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It is also possible that maternal genes alone do not confer risk of clefts to the newborn unless specific environmental exposures are also present.
Our results are also consistent with those of a larger study that investigated whether half sibships ascertained through an affected proband had a higher risk of clefts when the mother was the common parent [44].
We opted not to combine the Norwegian and Danish samples (although this would have boosted power) because we had no prior data to assume that the same haplotype(s) contribute to the risk of clefts in both populations.
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In recent years, reports have emerged indicating an increased risk of oral clefts (cleft lip and cleft palate) among infants born to mothers exposed to TPM during pregnancy.
Nutritional factors during early pregnancy, such as folate deficiency, as well as certain medicines taken during pregnancy (e.g., seizure medicines) may also increase the risk of cleft palate.
Sodium valproate has long been known to increase babies' risk of cleft palate and spina bifida.
The use of topiramate in pregnancy is associated with an increased risk of cleft lip/palate and low birth weight, especially when taken during first trimester [81].
Exposure to benzodiazepines during pregnancy has been associated with a slightly increased (from 0.06 to 0.07%) risk of cleft palate in newborns, a controversial conclusion as some studies find no association between benzodiazepines and cleft palate.
Except for FLNB, HIC1 and ZNF189, maternal genes did not appear to influence the risk of clefting in our data.
However, in Southern California, Texas, and the current study, O3 was not statistically associated with an increased risk of cleft lip/palate.
Table 5 shows the odds ratios for the risk of cleft lip/palate associated with ambient air pollution averaged over weeks 3 8 of pregnancy.
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