Fetal growth is affected by the maternal genetic environment. Women with certain metabolic polymorphisms are more susceptible to adverse effects of the environmental pollutants such as tobacco smoke. The CYP1AI gene, which catalyzes the metabolism of polycyclic aromatic hydrocarbons (PAHs), has been linked to adverse pregnancy outcomes. Objective: We investigated the genetic polymorphism of CYP1A1 metabolic enzyme, and its association with intrauterine fetal growth and gestational age. Design: A prospective case-control study was conducted in 2004-2005 amongst 244 mothers delivering singleton live births at the Liverpool Womens Hospital. The study included 61 cases (mothers with IUGR babies, <10th percentile), and 183 controls. Genomic DNA was extracted from maternal buccal smear and genotypes determined using the PCR-RFLP method. Results: Compared to controls, cases were more exposed to cigarette smoke during pregnancy (46.3% vs. 27.6% p<0.01) and had a lower mean hemoglobin level (11.9 vs. 12.4 g/dl, P<0.01). CYP1A1 genotype frequency (combined heterozygous wild type "Aa" and homozygous variant type "aa") was 63.4% in cases compared to 37.7% in controls (p=0.003). The prevalence of IUGR was 11.6% in mothers who were homozygous for the "A" allele (AA), compared to 17.4% in mothers with "Aa/aa" genotypes (p=0.003). The estimated reduction in mean birth weight and gestational age± (SD) were 326±28 grams and 4±0.5 days for "Aa/aa" compared to "AA" genotype groups (p<0.05). A logistic regression analysis adjusting for maternal age, cigarette and alcohol use, parity, hemoglobin levels, and marital and socio-economic status showed a significantly increased prevalence of maternal CYP1A1 (Aa/aa alleles) in mothers of babies with IUGR (adjusted OR=1.7; 95% CI: 1.2-3.5). Conclusion: The polymorphism of CYP1A1 that encodes the cytochrome P450 metabolic enzyme is associated with fetal growth retardation and reduced pregnancy duration.

Introduction: Two common polymorphisms in cytochrome P450; family 1, subfamily A, polypeptide 1 (CYP1A1); have been implicated as a risk factor of prostate cancer, but individual studies have been inconclusive or controversial. We reviewed studies on CYP1A1 polymorphisms in patients with prostate cancer.Materials and Methods: The strategy searching in the PubMed was based on combinations of prostate cancer, CYP1A1, CYP1A1 gene polymorphism, and genetic susceptibility. The last search update was May 2008. The retrieved articles and their bibliographies of were evaluated and reviewed independently by 2 experts. We shortlisted 19 studies, of which 14 on sporadic prostate cancer were analyzed Overall, 2573 patients with prostate cancer and 2576 controls, were analyzed.Results: The random effects odds ratio was 1.350 (95% confidence interval, 1.110 to 1.641; P=.003) for T/C polymorphism and 1.085 (95% confidence interval, 0.863 to 1.364; P=.49) for A/G polymorphism. The A/G polymorphism was not associated with increased risk of prostate cancer. However, the T/C polymorphism showed conflicting results in different studies, while overall, this polymorphism showed significant effects on the susceptibility to prostate cancer. There was no significant betweenstudy heterogeneity for both polymorphisms with respect to distribution of alleles.Conclusion: This meta-analysis suggests that while the CYP1A1 T/C polymorphism is likely to considerably increase the risk of sporadic prostate cancer on a wide population basis, the A/G polymorphism may not influence this risk. However, the association of polymorphisms may be significant with respect to smoking history, diet habits, ethnicity, and race.