Showing papers by "Vincent Cogliano published in 2009"

A review of human carcinogens--Part B: biological agents

Abstract: In February, 2009, 36 scientists from 16 countries met at the International Agency for Research on Cancer (IARC) to reassess the carcinogenicity of the biological agents classifi ed as “carcinogenic to humans” (Group 1) and to identify additional tumour sites and mechanisms of carcinogenesis (tables 1 and 2). These assessments will be published as part B of Volume 100 of the IARC Monographs. Hepatitis B virus (HBV) and hepatitis C virus (HCV) infect, res pectively, over 300 million and 170 million people worldwide, mainly in Asia and Africa. Chronic infection with these viruses is known to cause hepatocellular carcinoma. Suffi cient evidence is available to conclude that chronic infection with HCV can also cause non-Hodgkin lymphoma, especially B-cell lymphoma. In an inter vention study, patients with HCV infection and splenic lymphoma who were given the antiviral agent, interferon, showed regression of the lymphoma. Epstein–Barr virus (EBV) infects almost everyone and causes several types of cancer, including nasopharyngeal carcinoma, one of the most common cancers in southeastern Asia, and Burkitt’s lymphoma in children in Africa. New evidence points to a role for EBV in 5–10% of gastric carcinomas worldwide. EBV-positive gastric carcinoma develops early in life and has distinct histopathology, therefore it might belong to a separate clinical entity. In this subset of gastric tumours, presence of the viral genome in a monoclonal form and expression of EBV-transforming proteins are strong evidence for the involvement of EBV. Data from 22 cohort studies and 80 case–control studies show an association between Kaposi’s sarcoma herpes virus (KSHV) and Kaposi’s sarcoma, with relative risks higher than 10. Most studies are of transplant recipients and people infected with HIV-1. In both patients who are and are not infected with HIV-1, risk of Kaposi’s sarcoma increases relative to increasing titre of antibodies directed against KSHV, which are markers of the viral load. Evidence is suffi cient to show that KSHV causes primary eff usion lymphoma, a rare subgroup of B-cell non-Hodgkin lymphoma. Mechanistic data support an oncogenic role for KSHV in Kaposi’s sarcoma and in primary eff usion lymphoma—in individuals who are immunocompromised and in those apparently immunocompetent. KSHV is also associated with multicentric Castleman’s disease. Individuals who are infected with HIV-1 have a high risk of cancer. HIV-1 infection, mainly through immunosuppression, leads to increased replication of oncogenic viruses such as EBV and KSHV. Although antiretroviral therapy lowers the risk of many cancers associated with HIV-1, risks remain high. Cervical cancer is caused by types of human papillomavirus (HPV) that belong to a few phylogenetically related “high-risk” species (alpha-5, 6, 7, 9, 11) of the mucosotropic alpha genus. The types found most frequently in cervical cancer (HPV-16, 18, 31, 33, 35, 45, 52, 58) and four types less constantly found (HPV-39, 51, 56, 59) were classifi ed in

A review of human carcinogens--Part E: tobacco, areca nut, alcohol, coal smoke, and salted fish.

