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CancerCode.org

Code 7

Many aspects of general health can be improved, and certain cancers avoided, if you adopt a healthier lifestyle

:: Apply strictly regulations aimed at preventing any exposure to known cancercausing substances. Follow all health and safety instructions on substances which may cause cancer. Follow advice of national radiation protection offices.The prevention of exposure to occupational and environmental carcinogens has followed the identification of a substantial number of natural and man-made carcinogens, and has led to significant reductions in cancer occurrence. The message in this item of the code solicits responsible behaviour for individuals in three respects:

1) from those who have to provide timely and clear instructions, primarily legislators and regulators who should adapt scientific consensus evaluations into European Union law, and control compliance with these regulations;

2) from those who should follow these instructions and comply with the laws to protect the health of others, for instance, managers, hygienists and doctors in industry; and

3) from every citizen who in order to protect their own health and the health of others, ought to pay heed to the presence of carcinogenic pollutants and follow instructions and regulations aimed at mitigating or preventing exposure to carcinogens

The latter applies to a wide variety of circumstances such as traffic restrictions within cities, restrictions on smoking, use of personal safety devices and respecting validated procedures in the workplace. Application of regulations is particularly important in the working environment where carcinogens may be found in higher concentrations than in the general environment. The control of the prevalence and level of exposure to occupational and environmental carcinogens through general preventive measures has historically played a more important role in preventing cancers than individual measures of protection.

The cancers that have most frequently been associated with occupational exposures are those of the lung, urinary bladder, mesothelioma, larynx, leukaemia, angiosarcoma of the liver, nose and nasal cavity and skin (non-melanoma). Several other neoplasms have also been associated with occupational exposures but the evidence is less strong. They include cancers of the oral cavity, nasopharynx, oesophagus, stomach, colon and rectum, pancreas, breast, testis, kidney, prostate, brain, bones, soft-tissue sarcoma, lymphomas and multiple myeloma. Most known or suspected occupational carcinogens have been evaluated by the International Agency for Research on Cancer(IARC Lyon, France). Actually, 29 chemical or physical agents, groups of agents or mixtures that occur predominantly in the workplace, have been classified as human carcinogens (Group 1 of the IARC classification). In the same Group 1, IARC has classified 13 industrial processes or occupations, such as the rubber industry, painters, etc. In European Union countries, production or use of some of these chemicals has been banned and are only of historical interest (e.g. mustard gas, 2-naphthylamine), while some high-risk industries have stopped functioning (e.g. ‘Wismut’ uranium ore mining associated with exposure to ionising radiation). Exposure to other carcinogens such as metals and dioxins is still widespread.

Thirty-five agents or industrial processes are classified as probably carcinogenic to humans (Group 2A of the IARC). Many of the agents in this group are still widely used, for example 1,3- butadiene and formaldehyde. More than 200 agents, groups of agents or exposure circumstances are classified as possibly carcinogenic to humans (Group 2B) largely on the basis of carcinogenicity data from animal experiments. It has been estimated that in the early 1990s about 32 million workers (23% of those employed) in the European Union were exposed to carcinogenic agents at levels above background. Exposure to these agents is still widespread but occurs mostly at low levels. The more common occupational exposures are solar radiation, passive smoking, crystalline silica, diesel exhaust, radon, wood dust, benzene, asbestos, formaldehyde, polycyclic aromatic hydrocarbons, chromium VI, cadmium and nickel compounds. Extensive preventive measures in the workplace in recent decades have resulted in the prevention of many cancers related to workplace exposures. This has been well documented, for example for occupational bladder cancer after the ban on the use of beta-naphthylamine in the rubber and chemical industries. The delays in taking protective measures, however, and the long latency for many neoplasms will result, in certain instances, in a continuous increase in the number of occupational cancers during the coming years. An increasing number of mesothelioma cases due to past occupational exposure to asbestos is expected in many European Union countries for another 10–20 years, even though asbestos has been banned in some European Union countries since the early 1990s. The proportion of all cancers that can be causally attributed to carcinogens in the occupational environment and are therefore wholly or partially avoidable through exposure control, remains difficult to quantify reliably. An estimated 5% of cancers is attributable to the occupational environment. This proportion depends on the variable prevalence of the exposures by geographical areas, gender, socioeconomic status and periods of time, as well as on the concurrent prevalence of other dominant cancer causing factors, particularly tobacco smoking. Furthermore, the effect of specific occupational carcinogens, such as aromatic amines or polycyclic aromatic hydrocarbons, is also mediated by genetic factors, such as genetic polymorphisms of the NAT2 or GSTM1 genes. The distribution of these polymorphisms within the populations of the European Union is fairly uniform and genetic factors probably do not determine differences in the proportion of occupational cancers between populations in European Union countries.

