Document gDMDYg1X4BYVOz3pK63bQ4mj3

URL 04586 FIG. 3.10 CALCASIEU PARISH HAZARDOUS WASTE SITES. SOURCE: Attorney General's Office. 84 URL 04587 FIG. 3.11 EAST BATON ROUGE PARISH HAZARDOUS WASTE SITES. SOURCE: Attorney General's Office. 85 FIG. 3.12 Map 3: ASCENSION PARISH HAZARDOUS WASTE SITES. SOURCE: Attorney General's Office. These surveys have revealed potential problems associated with hazardous waste sites in Louisiana. Unrestricted access to the sites due to inadequate security has allowed cattle grazing, hunting and fishing on sites containing such chemicals as hexachlorobenzene and the carcinogenic polychlorinated biphenyls (PCB's). Degradation of plastic liners and soil levees has allowed site constituents to migrate in surface water. For example, chemicals such as polynuclear aromatic hydrocarbons (certain chemicals in this class are carcinogenic) at the BF1 Darrow site have migrated through the landfill cap and eventually into the Amite River and Lake Maurepas. Analysis of clams from Lake Ponchartrain has indicated the presence of chemicals from this waste site. The extent of chemical migration from this and other sites remains uncertain.**'^ Analyses of all drinking water supplies within three miles of 23 hazardous waste site hi Louisiana was performed in 1982 by the Department of Health and Human Resources, Office of Health Services and Environmental Quality. Examination of 79 different wells ranging from 20 feet to 2300 feet in depth identified no contamination due to migration from any of the waate sites monitored. Increased ground water analyses are performed statewide to assess possible contaminations. 27 The health hazards associated with hazardous waste sites remain of great concern, yet are unclear. Major episodes of chemical migration from waste sites containing known carcinogens across the nation (Love Canal, New York; Toone Chemical Dump, Tennessee; Rollins LogaOnff Township Facility, New Jersey) initially suggested extensive public health crises. Recent evidence indicates that relation ships between chemical migration and disease are not firmly established.^* It should be emphasized that recent conclusions do not support lack of public health hazards but the uncertainty of effects. More well-defined studies are required. The Gulf Coast is a transportation route from Texas and Louisiana to the Eastern United States. Of special importance is the Huey P. Long Bridge in New Orleans because it is the only major rail crossing over the Mississippi River south of Memphis, Tennessee. Therefore, for a great percentage of toxic chemicals produced in the South this bridge is a vital link over the Mississippi River between the Eastern and Western United States. In addition to truck traffic on Louisiana highways, railroad car passage and rail car storage pose significant sources for water pollution not yet IQ ffff fully appreciated. 0,03 The ability to adequately respond to chemical emergencies resulting from transportation accidents on highways, the rail system or waterways remains a %fin-ancial and workforce challenge.65 '66 87 URL 04590 References - THE COMMUNITY ENVIRONMENT 1. Guthrie FE, Perry JJ Eds. Introduction to Environmental Toxicology. New York, New York: Elsevier Press, New York, 1980. 2. DouII J, Klaassen CD, Amdur MO Eds. Toxicology, The Basic Science of Poisons. New York, New York: MacMillan Publishing Co, 1980. 3. Kraybill HF. Global distribution of carcinogenic pollutants in water. Annals of New York Academy of Science 298:80-89, 1977. 4. Smith P, Heath D, Paraquat. CRC Critical Reviews in Toxicology: p, 411-445, October, 1976. 5. Environmental Protection Agency (EPA). Industrial pollution of the lower Mississippi River in Louisiana. EPA, Dallas, Texas, 1972. 6. Environmental Protection Agency (EPA). Draft analytical report: New Orleans area water supply study. EPA, Cincinnati, Ohio, 1974. 7. Environmental Protection Agency (EPA).*yPreliminary assessment of suspected carcinogens in drinking water. Report to Congress. EPA, Washington, D.C., 1975. 8. DeRouen TA, Diem JE. Relationships between cancer mortality in Louisiana drinking-water sources and other possible causative agents. In: H Hiatt, J W -tson and J Winsten Eds. Origins of Human Cancer Cold Spring Harbor Laboratory, 1977. 9. Page T, Harris RH, Epstein S. Drinking water and cancer in Louisiana. Science 193:55-57, 1976. 10. Wilkins JR, Reiches NA, Kruse CW. Organic chemical contaminants in drinking water and cancer. American Journal of Epidemiology 110:420-448, 1979. 11. Marx JL Drinking water: Another source of carcinogens? Science 186:809-811, 1974. 12. Kraybill HF. Carcinogenesis induced by trace contaminants in potable water. In: Berchardt et al. Eds Virus and Trace Contaminants in Water and Waste Water, Ann Arbor, Michigan: Ann Arbor Science Pub., 1977. 13. Harris RH, Page T, Reiches NA. Carcinogenic hazards of organic chemicals in drinking water. In: H Hiatt, J Watson, J Winsten, Eds. Origins of Human Cancer. Cold Spring Harbor Laboratory, 1977. 14. Gottlieb MS, Carr JK, Clarkson JR. Drinking water and cancer in Louisiana. American Journal of Epidemiology 116:652-667, 1982. 15. Gottlieb MS, Carr JK, Morris DT. Cancfer and drinking in Louisiana: Colon and rectum. International Journal of Epidemiology 10:117-125, 1981. 88 URL 04591 16. Gottlieb MS, Carr JK. Case-control cancer mortality study and chlorination of drinking water in Louisiana. Environmental Health Perspectives. 48:169-177, 1982. 17. Hyman ES. The drinking water-cancer-carbon filtration problem. The Journal of the Louisiana State Medical Society. 131:11-32, 1979. 18. O'Neill M. Presentation to the Governor's Task Force on Environmental Health. Baton Rouge, LA. June 30, 1983. 19. Peaeocke S. Lake Providence toxic waste over limit. News-Star-World, August 30, 1983. 20. Parker V. Presentation to the Governor's Task Force on Environmental Health. Baton Rouge, LA., May 16, 1983. 21. Westrick JJ, Mello JW, Thomas RF. The Groundwater Supply Survey. Summary of Volatile Organic Contaminants Occurrence Data. Environmental Protection Agency, Cincinnati, Ohio, 1983. 22. Parker V. Presentation to the Governor'SvTask Force on Environmental Health. Baton Rouge, LA., May 16, 1983. 23. Parker V. Presentation to the Governor's Task Force on Environmental Health. * Baton Rouge, LA., May 16, 1983. 24. Knudson MO. Presentation to the Governor's Task Force on Environmental Health. Baton Rouge, LA. May 16, 1983. 25. Givens D. Presentation to the Governor's Task Force on Environmental Health. Baton Rouge, LA. May 16, 1983. 26. Keith LH, Telliard WA. Priority Pollutants: A Perspective View. Environmental Science and Technology. 13:416-423, 1979. 27. Parker V. Presentation to the Governor's Task Force on Environmental Health. Baton Rouge, LA., May 16, 1983. 28. Theis AR. Presentation to the Governor's Task Force on Environmental Health. Baton Rouge, LA., May 16, 1983. 29. Knochenmus D. Presentation to the Governor's Task Force on Environmental Health. Baton Rouge, LA., May 16, 1983. 30. Davis A. Presentation to the Governor's Task Force on Environmental Health. Baton Rouge, LA., April 27, 1983. 31. VonBodungen _G. Presentation to the Governor's Task Force on Environmental Health, April 27, 1983. 32. Environmental Protection Agency (EPA). Analysis of Organic- Air Pollutants by Gas Chromatography and Mass Spectroscopy^ Environmental Research Laboratory, Research Triangle Park, North Carolina, 1979. 89 URL 04592 33. Sheppard JB, Cancer in Louisiana. Louisiana State House of Representatives Commerce Committee, 1979. * 34. Office of Technology Assessment, United States Congress. Technologies and Management Strategies for Hazardous Waste Control: Summary. Washington, D.C., 1983. 35. Pojasek RB. Disposing of hazardous chemical wastes. Environmental Science and Technology 13:810-814, 1979. 36. Schwarzer CG. Recycling hazardous wastes. Environmental Science and Technology 13:166-171, 1979. 37. Healy GD. Presentation to the Governor's Task Force on Environmental Health. Baton Rouge, LA., June 30, 1983. 38. Fontenot W. Presentation to the Governor's Task Force on Environmental Health. Baton Rouge, LA., June 30, 1983. 39. Magnuson W. The poisoning of America. Time 116:58-71, 1980. 40. Laseter J. Presentation to the Governor's Task Force on Environmental Health. July 14, 1983. ^ 41. Thomas L (Chairman). Report of the Governor's Panel to Review Scientific Studies and the Develoment of Public Policy on Problems Resulting from Hazardous Wastes. New York, 1980. 42. Eckholm E. Unhealthy Jobs. Environment 19:29-38, 1977. 43. Anderson K and Scott R. Fundamentals of Industrial Toxicology. Ann Arbor, MI.: Ann Arbor Science Publishers, 1981. 44. Lehmann P. Occupational Cancer. Job Safety and Health, 3. United States Department of Labor, Occupational Safety and Health Administration, 1975. 45. Gottlieb MS, Stedman RB. Lung cancer in shipbuilding and related industries in Louisiana. Southern Medical Journal 72:1099-1101, 1979. 46. Rothschild H, Mulvey JJ. An increased risk for lung cancer mortality associated with sugarcane farming: Journal of National Cancer Institute 68:755-760, 1982. 47. Gottlieb MS, Pickle L, Blot WJ, Fraumeni JF. Lung cancer in Louisiana: Death certificate analysis. Journal of National Cancer Institute 63:1131-1137, 1979. 48. Gottlieb MS. Lung cancer and the petroleum industry in Louisiana. Journal of Occupational Medicine 22:384-388, 1980. 49. Pickle LW, Gottlieb MS. Pancreatic Cancer Mortality in Louisiana. American Journal of Public Health 70:256-259, 1980. 50. Gottlieb MS, Pickle LW. Bladder cancer mortality in Louisiana. The Journal of the Louisiana State Medical Society. 133:6-9, 1981. 90 51. Louisiana Department of Natural Resources. Louisiana Petrochemical Industry Assessment. 1983. 52. United States Department of Health and Human Services. Second Annual Report on Carcinogens. 1981. 53. Finkel JJ. Industrial Toxicology (9th ed.). Boston, Mass.: John Wright PSG Inc., 1983. 54. IARC Monograph on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Supplement I. IARC, Lyon, France, 1979. 55. Maltoni C, Scarnate C. First experimental demonstration of the carcinogenic effects of benzene. Med. Lavoro. 70:352-357, 1979. 56. Ott MG, Townsend JC, Fishbeck WA, Langner RA. Mortality among individuals occupationally exposed to benzene. Archives of Environmental Health. 33:3-10, 1978. 57. Aksov M, Erdems S, Dincol G. Leukemia in Shoe Workers exposed chronically to benzene. Blood. 44:837-841, 1974. "V 58. Occupational Safety and Health Administration. Exposure to coke oven emissions. Federal Register 41 206:46472-46790, 1976. 59. National Cancer Institute. Bioassay of 1,2-Dichlorethane for Possible Careinogenicity. Technical Report Series No. 55, DH^W Publication No. (NIH) 78-1361. Washington, D.C. Department of Health, Education and Welfare, 1978. 60. Swenberg JA, Kerns WD, Mitchell RI, Gralla EJ, Pavkov KL. Induction of squamous cell carcinoma of the rat nasal cavity by inhalation exposure to formaldehyde vapor. Cancer Research 40:3398-3401, 1980. 61. Alexander, V. Presentation to the Governor's Task Force on Environmental Health. Baton Rouge, LA., July 14, 1983. 62. Tri-State Delta Chemical, Inc. 1983 Agricultural Chemical Label Book. 63. Bagent J. Louisiana State University Extension Service. Communication, September 1983. Personal 64. Sanders D. Louisiana State University Extension Service. Communication, September 1983. Personal URL 04593 I 91 URL 04594 V IV. THE OCCUPATIONAL ENVIRONMENT THE NATURE OF OCCUPATIONAL EXPOSURES Work-related illness has been recognized since early Greek and Roman writings associated diseases peculiar to certain professions. The Italian physician, Bernardino Ramazzini, in his classical 1700 text, Diseases of Workers, first emphasized the importance of knowing one's occupation to complete a medical history. 1 The nature of chemical exposures in the workplace presents unique risks to the worker. The worker population is often limited and predictable. Normally, workers are between 18 and 65 years of age and in reasonably good health, unlike the spectrum of the general population. Conditions experienced by workers including job duties, temperature fluctuations, humidity, vibration and noise may all affect their responses to chemicals with which they work. For example, a worker exposed to an airborne toxicant while he/she is breathing heavily due to strenuous duties will probably inhale a larger dose than a co-worker not exerting as much effort. Additionally, workers are usually exposed to more than one chemical in the course of their employment. Few industrial operations generate just one toxicant. This often confounds the ability to discern appropriate biological effects of chemical exposures. Worker exposure to low concentrations of toxicants generally occurs over an entire work day for prolonged periods. This constitutes a chronic exposure. This differs from acute chemical exposures that can occur to the general population from a single high concentration of a toxicant. (See Table IV-1.) 92 > URL 04595 TABLE IV-1 OCCUPATIONAL CANCERS ORGANIC AGENTS Aromatic hydrocarbons Coal soot, coal tar, other products of coal combustion Petroleum, petroleum coke, wax, creosote, anthracene, paraffin, shale, mineral oils Benzene Aur&mine, benzidine, 1-naphthylamine 2-rtaphthylamine, magenta, 4-aminobiphenyl, 4-nitrobiphenyl Others Mustard gas Isopropyl oil Vinyl chloride Bis (chloromethyl) ether, chloromethyl methyl ether INORGANIC AGENTS (Metals) Arsenic compounds Cadmium Pagination Site of Cancer Manufacturers of coal gas; coal tar, and pitch workers; coke-oven workers; miners (uranium, fluorspar, hematite); still cleaners; chimney sweeps Lubricating, cooling, or fuel oil workers; coke, paraffin, wax, rubber and retort workers; textile weavers; diesel let testers Workers wiftt chemicals, glues, varnishes, explosives, rubber cement; distillers, dye workers, painters, and shoe workers Manufacture and use of dyestuffs; rubber workers, textile dyers, paint manufacturers Poison gas makers Isopropylene manufacturers PVC manufacturers, plastics workers Makers of ion-exchange resins, chemical workers Lung, larynx, skin, scrotum, bladder Nasal cavity, lung, larynx, skin, scrotum Bone marrow, leukemia Bladder Larynx, lung, trachea, bronchi Nasal sinuses Liver (angiosarcoma), brain Lung Gold miners, smelter workers; some vineyard workers; sheep dip manufacturers, tanners; insecticide makers and sprayers, chemical workers Cadmium-using industries Skin, lung, liver Prostate, bronchus TABLE IV-1 continued on next page 93 TABLE rV-1 (continued) OCCUPATIONAL CANCERS Iron oxide Agent Nickel PHYSICAL AGENTS ionizing radiation X-rays Uranium, radon, radium mesothorium Non-ionizing radiation Ultraviolet rays Fibers Asbestos Dusts Wood Leather Others Hypoxia Occupation Hematite miners, metal grinders and polishers, silver finishers, iron foundry workers Nickel refiners, electrolysis workers Site of Cancer Lung, larynx Nasal sinuses, lung Radiologists, medical personnel Radiologists, radiographers, miners of uranffl'm, fluor spar, and hematite; radium dial painters; radium chemists Farmers, sailors Miners, millers, textile insulation, and shipyard workers Wood workers Leather and shoe workers Caisson workers Skin, bone marrow (leukemia) Skin, bone, lung, bone marrow (leukemia) Skin Lung, pleural and peritoneal meso thelioma Nasal cavity and sinuses Nasal cavity and sinuses, bladder Bone 96Sf>0 Itin SOURCE: Adapted from Doll R. Introduction. In: Hiatt H H, et al., eds. Origins of Human Cancer. Cold Spring Harbor Conferences on Cell Prolifera tion. Vol. 4, Cold Spring Harbor, NY: Cold Spring Harbor Laboratory, 1977, p. 3, Table 4} Tomatfs-L, et al., Evaluation of tlte Carcinogencity of Chemicals: A Review of the Monograph Program of the International Agency for Research on Cancer (1971 to 1977), Cancer Research, 38:877-885, 1978, pp. 879, 880, Table 2; Cole P, Goldman M B, Occupation. In: Fraumeni J F Jr, ed. Persons at High Risk of Cancer. New York: Academic Press, 1975, pp. 172-176, Table 1. 94 URL 04597 Understanding occupational cancers poses unique difficulties. Due to the latent nature of the disease, worker exposure to a chemical carcinogen may not result in the occurrence of the disease until many years later (10-30 years) and often a multitude of other chemical exposures. Well known associations of chemical carcinogens with human cancers arising from the workplace include lung cancer in uranium miners, lung and lymphatic cancer in copper smelter workers, bladder cancer in dyeworkers and lung cancer in asbestos workers. Table IV-2 lists the chemical carcinogens produced in Louisiana. TABLE IV-2 CHEMICAL CARCINOGENS PRODUCED BY LOUISIANA INDUSTRY Acrylonitrile Benaene Carbon Black Coke Oven Emissions Carbon Tetrachloride Chloroform Ethylene Dichloride Ethylene Oxide Formaldehyde Trichloroethylene Vinyl Chloride Asbestos* * SOURCE: U.S. Department of Health and Human Services. Second Annual Report on Carcinogens. 1981. * Not produced, but significantly present in Louisiana Industry 95 URL 04598 INDUSTRIAL EXPOSURE TO CARCINOGENS IN LOUISIANA Some occupations in Louisiana have been associated with increased risks of certain cancers. Increased risks of lung cancer have been correlated with shipbuilding, sugarcane farming, mining, agriculture and those employed in the petroleum industry, such as welders, oilfield workers, operators, boilermakers and painters.^* Increased risk of pancreatic cancer has been associated with oil refining, paper Q milling, utilities work and agriculture. Increased riskQ of bladder cancer has been associated with workers in oil refineries and sawmills. Though definite cause and effect is difficult to establish in these cases, the information provides a framework for further study to isolate specific chemicals and characterize potential for carcinogenesis. Louisiana industry produces significant quantities of chemical carcinogens (16% of total state chemical production volume).* Appropriate control of workplace atmospheres and chemical disposal is essential to properly regulate human exposure to these chemical carcinogens. ^ Tables IV-3 and IV-4 rank the carcinogens described in the following pages according to volume and value, respectively, in comparison with other Louisiana TABLE IV-3 PRODUCT RANKING BY VOLUME Rank (out of 98) 6 8 14 17 28 45 47 48 56 67 Chemical Ethylene dichloride Vinyl chloride Benzene Ethylene oxide Carbon black Acrylonitrile Formaldehyde Trichloroethylene Carbon tetrachloride Chloroform % of total 6.2 4.1 2.0 1.8 0.7 0.2 0.2 0.2 0.1 0.1 15.6% SOURCE: Abstracted from Louisiana Department of Natural Resources data.* NOTE: Chemicals are ranked by total known state capacity. 96 TABLE IY-4 PRODUCT RANKING BY VALUE TO LOUISIANA INDUSTRY Rank (out of 98) 4 6 7 15 24 30 42 57 68 72 Chemical Vinyl chloride Ethylene dichloride Ethylene oxide Benzene Carbon black Formaldehyde Acrylonitrile Trichloroethylene Chloroform Carbon tetrachloride % of total 5.0 4.9 4.5 2.2 1.2 0.9 0.5 0.3 0.2 0.2 19.9% SOURCE: Abstracted from Louisiana-epartment of Natural Resources data. , NOTE: Chemicals are ranked based on total state capacity and list price as published by the Chemical Marketing Reporter. products. It can be seen that these carcinogens represent a significant portion of Louisiana industry. It is essential that industry provide effective worker protection for individuals associated in the manufacture and use of these chemical carcinogens. Workplace monitoring for these carcinogens can assure compliance with stan dards set for these chemicals by the Occupational Health and Safety Administration (OSHA), listed on Table IV-5.11 Though several of the standards established are for toxicity other than for cancer, industry can strive for the lowest possible level of exposure to these chemicals. Additionally, employers should provide proper instruction for careful handling of carcinogenic products and make protective clothing available. Eleven chemicals of Louisiana's ninety-eight major chemical products are recognized as carcinogens by the National Toxicology Program under the United States Department of Health and Human Services (Table IV-2).** These chemicals are not only generated as products but may be used as intermediates in other synthetic processes^ URL 04599 97 TABLE IV-5 OSHA STANDARDS POR WORKPLACE CARCINOGENS Chemical 8-hr Threshold Limit Value Ceiling Concentration Acrylonitrile Benzene Carbon black Coke Oven Emissions Carbon tetrachloride Chloroform Ethylene dichloride Ethylene oxide Formaldehyde Trichloroethylene Vinyl Chloride Asbestos 2 ppm 10 10 ppm 25 0.7 ppm 0.02 0.03 ppm -- 10.0 ppm 25 -- 50 50.0 ppm 100 50.0 ppm -- 3.0 ppm 5 100.0 ppm 200 1.0 ppm 5 2 fibers greater than 5 um/ml air ppm ppm ppm PAH* ppm ppm ppm ppm ppm ppm SOURCE: U.S. Department of Health and Human Services. Second Annual Report on Carcinogens. 1981. NOTE: Standards may be based on toxicity other than for cancer * Polycyclic aromatic hydrocarbons c*A <3. %s Knowledge of the sources, uses and specific cancers associated with these chemicals can enhance the understanding of the health risks to Louisiana workers. Therefore, a brief description is provided of these chemical carcinogens produced by Louisiana industry. Acrylonitrile Acrylonitrile is used for the manufacture of synthetic fibers, resins, plasties and rubber for such' consumer goods as textiles, dinnerware, food containers, toys, luggage, automotive parts, small appliances and telephones. Primary human exposure occurs during manufacture and production. Since the chemical is volatile, exposure 98 uwt-o itin occurs primarily by inhalation of vapors or skin absorption. Significant occupations associated with acrylonitrile exposure are acrylic resin makers, organic chemical synthesizers, pesticide workers, and makers of rubber, synthetic fiber and textile products. Direct consumer exposure to acrylonitrile through consumer products is low due to minimal migration of acrylonitrile from the product. 11*12 Acrylonitrile can produce cancer of the brain and stomach in laboratory animals. Significant increases in the rate of human lung and colon cancers have been associated with acrylonitrile workers, 13 although ongoing research indicates that only for lung cancer may the association be statistically significant. Acrylonitrile is produced in Louisiana by American Cyanamid Co., Westwego, and Nalco Chemical Co., Garyville.10 Benzene Benzene is a major raw material of thevchemical industry. Benzene is used as a solvent in chemical processes; as a starting material and intermediate in a variety of synthetic procedures. Benzene is used as an intermediate chemical in the production of nitrobenzene, phenol, detergent alkylate and a wide range of other chemicals. The manufacture of tires accounts for a significant quantity of the benzene used. It is also used as an octane booster in gasoline. Nylons, certain pesticides, adhesives, laminates, coatings, inks, paints, paint strippers, and varnishes are all end-products which use benzene in their production. General public exposure to benzene occurs primarily from gasoline and benzene-containing consumer products.25 Worker exposure occurs in petroleum and petrochemical refineries, chemical plants (in particular those that produce rubber products and solvents), and the steel industry. Printing press operators, lithographers, shoemakers, gasoline pump attendants, and professional artists and craftsmen are also an exposed group of workers.25 Workers may be exposed to benzene either during production processes or during use of substances containing benzene. Human exposure to benzene is primarily through inhalation of the vapors or by skin absorption. * In laboratory animals benzene produces leukemia, mammary gland and zymb&l (rodent) gland carcinomas.14 Increased acute non-lymphocytic leukemia has been associated with human exposure to benzene.1 5*1A Benzene is produced in Louisiana by American Hoechst, Baton Rouge; Cities Service Co., Sulphur; Dow Chemical, Plaquemine; Exxon Chemical Co., Baton Rouge; Gulf Oil Chemicals Co., Alliance; Pennzoil Co., Shreveport; Tenneco Inc., Chalmette; and Union Carbide Corp., Taft. 99 URL 04602 Carbon Black Carbon black consists of elemental carbon in the form of near spherical colloidal particles and is obtained by partial combustion or thermal decomposition of liquid or gaseous hydrocarbons. Carbon black may contain traces of sulfur ash and 0.11.5% polycyclic aromatic hydrocarbons including benzopyrene. These components increase the carcinogenic potential of carbon black. Only when carbon black is contaminated with certain polycyclic aromatic hydrocarbons are carcinogenic properties found. Carbon black is used for deodorizing, filtering, pigment for rubber tires, printing, stencilling and drawing inks, leather goods, stove polish, phonograph records, and electrical insulating apparatus. Activated charcoal, a product from carbon black processing, has been used in medicine for antidotal purposes. Epidemiological studies in North America have revealed no significant occurrence of malignancies in carbon black workers1^2 Carbon black is produced in Louisiana by Ashland Chemical Co., Shreveport; Cabot Corp., Franklin and Lottie; Columbian Chemicals Co., Sulphur and Lake Charles; Sid Richardson Carbon Co., Addis.10 Coke Oven Emissions Coke oven emissions are complex mixtures of coal and coke particles (nonvol atile coal residues), vapors, gases and tars that include potentially carcinogenic polycyclic aromatic hydrocarbons. Most of the coke produced in the United States is used in the extraction of metals from their ores. As a raw material, coke is used in the synthesis of calcium carbide and in the manufacture of graphite and electrodes.11 Oven-charging operations and leakage around poorly sealed coke oven doors are major sources of exposure to workers. Coke oven workers have an increased risk of lung and urinary tract cancers. Studies in animal and human populations also suggest that skin tumors may be associated with coke oven emissions. 17 Calcined petroleum coke is produced in Louisiana by Kaiser Aluminum and Chemical Corp., Lottie; and Reynolds Metals Co., Baton Rouge.10 100 Carbon Tetrachloride Carbon tetrachloride is a volatile liquid used for the manufacture of fluorocarbons and useful in industrial degreasing operations as a general solvent and grain fumigant. Human exposure can occur by inhalation of vapors or by skin absorption. Carbon tetrachloride is carcinogenic in mice and rats, primarily causing liver tumors. Several cases of liver tumors in humans have been associated with worker exposure to carbon tetrachloride. Carbon tetrachloride is produced in Louisiana by Dow Chemical Co., Plaquemine; and Vulcan Materials Co., Geismar.L Chloroform Chloroform, a highly volatile liquid, is used primarily as an intermediate in the manufacture of fluorocarbons, dyes, drugs and pesticides; as a solvent in the extraction and purification of antibiotics,'Titamins and flavors; as an industrial solvent in photography and dry cleaning. Chloroform produces hepatomas and hepatocellular carcinomas in mice, malignant kidney tumors in male rats and thyroid tumors in female rats.*"* Chloroform is produced in Louisiana by Dow Chemical Co., Plaquemine; and Vulcan Materials Co., Geismar. URL 04603 Ethylene Dichloride (1.2-Dichloroethane) Ethylene dichloride is used as a solvent intermediate in the production of vinyl chloride, chlorinated solvents, and ethylene amines; as a component of leaded fuel, insect fumigant, solvent, upholstery cleaner, and metal degreaser; and as an extractant in certain food processes.11*12 Human exposures can occur through skin absorption, inhalation or ingestion. Workers may be exposed in chemical manufacturing and processing industries. Ethlylene dichloride has produced in laboratory animals benign and malignant lung tumors, malignant lymphomas, hepatocellular carcinomas, uterine adenocarcinomas, stomach carcinomas, benign and malignant mammary tumors and hemangiosarcomas. 18 Ethylene dichloride is produced in Louisiana by Borden Chemical, Geismar; Conoco Chemicals Co., Lake Charles; Convent Chemical Corp., Convent; Formosa Plastics Co., Baton Rouge; Georgia Pacific Corp., Plaquemine; PPG Industries, Lake Charles; Shell Oil/Chemical Co., Norco; Union Carbide Corp., Taft; and Vulcan Materials Co., Geismar.