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Improved Communication -HYQIENIC STANDARDS FOR DAILY INHALATION- 7^ "DaKdCd 5- '?He*H<vUcil ^cctcvie HENRY FIELD SMYTH, JR,, Ph.D. Mellon Institute end Union Carbide and Carbon Corporation Pittsburgh, Pennsylvania 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 our ability to communicate, crets of nature, feeling no need we may be well on the way and finding no opportunity to toward emerging into a new 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 Hanry F. Smyth, Jr. from the current division of labor, of experience, and of rection has been made during the past ten knowledge. Each one of us 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, Presented at the Seventeenth Annual Meeting of the American Industrial Hygiene Association, Philadelphia, April 25, 1956. "We must provide a fluid and effective means of communication between the chem ist, the engineer, the physicist, the toxicolo- 'TVS l-V* UCC - 109566 130 June, 1956 gist, the physician, and the other special ists brought into industrial hygiene. There must result from this interchange of ideas not only an appreciation of each team mem ber's contribution, but an ability actually to bridge the gap between the disciplines, to synthesize, from the offerings of each of the fields, the solutions to the ever more com plicated problems. Each member specialist must not only contribute the information he is most qualified to give, but also must en courage a sympathetic, intelligent, and mu tual understanding." In this matter of mutual understanding, we are very much like the inhabitants of Looking Glass Land. You remember that the White Queen told Alice, "Now here, you see, it takes all the running you can do, to keep in the same place. If you want to get somewhere else, you must run at least twice as fast as that." With the entry of new people into our profession and the recogni tion of new constituent specialties such as health physics and atmospheric pollution control, each with a tendency to keep to it self, are we running fast enough even to stay in the same place? We all feel there are too many conferences and too many com mittees to leave us time to do our daily work. On the other hand, if we are to do our work as well as it can be done, we must be in constant communication with related spe cialists, because each one of us fully knows only one facet of his own problems. Communication is not a simple process. It requires an informed speaker or writer who can express himself at the level of compre hension of his audience. It requires an audi ence which wishes to receive communica tion. It must be carried on with words, those abstract symbols for reality, each of which has a different meaning to each in dividual, shaded by his entire past experi ence. Only a newly coined word is free from ambiguity, and it remains new for only a brief interval. Most important of all, suc cessful communication requires what is to day known as feed-back. By this, the speaker hears his audiences' impressions. He can correct and amplify his words until he thinks his audience truly perceives his mean ing. A leisurely conversation can be effective communication through f.eed-back; an arti cle in a journal is likely to'be poor communi cation because feedback isunadequate. The relatively new specialty of industrial toxicology has already contributed to the equally new profession of industrial hy giene by means of communication. The toxi cologists are doing an acceptable job for those people who recognize their need for toxicological information and opinion. The job could be done better, but it is at least ac ceptable. Success is by no means as great in helping those people who do not recognize their need for help. Once more communica tion cannot succeed unless the audience de sires to receive communication. Acceptable Concentrations 'J'he most important communication within industrial hygiene, and between our profession and others, may be the collection of judgments upon acceptable concentra tions of contaminants in working atmos pheres. During what may be called the age of chaos, every experienced industrial hy gienist had a few values uniquely his own, drawn from his own experience. For less familiar substances, he borrowed more or less judiciously from the values cherished by his professional colleagues. Some degree of unanimity was brought about when the United States Public Health Service values, based on its long-time collective experience in industrial hygiene, were published in a manual (USPHS 1943). Further unanimity followed publication of the values collected and extended by Cook (1945). In 1947 the American Conference of Governmental In dustrial Hygienists published its first list in the Industrial Hygiene Newsletter (ACGIH 1947). In the next two. years (ACGIH 1948, ACGIH 1949) revised lists were privately circulated to the members of the Association. Then (ACGIH 1950) pub lication took place in a scientific journal, and each year thereafter a revised list of threshold limit values has appeared in the scientific literature, and has been general ly accepted. The contributions of Cook (1945) in uni fying opinion, and in weighing threshold limit values then in use, judging new data and proposing a list of 129 values, are worthy, of high regard. Among the 238 values for substances other than mineral dusts in the current list (ACGIH 1966) of established and tentative threshold limit values are 54 of those which were first pro- , *t. vV ' *- Jl'T-'V'Ltv lm POM tab UCC - 109567 Industrial Hygiene Quarterly IS1 posed in Cook's list, some as definitely es tablished, others to be used cautiously until verified by actual experience. Not since Cook has anyone published a summary of the data which serve as bases for the selection of specific threshold limits. The privately circulated documents which give some of these data (ACGIH 1953b, 1954b, 1955b) cannot be considered to be publication, although they are freely avail able to any person. Threshold limits are, and must continue to be the products of judgment, important if true. Some few truly represent their defi nition and are approximations of the maxi mum concentrations which can be inhaled continuously and repeatedly without injury to health. These may possibly be fit para meters for incorporation into codes and regulations. Many of the threshold limits are well below concentrations which can in jure health. They represent current judg ment as to concentrations to which, good practice dictates, men may be expected to subject themselves. These do not seem fit parameters for regulations. In a particular operation, if possible, it is desirable to maintain concentrations below the bench mark by reasonable ventilation and precau tion. It is always best to reduce exposure to chemicals to the lowest practical level. 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 prais ing the development of threshold limits, and to suggesting ways in which their presenta tion could be made more useful. Since that report, two developments have taken place along lines desired by the Committee. The annual table of the Threshold Limits Com mittee of the American Conference of Gov ernmental Industrial Hygienists is now pub lished in the Archives of Industrial Health, removing the earlier implication of 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 jind 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- y mum, threshold and limit. These words all l A ucc 132 June, 1956 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 without injury to health." Careful study of the data which support the currently ac cepted values suggests that no such de scription can be truthfully attached to most of them. Industrial hygienists recognize this. They are accustomed to emphasize that the values should be regarded simply as bench marks, guides to good practice. In deed, the Threshold Limits Committee it self confusingly warns "Threshold limits . . . should not be regarded as fine lines be tween safe and dangerous concentrations." (ACGIH 1956) The term maximum acceptable concentra tion being used in revisions of standards by the American Standards Association Z-37 Committee is objectionable only because it will be abbreviated M.A.C. Many will in terpret this abbreviation as maximum al lowable concentration, and nothing will have been gained by the change from allowable to acceptable. I conclude that the names maximum al lowable concentration and threshold limit are misleading. They convey a wrong im pression to those who are not already famili ar with the concepts behind the values. The name suggested in 1949, hygienic standard, is not misleading. Standards of good prac tice are familiar to all of us in many fields. Looking toward the future provision of a variety of hygienic standards, a series of values should be selected, to be known as hygienic standards for daily inhalation. The third suggestion is more far-reach ing. The Committee on Chemical Agents (1949) pointed out that there has been no simple or uniform relation between the ef fects of a substance and the numerical value chosen for tabulation. The Committee con cluded that concentrations have been se lected on the basis of one of four concepts of the level best suited to hygienic control of inhalation, the choice having been governed by the nature of the toxic response and by 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 of toxic effect in any workman during a lifetime of industrial exposure. c. Bench mark: A concentration based on the belief that any unnecessary ex posure is undesirable--a concentration lower than that of a or b, one as low as is consistent with practical engineering con trol. d. Comfort: A concentration lower than a or b, representing the maximum which in a short time is not objectionable to 9 out of 10 of a group of persons not accustomed to inhalation of the substance. Note well that these four concepts were judged to be those already used for the se lection of hygienic standards for daily in halation. All four were judged consistent with the goals of industrial hygiene. Hygienic Standards for Daily Inhalation 'J'he subject of hygienic standards for daily inhalation should be re-examined, the concepts represented by the values should be restated in more realistic toxi cological terms, and more consistent and more informative standards should be pre pared. Such a step will not undo any of the accomplishments of the profession of in dustrial hygiene or of any organization. Rather, it will supply informative standards to supplement the accumulation of naked numbers now accepted, some of which have not been critically re-examined for a decade. It is certainly imperative that the inhala tion of substances during the working day shall not be allowed to result in any injury to the physical well-being of workmen. It is furthermore imperative that inhalation shall not increase the probability of acci dents through the mental distress occa sioned by objectionable eye, nose or throat irritation, transient though it may often be, nor through the impaired judgment and delayed reaction time of light narcosis. It is desirable that-inhalation shall result in no degree of discomfort whatsoever. On. the 4 In cisio comj A shou with to be cone* no ii work it ma irritj prodi versi these how serve curve injur range men, not a Ad. stand periei of wc ucc 109569 Industrial Hygiene Quarterly 133 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 stiff re versible and non-progressive effects. From these two concentrations, one can at once see how strictly the standard should be ob served, the steepness of the dosage-response curve, the breadth of the plateau of noninjurious concentrations. Despite the wide range in individual susceptibilities of work men, such values can be selected for most, if not all, substances. Adequate data for preparing this sort of standard consist of appropriate human ex perience, or repeated medical examinations of workmen in atmospheres whose concen tration has been frequently estimated. Sterner (1955) discussed this point in de tail. Experiments upon animals, verified by biochemical and physiological studies in humans, may demonstrate conclusively that a substance has an effect during one period of inhalation which does not progress dur ing oft-repeated inhalation. For such a sub stance, satisfactory data can be obtained from objective study and secretly recorded subjective effects of a group of humans in haling known concentrations for substan tially eight hours. Any lesser body of data should result in a hygienic standard being designated as tentative. Categories of Objectionable Action udgments should be made to determine J which hygienic standards for daily in halation must be carefully observed, and which may be exceeded when it is im practical to observe them. These judgments will be most consistent if we first decide for each substance what objectionable action we are guarding against by the standard. Every toxicologist will realize that the ac tion at a low concentration which it is most important to guard against, may not be the same as the menace to life to be expected at a high concentration. In a tentative fashion, the writer has made these decisions for the 238 substances, exclusive of the mineral dusts, included in the 1956 tables of pro posed accepted and tentative standards (ACGIH1956). The decisions can be divided into the following nine categories on the basis of the nature of human response. Chronic toxicity. The most dangerous ef fect of some substances is a progressive systemic injury, increasing in severity with continuing inhalation. Benzene, carbon di sulfide, carbon tetrachloride and lead are the most familiar examples. The lower stand ard for these substances should be a concen tration believed not to produce any effect in any workman, and no considerations of practicality are sufficient to justify inhala tion in excess of the standard. Close medical supervision is required for safe use of these substances. The standard for chronically toxic substances should refer to the timeweighted average concentration throughout a working day. Brief peaks of a few times the standard have no significance, save as they increase the average. 134 June, 1956 Acute toxicity. Some substances do not produce an injury progressing with re peated inhalation. Such systemic injury as they may cause takes place as the result of one excessive inhalation, or not at all: Familiar examples are carbon monoxide and hydrogen cyanide. The standards for acute ly toxic substances should be interpreted in the same light as those for chronically toxic substances. Narcosis. The most dangerous effect of some substances is narcosis, which becomes anesthesia in its extreme stage. At a rather low concentration they induce accidents by impairing judgment and delaying reaction time. Familiar examples are ethyl alcohol, ethyl ether and gasoline. The lower stand ard for a narcotic substance should be a concentration which produces no detectable effect upon judgment and reaction time af ter eight hours inhalation. It should refer to the average concentration existing during some appreciable period of time, the length of which can be estimated from absorption and elimination data. No considerations of practicality can justify exceeding the stand ard for a narcotic substance. Irritation. The most dangerous effect of some substances is irritation. Eye, nose and throat are irritated at a low concentration, the bronchi at a higher concentration, and fatal lung edema may be the result of inhal ing an extreme concentration. The alde hydes, halogens and acids are familiar ex amples. Highly odorous substances may also be considered in this category. The lower standard for an irritant substance should be a concentration which is detectable, but is not objectionably irritating to the majority of unhardened subjects who are exposed for a substantial part of a working day. The higher standard should be set at a concen tration which is well under one injuring bronchi or lungs, arid which is justifiable when it is impractical to keep concentra tions at the lower standard. Standards for irritating substances should refer to concen trations existing for even a brief period during a work day. Asphyxiation. Some substances are inert in the body and can injure only by asphyxia at extremely high concentrations, exclud ing the oxygen of the atmosphere. Familiar examples are the fluorochloro refrigerants. The lower standard for these asphyxiants should be a nominal bench mark of good en gineering practice, such as the 1000 ppm concentration now quoted. The inert nui sance dusts like iron oxide might well be placed in this same category, and the cur rently used bench mark of 15 mg./cu.m. seems an appropriate level. The standard should refer to the concentration existing during any brief period, but it should be recognized that higher concentrations are justified when it is impractical to keep below the standard. Fume fever. The most important effect of some substances is a transient influenza like condition known as fume fever. A familiar example is zinc oxide fume. The lower standard for a fume fever producer should be a concentration which will not produce that distressing but not menacing condition in any workman, and it should apply to an appreciable period, such as half an hour. No considerations of practicali ty can justify exceeding the standard for fume fever producing substances. Eye pigmentation. The most important effect of two substances, quinone and hydroquinone, appears to be a slowly develop ing pigmentation of the sclera, which may reduce visual acuity, or even lead to blindness. The lower standard for these substances should be a concentration which produces no pigmentation after years of exposure, and it should refer to the timeweighted average concentration throughout the day. For a few days at a time, conditions of practicality should justify exceeding the standard. Cancer. One substance is reasonably well established as a cause of respiratory tract cancer. This is nickel carbonyl. It appears probable that the minimum cancerigenic ex posure will never be defined. At this time it is prudent to set the standard for a can cerigenic substance substantially at zero, as has already been done for nickel carbonyl, and no considerations can justify allowing the inhalation of any concentration which is avoidable. Allergy. Some substances are known to sensitize an appreciable proportion of ex posed workmen. They may produce distress ing and menacing asthma-like attacks when a sensitized person inhales a low concentra tion. Examples are ethylene diamine and the diisocyanates. At this time there is no t V S` H, \ \ ucc 109571 Industrial Hygiene Quarterly 135 rational experimental basis for defining a 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 "NUo new values for standards are sug gested at this time. The available data upon which the 238 values in the 1956 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, pyrolysis 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 ly 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 notoriously 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 hy gienists and toxicologists. Not one of these but will object to some among the thousand personal judgments entered. However, the 136 June, 1956 annual threshold limit tables are consulted by upwards of twenty thousand other per sons who do not have access to original sources and extensive experience. These peo ple rightly regard the threshold limits as a presentation of the best available judgment, and they may wrongly regard them as every thing they need to know about safe use of a substance. Despite specific disclaimers, printed with each year's table, these readers tend to regard each threshold limit as de fining the line between safety and injury. Table I is presented as a beginning in the extensive job of improving communica tion by developing a rational and informa tive series of hygienic standards for daily inhalation. Summary of Underlying Data 'J'he data relied upon for the interpretations entered in Table I are summarized and briefly commented upon in the pages which follow. It is believed that the most significant published information is in cluded, but no attempt has been made to list all pertinent articles. Certain hitherto un- published observations are included when they appear to confirm or supplement ma terial in the literature. The term "most im portant effect" used with 'every substance, refers to the possible effect of inhalation of concentrations a few times the threshold limit, not necessarily to the possible effects at very high concentrations. Acetaldehyde. Cook (1945) quotes the 1911 report of Iwanoff that cats inhaling 280 ppm for seven hours were not noticeably affected. The unacclimated subjects of Sil verman, Schulte and First (1946) found 25 ppm objectionable, 50 ppm irritating to the eyes, but even 200 ppm not irritating to the throat. Fairhall (1949, p. 199) describes the effects as irritation, narcosis, bronchitis, albuminuria, fatty liver and lung edema. He concludes that inhalation does not cause chronic poisoning, and that death is due to anesthesia when prompt, or to lung edema when delayed. Smyth (1937-65) found rats survive four hours inhalation of 8000 ppm but die from 16,000 ppm. The liquid causes severe corneal injury, irritates the skin and may sensitize some persons. Mnemonic abbreviations used in Table I. acn^-- chloracne from continued skin contact. acute-- acute toxicity, with little or no increase in all-- severity from continued inhalation. allergenic. Dermatitis and asthma-like sen- sitization may result. allergenic. Dermatitis and asthma-like sen* sitization are likely. asphyxia---asphyxiation at very high concentrations. bur-- burn of the skin. BUR-- very severe burn of skin. cancer^ cancer reported in humans. chronic-- chronic toxicity, with increase in severity from continued inhalation. clin-- clinical examination of workmen was cor- v cns-- related with their exposure. central nervous system stimulation, such as cy-- tremors or convulsions. cyanosis (blue skin) may be evident. CY-- cyanosis (blue skin) may be marked. 