ENVIRONMENTAL

CHEMICALS
HUMAN & ANIMAL HEALTH
3rd Annual Conference
1974

Proceedings
               U.S. Environmental Protection Agency
                 Office of Pesticide Programs
                   Washington, D.C.

-------
        ENVIRONMENTAL  CHEMICALS
        HUMAN  AND  ANIMAL  HEALTH
 Proceedings  of  3rd  Annual  Conference
             Sponsored  by
       Colorado  State University
    College  of Veterinary  Medicine
        and  Biomedical  Sciences
Institute of Rural  Environmental  Health

                  and

 U.S.  Environmental  Protection Agency
     Office  of Pesticide Programs
          Operations Division
       Edited  by  El don  P.  Savage
                Held  at
       Colorado State University
        Fort Collins, Colorado
           July 15-19,  1974

-------
                            CONTENTS

                                                             Page

Contents	     i

Preface	   iii

Conference Participants 	     v

Current Trends in Chemical Usage
     Donald A. Spencer	     1

Pesticide Usage in Pennsylvania Agriculture
     William Wills, Gary E. Jones and William Apgar ....    17

Pesticide Products Sold in Retail Food
  Establishments in Kentucky, 1972
     Edsel Moore	    29

Military Pest Control
     Walter W. Barrett	*	    69

Pesticides and Wildlife
     William D. Fitzwater 	    79

Human Health Aspects of Pesticides
     Eldon P. Savage	    93

An Epidemiological Approach to Pesticide Poisoning
     Wilton A. Williams	   101

Occupational Pneumoconiosis
     Bobby J. Gunter	   Ill

Environmental Chemicals of Contemporary Interest
     Frank S. Lisella	   115

Pesticide Residues in Laundered Clothing
     J. W. Southwick, H. D. Mecham, P. M. Cannon
     and M. J. Gortatowski	   125

A Comparative Study of Cholinesterase Values and
  Urinary Alkyl Phosphate Excretion Levels from
  Organophosphate Exposed and Non-Exposed Males
     Herbert Starr and Sara Borthick	   133

Assessing the Environmental Impact of Chemicals
     G. U. Ulrikson, Anna S. Hammons and
     James Edward Huff	   143

-------
                                                             Page

Interim Region VIII Pesticides Land Storage and
  Disposal Guidance, January 1974
     Dan W. Bench		     161

Degradation of Pesticides
     Frederick Applehans 	     171

Referral Process for Coordinated Environmental and
  Land Use Decisions
     Lane Kirkpatrick, Steve Weiner and
     Donald Shanfelt	     181

Mycotoxins
     Frederick W. Oehme	     191

An Iimnunological Approach to Population Control
     Lloyd C. Faulkner .	i	     211

Arsenics
     Arthur A. Case	     217

Chemical Safety - Pesticides
     Homer R. Wolfe	     233

Analytical Development
     Lionel A. Richardson	     257

Avian Salt Glands - An Index to Effects of
  Environmental Pollution
     Milton Friend and John H. Abel, Jr	     259

Environmental Concerns in Fish Management
     Charles R. Walker	     269

Air Sampling for Pesticides
     David L. Spencer	     271

PCBs - Their Origin and Fate in a River Ecosystem
     Richard E. Johnsen and Lorreta Y. Munsell 	     273

Asbestos:  An Overview
     J. E. Huff	     293
                                 ii

-------
                            Preface


     The Third Annual Conference on Environmental Chemicals:  Human

and Animal Health was held on the campus of Colorado State University

during the week of July 15-19, 1974.

     The purpose of this Conference is to explore the environmental,

ecological, human and animal health effects of environmental chemicals,

Over 100 people representing 30 states and Canada attended the 1974

Conference.

     As co-chairman of the Conference, with Mr. William Fitzwater, of

the Environmental Protection Agency, I wish to express our sincere

appreciation to fellow staff members of Colorado State University and

the Environmental Protection Agency for assistance in the program.

I wish to thank Virginia Moroney for typing the Proceedings of this

Conference.
                                            E.  P.  Savage
                                            Editor
                               iii

-------
iv

-------
                     CONFERENCE PARTICIPANTS
Abrahamson, Lawrence, Ph.D., U.S. Forest Service, Pesticide Specialist
    1720 Peachtree Road, N.W.,  Suite 710, Atlanta, Georgia 30009.

Applehans, Fred M., B.S., M.S., Colorado Epidemiologic Pesticide Studies
    Center, Institute of Rural Environmental Health, Department of
    Microbiology, Spruce Hall^  Colorado State University, Fort Collins,
    Colorado 80523.

Bagby, John R., Jr., M.S., Ph.D., Director, Institute of Rural Environ-
    mental Health, Professor of Microbiology, Department of Microbiology,
    Colorado State University,  Fort Collins, Colorado 80523.

Barrett, Walter W., Entomologist, Headquarters,  United States Air Force
    (TREV), Washington, D.C.

Bench, Dan, Pesticide Disposal Coordinator, Environmental Protection
    Agency, Region VIII, 1860 Lincoln, Denver, Colorado 80202.

Bennett, C. Willard, Southern Division, Naval Facilities, Engineering
    Command, Senior Entomologist, P.O. Box 10068, Charleston, South
    Carolina 29411.

Bohmont, Bert L., Ph.D., Agricultural Chemicals  Coordinator, College
    of Agricultural Sciences, Colorado State University, Fort Collins,
    Colorado 80523.

Boyes, Virginia, Colorado Epidemiologic Pesticide Studies Center,
    Institute of Rural Environmental Health, Department of Microbiology,
    Spruce Hall, Colorado State University, Fort Collins, Colorado
    80523.

Buchan, Roy M., Ph.D., Institute of Rural Environmental Health, Department
    of Microbiology, Colorado State University,  Fort Collins, Colorado
    80523.

Buffaloe, William B., Chief Pesticide Officer, Pest Control Division,
    N. C. Department of Agriculture, P.O. Box 27647, Raleigh, North
    Carolina 27611.

Byrne, Martin, Environmental Protection Agency,  Region VIII, 1860 Lincoln,
    Denver Colorado 80202.

Campbell, Dr. Kirby I., Environmental Toxicology Research Lab, National
    Environmental Research Center, Environmental Protection Agency,
    1055 Laidlaw Avenue, Cincinnati* Ohio 45237.

Campt, Doug, Environmental Protection Agency, Washington, D. C.

Carey, Ann E., Soil Scientist,  Technical Services Division (WH-569),
    Environmental Protection Agency,  401 M  St.,  S.W., Washington, D.C.
    20460.

-------
Case, Arthur A., M.S., D.V.M., Professor of Veterinary Medicine and
    Surgery, University of Missouri, Columbia,  Missouri.

Cholas, Gus, D.V.M., M.P.H., Associate Professor of Microbiology,  Department
    of Microbiology, Colorado State University, Fort Collins,  Colorado
    80523.

Collier, John R., D.V.M., M.S., Ph.D., Institute of Rural Environmental
    Health, Professor of Microbiology, Department of Microbiology,
    Colorado State University, Fort Collins, Colorado 80523.

Conway, Thomas, M.S., P.E., Colorado Epidemiologic Pesticide  Studies
    Center, Institute of Rural Environmental Health, Department of
    Microbiology, Spruce Hall, Colorado State University, Fort Collins,
    Colorado 80523.

Coon, M. J., Department of Biological Cehmistry, Medical School, University
    of Michigan, Ann Arbor, Michigan 48104.

Crawford, Richard K., Pesticides Inspector, Environmental Protection
    Agency, P.O. Box 885, Slidell, La. 70458.

Davidson, Darrell C., Labor Foreman, Rocky Flats, Box 888, Golden, Colorado
    80401.

Davison, Kenneth L., USDA, Agricultural Research Service, Metabolism and
    Radiation Research Lab, State University Station, Fargo,  North Dakota
    58102.

DePriest, Clarinda, Colorado Epidemiologic Pesticide Studies  Center,
    Institute of Rural Environmental Health, Department of Microbiology,
    Spruce Hall, Colorado State University, Fort Collins, Colorado 80523.

Dodson, I., Environmental Protection Agency, Region VIII, 1860 Lincoln,
    Denver, Colorado 80202.

Donaldson, Donald A., Pesticide Operations Officer, Environmental Protection
    Agency, Region X, 1200 6th Avenue (M/S 537), Seattle, Washington 98101.

Drake, Earl, D.V.M., University of Nevada, Extension Veterinarian, 107
    Anderson Health Science Bldg., Veterinary Science, Reno,  Nevada 89507.

Elliott, John, Specialist in Pesticide Education, Cooperative Extension
    Service,  Auburn University Extension Cottage, Auburn, Alabama 36830.

Faulkner, Lloyd, Ph.D., D.V.M., Professor and Chairman, Physiology and
    Biophysiology Department, Colorado State Univeristy, Fort Collins,
    Colorado 80523.
                                   vi

-------
Fechner, Walt, D.V.M., Director, Meat Inspection Division,  Arkansas
    State Department of Health, 4815 W. Markham Street,  Little Rock,
    Arkansas 72201.

Fergin, Truman J., Denver Wildlife Research Center, Wildlife Biologist,
    Building 16, Federal Center, Denver, Colorado 80225.

Fitzwater, William, Senior Biologist, Office of Pesticide Programs,
    Environmental Protection Agency, 401 M Street, S.W., Washington,
    D.C. 20460.

Flake, Harold, Pesticide Coordinator, USDA Forest Service,  Federal
    Building, Missoula, Montana 59801.

Freden, Greg, Colorado Epidemiologic Pesticide Studies Center, Institute
    of Rural Environmental Health, Department of Microbiology, Colorado
    State University, Fort Collins, Colorado 80523.

Fresh, Richard W., O.M. Scott & Sons Company, Environmental Advisor,
    Landscape Office, Marysville, Ohio 43040.

Fredrickson, Luther E., D.V.M., Director, Veterinary Medicine, Tennessee
    Department of Pu.blic Health, 101 Capitol Towers, Nashville, Tennessee
    37219.

Frick, John H., Entomologist, Department of the Army Civilian, U.S.
    Army Environmental Hygiene Agency, Attn:  USAEHA-SWMD,  Aberdeen
    Proving Ground, Md. 21010.

Friend, Milton, Ph.D., United States Fish and Wildlife Service, Federal
    Center, Denver, Colorado.

Frost, Margaret Nancy, Chemist, Environmental Protection Agency, Region
    IX, Pesticide Product Laboratory, 50 Fulton Street,  Room 545, San
    Francisco, California 94102.

Gebhart, William A., 104B1, Entomologist, Naval Facilities Engineering
    Command, 200 Stovall Street, Alexandria, Virginia 22332.

Greenman, David L., Ph.D., National Center for Toxicological Research,
    Pharmacologist, Food and Drug Administration, Jefferson, Arkansas
    72079.

Griffith, Jack, Ph.D., HM-569, Technical Services Division, OPP, Environ-
    mental Protection Agency, Room 315, Waterside Mall,  East Towers
    401 M Street S.W., Washington, D.C. 20460.

Grosso, Louis S., Accident Investigator, Environmental Protection Agency,
    Region III, 6th & Walnut Streets, Philadelphia, Pennsylvania 19106.

Gundlach, Charles E., VMD, HEW, Food & Drug Administration/BVM, 6800
    Caneel Court, Springfield, Virginia 22152.
                                vii

-------
Gunter, Bobby J., Ph.D., Regional Industrial Hygienist, National Institute
    for Occupational Safety and Health, Department of Health, Education,
    and Welfare, 11023 Federal Building, Denver, Colorado 80225.

Haegele, Max A., Denver Wildlife Research Center, Wildlife Biologist,
    Building 16, Federal Center, Denver, Colorado 80225.

Hager, Lura, Colorado Epidemiologic Pesticide Studies Center, Institute
    of Rural Environmental Health, Department of Microbiology, Spruce
    Hall, Colorado State University, Fort Collins, Colorado 80523.

Hammons, Anna S., Oak Ridge National Laboratory, Union Carbide Corporation,
    P.O. Box Y, Oak Ridge, Tennessee.

Hansen, Gary, Environmental Protection Agency, 1860 Lincoln, Denver,
    Colorado 80202.

Harding, Dr. Wallace C., Jr., Extension Entomologist and Pesticide
    Coordinator, University of Maryland, Department of Entomology,
    College Park, Md. 20742.

Hawes, Ralph W., Dow Chemical Research Engineer, Rocky Flats Division,
    P.O. Box 888, Golden, Colorado 80401.

Hess, Archie D., Ph.D., Institute of Rural Environmental Health, Depart-
    ment of Microbiology, Colorado State University, Fort Collins,
    Colorado 80523.

Honing, Frederick W., Assistant Director of Forest Pest Control, USDA
    Forest Service, 14th and Independence Avenue, S.W., Washington,
    D.C. 20250.

Hueneberg, Carl, Superintendent, Sanitation Section, 824 Civil Engineering
    Squadron, PSC Box 25279, APO San Francisco, California 96230.

Huff, James E., Ph.D., Oak Ridge National Laboratory, Union Carbide
    Corporation, P.O. Box Y  Oak Ridge, Tennessee.

Hughes, Duane, Chemist, Food and Drug Administration, 1009 Cherry,
    Kansas City, Missouri 64106.

Humphrey, Harold, Michigan Department of Public Health, 3500 North
    Logan, Lansing, Michigan.

Ingram, Temple B., Jr., Pesticide Accident Investigation Officer, Environ-
    mental Protection Agency, Region I, Categorical Programs Division,
    Pesticides Branch, JFK Federal Building, Boston, Mass. 02203;

Johnson, Terry, Pesticide Coordinator, Ohio Environmental Protection
    Agency, 361 East Broad Street, Columbus, Ohio 43215.

Kanof, Elizabeth P., M.D., Physician-Dermatologist, 1300 St. Marys St.,
    Raleigh, North Carolina 27605.
                               viii

-------
Kirkpatrick, Lane, Air Pollution Control Commission, Colorado Department
    of Health, 4210 East llth Avenue, Denver, Colorado.

Kreigh, Kyle R., Environmental Protection Agency, Program Specialist,
    1 N. Wacker Drive, Chicago, Illinois 60606.

Levine, Dr. Ronald H., Assistant Director, Division of Health Services,
    North Carolina Department of Human Resources, P.O. Box 2091, Raleigh,
    North Carolina 27602.

Levy, Morris R., D.V.M., J.D., U.S. Food and Drug Administration,
    Regional Veterinary Medical Officer, Room 900, U.S. Customhouse
    Bldg., 2nd and Chestnut Streets, Philadelphia, Penn. 19106.

Lewis, Dr. R. G., Chief, Analytical Services, PTSEL, Environmental
    Protection Agency, National Environmental Research Center, Room
    138, Monsanto Building, Research Triangle Park, North Carolina
    27711.

Lisella, Frank S., Ph.D., Chief, Program Development Branch, Environmental
    Health Services Division, Department of Health, Education, and Welfare,
    Public Health Service, Center for Disease Control, Atlanta, Georgia.

Lister, Ken, U.S. Forest Service, Denver Federal Center, Building 85,
    Denver, Colorado  80225.

Lund, CMSgt John L.,  Sr., NCOIC, Environmental Health Branch, Brooks
    AFB, Texas 78235.

Malberg, Joe, Colorado Epidemiologic Pesticide Studies Center, Institute
    of Rural Environmental Health, Department of Microbiology, Spruce
    Hall, Colorado State University, Fort Collins, Colorado 80523.

Maloney, Kathleen A., Environmental Protection Specialist, Pesticides
    Branch, Environmental Protection Agency, 100 California Street,
    San Francisco, California 94111.

Marano, Donald, National Institute for Occupational Safety and Health,
    Cincinnati, Ohio.

Matzke, Tim, Quality  Control Coordinator, Environmental Protection Agency,
    1600 Patterson, Dallas, Texas 75201.

McAlister, Robert L., Oklahoma Department of Health, Room 803, NE 10th
    and Stonewall, Oklahoma City, Oklahoma 73105.

Miller, Charles W., Ph.D., Field Studies Coordinator, Epidemiologic
    Studies Program,  Colorado State University, Fort Collins, Colorado
    80523.

Moore, Edsel E., Director, Pesticides Program,  Division of Environmental
    Services, Kentucky Department of Health, Frankfort, Kentucky.
                                ix

-------
Morrison, William P., Pesticide Coordinator, N.M. Department of
    Agriculture, Acting Chief, Division of Pesticide Control, Box
    3189, Las Cruces, New Mexico 88003.

Mounce, Lawrence, Colorado Epidemiologic Pesticide Studies Center,
    Institute of Rural Environmental Health, Colorado State University,
    Fort Collins, Colorado 80523.

Murray, William S., Ph.D., Directorj Technical Services Division, Office
    of Pesticide Programs, Environmental Protection Agency, 401 M Street,
    S.W., Washington, D.C. 20460.

Oehme, Frederick W., D.V.M., Ph.D., Professor of Toxicology and Medicine,
    Director, Comparative Toxicology Laboratory, Department of Surgery
    and Medicine, Kansas State University, Manhattan, Kansas.

Ogg, James E., Ph.D., Professor and Head, Department of Microbiology,
    Colorado State University, Fort Collins, Colorado 80523.

Oglesbee, Paul B., Jr., EPA-TSD Chemistry Lab Supervisor, Building
    1105, MTF, Bay St. Louis, Ms. 39520.

Osteryoung, Janet G., Ph.D., Institute of Rural Environmental Health,
    Associate Professor, Department of Microbiology, Colorado State
    University, Fort Collins, Colorado 80523.

Patterson, Barry, New Mexico Department of Agriculture, Box 3189,
    Las Cruces, New Mexico 88003.

Perez, MaryIn K., Assistant to the Associate Director for Sciences,
    Bureau of Foods, 200 "C" Street, S.W., Food and Drug Administration,
    HEW, Room 2117, Washington, D.C. 20204.

Powers., William J., Entomologist, Environmental Protection Agency
    Headquarters, WSME 234, Washington, D.C. 21044.

Reeves, Robert G., Chemist, USDA, APHIS, PPQ, Environmental Quality
    Lab, P.O. Box 3296, Brownsville, Texas 78520.

Richardson, Lionel A.» Ph.D., Operations Division, Office of Pesticide
    Programs, Environmental Protection Agency, Washington, D.C.

Richmond, Merle L., Wildlife Biologist, Denver Wildlife Research Center,
    Building 16, Federal Center, Denver, Colorado 80225.

Robertson, Suzanne, Royal Commission on Pesticides and Herbicides,
    5760 Toronto Road, Vancouver, B.C., Canada V6T1L2.

Savage, Eldon P., M.P.H., Ph.D., Director,- Colorado Epidemiologic
    Pesticide Studies Center, Chief, Chemical Epidemiology Section,.
    Institute of Rural Environmetnal Health; Associate Professor, De-
    partment of Microbiology, Colorado State University, Fort Collins,
    Colorado 80523.

-------
Savarie, Peter J., Ph.D., Pharmacologist,  U.S.  Fish and Wildlife Service
    Building 16, Federal Center,  Denver,  Colorado 80225.

Schoenherr, W. H., Lauhoff Grain Company,  Vice  President,  P.O.  Box
    571, Danville, Illinois 61832.

Smith, Dr. Harry G., Pesticide Specialist, University of Nevada, College
    of Agriculture, Reno, Nevada 89507.

Smith, Dr. James Allbee, Residue Chemist,  West  Virginia Department of
    Agriculture, Laboratory Services Division,  Charleston, West Virginia
    25305.

Sorensen, Stephen L., Department of Environmental Protection,  Environ-
    mental Sanitarian, Building #2, Pierre, South Dakota 57501.

Southwick, J. Wanless, Ph.D., Chief, Health Effects Section, Division
    of Health, 44 Medical Drive,  Salt Lake City,  Utah.

Spencer, David, Colorado Epidemiologic Pesticide Studies Center, Institute
    of Rural Environmental Health,  Department of Microbiology,  Spruce
    Hall, Colorado State University, Fort Collins, Colorado 80523.

Spencer, Dr. Donald A., Consulting Ecologist for the National  Agricultural
    Chemicals Association, 1155 15th Street N.W., Washington,  D.C.

Starr, Herbert G., Jr., Public Health Chemist,  Colorado Epidemiologic
    Pesticide Studies Center, Institute of Rural Environmental Health,
    Department of Microbiology, Colorado State  University, Fort Collins,
    Colorado 80523.

Svetich, Edward, Sanitarian, Scott County Health Department,  416 West
    4th Street, Davenport, Iowa 52801.

Swift, Dr. John E., Statewide Coordinator, Pesticides, Agricultural
    Extension Service, University Hall,  2200 University Avenue, Univer-
    sity of California, Berkeley, California 94720.

Tennis, Carlyle R., Pesticide Inspector,  Environmental Protection Agency,
    Region IX, S & A Division, 100 California Street, San  Francisco,
    California 94111.

Tessari, John, Colorado Epidemiologic Pesticide Studies Center, Institute
    of Rural Environmental Health,  Department of Microbiology,  Spruce
    Hall, Colorado State University, Fort Collins, Colorado 80523.

Thomas, William L., U.S. Fish & Wildlife Service, Pesticide Staff
    Specialist, 17 Executive Park Drive,  N.E.,  Atlanta, Georgia 30329.

Tietz, William J., D.V.M., Dean,  College of Veterinary Medicine and
    Biomedical Sciences, Colorado State University, Fort Collins, Colorado
    80523.
                                xi

-------
Turner, William D., Project Coordinator, Tennessee Pesticide Project,
    Memphis Shelby County Health Department, 814 Jefferson Avenue,
    Memphis, Tennessee 38105.

Vallejo, Roberto G., Pesticides Specialist, Environmental Protection
    Agency, 1600 Patterson Street, Dallas, Texas 75201.

Von Sumpter, D. Thomas, II, Pharmacologist, Environmental Protection
    Agency, 2105 Spruce Drive N.W., Washington, D.C. 20012.

Walker, Charles R., Office of Environmental Assistance,  Fish and Wild-
    life Service, U.S. Department of Interior, Washington, D.C.

Warnick, Stephen L., Ph.D., Intermountain Laboratories Inc., 870 East
    7200 South, Midvale, Utah 84047.

Western, Evan, Utah State Health Department, Pesticides  Project, 44
    Medical Drive, Salt Lake City, Utah.

Wheeler, Richard H. HEV-10, Ecologist - Federal Highway  Administration,
    400 7th Street, S.W., Washington, D.C. 20590.

Wheeler, William, B.S. , Colorado Epidemiologic Pesticide Studies Center,
    Institute of Rural Environmental Health, Department  of Microbiology,
    Spruce Hall, Colorado State University, Fort Collins, Colorado 80523.

Whitcomb, Dr. Donald, Arizona State Department of Health, 1716 West
    Adams Street, Phoenix, Arizona 85007.

Whittemore, F. W., Environmental Protection Agency, Washington, D.C.

Wiersma, G. Bruce, Ph.D., Chief, Ecological Monitoring Branch, National
    Environmental Research Center, Environmental Protection Agency,
    Las Vegas, Nevada.

Williams, Leslie P., D.V.M. , M.P.H., Dr.P.'H., Chief, Epidemiology and
    Zoonoses Section, Institute of Rural Environmental Health, Associate
    Professor, Department of Microbiology, Colorado State University,
    Fort Collins, Colorado 80523.

Williams, W. A., Pesticides Epidemiologist, Pesticides Program, North
    Carolina Department of Human Resources, P.O. Box 2091, Raleigh,
    North Carolina.  >

Wills, William, Director-, Entomology Laboratory, Bureau  of Community
    Environmental Control, Department of Environmental Resources, P.O.
    Box 2063, Harrisburg, Pennsylvania.

Wolfe, Homer R., Field Studies Section, Environmental Protection Agency,
    Wenatchee, Washington.
                               xii

-------
Yert, Louise, Research Chemist, Toxicology Branch, Center for Disease
    Control, 1600 Clifton Rd., N.E., Atlanta, Georgia 30^33.

Young, Nick, Department of Microbiology, Colorado State University,
    Fort Collins, Colorado 80523.                            V-\,

Younger, Dr. R. L., Veterinary Medical Officer, Veterinary Toxicology
    & Entomology Research Laboratory, ARS, USDA, Post Office Drawer
    GE, College Station, Texas 77840.
                             xiii

-------
                CURRENT TRENDS IN CHEMICAL USAGE




                       Donald A.  Spencer




          National Agricultural Chemicals Association






     Two years ago "El Nino" re-occurred with a vengence off the coast




of Peru, as it has on at least seven other occasions since 1891 (1).




The up-welling of mineral-rich water from the ocean's depths having




ceased, the food chain that supported an annual harvest of 8-10 million




tons of anchovies (small fish) also collapsed.  The millions of seabirds




that shared this resource declined drastically.  The effects were far




reaching.  The poultry raiser in Delaware and the catfish farmer in




Arkansas felt the pinch when 42 percent of the world's fishmeal was




abruptly unavailable.  In a protein-starved world this event was a major




catastrophe.




     Aside from localized areas where ocean currents return mineral




wealth, the surface waters of our oceans are surprisingly deficient in




life-support chemicals.  Even the run-off contributions from land reach




no great distance at sea.  The research vessels of the Woods Hole Ocean-




ographic Institute collected surface water samples.at varying distances




off-shore from Cape Cod to the Florida Keys.  The report of these studies




shows that the total suspended solids six miles off-shore averaged only




1.0 ppm (2).  Beyond this the suspended solids diminished to an average




of only 0.1 ppm.  They also produced evidence that the movement of bottom




sediments on the Continental shelf' and in estuaries of the Atlantic




seaboard was predominantly landward rather than seaward.




     An even more dramatic account of nutrient deficiency in ocean waters




(9) is the research on the use of bacteria that can utilize an oil slick

-------
as a source of energy.  Because of recurrent oil spills and deliberate




discharge of oil wastes in bays and in-shore marine areas, Dr. "Richard




Bartha (3) found that bacteria were often present to perform an oil re-




moval service, but their numbers increased too slowly to handle most




problem spills.  The New Jersey scientist distributed oil-soluble nitrates




and phosphates over an oil slick with the result that bacteria chomped-




away at the oil at a pace ten times as fast.




     Two years ago, tropical storm Agnes came raging up the east coast




of the United States, pausing over Virginia, Maryland, and Pennsylvania




to dump prodigious amounts of rain.  The upper part of Chesapeake Bay -




the largest estuary along the Atlantic Coast - became temporarily a fresh




water lake.  The saline content of the Bay's waters were altered to the




point where clams and oysters which could not flee their fixed habitation




suffered heavy mortalities.




     A serious cause of mortality in fish called "gas bubble disease"




is plaguing the economically important salmon fisheries of the Pacific




Northwest.  At peak flow along the Snake and Columbia Rivers water plunging




over the spillways of dams entrains air which is carried into deep pools




at the base.  Under plunging pressure water becomes super-saturated with




air (80% nitrogen) causing a condition in fish not unlike the bends in




human divers if they surface too fast.  Costly re-design of these spill-




ways is being undertaken. .




     Contrast the above situation of "too much air" with the incident at




a power dam on the lower Susquehanna River.  Here several turbines were




shut down over the weekend when there was no electrical demand.   An




oxygen sag occurred in the area below the dam resulting in a massive




kill of menhaden that had congregated there.  Water passing through the




turbines contributed importantly to relief of an oxygen deficiency




existing in the tailrace.

-------
     In parts of the northern Great Plains the soils  embody natural




occurring amounts of selenium.  Certain plants translocate selenium




to the degree that on being grazed by livestock sickness or death can .




result.  On the other hand, the U.S. Food and Drug Administration has




recently approved the addition of this toxic metal at 0.1 ppm to blended




feeds for swine and broiler chickens.  It is a trace  element necessary




for healthful development.




     From time to time,deaths occur among cattle that feed on moldy




sweet clover hay.  Death is preceded by hemorrhage.  Dr. Karl Paul




Link, University of Wisconsin,subsequently traced the cause to a. natural




occurring toxin in moldy hay - dicoumarin.  Dicoumarin seemed to have




promise as a rodenticide and among the analogs studied was one given




the name of "Warfarin"t  Today Warfarin and other members of the anti-




coagulant family are the principal means by which man holds populations




of house rats and mice in check.  Yet this very rat poison is an in-




dispensable tool in directly saving human lives.  After major surgery




it is a "must" to control clotting.of blood.  Warfarin does yeoman




service in the treatment of certain types of heart ailments.




     These random examples would seem to be an unusual way of introducing




a discussion of environmental chemicals and their effect on human and




animal health.  But they serve to emphasize that environmental chemicals




are not restricted to man-synthesized products, that  both air and water




can be lethal pollutants under some circumstances, and that chemical




hazard is almost without exception dose-related.




     The general public - and I am referring to the 93 percent of .us




that live in urban centers - re-discovered contaminating chemicals in




the food supply, in the environment, and as residues  in wildlife in  the

-------
early 1960's.  Initially attention was focused on blanket aerial




application of insecticides that included the urban area.  Involved




were the control of Dutch Elm Disease that was stripping many a north-




eastern town of a valued shade tree; the continuing effort to contain




the west and southerly spread of the destructive gypsy moth; and the




mosquito abatement programs.




     Progressively the concern about "hard pesticides" spread further




and further away from the urban doorstep.  Large scale government pest




control programs, like the fire ant project in the Gulf States, proved




susceptible targets.  Concern rather promptly escalated to include the




so-called "indiscriminate" use of pesticides by farmers and the ir-




responsible attitude of chemical companies.




     Pesticides were a natural for openers, because any number of them




were toxic and hazardous if misused.  But it was as though Pandora's




box had been opened.  Environmental quality became a watchword and now




no identificable pollutant is ignored.  Confused and alarmed by the




array of problems, the concerned citizens crowded their Federal and




State Legislatures into passing a series of environmental protection




laws, one of which defined a pollutant as, "the man-made or man-induced




alteration of the chemical, physical, biological, and radiological




integrity of water," (4) and then set fixed dates for zero discharge.




Over-reactions often ignore the feasibility of the time schedule and




the impact on the economy.  Like a kaleidoscope, chemical problems of




widely differing origins began to flash across the front pages of the




press:   a plasticizing agent in broiler chickens, a heavy metal in fish,




a fire retardant chemical in dairy feed, and two different synthetic




chemical intermediates - one in range cattle,  one a hazard in the human

-------
community, just to name a few.




     Even today, most of the "involved public" consider themselves neither




at blame, nor responsible for environmental clean-up.   But slowly, in-




exorably, the individual protesting from the sidelines is finding him-




self swept into a frustrating maelstrom of his own making.  There is




absolutely nothing wrong with the goals for a well-managed environment




and an insistence on a benefit/risk evaluation on new projects.  The




error is that a reasonable course for its achievement has not been




charted.




     Man, progressively, over the tens of thousands of years of his




existence on this planet, has learned to develop the potential of his




environment in ways seldom matched in natural processes.  Today we




live in a chemically oriented society.  In the study of plants, animals,




and physical processes about us we have identified elements and chemical




compounds for which we have need.  Initially, man turned to natural




resources for these products - sources often too limited for his needs.




Today, in ever increasing numbers we synthesize the required products




from other more abundant raw materials.  Man progressed from clothing




himself in animal skins, crude cloth woven from bird feathers and silk




from insect cocoons; to the cultivation of cotton, flax and hemp for




textile fibers; to the chemical miracle of making large organic molecules




which can be extruded into fibers of many characteristics from simple




liquid and gaseous monomers.




     The human population growth is posing a serious burden on our




capability to feed ourselves.  Not only is there a world wide shortage




of food per se, but the nutritional deficiency of the available food




deeps a number of under-developed nations on the threshold of physical

-------
deterioration.  Scientists at various agricultural experiment stations




are making exceptional progress in the genetic manipulation of food




plant species to produce varieties of improved nutritional value.  The




development recently of a high lysine sorghum by research teams at




Purdue University is an example (5).  But concurrently chemists have




succeeded in synthesizing several important amino acids by nonagricultural




chemical processes.  Lysine and methionine, now that they are in large




scale production,are used widely to fortify cereal foods.  Chemists have




worked out a chemical synthesis for tryptophan and a method exists for




producing threonine by fermentation.  However, cost is still a hurdle




in the case of the last two named protein building blocks (6).




     But chemicals are not just a means of fortifying or adding to our




food supply - they function to make it possible for us to produce more




food on fewer acres and assure its reaching our tables in good quality




and in a non-seasonal pattern.  In fact, chemical input into the "food




assembly line" is nothing short of astounding.  Fertilizers, pesticides,




and veterinary medicines come easily to mind, as may also the fumigants




that protect the grain and other raw agricultural, products in storage,




plus the sanitizing agents that are associated with every step of food




processing from the flour mill, to the bakery, the retail store and the




restaurant.  But this fiood production technology also requires tractors,




plows, combines, trucks and much sophisticated machinery that require




chemical tools at the mine, the ore concentrating mill, the smelter,




the steel mill, and the fabricating plant.  For energy to.operate this




equipment there are oil and gas wells, refineries, rail, truck and




pipeline transport - all with requirements for differing chemicals.




As for that electric power plant which is very much involved in the

-------
operation of this "food assembly line," selection is made from over 150




different chemical compounds to process water used for steam and to




control raw water in the cooling system (6).   Frozen foods have come




rapidly to the fore in recent years.   The refrigeration systems at the




food processor, in mobile transport,  at the retail outlet, and in the




home require the production in the United States of some 700 million




pounds annually of fluorocarbon refrigerants  (7).  Then there is pack-




aging; with wood from the forests converted by chemical process to paper,




plastics that are polymerized from simple chemical compounds, glass




containers, (the U.S. glass industry makes and ships more than 25 billion




pounds of various glass products each year),  "tin" and aluminum cans,




and don't forget the dyes, inks, paint and glue used in labeling.




Lastly, water supply is a critical factor throughout the entire food




assembly line.  Whether for irrigation or potable uses it must be im-




pounded behind dams or pumped from the ground.  In the clean-up process,




for example, processing of public water for Montgomery and Prince George




Counties in Maryland during fiscal year 1972-73 required 883.9 tons of




chlorine, 100 tons of sodium silicofluoride,  10.6 tons of sodium bi-




sulphite, 3,278 tons of alum, and 2,136 tons  of lime.  All of these




processes produce wastes that must be re-acted with millions of pounds




of man-produced chemicals if they are to be removed before discharge




of effluents into air or water.




     Our requirements for chemicals are unbelieveably large.  The




American Chemical Society reports that, "Among the top 100 organic




chemicals in production value, annual output  ranges from 3 billion




pounds to 10 million pounds or less."  Close to 90% of organic inter-




mediates today are made from petroleum and natural gas.  Most of the

-------
remainder come from coal tar, produced by the steel industry's coke




ovens, and a very small amount is made from animal fats, vegetable oils,




rosin and grains."  On the otherhand, from naturally occurring mineral




ores and brines we recover or porduce huge tonnages.  Of the chemicals




produced in the largest tonnages in the U.S., inorganics occupy 9 of




the first 10 places (7).




     This vast array of chemicals and chemical products range from




those that are relatively non-reactive and comparatively safe to handle




to highly toxic, highly reactive, even explosive chemicals.  Over the




years we have acquired the knowledge of how to avoid, contain, or min-




imize the hazardous characteristics of an otherwise useful chemical




tool.  No claim of absolute safety can be made for any of these products -




nor is there any need to do so.  Man will continue, as he has in the




past, to apply a risk/benefit evaluation to each of his activities.




A serious problem may call for heroic measures and we will be grateful




for an effective counter weapon that in more normal circumstances we




would not choose to employ.  With an outbreak of encephalitis or a wheat




crop threatened by a rapidly spreading disease, no formerly registered




pesticide is so objectionable that we would hesitate to use it.  We




can expect a changing status of acceptability in chemical tools as the




pressures against our way of life shift.                 :




     One approach to minimizing the potential hazard from using chemicals




of high toxicity has been the proposal to limit the number available




for use.  For purposes of registration or retaining registration, the




question might be, is it essential?  Is there an alternate product




available?  Such a solution to the problem ignores basic principles in




the management and control of plant and animal life, including veterinary




and human medicine.  A chemical agent achieves its purpose by interrupting
                                 8

-------
some specific biological process.  Subjecting a population of a plant




or animal species to a given pesticide rarely, if ever, eliminates 100




percent of the individuals within that population.  By reason of slight




genetic differences some individuals may not be stressed arid live to




re-establish the species.  In other words, "chemical selection" is




similar to "natural selection" in the plan of survival of the species.




Another chemical pesticide differing little in overall effectiveness,




exerts pressure against an entirely different biological process, re-




sulting in an entirely different set of individuals escaping the screen.




Thus, there is need to maintain as wide a selection in our kit of chemical




tools as our technology can originate, if we are to successfully mani-




pulate the plant cover and minimize the pressures of competing animal




species.




     Any number of examples of the above principle will occur to you.




For example, prior to the early 1940*s we relied heavily on the heavy




metals for insect control (calcium arsenate, lead arsenate) until the




codling moth had reestablished a tolerant strain.  Then came DDT and




related chlorinated hydrocarbons that worked on an entirely different




biological system.  This was followed by the organophosphorus and car-




bamate insecticides that essentially worked on one system - anticho-




linesterase.  Each has had an effective period.  Unfortunately, they




were not used interchangeably, largely due to progressive development.




     Another problem area in the pesticide field is vertebrate control.




Largely because of high toxicity, one after another of the vertebrate




control chemicals have been removed from registration or have had their




use severely restricted.  Thus, in the field of house rat and mouse




control, we have available today a dangerously low selection of chemical

-------
tools.  Warfarin, pival, diphacinone and related rodenticides all




work on one system governing the coagulation of the blood.  .Other than




this, the choice is red squill, or zinc phosphide.  We have dropped




phosphorus pastes, arsenic, thallium, compound 1080.  Strychnine is




under study for deletion.




     Persistence of chemicals after release into the environment has




been another difficult problem for administrators.  Now persistence




per se is not necessarily an undesirable feature of chemicals.  For '  -.




example, chemicals are used to prolong the life and utility of products




already grown or manufactured, such as a railroad tie from attack from




insects and decay, the life of a boiler tube from rust and corrosion




or the period of protection of a home against termites.  In shorter




range a farmer would prefer to get season-long weed control from one




application.  We desperately need an insecticide that will provide




control of the Gypsy Moth over a 6-week period from a single application.




In Pennsylvania the eggs of this moth hatch over such a period.  The




problem is to have effective chemical action over a given time span and




still be able to "cut it off," such as effective weed control for the




growing period of the crop and still not have significant residues




carry over to another season.  This is entirely possible in the organic




chemical field where degradation may result from light, heat, chemical




action, and metabolism in plants and animals (particularly micro-organisms).




Heavy metals such as mercury, lead, arsenic, copper, cadmium, etc.,




are truly persistent, do not degrade (within the concept of this discussion),




and are merely shuffled about.




     Persistence is directly linked to still another problem with environ-




mental chemical - their movement from point of release or application.
                              10

-------
Obviously, nothing in this category stays put.   All chemicals  exhibit




vapor pressure although exceedingly limited in some cases.   Under high




temperatures, such as incineration, the conversion to a gaseous phase




may take place readily.  PCBs may be volatilized from urban trash,




mercury and other metals from fossil fuels.  Dirft of aerially applied




sprays are a short distance phenomena.  Wind and water transport perhaps




account for the greatest movement.  Biological transport can also be




demonstrated.  Insects feeding in a contaminated zone are often free




to move out of the area carrying residues with them.  Long distance




transport occurs when waterfowl wintering about the Gulf of Mexico




migrate to northern Canada or Alaska to nest.  Arctic predators who




have never left that region may acquire a body residues from their




mirgatory prey.




     In water and air transport of environmental chemicals, mineral




soil and organic debris play a significant role.  DDT, for example,




is one of the world's most water-insoluble compounds, its solubility




in distilled water approximately 1.0 ppb.  Nevertheless, in passing




through clay minerals even this small amount can be reduced below the




sensitivity of our means to measure it.  When DDT in solution was




injected into a test well at Ada, Oklahoma it could not be recovered




at the nearest well used for measuring movement in the underground




aquifer, although nitrates similarly injected were detected (8).  But




even more efficient at immobilizing the chlorinated hydrocarbons are




the resins, waxes, oils and fats associated with both living and dead




organic matter.  DDT is millions of times more soluble in certain oils




than in water.  DDT spray falling on the epicuticular wax layer that
                              11

-------
protects most green plants, goes into solution in the wax.   Soluble

chemicals may also be either adsorbed, or chemically bound  by soil

and organic debris.  Thus a large percent of environmental  chemicals

escape the area of their release riding piggy-back on wind-born dust

and water suspended silt.

     The control of soil erosion features very prominently  in environ-

mental management to contain chemical pollutants.  A most enlightening

study has just been completed in the N.E. segment of Chesapeake Bay

by the Westinghouse Ocean Research Laboratory and the State of Maryland

Department of Natural Resources (9).  They selected the Chester River,

whose drainage basin is intensively used for agriculture, on the sup-

position that this farming would contribute importantly to  the pesticide

and other chemicals to be found in the river water and in the silts of

its bed.  They early determined that:

         "Both trace metals and the insecticides and PCBs
         are carried on the surfaces of sediments, there
         being an inverse relationship between the amount
         of these materials and the mean grain-size of
         the sediments."

         "The insecticides, DDT, ODD, DDE, cholrdane and
         PCBs (primarily Aroclor 1242) were found routinely
         in biological samples and sediment samples from
         the Chester River, but at levels far below those
         considered hazardous to humans." (9)

Then came the surprise finding:

         "Most of the measured chlorinated hydrocarbon
         pollutants are entering the Chester River from
         the upper Bay rather than from the river drainage
         area itself."

         "The fine sediments carpeting the bottom of the
         river are derived in large part from the upper
         Bay based on mineralogical composition and the
         presence of a unique clay type not common in the
         sediments drained by the river." (9)
                               12

-------
This is to say that soil erosion elsewhere in the Chesapeake Bay area




completely overshadows anything from the better managed agricultural




area along the Chester River.




     A fairly recent agricultural program is variously designated as




"mulch tillage", "minimum tillage" and even "no till".  Coupled with




land terracing, sodded drainageways, controlled irrigation and other




conservation practices soil erosion is minimized and fertilizer and




pesticide loss contained.  While it keeps chemicals where they are being




used, this minimum tillage practice will actually require more chemicals




to replace weed control formerly handled by cultivation.  In addition,




retaining crop residues to mulch the soil surface means a greater hazard




of carrying over from one season to the next insects and disease.  It




follows that more fungicides and insecticides will be needed than in the




instance when stubble and plant debris was destroyed by burning or




removal.




     A problem that creates much public controversy is that in using




broad spectrum chemicals beneficial insects are often killed along with




the target pest species.  Conservationists are pressing for research




and development of chemicals that are specific for a given problem -




a given insect of family of insects.  On the surface this may seem a




very desirable course for us to take.  However, the minimum cost of




developing such specific control item is at least $5 million and the...




research requires from 5-7 years.  The problem to be solved will have




to be large to cover this investment.  This approach will require more




labor and time on the part of the farmer for he must now make a number




of separate applications.  The larger number of differing compounds and




their interactions may be just as great a problem.
                              13

-------
    In conclusion, it must now be obvious that we cannot expect




solutions to chemical problems that preclude every undesirable effect.




The risk/benefit evaluations we make must be the product of thoughtful,




professional judgement.  In the United States we have created the frame-




work that should require just such careful judgements.  Environmental




Impact Statements must be prepared for interdisciplinary review before




starting new projects and programs on Federal Lands, or programs re-




ceiving Federal cost sharing, or government licensing.  The task of




researching and preparing an environmental impact statement is time




consuming and often quite costly.  For example, the environmental impact




statement prepared for the U.S. Atomic Energy Commission before the




underground "Cannikin" test on Amchitka cost $5 million.  Nevertheless,




most decisions to deny a program are based on the inadequacy (incomplete-




ness) of the environmental study.  It is frustratingly difficult to




consider every change that might take place in the physical and living




environment under all of the alternative solutions to the problem.




Time consuming as the preparation of environmental impact statements




is, the time each involved agency must take to review and comment on




the thousands of EIS has literally "snowed under" Federal Agencies.




Unfortunately, the thrust of the program thus far has been as a tool




to delay or prevent new projects rather than as a vehicle to encourage




the best planning.




    For the most part, the options we have today are how to best use




our chemical technology, riot whether to place it in "mothballs".
                              14

-------
                           References






1.  Loftas, T,  Where have all the anchoveta gone?  New Scientist:




    583-586, September 26, 1972.




2.  Manheim, F. T., R. H. Meade and G. C. Bond.  Suspended matter in




    surface waters of the Atlantic Continental Margin from Cape Cod




    to the Florida Keys.  Science:  167(3917):371-376, January 23, 1970.




3.  Anonymous.  Oil and troubled waters.  Re:  Search, New Jersey Agri-




    cultural Experiment Station:  6(2):2-3, Spring 1973.




4.  The Federal Water Pollution Control Act of 1972; Public Law 92-500:




    Section 502(19).




5.  Rhoad, D. L.  Milk in my mouth.  (High lysine sorghum).  War on




    Hunger, U.S. Agency for International Development, Washington, D.C.




    8(3):6-10, March 1974.




6.  Becker, C. D. and T. 0. Thatcher.  Toxicity of power plant chemicals




    to aquatic life.  U.S. Atomic Energy Commission:  200 p., June 1973.




7.  ACS Committee on Chemistry and Public Affairs.  Chemistry in the




    economy.  Amer. Chemical Society, Washington, B.C., Book, 600 p.,




    1973.




8.  Scalf, M. R., et al.  Fate of DDT and Nitrate in ground water.




    USDI, Fed. Water Control Admin., Ada, Oklahoma and USDA, S.W.




    Great Plains Research Center, Bushland, Texas: 46 p., 1968.




9.  Clarke, W. D. and L. C. Murdock.  Chester River Study, Vol. 1




    Westinghouse Electric Corp. and Maryland Dept.. Natural Resources,




    38 p., 1972.
                              15

-------
16

-------
          PESTICIDE USAGE IN PENNSYLVANIA AGRICULTURE




         William Wills, Gary E. Jones and William Apgar




       Pennsylvania Department of Environmental Resources






    Present information on agricultural pesticide usage in Pennsylvania




currently comes from three sources:  1) Quantities of Pesticides Used




by Farmers in 1966 and 1968, U.S.D.A., E.R.S., 2) 1969 Agricultural




Census, U.S.D.A., and 3) Adams County Profile Study.  The first two




are severely limited from a statistical standpoint and are inadequate




to reflect agricultural pesticide usage on a statewide basis, whereas




the third was a county study.  It, therefore, became necessary to design




a statistically valid survey of the agricultural community in Penn-




sylvania to determine the following scope of information:




    1.  To obtain necessary information regarding the use of pesticides




    by Pennsylvania's agricultural producers so that appropriate goals,




    objectives and methods can be developed in the Statewide comprehensive




    environmental plan for the protection and conservation of the environ-




    ment and the health of agricultural workers.




    2.  To adequately determine the types and quantities of pesticides




    currently being used by the State's farming population.




    3.  To determine the nature and extent of occupational exposure to




    pesticides in Pennsylvania agriculture.




    4.  To more adequately determine the extent and nature of pesticide




    waste disposal problems as it relates to Pennsylvania agriculture




    and solid waste management.




    5.  To learn the sources of information relating to pesticide usage




    presently utilized by. the State's farmers.
                             17

-------
                    Pennsylvania Agriculture




    Although Pennsylvania is considered to be primarily an industrial




state, the total value of the agricultural industry in the State in-




cluding capital assets is currently about five billion dollars.  Penn-




sylvania ranks 33rd in total area and 36th in farm acreage; it is,




however, 19th among all states in cash receipts from farm products.




    The State's farmland is ideal for producing a. great variety of




crops.  The elevation ranges from practically sea level to 3,000 feet




and the crop-growing season from 80 to 207 days.  This range makes




possible the general cultivation of fruits, vegetables and grain.




Climate and rainfall generally are favorable to grassland farming.




    With the possible exception of the fruit and mushroom industries,




the agricultural community is characterized by highly diversified farms




averaging 145 acres each.  A total of 10,450,000 acres are currently




devoted to agriculture in the State, of which approximately 4,545,000




acres are employed in the production of forage and field crops.




                          Methodology




    The total number of farms to be surveyed was determined on the basis




of the number required to attain a 95% confidence interval when based




on a 50% probability of obtaining either a yes or no answer to the




questions on the survey.  It was determined that the survey should




encompass approximately 800 of the State's 73,000 farms.




    The actual determination of the specific farms to be contacted was




based on a three-stage cluster-type design.  This was done in order to




minimize expenses and manpower requirements.




    In accordance with this method, 10% of the State's 67 counties (seven




actually chosen) were selected by a process of randomized allocation




(Figure 1).  This process essentially entailed a randomized listing of






                              18

-------
                                  Figure 1




                        COMMONWEALTH OF PENNSYLVANIA




Counties Surveyed in the 1973 Statewide Agricultural Pesticide Usage  Survey

-------
the counties by region followed by a determination of the counties to




be surveyed.  This was done by dividing the number of farms in the State




(73,000) by the seven counties to be surveyed.  By adding the resulting




10,430 to a randomly selected number (6,472)j the first county (Berks)




was selected.  The next county was then determined by totalling the




number of farms until the next increment had been reached (16,902 +




10,430 = 27,332).  The remaining five counties were selected in a




similar manner.  The seven counties thus chosen to be surveyed were




Berks, Tioga, Lancaster, Snyder, Cambria, Washington and Lawrence.




    Each chosen county was then divided into blocks utilizing navigational




meridians.  After numbering the blocks in a serpentine fashion, one-




third were selected.  All of the farms in each of the selected blocks




were then numbered and the specific farms to be contacted were determined




by randomly distributing the 800 units among the 67 blocks chosen, taking




into consideration the relative number of farms in each county.




    Each of the selected units were subsequent contacted by one of three




enumberators and a questionnaire completed.  All data was entered onto




punch cards.  The survey began on July 6, 1973 and was completed on




September 14, 1973.




                     Results and Discussion




    Of the 800 original farms picked to be surveyed, 774 were actually




contacted.  This represents approximately 1.09% of the estimated 73,000




farms in Pennsylvania.  The total acreage of the farms surveyed, based




on land that was either owned, rented or leased was 96,153 acres.  This




acreage represents approximately .92% of the total estimated acreage,




being farmed in Pennsylvania.
                                20

-------
     The average acreage per farm surveyed was 125 acres.   Farms ranged




in size from 10 acres to.1,034 acres.  Farms were grouped as small (-99),




medium (100-199) and large farms (1200).  Small and medium sized farms




made up 87.7% of the farms surveyed.  Ninety-three percent of the farms




surveyed were family owned.  Commercially owned farms and farm rentals




each made up approximately 2.5% of farm ownership.




     Eighty-two percent of the farms contacted indicated that they used




pesticides as part of their operation for 1973, while 18% of the farms




did not use any pesticides in their farming operations.




     As the size of the farms increased, the percentage of farms using




pesticides also increased.  Seventy-five percent of the small acreage




farms used pesticides, while 84% of the medium acreage farms and 92% of




the large acreage farms used pesticides in their farming operations.




                            Pesticides




     Herbicides are the major group of pesticides used on crops in




Pennsylvania.  Approximately 95% of the total crop acreage treated with




pesticides was treated with herbicides (Table 1).  Insecticides were the




other major group of pesticides used on crops.  All other pesticides com-




bined were applied to less than 5% of the total acreage treated.




     Farm usage of pesticides during 1973 as compared with the previous




five years is shown in Table 2.  A majority of the farms did not have an




increase in the quantities of pesticides used during that period.




     Crops.  Corn was the major crop treated with pesticides in Pennsylvania




(Table 3).  All other crops combined make up less than 20% of the total




acreage treated with pesticides.




     Livestock.  Approximately 30% of the users applied pesticides (the




vast majority of which were insecticides) to livestock and/or livestock




shelters.




                               21

-------
Table 1.  Types of Pesticides Used on Crops

                    % of Total Acreage Treated       % of Users

Herbicides                     94.8                    94.3

Insecticides                   27.2                    26.5

Plant Regulators                1.3                     7.1

Fungicides                      2.0                     2.4

Other                          <1                      <1
Table 2.  Comparison of Quantities of Pesticides Used During 1973 with
          Previous Five Years

                                    % of Users

1.  Same                               70

2.  More                               20

3.  Less                                6

4.  Unknown                             4
                                 22

-------
     Suppliers.  Feed and seed stores were the major suppliers of pesticides




to farmers (Table 4).




     Application.  Sixty percent of the farmers who used pesticides did




all of the application of the pesticides themselves.  Twenty-four percent




of the users had custom application only, while 16% of the users applied




some of the pesticides themselves and had some custom application.  There-




fore, approximately 76% of the users applied some or all of their pesticides,




     Label specifications.  Of the farmers who apply their own pesticides,




40% stated they "always" follow label specifications, 52% stated they




"sometimes" follow label specifications, and none of the farmers replied




with "never" (the other 8% gave no answer).  Many of the farmers who




answered with "sometimes" explained that they used lower rates than the




label recommended.




     Storage.  Forty-five percent of the users stated that they stored




pesticides on their farms.  ,Most of the farmers stored their pesticides




in the barn (60% of farmers who store).  Utility rooms ranked second as




a storage area (24%), while garages (6%) and shops (4%) were some of the




less common areas in which pesticides were stored.  Only 7% of all the




storage areas were kept locked.




     Source of the most information.  Farm magazines and journals were




the most common source of information on pesticides listed by the users




(Table 5) and thus would be a very useful tool in disseminating information




to the farmers.




     Training.  Of the farms that applied some or all of their pesticides,




only 19% had one or more personnel handling pesticides that had attended




a training course on the safe use and selection of pesticide material.
                                 23

-------
Table 3.  Crops Treated with Pesticides
Crop % of Total Acreage Treated
Corn 86.9
Small grains 4.3
Alfalfa 2.3
Tobacco 2.0
Soybeans 1.9
Potatoes 1.5
Fruit ~ 1 . 0
Vegetables <1.0
Hay . <1.0
Other <1.0
Table 4. Suppliers of Pesticides to Farmers
% of Users
Feed and seed store 80.9
Chemical company store 5.8
Custom 4.6
Salesman 3.3
Variety store 1.6
Other 5.3
% of Users
92.3
8.7
4.3
10.1
3.5
1.4
1.4
                                . 24

-------
     Precautions.  The following precautions were taken by farmers when



applying their own pesticides:  wash after use (87%), no eating or smoking
                                                     o


when applying (39%), gloves (13%), respirator (6%),  protective clothing



(4%), protective glasses (2%).



     Pesticide wastes.  Fifty-six percent of the farms using pesticides



stated that they generated pesticide wastes.  Forty-five percent of these



farms indicated they would take wastes to a centralized county disposal



site if such a site were set up by the State.



     The following types of wastes were disposed of  by farmers:  small



cans (<5 gal.) (40% of farmers disposing), bags and  other flammable con-



tainers (37%), metal drums (2%).  None of the farmers stated they disposed



of surplus pesticides.



     Table 6 lists the method of disposal of pesticide containers.  The



majority of farmers disposed of pesticide containers on their farms.



     Highly toxic pesticides.   Fifteen percent of the farms using pesticides



used highly toxic or hazardous pesticides.  The most commonly used highly



toxic pesticides were aldrin,  carbofuran, phorate, dyfonate, paraquat and



parathion.  Sixty-one percent of these farms applied the pesticides them-



selves, while 39% hired a custom applicator.



     Forty-five percent of the farms using highly toxic pesticides stored



them on their farms.  None of these farms had their  storage areas locked.



