Unexposed Mothers Research Articles

Mother's environmental tobacco smoke exposure during pregnancy and externalizing behavior problems in children

BackgroundWhile the impact of active maternal smoking during pregnancy on child health has been well investigated, the association between maternal passive smoking, or environmental tobacco smoke (ETS), or second-hand smoke, and behavioral development of offspring is less clear. This study examines the association between maternal ETS exposure during pregnancy and child behavior problems. MethodsCross-sectional data of 646 mother–child pairs from the Jintan China Cohort Study were used in the analyses. Mother's exposure to tobacco smoking at home, the workplace, and other places during pregnancy (for the determination of maternal ETS exposure) and children's behaviors (via Child Behavior Checklist) were assessed when the children were 5–6 years old. Logistic regression models were constructed to examine associations between maternal exposure to ETS during pregnancy and internalizing and externalizing behavior problems, adjusting for potential cofounders including child sex and parental characteristics. Results37% of mothers reported ETS during pregnancy. Children of mothers exposed to ETS during pregnancy had higher scores for externalizing and total behavior problems, with 25% of children whose mothers were exposed to ETS compared to 16% of children of unexposed mothers. After adjusting for potential confounders, ETS exposure was associated with a higher risk of externalizing behavior problems in offspring of exposed mothers (OR=2.08, 95% confidence interval [CI] 1.27–3.43). Analysis after multiple imputations and sensitivity analysis further verified the association, but no dose–response relationship was found. ETS exposure, however, was not associated with internalizing or total behavior problems. ConclusionThis study suggests that maternal ETS exposure during pregnancy may impact child behavioral development, particularly externalizing behaviors.

Effects of dimethoate on rotifer Brachionus calyciflorus using multigeneration toxicity tests

As important members of the zooplankton community and sources of food for fish, rotifers are used extensively in ecotoxicological research to assess the health of the environment and safety of compounds. However, most rotifer toxicity tests are only conducted using rotifer neonates derived from unexposed mothers, thus ignoring the potential transfer of contaminants from mother to offspring. To understand better the mother to offspring exposure, a multigenerational study was conducted using three successive generations (F0, F1 and F2) of the common freshwater rotifer Brachionus calyciflorus to investigate the toxic effects of the widely used organophosphate pesticide, dimethoate (O, O-dimethyl S-methylcarbamoylmethyl phosphorodithioate). When the F0 generation was exposed to five pesticide concentrations, the population growth rate (r) displayed symptoms of hormesis, characterized by the conversion of low-concentration stimulation to high-concentration inhibition. Despite this observation, the exposure to any given concentration of dimethoate reduced the population growth rates of the F1 and F2 generation rotifers. Significant differences existed between the F0, F1 and F2 rotifers for the population growth rate under dimethoate stress: F2 individuals were more sensitive than F1, whereas the F1 individuals were more sensitive than F0. The results indicated that the parental exposure to a given toxic stress could result in increased sensitivity and decreased fitness in the offspring. This study illustrates the utility of multigenerational toxicity tests, which may better reflect and more accurately predict the effects of long-term pesticide exposure to aquatic organisms at the population level.

Maternal predator-exposure has lifelong consequences for offspring learning in threespined sticklebacks.

Learning is an important form of phenotypic plasticity that allows organisms to adjust their behaviour to the environment. An individual's learning performance can be affected by its mother's environment. For example, mothers exposed to stressors, such as restraint and forced swimming, often produce offspring with impaired learning performance. However, it is unclear whether there are maternal effects on offspring learning when mothers are exposed to ecologically relevant stressors, such as predation risk. Here, we examined whether maternal predator-exposure affects adult offsprings' learning of a discrimination task in threespined sticklebacks (Gasterosteus aculeatus). Mothers were either repeatedly chased by a model predator (predator-exposed) or not (unexposed) while producing eggs. Performance of adult offspring from predator-exposed and unexposed mothers was assessed in a discrimination task that paired a particular coloured chamber with a food reward. Following training, all offspring learned the colour-association, but offspring of predator-exposed mothers located the food reward more slowly than offspring of unexposed mothers. This pattern was not driven by initial differences in exploratory behaviour. These results demonstrate that an ecologically relevant stressor (predation risk) can induce maternal effects on offspring learning, and perhaps behavioural plasticity more generally, that last into adulthood.

