acute odor 3. chronic-lung irr 1. lung none 0.05 chronic-lung none 20. lung irr-odor Hydroqulneae m-2. Iodine 0.1 Iron oxide fume m-15. Tsophorone 26. Isopropyl*mine 5. eye pig lung none irr fume-lung chronic- narcosis none irr-odor Jung odor IRR TOX eye-Iung*tox irr-iung lung-odor-tox eye pig IRR lung-tox vis eyc-lung fumc-irr limy IRR-nar-tox irr eye Lead Lead arsenate Lindane Magnesium oxide fame Malathon m-0.15 chronic m-0.16 T chronic m0.5 chronic m-15. m-15. fume acute toxT none none none none tox none none TOX irr irr fume-irr lung tox Manganese Mercury Mercury, organic Mesityl sMv MethoxycUor m-6. m-0.1 m-0.01 no. m-15. chronic chronic chronie narcosis chronic Methyl acetate Methyl acetylene Methylal Methyl acrylate Methyl alcohol 200. 1000. 1000. 10. 200. narcosis lung chronic Thine narcosis none none toxT irr-odor none odor none odor none none none tox nar irr-tox irr odor irr odor odor tox TOX tox IRR-lung nar lung-nar lung-tox irr-nar irr-nar-tox? Methyl bromide Methyl CELLOSOLVE 20. chronic 25. chronic none none ens-odor irr-tox odor-toxf irr-nar-tox Hazards Other Than from Inhalation Nature- of Interpretive Data Year Proposed SKP hu est hu 1945 1956 1941 hu-sg! 1947 bur-eye bur-eye bur-eye SKP BUR-EYE BUR-EYE bur-eye BUR-EYE nll-skp SKP pyr hu-sgl rpt hu ind-rpt hu-sg] ind-rpt 3947 1955 1955 1943 1913 1943 rpt hu-ind-rpt clin-sgl din ind din hti-rpt ms 1948 1943 1955 1948 1947 1945 ind-sgl elin rpt rpt HU est-clin clin clln-rpt clin-agl hu-rpt SKl cst-sg) rpt rpt rpt rpt clin-rpt 1955 1943 1956 1954 1946 1954 1945 1943 1954 1945 1954 1948 1955 1958 1956 1943 194S clin-rpt 1947 Industrial Hygiene m \ r r rw <a <D Substance Methyl Threshold Limit E ppm Imp. or Kir* ---- -mg./eu.m. -- Jh<- CELLOSOLVE acetate Methyl 25. chloride M.lhyl 100. chloroform 500. jr. Methyl eyclo~ hex?no Methyl cyciohexnnol Methyl cyetohexanene Methylene chloride Methyl formate 550. 100. DO. 500. 100. firm nr chiu Methyl i<*obu- tyi rarbinoi (methylamyl alcohol) Methyl 25. n.iu mercaptan Molybdenum SO. T lun;. (soluble) Molybdenum (insoluble) Naphtha m-5. m-15. chn. ch ix (coal tar) 200. Naphtha (petroleum) 500. Nickel nar. carbonyl Nicotine Nitric acid p-Nitroatuline 0-001 can. m-0.5 Pehn 10. T Junfc 1. chn Nitrobenzene Nitroethane Sitmzen dioxide Nitroglycerine Nitromethane 1. JOO. A, 0.5 100. chn itcu^ lur* acu acu 2*Ntropro- pane Nitrotoluene Octane Ozone Parathion 50. S. .00. 0.1 m-0.1 aeui eh n nar luni acu Pentaborane Pentachloro. 0.01 Tacu naphthalene m-0.5 Pentachloro* phenol Pentane m-0.5 1900. Pentanone (methyl pro pyl ketone) too. ehn nar nar Peichloroethylene PerehVoromethyl \ 200. har mercaptan 0.1 T Jun ? M^y .' i*v June, 1956 Nature of Interpretive Year Data Proposed 1945 1966 hu 1947 r hu-sgl 1947 hu-sgl rpt hu ind-rpt hu-sgl ind-rpt 1947 1969 1965 1948 1948 1948 rpt hu-ind-rpt clin-sgl clin d n'n hu-rpt 1995 1948 1943 1955 1948 1947 1945 ind-sgl clin rpt rpt HU cst-clin clin elin-rpt clin-sgl hu-rpt sgl est-sgl rpt rpt rpt rpt clin-rpt 1955 1943 1956 1954 1946 1954 1945 . 1943 1954 1945 1964 1948 1966 1962 1966 1943 1945 clin-rpt 1947 Industrial Hygiene Quarterly 111 Table I--Continued Substance Threshold Limit ppm or mg./cu.m. Methyl CELLOSOLVE acetate Methyl chloride Methyl chloroform 25. 100. 600. Most Important Effect of Inhalation chronic chronic narcosis Predicted Effect* of Daily eight-hour Inhalations At Threshold Limit Additional At Twice Threshold Limit Additional At Ten Times Threshold Limit none none odor odor-tox irr-nar-tox odor ens-nar nar NAR Methyl cyclo hexane Methyl cyclohexano! Methyl cyclohexanone Methylene chloride Methyl formate 500. 100. 100. 500. 100. narcosis narcosis narcosis chronic narcosis odor irr-odor irr-odor none none nar irr-NAR-tox nnr-tox IRR-NAR IRR-nar odor nar irr-odor nar Methyl isobu- tyl carbinol (methylamyl alcohol) 25. Methyl mercaptan 50. Molybdenum (soluble) m-5. Molybdenum (insoluble) m-15. Naphtha (coal tar) 200. narcosis T lung chronic chronic narcosis none irr-odor IRR-nar ODOR eye-irr-lung 7 none irr-tox none none irr-tox irr-nar?-odor NAR Naphtha (petroleum) Nickel carbonyl Nicotine Nitric acid p-Nitroaniline Nitrobenzene Nitroethane Nitrogen dioxide Nitroglycerine Nitromethane 500. narcosis odor 0.001 cancer-lung m-0.5 T chronic 10. T lung .1 chronic .1 chronic 100. acute none none irr none none none 5. 0.5 100. Jang acute acute odor head none irr-nar NAR none JRR irr-odor none tux lung tox tox nur-tox irr irr-odor LUNG tox nar-tox 2-Nitropropane Nitrotoluene Octane Ozone Parath ion 60. 5. 500. 0.1 m-0.1 acute chronic narcosis lung acute nau-tox 7 none odor odor none tox 7 irr-nar odor-tox tox NAR irr-lung tox Pentaborane 0.01 T acute Pentachloro- naphthalene m-0.5 chronic Pentachloro- phenol m-0.5 acute Pentane 1000. narcosis Pentanone (methyl pro pyl ketone) 200. narcosis none none none odor irr-odor tox7 irr IRR none tox irr-tox nar nar Peiehloroethylene \ Perchloro- methyl mercaptan narcosis 0.1 T lung odor irr-NAR Hazards Other Than from Inhalation Nature of Interpretive Data Year Proposed pyr pyr pyr est 1947 rpt 1947 rpt 1963 rpt 1947 rpt 1946 rpt 1946 rpt 1946 1947 SKP HUR-EYE skp SKP SKP SKP SKP acne bur-skp bur-EYE hu-sgl egl rpt rpt est est ind-sgl est est est-ind est rpt ind-rpt clin rpt clin-sgl est est rpt clin-est rpt rpt est hu hu-sgl med-rpt sgl 1954 1954 1965 1966 1945 1945 1964 1968 1955 1954 1947 1947 1945 1946 1947 1947 1943 1946 1954 195S 1956 1946 1947 1947 1947 19 O June, 1956 IAS ITable --Continued Predicted Effects of Daily eight-hour Inhalations Important Threshold Limit ppm or Substance Phenol mg./cu.m. 6. Phenylhydra- 5. Phosgene 1. Phosphine Phosphorous (yellow) 0.05 m-0.1 Most Important Effect of Inhalation chronic chronic lung chronic chronic At Threshold Limit odor none none Additional At Twice Threshold Limit irr Additional At Ten Times Threshold Limit lung-tox cy-TOX LUNG-odor none none tox? Hasards Other Than from Inhalation Nature of Interpretive >ata Year Proposed 11UR-EYE-SKP hu-rpt 2962 all-SKP bur* EYE sgl HU-rpt rpt 1954 1945 1941 ind 1947 Phosphorous pentachlor- ide Phosphorous pentasulfide Phosphorous trichloride m-1. m-1. 0.5 .picric acid m-0.1 Propyl acetate 200 lung lung lung chronic narcosis none none none none irr-odor irr-lung irr-lung irr lung-odor irr tox lRR-nur NAR bur-EYE bur* EYE sll-shp sffi est sgl ciin est-sffl 1947 1947 3945 1954 1945 propyl alcohol (isopro panol) Propylene di chloride 400. 75. narcosis chronic irr-odor tox 7 1RR-NAR nar-odor TOX est-htt pyr rpt bur-EYE-SKP sgl 1945 1847 1955 25. acute-lung odor -------------------------------~"Pt ' 1945 !! Propyl ether Pyrethrum Pyridine Quinone Rotenone 500. narcosis m-2. T lung 10. chronic 0.1 eye pig m-5. T lung irr-odor none cns?*odor none none IRR eye-pig NAR irr irr-tox vis irr rpt ind-med clin est 2956 1954 1955 1956 Selenium compounds, clin-est 1947 as Se rn*0.1 chronic .none fl Sodium hy droxide Stibine m-2. 0.1 irr irr chronic-lung none Stoddard sol vent Strychnine 500. narcosis m-0.16 T acute odor none irr-nar IRR lung?-tox? NAR tox bur-EYE ind sgl hu est 1954 1947 1945 1956 Styrene monowor Sulfur dioxide 200. 10. Sulfur hexa fluoride Sulfuric acid 1000. m-1. chloride 1. narcosis hmg asphyxia lung lung odor irr-odor none irr none irr ilUl irr IRlt-nar lung none IRK-iung pyr bur-EYE bur-EYE hu-rpt ctiit-hu 4gl HU-iiul-sgl Ind-agl 1947 194$ 1954 194$ Sulfur penUfluoride TEDP Tellurium TEPP 0.025 m-0.2 m-0.1 m-0.06 lung acute chronic acute none none % none none none irr-lung tox irr-tox ? tox bur-EYE sgl est clin cat 1954 1954 1947 1954 p-Tertisry butyl toluene 10. chronic odor irr-nar-tox hu-rpt 1955 ethane Tetrahydro* furan Tetranitrome- thane Tetry) Thallium (soluble) 5. chronic 200. T narcosia 1. m*1.5 acute chronic m-0.15 T chronic tox? irt none tox odor Irr odor*TOX irr tox tox skp all-skp rpt rpt clin est 196$ 1955 194$ 195$ Industrial Hygiene Quart : t Subntance Threshold Limit ppm or m*./cu.m. ?. | Most r JmporUife Effect of Thiram Titanium dioxide Toluene o-Toluidine Trichloro- ethylene m-5. T chronic , m-15. 2*0. 5. lung narcosis chronic 200. nurcuei* * Trichloro* naphthalene T riuuoromon. obromo* methane Triritrotoluem Turpentine Uranium (soluble) m-5. 1000. m-1.5 100. m-0.05 chronic narcosis chronic narcosis' chronic Uranium (insoluble) Vanadium (VtOi dust) Vanadium ( VrOs fume) Vinyl chloride Warfarin m-0.25 chronic m-O.o lung m-0.1 'ting 00. natvosW m 0.5 T chronic Xylene Zinc oxide fume Zirconium 200. iiarcosu m-lo. fomc m-5. T lung The most important efF* inhalation is irritation of tract, bronchi and even I threshold limit can be human sensory data. It to prevent lung: injury. Acetic acid. Sterner (1 ppm is reasonably ih>jihnsis of industrial i-xpcri 11, p. 8S6) finds 800 to able. Smyth (1937-55) 10,000 ppm by ruts for one of six. The liquid cai injury. Vigliani and Zu workers exposed seven t centrations of GO ppm, w at 100 to 2G0 ppm, hat slight irritation of the stomach and skin. They r as without danger. The only important e1. inhalation is irritation, eyes, then in the upper bronchi and even lung. rj old limit can be interp BFG36776 i June, 1956 f ture of rpretive Data -rpt Year Proposed 1952 U-rpt 1954 1943 1947 d 1947 ;1 it el et-sgl 1947 1947 1946 1954 1945 *3t-hu rpt 5*1 rpt est 1945 1947 1966 1945 1966 1954 1955 1956 eat 9*1 est 1947 1954 1947 1945 1956 hu-rpt clin-hu $r! HU-ind-sgl ind-agl 1947 1943 19S4 1948 1945 3gl est clin est 1954 1954 1947 1954 hu-rpt ind-sgl rpt rpt clin est 1956 1947 1956 1955 1943 1956 r { Industrial Hygiene Quarterly us Substance Th resholil Limit ppm or mg./cu.m. Most Important Effect of Inhalation Thiram Titanium dioxide Toluene o-Toluidlne Trichloro ethylene m-5. T chronic m-15. 200. 5. lung narcosis ?h ronic 200. narcosis Trichloronaphthalene Trifluoromonobromomethane Trinitrotoluene Turpentine Uranium (soluble) ni-5. 1000. m-1.6 10C. m-0.05 chronic narcosis chronic narcosis chronic Uranium (insoluble) Vanadium (VsOs dust) Vanadium (V:Oi fume) Vinyl chloride Warfarin m-0.25 chronic m-0.5 lung m-0.1 lung 500. narcosis m- 0.5 T chronic Xylene Zinc oxide fume Zirconium 200. nArcosis m-15. fume m-5. T lung Table I--Continued Predicted Effects of Daily eight-hour Inhalations At Threshold Limit Additional At Twice Threshold Limit Additional At Ten Times Threshold Limit none none narT-odor none irr cy irr-lung NAU CY-tox nnr-nau-odor irr-NAR none (ox none tox T irr-odor none none none none tox? IRR-nar irr-nar irr-tox NAR-tox tox tox lung none none none lung irr-nnr ?-odor nnr nar tox NAR fume none fume-trr lung lung Important Hazards Other Than from Inhalation Nature of Interpretive Data cst-ngl Proposed Year 1956 SKP n>t rlin-hu-rpt Mfl 1954 1943 1943 pyr intl-m etl.rpt 1943 ncnc rpt 1945 pyr skp rad rad rpt clin-rpt hu-rpt rpt rpt rpt 1956 1943 1945 1953 1953 1954 rpt 1954 pyr s*l 1947 cat 19*6 hu 1943 HU 1943 rpt 1955 The most important effect of acetaldehyde inhalation is irritation of upper respiratory tract, bronchi and even lung. The 200 ppm threshold limit can be interpreted from human sensory data. It is sufficiently low to prevent lung injury. Acetic acid. Sterner (1943) concludes 10 ppm is reasonably non-irritating on the basis of industrial experience. Patty (19489, p. SS6) finds 800 to 1200 ppm intoler able. Smyth (1937-55) found inhalation of 16,000 ppm by rats for four hours killed one of six. The liquid causes severe corneal injury. Vigliani and Zurlo (1955) report workers exposed seven to 12 years to con centrations of 60 ppm, with one hour daily at 100 to 260 ppm, had no injury except slight irritation of the respiratory tract, stomach and skin. They regard 20 to 30 ppm as without danger. The only important effect of acetic acid inhalation is irritation, first evident in the eyes, then in the upper respiratory tract, bronchi and even lung. The 10 ppm thresh old limit can be interpreted from uncon trolled human sensory data. It is low enough to prevent lung injury. Acetic anhydride. Henderson and Hag gard (1943, p. 130) mention eye, nose and throat irritation and suggest that bronchial and lung injury are likely. Fairhall (1949, p. 203) considers it a lacrimator and finds systemic efFects unlikely. McLaughlin (1946) discusses serious corneal injury from the liquid in industry. Smyth (1937-55) found rats inhaling 1000 ppm for four hours survived, but 2000 ppm was fatal. The liquid causes skin burns. The only important effect of acetic an hydride inhalation is irritation, first evident in the eyes, then in the upper respiratory tract, bronchi and even lung. The 5 ppm threshold limit can be interpreted from an alogy with acetic acid. In view of rat mor tality from the two vapors, a lower value would be more consistent, although it is undoubtedly low enough to prevent lung in jury. Aceione. Nelson, Ege, Ross, Woodman and Silverman (1943) found slight eye, 24960016 it & s June, 1956 .Industrial Hygiene Quart 114 nose and 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. Vigliani 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, Schrenk, 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 .nd Haggard (1943, p. 138) conclude the main attack is on the upper respiratory tract, but that a high concentration can Wilson (1944) in exposed workmen, found evidence of skin penetration and effects ref erable to liver injury. Smyth's (1937-65) rats survived four hours at 509 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 ppm 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, 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 it can be interpreted from the results of examination of exposed workmen. It is low * V t 1 interpreted from a report ffl tion and results of repeated tion. It is probnbly low ena injury, but may be slight? some. | Allyl chloride. Adams, Sj (1940) found rats survive)/ halation of 290 ppm, whf killed all. Injury was chiej with some kidney effects;? weak but mucous membrane prominent. % The most important effect inhalation is irritation of th? tory tract, bronchi and lung, tative threshold limit can. from single inhalations by analogy with chloroprene. - enough to prevent injury. - Allyl propyl disulfide. Fej Baliff (1946) surveyed an ing plant and found prono; of eye, nose and throat at 3 calculated as this disulfide, tation at 2 ppm. Acclimiti dent. The most important effcv; disulfide inhalation is in upper respiratory tract and threshold limit can be inter results of complaints from men. It appears low ettoiig) jury. Animate. ACGIH (1P5H 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 ali die from 16 ppm. The liquid causes severe corneal injury and burns of enough to prevent injury. Alhjl alcohol. McCord (1932) found some human irritation at 5 ppm. The review by von Oettingen (1943, p. 138) shows cats die during 30 seven-hour inhalations of 50 ppm, with pulmonary edema, gastroenteritis, hematuria and nephritis. Smyth (1937-55) 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 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 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. dangerous, and skin contact causes bums when evaporation is prevented. The most important effect of allyl alcohol inhalation is irritation, manifest a3 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 single dose LD-,, for as mg. kg. justifies no more e. tion than is required fur sance dust. The most important eitee; inhalation is the low grad substantially inert dust. T threshold limit can be ini. analogy. It appears low er injury. Ammonia. Lehmann (1 100 ppm is tolerable, am dustrial experience has bee derson and Haggard (IPincapacitating temporary respiratory arrest from a tion. They state 53 ppm is smelled, but Smyth (1937detected and identified by C.0 give 408 ppm as irritatii (J) 698 ppm irritating to the Q O V* June, 1956 v^-.anen, found and effects refrth's (1937-55) t 500 ppm but . of acrylonitrile ng, due to hyide. The 20 ppm .preted from reihalation studies accepted 10 ppm en cyanide. It is ybeck (1951) exo three years exn. aldrin and reclinical evidence reviewing human Is aldrin and linAcutely they in stem irritability, ronically they ins also on kidney, and they sensitize 54b) finds aldrin icutely as lindane, ashold limit of the jpriate. feet of aldrin inn;og centering in threshold limthe results of vorkmen. It is low f1932) found some >m. The review by 38) shows cats die alatiens of 50 ppm, i, gastroenteritis, . Smyth (1937-55) hour at 500 ppm, The vapors irritate fficiently so to premcentration which ; man through deChronic toxicity is skin penetration is ntact causes burns svented. fleet of allyl alcohol , manifest as disd pulmonary edema, ganic effects someand narcosis overresbold limit can be j ( t t ( Industrial Hygiene Quarterly H5 interpreted from a report of human irrita tion and results of repeated animal inhala tion. It is probably low enough to prevent injury, but may be slightly irritating to some. Allyl chloride. Adams, Spencer and Irish (1940) found rats survive three hours in halation of 290 ppm, while eight hours killed all. Injury was chiefly in the lung, with some kidney effects. Narcosis was weak but mucous membrane irritation was prominent. The most important effect of allyl chloride inhalation is irritation of the upper respira tory tract, bronchi and lung. The 5 ppm ten tative threshold limit can be interpreted from single inhalations by animals and by analogy with chloroprene. It appears low enough to prevent injury. Allyl propyl disulfide. Feiner, Burke and Baliff (1946) surveyed an onion dehydrat ing plant and found pronounced irritation of eye, nose and throat at 3.4 ppm onion oil calculated as this disulfide, with some irri tation at 2 ppm. Acclimitization was evi dent. The most important effect of allyl propyl disulfide inhalation is irritation of eye, upper respiratory tract and lung. The 2 ppm threshold limit can be interpreted from the results of complaints from exposed work men. It appears low enough to prevent in jury. Animate. ACGIH (1954b) concludes the single dose LD5U for animals of 2000 mg./kg. justifies no more control on inhala tion than is required for a non-toxic nui sance dust. The most important effect of animate dust inhalation is the low grade irritation of a substantially inert dust. The 15 mg./cu.m. threshold limit can be interpreted only by analogy. It appears low enough to prevent injury. Ammonia. Lehmann (1886) suggested 100 ppm is tolerable, and subsequent in dustrial experience has been favorable. Hen derson and Haggard (1943, p. 125) note incapacitating temporary blindness,- and respiratory arrest from a high concentra tion. They state 53 ppm is the least amount smelled, but Smyth (1937-55) found 1 ppm detected and identified by 10 subjects. They give 408 ppm as irritating to the throat, 698 ppm irritating to the eye, 2500 to 6500 ppm dangerous to life in 30 minutes. Fairhall (1049, p. 20) notes eye and upper respiratory tract irritation, salivation, bronchial irritation and lung edema, but no chronic systemic effect. Elkins (1950, p. 84) found 55 ppm not objectionable in industry but 125 ppm irritating. Silverman, Whittenberger and Muller (1949) found 500 ppm stimulated human