* 101 URL 04604 Ethylene Oxide Ethylene oxide is an effective and widely used sterilant for drugs and medical supplies. The chemical is used as an intermediate in the production of ethylene glycol and surface active agents. Ethylene oxide mutagenicity has been demonstrated in several plant and invertebrate systems as well as mammalian germinal cells. Increased cases of leukemia, and gastrointestinal and urogenital tract malignancy have been reported in workers exposed to ethylene oxide gas. 12 Forty percent of total American capacity for ethylene oxide production is located in Louisiana. Ethylene oxide is produced by BASF Wyandotte, Geismar; Calcasieu Chemical Corp., Lake Charles; Dow Chemical Co., Plaquemine; Shell Chemical Co., Geismar; Union Carbide Co., Taft.10 Formaldehyde Formaldehyde is a high volume chemical used for the production of phenolic, urea, melamine and acetal resins with wide usage in the construction (insulation), automotive and appliance industries. Formaldehyde has also been used in textiles, embalming fluids, fungicides, bactericides, and cosmetics.11 Human exposure to formaldehyde is primarily through inhalation and skin absorption. Inhalation of formaldehyde has resulted in nasal carcinomas in laboratory animals.19 Formaldehyde is produced in Louisiana by the Borden Chemical Co., Geismar.10 Trichloroethylene Trichloroethylene is used in large quantities as a metal degreaser and dry cleaning agent. Minor quantities have been used for extraction of fats from fish meal and caffeine from coffee. Also, the chemical is used in the manufacture of adhesives, industrial paints and dewaxing of lubricating oils. 12 Trichloroethylene is readily absorbed in the lungs and gastrointestinal tract of humans. In experimental animals trichloroethylene has produced significant increases in hepatocellular carcinomas after long term feeding. 12 Trichloroethylene is produced in Louisiana by Ethyl Corp., Baton Rouge; and PPG Industries, Lake Charles.10 102 URL 04605 Vinyl Chloride Vinyl chloride is primarily used in the production of plastics. Vinyl chloride is a chemical composed of a single molecule (monomer) and can be formed into plastic by the polymerization of vinyl chloride (VC) to polyvinyl chloride (PVC). PVC is used to make phonograph records, wire and cable insulation, floor coverings, garden hoses, furniture, upholstery fabrics, automobile bodies, containers, bottles, and plastic food wrappings. Human exposure primarily occurs through inhalation, though skin absorption can occur.11 Vinyl chloride has produced cancer in animals and humans. Target organs include the liver, brain, lung and hemo-lymphopoietic system. 13 Vinyl chloride is produced in Louisiana by Borden Chemical Co., Geismar; Conoco Chemicals Co., Lake Charles; Dow Chemical Co., Plaquemine; Ethyl Corp., Baton Rouge; Formosa Plastics Co., Baton Rouge; Georgia Pacific Corp., Plaquemine; W. R, Grace and Co., Lake Charles; PPG Industries, Lake Charles; and Shell Oil/Chemicals Co., Norco.10 "V Asbestos Asbestos, a potent carcinogen, is a general term used to describe a group of silicate minerals that have common properties. These minerals are fibrous and possess electrical and thermal insulating properties as well as flexibility which allows the fibers to be woven into fabric. Other than the mining and milling of asbestos, exposures to asbestos are found during industrial uses in construction (cement products, floor tiles, paper products, insulation, paint, caulking), textiles, plastics and transportation (brake linings). Approximately 8896 of asbestos use is in the construction industry. More than 5,000 products contain asbestos though production is expected to decline in the 1980s.11*1^ Significant human exposure may occur through inhalation or ingestion and can result in one of several types of cancer. Such cancers include gastrointestinal and respiratory (bronchiogenic carcinoma, mesothelioma) cancers. 13 The risks associated with developing cancer from asbestos exposure apparently depend upon relationships between asbestos' air concentration and the duration of worker exposure. Intense workplace exposure for a period as short as 30 days may be associated with an elevated risk of asbestos-related disease 30-40 years later. However, mesothelioma may occur w- hen lower levels of asbestos exposure occur over long periods of time.20 103 URL 04606 Essentially all workers who handle asbestos products or those in the vicinity of workers who handle asbestos products have elevated risks. This may even include family members of asbestos workers, due to asbestos-contaminated clothing which may be brought into the home. Asbestos fibers do not degrade in the environment or settle out for collection purposes. These risks are especially relevant to the chemical, shipbuilding and construc tion industries common to Louisiana which have used asbestos-containing materials. Due to the latency of asbestos-related cancers, the impact of asbestos in these industries may not be fully evident until the year 2000 and the problem will not end unless asbestos use is terminated. Though asbestos is not presently used in the shipbuilding industry (in which approximately 300,000 Louisiana citizens have been involved over 30 years), repair operations of old ships may still pose occupational hazards unless protective measures are taken. The renovation of older buildings can also represent a hazardous exposure to asbestos. Additionally, as a result of past asbestos use in industry (specifically in construction and vehicle brake linings), asbestos is found in the air, water and soil; however, the health risks of this non-occupational exposure are unclear.24 Asbestos is regulated as a hazardous pollutant by the Environmental Protection Agency. AGRICULTURAL EXPOSURES TO CARCINOGENS IN LOUISIANA Known carcinogenic pesticides are not currently produced by major Louisiana industry;21 however, the potential hazard to pesticide formulators and applicators has been traditionally significant. Organochlorine insecticides such as DDT, Chlordane, Aldrin, Dieldrin, Heptachlor, Toxaphene, Mirex, Kepone and Lindane were heavily used in past agricultural practices. Due to their chemical persistence, these pesticides still pose a problem of environmental contamination. Due to evidence of carcinogenicity for the majority of these chemicals, they are currently used only in minor amounts for insect control with livestock, domestic housing and pecan farming. In these cases, extreme caution should be exercised to protect workers. The major commodities in Louisiana (cotton, soybeans, sugarcane and rice) are currently protected against insects by applications of pyrethroid, organophosphate or carbamate insecticides. These specific agents used have yet to be proven carcinogenic.22 (See Figure 4.1.) 104 No herbicides currently used in Louisiana on soybeans, cotton, rice and sugarcane have yet been proven carcinogenic. Concern has been prevalent, however, regarding the use of 2,4,5-Trichlorophenoxyacetic acid (2,4,5-T) which may contain trace levels of thetesatogen dioxin (TCDD), an indicted carcinogen. The toxicological properties of 2,4,5-T and dioxin are still under investigation. In order to control water hyacinth which heavily infests certain areas of Louisiana's wetlands, herbicide spraying of infested areas began in Louisiana in 1949 and continues today. The herbicide used in the water hyacinth control program is dimethylamine salt formulation of 2,4-Dichloraphenoxyacetic acid (2,4-D).., One gallon (four pound acid equivalent) per 200 gallons of water is sprayed for each acre of water hyacinth, and the spraying is performed by the U.S. Army Corps of Engineers and the Louisiana Department of Wildlife and Fisheries. The application rate of four pounds/acre will cause levels of 2,4-D in waters upward of 155 ppb., a level which surpasses both proposed and old federal water quality criteria limits for 2,4-D. Upper A/* portions of Bayou Lafourche are sprayed near community water sources. The California Department of Health Services in 1980 issued a Hazard Alert for the herbicide 2,4-D and recommended that because "the scientific data are sufficiently suggestive of a carcinogenic effect and demonstrate a weak teratogenic effect, that 2,4-D use should be restricted to areas in which human exposure can be kept to a minimum. Contamination of open water must be monitored and prevented. Broadcast methods of application that could directly expose the general population should be strongly discouraged. Greater consideration must be given to alternative methods for removing unwanted plants." 27 ADVANCES IN DETECTION TECHNOLOGY Few substances in nature are truly pure. Water in a stream, for example, will contain: chemicals such as nitrogen and phosphorus; metals such as zinc, manganese, and iron; and natural chemical substances such as the organic humic and fulvic acids. The air contains particles and aerosols required as nuclei for cloud formation. These perpetuate the cycle of thunderstorms complete with rain and lightning, which produces available nitrogen for plants. Many of these substances are regarded as pollutants if they are found in concentrations above the level found in the natural systems. For example, nitrogen and phosphorus in rivers and streams are necessary for aquatic plant growth, which in turn is the basis of the aquatic food chain. The aquatic food chain ends with oysters, shrimp, fish and other species important for human URL 04607 105 URL 04608 -AGRICULTURAL REGIONS predominant crop listed first Truck Forms t Dairy, Beef, Woodland 52 Beef and Woods or Marsh IS Rice, Beef 111 Sugarcane D Cotton, Soybeans Soybeans, Cotton PESTICIDE USE IN LOUISIANA O Parish with less than 500 ocres in crops 0 5000 to 100,000 lbs. ffiD 101,000 to 300,000 lbs. 301.000 to 600,000 lbs. 601.000 to 1,000,000 lbs. ,000,000 plus lbs. FIG. 4.1 AGRICULTURAL REGIONS AND PESTICIDE USE IN LOUISIANA SOURCE: Agricultural regions: Newton B Je. Atlas of Louisiana: a Guide for Students. Baton-Rouge, La.t Louisiana State University School of Geoscience, p. 114. 1972, Pesticides: Pesticide Use Patterns on Major Crops in Louisiana. Louisiana Department of Agriculture. 1979, map compiled by S. Watkins. 106 URL 04609 consumption. If the chemical nutrients are introduced in relatively high levels then serious water quality problems can result, leading to eutrophication with ensuing bluegreen algal blooms, low oxygen levels, and fish kills. Some metals such as iron, copper, and zinc are essential to life in trace amounts; other metals are toxic and hazardous to life even at trace levels (mercury, cadmium, arsenic, lead, silver, and nickel for example). There also exist other persistent substances (PCB's, halogenated hydrocarbons and many pesticides) which are hazardous when they are introduced into the environment, although the range of toxic potency for these various chemicals can be very large. The magnitude of environmental contamination is generally expressed in terms of parts per million (ppm), parts per billion (ppb), and in some instances, parts per trillion (ppt). Known carcinogenic chemicals have potencies which range from a millionth of a gram to as much as ten grams. The order of magnitude of concentration of a chemical for which a health professional need be concerned varies with each chemical and also with the species or form in which that chemical is found. For example, elemental selenium is not toxic, whereas its hydride, oxide, or salts are extremely toxic and potentially carcinogenic. The science of chemical analysis has become highly refined within the past ten years. Technology of mass spectrometry combined with gas chromatography has allowed the identification of over 35,000 molecular species with a sensitivity of the measurements advancing from ppm to ppt range, a millionfoid increase. Although the very sophisticated analyses performed by atomic absorption spectroscopy and gas chromatography-mass spectrometry provide the basic data used in judging environ mental quality, a number of other analytic techniques are employed. Asbestos is identified and its fibers counted by polarized light and phase contrast microscopy. For detecting asbestos fibers in the parts per trillion range scanning electron microscopes have proven more sensitive than the phase contrast analytic techniques. A closed loop stripping technique has recently been developed for concentration of volatile organics that have previously been missed by other concentration methods. This technique is selective for many industrial solvents which are very volatile such as tetrachloroethylene, tetrachloroethane, dichlorobenzene, etc. Its application is extremely valuable for identifying volatile organics found in drinking water due to the chlorination process, and in groundwater contaminated by industrial solvents. Additionally,' conventional wet chemical methods are sometimes used, including biochemical oxygen demand (BOD) and biotoxicity studies. 107 ovawnan Due to the development of these techniques in the past few years it has become possible to determine with more certainty trace amounts of inorganic and organic species present in the environment. Measurements in the parts per billion to parts per trillion range are now made routinely . The values determined are made reliable by quality assurance and quality control programs. The American Industrial Hygiene Association accredits only those laboratories that meet repeated, rigorous inspections and successfully participate in its program of proficiency tests. Although the EPA does not give any certification to laboratories, it does carefully inspect facilities and does provide standard test species and samples for use in calibrating analytic instruments and laboratory performances. State agencies require their laboratories and any commerical laboratories performing state work to meet rigorous standards of capability and performance. Detection of water and air contamination is now possible which in the past would have gone unnoticed. In many ewes, the scientific data base does not exist to determine the health effects at the ppt range, although some chemical carcinogens are active at this level. Detection technology is expected to continue to advance faster than the knowledge of the possible adverse health effects of small amounts of persistent chemicals and trace metals. This uncertainty leads to the question of risk assessment. (See Section VI.) OCCUPATIONAL SAFETY WITHIN THE LOUISIANA CHEMICAL INDUSTRY Occupational Health Surveillance Programs The following discussion of industrial hygiene is written from the perspective of large chemical manufacturing facilities. This is not intended to minimize the occupational safety concerns created for workers in the numerous smaller establishments such as machine shops, plating companies, spray painting and others who use a variety of toxic and potentially carcinogenic substances. Exposures to workers in these smaller establishments are often more problematic than exposures at larger facilities that frequently have a physician at the facility and ongoing industrial hygiene programs. The emission of wastes into the community environment by the numerous smaller establishments can have a substantial cumulative effect, despite modest total volumes from each individual facility. The objective of any industrial occupational health program is essentially twofold; to safeguard employees from known physical, chemical or biologic hazards 108 URL 04611 and to meet the obligations of occupational health regulations. Industries use various practices to achieve these objectives. The surveillance programs include pre placement and periodic medical examinations, clinical and lab tests and epidemiological investigations. A pre-placement medical examination serves several functions. First, it helps establish that individuals are medically capable of performing the duties of the job. it assures placement of persons in jobs most appropriate to their physical, mental and emotional health. It establishes a profile of the health of an individual as he enters employment, which allows subsequent comparative measurement. The pre-placement examinations are conducted in the context of a person's past medical history, the nature and essential work activity of the job in consideration, and any special environmental conditions in the workplace. In some cases periodic examinations are required by law, and in others may be required by the employer. They provide a regular opportunity to observe possible health effects caused by workplace exposures. After the physical examination and completion by the worker of a comprehensive health questionnaire, the examining physician can make sound recommendations as to whether the employee can continue to perform his/her work assignments safely. Clinical and laboratory testing are critical elements in an employee medical examination program. Clinical and laboratory tests are performed during the initial pre-placement examination and during subsequent periodic examinations. Testing provides information about long-term employee health and is required for epidemiologic investigations, which may provide the initial identificat exposure problems. Standard clinical tests used in an occupational health exam respiratory tests to determine if a respirator can be safely used by electrocardiograms to assess cardiovascular function, chest X-rays, ai tests. Laboratory tests, such as a complete blood count, a complete selective serum chemistries would also be included in the examination. Workplace Monitoring The objective of industrial hygiene programs is to minimize pot* exposure to chemicals, to protect employees on the job, and to extenc to workers'families and communities. Various forms of monitori: 109 industries to detect the presence or absence of chemicals. The monitoring programs include periodic air monitoring. An area-job classification scheme groups individuals by common environmental conditions at work and provides the basis for evaluation of on-the-job exposure criteria by a class of job. This is thought to provide more information than individualmeasurements. The criteria for establishing area-job classifications include work similarities, exposure similarities, and similarities in workplace environment (which would take working conditions into account). Area-job classification facilitates the development of reliable sampling strategies, worker protection and training requirements, medical surveillance, and evaluation of existing engineering controls for the designated area. Employee exposure monitoring serves two basic purposes. In determining employee exposure status relative to OSHA permissible exposure levels and to a company's own industrial hygiene guide values. Monitoring programs are generally built around a formal sampling strategy, an organized method of data collection (where area-job classification plays an important role) and well-defined reporting and record-keeping requirements. The successful periodic air monitoring program will allow proper identification of contaminants and their sources, determine workplace exposures prior to and as a result of worker complaints, and serves as a check on the effectiveness of engineering and administrative controls. Control and Protection Programs In addition to worker health surveillance programs and workplace monitoring, some industries use other means of minimizing potential workplace exposures to chemicals. These other means include the safest possible design of industrial processes and the provision of protective equipment. For the processes and equipment to be used to their best advantage workers must be fully aware of their protective potential. Many industries have education and training programs. Engineering controls used to provide protection include proper design of workplace ventilation, minimizing material loss from process equipment, and any physical workplace changes that would reduce exposures. Administrative controls include enforcement of proper work practices, appropriate maintenance of monitoring devices, and employee training. Employees play an important part in the administrative control effort. Safe work practices cannot be dictated; they must be implemented on the job by the 110 employee. Often the individual employee can best identify a potential safety problem and suggest the proper solution. Periodic reviews are essential in maintaining commitment and currency in safe work practices. Various types of personal protective equipment and supplies have been developed. The most common are respirators, plastic safety glasses, chemical sampling badges and pumps, and flame-resistant clothing. Use of this equipment is one of the basic elements of a serious employee health protection program. Proper use is based on employee understanding and safety training. It has been noted that there are significant problems associated with the use of respirators in routine work exposure situations. Poor fit, lack of training, adverse environmental conditions and improper respirator maintenance have created problems for users. Educational programs may include roundtable discussions, lectures, hands-on practice with protective equipment, and the development of manuals which include a detailed safety analysis for each operating position in a plant, and its specific potential hazards. Some industries have education and training programs that extend to community public safety operations lik^Tire and police departments. The programs are given to large groups or are personalized where needed. A majority of chemical companies have employee information programs. The programs include training in proper material handling techniques and medical emergency training. A Material Safety Data Sheet (MSDS) on ar. individual product or chemical provides detailed information about its relative hazards and safety measures. A standard MSDS contains information in plain language on the chemical name, trade name and synonyms; physical and chemical properties; chemical reactivity; fire and explosion hazards; short and longterm health effects; potential routes of exposure; signs and symptoms of overexposure; handling precautions to take and protective equipment to use; and the procedures for handling spills, fire and first aid relative to the product. The MSDS also lists an emergency phone number to call for more detailed information. MSDSs should be kept at the worksite and accompany product shipments, although access to this information has been a source of controversy at various times in the past. W i 04613 I i i i j Ill URL lWb*H References - OCCUPATIONAL ENVIRONMENT 1. Eckholm E. Unhealthy Jobs. Environment 19:29-38,1977. 2. Anderson K, Scott R. Fundamentals of Industrial Toxicology. Ann Arbor, MI, Ann Arbor Science Publishers, 1981, 3. Lehmann P. Occupational Cancer. Job Safety and Health, 3. United States Department of Labor, Occupational Safety and Health Administration. 1975. 4. Gottlieb MS, Stedman RB. Lung cancer in shipbuilding and related industries in Louisiana. Southern Medical Journal 72:1099-1101, 1979. 5. Rothschild H and Mulvey JJ. An increased risk for lung cancer mortality associated with sugarcane farming. Journal of National Cancer Institute. 68: 755-760, 1982. 6. Gottlieb MS, Pickle L, Blot WJ, Fraumeni JF. Lung cancer in Louisiana: Death certificate analysis. Journal of National Cancer Institute. 63:1131-1137, 1979. 7. Gottlieb MS. Lung cancer and the petroleum industry in Louisiana. Journal Occupational Medicine. 22:384-388, 1980. 8. Pickle LW, Gottlieb MS. Pancreatic Cancer Mortality in Louisiana. American Journal of Public Health. 70:256-259, 1980. 9. Gottlieb MS, Pickle LW. Bladder cancer mortality in Louisiana. The Journal of the Louisiana State Medical Society. 133:6-9, 1981, 10. Louisiana Department of Natural Resources. Louisiana Petrochemical Industry Assessment. 1983. 11. United States Department of Health and Human Services. Second Annual Report on Carcinogens. 1981. 12. Finkel JJ. Industrial Toxicology (9th ed.). Boston, MA, John Wright PSG Inc., 1983. 13. IARC Monograph on the Evaluation of the Carcinogenic Risk of Chemicals to Humans, Supplement I. IARC, Lyon, France, 1979. 14. Maltoni C. Scarnate, C. First experimental demonstration of the carcinogenic effects of benzene. Med. Lavoro 70:352-357, 1979. 15. Ott MG, Townsend JC, Fishbeck WA, Langner RA. Mortality among individuals occupationally exposed to benzene. Archives of Environmental Health 33:3-10, 1978. 16. Aksov M, Erdems S, Dincol G. Leukemia in Shoe Workers exposed chronically to benzene. Blood 44:837-841, 1974. 112 % 17. Occupational Safety and Health Administration. Exposure to coke oven emissions Federal Register 41:(206), 46472-46790, 1976. 18. National Cancer Institute. Bioassay of l2-Dichlorethane for Possible Carcinogenicity. Technical Report Series No. 55, DHEW Publication No. (NIH1 78-136l" Washington, D.C. Department of Health, Education and Welfare. 1978. 19. Swenberg JA, Kerns WD, Mitchell RI, Gralla EJ, Pavkov KL. Induction of squamous cell carcinoma of the rat nasal cavity by inhalation exposure to formaldehyde vapor. Cancer Research 40:3398-3401, 1980. 20. Alexander V. Presentation to the Governor's Task Force on Environmental Health. Baton Rouge, LA, July 14, 1983. 21. Tri-State Delta Chemical, Inc. 1983 Agricultural Chemical Label Book. 22. Bagent J. Louisiana State University Extension Service. Communication, September 1983. Personal 23. Sanders D. Louisiana State University Extension Service. Communication, September 1983. Personal 24. Doull J, Klaassen CD. and Amdur MO, Eds. MacMillan Publishing Co., Toxicology, The Basic Science of Poisons. New York, N.Y., 1980. 25. Epstein, S. The Politics of CancerJSierra Club Books: San Francisco, CA, 1978. URL 04615 113 URL 04618 THE NATURE OF PERSONAL CHEMICAL EXPOSURES Chemical exposures associated with the personal environment are unique in several ways from exposures in the workplace or community/global environments. (See Section III Community Environment, and Section IV Occupational Environment). Primarily, the aspect of choice is a significant difference. Intake of chemicals from the diet, cigarette smoke, alcohol, drugs and household chemicals is often a matter of an individual's knowledge and volition. The type and amount of exposure often reflects personal choice of lifestyle and habits. Workplace and community exposures are less controlled than these exposures encountered in the personal environment. With increased control of chemical exposures, the ability to reduce or prevent adverse chemical effects is more attainable within the personal environment. In this regard it is important to note that most chemical related deaths in American adults are associated with chemicals common to the personal environment (drugs, alcohol).* Also, the most significant etiological factor (cigarette smoking) related to the o development of lung cancer is associated within the personal environment, (See Section VI Cancer Rates and Risk Factors in Louisiana.) The primary route of chemical exposure in the personal environment is also different. Chemicals are more often ingested than inhaled as is characteristic of the community and occupational environments. Associated with ingestion is the significant influence of liver metabolism prior to systemic distribution of the ingested chemicals. 114 A* i4 as U fiL 04617 The action of the liver may have either a helpful or a harmful effect, depending upon the food eaten. Since the liver serves to activate many chemicals to more toxic forms (including carcinogens), oral exposures are associated with increased toxicities for those chemicals where metabolism is prerequisite to toxicity. Conversely, the liver may detoxify certain chemicals and this first passage through the liver after oral exposure may be a valuable defense mechanism. Many additional factors may affect the extent to which ingested chemicals are absorbed. These factors include acidity of the gastrointestinal tract, activity of the intestinal microflora which metabolize many chemicals, and food patterns.3 * Aside from suicide or accidental chemical exposures where concentrations are high, chemical exposures to carcinogens in the personal environment are usually lower and chronic in nature. (See the discussion of promoters and inducers in Section 1). Since most toxicity studies are designed to characterize measurable chemical effects, the risks of chronic exposures to low levels of carcinogens are traditionally difficult to assess due to occurrence of minimal effects at low doses. It is even more difficult to define dose-response relationships for diet, smoking and alcohol effects on development of cancer from exposures in the occupational and community environments. These factors contribute to the uncertainty regarding chronic effects of chemicals in the personal environment. As more scientific data are provided on the relationship between cancer and chemicals in the personal environment the role of individual responsibility for cancer prevention will surely be significant. DIETARY EXPOSURES IK LOUISIANA The role of diet and nutrition in the etiology of cancer has become a relevant area for scientific research. The possible relationship between diet and cancer has caused public anxiety yet this has also suggested new hope for the prevention of 4 cancer through appropriate dietary habits. Some scientists have estimated that diet (if defined as "everything that is put into the mouth and swallowed") may be responsible for 30-40% of cancers in men and 60% of cancers in women.5 Table V-l lists possible ways that diet may influence the 2 incidence of cancer. The connection between diet and cancer not only involves contamination of food . with direct acting carcinogens but also includes the potential of synergistic or promoting effects of dietary components with carcinogens of non-nutrient value. 