Analysis of selected maternal exposures and non‐syndromic atrioventricular septal defects in the National Birth Defects Prevention Study, 1997–2005.

Although the descriptive epidemiology of atrioventricular septal defects (AVSDs), a group of serious congenital heart defects (CHDs), has been recently reported, non-genetic risk factors have not been consistently identified. Using data (1997-2005) from the National Birth Defects Prevention Study, an ongoing multisite population-based case-control study, the association between selected non-genetic factors and non-syndromic AVSDs was examined. Data on periconceptional exposures to such factors were collected by telephone interview from 187 mothers of AVSD case infants and 6,703 mothers of unaffected infants. Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were estimated from logistic regression models. Mothers who reported cigarette smoking during the periconceptional period were more likely to have infants with AVSDs compared with non-smokers, independent of maternal age, periconceptional alcohol consumption, infant gestational age, family history of CHDs, and study site (aOR 1.5, 95% CI 1.1-2.4). The association was strongest in mothers who smoked more than 25 cigarettes/day. In addition, mothers with periconceptional passive smoke exposure were more likely to have infants with AVSDs than unexposed mothers, independent of maternal age, active periconceptional smoking, infant gestational age, and family history of CHDs (aOR 1.4, 95% CI 1.0-2.0). No associations were observed between AVSDs and maternal history of a urinary tract infection or pelvic inflammatory disease, maternal use of a wide variety of medications, maternal occupational exposure, parental drug use, or maternal alcohol consumption. If the results of this preliminary study can be replicated, minimizing maternal active and passive smoke exposure may decrease the incidence of AVSDs.

Maternal exposure to predation risk decreases offspring antipredator behaviour and survival in threespined stickleback

1. Adaptive maternal programming occurs when mothers alter their offspring's phenotype in response to environmental information such that it improves offspring fitness. When a mother's environment is predictive of the conditions her offspring are likely to encounter, such transgenerational plasticity enables offspring to be better-prepared for this particular environment. However, maternal effects can also have deleterious effects on fitness.2. Here, we test whether female threespined stickleback fish exposed to predation risk adaptively prepare their offspring to cope with predators. We either exposed gravid females to a model predator or not, and compared their offspring's antipredator behaviour and survival when alone with a live predator. Importantly, we measured offspring behaviour and survival in the face of the same type of predator that threatened their mothers (Northern pike).3. We did not find evidence for adaptive maternal programming; offspring of predator-exposed mothers were less likely to orient to the predator than offspring from unexposed mothers. In our predation assay, orienting to the predator was an effective antipredator behaviour and those that oriented, survived for longer.4. In addition, offspring from predator-exposed mothers were caught more quickly by the predator on average than offspring from unexposed mothers. The difference in antipredator behaviour between the maternal predator-exposure treatments offers a potential behavioural mechanism contributing to the difference in survival between maternal treatments.5. However, the strength and direction of the maternal effect on offspring survival depended on offspring size. Specifically, the larger the offspring from predator-exposed mothers, the more vulnerable they were to predation compared to offspring from unexposed mothers.6. Our results suggest that the predation risk perceived by mothers can have long-term behavioural and fitness consequences for offspring in response to the same predator. These stress-mediated maternal effects can have nonadaptive consequences for offspring when they find themselves alone with a predator. In addition, complex interactions between such maternal effects and offspring traits such as size can influence our conclusions about the adaptive nature of maternal effects.