8t-- estimate from experience and analogy. eye-- eye irritation severe enough to require medical treatment. EYE-- eye burn mty be .evereu eye pig--* eye pigmentation without injury. fume fever. head-- Headache. This symptom has not been en- hu-- tered every time it may occur. human sensory data. HU-- human toxicological or physiological data. ind-- industrial complaints or observations, less quantitative than clinical examinations. irr-- irritation of eye* nose or throatin soma, IRR-- irritation of eye, nose or throat marked, `, lungf-- minor irritation of bronchi (coughing) or lungs. lung-- definite irritation of bronchi or lungs with injury of lungs possible. LUNG-- dangerous injury of lungs with little warn- ing. m-- the quantity is expressed in milligrams per cubic meter (mg./ou.m.), not in ppm. med-- medical usee yield some information. narcosis-- narcosis, ranging from impaired coordina- tion through dizziness, to anesthesia. narT-- faint narcosis, somewhat impaired reaction time and judgment. nar-- narcosis definite, short of dizziness. NAR-- narcosis marked, dizziness to unconscious* ness. n&U-- nausea. This symptom has not been entered every time it may occur. none-- no effects are expected. odor-- odor may be perceptible. ODOR-- odor marked. pyr-- pyrolysis to lung injuring- halogen com* pounds in a flame, or on hot metaL r*d-- radiation injury is possible. rpt-- repeated animal inhalation results* agl-- single animal inhalation results. akp-- skin penetration may cause symptoms. SKF-- skin penetration of liquid is dangerous. T-- tentatively proposed. tox?-- toxic symptoms may arise very slowly. tox-- minor toxic symptoms. TOX-- major toxic symptoms. via-- visual acuity loss Cad: Calc ucc . 109573 Industrial Hygiene Quarterly 137 Table I. 1956Interpretation of Threshold Limit Values Proposed for Exclusive of Mineral Dusts (Mnemonic abbreviations explained at foot of table) Substance Threshold Limit Dpm or mg./cu.m. 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 AUyl alcohol Allyl chloride Ally! propyl disulfide 20- acute m-0-25 chronic 6. EY E-lung 6. T lung 2. lung Ammate Ammonia Amyl acetate Amyl alcohol Aniline m-15. 100. 200. 100. 6. lung lung narcosis narcosis chronic Antimony ANTU Armenia Arsine Barium (soluble) m-0.5 chronic m-0.3 T chronic m-0.6 chronic 0.05 acute-lung m-0.5 acute-lung Benzene Benzyl chloride Bromine Butadiene Butanone (methyl ethyl ketone) 86. chronic 1. * lung 1. 1000. lung narcosis 25 0. narcosis Butyl acetate Butyl alcohol Butyl amine Butyl CELLOSOLVE Butyl mercaptan 200. 100. 6. narcosis narcosis lung 200. chronic 10. T lung Predicted Effects of Daily eight-hour Inhalations At Thteshold 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 eye-IRR-lung NAR lung tox irr-tox eye-lung irr-odor irr none irr-odor irr-odor irr-odor none none none none none IRR IRR-nar IRR-nar cy none tox? lung IRR-lung NAR NAR CY-tox tox tox tox lung?-tox none tox? irr tox odor tox nar-odor-TOX IRR-lung irr-odor none odor IRR-lung nar irr-odor irr-odor odor odor IKR-nau IRR-nar irr irr nar NAR ' IRR-NAR eye odor-tox ? ODOR nar-tox frr-nar-TOX eye-irr-lung ? Important Hazards Other Than from Inhalation ali-EYE bur-EYE Nature of Interp retive Data hu-sgl hu-ind-sg] Year Proposed 1945 1945 bur-EYE bur-EYE skp all-skp bur-EYE pyr sgl HU-ind hu-sgl rpt clin itid-sgi sgl 1947 1953 1945 1943 1964 1954 1966 bur-eye SKP ind est HU-ind-sgl hu-Sgl hu-sgl rpt clin-rpt est clin-est ind-sgl 1954 1954 1943 1945 1945 1943 1948 1956 1948 1947 EYE est clin-rpt 3gl 1943 1948 1954 BUR-EYE ind-sgl hu-rpt 1945 1947 BUR-EYE skp hu-sgl hu-sgl clin ind-sgl rpt sgl 1948 1945 I960 1955 1945 1954 Cadmium oxide fume Calcium arsenate Carbon dioxide Carbon disulfide Carbon monoxide m-0.1 acute-lung m-0,1 T chronic 5000. asphyxia 20. chronic 100. acute none none none none none odor tox none nar nar-tox TOX ind-rpt eat HU clin-rpt clin-HU 1948 1956 1948 1948 1943 Carbon tetrachloride CELLOSOLVE CELLOSOLVE acetate 26. 200. 100. chronic chronic chronic tox? odor odor tox nar-tox nar-odor-TOX irr-nar-tox pyr itr-tox IRR-nar-tox clin-ind-rpt rpt 1953 1946 rpt 1945 ucc 109574 138 June, 1956 Table I--Continued Substance I.imit 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 Chlorobenzene Chlorobromo- methane m-0.5 1, chronic lung 0.1 lunar 75. narcosis 400. T narcosis Chlorodl- pheny) (42% Cl) m-1. Chlorodiphenyl (64% Cl) m-0.5 Chloroform 100. l-Chloro*l- nitropro- pane 20. Chloropicrin 1. chronic T chronic chronic lung T lung Predicted Effects of Daily eight*hour Inhalations At Threshold Limit Additional Additional At Twice At Ten Times Thi eshold - Threshold Limit Limit none none irr-tox none tox none odor none odor none tox 7 irr irr-tox nar tox IRR-lung irr-lung nar tox none none odor-tox ? none tox? nar-tox tox? tox TOX none odor irr-lung-tox irr lung Chloroprene Chromic acid, chromates aa CrOi CRAG herbicide Creaol Cyanide ae CN 25, m-0.1 m-16. . m-6. chronic irr chronic chronic acute none none none odor none nar-tox TOX irr none irr IRR irr-tox? lung.tox tox Cyclohexane Cydohexanol 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-NAR-tox IRR-NAR IRR-nar irr-NAR-tox irr-NAR 2,4-D DDT Decaborane Diacetone alcohol Diborane irv-10. chronic m-1. T chronic 0.06 T acute 50. narcosis 0.1 cns-lung none none none irr none none none odor irr-tox 7 irr-tox odor IRR-nar lung-tox? o-Dichloro* benzene Dlchlorodlfluoromethane 1,1-DicbkuDethane l,2*Dichk>ro* ethylene Ditbloroethyl ether 60- 1000. 100. 200. 16. chronic odor-tox 7 asphyxia chronic narcosis lung none odor none none irr-tox nar none none nar-tox odor irr-nar irr-odor lun Dichloromonofluoromethsne 1,1-Dichloro1-nittoethane 1000. 10, asphyxia none lung none none irr none lung-tox Hazards Other Than from Inhalation all-skp Mature of Interpretive Data clin Year Proposed 1954 all-skp est 1956 acne bur-EYE bur-EYE pyr pyr rpt hu-rpt rpt e*t-6gl rpt 1955 1948 1956 1943 1966 acne acne pyr rpt rpt est-med-sgl 1946 1956 1946 pyr-skp sgl clin rpt 1946 1956 1945 bur-EYE clin est BUR-EYE-SKP wt-sEl est rpt hu-rpt hu-rpt sgl est-med est skp est rpt hu-ggl clin-rpt pyr ind-sgl 1943 1964 1962 1947 1946 1945 1946 1946 1947 1964 1964 1966 1954 1965 1947 pyr rpt 1947 pyr rpt 1945 pyr Sgl 1946 skp hu-sgl 1945 pyr sgl 1947 rpt 1945 Ind Diniti zem Diniti ere* Diniti Dioxa EPN Ethyl Ethyl Ethyl EthyU Ethyl Ethyl Ethyl Ethyk chlo Ethyle dian EthyU dibr Ethyle dich Ethyle imir Ethyle Ethyl Ethyl Ethyl men Ethyl Ferbar Ferro um Fluoric Fhiorii ' Fluoro. Fluoro cbloi meth Forma Furfur Furfur alcoh GmoHd :c UCC - 109575 56 46 45 143 >47 947 1947 1946 industrial Hygiene Quarterly 189 Table I--Continued Substance Threshold Limit ppm or mg./cu.m. Most Important Effect of Inhalation Predicted Effects of Daily eight-hour !Inhalations At Threshold Limit Additional At Twice Threshold Limit Additional At Ten Times Threshold Limit Dichlorotetrafluoro- methane Dieldrin Diethylamine 1000. m-0.25 25. chronic asphyxia lung none none odor 0 none none ?ye*irr none irr IRR-lung Diftuorodibromomethane Diisobutyl ketone Diisocyano toluene Dimethylaniline Dimethylsulfate 100. chronic none 50. narcosis irr-odqr 0.1 T ALL-Iung all 6. chronic none .1 acute-LUNG none none cy irr-nar-tox IRR-nar ALL CY-tox LUNG-TOX Important Hazards Other Than from Inhalation Nature of Interpretive Data pyr all-skp bur-EYE sgl clin sgl pyr rpt hu-rpt ind SKP *gi BUR-EYE-SKP sgl Dinitrobeuzene Dinitro-oc resol Dinitrotoluene Dioxane EPN m-1. T chronic m-0-2 m-1.5 100* m-O.G acute chronic chronic acute none none tox? none none Ethyl acetate Ethyl acrylate Ethyl alcohol Ethylamina Ethyl benzene 400. 25. 1000. 26. 200. narcosis T lung narcosis lung narcosis irr-odor odor irr-odor odor narT-odor Ethyl bromide Ethyl chloride Ethylene chlorhydrin Ethylene diamine Ethylene dibromide 200. 1000. 5- 10. 25. lung , narcosis none odor acute none ALL-lung odor chronic-lung none tox tox? nar-odor nar irr nar eye-irr irr irr-odor irr-tox irr-tox irr-NAR-tox tox IRR-NAR lung IRR-NAR IRR-lung NAR lung nar toxt irr odor-tox eye irr-odor lung-tox skp est skp skp bur-EYE pyr pyr sgl est hu-rpt est hu-sgl rpt HU sgl hu-sgl sgl Sgl SKP ind-sgl ALL-bur-EYE ind-rpt pyr rpt Ethylene dichloride Ethylene inline Ethylene oxide 100- 6. 100. Ethyl ether 400. Ethyl formate 100. chronic odor-tox? acute-lung lung-nar- costs narcosis narcosis odor odoT-nar irr-odor none nar-nau TOX pyr lung-TOX bur-eye-SKP irr IRR-LUNG-NAR bur IRR NAR irr-odor nar ind-rpt hu-sgl hu-rpt HU-med Sgl Ethyl mercaptan 250. T lung Ethyl silicate 100. acute-lung Ferbam m-16. TIung Ferro vanadi- um dust lung Fluoride dost m-2.6 chronic Fluorine Fluoroaeetates Fluorotri- chloro- methane Formaldehyde Furfural 0.1 m-0.1 1000* 6. 6. lung T acute asphyxia lung TIung Furfuryl alcohol Gasoline 60. T narcosis 600. nnreoai. ODOR odor none none toil none none none Irr irr odor odor irr-tox irr eye-irr-lung IRR IRR none irr-tox Irr-hmgT-tox T tox nil BUR-EYE none odor none IRR-lung IRR-lung irr-nr - irr-nar IRR-NAR NAR pyr -11-EYE .11-EYE Sgl hu-rpt eat rpt clin-HU clin-rpt est el Ind-egl ind-egl rpt hu-ind Year Proposed 1947 1954 1952 1955 1954 1956 1943 1945 1956 1949 1943 1947 1964 1945 1956 1945 1962 1945 mi 1947 1947 1966 1963 1953 1956 1945 1947 1947 1954 1946 1955 1954 1947 1963 1965 1945 1948 1954 1955 1946 UCC 109576 140 June, 1956 Substance Threshold Limit ppm or mg./cu.m. Most Important Effect of inhalation Table I--Continued Predicted Effects of Daily eight-hour Inhalation* At Threshold Limit Additional At Twice Threshold Limit Additional At Ten Times Threshold Limit Heptane HETP Hexane 500. narcosis m-Q.i T acute 500. narcosis odor none odor irr-nar irr NAR tox irr-nar-nau Hexanone (methyl butyl ketone) Hexone (methyl isobutyl ketone) Hydrasine Hydrogen bromide Hydrogen chloride 100. narcoBiB odor 100. narcosis odor 1. lung none 5. lung irr 5. him irr irr nar irr IRR IRR nar cns-irr-lung eye-lung eye-lung Hydrogen cyanide Hydrogen fluoride Hydrogen peroxide. 90% Hydrogen selenide Hydrogen sulflde 10. acute odor 3. chronic-lung trr 1. lung none , 0,06 chronic-lung none 20. lung irr-odor IRR TOX eye-lung-tox irr-lung lung-odor-tox lung-tox Hydroquinone Iodine Iron oxide fume Isophorone m-2. 0.1 m-16. 26. Isopropylamine 6. eye pig lung none irr fume-lung chronic- narcosis none irr-odor lung odor Lead Lead arsenate Lindane Magnesium oxide fume Malathon m-0.16 chronic m-0.16 T chronic m-0.6 chronic m-16m-16. fume acute tox? none none none none Manganese Mercury Mercury, organic Mesityl oxide Methoxychlor m-6. m-0.1 m-0.01 50. m-16. chronic chronic chronic narcosis chronic none none tox 7 irr-odor none eye pig vis IRR eye-lung fume-irr lung TRR-nar-tox irr tox none none eye TOX irr irr fume-irr lung tox none tox tox TOX nar Irr-tox tox ZRR-lung Methyl acetate Methyl acetylen* Methylal 200. 1000. 1000. narcosis lung chronic odor none odor irr odor Irr nar lung-nar lung-tox acrytate 10. T Ion, Methyl alcohol 200. narcosis none none odor odor irr-nar irr-nar-tox 7 Methyl bromide Methyl CELLOSOLVE 20. chronic none 25. chronic 'none cns-odor Irr-tox odor-tox? irr-nar-tax Important Hazards Other Than from Inhalation SKP bur-eye bur-eye bur-eye SKP BUR-EYE 1 BUR-EYE bur-eye BUR-EYE all-akp SKP pyr Nature of Interpretive Year Data Proposed hu 1946 est 1956 hu 1947 hu-sgl 1947 hu-sgl rpt hu ind-rpt hu-sgi ind-rpt 1947 1955 1965 1948 1948 1943 rpt hu-ind-rpt clin-sg! clin ind clin hu-rpt 1955 1948 1943 1955 1948 1947 1945 ind-sgl clin rpt rpt HU est-clin clin clin-rpt clin-egl hu-rpt gl est-sgl rpt rpt rpt rpt clin-rpt 1956 1943 1966 1954 1946 1954 1946 1943 1964 1946 1654 1948 1965 1662 1956 1642 1945 clin-rpt 1947 lUCC - 109577 Industrial Hygiene Quarterly U1 Table I--Continued Predicted Effects of Daily eight-hour Inhalations Substance Limit ppm or mg./cu.m, Most Important Effect of Inhalation At Threshold Limit Additions! At Twice Threshold Limit Additional At Ten Times Threshold Limit Methyl CELLOSOLVE acetate Methyl chloride Methyl chloroform 25. 100. 600. chronic chronic narcosis none none odor odor-tox irr-nar-tox odor ens-nar nar NAR Methyl cyclo- hexane Methyl cyclo- bexanol Methyl cyclo- hexanone 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 nar-tox IRR-NAR IRR-nar odor nar irr-odor nar Methyl isobu- tyl c&rbinol (methylamyl alcohol) Methyl 25. mercaptan 5Q. 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? none irr-tox none none irr-tox irr-nar?-odor NAR Naphtha (petroleum) Nickel carbonyl Nicotine Nitric acid p-Nitroaniline 500. narcosis odor 0.001 cancer-lung none m-0.5 T chronic none 10. T lung irr 1, chronic none irr-nar none IRR NAR none tox lung tox Nitrobenzene Nitroethane Nitrogen dioxide Nitroglycerine Nitromethane 2-Nitropropane Nitrotoluene Octane Ozone Parsthlon 1, 100. 5. 0.5 100. 50. 5. 600. 0,1 m-0,1 chronic acute lung acute acute acute chronic narcosis lung acute none none odor head none nau-tox ? none odor odor none tox irr-odor nar.tox irr irr-odor LUNG tox nar-tox tox? irr-nar odor-tox tox NAR irr-lung tox Fentaborane 0.01 T acute Pentachloro- naphthalene m-0.5 chronic Pentachloro* phnol 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 1 rr-tox nar nar Perchloro* etbylen* Perchloromethyl mercaptan zoo. narcosis 0.1 Thing odor none nar irr-NAR irr Hazards Other Than from Inhalation pyr pyr pyr SKP BUR-EYE Skp SKP SKP SKP SKP acne bur-ekp pyr bur-EYE Nature of Interpretive Data Year Proposed est 1947 rpt 1947 rpt 1953 rpt 1947 rpt 1945 rpt 1945 rpt 194$ sgj 1947 hu-sg] Sgl rpt rpt est est ind-sgl est eat est-ind est rpt ind*rpt clin rpt clin-Hgl est est rpt clin-est rpt rpt est hu hu-sgl med-rpt ffl 1954 1954 1955 1955. 1945 1945 1954 1966 1966 19S4 1947 1947 1946 1946 1947 1947 1943 1945 1954 1953 1966 1946 1947 1947 1947 1951 1954 I n& June, 1956 Table I--Continued Substance Limit ppm or mg./cu.m. Most Important Effect of Inhalation Phenol Phenylhydrasine Phosgene 6. chronic 5, chronic 1. lung Phosphine Phosphorous (yellow) Phosphorous pentachloride Phosphorous pentasulflde Phosphorous trichloride 0.05 m-0.1 m-1. m-1. 0.6 chronic chronic lung lung lung Picric acid Propyl acetate Propyl alcohol (isopro* panol) Propylene dichloride Propylene imine m-0.1 200. 400. 16. 26. chronic narcosis narcosis chronic acute-lung Predicted Effects of Daily eight-hour Inhalations At Threshold Limit Additional At Twice Threshold Limit Additional At Ten Times Threshold Limit odor irr lung-tox none none ey-TOX LUNG-odor none none tox7 none none none none irr-odor irr-Jung irr-lung irr irr IRR-nar lung-odor tox NAR irr-odor tox 7 odor nar IRR-NAR nar-odor TOX lung-TOX Propyl ether Pyrethrum Pyridine Quinone Rotenone 500. m-2. 10. 0.1 m6. narcosis T lung chronic eye pig T lung irr-odor none cns7-odor none none Selenium compounds, as Se Sodium hy* droxide Stibine Stoddard sol- vent Strychnine m-0.1 chronic none m-2. 0.1 irr irr chronic-lung none 500. narcosis m-0.16 T acute odor none Styrene monomer 200. Sulfur dioxide 10. Sulfur hexa- fluoride 1000. Sulfuric acid m-1. Sulfur mono- chloride 1. narcosis lung asphyxia lung lung odor irr-odor none irr none Sulfur pentafluoride TEPP Tellurium TEPP p-Tertiary butyl toluene 0.026 lung m-0,2 acute m-0.1 chronic m-0.06 acute 10. chronic none none none none odor Tetrachloro- ethane Tetrahydro- furmn Tetranltrome- than* Tetryl Thallium (soluble) 6. chronic 200. T narcosis 1. m-1.6 acute chronic m-0.16 T chronic toxT none irr none IRR eye-pig NAR irr irr-tox ` vis irr irr-nar tox IRR lungT-tox? NAR tox Irr IRR none irr IRR-nar lung none IRR-Iung IRR-lung none irr-lung tox irr-tox 7 tox irr-nar-to* tox odor irr r odor-TOX irr tox tox Important Hazards Other Than from Inhalation Nature of Interpretive Year Data Proposed BUR-EYE-SKP hu-rpt 1962 all-SKP bur-EYE sgl HU-rpt rpt 1964 1943 1947 ind 1947 bur-EYE bur-EYE all-skp sgt eat sgl clin est-sgl 1947 1947 1946 1964 1946 est-hu pyr rpt bur-EYE-SKF \ sgl rpt rpt ind-med clin est 1946 1941 1966 1946 1966 1964 1966 1956 bur-EYE ' pyr bur-EYE bur-EYE bur-EYE clin-est ind sgl hu est hu-rpt clin-hu i HU-ind-agl ind-Bgl sgl est clin est 1947 1964 1947 1946 1966 1947 194ft 1964 1948 1946 1964 1954 1947 12(4 pyr skp all-skp hu-rpt ind-sgl rpt rpt clin est 1956 1247 1966 1956 1948 1966 Ind Subst Thira Titan dio: Tolue o-Toh Trich cth> Trichl nap Triflu' obrc met Trimt Turpe Urani (sol Uranii (ins Vanad (Vj< Vanad <V:( funii Vinyl Warfa Xylene Zinc < fume Zircon Th inhal tract, thres huma to pr< Aa ppm basis 9, p. able. 16,00< one o: injur; workt centr; at 10 slight stoma as wit The inhals eyes, bronc] old li: IX UCC - 109579 Industrial Hygiene Quarterly US Substance Limit ppm or mg./eu,m. Most Important Effect of Inhalation Thiram Titanium dioxide Toluene o>Toluidine Trichloro* ethylene m-5. T chronic m-15. 200. 5. lung narcosis chronic 200, narcosiB Trichloro- naphthalene m-5. Trifluoromon- obromo* methane 1000. Trinitrotoluene m-1.5 Turpentine 100. Uranium (soluble) m-0.05 chronic narcosis chronic narcosis chronic Uranium (insoluble) Vanadium (VaOa dust) Vanadium (VjOa fume) Vinyl chloride Warfarin m-0.25 chronic m-0.5 lung m-0.1 lung 600- narcosis m-0.fi T chronic Xylene Zinc oxide fume Zirconium 200, narcosis ro-16. fume m-6. 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 nar?-odor none irr-lung irr ' NAR cy CY-tox nar-nau-odor irr-NAR none tox none tox? irrn>dor none none none none tox 7 IRR-nar irr-nar irr-tox NAR-tox tox tox lung none none none lung irr-nar ?*odor nar nar tox NAR fume none fume-irr lung lung Hazards Other Than from Inhalation Nature of Interpretive Proposed Data Year est-sgl 1956 SKP pyr rpt clin-hu-rpt 3gl ind-med-rpt 1954 1943 1945 1948 acne rpt 1945 pyr skp rad rad rpt clin-rpt hu-rpt rpt rpt rpt 1956 1943 1945 1953 1953 1964 rpt 1964 pyr sgl 1947 est 1966 hu 1943 HU 1943 rpt 1956 The most important effect of acetaldehyde inhalation is irritation of upper respiratory tract, bronchi and even lung. The 200 ppm threshold limit can be interpreted from human sensory data. It is sufficiently low to prevent lung injury. Acetic acid. Sterner (1943) concludes 10 ppm is reasonably non-irritating on the basis of industrial experience. Patty (19489, p. 886) 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 (1937-66) found rats inhaling 1000 ppm for four hours survived, but 2000 ppm was fatal. The liquid causes skin burns. The only important effect of acetic an hydride inhalation is irritation, first evident in the eyes, then in the upper respiratory tract, bronchi and even lung. The 5 ppm threshold limit can be interpreted from an alogy with acetic acid. In view of rat mor tality from the two vapors, a lower value would be more consistent, although it is undoubtedly low enough to prevent lung in jury. Acetone. Nelson, Ege, Ross, Woodman and Silverman (1943) found slight 'eye, iu June, 1956 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 y3 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 and Haggard (1943, p. 138) conclude the main attack is on the upper respiratory tract, but that a high concentration can cause lung edema. They report 10 ppm to be lethal in a short time. Systemic effects are not to be expected. Smyth (1937-55) found four hours inhalation of 8 ppm kills one of six rats and all die from 16 ppm. The liquid causes severe corneal injury and burns of the skin. The only important effect of acrolein in halation is irritation, first evident in the eyes, then in the upper respiratory tract, bronchi and even lung. The 0.5 ppm thresh old limit can be interpreted from human sensory data. It is low enough to prevent lung edema. Acrylonitrile. Dudley, Sweeney and Miller (1942) found repeated inhalation of 153 ppm injurious to animals, but believed the effect not chronic toxicity. Dudley and Neal (1942) concluded injury is due to formation of cyanide in the body. The 10 ppm hydrogen cyanide threshold limit is equivalent to 20 ppm, acrylonitrile, if conversion is complete. Wilson (1944) in exposed workmen, found evidence of skin penetration and effects ref erable to liver injury. Smyth's (1937-55) rats survived four hours at 500 ppm but were killed at 1000 ppm. The most important effect of acrylonitrile inhalation is acute poisoning, due to hy drolysis in the body to cyanide. The 20 ppm threshold limit can be interpreted from re sults of repeated animal inhalation studies and its relationship to the accepted 10 ppm thz-eshold 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 enough to prevent injury. Allyl 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) found rats survive one hour at 500 ppm, but die from 1000 ppm. The vapors irritate eye and nose, but not sufficiently so to pre vent exposure to a concentration which temporarily blinded one man through de layed corneal necrosis. Chronic toxicity is not to be expected, but skin penetration is dangerous, and skin contact causes bums when evaporation is prevented. The most important effect of allyl alcohol inhalation is irritation, manifest as dis abling corneal injury and pulmonary edema, with non-progressive organic effects some what less important and narcosis over shadowed; The 5 ppm threshold limit can be Industrial interpretei tion and r tion. It is injury, bi some. Allyl ch (1940) fo halation c killed all. with soim weak but prominent The mos inhalation tory tract, tative thr from sing analogy w enough to Allyl pr Baliff (19ing plant of eye, nos calculated tation at dent. The mot disulfide i upper resp threshold 1 results of men. It ap jury. Ammate single do: mg./kg. ju tion than sanqe dust The mos inhalation substantia threshold analogy, I injury., Animom 100 ppm dustrial ex derson an incapacital respirator; tion. They smelled, bi detected ai give 408 ] 698 ppm i: 1 ound ref'-55) but itrile > hyppm n reudies ppm It is ) ex 's exid redence uman d linly insility, ey inidney, isitize aldrin idane, of the dts of is low 1 some ew by its die 3 ppm, teritis, 37-65) ) ppm, rritate to prewhich gh de city is tion is burns alcohol is disedema, ; some; over can be Industrial Hygiene Quarterly U'5 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 luirg, 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. Ammate. ACGIH (1954b) concludes the single dose LD50 for animals of 2000 mg./kg. justifies no more control on inhala tion than is required for a non-toxic nui sance dust. The most important effect of ammate dust inhalation is the low grade irritation of a substantially inert dust. The 16 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. 