Document BRLEDMzQneapKYobgnYjEaDMJ

Vista Chemical Company August 2, 1988 15990 North Barker's Landing Road Post Office Box 19029 Houston, Texas 77224 Phone (713)531-3200 TGG: JCL: MMG: RF XF:__ _________ Mr. Steve Freese B. F. Energy 359 San Miguel, Suite 204 Newport Beach, CA 92660 Dear Steve: Enclosed is a copy of the skin irritation study on Vista 47 Ink Solvent. The testing produced a maximum irritation index of 3.7 out of 8, which classes it as a moderate irritant. This study is done by causing constant contact on the skin of rabbits for four hours. From a regulatory standpoint an irritation score of 5.0 or greater as defined in the Hazard Communication Standard is considered a skin irritant by OSHA. However, proper precautions should be taken by users of this product to avoid prolonged or repeated skin contact. Please contact me if you have any questions regarding the details of this study. Sincerely, Thomas G. Grumbles, C.I.H. Environmental Quality Manager dlj Enclosures VVV 000008717 Thomas G. Grumbles To ^V tf2oC\ rr\<2>A \ VISTA (\^aeVe.t> as a c^o-ot^ \^od'c\^V- or\ cxVe^s^ eAd. ~+ V\G.^e, 3^m e_ V\qA^><-A lA^t>ZsftOccf'W/\ $> YR- C_CrA Aa^/lltcL^W/x VVV 000008713 vvv 000008719 The American Council on Science and Health (ACSH) is a national consumer education association directed and advised by a panel of scientists from a variety of disciplines. ACSH is committed to providing consumers with scientifically balanced evaluations of issues relating to food, chemicals, the environment, and health. ACSH is a nonprofit association exempt from federal income tax under Section 501 (cl (3) of the Internal Revenue Code. All contri butions are tax-deductible as provided by law. Individual copies of this report are available at a cost of $2.00. Reduced prices for 10 or more copies are available on request. June 1988 American Council on Science and Health 1995 Broadway (18th floor) New York, NY 10023 (212) 362-7044 CANCER IN THE UNITED STATES: Is There an Epidemic? This report was written by Alan C. Fisher, Dr.P.H., and Wendy Worth, Ph.D. The American Council on Science and Health (ACSH) gratefully acknowledges the comments and contributions of the following individuals who reviewed this report: Donald F Austin, M.D., M.P.H. California Department of Health Services Stephen Barrett, M.D. Lehigh Valley Committee Against Health Fraud Norman E. Borlaug, Ph.D. Texas A&M University Joseph F. Borzelleca, Ph.D. Medical College of Virginia Julius Coon, M.D., Ph.D. Thomas Jefferson University James E. Enstrom, Ph.D. University of California, Los Angeles Lloyd Jackson Filer, Jr., M.D., Ph.D. University of Iowa Ralph W. Fogleman, D.V.M. Upper Black Eddy, PA F.J. Francis, Ph.D. University of Massachusetts Roger E. Gold. Ph.D. University of Nebraska Saxon Graham, Ph.D. State University of New York at Buffalo Alfred E. Harper, Ph.D. University of Wisconsin Victor Herbert, M.D., J.D. Bronx VA Medical Center Mt. Sinai School of Medicine Howard D. Maccabee, Ph.D., M.D. Radiation Oncology Center Walnut Creek, CA W.W. Melvin, M.D.. Sc.D., M.P.H. Colorado State University Thomas Mllby, M.D., M.PH. Lafayette, CA J.A. Milner. Ph.D. University of Illinois VVV 000008720 Grace P. Monaco, J.D. White. Fine & Verville Robert E. Olson, M.D., Ph.D. State University of New York at Stony Brook Edward G. Remmers, Sc.D. American Council on Science and Health Sidney ShindeU, M.D., LL.B. Medical College of Wisconsin Fredrick J. Stare, M.D., Ph.D. Harvard School of Public Health Stephen S. Sternberg, M.D. Memorial Sloan-Kettering Cancer Center Elizabeth M. Whelan, Sc.D., M.P.H. American Council on Science and Health The opinions expressed in ACSH publications do not necessarily represent the views of all ACSH Directors and Advisors. 2 Part I: Cancer Statistics and Trends Introduction Cancer is a disease that should concern all Americans. Actually, cancer comprises a group of more than 100 dif ferent diseases. Although their form and symptoms vary, all cancers begin with an alteration in a normal cell that in turn replicates itself millions of times resulting in the unregulated growth and spread of abnormal cells. Our concern over the disease is justifiable. Approximately 22 percent of all deaths in this country are now due to can cer. It is estimated that in 1987 there were 483,000 can cer deaths and 965.000 new cases of cancer in the United States. Many Americans believe that we are currently experienc ing a cancer epidemic. With the notable exception of lung cancer, this is not true. An "epidemic-' is a significant increase in the frequency of a disease. In the case of can cer. what is excessive can be determined by a comparison of cancer rates over time, among different countries, and even among different groups within the same country. As will be seen, such comparisons do not reveal an overall cancer epidemic in the U-S. today. Part 1 of this report focuses on these comparisons. Part II focuses on the known causes of human cancer and what one can do to reduce his/her risk of developing any of these many diseases. Before looking at these compari sons. however, it is necessary to have a working under standing of how cancer statistics are typically calculated and the limitations of the sources from which they are obtained. Ways of Looking at Cancer Data: Terminology Epidemiology is the scientific study of the distribution and determinants of disease frequency within and between human populations, and the application of this study to the control of health problems1. Cancer epidemiology is a subspecialty of this discipline, which uses standard statisti cal techniques to compare cancer data from place to place, time to time, or group to group. This report will focus only on those techniques that are most useful for addressing the issue of a cancer epidemic in the United States. An important concept in cancer epidemiology is inci dence--the number of new cases diagnosed in a given geographic place during a specific period of time. To compensate for variations in number of inhabitants in dif ferent areas, incidence is divided by the total population 3 VVV 000003721 to yield the incidence rate. The measure thus formed is not influenced by population size and can be used for comparison. Another important concept is cancer mortality or death. This is how many people in a given geographic place, during a specific period of time, die of cancer. Usually one wants to compare cancer deaths, and therefore cal culates mortality or death rates by dividing the number of deaths by the total population of the geographic location. Theoretically, epidemiologists prefer incidence rates to death rates. Incidence rates are more closely associated with the occurrence of a disease and its causes. By con trast, mortality data are the end result of the disease and are therefore further removed from its causes. Such data are also influenced by changes and advances in treat ment. However, death rates for cancer are more readily available than incidence rates, because the cause of death appears on every death certificate. Thus, epidemiologists frequently use cancer death rates to indicate incidence rates. Death rates most closely resemble incidence rates when the average survival time for a form of cancer is short. Lung cancer is one instance where incidence and death rates are similar. Despite the theoretically valid argument just outlined, some evidence points to unreliability of incidence rates for studying recent trends in cancer. With respect to some cancers, recent trends show either sharp increases or sub stantial fluctuations from year to year. The following sec tion deals with the `'biases'' (or systematic departures from true values) believed responsible for these statistical artifacts (exception: lung cancer). Occasionally, incidence rates and death rates are stand ardized or "adjusted" for an additional factor, namely age. The adjusted rate is composed of a weighted aver age of rates for specific age groups. The amount of weight given to each age group is determined by refer ence to a standard population, Since the risk of cancer increases with age and people in the United States are liv ing longer today, failure to either adjust cancer rates by age or look at different age groups separately (age-spe cific rates) can convey the impression of an overall increase in cancer when in fact there is none. Therefore, when one compares cancer rates over time, between places, or among racial and ethnic groups, where the age distribution varies, one generally adjusts the rates statisti cally to a standardized age distribution so as to make them comparable. Thus, changes in cancer frequency over and above those influenced by a changing age distri bution become detectable. Incidence rates and death rates are often reported per 100,000 persons. Also, it is common to report rates for a one-year period corresponding to a given calendar year. 4 The United States Sources of Cancer Data In the United States there is one primary source of data for incidence rates and one for death rates. The National Cancer Institute (NCI) has conducted sur veys of cancer incidence in the past (1937. 