For human complex traits, non-additive genetic variation has been invoked to explain “missing heritability,” but its discovery is often neglected in genome-wide association studies. Here we propose a method of using SNP data to partition and estimate the proportion of phenotypic variance attributed to additive and dominance genetic variation at all SNPs ( and ) in unrelated individuals based on an orthogonal model where the estimate of is independent of that of . With this method, we analyzed 79 quantitative traits in 6,715 unrelated European Americans. The estimate of averaged across all the 79 quantitative traits was 0.03, approximately a fifth of that for additive variation (average = 0.15). There were a few traits that showed substantial estimates of , none of which were replicated in a larger sample of 11,965 individuals. We further performed genome-wide association analyses of the 79 quantitative traits and detected SNPs with genome-wide significant dominance effects only at the ABO locus for factor VIII and von Willebrand factor. All these results suggest that dominance variation at common SNPs explains only a small fraction of phenotypic variation for human complex traits and contributes little to the missing narrow-sense heritability problem.