115 TABLE V-l MECHANISMS WHEREBY DIET MAY AFFECT CANCER INCIDENCE Mechanism Example 1. Ingestion of potent, direct acting carcinogen or precursor 2. Factors affecting carcinogen formation in the body 3. Factors affecting transport, activation, deactivation of carcinogens. 4. Factors enhancing promotion of initiated cells 5. Overnutrition Carcinogens in natural foodstuffs Carcinogens produced by cooking Carcinogens produced by microorganisms during storage Ingestion of substances enhancing carcinogen formation (nitrosamine) Alteration of fat metabolism Alteration of gut microflora Alteration of fecal concentration of carcinogens (fiber effects) Alteration of carcinogen transport Enzyme induction Enhanced deactivation (Vitamins A, C,E, selenium, beta-carotene). Vitamin A deficiency Adipose-tissue-derived estrogens URL 0461 oz> SOURCE! Doll and Peto2 Natural Foodstuffs The nature of the diet in regard to intake of major food groups may be a significant factor in carcinogenesis. Though total caloric intake, total ingested lipids, protein, carbohydrate, dietary fiber and vitamins may not be causative agents, these dietary components may promote carcinogenesis either by dietary deficiency or excess. e Though the data are incomplete, many epidemiological studies have demonstrated an association between dietary fat and occurrence of breast, prostate and colon cancers.5'7*8 Many foods popular in Louisiana are high in fat. Pork is very popular throughout the state not only as a roast but as slab bacon used for seasoning meat and vegetables. The large amount of cooking oil and lard used in meal 116 preparation is also a significant source of dietary fat. Home cooked meals in Louisiana which include fried foods, cornbread, biscuits, pies and roux-based sauces a often contain higher fat content than the equivalent commercial products. Chicken, a lean meat, was reported to be the most popular food of all Louisiana residents sampled; however, steak was more popular with northern residents than southern Louisiana residents. Pork consumption was greater among Louisiana blacks than whites.10 The role of Vitamins A,C, and E in the prevention of cancer has continued to generate scientific interest. Epidemiological evidence suggests that there is an inverse relationship between risks of lung, larynx and bladder cancers and ingestion of Q foods containing Vitamin A or its precursors (such as beta-carotene). These foods include liver, and green and yellow vegetables (broccoli, carrots, spinach, squash, sweet potatos and brussel sprouts). Evaluation of the nutritional status of Louisiana residents has suggested relation ships between Vitamin A deficiency and increased incidence of lung cancer. Com parison of lung cancer cases with octroi cases indicated significantly less serum retinol and beta-carotene in cancer patients than in controls. Beta-carotene may serve to prevent cell injury by reacting with carcinogens. Correlation coefficients were calculated for comparisons between Vitamin A levels and lung cancer incidence. (See Figure 5.1) A negative correlation was established between Vitamin A intake and incidence of lung cancer mortality in white males.11 Historically, Louisiana has had problems with malnutrition. During World War n more Louisiana men were rejected Q from military service because of malnutrition than any other state's men. Nutrition surveys conducted in Louisiana have indicated that 8% of Louisiana residents are significantly deficient in Vitamin A and this places them in high risk categories for the development of disease.11 Geographic differences in Vitamin A intake exist. North Louisianians ingest approximately two times more Vitamin A (5886 International Units) than do south Louisiana residents (2581 International Units).11 This may be related to increased availability of fresh fruits and vegetables in the north. Intake of fresh fruit and vegetables by residents of 29 Louisiana parishes has been negatively correlated with lung cancer risks.12 Particularly significant in reduced cancer risk were broccoli, lettuce, carrots, bananas, oranges and fruit juice. URL 04619 i 117 19 Year Incidence of Long cancer in Men URL 04620 FIG. 5.1 BETA-CAROTENE LEVELS AND LUNG CANCER INCIDENCE. SOURCE: ShekeUe RB et al. Dietary Vitamin A and risk of cancer in the Western Electric Study. The Lancet. Sat. 28 Nov. p. 1186-87, 1981. The consumption of fresh fruit and vegetables provides an increased amount of Vitamin C (ascorbic acid). Decreased risks of gastric and esophageal cancers have been associated with high Vitamin C intake. Vitamin C (and E) may inhibit formation of N-nitroso compounds and other carcinogens in vivo.598 Ingestion of fruits and vegetables has been considered to be. the most healthy food habit by Louisiana residents. Northern Louisiana residents prefer these food items (green vegetables and citrus fruit) more than the residents of southern Louisiana do.10 The most popular vegetables throughout the state have been corn, green peas, q green beans and tomatoes.' Evidence has suggested that dietary fiber present in certain fruits, vegetables, grains and cereals may protect against colo-rectal cancer in humans. Generally, the Louisiana population has a low consumption of whole wheat or whole grain breads. For example, cornbread and hush puppies popular in northern parishes are often made from white meal. French bread, popular in South Louisiana is made primarily from white flour.9 118 Naturally-Occurring Carcinogens In Food Many food sources, particularly plants, contain a variety of mutagens. Table V-2 provides a selection of food sources and mutagens that have been identified in them. (See discussion of mutagens in Section I.) Many of these chemicals can injure DNA and potentially result in cancer. Most biological systems, however, possess defense mechanisms whereby these injuries may be repaired. It is often the balance between injury and repair that prevents cancer development. It is important to note that chemicals promoting defense mechanisms are also found in the diet and their intake is essential to optimum health. Such TABLE V-2 NATURALLY-OCCURRING MUTAGENS IN FOODS Chemical Safrole Hydrazines Psoralen derivatives Solanine Anthraquinone derivatives Theobromine AUyl isothiocyanate Gossypol Malvalic acid Phorbol esters C anavanine rv Food Source Oil of Sassafras Black Pepper r Mushrooms (Qyromitra esculents, 3-} Agaricus bisporus) Celery, parsnips, figs, parsley. Diseased, bruised potatoes Rhubarb Cocoa powder, teas Oil of Mustard, horseradish Cottonseed oil * < T Herbal teas Alfalfa sprouts SOURCE: Ames8 119 la n --'.sir protective components include antioxidants that prevent action of chemicals such as free radicals which damage DNA and cell membranes. Such antioxidants include Vitamins E, C, beta-carotene, selenium and various phenols. In addition to chemicals naturally found in foods, carcinogens may be formed during cooking or browning processes. Carcinogens such as benzo(a)pyrene and other polycyclic aromatic hydrocarbons can be produced by pyrolysis (2500 F temperatures) when meat or fish is broiled, barbecued, smoked or fried in fat.14 The popularity of charcoal gTilled meat is high in Louisiana due, in part, to the q long summer season. Steak, ground beef and roast have been preferred by North Louisiana white residents compared to wild game, seafood and fish preferred by white individuals in South Louisiana. Higher levels of fried pork or bacon in the diets of Louisiana blacks may be a significant source of mutagens related to cooking.1 Though the potential exists for mutagen formation in cooking processes, epidemiological relationships between such mutagens and gastric and other cancers have been weak. Carcinogens may be formed within the body if certain precursors are ingested within the diet. Some of the most powerful carcinogens known are produced in this manner. N-nitroso compounds (including nitrosamines) have been found in gastric juices. These compounds may be formed in the digestive tract following reactions between ingested nitrites and any compound to which the nitrite may bond; that is, a nitrosable compound. These nitrosable compounds are usually secondary amines or Nsubstituted amides. Nitrosable compounds are commonly found in fish and meat, pesticide residues or drugs, or may be formed from endogenous amino acids. Nitrite is commonly found in food as a preservative, color or flavor enhancer. Nitrite may be formed in vivo from nitrate ingested in vegetables and drinking water. Though laboratory evidence is clear in defining nitrosamine potency, epidemiological data is lacking to define a role in human cancer. 2*5 y 15 Food Contaminants In addition to nutrients, many non-nutrient chemicals are found in foods that ' cause mutations and possibly cancer. Potent carcinogenic contaminants inelud 3 metabolites such as the aflatoxins which cause liver cancer. Conditio contamination of foodstuffs with microorganisms that produce mu' involve storage conditions at high temperatures and humidity. Grair fruits and vegetables are susceptible to these conditions, f* Louisiana are conducive to these types of contamination, tho. <r 120 the United States suggest that aflatoxins make up a minimal amount of the diet. However, the hazard of these contaminants remains to be fully defined. Of the numerous minerals normally present in the human diet, no firm conclusions can be drawn relating them to risks of cancer. This includes arsenic, cadmium and lead, the laboratory data for which indicates development of cancer at concentrations higher than found in the diet.^ Concern has been generated regarding arsenic concentrations in shellfish in Louisiana waterways; however, effects on health have not been documented. Food Additives Chemicals occurring in foods that are synthetically processed include food additives and pesticide residues. Nearly 3000 substances are intentionally added to foods during processing in the United States. (See Table V-3) Approximately 12,000 chemicals are unintentionally added as a^result of processes such as packaging.5 Of the intentionally added chemicals, all of those found in laboratory animals to be carcinogenic, except saccharin, have been banned in accord with the "Delaney Clause" of the Federal Food, Drug, and Cosmetic Act. Saccharin-containing artificial sweetener products are found throughout Louisiana in supermarkets and restaurants. In laboratory animals saccharin has caused bladder cancer; however, the mechanism is 2 unresolved. As summarized by Doll and Peto, the results of the best epidemiological URL 04623 Compound TABLE V-3 FOOD ADDITIVES Target Organ/Cancer Risk saccharin nitrites,nitrates, nitrosamides nitrosamines cycasin SOURCE: Oppenheimer.^1 bladder stomach gastrointestinal tract, liver, bladder, lung, kidney liver 121 studies in humans (Table V-4) evaluate the risks of bladder cancer with use of artificial sweeteners. From these studies, Doll and Peto concluded that the proportion of human bladder cancers attributable to the use of artificial sweeteners is negligible. However, more time may be required to characterize the long term effects of this weak animal carcinogen.2-5-16-17.18-19.20 Cancer incidence from unintentional additives in foods such as vinyl chloride from PVC food wrappings as well as chlorinated hydrocarbon insecticides from agricultural applications has not been well defined. Though epidemiological evidence does not support increased incidence of liver cancers that were associated with these chemicals in the laboratory, their role as potential synergists is unclear. 2 5 URL 04624 TABLE V-4 RISK OF BLADDER CANCER WITH USE OF ARTIFICIAL SWEETENERS Authors Patients (Number) Table Top Sweeteners Relative Risk* Diet Beverages Artificial Sweeteners (Any Form) Howe et al.*** Kessler and Clark 17 Hoover et al.* Morrison and Buring19 Wynder and Stellman 20 Male Female Male Female (408) (152) (365) (154) Male (2226) Female (744) Male (469) Female (197) Male (302) Female (65) 1.6 0.6 0.88 0-91 1.04 1.04 0.8 1.5 0.93 0.62 0.8 0.9 0.95 1.00 0.95 0.97 0.8 1.6 0.85 0.60 -- 0.97 (1.08)* 1.00 (0.87) 0.99 1.01 --- --- SOURCE: Doll and Peto.2 * Values greater than 1 suggest increased risk of bladder cancer. ** Specifically saccharin. 122 sap INDOOR POLLUTION Another significant type of chemical exposure associated with the personal environment is indoor pollution. Indoor pollution is pollution found within residential buildings at levels that affect human health. It is, primarily, created by the personal habits of the individual in the home, the consumer products used indoors, the building materials of the structure, and the nature of the home's heating system. 22 Indoor pollution may pose a greater threat to human health than outdoor pollution because the air pollutant concentration may become significantly higher indoors and because people spend most of their time indoors. This becomes especially true with home "weatherizing" which reduces to a minimum exchange between outdoor and indoor air. 23 Examples of common indoor pollutants found in homes are radon, certain combustion products, formaldehyde, asbestos and tobacco smoke. Each of these is a known or suspected human carcinogen. For the source, risk, and level of these 'v pollutants see Table V-5. Some inadvertent exposures to carcinogens are thought to occur to homeowners from improper applications of pesticides. Exposures to these substances indoors have not been regulated. 4 URL 04625 CARCINOGENIC DRUGS AND MEDICAL TREATMENT . There are a number of drugs prescribed in the course of medical practice which are associated with human cancers. (See Table V-6) Medical treatment which o increases cancer risk is the use of ionizing radiation (X-rays). Doll and Peto estimate that the medical use of ionizing radiation results in 0.5% of all U.S. cancers. They state, "this number is distressingly large, and any reduction in the frequency of use or the dosage of diagnostic irradiation, especially for fetuses (and perhaps children), might eventually prevent a few hundred cancer deaths per year." The use of some of these carcinogenic drugs continues because the benefits of the chance of saving a life may outweigh the possible development of an iatrogenic (doctor caused) cancer caused by the drug. 123 - otu^O TABLE Y-5 INDOOR POLLUTION Type of Pollutant 1) Radon Source concrete and brick building materials; natural gas used in home Risk Levels Found in Home human carcinogen (According to EPA, radon exposure inside building may account for as much as 10% of all lung cancer deaths in U.S.) .004 to .02 working levels (Mine and Safety Standard is 1 working level) 2) Combustion products (polycyclic aromatic hydrocarbons) woodstoves, fireplaces, kerosene space heaters, and gas clothes dryers, gas cooking appliances human carcinogen less than 1 to 200 ng/m^ 3) Tobacco smoke (polycyclic aromatic hydrocarbons) personal and passive smoking human carcinogen particulate matter level 30-700 micrograms/meter (Clean Air Act maximum exposure is 150 microgram/ 3 m at any instant) 4) Formaldehyde urea formaldehyde insulation, particle board, plywood, floor coverings, cosmetics serious respiratory and skin irritant, possible human carcinogen 0 to 3ppm (occupational exposure limit is 3ppm) Table V-5 continued on next page 124 TABLE V-5 (continued) INDOOR POLLUTION 7 Type of Pollutant Source Risk Levels Found in Homt 5) Asbestos 6) Chlordane/ Heptaehlor roofing and flooring materials, textiles, papers, filters and gaskets, cement pipes, coating materials, and thermal and acoustic insulation 'V spraying for termite control human carcinogen 0 to 80 fibers/ml* (occupational exposure limit 2 fibers/ml on eight hour average basis and 10 fibers/ml at any given moment) suspected human carcinogen (banned by EPA in 1978 for agricultural use but no limit set on domestic use of C/H for termite control** no published information on levels following treatment for termite infestation** (JRL 04627 -- SOURCE: Kirseh. * 80 fibers/ml exposure to person stripping a ceiling. * * Epstein. 125 Drug TABLE VHS CARCIWOGEW1C DRUGS Human Cancer Associated With Heavy Use Cyclophosphamide Coal tar ointments Diethylstilbestrol(DES) Arsenic-containing M elphalan Oxymetholone N,N, - Bis (2-chloroethyl) 2-Napthylamine Phenytoin C hloramphenicol Bladder Skin, stomach, colon, rectum Uterus, vagina Skin, lung, liver Leukemia Liver Bladder Lymphoreticular cancer Leukemia SOURCE: Oppenheimer.2* USE OF HORMONES Female sex hormones are the most commonly prescribed drugs in America today, second only to tranquilizers.24 Studies of the use of the hormone estrogen for menopause treatment found that cancer of the uterus was 20 to 60% more common in women being treated than for those not receiving treatment. (See Figure 5.2 and Table V-7).25*21 There has been a significant correlation between vaginal cancers in the daughters of DES-treated women as well as excess breast cancer in the treated women, themselves.24 DES is a synthetic estrogenic drug that was widely used from 1945 to 1970 for the prevention of miscarriages. Use of the oral contraceptive pill is associated with excessive risks of rare liver tumors. The same association suggests evidence of increased risk of cervix and breast cancer for women using oral contraceptives. URL 04628 126 90 90 Estrogen sales millions of dollars 0 1_______ l_____________ L_ I960 1965 1970 Year __ I__ 1975 0 FIG. 5.2 ESTROGEN SALES AND CORPUS CANCER. Age-adjusted (1950 U.S.) incidence rates in white females. SOURCE: Council on Environmental Quality. 95 127 URL 04630 Site Endometrium Breast Prostate Ovarian epithelium Testis Thyroid Osteosarcoma TABLE V-7 HORMONE-RELATED CANCERS Hormone Estrogen Estrogen and prolactin Testosterone Gonadotropins Estrogens, follicle-stimulating hormone Thyroid stimulating hormone Skeletal growth stimulating hormones (pituitary growth hormone, thyroid hormone, androgens, estrogens) SOURCE: Oppenheimer.21 USE OF ALCOHOL IN LOUISIANA Epidemiologic studies in several countries have shown that alcohol intake considerably increases the risk of certain cancers, especially those of the mouth, pharynx, larynx and esophagus. The mechanism of action has not been clear because alcohol per se has not been found to induce DNA damage or cancer in any experimental system. The role of alcohol seems to be closely linked to that of tobacco and there is good proof that both agents increase the cancer risk in a multiplicative (synergistic) pattern; that is, each agent potentiates the effect of the other. (See Figure 5.3.) It has recently been reported that alcohol interferes with the "first pass clearance" of certain carcinogens, especially nitrosamines. First pass clearance refers to the drastic reduction in the blood level of toxic substances after they pass once through the tissues and are acted upon by detoxifying enzymes, especially in the liver. It therefore appears that alcohol interferes with some enzyme systems and will prolong the contact of carcinogens with their target tissues. 128 Relative Risks of Larvnx Cancer cigarettes per day Relative Risks at Oral Cavity Cancer 384 4725 239 4725 FIG. 5.3 SMOKING AND CANCER SOURCE; Surgeon General's Office.40 129 &9H) 7y0 Alcoholic beverages are part of the culture in most human populations but there are marked differences in the amounts consumed. Contrasting consumption patterns are found in Louisiana: the predominant cultural pattern in North Louisiana discourages alcohol use while in South Louisiana alcohol is an important component of the "joie de vivre" philosophy. A recent survey has reported that the amount of alcoholic beverages consumed by South Louisianians (whites and blacks) is about double that of the north. USE OF TOBACCO IN LOUBIANA Tobacco is one of the biggest killers in the United States today. It is responsible for 30% of all cancer deaths and for an even great** number of deaths from heart disease. The amount of suffering due to smoking is incalculable but is well shown by the thousands of patients who die each year from emphysema: they spend the last 2 to 10 years of their lives gasping for breath. The addiction to this toxic drug causes much more suffering, disease and death than marijuana, cocaine, morphine and all other drug addictions put together. This drug addiction is tolerated by our society because when it started, its effects on health were not known and it developed into a multi-billion dollar industry with some of the best organized lobbies in all "developed" countries. Tobacco is not regulated by the Food and Drug Administration because it conveniently ignored the fact that nicotine is an addiction-causing drug. The habit is forced onto society by a propaganda campaign which costs well in excess of one billion dollars per year, much more than the entire budget of the National Cancer Institute. Mortality rates for cancer of the bronchus, trachea and lung quadrupled for males from 1950 to 1975 (See Figure 5.4). Thousands of scientific articles have documented beyond any reasonable doubt the deleterious effects of smoking on human health, well summarized in Smoking and Health, in two volumes,30 and the many other publications of the Office of Smoking and Health of the U.S. Department of Health, Education and Welfare. Their last report estimates that 129,000 Americans died of smoking-related cancers in 1982. The best documented effects of cigarette smoking are on lung cancer, which affected 2,300 and killed 2,100 Louisianians in 1982. Approximately 9096 of lung cancer deaths could be prevented by avoiding smoking. Cigarette smoking is also the major cause of cancers of the oral cavity, larynx and esophagus; all of these cancers are excessive in Louisiana. Smoking is also a contributory cause of cancer of the bladder, kidney, pancreas, stomach and cervix uteri, all relatively excessive in Louisiana. 130 e9i,0 7fc0 Age-od]ustd Mortality Rata for coneor of 1t BrondWi Ling aid TrachaOt by Roc* aid Sax Unitad States Statistics I9SCLI977 FIG. 5.4 BRONCHUS, TRACHEA AND LUNG CANCER RATES. Age-adjusted mortality rates (1970 U.S.) SOURCE: Surgeon General's Office.40 131 -'SM.. im TABLE V-8 COMPARISON OF SMOKING HABITS IN LOUISIANA* 29 * * * 33 % current smokers % smokers starting after age 20 % smokers using filter cigarettes % whose father smoked % whose mother smoked White South North 38.7 17.4 75.9 39.3 6.5 34.7 20.2 84.9 28.0 5.2 Black South North 54.0 19.3 73.8 29.7 3.9 46.9 19.4 74.6 28.7 5.9 SOURCE: Correa and Johnson.^9 The smoking habits of Louisianians are again determined by the cultural patterns. North Louisiana's pattern is similar to that of the rural south of the United States: smoking became prevalent after World War I but the pace at which it was picked up by the rural communities was somewhat slower than in the big cities. This correlates with lung cancer rates approximately 30 years later: they first were highest in the big cities and later in the rural areas. South Louisianians have not followed that pattern. Their smoking habits resemble Mediterranean patterns. The differences between north and south are summarized in Table V-8, the result of a recent survey of Louisiana males. 29 South Louisianians are more frequently smokers, start earlier and more frequently use high tar, non-filter cigarettes. These differences have been present for at least two generations and appear even more accentuated in the past: there was more than 10% excess of smokers among the fathers of the present generation. These findings are probably related to the very high lung cancer rate observed in South Louisiana as far back as reliable statistics go. Smoking is no longer considered a personal habit concerning only the smokers. The smoker forces his/her companions to inhale the smoke of his/her cigarette, pipe or cigar. (See Table V-9.) Non-smoking Louisiana women married to heavy smokers have 3 times the lung cancer risk of those married to non-smokers. The smoke not inhaled during active smoking, so-called sidestream smoke, is considerably more toxic than the mainstream smoke. Table V-10 shows that some nitrosamines are much more concentrated in sidestream smoke which is inhaled by the smokers companions. 33 132 - 'JUi. --`..XtCZ TABLE V-9 LUNG CANCER DEATHS AMONG NONSMOKING WOMEN WITH CIGARETTE SMOKING HUSBANDS Parameter Observed deaths Expected deaths Mortality ratio Husband did not smoke 65 65.00 1.00 Husband smoked <20 cigarettes per day 39 30.67 1.27 Husband smoked^20 cigarettes 49 44.67 1.10 SOURCE: Budbord.36 NOTE: Based on American Cancer Society Study, 1960-1972. "V Inhaled cigarette smoke is absorbed by the lungs and many of its chemicals, some of them carcinogenic, cross the placental barrier into the unborn fetus. This increases the susceptibility to cancer in experimental animals. A Louisiana patient with lung cancer whose mother was a smoker had an elevated relative risk (1.4 times higher) than one whose mother was not a smoker. REPRODUCTIVE AND SEXUAL BEHAVIOR Increased cancer of the cervix, which accounts for 1.5% of all U.S. cancer deaths, has been correlated with multiple sexual partners. The present evidence suggests that one of the primary causes of this particular cancer is an agent, possibly a virus, passed between partners during intercourse. Pregnancy and childbirth play a significant preventative role in cancers of the endometrium, ovary, and breast. These conditions are less common in women who bear children early than in women who have had no children. Women are progressively less likely to develop breast cancer as the age of first pregnancy decreases, by a late onset of menstruation, and by an early menopause. 2 URL 04635 133 , URL 04636 TABLE V-10 SOME CARCINOGENS IN CIGARETTE SMOKE (Nanograras/cigarette) Benzo(a)pyrene Dimethylnitrosamine Methylethylnitrosamine Diethylnitrosamine N-nitrosonornicotine 4-(N-methy1-N-nitrosam ino)- l-(3-pyridyl)-l-butanone Mainstream Smoke (MS) 20-40 5.7-43 0.4-5.9 1.3-3.8 100-550 80-220 N i tr osopyrr oli d i n e Quinoline Methylquinolines Hydrazine 2-naphthylamine 4-aminobiphenyl 0-toluidine 5.1-22 1700 700 32 1.7 4.6 160 Sidestream Smoke (SS) 68-136 680-823 9.4-30 8.2-73 500-2750 800-2200 204-387 18000 8000 96 67 140 3000 SS:MS ratio 3:4 19-129:1 5-25:1 2-56:1 5:1 10:1 9-76:1 11:1 11:1 3:1 39il 30:1 19:1 SOURCE: Stock33 COST OF CANCER Cancer produces serious economic and social costs. The direct economic costs of cancer include money spent on prevention, diagnosis, and treatment. Hospital and nursing care, doctor services, drugs, medical research, training personnel, and insurance all contribute to the cost of disease for cancer patients and their families. Illness and death due to cancer prevent people from leading productive lives and this loss is included in estimates of indirect costs. Every cancer death costs an equivalent of 16 years of life. In 1980, twenty-six (26) million hospital days and approximately twenty-eight (28) million visits to physicians were attributed to cancer.37 According to the National Cancer Institute, the total national cost of cancer was approximately $50 billion with medical expenditures amounting to $13.6 billion (1980 figures). TABLE Y-ll ESTIMATED MEDICAL CARE EXPEWDITORES FOR CANCER IN LOUISIANA, 1980 (in Millions of Dollars) Site Digestive Organs and Peritoneum Trachea, Bronchus and Lung Breast Female Genital Organs Other Genitourinary Organs Lymphatic and Hematopoietic Tissues Other and Unspecified Sites TOTALS TOTAL MALE AND FEMALE: $176 Million Male $ 17.2 18.1 14.3 7.6 27.9 $ 85.1 Female $ 13.3 10.1 16.4 12.8 3.1 9.3 25.9 $ 90.9 SOURCE: Correa.39 TABLE V-12 ESTIMATED LOST EARNINGS DUB TO CANCER IN LOUISIANA. 1977 (in Millions of Dollars) Site Digestive Organs Respiratory Organs Breast Female Genital Organs Other Genitourinary Organs Lymphatic and Hematopoietic Tissues Other and Unspecified Sites TOTAL Loss $ 77.9 111.2 39.2 21.7 21.8 45.1 93.5 $410.4 SOURCE: Correa.39 135 The total medical care expenditures for cancer in Louisiana were estimated to be $176 million dollars for 1980 (direct cost). The total loss of earning resulting from cancer in Louisiana was estimated at over $410 million dollars for 1977. Cancer of the respiratory system resulted in the highest total earnings loss in Louisiana in 1977, followed by the digestive organs, lymphatic tissue and hematopoietic tissue.^ (See Tables V-ll and V-12.) PREVENTION The complex, multifactorial causes of cancer (for discussion of multifactorial processes, see Section I) smoking, diet, environmental contaminants, occupational exposure to carcinogens, therapeutic and diagnostic agents, ultraviolet radiation, etc.