Environmental exposures usually refer to exposures of the general population that cannot be directly controlled by the individual. They include air-pollution, drinking water contaminants, passive smoking, radon in buildings, exposure to solar radiation, food contaminants such as pesticide residues, dioxins or environmental estrogens, chemicals from industrial emissions, and others. Exposure may be widespread, as is the case for air pollution, or could be restricted, as would be the case of populations living in the vicinity of a contaminating industry. These exposures have been associated with a variety of neoplasms, including cancers of the lung, urinary bladder, leukaemia and skin. The impact of several environmental carcinogenic exposures, such as arsenic in drinking water, has not been quantified, though exposure to arsenic is likely to affect only limited population groups. Air pollutants, such as fine particles, have been associated in several studies with a small increased risk of lung cancer even at current low-level urban exposure levels. The evidence on other exposures that are widespread, such as disinfection by-products in drinking water, is still inconclusive. Agents in the general environment to which a large number of subjects are exposed for long periods, such as passive smoking or air-pollution, although increasing only modestly the relative risk for certain cancers may be at the origin of several thousand cases per year in the European Union.

It is essential that for any agent liable to present a risk, the nature, degree and duration of such risk must be determined in order to define what measures need to be taken to prevent or reduce the exposure. Among these measures, suitable operating procedures and methods are of utmost importance. Instructions to be followed may take the form of quantitative control limits of exposure, derived empirically or through formal procedures, which still leaves much to be desired. The specification of a quantitative control limit of exposure in the general and occupational environment combines two elements: the quantitative estimate of the risk associated with a given level of exposure and the level of risk regarded as socially “acceptable”, with consideration of the technical feasibility, and human and economic costs of various degrees of control.

Related:

Ionising and Non-Ionising Radiation

Cosmic Radiation And Cancer

Radioiodine and thyroid cancer

Nuclear workers

Populations living near nuclear installations

Power lines and cancer

Cellular telephones and cancer

Ben Foster

Table 6

BIG RISK, especially among those who start smoking cigarettes regularly in their TEENAGE years: if they keep smoking steadily then about HALF will eventually be killed by tobacco (approximately one-quarter in old age plus one-quarter in middle age)

  • Those killed by tobacco in MIDDLE age (35-69 years) lose an average of 20-25 YEARS of non-smoker life expectancy
  • Throughout the European Union, tobacco is much the greatest single cause of death. In non-smokers, cancer mortality is decreasing slowly and total mortality is decreasing rapidly
  • Most of those killed by tobacco were not particular “heavy” smokers

STOPPING SMOKING WORKS: Even in middle age, stopping before having cancer or some other serious disease avoids most of the later excess risk from tobacco, and the benefits of stopping at earlier ages are even greater

Ben Foster

Code 1

Many aspects of general health can be improved, and certain cancers avoided, if you adopt a healthier lifestyle

:: Do not smoke; if you smoke, stop doing so. If you fail to stop, do not smoke in the presence of non-smokers

It is estimated that between 25 and 30% of all cancers in developed countries are tobacco-related. From the results of studies conducted in Europe, Japan and North America, between 87 and 91% of lung cancers in men, and between 57 and 86% of lung cancers in women, are attributable to cigarette smoking. For both sexes combined the proportion of cancers arising in the oesophagus, larynx and oral cavity attributable to the effect of tobacco, either acting singly or jointly with the consumption of alcohol are between 43 and 60%. A large proportion of cancers of the bladder and pancreas and a small proportion of cancers of the kidney, stomach, cervix and nose and myeloid leukaemia are also causally related to tobacco consumption. Because of the length of the latency period, tobacco-related cancers observed today are related to the cigarette smoking patterns over several previous decades. On stopping smoking, the increase in risk of cancer induced by smoking rapidly ceases. Benefit is evident within 5 years and is progressively more marked with the passage of time.Smoking also causes many other diseases, most notably chronic obstruction pulmonary disease (commonly called chronic bronchitis) and an increased risk of both heart disease and stroke. The death rate of long-term cigarette smokers in middle age (from 35 to 69 years of age) is three times that of life-long non-smokers and approximately half of regular cigarette smokers, who started smoking early in life, eventually die because of their habit. Half the deaths take place in middle age when the smokers lose approximately 20 -25 year of life expectancy compared to non-smokers; the rest occur later in life when the loss of expectation of life is 7-8 years. There is, however, now clear evidence that stopping smoking before cancer or some other serious disease develops avoids most of the later risk of death from tobacco, even if cessation of smoking occurs in middle age Table 6. While the rate at which young people start to smoke will be a major determinant of ill-health and mortality in the second half of this century, it is the extent to which current smokers give up the habit that will determine the mortality in the next few decades and which requires the urgent attention of public health authorities throughout Europe.

