Heidi Mattock

The carcinogenicity of outdoor air pollution

Monograph Working Group Members J Samet (USA)–Chair; P H N Saldiva (Brazil); M Brauer, G Chen, P White (Canada); W Huang (China); L E Knudsen, P Møller, O Raaschou-Nielsen (Denmark); U Heinrich (Germany); K Balakrishnan (unable to attend; India); F Forastiere (Italy); T Yorifuji (Japan); D H Phillips, P Vineis (UK); J Chow, D M DeMarini (unable to attend), R Henderson, F Laden, D L Morgan (unable to attend), J J Schauer (USA)

Carcinogenicity of consumption of red and processed meat

In October, 2015, 22 scientists from ten countries met at the International Agency for Research on Cancer (IARC) in Lyon, France, to evaluate the carcinogenicity of the consumption of red meat and processed meat. These assessments will be published in volume 114 of the IARC Monographs.

Carcinogenicity of tetrachlorvinphos, parathion, malathion, diazinon, and glyphosate

DOI: http://dx.doi.org/10.1016/S1470-2045(15)70134-8 Article Info  Summary  Full Text  Tables and Figures  References In March, 2015, 17 experts from 11 countries met at the International Agency for Research on Cancer (IARC; Lyon, France) to assess the carcinogenicity of the organophosphate pesticides tetrachlorvinphos, parathion, malathion, diazinon, and glyphosate (table). These assessments will be published as volume 112 of the IARC Monographs.

Carcinogenicity of polychlorinated biphenyls and polybrominated biphenyls

Monograph Working Group Members V J Cogliano (USA)–Chair; K Aronson, H Tryphonas (Canada); Y L Guo (Taiwan, China); M Machala (Czech Republic); E C Bonefeld-Jørgensen, K Vorkamp (Denmark) J P Cravedi, B Le Bizec, J F Narbonne (France); H Esch (Germany); P Cocco, F Merletti (Italy); R Vermeulen (unable to attend; Netherlands); A Agudo (Spain); N Johansson (Sweden); H Fiedler, N Hopf (Switzerland); H P Glauert, R A Herbert, M O James, G Ludewig, L Robertson, A Ruder, N Walker (USA)

Carcinogenicity of trichloroethylene, tetrachloroethylene, some other chlorinated solvents, and their metabolites

In October, 2012, 18 experts from seven countries reassessed the carcino genicity of several chlo rinated solvents and some of their metabolites at the International Agency for Research on Cancer (IARC), Lyon, France (table). These assess ments will be published as volume 106 of the IARC Monographs. Trichloroethylene (TCE) was widely used for degreasing metal parts until the 1990s, and in dry cleaning from the 1930s to 1950s. It is still used for stain removal, but its main use is in chlorinated chemical production. An estimated 276 000 workers in the European Union were exposed to TCE in the early 1990s, although occupational exposure levels are decreasing. The general population is exposed through consumer products—including food— and contaminated water. The Working Group classifi ed TCE as carcinogenic to humans (Group 1). Biotransformation of TCE, well characterised in humans and animals, occurs primarily through oxidative metabolism by cytochrome P450 enzymes and also via glutathione conjugation by glutathione S-transferase enzymes. The main oxidative metabolites are dichloroacetic acid (DCA), trichloroacetic acid (TCA), and chloral hydrate (CH). Metabolites of TCE formed via glutathione conjugation are genotoxic, particularly in kidney cells in which in-situ metabolism occurs. Case-control studies provide convincing evidence for a positive association between exposure to TCE and renal-cell carcinoma. Two studies have evaluated confounding for several kidney cancer risk factors, and provided evidence of an exposure–response relationship. A French study, done in an area with high prevalence of occupational exposure to TCE, reported an odds ratio (OR) of 2·16 (95% CI 1·02–4·60) for people with high cumulative exposure after adjusting for smoking and body-mass index, and 1·96 (0·71–5·37) when also adjusted for exposure to cutting fl uids and other petroleum oils. An eastern European study was larger than the French study but had lower exposure prevalence. The OR was 1·63 (95% CI 1·04–2·54) for any exposure to TCE and 2·34 (1·05–5·21) in the highest category of exposure intensity. Consistent with the importance of glutathione conjugation for kidney carcinogenesis, TCE-exposed people with an active GSTT1 enzyme had an increased risk (OR 1·88, 95% CI 1·06–3·33), but people without GSTT1 activity did not (0·93, 0·35–2·44). Cohort studies of aircraft and aerospace workers in the USA and a Danish study of workers in industries using TCE have reported modestly increased relative risks (RRs) of kidney cancer, with indications of an exposure–response relationship. Three small, independent cohorts of Nordic workers who were monitored biologically by TCA in urine show little evidence of an increased risk of kidney cancer. However, level of exposure varied widely and few measurements per worker were available. A meta-analysis also reported signifi cant RRs of kidney cancer; 1·3 overall and 1·6 for high-exposure groups. Confounding by smoking is unlikely to account for the increased risk of kidney cancer, since RRs for lung cancer were not increased in most cohorts or in the meta-analysis. Furthermore, case-control studies generally adjusted for smoking and other potential confounders, with little eff ect on risk estimates. The epidemiological evidence for the association between TCE exposure and non-Hodgkin lymphoma (NHL) or liver cancer was limited. The cohort studies, including the biologically monitored Nordic cohorts, and several case-control studies reported slightly increased risks of NHL, with weak indication of an exposure–response relationship. Several genotoxic and non-genotoxic TCE-induced