The most common storage areas were the barn (60% of  users that store),



utility room (22%), shop (11%), garage (4%) and outside (4%).



     Highly persistent pesticides.  Ten percent of the farms using pest-



icides applied persistent pesticides to their crops.  The most common



persistent pesticides used were aldrin (54% of farms using persistent



pesticides), chlordane (23%),  lindane (16%) and lead arsenate (5%).





                                  25

-------
Table 5.  Sources of the Most Information on the Safe and Proper Use
          of Pesticides by Farmers Who Apply Pesticides
1.  Farm magazine and journal

2.  Pesticide dealer

3.  State extension service

4.  State Department of Agriculture

5.  Manufacturer and/or agent

6.  Friends and neighbors

7.  University experimental station

8.  Other
of Farmers Applying Pesticides

            71.0

            45.6

            32.4

            15.8

             5.0

             3.5

             1.7
Table 6.  Disposal of Pesticide Containers

                                     % of Farms Disposing
Container
Large drums
Small metal cans
(5 gal.)
Bags and other
flammable containers
Burn
0
0

53.8
Dump
on Farm
1.8
56.1

7.1
Dump off Keep for
of Farm other uses

-------
                             Summary




     Eighty-two percent of some 70,000 farms in Pennsylvania use pesticides




as part of their farming operation.   Based on acreage treated,  herbicides




were the major group of pesticides used in Pennsylvania while corn was the




major crop treated.




     The major suppliers of pesticides to farmers were feed and seed stores.




Farm magazines and journals were the most common source of information on




pesticides.  Only 19% of the farms using pesticides had one or more per-




sonnel handling pesticides that had attended a training course on the safe




use and selection of pesticide material.




     The major type of pesticide wastes disposed of by farmers were small




metal cans and bags and other flammable containers.  The most common place




of disposal of pesticide containers was on the farm.




     Of the farms using pesticides, 15% used highly toxic or hazardous




pesticides, and 10% used highly persistent pesticides on their crops.
                                 27

-------
28

-------
                PESTICIDE PRODUCTS SOLD IN RETAIL




               FOOD ESTABLISHMENTS IN KENTUCKY,  1972




                           Edsel Moore




                   Kentucky Department of Health






                           Introduction




     It has been estimated that 15% of all pesticides manufactured in




the United States for domestic use is destined for the urban-suburban user (1).




It is, therefore, not unreasonable, to expect that at least 25% of the total




dollar volume of pesticide sales in the United States are destined for




the home, lawn, and garden market.  These small package pesticide chemicals,




generally in low concentration, may be purchased at innumerable retail




establishments.  It is known that retail food establishments (grocery




stores) handle, store, display, and sell approximately 100 different




pesticide chemicals for the above market (2).




     A survey of 217 retail food establishments was conducted in Kentucky




during 1972 to determine the manner in which pesticides were received,




stored, handled, and displayed in relation to food items in permeable




containers and to determine if these practices constituted a potential




public health hazard.  Additionally, the study was conducted to determine




the extent to which concentrated toxic pesticides were handled and sold




at rural retail food establishments serving the farm community.  Further,




the study was designed to initiate surveillance for the presence of any




misbranded or non-federally registered products and to determine vector




control practices in retail food establishment operations.




     The results obtained from the survey were separated both by store size




and by rural-urban location in order to identify more specifically the
                                      v



problem areas, when they exist.




                                 29

-------
                            Procedure




     The sample selection of grocery stores from the population of grocery




stores throughout the state of Kentucky, after considering several alternatives,




was accomplished in September by a systematic selection procedure from an




up-to-date list of all known operating grocery stores.  The sample consisted




of 217 retail food establishments located in 80 of Kentucky's 120 counties,




as can be seen in Figure 1.  The acutal survey was then undertaken in late




October and early November following forms testing and strategy sessions.




     In the present study a grocery store is defined as one generally




handling a complete line of food items and household goods.  An urban store




is defined as one located in an area of greater than 2500 in population.




A possible weakness of the present sample selection exists where prestrat-




ification of the grocery store population by size and rural-urban location




was not accomplished.  Lack of information as to store size and exact




location within the designated county prevented this procedure.  While




it whould be noted that systematic selection of grocery stores, after




first dividing the stores by county, can be expected to give a rather




accurate distribution of the selected sample by store size and rural-




ruban location, it should also be noted that relatively small numbers




within some of the store size and rural-urban categories give less reliabil-




ity to statistical results.




     Divisions of retail establishments by store size (based on number of




employees) and by rural-urban location were considered to be the most




appropriate approach to grocery store comparisons.  There were originally




four store sizes; 1-7 employees, 8-19 employees, 20-49 employees, and 50-




99 employees.  For the total and urban area, store sizes 3 and 4 (20-49




employees and 50-99 employees) were combined due to the small number of
                                  30

-------
Figure 1.  Location (Lined Counties) of retail food establishments




             among 80 of 120 counties,  Kentucky, 1972

-------
stores of size 4.  For the rural area, store sizes 2 and 3 (8-19 employees




and 20-49 employees) were combined due to the small number of stores of




size 3.  There were no stores of size 4 in the rural area.




     A chi-square procedure is used to make the various comparisons for




each of 25 questions (See Questionnaire Items) concerning pesticides




within grocery stores.  In the present case it is used to test whether an




observed series of frequencies (See Tables 1,2, and 3) differ between




themselves to a greater degree than might be expected to occur by chance,




as denoted by the P-values in Tables 4 and 5.  Comparisons by store size




for all stores combined, for both rural, and urban stores are first con-




sidered (Table 4) followed by rural-urban comparisons at each of two




store-size categories (Table 5).   Occasionally, where numbers within




a row category were below a minimum, categories were combined before




computing the chi-square value; e.g., question 1 elicited no responses




to answer 1 and only two responses to answer 5 (See Table 3 as well as




Questionnaire Items) so that the computer program combined answers 1




and 2 as well as answers 4 and 5 before computing a chi-square value.




In most cases this combining of row categories had little effect on the




chi-square results as well as on the interpretation of the results.






                            Discussion




     Results of the first question, "How Pesticides are Shipped" is




shown in Table 1.  Approximately 53% of the grocery stores received




pesticides with nonperishable goods.  This compared to 34% of stores




that received pesticide products along with both nonperishable and




perishable goods. .The overall percentages appear to be very similar




for both the rural (Table 2) and urban (Table 3) locations.  However,




Table 4 shows different results for rural and urban locations when comparing






                                 32

-------
store size within each area.  For the rural area, p = .95 indicates




there is no difference in shipping practices with regard to store size.




Note that the percentage distributions in Table 2 are very similar.  In




contrast, for the urban area p = .05, suggests a somewhat different




practice in the shipment of pesticides to various size stores.   For the




total, or combined rural and urban, p =* .1 suggests only slight  differences




in shipping practices.  By comparing rural versus urban for each of two




store sizes (1-7 employees and 8-19 employees), we find that no significant




differences occur for either small or medium size stores (See Table 5




where p = .2 and p = .98 respectively).




     The chi-square results from Table 4, as well as the table of percentage




distributions, seem to suggest a tendency to ship pesticides more often




with nonperishables to larger stores in urban areas (note the direct




relationship in Table 3 between percentages for answer 2 and store size)




and separately to small urban stores (note the percentage decrease from




small to medium size stores for answer 4).  This practice may be due to




the fact that smaller stores are more often serviced by wholesale supply




companies or pesticide company representatives while larger chain stores




often have their own trucks and distribution centers.  Nevertheless, it




is important to ntoe from Table 1 the relatively high percentages for the




various stores which receive pesticides with perishable and nonperishable




goods (38%, 33%, and 29%).




     The percentage distributions in Table 1 for the second question




concerning "Disposal Procedure for Spillage or Breakage at the Receiving




Area" show that 60% of all stores returned damaged pesticide products




while 28% placed the damage products in the same storage receptacles




as garbage.  Similar percentages can be observed for the rural and urban




area stores (Tables 2 and 3 respectively).  Table 2 suggests that for





                                 33

-------
the rural area stores there is a slight tendency to "return" more and




"put in garbage" less with increase in store's size.  However,  the reverse




exists with stronger significance for the total and urban categories




(p = .05 and .01 respectively in Table 4) suggesting that as store size




increases the tendency is to "put in garbage" any breakage or spillage.




     By testing rural versus urban at each of two store sizes for this




second question, we find that no difference exists for store size 1 while




rather high significance exists for store size 2 (Table 5).  Within store




size 2 we can see from Tables 2 and 3 that rural areas tend more often




to "return" breakage (89% versus 45% for urban area stores) and less




often to place open containers into garbage containers (11% versus 43%




for urban area stores).




     Question 3 relates to the storage distance (in feet) from food items




in permeable packages in the stockroom.  Table 1 shows the largest percentage




for answer four (over 15 feet) with a relatively large percentage of stores




showing no stockroom (27%).  A surprisingly greater percentage of urban




area stores show no stockroom (29% versus 19% for the rural area).  Table




4 shows significance for the combined total and for the urban area while




it shows nonsignificance for the rural area.  Two things appear to be the




cause for significance:  (1) in general, as store size increased the distance




away from food items in permeable packages increased, and (2) the percentage




of "no stockroom" decreased with increased store size (See Tables 1, 2,




and 3 and the Questionnaire Items).  Although more space may be available




for storage in larger stores, the increasing distance from food items may




also be due to an increase in concern for possible contamination within  .




these stores.
                                 34

-------
     Rural versus urban location at each of two store sizes (Table 5)




shows no significance indicating that storage practices away from food




items are generally the same within a given store size for both rural  and




urban locations.




     For question 4 relating to designated or undesignated area in the




stockroom for pesticide storage, Table 1 shows that the storage of pest-




icides in the stockroom was ordinarily accomplished in 133 establishments




(62%) by separation of these items in a designated area away from food in




permeable containers while 58 establishments (27%) did not have a stockroom.




The potential contamination of food items in permeable containers in the




stockroom was therefore considered minimal, involving only 23 establishments




(11%).  Table 4 shows significance for the total and urban area stores,




and this significance appears to be mostly due to the large percentage




of "not applicable" for store size 1 in the urban area; i.e., the largest




percentage with no stockroom.




     Results from Tables 1, 2, and 3 for question 5 are difficult to




interpret since most (60%) stores responded to answer 5, "two or more of




above".  However, based on the percentages for the first four answers,




we can expect that most of the 129 stores responding to answer 5 have




prescribed decontamination procedure.  Significance for question 5 is




similar to that for the previous question (significance for the total




and the urban area and nonsignificance elsewhere) and again, mainly due




to the relatively high percentage of "not applicable" for store size 1.




However, percentage distribution for the first answer  (prescribed de-




contamination procedure) also affects significance where we find 0%,




16%, and 8% respectively for store sizes 1, 2, and 3 under total.  Pre-




scribed decontamination procedures are not expected in small stores since
                                 35

-------
these facilities generally do not have a stockroom and do not accept




broken or damaged pesticide products.




     Results from Table 1 for questions 6,  7,  and 8 show that relatively




few grocery stores used DDVP strips and automatic time-metered insecticide




devices in either the stockroom, the meat preparation area,  or the vegetable




preparation area.  In addition, questions 6,  7,  and 8 give little or  no




significance between store size or between rural-urban location as can be




seen from Tables 4 and 5.  However, it  should be  noted that the survey




team found a total of 73 instances where the above control measures were




in use in various areas throughout the stores, 50 of which were found to




be in violation of label restrictions.




     Results from Tables 1, 2 and 3 for question 9 show that most stores,




regardless of location, have a pest control contract.  Table 4 shows  the




percentage distribution in Table 3 that store size 1 appears to be signif-




icantly different from the other store sizes,  suggesting a greater like-




lihood of having a pest control contract as store size increases.  Perhaps




this situation is due to greater vector control  consciousness on the  part




of larger stores in primarily urban areas.   The  survey team further found




that 29 of the 190 stores under pest control contract, applied additional




insecticides and/or rodenticides.




     Questions 10 through 14 are also  concerned  with pesticide use within




the store.  For question 10, we see from Tables  3 and 4 that in urban areas,




insecticide and rodenticide use is significantly more prevalent in larger




stores while "other" means are more prevalent in smaller stores.  No




significant difference exists between  rural-urban comparisons for a




particular store size.  Question 11, concerning  any application by employee,
                                 36

-------
also shows no significance for any comparison.   However,  when employee




application is the case, question 12 of the survey results revealed in-




secticide use increases with increase in store size,  as was noted from




question 10, the combination of insecticide-rodenticide use is solely




that of the small urban store.  Questions 13 and 14 show  little difference




in results where it appears that there is no specific area treated or




left untreated and we find mostly monthly treatment among all stores.




     Results from questions 15 through 18 show no surprises for the total




and the urban area where we can see from Tables 1, 2, 3,  and 4 that store




size and percentage annual sales are directly related.  Even for the rural




area, which gives only a probability value of .1 in Table 4 for questions




15 through 17, we can note from the percentage distributions that a direct




relationship also exists.  By considering rural versus urban at each of




two different store sizes, we can see from Table 5 that there are different




rural-urban percentage distributions for small stores at  questions 15, 16,




and 18 (small rural stores appear to handle greater volumes of pesticide




products in cans and cartons than do small urban stores)  but only signif-




icance at question 18 for large store distributions where cartons appear




to be more popular among rural stores.  The survey team found that most




small urban and rural stores maintained a low inventory of pesticide




selections, particularly those pesticides in glass bottles.  This practice




was followed for several reasons such as limited space, high risk of




breakage, less demand, etc.  It should also be noted that the survey




team found a surprising 43,086 containers on display considering the survey




was conducted during the non-peak season.  The products recorded represented




86 different manufacturers.  Some 399 different containers were observed,




many with same ingredient(s) but a size or brand variance.  Four broad




categories of pesticides were found as follows:  herbicides, fungicides,







                                 37

-------
rodenticides, and insecticides that included chlorinated hydrocarbons,




organophosphates, cargamates, botanicals, and other miscellaneous insecticides.




     Results from question 19 concerning where pesticides are displayed




show that most stores display the products in the area of miscellaneous




goods or household goods.  No significance occurs for either Table 4 or




Table 5; however, for the urban area slight differences in display practices




appear between store size 3 and smaller stores where there is a tendency




of large stores to display pesticides nearer to the area of household




goods.




     The percentage distributions for question 20 in Tables 2 and 3 are




almost identical indicating no overall difference between rural and urban




stores with regards to accessibility of pesticides to children.  Table




5 also indicates no rural-urban differences at either store size 1 or store




size 2.  However, results from Table 4 indicate,  especially for the urban




area, that pesticides become more accessible to small children as store




size increases.  While significance is not as great for the rural area,




the trend is still evident.  The survey team found in larger establishments




that pesticides displayed on racks and shelves extending to floor level




constitutes a larger volume of containers accessible to preschool age




children.  As can be noted from Table 1 for large stores, pesticides were




displayed within easy reach of preschool age children (three feet or less




from floor) in 52 (84%) of the establishments.




     The percentage distributions for question 21 in Tables 2 and 3 are




again very similar indicating little overall difference between rural and




urban stores with regards to pesticide display in relation to food items.




Only slight significance occurs in the total category of Table 4 concerning




store size comparisons.  The reason for any significance here would be
                                 38

-------
due mostly to answer number 8 of Table 1 (completely separated)  which




shows a percentage increase with increasing store size.   An important




point to note for the present question is that the display of pesticides




directly above, below, or beside (or a combination of these) food items




in permeable containers (answers 1 through 7) was found in 81 (38%) of




the retail establishments.




     The percentage distributions in Table 1 for question 22 show that most




stores displayed pesticides away from fruits, vegetables, meats, and




bakery items.  However, vegetables and bakery items were displayed nearest




to pesticides in 12% and 14% of the stores, respectively.  No significance




appears in Tables 4 and 5 indicating that there is no consistency as to




where pesticides are displayed with regards to food items in permeable




containers.  Results from Table 4 relating to question 23, however, do




indicate that the distance from food items in permeable containers increases




with increasing store size.  The total percentages in Table 1 show that




99 (46%) of the stores displayed food items in permeable containers within




0-5 feet of pesticides.




     Results from Table 1 for question 24 show that a relatively large




percentage (63%) of stores had all three types of containers (carton,




bottle, and can) on display and that there was little difference between




rural and urban stores, as noted in Table 5.  However, significance in




Table 4 for total and urban indicates a situation where combinations of




types as opposed to single types become more prevalent as store size in-




creases.




     The final question related to bagging of pesticides at checkout and




results of the comparisons show little or no significance.  However, it




is interesting to note from the percentage distributions in Tables 1, 2,




and 3 that middle size stores with 8-19 employees (in Table 2 only five




                                  39

-------
stores had more than 19 employees) appear to perform slightly better with




regards to placing pesticides in a separate bag at checkout.  Three possible




reasons for better performance among middle size stores are as follows:




(1) small stores of 1-7 employees cannot afford extra bags and possibly




have less knowledge of potential dangers; (2) large stores of 20-99 em-




ployees often use high school age kids for bagging who are unfamiliar




with potential hazards, and due to the volume of traffic and other




distractions even the more experienced employees sometimes violate bagging




instructions; and (3) medium size stores often have managers and owners




(or owner's wives) for bagging and can afford extra bags.  It should




also be noted from Table 1 that 28% of all stores indicated the practice




of placing pesticides in the same bag with groceries.




     Although the present survey included a question relating to types




(brand name) and volume of pesticides on display, the results are not




included.  However, it should be noted that several rural establishments




offered for sale sodium flouride, strychnine treated grains, 74% technical




chlordane, concentrated paraquat, and other highly toxic pesticides that




were not observed in urban areas.  Also, it was found that five different




insecticide brands observed in three establishments were not properly




labeled or federally registered.






                           Conclusions




     Pesticide products can be found in most retail food establishments




whether large or small, rural or urban.  In the present survey only three




establishments did not handle pesticides for sale.  These products are




received in cans (aerosol), bottles (plastic and glass), paper cartons,




and other types generally by way of trucks carrying both nonperishable and
                                 40

-------
perishable goods.  These products may be stored,  before being shelved,




in a designated or an undesignated area in the stockroom or within the




main part of the store depending upon the circumstances.  It was found




that 34% of all stores receive pesticides with both nonperishables and




perishables and that 38% of all stores either stored pesticide products




in any available area in the stockroom or directly inside the stores.




Any undiscovered breakage or spillage would be potentially hazardous both




during delivery as well as during temporary storage.  While the majority




of stores (37%) stored pesticides over 15 feet away from permeable food




items in the stockroom, 63% of all stores either  had no stockroom or .stored




them less than 15 feet away from permeable food items within the stockroom.




Again, we have a potentially hazardous situation  from any undiscovered




leakage or breakage.




     Table 4 shows significant p-values under urban for each of the first




five questions relating to the stockroom area. A close look at the small




urban area store (1-7 employees) reveals the following:  (1) it more




often receives pesticides in shipments containing perishable foods; (2)




it more often "returns" pesticide breakage or spillage as opposed to




"putting in garbage" (possibly a greater potential hazard since the broken




product is not immediately discarded); (3) it stores pesticides in the




stockroom in closer contact with food items in permeable bags or cartons;




(4) it more often has no stockroom for:storage (hence, temporary storage




in main part of store); and (5) it is probably less likely to have any




prescribed decontamination procedure because of the tendency to "return"




breakage.




     While the display of pesticide products was  found to be generally




located within the area of miscellaneous or household goods, a surprisingly
                                 41

-------
 large overall percentage  (46%) of all stores displayed these products




 within  0-5 feet of food items in permeable containers.  As can be expected,




 however, distance away from food items in permeable containers is directly




 related to store size.  Another somewhat surprising finding was that the




 accessibility of pesticides to small children increases with increasing




 store size, mainly due to the display of pesticide products in larger




 stores  on racks and shelves extending to floor level.




     Vector control practices (pest control contract plus additional control




 measures) were found to be rather common where 190 (89%) of all stores




 were under contract with additional insecticides and/or rodenticides being




 applied by 29 of these stores.  The survey team also found some 73 instances




 where DDVP strips and/or automatic time-metered insecticide devices were




 used in various parts of the store, 50 of which were in violation of label




 restrictions.




     The sale of concentrated toxic pesticides by rural retail food establish-




 ments is considered to be relatively high since several stores were observed




 as having such items as sodium flouride, strychnine treated grains, 74%




 technical chlordane, concentrated paraquat, and other highly toxic pest-




 icides.  The potential health hazards could be significant among these rural




 establishments where special precautions are not ordinarily taken.




     Improper labeling of pesticide products appears to be of little




 significance.  The survey team found only five different insecticides with




 improper labels among three retail food establishments.




     Finally, it should be important to point out that from Tables 4 and 5




most significant chi-square differences occur under urban and total where




 store-size comparisons are made.   These results along with the results of




 Table 3 suggest the need for a further look at the small retail food establishment.
                                 42

-------
                            References






1.  Patterns of pesticide use and reduction in use as related to social




    and economic factors, Pesticide Study Series - 10, Office of Water




    Programs, Environmental Protection Agency, Washington, D. C., Pages




    9-10.




2.  Proceedings of National Working Conference on Pesticide Disposal,




    National Agricultural Library, Beltsville, Maryland, June 30 and




    July 1, 1970, page:4.
                                43

-------
                       QUESTIONNAIRE ITEMS
1.  flow Pesticides are Shipped

    1.  With perishable goods
    2.  With nonperishable goods
    3.  Both 1 and 2
    4.  Separately
    5.  Other

2.  Disposal Procedure for Spillage or Breakage at the Receiving Area
    1.  Returned
    2.  Repackaged for sale
    3.  Put in garbage
    4.  1 and 2
5.  1 and 3
6.  2 and 3
7.  1, 2, and 3
8.  Other (specify)
3.  Storage Distance from Food Items in Permeable Bags or Cartons in Stockroom

    1.  0-5 feet
    2.  6-10 feet
    3.  11-15 feet
    4.  Over 15 feet
    5.  No stockroom

4.  Storage in Stockroom

    1.  Designated area
    2.  Any available area
    3.  Not applicable

5.  Disposal and/or Cleanup Procedure for Spillage or Breakage in Stockroom

    1.  Prescribed decontamination procedure
    2.  Container put in garbage
    3.  Disposal of contaminated food
    4.  Other (specify)
    5.  Two or more of above
    6.  Not applicable
6.  Pesticides Used in Stockroom

    1.   DDVP strips
    2.   Automatic time-metered
        insect devices
    3.   Other (specify)
    4.   1 and 2
5.  1 and 3
6.  2 and 3
7.  1, 2, and 3
8.  None
9.  Not applicable
                               44

-------
 7.  Pesticides Used in Meat Preparation Area

     1.  DDVP strips                 5.  1 and 3
     2.  Automatic time-metered      6.  2 and 3
         insecticide devices         7.  1, 2, and 3
     3.  Other (specify)             8.  None
     4.  1 and 2

 8.  Pesticides Used in Vegetable Preparation Area

     1.  DDVP strips                 5.  1 and 3
     2.  Automatic time-metered      6.  2 and 3
         insecticide devices         7.  1, 2, and 3
     3.  Other (specify)             8.  None
     4.  1 and 2

 9.  Have Contract with Pest Control Operator?

     1.  Yes
     2.  No

10.  If Yes to Above, What is Used?

     1.  Insecticide
     2.  Rodenticide
     3.  Other (specify)
     4.  Both 1 and 2

11.  Application of Pesticide by Employee

     1.  Yes
     2.  No

12.  If Yes to Above, What is Used?

     1.  Insecticide
     2.  Rodenticide
     3.  Other (specify)
     4.  Not applicable
     5.  Both 1 and 2

13.  Areas, if Any, Treated by Pesticides

     1.  Stockroom                   5.  Display area
     2.  Meat preparation area       6.  Other (specify)
     3.  Vegetable preparation area  7.  More than one above
     4.  Sales area

14.  Frequency of Treatment, if Any

     1.  Weekly                      4.  Annually
     2.  Monthly                     5.  Other (specify)
     3.  Quarterly
                                45

-------
15.  Estimated Annual Gross Dollar Volume of Pesticide Sales

     1.  Less than $100              4. "$1500 or greater
     2.  $100 to $499                5.  None
     3.  $500 to $1499               6.  Other

16.  Number of Cans of Pesticides Sold Annually

     1.  Less than 50                4.  750 or greater
     2.  50 to 249                   5.  None
     3.  250 to 749                  6.  Other

17.  Number of Bottles of Pesticides Sold Annually

     1.  Less than 50                4.  750 or greater
     2.  50 to 249                   5.  None
     3.  250 to 749                  6.  Other

18.  Number of Cartons of Pesticides Sold Annually

     1.  Less than 50                4.  750 or greater
     2.  50 to 249                   5.  None
     3.  250 to 749                  6.  Other

19.  General Area Where Pesticides are Displayed

     1.  Vegetable                   6.  Miscellaneous goods
     2.  Dry goods                   7.  Household goods
     3.  Can goods                   8.  Two or more of above
     4.  Hardware                    9.  Other
     5.  Bakery goods

20.  Are Pesticides Accessible to Small Children?

     1.  Yes
     2.  No

21.  Display of Pesticides in Relation to Food Items

     1.  Above                       6.  2 and 3
     2.  Below                       7.  1, 2, and 3
     3.  Beside                      8.  Completely separated
     4.  1 and 2                     9.  Unknown
     5.  1 and 3

22.  Nearest Displayed Food Item in Permeable Container

     1.  Fruit                       4.  Bakery items
     2.  Vegetable.                   5.  Other (specify)
     3.  Meat
                                46

-------
23.  Distance of Nearest Displayed Food Item in Permeable Container

     1.  0-5 feet
     2.  6-10 feet
     3.  11-15 feet
     4.  Greater than 15 feet
     5.  Unknown

24.  Types of Pesticide Containers on Display

     1.  Paper carton                5.  1 and 3
     2.  Bottle                      6.  2 and 3
     3.  Can                         7.  1, 2, and 3
     4.  1 and 2                     8.  Other (specify)

25.  Bagging of Pesticides at Checkout

     1.  Placed in separate bag
     2.  Placed in same bag with other groceries
     3.  Both 1 and 2
     4.  Other.
                                47

-------
                                TABLE 1

          NUMBER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
      FOR ALL STORES COMBINED, BY SIZE OF STORE, KENTUCKY, 1972
f
QUESTIONNAIRE ITEMS

1. How shipped
1.
o
^ •
3.
4.
5.
2. Disposal
1.
2.
3.
4.
5.
6.
7.
8.
3. Storage
1.
2.
3.
4.
5.
4. Storage
1.
2.
3.
5. Disposal
1.
2.
3.
4.
5.
6.

*
TOTAL
TOTAL
NUMBER
*
214
0
114
73
25
2

128
0
60
0
20
1
1
4

14
33
29
80
58

133
23
58

14
11
2
5
129
53



%

100
0
53
34
12
1

60
0
28
0
10
0
0
2

7
15
14
37
27

62
11
27

7
5
1
2
60
25

1-7 EMPLOYEES.
NUMBER

97
0
43
37
15
2

68
0
17
0
9
0
0
3

9
13
9
29
37

49
8
40

0
4
o •
3
53
37


%

100
0
44
38
16
2

70
0
18
0
9
0
0
3

9
14
9
30
38

51
8
41

0
4
0
3
55
38



8-19 EMPLOYEES
NUMBER

55
0
34
18
3
0

31
0
19
0
4
0
0
1

4
6
10
24
11

38
8
9

9
3
0
1
33
9



%

100
0
62
33
5
0

56
0
35
0
7
0
0
2

7
11
18
44
20

69
15
16

16
6
0
2
60
16



20-99 EMPLOYEES
NUMBER

62
0
37
18
7
0

29
0
24
0
7
1
1
0

1
14
10
27
10

46
7
9

5
4
2
1
43
7



%

100
0
60
29
11
0

47
0
38
0
11
2
2
0

2
23
16
43
16

74
11
15

8
7
3
2
69
11



Three stores from the sample of 217 stores  did not  handle  pesticide  products
for sale.
                                      48

-------
                      TABLE 1 (COK'T)

    NUMBER AMD PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR ALL STORES COMBINED, BY SIZE OF STORE, KENTUCKY, 1972
QUESTIONNAIRE ITEMS
. 6. Pesticides
1.
2.
3.
4.
5.
6.
7.
8.
9.

7. Pesticides
1.
2.
3.
4.
5.
6.
7.
8.
8. Pesticides
1.
2.
3.
4.
5.
6.
7.
8.
9. Contract
1.
2.

TOTAL
TOTAL
NUMBER

13
18
1
1
0
0
0
168
13


16
7
0
0
0
0
0
191

14
5
0
0
0
0
0
195

190
24

%

6
9
0
0
0
0
0
79
6


8
3
0
0
0
0
0
89

7
2
0
0
0
0
0
91

89
11

1-7 EMPLOYEES
NUMBER

6
3
0
1
0
0
o.
80
7


9
0
0
0
0
0
0
88

6
1
0
0
0
0
0
90

77
20

%

6
3
0
1
0
0
0
83
7


9
0
0
0
0
0
0
91

6
1
0
0
0
d
0
93

79
21

8-19 EMPLOYEES
NUMBER.

6
7
0
0
0
0
0
39
3


5
4
0
0
0
0
0
46

5
1
0
0
0
0
0
49

52
3

o/

11
13
0
0
0
0
0
71
5


9
7
0
0
0
0
0
84

9
2
0
0
0
0
0
89

95
5

20-99 EMPLOYEES
NUMBER

1
8
1
0
0
0
0
49
3


2
3
0
0
0
0
0
57

3
3
0
0
0
0,
0
56

61
1

%

2
13
2
0
0
0
0
78
5


3
5
0
0
0
0
0
92

5
5
0
0
0
0
0
90

98
2

                                 49

-------
                      TABLE 1 (CON'1!)

    NUMBER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR ALL STORES COMBINED, BY SIZE OF STORE, KENTUCKY, 1972
QUESTIONNAIRE ITEMS
10. What Used
1.
2.
3.
4.
11. Application
1.
2.
12. What Used
1.
2.
3.
4.
5.
. 13. Areas Treated
1.
2.
3.
4.
5.
6.
7.
14. Frequency
1.
2.
3.
4.
5.
TOTAL
TOTAL
NUMBER

13
0
22
179

53
161

36
8
1
161
8

3
0
0
0
0
1
210

2
175
4
0
33
%

6
0
10
84

25
75

17
4
0
75
4

2
0
0
0
0
0
98

1
81
2
0
16
1-7 EMPLOYEES
NUMBER

3
0
18
76

23
74

10
5
1
73
8

2
0
0
0
0
1
94

2
'78
2
0
15
%

3
0
19
78

24
76

11
5
1
75
8

2
0
0
0
0
1
97

2
80
2
0
16
8-19 EMPLOYEES
NUMBER

1
0
3
51

12
43

12
0
0
43
0

1
0
0
0
0
0
54

0
47
1
0
7
%

2
0
5
93

22
78

22
0
0
78
0

2
0
0
0
0
0
98

0
85
.2
0
13
20-99 EMPLOYEES
NUMBER

9
0
1
52

18
44

14
3
0
45
0

0
0
0
0
0
0
62

0
50
1
0
11
%

14
0
2
84

29
71

23
5
0
72
0

0
0
0
0
0
0
100

0 .
80
2
0
18
                              50

-------
                      TABLE 1 (CCN'T)
    NUMBER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR ALL STORES COMBINED, BY SIZE OF STORE,  KENTUCKY,  1972
QUESTIONNAIRE ITEMS
15. Sales
1.
2.
3.
4.
5.
6.
16. Cans Sold
1.
2.
3.
4.
5.
6.
17. Bottles Sold
1.
2.
3.
4.
5.
6.
18. Cartons Sold
1.
2.
3.
4.
5.
6.

TOTAL
TOTAL
NUMBER

29
86
70
23
3
3

22
74
69
40
6
3

95
70
19
2
25
3

76
80
31
14
10
3

%

14
40
33
11
1
1

10
35
32
19
3
1

44
33
9
1
12
1

36
37
14
7
5
1

1-7 EMPLOYEES
NUMBER

28
53
13
0
3
0

22
48
18
3
6
0

55
19
1
0
22
0

55
27
5
0
10
0

%

29
55
13
0
3
0

23
49
19
3
6
0

56
20
1
0
23
0

57
28
5
0
10
0

8-19 EMPLOYEES
NUMBER

0
23
27
4
0
1

0
18
27
9
0
1

21
26
6
0
1
1

14
25
11
4
0
1

%

0
20-99 EMPLOYEES
NUMBER

1
42 10
49 30
7 j 19
0 ! 0
2

0
33
49
16
0
2

38
47
11
0
2
2

25
46
20
7
0
2

2

0
8
24
28
0
2

19
25
12
2
2
2

7
28
15
10
0
2

%

2
16
48
31
0
3

0
13
39
45
0
3

31
40
20
3
3
3

12
45
24
16
0
3

                               51

-------
                      TABLE 1 (CONrT)

    KUMBER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR ALL STORES COMBINED, BY SIZE OF 'STORE, KENTUCKY, 1972
i
1
1
!
QUESTIONNAIRE ITEMS

19. Area Displayed
1.
2.
3.
4.
5.
6.
7.
8.
9.
20. Accessible
1.
2.
21. Display
1.
2.
3.
4.
5.
6.
7.
8,
9.
22. Displayed
1.
2.
3.
4.
5.
TOTAL
TOTAL
NUMBER


7
1
4
5
7
47
70
70
3

152
62

16
10
32
4
8
4
7
131
2

2
25
20
30
137
%


3
0
2
3
3
22
33
33
1

71
29

7
5
15
2
4
2
3
61
1

1
12
9
14
64
1-7 EMPLOYEES
NUMBER


4
0
4
0
5
24
31
27
2

57
40

7
8
16
4
5
2
2
52
1

1
10
7
17
62
%


4
0
4
0
5
25
32
28
2

59
41

7
8
17
4
5
2
2
54
1

1
10
7
18
64
8-19 EMPLOYEES
NUMBER
%
|
!
2 4
1 2
0
4
1
13
11
22
1

43
12

5
1
10
0
3
2
0
34
0

1
10
6
8
30
0
7
2
23
20
40
2

78
22

9
2
18
0
5
4
0
62
0

2
18
11
15
54
20-99 EMPLOYEES
NUMBER


1
0
0
1
1
10
28
21
0

52
10

4
1
6
0
0
0
5
45
1

0
5
7
5
45
%


2
0
0
2
2
16
45
33
0

84
16

6
2
10
0
0
0
8
72
2

0
. 8
11
8
73
                            52

-------
    MUV2ER A*n) PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR ALL STORES COMBINED, BY SIZE OF STORE, KENTUCKY, 1972
QUESTIONNAIRE ITEMS

23. Distance
1.
2.
3.
4.
5.
24, Types
1.
2.
3.
4.
5.
6.
7.
8.
25. Bagging
1.
2.
3.
4.
TOTAL
TOTAL
NUMBER


99
51
18
42
4

2
3
8
1
46
9
135
10

129
60
21
4
%
;
1-7 EMPLOYEES
NUMBER
i

46
24
8

53
24
8
20 . 9
2 3

1
1
4
0
22
4
63
5

60
28
10.
2

1
3
7
1
19
7
53
6

54
32
8
3
%


55
25
8-19 EMPLOYEES
NUMBER


25
16
8 4
9
3

1
3
7
1
20
7
55
6

56
33
8
3
10
0

0
0
%


46
29
7
18
0

0
0
1 2
0
9
2
42
1

38
11
6
0
0
16
4
76
2

69
20
11
0
20-99 EMPLOYEES
NUMBER


21
11
6
23
1

1
0
0
0
18
0
40
3

37
17
7
1
%


34
17
10
37 |
2

2
0
0
0
29
0
64
5

60
27
11
2
                               53

-------
                      TABLE 2

  NUMBER A'lD PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR RURAL AREA STORES, BY SIZE OF STORE, KENTUCKY, 1972
1
t
QUESTIONNAIRE ITEMS
1. How Shipped
I 1'
: 2.
3.
4.
5.
2. Disposal
1.
2.
3.
4.
5.
6.
7.
8.
3. Storage
1.
2.
3.
4.
5.
- 4. Storage
1.
2.
; 3,
5 . Disposal
1.
2.
3.
RURAL
TOTAL
NUMBER
32
0
18
13
1
0

25
0
6
0
1
0
0
0

2
7
5
12
6

19
7
6

3
2
0
4. 0
5. 22
6. 5

/o
100
0
56
41
3
0

78
0
19
0
3
1-7 EMPLOYEES
NUMBER
14
0
8
6
0
0

9
0
4
0
1
0 \ 0
0
0

6.
22
16
37
19

59
22
19

9
6
0
0
69
16

i
0
0

2
3
1
4
4

7
2
5

0
1
0
0
9
4


%
100
0
57
8-49 EMPLOYEES
•: NUMBER
18
0
10
43 ! 7
0
0

64
0
29
0
7
0
0
0

14
21
7
29
29

50
14
36

0
7
0
0
64
29

1
0

16
0
2
0
0
0
0
0

0
4
4
8
2

12
5
1

3
1
0
0
13
1

%
100
0
55
39
6
0

89
0
11
0
0
0
0
0

0
22
22
45
11

66
28
6

16
6
0
0
72
6

i |
                           54

-------
                  TABLE 2 (CON'T)

  NUMBER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR RURAL AREA STORES, BY SIZE OF STORE, KENTUCKY, 1972
QUESTIONNAIRE ITEMS

6. Pesticides
1.
2.
3.
4.
C
mJ •
6.
7.
8.
9.
7 . Pesticides
1.
2 .
3.
4.
5.
6.
7.
8.
8. Pesticides
1..
2.
3.
4.
5.
6.
7.
8.
9. Contract
1.
2.
RURAL
TOTAL
NUMBER 1 %


6


19
3 !• 9
0
0
0
0
0
19
4

4
0
0
0
0
0
0
28

4
1
0
0
0
0
0
27

29
3
0
0
0
0
0
59
13

13
0
0
0
0
0
0
87

13
3
0
0
0
0
0
84

91
9
1-7 EMPLOYEES
NUMBER


2
2
0
0
0
0
0
7
3

3
0
0
0
0
0
0
11

2
1
0
0
0
0
0
11

12
2
%


14
14
0
0
0
0
0
50
22

21
0
0
0
0
0
0
7.9

14
7
0
0
0
0
0
79

86
14
8-49 EMPLOYEES
NUMBER


4
1
0
0
0
0
0
12
1

1
0
0
0
0
0
0
17

2
0
0
0
0
0
0
16

17
1
%


22
6
0
1
0
0
0
0
66
6

6
0
0
0
0
0
0
94

11
0
0
0
0
0
0
89

94
6
                          55

-------
                  TABLE 2 (CON'T)
         AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR RURAL AREA STORES, BY SIZE OF STORE, KENTUCKY, 1972
!
l
i
I
j QUESTIONNAIRE ITEMS
10. What Used
1.
2.
3.
4.
|
11. Application
1.
2.
12. What Used
1.
RURAL
t
TOTAL 1-7 EMPLOYEES
NUMBER

0
0
3
29


6
26

5
2. 1 1
3. 1 0
4.
5.
13. Areas Treated
1.
2.
3.
4.
5.
6.
7.
14 . Frequency
1.
2.
3.
4.
5-
26
0

3
0
0
0
0
0
29

0
27
1
0
. 4
%

0
0
9
91


19
81

16
3
0
81
0

9
0
0
0
0
0
91

0
84
0
3
13
NUMBER! %

0
0
2
12


2
12

1
1
0
12
0

2
0
0
0
0
0
12


0
0
14
86


14
86

7
7
0
86
0

14
0
0
0
0
0
86

0 0
12 86
0 0
0
2
0
14
8-49 EMPLOYEES
NUMBER

0
0
1
17


4
14

4
0
0
14
0

1
0
0
0
0
0
17

0
15
1
0
2
V
/3

Q
0
6
94


22
78

22
0
0
78
0

6
0
a
C
0
0
94

0
83
6
0
11
                            56

-------
                  TABLE 2 (CON'T)

  SUTLER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR RURAL AREA STORES, BY SIZE OF STORE, KENTUCKY, 1972
i i
i 1
i
QUESTIONNAIRE ITEMS
15. Sales
1.
2.
3.
4.
5.
6.
16. Cans Sold
1.
2.
3.
4.
5.
6.
17, Bottles Sold
1.
2.
3.
4.
5.
6.
• 18. Cartons Sold
1.
2.
3>
4.
5.
6.

RURAL
: 1
TOTAL 1-7 EMPLOYEES j 8-49 EMPLOYEES
NUMBER

0
17
13
2
0
0

0
8
19
5
0
0

15
11
3
0
3
0

0
18
11
3
0
0

%

0
53
41
6
0
0

0
25
59
16
0
0

47
35
9
0
9
0

0
56
35
9
0
0

NUMBER

0
10
4
0
0
0

0
6
7
1
0
0

8
2
1
0
3
0

0
9
5
0
0
0

% i NUMBER

0
71
29
0
0
0

0
43
50
7
0
0

57
14
7
0
22
0

0
64
36
0
0
, 0


0
7
9
2
0
0

0
2
12
4
0
0

7
9
2
0
0
0

0
9
6
3
0
0

%

0
39
50
11
0
0

0
11
67
22
0
0

39
50
11
0
0
0

0
50
33
17
0
0

                            57

-------
                  TABLE 2 (CON'T)

  NUMBER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR RURAL AREA STORES, BY SIZE OF "STORE, KENTUCKY, 1972
QUESTIONNAIRE ITEMS
RURAL
TOTAL
• NUMBER
••
! .
19. Area Displayed!
1. 1
2 . 0
3.
A
~r »
5.
6.
7.
8.
1
3
2
1
5
19
%


3
1-7 EMPLOYEES
NUMBER


1
0 I 0
3 1
9
6
3
16
60

9.
20. Accessible
1.
o
i. *

21. Display
1.
2.
3.
4.
5.
6.
7.
8.
9.
22. Displayed
T__
2.
3.
*.
0

23
9


3
2
5
0
1
0
2
19
0

0
6
2
3
5. 21
0

72
28


0
; 2
0
4
6

0

8
6


9 ! 1
6 2
16 1
0 0
3 ! 1
0
6
60
0

0
0
9
0

o' 1 o
19 2
6
9
1
1
66 10
. .
%


7
0
7
0
14
0
29
43

0

57
43


7
14
7
0
7
0
0
65
0

0
14
7
7
72

8-49 EMPLOYEES
NUMBER


0
0
0
3
0
1
1
13

0

15
3


2
0
4
0
0
0
2
10
0

0
. 4
1
2
11

-.
%


0
0
0
16
0
6
6
72

0

83
17


11
0
22
0
0
0
11
56
0

0
22
6
11
61

                           58

-------
                  TABLE 2 (CON'T)

  NUMBER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR RURAL AREA STORES, BY SIZE OF STORE, KENTUCKY, 1972
QUESTIONNAIRE ITEMS
23. Distance
1. •
2.
3.
4.
5.
24. Types
•1.
2.
3.
4.
5.
6.
7.
8.
25. Bagging
1.
2.
3.
4.
RURAL
TOTAL
NUMBER

13
11
3
5
0

0
0
0
0
6
0
26
0

25
4
3
0
%

41
34
9
16
0

0
0
0
0
19
0
81
0

78
13
9
0
1-7 EMPLOYEES
NUMBER

5
5
%

36
36
1 7
3
0

0
0
0
0
3
0
11
0

10
2
2
0
21
0

0
0
0
0
21
0
79
0

72
14
14
0
8-49 EMPLOYEES
NUMBER

8
6
2
2
0

0
0
0
0
3
0
15
0

15
2
1
0
. %

45
33
11
11
0

0
0
0
0
17
0
83
0

83
11
6
0
                            59

-------
                      TABLE 3

  NUMBER AIT!) PERCENT RESPONSE TO QUESTIONNAIRE  ITEMS
FOR URBAN AREA STORES, BY SIZE OF STORE, KENTUCKY,  1972
r i
QUESTIONNAIRE ITEMS
1. How Shipped
1.
o %
j. ,
/
hi B
5.
2. Disposal
URBAN
TOTAL
NUMBER
. 182
0
96
60
24
2

1. i 103
; 2. '
3.
4.
5.
6,
7.
8.
3. Storage
1.
2.
3.
. 4.
5.
.4. Storage
1.
2.
o
5. Disposal
i^
2.
3.
4.
0
54
0
19
1
1
4
12
26
24
68
52
114
16
52
11
9
2
5
5. 107
6. 48
j
-
%
100
0
53
1-7 EMPLOYEES
NUMBER
83
. o
35
%
100
0
42
8-19 EMPLOYEES
NUMBER 7-.
42
0
26
33 31 37 ! 14
13 15
1

56
0
30
0
10
1
1
2
7
14
13
37
29
63
9
28
6
5
1
3
59
26
2

59
0
13
0
8
0
0
3
7
10
8
25
33
42
6
35
0
3
0
3
44
33
|
18
3

71
0
16
0
10
0
0
3
8
12
10
30
40
51
7
42
0
4
0
4
53
39

2
0

19
0
18
100
0
62
33
5
0

45
0
43
0 0
4
0
10
0
0 i 0
1
4
4
7
18
9
29
5
8
6
2
0
1
25
8
.
2
10
10
16
43
21
69
12
19
14
5
0
2
60
19

20-99 EMPLOYEES
NUMBER
57
0
35
15
7
0

25
0
23
0
7
1
1
0
1
12
9
25
10
43
5
9
5
4
2
1
38
7

V
/••>
100
0
62
26
12
0

44
0
40
, 0
12
2 •
2
0
2
21
16 \
44
17
75
9
16
9
7
3
2
67
12

                             60

-------
                    TABLE 3 (CCN'T)

  NUMBER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR URBAN AREA STORES, BY SIZE OF STORE, KENTUCKY, 1972
QUESTIONNAIRE ITEMS
6. Pesticides
1.
2.
3.
4,
5.
6.
7.
8.
9.
7. Pesticides
^
2.
3.
4.
5.
6.
7.
8.
8. Pesticides
1.
2.
3.
4.
^
— •< *
6.
7.
8..
| '9. Contract
I
1.
2.
URBAN
TOTAL
NUMBER

7
15
1
1
0
0
0
149
9

12
7
0
0
0
0
0
163

10
4
0
0
0
0
0
168

161
21
%

4
8
1
'1
0
0
0
81
5

7
4
0
0
0
0
0
89

5
2
0
0
0
0
0
93

88
12
1-7 EMPLOYEES
NUMBER

4
1
0
1
0
0
0
73
4

6
0
0
0
0
0
0
77

4
0
0
0
0
0
0
. 79

65
18
%

5
1
o •
1
0
0
0
88
5

7
0
0
0
0
0
0
93

5
0
0
0
0
0
0
95

78
22
8-19 EMPLOYEES
. NUMBER

2
7
0
0
0
0
0
31
2

4
4
0
0
0
0
0
34

3
1
0
0
0
0
0
38

40
2
%

5
16
0
0
0
0
0
74
5

10
10
0
0
0
0
0
80

7
2
0
0
0
0
0
91

95
5
1
20-99 EMPLOYEES
NUMBER

1
7
1
0
0
0
0
45
3

2
3
0
0
0
0
0
52

3
3
0
0
0
0
0
51

56
1
"/
/a

2
12
2
0
0
0
0
79
5

2
4
0 .
0
0
0
0
94

5
5
0
0
0
0
0
: 90

98
2
                            61

-------
                    TABLE 3 (CCN'T)

  NUMBER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR URBAN AREA STORES, BY SIZE OF STORE,  KENTUCKY, 1972
QUESTIONNAIRE ITEMS
10. What Used
1.
2.
3.
4.
11. Application
1.
2.
12. What Used
1.
2.
3.
4.
5.
13. Areas Treated
1.
2.
3.
4.
5.
6.
7.
14. Frequency
1.
2.
3.
. 4.
5.

URBAN
TOTAL
NUMBER

13
0
19
150

47
135

31
7
1
135
8

0
0
0
0
0
1
181

2
148
3
0
29

%

7
0
10
83

26
74

17
4
1
74
4

0
0
0
0
0
1
99

1
81
2
0
16
'-- - -
1-7 EMPLOYEES
NUMBER

3
0
16
64

21
62

9
4
1
61
8

0
0
0
0
0
1
82

2
66
2
0
13

%

4
0
19
77

25
75

11
5
1
73
10

0
0
0
0
0
1
99

2
80
2
0
16

8-19 EMPLOYEES
NUMBER

1
0
2
39

9
33

9
0
0
33
0

0
0
0
0
0
0
42

0
37
0
0
5

%

2
0
5
93

21
79

21
0
0
79
0

0
0
0
0
0
0
100

0
88
0
0
12

20-99 EMPLOYEES
.NUMBER

9
0
1
47

17
40

13
3
0
41
0

0
0
0
0
0
0
57

0
45
1
0
11

%

16
0
2
82

30
70

23
5
0
72
0

0
0
0
0
0
0
100

0
79
2
0
19

                            62

-------
                    TABLE 3 (CGK'T)

  NUMBER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR URBAN AREA STORES,'BY SIZE OF STORE,  KENTUCKY,  1972
i
QUESTIONNAIRE ITEMS
15. Sales
1.
2.
3.
4.
5.
6.
16. Cans Sold
1.
2.
3.
4.
5.
6.
17. Bottles Sold
1.
2.
3.
4. .
5.
6.
18. Cartons Sold
1.
2.
3.
4.
5.
6.
URBAN
TOTAL
NUMBER

29
69
57
21
3
3

22
66
50
35
6
3

80
59
16
2
22
3

76
62
20
11
10
3
%

16
38
31
11
2
2

12
36
28
19
3
2

44
32
9
1
12
2

42
34
11
6
5
2
1-7 EMPLOYEES
NUMBER

' 28
43
9
0
3
0

22
42
11
2
6
0

47
17
0
0
19
0

55
18
0
0
10
0
%

34
51
11
0
4
0

27
51
13
2
7
0

57
20
0
0
23
0

66
22
0
0
12
0
8-19 EMPLOYEES
NUMBER

°
18
20
3
0
1

0
16
19
6
0
1

17
18
9
0
1
1

14
19
7
1
0
1
. %

0
43
48
7
0
2

0
38
45
15
0
2

41
43
12
' 0
2
2

34
45
17
2
0
2
20-99 EMPLOYEES
NUMBER

1
8
28
18
0
2

0
8
20
27
0
2

16
24
11
2
2
2

7
25
13
10
0
«-\
%

2
14
49
31
0
4

0
14
35
47
0
4

28
41
19
4
4
4

12
44
23
17
0
4
                             63

-------
                    TABLE 3 (CON'T)

  NUMBER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR URBAN AREA STORES, BY SIZE OF STORE, KENTUCKY, 1972
QUESTIONNAIRE ITEMS
19. Area Displayed
-L •
2.
3.
4.
5.
URBAN
TOTAL
NUMBER

6
1
3
2
5
6. I 46
7.
8.
9.
' 20. Accessible
1.
2.
21. Display
1.
2.
3.
4.
5.
6.
7.
8.
9.
22. Displayed
1.
2.
65
51
3

129
53

13
8
27
4
7
4
5
112
2

2
19
3. IS
4. i 27
5. | 116
i
i ;
i '
%

3
1
2
1
3
25
35
28
2

71
29

7
4
15
2
4
2
3
62
1

1
10
10
15
64



1-7 EMPLOYEES
NUMBER

3
0
3
0
3
24
27
21
2

49
34

6
6
15
4
4
2
2
43
1

1
8
6
16
52



%

4
0
4
0
4
29
32
25
2

59
41

7
7
19
5
5
2
2
52
1

1
10
7
19
63



8-19 EMPLOYEES
NUMBER

2
1
0
1
1
12
10
14
1

33
9

3
1
6
0
3
2
0
27
0

1
7
6
6
22


%

5
2
0
2
2
29
24
34
2

79
21

7
2
14
0
7
5
0
65
0

2
17
14
14
53


20-99 EMPLOYEES
NUMBER

1
0
0
1
1
10
28
16
0

47
10

4
1
6
0
0
0
3
42
1

0
4
6
5
42


1
	 -It 	 	 _ -._.'.--.. --. 	 (-__-.-.__„ 	 _. . 	
%

2
0
0
2
2
17
49
28
0

82
18

7
2
10
0
0
0
5
74
2

0
7
11
9
73



                           64

-------
                    TABLE 3 (CON'T)

  NUMBER AND PERCENT RESPONSE TO QUESTIONNAIRE ITEMS
FOR URBAN AREA STORES, BY SIZE OF STORE, KENTUCKY, 1972
QUESTIONNAIRE ITEMS
23. Distance
1.
2.
3.
4.
5.
24. Types
1.
2.
3.
4.
5.
6. .
7.
8.
• URBAN :
TOTAL
NUMBER %

86
40
15
37
4

2
3
8
1
40
9
109
10
i
25. Bagging
1.
2.
3.
4.

104
56
18
4

47
22
8
21
2

1
2
4
1
22
5
60
5


57
31
10
2
1-7 EMPLOYEES
NUMBER

48
19
7
6
3

-i
3
7
1
16
7
42
6


44
30
6
3
%

58
2.3
8
7
4

1
4
9
1
19
8
51
7


53
36
7
4
8-19 EMPLOYEES
NUMBER

19
11
3
9
0

0
0
1
0
8
2
30
1


27
10
5
0
%

45
26
7
22
0

0
0
2
0
19
5
72
2


64
24
12
0
20-99 EMPLOYEES 1
NUMBER

19
10
5
22
1 .

1
0
0
0
16
0
37
3


33
16
•7
1
1
%

33 ]
16
9
39
2

2
0
0
0
28
0
65
5


58
28
12
2
                           65

-------
                                    TABLE 4

    OBSERVED CHI-SQUARE VALUES AND PROBABILITY VALUES  (SIGNIFICANCE)  TESTING
     INDEPENDENCE BETWEEN STORE SIZE CATEGORIES WITH REGARDS  DISTRIBUTION OF
     ANSWERS TO QUESTIONNAIRE ITEMS, BY RURAL-URBAN LOCATION, KENTUCKY,  1972
Item
No.
1
2
3 .
4
5
6
7
8
9
10
11
12
13
14
15
15
17
. 18
19
20
21
22
23
24
25
TOTAL
Chi-Sq.
Value
7.83
11.47
19.78
18.42
30.02
10.43
2.49
0.66
16.19
23.44
0.92
17.53
0.0
0.48
92.52
90.35
46.85
59.85
11.71
13.43
16.44
8.30
17.96
20.53
3.30
Prob. Value (P)
.1(90% Level)
.05(95% Level)
.02(98% Level)
.01
.001
, 2
.3
.8
.001
.001
.7
.01
—
.8
.001
.001
.001
.001
.1
.01
.1
.3
.01
.01
.7
RURAL
Chi-Sq.
Value
0.0081
2.79
3.47
4.84
3.89
0.0025
0.0
0.64
0.0
0.0
0.33
0.33
0.0
0.04
3.35
4.69
4.76
0.65
4.35
2.67
1.78
0.42
0.29
0.12
0.65
Prob. Value (P)
.95
.1
.5
.1
.2
.98
—
.5
—

.7
.7
__
.9
.1
.1
.1
.5
.2
.1
.5
.8
.9
.7
.5
URBAN
Chi-Sq.
Value
9.55
16.10
16.21
14.34
23.45
5.49
4.41
1.81
15.61
21.21
0.91
2.52
0.0
1.42
87.51
88.77
40.53 .
72.59
8.92
10.55
10.50
8.81
18.39
18.93
2.49
Prob. Value (P) '
.05
.01
.05
.01
.001
.3
.2
.5
.001
.001
.7
.3
—
.5
.001
.001
.001
.001
.2
.01
.3
.2
.01
.02
.7
14 Significant Chi-Sq.
   (?95% Level)
No Significant Chi-Sq.
14 Significant Chi-Sq.
     Values
                                         66

-------
                               TABLE 5

OBSERVED CEI-SQUARE VALUES AND PROBABILITY VALUES (SIGNIFICANCE) TESTING
  INDEPENDENCE BETWEEN RURAL-URBAN LOCATION WITH REGARDS DISTRIBUTION
   OF AKSi.TRS TC QUESTIONNAIRE ITEMS, BY STORE SIZE, KENTUCKY, 1972
ITEM NO.