Tobacco smoke released to the environment by smokers, commonly referred to as environmental tobacco smoke (ETS) and which may be said to give rise to enforced ‘passive smoking’, has several deleterious effects on people who inhale it. It causes a small increase in the risk of lung cancer and also some increase in the risk of heart disease and respiratory disease and is particularly harmful to small children. Smoking during pregnancy increases the risk of stillbirth, diminishes the infant’s birth weight, and impairs the child’s subsequent mental and physical development while smoking by either parent after the child’s birth, increases the child’s risk of respiratory tract infection, severe asthma, and sudden death.

Although the greatest hazard is caused by cigarette smoking, cigars can cause similar hazards if their smoke in inhaled and both cigar and pipe smoker cause comparable hazards of cancers of the oral cavity, pharynx, extrinsic larynx, and oesophagus.

Worldwide, it is estimated that smoking killed four million people each year: in the 1990s and that altogether some 60 million deaths were caused by tobacco in the second half of the Twentieth century. In most countries, the worst consequences of the “Tobacco Epidemic” are yet to emerge, particularly among women in developed countries and in the populations of developing countries, as, by the time the young smokers of today reach middle or old age, there will be approximately ten million deaths each year from tobacco (three million in the developed, seven million in the developing countries). If the current prevalence of smoking persists, approximately 500 million of the world’s population today can expect to be killed by tobacco, 250 million in middle age.

The situation in Europe is particularly worrying. The European Union is the second largest producer of cigarettes (749 billion in 1997/98) after China (1675 billion in 1998) and the major exporter of cigarettes (400 billion). In Central and Eastern Europe, there has been a major increase in the smoking habit. Of the six World Health Organisation (WHO) regions, Europe has the highest per capita consumption of manufactured cigarettes and faces an immediate and major challenge in meeting the WHO target for a minimum of 80% of the population to be non-smoking. In 1990-1994 34% of men and 24% of women in the European Union were regular smokers. In women the rates were reduced by the low rates in southern Europe, but the rates there are rising and seem set to continue to rise over the next decade. In the age range 25-39 years the rates are higher (55% in men and 40% in women) and this can be expected to have a profound influence on the future incidence of the disease. It is particularly disturbing that in many parts of Europe, the prevalence of smoking remains high among General Practitioners, who should set an exemplary lifestyle in terms of health. This should be a target for immediate action.

It has been shown that changes in cigarette consumption are affected mainly at a sociological level rather than by actions targeted at individuals (for example, individual smoking cessation programmes). Actions such as advertising bans and increases in the price of cigarettes influence cigarette sales particularly among the young. A “Tobacco Policy” is, consequently essential to reduce the health effects of tobacco, and experience shows that this should be aimed at both stopping young people from starting to smoke and helping smokers to stop. To be efficient and successful, a tobacco policy has to be comprehensive and maintained over a long time period. Increased taxes on tobacco, total bans on direct and indirect advertising, smoke-free enclosed public areas, prominent health warning labels on tobacco products, a policy of low maximum tar levels in cigarettes, education about the effects of smoking, encouragement of smoking cessation, and health interventions at the individual level, all need to be implemented. It must be recognized that nicotine is an addictive drug and that some smokers who are heavily addicted need medical help to overcome the addiction.

The importance of adequate intervention is shown by the low lung cancer rates in those Nordic countries which, since the early 1970’s, have adopted integrated central and local policies and programmes against smoking. In the UK, tobacco consumption has declined by 46% since 1970 and lung cancer mortality among men has been decreasing since 1980, although the rate still remains high. In France, between 1993 and 1998, there has been a 11% reduction in tobacco consumption due to the implementation of anti-tobacco measures introduced by the Loi Evin.