126) note incapacitating temporary blindness, and respiratory arrest from a high concentra tion. They state 63 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 (1949, p. 20) notes eye and upper respiratory tract irritation, salivation, bronchial irritation and lung edema, but no chronic systemic effect. Elkins (1950, p. 84) found 55 ppm not objectionable in industry but 125 ppm irritating. Silverman, Whittenberger and Muller (1949) found 500 ppm stimulated human respiration, irritated eye and throat, caused lacrimation. Smyth (1937-55) found rats survive four hours at 2000 ppm, die at 4000 ppm. Solutions irri tate the skin, erode mucous membrane and severely injure the cornea. Vigliani and Zurlo (1955) in workers inhaling 100 ppm, found irritation of the respiratory tract and conjunctiva. Even 20 ppm caused com plaints until workers became hardened. The most important effect of inhalation of ammonia gas is respiratory tract irritation, with lung edema or respiratory arrest the maximum injury. The 100 ppm threshold limit can be interpreted from human sen sory and physiological data. It is low enough to prevent injury. Amyl acetate. Patty, Yant and Schrenk (1936) found 2000 ppm does not injure guinea pigs in several hours, while a concen tration killing in 60 minutes can not be ob tained. Symptoms consisted of eye and nose irritation and narcosis. Nelson, Ege, Ross, Woodman and Silverman (1943) found slight throat irritation in unacclimated sub jects at 100 ppm, mild eye and nose sensa tion and severe throat irritation at 200 ppm. Smyth (1937-55) with rats inhaling substantially saturated vapors found anes thesia in two hours and death in eight hours. Chronic toxicity is not to be expected. The most important effect of amyl acetate inhalation is narcosis. The 200 ppm thresh old limit can be interpreted from human sensory data and single inhalations by animals. It is low enough to prevent definite narcosis. Amyl alcohol (isoamyl alcohol.) Nelson, Ege, Ross, Woodman and Silverman (1943) found slight throat irritation in unac climated subjects at 100 ppm, and objection able eye, nose and throat irritation at higher concentrations. Haggard, Miller and Greenberg (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 t1, ijr* f < * Vs*1 ' pM ucc 109582 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 electrocardiographically. Dernehl, Nau and Sweets (1945) exposed guinea pigs to anti mony oxide of one micron diameter at 45 mg./cu.m., three hours a day for several months. One-sixth died of pneumonitis with severe liver injury and white blood cell changes, but hearts remained normal. Electrocardigrams on the animals and on a few industrially exposed workmen were normal. Brieger, Senisch, Stasney and Piatnek (1945) in an industrial operation where antimdny trisulfide concentrations ranged from 0.58 to 5.5 mg./cu.m., found abnormali ties in blood pressure, electrocardiographic changes and two deaths from chronic throm bosis. The most important effects of inhalation of antimony dust are chronic poisoning marked by electrocardiographic changes, pneumonitis and liver injury. The 0.5 mg./cu.m. threshold limit can be interpreted from the results of repeated inhalations and examination of workmen. It appears low enough to prevent injury. ANTU (alphanaphthylthiourea). McClosky and Smith (1945) found consider able species differences in acute oral toxici ty. The LDS0 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 (1943, p. 241) describe acute arsine poisoning as due to hemolysis of red blood cells with re sulting anemia and kidney damage, and lung Industn edema. r is fatal, toms in an indu limit of (1950, ] fatal ca: The n halation edema. r interpre experien prevent Bariu (1949, p ble bari with gas sympton from ba action o The n of solubl ritation, 0.5 mg./ preted o pears lo Benze a limit > aminatit inhalatii poisonin centrath slowly t medical moval fi ing is f; ing is pj Benzene effects c all expo of a hif be fatal 100 ppm p. 228) exposuri 40 to 80 The n halation the bon limit ca aminati< quantity appears ment of Benzi Industrial Hygiene Quarterly U7 edema. They state 250 ppm for 30 minutes mator, irritating to eye, nose and throat, and is fatal, and 3 to 10 ppm can cause symp capable of causing lung edema. Flury and toms in a few hours. Nau (1948) reported Zernik (1931, p. 538) conclude 170 ppm is an industrial episode showing the earlier dangerous to cats in eight hours and 16 ppm limit of 1 ppm was too high, and Elkins intolerable to man in one minute. It may be (1950, p. 67) reported briefly on a non- inferred that the liquid causes severe fatal case at a level of about 0.5 ppm. corneal injury. The most important effect of arsine in The only important effect of benzyl chlor halation is acute poisoning, largely lung ide inhalation is irritation, first evident in edema. The 0.05 ppm threshold limit can be the eyes, then in the upper respiratory tract, interpreted from the results of industrial bronchi and even lung. The 1 ppm threshold experience. It appears to be low enough to limit can be interpreted from older human prevent injury. sensory data. It is undoubtedly low enough Barium (soluble corn-pounds). Fairhall to prevent lung injury. (1949, p. 32) records the fatal dose of solu Bromine. Flury and Zernik (1931) quote ble barium compounds as 0.8 to 0.9 grams Lehmann that 0.75 ppm in a workroom with gastro-intestinal disturbance the chief caused no symptoms in six hours. Hender symptom. He notes bronchial irritation son and Haggard (1943, p. 133) state bro from barium carbonate dust, and depilatory mine acts as a respiratory irritant leading to action of barium sulfide. lung edema. They state 40 to 60 ppm is The most important effect of inhalation dangerous on short inhalation, and 4 ppm of soluble barium compounds is bronchial ir allowable for 30 to 60 minutes. Elkins (1950, ritation, with acute poisoning possible. The p. 87) found 1 ppm excessively irritating. 0.5 mg./cu.m. threshold limit can be inter Severe burns of skin and cornea result from preted only by analogy with antimony. It ap the liquid. Patty (1948-9, p. 554) concludes pears low enough to prevent injury. 0.3 ppm is not objectionably irritating. Benzene, Winslow (1927) first proposed The most important effect of inhalation a limit of 100 ppm, based on extensive ex of bromine vapor is respiratory tract irrita amination of exposed workmen and animal tion, with lung edema the maximum effect. inhalation. He recognized that chronic The 1 ppm threshold limit can be inter poisoning would develop in some at this con preted from industrial experience. It ap centration, but believed it would progress pears low enough to prevent injury. slowly enough to be detected by periodic Butadiene. Von Oettingen (1940) quotes medical examinations, and arrested by re repeated animal exposures at 64,000 ppm moval from exposure. Acute benzene poison which caused bronchial and lung irritation ing is fatal anesthesia, and chronic poison and some hyperplasia of bone marrow. ing is primarily injury to the bone marrow. Carpenter, Shaffer, Weil and Smyth (1944) Benzene is particularly insidious because its found animals not affected by repeated in effects can progress to a fatal outcome after halation of 2300 ppm, while 6700 ppm all exposure ceases. Even brief inhalation slightly retarded growth and there were of a high non-anesthetic concentration can minor liver effects. Two humans found be fatal. Patty (1948-9, p. 757) states that psychomotor effects of early narcosis from 100 ppm has only a faint odor. Elkins (1950, 8000 ppm, equivalent to those from 200 p. 228) investigated a fatal case whose ppm toluene. exposure he was convinced had been only to The most important effect of butadiene 40 to 80 ppm. vapor inhalation is narcosis. The 1000 ppm The most important effect of benzene in threshold limit can be interpreted from re halation is chronic poisoning centering in sults of repeated animal inhalation and the bone marrow. The 35 ppm threshold single human inhalation. It is low enough limit can be interpreted from extensive ex to prevent any degree of narcosis. amination of exposed workmen, and was Butanone (methyl ethyl ketone). Patty, quantitatively defined by one fatal case. It Schrenk and Yant (1935) found guinea pigs appears low enough to prevent the develop tolerated 3000 ppm for several hours, and ment of irreversible poisoning. men found it irritating to nose and eyes. Benzyl chloride. This is a potent lacri- Nelson, Ege, Ross, Woodman and Silverman 148 June, 1956 (1943) found slight throat irritation in un acclimated subjects at 100 ppm, irritation of eyes at 200 ppm and objectionable irrita tion at 300 ppm. Elkins (1950, p. 118) found complaints of nausea at 500 ppm, irritation at 300 ppm, but no ill effects at 700 ppm. Smyth (1937-55) found rats survived two hours at 2000 ppm but 4000 ppm killed four of six. He found that an episode of indus trial eye injuries during inhalation of 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. Butyl acetate. Sayers, Schrenk and Patty (1936) found guinea pigs are not affected by several hours inhalation of 3300 ppm. Nelson, Ege, Ross, Woodman and Silverman (1943) found throat irritation in unaccli mated subjects at 200 ppm, severe at 300 ppm. Henderson and Haggard (1943, p. 222) conclude the ester shows no chronic toxicity. Smyth (1937-56) found rats inhaling sub stantially saturated vapors are not killed in four hours, but died within an eight-hour inhalation period. The most important effect of butyl acetate inhalation is narcosis. The 200 ppm thresh old limit can be interpreted from human sen sory response and single inhalations by animals. It is low enough to prevent defi nite narcosis. Butyl alcohol (n-butanol). Tabershaw, Fahy and Skinner (1944) reported eye in flammation in workmen above 50 ppm, but no systemic effects below 100 ppm. Sterner, Crouch, Brockmyre and Cusack (1949) fol lowed workmen for 10 years with butyl al cohol concentrations held to 100 ppm, and for a briefer period to 200 ppm. Neither ir ritation nor systemic effects were found at 100 ppm, but there was some eye irritation at 200 ppm. Smyth (1937-55) found rats are not killed in four hours at 8000 ppm. The most important effect of butyl al cohol inhalation is narcosis. The 100 ppm threshold limit can be interpreted from an extensive study of workmen under condi tions of known peak exposure-. No narcotic or irritative effects are to be anticipated. Butyl amine. Hanzlik (1923) reported central nervous stimulation, convulsions, then depression and narcotic death with pul monary edema. Smyth (1937-55) found rats survive four hours at 2000 ppm but die from 4000 ppm. Injury to skin and cornea from the liquid is severe. Unreported industrial experience suggests skin injury is the great est practical hazard. ACGIH (1955b) cites unpublished industrial experience that levels above 5 ppm tend to be irritating. The most important effect of butyl amine inhalation is respiratory tract irritation, with lung edema the maximum injury. The 5 ppm threshold limit can -be interpreted from analogy with ethyl amine. It is prob ably low enough to prevent injury. Butyl CELLOSOLVE (2-butoxyethanol). Werner, Nawrocki, Mitchell, Miller and von Oettingen (1943) found 300 to 400 ppm, in repeated inhalation produced only small ef fects on rats, particularly on the blood pic ture. Werner, Mitchell, Miller and von Oet tingen (1943a, b) reporting on single in halations by rats and repeated by dogs, make it clear that the butyl ether produces somewhat greater blood cell changes than do the methyl or ethyl ethers. They also found hemoglobinuria, with lung, liver and kidney changes. Smyth (1937-55) found in rats fractional mortality from as little as 500 ppm inhaled eight hours, with hematuria a prominent symptom. The liquid penetrates the skin readily and is sufficiently toxic so that this is dangerous. The most important effect of butyl Cellosolve inhalation is chronic poisoning, centering in the blood cells and kidney. The 200 ppm threshold limit can be interpreted from results of repeated animal inhalation studies. Based on reports from simultaneous studies of CELLOSOLVE and butyl CELLOSOLVE it is obvious that the threshold limit for the latter should be lower than for the former if equal degrees of protection are. to be at tained. Butyl mercaptan. Fieldner, et al. (1931) reports 733 ppm to be lethal to dogs in 30 minutes, indicating 20 times the acute toxicity of ethyl mercaptan. Effects like those of hydrogen sulfide are to be expected. The most important effect of butyl mer captan is eye and respiratory tract irrita tion. The 10 ppm tentative threshold limit can be interpreted from the results of lim ited single inhalations by animals and an alogy with hydrogen sulfide. It appears, low Ind jurj tant not pois imp< thre the calci old 1 tent dust Ci quot ppm hour 52) 30,0' inert deer sym; for ; toxit jurn tion: hala jSSsd. i.' |UCC 109585 1 puli rats from from strial jreatcites levels imine ition, . The reted prob- mol). i von m, in 11 efl pic- Oete in dogs, duces an do bund idney rats ; 500 ic so Celning, . The reted ation leous SOLVE r the rmer e at- .931) in 30 acute like icted. merritalimit liml ani low Industrial Hygiene Quarterly ng 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. Fairhall (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. ACGIH (1954b) bases the tentative threshold limit upon a rat oral LD50 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 central 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 Zurlo (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 tetrachlorideElkins (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 150 June, 1956 kidney injury, while early narcosis occurs at a low concentration. Chronic toxicity is chiefly marked by liver injury. The most important effect of carbon tetra chloride inhalation is chronic toxicity cen tering in the liver. The 25 ppm threshold limit can be interpreted from the results of repeated animal inhalations and industrial experience. It is low enough to prevent ir reversible injury, but perhaps it will allow minor injury, Cellosolve (2-ethoxyethanol). Werner, Nawrocki, Mitchell, Miller and von Oettingen (1943) found rats repeatedly inhaling 300 to 400 ppm showed small but measur able blood cell effects. Werner, Mitchell, Miller and von Oettingen (1943b) found dogs inhaling 800 ppm repeatedly developed small blood cell effects. Smyth (1937-55) found rats survive four hours at 2000 ppm, but half are killed by 4000 and all are killed by eight hours at 4000 ppm, close to satura tion. Death is marked by severe kidney dam age. The most important effect of cellosolve inhalation is chronic poisoning centering in the red blood cells. The 200 ppm threshold limit can be interpreted from results of re peated animal inhalation studies. It appears to be low enough to prevent injury. There are no data to judge the degree of eye and nose irritation it allows. Cellosolve acetate (2-ethoxyethyl ace tate). Smyth (1937-66) 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 1600 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 irritationdt allows. CHLORDANE. Princi and Spurbeck (1961) 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 LD50 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 camphene 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 (193765) 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 Indust to 60 p edema, throat Patty ( is toler The of chlo tion, w The 1 p from rc sensory injury. Chloi (1955) tant. R ppm, wl pea ted 13 was inci Acuity i Horn ai halation jured oi monia. The r of chloi tract iri mum eff be inter) tion. It jury. Chlori conclude benzene, poetic ef The n zene ini threshok rough es chlorinat enough t Chloro Alford ar ppm ,to t inhalatio dogs to days a w out effect found fr< kidney re inhalatioi light nar< ppm for . ppm was nary eder The me ucc 109587 Industrial Hygiene Quarterly 151 to 60 ppm may lead to pneumonitis and lung chlorobromomethane is narcosis with non edema, 30 ppm causes coughing, 15 ppm progressive effects on liver and kidney. The throat irritation and 3.5 ppm can be smelled. 400 ppm tentative threshold limit can be in Patty (1948-9, p. 547) concludes 1 to 2 ppm terpreted from the results of repeated in is tolerable, 3 to 6 ppm irritating. halations with animals. It appears low The most important effect of inhalation enough to prevent injury. of chlorine gas is respiratory tract irrita Chlorodiphenyl (42% chlorine). After ex tion, with lung edema the maximum effect. tensive inhalation studies with rats. Drink The 1 ppm threshold limit can be interpreted er (1939) concluded that 10 mg./cu.m. of a from repeated animal inhalation and human ' sample 68% chlorine, but free from chlorin- sensory data. It is low enough to prevent ' ated diphenyl benzene, would lead to no injury. systemic injury, but that the presence of Chlorine trifluoride. Horn and Weir chlorinated diphenyl benzene reduced the (1955) found it an extremely active irri permissible limit to 0.5 mg./cu.m. Smyth tant. Rats are killed in 40 minutes at 96 (1937-55) found the material penetrates the ppm, while rats and dogs inhaling 5 ppm re skin, and repeated contact leads to chlor- peatedly are severely injured. Pneumonia acne. Treon, Cleveland, Cappel and Atchley was increased and there was respiratory dif (1956) reported that inhalation of 8.6 ficulty in all. The vapors injure the cornea. mg./cu.m. for 24 seven-hour periods did not Horn and Weir (1956) found repeated in affect four species of animals, and 1.9 halation of 1.17 ppm by rats and dogs in mg./cu.m. for 160 periods also was without jured only by increased incidence of pneu effect. monia. The most important effect of chloro The most important effect of inhalation diphenyl inhalation is chronic poisoning, of chlorine trifluoride gas is respiratory centering in the liver. The 1 mg./cu.m. tract irritation, with lung edema the maxi threshold limit can be interpreted from the mum effect. The 0.1 ppm threshold limit can results of repeated animal inhalations. It is be interpreted from repeated animal inhala low enough to prevent injury. tion. It appears low enough to prevent in Chlorodiphenyl, 54% chlorine, Treon, jury. Cleveland, Cappel and Atchley (1956) re Chlorobenzene. Fairhall (1949, p. 260) ported that repeated inhalation over a seven- concludes it is somewhat more toxic than month period of 1.6 mg./cu.m. caused some benzene, but finds no evidence of hemato- minor liver injury in four species of rodents. poetic effect. The most important effect of inhalation of The most important effect of chloroben chlorodiphenyl (54% chlorine) is chronic zene inhalation is narcosis. The 75 ppm toxicity centering in the liver. The 0.5 threshold limit can be interpreted only as a mg./cu.m; tentative threshold limit can be rough estimate. By comparison with other interpreted from the results of repeated in chlorinated hydrocarbons, it appears low halation by animals. It appears to be slight enough to prevent injury. ly below an injurious concentration. Chlorobromomethane. Svirbely, Highman, Chloroform. Fairhall (1949, p. 264) con Alford and von Oettingen (1947) found 3000 cludes . it acts much like carbon tetrachlor ppm ito be the LC50 for mice in eight-hour ide, and that anesthetic use has led to liver inhalations. Exposures of rats, rabbits and injury, but