world cancer report - iarc

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cating that exposure to asbestos caused lung cancer accumulated from the 1930s and the evidence became conclusive during the 1950s and 1960s. However, only during the late 1970s were effective steps for limiting exposure initiated in some countries [4]. Even so, relatively little action concerning asbestos-induced cancer has been taken in many countries (notably in the developing world, see below) until recently. After introduction of preventive measures, a progressive decrease in the risk of cancer among relevant workers may be evident. This may be seen by comparing groups of workers who were employed in different time periods. For example, the risk of lung cancer decreased among cohorts of American workers who were potentially exposed to chloromethyl ethers. This hazard was reduced after 1971, when a closed manufacturing system was introduced [5]. Among relevant workers, lung cancer incidence was greatest in the 1960s, and decreased after 1974. Change in risk of cancer is also evident amongst Norwegian workers employed in a nickel refinery smelter from the beginning of operation in the 1910s until the 1960s [6] (Fig. 4.9). Major changes in the process occurred during this time, particularly after 1950. [7]. Risk of nasal cancer has decreased; excess risk of lung cancer has also decreased but to a lesser degree, which may be attributable to the effects of increased smoking. The situation in developing countries Most documented examples of successful prevention of occupational cancer involve developed countries. To some extent, these examples have also led to improvement in conditions of occupational hygiene in developing countries. The quality of industrial hygiene in the Chinese chemical industry improved markedly during the 1970s such that by 1981, air concentrations of vinyl chloride monomer were similar to those in industries in Europe and North America [8]. However, lack of economic resources and health services may limit the adoption of preventive measures. Often, exposure levels in the informal employment sector and in small workshops, where a large propor- Fig. 4.9 Risk of lung cancer among nickel refinery workers, by year of first employment. Fig. 4.10 UK asbestos imports and predicted mesothelioma deaths in British men. Mortality from mesothelioma reflects past exposure to asbestos. Despite the ban on the use of asbestos in the early 1990s, mesothelioma cases will continue to increase, with approximately 250,000 expected deaths in Europe over the next 35 years. tion of workers are located in developing countries, are high compared to “best practice” adopted in large facilities [9]. Protective clothing may have limited effectiveness in some developing countries because of discomfort arising from its use in hot, humid climates. Exposure to asbestos, crystalline silica and pesticides are recognized priorities for control of occupational cancer hazards in developing countries. The greatest impact in terms of prevention of disease is likely to come from the establishment and enforcement of national and international regulatory controls. Child labour is another cause for concern. Even where regulations to protect workers from exposures to carcinogens are adopted, such regulations may not apply to children, who are often not employed legally [8]. Some nations have established legislation that applies specifically to the employment of children: for example, a detailed list of Reduction of occupational and environmental exposures 137
industries, processes and occupations that are deemed to be dangerous for children has been set out by the Philippines. Prevention of occupational cancer may positively affect general environmental conditions. A study of conditions at the Huannan coal mine, China, established that from 1953 to the 1980s underground dust Pollutant Decrease Carbon monoxide (CO) 37% Lead 78% Nitrogen dioxide (NO 2) 14% Ozone 6% Particles of ≤10 µm diameter (PM-10) 22% PM-10 measurements began in 1988 Sulfur dioxide (SO 2) 37% Table 4.5 Percent decrease in air concentrations of six key air pollutants, USA (1986-1995). 138 Prevention and screening levels decreased from 266 mg/m 3 to 1.3 mg/m 3, and this coincided with marked improvement in housing conditions, water quality, nutrition and sanitation [8]. Environmental pollution The prevention of cancer caused by environmental pollution might be expected to follow the same principles and approaches adopted for prevention of occupational cancer. However, control of carcinogenic hazards in the general environment is usually more complex than at the workplace. Among other things, environmental pollution usually derives from many sources. Moreover, exposure levels vary greatly over space and time. Measures to reduce pollution can rarely be correlated with reduced cancer incidence. A decreased incidence of lung cancer, for example, cannot be attributed to reduced air pollution against a high background of tobac- Compound Average ambient Cancer associated IARC classification air concentration [mg/m 3] Acetaldehyde 5 Nasal tumours in rats 2B Acrylonitrile 0.01 - 10 Lung cancer in workers 2A Arsenic (1 - 30) x 10 -3 Lung cancer in humans 1 Benzo[a]pyrene No data Lung cancer in humans 1 Bis(chloromethyl)ether No data Epitheliomas in rats 1 Chloroform 0.3-10 Kidney tumours in rats 2B Chromium VI (5 - 200) x 10 -3 Lung cancer in workers 1 1,2-Dichloroethane 0.07 – 4 Tumour formation in rodents 2B Diesel exhaust 1.0 - 10.0 Lung cancer 2A Nickel 1 - 180 Lung cancer in humans 1 Polycyclic aromatic (1 - 10) x 10 -3 Lung cancer in humans 1 hydrocarbons (benzo[a]pyrene) 1,1,2,2-Tetrachloroethane 0.1 - 0.7 Hepatocellular carcinomas in mice 3 Trichloroethylene 1 – 10 Cell tumours in testes of rats 2A Vinyl chloride 0.1 – 10 Haemangiosarcoma in workers 1 Liver cancer in workers Table 4.6 WHO guidelines (1999) for air pollutants with carcinogenic health end-points. These substances have been classified by IARC as either human carcinogens (Group 1), probable human carcinogens (Group 2A) or possible human carcinogens (Group 2B).endpoints
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WORLD HEALTH ORGANIZATION WHO OMS I
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WORLD CANCER REPORT Editors Bernard
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CONTENTS Foreword 9 1 The global bu
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The global burden of cancer Cancer
