Document YDLGx2B146NQxpJ3orevRRQby

TRANSACTIONS OF THE THIRTY SIXTH ANNUAL MEETING OF THE AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS Miami Beach, Florida MAY 13-17, 1374 FUTURE CONFERENCES June 1-6, 1975 Leamington Hotel Minneapolis, Minnesota May 16-21, 1976 Marriott Hotel Atlanta, Georgia May 22-27, 1977 Fairmont Hotel New Orleans, Louisiana May 7-12, 1978 Biltmore Hotel Los Angeles, California May 27-June 1, 1979 Palmer Hous Chicago, Illinois May 18-23, 1980 Hyatt Regency Houston, Texas 1 TABLE OF CONTENTS Annual Meetings and Officers ................................................................ Board of Directors 1974-75 ACGIH Committees for 1974-75 ................................................................ Business Session May 13, 1974................................................................ Secretary-Treasurers Reports Publications........................................................................................................ Nominations....................................................................................................... Financial ....................................................................................................... Executive Secretarys Comments............................................................... Chairmans Comments...................................................................................... Reports from Committee Chairmen TLV (airborne).................................................................................................. TLV (physical agents)................................................................................. Industrial Ventilation ........................................................ Secretarys Summary of Reports from: Agriculture ........................................ Air Pollution....................................................................................................... Air Sampling Instruments..................................................................... Aerosol Hazards Evaluation............................................................... Analytical Methods...................................................................................... Mining Environment . ................................................................................ Chairmans Acknowledgements............................................................... Chairman-Elects Comments..................................................................... Adjournment 11:45 A. M.................................................................................. 1 2 4 12 12 14 14 15 16 16 19 20 21 22 22 22 22 23 23 24 26 Annual Reports Publication Office Sales........................................................................... 27 ACGIH Financial Statement 1973-74 .............................................. 28 Auditors Certificate...................................................................................... 31 Ventilation Committee................................................................................. 32 Financial Statement........................................................................... 33 Auditors Certificate........................................................................... 35 Air Sampling Instruments..................................................................... 36 Aerosol Hazard Evaluation..................................................................... 36 TLV (airborne)................................................................................................. 37 TLV (physical agents)........................................................................................40 Report of Awards Committee............................................................................ 41 Presentation of Award.............................................................................................42 1974 ACGIH Banquet...................................................................................................44 1974 Conference Activities 45 11 Panel Discussion: Industrial Cold Stress.......................................................................... 51 Health Hazard Evaluation - An Overview...................................85 J. P. Flesch Carbon Disulfide in Viscose Rayon Manufacturing ... <R. E. Rosensteel, Steven K. Shama, M. D. 92 Diethylstillbestrol, N-acetyl Sulfanilyl Chloride in Chemical Manufacturing............................ D. J. Burton, Edward Shmunes, M. D. 103 Isocyanates in Plastic Manufacturing...................................................115 R. Vandervort, M. S. , Steven K. Shama, M. D. Epoxies in Sporting Goods Manufacturing....................................... 125 J. B. Lucas, M. D. , Bobby J. Gunter Chromic Acid in Electroplating ..............................................................131 Steven R. Cohen, M. D. , RichardS. Kramkowski The Safety Specialist Role in Industrial Hygiene .... 141 Ronald R. Ott -1- Year 1938 1939 1940 1941 1942 1943 1944 1946 1947 1948 1949 1950 1951 1952 1953 1954 1955 1956 1957 1958 1959 I960 1961 1962 1963 1964 1965 1966 1967 1968 1969 1970 1971 1972 1973 1974 AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS THIRTY-SIXTH ANNUAL MEETING May 12-17, 1974 FONTAINEBLEAU HOTEL MIAMI BEACH, FLORIDA PAST MEETINGS AND OFFICERS City Chairman Sec. /Treas. Washington, D. C. t! Bethesda, Md Washington, D.C. ff Rochester, N, Y, St. Louis, Mo. Chicago, 111. Buffalo, N. Y. Boston, Mass. Detroit, Mich. Chicago, 111. Atlantic City, N. J. Cincinnati, Ohio LosAngeles, Cal. Chicago, 111 Buffalo, N. Y. Philadelphia, Pa St. Louis, Mo. Atlantic City, N. J. Chicago, 111. Rochester, N. Y. Detroit, Mich. Washington, D. C. Cincinnati, Ohio Philadelphia, Pa. Houston. Texas Pittsburgh, Pa. Chicago, 111. St. Louis, Mo. Denver, Colorado Detroit, Mich Toronto, Canada San Francisco, Cal. Boston, Mass. Miami Beach, Fla. A. S. Gray, M. D. J. J. Bloomfield W. S. Johnson 11 M. H. Kronenberg, M. D, f1 C. L. Pool 1I C. A. Nau, M. D. 11 M. F. Trice 11 P. A. Brehm, M. D. 11 P. A. Brehm, M. D. 1! K. M. Morse M L. W. Spolyar, M. D. 1t H. G. Dyktor I1 K. E. Markuson, M. D. L. J. Cf-alley, Ph. D J. J. Bloomfield L. M. Petrie, M. D. J. C. Soet J. Shilen, M. D. H. B. Ashe J. E. Flanagan, Jr. it it 11 11 R. R. Sullivan, M. D. W. G. Fredrick, D. Sc. T. F. Mancuso, M. D. C. E. Couchman A. L. Coleman A. L. Coleman W. L. Wilson, M. D. C.D. Yaffe 11 ir 11 11 if 11 E. L. Sc hall C. Einert, M. D. L. J. Cralley, Ph. D. B. D. Bloomfield R. H. Duguid, M. D. Henry N. Doyle A. D. Hosey ff 11 11 11 11 Edward J. Baier Marcus M. Key, M. D. Andrew D. Hosey V. E. Rose 1t 1I H. E. Ayer W. D. Kelley E. Mastromatteo, M. D. 11 Fred Keppler tl -2- AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS Board of Directors 1974-75 Chairman, JEREMIAH R. LYNCH NIOSH, U. S. Postoffice & Courthouse Cincinnati, Ohio 4520 2 (513) 684 2541 Vice Chairman, JAMES C. BARRETT Division of Occupational Health Michigan Department of Health 3500 North Logan Street Lansing, Michigan 48914 (517) 373 1410 Vice Chairman-elect, DARRELL D. DOUGLAS University of California Los Alamos Scientific Lab. H-5 P.O.Box 1663 Los Alamos, N. M. 87544 (505) 667 6235 Past Chairman, J. FREDERICK KEPPLER OSHA, DOL 46 East Ohio Street Indianapolis, Indiana 46204 (317) 633 7384 Director, FRED OTTOBONI, Ph. D. Bureau of Occupational Health California Dept, of Public Health 2151 Berkeley Way Berkeley, California 94704 Director, MARSHALL E. LA NIER NIOSH, U. S. Postoffice & Courthouse Cincinnati, Ohio 45202 Director, RONALD R. OTT OSHA, DOL Federal Building 450 Golden Gate Ave. P. O. Box 36017 San Francisco, Calif. 94102 Secretary-Treasurer, WILLIAM D. KELLEY NIOSH, P. O. Box 1937 Cincinnati, Ohio 45 201 (513) 684 2535 Norman G. White, Ph. D. , Executive Secretary 4111 Grennoch Lane Houston, Texas 77025 (713) 664 2517 -3- 1974-75 BOARD OF DIRECTORS KELLEY LA NIER BARRETT OTT KEPPLER LYNCH DOUGLAS Not present- OTTOBONI -4- MEMBERS OF COMMITTEES 1974-75 AGRICULTURAL SAFETY & HEALTH Mr. Jeffrey S. Lee, Chairman. NIOSH Dr. Clyde Berry, University of Iowa Dr. William R. Burg, Ph. D. University of Cincinnati Mr. Paul Caplan, NIOSH Dr. Harry Hays, USD A Dr. Ephriam Kahn, M. D. Calif. Dept, of Health Dr. Keith T. Maddy, Calif. Dept, of Food & Agriculture AIR POLLUTION Mr. Robert P. Miller, Chairman. Mich. Dept, of Natural Res. Mr. C. Fred Berghout, Edgewood Arsenal Mr. James Hambright, Penn. Dept, of Environmental Resources Mr. Lee E. Jager, Michigan Dept, of Natural Resources Mr. Clements Lazenka, Philadelphia Dept, of Public Health Mr. Peter Loquercio, Cook County Air Pollution Bureau Mr. Otto Paganini, Texas Dept of Health Mr. Louis J. Proulx, Conneticut State Dept, of Health AIR SAMPLING INSTRUMENTS Dr. Morton Lippmann, Chairman. New York University Mr. Paul E. Caplan, NIOSH Mr. Irving H. Davis, Michigan Dept, of Health Dr. Robert T. Drew, NIEHS Maj. Victor Furtado, Ph. D. , U. S. Air Force Mr. John S. Nader, EPA Mr. Leonard Pagnotto, Massachusetts Dept, of Labor & Industry Mr. William H. Perry, NIOSH Mr. G. S. Rajhans, Ontario Ministry of Health Dr. Bernard E. Saltzman, University of Cincinnati Mr. Grlen Sutton, U. S. Bureau of Mines Dr. David Swift, John Hopkins University ANALYTIC METHODS Mr. Alvin VanderKold, Mr. John R. Carlberg, Chairman. NIOSH Michigan Dept, of Health Mr. George L. Corte, Ontario Dept, of Health & Welfare Mr. Robert J. Graul, California Dept, of Public Health Mr. Martin W. Jeremias, New York State Dept of Labor Mr. Mr. Ms. Lee E. Monteith, University of Washington Leonard Pagnotto, Massachusetts Dept, of Labor & Industries Virginia M. Vought, Penn. Dept, of Environmental Resources Mr. Jack C. Wells, Indiana State Board of Health -5- AWARDS Dr. Bobby F. Craft, Chairman. NIOSH Mr. James C. Barrett, Michigan Dept, of Health Mr. Darrell D. Douglas (Comm. Coordinator) U. Of Cal. LosAlamos Mr. John C. Lumsden, North Carolina Board of Health Mr. Hugh Parker, Georgia Dept, of Health Mr. George F. Sprague, III, Forest Hill, Maryland INDUSTRIAL HYGIENE OPERATIONS Mr. James C. Barrett, Chairman. Michigan Dept, of Public Health Mr. Charles E. Adkins, OSHA DOL M,r. Hugh C. Colman, NIOSH Mr. Albert Edwards, OSHA DOL Mr. Arthur E. Johnston, NAVORD Mr. John D. McKichan, OSHA DOL Dr. Fred L. Ottoboni, California Dept, of Public Health Ms. Claudia S. Prieve, OSHA DOL Mr. Russel G. Scovill, Michigan Dept, of Public Health Mr. Barkev Siroonian, OSHA DOL Mr. George B. Stanton, Jr. New Jersey Dept, of Labor & Industry Mr. Robert Vandervort, NIOSH Mr. Robert H. Wolle, Tennessee Dept, of Health INDUSTRIAL VENTILATION Mr. Marvin M. Schuman, Chairman. Michigan Dept, of Health Mr. James C. Barrett, Michigan Dept, of Public Health Mr. William M. Cleary, Michigan Dept, of Public Health Mr. Louis Dickie, American Air Filter Co. (Consultant) Mr. George Hama, Wayne State University Dept of Health (Consult. ) Mr. Richard Hibbard, University of Washington Mr. Jbremiah R. Lynch, NIOSH Mr. Knowlton J. Caplan, University of Minnesota Mr. Gyan S. Rajhans, Ontario Dept, of Health Mr. Robert H. Wolle, Tennessee Dept, of Public Health SYMPOSIUM Dr. Alan D. Stevens, Chairman. NIOSH Prof. B. Dwight Culver, University of California Mr. Grover Wrenn, OSHA Dr. Ralph Vernon, Texas A & M Lt. Col. Wwen H. Kittilstad, USAF -6- NURSING SERVICES IN OCCUPATIONAL HEALTH Mrs. Helen O. Coburn, Chairman. Connecticut Dept, of Health Ms. Dorothy Benning, Ohio Dept, of Health Ms, Catherine Chambers, Wisconsin Dept, of Health Ms. Ruth E. ..Reifschneider, NIOSH Mr. Morris A. Wolf, New York State Dept, of Labor THRESHOLD LIMITS FOR AIRBORNE CONTAMINANTS Dr. Herbert E. Stokinger, Chairman. NIOSH Dr. Hector P. Blejer, California Dept, of Health Mr. Paul Caplan, NIOSH Dr. Hervey B. Elkins, Massachusetts Dept, of Labor & Industries Dr. William G. Frederick, Wayne State University Mr. Bernard Grabois, New York State Dept, of Labor Dr. Paul Gross, Industrial Hygiene Foundation Dr. Elliott S. Harris, NIOSH Mr. John W. Knauber, Penn. Dept, of Environmental Resources Mr. Jessee Lieberman, Philadelphia Naval Shipyard Dr. Keith Long, University of Iowa Mr. Frederick T. McDermott, Michigan Dept, of Health Mr. Ronert Mahon, DOL-NIOSH Liaison Col. Walter W. Melvin, Jr. USAF Mr. James F. Morgan (Industry liaison) Mr. David Padden (Labor liaison) Mr. Meier Schneider, LosAngeles City Health Dept. Dr. Marshall Steinberg, U. S. Army EHA Mr. Gordon J. Stoops, Ontario Health Dept. Mr. John F. Summersett, Kentucky Dept, of Labor Dr. Theodore R. Torkelson (Industry liaison) Mr. William Wagner, NIOSH Mr. Ralph Wands, Advisory Center on Toxicology, NAS Dr. Mitchell R. Zavon, (Industry liaison) THRESHOLD LIMIT VALUES FOR PHYSICAL AGENTS Mr. Herbert H. Jones, Chairman. Central Missouri State University Mr. Peter A Breysse, University of Washington Dr. Gerald V. Coles, London School of Hygiene & Tropical Medicine Mr. Thomas Cummings, Ontario Ministry of Health Mr. Irving H. Davis, Michigan Dept, of Health Mr. R. Denny Dobbin, London School of Hygiene & Tropical Medicine Dr. David A. Fraser, University of North Carolina Maj. George Kush, USAF Mr. Wordie H. Parr, NIOSH Mr. David H. Sliney, U. S. Army Dr. Robert N. Thompson, F. A. A. Dr. Robert T. Wagemann, U. S. Army Mr. Thomas K. Wilkinson, National Institute of Health Mr>. Eugene G. Wood, OSHA DOL -7- HISTORY OF INDUSTRIAL HYGIENE Mr. Charles D. Yaffe, Chairman Dr. Jean S. Felton, M. D. Mr. Henry Doyle, Vice chairman Dr. William G. Fredrick Mr. J. J. Bloomfield Mr. Bruce J. Held Prof. William A. Burgess Mr. Andrew D. Hosey Frof. Jacob Cholak Mrs. Mary Fouse Peyton Mr. Irving H. Davis Mr. Kenneth E. Robinson TRAINING COMMITTEE Mr. Darrell D. Douglas, Chairman Dr. Clyde M. Berry Dr. Ralph G. Smith Mr. Peter A. Breysse Mr. William W. Steffan AD HOC COMMITTEES ARSENIC Dr. E. Mastromatteo, Chr. Mr. John W. Knauber Mr. C. Fred Berghout Dr. Ralph G. Smith Ms Therese Donovan Mr. Alvin L. VanderKolk CHLOROFORM Dr. Edward A. Emmett, M. D. Dr. Souheil Laham Dr. Ted Torkleson (Consultant) Dr. Sanford W. Horstman, Jr. Dr. Norman G. White COTTON DUST Dr. E. Mastromatteo, Chr. Mr. C. Fred Berghout Mr. Edwin J. Kloos Mr. Morton Lippman Mr. Marvin M, Schuman ETHYLENE DICHLORIDE Mr. Ralph Griffin Dr. Paul Sneeringer Mr. John Summer sett HEXAVALENT CHROMIUM Dr. Marshall Steinberg, Chr. Dr. Hervey B. Elkins Dr. Thomas F. Mancuso Mr. Alvin L. VanderKolk HYDROGEN CYANIDE Mr. J. Brennan Gisclard Mr. Sam Goldberg Mr. FredHertlein PAR ATHLON Mr. Darrel D. Douglas, Chr. Dr. Hector P. Blejer Dr. G. Quimby* Dr. B. Stevenson* Dr. Mitchell R. Zavon* * Consultant -8- AD HOC COMMITTEES (Cont. ) SODIUM HYDROXIDE Mr. Otto Paganini Dr. Paul Sneeringer Dr. Norman G. White Mr. Alvin L. VanderKolk SULFURIC ACID AND SULFUR DIOXIDE Mr. William G. Frederick, Chr. Dr. Ralph G. Smith Dr. Ernest Mastromatteo Dr. Mitchell R.Zavon* Mr. Frederick T. McDermott * Consultant TOLUENE Dr. E. Mastromatteo, Chr. Mr. C. Fred Berghout Ms. Therese Donovan Mr. John W. Knauber Dr. Ralph G. Smith Mr. Alvin L. VanderKolk TRICHLOROETHYLENE Dr. Hervey B. Elkins, Chr. Mr. Harold Bovley Mr. Fred Berghout Dr. William A. Burgess Ms. Therese Donovan Dr. William G. Frederick AMERICAN BOARD OF INDUSTRIAL HYGIENE ACGIH AIHA Mr. E. J. Baier Mr. James D. Barrett Mr. Knowlton J. Capian Mr. Charles R. Cheever Mr. John C. Lumsden Mr. Jack C. Rogers Mr. Vincent Castrop Mr. Melvin W. First Mr. Nathan V. Hendricks Mr Henry Muranko Dr. Verald K. Rowe Dr. Henry F. Smyth, Jr. Mr. Paul Toth JOINT COMMITTEES WITH AMERICAN INDUSTRIAL HYGIENE ASSOCIATION AEROSOL HAZARDS EVALUATION Dr. Morton Lippmann, Chairman ACGIH AIHA Mr. Howard E. Ayer Dr. J. Leroy Balzer Mr. Harry J. Ettinger Mr. Murray Jacobson Mr. William C. Janes Dr. William H. Krebs Mr. Geoffrey Knight Mr. Paul Lange Mr. Sidney Laskin Mr. Eric B. Sans one Mr. Jeremiah R. Lynch Mr. R. W. VanHouten Mr. Milton Scheinbaum Dr. W. R. Van Pelt Mr. Glen W. Sutton -9- JOINT COMMITTEES WITH AMERICAN INDUSTRIAL HYGIENE ASSOCIATION (Continued) DIRECT READING GAS DETECTING TUBE SYSTEMS * Dr. Richard B. Konzen, Chrairman ACGIH Mr. LeRoy L. Garcia Mr. Nelson A. Leidel Mr. Mr. Michael Roder Mr. Alvin VanderKolk Mr. Leon T. Gonshor AIHA Mr. Gene X. Kortsha, V. Chr, Mr. Meliton M. Garcia Mr. Arthur E. Johnston Mr. Joseph W. Klinsky Mr. Adrian L. Linch Mr. H. W. Speicher MINING ENVIRONMENT * Mr. G. Reub Yourt, Chairman ACGIH AIHA Mr. Wm. A. Bardswich Mr. J. E. Cleveland Mr. Ployd C. Bossard Mr. R. B. Gresham Mr. Alfred J. Breslin Mr. Murray Jacobson Mr. E. J. Harris Mr. F. J. Laird, Jr. Dr. E. Mastromatteo Mi-. Kenneth M. Morse Mr. Glen W. Sutton Mr. J. G. Rutherford RESPIRATOR COMMITTEE *Mr. Bruce J. Held, Chairman ACGIH AIHA Dr. William A. Burgess Mr. Ronald L. Guinn Mr. Jerrold L. Caplin Mr. C. R. E. Merkle, Jr. Mr. Alan K. Gudeman Mr. J. F. Morehead Ms. Patricia Gussey Mr. George L. Morse Mr. E. C. Hyatt Mr. William H. Revoir Mr. Edwin J. Kloos Mr. L. N. Rodenhouse Mr. Ross N. Kusian Mr. W. H. Speicher Mr. Stuart G. Luxon Mr. George M. Tomer Mr. J. P. O'Neill Mr. John M. White Mr. Charles J. Shoemaker Mr. Ronald J. Uhle REPRESENTATIVES ON COMMITTEES OF AMERICAN SOCIETY FOR TESTING AND MATERIALS ASTM D-22 Dr. Ralph Smith (atmospheric sampling and analysis) ASTM D-26 Mr. Robert Vandervort (halogenated solvents) REPRESENTATIVES ON INTERSOCIETY COMMITTEES Guidelines for Noise Exposure Control- Mr. Herbert H. Jones Dr. Floyd A. VanAtta Air Sampling and Analysis - Mr. John V. Crable -10- REPRESENTATIVES ON COMMITTEES OF AMERICAN NATIONAL STANDARDS INSTITUTE All - Mr. J. Baliff (industrial lighting) K13.1 - Mr. E. C. Hyatt (identification of gas mask cannisters) N12 - Mr. Donald E. Van Farowe (nuclear energy) N13 - Mr. Donald E. Van Farowe (radiation protection) N42 - Mr. Jesse Lieberman (radiation instrumentation) N43 - Dr. Robert H. Duguid (equip, for non-medical radiation applications N44 - Dr. Adam Rapolski - Dr. Jacqueline Messite, alternate (equipment and materials for medical radiation applications) N46 - Mr. Harold J. McAlduff, Jr. (nuclear reactor fuel cycle) N101 - Mr. Howard E. Chaney and Mr Ronald E. Bales, Alternate (atomic industry facility design) S3 - Major Donald C. Gasaway (bioacoustics) Z4 - Mr. William T. Ingram, Chr. (Subcommittee: Fernando J. Castro, Frank W. Mackison) Z8 - Mr. Irving Davis (laundry and dry cleaning) Z9 - Mr. Robert Hughes and Mr. A1 Gudeman ( safety code for exhaust systems) Z16 - Mr. V. Rose and Mr. David F. Stetzer, Alternate ' '(work injury experience ) Z37 - Dr. Herbert E. Stokinger (threshold limits) Z88 - Mr. Edwin C. Hyatt and Mr. Jeremiah R. Lynch, Alternate ( respiratory protection) Z105 - Mr. James Barrett and Mr. L. E. Jager, Alternate(air and gas cleaning) Z117 - Mr. Peter Breysse (safety requirements for working in tanks and confined spaces) Z136 - Dr. Chas H. Powell and Mr Vernon E. Rose, Alternate (lasers) Z137 - Mr. William Steffan and Mr, Herbert Jones, Alternate( hearing protection) REPRESENTATIVES ON INTERSOCIETY SUBSTANCES COMMITTEES Sulphur Compounds - Mr. John B. Pate Halogen Compounds - Mr. John D. Strauther Oxidants and Nitrogen Compounds - Dr. John E. Cuddebach Carbon Compounds - Dr. Ralph G. Smith, Chr. Hydrocarbon Compounds - Mr. Lowell D. White Heavy Metals - Dr. Janet C. Haartz Metals 11 - Mr. L. Dubois Radioactive Compounds - Mr. D. E. Van Farowe Laboratory Techniques and Precautions - Mr. A. L. VanderKolk Particulates - Mr. Edward Stein Stationary Source Sampling - Mr. Jerry Flesch Standardization and Coordination- Mr. William D. Delley -11- REPRESENTATIVE TO ISO/TC 146 ON AIR QUALITY Mr. Benjamin Levadie OCCUPATIONAL HEALTH INSTITUTE, TO ACCREDITATION COMMISSION Mr. Jeremiah R. Lynch ACGIH REPRESENTATIVE LOCAL ACGIH CHAPTERS Keystone (Commonwealth of Pennsylvania) Woodrow W. Wending, M. D., Chairman Puerto Rico Jose E. Sanchez, Chairman Southern California Anastracio G. Medina, Chairman -12- BUSINESS SESSION - MAY 13. 1974 J. Frederick Keppler, Chairman, Presiding The Annual Business Meeting of the American Conference of Govern mental Industrial Hygienist was held on Monday, May 13, 1974 in the Fontaine Room of the Fontainebleau Hotel, Miami Beach, Florida. The meeting was called to order at 10:40 o'clock a.m. by Chairman J. Frederick Keppler. CHAIRMAN J. FREDERICK KEPPLER: Could we get started please? I would like to open the meeting for the 1974 ACGIH business session. And to start things off, let's first have the secretary's report from Bill Kelly. SECRETARY-TREASURER WILLIAM D. KELLY: Thank you, Fred. First of all, I would like to express my personal appreciation to the people who have made possible, really, the functioning of the secretarytreasurer's office-----specifically: Mrs. Ruth Duffy. Ruth if you will stand up. Jerry Lynch. Ruth used to be my secretary. She is now Jerry's secretary, but he still allows me to use her as secretary to the secretary-treasurer. I would also like to mention Evelyn Jones who is currently my sec retary, but not here; and the person who most of you have come in contact with at least by correspondence, Kim Stewart, manager of the publications office. Since we are into publications, I would like to summarize some of the significant activity in the publications area with, really, the announcement of several new publications. The first is "The Process Flow Diagrams and Air Pollution Emission Estimates," which has just been published by the Air Pollution Com mittee. It is now available. There will be several copies on dis play at the ACGIH exhibit booth which, by the way will be in the Grand Galleries outside the exhibit hall. The new publications list which will also be available will have it documented, and with a convenient order form for you. The second publication is, of course, one of our standards, "The Air Sampling Instruments Manual." Some 701 copies were sold during the fiscal year, and as an indication as to current interest, some 53 copies were sold just during the current month of April. "The Air Sampling Instruments Manual" is at the printers for a second printing with a significant addendum, including corrections, updat ing. And for those of you that do have the current edition, you will be able to order the addenda as a separate. -11- REPRESENTATIVE TO ISO/TC 146 ON AIR QUALITY Mr. Benjamin Levadie OCCUPATIONAL HEALTH INSTITUTE, TO ACCREDITATION COMMISSION Mr. Jeremiah R. Lynch ACGIH REPRESENTATIVE LOCAL ACGIH CHAPTERS Keystone (Commonwealth of Pennsylvania) Woodrow W. Wending, M. D., Chairman Puerto Rico Jose E. Sanchez, Chairman Southern California Anastracio G. Medina, Chairman -12- 3USINESS SESSION - MAY 13. 1974 J. Frederick Keppler, Chairman, Presiding The Annual Business Meeting of the American Conference of Govern mental Industrial Hygienist was held on Monday, May 13 197^ in the Fontaine Room of the Fontainebleau Hotel, Miami Beach, Florida. The meeting was called to order at 10:40 o'clock a.m. by Chairman J. Frederick Keppler. CHAIRMAN J. FREDERICK KEPPLER: Could we get started please? I would like to open the meeting for the 197^ ACGIH business session. And to start things off, let's first have the secretary's report from Bill Kelly. SECRETARY-TREASURER WILLIAM D. KELLY: Thank you, Fred. First of all, I would like to express my personal appreciation to the people who have made possible, really, the functioning of the secretarytreasurer 's office---- specifically: Mrs. Ruth Duffy. Ruth if you will stand up. Jerry Lynch. Ruth used to be my secretary. She is now Jerry's secretary, but he still allows me to use her as secretary to the secretary-treasurer. I would also like to mention Evelyn Jones who is currently my sec retary, but not here; and the person who most of you have come in contact with at least by correspondence, Kim Stewart, manager of the publications office. Since we are into publications, I would like to summarize some of the significant activity in the publications area with, really, the announcement of several new publications. The first is "The Process Flow Diagrams and Air Pollution Emission Estimates," which has just been published by the Air Pollution Com mittee. It is now available. There will be several copies on dis play at the ACGIH exhibit booth which, by the way will be in the Grand Galleries outside the exhibit hall. The new publications list which will also be available will have it documented, and with a convenient order form for you. The second publication is, of course, one of our standards, "The Air Sampling Instruments Manual." Some 701 copies were sold during the fiscal year, and as an indication as to current interest, some 53 copies were sold just during the current month of April. "The Air Sampling Instruments Manual" is at the printers for a second printing with a significant addendum, including corrections, updat ing. And for those of you that do have the current edition, you will be able to order the addenda as a separate. -13- The new edition of "The Air Sampling Instruments Manual" will "be scheduled sometime during 1975 or 1976, which year I guess depend ing on how hard Dr. Lippman can crack the whip on his committee. The next publication I would like to mention is that of "The Analy tical Methods Manual." Some 148 copies were sold last year, and there will be a significant new activity in that area which we will report later. The next publication is "The Round Table Proceedings for the Analy tical Techniques for Quartz." This round table was held in Decem ber of 1972. The proceedings are available. Probably "The Silica Criteria Document" will be out this summer, which will certainly spark interest in this publication. The standby publications, of course, are the TLV's. During this past fiscal year some 6,000 copies of the *72 TLV and over 37,000 copies of the '73 TLV were sold. So for the fiscal year, which obviously kind of laps the two publishing year, over 43,000 copies have been sold which, of course, is a new record. As a matter of fact, we had to go to a second printing of 5,000 copies of the ' 73's to carry us until the '74's will be available. The documentation of the TLV's, some 605 copies were sold. The '71 and '72 supplements sold about 175 and 270 copies respectively. Again there will be a reprinting of the current edition of the doc umentations which, again, will be available either as part of the second printing or separate. I am sure you believed it would never come, and perhaps to some of you it may not have yet, but the transactions of last year's meet ing were mailed on the 2nd of May. And my personal apologies for the gross delays in getting it out. However, as a bonus, those of you who did get the transactions also got, for free, a copy of "The Guide for Control of Lazer Hazards," which under other circumstances is $2.75* This is, of course, the result of the Committee on Physical Agents and represents a complete updating of the original guide, and according to Herb Jones is much better and a lot cheaper than the ANSI document. One last note on publications, and that is the membership book. Kim has sworn I am not sure at us or just about us-----but she will guar antee that at least half the membership has moved at least once dur ing this past year. So please, if you have moved recently, if you have not submitted a change of address, if what is in the membership book is not current, please get it to Kim very shortly because we will be going to press with the new membership book next month, and so the deadline is getting close, or we will be behind another year on the membership book. As far as nominations, the Nominations Committee was under the dir ection of Mr. Ed Largent. -14- The nominations for vice-chair-elect were: Mr. Darrell Douglas, and Mr. John Pasco. Nominations for director were: Mr. Ron Ott and Mr. Bud Siroonian. The nominations for secretary-treasurer were: myself-------I think against the "withelds." The chairman will announce the results of the election later. Mr. Chairman, I move that the secretary's report he accepted. CHAIRMAN KEPPLER: A motion has been made that the secretary's re port be accepted. Is there a second to this motion? MEMBER: I second it. CHAIRMAN KEPPLER: It has been moved and seconded that the secretary's report be accepted. Is there any discussion? If not, all in favor of accepting the secretary's report signify by saying Aye. Contrary. Motion carried. Now we will have the most important report, that of the treasurer's report by Bill Kelley. SECRETARY-TREASURER KELLEY: Somehow it always gets down to this, doesn't it? As you are all aware, the full financial statement of the Conference has been audited by Mr. Charles Gehler and the audited, certified statement will appear in the transactions. I would like to summarize some of the significant sources of income and expenses to just give you kind of a feel for the operations. In terms of cash receipts, the most significant sources were, ob viously, our publications, including "The Air Sampling Instruments Manual," $8,600; the TLV's, $23,000; the documentations, $9,000; the receipts from the Ventilation Committee from the sale of ventilation manuals was $13,600 last year; the receipts from the conference in Boston were $8,6000 in receipts, but that was not profit in that there was $3,000 in direct expenses due to the banquet plus the other ex penses. The cash receipts were $71,781.81. With interest on sav ings accounts the total cash receipts were $74,957*22. That is where it came from. Now, where did it go? The Conference expenses, Board expenses, and so forth amounted to $6,900, including the banquet last year; print ing costs, since that, of course, is the principal activity of the Conference, was the principal source of income and principal source of expenses, $23,000; the committee meeting expenses, $8,000. And of course, it is through the committee expenses, if you will, the support of committee activities, that the publications are generated which support the Conference, and so that $8,000 is, I think you will see, a very good investment. Office expenses, including the office of the executive secretary, the publication office, secretarial assis tance, the bulletin board, which was $4,400; postage, $2,100. All of these office expenses came to $21,000, for a total cash disbursement of $59,132.12. -15- Now, the magic number, the excess of cash receipts over cash dis bursements, $15,825.10. That is the summarization of the treasur er's report. As I indicated, the details with the CPA's certifi cation will be in the transactions. Mr. Chairman, I move the acceptance of the treasurer's report. CHAIRMAN KEPPLER: It has been moved that the treasurer's report be accepted. Is there a second. MR. HUFFMAN: Second. CHAIRMAN KEPPLER: Mr. Huffman seconded. Is there any discussion? All in favor of accepting the treasurer's report signify by saying Aye. Contrary, the same. Report is carried. Probably the main project of last year was the hiring of an execu tive secretary. Since this is my first term in office, I cannot possibly understand how we could operate previously without an exe cutive secretary. It has been a godsend to me, and I am sure it will be to the officers in the fu-ture. I think most of you know Norm White, our executive secretary, and maybe he would like to say a word or two. Norm. EXECUTIVE SECRETARY NORMAN G. WHITE: I think you can hear me with out going to the mike. I would just like to state I am happy to be aboard. I will strive to keep you all informed properly and prom ptly, get your bulletin boards out on time, and hopefully get the transactions out earlier this year. The way things are going, on the basis of the load as it has deve loped up to this point, why, who knows, I may have an assistant one of these days. But I will be in need of information from a lot of you people. I will probably need more assistance in this first year than I will be able to give. From now on, the buck passes and stops here. Thank you gentlemen. CHAIRMAN KEPPLER: Thank you, Norm. Bill has covered our publicat ions very well. I was going to mention it a little bit. First of all, we have sold over 40,000 TLV booklets last year. That is pretty big business. Next year's meeting, as you know, will be in Minneapolis, and we hope that you all plan to attend next year. We are going to begin a membership drive. Since we have an executive secretary and since his fee is so high, we are going to have to get more membership in order to keep solvent. So we think we ought to be able to get three or four hundred new members. We are planning a midyear topical symposium on cotton dust. This will probably be held sometime in November of this year, and it will be a two- or three-day symposium. The location has not been selected. -16- And the registration fee, including a copy of the transaction, will probably be around $15- So look for further information on this symposium. As I indicated earlier this morning, Number 1; we are working with AIHA in an effort to shorten our meeting, our Conference meeting, and Number 2, we are attempting to have one combined banquet rather than two banquets, so this may be our last individual ACGIG banquet. We would certainly hope that you would attend our banquet Tuesday night. We do have a real good speaker, a humorous speaker, and we think that you will enjoy this. I think the next order of business is our committee reports, And first let's hear from the TLV Committee, Herb Stokinger. Herb. DR. HERBERT E. STOKINGER: Thank you. Here I seem to be again, for the umpteenth time. Well, if you have been following the events in occupational health throughout the year-----and I can't.imagine who hasn't----- and if you cast your one good eye on the TLV Committee report that you have, consisting of three pages, you can see that this year has been a very busy year the the Threshold Limit Committee. And if you look at the committee report, you will see that on Page 1, 20 changes have been made for the 197^ edition of the TLV book let. And in addition, we have made 23 transfers to the adopted list which is on Page 3. This now constitutes the largest number of actions ever taken in the history of the TLV Committee. And as the year rolled on, first came the news in the early part of '73 of the ketone involvement with neuropathies. And this brought into question, you see, the validity of the TLV for methyl ethyl ketone, methyl butyl ketone, and methyl isobutyl ketone. And while these were under scrutiny by the committee, the story broke on the angiosarcoma of the liver of workers exposed to vinyl chloride. And this, of course, resulted in adding vinyl chloride to the fast-increasing list of industrial carcinogens. And while all this is going on, a proposed draft of NIOSH, which is acceptable to the TLV Committee, to replace benzene solubles as an index of coal tar pitch volatiles with benz (a) pyrene, this was found unacceptable to the industry after a series of, I would say, rather involved meetings, four in number. Then the theory----- I am sorry, I meant the thorny question of indus trial carcinogens were continually on the minds of the committeemen in regard as to how to define and categorize industrial carcinogens and what criteria are we going to use for establishing a threshold and the TLV. This is the basis of a very difficult question, because there are two bodies of thought on this matter, those who believe there is no -17- such thing as a threshold for carcinogens and those who believe her is. And of course, being on the TLV Committee, we must take the latter as the basis for making a TLV for these carcinogens. So I will just take time to review briefly what the major actions of the more prominent items were that were taken by the committee. These were seven in number. And of course, first and foremost, vinyl chloride. The present TLV of 200 parts per million was retained because of an ongoing investigation that is soon to be concluded. We thought it was undesirable to try to force the issue and come up with some poorly defined limit,-----rather wait until all the information was in. However, we did put it into a new carcinogen category called Ale that you will see in the Appendix in recognition of the human car cinogenic potential, and which is added the uncertain state of knowledge, and this takes it out of the regular place where most of the; human carcinogens are placed. Now, the coal tar pitch volatiles. The present TLV of 200 micro grams of benzene solubles is also retained pending the development of analytic methods that are more acceptable to the industries in volved. And as I mentioned before, the NIOSH draft proposal to use benzo (a) pyrene at 0.1 microgram per cubic meter as an index of exposure was found unacceptable. Industry is supposedly work ing on some analytic methods that will be more comprehensive and more satisfactory for their activities. Now, the third one is methyl butyl ketone, and here agin the present TLV of 100 parts per million was retained, because we are waiting for positive identification that MBK was the true cause of the human neuropathies and we have to find out the levels at which they have occurred. We are of the opinion, as a committee, that they must have occurred at levels well in excess of the 100 parts per million. Now as to dioxane, the TLV was reduced two years ago to 50 parts per million, and it was transferred to the list of adopted values following animal experimental evidence that a considerable factor of safety for tumor induction at the 50 parts per million level. The fifth one, bis-chloromethyl ether. Now, the TLV of one part per billion for this suspected human carcinogen was retransferred to the list of adopted values after the committee had learned of experimental evidence of a considerable margin of safety in this TLV, and also that there was no evidence that levels around this value can induce human cancer. The evidence that came out of ex perimental work at Dow Chemical showed that whereas 95 percent of the animals had tumors at 100 parts per billion, there was not an animal that had one at ten and, of course, one part per billion, which is the present limit. In the field of carcinogens, we have the Subcommittee on Carcin- -18- ogens whose chairman is Dr. Zavon, who has had personal, longtime experience with carcinogens. He is developing a philosophy and a procedure for establishing substances as carcinogens that are both experimental and human, how to divide them and separate them. And he is developing criteria for establishing a threshold and a TLV for such substances. The Committee on Short-Term Limits, whose chairman is Paul Caplan, is developing a report defining STL's and proposing such limits for appropriate substances in the TLV list, and this is going to constitute quite a number. And finally, the committee got a pleasant surprise,----- after nearly a quarter of a century of asking for information from industry, the Subcommittee on Hydrocarbons received six inches of reports of in vestigations from work that was sponsored by American Petroleum In stitute over the past five years, and from which the subcommittee was able thus far to develop recommended limits for six. And I want to point out before I conclude, these reports represent the greatest criteria to the TLV Committee. And I guess the publication line has already been covered amply, and so I have nothing more to do than to recommend that the items listed on three pages of the handout be adopted by the Conference. Do we hear any seconds to the motion, or otherwise? MEMBER: I will second it. CHAIRMAN KEPPLER: It has been moved and seconded that we accept the TLV report. Is there any discussion? Are we ready for the question? Yes, sir. MR. KENNETH R. SCHRAG: With respect-- CHAIRMAN KEPPLER: Would you get over to the microphone so we can hear you please? Please give your name and where you are from. MR. SCHRAG: Ken Schrag from Vancouver. With respect to the arc welding TLV, is that based on the iron TLV? DR. STOKINGER: Yes, we are going to adopt a procedure of putting such generic things into a separate appendix which involves consid eration of analyzing for such things as the constituents of welding fumes and then from this analysis determine what TLV's actually apply; and the iron oxide is, of course, a major component of most welding fumes and this will be taken care of in a separate manner. CHAIRMAN KEPPLER: Are you ready for the question? All in favor of accepting this report signify by saying Aye. Contrary, the same. Report is accepted. Thank you, Herb. We will now have the TLV report on physical agents by Herb Jones. MR. HERBERT H. JONES: Well, the report from the Physical Agents -19- Committee of this year is much chorter than the one Herb Stokinger just have you from the chemical agents. And it has been pointed out earlier we do have one new publication, that is "A Guide for the Control of Laser Hazards," and I think you are all familiar with the TLV for lasers and are aware that it becomes a wee bit complicated, a little difficult to work with, and also an inadequ ate supply of instrumentation in this area. I think by using the guide and a classification scheme of lasers that in a majority of the cases it would be possible to control hazards from lasers with minimal ammount of effort. If you do have a laser problem, I would strongly recommend the guide. The committee does have the following recommendations for changes in TLV: Item 1, to extend the coverage of the UV-TLV to include solar radia tion. This has been on the notice of intended changes, and we would recommend that this be included in the permanent UV-TLV. Second, that in the UV-TLV that we add an additional statement which reads as follows: "Conditioned (tanned) individuals can tolerate skin ex posure in excess of the TLV without erythmeter effects. However, such higher levels may not protect persons against skin cancer." We are still lacking much information as to exposure levels which might produce skin cancer. Third, the noise TLV remains as a notice of intended change for another year. It is the committee's feeling that it should remain on the intended change list for one more year. And the fourth item, to add to the noise TLV the following statement It should be recognized that the application of the TLV for noise will not protect all workers from the adverse effects of noise exposure. A hearing conservation pro gram with audiometric testing is necessary when workers are exposed in excess of the TLV. I move for the acceptance of these recommendations. CHAIRMAN KEPPLER: It has been moved that we accept the report of the TLV Committee on Physical Agents. Is there a second? MEMBER: Second. CHAIRMAN KEPPLER: It has been seconded. Do you have any questions or is there any discussion on this? If not, all in favor of accept ing this report signify by saying Aye. Contrary, the same. The re port is accepted. -20- The next committee report is the one on ventilation, and Norm Schuman will give this report-----Marv Schuman, I am sorry. MR. MARVIN M. SCHUMAN: Thank you, Fred. I would like to make a short report for the Ventilation Committee. We are active, and we made our largest sale this year of any year that we have had. We have sold over 12,000 copies of "The Industrial Ventilation Manual." Previous to this time we have sold over the last 25 years 100,000 copies, and at the rate we are going I think we should reach the 200,000 mark by another ten years or less. It looks like our sales are going up about ten percent a year. The committee is still active trying to improve the manual by changes which, of course, do not compare with the TLV Committee. And as new criteria are developed by NI0SH, we are going to try to include them in the manual. A couple of weeks ago the secretary called me and said we had a little bit of money in our account that we should not need for publications, so at this time I would like to present Fred a check for $12,000 which is in excess of what we need. I move the report be accepted. Thank you. CHAIRMAN KEPPLER s How can you----- SECRETARY-TREASURER KELLEY: As treasurer, I will second that. CHAIRMAN KEPPLER: And how can you reject not passing this on with the check for $12,000? SECRETARY-TREASURER KELLEY: Thank you, Fred. CHAIRMAN KEPPLER: All in favor of accepting the check and the report signify by saying Aye. Contrary, the same. Yes, sir? MR. PAUL CAPLAN: Yes, I would like to break that into two parts. I would like to accept the check, but I also have a question about the new recommendation in the manual that recommends recirculation of contaminated air. I imagine you have had some comments about that, and I wonder what the justification was and what actual fail-safe types of recommendations you can put into the manual on that line; re circulation of contaminated toxic materials. Paul Caplan, NI0SH. MR. SCHUMAN: If any of you have seen the 13th edition and have looked through it, you will notice the equation in there for re circulation. And we believe it is technically correct and that it does have a safety factor built into it which will protect the worker and keep the TLV at the worker's station below that which is recommended. -21- Now, we did this for a number of reasons. First is for conservation of energy, and we are presently trying to do more in this respect. Second, we thought it was an approach in this direction, and we were putting this in the manual. We did feel that it had enough safety built into it and it was a good approach, at least in the work that had been done. MR. CAPLANs Well, my concern is that in the practical world that often the systems may be designed proplerly but that in the mainten ance of them they often have a lot to be desired. And I think that there should be something written into the manual concerning fail-safe operation so that there definitely--well, the filtration system does not operate, there is postive action in some way that will require action to be taken to repair the system rather than letting it degrade, which normally happens in a ventilation sys tem normal degradation. It may start out being a good control system but unless you have a fail-safe system in it, it does not often work. MR. SCHUMAN: I think if you read this that you will find that there are indicators supposedly on the system. They are supposed to be put on the system to indicate when the system is not operating as it should. CHAIRMAN KEPPLERs Are there other discussions on this? Then all in favor of accepting the ventilation report signify by saying Aye. Those opposed, the same. The report is accepted. We will now have Bill Kelley summarize the other committee reports. Bill. SECRETARY-TREASURER KELLEY: Thank you, Fred. I will run through these in alphabetical order rather than in any other; the first being the report of the Agricultural Committee. Dr. Mitchell Zavon has been chairman. I would like to read you his report. Dear Bill: It is with a great deal of regret that after some two decades of membership in the ACGIH I have to ten der my resignation as I no longer have any governmental affiliation. Having become medical director of the Ethel Corporation, I find it inappropriate to continue, and under the rules of the Conference, I think I would be unable to continue membership. As chairman of the Committee on Agricultural Health, I wish to report that the committee has been working on the question or reentry times. After a considerable period of time occassioned by the need to write back and forth, it is evident that reentry into fields which have been treated with pesticides is a very specialized problem which does not appear to be of widespread import in the United States. -22- Based on the best of our information, it appears this is a problem in California, although it is not clear how big a problem it actually is there. It does not appear to be a significant problem in other parts of the United States. With the submission of the report, we were fortunate to have a vistor down at the Board of Directors' meeting, and I am not sure he considers it as fortunate, but Bill Steffan was there. And Bill Steffan volunteered to be interim chairman of the Agricultural Com mittee until such time as membership and a new chairman, new perma nent chairman can be found and will accept. So really the first activity of the reconstituted Agricultural Committee under the temp orary chairmanship of Bill Steffan is a call for volunteers. As to the Air Pollution Committee, as we indicated earlier, the cul mination of many years of effort in revising the earlier air pollu tion flow sheets was the publication which, again, is entitled "Process Flow Diagrams and Air Pollution Emission Estimates." And the activity of the committee will continue to update and expand this publication. Mr. Lee Jaeger has been chairman, and with a recommend ation for Mr. Bob Miller as new chairman of the committee. Dr. Lippman, as chairman of both the Air Sample Instruments Committee and the Joint Committee on Aerosol Hazards, presented both in writing and orally his reports. As to the Air Sampling Instruments Committee, essentially we had summarized this earlier in terms of the publications, the activity being the completion of the addenda for the current edition and the in-progress work of reprinting this. And then at this meeting the committee will be very actively involved in the preparation of the new edition of the manual which will come out in either 1975 or '76. As to the Aerosol Hazards Evaluation Committee, the major countinuing effort during the past year has been to complete the preparation of a guide and documentation paper on sampling and counting asbestos fibers for occupational exposure evaluations. Upon favorable committee action, the guide and documentation paper will be submitted for publication in the AIHA Journal, subject to appropriate review and approval. The committee intends to update the guide and documentation paper on respirable mass sampling in 1970 by one of its predecessors, the AIHA Aerosol Technology Committee. This will be the next major activity of the committee. The Analytical Methods Committee, under Mr. Alvin Vanderkolk as chair man, has not met as a group since its meeting last year at the Boston meeting. However, during the past year a total of 13 methods were either newly written or rewritten to fit their new format. In addition, there are some 21 assignments of additional methods which are in various stages of completion. The committee will be undertaking the finalization of these and the publication of a new analytical -23- methods manual. The report of the Joint Mining Environment Committee was submitted by Mr. Yourt, chairman. The committee has met once during the past year, and this has resulted in the culmination of their efforts to draft a manual. I was fortunate enough to see the draft of this manual last evening and it should be a fine addition to the publication when it becomes finally available. No specific action was requested by the Board. The Awards Committee report will become public, of course, at the banquet with the presentation of the annual awards. Mr. Chairman, I move the acceptance of the committee reports. CHAIRMAN KEPPLER: It has been moved that the remaining committee reports be accepted. Is there a second? MEMBER: I will second it. CHAIRMAN KEPPLER: Is there any discussion on any of these reports? If not, all in favor of a acceptance of the remaining committee re ports signify by saying Aye. Contrary, the reverse. The reports are accepted. During the past year our former Conference chairman, John Soet, passed away. Does anyone else, any of the other members, have information as to members who have passed away during the past year? Then could we have just a second of silence in memory of John Soet. (Members stood in silence.) CHAIRMAN KEPPLER: ACGIH would particularly like to thank Bill Deich mann and Bill McDonald, the Conference chairman, and all of the other members for the terrific job that they have done here on the conferece. We would also like to thank our chairman representing ACGIH, Jack McKichan. Is Jack present? At any rate, Jack did a real good job for us and we certainly do appreciate it. We have two retiring members from our Board, Darrell Douglas and Ernie Mastromatteo. Darrel and Ernie, would you stand up? I think they need a big hand. (Applause) In our election, our newly elected member of the Board is Ron Ott. Ron would you stand up please? (Applause) Vice-president-elect, DarreJ Douglas# (Applause) And secretary-treasurer, Bill Kelley was running against "withheld". I do not know who that is, but "withheld" got 37 votes. But at any rate, we could not get along without Bill, so we are real -24- happy that Bill was reelected our secretary-treasurer. (Applause) Is there any new business to be brought before our meeting? Does any one have any new business? If not, Jerry, would you come forward? It is really with great pleasure that I present the gavel-----that I do not have----- to you as the new chairman for the following year. And I can assure you that the chairmanship is in excellent hands. (Applause) CHAIRMAN-ELECT JEREMIAH R. LYNCH: Thank you. Thank you, Fred. It was pointed out to me that at the Board meetings that we never have any embarrasing silences while I am there, since I have the reputa tion of talking rather a lot. But you are not going to hear a great deal from me this morning because I have a sore throat. I would like you to think a bit about the way our Conference is oper ated. Over the years each of the chairmen has in his own way had some particular thing that he wished to do during his year as chair man of the Conference. Ernie convened