world cancer report - iarc

More documents

Recommendations

Info

der cancer of the order of 50% is plausible. Several other groups of pollutants of drinking water have been investigated as possible sources of cancer risk in humans [14,17]. They include organic compounds derived from industrial, commercial and agricultural activities and in particular from waste sites, as well as nitrites, nitrates, radionuclides and asbestos. For most pollutants, the results are inconclusive. However, an increased risk of stomach cancer has been repeatedly reported in areas with high nitrate levels in drinking water, and an increased risk of leukaemia REFERENCES 1. Tomatis L, Aitio A, Day NE, Heseltine E, Kaldor J, Miller AB, Parkin DM, Riboli E, eds (1990) Cancer: Causes, Occurrence and Control (IARC Scientific Publications, No. 100), Lyon, IARCPress . 2. Doll R, Peto R (1981) The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J Natl Cancer Inst, 66: 1191-1308. 3. Harvard Center for Cancer Prevention (1996) Harvard report on cancer prevention. Causes of human cancer. Environmental pollution. Cancer Causes Control, 7 Suppl 1: S37-S38. 4. Health Effects Institute (1991) Asbestos in Public and Commercial Buildings: A Literature Review and Synthesis of Current Knowledge, Boston, MA, Health Effects Institute. 5. Bruce N, Perez-Padilla R, Albalak R (2000) Indoor air pollution in developing countries: a major environmental and public health challenge. Bull World Health Organ, 78: 1078-1092. 6. WHO European Centre for Environment and Health (1995) Air pollution. In: Concern for Europe's Tomorrow: Health and the Environment in the WHO European Region, Stuttgart, Wissenschaftliche Verlagsgesellschaft, 139-175. 7. Katsouyanni K, Pershagen G (1997) Ambient air pollution exposure and cancer. Cancer Causes Control, 8: 284- 291. 8. Williams FL, Lloyd OL (1988) The epidemic of respiratory cancer in the town of Armadale: the use of long-term epidemiological surveillance to test a causal hypothesis. Public Health, 102: 531-538. 9. EPA (1999) National Air Quality and Emissions Trends Report, 1999. Office of Air Quality Planning & Standards. United States Environmental Protection Agency. 42 The causes of cancer has been observed among residents in areas with elevated levels of radium in drinking water. The atmosphere, and more particularly water and soil, may be polluted by a range of toxic organic compounds specifically including persistent pesticides, by-products of combustion, such as polychorinated dibenzo-p-dioxins (2,3,7,8-tetrachlorodibenzodioxin, TCDD, being of greatest concern) and dibenzofurans, and industrial products, such as polychlorinated biphenyls (PCBs) and polybrominated biphenyls (PBBs). These compounds are 10. Zhong L, Goldberg MS, Parent ME, Hanley JA (1999) Risk of developing lung cancer in relation to exposure to fumes from Chinese-style cooking. Scand J Work Environ Health, 25: 309-316. 11. World Health Organization (2000) Fact Sheet No. 187: Air Pollution, WHO, Geneva. 12. IARC (1991) Chlorinated Drinking-Water; Chlorination by-Products; Some Other Halogenated Compounds; Cobalt and Cobalt Compounds (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 52), Lyon, IARCPress. 13. Morris RD, Audet AM, Angelillo IF, Chalmers TC, Mosteller F (1992) Chlorination, chlorination by-products, and cancer: a meta-analysis. Am J Public Health, 82: 955- 963. 14. Cantor KP (1997) Drinking water and cancer. Cancer Causes Control, 8: 292-308. 15. IARC (1987) Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42 (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Suppl. 7), Lyon, IARCPress. 16. Kurttio P, Pukkala E, Kahelin H, Auvinen A, Pekkanen J (1999) Arsenic concentrations in well water and risk of bladder and kidney cancer in Finland. Environ Health Perspect, 107: 705-710. 