Application of a Novel Hybrid Study Design to Explore Gene‐Environment Interactions in Orofacial Clefts

Orofacial clefts are common birth defects with strong evidence for both genetic and environmental causal factors. Candidate gene studies combined with exposures known to influence the outcome provide a highly targeted approach to detecting GxE interactions. We developed a new statistical approach that combines the case-control and offspring-parent triad designs into a "hybrid design" to search for GxE interactions among 334 autosomal cleft candidate genes and maternal first-trimester exposure to smoking, alcohol, coffee, folic acid supplements, dietary folate and vitamin A. The study population comprised 425 case-parent triads of isolated clefts and 562 control-parent triads derived from a nationwide study of orofacial clefts in Norway (1996-2001). A full maximum-likelihood model was used in combination with a Wald test statistic to screen for statistically significant GxE interaction between strata of exposed and unexposed mothers. In addition, we performed pathway-based analyses on 28 detoxification genes and 21 genes involved in folic acid metabolism. With the possible exception of the T-box 4 gene (TBX4) and dietary folate interaction in isolated CPO, there was little evidence overall of GxE interaction in our data. This study is the largest to date aimed at detecting interactions between orofacial clefts candidate genes and well-established risk exposures.

Prenatal exposure to selective serotonin reuptake inhibitors and risk of childhood overweight

The objective was to investigate the association between prenatal selective serotonin reuptake inhibitor (SSRI) exposure and overweight in offspring at 4-5 years of age. We conducted a retrospective cohort study using linked records from the Women's and Children's Health Network in South Australia, Australia. Women were eligible to participate if they gave birth to singleton, live-born infants between September 2000 and December 2005. Women were excluded if they received a dispensing for an antidepressant other than SSRIs or an antipsychotic or an anti-epileptic or had a chronic medical condition. Of the 6560 eligible women, 71 received a dispensing for an SSRI (exposed), 204 had a reported psychiatric illness but did not receive a dispensing for any antidepressant (untreated psychiatric illness) and 6285 did not have a reported psychiatric illness and did not receive a dispensing for any antidepressant (unexposed). Childhood overweight was classified as a body mass index >85th percentile, based on age and sex. At 4-5 years of age, female offspring of exposed mothers were less likely to be overweight compared with female offspring of mothers with an untreated psychiatric illness [adjusted Prevalence Ratio (aPR) 0.23; 95% confidence interval (CI) 0.05-0.98] and female offspring of unexposed mothers (aPR 0.27; 0.07-0.99). No association with overweight was observed among male offspring of exposed mothers compared with male offspring of mothers with an untreated psychiatric illness (aPR 1.17; 0.54-2.51) and male offspring of unexposed mothers (aPR 0.93; 0.52-1.67). Further research is required to confirm these findings and examine the potential mechanisms behind the sex-specific differences.

Association between cocaine abuse in pregnancy and placenta-associated syndromes using propensity score matching approach

AimsWe used propensity scores matching techniques to assess the association between maternal cocaine abuse in pregnancy and the occurrence of placenta-associated syndromes (PAS). Study designMothers who abused cocaine (n=5026) were matched to controls (n=5026) from a sample of 1,693,197, unexposed mothers in Florida from 1998 to 2007. Cocaine abuse was identified using the ICD-9 principal and secondary diagnosis codes (304.2 for cocaine dependence and 305.6 for cocaine abuse). The outcome of interest, PAS, was identified as any indication in diagnosis field of ICD-9-CM codes for: placental abruption (641.2), oligohydramnios (658.0), placental infarction (656.7, 656.8, 656.9), gestational hypertension (642.3, 642.9), preeclampsia (642.4, 642.5, and 642.7) or eclampsia (642.6). ResultsNearly 6% of mothers in the study sample experienced a condition associated with PAS prior to matching. Women who abused cocaine were 58% more likely to have PAS when compared to women who did not (OR=1.48, 95% confidence interval: 1.33, 1.66). Women who abused cocaine were at elevated odds for placental abruption, placenta infarction and preeclampsia with the most pronounced odds noted for placental abruption (OR=2.79, 95% confidence interval: 2.19, 3.55). ConclusionsThese findings indicate that cocaine abuse during pregnancy is associated with more placenta-related disorders than previously reported.