a Conference in Toronto at which we came together and decided who we were, really. I think that is the main thing, and what the importance of the American Conference of Governmental Industrial Hygienist was. And the deliberations of that Toronto meeting have permeated through all of the thinking that has gone on in the Board since then. During Fred's term, many of the----- I will say problems, although also opportunities----- that we had with relation to the AIHA have been re solved, also we had found our need, which had been apparent for some time, for an executive secretary, and as a consequence, during Fred's term, Norm came with us. As I enter my term as chairman of this Con ference, I find things to be in excellent shape. I think that many of the problems that we saw when OSHA was passed when we felt perhaps the TLV Committee was threatened, those prob lems have vanished, thanks to Norm and the other able people who have been working on this. And I think you recognize the financial con dition of the Conference is excellent. And the vitality of the member ship; that above all has been magnificent. So here I am presented with this opportunity, and what am I going to do with it? Well, I want to mention several things. Several of them Fred has already alluded to. To begin with, I feel that every single governmental industrial hy gienist should be a member of this Conference. It is not so much a matter of having additional numbers on our rolls as it is that we are the unique organization which represents him, the governmental indus trial hygienist, and we need him, every single one of them. And we are going to try in all of the ways that we can think of to find these people, the few----- I think there are only a few----- who are not members, and to bring them into the fold. -25- Secondly, as Fred mentioned, we have begun a program of having mid year topical symposiums. There probably will be some revision of the format of the annual conference. We and the AIHA will continue to participate jointly in that. But in addition, the American Conference of Governmental Industrial Hygienists will sponsor an annual meeting at which there will be a single topic. We have chosen cotton for this year, and we have suggestions for future years. We will have trans actions, a transcript of that meeting. And it will be an additional publication to add to our already magnificent library of publications. This is one of the things that I feel will be, perhaps in small part, my contribution during my year here. One of the most important things about this Conference is our commit tees and what they do. And I want to announce that we have a couple of new committees. We have decided to have a Committee on Industrial Hygiene Operations. Since we are the organization to which the people who have the respon sibility for industrial hygiene compliance operations belong, I feel that it is our responsibility to develop uniform standards for com pliance operations if they are to be developed. Not only this, these guidelines for compliance operations in indus trial hygiene would be recommended by the Conference for use by the federal government and by the states, since inevitably it is the intent of the federal government that the states take over this activity. We may or may not agree with the concept of industrial hygiene com pliance, but it is upon us. And it is important that it be done well. And we above all are the group who know how to do it and set down the correct way of doing it if it must be done. That is one of the com mittees . Another committee, a special joy of mine, and although it may seem somewhat frivolous, I think it is very important, and that is the Com mittee on History of Industrial Hygiene. We intend by that committee to identify and perhaps collect artifacts, oral history from some of the old-timers who are still with us, identify and collect documents, perhaps put together an exhibit. Now, I am going to conclude just with this point. The one thing I want to say is I need to hear from you. We have, thanks to the bul letin board and all Norm's efforts, a very excellent means of my talk ing to you. Now, what I need is for you to talk to me. I think that one of the most important things I can do is try to in crease Conference member participation in the operations of the Con ference during my year on the Board. And so in any way, either grab hold of me or any of the other Board members or say something now or write me a letter, but however you do it, please let me hear from you. And I want especially to know those of you who have interest in com mittee activities and would like to do that work. That is what I am asking for. I want to hear from those people especially who would -26. like to work, because this is the thing we do. And we do it very well. Thank you. (Applause) SECRETARY-TREASURER KELLEY: There are a couple of announcements I would like to make before we let Jerry carry out his most important function as incoming chairman. And the first announcement is one of great importance. Prior to the banquet tomorrow evening there will be a cash bar in the Garden Lobby from 5*30 o'clock p.m. to 6:30 o'clock p.m. Secondly, in a little less serious vein, Dr. Mastromatteo has in dicated that there will be an International Symposium on Practical Applications of Ergonomics in Industry, Agriculture and Forestry, Septemeber 17-20, 197^ in Bucharest. There will be copies of the information at the ACGIH booth this week, and I am sure Ernie would love to talk to you about it. For those of you who want to plan ahead, I would like to just out line the upcoming conferences. Now, as was mentioned, next year's is in Minneapolis. It will be at the Lemington Hotel as the conference headquarters, and the week will be different. It will be the week of June 1 to 5- So keep the first week in June open next year. In 1976 the conference will be in Atlanta; in 1977 New Orleans; 1978, Los Angeles; 1979 Chicago; and 1980, Houston. Mr. Chairman. CHAIRMAN LYNCH: Do I hear a motion that the meeting be adjourned? Second? All in favor. Thank you. (Applause) (Whereupon the meeting adjourned at 11:^5 o'clock a.m.) -27- PUBLICATIONS OFFICE STATEMENT OF VOLUME SALES FISCAL YEAR 4/1/73 TO 3/31/74 Air Pollution Control Process Flow Sheets - 1961 fi rr n n nn 1974 16 43 Air Pollurtion Reference Library (temporily out of print) 88 Air Sampling Instruments Manual 701 Analytical Methods Manual 148 Bibliography of Radiation Protection Organizations (discontinued) 4 Documentation of TLV's, 3rd Edition 1971 605 Supplemental Documentation, 1971 174 " " 1972 264 Other Yearly Documentations 5 Guide to Records for Health Services in SmallIndustries 23 ( discontinued this year) Guide to Uniform Industrial Hygiene'Codes or Suppliment #1 Suppliment #6 Laser (Codes discontinued this year) Regs.Full set 14 1 1 7 Guidelines for Noise Exposure Control (temporarily out of print) 107 Quartz Roundtable Proceedings Standard Reports of Occupational Health Activities Among 62 State and Local Agencies (discontinued this year) Threshold Limit Values, 1973 Threshold Limit Values , 1972 Trade Names Index, Supplement #1 8 36, 954 6, 372 10 Supplement #2 Transactions of Annual Meetings Miscellaneous Publications (single DOCs. *7.0 TLV-PA, etc.) 14 26 20 -28- Statement of Financial Transactions Fiscal Year 4/1/73 to 3/31/74 American Conference of Governmental Industrial Hygienist Cash Receipts Sale of Air Sampling Instruments Manual (Published and expenses 1972) $ 8,564.90 Sale of Analytical Methods Manual (Puglished 1958 and supplement 1961, expensed 1958, 1961, 1963, 1967, 1969 and 1972) 1,169.25 Sale of Threshold Limit Values for 1972 and 1973 21,176.95 Sale of Documentation of Threshold Limit Values (Published and expensed 1971) 9.057.50 Sale of Supplemental Documentation for 1971 and 1972 (Published and expensed 1971 and 1972) 364.25 Sale of Guide to Uniform Industrial Hygiene Codes or Regulations and Supplements 28.25 Sale of Process Flow Sheets and Air Polution Control (Published 1961 and expensed 1961, 1964, 1966 and 1972 40.50 Sale of Process Flow Sheets and Air Polution Controls (Published 1974 and partially expensed 1974) 40.25 Sale of Quartz Roundtalbe Proceedings (Published and expensed 1974) 239*50 Sale of Trade Names Index Supplement No. 1 (Published and expensed 1967) 26.00 Sale of Trade Names Index Supplement No. 2 (Published and expensed 1968) 54.00 Sale of Transactions (1972 and previous years) 155-00 Received from Ventilation Committee from Sale of Ventilation Manuals 13,640.50 Received from Respirator Committee from Sale of Respirator Manual (Published and expensed 1963 1,215*00 Membership Dues (Net of Foreign Exchange) 6,239*10 Share of Receipts from 1973 American Industrial Hygiene Conference - Boston 8,599*00 Sale of Miscellaneous Publications 582.17 State of Ohio Sales Tax Collections 32.27 Miscellaneous Income Received (Postage and Travel Rebates) 390.42 Collections on Prior Receipts Expensed 67.00 Total Interest Earned - Eagle Savings and Loan Account 792.64 Interest Earned - First National Bank of Cincinnati 486.39 Interest Earned - Mercantile Bldg, and Loan Account 591*15 Interest Earned - P.H.S. Credit Union Account 442.72 Interest Earned - Provident Bank Account 115*84 Interest Earned - Spring Garden Savings & Loan Account 746.67 $71,781.81 3.176.41 TOTAL CASH RECEIPTS $74.967.22 -29- Cash Disbursements Expenses for Secretary-Treasurer to 1973 Conference Expenses for Mps. Duffy to 1973 Conference Miscellaneous 1973 Conference Expenses Board of Directors Expenses Recording of Business Meeting Board of Directors Banquets Conference banquet Photographer and Plazques Flowers for Guest Speaker Dr. Warren A. Cook (Meritorious Service Award) Miscellaneous 1974 Pre-Conference Expenses $ 228.52 173-18 1,334.39 15.00 646.99 3,740.63 179.88 5.15 294.69 320.60 $ 6,939.03 Printing Costs 1973 Membership Directory 1973 Threshold Limit Values 1973 Transactions Quartz Rountable Proceedings Guide for Control of Laser Hazards Process Flow Sheets and Air Pollution Controls Official Publication List Stationery, Envelopes, etc. Comm-i_ttee Meeting Expenses Board of Directors Meetings Air Pollution Air Sampling Instruments Analytical Methods API Committee on Toxicology ASSE Parathion Review Physical Agents Threshold Limit Values (Two Meetings) Other Committee Expenses Executive Committee Travel Office Expenses Audit of Treasurer's Report and Tax Returns Surety Bonds for Secretary-Treasurer & Bookkeeper Ohio Sales Tax Executive Secretary's Salary Executive Secretary's Expenses Rebates on Dues and Publications Multilithing, Addressing, etc. of Bulletin Board Postage (Including Truck Shippings) Bank Collection Charges on Receipts Secretarial Help Miscellaneous Office Expenses Exhibit Booth Expenses Miscellaneous Printing Business Office Expense: Salary $ 4,981.20 Office Expenses 1,918.68 Total Cash Disbursements $ 1,956.20 7.683.00 4.141.53 3.766.53 3.150.00 250.00 43i.ll 1,760.35 23,138.72 2,516.17 754.41 110.42 486.98 160.00 133.78 122.15 33309 3,360.73 7,978.03 98.20 98.20 350.00 165.00 49.25 2,500.00 1,084.82 109.95 4,423.97 2,111.26 109.50 574.22 258.00 1,759.19 583.10 6.899.88 20.978.14 $69.132.23 -30- Excess of Cash Receipts over Cash Disbursements Addi Balance in Checking Account 4/1/73 Balance in Savings Account 4/1/73 Cash Balance as of 3/31/74 $ 15,825.10 $41,446.19 45.908.79 87,354.98 $103.180.08 Represented bys The Provident Bank, Cincinnati, Ohio, Checking Account $ 16,237.42 Cincinnati, PHS Federal Credit Union Account - 5 3A# 8,036.20 Eagle Savings & Loan, Cincinnati, Ohio, Savings Acct - 5%fo 15,000.00 First National Bank of Cincinnati, Ohio, Savings Acct - 4 3/ Vfo 10,000.00 Mercantile Bldg. & Loan, Cincinnati, Ohio, Savings Acct - 5i' S 11,906.46 Spring Garden Savings & Loan, Cincinnati, Ohio, Savings Account - 6% 20,000.00 Standard Federal Savings & Loan, Cincinnati, Ohio, Savings Account - 7 l/4?S 20,000.00 The Provident Bank, Cincinnati, Ohio, Savings Account 5 3A ,2 000.00 Total 103,180.08 -31- C O P Y AUDITORS CERTIFICATE I have examined the Statement of Financial Transactions for the fiscal year 4/1/73 to 3/31/74 of the American Conference of Governmental Industrial Hygienists as submitted hy the Sec retary-Treasurer of the organization. I did not make a formal audit of the transactions. Based on the records maintained and the information furn ished to me, the above statement presents correctly the financial transactions for the above organization for the period as stated. May 1, 1974 (Signed) Certified Public Accountant Charles Gehler 1801 Carew Tower Cincinnati, Ohio 45202 -32- ANNUAL REPORT FOR COMMITTEE ON INDUSTRIAL VENTILATION 1974 The Committee has met twice during the past year to review material writ ten for additions to the manual, to discuss possible changes for clarifica tion of sections and what material could or should be considered for future editions. The make-up air section was extensively revised as proposed in our previous report. We expect to consider ventilation for cotton machinery and review material submitted for push-pull ventilation methods since this was not received in sufficient time for the 13th Edition. The recommendation by the Board was considered during our meeting in May, which asked the Ventilation Committee to review the various ventilation standards published by OSHA. The committee concluded that because of the various assignments for committee members and other activities it would be impossible for the committee as a whole to review the standards. The com mittee felt that if a member was so inclined, that it should be up to his discretion to do this as an individual rather than as a committee member. Sales have been up to expectations with a total of 12, 759 copies sold dur ing the fiscal year, thehighest sales for any single year to date. To help account for these sales, over 2, 000 copies were sold to SMCNA bringing our total to this organization to more than 12, 000. The 13th Edition was printed in February and with the present sales we expect our growth rate to continue at approximately 10% per year. The Industrial Ventilation Conferences, particularly the one at Michigan State University, have a pro found affect on the sales of the Manual, with usually twice the normal sales in February during the conference. The Committee plans to go forward, as in the past, changing material where new information has become available and to add to areas where interest has been shown. One area of major concern and expanded upon in the 13th Edition is air recirculation. As information becomes available, we hope to expand this section for the conservation of available energy. Respectfully submitted, (signed) Marvin M. Schuman, Chairman Committee on Industrial Ventilation -33- COMMITTEE ON INDUSTRIAL VENTILATION Statement of Income and Expense for the year ended March 31, 1974 Sales Cost of Materials Sold Gross Margin $ 57, 835. 99 26, 648. 97 $ 31, 187. 02 Expens es: Secretarial $3, 401. 85 Postage Office Supplies Committee Expense 3, 733. 84 1. 373. 78 842. 16 Sales & Income Taxes 304. 15 Advertising 209. 00 Accounting Services 195. 00 Bad Debts 76. 00 Net Operating Income Interest on Savings Account Net Income Submitted to A. C. G. I. H. Due to A. C. G. I. H. Increase in Net Worth $ 11, 815. 50 1, 774.00 10, 135. 78 $ 21, 051. 24 83. 85 $ 21, 135.09 13, 589. 50 $ 7, 545.59 -34- COMMITTEE ON INDUSTRIAL VENTILATION Statement of Assets, Liabilities and Net Worth March 31, 1974 Cash: In Bank and on Hand In Savings Account Accounts Receivable Inventory Supple s: Packing Materials Postage ASSETS $ 18, 733.97 2, 166. 00 $ 20, 899.97 6, 171.00 15, 929. 90 $ 171.04 357. 67 528.71 $43, 529. 58 LIABILITIES AND NET WORTH Accounts Payable Accrued Secretary's Bonus Sales and Payroll Taxes Payable Due to A, C. G. I. H. Net Worth: Balance, April 1, 197 3 Increase for the Year $32, 497. 26 7, 545. 59 $ 132.11 1, 301. 85 278.77 1,774.00 $ 3,486.73 40, 042. 85 $ 43, 529. 58 -35- April 30, 1974 Committee on Industrial Ventilation 759 Tarleton East Lansing, Michigan C O P Y Gentlemen: I have examined the records of the Committee on Industrial Ventilation, together with the Statement of Assets, Liabilities and Net Worth as of March 31, 1974, and the Statement of Income and Expense for the year then ended. The examination included a review and tests of the records maintained by the Secretary as considered necessary in the circumstances. In my opinion, the accompanying statements present fairly the financial position of the Committee on Industrial Ventilation as of March 31, 1974, and the results of its operations for the year then ended, in conformity with generally accepted accounting principles applied on a basis consistent with that of the preceding year. (Signed) Stephen H. Terry Certified Public Accountant -36- ANNUAL REPORT Air Sampling Instruments Comm. A second printing of 1000 copies of the 4th Edition of "Air Sampling Instruments" was ordered since the first printing of 2900 was completely sold out early in 1974. A revised Addenda section was included in the second printing, noting changes in instrument sources and availability since the preparation of the 4th Edition. The Committee and its consultants are at work on the prepar ation of the 5"th edition, which is scheduled for publication in 1975. All present members of the Committee should be reappointed. In addition, Leonard Pagnotto should be appointed to the Committee. ANNUAL REPORT Aerosol Hazards Evaluation Committee The major continuing effort guring the past year has been to com plete the preparation of a "Guide" and documentation paper on sampling and counting asbestos fibers for occupational exposure evaluations. The "Guide" has gone through several revisions and will be up for final committee approval at the annual meeting. The documentation paper is nearing completion, and a complete draft will be distributed to the full committee before the annual meeting. If is not likely that this draft will be in sufficiently final form for committee approval in May. If not ready in May, it should be ready for committee approval by mail ballot within the next few months thereafter. Upon favorable Committee action, the Guide and documentation paper will be submitted for publication in the AIHA Journal, subject to whatever review and approvals are required by AIHA. The Committee intends to update the Guide and documentation paper on Respirable Mass Sampling published in 1970 by one of its pred ecessor's, the AIHA Aerosol Technology Committee. This will be the next major activity of the Committee. The present Committee membership list should be continued for next year without additions or deletions. -37- REPORT OF THE ACGIH COMMITTEE ON THRESHOLD LIMITS FOR THE AIR OF WORKPLACES ANNUAL BUSINESS MEETING, ACGIH Miami, Florida May 13, 1974 At the second semi-annual, plenary meeting of the TLV Committee (April 16 and 17), the following changes and additions to the 1973 listings for air borne contaminants in the workplace were recommended for adoption by the Conference. RECOMMENDED CHANGES ITEM Arsenic, (Inorganic compounds, as As) Benzene Butane n-Butyl alcohol n-Butyl lactate Cadmium (metal dust & salts, as Cd) Carbofuran (FuradanQD) Dimethyl sulfate Dioxane Ethylene chlorohydrin Heptane Hexane Isobutyl alcohol Methylcyclohexane Octane Pentane Phosgene Stoddard solvent Vinyl bromide Vinyl chloride From 1973 3 0.5 mg/m C 25 ppm 500 ppm 100 ppm 1 ppm 3 0.2 mg/m 0.05 mg/m3 1 ppm (A2) 50 ppm 5 ppm 500 ppm 500 ppm 100 ppm 500 ppm 400 ppm 500 ppm 0.1 ppm 200 ppm 250 ppm 200 ppm To 1974 3 0.25 mg/m 10 ppm 600 ppm 50 ppm 5 ppm 3 0.05 mg/m 0.10 mg/m3 0.01 ppm (A2) 50 ppm (A2) C 1 ppm 400 ppm 100 ppm 50 ppm 400 ppm 300 ppm 600 ppm C 0.05 ppm 100 ppm A- refers to TLV booklet Appendix Alc - "No new TLV assigned pending investigations under way" -38- Annual Report - 2 ADDITIONS TO TENTATIVE LISTINGS ITEM Arc-welding Fume (Total Particulate) Calcium cyanamide Calcium hydroxide Captan Dicyclopentadien e Disulfuram 2,6-Ditert.-butyl-p-cresol Dursban (Chlorpyrifos) Dyfonate Fensulfothion (Dasanit) Glutaraldehyde Glutaraldehyde (Alkaline-"Activated") Hexylene glycol Hydrogenated terphenyls Iodoform Nonane Resorcinol Sodium azide Succindialdehyde (see Glutaraldehyde) A,A'-Thiobis(6-tert.butyl-m-cresol) Triphenyfamine m-Xylene, a, ex'-diamine PPm 5 C2 25 0. A 0.2 200 10 C 0.1 mg/m3 5 0.5 2 5 30 2 10 0.2 0.1 0.1 C8 C 0.25 125 4.A 3 1050 A5 C 0.3 10 5 0.1 All changes and additions that are listed are based on documented evidence which is available from the chairman. -39- Annual Report - 3 TRANSFERS FROM STATUS OF TENTATIVE LISTING TO ADOPTED VALUES FOR 1974 (In accordance with general policy of transfer after 2-year period without indication of action otherwise.) ITEM TLV Asbestos, all forms..........5 fibers/cc > 5 JJm long (A las Baygon ..................................... 0.5 mg/m3 Caprolactam Dust ..................................... 1 mg/m3 Vapor ................................... 5 ppm bis-Chloromethyl ether.. 1 ppb (Ala) o-Chlorotoluene ................. 50 ppm . Cotton dust, raw.............. 0.2 mg/m3 Cyclohexylamine ................ 10 ppm Dioxane ................................. 50 ppm Disyston................................. 0.1 mg/m3 Ethylidene norbomene .. C 5 ppm Furfuryl alcohol ....... 5 ppm Hexachlorocyclopentadiene 0.01 ppm Manganese cyclopentadienyl tricarbonyl (as Mn)... 0.1 mg/m3 4,4 ^ Methylene bis(2-chloro- aniline) ... 0.02 ppm (A2) Methylene bis(4-cyclo- hexylisocyanate) ..... C 0.01 ppm Methyl ethyl ketone peroxide 0.2 ppm Mineral wool fiber.......... 10 mg/m3 Paraffin wax fume .......... 2 mg/m3 Phorate (Thimetw) .... Potassium hydroxide .... 0.05 me/m3 C 2 mg/m3 Silicon tetrahydride (Silane) 0.5 ppm Tripoli ................................... Use respirable mass formula for quartz efoorofa * Capital letters refer to Appendices. m) Lint-free dust, measured according to specifications. -40- ANNUAL REPORT TLV Physical Agents Committee, 1973-7^ The Committee published "A Guide for Control of Laser Hazards" and this is available from the Secretary-Treasurer's office and will sell for $2.75* The Committee makes the following recommendations for changes in TLV: 1. Extend the coverage of the UV-TLV to include solar radiation as given in the notice of Intended changes (1973). 2. Insert the following statement in the UV-TLV, "Con ditioned (tanned) individuals can tolerate skin ex posure in excess of the TLV without erythmeter effects. However, such higher levels may not protect persons against skin cancer. 3- The noise TLV remain as a notice of Intended changes for another year. k-. Add the following paragraph to the noise TLV, "It should be recognized that the application of the TLV for noise will not protect all workers from the ad verse effects of noise exposure. A hearing conser vation program with audiometric testing is necessary when workers are exposed in excess of the TLV. -41- REPORT OF THE COMMITTEE ON AWARDS The Bill of Particulars for the Awards Committee suggests the citing of an individual, a group, or both for meritorious achievement. This year your Committee has selected a group - the U. S. Army Envi ronmental Hygiene Agency at the Aberdeen Proving Ground, Maryland to be the recipient of the Meritorious Achievement Award. This organization was authorized by the Secretary of War on January 5, 1942, to establish a central Industrial Hygiene Laboratory with a budget not to exceed $3, 000. 00 and a staff of three industrial hygiene engineers at the Walter Reed Army Medical Center as an inte gral part of the expanded Army Industrial Hygiene Laboratory was trans ferred to Johns Hopkins University. The activities of the Laboratory necessitated that surveys and investigations be conducted at Army instal lations throughout the continental United States and at Army Air Force industrial installations. The activities of the Industrial Hygiene Laboratory grew rapidly, and at the peak of WW II activity, the Laboratory had 23 Sanitary Corps officers, 2 Medical Corps officers, 1 WAC officer, 2 enlisted men, and 13 civilian employees. A few weeks after V-J Day in 1945 the Industrial Hygiene Laboratory was moved from Baltimore to the Army Chemical Center, Md. , now the Edgewood area of Aberdeen Proving Ground. In I960 the Laboratory became the Army Environmental Hygiene Agency. In 1967 the Laboratory was moved into a modern 4-story building. The facility has special ventilating systems for environmental studies; there are insectories which permit control of environmental conditions includ ing varying degrees of light that may exist in any part of the world; there are calibration facilities for radiological, chemical, and physical mea surement instruments; and a complete animal-care facility. It has a 20,000 volume library, a modern communications system, electronic data-processing facilities, and is equipped to perform acute and chronic toxicologic investigative studies. Activities are directed in four basic scientific areas, namely: medical services, including industrial hygiene; environmental quality services; radiation services; and laboratory services. Agency experts are available to Army and certain Defense Department installations world wide. Two pieces of federal legislation, the Federal Civilian Employees Health Act of 1946 and the Occupational Safety and Health Act of 1970 have had a tremendous impact with respect to the damand for the Agency's ser vices. At present there are 86 officers, 40 enlisted personnel and 180 civilians. The working budget for FY-1975 is 5. 5 million dollars exclu sive of military salaries. It is interesting to note that 24 of the present staff including the pre sent commander, COL James E. Anderson, are members of ACGIH (six are Board Certified in Industrial Hygiene). Many former members -42- Lt. Col. Manmohan Ranadive, M. D. , Director of Occupational Health, accepts the 1 97 4 ACGIH Meritorious Achievement Award for the U. S. Army Environmental Hygiene Agency Aberdeen Proving Ground, Md. p resented by Bobby Craft, Ph. D. -43- of the Agency have retained their affiliation with the ACGIH. Three, Dr. Robert H. Duguid, Mr. Marion F. Trice, and the late Charles Couchman have served as Chairmen of ACGIH. Of the present 24 ACGIH members at the Agency, five have worked there more than 25 years each with a total of more than 143 years. Four of these veterans expect to retire during 1974. They are Mr. Harry H. Ackerman, Mr. Christian F. Berghout, Dr. Robert H. Duguid, and Mr. George F. Sprague, III. The fifth veteran, Mr. Walter R. Halpin, the youngest in age but with the longest uninterrupted tenure, expects to continue his dedicated service. These gentlemen have served the profession in an outstanding manner and have done much to establish the stature of USAEHA. Each has served on various committees of ACGIH and of AIHA also on various ANSI Commit tees. They have authored or co-authore numerous Army technical bulletins and technical guides and have directed on-the-job training for newly-assign ed personnel. They have been invited as guest lecturers at professional conferences and short courses in various parts of the country. Throughout the years they have given numerous papers at Industrial Hygiene Conferen ces. They have also assisted in the review of numerous hygienic guides and of NIOSH Criteria Documents. The Awards Committee of the American Conference of Governmental Industrial Hygienists takes great pleasure in presenting this placque to the U. S. Army Environmental Hygiene Agency and a certificate of recognition to the five employees with 143 years service with USAEHA-Dr. Duguid, Messrs. Ackerman, berghout, Sprague, and Halpin. -44CX -45- AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS Conference Activities Sunday, May 12, 1974 9:00 A. M. - 5:00 P. M. Round Table Sessions 3:00 P. M, - 5:00 P. M. NIOSH-OSHA Open Meeting with State and Local Programs Monday, May 13, 1974 9:00 A. M. - 10:30 Chairman, C. E. Adkins OSHA, Kansas City, Mo. Monitor, W. E. Murray NIOSH, Cincinnati, Oh. 9:00 A. M. - Welcome - ACGIH Opening Session J. Fred Keppler, Chairman, ACGIH 9:15 A. M, - Eye and Face Protection J. I. Kamin, NIOSH, Cincinnati, Oh. 9:35 A. M. - Classification of Analytical Methods J. V. Crable, D. G. Taylor, & R. G. Smith NIOSH, Cincinnati, Oh. 10:00 A, M. Progress in Accreditation J. C. Barrett, Michigan Dept, of Health Lansing Michigan H. T. Walworth, Lumberman's Mutual Long Grove, 111. 10:30 A. M. ACGIH Business Meeting 1:30 - 4:00 P. M. Chairman, Austin Henschel, Ph. D. NIOSH, Cincinnati, Oh. Monitor, S. N. Dereniuk NIOSH, Cincinnati, Oh. Panel Discussion INDUSTRIAL COLD STRESS Moderator - Austin Henschel, Ph. D. Panel Members: (Continued ) - 46- Banquet Speaker - Win Pendleton Humorous - with a Message ! -47- Monday May 13, 1974 (Con'd) Panel Members: E. Buskirk, Ph. D. Pennsylvania State University University Park, Pa. S. Horvath, Ph. D. University of California Santa Barbara, Calif. R. Goldman, Ph. D. Army Research Institute Natick, Massachusetts W. Doolittle, M. D. Tanana Valley Medical Fairbanks, Alaska F. N! Dukes-Dobos, M. D. NIOSH, Cincinnati, Oh. Tuesday, May 14, 1974 9:00 A. M. - 12:00 NIOSH HAZARD EVALUATION HIGHLIGHTS Session Arranger - J. P. Flesch NIOSH, Cincinnati, Oh. 9:00 A. M. 9:20 A. M. 9:40 A. M. 10:00 A. M. 10:20 A. M. 10:40 A. M. 11:00 A. M. 11:20 A. M. 11:40 A. M. Chairman - M. E. LaNier NIOSH, Cincinnati Monitor - Loren Canada OSHA, Macon, Ga. Health Hazard Evaluation - An Overview J.P. Flesch, NIOSH Carbon Disulfide in Viscose Rayon Manufacturing R. E. Rosensteel, NIOSH, Cincinnati Diethylstilbestrol, N-acetyl Sulfanilyl Chloride in Chemical Manufacturing D. J. Burton, NIOSH, Salt Lake City, Ut. Isocyanates in Plastics Manufacturing R. Vandervort, NIOSH, Cincinnati Break Epoxies in Sporting Goods Manufacturing J. B. Lucas, M. D. , NIOSH, Cincinnati Polyvinyl Chloride Film in Meat Wrapping P. L. Polakoff, M. D. , NIOSH, Cincinnati Trichloroethylene in Electronic Components Mfr. M. T. Okawa, NIOSH, SanFrancisco, Ca. Chromic Acid in Electroplating S. R. Cohen, M. D. , NIOSH, Cincinnati -48- Tuesday, May 14, 1974 1:10 P. M. - 3:20 P. M. - JOINT ACGIH- AIHA SESSION 1:H0 P. M. 1:15 P. M. 1:20 P. M. 1:40 P. M. 2:00 P. M. 2:20 P. M. 2:40 P. M. 3:00 P. M. 3:20 P. M. INDUSTRIAL HYGIENE COMPLIANCE STRENGTH AND WEAKNESSES Session Arrangers - E. J. Baier, NIOSH Rockville, Md. J. R. Lynch, NIOSH Cincinnati Chairmen: J. T. Siedlecki Standard Oil of Indiana J. F. Keppler OSHA, Indianapolis, Ind. Monitors- C. H. Moline, NIOSH C. J. Carstens, Occ. Health Raleigh, N. C. Welcome and Remarks J, T. Siedlecki, President, AIHA Welcome and Remarks J. F, Keppler, Chairman, ACGIH What is an OSHA Industrial Hygienist V. E.Rose, NIOSH Rockville, Md. Inspection Experiences R. Tremblay, OSHA Atlanta, Ga. The Operations Manual J. R. Lynch, NIOSH, Cincinnati Break The Safety Specialist Role in Industrial Hygiene R. R. Ott, OSJdA SanFrancisco, Ca. Statistics in Compliance M. A. Leidel, NIOSH, Cincinnati Defects in Enforceable Standards B. D. Tebbins, Sc. D. , University of California Berkeley, Calif. 6:30 P. M. ACGIH Banquet Speaker, Win Pendleton Presentation of the Meritorious Achievement Award -49- P la c q u e b e in g p re s e n te d b y in c o m in g yn ch , to o u tg o in g C h a irm a n K e p p le r -51- MONDAY AFTERNOON SESSION - MAY 13, 1974 Austin Henschel, Ph.D., Chairman, Presiding The 1974 American Conference of Governmental Industrial Hygienists convened at 1:38 o'clock p.m. in the Fontaine Room of the Fountainebleau Hotel, Miami Beach, Florida, Austin Henschel, Ph.D., Chair man, presiding. CHAIRMAN HENSCHEL: Good afternoon, ladies and gentlemen. I think we should get our panel discussion started. I would like first to lay out some of the rules that we are going to follow in our discussion this afternoon. First, we will have five presentations of approximately 15 minutes each. I would like to have you hold your questions until all five speakers have pre sented their material. We will have then an hour which will be available for discussion. All of the remarks that we are making, and that anyone else who wants to.talk will be making, are being recorded, so we will have a transcript of the information that has been presented during the meeting. If you have a question or comments, we have two microphones down on the floor, and if you would, come to the microphone, give your name, affiliation and where you live so that we can again identify you in the records, because we may want to get in touch with you. What are we interested in? From the audience participants we would like to hear of the experiences you have had, your companies have had or your unions have had in cold operations, whether it is in doors or outside. We would like to know your experiences and the work practices that you may have put into effect to alleviate the effects of the cold upon the individual. We have had to make a few changes in the program since it was print ed. Unfortunately, two of the scheduled speakers have had very ser ious illness's in their immediate families and were not able to be here. We have done some rearranging and we hope that we will be able to do what we had planned to do. I would like also to impress upon you that the remarks that the ex perts are going to make are their own. This does not necessarily mean that they are the beliefs or the policy of the National Ins titute of Occupational Safety and Health. It is their own remarks. Sometimes some of the people may give conflicting evidence or imp ressions, but this is part of it. In the end, we are committed to prepare a criteria document of work practicies for cold weather operation. There are many occupations and industries in which cold exposure is common. Practically any area in this country at some time in the year involves cold weather operations. In parts of the country the cold weather operations will cover a large part of the year. There are industries in which cold exposure extends during much of the year as part of the require -52- ments of the process itself. We would like today to highlight a few of the various problems. We are interested in cold weather and cold exposure, but what is cold? Cold depends upon, among other things; on the individual, what the individual is doing and the clothing being worn. For the little old lady sitting in a light calico dress in her rocking chair, 80 de grees might be the beginning of cold exposure; for the person in an office with light office clothing, 60 degrees may be cold weather; for a person lightly dressed, or dressed as we are, who is outside doing light work, 40 degrees may be cold weather; for an individual who is working moderately hard, with even fairly good cold weather clothing, 20 degrees can be cold weather. So cold weather and cold exposure are relative. It depends on many factors, some of which we hope to bring out today. In thinking about cold, we have to consider the various types of cold exposure. There is "acute exposure," where the individual may be exposed for only very short periods'of time. The effects may be quite different from those for the individual who is exposed eight hours a day, day after day, for a lifetime. There are the specific effects of the cold itself, such as frostbite. There are also other consequences. If cold interferes with the other senses, it may have rather serious safety implications. If it has an effect upon other factors that are present in the environment, this in itself, may have other implications. We will try to summarize what we know at the moment, and try to put this in the framework of a practical approach to the solution of the problems. On your program Dr. Horvath from the University of California was listed as the individual who would talk about the physiology of cold exposure.responses to cold and aspects of cold acclimatization. Dr. Horvath could not be here. Dr. Goldman from the Army Research In stitute of Environmental Medicine up in Natick, who has had 19 years of cold weather experience volunteered to review these problems for us. Ralph. DR. RALPH GOLDMAN (Army Research Institute of Environmental MedicineNatick, Massachusetts): I am going to start by pointing out that man's ability to get along in the heat' or cold is a matter of bal ance. Factors increasing heat production include: resting heat pro duction, the specific dynamic action of food, various diseases, the state of consciousness, tension of muscles, and exercise or shiver ing. All of these help increase the heat production and therefore lower the temperature at which man can be comfortable. The more heat you are producing, the better off you are in a cooler environment. On the heat loss side of the balance, of course, wind speed plays a tremendous role in heat loss by convection. Surface area is import ant; those who have seen pictures of Alaskan sled dogs or people, sleeping in the cold, may have noted that they tend to curl up in a -53- tight little ball. This reduces surface area, therefore reducing heat loss. Evaporation can be an important avenue of heat loss. You would like to prevent sweating, because when a man is heavily clothed, the sweat produced at the skin is difficult to evaporate, and if clothing gets sweat wetted, sweat remains to be evaporated, in many cases, after the need for evaporative cooling has passed. Specific mechanism for increasing heat loss include, of course, in creasing the circulation to the skin. Conversely, to decrease heat loss, vasocontriction, the reduction of the blood flow to the skin, becomes a major feature. In the heat we depend on sweat evaporation for heat loss. In the cold, we still lose some 25 percent of our calories by evaporation; half from diffusion of moisture from the skin; the other half comes from the respiratory tract. Indeed, respiratory heat loss becomes an increasing avenue of heat loss as a man works in the cold. These, then are some of the specific factors in cold tolerance. First of all, increasing heat production by muscular activity, in creased muscle tone or frank'Shivering. Slight shivering isn't terribly effective, although shivering can increase your heat pro duction by a factor of bur or even five. However, a man who is shivering at 400 to 500 Calories an hour is no longer functioning. He is just standing there shaking. Voluntary contractions, e.g., isometric exercise, don't work terribly well; if you just sit down and do static contractions it is not a very effective way to in crease heat production. Thus, the trick must be more on the de crease of heat loss than the increase of heat production. There are some long term changes that take place; biochemical ef fects of cold acclimatization, and circulation changes witch de crease heat loss by decreasing the blood flow to the skin. The noncirculatory factors include any decrease in body surface area; and perhaps laying down a little bit more fat. When the mini skirt first came into style, everbody was talking about the fat knees the girls might develop. Animals get a little better fur in winter, but man has already lost most of his fur. One of the problems of cold protection is the variability of heat production. Sleeping, you have a low heat production, at office work a bit more, and obviously people who routinely work as carpen ters, stone workers, etc., know they have to be reasonably fit for such work. However, if you suddenly move the worker to a cold en vironment, and add 20, 30, or 40 pounds of clothing to the weight the man must carry around, this increases the work, and also mov ing in such multilayered, bulky clothing, can effectively add 15 percent to the energy cost above the c&st of the added weight. In addition, if you have weight carried out on the extremities, i.e., out on the end of the lever arm, your energy cost is dis proportionate. If you are wearing appropriate shoes for the cold (sox and boots that weigh two or three pounds each) you multiply -54- that by five, and if you are wearing the six pounds of footwear which you may very well need in the Arctic, that is like carrying 30 pounds on your back. So the means of protecting the man against the environ ment have a cost in terms of the physical work, and the worker who may be getting along reasonably well otherwise, when faced with walking through deep snow with the energy cost increasing by a factor of six, seven or eight, depending on the depth of the snow and whether the man sinks in, may get into difficulty. This has to be addressed in selecting men for work in a heavy work occupation; when suddenly hav ing to have all this protection they find it costs something to carry it. Turning to the specifics of body temperature, we have depicted the body temperatures of man, across a wide span of air temperatures. No tice that the rectal temperature doesn't fall too much, but there is a distribution of temperatures across the body surface when man goes from warm to cold. The head temperature falls; the hand falls rather dramatically; the feet are among the most critical areas to keep warm, in part because they are at the end of the pipeline, with tremendous counter current heat exchange between the arteries bringing warmer blood from the central body and the veins coming back from the feet with the cooled blood. When we look at this in man we can define two areas, a rather narrow periphery which is basically the layer from the subcutaneous fat, plus the layer with the circulatory flow next to the skin, to the skin its elf; there is also a film of still air and/or clothing next to the skin which can sometimes be considered part of the shell. The second area in the core, where most of the heat is produced, and is then trans ferred out to the skin by the circulation, through the fat. Once you vasoconstrict and thus cut down the flow of circulatory heat through the fat layer, the more fat you have the more insulation you have. We can study whole body heat loss most effectively in water, because to get air temperature cold enough to drop the deep body temperature, you usually wind up freezing the skin first. Much of the results from studies on water immersion relate to cooling in air. Sitting still, nude, in unstirred water, your drop in rectal temperature in cold water might be some 1.2C although you would produce about 4 l/2 Calories a minute. When you start work, you do increase your heat production, but you are also cooling more rapidly. Why? Very simply, you are disrupting whatever still water layer you have next to your skin and also disrupting your vasoconstriction; i.e., you are shunting more blood from the core, where heat is produced, out to the skin and, if dressed, you are a little bit better off then you were, if dressed, at rest. However, if you are nude, even working 9 Calories a minute, which is an exhausting level, you still, on balance, lose more heat and cool more rapidly than you do sitting quietly. Of course, if you sit still and have clothing on, there is quite a benefit; you lose much less heat with clothing and even working, as long as you are reasonably clothed you can retain a great deal of the body heat production and the heat loss as affected by vasoconstriction and clothing. -55- When you lose too much heat (i.e., suffer whole body hypothermia) fatigue is acute and much more than expected; there is muscular weakness, abnormal behavior; people do very funny things when they are throughly chilled; there may be a depression of con sciousness; cessation of shivering is one of the signs that you may already be in the area where temperature regulation mech anisms are over stressed. Of course, the usual problem in the cold is not a fall in deep body temperature but in the extremities. When reasonably act ive, at minus 20 degrees fahrenheit man needs mittens, the best possible mittens, but they only give him two or three hours of protection if he is not active. If you put the man in a pair of shorts and gave him insulation around his hands, it would probably do considerably more good then if you put it around his torso; so the problem really is the extremities and the vasoconstriction which reduces heat in put . Specific protective mechanisms include cold acclimatization, and here we have some temperatures of the fingers in a cold room. Fingers cool quite rapidly until interrupted by a cyclic rewarming; this mechanism is called a cold induced vasodilat ation, it is a CIVD. The hand cools toward ambient tempera ture, but eventually the cooling pattern is interrupted, if you are reasonably warm on your torso The white man outdoors throughly chilled will exhibit this CIVD response, but the Eskimo doesn't show as much of it. Why not? He has a better deve loped protective mechanism; one aspect of cold acclimatization is that you routinely flow more heat to the skin. His finger doesn't cool as much, to begin with. In addition, he may not shiver as much, because he has another mechanism, "Nonshiver ing thermogenesis". It is a mechanism whereby a chemical change in the way the body metabolized fuel, supplies extra heat to make up for the shivering, so that you don't have to shiver as much. In essence, man may acclimatize to cold. However, probably the single most important aspect is getting used to the cold is learning how to live in cold, how to use protec tive equipment, and perhaps keeping your skin dry add cloth ing dry. Here is another example, from a hand immersed in ice water, showing just how important and massive this cold-induced vasod ilation (CIVD) can be. As long as this continues, you will not get frozen fingers, in our experiences in an experimen tal setting, once cold-induced vasodilation started it was difficult to freeze the finger. Now, we are talking about heat loss, and here we have a study in which we gave a man alcoholic drinks, hot drinks, room temperature water, or he smoked two cigarettes. Here is his actual heat flow; i.e., the heat loss available .to the hand. -56- The alcohol does increase the blood flow. Smoking does de crease circulatory heat flow by a bit more than the cool water control, at least in the first fifteen minute period By the second 15 minute period the benefits of the hot drink are lost, the alcohol is still helping keep the man's hands warmer, and smoking still is a disadvantage. However, by the end of an hour, except for smoking, there really isn't too much difference. This temporary additional heat to the hand is being faken from the body's core, so the man who has had the alcoholic drink is actually losing his body heat at a greater rate. Thus, if one has to stay out in the cold it is dangerous to have alcoholic beverages. On the other hand, if one has to go out and work for an hour, a little alcohol is not necessarily a bad thing. The heat to the hand benefit surpasses the colder core, and also the pain/discomfort sen sation is a little numbed; however, if there is prolonged ex posure, the man has a much greater risk of hypothermia, if he has an alcoholic beverage. Here you see two cooling curves of .the same finger; actually, it was mine. In the one case, we had arubber band completely occluding the blood flow, so that therewas no way I could get any circulatory heat to the fingertip, and in the other I was thoroughly chilled, but I was getting my normal heat flow. When you are thoroughly chilled, you may get seven Calories per square meter of surface area per hour, and v/hen you are exercising you can get up to 440 Calories. So the range of blood flow to an extremity is tremendous, depending on the activity. We have an experimental situation where we can pull tempera tures from a refrigerated chamber at any temperature and wind speed we would like, and expose a finger and look at the risk. A finger so exposed, starts in cooling but then may start warming. The cooling is interrupted in about 12 minutes by a CIYD, a warming response. You can characterize an individual as a good rewarmer if he rewarms in something between three to five minutes; the average is five to eight, and slow is about ten mintues. So this is a slow rewarming, and other in dividuals under the same circumstances, may actually cool and then suddenly freeze. This is frostnip and the sudden temperature jump is the heat released by ice crystallization. Notice that you don't freeze at 0C (32F; the skin is dry, and can be supercooled quite appreciably. However, if the skin is wet, you can freeze at -0.6C. So keeping the skin dry is very important, indeed one of the most important feat ures of any cold exposure. Constant cold injury shoud be mentioned. We work on this extensively, as a function of the temperature of the metal surface and the exposure duration. You can talk about time limited tolerances. It is very important not to touch bare metal at -20C with your hand, and if your hand is cold you will freeze to the cold surf-ce and have an instant frost- -57- bite. If your hand is wet, even taking ice cubes out of the freezer, you can freeze right to the tray. Finally, sleeping in the cold is sometimes a problem. One of the problems is cold diuresis; in the cold, the shunting of the blood to the core increases renal blood flow, and the need to go to the bathroom increases. Those of you who camp in the winter know that if you don't go to the bathroom before you crawl in your sleeping bag, you are almost sure to have to get out to do so before morning. So, some of the various things that compound a man's staying in the cold, are compromised by frequent urination and possible dehydration. CHAIRMAN HENSCHEL: Thank you Ralph. Dr. Doolittle was to have given a talk on some of the medical considerations. Dr. Doolittle was the Commanding Officer of the Arctic Medical Research Laboratory at Fairbanks. He also had an illness in his immediate family and was not able to get here. We were fortunate to have Captain Hamlet, who spent three years working with Dr. Doolittle in Fairbanks, and who knows the problems of operating in the cold, to speak to us on some of the medical problems in the cold. Captain Hamlet. CAPTAIN MURRAY P. HAMLET, YC, USA (Director, Experimental Pathology Laboratory - U. S. Army Research of Environmental Medicine): Thank you very much. It is too bad that Dr. Doolittle could not be here. He could add a great deal to any presentation on cold injury. I think the green suit should impress you about one thing, and that is one of the major sources of information about man's functions in severe climate is in the army----- or military in general. Some of the statistics and figures that I will read to you a little later will impress upon you the continuing effort that the Army has and the continuing effort that is being placed in research for maintaining the function of the soldier. Much that is gleaned from war time situations in which men don't have much choice about where they play war, but some of the epidemiological studies have been done in Alaska. What exactly is a cold injury? The first illustration is a case of a mild frostnip. This was produced in our laboratory, a frostnip of the digit in that experimental model. This is a freezing injury, one in which the surface is frozen. There is crystal formation within the skin, but no serious loss of tissue. Next is a case of frostbite of the knees, of a fellow while changing tires on his car in Alaska. This is a frostbite -58- of the hands of the same individual who had the frozen fingers trying to work on his automobile. And this is the same in dividual with a frostbite .of the feet, with the subsequent loss of digits and function. The non-freezing cold injuries that I am talking about today are Raynaud's phenomenon and angina pectoris, associated with coronary constriction. Some of the other problems in the cold are accidental hypothermia, trench foot, increased heart rate and asthma. There are things that we should all be aware of. They are. all intensified by cold exposure, and hopefully with in the next few years there will be more work done on them. The military requirement is somewhat different from the in dustrial requirement, but the knowledge is easily applicable to both areas. It has the potential for being very important in the next 20 years, as we develop more and more of our Arctic and northern mineral potential. There are many jobs that are now cold exposure type jobs, and I hope to touch on some of their problems as the lineman, who are in cold environments. It is hard to tell just how much the cold has affected their function up to this point. Again, I would encourage you to comment on this. Anytime man is forced or enticed to function in severe weather conditions, casualties can occur. In a military situation this decreases the operational capability of the fighting unit. In industry there will be a severe decrement of performance, and if key individuals are involved, this can lead to lengthy de lays and disruption of production. Let me read you some figures that you should think about. There were over 90,000 cold injury casualties in World Ware II, not counting the people killed because they were cold injured be fore they died. We had 9,000 casualties in Korea, and the coldest it got was a minus 10 degrees farenheit. Most of these were under very serious conditions. People pinned down for very long periods of time, but it points up the fact that a frostbite is a major military medical problem. Eighty-five percent of the cold injury casualties at Fort Wainwright, Alaska and Fairbanks in one year were incurred by persons with out adequate clothing or persons who were not wearing the clothing properly. Keep in mind that