-preclude a simple cancer prevention program. An overall cancer prevention program must be multidisciplinary in approach and needs to include: (1) further identification of agents and factors responsible for cancer, (2) removal or reduction of carcinogenic agents and factors from the environment, and (3) change in personal habits through education in order to lower cancer risk. Steps 1 and 2 are preventative measures within the scope of governmental responsibility. Risk identification and reduction require state and federal funding and legislation to insure that exposure to ambient environmental and occupational carcinogens is kept to a minimum. The risk-benefit assessments on which such policies are based should protect the overall interests and welfare of the general public. It has been recommended that a state or community cancer prevention plan should ensure that exposures are controlled where substitutes are not available for essential chemicals and should be based on the grounds that modern society can act coopera tively and not as warring factions. Exposures of this nature are not within the individual's range of controllable risk factors. PERSONAL CANCER PREVENTION PLAN Many risk factors for cancer are, however, directly related to an individual's lifestyle and personal habits, and, to a large measure, these risks are avoidable. The estimates of the relative role of various risk factors in cancer causa ion are a matter of debate. Figure 1.5 gives two different estimates of the relative magnitude of risk factors such as smoking, diet and nutrition, occupation and environment, heredity, as a percent of all cancer deaths. The range of estimates for risk factors which are c: ^ S ao Lryjr.~ 136 URL 04639 4o~ o KEY: c o Continuing smokers Ex-smokers o ft> Non-smokers 0> o o0) Q Number of years FIG. 5.5 PREVENTION POTENTIAL FOR LUNG CANCER RATES BY CESSATION OF SMOKING. SOURCE: Cairns J. Cancer: Science and Society. San Francisco, CA: W. H. Freeman. 1978. 137 URL 04640 lifestyle-related falls within sixty and seventy percent. These estimates show that the individual can eliminate or reduce many cancer risks through lifestyle modification and development of a personal cancer prevention plan (Table V-13) which includes smoking cessation and dietary changes. The American Cancer Society states that cigarette smoking is responsible for one in every five cancer deaths in the United States. Doll and Peto (1981) estimate it to be responsible for as much as 30% of cancer deaths. Cigarette smoking, as previously mentioned, is linked to lung cancer, and cancer of the larynx, pharynx, oral cavity, esophagus, pancreas, and bladder. The prevention potential from smoking cessation is extremely great and is assisted by the fact that, unlike most carcinogens, damage from exposure to tobacco smoke appears to be reversible at early stages. (See Figure 5.5.) Local smoke cessation clinics and workshops by the American Cancer Society can help smokers give up their habit. TABLE V-13 PERSONAL CANCER PREVENTION PLAN Stop smoking Avoid excessive exposure to sun (use sunscreens where necessary) Avoid exposure to known carcinogens in food (such as those given in this report) Reduce consumption of fats and increase consumption of foods containing fiber Consume foods rich in beta-carotene (Vitamin A derivative), Vitamin C, and Vitamin E Reduce consumption of salt-cured, salt pickled, smoked, and charred foods Maintain a lifestyle that prevents obesity Avoid or attempt to control psychological stress Consume alcoholic beverages in moderation, if at all 01 SOURCE: Oppenheimer. i 138 URL 04641 State government has various options to promote smoking prevention. One is a higher tax on cigarettes. This has two effects; one is to reduce the amount of cigarette consumption among smokers, an effect that directly translates into lives saved. The second effect is to reduce the likelihood that young people will become regular smokers because of the increased need for financial resources that it places on them. Another option for state government to persue is the inclusion of health education courses in schools regarding tobacco use. The state could also limit tobacco advertising within the state or require a health message on all in-state tobacco advertising. This has been done by some local governments in other states. Studies, mentioned previously in this report, have linked certain dietary factors to an increased risk of cancer. A recently released report on diet, nutrition, and cancer issued by the National Research Council of the National Academy of Science (1982)38 suggests the following dietary guidelines: 1. Reduce the intake of fat to 30% of total dietary calories. This includes both saturated and unsaturated fats. 2. Increase the intake of fruits, vegetables, and whole grain cereal products in the daily diet. 3. Reduce the intake of food preserved by salt curing, salt-pickling, or smoking. 4. Minimize the intake of foods contaminated with carcinogens from any source. 5. Identify mutagens in food to expediate testing for their carcinogenicity and, where feasible and prudent, removal of the mutagens. 6. Consume alcoholic beverages in moderation, if at all. The ingestion of particular agents, such as Vitamins A (beta-carotene), C, E (tocopherol), and riboflavin, has been experimentally shown to act as a defense mechanism against cancer. See Table V-14 for a list of selected anticancer agents. Foods rich in Vitamin A (beta-carotene) are broccoli, carrots, greens, spinach, cantaloupe, and certain squashes (See Table V-15.) 139 URL 04642 TABLE V-14 CHEMOPREVEHTION OF CANCER: SOME EXPERIMENTAL RESULTS Anticancer agent Type of Inhibition Vitamin A and derivatives, beta-carotene Vitamin C Vitamin E Riboflavin, a factor of the Vitamin-B complex Inhibits chemically-induced carcinomas in a variety of laboratory animals and at a variety of anatomical sites. Dietary deficiency of Vitamin A enhances susceptibility to chemical carcinogenesis. Human population groups ingesting low levels of Vitamin A are at increased risk for developing lung and bladder cancers. Blocks nitrosamine formation Helps reduce level of mutagens in human intestine Inhibits chemically-induced liver cancers SOURCE: Oppenheimer.^1 Obesity is a risk factor in the development of cancers of the endometrium (mucus membrane lining of the uterus). In addition to cancer, obesity has been associated with numerous health problems, especially heart disease. Maintenance of a lifestyle that prevents excessive overweight is prudent. Avoiding excessive exposure to sunlight reduces an individual's risk of skin cancer, the most common of all cancers. Avoidance of unnecessary X-rays would reduce cancer risk; however, the benefit of most medical, diagnostic X-rays usually outweighs the risk. Finally, avoidance or control of stress possibly effects cancer risk reduction. Recent studies on mice subjected to controlled stressful conditions suggest that stress leads to destruction of important elements of the immune system. 140 Food TABLE V-15 BETA ~ CAROTENE IK FOODS Serving Size Acorn Squash Apricot (fresh) Broccoli But > nut squash Cantaloupe Carrots Collard greens Hubbard squash Peach Prunes Spinach, cooked Watermelon Zucchini 1 cup 1 1 cup 1 cup 1/2 1 raw 1 cup 1 cup 1 large ^ 1 cup 1 cup 1 cup 1 cup SOURCE: Center for Science in the Public Interest. Nutrition Action Carotene (micrograms) 1,722 1,734 2,320 7,872 5,544 4,758 8,892 5,904 1,218 ; 1,302 8,748 564 432 c uI-- ou 2OJ 141 URL 04644 References - PERSONAL ENVIRONMENT 1. Loomis TA. Essentials of Toxicology (3rd ed.) Philadelphia, PA.: Lea and Febiger. p 10-11, 19?^ " ** 2. Doll R and Peto R. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. Journal of National Cancer Institute 66:1192-1308, 1981. 3. Doull J, Klaassen CD, Amdur MO. Eds. Toxicology, The Basic Science of Poisons. MacMillan Publishing Co,, New York, 1980. 4. Weinhouse S. Opening Remarks: Workshop Conference on Nutrition in Cancer Causation and Prevention. Cancer Research 43:2391, 1983. 5. National Research Council, Assembly of Life Sciences, Committee on Diet, Nutrition and Cancer. Washington, D.C., National Academy Press. 1982. 6. Enstrom JE. Reassessment of the role of dietary fat in cancer etiology. Cancer Research 41:3722-3723, 1981. 7. Hill MJ. The role of unsaturated bile acids in the etiology of large bowel cancer. In: Hiatt JJ, Watson JD, Winsten JA, Eds. Origins of Human Cancer. Cold Springs Harbor, New York: Cold Springs Harbor Press, 1627-1640, 1977. 8. Ames BN. Dietary carcinogens and anticarcinogens. Science 221:1256-1264, 1983. 9. Langham RA. Presentation to the Governor's Task Force on Environmental Health, New Orleans, LA., September 13, 1983. 10. Steelman VP. The Cultural Context of Food. A Study of Food Habits and their Social Significance in Selected Areas of Louisiana. Bulletin No. 681: Louisiana State University, Center forAgriculturalTSciences and Rural Development. 1974. 11. Lopez A. Presentation to the Governor's Task Force on Environmental Health. New Orleans, LA., September 13, 1983. 12. Correa P, Pickle L, Fontham E, Dalager N, Lin Y, Haenszel W, Johnson WD, The causes of lung cancer in Louisiana. Presentation to the Governor's Task Force on Environmental Health. New Orleans, LA., September 13, 1983. 13. Gori GB. Dietary and nutritional implications in the multifactorial etiology of certain prevalent human cancers. Cancer 43:2151-2162, 1979. 14. Sugimura T, NagaoM, Kawachi T, Honda M, Yahagi T, Seino Y, Sato S, Matsukura N, Matsushima T, Shirai A, Sawamura M, Matsumoto H. Mutagen-carcinogens in food with special reference to highly mutagenic pyrolytic products in broiled foods. Hiatt JJ, Watson JD, Winsten JA^Eds. In: Origins of Human Cancer. Cold Harbor Springs, New York. Cold Harbor Springs Press, p. 1561-1578, 1977. 142 URL 0464 15. Lijinsky W, Taylor HW. Nitrosamines and their precursors in food. Hiatt JJ, Watson JD, Winsten JA, Eds. Ins Origins of Human Cancer. Cold Harbor Springs, New York. Cold Harbor Springs Press, p. 1579-1590, 1977. 16. Howe GR, Burch JD, Miller AB, et al. Artificial sweeteners and human bladder cancer. Lancet 2:578-581, 1977. 17. Kessler II, Clark JP. Saccharin, cyclamate and human bladder cancer. No evidence of an association. Journal American Medical Association 240:349-355, 1978. 18. Hoover R et al. Progress report to the Food and Drug Administration from the National Cancer Institute concerning the national bladder cancer study. Lancet 1:837-840, 1980. 19. Moorison AS, Buring JE. Artificial sweeteners and cancer of the lower urinary tract. New England Journal of Medicine 302:537-541, 1980. 20. Wynder EL, Stellman SD. Artificial sweetener use and bladder cancer. Science 207:1214-1216, 1980. 21. Oppenheimer SB. Prevention of Cancer. American Laboratory 71:66-72, February, 1983. 22. Spengler JD, Sexton K. Indoor Air Pollution: A Public Health Perspective. Science Vol. 221, No. 4605:9-116, July, 1983. 23. Kirsch LS. Behind Closed Doors: The Problem of Indoor Pollutants. Environment Vol. 25, No. 2:17-42, 1983. 24. Forrestal G. Estrogen Hurting, Coricoid Healthy. Chemical Week, p. 23, November 23, 1977. 25. Council on Environmental Quality. Environmental Quality - 1979. U. S. Government Printing Office, 1980. 26. Epstein SS. The Politics of Cancer. Garden City, New York: Anchor Press, Doubleday, 1979. 27. Tuyns AJ, Peguignot G, Abbatucci JS. Oesophageal cancer and alcohol consumption: Importance of type of beverage. International Journal of Cancer 23:443-447, 1979. 28. Swann PF. Metabolism of nitrosamines: Observations on the effect of alcohol on nitrosamine metabolism and on human cancer. Magee, PN., Ed. In: Nitrosamines and Human Cancer. Banbury Report No. 12 Cold Springs Harbor, New York. Cold Springs Harbor Press, p. 53-68, 1982. 29. Correa P, Johnson WD. Cancer and lifestyle in Louisiana. Journal Louisiana State Medical Society p. 4-6, March 1983. 30. U.S. Department of Health and Welfare. Smoking and Health <2 vols.) HEW Public Health Service Publication No. 1103 (vol. l) 1964 and No. 79-50066, 1979. Washington, D.C.: U. S. Government Printing Office. 143 31. American Cancer Society. Cancer Facts and Figures, 1982. New York, New York, 1982. 32. Blot WD, Fraumeni JF Jr. Changing patterns of lung cancer in the United States American Journal of Epidemiology 115:664-673, 1982. 33. Stock SL. Risks the passive smoker runs. Lancet 2:1082, 1980. 34. MacMahon B, Cole P, Brown J. Etiology of breast cancer, a review: Journal of National Cancer Institute 50:21-42, 1973. 35. Hartunian NS, Smart CN, Thompson MS. The Incidence and Economic Costs of Major Health Impairment. Lexington Books, 1981. 36. U. S. Department of Health, Education, and Welfare. Disease Prevention and Health Promotion: Federal Programs and Prospects, Report of the Departmental Task Force on Prevention. Department of Health, Education, and Welfare (PHS) Pub. No. 79-55071 B. 1978. 37. Higginson J. "A hazardous society? Individual versus community responsibility in cancer prevention." American Journal of Public Health. Vol. 66:4, 359-366. 1976. 38. . National Research Council. Diet, Nutrition, and Cancer. Washington, D.C., National Academy Press, 1982. 39. Correa P, Chen VW, Craig JF, Ballinger T, Campbell W, Zavala D. Cancer in Louisiana: Louisiana Tumor Register, New Orleans, LA: Office of Health Services and Environmental Quality, Louisiana Department of Health and Human Resources, 1983. 40. Surgeon General's Office. The Health Consequences of Smoking: Cancer. U. S. Department of Health and Human Resources. Office on Smoking and Health. Washington, D.C.: Government Printing Office, 1982. c: ? g g co URL 04647 VI. CANCER RATES AND RISK FACTORS IN LOUISIANA INTRODUCTION Louisiana has unusually high rates for certain types of cancer. Cancer is one of the most serious health problems in the state. In 1983, an estimated 7,600 persons will die of cancer and another 14,800 persons will be diagnosed with the disease. Approximately 30% of all Louisianians will have cancer in their lifetimes.1 To understand the cause{s) or etiology of cancer, risk factors for cancer in Louisiana have been identified by epidemiologists and cancer researchers. The risk factors that have been identified and studied to date are: tobacco smoking, nutrition, occupation, climatic - geographic conditions, ethnic considerations, and environmental pollution. This section of the report will focus on Louisiana's cancer rates and associated risk factors. LOUISIANA CANCER RATES Cancer Excess An excess of mortality from cancer has been observed in Louisiana compared to national mortality figures or to other southern states. 1'2 As far back as 1930, national mortality statistics showed an excess of cancer in Louisiana. Cancer incidence was first measured in Louisiana in 1947. New Orleans was one of the cities that participated in a ten-metropolitan area cancer incidence survey 144 of 1947. The study found the incidence of cancer in New Orleans exceeded the other nine cities for cancers of all sites. Of particular concern were cancers of: the oral cavity and stomach in non-white males; liver, pancreas and prostate in white males; larynx, lung and bronchus in all males; breast, uterine cervix and corpus in white females; kidney in whites; bladder in all but non-white males; skin and brain in females; and lymphomas (See Table VI-1). Cancer incidence rates reflect exposure from 10 to 20 years earlier and are reported as new cases per year per 100,000 population. Mortality rates impose the additional time period of survival following detection and therefore reflect prior exposure from 20 to 30 years. The exposure period of interest for the purposes of this study, 1940-60, follows the control of major infectious diseases, and coincides with the new chemical industrialization. This exposure period reflects incidence rates of the 1950s and 1960s and mortality rates in the 1960s and 1970s. Typhoid fever was controlled in the 1930s and 1940s; malaria and yellow fever were controlled by insecticides controlling insect populations; tuberculosis began its decline in the 1940s and declined even further with specific pharmacologic therapy in the 1950s. Polio was brought under control as recently as the late 1950s. There was no comparable cancer morbidity data for the rest of Louisiana in the 1930s and 1940s. The National Cancer Institute's compilation of Cancer Mortality Rates for U.S. Counties 1950-69 was the first time relatively small geographic areas could be studied with sufficient statistical stability for confidence. These data reflect mortality from an exposure time (accounting for a survival of ten years following diagnosis) comparable to that used in the 1947 incidence survey. Louisiana was again noted to rank higher for several cancer sites and for several parishes. See Table Vl-2 for comparison with the 1947 incidence rates. The availability of the average annual 20-year cancer mortality rates for all parishes in Louisiana was of importance. The parishes in the southern part of Louisiana reflect mortality rates for several cancers that are higher than elsewhere in the United States.1 The age-adjusted (U.S. 1960 standard) lung cancer mortality rate (1950-69) in Louisiana of 51.97 per 100,000 white men was 37% above the national average of 37.98 per 100,000. Over 3,000 counties in the United States were studied. Thirteen of the 31 counties with the highest lung cancer mortality rates were for white men in Louisiana. Thirty-eight of the 64 Louisiana parishes (counties) were in the upper 10% of the counties for lung cancer deaths among white men. 145 TABLE VI-1 CANCER INCIDENCE RATES 1947 All Sites Oral cavity Stomach Liver Pancreas Larynx Lung & bronchus Breast Cervix uteri Corpus uteri All cities South New Orleans All cities South New Orleans All cities South New Orleans All cities South New Orleans All cities South New Orleans All cities South New Orleans All cities South New Orleans All cities South New Orleans AU cities South New Orleans All cities South New Orleans AH Persona 328.0 370.7 410.7 12.8 14.7 15.3 26.4 20.7 30.5 4.6 4.5 6.2 7.4 7.4 8.1 3.9 4.2 8.1 17.6 16.0 22.0 36.9 35.0 45.5 18.9 28.9 32.9 5.2 6.7 8.5 White Male 338.3 426.2 485.5 21.1 26.5 30.2 34.1 23.0 37.8 4.9 4.9 6.5 9.3 11.4 13.3 7.6 8.1 19.0 29.5 30.3 45.1 O.'S 0.5 0.6 Non-White Male White Female Non-White Female 252.6 221.3 280.0 10.9 10.2 13.5 39.6 37.6 58.4 5.3 6.1 13.0 11.6 9.5 9.1 5.7 7.6 14.1 25.4 19.3 41.9 0.2 0 0 333.4 395.6 442.5 6.3 9.4 8.9 18.3 13.6 17.5 4.2 3.0 4.6 5.5 4.9 5.3 0.6 0.9 1.0 6.5 5.B 4.7 72.6 70.7 94.8 32.8 48.6 57.4 10.3 12.1 16.0 293.0 277.8 310.7 5.3 5.4 9.3 22.8 20.3 31.7 2.7 3.3 3.7 6.4 3.7 4.7 0.6 0.6 1.1 5.8 3.7 2.5 53.9 51.9 49.5 70.4 74.9 72.2 URL 04649 TABLE VI-1 continued on next page TABLE VI-1 (continued) CANCER INCIDENCE RATES 1947 Prostate Kidney Bladder Skin Brain Lymphoma AU cities South New Orleans All cities South New Orleans AU cities South New Orleans AU cities South New Orleans AU cities South New Orleans AU cities South New Orleans An PeraoM 16.3 18.6 18.8 4.2 4.3 5.1 12.5 11.5 21.2 43.1 89.2 68.9 %.6 5.7 4. S 9.0 9.0 11.7 White Mite Non-White Mite White Female Non-White Female 5.6 6.4 7.5 18.6 17.8 34.6 56.1 143.3 122.4 5.9 7.6 5.2 10.8 11.7 13.2 3.1 3.0 3.1 1.8 4.3 2.5 8.0 9.1 17.6 7.9 8.0 14.6 39.5 88.0 65.3 3.1 3.8 2.2 5.7 1.2 4.9 6.0 8.5 9.7 2.7 3.4 3.2 9.3 7.5 9.4 7.1 6.5 13.7 6.7 7.1 8.5 SOURCE: Dorn.3 NOTE: Age-adjusted incidence per 100,000 population in a ten-metropolitan area cancer incidence survey. URL 04650 i 147 TABLE VI-2 CANCER MORTALITY RATES 1950-1969 Site Stomach Liver and biliary passages Pancreas Larynx Trachea: bronchus Breast Cervix Uteri Corpus Uteri Other parts of Uterus Kidney Bladder & Urinary Brain & CNS Lymphoma White Males Won-White Males Wo. Rate Wo. Bate La. 2,206 13.35 2,380 31.29 US 222,524 15.22 33,606 24.03 White Females Won-White Females Wo. Rate Wo. Rate 1,334 6.50 137,254 7.70 1,161 13.53 16,725 10.69 La. 1,003 US 76,070 5.94 543 7.23 5.16 10,021 6.91 811 3.96 94,229 5.34 363 4.20 7,261 4.59 La. 1,985 US 142,333 11.77 9.63 734 9.85 14,416 10.17 1,226 102,899 6.00 5.83 484 5.68 9,650 6.17 La. 592 US 37,954 La. 9,191 US 571,226 3.44 2.54 51.97 37.98 192 2.57 3,898 2.67 2,885 38.46 53,910 36.67 60 4,141 1,438 108,326 0.29 0.24 6.97 6.29 29 607 526 10,222 0.34 0.37 6.13 6.27 La. 37 0.22 US 4,131 0.28 25 0.34 4,454 21.45 527 0.37 436,618 25.51 1,878 21.81 36,926 22.10 La. 1,589 7.62 1,652 19.12 US 131,240 7.79 32,329 18.92 La. 1,079 5.24 1,066 12.34 US 106,455 6.13 32,329 11.30 La. 614 US 57,780 La. 1,138 US 98,304 La. 843 US 67,751 La. 833 US 73,475 3.43 3.86 7.12 6.78 4.22 4.42 4.46 4.89 179 4,072 430 7,001 174 4,154 221 5,277 2.28 2.76 5.80 5.05 2.04 2.34 2.80 3.38 429 34,204 490 43,095 498 47,192 572 55,658 2.08 1.99 2.39 2.39 2.33 2.91 2.76 3.25 118 2,429 331 4,758 127 3,022 170 3,283 1.29 1.42 3.85 3.05 1.29 1.54 1.87 1.91 2 SOURCE: Mason. NOTE: Age-adjusted per 100,000 population malignant neoplasms URL 04651 148 URL 04652 o The Atlas of Cancer Mortality of U.S. Counties, 1950-69, contains maps of total cancer mortality and lung cancer for white males; and all cancers for non-white males for 1950-54 (Figure 6.1). These maps show that the parishes with high lung cancer mortality rates are aggregated along the Mississippi River and in the southern part of the state. The map for lung cancer mortality 1970-79 shows that high concentrations of lung cancer mortality for white males has shifted from the northeast down to the southeast (See Figure 6.2).** Mortality statistics in recent decades have consistently shown. "excessive" (higher than expected) rates in Louisiana for several cancer sites . Recent data have shown excessive rates for oral cavity and pharynx, esophagus, stomach, and lung, as seen in Table VI-3. For white males the incidence rate for cancer of the mouth in New Orleans is 38% higher than the SEER Program rates which are used as the national incidence rates (23.2 vs. 16.8) in the Surveillance, Epidemiology and End Results (SEER) program of the National Cancer Institute.5 However, the mortality rate for mouth cancer is 169% higher in Louisiana than in the United States (7,0 vs. 2.6). To interpret this discrepancy the comparative accuracy of incidence and mortality rates for the United States and Louisiana need to be examined as do the comparability of access to medical care systems in Louisiana versus the rest of the nation. The Louisiana Tumor Registry has been collecting population-based incidence cases of cancer for Orleans, Jefferson and St. Bernard parishes since 1974. It has been estimated that there is greater than 95% case ''ascertainment" by this program, making the data very accurate and useful. Although the geographic area of data collection is limited, observations on incidence for one area, if consistent with mortality data and other observations, can serve to reinforce the credibility of mortality data for the other areas where incidence data is not readily available. To obtain population-based incidence data is an expensive undertaking. The SEER Program For 1974-78, the national average annual age-adjusted incidence rates of malignant neoplasms for New Orleans was 349.7 per 100,000 population compared to 331.5 per 100,000 for the SEER (Surveillance, Epidemiology and End Results-National Cancer Institute) program. (See Table VI-4.) SEER represents a 10% cross-section of the population of the United States.5 An individual from New Orleans has a 33.1% lifetime (age 0-74 years) likelihood of developing cancer compared with a 30.8% likelihood for an individual from the SEER area elsewhere. The most striking comparison is seen for white males, who have 435.8 per 100,000 cancer 149 WHITE MALES BBUi Significantly High; in highest decile :iijiiilii In Highest Decile; not significant No Signiheant Difference from U. S. Average Significantly Lower than U.S. Average la n Significantly High; in highest decile Significantly Highs not in highest decile In Highest Decile; not significant F / / A No Significant Difference from U.S. Average I ~ I Significantly Lower than U.S. Average FIG. 6.1 U.S. CANCER MORTALITY RATES FOR MALES BY RACE: 1950-1969. SOURCE: Mason et al,2 p. 42. 150 KEY: Highest 10% Higher thi U.S. Average Same as United States Averoge Lower than U.S. Averoge Lowest 10% KEY: Highest 10% Hiqher than U.S. Averoge Same as United States Averoge Lower than U.S. Average Lowest 10% FIG. 6.2 GEOGRAPHIC SHIFT IN LUNG CANCER MORTALITY RATES. SOURCE: Correa et al,4 p. 88-89. 151 URL 04655 TABLE VI-3 CANCER MORTALITY RATES IN THE UNITED STATES (1968-77) AND LOUISIANA STATE (1968-78) Primary Site All Sites U.S. La, Buccal Cavity and Pharynx U.S. La. Esophagus U.S. La. Stomach U.S. La. Colon U.S. La. Rectum U.S. La. Liver and Biliary Ducts U.S. La. Pancreas U.S. La. Larynx U.S. La. Trachea, Bronchus and Lung U.S. La. Malignant Melanoma U.S. La. Breast U.S. La. Uterine Cervix U.S. La. Uterine Corpus U.S. La. White Male 901 .0 219.8 2.6 7.0 4.3 4.1 9.6 8.1 19.5 16.3 6.2 4.6 3.2 2.9 11.0 12.6 2.8 3.0 61.2 78.6 2.2 2.1 __ -- __ -- __ -- White Female Non-White Non-White Male Female 131.0 125,4 239.7 248.8 143.8 147.6 0.7 3.9 2.0 8.3 1.0 2.6 1.4 12.7 1.0 10.3 3.2 2.6 4.7 17.7 4.0 20.6 7.8 9.7 16.4 14.0 16.5 14.0 15.7 13.6 3.6 5.5 2.7 4.9 3.7 4.0 3.0 4.8 1.9 2.8 2.7 1.7 6.7 12.7 7.5 12.3 8.0 6.7 0.3 3.8 0.4 3.9 0.5 0.5 13.4 15.5 68.7 73.0 13.4 13.9 1.4 1.4 26.9 23.6 4.6 4.1 1.8 1.0 0.6 0.6 __ -- __ -- __ -- 0.3 0.3 24.4 24.0 12.1 13.0 2.5 2.2 Table VI-3 continued on next page 152 TABLE VI-3 (continued) CANCER MORTALITY RATES IN THE UNITED STATES (1968-77) AND LOUISIANA STATE (1968-78) Primary Site White Male White Non-White Non-White Female Male Female Prostate Kidney, Pelvis and Ureter Bladder and Other Urinary Organs Brains and Central Nervous System Thyroid Multiple Myeloma Lymphoma Leukemia U.S. La. U.S. La. U.S. La. U.S. La. U.S. La. U.S. La. U.S. La. U.S. La. 19.9 19.4 4.6 4.3 7.4 6.8 5.0 4.8 O.*' 0.3 2.6 2.5 7.8 7.1 9.1 9.7 -- -- 2.1 2.1 2.2 2.2 3.4 3.1 0.5 0.5 1.8 1.7 5.2 5.0 5.5 6.0 35.1 35.7 3.4 3,1 5.7 5.5 2.8 2.9 0.4 0.5 4.7 4.1 5.4 4.8 6.8 7.7 -- -- 1.6 1.1 3.0 3.2 1.9 1.8 0.6 0.6 3.2 3.1 3.1 2.5 4.4 5.1 SOURCE: Correa4 NOTE: Average age-adjusted (US 1970) mortality rates per 100,000 population. URL 04656 153 URL 04657 TABLE VI-4 CANCER INCIDENCE RATES IN ALL SEER AREAS (1973-77) AND METROPOLITAN NEW ORLEANS (1974-78) Primary Site All Sites SEER N.O. Buccal Cavity and Pharynx SEER N.O. Esophagus SEER N.O. Stomach SEER N.O. Colon SEER N.O. Rectum and Anal Canal SEER N.O. Liver and Biliary Ducts SEER N.O. Pancreas SEER N.O. Larynx SEER N.O. Trachea, Bronchus and Lung SEER N.O. Malignant Melanoma SEER N.O. Breast SEER N.O. Cervix SEER N.O. Uterine Corpus SEER N.O. White Male White Next-White Non-White Female Male Female 371.6 437.6 301.2 284.7 454.3 488.7 288.7 298.5 16.8 23.2 6.0 19.3 6.8 24.5 7.0 7.1 4.8 '.6 16.9 4.5 5.1 i.8 16.8 3.3 12.7 10.0 36.7 38 6 <y 5.6 5.2 31.0 27.3 22.4 27.4 36.3 31.3 9.9 12.6 30.6 33.0 19.6 21.3 12.2 10.6 14,0 19,1 11.4 12.3 5.2 4.1 7.4 4.1 5.7 3.6 9.2 5.0 11.9 13.0 7.7 17.5 9.3 18.7 11.9 9.4 8.3 11.3 1.3 12.1 2.0 14.1 1.9 2.3 77.5 112.5 22.1 29.0 110.7 129.0 24.6 28.1 6.7 6.0 0.6 0.7 8.3 5.7 0.8 0.4 0.8 85.6 1.4 72.0 1.0 79.3 1.2 70.6 __ 10.9 __ 25.7 -- 10.5 -- 26.0 __ 29.9 -- 14.6 -- 13.0 -- 13.6 Table VI-4 continued on next page 154 TABLE VI-4 (continued) CANCER. INCIDENCE RATES IN ALL SEER AREAS (1973-77) AND METROPOLITAN NEW ORLEANS (1974-78) Primary Site White Male White Female Non-White Non-White Male Female Prostate Kidney, Pelvis and Ureter Bladder and Other Urinary Organs Brain and Central Nervous System Thyroid Multiple Myeloma Lymphomas Leukemias SEER N.O. SEER N.O. SEER N.O. SEER N.O. SEER N.O. SEER N.O. SEER N.O. SEER N.O. 66.2 57.6 10.2 12.5 27.4 32.3 6.7 6.7 2.4 3.1 4.3 3.8 14.3 16.3 13.0 12.3 -- 4.8 6.0 7.3 9.0 4.6 4.7 5.3 5.9 3.0 2.8 10.7 11.4 7.7 6.6 108.9 105.7 8.7 8.4 14.0 13.1 4.2 3,8 1.3 1.2 9.6 8.8 10.3 10.8 11.1 10.4 '-- 4.6 4.0 6.0 5.3 2.7 3.9 4.0 3.2 6.7 7.7 5.8 7.6 6.8 6.5 URL 04653 SOURCE: Correa P,4 p. 139. NOTE: Average annual age-adjusted (U.S. 1970) incidence rates per 100.000 population. i 155 URL 04659 incidence for New Orleans compared with 371.6 per 100,000 for the SEER program areas (or 17% higher than the combined SEER areas which include New Orleans) and a 40.1% lifetime cancer risk compared to a 33.4% lifetime risk for the areas contributing to the SEER program. For white females, New Orleans residents have a lower cancer incidence than white females in the other SEER areas. New Orleans residents also have lower incidence rates than other SEER cities residents for cancers of the breast and uterine corpus, and prostate. For cancers of the trachea, bronchus and lung, buccal cavity and pharynx and larynx, New Orleans residents have a higher incidence than the other SEER areas combined for all four race/sex groups; for cancer of the kidney, ureter, bladder and urinary organs for males; for rectum, anoreetum and liver for males and non-white females; for pancreas for males and white females; and for stomach among non-white males and females (Table Vl-4).