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4. IARC monographs: 40 years of evaluating carcinogenic hazards to humans.

Author

Pearce, Neil, Blair, Aaron, Vineis, Paolo, Ahrens, Wolfgang, Andersen, Aage, Anto, Josep M, Armstrong, Bruce K, Baccarelli, Andrea A, Beland, Frederick A, Berrington, Amy, Bertazzi, Pier Alberto, Birnbaum, Linda S, Brownson, Ross C, Bucher, John R, Cantor, Kenneth P, Cardis, Elisabeth, Cherrie, John W, Christiani, David C, Cocco, Pierluigi, Coggon, David, Comba, Pietro, Demers, Paul A, Dement, John M, Douwes, Jeroen, Eisen, Ellen A, Engel, Lawrence S, Fenske, Richard A, Fleming, Lora E, Fletcher, Tony, Fontham, Elizabeth, Forastiere, Francesco, Frentzel-Beyme, Rainer, Fritschi, Lin, Gerin, Michel, Goldberg, Marcel, Grandjean, Philippe, Grimsrud, Tom K, Gustavsson, Per, Haines, Andy, Hartge, Patricia, Hansen, Johnni, Hauptmann, Michael, Heederik, Dick, Hemminki, Kari, Hemon, Denis, Hertz-Picciotto, Irva, Hoppin, Jane A, Huff, James, Jarvholm, Bengt, Kang, Daehee, Karagas, Margaret R, Kjaerheim, Kristina, Kjuus, Helge, Kogevinas, Manolis, Kriebel, David, Kristensen, Petter, Kromhout, Hans, Laden, Francine, Lebailly, Pierre, LeMasters, Grace, Lubin, Jay H, Lynch, Charles F, Lynge, Elsebeth, 't Mannetje, Andrea, McMichael, Anthony J, McLaughlin, John R, Marrett, Loraine, Martuzzi, Marco, Merchant, James A, Merler, Enzo, Merletti, Franco, Miller, Anthony, Mirer, Franklin E, Monson, Richard, Nordby, Karl-Cristian, Olshan, Andrew F, Parent, Marie-Elise, Perera, Frederica P, Perry, Melissa J, Pesatori, Angela Cecilia, Pirastu, Roberta, Porta, Miquel, Pukkala, Eero, Rice, Carol, Richardson, David B, Ritter, Leonard, Ritz, Beate, Ronckers, Cecile M, Rushton, Lesley, Rusiecki, Jennifer A, Rusyn, Ivan, Samet, Jonathan M, Sandler, Dale P, de Sanjose, Silvia, Schernhammer, Eva, Costantini, Adele Seniori, Seixas, Noah, Shy, Carl, Siemiatycki, Jack, and Silverman, Debra T

Subjects
Humans, Neoplasms, Carcinogens, Environmental, Public Health, Biomedical Research, Publications, International Agencies, Environmental Sciences, Medical and Health Sciences, Toxicology
Abstract

BackgroundRecently, the International Agency for Research on Cancer (IARC) Programme for the Evaluation of Carcinogenic Risks to Humans has been criticized for several of its evaluations, and also for the approach used to perform these evaluations. Some critics have claimed that failures of IARC Working Groups to recognize study weaknesses and biases of Working Group members have led to inappropriate classification of a number of agents as carcinogenic to humans.ObjectivesThe authors of this Commentary are scientists from various disciplines relevant to the identification and hazard evaluation of human carcinogens. We examined criticisms of the IARC classification process to determine the validity of these concerns. Here, we present the results of that examination, review the history of IARC evaluations, and describe how the IARC evaluations are performed.DiscussionWe concluded that these recent criticisms are unconvincing. The procedures employed by IARC to assemble Working Groups of scientists from the various disciplines and the techniques followed to review the literature and perform hazard assessment of various agents provide a balanced evaluation and an appropriate indication of the weight of the evidence. Some disagreement by individual scientists to some evaluations is not evidence of process failure. The review process has been modified over time and will undoubtedly be altered in the future to improve the process. Any process can in theory be improved, and we would support continued review and improvement of the IARC processes. This does not mean, however, that the current procedures are flawed.ConclusionsThe IARC Monographs have made, and continue to make, major contributions to the scientific underpinning for societal actions to improve the public's health.