1947. 196971). It was not until 1973. however, that it began to con stantly monitor cancer incidence through the Surveillance. Epidemiology, and End Results (SEER) Program. This program involves collection of data from cancer registries in different geographic areas. The areas presently covered are the entire states of Connecticut. Hawaii, Iowa. New Mexico, Utah, and New Jersey, as well as the Commonwealth of Puerto Rico. Also included are metropolitan Atlanta, Detroit, and the San FranciscoOakland and Seattle-Puget Sound areas. The areas cov ered by SEER have changed slightly over the years. Mortality data on cancer come from the National Center for Health Statistics (NCHS) and are obtained from death certificates throughout the U.S. Such data have been available since 1933. Every year the American Cancer Society (ACS) uses data from the NCI and NCHS to compile estimates of both cancer incidence and mortality for the upcoming year. The annual ACS publication presenting this infor mation is called Cancer Facts and Figures.- A. Accuracy. All three sources of cancer data have limitations, some of which are inherent in the data and can cause bias during examination of statistics for a specified period. In other circumstances, biases cause concern when we compare data from different time periods. Different kinds or degrees of bias may characterize each period. The major limitation of the recent NCI data (SEER) is that the geographic areas covered in the Survey do not repre sent the United States as a whole, but were chosen because they represent epidemiologically diverse popula tions. Information included for incidence rates by site, age, race, and ethnicity allows epidemiologists to monitor changes in incidence over time and make comparisons among groups. In fact, mortality rates by cancer site, for the SEER areas and the U.S. as a whole, correspond closely, especially for whites. Thus, cancer incidence rates by site obtained from SEER may be representative for the white population. In comparing incidence rates over time for NCI data, a number of important biases are relevant. First, there has been a change in the geographic areas covered. Although some overlap occurs among the first three NCI VVV 000008722 studies and the areas covered by SEER, there is also a significant difference in the areas covered by the earlier studies compared to those covered by SEER. A second bias stems from differences in the accuracy of area popu lation estimates at different time periods. Another impor tant problem likely to have varied over time lies in the care taken to include each cancer patient only once in the study and to include only new cases of cancer for the per iod under study. Accompanying this is the bias intro duced by changes in the effort and motivation of physi cians in registering cases of cancer incidence. Furthermore, over the years there have been technical changes in the definition of exactly what constitutes a cancer as well as changes in the methods and ability to diagnose many forms of the disease. Many experts believe that current cancer incidence rates are being inflated by a significant number of cases of "overdiagnosis''--growths that are biologically malignant but do not spread quickly and threaten the individual's health. In a recent report. the National Cancer Advisory Board identifies this problem as inflating some cancer rates. Data on death rates from the National Center for Health Statistics (NCHS) are subject to several kinds of prob lems. Since the source of these data (death certificates) has remained constant, biases in current data and those arising from comparisons with past data will be discussed together. Rules governing the registration of deaths from one state to another may vary over time, thus introducing a source of bias and making comparisons more difficult. Classifica tion systems used in the reporting of deaths have varied over time. Even when the exact type of cancer is detected while the patient is alive, the correct information may not appear on the death certificate. In addition. often only one underlying cause of death appears on a death certifi cate, and therefore some cancer deaths are incorrectly attributed to secondary causes or even missed entirely. Such errors are more likely to occur in elderly patients, and have been more of a problem in the past than now. In cases where the patient has widespread cancer, the pri mary site of the disease may not be known and/or prop erly recorded and thus the type of cancer is not specified on the death certificate. When cancer has spread, the death certificate may contain incorrect information as to its primary source. Sometimes a misdiagnosis of the cell type of cancer occurs. Many such errors can also affect incidence rates. The annual Cancer Facts and Figures from the American Cancer Society (ACS) is a major source of cancer infor mation disseminated to the public. It is thus fair to ask if the estimates of cancer death and incidence contained in this publication are accurate. Because it takes time to compile nationwide information 6 from death certificates, the ACS uses death rates three to five years old to project trends for the coming year. In general, their track record has been very good. One study12 found that when actual data become available and are compared to ACS estimates for specific sites, esti mates are off by only two to four percent. The more com mon the type of cancer, the better the estimate tends to be. Estimates for sites with rapidly changing mortality (i.e., lung cancer in women) have been consistently low. ACS estimates of incidence tend to be less accurate than death estimates, partly because actual rates from which estimates are made are limited to locations covered by SEER. Yet, estimates for incidence rates are made for the whole country. These estimates are also dependent upon the accuracy of population and mortality projections which may contain errors. Incidence estimates for states covered by SEER, and for cancer sites, have been in error by as much as 22.3 percent, though, in fairness, they have also been within one percent of actual figures. However, it is not uncommon for these estimates to be off by 15 to 20 percent. One problem with all of the above sources of data is their comparability. For example, the ACS often reports data in actual numbers rather than rates, while the SEER and NCHS figures are reported as rates. In addition, when rates are adjusted by age they are not necessarily stand ardized to the same base population. This creates addi tional error. Thus, comparison of cancer statistics between publications or over time must be made with caution. Time Trends in the (J.S.: Incidence and Mortality An important way of examining the issue of whether there is a cancer epidemic in the United States today is to look at patterns over time for cancers of specific sites. As mentioned above, incidence rates are theoretically pref erable to death rates for this type of comparison. But. as noted, in recent years the incidence for some cancers has shown substantial fluctuations not easily explained by the nature of the disease. These variations seem likely to be statistical artifacts produced by a combination of over diagnosis and improved reporting of cancer cases. Breast and prostate cancer are believed to be examples of this situation. In light of these biases, both incidence and mortality data over time are presented. A. Incidence The availability of data on incidence rates over time is lim ited. As mentioned earlier, there were three nationwide NCI cancer studies before the SEER program, covering the years 1937, 1947, and 1969-71. Using these three points in time and the SEER results, the following trends for cancer incidence emerge: 7 VVV 000008723 FIGURE 1 FIGURE 2 AGE--ADjJSTED CANCER INCIDENCE RATtS FOR SElECED SiTES MALE. uN'TEC STATES AGE-ADJUSTED CANCER INCIDENCE R-^ES FDR Sl-ET'E: D E; F-MAi ~ Tt3 STATES ; 60 i Source: Data from NCI cancer incidence surveys (1937. 