Abstract: www.thelancet.com/oncology Vol 10 November 2009 1033 In October, 2009, 30 scientists from 10 countries met at the International Agency for Research on Cancer (IARC) to reassess the carcinogenicity of tobacco, areca nut, alcohol, coal smoke, and saltpreserved fi sh, and to identify additional tumour sites (table) and mechanisms of carcinogenesis. These assessments will be published as part E of Volume 100 of the IARC Monographs. Tobacco smoking is the single largest cause of cancer worldwide. More than 1 billion people around the world are current smokers. New evidence con tinues to add to the extensive list of tobacco-related cancers (table); there is now suffi cient evidence that tobacco smoking causes cancer of the colon and of the ovary. More than 150 epi demiological studies of tobacco smoking and breast cancer were reviewed. Large cohort studies published since 2002 consistently show a small positive association (relative risks 1·1–1·3). Many chemicals in tobacco smoke cause mammarygland tumours in animals, and these carcinogens are stored in breast adipose tissue in women; therefore, the Working Group concluded that there is limited evidence that tobacco smoking causes breast cancer. A causal link between parental smoking and childhood cancers has been established. Four recent studies showed that children born of parents who smoke (father, mother, or both, including the preconception period and pregnancy) are at signifi cantly higher risk of hepatoblastoma, a rare embryonic cancer. The UK Childhood Cancer Study reported a relative risk of 1·86 for paternal smoking only and 2·02 for maternal smoking only, increasing to 4·74 (95% CI 1·68–13·35) when both parents smoke. For childhood leukaemia, a meta-analysis reported an associ ation with paternal smoking before pregnancy (summary relative risk 1·12, 1·04–1·21). Second-hand smoke causes lung cancer. There is now limited evidence for an association with cancers of the larynx and the pharynx, whereas evidence for female breast cancer remains inconclusive. Since secondhand smoke contains most of the constituents of mainstream smoke, it might also be associated with other cancer sites. Many types of smokeless tobacco are marketed and all contain nicotine and nitrosamines. Hundreds of millions of people use smokeless tobacco, mainly in India and southeast Asia, but also in Sweden and the USA. Earlier fi ndings showed a causal association between use of smokeless tobacco and cancers of the oral cavity and pancreas, and there is now suffi cient evidence for cancer of the oesophagus. All of the forms of tobacco discussed above induce malignant tumours in laboratory animals. Among the many carcinogens present in tobacco are nitrosamines, including the tobaccospecifi c nitrosamines 4-(methyl nitrosamino)-1-(3-pyridyl)-1-butanone Special Report: Policy A review of human carcinogens—Part E: tobacco, areca nut, alcohol, coal smoke, and salted fi sh

A review of human carcinogens--part D: radiation.

Abstract: In June 2009, 20 scientists from nine countries met at the International Agency for Research on Cancer (IARC) to reassess the carcinogenicity of the types of radiation previously classified as “carcinogenic to humans” (Group 1) and to identify additional tumour sites and mechanisms of carcinogenesis (table and panel). These assessments will be published as part D of Volume 100 of the IARC Monographs. Alpha particles, consisting of two protons and two neutrons, are a densely ionising type of radiation with low capacity to penetrate living tissue (less than 0·1 mm). Beta particles are electrons or positrons that are less ionising, but more penetrating (up to a few milimetres). The health hazards resulting from radionuclides that emit these particles largely occur after internal deposition. Epidemiological evidence shows a number of radionuclides that emit alpha or beta particles increase cancer risks at several anatomical sites (table). The Working Group reaffirmed the carcinogenicity of internally deposited radionuclides that emit alpha or beta particles (Group 1). After the Chernobyl accident, a sharp increase in the risk of thyroid cancer was found with exposure to radioiodines, particularly iodine-131, during childhood and adolescence. This increased risk might be due to higher milk intake per unit of body weight among children; a higher thyroid dose per unit of iodine-131 intake from milk; a higher susceptibility per unit of thyroid dose; or a combination of these. Radon exposure occurs mainly through contamination of indoor air by radon released from soil and building materials. Combined analyses of case–control studies now estimate that residential exposure to radon gas is the leading cause of lung cancer after tobacco smoke (8–15% attributable risk in Europe and North America). X-rays and gamma-rays are sparsely ionising electromagnetic radiation that penetrate living tissue, typically producing fast electrons that deposit energy, resulting in tissue damage. Extensive study of atomicbomb survivors shows increased cancer risks at multiple anatomical sites. Current evidence adds to the list of tumours caused by x-rays and gamma-rays (table), and also establishes that in-utero exposure increases the risk of cancer at multiple sites. The Working Group reaffirmed the carcinogenicity of x-radiation and gamma-radiation (Group 1). Neutrons are produced by nuclear reactions and are a main component of cosmic radiation. They are highly penetrating and interact with the traversed tissue, producing protons, other charged particles, and gamma-radiation. Epidemiological evidence is inadequate to assess the carcinogenicity of neutrons, because of co-exposures to other types of radiation. However, the evidence of cancer in experimental animals is sufficient, and mechanistic data show that neutrons transfer their energy in clusters of ionising events— resulting in similar, but more severe, local damage than that induced by x-rays or gamma-rays. On the basis of this evidence, the Working Group reaffirmed the carcinogenicity of neutron radiation (Group 1). Each type of ionising radiation (panel) transfers energy in the form of highly structured tracks of Upcoming meetings Sept 29–Oct 6, 2009 Lifestyle Factors