The first point of the European Code Against Cancer should consequently be:

DO NOT SMOKE. Smoking is the largest single cause of premature death.

SMOKERS: STOP AS QUICKLY AS POSSIBLE. In terms of health improvement, stopping smoking before having cancer or some other serious disease avoids most of the later excess risk of death from tobacco even if smoking is stopped in middle age.

DO NOT SMOKE IN THE PRESENCE OF NON-SMOKERS. The health consequences of your smoking may affect the health of those around you.

Ben Foster

Cancer Control

The diseases grouped under the title “cancer” are remarkably common and of major public health importance since more than half the people who develop cancer die from their disease. Thus, the concept of “cancer control” has been developed to attack the cancer problem at various points in its evolution, with the overall goal of reducing cancer related suffering and death

Primary Prevention

The most obvious ways to prevent people dying from cancer are either to find cures for the different forms of the disease or to find ways to stop the development of clinical cancer in the first instance. At the present time, cancer prevention involves determining the causes of cancer (risk determinants) among those factors shown to be associated with the development of the disease by epidemiological studies (risk factors). Avoiding a changing exposure to risk determinants would result in a reduction in cancer risk.

The evidence that cancer is preventable is compelling. Different populations around the world experience different levels of different forms of cancer[4], and these levels change with time in orderly and predictable manners[5]. Groups of migrants quickly leave behind the cancer levels of their original home and acquire the cancer pattern of their new residence sometimes within one generation[6-7]. Thus those Japanese who left Japan for California left behind the high levels of gastric cancer in their homeland and exchanged it for the high levels of breast and colorectal cancer present among inhabitants of their new home. Furthermore, groups whose lifestyle habits differentiate themselves from other members of the same community frequently have different cancer risks (c.f. Seventh Day Adventist and Mormons[8]).

For reasons such as these, it is estimated that upwards of 80 per cent, or even 90 per cent, of cancers in western populations may be attributable to environmental causes[9] defining “environment” in its broadest sense to include a wide range of ill-defined, dietary, social and cultural practices. Although all of these avoidable causes have not yet been clearly identified, it is thought that risk determinants exist for about one half of cancers. Thus, primary prevention in the context of cancer is an important area of Public Health.

Secondary Prevention

It is very frequently the case that the probability of successful treatment of cancer is increased, sometimes very substantially, if the cancer can be diagnosed at an early stage. Awareness of the significance of signs and symptoms is important, but all too frequently cancers which exhibit symptoms are at an advanced stage. Screening is a term frequently applied to the situation where tests are used to indicate whether an (generally asymptomatic) individual is at a high or low chance of having a cancer. Detecting cancers at an early, asymptomatic stage could lead to decreases in the mortality rate for certain cancers.

Tertiary Prevention

An obvious way to prevent cancer death is to cure those cancers which develop. However, there have been few major breakthroughs in cancer treatment in the sense of turning a fatal tumour into a curable one. Notably successes have been in Testicular Teratoma[10], Hodgkin’s Disease[11], Children’s Leukaemia, Wilm’s Tumour and choriocarcinoma. Progress in survival of the major cancers has been very much less than hoped. Adjuvant chemotherapy and Tamoxifen have improved survival in breast cancer[12], adjuvant chemotherapy has also contributed to improvements in prognosis of ovarian cancer and colorectal cancer[13] and there have been some other progress which could be attributed specifically to certain treatments.

General progress in medical science has led to modern anaesthesia making more patients to be candidates for surgery and surgery safer, better control of infection and bacterial diseases, better imaging has improved tumour localisation and staging, and better devices are available to deliver the appropriate doses of radiation and drugs. Thus, more patients can get better and more appropriate therapy and, hence, have a better prognosis.

The quality-of-life issue has not been neglected with breast conservation therapy now almost supplanting traditional, radical mastectomy in the majority of women; more plastic breast reconstruction; less amputation of limbs for bone and soft-tissue sarcomas; and better colostomies, being some important advances.

Against this background of Cancer as an important Public Health problem which is one of the commonest causes of premature and avoidable death in Europe, the European Code Against Cancer was introduced to be a series of recommendations which, if followed, could lead in many instances to a reduction in cancer incidence and also to reductions in cancer mortality.

