Maternal occupational exposure to polycyclic aromatic hydrocarbons and risk of neural tube defect‐affected pregnancies

Langlois, Peter H.; Hoyt, Adrienne T.; Lupo, Philip J.; Lawson, Christina C.; Waters, Martha A.; Desrosiers, Tania A.; Shaw, Gary M.; Romitti, Paul A.; Lammer, Edward J.

doi:10.1002/bdra.23045

Cited by 44 publications

(47 citation statements)

References 25 publications

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“…Maternal occupational exposure to PAHs was associated with increased risks of congenital heart defects (Lupo et al, 2012b), gastroschisis (Lupo et al, 2012a) and NTDs (Langlois, Hoyt, 2012). In our previous study, maternal passive smoking and exposure to indoor coal combustion had been shown to be associated with an elevated NTD risk.…”

Section: Discussionmentioning

confidence: 99%

“…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.…”

Section: Introductionmentioning

confidence: 99%

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Levels of PAH–DNA adducts in cord blood and cord tissue and the risk of fetal neural tube defects in a Chinese population

Yuan

Jin

et al. 2015

NeuroToxicology

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Introduction 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. Objectives We aimed to examine the relationship between the levels of PAH-DNA adducts in cord blood and cord tissue and the risk of NTDs. Methods From 2010 to 2012, sixty NTD cases and 60 healthy controls were recruited from a population-based birth defects surveillance system in five counties of Shanxi Province in Northern China, where the emission of PAHs remains one of the highest in the country and PAHs exposure is highly prevalent. PAH-DNA adducts in cord blood of 15 NTD cases and 15 control infants, and in cord tissue of 60 NTD cases and 60 control infants were measured using the 32P-postlabeling method. Results PAH-DNA adduct levels in cord blood tend to be higher in the NTD group (28.5 per 108 nucleotides) compared with controls (19.7 per 108 nucleotides), although the difference was not statistically significant (P=0.377). PAH-DNA adducts in cord tissue were significantly higher in the NTD group (24.6 per 106 nucleotides) than in the control group (15.3 per 106 nucleotides), P=0.010. A positive dose-response relationship was found between levels of PAH-DNA adducts in cord tissue and the risk of NTDs (P=0.009). When the lowest tertile was used as the referent and potential confounding factors were adjusted for, a 1.03-fold (95% CI, 0.37–2.89) and 2.96-fold (95% CI, 1.16–7.58) increase in the risk of NTDs was observed for fetuses whose cord tissue PAH-DNA adduct levels were in the second and highest tertile, respectively. Conclusions High levels of PAH-DNA adducts in fetal tissues were associated with increased risks of NTDs.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Levels of PAH–DNA adducts in cord blood and cord tissue and the risk of fetal neural tube defects in a Chinese population

Yuan

Jin

et al. 2015

NeuroToxicology

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“…Several derivatives of PAHs have been shown to be teratogenic in animal models, producing NTDs and a variety of other malformations in the exposed embryos [5]. There is also growing evidence from human environmental and occupational studies on risks of NTDs in association with prenatal exposure to PAH [6-9]. PAHs can exert genotoxic effects through metabolic activation and subsequent binding to DNA, thus forming bulky PAH-DNA adducts, a widely used indicator of DNA damage that has been associated with increased cancer risk [10-12].…”

Section: Introductionmentioning

confidence: 99%

Levels of PAH–DNA adducts in placental tissue and the risk of fetal neural tube defects in a Chinese population

Yuan¹,

Jin²,

Wang³

et al. 2013

Reproductive Toxicology

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We examined the relationship between PAH-DNA adduct levels in the placental tissue, measured by a highly sensitive 32P-postlabeling assay, and the risk of fetal neural tube defects (NTDs). We further explored the interaction between PAH-DNA adducts and placental PAHs with respect to NTD risk. Placental tissues from 80 NTD-affected pregnancies and 50 uncomplicated normal pregnancies were included in this case-control study. Levels of PAH-DNA adducts were lower in the NTD group (8.12 per 108 nucleotides) compared to controls (9.92 per 108 nucleotides). PAH-DNA adduct concentrations below the median was associated with a 3-fold increased NTD risk. Women with a low PAH-DNA adduct level in concert with a high placental PAH level resulted in a 10-fold elevated risk of having an NTD-complicated pregnancy. A low level of placental PAH-DNA adducts was associated with an increased risk of NTDs; this risk increased dramatically when a low adduct level was coupled with a high placental PAH concentration.

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“…This expert review strategy was based on an approach previously developed and used in the Baltimore-Washington Infant Study (Jackson et al, 2004) and described previously (Langlois et al, 2012). Specifically, as part of the NBDPS occupational exposure assessment, industrial hygienists involved in the project participated in a training session before reviewing the job histories.…”

Section: Methodsmentioning

confidence: 99%

“…Additionally, studies in humans suggest maternal occupational and environmental exposure to PAHs is associated with structural birth defects including neural tube defects (Naufal et al, 2010; Ren et al, 2011; Langlois et al, 2012) and gastroschisis (Lupo et al, 2012). Despite this evidence, to our knowledge there have been no studies evaluating the potential association between maternal occupational exposure to PAHs and CHDs among offspring.…”

Section: Introductionmentioning

confidence: 99%

Maternal occupational exposure to polycyclic aromatic hydrocarbons and congenital heart defects among offspring in the national birth defects prevention study

Lupo

Symanski

Langlois

et al. 2012

Birth Defects Research

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BACKGROUND There is evidence in experimental model systems that exposure to polycyclic aromatic hydrocarbons (PAHs) results in congenital heart defects (CHDs); however, to our knowledge, this relationship has not been examined in humans. Therefore, we conducted a case-control study assessing the association between estimated maternal occupational exposure to PAHs and CHDs in offspring. METHODS Data on CHD cases and control infants were obtained from the National Birth Defects Prevention Study for the period of 1997 to 2002. Exposure to PAHs was assigned by industrial hygienist consensus, based on self-reported maternal occupational histories from 1 month before conception through the third month of pregnancy. Logistic regression was used to evaluate the association between maternal occupational PAH exposure and specific CHD phenotypic subtypes among offspring. RESULTS The prevalence of occupational PAH exposure was 4.0% in CHD case mothers (76/1907) and 3.6% in control mothers (104/2853). After adjusting for maternal age, race or ethnicity, education, smoking, folic acid supplementation, and study center, exposure was not associated with conotruncal defects (adjusted odds ratio [AOR], 0.98; 95% confidence interval [CI], 0.58–1.67), septal defects (AOR, 1.28; 95% CI, 0.86–1.90), or with any isolated CHD subtype. CONCLUSIONS Our findings do not support an association between potential maternal occupational exposure to PAHs and various CHDs in a large, population-based study. For CHD phenotypic subtypes in which modest nonsignificant associations were observed, future investigations could be improved by studying populations with a higher prevalence of PAH exposure and by incorporating information on maternal and fetal genotypes related to PAH metabolism.

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Maternal occupational exposure to polycyclic aromatic hydrocarbons and risk of neural tube defect‐affected pregnancies

Cited by 44 publications

References 25 publications

Levels of PAH–DNA adducts in cord blood and cord tissue and the risk of fetal neural tube defects in a Chinese population

Levels of PAH–DNA adducts in cord blood and cord tissue and the risk of fetal neural tube defects in a Chinese population

Levels of PAH–DNA adducts in placental tissue and the risk of fetal neural tube defects in a Chinese population

Maternal occupational exposure to polycyclic aromatic hydrocarbons and congenital heart defects among offspring in the national birth defects prevention study

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