Published
2015

9. Increased Lung and Bladder Cancer Incidence in Adults after In Utero and Early-Life Arsenic Exposure

Author

Steinmaus, Craig, Ferreccio, Catterina, Acevedo, Johanna, Yuan, Yan, Liaw, Jane, Durán, Viviana, Cuevas, Susana, García, José, Meza, Rodrigo, Valdés, Rodrigo, Valdés, Gustavo, Benítez, Hugo, VanderLinde, Vania, Villagra, Vania, Cantor, Kenneth P, Moore, Lee E, Perez, Saida G, Steinmaus, Scott, and Smith, Allan H

Subjects
Epidemiology, Health Sciences, Endocrine Disruptors, Urologic Diseases, Prevention, Lung Cancer, Clinical Research, Foodborne Illness, Cancer, Lung, 2.2 Factors relating to the physical environment, 2.1 Biological and endogenous factors, Adult, Aged, Arsenic, Arsenic Poisoning, Chile, Environmental Exposure, Female, Humans, Incidence, Lung Neoplasms, Male, Middle Aged, Pregnancy, Prenatal Exposure Delayed Effects, Urinary Bladder Neoplasms, Water Pollutants, Chemical, Water Pollution, Chemical, Medical and Health Sciences, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundFrom 1958 to 1970, >100,000 people in northern Chile were exposed to a well-documented, distinct period of high drinking water arsenic concentrations. We previously reported ecological evidence suggesting that early-life exposure in this population resulted in increased mortality in adults from several outcomes, including lung and bladder cancer.MethodsWe have now completed the first study ever assessing incident cancer cases after early-life arsenic exposure, and the first study on this topic with individual participant exposure and confounding factor data. Subjects included 221 lung and 160 bladder cancer cases diagnosed in northern Chile from 2007 to 2010, and 508 age and gender-matched controls.ResultsORs adjusted for age, sex, and smoking in those only exposed in early life to arsenic water concentrations of ≤110, 110 to 800, and >800 μg/L were 1.00, 1.88 [95% confidence interval (CI), 0.96-3.71], and 5.24 (3.05-9.00; P(trend) < 0.001) for lung cancer, and 1.00, 2.94 (1.29-6.70), and 8.11 (4.31-15.25; P(trend) < 0.001) for bladder cancer. ORs were lower in those not exposed until adulthood. The highest category (>800 μg/L) involved exposures that started 49 to 52 years before, and ended 37 to 40 years before the cancer cases were diagnosed.ConclusionLung and bladder cancer incidence in adults was markedly increased following exposure to arsenic in early life, even up to 40 years after high exposures ceased. Such findings have not been identified before for any environmental exposure, and suggest that humans are extraordinarily susceptible to early-life arsenic exposure.ImpactPolicies aimed at reducing early-life exposure may help reduce the long-term risks of arsenic-related disease.

Published
2014

10. Disinfection By-Products in Drinking Water and Bladder Cancer: Evaluation of Risk Modification by Common Genetic Polymorphisms in Two Case-Control Studies

Author

Freeman, Laura E. Beane, Kogevinas, Manolis, Cantor, Kenneth P., Villanueva, Cristina M., Prokunina-Olsson, Ludmila, Florez-Vargas, Oscar, Figueroa, Jonine D., Ward, Mary H., Koutros, Stella, Baris, Dalsu, Garcia-Closas, Montserrat, Schwenn, Molly, Johnson, Allison, Serra, Consol, Tardon, Adonina, Garcia-Closas, Reina, Carrato, Alfredo, Malats, Nuria, Karagas, Margaret R., Rothman, Nathaniel, and Silverman, Debra T.

Subjects
Toxicogenomics -- Research, Drinking water -- Contamination -- Health aspects, Bladder cancer -- Risk factors -- Environmental aspects -- Genetic aspects, Single nucleotide polymorphisms -- Health aspects, Trihalomethanes -- Environmental aspects -- Health aspects, Environmental issues, Health
Abstract