1947. and 1969-71) and SEER (1977. 1983), adjusted to the age distribution of the I960 U.S. Census population. Figures 1 and 2 display incidence rates for the three national cancer surveys and for two years from the recent SEER studies. The data are available for white males and females from 1937 to 1983. We see that during this per iod there were sharp decreases in stomach and cervical cancer. Lung, breast, and prostate cancer all show increases. In males, bladder and kidney cancer increased. The increase in breast cancer occurred between the 1969-71 and 1973-77 studies. As seen in Table 1, the 8 SITESEX *+* CSDPHUUIS WWW IFf.T'JU $$$8REAST O0OOM1 a<HHeBt-P*S(sNrOiCoUA^rC*rSt .rcsi *H>B*H* CLJ1HXC0K ^^cwpiis jter: Source: Data from NCI cancer incidence surveys (1937. 1947. and 1969-71) and SEER (1977. 1983), adjusted to the age distribution of the 1950 U.S. Census population incidence rate peaked in 1974. and until the last few years showed an erratic pattern. It is believed that the 1974 peak is due to early disease detection and over diagnosis. In that year, greatly heightened public aware ness of breast cancer followed the announcement that the wives of President Ford and Vice President Rockefeller had the disease. Because no known environmentally induced factor can explain this sudden rise and subse quent variations for breast cancer, it is reasonable at present to attribute this finding to a statistical artifact--a climate of increased public awareness. However, increases during the last few years suggest that such a conclusion may not apply to the most recent data. 9 VVV 000008724 TABLE 1 U.S. Incidence Rate per 100,000 for Female Breast Cancer, Whites, 1973-83* Year 1973 1974 1975 1976 1977 1978 1979 1980 1981 1982 1983 Rate 79.8 90.9 84.6 82.7 80.8 81.1 81.3 81.4 85.0 85.2 87.8 Age adjusted to the 1950 U.S. population. Source: SEER, unpublished computer run. Cancer of the prostate shows a consistent increase in the period covered. As in the case of breast cancer, this may also be due to a statistical artifact. Doll and Peto' believe this pattern to be the result of a "vigorous search for lumps" resulting in overdiagnosis of the disease in cases where it is associated with old age and is not lifethreatening. Frequently, this apparent increase is detected as a result of biopsies for noncancerous condi tions. The average age at diagnosis of prostate cancer is about 73. Over the years the frequency and accuracy of autopsies have increased, and incidental findings of pros tate cancer have been added to incidence cases. Thus, the recorded increase in prostate cancer may reflect increased biopsy and autopsy findings of cancers in men without any symptoms of the disease. At this time, it is not known whether the increases in male bladder and kidney cancer are real or an artifact resulting from different methods of diagnosis and data collection in the different periods. 10 FIGURE 3 Age-Adjusted Cancer Death Rates * for Selected Sites' Males. United States. 1930-1982 ol f)ii* U8 National Cuntrr toi MAh'tc> .Wij L ^ Rufuau wi th* Hi the aye Wi huii>n *,| thi* H7 !' s t The conclusion from these incidence data is that there is an epidemic of lung cancer in the United States today. However, the most recent NCI data indicate that between 1982 and 1983 the incidence rate for lung cancer in white men decreased from 73.0 to 70.0 per 100.000. adjusted to the 1950 population distribution (82.7 to 79.3 per 100,000 adjusted to the 1970 distribution}. This is the first such decrease in 50 years and corresponds to a substantial decrease in smoking patterns among men about 20 years ago. Among women the story is different. No such decrease is expected for 15 to 20 years because younger women are smoking more. B. Mortality Figures 3 and 4 present death rates for males and females from 1930 until 1982 (the latest data available as of this writing). An important advantage of these data is availa bility throughout the period. These data support the con clusions based on examination of incidence data. For males, the sharp increase in deaths from lung cancer is apparent, as is the sharp decrease in deaths due to stomach cancer. The other forms of cancer tend to show steady death rates, especially in recent years. There is no 11 vvv 000008725 FIGURE 4 Age-Adjusted Cancer Death Hates' for Selected Sites Females, United States, 1930*1982 Sources: Cancer Rales and Risks. N!H publication 85-691 and Cancer Incidence and Mortality. NIH publication 85-1837. marked increase in mortality from prostate cancer. This supports the argument that increases in incidence are largely artifactual. As for females, the increase in deaths due to lung cancer occurs later, as expected. Breast can cer mortality does not increase markedly, again suggest ing that increases in past incidence data are artifactual. Death rates from stomach and cervical cancer also declined over the entire period, and those for colon and rectal cancer show a downward trend. Deaths from other cancers indicate a steady rate in recent years. Current Cancer Patterns in the U.S.: Incidence and Mortality Examination of current cancer patterns is an important step in addressing the issue of whether there is a cancer epidemic. For example, by comparing racial and ethnic groups at the same point in time we can specify which groups have high rates for specific cancers. This may indi cate trends toward an epidemic and further clarify the nature of the epidemic of lung cancer discussed in the previous section. These comparisons have been exam ined for men and women from the 1930s until the early 1980s. Comparing groups at the same point in time allows us to eliminate biases in the data attributable to 12 changes in recording procedures and diagnoses with the passage of time. Before looking at comparisons of cancer rates for racial and ethnic groups, it is important to stress that cancer incidence (and mortality) increases significantly with advanced age. In fact, more than half of the cancer cases diagnosed today are among people 65 or older. Figure 5 displays this trend for white males, white females, black males, and black females. The sharp increase in inci dence evident for all four groups after the age of forty is to be expected, as is the higher incidence of cancer among males. It does not indicate an overall epidemic, but rather explains how our mistaken perception of an epidemic may have come about. FIGURE 5 Average Annual Age-Specific Cancer Incidence per 100,000, U.S. Population, All Sites Combined, 1973-77 'll* Q*r 100 000 mhm eiiu. mii ftlfCl F"*alM Source: Unpublished data ftom SEER. vvv 000008726 13 Primary Site All sites Bladder Breast. Female Ages < 40 Ages 40 + Cervix Uteri Colon Rectum TABLE2 Average Annual Age-Adjusted Cancer Incidence Rates per 100v000 by Primary Site and Racial/Ethnic Group, U.S. SEER Program, 1978-81 Whites 335.0 15.4 86 5 8.2 221.1 8.8 34.6 15.0 Blacks 372.5 86 71.9 10.7 179.3 20.2 37.9 11.7 Hispanics* Japanese 246.2 8.2 54 1 7.9 134.9 17.7 15.8 9.4 247.8 7.7 53.1 8.6 146.5 7.6 34.0 16.4 Chinese 252.9 77 54.0 7.4 141.0 11.2 27.7 13 1 Filipinos 222.4 5.1 43.4 7.1 117.0 8.8 17.7 12.4 Native American Hawaiians Indians 357.9 8.2 111.1 7.1 300.0 14.1 18.4 14.3 164.2 1.1 28.5 4.0 71.4 22.6 8.0 19 VVV 000008727 Corpus Uteri Esophagus Larynx Lung. Male Lung. Female Multiple Myeloma Ovary Pancreas Prostate Stomach 25.1 3.0 4.6 81.0 28.2 3.4 13 6 8.9 75.1 8.0 13.4 11.5 06 119.0 30 5 7.9 9.5 13 6 120.3 13 8 111 1.6 2.6 34.3 13.0 2.5 10.4 10.8 76.5 15.7 18.6 2.4 26 45 1 14 1 1.2 8.7 7.4 44 2 27.9 17.6 3.4 1.9 62.6 31.2 1.6 9.1 9.3 26.1 9.0 11.7 3.6 1.8 38.1 18.4 4.1 94 6.7 48.9 7.0 27.1 6.4 5.2 100.9 38.6 5.5 13.5 10.0 57.9 32.4 2.6 24 0.9 14.6 3.1 2.8 3.2 6.0 45.4 19 3 * Cancer incidence data for Hispanics come from New Mexico only. Source: Baquel. C.R et al. Cancer Among [Hacks & Other Minorities: Statistical Profiles NIH Publication No. 86-2785 Bethesda. Md , National Cancer Institute. March 1986. page 9 o> TABLE 3 Average Annual Age-Adjusted Cancer Mortality Rates per 100,000 by Primary Site and Racial/Ethnic Group, U.S. Total United States, 1978-81* Primary Site All sites Bladder Breast, Female Ages < 40 Ages 40 + Cervix Uteri Colon Rectum Corpus Uteri Whites ' 163.6 3.9 26.6 16 70.2 3.2 18.1 3.5 3.9 Blacks 208.5 3.8 26.3 2.5 68.1 8.8 18.8 3.5 6.6 Japanese 104.2 1.8 9.9 1.1 25.2 2.7 13.6 3.6 3.9 Chinese 131.5 1.7 13 0 0.8 34.6 2.9 15.5 3.8 4,3 Filipinos 69.7 15 8.0 0.9 20.6 1.6 58 23 2.0 Native Hawaiians 200.5 16 33.0 1.2 88.7 4.2 11.4 3.6 3.0 American Indians 87.4 1.0 8.2 1.1 20.6 5.8 6.8 1.8 1.8 VVv 000008728 Esophagus Larynx Lung. Male Lung, Female Multiple Myeloma Ovary Pancreas Prostate Stomach 2.6 13 69.3 20.2 2.4 8.1 8.4 21.0 5.3 9.2 25 91.4 20.1 5.0 6.4 11.0 43.9 10.0 1.9 . 