Table 4.
Outcome and SNP | TEQ tertiles | 0 minor alleles | 1 or 2 minor alleles | |||||
---|---|---|---|---|---|---|---|---|
HR (95% CI) | HR (95% CI) | |||||||
G2 pubertal onset | ||||||||
rs258747 (GR) | ||||||||
G2, p G×E = 0.0001a* | 1 | 1 (Reference) | 0.57 (0.39, 0.84) | |||||
2 | 0.39 (0.25, 0.62) | 0.52 (0.35, 0.79) | ||||||
3 | 0.31 (0.17, 0.55) | 0.41 (0.25, 0.66) | ||||||
rs1866388 (GR) | ||||||||
G2, p G×E = 0.0005a* | 1 | 1 (Reference) | 0.47 (0.33, 0.68) | |||||
2 | 0.46 (0.32, 0.66) | 0.54 (0.38, 0.79) | ||||||
3 | 0.36 (0.23, 0.57) | 0.45 (0.28, 0.72) | ||||||
rs12212176 (ESR1) | ||||||||
G2, p G×E = 0.0009a* | 1 | 1 (Reference) | 0.71 (0.47, 1.06) | |||||
2 | 0.62 (0.45, 0.86) | 0.76 (0.52, 1.11) | ||||||
3 | 0.50 (0.34, 0.74) | 0.84 (0.52, 1.37) | ||||||
TV pubertal onset | ||||||||
rs258747 (GR) | ||||||||
TV, p G×E = 0.04a | 1 | 1 (Reference) | 0.72 (0.49, 1.06) | |||||
2 | 0.49 (0.31, 0.78) | 0.69 (0.46, 1.04) | ||||||
3 | 0.44 (0.25, 0.79) | 0.43 (0.26, 0.70) | ||||||
rs1866388 (GR) | ||||||||
TV, p G×E = 0.12a | 1 | 1 (Reference) | 0.74 (0.51, 1.07) | |||||
2 | 0.58 (0.40, 0.83) | 0.82 (0.56, 1.19) | ||||||
3 | 0.50 (0.32, 0.79) | 0.43 (0.27, 0.71) | ||||||
rs12212176 (ESR1) | ||||||||
TV, p G×E = 0.28a | 1 | 1 (Reference) | 0.88 (0.59, 1.31) | |||||
2 | 0.68 (0.49, 0.95) | 0.88 (0.60, 1.29) | ||||||
3 | 0.56 (0.37, 0.85) | 0.49 (0.29, 0.82) | ||||||
Abbreviations: G×E, gene–environment interaction; HR, hazard ratio. aGene–environment p-values shown here were calculated in models with additive genotype coding (as shown in Table 3), not in the model with tertile indicators presented here. In each model the reference group consists of the boys in the lowest TEQ tertile and with 0 minor alleles. All models adjusted for lead and PCB serum concentration and diet (total calories, percent calories from protein, fat, and carbohydrate) at 8–9 years of age, and parental education. *FDR q < 0.2. |