respiration, irritated eye and throat, caused lacrimation. Smyth (1937-55) found rats survive four hours at 2000 ppm, die at 4000 ppm. Solutions irri tate the skin, erode mucous membrane and severely injure the cornea. Vigliani and Zurlo (1955) in workers inhaling 100 ppm, found irritation of the respiratory tract and conjunctiva. Even 20 ppm caused com plaints until workers became hardened. The most important effect of inhalation of ammonia gas is respiratory tract irritation, with lung edema or respiratory arrest the maximum injury. The 100 ppm threshold limit can be interpreted from human sen sory and physiological data. It is low enough to prevent injury. Amyl acetate. Patty, Yant and Schrenk (1936) found 2000 ppm does not injure guinea pigs in several hours, while a concen tration killing in 60 minutes can not be ob tained. Symptoms consisted of eye. and nose irritation and narcosis. Nelson, Ege, Ross, Woodman and Silverman (1943) found slight throat irritation in unacclimated sub jects at 100 ppm, mild eye and nose sensa tion and severe throat irritation at 200 ppm. Smyth (1937-55) with rats inhaling substantially saturated vapors found anes thesia in two hours and death in eight hours. Chronic toxicity is not to be expected. The most important effect of amyl acetate inhalation is narcosis. The 200 ppm thresh old limit can be interpreted from human sensory data and single inhalations by animals. It is low enough to prevent definite narcosis. Amyl alcohol (isoamyl alcohol.) Nelson, Ege, Ross, Woodman and Silverman (1943) found slight throat irritation in unac climated subjects at 100 ppm, and objection able eye, nose and throat irritation at higher concentrations. Haggard, Miller and Green berg (1945) found the toxicity 12 times that of ethyl alcohol for anesthetic death. No chronic systemic toxicity is to be ex pected. Smyth (1937-55) found rats not 24900018 ? s U6 June, 1956 Killed" by eight hours at 2000 ppm, close to saturation. The most important effect of amyl al cohol inhalation is narcosis. The 100 ppm threshold limit can be interpreted from human sensory data and analogy with butyl alcohol. It is low enough to prevent signifi cant narcosis, but not to prevent slight irri tation. Aniline. Henderson and Haggard (1943, p. 227) conclude 7 to 25 ppm gives slight symptoms in several hours, 100 to 160 ppm for one hour causes serious disturbance. Aniline is a chemical asphyxiant, causing methemoglobin cyanosis through its meta bolite, p-aminophenol. This can lead to anemia, but death from a single exposure is due to central nervous effects leading to respiratory paralysis. Skin penetration is more an industrial hazard than inhalation. Smyth (1937-55) found 340 ppm, substan tial saturation, did not kill rats in two hours but was fatal in four, with their hemoglobin 54% converted to methemoglobin. Oberst, 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 that exposed workmen should be followed eleetrocardiographically. 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. ANTU (alphanaphtlnjlthiourea). McClosky and Smith (1945) found consider able species differences in acute oral toxici ty. The LD50 for rats, the most susceptible species, was about 0.03 gm./kg. Death was due to pleural efusion. Repeated doses caused liver injury. Fitzhugh and Nelson (1947) found rats are not affected by 50 ppm in their diet over a two-year period. Tolerance developed. The most important effect of ANTU in halation is chronic poisoning centering in the liver. The 0.3 mg./cu.m. tentative threshhold 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 McCaughey (1945) found workers exposed to 0.007 to 0.60 mg./cu.m. showed no symp toms. Chronic arsenic poisoning causes varied symptoms (I.L.O., 1930, I, p. 161): digestive disturbance, hyperemia, skin erup tion, pigmentation, keratosis, epithelial cancer, polyneuritis, cirrhosis, confusion, delirium, irritation of eyes and respiratory tract. Arsenic is stored in the body, but not to the extent of lead. The most important effect of inhalation of arsenic compounds is chronic poisoning. The 0.5 mg./cu.m. threshold limit can be in terpreted from the-results of examinations of exposed workmen. It appears low enough to prevent injury. Arsine. Henderson and Haggard 11943, p. 241) describe acute arsine poisoning as due to hemolysis of red blood cells with re sulting anemia and kidney damage, and lung Industrial Hygiene Quarts edemn. They state 250 ppn is fatal, and 3 to 10 ppm toms in a few hours. Nau * an industrial episode show limit of 1 ppm was too b| ]| (1950, p. 67) reported bi| fatal case at a level of ab$ The most important effci halation is acute poisoning edema. The 0.05 ppm thresli interpreted from the result experience. It appears to b| prevent injury. ^ Barium- (soluble canipoi (1949, p. 32) records the fr,' ble barium compounds as C with gastro-intestinal distu,1 symptom. He notes brom from barium carbohnte dust action of barium sulfide. ; The most important effe.' of soluble barium compound; ritation, with acute poisonir 0.5 mg./cu.m. threshold lim preted only by analogy with pears low enough to proven: Benzene. Winslow (1927, a limit of 100 ppm, based > nmination of exposed work: inhalation. He recognizee poisoning would develop in ; centration, but believed it slowly enough to be detec medical examinations, and moval from exposure. Acute ing is fatal anesthesia, and ing is primarily injury to ti Benzene is particularly insk effects can progress to a fat all exposure ceases. Even of a high non-anesthetic ci be fatal. Patty (1948-9, p. 100 ppm has only a faint od p. 22S) investigated it r\- exposure he was convinced 40 to 80 ppm. The most important effet halation is chronic poison: the bone marrow. The 3c limit can be interpreted fr animation of exposed woi f'Squantitatively defined by o yfaappears low enough to pre tOnent of irreversible poisoi Benzyl chloride. This is w? > June, 1956 r jperation where oncentrations ranged i.m., found abnormali, electrocardiographic s from chronic throm- t effects of inhalation re chronic poisoning irdiographic changes, /er injury. The 0.5 mit can be interpreted peated inhalations and anen. It appears low ljury. ohthylthiourea). Mc1945) found consideres in acute oral toxicis, the most susceptible 03 gm./kg. Death was sion. Repeated doses Fitzhugh and Nelson ire not affected by 50 ver a two-year period. nt effect of ANTU in poisoning centering in /cu.m, tentative threshterpreted from the reil doses to rats. It corium daily absorption of ? * 0.05 mg./kg. This event injury, arner limit of 0.15 1 upon supposed quantilead. Watrous and Mcind workers exposed to .u.m. showed no sympenic poisoning causes i.L.O., 1930, I, p. 161): e, hyperemia, skin erup, keratosis, epithelial 3, cirrhosis, confusion, of eyes and respiratory red in the body, but not T j i ,^ ) l J f 1 | J j nt effect of inhalation of s chronic poisoning. The shold limit can be in results of examinations i. It appears low enough on and Haggard d943, lute arsine poisoning as : red blood cells with re kidney damage, and lung Industrial Hygiene Quarterly U7 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 mnrrow. 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, ku Schrenk and Yant (1935) found guinea pigstO tolerated 3000 ppm for several hours, and men found it irritating to nose and eyes. Q Nelson, Ege, Ross, Woodman and Silverman o % ,1 1-4S June, 195S Industrial Hygiene Q (1943) found slight throat irritation in un acclimated subjects at 100 ppm, irritation of eyes at 200 ppm and objectionable irrita tion at 300 ppm. Elkins (1950, p. 118) found complaints of nausea at 500 ppm, irritation at 300 ppm, but no ill effects at 700 ppm. Smyth (1937-55) found rats survived two hours at 2000 ppm but 4000 ppm killed four of six. He found that an episode of indus trial eye injuries during inhalation of butanone was caused by an unsaturated ketone impurity accidently present. The most important effect of butanone inhalation is narcosis. The 250 ppm thresh old limit can be interpreted from human sensory data. It appears low enough to pre vent definite narcosis. then depression and narcotic death with pul monary edema. Smyth (1937-55) found rats survive four hours at 2000 ppm but die from 4000 ppm. Injury to skin and cornea from the liquid is severe. Unreported industrial experience suggests skin injury is the great est practical hazard. ACGIH (1955b) cites unpublished industrial experience that levels above 5 ppm tend to be irritating. The most important effect of butyl amine inhalation is respiratory tract irritation, with lung edema the maximum injury. The 5 ppm threshold limit can be interpreted from analogy with ethyl amine. It is prob ably low enough to prevent injury. Butyl CELLOSOLVE (2-butoxyethanol). Werner, Nawrocki, Mitchell, Miller and von r h enough to prevent injurjfc Cadmium oxide fwme.\ the basis of anima) ex^: it is as toxic as lead. Sp Porter (1944) reported'^ ing and fatalities from f to the fume. Fairhall \ eludes inhalation cause: tion and pneumonitis, w duces gastro-intestinal C The most important of cadmium oxide fume jury, with systemic po; tant. The 0.1 mg./cu.m. i not be interpreted qua appears low enough to pr Calcium Arsenate. AQ 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 stantially saturated vapors are not killed hemoglobinuria, with lung, liver and kidney in four hours, but died within an eight-hour changes. Smyth (1937-55) found in rats inhalation period. fractional mortality from as little as 500 The most important effect of butyl acetate . ppm inhaled eight hours, with hematuria a f the tentative threshold' oral LD,0 of 100 mg./kgv. rats fed 5 mg., kg. for 45* The most important eii calcium arsenate dust poisoning, with broncl; important. The 0.1 r threshold limit should b the threshold limit for ; calcium arsenate is 20?. old limit of 2.5 mg./cu.r tent with the accepted dusts. 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 Cerfton dioxide. Flury quote Lehman-Hess to i sory response and single inhalations by that this is dangerous. ppm causes no noticeab animals. It is low enough to prevent defi The most important effect of butyl Cel- hours. Aero Medical A: nite narcosis. losolve inhalation is chronic poisoning, 52) considers the gas Butyl alcohol (n-butanol). Tabershaw, centering in the blood cells and kidney. The 30,000 ppm increasing Fahy and Skinner (1944) reported eye in 200 ppm threshold limit can be interpreted increasing pulse and 1 flammation in workmen above 50 ppm, but from results of repeated animal inhalation decreasing acuity of 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 symptoms arise above t1 for 30 minutes giving t lowed workmen for 10 years with butyl al it is obvious that the threshold limit for the toxication, and 70,000 t is 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 r: r t .1 ritation nor systemic effects were found at tained. 100 ppm, but there was some eye irritation Butyl mercaptan. Fieldner, et al. (1931) ing unconsciousness in The most important oxide inhalation is as; concentrations. The 5 at 200 ppm. Smyth (1937-55) found rats reports 733 ppm to be lethal to dogs in 30 n are not killed in four hours at 8000 ppm. minutes, indicating 20 times the acute 1 * The most important effect of butyl al toxicity of ethyl mercaptan. Effects like limit can be interpretei extensive human expi enough to prevent noth i f cohol inhalation is narcosis. The 100 ppm those of hydrogen sulfide are to be expected. Carbon disulfide. Wi threshold limit can be interpreted from an The most important effect of butyl mer Oettingen (1936) foun extensive study of workmen under condi captan is eye and respiratory tract irrita S: tions of known peak exposure. No narcotic tion. The 10 ppm tentative threshold limit &t' or irritative effects are to be anticipated. can be interpreted from the results of lim of 30 ppm has no : animals. Barthelemy juries to rayon workr Butyl amine. Hanzlik (1923) reported ited single inhalations by animals and an tions were kept below central nervous stimulation, convulsions. alogy with hydrogen sulfide. It appears low halations, it is mnrkc N June, 1956 . c with pul1-5aj found rats pm but die from ind cornea from iorted industrial ury is the greatH (1955b) cites rience that levels tating. :t of butyl amine tract irritation, mim injury. The n be interpreted mine. It is probt injury. 2-butoxyethanol). II, Miller and von 00 to 400 ppm, in :ed only small efon the blood piciller and von Oeting on single inepeated by dogs, tyl ether produces ill changes than do 3. They also found i, liver and kidney 5) found in rats n as little as 500 with hematuria a ; " nid penetrates ently toxic so ffect of butyl Celchronic poisoning, 11s and kidney. The can be interpreted 1 animal inhalation . from simultaneous d butyl Cellosolve eshold limit for the han for the former ection are to be at- l -J ^ i I \ j j jL f I ( j J j Idner, et al. (1931) lethal to dogs in 30 ) times the acute aptan. Effects like e are to be expected, effect of butyl meriratory tract irritaitive threshold limit i the results of limby animals and anilfide. It appears low \ Industrial Hygiene Quarterly 149 enough to prevent injury and eye irritation. Cadmium oxide fume. Prodan (1932) on the basis of animal experiment concluded it is as toxic as lead. Spolyar, Keppler and Porter (1944) reported on serious poison ing and fatalities from industrial exposure to the fume. Fairhail (1949, p. 45) con cludes inhalation causes bronchial irrita tion and pneumonitis, while ingestion pro duces gastro-intestina! disturbances. The most important effect of inhalation of cadmium oxide fume is severe lung in jury, with systemic poisoning less impor tant. The 0.1 mg./cu.m. threshold limit can not be interpreted quantitatively, but it appears low enough to prevent injury. Calcium Arsenate. ACG1H (1954b) bases the tentative threshold limit upon a rat oral LD,,W of 100 mg./kg., and blind litters.in rats fed 5 mg./kg. for 45 days. The most important effect of inhalation of calcium arsenate dust is chronic arsenic poisoning, with bronchial irritation less important. The 0.1 mg./cu.m. tentative threshold limit should be interpreted from the threshold limit for arsenic dusts. Since calcium arsenate is 20% arsenic, a thresh old limit of 2.5 mg./cu.m. would be consis tent with the accepted limit for arsenic dusts. Carbon dioxide. Flury and Zernik (1931) quote Lehman-Hess to the effect that 5500 ppm causes no noticeable symptoms in six hours. Aero Medical Association (1953, p. 52) considers the gas as weakly narcotic, 30,000 ppm increasing respiration by 90%, increasing pulse and blood pressure, and decreasing acuity of hearing. Subjective symptoms arise above this level, 50,000 ppm for 30 minutes giving the first signs of in toxication, and 70,000 to 100,000 ppm caus ing unconsciousness in a few minutes. The most important effect of carbon di oxide inhalation is asphyxia at very high concentrations. The 5000 ppm threshold limit can be interpreted from the results of extensive human experiments. It is low enough to prevent noticeable effects. Carbon disulfide. Wiley, Hueper and von Oettingen (1936) found repeated inhalation of 30 ppm has no significant effect on animals. Barthelemy (1939) found no in juries to rayon workmen when concentra tions were kept below 30 ppm. In single in halations, it is markedly narcotic, and in repeated exposure the effects may be neuro logical, not recognized by the victim. Hen derson and Haggard (1943, p. 223) state that 480 to 1600 ppm is the maximum breathable for one hour without serious dis turbance. The most important effect of carbon di sulfide inhalation is chronic poisoning with centra! nervous system effects. The 20 ppm threshold limit can be interpreted from the results of repeated animal inhalations and examination of exposed workmen. It is low enough to prevent injury. Carbon monoxide. Henderson, Haggard, Teague, Prince and Wunderlich (1931) sug gested a limit of 100 ppm on the basis of extensive human experiment. Sayers, Yant, Levy and Fulton (1929) showed 200 ppm caused slight symptoms in humans. Sievers, Edwards, Murray and Schrenk (1942) found 70 ppm over a 13-year period had not affected health. Carbon monoxide is a chemi cal asphyxiant, acting by combining with hemoglobin. Henderson and Haggard (1943, p. 167) define its effects in terms of the product of time and concentration, 100 ppm for three hours producing no effect; for six hours, a just appreciable effect; for nine hours, headache and nausea; and for 15 hours, danger. One hour at 4000 ppm may be fatal. Vigliani and ZurJo (1955) study ing 100 workers found no injury to health at 100 ppm for eight hours every day. In the United States chronic poisoning is not considered a reality. The most important effect of carbon mon oxide inhalation is chemical asphyxia, re ducing the oxygen carrying power of the blood. The 100 ppm threshold limit can be interpreted from the results of extensive human experiment and examination of ex posed workman. It will prevent injury, but will allow a recognizable effect if inhaled for eight hours. Carbon tetrachloride. Elkins (1950, p. 229) on the basis of industrial experience, concluded the earlier figure of 100 ppm was too high and suggested 40 ppm. Adams, Spencer, Rowe, McCollister and Irish (1952) in extensive animal studies, found some ef fect on the liver in some species at all con centrations above 5 ppm. Smyth (1937-55) found rats survive eight hours at 3000 ppm, but 8000 ppm is fatal. Human anesthesia, or near anesthesia, is usually fatal from 2200966-2 150 June, 1956 ;idney 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. Rats 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. Chlordane. 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. showed no clinical evidence of effect. Alvarez and Hyman (1953) examined men in another producing plant with up to five years ex posure and found no effects, but concentra tions were not measured. Ingle (1953) shows that early reports of inhalation in jury in animals were due to a volatile un reacted intermediate in the early product, and that 14 days continuous inhalation of saturated air does not injure mice. ACGIH (1954b) bases its tentative threshold limit on a rat oral LD-,, of 590 mg./kg. The most important effect of chlordane inhalation is chronic poisoning-centering in the liver. The 2 mg./cu.m. threshold limit can be interpreted from the results of ex aminations of exposed workmen. It is low enough to prevent injury. Chlorinated camphene, 60% (toxaphene). Lackey (1949) found an oral dose of 10 mg./kg. caused convulsions in dogs while 15 mg./kg. was fatal. A daily dose of 4 mg./kg. for 106 days was not fatal, but at times con vulsions were seen. Liver and kidney changes resulted. The most important effect of chlorin ated cnmphene is chronic poisoning center ing in the liver. The 0.5 mg./cu.m. tentative threshold limit can be interpreted from the results of single and repeated oral doses, and by analogy with the similar but less toxic DDT. It appears low enough to pre vent injury. Chlorinated diphenyl oxide. After exten sive inhalation studies with rats. Drinker (1949) concluded that 0.5 mg./cu.m. is a permissible concentration which will not lead to systemic injury'. Liver injury is the effect of chronic poisoning. Smyth (193755) found the material penetrates the skin, and repeated contact leads to chloracne. The most important effect of chlorinated diphenyl oxide 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. Chlorine. Sklyanskaya and Rappaport (1935) found lung injuries and increased in cidence of pneumonia in guinea pigs re 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 Industrial Hygiene Qua to 60 ppm may lead to pna T edema, 30 ppm causes 9 \ throat irritation and 3.5 p| I Patty (1943-9, p. 547) co| is tolerable, 3 to 6 ppm In The most important e* of chlorine gas is respire r tion, with lung edema th<* The 1 ppm threshold limit* from repented animal inhs V sensory data. It is low injury. ; Chlorine trifluoride. 