ENVIRONMENTAL
CHEMICALS
HUMAN & ANIMAL HEALTH
3rd Annual Conference
1974
Proceedings
U.S. Environmental Protection Agency
Office of Pesticide Programs
Washington, D.C.
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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
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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
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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
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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
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iv
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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
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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.
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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
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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
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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
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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
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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
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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
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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
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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
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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
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16
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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
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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
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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
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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
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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
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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
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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
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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
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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
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28
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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
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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.
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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.)
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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).
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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
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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 areassterile 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.
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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
annuallyfour 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
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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
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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
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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
formsoffspring 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
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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 presentationthe 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
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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.
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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
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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.
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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 ppma 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.
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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.
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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.
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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
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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
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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
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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
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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
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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
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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
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100
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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
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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
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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
11 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
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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
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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
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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
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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
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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
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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 formssimple 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
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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
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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
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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
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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
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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
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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
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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.
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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.
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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
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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.
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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
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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.
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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
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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.
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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.
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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
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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
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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
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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
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132
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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.
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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
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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
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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
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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
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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
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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
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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
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142
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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 viewfor 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
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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 accesschlorinated dibenzo-p-
dioxins and chlorinated dibenzofurans, asbestos, mercury, cadmium, lead,
and others.
HandbooksFactual 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 describedthrough 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
purposesthe 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,
andin 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
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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
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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
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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
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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
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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
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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
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170
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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
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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
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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
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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
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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
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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
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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
industrycurrent 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
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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
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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.
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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
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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
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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
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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
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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.
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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
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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.
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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
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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.
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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
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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.
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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
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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.
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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
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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
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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).
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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
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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
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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,
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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
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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
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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
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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
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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
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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,
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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.
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15. Munro, I. C., Scott, P. M., Hoodie, C. A. and Willes, R. G. Ochra-
toxin AOccurrence 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.
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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
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210
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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(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
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t '
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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.
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29. Hayes, F. A., Greer, W. E., Shotts, E. B. A Progress Report from
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30. Horvath, D J. Limits for Sewage Recycling. Interface 3(2):18. 1974.
31. Jones, L. Meyer. Veterinary Pharmacology and Therapeutics, 3rd Ed.
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32. Kinsley, A. T. Arsenical Poisoning, Vt. Med. 24:445. 1929.
33. Krocza, W. and Schuh, M. Arsenic Residues in the Carcasses of Slaughter
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34. Ledet, A. E. cited by Buck. Clinical Toxicological, and Pathological
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35. Ledet, A. E., Duncan, A. E., Buck, W. B. and Ramsey, F. K. Clinical
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36." Lenihan, J. M. A. Technology and Humanity. Proceed. First Annual
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37. Lenihan, J. M. A. and Smith, H. Nuclear Activation Techniques in the
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28. Liebig, G. F., Jr. cited by Selby, et al (1974). Arsenic, Chapter 2
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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.
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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.
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46. Moxon, A. L. Alkali Disease or Selenium Poisoning So. Dakota Agri.
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Elements: Preferential Concentration in Respirable Particles. Science
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48. Oliver, W. T. and Rose, C. K. Arsanilic Acid Poisoning in Swine.
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49. Peoples, J. S. Metabolic Fate of Arsenic Acid in Dairy Cows. Fed.
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50. Peoples, J. S. Arsenic Toxicity in Cattle. Annals N.Y. Acad. Sci.
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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-
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of Vegetation, of Missouri, Plans and Progress for the sixth 6-months
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55. Scheidy, S. F., Wilcox, P. W. and Creamer, A. A. Residual Arsenic in
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Hazards Associated with Arsenic Poisoning in Cattle. J.A.V.M.A.
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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
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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
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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.
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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,
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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
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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
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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.
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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
protectionperhaps 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.
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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
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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.
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"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
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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.
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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
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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.
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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256
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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
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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
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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
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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
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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 functionconcentration 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
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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
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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
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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
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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.
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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
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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
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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
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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
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270
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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
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272
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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
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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
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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
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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.Joo*~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
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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
detectedsensitivity 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
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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
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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
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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
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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
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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
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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
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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
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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).
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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
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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).
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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