Background characteristics and exposure distributions among those children who had (n ¼ 324) and those who had not (controls,
n ¼ 930) developed T1D are shown in Table 1. Children with T1D
had more often been exposed prenatally to the highest NOx
quartile (18%) than those without T1D (14%). When restricting to children in the DiPiS dataset, 16% of the cases and 14% of the controls were exposed to the highest NOx exposure category.
When we performed gene-matched case-control logistic re-
gressions the effects were more pronounced. Regarding NOx ex- posure the ORs were above one for all three trimesters (1.36, 1.38 and 1.58, respectively, Table 2) when we compared the highest exposure category with the reference category. However, it was only exposure during the third trimester that reached statistical significance (OR 1.58 95% CI 1.06–2.35). When only the exact HLA- matched case-control sets were included in the analyses the cor- responding OR was 1.47 (95% CI 0.96–2.24). The estimates only changed marginally when we performed the sensitivity analyses (data in Table 3). In multivariate analyses the adjusted ORs for developing T1D when comparing highest with lowest category of exposure were 1.38 (95% CI 0.98–1.93) for NOx (data in Table 4).
For ozone exposure during the second trimester an association,
albeit not statistically significant, with T1D was observed when the highest exposure quartile was compared with the reference cate- gory (OR 1.62, 95% CI 0.99–2.65; Table 2). When only the exact HLA-matched case-control sets were included in the analyses the corresponding OR was 1.71 (95% CI 1.00–2.93). No significant as- sociations were observed for ozone exposures during trimester
1 and trimester 3, although the corresponding ORs were above one. Again, the estimates only changed marginally when we per- formed the sensitivity analyses (data in Table 3). In multivariate analyses the adjusted ORs for developing T1D when comparing highest with lowest quartile of exposure were 1.56 (95% CI 1.04–
2.35) for ozone (data in Table 4).
Background characteristics and exposure distributions among those children who had (n ¼ 324) and those who had not (controls, n ¼ 930) developed T1D are shown in Table 1. Children with T1Dhad more often been exposed prenatally to the highest NOxquartile (18%) than those without T1D (14%). When restricting to children in the DiPiS dataset, 16% of the cases and 14% of the controls were exposed to the highest NOx exposure category.When we performed gene-matched case-control logistic re-gressions the effects were more pronounced. Regarding NOx ex- posure the ORs were above one for all three trimesters (1.36, 1.38 and 1.58, respectively, Table 2) when we compared the highest exposure category with the reference category. However, it was only exposure during the third trimester that reached statistical significance (OR 1.58 95% CI 1.06–2.35). When only the exact HLA- matched case-control sets were included in the analyses the cor- responding OR was 1.47 (95% CI 0.96–2.24). The estimates only changed marginally when we performed the sensitivity analyses (data in Table 3). In multivariate analyses the adjusted ORs for developing T1D when comparing highest with lowest category of exposure were 1.38 (95% CI 0.98–1.93) for NOx (data in Table 4).For ozone exposure during the second trimester an association,albeit not statistically significant, with T1D was observed when the highest exposure quartile was compared with the reference cate- gory (OR 1.62, 95% CI 0.99–2.65; Table 2). When only the exact HLA-matched case-control sets were included in the analyses the corresponding OR was 1.71 (95% CI 1.00–2.93). No significant as- sociations were observed for ozone exposures during trimester1 and trimester 3, although the corresponding ORs were above one. Again, the estimates only changed marginally when we per- formed the sensitivity analyses (data in Table 3). In multivariate analyses the adjusted ORs for developing T1D when comparing highest with lowest quartile of exposure were 1.56 (95% CI 1.04–2.35) for ozone (data in Table 4).
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