1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
• 22
23
24
25

STORE SIZE 1
CHI- SO. VALUE

3.57
0.26
1.01
0.002
0.64
0.0
0.0
0.0
0.40
0.52
0.80
- 0.06
0.0
0.12
7.01
8.90
0.02
21.43
1.37
0.02
1.99
1.22
2.37
2.16
1.65

(1-7 IMP.)
PROB. VALUE (P)

.2(80% Level)
.7
.7
.95
.5
—
—
—
.5
.5
t;
• _/
.8
—
.7
.05(95% Level)
.02(98% Level)
.99
.001(99.9% Level)
.5
.9
.5
.7
.3
.2
. .2

STORE SIZE 2 (8-19 EMP.)
CHI-SO. VALUE

0.0006
8.94
0.50
0.0002
1.16
0.48
0.94
0.0
0.0
0.0
0.02
0.02
0.0
0.0
0.08
2.33
0.40
7.92
3.12
0.02
0.46
0.91
1.19
1.99
1.92

PROB. VALUE (P)

.98
.01(99% Level)
.95
.99
.7
.5
.4
—
—
—
.9
.9
—
—
.8
.3
.5
.02(98% Level)
.2
.9
.5
.7
.4
.2
.2

    Store Size 1-3 Sig. Chi-Sq.
             Values
Store Size 2-2 Sig. Chi-Sq.
         Values
                                     67

-------
68

-------
                      MILITARY PEST CONTROL




                        Walter W.  Barrett




                         U. S. Air Force






     Insects and other pests have created problems for nearly every




army that existed, from biblical times to the present.




     References in the Bible reveal that pestilence and famine were




common in the lands around Galilee.  Despite mankind's best efforts,




many of the same pests still abound.  Note, for example, the locust problem




which is graphically portrayed in the commercial motion picture film,




"The Rival World."




     Alexander the Great knew nothing but victory when facing human foes,




yet his empire disintegrated when he died at age 33, a victim of mosquito-




borne malaria.




     In 1528, an Italian army was surrounded by the French at Naples.




That time, pestilence came to the aid of the Italians. . The siege was




lifted after over half of the French army succumbed to the typhus fever.




     In more recent history, 1943 saw a repeat of the typhus epidemic




in Italy, creating the unforgettable scene of power delousers treating




thousands of people with DDT dust.




     As Napoleon fought against Russia, typhus and cold weather combined




to defeat him.  Another interesting sidelight of Napoleonic history and




the part that pestilence played in making our own nation took place when




Napoleon was battling on two fronts - fighting England while also attempt-




ing to settle in Louisiana.  Yellow fever weakened so many of his men




that he was forced to sell out in Louisiana.  This resulted in the Louisiana
                                  69

-------
Purchase Agreement - for $7,000,000 or about $.03 per acre.




     Yellow fever is still around today, with the failure of the.1963-




1966 eradication campaign against the Aedes aegypti mosquito only a faint




memory.  Funding problems brought this eradication concept to an early




end, before many of its lofty goals were reached.




     A National Cemetery display at Frederickburg, Virginia reveals that




over 600,000 casualties resulted in that area.  There were many pitched




battles on both sides of the Rappahanock River.  Of the 600,000 casualties,




diseases (including malaria and Yellow fever) caused 2 to 3 times as many




deaths as bullets and cannon.




     A prime example of an economic pest - termites - illustrates the




damage caused by this pest.  On the Island of Guam, termite damage to nearly




1300 homes at a USAF base resulted in a commercial pest control contract




for $469,000.  Repair costs very likely were estimated to be an additional




$600,000.




     We have accurate data on World Wars I and II, the Korean and Vietnam




conflicts.   Lice and the diseases associated with lice played prominent




roles in each of these wars.




     Malaria also was a significant factor in loss of lives and manhours




in past wars.  Malaria is usually associated with the South Pacific areas




where it had a tremendous impact on troop strength, medical manhours




expended, as well as the tragic numbers of deaths.  Few people realize




the impact of malaria in the European area, particularly the Mediterranean-




Campaigns.   On the Island of Corsica, for example, estimates of the Italian




malarial rates ranged as high as 90% of the troop strength.  Imagine if




you will, the diminished fighting ability of a squadron with 90% of its




pilots, mechanics, and armorers down with malaria.
                                 70

-------
     Organization of the military pest control program from the Washington




level follows down to base levels in a rather straight pattern.  At DOD




level, the Assistant Secretary for Health and Environment controls or is




responsible for medical aspects and also is the agent to which the Armed




Forces Pest Control Board reports.  The Assistant Secretary for Installa-




tions and Logistics is responsible for the maintenance of facilities.  In




general, the lines follow similarly for each service, with medical and




survey responsibilities assigned to the Surgeon General of each service




and engineering and control responsibilities assigned to the Director




of Civil Engineering or Public Works in Washington, then to similar set-




ups at command and base levels.




     The Armed Forces Pest Control Board functions as a coordinating




office for the Department of Defense.  It has a separate office maintained




at the Walter Reed Army Medical Center's Annex.  The Board has a staff




of 15 persons, including clerical assistants, to review military programs,




decide on new pesticides/equipment and resolve problems of mutual concern




to DOD components.  It includes the Military Entomology Information Service




(MEIS) which abstracts pertinent articles for retrieval and use by in-




terested people.  Not much is known of this service by outsiders, but




as one example of its usefullness, MEIS is invaluable for determining




effectiveness of materials or resistance of pests to specific chemicals




in nearly any country in the world.  Print-outs are available on nearly




any subject of medical or economic importance, with only one caution.




Don't ask for general information on termites in the U.S. or similar




general questions.  Why?  You would be swamped with references if you




did.   An ideal example would be "Do you have a listing of references




on Hippelates ghat control by aircraft1?"  In other words, be specific.
                                71

-------
I have included the address of this service in the appendix to this




speech, as well as in the leaflets at the rear of this room.




     Training will be cpvered in detail here, primarily because the




military has placed great stress on training in the past and will continue




to do so in the future.  One thread that is woven into all DOD philosophy




is the concept that well-trained personnel hold the key to the best usage




of various control techniques and the best way to prevent mis-use of




pesticides.  Training is considered to be a basic part of the DOD certifica-




tion procedure.  These procedures will be covered in depth during this




conference since Public Law 92-516 has stated very clearly the dates when




all agencies must have approved certification requirements for pesticide




applicators.




     All services (except the Marine Corps which comes under the Navy




Medical Corps for vector control) have established schools for training




civilian and military personnel.




     The Army has a program for eight 5-week courses and three to four 1-




week courses in FY 1975, the latter designed as recertification courses.




They are all system-engineered and are held at the newly-formed Health




Service Command at San Antonio, Texas.  Class size is 20-25.




     Courses for the control of economic pests as well as medical pests




are taught at Fort Sam Houston, Texas.  They provide a borad spectrum of




training, such as:




     Program Administration                        11 Hours




     Pesticide Usage and Safety                    13 Hours




     Equipment                                      9 Hours




     Biology, Identification, Surveys              31 Hours
                                 72

-------
     Concepts of Control Procedures                26 Hours




     Field Control Problems                        43 Hours




     The Navy has had formal courses longest, having initiated a 4-week




Disease Vector and Economic Pest Control Course at Jacksonville, Florida




in 1956.  It expanded this to Alameda, California in 1957.  The Navy,




as well as other services, realizes the importance of training and




cooperated for nearly 12 years in training Air Force personnel at both




locations.  Well over 600 Air Force personnel completed the Navy course




at the Florida and California locations.  Both schools are manned with




professional entomologists, including Ph.D. Officers-in-Charge, and a




complement of petty officers and civilians trained in all aspects of




pest control.




     The general approach for the Navy is three-fold:




     a.  Importance, biology, and recognition of pests.




     b.  Practical experience in identifying pests.




     c.  Survey and control methods and equipment.




     The Navy courses, as well as the Army and Air Force courses, do




stress integrated control, a procedure that will be covered later in




this conference.




     Intensive Navy pest control programs were initiated in the late




1950's, primarily to protect personnel and also protect a sizeable invest-




ment in shore facilities.  The fleet was not neglected either, since the




training is available to ships personnel - for tips on safe control of




roaches, rodents, and other pests which delight in living aboard warm




ships and find the many hiding places to their liking.
                               73

-------
     Correspondence courses are available from Navy sources and are




recommended for personnel unable to get quotas to the formal courses




or for preparation for the formal courses.




     The Navy courses are open to all active duty officers and enlisted




personnel of DOD, as well as other Federal Agencies.  Permission of the




Officer-in-Charge is required because priority is assigned to Navy and




other DOD personnel.  Air Force personnel must receive approval of ATC




(ATTMC) officers at Randolph AFB, Texas 78148.




     The Air Force program closely follows the subjects covered in the




Navy courses, but several innovations have been added.




     The Air Force has basic courses in pest control at Sheppard AFB,




Texas but it also features mobile training temas and specialized teams




for unique problems.  For brevity in this speech, the courses are listed




in Appendix 2.




     For all military personnel if you have not attended a formal course,




or completed a correspondence course, or obtained your certification,




I highly recommend a visit to your base personnel/education officer upon




your return, for additional details on these courses or certification




procedures.




     Certification procedures are delegated to major commands for all




DOD components.   These have been in effect since 1955, so there's been




a wealth of experience in formulating tests, observing on-the-job competency,




establishing necessary training courses, and refining the systems.   In




general,  these certification procedures require:




     a.   Successful completion of a formal course.




     b.   Satistactory on-the-job evaluation.




                      OR
                                74

-------
     a.   Successful completion of written examinations.
     b.   Recommendation by the Base Civil Engineer,  with comments on the
candidates training, safety habits, and other pertinent information.
     DOD employs professional entomologists to assure the adequacy of
training, survey and control procedures as well as to conduct research
and assist in monitoring of pesticide usage.


     Army                 82 military + 13 civilians as medical
                          entomologists
                          5 civilian engineer entomologists

     Navy                 21 medical entomologists
                          23 civil engineer entomologists

     Air Force            16 medical entomologists
                          5 civilian engineer entomologists

     In summary, military pest control programs are designed to secure
intelligent, qualified personnel; to train them in the latest and best
procedures available; and to certify successful candidates to achieve
our goal of protecting health and property.

                            References
1.  Bunn, Lt. Col. R. W., US Army; Cdr. K. L. Knight, US Navy; and Lt.
    Col. W. J. LaCasse, US Air Force,  The role of entomology in the
    preventive medicine program of the armed forces.  Military Medicine.
    116(2), February 1955.
2.  Holway, Capt. R. T., USN.  Contributions of insecticides to national
    defense.  Proceedings Entomology Society of America, Armed Forces
    Pest Control Board, Washington D. C., 1960.
                               75

-------
3.  Bayne-Jones, S., M.D.  The evolution of preventive medicine in the




    U.S. Army, 1607-1939.  Office of the Surgeon General, Department of




    the Army.  Library of Congress Catalog: 60098.  1968.




4.  Bunn, Col. R. W., MSC and Col. Joseph E. Webb, Jr. MSC.  History of




    the U.S. Army Medical Service Corps, Chapter XIII, Laboratory Special-




    ties, Section 7, Entomology.




5.  AFM 91-16, Military Entomology Operational Handbook.




6.  TM 5-632, Military Entomology Operational Handbook.






                            Appendix 1




Addresses:




1.  Military Entomology Information Service, Armed Forces Pest Control




    Board, Forest Glen Section (WRAMC), Washington, DC 20012.




2.  List of Air Force Training Courses.






                            Appendix 2




List of Air Force Courses:




    The following courses are offered by ATC at the Sheppard AFB, Texas




Technical Training Center, as well as other locations in the case of the




travelling teams.




    3 ABR 56630 - 6 weeks, Sheppard AFB, Texas (Seven students every 11




weeks with plans to increase this to 12 students per class every 10 weeks).




    3 AB 56650 - 4 weeks + 2 days, Sheppard AFB, Texas (Class of 10




students every 5 weeks).




    2 ASR 56650-2 - 2 weeks, Sheppard AFB, Texas (Not too active, was




designed as refresher course for SEA-bound personnel.  May be dropped.)




    2 ASR 56650-3 - 3 weeks, Sheppard AFB, Texas (Application of Herbicides,




scheduled irregularly, with class size of 9-12 students.   AFSCs 566X0 and




551XX are eligible.)





                               76

-------
    4 AST 56650-1 - 2 weeks, Mobile Training Team (Annually in USAFE,




generally in Germany, with 2 classes of 15 each).




    4 AST 56650-2 - Aluminum Phosphide Fumigation Special Course, 2 days,




at selected locations. (Class size from 10-15 students, may be dropped




as subject is now covered in basic courses).
                               77

-------
78

-------
                      PESTICIDES AND WILDLIFE




                        William D. Fitzwater




               U. S. Environmental Protection Agency






Introduction




     Humans have great impact on the fellow creatures sharing the planet




with them.  Most important is the destruction and/or improvement of the




habitat supporting various life forms.   Of lesser importance is the intro-




duction of foreign species to new areas or new causes of mortality to




resident species.  Man, by his.market and/or sport hunting pressures,




can also cause severe disruption to a particular species.  These and other




pressures may result in the complete extinction of a particular life




form.  The role of pesticides, while important in regulating animal




numbers, has generally been exaggerated.  Pesticides do, however, affect




the lesser animals in several ways.  Direct mortality, while very evident,




is probably not as important as the more insidious effects on reproduction,




behavioral changes, growth rates, food quality changes and disease sus-




ceptibility.  Other factors determining the extent of pesticide impact




are biological accumulation, persistence and the development of pesticide




resistence.






Impact of Man on Wildlife




     The greatest effect man has on his brother creatures is the




alteration of the habitat common to both.  As there is only a finite




amount of living space on this globe, the demands of an exploding




human population are rapidly shrinking the environment suitable for




many other species.  Foremost factor in this habitat destruction is




"urban sprawl".  The expansion of man's steel and concrete tentacles




favor a few species but destroy most others.  It is estimated that
                                  79

-------
420,000 acres are gobbled up annually to create living space for




humans.  Another 160,000 acres are made "unproductive" by conversion




into highways and airports (16).




     As an example of this trend, Los Angeles County in ten years




dropped from the fourth most agriculturally productive county to




eleventh in California.  On the other end of the Los Angeles-San




Francisco megalopolis, the plum orchards below San Jose have been




rooted up to furnish a non-productive (agriculturally at least)




bedroom annex for San Francisco.  This county, Santa Clara, has




dropped from fifteenth to below twenty-first in the state (4).




     Current agricultural philosophy for supplying the expanding




human population depends on "monoculture".  This, in turn, creates




vast tracts of homogenous land use areas—sterile deserts to many




forms of life though vertiable paradises to others.  The inefficient




hedgerows that offered food and security to many animals in the




early part of this century have given way to sterile wire fences.




Marsh areas, the important life zones of many creatures, are system-




atically being drained and plowed into production to feed the swelling




human demand.




     As the Arab oil confrontation lead to our being more energy




conscious, the rooting for buried mineral resources has proliferated.




The moon-like landscapes resulting from this despoilation will support




only a fraction of the life biomass that existed before man's inter-




vention.  Disposal of the wastes of civilization has created a problem




of global pollution that further destroys the habitat for more sensitive




species than Homo sapiens.  These,then,are the forces of man's greatest




impact on wildlife.
                               80

-------
     To give the devil his due, man has improved the environment for




some species.  When the first Europeans came to this country,  the




deer herd was estimated at around one million (20).   Cutting the




mature forests opened the ground beneath them to start anew suc-




cessional changes and bring more food within reach of these animals.




In Texas and California alone, over four million deer are harvested




annually—four times the number of the original herd.




     Artificial feeding programs like hay to Jackson Hole elk, water




guzzlers to desert valley quail and backyard feeding stations have




enabled some species to expand beyond previous limits in a given area.




Wildlife have also benefited from man's fight against diseases of




direct effect to himself.  Mosquito-spraying programs have eliminated




malaria and several other mosquito-borne diseases that affect the




lower animals.  The development of vampire bat control measures in




Central America has reduced their rabies potential,  thus diminishing




exposure to this disease for other warm blooded animals besides




domestic stock (13).




     In general, man's insatiable desire to upset nature by bringing




in forms foreign to a given area has been disastrous.  Domestic stock




has preempted range, both existing and potential, from native grazers




and browsers.  Another example is that cosmopolitan family - the Muridae




or "Old World rats and mice".  Originally an obscure desert rodent,




the roof rat has been carried over the world to wreck almost as much




havoc on some native fauna as the human animal.




     Not all of these introductions have been as unintentional as




rats and mice.  We are "blessed" today with a plague of starlings.




This is all because one man thought it would be "nice" to bring over
                                81

-------
all the birds mentioned by Shakespeare in his plays.  Would: that the




ol' bard had never penned the line, "I'll have a starling shall be




taught to speak nothing but 'Mortimer'" [Henry IV] (23).  But the




prize for the most bungling of importations of unsuited vertebrate




guests must go to Australia and New Zealand.




     While most of man's meddling has been unfortunate, there have




been some notable exceptions such as the ring-necked pheasant and




Barberry sheep.  These species have filled ecological niches not




effectively occupied by native species.




     Another direct detrimental effect man has exerted on wildlife




is the introduction of various mortality factors into wildlife eco-




systems.  Diseases have been brought in, usually via domestic live-




stock.  Plague from our friend, the rat, became established on the




West Coast and has moved as far east as Nebraska*  While human cases




are held to a couple per year, the disease destroys many colonies of




native rodents until it has run its course.   Other- diseases,  such as.




Newcastle, foot and mouth disease, leptospirosis and rabies have




been brought in by man to infect resident wild species.  The same




problem has occurred with foreign parasites.  Trichimoniasis brought




over by the feral pigeon is supposed to have been a factor in wiping




out the once abundant passenger pigeon (18).  Predators, such as




feral cats and dogs, introduced into new ecosystems,  are responsible




for much loss of wildlife.




     Other byproducts of civilization have destroyed large numbers




of animals.   There are 8,000 oil spills reported yearly in the United




States alone, mostly in the coastal waters.   It is estimated that




over five million tons of oil wastes are dumped yearly in the oceans
                               82

-------
of the world from bilge,  tankers,  offshore industries,  etc.   These




oil slicks play havoc with all marine life.   The 25,000 wells dumping




some 1.1 million barrels  of oil in the Gulf  of Mexico annually are




tainting shell fish and destroying their beds (1).   Dispersants to




clean up oil slicks may cause worse damage than the oil itself, as




it makes it easier for marine animals to ingest these hydrocarbons.




     Besides the disruption of the complex marine food chain, there




is the actual destruction of the larger marine animals, particularly




birds.  Those that come in contact with oil lose flight capability.




Despite publicized effort to save these birds, only a very small




fraction can be salvaged as the methods used to remove the oil, also




remove the waterproofing from the feathers.   The birds must molt




before they are capable of functioning normally again.




     Man-made structures, such as lighthouses, have confused migratory




fowl causing collisions in stormy weather, resulting in the spectacular




loss of large numbers of birds.  Highway mortality runs into countless




numbers per year as subhuman pedestrians tempt fate on the concrete




bowling alleys.  In Minnesota, highway mortality accounts for 63.6%




of the deer killed other than by legal hunting.  Poachers at 14.8%




are the next highest cause of loss (3).




     The intentional killing of wild animals by shooting, trapping




or fishing is another point of impact.  However, with some notable




exceptions, this is not important.  Wild animal populations are a




renewable resource which the sport hunter harvests.  The habitat




will sustain life for only so many mice, squirrels, fox or elk.




Annual production is usually much in excess of these numbers so the




populations must be limited in one way or another.   Shooting is







                                83

-------
probably one of the least traumatic of these methods.




     Market hunting, however, is another matter.  The American bison




herd was brought from 60,000,000 animals to 300 individuals in one




century.  Beaver and egrets were fast disappearing until fashion




changes halted their exploitation.  The pet trade that sees over




120,000,000 animals imported into this country represents only a




partial fraction of this wastage of animal life (2).  Take the case




of primates.  Native monkey collectors in India shoot the females




carrying young as this is the most feasible way of catching a market-




able animal for the pet trade.  Besides the evident reduction in the




breeding crop, many of the animals collected are too young to success-




sully survive without a mother's care.




     The endangered species problem has received much ballyhoo.  While




it certainly would be a drab life if our only wild animal contact was




with starlings, pigeons, mice and coyotes (the species who seem most




likely to succeed in spite of man), life is a dynamic force.   Since




its advent on this planet, many, many, many forms have appeared only




to disappear as not fitted to survive the constantly changing condi-




tions imposed by the habitat.  While some 94 species of birds and 76




species of mammals have disappeared since 1600, this is only 1% of




all the known species (16).  In most cases these have been relict




forms—offspring from an aberrant ancestor who enabled an eager




taxonomist to publish a paper.  The loss, for example, of the San




Francisco garter snake (claim to fame is a red stripe down its sides)




presents no practical problem.




     We do have more obligation to prevent the disappearance of a




species from the face of the earth because of human greed and lack
                               84

-------
of foresight, but this must be tempered with a true understanding of




biological principles.  The disappearance of the red wolf in the




Southcentral states is a taxonomist's dilemna.  The influx and sub-




sequent interbreeding with the coyote poses a bigger threat to the




survival of the species than the U.S. Fish and Wildlife's predator




control program.




     We finally come to the main thesis of this presentation—the impact




of pesticides on wildlife.  Pesticides have been a public whipping




boy since Rachael Carson's (1962) Silent Spring.  Pesticides do play




an important role in the loss of much animal life, directly and in-




directly.  Much of this loss has been due to the almost criminal




misuse of toxic chemicals and complete disregard for their total ef-




fects.  But at present they are indespensible in achieving food and




fiber production and protection of human health.  Hopefully, future




technology may obviate this need, but this will not happen tomorrow,




despite all the legislation Congress can pass.




                Impact of Pesticides on Wildlife




     Pesticides exert an impact on wild animal numbers in many ways:




Direct Mortality




     This is the most evident effect.  As the public media casts about




for more grist for their mills, fish kills or the loss of several hun-




dred Canada geese in Oregon in a field mouse poisoning program make




good space fillers.  However, this is in actuality one of the least




important aspects of the pesticide-wildlife interaction.




     Pesticides used intentionally for vertebrate pest control are




a minor entity.  Take for example the "dread" ten-eighty (sodium




monofluoroacetate).  The last year before its banning as a coyote
                               85

-------
control agent, the U. S. Fish and Wildlife Service used a total of




17 pounds in its coyote control program over the entire country.




Admittedly a toxic material, any thinking spectator would have to




question the charge the West was being covered with poison at this




rate.




     Artificial reduction in numbers of predatory animals may have




an effect on the numbers of prey or lesser predators produced.  The




treatment of an Alaska stream with toxaphene to kill sculpins which




preyed on pink salmon fry had the ability to increase the annual




production run of the latter species significantly.  The advent of




more effective coyote controls (coyote getter and 1080 stations)




temporarily depressed coyote populations with a compensating increase




in lesser predator populations of badger, fox and bobcat in the same




areas (17).  However, predator numbers are more apt to be influenced




by the numbers of prey rather than prey being affected by the predators




as shown by Elton's classic study (1935) on the lynx-snowshoe hare




relationship.  Depression of rodent populations is only a brief




respite before the biological potential replaces the losses.




     Most losses of "non-target" vertebrate animals, such as a 1958




Illinois study (19), are of short-lived duration.  Dieldrin applied •




at the rate of 3 pounds per acre in an effort to eradicate Japanese




beetle over a wide area did kill a number of vertebrate animals.




However, the investigators reported populations had recovered by the




next year.




Reproduction




     Of more significance is the indirect effect pesticides have on




the reproduction of some vertebrates, particularly fish-eating birds.
                                86

-------
Laboratory studies have shown various pesticidal chemicals at certain




levels can depress reproduction by increasing ovulation time, eggshell




thinning,'embryonic and infant mortality (15).  However, in the field these




effects are not as clearcut (9).  The complexity of nature makes it nearly




impossible to single out any one factor as being the sole cause.  Egg shells




are apparently thinner since 1946 with the advent of widescale use of DDT




and certain other chemicals.  This thinning is blamed for the disappearance




of the bald eagle in the East and the brown pelican off the coast of Calif-




ornia.  While undoubtedly a factor, what importance does it have in the




total picture where prime eagle habitat is being preempted by condominiums




and the pelicans are being disturbed by flat-footed biologists taking




frequent head-counts?




Behaviorial Changes




     Another insidious effect is the change in behaviorial patterns, again




as shown by laboratory studies.  Pesticides have been shown to affect




visual discrimination  (21), learned avoidance response  (11) and feeding




behavior (10).




Growth Rates




     Pesticidal chemicals may have a differential effect on growth.  White-




tailed deer on a sublethal dieldrin intake grew more slowly than the controls




over a 3-year period (14).  Conversely, sublethal doses of endrin increased




the weight of rats (6) mainly through the increase in the lipids content.




Food Quality Changes




     Agricultural chemicals may alter the quality of the food available to




animals.  Application of 2,4-D and other herbicides has a very decided




effect on the number of pocket gophers who can survive  in a treated area




without broadleaved weeds (12).  This herbicide also increases sugar content
                                 87

-------
making the toxic ragwort plant more attractive to cattle.  The facility of




increasing the presence of some elements and decreasing others could exert




a very subtle effect on the herbivores in an ecosystem.  There is also the




direct loss of food as in the case of the complete elimination of a caddis




fly hatch for fish food because of phosphomidion spraying in a spruce budworm




infestation (8).




Disease Susceptibility




     PCBs have demonstrated an ability to increase the susceptibility of




ducklings to duck hepatitis.  In the same way, 2,4-D and carbaryl have




been able to lower the resistance of fish to a microsporian parasite.




On the other hand, Allison, et al (1964) have shown cut-throat trout surviving




DDT applications had a 50% less infection incidence than the controls..




Pesticide Resistance




     While the generation gap in vertebrates is further apart than with in-




vertebrates, vertebrate animals can develop resistence to pesticides too.




The house mouse can double its resistance to DDT in 10 generations.  Pine




mice surviving in treated orchards are twelve times more resistant to endrin




(22).  The big worry in Norway rat control is the increasing evidence of




the development of anticoagulant resistant strains of rats appearing world-




wide to the frustration of rodent control specialists.




Biological Accumulation




     As the chain of life consists of big forms eating smaller ones,




pesticidal chemicals can be passed along this chain.  The potential of




accumulations in animals higher up on the: chain depends upon the chemical




persistence of the pesticide and the ability of the host to metabolize




or excrete it.   Thus we find oysters in water containing 1 ppb DDT




are able to concentrate that chemical 70,000 times in their own bodies.
                                 88

-------
Another study showed that DDT at 9.9 ppm in the soil was concentrated




at 141 ppm in earthworms living in that soil.   Further up the food chain,




robins eating the earthworms contained 444 ppm—a lethal dosage,




Persistence




     Persistence is essentially a part of the above phenomena.  If




pesticides were not persistant chemical entities, they would not be




as important in the complex web of life that shapes this world.   DDT




applied at one pound per acre has an estimated life span of thirty years




in a protected forest site.  The half life of some organic phosphate




materials is measured in hours.  A final consideration is the state of




the art of analytical chemistry.  For over ten years, chemists reported




the world-wide distribution of DDT only to find that at least half of




the DDT determinations involved PCBs of nonpesticidal origin.




     While not negating the impact of pesticides on wildlife, the total




picture would indicate that "Silent Spring" will not arrive if thoughtful




use of pesticides can be achieved.






                            References




1.  Anderson, Jack.  Study describes oil-waste damage.  Washington Post,




    May 30, 1974, p. C7.




2.  Anonymous.  Wildlife imported into the United States in 1972.  U.S.




    Dept. of the Interior, Bur. of Sport Fish, and Wildlife, WL-502.  1973,




3.  Burcalow, D. W.  Minnesota's deer traffic toll.  The Conservation




    Volunteer, 5(25):14-16.  1942.




4.  Carpenter, G. Alvin.  Economic briefs for California agricultural




    extension personnel.  Univ. Calif. Berkeley New Notes, June 15 , 1969,




    p. 2116-2120.




5.  Carson, Rachael.  Silent Spring^  Houghton Mifflin Co., Boston, Mass.




    368 p.  1962.




                                 89

-------
 6.  Deichmann, W. B. and LeBlanc, T. J.  Determination of the approxi-




     mate lethal dose with about six animals.  Journ. Industrial Hygiene




     and Toxicology.  25(9):415-417.  1943.




 7.  Elton, C. E.  Animal ecology.  Macmillan Co., New York, 209 p.  1935.




 8.  Ferguson, Denzel E.  The effects of pesticides on fish:  Changing




     patterns of specisation and distribution.  Iri James W. Gillett (The




     biological impact of pesticides on the environment) pp. 83-86.  1970.




 9.  Fowler, J. F., Newsom, L. D., Graves, J. B., Bonner, F. L. and




     Schilling, P. E.  Effect of dieldrin on egg hatchability, chick




     survival and eggshell thickness in purple and common gallinules.




     Bull, of Environmental Contamination and Toxocology, 6(6):495-501,




     1971.




10.  Grant, B. F. and Mehrle, P. M.  Chronic endrin poisoning in goldfish,




     Carassius auratus.  Journ. Fisheries Research Board of Canada, 27




     (12):2225-2232.  1970.




11.  Hatfield, C. T. and Anderson, J. M.  Effects of two insecticides on




     the vulnerability of Atlantic salmon (Salmo salar) Parr to brook




     trout (Salvelinus fontinalis) predation.  Journ. Fisheries Research




     Board of Canada, 29(l):27-29.




12.  Keith, J. 0., Hansen, R. M. and Ward, A. L.  Effect of 2,4-D on




     abundance and foods of pocket gophers.  Journ. Wildlife Management,




     23(2):137-145.  1959.




13.  Linhart, S. B., Crespo,  R. F. and Mitchell, G. C.  Control of vampire




     bats by topical application of an anticoagulant, chloropacinone.




     Boletin de la Oficina Sanitaria Panamaericana, 6(2):31-38.  1972.




14.  Murphy, D. A., and Korschgen, L. J.  Reproduction, growth and tissue




     residues of deer fed dieldrin.  Journ. Wildlife Mangement, 34(4):




     887-903.  1970.





                                  90

-------
15.  Neill, D. D., Muller, H.  D.  and Shutze,  J.  V.   Pesticide effects




     on the fecundity of the gray partridge.   Bull,  of Environmental




     Contamination and Toxicology, 6(6):546-551.  1971.




16.  Nobile, P. and Deedy, J.   The complete ecology fact book.  Anchor




     Books, Doubleday and Co., Inc., Garden City, N.Y., 472 p.  1972.




17.  Robinson, Weldon B.  Population changes of  varnivores in some coyote-




     control areas.  Journ. Mammalogy, 42(4):510-515.  1961.




18.  Schorger, A. W.  Introduction of the domestic pigeon.  AUK, 69(4):




     462-463.  1952.




19.  Scott, T. G., Willis, Y.  L.  and Ellis, J. A.  Some effects of a




     field application of dieldrin on wildlife.   Journ. Wildlife Manage-




     ment, 23(4):409-427.  1959.




20.  Trefethen, J. B.  The return of the white-tailed deer.  American




     Heritage, 21(2):97-103.  1970.




21.  VanGelder, G. A., Smith,  R.  M. and Buck, W. B.   Behavioral toxicology:




     Do toxicants alter behavior?  Iowa State Univ.  Veterinarian, 34(1):




     17-22.   1972.




22.  Webb, R. E. and Horsfall, F., Jr.  Endrin resistance in pine mouse.




     Science, 156(3783):1762.   1967.




23.  Webster, G.  Codfish, cats and civilization.  Doubleday and Co.,




     Inc.  (N.Y.) 263 p.  1959.
                                   91

-------
                HUMAN HEALTH ASPECTS OF PESTICIDES




                         Eldon P. Savage




                    Colorado State University






     Much of our current knowledge about the effects of pesticides in




man have been obtained from accidental poisoning cases, long term studies,




the use of volunteers and through the extrapolation of data from laboratory




animals to man.




     One of the major problems still encountered in studies of pesticides




on man is the measurement of the true dosage and exposure of man to pest-




icides.  The most important single item in considering the effects of




pesticides on man is the size of the dose of the compound.  No chemical




is entirely safe nor is any chemical entirely toxic.  For example, in




Binghampton, New York several infants died a few years ago when a person




mixing formula inadvertently mixed salt in the formula instead of sugar.




     Another important item is the toxicity of the compound.  Toxicities




are usually expressed as an LD,... value.  The LD,-,. value is a statistically




calculated value which estimates the best estimation of the dose required




to produce death in 50 percent of the animals (1).




     In addition to the dose and the toxicity of the pesticide, the in-




dividual susceptibility is important in the response, of the individual




to the pesticide exposure.  Factors involved in the individual's suscept-




ibility includes age, sex, nutritional state, general health, and hereditary




factors.  Most scientists agree that age is an important factor and that




the newborn and very young may not have some detoxification mechanisms




developed as well as they are in adults.  In spite of this general concept,




some authors have noted that microsomal enzymes involved in DDT metabolism
                                 93

-------
are probably fully functional at birth, but there are no direct studies




available to support this concept.




     In establishing LD   values in rats, it is generally assumed that




sex differences do occur in detoxification of some compounds.  Nutritional




status of the exposed individual is of importance in the individual sus-




ceptibility ot exposure.  The amount of body fat an individual has is




of importance in the storage of lipid soluable chemicals.  For example,




this is the main site of storage of important persistent chlorinated




hydrocarbon pesticides.  General health is also an important factor in




assessing individual variation to exposure to pesticides.  It has been




recognized for a number of years that chronic alcoholics are much more




susceptible to pesticides than non-alcoholics doing the same type of




work.  Since the liver is a main biotransformation site, individuals




suffering from any type of illness effecting the liver's function should




probably be considered more susceptible to illness from exposure to




pesticides than their healthy counterparts.  Thus, a person suffering




from disease state such as hepatitis is probably more susceptible to




pesticide exposure.  Another important factor in the individual's ability




to handle pesticide exposure may be due to heredity.  In some individuals




there may be hereditary defects in their ability to metabolize compounds.




As a result, an individual reaction to the exposure may occur.  Another




important factor in pesticide exposure is that of simultaneous exposure.




     Hayes noted several years ago that the vast majority of injuries




caused by pesticides involve straightforward poisoning usually associated




with gross carelessness (2).



     Most researchers agree that there are three types of intoxification.




Type 1 is an acute convulsive intoxification, resulting from one or a few
                                94

-------
gross overexposures.   This type of exposure usually tends to occur with




highly toxic and less persistent compounds.  Type 2 is accumulative in-




toxification caused from a number of smaller doses of an insecticide




with a lower acute toxicity, but causing an accumulative intoxification.




Type 3 is a combination of 1 and 2, where an acute intoxification is




superimposed upon a subclinical accumulative intoxification.




     Information of pesticide morbidity is not recorded as systematically




as mortality data.  Up to this time, the number of cases of non-fatal




poisonings have been estimated from the ratio of non-fatal to fatal cases




in special studies.  Severity of illness is the chief variable leading




to the very different estimates of the ration of non-fatal to fatal cases.




Some research personnel will count every report as a case, while other




investigators will count only cases of significant illness.




     In the United States, the mortality rate for pesticides has been




given as 1 per 1 million, and the ratio of fatal to non-fatal poisonings




has been expressed as 1 to 13 in one study and 1 to 75 in another study




(3,4).




     Pesticides may be either stored, detoxified, or excreted.  In the




past monitoring, long term studies and studies of occupational exposed




have been used to determine these storage levels.  Hayes studied volunteers




in a national monitoring program.  Studies have also been done on human




milk.  In a study in our laboratory, we found 100% of the people to store




DDE, the metabolite of DDT and only 20% stored PCB's.




     Much of our knowledge of pesticides have come through the study of




acute poisonings.




     Exposure of humans to chlorinated hydrocarbons can be estimated from




the storage level of the compounds or of their metabolites in adipose




tissue or in some cases, from excretion of biotransformation products





                                95

-------
in urine.  Exposure to the organophosphate compounds has been limited to




clinical symptomology and laboratory analysis of the.blood for depression




of the enzyme acetylcholinesterase.  Since all organophosphate insecticides




yield one to three of the six alkyl phosphate metabolites, urine has been




used recently to determine if the analysis of urinary alkyl phosphate




metabolites of organophosphates as a sensitive and accurate measure of




chronic and low level exposure.




     In the past, diseases that have been attributed to pesticides include




aplastic anemia and other blood dyscrasis.  It has also been suggested




that pesticides cause leukemia and renal dysfunction.




     Much information has come from studies of the occupationally exposed.




Allergies and skin dermatitis are reactions that have been observed.




This is an area that will probably also pay dividends in the future.




     In 1775, the British surgeon Percivall Pott, in a paper entitled,




"The Cancer of the Scrotum" realted the occurrence of cancer in chimney




sweeps caused by soot lodged in the crevices of the skin of male genitalia.




Approximately 150 years later, in 1918, the Japanese induced skin cancer




in rabbits by repeated painting of the inner surface of the earlobe with




tar.  Identification of cancer-porducing environmental agents is difficult




and many years elapse between exposure to a pollutant and the visible




signs of cancer.  Furthermore, the problem of establishing that the disease




has been caused by a particular pollutant is very complex.  For example,




the industrial chemical vinyl chloride was used for several years and was




usually considered to be relatively nontoxic.  The TLV for years was 5.00 ppm




and is now 2.00 ppm.  Once the material was considered as an anesthetic.




The 11 confirmed cases in the U.S. and the twelfth confirmed case in




England has harsh implications for thousands of workers for industry
                                96

-------
facing the immediate need to change production methods.   The B.  F.  Goodrich




plant in Louisville, Kentucky alerted by plant physicians,  informed




government officials that four liver angiosarcoma deaths had occured




among former employees involved in producing polyvinyl chloride from VC.




Further search showed five deaths and two workers with the  disease, but




still alive, at Louisville; three deaths at the Goodyear plant in Niagara




Falls, New York; and one death at the Union Carbide plant in South Charleston,




West Virginia.  In February, an Italian researcher presented results that




showed that VC produced angiosarcoma of the liver in rats at 250 ppm (7).




     Most of the people who have worked with pesticides recall that the




EPA and FDA asked manufacturers to volluntarily pull VC propelled products




from the nation's store shelves.  Recent animal studies have shown that mice




exposed to only 5.0 ppm of VC can develop angiosarcoma of the liver.  The




vinyl chloride experience may offer important leads for closer scrutiny




of pesticide industries.  The Federal Government will undoubtedly increase




their efforts to monitor industry and to conduct epidemiological studies




of the occupationally exposed, especially those working in  manufacturing




plants.  In addition, the centrifugal spread of disease around a manufactur-




ing area may take on new emphasis.  For years, researchers  have recognized




that people living in the areas along transportation routes away from plants,




homes of workers near plants, and those living near fallout from plumes from




certain type plants were subject to prolonged exposures of  the materials




in question.  People living in these areas may offer a rich source for




future investigation of chronic exposure to pesticides.




     In addition to occupationally exposed in manufacturing plants, the




migrant field worker may have the highest exposure to pesticides.
                                  97

-------
     Although much attention has been given to the health of migrant




field workers, comparatively little research has been done on the exposure




and potential effects of pesticides on these populations.  Because of




their mobile life style, migrant and seasonal field workers have not




generally been included in the long term study of occupationally exposed




workers conducted by the community studies on pesticides.  The life




expectancy of migrant field workers is believed to be about 46 years.




Studies done by our laboratory on the upper respiratory ailments of migrants




show significantly higher occurrence of these ailments than in matched




non-migrant counterparts.




     Recently, I have participated in three training activities to train




migrant leaders in environmental health.  In every migrant stream they are




familiar with strawberry itch and pesticide dermatitis.




     The problem of teratogenesis was brought to everyone's attention




following the publication of the studies on 2,4,5,-T and contaminant




dioxin.  Prior to this episode, this compound had been responsible for




production of chloracne in a number of workers involved in the synthesis




of 2,4,5-T.  The results of followup studies showed the increased incidence




of defects and fetal mortality in the rat to be entirely blamed on the




impurity dioxin.  Tests following the 2,4,5-T experiment showed Sevin,




Captan, Folpet and others to be teratogenic (8).




     To date, the health effects of pesticides on human health are not




clearly understood.  In the future, new and expanded research efforts




to determine the health aspects of pesticide useage on human health should




help to determine the short and long term effects, if any, that pesticides




may have on health of man.
                                98

-------
the health aspects of pesticide usage on human health should help to deter-

mine the short and long term effects, if any, that pesticides may have on

health of man.


                              References

1.  Hayes, W. J., Clinical Handbook on Economic Poisons, USDHEW-PHS, 144 pp.

2.  Hayes, W. J., Pesticides and Human Toxicity, Annals of the New York

    Academy of Sciences, Vol. 160, Article 1, pp. 40-54, June 23, 1969.
                             ;
3.  Hayes, W. J. and C. I. Pirkle.  Mortality From Pesticides in 1961.  Arch.

    Env. Health, Vol. 12, pp. 43-56, Jan. 1966.

4.  Hayes, W. J., Effect of Pesticides on Human Health, Science and Man
                                  £••
    Symposium.  Nature, Man and Pesticides, Washington, D.C., Aug. 20, 1963.

5.              , Report of the Secretary's Commission on Pesticides and

    Their Relationship to Human Health, USHEW, Dec. 1969.  Supt. Documents

    pp. 676.

6.  	, Environment, April 1974, Vol. 16, No. 3, 44 p.

7.  	, Environmental Health Perspectives.  Perspective on

    Chlorinated Dibenzodioxins and Dibenzofurans.  Exp. Issue No. 5,

    Sept. 1973, 313 p.
                                 99

-------
100

-------
       AN EPIDEMIOLOGICAL APPROACH TO PESTICIDE POISONING




                        Wilton A. Williams




           North Carolina Department of Human Resources






    Chemical pesticides have become ubiquitous in our society in recent




decades, yielding significant contributions to disease control, food and




fiber production, property protection, and personal comfort necessary to




sustain our standard of living.  However; because of their inherent toxic




properties, pesticides also possess the potential for adverse effects to




other non-target segments of the total environment including the poisoning




of man.




    Indeed, such events do occur as evidenced by the tremendous amount




of publicity, controversy, and concern over pesticides in recent years.




However, in many instances, adverse episodes are not adequately investigated




and factually documented, a practice that has led to erroneous conclusions




and ill-founded courses of action.




    In 1969, a Federally sponsored Pesticides Surveillance Program was




established in the State Health Department of North Carolina.  This program




is administered by and operates within the Epidemiology Section of the




agency.




    One may ask, why put a program dealing with pesticides in Epidemiology;




why not Sanitary Engineering, Environmental Health or Agriculture?




    Let's first take a look at what "epidemiology" means.  It has been




defined as "the study of the distribution and determinants of disease




frequency in man ."  Commonly thought of as applying only to large striking




outbreaks of diseases such as plague, cholera, typhoid, and yellow fever,




the concept of epidemiology has broadened and its principles are equally




useful in studying other maladies of man and his surroundings.





                               101

-------
    When the North Carolina pesticides project was initiated, little was
                        't

known about pesticide poisoning in our state.  Poison Control Center


statistics indicated that pesticide-associated illnesses and deaths were


occurring but detailed information of cases was non-existent.


    Following Federal guidelines for initial operation, the North Carolina


Pesticide Program's early activities were centered around air monitoring,


submitting autopsy tissue specimens for chlorinated hydrocarbon residue anal-


ysis, and reviewing existing legislation and regulations relevant to pesticide


control.  Over a five-year period, the program has expanded into an agressive


epidemiological attack on many health-related problems of pesticides.


    During the Spring of 1970, a human pesticide poisoning reporting system


was developed.  A form requiring only basic information is distributed


periodically to the State's hospitals, local health departments, and 1,700


of its practicing physicians.  Recipients are asked to voluntarily complete


and forward these report forms when pesticide cases occur.


    Since the Summer of 1970, over 550 cases of pesticide exposure have


been reported through this system.   The cards are used as access to detailed


investigation where indicated.
DH3 FORM >9S3 REV. 3-74 N. C. DepT OF HUMAN RESOURCES
PESTICIDES PESTICIDE CASE REPORT CARD
PATIENT'S
NAME LAST FIRST MIDDLE
ADDRESS:
ST. on RFD NO. CITY COUNTY
AGE OF SEX: Q MALE RACE: Q WHITE Q BLACK
PATIENT: [] FEMALE Q INDIAN Q OTHER
DATF o" li i N^RI r>N«?T: i**7. ,. , DAT o* RFPORT^ 107

CASE SEVERITY: HOSPITALIZED n YES ^ » •
n N CD TRE*TED IN ER n PHYSICIAN'* OFFICE
PpBTinnF P"nr>UCT lN"O'.VFn;

TYPE CASE: Q ACCIDENTAL INGESTION USAGE ACCIDENT! Q DOMESTIC rj OTHER
Q SUICIDE ATTEMPT [j AGRICULTURAL
REPORTED BY: ADDRESS:
ATTENDING PHYSICIAN (IF DIFFERENT FROM ABOVE)


•z.
p
3 fl
> B) CO
«. X-.
r ^^ Q
£ o "> o
1^3=!,
• r*
• o S, (o
wO = ^
0) 3 2
0 3 <
re °
w 8>
.0
W





o'

en
3
TO
3





                            102

-------
  PESTICIDE POISONING  INVESTIGATION REPORT
ame
ddress

arent
mployer_

ddress
 hysician_

 ddress
 ospital

 ddress
.gent  Involved

ormulator
:egistration Number_

:ommon Name
"•hemical  Name
'.hemical  Class
\ctive Ingredients	

'orm of_ Product:

    Bemulsifiable concentrate   Qdust
    liquid                     LJ granular
 Liwettable powder            U other
Source of_ Product:

     Purchased at
     Address
E
grocery store
rural general store
service station
hardware store
                           M
farm supply
pharmacy
variety store
other type store
                                                          DEPARTMENT OF HUMAN RESOURCES
                                                           DIVISION OF HEALTH SERVICES
                                                              EPIDEMIOLOGY  SECTION
                                                               PESTICIDES PROGRAM
                                                        Case  Number_

                                                        County	
                                                         Interviewer_

                                                         Date
                                                   Age
                                                   Weight
                                         Race:

                                      LJ  white
                                          black
                                          Indian
                                          other
                            Sex:

                           Dmale
                           CD female
                                                   Type of Pesticide:
                                                                 Insecticide
                                                                 Herbicide
                                                                 Nematocide
                                                                 Acaricide
                                                                 Fungicide
                                                                 Soil  Fumigant
                                                                 Growth Regulator
                                                                 Defoliant
                                                                 Desiccant
                                                                 Rodenticide
                                                                 Germicide
                                                   Type of_ Container:

                                                  L original  container; .labeled, numbered
                                                  L original  container; labeled, unnumbered
                                                  L original  container., unlabeled
                                                  LJ other container	

                                                  D paper            LI aerosol

                                                  Dmetal            D glass

                                                  D plastic

                                                   Area Agent Stored:
shed or barn
garage or carport
kitchen
closet
bathroom
other
DHS Form 2004 (5-74)

-------
 Type o£ Use;

L=  crop	
L  home garden
L=  household
LJ  greenhouse
LJ  governmental
1—1  farm buildings
    industrial
    institutional
    commercial pest control
                           Type of Accident:
                             agricultural
                             domestic
                             occupational
                             suicidal
                             homicidal
                             other
                       primary
                   Route of Exposure;
                      oral
                      dermal
                      inhalation
           Previous  Poisonings

              Hno
              yes  (explain
                   below)
 Symptoms:   Date and Hour of Onset
                                      (month)
                                                (date)
                               (hour)
D
abdominal pain
blurred vision
chest tightness/difficulty  breathing
diarrhea
headache
increased salivation
increased sweating
increased tearing
                                                    runny nose
                                                    1 ight-headed/dizzy/faint
                                                    muscle twitching or tremors
                                                    nausea/vomiting
                                                    weakness
                                                    slurred speech  .
                                                    other
 Signs (before treatment)

=J  coma
    convulsions
    constricted pupils
    dilated pupils
    fever
         (specify)


 Therapy:  Date and Hour Begun
                                    rash
                                    skin flushed
                                    skin pale
                                    cyanosis
                                    pulmonary edema
                                    other
                                                             Treatment:
                                none
                                physician's office
                                emergency room
                                hospitalized
B
                                                                          a
                                   (month)
                                                 (date)
                                  (hour)
                                               CdaysT

                                             a.m.
                                             p.m.
D
D
    none
    decontamination
    ernes is  or  lavage
    Atropine  (dose)_
    2-PAM  (dose)
                                                        Outcome:
other medication (specify!
Respiratory support (specify)_
Other (specify)	~
                                                       n
                                                           u
                           recovery
                           residual
                           fatality
 Laboratory  Analyses;
s
    none
    blood  ChE
blood residue_
urine	~
gastric	
 See Reverse for Case Summary
product 	
environment
tissue
radiologic
other
  Diagnostic  Complications:

  CZJnone
  Dmedication prior to
       illness  (explain)
    narcotics  (explain)
    intoxication
    other (explain)
                                            104

-------
    The usual sequence of events followed by our program is:




    (1)  Receive report of case either by a phone call from the physician




while the patient is under medical care or from the mailed-in case report




card.




    (2)  Contact the reporting physician by phone or personal visit to




obtain permission to interview his patient or the victim'.s family in




fatal cases.




    (3)  Obtain medical records of diagnosis and treatment from the




physician and the hospital involved.




    (4)  Personally interview the poisoning victim and/or knowledgeable




associates to document the circumstances of exposure, the pesticide involved,




and sequence of events from exposure through illness onset and resolution.




    (5)  Document by completing investigation forms  (see appended example




form)  and distributing them to concerned agencies such as the North Carolina




Agriculture Department, North Carolina State University, and the Pesticide




Accident Surveillance System of EPA.




    Why could we not just make the report card a little more detailed and




use it as documentation of the poisoning and eliminate the time, bother,




and expense of our field investigation and personal interviews?




    In 1973, we received reports of 162 human cases.  Through epidemiological




investigations, 128 of these were confirmed and documented.  Thirty-four




were concluded not to be legitimate pesticide cases.




Case 1




    E. S., adult male, was reported as hospitalized from poisoning by TEMIK,




an extremely tosic carbamate insecticide.  Investigation revealed that he




was indeed hospitalized with severe abdominal cramps and pain and had, on
                               105

-------
the day of illness onset been loading and applying TEMIK.  However, from




interview with his employer, it evolved that he was using granular TEMIK




in which the active compound is encapsulated in a coating that requires




moisture to be dissolved and released.  Others who worked with the patient,




including the farmer, stated the sick man's exposure was no different




from their own.  Other expected symptoms of carbamate poisoning such as




excessive secretions, pin-point pupils, chest tightness, and muscle in-




coordination were absent.  Further diagnostic efforts by the attending




physicians disclosed an intestinal block, completely disassociated from




the presticide exposure history, and corrective surgery was performed




accordingly.




    The reverse can also occur as in the following case example from our




files:




Case 2




    A 7-year-old girl was in a comatose state when admitted to the hospital.




She had experienced nausea and vomiting the evening before admission.




She was treated symptomatically.  After a restless evening, the patient




lost her ability to walk, complained of difficulty seeing, and became




progressively unresponsive.  Physical signs including miosis, rales in




both lung fields, and minimal response to painful stimuli.  While the




possibility of poisoning was considered, no history of exposure could be




obtained despite careful.questioning of her parents.  An immediate in-




spection of her home revealed a discarded 5-gallon drum collecting rainwater




in the backyard.  The label identified the original contents as Dasanit,




a potent organic phosphate insecticide.  Neighborhood children reported




that the girl had been making mud pies using a plastic bottle filled with
                                106

-------
water from the pesticide drum on the day she became ill.   She had sprayed




some of the water into her mouth.  Her diagnosis was confirmed by a




depressed blood cholinesterase level, and she had a dramatic clinical




response to atropine and 2-PAM.




    Both the foregoing cases indicate the value of epidemiologic support




in obtaining true incidence and cause.  Investigation of reported incidents




can become even more involved and revealing as in the following case:




Case 3




    J. H., 59-year-old male, died on September 1, 1973.  His death cer-




tificate listed cause of death as acute parathion poisoning, exposure




occurring while farming.  The local Medical Examiner's Report read:




"the decedent was working in a field and was exposed to Ethyl-Methyl




Parathion insecticide spray used to spray cotton from a helicopter."




The death was ruled accidental.




    When we investigated, sometime later, the vicitm's wife was interviewed




and told us an aerial pesticide applicator had sprayed her husband with




parathion as he stood in his garden adjacent to a cotton field.  He became




gravely ill and she carried him to the doctor 15 hours later.  Her story




seemed illogical.  We visited the local physician who stated he treated




the patient unsuccessfully for organophosphate poisoning following her




statement of his exposure and transferred him to a larger hospital.




Because of the described history, they also treated for parathion poisoning




with atropine.  Review of medical records indicated the patient did not




experience some of the classic organophosphate symptoms and made little




or no response to atropine therapy.  An interview with a neighbor indicated




domestic problems had occurred in the deceased's household.  We developed




a strong suspicion of foul play in the case and notified the State Chief
                                107

-------
Medical Examiner and the State Bureau of Investigation.  The victim's




body was exhumed and laboratory analysis indicated extremely high arsenic




levels.  Under questioning, the wife admitted poisoning her husband with




Singletary's Pest Control  (Arsenic Trioxide).  She is now confined in a




North Carolina prison.




    Thus, a reported and erroneously documented, accidental agriculturally-




oriented death proves to be still a pesticide case, but goes into the




correct category of an arsenical-product homicide statistic.




    The value of valid, reliable statistics achieved through thorough field




investigation is that problem areas can be accurately defined and workable




measures instituted in the public interest.  Epidemiological data we




have gathered has enabled us to publish monthly newsletters and poison




control notes which supply physicians with up-to-date information, in-




cluding treatment and advice about morbidity patterns which occur through-




out the state.  Our data has helped provide impetus for state legislation




creating tighter controls on pesticides.




    The North Carolina General Assembly has recognized that the area of




pesticides involves many viewpoints and has in its "Pesticide Law of 1971"




created a Regulatory Board and Technical Advisory Committee thereof




comprised of balanced representation from agricultural, health education,




environmental and industrial interests.  Members of our staff sit on




both these gorups responsible for regulating all aspects of pesticides




used in North Carolina.




    Under this arrangement and close, daily working relationships with




the North Carolina Department of Agriculture, North Carolina State University,




and EPA, we feel a reduction in adverse pesticide effects is already in




progress in our state.
                                 108

-------
    Two recent episodes episodes exemplify a cooperative effort toward




this goal:




Case 4




    L. Z., 51-year-old female, was working in a tobacco plant bed "pulling"




plants for the field setting of tobacco.  About mid-morning,  she went




to her employer's truck nearby for a drink of water.   A jug of pesticide




was mistaken for water, she drank a small swallow of  it and was pronounced




dead approximately 9,hours later despite vigorous medical efforts to




save her.




