Dana Loomis
International Agency for Research on Cancer
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Publication
Featured researches published by Dana Loomis.
Lancet Oncology | 2013
Dana Loomis; Béatrice Lauby-Secretan; Fatiha El Ghissassi; Véronique Bouvard; Lamia Benbrahim-Tallaa; Neela Guha; Robert Baan; Heidi Mattock; Kurt Straif
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)
Lancet Oncology | 2015
Véronique Bouvard; Dana Loomis; Kathryn Z. Guyton; Fatiha El Ghissassi; Lamia Benbrahim-Tallaa; Neela Guha; Heidi Mattock; Kurt Straif
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.
The New England Journal of Medicine | 2016
Béatrice Lauby-Secretan; Chiara Scoccianti; Dana Loomis; Franca Bianchini; Kurt Straif
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.
Lancet Oncology | 2012
Lamia Benbrahim-Tallaa; Robert Baan; Béatrice Lauby-Secretan; Fatiha El Ghissassi; Véronique Bouvard; Neela Guha; Dana Loomis; Kurt Straif
Benbrahim-Tallaa, Lamia Baan, Robert A Grosse, Yann Lauby-Secretan, Beatrice El Ghissassi, Fatiha Bouvard, Veronique Guha, Neela Loomis, Dana Straif, Kurt News England Lancet Oncol. 2012 Jul;13(7):663-4.
Environmental Health Perspectives | 2014
Ghassan B. Hamra; Neela Guha; Aaron Cohen; Francine Laden; Ole Raaschou-Nielsen; Jonathan M. Samet; Paolo Vineis; Francesco Forastiere; Paulo Hilário Nascimento Saldiva; Takashi Yorifuji; Dana Loomis
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-μg/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.
Epidemiology | 1999
Dana Loomis; Margarita Castillejos; Diane R. Gold; William McDonnell; Víctor Hugo Borja-Aburto
Historic air pollution episodes of the 1950s led to acute increases in infant mortality, and some recent epidemiologic studies suggest that infant or child mortality may still result from air pollution at current levels. To investigate the evidence for such an association, we conducted a time-series study of infant mortality in the southwestern part of Mexico City in the years 1993 to 1995 using mortality data from death registrations and air pollution measurements from a monitoring station we operated. Excess infant mortality was associated with the level of fine particles in the days before death, with the strongest association observed for the average concentration of fine particles during the period 3 to 5 days previously: a 10-microg m(-3) increase in the mean level of fine particles during these 3 days was associated with a 6.9% excess of infant deaths (95% confidence interval 2.5-11.3%). Infant mortality was also associated with the levels of nitrogen dioxide and ozone 3 to 5 days before death, but not as consistently as with particles.
The New England Journal of Medicine | 2015
Béatrice Secretan; Chiara Scoccianti; Dana Loomis; Lamia Benbrahim‑Tallaa; Véronique Bouvard; Franca Bianchini; Kurt Straif
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.
Lancet Oncology | 2015
Kathryn Z. Guyton; Dana Loomis; Fatiha El Ghissassi; Lamia Benbrahim-Tallaa; Neela Guha; Chiara Scoccianti; Heidi Mattock; Kurt Straif
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.
Lancet Oncology | 2013
Béatrice Lauby-Secretan; Dana Loomis; Fatiha El Ghissassi; Véronique Bouvard; Lamia Benbrahim-Tallaa; Neela Guha; Robert Baan; Heidi Mattock; Kurt Straif
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)
Environmental Health Perspectives | 2012
Elizabeth A. Maull; Habibul Ahsan; Joshua R. Edwards; Matthew P. Longnecker; Ana Navas-Acien; Jingbo Pi; Ellen K. Silbergeld; Miroslav Styblo; Chin-Hsiao Tseng; Kristina A. Thayer; Dana Loomis
Background: Diabetes affects an estimated 346 million persons globally, and total deaths from diabetes are projected to increase > 50% in the next decade. Understanding the role of environmental chemicals in the development or progression of diabetes is an emerging issue in environmental health. In 2011, the National Toxicology Program (NTP) organized a workshop to assess the literature for evidence of associations between certain chemicals, including inorganic arsenic, and diabetes and/or obesity to help develop a focused research agenda. This review is derived from discussions at that workshop. Objectives: Our objectives were to assess the consistency, strength/weaknesses, and biological plausibility of findings in the scientific literature regarding arsenic and diabetes and to identify data gaps and areas for future evaluation or research. The extent of the existing literature was insufficient to consider obesity as an outcome. Data Sources, Extraction, and Synthesis: Studies related to arsenic and diabetes or obesity were identified through PubMed and supplemented with relevant studies identified by reviewing the reference lists in the primary literature or review articles. Conclusions: Existing human data provide limited to sufficient support for an association between arsenic and diabetes in populations with relatively high exposure levels (≥ 150 µg arsenic/L in drinking water). The evidence is insufficient to conclude that arsenic is associated with diabetes in lower exposure (< 150 µg arsenic/L drinking water), although recent studies with better measures of outcome and exposure support an association. The animal literature as a whole was inconclusive; however, studies using better measures of diabetes-relevant end points support a link between arsenic and diabetes.