^ Changes in Cancer Over Time Patterns of cancer occurrence have changed in Louisiana. The best data to use to analyze occurrence patterns would be incidence data. Incidence data are only available on a population basis for the New Orleans area. However, for certain cancer sites mortality data approximates incidence data because of short survival following diagnosis. These cancer sites include lung, bronchus and trachea, pancreas, and liver, all of which are of concern to Louisiana. Figure 6.3 shows tendencies for the most common tumors. Mortality from cancer of the trachea, bronchus and lung has increased an ageadjusted average of 396 a year between 1968 and 1978 for all sex and racial groups and was greatest among females (white females 6.27% and non-white females 9.24% per year). In white females lung cancer has surpassed all other cancers as a cause of death since 1980. For cancer of the pancreas, the greatest increase was noted in white females, who experienced an average increase of deaths of 2.04% per year from 1908 to 1978. Also notable is an average annual increase of 5.19% for white males in age-adjusted (to 1940) mortality rates for cancer of the liver from 1968 to 1978. Small numbers and e diagnostic difficulties make data for liver and pancreas cancers somewhat unreliable. There appeared to be a decrease in average annual age-adjusted mortality for cancer of the urinary bladder. This was almost completely attributable to the 156 Death Rate per 100,000 90 white males 0 H_____,------------- ------------------------ ------- --------- 1960 1970 Year 1990 Lung Breast Colon Pancreas Stomach Cervix Death Rate per 100,000 Year 0 1960 1970 Year FIG. 6.3 CHANGING PATTERNS OF CANCER OCCURRENCE. Louisiana Age-Adjusted (U.S. 1970) Cancer Mortality Rates. SOURCE: Correa etal,4 p. 38-41. 1980 157 / URL 04661 observation for non-white females. However, age-adjusted average annual mortality rates for cancer of the kidney increased overall by 2.9396 per year from 1968 to 1978, and for all groups other than non-white females (white males, 3.18%; white females, g 3.22%; and in non-white males, 6.72%). There is a clear excess of oral cavity cancer deaths in Louisiana (1968-78) for all sex-race categories. Stomach cancer mortality rates for non-whites in Louisiana (1968-78) are well above the U.S. average, while slightly lower in Louisiana whites. Other sites with increasing age-adjusted average annual mortality rates are as follows: cancer of the pharynx in non-whites; rectal cancer for non-white females; esophagus in all but non-white females; thyroid cancer in non-whites; retroperitoneum and peri toneum in males; brain tumors for white males and myelogenous leukemia in all but ig non-white males. CANCER RISK FACTORS IN LOUISIANA Epidemiological studies have determined major geographic differences in cancer distribution in the United States (and the world), confirming the influences which varying modes of lifestyle (food, occupation, smoking habits of a particular population) and environmental conditions have on this disease. The National Cancer Institute's Atlas of Cancer Mortality of U.S. Counties shows variances within the o United States. The existence of differences in cancer mortality and incidence within a county or state, between occupational and ethnic groups, and over time may reflect differences in the nature and/or degree of exposure to environmental carcinogens y (including personal environmental factors such as smoking and diet). Epidemiological studies of cancer in Louisiana have examined correlations of risk factors and rates in Louisiana populations, and have performed case-control studies (See Glossary). Correlation between cancer frequency and factors in the environment or the host which may be related to a particular cancer constitute a first attempt to study the causes of cancer. Case-control studies, some based on death certificates and some on direct interviews with patients or their next of kin, provided additional information on the significance of cancer risk factors. These studies are described in detail below. 158 t/R L 0 4 0 6 2 Smoking Correlations between lung cancer rates and cigarette sales as measured by tax revenues have been attempted but are considered unreliable because of insufficient information on cigarette sales. Studies based on the incident cases of lung cancer and personal interviews have been conducted in Louisiana. One study reported cigarette smoking as the major Q cause of the disease (90% for males, 75% for females). This study also reported increased risk associated with passive smoking (See Glossary). Non-smoking women married to heavy smokers had an increased risk. Maternal (but not paternal) smoking increased the lung cancer risk of the offspring. Risk for cigarette smoking was noted to decrease for exposed individuals whose diets contained significant quantities of o fruits and vegetables. From these and other studies it appears that cigarette smoking may be the single most important and clearly demonstrated cause of lung cancer; however, there appear to be other factors contributing to the observed mortality. A discussion of these factors fellows. : Nutrition A national nutrition survey reported low levels of Vitamin A in Louisiana diets. A negative correlation between lung cancer and beta-carotene (a precursor of Vitamin Q A) intake has been reported in Louisiana. For further discussion of dietary habits in Louisiana and nutrition see discussion in Section V. Occupation Certain occupations manifest excessive risks of cancer and several of these are important in Louisiana. (See Table IV-1 in Section IV.) Studies by the National Cancer Institute, using aggregate data, demonstrated positive associations between the percent of the parish population employed in petroleum, chemical, paper and transportation industries and lung cancer mortality.10 The excessive risk of lung cancer found among petroleum workers in rural areas is particularly significant.11 A study of lung cancer deaths compared to non-cancer deaths among people employed in petroleum mining in Louisiana (1960-1975) revealed that workers employed as welders, operators, boilermakers, painters, and oilfield workers had a greater risk of lung cancer.1^ 159 99ki ian 10% of orea covered by standing water age-adjusted mortality significantly high. FIG. 6.4 CORRELATION OF RESPIRATORY CANCER AND WETLAND RESIDENCY. SOURCE: Voors et al.19 Climatic-Geographic Conditions A positive correlation has been reported between age-adjusted respiratory cancer mortality rates and wetland residency for men.19 (See Figure 6.4.) Analogous associations of respiratory cancer and wetland residency have been found elsewhere in the United States. (See Figure 6.5.) The observed association between cancer mortality and wetland residency is confined to men. Since men smoke much more than women, this suggests a wetlands-associated substance promotes respiratory cancer in smokers. The authors hypothesized the association was due to one or more of the following: (1) a mycotoxin in the wetland, 160 *99^ (2) industrial and agricultural activities in wetlands which may cause pol lution of the water resulting from halogenated hydrocarbons which act as tumor promotors in the respiratory tract, (3) inhaled asbestos, (4) peaty water-logged soils which may promote nitrosamine formation in locally grown foods, (5) unknown carcinogenic arbovirus transmitted by swamp insects (no known precedent), (6) high humidity of the air increasing the amount of moisture in the lung, and thus acting as a solvent for carcinogens. Ethnic Considerations Louisiana has a culturally diverse population including groups who have main tained some degree of cultural isolation. (See Figure 6.6.) The northern part of the state reflects the basic character of the states that surround it: a southern culture, largely agricultural, and predominantly Protestant. The southern half of the state, particularly the mid-south, was largely settled in the eighteenth century by the Catholic French settlers who were called Acadians, namely those displaced from Nova Scotia. A study based on death certificates of 19 parishes in north and south Louisiana reported the industry of occupation in males who died of lung cancer from 1960 through 1975, and compared these deaths to deaths from other causes. Significantly more of those deaths from lung cancer reported primary employment in transportation equipment manufacturing industries (shipbuilders), the fishing industry, and auto repair. Also increased, but not as significant, were rates for those employed in crude oil extraction, oil refining and metal machinery manufacturing industries. 13 Shipbuilders had a significantly increased risk (greater than two-fold) of dying of lung cancer. Seamen and longshoremen also had increased risks of lung cancer death. The increased risk may be partly due to asbestos exposure, which is an accepted causal factor in lung cancer. During the early 1940s many men in southern 161 URL 04665 CANCERS OF LUNG BRONCHUS AND TRACHEA Quortiles 1950-1969 FIG. 6.5 WETLANDS AND RESPIRATORY CANCER MORTALITY IN LOUISIANA. SOURCE: Voors et al.19 162 i Louisiana were involved in shipbuilding. They were likely to have been heavily exposed to asbestos fibers. There were asbestos manufacturing plants in New Orleans until very recently* this provided another source of exposure. Many of the large pipes used in petrochemical plants are asbestos-lined. 14 Work based on death certificate studies and next-of-kin interviews found elevated risks for lung cancer and mesotheliomas for people employed in sugar cane farming.15 They hypothesized that burning the cane after harvesting causes lung irritation which could increase susceptibility to other carcinogens. It was also hypothesized that exposure to specific carcinogenic herbicides and pesticides may increase cane workers' risks. A possible association with low socioeconomic level and limited access to health care was also hypothesized. ^ i 999W IHn FIG. 6.6 CULTURAL REGIONS OF LOUISIANA. SOURCE: Gottlieb and Pickle.16 163 Urinary bladder cancer has excessive mortality rates in southern Louisiana. A case-control study based on death certificate analysis showed oil refinery workers more frequent in cases than in control groups. Transport equipment operators, auto mechanics, and young farmers showed some increased risk of bladder cancer. White farmers in certain southern parishes had increased risks ranging from three- to six- fold. Individuals employed in chemical plants and petrochemical operations as operating engineers in Louisiana and Texas have been shown to have an excess risk of brain tumors. This risk is largely associated with employment in three large facilities in these two states. 17 High pancreatic cancer mortality rates for white males in certain Louisiana parishes were investigated. A two-fold increased risk was found for workers in oil refining and paper manufacturing industries. 16 Of special interest is the contrast between inhabitants of high cancer risk areas in the industrialized south and low cancer risk areas in the rural north. (Note: several parishes in North Louisiana do have high cancer mortality). The northern part of the state is dominated by the Protestant Puritanic culture while the south is dominated by the "joie de vivre" so typical of the Cajun culture. A recent survey showed that, compared to the north part of the state, South Louisianians have less formal education but have a higher income, start smoking earlier, smoke more, more frequently use non- filter, high-tar cigarettes, drink alcoholic beverages more frequently, and work more frequently in oil, petrochemical, fishing and shipbuilding jobs.* In a 1979 study by Gottlieb et al., Acadian ancestry was associated with a higher risk of lung cancer among older men and women, but this was not true for young Acadians. Males of Acadian background demonstrated a two-fold risk of urinary bladder cancer which cannot be explained by industrial or occupational exposures. 16 Environmental Pollution Most of Louisiana is a flat lowland with abundant bodies of water from lakes, bayous and the Mississippi River. Originally the state had an agrarian economy until the industrial revolution occured in the South during the last 50-70 years. The Mississippi River serves major industries and receives industrial and agricultural wastes from the heartland of the United States. Establishment and expansion of the petrochemical industry created a need to locate new refineries and processing plants 164 V along the Mississippi River. Today, Louisiana has one of the world's largest concentrations of petrochemical industries, primarily along the Mississippi River from Baton Rouge to New Orleans which is known as the industrial corridor. Industrialization in Louisiana was not accompanied by regulations to create appropriate discharge facilities for the industrial wastes. The most convenient choice for industrial waste disposal was the rapidly flowing river or on land not contemplated for building purposes because it was too wet. These wetland waste disposal sites could readily flood and the discharge would flow into the river or into other waters which might be drinking water supply sources. In the past, pollution of the water by these wastes was not of great concern because the major health problems were still infectious diseases; typhoid fever, polio, tuberculosis and malaria. There was little scientific knowledge of the nature of the organic compounds being processed and produced, and less awareness or concern for potential health effects. Rivers and wetlands had previously provided satisfactory sites for disposal of wastes. There was no reason to think they could not continue this service to people. In general, people were not living long enough to see effedts of diseases requiring long latency periods for expression. Sanitary conditions and the standard of living improvements, and efforts to control typhoid fever and tuberculosis dominated public health policy. Malaria could be controlled through the use of residual insecticides. There was little concern about run-off into potable water supplies. To increase agricultural productivity of rice, cotton and sugar cane, herbicides, insecticides and rodenticides, all products of the new organic compound era, were a boon. Practices such as these in the past, have an effect on cancer rates today due to the latency period of cancer. Several studies relating ambient environmental pollution to cancer rates in Louisiana have been completed. A study using aggregate mortality data for parishes with populations taking their drinking water from the Mississippi River found an association with increased rates of gastrointestinal and genitourinary cancers. 20 Although the multivariate method of analysis controlled for variables such as industrialization, the observations were not completely accepted because socio cultural confounders which are known to have a significant association with gastrointestinal cancers were not introduced into the model. 21 In recent years several studies have examined the relationship of drinking water and cancer in Louisiana. The distribution of parishes having high mortality from lung cancer are mainly clustered along the Mississippi River. A study of 20 parishes from southern Louisiana which compared deaths from 17 sites of cancer to matched control 165 URL 04668 URL 04669 deaths noted a significant risk associated with lung cancer and surface water as a drinking water source reported at death. However, the excess risk was no longer noted when the data were examined in terms of estimated lifetime use of surface water as the drinking water source. This would imply a social class variable as a confounder. However, a consistent, significantly increased risk for rectal cancer mortality was noted for males and females having lifetime use of surface water as a drinking water source, and some increased risk was noted for kidney cancer. Moreover, the risk for rectal cancer mortality was noted to be independently associated with the chlorination level of the water. This also appeared to be associated with breast cancers. The effects of living in the vicinity of polluting industrial plants may play an Q important role m Louisiana lung cancer rates. A study of lung cancer deaths (196075) in residents of twenty parishes was compared to a control group matched for age, sex, year of death, and parish of residence. Residents living within one mile of petroleum and chemical industries had an increased risk of lung cancer compared with these residing within one to three miles of the site. For the petroleum industry, the risk was shown in the group with ten or more years of residential exposure. Residential risk was found to be independent of length of exposure for those living in proximity to the chemical industry and held true for people employed in low risk occupations. The results suggest that residential proximity to petrochemical OO industries may make a contribution to lung cancer mortality in Louisiana. CONCLUSION It must be emphasized that today's cancer rates reflect carcinogenic exposure of the previous 10 to 30 years. Any cancers produced by today's carcinogenic exposure (both life-style and environmentally related) will be detected years later. The elevated cancer rates of South Louisiana represent a complex problem not yet well understood. For some cancers, such as lung cancer, the problem is not the lack of factors which may be causes but the fact that a number of factors have been pointed out by several studies. The exact contribution of each factor cannot be assigned with certainty but there are reasonably good bases to assign approximate relative roles to several factors for some cancers. For other cancers, such as oral cavity, esophagus, stomach, liver and bladder, not enough data based on Louisiana studies are available but some inferences can be advanced, mostly based on studies done in other communities. (See the discussion of various risk factors in Section I.) 166 'JY J* URL 04670 Concerning lung cancer, there is general agreement that cigarette smoking is an overwhelming cause. It has been postulated that, in the hypothetical situation of a total suppression of smoking by the population, 30% of all cancer will be prevented Q (90% of lung cancers in males, 75% in females). Whether excessive smoking alone can explain the excess in lung cancer in South Louisiana is controversial. Another important contribution to lung cancer in South Louisiana is inadequate nutrition, especially the inadequate intake of fresh fruits and fresh vegetables. Industrial development, through exposure of workers in specific occupations and through environmental pollution, appears to contribute somewhat to lung cancer causation in Louisiana; it is likely to increase the risk for smokers and may provide the risk for non-smokers. The magnitude of that contribution is quite controversial. Genetic (hereditary) predisposition has not been found to contribute to lung cancer in Louisiana. All races and genetic groups are susceptible to lifestyle and environmental carcinogens. Rectal cancer may be associated with the intake of polluted drinking water. However, it represents a very small risk: less than 2% of the subjects living to age 74 will develop the disease. Due to the large number of potentially carcinogenic substances and their byproducts in the water, it is unlikely that the specific carcinogen for a specific cancer in the water supply could be identified. No definite information is yet available concerning cancer risk associated with specific exposure in the water supply. That, though, is probably not the issue. The total effect on the human body of all types of exposures is most critical. Reasons for excessive rates of hepatic, pancreatic and bladder cancer in Louisiana are obscure but studies have shown certain occupations to be at higher risk. No Single Cause The available data suggest that a single causative factor cannot explain the high incidence of cancer in Louisiana. A combination of factors is suggested as the most logical explanation. These factors fall into two categories: those associated with life-style and those related to the external environment. Lifestyle factors include primarily: smoking, excessive alcohol consumption and a diet high in fats and deficient in the protective substances found in fresh fruits and vegetables. The other factors which are less controlled by an individual relate principally to occupational exposures and pollution of the air and drinking water. 167 URL 04671 There are some factors which combine to increase the risk of cancer either in an additive or synergistic (multiplicative) fashion. Those interactions have not been well studied in Louisiana. Examples of interactions are the multiplicative effects of asbestos exposure (occupational) and smoking (lifestyle) factors. Poor nutrition appears to increase the risk of the other factors, for both environmental and lifestyle factors. Due to the multiplicity of sources of carcinogenic exposures a sound cancer prevention policy must include a variety of programs. State and community cancer prevention plans should focus on the removal or reduction of carcinogens in the community and occupational environment where feasible. The individual shares responsibility in cancer prevention and can greatly reduce his/her risk by following the Personal Cancer Prevention Plan. To further examine these potential risks in Louisiana, several studies are necessary: long-term follow-up of exposed and non-exposed industrial groups, population-based personal interviews for incidence studies, properly selected controls on case-controlled studies for selected cancer sites, and an ongoing population-based surveillance system to detect any significant change in incidence patterns for all cancers (a tumor registry). Monitoring carcinogenic pollutants in the environment is needed, including measures of the human body burdens of such substances. 168 Idn References - CANCER AND RISK 1. American Cancer Society. Cancer Facts and Figures, 1983. New York, New York, 1983. 2. Mason TJ, McKay FW, Hoover R. Atlas of Cancer Mortality for U. S. Counties 1950-1969. Washington, D.C.; U. S. Government Printing Office, 1975. 3. Dorn HF and Cutler SJ. Morbidity from Cancer in the United States. Public Health Monograph No. 56, Washington, D.C.: U. S. Government Printing Office, 1959. 4. Correa P, Chen VW, Craig JF, Ballinger T, Campbell W, Zavaler DE. Cancer in Louisiana: Louisiana Tumor Registry. Department of Health and Human Resources in collaboration with Department of Pathology, Louisiana State University Medical Center. 1983. 5. Young JL, Percy CL, Asire AJ, Eds. Surveillance Epidemiology and End Results: Incidence and Mortality Data, 1973-77. National Cancer Institute Monograph, NIH Publication No. 81-2330, Bethesda, 1981. 6. Ballinger T. Vital Statistics, personal communication. 1983. *V T 7. Muir CS. Limitations and Advantages of Epidemiological Investigations In Environmental Carcinogenesis. Annals of New York Academy of Science, p.153-164, 1979. 8. Correa P. NCI/EPA Collaborative Program: A case-control study of lung, pancreas and stomach cancer in Southern Louisiana, NCI-CP-FS-81036-65, 1979. 9. Lopez A, Yates B, Johnson WD, Nge R. The role of Vitamin A and ascorbic acid in relation to respiratory system cancer, American Society Clinical Nutrition Abstracts: p.553, 1979.. 10. Blot WJ, Fraumeni JF. Changing patterns of lung cancer in the United States. American Journal of Epidemiology 115:664-673, 1982. 11. Blot, WJ, and Fraumeni JF. Geographic patterns of lung cancer: industrial correlations. American Journal of Epidemiology 103:539-550, 1976. 12. Gottlieb MS. Lung cancer and the petroleum industry in Louisiana. Journal of Occupational Medicine 22:384-388, 1980. 13. Gottlieb MS, Pickle L, Blot WJ, Fraumeni JF. Lung cancer in Louisiana: Death certificate analysis. Journal National Cancer Institute 63:1131-1137, 1979. 14. Gottlieb MS, Stedman RG. Lung cancer in shipbuilding and related industries in Louisiana. Southern Medical Journal 72:1099-1101, 1979. 15. Rothschild H, Mulvey JJ. An increased risk for lung cancer mortality associated with sugarcane farming. Journal National Cancer Institute 68:755-760, 1982. 169 16. Gottlieb MS, Piekle LW. Bladder cancer mortality in Louisiana. The Journal of the Louisiana State Medical Society 133:6-9, 1981. 17. Nicholson WJ, Seidman H, Selikoff IJ, Tarr D, Clark E. Brain tumors among operating engineers in the chemical and petrochemical industry in Texas and Louisiana. Annals of New York Academy of Science 381:172-180, 1978. 18. Pickle LW, Gottlieb MS. Pancreatic cancer mortality in Louisiana. American Journal of Public Health 70:256-259, 1980. 19. Voors AW, Johnson WD, Steele SH, Rothschild H. Relationship between respiratory cancer and wetlands residency in Louisiana. Archives of Environmental Health: 124-128, May/June, 1978. 20. Harris RH. The implication of cancer-causing substances in Mississippi River water. Washington, D.C., Environmental Defense Fund, 1974. 21. DeRouen TA, Diem JE. Relationships between cancer mortality in Louisiana and drinking water source and other possible causative agents. In: Origins of Human Cancer. Cold Harbor Springs, New York. Cold Springs Harbor Laboratory, 331-345, 1977. 22. Gottlieb MS, Shear CL, and Seale DB. Lung Cancer Mortality and Residential Proximity to Industry. Environmental Health Perspectives 45:157-164, 1982. 23. Louisiana Department of Natural Resources. Louisiana Petrochemical Industry Assessment, 1983. URL 04673 ^jjOBSBwT 170 r`- .^hSaJs GLOSSARY adsorption: the surface retention of a substance by a solid or a liquid, as opposed to absorption which is the penetration of a substance into the bulk of the solid or liquid. absorption spectroscopy; the study of spectra obtained by the passage of radiant energy from a continuous source through a cooler, selectively absorbing medium. acceptable risks the risk that has minimal detrimental effects, or for which the benefits outweigh the potential hazards. Epidemiologic studies have pro' ^ed data for calculation of risks associated with occupational and environmental exposures. aerosol: suspension of particles or droplets in a gaseous medium. -V aflatoxin: a mold metabolite which is a potent carcinogen. age-adjustment: a summarizing procedure for rates of association in which the effects of differences in age composition among populations being compared have been removed by mathematical procedures. Ames Test: a short-term test to identify chemicals that alter the genetic structure of cells using the microorganism, Salmonella typhimurium. Chemicals that we mutagenic are usually also cancer-causing. amines: one of a class of organic compounds derived from ammonia by replace ment of one or more hydrogens by an organic group. animal model: a study in a population of laboratory animals that uses conditions of animals analogous to human conditions to model processes comparable to those that occur in human populations. anticarcinogen: a substance that inhibits or eliminates the activity of a carcinogen. 