    Upon immediate investigation, we discovered the material was Vydate-L




(oxymyl) a new highly toxic carbamate insecticide-nematocide by DuPont.




It had been marketed recently in two forms:  a clear  liquid under an




experimental label and an amber liquid under full EPA registration, both




packaged in one-gallon transparent plastic containers.  While still in




the field investigating this case, we collaborated extensively with the




North Carolina Department of Agriculture and the manufacturer regarding




the product, its registration, and marketing status.   An emergency meeting




was held the following day with representatives from our office, the




North Carolina Department of Agriculture, and DuPont.  The case was dis-




cussed and as a result, DuPont representatives collected all the remaining




clear form of the product from our state within 48 hours.




    Two weeks later:




Case 5




    V. R., 74-year-old male, while working transplanting tobacco, went




to the supply trailer for a drink of water.  Possessing rather poor




eyesight, he picked up a jug of the amber-colored Vydate in a container
                                    109

-------
very similar to a familiar one he had gotten water from previously,




poured some of the liquid into a smaller drinking vessel and drank a




swallow of it before recognizing the mistake.  Within ten minutes, he was




unconscious with acute carbamate poisoning.  After vigorous medical treat-




ment by alerted physicians, this victim survived.




    Following investigation of this case, another meeting between our




staff and the North Carolina Department of Agriculture terminated in a




conclusion that, because of use circumstances, the product in its current




form and packaging presented extreme hazard.  DuPont was contacted and




voluntarily agreed to completely recall the product immediately.




    We are now in the process in North Carolina of approaching epidemiolog-




ically other non-human pesticide adverse effects such as animal, wildlife,




and fish kills, water and other environmental substrate contamination and




crop damage.  This will hopefully be accomplished by inter-agency cooperation




of our Department, North Carolina Department of Agriculture, North Carolina




Department of Natural and Economic Resources, the Extension Service of




North Carolina State University, and EPA.  Case access reporting systems




will be established for these incidents modeled after our human poisoning




system.  Training of field personnel in the agencies mentioned is planned




to insure reliable investigation and documentation of all incidents.




    Once these systems are in full effect, our Pesticide Board will be




afforded necessary knowledge to completely regulate pesticides in the best




interests of the people of our state, knowledge epidemiologically gained




that "is" rather than "appears to be."
                                  110

-------
                    OCCUPATIONAL PNEUMOCONIOSIS




                         Bobby J. Gunter




       National Institute for Occupational Safety and Health






    At the present time there is no universal definition of pneumoconiosis.




For convenience I will refer to pneumoconiosis as any disease of the




respiratory system caused by inhalation of either a dust or fiber.  Not




all dust produces pneumoconiosis.  A large number of dust are inert and




are .easily removed by the various defense mechanisms of the respiratory




tract.  The physical and biological factors that are responsible for a




particle being deposited in the lungs include size, density, biological




reactivity, and the physical shape, of the human lung where the particle




is deposited.  Usually particles less than 3 microns in diameter reach




the alveoli.  A majority of these particles are less than 1 micron.  When




these particles are deposited in the lungs, they are moved out of the lungs




by celia until they reach the terminal air spaces in the lungs; and here




many of the dust particles are englufed by mast cells and phagocyte cells




which engulf them and deposit them in the lymphatic system.  During the




passage through the upper respiratory tract to the final deposition of




these particles in the lymphatic system, it is possible for many occupational




diseases to occur.




    Three types of pneumoconioses which have received most attention £rom




the occupational health viewpoint are:




    (1) Silicosis




    (2) Coal miners pneumoconiosis (Black Lung)




    (3) Asbestosis




    There are many other chemical and physical agents which produce




pneumoconiosis such as beryllium, cotton dust, and iron oxide.






                             Ill

-------
Silicosis




    Silicosis has been an occupational health problem in the mining




industry throughout its history.  Exposure to free silica is world wide.




It is found in everything from sand blasting operations to monument




engraving.  The response of the lungs to free silica is reflected by




the size of the respired free silica.  It is believed that the lungs'




response to particles ranging from 0.2 to 5 microns is characterized




radiographically by silicotic nodules throughout the lungs.  Silicosis




may occur very rapidly, depending upon the dust concentration and the




percentage of free silica in the dust.  Disabling silicosis can occur in




a 2-3 year period.  Exposure to free silica has been decreased by employing




wet techniques to rock quarry operations and proper ventilation of under-




ground mining operations.  Glove box sand blasting operations are often




times responsible for a worker receiving a high exposure of free silica.




Substitution of aluminum oxide for sand has eliminated the potential for




free silica exposure in many operations.




    Prevention is particularly important in the case of silicosis, since




there is no therapeutic treatment for the pulmonary lesions caused by




silicosis.




Coal Miners Pneumoconiosis (Black Lung)




    Coal miners pneumoconiosis may be simply defined as the occupational




disease caused by retention of coal dust in the lung.  Coal miners




pneumoconiosis exists in two forms—simple and complicated.  Complicated




is often referred to as a progressive, massive fibrosis of the lung tissue.




    In 1969, the Federal Coal Mine Health and Safety Act was passed to




eliminate Black Lung and to compensate workers who had been disabled from




Black Lung.  As a result of this Act, many coal miners have been compensated;
                             112

-------
and work conditions in underground coal mines have been greatly improved.




In many aspects, coal miners pneumoconiosis is very similar to silicosis,




since coal dust is infiltrated with large quantities of free silica.




Roof bolters in coal mines have a high percentage of silicosis, since




their job is screwing bolts into the coal mine roof and thus exposing




them to high levels of silica.




     Prevention of coal miners pneumoconiosis is the only effective




preventive measure, since there is no therapy (1).




Asbestosis




     The epidemiology of asbestos exposure has been under investigation




by numerous organizations over a period of fifty years.  The specific




diseases associated with asbestos exposure are asbestosis (a form of




fibrosis of the lung), cancers of the bronchi, pleura, and peritoneum.




Asbestos corns on the hands and forearms also occur frequently.  Clubbing




of the fingers is also evident among asbestos workers.




     Bronchial cancer caused by exposure to asbestos was discovered




in the 1930's and was found among textile workers.  It was also observed




that asbestos textile workers who smoked has a much higher incidence




of mesothelial tumors.  Mesothelioma is a diffuse cancer spreading




over the entire surface of the lung and is found occasionally in the




peritoneum.  Cigarette smoking has not been found to be a contributing




factor to mesotheliomas.  Asbestos exposure does seem to increase the




incidence of mesothelioma.




     An occuptional standard of 2 fibers per cc greater than 5 microns




in length was put into effect on July 1, 1974.  At this concentration




a worker should not contract asbestosis or any other disease associated




with asbestos.
                            113

-------
    Those persons responsible for evaluation and control of industrial




environments that produce respiratory injury should have (1) knowledge




of the anatomy of the respiratory system; (2) an understanding of the




factors governing entry, deposition, removal, and retention of gases and




particulates entering the respiratory system; and (3) some knowledge of




how respiratory tissue reacts to physical and chemical irritants.




    Two additional concepts of the action of particulates deposited on




the surface of the lung should be understood:




    (1) Residence time, which can either be minutes or hours, during




which the biological effects leading to chronic bronchitis and cancer




could be initiated (2).




    (2)  The second concept is combined exposure.  An example of this




would be an inert or biologically inactive particle combining with a




harmful agent in depositing it in the lung such as an alpha particle




deposited in the lungs from an inert dust particle.






                            References






1.  Occupational Health and Safety, Volume 1.  International Labor Office,




    Geneva, pages 307-309.




2.  The Industrial Environment - Its Evaluation and Control.  NIOSH, p.




    495, 1974.
                             114

-------
          ENVIRONMENTAL CHEMICALS OF CONTEMPORARY INTEREST




                          Frank S. Lisella




            Department of Health, Education and Welfare




                     Center for Disease Control






     During the past ten years, considerable public attention has been




focused upon the concerns associated with the dissemination of chemicals




throughout our environment.  Many of these concerns have been vocalized




by the younger segment of our society because these individuals are among




the first persons to be raised in an era which has witnessed significant




reductions in the prevalence of many communicable diseases.  Marked improve-




ments, for example, have been noted in the control of tuberculosis, diph-




theria, typhoid fever, and many of the vector-borne diseases.  These im-




provements were, to a large measure, associated with the use of various




types of a chemical product, either as medicinal agents or as pesticides.




Advances such as those noted and a plethora of others in our society have




created a paradox for the scientist.  He is confronted with the almost




formidable task of developing products to meet societal demands and then




ascertaining that the products will not adversely effect man, animals, or




the environment.




     Today humans are exposed to an astounding array of chemical compounds




in the home or on the farm.  These include drugs; cosmetics; fertilizers;




antibiotics; vitamins; pesticides; cleaning, polishing, and disinfecting




agents; alcohol; gasoline; solvents; thinners; and other materials, to mention




a few.  There are reported to be more than 250,000 chemical products which




are capable of causing human illness, death, or contamination to wildlife




and the environment.  An estimated 40,000-50,000 new potentially poisonous




chemical products enter the market place each year.






                               115

-------
     This discussion will be concerned with two environmental toxicants




namely, carbon monoxide and lead-based paints.           '







                          CARBON MONOXIDE




     While there are many poisonous gases that are likely to have a




deleterious effect on man and animals, carbon monoxide (CO) is the most




widely encountered.  The gas is colorless, odorless, tasteless, and non-




irritating, and results from the incomplete combustion of organic matter.




The gas may result whenever a flame touches a surface that is cooler than




the ignition temperature of the gaseous part of the flame (1).  Fuel fired




clothes dryers, water heaters, gas and coal space heaters can be significant




cources of carbon monoxide if they are not vented effectively.  Many appli-




ances such as gas heaters, although they may be properly adjusted when




installed, may become hazardous sources of carbon monoxide if not properly




maintained.




     External to the home environment, automobile exhaust gas in garages is




probably the most familiar source of carbon monoxide exposure.  Additional




concern has been shown with respect of the use of "catalytic" heaters in




tents and camping vehicles as potential producers of this agent.  In the




occupational environment, potential sources of the chemical occur in opera-




tions conducted near furnaces, ovens, stoves, forges, kilns, and other areas.






Toxic Properties




     Carbon monoxide is absorbed only through the lungs and its toxicity




is due to the fact that it combines with hemoglobin to form carboxyhemoglobin




(COHb).  Hemoglobin in this form is unavailable for the transport of oxygen.




Hemoglobin combines with the same amount of CO as it does with Oxygen, and
                                116

-------
both gases react with the same group in the hemoglobin molecule (2).   Up




to the point where CO enters the red blood cell, however, its behavior




differs sharply because its affinity for hemoglobin is approximately 210




times as great as that of oxygen.  Thus, in the presence of CO alone, the




blood takes up 210 times as much CO per unit of partial pressure (3).




Death is likely to occur when the blood is saturated with 60-80 percent




carboxyhemoglobin.  If the poisoned individual is rendered unconscious and




survives, damage to the brain, central nervous system, and circulatory




system may occur.  A presumptive diagnosis of acute CO poisoning is often




made on the basis of the circumstances under which the victim is found and




his appearance.  Since COHb is bright red in color> the victim typically




has a "cherry-red cyanosis" accompanied by bright red coloration of the




fingernails and mucous membrances.  Confirmation of the diagnosis is made




on the demonstration of COHb in the blood.




     In the absence of environmental exposure to carbon monoxide, endogenous




production of the gas by heme catabolism is sufficient to produce COHb levels




in the range of 0.3 to 0.7 percent.




     The level in pregnant women is typically higher than that found in other




segments of the population.  The level of 2 percent COHb is one at which




no medical risk, or limitation of activity of function, is anticipated.  In




the range between 2.6 and 5 percent COHb, some investigators have found




evidence for encroachment on the functional reserve of the heart and brain,




without permanent damage.  Impaired myocardial function in patients with




coronary artery disease appears to be the most important finding at this




time.  Subtle changes of mental function have been suggested but need addi-




tional investigation.  Above 5 percent COHb the changes of body functions




appear to be definite and undesirable (4);
                                117

-------
     Evidence regarding long-term low-level exposure to the agent and its

impact on human health is conflicting.  This is particularly true with

regard to the assoication between carbon monoxide and various types of

cardiovascular disease (4).  The question of significant changes in mental

function produced by carboxyhemoglobin is equally controversial.  Investigators

have been unable to corroborate some of the studies which purported to

demonstrate a relationship between the performance of cognitive tasks and

carbon monoxide exposure.  Others failed to demonstrate any decrement in

tracking tests, eye-hand coordination tests, or reaciton time tests and
   i
elevated carboxyhemoglobin levels.  It has been suggested that maternal

carboxyhemoglobin levels between 3 and 10 percent correlate with an increased

incidence of fetal and perinatal morbidity (4).  With regard to manual

coordination, exposures producing carboxyhemoglobin saturation greater

than 15 to 20 percent resulted in delayed headaches, changes in visual

evoked response, and impairments of manual coordination (5).



Existing Environmental Standards

     Several agencies have been confronted with the difficulties associated

with the development of standards for carbon monoxide.  The National In-

stitute for Occupational Safety and Health has proposed a limit of 35 PPM

for an 8-hour exposure in the occupational environment.  The Environmental

Protection Agency, under provisions of the Clean Air Act, promulgated national

primary and secondary air quality standards on April 30, 1971.  These

standards are:

     (A)   10 milligrams per cubic meter (9 PPM) maximum 8-hour concentration

          not to be exceeded more than once per year.

     (B)   40 milligrams per cubic meter (35 PPM) maximum 1-hour concentration

          not to be exceeded more than once per year.


                                118

-------
     Attempts to establish standards such as those indicated above are




fraught with technical difficulties.  Efforts must be directed toward




ascribing long-term, low-level exposure to the development of specific




sequelae.







Morbidity and Mortality




     In 1969 (the latest year for which data is available) the National




Center for Health Statistics reported 1,482 deaths as the result of an




accidental exposure to carbon monoxide.  An additional 2,041 deaths were




reported to have been suicidal in origin.




     Morbidity from carbon monoxide, like illness associated with any chemical




agent, is difficult to estimate because of the lack of uniform reporting




procedures.  However, it has been stated in several reports that approx-




imately 10,000 individuals are made ill annually because of exposure to




this agent (6).  On the basis of the available data, as many as 100,000




to 2,500,000 persons may be potentially at risk from the hazards associated




with carbon monoxide, primarily because they reside in a deteriorating




or dilapidated housing unit, most likely to have defective heating facil-




ities.  Of special concern in the risk categories are infants, the aged,




infirm persons, and individuals with coronary heart disease, smokers,




pregnant women, and persons with anemia or respiratory conditions and




also individuals residing at high altitudes.




     The insidious nature of carbon monoxide requires that health and




housing personnel maintain constant vigilance with regard to the detection




of this agent in the environment.  Educational measures must be instituted




during the fall and winter months to alert the public to the potential




hazards assoicated with this chemical.
                                119

-------
                                LEAD




     Emphasis by many public officials today is directed toward the




 resolution of problems associated with the distribution of this heavy




 metal in  the environment.  Lead occurs naturally in the earth's crust




 and is also found in the atmosphere due to airborne dust and to gases




 diffusing from the earth's crust (7).  Contamination of the soil and




 vegetation from airborne deposits of lead is a funciton of vehicular




 traffic volume.  Only a small portion of the lead released from vehicle




 emissions actually settles or accumulates in the vicinity of roadways.




 The majority of the chemical is transported by atmospheric currents and




 ultimately settles on the soil and foilage.  Lead which has been extracted




 from surface waters has been attributed to gasoline.  This may subsequently




 result in the accumulation of the metal in the tissues of fish.




     The  use of lead in paints and the potential poisoning problems




 assoicated with this practice provided the thrust for Congress to pass




 the Lead-Based Paint Poisoning Prevention Act in 1971.  This legislation,




 among other provisions, authorizes grants for the detection and treatment




 of children with elevated blood lead levels.  Further, allowances are




made for  the elimination of lead-based paint in housing units.




     At present, 42 projects are being supported in 23 states and the




District  of Columbia through the Childhood Lead Poisoning Control program




at the Center for Disease Control (Table 1).  The emphasis in these projects




 is on the detection of children with elevated blood lead levels and follow-




up and referral activities as appropriate.  Each of the projects is expected




to secure local funds and assistance from local agencies to insure the




proper treatment of poisoned children and the reduction of hazards associated




with deteriorating dwellings.
                                 120

-------
Table 1.  Location of Funded Lead Projects, United States, 1974



California (Los Angeles County, Sacramento)



Colorado (Denver)



Connecticut (Hartford)



Delaware (Wilmington)



District of Columbia



Georgia (Savannah)



Illinois (Chicago, Peoria, Rockford, Springfield)



Iowa (Burlington, Des Moines)



Louisiana (New Orleans)



Maryland (Baltimore)



Massachusetts (Boston, Chelsea, Lowell, Sommerville, Waltham)



Michigan (Detroit)



Missouri (St. Louis)



New Jersey (Hoboken, Newark)



New York (Albany Co., Erie Co., New York City, Onondaga County)



Ohio (Cincinnati, Cleveland, Toledo)



Oklahoma (Tulsa)



Oregon  (Portland)



Pennsylvania  (Allegheny Co., Philadelphia)



South Carolina (Charleston, Greenville)



Tennessee (Chattanooga, Nashville)



Texas (Houston)



Virginia (Norfolk)



Wisconsin (Milwaukee)                    „          .„  0
          v                              Summary:  42  Grantees


                                                   42  Communities
                                                    23  States  and  District

                                                       of  Columbia
                                 121

-------
     Since the program began in June 1972, a total of 479,013 children




in the project areas have been screened at least once.  Overall, 9.7




percent of these children (46,271) have been confirmed as having elevated




blood lead levels (>40 ugm) (8).  Of those children screened, 7,466 (1.6




percent) have received chelation therapy.




     This data is to be compared with the best estimates of the extent




of the problem:  2.5 million children ages 1-6 years at risk, 600,000




with elevated blood lead levels, 125,000 with lead poisoning, 6,000 with




neurological damage and 200 deaths per year (8).




     Overall, 42,050 housing units have been inspected for lead-based




paint in this program.  Sixty-four percent of those units were positive




for lead-based paint, and hazard reduction has been achieved in 60 per-




cent of the positive units.   Hazard identification in housing is usually




by XRF analyzer, and occasionally by chemical laboratory analysis.  How-




ever, the XRF analyzer does not reliably detect lead concentrations below




2 mg/cm2, which still may pose a health hazard to children.






Research Activities




     At the present time, the following research projects are being




supported in this program area:




     1.   Free Erythrocyte Protoporphyrin (FEP) Analysis.  Results of this




         micro blood test reflect the toxic effects of lead on hemoglobin




         synthesis.   Thus,  it tends to select children who have physiologic




         changes from lead,  is less subject to contamination, and fluctua-




         tion than blood lead levels and may be cheaper than blood lead




         determinations.
                                 122

-------
     2.  The absorption, retention, and effects of different lead compounds




         in animals are being investigated.   Included in these studies




         are the effects of dietary factors  such as the ratios of carbo-




         hydrates, fats, and protein on lead absorption.




     3.  The criteria and methodology for the self-evaluation of grant




         programs are being developed and tested in two project cities.




         Elements to be evaluated include screening, followup, educational




         and laboratory capacities which are Internal to the program,




         as well as relevant external factors such as population mobility




         and changes in housing characteristics.  Baseline and resurvey




         prevalence rates of lead-based paint poisoning and undue lead




         exposure in children 1-6 years will be examined to determine




         their relationship to the impact of those external and internal




         factors.




     While some emergency treatment and hazard reduction activities are




conducted directly under project auspices, other community resources are




mobilized and encouraged to undertake specific corrective procedures.




The elimination of poisonings assoicated with lead-based paint is predicated




upon the successful blending of casefinding  efforts, abatement .of hazardous.




conditions, and adequate housing code enforcement at the local1level.






                             References




1.  Patty, Frank A.  Industrial Hygiene and  Toxicology.  Volume II.




    Interscience Publishers, p. 924-936, 1963.




2.  Goodman, Louis S. and Gilman, Alfred.  The Pharmacological Basis of,




    Therapeutics, 3rd Edition, the Macmillan Co., N. Y., p. 915, 1965.




3.  Ruch, Theodore C. and Patton, Harry 0.  Physiology and Biophysics,




    19th Edition, W. B. Saunders Co., Philadelphia, p. 774-776, 1966.





                                 123

-------
4..  DuBois, Arthur B. e_t auL.  Report to the Bureau of Community Environ-




    mental Management on Carbon Monoxide, (unpublished report), June




    26, 1973.




5.  Stewart, Richard D.; Peterson, Jack E.; Baretta, Edward D.; Bachand,




    Romeo T.; Hosko, Michael J.; and Herrmann, Anthony A.  Experimental




    exposure to carbon monoxide.  Archives of Environmental Health,




    Vol. 21, 1970.




6.  Lehr, E. L.  Better Standards for Home Heating Needed.  96th Annual




    Meeting of the American Public Health Association.  Editorial summary




    in Public Health Reports, Vol. 84, p. 286, March 1969.




7.  Hardy, H. et al.  Lead as an environmental poison.  Clinical Pharmacology




    and Therapeutics.  Vol. 12, p. 982-1002, November 1971.




8.  Hopkins, Donald R.  Briefing on lead-based paint poisoning prevention




    activities of the Department of Health, Education and Welfare.  (un-




    published report).  Environmental Health Services Division, CDC,




    Atlanta, Georgia, May 1974.
                                 124

-------
             PESTICIDE RESIDUES IN LAUNDERED CLOTHING




 J. W. Southwick, H. D. Mecham, P. M. Cannon and M.  J.  Gortatowski




                  Utah State Division of Health






Example of Hazard in Pesticide Contaminated Clothing




    A 70 year old white male was admitted July 10, 1972, to a Salt Lake




City hospital.  He had been spraying fruit trees and a backyard garden




for about two hours on July 10 using four-pound-per-gallon parathion




liquid concentrate in a spray unit that attached to the garden hose.




    His clothing included long sleeved shirt, bib overalls, and goggles,




but no respirator.  Apparently, he sprayed the trees while the wind was




blowing and became saturated with the mixture.  While wearing the same




clothing, he prepared supper and ate.  After getting ready for bed he




became extremely weak and diaphoretic.  He vomited and was then taken




to the hospital at 9:40 P.M.




    At the emergency room he was very weak, disoriented, with muscle




twitching.  Atropine (4 mg IV) and Protopam (1.0 gram IV) were given




with good clinical response; he became oriented, pulse went from 88 to




140, and pupils became dilated.  Laboratory values revealed hypocholin-




esterase:  0.6 units (normal 2.5 - 6.5).  Liver and renal function along




with the CBC (hematocrit and WBC) were essentially normal.  A portable




chest x-ray was normal, and the EGG revealed many multifocal PVC's.




    The patient gradually improved.  At 2:QO A.M. on July 11, 1972, Protopam




(500 mg IV) was again given and Atropine (0.8 mg IV, approximately Q6H).




He continued to feel stronger and wanted to go home.  He was discharged




at 9:30 A.M., July 12, 1972.




    At home he continued to improve, and he even began doing some light




work in the backyard.  An office visit to his doctor on July 18, six days






                               125

-------
after leaving the hospital, indicated good progress.  Except for mild




nervousness, the patient had no complaints.  His blood pressure was 200/100.




    On July 28, 1972, the patient worked in a basement room panneling a




wall.  He wore the same bib overalls that had been previously soaked with




the parathion spray and subsequently laundered.  He developed nausea and




vomited.  He went to bed but was restless and unable to sleep.  At 6:00




A.M. the following morning (July 29) we was unconscious and had vomited




in bed.  He was taken directly to a hospital emergency room.  Upon arrival




he was still comatose; blood pressure was 130/90, pulse 92, pupils pinpoint;




he had marked diaphoresis with copious secretions.




    X-rays confirmed the suspicion of aspiration pneumonia.  EGG showed




atrial fibrillation with multiple PVC's; laboratory values revealed acidosis




with serum pH 7.11 (normal 7.4), mild dehydration, leukocytosis, and a




cholinesterase of only 0.013 units (normal 2.5 - 6.5).




    He showed minimal improvement with IV fluid, Protopam (1.0 gram IVx2),




Digoxin (0.5 mg IV), Decadron (4 mg IV), and NaHC03 (4.4 mEq IV).  Despite




this vigorous treatment, the patient had cardio-pulmonary failure and




expired July 29, 1972, at approximately 10:30 A.M.




    The pathologist concluded that the patient's primary cause of death




was due to organophosphate poisoning because of the history of exposure




to parathion, the severely depressed cholinesterase levels, and the




absence of other pathology.  Laboratory analysis of the bib overalls




showed a large residual (about 2,500 ppm) of parathion remaining, despite




previous laundering.   This finding of an exceptionally high parathion




level in the laundered overalls suggested that sufficient parathion could




have been absorbed through the skin from the overalls to bring about the




second cholinesterase depression,  which contributed to his death.
                               126

-------
Levels of Contamination in Clothing




    When we obtained the man's overalls they had the appearance of  a




freshly laundered garment.  They may have been laundered twice, but at




least once, in an automatic washer with detergent.   They were dried




by hanging on an outdoor clothesline.




    The contaminated overalls were laundered with other old work clothes.




Other samples of his clothing were obtained and analyzed for pesticide




residues.  Table 1 shows that parathion contaminated these clothes  also




but to a lesser degree.  The contamination may have come from association




in laundering with the sprayed clothes.




    Table 1.  Pesticide contamination of clothes associated with an




              organophosphate poisoning death (in parts per million)







                  Clothes                        Parathion





              Bib overalls worn while spraying      2,552




              Pooled sample of 3 other pants          377




              Pooled sample of 2 pair underwear       324





    Concern about the hazard of pesticide contaminated clothing caused




us to "spot check" clothing worn by pest control operators.  We obtained




a set of work coveralls from each of three pest control operators.   Each




of the coveralls were cut apart at the mid seam, one half was laundered,




and the other half was kept as a control.  The extracts from the laundered




and unlaundered halves were analyzed for pesticide residues.




    Table 2 shows that about half of the chlorinated hydrocarbon residues




were removed by laundering.  The organophosphates (dursban and diazinon)




seemed to be removed somewhat more by laundering than were the chlorinated




hydrocarbons.
                               127

-------
    Table 2.  Pesticide residues (in parts per million) found in spray




              clothing of pest control operators both before and after




              the clothes were laundered.

Total DDT
Aldrin
Dieldrin
a Chlordane
Diazinon
Dursban
Effects of
PCO
Before
8.77
44.62
.85
7.04
.79
11.43
Laundering
#1
After
5.69
23.08
.56
3.24
—
5.43

PCO
Before
90.14
.62
12.16
14.86
.60
472.44

n
After
37.90
1.05
9.94
7.42
—
5.64

PCO
Before
67.39
6.74
10.37
7.77
47.25
—

#3
After
38.68
2.77
5.16
4.26
5.46


    Experiments were conducted to evaluate the effectiveness of laundering




to remove parathion contamination from clothing.  Several square foot




samples of new denim were treated with parathion.  Several untreated




pieces of denim were also used as controls in the experiment.




    A denim square treated with concentrated parathion measured 20,740




ppm parathion before washing.  A similarly contaminated square of denim




was laundered together with a noncontaminated square of denim using A.11




as the detergent in an automatic washer.




    After laundering, the contaminated piece still contained 4,273 ppm




parathion and the noncontaminated piece contained 633 ppm of parathion.




About four-fifths of the parathion was removed in the laundering process.




In addition, the noncontaminated denim picked up parathion from the wash




waters.  Hot water from the wash cycle contained 43 ppm parathion and




the rinse water contained about 11 ppm.
                                128

-------
    In a second experiment, dilute parathion was used to treat two more




denim squares; one contained 3,646 ppm without laundering,  the other




contained 1,723 ppm after laundering.




    Again a noncontaminated piece of denim was included in the laundering




process.  This time it picked up 153 ppm parathion from the wash water.




Only about one-half the parathion was removed in the laundering process,




and the uncontaminated piece picked up substantial parathion.




    The above findings are similar to those observed in the circumstances




surrounding the death of the 70 year old man.  Ordinary laundering of




parathion contaminated clothing with detergent may not remove sufficient




parathion to make them safe to wear.




Comparisons^ of Laundry Methods




    A technique has been developed to evaluate the effectiveness of removing




pesticide contaminants from clothing by laundering.  Cotton denim squares,




which simulated pesticide user's work clothing, were uniformly treated




with a solution of a radioisotope and nonlabeled parathion.  The radio-




isotope acted as a marker for determining uniform application of pesticide




to cloth.




    Denim squares were air dried, counted for radioisotope content,




laundered, and then analyzed for parathion residue retention.  Laundering




involved four methods:  (1) water wash, (2) bleach, (3) cationic detergent,




and (4) anionic detergent.  As a control, pesticide treated but unlaundered




denim was analyzed.




    Thus far two groups of cloths have been processed.  The first group




was laundered in several washing machines at a laundromat.   Since the




variation between washing machines was too great, the second group was
                                129

-------
laundered in the laboratory using flasks and a shaker to simulate the




machine washing.




    Results from both groups of cloth indicated that after laundering




with either anionic or cationic detergents, less than 50 percent of the




parathion was removed.  The bleaching agent, however, was more effective




in decreasing the concentration of parathion retained in denim (see Table 3).




    Table 3.  Preliminary comparison of laundry methods testing the




              effectiveness of parathion removal from cotton denim.
Laundry method
Control
(no washing)
Laundered Control
(water only)
Bleach
Cationic Detergent
Anionic Detergent
Percentage
Laundromat
Washing Machines
0%
53%
81%
14%
27%
of parathion removed
Laboratory Simulation
of Washing Machine
0%
28%
95%
15%
49%
    These preliminary observations indicate the need for further investigation.




Summary and Conclusions




    Substantial evidence indicated that laundered but, nonetheless, parathion




contaminated clothing contributed to the death of a 70 year old man who




had been previously treated with Atropine and 2-PAM for organophosphate




(parathion) poisoning.  This example of an insidious fatal exposure to




parathion shows the need to evaluate the efficacy of various laundering




methods for decontamination of clothing used ,in pesticide spraying.
                                130

-------
    Experimentation indicates that potentially hazardous amounts of




parathion can persist in clothing after laundering with detergent.   Bleach




was more effective in decreasing parathion residual in contaminated cloths.




    Additional experimentation is planned to evaluate other laundering




methods, various types of pesticide contamination, and a variety of




fabrics commonly used in work clothing.
                                131

-------
132

-------
A COMPARATIVE STUDY OF CHOLINESTERASE VALUES AND URINARY ALKYL PHOSPHATE




 EXCRETION LEVELS FROM ORGANOPHOSPHATE EXPOSED AND NON-EXPOSED MALES




                 Herbert Starr and Sara Borthick




                    Colorado State University






Background




     The determination of cholinesterase (ChE) depression has been




used as an index for evaluating the extent of acute exposure and for




monitoring chronic exposure to organophosphate compounds for a number




of years.  Although this method has the advantage of being a rapid




procedure requiring a relatively modest equipment investment, it has




the following disadvantages:




     1.  Since the range of normal values is wide, a baseline or pre-




         exposure level of activity should be established for each




         invidivual for comparison with future assays.




     2.  ChE values give no information about the causative agent other




         than its ability to inhibit cholinesterase.  This could be a




         serious disadvantage in cases of poisoning by an unkwnown compound.




     3.  Low to moderate OP exposure may not produce a significant decrease




         in ChE activity.




     4.  The test requires a blood sample.




     Current test methods allow for the separation and quantification




of a variety of dialkyl phosphates, the metabolites and urinary hydrolysis




products of OP compounds, in human urine.  The gas chromatographic analysis




has the following advantages:  detects lower OP exposure levels than




those resulting in ChE depression (1); indicates the general class of




OP compound involved; does not require a blood sample; and, is not




dependent on pre-established values.
                                133

-------
     A study was conducted to evaluate these two methods in terms of




ability to identify an OP exposed individual or group.




Methods and Procedure




     The study population included both a highly-exposed group and an




occupationally non-exposed group from the general population.




     The exposed study population consisted of 16 males who were employed




by a chemical company operating three formulating plants in Greeley,




Colorado.  Table 1 shows the production and chemical class of products




formulated by each of the plants.  One of the formulators worked year-




round at Plant 1; the rest of the men worked primarily at Plant 2 with




the exception of 2 men who, during the summer months, worked at Plant 3.




The length of employment of the study group ranged from 2 months to 10




years with an average time of 3 years.  Ages ranged from the early twenties




to the late fifties with a median age of 33 years.




     Blood and urine samples were collected at random times throughout




the two-year period resulting in as many as 9 sets of data on some of




the men and as few as 2 sets of data on the 2 men who had only been




employed 2 months.




     The non-exposed group consisted of a group of 57 men who were not




occupationally exposed to pesticides.  From 1 to 3 sets of data were




collected on each of these men during the same two-year time period.




Data from this group were used to establish a normal range for ChE




activity and to indicate background levels of alkyl phosphate excretion




for Colorado males.




     ChE activity was determined by the pH Stat method using acetyl-




choline iodide as the substrate (2).  Measurements were made with a




Radiometer Titrator, Titrigraph and syringe buret.  Random urine samples,




collected at the same time as the blood samples, were assayed for alkyl






                                134

-------
Table 1.  Chemical Class of Pesticide Products Formulated by Three Plants

          of a Chemical Company in Greeley, Colorado 1973.
Plant
                                     Products formulated
Organophosphates    Chlorinated Hydrocarbons  Other
No. 1

No. 2
No. 3
Co-Ral

Thimet


Di-Syston


Dasanit

Parathion


Malathion

Parathion

Malathion
Bladex
Toxaphene

2,4-D

Thiodan

Chlordane

Endrin
Polyram
(carbamate)

Zineb
(carbamate)

Dipel
(microbial product
of B. Thuring-
inensis)
                                135

-------
Table 2.  Date and Plant Activity for Test  Periods  in Fig.  2A and  2B
Test Period




     1




     2




     3




     4




     5




     6




     7




     8




     9
     Date




Jan. 31, 1972




June 7, 1972




Oct. 13, 1972




Dec. 6, 1972




Jan. 25, 1973




March 19, 1973




March 27, 1973




July 19, 1973




Aug. 3, 1973
   Plant Activity




Formulating Thimet




Formulating Thimet




Slack Period




Slack Period




Formulating Dasanit




Formulating Thimet




Formulating Thimet




Drum Washing




Drum Washing
                                136

-------
          A
     7.0
   E 5.0
   c
  I
  2 3.0
  o
     1.0-
•* * *Artl(jl*«*«*»*«*«*»*«*«*«<

KI>/   iMi>'(ini(
-------
phosphates by a modified gas chromatographic method utilizing a flame




photometric detector  (2).  The procedure permits the quantitation of




6 major metabolites and hydrolysis products of organophosphorus pesticides.




Results and Discussion




     Statistical analysis indicated that the distribution of non-exposed




sample values for plasma and RBC ChE did not differ significantly from




that of normal distribution.  Based on the assumption of a normal frequency




distribution, a two-sided tolerance interval was constructed.  At the




95% confidence level, 95% of the male population would fall within the




following limits:




             Plasma ChE 	 2.26  -  6.80 micromoles/min./ml.




             RBC ChE    	 8.73  - 17.29 micromoles/min./ml.




     Mean excretion levels (ppm) of the non-exposed group for each of the




six metabolites were:




             o,o-dimethyl phosphate (DMP)	< .01




             o,o-diethyl phosphate. (DEP)	01




             o,o-dimethyl phosphorothionate (DMTP)	01




             o,o-diethyl phosphorothionate (DETP)	< .01




             o,o-dimethyl phosphorodiothionate (DMDTP)	01




             o,o-diethyl phosphorodithionate (DEDTP)	00




     Data from the Human Monitoring Program (3) indicate that general




population levels of these six metabolites are not significantly different




from the non-exposed study group.




     Figures 1A and IB show plasma ChE and total urinary metabolites




(i.e.  DEP + DMP + DEDT + DMTP + DEDTP + DMDTP) for each of 9 men sampled




during January, 1973.  Di-Syston and Thimet were being formulated at




that time.  The wide range of normal activity of plasma ChE can be seen,




and although 6 of the 9 men have ChE values below the mean, none are






                                 138

-------
below  the lower range of normal.  Without pre-exposure levels for com-




parison  it would be impossible to say if any one of these men was exposed




.to OP  compounds.  By contrast, in Figure IB, 8 of the 9 men had a total




urinary  metabolite  (TUM) excretion level highly elevated from the mean




of the non-exposed group.




     Figures  2A and 2B show respectively plasma ChE and TUM excretion




for one  man tested 9 times over an 18 month time period.  Table 3 lists




the dates and plant activities for each of the test periods.  The rise




in plasma ChE parallels the decrease in TUM excretion during the slack




period 3 and  4.  It is interesting to note that even during the slack




periods  when  plasma ChE activity is at its .peak, excretion of DEP is




moderately elevated indicating continuing low-level OP exposure.  The




excretion pattern and levels  (ppm) for test periods 3 and 4 were as




follows:




     Test Period     DMP    DEP    DMTP    DETP   DMDTP    DEDTP




       3            .03    .11     0       .02     .03      0




       4            .01    .11     .02     .06   <.01      0




     The significant drop in  plasma ChE and the dramatic rise in TUM




excretion levels during test  periods 7 and 8 are evidence of increased




exposure associated with the  drum washing procedure.  The drums contained




concentrated  liquid OP chemicals used for the various formulations.




Disposal regulations require  these containers to be washed and crushed.




Even though most of this operation was carried out in the open air out-




side the plant, the drum washing procedure provided a significant source




of exposure.




     Figure 2A also illustrates the need for determining a pre-exposure




level  of ChE  activity.  Since all values are within the normal range,
                                 139

-------
           A
      7.0
   E  5.0-
   \
   c
   1
   "o
   E
      1.0-
                    i • • • • # i
234567
          Test  Period
                                                             89
           B
      1.4
      1.0
   E
   a
   a
      0.6
     0.2
           OIIIIIIIIIBIIIBIIIIIIIIIIIDIIIIIIIIllIllllllBllliBlQIllllllBllliailBIIIllllllllEimiDII
                             3     4      56
                                Test Period
                                      3     9
Figure  2.   Plasma  ChE values  (A)  and total urinary metabolite excretion
            levels  (B) for one OP  exposed man who was sampled 9 times
            over a  20  month time period.

            Plasma  CKE tolerance interval X'X
            Mean uiaa
                                  140

-------
any single value would be of little help in assessing this man's exposure




to OP compounds.




     Data from 10 of the exposed men who had been sampled at least 5




different times were analyzed individually to see if there was any




correlation between plasma ChE, RBC ChE and total urinary metabolites.




Recognizing the small sample size, the analyses suggest a negative




correlation between plasma ChE and RBC ChE, and a negative correlation




between plasma ChE and total urinary metabolites.  No pattern of cor-




relation could be established between RBC ChE and total urinary metabolites.




     Results of this study indicate that determination of urinary alkyl




phosphates may be an excellent tool for assessing body burden of OP




compounds and for identifying OP exposed groups and individuals in




either acute or chronic exposure situations.




References




1.  Shafik, M. T., D. Bradway and H. F. Enos.  A Cleanup Procedure for




    the Determination of Low Levels of Alkyl Phosphates, Thiophosphates,




    and Dithiophosphates in Rat and Human Urine.  Ag. and Food Chem.




    19:885-889, 1971.




2.  Thompson, J. F., ed.  Analysis of Pesticide Residues in Human and




    Environmental Samples.  Primate and Pesticides Effects Laboratory,




    EPA, Perrine, Florida, Sec 6A, 1972.




3.  Colorado Community Study on Pesticides, Colorado Department of Health,




    Quarterly and Annual Report No. 35, Jan. 25, 1974.
                               141

-------
142

-------
          ASSESSING THE ENVIRONMENTAL IMPACT OF CHEMICALS




        G. U. Ulrikson, Anna S. Hammons and James Edward Huff




                    Oak Ridge National Laboratory







Introduction




    As more and more chemicals are introduced into the environment by




both industry and the general public, the need for evaluating the overall




effects of these chemicals becomes increasingly important.  New chemicals




are sometimes hurriedly released for consumer use before sufficient time




has elapsed for thorough longterm toxicity testing.  Oftentimes we dis-




cover belatedly that old familiar chemicals we have used for years, with




caution but without worry, are in actuality serious health hazards.




Reasons for this can be numerous but, in general, are primarily because of




increasing residue buildup or bioaccumulation.  Some recent examples are




the "sudden scares"connected with the use of DDT, mercury, asbestos, and




 vinyl chloride.




    The overwhelming volume of data generated on chemicals and their




resultant effects on man and his environment necessitate easy access to




an efficient system for gathering and disseminating specific information.




This need is particularly great for persons involved in assessing data




from a multidisciplinary view—for example, chemical and physical prop-




erties, environmental effects, and toxicology.




    The Environmental Information System Office (EISO), a part of the




Information Division of the Oak Ridge National Laboratory (ORNL), has




developed an information search and retrieval program that Is service-




oriented to individual requestor needs.  EISO also provides data eval-




uation and subsequent reviews and state-of-the-art documents.
                               143

-------
    The primary.functions of EISO are to develop and correlate information




activities of environmental research projects currently underway at ORNL,




and to systemize operations for maximum responsiveness to its funding




agencies and user community.






EISO Component Center .Functions




    There are several information centers within EISO, each with individual




responsibilities but interacting to provide a wider range of information




analysis and synthesis for an overall more balanced and effective system.




Organization of information centers within EISO and the overall structure




is demonstrated in Figure 1.  Funding and core support emanate from a multi-




agency base.




    Most of the biomedically-dependent activities reside in the Biomedical




Sciences Section (BIOSCI):




      -  The Biomedical Studies Group (BMS) is engaged primarily in data




         extraction and analysis, specialized data base building, and




         preparing annotated literature collections and state-of-the-art




         reviews.




      -  The Environmental Mutagen Information Center (EMIC) maintains an




         updated literature and data bank containing 15,000 records on




         chemically-induced mutations; each record comprises multiple




         entries — complete bibliographic reference, chemical agent,




         Chemical Abstracts Registry Number, taxonomic organism, test




         object, and author's comments.




      -  The Toxicology Information Response Center (TIRC) prepares in-depth




         literature searches, using computerized data bases and extensive
                               144

-------
                                                                              ORNL-DWG 74-7156
                             I ENVIRONMENTAL INFORMATION SYSTEM OFFICE |
BIOMEDICAL SCIENCES
SECTION

^^Vl
t^mm

BIOMEDICAL
STUDIES
GROUP

ENVIRONMENTAL
MUTAGEN
INFORMATION
CENTER

TOXICOLOGY
INFORMATION
RESPONSE



ECOLOGICAL AND
ENVIRONMENTAL SCIENCES


Wl
mum

TOXIC
MATERIALS
INFORMATION
CENTER

ENVIRONMENTAL
RESPONSE AND
REFERRAL
SERVICES GROUP

ECOLOGICAL
SCIENCES
CENTER
                                           PHYSICAL AND
                                           CHEMICAL SCIENCES
                                         SOCIAL AND
                                         ECONOMIC SCIENCES
                                                ENERGY
                                                INFORMATION
                                                CENTER
INFORMATION STORAGE
        AND
RETRIEVAL PROCESSES
                                                ENERGY
                                                R AND D
                                                INVENTORY
                                              REGIONAL AND
                                              URBAN STUDIES
                                              TECHNICAL
                                              INFORMATION
                                              CENTER
     DOCUMENT
     ACQUISITION
     AND
     CONTROL
                                                                   DATA
                                                                   PROCESSING
                                                                   CENTER
                                                                                         PRODUCTION
INFORMATION
CENTER
                   F1g. 1.  Environmental Information System Office  Organization

-------
         library facilities:; answers specific toxi.cological questions




         (about 500 requests per year) posed by the scientific community,




         government agencies, industry, and others; and publishes topical




         bibliographies.




    The. Ecological and Environmental Sciences Section is concerned mainly




with the impact of technology on the environment:




      -  The Toxic Materials Information Center (TMIC) collects, stores,




         and disseminates pertinent information on materials in^the environ-




         ment, with particular emphasis on metals and organometallic com-




         pounds.  The NSF-RANN Trace Contaminants Abstracts and newsletter




         covering the activities of the nationwide Trace Contaminants




         Program of NSF and the indexed directory to all NSF-RANN Trace




         Contaminants Program participants are periodic publications of




         this center.




         The Environmental Response and Referral Service Group (ERRS) responds




         to requests for environmental information from all sources all




         over the world.  This group also provides information services      '




         to ORNL research teams engaged in preparing environmental impact




         statements for nuclear power plants; in establishing various




         environmentally oriented Forest Service data bases; maintains a




         computerized record of all documents ordered for ORNL's environ-




         mental scientists; maintains a small but selective environmentally-




         oriented resource center with, for example, a complete set of




         environmental impact statements for all nuclear power plants;




         maintains a directory of technical environmental specialists and




         centers by location, telephone numbers, discipline, training, and
                               146

-------
interest; and prepares state-of-the-art or generic documents as required.




      -  The Ecological Sciences Information Center (ESIC)  provides information




         support to ecological research sponsored by AEC's Division of




         Biomedical and Environmental Research, to ORNL's Environmental




         Sciences Division, and to other institutions by establishing com-




         puterized information files on selected Topics such as bioenviron-




         mental aspects of uranium, neptunium, and other transplutonic




         elements; radioecology; and thermal effects.




    EISO information activities in the area of physical and chemical sciences




center on the Energy Information Center and the Energy Research and Develop-




ment Inventory:




      -  The Energy Information Center (EIC)  serves as a nucleus for the emerging




         energy information complex at ORNL.   This energy data base now




         includes 2,800 bibliographic entries, covering such topics as:




         conservation, supply and demand studies, economic studies, fore-




         casting, policy, electric power generation, transmission and dis-




         tribution, environmental effects of energy and energy uses.




         The Energy Research and Development Inventory  (ERDI) data base and pub-




         lication surveys government agencies, academic institutions, private




         industry, and other sponsored research.  The scope of research




         projects of interest include:  (1) all types of energy sources -




         fossil fuels, nuclear, hydro-electric, solar, geothermal, tidal,




         wind, wood, plant, animal materials, and waste products; (2)




         electric power - generation, transmission, distribution, and




         storage; and  (3) energy uses - residential, commercial, industrial,




         transportation, agricultural, and specialized applications.
                               147

-------
     The Social and Economic Sciences Section is composed of the Regional


and Urban Studies Technical Information Center (RUSTIC):


     -1  RUSTIC is an experimental program organized to provide data services


        to local, regional, and state governments.   RUSTIC represents an

                                                                        'i
        effort On the part of the Department of Housing and Urban Develop-


        ment to determine the degree to which a technical data service center


        can respond to state, regional, and local information needs and


        difficulties.


        All information storage and retrieval processes are performed by


        a centralized data processing and computer production group working


        in conjunction with the Computer Sciences Division.


        The Data Processing Center is responsible for the input of biblio-


        graphic, abstract, index, numeric, questionnaire, and other forms


        of data.


     -  The Computer Production Group (COMPRO) has the responsibility for


        job submission and follow-up as well as other activities involved


        in the computer job aspects of data management, publication and


        indices production, searches, and other information areas required by


        EISO and several other ORNL groups.


Information Sources


Bibliographies, Directories, and Inventories


     The most valuable sources of information for the research investigator


and science administrator are listed in Table 1.  A good  beginning for the


selection of available literature sources is always with  bibliographic


references.  However, the researcher or administrator interested in inter-


disciplinary data is hampered by the single objectiveness of most biblio-


graphic services.  Chemical Abstracts (1) and Biological  Abstracts (2) are
                                148

-------
Table 1.  Environmental Information Needs
     Bibliographic References

     Annotated and Keyworded Literature Collections

     Directories and Inventories of Current Researchers and
        Research Projects

     Factual Information

     Numerical Data

     Assessment of Information


excellent examples of disciplinary sources.  As a result, complete literature

coverage of multifaceted problems, including most environmental concerns,

involves extensive time and effort to scan several bibliographic references

and select relevant material.

     EISO has ready access to many computer searchable bulk data bases containing

bibliographic information related to chemicals and their behavior.  Most of

these are illustrated in Tables 2 and 3.  The MEDLINE and TOXLINE data bases

are accessible through the National Library of Medicine (NLM).

     The most expedient way for an investigator to gather specific information    '<

from these data bases is to discuss requirements with a resident information

scientist; with full understanding of the needs of the requester the specialist

can search pertinent data bases for sepcific information through strategical

keywording.  The information retrieved can then be repackaged into an inter-

disciplinary data base considerably more beneficial to the user.

     Journal listings selected from bibliographic references lead the searcher

to areas of relevant published material, enabling him/her to provide the user

with specific documents and special order bibliographies.  Sources not in-

cluded in these data bases are frequently manually searched.
                                149

-------
                  TABLfc, 2  v-UMKjrERl/LtD AND MANUALLY-SEARCHABLE
                          .   INFORMATION SOURCES AVAILABLE TO EISO
                               ORNL-Produced On-Lintf Data Sources
   Ecological  Sciences Information Center*
   Ecosystems  Analysis Data Base*
   Energy Dora Base*
   Environmental Law Abstracts*
   Environmental Mutagtsn Information Center*
   Environmental Plutonium Data Base*
   IBP Data Base*
   Liquid Waste Data Base**
      (Urban Technology)
   Materials Resource* and Cycling*
   Mercury Data Base*
                                        11.   Nuclear Safety Information Center
                                        12.   Radiation Shielding Information Center
                                        13.   Radionuclide Cycling — Soils and Plants*
                                        14.   Regional Modeling *
                                        15.   Regional Systems Information Center*
                                        16.   Solid Waste Data Base*
                                        17.   Thermal Effects Data Base*
                                        18.   Toxic Materials  Information  Center*
                                        19.   Toxicology Information Response Center*
I.   Accelerator Information Center
2.   Charged Particle-Cross Section Data Center
3.   Controlled Fusion Atomic Data Center
        ORNL-Produced Non-Computerized Data Sources

                                         4.   Criticaliry Data- Center
                                         5.   Health Physics Information Center
                                         6.   Research Materials Information Center
                               Non-ORNL Computerized Data Sources
a.
b.
c.
d.
e.
f.
g.
h.
                                                           First Count, File A , all states
                                                           First Count, File B, all states
                                                           Second Count, File A, all states
                                                           Second Count, File B, all states
                                                           Geographic Area Code Index (GAG)
                                                           Master Enumeration District List
                                                                               in a
                                                                 ICO)
1.  Analytical Methodology Information Center,
2.  Biological Abstracts**
3.  oioResearch Index**
4.  CA-Condenvates, Chemical Abstracts**
5.  Cea-ius and Social Science Data**
        1970 Census of Population and Housing:
        1970 Census of Population and Housing:
        1970 Census of Population and Housing:
        1970 Census of Population and Housing:
        1970 Census of Population and Housing:
        1970 Census of Population and Housing:
        Extended with Coordinates (MED-X)
        1970 Census of Population and Housing:  Master Area Tract Identification
        Latitude and Longitude Descriptive Array (MATILDA)
     i.  I960 Census of Population and Housing:  Public Use Sample  (1
     j.  1960 Census of Population and Housing:  Tracted areas, all states
     k.  Continuous Work History Sample of the Social Security Administration:
         LEED, 1957-1966                                      .        -
     I.  1962 City-County Data
     m. 1967 City-County Data
     n.  1964 County Business Pcttsrro
     o.  1967 County Business Patterns
     p.   1969 County Business Patterns
     a.  Migrcuion matrix of the 509 Stats Economic Areas
 6.  Chemical-Biological Sections,   Chemical Abstracts**
 7.  Government Research Announcements**
 8.  MEDLINE (National Library of Medicine)**
 9.  MetoIs Abstracts**
10.  Name-Match System, Chemical  Abstracts**                    .
11.  Nuclear Science Abstracts (USAEC, RECON system)**
12.  Searchable Physics Information Notices (SPIN)**
                                                                                       1%
    *EISO-affiliated, on ORLOOK (on-line "Oak Ridge look")
   **Machine readible on demand at ORNL    .      150

-------
                                            ORNL-DWG  74-7157
Table 3.
DATA BASES AVAILABLE FOR SEARCHING AT ORNL
Data Base
BA (Biological Abstracts)
BRI (Bio-Research Index)
CAE (Chemical Condensates -
Even Issues) \
CAIN (Catalog and Indexing
System)
CAO (Chemical Condensates -
Odd Issues)
CBAC (Chemical -Biological
Activity
MEDLINE (National Library •
of Medicine)
NSA (Nuclear Science
Abstracts)
SPIN (Searchable Physics '
Information Notices)
TOXLINE (National Library
of Medicine)
USG (Government Reports
Date of
Coverage
Jan.
Jan.
Nov.
1970
Dec.
Jan.
Jan.
Aug.
June
Jan.-
Jan.
1971
1971
1972
1972
1971
1970
1971
1970
1965
1972
Approximate
Total No. of
Records Thru
April 1974
484,230
315,600
240,720
513,720
183,500
90,000
800,000
176,000
156,000
350,000
130,000
   Announcements)
                         151

-------
      Other useful sources of information supplied by information centers




are up-to-date directories of people and places involved in research




projects in the area of interest.  The EISO computerized directory in-




cludes names and addresses and other identifying notations of approxi-




mately 20,000 people engaged in environmental, toxicological, and peri-




pheral research.




      A number of inventory files listing current research projects are




available including the Environmental Protection Research Catalog (3),




Summaries of USAEC Environmental Research and Development (4), and two




ETSO files - the Inventory of Current Energy Research and Development (5)




and the NSF-RANN Trace Contaminants Abstracts (6).  A number of topical




files are built and maintained for ready access—chlorinated dibenzo-p-




dioxins and chlorinated dibenzofurans, asbestos, mercury, cadmium, lead,




and others.




Handbooks—Factual and Numerical Data                                       I




      Available handbooks such as the CRC Handbook of Chemistry and Physics




(7), and the Biology Data Book (8) are single objective data references—




valuable but time-consuming sources for review and evaluation of inter-




disciplinary problems.