regression is more likely than dogs to 1000 ppm seven hours a day five with carbon tetrachloride. A concentration days a week for fourteen weeks were with of 4000 ppm causes slight symptoms after out effect. Non-progressive liver injury was several hours exposure. Patty (1948-9, p. found from single inhalations, but liver and 793) concludes the least concentration kidney remained normal during the repeated smelled is 200 to 300 ppm. Smyth (1937-55) inhalations. Comstock et al. (1952) found found one of six rats die from four hours at light narcosis in rats and mice inhaling 3000 4000 ppm, and all from 8000 ppm. ppm for 10 to 15 minutes, and about 30,000 The most important effect of inhalation of ppm was fatal within 15 minutes. Pulmo chloroform is chronic poisoning centering in nary edema was present in animals dying. the liver. The 100 ppm threshold limit ^can The most important effect of inhalation of be interpreted from the results of single 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-lnitroethane is lung injury. The 20 ppm threshold limit can be interpreted from the results of single animal inhalations. It ap pears low enough to prevent injury. Chloropicrin. Fairhall (1949) concludes it is an irritant gas, producing bronchial and lung injury. He concludes 20 ppm produces lesions within one to two minutes and that 4 ppm will incapacitate a man. The most important effect of chloropicrin is respiratory tract irritation with lung in jury probable. The 1 ppm tentative thresh old limit can be interpreted from sum maries of studies of its use as a war gas. It appears, low enough to prevent serious in jury. Chloroprene (2-chlorobutadiene). Von Oettingen, Hueper, Deichmann-Gruebler and Wiley (1936) made repeated inhalation studies with animals. A concentration of 83 ppm caused some respiratory irritation, cen tral nervous system depression, and effects on liver, kidney and vascular system. Skin penetration was dangerous. The most important effect of chloroprene inhalation is chronic poisoning, centering in the liver. The 25 ppm threshold limit can be interpreted from the results of repeated animal inhalations. It appears low enough to prevent injury. Chromic acid. Bloomfield and Blum (1928) and Riley and Goldman (1937) dem onstrated in industrial surveys that per foration of the nasal septum and other up per respiratory tract effects of chromic acid mists are not found at a concentration of about 0.1 mg./cu.m. Other effects are not produced. Vigliani and Zurlo (1955) found ulcerated nasal septum, inflamed larynx, chronic bronchitis and two respiratory tract cancers among 150 workers exposed to 0.11 to 0.15 mg./cu.m. The most important effect of inhalation of chromic acid aerosol is upper respiratory tract irritation, leading to perforation of the nasal septum. The 0.1 mg./cu.m. thresh old limit can be interpreted from studies of exposed workmen. It is low enough to pre vent injury. CRAG herbicide. ACGIH (1954b) sug gests on the basis of a general low toxicity and a rat oral LD50 of 1500 mg./kg., that 10 mg./cu.m. is a fit limit. Smyth (1937-55) found death from a single oral dose due to respiratory paralysis with injuy to liver and kidney. Rats are not affected by 0.02% in their diet for two years, and 0.06% causes minor effects on liver and kidney. The most important effect of CRAG her bicide inhalation is chronic poisoning cen tering in the liver. The 15 mg./cu.m. thresh old limit can be interpreted from the results of single and repeated oral doses to animals. It appears low enough to prevent injury. Cresol. Fairtyall (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 hdmatopoetic changes. Patty Ini (If tin< inh org it i pea to ] C mil tioi cal the Eg* fou nos' sub kill stai T inh; org. thr* suit hun prenot C Kit; fou; Egt fou and ject fou cau: T non thrt pea sor: pre- C clue anil ane; gre; T inh; old sing to p C viev thes Industrial Hygiene Quarterly 15S (1948-9, p. 769) reports 300 ppm has no dis ard in industrial use. The most important '-;f- tinct odor or irritation. fect of cyclopropane gas inhalation is narco The most important effect of cyclohexane sis. The 400 ppm threshold limit can be in inhalation is narcosis, with non-progressive terpreted from analogy with cyclopentane, organic effects. The 400 ppm threshold lim and by human surgical use. It is probably it can be interpreted from results of re low enough to prevent definite narcosis peated animal inhalation. It is low enough 3,4-D. Rowe and Hymas (1954) conclude to prevent definite narcosis. that it has a low degree of rhronicity, and Cyclohexanol. Treon, Crutchfield and Kitz- ,the acute LD50 values range from 300 to miller (1943) reported that repeated inhala 1000 mg./kg, for various species. tion of 693 ppm caused minimal pathologi The most important effect of 2,4-D inhala cal changes in a monkey, and 145 ppm in tion is chronic poisoning centering in the the livers and kidneys of rabbits. Nelson, liver. The 10 mg./cu.m. threshold limit can Ege, Ross, Woodman and Silverman (1943) be interpreted from the results of single and found 100 ppm causes objectionable eye, repeated oral doses to animals. It appears nose and throat irritation in unacclimated low enough to prevent injury. subjects. Smyth (1937-55) was unable to DDT. Barnes (1953) finds no incidence of kill rats by eight hours inhalation of sub illness among workers using it throughout stantially saturated vapors. the world. Poisoning from accidental inges The most important effect of cyclohexanol tion is marked by abdominal pain, vomit inhalation is narcosis, with non-progressive ing, dizziness and weakness. Long repeated organic effects less prominent. The 100 ppm doses of 25 to 50 mg./kg. are required to threshold limit can be interpreted from re poison animals, although man is probably sults of repeated animal inhalations and more sensitive. human sensory data. It is low enough to The most important effect of DDT inhala prevent significant narcosis or injury, but tion is chronic poisoning centering in the not to prevent irritation. liver. The 1 mg./cu.m. tentative threshold Cyclohexanone. Treon, Crutchfield and limit can be interpreted from the results of Kitzmiller (1943) in animal experiments repeated oral doses to animals. It appears found only narcosis and irritation. Nelson, low enough to prevent injury. Ege, Ross, Woodman and Silverman (1943) Decaborane. Svirbely (1954a,b) found found 50 ppm caused objectionable eye, nose the LC50 for mice inhaling vapors for four and throat .irritation in unacclimated sub hours to be 25.7 ppm. Symptoms included jects. Smyth (1937-55) did not kill rats by central nervous excitability and corneal four hours at 4000 ppm, but 8000 ppm opacity. Six-hour inhalations of 20 ppm by caused anesthetic death. rats, repeated 20 times, killed some with The most important effect of cyclohexa fatty livers and central nervous excitability. none inhalation is narcosis. The 100 ppm Comstock and Oberts (1953) report that threshold limit can be interpreted from re the median detectable odor is 0.35 mg. 'eu.m. peated animal inhalations and human sen (0.07 ppm), described as foul or chocolate sory response. It is probably low enough to like. prevent definite narcosis. The most important effect of decaborane Cyclohexene. Fairhall (1949, p. 279) con inhalation is acute toxicity involving the cludes that 9000 ppm causes mild narcosis in central nervous system, with liver injury animals, while 13,500 to 15,000 ppm gives less important. The 0.05 ppm tentative anesthetic death. This indicates a toxicity threshold limit can be interpreted from lim greater than that of cyclohexane. ited animal inhalations. It appears to allow The most important effect of cyclohexene an adequate margin of safety. inhalation is narcosis. The 400 ppm thresh Diacetone alcohol. Von Oettingen (1943, old limit can be interpreted from results of p. 138) reports animals at 2100 ppm are single animal inhalations. It is low enough restless, irritation and kidney effects are to prevent definite narcosis. noted. He concludes it is twice as toxic as Cyclopropane. Fairhall (1949, p. 280) re acetone. Silverman, Schulte and First views reports of experience in surgical anes (1946) found 100 ppm irritating to eyes, thesia and concludes there is no toxic haz nose and throat but not intolerable in un- acclimated subjects. Smyth (1937-55) found difluoromethane inhalation is asphyxia from 1500 ppm, approaching saturation, did not extremely high concentrations. The 1000 I kill rats in eight hours. ppm threshold limit can be interpreted from 5 t The most important effect of diacetone al the results of repeated animal inhalations. cohol inhalation is narcosis. The 50 ppm It represents good engineering control threshold limit can be interpreted from rather than a hazard limit. single animal inhalations and human re 1.1- Dichloroethane. Henderson and Hag sponse. It appears low enough to prevent gard (1943, p. 207) conclude it is similar to definite narcosis. carbon tetrachloride. Smyth (1937-55) Diborane. Rozendaal (1951) reported on found rats survive eight hours at 4000 ppm, five human injuries from inhalation of but are killed at 16,000 ppm, an acute toxici 1. diborane and other boron hydrides. Dibor ty half that of carbon tetrachloride. In re ane produced symptoms like metal fume peated inhalations by rats and dogs, chron fever and severe central nervous system ir ic toxicity somewhat less than that of car ritation. Krachow (1953) reported that bon tetrachloride was likewise found. single inhalations of 50 ppm may be fatal to The most important effect of 1,1-dichlor- rats, resulting in lung injury, while 6 ppm oethane inhalation is chronic poisoning, repeatedly for three weeks causes lung centering in the liver. The 100 ppm thresh damage, and 2 ppm causes some lung injury old limit can be interpreted from single and within four weeks. Kidney effects are also repeated animal inhalations. It may be low noted. He finds diborane about as injurious enough to prevent injury, but new data are as phosgene. Odor is evident at 2 to 4 ppm. desirable in view of current views on car The most important effects of diborane bon tetrachloride. inhalation are central nervous system irri 1.2- Dichloroethylene. Fairhall (1949, p. tation and lung injury. The 0.1 ppm thresh 292) concludes 39,Odo to 50,000 ppm is lethal old limit can be interpreted from the effects to guinea pigs, and 18,000 ppm produces of repeated animal inhalation and clinical narcosis. Acute poisoning consists of narco studies on accidental human injuries. It is sis with central nervous system irritation. apparently low enough to prevent injury. No liver injury has been found. The vapors O-Dichlorobenzene. Cameron, Thomas, are irritating. Smyth (1937-55) found the Ashmore, Warren, Buchan, and Kenny- cis isomer did not kill nor anesthetize rats Hughes (1937) found 30 minutes inhalation in four hours at 8000 ppm, while 16,000 ppm of 390 ppm caused in animals, liver necro anesthetized in eight minutes and killed in sis and minor kidney injury. They concluded four hours. The trans isomer was twice as it is more toxic than chlorobenzene. Fairhall toxic and anesthetic. (1949, p. 284) points out its narcotic The most important effect of 1,2-dichlor- properties. Elkins (1960, p. 147) reports oethylene inhalation is narcosis. The 200 some irritation of eye and respiratory tract ppm threshold limit can be interpreted from from 100 ppm, without other effects. the results of single animal inhalations. It The most important effect of o-dichloro- is low enough to prevent definite narcosis. benzene inhalation is chronic poisoning cen Dichloroethyl ether. Schrenk, Patty and tering in the liver. The 50 ppm threshold Yant (1933) found 500 to 1000 ppm killed limit can be interpreted from the results of guinea pigs in 30 to 60 minutes with lung single animal inhalations and human sensory hemorrhage and edema, while 35 ppm pro response data. It does not appear t6 allow duced slight irritation in several hours. This sufficient margin to prevent human in concentration can be smelled but is not im jury from continuous inhalation. mediately irritating to man, while 500 to Dichlorodifluoromethane. Sayers, Yant, 1000 ppm is lacrimating. Smyth (1937-55) Chornyak and Shoaf (1930) found animals found rats survive four hours at 125 ppm, exposed repeatedly to 200,000 ppm developed but are killed by 250 ppm. Skin penetration a generalized tremor and ataxic gait, but no is moderately dangerous. gross pathology. Fairhall (1949, p. 347) The most important effect of dichloroethyl notes it has little, if any anesthetic or toxic ether inhalation is lung injury. The 15 ppm action. threshold limit canfire interpreted from the The most important effect of dichloro results of single animal inhalations. It Industn seems t< Dichh (1933) other fl They ar The i monoflui from ej 1000 pf preted I refriger control 1,1-Di Treon, found 2f of 204 tated ey jury to 1 Then 1-nitroe' 10 ppm from th tions. I injury. Dichh (1933) ; found o: exposed ic effect: ologicall The i tetrafluc very hi threshol results i pears tc level. Dieldi and Spu dustrial cides in< of the o dence of (1955) two yea are mos Chronic acute pt ritation the skin The r halation the liver can be peated < UCC 109591 cia from le 1000 ed from dations. control id Hagmilar to 937-55) 00 ppm, e toxici- In re, chronof carid, dichlorisoning, threshlgle and be low lata are on car- :949, p. is lethal iroduces f narcoitation. )00 ppm rilled in wice as dichlor'he 200 ed from ions. It cosis. tty and n killed th lung pm prors. This not im- 500 to 937-55) 15 ppm, stration iroethyl 15 ppm rom the ons. It Industrial Hygiene Quarterly lSfi seems to be low enough to prevent injury. Dichloromonofluoromethane. 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 dichloro monofluoromethane inhalation is asphyxia from extremely high concentrations. 'The 1000 ppm threshold limit can be inter preted by analogy with other fluorocarbon refrigerants. It represents good engineering control rather than a hazard limit. 1 ,l~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. Dichlorotetrafiuoroethane. N u c k o 11 s (1933) and Yant, Schrenk and Patty (1932) found only transient discomfort in animals exposed two hours to 25,000 ppm. No chron ic effects are to be expected from this physi ologically inert material. The most important effect of dichlorotetrafluorethane inhalation is asphyxia from very high concentrations. The 1000 ppm threshold limit can be interpreted from the results of single animal inhalations. It ap pears to be far below a possible injurious level. Dieldrin. The workers examined by Princi and Spurbeck (1951) after three years in dustrial exposure to several related insecti cides including dieldrin with concentrations of the order of 6 mg./cu.m., showed no evi dence of clinical effect. Treon and Cleveland (1955) found 25 ppm in the diet of rats for two years did not shorten their lives. Dogs are most sensitive, tolerating'only 3 ppm. Chronic toxicity centered in the liver. In acute poisoning, central nervous system ir ritation is prominent. Dieldrin penetrates the skin. The most important effect of dieldrin in halation is chronic poisoning centering in the liver. The 0.25 mg./cu.m. threshold limit can be interpreted from the results of re peated oral doses to animals and results of examination of exposed workmen. It is low enough to prevent injury. Diethylamine. Brieger and Hodes (1951) exposed rabbits repeatedly to 50 ppm and found lung and corneal injury, but animals survived with some liver injury. Smyth (1937-55) found rats suffer fractional mor tality from four hours at 2000 and 4000 ppm, while 8000 is lethal to all. The liquid is extremely injurious to the cornea. The most important effect of diethylamine inhalation is respiratory tract irritation, with lung edema the maximum injury. The 25 ppm threshold limit can be interpreted from results of repeated animal inhalation. It appears low enough to prevent injury. Difluorodibromomethane. ACGIH (1955b) quotes Chemical Corps Medical Laboratories Research Report No. 180, 1953. This shows six weeks daily inhalation of 2300 ppm kills some animals with lung injury, liver and central nervous system damage. The most important effects of difluoro dibromomethane inhalation are chronic toxicity and respiratory tract irritation. The 100 ppm threshold limit can be interpreted from the results of single animal inhalations, in comparison with carbon tetrachloride, ethyl and methyl bromide. It appears low enough to prevent injury. Diisobutyl ketone. Silverman, Schulte and First (1946) found concentrations above 25 ppm give eye irritation in unacclimated sub jects. Carpenter, Pozzani and Weil (1953) feund single eight-hour inhalations of 200 ppm killed some rats by anesthesia, re peated inhalation of 1650 ppm killed some and caused liver, kidney and lung injuries, while 125 ppm was without effect. Two humans found 50 ppm satisfactory for work during a three-hour period, but were un comfortable at 100 ppm. The most important effect of diisobutyl ketone inhalation is narcosis. The 50 ppm threshold limit can be interpreted from re peated animal inhalations and human sen sory response. It is low enough to prevent definite narcosis. 2A-Diisocyanotoluene. Swenson, Holmquist and Lundgren (1965) quote French animal inhalations in which 1 to 2 gm./cu.m. (140 to 280 ppm) caused only respiratory tract irritation. They report three human industrial cases featuring upper respiratory tract irritation followed by sensitization ucc 109592 156 June, 1956 and asthma-like attacks. Unpublished The most important effect of inhalation of American experience features sensitization. dinitrobenzene is chronic poisoning. The 1 The most important effect of 2,4-di- mg./cu.m. tentative threshold limit appears isocyanotoluene inhalation is respiratory to be based on the reasonable assumption tract irritation, followed by sensitization. that dinitrobenzene is five times as toxic as The 0.1 ppm tentative threshold limit cannot nitrobenzene. be interpreted quantitatively. It is probably Dinitro-o-cresol. Baltimore (1943) re not low enough to prevent an attack in a ports a non-fatal case from inhalation of sensitized person. 4.7 mg./cu.m. Spencer, Rowe, Adams and Dimethyl aniline (E-dimethyl aniline), Irish (1948) in animal experiments, found Henderson and Haggard (1943, p. 227) con- 10 to 50 mg./kg. is a fatal dose for animals. elude that the alkyl anilines are less toxic It is a rapidly acting metabolic stimulant, than aniline, but von Oettingen (1941, p. increasing body temperature to the point of 15) concludes dimethyl aniline has a greater heat stroke. Cataracts are produced in sus depressant effect than aniline. It forms ceptible species, but chronicity is low. methemoglobin in the blood. He cites two The most important effect of dinitro-o- human poisonings with symptoms like ani cresol inhalation is acute poisoning, marked line. by metabolic stimulation with rise of body The most important effect of dimethyl temperature. The 0.2 mg./cu.m. threshold aniline inhalation is poisoning like that limit can be interpreted from the facts of from aniline. The 5 ppm threshold limit can one industrial accident. It appears low be interpreted by analogy with aniline. It enough to prevent injury. appears low enough to prevent injury. Dinitrotoluene, Von Oettingen (1941, p. Dimethyl sulfate. Fiury and Zernik 110) concludes this is similar to trinitro (1931) report that 13 ppm severely poisoned toluene but less toxiij when pure. The dust cats in 20 minutes. Patty (1948-9, p. 925) causes mucous membrane irritation. I, states it has only a faint odor and there is a The most important effect of dinitro considerable latent period before effects are toluene inhalation is chronic poisoning, evident. Fairhall (1949, p. 309) concludes it marked by central nervous system, liver is a powerful irritant upon inhalation, the and red blood cell changes. The 1.5 mg./cu.m. liquid causes severe skin burns and corneal threshold limit can be interpreted from an injury, and when swallowed, marked central alogy with trinitrotoluene. It does not ap nervous system effects such as convulsions pear low enough to prevent all injuries. and delirium result. Smyth (1937-55) Dioxane. Fairley, Linton and Ford-Moore found rats survive four hours inhalation of (1934) found liver and kidney injury in 15 ppm but die from 30 ppm. animals repeatedly inhaling 1000 ppm, and The most important effect of dimethyl from skin absorption. Silverman, Schulte sulfate inhalation is delayed irritation of and First (1946) found eye, nose and throat bronchi, and lung edema, not preceded by irritation at 300 ppm in unacclimated sub promptly evident irritation of eye and upper jects. Patty (1948-9, p. 957) concludes there respiratory tract. Very high concentrations is only a faint odor at 200 ppm. Smyth may cause convulsions and delirium, then (1937-55) found rabbits particularly sus coma. The 1 ppm threshold limit can be in ceptible, repeated inhalation at 800 ppm terpreted from results of single animal in killing some with kidney injury within 30 halations. It appears to be low enough to days. protect against lung injury, but available The most important effect of dioxane in data do not indicate that it will prevent halation is chronic poisoning, centering in bronchial irritation. the liver and kidney. The 100 ppm thresh Dinitrobenzene. Fairhall (1949) con old limit can be interpreted from results of cludes the chief effect of dinitrobenzene is repeated animal exposure studies. It ap the production of methemoglobin, leading pears to be low enough to prevent injury. to anoxia and anemia. Von Oettingen (1941) EPN, Hodge, Maynard et al (1954) found in a review of the literature finds chronic the acute oral LD50 for rats ranges from 7 liver injury and cites opinions that Tt is to 33 mg./kg., while 75 ppm in the diet is more toxic than nitrobenzene. , without effect during two years. The ma- Industru terial m symptom to excita be Vs to The me tion is th The 0.5 interpret i doses to thion. It jury. Ethyl < of Nelson man (194 odor at 2 irritation gard (19 20,000 p] posures. 