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 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.
Exposure to traffic-related air pollutants is an important public health issue. Here, we present a systematic review and meta-analysis of research examining the relationship of measures of nitrogen ...oxides (NOx) and of various measures of traffic-related air pollution exposure with lung cancer.
We conducted random-effects meta-analyses of studies examining exposure to nitrogen dioxide (NO2) and NOx and its association with lung cancer. We identified 20 studies that met inclusion criteria and provided information necessary to estimate the change in lung cancer per 10-μg/m3 increase in exposure to measured NO2. Further, we qualitatively assessed the evidence of association between distance to roadways and traffic volume associated with lung cancer.
The meta-estimate for the change in lung cancer associated with a 10-μg/m3 increase in exposure to NO2 was 4% (95% CI: 1%, 8%). The meta-estimate for change in lung cancer associated with a 10-μg/m3 increase in NOx was similar and slightly more precise, 3% (95% CI: 1%, 5%). The NO2 meta-estimate was robust to different confounding adjustment sets as well as the exposure assessment techniques used. Trim-and-fill analyses suggest that if publication bias exists, the overall meta-estimate is biased away from the null. Forest plots for measures of traffic volume and distance to roadways largely suggest a modest increase in lung cancer risk.
We found consistent evidence of a relationship between NO2, as a proxy for traffic-sourced air pollution exposure, with lung cancer. Studies of lung cancer related to residential proximity to roadways and NOx also suggest increased risk, which may be attributable partly to air pollution exposure. The International Agency for Research on Cancer recently classified outdoor air pollution and particulate matter as carcinogenic (Group 1). These meta-analyses support this conclusion, drawing particular attention to traffic-sourced air pollution.
Hamra GB, Laden F, Cohen AJ, Raaschou-Nielsen O, Brauer M, Loomis D. 2015. Lung cancer and exposure to nitrogen dioxide and traffic: a systematic review and meta-analysis. Environ Health Perspect 123:1107-1112; http://dx.doi.org/10.1289/ehp.1408882.
Particulate matter (PM) in outdoor air pollution was recently designated a Group I carcinogen by the International Agency for Research on Cancer (IARC). This determination was based on the evidence ...regarding the relationship of PM2.5 and PM10 to lung cancer risk; however, the IARC evaluation did not include a quantitative summary of the evidence.
Our goal was to provide a systematic review and quantitative summary of the evidence regarding the relationship between PM and lung cancer.
We conducted meta-analyses of studies examining the relationship of exposure to PM2.5 and PM10 with lung cancer incidence and mortality. In total, 18 studies met our inclusion criteria and provided the information necessary to estimate the change in lung cancer risk per 10-μg/m3 increase in exposure to PM. We used random-effects analyses to allow between-study variability to contribute to meta-estimates.
The meta-relative risk for lung cancer associated with PM2.5 was 1.09 (95% CI: 1.04, 1.14). The meta-relative risk of lung cancer associated with PM10 was similar, but less precise: 1.08 (95% CI: 1.00, 1.17). Estimates were robust to restriction to studies that considered potential confounders, as well as subanalyses by exposure assessment method. Analyses by smoking status showed that lung cancer risk associated with PM2.5 was greatest for former smokers 1.44 (95% CI: 1.04, 1.22), followed by never-smokers 1.18 (95% CI: 1.00, 1.39), and then current smokers 1.06 (95% CI: 0.97, 1.15). In addition, meta-estimates for adenocarcinoma associated with PM2.5 and PM10 were 1.40 (95% CI: 1.07, 1.83) and 1.29 (95% CI: 1.02, 1.63), respectively.
The results of these analyses, and the decision of the IARC Working Group to classify PM and outdoor air pollution as carcinogenic (Group 1), further justify efforts to reduce exposures to air pollutants that can arise from many sources.
Background: Particulate matter (PM) in outdoor air pollution was recently designated a Group I carcinogen by the International Agency for Research on Cancer (IARC). This determination was based on ...the evidence regarding the relationship of PM2.5 and PM10 to lung cancer risk; however, the IARC evaluation did not include a quantitative summary of the evidence. Objective: Our goal was to provide a systematic review and quantitative summary of the evidence regarding the relationship between PM and lung cancer. Methods: We conducted meta-analyses of studies examining the relationship of exposure to PM2.5 and PM10 with lung cancer incidence and mortality. In total, 18 studies met our inclusion criteria and provided the information necessary to estimate the change in lung cancer risk per 10- mu g/m3 increase in exposure to PM. We used random-effects analyses to allow between-study variability to contribute to meta-estimates. Results: The meta-relative risk for lung cancer associated with PM2.5 was 1.09 (95% CI: 1.04, 1.14). The meta-relative risk of lung cancer associated with PM10 was similar, but less precise: 1.08 (95% CI: 1.00, 1.17). Estimates were robust to restriction to studies that considered potential confounders, as well as subanalyses by exposure assessment method. Analyses by smoking status showed that lung cancer risk associated with PM2.5 was greatest for former smokers 1.44 (95% CI: 1.04, 1.22), followed by never-smokers 1.18 (95% CI: 1.00, 1.39), and then current smokers 1.06 (95% CI: 0.97, 1.15). In addition, meta-estimates for adenocarcinoma associated with PM2.5 and PM10 were 1.40 (95% CI: 1.07, 1.83) and 1.29 (95% CI: 1.02, 1.63), respectively. Conclusion: The results of these analyses, and the decision of the IARC Working Group to classify PM and outdoor air pollution as carcinogenic (Group 1), further justify efforts to reduce exposures to air pollutants that can arise from many sources. Citation: Hamra GB, Guha N, Cohen A, Laden F, Raaschou-Nielsen O, Samet JM, Vineis P, Forastiere F, Saldiva P, Yorifuji T, Loomis D. 2014. Outdoor particulate matter exposure and lung cancer: a systematic review and meta-analysis. Environ Health Perspect 122:906-911; http://dx.doi.org/10.1289/ehp.1408092
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).
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.
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.3-5 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. Welding, welding fumes and some related chemicals IARC Monograph Working Group Members L T Stayner (USA)--meeting chair; E Milne (Australia); S Knasmüller (Austria); A Farah, L F Ribeiro Pinto (Brazil); D W Lachenmeier (Germany); C Bamia (Greece); A Tavani (Italy); M Inoue (Japan); N Djordjevic (Serbia); P C H Hollman, P A van den Brandt (Netherlands); J A Baron, E Gonzalez de Mejia, F Islami (unable to attend); C W Jameson, F Kamangar, D L McCormick, I Pogribny, I I Rusyn, R Sinha, M C Stern, K M Wilson (USA) Declaration of interests MI is the beneficiary of a financial contribution from AXA Research fund as chair holder of the AXA Department of Health and Human Security, Graduate School of Medicine, The University of Tokyo from Nov 1, 2012.
PDF