A review of human carcinogens—Part C: metals, arsenic, dusts, and fibres

Abstract: In March, 2009, 27 scientists from eight countries met at the International Agency for Research on Cancer (IARC) to reassess the carcinogenicity of metals, arsenic, dusts, and fi bres previously classifi ed as “carcinogenic to humans” (Group 1) and to identify additional tumour sites and mechanisms of carcinogenesis (table). These assessments will be published as part C of Volume 100 of the IARC Monographs. Inhalation is the primary route of exposure to arsenic in the workplace and happens in industries such as nonferrous smelting, arsenic pro duction, wood preservation, glass manu facturing, production and application of arsenic-based pesticides, and electronics. Non-occupational exposure to arsenic is mainly through food, except in areas with high levels of arsenic in the drinking water—eg, Taiwan, Bangladesh, West Bengal (India), northern Chile, and Cordoba Province (Argentina). Epidemiological studies have shown that exposure to arsenic through inhalation or drinking-water causes cancer of the lung, skin, and urinary bladder. Evidence suggests an association between exposure to arsenic in drinking water and the development of tumours at several other sites; however, various factors prevent a conclusion. Analytical studies have provided only limited information to support an association with kidney cancer, causes of liver cancer can be diffi cult to elucidate in groups that are high-risk for hepatitis B, and data on prostate cancer and arsenic exposure are not consistent between countries. Overall, the Working Group classifi ed arsenic and inorganic arsenic compounds as “carcinogenic to humans” (Group 1). The organic arsenicals monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) are the active ingredients of some herbicides and are metabolites of inorganic arsenic. On the basis of suffi cient evidence of cancer caused by DMA in experimental animals, and because MMA is extensively metabolised to DMA, both compounds are classifi ed as “possibly carcinogenic to humans” (Group 2B). Arsenobetaine and other organic arsenic compounds that are not metabolised in humans are “not classifi able” (Group 3). The Working Group reaffi rmed the classifi cation of beryllium and its compounds, cadmium and its compounds, chromium (VI) compounds, and nickel compounds as “carcinogenic to humans” (Group 1). Studies involved complex occupational exposures to a metal and its compounds, making it impossible to separately assess their carcinogenicity. Globally, an estimated 125 million people are still exposed to asbestos in the workplace. Although asbestos has been banned or restricted in most of the industrialised world, its use is increasing in parts of Asia, South America, and the former Soviet Union. Naturally occurring sources of asbestos, its use in brake linings, and deterioration of asbestos-containing products all contribute to environmental exposure worldwide. Exposure may also come from fi bres carried home on the clothing of asbestos workers. Upcoming meetings June 2–9, 2009 Radiation

A review of human carcinogens--Part F: chemical agents and related occupations.