0.2 32.7 8.6 1.2 4.3 70 88 17.5 3.3 07 48.2 21.2 1.2 4.2 7.4 7.5 7.8 1.9 0.4 20.0 6.8 1.2 2.8 3.3 8.2 3.3 6.5 14 88.0 31.5 2.8 7.0 10,9 11.6 25.3 2.1 0.9 28.0 8.6 1.9 3.3 4.5 15.5 6.2 * The Naliona! Center for Health Statistics from which these data are derived does not code ethnicity for Hispanics Source: Baquet, C.R. et a!. Cancer Among Blacks & Other Minorities: Statistical Profiles NIH Publication No 86-2785 fiethesda. Md . National Cancer Institute, March 1986, page 10 *J People are living longer than ever. Earlier in the century infectious diseases were the big killers but modern medi cine and improved health measures have eliminated them as major causes of death and allowed many people to live long enough to get cancer, a disease that often takes several decades to develop. Also, the population has not only grown, but grown older. Therefore, if one looks only at the "crude figures." i.e., the number of can cer cases and impressions gained from media reports and personal knowledge of cancer victims, it may appear that there is an epidemic. However, if one converts these fig ures into rates (thus controlling for the size of the popula tion) and statistically adjusts them to a standardized age distribution, they become more meaningful. As seen in the previous section, with the exception of lung cancer, they do not reveal any evidence of an epidemic. Incidence and Mortality among Racial and Ethnic Groups As discussed, SEER data are collected so as to include different racial and ethnic groups and thus allow for com parisons of cancer rates among these groups. Table 2 presents incidence rates for eight different groups and includes information by sex. Overall cancer rates vary considerably among the groups. Blacks have the highest cancer incidence rate, followed by native Hawaiians. American Indians have the lowest. Blacks have the highest rates for cancer of the breast (women under 40). esophagus, colon, larynx, lung (male). pancreas, prostate, and multiple myeloma. They also have a high rate for cancer of the cervix. Based on SEER data, whites have the highest rate for cancer of.the bladder and ovary. American Indians have the highest rate for cervical cancer and native Hawaiians the highest rate for cancers of the breast in women over 40. andfor cancers of the uterine corpus (cancer of the endometrium or lining of the uterus), stomach, and lung (female). Japanese Americans have the highest inci dence rates for cancer of the rectum. These data indicate that there is a cancer epidemic among blacks in this country as compared to other sub groups of the population. They further specify which types of cancer account for this epidemic. The explana tion of this epidemic is beyond the scope of this report but the causes of cancer discussed in Part II will suggest some answers. Of particular relevance to blacks may be the risks associated with diet and smoking as well as other aspects of lifestyle. Mortality data confirm this demographic pattern (Table 3). Blacks have the highest overall cancer mortality. Black mortality is highest for all cancers in which they have the 18 highest incidence rate: cancer of the breast (women under 40), esophagus, colon, larynx, lung (male), pan creas, prostate, multiple myeloma, cervical cancer and cancer of the uterine corpus. Thus, mortality data confirm a cancer epidemic among blacks in the U ,S. Another Way of Looking at Current Patterns: Gender Figures 1-4 display differences in cancer rates between males and females. Incidence rates are from 1937. 1947. 1969-71, 1977, and 1983. Mortality rates are from 1930 through 1982. Another approach to current male-female cancer patterns is to look not at rates but at only the per centage distribution of deaths for the major forms of can cer among individuals who have the disease. Each year, the American Cancer Society prepares esti mates of the percentage distribution of cancer incidence and death by site and sex for the upcoming year. Since their projections for mortality tend to be much more accurate than those for incidence, only the mortality esti mates are presented here (Figure 6). The high percentage of expected death from lung cancer for men is readily apparent. Of the men expected to die FIGURE 6 Estimated Percentage of Cancer Deaths by Site. Male and Female. 1986 SKIN ORAL LUNG COLON & RECTUM PANCREAS PROSTATE URINARY LEUKEMIA & LYMPHOMAS ALL OTHER Source: American Cancer Society SKIN ORAL BREAST LUNG COLON & RECTUM PANCREAS OVARY UTERUS URINARY LEUKEMIA & LYMPHOMAS ALL OTHER 19 VVV 000008729 from cancer in 1986. 35 percent were projected to die from iung cancer! For women, the corresponding figure is 19 percent. The latter figure is of particular significance because it represents the first time that lung cancer will surpass breast cancer as the leading killer of women. (It has already done so in at least 15 states.) Thus, by look ing only at cancer victims we have again confirmed the presence of a lung cancer epidemic. International Sources of Data The major source of data for international disease inci dence and mortality rates is the World Health Organiza tion (WHO), specifically its affiliate the International Agency for Research on Cancer (IARC). Periodically. IARC publishes international incidence data, the latest volume being Cancer Incidence in Five Continents. Vol ume IV {1982). This volume contains data from 58 can cer registries, although it does not cover all countries on every continent. WHO also publishes updated data on mortality. International Comparisons of Cancer Statistics Comparison of cancer incidence and mortality among countries'presents many potential sources of error. Data for each country are subject to the kinds of errors for inci dence and mortality discussed earlier for the United States. Since the type of errors can vary by country and registry, comparisons can serve to magnify errors. Of particular importance is the fact that incidence data are usually based on a small number of registries in a par ticular country. The data fall into specifically identified regions, states, counties, and metropolitan areas, and it is unclear how representative these registries are for the total population of the country. In addition, the extent to which people use medical services (often varying accord ing to age), the availability and affordability of these serv ices, the level of diagnostic ability, and the quality of data in the registry--compliance in reporting, careful checks and "cleaning" of the data--may all differ by registry and country. A major problem with mortality rates is that the level of technology used in diagnosis and the medical treatment given to the patient can affect lifespan. Therefore, a high or low mortality rate may not truly reflect cancer mortal ity, but rather the influence of the level of diagnosis and treatment. Because of these limitations we will primarily rely on the international data to help confirm the epidemics of lung 20 cancer and cancer among blacks already found in the time comparisons and racial and ethnic comparisons, respectively. Of course, there is also the possibility that the U.S. data for a particular site will not reveal an epi demic when in fact international comparisons do. Because of the serious limitations of international data, evaluation of these findings is beyond the scope of this report. Internationally compared cancer incidence and mortality data are age-standardized to a world standard popula tion. Sometimes different world standard populations are used for different continents. However, despite this pre caution the influence of age can exert an effect on the data through such processes as differential use of diag nostic and treatment facilities by various age groups. The IARC volume presents cancer incidence