      EISO prepares specialized handbooks of factual and numerical informa-




tion based on data descriptors such as those shown in Figure 2.  Each




horizontal line of blocks represents a set ot table of specific information;




the blocks in each line denote column headings.  The titles and column




headings or data elements are selected after thorough discussions between




the user and the information specialist.  These discussions determine the




type of information gathered, the extent of literature coverage, and the




format adopted (Table 4) .
                                  152

-------
                                                                                                                                                                               ORNL DWG 74-5738
SUBSTANCE IDENTIFICATION
SUBSTANCE
COMMON NAME
CHEMICAL NAME
SYNONYMS
NATURAL
OCCURRENCES
DISCOVERER
MOLECULAR
WEIGHT
MOLECULAR
FORMULA
ENVIRONMENTAL PROTECTION
AGENCY REGISTRY NUMBER
CHEMICAL ABSTRACTS
REGISTRY NUMBER
WISWESSEB
LINE - FORMULA
NOTATION
COMMENTS
CHEMICAL AND PHYSICAL PROPERTIES
SUBSTANCE
FORM
COLOR
TASTE ODOR
FLAMMABILITY
VAPOR PRESSURE
MELTING POINT
BOILING POINT
SPECIFIC GRAVITY
SOLUBILITY
EXPLOSIVITY STABILITY
ANALYTICAL METHODS
COMMENTS
HAZARDOUS DATA
SUBSTANCE
FIRE AND EXPLOSION
HAZARDS
LIFE HAZARD
PERSONAL PROTECTION
FIRE FIGHTING PHASES
USUAL SHIPPING CONTAINERS
STORAGE
SOURCE
COMMENTS
PRODUCTION/APPLICATIONS
SUBSTANCE
TRADE NAME
MANUFACTURER LOCATION
ANNUAL PRODUCTION
COMMON USES
FORMULATION
TARGET ORGANISMS
MODE OF ACTION
METHOD OF APPLICATION
SOURCE
COMMENTS
EXISTING CRITERIA LEVELS
SUBSTANCE
ORGANISM
ENVIRONMENTAL
PROTECTION AGENCY
NATIONAL ACADEMY
OF SCIENCES
NATIONAL TECHNICAL ADVISORY
COMMITTEE TO THE SECRETARY
OF THE INTERIOR. 1968
NATIONAL INSTITUTE OF
OCCUPATIONAL SAFETY
AND HEALTH
AMERICAN CONFERENCE
OF GOVERNMENTAL
INDUSTRIAL HYGIENISTS
AMERICAN INDUSTRIAL
HYGIENE ASSOCIATION
WATER QUALITY
CRITERIA
COMMENTS
HUMAN TOXICITY
SUBSTANCE
STUDY TYPE
SEX AGE '.'.'EIGHT
PREPARATION OF DOSE
ROUTE OF ADMINISTRATION
VALUE
DURATION .OF EXPERIMENT
EFFECTS
SOURCE
COMMENTS
CLINICAL OBSERVATIONS
SUBSTANCE
INTAKE
EXCRETION
DISTRIBUTION
ACUTE
INCIDENCE
ACUTE SIGNS AND
SYMPTOMS
ACUTE
TREATMENT
LETHAL DOSE
CHRONIC
INCIDENCE
CHRONIC SIGNS AND
SYMPTOMS
CHRONIC
TREATMENT
DIAGNOSIS
CLINICAL TOXICOLOGY OF
COMMERCIAL PRODUCTS - TOXICITY
RATING
SOURCE
OCCUPATIONAL HAZARDS
SUBSTANCE
OCCUPATION
PRECAUTIONS
INHALATION TOXICITY
DERVAL PENETRATION
DISPOSAL METHODS
THRESHOLD LIMIT VALUE
SOURCE
COMMENTS
PATHOCENICITY
SUBSTANCE
SPECIES
TREATVENT CONDITIONS
EFFECTS
SOURCE
COMMENTS
TOXICITY TO MAMMALS
SUBSTANCE
STUDY TYPE
SPECIES
STRAIN
SEX AGE '.'.EIGHT
PREPARATION
OF DOSE
ROUTS
VALUE
DURATION OF
EXPERIMENT
EFFECTS
SOURCE
COMMENTS
                                                       Figure  2.     Biomedical and Environmental Handbook
                                                                                       DATABASE FILE

-------
                                                                                                                                                                                OBNL OWG 74-5790
    CARCINOGENICITY
SUBSTANCE
ORGANISM
STRAIN
SEX AGE '.'.'EIGHT
PREPARATION
OF DOSE
ROUTE
PATHOLOGICAL EXAMINATION
LEVEL
ANIMALS WITH
TUMORS
EFFECTS
SURVIVAL
DURATION OF
EXPERIMENT
SOURCE
COMMENTS
    TERATOGENICITY
SUBSTANCE
ORGANISM
STRAIN
SEX AGE WEIGHT
PREPARATION
OF DOSE
ROUTE
EFFECTS
AUTHOR'S COMMENTS
SOURCE
     MUTAGENICITY
SUBSTANCE
ORGANISM
STRAIN
SEX AGE WEIGHT
ASSAY
TREATMENT
DOSE
CONCENTRATION
DOSE TIME
DOSE
TEMPERATURE
BIOLOGICAL
EFFECT
AUTHOR'S COMMENTS
SOURCE
     BIOLOGICAL ACTIVITY
SUBSTANCE
ORGANISM
STRAIN
SEX AGE WEIGHT
TREATMENT
CONDITIONS
BIOCONCENTRATION
TISSUE
ACCUMULATION
ELIMINATION
HALF LIFE
METABOLISM
EFFECTS
TOTAL BODY
BURDEN
SYNERGISTIC
EFFECTS
SOURCE
COMMENTS
     AQUATIC TOXICITY
Ul
SUBSTANCE
STUDY TYPE
SPECIES
VARIETY
TREATMENT
VALUE
DURATION OF
EXPERIMENT
EFFECTS
SOURCE
COMMENTS
     PHYTOTOXICITY
SUBSTANCE
STUDY TYPE
SPECIES
TREATMENT
DURATION OF
EXPERIMENT
EFFECTS
SOURCE
COMMENTS
     ENVIRONMENTAL MONITORING AND HAZARDS
SUBSTANCE
EMISSION SOURCE FORM
MOBILITY
SUSCEPTIBLE GROUPS IN
RECEPTOR POPULATION
UBIQUITY
PERSISTENCE
DEGRADATION
ACCUMULATION
COLLECTION METHOD TIME
SOURCE
COMMENTS
     ENVIRONMENTAL STANDARDS
SUBSTANCE
AIR AVBIENT
AIR EMISSION
XVATER GENERAL
WATER EFFLUENT
WATER DRINKING
SOURCE
COMMENTS
                                                          Figure  2.
Biomedical and Environmental  Handbook
             DATA BASE FILE

-------
    The data bases may be generated in a tabular format for easy and rapid

information comparison (see Figure 3).

    Current plans are for incorporation of all similar data.files into the

more general Biomedical and Environmental Handbook.  This will ultimately

establish a large integrated data base encompassing numerous areas of study

and including current recommended criteria and established standards for

the presence of certain chemicals in various environmental media.
Table 4.  Sequential Development of the Biomedical and Environmental
          Data Base File.
       Selection of:

         1.  key field descriptors,

         2.  specific data elements,

         3.  agents or compounds of current interest and concern
             for data base inclusion,

         4.  a core listing of secondary source documents,

         5.  current primary research literature,

         6.  proper computer input, display, and output features,

         7.  data from these sources for analysis and computerization,

         8.  tabular display for easy and rapid data comparison,

         9.  data base subsets for publication.



Data Extraction

    Literature coverage for search request and data extraction is partially

accomplished by computer scanning profiles of the bibliographic data bases

mentioned earlier.  Manual scanning is required of bibliographic tools not

available in these data files.  Relevant articles are then selected for

preparation of a specialized bibliographic data base with an author and
                                 155

-------
KISS
150 ppa in  drinking  vatec
for 6 nonths
1.0 rg of cadaiun sulfate  3
tines-a voek foe S sooths.
(2-3 oq Cd/kq body vcight).
Subcutaneous injections.

10, SO,- and  300 ppa in
drinking water.
160 fpa is drinkioq vatec
Bean exposure of 15.5 ag
Cd/kg body veight per day
for $ aonths.
 Daily doses of 5 and 20 ig
 of C4 per rabbit - In valet
 for cne year.
 10  ffj in drinking vatcr
 for  one  jc.ir.
                                        E?F£CTS
                             Bronchopnouaonia resultinq in
                             death 5 days after tho
                             accident. Bed h?pati:jtion of
                             the loner lobas of both lnnqr.
                             and »irkcd fatty degeneration
                             of the li»er.
Sabendocacdial hemorrhage and
fibcosis vith sutiepicic J ill
petechiae and ayocarJial
perivisculjr aono^uclear
infiltration.  The treataent
va's fatal in one of the three
cases.

•Cn-stroint-ostical catarrh.
TiiSney deqenoratioa, edeaa,
polynenritis, liver
cirrhosis, bon« aarrov injury
and exfoliate deraatitis.

Liver depletion of collaqen,
increases in caloplis-ic
reticulua, iaflasaatory cell
infiltrates  in portal rcqions
and biliary  Kyperpla'sia.

Proteinuris  appeared after
one aonth.   Gloaer'ilar and
tubular  lesioas aft«r one
soath.  -

5inor chanq'js ia the kidneys
»ere noticed after 6 to 12
veeks in th? 10 ppa qroap.
Hfter 10 vfieks sliqht but
obvious  chaajes vern se^n,
such as  svollen aitochoadria
and vacuoles contaiaiaq call
debris.  At  high dose levels
obvious  cbanqes v»re r.oted
after 6  to 12 veeks an4
pronounced ai tocton-jrial
changes  after 24-UO v«o'. 1.1
                                                             « (101)
                                                             p. 27
                                                             56
• (101)
p.  as
» (101)
p.  81
• (901)
p.  80
o. 81
•(HOI)
p. R5
• (101)
p. 85
                                                                                 CO.»..1»S73
          The liver vjs found to
          contain 3.0 p;i of arsenic
          tcioxldc, the hiir 3.0 p?a,
          and the urine present in  the
          bladder 3.5 p?:.  Th° higher
          llvf-r content vis interpreted
          as absorption over a period
          of tine, proSjblj through the
          ckin.

          ?vo patients reqcesssl
          coincid-entall y vi'h clinical
          recovery sugqsslinq an acute
          pharsacologic cardiac Insult.
                                                                       SISS
HISS
HISS
HISS
          xrss
           NISS
 The  diet  in  these anisals va:
 lov  in  calci'ji.  Vhether the?
 bone changes vete 4u-> to tht?
 changes in renal function or
 du»  to  an effect of ctJaiua
 oo "intoATinal  a'isirptlori" of
 calciua is not  kaovn.
                              (SE1T PAGi)
  Figure  3.    Example  of Tabular  Data  Display
                              156

-------
keyworded index or for acquisition for data extraction to be used in hand-




books, reviews, or eventual state-of-the-art documents.   Other sources,




such as available handbooks and textbooks, are also collected and reviewed




for possible data extraction.




    The selection of sources and information is necessarily based on the




needs of the user, which are discussed with the information specialist




before searches are begun.  Some users specify their preference of sources




to be searched.




State-of-the-Art




    Factual data base files and repackaged specialized bibliographic files




are passed on to the user for evaluation; however, we can and do play a




direct role in assessing the data collected.




    In preparing reviews and state-of-the-art documents we cover the liter-




ature as previously described—through planned search and retrieval strategy—




and select relevant material for acquisition and review.  An annotated




and keyworded specialized bibliographic data file is usually completed




before data is gleaned for state-of-the-art documents.  This serves two




purposes—the production of a useful bibliographic data base and the famil-




iarization of the information specialists with the available literature.




This enables her/him to intelligently select and evaluate the literature sources.




    The EISO staff encompasses a wide variety of academic backgrounds.




Whenever possible preparation of these documents is assigned to the spe-




cialist whose background experience is most compatible with the area under




review.  This not only makes the work more enjoyable for the specialist




but creates a more valuable document for the user.
                               157

-------
Conclusion




    Information centers, by definition, function as a support service for




the scientific community; however, because the EISO Scientific Staff




possesses such diverse and extensive research backgrounds, numerous original




state-of-the-art reports and reviews are generated "in house".  The multi-




center, interactive approach used to create EISO brings to the complex




not only a community capable of sorting, supplying, repackaging, and dis-




pensing available information, but one that evaluates, analyzes, digests,




and—in essence—"creates" new data by assimilating the published informa-




tion into a comparative and more useful form.




References




1.  Chemical Abstracts, American Chemical Society, Columbus, Ohio.




2.  Biological Abstracts, Biosciences Information Service, Philadelphia,




    Pennsylvania.




3.  Environmental Protection Research Catalog, Parts 1 and 2, U.S.  Environ-




    mental Protection Agency, Office of Research and Monitoring, Research




    Information Division, Washington, B.C., January 1972.




4.  Summaries of the USAEC Environmental Research and Development TID-4065-




    Rl, Office of Information Services, Technical Information Center, Oak




    Ridge, Tn., August 1973.




5.  Caton, G. M., J. M. Chilton, J. K. Huffstetler, B. W.  Kline and D.  C.




    Michelson, Inventory of Current Energy Research and Development, En-




    vironmental Information System Office, Oak Ridge National Laboratory,




    ORNL-EIS-73-63, December 1973; three volumes reprinted under the same




    title as Congressional Committee Print (Serial J), January 1974, ob-




    tainable through U.S. Government Printing Office.
                                158

-------
6.  Copenhaver, E. D. (ed.), NSF-RANN Trace Contaminants Abstracts, Toxic




    Materials Information Center, Environmental Information System Office,




    Oak Ridge National Laboratory, ORNL-EIS-60, Nos. 1-4, 1973-74.




7.  Weast, R. C. (ed.)»  CRC Handbook of Chemistry and Physics, Chemical




    Rubber Company, 53rd edition, 1972-1973.




8.  Altman, P. L., and D. S. Dittman (eds.), Biology Data Book, Federation




    of American Society for Experimental Biology, Bethesda, Maryland.
                               159

-------
160

-------
           INTERIM REGION VIII PESTICIDES LAND STORAGE




               AND DISPOSAL GUIDANCE, JANUARY 1974




                           Dan W. Bench




            U. S. Environmental Protection Agency






I.  Landfilling - Generaj.




     Most excess pesticides and pesticide containers can be placed in




individually designed sanitary landfills.  However, not all sites used




in Region VIII today can be used for pesticides unless these sites are




specially designed and constructed for that purpose.




     While it is possible to construct a sanitary landfill on nearly




all topographies, some land formations are more difficult than others




to use, therefore, soil reinforcement may be necessary for pesticide




wastes.  This makes each sanitary landfill distinctive.  It would be




impossible to standardize all techniques required at every potential




disposal site.  This discussion is intended to'cover those features




and procedures that are intrinsic to a good sanitary landfill operation




for pesticide land storage and disposal.




     These interim guidelines will not supersede the proposed guidelines




for "Land Disposal of Solid Wastes" or the proposed guidelines for




"Disposal and Storage of Pesticide Related Wastes" being developed under




Section 209 of the Resource Recovery Act and Section 19 of the Federal




Insecticide, Fungicide and Rodenticide Act of 1972.




     The following criteria are essential for landfilling pesticide




wastes:




     A.  All cells should be designed and constructed for a particular




         stockpile of ingredients.




     B.  All cells should be constructed, filled and covered as rapidly




         as possible to maintain the integrity of the structure.






                                161

-------
    .C.   Wastes whould be temporarily stored until there is a sufficient




         quantity to warrant the design and construction of a cell.




     D.   A.detailed site description and a plat of the completed landfill




         should be permanently recorded in the appropriate office of




         legal jurisdiction.




II.   Landfilling - Specifications




     A.   Site Location Requirements




         It is important that the structure:




         1.  Be readily accessible for construction, operation, and




             maintenance;




         2.  Conform to zoning and land use requirements and plans of




             the area;




         3.  Not be located in a known flood plain;




         4.  Not be in an area where the ground water table is High;




             and




         5.  Contain sufficient and suitable cover material.




     B.   Site Design




         Site development plans should include a topographic map showing




         land use and zoning within one mile of the disposal site.  The




         map should show all homes, buildings, wells, watercourses,  dry




         runs, rock outcroppings, roads, and other pertinent data, i.e.,




         USGS 7 1/2 minute quadrangle map.  Additional site detail should




         show the location of all soil borings to a depth sufficient to




         allow evaluation of water quality protection, location of pro-




         posed buildings, area roads and fences, and detailed contours or




         cross sections of proposed structures.




         A report accompanying the plans and specifications should document




         the following:
                                162

-------
    1.   The volume and comprehensive description of the waste




        materials which may be accepted for disposal;




    2.   The types of hazardous waste materials which can be stored




        together;




    3.   The geology, hydrology, and soil testings;




    4.   The interpretation and classification of all materials




        encountered in the site area using the Unified Soil Classifica-




        tion System;




    5.   The method of soil placement and/or structural additives;




    6.   The schedule of periodic inspections;




    7.   The responsible agency for construction and maintenance;




        and




    8.   The method of control of off/on site, surface and subsurface




        drainage.




C.  Structural Parameters




    1.   Soil characteristics of the disposal site should have:




        a.  Classifications of CL, CH or OH by the USCS or some




            combination thereof.




        b.  A fine grained texture (more than 50% passing the number




            200 sieve,size - U.S. standard) as determined by testing




            procedures of AASHO T88.




        c.  A Plasticity Index  (PI) greater than 20 by ASTM Test




            D424 or AASHO T90.




        d.  A permeability less than 10-8 cm/sec or 0.2 feet per




            year, whichever is less.




    2.   For structural integrity, soil should be placed in six inch




        layers and compacted with a sheeps foot roller of more than
                             163

-------
        4,000 pounds per lineal foot,  to a density of 95% of modified

        proctor at optimum moisture content (ASTM Test D1557 or  .

        AASHO T180).  Cell bottoms and sides should be constructed

        in a continuous operation.

    3.   Depth requirements of compacted backfill surrounding the

        material will vary with wastes placed in the structure.

        Using the EPA, Office of Pesticide Programs  classification,

        the following should serve as a guide until more complete

        data is accumulated:

                Hazardous Waste Class             !_  1_I III IV  V

                (depth in fill necessary in ft.)  5   5   4   2   2

    4.   Soil types mentioned above may not be available in all

        areas of the United States.  Therefore, reinforcements
                                                           i
        may be used to upgrade the soil characteristics, i.e.,

        soil, cement, asphaltic materials, concrete bentonitic

        clays, impervious membranes, etc.  When reinforcements

        are used, the recommended compacted soil depths may be

        reduced significantly.

    5.   The cell shall be capped with a minimum of 2 feet of

        compacted soil.

D.  Moisture Content

    The water content of the earthfill materials prior to and during

    compaction should be distributed uniformly throughout each

    layer of the material.  The soil water content should allow

    maintenance of the modified proctor laboratory condition.

    (This optimum water content is defined as that water content

    which results in a maximum dry unit weight of soil when subject

    to the modified proctor compaction test).  The proctor compaction


                             164

-------
    tests should be conducted by a qualified person using the




 ~   appropriate ASTM designation D1557 or standard AASHO T180 method.




    The material should contain the proper moisture content in the




    borrow pit before excavation.  Supplementary water, if required,




    should be added to the material by sprinkling on the earthfill




    and should be mixed uniformly throughout the layers.




E.   Rollers




    Tamping rollers should be used for compacting the earthfill.




    They should be furnished by the contractor and should meet




    the following requirements:




    1.  Roller drums - Each drum should have an outside diameter




        of not less than five feet and should not be less than




        four feet nor more than six feet in length.  The space




        between adjacent drums, when on a level surface, should




        not be less than twelve inches nor more than fifteen inches.




        Each drum should be free to pivot about an axis parallel




        to the direction of travel and should be equipped with a




        suitable pressure-relief valve.




    2.  Tamping Feet - At least one tamping foot should be provided




        for each 100 square inches of drum surface.  The space




        measured on the surface of the drum, between the centers




        of any two adjacent tamping feet, should not be less than




        nine inches.  The distance between the tamping foot and




        the outside surface of the drum should not be less than




        nine inches.  The cross-sectional area of each tamping foot




        should not be more than ten square inches at a plane normal




        to the axis of the shank six inches from the drum surface,
                               165

-------
              and should not be less than seven square inches nor more

              than ten square inches at a plane normal to the axis of

              the shank eight inches from the drum surface.

          3.   Roller Weight - The weight of the roller when fully loaded

              should not be less than 4,000 pounds per foot of drum

              length.   If more than one roller is used on any one layer

              of fill, all should be the same type and with the same

              dimensions.  During rolling, the contractor should keep

              the spaces between the tamping feet clear of materials

              which would impair tamping.

III.   Land filling - Construction

      A.   General

          1.   Access to the site should be controlled to keep unauthorized
                                                                 i
              persons out.

          2.   Open burning of waste should be prohibited.

          3.   Design provisions should ensure that no pollution of surface

              or ground water results from the operation.  Routine monitor-

              ing should be performed by qualified personnel.

          4.   Provisions should be made for on-site control of potential

              gas movement from the landfill.

      B.   Preparation of the Foundation

          No  material should be placed in any section of the earthfill

          portion of the storage site until the foundation for that section

          has been prepared and approved by a qualified person.  Test

          pits and all other existing cavities found within the area

          covered by the earthfill and which extend below the established

          lines of excavation for the structural embankment should be

          filled with material and compacted as specified for the earthfill.


                                      166

-------
        The foundation should be prepared by leveling and rolling




        so that subsurface material of the foundation will be as




        compacted and well bonded with the first layer of earthfiH




        as for each subsequent layer of earth.  All rock, shale, and




        other undesirable materials should be excavated from the founda-




        tion as indicated in the plans or directed by a qualified




        person.  Surfaces should be protected from air slacking and




        freezing.  Surfaces upon or against which the earthfill




        portions of the structural embankment are to be placed,




        should, be cleaned of all loose and objectionable materials




        in an approved manner by hand or other effective means




        immediately prior to placing the first layer of earthfill.




C.  Waste Placement and Covering




    1.  Placing




        The distribution and gradation of materials throughout the




        earthfill should assure that the fill is free from lenses,




        pockets, streaks, or layers of materials differing sub-




        stantially in texture or gradation from the surrounding




        materials.  Placing of materials should be subject to the




        approval of a qualified person who may designate the placing




        of individual loads.  Impervious materials should be placed




        in the central portion of the earthfill so that the permeability




        will gradually increase toward the outside.  Cobbles and rock




        fragments with a diameter greater than three inches should




        be removed from the structural material.




        Structural material should be placed in horizontal layers




        not more than six inches thick and then compacted.  If
                          167

-------
        the surface of the foundation or the rolled surface of any




        layer of earthfill is too dry or smooth to bond properly




        with the next layer of material, it should be moistened




        and/or worked with harrow, scarifier, or other suitable




        equipment to a sufficient depth to provide a satisfactory




        bonding surface before the next layer of earthfill material




        is placed.  If the rolled surface of any layer of earthfill




        is too wet for proper compaction with the next layer to be




        placed, it should be removed or dried until the water content




        is satisfactory for compaction before the next layer of




        earthfill is placed.




2.   Landfilling




    a.   All slopes at the working face should enable machinery to




        function properly and be 3:1.




    b.   Groups of hazardous materials should be in separate parti-




        tioned areas.




    c.   Liquid materials, in barrels or drums, should have an appropriate




        absorbent placed around the containers to retain the liquid




        if leakage occurs.




    d.   After all materials, pesticides, etc., have been placed,




        covering operations should proceed immediately.




    e.   After compacting the cover material, all exposed earth




        should be covered with topsoil and appropriate grass or




        shallow rooted shrubs planted.




    f.   Surface slopes on areas with intermediate or final cover




        should be at least two percent to facilitate surface runoff.
                           168

-------
g. . At least semiannually, each site should be inspected by




    a qualified person and a report presented to the appropriate




    regulatory agency.  Deficiencies, along with recommended




    corrective action, should be reported.
                       169

-------
170

-------
                   DEGRADATION OF PESTICIDES




                      Frederick Applehans




                   Colorado State University






     Following the increased usage of DDT and other pesticides after




World War II, the sales of pesticides have increased tremendously.




During the 1960's a surge in the production of total unformulated




pesticides was observed.  The dollar value of pesticide production




increased from about $450,000,000 in 1962 to around $1,300,000,000




in 1969 (1).  In recent years the use of the more persistent organo-




chlorine pesticides has declined, primarily due to their restricted




use.  Present trends are toward the usage of the less persistent




compounds; some of these are of low toxicity and others are highly




toxic.




     Pesticides can be grouped into four general chemical classes:




(1) organochlorine, (2) organophosphate, (3) carbamate, and (4) metalics,




The pesticides can be further divided into groups designated by their




target organism; (1) insecticide, (2) herbicide, (3) fungicide, (4)




rodenticide, (5) acaricide, (6) nematocide, and (7) miticide.




     Because of the tremendous usage of pesticides throughout the




world, we have become interested in the fate of these chemicals after




they enter our ecosystem.  Questions have been raised concerning the




persistence, toxicity and degradability of the compounds.




     There are several factors which may influence the degradation of




pesticide residues in the environment.  One must first consider the




chemical structure of the compound for this factor alone can determine




the speed and ultimate success or failure of the degradation pathway.
                                171

-------
The physical size of complex molecules  often limits  the approach of




enzymes and reduces the rate at which organisms  can  break down the




compound.  Aliphatic compounds are, in  general,  more degradable than



...	 I	;...,.	1	1 t-l,,	l,,.t- 4 •-,.». t .-..  -I  .. 1 _„,,-,.•.	i-l,.-,.  «-!.-,,, -.-,»•(	




in the molecular chain often makes the  compound  more resistant.   Esters




and epoxides, salts, etc. are more resistant  than  the  base pesticidal




compound.  Compounds in emulsified or chelated forms are not  readily




degraded by microorganisms.




     Other factors affecting pesticide  degradation are (1) the concen-




tration of material applied, (2) formulation  - granular more  persistent,




(3) type of soil - some clays tend to absorb  compounds thus making them




unavailable to microorganisms - sandy soils  are  also poor, (4)  high




organic matter content in soil will also enhance the degradation process,




(5) pH - basic conditions are the best; however, degradation  does occur




in a pH range of 5 to 9.  Extensive degradation  is also known to occur




at pH in excess of 13.0,  (6) climatic factors -  temperature effects




on the microbial systems are very significant -  summer - high activity




and during winter low activity.  Good degradation usually will occur




at around 30-35 C and high moisture levels are ideal.




     Agents which perhaps play the most important role in the ultimate




dissipation of pesticide residues from  the environment are microorganisms,




animals, plants, and U.V. light rays from the sun.   Naturally,  the




relatively unstable pesticides undergo  degradation rather  rapidly and




the more stable ones may require more time or, in some cases,  extreme




physical conditions such as high temperatures or harsh pH for degradation




to be accomplished.  Examples of pesticide persistence in  soils  are




listed in Table'1.
                                  172

-------
Table 1.  Examples of Pesticide Persistence in Soils
Chlordane
DDT
BHC
Dieldrin
Heptaclor


6 years
4 years
3 years
3 years
2 years


Picloram
Simazine
2,3,6 TEA
Atrazine
Trifluralin
2,4,5-T
2,4-D
18 months
12 months
12 months
10 months
6 months
5 months
1 month
                  Diazinon




                 .TCA




                  Disulfaton




                  Phorate




                  Barban




                  Malathion




                  Parathion
 12 weeks




 10 weeks




  4 weeks




  2 weeks




  2 weeks




1-2 weeks




1-2 weeks
                              173

-------
     Perhaps the most researched agent affecting pesticide degradation




is that of microorganisms, particularly the soil inhabitants.  Depending




on the chemical nature of the pesticide and the requirements and




'capabilities of. the particular microorganism  (be it an actinomycete,




fungus, or bacterium) a pesticide can be degraded via ester hydrolysis,




amide hydrolysis,  3-oxidation, ether cleavage, alcohol and aldehyde




oxidation, hydroxy.lation, dealkylat i.ori, dehalogenation,  etc.  (2).




Microorganisms mostly utilize a reductive system in metabolizing




pesticide residues  (3,4).  Some microorganisms are even  capable of




utilizing pesticide residues as a sole carbon source  (5), but  this




is usually a laboratory phenomena more so than an enivronmental rule.




     The degradation pathway for DDT has been reported by several




researchers  (5,6,7,8,9,10).  The major microbial metabolic steps in-




volved are the reductive dechlorination reaction and  the oxidative




system.  DDT is degraded mainly to give a series of: dechlorinated




analogues, namely DDT; DDMU  (l-ch.loro-2,2-bis[p-chlorophenyl]  ethylene) ;




DDM.S (:i-chloro-2,2-bis[p-chlorophenyl] ethane); DDNU  (unsym~bis[p-




cliloropheny.1 ] ethylene); DDA (2,2-bis[p-chlorophenyJ ] acetate); and




.DBF  (4,4'-dichlorobenzophenone) (7).




     I'ocht and Alexander  (11) published work  indicating  that  the p,p'Cl




positions on DDT and its analogues were responsible, for  DDT's  resist-




ance to immediate microbial degradation.  Removal of Cl  from the para




positions allowed the compounds to be readily degraded to phenol and




benxoic acid.




     Perhaps some of the most resistant pesticides to microbial de-




gradation are the cyclodiene insecticides.  Included in  this group




of compounds are dieldrin, aldrin, heptachlor, and chlordane.  As




illustrated in Figure 1, the chlorine containing ring is particularly





                               174

-------
    Figure 1. Biological and U.V. Light Transformation of Aldrin (2).
          C1C!
ALDRIN  Ci
BIOLOGICAL CI
            CI.CI
              CI
                  OXIDATION   Hf
                 MICROS IAL AND_
             ULTRAVIOLET ACTION
            V
           H
                 BIOLOGICAL^
                 OXIDATION
DIELDRhN,
   PHOTO ALDRIN
             H   '0

           PHOTO  DIELDRIN
                     175

-------
stable and the major microbial attack may be on the non-chlorinated

rings(2).  Also noted in the Figure is the biological oxidation of

aldrin and photo-aldrin to dieldrin and photo-dieldrin respectively.

This type of natural epoxidation results in the transformation of a

persistant compound into one that is more resistant to microbial attack.

Other natural epoxidation reactions include the transformation of

heptaclor to heptaclor epoxide and endrin to isodrin.

     Unlike DDT and the cyclodiene insecticides, BHC has been known

to disappear relatively quickly from soil.  A combination of soil

microorganisms and soil alkalinity may play key roles in the degradation

of BHC (2).  Indications are that a dechlorination process appears

to play an important tole, with the major metabolic product of A-BHC

being A-pentachlorocyclohex-1-ene (A-PCCH).  Further dehydrochlorination

of PCCH may result in the formation of 1,2,3,5-tetrachlorobenzene.

     The organophosphates, a chemical class of pesticides containing

some of the most highly toxic compounds used for insect control, are

generally considered to be readily attacked by microorganisms.  These

pesticides include parathion; di-syston; thimet, TEPP; and malathion,

the latter being relatively nontoxic.  A common mechanism employed by
                                                                      i
microorganisms to degrade OP insecticides 1s the hydrolysis process

through esterases (2).  This is opposed to the oxidative process

important in higher animal metabolism.  Through the microbial reductive

degradation system, aminoparathion is formed from parathion.

     Generally, the phenoxyacetic acid herbicides such as 2,4-D, MCP,

and 2,4,5-T are readily degraded by soil microorganisms.  The site

of attack on the herbicides is the ether linkage between the ring

and fatty acid of phenoxyalkanoic acid (2).  Through this process,

the herbicidal activity of the compound is diminished.  A Flavobacterium


                               176

-------
sp (12) and an Arthrobacter sp (13) are known to degrade 2,4-D via this




route.  3-oxidation, occurring naturally in soil and in microbial




cultures, is also an important process for this group of compounds.




Probably, the herbicides in the odd numbered aliphatic acid become




phehoxypropionic acid derivatives and those having even numbered acids




will form corresponding phenoxyacetic acids (2).  Ring hydroxylation




of 2,4-D and MCPA by Aspergillus niger (14) and Pseudomonas respectively,




has also been reported.




     The ultraviolet portion of sunlight appears to have the most




significant impact on the degradation of pesticides in the environment




of all known physical factors (eg. air, moisture, pH, etc.).  Ultraviolet




light rays reaching the earth's surface have a wavelength of between




295 and 300 nanometers.  Many pesticides are substituted aromatic




compounds having absorption maxima between 200 and 350 nm.  An important




factor affecting the rate of pesticide degradation by sunlight is the




presence of photosensitizers (2).  These photosensitizers are other




chemicals which expedite the transfer of light energy into the receptor




chemicals.  In 1956 Bell reported that the photodecomposition of




2,4-D was photosensitized by the presence of riboflavin (2).  Other




photosensitizers known are:  benzophenone, riboflavin-5'-phosphate,




rotenone, and anthraquinone.




     Four photochemical reactions may occur when aromatic pesticides




are exposed to U.V. light.  These are:  ring-substitution, hydrolysis




(when water is present), oxidation, and polymerization.




     Examples of dxidative photochemical reactions are:  chlorobenzoic




acid ->• benzaldehyde; parathion -* paraoxon and other oxo-analogues of




parathion; and DDT ->• 4,4'-dichlorobenzophenone.







                               177

-------
     Examples of polymerization are:  (1) the loss of 2 chlorine




atoms from DDT and the formation of a dimer without air in the presence




of U.V. liRht; (2) for the chlorinated aniline derivatives, the initial



reaction is the .tormation of diazobenzene analogue, which reacts with




another molecule of the parent compound to form the corresponding




trimer in presence of the photosynthesizer, riboflavin-5-phosphate




salt (2).




Summary




     The degradation process of pesticides by biological or physical




agents is sometimes difficult to understand, particularly when one




sets out to determine the metabolic pathways as they would occur in




nature, that is, the interreaction of microbes, soil enzymes, U.V.




light, and other physical factors.




     Matsumura (2 ) points out that it is important to consider first,




whether such degradation products are stable enough to become "terminal




residues", second, if such residues have a strong affinity to biological




materials so as to cause them to become biologically magnified, and




third, are any of the products formed harmful to any form of biological




system.




                           References




1.   Environmental Protection Agency.  The pesticide manufacturing




     industry—current waste treatment and disposal practices.  U.S.




     Government Printing  Office, Washington,  D.C.   1972.




2.   Matsumura, F.  Degradation  of  pesticide residues  in  the  environment,




     Chapter  13.   In  C. A.  Edwards  (ed.), Environmental pollution  by




     pesticides.   Plenum  Press,  N.  Y.  1973.
                                178

-------
 3.   Plimmer, J.  R.,  P.  C.  Kearney, and D. W. VonEndt.  Mechanism of




     conversion of DDT to DDD by Aerobacter aerogenes.  J. Agr. Food




     Chem. 16:594.  1968.




 4.   Matsumura, F. and G. M. Boush.  Degradation of insecticides by




     a soil fungus,  Trichoderma viride. 61:610.  1968.




 5.   Focht, D. D. and M. Alexander,  Aerobic cometabolism of DDT analogues




     by Hydrogenomonas sp.  J. Agr. Food Chem. 19:20.  1971.




 6.   Pfaender, F. K.  and M. Alexander.  Extensive microbial degradation




     of DDT in vitro and DDT emtabolism by natural communities.  J.




     Agr.  Food Chem.  20:842.  1972.




 7.   Wedemeyer, G. Dechlorination of l,l,l-trichloro-2,2-bis(p-chloro-




     phenyl) ethane by Aerobacter aerogenes.  Appl. Microbiol. 15:569.




     1967.




 8.   Focht, D. D.  Microbial degradation of DDT metabolites to carbon




     dioxide, water,  and chloride.  Bull. Environ. Contain. Toxicol.




     7:52.  1972.




 9.   Glass, B. L.  Relation between the degradation of DDT and the iron




     redox system in soils.  J. Agr. Food Chem. 20:324.  1972.




10.   Guenzi, W. D. and W. E. Beard. Anaerobic conversion of DDT to




     DDD and aerobic stability of DDT in soil, Soil Sci. Soc.  Amer.




     Proc.  32:522.   1968.




11.   Focht, D. D. and M. Alexander.  DDT metabolites and analogs:




     ring fission by Hydrogenomonas.  Science 170:91.




12.   MacRae, I. C. and M. Alexander.  Metabolism of phenoxyalkyl carboxylic




     acids by a Flavobacterium species.  J. Bacteriol. 86:1231.  1963.




13.   Loos, M. A., R.  N.  Roberts, and M. Alexander.  Metabolism of




     2,4-D by an Arthrobacter species.  Bacteriol. Proc. 65:3,A15. 1965.
                                 179

-------
14.  Faulkner, J. K. and D. Woodcock.  Metabolism of 2,4-Dichloro-




     phenoxyacetic acid ('2,4'D') by Aspergillus niger van Tiegh.




     Nature 203:865.  1964.
                                180

-------
                 REFERRAL PROCESS FOR COORDINATED
               ENVIRONMENTAL AND LAND USE DECISIONS

                  Lane Kirkpatrick and Steve Weiner

             Colorado Air Pollution Control Commission

                         Donald Shanfelt

                   City of Lakewood, Colorado


     In state, local and regional government, there is a need for more

coordinated and integrated environmental decision-making, implementation

and relating environmental programs to the more comprehensive matters

of land use and transportation control.  Though this problem is broader

than described here, the need can be acute at all three levels of

government.  First, it is essential that all state agencies in the

environmental and land use areas cooperate in developing overall state

goals, integrating individual agency goals and objectives as part of

the overall concept.  It is equally important that a process be developed

which enables coordinated implementation of these goals on a day by

day basis by all agencies concerned, including regional and local

agencies.

     The urgency of this need is exemplified by state legislation

that often requires state air and water quality and solid waste control

programs to relate to broader land use considerations when approving

or denying new construction.  In air quality, auto traffic generation

must often be evaluated against air quality objectives; in water quality,

growth may be limited unless proper sewage treatment plant capacity

exists; and in solid waste, disposal facilities must be able to handle

new development.  The complexity of these evaluations is further

compounded by the need to maintain perspective with other community

needs as social, economic, energy, and transportation factors.

                                181

-------
     Recently, the City of Lakewood, Colorado developed the "referral




process" to answer such a need on the local level.  This process can




easily be modified to satisfy the analogous needs of state government




and is currently being considered by the Colorado Department of Health.




     This approach combines the procedures used in reviewing Environ-




mental Impact Statements with an efficient industry decision-making




process.  The result is a "procedural impact analysis" for any proposed




development that must be reviewed by a multitude of governmental agencies.




How to Assess Impact;




     Since the passage of the Environmental Policy Act in 1969, federal




agencies have been required to produce an Environmental Impact Statement




for all federal projects or those using federal land.  These document




a given decision, such as the consideration for construction of a coal




fired power plant.  Contained in this law is a decision checklist




called the EIS outline.  Although many use just such a mental pro-




cedure, the Environmental Policy Act requires that (1) Assumptions




and conclusions be substantiated and verified; (2) Those people or




groups to be affected are made part of the decision-making process;




and (3) The total decision-making process is put down in writing and




made available to the public.




     This process is herein expanded into a total decision-making




process.  Although in many environmental health departments, traditional




environmental concerns such as air quality and ecology have been addressed,




contemporary statements inevitably must also address social, legal,




economic and cultural aspects.  The sudden awareness then is the fact




that our total environment must be evaluated to arrive at an informed,




complete decision.






                              182

-------
           This referral process Is not completely new.  In fact, most

      communities refer development proposals to other agencies for comment

      on all rezoning  (change in land use) applications.  However, the

      present system suffers from lack of standardized objective criteria

      and from the absence of meaningful responses from most referral agencies,

           By incorporating the concepts of the Environmental Impact State-

      ment outline (Table 1) and project management system (Table 2),  the

      process has been easily upgraded and explained to the level that

      agencies can use it to obtain more coordinated and comprehensive

      environmental and land use decisions.
      Table 1.   Environmental Impact Statement Requirements  Outlined
                (1969 National Environmental  Policy  Act)

                 I.   Project  Purpose
                II.   Project  Description
               III.   Existing Environment
                IV.  'Impact of Proposed Action
                 V.   Favorable Effects
                VI.   Adverse  Effects  Which Cannot be Avoided
               VII.   Alternatives to  Proposed  Action
             VIII.   Short-Term Local vs. Long-Term  Productivity
                IX.   Irreversible/Irretrievable Committment of Resources

     Table  2.   Project Management System

          In this system a project manager utilizes and coordinates the
     expertise  of many programs as shown below to evaluate development
     proposals  or to develop  programs so better overall decisions are made.
                                 PROJECT
LOCAL STREET
 S DRAINAGE
ENGINEERING
   REGIONAL
TRANSPORTATION
   DISTRICT
MANA
;ER
DEVELOPMENT
PROPOSAL
EVALUATION.
   LOCAL
  HOUSING
AUTHORITY
  STATE
 HEALTH
  DEPT.
   FEDERAL
ENVIRONMENTAL
  PROTECTION
    AGENCY
.  ETC.
                                  183

-------
     The referral process consists of two phases.  First, the developer's




conceptual design problems are reviewed by the concerned agencies and




preliminary plans are formulated.  Second, formal detailed plans of




the proposed development are submitted to the lead program or agency,




and written plan review is completed by all concerned agencies.




     Although it is strongly urged that complementary use of this




referral process be made by all levels of state and local government




involved with land use and environmental matters, the following illus-




trates application to an environmental health department (Table 3).






Table  3.
                             Phase 1
Step 1
Informal Consultation
Developer receives agency
Checklist of Environment
Regulations, guidelines
and other requirements.
Step 2
Developer Requests
Pre Planning conference
Developer submits concep-
tual plan.
Plan referred to conoarned
programs for review.
Step 3
Site Inspection
by program represen-
tatives.


Step 4
Pre Planning Conference




Phase 2 \f .

Step 5
Formal submit tal of de-
tailed plan by developer
and referral of detailed
plans to concerned pro-
grams
Step 6
Referral Programs Respond
.

'

Step 7
Negotiation
•'
—
I

Step 8
Staff Recommendations
and Decisions

•

                                                                     1
                                                                  Step 9




                                                             • Board Decisions
                              184

-------
                                                 Phase 1
             Step 1
       Informal  Consultation

     Developer receives agency
     Checklist of Environment
     Regulations, guidelines
     and  other requirements.
                                      Step 2
                                    Developer Requests
                                Pre  Planning  Conference
                              Developer submits concep-
                              tual  plan.
                              Plan  referred  to concerned
                              programs for review.
      Step 3
   Site Inspection

by program represen-
tatives .
       Step 4
Pre Planning Conference
                                                 Phase 2
oo
        Step 5
Formal submittal of de-
tailed plan by developer
and referral of detailed
plans to concerned pro-
grams
                                           Step 6
                                    Referral  Programs Respond
      Step 7
   Negotiation
       Step 8
Staff Recommendations
and Decisions
                                                                                                     \f
                                                                                                 Step 9
                                                                                           Board Decisions

-------
                          - Step 1 -




     A developer proposing an activity involving environmental problems




contacts an environmental coordinator within the department and receives




copies of individual program requirements, and if requested, receives




consultation thereto.  In addition, he may be referred to other appro-




priate agencies for information.




                          - Step 2 -




     When the developer has a conceptual plan prepared, it is submitted




to the Environmental Coordinator's office and a date is set for a




pre-planning conference.  The plan is then distribured to concerned




environmental health department programs for review.and comment.




                          - Step 3 -




     This process encourages joint site inspection by concerned programs




so as to enhance the relevance and quality of the overall environmental




decision.




                          - Step 4 -




     A representative of the Environmental Coordinator's office chairs




a meeting of representatives from each concerned program (air, water,




solid waste, radiological health, etc.) and the developer.  The objective




is to identify problems evidenced in the preliminary plan review and




site inspection as related to all environmental control requirements




of the environmental health department and to seek complementary solutions.




     If no problems are seen at this point, the developer is encouraged




to submit detailed plans.  If substantial problems exist, these are




pointed out to the developer, and recommendations are made for solutions.




Although the developer can submit plans still containing the problems,




it would be to his benefit to correct the shortcomings in advance.







                             186

-------
     The second phase closely parallels procedures used in environmental

health departments with the addition of a written review checklist

used in the detailed review.  Each referral agency gives project data,

outlines criteria and evaluation procedure, analyzes problem areas,

and gives its recommendations on a common review checklist.

     This procedure offers several advantages over the present system
                /
used by most environmental programs.  It allows each program to set

its own criteria and evaluation procedures.  All programs would have

greater input to the decision-making process, and each opinion would

be given equal weight.  So, the political problem of the "lead agency"

or program is eliminated along with the demand that all programs be

expert in all areas.

     This process allows citizen goals to be realized through a detailed

and concise review of all developments which also allows control and

greater flexibility at the same time.  Criteria are pre-established.

Thus, development consistent with program goals and citizen concerns

is encouraged.

                          - Step 5 -

     At some later date, the developer submits his plan for consideration

by the Environmental Coordinator's office.  This plan is far more

detailed than the previous plans, and his chance of denial is lower

because he was guided by the overall and individual program goals

during the site visit and pre-planning conference.  This process saves

the developer time and money and saves the environmental coordinator's

office staff time and effort because environmental concerns are generally

reflected in the detailed plan.
                             187

-------
     The Environmental Coordinator's office distributes the detailed




plan to concerned programs as in Step 2.  The programs now, however,




are required to submit written evaluations based on written and adopted




program rules, regulations, and other requirements.




                          - Step 6 -




     In addition to evaluating development plans on the basis of written




program requirements, individual programs should list specific problem




areas and suggest reasonable solutions if possible.




                          - Step 7 -




     All referral programs forward their written evaluations to the




Environmental Coordinator's office who informs the developer in detail




of any or all environmental problems discovered.  If necessary, a




meeting is arranged between the developer and the appropriate programs,




or appropriate correspondence is written encouraging problem resolution




between the parties.




                          - Step 8 -




     If all problems  are satisfactorily resolved between the developer




and the enforcement staffs involved, within the legal and policy con-




straints, the project is approved.  If problems cannot be mitigated,




the plans can be appealed to the appropriate policy-setting board.




     Ideally, one Board would have comprehensive policy-setting respon-




sibilities on all environmental matters; however, many agencies have




several Boards involved in environmental matters, so the Environmental




Coordinator should provide coordination between the Boards and en-




forcement programs and arrange joint meetings when necessary to make




final decisions.
                            188

-------
Benefits of the^ Referral Process:


     To the Citizen:


          1.  Gains control of his environment and quality of life.


          2.  Is included in decision-making process.


          3.  Evaluation requirements and procedure is readily


              available to him.


     To the Developer:


          1.  Knows requirements beforehand.


          2.  Saves time and money.

                                                      *
          3.  Encourages flexibility and design creativity.


          4.  Product is better suited to community needs.


     To the Environmental Health Agency:


          1.  Knows requirements beforehand.


          2.  Streamlines evaluation.


          3.  Produces objective evaluation.


          4.  Systematizes decision-making


          5.  Maintains autonomy - avoids lead agency problem


          6.  Encourages agency definition of goals.


          7.  Allows evaluation criteria update for viability.


          8.  Project management process facilitates developer under-


              standing


          9.  Defines ideas in written form.


         10.  Encourages development by responsible firms.


Broader Application of Referral Process;


     The foregoing illustrates the application of the referral process


for coordination of environmental permit reviews in a typical state


health department or environmental agency.  There usually exists the


need to coordinate the review of proposed development plans with other

                            189

-------
environmental programs scattered through the state government, local




and regional agencies and planning agencies.  The referral process




can be used for interagency and intergovernmental level plan reviews.




For example, a development proposal submitted at the state level,




affecting a city could be referred to that city's government for




evaluation.  Conversely, a local proposal affecting state concerns




cas be referred to appropriate state agencies, and all of this can be




accomplished without major governmental reorganization.




     The trend toward development of national and state level use




legislation provides further opportunities and benefits to be derived




from the referral process for coordinating land use laws with environ-




mental concerns.  Since the way in which we allow our land to be used




is the major determinant of the quality of our total environment,




envisioned land use planning and control agencies may become the




major focal point for reviewing a developer's plan which could then




be referred to sub-focal points as health departments and planning




agencies at all concerned levels of government for comprehensive and




systematic evaluation.
                             190

-------
                             MYCOTOXINS  •




                          Frederick W. Oehme




                      Kansas State University






     Some of the lower members of the plant family, the fungi, arts




capable of producing a variety of toxins as by-products of their growth.




These fungal metabolites that are capable of producing a harmful effect




upon man or animals have been called mycotoxins (1,10,22).  Although




investigations of the mycotoxins have become a focal point for scientific




studies during the past decade, only a few of the many potential fungal




toxins have been associated with disease syndromes and even fewer have




been isolated and chemically characterized.  The purpose of this presenta-




tion is to review the known mycotoxins by specific chemical form, to




describe the clinical syndromes associated with the unidentified fungal




toxins, and to offer some projections of possible unrecognized mycotoxic




effects and concerns.




Importance




     Except in rare situations, mycotoxicosis is a subtle and insidious




syndrome that often defies routine diagnostic procedures (12,18,22).




Most fungal toxins produce clinical disorders that are not unique and




that often mimic other conditions associated with chronic metabolic




dysfunction, insidious organ pathology, or mild digestive disturbances.




These various effects are usually vague and may affect the liver, kidney,




or blood, and may produce deficiencies or malfunctions related to




utilization of protein and vitamins or may be associated with the develop-




ment of cancer or congenital defects.  The subtleness of most mycotoxicoses




results in many affected individuals not being presented for evaluation




until late in the disorder.  Complicating conditions are usually present







                                191

-------
at that time and definitive, accurate patient evaluation and diagnosis




is usually slow and arbitrary.  Specific diagnoses tests are not available,




although recent publications and symposia (3,22) have attempted to present




the current findings of laboratory investigations to the practicing




veterinarian and physician.  The reluctance of most practitioners to use




mycotoxins as a "catch-all" diagnosis further complicates control of




this situation.  The difficulty in identifying mycotoxins as etiologic




agents in clinical situations presents the most important and difficult-




to-solve problem to controlling the disease syndromes produced by this




group of compounds.  Animal and public health concerns are thus justified




when the potential for feeds or foods containing mycotoxins is ever present.




Occurrence




     Since mycotoxins are associated with fungal growth, they are potentially




found wherever fungi propagate and develop.   The wide distribution of




fungi illustrates the potential hazards of their toxic metabolites,




since one study showed that 36.6 percent of fungal isolates produced




crude extracts that were toxic to mice or cell culture (19).  As with




most growing things, a source of nutrition and proper amounts of moisture




and heat must be present to support fungal growth.  For optimal mycotoxin




production, moisture in excess of 20 percent, a temperature between 70




and 80 degrees F., and a substrate which provides a ready source of




energy are necessary (13,14).  Under such suitable conditions, fungal




growth will result and in the growth process these fungi will produce




toxins.  Hence, the mycotoxins are products  of fungal growth; the mere




presence of the fungus does not necessarily  indicate that a particular




toxin is also present.   Conversely, the toxin may be present and viable




fungi may no longer exist in the sample.
                               192

-------
     Mold toxins commonly develop in stored grains and on certain feed-


stuffs subjected to unusual weathering or storage conditions.  Although


moldy feed is usually grossly identifiable, the spoiled feed may be


mixed into a ration or otherwise offered for human or livestock con-


sumption through ignorance or by intent.  Animals will often reject


extremely spoiled feed, but well-diluted feeds or rations offered hungry

                 i                                      •
animals may result in acceptance and toxicity.


     There are many sources of mycotoxins, as there are many types of


fungi and clinical syndromes produced by the mycotoxins (14).  There


are approximately 50,000 fungal species (8), of which approximately


100 are toxic (13).  These 100 fungi produce over 200 mycotoxins, 20


of which have been already shown to be associated with disease conditions


(20).  Conditions of growth are critical for the production of specific


mycotoxins.  Variations in moisture content or temperature may be


sufficient to vary the production of toxins from lethal to insignificant.


Since mycotoxins are uniformly present as dietary contaminants, the


concentration of toxin present in the diet and the duration of consump-


tion will greatly affect the clinical syndrome produced.   Such variations


surve to further complicate the evaluation of clinical effects observed


from specific fungal ingestion.


     Because of these variations and fluctuations in clinical effects


depending upon environmental circumstances, the correlation of clinical


signs with specific fungi and their mycotoxins is often difficult.


Diagnosis of mycotoxicosis is therefore dependent upon the isolation of


specific fungal principles or previously identified mycotoxins in the


diet.  Unfortunately, there have been few actual isolations and even
                               193

-------
fewer chemical characterizations of specific mycotoxin principles (6,

10,25).  Hence, the clinical diagnosis of mycotoxicosis and the appli-

cation of control measures is largely dependent upon astute observation

of clinical signs and circumstances surrounding intoxications and the

elimination of other possible etiologies and, where applicable, the isola-

tion and confirmation of those mycotoxins for which standards and lab-

oratory procedures for -diagnosis are available.

                     The Clinical Mycotoxicoses

     A wide range of clinical disorders and syndromes are produced by

or associated with the ingestion of mycotoxins in man and animals.

Most fungal toxins affect the liver and produce lesions varying from
                                                                        r
frank necrosis to biochemical interference with enzymes or blood co-

agulation mechanisms.  Digestive tract disturbances, photosensitization,

poor feed utilization, abortions, and reporductive failures have also

been associated with mycotoxin consumption.  The clinical disorders

produced by mycotoxins will be categorized and briefly reviewed accord-

ing to type of fungus involved, specific mycotoxin (if known), or by

clinical disorder produced.  Each syndrome will be briefly described

with references offered for the securing of more detailed information.

Mushrooms

     Mushroom poisoning occurs in humans and animals and is primarily

produced by Amanita species (usually phalloides or muscaria).  These

larger fungi produce a characteristic syndrome of initial acute gastro-

digestive disturbances followed in several days by evidence of liver

dysfunction (6,10).  The syndrome in animals is similar to that in

humans, with somewhat more digestive tract irritation being observed

in dogs.  Lesions observed on post-mortem examination include degen-

eration and necrosis of liver and kidney and a hemorrhagic enteritis.


                               194

-------
 Many individuals recover from the digestive tract  syndrome only to


 succumb to the liver degeneration and resulting hepatosis.


 Ergotism


      The ingestion of sclerotia formed by Claviceps  sp.  infecting the


 seeds of grain and grasses has produced poisoning  in humans and animals


 throughout the centuries.   "Saint Anthony's fire"  resulted from the


 consumption of rye and other cereals parasitized by  this fungus.   The


 alkaloids of ergot are amides or polypeptides formed from lysergic acid


 and have a direct stimulatory action on smooth muscle or have  an inhibi-


 tory action on sympathetic functions of the autonomic nervous  system



'(4).   •       .


      Gangrenous form.  This chronic condition results in gangrene of
                                   r

 the extremities caused primarily by peripheral thrombosis of the  arteries.


 It occurs in man and animals and produces lameness and dry gangrene of


 limbs,  ears, tail, and teats.   Reproductive failures are commonly reported


 and lack of lactation are a common complaint due to  the  circulatory


 disruption in peripheral vessels (4,6).


      Nervous form.  This acute form of ergot poisoning is a result of


 injury to the central nervous system which produces  numbness,  blindness,


 deafness, convulsive seizures,  and ultimately paralysis.   The  disorder


 is acute with signs developing in a matter of days following exposure


 to the ergotized grain.   The incoordination and nervous  signs  have


 resulted in the condition being called "Paspalum Staggers"  (9).   Cattle


 are especially affected  arid may develop  trembling  and ataxia if moved.


 Tremorgen Intoxication


      As metabolites from the Penicillium mold (9), the "tremorgens"


 have  not been chemically characterized,  but there  is  some evidence  that
                               195

-------
they are related to the ergot  alkaloids  (8).   Intoxication resulted




 in trembling,  staggering,  cyanosis  and  death.   In experimental animals




 it produced death with convulsions  when given intraperitoneally.




 Aflatoxins




      The aflatoxins are the most  studied of  all the mycotoxins.   Initially




 isolated from  strains  of Aspergillus  flavus,  these metabolites have  also




 been found in  Penicillium  species and other  genera of Aspergillus.   At




 least 12 different aflatoxins have  been isolated and they have been




 found to affect almost all species  of animals,  including man.   They




 appear to be the most  potent  of the currently recognized mycotoxins,




 with concentrations in the diet as  low  as 50 parts per billion aflatoxin




 B,  producing hepatic damage in laboratory animals.  In swine,  aflatoxin




 BI  dietary levels of 0.5 parts per  million result in growth retardation




 and abortions.   Feed levels of 1  -  2  parts per million or more are




 capable of causing acute death.   The  potency and liver specificity




 of aflatoxins  are frightening.  Hence governmental regulations place




 the maximum safe levels of aflatoxin  for most animals at significantly




 less than 1 part per million.  For  man,  the  permissible  limit  is  0.02




 parts per million.




