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The International Agency for Research on Cancer convened a workshop on the relationship between body fatness and cancer, from which an IARC handbook on the topic will appear. An executive summary of the evidence is presented. In April 2016, the International Agency for Research on Cancer (IARC), based in Lyon, France, convened a working group to reassess the preventive effects of weight control on cancer risk. (The members of the working group for volume 16 of the IARC Handbooks are listed at the end of the article; affiliations are provided in the Supplementary Appendix, available with the full text of this article at NEJM.org.) Overweight and obesity are the abnormal or excessive accumulation of body fat that present a risk to health. The body-mass index (BMI, the weight in kilograms divided by the square of the height . . .

The International Agency for Research on Cancer concluded that screening for colorectal cancer with stool-based tests and with lower endoscopy (either colonoscopy or sigmoidoscopy) saves lives. Comparative effectiveness data were inconclusive.

The recognition of occupational carcinogens is important for primary prevention, compensation and surveillance of exposed workers, as well as identifying causes of cancer in the general population. This study updates previously published lists of known occupational carcinogens while providing additional information on cancer type, exposure scenarios and routes, and discussing trends in the identification of carcinogens over time. Data were extracted from International Agency for Research on Cancer (IARC) Monographs covering the years 1971–2017, using specific criteria to ensure occupational relevance and provide high confidence in the causality of observed exposure-disease associations. Selected agents were substances, mixtures or types of radiation classified in IARC Group 1 with ‘sufficient evidence of carcinogenicity’ in humans from studies of exposed workers and evidence of occupational exposure documented in the pertinent monograph. The number of known occupational carcinogens has increased over time: 47 agents were identified as known occupational carcinogens in 2017 compared with 28 in 2004. These estimates are conservative and likely underestimate the number of carcinogenic agents present in workplaces. Exposure to these agents causes a wide range of cancers; cancers of the lung and other respiratory sites, followed by skin, account for the largest proportion. The dominant routes of exposure are inhalation and dermal contact. Important progress has been made in identifying occupational carcinogens; nevertheless, there is an ongoing need for research on the causes of work-related cancer. Most workplace exposures have not been evaluated for their carcinogenic potential due to inadequate epidemiologic evidence and a paucity of quantitative exposure data.

The International Agency for Research on Cancer (IARC) has updated its 2002 guidelines on screening for breast cancer, drawing on data from studies completed in the past 15 years. In November 2014, experts from 16 countries met at the International Agency for Research on Cancer (IARC) to assess the cancer-preventive and adverse effects of different methods of screening for breast cancer. (The members of the working group for volume 15 of the IARC Handbook are listed at the end of the article; affiliations are provided in the Supplementary Appendix, available with the full text of this article at NEJM.org.) This update of the 2002 IARC handbook on breast-cancer screening 1 is timely for several reasons. Recent improvements in treatment outcomes for late-stage breast cancer and concerns regarding overdiagnosis call for reconsideration. . . .

Background Aspartame is one of the world’s most widely used artificial sweeteners and is an ingredient in more than 5000 food products globally. A particularly important use is in low-calorie beverages consumed by children and pregnant women. The Ramazzini Institute (RI) reported in 2006 and 2007 that aspartame causes dose-related increases in malignant tumors in multiple organs in rats and mice. Increased cancer risk was seen even at low exposure levels approaching the Acceptable Daily Intake (ADI). Prenatal exposures caused increased malignancies in rodent offspring at lower doses than in adults. These findings generated intense controversy focused on the accuracy of RI’s diagnoses of hematopoietic and lymphoid tissue tumors (HLTs). Critics made the claim that pulmonary lesions observed in aspartame-exposed animals were inflammatory lesions caused by Mycoplasma infection rather than malignant neoplasms. Methods To address this question, RI subjected all HLTs from aspartame-exposed animals to immunohistochemical analysis using a battery of markers and to morphological reassessment using the most recent Internationally Harmonized Nomenclature and Diagnostic (INHAND) criteria. Findings This immunohistochemical and morphological re-evaluation confirmed the original diagnoses of malignancy in 92.3% of cases. Six lesions originally diagnosed as lymphoma (8% of all HLTs) were reclassified: 3 to lymphoid hyperplasia, and 3 to chronic inflammation with fibrosis. There was no evidence of Mycoplasma infection. Interpretation These new findings confirm that aspartame is a chemical carcinogen in rodents. They confirm the very worrisome finding that prenatal exposure to aspartame increases cancer risk in rodent offspring. They validate the conclusions of the original RI studies. These findings are of great importance for public health. In light of them, we encourage all national and international public health agencies to urgently reexamine their assessments of aspartame’s health risks - especially the risks of prenatal and early postnatal exposures. We call upon food agencies to reassess Acceptable Daily Intake (ADI) levels for aspartame. We note that an Advisory Group to the International Agency for Research on Cancer has recommended high-priority reevaluation of aspartame’s carcinogenicity to humans.

