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Nonsyndromic cleft palate (CP) is one of the most common human birth defects and both genetic and environmental risk factors contribute to its etiology. We conducted a genome-wide association study (GWAS) using 550 CP case-parent trios ascertained in an international consortium. Stratified analysis among trios with different ancestries was performed to test for GxE interactions with common maternal exposures using conditional logistic regression models. While no single nucleotide polymorphism (SNP) achieved genome-wide significance when considered alone, markers in  SLC2A9  and the neighboring  WDR1  on chromosome 4p16.1 gave suggestive evidence of gene-environment interaction with environmental tobacco smoke (ETS) among 259 Asian trios when the models included a term for GxE interaction. Multiple SNPs in these two genes were associated with increased risk of nonsyndromic CP if the mother was exposed to ETS during the peri-conceptual period (3 months prior to conception through the first trimester). When maternal ETS was considered, fifteen of 135 SNPs mapping to  SLC2A9  and 9 of 59 SNPs in  WDR1  gave  P  values approaching genome-wide significance (10 −6 < P <10 −4 ) in a test for GxETS interaction. SNPs rs3733585 and rs12508991 in  SLC2A9  yielded  P  = 2.26×10 −7  in a test for GxETS interaction. SNPs rs6820756 and rs7699512 in  WDR1  also yielded  P  = 1.79×10 −7  and  P  = 1.98×10 −7  in a 1  df  test for GxE interaction. Although further replication studies are critical to confirming these findings, these results illustrate how genetic associations for nonsyndromic CP can be missed if potential GxE interaction is not taken into account, and this study suggest  SLC2A9  and  WDR1  should be considered as candidate genes for CP.

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Evidence of Gene−Environment Interaction for Two Genes on Chromosome 4 and Environmental Tobacco Smoke in Controlling the Risk of Nonsyndromic Cleft Palate