Maria A Karalexi1, Nick Dessypris1, Jacqueline Clavel2, Catherine Metayer3, Friederike Erdmann4, Laurent Orsi5, Alice Y Kang3, Joachim Schüz6, Audrey Bonaventure7, Kathryn R Greenop8, Elizabeth Milne8, Eleni Th Petridou9. 1. Department of Hygiene, Epidemiology and Medical Statistics Medical School, National and Kapodistrian University of Athens, Athens, Greece. 2. INSERM U1153, Epidemiology and Biostatistics Sorbonne Paris Cité Center (CRESS), Epidemiology of Childhood and Adolescent Cancers Team (EPICEA), Paris-Descartes University, Villejuif, France; RNCE - National Registry of Childhood Cancers, Inserm, Villejuif and CHU de Nancy, Villejuif, France. 3. School of Public Health, University of California, Berkeley, 1995 University Avenue, Suite 460, Berkeley, CA 94704-1070, USA. 4. Section of Environment and Radiation, International Agency for Research on Cancer, Lyon, France; Childhood Cancer Research Group, Danish Cancer Society Research Center, Strandboulevarden 49, 2100 Copenhagen, Denmark. 5. INSERM U1153, Epidemiology and Biostatistics Sorbonne Paris Cité Center (CRESS), Epidemiology of Childhood and Adolescent Cancers Team (EPICEA), Paris-Descartes University, Villejuif, France. 6. Section of Environment and Radiation, International Agency for Research on Cancer, Lyon, France. 7. INSERM U1153, Epidemiology and Biostatistics Sorbonne Paris Cité Center (CRESS), Epidemiology of Childhood and Adolescent Cancers Team (EPICEA), Paris-Descartes University, Villejuif, France; Cancer Survival Group, Department of Non-Communicable Disease Epidemiology, London School of Hygiene and Tropical Medicine, London, UK. 8. Telethon Kids Institute, University of Western Australia, PO Box 855, West Perth, WA 6872, Australia. 9. Department of Hygiene, Epidemiology and Medical Statistics Medical School, National and Kapodistrian University of Athens, Athens, Greece; Department of Clinical Epidemiology, Department of Medicine, Karolinska Institute, Stockholm, Sweden. Electronic address: epetrid@med.uoa.gr.
Abstract
BACKGROUND: Dietary habits during pregnancy have been inconsistently linked to childhood acute myeloid leukemia (AML), given the putative intrauterine onset of the disease as a result of triggering events during the critical period of fetal hematopoiesis. We investigated the potential association of maternal coffee and tea consumption during pregnancy with childhood AML risk, pooling primary data from eight case-control studies participating in the Childhood Leukemia International Consortium. METHODS: Information on coffee and/or tea consumption was available for 444 cases and 1255 age- and sex-matched controls, on coffee consumption for 318 cases and 971 controls and on tea consumption for 388 cases and 932 controls. Categories for cups of daily coffee/tea consumption were created in order to explore potential dose-response associations. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression. RESULTS: Associations were found neither in the analysis on coffee or tea nor in the analysis on coffee only consumption (any versus no). A positive association with increasing coffee intake was observed (>1 cup per day; OR: 1.40, 95% CI: 1.03-1.92, increment of one cup per day; OR: 1.18, 95% CI: 1.01-1.39). No associations were observed with tea consumption. Interaction analyses showed non-significant associations between coffee/tea and smoking. Hyperdiploidy was inversely associated with tea consumption, with other cytogenetic markers having no association with coffee/tea. CONCLUSION: Given the widespread consumption of caffeinated beverages among pregnant women, our finding is of important public health relevance, suggesting adverse effects of maternal coffee consumption during pregnancy in the offspring.
BACKGROUND: Dietary habits during pregnancy have been inconsistently linked to childhood acute myeloid leukemia (AML), given the putative intrauterine onset of the disease as a result of triggering events during the critical period of fetal hematopoiesis. We investigated the potential association of maternal coffee and tea consumption during pregnancy with childhood AML risk, pooling primary data from eight case-control studies participating in the Childhood Leukemia International Consortium. METHODS: Information on coffee and/or tea consumption was available for 444 cases and 1255 age- and sex-matched controls, on coffee consumption for 318 cases and 971 controls and on tea consumption for 388 cases and 932 controls. Categories for cups of daily coffee/tea consumption were created in order to explore potential dose-response associations. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression. RESULTS: Associations were found neither in the analysis on coffee or tea nor in the analysis on coffee only consumption (any versus no). A positive association with increasing coffee intake was observed (>1 cup per day; OR: 1.40, 95% CI: 1.03-1.92, increment of one cup per day; OR: 1.18, 95% CI: 1.01-1.39). No associations were observed with tea consumption. Interaction analyses showed non-significant associations between coffee/tea and smoking. Hyperdiploidy was inversely associated with tea consumption, with other cytogenetic markers having no association with coffee/tea. CONCLUSION: Given the widespread consumption of caffeinated beverages among pregnant women, our finding is of important public health relevance, suggesting adverse effects of maternal coffee consumption during pregnancy in the offspring.
Authors: Anja Oechsle; Michel Wensing; Charlotte Ullrich; Manuela Bombana Journal: Int J Environ Res Public Health Date: 2020-11-20 Impact factor: 3.390