the military issues a very functional and very adequate clothing ensemble if worn properly. The average hospitalization time for the past year in the Army for cold injuries was eight days, and the current cost per day is $90.00. And this was without any amputation. In the last fiscal year there was no amputation of military persons. If severe tissue loss occurs and amputation is re quired, long convalescent periods are in order. None of -59- these figures take into account the second category of medical problems influenced by the cold. The 52 year old man has a myocardial infarction while shoveling his walk. The person who, when he is exposed to cold, can't seem to get his hands and feet warm. He experiences cold, pain, loss of dexterity and possibly frostbite. Very careful medical evaluation should be made of employees who may be subjected to cold exposure. That's meat processors, fishermen, linemen, underwater divers, outdoor workers, fuel handlers, pilots, oil workers and whoever. These are the in dividuals who require some extra attention in determining whether they are fit subjects to be exposed to the cold. Now let me describe some of the major medical problems and then cite an example which most of you have some familiarity with. The medical problems influenced by the cold include Raynaud's Disease or Phenomenon and angina pectoris, asthma, and some other allergies. Raynaud's Disease is a condition in which the sympathetic nervous system which controls peripheral vascular tone is aff ected by vibration or by cold. The term "occupational Raynaud's" has come into vogue to describe a peripheral vascular shut down associated with persons who subject their arms or their bodies to vibrations. This includes chain saw operators, jackhammer operators and so on. The ones we are most con cerned about are the individuals who, when subjected to cold have this same peripheral vascular shutdown. There are varing degrees of response, but these persons are at very great risk in the cold. Dr. Goldman showed you some CIVD response. Different individuals respond differently in that kind of situation, and we feel quite strongly that these should be screened out of the population to be exposed to any cold environment. The second condition, and one which will be receiving some effort in our laboratory in the future, is angina pectoris associated with inhalation of cold air. Angina is radiating upper chest pain, associated with decreased cardiovascular (nutritional blood flow to the heart muscles. There is clear evidence associated with this that if allowed to breath cold air, they will have bouts of angina. There is also some clinical evidence to support the idea that inhalation of cold air can bring about constriction of coronary vessels, increase the heart rate, increase the blood pressure and subsequent coronary embolism and mycardial infarction. It is standard procedure in cold for physicians to recommend -60- the use of a scarf or surgical mask, to help preheat the in haled air for their angina patients. There is even available a small battery-powered heated mask for angina sufferers. Again, these individuals should not be exposed to the cold in a working environment. Asthma patients also suffer bouts of their disease when at tempting to exercise or work in the cold, and depending on the severity of their condition, the degree of pulmonary path ology and other ongoing diseases, these individuals should be carefully evaluated for their ability to function properly in the cold. For sure, they will not be any better in the cold. Cold urticaria or rash or hives is not a common entity, but when it exists, it clearly limits the function of an individual in the cold. There is evidently humoral(antibody produced in these individuals against cold. It is an interesting dis ease, and one on which there is very little information avail able currently. We hope to do some more work on it ourselves. Let me now turn to the drugs. We are a drug-oriented society. We take a wide variety of medications and an equally large variety of prescription medications, for all kinds of illnesses and maladies. The use of these drugs is contra-indicated in the cold. Drugs that affect peripheral vascular tone, drugs that affect sweating, affect a person's mental function, are clearly contra-indicated in severe environments. The physician must take great pains to identify all medication used by the patients, either routinely or medications available to him for his use when he feels he might need them. Many will render him more susceptible to cold injury. Alcohol ingestion leads to peripheral vascular dilatation and increased core heat loss with impairment in judgment; none of which are advantageous in a cold environment. Smoking causes peripheral vascular constriction, decreasing blood flow to the extremities and renders an individual more susceptible to cold injury. There is a racial difference in susceptibility to cold injury. This comes from data in the second world war and Korea and from Alaska. Blacks are, statistically, more susceptible to frost bite. Blacks are, however, completely capable of functioning and carryingout their mission on the job when properly trained and properly motivated to follow the doctrine associated with maintaining one's clothing properly. Dehydration is a problem in the Arctic, because the thirst mechanism doesn't function properly. The field commander is taught to look at the color of the urinations around the tent and the camp, because people can become dehydrated over a short period of time. He should instruct the people to stand in line and drink a canteen cup of water three times a day in order -61- to maintain a decent state of hydration. Constipation going along with dehydration is a major problem and the nutritional problems, poor nutrition or low caloric in take increases the susceptibility to hypothermia and frostbite, but I will get into these a little later on. Let me speak for a moment now about things we know most about) that is frostbite and accidental hypothermia. The illustration I gave you attest that frostbite is not a minor problem, but one which can lead to severe disfigurement and subsequent loss of ability to work. Frostnip is a mild form of frostbite. I put this slide up to demonstrate or to show you some of the areas, pathogeneisis of how someone gets frostnip and frostbite. The ice crystal formation is one of the major problems. It has a severe phy sical disruptive effect on the cellular structure of the vessel walls, especially capillaries and you get a micro-vascular shutdown and subsequent loss of nutrition and oxygen and a build-up of cellular byproducts, and this causes the death of the tissue. I won't go into the treatment or other pro blems in describing frostbite. If anybody has any specific questions about this, I will be happy to try to help you out. I can tell you that there are no good treatments for frostbite, and to sum it up, all we do is rewarm and wait and see. It is not uncommon for a frostbite patient to be in the hospital many, many months. And early diagnosis of frostbite is something I should per haps tell you about. When this is incurred it is not a pain ful injury. As you warm them up it is painful, but when they get cold it is not. All there is is a blanching of the tissue, and most of the time they have something else on their mind, so they do not recognize that they are being frostnipped or bitten. Actually, in an experimental situation frostnip is a little tingling pain, but nothing that one would recognize if you had your mind elsewhere. Depending on the severity of the injury, there can be mild edema, swelling, a blister formation, and complete even necro sis of the tissue. All of the injuries, even the mild injur ies, often require physiotherapy. So here again, we are talk ing about a long term injury and not one that can be handled gracefully. There is the micro-vascular plugging, after frost nip. You can see plugs or breaks in the normal blood flow in the capillaries. Hypothermia is a little different problem. Under certain conditions, such as cold water emersion or with light clothing in excessive cold, the body's normal thermal regulatory mechanisms can be overcome. As the body tempera ture falls various things occur, including shivering and coma. When one is fatigued, which is very common in cold exposure, -62- actually you don't know you are getting cold. One has no perception of whole body cooling until shivering starts. There is muscle weakness, lassitude, abnormal behavior and mentation. People do very bizarre things when they get cold, and nobody, including the Russians know much about that. It is identified clearly in mountain climbing con ditions and survival-type situations, but no one knows just how much one's judgment is impaired in the cold. Extreme hypothermia patients are presented to a hospital essent ially dead. They have no palpable pulse, no audible heart beat. They are essentially dead. They do, however, many of them, have electrical activity still present in the heart and are completely capable of being resuscitated if one starts it early. We fee1 very strongly, after looking at the world's literature on resuscitation of hypothermics, that internal methods of rewarming are by far superior to external methods. The use of arterial-venous shunts or warm peritoneal dialysis and good clinical management has proven extremely successful in the resuscitation of persons whose body temperature has dropped to as low as 65 degrees farenheit. These people suffer no after effects of hypothermia, and once they have been re leased from the hospital they have no alteration in mental function or anything else. The key to success of functioning in the Arctic is the ability to prevent frostbite or hypothermia, and this is going to be your job and our job for the next few years, and I wish you all the luck, and I wish you would help us. Let me describe a situation that a large number of you or some of you may have some input to. What I am talking about is the projected development of the Alaskan pipeline, which will go from Prudhoe Bay across one major mountain range, down through Fairbanks, down across another mountain range, a major fault line, another mountain range, a major fault line, to the coast at Valdez. This is a monumental undertaking, and one in which a great number of people will be exposed to cold injury pro ducing conditions. People in the oil and pipeline industry are mostly from the south. Most of our oil has been developed in the south by people from Texas and Oklahoma, who have little or no under standing of what they are going to be confronted with in the Arctic. There are miles and miles of mountains, snow and cold, eight hundred miles in fact. In the path of the pipeline is the town called Wiseman. It is unbelieveable, but the tempera ture there can drop to minus 57F. Without experience one has no conception of what it is like, what functioning in that is like, unless you have been there. Two things are evident: First of all, the minus 57 is very oppressive. The other thing is the darkness and the ice fog. -63- Even at midday, noon in Fairbanks, Alaska, the ice fog which is the result of temperature inversion limits visability. The pollution levels are astronomical in Fairbanks, where people are working and the automobiles are going. This is going to be a very big problem and nobody knows how industry is going to function in that kind of environment. The work sites will be heated and at various times the indivi dual will have to travel from one site to another, and most of them will be exposed. There are other stresses in the Arctic which I won't dwell on at all, the long darkness, the subsequent alteration in the normal biological rhythm, iso lation, and in the summertime, the unbelievable mosquito pro= blem and things that we have never been confronted with before in industry but things that we are going to have to answer. The new comer to the Arctic is clearly more susceptible to cold injury problems than the person who has lived there for a number of years. If you put them all together, that is the novice, the enticement with money rather than motivation and desire, and the poorly equipped and marginally equipped, sit ting in that little town of Wiseman in the Brooks range at 50 below zero, you add a little alcohol to it, and you are a prime target for real problems. Let me say no one is comfor table at 50 below zero, but almost everybody can tolerate it if he is properly prepared mentally and physically. There is ready testimony that they can put up with this if they know what they are doing and have proper equipment and confidence in the equipment. CHAIRMAN HENSCHEL: Thank you, Dr. Hamlet. I would like to mention one other thing in relationship to the effects of drugs - the interaction between drugs and cold. Dr. Hamlet remarked about some of the effects of drug tolerance in cold. There is also some animal work that shows that cold weather increases the toxicity of the toxic materials. The toxicity may be increased manyfold when the temperature of the environment which the animal is exposed to is decreased. We will now go back to Dr. Goldman. He will talk to us about what he promised at first - the assessment of the cold environ ment and some of the protective devices that are available or should be made available. DR. GOLDMAN: Thank you. Well, as Captain Hamlet said, there are two domains most of us are used to working in, in the cold. Some have experience at perhaps 0C, and maybe -20C if you live in New England, but people can function reasonably well to about -30C, and when it gets below that, it is a whole new ballgame. -64 One of the terms I did not introduce before is something we measure with a heated copper man; it is the "CLO" unit of in sulation. The CLO concept was derived ini.the 19^0s, as an expression of the thermal resistivity of clothing to heat loss. The CLO consists of two components; the insulation of the clothing material itself (Iclo) and the insulation of the air layer around the surface (I^T- The CLO was defined as a fun ction of; a) the difference between the skin and air tempera tures b) for comfortable standard man c) in an office environ ment, d) wearing a standard business suit, and e) the heat he had to lose through the suit. The metabolic heat production, less the 25$ lost by evapora tion worked out mathematically that one CLO became defined as an insulation unit which allowed a heat loss of 5i Calories per square meter of surface area per hour for every C gradient between skin and air temperature. If you know the insulation of the clothing, you can pretty well definethe heat loss for any air temperature. If one is wearing one CLO, he will lose 5-5 Cal/1V[2/hr/C0, with two CLOs he will lose half as much, with three CLO 1/3 as much and so on. You can actually plot the heat loss value as a function of the insulation; a fatigue uniform plus helment and field pack, with out battle armor is 1.4CL0, and the same plus body armor 1.6 CLO. A man who at rest is producing 400 BTU an hour, and therefore would not like to loose more than 300 by radiation and convection through his clothing, (because he is going to lose 100 BTU or 25$ by evaporation) will be comfortable at 67 or 68F; but at rest with the armor, he will be comfortable down to 64 degrees. You can translate this same relationship all the way down to many degrees below zero. Unfortunately, as you start getting below about 30F, the best clothing we can deliver starts to be inadequate at rest. Activity is this a very important point in the relationship be tween the degree of frostbite and what the man was doing when he incurred frostbite. If he was a prisoner, 33 percent; if he was standing guard - a fairly low level activity -- 131 percent; walking, 179. riding 85; casually sleeping, 60. If he was pinned down, he was both afraid and sombody was shooting at him--and if you are afraid you don't show those spontaneous rewarming CIVD, ?nd so if you are thoroughly chilled and frightened you have increased risk of cold injury. So you see the activity is very important, since action is one way around the cold problem. The other critical point has to be clothing. Here is a percent distribution of injuries; 65$ of the people with cold injuries were inadequately clothed, 20%> didn't wear the clothing adequat ely worn; e.g. the good cap has ear flaps, but the ear flaps were open or the gloves were good but were wet. -65- Only 15% of the cold injuries had adequate clothing. So clothing seems to he one of the major solutions, and the gen eral principal for clothing is something called the layer principal You build your clothing system by adding layer on layer of insulation. This gives you flexibility. As you start to work you can start peeling off the clothing layers. This is essen tial, because if you don't you are going to overheat badly. In fact, the usual problem we talk about with the troops in the Artie is, "Let's get the troops in out of the hot cold." Soldiers don't stand around; they work. And when they are clothed so as to protect them at rest, then during work the sweat they produce sweat wets their clothing, reduces the insulation and wets the skin. This is very undesirable. Plus, of course, the weight of the material adds to their heat pro duction. Now insulation is thickness. In one of the new materials, fiber fill, a polyster, there is a great deal of loose bulk and the thickness provides good insulation. We are hoping to build a new, thick clothing systems using this type of in sulation which isn't very heavy. Now what does CLO do? Here we have, as a function going from 88F down to 58F. the dry heat loss, i,e. the radiation plus convection heat loss in Calories per hour. Assuming that a standard man has 1.8 square meters and must have, for comfort, a mean skin temperature equal to or above 32C (90F), if you are wearing one CLO, which is about what most of you in the audience are wearing, at +50F, you will lose perhaps 120 Calories an hour. If you are going to talk about temperatures below 0C (32F), and if you wouldn't like to lose more than about 100 Calories an hour, you already need up to five CLO. This exceeds the in sulation of the best uniforms we have ever issued, that a man could ever do any practical work in. How do these CLO insulation values compare to the actual heat loss? Here we have a study of 12 different sleeping bags, with bags arranged along a line in terms of bag insulation value, and here we have the mean heat debt. Note that the body tempera ture fell by a varied degree, and notice that if two bags have the same insulation, the men sleeping in them had the same loss. Heat loss follows insulation quite nicely, so these CLO insula tion values do relate to how much of a problem the man will have Now, in the cold environment there are two major factors you must consider. One, as we've already discussed, is temperature, but the other is the wind. Wind increases the rate of heat loss both by penetrating the clothing and by reducing the still -66- air insulation. Those of you who aren't familiar with this still air insulation, will suddenly sense a difference when you wave your hand (demonstrating with the hand), because when your hand is still it is surrounded by an air layer which traps the heat from your skin, and any even minor motion disrupts that still air layer. So wind is a major feature in accele rating heat loss. Over almost a hundred years, beginning from 1804 to 1826, the concept of the cooling power of wind grew, and was developed and extended, until finally today it exists most familiarly in the "Wind Chill index". The Wind Chill index is probably not the best index in the world. There are many things wrong with it, but it is widely recognized and used as a way to measure relative range of cooling in en vironments with different temperature and wind combinations. One takes the air temperature (from +80F to -80F) and the wind (from essentially zero to two, three, four, five, ten, and so forth miles per hour) and calculates Wind Chill by this rather complicated formula, which assumes a 91*4F mean skin temperature. So at any given temperature, as the function of the wind velocity you calculate the Wind Chill index in Cal ories per meter square per hour; e.g. 1400 Calories of Wind Chill level is one at which exposed flesh will supposedly freeze in about one hour. Now, how good is the index? In fact, the combination which calculates to 1400 Calories doesn't really represent 1400 Cal ories of actual cooling. It is not a good number, but it is true, and quite reliable, that a condition in which the Wind Chill is loOO is worse than one of 1500, which is worse than 140, etc., so it is a relative way to rank order the combined effect of cold and wind. It is the best thing around. At the 2200 level, exposed flesh will in fact freeze in less than one minute, and we used to say that if the Wind Chill was less than 1400 you were perfectly safe. Some of you may have picked up the Wind Chill cards handed out at the front desk, and you will notice that we have changed that "perfectly safe at less than 1400" to reflect the fact that in Korea we took most of the cold injuries between roughly the 600 and 900 level, but these took five to seven hours. This is still a practical work per iod. It was frequently a cold damp situation; not much below zero at all. Under these conditions, the man did not get the tremendous stimulus of "it's tremendously cold out; you'd better keep your gloves on; you'd better stay warm." And he also had wet clothing; down at very low temperatures we problably don't have wet clothing, but here clothing gets wet and stays yet. So Wind Chill is a useful index. It was used to calculate the number of cases of cold injuries as a function of the daily average Wind Chill. It has also been used, in our own studies with frostnip, to look at the Wind Chill in terms of the 1700, -67 1600, 1400 levels and the occurence of "frostnip". "Frostnip" is an experimental exposure which we can terminate safely, but if the subject leaves his finger in that wind tunnel a little longer (three to five minutes longer) we will actually get frost bit. At below 1400, we can almost never get frostnip, with one exception; if there is snow or blowing moisture, or if the skin is wet. In that case you don't supercool, you freeze shortly after cooling below 0C. You get to -0.6C rapidly and there isn't time for the CIVD phenomenon to start the rewarming pro cess before freezing occurs. Now, many of you are probably more familiar with Wind Chill in terms of the Wind Chill equivalent temperature, so let's talk a little bit about this equivalent temperature. Scientist translated these wind Chill curves back down to a zero wind speed, or a "calm air" speed. If the wind is ten miles per hour and the temperature plus 40F. the equivalent temperature is +28F; this means that you would cool as if you were in a 28F environment without wind. Your initial rate of drop will be as fast as if you were at the more severe equivalent tempera ture. So whether we talk "Wind Chill" or "Wind Chill Equiva lent Temperature", we are talking about the same thing. Where does frosbite occur? Twenty-six percent of the cases are fingers; twenty-one percent, toes; twenty percent, ears; forty percent, heel and foot; twelve percent, nose; two percent, face. All others amount to nine percent, and usually are associated with somebody spilling gasoline or other very cold liquid or kneeling on the frozen snow. Note that these are mostly the extremities, and these are the parts which have had their blood supply reduced by vasoconstriction. So protection must be afforded by protective clothing. A glove is good, but it has more surface area than a mitten; you've got five individual fingers all losing heat. A mitten is better. In a glove each finger is separate; in the mitten you can ball you hand up and reduce the heat loss and rewarm your fingers against the palm. You can't do this with a glove. Here is a man wearing no mittens, considered as "control or an Arctic mitten or a light mitten. If you take the bare hand "control" performance as 100 percent, wearing a light mitten knocks it down a little bit; however, wearing a full Arctic mitten on the hand cuts this down appreciably. If you are oper ating a radio control with a mitten, or are a switchboard oper ator, these effects of the protective clothing items are in fact worse than the temperature effects per se. If you look at the average efficiency at -25C for one hour or -4lC, the temperature effects produce a significant decrement in perfor mance, but it is no worse than if you kept the hand warm and wore the Arctic glove. So there is a price to be paid for avoidance of hand frostbite and cold injuries. You can pro vide the protection, but you lose the manual dexterity. We have not found a way around it. -68- The footwear we use is a vapor barrier boot. It is quite effec tive, but weighs three pounds. The newest boot under develop ment weighs 1.7 pounds, but even this is like carrying 16 to 17 pounds on the back. Fortunately, we don't have to worry about manual dexerity on the foot, but there is the problem of keep ing the sox dry, and this is a real problem. With a raukluk, i.e., a boot with normal vapor permeability, the sox can be thicker and hence warmer, providing more insulation, but the problem is that it gets wet. You have real problems then. Wet insulation has substituted water for the air which is the basic insulation; water is a beautiful conductor, so the mukluk, while it may be very good in extreme cold, probably in not accep table if temperatures are hovering from -10C on up to above freezing. Now on the face, the nose, of course, has a large surface area and has a high risk of cold injury. The flat check bones of the mongoloid type race are believed to be derived from the fact that the youngster with the sharper cheek bones got more cold injury, and no one would marry them.. If you put a face mask on, and this is reasonably easy, but it may be penetrated by wind, or you can put a parka hood on; this is the approach that is usually used in the Arctic. You design a wire rim in this parka hood, and you can reduce the air pentration rather appreciably. This is our current face mask. It does a little bit of rewarm ing of the inspired air. It has a bib, because keeping the neck warm is a real problem since the top of the jacket is usually open. Thus you can keep the face from being affected by high wind chills, but you pay a penalty. You can't hear very well. You can't see very well. The long range solutions are auxilliary heated suits (air vent ilated) but these are still prototypes, twenty or thirty thou sand dollars apiece. There are the auxilliary heated glove and sox, with battery vests, and this has enabled us to keep in active people comfortable, even in a wind of ten miles an hour at -70F as long as the battery power lasted; basically, six or seven hours. So there are technological solutions. But the major solution has got to come through training, and protective equipment - paying off the balance between activity and pro tective clothing. CHAIRMAN HENSCHEL: Thank you, Ralph. The next speaker is Dr. Buskirk, Professor of Applied Physio logy at the Laboratory of Human Performance, Pennsylvania State University. Dr. Buskirk has had experience in cold weather, having spent some time at the Laboratories in Natick, and has had experience with nutrition both in field and in laboratory studies in cold conditions. He will talk to us about the things that one can do to help out in the cold by proper nutrition. DR. E. BUSKIRK (Pennsylvania State University - University Park, Pennsylvania:5 Thank you Dr. Henschel. -69- Man's nutritional requirments have been extensively studied throughtout the years, including the Arctic and the Antarctic. The most widely followed recommendations are those prepared by the National Academy of Sciences National Research Council, with their recommended dietary allowances. This set of recomm endations provide only relatively brief comment about the impact of low ambient temperatures in their nutritional recommendations. The general conclusioni can be drawn, however, that cold, while an important modifier of food and water requirements, is of secondary consequences to those who adjust to the environment through behavioral modification of body heat loss, involving primarily housing, clothing or thermal protection by whatever means. Now, the major factors to be considered in preparing recommendations for thermal protection and other means for nut ritional allowances are; 1.) age, stage of growth, development and maturity; 2.) sex; j.) body size and compositon; 4.) physi cal activity; 5*) climate and thermal protection; and, of course, it doesn't apply to many of the people who worked in the Arctic in the past, but it's still an important consideration and that is; 6.) pregnancy and lactation. Of major concern here is the climate, particularly low ambient temperatures with or without high rates of air movement. Suffice it to say at the beginning, that a good mixed diet con taining the seven basic foods in sufficient quantity, if ad equate calorically, will satisify the nutritional requirements of those working in cold environments. There appears to be no special nutritional problems for man working in the cold other than to supply sufficient calories and related metabolic needs to support his daily energy expenditure requirements. The latter is set primarily by the type, intensity, frequency and duration of the work in which he is envoived. Prior to 1950 good cold weather clothing was difficult to ob tain and that available had relatively poor insulation. Sure you could get good quality clothing, but it was difficult to come by. But since then there has been a marked improvements in clothing. There is, of course, a variety of recreational clothing now that really is quite good and one could get down-filled clothing and new fiber filled clothing. I think in this general area we are much better today than we were just a few years ago. On the basis of current evidence, no more than five percent or (possibly to fifteen percent) increase in caloric allowance need be pro vided for adequately clothed persons working in cold environ ments to compensate for the environment itself; not for the phy sical activity, but just for the environment itself. A small increase in caloric demands exist that is associated with the hobbling effect of bulky clothing, including the necessity to wear bulky boots, uncertain or difficult footing on ice and snow and, of course, as has been alluded to, the possibility of periodic chilling. Now, what about physical activity? Dr. Goldman has talked a- -70- bout this in part, but I sould like to re-emphasize the fact that physical activity has a major impact on caloric require ments, and a summary of a number of investigations in this area will appear in the final criteria document material. Caloric requirements for a variety of activities and daily work regi mens from sedentary to extremely hard work, such as lumberjacking, can be put together and presented. And again, let me emphasize that intensity, type, frequency and duration of the activity is important. In an age where the daily energy ex penditures are generally reduced, there still remain.some jobs with high energy demands. For the most part, these jobs are in the laboring category and involve lifting, load carrying and bodyweight transport for six or more hours each day, and of course the transport of bulky clothing. Ironically, some jobs with the highest energy demands are in the sport fields; for example, football, basketball and hockey players, during their routine practive sessions are frequently forced to work hard for three to five hours per day. These high energy expenditure activities in cold regions would in clude dog sledding, cross country skiing, snow shoeing, fishnet hauling, pole climbing, snow shoveling and, of course, with pipeline activity, a variety of different mechanical and labor tasks. One thing that has been referred to here previously, in terms of fragmentation of the metabolism, is the basal met abolic rate. Numerous studies have been conducted to clarify the impact of climate per se on basal metabolic rate. Such im pact has not been clearly established, although a connection has frequently been made for temperature in tables for caloric allowance. Such a correction has been applied in establishing any recommendations made in this area. Actually, the basal metabolic rate only applies to a narrow range of time under rigorously defined postprandial conditions. The importance here is that the true measurement of the basal metabolic rate cannot be obtained if the subject is chilled or shivering. There is some evidence to suggest that resting metabolism may be elevated in those chronically acclimatized to cold, but the evidence is not indisputable. This is the socalled chemical regulation that was referred to earlier. Another factor in this general realm is what is called the specific dynamic action or the specific dynamic effect of food. A variety of terms have been applied to this metabolic incre ment associated with digestion, absorrition and intraconversion of foodstuffs. While only useful for the regulation of body temperature, this metabolic and eventually heat loss increment is a common feature of man's metabolism, depending on the diet, meal size,, type of food and pattern of meals eaten. This metabolic increment can range from 5 to 15 percent of the ingested calories. In the cold, this thermoganic effect of food remains, and as alluded to earlier, helps to maintain body temp- -71- ature when physical activity is either voluntarily maintained at a near resting level or for some reason cannot be increased; that is, the job demands mental concentration and little or no physical activity. The increase of heat production by nonmuscular body components,as in the liver, the spleen, has been termed "visceral" or "chemical" heat production, and is an identifiable feature of chronic acclimatization to cold in many laboratory animals, but not in man. This chemical in crement would presumably be additive to the specific dynamic effect. In a series of experiments on young men in the armed services, it was concluded that the major factor affecting resting energy expenditure during the day was the specific dynamic effect of food. Food exerted a greater effort on resting metabolism than either moderate physical activity or the natural environment, including cold environments, if the men were adequately clothed. Pre-and postprandial heat production data reveal that peak heat production was reached within 30 minutes after eating and declined steadily thereafter. When a three meal per day eating pattern was followed, resting metabolism followed a progressive upward saw-tooth pattern with abrupt increase in resting met abolism following each meal. Thus the normal individual follow ing regular meal habits exhibits a characteristic diurnal heat production pattern. Since this pattern is largely induced by non-muscular factors, it provides the baseline pattern under lying daily heat production, and is useful for maintaining body heat content in the cold. Since dietary protein elicits the longest specific dynamic effect, it has been postulated that dietary supplementation with single amino acids, such as glycerin; tyrosine, alanine and glutamic acid might be useful to the man working in the cold. While heat increments associated with the ingestion of these amino acids can be demonstrated, the practice would yield no higher heat production values than a mixed diet con taining the large amounts of protein in the diet consumed by most U.S. workers. Now, what about sleep? Food may be a useful adjunct in enhanc ing night time comfort in a cold environment, It has been shown that a 500 or 600 Calorie snack before going to bed may in crease the length of sleep, if thermal protection during the night is marginal or inadequate. Presumably, the extra heat production associated with the meal's specific dynamic effect serves a useful purpose. Sleep disturbance may be important if a person becomes chilled and must cool and/or shiver to keep warm. The necessity to void as a result of cold diuresis may also distrub the continuity of sleep. In other words, a person wakes up and then tries to figure out what to do. It is apparent that a threat to thermal equilibrium is imposed when caloric intake is markedly inadequate during cold exposure. Since shivering is an inefficient way of maintaining thermal -72 balance, the reduction or lack of the specific dynamic effect may be a contributing factor to the drop in body temperature brought about by undemutrition or starvation in the cold. What about preventative measures? Protection against cold can be practiced fairly effectively, particularly if individuals susceptible to cold injury are detected. In other words, you find them and get them out of the exposed population or take whatever measures are needed to protect them. Malnutrition and metabolic diseases such as diabetes, thyroidism, anemia and other circulatory diseases would be important. A supply of proper diet is paramount. Constipation was mentioned as a problem. Workers may allow themselves to become constipated if forced to work in the cold under adverse conditions, because of the inconvenience and dis comfort of relieving themselves. Changes in nutritional com ponents and failure to drink adequate amounts of fluids may be contributory causes. Provisions of warm comfort stations as well as natural food that provides some bulk, plus adequate water should minimize the problem. What about vitamin and nutritional supplements? Repeated ex posure to cold environments in the adequately fed and clothed workers clearly indicate that they can maintain normal neuro muscular function and mental efficiency, and that these fun ctions cannot be appreciably enhanced by giving excessive doses of vitamin C, Bi, B2 or nicotinic acid, or a variety of other things that you can think of, even if given well in the amounts above what is required for adequate nutrition. In other words, if the man is nutritionally well supplied, this is all that is required, presumably. Raising the caloric requirement by the initiation of hard work in a cold environment will raise the vitamin requirement, but the consumption of additional food will usually supply the necessary additional quantities, particularly if the diet is well balanced. Provisions of a balanced diet is essential, however, and you can underline that, because all of the nut ritional elements are needed. There is a tendency to want to depend on convenience foods or easily packaged foods, easily transported foods, but sometimes these foods are not well conceived nutritionally and are in adequate. Therefore, emphasis must be placed on receipt of the balanced diet. Now let's talk just briefly about water in closing here. Since cold acts as a diuretic, the water loss via the kidneys is abnormally high when man is exposed to cold. This water loss can be accentuated if diurectic drugs are taken for any reason, that is, if the person is taking them for relief of -73- hyper tens ion or to reduce blood volume in order to reduce heart work. Cold exposure also induces skin drying and water vapor loss from the respiratory tract. The vapor pressure falls to very low levels in extremely cold environments. The rate of water loss from the respiratory tract is proportional to the vapor pressure on the saturated surfaces of the upper air ways normally maintained between 33 to 37 degrees Centi grade and the vapor pressure of the environment. One appreciates the water loss via the respiratory tract in cold environments when the nasal passages cool. The expired water vapor condenses there and one's nose continues to drip. When hard work is performed in a cold environment, water loss via the respiratory tract increases appreciably because of respiratory ventilation increases. Water loss is proportional to the product of the vapor pressure gradient and the amount of air expired. Thus, water loss from the respiratory tract is proportional to the workload undertaken. About 13 to 33 milligrams of water are lost from the body for every liter of air expired, depending on the ambient conditions. In addit ion to this, and this was alluded to earlier by Dr. Goldman, sweating may be initiated by hard work in the cold because of the severity of the work or because the worker has overdressed, and his clothing creates a hot micro-climate within it. Sweat ing not only increases heat loss, but may also wet the cloth ing, thereby decreasing it thermal insulation. To the worker who can seek protective shelter or who has access to dry cloth ing, the wetted clothing may not be critical. But for the worker who must remain in the cola, the wetted clothing may pose a hazardous situation, for not only is the insultation of the clothing likely to be reduced, but water evaporating from the clothing also cools the worker further as does the evaporation of any sweat that remains on his skin surface. Now, in view of the above, it is imperative that attention be paid to the routes and quantity of body water lost in cold environments, Rates of water loss may be high, while thirst remains underdemanding or water unavailable. Under these conditions appreciable negative water balances can ensue with the largest portion of the body water loss coming from the plasma volume and other extracellular sources. Since effec tive plasma and blood volumes are necessary for convective heat transfer within the body, any appreciable negative water balance can predispose one to syncope and can adversely affect heat transfer and lead to extensive peripheral cold injury. In a dehydrated individual, these problems can become quite acute. Provision should be made for adequate fluid intake, and fluid is perhaps equally important as food; on a short time more important. Although soups and warm beverages maybe pre ferred, water is adequate for the prevention of dehydration. Provision of copious amounts of juices and other fluids, part -74- icularly with meals, is recommended. We thank you. CHAIRMAN HENSCHEL: Thank you, Dr. Buskirk. Dr. Frank Dukes-Dobos from NIOSH, will talk to you about the development of the work criteria document. He put together a few suggestions on what might be included in a work prac tice document. Frank is going to try some of these on for size now. DR. F. N. DUKES-DOBOS (NIOSH - Cincinnati, Ohio); Thank you, Dr. Henschel. I think that the right expression to use at this stage of the game is that we are trying our hands in drafting a standard which we would recommend for the purposes of safe guarding the worker's health in cold environments. As you could hear from the previous lecturers, a great deal is known about the hazards which develop while working in the cold, and also how the workers can be protected against these harmful effects. However, in order to do it correctly, you have to know exactly what the extent of cold exposure is and the ex tent of cold exposure depends not only on the environmental conditions, but also on the clothing and on the work intensity. So if you would like to go all the way and follow this logic, then we would have to require that not only the climatic ex posure that the work intensity and the insulation properties of the clothing should should be measured. It is believed, that at the present, industry would not be able to comply with such a standard, nor would the garment industry be able to supply insulation values of the clothing for all situations. Therefore, we believe that at this stage we should recommend a work practices standard which, if followed, would not require a great deal of detailed measurements. Compliance would re quire only the implementation of work practices, where and when pertinent. This list of work practices which I think would be satisfac tory to protect the workers is compiled in a rough draft. I have copies now here available for you for reviewing. The copies are right there in front of you, and I would suggest that each of you who is involved in the course of their work with health problems of cold exposure, in other words, indus trial hygienists who have to do with workers exposed to cold environment, please avail yoursleves of these copies, because we would like to ask you that after reviewing this draft you comment on the recommendations. We also left some blank spaces for certain environmental limit values and we would like to ask you to fill in the values you would suggest as limiting conditons for each work practive. We also would like to ask you to make any other recommendations you have. I would like to use just a few minutes to familiarize you with -75- the structure of the proposed work practices standard. I will wait until you have a copy and then you can follow my presentation. I am sorry if not everybody has a copy, but there was a limit to the number of copies I could bring with me. I do hope that most of you will have a copy and at least everyone will be able to follow me while I am discussing it. As you can see, the draft proposal consists of two main parts. The first part starts on the first page under "A" Provisions for Hand Protection and the second part is "B" Provision for Total Body Protection. Under capital "A" starting on Page 1, the Provisions for Hand Protection are divided into three major parts, according to the severity of the exposure and the requirements for protecting the hand. In each case, of course, it is mainly directed toward main taining manual dexterity, and under paragraph 1 you see a provision for not too severe conditions. Even if there is no danger of frostbite, certain provisions have to be made to warm the hand, such as providing hot air jets or radiator heaters or making available warm plates which the workers can warm their hands on. The second paragraph deals with more severe conditions, there gloves are required. The third paragraph deals with the cold conditions, the requirement is for mittens, because gloves can no longer protect the hands against harmful effect of the cold. Part "B" starts on Page 2, and deals with "Provisions for Total Body Protection". The first item deals with clothing. It is one of the most important considerations. And the subparagrapsh in this deal with such problems as protection against wind and drafts and protection against wetness. Under extrems conditions where the CLO insulation of the cloth ing does not provide satisfactory protection, the use of aux- illiary heating devices is recommended. If even this is un satisfactory, then the work must be suspended to prevent any harmful effects to the worker. The second major area for protection is protective shelters, which can provide satisfactory safeguards against wind. As you heard in the presentation before wind is one of the most important reasons for suffering harmful cold effects. Shelters could be tents, cabins, restroom, depending on the special situation at the industrial worksite or outside, and depending on what type of work we are talking about. The third item deals with certain work practices which, if followed, can prevent any harmful effect to the worker; nn example for instance is the buddy system. The worker should never be left completely alone in extreme cold. He should -76- be always under supervision, and if not by a specific super visor, at least by another coworker. Also, another consideration, as far as work practices is concerned, is that the work intensity should not be on such a high level that it would cause excessive.sweating, be cause this would wet the clothing and eliminate its insul ating value. Futhermore, there are certain recommendations to permit the worker to become accustomed to working conditions be fore he is exposed to the full severity of the working sit uation, and that would perhaps help to prevent the cold injuries. Another consideration is that the weight of the clothing, which sometimes reaches very high values, should be taken into consideration in judging how much clothing shall be worn because carring anything like 30 or 40 pounds of weight over an eight hour period is quite a workload, and it can not be required that the worker should work as hard with such heavy clothing as when wearing lighter garments. There are other recommendations which we gleaned from the literature which have been shown to have a good effect on preventing cold injuries. For instance, make sure that the worker does not sit constantly or stand constantly. Under working conditions, as in a refrigerating room, he should have the opportunity to change from sitting to standing periodically. Another important requirement is that the worker should receive proper instructions about the poten tial harmful effects of cold and also how he can protect himself from harmful effect, such as clothing practices, rewarming procedure, proper eating and drinking habits, how to recognize excessive cooling of the body when shivering does not occur. Safe work practices can be specified, but may be different in each special industrial situation, and last but not least, proper hygiene practices. Another item is to make sure that the workers have available satisfactory amounts of water to prevent dehydration and also, perhaps to, warm the workers with some hot drinks. There are some special recommendations for refrigerator rooms. The workers are exposed for quite a long period of time, perhaps regularly for eight hours, and the wind velo city of these rooms should be regulated to make sure that it should not cause unnecessarily excessive cooling to the worker. The next item on Page 5 is under Item 5. "Toxic Substances." In the literature we found evidence that cold exposure renders animals much more sensitive to some toxic effects. This information should be included in the work practices -77- stanaara, so that the workers are aware oi xne increased risk and that exposure to toxic substances should be considered very carefully. Eye protection is neccessary only where workers are in the outdoor environment, large areas covered with ice and snow where of course safety goggles have to be worn against snow blindness, against drifing ice particles. Under Item 7, you see a short paragraph on Record keeping. This is an area which is more significant from the point of view of enforce ment, and we did not go into great detail in that area. We think that compliance question can be solved without too much involvement for record keeping, nevertheless, they would have to be recommended. The great problem on the next page, Page 6, is when should we require mandatory environmental monitoring and which climatic variables should be measured. We think, that most of the time dry-bulb temperature would be satisfactory, however, under excessive cold conditions it would be necessary to measure wind velocity in addition to dry bulb temperature. In the next paragraph, No 9, certain medical require ments are mentioned. There are diseases which render the individual more sensitive to cold injuries, and of course, these individuals should be excluded from exposure in cold environments. Finally, on Page 7. there is a short paragraph on the question of protecting older individuals from being exposed to conditions which they wouldn't beable to tolerate satisfactorily. This is a sensit ive question but on the basis of the literature, , under extreme cold conditions such age limits are justified. Now I think that if you have any comments we can discuss these. CHAIRMAN HENSCHEL: If any of you have any comments or questions, please go to the microphone, give your name, affiliation, address and if it is a question, try to address it to one of the speakers. If there are general comments, we would like to hear them, too. The American National Standards Institute has set up a committee which is working on the development of some criteria for cold weather oper ation. Is anyone from that group here to report on what they have achieved so far? MR. YONG CHI WU (NBS-Washington, D.C.): Mr. Hook is not here today, but they have not started anything yet, so we have nothing to re port. But I would like to take this opportunity to address Dr. Hamlet on the question of cold injury. We know that cold injury is dependent on how fast and how much heat is removed from the tissue. If the heat removal is faster than the heat production, cold injury will occur. I would like to ask at what temperature this cold in jury will occur? CAPTIN HAMLETs If I understand correctly, I think that there is some cellular changes that occur only after frostbite, after the -78- freezing of the tissue. The glutination and coaguation of plate lets and white cells that eventually plug up the vessels occurs only after the freezing injury. We have two preparations we have used for studying this. One is the check pouch whiclri.is pulled out and spread over a stage, we visualise through a microscrop, and take movies, and then we have a technique for freezing this at the various rates and cooling i'; at certain rates and warming it at several rates, and then we do an electron-microscopic study on the tissue and combining all of these, we see that we can supercool that to about minus 10 to 3C with no effect. The freezing of the water and then rewarming it, that is when you start getting the emboli and the extravasation