5 (1955) found it an extre tant. Rats are killed in ppm, while rats and dogs i peatedly are severely inj was increased and there wt ficultv in all. The vapors j Horn and Weir (1956) & halation of 1.17 ppm by 1 jured only by increased ir monia. $ The most important efE r of chlorine triiluoride gr tract irritation, with lunc mum effect. The 0.1 ppm t! be interpreted from repear tion. It appears low enoujury. Chlorobenzene. FairhaH concludes it is somewhat, benzene, but finds no evi' poetic effect. ' The most important et: zene inhalation is narco C threshold limit can be int. i' rough estimate. Ry comp, chlorinated hydrocarbons, enough to prevent injury Chlorobromomcthane. 5' Alford and von Oettingen ppm to be the LCr,0 for n inhalations. Exposures of dogs to 1000 ppm seven days a week for fourteen out effect. Non-progressiv found from single inhalat: kidney remained normal di inhalations. Comstock et light narcosis in rats and : ppm for 10 to 15 minutes. .tvppm was fatal within 15 Qnary edema was present i: I The most important efft Ik June, 1956 _u.ml showed ct. Alvarez and men in another o five years ex5, but concentra. Ingle (1953) )f inhalation in to a volatile un,e early product, >us inhalation of ire mice. ACGIH e threshold limit ng./kg. :ect of chlordane ning-centering in 1. threshold limit ;he results of exirkmen. It is low >0% (toxaphene). oral dose of 10 3 in dogs while 15 dose of 4 mg./kg. , but at times coniver and kidney effect of chlorin. poisoning centerng./eu.m. tentative terpreted from the ted oral doses, similar but less ow enough to pre side. After extenwith rats, Drinker 0.5 mg./cu.m. is a in which will not Liver injury is the ing. Smyth (1937penetrates the skin, ds to chloracne. iffect of chlorinated n is chronic poisonr. The 0.5 mg./cu.m. nterpreted from the lal inhalations. It is ijury. /a and Rappaport ies and increased inin guinea pigs re0 1.7 ppm. Fairhall ; irritates eyes and atal lung irritation. 1 is rapidly fata], 40 l t Industrial Hygiene Quarterly 151 to 60 ppm may lead to pneumonitis and lung edema, 30 ppm causes coughing, 15 ppm throat irritation and 3.5 ppm can be smelled. Patty (194S-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 limit 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 3000 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 nonprogressive effects on liver ami 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 (42c,c 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 chloraene. 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, 5ic/c 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 & to 01 JS* 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. l-Chloro-l-nitropropane. Machle, Scott, Treon, Heyroth and Kitzmiller (1945) ex posed animals for six hours to 400 ppm. Ef fects were chiefly irritation of eye, nose bronchi and lung, with some injury to liver, kidney and vascular system, and 25% died. Simultaneous repeated studies on 1,1-dichloro-l-nitroethane showed little cumula tive action. The most important effect of 1-chloro-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 (19.49) 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- ury. Chloroprene (2-cMorobutadiene). Von Oettingen, Hueper, JDeichmann-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 (1956) 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 LDr>0 of 1500 mg./kg., that 10 mg./cu.m. is a fit limit. Smyth (1937-55) found death from a single oral dose due to respiratory paralysis with injuy to liver and kidney. Rats are not affected by 0.02% in their diet for two years, and 0.06% causes minor effects on liver and kidney. The most important effect of CRAG her bicide inhalation is chronic poisoning'cen tering in the liver. The 15 mg./cu.m. thresh old limit can be interpreted from the results of single and repeated oral doses to animals. It appears low enough to prevent injury. Cresol. Fairhall (1949, p. 271) concludes effects and practical hazards are like those of phenol. Smyth (1937-55) found rats sur vive eight hours inhalation of vapors sub stantially saturated at room temperature. The liquid penetrates the skin to a danger ous extent, and causes severe skin and cor neal injury. The odor appears to be some what more intense than that of phenol. Although cresol vapors are odorous and irritating, their major effect is chronic systemic poisoning. The 5 ppm threshold limit can be interpreted from analogy with phenol. It appears, to be low enough to pre vent chronic poisoning. Cyanide as CN. To the extent that cya nide dusts dissolve, their toxicity is that of hydrogen cyanide, with some added local ir ritation due to hydrolysis on moist tissue. Cyanide dust equivalent of the 10 ppm threshold limit for hydrogen cyanide is 11 mg./cu.m. The 5 mg./cu.m. threshold limit is about half that for hydrogen cyanide, and hence is conservative. Cyclohexane. Treon, Crutchfield and Kitzmiller (1943) found minor liver and kidney changes in animals repeatedly in haling 786 ppm, none at 434 ppm. Fairhall (1949, p. 273) concludes acute poisoning is anesthesia and that repeated inhalation causes no hematopoetic changes. Patty Industrial Hygiene Quarter^ (1948-9, p. 769) reports 300 y tinct odor or irritation. The most important effect^ inhalation is narcosiB, with n organic effects. The 400 ppnf it can be interpreted from?' peated animal inhalation. It* to prevent definite narcosis. * Cyclohexanol. Treon, Crutci miller (1943) reported that r tion of 693 ppm caused mir._ cal changes in a monkey, a*, the livers and kidneys of r! Ege, Ross, Woodman and Sib found 100 ppm causes obj; nose and throat irritation i subjects. Smyth (1937-55) kill rats by eight hours inh. stantialiy saturated vapors. ; The most important effect; inhalation is narcosis, with v organic effects less prominent threshold limit can be interp suits of repeated animal ii human sensory data. It is prevent significant narcosis not to prevent irritation. Cyclohexanone. Treon, C Kitzmiller (1943) in aninii found only narcosis and irri Ege, Ross, Woodman and Sif found 50 ppm caused objectii and throat irritation in un: jects. Smyth (1937-55) did four hours at 4000 ppm, caused anesthetic death. The most important effec none inhalation is narcosis, threshold limit can be inter peated animal inhalations a sory response. It is probabl; prevent definite narcosis. Cyclohexene. Fairhall (19 eludes that 9000 ppm causes animals, while 13,500 to 1C anesthetic death. This indi greater than that of cycloh The most important effec inhalation is narcosis. The old limit can be interpreted single animal inhalations. 1 to prevent definite narcosis Cyclopropane. Fairhall ( views reports of experience thesia and concludes there June, 1956 xt .ed to 0.11 of inhalation jer respiratory perforation of ./cu.m, thresh:rom studies of enough to pre- (1954b) sugral low toxicity ng./kg., that 10 lyth (1937-55) oral dose due h injuy to liver 'ected by 0.02% .rs, and 0.06% r and kidney, t of CRAG her. poisoning cenig./cu.m. threshfrom the results loses to animals, event injury. . 271) concludes Is are like those found rats suri of vapors sub orn temperature, sk'n to a danger- skin and cor<-. .s to be somenat of phenol, are odorous and effect is chronic 5 ppm threshold com analogy with nv enough to pre- : extent that cyatoxicity is that of me added local ir3 on moist tissue. of the 10 ppm gen cyanide is 11 m. threshold limit hydrogen cyanide, e. Crutchfield and l minor liver and als repeatedly in434 ppm. Fairhall acute poisoning is jpeated inhalation c changes. Patty r Industrial Hygiene Quarterly 155 (1948-9, p. 769) reports 300 ppm has no dis tinct odor or irritation. The most important effect of cyclohexane inhalation is narcosis, with non-progressive organic effects. The 400 ppm threshold lim it can be interpreted from results of re peated animal inhalation. It is low enough to prevent definite narcosis. Cyclohexanol. Treon, Crutchfield and Kitzmiller (1943) reported that repeated inhala tion of 693 ppm caused minimal pathologi cal changes in a monkey, and 145 ppm in the livers and kidneys of rabbits. Nelson, Ege, Ross, Woodman and Silverman (1943) found 100 ppm causes objectionable eye, nose and throat irritation in unacclimated subjects. Smyth (1937-55) was unable to kill rats by eighc hours inhalation of sub stantially saturated vapors. The most important effect of cyclohexanol inhalation is narcosis, with non-progressive organic effects less prominent. The 100 ppm threshold limit can be interpreted from re sults of repeated animal inhalations and human sensory data. It is low enough to prevent significant narcosis or injury, but not to prevent irritation. Cyclohexanone. Treon, Crutchfield and Kitzmiller (1943) in animal experiments found only narcosis and irritation. Nelson, Ege, Ross, Woodman and Silverman (1943) found 50 ppm caused objectionable eye, nose and throat irritation in unacclimated sub jects. Smyth (1537-55) did not kill rats by four hours at 4000 ppm, but 8000 ppm caused anesthetic death. The most important effect of cyclohexa none inhalation is narcosis. The 100 ppm threshold limit can be interpreted from re peated animal inhalations and human sen sory response. It is probably low enough to prevent definite narcosis. Cyclohexene. Fairhall (1949, p. 279) con cludes that 9000 ppm causes mild narcosis in animals, while 13,500 to 15,000 ppm gives anesthetic death. This indicates a toxicity greater than that of cyclohexane. The most important effect of cyclohexene inhalation is narcosis. The 400 ppm thresh old limit can be interpreted from results of single animal inhalations. It is low enough to prevent definite narcosis. Cyclopropane. Fairhall (1949, p. 280) re views reports of experience in surgical anes thesia and concludes there is no toxic haz ard in industrial use. The most important ef fect of cyclopropane gas inhalation is narco sis. The 400 ppm threshold limit can be in terpreted from analogy with cyclopentane, and by human surgical use. It is probably low enough to prevent definite narcosis. 2,4-D. Rowe and Hymas (1954) conclude that it has a low degree of chronicity, and the acute LDr,,, values range from 300 to 1000 mg./kg. for various species. The most important effect of 2,4-D inhala tion is chronic poisoning centering in the liver. The 10 mg./cu.m. threshold limit can be interpreted from the results of single and repeated oral doses to animals. It appears low enough to prevent injury. DDT. Barnes (1953) finds no incidence of illness among workers using it throughout the world. Poisoning from accidental inges tion is marked by abdominal pain, vomit ing, dizziness and weakness. Long repeated doses of 25 to 50 mg./kg. are required to poison animals, although man is probably more sensitive. The most important effect of DDT inhala tion is chronic poisoning centering in the liver. The 1 mg./cu.m. tentative threshold limit can be interpreted from the results of repeated oral doses to animals. It appears low enough to prevent injury. Decaborane. Svirbely (1954a,b) found the LC50 for mice inhaling vapors for four hours to be 25.7 ppm. Symptoms included central nervous excitability and corneal opacity. Six-hour inhalations of 20 ppm by rats, repeated 20 times, killed some with fatty livers and central nervous excitability. Comstock and Oberts (1953) report that the median detectable odor is 0.35 mg. cu.m. (0.07 ppm), described as foul or chocolate like. The most important effect of decaborane inhalation is acute toxicity involving the central nervous system, with liver injury less important. The 0.05 ppm tentative threshold limit can be interpreted from lim ited animal inhalations. It appears to allow an adequate margin of safety. Diacetone alcohol. Von Oettingen (1943, p. 138) reports animals at 2100 ppm are restless, irritation and kidney effects are noted. He concludes it is twice as toxic as acetone. Silverman, Schulte and First (1946) found 100 ppm irritating to eyes, nose and throat but not intolerable in un- G96&Z -i ii, 3 ' 154 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. Diborane 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. Fairhall (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-dichloroethane 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-diehlor- oethylene 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 threshold limit can be interpreted from the results of single animal inhalations. It Industrial Hygiene Q* seems to be low enouj Dichioromonoflnoron, (1933) showed it is 3 other fluorocarbons ir? They are practically is The most important monofluoromethane ini from extremely highy 1000 ppm threshold ; preted by analogy wistrefrigerants. It represe control rather than a 1 1,1-Dichloro-l-nitrot^ Treon, Heyroth and; found 25 ppm did not k of 204 hours inhalatlr tated eyes, nose, broncF jury to liver, kidney an. The most important r 1-nitroethane inhalatio'i 10 ppm threshold limit from the results of rep tions. It appears low injury. Dichlorotct rafiuaroec (19331 and Yant, Schrc found only transient d exposed two hours to 2 ic effects are to be expo ologically inert materi; The most importan; tetrafluorethane inhala very high concentrati threshold limit can be results of single anira pears to be far below level. Diehlrin. The workei and Spurbeck (1951) dustrial exposure to s< cides including dieldrii of the order of 5 mg./ dence of clinical effect (1955) found 25 ppm two years did not sho are most sensitive, ti. Chronic toxicity cent acute poisoning, centi citation is prominent the skin. The most importan halation is chronic p the liver. The 0.25 mg can be interpreted ft peated oral doses to ; June, 1956 I i jphyxia from atiuiis. The 1000 e interpreted from .nimal inhalations, gineering control it. nderson and Hagude it is similar to Smyth (1937-55) hours at 4000 ppm, pm, an acute toxici2traehloride. In re ts and dogs, chron3 than that of carrfewise found. fleet of 1,1-dichlorchronic poisoning, he 100 ppm thresh- ted from single and ons. It may be low y, but new data are :rent views on car- Fairhall (1949, p. 50,000 ppm is lethal .,000 ppm produces g consists of narcos system irritation, i found. The vapors 1937-55) found the p' ' anesthetize rats hile 16,000 ppm linutes and killed in isomer was twice as effect of 1,2-dichlor. narcosis. The 200 be interpreted from limal inhalations. It t definite narcosis. Schrenk, Patty and ) to 1000 ppm killed 0 minutes with lung i, while 35 ppm pron several hours. This nelled but is not im) man, while 500 to lg. Smyth (1937-55) r hours at 125 ppm, pm. Skin penetration is. effect of dichloroethyl X injury. The 15 ppm interpreted from the imal inhalations. It I *4 ( .f . : L f ! j I Industrial Hygiene Quarterly 155 seems to be low enough to prevent injury. Dichloromonofiuoromethane. Nuckolls (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. Dichlorotetrajhioroethane. Nuckolls (1933) and Yant, Schrenk and Patty (1932) found only transient discomfort in animals examination of exposed workmen. It is low enough to prevent injury. Dietltylamine. 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 mortality 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 diethylnmine 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. ACG1H (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, ? exposed two hours to 25,000 ppm. No chron in comparison with carbon tetrachloride, ic effects are to be expected from this physi ethyl and methyl bromide. It appears low ologically inert material. enough to prevent injury. The most important effect of dichloro- Diisobutyl ketone. Silverman, Schulte and tetrafluorethane inhalation is asphyxia from First (1946) found concentrations above 25 very high concentrations. The 1000 ppm ppm give eye irritation in unacclimated sub threshold limit can be interpreted from the jects. Carpenter, Pozzani and Weil (1963) results of single animal inhalations. It ap found single eight-hour inhalations of 200 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 pehetrates 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 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. 2,1-Diisocyanotolnene. Swenson, Holm- quist 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 bv sensitization ** V* 2? `i o 156 June, 1956 .nd' asthma-like attacks. Unpublished American experience features sensitization. The most important effect of 2,4-diisocyanotoluene inhalation is respiratory tract 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 (1043, 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. Von 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-o- cresol 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 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, and from skin absorption. Silverman, Schulte 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 ceptible, repeated inhalation at 800 ppm killing some with kidney injury within 30 days. The most important effect of dioxane in halation is chronic poisoning, centering in the liver and kidney. The 100 ppm thresh old limit can be interpreted from results of repeated animal exposure studies. It ap peal's to be low enough to prevent injury. EPN. Hodge, Maynard et al (1954) found the acute oral LD50 for rats ranges from 7 to 33 mg./kg., while 75 ppm in the diet is without effect during two years. The ma- Industrial Hygiene Q terial i3 a choiinestera symptoms of excess in ainj to excitability and treroc be Vs to Vs as toxic as paj The most important effe. tion is the reduction of bl& The 0.5 mg./cu.m. thresh interpreted from the resu doses to animals and arC thion. It appears low enou. jury. Ethyl acetate. The unac of Nelson, Ege, Ross, Wop man (1943) found an obj odor at 200 ppm and eye; irritation at 400 ppm. Her gard (1943, p. 222) ec; 20,000 ppm is dangerou poc.ures. It is mildly nare produce systemic effects. (: found rats inhaling 8000 p; survive, but 16,000 ppm k: The most important effe. inhalation is narcosis. The old limit can be interpret* sory data and results of r by animals. Ic apparently^ prevent definite narcosis. . Ethyl acrylate. Pozzani penter (1949) found 30 i: ppm injured lungs, liver rats and rabbits, while 70 jure rats. They found thai detectable by odor, and th. ppm is objectionable. Treon and Kitzmiller (1949) similar results. The most important effc ate inhalation is respirator The 25 ppm tentative thre; interpreted from repeatc tion results and limited hu: It appears low enough to Ethyl alcohol. Headers (1943, p. 219) consider its but not toxic. Only unde; cumstances can inhatatlor toxication. They estimab eight hours is not sufficie earliest stage of intoxicat (1945) stated that indus S3000 ppm has led only to n kEfcye irritation. Patty (19/ Swludes 6000 to 9000 ppm i C&blv irritating, but that n Oo June, 1956 ; u inhalation of >oisoning. The 1 >ld limit appears able assumption times as toxic as ore (1943) re>m inhalation of we, Adams and periments, found dose for animals. ;abolic stimulant, re to the point of produced in suscity is low. feet of dinitro-o>oisoning, marked with rise of body r./cu.m. threshold from the facts of It appears low .ttingen (1941. p. milar to trinitroen pure. The dust irritation, effect of dinitrohronic poisoning, ous system, liver .rrhe 1.5 mg./cu.m. reted from ant. It does not aplt all injuries. >n and Ford-Moore kidney injury in ing 1000 ppm, and lilverman, Schulte ye, nose and throat unacclimated sub57) concludes there . 