171 URL 04675 antioxidants a substance that retards oxidation. Examples include Vitamin C, Vitamin E, and BHA. ociatiore the degree of statistical dependence between two or more events or variables. These events or variables are associated when they occur more frequently together than one would expect by chance. It does not necessarily imply a causal relationship. benign tumor: a tumor that is confined to the territory in which it arises, i.e., it does not invade surrounding tissue or metastasize to distant organs. beta-carotenes (C40 H56) a carotenoid hydrocarbon pigment found widely in nature, always associated with chlorophylls; converted to vitamin A in the liver of many animals; a precursor of vitamin A found in such foods as carrots, broccoli, cantaloupe, squash, etc. <*v bloaccurr^*tinm the accumulation of certain substances up a food chain. bioaasay: determination of the relative effective strength of a substance (chem ical) by comparing its effect on a test organism with that of a standard prepara tion using living organisms to measure the effect of a substance, factor, or condition. bioavailabUitys the measurement of both the relative amount of a chemical that reaches the general circulation of the body and the rate at which this occurs. It is the extent of absorption of a chemical into the body. biochemical oxygen demands the dissolved oxygen required to decompose organic matter in water. It is a measure of pollution due to the fact that heavy waste loads result in high oxygen demand. biomagnifications the concentration of certain substances up a food chain. A very important mechanism in concentrating pesticides and heavy metals in organisms such as fish. 172 URL 04676 biomonitoring: the use of living organisms to test water quality at a discharge site or downstream area. carcinogens a chemical, physical or biological agent that produces cancer. case: in epidemiology, a person in a population or study group identified as having the particular disease or condition under investigation. case - control studlys study in which groups of individuals are selected in terms of whether they do (cases) or do not (controls) have the disease of which the cause is being investigated. The two groups are compared with respect to existing or past characteristics or exposures judged to be relevant to the cause of the disease. clustering: closely grouped cases of disease with well-defined distribution patterns in relationship to place and/or time. ^ cocarcinogens an agent which acts with another to cause cancer. complete carcinogens: substances which contain both initiators and promoters of the process of carcinogenesis. confoimdert a cause of a disease under study that is distributed unequally between the exposed and unexposed groups. The presence of a confounder can obscure whether increases in disease rates are actually due to the agent under investiga tion. For example, cigarette smoking is a confounder in occupational cancer studies. control (group): a comparison group comprising persons who have not been exposed to the disease or other variable whose influence is being studied. matched controls: controls who are selected so that they are similar to the cases in specific characteristics, such as age, sex, race, and socio economic status. covalent: a nonionic chemical bond formed by shared electrons usually a pair belonging originally to a different atom. 173 URL 04677 cumulative rate: a percentage measure of the risk an individual has of developing cancer during a certain age range. cytotoxic drugs; drugs which have a toxic effect upon cells. death certificate: a vital record signed by a licensed physician that includes cause of death, decedent's name, sex, birthdate, and place of residence and of death. Occupation, birthplace, and other information may be included. demography: the statistical study of the human vital statistics and population dynamics. determinant: any factor, whether event, characteristic or other definable entity, that brings about change in a health condition. diffusion: the process whereby particle^ of liquids, gases, or solids move from a region of higher concentration to one of lower concentration. PNA (deoxyribonucleic acid): carrier of genetic information, which is encoded in the sequence of bases; present in chromosomes and chromosomal material of cells. dose-response relationship: relationship in which a change in amount, intensity, or duration of exposure is associated with a change, either an increase, or a decrease, in a risk of a disease. effluent: the liquid waste of sewage or industrial processing. endemic: the usual frequency of disease occurance. epidemic: the occurence in a community or region of cases of a disease clearly in excess of normal expectancy; excessive prevalence of a disease. epidemiology: the study of the factors determining the occurrence of disease in populations and the distribution ofdisease frequency. 174 URL 04678 essential trace element: a chemical element required in trace quantities for the normal growth of an organism. estrogens a female sex hormone. etiology: cause of a disease. eutrophication: natural or artificial addition of nutrients to water bodies and the effects of these added nutrients. It often results in undesirable changes in water quality. familial predisposition: tendency for familial occurrence of a disease due to genetic transmission, intrafamilial transmission of infection or culture, interaction within the family, or the family's shared experience, including its exposure to a common environment. i feedstock: gaseous or liquid petroleum-derived Tfydrocarbons or mixtures of hydro iI carbons from which gasoline, fuel oil, and petrochemicals are produced by thermal or catalytic cracking. J J! food chain: the series of events which convert solar energy, by way of photosyn thesis, to food for plants and animals. More complex creatures consume plants and/or smaller organisms and so on in a chain of events involving ever-increasing i sizes and appetites of the consumers and ever-decreasing amounts of food available ) in the chain. gas chromatography: in analytical chemistry, a separation technique which involves i the passage of a gas through a column containing a fixed adsorbent material. This technique is used principally to quantify volatile compounds. i genetic material: the elements of the germ plasm which serve as specific trans mitters of hereditary characters and usually regarded as portions of DNA linearly arranged in fixed positions and as functioning through control of the synthesis of specific polypeptial chains. genotoarics damaging to genetic material. 175 halogenated hyfrocarbons one of a group of halogen derivatives of organic hydrogenand carbon-containing compounds; the group includes monohalogen compounds and polyhalogen compounds that contain the same or different halogenatoms. healthy worker effects a phenomenon observed in studies of occupational diseases. Workers usually exhibit lower overall death rates than the general population, due to the fact that the severely ill and disabled are ordinarily excluded from employment. Death rates in the general population may be inappropriate for comparison unless this is taken into account. histological; relating to the microscopic structure of the tissues of organisms. host: a species capable of being affected by a disease agent. humicss a chemical substance, an acid, formed from the dark natural organic material in soils. hydrocarbons: one of a very large group of chemical compounds composed only of carbon and hydrogen; the largest source of hydrocarbons is from petroleum crude oil. : C 33 6L9* iatrogenic: induced by a physician. immunologic factors: factors that affect the power of the body to resist disease. incidence: number of new cases of a disease in a defined population within a specified period of time. f a 4 r incidence rates: the rate at which new cases of disease occur within a general population during a specified period of time. Incidence rate * number of persons developing the disease per unit time. total number of persons at risk initiators: substances which can initiate the process of carcinogenesis. ionizing radiation: any radiation consisting of ionizing particles (particles which produce atoms that have a positive or negative electric charge.). 176 UHL 04680 4. lacto-ovo-vegetarian diet: a vegetarian diet which includes dairy products and eggs. latency (latent period): period of time between documented exposure to a car cinogen and evidence of tumor development. lymphomas: any tumor, usually malignant, of the lymph nodes or lymph tissue. macro molecules: very large molecules as of a protein, cellulose, or other natural or synthetic polymer. malignant tumor: a tumor which can invade neighboring tissue and/or spread to distant body sites. mass spectrometry: an analytical technique used for the identification of chemical structures, mixtures of chemicals and quantitative analysis. melanoma: a tumor of high malignancy that starts in a black mole and metasta sizes rapidly and widely. metastasize: spread of cancerous cells from original site to distant parts of the body. micronutrientss an organic compound essential in minute amounts only to the growth and welfare of an animal. migrant studies: studies taking advantage of migration to one country by those from other countries with different physical and biological environments, cultural background and/or genetic makeup, and different morbidity or mortality experience. Comparisons are made between the mortality or morbidity experience of the migrant groups with that of their current country of residence and/or their country of origin. Sometimes the experiences of a number of different groups who have migrated to the same country have been compared. morbidity; the condition of disease, refers to incidence or prevalence of a disease. 177 i -jyr) mortality rate: the rate at which members of a general population die of a disease during a specified period of time. Mortality rate = number of persons dying due to disease per unit time total number of persons in group multifactorial etiology: multiple interacting factors which affect the cause of a disease. The term is used to refer to the concept that a given disease may have more than one cause. multivariate analysis: a set of statistical techniques used when the variation in several variables has to be studied simultaneously. mutagens: chemical compounds which produce a change in genetic structure resulting in an altered expression of that gene (a mutation). mycotoxins toxin formed by a fungus. natural rate of increases increase of disease due to population growth in absence of migrations, live births during year - deaths x 1000 midyear population neoplasm (malignant): abnormal growth or tumor (cancerous). nitrosable compounds Initiates^ nitrites, nitroamines): compounds containing nitrogen in combined forms (NO^, NOg* NNOg) non-linear kinetics: an uptake rate of a substance which does not follow a linear pattern. non-point source: causes of water pollution that are not associated with a single point discharge, such as agricultural runoff and sediment from contruction. occurrence: in epidemiology, a term describing the frequency of a disease. oncogenic virus: tumor-causing or cancer-causing virus. 178 URL 04682 oncology? the study of tumors. organic chemicals: all compounds of carbon except such binary compounds as the carbon oxides; the total number of organic chemicals is indeterminate, but some 3,000,000 have been identified and named. Examples are straight-chained, alicyclic, and aromatic hydrocarbons (petroleum and coal-derived); aldehydes; betons, alcohols; ethers, pyrrells, organometallic compounds, and synthetic high polymers. organic matter: plant and animal residues at varying stages of decomposition. organochlorines; any compound of chlorine and carbon elements. pathological: relating to the anatomic and physiologic change from normal tissues in an organism to diseased tissue pertaining to disease. permissible exposure limit (PEL): an occupational health standard to safeguard employees against dangerous chemicals or contaminants in the workplace. pharmacokinetics: the study of the time course of chemical concentrations in different fluids, tissues, and excreta of the body and of the mathematical relationships required to develop models to interpret such data. phenotype: the detectable expression of the interaction of genotype and environ ment. photodecompoation: decomposition due to presence of sunlight or other radiant energy. point source: a stationary location where pollutants are discharged, usually from industries or municipalities. polychlorinated biphenyls (P JBs): a mixture of compounds composed of the biphenyl molecule which has been chlorinated to varying degrees; a class of organic compounds, most of which are carcinogenic. 179 ORL 04633 polycyclic aromatic hydrocarbons: hydrocarbon molecules with two or more nuclei. An example is naphthalene (in moth balls), C^Hg with two benzene rings side by side. These often originate from petroleum products, and at least some of which are carcinogens. precursors: a chemical that takes part in a chemical reaction resulting in the formation of one or more new pollutants. priority pollutants: toxic substance or categories of toxic substances identified by EPA. promoters: substances which enhance by their presence the carcinogenic action of other substances. P value (probability): a statement of the probability that the observed difference could have occurred by chance if the grougj are really alike. qualitative risk awawment: the characterization of toxicity to humans as deter mined from observations of human populations and/or experimental systems. quantitative risk awnnsnments the assessment of both hazard and exposure infor mation for purposes of estimating the likelihood that hazards associated with a substance will be realized as risks to exposed individuals or populations. radionuclides: a nuclide (atom) that exhibits radioactivity. retrospective study: a research design which is used to test etiologic hypotheses in which inferences about exposure to the causal factor are derived from data relating to events or experiences or characteristics in the past of the persons under study. riparian: association with river or stream-side. risk: in epidemiology risk refers to the probability of the occurrence of a disease in a population. 180  **' 9*r risk assessment: the process of evaluating the potential effects of a hazard, and involves both qualitative risk assessment and quantification. risk factor: an attribute or exposure that is associated with an increased proba bility of the occurrence of a disease. risk management: the process of evaluating alternative regulatory options and selecting among them. saturation kinetics: the rate of a reaction (v) produced by an enzyme when the substate concentration is high enough to saturate the enzyme and is related to the rate of reaction (u) at a lower substate concentration (c) and the constant Km (Michaelis constant); V=v(l+Km/c). selective migration: the migration into or out of a selected population due to identifiable factors, such as available health care facilities or decline in employ ment opportunities. simple Mendelian heredity: based on three fundamental concepts: (1) the organism is a mosaic of unit characters capable of separate hereditary transmission, (2) a unit character may mask a related unit character completely (dominance) when the potentialities for development of both are present in an individual. The masked character is said to be recessive, (3) unit characters are segregated during reproduction regardless of the combinations in which they have been associated. sites the location of a tumor on or in an organism. social class: a method of socially stratifying populations, e.g., according to educa tion, income, or occupation. somatic mutation: change originating in a somatic (body) cell due to genetic change. species (of a chemical): one of a class of chemicals having common characteristics and qualities. ^ % 181 standard incidence ratio (SIR): the observed incidence cases _____ age adjusted expected incidence cases X 100 = SIR statistical significance; refers to the frequency with which a difference as large as that observed in a study would be expected in taking repeated pairs of samples from identical populations. synergism: cooperative action of two agents (chemicals) such that the total effect is greater than the sum of the two effects taken independently. Two factors act synergistically if there are persons who will get the disease when exposed to both factors but not when exposed to either alone. threshold levels level at which an exposure to a particular substance (chemical) has no effect. toxicology; the scientific study of detection, occurrence, properties, effects and regulation of toxic substances. toxic substances any chemical which when present in excess of threshold concen trations causes harmful biological effects in living organisms. variables any attribute, phenomenon, or event that can have different values. vital statistics: systematically tabulated information concerning births, marriages, divorces, separation, and deaths based on registrations. URL 04685 182 URL 04686 LIST OF ACRONYMS CERCLA: Comprehensive Environmental Response Compensation and Liability Act of 1980. PHHRs Department of Health and Human Resources (Louisiana) EPA: Environmental Protection Agency (U.S.) 1ARC: International Agency for Research on Cancer LWRIC: Louisiana Water Resources Information Center NCAB: National Cancer Advisory Board NCI: National Cancer Institute 'V NESHADS: National Emissions Standards for Hazardous Air Pollutants NIHs National Institute of Health HIOSH: National Institute of Occupational Safety and Health HORS; National Organics Reconnassance Survey NPDBS: National Pollutant Discharge Elimination System HRDCs National Resources Defense Council NSWQAN: National Surface Water Quality Appraisal Network NTPs National Toxicology Program OHSBQt Office of Health Services and Environmental Quality (DHHR, Louisiana) RA: Quantitative Risk Assessment 183 URL 0468"? RCRA: Resource Conservation and Recovery Act SEER: Surveillance, Epidemiology and End Results (NCI) SIP; State Implementation Plans (Louisiana Department of Natural Resources) WPCD: Water Pollution Control Division (Louisiana Department of Natural Resources) 184 URL 04688 ANNOTATED BIBLIOGRAPHY I. GENERAL CANCER INFORMATION O Cancer Facts and Figures - 1983. American Cancer Society. 777 Third Avenue, New York, New York 10017 1982. This report covers basic data concerning cancer in the United States. Topics covered are cancer incidence, mortality, survival, treatment management, types of cancers and their risk factors, professional educational programs, service and rehabilitation programs, cancer and the environment, costs of cancer, available grants for cancer research, and information concerning the American Cancer Society. O An Evaluation of Chemicals and Industrial Processes Associated with Cancer irTHumans Based on Human and Animal Data: IARC Monographs Volume 1 Althonse R, Huff J, Tomatis L, and Wilbourn J. Unit of Chemical Carcinogenesis International Agency for Research on Cancer (IARC). 150 Cours Albert Thomas, 69372 Lyon Cedex 2 France. An international ad hoc Working Group of experts in cancer research met at the international Agency for Research on Cancer (IARC) in January 1979 to evaluate the data on human and experimental animal carcinogenicity for 54 chemicals, groups of chemicals, ar.d industrial processes. Monographs for these chemicals were published Vols. 1 to 20 of the IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Based on evidence from human studies, 18 of the 54 chemicals or industrial processes are human carcinogens. An additional 18 chemicals are probably carcinogenic for humans, although the data were considered not adequate to establish a causal association. The chemicals were further subdivided, with 6 chemicals exhibiting a high degree of evidence and 12 chemicals exhibiting a lower decree. Data on the remaining 18 chemicals were considered insufficient to allow any evaluation of carcinogenicity. The report summarizes the background, purpose, and overall conclusions of the Working Group. The evidence supporting the evaluations is given in the "Appendix.11 o Second Annual Report on Carcinogens. National Toxicology Program^ U.S. Department of Health and Human Services Public Health Service. Public Information Office. 18S National Toxicology Program. MD B2-04 Post Office Box 12233 Research Triangle Park, North Carolina 27709. December 1981. Annual report which lists all substances (88 included) which either are known to be carcinogens or which may be reasonably anticipated to be carcinogens and to which a significant number of persons roin the United States are exposed. Aiso provides information on the j - -..ire and degree of exposures to such carcinogens and the extent to which Federal regulations are effective in reducing the risk to the public health from exposures to these chemicals. D. UNITED STATES CANCER STUDIES O Cancer Mortality in the United States; 1950-1977. National Cancer Institute Monograph No, 59. c McKay F W, Hanson M R and Millay R W. NIH Publication NO. 82-2435. U.S. Department of Health and Human Services . jd o ^ Public Health Service g National Institutes of Health National Cancer Institute, Bethesda, Maryland 20205 April 1982. Graphic display of age-adjusted mortality rates of all malignant neo plasms in United States. 1950-1977 for white and non-white males and females. O Cancer Incidence and Mortality in the United States, 1973-77. National Cancer Institute Monograph NO. 57. Young J L, Percy C L, Ardyee, A J, Berg,J W, Cusano, M M, Gloeckler L A, Horm J W, Lourie W 1 Jr, Pollack E S, Shambaugh E M. National Cancer Institute Bethesda, Maryland 20205. 1980 Reports detailed information on the incidence of and mortality from cancer in the United States during the initial 5 years of the Surveil lance, Epidemiology, and End Results (SEER) Program, 1973-77. Data are classified according to race, age, sex, and residence of the patient, along with anatomic site and histologic type of cancer. O Mesothelioma in the United States. Incidence in the 1970s. Hinds M W. Journal of Occupational Medicine/20:7 469-471. July 1978. 186 * i URL 04690 Mesothelioma is a rare neoplasm, the occurrence of which has been clearly related to asbestos exposure. Data recently collected by population based cancer registries in Washington, Hawaii, New Mexico, Connecticut, Michigan, Utah, Louisiana, and Iowa were obtained for the determination of mesothelioma incidence rates. These registries repre sent a total population of over 16 million persons. Crude incidence rates were found to range from 3.0 to 7.1 per million per year. Age incidence rates showed a steady increase from the third through the eighth decade, with a more rapid increase for males than females. Sex specific incidence rates, age adjusted to the 1970 U.S. population, were found to range from 4.4 to 11.1 per million per year for males and from 1.2 to 3.8 million per year for females. The highest rates for both males and females were found in the New Orleans area of Louisiana and the Puget Sound area of Washington state, both with significant shipbuilding activity. O Geographic Patterns of Bladder Cancer in the United States. Blot W J, and Fraumeni J F. Journal of the National Cancer Institute 61:4. 1017-1023. October 1978. Age-adjusted rates of mortality during 1950-69 from bladder cancer were correlated with demographic and industrial for 3,056 counties of the contiguous U.S. ... Outside the Northeast, high rates were generally limited to urban areas, but clusters of elevated mortality occured among white males along the Illinois-Wiseonsin border, in parts of lower Michigan, and in southern Louisiana. Industrial factors may explain at least part cf the geographic clustering, inasmuch as rates among males were significantly higher in U.S. counties where the chemical industry is heavily concentrated. Increases were also associated with the printing industry, but correlations with 16 other major manufacturing industries were near or below expected levels. O Cancer Incidence and Mortality Trends in the United States: 1935-74. Devesa S S, and Silverman D T. Journal of the National Cancer Institute 60:3. 545-571. March 1978. Using incidence data from three national cancer surveys and mortality data for the entire United States, one can make several observations concerning the trends in cancer occurrence. Rates among males have been increasing, whereas those among females have been decreasing. In the past, cancer of all sites combined occurred more frequently among females; now males have rates higher than do females of the same race. White predominance has been replaced by a nonwhite excess in incidence and mortality rates among males and a nonwhite excess in female mortality; racial differences in incidence rates among females have been diminishing. Increases have occurred in cancers of the lung, prostate gland, breast among nonwhite females, pancreas, kidney, bladder among males, and esophagus among nonwhites; melanomas have increased among whites, and lymphomas have increased in each racesex group. The reported increases may be due partly to improvements in diagnosis, which probably varied for the different 187 URL 04691 primary sites and probably affected nonwhites more than whites. Meanwhile, decreases have occurred in cancers of the uterus (particularly cervix), stomach, and liver. Intestinal cancer has increased, whereas rectal cancer has decreased. Possible problems in specifying the site of origin of tumors arising in the area of the ociosigmoid junction make it difficult to determine how accurately the observed trends reflect the true situation. When intestinal and rectal cancers are considered together, the rates for nonwhites have been increasing toward the more stable level of the whites. The incidence of thyroid cancer has increased, whereas the mortality has decreased. Without lung cancer, the incidence of all cancer types combined among white males would be decreasing in recent years rather than increasing. The increases in overall incidence seen among nonwhite males are due primarily to increases in cancers of the lung, prostate gland, intestine, and esophagus. Among white females, the decrease in overall incidence is due to the decreases in cancers of the uterine cervix and the stomach; breast cancer rates are steady and continue to have a major impact. Except for breast cancer, the experience of nonwhite females is similar, with the declines of uterine cancer being greater and those in the other sites being less than the declines observed for white females. O Trends in Cancer Incidence and Mortality in the United States, 1969-76. Pollack K S, and Horm J W Journal of the National Cancer Institute 64:5. 1091-1103. May 1980. Trends in cancer incidence and mortality in the United States were analyzed over the period 1969 through 1976. The greatest increase in incidence among whites occurred for lung cancer among females (almost 9 percent/year), whereas the incidence of cancer of the uterine corpus increased 6 percent per year. Cancer of the cervix showed the greatest decrease in incidence, an average of 8 percent/year. Stomach cancer incidence and mortality showed a substantial decline for each sex, and rectal cancer incidence increased for each sex whereas mortality declined. The incidence of cancer of the female breast increased 1.8 percent per year without inclusion of the rates of 1974 and 1975, when an unusually large decrease occurred. Cancer mortality data were presented for the United States on the basis of data from the National Center for Health Statistics. Emphasis was focused on the comparability of cancer incidence data over the time period studied, given the fact that cancer incidence was measured by the Third National Cancer Survey for the period 1969-71 and by the Surveillance, Epidemiology, and End Results Program for the period 1973-76. 188 d URL 04692 ffl. ENVIRONMENTAL CANCER AND ITS EPIDEMIOLOGY O Developing Clues to Environmental Cancer: A Stepwise Approach With the Use of Cancer Mortality Data, Blot WT, Fraumeni J F Jr, Mason T J, and Hoover R N. Environmental Health Perspectives. Volume 32, 53-58. October 1979. This review article examines a stepwise approach for using cancer mortality maps, supplemented by correlation studies linking mortality rates with demographic and industrial data at the county level, to generate hypotheses to cancer etiology which can then be pursued by analytical epidemiological studies. The advantages and limitations of this approach and its application in the study of lung cancer in the United States are discussed. O Geographic Clues to High-Risk Groups in Cancer. Fraumeni J F Jr. The Cancer Bulletin, 29:6. 191-194. 1978 Review of geographic patterns of cancer in the United States. Geo graphic patterns provide useful clues to the identification of high-risk groups in directing attention to communities where further epidem iologic study should be concentrated in the search for environmental carcinogens. All combined cancers in males and females show high cancer death rates in the northeastern United States and in southern Louisiana. O Environmental Cancer. Hoover R. Annals New York Academy of Science. 1979 Article discusses the environmental risk factors of cancer, including occupational exposure, therapeutic drugs, ionizing radiation, air pol lution, water pollution, food additives, tobacco and alcohol consump tion, dietary factors, reproductive and sexual factors, endogenous biochemical factors, microbiological agents, and psychological factors. O Social Environment and Cancer Mortality in Men. Jenkins C D. The New England Journal of Medicine. 308:7 395-398. February 1983. Article examines the distribution of mortality rates from cancer with the focus on the variables of the social environment of neighborhoods, such as demographic composition, marital status, nature of housing, and family structure. 189 7^ URL 04693 o Milestones in Chemical Carcinogenesis. M iller E C and M iller J A. Seminars in Oncology. 6:4 445-460, December 1979. Review article which discusses the major findings in the studies on chemical carcinogenesis. O Limitations and Advantages of Epidemiological Investigations in Environmental Carcinogenesis. Muir C S. Annals New York Academy of Sciences, pp 153-164 1979. This article discusses epidemiological method and draws attention to the fact that, essential though epidemiological investigations are, there are very few trained chronic disease epidemiologists. Describes the different types of epidemiological studies, such as descriptive epidemiology, occupational mortality, case report, case-control and retrospective and prospective cohort studies; and discusses the advan tages and disadvantages of each. O Historic Milestones in Cancer Epidemiology. Petrakis N L. Seminars in Oncology, 6:4 433-444. December 1979. Review paper which discusses important milestones in statistical and epidemiologic methods and significant epidemiologic studies of a few specific cancer sites. 0 Thresholds for Environmental Cancer: Biologic and Statistical Considerations. Schneidermann M A, Decoufle P, and Brown C C. Annals New York Academy of Science. 92-127. 