      Routine assay of  feed grains frequently yields levels of  aflatoxins




 approaching or  in excess of the minimum level capable of causing  biochemical




 lesions.   With  grain shortage becoming  a more common reality,  and the




 constant threat of spoilage due to  adverse weather conditions  or  faulty




 storage facilities,  the possibility of  aflatoxins in the diets of




 animals or humans is increasing.  The underdeveloped areas are more




 susceptible to  aflatoxin poisoning  due  to the  lack of adequate food




 storage facilities  and primitive  means  of preparing foodstuffs.   Care
                               196

-------
in selecting food and feed materials is likewise less discriminatory




and the potential for real human and animal hazard is significant.




     Aflatoxins produce either acute liver necrosis or chronic liver




lesions which include fibrosis, bile duct hyperplasia, and eventual liver




failure.  Clinical effects are largely determined by the dose of afla-




toxin received, with chronic liver disease the most frequently observed




condition in man and animals.  Growth retardation, poor feed utilization,




interference with immune response and antibody production, and the




possibility of liver neoplasia are all significant aspects of the




toxicity produced by aflatoxins (11,17,18,21).




Fusariatoxin




     Species of Fusarium are capable of producing a variety of mycotoxins.




One of these, labeled as "T-2", produces a diffuse clinical disorder in




animals and man.  Humans develop symptoms that include nausea, vomiting,




drowsiness, ataxia or dizziness, diarrhea, and hemorrhage.   Cattle and




other ruminants undergo decreased clotting times with resulting hemorrhage




in muscles, and necrosis of skin (1,24).  This hemorrhagic disorder is




often associated with the feeding of moldy corn, but is not unique to




that grain.




Estrogenic Factor




     Another Fusarium species produces a metabolite called zearalenone




("F-2").  Usually assoicated with the feeding of moldy grain to pigs,




this syndrome involves vulvar hypertrophy, vaginal prolapse,  and mammary




hypertrophy.  The clinical situation is unique and does not usually




produce death, but the clinical condition is sufficiently  severe to




produce economic concern (6,14,16).
                               197

-------
Ochratoxin




     A product of either Aspergillus or Penicillium species of fungi,




this toxin has been isolated and chemically characterized.  Analytical




techniques are currently available for its detection in feed and food




materials.  The toxin is capable of causing diffuse hepatic and renal




damage; and clinical signs include weight loss, unthriftiness, repro-




ductive difficulties, abortion, and fetal resorptions (20).  Current




investigations with this toxin are extensive and future studies will




no doubt reveal much about its mechanism of action and potential human




hazard (2,6,14,15).




Rubratoxins




     This mycotoxin may be found alone in fungal isolates of Penicillium




rubrum (20) or may be assoicated with aflatoxin-producing fungi.  It




produces liver necrosis, but is especially known for its assoication




with profuse hemorrhages in the tissues of pigs.  Vomiting, refusal to




eat, diarrhea, jaundice, and liver lesions and widespread muscular hemor-




rhages have all been observed (27).  Large numbers of pigs have been




condemned upon slaughter in recent years due to the appearance of muscle




hemorrhages when the carcasses were being processed.




Sterigmatocystin




     This mycotoxin is similar or related to aflatoxin.   It is produced




by the Aspergillus mold (2), and currently has only been demonstrated




toxic in laboratory animals.  Investigations are continuing to determine




whether this specific mycotoxin is also a human health hazard.




Citrinin




     As a product of Penicillium molds (5), the metabolite has




been demonstrated to produce severe kidney lesions.  Nephrosis and unique




perirenal edema have been reproduced and documented in small laboratory




                                 198

-------
animals following feeding of this fungus (2).  Its role in human feeds




and possible health hazards has not been clarified.




Slaframine




     Red clover hay with "black patches" has been found to produce ex-




cessive and prolonged salivation when fed cattle (7,8).  The mold




Rhizoctonia was shown to produce a "slobber factor" which upon ingestion




by ruminants produces the unique salivation.  Animals may also develop




diarrhea, bloat, and stiff joints, although death is rare.  Cattle and




sheep may be affected; hence the fluid loss and resulting temporary




disability makes this mycotoxin a potential animal health hazard.




Alimentary Toxic Aleukia




     This name was given to a severe and often fatal disease of humans




and animals assoicated with the consumption of grain left under snow during




the winter months.  It has been particularly prevalnet during certain




years in which harvesting was delayed.  Primary toxic effects are on




the digestive tract and blood forming organs.  Diarrhea with blood in




the feces and leukopenia are common (8).  Acute degeneration may also




occur in kidneys and adrenal glands.




Facial Eczema




     The fungus Pithomyces chartarum produces a hepatotoxic metabolite




called sporidesmin.  This chemical produces severe liver lesions, photo-




sensitization, and death in sheep and cattle.  Large numbers of ruminants




have been lost in New Zealand and Australia due to this mycotoxicosis.




The condition is so severe that in New Zealand farmers are provided with




a warning service to alert them to periods when pastures are toxic.




Increased spore counts in warm wet weather invariably produces increased




hazard for sheep on pasture.  Affected animals suffer chronic liver
                                 199

-------
 damage and photosensitization when on high chlorophyll-containing rations.

 The production of  skin lesions may be delayed several months following

 ingestion of the mycotoxin and mortality rates can be quite high (6,8,

 23).

 Stachybotryotoxicosis

      Although this condition affects primarily horses, it also may involve

 cattle.   It is due to the consumption of hay or straw contaminated with
i
 toxic strains of Stachybotrys.  Following initial inflammation and swell-

 ing of the mouth and throat, progressive leukopenia,  impairment of blood

 clotting, and death follow.   On post-mortem examination there is wide-

 spread necrosis and hemorrhage in most body tissues.   Humans working with

 the contaminated forage may be affected by topical contact or by inhalation

 of the toxic metabolites (8).

 Equine Leukoencephalomalacia

      This condition is a chronic neuro-degenerative syndrome produced

 by mycotoxins of Fusarium species.   Horses are affected with a debilitat-

 ing and  progressive brain degeneration that eventually produces a dummy-

 like attitude and  eventual death.   On post-mortem examination the brain

 is found to contain necrotic areas of malacia (28).

 Sweet Clover Poisoning

      An  unidentified fungus apparently converts coumarin present in sweet

 clover (Melilotus   alba) into dicoumarol.   This is a  hemorrhagic substance

 that produces losses in cattle and sheep.   Prolonged  blood clotting times

 and severe internal hemorrhages are the major features of the toxicity (8).

 Hemorrhagic Syndromes

      Bleeding disorders due to fungi have been repeatedly documented in

 pigs, cattle, and  poultry.   They are associated with  growths of Aspergillus,
                                 200

-------
Penicillium, Fusarium, and Alternaria (8).  Moldy corn, other grains,

and mash have been the causative feeds with diffuse hemorrhages in the

muscle the most common clinical effect.  In birds, blood-tinged diarrhea,
      i                        .          .
paleness of wattles, hemorrhage and congestion of most body tissues, and

post-mortem lesions in liver, kidney, and bone marrow are characteristic.

This condition usually responds to the administration of vitamin K, , and

has resulted in many livestock rations containing increased quantities

of this vitamin.

Lupinosis

     Lupines fed as fodder to sheep and cattle have resulted in the

occasional animal losing weight, becoming jaundiced with occasional

photosensitization, progressing to aimless wandering, and severe cases

dying rapidly.  Post-mortem lesions are chronic liver disease with jaundice,

liver cirrhosis and fibrosis, and increased hepatic cell size.  Various

fungi have been suggested as being the etiologic agent for this condition

(8), but Phomopsis rossiana has recently been definitely incriminated.

Fescue Poisoning                                                        ,

     The plant Festuca arundinacea periodically produces a disease syndrome

characterized by sloughing of gangrenous extremities.  The similarity to

ergotism has led to the postulate that a mycotoxin is responsible  (6).

Although numerous species of fungi have been found on toxic grass, and

toxic constituents of several fungi have been isolated and identified,

it is still not known if any of these compounds is a causative agent

of fescue poisoning.

Effects on Immunity

     Recent studies (21) have documented that aflatoxin and some other

mycotoxins have a definite interference effect on the production of
                                 201

-------
immunity following the injection of antigens.  This effect is probably




related to the ability of some mycotoxins to bind to RNA and thereby




block the formation of antibodies in response to antigen exposure.  The




clinical significance of this observation remains to be established, but




experimental studies have shown significant interference with the estab-




lishment of an immune response.




Cancer Production




     Although cancer has never been described in clinical instances of




mycotoxicosis, the production of tumors by aflatoxins in some experimental




animals has produced concern over the concentrations of this toxin in




grains destined for human consumption (18).  The impracticality of attempt-




ing to eliminate all aflatoxins from human and livestock feeds poses




the question of what exposure level is to be tolerated.  The increased




concern over food production and availability of energy and protein sources




for human consumption will no doubt play an important role in establishing




aflatoxin concentration guidelines for future human foods.




Other Mycotoxin-Related Syndromes




     Photosensitivity.  Numerous field outbreaks of mycotoxicoses involving,




among other things, severe photosensitization, has established this




clinical sign as being produced by one or more mycotoxins (23).




     Abortions.  Aspergillus and Penicillium have been isolated from hay




which produced abortion in dairy cattle (8).  Ochratoxin A has been isolated




as one of the causative factors for this condition.  Other mycotoxins




have also been clinically suspected in field cases of bovine abortion.




     Gastroenteritis.  Digestive tract involvement is a common clinical




sign in cases of mycotoxicosis in cattle, sheep, swine, and occasionally
                                 202

-------
smaller animals.  Whether this is a primary effect of the causative myco-




toxin is currently unresolved; it may be that the digestive tract involve-




ment is secondary to debilitation produced by the toxin(s).  Further




work in this area is necessary to define the specific etiologic agent and




its direct effect (13).




     Poor Growth.  This vague clinical problem, also called "ill-thrift"




in some areas of the world, is most difficult to pinpoint as being produced




by one or more mycotoxins.  Lack of other etiologic agents and the finding




of potentially pathogenic fungi in the ration, suggests that a failure




to respond to normal dietary rations may indeed have a fungal base (8).




In some instances fungi present in high density have been shown to produce




highly toxic metabolites.  Large doses in ruminants have led to severe




hemorrhagic gastroenteritis, ulcerations of the fore-stomach, and death.




Daily small doses have led to weight loss with no adverse clinical signs.




     Hyperkeratosis.  The presence of toxic strains of Aspergillus in




hay and pelleted feed has been seen in outbreaks of this condition.  •




Lesions on the muzzle and mouth, hyperkeratosis of the cheeks and neck,




and degenerative changes in the liver are commonly produced.  Although




circumstantial evidence is strong, the metabolites isolated from this




fungus have not yet experimentally been connnected with the hyperkeratosis




syndrome  (8).




                        Public Health Concerns




     Since fungi are widely distributed and environmental conditions for




mycotoxin production occur commonly, the prevention of mycotoxin develop-




ment in feed and foodstuffs is most difficult.  This is especially so




in the developing countries which lack sophisticated storage systems and




elaborate regulatory mechanisms.  In the United States, the treatment of
                                 203

-------
grains during storage to prevent the development Of molds and,, potential




mycotoxin formation is a major industrial thrust (2).




     The ingestion of toxic quantities of mytoxins is best prevented




by not feeding foods or livestock feeds that contain potentially harmful




concentrations.  Quality control of human and animal diets is therefore




important.  Unfortunately, mycotoxins are so prevalent that many dietary




constituents would be discarded if the mere presence of potentially harm-




ful concentrations of mycotoxins was the sole criteria for their usefulness,




In human foods, public criteria and humane values usually govern the ac-




ceptability of food.  In developing countries and areas of food shortages,




these criteria are often overlooked, with the resulting increase in    '




mortality due to mycotoxins (18).  Livestock feeds are somewhat more




removed from human hazard, since metabolism by an intermediate animal




is required before human consumption of the animal product (meat or milk).




Animal feeds containing borderline concentrations of mycotoxins may,




therefore, be fed to older animals rather than the more sensitive young




or the feed may be diluted with other feed containing "safe" levels of




mycotoxins (13,26).  Prevention of mycotoxin development of consumption




is still the most improtant protection against mycotoxicoses in man or




animals.




     Only a few of the toxins of fungal origin have presently been iden-




ified, but methods for accurate and sensitive detection are available for




some mycotoxins (1,25).   Unfortunately, practicality makes the detection




and assay of mycotoxins relatively limited, since sophisticated laboratory




instrumentation and expertise is usually necessary to determine levels




of mycotoxins in foods and feeds.  Almost all forages and foods contain




some detectable mycotoxins, especially aflatoxins; but meats used for
                                 204

-------
human consumption are notably free from these chemicals since they are

not stored in the muscles of food-producing animals.  The greatest

danger appears to be from the utilization of grains and plant-source

protein in animal and human feeds.

     In addition to the laboratory procedures that are limited but avail-

able to detect and quantitate mycotoxins, feeding trials in experimental

animals may also be used to determine any interferences in normal growth

and development that might result from mycotoxin-contaminated feeds.

This type of detection is expensive, however, and economics frequently

require that this time-consuming procedure not be attempted.  The recent

and continuing development of rapid field procedures to detect toxic

levels of mycotoxins may also greatly assist in reducing the hazard

from these naturally-occurring dietary poisons.  Such field detection

methods may be utilized by laymen in feed-producing areas or mills,

with specific confirmation later provided by laboratory personnel on

feed samples that were preliminarily shown positive.

     Because of the subtleness of mycotoxin problems and their wide-

spread occurrence and potential for human and animal health hazard,

this threat to our food-producing population and ourselves should

be continually studied and documented.  Not only is an increased public
                                   r
and scientific awareness of this hazard necessary, but continual and

increasing funds for research studies are required (3). 'More study of

the variety of clinical syndromes produced in all species of animals

and in man under varying conditions is imperative, and documentation

of the minor subtle effects that often escape notice or diagnosis are

urgently called for (12,20).   Further concern is associated with potential

interaction of mycotoxins with themselves or even with other foreign
                               205

-------
or naturally occurring chemicals in the diet or environment (18,19,22).




Such interactions are extremely potentially hazardous since animals




and humans are being subjected to increasing numbers of chemical agents.




The interactions that may occur between one or more mycotoxins and




any number of the chemicals in our environment, used as therapeutic




agents, or added to diets should be studied and considered for pos-




sible harmful effects.




    Since mycotoxins are universal and political boundaries are in-




effective in preventing their spread or occurrence in feeds and foods,




the problem presented by mycotoxins is international in its significance




(8,26).  Although scientists generally recognize that toxins do not




discriminate based upon nationality or race, politicians and regulatory




officials need to be reminded that military strength or political




position is no deterrent to the harmful effects that mycotoxins and




other foreign chemicals may produce.  International cooperation to




investigate toxic syndromes and control their occurrence in all animals




and peoples of all nations is an important and vital step toward




protecting our own health.




Summary




    Mycotoxins are fungal metabolites capable of producing harmful affects




on biological systems.  Man, domestic and wild animals, and even plants




may be affected.  It has only been since the 1940?s that significant




progress has been made in understanding the mycotoxicoses.  Since




that time, however, and especially in recent years, a variety of disease




syndromes have been attributed to these fungal by-products.  Approx-




imately 100 species of molds are capable of producing these toxins.




The most heavily studied are the aflatoxins which produce hepatic




cell necrosis, increased clotting time and capillary permeability,





                            206

-------
and are carcinogenic.  Very small daily dosages will produce clinical




signs in young individuals, and more subtle effects, such as inter-




fering with the development of immunity, have also been documented.




MI hpr mvrot-oxlnq are capable of producing such clinical dlspasps as




hyperestrogenism, abortion, failure of conception, embryonic reabsorp-




tion, hypersalivation, photosensitization, nephrosis, and central nervous




system disturbances.  Since many of the clinical affects are similar




to those of other chemicals or infectious agents, diagnosis of mycotoxicosis




is difficult.  Reliable analytical methods are available for some, but




not all, of the toxins.  Fungal culture and the elimination of other




clinical possibilities are of diagnostic value.  A more specific under-




standing of the types of clinical syndromes and the biological effects




capable of being produced by fungal toxins is an important area for




investigation, especially due to the varied international nutritional




levels and the many potential subtle and complex disease entities.






                             References




1.   Bamberg, J. R.  The Biological Activities and Detection of Naturally




    Occurring 12,13-Epoxy-A9-Trichothecenes.  Clin. Toxicol. 5:495-516.




    1972.




2.   Berg, G. L.  Master Manual on Molds and Mycotoxins.  Farm Technology/




    Agri-Fieldman, Willoughby, Ohio, 1972.




3.   Buck, W. B., and Oehme, F. W., eds.  Symposium on Natural Toxins




    in Foods and Feeds.  Clin. Toxicol. 5:437-480.  1972.




4.   Burfening, P. J.  Ergotism.  J.A.V.M.A. 163:1288-1290.  1973.




5.   Carlton, W. W., Tuite, J. and Caldwell, R.  Penicillium viridicatum




    Toxins and Mold Nephrosis.  J.A.V.M.A., 163:1295-1297.  1973.
                                207

-------
 6.  Ciegler, A., Kadis,, S., and Ajl, S. J.  MIcrobial Toxins, Vol.




     6-8.  Academic Press, New York.  1971-1972.




 7.  Crump, M. H.  Slaframine (Slobber Factor) Toxicosis.  J.A.V.M.A.,




     163:1300-1302.  1973.




 8.  Culvenor, C. C. J.  The Hazard from Toxic Fungi in Australia.




     Australian Vet. J.  50:69-78.  1974.




 9.  Cysewski, S. J.  Paspalum Staggers and Tremorgen Intoxication in




     Animals.  J.A.V.M.A. 163:1291-1292.  1973.




10.  Forgacs, J. and Carll, W. T.  Mycotoxicoses.  Adv. Vet. Sci., 7:




     273-282.  1962.




11.  Goldblatt, L. A.  Aflatoxin.  Academic Press, New York, 1969.




12.  Goldblatt, L. A.  Implications of Mycotoxins.  Clin. Toxicol. 5:




     453-464.  1972.




13.  Herrick, J. B.  Mycotoxicosis in Animals.  Vet. Med./Sm. An. Clinician,




     69:483, 486.  1974.




14.  Lillehoj, E. B.  Feed Sources and Conditions Conducive to Production




     of Aflatoxin, Ochratoxin, Fusarium Toxins,, and Zearalenone.  J.A.V.




     M.A.  163:1281-1284.  1973.




15.  Munro, I. C., Scott, P.  M.,  Hoodie, C. A. and Willes, R. G.  Ochra-




     toxin A—Occurrence and Toxicity.  J.A.V.M.A. 163:1269-1273.  1973.




16.  Nelson, G. H., Christensen,  C. M. and Mirocha, C.  J.  Fusarium and '




     Estrogenism in Swine.  J.A.V.M.A.  163:1276-1277.  1973.




17.  Newberne, P. M.  Chronic Aflatoxicosis.  J.A.V.M.A.  163:1262-1267,




     1973.




18.  Newberne, P. M.  The New World of Mycotoxins-Animal and Human Health.




     Clin. Toxicol. 7:161-178.  1974.
                                 208

-------
19.  Ohtsubo, K.  Mycotoxins in Foodstuffs and Their Biological Action




     on Mammals.  Beitr. Path. Bd. 148:213:220.  1973.




20.  Pier, A. C.  An Overview of the Mycotoxicoses of Domestic Animals.




     J.A.V.M.A. 163:1259-1261.  1973.




21.  Pier, A. C.  Effects of Aflatoxin on Immunity.  J.A.V.M.A. 163:




     1268-1269.  1973.




22.  Proceedings of the Symposium on Mycotoxins and Mycotoxicoses.




     University of Missouri-Columbia, May 94 1972.




23.  Richard, J. L.  Mycotoxin Photosensitivity.  J.A.V.M.A. 163:1298-




     1299.  1973.




24.  Smalley, E. B.  T-2 Toxin.  J.A.V.M.A. 163:1278-1281.  1973.




25.  Stoloff, L.  Analytical Methods for Mycotoxins.  Clin. Toxicol.




     5:465-494.  1972.




26.  Messel, J. R. and Stoloff, L.  Regulatory Serveillance for Afla-




     toxin and Other Mycotoxins in Feeds, Meat, and Milk.  J.A.V.M.A.




     163:1284-1287.  1973.




27.  Wilson, B. J. and Harbison, R.  D.  Rubratoxins.  J.A.V.M.A.  163:




     1274-1276.  1973.




28.  Wilson, B. J., Maronpot, R. R.  and Hildebrandt, P.  K.  Equine




     Leukoencephalomalacia.   J.A.V.M.A.  163:1293-1295.   1973.
                                 209

-------
210

-------
        AN IMMUNOLOGICAL APPROACH TO POPULATION CONTROL




                       Lloyd C. Faulkner




                   Colorado State University






     The studies to be described were the subjects of doctoral




dissertations by Mauricio H. Pineda, D.V.M., M.S., Ph.D., John E.  Lunnen,




B.S., M.S., Ph.D. and Abbas Al-Kafawi, D.V.M., Ph.D.  Dr. Pineda has




returned to Colorado State University as a Postdoctoral Fellow after




experience as a member of the Faculty of Veterinary Medicine at the




University Austral in Chile and as a Postdoctoral Fellow with Dr.  Oliver




Ginther at the University of Wisconsin.  Dr. Lunnen is a member of the




faculty of the Department of Physiology, Kansas City College of Osteo-




pathic Medicine, Kansas City, Missouri.  Dr.  Al-Kafawi is a member of the




Faculty of Veterinary Medicine at the University of Baghdad in Iraq.




     Dr. Pineda's original objective was to define the role of luteinizing




hormone (LH) in regulating the function of the corpus luteum in cattle.




We proposed to produce antibodies against bovine LH in male rabbits.




The antibodies were to be transferred passively to cattle, where they




would neutralize endogenous LH and prevent the presumed luteotropic




activity of LH.  However, during the course of active immunization of




the rabbits, it became quite evident that the procedure was having a




profound effect on the testes of the rabbits.  The testes atrophied and




eventually ascended into the abdominal cavity.




     We repeated the experiment with doe rabbits and again produced




reproductive dysfunction and genital atrophy.  The production of anti-




bodies against a relatively purified preparation (NIH-LH-B3) of bovine
                             211

-------
 luteinizing hormone was associated with genital atrophy in both sexes



 of immunized rabbits.  The results were attributed to the neutralization



 of endogenous gonadotropin, presumably LH, by antibodies produced against



 bovine LH.  This postulate was supported by the demonstration of anti-



 bodies in the sera of immunized rabbits which precipitated some factor,



 presumably gonadotropins, in extracts of pituitary glands from rabbits.
                  /


 The extract of pituitary glands of rabbits formed a line of partial



.identity when tested with NIH-LH-B3 in microimmunodiffusion against



 the sera of immunized rabbits.  It appeared that bovine LH was suffi-



 ciently foreign, when administered with Freund's complete adjuvant,



 to stimulate the production of antibodies in rabbits.  The rabbits'



 own LH, however, was apparently sufficiently similar to the bovine



 LH that the antibodies neutralized the endogenous hormone, resulting



 in gonadal and genital atrophy.



     A series of studies was conducted to detect cross reactions of



 the antibodies in the sera of rabbits immunized against bovine LH with



 pituitary factors in the extracts of glands from a variety of animals.



 The pituitary glands of dogs and cats, among others, contained factors



 which were precipitated by the immune sera.  This raised the distinct



 possibility that antibodies produced against bovine LH in dogs and cats



 might neutralize endogenous gonadotropin and cause genital atrophy,



 giving us a non-surgical method of suppressing reproductive function.



     The bitch presents a very real problem as a subject for research



 on contraceptive technology because of the long interval between suc-



 cessive heats.  Reproductive function in male dogs, conversely, is con-



 tinuous.  Since we had already demonstrated that the genital atrophy
                             212

-------
in immunized rabbits was not specific to sex, we elected to use male


dogs in our exploratory studies.  Using males, we were able to monitor


continuously the association of immunologic response and reproductive


function.


     Semen was collected weekly by digital stimulation in the presence


of an estrogenized bitch.  Seminal ejaculates were collected as presperm,


sperm-rich and post-sperm fractions of the basis of visual observation


of the color and turbidity of the ejaculate during delivery.  The pre-


sperm fraction is delivered first and is thought to be the secretion


of urethral glands; it is nearly devoid of spermatozoa.  The second


fraction to be delivered contains most of the spermatozoa, while the


third fraction, primarily a prostatic secretion, contributes most of the


ejaculatory volume.  It was hoped that differential changes in some


measurable parameter in each fraction might indicate selective impair-


ment of specific portions of the reproductive system.


     Twenty-four male Beagles from 1^ to 4% years of age were randomly


assigned to six groups of four dogs:  untreated in a short-term study;


Freund's complete adjuvant (FCA) only in a short-term study; FCA + LH


in a short-term study; untreated in a long-term study; FCA only in a

                               v
long-term study; and FCA + LH in a long-term study.  Dogs in the short-


term study were autopsied 15 weeks after the start of treatments; those


in the long-term study were autopsied 52 weeks after the start of


treatments.


     Each LH-immunized dog was given a total of 33 mg bovine LH (NIH-


LH-B5) in 12 injections over a period of 94 days.  Freund's complete


adjuvant is quite effective in enhancing the immunologic response but
                              213

-------
has the distinct disadvantage of stimulating a rather severe inflam-




matory reaction at the site of injection.  The procedure we used in this




study was selected to demonstrate whether the immunologic approach to




suppressing reproductive function was possible and not for its practicality.




     Antibodies which bound a highly purified preparation (LER 1072-2)




of bovine luteinizing hormone were present in the sera of immunized




dogs but absent from the sera of untreated dogs and dogs treated with




the adjuvant alone.  Extracts of canine pituitary glands inhibited the




binding of purified bovine LH by the immune sera, indicating that anti-




bodies against bovine LH cross reacted with some factor in the canine




pituitary gland, presumably LH.  No ejaculates were obtained from the




immunized dogs when their sera, diluted 1:2000, bound more than about




20% of the purified bovine LH.




     The immunized dogs which were killed at week 15 had ceased to




ejaculate by the sixth week, and further attempts to collect semen




were unsuccessful.  The dogs which were killed at week 52 ejaculated




at only 23% of the attempted collections after the fifth week, and




65% of the ejaculates were collected from one dog which recovered




from the effects of immunization.




     Failure to ejaculate and the presence of antibodies against LH




were accompanied by a decrease in blood levels of androgens to levels




commonly observed in male castrates.  The weights of the testes, epi-




didymides and prostate glands were significantly less than those of




the untreated and adjuvant-treated dogs at autopsy at both 15 and 52




weeks.  Microscopic sections of these organs were characterized by




marked atrophy and fibrosis in all but the single dog which recovered




in the long-term study.  The weights and, microscopic morphologies of







                              214

-------
the reproductive tissues from the dog which recovered from the effects


of immunization were similar to those of the dogs in the control groups.


Treatment with the adjuvant alone did not produce detectable changes


in the testes or accessory sexual organs.


     Immunization against bovine LH caused no detectable changes in
                            /»

the adrenal or thyroid glands, measured by glandular weights, microscopic


morphology, and blood levels of adrenal and thyroid hormones.


     We had demonstrated that suppression of reproductive function by
                                          B>

immunization against gonadotropins was possible.  The next challenge


was to investigate methods of producing a prolonged suppression of


reproductive function by a single dose of a commercially available


gonadotropic antigen.


     Human chorionic gonadotropin (HCG) is widely available, very closely


related to luteinizing hormone in several species, and free of contamina-


tion with pituitary tropins which might cause undesirable side effects.


We had previously shown that antibodies produced in rabbits against


bovine LH did not react with HCG in microimmunodiffusion but decided


the possibility of success took precedence over the probability of failure.


     A single dose of HCG in adjuvant stimulated the production of


antibodies in bitches and males.  The Freund's complete adjuvant was


superior to a water in oil adjuvant in stimulating the production of


antibodies which bound HCG.  Unfortunately, the antibodies failed to


cross react jln vivo or jLn vitro with canine pituitary gonadotropins,


and reproductive function was unaffected.  We were encouraged, however,


by the production of antibodies in response to a single injection of


the antigen.
                              215

-------
     We searched in vain for a commercial preparation of bovine LH.




Dr. Pineda had successfully immunized and caused genital atrophy in




a single male dog with a series of injections of a commercial preparation




of ovine gonadotropins.  Three adult, male Beagles were injected with




a single dose of commercial ovine gonadotropin in Freund's complete




adjuvant.  All three failed to ejaculate by the second or third week




after inoculation and associated with the development of antibodies




which bound a highly purified ovine LH.  Levels of antibodies remained




elevated and the dogs failed to ejaculate for 20 to 30 weeks, then low




or absent levels of antibodies were associated with recovery of ejacula-




tory ability.  We are currently investigating methods of prolonging




immunity and sterility.




     Prepuberal bitches and male pups have been immunized with a single




injection of ovine gonadotropin in Freund's complete adjuvant.  We have




observed that puberty is delayed in both sexes, and the males develop




seemingly normal reproductive function.  The results of immunizing




prepuberal bitches are incomplete.




     We have shown that an immunological approach to controlling re-




production is technically possible.  Progress has been made toward




making this a practical approach, and several problems are being




attacked.
                               216

-------
                            ARSENICS




                         Arthur A. Case




                University of Missouri-Columbia






     Arsenical compounds may be the cause of intoxications in fowls




or animals.  Exposure to arsenicals could be due to natural environ-




mental influences but almost all are due to induced circumstances.




Poisoning by arsenicals may be acute and dramatic (2,7,21,45) or




chronic and insidious (2,26,60,66).  The type of animal production




management in use is also important in determining the nature and




extent of the loss as well as the potential hazard to human health




from subclinically poisoned fowls or animals entering the food chain.




Selby, et al., 1974 (58) as well as others deal in some length with




such possibilities (5,6,14,24,26,28,34,40,46,55).




     Arsenicals represent natural earth substances as well as potent




commercial compounds that are still in wide use in industry, as brush




killers and debarkers, herbicides, defoliants, wood preservatives,




and as by-products of mining or smelter industries, or other coal




burning industry (9,18,22,25,30,45,47,63,65).  The author works with




local veterinarians, extension area specialists, owners and producers,




feed industry representatives, and anyone else with an interest in




specific problems involving toxic substances, whether of natural or




artificial circumstances.




     Deliberate, malicious poisoning can happen but most instances of




poisoning of man or animals are accidental; most could have been pre-




vented or greatly ameliorated by careful management and judicious




operation of such equipment as field or orchard sprayers (15).
                              217

-------
     Arsenic compounds should be considered as toxic by all who use




them (3,9,19,45,51).  Arsenic (itself, non-toxic) and most of its com-




pounds (many are toxic) are derived from the earth's crust, hence,




are to be found in one form or another nearly everywhere in soils,




water, plants and animal tissues, in the air as well as the sea




(9,12,19,26,63).  Recent studies by geochemists. have shown that there




are few anomalously high amounts of arsenic in surficial soils or




waters although there may be exceptions (20,53,54) in the United




States.  Vinogradov (1959) (63) described in full, the geochemistry




and rare or dispersed elements in soils of Russia.




     Recent investigators have attempted to prove or disprove that




arsenic is an essential trace element but much remains to be proven




about the place of arsenic in vital plant or animal metabolism (6,36,




61,64).  It may well be that the requirements for arsenic are so low




that enough is supplied by the ubiquitous background amounts (5,36,




56,61).  That arsenic compounds may enhance nutrition and growth is




a matter of fact in amphibia (61), small rodents  (61), and in poultry




and swine (5,44,61).  It was the recycling of the waste (manure) from




poultry as well as other animal waste that led to the research reported




by Calvert (14) and several others (1,30).  Calvert published a dozen




tables summarizing what residues, and where such are found, in what




concentrations in litter, meat of cattle, sheep, milk, and kidney and




liver (14).   He also reported the withdrawal time-amounts and his




observations support that of some earlier as well as contemporary




authors (27,28,33,45,48,49,50,55,62,61,66).




     Toxicity of any arsenic compound depends upon solubility of the




compound as well as to how it is taken into the body (9,5,7,12,13,22,




23,61) and the form it is in (9,11,18,25).  Inhalation of microaerosol





                              218

-------
dusts (Natsuch, £t al., [l974] [4?]; Roberts and Goodman, cited by




Case.[l7]; Runnels, cited by Case [l?]) and gases  (Arsine)  (9) are




more likely to affect man (industrial hazards, laboratory hazards)




than animals (9,62,65).  However, fine dust fall-out from coal burning




power plants, smelters and refineries processing raw materials contain-




ing arsenic have been reported as sources for chronic .poisoning in




animals by Roberts and Goodman, cited by Case (17); Natsuch, et al.,




(1974) (47); and by Clarke and Clarke (18) as well as Buchanan (9).




Volcano gases may contain arsenic (9) as do sea and ocean waters  (9,61).




     Some arsenic compounds may be used in treatment of man or animals




(23,31) and some of these may be injected; poisoning can readily  follow




such medication, especially in the very sensitive person or animal




(Anon [2]; Buck [lO]; Case, citing Staples [l?]; Salisbury and Van




der Wauden [17]; Liebig [38]; Morehouse [43]; Buchanan [9]).  Arsenic




may be readily absorbed through abrasions and lacerations of the  skin




and such exposure may cause intoxications of severe intensity, especially




in sheep (66), cattle (18), horses (60), as well as man (9).  Arsenic




is still in use in some areas for control of external parasites of




animals, and combined with lead for control of tapeworms in sheep




(17,18,22,40,45,66).




     Organic arsenicals have been considered as less toxic than the




inorganic arsenic compounds and are in wide use for growth promoting




feed additives (fowls and swine)\ coccidiosis control, and for therapy




of swine enteric diseases (12,42,5,55,58,61).




     The inorganic arsenicals and their medical and toxic properties




have been known for several millenniums, perhaps longer, because
                              219

-------
Socrates and Aristotle were probably familiar wicn tne properties or




such compounds (9,18,38,58).  Paracelsus introduced inorganic salts




into 16th century Medicine (9), and there has been very extensive




industrial, agricultural and other use of arsenicals until very re-




cently (9),  Arsenic compounds are still in wide use as general herb-




icides (8,19,22,29) or selective herbicides (11,12,19,22).




     In the United States, the Environmental Protection Agency, United




States Department of Agriculture, and in situations which involve toxic




residues in human food, FDA set standards for the use of toxic sub-




stances, including arsenicals (3,4,6).  When some of the chlorinated hydro-




carbon pesticides were restricted or insects for which they were in use




developed resistance, the arsenicals were again used (29) and animals, in-




cluding deer were poisoned by the vegetation dusted or sprayed with arsenicals.




Previous heavy use of the arsenicals, some of which also contained copper




and lead in orchards left heavy contamination of soil and vegetation




which still persists (2,11,16,17,38,58).  Ellis (21) describes a sudden




loss of one-third of a herd of Brangus bulls worth an estimated $10,000;




6 were found dead, and 4 more died but 20 recovered following specific




treatment with BAL.  They ate calcium arsenate out of the container




which was easily available to the bulls in an old shed.  We could




describe several very similar "accidents" caused by carelessness in




storage of poisons, the improper disposal of surplus field or orchard




pesticides, or improper disposal of "empty" containers, or the reuse




of "empty" pesticide containers, including arsenicals.   Some fields,




orchards, or farmyards have been heavily contaminated by spills of




spray or dust materials, or by the "washings" in cleaning the equipment
                               220

-------
after use.  Such soil heavily saturated by arsenic will remain barren




for long periods of time (2,18,25,38,58,51).




     Selby, eit al. (1974) (58) described in detail several episodes of




arsenic poisoning in cattle in which barren soil was eaten by the cattle




(usually young cattle) or an owner left the animals in a pasture and




used an arsenical to kill pasture weeds (and his cattle'.).  Several




instances of losses due to arsenical poisoning (confirmed by demonstra-




tion of high levels of arsenic plus a typical acute intoxication syndrome)




are under investigation at present (2,43).'  All are the kind of situation




where the animals know where the poison is but the owner doesn't (43)1




On pastures or ranches comprising several hundred acres, especially




with recently acquired properties, one can have a difficult problem




discovering the source of the poison.  Old orchards may be gone with




little evidence of their previous existance.  Storage sheds may be




destroyed by fire or decay but the arsenic will still persist.  Dis-




carded grasshopper bait may be poisonous for many years beyond the time




its identity has disappeared into the soil;  very heavy rains may wash




it into a pond, several decades later (2).  Strip mining ponds or




"lakes" may carry higher than usual amounts of arsenic for many years




(20) but most arsenical ores are not surficial deposits in this country




(53).  An occasional exception occurs (54),  as in a high arsenic situation




near Pottersville, Missouri.  We have not recognized toxicity in animals




from that area (2,43).




     A common practice of using a general herbicide to kill all of the




vegetation along right-of-ways, on fairgrounds, about transformer and




switch yards has resulted in the poisoning of farm animals and wild-




life, especially when sodium arsenite was used (2,7,12,15,16,17,18,
                             221

-------
22,25,29,32,38,45,50,51,65,66).




     Drift of arsenical spray caused poisoning of cattle in the




instance described by Weaver (65).  Udall, citing Fincher mentions




arsenical poisoning and remarks upon the lack of decomposition of car-




casses over long periods (60) and we have observed that and used rumen




contents, liver and kidney, as well as bone for analysis to demonstrate




toxic levels of arsenic, lead or copper in carcasses that had been dead




more than a year.  The state of preservation due to toxic levels of




arsenic is remarkable:  the carcass mummifies and all sarcophagous




creatures including the putrefactive microorganisms are killed or




repelled (2,58,60).  Some of the barren earth spots described by Selby,




^t al. (58) as well as the conditions mentioned by Liebig (38) were




on places where the calves ate the barren earth and were killed,by




toxic amounts of arsenic.  Modern methods of analysis for arsenic




(37,39,47,53,54,61,62,62,33) are available and some of the older




classical tests for arsenic are still in use, especially for larger




amounts that would be expected in poisoning (12,16,17,18,23,24,25,




28,39).




     It should be noted that mere detection of a toxic trace element




in animal tissues or feeds is not of diagnostic significance unless




there is a syndrome of poisoning or other manifestation of intoxication




such as an interference syndrome, Case (17), and many others have made




the same observation (7,8,9,12,18,19,21,25,27,28,31,32,35,40,41,45,




48,50,51).




     Arsenicals of one kind or another have been blamed for causing




malignant neoplasia (52,9) but this has been disputed by some other




authors (56), (Frost, cited by Underwood [6l]); working with life-time
                             222

-------
medication using sodium arsenite or other arsenical, Schroeder and




Balassa (56) were not able to show any evidence of carcinogenicity in




small laboratory rodents although the rats and mice did accumulate




considerable arsenic in such tissues as the aorta and the red blood




cells.  It just may be that rats and mice have special reactions to




arsenic that are entirely different than other species of animals, or




man (56,62', 66) .




     Underwood (61) has recently reviewed and summarized the literature




regarding trace elements, including arsenic and a small book on arsenic




has been written by Buchanan (9).  New Zealand workers have written




comprehensive studies of the actions of arsenic, especially as it




pertains to ruminants (45) and thier findings support those of other




authorities (7,12,13,18,25,32,50).




     Regelson, et al. (52) found no relationship between tissue level




of arsenic and lesions assoicated therewith but in most instances of




acute and subacute poisoning of animals, intense gastroenteritis is




readily evident at necropsy (2,7,12,16,17,18,23,25,32,34,38,45,46,50




51,28).  Peracute poisoning in which the animals are killed within a




few hours may not show characteristic lesions of the digestive tract




and these could be mistakenly diagnosed as other conditions, both under




field conditions and in the necropsy laboratory unless the presence




of arsenic is suspected and analysis made to confirm its presence or




rule it out (2,8,12).




     Anyone working with animals under field conditions may be misled




easily:  arsenic poisoning in farm animals and wildlife may be unsus-




pected and conditions such as grass tetany, winter tetany, prussic
                             223

-------
acid poisoning, or peracute ammonia  (urea) and nitrite may be suspected




as more logical under a number of circumstances (2,12,28,29,32,34,51).




Owners also have a tendency to consider all loss of animals over a




period of years as "poisoning" if a single instance of arsenical or




other poisoning can be confirmed (2) and many may attempt to recover




damages from the veterinarian, a neighbor, an industry, or an insurance




company (2).  We have several such instances in our area at present,




and this is one reason that supportive diagnostic analysis is difficult




to obtain from those best able to render such help.  The author routinely




refers suspect medical-legal analysis to a commercial laboratory that




is willing to be involved in such proceedings but the veterinarian




still has to make the diagnosis in most situations which involve farm




animals, pets, or wildlife if the veterinarian is called into the




situation by an owner.  Many times, it is impossible to make other than




a tentative diagnosis; we have had occasion to defend such tentative




diagnosis in court, and we know from experience, one cannot have too




much supportive information (both, qualitative as well as quantitative




analysis, where possible).  Good supportive laboratory analysis is




expensive, and not always available to those who may need it most.




     Selby, at ad. (58) as well as others (49) have described very well




the possibilities of arsenic moving into human food chains but the




possibility may pose more of a problem than the acutal probability and




many other food substances such as marine (sea foods) are naturally




higher in arsenic content than most tissues of acutely poisoned food




animals such as poultry, swine, cattle and sheep,  as pointed out by




Selby (58) and a large number of other authors summarized by Underwood
                             224

-------
(61), Liebig (38), Krocza (33), Moxon (46), and Wahlstrom (64) were




aware of the interaction between arsenic and selenium more than 35




years ago and recently Thompson (59), Selby, &t_ al_. (57), and well as




Underwood (61) have dealt with interrelationships of trace and macro




elements and their influence on the nutrition of man and animals.




Under field conditions, it is the many uncontrolled variables that have




to be considered rather than standardized situations with one or two




variables.  To make field situations more complex, some of the possible




variables (such as arsenic) may not be readily recognized.  The plane




of nutrition, the time of year, climatic conditions, the kind of animals,




their age and sex, and many other variables may determine the clinical




field picture.  Determination of what is shown in that picture may




require much time, and detailed study of many fine points.
                              225

-------
                              References



  1.   Andersson,  A.  and Nilsson, K.  0.  1972.  Enrichment of Trace Elements

      from Sewage Sludge Fertilizer  in Soils and Plants.  Ambio 1:176, cited


      by Horvath, D.  J. (1974).
 t                  '
  2.   Anonymous:   Veterinary Clinic  Records, College of Veterinary Medicine,

      University of  Missouri, Columbia, Mo., 1968-1974.

  3.   Anon:  Summary of Registered Agricultural Chemical Uses Insecticides,

      Repellants, Acaricides, 3rd Ed. EPA, Washington, D.C.:lll-C-4 & 4.1.

      March,  1972.

  4.   Anon:  1972.  Code of Federal  Regulations.  21.

  5.   Anon:  Arsenics as Growth Promoters in Organic Form.  Nutr. Reviews

      14:206-209, 1956.

  6.   Berreth, Donald A.  Arsenic Tolerance Level. T73-44, FDA Press Office

      in Food Regulations.  1973.

  7.   Blood,  D. C. and Henderson, J. A.  Veterinary Medicine, 3rd Ed.,

      Williams & Wilkins Co., Baltimore, Md., pp. 758-849.  1968.

  8.   Boyce,  A. P.,  Verme, L. J.  Toxicity of Arsenic Debarkers to Deer in

      Michigan.  Proceed.  16th Midwest Wildlife Conference.  1954.

  9.   Buchanan, W. D.  Toxicity of Arsenic Compounds.  Elsevier Publ. Co..,

      New York, 155  pp.  1962.

 10.   Buck, W. B.  Untoward Reactions Encountered with Medicated Feeds.

      The Use of Drugs in Animal Feeds.  Nat. Acad. Sci., Wash., D. C.

      Publ. 1679:196-217.   1969.

 11.   Buck, W. B.  Pesticides in Food Chains.  Proceed. U.S.. Animal Health.


      Assoc.   73rd An. Meet. 221-226.  1969.

12.   Buck, W. B., Osweiler, G. D. and Van Gelder, G. A.  1973.  Clinical

     and Diagnostic  Veterinary Toxicology.  Kendall/Hunt, Dubuque, la.



                                  226

-------
13.  Bucy, L. L., Garrigus, U. S., Forbes, R. M., Norton, H. W. and Moore,




     W.' W.  Toxicity of Some Arsenicals Fed to Growing-fattening Lambs.




     J. Anim. Sci. 14:435-445. 1955.




14.  Calvert, C. C.  Feed Additive Residues in Animal Manure Processed




    .for Feed.  Feedstuffs (45):32-33, April 23, 1973..




15.  Case, Arthur A.  Toxicologic Problems in Large Animals.  J.A.V.M.A.




     149(12):1714-1719.  1966.




L6.  Case, Arthur A.  1972.  Heavy Metal Poisoning in Animals.  Proc.




     First Conf. Geochemistry and Health, Colorado State Univ., E.P.A.




     1972.




17.  Case, Arthur A.  Toxicity of Various Chemical Agents for Sheep.




     J.A.V.M.A.  164:277-283.  1974.




18.  Clarke, E. G. C., and Clarke, M. L.  Garners Veterinary Toxicology.




     3rd Ed., The Williams and Wilkins Co. pp. 44-54.  1967.




19.  Done, A. K. and Peart, A. J.  Acute Toxicity of Arsenical Herbicides.




     Clin. Tox. 4:343-355.  1971.




20.  Ebens, R. J.,.Erdman, J. A., Feder, G. L., Case, A. A., and Selby,




     L. A.  Geochemical Anomalies of a Claypit Area, Callaway County,




     Missouri, Related Metabolic Imbalance in Beef Cattle.  U.S. Geological




     Survey Prof.  Paper 807, U.S. Supt. of Docum. Wash., D.C.  1973.




21.  Ellis, H. R., and Herron, J. T.  A Busy Weekend:  Acute Arsenic Poison-




     ing in Brangus Bulls.  Arkansas Animal Morbidity Reports 6(6):1-2.  1961.




22.  Frear, D. E. H.  Chemistry of the Pesticides.  3rd Ed., D. Van Nostrand




     Co., New York, N. Y.  Arsenicals 239-268.  1955.               '




23. v  Goodman, L. S. and Oilman, A.  The Pharmacological Basis of Therapeutics.




     3rd Ed., The MacMillan Co.,  New York, pp. 944-951.  1966.
                                   227

-------
24.  Ham, W. E., Kline, E. A. and Ensminger, M. E.  Residual Arsenic and




     Strychnine in Tissues of Drug Treated Cattle.  Am. J. Vet. Res. 10:150.




     1949.                                           '        '




25.  Hammond, P. B.  toxic Minerals, cited by L. Meyer Jones, Veterinary




     Pharmacology and Therapeutics, 3rd Ed., 1965, 4th Printing 1970.




     Arsenic: 960-963.  1965.




26.  Harkins, W. D. and Swain, R. E.  Arsenic in Vegetation Exposed to




     Smelter Smoke.  J. Amer. Chem. Soc. 30:915.  1908.




27.  Harkins, W. D. and Swain, R. E.  The Chronic Arsenical Poisoning of




     Herbivourous Animals.  J. Amer. Chem. Soc. 30:928.  1908.




28.  Hatch, R. C.  Inorganic Arsenic Levels in Tissues and Ingesta of




     Poisoned Cattle.  Canad. Vet. J.  10:117-120.  1969.




29.  Hayes, F. A., Greer, W. E., Shotts, E. B.  A Progress Report from




     Southeast Cooperative Deer Disease Study.  Trans.  N. Amer. Wildlife




     Conference 21:133-136.  1957.




30.  Horvath, D J.  Limits for Sewage Recycling.  Interface 3(2):18.  1974.




31.  Jones, L. Meyer.  Veterinary Pharmacology and Therapeutics, 3rd Ed.




     Iowa State Univ. Press.  1965.




32.  Kinsley, A. T.  Arsenical Poisoning, Vt. Med. 24:445.  1929.




33.  Krocza, W. and Schuh, M.  Arsenic Residues in the Carcasses of Slaughter




     Animals.  Arsenruckstande im Fleisch von Schlachttieren.  Wiener




     Tierarztliche Monatsscrift  (1973) 60 Heft 12, 366-371.  Abstr. in




     Vet. Bulletin.  1974.




34.  Ledet, A. E. cited by Buck.  Clinical Toxicological, and Pathological




     Aspects of Arsanilic Acid Poisoning in Swine.  Ph.D. Thesis, I.S.U.,




     Ames, Iowa.  1970.
                                   228

-------
35.  Ledet, A. E., Duncan, A. E., Buck, W. B. and Ramsey, F. K.  Clinical




     Toxicology, 6(3):439-457.  1973.




36."  Lenihan, J. M. A.  Technology and Humanity.  Proceed. First Annual



     Conference on Trace BubsLauces in Environmental HeaLi.ii, Un i vetaiLy or




     Missouri-Columbia.  Dr. D. D. Hemphill, Ed.  Vol. 1:142-151.  1967.




37.  Lenihan, J. M. A. and Smith, H.  Nuclear Activation Techniques in the




     Life Sciences, IAEA, Vienna, cited by Underwood (183).  1967.




28.  Liebig, G. F., Jr.  cited by Selby, et al  (1974).  Arsenic, Chapter 2




     in Chapman, H. D., Ed.  Diagnostic Criteria for Plants and Soils:




     Riverside, Calif.  Univ. Div. Agric. Sci, pp. 13-23.  1966.




39.  Lisk, D. J.  Recent Developments in the Analysis of Toxic Elements.




     Science 184(4142):1137-1141.  1974.




40.  Maas, E. E. Arsenic Content in Urine of Cattle Dipped in Arsenic




     Solutions.  J.A.V.M.A. 110:249.  1947.




41.  McCulloch, E. C. and St. John, J. L.  Lead Arsenate Poisoning in




     Sheep and Cattle.  J.A.V.M.A.  96:321-326.  1940.




42.  Menges, R. W., Kintner, L. D., Selby, L. A., Stewart, R. W. and Marienfeld,




     C. J.  Arsanilic Acid Blindness in Pigs.  Vet. Med. SAC:565:568.  1970.




43.  Morehouse, L. G., Ed.  Annual Reports of Veterinary Diagnostic Laboratory,




     College of Veterinary Medicine, University of Missouri-Columbia.




     Reports for 1968-1973.




44.  Morehouse, N. F.  cited by Menges, et al'(!) Accelerated Growth in




     Chickens and Turkeys Produced by 3-nitro-4-phenylarsonic acid.  Poultry




     Sci.  28:375-384. 1949.




45.  Moxhan, J. W. and Coop, M. R. Arsenic Poisoning of Cattle and Other




     Domestic Animals,  N. Zeal. Vet. J. 16:161-165.  1968.
                                  229

-------
46.  Moxon, A. L.  Alkali Disease or Selenium Poisoning So. Dakota Agri.

     Exp. Sta. Bui. 311.  1937.

47.  Natsuch, E. F. S., Wallace,,J. R., Evans, C. A., Jr.  Toxic Trace

     Elements:  Preferential Concentration in Respirable Particles.  Science

     183:202-204.  1974.

48.  Oliver, W. T. and Rose, C. K.  Arsanilic Acid Poisoning in Swine.

     J.A.V.M.,A. 130:177-178.  1957.

49.  Peoples, J. S.  Metabolic Fate of Arsenic Acid in Dairy Cows.  Fed.

     Proc. 20:174.  1961.

50.  Peoples, J. S.  Arsenic Toxicity in Cattle.  Annals N.Y. Acad. Sci.

     Col. 111:644-649.  1964.

51.  Radeleff, R. D.  Veterinary Toxicology 2nd Ed.  Lea and Febiger,

     Philadelphia pp. 158-161. 1970.

52.  Regelson, W., Untae, Kim, Ospina, J. and Holland. J. F.  Hemangioendo-

     thelial Sarcoma of the Liver from Chronic Arsenic Intoxication by

     Fowler's Solution.  Cancer 21:514. 1968.

53.  Schacklette, H. T., Boerngen, J. G. and Keith, J. R.  Selenium, Fluorine,

     and Arsenic in Surficial Materials of the Conterminous United States,

     Geolog. Surv. Circ. 692:1-14, Washington, D.C.  1974.

54.  Schacklette, H. T., Erdman, J. A. and Keith, J. R.  Geochemical Survey
                                                                          f
     of Vegetation, of Missouri, Plans and Progress for the sixth 6-months

     period, June, 1972 f, pp. 58-63.  Open File Rpt. Publ. in 1973, U.S.

     1972.

55.  Scheidy, S. F., Wilcox, P. W. and Creamer, A. A.  Residual Arsenic in

     Swine Tissues Following Oral Administration. J.A.V.M.A. 123:341-342.

     1953.
                                 230

-------
56.  Schroeder, H. A., Balassa, J. J.  cited by Underwood; Selby.  Abnormal




     Trace Metals in Man:  Arsenic.  J. Chronic. Diseases 19:85, 573.  1966.




57.  Selby, L. A., Marienfeld, C. J., and Pierce, J. 0.  The Effects of




     Trace Elements in Human and Animal Health.  J.A.V.M.A.  157(11):1800-




     1808.  1970.




58.  Selby, L. A., Case, A. A., Dorn, C. R. and Wagstaff, D. J.  Health




     Hazards Associated with Arsenic Poisoning in Cattle.  J.A.V.M.A.




     164(9):918.  1974.




59.  Thompson, D. J.  Trace Elements in Animal Nutrition, 3rd Ed. International




     Minerals and Chemicals Corp.  Skokie, 111. (:25).  1970.




60.  Udall, D. H.  The Practice of Veterinary Medicine, 5th Ed., Pub. by




     the author at Ithaca, N.Y.  1947.




61.  Underwood, E. J.  Trace Elements in Human and Animal Nutrition, 3rd




     Ed. Academic Press, N. Y. and London. 543 pp.  1971.




62.  Vallee, B. L., Ulmer, D. D. and Wacker, W. E. C.  Arsenic Toxicity and




     Biochemistry.  Arch. Indust. Health 21:132.  1960.




63.  Vinogradov, A. P.  (Russian) Geochemistry of Rare and Dispersed Elements




     in Soils, 2nd ed. Eng. Trans, pub. by Consultants Bureau NSF, N.Y. and




     London.  1959.




64.  Wahlstrom, R. C., Kamstra, L. D. and Olson, 0.  E.  The Effect of




     Arsanilic Acid and 3-nitro-4-hydroxyphenyl-arsonic Acid on Selenium




     Poisoning in the Pig;  Journ. Anim. Sci.  14:105.  1955.




65.  Weaver, A. C.  Arsenic Poisoning in Cattle Following Pasture Contamination




     by Drift of Spray.  Vet. Rec. 74:249.  1962.









66.  White, I. E., Blood, D. C. and Whitten, J. H.  Arsenic Poisoning in




     Sheep.  Austral. Vet. J. 24:331-334.  1948.
                                  231

-------
232

-------
                  CHEMICAL SAFETY - PESTICIDES




                          Homer R. Wolfe




             U.S. Environmental Protection Agency






     People who become involved in activities requiring exposure




to pesticides should be aware of the potential hazards involved as




a result of absorption of toxic compounds.  If a person is know-




ledgeable about such hazards and understands the importance of taking




proper precautions, he can do much to insure the safety of himself




and others.  Although illnesses resulting from over-exposure to




toxic compounds do occur among applicators and other workers, most




are a result of carelessness or accident.  Experience has shown that




if proper precautionary measures are observed and directions on




the pesticide label are followed, even the more toxic compounds




can be used safely.  Exposure to less toxic compounds should not be




ignored.




