world cancer report - iarc

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Industry, occupation Cancer site/cancer (suspected cancer sites in parentheses) IARC Group 1 Aluminium production Lung, bladder Auramine, manufacture of Bladder Boot and shoe manufacture and repair Nasal cavity, leukaemia Coal gasification Skin, lung, bladder Coke production Skin, lung, kidney Furniture and cabinet making Nasal cavity Haematite mining (underground) with exposure Lung to radon Iron and steel founding Lung Isopropanol manufacture (strong-acid process) Nasal cavity Magenta, manufacture of Bladder Painter (mainly in the construction industry) Lung Rubber industry (certain occupations) Bladder, leukaemia IARC Group 2A Art glass, glass containers and pressed ware (Lung, stomach) (manufacture of) Hairdresser or barber (occupational exposure as a) (Bladder, lung) Non-arsenical insecticides (occupational exposures (Lung, myeloma) in spraying and application of) Petroleum refining (occupational exposures in) (Leukaemia, skin) IARC Group 2B Carpentry and joinery (Nasal cavity) Dry cleaning (occupational exposures in) (Bladder, oesophagus) Textile manufacturing industry (work in) (Nasal cavity, bladder) Table 2.9 Industries and occupations classified as carcinogenic to humans (IARC Group 1), probably carcinogenic to humans (IARC Group 2A) or possibly carcinogenic to humans (IARC Group 2B). workers were exposed to more than one such agent. Nonetheless, benzidinebased dyes and 4,4’-methylenebis (2-chloroaniline) (known as MOCA, a curing agent for plastics) are implicated. The manufacture of auramine has been shown to cause bladder cancer, but the causative agent is not known. Benzene Occupational exposure to benzene may occur in the chemical and petroleum industries; it is used as a solvent and intermediate. The compound is known to cause leukaemia, most relevant studies implicating non-lymphocytic leukaemia, and myelogenous leukaemia in particular [6]. 36 The causes of cancer Asbestos and other fibres Cancer caused by inhalation of asbestos dust has been recognized since the 1950s. All forms of asbestos, including chrysotile and the amphibole, crocidolite, cause lung cancer and mesothelioma, an otherwise rare tumour derived from the lining of the peritoneum, pericardium or pleura. Apart from asbestos miners, those exposed include construction, demolition, shipbuilding, insulation and brake workers. Fibre size is a crucial factor determining the carcinogenicity of asbestos. Evidence suggests that insulation glass wool, rock wool and slag wool, which are used as replacements for asbestos in some applications, do not cause increased risk of lung cancer or mesothelioma, although ceramic fibres and certain special-purpose glass wools are possible carcinogens [7]. Metals Cancer of the lung can be caused by exposure to inorganic arsenic in mining and copper smelting. An increased incidence of lung cancer has also been recorded among workers in chromateproducing industries and among chromium platers and chromium alloy workers. Increased risk is predominantly associated with hexavalent chromium compounds. Nickel refining carries a carcinogenic risk in processes involving nickel (sub)sulfides, oxides and soluble nickel salts. Coal tar, coal gas production and iron founding Coal tar pitches and coal tar vapour are encountered in a variety of occupations including coke production, coal gasification and roofing. These mixtures produce cancers of the skin and at other sites including the urinary and respiratory systems. Work in iron and steel founding is also associated with an elevated risk of lung cancer; in addition to coalrelated emissions, such work may involve exposure to silica, metal fumes and formaldehyde. Wood work Nasal adenocarcinomas are caused by exposures in the furniture- and cabinetmaking industry, mainly among people exposed to wood dust. Painting Approximately 200,000 workers worldwide are employed in paint manufacture, and several million are believed to work as painters, including in specialist painting such as in vehicle production and repair. Painters are exposed to hydrocarbon and chlorinated solvents, dyes, polyesters, phenol-formaldehyde and polyurethane resins. A 40% excess risk of lung cancer has been consistently recorded, and cannot be explained by smoking alone.