1979. A review paper which discusses statistical models developed for estimating threshold levels, along with dose-response studies. Con clusion is there is little or no evidence of thresholds in human cancer. Epidemiological data, both industrial exposure studies and cigarette smoking data are consistent with there being no threshold. O Epidemiology of Environmental Pollution: Drinking Water in Relation to Cancer and Heart Disease. Buncher C R, Kuzma R J, and Forcade C M. University of Cincinnati Medical College Cincinnati, Ohio 45267. Literature in this field is reviewed. Discuss the pros and cons of cancer mortality correlated to drinking water from Mississippi River. 190 URL 04694 O Contribution of the Environment to Cancer Incidence: An Epidemiologic Exercise. Wynder E L, and Gori G B. Journal of the National Cancer Institute 58:4 825-832. April 1977. Guest editorial which discusses epidemiological basis for estimates concerning environmental cancer incidence, and select environmental factors (tobacco, nutrition, air and water pollution, and occupational exposure, drugs) which contribute to human cancers. O The Politics of Cancer Epstein & & Anchor Press/Doubleday 1982. A review of information on the environmental causes of cancer and the political background of legislation concerning regulation of various carcinogens. O The Causes of Cancer Reif A E American Scientist 69. 437-447. August 1981. This paper reviews the present state of knowledge concerning the causes of the various types of cancer. It discusses genetics, chemicals, diet, industry, radiation, estrogens, viruses, as sources of cancer. O- Environmental Pollution and Cancer and Heart and Lung Disease: First Report to Congress by The Task Force on Environmental Cancer and Heart and Lung Disease. U.S. Environmental Protection Agency; National Cancer Institute; National Heart, Lung and Blood Institute; National Institute for Occupational Safety and Health; and National Institute of Environmental Health Sciences. Washington, D C August 1978. The First Annual Report of the Task Force presents an overview of the problem of environmentally related cancer, heart and lung disease, summarizes current Federal programs which address the problem, and describes Task Force objectives, actions and plans. 191 URL 04695 IV. OCCUPATIONAL - INDUSTRIAL CANCER O Cancer Mortality in U.S. Counties With Petroleum Industries. Blot W J, Brinton L A, Fraumeni J F, and Stone B J. Science. Volume 198. 51-53. October 1977. A survey of cancer mortality from 1950 to 1969 was conducted in United States counties where the petroleum industry is most heavily concentrated. Male residents of these counties experienced significantly higher rates for cancer of the lung, the nasal cavity and sinuses, and the skin (including malignant melanoma) compared to male residents of counties with similar demographic characteristics. Further study is needed to determine whether those patterns result from exposure to chemical carcinogens, including polycyclic hydrocarbons, involved in the manufacturing of petroleum. O Lung Cancer After Employment in Shipyards During World War n. Blot W J, Harrington J M, Toledo A, Hoover R, Heath C W, and Fraumeni J F. New England Journal of Medicine. 299:12 620-624. September 1978. A case-control study, undertaken to identify reasons for the exceptionally high rate of lung cancer among male residents of coastal Georgia, revealed a significantly increased risk associated with employment in area shipyards during World War n. The summary relative-risk estimate, adjusted for smoking, other occupations, age, race, and county of residence was 1.6 (95 percent confidence limits = 1.1 to 2.3). A synergistic relation was found between shipyard employment and cigarette smoking. These findings suggest that asbestos and possibly other shipyard exposures during wartime employment account for part of the excess mortality from lung cancer in certain coastal areas of the United States. 0 Occupational Risk for Laryngeal Cancer. Flanders W D, and Rothman K J. American Journal of Public Health. 72:4 369-372. April 1982. In a case-control analysis, the effects of type of employment on laryngeal cancer risk were studied using the interview data from the Third National Cancer Survey. Effects were measured relative to the risk for these employed in a group of arbitrarily defined industries and occupations with low risk. Females were excluded and age, tobacco use, alcohol use, and race were controlled for in the analysis. We found ratio estimates above 3.0 (increased risk) were found for workers in the railroad industry and the lumber industry; and for sheet metal workers, grinding wheel operators, and automobile mechanics. 192 URL 04696 O Epidemiologic Study of Refinery and Chemical Plant Workers. Hanis N M, Holmes T M, Shallenberger L G, Jones K E. Journal of Occupational Medicine. 24:3 March 1982. A dynamic retrospective cohort study was performed to examine the mortality experience of workers at Exxon's Baton Rouge, La., refinery and chemical plant. Included were 8,666 regular employees who worked at least one month during the period January 1, 1970 through December 31, 1977, and retirees who were alive as of January 1, 1970. Mortality from all causes of death was lower than expected when compared with that of the United States population of similar age, sex, and race. Analyses of mortality by specific site of cancer revealed elevated standardized mortality ratios (SMRs) for cancer of the kidney, testis, brain/eentral nervous system, pancreas, and lymphopoietic sites; none of these elevations was statistically significant. Because of the higher than average mortality from cancer of the pancreas in some Louisiana parishes and the observation that one additional death from cancer of the pancreas in this study would have resulted in a statistically significant SMR at the 95% confidence level, some emphasis was placed on this finding. No evidence was found to link cancer of the pancreas to a specific occupational group. An examination of mortality by occupational class revealed some elevated SMRs for further study. 0 Lung Cancer in Coastal Georgia: A Death Certificate Analysis of Occupation: Brief Communication. Harrington J M, Blot W J, Hoover R N, Housworth W J, Heath C W, and Fraumeni J F Jr. Journal of the National Cancer Institute. 60:2 295-298. February 1978. A comparison of death certificate statements on occupation for 858 white males who lived in coastal Georgia counties and who died of lung cancer during 1961-74 and for 858 controls who were of the same age and county residence revealed a twofold excess risk of lung cancer associated with the construction industry. No elevated risk of lung cancer was found for workers in the wood and paper industries in the urban areas of Savannah, Brunswick, or Waycross, but a threefold increase was uncovered for remaining coastal counties where the wood and paper industry was the largest employer. O Asbestos Disease In Maintenance Workers of the Chemical Industry. Lilis R, Baum S, Anderson H, Serata M, Andrews G, and Selikoff 1 J. Annals New York Academy of Science pp. 127-134. 1979. Chemical plant maintenance workers examined had experienced various degrees of asbestos exposures; chest x-ray abnormalities were relatively frequent and were characteristics of less intense asbestos exposure. Progression to severe disabling asbestosis less probable under such circumstances, the risk for lung cancer and mesothelioma remain. 193 URL 04697 O Geographic Patterns of Cancer Risk: A Means for Identifying Possible Occupational Factors. Mason T J. Epidemiology Branch National Cancer Institute Bethesda, Maryland 20014 Annals of the New York Academy of Sciences. Vol. 381, pp. 370-376. 1982. Occupational studies have identified carcinogens affecting the lung and bladder. Patterns of county mortality rates for these sites were examined for white males, and specific attention was given to counties in the United States with age-adjusted mortality rates in the top 1 percent of the distribution of these rates for all counties. Kidney cancer among white males, since this tumor has not been clearly linked to occupational agents, was also investigated. The feasibility of using these patterns as a means of identifying possible occupational factors was evaluated. O Brain Tumors Among Operating Engineers in the Chemical and Petrochemical Industry in Texas and Louisiana. Nicholson W J, Seidman H, Selikoff I J, Tarr D, and Clark E. Annals of the New York Academy of Sciences. Vol. 381, pp. 172-180. 1982. The results of a proportionate mortality analysis of the deaths among operating engineers in Texas and Louisiana reveals that these individuals employed in chemical plants and petrochemical operations have an excess risk of brain tumors. This risk is largely associated with employment in three large facilities in these two states and is confined to individuals employed as operators. Additionally, there is evidence that lung cancer may be elevated among individuals employed in chemical operations, although the data are less definitive. Data were not available that would help identify specific agents which could be associated with this excess malignant risk. O Mortality Among Individuals Occupationally Exposed to Benzene. Ott M G, Townsend J C, Fishbeck W A, and Langer R A. Archives of Environmental Health, pp. 3-10. January/February 1978. The mortality experience of 594 individuals occupationally exposed to benzene was investigated using a retrospective cohort design. Three hundred thirty-five of the employees began working in benzene areas prior to 1950, which provided a sound data base from which to examine latency. Data derived from work histories and industrial hygiene records permitted estimation of exposure intensities and cumulative dosages for each employee. No mortalities directly attributable to benzene exposure were observed. Several cases of leukemia and other blood disorders were noted and discussed. 194 UBL 04698 O Short-term Asbestos Work Exposure and Long-term Observations. Seidman H, Selikoff I J, and Hammond E C. Annals New York Academy of Science. 1979. Study found that work exposure to amesite asbestos for as short a period as one month showed a clear excess risk of cancer. With longer direct exposure (i.e. 2, 3, 6 months, and so on) the cancer risk became greater. O A Case-Control Method for Assessing Environmental Risks from Multiple Industrial Point Sources. Stinnett S S, Buffler P A, and Eifler C W. 1981. This study utilized a simple method based on inverse of distances from point sources of air pollution, weighted by annual average emissions, and created an industrial emissions score for each census tract in two industrialized Texas counties. In a case-control study of liver cancer mortality showed no difference between cases and controls in their residential proximity to industrial plants. No interaction between employment status and proximity scores were observed. O Mortality Among Workers Employed in Petroleum Refining and Petro-Chemical Plants. Thomas T L, Deconfle P, and Moure-Eraso R. Journal of Occupational Medicine. 22:2 97-103. 1980. The cause-specific mortality specific experience of 3,105 members of the Oil, Chemical, and Atomic Workers International Union of Texas was examined to determine if there were unusual patterns of fatal disease that may be indicative of hazardous agents in the work environment. Increased relative frequencies of stomach cancer, cancer of the brain, leukemia, and multiple myeloma were confined to white males who were refinery and petrochemical plant workers. Excess deaths from stomach cancer and brain cancer were found among white male members employed at one specific oil refinery and petrochemical plant in Texas. Proportionate mortality ratios for cancers of the liver, pancreas, lung, and skin were also elevated among refinery and petro chemical plant workers. Findings suggest workers may be at increased risk of certain cancers and indicates further investigation needed. O Influence of Dose and Fiber Type on Respiratory Malignancy Risk in Asbestos Cement Manufacturing. Weill H, Hughes J, and Waggenspack C. American Review of Respiratory Disease. Vol, 120: 345-354. 1979. 195 3 This study focused on risk of respiratory malignancy in relation to duration, degree, and fiber type of exposure to asbestos in a manu facturing cohort of 5,645 with long-term follow-up. Excess risk of respiratory cancer was detected in workers with moderate and heavy exposure, while low exposure to asbestos dust did not exhibit excess risk of respiratory malignancy. O Cancer in Children of Parents Exposed to Hydrocarbon-Related Industries and Occupations. Zach M, Cannon S, Loyd D, Heath C W Jr, Falletta J M, Jones B, Housworth J, and Crowley S. American Journal of Epidemiology. 3:3 329-336. 1980. Texas Childhood Cancer Study, 1976-1977, tested the hypothesis that parent's occupation is associated with the development of childhood malignancy. They found no association between job-related hydro carbon exposure and childhood cancer. This agrees with the findings of a Finnish Study) but not with those of a Quebec Study, which showed that children who died of malignant disease before five years of age were twice as likely as controls to have fathers who worked in hydrocarbon-related occupations (car mechanics, machinists, miners and painters) at the time of the child's birth. O Preliminary Analysis of Cancer Hates in Primary Organic Chemical-Producing Counties. USEPA EPA-600-1-79-022 June 1979. Study designed to determine whether there is an association between cancer mortality and the production of environmental carcinogens. Mortality rates of counties containing organic chemical production facilities are compared to rates of control counties. Twelve different cancer sites in lung, stomach, etc., and eight organic carcinogens were considered. Although a rigorous statistical analysis was not conducted, for most cancer sites mortality rates were found to be higher in counties of organic carcinogen production than in control counties. The study aids in the development of statistical techniques for determining the contribution of environmental contaminants to the rise in cancer rates. Research of this type assists in the identification of compounds that need to be regulated. 196 URL 04700 V. LIFESTYLE CANCER O Dietary Carcinogens and Anticarcinogens Oxygen Radicals and Degenerative Diseases. Ames N. Science. Vol. 221 1256-1262. 1983. The human diet contains a great variety of natural mutagens and carcinogens, as well as many natural antimutagens and anticarcinogens. Many of these mutagens and carcinogens may act through the genera tion of oxygen radicals. Oxygen radicals may also play a major role as endogenous initiators of degenerative processes, such as DNA damage and mutation (and promotion), that may be related to cancer, heart disease, and aging. Dietary intake of natural antioxidants could be an important aspect of the body's defense mechanism against these agents. Many antioxidants, such as vitamin E (tocopherol), B-carotene, selenium, and ascorbic acid, could be an important aspect of the body's defense mechanism against these agents. Many antioxidants are being identified as anticarcinogens. Characterizing and optimizing such defense systems may be an important part of a strategy of minimizing cancer and other related diseases. O Cancer and Lifestyle in Louisiana. Correa P, and Johnson W D. Journal of Louisiana State Medical Society. 135:3 pp. 4-6. March 1983. Results of a correlation study to investigate the possible link between cancer risk and lifestyle in Louisiana are given. O Passive Smoking and Lung Cancer. Correa P, Pickle L W, Fontharr. E, Lin Y, Haenszel W. The Laneet. pp 595-599. September 1983. Questions about the smoking habits of parents and spouses were asked in a case-control study involving 1338 lung cancer patients and 1393 comparison subjects in Louisiana. Non-smokers married to heavy smokers had an increased risk of lung cancer, and so did subjects whose mothers smoked. There was no association between lung cancer risk and paternal smoking. The association with maternal smoking was found only in smokers and persisted after controlling for variables indicative of active smoking. It is not clear whether the results reflect a biological effect associated with maternal smoking or the inability to control adequately for confounding factors related to active smoking. This preliminary finding deserves further investigation. 197 0 The Causes of Cancer: Quantitative Estimates of Avoidable Risks of Cancer in the United States Today. Doll R and Peto R. Journal of the National Cancer Institute. 66:6. June 1981. Evidence that the various common types of cancer are largely avoidable diseases is reviewed. Life-style and other environmental factors are divided into a dozen categories, and for each category the evidence relating those particular factors to cancer onset rates is summarized. Where possible, an estimate is made of the percentage of current U.S. cancer mortality that might have been caused or avoided by that category of factors. These estimates are based chiefly on evidence from epidemiology, as the available evidence from animal and other laboratory studies cannot provide reliable human risk assessments. By far the largest reliably known percentage is the 30 percent of current United States cancer deaths that are due to tobacco, although it is possible that some nutritional factor(s) may eventually be found to be of comparable importance. The percentage of United States cancer deaths that are due to tobacco is still increasing, and must be expected to continue to increase for some years yet due to the delayed effects of the adoption of cigarettes in earlier decades. Trends in mortality and in onset rates for many separate types of cancer are studied in detail in appendixes to this paper. Biases in the available data on registration of new cases produce apparent trends in cancer incidence which are spurious. Biases also produce spurious trends in cancer death certification rates, especially among old people. In (and before) middle age, where the biases are smaller, there appear to be a few real increases and a few real decreases in mortality from some particular types of cancer, but there is no evidence of any generalized increase other than that due to tobacco. Moderate increases or decreases due to some new agent(s) or habit(s) might of course be overlooked in such large-scale analyses. But, such analyses do suggest that, apart from cancer of the respiratory tract, the types of cancer that are currently common are not peculiarly modern diseases and are likely to depend chiefly on some long-established factor(s). (A prospective study utilizing both questionnaires and stored blood and other biological materials might help elucidate these factors.) The proportion of current United States cancer deaths attributed to occupational factors is provisionally estimated as 4 percent (lung cancer being the major contributor to this). This is far smaller than has recently been suggested by various United States Government agencies. The matter could be resolved directly by a "case-control" study of lung cancer two or three times larger than the recently completed United States National Bladder Cancer Study but similar to it in methodology and unit costs; there are also other reasons for such a study. A fuller summary of conclusions and recommendations comprises the final section of this report. 198 URL 04702 O Fallacies of Lifestyle Cancer Theories. Epstein S S and Swarz J B. Nature. Vol. 289 127-130. 1981. Cancer is a disease of multifactorial etiology to which occupational exposure and smoking can contribute importantly, sometimes interactively. There have been substantial recent increases in cancer rates which cannot be accounted for by smoking alone. Smoking is the major lifestyle factor of importance in cancer and evidence for the causal role of other lifestyle factors, particularly diet, is slender. The role of lifestyle factors has been exaggerated, by these with an economic or intellectual investment in this theory by largely excluding involuntary exposures to carcinogens and minimizing the role of occupational carcinogens. Cancer is essentially a preventable disease which requires intervention and regulation on several levels, particularly occupational and smoking. Failure to prevent cancer reflects major political and economic constraints which have been hitherto been largely unrecognized and discounted. O A Hazardous Society? Individual Versus Community Responsibility in Cancer Prevention. Higginson J. American Journal of Public Health. 66:4, pp. 359-366. April 1976. The Third Annual Matthew B. Rosenhaus Lecture which reviews the environmental and occupational hazards in cancer with specific emphasis on the role of the individual as well as that of the community in primary cancer prevention and control. O Behind Closed Doors: The Problem of Indoor Pollutants. Kirsch L S. Environment. 25:2, 17-42. 1983. An overview report concerning indoor pollutants. Describes what indoor pollutants are, where they originate, their health effects, and types of controls available. 0 Diet. Nutrition and Cancer. National Research Council; Committee on Diet, Nutrition and Cancer, Assembly of Life Sciences. Nutrition Today, pp. 20-25. August 1982. Executive Summary of report, verbatim transcript. Discusses American dietary patterns and food components; total caloric intake; lipids, proteins, carbohydrates, and dietary fiber in United States diet; the effects of various vitamins and minerals on cancer inhibition; alcohol consumption and cancer; naturally occurring carcinogens; mutagens in foods; food additives; environmental contamination; and the contribution of diet to overall risk of cancer. 199 URL 04703 O Appraisal of Diet, Nutrition, and Cancer Editorial* Mendeloff A I. The American Journal of Clinical Nutrition. 37: 495-493. March 1983. Editorial states that evidence Unking dietary factors and human cancer has not been truly demonstrated. O Prevention of Cancer. Oppenheimer S B. American Laboratory Journal, pp. 66-72. February 1983. Review article which discusses cancer risk factors; specific carcinogens associated with occupation, diet, drugs, hormone usage, and lifestyle factors; and list actions that should lead to substantial prevention of cancers. Examples are: stop smoking, avoid excessive exposure to sun, avoid exposure to known carcinogens, avoid heavy alcohol consumption, and initiate dietary changes, such as, increased vitamin A, C, E. O Indoor Air Pollution: A Public Health Perspective. Spengler J D and Sexton K. Science. 221:4605 9-16. Concerns about potential public health problems due to indoor air pollution are based on evidence that urban residents typically spend more than 90 percent of their time indoors, concentrations of some contaminants are higher indoors than outdoors, and for some pollutants personal exposures are not characterized adequately by outdoor measurements. The more important indoor contaminants associated with health or irritation effects are passive tobacco smoke, radon decay products, carbon monoxide, nitrogen dioxide, formaldehyde, asbestos fibers, microorganisms, and aeroallergens... An overall strategy should be developed to investigate indoor exposures, health effects, control options, and public policy alternatives. O The Health Consequences of Smoking: Cancer. A Report of the Surgeon General. U.S. Department of Health and Human Services Public Health Service Office of Smoking and Health Rockville, Maryland 20857 1982. Report concludes that cigarette smokers have overall mortality rates substantially greater than those of non-smokers. Overall cancer mortality rates among smokers are dose-related as measured by the number of cigarettes smoked per day. Heavy smokers (over one pack per day) have more than three times the overall cancer death rate of non-smokers. Cigarette smoking is the major cause (85%) of lung cancer in the United States and contributes to 309 percent of all cancer deaths. With increased duration of smoking cessation, overall cancer death rates decline, approaching the death rate of non-smokers. 200 URL 04704 O Colon Cancer and Diet, with Special Reference to Intakes of Fat and Fiber* Walker ARP. The American Journal of Clinical Nutrition. 29:1417-1426. December 1976. Colon cancer currently accounts for 2 to 4 percent of all deaths in Western populations. Evidence suggests the primary cause to be reduced intake of fiber-containing foods and increased fat intakes. O The Relationship Between the Geographic Distribution of Lung Cancer Incidence and Cigarette Smoking in Allegheny County, Pennsylvania! Weinberg G B, KullerL H, and Redmond C K. American Journal of Epidemiology. 115:1 40-58. 1982 The results of the Third National Cancer Survey have shown substantial variations in lung cancer incidence rates for white males within Allegheny County, Pennsylvania. The study showed that (1) most of the lung cancer risk between areas was due to cigarette smoking, (2) most of the lung cancer risk within each area was due to cigarette smoking, (3) air pollution effects are minimal, and (4) results emphasize the need to ascertain detailed smoking histories in occupational and air pollution studies. YL CANCER STUDIES IN LOUISIANA O Cancer in Louisiana: Monograph 1983. Correa~P, CheiTv, Craig J F, Bollinger T, Campbell W, and Zavala D E. Louisiana Tumor Registry Department of Health and Human Resources Office of Health Services and Environmental Quality and the Department of Pathology Louisiana State University Medical Center New Orleans 1983 Monograph presents data on the frequency of cancer in Louisiana. Graphs and maps of mortality rates for Louisiana covering the period 1968-78 are compared to the United States rates for the period 196877, while incidence rates for metropolitan New Orleans covering the period 1974-78 are compared to the SEER rates covering 1973-77. O Lung Cancer in Shipbuilding and Related Industries in Louisiana. Gottlieb M S, and Stedman R B. Southern Medical Journal. 72:9 1100-1101. September 1979. The relationship between shipbuilding and related industries and risk of fatal lung cancer (1960-1975) is1-described for selected Louisiana parishes. Deaths from lung cancer were matched to deaths not caused 201 URL 0470 by cancer. Shipbuilders had a significant increased risk (greater than twofold) of dying of lung cancer as compared with other causes. The risk of dying of lung cancer in related occupations (seamen and longshoremen) was also increased... The preponderance of deaths appears to be occurring in men with a greater number of years of exposure to this industry and in those aged 20 to 34 years in 1940. These common occupations in Louisiana could contribute to the high rate of lung cancer. O Lung Cancer in Louisiana: Death Certificate Analysis. Gottlieb M S, Pickle L W, Blot W J, and Fraumeni Jr. J F. Journal of the National Cancer Institute. 63:5. November 1979. A review was made of death certificates of residents in a cluster of Louisiana parishes, mainly in the southern part of the state where lung cancer mortality was high. A comparison of the statements on occupation for 3,327 patients with lung cancer and those of 3,327 controls (matched by sex, race, age, and parish of residence) during 1960-75 revealed an approximately twofold excess risk associated with transportation equipment, mainly shipbuilding and the fishing industry. Smaller elevations of lung cancer risk were found among older men who had been employed in petroleum exploration and production and among male and female residents of towns where the petroleum was a major employer. In addition, Acadian ancestry was associated with a higher risk of lung cancer among older male and female residents. O Lung Cancer and the Petroleum Industry in Louisiana. Gottlieb M S. Journal of Occupational Medicine. 22:6, pp. 384-388. June 1980. Death certificates from the period 1960 to 1975 for Louisiana were surveyed for lung cancer deaths and non-cancer deaths among people employed in petroleum mining and refining to determine if there were specific occupations within this industry associated with a higher risk of lung cancer. Workers employed as welders, operators, boilermakers, and painters and oilfield workers had the greatest risks. Oil field miners born outside Louisiana had a higher risk than native-born miners. Occupation as listed on death certificates provides a rapid means of identifying those with high risk, as a large part of the population can be rapidly screened, covering employees in many industries. O Pancreatic Cancer Mortality in Louisiana. Pickle L W, and Gottlieb M S. American Journal of Public Health. 70:3, pp. 256-259. 