of fluids in the tissue out of the capillaries. We are to the point now that we feel that these emboli are not as much a part of the eventual tissue loss as is the loss of vessel integrity. If you could visualize it as a series of fine tubes, capillary beds, you now have the frostbite and these tubes are broken up, and the fluid is trying to pass through. Picture it in the inerstitial space, and we tend to believe now----- and there will be a paper published on this in the next month or so----- that the emboli are probably not that big a problem in the out come of frostbite. We have looked at numerous chemicals and substances that alter this aggravation of platelets, and they didn't seem to alter the frostbite injury at all. Did that answer your question? MR. WU: Well, to an extent, yes, but I would like to know what temp erature it would have to get down to to have that kind of formation. CAPTAIN HAMLET: It has to be freezing. MR. WU: Below the freezing temperature, but how many degrees below and how long would it take? CAPTAIN HAMLET: Once ice crystals form, the ice crystals form in the tissue at zero or minus 5 to 10C we have little control over affects. Once the ice crystals form, injury is going to happen, but it depends on the depth that the crystal formation occurs. In mild injuries it probably occurs on the surface, and as we get deeper and deeper tissue injury, we get more and more loss. MR WU: Yes, but the initial temperature starts to decrease, though. CAPTAIN HENSCHELs When the intiacellular temperature reaches about minus 0.6C that's the point that the damage occurs. MR WU: But the problem is, when you have the tissue in vitro, you are not instantly going to get down to the minus whatever the temp erature is, but in order to reach the temperature what produces the crystals, and I thought you might have the extreme, and I would like -79- to know what temperature and then what would be some criteria to stop some kind of cold injury in a way that you can protect this in some way. CAPTAIN HAMLET: To be absolutely safe, I would say zero. MR WU: Well, we don't get frostbite----- CAPTAIN HAMLET; I think I would. We have cooled dry skin temperature down to minus 13 degrees and had no frostbite, however. MR WU: So therefore it is a temperature and time function. You take certain length of time and your body fluid at that temperature starts to freeze. I thought you might have some data that I could use in this way. CAPTAIN HAMLET: Why don't you talk to me afterwards. We have a lot of date, but we can maintain zero degrees skin temperature and tissue temperature and get no injury whatsoever for hours, but you take an other individual and you take his skin temperature to zero and you get crystalization and he is going to have a frostbite. CHAIRMAN HENSCHEL: Anyone else have comments or questions? MR. WILLIAM G. FREDERICK (Wayne State University-Detroit, Michigan): I wanted to make some comments with respect to this d&cument here. I certain have no familiarity with wind factors as far as the outdoor cold workers are concerned, but there are some practical difficulties. I think that in almost every large urban community it is surprising the number of coldroom operations that are involved. The freezing of ice cream, the storage of meat. People are in and out and they work in the coldroom a couple of hours and then go out and load a semi and then go back into the coldroom again, and it is not uncommon for meat storage workers to carry the carcasses out and load a truck and then come back in and then go back out again. It is also surprising the number of people in large cities that are involved in chain saw oper ation in connection with construction or tree trimming. There is an other consideration that after a certain age workers should not work in the cold, but some provision has to be made for people who have always worked in the cold and are well acclimated. They just can't be released at the age of I just wanted to comment that this is the sort of thing that is different from that in logging, lumbering and pipeline operations in the Arctic. Thank you. DR. DUKES-DOBOS: These are very valuable observations. As far as c changes from cold to heat and back from heat to cold, we found that these are the conditions \yhere most of the complaints among workers have been observed, that they have been required to go suddenly from the cold room to the outside during the summer where there was a hot temperature, and they had to do some work, whereby they sweated and then they have to go back to the cold area again in the wet clothing, and, of course, this caused them to be much colder than they would have been had they had dry clothing. This is why we recommended in this standard, that the workers should be permitted to take some add itional time when going from cold to heat or heat to cold. For in -80- stance, if they were in the heat, they should not be forced to go in wet clothing back into the cold. And the other way around, if they go from the cold to heat, they should have time enough to take off the clothing which was adequate for the cold situation, but which would be completely inadequate for the working in heat. What consequence this may have in practical situation, this is the re sponse we are asking you to tell us, if you have experiences in this area. What do you think, how these aims can best be achieved. As far as the Raynaud's Disease is concerned, we believe if a worker already has this disease he should not be required to work in the cold, particularly if this is connected with vibration tools, because this will exacerbate the disease and will cause capillary spasms in the finger tips, and in addition to being painful, it is also danger ous because the person loses his tactile sense and he will be much more prone to accidents. MR. FREDERICK: Well, from a practical standpoint, in Detroit the forestry group work out trimming trees and they get cold. They go sit in the truck cabuntil they warm up and then they go back out again. What is needed practicallyis some sort of heated glove at this stage of the game. You see, under union regulations you can't lay these people off. You see there .is a practical aspect to it, and that is what I was trying to get across. CHAIRMAN HENSCHEL; YEs, the next gentleman. MR. LEONARD KANIAN (Safety Coordinator, 312 3rd Ave. South, Minne apolis, Minnesota 55^15)* I am with the City of Minneapolis, and I think we are a little colder than they are in Detroit. However, in our Water Department for main construction people, those that dig ditches, put the mains in, we have arbitrarily set up a rule if it is 10F they work and if it is 9F they stop working. They don't look at the wind chill factor at all. For the forestry people that go up in the elevated baskets to trim trees it is left up to the men themselves. If they feel they can work they let them go ahead. If they feel it is too cold then they let them go home. Our sanitation people who collect the garbage--do so every day of the week, no matter what the weather is like. My question is, does 10F sound plausible or should we be using the wind chill rather than just reading the thermometer? CHAIRMAN HENSCHEL: There have been a number of suggestions so far. One of them is for people exposed outdoors, the wind chill is a feasible approach, because wind measurements are not too difficult. In many places in industry inside jobs, where you have localized variability in wind speed, then the wind becomes a very difficult parameter to measure, then there one might have to use just temperature. DR. GOLDMAN: One other point on that, of course, is that for garbage workers, if they are riding on the back of the truck--as they usually are with their hands out--you need more than just the wind and temp erature? you need to know what speed that truck is going, because it will add as much as 20 miles per hour to the wind speed. -81- MR. HANIANi I agree with you. The Water Department people go strict ly on the temperature reading, and sometimes they may be working when the wind chill is so much greater and they get more exposed. I would like to get something officially and bring it back wherein I could re commend that it is not so much a temperature reading as it is the wind chill reading where you can get frostbite easier and quicker. DR. BUSKIRK: One of the problems here, too, depends on where they are working. If they are down in the ditch digging, it could easily be warmer down there than it is on the surface, and there would be very little wind. If they are behind a building, they may be protected from the wind, and I think that this is where the portable instrumentation that Dr. Goldman referred to comes in. In many of these industrual sit uations it would be nice to have. some portable monitoring equipment for these ambient conditions, something that could be easily carried. A man working on a pole, let's say, hanging half out of a basket in a minus 20F weather in a thirty mile per hour wind, that is tough going up there, and perhaps, unless it is an absolute emergency, he should be relieved or taken off the pole. There has to be some common sense, I think in the structure of these recommendations. There is one point I would like to make, and that is that we need more monitoring equipment. MR. KANIANs Well, it hasn't been too big of a problem, because we have only had one case of frostbite with a garbage collector in the last 3 or 4 years, so we haven't actually had cases of disability as a result of cold. We are always having these discussions about when to work and when not to and it becomes an individual thing and an opinion rather than something that might have a good basis. DR. DUKES-DOBOS: Well, I would like to comment on this. Such infor mation as you just mentioned is very interesting to us in formulating our recommendations and we would appreciate it if you would let us know exactly what your regulation or recommendations are. The big question is at what temperature would we require that not only air temperature but the wind velocity be measured, and how we should evaluate it. Your information might be very valuable in helping us make the right decisions. MR. L.A. PENN (City of Milwaukee-Milwaukee, Wisconsin): My comment is that in our garbage department workers and the outdoor workers of the Department of Public Works have within their union contract the terms of wind chill factors, whether they work or do not work. And apparently up to this point it is successful, but I do have a question. When I was a youngster we used to get a non-disabling but rather miserable condition that we called chillblains, and I would like to know if that has been a factor up in the Arctic? DR. GOLDMAN: Usually chillblains is something that takes longer to de velop. One is apt to get it as a youngster out playing for any length of time, but if one is out working in the Arctic, one is usually out for no longer than one has to be. Chillblains usually result from a combination of things. If the foot is hanging down, a lack of circulation and cold for prolonged periods could cause the prolonged vascular constriction. -82- The incidence of chillblains is probably greater than is recognized, but it is not usually a disabling thing, it is temporary. CAPTAIN HAMLET: It is not considered a serious medical problem in the army. It is written in the standard documents, but I personally have ex perienced it only once. Dr. Goldman said, it is temporary, but it could enter into a serious problem for workers if they were sitting consis tently sedentary, in the cold, yes it could occur, but that has not been addressed scientifically very much since the second world war. CHAIRMAN HENSCHEL: All right, the back mike. DR. RODNEY R BEARD (Stanford Medical Center-Stanford, California 9^305)! I would like to comment on this draft, starting from the last page and going forward. I believe that any discrimination based on age in this manner is probably somewhat less justified than other age discrimina tions. I defy anyone here to set an arbitary age at which the risk of cold injury increases, which is going to be valid for all individuals or even for most individuals. I think at this time the decision has to be made on the basis of individual needs, individual requirements, not on the number of birthdays. Under the heading "Medical," I think that there is a mistaken approach in this matter, not only in this document but in others which I have seen. It is quite impossible to assess all of the medical conditions which ought to be considered in circumstances of this kind. The problem in trying to do this is that one inevitably leaves out a number which ought to be mentioned and invitably put in a number not really very important at all, and which ought to have a lot of qualifications. It all goes together with the idea that one can have medical examination done on some periodic basis, specified by regulations and get good results from that kind of approach. The consequence of it is of course, that one man gets disinterested physicians who do routine examinations which have no meaning for the examiners nor for the people. I believe the medical program should be devised which would be addressed to the needs of a particular situation and which should be cognizant of the needs of the particular workers. This is the only satisfactory and economical way to use medical service in the long run. You can't possibly, in the space of a few sentences, indicate all of the con sideration which should go into the decisions as to whether a given in dividual should be put on a job which may expose him to the cold. It is a complex medical and personal judgement. Now in this list there are a couple of things that I don't see any reason for. For example, hypothyroidism. There is no reason why a person with hypothyroidism can't work in the cold if he is adequately treated, and I am not sure that it does any harm if he isn't treated. I certainly would not agree that all of those who have suffered from cold injuries should be forever excluded from working in the cold, Certainly some of the people who have done the best work in the past would have been out of a job long ago. The other flaw in the list, cardiac arrhythmias am't mentioned and consideration isn't given to metabolic disease other than hypothyroidism, and certainly a person with a pituitary tumor, which will affect his urinary excretion, ought to be spared from this trauma. Psoriasis, I think this would be one of the diseases that would be ag gravated by cold. The decision has to be made not just on the name of the disease but on the individual, on the nature of the job which is to be done, the duration of exposure and a number of other factors. And then going back to the beginning, I would ask the experts up front, whether the matter of hand warming with hot air jets is a bad choice. If it is acceptable at all, shouldn't it be made the last choice rather than the first? Because of the drying of skin which would take place with hot air jets? Thank you. DR. GOLDMAN: One of the advantages to hot air jet is that fact that you can control the temperature, and one of the problems with the auxiliary heat, a glove for example, with the present auxiliary heating system, the wearer of this heating system may get a trace of wire heat and a gap between. There are new materials, conductor rubber, the fibers which are now conducting, that look promising, but they are not yet available. You are right, this does enhance the drying of the skin, depending on where you get your source of heat. Most of the heat is from heat ex changes, using the exhaust gas mixed with a certain amount of make-up moisture from the skin with the air flowing over the hand, and of course, you do extend the tolerance. CAPTAIN HAMLET: I hope I conveyed in my portion of the presentation that I was covering only some of the medical problems, and my comments about a strong medical coverage for workers exposed to the cold real izing, of course, the need for strong clinical management and under standing of the individual patient as to what he can tolerate. Clearly setting forth a list of all the diseases and all of the drugs that can affect your functioning in the cold would be a hopeless task. Again I believe a physician who has some understanding of the problem has some responsibility for seeing than an individual is not exposed. The cold injuries and the main things I talked about today were things that we identified routinely in Alaska. We have some experiance in looking at the workers that are now stationed on the Arctic slope. The number of diseases and disease incidence that we identified were from just routine histories and physicals. Short clinical follow-ups revealed that they had not received that kind of consideration before they were sent there. But again, someone has to be responsible, and I happen to feel that the physician is the one who must be responsible. MR. JACK WINDISH (Department of Nationial Health and Welfare-Ottawa, Canada): This is for Drs. Dukes-Dobos, Goldman or Hamlet. When you refer to the fact1- that at low temperature the toxicity of the sub stance seems to increase, I was wondering whether this was found to apply to all substances or certain types of substances, and at what temperature does it become important and do you have any order of magnitude of this type of thing? CHAIRMAN HENSCHEL: Yes, at least part of the information comes from animal work. The affects of the environment temperature on toxicity of toxic substance is an inverted U-shaped relationship with toxicity going up on both sides of the optimun of between 70 and 80 degrees for the animals used, which were rats. As the temperature increased or decreased, the toxicity increased as the environment temperature went up above the optimun of 70 to 80 degrees. CAPTAIN HAMLET: I might comment that the Russians have done some -84- extensive work on the alteration in toxicity of radio-active materials in hypothermia. There is a fairly good sized body of Russian lit erature on this and it should be available to you. To the best of my knowledge, my impression of the toxicity increase in cold would relate to compounds that their excretory process is slowed down but their toxicity is maintained in the cold. I don't know any specif ically, but I would suspect there are a number of them. It is just a question of someone having the scientific desire to look at them. MR. WILLIAM ELKINS (Acurex Corporation - Mountain View, California)! I just want to mention that we are currently doing work on both heating and cooling segmented portions of the body, hands and feet and total body heating and cooling. If anyone is interested in our techniques, we have a booth at display section 37. and I would be delighted to talk to anybody about our techniques; CHAIRMAN HENSCHELi Are there any other questions or any other points that anyone would like to bring up? If not, thank you, Captain Hamlet, Dr. Goldman, Dr. Buskirk, and Dr. Dukes-Dobos, Thank all of you for coming. (Thereupon at 3*^8 o'clock p.m. the meeting adjourned.) -85- The NIOSH Health Hazard Evaluation Program An Overview Jerome P Flesch, Chief, Hazard Evaluation Services Branch U.S. Department of Health, Education, and Welfare Public Health Service National Institute for Occupational Safety and Health Center for Disease Control U.S. Post Office Building Room 58 Cincinnati, Ohio 45202 Abstract: The history and development of the NIOSH Health Hazard Evaluation Program is presented, incorporating the legislative authorization and the regulations specifying its operational procedures and re quirements . The basic philosophy of the NIOSH "toxicity" determination and the salient investigative approaches followed are differentiated from those of the OSHA "compliance inspection" program. A summary of the current numbers, types and origin of requests is discussed, and selected findings of completed toxicity determina tion reports are presented. The overall utility of the Program will be reviewed; generation of human toxicological exposure information related to criteria for standard setting; identification of new problem substances and ana lytical methodologies; and recognition of efficient control measures *****# INTRODUCTION On behalf of NIOSH I would like to extend sincere appreciation and thanks to the American Conference of Governmental Industrial Hygien ists and in particular to Mr. Jeremiah Lynch, this year's Vice Chair man and Program Arranger, for their acceptance of our proposal last winter to present this program. During the three years of operation in the NIOSH Health Hazard Eva luation (HHE) Program, I believe much good has been accomplished. We are delighted to have an opportunity to present some highlights of this work for you today. Due to the energy crisis and resultant attendance ceiling which lim its the number of NIOSH personnel at this conference, three of our primary authors are not here tbday. Their papers will be presented instead by substitute or co-investigators. As will become evident from ensuing presentations, the conduct of the HHE Program enlists the support of many branches and divisions -86- throughout NIOSH. It is not feasible to acknowledge individually all of the many NIOSH investigators who have contributed to and support the Program hut could not he here today. Recognition and thanks are directed especially to NIOSH staff in the Hazard Evaluation Services and Medical Services Branches of the Division of Technical Services in Cincinnati and Salt Lake City, to the Regional Industrial Hygienists, and to the Division of Laboratories and Criteria Development. ORIGIN OF THE HHE PROGRAM In December 1970 Congress enacted the Occupational Safety and Health Act in order to provide safe and healthful working condidtions for all employees. To meet this end, the Act provides a legislative mandate to two separate Federal Departments giving each specific responsibilities: 1. To the Department of Labor (D.O.L.) and its Occupational Safety and Health Administration (O.S.H.A.), it gives the charge to both promulgate and enforce health arid safety standards in the workplace. 2. To the Department of Health, Education, and Welfare (D.H.E.W.) and its National Institute for Occupational Safety and Health (N.I.O.S.H.), it provides the directive to conduct research activities in order to develop valid criteria and aid in standard setting. One of the specific responsibilities given N.I.O.S.H. in this regard is the mandate contained in Section 20(a)(6) of the Act which provides for the conduct of "on-site toxicity determinations" in the workplace, or as it has come to be known - NIOSH Health Hazard Evaluations. Section 20(a)(6) provides an opportunity for both representatives of employers and representatives of employees who are covered by the Act to request and received from NIOSH an evaluation of their specified workplace. This evaluation will determine whether the chemical substances normally used or evolved in their process are potentially toxic to exposed employees in the concentrations or con ditions of use found. The development of this Program and the progress achieved to date are the subjects of our "Highlights Session" today. DEVELOPMENT OF THE HHE PROGRAM Our philosophy in approaching the conduct of an evaluation necessary to make a toxicity determination in a specific work environment is one which combines two aspects: First, an assessment of the actual employee exposures to the alleged potentially toxic substances, and second, an assessment of the toxic effects manifested in that work group. The program is responsive to requests regarding not only new substances, that is - those which do not have occupational health standards, but also to those substances currently having standards. Such promulgated -87- standard levels may not be sufficient to protect the worker from experiencing adverse health effects. Thus an investigatory approach is followed in this program which utilizes both environmental and medical aspects. Health Hazard Evaluations conducted for substances will, over a period of time, develop human exposure-toxicity data to aid in validating, reassessing, and establishing new criteria on which to base occupat ional health standards. In contrast to the NIOSH program it may be of interest to point out that requests directed to O.S.H.A. under the authority of Section 8(f) of the OSH Act will result in an environmental assessment only of current exposure to determine compliance or non-compliance with the current Federal standard level, which may be inappropriate. Regulations for the HHE Program were developed during the initial years of operations which define the requirements and procedures utilized. They are contained in the Code of Federal Regulations, Title 42, Part 85 and were published in November 1972. A brochure containing these Regulations and further descriptive aspects of the Program is available at the NIOSH display booth here at the conference, or at any NIOSH location. PROGRAM OPERATIONS Some of the salient features of HHE operations will be described here. The conduct of each Hazard Evaluation usually incorporates the follow ing four phases: I. Validation of Request II. Initial Field Investigation III. Follow-up Environmental-Medical Studies IV. Analysis/Determination of Toxcity 1. The initial phase in responding to requests received by the Hazard Evaluation Services Branch, headquartered in Cincinnati, is to determine the validity of the request. First, does the request pertain to an exposure to a CHEMICAL SUBSTANCE in the workplace? Specifically EXCLUDED from our authority to investigate are PHYSICAL AGENTS, such as noise, heat, and radiation. SAFETY HAZARDS are likewise excluded from coverage by this Section. Secondly, it must be demonstrated that the request was submitted by AUTHORIZED REPRESENTATIVE of either the employer or the employees, according to provisions contained in the REGULATIONS. -88- Thirdly, the applicability of the Act must encompass the ESTABLISHMENT/Employer identified on the request. EXCLUDED from NIOSH's jurisdiction are working conditions of employees of Federal, State, or political subdivisions. Of the 407 requests received to date, I65 or nearly 40$ were out side the scope of the Hazard Evaluation Program for various ex clusions described above. Aid has been extended to these prospec tive requesters by searching out and directing them to appropriate sources for the service or evaluation desired. II. Once the request has been validated and reviewed to assess the reported toxicity occurring or potential toxicity relative to sub stances identified, an industrial hygienist and/or physician con ducts an INITIAL Field Investigation. The purpose of this phase is to determine the condition of use on-site at the specific work place or process in question, to obtain information related to the potential exposure and toxic agents, and to record apparent or re ported adverse health effects in the work force. The following aspects of this survey incorporate: 1. Employer-Employee Representative Interview 2. Walk-Through Survey 3. Exposed Employee Interviews 4. Bulk-Air/Substance Sampling 5- OSHA Record of Illness and Injury III. Information obtained from this aspect is reviewed and a plan formulated for the conduct of environmental and medical studies as required to make a determination. These studies may be conducted at different times or concurrently, depending upon the utility to correlate exposure with effect. ENVIRONMENTAL EVALUATION Component approaches taken under the scope of the ENVIRONMENTAL EVALUATION are the following: 1. Identify Potentially Toxic Substances Methods of accomplishment include a review of the request, the process information submitted and obtained, the employer-employee interviews, and the walk-through survey of operations in the work place . 2. Assess Substances of Inportance Methods include an assessment of the quantity and frequency of usage, route of entry or contact with the substance, the con- -89- trols engineering, administrative, personal - existing and the time instituted, the collection of hulk samples and review of related toxicological criteria. 3. Measure Employee Exposure Methods incorporate personal breathing zone sampling for vapor/ gas and particulate (total/respirable fractions) concentration, work shift averages, short-term excursions and related observa tions of employee work practices. MEDICAL EVALUATION The MEDICAL EVALUATION usually encompasses the following five ap proaches with appropriate Methodologies. 1. Histories of Occupational Exposure are obtained and non-directed questionnaires are utilized in private employee interviews to elicit work related health effects including symptomatology occuring or reported by workers. 2. Physical examinations may be conducted to identify signs of ad verse effects, for example, relate to the cutaneous dermatologic or neurologic systems. 3* Biologic specimens, such as blood or urine, may be collected to detect excessive absorption, changes in metabolic function, or adverse effects upon various organ systems. 4. Diagnostic tests may be administered such as (a) Patch tests to demonstrate skin sensitivity and allergy, (b) Pulmonary function for respiratory disorders, (c) Chest X-ray for respiratory disease and (d) EKG for cardiac disorders. 5- A thorough review and analysis of records may be conducted to demonstrate unusual or excessive morbidity and/or mortality. IV. The fourth and final phase of the Hazard Evaluation is-------- ANALYSIS/DETERMINATION OF TOXICITY This consists of the followings 1. Review of Environmental-Medical Study Results 2. Comparison with Existing Criteria 3. Interpretation of findings and judgment of potential toxicity. 4. Basis for the Determination 5. Recommendations for control/solutions if appropriate. -90- SUMMARY While the actual field conduct of these Hazard Evalutions is usuallylimited to a few days of on-site testing, completion of the short term cross sectional study may require a number of months. Develop ment of sampling and analytical methods may he required before agents and exposures can be characterized. Seasonal variations can temper the occurrence of toxicity in the workplace, limitations in number of employees and variation in job duties and a host of var iables may complicate the operation and make toxicity determinations difficult. Those substances/exposure which result in acute or short-term toxi city are most favorably addressed by the Hazard Evaluation Program. The question of potential toxicity or long term CHRONIC TOXICITY is difficult to investigate. In this regard, referrals of such suspected cases for possible retrospective or prospective studies are directed to other NIOSH Divisions, for example the Division of Field Studies and Clinical Investigations which conducts long-term or industry wide-studies. STATUS OF PROGRAM A table offering a brief accounting of program status through April 1974 shows t Total Requests....................................................................................... 407 Valid.................................................................................................... 242 Invalid.......... ....................... 165 Determinations Completed........................................................ ...134 Toxic....................................... 58 # Substances...................................................................... 100 Not Toxic............................................................................................ 76 # Substances...................................................................... 295 Active Requests................................................. 104 UTILITY OF THE HHE PROGRAM The following benefits will potentially result from completion of health hazard evaluation studies. Outlined they consist of the following1 1. PROTECT THE HEALTH OF WORKERS AND PROVIDE ON SITE CONSULTATION TO EMPLOYERS -91- A. Identify Problems B. Recommend Solutions 2. PRECIPITATE RESEARCH AND DEVELOPMENT A. Sampling and Analytical Methods B. Toxicological Studies C. Epidemiological Studies D. Medical Procedures, Diagnostic Tests 3. DEVELOP HUMAN EXPOSURE-TOXICITY DATA A. Assess Validity of Existing Standards B. Criteria for New Standards C. Criteria for Combined Exposures With respect to the development of criteria for standards, a number of substances were determined toxic but do not currently have occupational health standards, or current standards which do exist appear inadequate to prevent the exposed workers from experiencing adverse health effects. Some of these INDIVIDUAL SUBSTANCES identified includet Diethylstilbestrol N-acetyl sulfanilyl chloride Salicylic acid Monoisopropanolamine Petroleum pitch Polyvinylchloride film Bisphenyl-A epoxy resin Trichloroethylene Chromic acid Carbon disulfide Toluene diisocyanate, TDI Additional, combined exposures to a number of substances have pro duced toxicity at levels below current standards. For example these include t Furfuryl alcohol, formaldehyde Styrene, Methylene bisphenyl isocyanate MDI Xylene, Toluene, Butyl Alcohol, Naptha Some of these substances and resultant study data will be discussed in subsequent papers. In conclusion, I would urge each of you, where appropriate, to utilize the service which the mechanism of Health Hazard Evaluations provide. Information developed will not only aid individuals directly affected but also the Institute in fulfilling its mandate under the Act. -92- CARBON DISULFIDE IN VISCOSE RAYON MANUFACTURING Robert E. Rosensteel Steven K. Shama, M.D. Jerome P. Flesch U. S, Department of Health, Education, and Welfare National Institute for Occupational Safety and Health Center for Disease Control U. S. Post Office Building Room 508 Cincinnati, Ohio *15202 Abstract The spinning and cutting areas of a large viscose rayon manufactur ing plant were studied. The study of population consisted of six spinnermen and eight' cuttermen; air samples for carbon disulfide were obtained for measuring exposure to acute, i.e., short term re latively high concentration as well as general room concentrations. Sample results were combined to determine shift time-weighted aver age exposures. Urine samples from cuttermen and spinnermen were collected at the beginning and end of the shift for analysis for met abolite (s) of carbon disulfide by the iodine azide method. Acute exposures for cuttermen ranged from less than 20 ppm to greater than 2000 ppn; fifty-two percent of these measurements were greater than 100 ppm. Shift time-weighted average concentrations ranged from 10 ppm to .1.30 ppm. Seventy-five percent of cuttermen had end of shift iodine azide values which were abnormal with seventy-eight percent of this group considered symptomatic from carbon disulfide exposure based upon medical questionnaires. The medical questionnaire was developed from the most common symptoms noted by Alice Hamilton in her classic study and the various symptom lists presented in Toxicology of Carbon Disulfide. Spinnermen were found to be exposed to much lower levels of carbon disulfide with three percent of this group having abnormal iodine azide tests while forty-two percent were found to be symptom atic . ****** i. PLANT PROCESS The operations which were involved in the initiation of a Request for Health Hazard Evaluation are located in the cutting and spinn ing areas of a viscose rayon plant. The spinning part of the pro cess is also referred to as regeneration and begins by pumping the viscose solution to headers on each side of the spinning bath. Metering pumps are located along each side of the spinning bath, one metering pump for each jet. The viscose is pumped through the metering pumps to the jets which are submerged in the acid solu tion of the spinning bath. Reaction between viscose and sulfuric acid results in the release of carbon disulfide (CSg). The bundle of fibers, called tow, which has been spun into the acid bath is wrapped around a driven wheel called a Godet which -93- serves as a holding point for the application of stretch to the fiber bundle, Spinnermen perforin a variety of jobs in the spin ning area consisting of lacing up machines, cleaning scraps of rayon from drains in the bath (cleaning hooks), changing jets, washing salt off machine parts, or performing routine process checks. Eight spinnermen on each shift would normally be ex posed to CS2- The tow is then fed over a reel at the cutting end of the machine and into a cutter which chops it into short lengths of staple. The cuttermen are responsible for patrolling their assigned mac hines, checking machine stretch sections, cutting wraps off takeup reels, clearing plugged cutters, pulling tow, clearing cutter sluice plugs, loading and emptying tow buggies. Seven cuttermen in each shift would normally be exposed to CS2- Industrial poisoning from carbon disulfide (CS2) has been recog nized for over 100 years. The major route of absorption of CS2 is inhalation1 and the standards have been established to limit high air levels. Single high- dose exposures may result in head ache, dizziness and narcosis. Repeated exposures may lead to nervousness, irritability, indigestion, insomnia, excessive fat igue, loss of appetite^, peripheral nerve damage and psychoses.3 Davidson and Feinleib^ cite reports of CS2 causing skin irrita tion, vision damage, hearing abnormalities, intestinal problems, blood abnormalities, and abnormalities of the adrenal glands and the testes. Of particular importance is the association of kid ney, heart, and blood vessel damage in workers exposed to CS2. Kidney damage may be secondary to a general atherosclerotic pro cess possibly induced by CS2-5 II. CRITERIA FOR EVALUATION OF WORKPLACE CONCENTRATIONS OF CSo The documentation of the TLV1 notes that air levels of 60 to 120 ppm and higher have been associated with chronic symptoms of CS2 over-exposure, e.g., mental fatigue, sleepiness and headaches with milder cases observed at 30-^0 ppm. Various sources have re commended average 8-hour exposure TLVa of ^5 ppm , 30 ppm< or 10 ppm>910. The ACGIH has established a TLV of 20 ppm for pro tection against serious systemic effects which is also the pre sent Federal Standard for an 8-hour exposure. III. ENVIRONMENTAL-MEDICAL PROTOCOL Although several preliminary visits to the plant were necessary to develop analytical methodologies and collect medical histories, a comprehensive environmental-medical study was conducted during December 1972. The last day of a shift sequence was selected as the day upon which to study the atmospheric concentrations of CS2 to which cut termen were exposed. The decision was based upon the need to ob tain biological samples expected to reflect the maximum total ex- -94- posure and retention of carbon disulfide which normally coincides with the last day of a shift sequence. Spinnermen being exposed to lower air concentrations were sampled on the next to the last day of the shift sequence. Two types of personal samples were obtained for both the spinner men and cuttermen reflecting either "acute" or "general room" ex posures. "Acute" exposures for cuttermen occur when work is per formed with the cutterhouse hood open, stretch section hood open, pulling tow, and emptying or pushing loaded tow buggies. Cutter men have instructions to wear respirators during any of these acute exposure periods, but on a number of occassions men were ob served working without protection. Spinnermen experience acute exposure when checking machine operation, cleaning hooks, lacing machines, making jet changes and taking up machines, although re spirators are not worn while performing these tasks. The acute exposures were measured by holding the inlet of a midget bubblerimpinger sampling train in the breathing zones of the cuttermen or spinnermen at the time of the exposure. General room samples were obtained in the cutting or spinning areas at least once per hour during each shift. The analytical method used involves the immediate stabilization of CS2 as the yellow cupric diethyldithiocarbamate with the amount of CS2 determined from an absorbence concentration calibration curve. A medical questionnaire was administered based upon the most com mon symptoms noted by Alice Hamilton in her clasic study of CS2 exposure and the symptom lists presented in various papers appea ring in Toxicology of Carbon Disulfidell. In order to correlate symptoms elicited from workers with an objective test of exposure, urine samples were taken on the last day of a work week and were analyzed using the iodine azide test originally described by Yoshidal2 and, developed further as a field test for CS2 exposure by Vasak.13.1^ Medical questionnaires were administered and urine samples were collected before and after the seventh day of the work week. Urine specimens were preserved with thymol and were analyzed at the plant site by NIOSH personnel. Samples were observed for five hours, if they did not convert during this period of time they were considered "normal." Exposure coefficients (E values) are reported either as "Normal" or E = -6.0; Borderline Abnormal 6.0 E 5-Os or Abnormal E 50. All cuttermen and spinnermen were involved in the evaluation. A special group of workers whose exposure was not measured but who were at times in the spinning area were also tested; these workers were in such job classifica tions as patrolmen, pumptesters, and filtermen. IV. RESULTS Table I contains the distribution of all acute CS2 measurements made in the breathing zones of the cuttermen studied. These data cover a very wide concentration range, from a minimum less than 20 ppm to a maximum greater than 2000 ppm. These acute exposures -95- exceed by far the limits which various investigators have sug gested for workroom air. Acute exposures of CS2 to spinnermen were at much lower levels than those of cuttermen. The acute exposure levels for all spinnermen varied from 0.9 to 127 ppm, with only the one sample exceeding 100 ppm. The results of the medical questionnaires and urine tests are summarized in Table II. Cuttermen as were expected showed the greatest number of symptomatic individuals. Comparing the spin nermen with the special group (known to have less time in CS2 atmospheres), the special group has a smaller percentage of symptomatic individuals. Workers were considered symptomatic if they admitted to at least symptoms of headaches, and dizziness on occasion. In most in stances symptomatic spinnermen and workers in the special group complained only of headaches and dizziness (the typical symptoms of acute high dose CS2 exposure). The men easily predicted when symptoms would occur, e.g.; on "bad days", "when fumes were heavy", when ventilation was poor or when spinnnermen were ex posed in the cuttermen's area. Symptomatic cuttermen rarely complained only about headaches and dizziness but often had associated sleep disturbances, fatigue, nervousness and poor appetite. The environmental data from acute and general room exposures were combined by time-weighting the data to obtain a shift timeweighted average exposure to CS2. Table III contains the results of environmental sampling, iodine azide results, and whether the worker was symptomatic on the day surveyed or in the past. Due to the method of sampling only two workers could be monitored per shift. A total of eight cuttermen and six spinnermen were mon itored environmentally during the study although all cuttermen and spinnermen participated in medical interviews and furnished urine specimens. The TWA acute exposure for cuttermen varied from a minimum of 23 ppm to a mazimum of 38O ppm. All except one of the TWA acute exposures for cuttermen exceeded the Department of Labor's max imum peak of 100 ppm for CS2 exposure. The time weighted aver age acute exposure for all cuttermen was found to be 186 ppm. These results serve to emphasize the very serious nature of the acute CS2 exposures existing at this plant especially for cutter men. The TWA acute exposure of spinnermen did not exceed Depart ment of Labor Standards for CS2 exposure. The range of general room exposure for cuttermen was from 6.3 to 47ppm. Four of the general room exposures of cuttermen were higher than the upper limit of 30 ppm which more liberal invest igators would suggest as a safe TWA shift exposure, and these four levels are also in excess of the 30 ppm ceiling - 30 minutes duration standard of the Department of Labor. Two of the remaing general room levels, 20.0 and 25.0 ppm, would be considered as borderline safe while the other values of 6.3 and 12.6 ppm would -96- be considered safe by most investigators. The level of the gen eral room exposure leads one to consider seriously the necessity for protection of cuttermen during the entire shift until adequ ate engineering controls are operating which will provide a safe environment in the cutting area. Since spinnermen were not wearing respirators, their TWA repres ents in all cases a full day's exposure and may be compared dir ectly to their iodine azide values. In only one case, the first spinnerman in Table III did have a borderline abnormal Eg with a TWA well below the Federal Standard of 20 ppm. Of interest is that he was the only one of two monitored who had two excursions above 30ppm during the day. These two mild excursions above the ceiling level may explain the E value. All other spinnermen had normal Eg and TWAs below the Federal Standards. Then general room TWA obtained in the spinning areas show values in a range of 3.0 to 5*5 ppm which would all be considered within safe limits. Table IV reveals the TWA for cuttermen who were environmentally monitored and assumes exposure to only general room air. We note that TWAs calculated place four of the eight cuttermen only sligh tly ablove the Federal Standard of 20 ppm ( 23*2-32.2), while E values are markedly abnormal in five of the eight. Carbon disulfide average exposures can be predicted from Eg values. Djuricl5 notes that his E values and active measured air exposures to CS2 showed good correlation with E calues. Values of 6.5 and 3.0 correspond approximately to 20 ppm and 60 ppm air concentra tions respectively. If we look at all Eg values from cuttermen who were monitored environmentally, the five which are abnormal all have an E value less than 3 which would place all exposure levels at greater than 60 ppm. Furthermore a total of 13 cutter men not monitored environmentally also had E values less than 3 indicating an average greater than 60 ppm. In a comparison of symptoms and the iodine azide test, non-tabulated data shows that 23 cuttermen had abnormal Eg values, and of the 23, four workers had symptoms of an acute (day of testing) nature while fourteen had symptoms of a chronic nature. .This would suggest that Eg is a good indicator (18 of 23 or 70%) of workers who are or have been symptomatic. Of all cuttermen only five members (five and seven of Table III and three not tabulated) had both abnormal Eg and Eg values. Three of these five had sym ptoms on the day of testing and all reported past symptoms. Making the assumption that cuttermen are exposed only to general room air and not to acute exposures because of respirator use, Table IV shows exposure averages which are slightly above the Fed eral Standard (23-32 ppm) while corresponding Eg are markedly ab normal, in fact the Eg would suggest concentrations above 60 ppm. The difference between the actual calculated TWAs in Table IV and those predicted from E values suggests that cuttermen were in fact exposed to high levels of CS2 whne standing near an "acute exposure operation" without wearing respirators or that the re -97- spirators or that the respirators were ineffective. CONCLUSION Based upon the results of the environmental-medical study, i.e., (a) the excessivley high environmental levels of CS2 detected, (b) abnormal iodine-azide biological tests observed in workers, and (c) significant occurrence of symptomatology, it was determined by the NIOSH investigators that the exposure to carbon disulfide vapors at the concentrations found in this work environment were toxic to cuttermen, chargehands, or others working in the cutter area. The respirator program in effect for cuttermen was found to be ineffec tive in protecting this group. Spinnermen, N-10 men, patrolmen, filtermen, and pumpters may occasionally be exposed to levels of carbon disulfide potentially toxic to them. -98- REFERENCES 1. Documentation of the Threshold Limit Values, ACGIH, 3rd Edition, pp. 39-40t Cincinnati, Ohio 1971 2. Fairhill, T. T. Industrial Toxicology, Williams and Wilkins, Bal timore, Md., P. 181, 1957 3. Vigliani, E. C., Brit. J. Ind. Med. 11,*235, 1954 4. Davidson, M. and M. Feinleib. American Heart Journal, Vol, 83, No. i pp. 100-114, January 1972 5* Browning, E. Carbon Disulfide, in Toxicity and Metabolism of Industrial Solvents, Amsterdam, Elsevier Publishing Company, pp 702-712, 1965 6. Vigliana, E. C. Industrial Medicine and Surgery, 19241, 1950 7. Barthelmey, H. 1. Journal of Industrial Hygiene and Toxicology, 21:141. 1939 8. Rubin, H.D., et al., Industrial Hygiene and Occupational Medi cine, 2:529 1950 9* Gordy, S. T., Trumper, M. Journal of American Medical Association, 110:1543, 1939 10. Klwindwls, M. and I. R. Tabershaw. Journal of American Medical Association, Vol. 1951 No. 7* pp 667, 1955 11. Brieger, H. and J. Teisinger: Editors. Toxicology of Carbon Disulfide-Proceedings, Amsterdam, 1967- Excerpta Medica Found ation. 12. Yoshida, I. J. Sci. Labor, Tokyo 31:209, 1955 13* Vasak, V. PracovLek., 15*143, 1963 14. Vasak, V., Vanecek, M. and B. Kimmelova, Pracov Lek. 15:145, 1963 15* Djuric, D.; Determination of carbon disulfide and its metabol ites in biological material, in Breiger, H. and J. Teisinger Editors: Toxicology of carbon disulfide proceedings, Amsterdam, Excepta Medica Foundation, pp. 52-59, 1967 T a b le - D i s t r i b u t i o n o f " A c u te " CS2 M easurm entsI from C u tte rm e n 's B re a th in g Zones -99- oH -p cd cd >P o -P ^ sj <o1) -P o <1) o d PQ) +a3> Ph ocd H OsIS-vnvO >-o OHNV0 4-OPr\ rH C^VOCO tH o oH -p cd p -p ao> mo<M o o 00000000 OO OOOCO^VO^r'OiCMOC1-H M CM H CO 1--1 cd to P -P dH H p t> to H CD d PS M -P to O Cl) H Eh P cd a) gd O *H -P tsl Pr^ <D C/2 H 1d 0 HM H d 0) 1--1 TO cd EH to g -P p r--1 0 P CO a) PS Q) -P to H a) rH EH p Q) <d d dP H 0 tSJ PP *! a) t--1 cd H g dP 00 H C CO r--i cd P d H t> H d H 0 H -P cd e 0 -p p >. ta CM VPiO rH H 1--I O O CM CMrin I CM rH 0CO) <U Pg !