The European Code Against Cancer was originally drawn-up and was subsequently endorsed by theEuropean Commission high-level Committee of Cancer Experts in 1987. In 1994, the European Commission invited the European School of Oncology to assemble a group of international experts to examine and consider revision of the scientific aspects of the recommendations given in the current Code. This exercise took place and a new version was adopted by the Cancer Experts Committee at its meeting of November 1994[1].

This publication constitutes the second revision, producing the third version of the European Code Against Cancer. The project was funded by the Europe Against Cancer programme of the European Commission. An Executive Committee was formed to guide the project and the Committee involved Public Health specialists, Oncologists as well as representatives of the Cancer Leagues and the Prevention Departments of Ministries of Health in Europe. A Scientific Committee was established comprising several independent experts and nominated Chairmen of the sub-Committees established to review recommendations on specific topics. Below the scientific rationale for each recommended point of the European Code Against Cancer is outlined as well as discussion of other factors which were considered but not included in the Code.

Ben Foster

References

1. Boyle P, Veronesi U, Tubiana M et al. European School of Oncology advisory report to the European Commission for the “Europe Against Cancer Programme” European Code Against Cancer. Eur J Cancer 1995; 31A: 1395–1405.

2. Cook PJ, Doll R, Fellingham SA. A mathematical model for the age distribution of cancer in man. Int J Cancer 1969; 4: 93–112.

3. Boyle P, Severi G. Epidemiology of prostate cancer chemoprevention.
Eur Urol 1999; 35: 370–376.

4. Parkin DM, Whelan S, Ferlay J et al. (eds). Cancer incidence in five continents, vol VIII. IARC Scientific Publication No. 155. Lyon, France:International Agency for Research on Cancer 2002.

5. Doll R, Fraumeni JF, Muir CS. Cancer Trends. Oxford, UK: Oxford University Press 1994.

6. Haenszel W, Kurihara M. Studies of Japanese migrants I. Mortality from cancer and other diseases among Japanese in the United States. J Natl Cancer Inst 1968; 40: 43–68.

7. Grulich AE, McCredie M, Coates M. Cancer incidence in Asian migrants to New South Wales, Australia. Br J Cancer 1995; 71: 400–408.

8. Cairns J. Cancer, Science and Society. Cold Spring Harbor, NY: Cold Spring Harbor Press 1980.

9. Doll R, Peto R. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J Natl Cancer Inst 1981; 66: 1191–1308.

10. Boyle P. Testicular cancer: the challenge for cancer control. Lancet Oncol (Submitted).

11. Boyle P, Soukop M, Scully C et al. Improving prognosis of Hodgkin’s disease in Scotland. Eur J Cancer Clin Oncol 1988; 24: 229–234.

12. Early Breast Cancer Trialists’ Collaborative Group. Systemic treatment of early breast cancer by hormonal, cytotoxic, or immune therapy. 133 randomised trials involving 31,000 recurrences and 24,000 deaths among 75,000 women. Lancet 1992; 339: 71–85.

13. Cunningham D, Findlay M. The chemotherapy of colon cancer can nolonger be ignored. Eur J Cancer 1993; 29: 2077–2079.

14. IARC. Non-ionizing radiation, part 1: static and extremely low frequency (ELF) electric and magnetic fields. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, vol 80. Lyon, France: International Agency for Research on Cancer 2002.

15. Boice JD Jr, McLaughlin JK. Epidemiologic studies of cellular telephones and cancer risk. SSI report 2002:16. Stockholm, Sweden: Swedish Radiation Protection Authority 2002.

16. Hennekens CH, Buring JE, Manson JE et al. Lack of effect on long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular diseases. N Engl J Med 1996; 334: 1145–1149.

17. Lee IM, Cook N, Manson JE, Hennekens H. £]-carotene supplementation and incidence of cancer and cardiovascular disease: the Women’s Health study. J Natl Cancer Inst 1999; 91: 2102–2106.

18. The Alpha-Tocopherol, Beta Carotene Prevention Study Group. The effectof vitamin E and beta carotene on the incidence of lung cancer and othercancers in male smoker. N Engl J Med 1994; 330: 1029–1035.

19. Omen GS, Goodman GE, Thornquist MD et al. Effect of combination of beta carotene and vitamin A on lung cancer and cardiovascular diseases. N Engl J Med, 1996; 334: 1150–1155.

20. Blot WJ, Li JY, Taylor PR et al. Nutrition intervention trials in Linxian, China: supplementation with specific vitamin/mineral combinations, cancer incidence, and disease-specific mortality in the general population. J Natl Cancer Inst 1993; 85: 1483–1492.