data by site and sex. For each site by sex appear high and low rates of incidence and the location of source registries. However, these comparisons are inappropriate for defining a cancer epidemic in the U.S. If a registry in a country is singled out as having the highest (or lowest) incidence for a par ticular cancer, it may or may not be representative of the rest of the country. Thus, international incidence data can best be used to help confirm patterns previously found. International mortality data may lend support to conclu sions from the incidence data. Table 4 presents international incidence data from "around" 1976 (the year of data collection varies slightly by country) for cancers discussed previously of which the United States has the highest incidence rate recorded. Among white males there is no evidence of an overall epidemic, but the rate for colon cancer is notably high. However, black males have the highest international rates for cancer of the pancreas, lung and bronchus, prostate, and multiple myeloma. Among females there is also no evidence of an overall U.S. cancer epidemic and no evidence for an epidemic among black females. Table 5 presents the other side of the coin: the interna tional comparisons for incidence for which the U.S. has the lowest rates. The low rate of stomach cancer among males is consistent with previous findings. Conclusion Mortality rates are available for 47 countries. Table 6 presents the U.S. world standardized rate and rank for all sites combined for eight major cancers. The overall rates and ranks indicate no evidence of a cancer epidemic for either sex. While the mortality data are consistent with an epidemic of lung cancer for both sexes, there is nonethe less no conclusive evidence of an overall cancer epidemic in the U.S. 21 VVV 000008730 rroo TABLE4 Comparison of International Incidence of Cancer per 100,000 for Selected Sites by Sex: Highs for the United States, around 1976 * Males High Low ( Site Population Rate Population Rate Ratio H/L j Colon U.S., Connecticut 32.3 India. Poona 3.1 10.4 f Pancreas U.S., Bay Area, Black 18.3 India, Bombay 2.0 9.2 Lung & Bronchus U. S., New Orleans, Black 107.2 U.S., New Mexico, Am. Indian 8.1 13.2 Prostate U.S., Alameda, Black 100.2 Shanghai 0.8 125.3 Kidney U S,, Hawaii, White 11.2 India, Bombay 1.3 8.6 Multiple Myeloma U.S., Bay Area, Black 8.4 India, Poona 0.6 14.0 VVV 000008731 Colon Pancreas Breast Corpus Uteri Bladder Multiple Myeloma U.S., Bay Area, Japanese U.S.. New Mexico, Am. Indian U.S., Hawaii. Hawaiian U.S., Alameda, White U.S., New Orleans, White U.S., Hawaii, Hawaiian Females 27.4 10.4 87.5 38.5 6.5 5.9 India. Poona India, Bombay Japan, Osaka, Rural Japan. Fukuoka, Rural Hungary. Szabolcs Poland, Katowice Age - standardised to the Standard Work! Population Source; Waterhouse et a!., 1982. troo 2 8 9.8 0.9 11 9 8.9 9.8 10 38.5 0.5 13.0 0.4 14.8 \0 CM r~. cd vO CM hi *VA* QS r- (-H d oo o ON ^ "5 ?I 01 & 0) 0) yc *J 3S O* a *2 irt c=> LU J CQ 2 va x e ge J5 0 V 75 2 cA _AcJ 2< 1c oo' s 0 5A. C J2 'xCl) 2 3 A <Z *3 ao c/5 CL d 12 _Ac 5 cd d (ft V * E u Li. 4p> J*" sx 5 cr =i *s (A O 0) e .- o cr> V--) _"O- (Q ^ fi. U 6 Ji o <j</> CM CM c rosl C w cq II 2,0 s Z zw c g. cd J a -C o id -g CM 03 3 5aSi a' c5 <75 CD 3 JoZ C o j= to a E? t/5l o2o _5j a a> -Aa .fcir CA S5 Ol jza aoi/i LU 4C1O <S0: < UO 24 TABLE 6 U.S. Mortality Rate per 100,000 and Rank Among 47 Countries for Cancer, Selected Sites by Sex, 1980-51" Alt Sites Oral Colon & Rectum Lung Breast Uterus Stomach Prostate Leukemia Male Rate 215.9 5.6 25.1 71.6 Rank 21 13 17 9 8.2 22.7 8.7 45 14 3 Female Rate 135.5 1.9 18.2 21.4 26.6 7,7 3.9 Rank 18 11 17 6 15 36 45 5.2 10 Age - standardized to the Standard World Population Source: World Health Statistics Annual. 1982-84. VVV 000008732 25 Part II: What Causes Human Cancer? While there is still an interest in the role of genetics in can cer risk, current research strongly suggests that external factors--aspects of our environment--cause most human cancers. The importance of environment in cancer causation has been illustrated dramatically by studies of migrants from one part of the world to another. They or their descen dants quickly take on the cancer patterns typical of their new home. It is also significant that dramatic changes in cancer rates sometimes occur in only a few decades. Genetic changes cannot account for this: environmental changes can. Since 1970. professional and popular articles have fre quently cited an estimate that "80 to 90 percent of all cancers are environmentally induced." This estimate was originally calculated by the International Agency for Research on Cancer (IARC). a World Health Organiza tion affiliate. It has often been misinterpreted, leading to the mistaken impression that 80 to 90 percent of all can cers are due to known environmental factors such as air and water pollution, industrial chemicals or food chemi cals and contaminants. This IARC estimate was derived by comparing the high est and lowest cancer death rates from around the world. In assessing the meaning of this controversial statement, we must emphasize two points. First, saying that 80 to 90 percent of cancer is environmentally caused is not the same as saying that we know what these factors are and that we can control them effectively. The specific causes of most cancers are unknown. For example, two well-known scientists who have addressed the risk posed by industrial pollution -- a widely suspected cause of cancer--estimate that only about two percent of all cancers are attributable to such pollution. (Doll. R. and R. Peto, The Causes of Cancer, Oxford University Press. New York: 1981). Second, our "environment" is not limited solely to our physical surroundings and man-made chemicals. Many scientists now believe that cultural and personal habits contribute more to cancer causation than environmental pollution or toxic chemicals. In its broadest sense, then, our environment encompasses such factors as smoking, diet, sexual and reproductive patterns, alcohol consump tion. sunbathing, and other aspects of lifestyle, as well as our purely physical surroundings. 26 Tobacco National incidence and mortality figures confirm the dras tic and unprecedented rise in lung cancer in the United States, Yet before 1930, lung cancer was a rare disease. In 1912, a physician commenting on U.S. disease pat terns wrote: "There is nearly a complete consensus of opinion that primary malignant neoplasms of the lung are among the rarest forms of disease." However, by 1950, clinical and statistical evidence clearly demonstrated a sig nificant increase in lung cancer among men. Since 1970. the same pattern of increasing incidence has also been observed among American women. Numerous clinical, epidemiological and laboratory studies have con firmed that the increase in lung cancer is directly related to cigarette smoking. It has been shown that lung cancer death rates are more than ten times higher among male cigarette smokers than among male nonsmokers. Although precise estimates of the number of lung cancer deaths caused by smoking vary, most experts agree that at least 80 and perhaps 90 percent of all lung cancer deaths are the result of cigarette smoking. Smoking acts to increase cancer risks for body sites in addition to the lung. Tobacco smokers have greater risks than nonsmokers for cancers of the mouth, throat, blad der. pancreas and kidney. Cigarette smokers have two to three times greater risk for developing bladder cancer than nonsmokers. Scientists have estimated that cigarette smoking and other tobacco use is responsible for roughly 30 percent of all cancers in the United States. Despite the clear association between smoking and can cer. the process by which cigarettes cause cancer has not been fully explained. Most research suggests that several chemicals found in tobacco smoke are the ultimate car cinogenic agents. However, other factors are equally important. These include the length of time a person has smoked, the total number of cigarettes consumed, how deeply the smoke is inhaled and. to a lesser extent, the brand of cigarette smoked. Cigarette smoking can also act to increase or "promote" the cancer causing potential Of other risk factors. It is known, for example, that drinkers of alcohol who also smoke heavily have greater risks for developing esopha geal cancer than would be predicted by simply adding the two risks together. This synergistic effect has also been found among smokers exposed to certain hazardous materials such as asbestos and radon. These facts prompted the statement made in the 1979 U.S. Surgeon General's Report: "Cigarette smoking is the single most important environmental factor contributing to premature mortality in the United States." 