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Fig. 1.2 Incidence and mortality of
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Central and Southern Europe differ
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Incidence of cancer in South Centra
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from documentation of disease to a
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TOBACCO SUMMARY >In addition to lun
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Fig. 2.3 Smoking by children is inc
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Cancers positively Sex Standardized
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PHARMACOLOGICAL APPROACHES TO SMOKI
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level the dose—response relations
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lipoprotein-associated cholesterol,
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Agent Cancer site/cancer Main indus
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Industry, occupation Cancer site/ca
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to occupational exposures in develo
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Air pollutant WHO Air Quality Guide
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der cancer of the order of 50% is p
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AFLATOXIN B 1 HEPATITIS VIRUS (chro
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Fig. 2.30 Correlation between regio
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MEDICINAL DRUGS SUMMARY > Certain d
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Drug or drug combination Cancer IAR
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Agent or substance Cancer site/canc
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sources of electromagnetic fields [
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CHRONIC INFECTIONS SUMMARY > Infect
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Infection Subclinical Mutagenic fac
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TUMOURS ASSOCIATED WITH HIV/AIDS Ap
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DIET AND NUTRITION SUMMARY > Up to
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Fig. 2.54 The age-adjusted mortalit
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OVERWEIGHT, OBESITY AND PHYSICAL AC
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IMMUNOSUPPRESSION SUMMARY >Persiste
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Fig. 2.64 Cancer following immunosu
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Syndrome Gene Location Cancer site/
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viduals, confirmation of a gene def
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REPRODUCTIVE FACTORS AND HORMONES S
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PHYTO-ESTROGENS AND CANCER PEVENTIO
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Indicator Number of oral contracept
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Mechanisms of tumour development Th
Page 81 and 82: The stages in tumorigenesis have be
Page 83 and 84: PRECURSOR LESIONS IN CHEMOPREVENTIO
Page 85 and 86: CARCINOGEN ACTIVATION AND DNA REPAI
Page 87 and 88: adducts, a few weeks or months for
Page 89 and 90: I Reactive oxygen species Methylati
Page 91 and 92: which remove the mismatched bases,
Page 93 and 94: Common human oncogenes Many common
Page 95 and 96: product of the RB1 gene (pRb) and a
Page 97 and 98: ates a molecular bridge between p53
Page 99 and 100: potential cancer genes altered thro
Page 101 and 102: One of the earliest genes to be ide
Page 103 and 104: Regulation of the cell cycle and co
Page 105 and 106: CELL-CELL COMMUNICATION SUMMARY > C
Page 107 and 108: Connexin genes and tumour suppressi
Page 109 and 110: APOPTOSIS SUMMARY > The term apopto
Page 111 and 112: Caspase-8 Caspase-3 c-FLIP Procaspa
Page 113 and 114: ways. Several options are under inv
Page 115 and 116: INVASION AND METASTASIS SUMMARY > T
Page 117 and 118: laminin, entactin and also heparan
Page 119 and 120: Target Example of agent Comments Ad
Page 121 and 122: organs, and to respond to local gro
Page 123 and 124: TOBACCO CONTROL SUMMARY > Tobacco-i
Page 125 and 126: Region Deaths due to % of total dea
Page 127 and 128: ipated, is primarily attributable t
Page 129 and 130: smoke. This may be achieved in part
Page 131: there is no evidence for the effica
Page 135 and 136: stoves arises in rural areas of dev
Page 137 and 138: Climbing plants on trellis at end r
Page 139 and 140: HEPATITIS B VACCINATION SUMMARY > P
Page 141 and 142: Fig. 4.17 Chronic active HBV-associ
Page 143 and 144: HUMAN PAPILLOMAVIRUS VACCINATION SU
Page 145 and 146: Vaccine Site of trial Number of pat
Page 147 and 148: prolonged use. Similar drugs, that
Page 149 and 150: aspirin and other non-steroidal ant
Page 151 and 152: SCREENING FOR BREAST CANCER SUMMARY
Page 153 and 154: Fig. 4.35 Cumulative mortality from
Page 155 and 156: SCREENING FOR PROSTATE CANCER SUMMA
Page 157 and 158: Fig. 4.39 Poster designed for an an
Page 159 and 160: is around 10% for cancer (out of ev
Page 161 and 162: 45 with one positive rehydrated FOB
Page 163 and 164: eing based on (i) time trends in th
Page 165 and 166: Fig. 4.48 Women at a clinic in Indi
Page 167 and 168: SCREENING FOR ORAL CANCER SUMMARY >
Page 169 and 170: India will provide useful informati
Page 171 and 172: cer incidence following cure of inf
Page 173 and 174: 100 50 25 10 5 2.5 1 Japan Males Fe
Page 175 and 176: Human cancers by organ site Maligna
Page 177 and 178: tobacco smoking: age at start, aver
Page 179 and 180: diagnosis is usually confirmed by h
Page 181 and 182: is frequent and survival rates are
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Fig. 5.14 Physician reading digital
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Markers of prognosis in breast canc
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cer in the contralateral breast (Ch
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100 50 25 10 5 2.5 1 Japan Chile Po
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depends on staging. Small intramuco
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Fig. 5.30 A diet rich in fresh frui
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ane protein involved in cell adhesi
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LIVER CANCER SUMMARY > About 560,00