In human beings, observational data showed slight but statistically significant associations with APC gene mutation or promoter methylation that were identified in 75 (43%) and 41 (23%) of 185 archival colorectal cancer samples, respectively.17 Consuming well done cooked red meat increases the bacterial mutagenicity of human urine. In three intervention studies in human beings, changes in oxidative stress markers (either in urine, faeces, or blood) were associated with consumption of red meat or processed meat.18 Red and processed meat intake increased lipid oxidation products in rodent faeces.13 Substantial supporting mechanistic evidence was available for multiple meat components (NOC, haem iron, and HAA).

ObjectivesInhalation of secondhand smoke (SHS) causes several diseases, including lung cancer. Tobacco smoking is a known cause of oral cancer; however, it has not been established whether SHS also causes oral cancer . The aim of this study was to evaluate the potential association between SHS exposure and the risk of oral cancer.MethodsA systematic review and meta-analysis study (following the PRISMA guidelines) was developed to examine the studies reporting on the associations of SHS and the risk of oral cancer, employing a search strategy on electronic databases (PubMed, Web of Science, Scopus, Cochrane Library, Open Grey, and ProQuest databases for dissertations) until 10 May 2020. Meta-analyses and sensitivity analyses were performed using random-effect models. The protocol was registered in PROSPERO (CRD42020189970).ResultsFollowing the application of eligibility criteria, five studies were included, comprising a total of 1179 cases and 5798 controls, with 3452 individuals exposed and 3525 individuals not exposed to SHS. An overall OR of 1.51 (95% CI 1.2o to 1.91, p=0.0004) for oral cancer was observed, without significant heterogeneity (I2=0%, p=0.41). The duration of exposure of more than 10 or 15 years increased the risk of oral cancer (OR 2.07, 95% CI 1.54 to 2.79, p<0.00001), compared with non-exposed individuals, without significant heterogeneity (I2=0%, p=0.76).ConclusionsThis systematic review and meta-analysis supports a causal association between SHS exposure and oral cancer. Our results could provide guidance to public health professionals, researchers, and policymakers to further support effective SHS exposure prevention programs worldwide.

Occupational use was associated with an increased risk of prostate cancer in a Canadian case-control study8 and in the AHS, which reported a significant trend for aggressive cancers after adjustment for other pesticides.9 In mice, malathion increased hepatocellular adenoma or carcinoma (combined).10 In rats, it increased thyroid carcinoma in males, hepatocellular adenoma or carcinoma (combined) in females, and mammary gland adenocarcinoma after subcutaneous injection in females.4 Malathion is rapidly absorbed and distributed. Red meat and processed meat Monograph Working Group Members A Blair (USA)--Meeting Chair; L Fritschi (Australia); J McLaughlin; C M Sergi (Canada); G M Calaf (Chile); F Le Curieux (Finland); I Baldi (France); F Forastiere (Italy); H Kromhout (Netherlands); A 't Mannetje (New Zealand); T Rodriguez [unable to attend] (Nicaragua); P Egeghy [unable to attend], G D Jahnke; C W Jameson; M T Martin; M K Ross; I Rusyn; L Zeise (USA) Invited Specialists C Portier (Switzerland) Representatives M E Gouze, for the French Agency for Food, Environment and Occupational Health and Safety (France); J Rowland, for the US Environmental Protection Agency (USA) Observers M K Boye Jensen, for Cheminova (Denmark); B Fervers, for the Léon Bérard Centre (France); E Giroux, for University Jean-Moulin Lyon 3 (France); T Sorahan, for Monsanto Company (USA); C Strupp, for the European Crop Protection Association (Belgium); P Sutton, for the University of California, San Francisco (USA) IARC/WHO Secretariat L Benbrahim-Tallaa; R Carel; F El Ghissassi; Sonia El-Zaemey; Y Grosse; N Guha; K Z Guyton; C Le Cornet; M Leon; D Loomis; H Mattock; C Scoccianti; A Shapiro; K Straif; J Zavadil For the Preamble to the IARC Monographs see http://monographs.iarc.fr/ENG/Preamble/index.php For declarations of interests see http://monographs.iarc.fr/ENG/Meetings/vol112-participants.pdf We declare no competing interests.