> CC H t/2 -P cd p H <u P N>AHHNHV4r-\NNHO-OMD\ tH rH o izj 1--I cd -P 00 O-VP\00 o CM CM tH CM EH Pr > PO PO Wd) -P cd O &o -3 O C/3 C/2 O -100- .Y OF ENVIRONMENTAL MEDICAL SURVEY- - DECEMBER 1 1 - 1 8 , 1972 i sPtaosrtv 1 + + 4- + + + + + l I + ra g o p ft 0 CO cd 0 i i i + i + i i i i i i i Q> P 3 CO ra p ra 0 P tH H Td T-\ p 00 ^ OOO O..................... &c gg ^3- o P p vnm .oo SVOVO EH CO W 0 Td H < 0 C H tj o PP g g g g g P P P P P P3- H CM P h A cd p so ao so sovnvA ^oso gg VO p On p p VO O OO O-S C-S S tN- M CO CO 1 0 g H EH 0 --W g cd ftp ft --- > o rcJ h 0 PP cd u t4 -p (D o c o o p H CO g o o PS i--! cd p0 0c o 0 p 3o << u o -P cd 0U ft o On o noooovo 00 tH O- On H cm OVOmt-HC'-CMCnvn CM T-t -j- CV CM ocnoooooco OCMNOOOOOOOVOISCM rIHrinn th cm rvj- vnvo cv-oo CM no rH On ON vn^}- n--i \o co vo !N~3- CM no On cnnnn ONvno o o cm CN-VOCM tH CM On CMHH rH cm vomo p o oooooooo wwmwww -101- TABLE IV TIME-WEIGHTED EXPOSURE OF CUTTERMEN TO CS2* DECEMBER 11-18, 1972 Cutterman Time-Weighted Average (Actual) Iodine Azide Start End 1 12.3 2 5-1 3 7.4 4 27.0 5 24.4 6 32.2 7 23.2 8 15-2 * Assumes only General Room Exposure Norm Norm Norm Norm 5.4 5.1 5-2 Norm 6.1 Norm 6.5 1.1 1.8 1.4 1.0 2.8 -102- -103- Diethylstilbestrol, N-Acetyl Sulfanilyl Chloride in Chemical Manufacturing David J. Burton Industrial Hygienist Western Area Occupational Health Laboratory Salt Lake City, Utah and Edward Shmunes, M.D. Columbia Skin Clinic Columbia, South Carolina #**** The Occupational Safety and Health Act of 1970 authorizes NIOSH following a request to determine whether any substance normally found in the place of employment has potentially toxic effects in concentrations as used or found. NIOSH received two such requests regarding exposures to Diethylstilbestrol (DES) and N-Acetyl Sulfanilyl Chloride (ASC). I. DES A. Toxic Effects of Des Diethylstilbestrol is a synthetic female hormone and is the source of various non-steroid estrogens. Its formula is C18H2002. It is thought to be irritant, an allergen, a car cinogen in certain situations in females, and a feminizing agent in males. It can be ingested, inhaled or absorbed through the skin. Typical physiological reactions in males include gynecomastia and impotency. Little is reported in the litera ture concerning dose-response relationships in males. B. Background Information and Manufacturing Process Diethylstilbestrol is made starting with a form of ethyldesoxyanizoin, which is reported not to cause hormonal-type re actions. In the particular process studied, this compound went through another stage of synthesis and the final product diethylstilbestrol was pumped in a water slurry into a room called the finish room. The water was drained off and the workers then shoveled the wet cake into a tank where it was dissolved into hot benzene. The DES was then filtered, de watered, cooled, and the benzene drained. It was then man ually shoveled into drying ovens. The consistency at this point was a rough lumpy powder. It was then milled to approxi mately 10 microns in size. Drums of DES were filled in the finish room, weighed and placed into a storage area. There were at any given time two people working in the operation. On a normal working day, 8 people per 24 hours were exposed. One man per shift worked in the finish room. This particular -104- job was rotated among the workers every six weeks or so. The following table supplied by the company shows the number of employee reactions to DES during a three year period. Spot checks with employees indicated that perhaps these figures did not accurately reflect the actual number of reactions exper ienced. Year 1959 1970 1971 Number of DES Reactions 10 11 02 The term "reaction" implies tenderness and enlargement of the male breast with or without accompanied periods of sexual impotency. All of those reported in the above table were re ferred to a physician. C. Environmental Studies and Results Measurements of employee exposures to diethylstilbestrol were obtained using personal air sampling equipment. During each shift 2 men worked in and around the diethylstil bestrol area. The outside man was called the "helper". The "finish" or "inside man" spent approximately 2 to 3 hours per day inside the finish room. While he was in the finish room the helper stood and watched him through a window. Before entering the finish room the finish man was helped into an air supplied plastic suit. He then entered a shower where he show ered, disconnected his air hose, and entered the finish room where he re attached his suit to an inside air supply. While the finish man was working in the finish room the helper was required to enter the finish room to deliver tools or to carry away filled containers. The helper was wearing no res pirator or any protective clothing. It was noted on one occasion that after the helper assisted the finish man, his gloves were contaminated with DES which he then proceeded to place in his rear pocket. As a drum was filled in the finish room it was brought to the outside, whereupon the helper washed the drum with water. The water-laden diethylstilbestrol was left on the ground. Equipment was observed to be brought in from other work areas to be used in the diethylstilbestrol operation and returned with out decontamination. Following his activity in the finish room the finish man again showered and went into the small locker room adjacent to the shower room, where the helper assisted him in removing the suit. Ventilation in the finish room consisted of two rudimentary systems. One was connected to a baghouse which collected some -105- of the residue from milling and drying operation. The other system consisted of a roof-mounted fan which when activated simply blew the diethylstilbestrol out onto the roof of the finish room. In spite of apparent employee fear of exposure to DES, there was surprisingly little attention or thought given to adequate housekeeping or the careful handling of DES. Spills were left untouched, usually until a maintenance man could be called. Decontamination, as a procedural practice, was absent. There was evidence of diethylstilbestrol leaking through the windows into the adjacent room. Results of sampling are shown in Table 1. Environmental sampling was limited to 9 samples. These consisted of 3 wipe samples, 4 personal samples, and 2 area samples taken in the building adjacent to the finish room. Of the 4 personal samples, 2 were taken while the man was in the special suit. Both of these samples showed DES exposure even while inside the suit. One personal sample was placed on the helper and he received a high exposure. This was due presumably to his entering the finish room without adequate protection. All three wipe samples showed contamination of DES at the loc ation tested. One was taken from the roof over the finish room and another was taken from the floor of the adjacent building. The last wipe sample, which did show positive results for DES, was taken on the drink dispenser in the lunch room. D. Medical Studies and Results As noted above, DES is a non-steroid estrogen with a potent capacity to induce feminizing symptoms in males. In the oral contraceptive industry, which uses steroidal forms of estrogen compounds, urine monitoring for 24 hour total estrogens is done periodically. When an individual begins to approach ranges of urinary estrogens that are known to correlate with feminizing symptoms, the individual is withdrawn from the ex posure area. A similar urine assay for the non-steriod estrogen, diethylstil bestrol was developed for this study. Recent interest in DES in cattle tissues by the FDA had led to a specific chemical assay for DES. The method was developed by Eli Lilly and adapted by the FDA for its analysis on beef liver. It was found that it could be easily adapted to human urine and air samples. Thus, all DES samples were analyzed using this method, by the WARF Institute, as a private laboratory in Madison, Wisconsin, that specializes in DES determinations. The medical studies consisted of three separate 24-hour urine samples taken from nine men working in the DES area during the Fall of 1972. The first samply was taken on the 17th day of -106- exposure . The majority of the workers were resampled with 24-hour urines on the 59th day of exposure, and the 93rd day of exposure which was several days after DES production was shut down. The closure of the DES production was in response to the FDA's action to ban DES in animal feeds. Additional 24-hour urine samples were collected at various times on a few individuals after termination of work in the DES area to study how long detectable quantities were excreted. In addition, eight control urines from selected key personnel and a samply of tap water were submitted for analysis. A measure of completeness of 24-hour urine specimens, total urine creatinine determinations were performed. Of the nine individuals employed in the DES area during the urine collections, five were finish room workers at some time and, four were helpers. Their ages ranged from 22 to 42 with an average age of 29- Seven of the nine had had previous DES reactions on other tours of duty. These data are summarized in Table II. Only one of the four helpers in the study had detectable levels by the 17th day which increased to a level of 27-0 ug/ml by the 47th day of exposure. This worker's activity did not differ knowingly from the other helpers (who at no time showed detec table levels.) His level at day 47 was lower than any of the finish room employees. He no longer had detectable levels by the 6th day post-shut-down. Controls, i.e., those with no exposure to the DES manufactur ing operations, showed no detectable levels of DES in urine. E. Conclusions The results of these studies indicated that there was a sign ificant hazard to the health and wellbeing of the workers ex posed to DES at this particular manufacturing facility. This finding was based upon the following evidence; (1) there had been a persistant history of DES reactions, year after year, (2) high urine levels and adverse reactions were found in work ers participating in the medical studies of this evaluation, and (3) there was found wide-spread DES contamination of build ings and equipment, extending as far away as the lunch room. It should be noted that our study led us to believe that much of the absorption of DES by employees was through the G.I. tract and the skin. This was brought about by the gross contamination of clothing, equipment, and skin by careless handling of DES and the lack of adequate decontamination procedures. For this reason no correlation between airborne exposure dose and physiological response had been attempted in this study. -107- The urine assay for DES used in this study produced consist ent data which could he used to predict exposures that are app roaching symptomatic levels. In the two individuals that de veloped DES reactions, levels had reached 40 ug/ml. It would seem prudent in a monitoring program to remove individuals that approach levels greater than the 30 ug/ml. II. ASC A. Toxic Effects ASC is an intermediate in the manufacture of sulfa drugs. There is no established standard for ASC. Little is reported in the literature regarding industrial exposures. The only pertinent industrial report in the literature involved workers with eczema, handling ASC in the preparation of sul fathiazole. Six out of thirteen workers developed positive allergic skin reactions on patch testing with ASC. Irritant symptomatology was not discussed in the report. These workers were exposed to other sulfa intermediates and gave positive patch testing responses to them as well, hut not to the fin ished product, sulfathiazole. The ASC reaction could represent cross sensitivity to the other allergens. B. Background Information and Manufacturing Process ASC manufacture starts with the combining of acetic acid and analine to make acetanilide, a flakey material, which is then manually dumped into a reactor in which it combines with chlorosulfonic acid to become acetyl sulfanilyl chloride. The ASC is then quenched in methylene chloride. The ASC is cooled, centrifuged, dried, packaged, and weighed. The employees on shift during the initial walk-through were interivewed by NIOSH physicians. Typical health complaints included! Bleeding noses, sore throat, eye irritation, dizzi ness, stuffiness, and skin inflammation. The company supplied a list of past ASC medical reactions as follows! 1969..........12 cases 1970.....21 cases 1971..........11 cases These reactions consisted mainly of serious contact dermatitis or conjunctivitis which were referred to a physician. C. Environmental Studies and Results Measurements of employee exposures to ASC were obtained using personal air sampling equipment using silver membrane filters -108- to collect ASC. Area samples were taken using sequential samplers. Maximum exposures occurred during dryer unloading operations. Ventilation was rudimentary and ineffective. Results for airborne levels of ASC averaged 2.1 mg/lvP for the general room air, and 51 mg/lvi3 for the time-weighted, fullshift, breathing zone samples of the centrifuge-dryer operators. D. Medical Studies and Results The medical evaluation of ASC exposure consisted of three parts: (1) primary irritation index patch testing in rabbits, (2) 48-hour occlusive patch testing of employees, and (3) a medical interview and dermatologic examination. Medical studies were conducted during July 1973* 1. Primary Irritation Index to Rabbits (Patch Testing) In order to decide on an appropriate concentration of ASC for human patch testing, the primary irritation index to rabbit skin was first determined. On the basis of this study, the Primary Irritation Index to rabbits was 10^ (the highest concentration not causing erythema) and a 10?? solution was prepared for human patch testing. Twenty-nine male employees, aged 18 to 4l, volunteered for the study. Thirteen of these individuals were current employees in the ASC area. Sixteen had been reassigned to a different area of the plant after having developed problems. Each participant was questioned about health problems during his employment in the ASC area, examined by a dermatologist, and given 48-hour occlusive patch tests to solutions of ASC and sulfacetamide. Forty-eight and 72-hour readings at patch test sites were performed. Patch testing did not show any allergic responses at the patch testing concentrations to the ASC or the sulfacetamide. Onethird of those tested did show some primary irritant response at the border of the cloth square. All workers in this study had been symptomatic while working in the ASC area, including current workers. The various symptoms represented systemic involvement of eyes, nose, skin, throat, and chest. The degree of symptomatology seemed to fall into two groups: those who became symptomatic when working the drier and those who eventually became symptomatic to small amounts of ASC dust. There were twenty employees who were symptomatic only when empting the drier and nine employees who developed symptoms when -109- they are anywhere in the building. One employee having been removed from the area has continued to react even if he hand les small quantities of dust on the outside of containers of ASC in a separate warehouse. The interval between employment and development of symptoms was as follows: 8 after one day, 8 after one week, 8 after 2-4 weeks, 3 after several months, and 2 employees developed symptoms approximately one year after working with ASC. Dermatitis reported was largely con fined to the face and neck, but involved a few other sites as well. E. Conclusions On the basis of the environmental and medical studies it was determined that ASC produced toxic effects as used and found in the ASC production area. Toxicity reactions included irrita tion to eyes, skin, and the upper respiratory tract. It also appears that certain individuals, after an interval of ex periencing irritation at the levels encountered in this area in the plant, became sensitive to small amounts of ASC and developed symptoms characteristic of immediate allergy (hives, sneezing, wheezing, facial swelling). Irritation not allergy, however, was responsible for the skin problems. No attempt was made to determine a threshold level at which no symptoms occur in any employee. ASC C o n c e n tr a tio n s , B u ild in g #2 ft PQ ON CM CM O i--1 o vn 3| 1--1 T-1 CM i--1 CM to s EH ft H a> ft CD ra -p CO ft a> O CD CD cd o o H O rH H C5 ft d a P ft S H fpt o ft ft o Ph <D EH Ph 0 o Ph (D rH t> rH -P a) g g M p >H > >3 i O cd ft Ph Ph Ph <j; e CD PPPP o Ph EH r--1 U <*! HP ft ft ft cd ft > a) a) 0 U Ph M ft rH i--l *--i a> CD EH P i--i r--1 r--1 G cd >3 CD Ph 3 CO O ft X rs CD < Me r--i * EH o- O P PS PS 3 a) Ph ON oj ft ft ft ft O < P 1--1 03 -P CO Pd Ph CD O >3 * u cd 3 Ph rs OOS to <JO M rH VO CM Os CS oo CM CM 4- H rH rH oo o O o ft o S 0 Ph O ft -P cd 03 -P CD cd Ph Ph ft a) CD ft Ph o - Ph Ph 0 ft CO W Q 0 pq ft o PQ PQ PQ PQ o o o o r--1 O EH O ft ft H fjj EH in Ph CD ft O Ph Ph O <D -p >3 cd Ph Ph rH cd ft o Ph CD -P >5 Ph ft l 0 W) PS ft H i--i cd C ft o ft ft CO fH ft Ph O PQ O ft ft 3 S o tH SO >- CO Os rH Os tH P <B ft 1O CD Ph W) O PS -P ft cd H CD s o rH -P ft ft PS -H O ft CO Ph P C 0 O O -P -p pT | ft H ft to Ph c3 -P ft C rH CD PS a co Ph d) Ph ft PS o o ft in 0 Ph 3 03 O ft r--) 1 1 oj 0O X i--i w PS ft EH ft H tH CM tH CM tH CM tH CM pq a 03 H E cd ps -p ft ft CO M PSho ft H ft ft H cd CO p rH o --1 i-H o H O rH S'H 3 ft ft ft l EH 0 H <rs EH cd ft O O O O EH Os Os tH r--I Os Os tH tH <; Q \ CM \ CM \ CM \ CM \ CM \ CM \ CM \ CM PQ O ft S * Ph 0 i> "01T -111- <D w aJ p 0C) o 00 o Ph VO CM O- VO 00 rH 4- <x> CM oo CM 'g. rH CM -p4- o P o H R e p o rte d Symptoms o f ASC W o rk e rs F o llo w in g E x p o s u re P h o to s e n s itiv ity 1 o rH pa s0 p -3- 0^ CM CO CMOOOOVO^J- <T\ 1 CM CM CM H P H m <D 1 P C<DO Xi o <H o CO 'd CO Ccd <CDO xi $ CD Xi W) -P rH p o *a W) W) c rH ctHsl H 0) cd a) PA W -112- TABLE 3 Distribution of Dermatitis for Men Working with ASC Site of RashNumber Face 8 Neck 7 Forearm 3 Groin 1 Wrist 1 Legs 1 Trunk 1 TABLE 1 . DIETHYLSTILBESTROL CONCENTRATIONS ee oo oo PS os rP p H 01 01 CO H <D P p H H rH ft ft H > +Po> 0} p 0P Pi 0 0 01 0 0 H Td Xi -P rl H o CO CO < pP M H 01 p CO P 0 6 O ft o CM 01 o H ps P P >H 0 0o EH rH rH H t--1 H H P >P P cd H& > EH O O " * << 1 P1 co CO Pro t CO sS o * B B p0 01 Td P H p H p p> p H p ft CN O -- P i--I 0 > ft 6 o o o o PS H EH < O o P 0) H CO H Pi 0 0 'd Pi H rH 0 (1) P H 0 TO H 01 O O P1 H 00 00 _p ft o oo o rH cm ft .P o p p p w ON O- CO CO CO o o o o Eh CM CM CM CM CM c^ c~\ c^ <a! \ \ \ \ \ \ \\ P VO NO NO NO NO NO NO NO NO W MP Ph Oj CO p 01 p 01 p 01 p cd 0 cd 0 000 ft ft ft >H O S Eh 0 ft 0 ft 0 ft 0 Ph p <s P < rl H Se H 3: CO S O H EH co ps,S W EH\ Qg M W PS o -3 o CO CM rH oo rH O CM O 00 * * * -3" rH NO i--1 NO i--1 - C^N rH o s o o p p p H * w p Ph Cj s s CO CM co On ON CM O cn o 'J'N NO On On 00 co co o CO H i--1 rH rH 1--1 I--I 1--1 1--1 CM -en- URINE-DES LEVELS VS. EXPOSURE TIME XM -P CD 0 O CD CD tH > rH Mg cd in X M -P CD CD -3- <D p p i=> u .p x 3 -P CD o O <D XH^ -3- cm * * 1--1 * & X CD W -P CD P o\> CQ CD i> CD PI CO wM Q Xi <D | lp a) CD vO ^ P lH P X * *jd \r0 0 i o> . Q X p 1--1 s vO Hvn vn l--I * * * * * Q X P o- x (TV <r\ PPp XXX ** ** CM CM CN- 0^ P * VO CM O- O- X -3" 3- Om P l>- CM X p X CO vn cn -3 [>- p pP o- CM vO D-- Ov vn, X rH 0~\ cn CM XX n a) CD CD CD CD CD Td d Td d d P CD p CD p 0 p 0 H rH H ft ft ft ft 0 CQ pP MM to P H CD P H CO P H rH CD X rH o X rH 0 w rH 0 X CD CD p >J CD 0 rH 6 ft 3 g S3 W tH CM 0^ vp vO ts* CO Ov -HI o d P P .P 0 P 0 p ch cd P o H oP P H o -P H cd -p P o0 cd ft 0o P -P 0 P 0 ft o CO W Q d o .p o -p ch o ch Po 0 -p p M ft 0 e 0 P o cd 3 -P ch o d d 1 p <d cd 0 -P H 0 0 P P P X ft i--l -p 0 0 c3 H o 0 fcuo 6 Pc -P p H i--1 0 p X 0 0 o ft O .H pp 3 P 0 is o pS 0o op ft ch 0d M 0 0 0 P d cd 0 r--1 X 0d O0 H o P 0 i--1 d p. cd ch o t> o PX >5 H 0 d 0 -p g 0 1--1 0 1 00 -P 0 P -P o p o0 cd cd 0 p oP 0g 0 H ft 0 00 0 d 0 o X >5 o ,X O p o p I--1 ft p ft P cd rpH. o H g ft H f= X co W m* * * w *+ P * ** ** X* -115- ISOCYANATES IN PLASTICS MANUFACTURING Robert Vandervort, M.S. Steven K. Shama, M.D. U. S. Department of Health, Education, and Welfare National Institute for Occupational Safety and Health Center for Disease Control U. S. Post Office Building Room 508 Cincinnati, Ohio 45202 Abstract! An insulated container manufacturing facility employing approxi mately 290 individuals was evaluated. A sample population composed of 29 exposed and 7 control was studied via air sampling and clini cal testing. All measured environmental concentrations of TDI were below 37 ug/1VI3* All measured workshift-time-weighted-average ex posures of TDI were well below the current, ceiling occupational health standard for TDI (0.14 mg/)VI3 or 0.02 ppm) promulgated by the U. S. Department of Labor, and below the recently recommended stand ard for 8-hour time-weighted-average exposure (0.035 mg/^3 or 0.005 ppm) contained in the NIOSH criteria document for toluene diisocyan ate . The study population was selected to contain historically sympto-' matic and asymptomatic individuals. The study cohort of sensitive individuals were found during this evaluation to experience mild asthma and hay fever-like symptoms which, in general, did not re sult in reduced pulmonary function test results over the course of one workshift's exposure. Only one sensitive individual experienced more severe symptoms including difficulty in breathing, chest tight ness and congestion, and was demonstrated to have a significant de crement 'in pulmonary function test results after one workshift's exposure to low levels of TDI. The group of asymptomatic employees did not show a significant change in pulmonary function test results after one workshift's exposure. The study determined that exposure to TDI in this facility was pot entially toxic to sensitive employees. It was not positively est ablished how sensitive employees acquired their sensitivity to TDI. Although past exposures to transient high levels of TDI resulting from spills of foam materials were considered an important cause for employee sensitivity, sensitivity in some cases may have resulted from chronic exposure to low levels of TDI. ***** I. INTRODUCTION In response to a request for evaluation of industrial exposures to toluene diisocyanate (TDI) submitted by an authorized repre sentative of employees, an insulated container manufacturing facility was studied. The request was precipitated by cases of employees symptomatology which necessitated movement of affected -116- II. III. employees to new jobs. In accordance with Section 20(a)(6) of the Occupational Safety and Health Act of 1970, the pur pose of this health hazard evaluation was to determine whether potentially toxic concentrations of TDI were present in this plant during normal operating condidtions. Description of Plant Process Insulated ice chests, picnic jugs, and metal vacuum bottles were being produced with shells and liners made from styrene plastic and metal. Compressed styrene beads, fiberglas, and polyurethane foam were employed as insulating materials. The polyurethane foam -utilized in this application was based on TDI. Liquid foam material was semi-automatically dispensed into container shells. A, liner was placed inside the shell over the foam and held in place by a form. The urethane foam was then allowed to expand and fill the space between the con tainer shell and liner. Approximately 200 employees were ex posed to airborne TDI generated by the container foaming pro cess. Study Progress and Design During the course of the evaluation, the manufacturing facility was visited on three separate occasions by NIOSH investigators. The first visit afforded preliminary evaluation of environ mental TDI concentrations and medical interviews with exposed and transferred employees. Interviews revealed that eight employees then working on foam lines were not symptomatic, but that fourteen of eighteen (14 of 18) transferred workers had had symptoms consistent with intolerance to TDI at the time they were transferred. Most of the transferred workers gave similar histories of being unable to work near foaming opera tions because of the onset within minutes to hours of a pro ductive cough, chest heaviness, and wheezing. All had been foam machine operators or maintenance personnel. Because many workers were found to have apparently developed sensitization to TDI, an in-depth evaluation of exposures and workers was planned. Due to the large number of employees and variety of exposure possibilities, it was apparent that a re presentative group of employees would have to be selected for s tudy. Intensive environmental sampling was conducted during a second visit to the plant. Thirty-three samples and appropriate blanks were analyzed at the plant by a NIOSH chemist. Results of this sampling showed that TDI levels were well below the federal occupational health standard for TDI in all departments sampled (Range 0.0 to 32 ug/1V[3 with the average of all samples at 4.8 ug/M3). Also during the second visit, all plant employees (290), re gardless of job description or exposure to TDI, were asked to -117- fill ou.t a questionnaire designed to elicit a history of TDI exposure and any symptoms that may have resulted from such ex posure. Questionnaires were screened for major chest symptoms associated with foaming operations (i.e., cough, chest tightness and wheezing) and minor, non-specific irritative symptoms (i.e., yey, nose, and throat irritation). Cohorts of workders were classified as either symptomatic or asymptomatic. Symptomatic workders were those reporting coughing and chest tightness with congestion, or coughing, chest tightness and wheezing in association with foaming operations. Symptomatic employees were regarded as sensitive to TDI in that they ex perienced symptoms even though their exposure to TDI was dem onstrated to be very low. Asymptomatic workers were those not ing either minor, non-specific irritative symptoms or no symptoms as related to foaming operation, Twenty-nine exposed workers were selected for study; 13 symptomatic and 16 asymptomatic workers. The exposed study population was subdivided into moderate and low dose exposure groups on the basis of measured TDI concentrations. The low exposure group contained those workers who were trans ferred because of alleged sensitization and whose exposure to TDI was incidental. With attention to age, sex, and smoking history, the exposed population of 29 workders was matched with a control population of 7 individuals. The third visit to the plant commenced on a Monday. Each mem ber of the study population was given pre- and post-shift pul monary function tests. Exposed workers were asked to wear per sonal sampling equipment for the period between morning and afternoon pulmonary function testing. The study population completed an extensive medical questionnaire and three shorter questionnaires. The shorter questionnaires were administered before, after, and the morning after the monitored shift and allowed better correlation of symptoms with exposure levels and pulmonary function data. Serum samples were obtained from 35 of 3^ individuals in the study population. An additional 47 serum samples were obtained from other workers who were not involved in the complete study. IV. Criteria for Evaluation of Workplace Concentrations of TDI The occupational health standard for TDI as promulgated by the U.S. Department of Laborl is a ceiling value and stipu lates that employees are not to be exposed to TDI concentrat ions in excess of 0.02 ppm or 0.14 mg/M3. This ceiling stand ard may also be expressed as 140 ug/1W3. Recently, NIOSH has gathered criteria for the recommendation calls for an eighthour time-weighted-average exposure level of 0.005 ppm or O.O35 mg/)W3 in additon to the present ceiling value. This recommended time-weighted-average standard may also be ex pressed as 35 ug/t/13. -118- V. Evaluation Methods 1. Toluene Diisocyanate (TDI) Air Sampling Employee exposures to TDI were measured using personal air sampling equipment. Utilizing midget impingers, both work area and breathing zone samples were obtained. Reagents and analytical procedures followed the "modified" Marcali method as reported by Grim and Linch.3 Absorbance measurements were made using a Beckman Du spectrophotometer. Samples were an alyzed within hours of collection by NIOSH chemist in the field at the plant. In order to accurately measure the low airborne TDI concen trations encountered in this plant, sampling duration, and thus samply volume were greatly increased. Average sampling duration was approximately 150 minutes (range 13 to 4-80 minutes) yielding an average air volume sampled of approxi mately 300 liters (range 2o to 960 liters). 2. Pulmonary Function Testing Each pulmonary function test required the employee to make two forced expiratory volume practive maneuvers after which three forced expiratory volume maneuvers (reproducible with in 5%) were recorded as flow volume loops. A waterless, high fidelity spirometer equipped with an air temperature probe was used. Flow volume loops were displayed on a storage oscilloscope and recorded on magnetic tape. Computer analysis of the flow volume loops provided the following parameters (corrected to body temperature and pressure, saturated with water vapor): forced expiratory volume in one second (FEVi), and forced vital capacity (FVC). For the purpose of calculat ing A.M. to P.M. difference in group mean FEVi and FVC values, each individual's best FEVi and best FVC of his A.M. and P.M. trials were used. 3. Immunologic Assay - Serum Antibody Tests Each employee serum sample was subjected to a battery of six immunologic test procedures.^ These developmental tests in cluded those specifically designed to detect various types of antibodies resulting from specific isocyanate antigens. VI. Evaluation Results It is important to mention that work operations where employees were exposed to TDI in this plant were highly repetitive. Under near normal conditions foam machine operators and other assem bly personnel were exposed to relatively constant levels of TDI which were reflected by air sampling conducted during this study. However, according to employee and employer represent atives, there had been incidents when foam machines and assoc iated equipment malfunctioned and "spills" of foam material re- -119- sulted. These incidents undoubtedly produced transient elevated levels of TDI in the plant. During the days of this evaluation an incident such as this did not occur. 1. Toluene Diisocyanate (TDI) Air Sampling In excess of 125 individual air samples were collected and analyzed in the course of this evaluation. All measured environmental concentrations of TDI were below 37 ug/M3- On the day of clinical testing all measured workshift timeweighted-average exposures were at or below 30 ug/tI3* (Refer to Table I.) Thus, environmental levels of TDI were well below the current ceiling occupational health standard for TDI, and below the recently recommended standard for 8-hour time-weighted-average (35 ug/ftl3) contained in the NIOSH criteria document for TDI. 2. Medical Evaluation Table II contains A.M. to P.M. difference in FEVi and FAC values for the control group and the exposed subgroups. For each of the exposed subgroups (II through V) and for the control group (I), pulmonary function test results were eva luated using "paired t test" analysis of A.M. to P.M. mean differences in FEVi and FVC values. At the 95$ confidence level, only subgroup III (Symptomatic Employees with Low Exposure) showed a significant change in A.M. to-.dP.M. mean differences in FEVi and FVC values. When these differences for subgroup III were compared with corresponding values for the control group (I) using the "student t test", a signifi cant difference was found at the 95$ confidence level. These two statistically significant findings for subgroup III were reviewed with the knowledge that subgroup III contained only four individuals all of whom were transferred to new jobs be cause of intolerance to TDI. One of these individuals, be lieved to be exquisitely sensitive for TDI, recorded the greatest individual change in FEVi and FVC even though his time-weighted-average exposure to TDI during the monitored shift was 0.2 ug/k3. The "statistical" significance of sub group Ill's data can be attributed to this one individual's results. A.M. to P.M. mean differences in FEVi and FVC values for all symptomatic employees (subgroups II and III combined) and for all asymptomatic employees (subgroups IV and V combined) were evaluated via "paired t test" analysis. No significant diff erences were demonstrated at the 95$ confidence level. Results from the developmental serum antibody tests were not entirely consistent, but in certain cases were of limited aid in the evaluation of exposed workders. Table III shows the reported occurrence of symptoms before, after, and the evening after the monitored workshift. As can be seen there were no significant findings for the control -120- group (I). Employees in subgroup II (Symptomatic Employees with Moderate Exposure to TDI)displayed a marked increase of symptomatology over the workshift. Subgroup III (Symptomatic Employees with Low Exposure to TDI), which included those in dividuals who had been transferred to jobs away from foaming operations because of intolerance to TDI, displayed a definite increase in symptomatology. All workers in subgroup IV (Asymptomatic Employees with Moderate Exposure to TDI) ex perienced minor, eye, nose, or throat irritation at some time during the day of clinical testing. Subgroup V (Asymptomatic Employees with Low Exposure to TDI) reported symptoms other than minor irritation, but these symptoms were of a very mild nature. In summary, the study cohort of symptomatic (sensitive( in dividuals were found during this evaluation to experience mild asthma and hay fever-like symptoms, which in general did nto result in reduced pulmonary function test results over the course of one workshift's exposure. Only one sensitive in dividual experienced more severe symptoms and was demonstrated to have a significant decrement in pulmonary function test re sults after one workshift's exposure to low levels of TDI. The group of asymptomatic employees did not show a significant change in pulmonary function test result after one workshift's exposure. VII. Toxicity Determination The health hazard evaluation determination report for this study stated that toluene diisocyanate (TDI) was potentially toxic to sensitive employees at the concentration found during the evaluation. Through the use of comprehensive medical and work histories an attempt was made to discover how sensitive employees acquired their sensitivity to TDI. Although past exposure to transient high levels of TDI resulting from spills of foam materials were considered an important cause for employee sensitivity, several sensitive employees denied ever being exposed to a foam spill. Thus, some cases of employee sensitivity may have resulted from chronic exposure to low levels of TDI. The re port consequently stated that presently unaffected employees may possibly become sensitive in the future as the result of chronic low level exposure. The report also stated recommendations regarding medical monitoring programs, engineering control, employee protective equipment, and work practices. T1TL. References 1. Federal Register, October 18, 1972, Title 29, Chapter XVII Subpart G, Table G-l. -121- 2. Criteria for a Recommended Standard....Occupational Exposure to Toluene Diisocyanate. U.S. Department of Health, Education, and Welfare, Public Health Service, National Institute for Occupational Safety and Health, 1973- 3. Grim, K.E., and A.L. Linch. Recent Isocyanate-in Air Analysis Studies. Am. Ind. Hyg. Assoc. J., Vol. 25, May-June, 1965* 4. Scheel, L.D., R. Killens, and A. Josephson. Immuno-chemical Aspects of Toluene Diisocyanate (TDl) Toxicity. Am. Ind. Hyg. Assoc. J., Vol. 25, (179) 1964. Table I Workshift Time-Weighted GROUP Is Controls (7) SUBGROUP II: Symptomatic with Moderate Exposure (9) SUBGROUP Ills Symptomatic with low Exposure (Transferred) (4) SUBGROUP IVs Asymptomatic with Moderate Exposure (8) SUBGROUP Vs Asymptomatic with Low Exposure (8) 0.0 to 0.2 ( 0.1) 0.6 to 23-2 (5-2) 0.4 to 1.1 (0.6) 6.2 to 30.0 (17-0) 0.6 to 3*0 (2.2) -122- TABLE II Pulmonary Function Test Results Difference (A.M. to P.M.) Paired t Test GROUP I Controls (7) FEVl (liters) FVC (liters) Range -.15 to +.12 -.25 to +.05 Mean -.06 -.04 NS (p = .164) NS (p * .507) SUBGROUP IIt Symptomatic with Moderate Exposure (9) FEVi (liters) FVC (liters) -.19 to +.32 -.17 to +.33 +.02 -.04 NS (p = .802) NS (p = .440) SUBGROUP Hit Symptomatic with Low Exposure (transferred)(4) FEVi (liters) FVC (liters) -.53 to +.11 -.61 to -.09 -.16 -.31 s (p = .024; S (p = .004) SUBGROUP IV t Asymptomatic with Moderate Exposure (8) FEVi (liters) FVC (liters) -.14 to +.07 -.10 to +.14 + .02 -.02 NS (p = .417) NS (p = .492) SUBGROUP Vt Asymptomatic with Low Exposure (8) FEVi (liters) -.10 to +.01 FVC (liters)________________ -.17 to -.01 NS = Not Significant at the 95$ confidence level S = Significant at the 95% confidence level -.04 -.08 NS (p = .383) NS (p = .080) NO TABLE III submitted -123- Employee Number Sex ____ TABLE IV Before Shift Reported Symptoms* After Evening Shift______ After Shift GROUP I: 1 2 3 4 5 6 Controls (7) M ------------------------ f p ------------------------ p -----------------------M M ------------------------ a a SUBGROUP IIs 8 9 Symptomatic with Moderate Exposure (9) m ------------------------ a,c F ------------------------ b a ,b, c a,b, c 10 F a aa 11 M ------------------------ d, e a, d, e a,b 12 F ------------------------ a.b.c.e a 13 F ------------------------ a, d d a,b,c,d,e 14 F ------------------------ bicie 15 F ------------------------ b, c a 16 M a a,b ,c a,b,c,e SUBGROUP Ills Symptomatic with Low Exposure (Transferred) (4) 17 M ------- -- ---------- a 1 b 1 c a1b1c 1e a, b, c , d 18 M ------------------------ a b, c, e a,b,c,d,e 19 M ------------------------ a, e a 20 F a,b,c,d,ea,d,e a,c,d,e SUBGROUP IVs Asymptomatic with Moderate Exposure (8) 21 M aa 22 M a 23 M aa a 24 F aa 25 M aa a 26 F a 27 F a a,c a 28 SUBGROUP Vs 29 F -----------------------Asymptomatic with Low Exposure (8) M ------------------------ 30 F 31 F ------------------------ aa a,b, c b 32 M 33 f aa aa a 34 m a 35 M ------------------------ 36 F ------------------------ b a,b, e Symptoms: a = Minor, non-specific eye, nose, or throat irritation b = Coughing c = Chest tightness, soreness, or heaviness d = Wheezing or whistling e = Shortness of breath -124- EPOXIES IN SPORTING GOODS MANFACTURING James B. Lucas, M.D., and Bobby J. Gunter, Ph.D. U. S. Department of Health, Education, and Welfare National Institute for Occupational Safety and Health Center for Disease Control U. S. Post Office Building Room 518 Cincinnati, Ohio 45202 Abstract This paper reviews the cutaneous hazards associated with epoxy re sin systems. The dermatitis potential of the various components & numerous additives are discussed. Allergic contact and primary irr itant dermatitis caused by these agents are contrasted. The combined medical, epidemiologic, and environmental Hazard Eva luation approach to a recent outbreak of "epoxy" dermatitis occuring among the employees in a moderate sized plant engaged in the manufacture of epoxy-fiberglas composite skis and other sports equipment is described in detail. The importance of patch testing in elucidating the cause of this dermatitis outbreak is stressed and the essential steps in performing valid patch tests is dis cussed. The principal preventative measures and the industrial management of workers who have developed allergic contact dermat itis are presented. ******** Despite the great variety of modem polymer systems employed in modern technology, relatively few have known significant toxicologic effects. In fact, the majority of NIOSH hazard evaluation requests dealing with plastics have been accounted for by only two system?-- the polyurethanes and epoxies. The polyurethanes have been discussed by the previous speaker. With recent revelations concerning the health effects of poly vinyl chloride and its precursor, it now seems certain that compound is destined to make a significant increase in the Health Hazard Evaluation caseload. Of far greater importance to the dermatologist are the epoxy resir^san extremely versatile class of plastics. Commercially available since World War 11, these compounds are considered technically super ior in many aspects to the older phenolic and polyester resins. It is probable that domestic consumption now approximates 200 million pounds annually. The epoxies account for approximately 90?S of the dermatitis attrib uted to the plastic systems and thus constitute the vast bulk of the occupational health problems encountered by industrial users of these systems. Typical commercial epoxy resins are prepared by reacting epichloro- -126- hydrin with hydroxyl containing compounds, most frequently, bisphenol A, resorcinol, substituted phenols or alcohols. Most commerical pro duction, in fact over 90f, today employs bisphenol A. The epoxies are named for the characteristic two carbon, one oxygen ring structure show here: R - C -C - R " \/ 0 The usual production reaction may be depicted as follows: EPICHLOHYDRIN BIS-PHENYL A C - C - C-Cl + o-<3-c-<3- o \/ 0 NaOH - c - c - c -o-O-c-7 \/ 0 -0 -c - c - c - 0 -O-C -< >-0 - C - C - C I V |-- \/ OH > ' 0 N + NaCl + H , When the total ratio of N groups is less than one, the resins are usually liquids. These are produced by running the reaction with a large excess of epichlohydrin. By varying the conditions of the reaction polymers of low, medium, or high molecular weight can be produced. This is important in terms of dermatitis since the liquid lower molecular weight resins are both primary irritants and skin sensitizers. Among the raw materials, Bisphenol A is a sensitizer and cross re acts with both organic silicones and diethylstilbestrol. Epichlorohydrin is a severe vesicant with blistering and pain occurring some hous after initial contact. It is only occasionally a sensitizer, but is known to cross react with propene oxide. However, most epoxy problems occur during the subsequent utilization and application of the compunds rather than in their basic manufacture. Conversion to the thermoset state curing can be accomplished by reacting the resin with well over fifty different classes of chemical compounds. These compounds are variously termed hardeners, catalysts or curing agents. The most frequently encountered moieties are the primary, secondary and tertiary amines of both the aliphatic and aromatic series, phenols, organic acids and the anhydrides of mono-and difunctional organic acids such as phthalic or maleic anhydride. Sensitivity to hardeners is less frequent than to the resins themselves. However, of the hardeners, the amines are both irritants, because of their high pH, and sensitizers, while the anhydrides much less commonly -127- present problems. Once fully cured, epoxy resins are inert and are not a cause of dermatitis. In addition, various modifiers are fre quently added to the resin-curing agent systems. Diluents to reduce viscosity commonly include dibutyl phthalate, pine oil and mono-epoxy compounds. Reactive diluents are often irritants and sensitizers. Chlorine or bromine containing compounds are used to impart flame re sistance and retardance to the finished cured system. Plasticizers may be added to improve adhesive strength and extenders or fillers such as various silicas, silicates, aluminum powder, calcium carb onate and clays are used to reduce cost or alter handling or curing properties. Pigments are commonly added to color the final product. Obviously by varyirg the type of resin, curing agent, and various addiitives, literally thousands of differing final polymers with an ex tremely wide range of useful properties can be produced. This list of ingredients should also suggest to you that the unraveling of an "epoxy dermatitis* problem can be both a complex and time consuming task requiring careful analysis. In addition, the mechanical irr itation due to airborne fibrous glass spicules generated by sawing, grinding or sanding operations performed on fully cured epoxy com posites must also be kept in mind. Major properties shared by this polymer group include resistance to thermal shock, heat resistance, low flammability, high dielectric constant, lack of shrinkage upon curing, great adhesive and comp osite strength, and high degrees of environmental resistance. The applications of epoxy systems are already numerous and continue to expand at a rapid rate. The largest application is probably as coating compounds (metal primers, floor and masonary coatings and paints). Other extremely important commerical uses include elec tronic potting and encapsulating operations (high voltage ignition coils, telephone components); molding (small parts, toys, etc.); adhesives (metal bonding, maintenance, laminates for printed cir cuits); composites with some form of fibrous reinforcement usually fibrous glass (sports equipment, piping, automobiles bodies, air frame and aerospace components); and as stabilizers in chlorine con taining plastics such as poly vinyl chloride (meat wrapping films, piping, etc.). A typical example of the 5>proach utilized in problems of this sort is illustrated by a recent hazard evaluation requested by an employer who manufactured a line of high quality, essentially hand-crafted, tennis rackets and snow skis. Following a preliminary walk-through performed by a NIOSH physician and regional industrial hygienist, it was concluded that a significant incidence of dermatitis was occurring among hourly employees. From an even larger number of substances found in the work place, twelve materials were tentat ively selected as possible causes for the outbreak. These included two polyamide resins, butyl carbitol, two epoxy resins (Epon 815 & Dow 330), a polyol urethane coating solution, a mold release agent, an isocyanate containing urethane coating, a foam core polyol, paint stripper, a foam core isocyanate, and a silk screen ink. It was decided that patch testing would be essential to determine -128- whether the dermatitis was due to irritation or from sensitization and which substance or substances were responsible. Since patch testing can only be carried out using concentrations which are known to be non-irritating, it was first necessary to determine a skin irritation index for each substance. This was determined by app lying concentrations of 100, 50, 25, 10, 1 and 0,1# to separate intact and abraded skin areas on each of six male albino rabbits. Each site is evaluated at 24 and 48 hours and graded on a 1 to 4 scale ranging from mild irritation to corrosive effects and the highest concentra tion failing to produce even mild irritation in a majority of animals (irritation index) determined. These tests were carried out by the staff of the Toxicology Branch, Division of Laboratories and Criteria Development. To avoid any possible irritant effects in hypersensitive subjects, final concentrations for patch testing were made up to 5? of the strength indicated by the irritation index, using appropriate non-irritating solvents. Prior to any clinical investigations, a second walk-through of the facility was made and the plant nurse and records consulted. As a result it was further determined that' the dermatitis problem was al most exclusively confined to the ski molding area in which only three suspect substances were used. In this area pre-cut and weighed strips of fiber glass cloth are laid in steel molds and coated by spatula application with activated, pre-weighed and mixed epoxy resin which is obtained for each pair of skis from an automatic dispenser. After the mold is closed it is heated in an oven for several hours to fac ilitate curing. After the molds are broken open, excessive cured epoxy material is scraped from the skis which are then transferred to a different department for the final finishing steps in manufacture. The three suspect substances used in the department were the mold re lease agent, which was chlorinated was dissolved in methylene chloride, epoxy resin-Dow 330, and polyamide resin V-40. Twenty employees from the area were determined by interview to either have or to have had dermatitis. These were then examined and in eight cases the dermatitis was found to either be due to an obvious cause or was on a pre-existing non-occupational basis, excluding any need for patch testing. Diagnoses in this group included psoriasis, acute chemical irritation, glove maceration, chronic hand eczema, acne, and mechanical irritation due to fiberglas spicules. The remaining 12 workers had histories or physical findings suggestive of occupational contact dermatitis consistent with either the irrit ative or allergic varieties. Standard patch tests using the final 3 suspect substances were applied to the mid-back areas along with app ropriate diluent controls. Test sites were read 48 hours after app lication and confirmed by a second reading 24 hours later. The results were clear-cut. Sex workers had positive tests to epoxy resin-Dow 330 and all 12 had negative tests to the mold release agent and the polyamide resin. -129- In conclusion, epoxy resin systems are capable of producingboth primary irritant and allergic contact dermatitis. In most instances patch testing is required to definitely identify the allergic worker. This is an important distinction since sensitized individuals can expect severe and repeated bouts of dermatitis following even minor skin contact. They must also try to avoid any vapor given off, es pecially during mixing operations since the hardening process is an exothermic one. Severe facial and neck dermatitis commonly result from such exposure. The demonstration of actual sensitivity does not necessarily preclude future work with the substance, but such persons require careful reindoctrination regarding work practices to prevent or minimize future recurrences and to insure that they understand their responsibility in prevention. In the example given, 50% of workers tested were found to be sen sitive to epoxy resin-Dow 330. Breaks in.work technique and the relatively crude hand processing involved in this department were undoubtedly responsible. An examination of various work character istics such as age, sex, atopic diathesis, etc., for both sensitized and non-sensitized workers revealed only one major difference, i.e., the length of service in the ski moulding area. Sensitized workers had an average length of service of 17 months compared with 7 months for the non-sensitized. This was expected since repeated exposure is important in initiating sensitization. Thus, the lack of sen sitization in a given worker in no way precludes its eventual deve lopment or negates the importance of personal protective measures. Ideally, epoxies should be handled with "no-touch" techniques. Un fortunately, this is rarely entirely practical for many of the app lications in today's technology, and in any event, accidental skin contamination is always a possibility. In addition to the use of disposable gloves and long sleeved gowns or smocks, shoe coverings are advisable. Bench tops or other work areas should be covered with disposable paper to facilitate good housekeeping. Personal cleanliness is essential. Adequate washing facilities should be provided in close proximity to the work site since the use of such a facility is inversely proportional to its distance from the worker. The prompt removal of occasional accidental skin contamination by washing with mild soap and water is of utmost importance. Prompt washing will almost always prevent or greatly minimize the elicitation of dermatitis even in highly sensitized individuals since skin ab sorption, a necessary precursor to allergic contact dermatitis, re quires a considerable but variable time in which to occur. Washing within 20 minutes is usually preventative. Workers developing frequent, recurrent, or especially severe der matitis should be considered for transfer to other plant areas. In our experience, once a worker understands his role in prevention, transfer is seldom necessary. -130- -131- CHROMIC ACID IN ELECTROPLATING Steven R. Choen, M.D. Medical Officer Medical Sevices Branch and Richard S. Kramkowski Industrial Hygienist National Institute for Occupational Safety and Health U.S. Department of Health, Education, and Welfare Cincinnati, Ohio, 45202 In considering the hazards to worker health associated with the use of chromic acid in the electroplating industry, it may be of value to briefly review the basic elements which tend to govern the conduct of the Health Hazard Evaluation. The first stage of an Evaluation is the IDENTIFICATION of the hazard. In the case under consideration - which is relatively typical - The National Institute for Occupational Safety and Health (NIOSH) received a joint request from both the labor and management members at a plant involved in the production of chromeplated auto accessories. NIOSH was called upon to investigate worker allegations of nasal and skin damage resulting from ex posure to a chemical (s) which was being used in the plating pro cess. The request was apparently generated after a considerable number of employees in the chrome plating department filed work men' compensation claims for their alleged occupationally-induced damage. There are several chemicals, (acids, alkalies) used in a chrome-plating operation that might cause the nasal and skin dam age described in the Request, however, an "a priori" description of this type pathology would tend to bias our identification of the hazard heavily in favor of a chromic acid etiology. INVESTIGATION of the hazard, which is the second stage of an evalua tion, consists of 1; a review of the literature concerning all chemicals which have been been identified as a potential hazard and 2; the conduct of an epidemiologic study regarding the workers and all environmental factors which might impinge on the determination of whether or not the alleged hazard is toxic as found in the plant. A review of the literature on chromic acid should lead one to a con sideration first of the parent element, chromium, and an understand ing of some of its properties. The word chromium is derived from the Greek work "chroma" meaning color, which probably relates to the wide variety of pigmentary applications for which the element has been utilized since ancient times. Elemental chromium is not found free in nature; its most important mineral occurrence is in the form of chromite which is a dark=brown to jet=black octahedral mineral containing interstitial (most magnesium silicates and other silicates). Chromium forms three series of compounds with other elements and -132- these can be represented in terms of the chromium oxides: chromium valence +2, chroraous oxide, CrO; chromium valence +3, chromic oxide, CroO^j and chromium valence +6 or hexavalent chromium, chromium trioxide also known as chromic anhydride or by its more familiar name, chromic acid, CrO^. The valence with which chromium is en countered in an occupational setting is of particular importance in that Samitz and Epstein-1- have demonstrated chromium to be a serious health hazard only in its hexavalent form. Chromic acid is considered to be a strong acid and a powerful oxidizing agent. Compounds containing chromium in the hexavalent state are used in many industrial operations, including the man ufacture of inorganic pigments (eg. lead chromes, milybdate oranges, zinc chromate yellow, chromium oxide green, and others), wood pre servatives, corrosion inhibition, tanning processes, dyeing of textiles and "decorative" and "hard" plating processes. Chromic acid is employed extensively to coat the surface of various objects with the bright, shiny chrome metal finish with which we are all quite familiar. The chemical reactions that take place in the chrome plating process are not well understood. It is known that hexavalent chromium is transformed into chromium metal per se in conjunction with the passage of an electric current from an insoluble lead anode to a cathode which itself is composed of the