1 produce s found rat: survive, b The mo inhalation old limit i sory data by animal prevent d< Ethyl o penter (1! ppm inju rats and i jure rats, detectable ppm is obj' and Kitzi similar re The mo: ate inhalat The 25 ppi interprets tion result It appears Ethyl a (1943, p. 2 but not tc cumstancei toxication. eight hour earliest st; (1945) stc 1000 ppm 1 eye irritat eludes 600( ably irrita- |UCC 109593 Industrial Hygiene Quarterly 157 terial is a cholinesterase inhibitor, and lows. Smyth (1937-55) found rats survive symptoms of excess in animals are confined eight hours at 16,000 ppm but some are to excitability and tremors. It appears to killed at 32,000 ppm. be y8 to y3 as toxic as parathion. The most important effect of ethyl alco The most important effect of EPN inhala hol inhalation is narcosis. The 1000 ppm tion is the reduction of blood cholinesterase. threshold limit can be interpreted from The 0.5 mg./eu.m. threshold limit can be human physiological data. It is low enough interpreted from the results of single oral to prevent significant narcosis, but some eye doses to animals and analogy with para irritation will result. thion. It appears low enough to prevent in- ' Ethyl amine. Brieger and Hodes (1951) jury. exposed rabbits repeatedly to 50 ppm and Ethyl acetate. The unacclimated subjects found lung and corneal injury, with some ef of Nelson, Ege, Ross, Woodman and Silver- fect on heart muscle. Smyth (1937-55) man (1943) found an objectionably strong found four hours at 4000 to 8000 ppm kills odor at 200 ppm and eye, nose and throat some rats, and 16,000 ppm kills all. Respira irritation at 400 ppm. Henderson and Hag tory tract irritation is prominent. The liquid gard (1943, p. 222) conclude 10,000 to is extremely injurious to the cornea. 20,000 ppm is dangerous for short ex The most important effect of ethyl amine posures. It is mildly narcotic but does not inhalation is respiratory tract irritation, produce systemic effects. Smyth (1937-55) with lung edema the maximum injury. The found rats inhaling 8000 ppm for four hours 25 ppm threshold limit can be interpreted survive, but 16,000 ppm kills. from results of repeated animal inhalation. The most important effect of ethyl acetate It appears low enough to prevent injury. inhalation is narcosis. The 400 ppm thresh Ethyl benzene. Yant, Schrenk, Waite and old limit can be interpreted by human sen Patty (1930) found only slight irritation in sory data and results of single inhalations guinea pigs breathing 1000 ppm for eight by animals. It apparently is low enough to hours. Fatalities from higher levels showed prevent definite narcosis. lung edema. Humans found 1000 ppm was Ethyl acrylate. Pozzani, Weil and Car initially irritating to the eyes and 2000 ppm penter (1949) found 30 inhalations of 300 caused throat irritation, constriction in the ppm injured lungs, liver and kidneys of chest and slight intoxication. Smyth (1937- rats and rabbits, while 70 ppm did not in 55) found rats not killed by four hours at jure rats. They found that 8 ppm is readily 2000 ppm, while 8000 ppm is fatal. There detectable by odor, and that the odor of 50 is general agreement that it does not exert ppm is objectionable. Treon, Sigmon, Wright the hematopoetic effects of benzene. and Kitzmiller (1949) obtained closely The most important effect of ethyl ben similar results. zene inhalation is narcosis, with irritation The most important effect of ethyl acryl of the entire respiratory tract contributing ate inhalation is respiratory tract irritation. to injury. The 200 ppm threshold limit can The 25 ppm tentative threshold limit can be be interpreted from results of single animal interpreted from repeated animal inhala inhalations and limited human sensory re tion results and limited human sensory data. sponse. It is low enough to prevent injury. It appears low enough to prevent injury. Ethyl bromide. Waite and Yant (1928) Ethyl alcohol. Henderson and Haggard found lung edema a prominent effect of (1943, p. 219) consider its vapors anesthetic guinea pig inhalation. Sayers, Yant, Thomas but not toxic. Only under exceptional cir and Berger (1929) found several hours in cumstances can inhalation cause slight in halation of 1700 ppm by animals was with toxication. They estimate 1064 ppm for out effect. Henderson and Haggard (1943, p. eight hours is not sufficient to produce the 207) note that vapors are not narcotic. earliest stage of intoxication in man: Cook The most important effect of ethyl bro (1945) stated that industrial exposure at mide inhalation is respiratory tract irrita 1000 ppm has led only to a few complaints of tion. The 200 ppm threshold limit can ;be in eye irritation. P,atty (1948-9, p, 861) con terpreted from the results of single animal cludes 6000 to 9000 ppm is initially intoler inhalations. It is probably low enough to pre ably irritating, but that acclimatization fol vent injury. '\ 158 June, 1956 Ethyl chloride. Sayers, Yant, Thomas and Berger (1929) found with animals that 150.000 to 300,000 ppm is rapidly fatal, death being due to anesthesia, that 40,000 ppm does not kill in 270 minutes, 20,000 ppm causes only moderate unsteadiness, and 10.000 ppm is without effect. The most important effect of ethyl chlor ide inhalation is narcosis. The 1000 ppm threshold limit can be interpreted from the results of single animal inhalations. It is low enough to prevent significant narcosis. Ethylene chlorhydrin. Dierker and Brown (1944) reported one fatality with estimated exposure of 305 ppm for two hours. Animal experiment produced kidney pathology from 365 ppm for two hours. Goldblatt (1944) and Goldblatt and Chiesman (1944) report 11 cases, two of them fatal. Nervous system, cardiovascular system and kidneys were affected, and no warning irritation was apparent. They found one hour at 1120 ppm killed animals, with evidence of poten tial chronic effect. They conclude no concen tration is safe for daily exposure. Smyth and Carpenter (1945) point out very rapid skin penetration of the liquid, the absence of warning skin irritation and the failure of rubber gloves to protect. The most important effect of ethylene chlorhydrin inhalation is acute poisoning, centering in the kidney. The 5 ppm thresh old limit can be interpreted from the re sults of single animal inhalations. It appears low enough to prevent injury. Ethylene diamine. Dernehl (1951) re lated industrial experience showing this is a sensitizer upon contact and inhalation. Pozzani and Carpenter (1954) exposed rats repeatedly to the vapors. All died within 20 days at 484 ppm, with loss of hair, injury to the kidney and lesser effects on liver and lung. There was no effect except loss of hair at 132 ppm, and none whatever at 59 ppm. Very brief human exposures found 100 ppm inoffensive, tingling of skin and nose at 200 ppm and intolerable sensory response at 400 ppm. Smyth (1937-55) found eight hours at 2000 ppm did not kill rats while 4000 ppm was fatal. Death was due chiefly to kidney injury, with some injury to lung. The liquid irritates the skin and severely in jures the cornea. The most important effects of ethylene diamine inhalation are respiratory tract 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 skin. It is painful in the eye, but causes 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 results of repeated animal inhalations. It is probably low enough to prevent injury. Ethylene dichtoride. Spencer, Rowe, Adams, McCollister and Irish (1951) study ing repeated inhalation by animals, found no effect from 100 ppm. Single dangerous inhalations irritate the lung and depress the central nervous system, while dangerous re peated inhalations injure liver and kidney. They feel chronic intoxication is unlikely because tolerated repeated inhalations are close to concentrations tolerated once. Con centrations sufficient to cause marked nar cosis are irritating to the upper respiratory tract. Adams, Spencer, Rowe, McCollister and Irish (1952) simultaneously studying carbon tetrachloride, found it at least four times as toxic as ethylene dichloride. Elkins (1950, p. 137) found complaints of nausea from industrial exposures to 100 to 150 ppm. Patty (1948-9, p. 805) finds little odor at 100 ppm, slight eye and nose irritation at 1000 ppm. The most important effect of ethylene dichloride inhalation is chronic poisoning, centering in the liver. The 100 ppm thresh old limit can be interpreted from the results of repeated animal inhalations and human response. It is low enough to prevent injury. Ethylene imine. Silver and McGrath (1948) and Carpenter, Smyth and Shaffer (1948) studied single inhalations in animals. The LC50 for mice in a 10-minute exposure Indus tr is 2236 to rats a eight he hours. I due to lung an smell 2 tate eye. skin, p burns, l The j inline ir ing in tl imports, be inter} inhalatn sory dal prevent tract in Ethyl' (1930) no symp Greater irritatio tation. low cone tion are Sexton ; ten tion with ser. with th< Smyth hours appm. H< ter and ! Iy inhal and son kidney, were no toleratei Feinsilv found si tion of feet. The j oxide in tion lea to liver 100 ppir from re studies, injury. Ethyl (1943, human 1 Ucc 109595 Industrial Hygiene Quarterly 159 is 2236 ppm, 500 ppm for one hour is fatal of 400 ppm is 0.018 gm./i., causing no in to rats and guinea pigs, 25 ppm kills some in toxication, while 2000 ppm will give a blood eight hours, and 10 ppm kills none in eight level of 0.09 gm./l., corresponding to insta hours. Symptoms and death are delayed, bility in some persons. They state 35,000 due to kidney tubular injury, with lesser ppm anesthetizes in 30 minutes, and a higher lung and liver injury. Humans can barely concentration kills by respiratory paralysis. smell 2 ppm, while 100 ppm begins to irri Experience in human anesthesia shows that tate eyes and nose. The liquid penetrates the pneumonitis may follow ether anesthesia, skin, produces severe skin and corneal but other injuries are unlikely. Nelson, Ege, burns, and sensitizes the skin. Ross, Woodman and Silverman (.1943) The most important effect of ethylene found nasal irritation at 200 ppm with unac imine inhalation is acute poisoning, center climated subjects, somewhat greater at 300 ing in the kidney, with lung injury of lesser ppm. importance. The 5 ppm threshold limit can The most important effect of ethyl ether be interpreted from results of single animal inhalation is narcosis. The 400 ppm thresh inhalation studies and limited human sen old limit can be- interpreted from human sory data. It is apparently low enough to physiological and sensory data. It is low prevent poisoning and upper respiratory enough to prevent definite narcosis. tract irritation. Ethyl formate. Flury and Zernik (1931) Ethylene oxide. Waite, Patty and Yant reported 330 ppm causes in man slight eye (1930) in single animal inhalations found irritation and rapidly increasing nasal irri no symptoms from eight hours at 250 ppm. tation, while 10,000 ppm is anesthetic and Greater concentrations caused eye and nose fatal. Fairhall (1949, p. 344) notes its ef irritation, narcosis, bronchial and lung irri fects are irritation and narcosis, and that tation. Sensory response is only moderate at there is no chronic toxicity. Smyth (1937- low concentrations, but eye and nose irrita 55) found rats survive four hours inhala tion are intolerable at high concentrations. tion of 4000 ppm but die from 8000 ppm. Sexton and Henson (1950) have called at The most important effect of ethyl for the tention to spectacular human skin injuries mate inhalation is narcosis. The 100 ppm with sensitization, which arise from contact threshold limit can be interpreted from with the liquid and its aqueous solutions. scanty human sensory data and single Smyth (1937-55) found rats survive four animal inhalations. It appears to be low hours at 4000 ppm but are killed by 8000 enough to prevent definite narcosis and irri ppm. Hollingsworth, Rowe, Oyen, McCollis- tation. ter and Spencer (1956) in animals repeated Ethyl mercaptan. Sayers, Fieldner, Yant, ly inhaling 204 ppm found lung irritation Leitch^and Pearce (1930) report the odor and some fatalities, with injury to liver, detectable at one part per billion and dis kidney, adrenal and testes. Rats and mice agreeable at one part per fifteen million. were not affected at 49 ppm, other species They quote that its effects are like those of tolerated 113 ppm. Jacobson, Hackley and hydrogen sulfide, and by analogy with butyl Feinsilver (1956) with dogs, rats and mice mercaptan they conclude more than 733 found some fatalities from repeated inhala ppm is required to kill in 30 minutes. Flury tion of 400 ppm, but 100 ppm had little af and Zernik (1931) quote 3000 ppm as harm fect. less to dogs and 10,000 ppm causing hema The most important effect of ethylene tologic and blood cell changes. oxide inhalation is respiratory tract irrita The most important effect of ethyl mer 4 tion leading to lung injury, while injury captan is eye and respiratory tract irrita m to liver and kidney are less important. The tion. The 250 ppm tentative threshold lim 100 ppm threshold limit can be interpreted it can be interpreted from the results of from results of repeated animal inhalation single inhalation by animals. It appears low studies. It appears low enough to prevent enough to prevent injury and eye irritation. I TM v ti*<c!'1 injury. Ethyl silicate. Smyth and Seaton (1940) Ethyl ether. Henderson and Haggard found eight-hour inhalation of 550 ppm the (1943, p. 195) estimate the maximum least fatal exposure for guinea pigs. Death human blood concentration from inhalation is due to lung injury, with some kidney `X" \j/f ucc 160 June, 1956 Indus 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 The chloro I 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 of na concei some kidney damage in rats repeatedly in age in the body occurs when as little as it car haling 125 ppm. Pozzani and Carpenter three milligrams per day fluoride in the single (1951) exposed rodents repeatedly. Some form of sodium fluoride is ingested, rough far be died within 30 days at 440 ppm with injury ly equivalent to inhalation of 0.3 mg./cu.m. For to lung, liver and kidney, but 88 ppm did soluble fluoride dust. (1943, not injure. The data suggest that repeated The most important effect of inhalation irritat inhalation at a given concentration is no of fluoride dust is chronic poisoning, cen ly the more injurious than a single inhalation. tering in the bones, with respiratory tract effects The most important effect of ethyl silicate irritation at high concentrations. The 2.5 to sol inhalation is lung injury, with non-progres mg./cu.m. threshold limit can be interpreted tract s sive kidney damage less important. The from results of examination of exposed Elkins 100 ppm threshold limit can be interpreted workmen and experimental studies of human workm from results of repeated animal inhalations fluoride retention. It is not low enough to tation and limited human sensory data. It can be prevent fluoride storage with resulting ef Smyth smelled, it is not irritating, and is low fects on the bones. hours enough to prevent lung or kidney injury. Fluorine. Machle and Evans (1940) ex by 250 Ferbam. Hodge, Maynard, Downs, Blan- amined workmen exposed intermittently to injury. chet and Jones (1952) reported the oral as much as 10 ppm and found no clinical evi The LD50 for rats to be over 17 gm./kg., with dence of damage, but there was some ac hyde ii guinea pigs and rabbits more sensitive. Rats cumulation in bones and teeth. Stokinger the eye tolerated 0.01% in their diet for 30 days (1949) found few toxic effects in dogs re bronch without effect while 0.5% was required to peatedly exposed to 0.5 ppm. Greater con limit c kill. Dogs were not injured by 25 mg./kg./ centrations injured lung and kidney. This is human day for six months. The mechanism of in apparently below the level which leads to to prev jury is not clear. bone abnormalities (Roholm 1937). Furf The most important effect of inhalation The most important effect of inhalation animal of Ferbam appears to be the upper respira of fluorine gas is respiratory tract irrita 280 ppr tory tract irritation of a substantially inert tion, with lung edema the maximum effect. brane dust. The 15 mg./cu.m. tentative threshold Chronic effect on bone metabolism is also acute ii limit is in accord with this. important. The 0.1 ppm threshold limit can ACGIH Ferro vanadium dust. Roshchin (1952) be interpreted from results of animal in nik, (j exposed rats two months to 1000 to 2000 halation and studies on exposed workmen. It effect t mg./cu.m. and found no effect beyond some is low enough to prevent injury. ache ar lung irritation. The author suggests a Fluoroacetates. Diekeand Richter (1946) jury is threshold limit of 1 mg./cu.m. Vanadium report the median lethal oral dose to be 0.22 analogy compounds irritate the upper respiratory mg./kg. for wild rats. The substance is skin ar tract, but Sjoberg (1951) found no chronic rapidly fatal through intervention in the found. general poisoning in workers exposed to tricarboxylic acid metabolic cycle. The r vanadium pentoxide dust, symptoms being The most important effect of fluoroaeetate halatior confined to respiratory difficulties and skin inhalation is acute toxicity. The 0.1 in the < allergies. mg./cu.m. tentative threshold limit can be tract, b: The most important effect of inhalation interpreted from acute oral toxicity data for tative i of ferrovanadium dust is respiratory tract rats. It corresponds to a maximum human from ui irritation. The 1 mg./cu,m. threshold lim intake of one milligram per day, apparently is suffici it can be interpreted from limited repeated well below a dangerous amount. Furfi animal inhalations and examination of ex Fluorotrichloromethane. Nuckolls (1933) found t posed workmen. It appears low enough to found in animals no more than occasional due to prevent injury. tremors and retching during two hours at thesia, a Fluoride dust, Roholm (1937) found fluor 22,000 to 25,000 ppm. No toxic effects are to reversib osis of human bone, but no other effects, af be expected from this physiologically inert cal Cor ter several years work in 2 to 3 ppm fluorine, material. Report I ucc 109597 Industrial Hygiene Quarterly 161 The most important effect of Huorotri- hours inhalation of 700 ppm killed 25 % of chloromethane inhalation is a minor degree a group of rats. of narcosis, and asphyxia from very high The most important effect of furfuryl al concentrations. The 1000 ppm threshold lim cohol inhalation is narcosis. The 50 ppm ten it can be interpreted from the results of tative threshold limit can be interpreted single animal inhalations. It appears to be from results of single animal inhalations. It far below a possibly injurious level. appears low enough to prevent injury. Formaldehyde. Henderson and Haggard Gasoline. Sayers, Fieldner, Yant and (1943, p. 128) conclude its action is chiefly' Thomas (1927) reported human dizziness irritation of all tissues contacted, particular at 700 ppm, and Drinker, Yaglou and War ly the respiratory tract, and that systemic ren (1943) found human respiratory tract effects are not important. Skin sensitization irritation and headache begin at 1000 ppm. to solutions is frequent and respiratory Elkins (1950, p. 99) found industrially no tract sensitization to the gas is not unlikely. sensory response to 660 to 800 ppm benzine, Elkins (1950, p. 231) reports irritation in and dizziness at 2000 to 3000 ppm. He con workmen inhaling 5 to 6 ppm, and eye irri cludes chronic effects do not occur when con tation of unhardened persons at lower levels. centrations are too low to cause narcosis, Smyth (1937-55) found rats survive eight but Hayhurst (1936) reported chronic hours inhalation of 125 ppm but are killed poisoning consisting of central nervous sys by 250 ppm. The liquid causes severe corneal tem effects and blood cell changes after injury. many years of exposure. This article does The most important effect of formalde not seem to be generally accepted. Henderson hyde inhalation is irritation, first evident in and Haggard (1943, p. 192) consider nausea the eyes, then in the upper respiratory tract, and incoordination the significant effects, bronchi and even lung. The 5 ppm threshold with anesthetic death at 20,000 to 30,000 limit can be interpreted from uncontrolled ppm. Aromatic hydrocarbons in gasoline human sensory data. It is sufficiently low from cracking operations may much reduce