     Much of the pesticide usage in this country involves insecticides,




acaricides, fungicides and herbicides.  The more extensively used




modern synthetic insecticide or acaricide compounds are the chlor-




inated hydrocarbons, organophosphorus and carbamate compounds.  The




acute toxicity of the organophosphorus compounds is, on the average,




somewhat greater than that of the carbamates or chlorinated hydro-




carbons.  Because chlorinated hydrocarbons are much more stable than




organic phosphorus or carbamate compounds, they can be more of a




residue problem.  Carbamate pesticides have been considered relatively




safe to use; however, certain of the newer compounds in this group




are relatively toxic to warm-blooded animals.   More experience with
                              233

-------
their use will allow better judgment as to their hazard to applicators




or other workers.




     With the exception of mercury compounds, most common fungicides




are less toxic than DDT.  Acute poisoning by organic mercury compounds




in man is rare in the United States, although such poisonings have




been reported.  However, in other countries there have been many




cases of chronic poisoning involving both inorganic and organic




mercury.  Most chronic cases have been associated with repeated




exposure from the manufacturing of organic mercury compounds, from




their use in treating seed, or from eating treated seed.




     Certain fungicides, particularly ziram, may occasionally cause




local irritations or dermatitis.  However, these cases are not




usually very severe.




     Most herbicides are less toxic than other types of pesticides.




Two of the most toxic older materials commonly used as herbicides




are arsenicals and dinitro-type compounds.  The arsenical herbicides,




although not particularly hazardous to spraymen by skin contact,




do have a poor safety record.  A dinitro compound (dinitrocresol)




used for weed control has caused occupational illnesses and deaths




in Europe (3).in contrast, tests have indicated that under the conditions




of use in the Pacific Northwest area of this country the hazard




associated with the application of dinitro compounds is minimal for




weed control (18).  This conclusion has been corroborated by use




experience.




     We do not often see acute illnesses as a result of exposure




to the newer herbicides.  Complaints are usually about skin disorders




or respiratory irritation or distress.  However, one of the newer
                             234

-------
herbicides, paraquat, is of considerable interest because only a




very small oral dose may produce irreversible lung fibrosis which




usually leads to death (2).  Response to antidotal procedures has




been rare.  Although many of the recorded deaths from paraquat have




been due to voluntary ingestion with suicidal intent, there have been




deaths following accidental ingestion of very small amounts of the




liquid concentrate.  In one case it was estimated that the quantity




of fluid consumed could not have exceeded three-quarters of a




teaspoon (8).  This compound is also somewhat caustic and may cause




chemical damage, especially to the eyes.  This emphasizes the im-




portance of avoiding splashing the concentrate into the mouth or




eyes during measuring and mixing operations.




     The other herbicide of most current toxicologic interest is




2,4,5,-T.  This compound, along with its dioxin contaminant, has




caused teratologic effects in experimental animals when given at




sufficiently high dosage levels (5).




     At one time or another practically every state in the nation




has published some type of listing of safety  precautions or recom-




mendations to follow when working with toxic  pesticides, and the




usual statements are common knowledge to most of those who have




worked with pesticides for any length of time.  Becuase of this,




there will be no attempt to enumerate all of  these in this discussion.




This presentation will cover some of  the more important safety




precautions related to worker exposure and, in addition, will touch




on some of the research related to exposure and safety carried out




at the Environmental Protection Agency,  Field Studies Section lab-




oratory during the last several years.
                              235

-------
     There are several important ways to insure safety of the worker




such as providing them with education and medical supervision, stress-




ing the importance of personal hygiene and cleanliness, emphasizing




the importance of not developing careless work habits, impressing




them with the necessity for reading and following recommendations




and directions on the pesticide label, and making sure they are




provided with proper protective gear and that they understand the




importance of their use and care.




Education of Workers




     It is essential that all workers who have intimate contact




with pesticides: have at least some knowledge of pesticides.  Well-




informed personnel are more likely to be more careful when handling




toxic materials and thus help to maintain a good pesticide safety




record.  Workers should be informed about the different classes




of pesticides, i.e., chlorinated hydrocarbon, organophosphorus,




carbamate, etc. and their relative toxicity or hazard.  Education




is one of the most important factors in pesticide safety.




Medical Supervision




     Regardless of the size of an operation, it is wise to arrange




some type of medical supervision.  This is particularly important




if exposure is to highly toxic chemicals.  A pre-employment physical




examination should include a blood cholinesterase test for employees




who may work with the more toxic cholinesterase-inhibiting compounds.




The test will provide some indication of the normal cholinesterase




activity level and may be useful later in determining whether an




illness is due to pesticide poisoning.  Personnel working with such




compounds, especially the highly toxic organophosphorus pesticides,
                             236

-------
should have their cholinesterase acitvity checked at regular intervals




in order to detect any appreciable deviation from normal which may




indicate impending danger of poisoning.  If significant reduction




in cholinesterase activity is noted, the employee should be removed




from the work situation, which might be a source of exposure to




pesticides, until the worker is advised by a physician that it is




safe to resume his regular duties.




Personal Hygiene and Cleanliness




     Even though the employer may provide a relatively safe working




environment, the worker should make an effort to protect himself




from excess absorption of pesticides through good personal hygiene




practices.  Applicators should change and launder clothing daily.




Workers in a formulating plant should remove street clothing and




put on clean work clothing before starting work.  Street clothing




should not be worn under work clothing.  At the end of the work shift




work clothing should be removed and placed in a bin to be laundered.




This should be followed by bathing in a shower, using plenty of




soap to thoroughly cleanse any pesticide from the skin before dressing




in street clothing to go home.




     If any worker, whether it be in the field or formulating plant,




should become excessively contaminated at any time with either dry




or liquid concentrate pesticide, he should immediately stop work,




bathe and change into clean work clothing before resuming his duties.




This is especially important if he has been working with the more




toxic organophosphorus compounds.   In such case he should be observed




for poisoning symptoms.




     Waterproof protective clothing should be cleaned daily.   It is




especially important that such protective gear be kept thoroughly






                            237

-------
clean on the inside as well as on the outside.




     Workers should never smoke, chew tobacco or gum, drink or eat




while working with pesticides.  These activities should take place




away from the pesticide exposure area.  The hands and face should




be washed prior to such activities.




Avoid Careless Work Habits




     Risk of injury or illness can be minimized by using the best




informed and most careful employees in work situations that are




potentially the most hazardous.  Unfortunately, this principle is




not always observed.  For example, in many pesticide formulating




plants the more hazardous jobs are usually dirtier, require more




physical effort and thus are less desirable than other jobs.  As




a consequence, new inexperienced personnel are often given the more




hazardous duties, while those with more seniority and knowledge of




pesticide safety move to the more desirable positions.  Careless




workers are not particularly difficult to detect.  Close observations




of workers quickly reveal any tendency toward carelessness.  Care-




less workers can jeopardize the health of other workers as well as




themselves.  They may also produce more contamination of the environ-




ment through careless application.




Follow Directions on the Pesticide Label




     Information on the pesticide label represents the results of




much research and legislation in the interest of safety to the user




and the general public.  However, it is the individual user who must




take personal responsibility to read the label and follow the direc-




tions.   If all directions are followed explicitly there should be




minimum hazard.  Anyone working with pesticides should be aware






                            238

-------
that the presence of a red skull and crossbones indicates a highly




toxic compound.  In applying pesticides to food plants and crops,




care should be taken to make sure the proper dosage recommended




on the label is being followed.




Use of Proper Protective Gear




     Direct protection of the routes of entry of chemical compounds




into the body as a means of preventing exposure is very important.




The routes of entry are dermal, respiratory and oral.  Protection




is afforded by the use of various items of protective gear, such




as special protective clothing, respirators, goggles, etc.




     Dermal route;  The dermal route is probably the most important




route of entry during the most exposure situations especially in




the field where liquid sprays are involved.  The insidiousness of




absorption by that route adds to its hazard.  Most persons are aware




of the danger of swallowing or breathing pesticides, but the possi-




bility of absorbing appreciable amounts of a poison chemical through




the intact skin is not so familiar.




     Although cloth overalls or trousers provide a reasonable amount




of dermal protection where pesticide does not easily penetrate clothing,




the wearing of waterproof trousers provides the best protection




for the lower trunk and leg areas and is especially recommended in




work situations where there is chance of liquid spillage, soaking




by continued contact with more dilute liquid sprays, or penetration




of clothing through excessive contact with dry pesticides.  Even




though regular clothing is covered by waterproof protective gear,




it is important that the workers change to freshly laundered clothing




each day in order to prevent contamination of skin areas.







                             239

-------
     In pesticide formulating plants it is especially important to

use proper protective gear because exposure is often to the more

concentrated forms of pesticides for prolonged periods of time.  The

waterproof apron is especially needed by the worker at the bagging

or mixing stations, as there is often considerable contamination

of the front of the clothing from the belt downward.  It is very

important that concentrate pesticide does not penetrate the clothing

to the scrotum because that area has been shown to be the area of

greatest absorption on man (7).  Protection of the upper trunk and

arms from contamination by toxic pesticides is important, especially

under field conditions where heavy spray drift may thoroughly wet

cloth shirts, coveralls, and underclothing or where concentrated

pesticides come in contact with clothing and skin.  Our studies

have shown that the greatest potential contamination of spraymen

in this general body area is the upper back, shoulders, and forearms

of workers operating equipment which propels spray up into the air

where it is more subject to drift.  Under these conditions a water-

proof jacket or raincoat provides the best protection for this general

body area..  This gear is usually worn during cooler conditions,

but as the temperature rises and the clothing becomes unbearably

hot to wear, workers tend to discard them and work with much less

protection—perhaps only a short-sleeved-T-shirt-type undershirt
                        !
on the upper trunk area.  Under such conditions workers should be

encouraged to at least wear a long-sleeved cloth jacket that will

not be easily penetrated by pesticide, and preferably one that can

be properly washed.
                             240

-------
     The wearing of long-sleeved, closely woven cotton shirts or

coveralls as outer clothing during hot weather, often with no under-

clothing, has been popular with many applicators even though this

is not a recommended practice.  Fortunately, these items of outer

clothing provide a reasonable amount of protection where spray drift

is light with very fine droplets that do not wet through to the skin.

Under such conditions the clothing should be changed and laundered

daily.  If clothing used during spraying such as shirts, jackets,

or coveralls are merely hung up to dry after work and used repeatedly,

as is often the practice, it doesn't take long for the pesticide
                                                                 •
material to work through where it will make contact with underclothes

or skin.

     In selecting protective clothing for workers it is important to

take into consideration the comfort of the individual when he wears

such items.  The conventional black or dark green rubberized or

plastic waterproof jackets in common use during past years are con-

sidered by many applicators to be uncomfortable to wear not only

because of greater heat absorption but also because they may be of

heavy grade material and not very flexible.  During recent years,

however, several jackets and jacket-trouser combinations that are

lighter in color and weight have been available.  Although less durable,

they are less costly to replace.  Nevertheless, there is still con-

siderable discomfort in wearing any waterproof clothing during hot

weather because of trapping of body heat.

     Observations of pesticide applicators have indicated that although

waterproof clothing items, and especially jackets, are usually carried
                            241

-------
by the worker, or readily available to him, he usually will not




wear the clothing until exposure to pesticide increases to the point




where he feels protection is necessary.  Unfortunately, by this time




there is often considerable contamination of skin and clothing.  The




covering of contaminated skin areas by waterproof clothing may create




conditions under which dermal absorption may be increased.  This may




be more important during hot weather where high temperatures and per-




spiration are involved.  Whether, or not there would be less absorption




under these conditions than if the clothing were left off entirely,




depends upon the potential exposure which might occur after the worker




puts on the clothing.  Although the increase of absorption of pest-




icide by covering contaminated skin with various items of protective




clothing is not known, it is important to emphasize the need to put




on protective gear before the skin has been contaminated to any great




degree.




     Where protection from downward drift is a factor during application




of liquid sprays it is important to wear headgear that provided maximum




protection to the entire head-face-neck area.  The headgear most




commonly used by pesticide applicators is the billed cap which provides




some protection for the face but very little for the remainder of the




head-neck area other than the scalp.  The conventional "Sou'wester"




rain hat, often used when heavy downward drift occurs, does not provide




exceptionally good protection for the face and sides of the neck.




This is because of the narrow brim in all areas except at the back




of the neck.  Metal or fiber "hard hats: are also used to some extent;




however, most have too narrow a brim to provide adequate protection.
                             242

-------
"Hard hats" which allow circulation of air over the head under the




hat should not be used where exposure is to toxic dusts.  Our studies




have shown that the greatest protection from downward drift of pest-




icides is afforded by some type of wide-brimmed hat, preferably made




of water-repellent material.




     Of particular interest in relation to exposure of the head-neck




area if the finding by Maibach et al. (7) that absorption of parathion




is relatively efficient (47% of applied dose) in the ear canal.  Ex-




posure in this area could occur through drift of fine pesticide mists




or dusts or by digging the the ear with the tip of a contaminated finger.




     It is of importance to note that wearing goggles and respirators




provides considerable protection to the face.




     Although a statement suggesting the use of goggles can be found




on certain pesticide labels, they are rarely worn except by pilots




who apply pesticides by aircraft.  Questioning of pilots has revealed




that they wear goggles not only to prevent poisoning and to keep wind




out of the eyes but also to prevent certain organophosphorus pesticides




that are direct inhibitors of cholinesterase from causing miosis;




This is understandable because it has been shown that unilateral con-




tamination of the eye with TEPP may cause pilots to inadequately




judge distance (9).  The incoordination which may accompany this




could be a serious threat to safety.




     The hands are often the body area having the highest exposure




to pesticides and they have a greater chance of coming in contact




with the more concentrate formulations.   They are also more subject




to cuts or abrasions, which allows a more direct route of entry through
                            243

-------
the skin.  High potential exposure to the hands brings attention to




the need for wearing gloves.  Some people who have worked with pesticides




feel it is better not to wear gloves than to wear gloves that are




contaminated on the inside; something which invariably occurs to some




degree.  Our research concerning the use of protective gloves indicates




that, unless there is gross contamination of the inside of the gloves,




the potential exposure is less when wearing gloves than when not




wearing them.  If gloves are kept clean on the inside there is very




little doubt concerning the value of their use when handling pesticides.




Unlined rubber gauntlet gloves provide the best protection because




the gauntlet covers the wrist area not normally covered by the jacket




sleeve and they can be turned wrong side out for proper cleansing of




the unlined inside surface.




     In order to provide proper protection to the feet, waterproof




shoes or boots should be worn when handling or applying pesticides




on a large scale.  When leather shoes become wet with spray material




they have a tendency to become cracked and dried out to the extent




that pesticide easily penetrates through to the sock or foot.  Both




leather and canvas shoes absorb chemicals and may hold them in contact




with the wearer.  Boots should be washed and dried thoroughly, inside




and out, as frequently as needed to remove any pesticide contaminant.




Rubberized boots are essential in formulation plants.  The legs of




coveralls should be worn outside the boot tops to prevent dry pesticide




from sifting into the footwear.




     Respiratory route;  Where toxic dusts and vapors or very small




spray droplets are prevalent, or where application is in confined




spaces, protection of the respiratory route is especially important.
                            244

-------
Extremely fine particles and droplets found in dusts and mists are




much more easily drawn into the respiratory system than the larger




droplets formed by most conventional dilute spray machines.  Our




tests have shown that when operating an 8X (eight times the normal




dilute concentration) concentrate airblast machine in fruit orchards




the potential respiratory exposure is nearly 3 times greater than




when operating the conventional dilute machine (11).




     The cartridge-type respirator provides adequate respiratory




protection in most types of application situations.  In certain




cases it is advisable to use gas masks with special canisters because




of their greater adsorbent capacity.  Applicator pilots who risk




the possibility of flying through drift of fine droplets or dusts




should use a face mask equipped with a filter canister attached




either to their belt or to the inside of the cockpit.  When fumigating




or applying highly toxic pesticides in confined spaces it is advisable




to use a respirator with a special compressed air supply tank so that




none of the contaminated ambient air is inhaled.




     If respirators are to be effective they must have proper care.




The rubber face-piece becomes hardened and the head straps lose their




elasticity with age and exposure to heat and sunlight.  These condi-




tions lead to poor fit and allow leakage around the face-piece.  Two




of the more common offenses in the care of respirators that we have




observed are (1) failing to occasionally wash the face-piece-with soap




and water and (2) neglecting to change the filter cartridges or can-




isters regularly.  Washing of the face-piece of a cartridge-type




respirator should not be attempted while the cartridges are in place
                            245

-------
as moisture may contact the activated charcoal filter material and




reduce its effectiveness in adsorption and absorption of pesticides.




Solvents should not be used as a cleaner for they may damage certain




parts of the respirator.  The general recommendation is that cartridges




should be changed after 8 hours of continuous exposure.  ,In most ap-




plication situations this leaves much up to the individual worker to




keep a record of his respirator exposure time.  In a formulating plant




where hours of exposure are more regular this is more easily controlled




under the guidance of a foreman.  Under conditions of intense exposure




the useful life of the cartridge is much shorter.  Thus, if the breath-




ing seems hampered, or if the odor of pesticide is detected, the filter




cartridges should be changed immediately.  If the outer filter pads




are separate removable units they should be changed more frequently




than the cartridges.




     During disucssions of the respiratory route of entry into the




body the question is often raised concerning the hazard of smoking




pesticide-contaminated cigarettes.  We have found it difficult to




measure such potential exposure with any great degree of accuracy.




The technique we have utilized thus far involves subjecting the cig-




arettes to normal handling through the process of removing them from




the pack and placing them in the mouth, lighting them, and smoking




one-half of the cigarette.  The remainder of the cigarette is then




analyzed for pesticide content.  The values obtained are based on the




assumption that pesticide on the cigarette will be volatilized before




being broken down by burning and that none of the volatile or partic-




ulate pesticide would be trapped in the butt end of the cigarette.
                               246

-------
In observing smoking by workers it was noted that the area of greatest




contamination of the cigarette was far enough from the butt end to allow




burning of the contaminated area in most cases.




     In studies of cigarette contamination by spraymen applying




endrin in orchards, the potential exposure through smoking during




application operations was calculated to be not more than 2 yg per




cigarette, even when the cigarettes were handled with hands wet with




the dilute spray (16).  In later studies (13) involving spraymen




applying parathion to apple orchards by airblast machines, up to




18.1 yg of parathion per cigarette could be recovered where they




were handled with hands contaminated with dilute spray.  Contamination




with hands that had contacted the concentrate formulation resulted




in values up to 235 yg per cigarette




     Even though values for potential respiratory exposure through




smoking contaminated cigarettes may not appear to reflect any great




hazard, two important points must be kept in mind:  (1) Pesticide




entering by the respiratory route is practically 100% absorbed, and




(2) There is no assurance that a more toxic breakdown product will




not be formed and inhaled as the high temperature of a burning cigarette




reaches the contaminated areas rather than complete destruction of




the compound by burning.  For example, in the case of parathion the




oxidation product, paraoxon, is estimated to be much more toxic than




the parent compound.  This could be an important factor as far as




hazard is concerned and emphasizes the need for recommending washing




of hands and face before smoking.




     Oral route;  Oral exposure is difficult to measure.   We are




studying techniques at the present time.  Analysis of saliva samples






                              247

-------
of exposed individuals appears to give some indication of contamination.

Splashing of liquid concentrate into the mouth while pouring and

measuring pesticides may produce the most serious oral exposure.

Contamination muy also occur through licking the llpn, by rubbing

the mouth with contaminated arms or hands, by careless actions such

as attempting to blow out clogged spray nozzles with the mouth, or

by eating or drinking with contaminated hands.

     We have attempted to measure the parathion contamination of

typical sack lunch items, such as sandwiches, cookies, and pickles

by workers whose hands had been contaminated while thinning fruit

in recently sprayed apple orchards.   A lunch consisting of four

half-sandwiches, two cookies, and one pickle was given to workers

who handled and ate one-half of each item with unwashed hands.  The

other half of each item was analyzed for parathion.  This provided

potential oral exposure values for lunch items.  A total of approx-

imately 103 yg of parathion was found on the typical lunch mentioned

above.  Although this is not a great amount of pesticide, it would

add to the total exposure of each individual; thus, workers should

wash hands and face before eating.

Exposure in Different Work Activities
                                                                        ;
     Degree of exposure in different work activities can be estimated

by both indirect and direct methods of measurement.  An example of

an indirect method of measurement that correlates quite well with

clinical effects is the determination of cholinesterase activity in

the blood of workers exposed to organophosphorus compounds.  Determina-

tion of urinary metabolites excreted following exposure to certain

pesticides is another example of indirect measurement of exposure.
                              248

-------
of exposed individuals appears to give some indication of contamination.




Splashing of liquid concentrate into the mouth while pouring and




measuring pesticides may produce the most serious oral exposure.




Contamination may also occur through licking the Ilpa, by rubbing




the mouth with contaminated arms or hands, by careless actions such




as attempting to blow out clogged spray nozzles with the mouth, or




by eating or drinking with contaminated hands.




     We have attempted to measure the parathion contamination of




typtoal sack lunch items, such as sandwiches, cookies, and pickles




by workers whose hands had been contaminated while thinning fruit




in recently sprayed apple orchards.   A lunch consisting of four




half-sandwiches, two cookies, and one pickle was given to workers




who handled and ate one-half of each item with unwashed hands.  The




other half of each item was analyzed for parathion.  This provided




potential oral exposure values for lunch items.  A total of approx-




imately 103 yg of parathion was found on the typical lunch mentioned




above.  Although this is not a great amount of pesticide, it would




add to the total exposure of each individual; thus, workers should




wash hands and face before eating.




Exposure in Different Work Activities




     Degree of exposure in different work activities can be estimated




by both indirect and direct methods of measurement.  An example of




an indirect method of measurement that correlates quite well with




clinical effects is the determination of cholinesterase activity in




the blood of workers exposed to organophosphorus compounds.  Determina-




tion of urinary metabolites excreted following exposure to certain




pesticides is another example of indirect measurement of exposure.
                              248

-------
These methods are used in estimating how much pesticide has actually




been absorbed by the body.  We have used levels of parathion and DDT




metabolites excreted in urine as an indicator of exposure of spraymen



  , '  : . ,  -I.  ,   i : .  : ,1 .... M -. \   r . , ,.|  ,r- 1 .... ,  I . .  r I !,.  ,„,.( ..,),,. I  ! |., .,



correlated well with direct exposure measurements.  Excretion  curves




for both metabolites showed diurnal variation during the period after




exposure had ended.  On the average for a specific exposure, more




parathion-derived material than DDT-derived material was recovered




in the urine.




     Direct methods for measurement are utilized to attempt to estimate




the amount of dermal or respiratory exposure to which the body is <




potentially subjected  (6).  Potential dermal contamination can be measured




by swabbing skin areas or by attaching special absorbent pads  to dif-




ferent parts of the body or clothing of workers.  Contamination of




the hands can be measured by rinsing them with a suitable solvent into




a polyethylene bag.  The amount of pesticide found on the dermal^'pads,




swabs,  or bag rinses will indicate the amount of pesticide that may




have accumulated on exposed skin areas during a specific period of




work activity.  Respiratory exposure can be estimated from the con-




tamination of special filter pads held in special single- or double-




unit respirators, from air concentration values determined by use of




impinger-type air samplers, or both.  Chemical analysis of respirator




pads or of air samples taken near the breathing zone of workers yields




values that can be used to calculate the potential respiratory exposure.




     The results of direct measuremetns of exposure to pesticides may




be used in evaluating the relative hazards  of different routes  of




exposure, different operational procedures, and different protective
                               249

-------
devices.  Results of our potential dermal and respiratory exposure




studies (4,10,12,14,16,17,19) for several different work situations




and compounds are shown in Table 1.  These calculated values are based




on the assumption that the workers were wearing short-sleeved shirts,




no gloves or hats, with clothing worn giving protection of the body




areas covered.  An important point illustrated by the Table is that




the potential for dermal exposure is generally greater than that for




respiratory exposure and sometimes it is very much greater.  In earlier




work at this laboratory (17) we found that potential respiratory exposure




to a number of pesticides ranged from 0.02% to 5.8%, with a mean of




only 0.75%> of the total dermal plus respiratory exposure.  Thus, we




feel that dermal exposure is more important than respiratory exposure




in many work situations, and especially during application of liquid




sprays in the field.  It should be understood that any given amount of




pesticide is more rapidly and more completely abosrbed by the oral or




respiratory routes; however, absorption of pesticides by these two




routes is probably too small a fraction of the total potential exposure




to be considered the main factor in most poisoning cases of workers




in the field.




     In one set of experiments, for example, we have calculated the




potential dermal exposure of orchard spraymen .to parathion to be 17.2




mg/hr; however, the potential respiratory exposure was calculated to




be only 0.02 mg/hr of exposure.  This indicates that there is potentially




over 800 times more dermal exposure than respiratory exposure to workers




in that type of application operation.   Thus, if only a small fraction




of the potential dermal exposure was to be completely absorbed it would




probably still be more than the respiratory exposure.
                               250

-------
     Table 1 also shows that the total percent of toxic dose potentially




received per hour of work, assuming all the pesticide was absorbed,




is very low for most exposure situations listed.  The higher values




obtained were for workers more heavily exposed to the more toxic organo-




phosphorus compounds or where extremely high potential dermal and




respiratory values were obtained for indoor house spraying with DDT.




The flagger for parathion crop dusting by air received the most toxic




dosage per hour of work.  This was because the worker made no effort




to move away from the drift of the toxic dust.  The high value is




consistent with our observations that air dust application flaggers and




loaders are often subjected to greater exposure than most workers in




field application situations.




     Improvements in quality and acceptability of gear for use in




protecting the routes of exposure are needed to bring about better




protection of workers.  People who work with toxic chemical compounds




must realize that even when using the best equipment there is some




element of risk involved.  Accidents occur, even among workers who




are careful.  In case of accidental gross contamination of skin with




a highly toxic compound every effort must be made to cleanse the




contaminated area as thoroughly as possible.  At our present state of




knowledge about dermal absorption we feel that the use of plenty of




soap and water is the best suggestion for removing skin contamination.




This must be done soon after contamination because absorption of




certain pesticides is relatively rapid.   Wash by rubbing with the hands




or with a piece of cloth.  Do not scrub  too vigorously or use a brush




because this may cause the outer layer of protective cells of the




skin to be abraded enough to allow more  rapid absorption of any pesticide
                              251

-------
 Table 1.   Potential Dermal and Respiratory Exposure of Workers to Pesticides
Exposure
Compound
DDT .
DDT
DDT
.DDT
Parathion
Parathion
Parathion
Parathion
Parathion
Parathion
Carbaryl
Carbaryl
Carbopheno-
thion
Ethion
Endosulfan
Endrin
Fenthion
Fenthion
Perthane
Activity
Spraying apples
Indoor house spraying
Outdoor house spraying
Formulating plant
Spraying apples
Spraying citrus
Spraying potatoes
Dusting potatoes
Thinning apples
Flagger: — crop dusting
Spraying apples
Formulating paint
Spraying orchards
Spraying orchards
Spraying apples
Spray orchard cover for mice
Mosquito spray
Hand granular
Spraying apples
Dermal
mg/hr
54
1,755
243
524.5
17.3
18.0 .
4.7
7.8
8.4
84.0
59.0
73.9
41.3
44.2
24.7
2.5
3.6
12.3
59.4
. Respiratory
mg/hr
0.10
7.10
0.11
14.11
0.02
0.03
0.01
0.16
0.06
0.02
0.09
1.10
0.11
. . 0.04
0.02
0.01
0.01
0.08
0.14
Total
% toxic
dose/hr
0.03
1.02
0.14
0.39
1.19
1.17
0.32
0.64
0.61
5.72
0.02
0.03
1.12
0.26
0.27
0.21
0.02
0.06
<0.01
aCalculated on the basis of the worker wearing a short-s.leeved, open-necked
 shirt, no gloves or hat, .with his clothing giving protection of the areas
 covered.
                                 252

-------
 not  removed.  A bar  of  soap,  towel,  and  container  of water  should be


 carried  on every  pesticide  application machine  or  accompanying vehicle


 for  use  in washing should a spillage occur.   In formulating plants


 emergency  showers and washing facilities should be relatively close


 to work  areas.  If pesticide gets  in the eyes they should be thoroughly


 flushed  with water for  several minutes.   If  a person should feel ill


 while working with pesticides he should  stop work  at once and get

                                   /
 medical  attention.


   1   In  general,  our research findings over  the last 20 years area


 consistent with the  idea that pesticides can be used safely provided


 recommended precautions are followed.  However,  the relatively high


 exposure values associated  with a  few of the more  toxic pesticides


 indicate that even minor lapses in adherence to safety precautions might


 be sufficient to  allow  poisoning to  occur.


                            References


 1.   Armstrong,  J. F., Wolfe,  H. R.,  Comer, S. W. and Staiff, D. C.


     Oral exposure of workers  to parathion through  contamination of.


     food items.   Bull.  Environ. Contam.  Toxicol.,  10:321-327, 1973.


 2.   Bullivant,  C. M.  Accidental poisoning by paraquat:  Report of


     two  cases in  man.   Brit. Med.  J., 1:1272-1273,  1966.


 3.   Bidstrup, P.  L. and Payne, D.  J. H.  Poisoning by dinitro-ortho-


     cresol.  Brit. Med. J., 2:16,  1951.


 A.   Comer,  S. W., Staiff, D.  C., Armstrong,  J. F.  and Wolfe, H. R.


     Exposure of workers to  carbaryl.  In preparation.


.5.   Courtney, K.  D., Gaylor, D. W.,  Hogan, M. D.,  Falk, H.  L.,  Bates,


     R. R. and Mitchell, I.   Teratogenic evaluation of 2,4,5-T.   Science


     168:864-866,  1970.
                               253

-------
 6.  Durham, W. F.  and Wolfe, H.  R. Measurement of the exposure of

     workers to pesticides.  Bull.  WHO, 26:75-91, 1962.

 7.  Maibach, H. I., Feldmann, R.  J.,  Milby, T. H. and Serat, W. F.

     Regional variation in percutaneous penetration in man.  Arch.

     Environ. Health, 23:208-211,  1971.

 8.  Masterson, J.  G. and Roche,  W. J.  Fatal paraquat poisoning.  J.

     Irish Med. Ass.  63:261-264,  1970.

 9.  Upholt, W. M., Quinby, G. E.,  Batchelor, G. S. and Thompson, J.

     P.  Visual effects accompanying TEPP-induced miosis.  AMA Arch.

     Ophtal. 56:128-134, 1956.

10.  Wolfe, H. R.  and Armstrong,  J. F. Exposure of formulating plant

    .workers to DDT.  Arch. Environ. Health, 23:169-176, 1971.

11.  Wolfe, H. R.,  Armstrong, J.  F. and Durham, W. F.  Pesticide exposure

     from concentrate spraying.  Arch. Environ. Health 13:340-344, 1966.

12.  Wolfe, H. R.,  Armstrong, J.  F. and Durham, W. F.  Exposure of mos-

     quito control workers to fenthion.  Mosquito News in press.

13.  Wolfe, H. R.,  Armstrong, J.  F., Staiff, D. C. and Comer, S. W.

     Potential exposure of workers ot parathion through contamination

     of cigarettes.  In preparation.

14.  Wolfe, H. R.,  Armstrong, J.  F., Staiff, D. C. and Comer, S. W.

     Exposure of spraymen to pesticides.  Arch. Environ Health 25:29-31

     1972.

15.  Wolfe, H. R.,  Durham, W. F.  and Armstrong, J. F.  Urinary excretion of

     insecticide metabolites.  Excretion of paranitrophenol and DDA as

     indicators of exposure to parathion and DDT.  Arch. Environ. Health

     21:711-716, 1970.

16i   Wolfe, H. R., Durham, W. F.  and Armstrong, J. F.  Health hazards

     of the pesticides endrin and dieldrin.  Arch. Environ. Health

     6:458-464, 1963.
                                   254

-------
17.  Wolfe, H. R.,  Durham, W.  F. and Armstrong, J. F.  Exposure of




     workers to pesticides.  Arch.  Environ.  Health, 14:622-633, 1967.




18.  Wolfe, H. R.,  Durham, W.  F. and Batchelor, G. S.  Health hazards




     of some dinitro compounds.   Arch. Environ. Health, 3:468-475, 1961.




19.  Wolfe, H. R.,  Walker, K.  C., Elliott, J.  W.  and Durham, W. F.




     Evaluation of  the health hazards involved in house-spraying with




     DDT.   Bull. WHO, 20:1-14, 1959.
                                  255

-------
256

-------
                        ANALYTICAL DEVELOPMENT




                         Lionel A. Richardson




                 U. S. Environmental Protection Agency






       The practice of analytical chemistry is based upon both the character-




istics of the entity under analysis and the characteristics of its immediate




environmental neighbors and relatives.  Thus, all analytical procedures




are devised to take advantage of specific physical properties.  While we




utilize such terms as physical, chemical, electrical, electronic and com-




binations thereof to assist us in the categorization of analytical schemes,




all of these terms, and the activities which they describe, are fundamentally




physical.  Thus, the fundamental basis of analysis has not changed over the




years, only the means of activating and using these properties in making




qualitative and quantitative analyses.




       Early methods of analysis utilized primarily reactivity and solubility,




at times, coupled with spectrophotometric detection systems.  With few




exceptions, such methods would be considered curde and inefficient in today's




laboratories principally because of their lack of sensitivity, limited




applicability and performance time.  Certain of these techniques, however,




are still valuable and preferable under the appropriate circumstances.




       To a large extent, analyses are currently performed using instrumenta-




tion which concerns itself with such molecular properties as electrochemical




relationships, time-related differential solubilities and electronic properties




(and changes therein) expressed through spectral development and interpretation.




Such sophisticated techniques are ultimately more sensitive and efficient




than their predecessors.   However, they have disadvantages:  (1) We often




need to combine two or more in order to provide both qualitatively and
                               257

-------
quantitatively dependable data, (2) acquisition of both instrumentation




and operators Is expensive, (3) meticulous sample preparation is often




required, and (4) analytical over-confidence sometimes develops.




       In the future we should utilize continuous monitoring systems as




well as the conventional analytical laboratory facilities.  Continuous




monitoring devices need to be developed and employed both for source




monitoring of specific species of known pollutants arid as advisors to




the presence of multi-pollutants and their interaction products.  These




latter systems must be property-specific rather than species-specific.




       The central laboratory facilities must serve the functions of




sophisticated qualitative and quantitative analysis and data interpreta-




tion necessary to ultimately define the pollution potential, determine




whether or not a problem does exist and contribute to ways and means by




which such problems can be resolved.
                                258

-------
AVIAN SALT GLANDS - AN INDEX TO EFFECTS OF ENVIRONMENTAL POLLUTION




                          Milton Friend




                 U. S. Fish and Wildlife Service




                               and




                        John H. Abel, Jr.




                    Colorado State University






     Evaluation of the effects on wildlife of pesticides and other




environmental pollutants is one of the many responsibilities of the




U. S. Fish and Wildlife Service.  Initially, our research efforts in




this area were primarily directed toward the more obvious questions




involving the death of animals in treated areas and the epizootiology




of pesticide intoxication of wildlife (32,33,34,35,36).  At our lab-




oratories considerable research effort was, and still is, expended in




determining the acute (LD.-Q) and chronic (LC  ) values for a wide variety




of pesticides (31,9).  Identification of diagnostic residue levels of




DDT and its metabolites (29,30) and dieldrin (29) in brain tissues has




allowed cause-and-effeet relationships to be established between exposure




and mortality for these compounds in the field.




     We have made a continuous effort to monitor large, widespread




programs of pesticide uses (20,5,18) and to help identify safer chemicals




with which to replace those of particular hazard (21,13,17,22).  Other




of our field studies have demonstrated the movement of some compounds




from the site of application (12) and concentration of organochlorine




pollutants through increasing trophic levels of natural ecosystems




(14,27).  As our knowledge grew, our research became more sophisticated




and focused on more complex relationships such as reduced reproductive
                              259

-------
success.  The thin eggshell phenomena in wild birds is well documented



(1) and our experimental studies have demonstrated the apparently



unique ability of DDE to cause thin eggshells in a variety of avian



species (8,38,15,19).



     We recognize that the results of exposure to an environmental



pollutant may be either modified or enhanced by a variety of physical



or biological events in the external or internal environment of the



animal and that the sequence of these events may be especially important.



It is these types of complex relationships that have resulted in our



selection of the avian salt gland system as a model for studying en-



vironmental pollution.



     I first became interested in the survival value of functional salt



glands when I read a report by Cooch (1964).  He concluded that water



birds living in the alkaline areas of the North American plains could



die simply from malfunction of the salt glands following exposure to



minimal doses of Type C botulinum toxin.  This reminded me of numerous



undiagnosed die-offs of marine birds, and shortly thereafter I had the



opportunity to investigate a die-off of wading birds on the Texas Gulf



Coast shortly after their island had been sprayed with malathion in an



attempt to eradicate mosquitos involved in the transmission of Venezuelan



equine encephalitis.  I caught several sick birds and inoculated them



intraperitoneally with 5% saltwater.  None of them produced detectable



salt gland secretions, as they should have if the system were functioning
                                       <-l


properly and all died within 30 to 45 minutes.



     With this bit of circumstantial evidence, I sought out individuals



with knowledge of the avian salt gland system and had the good fortune



to contact Dr. John Abel of the Department of Physiology and Biophysics
                              260

-------
here at Colorado State University.  Dr. Abel's area of research involves


osmoregulation in vertebrates in general and the avian salt gland system


in particular.  Together we designed the series of studies that led to


the development of our p  posed model.


     Before describing these studies, a brief description of the avian


salt gland system is in order.  Response to osmotic and ionic change


in the environment is a universal problem that must be faced by all


animals; their ability to solve it dictates whether they can survive


in a particular habitat.  Survival in extreme conditions, such as


marine, desert, and alkali environments, has required successful species


to develop specialized water-conserving and salt-secreting tissues and

                  •1
glands.  The avian salt gland system is particularly suitable for study


because of its simple function and easily measured response.


     Birds' salt glands have a single function—concentration and


excretion of excess salt from the body (24,25).  They can easily be


activated merely by salt-loading the bird.   The concentration and volume


of the resulting effluent are easily measured, and are a good index


of the organism's total adaptive capabilities because salt gland function


requires both corticosterone from the adrenal gland and cholinergic


innervations from the secretory nerves.  This means that both the central


nervous system and all the neuroendocrine mechanisms of the stress


axis must be working smoothly to produce a normal response.  Because


the neuroendocrine system required to activate the salt glands in birds


is similar to that for other animals and is essentially similar to the


stress axis described for man (26), this model has wide latitude.


Osmoregulatory processes transect classes within the animal kingdom,


and modification of the model should also permit study of the cold-




                              261

-------
blooded vertebrates, mammals, and a vareity of habitat conditions where




water conservation is essential for survival.  Janicki and Kinter have




previously reported DDT caused disruption of osmoregulatory events in




marine teleosts (1971a) and eels, Anguilla rostrata (1971b).




Laboratory Experiments




     In the first experiment, effects on salt gland function were studied




in 5-month-old pen-reared male mallards, Anas platyrhynchos, maintained




on either fresh or 1% salt (NaCl) drinking water and given 0, 10, 100




or 1,000 ppm DDE in the diet.  The rate of sodium chloride excretion by




the salt gland following injections of concentrated salt solutions was




not reduced (from that of controls) in DDE-treated birds maintained




on saltwater, but was significantly reduced in DDE-treated birds not




previously given salt (6).  Two points were obvious:  (1) increasing




levels of DDE exposure did not increase the magnitude of salt gland




function, and (2) stimulation of salt glands through saltwater exposure




prior to DDE exposure prevented DDE from interferring with salt gland




function.  This led us to believe that pesticide effects on salt gland




function might be an all-or-none type response once a threshold level




of exposure was reached and that the timing of pesticide exposure




(relative to salt gland development and initial salt stimulation) was




a critical factor.




     Before undertaking any detailed studies to further explore pesticide-




salt gland relationships, a variety of compounds representing the major




classes of environmental pollutants (organophosphates, carbamates, orgario-




chlorines, PCB's and heavy metals) were screened in mallard ducklings.




Ducklings replaced adults to increase the sensitivity of the test system.




The results of this screening indicated that organophosphates had the
                               262

-------
greatest effect on salt gland function.  This result was expected since


these compounds are potent inhibitors of cholinesterase activity (4).


Since the salt glands apparently require continuous stimulation with

acetylcholine during secretion, agents that inhibit the release of


acetylcholine are all potential inhibitors of salt gland function.


Even at low levels, exposure to these compounds resulted in significant


increases in mortality (over controls) following a severe osmotic stress;


for baytex and parathion increased mortality occurred at 1 pptn, for

bidrin at 4 ppm and for EPN at 15 ppm in the feed (chronic exposure).


     Following these preliminary studies, parathion was selected for more


detailed study.  Significant disruptions in salt gland function occurred

when ethyl parathion was administered in feed to newly-hatched mallards


at 25, 15, or 7.5 ppm.  Parathion was unexpectedly toxic to the test
                                                         i
birds, thereby supporting results obtained in the preliminary studies.


Despite a reported LCcg of 275 ppm for mallards (9) high mortality forced

termination of the 25-ppm experiment after the first severe salt stress


(intraperitoneal injection of 5% NaCl solution at 25 ml/kg of body weight)

and the 15-ppm experiment after the second of three planned salt stresses.

Significantly fewer parathion-treated birds responded to challenge in-


jections by producing measurable salt gland secretions at 25 and 15 ppm,

and those that responded secreted significantly smaller volumes and lower

sodium ion concentrations at 25 and 15 ppm and during the first challenge

at 7.5 ppm.  Parathion inhibited cholinesterase activity in the hypo-


thalamus and salt glands of both fresh and saltwater birds and increased

ATPase activity of salt glands of saltwater birds (7,37).  These results

clearly demonstrate that parathion exposure, even at very low levels,

does inhibit salt gland function in juvenile mallards.  In contrast
                               263

-------
with the results obtained for DDE (6), effects of parathion exposure

appeared to be dose-dependent for nearly all parameters measured.

Conclusions

     Our studies have rather broad implications.  The existence,

structure, and development of the salt, or nasal, gland has been

reported for a number of species (2,16,23,25), but it was not until

the late 1950's that its function as a major salt-secreting organ

was described (25).  Since these glands are the main route of

sodium chloride excretion in marine birds (25),  it follows that

suppression of salt gland function could be detrimental to survival

in habitats of high salinity.  The simplicity of the system coupled

with the specificity of the responses following a salt stress

leads us to believe that this system has great potential not only

as a sensitive bioassay system for detecting and measuring sub-
     s
lethal effects of organophosphate pesticides and possibly other

environmental pollutants, but also as a bioassay system that

closely reflects the ability of the test species to survive in a

marine environment.
                                264

-------
                              References






 1.  Anderson, D. W. and Rickey, J. J.  Eggshell changes in certain North




     American birds.  Proc.  XV Internatl. Omithoi. Congress,  pp. 514-540.




     The Hague.  1972.




 2.  Bock, W. J.   A generic  review of the plovers (Charadriinee, Aves).




     Harvard Univ. Bull. Mus. Comp. Zool.  118:27-97.  1958.




 3.  Cobch, F. G.  A preliminary study of the survival value of a functional




     salt gland in prairie anatidae.  Auk 81:380-393.  1964.




 4.  Fest, C. and Schmidt, K. J.  The chemistry of organophosphorous pest-




     icides, reactivity, synthesis, mode of action, toxicology.  Springer




     Verlag, N. Y.  339 pp.   1973.




 5.  Flickinger,  E. L. and King, K. A.  Some effects of aldrin-treated




     rice on Gulf Coast wildlife.  J. Wildl. Mgt. 36:706-727.  1972.




 6.  Friend, M.,  Haegele, M. A. and Wilson, R.  DDE:  Interference with




     extra-renal salt excretion in the mallard.  Bull. Environ.  Contam.




     Toxicol.  9:49-53.  1973.




 7.  Friend, M. and Abel, J. H., Jr.  Effects of parathion on salt gland




     function in mallard ducklings.  (In press).  1974.




 8.  Heath, R. G., Spann, J. W., and Kreitzer, J. F.  Marked DDE impairment




     of mallard reproduction in controlled studies.  Nature 224:47-48.




     1969.                                                   .   -   .




 9.  Heath, R. G., Spann, J. W., Hill, E. F. and Kreitzer, J. F.  Comparative




     dietary toxiciti.es  of  pesticides to birds.  B.S.F.W. Special Scientific




     Report-Wildlife No. 152.  57 pp.  1972.




10.  Janicki, R.  H. and Kinter, W. B.  DDT inhibits Na+, K+, Mg 2+-ATPase




     in the intestinal mucosae and gills of marine teleosts.  Nature (New




     Biology) 233:148-149.  1971 a.





                                  265

-------
11.  Janicki, R. H. and Kinter, W. B.  DDT:  Disrupted osmoregulatory


     events in the intestine of the eel Anguilla rostrata adapted to sea-


     water.  Science 173:1146-1148.  1971b.


12.  Keith, J. 0.  Insecticide contaminations in wetland habitats and


     their effects on fish-eating birds.  J. Appl. Ecol. 3 .-(Sup.pl.):71-85.  1966.


13.  Keith, J. 0. and Mulla, M. S.  Relative toxicity of five mosquito


     larvicides to mallard ducks.  J. Wild. Mgt.  30:553-563.  1966.


14.  Keith, J. 0. and Hunt, E. G.  Levels of insecticide residues in fish


     and wildlife in California.  Trans. 31st North Amer. Wildl. and


     Nat. Resourc. Conf.  pp. 150-177.  1966.


15.  Longcore, J. R., Samson, F. B. and Whittendale, T. W., Jr.  DDE thins


     eggshells and lowers reproductive success of captive black ducks.


     Bull. Environ. Contam. Toxicol. 6:485-490.  1971.
                                                                            /

16.  Marples, B. J.  The structure and development of the nasal glands


     of birds.  Proc. Zool. Soc. London.  Part 4:829-844.  1932.


17.  McEwen, L. C. and Brown, R. L.  Acute toxicity of dieldrin and malathion


     to wild sharp-tailed grouse.  J. Wildl. Mgt. 30:604-611.  1966.


18.  McEwen, L. C., C. E. Knittle, and M. L. Richmond.  1972.  Wildlife


     effects from grasshopper insecticides sprayed on short-grass range.


     J. Range Mgt. 25:189-194.  1972.


19.  McLane, M. A. R. and Hall, L. C.  DDE thins screech owl eggshells.


     Bull. Environ. Contam. Toxicol. 8:65-68.  1972.


20.  Pillmore, R. E. and Finley, R. B., Jr.  Residues in game animals


     resulting from forest and range insecticide applications.  Trans


     28th North Amer. Wildl. & Nat. Resourc. Conf. pp. 409-422.  1963.


21.  Pillmore, R. E., Flickinger, E. L. and Richmond, M. L.  Forest


     spraying of Zectran and its safety to wildlife.  J. Forest.  69:


     721-727.  1971,


                                  266

-------
22.  Pillmore, R. E.  Toxicity of pyrethrum to fish and wildlife.




     Jin Pyrethrum, the Natural Insecticide, J. E. Cassida, (Ed.).




     Academic Press, N. Y.  P. 143-164.  1973.




23.  Schmidt-Nielsen, D., and Fange, R.  Extrarenal salt secretion.




     Fed. Proc.  17:142.  1958.




24.  Schmidt-Nielsen, K., Jorgensen, C. B. and Osaki, H.  Secretion




     of hypertonic solutions in marine birds.  Fed. Proc. 16:113-114, 1957.




25.  Schmidt-Nielsen, K., Jorgensen, C. B. and Osaki, H.  Extrarenal




     salt excretion in birds.  Amer. J. Physiol. 193:101-107.  1958.




26.  Selye, H.  Studies on adaptation.  Endocrinology.  21:169-188. 1954.




27.  Stickel, L. F.  Organochlorine pesticides in the environment.




     B.S.F.W. Special Scientific Report-Wildlife No. 119.  32 pp. 1968.




28.  Stickel, L. F., Stickel, W. H. and Christensen.  Residues of DDT




     in brains and bodies of birds that died on dosage and in survivors.




     Science 151:1549-1551.  1966.




29.  Stickel, W. H., Stickel, L. F., and Spann, J. W.  Tissue residues




     of dieldrin in relation to mortality in birds and mammals.  In




     Chemical Fallout.  M. W. Miller and G. C. Berg (Eds.),  pp. 174-




     204.  Charles C. Thomas, Springfield, 111.  1969.




30.  Stickel, W. H., Stickel, L. F., and Coon, F. B.  DDE and DDD




     residues correlated with mortality of experimental birds.  JEn




     Pesticides Symposia.  W. P. Deichmann (Ed.),  pp. 287-294.  Helios




     and Assoc., Miami.  1970.




31.  Tucker, R. K. and Crabtree, D. G.  Handbook of toxicity of pesticides




     to wildlife.  B.S.F.W. Resource Publication No. 84. 131 pp.  1970.




32.  U. S. Fish and Wildlife Service.  Pesticide-wildlife review, 1959.




     Circular 84.  36 pp.  1960.
                                267

-------
33.  U.S. Fish and Wildlife Service.  Effects of pesticides on fish and




     wildlife.  Circular 143.  52 pp.  1962.




34.  U.S. Fish and Wildlife Service.  Pesticide-wildlife studies.  Circular




     167. 109 pp.  1963.




35.  U.S. Fish and Wildlife Service.  Pesticide-wildlife studies, 1963.




     Circular 199.  130 pp.  1964.



36.  U.S. Fish and Wildlife Service.  The effects of pesticides on fish




     and wildlife.  Circular 226.  77 pp.  1965.



37.  Verhage, H. G., Abel, J. H., Jr., Friend, M. and McClellan, M.



     Effects of parathion on cholinesterase and ATPase activity in the




     salt glands and hypothalamus of mallards.  (In press). 1974.




38.  Wiemeyer, S. N., and Porter, R. D.  DDE thins eggshells of captive




     American kestrels.  Nature 227:737-738.  1970.
                                  268

-------
               ENVIRONMENTAL CONCERNS IN FISH MANAGEMENT




            ^             Charles R. Walker




                   U. S. Fish and Wildlife Service






    Aquatic ecosystems are quite sensitive to environmental changes and




present complex problems in the management of fishery resources.




    The interaction of man's development actions and pollutants are often




hard to statistically quantitate from "natural variations" in the popula^-




tion dynamics of many species.  Yet we have made significant advances in




the understanding of subtle physiological stresses imposed by many pol-




lutants under controlled laboratory conditions and are now getting a




clearer picture of the trends indicated in monitoring studies of chemical




residues and biological field measurements of populations. • Our lab-




oratories are defining the effects of biocidal chemicals among various




trophic levels, specific effects on certain species relative to the




behavior, growth rate,, longevity, fecundity or reproduction, physiological




response to stresses.  The subtle long term effects are often quite dif-




ferent from the pathology and toxicological manifestations of acute and




intermittent dose response observations.
                                   269

-------
270

-------
                    AIR SAMPLING FOR PESTICIDES




                          David L. Spencer




                     Colorado State University







     During the past few years there has been an extensive effort to




monitor the environment for pesticide residues.




     The various sources of the pesticide residues detected in air




have been summarized by several investigators; however, comparatively




little data are currently available on residue incidence and levels




largely due to the lack of adequate air sampling methods.




     Several ambient air sampling devices are available and each has




its advantages and disadvantages.  Some of the more commonly used




samplers include:




          1.  Greenburg-Smith implngers




          2.  Midwest Research Institute Sampler (MRI)




          3.  High Volume Air Sampler




          4.  Nylon Cloth Screen




     We are currently evaluating an air sampler developed by the




Syracuse University Research Corporation (SURC).




     A discussion of results from an air sampler comparison and evalua-




tion study conducted by the Colorado Pesticide Center will be presented.
                                   271

-------
272

-------
         PCBs - THEIR ORIGIN AND FATE IN A RIVER ECOSYSTEM




             Richard E. Johnsen and Loretta Y. Munsell




                     Colorado State University






Introduction




     The serious ecological problems brought about by large-scale use




of persistent agricultural pesticides, particularly DDT, has focused




attention on a structurally-related group of industrial chemicals, the




polychlorinated biphenyls (PCBs).  The PBCs, with many diverse and im-




portant industrial uses, have in recent years been shown to be environ-




mental pollutants of worldwide distribution.  The pathways by which they




enter ecosystems are not resolved but must be divergent from that of




pesticides because of the different use patterns of the 2 chemical types.




The PCBs are never deliberately dispersed into the environment as are




pesticides.  Concern over the ecological implications of this contamination




is reflected in the fact that issue no. 1 of Environmental Health Per-




spectives  (April 1972) is devoted in its entirety to PCBs.




     The PCBs are chlorinated compounds manufactured by the,direct chlorina-




tion of biphenyl which results in a wide array of possible compounds




and isoiners (210), depending on the degree of chlorination.  They are




manufactured in the U.S. solely by the Monsanto Chemical Co. under the




trade name Aroclor.  They market 8 formulations based on their percent




chlorine by weight with formulations varying from 21 to 68% chlorine.




Aroclor 1242 and 1254, for example, contain 42 and 54% chlorine,by weight,




respectively.  Aroclor 1016, a recent formulation, is similar to 1242




but contains no compounds with 5 or more chlorines.  Their remarkable




range of industrial applications is due to their high dielectric constant,
                                   273

-------
inflammability, heat transfer abilities and their action as plasticizers.




A listing of applications can be found in Hubbard (1) and a brief resume




of PCB uses was made by Nisbet and Sarofim (2).  Several general reviews




of the PCB situation have been made (3-6) and Cook gave an overview of




PCB chemistry  (7).




     The fact that they have been manufactured since 1929 (1) and the




first reported environmental contamination not until 1966 from Sweden




(8) implies two things.  Firstly, they were never intentionally applied




to the environment, as was DDT for example, so no one was looking for them




in samples of fish, soil, birds, etc.  Secondly, since there was a 37




year gap between their initial use and reported environmental occurrence,




residues no doubt were present in the environment earlier but were con-




fused with chemicals known to be added to the environment such as DDT.




The PCBs present a more serious problem because of their very high chemical




stability.  They are not decomposed in concentrated acids or bases or




under incinerating conditions less than 2000°F.




     PCBs are thought to become environmental pollutants by incineration




of wastes through solid waste disposal programs, by leaks of PCB-containing




fluids or from sealed systems, by volatilization or weathering of PCB




residues in various products, by improper disposal of PCBs or PCB-containing




fluids and by passage through sewage treatment facilities.  The sources




of PCBs into these latter facilities are not known.  Other workers have




shown that PCBs in the environment, principally Aroclor 1254, are associated




with sewage treatment plants or disposal of sewage (9-13).




     Our laboratory has shown that PCBs, primarily Aroclor 1254, are found




in association with the 2 sewage treatment facilities of Fort Collins and




have been since at least mid-1969, the earliest sampling time (14).  The
                                  274

-------
identity of the residues in digested sewage sludge as Aroclor 1254 has




been confirmed using mass-spectrometry, both direct probe and coupled




with a gas-liquid chromatograph (GLC), by thin-layer chromatography,




infra-red spectrophotometry and GLC using the Coulson detector specific




for chlorine (14).   This report deals with the monitoring of PCB levels




in digested sewage sludge over the course of about 2 years and the analysis




of fish, water and sediment both upriver and downriver from the sewage




treatment plants in the Cache La Poudre River.  Attempts to determine




the source(s) of .PCBs into the treatment plants also were made.