object(s) to be plated. The reaction is carried out in a heated aqueous bath to which has been added small quantities of sulfuric acid, serving to enhance the uniformity of the chrome surfacing (i.e., enhance "throwing power"). However, even with the use of the acid and an elevated temperature bath the process is relatively inefficient at best. The result is the release of considerable amounts of hexavalent chromium, as chromic acid, into the workroom atmosphere were chrome electroplating is conducted. As might be expected, the presence of this contaminant was first suggested during the last 50-1 years by repeated findings of certain characteristic types of pathology in workers who had been exposed to such an environment. The immediate or acute effects of exposure to chromic acid, either as a solid or in concentrated solution, usually takes the form of a destructive action on body tissues. Contact with the eyes may re sult in irritation and conjunctivitis from dilute solutions, as well as potential loss of sight from contact with more concent rated solutions. Contact with breaks in the skin may cause "chrome sores," which appear as slow-healing, hard rimmed ulcers and leave the affected skin area vulnerable to infection from a secondary source shich as bacteria. Chromic acid dust or mist may irritate the nose, throat or lungs, taking the form of burning, itching, redness or "sneezing fits." Chemical bronchitis has been caused by high exposures. While severe internal distress may result from swallowing chromic acid, this would be an unlikely type of occupat ional exposure. Delayed or chronic effects of exposure to chromic acid, either to repeated or prolonged exposure to dust, mist or solutions, may -133- cause a primary skin irritation (appearing as redness and scaling at points of contact with clothing) or the development of an allergic condition (also called sensitization). Furthermore, repeated or prolonged exposure with mist of dust of chromic acid may result in damage to the mucous membranes of the nose, throat or lower res piratory tact....this may assume the form of irritation, erosion or ulceration of the membranes and in the case of the nasal septum, a perforation may result. However, the most serious potential threat of working with chromic acid relates to data on workers em ployed in the chromate-producing industry which have shown a greater incidence of cancer of the respiratory system in the latter group than in the general population. Such a grim conclusion has not been drawn from any employee population working only with chromic acid, nonethless the overall toxicity of this material is considerable and every attempt to prevent and control the occurence of the toxic effects should be undertaken by management and labor at a subject facility. The environmental control of chromic acid in the work room at mosphere should begin with an adequate ventilation system for open surface tanks (the criteria for such a system is provided in the Federal Register, October 18, 1972, Title 29, Chapter XVII, Sect. 1910,94, pp. 22154-57* Criteria have also been published by the American National Standard Institute and the American Conference of Governmental Industrial Hygienists). The preventive approach to dealing with any toxic material should incorporate a Safety program to deal with all aspects of the substance, as used in the particular plant. Employees should be apprised of correct procedures for hand ling, storage and spills of the chemical, as well as being supplied with and trained in the use of personal protective equipment (i.e., chemical goggles, safety glasses, gloves, sleeves, apron, and cover alls). All of the foregoing topics should be discussed thoroughly in an employee education program of an ongoing nature. In dealing with any material that is potentially hazardous to an employee's health and well being, it is essential that appropriate medical precautions be taken to prevent unnecessary employee risk. These precautions generally include medical examinations, the pro vision for employee education and consultation services, as well as the establishment of emergency protocols that can be utilized in the event of an acute intoxication. Once the basic toxicology of a given substance has been reviewed, the second phase of the hazard INVESTIGATION can be conducted with some degree of proficiency. In response to the request to NIOSH for assistance to evaluate potential chromic acid hazard, an in dustrial hygienist and a medical physician visited the'plant site. The first or preliminary visit was used to briefly interview most of the workers in the.facility, including management personnel while the industrial hygienist conducted a thorough examination of the work site and collected a few atmospheric measurements of potential contaminants. On the basis of the symptomatology elicited from the workers, it was felt that the complaints were quite suggestive of chromic acid toxicity. Therefore, in order to obtain more detailed -134- information from "both workers and their environment a second and third visit was planned. On each of our subsequent visits we administered formal medical questionnaires to each worker in the chrome plating area and to a selected group of workers from other areas (who were not expected to have any exposure to chromic acid) who might serve as a control population. We also contracted for the services of a dermatologist and otolaryngologist (ENT) from a nearby medical center to examine each of the workers who received a medical questionnaire. During this same period of time, environmental air samples were collected from the breathing zones of several workers in exposed and control areas. Additionally, a chemical spot test adapted from the method of Feigl^ was used to detect the presence of hexavalent chromium on various surfaces within the plant. A more detailed review of the analytical methods used in this study has been reported in a separate paper3. The demographic data (Table I) concering the electroplate workers in this study demonstrate that exposed and control groups are fairly well matched for age, race and length of employment in the plant. Although the groups are not correlated precisely for sex distribu tion, there is no known difference between the male and female bio logical response to chromic acid. The incidence of each index symptom (Table II) (that is a symptom consistent with chromic acid exposure) is higher for the workers in the chrome plating area than for workers in other areas of the plant. It is of interest that no worker in the control population complained of a nasal "sore" which was considered to be characteristic of chromic acid-type of exposure and was reported fairly frequently in the chrome platers. The mean length of time before a worker noted the appearance of any given symptom, on the average, was less in the control group than in the exposed group which suggests a completely different type of exposure in the former. In fact the control population was exposed to harsh acidic fumes emanating from a "pickling" operation in proximity to their work stations and workers in the chrome plating area were not so exposed. The results of the medical examinations showed that 35 of 37 (95f) workers in the chrome plating area had developed damage to the tissues in their noses, while a lesser number had developed skin damage (Tables III, IV, and V). The data collected statistically suggests that workers employed for longer periods of time had de veloped higher grade (i.e., more severe) lesions of the nasal mucosae. All except one worker in the control group had perfectly normal nasal tissues with no evidence of any damage and that one worker in the control population had a previous occupational history of probable exposure to chromic acid in a dyeing operation. How ever, while our medical data and examinations firmly established a presumptive etiology for the symptoms and pathology (i.e., chromic acid exposure), our environmental samplong (Table VI) showed atmospheric concentrations of the chemical to be present, but at very low levels. These measured levels were far too low to ex plain our medical findings using the current "criteria" that have -135- been established for a "safe exposure level" as found in the lit erature. Yet while our environmental air sampling was somewhat less than corroborative of the medical findings, the chemical spot test used to detect the presence of hexavalent chromium on workroom surfaces showed the chemical to be on virtually every surface tested, including not only work surfaces per se, but also eating tables, soda machine levers, rest room soap dispensers and faucet handles, etc. Our review of the scientific literature on chromic acid has revealed only five previous studies to date where an attempt has been made to correlate exposure (environmentally) to effect (medically)^-8. It is readily discernible (Table VII) that all previous studies had demonstrated much higher levels of chromic acid than found in our investigation. The resolution of this dilemma brings us to the last stage of the hazard evaluation, which ia an INTERPRETATION of the hazard.......... IS THE SUBSTANCE TOXIC AS USED OR FOUND? In this particular instance we considered the exposure to be toxic, in that we demonstrated occupationally induced nasal damage and skin damage in the chrome-platers and-not in the control group. However, we have also considered some possible explanations for the unusual environmental air levels in this study. Although another agent might be responsible for the findings in this study, it is very un likely in light of the fact that no other agent was detected in con centrations of a significant nature in the plant atmosphere. There may be industrial circumstances where this factor is of overriding importance, especially in an industry that is using new or unusual chemicals (for which no toxicology data exists), but such was not the case in this plant. It is possible that the present standard may be too hight to pre vent the occurrence of adverse health effects for exposure to chromic acid, The demonstration of a statistically positive association be tween the workers * length of exposure and the development of in creasingly severe nasal pathology in this study certainly suggests that very low concentrations of chromic acid in the atmosphere may, in fact, play such a role over long periods of time. This question and the question of whether we may be seeing the effect of low atmospheric levels of hexavalent chromium as measured in this plant can only be answered by looking with an epidemiologic eye at other facilities where similar conditions exist. This study, to the best of our knowledge, is the first study that has even examined levels of hexavalent chromium....previous studies report gross levels of chromic acid (which may have a considerable fraction of the toxic trivalent chromium in a given sample). Thus, the older liter ature may have reported high chromic acid levels without giving due consideration to the fraction of hexavalent chromium, More work is needed in this area to arrive at a meaningful conclusion to these queries. Finally, with regard to "other factors," there was, in particular, lack of emphasis on the principles of good industrial hygiene pract ice by both management and labor. These latter circumstances may be of greater importance in determining the etiologic factors con -136- tributing to the development of nasal lesions than the ambient levels of chromic acid. The transfer of chromic acid from the work surfaces to nasal tissues appeared to be a significant con sideration following our observation of the workers. The "transfer" or "direct contact" etiology seems to be born out by the results of our chemical spot testing for chromic acid on various workroom surfaces. Hexavalent chrome was detected on racks, parts, work tables, gloves (inside and outside) and the finger tips of a majority of workers in the chrome-plating area. A "direct contact" etiology for the development of nasal damage in such a facility (or similar industrial setting) may help to explain why the length of exposure prior to the development of nasal lesions has ranged so widely in the older literature and in the current investigation. Thus, a worker with good in dividual work practices and personal hygiene care may be free of pathology while working in the same plant stmosphere as a fellow employee who has a nasal perforation. The latter em ployee might be expected to have less than acceptable work habits and personal hygiene care. At any rate, our designation of this hazard evaluation as one in which there was considerable toxicity demonstrated among the exposed workers resulted from a careful INTERPRETATION of our findings in light of our IDENTIFICATION and INVESTIGATION of the hazard, both in the plant and in the literature. In orde to ameliorate the existing hazard at the facility under investigation it was recommended that the management establish an occupational health program to deal effectively with the current health and safety problems and the potential problems; and in keeping with the development of an occupation health program (as described elsewhere by the author9) it was recommended that the management institute the proposed program specifically en couraged in the recent NIOSH publication on the "Criteria for a Recommended Standard.......... to Chromic Acid."10 We also suggested that it migBnt be quite valuable for this facility to look into the work of Samitz and co-workers indicating that improved in dustrial hygiene practices and the utilization of chrome reduc ing solutions and ointments can help to successfully lower the incidence of cutaneous and nasal pathology in chromate exposed workers.111^ In that an estimated 15,000 American workers are potentially ex posed to chromic acid and since this Hazard Evaluation indicates that there is a need for up-dated work practice guidelines to govern the safe handling of chromic acid in the electroplating industry, it is appropriate that NIOSH review the current standard for a safe level of exposure to this chemical agent. -137- REFERENCES 1. Samitz, M.H. and Epstein, Es Experimental Cutaneous Chrome Ulcers in Guinea Pigs. Arch Environ Health, 5*^63 (1962) 2. Peigl, Fs Qualitative Analysis by Spot Tests, 3rd ed- P 262, Elsevier Publishing Company, New York 1946 3* Cohen, S.R., David, D.M. and Kramkowski, R.S.; Clinical In vestigations of Chromic Acid Toxcity - Nasal Lesions in Electro plate Workers, Cutis, April 1974 (in press). 4. Bloomfield, J.J. and Blum, W.: Health Hazards in Chromium Plating, Pub Health Rep. 43;2330 (1928. 5* Zvaifler, N. and Gresh, J.T.s Chromic Acid Poisoning Result ing from Inhalation of Mist Developed from Five Percent Chromic Acid Solution, J Ind Hyg Toxicol, 26:124 (Part 1 - Medical): 127 (Part 11 - Engineering) (1944). 6. Vigliani, E.C. and Zurlo, N: (Observations of the Clinica del Lavoro with Several Maxium Operating Position. Concentrations (MAK) of Industrial Poison.) Arch Gewerbepathol Gewerbyhyg. 13:528 (1955) (Ger). 7. Kleinfield, M. and Rosso, A.: Ulcerations of the Nasal Septum Due to Inhalation of Chromic Acid Mist, Ind Med Surg, 34:242 (1965) 8. Gomes, E.R.: Incidence of Chromium-Induced Lesions Among Electroplating Workers in Brazil, Ind Med. 41:21 (1972). 9. Cohen, S.R.: Another Look at the In-Plant Occupational Health Program, J. Occupat Med. 15:869 (1973)* 10. Criteria For A Recommended Standard....Occupational Exposure to Chromic Acid, U.S. Public Health Service Publication No. MSM 7311-21, Superintendent of Documents, U.S. Government Printing Office Washington, D.C. 20402 (1973). 11. Samitz, M.H., and Katz, S.: Protection Against Inhalation of Chromic Acid Mist. Arch Environ Health, 11:770 (1965) 12. Samitz, M.H., and Shrager, J.: Prevention of Dermatitis in the Printing and Lithographing Industries, Arch Dermatol, 94:307 (1966) -138TABLE I DEMOGRAPHIC DATA CONCERNING 52 ELECTROPLATE WORKERS WITH AND WITHOUT EXPOSURE TO CHROMIC ACID Sex Distribution Mean Age (years) male female Race Distribution Caucasian black Mean Length of Employment (months) Exposed (N=37) 7 30 29.1 (range 18-57) 36 1 26.9 (range O.3-I32) Non-Exposed (N=15) 9 6 31.1 (range I8-63) 15 0 26.1 (range 0.1-96) SYMPTOMS REPORTED FROM 5 2 ELEC TR O PLATE WORKERS iGoH f->i GftTc3d \o o CM CM o ca -0 -G B O-P II X H tH <1) CM w P ra ra 0 G 0) Go cao> H GP o cd oG H 0 PH o VPl rH CM CM CA VA ON 'A CA CA -4- H ft W) H*H G cd co o CO H >s cd o ,Q I-I oo p 0 MG ft G cd G rH 0 o *A o ft o oEH i--I d) rH CD G rOH G o W a) ft II g >A m o ft wX Eh PO 0 K EH M Ss o SC.M^ ca ca tH vr\ CM ca o o tH V--/ -N=Wt* CM o VO H ft ft AfCtD XS oo -p G oH ra MG fit! Ph cd xs gH GO P M O O *H cd cd rIIa w Eh g oEH oo /-s C^N O- <0s0^ >i*t 00 tH mD CM tH o CM CO >w* vO rH CA -d" rH CM tH i--I cd CO S3 o cd rcad Z ra 3 TO r0a H P G ft M .G GH G G no CD 0 GH GH oO 3 O O 0 0 l--1 &0 ra o CO 1--1 cd ra 3 G W GH CGO rH PQ o cd S3 CO og -- gpp ftp CD g G P So p ra g P fcUO CD GGG 0 *H O ra o ll CD -H CA GP ft CD o G M GP (D 0 ra G m G 0 H 0 G g3 tH O P oG ll CM * -6T -140- -141- THE SAFETY SPECIALIST ROLE IN INDUSTRIAL HYGIENE Ronald R. Ott, P.E., C.I.H. Occupational Safety and Health administration U. S. Department of Labor San Francisco, California 9^102 Ladies and gentlemen, may I first say how much I appreciate being asked by the Conference to attend this meeting and give this pre sentation. At the onset, however, I believe it best to say that the material given here is essentially my own under the auspices of the ACGIH and does not necessarily represent the policy or views of my employer. In considering the role of the safety specialist (S/) in dindustrial hygiene you may wish to think of this professional as if you were considering a sanitarian plant project engineer, or any other pro fessional with either an ancillary or parallel inspection role to that of an industrial hygienist. In this paper I would like you to follow a Safety Specialist on .what may be a typical governmen tal survey of an industrial plant. In this role the Safety Special ist will make a somewhat standardized safety inspection followed by a health hazard screening survey. In a closing discussion I will discuss professional and legal limitations that should assist establ ishment of boundaries of the safety specialist's role in indus trial hygiene. Various aspects of this survey have been simplified somewhat to emphasize principles involved. At the onset a safety specialist would proceed into a standard ized safety inspection. Initially pertinent information would be obtained at the plant office including, for examples 1. Accident frequency and severity records. 2. Pertinent air and medical monitor data. 3. General plant lay-out including raw material input versus product output as well as the number of employees at part icular work tasks. Once the office information gathering is finished, the safety special ist would start the preliminary walk-through survey. An audio re corder and/or written notes would be taken depending on both prefer ence and work conditions. During the walk-through survey the s/s could evaluate implementation of known safety performance standards as well as unsafe working conditions. Pertinent sketches and/or photographs of the plant would be made relative to safety violat ions as well as perspective lay-out photos for use during a sub sequent industrial hygiene survey. An evaluation of plant standard operational procedures (S.O.P.'s) would be made relative to over-all operation and maintenance. Separate or in conjunction with the S.O.P.'s, a visual and/or photographic eval uation of engineering controls and personal protective equipment -142- would also be made. As part of the walk-through survey general safety instrumentation determinations would also be made. These would include, for examples 1. Combustible gas indicator tests for verification of flam mability, or, safety performance standard enforcement. 2. Light meter to verify adequacy of lighting in regard to safety, i.e., trips, falls, etc. 3. Oxygen indicators for determination and evaluation of oxygen-deficient atmospheres (more complex cases usually need referral to an industrial hygienist). 4. Electrial safety instruments. 5. Air pressure gauge. Based upon this walk-through survey, safety control measures should obviate the necessity for subsequent health control measures where possible. For example, ignition points exposed to flammable gases and/or vapors should be controlled through in-process control or total exhaust ventilation rather than conbustion-proof lighting or electrical connections. Obviously total control at the source is the permanent engineering solution wherever safety or health is in volved. Sanitation is another area often ignored by all professionals, yet should be implemented to provide adequate washing and toilet facil ities, eating areas, etc., including housekeeping. The S/S may also either initially evaluate or implement controls relative to water supply and waste disposal. In regard to lighting, implementation of adequate lighting for both safety and health would further obviate the necessity for an addit ional follow-up survey by an industrial hygienist. The S/S could further implement the procurement and use of emergency respiratory equipment, general protective equipment, as well as emergency medical procedure including first aid, eye wash fountains and deluge showers. The final phase or secondary walk-through survey by the S/S will re quire applicable training of the S/S by an industrial hygienist. This phase is a hazard recognition and instrumental screening by the S/S. This survey may involve a further detailed analysis of com pany flow-diagrams and individual area or room processes. Also in cluded would be a detailed analysis and recording of specific phy sical and/or chemical agents that could be "unseen" hazards (such as labels. During the health screening survey an industrial hygiene screening form similar to that shown by Figure 1. is desirable. The use of the form itself can in turn consider suspect health hazards given by Figure 2, 3 and which a S/S should be readily trained to re -143- cognize. During such screening, the necessity for proper instrum entation is obvious. In specific cases involving exact performancetype health regulations or standards, particular violations could be cited (subject to final review by an industrial hygienist), where vio lations are later sent by mail. An example of two situations where conditions would be cited are the use of a light meter at specified locations (given in standard) in somewhat elementary situations, and use of a ventilation meter. The latter could be used at spec ified locations given in a standard, such as a spray paint booth (S/S trained in face velocity traverses). Smoke tubes may also be of considerable value, particularly in conjunction with photographs, in documenting insufficient capture velocities. As a health screening instrument, the combustible gas indicator, low scale; may be used for an "indication" of flammable vapors pre sent considerably below the LEL or lower explosive limit. As a rough estimate with pure solvents: {% LEL) X (fo concentration at LEL) = % Flammable vapors. A better estimate is possible if the meter manu facturer provides a "rough" conversion chart with the instrument. Obviously, although only an indication, this type of measurement together with chemicals involved, listed on the screening form, will be of great assistance to an industrial hygienist prior to an I.H. follow-up survey. The use of chemical indicator tubes with calibrated pumps may be of considerable value for gross determination of potential vapor/gas hazards, if hazards are known, for a more definitive referral to an industrial hygienist. In this regard the S/S should keep the supply of indicator tubes refrigerated when not in use to enhance or extend the life of the tubes. Calibrated tubes may also be used where chemicals are known to determine "trigger-level" concentrations. Such concentrations are those that would, in effect, "trigger" or require air monitoring of chemicals as well as certain medical tests for employees and necessary recordkeeping. The use of calibrated sound, level meters (SUVI's) with basic "A" weighted network (Type 2) could also be used for screening purposes, with documentation on the screening form. Dependent upon noise in tensities and time durations involved in exposure conditions, notes would be taken relative to basic administrative or engineering con trols in use, and hearing conservation program in force. DISCUSSION Professional and legal limitations must be considered for each S/S making health screening tests or actually citing health performance standard violations. Professionally, the S/S's technical education, experience, and time alloted for his/her over-all safety inspection must be considered. In some cases S/S's areas of expertise may some times excel those of an industrial hygiene generalist, considering both technical education and experience. In enforcement work professional organizations such as ACGIH and AIHA should continue to develop guidelines, establish precedents, so as to -144- establish qualified professional ethics for use in both general evaluation and strict legal areas. We must continually better de fine the make-up of professional duties of industrial hygienists versus safety specialists versus noise or other specialists. In dustrial hygienists should assume technical leadership in their areas of expertise for administrators, attorneys, judges, etc., and not be led by them. FINALE In closing, you can see then that the safety specialist's role in industrial hygiene must be that of a qualified professional working with a qualified professional. Neither should be subservient to the other----- both on equal terms. It is further obvious that industrial hygienists could do well to learn and better understand the safety specialist's over-all role including safety screening for him/her as may be applicable. -145- FIGURE I CSHO HEALTH REFERRAL Company____________ _____ _ Address________ Telephone:________________________ Inspection Date: 1. Name and title of employer's agent in charge: 2. Specify the particular building or worksite where alleged hazard is located: 3. Describe briefly the hazard which exist by completing the following information: Trade Name or Toxic Substance: Manufacturer and Address: Does material have a warning label? Yes No Physical Form: Dust_______ Gas_______ Liquid_______ Mist_______ Other Type of Exposure: Inhalation_______ Ingestion_______ Skin Contact No. of Employees Exposed: Length of Daily Exposure: Activities of Employees During Exposure_______________________________________________ 4. Describe the nature of conditions or circumstances which may produce illness or show symptoms of exposure.___________________________ ________________________________ 5. CSHO: (Rev. 1/74) -146- FIGURE 2 HEALTH HAZARDS EXPOSURE DETECTION GUIDE 1. TARGET HEALTH HAZARDS t A. Carbon Monoxide B. Asbestos (cutting, dry application) C. Lead D. Raw Cotton Dust E. Crystalline Silica (Quartz, Silica Sand, etc.) 2. SUSPECTED CARCINOGENS: Cancer-producing agents detection will depend on the employer-user's knowledge and his possible inquiries during the course of inspection. 3. POISONOUS GASES: A. Chlorine B. Fluorine C. Phosgene D. Hydrogen Cyanide, etc. 4. OXYGEN DEFICIENT ATMOSPHERES: Basically, closed and semi-closed spaces or non-vent ilated, closed work areas such as silos, tanks, etc. -147- FIGURE 3 HEALTH HAZARDS EXPOSURE DETECTION GUIDE 5. IONIZING RADIATION: (A. E. C. PERMITTEES ONLY) A. X-Ray B. Natural Radio Isotopes 6. NON-IONIZING RADIATION: A. Micraowave B. Lasers 7. EXCESSIVE NOISE: Steady, Intermittent, or impact. 8. COMBUSTIBLE GAS (es) USE: A. Methane B. Hydrogen C. Acetylene -148FIGURE 4 HEALTH HAZARDS EXPOSURE DETECTION GUIDE 9- SPRAY-PAINTING, LACQUERING OPERATIONSt (check ventilation and personal protective equip ment usage.) 10. SOLVENTS AND VAPOR DE-GREASING OPERATION: A. Contact dermatitis t>. Respiratory difficulties 11. OPEN-SURFACE VESSEL/TANK OPERATIONS: A. Plating Shops B. Acids, Alkalies C. Miscellaneous Corrosives 12. INADEQUATE ILLUMINATION: (Such as would hear on employee protection.) APENDIX DOCUMENTATION OF THE 1974 THRESHOLD LIMIT VALUES -149- -150- ARSENIC, INORGANIC SALT, ARSENIC TRIOXIDE AS As TLV, 0.25 mg/m3 as As In the roasting of copper ore in this country, crude arsenic trioxide, sulfur dioxide and other gases are driven off, the AS2O3 is condensed as a dust, reheated and cooled, and again condensed, and the purified AS2O3 is bagged or barreled. A typical analysis of this purified "white arsenic" is 97.3% AS2O3, 0.06% Pb, 1.9% 8620^ with traces of H20(l). Occupational exposures solely to As20g have been reported to result in contact dermatitis and sensitization, conjunctivitis, and ulceration and perforation of the nasal septum (1,3); cancers from exposure to arsenic have followed 1) the internal use of Fowlers Solution (4), an aromatic solution of potassium arsenite, 2) inhalation and skin contact exposure to sheep-dip dust (5) a mixture of sodium arsenite and sulfur, or 3) the combined in halation of AS2O3, sulfur dioxide and minor amounts of heavy metal oxides (1,2,6,7)*. Experimental cancers in animals have not been produced from AS2O3 despite several attempts (8,9,10), and the conclusion has been reached after an extensive review that "it is improbable that arsenic (per se) plays a significant role in the generation of cancer (10)." A search of the world literature reveals no reports of industrial or experimental exposures solely to AS2O3, which contain both environmental and toxicologic criteria from which a TLV can be unequivocally based. How ever, information helpful in arriving at a TLV for AS2O3 on a reasonable basis is available by estimating the exposure levels from the urinary arsenic values in smelter workers (2). [In this calculation, it is assumed that arsenical dermatitis, and not cancer, is the response from AS2O3 alone.] Total urinary As values among smelter workers averaged 0.8 mg/day over a period of years. If 12 to 14% of this value is dietary As, or 0.7 mg, and that, of the 8 m^ of air inhaled during a workshift, 50% is deposited in the body, and of that, 50% is retained in the tissues or excreted in the feces, a TLV of 0.25 mg As/m3 as a TWA is estimated to be a reasonable air limit. Reduction from the previous TLV of 0.5 mg/m^ seems warranted on the poss ibility that airborne AS2O3 contributed to the arsenical dermatitis reported (2). References: 1. Pinto, S.S., McGill, C.M.: Ind. Med. & Surg. _22, 281 (1953). 2. Pinto, S.S., Bennett, B.M. : Arch. Envir. Hlth. ]_, 583 (1963). 3. Birmingham, D.J. et al.: Arch. Derm. _91, 457 (1965). 4. Graham, J.H. et al.: J. Invest. Derm. 57, 317 (1961). 5. Hill, A.B., Faning, E.L.: Brit. J. Ind. Med. _5(1), 6 (1948). 6. Milham, S. Jr., Strong, T.: Envir. Res. (1974). 7. Lee, A.M., Fraumeni, J.F. Jr.: J. Natl. Cancer Inst. 42, 1045 (1969). 8. Hueper, W.C., Payne, W.W.: Arch. Envir. Hlth. 445 (1962). 9. Baroni, C. et al. : ibid. 7^, 668 (1963). 10. Vallee, E.L. et al.: Arch. Ind. Hlth., 21, 132 (1960). -151- BENZENE - Skin C6H6 TLV, 10 ppm (Approximately 30 mg/m^) Benzene as an acute poison produces narcotic effects comparable to those of toluene. Chronic intoxication by benzene is by far the most serious disease caused by the common hydrocarbon solvents. Its action is primarily on the bone marrow resulting in numerous blood changes and, in serious cases, aplastic anemia, with a frequently fatal outcome. It is unique among the hydrocarbons as a myelotoxicant, according to Gerarde (1). Elkins (2) stated that more than 140 fatal cases of benzene poison ing had been recorded prior to 1959. Vigliani and Saita (3) listed 26 deaths from chronic benzene poisoning in two provinces in Italy between 1960 and 1963. Eleven of these cases were diagnosed as leukemia, which frequently develops several years after cessation of exposure to benzene. Many of the deaths from benzene have resulted from exposures of the order of 200 ppm or more. Bowditch and Elkins (4) estimated that of eleven fatal cases, three resulted from concentrations in excess of 200 ppm, four from concentrations between 100 and 200 ppm, and three from concentrations judged to be below 100 ppm (but not measured). Greenburg et al. (5) described nine cases, with one death, in the rotogravure printing industry. Of 48 air analyses, 20 showed less than 100 ppm, and 15 more than 200 ppm. Savilahti (6) found that 107 of 147 workers in a shoe factory revealed blood abnormalities. The source of the benzene was cement, and concentrations were reported to have ranged from 318 to 470 ppm (these seem high for shoe cementing operations). One death occurred. Winslow (7), however, reported blood changes in workers where con centrations of benzene vapor below 100 ppm were found. Heimann and Ford (8) found one death and three cases with blood changes where air analysis for benzene showed a concentration of 105 ppm. Wilson (9) reported three fatal cases in a plant where the average concentration of benzene vapor was 100 ppm. Hardy and Elkins (10) recorded one death and several cases of blood changes in a plant where repeated air analyses indicated benzene vapor concentrations of about 60 ppm. Blaney (11) found little evidence of benzene intoxication in a group of 90 workers regularly exposed to benzene for about 13 years. Concen trations were generally low, but urinary phenol measurements indicated some exposures of the order of 25 ppm (12). Pagnotto et al. (13) found rubber-spreaders exposed to benzene concentrations ranging for the most part between 6 and 25 ppm. A limited number of blood studies showed some abnormalities, but no apparent correlation with exposure. So far as is known, none of this group developed serious blood dyscrasias. Deichmann et al. (14) found that rats exposed 5 hours per day, 5 days per week for from 5 to 8 weeks to benzene at concentrations of 44 and 47 ppm developed a moderate degree of leukopenia, but no leukopenia when exposed at con centrations of from 15 to 31 ppm, thus establishing an approximate threshold -152- for this blood dyscrasia for rats, at least under these conditions, of some level between 31 ppm and 44 ppm. Some substantiation for these findings was reported by Nau et al. (15) who found a decrease in the number of white blood cells of rats which had been exposed to benzene at 50 ppm for 756 hours on an exposure schedule of 8 hours per day, 5 days per week. The rats also showed reduced amounts of DNA in the white cells, a depression in myelocytic activity, and an increase in the relative number of red cell percursors in the bone marrow. Considering the borderline changes in the formed elements of the blood in both man and animals that occurred from not excessively long periods of exposure at levels only slightly above that of the 1973 TLV of C 25 ppm, a TLV of 10 ppm as a time-weighted average is recommended with a ceiling value of 25 ppm. Other recommendations: Cook (1945) 50 ppm; Smyth (1956) 35 ppm; Elkins (1959) 25 ppm; ANSI (1969) 10 ppm; USSR (1972) 3 ppm; Czechoslovakia (1969) 16 ppm. References: 1. Gerarde, H.W.: Toxicology and Biochemistry of Aromatic Hydrocarbons, Elsevier Publishing Co., NY (1960). 2. Elkins, H.B.: Chemistry of Industrial Toxicology, p. 103, Wiley & Sons, NY (1959). 3. Vigliani, E.C., Saita, G.: New Eng. J. of Med. 271, 872 (1964). 4. Bowditch, M., Elkins, H.B.: J. Ind. Hyg. & Tox. 21, 321 (1939). 5. Greenburg, L., Mayers, M.R., Goldwater, L., Smith, A.R.: J. Ind. Hyg. & Tox. 21, 395 (1939). 6. Savilahti, M. : Arch. Gewerbepath. u. Gewerbehyg. _15, 147 (1956). 7. Winslow, C.E.A.: J. Ind. Hyg. 9, 69 (1927). 8. Heimann, H., Ford., C.B.: NY Ind. Hyg. Bull. p. 224 (Nov. 1940). 9. Wilson, R.H.: J. Lab. Clin. Med. 27, 1517 (1942). 10. Hardy, H.L. Elkins, H.B.: J. Ind. Hyg. & Tox. 30, 196 (1948). 11. Blaney, L.: Ind. Med. & Surg. 19, 227 (1950). 12. Walkley, J.E., Pagnotto, L.D., Elkins, H.B.: Am. Ind. Hyg. Assn. J. 22, 362 (1961). 13. Pagnotto, L.D., Elkins, H.B., Brugsch, H.G., Walkley, J.E.: Am. Ind. Hyg. Assn. J. 22, 417 (1961). 14. Deichmann, W.B., et al.: Tox. Appl. Pharm. 5_, 201 (1963). 15. Nau, C.A., et al. : Arch. Environ. Hlth. _12, 382 (1966). BUTANE CH3CH2CH2CH3 600 ppm (Approximately 1,420 mg/m^) Butane, like other homologues in the straight chain, saturated aliphatic hydrocarbon series (pentane, hexane) is not characterized by its toxicity, but rather by its narcosis-producing potential at high exposure levels. A 10-minute exposure at 10,000 ppm (1 per cent) to -153- butane gas results in drowsiness, but no other evidence of systemic effect (1). The odor of butane is not detectable below a concentration of 5,000 ppm and thus does not provide any warning until levels greater than 10-fold the recommended TLV. No published report appears to be available indicating that butane is significantly irritating at moderate levels of exposure. The TLV of 600 ppm is recommended by analogy to pentane, the next higher homologue, whose properties it shares (2). References: 1. Gerarde, H.W., in Patty, F.A., Ind. Hyg. and Tox., Vol. II, p. 1198, Interscience, NY (1962). 2. Wirtschafter, Z.T., Bischel, M.G., Arch. Ind. Hlth., 21, 152 (1960). BUTYL LACTATE TLV, 5 ppm (Approximately 25 mg/m3) ' | N)(CH2)3CH3 OH Butyl lactate, a liquid acid having a boiling point of 160-190 C; slightly soluble in water and completely miscible with alcohol and ether, is used as a major vehicle component in paints and stamping processes. Prolonged exposures at levels around 7 ppm with short, peak expos ures of 11 ppm resulted in headache, irritation of the pharyngeal and laryngeal mucosa with coughing in all workers. Some workers complained nausea and vomiting was experienced. Complaints of irritation of the conjunctiva were not confirmed by examination. Routine blood and urin alysis showed nothing abnormal. Some of the symptoms of exposure (headache and coughing) and signs (pharyngitis) were related to air concentrations of 4 ppm measured with a personal monitoring device. When, however, exposure concentrations were below 1.4 ppm (7 mg/m^) no signs or symptoms of butyl lacate exposure occurred and medical exam inations were negative (1). Subsequent information (2), using improved sampling analytic method, indicated that, whereas levels of 7 ppm produced a readily discernible odor of butyl lacate, this concentration was not found to be objectionable or injurious. In view of these findings, a TLV of 5 ppm is recommended to prevent irritation of mucosal surfaces and headache. References: 1. Written communication to Committee Member from Drs. H. Zuidema and H.J. Pel, Philips Eindhoven, Netherlands, April 21, 1969. 2. Dr. D. Turner, British Petroleum Co., Ltd., dated March 27, 1972. -154- C BUTYL ALCOHOL (n-Butanol) - Skin C4H9OH TLV, 50 ppm (Approximately 150 mg/m^) Tabershaw, et al. (1) reported eye irritation in workmen in concen trations above 50 ppm, but no systemic effects below 100 ppm. Sterner, et al. (2) followed workmen for ten years exposed to butyl alcohol concen trations held at 100 ppm, and for briefer periods at 200 ppm. Neither irritation or systemic effects were found at 100 ppm, but there was some eye irritation at 200 ppm. Smyth (3), exposing rats, found that they were not killed in four hours at 8,000 ppm. He concluded that no narcotic or irritative effects are to be anticipated at 100 ppm. Nelson and associates (4) exposed human subjects to varying concentra tions of n-butanol vapor, and reported mild irritation at 25 ppm, which became objectionable and was followed by headaches at 50 ppm. More serious systemic effects in the form of auditory nerve and vestibular injury have been reported in workers outside the USA, France and Mexico. Seitz (5) reported severe vertigo, "vertiges gravis" in 5 workers exposed to butyl alcohol during the period 1929 to 1944. Velasquez (6) and Velasquez et al. (7) reported audiologic impairment from exposure to butyl alcohol. Of 11 workers exposed to n-butyl alsohol at a chromatographically measured concentration of 80 ppm, for from 3 to 11 years without personal protective equipment from noise, 9 experienced greater hearing loss (hypoacusia) in direct relation to the exposure time in comparison with a control group of 47 exposed to measured amounts of industrial noise of 90 to 110 dB, but not exposed to butyl alcohol. The averages in hearing loss in the exposed group were not large, but had central frequencies of 21.94 dB (11.59 dB min. and 32.39 dB max.) with a mean widening of the break between 3,000 and 4,000 Hz of 42.22 dB. There was a tendency to decrease as the frequencies moved away from the central zone. The age of the affected workers was from 20 to 39 years. In view of the apparent potential of n-butyl alcohol to increase hear ing loss in the younger age group of workers and to impair vestibular function at levels somewhat below 110 ppm, a TLV of 50 ppm as a ceiling value is recommended. Cook (1945) and Elkins (1959) recommended 50 ppm; Soviet limit (1966) 65 ppm; Czechoslovakia (1969) 30 ppm. References: 1. Tabershaw, I.R., Fahy, J.P., Skinner, J.B.: J. Ind. Hyg. & Tox. 26, 338 (194 ). 2. Sterner, J.H., Crouch, H.C., Brockmyre, H.F., Cusack, M.: Am. Ind. Hyg. Assoc. Quart. ^LO, 59 (1949). 3. Smyth, H.F., Jr.: Am. Ind. Hyg. Assoc. Quart. jL7, 148 (1956). 4. Nelson, K.W., Ege, J.F., Ross, M., Woodman, L.E., Silverman, L.: J. Ind. Hyg. & Tox. 25, 282 (1943). -155- 5. Seitz, B., Soc. Med. Hyg. du Travail: April 10, 1972. 6. Velasquez, J., Med. del Trabajo: _1, 43 (1964). 7. ibid, et al. Presented at the SVI International Congress Occup. Hlth. Tokyo, Sept. 21-28, 1969. CADMIUM DUSTS and SALTS -- as Cd TLV, 0.05 mg/m^ Inhalation overexposure to cadmium dusts, salts and fume* over a number of years results in chronic cadmium poisoning, a disease char acterized by a distinctive, nonhypertrophic emphysema with or without renal tubular injury, in which urinary excretion of a protein of molecular weight of 20,000 to 30,000 occurs. This protein does not react to routine proteinuria tests, and is by itself an indicative sign of early but reversible chronic poisoning. Further inhalation overexposure results in irreversible renal tubular damage, which may progress into a complete Fanconi syndrome with decreased tubular reabsorption of proteins, glucose, amino acids, calcium, phosphorus, and with decreased ability to acidify and concentrate the urine. Other reported toxic effects include anemia, eosinophilia, anosmia, chronic rhinitis, yellow discoloration of teeth and bone changes. (1,2,3,4) Princi (5) studied 20 American cadmium smelter workers exposed to concentrations of cadmium fume ranging from 6.59 to 0.98 mg/m^; cadmium oxide dust of 17.23 mg/m3; and cadmium sulfide of 31.30 mg/m^. They reported generally lower than expected hemoglobin concentrations and red blood cell counts, and an increased number of eosinophiles, as well as a yellow ring on teeth of 9 of the 15 workers who still had their own teeth. High urinary specific gravity values were found in all cases and ascribed to the higher urinary concentrations expected during the summer months of the study. Results of other routine clinical tests were not reported, although the boiling test for protein was negative in all cases (6). No special tests for cadmium proteinuria or pulmonary function studies were done. *See separate documentation for Cadmium Fune also. On the other hand, Friberg (7) reported anosmia, proteinuria of low molecular weight, pulmonary emphysema, yellow ring on the teeth, eosinophila, anemia, renal calculi, and other findings in workers with exposure of 20 years to concentrations between 3 and 15 mg/nr* of dusts of cadmium and its oxide, although average exposures were probably lower (4). Potts (8) reported urinary excretion of the low molecular weight protein, anosmia, glycosuria and other findings among British alkaline battery plant workers exposed for at least ten years to cadmium oxide dust. For the previous eight years, these exposures had seldome exceeded 0.1 mg/m^; and for seven years before that, 0.5 mg/m^. However, prior to those 15 years, cadmium oxide dust concentrations were measured at between 2.8 to 0.6 mg/m3 in two major work areas; and 236 mg/m-*, at a third. -156- Kazantzis et al (9) reported pulmonary emphysema and renal damage of definite tubular nature among British cadmium pigment workers exposed to the insoluble sulfide and sulfoselenide salts of cadmium. Hypercalciuria, renal calculi and colic, and nephrocalcinosis were reported also among these workers. No data on air concentrations of cadmium were reported. Nicaud et al (10) reported skeletal changes, osteoporosis and pseudofactures in 4 female and 2 male workers with an average exposure of ten years to cadmium oxide dust at an alkaline accumulator factory in France. These changes were reversed by administration of calcium and vitamin D. Anemia and eosinophilia also were reported, but not so any data on air concentrations of cadmium oxide dust. Suzuki et al (11) reported proteinuria and glycosuria among 27 Japanese vinyl chloride film plant workers examined in 1963 and exposed to cadmium stearate dust concentrations ranging from 0.69 to 0.03 mg/m^ for 80 minutes per eight-hour work shift. A year later, these authors (11) examined 19 men exposed to cadmium stearate dust, including 17 examined in 1963, and 24 unexposed controls, all working at the same factory. Concentrations of cadmium stearate dust had been lowered and ranged from 0.24 to 0.02 mg/m^, with average exposures of the same duration as the previous year. Proteinuria was reported in 12 of the 19 exposed workers. Among the 17 men reexamined, a greater amount of proteinuria was found in 8, and 5 new cases of proteinuria had developed. Glycosuria was reported in six of the exposed workers. No difference was found in the frequency of occurrence of respiratory symptoms or in results of pulmonary function tests between the exposed and control groups. Most of the above reports indicate cadmium concentrations grossly in excess of recent TLVs. In many such cases, simultaneous exposure occurred to various cadmium chemicals with probably different degrees of absorption and chronic toxicity; and also to noncadmium compounds with different, possibly even synergistic or antagonistic effects. Additionally, extraneous malnutritional factors in one of the original studies (10) were not evaluated properly, which led to erroneous inclusion of the bone findings reported as specific toxic effects of cadmium in chronic occupational poisoning, confusing this area for decades. Chronic cadmium poisoning is an insidious disease which once established may progress despite no further cadmium exposure: Consequently, the development of new cases of chronic poisoning in the storage battery, cadmium pigment and other industries a decade or more after the reduction of cadmium concentrations to 0.1 mg/m^ or lower was most likely the result of continuing toxic effects from those gross overexposures prior to the installation of proper industrial hygiene control systems. However, Lauwerys et al (12) reported in 1974 on the first published epidemiological investigation of the effects of occupational longterm, low level exposure to cadmium dusts. They studied 80 workers exposed to cadmium dusts in three plants: An electronic workshop, a nickel-cadmium storage battery factory, and a cadmium-producing plant. The workers were divided into three study groups: 1) 31 women, and 2) 27 men with less -157- than 20 years exposure; and 3) 22 men with exposures of 21 to 40 years. In each factory a control group was chosen to match the exposed group with respect to sex, age, weight, smoking habits and socioeconomic status. Total airborne cadmium concentrations were determined for approximately four hours in the operators' breathing zones at different work sites for the exposed and control groups, and they were repeated four to five times. Data analyses revealed that Group 1 workers had had a mean inhalation exposure dust period of 4.1 years to average total and respirable cadmium dust concentrations of 0.031 and 0.0014 mg/m3, respectively. Group 2 workers had experienced a mean inhalation exposure period of 8.6 years to an average total cadmium dust concentration of 0.134 tng/m^. (The average respirable cadmium dust concentration at the most polluted work site for Group 2 was 0.088 mg/m3.) The 22 workers in Group 3 had been exposed for an average of 27.8 years to mean total and respirable cadmium dust con centrations of 0.066 and 0.021 mg/m^, respectively. Results of biological tests showed that among smokers and nonsmokers in Group 2 all the pulmonary function indices were lower than in the corresponding controls, although none of the differences were statistically significant. However, in Group 3 workers a slight but significant reduction in forced vital capacity, forced expiratory volume in one second, and peak expiratory flow rate was found, as compared with the control group. Kidney damage was more pre valent, since excessive proteinuria was observed in 15 percent of Group 2 and 68 percent in Group 3 workers. The latter group also showed slight but statistically significant changes in the level of three blood enzymes (plasma {$-galactosidase, plasma lactate dehydrogenase, and erythrocyte acetylcholinesterase); as well as significantly lowered hematocrit (hemo globin) results, as compared with the corresponding control group. The investigators commented that the study results showed the kidney to be more sensitive than the lung to the toxic effects of cadmium, although the methods used were more likely to demonstrate a kidney lesion than a lung function impairment. It was noted that no major modifications had occurred in the different industrial processes since their installation in these three factories, and that the levels of airborne cadmium dusts measured in this study could thus be adjudged to be quite representative of past exposure. Consequently, they also commented that their data results supported a TLV of 0.05 mg/m3 for cadmium dusts. In 1963, Stokinger (2) stated that on a chronic cadmium accumulation basis, a TLV limit of 0.1 mg/m3 might not provide the desired factor of safety. Basing their conclusion on nonoccupational data, Friberg, Piscator and Nordberg (13) recommended in 1971 a TLV reduction to 0.008 mg/m^ for exposures not exceeding 25 years. A TLV of 0.05 mg/m^ for cadmium dusts and salts based on the occupational data reviewed above currently would appear to provide adequate protection against the possibility of systemic effects of chronic cadmium poisoning. The Soviet Union (1967) and Czechoslovakia (1969) both recommend 0.1 mg/m^, Finland (1972), 0.02 mg/m3 for cadmium dust. References: 1. Browning, E.: Toxicity of Industrial Metals, p. 103, Appleton-CenturyCrofts, New York (1969). -158- 2. Stokinger, H.E.: The Metals (Excluding Lead), in Patty, F.A., Industrial Hygiene and Toxicology, Vol. II, E. W. Fassett and D.D. Irish, eds.. Chapter 25, p. 1016, Interscience, New York (1963). 3. Blejer, H. P., Caplan, P. E.: Occupational Health Aspects of Cadmium Inhalation Poisoning, 2nd edition, p. 8, California State Department of Public Health, Berkeley (1971). 4. Fassett, D. W.: Cadmium, in Metallic Contaminants in Human Health, D.H.K. Lee, ed.. Chapter 4, p. Ill, Academic Press, New York (1972). 5. Princi, F.: J Ind. & Tox 29: 315 (1947). 6. Princi, F., personal communication to Lars Friberg, quoted in: Friberg, L., Piscator, M., Nordberg, G.: Cadmium in the Environment, p. 81, CRC Press, Cleveland (1971). 7. Friberg, L.: Acta Med Scand 138, Suppl. 240 (1950). 8. Potts, C.L.: Ann Occup Hyg _8:55 (1965). 9. Kazantzis, G., Flynn,.F.V., Spowage, J.S., Trott, D.G.: Quart J Med 32:165 (1963). 10. Nicaud, P., Lafitte, A., Gros, A.: Arch Mai Prof ^t:192 (1942). 11. Suzuki, S., Suzuki, T., Ashizawa, M.: Ind. Health ^:73 (1965). 12. Lavwerys, R.R., et al: Arch Env. Health 28: 145 (1974). 13. Friberg, L., Piscator, M., Nordberg, G.: Cadmium in the Environment, p. 105, CRC Press, Cleveland (1971). CALCIUM CYANAMIDE (Calcium Carbimide) N Ca * C || N TLV, 0.5 mg/m3 Mol. Wt. 80.11 Calcium cyanamide is also known as "cyanamide". The name "cyanamide", however has been used more in reference to hydrogen cyanamide. (Consequently the compound listed in the TLV list as cyanamide will be used to refer to hydrogen cyanamide - H2NC = N). Calcium cyanamide is crystalline with a melting point of about 1200 C. Commercial grades occur as grayish-black lumps and powder. Commercial grades may contain small amounts of calcium carbide, calcium hydroxide, carbon and other impurities. (1) It decomposes in water liberating ammonia. The compound is used as a fertilizer, defoliant, and herbicide. It is also used in the manufacture of iron, calcium cyanide, melamine and dicyandiamide. The acute toxicity of this compound is low. Exposure to airborne dust produces irritation of the exposed skin and mucous membrane. Exposed workers develop transient vasomotor disturbance of the upper part of the body. Calcium cyanamide is not converted to cyanide. Its method of action is not fully known. (2) Glaubach (3) suggested that it may react with the sulfur groups of glutathione and thus influence catalytic oxidation-reduction reactions. There appears to be a wide variation in the vasomotor response. Flury and Zernik (4) noted that the vasomotor effect is enhanced with simultaneous alcohol intake. The "antabuse like" effect of this industrial chemical in workers has been reported (5,6). -159- Calcium cyanamide is used medically because of its "antabuse effect" in the treatment of alcoholism. Maintenance dose in adults is 50 to 100 mg per day. Environmental data on airborne levels encountered by industrial workers is lacking on the basis of the available toxicological information a TLV of 0.5 mg/m^ is suggested. This concentration is considered sufficiently low to prevent irritation of the eyes and respiratory tract and also prevent any "antabuse-like" effect in exposed workers consuming alcoholic beverages after work hours. References: 1. The Merck Index. Eighth Edition, 1968. 