Parental alcohol consumption and risk of leukemia in the offspring: a systematic review and meta-analysis

Abstract

Parental alcohol consumption before and during pregnancy has been linked to adverse outcomes in the offspring including leukemogenesis. We, therefore, aimed to systematically assess and quantitatively synthesize published data on the association of paternal consumption during preconception and maternal consumption during pregnancy with leukemia risk in childhood (0-14 years). Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, we searched PubMed (until February 2016) and the reference lists of the relevant studies. Observational studies examining the association between parental alcohol consumption and childhood leukemia were considered eligible. Data extracted from 39 case-control studies (over 16 000 leukemia cases and 30 000 controls) were pooled and summary-effect estimates were calculated. Subgroup analyses were carried out by main acute leukemia type [lymphoblastic or myeloid), cytogenetics/genetic polymorphisms, and specific alcohol beverages. We found a statistically significant dose-response association of any level of maternal alcohol consumption compared with nondrinking during pregnancy exclusively with acute myeloid leukemia (AML) [odds ratio (OR)moderate consumption: 1.64, 95% confidence intervals (CIs): 1.23-2.17 and ORhigh consumption: 2.36, 95% CI: 1.60-3.49]. In contrast, no association of paternal preconception consumption with any leukemia type was noted. In beverage-specific analyses, only a positive association of maternal wine drinking with childhood AML was found, which was more pronounced in analyses including only studies on infant leukemia (ORwine: 2.12, 95% CI: 1.16-3.90). The largest ever meta-analysis shows a sizeable, statistically significant dose-response association of maternal alcohol consumption during index pregnancy with AML risk. Future research exploring the role of genetic polymorphisms is anticipated to shed light on the underlying pathophysiology.

Advanced parental age as risk factor for childhood acute lymphoblastic leukemia: results from studies of the Childhood Leukemia International Consortium

“…Moreover, the numbers in the extreme parental age discordant cells were rather limited to allow firm conclusions on the seemingly higher contribution of the advanced paternal compared to the maternal age on ALL risk. Lastly, information on genetic markers and maternal risk factors such as alcohol consumption [33] or maternal diabetes [34] was not currently contributed by the majority of studies to further enlighten underlying pathophysiological mechanisms. Similarly, information on breastfeeding, a proposed protective factor against childhood ALL [35] was actually missing in 3 out of 5 NCC studies, thus precluding meaningful analyses; nevertheless, sensitivity analyses restricted to studies availing this information showed similar results.…”

Is There Etiologic Heterogeneity between Subtypes of Childhood Acute Lymphoblastic Leukemia? A Review of Variation in Risk by Subtype

“…95). The associations with maternal alcohol use (65) and smoking during pregnancy and ALL overall are null (80).…”

Exploring a potential mechanistic role of DNA methylation in the relationship between in utero and post‐natal environmental exposures and risk of childhood acute lymphoblastic leukaemia

“…Various in utero and early childhood exposures have been investigated in the aetiology of childhood ALL [9, 10]. These include breast feeding [11], infection history [12], childcare/day care attendance [11, 12], maternal smoking [13, 14], alcohol [15, 16], caffeine [15, 17], folic acid [18, 19], iron [20], radiation [8], household paints [21], chemicals [22], pesticides [23, 24], and herbicides [25]. The weight of supporting evidence for the role of each exposure in the aetiology of childhood ALL varies.…”