Methods and Materials




Study Area




     The area of Fort Collins, in Larimer County, is a region of rapidly




increasing human population and growing industry.  The 2 sewage treatment




plants, because of this growth, have been hard-pressed to maintain adequate




treatment with the increasing load of waste waters.  As a result, the




Poudre River, which runs through the Northeast portion of the city, has




become polluted due in large part to the effluents from these plants.




Plant No. 1, located off Colorado Highway 14, is an old plant employing




a sedimentation tank with the settled solids  (sludge) going to one of




the two anaerobic digesters and the liquids through a trickling filter




bed.  Plant No. 2, located off east Drake Road, is about 3.1 miles down-




river from Plant No. 1 and came on-stream in 1969.  It employs an activated




sludge process with the sludge eventually going to one of two anaerobic




digestors.  After chlorination, the effluent waters from both plants




are discharged into the river which is part of the South Platte River




drainage system.
                                   275

-------
 Sampling




     Samples of digested sludge were obtained by pooling about 16




 subsamples from the drying beds, air-drying them in a hood, grinding




 them to pass a 16-mesh sieve and storing them in glass bottles with




 Teflon-lined lids.  Samples of sediment were obtained along the river




 and processed and stored similarly.  Samples of water from the outfall




 were obtained directly in 4-1 glass bottles while other water samples




 were obtained in similar bottles by immersion below the water surface.




 Fish samples were obtained initially by netting and later by electro-




 shocking.  They were sorted, representative specimens preserved in




 formalin for later identification and the remainder frozen.  Samples




 of various materials were also collected from other sources, such as




 industries, and stored in glass bottles until analyzed.




 Extraction




     Sludge and sediment samples, 5 and 40 g, respectively, were extracted




 using acetone in an ultrasonic device (15).  The acetone extract was




 diluted with water and the PCBs partitioned into hexane.  The acetone-




 water solution was re-extracted twice with hexane, the hexane extracts




 combined, washed with water, dried by passage through a column of




 anhydrous Na.SO,, and reduced in volume to about 10 ml on a rotary evaporator.




 Water samples were batch-extracted with hexane unless there were excessive




 amounts of particulate matter when samples were filtered prior to extraction.




 These filters then were extracted on a Soxhlet apparatus using an azeotrope




 of hexane-acetone.   These extracts were treated as above.  The fish samples




were thawed, ground with anhydrous Na?SO,  and extracted with hexane three




 times in a blender.   The extracts were combined and reduced to a standard
                                 276

-------
volume.  The PCBs then were partitioned into acetonitrile by three extrac-




tions of the hexane, thus removing most of the lipids.  The acetonitrile




extracts were combined, water added and the PCBs back-extracted into hexane.




The aqueous phase was discarded and the hexane phase washed, dried and




reduced in volume as above.




Cleanup




     Prior to GLC analysis, all extracts had organic impurities removed




by liquid chromatography.  The concentrated extract was added, with rinsings,




to a 2 cm ID glass column containing 10 g of activated Florisil preceded




and followed by about 2 cm of anhydrous Na«SO, which was pre-rinsed with-




50 ml of hexane.  The PCBs were recovered by eluting the columns with 200




ml of hexane.  The eluant then was reduced in volume and made up to the




appropriate volume for GLC analysis.  If additional cleanup was required,




the extract was chromatographed similarly on a column of Al.O-.




Instrumentation




     All GLC analyses were performed using a Tracor MT-220 equipped with




dual ^Ni-electron capture detectors and 4 glass columns (6 ft x,l/4 in OD).




The column packing used most often was 3% SP-2100 on 80,100 mesh Supelcon




AW-DMCS.  Others used were 1.5% SP-2250 + 1.95% SP-2401 and 4% SE-30 +




6% SP-2401, both on 100/120 mesh Supelcon AW-DMCS, and 3% SP-2250 on




80/100 mesh Supelcoport (all packings were from Supelco, Inc., Beliefonte,




Pa. 16823).  The carrier gas was pre-purified ^ maintained at 40 ml/min




and the injector, column and detector temperatures were 215, 190 and 265°C,




respectively.  Injections were in the range of 1-5 ul.




Analysis




     Most of the extracts cited above gave GLC fingerprints closely re-




sembling Aroclox 1254 by their relative peak heights and retention times.
                                   277

-------
Although specific chemical confirmation of PCB presence was not made for


each sample, earlier work with similar samples cited above (14) showed
                                                i

that similar peak patterns were due to PCBs.  Quantitation of the data


wan flfM'nmpI Inlipd hv roropsHng thp tnt^l sren of "j protolnenfr. peaks of


Aroclor 1254 with that of 5 similar peaks of the extract.  Occasionally,


samples contained earlier eluting peaks which more closely resembled


Aroclor 1242.  By admixture of portions of extracts with similar portions


of Aroclors, the resulting additive peaks gave additional evidence for the


presence of PCBs.  Although the clorinated naphthalenes (Halowaxes)


also can ha.ve complex chromatograms, similar admixture of extracts and


Halowaxes did not give additive GLC chromatograms except for possibly


some peaks.  This by itself did not preclude the presence of Halowaxes.


Previous work had shown that recoveries of Aroclor 1254 carried through


the analytical schemes were essentially quantitative (90-100%).  The data


reported herein have not been corrected for any slight loss.



Results and Discussion


Sewage Sludge


     The results of the analysis of 57 samples of sewage sludge are pre-


sented in Table 1.  Oftentimes, digested sludge was pumped into different


drying beds on the same day from different anaerobic digestors.  These


results, from the two samples with the same dates, were averaged and were


used in Figure 1.  From these data, it is apparent that since June 1969,


the levels of PCBs (Aroclor 1254 specifically) for Plant No. 1 have de-


creased from a high of over 30 parts per million (ppm or ug/g) to 15-20


ppm in 1972 and half of 1973 to a plateau level of 5-7 ppm for the remainder


of 1973 to the last sampling in June 1974.  For Plant No. 2, the PCB


levels were never higher than 22 ppm and remained at 15-22 ppm and remained



                                   278

-------
Table 1.  PCB Levels in Sewage Sludge in ppm at Various Time Intervals in
          Fort Collins, Colorado.
Date
6-24-69
1-12-71

10-16-72


12-22-72
12-28-72

1-30-73

5-26-73

6-4-73


6-26-73

7-24-73


8-13-73

8-23-73

11-6-73

11-21-73
1-29-74



2-19-74

5-26-74

6-3-74

Plant No.
Digester
-
—

2
3

.3
2

2
3
2
3 .
2
3

2
3
2
3

2
3
-2
3
2
3
Composite
2
3


2

-

2
3
1 (Colo.
ppm PCB
31.8
35.6

18.3
18.3

18.7
14.5

17.7 ,
17.3
16.2
19.7
12.5
15.0

13.2
10.6
* 10.7
10.4

8.0
5.8
5.4
6.6
7.8
6.5
7.2
6.9
7.2


6.0

5.0

5.9
6.1
14)
Avg.



18.3





17.5

18.0

13.8


11.9

10.6


6.9

6.0

7.2


7.0.



. 6.0



6.0

Date
6-24-69
-11-20-72


12-20-72

1-15-73
2-2-73


6-7-73
6-13-73

6-23-73

7-11-73

7-17-73
7-20-73

7-31-73

8-29-73
9-21-73

10-16-73

10-18-73
11-1-73

12-3-73


2-11-74

6-3-74

.< 6-20-74
Plant No.
Digester
'
1
2

-

-
1
2

-
1
2
_

-

-
—

'

-
1
2
1
2
-
. —

1
2

-

-

-
2 (Drake Road)
ppm PCB
21.5
22.0
20.2

15.8

19.0
21.8
20.7

15.7
21.4
13.3
12.3

11.2

10.8
12.1

11.5

7.6
6.5
7.4
7.8
7.4
6.7
6.5

6.4 .
6.8

7.0

6.6

6.6
Avg.

21.1



\

21.2



17.4











7.0

7.6




6.6







                                   279

-------
                                            FIGURE 1.  PCB LEVELS IN SEWAGE SLUDGE AT VARIOUS
                                                       Tint INTERVALS IN FORT COLLINS,  COLORADO
                                            PLANT No. 1 (CoLO, IK)
                                            PLANT No. 2 (DRAKE fto.Jo—o*~o
                                                    8-73   Id-Mi   12-73  '  2-74    4-7f    .6-74
01	„	L_,,J	L	I	1 .... I	I	I	    I
6-6
-------
at 15-22 ppm until mid 1973 when they too declined to a plateau level




of 6-8 ppm.  These plateau levels appear to be relatively low values but




it should be remembered that many tons of digested sludge are produced




monthly be each plant and most of this sludge is used for soil amendments




or low quality fertilizers.




     It is not known what percentage of incoming PCBs are retained by




the sludge and how much is released in the effluent water to be picked




up by aquatic organisms.  This is dependent on the efficiency of the




gravity settling of the sludge in the settling tanks.  We know that be-




cause of the very low water solubility of the PCBs, and PCBs in the ef-




fluent water are found adsorbed onto particulate matter.  The more efficient




the settling of sludge, the less particulate matter there will be in the




effluent water and hence less PCBs.  Dube, et al. (1974) (13) estimated




that at least 70% of PCBs in incoming waste are removed by treatment




of the waste waters as reflected by the comparatively high PCB levels




in the sludge.




     To determine that PCBs were not coming from the plant itself, such




as in sealing compounds used on the digestors, a 2-1 sample of waste-




activated sludge (undigested) was collected on June 25, 1973 from Plant




No. 2, analyzed and found to contain 35.8 ug for an overall level of about




0.02 ppm.  This appears low except that this sludge is largely water (only




2400 mg solids) and does not reflect the concentration of pollutants that




occurs during digestion followed by the dewatering of the digested sludge.




This level indicated that PCBs are present in influent waste waters.  Dube




et al. (13) has shown that PCBs are present in influent waters in numerous




Wisconsin cities examined and from a single sewage plant, the PCB levels




fluctuated between 0.54 to 3.1 ug/1 during a single day.






                                   281

-------
     The decline and stabilization of residues, as shown by the sludge




data, may be due to efforts by Monsanto who withdrew PCBs from sale for




other than closed system applications on or about August 1970 (16).




Since no laws have been legislated controlling PCB usage, and since Mon-




santo 's efforts are voluntary, few data have been published on whether




environmental residues are diminishing besides those in sludge herein




reported.  Veith (17) reported a sharp decline in PCB residues in river




waters in Wisconsin from 1970 to 1971, possibly due to these sales




restrictions by Monsanto.  Our results with sludge showed a sizable




decrease commencing in mid-1973.




     Figure 2 presents the GLC chromatograms of 2 sludge extracts from




Plant No. 2, one collected in June 1969 and one collected in June 1974,




with a comparison to the standard Aroclor 1254.  Both samples were ex-




tracted on the same date.  One can readily see the similarities of the




sludge extracts with that of Aroclor 1254,  The earlier peaks have been



shown to be due primarily to Aroclor 1242. : It is, apparent ..th^fome/subtle




changes have occurred in the peak patterns form the sample of 1969 to




the one in 1974.  Similar samples from Plant No. 1 show less divergence .




from Aroclor 1254 for both 1969 and 1974.  The fact that each plant handles




the waste waters from different secitons of the city with their own




associated industries, and since PCB levels have been quite similar for




the past year, implies that PCBs are coming from possibly numerous sources




at relatively low levels rather than from a single point.  The fact that




the chromatograms of sludge, for example Figure 2 (A) and (C), are so




similar to 1254, leads one to conclude that metabolism of 1254 under the




anaerobic conditions in the digesters is minimal if any.
                                    282

-------
                                                   ^N-wy U"
:1GURE 2.  Gas-liquid chrornatograms of an extract of sewage sludge from
          1969  (A), one from 1974 (3) and comparison with the Aroclor 1254
          standard  (C).

-------
Fish

     Although numerous fish samples are yet to be analyzed, the data from

those analyzed are presented in Table 2.  It is apparent by comparing the

number of specimens with the total weight that, with the exception of the

green sunfish and a group of longnose daces, all the specimens weighed less

than 1 g and were young to very young specimens.  The table also includes

data for two groups of insects (cranefly larvae), which indicates an overall

low level of PCBs but also considerably higher (50%) for those downriver

from the outfall.  Since the sample weights were small, the results are all

expressed in ppm on a whole-body, wet-weight basis.  It is evident that

levels exceeding 1 ppm were found only with longnose daces arid sunfish,

perhaps due to their older age than the other samples.  Figure 3 presents

a GLC chromatogram of an extract of longnose daces with comparison to 1254.

The similarity to 1254 is apparent but numerous earlier peaks are present,

similar to 1242.  This chromatogram (A) is very similar to that of the sludge

in Figure 2 (B).  Samples of carp and suckers, of varying size up to almost

two feet long, await analysis.  Results from these species should indicate

better the possible buildup of PCB residues with time.

     All the species analyzed contained PCBs, especially 1254, but also

had additional peaks attributed to other PCBs.  The analytical procedure

eliminates most possibly contaminating insecticides, except p,p'-DDE, but

various tests have shown this to be insignificant or absent.  It is difficult

at this time to make any conclusion regarding fish other than all samples

analyzed did contain PCBs.

Water and Sediment

     Besides those samples from the river itself, we collected water and

sediment samples from three sewage lagoons belonging to two local

sanitation districts, whose effluent waters also empty into the Poudre

River.  Surprisingly, the three water and three sediment samples were negative

for PCBs.  These districts, however, serve essentially no industry but rather
                                  284

-------
       Table 2.  PCB Levels in Fish and Cranefly Larvae From the Poudre River, Fort Collins, Colorado.
00
01
Sample
No.
I
2
3
4
5
6
7
8
9
10
11
12
Source
Plant No. 1
250 yds. upstream
100 yds. downstream
2 miles downstream
„ „
it n it
Plant No. 2
100 yds. upstream
„ ,,
n n n
n n n
n n n
2 miles downstream
4 miles downstream
aCranefly larvae, Family Tipulidae
Rhinichthys cataractae; Northern
promelas;
green sunfish, Lepomis
Collection
Date
3-13-73
9-6-73
3-13-73
8-30-73
8-30-73
8-23-73
8-23-73
8-23-73
3-13-73
8-23-73
9-10-73
9-10-73
, . Holorusia
Creek Chub,
cyanellus .
Species3
Cranefly larvae
White sucker
Cranefly larvae
Longnose dace
Longnose dace
Creek chub
White sucker
Fathead minnow
Green sunfish
Green sunfish
White sucker
Fathead minnow
grandis; white sucker,
Semotilus atromaculatus

Number
20
25
13
4
55
9
23
10
1
1
6
9
Total
Wt.(g.)
16.8
5.9
10.6
7.6
49.2
15.1
10.7
5.2 .
5.4
7.6
4.6
6.2
Catostomus commersoni ; longnose
atromaculatus ;

fathead minnow,
ppm
PBCb
0.06
0.17
0.09
1.50
1.99
0.30
0.27
0.62
1.33
0.46
0.37
0.48
dace ;
Pimephale
       "Level expressed on whole body, wet-weight basis as Aroclor 1254.

-------
                              -'!  '•'• j    '{ i :': SR-'H::-'.;--I-"- i '	{'-•
                              I   . I. 1    .L.  -. 1...3.,. ._j - ..-v. .'_. ...    I
                              A	_-; i.-!    ^|. - : jSj-r.--f^^:P"-J: i '	i_{_4.
                                         BaaiW!^
FIGURE 3.   Gas  liquid  chromatograms of an extract of Longnose Dace fishes
          (A) and  comparison with the Aroclor 1254 standard (B).
                                 286

-------
small residential areas.




     All the water and sediment samples have been processed and analyzed




by GLC.  Almost all of these samples are in the process of being re-




analyzed because of the presence of interfering co-extracted substances




even after extensive cleanup.  In addition, many of the GLC peak patterns




were atypical of any one Aroclor standard or of several of the mixtures




we tested.  The problem of quantitation, because of these considerations,




has been very difficult.  One continuing problem has been the presence




of inorganic sulfur in our extracts, which went unrecognized until fairly




recently, which in turn obscures many of the early peaks.  This problem




has been resolved by using reactive copper to remove the sulfur.  It has




also recently been found that other interferences can be removed by re-




chromatographing the extracts on micro-columns containing Florisil with




hexane elution.  So, at this time, many of our extracts have not yet




been adequately quantitated to our satisfaction.  The possibility of selec-



tive metabolism of various isomers by microorganisms which results in an




atypical GLC tracing cannot be ruled out even though this is not indicated




by the sludge data.




     We can conclude from the water samples analyzed so far that the six




samples collected upstream at varying distances, up to 30 miles upstream




toward the headwaters of the Poudre River, were negative for PCBs.  Only




with water samples from the outfall of Plant No. 1 or up to 100 yards




downriver are PCBs detectable.  At the Plant No. 1 outfall, levels of




up to 2 yg/1 Aroclor 1254 were found whereas at 100 yards downriver, levels




were about 0.05 pg/1.  No PCBs were detectable in water farther downstream




due to dilution by river water.  At Plant No. 2, similar but lower levels




were in the outfall water and 100 yards downstream but none were found




in samples collected as far as four miles downstream.




                                  287

-------
     Of those sediment samples completed to date, the results are presented


in Table 3.  It is apparent that residue levels fluctuated upward for the


two samples collected from the same site at different times.  It is too
             i

early to make any generalization on this apparent trend.  The fact that


levels were higher from both plants at 100 yards downstream rather than


closer to the outfall may be due to lack of sedimentation of PCB-bearing


partic.ulate matter so close to the outfall.  It was surprising to find


a level of 0.4 ppm at 2 miles downstream.  This site may be a natural


sink for particulate matter.  The fact that PBCs were detected upstream


of Plant No. 2 indicates that residues are being carried that far downstream.
                                             i


Table 3.  Levels of PCBs as Aroclor 1254 in ppm in river sediment.
Location3
Plant No. 1

100 yards upstream
25 feet downstream
100 yards downstream
2 miles downstream
2 miles downstream
Date


9-5-73
3-13-73
3-13-73
3-13-73
8-30-73
ppm in sediment

b
N.D.
0.50
0.61
0.01
0.04
   Plant No. 2


100 yards upstream                     3-13-73        0.03


100 yards upstream                     8-23-73        0.27



15 feet downstream                     3-13-73        0.10


100 yards downstream                   3-13-73        0.14


2 miles downstream                     3-13-73        0.40

aLocation refers to distance from outfall
     detected—sensitivity of method for 40g sample is 0.005 ppm
                                 288

-------
That the PCB levels at 100 yards downstream was considerably higher at

Plant No. 1 than No. 2 may be an indication that Plant No. 1 has been

in operation many years longer and such a buildup need not be unexpected.

It is not known what effects the spring snow melts have on sediment

redisue levels since a lot of particulate matter is carried downriver

by the much greater volume of river water.  Final results from the other

samples will help clarify the residue picture and perhaps allow some

conclusions to be drawn.

Miscellaneous Samples

     As mentioned earlier, the sources of PCBs into sewage systems are

unknown.  In attempts to find the sources, we collected a number of

samples from various sources and sites within the city and interviewed

various industry managers in attempts to. determine if their processes

might be contributing PCBs.  For the most part, the results have been

negative.  Since PCBs are present in sludge at a somewhat steady level,

there must be a continuous input rather than single incidents.  Analyses

of samples of service station grease and floor scrapings were negative.

Although all printing companies visited used dry processes and had no

significant input into the sanitary sewer, an oily rag from the newspaper

used to wipe printing machinery, was strongly positive for Aroclor 1254

(189 yg recovered), and also 1248, 1242 and possibly some chlorinated

terphenyls (PCTs).  A similar rag from an industry employing plastics and
                                               t
plastic molding machines was negative.  A wax sample scraped from the

floor of a campus building and 1 g analyzed was found to contain 181.8

ppm of Aroclor 1254.  This may be indicative of a widespread, low-level

contamination from many sources.  There has been unpublished data cited

reporting PCBs in dishwasher detergents and aluminum foil (13) which points
                                 289

-------
out this possibility.  Additional sampling may throw more light on this




aspect.




Summary and Conclusions




     The findings of this study to date show that PCBs, primarily Aroclor




1254, are found in the digested sewage sludge from both sewage plants in




Fort Collins, Colorado.  The PCBs were at levels of about 30 ppm in 1969




and have decreased to a plateau level of about 6 ppm in late 1973 and




1974.  PCBs also are found in river sediment at least 2 miles downstream




from the second sewage plant along the river and also have been found in




all the small fish analyzed as well as two samples of insect larvae.  It




is evident that PCBs are escaping from the treatment plants in the effluent




waters of the outfalls and are being picked up by the river fauna.  Deter-




mination of the sources of PCBs have not been ascertained but may be due




to many low-level inputs.




     The fact that PCBs are present in these various samples indicates




a problem of not only regional but national concern.  A solution to the




problem is elusive and further generalizations may be able to be made only




after all the samples are analyzed, the sample data are quantitated, and




the data have been evaluated.






                              References




1.  Hubbard, H. L.  Chlorinated biphenyl and related compounds.  In




    R. E. Kirk and D. F. Otherm (eds.).  Encyclopedia of Chemical Tech-




    nology, 2nd rev. ed. 5:289.  1964.




2.  Nisbet, I. C. T. and Sarofim, A. F.  Rates and routes of transport of




    PBCs in the environment.  Environ. Hlth. Persp. 1:21.  1972.




3.  Edwards, R.  The PCBs, their occurrence and significance - A review.




    Chem. Ind. (London) 20:1340.  1970.
                                 290

-------
                      ASBESTOS:  AN OVERVIEW*
      James Edward Huff, Anna S. Hammons, Carolyn- A. Dinger,
          Bradford L. Whitfield, and Gerald U. Ulrikson

          Information Center Complex/Information Division
                  Oak Ridge National Laboratory
                   Oak Ridge, Tennessee  37830
                    Freedom'4 juAt anotheA. wold
                       ($01 nothin' tzfit to Lot>e.

                    No thin' ain't wovtk notion1
                       but it't>
    Asbestos fibers are present in the air we breathe, the food and

beverages we consume, and the water we drink.  No longer does asbestos

represent just an occupational hazard but one of vast environmental

magnitude portending at least some exposure for us all.  The formerly

localized ailment of minor proportion has metastasized so widely as to

create an issue of greatest public concern — one that urgently cries

out for resolution.
*Work supported jointly by the Toxicology Information Program, National
Library of Medicine; the Solid and Hazardous Waste Research Laboratory,
U.S. Environmental Protection Agency; and Division of Biological and
Environmental Research, U.S. Energy Research and Development
Administration, under contract with the Oak Ridge National Laboratory
operated by Union Carbide Corporation Nuclear Division for the
U.S. Energy Research and Development Administration.
                                  293

-------
     Presently available data are overwhelmingly conclusive — asbestos



is indeed hazardous to human health!   Asbestos exposure is pathogenic



to humans, causing asbestosis, lung cancer,  mesotheliomas, and pleural



lesions; both experimental  animal data and human clinical  studies



support these findings.  Yet, one particular aspect — ths potential



harmfulness of asbestos ingestion — remains unresolved and contro-



versial.  The overall  problem awaits solution through the expanding



experimental, epidemic logical, and clinical  investigations now being



conducted..



     This overview of  the asbestos problem highlights historical



developments, summarizes the reference literature, reviews physical and



chemical properties,  lists production amounts and uses, sketches biologic



aspects, examines environmental contamination, and presents conclusions



based on assimilation of the literature.



                               HI STORY



     As can be imagined from Table 1, asbestos surely possesses an



enigmatic history.  Just for a moment, try to fathom what the ancients



conjured as use after different use was chanced upon for this virtually



i ndestruct i bIe mater i a I.



     In 1938, a book edited by Lanza documented the medical history of



asbestosis.  Written by investigative pioneers, these authors blazed  a



trail for future scientists to follow.
                                  294

-------
                 Table 1.   ASBESTOS HISTORY
4000 Years Ago   -  Regarded as a treasure.

Centuries B.C.   -  Fire-proof fabrics.

450 B.C.         -  Cremation cloth mentioned by Herodotus.

1st Century A.D.  -  Described in literature by Pliny and Plutarch.

1725                Benjamin Franklin gave the oldest known  woven
                    asbestos article —  a small  purse made of
                    tremolite — to Sir  Hans Sloan.   On exhibit
                    in the National History Museum.

1878                Commercial production in Quebec.

1900                Establishment of fabricating industry and
                    markets in America.

1900                First reported death resulting from asbestos
                    dust inhalation.

1910                Notable asbestos-mining facilities established
                    in present-day leading centers.

1930                First asbestos is cases reported  in the
                    United States.

1930                First investigation  of the asbestos industry.

1964                New York Academy of  Sciences hosted National
                    Conference on asbestos.

1972                National Institute for Occupational Safety and
                    Health recommended standard.

1974                National Institute of Environmental Health
                    Sciences gathered world's experts on asbestos.
                                  295

-------
                              LITERATURE




     The asbestos literature is no exception to the general  axiom that




most published literature — even that reporting on a single,  well  de-




fined subject area — appears scattered throughout the world in myriad




sources.  To reduce this seemingly endless and repeated exercise of




periodically attacking the literature, a computerized annotated




literature collection was started (Huff et al., 1974).  The initial




549 records represent a cross section of the total asbestos literature —




emphasizing human health hazards and clinical aspects for the period




from 1960 into 1974.



     Interest in the health aspects of asbestos has gained both




scientific and social momentum in recent years.  Witness that two major




national meetings have been convened on the adverse health hazards and




ultimate consequences of asbestos:  the first was held at the New York



Academy of Sciences  in 1964 whereas the second took place ten years



later at the National Institute of Environmental Health Sciences in



1974.  Planned is the Third International  Conference on the Physics and




Chemistry of Asbestos Minerals to be held at Laval University, Quebec



City, August 17-21,  1975.  Sections of many other gatherings addressed




the asbestos question; in others, numerous peripheral discussions



centered on meeting obligations — legal, social, economic, scientific,



and medical.



     References detailing asbestos research are abundant — and



multiplying.  A few significant topical examples comprise air pollution




(Air Pollution Control Office, 1971; National Academy of Sciences, 1971;



Office of Air and Water Programs, 1973; Sullivan and Athanassiadis, 1969),






                                  296

-------
geology (Brobst and Pratt, 1973; Bureau of Mines, 1970),  occupational




criteria (National Institute for Occupational  Safety and  Health,  1972;



Ruby and Buchan, 1974), carcinogenic risk (International  Agency for



Research on Cancer, 1973), literature collections (Huff et al., 1974;




Kenton, 1973), a recent synopsis (Hammons and  Huff,  1975), conference




proceedings (National   Institute for Environmental Health  Sciences,  1974;




New York Academy of Sciences, 1965), an environmental  background



document (Dinger et a I., 1975), as well  as a popular  account (Brodeur,




1972).



                   PROPERTIES, PRODUCTION, AND USES




     Asbestos — that "magic mineral" — refers to a group of hydrated,



silicate minerals which possess a fiber-like structure, the only




mineral capable of being woven  like and into cloth.   Widespread commer-



cial use of asbestos stems particularly from its natural  properties,



such as flexibility and high tensile strength  (Table 2),  which are



imparted by the chemical composition and crystal structure of the fibers.



Asbestos minerals consist of two main types (Table 3)  as  determined by



their crystal  structures: the serpentine class contains chrysotile, a



pure magnesium silicate that comprises 90-95?  of the world's asbestos




production; the amphibole class includes five  varieties in which  the



magnesium component is partially or wholly replaced  by other cations.




Differences in the chemical composition and in the crystal morphology



account for slight variations in physical  properties among different



types of asbestos (Table 4).
                                  297

-------
                                          Table 2.   ASBESTOS
Types and Percentage Use
                                  Favorable Properties
                                          Major Uses
CD
   Chrysotile      90-95


  *Crocidolite       3-4


  *Amos i te           2-3



   AnthophylIite     < 1

   Tremolite          < 1
FI ex!b iIi ty

Length of  Fiber

Tens!le Strength

Chemical  Reactivity

Resistance to Heat

Electrical Conductance

Filtration Characteristics
                                                                    Asbestos-Cement Building
                                                                    Materials                   10%
                                                                    Asbestos-Cement Pipe
                                                                    Floor Ti le
                                                                    Brake Linings,  Gaskets,
                                                                    Clutch Facings, Paints,
                                                                    Electrical  and  Heat         20$
                                                                    Insulations,  Steam-Pipe
                                                                    Coverings and Others
     Note:

     ^Possesses particular properties that would favor greater use if  they occurred more universally and in
     larger amounts.

-------
                   Table 3.  ASBESTOS NOMENCLATURE
Asbestos:   A generic term for naturally fibrous silicates that
            are amenable to mechanical  separation into fine
            filaments of considerable tensile strength and
            flexi biIity.
                               Asbestos
        Serpentine

           *Chrysotile

              (white asbestos)
Amphiboles

   Actino Iite

  *Amosite

  *AnthophylIite

  *Crocidolite

     (blue asbestos)

   Tremolite
Note:
*CommerciaIly important types.
                                 299

-------
                                Table 4.  ASBESTOS PROPERTIES
o
o

Compos it
Chemical
formu la
Color
Length
Texture
Note:
Chemica
Source:
Chrysoti le
( 1 2001 -29-5 )a
ion Hydrous silicates
of magnesia
Mg3Si205(OH)4
White, grey,
green, ye I lowish
Short to long
Soft to harsh;
a I so s i I ky

I Abstracts Service Reg

Amosite
(12172-73-5)
Si 1 icate of Fe
and Mg
(Fe2+Mg)7-
Sig022(OH)2
Ash gray,
greenish, or
brown
Long
Coarse, but
somewhat pi iable

istry Number.

AnthophyJ 1 tte
(17068-78-9)
Mg si I icate with
iron
(MgFe2+)?-
Greyish-white,
brown-grey or
green
Short
Harsh



Croc idol ite
(12001-28-4)
S i I icate of Na and
Fe with water
2+ 3+
Na^Fe, Fe«
Lavender, blue
green i sh
Short to long
Soft to harsh



      International Agency for Research on Cancer  (1973).

-------
     Because the industrial  uses of asbestos depend on the physical




characteristics of the fibers and because evidence indicates that harm-



ful effects in the body are related to the dimensions of the fibrils,




recent work has emphasized use of the electron microscope.  For instance,




chrysotile fibrils are approximately hollow cylinders with varying




amounts of an amorphous material on the inside and outside of the tubes




— estimated diameters averaged 20-25 nm for the outside and 2-5 nm for



the inside (Pundsack, 1961).



     World production amounts are listed in Table 5.   The three-year



trends show relative stability; production giants include Canada >




U.S.S.R. > South Africa > China > Italy > United States > Rhodesia >



Swaziland.  North America remains the leading source of asbestos.



     United States domestic production stems from four main areas



(Table 6).  California remains the overwhelming leader for mining



asbestos — about 70 percent of the total  — followed by Vermont,



Arizona, and North Carolina.



     In the last six decades, global use of asbestos has increased more




than 100-fold — from 30,000 tons to four million tons; in 1972, the




100th year of commercial  asbestos use in the United States, we consumed



nearly 20 percent of the world's total production.  Considering the



thousands of known end uses,  eight major categories consume 85 percent



of the asbestos used in this country, with the remaining 15 percent



devoted to "other" uses (Table 7).
                                  301

-------
               Table 5.  ASBESTOS WORLD PRODUCTION
                            (short tons x 1000)

North America
Canada
6United States
Latin America
^Argentina
Brazi 1
Europe
Bu Igaria
Fin land
France
5 1 ta 1 y
Portuga 1
2U.S.S.R.
Yugoslavia
Africa
Egypt
Mozambique
Rhodesia
3South Africa
Swazi land
Asia
4China
Cyprus
1 nd ia
Japan
Korea, South
Phi 1 ippnes
Taiwan
Turkey
Oceania
Austral ia
Total
1970

1,662
125

.390
18

3.3
15
.550
131
.223
1,175
13

.495
.251
88
320
36

190
28
11
23
1.5
1.3
3.1
3.6

.815
3,851
1971

1,635
131

.433
22

3.3
11
.550
132
.140
1,270
17

.077
1.6
88
355
39

175
31
12
20
—
—
2.6
4.3

.990
3,951
1972

1,629
132

.440
36

3.3
7.0
.550
146
—
1,345
12

.080
.589
88
356
37

220
31
14
16
2.2
—
3.0
4.4

1.0
4,083
Note:
Superscript numbers indicate rank order.
Source:
Bureau of Mines (1974).
                                 302

-------
                   Table 6.  DOMESTIC PRODUCTION
  State and Company
                             Name of  Mine
                   Type of Asbestos
Arizona
  Asbestos Manufacturing
    Co.

  Jaquays Mining Corp.

  Metate Asbestos Corp.


CaI ifornia
  Atlas Asbestos Corp.

  Coalinga Asbestos Co.
    Inc.

  Pacific Asbestos Corp.

  Union Carbide Corp.
1
Phi I Iips


Chrysotile

Lucky Seven



Santa Cruz

Christie (or
  CoaI inga)

Pacific Asbestos

Santa Rita (or
  Joe No.  5)
Chrysotile


Chrysotile

Chrysotile



Chrysotile

Chrysotile


ChrysotiIe

Chrysotile
North Carolina
  Powhatan Mining Co.


  Powhatan Mining Co.
                             BurnsviIle (or
                                Hippy)

                             Boot Hill
                     AnthophylI ite


                     AnthophyI Iite
Vermont
  GAP Corp.
                             Lowe I I
                     Chrysotile
Note:

Superscript numbers indicate rank order.

Source:

Bureau of Mines (1974).
                                 303

-------
    Table 7.  UNITED STATES CHRYSOTILE ASBESTOS CONSUMPTION,  1972
   End uses                 Short tons              Percentage
Construction
Floor tile
Friction products
Paper
Asphalt felts
Packing and gaskets
Insu lation
Texti les
Other
Total
323,400
84,700
77,000
69,300
46,200
30,800
15,400
7,700
115,500
770,000
42
11
10
9
6
4
2
1
15
100
Source:
Bureau of Mines (1974).
                                 304

-------
                          BIOLOGICAL ASPECTS




Plants. Protozoa and Bacteria



     Unfortunately, no information was found during our extensive




search of the literature on the effects of asbestos on plants,  protozoa,



or bacteria.  Future research plans should include this barren  area —




and most likely projects of this nature are either being started or




contemplated.



Animals in Natural  Habitat



     Similarly, almost no data have been published on exposure  of



animals to asbestos in the natural environment as opposed to the large



amount of data from experimental studies.  Some few examples follow:



     Schuster (1931) reported a case of asbestosis in a dog that lived




in an asbestos factory for 10 years.  No asbestos bodies were found in



the  lungs although the histology was typical of asbestosis.  The dog



was exposed to an unknown dose of white, blue, and brown asbestos and



survived for eight years before symptoms appeared.




     Kiviluoto (1965)  found anthophyI Iite asbestos fibers in the lungs



of a cow living near an asbestos mine.



     Interstitial fibres is, asbestos fibers, and asbestos bodies were



found  in the lungs of  a donkey that had worked 10 years at a amosite



mine and in the  lungs  of a baboon that  lived near a crocidolite mill



(Webster, 1963).  Asbestosis was also found in field rats trapped



around the same crocidolite mill.



Animals in Experimental Climate




     The primary goal  of most animal research with asbestos centers on




deciphering the reason(s) and mechanism(s) of the pathogenic effects.
                                 305

-------
Unfortunately, existing information leads only to possible answers and



hypotheses because often corroborative data are absent or conflicting




as well as controversial data abound.



     An ideal summation of animal  data would be a dose-response curve




showing the dose of various types of asbestos plotted against the




incidence of asbestosis and cancer in  different experimental  animals;




hopefully, one could then extrapolate  the results to humans.   Discour-




agingly, these investigative data do not yet exist.   We can conclude




from available data, however, that all commercially important types of




asbestos have the potential to produce asbestosis and cancer in all



commonly used laboratory animals — including mice,  rats, hamsters,




guinea pigs, and monkeys.



     Much of the following information has been summarized from the




comprehensive report by Dinger et a I.  (1975) and the computerized



annotated literature collection by Huff et al. (1974).  Resultantly,



reference to specific works has been avoided in the following sections



to allow not only clarity but, most importantly, brevity.  An edited




and updated revision of this report will appear in the future as an



EPA document.




     Species differ in the intensity and speed with which they respond




to asbestos exposure.  The fibrotic response in the rat usually is



multifocal and nonprogressive unless a chronic infection is present.



In guinea pigs, fibrosis is diffuse and progressive.



     Considerable controversy exists concerning the fibrogenic poten-



tial  of various asbestos types and fiber sizes.  For example, the



fibrotic response in the guinea pig was greater following intratracheal
                                 306

-------
injection of chrysotile fibers averaging 10 microns in length than  to




those averaging 5 microns.  However, fibrosis has also been produced in




guinea pig lung by very fine particles of asbestos, for instance,  1  micron




or less.  Chrysotile was more fibrogenic than amosite in rats, but  amosite




was more fibrogenic than chrysotile in guinea pigs, Vervet monkeys,




and rabbits.  The large number of physical  and chemical  variables which




may influence the pathogenicity of asbestos make firm conclusions about



pathogenic mechanisms seemingly impossible.



     A problem also exists when drawing conclusions about the carcino-



genic potential of asbestos; neither mechanisms of action nor quantita-



tive dose-response relationships have been defined.  Lung cancer and



mesothelioma induction are positively associated with asbestos exposure



as shown in many epidemiological investigations of humans.  Most meso-



theliomas in humans are associated with crocidolite inhalation; however,




in animal experiments, chrysotile, amosite, and silica as well as



crocidolite will produce mesotheliomas when injected intrapleuraIly




into rats.  Mesotheliomas have not been induced following inhalation



exposure of animals to any of the asbestos dusts.  Qualitatively, the



data clearly show that asbestos exposure can lead to asbestos is, lung




cancer, and mesothelioma  in animals but quantitative dose-response



relationships have not been obtained.



Human Evidence



     Asbestos inhalation causes several interrelated respiratory



diseases in humans (Table 8, 9, and 10).  The most prevalent is



asbestos is — a chronic, progressive disease characterized by pleura I



lesions and interstitial pulmonary fibrosis with functional impairment
                                 307

-------
             Table 8.  CONDITIONS CAUSED BY ASBESTOS
Asbestos is:


Pleural  calcification:

Pleural  plaques:
Pleural  and peritoneal
  mesothelioma:

Lung cancer:
Lung fibrosis caused by inhalation of
asbestos dust.

Hardening of pleural tissue.

A patch or small differentiated area
on the surface of the pleura.

A rare neoplasm derived from the lining
cells of the pleura and peritoneum.

Various types of malignant neoplasms,
most of which invade surrounding
tissues, that may metastasize to
several sites.
                                 308

-------
         Table 9.  ASBESTOS-RELATED HEALTH PROBLEMS
                     Signs and symptoms

Cough                                 Reduced lung function

Dyspnea                               Pulmonary fibrosis

Rales                                 Pleural effusion

Emphysema                             Pleural thickening

Pleuritis                             Finger clubbing

Altered serum                         Pleural plaques
  protein concentrations



                         Diagnosis

                  History of exposure

                  Biopsy

                  X-ray

                  Asbestos bodies in sputum,
                    tumor, or lung tissue

     i

                         Treatment

                  Remove from exposure

                  Symptomatic
                             309

-------
Table 10.  POSSIBLE MECHANISMS OF PATHOGEN ICITY



     Mechanical  properties of the fiber.

     Trace metals associated with the fiber.

     Polycyclic aromatic hydrocarbons associated
       with the fiber.

     Additives originating from the mining,  milling,
       and processing of asbestos.

     Cigarette smok acting in conjunction with
       asbestos exposure.
                      310

-------
of the lungs; symptoms include cough, weight loss, and shortness of


breath.  No effective treatment has been formulated for asbestosis or


its complications.  Once asbestos fibers reach the deep lung passages


they induce diffuse fibrous degeneration, primarily in the lower lobes;


this may develop as early as 3-6 years after initial  exposure and


continues to progress even after exposure has ceased.   The gradual


progression of fibrosis results in the distortion of  terminal bron-


chioles and air spaces, leading eventually to severe  pulmonary insuffi-


ciency and death.


     Abnormalities of the pleural  lining surrounding  the lungs commonly
         i

accompany asbestotic lung fibrosis.  The main pleural  lesions involved


are hyaline plaques., which are layers of hyalinized fibrous protein


formed by the proliferation of connective tissue fibers.  This fibrous


response is attributed to the abrasive action of asbestos fibers that


reach the pleural via penetration of lung tissue.


     Dose-response relationships between asbestos inhalation and


asbestosis are poorly defined for humans; nearly all  of the positive


evidence linking asbestos with human effects comes from epidemiological


and clinical studies, most of which  lack quantitative exposure histories.


Consequently, only a minimal association exists between human epide-


miological  data and environmental  exposure, and even  this reflects a


noticeable  lack of definitive information concerning  causal relation-


ships.  Generally, the development of asbestosis appears to be closely


related to the dose and duration of asbestos exposure as well as to the


length of asbestos residence in the  lungs; the incidence increases with


increasing dose and/or duration.  However, a 3Q%  incidence of asbestosis
                                 311

-------
has been reported in 101 shipyard workers exposed to a small  dose of




approximately 5 million particles per cubic foot (mppcf) for more than




20 years.  These results suggest that prolonged exposure to low concen-




trations is hazardous and that the current threshold limit value (TVL)




of 5 f/ml should be lowered.




     Other studies show that the inhalation of large doses for short




durations can be as harmful as the cumulative effect of low concentra-




tions over many years of exposure.




     Several types of human cancer have been attributed to asbestos




inhalation.  A recent report estimates that 50% ©f the persons with




asbestosis also develop lung cancer.  Mesotheliomas of the pleural  and




peritoneal  tissues are extremely rare primary tumors of the serosa,




approximately 80$ occurring in persons exposed to asbestos.  Prognosis



for mesothelioma in either site is poor; tumor progression may result



in encasement of the entire thoracic cavity by pleural  mesothelioma



or obliteration of the abdominal cavity by peritoneal  mesothelioma.



     Asbestos inhalation and ingestion may enhance the risk of cancer



of the stomach and colon.  Persons with asbestosis demonstrate an in-




creased  incidence of gastrointestinal cancer.  Also, the extremely



high rate of stomach cancer among the Japanese may result from the



ingestion of rice that  is treated with asbestos-contaminated talc.



Asbestos contamination of drinking water in Duluth, Minnesota has not




yet produced any apparent increases  in cancer mortality within the



surrounding population; asbestos-like fibers in industrial waste first



entered this water supply in 1955.   In the next 14 years, according to



Masson, McKay, and Miller (1974), no carcinogenic effect was apparent
                                 312

-------
in the patterns of cancer mortality among persons of all  ages,  nor



among children.  Obviously this observation period is short relative




to the latent period for occupationally induced carcinogenesis  from




asbestos.  Later, Gross et al. (1974)  reported that animals fed asbestos




over much of their lifetime and allowed to live to the age of cancer




production, failed to provide evidence of a cancerogenic  effect.   Never-




theless,  the findings are inconclusive because cancer induction requires



many years, and there is a significant paucity of experimental  and



epidemiological information concerning the effects of asbestos  ingestion



in humans.



     Well defined dose-response relationships between asbestos  exposure



and cancer induction cannot be derived readily from available data.



The greatest risk occurs with long, heavy exposure — most likely



occurring  in industrial  situations; an exception may be the development




of carcinoma in one patient exposed to asbestos for only  12 months.




Mesotheliomas have been reported in persons who were indirectly exposed



to asbestos through contact with clothing of occupationally exposed



relatives as well as in persons who live in the vicinity  of asbestos



industries.



     There are definite differences in the carcinogenic potential of



the various asbestos types.  Most epidemiological studies indicate that



crocidolite is more carcinogenic than  other types of asbestos;  it is



associated with a higher incidence of  mesothelioma and lung cancer than



are chrysotile, amosite, and anthophylIite.




     Cigarette smoking may be a cofactor in cancer induction by asbestos.



Asbestos   inhalation combined with cigarette smoking significantly
                                 313

-------
increases lung cancer incidence over that caused by exposure to.either



factor alone.



     Until 1969, diseases associated with asbestos exposure were



considered only as occupational hazards.  More recently, investigators



have realized that exposure of the general population to environmental



asbestos pollution also may be hazardous, particularly in urbanized



areas.  Asbestos bodies commonly are found in the lungs of urban



residents, both in Europe and the United States.  Data are insufficient



to indicate the significance of the concentrations detected; no evidence



suggests that the presence of asbestos bodies or fibers in the lungs



of nonoccupationally exposed persons increases the risk of pulmonary



disease.  Nevertheless, reports of mesotheliomas and pleural lesions



in persons who reside in the vicinity of asbestos industries indicate



that pollution of the environment by asbestos may be a serious human



health hazard.



                        ENVIRONMENTAL ASPECTS



     One potential devastatingly negative result from the industrial



popularity of the "mineral with thousands of uses" is widespread



dissemination in the environment — leading  to the supposition that



asbestos is everywhere.



     Asbestos particulates are released into water, air, and soil, mainly



from industrial  sources — losses during manufacture, transportation,



use, and waste disposal — and are moved readily by wind or water.



Contamination occurs also from nature, processes such as erosion of



asbestos outcrops, farming of asbestos-laden soils, and passage of water



through asbestiform rocks.  Asbestos fibers, easily disseminated by
                                 314

-------
wind and water, are generally regarded as being persistent in the

environment.  Degradation rarely occurs except under extremes of heat,

mechanical stress, or acidity.  However, conditions severe enough to

cause alteration of the mineral  usually are not encountered in the

normal human environment.

     Because of technical difficulties in monitoring concentrations and

distribution of asbestos in the environment — collecting, identifying,

and quantifying fibers in air, water, soil  — data are not available

concerning types, amounts, and sizes of asbestos fibers that contaminate

the environment.  Ambient air concentrations in urban areas are

considerably higher than for nonurban sites.  Contamination of North

American water resources is widespread; asbestos particles have been

detected  in drinking water samples from various cities in Canada and

the United States.  In addition, significant concentrations of asbestos

contaminate beverages, foods, and drugs that are processed through

asbestos filters during manufacture.

                              INFERENCES

     Although the general population is widely exposed to asbestos —

both by inhalation and ingestion — the hazards of chronic, environmental

exposure have not been determined:  reasons conflict but are attributed

in part to a paucity of  information on human dose response, effects of

asbestos  ingestion, ambient concentrations and distribution of asbestos

in the environment, the environmental cycling of asbestos, and related

biological  interactions  including transmission through food chains.

     As distilled from the world's asbestos literature, conclusions

representing a majority opinion are  listed for convenience and ready

reference:
                                  315

-------
•    All  asbestos types are pathogenic  in  animals



    and  humans, causing asbestosis,  lung  cancer,



    mesotheliomas,  and pleural  lesions.



    Due  to the large number of  variables  which



    influence the effects of asbestos,  the  mechanisms



    of pathogenicity are poorly understood.   The



    etiological significance of fiber  size  or type



    is controversial, and the physicochemical



    properties of various asbestos types  as related  to



    biological  effects are incompletely defined.



    Little is known about the clearance rates of



    asbestos  from tissues, the transport  of asbestos



    within the organism, or the metabolic alteration



    of asbestos in  the body.



    Animal models necessary to accurately predict the



    potential  effects of asbestos in  humans have  not



    been developed.



    Quantitative dose-response relationships between



    asbestos  inhalation and related diseases have



    not  been  determined for animals or humans,  and



    minimal exposure levels required  to cause disease



    are  not known.   Generally,  however, the



    greatest  incidence of asbestosis  and  cancer



    among occupationally exposed persons  increases



    with increasing dose and/or duration  of exposure;



    the  inhalation  of high concentrations for short






                         316

-------
durations is as harmful  as prolonged exposure to




low concentrations.



Malignancies arise primarily after long-term



occupational exposure of 20 years or more;




however, they also reportedly result from indirect,



nonoccupationaI  exposure in the vicinity of




asbestos industries.



An adverse causal relationship between gastro-




intestinal  cancer and asbestos ingestion has not




been established unequivocally.  The potential




effects of  ingested asbestos — either directly



into the gastrointestingl tract or indirectly



via lung clearance mechanisms — are only scantily




(often peripherally and speculatively) mentioned



in a limited number of reports.



Pathogenic synergism between asbestos and smoking



as well as environmental pollutants is poorly



defined.  Apparently tobacco smoking increases the



incidence of asbestos is and lung cancer among



asbestos workers.



Available data indicate that asbestos is a  wide-



spread environmental pollutant in air, water, soil,



food, drugs, and beverages.  However, efficient




methods for quantitatively identifying the




concentrations, size distributions, and types of



asbestos fibers  in the environment have not been
                    317

-------
developed adequately with uniform scientific



acceptance.



The human health hazards of chronic environmental



exposure to asbestos are not known.  This is due



to the paucity of information concerning human



dose responses, ambient concentrations and distri-



bution of asbestos in the environment, the



transmission of asbestos through food chains, and



the effects of asbestos ingest ion.



Because any asbestos standard must be based on



accurate knowledge of environmental levels and



related hazards, the available environmental and



biological  data may be insufficient at present to



enable the scientifically based promulgation of



such permanent standards.  Evidence clearly



indicates,  however, that personal health protection



both for asbestos workers and for the general



population — demands more attention for the safe



mining, processing, utilization, and waste disposal



of asbestos as well as establishment of strict



preliminary standards.



Persons working in potentially hazardous dust



areas should have thorough physical examinations



routinely;  new employees should be examined at



the start of employment and periodically thereafter.
                    318

-------
              Asbestos literature to date is confusing.  To
              present dependable, clinical  lung function data of
              asbestos-related disease is difficult; reports
              rarely supply complete data.

                         ACKNOWLEDGEMENTS

     Appreciation is expressed to P.  B.  Hartman, A.  B.  Gill,  and
B. K. Stevens for editorial and  technical assistance in preparation
and production of this paper.
                          "LAWS OF  ECOLOGY"

                The. fiAAt Law 0(J Ecology:
                     EveAythi.ng *A connected to  e.veAytking

                The. Second Law 0(J  Ecology:
                     EveA.ythi.ng muAt go

                The. Tkvid Law o& Ecology:
                     Nature, know
The. fouAth Law o& Ecology:
            no *u.ch tkui  06 a
                                                       lunch.
                                                     BaAAy CommoneA
                                 319

-------
                       SELECTED REFERENCES




1.    Air Pollution Control  Office, 1971.   Asbestos and  Air




      Pollution:   An Annotated Bibliography.   Publication




      AP-82, Office of Technical  Information  and Publications,




      Environmental Protection Agency,  Research Triangle Park,




      North Carolina, 101  pp.



2.    Brobst, D.  A., and W.  P. Pratt (eds.),  1973.   United States




      Mineral Resources, Geological Survey Professional  Paper 820,



      GPO, Washington, D.C., 722 pp.



3.    Brodeur, P., 1972.  Asbestos and  Enzymes, Ballantine Books,



      New York, pp. 1-52.




4.    Bureau of Mines, 1970.  Mineral  Facts and Problems,




      Bulletin 650, GPO, Washington, D.C., 1291 pp.



5.    Bureau of Mines, 1974.  Asbestos.  Preprint from the 1972




      Bureau of Mines Minerals Yearbook,  GPO, Washington, D.C.,



      12 pp.




6.    Dinger, C.  A., B.  L. Whitfield,  A.  S. Mammons, J.  E. Huff,




      1975.  The Environmental Impact  of  Asbestos.   Submitted



      to Solid and Hazardous Waste Research Laboratory/Environmental



      Protection Agency.




7.    Gross, P.,  R. A. Harley, L.  M. Swinburne, J.M.G. Davis, and



      W. B. Greene, 1974.   Ingested Mineral Fibers.  Do They



      Penetrate Tissue or Cause Cancer?  Arch. Environ.  Health,



      29(65:341-347.
                                  320

-------
8.    Hammons, A. S., and J.  E.  Huff,  1975.   Asbestos:   World



      Concern, Involvement, and  Laissez-Faire.   Intern.  J.  Environ.




      Studies (In press).




9.    Huff, J. E., C. A. Dinger, B. W. Kline, B. L. Whitfield, and




      A. S. Hammons, 1974.  A Health View of Asbestos:   An




      Annotated  Literature Collection - 1960-1974.  Environ. Health



      Perspect. £: 341-462.




10.   International Agency for Research on Cancer, 1973.  Asbestos



      Monograph, pp. 17-47.  In:  Evaluation of Carcinogenic Risk




      of Chemicals to Man.  Some Inorganic and OrganometalIic



      Compounds, Vol. 2,  IARC, Lyon, France, 181 pp.



11.   Kenton, C., 1973.  Asbestos Toxicity.   Lit. Search No. 73-31




      National Library of Medicine, Washington, D.C., 22 pp.



12.   Kiviluoto, R., 1965.  Pleural Plaques and Asbestos:




      Further Observations on Endemic and Other Nonoccupational



      Asbestos is.  Ann. N.Y.  Acad.  Sci., 132(1):235-239.



13.   Lanza, A. J. (ed.), 1938.   Silicosis and Asbestosis,



      Oxford University Press, London, 439 pp.



14.   Masson, T.  J., F.  W. McKay,  and R. W.  Miller,  1974.



      Asbestos-Like  Fibers  in Duluth  Water  Supply.   Relation



      to Cancer  Mortality. J. Am.  Med.  Assoc.,  228(8):1019-1020.




 15.   National  Academy  of  Sciences,  1971.   Asbestos.  The Need



      For  and  Feasibility of Air Pollution  Controls.  NAS,




      Washington,  D.C.,  40 pp.
                                  321

-------
16.   National Institute for Environmental  Health Sciences, 1974.




      Proceedings of the Joint NIEHS-EPA conference on



      "Biological Effects of Ingested Asbestos".  Environ.




      Health Perspect. 9.: 113-462.




17.   National Institute for Occupational  Safety and Health, 1972.




      Criteria for a Recommended Standard...Occupational  Exposure



      to Asbestos, HMS 72-10267, GPO, Washington, D.C., 136 pp.




18.   New York Academy of Sciences, 1965.   Biological Effects of




      Asbestos.  Ann. N.Y.  Acad. Sci., 132(1):1-766.



19.   Office of Air and Water Programs, 1973.   Control Techniques




      for Asbestos Air Pollutants.  Publication AP-117, Office




      of Air Quality Planning and Standards,  Environmental




      Protection Agency, Research Traingle Park, North Carolina,



      112 pp.



20.   Pundsack, F. L., 1961.  The Pore Structure of Chrysotile




      Asbestos.  J. Phys. Chem., 65_:30-33.



21.   Ruby, D. L., and R. M. Buchan, 1974.   Critique of the




      Proposed Standard of  the NIOSH Criteria  Document on



      Asbestos.  J. Environ. Health, 37.(2): 165-166.



22.   Schuster, N. H., 1931.  Pulmonary Asbestosis in a Dog.



      J. Pathol.  Bacteriol., 3£:751-757.



23.   Sullivan, R. J., and  Y. C. Athanassiadis, 1969.



      Preliminary Air Pollution Survey of  Asbestos.  A




      Literature Review, Publication APTD-69-27, National




      Air Pollution Control Administration,  Public Health Service,



      Raleigh, North Carolina, 94 pp.
                                 322

-------
24.   Webster, I., 1963.  Asbestosis in Non Experimental  Animals



      in South Africa.  Nature, 197(4866):506.
                                  323

-------