21. Correa P, Fonthan ETH, Bravo JC et al. Chemoprevention of gastric dysplasia: randomized trial of antioxidant supplements and anti-Helicobacter pylori therapy. J Natl Cancer Inst 2000; 92: 1881–1888.

22. Greenberg ER, Baron JA, Stukel TA et al. A clinical trial of beta carotene to prevent basal-cell and squamous-cell cancers of the skin. The Skin Cancer Prevention Study Group. N Engl J Med 1990; 323: 789–795.

23. Clark LC, Combs GF, Turnbull BW et al. Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. A randomized controlled trial. Nutrition Prevention of Cancer Study Group. JAMA 1996; 276: 1957–1963.

24. Li JY,Taylor PR, Li B et al. Nutrition intervention trials in Linxian, China: multiple vitamin/mineral supplementation, cancer incidence, and diseasespecific mortality among adults with esophageal dysplasia. J Natl Cancer Inst 1993; 85: 1492–1498. 1000

25. McKeown-Eyssen GE, Bright-See E, Bruce WR et al. A randomized trial of a low fat high fibre diet in the recurrence of colorectal polyps. Toronto Polyp Prevention Group. J Clin Epidemiol 1994; 47: 525–536.

26. Schatzkin A, Lanza E, Corle D et al. Lack of effect of a low-fat, high-fibre diet on the recurrence of colorectal adenomas. N Engl J Med 2000; 342: 1149–1155.

27. MacLennan R, Macrae F, Bain C et al. Randomized trial of intake of fat, fiber, and £]-carotene to prevent colorectal adenomas. The Australian Polyp Prevention Project. J Natl Cancer Inst 1995; 87: 1760–1766.

28. Alberts DS, Martinez ME, Roe DJ et al. Lack of effect of a high-fiber cereal supplement on the recurrence of colorectal adenomas. N Engl J Med 2000; 342: 1156–1162.

29. Bonithon-Kopp C, Kronborg O, Giacosa A et al. Calcium and fibre supplementation in prevention of colorectal adenoma recurrence: a randomised intervention study. European Cancer Prevention Organisation Study Group. Lancet 2000; 356: 1300–1306.

30. Baron JA, Beach M, Mandel JS et al. Calcium supplements for the prevention of colorectal adenomas. Calcium Polyp Prevention Study Group. N Engl J Med 1999; 340: 101–107.

31. Hofstad B, Almendingen K, Vatn M et al. Growth and recurrence of colorectal polyps: a double-blind 3-year intervention with calcium and antioxidants. Digestion 1998; 59: 148–156.

32. Giardiello FM, Hamilton SR, Krush AJ et al. Treatment of colonic and rectal adenomas with sulindac in familial adenomatous polyposis. N Engl J Med 1993; 328: 1313–1316.

33. Steinbach G, Lynch PM, Phillips RK et al. The effect of celecoxib, a cyclooxygenase-2 inhibitor, in familial adenomatous polyposis. N Engl J Med 2000; 342: 1946–1952.

34. Ladenheim J, Garcia G, Titzer D et al. Effect of sulindac on sporadic colonic polyps. Gastroenterology 1995; 108: 1083–1087.

35. Calaluce R, Earnest DL, Heddens D et al. Effects of piroxicam on prostaglandin E2 levels in rectal mucosa of adenomatous polyp patients: a randomized phase IIb trial. Cancer Epidemiol Biomarkers Prev 2000; 9: 1287–1292.

36. Thun MJ, Henley J, Patrono C. Nonsteroidal anti-inflammatory drugs as anticancer agents: mechanistic, pharmacologic, and clinical issues. J Natl Cancer Inst 2002; 94: 252–266.

37. Veronesi U, Maisonneuve P, Costa A et al. Prevention of breast cancer with tamoxifen: preliminary findings from the Italian randomised trial among hysterectomised women. Lancet 1998; 352: 93–97.

38. Powles TJ, Eeles R, Ashley S et al. Interim analysis of the incidence of breast cancer in the Royal Marsden Hospital tamoxifen randomised chemoprevention trial. Lancet 1998; 352: 98–101.

39. Fisher B, Costantino JP, Wickerham DL et al. Tamoxifen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study. J Natl Cancer Inst 1998; 90: 1371–1387.

40. IBIS investigators. First results from the International Breast Cancer Intervention Study (IBIS-I): a randomised prevention trial. Lancet 2002;360: 817–824.