27 VVV 000008733 Diet There is substantial scientific evidence suggesting that diet may be an important factor in human cancer develop ment. However, the exact roles played by specific aspects or components of the diet are still very uncertain. The resuits of some scientific studies suggest that a highfat diet may be associated with increased rates of cancers of the breast and colon-rectum. However, other studies have failed to support this conclusion. Still other studies point to increased calories from any source, rather than to fat per se. There are similar discrepancies in the results of studies on the possible protective effect of dietary fiber against colon cancer. If there is such an effect, specific fiber compo nents such as the pentosan fraction, rather than fiber as a whole, may be responsible. Different fiber components have different physiological effects in the intestine. Thus, attributing effects to fiber in general may be highly mis leading. Obesity has been associated with an increased risk of can cer at several body sites in some studies. Vegetables, fruits, vitamins A, C. and E, and the mineral selenium are all being investigated for possible protective effects, but their benefits have not been shown in humans. Experts warn against the use of high-dose sup plements of individual nutrients. Such supplements may be unsafe and have not been shown to be effective. International epidemiologic studies have linked the smoked and cured foods popular in Japan, China, and Iceland with increased rates of stomach and esophageal cancers. The very different types of smoke-flavored and cured foods consumed in the U.S. have not been simi larly implicated. A large number of substances that occur naturally in foods have been found to be carcinogenic when evalu ated by standard laboratory methods and criteria. Many additional carcinogens are produced in food by cooking or by the actions of microorganisms, The evidence cur rently available does not indicate that any of these sub stances has a measurable effect on cancer incidence in the U.S. Food additives and agricultural chemicals have not been found to have an impact on U.S. cancer rates. Alcohol Although alcohol is at most a weak carcinogen, heavy alcohol consumption has been implicated in human can cers. Consumption of large amounts of alcohol in combi nation with heavy cigarette smoking synergisticaily increases the risks of cancers of the mouth and throat. 28 Heavy alcohol consumption alone may also have an indi rect effect on liver cancer because it is capable of inducing cellular changes in liver tissue and this in turn may increase liver cancer risk. The effects of alcohol consump tion are closely related to the extent and duration of use and the type of alcoholic beverage consumed. Ionizing Radiation Exposure to ionizing radiation, for example medical x-rays, increases the risk of developing leukemia and skin cancer. As early as 1944. researchers noted that radiologists were more likely than other physicians to develop leukemia. Recent attention to this cancer risk has resulted in recom mendations against the use of x-rays as a routine medical practice. However, experts agree that when x-rays are used prudently, their diagnostic and therapeutic benefits far outweigh their small cancer risk. Drugs In rare cases, certain drugs have contributed to an increase in cancer risk. The most prominent example is DES' (diethylstilbestrol), a drug that was widely pre scribed to prevent miscarriages. In 1974 an obstetrician noted a rare form of vaginal cancer in women whose mothers had taken large doses of the drug during preg nancy. Although widely publicized, the actual number of cases of cancer caused by the use of DES as a human drug is small. Postmenopausal estrogens are a risk factor for endome trial cancer. Extended use (more than two years) of these drugs has been shown to increase the risk of cancer of the lining of the uterus, the endometrium. This risk must be weighed against the potential benefits of the drug, For some women, the protective effect of estrogens against loss (osteoporosis) far outweighs their cancer risk, estrogens are used as short-term therapy, they ntly do not increase cancer risk and are effective in treating certain menopausal symptoms such as hot flashes and genital atrophy. Other drugs used to treat tuberculosis and, ironically, some forms of cancer have also shown an increased risk potential. Yet for these drugs, the risks of not using them are far more serious than their cancer risk. For this it is important to weigh carefully both the risks and benefits of any drug before use.* * Until recently DES was also used as a cattle growth stimulant, but was discontinued after trace amounts were found in the livers of some animals. There is no evidence that these trace amounts were a risk to human health. 29 VVV 000008734 Sexual and Reproductive Patterns Intercourse at an early age and multiple sexual partners have been linked to an increased risk of cervical cancer. Strong evidence suggests that cervical cancer may be caused by a sexually transmissible disease. AIDS, another sexually transmitted disease, is also asso ciated with cancer. Kaposi's sarcoma, a rare type of can cer. occurs frequently among victims of AIDS. Other can cers. such as those of the lymphatic system, may also be unusually common among individuals who have AIDS. Sunlight The most widespread environmental carcinogen, accounting for the majority of superficial skin cancers and for some types of melanoma, is ultraviolet radiation from the sun. Superficial skin cancers are rarely fatal and are not included in most statistical estimates of U.S. cancer patterns. Melanoma is more serious, but overall, the out come of treatment of this cancer is good when it is discov ered early. Among light-skinned people, sunlight-related cancers are more common in tropical areas than in colder climates because the sun s rays are most intense near the equator There are also individual differences in susceptibility to the effects of the sun. with people who tan poorly and sunburn easily being most at risk. Sun exposure can cause cancer in two ways. Total expo sure. over many years, increases the risk of superficial skin cancer and at least one type of melanoma. Intense, occasional exposures, especially in childhood and ado lescence, increase the risk of two other types of mela noma. Limiting exposure to the sun and to other sources of ultraviolet light is the simplest and most effective means of reducing this cancer risk. It is best not to cultivate a suntan or to patronize sun tanning parlors. It is helpful to use sunscreen products and to wear protective clothing, especially when exposed to midday summer sun. Occupation High dose, long-term exposure to a number of industrial chemicals and manufacturing processes, including asbes tos, vinyl chloride, nickel refining, and dye manufactur ing, can increase risk for several types of cancer. To date, approximately 20 industrial chemicals have been con firmed as human carcinogens. An additional 200-300 are suspected carcinogens on the basis of animal evidence. As with other cancer risks, occupational risks depend on the length and degree of exposure, the potency of the chemical agent, possible interactions with other chemi cals, and lifestyle factors such as cigarette and alcohol 30 consumption. Most experts estimate that between one and five percent of all cancers m the U.S. are related to occupation. Air Pollution? The findings of trace amounts of carcinogens in urban and suburban air samples and the differences in cancer death rates between urban and rural areas have led many to conclude that pollution is a serious cancer risk. How ever, the case for air pollution as an important cause of human cancer remains unconvincing. A number of reviews of the relationship between air pol lution and lung cancer have reported no evidence of an association. Differences in lung cancer death rates between urban and rural people can be explained by dif ferences in smoking habits. A recent study