Maternal occupational exposure to ionizing radiation and birth defects

So far, only a few studies investigated occupational exposure to ionizing radiation in pregnancy to cause birth defects (BDs). No association between BDs and ionizing radiation, although described for high-dose exposure, could ever be confirmed for employees, or specific job titles. Here, an explorative analysis of a prospective population-based birth cohort used to quantify the prevalence of BDs in infants between 1/2007 and 2/2008 is presented. An active examination of all livebirths by specially trained paediatricians in two defined areas was performed. Additionally, a study-specific questionnaire distributed among all becoming mothers in the surveyed regions included questions on maternal occupational exposure to ionizing radiation within the first trimester of pregnancy. In 3,816 births (including 165 infants with BDs; 4.3%), maternal answers concerning possible exposures to medical and occupational ionizing radiation were available. Relative risk (RR) estimates in mothers surveyed for occupational exposure to ionizing radiation (wearing a radiation dosimeter) and BDs in the offspring were calculated exploratively. A higher prevalence of infants with BDs (n=4; 13.8%) was documented in newborns of the 29 surveyed mothers compared to that in 3,787 births from unexposed mothers (n=161; 4.3%), corresponding to a RR of 3.2 (1.2-8.7). Excluding deformations, the RR increased to 4.0 (1.5-10.7). Adjustment for possible confounders did not change the results substantially.

Germline minisatellite mutations in survivors of childhood and young adult cancer treated with radiation

Purpose: To investigate minisatellite germline mutation rates in survivors of childhood and young adult cancer who received radiotherapy.Materials and methods: DNA samples from 100 families, where one parent was a cancer survivor, were analysed for mutations at eight hypervariable minisatellite loci (B6.7, CEB1, CEB15, CEB25, CEB36, MS1, MS31, MS32) by Southern hybridisation.Results: No significant difference was observed between the paternal mutation rate of 5.6% in exposed fathers with a mean preconceptional testicular dose of 1.23 Gy (56 mutations in 998 informative alleles) and that of 5.8% in unexposed fathers (17 in 295 informative alleles). Subgrouping the exposed fathers into dose groups of <0.10 Gy, 0.10–0.99 Gy, 1.00–1.99 Gy, ≥2.00 Gy revealed no significant differences in paternal mutation rate in comparison with the unexposed fathers. Maternal mutation rates of 1.6% in cancer survivor mothers with a mean preconceptional ovarian dose of 0.58 Gy (five mutations in 304 informative alleles) and 2.1% in unexposed mothers (21 in 987 informative alleles) were not significantly different. There were no differences in minisatellite mutation rates associated with treatment with chemotherapeutic agents.Conclusions: This study provides evidence that preconception radiotherapy for childhood or early adulthood cancer does not increase the germline minisatellite mutation rate.

Birth defects in the sons and daughters of women who were exposed in utero to diethylstilbestrol (DES)

Prenatal exposure to diethylstilbestrol (DES) is associated with adverse health outcomes, including anatomic anomalies of the reproductive tract in women and of the genitourinary tract in men. The mouse model, which replicates many DES-related effects seen in humans, suggests that prenatal DES exposure causes alterations that may affect the next generation of offspring. We asked women participating in a large, multi-centre study of prenatal DES exposure to report birth defects occurring among 4029 sons and 3808 daughters (i.e., the third generation). A subcohort of 793 third generation daughters was also queried for birth defects. We used logistic regression models to generate odds ratio and 95% confidence intervals for the association between prenatal DES exposure in the mother and birth defects in the offspring. Based on the mothers' reports, overall birth defects were elevated in the sons (OR = 1.53; 95% CI = 1.04, 2.23) and in the daughters (OR = 2.35; 95% CI = 1.44, 3.82). Most estimates of association were imprecise, but daughters appeared to have an excess of heart conditions (OR = 4.56; 95% CI = 1.27, 16.34). Our data suggest a possible association between the mother's prenatal DES exposure and birth defects in their offspring, particularly in daughters. We cannot, however, rule-out the possible influence of reporting bias. In particular, the exposed daughters' elevated risk of cardiac defects may be as a result of the underreporting of these conditions by unexposed mothers.