Agent Cancer site/cancer IARC Group 1 Aflatoxins Liver Chronic infection with hepatitis B virus Liver Chronic infection with hepatitis C virus Liver Erionite Lung, pleura Radon and its decay products Lung Solar radiation Skin Environmental tobacco smoke Lung IARC Group 2A Diesel engine exhaust Lung, bladder Ultraviolet radiation A Skin Ultraviolet radiation B Skin Ultraviolet radiation C Skin Table 2.10 Agents and mixtures which occur mainly in the general environment but to which exposure may also occur in an occupational context. A worldwide problem Evidence on occupational cancer has been obtained mainly in developed countries. To a large extent, the critical data concern the effects of high exposure levels as a consequence of industrial practice during the first half of the 20th century. Few studies have been conducted in developing countries, other than some in China. Since the period, twenty to thirty years ago, to which most studies pertain, there have been major changes in the geographical distribution of industrial production. These have involved extensive transfer of technology, sometimes obsolete, from highly-industrialized countries to developing countries in South America and in Asia. For example, the manufacture of asbestos-based products is relocating to countries such as Brazil, India, Pakistan and the Republic of Korea, where health and safety standards and requirements may not be so stringent (Reduction of occupational and environmental exposures, p135). Occupational exposures to carcinogenic environments are increasing in developing countries as a result of transfers of hazardous industries and the establishment of new local industries as part of a rapid global process of industrialization [8]. A particular problem in developing countries is that much industrial activity takes place in multiple small-scale operations. These small industries are often characterized by old machinery, unsafe buildings, employees with minimal training and education and employers with limited financial resources. Protective clothing, respirators, gloves and other safety equipment are seldom available or used. The small operations tend to be geographically scattered and inaccessible to inspections by health and safety enforcement agencies. Although precise data are lacking, the greatest impact of occupational carcinogens in developing countries is likely to be in the less organized sectors of the relevant industries. Examples include the use of asbestos in building construction, exposure to crystalline silica in mining and mining construction, and the occurrence of polycyclic aromatic hydrocarbons and heavy metals in small-scale metal workshops and in mechanical repair shops. The most generally accepted estimates of the proportion of cancers attributable Fig. 2.19 Asphalt road-workers (shown here in India) are exposed to polycyclic aromatic hydrocarbons. Fig. 2.20 In modern mines (such as those of Charbonnages de France), the prevention of occupational risk is a major concern, which is being addressed on both collective (reduction of dust, organization of transport) and individual (use of suitable protection equipment) levels. Fig. 2.21 Textile dyeing in Ahmedabad, India. Protection against occupational exposures is often suboptimal in developing countries. Occupational exposures 37
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 34 and 35: to occupational exposures in develo
Page 36 and 37: Air pollutant WHO Air Quality Guide
Page 38 and 39: der cancer of the order of 50% is p
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
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PRECURSOR LESIONS IN CHEMOPREVENTIO
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CARCINOGEN ACTIVATION AND DNA REPAI
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adducts, a few weeks or months for
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I Reactive oxygen species Methylati
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which remove the mismatched bases,
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Common human oncogenes Many common
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product of the RB1 gene (pRb) and a
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ates a molecular bridge between p53
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potential cancer genes altered thro
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One of the earliest genes to be ide
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Regulation of the cell cycle and co
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CELL-CELL COMMUNICATION SUMMARY > C
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Connexin genes and tumour suppressi
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APOPTOSIS SUMMARY > The term apopto
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Caspase-8 Caspase-3 c-FLIP Procaspa
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ways. Several options are under inv
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INVASION AND METASTASIS SUMMARY > T
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laminin, entactin and also heparan
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Target Example of agent Comments Ad
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organs, and to respond to local gro
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TOBACCO CONTROL SUMMARY > Tobacco-i
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Region Deaths due to % of total dea
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ipated, is primarily attributable t
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smoke. This may be achieved in part
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there is no evidence for the effica
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industries, processes and occupatio
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stoves arises in rural areas of dev
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Climbing plants on trellis at end r
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HEPATITIS B VACCINATION SUMMARY > P
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Fig. 4.17 Chronic active HBV-associ
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HUMAN PAPILLOMAVIRUS VACCINATION SU
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Vaccine Site of trial Number of pat
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prolonged use. Similar drugs, that
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aspirin and other non-steroidal ant
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SCREENING FOR BREAST CANCER SUMMARY
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Fig. 4.35 Cumulative mortality from
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SCREENING FOR PROSTATE CANCER SUMMA
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Fig. 4.39 Poster designed for an an
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is around 10% for cancer (out of ev
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45 with one positive rehydrated FOB
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eing based on (i) time trends in th
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Fig. 4.48 Women at a clinic in Indi
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SCREENING FOR ORAL CANCER SUMMARY >
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India will provide useful informati
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cer incidence following cure of inf
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100 50 25 10 5 2.5 1 Japan Males Fe
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Human cancers by organ site Maligna
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tobacco smoking: age at start, aver
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diagnosis is usually confirmed by h
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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
Page 273 and 274:
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.
Page 289 and 290:
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
Page 339 and 340:
Microarray, 240 Micronutrients, 65,
Page 341 and 342:
S Saccharin, 64, 85 Salicin, 153 Sa
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