of lung cancer by the American Cancer Society concluded: "General air pollution had little effect in a comparison between urban and rural people. Smoking is the key factor.'' This is not to suggest that pollution should not be con trolled. There may be other health and aesthetic reasons to minimize environmental pollution. Some preliminary evidence suggests that certain types of air pollution may exacerbate acute respiratory illnesses such as asthma and bronchitis. Yet at present, the threat of cancer does not appear to be associated with general pollution. Recently, attention has focused on the possibility that indoor air pollution may pose a threat to health. Some scientific studies suggest that prolonged exposure to one indoor air pollutant, environmental tobacco smoke, may be associated with an increase in lung cancer risk. The possible role of radon is also under investigation. Cancer and the Environment: An Overview The age-adjusted death rates for most forms of cancer have decreased or remained constant for the past 50 years. Lung cancer is a notable exception. This disease, caused primarily by cigarette smoking, has increased dra matically in both sexes. Black Americans have higher cancer rates than other ethnic and racial groups; lifestyle factors, particularly smoking, may be responsible. The exact number of cancers that can be eliminated by sound preventive methods is unknown, but the percent age is undoubtedly substantial. Eliminating the effects of cigarette smoking alone would eventually reduce cancer incidence and mortality between 15 and 35 percent. Some experts believe that when the dietary factors that may influence cancer risk are fully understood, a similar reduction might be achieved by changes in eating habits. However, other authorities consider this much too opti mistic. Some cases will likely be prevented as a result of 31 VVV 000008735 reductions in occupational exposures to toxic chemicals. If it became unfashionable to cultivate a suntan, the rates of skin cancer and melanoma might be substantially reduced. Effective preventive measures can successfully reduce our cancer burden or at least postpone cancer until very late in life. To this end. current scientific knowledge sug gests that our preventive efforts should be focused on personal activities, especially smoking, sunbathing, and excessive alcohol consumption. REFERENCES 1. MacMahon. B. and T.F Pugh. EPIDEMIOLOGY. Principles and Methods. Boston: Little, Brown & Co.. 1970. 2. American Cancer Society, 1986 Cancer Facts and Figures. New York, 1986. 3. Bailar. J.C. Ill, and E.M. Smith, "Progress against Cancer?". The New England Journal of Medicine 314 (19): 1226-1232, 8 May 1986. 4. Baquet, C.R., et a(. Cancer among Blacks and other Minorities: Statistical Profiles. N1H Publication No. 86-2785, Bethesda, Md., National Cancer Institute, March 1986. 5. Doll. R.. and R. Peto. The Causes of Cancer. New York: Oxford University Press. 1981. 6. DeVita. V.. "Annual Cancer Statistics Update." National Cancer Institute, Office of Cancer Com munications. 2 December 1985. 7. Horm, J.W., et al (eds), SEER Program: Cancer Inci dence and Mortality in the United States. 1973-81 NIH Publication No 85-1837. Bethesda. Md.. National Cancer Institute. November 1984. 8. Newell. G.R., "Epidemiology of Cancer" in P. Calabresi, R Schein. and S. Rosenberg (eds). Medical Oncology: Basic Principles and Clinical Management of Cancer. New York: Macmillan. 1985. 9. Page. H.S.. and A.J. Asire, Cancer Rates and Risks. NIH Publication No. 85-691. Bethesda. Md., National Cancer Institute. 1985. 10. Schottenfeld. D., and J. Fraumeni. Jr.. Cancer Epi demiology and Prevention. Philadelphia: W.B. Saunders Co.. 1982. 11. Silverberg. E.. and J. Lubera. "Cancer Statistics, 1986." Ca-A Cancer Journal for Clinicians 36 (1), January/February 1986. 12. Silverberg, E., and J. Lubera, "A Review of Ameri can Cancer Society Estimates of Cancer Cases and Deaths." Ca-A Cancer Journal for Clinicians 36 (1), January/February 1983. 13. Sondik, E.J., etal. 1985 Annual Cancer Statistics Review. NIH Publication No. 86-2789. Bethesda. Md., National Cancer Institute. March 1986. 32 33 VVV 000008736 SUPPLEMENTARY REFERENCES Epidemiology Ahlbom, A., and S. Norell, Introduction to MODERN EPIDEMIOLOGY. Chestnut Hill. Mass.: Epidemiol ogy Resources, 1984. Benenson. A.S. (ed), Control of Communicable Dis eases in Man. New York: American Public Health Association, 1980. Kelsey, J.L., Thompson W.D.. and A.S. Evans. Methods in Observational Epidemiology. New York: Oxford University Press. 1986. Mausner. J.S., and S. Kramer. EPIDEMIOLOGY--An Introductory Text. Philadelphia: W.B. Saunders Co., 1985. Weiss. N.S.. Clinical Epidemiology: The Study of the Outcome of Illness. New York: Oxford University Press. 1986. Cancer Epidemiology Magnus. K. (ed), TRENDS IN CANCER INCIDENCE. Causes and Practical Implications. Washington. D.C.: Hemisphere Publishing Corp., 1982. Mathe. G.. and P Reizenstein. PATHOPHYSIOLOGI CAL ASPECTS OF CANCER EPIDEMIOLOGY. Oxford: Pergamon Press, 1985. Wellington. D.G., Macdonald E.J.. and P.F. Wolf. CANCER MORTALITY. 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Ph.D. University of Kentucky Glenn Froning, Ph.D. University of Nebraska, Lincoln LaNeBe E. Geddas. Ph.D.. R.N. Purdue University WIHiam Paul Glezen. M.D. Baylor College of Medicine Roger E. Gold. Ph.D. University of Nebraska. Lincoln Leonard J. Goidwater. M.D. Chapel Hill, NC Vincent P. Gotz. M.S.. R.Ph. University af Florida Saxon Graham. Ph.D. SUNY at Buffalo Jamas Ian Gray. Ph.D. Michigan State University Jesse F. Gregory III. Ph.D. University 0* Florida Helen A. Guthrie. Ph.D. Pennsylvania State University Wayland J. Hayes. Jr.. M.D.. Ph.D. Vanderbilt University School of Medicine Virgil Hays. Ph.D. University af Kentucky William E. Hazeitina, Ph.D. Butte County, California Mosauito Abatement Oistrict Norman Heidelbaugh, V.M.D.. M.PH..Ph.D. Texas A&M University L. M. Henderson. Ph.D. Sandy, UT Victor Herbert. M.D,, J.D. Bronx va Medical Center Ststa University of New York D. Born* Hiscoe. M.D. Healtn Central Lansing, Ml Helens. Hiscoe. Ph.D. Michigan State University John Holbrook. M.O. University of Utah Robert M. Hollingworth. Ph.D. Purdue University C. Stuart Houston. M.D. University Hoso'tal. Saskatchewan Lucian R. Jacobs, M.D. University of California Wflliam T. Jarvis. Ph.D. Lome Linda University Norge Jerome. Ph.D. University of Kansas Michael Kamrin. Ph.D. Michigan State University Edward Harold Kass. M.O , Ph.D. Harvard Medical School Philip Keeney. Ph.O. Pennsylvania State University G.A. Keyworth, II, Ph.O. Chairman. Keyworth Co. Washington. DC. John Kinsella. Ph.D. Cornet! University Kathryn M. Kolaea, Ph.D.. R.D. East Carokna University David Kritcheveky. Ph.O. The Wistar institute. Philadelohie Manfred Kroger, Ph.D, Pennaylvenia State University Leonard T. Kuriand, M.D.. Dr.P.H. Mayo Clinic, Rochester Carolyn Lackey, Ph.D.. R.D. North Carolina State University J. Claybum LaForce, Ph.D. Univarsity of California. Los Angelas Lawrence E. Lamb. M.D. Ccrrwnumcationa Inc., TX 38 Bernard J. Liska, Ph.D. Purdue University James A. Lowell. Ph.D. Prma Community College Albert Pearson. Ph.D. Michigan State University Timothy Dukes Phillips. Ph.D. Texas A&M University Daryl Lund. Ph.O. University of Wisconsin Howard D. Maccabee. Ph.D.. M.D. Radiation Oncology Center Walnut Creek. CA Roger P. Maickel. Ph.D. Purdue University Henry G. Manna. J.S.D. Emory University Mary Frances Picciano, Ph.O University of Illinois John J. Powers. Ph.D. University of Georgia William 0. Powrie. Ph.D. University of Bntisn Columbia John Renner, M.D. St. Mary's Hospital Kansas City. MO KariMaramorosch. Ph.D. Rutgers University John McKetta. P.E.. Ph.D. University of Texas at Austin w. W. Melvin. M.D., Sc.D.. M.P.H. Colorado State University Robert Menzer, Ph.D. University of Maryland Thomas Milby. M.D.. M.P.H. Larayerte. CA Joseph M. MiHer. M.P., M.P.H. New Hampton, nh W.J. Miller, Ph.D. University of Georgia J.A. Milner. Ph.D. University of Illinois Dade W. Moeller. Ph.O. Harvard School of Public Health A. Alan Moghissi, Ph.D. Institute of Regulatory Science. VA Grace P. Monaco. J.D. White. Fine & Verviiie Eric W. Mood. LL.O.. M.P.H. vale University John P. Morgan. M.D. City College of New York StepKen J. Moss. D.D.S.. M.S. New York University Dental Center Philip Nelson, Ph.D. Purd.ue University John Neuberger. Or. PH. University