Study characteristics are described in Table 1 and Supplemental Table 3. Table 2 shows the marginal results for each SNP. As we have previously reported using an overlapping set of subjects (10), 8 of the 10 loci show statistical evidence for association with CRC with nominal p-values ranging from 0.03 to 4.1×10⁻⁷. One SNP (rs16892766) had a heterogeneity p-value of 0.03; the heterogeneity p-value for all other SNPs ranged from 0.18–0.96, indicating little evidence for heterogeneity in the main effects of SNPs across studies. The two established SNPs not showing statistical evidence for association are rs10795668 at 10p14 and rs10411210 at 19q13; however, both showed a statistically non-significant odds ratio in the same direction of association as previous reports (Table 2). Our model selection procedure indicated a recessive model for rs6983267 (8q24): the OR for the AA genotype (homozygous for the minor allele) compared to the AC+CC genotype was 0.82 (0.78–0.89, p = 1.55 × 10⁻⁶). Focusing on marginal effects for the environmental risk factors (Figure 1), we observed statistical support for an increased risk of CRC with increased processed meat and red meat consumption (both derived as quartiles and as median cut points), increasing BMI, ever smoking, and increasing number of pack-years of smoking. We observed statistical evidence for a decreased risk for CRC with increased vegetable consumption (both quartiles and median cut), high fruit consumption, increased dietary folate, and any aspirin/NSAID use. Alcohol consumption showed a reduced risk for light drinkers (1–28 g/day) and increased risk for heavy drinkers (>28 g/day) compared to those who consumed less than 1 gram of alcohol per day. The main effects for quartiles of fiber and fruit intake were not statistically significant, but showed expected trends towards inverse associations. We did not investigate sex as a main effect, because most of the studies either matched on sex, or were restricted to one sex.