Carcinogenicity of lindane, DDT, and 2,4-dichlorophenoxyacetic acid

Lancet Oncology, The - In Press.Proof corrected by the author Available online since mercredi 24 juin 2015

Carcinogenicity of drinking coffee, mate, and very hot beverages

www.thelancet.com/oncology Published online June 15, 2016 http://dx.doi.org/10.1016/S1470-2045(16)30239-X 1 In May, 2016, a Working Group of 23 scientists from ten countries met at the International Agency for Research on Cancer (IARC) in Lyon, France, to evaluate the carcinogenicity of drinking coff ee, mate, and very hot beverages. These assessments will be published in volume 116 of the IARC Monographs. Coffee is one of the world’s most widely consumed beverages. It contains many diff erent compounds and its composition varies depending on how it is produced and prepared for drinking. After consumption, caff eine, chlorogenic acids, and other compounds contained in coffee are absorbed and distributed throughout the body. The carcinogenicity of coff ee drinking was last assessed by IARC in 1991. At that time coffee was classified as “possibly carcinogenic to humans“ (Group 2B) based on limited evidence of an association with cancer of the urinary bladder from case-control studies, and inadequate evidence of carcinogenicity in experimental animals. However, there was also evidence suggesting a lack of carcinogenicity for cancers of the female breast and the large intestine. For this re-evaluation, a much larger database of more than 1000 observational and experimental studies was available. In assessing the accumulated epidemiological evidence, the current Working Group gave the greatest weight to well-conducted prospective cohort and population-based case-control studies that controlled adequately for important potential confounders, including tobacco and alcohol consumption. For bladder cancer, there was no consistent evidence of an association with drinking coffee, or of an exposure–response gradient from ten cohort studies and several population-based case-control studies in Europe, the USA, and Japan. In several studies, relative risks were increased in men but were null or decreased in women, consistent with residual confounding from smoking or occupational exposures among men. The Working Group concluded that positive associations reported in some studies could have been due to inadequate control for tobacco smoking, which can be strongly associated with heavy coff ee drinking. By contrast, for endometrial cancer, the fi ve largest cohort studies showed mostly inverse associations with coff ee drinking. These results were supported by the fi ndings of several case-control studies and a meta-analysis. Inverse associations with coff ee drinking were also observed in cohort and case-control studies of liver cancer in Asia, Europe, and North America. A meta-analysis of prospective cohort studies estimated that the risk of liver cancer decreases 15% for each 1 cup per day increment. More than 40 cohort and case-control studies and a meta-analysis including nearly 1 million women consistently indicated either no association or a modest inverse association for cancer of the female breast and coffee drinking. Similarly, numerous cohort and case-control studies of cancers of the pancreas and prostate consistently indicated no association between these cancers and coffee drinking. Data were also available for more than 20 other cancers, including lung, colorectal, stomach, oesophageal, oral cavity, ovarian, and brain cancers, and childhood leukaemia. Although the volume of data for some of these cancers was substantial, the Working Group judged the evidence to be inadequate for all of the other cancers reviewed for reasons including inconsistency of findings across studies, inadequate control for potential confounding, potential for measurement error, selection bias or recall bias, or insuffi cient numbers of studies. The combination of evidence suggesting lack of carcinogenicity for cancers of the female breast, pancreas, prostate, uterine endometrium, and liver, with inverse associations for the latter two and inadequate evidence for all the other sites reviewed led to the conclusion that there is inadequate evidence in humans for the carcinogenicity of coff ee drinking. Coffee has been evaluated for carcinogenicity in several long-term studies in mice and rats, and has been tested for both tumour-promoting and cancer-preventing activity in a number of co-carcinogenicity studies in rats and hamsters. The Working Group concluded that these studies provided inadequate evidence in experimental animals for the carcinogenicity of coff ee. Coffee drinking exhibited strong antioxidant effects in studies in humans, including in randomised controlled trials. Results for genotoxicity from studies in humans were inconsistent, and coffee did not induce chromosomal damage in rodents. Nonetheless, coffee gave positive results in bacterial mutagenesis assays, but only without metabolic activation. Coff ee promoted apoptosis in human cancer cell lines. Moderate evidence of an association of coffee drinking with reduced risk of colorectal adenoma was noted. Coff ee has also been associated with benefi cial eff ects on liver fi brosis and cirrhosis. Overall coffee drinking was evaluated as unclassifiable as to its carcinogenicity to humans (Group 3). Mate is an infusion made from dried leaves of Ilex paraguariensis. It is consumed mainly in South America and to a lesser extent in the Middle East, Europe, and North America. Mate is traditionally drunk very hot (>65°C), but it can also be consumed warm or cold. The carcinogenicity of mate was previously evaluated in 1991, when Carcinogenicity of drinking coff ee, mate, and very hot beverages

Some chemicals that cause tumours of the urinary tract in rodents

IARC Monograph Working Group Members B W Stewart (Australia)— meeting chair; A P de Melo Loureiro, F J Paumgartten (Brazil); A Afghan, M Baril, C Hilts (unable to attend), C M Sergi (Canada); D W Lachenmeier (Germany); K Ogawa (Japan); C Svendsen (Norway); I M Ferreira (Portugal); J W Cherrie (UK); F A Beland, J V Bruckner, J K Dunnick, G Gamboa da Costa, K A Houck, C W Jameson, L H Lash, R L Melnick, K L Witt (USA)