Maternal Bisphenol A Exposure Promotes the Development of Experimental Asthma in Mouse Pups

BackgroundWe recently reported that various environmental estrogens induce mast cell degranulation and enhance IgE-mediated release of allergic mediators in vitro.ObjectivesWe hypothesized that environmental estrogens would enhance allergic sensitization as well as bronchial inflammation and responsiveness. To test this hypothesis, we exposed fetal and neonatal mice to the common environmental estrogen bisphenol A (BPA) via maternal loading and assessed the pups’ response to allergic sensitization and bronchial challenge.MethodsFemale BALB/c mice received 10 μg/mL BPA in their drinking water from 1 week before impregnation to the end of the study. Neonatal mice were given a single 5 μg intraperitoneal dose of ovalbumin (OVA) with aluminum hydroxide on postnatal day 4 and 3% OVA by nebulization for 10 min on days 13, 14, and 15. Forty-eight hours after the last nebulization, we assessed serum IgE antibodies to OVA by enzyme-linked immunosorbent assay (ELISA) and airway inflammation and hyperresponsiveness by enumerating eosinophils in bronchoalveolar lavage fluid, whole-body barometric plethysmography, and a forced oscillation technique.ResultsNeonates from BPA-exposed mothers responded to this “suboptimal” sensitization with higher serum IgE anti-OVA concentrations compared with those from unexposed mothers (p < 0.05), and eosinophilic inflammation in their airways was significantly greater. Airway responsiveness of the OVA-sensitized neonates from BPA-treated mothers was enhanced compared with those from unexposed mothers (p < 0.05).ConclusionsPerinatal exposure to BPA enhances allergic sensitization and bronchial inflammation and responsiveness in a susceptible animal model of asthma.

Prenatal exposure to tetrachloroethylene-contaminated drinking water and the risk of congenital anomalies: a retrospective cohort study

BackgroundPrior animal and human studies of prenatal exposure to solvents including tetrachloroethylene (PCE) have shown increases in the risk of certain congenital anomalies among exposed offspring.ObjectivesThis retrospective cohort study examined whether PCE contamination of public drinking water supplies in Massachusetts influenced the occurrence of congenital anomalies among children whose mothers were exposed around the time of conception.MethodsThe study included 1,658 children whose mothers were exposed to PCE-contaminated drinking water and a comparable group of 2,999 children of unexposed mothers. Mothers completed a self-administered questionnaire to gather information on all of their prior births, including the presence of anomalies, residential histories and confounding variables. PCE exposure was estimated using EPANET water distribution system modeling software that incorporated a fate and transport model.ResultsChildren whose mothers had high exposure levels around the time of conception had an increased risk of congenital anomalies. The adjusted odds ratio of all anomalies combined among children with prenatal exposure in the uppermost quartile was 1.5 (95% CI: 0.9, 2.5). No meaningful increases in the risk were seen for lower exposure levels. Increases were also observed in the risk of neural tube defects (OR: 3.5, 95% CI: 0.8, 14.0) and oral clefts (OR 3.2, 95% CI: 0.7, 15.0) among offspring with any prenatal exposure.ConclusionThe results of this study suggest that the risk of certain congenital anomalies is increased among the offspring of women who were exposed to PCE-contaminated drinking water around the time of conception. Because these results are limited by the small number of children with congenital anomalies that were based on maternal reports, a follow-up investigation should be conducted with a larger number of affected children who are identified by independent records.