17. Cantor KP (1996) Arsenic in drinking water: how much is too much? Epidemiology, 7: 113-115. chemically stable, are often passed along the food chain and may accumulate in fatty tissue. In most case, they were recognized as a carcinogenic hazard to humans on the basis of increased cancer risk in small but relatively heavily exposed groups who were occupationally exposed, in some cases as a result of industrial breakdowns or malfunctions (Occupational exposures, p33). Therefore the hazard posed to the general population can only be determined on the basis of extrapolation using mathematical models. WEBSITES United States Environmental Protection Agency: http://www.epa.gov/ The Health Effects Institute (a partnership of the US Environmental Protection Agency and industry): http://www.healtheffects.org/index.html United Nations Environment Programme: http://www.unep.org/
FOOD CONTAMINANTS SUMMARY > Food may be contaminated by natural or man-made toxins, including substances shown to be carcinogenic in experimental animals and, in some cases, in humans. > Naturally-occurring carcinogens include mycotoxins, particularly aflatoxins, which contribute to causation of liver cancer in Africa and Asia. >Food can be contaminated by residual pesticides. Small quantities of heterocyclic amines, which are mutagenic and carcinogenic in experimental animals, can be generated during food processing and cooking. > Means to reduce and, in some cases, eliminate food contamination include storage hygiene, appropriately enforced by regulation. > The burden of cancer attributable to food contamination is difficult to quantify, except in some defined instances (e.g. aflatoxin B1). Differences between diets eaten by diverse communities, in terms of amount and relative proportion of the major food groupings (vegetable content, fat content etc) exert a major influence on the distribution of cancers of the digestive tract and some other organs (Diet and nutrition, p62). By comparison, only a very minor part of the worldwide burden of cancer is attributable to contamination of foodstuffs by toxins recognized to be chemical carcinogens. Despite this global perspective, the issue warrants close attention because it may be a serious concern for particular communities and, irrespective of demonstrated cancer causation, food contamination can be rectified. Removal of carcinogenic contaminants requires that such contaminants are identified, and that ways are found to avoid their inclusion, or generation, in food. Such public health aims are amenable to regulation. Contamination of water is not included in the present discussion, but is considered elsewhere (Environmental pollution, p39). Contamination of food may occur directly during its production, storage and preparation. For example, grains and cereals are subject to fungal growth and contamination by mycotoxins. Indirect contamination of food can occur when animals have been given contaminated feed or been otherwise treated with various products. The most contentious residues occurring in meat, milk and eggs are antibacterial drugs, hormonal growth promoters and certain pesticides, heavy metals and industrial chemicals. An additional category of contaminants comprises those generated in the course of food preparation. Naturally occurring contaminants Food may be contaminated by mycotoxins, the presence of one such agent being indicative of the possibility that others are also present. A single fungus can produce several mycotoxins and food or feed can be contaminated by several varieties of mycotoxin-producing fungi. Only a small number of mycotoxins have been categorized as carcinogenic hazards. Aflatoxins Aflatoxins are a family of related compounds (designated B 1, B 2, G 1, G 2 and M) which occur as food contaminants in hot, humid parts of the world, with particularly high levels in traditional diets based upon maize and groundnuts (peanuts) of sub- Saharan Africa, South-East Asia and South America. Aflatoxins are products of the Aspergillus fungi and particularly accumulate