to prevent lung injury. safety. Furfural, Fairhall (1949, p. 354) quotes The most important effect of gasoline in animal experiments in which inhalation of halation is narcosis. The threshold limit of 280 ppm resulted only in slight mucous mem 500 ppm can be interpreted from human sen brane irritation, while 2800 ppm caused sory data, both experimental and indus acute irritation, prostration and lung edema. trially observed. It is low enough to prevent ACGIH (1954b) quotes Korenman and Res- definite narcosis. nik, {Arch. Hyg., 104:344, 1931) to the Heptane. Patty and Yant (1929) reported effect that 2 to 14 ppm causes human head slight htiman dizziness from 1000 ppm. The ache and eye irritation. Severe corneal in paraffin hydrocarbons are anesthetic agents jury is to be expected from the fluid, and and irritate mucous membrane, but they do analogy with other aldehydes suggests that not cause systemic toxicity. skin and respiratory sensitization may be The most important effect of heptane in found. halation is narcosis. The 500 ppm thresh The most important effect of furfural in old limit can be interpreted from limited halation seems to be irritation, first evident human sensory data and by analogy with the in the eyes, then in the upper respiratory better studied gasoline. It is probably low tract, bronchi and even lung. The 5 ppm ten enough to prevent definite narcosis. tative threshold limit can be interpreted HETP (hexaethyltetraphosphate). This from uncontrolled human sensory data. It material is substantially identical in quanti is sufficiently low to prevent lung injury. tative and qualitative effect with the cholin Furfuryl alcohol. Fine and Wills (1950) esterase inhibitor TEPP. Apparently no found that death from furfuryl alcohol is data specifically upon inhalation have been due to the respiratory paralysis of anes published. thesia, and that short of death, its effects are The most important effect of HETP is reversible. ACGIH (1955b) quotes Chemi reduction of blood cholinesterase. The 0.1 cal Corps Medical Laboratories Research mg./cu.m. tentative threshold limit can be Report No. 139,1942, to the effect that eight interpreted by analogy with parathion. It 'I I slitr ,'f ii I UCC - 109598 162 June, 1956 appears to be consistent with that value. Hexane. Nelson, Ege, Ross, Woodman and Silverman (1943) with unacelimated subjects found no irritation at 500 ppm. Drinker, Yaglou and Warren (1943) found human nausea, headache, eye and throat ir ritation at 1400 to 1500 ppm. The paraffin hydrocarbons anesthetize and irritate mu cous membrane, but do not cause systemic toxicity. The most important effect of hexane in halation is narcosis. The 500 ppm thresh old limit can be interpreted from human sensory data. It is low enough to prevent definite narcosis. Hexanone (methyl butyl ketone). Simple ketones are irritant and narcotic, but not chronically toxic. Schrenk, Yant and Patty (1936) found guinea pigs tolerate 1000 ppm with slight or no symptoms for several hours, a concentration with a strong odor, moderately irritating to human eyes and nose. Death from higher levels is anesthetic respiratory paralysis. Specht, Miller, Valaer and Sayers (1940) found it more depressant than acetone, butanone or pentanone. Smyth (1937-56) 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 (1937-65) found rats sur vive four hours at 2000 ppm, but die from 4000 ppm. Silverman, Schulte and First (1946) found the odor objectionable at 200 ppm, eye irritation evident, but no nose and throat irritation with unacclimated subjects. The most important effect of hexone in halation is narcosis. The 100 ppm threshold limit can be interpreted from results of single animal inhalations and human sen sory response. It is low enough to prevent definite narcosis. Hydrazine, Comstock, Lawson, Greene and Oberst (1954) found in animals dam age to lung and liver, tremors and' convul sions, irritation of eye, nose and throat. Most of the animals repeatedly inhaling 20 ppm died by 30th day. During six month's inhalation of 5 ppm, only minor changes in the lungs of rats and dogs were found. The most important effect of inhalation of hydrazine is respiratory tract irritation. The 1 ppm threshold limit can be interpreted from results of repeated animal inhalation. It is probably low enough to prevent injury. Hydrogen Bromide. ACGIH (1955b) quotes unpublished human response data from the Connecticut Bureau of Industrial Hygiene. Odor was evident at 2 ppm, nose and throat irritation began to be evident at 3 ppm, and eye irritation was not evident at 6 ppm. The most important effect of hydrogen bromide inhalation is respiratory tract ir ritation, with lung edema the maximum ef fect. The 5 ppm tentative threshold limit can be interpreted from analogy with hydrogen chloride and human sensory response. It is probably low enough to prevent injury. Hydrogen chloride. Machle, Kitzmiller, Scott and Treon (1942) found animals not affected by repeated inhalation of 34 ppm. Henderson and Haggard (1943, p. 126) con sider it an irritant without systemic effect. They state 1000 to 2000 ppm is dangerous to life through lung edema in a short time. Elkins (1950, p. 79) finds 10 ppm highly irri tating to humans although immunity seems to develop; 5 ppm immediately irritating; and even lower levels can erode the teeth. The most important effect of hydrogen chloride inhalation is respiratory tract irri tation, with lung edema the maximum ef fect. The 5 ppm threshold limit can be interpreted 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 O.fi ppm, and recognizable at 2 to 5 ppm. 1 , 1 ; > ? Indust The cyanidt chemic. limit c older ; some h to prev Hyd> found ; causing testis cl Animal pirator; sure. El at 0.4 1 finds 0.' taring a smarts, ing skii All solu metabol tooth at The i fluoride ritation, feet. Ch also imj can be i animal i It is low Hydrt stock an vive eigl sympton are four months the skin tated. T to skin : The n peroxide tract inmum effi be inter animal ii vent injr Hydro (1941) 3 hours at and char nose irri man, but ception t (1947) r than 0.2 X 20 ith's s in n of don. eted -ion. ury. 15b) lata ;rial lose t at t at gen irefcan gen t is Her, not pm. lonect. ems ng; h. gen rri- ;ion i to nik six and r is r is l is i in ves one the 3-9, at Industrial Hygiene Quarterly 163 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 fluoride inhalation is respiratory tract 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 injury. The most important effect of hydrogen selenide 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 low enough to prevent injury Hydrogen sulfide. Henderson and Hag gard (1943, p. 140, 243) 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 600 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.ra. The most important effect of hydro quinone inhalation 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 be inter preted from the results of examination of exposed workmen. It appears low enough to prevent effect. l~ ttii/t'v rir'* ' r ``S 1G4 June, 195G Iodine. Henderson and Haggard (1943, p. 133) state it is a respiratory tract irri tant with more effect on the lungs than chlorine and bromine. They quote an 1889 thesis by Matt to the effect that 0.1 ppm does not disturb workers. Fairhall (1949, p. 90) points out that excessive absorption can disturb the metabolism through effect on the thyroid. The most important effect of iodine vapor inhalation is respiratory tract irritation, with lung edema the maximum injury. The 0.1 ppm threshold limit can be interpreted from analogy with chlorine. It appears low enough to prevent injury. Iron oxide fume. Fairhall (1949, p. 92) reviews several articles. Inhalation of iron oxide dust for 5 to 10 years can lead to a benign pneumoconiosis, siderosis, revealed by x-ray but not injurious. U.S. Department of Labor (1941) in studies of welders, con cluded iron oxide fume below 30 mg./cu.m. was without effect, while in excess of this level a chronic bronchitis may result. The most important effect of inhalation of iron oxide fume is bronchitis or metal fume fever. The 15 mg./cu.m. threshold limit can be interpreted by analogy with zinc oxide fume. It is low enough to prevent injury. Isophorone. Smyth, Seaton and Fischer (1942) found no effect upon animals from repeated inhalation of 25 ppm, while 50 ppm caused some lung and kidney injury. Single inhalation of 4600 ppm (saturation) for eight hours injured the lung but did not anesthetize or kill. Silverman, Schulte and First (1946) found odor objectionable at 10 ppm and eye, nose and throat irritation at 25 ppm with unacclimated subjects. The most important effects of isophorone inhalation are lung and kidney injury. The 25 ppm threshold limit can be interpreted from the results of repeated animal inhala tion and human sensory data. It seems low enough to prevent injury. Isopropylamine. Smyth, Carpenter and Weil (1951) reported that rats survive four hours inhalation of 4000 ppm, but die from 8000 ppm. This is half the acute toxicity Smyth (1937-55) found for butyl amine. ACGIH (1955b) cite unpublished industrial experience that levels above 5 ppm tend to be irritating. The most important effect of isopropyla mine inhalation is respiratory tract irrita tion, with lung edema the maximum injury. The 5 ppm threshold limit can be inter preted from analogy with ethyl amines. It is probably low enough to prevent injury. Lead. Russell, Jones, Bloomfield, Britten and Thompson (1933) after a survey of a storage battery plant, proposed that the threshold limit be reduced from 0.5 to 0.15 mg./cu.m. At this level disabling lead poisoning does not occur, and mild poison ing is rare. The most important effect of lead dust inhalation is chronic poisoning. The 0.15 mg./cu.m. threshold limit can be interpreted from the results of examinations of ex posed workmen. It is low enough to prevent disabling poisoning, but not to prevent some mild cases. Lead arsenate. Fairhall and Miller (1941) and Fairhall, Miller and Weaver (1943) found the arsenate in lead arsenate de creases lead absorption or increases lead excretion, and reduces lead storage. The most important effect of inhalation of lead arsenate is chronic arsenic poison ing. The 0.15 mg./cu.m. tentative threshold limit can be interpreted from the results of biochemical studies on animals. It ap pears to have been selected by analogy with the limit for lead, while analogy with ar senic would yield a much higher figure. Lindane. A.M.A. (1951) in a summary, states lindane in large doses acts as a cen tral nervous system stimulant, leading to hyperirritability, convulsions and death. Animals exposed several months to saturated vapors were not affected, but 10,000 mg./cu.m. dust for one hour killed one of two mice. ACGIH (1954b) quotes an unpub lished 1951 report by J. F. Treon et al. A year of repeated inhalation of 0.7 mg./cu.m. caused minimal pathology in animals. An unpublished 1952 thesis by Spear is quoted to the effect that 655 days at 0.19 mg./cu.m. 24 hours a day did not result in pathology in rats. The most important effect of lindane in halation is chronic poisoning centering in the liver. The 0.5 mg./cu.m. threshold limit can be interpreted from the results of re peated animal inhalations. It appears low enough to prevent injury. Magnesium oxide-fume. Drinker, Thom son and Finn (1927) reported that experi- Industria mental fi cessive in a concent dition is lar pain, munity is The m. of magne fume fe\ limit can extensive enough t< Malath Cassaday conclude as toxic * (1954) r toxicity i many oth ver, Capl. group of posure al mg./cu.m cu.m. Th esterase. The me halation esterase, can be in doses to of expose to preven Manga'. (1951) d. the basal from wea mask-like ances, bu an ore-cr toms in less and be effect! The m of manga 6 mg./cu preted fr exposed t vent inju Mercwt the felt I of mercui concentra 0.1 mg./c psychic pallor, s; ucc 109601 Industrial 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 Cassaday (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 cholin esterase. 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. Lundgren 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, but 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 60 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. Methoxychlor. Haag, Finnegan, Larson, Riese and Dreyfuss (1950) found methoxy- . it* x ucc 109602 166 June, 1956 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 and Blanchet (1952) found no effect on rats for chronic effects is 11,300 ppm. in two years at 0.020% in the diet and no The most important effect of methylal in mortality or histological changes at 0.16%. halation is chronic poisoning, centering in Little accumulates in body fat. liver and kidneys, with narcosis and lung The most important effect of methoxy- injury less important. The 1000 ppm thresh chlor inhalation is chronic poisoning cen old limit can be interpreted from results of 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 of repeated oral doses to animals. It appears there are no data to judge the degree of ir low enough to prevent injury. ritation and narcosis it allows. Methyl acetate. Fairhall (1949, p. 375) Methyl alcohol. Sayers, Yant, Schrenk, notes irritation of eye and respiratory tract, Chornyak, Pearce, Patty and Linn (1942) narcosis less prominent than from higher found no effect on dogs from repeated inhal acetates, but fatal dose close to anesthetic ation of 450 to 500 ppm. Henderson and dose, and symptoms persistent after appre Haggard (1943, p. 218) stress slow elimina ciable narcosis. Death is due to anesthesia, tion, leading to progressive rise in blood but lung%njury also occurs. Smyth (1937- level from daily inhalation. At 200 ppm 0.87 55) found rats survive four-hour inhalations grams can be absorbed by a human in eight of 16,000 ppm, but die from 32,000 ppm. hours, but only part of this can be elimi The most important effect of methyl ace nated before the next day. Methanol is pri tate inhalation is narcosis. The 200 ppm marily a narcotic agent, but it may injure threshold limit can be interpreted by an retina and optic, nerve, leading to cloudy alogy with ethyl acetate, allowing a margin vision or blindness. There is some irrita for greater irritation and for the slow tion of mucous membranes. Elkins (1950, t ji metabolism of methyl alcohol. It apparently p. Ill) found industrial exposures ranging is low enough to prevent narcotic symptoms. from 100 to 1700 ppm with no evidence of Methyl Acetylene. AGGIH (1955b) cites poisoning. Smyth (1937-55) found rats sur Horn, Chemical Corps Medical Laboratories vive eight-hour inhalations of 32,000 ppm, Contract Report #35, 1954. For six months and only a fraction are killed by 64,000 ppm. dogs and rats inhaled 28,700 ppm repeatedly. The most important effect of methyl al A few died. There was lung irritation and cohol inhalation is narcosis, with injury to some central nervous system excitation. retina and optic nerve likely only from quite The most important effect of methyl acet excessive inhalation. The 200 ppm threshold ylene inhalation is lung injury. The 1000 limit can be interpreted from results of re ppm threshold limit can be interpreted from peated animal inhalations. It will not cause results of repeated animal inhalations. It is significant narcosis, but continuous inhala low enough to prevent injury. tion will cause a daily rise in the degree of Methyl acrylate. Treon, Sigmon, Wright early narcosis, due to slow elimination. and Kitzmiller (1949) exposed animals re Methyl bromide. Irish, Adams, Spencer peatedly to vapor. They found that 180 and Rowe (1940) found no effect from re seven-hour inhalations of 31 ppm had no ef peated inhalation at 17 ppm, and 34 ppm in fect upon four species, except some loss in jured only rabbits. Watrous (1942) found weight. Higher concentrations caused re mild symptoms in one-third of 90 workers in spiratory tract irritation and some narcosis. concentrations generally under 35 ppm. In The most important effect of methyl acryl gram (1951) found injuries where workers ate inhalation is respiratory tract irritation. were exposed to 100 to 1000 ppm. After The 10 ppm tentative threshold limit can be improvements reduced exposure to about interpreted from repeated animal inhala 20 ppm, injuries ceased. Fairhall (1949, 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 Methylal (dim ethoxymethane)^ Weaver, system poison leading to delirium, convul Hough, Highman and Fairhall (1951) found sions and even mania. It is rapidly metab that high concentrations produce fatty olized and eliminated. Indu Th brom cente liver, terpr mal i work set a tolerr Me Donlc (1931 gram posur CELLO Burk< centr; after of the and v ments toxici blood peate< cepha 336) ritatii chang vive f eight The CELLO; center The 2 pretec ful va and fi halatii to pre Met oxyetf, the' b( acid, a tating The CELLOS poison LOSOLr interp LOSOL^ Met and B ppm p pigs. repeat ucc 109603 Indiietrial 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 (methoxyethanol). Donley (1936) and Parsons and Parsons (1938) reported toxic encephalopathy with granulopenic anemia from industrial ex posure to a mixed solvent containing methyl gellosolve. 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 Oettingen (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 rats 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 (B-methoxyethyl 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 2886 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 cyclohexanol. 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 are evident at 500 ppm. The most important effect. of methyl cyclohexanol inhalation is narcosis, with non-progressive organic effects less promi- : l! 168 June, 1956 nent. The 100 ppm threshold limit can be in The most important effect of methyl terpreted from results of repeated animal isobutyl carbinol inhalation is narcosis. The inhalation. It is low enough to prevent sig 25 ppm threshold limit can be interpreted fi; 1 nificant narcosis, and probably to prevent from human sensory data. It is low enough minor effects on liver and kidneys. to prevent significant narcosis and irrita Methyl cyclohexanone. Treon, Crutchfield tion. and Kitzmiller (1943) found no effect on Methyl mercaptan. ACGIH (1954b) rabbits from 300 hours at 182 ppm, slight quotes de Rikowski who in 1893 found eye irritation at 514 ppm, while 1822 ppm methyl mercaptan similar to but somewhat caused some narcosis and eye irritation. less toxic than hydrogen sulfide. The most important effect of methyl The most important effect of methyl mer cyclohexanone inhalation is narcosis. The captan is eye and respiratory tract irrita ! r 100 ppm threshold limit can be interpreted tion. The 50 ppm tentative threshold limit from results of repeated animal inhalations. can be interpreted by analogy with hydro It appears low enough to prevent definite gen sulfide. It appears low enough to prevent narcosis. injury and eye irritation. Methylene chloride. Heppel, Neal, Perrin, Molybdenum. Fairhall, Dunn, Sharpless Orr and Porterfield (1944) found repeated and Pritchard (1945) in animal experi inhalation of 10,000 ppm caused moderate ments, found some bronchial and alveolar narcosis in animals, some deaths from lung irritation, with fatty changes in liver and edema and liver damage. A concentration kidneys. Animals survived repeated expo of 5000 ppm for six months had no effect sure one hour daily to 53 mg./cu.m. molyb- upon four species, but reduced the voluntary dic oxide fume and only one of a group was activity of rats, indicative of a very early killed by 286 mg./cu.m. molybdenite dust. stage of narcosis not usually detected in The Industrial Hygiene Digest (16:1083, animals. Fairhall (1949, p. 296) mentions a 1952) abstracts Mogilevskaya to the effect human fatality after accidental anesthesia. that histopathological changes in rat heart, The most important effect of inhalation of liver and kidney are found after repeated methylene chloride is chronic poisoning cen inhalation of 3 to 10 mg./cu.m. molybdenum tering in the liver. The 500 ppm threshold oxide aerosol. limit can be interpreted from the results of The most important effect of inhalation of repeated animal inhalations. It is low molybdenum compounds is chronic poison enough to prevent injury. ing, centering in liver and kidney. The Methyl formate. Schrenk, Yant, Chornyak threshold limits of 5 mg./cu.m. for soluble and Patty (1936) found guinea pigs toler and 15 mg./cu.m. for insoluble molybdenum ate 1500 to 2000 ppm for several hours with compounds can be interpreted from the re out disturbance, and 5000 ppm for one hour. sults of repeated animal inhalations. They Symptoms of higher concentrations were appear low enough to prevent injury, but nose and eye irritation, lung irritation, nar slight toxic effects may result from soluble cosis and anesthetic death. compounds. The most important effect of methyl for Naphtha (coal tar). A mixture of toluene mate inhalation is narcosis. The 100 ppm and xylene chiefly. The predominantly nar threshold limit can be interpreted from re cotic effects of these closely similar ma sults of single inhalations by animals. It terials are additive and a mixture is no more appears to be low enough to prevent definite injurious than the sum of its components. narcosis. Cook (1945) points out that if a sample has Methyl isobutyl carbinol (methyl amyl a low boiling point, an appreciable content alcohol). Silverman, Schulte and First of benzene is to be suspected, and working (1946) at 50 ppm found eye irritation in concentrations should be reduced according unacclimated subjects, although the odor ly. was not objectionable. Experience, with Being composed chiefly of toluene and other alcohols indicates systemic effects are xylene, the most important effect of coal tar not to be expected. Smyth (1937-55) found naphtha inhalation, when free from ben rats inhaling 1000 ppm for eight hours are zene, is narcosis with irritation of the res not killed, but 2000 ppm is fatal. piratory .tract less important. The 200 ppm Industrii threshok alogy wi low enoi Naph t affin hy molecula sion uiic Nickel quotes A a deposit piratory lung edei inferencf nating ir and Sunc 10 ppm k they sug; weight, \ tions. T1 liver inj( five and man an< human c; delayed, The ir vapor in layed ec nasal sin time expi it is app designed to prevei feet, but fectivene Nicoti't diets cor for a 60 on 0.05 % by 0.006' body wei tion redu tirely tc (1949) e 60 millig The m. halation The 0.5 j can be i studies c mum hui day, app level. Nitric eludes it ritant, ii 'J UCC - 109605 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) quotes 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. Sunder man 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% 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. 