41. Cauley JA, Norton L, Lippman ME et al. Continued breast cancer risk reduction in postmenopausal women treated with raloxifene: 4-year results from the MORE trial. Multiple outcomes of raloxifene evaluation. Breast Cancer Res Treat 2001; 65: 125–134.

42. Cuzick J, Powles T, Veronesi U et al. Overview of the main outcomes in breast-cancer prevention trials. Lancet 2003; 361: 296–300.

43. IARC. Hormonal contraception and post-menopausal hormonal therapy. IARC Monographs on the Evaluation of the Carcinogenic Risks to Humans, vol 72. Lyon, France: International Agency for Research onCancer 1999.

Ben Foster

The Present

Since the previous version of the European Code Against Cancer was created[1], the European Union has expanded its number of Member States and next year, in 2004, will see a further and dramatic expansion as 10 new Member States join (Cyprus, Czech, Hungary, Estonia, Malta, Latvia, Lithuania, Poland, Slovenia and Slovakia). Additionally, it is currently anticipated that Bulgaria and Romania will join in 2007 followed at a later date by Turkey. These expansions enlarge the Union to incorporate a greater diversity of peoples with a much larger degree of heterogeneity present in lifestyle habits and disease risk. The contrast between the Mediterranean countries, the Nordic countries and those countries of Central and Eastern Europe is considerable. In view of the accession of New Member States, an important aspect of the revision of this Code was to take into consideration the new Member States.

For the purposes of this text, the European Union shall be defined as the current 15 Member States (Austria, Belgium, Denmark, Finland, France, Germany, Greece, Ireland, Italy, Luxembourg, the Netherlands, Portugal, Spain, Sweden and the United Kingdom) plus the 10 Candidate Countries scheduled for entry in 2004 (Cyprus, Czech, Hungary, Estonia, Malta, Latvia, Lithuania, Poland, Slovenia and Slovakia).

Cancer Burden

In the European Union in 2000 it is estimated that there were 1.892.000 incident cases of all forms of cancer (excluding non-melanoma skin cancers diagnosed): this burden was shared almost equally by each gender although there was a slight excess in men (1.014. 000 cases) than in women (878.000 cases). In 2000, it is estimated that there were 1.156.000 deaths where cancer was the underlying cause in the European Union. Of these table 1. 651.000 were of men and 504.000 women.
The commonest form of cancer diagnosed in the European Union in 2000 was colorectal cancer, with an estimated total of 258,038 new cases. Of these, 123.000 were diagnosed in men while 135.000 were diagnosed in women table 2. There was a total of 138.000 deaths caused by colorectal cancer in the European Union, of which 70.000 were in men and 68.000 in women table 2
In 2000, it is estimated that there are 241.191 incident cases of lung cancer, with the majority diagnosed in men (192.000 cases) and fewer in women (48.901 cases) table 3 . In the same year, it is estimated that there are 231.000 deaths in the European Union caused by lung cancer. Of these, 183.000 occurred in men and 49.000 in women.
There was an estimated 95.500 incident cases of stomach cancer diagnosed in 2000, of which 57,000 were diagnosed in men and 38.000 in women table 4. There was an estimated total of 78.000 deaths caused by stomach cancer: 45.500 in men and 32.500 in women table 4.
In women, there was an estimated 244.500 new cases of breast cancer diagnosed in the year 2000 and there were 91.000 deaths caused by breast cancer table 5. In men, there was an estimated total of 157.000 incident cases of prostate cancer diagnosed in the European Union in 2000 and an estimated 66.500 deaths caused by this disease.
The age-adjusted risk of cancer increases quite quickly with age [2]: there is a difference of at least two orders of magnitude between the risk of developing cancer in the fourth decade of life and the eighth decade of life. Even if age-specific cancer rates remain fixed at 1980 levels, it is to be expected that there will be large increases in the numbers of cases of cancer diagnosed for the first two decades of the twenty-first century. This is simply a consequence of the ageing population; more and more men and women living to older and older ages. The post-World War II “baby-boom”, the first generation in western Europe to have had the benefit of modern medicine and not to have endured a major war, will reach ages where cancer is an important problem from the early days of next century. The effect on the absolute numbers of cases will be quite dramatic, particularly for cancers sites such as prostate cancer where the median age at diagnosis current is around 75 years in the European Union [3].

Ben Foster

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