during storage of grains. In many countries, including Europe and North America, aflatoxin contamination is recognized as a hazard and aflatoxin levels in susceptible foods are subject to monitoring and associated regulatory control. The detection of aflatoxin adducts on serum albumin is indicative of human exposure and, in regions where aflatoxins are a common food contaminant, such adducts are detectable in up to 95% of the population. In these regions, chronic hepatitis virus infection (essentially involving hepatitis B virus, HBV) occurs in up to 20% of the population. Together, aflatoxin exposure and HBV infection are the main risk factors accounting for the high incidence of hepatocellular carcinoma in some regions of Africa, Asia and South America [1]. Aflatoxin B 1 (the most common aflatoxin) causes liver cancer in experimental animals. In liver cells, aflatoxin B 1 is metabolized to form an epoxide which binds to the N7 position of specific guanines, leading to the formation of G to T transversions [2] (Carcinogen activation and DNA repair, p89). Mutations induced by aflatoxin B 1 are found in several genes involved in hepatocellular carcinogenesis. In particular, aflatoxin B 1 induces a typical Fig. 2.27 Groundnuts (peanuts) are particularly susceptible to contamination with aflatoxins in some regions, such as West Africa. Food contaminants 43
Page 2 and 3: WORLD HEALTH ORGANIZATION WHO OMS I
Page 4 and 5: WORLD CANCER REPORT Editors Bernard
Page 6 and 7: CONTENTS Foreword 9 1 The global bu
Page 8 and 9: The global burden of cancer Cancer
Page 10 and 11: Fig. 1.2 Incidence and mortality of
Page 12 and 13: Central and Southern Europe differ
Page 14 and 15: Incidence of cancer in South Centra
Page 16 and 17: from documentation of disease to a
Page 18 and 19: TOBACCO SUMMARY >In addition to lun
Page 20 and 21: Fig. 2.3 Smoking by children is inc
Page 22 and 23: Cancers positively Sex Standardized
Page 24 and 25: PHARMACOLOGICAL APPROACHES TO SMOKI
Page 26 and 27: level the dose—response relations
Page 28 and 29: lipoprotein-associated cholesterol,
Page 30 and 31: Agent Cancer site/cancer Main indus
Page 32 and 33: Industry, occupation Cancer site/ca
Page 34 and 35: to occupational exposures in develo
Page 36 and 37: Air pollutant WHO Air Quality Guide
Page 40 and 41: AFLATOXIN B 1 HEPATITIS VIRUS (chro
Page 42 and 43: Fig. 2.30 Correlation between regio
Page 44 and 45: MEDICINAL DRUGS SUMMARY > Certain d
Page 46 and 47: Drug or drug combination Cancer IAR
Page 48 and 49: Agent or substance Cancer site/canc
Page 50 and 51: sources of electromagnetic fields [
Page 52 and 53: CHRONIC INFECTIONS SUMMARY > Infect
Page 54 and 55: Infection Subclinical Mutagenic fac
Page 56 and 57: TUMOURS ASSOCIATED WITH HIV/AIDS Ap
Page 58 and 59: DIET AND NUTRITION SUMMARY > Up to
Page 60 and 61: Fig. 2.54 The age-adjusted mortalit
Page 62 and 63: OVERWEIGHT, OBESITY AND PHYSICAL AC
Page 64 and 65: IMMUNOSUPPRESSION SUMMARY >Persiste
Page 66 and 67: Fig. 2.64 Cancer following immunosu
Page 68 and 69: Syndrome Gene Location Cancer site/
Page 70 and 71: viduals, confirmation of a gene def
Page 72 and 73: REPRODUCTIVE FACTORS AND HORMONES S
Page 74 and 75: PHYTO-ESTROGENS AND CANCER PEVENTIO
Page 76 and 77: Indicator Number of oral contracept
Page 79 and 80: 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 and 132:
there is no evidence for the effica
Page 133 and 134:
industries, processes and occupatio
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
Page 183 and 184:
Fig. 5.14 Physician reading digital
Page 185 and 186:
Markers of prognosis in breast canc
Page 187 and 188:
cer in the contralateral breast (Ch
Page 189 and 190:
100 50 25 10 5 2.5 1 Japan Chile Po
Page 191 and 192:
depends on staging. Small intramuco
Page 193 and 194:
Fig. 5.30 A diet rich in fresh frui
Page 195 and 196:
ane protein involved in cell adhesi
Page 197 and 198:
LIVER CANCER SUMMARY > About 560,00
