Maternal occupational exposure to polycyclic aromatic hydrocarbons and risk of neural tube defect-affected pregnancies
ABSTRACT This study evaluated whether there is an association between maternal occupational exposure to polycyclic aromatic hydrocarbons (PAHs) and neural tube defects (NTDs) in offspring. This is the first such study of which the authors are aware.
Data were analyzed from 1997 to 2002 deliveries in the National Birth Defects Prevention Study, a large population-based case-control study in the United States. Maternal interviews yielded information on jobs held in the month before through 3 months after conception. Three industrial hygienists blinded to case or control status assessed occupational exposure to PAHs. Crude and adjusted odds ratios (ORs) with 95% confidence intervals (CIs) were estimated using unconditional logistic regression.
Of the 520 mothers of children with NTDs, 5.0% were classified as exposed to occupational PAHs, as were 3.5% of the 2989 mothers of controls. The crude OR for PAH exposure was 1.43 (95% CI, 0.92-2.22) for any NTD and 1.71 (95% CI, 1.03-2.83) for spina bifida. Adjusted ORs were smaller in magnitude and not significant. Among women who were normal weight or underweight, the crude OR for spina bifida was 3.13 (95% CI, 1.63-6.03) and adjusted OR was 2.59 (95% CI, 1.32-5.07). Based on estimated cumulative exposure, a statistically significant dose-response trend was observed for spina bifida; however, it was attenuated and no longer significant after adjustment.
Maternal occupational exposure to PAHs may be associated with increased risk of spina bifida in offspring among women who are normal weight or underweight. Other comparisons between PAHs and NTDs were consistent with no association. Birth Defects Research (Part A) 94:693-700, 2012. © 2012 Wiley Periodicals, Inc.
- SourceAvailable from: Richard H Finnell
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- "In laboratory animals, embryos exposed to derivatives of PAHs have been shown to present with NTDs (Barbieri et al., 1986; Incardona et al., 2004). Human studies have also indicated that maternal prenatal exposure to PAHs was associated with an elevated risk for NTDs in offspring, using residence location or biomarkers of exposure (Demetriou et al., 2012; Langlois et al., 2012; Rankin et al., 2009). Previously we demonstrated that indoor air pollution from coal combustion was a potential risk factor for NTDs in Shanxi Province, where the concentration of PAHs emissions is amongst the highest in the country. "
ABSTRACT: Maternal exposure to polycyclic aromatic hydrocarbons (PAHs) has been shown to be associated with an elevated risk for neural tube defects (NTDs). In the human body, PAHs are bioactivated and the resultant reactive epoxides can covalently bind to DNA to form PAH-DNA adducts, which may, in turn, cause transcription errors, changes in gene expression or altered patterns of apoptosis. During critical developmental phases, these changes can result in abnormal morphogenesis.NeuroToxicology 12/2014; 46. DOI:10.1016/j.neuro.2014.12.003 · 3.05 Impact Factor
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- "experiments (Barbieri et al., 1986) and a human epidemiological study on occupational exposure to polycyclic aromatic hydrocarbons (Langlois et al., 2012). Organochlorine pesticides (OCPs) were extensively used in agriculture throughout the world between 1950 and 1970 (Li and Macdonald, 2005). "
ABSTRACT: Organochlorine pesticides (OCPs) in placental tissue have been reported to be associated with an increased risk for fetal neural tube defects (NTDs). Our case-control study was performed to explore the association between maternal serum OCP concentration and NTD risk in offspring. Serum samples were collected from 117 mothers who delivered NTD infants (case group) and 121 mothers who delivered healthy infants (control group). Only three of the 25 OCPs were detected in more than half of the maternal serum samples. The median concentration of total OCPs in the case group was significantly higher than that of the control group. However, no dose-response relationships between higher levels of any individual OCPs or total OCPs and the risk of NTDs or subtypes were observed in either the unadjusted binary unconditional logistic regression model or the model adjusted by potential confounders. We conclude that no clear association between maternal serum OCP residues and NTD risk in offspring was observed in this population.Science of The Total Environment 06/2014; 490C:1037-1043. DOI:10.1016/j.scitotenv.2014.05.075 · 4.10 Impact Factor
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- "Recent epidemiological studies found that maternal exposure to indoor air pollution from coal combustion and occupational polycyclic aromatic hydrocarbons (PAHs) was associated with an increased risk of fetal NTDs (Li et al., 2011; Langlois et al., 2012). In addition, higher levels of PAHs in maternal blood and placental tissue were observed in NTD case mothers than in healthy control mothers (Naufal et al., 2010; Ren et al., 2011). "
ABSTRACT: Maternal exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with the risk of fetal neural tube defects (NTDs). Whether maternal genetic variants related to PAH metabolism contribute to the development of fetal NTDs remains unclear. We conducted a case-control study in a Chinese population to examine the association of selected maternal genetic variants of phase II enzymes involved in the elimination of the metabolic intermediates of these chemicals with fetal NTD risk, and to evaluate possible interaction of the genetic variant and maternal exposure to indoor air pollution from coal combustion and smoking (IAPCC). Blood samples were collected from 534 NTD case mothers and 534 control mothers and assayed for 12 polymorphisms of 5 genes encoding phase II enzymes. We found that the rs9282861 GG genotype of SULT1A1 was associated with an elevated risk of total NTDs (odds ratio [OR] = 2.12, 95% confidence interval [CI]: 1.49-3.00), compared with the GA genotype. The SULT1A1 rs9282861 variant showed a significant additive interaction with maternal exposure to IAPCC for NTD risk, with a relative excess risk of interaction of 1.20 (95% CI 0.23-2.18), and the OR for the joint effect of high-level IAPCC exposure and the GG genotype was 8.37 (95% CI: 3.63-19.28). Maternal SULT1A1 polymorphism is associated with the risk of fetal NTDs, and has an additive-scale interaction with maternal IAPCC exposure for NTD risk. Birth Defects Research (Part A), 2013. © 2013 Wiley Periodicals, Inc.Birth Defects Research Part A Clinical and Molecular Teratology 01/2014; 100(1). DOI:10.1002/bdra.23196 · 2.21 Impact Factor