200 ppm. Smyth s particularly susation at 800 ppm y injury within 30 ffect of dioxane inoning, centering in le 100 ppm thresh;ted from results of ire studies. It ap;o prevent injury, ietal (1954) found rats ranges from 7 ppm in the diet is wo years. The ma- 1 (*- . ( V ./ ' ' -lndustrial Hygiene Quarterly 157 terial is a cholinesterase inhibitor, and symptoms of excess in animals are confined to excitability and tremors. It appears to be Vs to Vs as toxic as parathion. The most important effect of EPN inhala tion is the reduction of blood cholinesterase. The 0.5 mg./cu.m. threshold limit can be interpreted from the results of single oral doses to animals and analogy with para thion. It appears low enough to prevent in jury. Ethyl acetate. The unacclimated subjects of Nelson, Ege, Ross, Woodman and Silverman (1943) found an objectionably strong odor at 200 ppm and eye, nose and throat irritation at 400 ppm. Henderson and Hag gard (1943, p. 222) conclude 10,000 to 20,000 ppm is dangerous for short ex posures. It is mildly narcotic but does not produce systemic effects. Smyth (1937-55) found rats inhaling 8000 ppm for four hours survive, but 16,000 ppm kills. The most important effect of ethyl acetate inhalation is narcosis. The 400 ppm thresh old limit can be interpreted by human sen sory data and results of single inhalations by animals. It apparently is low enough to prevent definite narcosis. Ethyl acrylate. Pozzani, Weil and Car penter (1949) found 30 inhalations of 300 ppm injured lungs, liver and kidneys of rats and rabbits, while 70 ppm did not in jure rats. They found that 8 ppm is readily detectable by odor, and that the odor of 50 ppm is objectionable. Treon, Sigmon, Wright and Kitzmiller (1949) obtained closely similar results. The most important effect of ethyl acryl ate inhalation is respiratory tract irritation. The 25 ppm tentative threshold limit can be interpreted from repeated animal inhala tion results and limited human sensory data. It appears low enough to prevent injury. Ethyl alcohol. Henderson and Haggard (1943, p. 219) consider its vapors anesthetic but not toxic. Only under exceptional cir cumstances can inhalation cause slight in toxication. They estimate 1064 ppm for eight hours is not sufficient to produce the earliest stage of intoxication in man. Cook (1945) stated that industrial exposure at 1000 ppm has led only to a few complaints of eye irritation. Patty (1948-9, p. 851) con cludes 6000 to 9000 ppm is initially intoler ably irritating, but that acclimatization fol- lows. Smyth (1937-55) found rats survive eight hours at 16,000 ppm but some are killed at 32,000 ppm. The most important effect of ethyl alco hol inhalation is narcosis. The 1000 ppm threshold limit can be interpreted from human physiological data. It is low enough to prevent significant narcosis, but some eye irritation will result. Ethyl amine. Brieger and Hodes (1951) exposed rabbits repeatedly to 50 ppm and found lung and corneal injury, with some ef fect on heart muscle. Smyth (1937-55) found four hours at 4000 to 8000 ppm kills some rats, and 16,000 ppm kills all. Respira tory tract irritation is prominent. The liquid is extremely injurious to the cornea. The most important effect of ethyl amine inhalation is respiratory tract irritation, with lung edema the maximum injury. The 25 ppm threshold limit can be interpreted from results of repeated animal inhalation. It appears low enough to prevent injury. Ethyl benzene. Yant, Schrenk, Waite and Patty (1930).found only slight irritation in guinea pigs breathing 1000 ppm for eight hours. Fatalities from higher levels showed lung edema. Humans found 1000 ppm was initially irritating to the eyes and 2000 ppm caused throat irritation, constriction in the chest and slight intoxication. Smyth (193755) found rats not killed by four hour's at 2000 ppm, while 8000 ppm is fatal. There is general agreement that it does not exert the hematopoetic effects of benzene. The. most important effect of ethyl ben zene inhalation is narcosis, with irritation of the entire respiratory tract contributing to injury. The 200 ppm threshold limit can be interpreted from results of single animal inhalations and limited human sensory re sponse. It is low enough to prevent injury. Ethyl bromide. Waite and Yant (1928) found lung edema a prominent effect of guinea pig inhalation. Sayers, Yant, Thomas and Bferger (1929) found several hours in halation of 1700 ppm by animals was with out effect. Henderson and Haggard (1943, p. 207) note that vapors are not narcotic. The most important effect of ethyl bro mide inhalation is respiratory tract irrita tion. The 200 ppm threshold limit can be in terpreted from the results of single animal inhalations. It is probably low enough to pre vent injury. Qi 158 June, 1956 Industrial Hygiene Q 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 irritation, kidney damage and sensitiza tion. The 10 ppm threshold limit can be in terpreted from results of repeated animal inhalation and human sensory data. It is low enough to prevent irritation and in jury, but probably not to eliminate re sponse by persons already sensitized. Ethylene dibromide. Rowe, Spencer, McCollister, Hollingsworth and Adams (1952) found four species of animals tolerated re peated inhalation of 25 ppm, but not 50 ppm. Major injury was in lung and liver, with kidney and central nervous system less prominent. The liquid penetrates the is 2236 ppm, 500 ppm to rats and guinea pigs, eight hours, and 10 ppi hours. Symptoms and due to kidney tubula lung and liver injury smell 2 ppm, while lOttv tate eyes and nose. TheS skin, produces severe^ burns, and sensitizes tjf The most important imine inhalation is ncuV ing in the kidney, with J? importance. The 6 pprrf exposure of 305 ppm for two hours. Animal skin. It is painful in the eye, but causes be interpreted from rest 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 only transient injury. The odor of a con centration dangerous to life is definite and sickening. The most important effects of ethylene dibromide inhalation are respiratory tract irritation and liver injury. The 25 ppm threshold limit can be interpreted from the inhalation studies and*; sory data. It is nppar<? prevent poisoning an<f tract irritation. h Ethylene oxide. Wait (1930) in single anima no symptoms from eigh'; ppm killed animals, with evidence of poten results of repeated animal inhalations. It fi4 3 tial chronic effect. They conclude no concen is probably low enough to prevent injury. tration is safe for daily exposure. Smyth Ethylene dichloride. Spencer, Rowe, Greater concentrations ; irritation, narcosis, bro tation. Sensory response r\t and Carpenter (1945) point out very rapid Adams, McColiister and Irish (1951) study skin penetration of the liquid, the absence ing repeated inhalation by animals, found low concentrations, but tion are intolerable at of warning skin irritation and the failure of no effect from 100 ppm. Single dangerous rubber gloves to protect. inhalations irritate the lung and depress the Sexton and Henson (If tention to spectacular I The most important effect of ethylene central nervous system, while dangerous re with sensitization, whici chlorhydrin inhalation is acute poisoning, peated inhalations injure liver and kidney. with the liquid and it.- centering in the kidney. The 5 ppm thresh They feel chronic intoxication is unlikely Smyth (1937-55) foum old limit can be interpreted from the re because tolerated repeated inhalations are hours at.4000 ppm but sults of single animal inhalations. It appears close to concentrations tolerated once. Con ppm. Hollingsworth, Iti low enough to prevent injury. centrations sufficient to cause marked nar ter and Spencer (1956) Ethylene diamine. Dernehl (1951) re cosis are irritating to the upper respiratory ly inhaling 204 ppm f< lated industrial experience showing this is a tract. Adams, Spencer, Rowe, McColiister and some fatalities, w sensitizer upon contact and inhalation. and Irish (1952) simultaneously studying kidney, adrenal and to Pozzani and Carpenter (1954) exposed rats carbon tetrachloride, found it at least four were not affected at 4`. repeatedly to the vapors. All died within 20 times as toxic as ethylene dichloride. Elkins tolerated 113 ppm. Jm days at 484 ppm, with loss of hair, injury to (1950, p. 137) found complaints of nausea Feinsiiver (1956) with the kidney and lesser effects on liver and from industrial exposures to 100 to 150 ppm. found some fatalities f: lung. There was no effect except loss of hair Patty (1948-9, p. 805) finds little odor at at 132 ppm, and none whatever at 59 ppm. 100 ppm, slight eye and nose irritation at tion of 400 ppm, but It feet. 9 Very brief human exposures found 100 ppm 1000 ppm. inoffensive, tingling of skin and nose at The most important effect of ethylene The most importani oxide inhalation is resj 200 ppm and intolerable sensory response at dichloride inhalation is chronic poisoning, 400 ppm. Smyth (1937-55) found eight centering in the liver. The 100 ppm thresh tion leading, to lung i to liver and kidney ari hours at 2000 ppm did not kill rats while old limit can be interpreted from the results 100 ppm threshold lim 4000 ppm was fatal. Death was due chiefly of repeated animal inhalations and human from results of repeat to kidney injury, with some injury to lung. response. It is low enough to prevent injury. studies. It appears lot The liquid irritates the skin and severely in Ethylene imine. Silver and McGrath JO >njury. jures the cornea. (1948) and Carpenter, Smyth and Shaffer Is, Ethyl ether. Ilendi The most important effects of ethylene (1948) studied single inhalations in animals. ll Idiamine inhalation are respiratory tract The LC.,o for mice in a 10-minute exposure (1943, p. 195) estii ^ human blood concentri Sr W tO J June, 1956 incL sensitiza)1q limit can be in>f repeated animal ensory data. It is irritation and in: to eliminate rey sensitized. (owe, Spencer, Mcand Adams (1952) limals tolerated re; ppm, but not 50 in lung and liver, al nervous system [uid penetrates the he eye, but causes The odor of a conto life is definite effects of ethylene e respiratory tract jury. The 25 ppm nterpreted from the mal inhalations. It , to prevent injury. Spencer, Rowe, Irish (1951) studyi by animals, found n. Single dangerous lung and depress the while dangerous re- 'iver and kidney, ition is unlikely ited inhalations are tolerated once. Coni cause marked narhe upper respiratory , Rowe, McCoilister rltaneously studying jund it at least four ne dichloride. Elkins ;omplaints of nausea :es to 100 to 150 ppm. i finds little odor at ad nose irritation at t effect of ethylene ;s chronic poisoning. The 100 ppm thresheted from the results halations and human igh to prevent injury. .ilver and McGrath , Smyth and Shaffer nhalations in animals, a 10-minute exposure * H i l .( j" ] I I j <\ 1 Industrial Hygiene Quarterly 159 is 2236 ppm, 500 ppm for one hour is fatal to rats and guinea pigs, 25 ppm kills some in eight hours, and 10 ppm kills none in eight hours. Symptoms and death are delayed, due to kidney tubular injury, with lesser lung and liver injury. Humans can barely smell 2 ppm. while 100 ppm begins to irri tate eyes and nose. The liquid penetrates the skin, produces severe skin and corneal burns, and sensitizes the skin. The most important effect of ethylene imine inhalation is acute poisoning, center ing in the kidney, with lung injury of lesser importance. The 5 ppm threshold limit can be interpreted from results of single animal inhalation studies and limited human sen sory data. It is apparently low enough to prevent poisoning and upper respiratory tract irritation. Ethylene oxide. Waite, Patty and Yant (1930) in single animal inhalations found no symptoms from eight hours at 250 ppm. Greater concentrations caused eye and nose irritation, narcosis, bronchial and lung irri tation. Sensory response is only moderate at low concentrations, but eye and nose irrita tion are intolerable at high concentrations. Sexton and Henson (1950) have called at tention to spectacular human skin injuries with sensitization, which arise from contact with the liquid and its aqueous solutions. Smyth (1937-55) found rats survive four hours at.4000 ppm but are killed by 8000 ppm. Hollingsworth, Rowe, Oyen, McColIister and Spencer (1956) in animals repeated ly inhaling 204 ppm found lung irritation and some fatalities, with injury to liver, kidney, adrenal and testes. Rats and mice were not affected at 49 ppm, other species tolerated 113 ppm. Jacobson, Hackley and Feinsilver (1956) with dogs, rats and mice found some fatalities from repeated inhala tion of 400 ppm, but 100 ppm had little af fect. The most important effect of ethylene oxide inhalation is respiratory tract irrita tion lending to lung injury, while injury to liver and kidney are less important. The 100 ppm threshold limit can be interpreted from results of repeated animal inhalation studies. It appears low enough to prevent injury. Ethyl ether. Henderson and Haggard (1943, p. 195) estimate the maximum human blood concentration from inhalation of 400 ppm is 0.018 gm.-l., enusing r.o in toxication, while 2000 ppm will give n blood level of 0.09 gm./l., corresponding to insta bility in some persons. They state 35,000 ppm anesthetizes in 30 minutes, and a higher concentration kills by respiratory paralysis. Experience in human anesthesia shows that pneumonitis may follow ether anesthesia, but other injuries are unlikely. Nelson, Ego, Ross, Woodman and Silverman (1913) found nasal irritation at 200 ppm with unac climated subjects, somewhat greater at 300 ppm. The most important effect of ethyl ether inhalation is narcosis. The 100 ppm thresh old limit can be interpreted from human physiological and sensory data. It is low enough to prevent definite narcosis. Ethyl formate. Flurv and Zernik (1931) reported 330 ppm causes in man slight eve irritation and rapidly increasing nasal irri tation, while 10,000 ppm is anesthetic and fatal. Fairhall (1919, p. 341) notes its ef fects are irritation and narcosis, and that there is no chronic toxicity. Smyth (193755) found rats survive four hours inhala tion of 4000 ppm but die from 8000 ppm. The most important effect of ethyl for mate inhalation is narcosis. The 100 ppm threshold limit can be interpreted from scanty human sensory data and single animal inhalations. It appears to be low enough to prevent definite narcosis and irri tation. Ethyl mercaptan. Sayers, Fieldner, Yant, I.eitch and Pearce (1930) report the odor detectable at one part per billion and dis agreeable at one part per fifteen million. They quote that its effects are like those of hydrogen sulfide, and by analogy with butyl mercaptan they conclude more than 733 ppm is required to kill in 30 minutes. Flury and Zernik (1931) quote 3000 ppm as harm less to dogs and 10,000 ppm causing hema tologic and blood cell changes. The most important effect of ethyl mer captan is eye and respiratory tract irrita tion. The 250 ppm tentative threshold lim it can be interpreted from the results of single inhalation by animals. It appears low enough to prevent injury and eye irritation. Ethyl silicate. Smyth and Seaton (1940) found eight-hour inhalation of 550 ppm the least fatal exposure for guinea pigs. Death is due to lung injury, with some kidney CO <5> O Pc*> I t* '-i 5 t i ? f :j $ 160 June, 1956 damage. Humans found 85 ppm detectable equivalent to 1.5 to 2.3 mg./cu.m. soluble by odor, 250 ppm slightly irritating to eye fluoride dust. Higher concentrations provide and nose, and 3000 ppm extremely irritat respiratory tract irritation and effects on ing. Rowe, Spencer and Bass (1948) found liver and kidney. Largent (1952) found stor some kidney damage in rats repeatedly in age in the body occurs when as little as haling 125 ppm. Pozzani and Carpenter three milligrams per day fluoride in the (.1951) exposed rodents repeatedly. Some form of sodium fluoride is ingested, rough died within 30 days at 440 ppm with injury ly equivalent to inhalation of 0.3 mg./cu.m. to lung, liver and kidney, but 88 ppm did soluble fluoride dust. not injure. The data suggest that repeated The most important effect of inhalation inhalation at a given concentration is no of fluoride dust is chronic poisoning, cen more injurious than a single inhalation. tering in the bones, with respiratory tract The most important effect of ethyl silicate irritation at high concentrations. The 2.5 inhalation is lung injury, with non-progres mg./cu.m. threshold limit can be interpreted sive kidney damage less important. The from results of examination of exposed 100 ppm threshold limit can be interpreted workmen and experimental studies of human from results of repeated animal inhalations fluoride retention. It is not low enough to and limited human sensory data. It can be prevent fluoride storage with resulting ef smelled, it is not irritating, and is low fects on the bones. enough to prevent lung or kidney injury. Fluorine. Machle and Evans (1940) ex Ferbam. Hodge, Maynard, Downs, Blan- amined workmen exposed intermittently to chet and Jones (1952) reported the ora! as much as 10 ppm and found no clinical evi LD50 for rats to be over 17 gm./kg., with dence of damage, but there was some ac guinea pigs and rabbits more sensitive. Rats cumulation in bones and teeth. Stokinger ( tolerated 0.01% in their diet for 30 days fl949) found few toxic effects in dogs re without effect while 0.5% was required to peatedly exposed to 0.5 ppm. Greater con kill. Dogs were not injured by 25 mg. kg./ centrations injured lung and kidney. This is day for six months. The mechanism of in apparently below the level which leads to jury is not clear. bone abnormalities (Roholm 1937). The most important effect of inhalation