Biomarkers of exposure to tobacco smoke and environmental pollutants in mothers and their transplacental transfer to the foetus. Part I: Bulky DNA adducts

32P-postlabelling and PAH-ELISA using the antiserum #29 were employed to analyze DNA adducts in venous and umbilical cord blood and the placenta of 79 mothers giving birth to 80 living babies in Prague (Czech Republic). Ambient air exposure was measured by stationary measurements of basic air pollutants (PM2.5, c-PAHs) during the entire pregnancy. Tobacco smoke exposure was assessed by questionnaire data and by plasma cotinine levels. The total DNA adduct levels in the lymphocytes of mothers and newborns were elevated by 30–40% ( p < 0.001) compared with the placenta. B[a]P-like DNA adduct (adduct with the identical chromatographic mobility on TLC as major BPDE derived DNA adduct) levels were elevated in the blood of mothers compared with the placenta and the blood of newborns ( p < 0.05 and p < 0.01). In tobacco smoke-exposed mothers, higher DNA adduct levels in the blood of mothers and newborns compared with the placenta were found ( p < 0.001), whereas the total and B[a]P-like adduct levels were comparable in the blood of mothers and newborns. B[a]P-like adducts were elevated in the blood of mothers unexposed to tobacco smoke compared with that of corresponding newborns and the placenta ( p < 0.01). Total and B[a]P-like DNA adducts were increased in the placenta of tobacco smoke-exposed compared with unexposed mothers ( p < 0.001 and p < 0.01). In lymphocytes of tobacco smoke-exposed mothers, the comparison of total adduct levels (1.18 ± 0.67 vs. 0.92 ± 0.28) and B[a]P-like DNA adducts (0.22 ± 0.12 adducts/10 8 nucleotides vs. 0.15 ± 0.06 adducts/10 8 nucleotides) with newborns indicated a 30–40% increase of adducts in mothers. Almost equal PAH–DNA adduct levels were detected by anti-BPDE-DNA ELISA in the placenta of tobacco smoke-exposed and -unexposed mothers. Our results suggest a protective effect of the placental barrier against the genotoxic effect of some tobacco smoke components between the circulation of mother and child. We found a correlation between adduct levels in the blood of mothers and newborns.

Prenatal Exposure to Tetrachloroethylene-Contaminated Drinking Water and the Risk of Adverse Birth Outcomes

BackgroundPrior studies of prenatal exposure to tetrachloroethylene (PCE) have shown mixed results regarding its effect on birth weight and gestational age.ObjectivesIn this retrospective cohort study we examined whether PCE contamination of public drinking-water supplies in Massachusetts influenced the birth weight and gestational duration of children whose mothers were exposed before the child’s delivery.MethodsThe study included 1,353 children whose mothers were exposed to PCE-contaminated drinking water and a comparable group of 772 children of unexposed mothers. Birth records were used to identify subjects and provide information on the outcomes. Mothers completed a questionnaire to gather information on residential histories and confounding variables. PCE exposure was estimated using EPANET water distribution system modeling software that incorporated a fate and transport model.ResultsWe found no meaningful associations between PCE exposure and birth weight or gestational duration. Compared with children whose mothers were unexposed during the year of the last menstrual period (LMP), adjusted mean differences in birth weight were 20.9, 6.2, 30.1, and 15.2 g for children whose mothers’ average monthly exposure during the LMP year ranged from the lowest to highest quartile. Similarly, compared with unexposed children, adjusted mean differences in gestational age were −0.2, 0.1, −0.1, and −0.2 weeks for children whose mothers’ average monthly exposure ranged from the lowest to highest quartile. Similar results were observed for two other measures of prenatal exposure.ConclusionsThese results suggest that prenatal PCE exposure does not have an adverse effect on these birth outcomes at the exposure levels experienced by this population.