Page 199 and 200:
Fig. 5.39 A woman in the Gambia pre
Page 201 and 202:
REFERENCES 1. Ferlay J, Bray F, Par
Page 203 and 204:
Certain Possible Uncertain Age Andr
Page 205 and 206:
Management The dramatic division be
Page 207 and 208:
TUMOUR NORMAL Gastrula PGC 2n Impri
Page 209 and 210:
CANCERS OF THE FEMALE REPRODUCTIVE
Page 211 and 212:
Fig. 5.62 Five-year relative surviv
Page 213 and 214:
Inheritance of high-penetrance gene
Page 215 and 216:
invasive malignant. Malignant germ
Page 217 and 218:
OESOPHAGEAL CANCER SUMMARY >Cancer
Page 219 and 220:
Fig. 5.76 A radiographic view of an
Page 221 and 222:
with a stent; laser recannulation,
Page 223 and 224:
Fig. 5.82 Risk of bladder cancer am
Page 225 and 226:
Partial cystectomy is appropriate f
Page 227 and 228:
poorly known since hypopharyngeal c
Page 229 and 230:
Fig. 5.92 Oral leukoplakia with mil
Page 231 and 232:
LYMPHOMA SUMMARY > Malignant lympho
Page 233 and 234:
T Fig. 5.101 Nuclear magnetic reson
Page 235 and 236:
Fig. 5.106 Five-year relative survi
Page 237 and 238:
Fig. 5.109 The immediate aftermath
Page 239 and 240:
A B Fig. 5.113 Acute myeloid leukae
Page 241 and 242:
Fig. 5.118 Five-year relative survi
Page 243 and 244:
Fig. 5.120 Age-specific incidence a
Page 245 and 246:
Hereditary condition Mode of inheri
Page 247 and 248:
MELANOMA SUMMARY > Approximately 13
Page 249 and 250:
Fig. 5.131 Primary melanoma with a
Page 251 and 252:
THYROID CANCER SUMMARY > Cancer of
Page 253 and 254:
Papillary carcinoma RET/PTC TRK BRA
Page 255 and 256:
KIDNEY CANCER SUMMARY > Cancer of t
Page 257 and 258:
Stage Clear cell carcinoma Papillar
Page 259 and 260:
TUMOURS OF THE NERVOUS SYSTEM SUMMA
Page 261 and 262:
ing the optic tract, brain stem and
Page 263 and 264:
mut = mutant p53 wt = wildtype p53
Page 265 and 266:
SURGICAL ONCOLOGY SUMMARY > Surgica
Page 267 and 268:
Year Radical mastectomy (%) Modifie
Page 269 and 270:
TELEMEDICINE The prospects for tele
Page 271 and 272:
Equipment Energy 50% depth dose App
Page 273 and 274:
CANCER EDUCATION IN MEDICAL COURSES
Page 275 and 276:
Fig. 6.10 Crystals of cisplatin: mo
Page 277 and 278:
Responsiveness Cancer (in decreasin
Page 279 and 280:
Most of the world’s most common c
Page 281 and 282:
treatment of cancer. The problems l
Page 283 and 284:
duction. It is clear that tumour ce
Page 285 and 286:
REHABILITATION SUMMARY > Rehabilita
Page 287 and 288:
cer and its associated disability.
Page 289 and 290:
REFERENCES 1. Garden FH, Gillis TA
Page 291 and 292:
Cancer pain relief varies and in so
Page 293 and 294:
EMERGING ISSUES IN PALLIATIVE CARE
Page 295 and 296:
Cancer control The negative impact
Page 297 and 298:
priority to cancer control activiti
Page 299 and 300:
Prevention of cancer Every country
Page 301 and 302:
- Assessing the magnitude of the ca
Page 303 and 304:
high-risk women. Further details on
Page 305 and 306:
ecords departments are either rudim
Page 307 and 308:
THE INTERNATIONAL AGENCY FOR RESEAR
Page 309 and 310:
in the capitals/urban areas of four
Page 311 and 312:
in the overall cancer strategy. WHO
Page 313 and 314:
68% 1955 1975 1995 2025 32% 40% by
Page 315 and 316:
Fig. 7.15 A grandfather at work in
Page 317 and 318:
Fig. 7.17 Main causes of death in d
Page 319 and 320:
Contributors and Reviewers Sources
Page 321 and 322:
Dr Vera Luiz da Costa e Silva Tobac
Page 323 and 324:
Georgia Moore Centers for Disease C
Page 325 and 326:
REVIEWERS Dr Sandra E. Brooks 405 W
Page 327 and 328:
2.53 T. Norat and E. Riboli, IARC 2
Page 329 and 330:
Gastroenterology, 118(2 Suppl 1): S
Page 331 and 332:
5.106 & 5.107 IARC/SEER/Osaka Cance
Page 333 and 334:
4.17 R. Lambert, IARC/Adapted from
Page 335 and 336:
Brain cancer, see nervous system tu
Page 337 and 338:
Fibroblast growth factor (FGF), 117
Page 339 and 340:
Microarray, 240 Micronutrients, 65,
Page 341 and 342:
S Saccharin, 64, 85 Salicin, 153 Sa
show all

world cancer report - iarc

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?