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Fig. 5.39 A woman in the Gambia pre
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REFERENCES 1. Ferlay J, Bray F, Par
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Certain Possible Uncertain Age Andr
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Management The dramatic division be
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TUMOUR NORMAL Gastrula PGC 2n Impri
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CANCERS OF THE FEMALE REPRODUCTIVE
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Fig. 5.62 Five-year relative surviv
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Inheritance of high-penetrance gene
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invasive malignant. Malignant germ
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OESOPHAGEAL CANCER SUMMARY >Cancer
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Fig. 5.76 A radiographic view of an
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with a stent; laser recannulation,
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Fig. 5.82 Risk of bladder cancer am
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Partial cystectomy is appropriate f
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poorly known since hypopharyngeal c
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Fig. 5.92 Oral leukoplakia with mil
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LYMPHOMA SUMMARY > Malignant lympho
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T Fig. 5.101 Nuclear magnetic reson
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Fig. 5.106 Five-year relative survi
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Fig. 5.109 The immediate aftermath
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A B Fig. 5.113 Acute myeloid leukae
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Fig. 5.118 Five-year relative survi
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Fig. 5.120 Age-specific incidence a
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Hereditary condition Mode of inheri
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MELANOMA SUMMARY > Approximately 13
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Fig. 5.131 Primary melanoma with a
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THYROID CANCER SUMMARY > Cancer of
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Papillary carcinoma RET/PTC TRK BRA
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KIDNEY CANCER SUMMARY > Cancer of t
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Stage Clear cell carcinoma Papillar
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TUMOURS OF THE NERVOUS SYSTEM SUMMA
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ing the optic tract, brain stem and
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mut = mutant p53 wt = wildtype p53
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SURGICAL ONCOLOGY SUMMARY > Surgica
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Year Radical mastectomy (%) Modifie
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TELEMEDICINE The prospects for tele
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Equipment Energy 50% depth dose App
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CANCER EDUCATION IN MEDICAL COURSES
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Fig. 6.10 Crystals of cisplatin: mo
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Responsiveness Cancer (in decreasin
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Most of the world’s most common c
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treatment of cancer. The problems l
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duction. It is clear that tumour ce
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REHABILITATION SUMMARY > Rehabilita
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cer and its associated disability.
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REFERENCES 1. Garden FH, Gillis TA
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Cancer pain relief varies and in so
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EMERGING ISSUES IN PALLIATIVE CARE
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Cancer control The negative impact
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priority to cancer control activiti
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Prevention of cancer Every country
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- Assessing the magnitude of the ca
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high-risk women. Further details on
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ecords departments are either rudim
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THE INTERNATIONAL AGENCY FOR RESEAR
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in the capitals/urban areas of four
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in the overall cancer strategy. WHO
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68% 1955 1975 1995 2025 32% 40% by
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Fig. 7.15 A grandfather at work in
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Fig. 7.17 Main causes of death in d
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Contributors and Reviewers Sources
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Dr Vera Luiz da Costa e Silva Tobac
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Georgia Moore Centers for Disease C
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REVIEWERS Dr Sandra E. Brooks 405 W
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2.53 T. Norat and E. Riboli, IARC 2
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Gastroenterology, 118(2 Suppl 1): S
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5.106 & 5.107 IARC/SEER/Osaka Cance
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4.17 R. Lambert, IARC/Adapted from
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Brain cancer, see nervous system tu
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Fibroblast growth factor (FGF), 117
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Microarray, 240 Micronutrients, 65,
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S Saccharin, 64, 85 Salicin, 153 Sa
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