The most important effect of inhalation of Ferbam appears to be the upper respira of fluorine gas is respiratory tract irrita tory tract irritation of a substantially inert tion, with lung edema the maximum effect. dust. The 15 mg./cu.m. tentative threshold Chronic effect on bone metabolism is also limit is in accord with this. important. The 0.1 ppm threshold limit can Ferro vanadium dust. Roshchin (1952; be interpreted from results of animal in exposed rats two months to 1000 to 2000 halation and studies on exposed workmen. It mg./cu.m. and found no effect beyond some is low enough to prevent injury. lung irritation. The author suggests a Fluoroacetates. Dieke and Richter (1946) threshold limit of 1 mg./cu.m. Vanadium report the median lethal oral dose to be 0.22 compounds irritate the upper respiratory mg./kg. for wild rats. The substance is tract, but Sjoberg (1951) found no chronic rapidly fatal through intervention in the general poisoning in workers exposed to tricarboxylic acid metabolic cycle. vanadium pentoxide dust, symptoms being The most important effect of fluoroacetate confined to respiratory difficulties and skin inhalation is acute toxicity. The 0.1 allergies. mg./cu.m. tentative threshold limit can be The most important effect of inhalation interpreted from acute oral toxicity data for of ferrovanadium dust is respiratory tract rats. It corresponds to a maximum human irritation. The 1 mg./cu.m. threshold lim intake of one milligram per day, apparently it can be interpreted from limited repeated well below a dangerous amount. animal inhalations and examination of ex Fluoroirichloromethane. Nuckolls (1933) posed workmen. It appears low enough to found in animals no more than occasional prevent injury. tremors and retching during two hours at Fluoride dust. Roholm (1937) found fluor 22,000 to 25,000 ppm. No toxic effects are to osis of human bone, but no other effects, af be expected from this physiologically inert ter several years work in 2 to 3 ppm fluorine, material. Industrial Hygiene QS The most important chloromethanc inhnlatst of narcosis, and asphy concentrations. The 100 it can he interpreted?, single animal inhalntijfar below a possibly inJ Formaldehyde, llenti U9-13, p. 128) conclude irritation of all tissues c ly the respiratory true, effects are not importay to solutions is frequ'i tract sensitization to tit Elkins (1950, p. 2311 workmen inhaling 5 to tation of imhardencd pc Smyth (1937-55; fount hours inhalation of 12f by 250 ppm. The liquid'' injury. The most important hyde inhalation is irriti the eyes, then in the up/ bronchi and even lung', limit can be interpret? human sensory data. to prevent lung injury. Furfural. Fairhall ( animal experiments in 280 ppm resulted only, i: brane irritation, whi! acute irritation, prostr; ACGIII (1951b) quote; nik, l Arch, llilf)., 10 effect that 2 to 14 ppm ache and eye irritntio; jury is to be expected analogy with other aid skin and respiratory found. The most important halation seems to be it in the eyes, then in t tract, bronchi and ever tative threshold limil from uncontrolled hu: is sufficiently low to p Furfurijl alcohol. F found that death fro due to the respiratoi thesia, and that short > reversible. ACGIII ( cat Corps Medical I Report No. 139, 1912. June, 1956 J !.l g./cu.m. soluble oncentrations provide :ation and effects on nt (1952) found storrs when as little as day fluoride in the le is ingested, roughition of 0.3 mg./cu.m. t effect of inhalation ironic poisoning, cenvith respiratory tract ncentrations. The 2.5 mit can be interpreted mination of exposed ental studies of human is not low enough to ige with resulting ef- ii *L ? T I nd Evans (1940) exosed intermittently to d found no clinical evit there was some ac- and teeth. Stokinger xic effects in dogs re3.5 ppm. Greater conng and kidney. This is ; level which leads to Roholm 1937). at effect of inhalation atory tract irrita. ,e maximum effect, me metabolism is also pm threshold limit can results of animal inm exposed workmen. It vent injury. jke and Richter (1946) hal oral dose to be 0.22 ats. The substance is ;h intervention in the tabolic cycle. it effect of fluoroaeetate e toxicity. The 0.1 threshold limit can be te oral toxicity data for to a maximum human am per day, apparently >us amount. thane. Nuckolls (1933) 3 more than occasional g during two hours at i. No toxic effects are to lis physiologically inert j \ 1 1 Industrial Hygiene Quarterly 161 The most important effect of lluorotrichloromethane inhalation is a minor degree of narcosis, and asphyxia from very high concentrations. The 1000 ppm threshold lim it can be interpreted from the results of single animal inhalations. It appears to be far below a possibly injurious level. Formaldehyde. Henderson and Haggard (1943, p. 128) conclude its action is chiefly irritation of all tissues contacted, particular ly the respiratory tract, and that systemic effects are not important. Skin sensitization to solutions is frequent and respiratory tract sensitization to the gas is not unlikely. Elkins (1950, p. 231) reports irritation in workmen inhaling 5 to 6 ppm, and eye irri tation of unhardened persons at lower levels. Smyth (1937-55) found rats survive eight hours inhalation of 125 ppm but are killed by 250 ppm. The liquid causes severe corneal injury. The most important effect of formalde hyde inhalation is irritation, first evident in the eyes, then in the upper respiratory tract, bronchi and even lung. The 5 ppm threshold limit can be interpreted from uncontrolled human sensory data. It is sufficiently low to prevent lung injury. Furfural. Fairhall (1949, p. 354) quotes animal experiments in which inhalation of 280 ppm resulted only in slight mucous mem brane irritation, while 2800 ppm caused acute irritation, prostration and lung edema. ACGIII (1954b) quotes Korenman and Resnik, (Arc/;. Hyg., 104:344, 1931) to the effect that 2 to 14 ppm causes human head ache and eye irritation. Severe corneal in jury is to be expected from the fluid, and analogy with other aldehydes suggests that skin and respiratory sensitization may be found. The most important effect of furfural in halation seems to be irritation, first evident in the eyes, then in the upper respiratory tract, bronchi and even lung. The 5 ppm ten tative threshold limit can be interpreted from uncontrolled human sensory data. It is sufficiently low to prevent lung injury. Furfuryl alcohol. Fine and Wills (1950) found that death from furfuryl alcohol is due to the respiratory paralysis of anes thesia, and that short of death, its effects are reversible. ACGIII (1955b) quotes Chemi cal Corps Medical Laboratories Research Report No. 139, 1942, to the effect that eight hours inhalation of 700 ppm killed 25'r of a group of rats. The most important effect of furfuryl nlcohol inhalation is narcosis. The 50 ppm ten tative threshold limit can be interpreted from results of single animal inhalations. It appears low enough to prevent injury. Gasoline. Sayers, Fiddlier, Yant and Thomas (1927) reported human dizziness at 700 ppm, and Drinker, Yaglou and War ren (1943) found human respiratory tract irritation and headache begin at 1000 ppm. Elkins (1950, p. 99) found industrially no sensory response to GOO to S00 ppm benzine, and dizziness at 2000 to 3000 ppm. He con cludes chronic effects do not occur when con centrations are too low to cause narcosis, but Hayhurst (1936) reported chronic poisoning consisting of central nervous sys tem effects and blood cell changes after many years of exposure. This article does not seem to be generally accepted. Henderson and Haggard (1943, p. 192) consider nausea and incoordination the significant effects, with anesthetic death at 20,000 to 30,000 ppm. Aromatic hydrocarbons in gasoline from cracking operations may much reduce safety. The most important effect of gasoline in halation is narcosis. The threshold limit of 500 ppm can be interpreted from human sen sory data, both experimental and indus trially observed. It is low enough to prevent definite narcosis. Heptane. Patty and Yant (1929) reported slight human dizziness from 1000 ppm. The paraffin hydrocarbons are anesthetic agents and irritate mucous membrane, but they do not cause systemic toxicity. The most important effect of heptane in halation is narcosis. The 500 ppm thresh old limit can be interpreted from limited human sensory data and by analogy with the better studied gasoline. It is probably low enough to prevent definite narcosis. HETP (hexacthyltetraphosphalcj. This material is substantially identical in quanti tative and qualifative effect with the cholin esterase inhibitor TEPP. Apparently no data specifically upon inhalation have been published. The most important effect of HETP is reduction of blood cholinesterase. The 0.1 mg. cu.m, tentative threshold limit can be interpreted by analogy with parathion. It ^00965^ 12 June, 1956 appears to be consistent with that value. Hexane. Nelson, Ege, Ross, Woodman and Silverman (1943) with unsicclimated 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 (193G) 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, Vainer 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 unnccHmated 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 Trcon (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 gases 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. Industrial Hygiene Qua'. The most important J cyanide inhalation is tut chemical asphyxia. The f limit can be interpreted; older single animal in6; some human sensory datji to prevent injury. - J. Hydrogen fluoride, p found 30 ppm is highly*; causing pulmonary dam testis changes and increa.-i Animals tolerated 7 ppm % piratorv tract irritation) sure. Elkins (1950, p. 73): at 0.4 to 0.7 ppm. Patty !' finds 0.026 mg. 1. <22 pp I tatinp and at 0.1 mg., !. ( smarts. The liquid causes ing skin injuries, and dc All soluble fluorides iuU: metabolism and an excess tooth abnormalities. r The most important c fluoride inhalation is rc ritation. with Jung edent: feet. Chronic effect oil L also important. The .3 p- can be interpreted from animal inhalation and hr It is low enough to prev Hydrogen peroxide, !> stock and Hnektev (190- vivo eight hours at 250 : symptoms, hut irritation are found in the lungs, months at 7 ppm witliu the skin was thickened luted. The liquid is ex to skin and cornea. The most important peroxide aerosol inhal: tract irritation, with lu mum effect. The i ppm be interpreted from : animal inhalation. It is vent injury. Itydropeit sclrnide. (1941) found animals hours at 0.3 to 1.2 ppm, and changes in liver ; nose irritation made t man, but 0.3 ppm is tu 8 caption of its odor i 11917) reported indusf 8 than 0.2 ppm, with Hvi 2 2 u) LA June, 1956 se ._a throat. lly inhaling 20 ng six month's nor changes in were found, of inhalation of ract irritation, n be interpreted imal inhalation. prevent injury. :GIH (1955b) response data ru of Industrial at 2 ppm, nose to be evident at is not evident at ect of hydrogen iratory tract irhe maximum efn-eshold limit can y with hydrogen y response. It is event injury. chle, Kitzmiller, mnd animals not ation of 34 ppm. 1943, p. 126) cont systemic effect. >pm ;s dangerous i short time. 0 t,^.n highly irri- immunity seems lately irritating; arode the teeth, feet of hydrogen iratory tract irri:he maximum ef1 limit can be inanimal inhalation t is low enough to ury and Zernik is tolerable for six . Henderson and ;onclude injury i3 hronic toxicity is state 3000 ppm is opm dangerous in to 40 ppm gives hours. This is one :an penetrate the ts. Patty (1948-9, rely detectable at at 2 to 5 ppm. \ l *l .j 1 , i j j | j i Industrial Hygiene Quarterly 1G3 The most important effect of hydrogen cyanide inhalation is acute poisoning, a chemical asphyxia. The 10 ppm threshold limit can be interpreted from results of older single animal inhalation data and some human sensory data. It is low enough to prevent injury. Hydrogen fluoride. Stokinger (1949) found 30 ppm is highly toxic to animals, causing pulmonary damage, kidney and testis changes and increases in bone fluoride. Animals tolerated 7 ppm with only mild res piratory tract irritation in repeated expo sure. Elkins (1950, p. 73) reports nosebleeds at 0.4 to 0.7 ppm. Patty (1948-9, p. 543) finds 0.026 mg./l. (22 ppm) is slowly irri tating and at 0.1 mg./l. (120 ppm) the skin smarts. The liquid causes severe slowly heal ing skin injuries, and destroys the cornea. All soluble fluorides interfere with calcium metabolism and an excess produces bone and tooth abnormalities. The most important effect of hydrogen iluoride inhalation is respiratory tr.net ir ritation, with lung edema the maximum ef fect. Chronic effect on bone metabolism is also important. The 3 ppm threshold limit can be interpreted from results of repeated animal inhalation and human sensory data. It is low enough to prevent injury Hydrogen peroxide, 90%. Oberst, Com stock and Hackley (1954) found rats sur vive eight hours at 250 to 300 ppm without symptoms, but irritation and areas of edema are found in the lungs. Dogs survived six months at 7 ppm without injury, although the skin was thickened and the lungs irri tated. The liquid is extremely destructive to skin and cornea. The most important effect of hydrogen peroxide aerosol inhalation is respiratory tract irritation, with lung edema the maxi mum effect. The 1 ppm threshold limit can be interpreted from results of repeated animal inhalation. It is low enough to pre vent injury. Hydrogen, selenide. Dudley and Miller (1941) found animals are killed in eight hours at 0.3 to 1.2 ppm, with lung irritation and changes in liver and spleen. Eye and nose irritation made 1.5 ppm intolerable to man, but 0.3 ppm is not irritating and per ception of its odor is soon lost. Buchan (1947) reported industrial cases due to less than 0.2 ppm, with liver injuiy. The most important effect of hydrogen seietiide is acute poisoning, largely lung edema at high concentration, and chronic poisoning centering in the liver. The 0.05 ppm threshold limit can be interpreted from the results of single animal inhalations and industrial accidents. It appears !<m- enough to prevent injury Hydrogen sulfide. Henderson and Hag gard (1943, p. 140, 213) state hydrogen sulfide may cause very rapid death from respiratory paralysis, or delayed death from lung injury. It is not cumulative. Low con centrations irritate the cornea. A concentra tion fatal in 30 minutes is GOO ppm, while 70 to 150 ppm causes slight symptoms in several hours. Barthelemy (1939) found no injury among viscose workers during 10 years, with control at about 20 ppm. Elkins (1950. p. 232) found eye irritation in indus try at 10 ppm and some complaints even at 5 ppm. Patty (1948-9, p. 590) concludes 0.3 ppm can be smelled, 3 to 5 ppm is offensive. The most important effect of hydrogen sulfide inhalation is acute toxicity, marked by respiratory paralysis or lung edema. The 20 ppm threshold limit can be interpreted from the results of examination of exposed workmen. It is low enough to prevent in jury. Hydroquinone. Sterner, Oglesby and Anderson (1947) reported on several years industrial experience with men exposed to quinone vapor and hydroquinone dust. No systemic effects could be found, but high concentrations caused transient eye irrita tion, and after several years, a pigmentation of cornea and conjunctiva was apparent, due to local action on the exposed tissue. Loss of vision has followed pigmentation in some cases, according to Oglesby (1956). It is uncertain whether the vapor or the dust was responsible. Hydroquinone dust ranged from 0.12 to 13 mg., cu.m. After comparing exposure with concentration, the authors conclude hydroquinone dust should be kept below 2 to 3 mg./cu.m. The most important effect of hydro quinone inhiilntion is transient eye irrita tion and a slowly developing pigmentation in the eye. Visual disability can result. The 2 mg./cu.m. threshold limit can he inter preted from the results of examination of - exposed workmen. It appears low enough prevent effect. to o June, 1956 y tract irrita2 maximum injury. mit can be inter im ethyl amines. It to prevent injury. Bloomfield, Britten fter a survey of a proposed that the 2d from 0.5 to 0.15 ^el disabling lead r, and mild poison- effect of lead dust oisoning. The 0.15 t can be interpreted :aminations of exi enough to prevent not to prevent some 11 and Miller (1941) rid Weaver (1943) lead arsenate deor increases lead lead storage. effect of inhalation mic arsenic poison- ' tentative threshold d from the results on animals. It apted by analogy with - analogy with ar- igher figure. oj.) in a summary, doses acts as a cenimulant, leading to ulsions and death, months to saturated ;d, but 10,000 mg./r killed one of two quotes an unpubr. F. Treon et al. A ;ion of 0.7 mg./cu.m. ogy in animals. An \ by Spear is quoted tys at 0.19 mg./cu.m. esult in pathology in effect of lindane insoning centering in ru.m. threshold limit m the results of reons. It appears low ry. me. Drinker, Thomeported that experi- \ ] ^ .(, \ ;. 1 , 1 i Indnstrial Hygiene Quarterly 165 mental fume fever in man results from ex cessive inhalation, but does not occur below a concentration of 15 mg./cu.m. This con dition is transient fever with chills, muscu lar pain, nausea and vomiting. An im munity is apparently build up. The most important effect of inhalation of magnesium oxide fume is transient metal fume fever. The 15 mg./cu.m. threshold limit can be interpreted from the results of extensive human experiment. It is low enough to prevent injury. Malathon. Johnson, Fletcher, Nolan and Cnssaday (1952) reviewed toxicity data and conclude malathon is about one-hundredth as toxic to mammals as parathion. Tousey (1954) reviews data and confirms that its toxicity is considerably lower than that of many other cholinesterase inhibitors. Cul ver, Caplan and Batchelor (1955) found a group of entomologists with maximum ex posure about five hours at a peak of 56 mg./cu.m. and an average of about 3.3 mg./ cu.m. This had no effect on blood cholin esterase. The most important effect of malathon in halation is the reduction of blood cholinestei'ase. The 15 mg./cu.m. threshold limit can be interpreted from the results of oral doses to animals and limited examinations of exposed workmen. It appears low enough to prevent injury. Manganese. Flinn, Neal and Fulton (1951) describe poisoning as an effect upon the basal brain ganglia, leading to disability from weakness in the legs, spastic gait, stolid mask-like expression and emotional disturb ances, but not ordinarily shortening life. In an ore-crushing plant, they found no symp toms in men exposed to 30 mg./cu.m. or less and they concluded concentrations can be effectively limited to 6 mg./cu.m. The most important effect of inhalation of manganese dust is chronic poisoning. The 6 mg./cu.m. threshold limit can be inter preted from the results of examination of exposed workmen. It is low enough to pre vent injury. Mercury. Neal et al. (1941) in a study of the felt hat industry, found the incidence of mercurialism proportional to atmospheric concentrations, with no cases found below 0.1 mg./cu.m. Chronic symptoms consist of psychic disturbances, timidity, tremors, pallor, salivation and tenderness of the gums. Ashe, Largent, Dutra, Hubbard and Blackstone (1953) in repeated inhalations by animals, found no effects at 0.1 mg.'cu.