2. Fasset, D.W. in Industrial Hygiene and Toxicology, Second Edition. Interscience Publishers Vol. II p. 2002. 1973. 3. Glaubach, S: Arch. Expert. Pathol. Pharmakol. 117:247 (1926). 4. Flury, F. and Zernik, F.: Schadliche Gase, Springer, Berlin, 1931. Quoted in Industrial Hygiene and Toxicology. Interscience Publishers Vol. II p. 2002. 1963. 5. Hald, J; Jacobson, E; and Varson, V. Acta Pharmacol. Toxicol. 8^:329 (1952). 6. Mastromatteo, E. Personal Communication to TLV Committee, (1973). CALCIUM HYDROXIDE Ca(OH)2 TLV, 2 mg/m3 The hydroxide of calcium, an alkaline earth element, is a less strong base than the alkali metal, sodium [pH of normal solution of Ca(0H)2 is 12.4 vs 14 for NaOH]; hence, its corrosiveness for body tissues is less. To protect against upper respiratory tract and skin and eye irritation, a TLV for Ca(0H)2 of 2 mg/m^ as a time-weighted average is recommended. CAPTAN N-(Trichloromethylthio)-4-cyclohexane-1,2-dicarboximide 5 mg/M^ /h2 P CH SCH-C 91 II I Vs-9-ci CH /CH-C Cl NCH2 0 C9 Hg CI3 N02S Mol. Wt. 300.61 Captan was introduced for use in agriculture as a protective fungicide in 1949. The pure material is white, crystalline, odorless solid with a -160- melting point of 175 C. The technical product (93 to 95 percent) is a yellow amorphous powder with a pungent odor and a melting point of 160 to 170 C. It has a low solubility in water and petroleum solvents. It may be used as a 3-1/2 to 5 percent dust for agricultural use or as a 75 percent powder for seed treatment as a protectant fungicide. There are other formulations available (1,2,3). The acute oral LC50 in rats is reported as 12.5 + 3.5 g/kg, with death mostly occuring during the third and fourth days (1,2,3,4,5). Long term feeding studies showed no effect in dogs fed 300 mg/kg/day for 66 weeks (1) or in rats fed 1000 mg/kg/day for 2 years (2). Animals become markedly more susceptible to the acute oral toxic effects of Captan as the dietary protein is progressively lowered (6). Boyd and Carsky administered Captan by gavage tube in a range of doses to young male albino rats for 100 days; the daily dose which killed 50 percent of rats over this period is reported as 0.92 + 0.23 g/kg/day. These results tend to indicate that Captan has a low order of acute toxicity, but a moderately high order of chronic toxicity. The World Health Organization estimates the acceptable daily intake for man at up to 0.1 mg/kg/day (5). Skin application in experimental animals in the range of 9000 mg/kg is reported to cause slight skin irritation. Some authors consider that Captan may cause skin irritation in some workers (2); however, Captan has a low order of dermal toxicity. Acute or long term inhalation studies are not available. Epstein and Legator in their review of the mutagencity of pesticides reported that Captan acted as an alkylating agent and induced chromosome rearrangements in rats and point mutations in Neurospora crassa. They quoted their own earlier work. In 1968 Epstein and Shafner reported that doses of 9 mg/kg and 500 mg/kg of Captan caused no changes in mice sperm cells. In 1969 Legator et al reported that a concentration of 10 mcg/ml inhibited DNA in human embryo cells (L-132 cells); concentrations of 1.5 to 5 mcg/ml produced chromosomal aberrations in somatic and germ cells in kangaroo rats. The significance and relevence of this work to occupational exposure is not at all clear. There have not been reports of mutagenic effects in humans handling Captan or ingesting food contain ing residues of it. Menzie reviewed the metabolism of pesticides. Thiophosgene is produced as an intercellular breakdown product of Captan and this substance is capable of inhibiting certain enzyme systems that have cocarboxylase as a co-enzyme. Captan reacts with sulfhydryl groups such as cysteine and glutathione. There have not been reports of any metabolic disorders in workers exposed to Captan. On the basis of the toxicity data available, a TLV of 5 mg/M^ is recommended. -162- DICYCLOPENTADIENE CH /\ HC CH------- CH II ch2 I II HC CH CH \ /\ / CH CH2 TLV, 5 ppm (approximately 30 mg/m3) According to Gerarde (1), leucocytosis followed subcutaneous dosage of rats with dicyclopentadicne (DCPD). Gage reported that rats showed no toxic signs after 15 six-hour exposures at 100 ppm (2), but were seriously affected by 10 exposures at 250 ppm. Kinkead et al found LC50 values for single 4-hour exposures to vary from 145 ppm for mice to 770 ppm for rabbits (3). Repeated 7-hour exposures five days a week for a total of 89 exposure days at 74 and 34 ppm resulted in kidney lesions in rats. Similar exposures of dogs were followed by minimal changes in biochemical test values. At 32 ppm BUN values were increased, and at 24 ppm SG0T and acid phosphatase values were increased. The no-ill-effect level for rats was judged to be below 35 ppm and possibly below 20 ppm. The no-ill-effect for dogs appeared to lie be tween 24 and 9 ppm. Human subjects reported an odor threshold of about 0.003 ppm, and slight eye or throat irritation at 1 and 5.5 ppm. During the five month period of investigation workers inadvertently exposed experienced transitory headaches during the first two months, but none thereafter. Reports of increased frequency of urination by workers exposed to DCPD were mentioned as possibly being associated with the kidney lesions observed in exposed rats (Documentor's note - wouldn't this indicate bladder rather than kidney effects?). Kinkead et al cite two Soviet papers, from which the USSR limit is derived? (4) (5). The hygienic standards suggested by the above noted investigators vary from 100 ppm (Gerarde), 20 ppm (Gage), 5 ppm (Kinkead et al) to 0.18 ppm (Karbakova, U.S.S.R.). A ceiling TLV of 5 ppm is recommended to prevent significant irritation and possible chronic toxic effects. References: 1. Patty, F.A.: Industrial Hygiene and Toxicology, Vol II, p. 1216. Interscience, New York, (1963). -161- References: 1. Martin, H: Pesticides Manual. Second Edition British Crop Protection Council (1971). 2. Spencer, E.Y.: Guide to the Chemicals Used in Crop Protection. Canada Department of Agriculture (1968). 3. The Merch Index. 8th Edition (1968). 4. Thompson, W.T.: Thompson Publication, Davis California (1967). 5. Boyd, E.M. and Carsky, E.: Acta Pharmacol et Toxicol. 29, 226 (1971). 6. Boyd, E.M. : Dietary Protein and Pesticide Toxicity in Male Weanling Rats. Bull. Wld. Hlth. Org., 40, 801-805 (1969). CARBOFURAN (FURADAN ) (2,3-dihydro-2,2-dimethyl-7-benzofuranyl methylcarbamate) TLV, Q.10 mg/m3 The oral LDjg of carbofuran is 8.7 and 8.0 mg/kg in male and female rats, respectively (1). Dermal dosing at 1000 mg/kg caused no deaths and only minimal symptoms in rats of both sexes. Thus, although the oral toxicity of carbofuran is quite high, it has a dermal toxicity of a low order of magnitude. The inhalation toxicity of carbofuran is also relatively great. The LC5Q of the 50 percent water wettable powder was 108 and 133 mg/m3 for male and female rats, respectively (2). Seventy-five percent water wettable powder had a respiratory LC5Q to guinea pigs (mixed sexes) of 53 mg/m3 (2). At all concentration levels equivalent to 0.56 mg/m3 of carbofuran 75% wettable powder, no cholinesterase depression was noted in the Rhesus monkey following a six-hour exposure. Slight but signif icant cholinesterase depression occurred at 0.86 mg/m3. In a chronic feeding study in the rat, the highest dietary level having no effect was 25 ppm; for the dog, 20 ppm (2). Dietary levels of 50 ppm produced significant inhibition of plasma, erythrocyte, and brain cholinesterase levels (1). As with other carbamate-type anticholinesterases, there is a very short time lag between exposure and onset of symptoms for carbofuran. Atropine is an effective antidote, but use of oximes, such as pralidoxime chloride, is contra-indicated. Tobin has suggested a TLV of 0.25 mg/m3 for carbofuran (2). However, in view of the high acute oral and respiratory toxicity of the compound, it is believed that a more conservative value of 0.10 mg/m3 should be adopted to prevent poisoning. References: 1. Gaines, Thomas B.: Unpublished data. 2. Tobin, J.S.: J. Occ. Med. 12, 16 (1970). -163- 2. Gage, J.C.: Brit. J. Ind. Med. 2J_, 1 (1970). 3. Kinkead, E.R., Pozzani, U.C., Geary, D.L., Carpenter, C.P., Toxicol. Appl. Pharmacolo 20, 552 (1971). 4. Karbakova, A.I.: - Vestn. Akad. Med. Nauk. SSSR 3J), (7) 17 (1964) Cited in Chem. Abstr. 61: 16694c. 5. Shashkina, L.F.: Gig. Truda of Prof. Zabolevaniya, j), (12): 13 (1965). Cited in Chem. Abstr. 64: 20509c. DIMETHYL SULFATE - Skin (ch3)2so4 TLV, 0.01 ppm (Approximately 0.05 mg/m^) A2 Smyth (1) found rats survive a four-hour inhalation at 15 ppm but die at 30 ppm in the same period. Flury and Zernik (2) found that 13 ppm seriously poisoned rats in 20 minutes. Browning (3) quoted work in which cats died in one and one-half weeks at 195 ppm exposures; monkeys, however, lived only three days at 26 ppm. Fairhall (4) noted that several cases of occupational poisoning by dimethyl sulfate, some of them fatal, were reported. Littler and McConnell (5) described two such cases. Distrubances in vision were among the first signs, followed by respiratory symptoms. Subsequently (1957-1962) cases of dimethyl sulfate poisonings in industrial workers were reported in the Italian, German and French literature. (6,7,8) Signs and symptoms uniformly found after exposure, began with headache and giddiness with burning of the eyes, reaching maximal intensity in from 2 to 10 hours after the first eye effects. The condition becomes progressively worse with painful, reddening eyes, photophobia, irritation of nose and throat, hoarseness and loss of voice, cough, oppression in the chest, difficult breathing and swallowing, vomiting, diarrhea and scalding micturition. Dysuria persists for 3 to 4 days, and congestion of mucous membranes and edema of the larynx may persist for two weeks. In some of the cases examined 6 years later, there was some impairment of liver function and reduction in the visual fields for various colors. When death occurs, the signs indicate circulatory failure. The eye effects are probably attributable to the metabolism of dimethyl sulfate to methanol and sulfuric acid. (8) In 1966 Druckrey et al. (9) reported the tumorigenic action of dimethyl sulfate in rats, albeit from extremely high doses; of 18 treated, 12 had local sarcomas from subcutaneous injections. Druckrey also associated an oat-cell bronchial carcinoma with metastases with apparent exposure of a chemical worker to dimethyl sulfate for 15 years. Preussmann (10) in testing a series of homologous alkyl sulfate esters, confirmed the sarcomagenic potency of dimethyl sulfate for rats, but Thiess et al. (11) found no clinical or X-ray evidence of lung cancer among 24 men who had worked for at least 3 years with dimethyl sulfate, although 4 cases of lung cancer were found in 368 men who had at one time worked with dimethyl sulfate, a number too small for statistical significance. -164- In the German list of Maximal Arbeitsplatzkonzentratione (MAKs) issued by the Commission on the Testing of Toxic Workplace Materials, dimethyl sulfate is not included in Section 6(a) among other materials known through experience to be capable of producing cancer in man. Presumably, this exclusion is based on the lack of overt cases of lung cancer among workers who have or have had contact with dimethyl sulfate at Badische anilinand Soda-Fabrik where the workers receive annual clinical examinations. A similar experience has been found at E. I. du Pont's three plants manu facturing dimethyl sulfate in a 1972 epidemiologic study covering a period of 15 years. (12) Accordingly, in keeping with the convention of assigning a TLV for an experimental carcinogen to control exposures "below the limit of sensitivity of the analytic method" (Appendix A, TLV Booklet 1973), a TLV of 0.01 ppm (0.05 mg/m3)* is recommended for dimethyl sulfate. This limit is that recommended by the Commission on the Testing of Toxic Workplace Materials of the Federal Republic of West Germany.* References: 1. Smyth, H.F., Jr.: Am. Ind. Hyg. Assn. Quart. L7, 129 (1956). 2. Flury, F., Zernik, F.: Schadliche Gase und Dampfe, p. 369, J. Springer, Berlin (1931). 3. Browning, E.: Toxicity of Industrial Organic Solvents, p. 396, Her Majesty's Stationery Office, London (1952). 4. Fairhall, L. T. : Industrial Toxicology, p. 227, Williams & Wilkins, Baltimore (1957). 5. Littler, T. R., McConnell, R. B.: Brit. J. Ind. Med. 12, 54 (1955). 6. Bartalini, E. et al.: Med. lavoro, 48, 329 (1957). 7. Nebelung, W. : Arch. Gewerbespathol, Gewerbehyg. 15, 581 (1957). 8. Roche, L., et al.: Arch, maladies profess. 23, 391 (1962). 9. Druckrey, H., et al.: Zeit, f. Krebsforsch. ^68, 103 (1966). 10. Preussman, R.: Food Cos. & Toxicol. 6^ 576 (1968). 11. Thiess, A.M. et al.: Zentralbl. Arbmed. Arbschutz. JJ), 97 (1969). 12. Pell, S. Epidemiologic Study of Dimethyl sulfate and Cancer of the Respiratory System (du Pont, Sept. 1972). *The sensitivity of this method has not been confirmed in the USA to date (Jan. '75). DISULFURAM Bis (diethylthiocarbamoyl) disulfide SS (c2h5)2 nC-s-s-An (c2h5)2 TLV, 2.0 mg/m3 C10 H20 N2 S4 Mol. Wt. 296.54 Disulfuram is a crystalline solid which has a melting point of 70 C. It is practically insoluble in water. The compound has a low order -165- of acute oral toxicity (Oral LD50 in rats is 8.6 g/kg) (1). Disulfuram is widely used as a rubber accelerator, rubber vulcanizer, seed disinfectant and fungicide. It is also used as a medication in the treatment of alcoholism. Persons consuming alcohol while taking this medication suffer intense vasodilatation of the face and neck, tachycardia and tachypnea followed by nausea, vomiting, pallor and hypotension. This is referred to as the "Antabuse-effect". Occasionally convulsions, cardiac arrythmias and myocardial infarction may occur. Other side effects of this compound which have been reported are: metallic or garlic taste in the mouth, polyneuropathy, peripheral neuritis and skin eruptions (2). More recently optic neuritis has been reported in a patient receiving this medication (3). The usual maintenance dose once adequate blood levels are attained is from 125 to 500 mg. per day. Industrial workers manufacturing and handling this compound have developed "antabuse effects" (4). Unfortunately concentrations of disul furam in air were not determined. On the basis of the oral dose recommended for maintenance therapy in the treatment of alcoholism a TLV of 1.25 mg/M3 is recommended. This TLV should be adequate to prevent "antabuse-like" effects to workers exposed to airborne concentrations of this substance. References:1 2 3 4 1. The Merck Index, Eighth Edition 1968. 2. Compendium of Pharmaceuticals and Specialties, Fourth Edition 1968. 3. Norton, A.L. and Walsh, F.B. Trans. Amer. Acad. Ophthamol. & Otolaryngol. J76:1263 (1972). 4. Mastromatteo, E. Personnel Communication to TLV Committee October 31, 1973. DYFONATE - SKIN (0-ethyl-S-phenyl ethylphosphonodithioate) TLV, 0.1 mg/m3 CH3CH20, CH3CH2 The average acute oral LD3q of technical dyfonate in male rats is 13.2 mg/kg (range of 6.81 to 17.5 mg/kg) (1). The average acute oral LD50 of technical dyfonate in female rats is 3.4 mg/kg (range of 3.16 to 3.69 mg/kg) indicating a sex-related difference in acute lethality. The acute oral LD50 of technical dyfonate in mongrel dogs (mixed sex) is 3 to 4 mg/kg, while the acute oral LD50 to albino rabbits is 134 mg/kg and to albino guinea pigs is 278 mg/kg, indicating a significant -166- difference in the dermal susceptibility between rabbits and guinea pigs. 0. 1.ml of technical dyfonate instilled into the eye of albino rabbits causes death, usually during the first 24 hours after administration of the chemical. The local eye irritation was reported to be negligible. Dietary feeding of dyfonate to groups composed of 2 male and 2 female dogs each for 14 weeks IndJested s no-effect level of 8 ppm (0.2 mg/kg). At the next higher done level (lb ppm) there was moderate Inhibit ion *l red blood cell cholinesterase activity, slight inhibition of brain cholinesterase activity, and convulsive siezure of one dog during the second week with recovery. Dyfonate was fed to groups of 15 male rats and 15 female rats for 13 weeks. The authors concluded that there were no effects related to the administration of dyfonate at levels as high as 31.6 ppm and with the exception of moderate inhibition of serum and red blood cell cholinesterase activity at 100 ppm levels no compound related effects were noted. Intramuscular administration to rats of greater doses of dyfonate indicated that atropine and 2-PAM chloride are effective antidotal treatments. Dyfonate incorporated into the diet of four groups of male and female Charles River Strain rats for 105 weeks produced a no-effect level of 10 ppm (2). Effects associated with the administration of dyfonate at the next highest level (31.6 ppm) indicated moderate inhibition (about 50%) of erythrocyte cholinesterase, and slight or no plasma cholinesterase inhibition except at the 26 and 52 week intervals where inhibition was moderate. It was concluded as a result of this study, that dyfonate did not show any carcinogenic effects. When Dyfonate was incorporated into the diet of pure bred beagles for 106 weeks, 8 ppm was considered to be no-effect level. A three generation reproduction study conducted in rats at dietary levels of 10 ppm and 31.6 ppm indicated that there were no adverse effects noted at either level on overall reproductive performance among the parental animals, or on the numbers, well being or integrity of the offspring, as compared with untreated controls. Based upon the cholinesterase inhibiting properties of this compound, it is recommended that a TLV of 0.1 mg/kg be applied. References: 1. Hoffman, L.J., Ford, I.M., Meun, J.J., Pesticide Chemistry and Physiology JL, 349-355 (1972). 2. Written Communication to committee member from Stauffer Chemical Company, Jan, 1974. C ETHYLENE CHLOROHYDRIN - Skin ch2ohch2ci 1 ppm (Approximately 3 mg/m^) Koelsch (1) subjected animals to a few (two to eight) repeated ex posures of ethylene chlorohydrin in concentrations ranging from 700 to 800 ppm with fatal results in all cases. Goldblatt (2) found that repeated exposures of 15 minutes a day at concentrations of 900 to 1000 ppm were fatal to rats within a few days. -167- Dierker and Brown (3) reported a fatal case of ethylene chlorohydrin poisoning resulting from a two-hour exposure to a concentration estimated at 300 ppm. Goldblatt and Chiesman (2) investigated two fatal and several nonfatal cases of intoxication by ethylene chlorohydrin. The average concentration in the nonfatal cases was 18 ppm. Nonfatal cases showed signs of circulatory shock, incoordination, repeated vomiting, epigastric pain, headache, polyruia, cough and erythema of the skin. They suggested 2 ppm as a target concentration. Bush et al. (4) described one fatal and several non-fatal cases of poisoning by ethylene chlorohydrin. The autopsy showed severe damage to the liver and brain and changes in many other organs. The survivors had nausea, vomiting, and irritation of eyes, nose and lungs. The concen trations at which workers were exposed (for unspecified periods) were estimated to be between 300 and 500 ppm. A limit of 2 ppm was suggested. Ambrose (5) reported concentrations of 7.5 ppm for one hour as being lethal to rats. Goldblatt (2) reported on LD50 of 72 mg/kg in rats by the oral route and 56 mg/kg by the intraperitoneal route. These results are comparable to the LD50 of ethylene chlorohydrin evaluated in mice, rats, rabbits, and guinea pigs by Lawrence et al (6) that range between 64 and 98 mg/kg. The mean time of death from vapors of the compound was calculated to be 13.3 minutes when mice were used as the test animals. The authors estimate that if the dermal LD50 for rabbits of 67.8 mg/kg could be extra polated to man, a volume slightly more than a teaspoonful could be lethal to the average (70 kg) man if it contacts the skin and is not washed off immediately. In a subacute toxicity study of rats by Lawrence et al (7), no adverse effects were observed in a one month study from 6.4 mg/kg daily (onetenth of the acute LD5Q), or from 12.8 mg/kg administered three times a week for 3 months. A ceiling limit of 1 ppm is recommended in view of the serious systemic responses to ethylene chlorohydrin. References; 1. Koelsch, F. : Zentr. Gewerbehyg. Unfallverhut. 14, 312 (1927). 2. Goldblatt, M.W., Chiesman, W.E. : Brit. J. Inc. Med. 1_, 207 (1944). 3. Dierker, H., Brown, P.G.: J. Ind. Hyg. & Tox. Z6, 277 (1944). 4. Bush, A.F., Abrams, H.K., Brown, H.V.: J. Ind. Hyg. & Tox. _31, 352 (1949) 5. Ambrose, A.M., Arch. Ind. Hyg. Occup. Med., 21, 591 (1950). 6. Lawrence, W.H., Turner, J.E., Autian, J.J.: J. Pharm. Sci. J50, 568 (1971) 7. Lawrence, W.H., Itoh, K., Turner, J.E., Autian, J.J.: J. Pharm. Sci. 60, 1163 (1971). -168- FENSULFOTHION (Dasanit) - Skin (0, O-diethyl-O-(4-methylsulphinyl-phenyl)-monothiophosphate) TLV, 0.1 mg/m3 c2h5o -0-/ c2h5o Fensulfothion is the common name of the insecticide 0, 0-diethyl0-(4-methylsulphinyl-phenyl)-monothiophosphate also named 0, 0-diethyl 0-(p-(methylsulfinyl) phenyl) phosphorothioate. The acute oral LD50 in male rats is approximately 4 mg/kg and in female rats is approx imately 1.8 mg/kg. Following inhalation of fensulfothion aerosols, the LC50 for male rats, 1 hour exposure, is 113 mg/M^ and for a 4 hour exposure is 29.5 mg/M^ (1). Species differences to the toxic effects of fensulfothion are not as noteworthy as sex differences where females were found to be more susceptible to the toxic effects. The symptoms produced by fensulfothion are typical of those caused by other organic thiophosphates and are due to its cholinesterase inhibiting properties. Although the active ingredient has a relatively high level of dermal toxicity (male rats' dermal LD50 ranges from 14.0 to 30.0 mg/kg and female rats from 3.5 to 3.0 mg/kg) (2) the results of skin absorption experiments using a 5 percent granular formulation applied airtight for two hours twice each day to the forearm of three persons for 5 consec utive days, produced skin irritation but no decrease in whole blood cholinesterase activity attributable to exposure to the formulation. However, good absorption via the lungs, has been demonstrated following inhalation of fensulfothion aerosols. Acute poisoning in rats and hens has been shown to be antidoted by atropine sulfate, 2-PAM, or T0X0G0NIN. Combined administration of atropine sulfate and 2-PAM or atropine sulfate and T0X0G0NIN gave better results than any of the individual drugs. Oral administration of fensul fothion to pregnant rabbits caused no embryotoxic effects and did not result in any malformation. Dominant lethal mutations were not produced in acute tests on mice. The "no effect" dietary level in subchronic feeding studies was found to be 1 ppm for rats and 2 ppm for dogs. Chronic oral application to rats for a period of 17 months had no damaging effect on the internal organs and the "no effect" level based on cholinesterase activity in this study was found to be 1 ppm. The major physiologic effect on fensulfothion on dogs maintained for two years on diets containing the compound was cholinesterase inhibition and in this study the "no effect" level was also 1 ppm. In a generation study on mice, inclusion of 2 or 4 ppm or fensulfothion in the diet was not observed to have any dilitarious effects on reproduction. Based on the cholinesterase inhibiting properties of this compound, it is recommended that a TLV of 0.1 mg/M^ be applied. \ ;-s-ch3 -169- References : 1. Luser, E., Kimmerle, G.: Pflanzenschutz - Nachrichten 24, 407 (1971). 2. The Toxic Substances List 1973 Edition, DHEW. C Glutaraldehyde 0 = C -(CH2)3 C = 0 HH TLV, 2 ppm (Approximately 8 mg/M3) (skin) C Alkaline ( Activated ) Glutaraldehyde (As glutaraldehyde) TLV, 0.05 ppm (Approximately 0.25 mg/M^) (skin) Glutaraldehyde: Molecular Weight: Melting Point: Boiling Point: Vapor Pressure: 17 mm Hg ( 1 mg/liter: 1 ppm: 100.0 97C 187C 20C 245 ppm 4.1 mg/m^ Glutaraldehyde, an aliphatic dialdehyde which forms colorless crystals, is soluble in water, alcohol and ether. It is a relatively strong irritant to the skin and eyes, (1) and can also cause skin sensitization (allergic contact dermatitis) from occassional or incidental occupational contact. (2) Oral LD50S in rats have been reported to range from 250 to 820 mg/kg. (3,4) Aqueous solutions of glutaraldehyde are stable for long periods of time, have mildly acid pH, a negligible odor, and are not potently antimicrobial. (3) When aqueous solutions of glutaraldehyde are bu^QAe.d to an alkaline pH of 7.5 to 8.0 upon the addition of sodium bicarbonate, they are actifated and their antimicrobial (sporocidal/bactericidal/viricidal/ fungicidal) activity is greatly enhanced, but for periods of up to only 14 days of so. (3) Glutaralydehyde itself has two active carbonyl (0=) groups, which under proper conditions can singly or together be further activated to undergo typical aldehyde reactions to form acetals, cynohydrins, oximes, and hydrazones; morever, through a cross-linking reaction, the carbonyl groups react with tissue protein. (3,5) Consequently, alkaline, ( activated ) glutaraldehyde solutions are being used as very effective cold-sterilizing disinfectants in a variety of medical-surgical and hospital uses because of their antimicrobial activity. katA,\)aX.<Ld glutaraldehyde retains the skin sensitizing properties of pure glutaraldehyde. (2) Furthermore, the relatively strong VVuXxmt effect on the skin, eyes, nasal passages and upper respiratory tract of pure glutaraldehyde are definitely enhanced when this dialdehyde is activated. Results of two studies demonstrate this increased irritant effect. In an experimental study, mice were exposed to 8 and 33 ppm -170- (33 and 133 mg/M^) of alkalinized glutaraldehyde for 24 hours: The animals reacted with distinctly nervous behavior, panting and washing of the face and limbs, with symptoms disappearing after a few hours. Half of each group were sacrificed immediately postexposure, and the rest a day later: Lungs and kidneys showed no histopathological damage, but the livers of the mice exposed to 33 ppm showed definite signs of toxic hepatitis, possibly still reversible, since it was present to a somewhat lesser degree in the animals autopsied one day post exposure. (6) In a second study, simulating a complete cold sterilizing procedure lasting 12 minutes, the integrated sample of activated 2 percent aqueous solution contained 0.38 ppm of glutaraldehyde measured at the operator's breathing zone (OBZ). Although some irritation had been felt throughout this procedure, it was not until the last part, when the equipment being sterilized was being air-hosed dry, that severe eye, plus nose and throat irritation were felt by the operator and the investigators, who also experienced sudden headache. (7) In view of the lower vapor pressure of aliphatic dialdehydes, glutaraldehyde per se would appear to be less hazardous than formalde hyde, with respect to inhalation, because it would not be expected to vaporize significantly enough to reach the operator's breathing zone under normal work procedures. However, the types of precautions needed under the many kinds of occupational use and exposure conditions indicate that glutaraldehyde and similar dialdehydes should be considered generally as toxic as formaldehyde and other lower molecular weight monoaldehydes if they reach the OBZ. (8) Other special uses and conditions such as the activiation and aerosolization of glutaraldehyde accentuate the tbxic hazard. A ceiling limit of 2 ppm appears to afford protection against the acutely irritating effects of glutaraldehyde per se; and a ceiling limit of 0.05 ppm, against the same effects of activated glutaraldehyde. References: 1. Fassett, D. W.: "In" Patty, F. A., Industrial Hygiene and Toxicology, Vol. II, p. 1980, Interscience, N.Y. (1963). 2. Jordan, W. P., et al.: Contact Dermatitis from Glutaraldehyde, Arch. Derm., 105:94 (1972). 3. Stonehill, A.A., et al: Buffered Glutaraldehyde -- A New Sterilizing Chemical Solution, Amer. J. Hosp. Pharmacy, J20:458 (1963). 4. Smyth, H. F.: Unpublished Data, Mellon Institute, Pittsburgh, Penn., quoted by Fassett, D. W., "In" Patty, F.A., opus cit., p. 1981. 5. Snyder, R. W., and Cheatle, E. L.: Alkaline Glutaraldehyde, An Effective Disinfectant. Amer. J. Hosp. Pharmacy, 22_:321 (1965). 6. Varpela, E., et al: Liberation of Alkalinized Glutaraldehyde by Respirators After Cold Sterilization, Acta Anaesth. Scand., 15:291 (1971). 7. Schneider, M., and Blejer, H.P.: In-House Report No. SU-171, Occupational Health Section, California State Department of Health, Los Angeles (December, 1973). Communicated to the TLV Committee. 8. Fasset, D.W.: Ibid., p. 1984. -171- HEPTANE CH3(CH2)5CH3 TLV, 400 ppm (Approximately 1600 mg/m^) Fuhner (1) reported that in concentrations of 10,000 to 15,000 ppm, heptane produced narcosis in mice within 30 to 50 minutes. At higher concentrations, 15,000 to 20,000 ppm, 30 to 60 minutes exposure caused convulsions and death in mice; 48,000 ppm caused respiratory arrest in 3 of 4 head-exposed mice in 3 minutes (6). Patty and Yant (2) reported 1,000 ppm to cause slight dizziness in man after exposure of six minutes; higher concentrations for shorter periods resulted in marked vertigo, incoordination and hilarity. The signs and symptoms of central nervous system involvement occurred in the absence of noticeable mucous membrane irritation and were first noticed on enter ing an uncontaminated atmosphere. Brief exposures (four minutes) to high levels (5,000 ppm) produced complaints of nausea, loss of appetite and a gasoline taste that persists for several hours after exposure. Flury and Zernik (3) also gave the fatal concentration as 16,000 ppm. A summary of published effects of heptane and other paraffinic hydrocarbons was prepared by Gerarde (4). Although chronic nervous system effects have not been attributed to heptane itself, Cavigneaux (5) stated that numerous cases of poly neuritis have been reported following prolonged exposure to a petroleum fraction with boiling range between 70 and 100C. Such a fraction would normally contain various isomers of heptane as major ingredients. In order to ensure the absence of chronic injury, as well as early stages of narcosis and irritation of respiratory passages or eyes, a reduction in the TLV of heptane (all isomers) from 500 to 400 ppm is recommended. References: 1. Fuhner, H.: Biochem. Z. 115, 235 (1921). 2. Patty, F.A., Yant, W.P.: U.S. Bureau of Mines Rep. of Invest. No. 2979 (1929). 3. Flury, F., Zernik, F.: Schadliche Gase, pp. 257-264, Springer, Berlin (1931). 4. Gerarde, H., In Patty, F.A.: Industrial Hygiene and Toxicology, Vol. II, 2nd Ed., p. 1198, Interscience, NY (1963). 5. Cavigneaux, A. Securite et hygiene de travail, 2nd quarter, 1972, p. 199. 6. Swann, H.E., et al. Am. Ind. Hyg. Assn. J.: J35, 511 (1974). -172- HEXANE (n-Hexane & Various Isomers) CH3(CH2)4CH3 TLV, 100 ppm (Approximately 350 mg/m^) Hexane is thrice as toxic to mice as is pentane; concentrations of 30,000 ppm produced narcosis in mice within 30 to 60 minutes; convulsions and death resulted from 35,000 to 40,000 ppm (1,11). In man, 2,000 ppm for ten minutes resulted in no effects, but 5,000 ppm caused dizziness and a sense of giddiness (2). Drinker et al. (3) found slight nausea, headache, eye and throat irritation at 1,400 to 1,500 ppm. Nelson and co-workers (4) found no irritation at 500 ppm in unacclimated subjects. Various isomers of hexane are major components of petroleum ether and other volatile petroleum solvents which have widespread industrial use. Narcotic symptoms, such as dizziness, have been observed frequently when concentrations exceeded 1,000 ppm, but not from levels below 500 ppm (5). Until recently chronic effects from hexane and similar paraffin hydrocarbons had rarely been reported. In 1967, however, Yamada (6) reported 17 cases of polyneuritis among workers exposed to n-hexane. Although alkyl titanium compounds were present where six of the cases occurred, the only apparent exposure in the other eleven cases was to n-hexane of 95% purity, in concentrations found to be between 500 and 1,000 ppm. Inoue et al. (7) followed this investigation with animal experiments which showed functional disturbances of the peripheral nerves of mice at 250 ppm, but not at 100 ppm. An additional 93 persons engaged in home work on vinyl sandal manu facture were found to suffer from polyneuropathy (8). Concentrations of n-hexane from the adhesives used were between 500 and 2,500 ppm. As a result of the above findings, the Japanese TLV for n-hexane was reduced to 100 ppm. Herskowitz et al (9) reported three cases of n-hexane neuropathy among workers in an American furniture plant, where concentrations of n-hexane averaging 650 ppm were found, with peaks of 1,300 ppm. Cavigneaux (10) noted the occurrence of numerous cases of (occupational) polyneuritis in several countries, and in many the incriminated agent was n-hexane in high concentrations. In view of the above reports, a reduction in the TLV for hexane from 500 to 100 ppm is recommended. References: 1. Flury, F., Zernik, F.: Schadliche Gase, p. 258, J. Springer, Berlin (1931). -173- 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. Patty, F.A., Yant, W.P.,: U.S. Bureau Mines Rep. Invest. No. 2979 (1929). Drinker, P. Yaglou, C.P., Warren, M.F.: J. Ind. Hyg. & Tox. Z5, 225 (1943). Nelson, K.W., Ege, J.F. Jr., Ross, M., Woodman, L.E., Silverman, L.: J. Ind. Hyg. & Tox. 25, 282 (1943). Elkins, J.B.: Chemistry of Industrial Toxicology, p. 101, Wiley and Sons, New York (1959). Yamada, S.: Japanese J. of Industrial Health, 9, 651 (1967). Inoue, T., Yamada, S., Miyagaki, H. Takeucki, Y.: Presentation at XVI Congress on Occ. Health, Tokyo, Sept. 22-27 (1069). Inoue, T. et al.: Japanese J. of Ind. Health 12, 73 (1970). Herskowitz, A., Ishii, N., Schaumburg, H.: New Eng. J. of Med. 285, 82 (1971). Cavigneaux, A.: Securite et Hygiene du Travail 67, 199 (1972). Swann, H.E. et al.: Am. Ind. Hyg. Assn. J.: S5, 511 (1974). C HEXYLENE GLYCOL (ch3)2-cohch2-choh-ch3 2-Methyl-2, 4-Pentanediol TLV, 25 ppm (Approximately 125 mg/m^) Hexylene glycol is prepared commercially by the catalytic hydro genation of diacetone alcohol. It is used as a chemical intermediate, as a selective solvent in petroleum refining, a component of hydraulic fluids, a solvent for inks and as a cement additive. It has a vapor pressure of 0.05 mm Hg (20 C), a boiling point of 198 C (760 mm Hg) and a specific gravity of 0.9234 (20/20 C.). Studies supported by the Shell Chemical Corporation and reported in their Industrial Hygiene bulletins (1) define hexylene glycol as inert, although central nervous system depression was produced by oral administration. Signs of toxicity resemble those seen with general anesthetics with excitement preceding profound depression. Mild to moderate irritation is produced by application of the liquid to the skin, however there appears to be no systemic absorption. Industrial use of hexylene glycol at normal room temperature does not normally create any vapor hazard due to its low vapor pressure and hygroscopic natue. Atmospheric contamination which may occur in the handling of hexylene glycol at high temperatures may produce pronounced irritation of the eyes. Sensory response evaluation resulted in the following information: Atmospheric concentrations of 50 ppm for 15 minutes produced slight odor with most people noticing slight eye irritation. At 100 ppm for 5 minutes the odor was plainly detectable and slight -174- nasal and respiratory discomfort was noticed by unacclimated and sensitive subjects. At 1,000 ppm for 5 minutes various degrees of eye irritation and throat and respiratory discomfort was noted. The LD^q for mice is 3.8 ml/kg and for rats it was found to be 4.79 g/kg. Hypnosis occurred in mice following single dose of 2.0 ml/kg; with higher doses it was profound. (2) Undiluted material, when intro duced into the rabbit's eye, caused appreciable irritation and corneal injury that was slow to heal. In order to prevent eye irritation it is recommended that the ceiling threshold limit value of 25 ppm be adopted. References: 1, Shell Chemical Corporation, New York, New York, Industrial Hygiene Bulletins SC: 57-101 and SC: 57-102. 2. H.F. Smyth, Jr. and C.P. Carpenter, J. Ind. Hyg. Toxical 30, 63, (1948). H2 .___ h2 HYDROGENATED TERPHENYLS TLV, 0.4 ppm (Approximately 4.4 mg/m3) o-Terphenyl, approx 40% hydrogenated The hydrogenated terphenyls are complex mixtures of ortho-, metaand para-terphenyls in various stages of hydrogenation. Five such stages exist for each of the three isomers, ortho, meta, and para. The structural formula for the approximately 40% hydrogenated ortho isomer is shown. The hydrogenated terphenyls are used as heat-transfer media and plasticizers. As coolants, they are 40% hydrated (HB-40). Potential acute hazards consist of damage to the lungs and damage to skin and eye from burns from the hot coolant; potential chronic hazards comprise damage to liver, kidney and blood-forming organs, with the possibility of induction of metabolic disorders and cancer. The basis for these concerns arose from toxicologic investigations on unhydrogenated terphenyl isomers. Although Cornish et al. (1) found the acute oral toxicity of the three isomers of terphenyl for rats to be low (LD50 ortho, 1,900; meta, 2,400; para, 10,000 mg/kg), continued ingestion at 500 mg/kg per day for 30 days indicated the possibility of liver and kidney damage from observation of increased liver and kidney to body-weight ratios and decreased weight gain. On a diet of 100 mg/kg of each isomer, body-weights were equal to those of the controls. Petkau -175- and Hoogstraaten (3) and Young, et al. (4), have confirmed the nephrotox icity of unirradiated terphenyl isomers, and the latter has shown hepatic damage in rats fed 33 mg/kg or more. Previously, Haley et al. (2), had found that inhalation of the ortho and meta, but not the para isomer resulted in bronchopneumonia. The isomers of terphenyls are metabolized in varying amounts to glucosiduronic acids and phenols(1). All three isomers gave no sign of skin irritation in rabits follow ing a 24-hour contact (1). The acute oral LDcq for rats of 40% hydrogenated terphenyls (reactor coolant) was found to be 17,500 mg/kg and 12,500 mg/kg for the mouse; for irradiated coolant, 6,000 mg/kg for rat and mouse (5). It is thus app arent that the irradiated 40% hydrogenated terphenyl mixture is about three-fold more toxic acutely by ingestion than is the nonirradiated. The results of 16 weeks of chronic ingestion confirmed the greater toxicity of the irradiated terphenyl particularly at high dose levels (5). At 1,200 mg/kg, the irradiated mixture was lethal to mice, whereas irreversible interstitial nephritis resulted from the nonirradiated. At 600 mg/kg, the irradiated resulted in irreversible renal lesions, which, for the nonirradiated, the renal lesions were reversible. At 250 mg/kg no lesions were apparent for either mixture at the 16-week period of exposure. In relatively brief, 8-day inhalation exposures of mice to non irradiated hydrogenated terphenyl at a level, 500 mg/m^, only slightly exceeding that around the reactor, the only changes were in the Type II cells of the alveolar epithelium, and these were transient (6). In a longer, 8-week exposure of mice to the irradiated mixture at 2,000 mg/m^ the same findings in the lung were made, and there was some proliferation of the smooth endoplasmic reticulum in the liver (7). In view of the findings of Henderson and Weeks (8) that the irradiated mixture proved carcinogenic in the skin of mice, and the relatively short, 8-week exposure period for testing carcinogenicity, it is not possible to interpret the significance of the changes seen in the mouse lungs from inhalation. The rapid rate of clearance (24 hours) of particles of the hydrogenated terphenyls from the mouse lung, shown by Adamson and Furlong (9), would tend to argue against a carcinogenic effect on the lung, although the relatively large particle size (1-20 }im) tends to speed clearance. Clearance from the gut, kidney and liver, where the lung-cleared particles are deposited, was considerably slower, however (14 days). Using the above-quoted data sources, and making certain assumptions of long-range potential from the available short-range studies, the employing safety factors for translation of effects from mouse to man, a suggested occupational exposure limit approximating 0.4 ppm or 4.4 mg/m^,* presumably as a time-weighted average of either or both of nonirradiated or irradiated 40% hydrogenated terphenyls was made. In view of the lack of information on long-range potentials, this limit must be considered highly tentative until this information has been developed. -176- *Assuming an average molecular weight of 241. References: 1. Cornish, H.H., Am. Ind. Hyg. Assn. J.: 23, 372 (1962). 2. Haley, T.H., et al., Tox. Appl. Pharm.: _1, 515 (1959). 3. Petkau, A., Hoogstraaten, J., Am. Ind. Hyg. Assn. J.: 26, 380 (1965). 4. Young G., et al., ibid.: 30, 7 (1969). 5. Adamson, I.Y.R. and Weeks, J.L., Arch. Envir. Hlth.: 27, 69 (1973). 6. Adamson, I.Y.R., et al., ibid.: 19, 499 (1969). 7. Adamson, I.Y.R., ibid.: 26_, 192 (1973). 8. Henderson, J.S., Weeks, J.L., Ind. Med. Surg.: 4^, 10 (1973). 9. Adamson, I.Y.R., Furlong, J.M., Arch. Envir. Hlth.: 2?3, 155 (1974). 10. Weeks, J.L., A Toxicologic Assessment of Organic Reactor Coolants, Whiteshell Nuclear Research Establishment, Pinawa, Manitoba ROE 1L0, Dec. 1973. IODOFORM - Skin TLV, 10 mg/m3 (Approximately 0.6 ppm) Iodoform (triiodomethane), CHI3, is a yellow or greenish-yellow crystalline solid which has a very characteristic pungent odor. Odor thresholds of 6.1 to 8.0 \ig/m3 have been reported (1,2). For many years it enjoyed significant medical interest because of its germicidal action. More effective germicides have now largely dis placed it. CHI3 has a molecular weight of 393.78 and is 96.69% iodine. It has a melting point of 119 C; d]p is 4.008. The solubility in g/100 ml of solvent is: water 0.01 at 25 C, 7.8 at 78 C in ethyl alcohol and 13.6 at 25 C in ether. It is soluble in chloroform, benzene and glycerine (3). Toxicologic data on iodoform is very limited and a generally accepted industrial air standard is not available. Data by Kutob and Plaa (4) indicate that on a mole basis the toxicity (based on lethality, barbiturate sleeping time and bromsulfalein (BSP) retention time) of iodoform to mice is of the same order as methyl iodide. A Threshold Limit Value (TLV) for methyl iodide of 5 ppm or 28 mg/m^ has been established (5). On a mole basis of iodine, it would then seem that as much iodoform iodine could be allowed in the workroom air as methyl iodide or approximately 10 mg/m3 of iodoform. Conservatively, a trial level of 10 mg/m^ or 0.6 ppm of iodoform seems prudent. References: 1. Staub-Reinhalt. Luft. Volume 32, No. 10, Oct 1972. p. 30. 2. Summer, W., Odor Pollution of the Air, Causes and Control CRC Press (1971) p. 22. 3. Kirk-Othmer, Encyclopedia of Chemical Technology, Volume II (1966( p. 864. -177- 4. Kutob, S. David and Gabriel L. Plaa, "A Procedure for Estimating the Hepatotoxic Potential of Certain Industrial Solvents," Toxicol. Appl. Pharm., 4:354-361, 1962. 5. "Threshold Limit Values for Chemical Substances and Physical Agents in the Workroom Environment with Intended Changes for 1973." American Conference of Governmental Industrial Hygienists. ISOBUTYL ALCOHOL (2-Methyl propanol) (CH3)2CHCH2OH TLV, 50 ppm (Approximately 150 mg/m^) Limited data (1,2) on the acute experimental inhalation toxicity of isobutyl alcohol indicate it to be somewhat more toxic than n-butyl al cohol; a 4-hour LC^q exposure by inhalation for the rat was 8000 ppm vS greater than 8000 ppm for n-butyl alcohol. Isobutyl alcohol was slightly more acutely toxic to the rabbit orally (3.75 g/kg vs 4.25 g/kg for butyl alcohol). As the LD50 from skin application was 4.2 g/kg, no "Skin" designation is required for isobutyl alcohol, as this exceeds 2 g/kg, the suggested cut-off value for percutaneous "absorbable" substances (3). A narcotic dose for mice by inhalation for a total of 136 hours was reported by Weese (4) to be 6,400 ppm; no deaths occurred from repeated narcotizing doses. Slight organic changes in the liver and kidney were, however, found; whether they were reversible was not reported. Although isobutyl alcohol is stated to be a skin irritant as evidenced by slight erythema and hyperemia upon application to human skin (5,6), no data are available on the effects of isobutyl alcohol vapor on the eyes. The injury to the eye caused by the liquid, however, is comparable to that from n-butanol. As no reports of isobutyl alcohol causing either auditory impairment or vestibular damage have come to the attention of the TLV Committee. The recommended TLV of 50 ppm, as a time-weighted average, must be based on its slightly greater acute toxic potential than n-butanol whose former TLV of 100 ppm was based on its acute toxic response. Neither the MAK list of the USSR (1970), of the West German Republic (1971) nor of Czechoslovakia (1969) contains an industrial air standard for isobutyl alcohol. References: 1. Smyth, H.F., Jr., Carpenter, C.P., Weil, C.S.: Arch. Ind. Hyg. & Occ. Med. 4, 119 (1951). 2. Smyth, H.F., Jr., Carpenter, C.P., Weil, C.S., Pozzani, U.C.: Arch. Ind. Hyg. & Occ. Med. 10, 61 (1954). 3. Stokinger, H.E.: Chapter II, "Occupational Exposure" in Occupational Disease-Chemical, Physical and Biologic Agents -- A Physicians Guide to Etiology, U.S. Government Printing Office, 1975. 4. Weese, H., Arch. Exptl. Path. Pharm. 135, 118 (1928). -178- 5. Schwartz, L. , Tulipan, L., A Testbook of Occupational Diseases of the Skin, Lea & Febiger (1939). 6. Oettel, H., Arch. Exptl. Path. Pharm. 183, 641 (1936). C ISOPHORONE TLV, 5ppm (Approximately 25 mg/m^) Smyth and associates (1) concluded from their work on experimental animal exposure that no effect whatever resulted from exposure at 25 ppm of isophorone vapor. Animals, 10 rats and 10 guinea pigs, were exposed for 30, eight-hour days to concentrations ranging from 25 to 500 ppm. Isophorone, in higher concentrations, in jured primarily as a kidney poison. CH2--------c(ch3)2 0C CH. CH---. X CH3 Smyth and Seaton (2) reported that men exposed at 40, 85, 200 and 400 ppm isophorone experienced eye, nose and throat irritation. A few complaints of nausea, headache, dizziness, faintness, inebriation and a feeling of suffocation resulted from 200 and 400 ppm. Symptoms of irritation and narcotic action decreased at concentrations of 40 and 85 ppm. Useful warning properties existed only at 200 and 400 ppm. On the basis of the above material, a TLV of 25 ppm was proposed to prevent irritative and narcotic effects. Silverman et al., (3) however, reported isophorone vapor was irritating to unconditioned volunteers at 25 ppm. According to Rowe and Wolfe, (4) moreover, the experiments of Smyth et al, (1,2) were made with impure material. In their opinion the concentrations given in some cases exceeded possible levels, others were higher than actually present, and the results were not valid. They recommended a TLV of 10 ppm in conformity with the recommendation of Silverman et al. Subsequently, information was reported to the Committee (5) that a TLV of 10 ppm was not sufficiently low to prevent complaints of fatigue and malaise after a month's work at isophorone levels of from 5 to 8 ppm. When, however, the air levels were reduced to shop levels of from 1 to 4 ppm, no further complaints were received. The ceiling TLV of 5 ppm was reported to be easily achievable by exhause ventilation. References: 1. Smyth, H.F., Jr., Seaton, J., Fischer, L. : J. Ind. Hyg. 6 Tox. _24, 46 (1942). 2. Smyth, H.F., Jr., Seaton, J.: J. Ind. Hyg. & Tox. 22:, 477 (1940). 3. Silverman, L., Schulte, H.F., First, M.W.: J. Ind. Hyg. & Tox. 28, 262 (1946). 4. Rowe, V.K., Wolfe, M.A., in Patty, F.A.: Industrial Hyg. & Tox., Vol. II, 2nd Ed., p. 1765, Interscience, N.Y. (1963). 5. Communication of June 26, 1973, from G. D. Ware, Western Electric Co. (Kearny) to Chairman, TLV Committee. -179- methylene CHLORIDE (Dichloromethane) ch2ci2 TLV, 200 ppm (Approximately 720 mg/m3) According to Lehmann and Flury (1), slight narcosis occurs at 4000 to 6100 ppm in several species of animals. The fatal concen tration for seven hours' exposure is given by many authorities as about 15,000 ppm (1,2,3). Rats exposed 75 days (8 hours a day) at 1300 ppm showed slight liver changes which were not found at 50 days (1). Cats exposed four to eight hours a day at 7200 ppm for four weeks were found to have kidney and liver changes. Heppel and associates (4) found that daily seven-hour exposures at 5000 ppm for six months had no discernible effect on dogs and rabbits, and only reduction in the rate of growth of guinea pigs. At 10,000 ppm, four hours a day for seven and one-half weeks dogs and guinea pigs, but not monkeys, rabbits or rats, developed liver injury. Moskowitz and Shapiro (5) reported four cases of poisoning with one fatality, apparently due to narcotic action. Collier (6) reported two cases of poisoning in painters who suffered from headache, giddiness, stupor, irritability, numbness and tingling in the limbs. Kuzelova and Vlasak (7) noted complaints of headache, fatigue and irritation of the eyes and respiratory passages by workers exposed at concentrations up to 5000 ppm. Neurasthenic disorders were found in 50%, and digestive distrubances in 30% of the persons exposed. Three acute poisonings, one involving loss of consciousness, were recorded without serious after-effects. Weiss (8) stated that a chemist after a year's exposure developed toxic encephalosis with acoustical and optical delusions and hallucin ations. Concentrations frequently exceeded 500 ppm; values of 660 ppm, 900 ppm, and, near the floor, 3600 ppm were noted. Golubovskii and Kamchatnova (9) found liver disease in workers exposed to methylene chloride and methanol which they attributed to the former. In the early 1940s methylene chloride was considered the least toxic of the chlorinated hydrocarbon solvents when a safe industrial air limit of 500 ppm was proposed by Heppel et al. (4), and later adopted by the TLV Committee as protective enough to prevent any significant narcotic effects or liver injury. Recently, however, Stewart et al. (10), reported that significant quantities of carbon monoxide and carboxyhemoglobin were produced in humans receiving single exposures at 500-1000 ppm of methylene chloride. The carboxyhemoglobin concentrations reported by Stewart approximated those considered objectionable if due to inhalation of carbon monoxide. -180- More extensive examination of CO production from methylene chloride was later reported by the same investigators (11). Human volunteers exposed to methylene chloride at 1000 ppm for two hours (2000 ppm-hours, one-half of the Ct permitted for an 8-hour exposure at 500 ppm) resulted in carboxyhemoglobin levels in excess of those permitted in industry from exposure to CO alone. Moreover, exposures which did not exceed permissible industrial air limits produced signs and symptoms of central nervous system depression. This finding of the body's capacity to metabolize methylene chloride to CO was confirmed in a group of workers exposed at 180 to 200 ppm methylene chloride by Ratney, Wegman and Elkins (12). Such daily, repeated 8-hour exposures resulted in equilibrium blood concentrations of carboxyhemoglobin of 9% that decreased to half that value by next day's start of work. The differential increment in percent carboxyhemo globin of 4.5% from a day's exposure at 180 to 200 ppm of methylene chloride is approximately the same as that developed from a daily exposure to CO at its TLV of 50 ppm. Thus industrial findings lend support to a TLV of 200 ppm for methylene chloride as a time-weighted average. Other recommendations: Cook (1945) and Smyth (1956) 500 ppm; Elkins (1959) 200 ppm; ANSI (1969) 500 ppm; USSR (1970) 15 ppm; Czechoslovakia (1969) 140 ppm. References: 1. Lehmann, K.B., Flury, F.: Toxicology and Hygiene of Industrial Solvents, pp. 134-138, Williams & Wilkins, Baltimore (1943). 2. Von Oettingen, W.F.: Halogenated Hydrocarbons, Toxicity and Potential Dangers, pp. 35-41; Pub. Health Service Publ. #414 (1955). 3. Svirbely, J.L., Highman, B., Alford, W.C., von Oettingen, W.F.: J. Ind. Hyg. & Tox. 29, 382 (1947). 4. Heppel, L.A., Neal, P.A., Perrin, T.L., Orr, N.L., Porterfield, V.T.: J. Ind. Hyg. & Tox. 26^, 8 (1944). 