1980. As a preliminary step in the investigation of high pancreas-cancer mortality among white males in a cluster of Louisiana parishes, we 876 pairs of certificates of death were examined which occurred in this 202 URL 04706 area during 1960-75. The pancreas-cancer death records were matched to controls by age, race, sex, year of death, and parish of residence. The odds ratios were increased about two-fold for workers in the oil refining and paper manufacturing industries, and slight elevations were seen among residents near refineries and food processing plants. Despite the limited residential and occupational information available on death certificates, this study suggests leads to environmental factors that can be further investigated by a case-control interview study in Louisiana. O Lung Cancer Mortality and Residential Proximity to Industry. Gottlieb M S, Shear C L, and Seale D B. Environmental Health Perspectives. Vol. 45, pp. 157-164. 1982 A potential causal relationship has been suggested by other studies between air pollution and lung cancer. To attempt to define the risk of lung cancer associated with residential proximity to industry by type in Louisiana, lung cancer deaths occurring between 1960 and 1975 in residents of 20 parishes were compared to controls matched on age, sex, year of death and parish of residence. The comparisons were limited to cases (N=1418) and controls (N*1429) with known length of exposure to and residing within"3.99 mile Exposed and 1.0 to 3.0 miles (unexposed) radius of an industry type. Of the 13 industry types evaluated, the petroleum and chemical industries showed the highest consistent elevations in risk associated with closeness of residence to industry, whereas possible risks shown for food, grain, canning, and paper industries are less defined. For the petroleum industry, the risk was demonstrated in the group with 10 or more years of residential exposure to the industry in question. For the chemical industry, the residential rfck was found in people employed in low risk occupations, who were exposed to large individual industries and was independent of length of exposure as determined for less or more than ten years, (RR=4.5). The results suggest that residential proximity to petro chemical industries may make a contribution to the lung cancer mortality in Louisiana. O Trends in Respiratory System Cancer Mortality in Louisiana: Geographic Distributions in 1950-1969 and 1967-1976 Compared. Rothschild H, Voors A W, Weed B A, Vial L J, Welsh R A, and Johnson W D. American Journal of Public Health. 69:4, pp. 380-381. April 1979. When 1967-1976 data compared with Mason and McKay's data (19501969), mortality attributable to respiratory system cancers (RCS) increased for Louisiana as well as for most parishes. In contrast to the trend for the United States, a greater rate increase was observed for whites than for nonwhites. Changes in age composition did not contribute to the observed increases in Louisiana, when compared with the rest of the nation nor when compared with the rest of the United States nor when compared with the previous data period, because rates were adjusted to the same (1960) United States age distribution. Men in southern Louisiana continued to rank high in mortality due to RSC. 203 URL 04707 O An Increased Risk for Lung Cancer Mortality Associated With Sugarcane Farming. Rothschild H and Mulvey J J, Journal of the National Cancer Institute. 68:5, pp. 755-760. May 1982. In a study to determine reputed occupation-related factors responsible for the excessive mortality due to lung cancer in southern Louisiana, the next of kin were interviewed of 284 of 400 persons (71%) randomly sampled from a total of 815 persons who died of lung cancer during 1971 through 1977 and had lived in any of 10 parishes (counties) of southern Louisiana. Of the decedents , 108 (38%) had been employed for at least 6 months as sugarcane farm workers at some time during their lives. Logistic regression analysis indicated this industrial involvement differed significantly (P 0.0001) from that of a control group, consisting of persons who had died of any cause other than lung cancer and who were matched for year of death, age, sex, race, and parish of residence; only 58 (20%) matched controls had had sugarcane farm employment (odds ratio=2.4; 95% confidence interval, 2.0-2.9). Employment in other industries or tobacco consumption could not account for the elevated risk of lung cancer mortality associated with sugarcane farming. After adjustment for smoking, the relative risk estimate of lung cancer mortality for sugarcane farm workers was 2.4 (95% confidence limits, 1.7-3.6). The sugarcane farmers who died with lung cancer had worked for longer periods in the sugarcane farm industry than did those sugarcane farmers in whom lung cancer did not develop (P=0.006). No specific histopathologic cell type was noted to be increased in persons who had been employed in sugarcane farming; however, 2 sugarcane farmers had had mesotheliomas. O Evidence for Space-Time Clustering of Lung Cancer Deaths. Shear C L, Seale D B, Gottlieb M S. Archives of Environmental Health. 35:6, pp. 335-343. November/December 1980. One parish in Louisiana has the highest reported incidence of lung cancer in the United States. Statistically significant space-time clustering (P .01) was present among lung cancer deaths (1960-1975) in residents of the urban portion of this parish. The spatial distribution of cancer deaths in the urban portion of the parish was compared to age, year of death, race, and sex matched control deaths to determine the risk of lung cancer associated with residential proximity to industry. For industries with independently increased risks, the combination of industries produced risks of 1.9 to 3.2 (P .05) for residing within 1.2 km of one or more industries to three or more industries, respectively. The results suggest residential exposure to industrial effluents is a factor contributing to the rate of lung cancer. O Relationship Between Respiratory Cancer and Wetlands Residency in Louisiana. Voors A W, Johnson W D, Steele S H, Rothschild H. Archives of Environmental Health, pp. 124-129. May/June 1978 204 URL 04708 Cancer mortality is high among white men residing in southern Louisiana parishes (counties). In an effort to elucidate this phenomenon, we studied three environmental correlates of cancer- namely, smoking, residence in urban communities, and residence in the wetlands were studied. Multiple regression analysis was applied to cancer mortalities adjusted for age and urban residency, and specific for race, sex, amount of standing water area in the parish, and cancer site. Cancer sites were grouped according to their correlation with smoking: strong, moderate, and no correlation. For men, the smokingrelated cancer mortality not only showed an association with residence in wetlands but also was higher in the Louisiana wetlands than in the remainder of the United States. ML AIR POLLUTION O Air Pollution, Demography, Cancer: Houston, Texas. Patterns of mortality In 15 regionsin Houston suggest a relationship to industrial pollution. McDonald E J. The University of Texas System Cancer Center 6723 Bertner Avenue, Houston, Texas 77030 Journal of the American Medical Women's Association, 31:10, pp. 379-395. Epidemiological investigations of the pattern of cancer mortality in Houston, Texas, was compared with patterns of industrial and ambient pollution. Evidence of a positive relationship was found. O Analysis of Organic Air Pollutants by Oas Chromatography and Mass Spectroscopy: Final Report. Pelllzzari E D. U.S. E.P.A. Environmental Sciences Research Laboratory Research Triangle Park N.C. 27711 EPA-600/2-79-057 March 1979. Three major geographical areas were selected for this study: Plaquemine, Geismar and Baton Rouge, Louisiana; Linden, Deepwater and Camden, New Jersey; and Philadelphia, Pennsylvania. The program was designed to delineate the strengths and weaknesses of the collection and analysis system for vapor phase organic compounds utilizing techniques of hrgc/ms/comp. Over 30 h&logenated hydro carbons were identified from the Plaquemine sampling site and a total of 18 halogenated hydrocarbons and 25 oxygenated compounds were identified in Baton Rouge ambient air. VOL O WATER The New Orleans Drinking Water Controversy: A Statistical Perspective. De Rouen T a7 and Diem J E. American Journal of Public Health. 65:10, pp. 1060-1062. 1975. 205 URL 04709 Report reviews Environmental Defense Fund report on drinking water and cancer in New Orleans. Concludes that although the theory is a plausible one, the evidence in support of it is not strong. O Variations in Drinking Water Quality and the Possible Effects on Human Health. Feder G L and Hopps H C. Trace Substances in Environmental Health - XV: A Symposium. University of Missouri, Columbia pp. 96-103. 1981. Many natural, potable waters can act as important supplements to food, contributing in a substantial way to the daily dietary requirements of several essential macro and micro elements. This is subject to marked geographic variation, however, because the chemical characteristics of natural waters vary greatly among various geologic terranes. This variation is not limited to the horizontal plane, but has a vertical component as well. For example, waters from wells adjacent to each other but completed at different depths often show marked variations. The range in concentration of chemical constituents in waters from different geologic terranes often varies from one to 3 orders of magnitude. Because of this, statements about the nutritional qualities of water must take into account the source of the water being considered. For example, many water supplies contain over 100 mg/1 magnesium, and can provide a major part of the recommended daily requirement (350 mg/day). A recent collaborative study between scientists of the U.S. and the USSR has shown that, at least in some circumstances, distilled (desalinated) water is not a suitable sole source of drinking water for animals, including human beings. We are proceeding with studies to determine the desirable amounts of various inorganic chemicals that would enhance desalinated water in terms of health benefits. In this context, health benefits include the provision of important nutrient elements as well as the exclusion of toxic ones. Results of this research could also provide information of potentially great value in enhancing the chemical composition of natural water supplies that are of suboptimal chemical quality. O Cancer and Drinking Water in Louisiana: Colon and Rectum. Gottlieb M S, Carr J K, and Morris D T. International Journal of Epidemiology. 20:2, pp. 117-125. 1981 A case-control mortality study conducted in 20 parishes (counties) of South Louisiana to determine what relationship drinking Mississippi River water might have on mortality from colon or rectal cancer, found a significant risk for rectal cancer associated with surface water. Rectal and colon cancer deaths (692 and 1167) from 1969 to 1975 were matched to non-cancer deaths by age at death (15 years), year of death, \ 206 URL 04710 sex and race, and within groups of parishes with similar industrial and urban-rural characteristics each group being defined so as to ensure that it included as nearly as possible equal populations using water from ground and surface sources, based on the 1970 census. Colon cancer did not relate significantly to any water variable, but rectal cancer associated strongly with surface, or Mississippi River, water. The odds ratio for rectal cancer between those who were born and died on ground water was 2.07 with 95% Cl (1.49-2.88). A multi-dimensional contin gency table analysis found the association between rectal cancer and surface water significant at the .0001 level and not dependent on age, race, sex or year of death. The risk for men was slightly higher than for women, but both sexes showed an increased risk. Chlorination also associated significantly with rectal cancer. Among those who used river water, the risk increased inversely as the distance from the mouth, with greater risk downstream from the many industries which line the river. O Case-Control Cancer Mortality Study and Chlorination of Drinking Water in Louisiana. Gottlieb M S, and Carr J K. Environmental Health Perspectives. 46, pp. 169-177. 1982. Several Louisiana parishes (counties) using the Mississippi River for their source of public drinking water have the highest mortality rates (1950-69) in the United States for several cancers. Therefore, a casecontrol mortality study on cancer of the liver, brain, pancreas, bladder, kidney, prostate, rectum, colon, esophagus, stomach, non-Hodgkin's lymphoma, multiple myeloma. Leukemia, Hodgkin's disease, lung, breast and malignant melanoma, from 1960 to 1975 in South Louisiana parishes grouped for similarities in industrial characteristics, having approximately equal exposure of the population to surface and groundwater, was conducted. Noneancer deaths were randomly selected as controls and matched to the case death on age, race, sex, and year and parish group of death. Water source at death was assigned based on the residence at death and described as surface or ground and chlorinated or nonchlorinated. A significantly increased risk for surface, chlorinated water use was noted for rectal cancer. No risk could be demonstrated for colon cancer. The risk noted for bladder cancer by other investigators is not substantiated. Brain cancer risk appears to be associated with chlorinated groundwater, but this may be industrial confounding. Breast cancer demonstrated a slight, but signif.eant, risk associated with surface chlorinated water. This risk, however, might be due to confounding of rural life style, early childbearing and large families with nonchlorinated water found in these settings. Chlorination risk for kidney cancer was not significant. No risk was observed in association with surface water for other cancers of the gastrointestinal or urinary tract. Multiple myeloma was significantly associated with a risk from ground water. 207 O Drinking Water arid Cancer in Louisiana; A Retropective Mortality Study. Gottlieb M S, Carr J K, and Clarkson J R. American Journal of Epidemiology. 116:4, pp. 652-667. 1982. Thirteen Louisiana parishes (counties) using the Mississippi River as a source of potable water have the highest mortality rates (1950-1969) in the United States for several cancers. To assess a possible relationship with drinking water source, a comparison of cancer deaths and noncancer deaths from 1960-1975 in selected southern Louisiana parishes was conducted. Parishes were grouped for similarities in industrialization and approximately equal exposure of the population to surface water and ground water. Cancers were studied in groups by hypothesized risk: high for bladder, colon, kidney, liver, lymphoma, rectum, and stomach; low for Hodgkin's lymphoma, leukemia, lung, malignant melanoma, multiple myeloma, and prostate; and questionable for breast, brain, esophagus, and pancreas. Noncancer deaths were randomly selected and matched 1:1 to cancer deaths on age, race, sex, residence at death, surface or gound water, and chlorinated or nonchlorinated water. The risk associated with using surface water least likely due solely to chance occurred for cancer of the rectum. Other risks which were lower but still greater than 1.0 occurred for cancer of the kidney and breast. No risk was observed for other cancers of the gastrointestinal or urinary tract. Risk for multiple myeloma was associated with use of ground water. O Carcinogenesis Induced by Trace Contaminants in Potable Water. KraybiU H F. Bulletin of New York Academy of Medicine. 54:4, pp. 413-427, April 1978. Some organic biorefractories in drinking water have been identified as carcinogens by reference to the literature, where some of these chemicals have been bioassayed in standard procedures using the rodent, other species, or both. Similarly, some inorganic water contaminants have been classified as carcinogens from experimental studies. Epidemiological studies have been conducted on inorganic contaminants which attempt to show, on a regional basis, possible relations to cancers in man in various organs and tissues. Some of these studies raise questions which require further investigation. In addition to corroborative evidence from carcinogenicity bioassays of various organic chemicals using typical rodent-feeding and inhalation studies over a two-year period, other approaches are suggested to determine carcinogenicity. The use of bacterial systems and cell cultures are recommended to determine mutagenicity and determine cell trans formation in in vitro bioassays to augment the in vivo procedures. Assessment of the role of aquatic carcinogens in the induction of human cancer is a complex area for research and requires a multidiscipline approach. Progress is being made because water, as an environmental stress system, is perhaps better identified, classified, and monitored than other human exposure. While carcinogenic stress may not depend on a microlevel of any one molecular species, inevitably the total dose from multiple biorefractories, contaminants, or both may possibly initiate cancer after a latency period of many years. 208 URL 04712 Evaluation of Public Health Aspects of Carcinogenic/Mutagenie Biorefractories in Prinking Water, Kraybill H F. Preventive Medicine. Vol. 9, pp. 212-218. 1980. At the turn of the century, concern over the contamination of drinking water was focused on that caused by viruses, bacteria, and parasites. However, in the developed countries attention is currently focused on organic chemical contaminants and, to a lesser extent, the inorganic chemicals. Of the wide spectrum of organic biorefractories in potable water, an identification and classification of a list of 309 in 1977 revealed 23 carcinogens and 30 mutagens. A current list updating such information may reveal a larger number. While some chemicals in drinking water, such as arsenic and nitrite, were incriminated in studies some years ago with regard to cancer, current studies on organic biorefractories are inconclusive. Some experimental studies in systems, in vitro and in vivo, would indicate some mutagenic and carcinogenic activity, however, more comprehensive studies are needed to provide more convincing evidence on cause and effect. Similarly, there have been 12 reported epidemiological studies of various types, some of which suggest interesting statistical associations. The studies, however, are limited with some uncontrolled variants. Future studies will have to correct for certain deficiencies. While the experimental and epidemiologic studies provide some presumptive evidence, one cannot establish, with any degree of assurance as yet, any causality relevant to cancer from these mieropollutants. There is serious concern, however, about those contaminants with the realization that the ingested carcinogenic-mutagenic biorefractories may contribute to the total cancer burden. Thus, control and reduction technologies in water treatment are recommended. Organics at the Air-Water Interface of Lake Pontchartrain. McFall J A, Huang W Y, and Laseter J L. Bulletin of Environmental Contamination and Toxicology, pp. 80-87. 1979. A wide variety of organics have been characterized by GC-MS in our samples collected from the air-water interface of Lake Pontchartrain. These include chlorinated hydrocarbons, aromatic hydrocarbons, fatty acids, alcohols, phenolic compounds, and phtalic acid esters. Although some are clearly biological in origin, a large number of the organic compounds present are of industrial origin that enter the lake from industrial effluents, domestic sewerage, atmospheric fallout, and agricultural runoff. These organics potentially have an effect on the biological processes in the environment. Therefore many of the organic compounds appear on the USEPA Priority Pollutant List and can be toxic to the aquatic organisms present and can also affect the health and well-being of humans deriving food products from Lake Pontchartrain. Studies are presently underway to determine the origin of these organics. Additionally, investigations into the nature of the primary uncharacterized organics are being carried out. 209 O Drinking Water and Cancer Mortality in Louisiana. Page T, Harris R H, and Epstein S S. Science. Vol. 193, pp. 55-57. July 1976. Multivariant regression analysis Indicates a statistically significant relationship between cancer mortality rates in Louisiana and drinking water obtained from the Mississippi River. This is true for total cancer, cancer of the urinary organs, and cancer of the gastrointestinal tract. 'A i O Reversion of Mutant Strains of SnhmnwHn Typhlinuriumby Knw im<l FinlMFuvd ftajerw froTn'BouIhcmw 1orn LouIfTTnnn. I'cTmu W, Whitman n F, Ho/mlcy 'lrVfl, mid Lonloy 1) I?. ItnvlromuohUI Inlornat loiml. Vol. *4, pp. rtU-75. Hinnplori of ruw und flnlslmd wutor wore collected from water treat ment plants in southeastern Louisiana between January 1975 and May 1976. The water source for each plant is the Mississippi River. Finished water samples also were obtained at water treatment plants at St. FranclsviUe, LA. and Baton Rouge, LA. where deep wells serve as sources of water. All samples were assayed for mutagens using histidine dependent mutant strains of Salmonella typhimurium. Almost twice as many of the finished water samples collected at Luling, Jefferson and New Orleans induced reversions than did the corresponding raw water samples. Often reversion of finished water samples occurred only with metabolic activation. When samples from Belle Chasse and Port Sulphur were assayed, the number of finished water samples inducing reversion were comparable or less than comparable to those with raw water. Nearly equal numbers of finished water samples from St. Francisville and from Baton Rouge induced genetic change. However, the majority of the samples from Baton Rouge which caused reversion, did so only with liver enzyme activation. Discussed is the significance of these findings, as well as the possible role of chlorination procedures in halogenating hydrocarbons into compounds which are mutagenic and/or carcinogenic. URL 0471 t OJ O Organic Chemical Contaminants in Drinking Water and Cancer. Wilkins J R Ill, Reiches N A, Kruse C W. American Journal of Epidemiology. 110:4, pp. 420-448. 1979. The discussion presented here reviews the epidemiologic evidence that has been advanced to evaluate the drinking water - cancer hypothesis. O Halogenated Hydrocarbons in New Orleans Drinking Water and Blood Plasma. Dowtz B, Carlisle D, Laseter J L, and Storer J. Science 187. 75-77. January 1975. Volatile organics from New Orleans drinking water and pooled plasma were collected on a solid phenyl ether polymer and analyzed by gas 210 URL 04714 chromatographic and mass spectrometric techniques. Thirteen halogenated hydrocarbons were identified in the drinking water. Five halogenated compounds were found in the plasma. Tetrachloroethylene and carbon tetrachloride were found in both the plasma and the drinking water. Considerable variation in the relative concentrations of the halogenated hydrocarbons was noted from day to day in the drinking water. DC. UK ASSESSMENT O Risk Assessment in the Policy-Making Process: Environmental Health and Safety Protection. Regens J L, Dietz TM, and Rycroft R W. Public Administration Review, pp. 137-145. This article examines the extent to which differences exist in the relative degree of discretion permitted by the statutory mandates under which health risk assessments are conducted as a basis for regulatory action. Attention is focused on the Environmental Protection Ageney and the Food and Drug Administration, because they are the lead federal regulatory agencies on most environmental health matters. The statutes are found to define risk, consider effects, identify target populations, and use benefit-cost analysis in a flexible way. But the burden of proof of risk typically is assigned in a more direct and stringent fashion. Overall, however, agencies are found to have substantial discretion in the manner in which risk assessments are incorporated into the policy process. A number of examples of efforts to reduce this flexibility are outlined and their implications for the future of the analysis of risks are delineated. O Cost-Effective Priorities for Cancer Prevention. Weinstein MC. Science. Vol. 221, pp. 17-23. July 1983. Faced with limited resources, the United States must set priorities for research to identify preventable causes of cancer. A quantitative approach to priority setting, based on principles of decision analysis and cost-effective analysis, can offer guidance in this process. An illustra tive application of such a model suggests that the National Institutes of Health-supported clinical trial of dietary B-carotene offers a greater expected reduction in cancer mortality per research dollar than Car cinogen bioassays of high-volume industrial chemicals such as pdichlorabenzene. National research priorities should reflect the relative cost-effectiveness of such investments. 211 *L~ URL 04715 o Risk Assessment in the Policy-Making Process: Environmental Health and Safety Protection, Regens J L, Dietz T M, Rycroft R W. Public Administration Review, pp 137-145. March/April 1983. This article examines the extent to which differences exist in the relative degree of discretion permitted by the statutory mandates under which health risk assessments are conducted as a basis for regulatory action. Attention is focused on the Environmental Protection Agency and the Food and Drug Administration, because they are the lead federal regulatory agencies on most environmental health matters. The statues are found to define risk, consider effects, identify 'target populations, and use benefit-cost analysis in a flexible way. But the burden of proof of risk typically is assigned in a more direct and stringent fashion. Overall, however, agencies are found to have substantial discretion in the manner in which risk assessments are Incorporated into the policy process. A number of examples of efforts to reduce this flexibility are outlined and their implications for the future of the analysis of risks are delineated. 0 Cost-Effective Priorities for Cancer Prevention. Weinstein, M Science, Vol. 221, pp. 17-23 July 1983. "Faced with limited resources, the United States must set priorities for research to identify preventable causes of cancer. A quantitative approach to priority setting, based on principles of decision analysis and cost-effective analysis, can offer guidance in this process. An illustrative application of such a model suggests that the National Institutes of Health-supported clinical trial of dietary B-carotene offers a greater expected reduction in cancer mortality per research dollar than carcinogen bioassays of high-volume industrial chemicals such as p-dichlorabenzene. National research priorities should reflect the relative cost-effectiveness of such investments." O Evaluation of Tests for Mutagenicity as Indicators of Environmental Mutagens and Carcinogens. deSeries F J. Annals New York Academy of Science. Vol. 329, pp 75-84. 1979. Reviews the progress made in the field of testing for mutagens as an effective mechanism for rapid identification and elimination of hazardous chemicals from the environment. Discusses the development of genetic tests that can be made on high-risk worker populations or on other high-risk groups. 212 TZ i.;r = URL 04716 0A)9]OOS jo sjuaiuSas SuiAjba q pdUtjap S9 Hijjauaq/>|su,4 pue 44>(su d{q&idaa>Bu jo sideouoo am jo MaiAjaAo uy 'ZLZ-L9Z <W *$ZV *IOA 'saouaiog jo Xuiapuoy *6^61 stauuy 'M S siammss sisA'i^uy jTjaudQ/>(SiH jo sapetl^jl aqx O - .- - k This public document was published at a total cost of $42,898. 2,500 copies-of this public document were published in the first printing at a cost of $9,220. The total cost of all printings of this document including reprints is $42,898. This document was published for the Governor's Task Force on Environmental Health by the Louisiana State University, Print Shop, 3555 River Road, Baton Rouge, Louisiana 70803 to provide information on cancer in Louisiana under the Executive Order 83-1. This material was printed in accordance with the standards for printing by state agencies established pursuant to R.S. 43:31. Printing of this material was purchased in accordance with the provisions of Title 43 of the Louisiana Revised Statutes. LU M Ibn ERF AT A <r ------- v This public document was published at a total cost of $42,772. 5,000 copies of this public document were published in the first printing at a cost of $9,095. The total cost of all printings of this document including reprints is $42,772. This document was published for the Governor's Task Force on Environmental Quality by the Louisiana State University, Print Shop, 3555 River Road, Baton Rouge, Louisiana 70803 to provide information on cancer in Louisiana under the Executive Order 83-1. This material was printed in accordance with the standards for printing by state agencies established pursuant to R.S. 43:31. Printing of this material was purchased in accordance with the provisions of Title 43 of the Louisiana Revised Statutes. URL 04717.01