Abstract: In October, 2009, 23 scientists from six countries met at the International Agency for Research on Cancer (IARC) to reassess the carcinogenicity of several chemical and occupational exposure circumstances previously classifi ed as ”carcinogenic to humans” (Group 1) and to identify additional tumour sites and mechanisms of carcinogenesis (table). These assessments will be published as the sixth and last part of Volume 100 of the IARC Monographs. Four aromatic amines and two related industrial processes were reaffi rmed as Group-1 carcinogens based on suffi cient evidence that they cause urinary bladder cancer in humans. The Group-1 classifi cation of dyes metabolised to benzidine and of 4,4’-methylenebis(2-chloroaniline) was based on suffi cient evidence in animal models and strong mechanistic evidence. Exposure to polycyclic aromatic hydro carbons (PAHs) causes cancers of the skin and lung in humans. Various PAH-related industries and PAHcontaining complex mixtures were confi rmed as Group-1 carcinogens. Although there are no epidemiological studies of benzo[a]pyrene, carcinogenicity in many animal species and strong mechanistic evidence justifi ed its classifi cation in Group 1. The carcinogenicity to humans of other chemicals and exposure scenarios was reaffi rmed (table). For ethylene oxide, the epidemiological evidence was limited, but there is suffi cient evidence for its carcinogenicity in rodents. Additionally, ethylene oxide is genotoxic and mutagenic in many in-vitro tests and in-vivo studies in animals, and its cytogenetic eff ects in lymphocytes of exposed workers provided strong support for its classifi cation in Group 1. Workers in the rubber-manufacturing industry have an increased risk for leukaemia, lymphoma, and cancers of the urinary bladder, lung, and stomach. Due to the diversity and com plexity of the exposures in this industry, it is diffi cult to identify causative agents, but there is strong evidence of genotoxic eff ects in these workers. The Working Group reviewed more than 100 epidemiological studies of benzene and confi rmed its carcinogenicity, with suffi cient evidence for ANLL, and limited evidence for ALL, CLL, MM, and NHL (for abbreviations, see table footnote). The Working Group also found limited evidence of an association between maternal exposure to painting—before and during pregnancy—and an increased risk of childhood leukaemia in the off spring. Dioxin (2,3,7,8-tetrachlorodibenzopara-dioxin, TCDD) was classifi ed in Group 1 in 1997, based on limited evidence of carcinogenicity in humans, For more on the IARC Monographs see http:// monographs.iarc.fr

Improving prediction of chemical carcinogenicity by considering multiple mechanisms and applying toxicogenomic approaches.

Abstract: While scientific knowledge of the potential health significance of chemical exposures has grown, experimental methods for predicting the carcinogenicity of environmental agents have not been substantially updated in the last two decades. Current methodologies focus first on identifying genotoxicants under the premise that agents capable of directly damaging DNA are most likely to be carcinogenic to humans. Emphasis on the distinction between genotoxic and non-genotoxic carcinogens is also motivated by assumed implications for the dose-response curve; it is purported that genotoxicants would lack a threshold in the low dose region, in contrast to non-genotoxic agents. However, for the vast majority of carcinogens, little if any empirical data exist to clarify the nature of the cancer dose-response relationship at low doses in the exposed human population. Recent advances in scientific understanding of cancer biology-and increased appreciation of the multiple impacts of carcinogens on this disease process-support the view that environmental chemicals can act through multiple toxicity pathways, modes and/or mechanisms of action to induce cancer and other adverse health outcomes. Moreover, the relationship between dose and a particular outcome in an individual could take multiple forms depending on genetic background, target tissue, internal dose and other factors besides mechanisms or modes of action; inter-individual variability and susceptibility in response are, in turn, key determinants of the population dose-response curve. New bioanalytical approaches (e.g., transcriptomics, proteomics, and metabolomics) applied in human, animal and in vitro studies could better characterize a wider array of hazard traits and improve the ability to predict the potential carcinogenicity of chemicals.

Lung cancer risk in painters: a meta-analysis.

Abstract: ObjectiveWe conducted a meta-analysis to quantitatively compare the association between occupation as a painter and the incidence or mortality from lung cancerData sourcesPubMed and the reference

Identifying tumour sites in the IARC Monographs.

Abstract: The letter from Drs Huff and Infante1 provides an opportunity to correct some misperceptions that have developed about the IARC Monographs . First, Huff and Infante call on IARC to make “appropriate adjustments” and “properly amend” the summaries for formaldehyde and other monographs. It is important to understand that IARC does not change summaries, which are developed by independent working groups of scientists who conducted the original research. This principle is meant to ensure confidence that IARC evaluations are free from the pressures that interested parties often use to influence public agencies. A second point concerns the temporal relationship between the formaldehyde monograph and IARC’s amended guidelines (the preamble). The formaldehyde working group met and developed its conclusions in June 2004. The preamble amendment process2 began in March 2005 and IARC posted the …