- m., but damage to kidney and brain at 0.86 mg./cu.m. The most important effect of inhalation of mercury is chronic poisoning. The 0.1 mg./cu.m. threshold limit can be interpreted from the results of repeated animal inhala tion and examination of exposed workmen. Mercury (organic compounds). Ahlmark (1948) on the basis of Swedish industrial experience suggests a limit of 0.01 mg.'cu.m. Ltmdgren and Swensson (1949) consider concentrations fluctuate so widely that an alysis does not detect important peaks, and that an M.A.C. cannot be defined. Organo mercurials produce effects like mercury, hut they have the added hazard of ready pene tration of the skin. Trakhtenberg, (ab stracted from the Russian in Chemical Ab stracts 44:10162g, 1950) reported mice die at 10 to 30 mg. cu.m, within three to five hours and concludes 0.01 mg./cu.m. should not be tolerated for repeated human expo sures. The most important effect of inhalation of organo mercurials is chronic mercury poi soning. The 0.01 mg. cu.m, threshold limit can be interpreted from the results of indus trial experience and single animal inhala tions. It is probably low enough to prevent injury. Mesityl oxide. Smyth, Seaton and Fischer (1942) found no effect upon animals from repeated inhalation of 50 ppm, while higher concentrations killed by anesthesia, with minor lung, kidney and liver injuries. In single inhalations, 100 ppm did not injure in eight hours, 500 killed some and 2,500 killed all, and in one hour 13,000 ppm (saturation) was fatal by anesthesia. Little cumulative action was revealed. Silverman. Schulte and First (1946) found some eye irritation at 25 ppm, and .at 50 ppm nose irritation and a persistent unpleasant taste in unacclimated subjects. The most important effect of mesityl oxide inhalation is narcosis. The 50 ppm threshold limit can be interpreted from the results of repeated animal inhalations and human sensory response. It is low enough to prevent definite narcosis. Methoxychlnr. Haag, Finnegan, Larson, Itiese and Dreyfuss (1950) found methoxy- 1 A > X X t i 5 8F0098F3 Wr. \ , `-*&k BFG36799 4fir 166 June, loss Industrial Hygiene t r chlor acts similarly to DDT in animals, and changes in liver, kidney and heart of ani is less toxic by inhalation. Hodge, Maynard mals, with lung irritation. The threshold n The most import bromide inhalation and Blanchet (1952) found no effect on nits for chronic effects is 11,300 ppm. centering in the cent in two years at 0.020% in the diet and no The most important effect of methylal in liver. The 20 ppm th mortality or histological changes at 0.16%. halation is chronic poisoning, centering in terpreted from the r Little accumulates in body fat. liver and kidneys, with narcosis and lung mal inhalations and The most important effect of methoxy- injury less important. The 1000 ppm thresh workmen. It appears chlor inhalation is chronic poisoning cen old limit can be interpreted from results of set at the maximum tering in the liver. The 15 mg./cu.m. thresh repeated animal inhalation studies. It ap old limit can be interpreted from the results pears low enough to prevent injury, but T (ok'ratc without effiM ethyl CKLLOSO, of repeated oral doses to animals. It appears there are no data to judge the degree of ir Donlcv (1936) and low enough to prevent injury. ritation and narcosis it allows. (193?) reported tox Methyl acetate. Fairhall (1949, p. 375) Methyl alcohol. Sayers, Yant, Schrenk, granulopenic ancmi; notes irritation of eye and respiratory tract, Chornyak, Pearce, Patty and Linn (1942) i posure to a mixed sol narcosis less prominent than from higher found no effect on dogs from repeated inhal cellosolve. Greenbe acetates, but fatal dose close to anesthetic ation of 450 to 500 ppm. Henderson and Burke and Moskowit; dose, and symptoms persistent after appre Haggard (1943, p. 218) stress slow elimina centrations in the e.- ciable narcosis. Death is due to anesthesia, tion, leading to progressive rise in blood after the cases deveh but lung injury also occurs. Smyth (1937- level from daily inhalation. At 200 ppm 0.87 of the glycol ether. V 55) found rats survive four-hour inhalations grams can be absorbed by a human in eight and von Octtingen of 16,000 ppm, but die from 32,000 ppm. hours, but only part of this can be elimi meats on (logs did no The most important effect of methyl ace nated before the next day. Methanol is pri toxicity suggested b> tate inhalation is narcosis. The 200 ppm marily a narcotic agent, but it may injure blood cell effects \v< threshold limit can be interpreted by an retina and optic nerve, leading to cloudy peated inhalation of alogy with ethyl acetate, allowing a margin vision or blindness. There is some irrita cephnlopnthy was fo: for greater irritation and for the slow tion of mucous membranes. Elkins (1950, 336) concludes the v: metabolism of methyl alcohol. It apparently p. Ill) found industrial exposures ranging ritating, and produc is low enough to prevent narcotic symptoms. from 100 to 1700 ppm with no evidence of changes. Smyth (19: Methyl Acetylene. ACGII1 (1955b) cites poisoning. Smyth (1937-55) found rats sur vivc four hours at 2' Horn, Chemical Corps Medical Laboratories vive eight-hour inhalations of 32,000 ppm, eight hours. Contract Report #35, 1954. For six months and only a fraction are killed by 64,000 ppm. The most import. dogs and rats inhaled 28,700 ppm repeatedly. The most important effect of methyl al CELLOSOLVE inhalatio: A few died. There was lung irritation and cohol inhalation is narcosis, with injury to l centering in the bra: some central nervous system excitation. retina and optic nerve likely only from quite 1 The 25 ppm thrcslu- The most important effect of methyl acet excessive inhalation. The 200 ppm threshold preted from nlmospk ylene inhalation is lung injury. The 1000 limit can be interpreted from results of re h ppm threshold limit can be interpreted from peated animal inhalations. It will not cause fill validity after him and from the results f, results of repeated animal inhalation?. It is significant narcosis, but continuous inhala halations. It appears !. low enough to prevent injury. tion will cause a daily rise in the degree of to prevent injuries. Methyl acrylate. Treon, Sigmon, Wright early narcosis, due to slow elimination. Methyl CKLLOSO. and Kitzmiller (1.949) exposed animals re Methyl bromide. Irish, Adams, Spencer nryethyl acetate.) Tl. peatedly to vapor. They found that 130 and Rowe (1940) found no effect from re the body to methyl seven-hour inhalations of 31 ppm had no ef peated inhalation at 17 ppm, and 34 ppm in acid, and its vapors a: fect upon four species, except some loss in jured only rabbits. Watrous (1942) found tating than those of I weight. Higher concentrations caused re mild symptoms iii one-third of 90 workers in The most import: spiratory tract irritation and some narcosis. concentrations generally under 35 ppm. In cellosolve acetate The most important effect of methyl acryl- ' gram (1951) found injuries where workers poisoning due to hyd ate inhalation is respiratory tract irritation. were exposed to 100 to 1000 ppm. After LOSOLVE. The 25 ppm The 10 ppm tentative threshold limit can be improvements -reduced exposure to about interpreted from ana interpreted from repeated animal inhala 20 ppm, injuries ceased. Fairhall (1949, losolve. It is low cno tions. It appears to be low enough to pre p. 376) notes it is a respiratory tract irri vent injury. tant, a liver injurant, and a central nervous m Methyl chloride. S and Berger (1929) I Methylal (dim ethoxymethane). Weaver, system poison leading to delirium, convul ppm produce no scrii Hough, Highman and Fairhall (1951) found sions and even mania. It is rapidly metab pigs. Smith and von C that high concentrations produce fatty olized and eliminated. repeated inhalation L June, 1956 ir eart of anin. ie threshold 0 ppm. >ct of methylal inling, centering in larcosis and lung 1000 ppm thresh ed from results of >n studies. It apevent injury, but e the degree of ir- Uows. 5, Yant, Schrenk, and Linn (1942) om repeated inhaln. Henderson and tress slow eliminasive rise in blood n. At 200 ppm 0.87 r a human in eight this can be elimiy. Methanol is pribut it may injure leading to cloudy re is some irritanes. Elkins (1950, exposures ranging nth no evidence of 55) found rats sur ras of 32,000 ppm, lied by 64,000 ppm. r v of methyl al.. with injury to :ely only from quite ; 200 ppm threshold from results of res. It will not cause continuous inhala,se in the degree of jw elimination, h, Adams, Spencer no effect from reipm, and 34 ppm inrous (1942) found ird of 90 workers in under 35 ppm. In- iries where workers 3 1000 ppm. After exposure to about ;d. Fairhall (1949, jpiratory tract und id a central nervous ;o delirium, convul!t is rapidly metab- 1i i Industrial Hygiene Quarterly 167 The most important effect of methyl bromide inhalation is chronic poisoning, centering in the central nervous system and liver. The 20 ppm threshold limit can be in terpreted from the results of repeated ani mal inhalations and examination of exposed workmen. It appears to be rather precisely set at the maximum concentration humans tolerate without effect. Methyl CELLOSOLVE (m ethoxyethanol). Donley (1936) and Parsons and Parsons (1938) reported toxic encephalopathy with granulopenic anemia from industri.nl ex posure to a mixed solvent containing methyl CELLOSOLVE. Greenberg, Mayers, Goldwater, Burke and Moskowitz (1938) estimated con centrations in the establishment some time after the cases developed, and found 25 ppm of the glycol ether. Werner, Mitchell, Miller and von Octtingcn (1943, a,b) in experi ments on dogs did not confirm the degree of toxicity suggested by the human cases. The blood cell effects were obtained from re peated inhalation of 500 ppm, but no en cephalopathy was found. Fairhall (1949, p. 336) concludes the vapors are somewhat ir ritating, and produce narcosis and kidney changes. Smyth (1937-55) found rnts sur vive four hours at 2000 ppm, but die from eight hours. The most important effect of methyl cellosolve inhalation is chronic poisoning, centering in the brain and red blood cells. The 25 ppm threshold limit can be inter preted from atmospheric analyses of doubt ful validity after human industrial injuries, and from the results of repeated animal in halations. It appears lower than is required to prevent injuries. Methyl CELLOSOLVE acetate (2-meth- oxyethyl acetate.) This ester hydrolyzes in the body to methyl cellosolve and acetic acid, and its vapors are somewhat more irri tating than those of the former. The most important effect of methyl cellosolve acetate inhalation is chronic poisoning due to hydrolysis to methyl cel losolve. The 25 ppm threshold limit can be interpreted from analogy with methyl CEL LOSOLVE. It is low enough to prevent injury. Methyl chloride. Sayers, Yant, Thomas and Berger (1929) found 10 hours at 400 ppm produce no serious injuries in guinea pigs. Smith and von Oettingen (1947) found repeated inhalation of 300 ppm by six species has no effect, but 500 ppm causes central nervous system effects. Complete re covery from injury is slow. Fairhall (1949, p. 379) concludes it acts chiefly by narco sis, but liver, kidney and bone marrow in juries are found. The most important effect of methyl chloride inhalation is central nervous sys tem injury, with less important chronic poisoning. The 100 ppm threshold limit can be interpreted from the results of repeated animal inhalations. It is low enough to pre vent injury. Methyl chloroform. Adams, Spencer, Rowe and Irish (1950) found in repeated exposures that 650 ppm retarded guinea pig growth, and 3000 ppm caused slight liver effects. Three other species were less sensi tive. Rats were mildly narcosed in one hour at 5000 ppm. The level tolerated in repeated inhalation was close to that tolerated in a single exposure. They concluded it is close to methylene chloride in toxicity and less toxic than trichloroethylene. The most important effect of methyl chloroform inhalation is narcosis. The 500 ppm threshold limit can be interpreted from the results of repeated animal inhalation. It is low enough to prevent definite narcosis. Methyl cyclohexane. Treon, Crutchfield and Kitzmiller (1943) found no effect on rabbits exposed 300 hours to 1162 ppm, slight kidney and liver changes from 90 hours at 2S86 ppm .and fractional mortality, eye and entire respiratory tract irritation and narcosis at 7308 ppm. Patty (1948-9, p. 770) concludes the odor is weak at 500800 ppm. The most important effect of methylcyclohexane inhalation is narcosis, with non- progressive organic changes. The 500 ppm threshold limit can be interpreted from re sults of repeated animal inhalation. It is low enough to prevent definite narcosis. Methyl cyclohcxanot. Treon, Crutchfield and Kitzmiller (1943) found 300 hours at 121 ppm causes slight liver and kidney changes in rabbits, and 300 hours at 503 ppm causes eye irritation with some nar cosis, but does not kill. Patty (1948-9, p. 881) concludes that odor and irritation arc evident at 500 ppm. The most important effect of methyl cyclohexanol inhalation is narcosis, withVJ non-progressive organic effects less nromiy^ 168 June, 1956 nent. The 100 ppm threshold limit can be in terpreted from results of repeated animal inhalation. It is low enough to prevent sig nificant narcosis, and probably to prevent minor effects on liver and kidneys. Methyl cyclohexanone. Treon, Crutchfield and Kitzmiller (1043) 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 King 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 ami/I 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) (liiotes 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 repented 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 i*epeated animal inhalations. They appear low enough to prevent injury, but slight toxic effects may result from soluble compounds. Naphtha (coal tar). A mixture of toluene and xylene chiefly. The predominantly nar cotic effects of these closely similar ma terials are additive and a mixture is no more injurious than the sum of its components. Cook (1945) points out that if a sample has a low boiling point, an appreciable content of benzene is to be suspected, and working concentrations should be reduced according ly. Being 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 Industrial Hygiene Qua threshold limit can be alogy with those of tolu low enough to prevent Naphtha (petroleum). affin hydrocarbons of! molecular weight than g sion under gasoline apj Nirkil carbonyl. Fnir ({notes Armit to the effee a deposit of finely divid\ pirntory tract, lending lung edema. Ilueper (19 inferences that it prod nating in the nasal sinus and Sunderman (1953) ; 10 ppm killed mice, 270 ; they suggest toxicity m weight, with man surviv tions. They found lung liver injury, hut conclut tive and that a toleranc t man and Kincaid (19 human cases, lwo fatal, I I delayed, due to lung ed< The`immediate effect vapor inhalation is lun; laved edema. Cancer nasal sinuses has been time exposure. The 0.00' it is apparently an npp designed to prevent earn to prevent all possibiltl feet, but there arc no c fectiveiiess in prevent! Nicotine. Wilson and diets containing nicoti for a 60-day period. II oil 0.05*7 nicotine. Rnf by 0.006"> nicotine, eqi body weight per day. tion reduced growth, du tirely to reduced fin < 1949) estimates the f 60 milligrams. The most important halation is iil-defincd The 0.5 mg. cu.m, tent can be interpreted fre studies on rats. It cor mum human intake of day, apparently well level. 8 Nitric acid. Fairhall eludes it is an upper LO ritant, injuring the bi 8 BFG36802 June, 1956 :t -of methyl oil .s narcosis. The can be interpreted a. It is low enough arcosis and irrita- ACGIH (1954b) ho in 1893 found ir to but somewhat sulfide. ffect of methyl mer- ratory tract irrita- tive threshold limit malogy with hydrow enough to prevent n. 11, Dunn, Sharpless in animal experimchial and alveolar hanges in liver and ived repeated expo53 mg./cu.m. molyb- one of a group was l. molybdenite dust. ie Digest (16:1083, vskaya to the effect hanges in rat heart, ound after repeated g./cu.m. molybdenum ,:J,. r * j d , ,) 1 , of inhalation of ; chronic poisonix and kidney. The ng./cu.m. for soluble nsoluble molybdenum trpreted from the relal inhalations. They prevent injury, but y result from soluble A mixture of toluene e predominantly nar- closely similar ma1 a mixture is no more m of its components. t that if a sample has n appreciable content spected, and working be reduced according- 'I ' liefly of toluene and rtant effect of coal tar vhen free from benirritation of the resportant. The 200 ppm ' Industrial Hygiene Quarterly 169 threshold limit can be interpreted by an alogy with those of toluene and xylene. It is low enough to prevent injury. Naphtha (petroleum). A mixture of par affin hydrocarbons of somewhat higher molecular weight than gasoline. The discus sion under gasoline applies. Nickel carbonyl. Fairhall (1949, p. 114) iiuotes Armit to the effect that this produces a deposit of finely divided nickel in the res piratory tract, leading to irritation and lung edema. Hueper (1950) summarizes the inferences that it produces cancer, origi nating in the nasal sinuses. Kincaid, Strong and Sunderman (1953) found 30 minutes at 10 ppm killed mice, 270 ppm killed cats, and they suggest toxicity may be related to body weight, with man surviving high concentra tions. They found lung edema and severe liver injury, but conclude it is not cumula tive and that a tolerance develops. Sunderman and Kincaid (1954) report on 36 human cases, two fatal. The fatalities were delayed, due to lung edema. The'immediate effect of nickel carbonyl vapor inhalation is lung irritation and de layed edema. Cancer originating in the nasal sinuses has been reported from long time exposure. The 0.001 ppm threshold lim it is apparently an approximation of zero, designed to prevent cancer. It is low enough to prevent all possibility of immediate ef fect, but there are no data to judge its ef fectiveness in preventing cancer. Nicotine. Wilson and De Eds (1936) fed diets containing nicotine to growing rats for a 60-day period. Rats did not survive on 0.05(r nicotine. Rats were not affected by 0.006% nicotine, equivalent to 4 mg./kg. body weight per day. A greater concentra tion reduced growth, due largely but not en tirely to reduced food intake. Lehman (1949) estimates the fatal human dose to be 60 milligrams. The most important effect of nicotine in.halation is ill-defined chronic poisoning. The 0.5 mg./cu.m. tentative threshold limit can be interpreted from repeated feeding studies on rats. It corresponds to-a maxi mum human intake