8i) 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 Ioflf enough to prevent injury. Nitroethane. Machle, Scott and Treon (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 ppm causes immediate throat irritation, 300 ppm coughing and 100 to 160 ppm is danger- ucc 109606 170 June, 1956 Industrial ous for 30 to 60 minutes. Fairhall (1949,.p. Machle, Scott and Treon (1940) concluded that enzyi 117) finds the vapor irritates the entire res that in the nitro paraffins toxicity increases and Bush piratory tract, leading to delayed lung with molecular weight. Thus, 2-nitropropane workers fi edema. There is some reduction in blood should be more toxic than nitroethane. Skin cu.m, cans pressure, causing headache. Gray, McNamee ner (1947) found workmen in concentra linesterase and Goldberg (1952) found respiratory tions of 10 to 30 ppm were not affected, but (1955) on tract inflammation in rats, inhaling 9 ppm 20 to 45 ppm caused anorexia, nausea, vom tion conch for a total of 48 hours in 10 days. Patty iting and diarrhea. to 0.12 mt (1948-9, p. 610) reports 5 ppm is evident The most important effect of 2-nitropro The mo by odor, 10 to 20 ppm is irritating to eyes pane inhalation is acute poisoning accom inhalation and nose. Vigliani and Zurlo (1955) in panied by narcosis and irritation. The 50 esterase. ' workers exposed several years to 30 to 35 ppm threshold limit can be interpreted from can be inti ppm found no symptoms. They regard a results of repeated animal inhalation and ination of threshold limit of 15 ppm satisfactory when industrial experience. It is probably low tain that ozone is absent. enough to prevent injury, but not to pre urable re The most important effect of nitrogen vent disturbing symptoms. but it is 1 dioxide inhalation is respiratory tract irri Nitrotoluene. Von Oettingen (1941) re Pentabc tation, with delayed lung edema probable. viewed the literature and could find no clear the LCso The 5 ppm threshold limit can be inter distinction between the toxicities of nitro hours to 1 preted from results of repeated animal in toluene and nitrobenzene. tral ner halation and human sensory data. It ap The most important effect of nitrotoluene opacity, f pears low enough to prevent injury. inhalation is chronic poisoning, marked by by rats k Nitroglycerim. Cook (1945) quotes U. S. reduced blood pressure and cyanosis. The 5 Comstock Public Health Service experience of no ppm threshold limit appears to be an esti the media systemic effects from 10 ppm, but with as mate without quantitative support. It is (0.5 ppm little as 0.5 ppm causing severe headache doubtful whether the difference between sweet. upon return to work after a week-end. nitrobenzene and nitrotoluene is sufficient The mo Fairhall (1949, p. 406) notes headache from to justify the difference in threshold limits. inhalation lowered blood pressure, excitement, dizzi Octane. No useful published data spe central ne ness, fainting, cyanosis, death from res cifically upon octane were found, but analogy tive thres piratory paralysis. Acclimatization is prom with heptane and gasoline is close. limited r< inent, skin penetration is a major hazard. The most important effect of octane in appears t Elkins (I960, p. 160) found some headaches halation is narcosis. The 500 ppm threshold Pentad at 0.04 ppm. limit can be interpreted only by analogy inhalation The most important effect of nitroglycer with pentane and gasoline. It is probably (1939) c< ine inhalation is acute poisoning, marked by low enough to prevent definite narcosis. in the li\ reduced blood pressure. The 0.5 ppm thresh Ozone. Fairhall (1949, p. 122) quotes for repea1 old limit can be interpreted from studies on McDonnell's incompletely reported work to solid mat' exposed workmen. It is sufficiently low to the effect that daily inhalation of 0.1 ppm the skin, prevent injury, but not to prevent headache. killed guinea pigs with pneumonia, higher chloracne Nitromethane. Machle, Scott and Treon concentrations leading to lung edema. He The mi (1940) found animals not affected by 500 notes respiratory tract irritation with fatal naphthali ppm for a total of 140 hours, but 1000 ppm pneumonitis or lung edema, but no systemic ing cente was fatal. The vapors are eye and respira poisoning. He quotes a statement that 0.015 threshold tory irritants and mildly narcotic. Central ppm can be smelled, and any higher concen results oi nervous system irritation and lung edema tration is irritating. low enouj result. Toxic symptoms are evident before The most important effect of ozone in Pentac narcosis. halation is respiratory tract irritation, with Gruebler The most important effect of nitromethane lung edema the maximum effect. The 0.1 evidence inhalation is acute poisoning, accompanied ppm threshold limit can be interpreted from the small by narcosis and irritation. The 100 ppm results of limited repeated animal inhala mg./kg. 1 I, threshold limit can be interpreted from re tions and human sensory data. It appears temal in y. sults of repeated animal inhalation. It ap low enough to prevent injury. 4 system v # pears low enough to prevent injury. Parathion. The earliest effect of this 2-Nitropropane. The animal work of cholinesterase inhibitor is a reduction of The m ophenol i ucc 109607 Industrial Hygiene Quarterly 171 that enzyme activity in the blood. Brown ing in the circulatory system. The 0.5 mg./ and Bush (1950) in tests on industrial cu.m, threshold limit can be interpreted workers found inhalation of 0.1 to 0.8 mg./ from the results of repeated doses to ani cu.m, causes definite reduction in blood cho mals. It appears low enough to prevent in linesterase activity. Vigliani and Zurlo jury. (1955) on the basis of cholinesterase reduc Pentane. Patty and Yant (1929) found no tion conclude that a threshold limit of 0.07 effect on humans from 10 minutes inhala to 0.12 mg./cu.m. is satisfactory. tion of 5000 ppm. Fairhall (1949, p. 358) The most important effect of parathion concludes that only narcosis and irritation inhalation is the reduction of blood cholin- . are produced. esterase. The 0.1 mg./cu.m. threshold limit The most important effect of pentane in can be interpreted from the results of exam halation is narcosis. The 1000 ppm thresh ination of exposed workmen. It is not cer old limit can be interpreted from limited tain that it is low enough to prevent meas human sensory data and analogy with the urable reduction of blood cholinesterase, better studied gasoline. It is probably low but it is low enough to prevent injury. enough to prevent definite narcosis, Pentaborane. Svirbely (1954a,b) found Pentanone (methyl propyl ketone). Yant, the LC,TM for mice inhaling vapors for two Patty and Schrenk (1936) found 30,000 to hours to be 10.9 ppm. Symptoms were cen 50,000 ppm killed guinea pigs in 30 to 60 tral nervous excitability and corneal minutes; 1600 ppm caused slight or no opacity. Six-hour inhalations of 3.3 ppm symptoms in several hours and was strongly by rats killed all within four repetitions. odorous and irritating to human eye and Comstock and Oberst (1953) report that nose. Death was anesthetic. Smyth (1937- the median detectable odor is 2.5 mg./cu.m. 55) found four hours at 2000 ppm killed (0.5 ppm), described as garlic or slightly part of a group of rats. sweet. The most important effect of pentanone The most important effect of pentaborane inhalation is narcosis. The 200 ppm thresh inhalation is acute toxicity involving the old limit can be interpreted from the results central nervous system. The 0.01 ppm tenta of single animal inhalation and limited tive threshold limit can be interpreted from human response data. It is low enough to limited repeated inhalations by animals. It prevent definite narcosis. appears to be a conservative estimate. Perchloroethylene. Carpenter (1937) Pentachlomaphthalene. After extensive found rats inhaling 230 ppm for 150 days inhalation studies with rats, Drinker showed slight non-progressive liver and (1939) concluded that injury is exclusively kidney effects, while 70 ppm had no effect. in the liver and that the permissible limit Humans perceived the odor at 50 ppm, slight for repeated inhalation is 0.5 mg./cu.m. The eye irfitation at 500 ppm, light narcosis at solid material or its oil solutions penetrates 1000 ppm, nausea at 5000 ppm. Rowe, Mc- the skin, and repeated contact leads to Collister, Spencer, Adams and Irish (1952) chloracne. found repeated inhalation of 400 ppm does The most important effect of pentachlor- not affect rats, rabbits and monkeys, while naphthalene inhalation is chronic poison 100 ppm does not affect guinea pigs. Hu ing centering in the liver. The 0.5 mg./cu.m. mans found no symptoms at 100 ppm, mini threshold limit can be interpreted from the mum narcosis at 200 ppm, eye and nose irri results of repeated animal inhalations. It is tation at 600 ppm, painful irritation at 1000 low enough to prevent injury. ppm. Pentachlorophenol. Kehoe, Deichmann- The most important effect of perchloro Gruebler and Kitzmiller (1939) found no ethylene inhalation is narcosis. The 200 ppm evidence of chronic poisoning in rabbits, and threshold limit can be interpreted from the the smallest lethal intravenous dose was 22 results of repeated animal inhalations and mg./kg. It penetrates the skin readily. In human response. It appears low enough to ternal injury is primarily to the vascular prevent significant narcosis. system with heart failure. Perchloromethyl mercaptan. ACGIH The most important effect of pentachlor (1954b) cites Flury and Zernik (1931) to ophenol inhalation is acute poisoning center the effect that after 15 minutes inhalation of l'1 ; ucc 109608 172 June, 1956 45 ppm, mice and cats die within two days. The most important effect of perchlor- omethyl mercaptan inhalation is eye and respiratory tract irritation. The 0.1 ppm tentative threshold limit can be interpreted on the basis of limited single inhalations by animals. It appears to be low enough to pre vent injury. Phenol. Deichmann, Kitzmiller and Witherup (1944) found guinea pigs are severely injured by 20 days inhalation of 25 to 50 ppm, rabbits suffer lung injury in 63 days, but rats are not affected. They con clude human injury from repeated inhala tion is marked by digestive disturbance, nervous disorders, skin eruption and liver and kidney damage. The liquid penetrates the skin to a dangerous extent, and causes severe skin and corneal injury. Patty (19489, p. 1034) reports that 5 ppm can be recog nized by odor. Smyth (1937-55) found rats survive eight hours inhalation of vapors saturated at room temperature. Although phenol vapors are odorous and irritating, their major effect is chronic sys temic poisoning. The 5 ppm threshold limit can be interpreted from results of repeated inhalations by animals. It appears to be low enough to prevent chronic toxic effects. Phenylhydrazine. 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 Barillet to the effect that phosphorous pentasulfide is somewhat less hazardous than phosphorous pentachloride. The most important effect of phosphorous pentasulfide inhalation is respiratory tract Indit irrit; is ap tive . vent Ph Hagg tant as raj mum distu. findin in an Th< trichi' ritatii feet, interp data, jury. Pici scribe, enteri titis. (1945 inn pi. 0.1942 piratoi fects t The inhalat mg./cu from o is low but not sitizati Prop conclud acetate acetate: tract ir Death . narcosi: (1937-5 32,000 The i tate ini threshol alogy v appears narcosis Prop% Woodms ppm can throat, acclimat L ucc 109609 ;ne in1 with ppm >m reigh to ggard tfatal imum oance. to the -hour i, but Acute sions, ng is sturfa cades phine 0.05 from ation. iry, 49, P. ffects cnetalinful s one 1. orous ng in limit srms. arson this and hlorkely. m. >rous tract The ently rt. It 1949, that less ride. irous tract Industrial Hygiene Quarterly 173 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 at vent injury. 12,000 ppm, but half are killed in eight Phosphorous trichloride. Henderson and hours. Haggard (.1943, p. 134) consider it an irri The most important effect of isopropyl tant and lung injurant. They cite 600 ppm alcohol inhalation is narcosis. The 400 ppm as rapidly fatal, and 2 to 4 ppm as the maxi threshold limit can be interpreted from mum for 30 to 60 minutes without serious human sensory data and analogy with ethyl disturbance. Cook (1945) quotes Butjog as alcohol. It is low enough to prevent signifi finding 0.7 ppm causes only slight irritation cant narcosis, but some irritation will result. in animals. Propylene dichloride. Heppel, Neal, High- The most important effect of phosphorous man and Porterfield (1946) found repeated trichloride inhalation is respiratory tract ir inhalation of 1000 ppm by 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 appears low enough to prevent in tetrachloride. jury. The most important effect of propylene Picric acid. Fairhall (1949, p. 423) de dichloride inhalation is chronic poisoning scribes systemic poisoning as gastro centering in the liver. The 75 ppm thresh enteritis, hemorrhagic nephritis and hepa old limit can be interpreted from the results titis. Sunderman, Weidman and Batson of repeated animal inhalations. It appears (1945) studied workers handling ammoni low enough to prevent injury. um picrate in atmospheres from 0.0088 to Propylene imine. Carpenter, Smyth and 0.1942 mg./cu.m. They found little res Shaffer (1948) found rats and guinea pigs 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 Mjth 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 v* (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 1.6 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 Pyrethrum. There is little published on throat, and 800 ppm is no more severe in un the toxicity of pyrethrum but many years acclimated subjects. Fairhall (1949, p. 429) of wide use as an insecticide indicates a low gI'Uiffl /'\j ucc 109610 m June, 1956 degree of hazard, except for some slight skin sensitizing property. Carpenter, Weii, Pozzani and Smyth (1950) found the rat oral LD5U of two samples to be 0.82 and 1.87 gm./kg. Inhalation studies were made with an insecticidal aerosol containing 10% pyrethrum and 90% peanut oil and a Freon propellant. Rats inhaled a concentration of 6000 mg./cu.m. pyrethrum with 10 times as much peanut oil for 30 minutes, and only moderate lung congestion resulted. Rats and dogs inhaled a concentration of 16 mg./cu.m. pyrethrum with 10 times as much peanut oil for 40 thirty-minute periods dur ing 31 calendar days, without injuries greater than those in peanut oil controls. Lehman (1949) estimates the fatal human dose to be 100 grams. The most important effect of pyrethrum inhalation is irritation of the upper respira tory tract. The 2 mg./cu.m. tentative thresh old limit can be interpreted from limited repeated animal inhalation data. It appears low enough to prevent injury. Pyridine. Pollock, Finkelman and Arieff (1943) using pyridine for human therapy, found no toxic symptoms after daily doses of 0.31 to 1.54 ml., but 1.85 to 2.46 ml. was toxic, with one death of liver and kidney injury. Fairhall (1949, p. 434) considers small repeated doses affect the bone marrow, increasing the platelet count. Elkins (1950, p. 167) quotes a Czech report of mild central nervous symptoms at 6 to 12 ppm. The most important effect of pyridine in halation is chronic poisoning, centering in liver, kidney and bone marrow. The 10 ppm threshold limit can be interpreted from limited human symptom data. Mild symp toms may be found. Quinone, Sterner, Oglesby and Anderson (1947) reported on several years industrial experience with men exposed to quinone va por and hydroquinone dust. No systemic ef fects could be found, but high concentration caused transient eye irritation, and after several years a pigmentation of cornea and conjunctiva was apparent, due to local ac tion on the exposed tissue. Loss of vision has followed pigmentation in some cases, ac cording to Oglesby (1956). It is uncertain whether the vapor or the dust was responsi ble, Concentrations from 0.01 to 8.2 ppm quinone were found in the plant. The odor of quinone is perceptible at about 0.1 ppm. definite at about 0.15 ppm, irritating at 0.5 ppm and markedly irritating at 3 ppm. After comparing exposure with concentra tion, the authors conclude quinone vapor should be kept below 0.1 ppm. The most important effect of quinone in halation is transient eye irritation and a slowly developing pigmentation in the eye. The 0.1 ppm threshold limit can be inter preted from the results of examination of exposed workmen. It appears low enough to prevent effect. Rotenone. On the basis of the literature and his own work, Lehman (1949) esti mates the fatal human dose to be 200 grams by mouth. The most important effect of rotenone in halation is irritation of the upper respira tory tract. The 5 mg./cu.m. tentative thresh old limit can be interpreted by analogy with pyrethrum. It appears low enough to pre vent injury. Selenium compounds (as Se). Fairhall (1949, p. 145J summarizes experimental studies which stress oral doses of selenium dioxide and inhalation of hydrogen selenide. Even at 3 ppm dioxide in the diet rats are injured, while 10 ppm kills within eight weeks. Dudley and Miller (1941) found ani mals killed in eight hours at 0.3 to 1.2 ppm hydrogen selenide, primarily due to lung in jury, with changes in liver and spleen. Buchan (1947) reports industrial cases due to less than 0.2 ppm (0.65 mg./cu.m.) hy drogen selenide, with symptoms largely referable to the liver. The most important effect of inhalation of selenium-bearing dusts is chronic poison ing, centering in the liver. The 0.1 mg./cu.m. threshold limit can be interpreted from the results of repeated feeding to animals and by analogy with hydrogen selenide. This is probably low enough to prevent injury. Sodium hydroxide. Elkins (1950, p. 84) states inhalation of mists result in upper respiratory tract irritation leading to ulceration. Patty (1949, p. 661) on the basis of experience with caustic mists from 1 to 40 mg./cu.m., concludes a concentration of 2 mg./cu.m. is noticeably but not excessively irritating. The most important effect of sodium hy droxide mist or dust inhalation is upper respiratory trffct irritation, leading to ul ceration. The 2 mg./cu.m. threshold limit $4 In ppr unc Wo ppn clin cok vapo limil resu hum prev Sn and . conti fouri irrit; p. II syste as d; ucc 109611 Industrial Hygiene Quarterly 175 at 0.5 can be interpreted from observations upon tating the eye and causing coughing, 8 to 12 ppm, exposed workmen. It appears low enough to ppm irritating the throat, and 3 to 5 ppm icntra- prevent injury. detectable by odor. Elkins (1950, p. 81) vapor Stibine. Webster (1946) finds stibine a finds slight human irritation at 2 ppm and lung injurant and powerful hemolytic agent, objectionable irritation at 10 to 30 ppm. one in- injuring liver and kidney as well. Some The most important effect of sulfur diox ;md a animals die after one hour inhalation of 40 ide inhalation is respiratory tract irrita he eye. ppm. Its action resembles that of the better tion, with lung edema or respiratory arrest inter- understood arsine. the maximum effect. The 10 ppm threshold tion of The most important effect of stibine in limit can be interpreted from human sensory enough halation is acute poisoning, largely lung data and examination of exposed work edema. The 0.1 ppm threshold limit can be men. It is low enough to prevent injury. erature interpreted by analogy with arsine. It ap Sulfur hexafluoride. Lester and Green ) esti- pears low enough to prevent injury. berg (1950) found that it is a physiological grams Stoddard Solvent. Nelson, Ege, Ross, ly inert gas, rats inhaling 800,000 ppm in Woodman and Silverman (1943) found 400 oxygen for 16 to 24 hours were not affected. one in- ppm produced no marked effects on unac The most important effect of sulfur hexa espira climated subjects. This solvent is toxi- fluoride inhalation is asphyxia from very th resh- cologically identical with gasoline and re high concentrations. The 1000 ppm thresh ;y with marks under that material apply. old limit can be interpreted from the re to pre- Strychnine. McNally (1937) reports that sults of prolonged animal inhalations. It is a human death has resulted from swallow so far below any possible injurious level ''airhall ing 30 milligrams. It is a convulsive poison. that it represents good engineering control, i mental The most important effect of strychnine rather than a hazard limit. ilenium inhalation is acute poisoning. The 0.15 Sulfuric acid. Fairhall (1949, p. 83) elenide. mg./cu.m. tentative threshold limit can be considers it an upper respiratory tract ir ats are interpreted from the known human fatal ritant with lung injury possible. It is cor i eight dose. It corresponds to a maximum intake of rosive to the skin and eyes, and erodes the 1.5 milligrams in a working day, apparently teeth. Amdur, Silverman and Drinker low enough to prevent injury. (1952) with normal human subjects, found Styrene monomer. Spencer, Irish, Adams changes in respiration at a concentration as spleen, and Rowe (1942) found immediate animal low as 0.35 mg./cu.m., and pronounced de ses due n.) hy- death was anesthetic, delayed death was due crease in minute volume at 5 mg./cu.m. to lung injury. Blood cells were not affected. Elkins (1950, p. 82) considers concentra largely Repeated inhalation of 650 ppm had no tions above 1 ppm (4 mg./cu.m.) are irri effect on animals. Humans found 1300 ppm tating. Sterner (1943) considered 5 mg./ ation of poisong./cu.m. extremely irritating to eye and nose, and cu.m, as tolerable. 