5. Moskowitz, S., Shapiro, H.: Arch. Ind. Hyg. & Occ. Med. j6, 116 (1952). 6. Collier, H.: Lancet 1, 594 (1936). 7. Kuzelova, M., Vlasak, R.: Pracovni lekarstvi 18, 167 (1966); abstr. in Scientific Reports on Industrial Hygiene and Occupational Diseases in Czechoslovakia, p. 69, Prague (1966). 8. Weiss, G. : Zentralblatt Arbeitsmed. u. Arbeitsschutz _17, 282 (1967). 9. Golubovskii, I.E.: Kamchatnova, V.P.: cited in Hygiene and Sanitation (USSR) 29, 145 (1964). 10. Stewart, R.D., Fisher, T.N., Hosko, J.J., Peterson, J.E., Baretta, E.D., and Dodd, H.C.: Science 176, 295 (1972). 11. Stewart, R.D., et al.: Arch. Environ. Hlth. 2j>, 342 (1972). 12. Ratney, R.S., Wegman, D.H., Elkins, H.B.: Arch. Environ. Hlth. 28, 223 (1974). -181- METHYL CYCLOHEXANE >CH2-CHo CH3CHQ \ch2 \ch2-ch^ TLV, 400 ppm (Approximately 1600 mg/m3) Lazarew (1) found that inhalation at a concentration of 7500 to 10,000 ppm for two hours caused prostration in white mice, and 10,000 to 12,500 ppm was fatal. Data cited by Lehmann and Flury (2) indicated that the acute toxicity of methylcyclohexane was greater than that of heptane, but less than that of octane. Treon and associates (3) reported 1200 ppm to be innocuous for rabbits. Prolonged exposure at 3700 ppm appeared to be harmless to monkeys. The histologic changes of animals exposed to methylcyclohexane resemble those from cyclohexane. In general, the alicyclic hydrocarbons are less irritating than the corresponding aromatic compounds. The TLV of 400 ppm, the same as that for heptane, which has comparable acute toxicity, should afford an exposure without significant narcosis and be will below the level causing other toxic effects (4). References: 1. Lazarew, N.W.: Arch. exp. Path. Pharmakol. 143, 223 (1929). 2. Lehman, K.B., Flury, F.: Toxicology and Hygiene of Industrial Solvents, p. 95, Williams & Wilkins, Baltimore (1943). 3. Treon, J.T., Crutchfield, W.E., Kitzmiller, K.V.: J. Ind. Hyg. & Tox. 25, 323 (1943). 4. Patty, F.A.: Industrial Hygiene and Toxicology, Vol. II, 2nd Ed., p. 1212, Interscience, NY (1963). Nickel, soluble inorganic salts (as Ni) TLV, 0.1 mg/m3 The soluble inorganic salts of nickel of industrial importance are nickel sulfate (NiSO^-6H20), nickel chloride (NiCl2-6H20) and nickel nitrate (Ni(NO3)2*6^0) . Nickel sulfate presents an exposure from its use in electroplating baths; nickel chloride and nitrate, from electro plating baths and in the preparation of nickel catalysts. Soluble nickel salts are highly toxic acutely; single intravenous doses of 10 to 20 mg/kg were lethal to dogs (1), with the heart and respiratory nerve centers being afftectd. Gross changes, from near lethal doses, consist of pulmonary edema and hemorrhage, and degeneration of heart muscle, brain, lung, liver and kidney (2). Subcutaneous, lethal doses are reported (2) to be 7 to 8 mg/kg for rabbits, 9 to 16 mg/kg for cats. Orally in drinking water 0.54 mg/kg daily, for 160 days, nickel sulfate caused severe damage to the myocardium and liver parenchyma of rabbits (3). -182- NiCl2 has been shown to affect glucose metabolism (4), either by intraperitoneal (8 mg/kg) or intratracheal (0.5 mg) administration or by long-term ingestion in drinking water (225 ppm, 4.5 mg/day) in rats and guinea pigs. A single intraperitoneal injection caused a rapid, 4-fold increase in serum glucose with resulting glucosuria, and ass ociated hyperlipidemia, insulin resistance, and increased pancreatic insulin level. Nickel dermatitis, "nickel itch" constitutes the most common affection among nickel platers (5,6). It has two components, a simple dermatitis localized to the area of contact, and a chronic eczema or neurodermatits without apparent connection to such contact (7,8). Nickel salts have long geen recognized (9,10) as substances producing sensiti zation; the elevated temperatures around the nickel-plating baths is considered to be a predisposing factor (11). Animals have been exper imentally sensitized to nickel salts (12). Exposure of rats by 12-hour daily inhalation for several weeks to nickel chloride at approximately one-tenth the TLV of lpppm as Ni, produced microscopically visible changes in the bronchial epithelium as evidenced by hyperplasia and marked mucus secretion (13). Although the duration of the daily exposures exceeded the normal work-day shift, the exposure level was sufficiently low to question the appropriateness of the 1 mg/m3 TLV. A further test of the appropriateness of the TLV was made by exposing rats and guinea pigs to a mist of NiCl2 7 hours daily, 5 days per week for 6 months at the TLV of 1 mg/m^ ad Ni (14). The lung weights of both rats and guinea pigs were significantly increased at both 3 and 6 months. In conformity with this finding were pulmonary lesions consisting of increased cellularity of alveolar walls, with macrophages in alveolar spaces near the respiratory bronchioles. As these lesions occurred to a lesser extent in unexposed animals, it was concluded that NiCl2 exacer bated a pre-existing lesion. From the nature of the lesion, it was also concluded that the lesions were probably reversible. No evidence was found of either metaplasia or neoplasia from this soluble nickel salt under the conditions of the exposure. Accordingly, in view of the observed changes in the lungs of animals exposed to a soluble nickel salt under conditions simulating the ordinary work week, though mild and probably reversible, a TLV of 0.1 mg/m^ as Ni is recommended as a time-weighted average. References: 1. Caujoulle, J. , Canal, G.J. Pharm. Chim.: 2!9, 391, 410 (1939). 2. Armit, H.W., J. Hyg. : 1_, 525 (1907); 8, 565 (1908). 3. Grusko, Y.M. et al., Farmicol. i Toksikol: 16 , 47 (1953) (Abstract, translation). 4. Clary, J.J., Vignati, L., Tox. Appl. Pharm.: 25, 467 Dec. (1972). 5. Mullschitzky, A., Wien, Med. Wochscht. : 89^, 717 (1939). 6. White, R.P., The Dermatogoses, 4th Ed., Lewis, London, 1934, p. 193. -183- 7. Calnan, C.D., Brit. J. Dermatol.: j38, 229 (1956). 8. Cvells, G.C., ibid.: 68, 237 (1956). 9. Rostenberg, A. Jr., Sulzberger, M.B., Arch. Dermatol. Syphilol.: 35, 433 (1937). 10. Johnson, H.H., ibid.: 43, 575 (1941). 11. Bulmer, F.M.R., Mackensie, E.A.: J. Ind. Hyg.: _8, 517 (1926). 12. Haxthausen, H., Arch. Dermatol, u. Syphilis: 174, 17 (1936). 13. Bingham, E. et al.. Arch. Environ. Hlth.: 25, 406 (1972). 14. Clary, J.J., et al., Tox App.: Pharm.: jy._______ (1975). NONANE C9H20 CH3(CH2)7CH3 TLV, 200 ppm (Approximately 1040 mg/m^) In the absence of published data on the toxicology of nonane, a TLV can be estimated from the relative toxicities and TLVs of the lower mem bers of the paraffin hydrocarbon series. The acute toxicities increase sharply with an increase in carbon atoms, as indicated in the following table on experiments with mice (1,2): Lethal Narcotic Isonarcotic Concentration Concentration (a) Concentration (b) (a)(b) Hexane Heptane Octane 30,000 ppm 12,000 ppm 10,000 ppm 42.000 ppm 16.000 ppm 8,000 ppm 37.000 ppm 16.000 ppm 52.000 ppm 16.000 ppm 13,500 ppm Since it is known that in general the higher boiling hydrocarbon mixtures are more toxic than the lower boiling ones (2), it is fairly safe to assume a higher acute toxicity for nonane than for octane. Until additional information is available, particularly on chronic toxicity, a limit of 200 ppm, in comparison with 300 ppm for octane, is recommended for all isomers of nonane. References: 1. Patty, F.A.: Industrial Hygiene and Toxicology, Vol. II, 2nd Ed., p. 1198, Interscience, NY (1963). 2. Flury, F., Zernik, F.: Schadliche Gase, pp 257-264, J. Springer, Berlin (1931) . OCTANE ch3(ch2)6ch3 TLV, 300 ppm (Approximately 1,400 mg/m^) Mice exposed at concentrations of 6,600 to 13,700 ppm octane demon strated narcosis in 30 to 90 minutes (1), and respiratory arrest at -184- 16,000 (1 of 4) to 32,000 ppm (4 of 4) in 5 to 3 minutes respectively (iso-octane) (5). Patty and Yant (2) state that the narcotic con centration is 10,000 ppm, while Flury and Zernik (3) put the narcotic concentration at 8,000 ppm and the fatal concentration at 13,500 ppm. From these data on actue toxic response, it can reasonably be inferred that octane is from 1.2 to 2 times more toxic than heptane for which a TLV of 400 ppm is recommended. On the basis of this comparison and by analogy with other paraffinic hydrocarbons, a TLV of 300 ppm is recommended. Gerarde (4) has summarized the available toxicologic information on octane and other paraffins in which narcosis and mucous membrane irritation are noted as common proper ties progressing in intensity with increasing molecular weight. References: 1. Fuhner, H., Biochem. Z.: 115, 235 (1921). 2. Patty, F.A., and Yant, W.P., U.S. Bur. Mines Rept. Invest. No. 2979 (1929). 3. Flury, F. and Zernik, F., Schadliche Gase, J. Springer, Berlin (1931) PP. 257-264. 4. Gerarde, H.W., In Patty, F.A.: Industrial Hygiene & Toxicology, Vol. II, 2nd Ed., p. 1198, Interscience, NY (1963). 5. Swann, H.E., et. al. Am. Ind. Hyg. Assn. J.: 35, 511 (1974). PENTANE ch3(ch2)3ch3 q TLV, 600 ppm (Approximately 1,800 mg/m ) Like other simple paraffinic hydrocarbons, pentane is not a toxic substance, but does cause narcosis at high concentrations. In the range from 90,000 to 120,000 ppm, narcosis results in 5 to 60 minutes (1). Human exposures for 10 minutes at 5,000 ppm did not cause mucous mem brane irritation or other symptoms (2). According to Flury and Zernik (3), and Swann et al. (6), a concentration of 130,000 ppm is fatal. Fairhall (4) concluded that narcosis and irritation were the only effects of pentane. Gerarde (5) summarized available toxicological information on pentane and other paraffins. On the basis of these limited data and the belief of experienced personnel that exposure should be limited to a level where odor and irritation do not constitute a nuisance during prolonged exposure, a TLV of 600 ppm is recommended as a time-weighted average. This limit is consistent with the recognized decrease in effects as the paraffinic carbon chain length decreases (nonane, TLV 200; octane TLV, 300; heptane, TLV, 400 ppm). References: 1. Fuhner, H.: Biochem. Z. 115, 235 (1921). -185- 2. Patty, F.A., Yant, W.P.: U.S. Bur. Mines Rept. Invest. #2979 (1929). 3. Flury, F., Zernik, F.: Schadliche Gase, pp. 257-284, J. Springer, Berlin (1931). 4. Fairhall, L.T.: Industrial Toxicology, 2nd Ed., p. 268, Williams & Wilkins, Baltimore (1957). 5. Patty, F.A.: Industrial Hygiene and Toxicology, Vol. II, p. 1198, Interscience, NY (1963). 6. Swann, H.E., Am. Ind. Hyg. Assn. J.: _35, 511 (1974). C PHOSGENE (CARBONYL CHLORIDE) coci2 TLV, 0.05 ppm (Approximately 0.2 mg/M3) Phosgene is a colorless gas with a suffocating odor; and when much diluted by air it has an odor reminiscent of moldy hay. The vapors are irritating to the eyes. Phosgene condenses at 0 to a clear colorless, fuming liquid and has a boilding point of 8.2 C. Gross and Associates reported that concentrations of phosgene as low as 0.5 ppm for 2 hours caused definite pathological changes in the lungs of rats sacrificed 96 hours postexposure. (1) Some abnormalities were considered by the investigators to be present 3 months after rats had been exposed at 2 ppm for 80 minutes. Cameron and associates reported that exposure at 0.8 mg/M^ (0.2 ppm) of phosgene for 5 hours per day for 5 consecutive days caused evidence of pulmonary edema in 41 percent of the animals exposed (goats, cats, rabbits, guinea pigs, rats, mice), extensive lung lesions were present in 4 percent of the animals and is a major consideration in setting this standard. Exposure of the same species at 4 mg/M^ (1 ppm) 5 hours daily for 5 con secutive days depressed ciliary function and caused lesions in the lung that were "likely to give rise in man to serious clinical symptoms". (2,3) Guinea pigs treated with low doses of phosgene + 10 mg/M^ (1.5 ppm) x 10 min. (1) for 7 days became relatively resistant to toxic levels + 140 mg/M^ (35 ppm) x 10 min. (4) Repeated exposure of cats to phosgene, 10-15 mg/M^ (1.5-3.8 ppm) or 20-25 mg/M3 (5-6 ppm), for 10 minutes every day caused no greater lung damage after 40 days than after 2 days. (5) Box and Cullumbine (6) performed experiments in animals that sug gested that phosgene inhaled at low concentrations resulted in a lessened susceptibility to subsequent, and otherwise acute, edemagenic doses. This was later confirmed by Henschler and Laux (7), who showed that phosgene at 1 ppm for 6 hours not only induced tolerance against the acute effects of itself but protected the host also against other edemagenic agents such as ozone and nitrogen dioxide. This development of tolerance against the acute edemagenic effects of phosgene has been shown to be a common property and action of edemagenic agents generally. (8) The development of tolerance, however, is believed to be the triggering mechanism of chronic, irreversible pulmonary changes of emphysema and fibrosis from prolonged daily exposure at concentrations that produce no ostensible acute response. (9) -186- Observers in World War I estimated LCtjjQ for man to be 3,200 mg min/M^ (2-minute exposure) (400 ppm). (10,11) Data obtained by the Chemical Warfare Service prior to 1921 indacated that 1 ppm of phosgene may be considered safe for prolonged exposure. (12). Cucinell states, based upon clinical data, that effects of chronic low doses of phosgene upon the lung in animals or man in situations where there are no acute symptoms from phosgene are not known. (13) It is generally accepted that phosgene may cause chronic lung disease in man, as well as obliterative bronchiolitis in dogs. (14) There are no quantitative data available on what dosage might cause permanent lung damage in man. No data have been generated to indicate that people with chronic respiratory diseases have an increased susceptibility to acute or chronic phosgene poisoning. It is assumed that people working around phosgene will have been prescreened and will not have, or be subject to, respiratory diseases (as estimated by having a measured normal alphatrypsin inhibitory factor in blood). (15) Some industrial operations using phosgene follow a "work practice" procedure wherein an attempt is made, using engineering techniques to preclude exposure to phosgene. Under this practice, detection of any level of phosgene is considered as evidence that a condition for potential exposure has occurred. Anyone suspected of being exposed under these circumstances to any level is medically evaluated and treated if required. Personnel are trained to recognize the odor of phosgene (odor detection limit is considered to be 0.5 ppm) and report any effluvium. (16) The National Academy of Sciences lists a 90 day atmospheric limit for use in submarines of 0.05 ppm and a Douglas aircraft continuous atmospheric limit of 0.04 ppm. (17) Because of its irritating effect on the respiratory tract, with particular regard being given to Cameron's work a ceiling limit of 0.2 mg/M^ (0.05 ppm) is recommended. References: 1. Gross, P., Rinehart, W.E., and Hatch, T., Arch. Environ. Health. 10, 768-775 (1965). 2. Cameron, G.R., Courtice, F.C., Foss, G.L., Short, R.H.D., Calder, R.M. , Bamford, R., Burgess, Allen, Fairley, A., Watkinston, G.L., and Williams, L.T.D. Minstry of Defense, UK. Proton Report 2349. First Report on Phosgene Poisoning. Part II. April 1942. UNCLASSIFIED Report. 3. Cameron, G.R., Courtice, F.C., Foss, G.L., Short, R.H.D., Calder, R.M., Bamford, R., Burgess, Allen, Fairley, A., Watkinston, G.L,, and Williams, L.T.D. Ministry of Defense, UK. Proton Report 2349. First Report on Phosgene Poisoning. Part VIII. April 1942. UNCLASSIFIED Report. -187- 4. Cordier, D., and Cordier, G. , Compt. Rend. Soc. Biol. 147, 327-330 (1952). 5. Cordier, D., and Cordier, G,, J. Physiol. 4_5, 421-428 (1953). 6. Box, G.E.P. , Cullumbine, H. Brit. J. Pharm. 2^, 38 (1947). 7. Henschler, D., Laux, W. Naunyn-Schmied. Arch. exp. Path. u. Pharmak. 239, 433 (1960). 8. Stokinger, H.E. Proceedings 13th Int. Congress on Occup. Health, New York City (1960). 9. Stokinger, H.E., Wagner, W.D., Dobrogorski, O.J. Arch. Ind. Health, 16, 514 (1957). 10. Medical Division Status Summaries. CWS Field Lab Memo 1-4-5, p. 305. 1944. UNCLASSIFIED Report. 11. Chasis, H. Phosgene. Review of the Literature on the Effect of Exposure in Man and Experimental Animals. Contract W-49-036-CWS-1. 1944. UNCLASSIFIED Report. 12. Fasciculus on Chemical Warfare Medicine. Volume II. Respiratory Tract. Chapter XX. Freeman, S., Grodins, F.S. and Kosman, A.J. Temperature and Humidity in the Treatment of Phosgene Poisoning. National Research Council. Committee on Treatment of Gas Casualties. 1945. UNCLASSIFIED Report. 13. Cucinell, S. Review of the Toxicity of Long-Term Phosgene Exposure, Arch. Environ. Health. .28, 270-275 (1974). 14. Caldston, M., Leutscher, J.A., Longcope, W.T., and Ballich, N.L., J. Clin. Invest. 2j>, 169-181 (1947). 15. Stokinger, H.E., Mountain, J.T., and Scheel, L.D., Ann. N.Y. Acad. Sci.- 151, 968-976 (1968). 16. Verbal Communication to committee member from industrial represent ative, Jan 1974. 17. Report of the Panel on Air Standards for Manned Space Flight of the Space Science Board; National Academy of Sciences 36 (1968), RESORCINOL C6H4(0H)2 O TLV, 10 ppm (Approximately 45 mg/m ) During a 1965-66 survey, none of 180 men employed in production and maintenance work involving explsure to resorcinol, complained of any irritation or discomfort at exposure levels of 10 ppm (1). In subacute animal exposure studies, no evidence of toxic effects was noted when rats, guinea pigs, and rabbits were exposed six hours per day for a period of two weeks to resorcinol concentrations of 34 mg/m^ (8 ppm) and in acute inhalation toxicity tests (2), aerosol (resorcinolwater) concentrations as high as 7800 mg/np (1733 ppm) for a one-hour period and as high as 2800 mg/m^ (625 ppm) for an eight-hour period caused no toxic signs or symptoms in the exposed animals. Range finding studies show resorcinol to be less toxic than phenol or catechol by ingestion or skin penetration (2,3). On the basis of the above data, a threshold limit value of 10 ppm for resorcinol is recommended. -188- References: 1. Koppers Company. Correspondence to Threshold Limit Values Committee, April 1, 1974. 2. ibid., April 10, 1974. 3. Von Oettingen, W.F, Phenol and Its Derivatives, NIH Bulletin 190, U.S. Govt. Printing Office (1949), C SODIUM AZIDE (Hydrazoic acid) N Na-N || \n N [ H-N7!) 1 XN TLV, 0.1 ppm (Approx. 0.2 mg/m^ as HN3) Sodium azide, socium azoimide, is a stable crystalline solid, highly soluble in water from which hydrazoic acid is released. Hence, most of the industrial exposures are to hydrazoic acid, as this is one of the chief uses of sodium azide. As an intermediate in organic synthesis is another use. An incidental use is as an agent in the urinary azide-iodine test for exposure to carbon disulfide (1). Sodium azide appears to be only slightly less acutely toxic than the corresponding cyanide (2,3), although testing by strictly comparable species and routes has not been done. Hydrazoic acid vapor, claimed (2) to have essentially the same degree of acute toxicity as sodium azide, as determined by intraperitoneal injection in mice, was about 8 fold less toxic after a 60-minute inhalation (4); (HCN concentration fatal after 60 minutes, 135 ppm vs 1024 ppm for HN3). The acute effects in man breathing HN3 vapor are eye irritation, bronchitis, headache, a fall in blood pressure, and weakness and collapse (4,5), Similar hypotensive effects are produced by sodium azide; as little as 1 mg/kg intravenously will produce hypotension in cats, which increases when the dose is repeated (5). Repeated intraperitoneal injections in rats of 5 to 10 mg/kg result in severs intoxication, with survivors showing demyelination of the nerve fibers of the central nervous system, but no damage to the liver or kidney (6). In the early 1950s sodium azide was tested as a hypotensive agent in hypertensive patients (7). Thirty hypertensive patients were treated with from 0.65 to 3.9 mg by mouth daily for periods up to 2.5 years. Apart from the lowering of the blood pressure and a transient pounding sensation in the head, the majority of the patients showed improved subjective symptoms and no organic damage. In 20 patients, however, continued treatment with sodium azide was followed by increased sensit ivity to the drug, which necessitated reducing the daily dosage from 0.5 to 0.25 mg/day. It is apparent from these medicinal uses of sodium azide that exposures must be controlled to very low levels, if hypotension is to be avoided. -189- Estimation of a maximal intake of sodium azide for a daily 8-hour work shift, assuming 10 m3 of air inhaled and a 75% retention for a daily oral intake of 0.75 mg results in a level of about 0.1 mg/m^. This value is consistent with the estimated value in the report (8) "that hydrazoic acid vapors at a concentration as low as 0.5 ppm can cause some discom fort to laboratory personnel". In order that the permissible limit of exposure to sodium and hydrogen azides incorporate a reasonable factor of safety against head ache discomfort, and protect against significant lowering of blood pressure, A TLV of 0.2 mg/m^ of sodium azide, or 0.1 ppm hydrazoic acid vapor is recommended. References: 1. Djuric, D. et al., Brit. J. Ind. Med,: 22_, 321 (1965). 2. Graham, J.D.P. et al. , J. Ind, Hyg. Tox. : jlO, 98 (1948). 3. Chen, K.K. et al., J. Am. Med. Assn. 100, 1920 (1933). 4. Fairhall, L.T., et al.. Public Hlth. Repts. U.S.: 58^, 607 (1943). 5. Graham, J.D.P., Brit. J. Pharm.: 4., 1 (1949). 6. Hicks, S.P., Arch. Path.: 5, 545 (1950). 7. Black, M.M. , et al., Proc. Soc. Exptl. Biol, Med.: 8^5, 11 (1954). 8. Haas, J.M., Marsh, W.W. Jr., Am. Ind. Hyg. Assn. J.: _31, 318 (1970). STODDARD SOLVENT TLV, 100 ppm (Approximately 600 mg/m^) "Regular" Stoddard Solvent has a flash point around 43 C (109 F) (1). The boiling range is normally between 150 and 210 C (2). It contains 15 to 20% aromatic hydrocarbons, with the remainder consisting chiefly of paraffin and naphthenic hydrocarbons. The normal paraffin hydrocarbons with boiling points closest to the 50% distillation point of a typical Stoddard Solvent (157-170 C) are nonane (150) and decane (173). Several isodecanes have boiling points between 150 and 160, Available data indicate that the aromatic hydrocarbons present in greatest quantity in Stoddard Solvent are the trimethyl benzenes, which compose 25-40% of the total aromatic content (3). As a first approximation for calculating a TLV, Stoddard Solvent may be considered a mixture of 80-85% nonane and isodecane and 15-20% trimethyl benzene. TLVs of 400 and 300 ppm, respectively, have been set for heptane and octane. While comparable toxicity date have not been published for nonane and decane, the following tables of acute toxicity have been reported for pentane, hexane, heptane and octane. -190- CONCENTRATION NARCOTIC (MICE) CONCENTRATION LETHAL (MICE) REFERENCE Hexane Heptane Octane 30,000 ppm 12,000 ppm 10,000 ppm 37,000 ppm 16,000 ppm Patty (4) 11 11 CONCENTRATION ISONARCOTIC (MICE) CONCENTRATION FATAL (MICE) REFERENCE Pentane Hexane Heptane Octane 130,000 ppm 42,000 ppm 16,000 ppm 8,000 ppm 130,000 ppm 52,000 ppm 16,000 ppm 13,500 ppm Flury & Zernik (5) if tr II it it If if ii 11 These data indicate a rapid increase in toxicity as the number of carbon atoms (and concurrently. the boiling point) increase. A TLV of not more than 200 ppm for nonane and isodecane would be a reasonable extrapolation of these date (in the absence of information on chronic effects, we are forced to rely on acute toxicity data in developing the TLV). TLVs of 25 ppm have been recommended for the various trimethyl benzenes based in large measure on the reports of human experience with mesitylene and pseudocumene exposure (6). Toxicological data on the higher members of the naphthenic hydro carbon series are even more meager than those on the paraffin series, but the information that we have for the most part indicates that the toxicities of compounds of similar boiling points in the two series have comparable toxicities. If a TLV of 25 ppm is accepted for the aromatic components in the mixture, and the value of 200 ppm is taken as the TLV for the non-aromatic portion, the TLV of the Stoddard Solvent can be calculated. In the case of a mixture with an aromatic content of 15%, the calculation would be: 1/TLV = 0.15/25 + 0.85/200 = 0.0103. TLV = 1/0.103 = 97 ppm If an aromatic content of 20% is assumed, the resulting TLV is 83 ppm. This reasoning is in general agreement with the statement of Flury and Zernik (4) that heavy benzene (boiling range 102-160 C) is one and one-half times as toxic as light benzene (boiling range 50-100 C), although their data indicated a two-fold ratio of toxicity or even more if concentration is based on parts per million rather than milligrams per liter. Relatively few data are available on industrial exposures to Stoddard Solvent. Oberg, in a survey of thirty drycleaning plants in Detroit, found an average concentration of 65 parts per million (weighted exposures, 35 ppm) -191- for solvents with flash point 105 F (7), The worst plant had an est imated average exposure of 135-200 parts per million. Lower concen trations were found with Stoddard solvents of higher flash points. Davis, Schafer and Bell (8) reported on unleaded gasoline exposure experiments on men. Ten men were exposed 30 minutes at concentrations of 200, 500, and 1,000 ppm of three different gasolines. (A-25% paraffin, 30% naphthenes, 65% aromatics.) The majority of subjects re ported itching or burning of eyes at 500 ppm. Before-and-after-photographs of the eyes were evaluated for injection of conjunctival vessels and the majority of the subjects showed slight change at 500 ppm. Based on the projected toxicities of the major aliphatic components and the TLV for the most abundant aromatic ingredients, with the latter present in amounts between 15 and 20%, a TLV of 100 ppm is recommended for regular Stoddard Solvent, to prevent narcotic, irritant and chronic responses. The same limit should apply to "Low End Point Stoddard Solvent." Stoddard Solvents with higher flash points than about 45 C (or 115 F) should have TLVs somewhat below 100 ppm. Note: In the above discussion, the units of composition are not listed. Actually, percentages should be in terms of molecular fractions. In practice, use of per cent by weight or volume does not make a great deal of difference among the hydrocarbons, since in general, these compounds of similar molecular weight have boiling points and densities of the same order. References: 1. National Institute of Drycleaning: The Four Classes of Stoddard Solvent. Technical Bulletin, March 1969. 2. National Paint, Varnish & Lacquer Assn. Petroleum Thinner Index (1953). 3. Runion, H.E.: Private communication (1967). 4. Patty, F.A.: Industrial Hygiene and Toxicology, Vol. II, 2nd Ed., p. 1198, Interscience, NY (1963). 5. Flury, F., Zernik, F.: Schadliche Gase, pp. 257-264, J. Springer, Berlin (1931). 6. Battig, K., Grandjean, E., Turrian, V.: Z. Prev. Med, .1, 389 (1957). 7. Oberg, M.: Am. Ind. Hyg. Assn. J. 29_, 547 (1968). 8. Davis, A., Schafer, L.J., Bell, X.G.: Arch. Env. Health ^L, 548 (1960). 4,4'-THIO-bis(6-tert.-BUTYL-m-CRESOL) TLV, 10 mg/m3 ch3 4,4'-Thio-bis(6-tertiary butyl metacresol) or 4,4'-Thio-bis(3-methyl6-tertiary butyl phenol) is an antioxidant for polyolefines, high- and low-pressure polyethylenes and polypropylene, and is marketed under the -192- trade name, Santonox. It is soluble in methanol to the extent of 79%; in acetone, 20%; in benzene, 5%, and water, 0.08%, Available toxicity data relate to the oral route in rats and consist of an approximate lethal dose, and 30- and 90-day feeding studies (1); no inhalation studies were per formed . The approximate lethal oral dose was 5 g/kg, with gastroenteritis being the chief symptom noted. Rats ingesting diets containing 0.05 and 0.25 per cent for 30 days showed normal weight gain at the 0.05% level (500 ppm), but retarded weight gain and enlarged livers at 5-fold this level. In the 90-day feeding studies, no apparent signs of toxicity resulted at the 0.005% level (50 ppm) but male rats on the 0.05% diet ate and grew slightly less than the other group, although no pathologic changes were observable. In the absence of information on the toxicity via the respiratory route, the TLV must be based upon the essential absence of effects by ingestion up to levels of 500 ppm. It would seem accordingly that a TLV of a "nuisance" particulate of 10 mg/m3 as a time-weighted average would be appropriate. Reference: 1. "Practical Toxicology of Plastics," Rene Lefaux, Iliffe Bks., Ltd. 1968, pp. 399-400. TRIPHENYL AMINE TLV, 5 mg/m3 Triphenyl amine has the formula (C6H5)3N and has a molecular weight of 245.3. It forms colorless monoclinic prisms, has a melting point of 127-129 C and a boiling point of 347 C. It is slightly soluble in ethyl alcohol and soluble in benzene and ether. It may be formed by the following reaction: 2 (C6H5)NH + 2C6H5I + K2C03Boiling CfiH5N02 2(06^) 3N + 2K1 + H2) + C0? 5J-T5% * The Eastman Kodak Company is apparently the only producer of the com pound and production data are not available. Its primary use is as a primary photoconductor and it is coated on film bases. Screening test in rats indicated that the oral LD^q in rats to be between 3200-6400 mg/kg while in mice the LD50 varied from 1600-3200 mg/kg. Intraperitoneally in both species the LD50 was greater than 6400 mg/kg. Deaths occurred in the case of oral administration in rats up to six days after administration and up to two days in the case of mice. Intraperit oneally no deaths occurred at the 6400 mg/kg level. -193- A 10% solution of the compound in a mixture of 9:1 acetone: corn oil applied to the depilated skin of the guinea pig under an occlusive covering at concentrations of 5-20 ml/kg for 24 hours produced only slight erythema without edema. Crystals of the solid compound placed in the conjunctival sac of the rabbit's eye produced no evidence of damage at any time during a two week period. Triphenyl amine was found not to be skin sensitizer in the guinea pig. (1) Information made available by the Eastman Kodak Company reveals that no injuries have occurred as a result of handling of the compound and that no special precautions are necessary other than those used for the routine handling of organic compounds. (1) References: 1. Personal communication from Robert L. Roudabush, Director of Health and Safety Laboratory, Eastman Kodak Company. Letter dated April 12, 1973. VINYL CHLORIDE CH2=CHC1 APPENDIX A/c Since vinyl chloride (chloroethene, CR2-CHC1) is a gas at room temperature and pressure, the common route of toxic exposure is by inhalation. As with many liquified gases, contact of the skin or eyes with escaping compressed vinyl chloride can produce freezing and frostbite(l). Vinyl chloride has long been considered to be very low in toxicity by acute inhalation. Lehmann and Flury (2) summarized the literature and reported work by Schauman who considered vinyl chloride to be a candidate surgical anesthetic. Schauman reported little pathological changes even after repeated exposure to anesthetic concentrations. Further work on the anesthetic potential of vinyl chloride indicated that vinyl chloride was unsafe for use as a surgical anesthetic in dogs and that because of its flammability, poor efficacy and its ability to cause cardiac irregularities at anesthetic concentrations vinyl chloride was not suitable for use as an anesthetic in humans. Despite the early reports ascribing low toxicity to vinyl chloride, injury during the production of polyvinyl chloride (PVC) resins was reported as early as 1949. Signigicantly this report came from Europe where production of PVC in Europe preceded U.S. production by several years and today the quantity produced in Europe still exceeds U.S. production by about two fold. In 1949, Tribuhk et al, (3) reported numerous effects in PVC workers in what by today's standards must be considered as primitive production facilities. These authors found a "considerable number of cases of hepatitis among workers" but were -194- more concerned with other hepatotoxic chemicals such as chlorinated diphenyl and chlorinated naphthylene (Holowax (sic)) than they were with vinyl chloride. As a result of two deaths in Canada, the acute inhalation toxicity of vinyl chloride was studied by Mastromatteo et al, (4) who reported that exposure of mice, rats, and guinea pigs to 10, 20, and 30 volume percent vinyl chloride caused the following mortality: NUMBER OF DEATHS IN DIFFERENT GROUPS OF FIVE MICE, RATS AND GUINEA PIGS EXPOSED FOR THIRTY MINUTES TO VARYING CONCENTRATIONS OF VINYL CHLORIDE IN AIR Vinyl Chloride concentration (percent by volume in air) _______ Laboratory animal_____________ Mice Rats Guinea pigs TOTAL 10 0/5 0/5 0/5 0/15 20 1/5 0/5 0/5 1/15 30 5/5 5/5 1/5* 11/15 40 ---- 2/5* 2/5 * A delayed death occurred within 24 hours following exposure. Some pulmonary hyperemia and engorgement was observed by these in vestigators, but liver and kidney injury were remarkably low. Deaths were due to narcosis. The first report of studies to determine the effect of long-term repeated exposure (6 months) were summarized by Torkelson, Oyen and Rowe (1) as follows: "Repeated exposures of laboratory animals to several concentrations of vinyl chloride in air were conducted to determine the chronic toxicity of this material towards animals in order to assess the hazard to humans. Vinyl chloride was found to have a slight capacity to cause liver and kidney injury on repeated exposures, Male and female rats showed micropathological changes after repeated daily 7-hour exposures at 500 ppm for 4.5 months. Repeated 7-hour exposures at 200 ppm for six months resulted in micropathological changes in the livers of rabbits and statistically significant increases in the average weight of the livers of male and female rats, but no detectable changes in dogs and guinea pigs. Repeated 7-hour exposures at 100 ppm resulted in slight increases in the average weight of rat livers, the other species were not affected. All species studied tolerated repeated daily 7-hour exposures to 50 ppm for six months with no detectable injury. -195- Repeated daily 1-hour exposures at 200 and 100 ppm of vinyl chloride were without effect, longer exposures caused a slight increase in liver weight. The standard for evaluating regular daily 7 to 8-hour exposures may be defined as the concentration below which practically all analytical results must fall. The value of 100 ppm is suggested as this standard for vinyl chloride, with a time-weighted average for all exposures not to exceed 50 ppm." Lester, Greenberg, and Adams (5) took exception to the conclusion of Torkelson et al (1961) that 50 ppm should be a maximum time weighted average exposure for workers. On the basis of 3 months exposure of rats to 2 volume percent and 19 days to 5 volume percent, they concluded that 500 ppm was acceptable as a TLV despite minor changes which they observed in rat livers and which they considered "were within the normal range and were not pathologic in nature". Since 1949 numerous articles describing conditions and problems in PVC production plants have appeared particularly in the Eastern European literature. Filatova and Gronsberg (6), Gabor et al (7), Suciu et al (8), Gabor et al (9), Grigorescu and Toba (10), Antonyuzhenko (11), and Kudryavtseva (12), have all described the effects of apparently gross chronic exposure. These papers and abstracts are difficult to interpret since there are generally inadequate descriptions of the exposure conditions and analysis of the workroom air, so no dose-response relationship can be determined. The injuries and effects described by the authors are not consistent with the levels of exposures claimed by the authors nor are the levels of exposure consistent with past or even present-day chemical technology. Furthermore, mistures of chemicals are involved making it possible to ascribe the effect to any one of them. For example, Suciu et al (8) (through Translation) described nervous disorders including euphoria with whistling and laughing, incoordination and dizziness similar to alcohol intoxication. However, Suciu et al ascribes these results to exposure of the order of 5.5 mg/m^ (2 ppm v/v) which is not consistent with other publications which indicate these effects will be apparent only if concentrations greatly exceed 10,000 to 20,000 ppm v/v. Therefore, the following conclusions by the authors can be construed as being the result of massive and apparently repeated exposures 1. Vinyl chloride and the vinyl monomers possess a narcotic action and produce, depending upon concentration, in addition to characteristic neurologic manifestation, a state of euphoria (12%), followed by a state of inebriation similar to that of alcohol intoxication. In certain cases narcosis can appear. After leaving the working environment, a state of somnolence (45%) persists, with hypersomnia. Vinyl chloride acts on the skin and produces a sensation of formication and of heat. 2. After repeated exposure, a neurologic asthenia sets in in which somnolence predominates. -196- 3. After a variable period of time, dyspeptic distrubances are added to the neurologic manifestations; these are at first not character istic; they are in the form of epigastric pains (16%), swelling, discomfort, feeling of heaviness in the right hypochondrium (7%) or the left (5%) with anorexia, particularly for fats. In 30.2% of the cases, congentive hepatomegaly appears, which may mimic toxic hepatitis without jaundice; some cases may become chronic. In 6% of the cases, the hepatomegaly is accompanied by splenomegaly. The proteinogram and the aldolases are the most sensitive tests and show changes similar to those of acute hepatitis: increase in aglobulins and of the ft- and y-globulins; and thymol test, Greenstedt's reaction and the zinc sulfate test are positive only in few of the cases. 4. After 3 years of exposure in 9% of the cases a syndrome typical of ulcer without radiologic changes becomes manifest. 5. In 6% of the cases the Raynaud syndrome has appeared, particularly among the young men. Plethysmography shows in half of the cases an inhibition of the vasomotor centers. 6. In addition, allergic dermatitis in 4.4% of the cases, and scleroderma in 3.6%, has been observed. 7. The clinical and laboratory findings are of great importance in occupational pathology because in numerous cases diseases appear in man that cannot be reproduced in the animal (Raynaud's syndrome and scleroderma). The sudden and frequent appearance of these manifestations in the PVC division of several plants, and in certain divisions in normal individuals who are still relatively young, and their disappearance in the majority of the cases after the institution of protective measures and change of work, have shown us decisively that vinyl chloride and the vinyl monomers have played a part in the production of these manifestations. (End of author's summary). In 1967, reports appeared in the literature describing a condition known as acroosteolysis in workmen engaged in polymerization of vinyl chloride to polyvinyl chloride. Harris and Adams (13) reported on two cases in Europe. Wilson et al (14), reported on 37 cases in the B.F. Goodrich Company. Julie et al (15) described a syndrome consisting of (arranged in decreasing order of occurrence) thrombopenia, splenomegaly, liver damage, obstruction of ventillation, circulatory obstruction, and skin and bone alteration. As a result of this problem, the University of Michigan in 1967 was retained by the Manufacturing Chemists Association to investigate acroosteolysis in sponsoring American companies. The results of a large scale epidemiological study of workers then currently employed in vinyl chloride and polyvinyl chloride production were reported in three pub -197- lications by this group Dinman et al, (16) Cook et al, (17), and Dodson et al, (18). Dinman et al (16) summarized the study as follows: "An epidemiological study was performed covering 5,011 employees with 21,510 man-years experience in various phases of vinyl chloride (VC) and polyvinyl chloride (PVC) manufacturing in 32 plants throughout the United States and Canada. The total number of definitive cases of acroosteolysis (AOL) was 25; 16 other individuals were under suspicion. This condition is clearly associated with the hand cleaning of polymerizers. Workers engaged in other phases of VC or PVC manufacturing do not appear to be at risk of developing AOL. The importance of Raynaud's phenomenon as a concomitant of AOL is emphasized. Several statistical approaches for rapid medical survey are^suggested. Acroosteolysis appears to be a systemic rather than local disease. Presently, neither the etiological agent nor its portal of entry is known." Cook et al (17) describes thepolyvinyl chloride production process in considerable detail. They condluded that although no etiological agent could be identified, "There appeared to be a correlation between the extent of degassing prior to entry into the reactor" and the incidence of acroosteolysis. Mutchler and Kramer (19) presented a paper at the 1968 Gordon Research Conference which was subsequently published (1972), which reported on "The Correlation of Clinical and Environmental Measurements for Workers Exposed to Vinyl Chloride", The authors drew the following conclusion: "Our findings suggest that repeated exposure to vinyl chloride at TWA levels of 300 ppm or above for a working lifetime together with a very low level of vinylidene chloride may result in slight changes in certain physiologic and clinical laboratory parameters. The possibility of some impairment in liver function tests must be considered, even though no overt clinical disease was evident in any of the individuals studied. We shall continue our study, but suggest that similar studies to help clarify the effects of this material be performed for other worker pop ulations exposed to vinyl chloride alone." P.O. Viola, in an attempt to produce acroosteolysis in animals, exposed rats 4 hours per day, 5 days per week to 30,000 ppm (3%) vinyl chloride vapor. In his first report on the results of 12 months exposure, he described metaplastic changes in the bones which he considered similar to the human disease acroosteolysis. He made no mention of having obser ved cancer in these animals until the Tenth International Cancer Congress in May, 1970. In the abstracts of this meeting, and subsequently in May, 1971, Viola, Bigotti and Caputo (21) reported tumors of the skin, lungs and bones occurring first after 10 months of exposure. The authors summarized this work as follows: "Rats (Ar/IRE Wistar strain) exposed for 12 months to vapors of vinyl chloride developed tumors of the skin, lungs, and bones. The -198- cutaneous tumors, which always appeared in the area in which submaxillary and parotid glands are located, have been histologically recognized as epidermoid carcinomas, papillomas, and mucoepidermoid carcinomas. The morphological characteristics of lung tumors, which occurred in a lower percentage, were mainly of the adenocarcinoma type, with the exception of a single epidermoid tumor originating from the epithelial covering cells. In a minor number of rats, a large proliferation of cartilaginous tissue diagnosed as osteochondroma developed in the metacarpal and meta tarsal regions of the four limbs." The report by Viola et al (21) is apparently the earliest publication in which carcinogenic activity has been ascribed to vinyl chloride in man or animals. Although there were obvious deficiencies in Viola's study, such as his very impure sample, the presence of food and bedding in the exposure chamber, the excessive exposure concentration as well as in the statistical evaluation and interpretation of the lesions, the report was of serious concern and resulted in additional animal and epidemiological studies which are currently underway in Italy Maltoni (22), Maltoni and Lefemine, (23,24) and the U.S, Keplinger et al (25). On January 22-23, 1974, the B.F, Goodrich Company notified its employees, NIOSH, the Kentucky State Department of Labor, and the public, that three workers had died of angiosarcomas of the liver. The case reports of the first subject has been published by Creech and Johnson (26). The subject, a 36 year old male, was hospitalized January 5, 1970 and subsequently succumbed September 27, 1971. He had worked in PVC production from November 1955 until his illness. The history, clinical course and pathologic findings are consistent with the others who died of angiosarcoma. The work of Maltoni and Lefemine (23,24) has been reported publicly at the OSHA hearing, Washington, D.C., February 15, 1974, and included in the 1974 publication of the Second International Symposium on Cancer De tection and Prevention, Bologna, Italy, April 9-12, 1973. In these studies groups of rats as well as mice and hamsters have been exposed to concen trations of 10,000 to 50 ppm vinyl chloride vapor. Maltoni and Lefemine (1974) reported carcinomas of the Zymbal glands, nephroblastoma and angiosarcomas of the livers of rats at concentrations of 250 ppm to 10,000 ppm but not at 50 ppm. Subsequent unpublished information (August 31, 1974) reported "1 liver angiosarcoma, 1 extrahepatic angiosarcoma and 1 nephroblastoma, in three animals of the first experiment, exposed to 50 ppm of VC for 1 year, and surviving 135 weeks from the beginning of the treatment." The authors conclude that "a dose-response relationship clearly emerges, as far as angiosarcomas and nephroblastomas are concerned, in the lower dose ranges: from 500 ppm to 50 ppm for angiosarcomas, and from 250 ppm to 50 ppm for nephroblastomas. A comparison of the results available at the present moment in rats exposed for 12 months and 4 months (BT1 and BT3 experiments) shows that the neoplastic response, as far as angiosarcomas and nephroblastomas are concerned, is affected by the length of exposure to VC." In their experiment BT3 Maltoni and Lefemine reported possible in utero production of angiosarcomas in offspring of pregnant rats exposed to 10,000 and 6,000 ppm. -199- Keplinger et al (25) in a study sponsored by American companies have confirmed the findings of Maltoni and Lefemine. In this study groups of 100 rats, mice and hamsters of each sex are being exposed seven hours per day, five days per week to either 2,500, 200 to 50 ppm vinyl chloride monomer. After seven months of exposure angiosarcoma and lung adenomas have been observed in mice at all exposure levels. Although the data are preliminary in nature and require confirmation, angiosarcomas were apparently also observed in rats at 2,500 and 200 ppm and in a single hamster at 2,500 ppm. This study is still in progress and will not be completed until 1976 or 1977. Epidemiological studies on U.S. workers have been conducted by Tabershaw-Cooper Associates for the Manufacturing Chemists Association (27). The summary of this study is as follows: 1. This historical prospective mortality study of 8384 men who had at least one year of occupational exposure to vinyl chloride before December 31, 1972, demonstrated that cancers of the digestive system (primarily angiosarcoma), respiratory system, brain, and cancers of unknown site, as well as lymphomas, occurred more often than expected in those members of the study population with the greatest estimated exposure. The mortality from other cancers was lower than that of the general male population, with the exception of cancers of the buccal cavity and pharynx. The explanation for the latter finding is not apparent. The other major findings of the study are: (1) The overall mortality of the study population was approximately 75% of what would be expected in a comparable population of U.S. males; (2) No cause of death showed a statistically significant excess over what would be expected in a com parable U.S. male population; and, (3) No deaths identified as angiosarcoma of the liver were found other than those previously identified. This is the first epidemiological study which suggests that in humans vinyl chloride may also be associated with cancer of multiple sites. Vinyl chloride is tentatively assigned to Appendix A/c, "Substances awaiting reassignment of TLV because of recently discovered carcinogenicity," References:1 2 3 4 5 6 7 8 9 1. Torkelson T.R, et al.: AIHAJ 22, (5), 354 (1961). 2. Lehman, K.B. and Flury, F.: Toxicology & Hygiene of Industrial Solvents (1938). 3. Tribukh, et al.: Arg. Sanit _10, 38 (1949). 4. Mastromatteo, E., et al.: AIHAJ ^1(5), 394 (1961). 5. Lester, D. et al.: AIHAJ 24 265 (1963). 6. Filatova, V.S. and Gronsberg, E. S.: Giegiena i Sanit 22^(1), 38, Abstract (1957). 7. Gabor, S. et al.: Prom. Toksikol. i Klinika Prof. Zabolevanii Khim. Etiol. Sb. 221, Abstract (1962). 8. Suciu, I. et al.: Medicina Interna (Bucharest), XV(8), 967 (1963), 9. Gabor S. et al: Ingiena Bucharest 11(5), 409, Abstract (1964). -200- 10. Grigorescu, I. and Toba, G.: Rev. Chim. 17/8), 499, Abstract (1966). 11. Antonyuzhenko, V.A.: GIG TR Prof Zabol 12/3), 50, Abstract (1968). 12. Kudryavtseva, O.F. GIG TR Prof Zabol 14/8), 54, Abstract (1970). 13. Harris, D.K. and Adams, W.G.F.: Brit. Med. J. 5567, 712, Abstract (1967) 14. Wilson, R.H. et al.: JAMA 201(8), 577 (1967). 15. Juhe, S, et al.: Dtsch. med. Wschr. 98, 2034 (1973). 16. Dinman, B.D. et al.: Arch. Environ. Hlth. 22, 61 (1971)* 17. Cook, W.A. et al.: Arch. Environ. Hlth. 22^, 74 (1971). 18. Dodson, V.N. et al.: Arch, Environ. Hlth 22_, 83 (1971). 19. Kramer, C.G, and Mutchler, J.E.: AIHAJ 33(1), 19 (1971). 20. Viola, P.L.: Medicina del Lavoro 61(3), (March 1970). 21. Viola, P.L. et al.: Cancer Research 31, 516 (1971). 22. Maltoni, C.: Proc. 2nd Inti. Symp. on Cancer Detection & Prevention, Bologna, 1973, Excerpta Medica, Amsterdam (1974). 23. Maltoni, C. and Lefemine, G. Lincei-Rendieonte Della Classe di Science, Tesiche, Mathmatische Naturalo, ^56, 1 (1974). 24. Maltoni, C. and Lefemine, G.: Carcinogenic Bioassays of Vinyl Chloride, Unpublished Data (1974). 25. Keplinger, M.L. et al.: Annals of NY Acad, of Sciences Working Group, May 10, 1974 (In preparation, 1974). 26. Creech, J.L. and Johnson, M.N.: JOM 16(3), 150 (1974). 27. Tabershaw, I.R. and Gaffey, W.R.: JOM 16(8), 508 (1974). 28. Patty, F.A. et al.: U.S. Public Health Reports 45, 1963, Abstract (1930) WELDING FUMES N.O.C.* Appendix TLV, 5 mg/m3 In electric or oxy-gas welding or iron or sheet, galvanized iron or aluminum, the chief components of the fume are ordinarily oxides of iron, zinc or aluminum. Other fumes, as well as toxic gases, may be present in significant amounts, however. Manganese, silicate and organic binders are commonly present in the coatings of welding rods for ferrous metals; fluoride in those for aluminum. And elements such as arsenic, copper, are sometimes found. Many aluminum rods contain appreciable quantities of silicon, and some have traces of beryllium. In shielded arc-welding, ozone is often formed, and carbon monoxide has been reported when CO2 was utilized as shield gas. Oxides of nitrogen are more likely to be associated with oxy-gas than with electric arc welding (1,2). Because of the additional hazard created by toxic gases and traces to small amounts of fumes of more toxic elements, the total fume con centration, when welding iron, mild steel or aluminum, should not exceed 5 mg/m3 in the breathing zone of the welder or others in the area. The fumes from stainless steel, cadmium- or lead-coated steel, and other metals such as copper and nickel are considerably more toxic and concentrations should generally be kept at a lower level, depending on the TLVs of the metals involved. In addition, in the shielded arc-welding of aluminum, relatively large amounts of ozone may be generated, and the -201- concentration of this gas may largely determine the health hazard. *Not Otherwise Classified References: 1. Emergency Control of Welding Fumes, NIOSH Research Rept., Div. Labor atories and Criteria Development, Cincinnati, OH. 2. The Welding Environment, American Welding Society, September 4, 1974, 2501 Northwest 7th Street, Miami, FL 33125, 1973. C m-XYLENE, a,a*-DIAMINE TLV, 0.1 mg/m13-2Skin H2NH2C \ ch2nh2 Determination of experimental toxicity of m-xylene Mol. wt., 136 diamine is limited to acute oral, and skin irritation Freezing pt., 14.7 C and sensitization (1). The approximate oral lethal dose Boiling pt. ,i> 200 C for male rats was 1.5 g/kg body weight indicating a low Decomposes 250 C acute oral toxicity. The compound appears to act as a Vapor Press. 3.2 mmHg gastrointestinal irritant because of its basic caustic- @ 119 C ity. The undiluted compound was corrosive to guinea pig skin; severe irritation resulted from the application of a 50% emulsion in a 1:1 acetone: dioxane mixture containing 13% guinea pig fat, and 10% and 5% concentrations of the compound produced mild and negligible irritation, respectively, Application of aqueous solutions either showed similar or slightly less irritation at the same concentrations. Repeated application to the skin resulted in mild sensitization in all 10 guinea pigs tested. On the basis of its close relation to the causticity and sensitization of phenylene diamine (which see), a TLV of 0.1 mg/m3 is recommended as a ceiling value. Reference: 1. Communication from Haskell Laboratory, E.I. DuPont, Wilmington, DE, April 24, 1973.