ol Kansas Richard Oksas, M.P.H.. Pharm. D. South Bay Free Clinic, CA J.E. Oldfield. Ph.O. Oregon State University Jane Orient. M.D. Tucson, AZ Robert Oseasohn. M.O. University of Texaa Grace L. Ostenso. Ph.D. Comimirre# on Science and Technology U.S. House of Representatives M. ABceOttoboni, Ph.D. Berkeley. CA Rosa Marie Pangbom, M.S. University of California. Davis Michael Pariza. Ph D. University of Wisconsin Rita Ricardo-Campbell. Ph.O. Hoover Institution. Stanford University Oavid 8. Roll, Ph.O. University of Utah Dale R. Romsos. Ph.O. Michigan State University Sheldon Rovin. D.D.S.. M.S. University of Pennsylvania Edward Runge. Ph.D. Texas A&M University Paul D. Saltman, Ph.D. University of California. San Diego Herbert P. Sarett. Ph.D. Sarasota. FL Lowell D. Satterlee, Ph.D. University of Nebraska Frank 0. Schaumberg, Ph.D. Oregon State University B,S. Schweigert. Ph.D. University ol California. Davis David P. Sheridan. M.D.. M.S. Medical College of Wisconsin Sarah Short. Ph.O . Ed D.. R.D. Syracuse University A. J. Siedler. Ph.O. University of Illinois John Silliker. Ph.D. S'liiker Laboratories. CA Julian L. Simon. Ph.D. University of Maryland S. Fred Singer. Ph.D. University of Virginia Roy F. Spalding. Ph.D. University of Nebraska Robert R. Spitzer, Ph.D. Milwaukee School ol Engineering Ronald T. Stanko. M.D. University Of Pittsburgh School of Medicine James H. Steele. D.V.M.. M.P.H. University of Texas JudithS. Stem, Sc.D. University of California. Davis Elizabeth F. Stier. Ph.D. Rutgers University Martha Barnes Stone. Ph.D. Kansas State University SltaP. Tatini. Ph.O. University of Minnesota V vvy OOOOO8739 Zerie L. Carpenter, Ph.D. Texas A&M University System C. Jelleff Can. Ph.O. Columbia, MO Robert G. Caaeens, Ph.D. University of Wisconsin James J. Cerda. M.D. University of Florida Bobbe L. Christensen. Ph.D. University 0< Texas F.M. Clydesdale. Ph.D. University of Massachusetts Bernard L. Cohen. D.Sc. University ot Pittsburgh Neville Colman. M.D,. Ph.D. Mount Sinai School of Medicine Julius M. Coon. M.D.. Ph.D. Thomas Jefferson University Bernard D. Davis. M.D. Harvard Medical School Thomas ft. OeGregori. Ph.D. University ot Houston Robert M, Devlin, Ph.O. University of Massachusetts John Dieboid The Dieboid Group. Inc. Theron Downes. Ph.D. Michigan State University Henry Dymsza. Ph.D.. R.D. University of Rhode island James E. Enstrom. Ph.O. University of California, Los Angeles Myron E. Essex. O.V.M.. Ph.D. Harvard School of Pudlic Health Owen ft, Fenneme. Ph.O. University of Wisconsin Lloyd Jackson Filer, Jr.. M.D.. Ph.O. University of Iowa Dean C. Fletcher. Ph.D. Washington State University Ralph W. Fogleman. O.V.M. Upoe' Black Eddy, PA J. D. Fox. Ph.O. University of Kentucky Glenn Froning. Ph.D. University ot Nebraska. Lincoln LaNeile E. Geddea. Ph.D.. R.N. Purdue University WHMam PauIGtezen. M.D. 8aylor College ot Medicine Roger E. Gold. Ph.D. University of Nebraska. Lincoln Leonard J. Goidwater. M.D. Chapel Hill. NC Vincent P. Gotz, M.S.. R.Ph. University of Florida Saxon Graham. Ph.D. SUNT at Buffalo James Ian Gray, Ph.D. Michigan State University Jasse F. Gregory III. Ph.D. University of Florida Helen A. Guthrie. Ph.D. Pennsylvania State University Waylend J. Hayes. Jr.. M.D.. Ph.O. Vanderbilt University School of Medicine Virgil Hays. Ph.D. University 0< Kentucky William E. Hazeltine. Ph.D. Butte County. California Mosquito Abatement Oistnct Norman Heidelbaugh. V.M.O.. M.P.H., Ph.D. Texas A&M University L. M. Henderson. Ph.D. Sandy, UT Victor Herbert. M.D.. J.D. Bronx VA Medical Center State University of New Vark D. Bonta Hiscoe. M.D. Healtn Central Lansmg, Ml Helen B. Hiscoe. Ph D. Michigan State University John Hoibrook. M.D. University of Utah Robert M. Hofllngworth, Ph.D. Purdue University C. Stuart Houston. M.D. University Hospital. Saskatchewan lucien R. Jacobs. M.D. University of California William T. Jarvis, Ph.D. Lome Linda University Norge Jerome. Ph.D. University of Kansas Michael Kamrin, Ph.O. Michigan State University Edward Harold Kass, M.D.. Ph.D. Harvard Medical School PhflipKeeney. Ph.D. Pennsylvania State University G.A. Keyworth. II. Ph.D. Chairman. Keyworth Co. Washington. D.C. John Kinseila. Ph.D. Corned University Kathryn M. Kolaea, Ph.D.. R.D. East Caroline University David Kritchevsky, Ph.D. The Wister institute. Philadelphia Manfred Kroger. Ph.D. Pennsylvania State University Leonard T. Kurland. M.D., Dr.P.H. Mayo Clinic. Rochester Carolyn Lackey, Ph.D., R.D. North Carolina State University J. Claybum LaForce. Ph.D. University ot California. Los Angeles Lawrence . Lamb, M.D, Communications Inc., TX 36 Bernard J. Liska. Ph.D. Purdue University James A. Lowell. Ph.D. Pima Community Coilege Daryl Lund. Ph.D. University of Wisconsin Howard D. Maccabee, Ph.D., M.D. Radiation Oncology Center Walnut Creek. CA Roger P. Maickei, Ph.O. Purdue University Henry G. Manne, J.S.D. Emory University Karl Maramorosch, Ph.O. Rutgers University John McKaita. P.E.. Ph.O. University of Texas at Austin W. W. Melvin. M.D.. Sc.D.. M.P.H. Colorado State University Robert Menzer. Ph.O. University of Maryland Thomas Milby, M.O., M.P.H. Lafayette. CA Joseph M. Miller. M.D., M.RH. New Hampton, NH W.J. Miller. Ph.D. University of Georgia J.A. Milner. Ph.D. University of Illinois Oade W. Moeller. Ph D. Harvard School of Public Health A. Alan Moghisai, Ph.O. Institute of Regulatory Science. VA Grace P. Monaco, J.D. White, Fine & Verville Eric W. Mood. LL.D.. M.P.H. Yale University JohnP. Morgan. M.D. City College of New York Staphen J. Moss. D.D.S.. M.S. New York University Dental Center Philip Nelson, Ph.D. Purdue University John Neuberger, Dr. P.H. University of Kansas Richard Oksas. M.P.H., Pharm. D. South Bay Free Clinic. CA J.E. Oldfield. Ph.D. Oregon State University Jane Orient. M.D. Tucson. AZ Robert Omeasohn. M.O. University of Texas Grace L. Ostenso. Ph.D. Committee on Science and Technology U.S. House of Representatives M. Alice Ottoboni, Ph.O. Berkeley. CA Rose Marie Pangbom, M.S. University of California. Daws Michael Pariza, Ph.O. University of Wisconsin Albert Pearson, Ph.D. Michigan State University Timothy Dukes Phillips. Ph.D. Texas A&M University Mary Frances Picciano. Ph.O. University of Illinois John J. Powers. Ph.D. University of Georgia WilHam O. Powrie, Ph.D. University of British Columbia John Renner, M.D. St. Mary's Hospital Kansas City. MO Rita Ricardo-Campbeil. Ph.D. Hoover Institution. Stanford University David B. Roll. Ph.D. University of Utah DaleR. Romsos, Ph.D. Michigan State University Sheldon Rovin. D.D.S.. M.S. University of Pennsylvania Edward Runge. Ph D. Texas A&M University Paul D. Saltman. Ph.D. University of California. San Diego Herbert P. Sarett. Ph.O. Sarasota. FL Lowed D. Setterlee. Ph D. University of Nebraska Frank D. Schaumberg. Ph.D. Oregon State University B.S. Schweigert. Ph.D. University of California. Davis David P. Sheridan. M.D.. M.S. Medical College of Wisconsin Sarah Short. Ph.O.. Ed.D.. R.D. Syracuse University A.J. Siedler. Ph D. University of ilt<no<s John Silliker. Ph.O. Silliker Laboratories. CA Julian L. Simon. Ph.D. University ot Maryland S. Fred Singer, Ph.D. University of Virginia Roy F. Spalding. Ph.D. University of Nebraska Robert R. Spitzer. Ph.O. Milwaukee School of Engineering Ronald T. Stanko, M.D. University of Pittsburgh School of Medicine James H. Steele. D.V.M.. M.P.H. University of Texas Judith S. Stem. Sc.O. University of California. Davis Elizabeth F. Stier. Ph.O. Rutgers University Martha Barnes Stone, Ph.D. K anees State University Sita R. Tatini, Ph.D. University of Minnesota 0qOQqq ?40 Steve L. Taylor, Ph.D. University ot Nebraska -- Murray M.Tuckennan, Ph.D. impla University John W. Tumor. M.D. Bay state Medical Center So'ingfield. U4 VarroE. Tylar. Ph.D. Purdue University Robert P. Upchurch. Ph.D. University ot Arizona W.F. Wardowski. Ph.D. University of Florida Miles Weinberger. M.D. University of lows Philip L. White. Sc.D. American Medical Association C. K. Whitehair. D.V.M., Ph.D. Michigan Stare University Carol Whitlock. Ph.D.. ft.D. Rochester Inst, ot Technology Christophar Wilkinson. Ph.D. Cornell University Warren Winkeletefn. Jr.. M.D.. M.P.H. University of California. Berkeley Virgil Wodicka. Ph.D. Fuilerton. CA Georga T. Woods. D.V.M. University of Illinois James Harvey Young, Ph.D. Emory University Panayiotis Michael Zavos. Ph.D. University of Kentucky VVV 000008741 WV 000008742