of five milligrams per day, apparently well below an injurious level. Nitric acid. Fairhall (1949, p. 81) con cludes it is an upper respiratory tract ir ritant, injuring the bronchi and even the lungs in high concentration. It also erodes the teeth. He suggests a threshold limit of 10 ppm. The most important effect of inhalation of nitric acid is upper respiratory tract irritation. The 10 ppm tentative threshold limit appears to be based upon undocu mented analogy with other acid gases. p-Nitroaniline. Fairhall (1949, p. 402) concludes p-nitroaniline is more toxic than aniline, causing headache, nausea and cyano sis. This is based on British industrial ex perience. The most important effect of p-nitro aniline inhalation is acute poisoning. The 1 ppm threshold limit is apparently an esti mate based on analogy with aniline. It ap pears low enough to prevent injury. Nitrobenzene. Henderson and Haggard ( 1943, p. 227) note that injury by skin ab sorption is more, frequent than by inhala tion. The compound is an anesthetic, pro ducing methemoglobin and reducing blood pressure. Acute toxicity is marked by head ache, narcosis, cyanosis, and death from respiratory paralysis. Chronic absorption results in anemia, cyanosis, muscular weak ness, bladder irritation. The maximum con centration which gives no serious dis turbance in one hour is 200 ppm, and 40 to 80 ppm cause symptoms in several hours. The most important effect of nitrobenzene inhalation is chronic poisoning, marked by reduced blood pressure and cyanosis. The 1 ppm threshold limit can be interpreted from results of single animal inhalation. It ap pears low enough to prevent injury. Nitroethane. Machle, Scott and Troon (1940) found guinea pigs inhaling 500 ppm for a total of 140 hours are not injured, but some die from 1000 ppm. Eye and nose ir ritation, narcosis, central nervous system irritation and lung edema are produced. Toxic symptoms are evident before narco sis. The most important effect of nitroethane inhalation is acute poisoning accompanied by narcosis and irritation. The 100 ppm threshold limit can be interpreted from re sults of animal inhalation. It appears low enough to prevent injury. Nitrogen dioxide. Henderson and Hag gard (1943, p. 137) state that 62 ppnJO causes immediate throat irritation, 30(fck ppm coughing and 100 to 150 ppm is dangc^Q o & i 3 p`V? 170 June, 1956 ou3 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-Nitropropane. The animal work of Machle, Scott and Treon (1940) concluded that in the nitro paraffins toxicity increases with molecular weight. Thus, 2-nitropropane should be more toxic than nitroethane. Skin ner (1947) found workmen in concentra tions of 10 to 30 ppm were not affected, but 20 to 45 ppm caused anorexia, nausea, vom iting and diarrhea. The most important effect of 2-nitropro pane inhalation is acute poisoning accom panied by narcosis and irritation. The 50 ppm threshold limit can be interpreted from results of repeated animal inhalation and industrial experience. It is probably low enough to prevent injury, but not to pre vent disturbing symptoms. Nitrotolnene. Von. Oettingen (1941) re viewed the literature and could find no clear distinction between the toxicities of nitrotoluene and nitrobenzene. The most important effect of nitrotolnene 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 halation is respiratory tract irritation, with lung edema the maximum effect. The 0.1 ppm threshold limit can be interpreted from results of limited repeated animal inhala tions and human sensory data. It appears low enough to prevent injury. Parafhion. The earliest effect of this cholinesterase inhibitor is a reduction of Industrial Hygiene Q that enzyme activity: and Rush (1950) in workers found iilhalai cu.m, causes definite r linesterase activity. 11955) on the basis of tion conclude that a t to 0.12 mg., cu.m, is s; The most importar inhalation is the redo esterase. The 0.1 mg. can be interpreted fro ination of exposed wt tain that it is low cni urnble reduction of but it is low enough : Pentaborane. Svirl the LC-(, for mice ini hours to be 10.9 ppm. tral nervous excit: opacity. Six-hour ini by rats killed all wii Comstock and Obersi the median detectable (0.5 ppm), described sweet. The most important inhalation is acute i central nervous s.vstei. tive threshold limit ca limited repeated inha appears to be a conS' Pcntnchlurnaphthui inhalation studies (1939) concluded tha in the liver and (hat for repented inhalatio solid material or its c the skin, and repca chloracne. The most importar naphthalene inhabit! ing centering in the 1 threshold limit can b results of repented m low enough to proven Pentachlorophenol. Gniebler and Kitzm evidence of chronic pi the smallest lethal in mg. kg. it penetrate ternal injury is prii system with heart f The most importn ophenot inhalation is 8 June, 1956 .0) .concluded tu^icity increases us, 2-nitropropane nitroethane. Skinlen in concentrae not affected, but 3xia, nausea, vom- ect of 2-nitropropoisoning accomirritation. The 50 e interpreted from ial inhalation and is probably low !, but not to pres. tingen (1941) recould find no clear oxicities of nitro- ect of nitrotcluene zoning, marked by id cyanosis. The 5 ;ars to be an estive support. It is lifference between >Iuene is sufficient n threshold limits, tblished data spefound, but analogy < ;s close. t of octane in,o0 ppm threshold 1 only by analogy ne. It is probably definite narcosis. 9, p. 122) quotes r reported work to alation of 0.1 ppm pneumonia, higher o lung edema. He rritation with fatal na, but no systemic :atement that 0.015 any higher concen- effect of ozone in tact irritation, with am effect. The 0.1 be interpreted from ted animal inhalay data. It appears injury. est effect of this is a reduction of ^f i Industrial Hygiene Quarterly 171 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. Viglinni 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 LCr,,, 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 appeal's 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 pentachlornaphthalene 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. Pentachlornphenol. 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 pentachlorophenol 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 appeal's low enough to prevent in jury. Pentane. Patty and Yant (1929) found no effect on humans from 10 minutes inhala tion of 5000 ppm. Fairhali (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 perchloroethvlcne 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 17S June, 1956 45 ppm, mice and cats die within two days. The most important effect of perchlor- omethyl mercaptan inhalation is eye and respiratory tract irritation. The 0.1 ppm tentative threshold limit can be interpreted on the basis of limited single inhalations by animals. It appears to be low enough to pre vent injury. Phenol. Deichmann, Kitzmiller and Witherup (1944) found guinea pigs are severely injured by 20 days inhalation of 25 to 50 ppm, rabbits suffer lung injury in 63 days, but rats are not affected. They con clude human injury from repeated inhala tion is marked by digestive disturbance, nervous disorders, skin eruption and liver and kidney damage. The liquid penetrates the skin to a dangerous extent, and causes severe skin and corneal injury. Patty (19489, p. 1034) reports that 5 ppm can be recog nized by odoi\ Smyth (1937-55) found rats survive eight hours inhalation of vapors saturated at room temperature. Although phenol vapors are odorous and irritating, their major effect is chronic sys temic poisoning. The 5 ppm threshold limit can be interpreted from results of repented inhalations by animals. It appears to be low enough to prevent chronic toxic effects. Phenylhydrazine. Von Oettingen (1941, p. 158) concludes death from a large dose is due to respiratory paralysis. There is hemo lytic anemia, formation of methemoglobin, injury to the liver and heart muscle. Skin penetration is rapid and dermal sensitiza tion takes place. The fatal oral dose for rats is of the order of 0.04 gm./kg. The most important effect of phenyl hydrazine inhalation is chronic poisoning, centering in the red blood cells. The 5 ppm threshold limit can be interpreted from analogy with aniline. Quantitative data are not available to judge the effectiveness of the limit. Phosgene. Fieldner, Katz and Kinne (1921) cite the Chemical'Warfare Service as authority for a 1 ppm allowable concen tration for prolonged exposure, based on human tests. Henderson and Haggard (1943, p. 137) consider phosgene a lung injurant producing delayed edema. They say 3.1 ppm is immediately irritating to throat, 4 ppm to eyes, 4.9 ppm causes cough ing, 5.6 ppm detectable by odor and 50 ppm rapidly fatal. The most important effect of phosgene in halation is respiratory tract irritation with delayed lung edema probable. The 1 ppm threshold limit can be interpreted from re sults of human studies. It is low enough to prevent injury. Phosphine. Henderson and Haggard (1943, p. 243) report 1000 to 2000 ppm fatal in 30 minutes, 100 to 200 ppm the maximum for one hour without serious disturbance. Fairhall (1949, p. 127) quotes Muller to the effect that animals die from two four-hour inhalations of 20 ppm, or 7 of 10 ppm, but two months at 5 ppm did not injure. Acute poisoning is rapidly fatal with convulsions, paralysis and coma. Chronic poisoning is marked by anemia and nervous disturb ances. Patty (1948-9, p. 576) concludes there is only a faint odor at 1 ppm. The most important effect of phosphine inhalation is chronic poisoning. The 0.05 ppm threshold limit can be interpreted from the results of repeated animal inhalation. It appears low enough to prevent injury. Phosphorous /yellow). Fairhall (1949, p. 131) summarizes the literature. The effects of chronic poisoning are upon bone meta bolism. They may be noticed first as painful swollen gums, or as spontaneous fractures of the long bones. They develop into peri ostitis and necrosis of the lower jaw, with secondary infection. In single exposures one milligram per kilogram is usually fatal. The most important effect of phosphorous inhalation is chronic poisoning, centering in the bones. The 0.1 mg./cu.m. threshold limit cannot be interpreted in quantitative terms. Phosphorous pentachloride. Henderson and Haggard (1943, p. 134) conclude this material is an irritant to nose, throat and lungs through hydrolysis to hydrogen chlor ide. Skin burns from the solid are likely. Mice are killed in 10 minutes by 120 ppm. The most important effect of phosphorous pentachloride inhalation is respiratory tract irritation, with lung edema possible. The 1 mg./cu.m. threshold limit is apparently an estimate without quantitative support. It appears low enough to prevent injury. Phosphorous pentasulfide. Fairhall (1949, p. 131) quotes Bardlet to the effect that phosphorous pentasulfide is somewhat less hazardous than phosphorous pentachloride. The most important effect of phosphorous pentasulfide inhalation is respiratory tract Industrial Hygiene Qtu '' irritation. The 1 mg./c is apparently an estinus live support. It appears rent injury. Phosphorous trichlor Haggard (1913, p. 134 taut and lung injurant, as rapidly fatal, and 2 t mum for 30 to 60 mim disturbance. Cook (194 finding 0.7 ppm causes - i\ in animals. The most important t trichloride inhalation is ritation, with lung ede: feet. The 0.5 ppm th: interpreted from limit' data. It appears low er jury. Pierie acid. FairhuU l scribes systemic po: enteritis, hemorrhagic titis. Sunderman, Wc (1945) studied worker um picrate in atmosph 0.19-12 mg. cu.m. The piratory tract irritatifects but considerable The most important inhalation is chronic mg./cu.m. threshold lint from observations on c is low enough to prev but not respiratory trai situation. Propyl acclnte. Fair concludes it is more i acetate, more narcotic acetates, but less loth; tract irritation and liv Death is due to anestl narcosis may leave no (1937-55) found four 32,000 ppm kills four The most important late inhalation is nar threshold limit can b( alogy with ethyl ncet appears to be low enoui narcosis. Propyl alcohol, iso. Woodman and Silverm ppm causes mild irrita JO throat, and 800 ppm is acclimated subjects. Fi <r> o o cn June, 1956 f phosgene inv.. irritation with able. The 1 ppm arpreted from reis low enough to and Haggard to 2000 ppm fatal ppm the maximum rious disturbance, totes Muller to the om two four-hour 7 of 10 ppm, but not injure. Acute with convulsions, onic poisoning is nervous disturb). 576) concludes at 1 ppm. fifect of phosphine isoning. The 0.05 *e interpreted from animal inhalation. > prevent injury. Fairhall (1949, p. trature. The effects ; upon bone metaced first as painful ntaneous fractures develop into periho lower jaw, with le exposures one ,, usually fatal, feet of phosphorous soning, centering in u.m. threshold limit quantitative terms. iloride. Henderson 134) conclude this to nose, throat and 3 to hydrogen chlorhe solid are likely, lutes by 120 ppm. ffect of phosphorous is respiratory tract dema possible. The limit is apparently ntitative support. It prevent injury. fide. Fairhall (1949, : to the effect that le is somewhat less orous pentachloride. ffect of phosphorous is respiratory tract 4 1 Industrial Hygiene Quarterly 17a 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 tive support. It appears low enough to pre (1937-55) found rats survive four hours nt vent injurv- 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 39 to 60 minutes without serious disturbance. Cook (1945) quotes Butjog as finding 0.7 ppm causes only slight irritation in animals. human sensory data and analogy with ethyl alcohol. It is low enough to prevent signifi cant narcosis, but some irritation will result. Propylene dichloride. Heppel, Neal, High- The most important effect of phosphorous man and Porterfield (1946) found repeated trichloride inhalation is respiratory tract ir inhalation of 1000 ppm by animals killed 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 appeal's 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. um picrate in atmospheres from 0.008S to Propylene inline. Carpenter, Smyth and 0.1942 mg.,cu.m. They found little res Shaffer (1948) found rats and guinea pigs 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 th the acute The most important effect of picric acid toxicity of ethylene imine in simultaneous 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 sitization. limit can be interpreted from results of 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 seem low enough to prevent definite Woodman and Silverman (1943) found 400 narcosis. ppm causes mild irritation of eye, nose and Pyrethrnm. 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 m June, 1956 Industrial Uyuient C, degree of hazard, except for some slight skin definite at about 0.15 ppm, irritating at 0.5 sensitizing property. Carpenter, Weil, Poz- ppm and markedly irritating at 3 ppm. can be interpreted ft exposed workmen. It zani and Smyth (1950) found the rat oral After comparing exposure with concentra prevent injury. LDC0 of two samples to be 0.82 and 1.87 tion, the authors conclude quinone vapor Stthine. Webster ( gm./kg. Inhalation studies were made with should be kept below 0.1 ppm. lung injurant and pov an insecticidal aerosol containing 10% The most important effect of quinone in injuring liver and 1 pyrethrum and 90% peanut oil and a Freon halation is transient eye irritation and a tpropellant. Rats inhaled a concentration of slowly developing pigmentation in the eye. animals die after one ppm. Its action resem 6000 mg./cu.m. pyrethrum with 10 times The 0.1 ppm threshold limit can be inter understood arsine. as much peanut oil for 30 minutes, and only preted from the results of examination of The most importar moderate lung congestion resulted. Rats exposed workmen. It appears low enough halation is acute p<j and dogs inhaled a concentration of 16 to prevent effect. edema. The 0.1 ppm mg./cu.m. pyrethrum with 10 times as much Rotenone. On the basis of the literature interpreted by aualov peanut oil for 40 thirty-minute periods dur and his own work, Lehman (1949) esti pears low enough to l ing 31 calendar days, without injuries mates the fatal human dose to be 200 grams Stoddard Solvent. greater than those in peanut oil controls. by mouth. Woodman and Silverr Lehman (1949) estimates the fatal human The most important effect of rotenone in ppm produced no me dose to be 100 grams. halation is irritation of the upper respira climated subjects. 1 The most important effect of pyrethrum tory tract. The 5 mg./cu.m. tentative thresh coiogicall.v identical ' inhalation is irritation of the upper respira old limit can be interpreted by analogy with marks under that mat tory tract. The 2 mg./cu.m. tentative thresh pyrethrum. It appears low enough to pre & Strychnine. McNall old limit can be interpreted from limited vent injury. a human death has r repeated animal inhalation data. It appears Selenium compounds (as Se). Fairhall ing 30 milligrams. It low enough to prevent injury. (1949, p. 145) summarizes experimental The most importan Pyridine. Pollock, Finkelman and Ariell studies which stress oral doses of selenium inhalation is acute (1943) using pyridine for human therapy, dioxide and inhalation of hydrogen selenide. nig. cu.m, tentative t found no toxic symptoms after daily doses Even at 3 ppm dioxide in the diet rats are interpreted from the of 0.31 to 1.54 ml., but 1.85 to 2.46 ml. was injured, while 10 ppm kills within eight dose. It corresponds toxic, with one death of liver and kidney weeks. Dudley and Miller (1941) found ani 1.5 milligrams in a w< injury. Fairhall (1949, p. 434) considers mals killed in eight hours at 0.3 to 1.2 ppm low enough to prevent small repeated doses affect the bone marrow, hydrogen selenide, primarily due to lung in Styrene monomer. increasing the platelet count. Elkins (1950, jury, with changes in liver and spleen. and Rowe (1912) foi p. 167) quotes a Czech report of mild central Buchan (1947) reports industrial cases due death was anesthetic, nervous symptoms at 6 to 12 ppm. to less than 0.2 ppm (0.65 mg./cu.m.) hy to lung injury. Itlood < The most important effect of pyridine in drogen selenide, with symptoms largely Repeated inhalation halation is chronic poisoning, centering in referable to the liver. effect on animals. Hu liver, kidney and bone marrow. The 10 The most important effect of inhalation of ppm threshold limit can be interpreted from selenium-bearing dusts is chronic poison * extremely irritating I00 ppm had an ubjec limited human symptom data. Mild symp ing, centering in the liver. The 0.1 mg./cu.m, irritation. Carpenter toms may be found. threshold limit can be interpreted from the Smyth (1941) found Quinone. Sterner, Oglesby and Anderson results of repeated feeding to animals and narcosis in humans at (1947) reported on several years industrial by analogy with hydrogen selenide. This is experience with men exposed to quinone va probably low enough to prevent injury. vapor inhalation is ni por and hydroquinone dust. No systemic ef Sodium hydroxide. Elkins (1950, p. 84) limit of 200 ppm ca: fects could be found, but high concentration states inhalation of mists result in upper results of repeated a; caused transient eye irritation, and after respiratory tract irritation leading to human sensory respon several years a pigmentation of cornea and ulceration. Patty (1949, p. 561) on the basis prevent definite narco conjunctiva was apparent, due to local ac of experience with caustic mists from 1 to Sulfur dioxide. Keh tion on the exposed tissue. Loss of vision has 40 mg./cu.m.', concludes a concentration of and LeRlanc 11932) s followed pigmentation in some cases, ac 2 mg./cu.m. is noticeably but not excessively continuously exposed cording to Oglesby (1956). It is uncertain irritating. found only upper res] whether the vapor or the dust was responsi The most important effect of sodium hy irritation. Henderson j; ble. Concentrations from 0.01 to 3.2 ppm droxide mist or dust inhalation is upper p. 131) conclude it i j quinone were found in the plant. The odor of respiratory tract irritation, leading to ul systemic effect. They toi quinone is perceptible at about 0.1 ppm, ceration. The 2 mg./cu.m. threshold limit as dangerous in a she o BFG36808 ITS June, 195S 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 penta- fluoride vapor inhalation is lung injury. The 0.025 ppm threshold limit can be interpreted from results of repeated animal inhalation. It is probably low enough to prevent injur}'. 