Background: By-products are formed when disinfectants react with organic matter in source water. The most common class of disinfection byproducts, trihalomethanes (THMs), have been linked to bladder cancer. Several studies have shown exposure-response associations with THMs in drinking water and bladder cancer risk. Few epidemiologic studies have evaluated gene-environment interactions for total THMs (TTHMs) with known bladder cancer susceptibility variants. Objectives: In this study, we investigated the combined effect on bladder cancer risk contributed by TTHMs, bladder cancer susceptibility variants identified through genome-wide association studies, and variants in several candidate genes. Methods: We analyzed data from two large case-control studies--the New England Bladder Cancer Study (n/n = 989 cases/1,162 controls), a population-based study, and the Spanish Bladder Cancer Study (n/n = 706 cases/772 controls), a hospital-based study. Because of differences in exposure distributions and metrics, we estimated effects of THMs and genetic variants within each study separately using adjusted logistic regression models to calculate odds ratios (ORs) and 95% confidence intervals (CI) with and without interaction terms, and then combined the results using meta-analysis. Results: Of the 16 loci showing strong evidence of association with bladder cancer, rs907611 at 11p15.5 [leukocyte- specific protein 1 (LSP1 region)] showed the strongest associations in the highest exposure category in each study, with evidence of interaction in both studies and in metaanalysis. In the highest exposure category, we observed OR= 1.66 (95% CI: 1.17, 2.34, p- trend = 0.005) for those with the rs907611-GG genotype and p-interaction = 0.02. No other genetic variants tested showed consistent evidence of interaction. Discussion: We found novel suggestive evidence for a multiplicative interaction between a putative bladder carcinogen, TTHMs, and genotypes of rs907611. Given the ubiquitous exposure to THMs, further work is needed to replicate and extend this finding and to understand potential molecular mechanisms. https://doi.org/10.1289/EHP9895, Introduction Worldwide, bladder cancer ranks as the ninth most common incident cancer and the 13th in mortality, with ~400,000 cases diagnosed each year. (1) Approximately 75% of incident cases occur [...]

Published
2022
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33. Data from Increased Lung and Bladder Cancer Incidence in Adults after In Utero and Early-Life Arsenic Exposure

Author

Steinmaus, Craig, primary, Ferreccio, Catterina, primary, Acevedo, Johanna, primary, Yuan, Yan, primary, Liaw, Jane, primary, Durán, Viviana, primary, Cuevas, Susana, primary, García, José, primary, Meza, Rodrigo, primary, Valdés, Rodrigo, primary, Valdés, Gustavo, primary, Benítez, Hugo, primary, VanderLinde, Vania, primary, Villagra, Vania, primary, Cantor, Kenneth P., primary, Moore, Lee E., primary, Perez, Saida G., primary, Steinmaus, Scott, primary, and Smith, Allan H., primary

Published
2023
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34. Supplementary Tables 1 through 3 from Increased Lung and Bladder Cancer Incidence in Adults after In Utero and Early-Life Arsenic Exposure

Author

Steinmaus, Craig, primary, Ferreccio, Catterina, primary, Acevedo, Johanna, primary, Yuan, Yan, primary, Liaw, Jane, primary, Durán, Viviana, primary, Cuevas, Susana, primary, García, José, primary, Meza, Rodrigo, primary, Valdés, Rodrigo, primary, Valdés, Gustavo, primary, Benítez, Hugo, primary, VanderLinde, Vania, primary, Villagra, Vania, primary, Cantor, Kenneth P., primary, Moore, Lee E., primary, Perez, Saida G., primary, Steinmaus, Scott, primary, and Smith, Allan H., primary

Published
2023
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36. Water Contaminants

Author

Cantor, Kenneth P., primary, Steinmaus, Craig M., additional, Ward, Mary H., additional, and Beane Freeman, Laura E., additional

Published
2017
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39. Disinfection By-Products in Drinking Water and Bladder Cancer: Evaluation of Risk Modification by Common Genetic Polymorphisms in Two Case–Control Studies

Author

Beane Freeman, Laura E., primary, Kogevinas, Manolis, additional, Cantor, Kenneth P., additional, Villanueva, Cristina M., additional, Prokunina-Olsson, Ludmila, additional, Florez-Vargas, Oscar, additional, Figueroa, Jonine D., additional, Ward, Mary H., additional, Koutros, Stella, additional, Baris, Dalsu, additional, Garcia-Closas, Montserrat, additional, Schwenn, Molly, additional, Johnson, Allison, additional, Serra, Consol, additional, Tardon, Adonina, additional, Garcia-Closas, Reina, additional, Carrato, Alfredo, additional, Malats, Nuria, additional, Karagas, Margaret R., additional, Rothman, Nathaniel, additional, and Silverman, Debra T., additional

Published
2022
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