400 ppm had an objectionable odor but little The most important effect of sulfuric acid irritation. Carpenter, Shaffer, Weil and inhalation is respiratory tract irritation, rom the Smyth (1944) found irritation and early with lung edema possible. The 1 mg./cu.m. tals and narcosis in humans at 800 ppm. threshold limit can be interpreted from This is iury. p. 84) a upper The most important effect of styrene vapor inhalation is narcosis. The threshold limit of 200 ppm can be interpreted from results of repeated animal inhalations and human sensory and physiological data. It is low enough to prevent injury. Sulfur monochloride. Henderson and Haggard (1943, p, 130) consider it an upper ling to human sensory response. It is low enough to respiratory tract' irritant through release he basis prevent definite narcosis. of hydrochloric acid, but rarely a lung in om 1 to Sulfur dioxide. Kehoe, Machle, Kitzmiller jurant. Mice die from one minute inhala ation of 1 and LeBlanc (1932) studied many workmen tion of 150 ppm, cats from 16 minutes at 48 essively continuously exposed to sulfur dioxide and ppm. Fairhall (1949, p, 160) concludes fouiid only upper respiratory tract chronic chronic systemic effects do not occur. Elkins ium hys upper irritation. Henderson and Haggard (1943, (1950, p. 81) found 2 to 9 ppm mildly irri p. 131) conclude it is an irritant without tating to humans. g to ul- systemic effect. They give 400 to 500 ppm The most important effect of sulfur mono ld limit as dangerous in a short time, 20 ppm irri chloride vapor inhalation is respiratory 176 June, 1956 tract irritation. The 1 ppm threshold limit The 0,05 mg./cu.m. threshold limit can be can be interpreted from results of single interpreted only by analogy with parathion. animal inhalations and human sensory data. It appears low enough to prevent injury. It is low enough to prevent injury. p-Tertiary butyl toluene. Hine et al. Sulfur pentafluoride. Greenberg and Les (1954) in repeated animal inhalations, ter (1950) found this to be a lung injur found narcosis, respiratory tract irritation, ant. Rat lungs were severely injured by one liver and kidney changes, blood cell changes hour at 10 ppm, less severely injured at 1 like those from benzene, and degenerations ppm and not affected at 0.1 ppm. Sixteen in spinal cord and brain. Rats are killed in hours at 1 ppm was lethal, due to lung in one hour by about 900 ppm, and slight evi jury, while 18 hours at 0.5 ppm injured dence of effect was found in animals re lungs but did not kill. peatedly inhaling 25 ppm. Humans detect 5 The most important effect of sulfur penta- ppm by odor, 80 ppm was unpleasantly ir fluoride vapor inhalation is lung injury. The ritating and some giddiness was noted at 0.025 ppm threshold limit can be interpreted 160 ppm. from results of repeated animal inhalation. The most important effect of p-tertiary It is probably low enough to prevent injury. butyl toluene inhalation appears to be TEDP. This cholinesterase inhibitor is chronic toxicity, combining effect on blood about half as toxic in single doses to animals cells, central nervous system, liver and kid as parathion, and the class of cholinesterase ney. The 10 ppm threshold limit can be in inhibiting compounds manifests little ten terpreted from results of repeated animal dency to chronic effect. inhalations and human sensory data. It ap The most important effect of TEDP in pears to be low enough to prevent significant halation is the reduction of blood cholin toxic effect. i esterase. The 0.2 mg./cu.m. threshold limit 1,1,2,2-Tetrachloroethane, Fairhall ("1949, can be interpreted only by analogy with p. 440) concludes this is the most toxic parathion. It appears low enough to prevent chlorinated hydrocarbon, nine times as toxic injury. as carbon tetrachloride. It is a narcotic and Tellurium. Steinberg, Massari, Miner and produces liver damage, polyneuritis and Rink (1942) examined workmen exposed to white blood cell changes. Elkins (1950, p. tellurium fume ranging from 0.01 to 0.1 139) refers to an unpublished report of ill mg./cu.m., with a peak of 0.74 mg./cu.m. ness from a concentration below 10 ppm. in one sample. The symptoms found were Smyth (1937-55) found rats survive four garlic odor of breath and sweat, dryness of hours at 500 ppm but are killed by 1000 ppm. mouth, metallic taste and somnolence. No The most important effect of 1,1,2,2-tetra- signs of poisoning were found. Excessive chloroethane inhalation is chronic poisoning absorption would have been shown by gas centering in the liver. The 5 ppm threshold trointestinal disturbances, reduction in red limit can be interpreted from industrial ex blood cells, diminished reflexes, and tremor. perience. It is uncertain whether it is low The most important effect of inhalation of enough to prevent some degree of injury. tellurium-containing dusts is chronic poison Tetrakydrofuran. Lehman and Flury ing centering in the liver. The 0.1 mg./cu.m. (1943, p. 269) report it a narcotic, irri threshold limit can be interpreted from the tating mucous membrane and injuring the results of examination of exposed workmen. kidneys. In animals 3400 ppm for eight It appears low enough to prevent injury. hours daily for 20 days caused some mucous TEPP. This cholinesterase inhibitor is membrane irritation and light narcosis, about twice as toxic in single doses to ani with albuminuria, lung and kidney injury mals as parathion, and the class of cholin and lung irritation in one animal each. esterase inhibiting compounds manifests ACGIH (1955b) quotes John A. Zapp, Jr. to little tendency to chronic effect. Vigliani and the effect that repeated inhalation of 200 Zurlo (1955) on the basis of cholinesterase ppin, then 400 ppm, slightly affected the reduction in workmen, consider 0.0007 pulse pressure of dogs, but resulted in no mg./cu;m. a satisfactory threshold limit. histopathology. Hoffmann and Oettell The most important effect of tepp inhala-, (1954) in rabbits and cats found some nar tion is the reduction of blood cholinesterase. cosis and mucosal irritation after six hours Industrial | ( / I | \ ^ > ( ^ 5; i* inhalation or kidney 60,000 ppi The mo: furan inh portant in ppm tent: terpreted inhalation to prevent Tetranii Gay and ] ritation o lung edem to liver ai to 25.2 pp 0.1 to 0.4 i two expos peated ini rats died dogs was t The me tromethan panied by limit can 1 peated ani to prevent tation. Tetryl. years' exp. more than trations k stant dilig quent but Hardy anc and eight the most p respirator; skin sensit tizations. 17.7 mg./c The mos tion is chi trotoluene, sensitizatii limit can with expo to prevent ThoUiun literature, chronic to. Useful qu; pear to be The mos halation i .949, :oxic ;oxie ppm. four ppm. etraning shold .1 ex. low iry. "lury irrif the right icous :osis, ljury each, fr. to ' 200 ! the n no ettell narlours Industrial Hygiene Quarterly 177 inhalation of 3400 ppm. There was no liver mg./cu.m. tentative threshold limit appears or kidney injury from inhalation of even to be based on a quantitative analogy with 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 appears to be an ill-defined chron ritation of eyes, upper respiratory tract, ic toxicity. The 5 mg./cu.m. tentative thresh lung edema, methemoglobinuria and injury old limit cannot be interpreted from pub to liver and kidney. Concentrations of 3.3 lished data found by the writer, but it ap 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. i: 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. f *- r[aftft:; UCC - 109614 178 June, 1956 Indus tr O-Toluidine. Henderson and Haggard IS weeks had no toxic or lung injuring ef mg./cu.r (1943, p. 228) quote slight symptoms after fects on dogs or rats. from th< several hours at 6 to 23 ppm, and for aniline The most important effects of trifluoro tions. It they give 7 to 53 ppm. Fairhall (1949, p. monobromomethane inhalation are narcosis Urani 450) find symptoms are like those from and respiratory tract irritation. The 1000 Neuman aniline. Smyth (1937-55) found rats not ppm threshold limit can be interpreted from on inha killed by eight hours inhalation of sub the results of repeated animal inhalations. uranium stantially saturated vapors. It appears low enough to prevent injury. ard thai The most important effect of o-toluidine Trinitrotoluene. Von Oettingen et al uranium inhalation is poisoning like that from ani (1944) in experiments on dogs found only animal t line. The 5 ppm threshold limit can be in tracheal irritation and some effects on red mg./cu.n terpreted by analogy with aniline. It ap blood cells from daily intratracheal insuf ty over pears low enough to prevent injury. flation of 50 mg./kg. This daily dosage by The m Trichloroethylene. Morse and Goldberg mouth did not kill in three months but re insoluble (1943) found headache, nausea and dizzi sulted in definite central nervous system, ing een ness common in industrial exposures well liver and blood cell effects. The material mg./cu.n under the 200 ppm figure proposed by penetrates the skin. Eddy (1944) reports from the USPHS (1943) on the basis of European fatal aplastic anemia in three humans at tions. It opinion. Adams, Spencer, Rowe, MeCollister concentrations of 1 to 3.5 mg./cu.m. Vanad and Irish (1951) found no adverse effects The most important effect of trinitrotolu to vanad from repeated inhalation by monkeys at ene inhalation is chronic poisoning marked mg./cu.n 400 ppm, in rats and rabbits at 200 ppm, or by central nervous system, liver and red three mo in guinea pigs at 100 ppm. Single massive blood cell changes. The 1.5 mg./cu.m. thresh for one exposures kill by anesthesia. Even 3000 ppm old limit can be interpreted from a report of lost some inhaled repeatedly causes no more than very industrial fatality. It is probably not low tion. Soi minor organic changes in the liver. They enough to prevent all injuries. was seen found almost identical effects from single Turpentine. Smyth and Smyth (1928) of the di and repeated inhalation of a single concen found that repeated inhalation of 750 ppm 70 to 80 tration, and concluded the effects are chiefly did not injure animals. Nelson, Ege, Ross, suggests those of narcosis. Voluntary habituation Woodman and Silverman (1943) with un for fume has been found in industry. acclimated subjects found nose and throat The m The most important effect of trichloro irritation at 75 ppm, while 175 ppm was of vanad ethylene inhalation is narcosis. The 200 ppm judged intolerable. Fairhall (1949, p. 464) injury. T threshold limit can be interpreted from the notes irritation, narcosis, and kidney injury. for dust results of repeated animal inhalations and The most important effect of turpentine interpret observations in industry. It is not low inhalation is narcosis, but irritation of the animal in enough to prevent significant narcosis, respiratory tract is more frequently en to prever Trichloronaphthalene. After extensive in countered. The 100 ppm threshold limit can Vinyl halation studies with rats, Drinker (1939) be interpreted from results of repeated ani (1930) 1 concluded injury is exclusively in the liver mal inhalations and human sensory data. It guinea pi and that the permissible limit for repeated is low enough to prevent injury. hours. Hi inhalation is 5 mg./cu.m. The solid material Uranium (soluble). Uranium is a radio narcosis, or its oil solution penetrates the skin and logical hazard through emission of alpha as a slig repeated contact leads to chloracne. particles, and a toxicological hazard prima dizziness The most important effect of, trichloro rily through injury to kidney tubules. naphthalene inhalation is chronic poisoning Hodge, Stokinger and Neuman (1949) show The me ) ' ide inhal centering in the liver. The 5 mg./cu.m. that on inhalation, the toxicological hazard threshold threshold limit can be interpreted from the is much greater than the radiological haz results o results of repeated animal inhalations. It ard. In repeated animal experiments, they human re is low enough to prevent injury. find that 0.5 mg./cu.m. allows a reasonable prevent s: Trifluoromonobromomethane. ACGIH margin of safety over the level producing Warfar (1955b) quotes Chemical Corps Medical kidney injury. and Bay Laboratories Research Report No. 180,1953. The most important effect of inhalation mg./kg. f This shows that the material is narcotic at of soluble uranium "dusts is chronic poison group of high concentrations, but that 23,000 ppm for ing, centering in the kidney. The 0.05 100 mg./k ucc 109615 rifluoronarcosis he 1000 ;ed from alations. jury. et al md only j on red .1 insufisage by but re system, material reports nans at itrotolumarked and red .thresheport of not low (1928) r50 ppm e.^pss, was p, 464) injury, -pentine i of the ltly enmit can ted anidata. It a radio>f alpha . primatubules. 9) show hazard cal hazts, they isonable oducing aalation poisonle 0.05 Industrial Hygiene Quarterly 179 mg./cu.m. threshold limit can be interpreted from the results of repeated animal inhala tions. It is low enough to prevent injury. Uranium (insoluble). Hodge, Stokinger, Neuman, Bale and Brandt (1949) show that on inhalation, the toxicological action of uranium on the kidney is much more a haz ard than the alpha radiation hazard of the uranium stored in the bones. In repeated animal experiments, they find 0.20 to 0.25 mg./cu.m. allows reasonable margin of safe ty over the level producing kidney injury. The most important effect of inhalation of insoluble uranium dusts is chronic poison ing centering in the kidney. The 0.25 mg./cu.m. threshold limit 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 80% mortality. One human fatality arose from the consumption of a total of 750 mg. over a 15-day period. The most important effect of warfarin in halation is chronic poisoning centering in the blood coagulation mechanism. The 0.5 mg. cu.m, tentative threshold limit cannot be interpreted in quantitative terms. It in volves a maximum daily absorption of 5 mg., about one-tenth the amount which was fatal to one man. Xylene. Nelson, Ege, Ross, Woodman and Silverman (1943) found 200 ppm definitely irritating to eye, nose and throat. Fairhall (1949, p. 468) concludes the effects are like those of toluene, narcosis without damage to red blood cells. The most important effect of xylene in halation is narcosis. The 200 ppm thresh old limit can be interpreted from human sensory data. It is irritating to eye, nose and throat. There are no data to show whether or not significant narcosis occurs at this concentration, but since narcotic ac tivity is greater than that of toluene it is to be anticipated. Zinc oxide fume. Drinker, Thomson and Finn (1927b) reported that experimental fume fever from zinc oxide in man results from excessive inhalation, but does not oc cur below 15 mg./cu.m. In industry it was found that 14 mg./cu.m. caused no reaction after eight hours, and in the laboratory 45 mg./cu.m. was without effect in 20 minutes. This condition is a transient fever with chills, muscular pains, nausea and vomitting. An immunity is apparently built up. The most important effect of zinc oxide fume inhalation is transient metal fume fever. The 15 mg./cu.m. threshold limit can be interpreted from the results of extensive human experiment and experience in indus try. It is low enough to prevent injury. Zirconium. ACGIH (1955b) quotes un published data from the University of Rochester A.E.C. Project. Four species of animals inhaled the following, all expressed in terms of contained zirconium: Zirconi um oxide, 1.6 micron dust, 75 mg./cu.m. for 30 days, 11 mg./cu.m. for 60 days, 3.5 mg./cu.m. for one year; zirconium tetra chloride, 0.6 micron dust, 6 mg./cu.m. for 60 days, 3.5 mg./cu.m. for a year. Only the higher concentration of tetrachloride had any effect, presumably due to liberated hy drochloric acid. .. ucc 180 June, 1956 The effect of zirconium dust inhalation is that of an inert nuisance dust when insolu ble, and possibly bronchial and lung irrita tion when soluble. The 5 mg./cu.m. tentative threshold limit can be interpreted from the results of repeated animal inhalations. It appears low enough to prevent injury. Bibliography ACGIH (1947): 1947 M.A.C. values, Ind. Hyg. Newtletter, 7:15-16, August. ACGIH (1948) : Threshold limit values adopted at April, 1948 meeting (privately circulated). ACGIH (1949) : Threshold limit values adopted at April 1949 meeting (privately circulated). ACGIH (1950): Threshold limit values. Arch. Ind. Hyg. & Occup, Med., 2:98-100. ACGIH (1951); Threshold limit values for 1951. Arch.. Ind. Hyg. A Occup. Med., 4:398-400. ACGIH (1952): Threshold limit values for 1952. Arch. Ind, Hyg. & Occup. Med., 6:178-180. ACGIH (1958): Threshold limit values for 19*53. Arch. Ind. Hyg. & Occup. Med., 8:296-29S. ACGIH (1953b): Privately circulated document giving support for many earlier adopted threshold limits, and those proposed in 1953. ACGIH (1954) : Threshold limit values for 1954. Arch, Ind. Hyg. A Occup. Med.t 9:530-534. ACGIH (1954b): Privately circulated document giving support for threshold limits newly proposed in 1954. ACGIH (1955): Threshold limit values for 1955. AMA Arch. Ind. Health; 11:621-524. ACGIH (1955b): Privately circulated document giving support for threshold limits newly proposed in 1955. ACGIH (1956): Proposed threshold limit values for 1956, presented April 23, 1956 to the Philadelphia, an nual meeting. Privately circulated in advance of pub lication. Adams, E. M.; Spences, H. C., and Irish, D. D. (1940): The acute vapor toxicity of aHyl chloride. J. Ind. Hyg. A To*., 22:76-86. Adams, E. M.; Spencer, H. C.; Rows, V. K., and Irish, D. D. 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(1936): On the toxic effects of low concentration of carbon disulfide. J. Ind, Hyg. A Tox,, 18:733-740. 0 Wilson, R. H., and DeEds, F. (1936): Chronic nicotine toxicity, J. Ind. Hyg* A Tox., 18:553-564. Wilson, R. H. (1944) : Health hazards encountered in manufacture of synthetic rubber, J.A.M.A., 124:701*703. Winslow, C-E. A. (1927): Summary of the National Safety Council study of benzene poisoning. J. Ind. Hyg*, 9:61-74. Yant, W. Schrenk, H. H.; Fatty, F. A,, and Sayers, R. R. (1930): Acrolein as a warning agent for detecting leakage of methyl chloride from refrigerators. U. S. Bur. Mineb Kpts., Investigations 3027. Yant, W. P., Schrenk, H, H.; Waite, C- P.. and Patty, F. A, (1930) : Acute response of guinea pigs to vapors of some new commercial organic compounds. II--Ethyl benzene. U. S Public Health Service, Pub. Health Rpte., 45:1241-1250, Yant, W. P.; Schrenk, H. H.: and Patty, F. A. (1932) : The toxicity of dichlorotetrafluorethane, U. S. Bur. Mines Rpt$,, Investigations 3185. Yant, W. P.; Patty F, A., and Schrenk, H. H. (1936) : Acute response of guinea pigs to vapors of some new commercial organic compounds, IX--Pentanone (methyl propyl ketone). U, S. Public Health Service, Pub. Health Rpte., 51:392-399. Reprints Available eprints of the preceding Cummings Memorial Lecture may R be obtained from GEORGE d. Clayton, Executive Secretary, AMERICAN INDUSTRIAL HYGIENE ASSOCIATION, 14125 Prevost, De troit 27, Michigan, at $1.50 each. The price of this issue of the AIHA QUARTERLY is $2.00. W Dr. H.nry Field Smyth, Jr., receiving the Cummings Memorial Awerd from N. V. Hendrick,, President of the American Industrial Hygiene Association. The presentation wa, made at the banquet of the Associa tion's Seventeenth Annual meeting in Philadelphia, Wednesday, April 25. is S.-,C- - ucc 109622