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 trointestinal 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 cholinesteriise inhibitor is about twice as toxic in single doses to ani mals as parathion, and the class of cholin esterase inhibiting compounds manifests little tendency to chronic effect. Vigliani and Zurlo (1955) on the basis of cholinesterase reduction in workmen, consider 0.0007 mg./cu.m. a satisfactory threshold limit. The most important effect of TEPP inhala tion is the reduction of blood cholinesterase. The 0.05 mg./cu.m. threshold limit can be interpreted only by analogy with parathion. It appears low enough to prevent injury. p-Terliary butyl toluene. Hine et al. (1954) in repeated animal inhalations, found narcosis, respiratory tract irritation, liver and kidney changes, blood cell changes like those from benzene, and degenerations in spinal cord and brain. Rats are killed in one hour by about 900 ppm, and slight evi dence of effect was found in animals re peatedly inhaling 25 ppm. Humans detect 5 ppm by odor, 80 ppm was unpleasantly ir ritating and some giddiness was noted at 160 ppm. The most important effect of p-tertiary butyl toluene inhalation appears to be chronic toxicity, combining effect on blood cells, central nervous system, liver and kid ney. The 10 ppm threshold limit can be in terpreted from results of repeated animal inhalations and human sensory data. It ap pears to be low enough to prevent significant toxic effect. 1,1,2,2-Tetrachloniethanc. Fairhall (1949, p. 440) concludes this is the most toxic chlorinated hydrocarbon, nine times as toxic as carbon tetrachloride. It is a narcotic and produces liver damage, polyneuritis and white blood cell changes. Elkins (1950, p. 139) refers to an unpublished report of ill ness from a concentration below 10 ppm. Smyth (1937-55) found rats survive four hours at 500 ppm but are killed by 1000 ppm. The most important effect of 1,1,2,2-tetrachtoroethane inhalation is chronic poisoning centering in the liver. The 5 ppm threshold limit can be interpreted from industrial ex perience. It is uncertain whether it is low enough to prevent some degree of injury. Tetrahydrofuran. Lehman and Ftury (1943, p. 269) report it a narcotic, irri tating mucous membrane and injuring the kidneys. In animals 3400 ppm for eight hours daily for 20 days caused some mucous membrane irritation and light narcosis, with albuminuria, lung and kidney injury and lung irritation in one animal each. ACGIH (1955b) quotes John A. Zapp, Jr. to the effect that repeated inhalation of 200 ppm, then 400 ppm, slightly affected the pulse pressure of dogs, but resulted in no histopathology. Hoffmann and Oettell (1954) in rabbits and cats found some nar cosis and mucosal irritation after six hours Industrial Hygiene Qnm inhalation of 3400 ppm. or kidney injury from 60,000 ppm. The most important et furan inhalation is narc portant injury to liver hr ppm tentative threshold ! terprctert from results < inhalation studies. It ai to prevent injury. Tetranitromcthane. i Gay and Monaco (1947; ritation of eyes, upper lung edema, methemoglo to liver and kidney. Cot to 25.2 ppm were severe 0.1 to 0.4 ppm caused on! two exposures. Horn (1 peated inhalation of 6.1 rats died from pticumo dogs was transient (more. The most important tromethnne inhalation is panied by irritation. Th limit can be interpreted peated animal inhalation to prevent injury, hut nor tation. Tetryt. Bergman (195 years' experience in an o more than 1000 exposed v trations kept below 1.5 stant diligence. Skin set quent but no systemic pc Hardy and Mnloof (195( and eight non-fatnl case the most prominent effec respiratory trnct irritat skin sensitization and a f tizations. Concentration 17.7 mg./cu.m. The most important ef) tion is chronic poisonini trotoluene, but the mos sensitization. The 1.5 i limit can be interpret* with exposed workmen, to prevent injuvy but n< Thallium. Fairhall (1 literature, concludes tti A CO chronic toxicity greater Useful quantitative dat pear to be lacking. oO) The most important c halation is chronic pi 2 CO June, 1956 u,- limit can be y with parathion. revent injury. ne. Hine ct al. mal inhalations, y tract irritation, blood cell changes md degenerations Rats are killed in m, and slight evid in animals re- Humans detect 5 s unpleasantly iress was noted at feet of p-tertiary i appears to be ig effect on blood em, liver and kidid limit can be inf repeated animal ;nsory data. It apprevent significant ie. Fairhall (1949, is the most toxic nine times as toxic t is a narcotic and polyneuritis and . Elkins (1950, p. d report of illv. oelow 10 ppm. rats survive four killed by 1000 ppm. ect of 1,1,2,2-tetras chronic poisoning ae 5 ppm threshold from industrial ex. whether it is low degree of injury, hman and Flury it a narcotic, irrie and injuring the .00 ppm for eight :aused some mucous nd light narcosis, and kidney injury one animal each. John A. Zapp, Jr. to l inhalation of 200 ightly affected the but l-esulted in no ann and Oettell its found some nartion after six hours Industrial Hygiene Quarterly 177 inhalation of 3400 ppm. There was no liver mg./cu.m. tentative threshold limit appenrs or kidney injury from inhalation of even to be based on a quantitative analogy with 60,000 ppm. lead. Its propriety cannot be judged. The most important effect of tetrahydro- Thiram. Meagre data have been found on furan inhalation is narcosis, with less im this substance. Smyth (1937-55) found the portant injury to liver and kidneys. The 200 rat oral LD50 to be 1.30 gm./kg. Rats sur ppm tentative threshold limit can be in vived four hours inhalation of a dense dust terpreted from results of repeated animal cloud, unmeasured but estimated to be at inhalation studies. It appears low enough least 500 mg./cu.m., with no effect but some to prevent injury. brief retardation of growth. Tetranitromethane. Sievers, Rushing, The most important effect of inhalation Gay and Monaco (1947) found in cats ir of thiram appenrs to be an ill-defined chron ritation of eyes, upper respiratory tract, ic toxicity. The 5 mg.'cu.m, tentative thresh lung edema, methemoglobinuria and injury old limit cannot be interpreted from pub to liver and kidney. Concentrations of 3.3 lished data found by the writer, but it ap to 25.2 ppm were severely injurious, while pears to be reasonable. 0.1 to 0.4 ppm caused only mild irritation in Titanium dioxide. Fairhall (1949, p. 180) two exposures. Horn (1954) found in re concludes titanium dioxide is chemically peated inhalation of 6.35 ppm that some , -inert and is not toxic. Lenzi (1936) found rats died from pneumonia. The effect on a pneumoconiosis in guinea pig lungs dogs was transient anorexia. after prolonged inhalation of high concen The most important effect of tetrani- trations. tromethane inhalation is poisoning, accom Inhaled titanium dioxide acts as an inert panied by irritation. The 1 ppm threshold dust, with only a slight tendency to produce limit can be interpreted from results of re pneumoconiosis. The 15 mg./cu.m. threshold peated animal inhalation. It is low enough limit is an arbitrary figure uniformly ap to prevent injury, but not to prevent all irri plied to inert nuisance dusts. It appears low tation. enough to prevent injury. Tetryl. Bergman (1952) summarizes ten Toluene. Von Oettingen, Neal and Dona years' experience in an ordnance plant with hue (1942) in repeated exposure of animals, more than 1000 exposed workers and concen found no blood cell changes or other toxic trations kept below 1.5 mg./cu.m. by con effects at 800 ppm. Humans inhaling 200 stant diligence. Skin sensitization was fre ppm for an eight-hour period found the quent but no systemic poisoning was found. earliest signs of impaired coordination and Hardy and Maloof (1950) report two fatal lengthened reaction time, while the effects and eight non-fatal cases with liver injury were more prominent and more prompt at the most prominent effect. There was upper 600 to 800 ppm. Fairhall (1949, p. 447 ) con respiratory tract irritation, very frequent cludes it is a narcotic with irritating proper skin sensitization and a few asthmatic sensi ties, but manifests no chronic effects. Elkins tizations. Concentrations were as high as (1950, p. 108) cites Greenburg's examina 17.7 mg./cu.m. tion of over 100 workers in atmospheres of The most important effect of tetryl inhala 100 to 1100 ppm without marked symptoms. tion is chronic poisoning like that of trini Smyth (1937-55) found rats survive four trotoluene, but the most frequent effect is hours at 4000 ppm, but die from 16,000 ppm. sensitization. The 1.5 mg./cu.m. threshold Commercial toluene may contain significant limit can be interpreted from experience amounts of benzene and may be more toxic with exposed workmen. It is low enough than these data indicate. to prevent injury but not sensitizations. The most important effect of toluene in Thallium. Fairhall (1949) reviewing the halation is narcosis. The 200 ppm threshold literature, concludes that thallium has a limit can be interpreted from results of re chronic toxicity greater than that of lead. peated animal inhalation, studies of human Useful quantitative data on inhalation ap narcosis and examination of exposed work pear to be lacking. men. It appears to be low enough to prevent The most important effect of thallium in all effects except the earliest signs of nar halation is chronic poisoning. The 0.15 cosis. GS0096F2 BFG36811 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, McColtister and Irish (1951) found no adverse effects from repeated inhalation by monkeys at 400 ppm, in rats and rabbits at 200 ppm, or in guinea pigs at 100 ppm. Single massive exposures kill by anesthesia. Even 3000 ppm inhaled repeatedly causes no more than very minor organic changes in the liver. They found almost identical effects from single and repeated inhalation of a single concen tration, and concluded the effects are chiefly those of narcosis. Voluntary habituation has been found in industry. The most important effect of trichloro ethylene inhalation is narcosis. The 200 ppm threshold limit can be interpreted from the results of repeated animal inhalations and observations in industry. It is not low enough to prevent significant narcosis. Trichloronaphthalene. After extensive in halation studies with rats. Drinker (1939) concluded injury is exclusively in the liver and that the permissible limit for repeated inhalation is 5 mg./cu.m. The solid material or its oil solution penetrates the skin and repeated contact leads to chloracne. The most important effect of trichloro naphthalene inhalation is chronic poisoning centering in the liver. The 5 mg./cu.m. threshold limit can be interpreted from the results of repeated animal inhalations. It is low enough to prevent injury. Trifluoromonobromomethane. A CGIH (1955b) quotes Chemical Corps Medical Laboratories Research Report No. 180,1953. This shows that the material is narcotic at high concentrations, but that 23,000 ppm for 18 weeks had iio toxic or lung injuring ef fects on dogs or rats. The most important effects of trifluoromonobromomethane inhalation are narcosis and respiratory tract irritation. The 1000 ppm threshold limit can be interpreted from the results of repeated animal inhalations. It appears low enough to prevent injury. Trinitrotoluene. Von 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 of soluble uranium dusts is chronic poison ing, centering in the kidney. The 0.05 Industrial Hygiene Qi mg./cu.m. threshold Ur from the results of re (ions. It is low enough Uranium (insoluble Neuman, Bale and Bra on inhalation, the to uranium on the kidne; V nrd than the nlpha ra uranium stored in th animal experiments, ? mg. cu.m, allows reuse tv over the level pro. The most important (# insoluble uranium du ing centering in tl mg./cu.m. threshold li. from the results of re tions. It is low enough Vanadiuin. Roshchi. to vanadium pen toxic mg./cu.m. for two hou three months, and to d for one hour daily ft lost some weight and ; tion. Some evidence was seen from the fun of the dust was inju. 70 to 80 mg./cu.m. v. suggests a threshold for fume and 0.5 mg. The most importa; of vanadium dusts s injury. The threshold for dust and 0.1 mg., interpreted from th animal inhalations. T to prevent injury. Vinyl chloride. Pr. (1930) found no s. guinea pigs inhaling hours. Higher concert narcosis. In humans, as a slight odor am dizziness is evident. The most importa; ide inhalation is n: threshold limit enn !; results of single ni human response. It : prevent significant n; Warfarin. Saunck and Bay (1955) ft mg./kg. for five days group of rats, while } 100 mg./kg. caused o BFG36812 June, 1956, injuring ef- ;cts of trifluorotion are narcosis tation. The 1000 interpreted from imal inhalations, irevent injury. Oettingen et al dogs found only me effects on red .ratraeheal insuf5 daily dosage by >e months but re- nervous system, t3. The material y (1944) reports three humans at mg./cu.m, ect of trinitrotolupoisoning marked >m, liver and red mg./cu.m. thresh ed from a report ot probably not low afsmyth (1928) ilation of 750 ppm Nelson, Ege, Ross, i (1943) with un nose and throat e 175 ppm was hall (1949, P- 464) and kidney injury. Lffect of turpentine ut irritation of the ore frequently enthreshold limit can ilts of repeated aninan sensory data. It t injury. Jranium is a radio emission of alpha igical hazard primato kidney tubules, ieuman (1949) show toxicological hazard :he radiological hazil experiments, they allows a reasonable the level producing effect of inhalation ts is chronic poison: kidney. The 0.05 Industrial Hygiene Quarterly 179 mg./cu.m. threshold limit can be interpreted from the results of repented animal inhala tions. It is low enough to prevent injury. Uranhnn (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 can 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. Fairhali (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 arc 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 hydrochloric acid. I izi. * ISO June, 195$ Industrial Hygiene Qua - Lr The effect of zirconium dust inhalation is that of an inert nuisance dust when insolu Rnltimore City Health Department (1943), Division of Industrial Hygiene: Baltimore Health New*. 20: Sep tember, 1943. uriciimanx, w. b.j Kitsmbu S. (1944): Phenol atudlee VI ble, and possibly bronchial and lung irrita Barnes. J. M. (1953): Toxic hazards of certain pesti inf, with special referent* ` perlmental anlmak of the 1^ tion when soluble. The 5 mg./cu.m. tentative cides to man. World Health Organisation, Geneva. Am. J. Clin. Path* threshold limit can be interpreted from the results of repeated animal inhalations. It Monograph 16. Barthelemy. H. L. (1939): Ten years experience with industrial hygiene in connection with the manufacture Dernehu C- U.; Nau. C. A* %s Animal studies on the toxteUi oxide, J. lnd. Hyg. if Tox., i appears low enough to prevent injury. Bibliography of viscose rayon. J. Ind. Hyg. & Tox., 21:141-151. nERRMAN. IL B. (1952) : Tetryl toxicity. Arch. lnd. Hyg. A Occup. Med.. 6:10-20. Bloomfield, J. J.. and Blum. W. (1928): Health h&tards in chromium plating. U.S. Fubtic Health Service, rub. 7 Dernehu C. U. (1961): CHafc sure* to ethylene amlnea, lnd. DtEKR. S. H.. and RtctnKk, c. Assays of roOentlcidm on vlld ACflIH (1947): 1947 M.A.C. vnluoa. tad. Hyg. Netr*<tter, JJrnUh Rpt*., 43:2330-2351. Health Service, Health ; 7:15-16, August. Bradley, W. R.. and Fredrick, \V. G. (1941): The toxicity Dirrkkx. II.. and Brown, P, G. ACGIH (1948): Threshold limit values adopted at April, 1948 meeting (privately circulated). ACGIH (1949) : Threshold limit values adopted at April of antimony: Animal studies, lnd. Med., 10, Ind. Hyg. Sec.. 2:15-22. Braxdt. A. D. (1947) : Industrial Health Engineering. l rase of ethylene chhrhyilrlR ; Tor., 26:277-279. ; Doxutv. D. K. 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Arch. lnd. Hyg. A Oe- Metal fume fever. IV. Thre* ACGIH (1953b): Privately circulated document giving support for many earlier adopted threshold limits, and rthose proposed in 1963. cup. Med.. 1 :623-636. Buchan, R. F. (1947): Industrial selcnosis. Occup. Med., 3:439-436. preventive measure* and the exposures. J. !d. Hyg., 9:3. Drinker. P.: Yaclou. C. P., an ACGIH (1954) : Threshold limit values for 1954. Arch. Cameron. G. R.; Thomas. J. C.: Ashmore, S. A.; War The threshold toxieity of gsao lnd. Hyg. Occup. Med., 9:530-534. ren, E. H.; Buchan, J. L., and McKsnny-Huoties, Tox.. 25:225*232. ACGIH (1964b); Privately circulated document giving A. W. (1937): The toxicity of certain chlorine deriva Dudley. H. C-. and Mill**. . support for threshold limits newly proposed in 1954. ACGIH (1955): Threshold limit values for 195*. AMA tives of benzene, with special reference to o-dichlorobenxene. J. Path. I3act,, 44:231-296. subacute exposure to hydroge Tox.. 23:470-477. Arch. Ind. 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Reprints Available REPRINTS of the preceding Cummings Memorial Lecture may be obtained from GEORGE D. clavton, Executive Secretary, AMERICAN INDUSTRIAL HYGIENE ASSOCIATION, 14125 Prevost, De troit 27, Michigan, at $1.50 each. The price of this issue of the AIIU QUARTERLY is $2.00. it Ai Dr. H.nry Fiald SmytH, Jr., r.csiving fh Cummings Mamorial Award From N. V. Hendricks, Presidant of tha American Industrial Hygl.n. Association. Tho presentation was mad. at tfia banquat of tha Associ.* tion's Sov.ntaanth Annual maating in Pfsilacfafphia, Wadn.sday, April 25. $ $ o p? 00 Xi 1:: '