Effectiveness of Repeat Single-Dose Nevirapine for Prevention of Mother-to-Child Transmission of HIV-1 in Repeat Pregnancies in Uganda

Single-dose nevirapine (SDNVP) is widely used to prevent mother-to-child HIV transmission in resource-limited settings. Given detection of resistant mutants among women who receive SDNVP, concerns have arisen over the efficacy of SDNVP in repeat pregnancies. Retrospective data were collected from SDNVP-exposed and -unexposed women from the HIV Network for Prevention 012 trial who subsequently received SDNVP in another pregnancy. Prospective data were collected from pregnant women who were SDNVP exposed or unexposed before delivery. Kaplan-Meier and Cox regression analyses were used to estimate rates of HIV infection and HIV-free survival among infants born to women with or without prior SDNVP exposure. In the retrospective cohort, the infection rates were 11.3% and 16.7% for 104 infants of NVP-exposed and -unexposed mothers, respectively (P = 0.41). In the prospective cohort, among 103 infants of NVP-exposed and -unexposed mothers, the 12-month infant HIV infection rates were 20.5% and 18.7% (P = 0.81) and HIV-free survival rates were 74.4% and 78.1% (P = 0.66), respectively. There was no increased risk of infant HIV infection among SDNVP-exposed women compared with -unexposed women. These findings support current international guidelines to offer SDNVP to HIV-infected pregnant women, regardless of previous SDNVP exposure, when more complex prophylaxis regimens are not available.

Maternal Exposure to Greenhouse Work During Pregnancy, PON1 Polymorphisms, and the Risk of LBW

ISEE-456 Objective: To assess the association between maternal exposure to greenhouse work during pregnancy and the risk of low birth weight (LBW; <2500 g) in their offspring, as well as to evaluate the interaction between this exposure and maternal genotype for PON1-192 polymorphisms. Material and Methods: In Mexico, a retrospective study was carried out in 2 states presenting high frequencies of greenhouse activity: Estado de México and Morelos. We interviewed and collected blood samples from 264 female (greenhouse workers or greenhouse workers couples) who became pregnant during the 10 years before interview; the questionnaire included questions on socioeconomic characteristics, tobacco and alcohol use, diseases, and occupational and reproductive history. We obtained information about 527 pregnancies. We extracted DNA from white cells, and determined PON1 genotype for 192 polymorphisms by PCR-RFLP. We analyzed the results with generalized latent and linear mixed models, generalized estimating equations and logistic regression models. Results: After adjusting for potential confounders, the risk from the 192RR homozygote mothers who were exposed to greenhouse work during pregnancy was significantly higher than that from unexposed mothers with 192QR or 192QQ genotype (OR 6.5, 95% CI 1.2–33.8). Conclusions: This result suggests that interaction between maternal occupational exposure to pesticides during pregnancy and 192RR PON1 genotype increase the probability of having children with LBW.

Limits of usual biochemical alcohol markers in cord blood at term: a fetal/maternal population-based study

After maternal alcohol consumption during pregnancy, many neonates affected by less apparent forms of fetal alcohol syndrome disorder (FASD) do not receive proper diagnosis or treatment. There is thus a need for laboratory markers for early detection of alcohol-exposed neonates. The aim of our study was to assess the efficiency of the usual alcohol biomarkers measured in cord blood to identify alcohol-exposed neonates immediately after birth. A 1-year study was conducted in the labor wards of the maternity units of the Auvergne, Central France at the time of term delivery. The patients answered an anonymous self-completion survey concerning alcohol use (Alcohol Use Disorder Identification Test; AUDIT) during their pregnancy. Aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyltransferase concentrations and the percentage of carbohydrate-deficient transferrin were measured in maternal and cord blood. We collected 870 maternal-fetal sample pairs. Two cases (0.2%) of typical FASD were detected. We report a non-significant correlation between maternal and cord blood biomarkers. None of the cord blood biomarkers differed significantly between newborns of alcohol-exposed and unexposed mothers. We demonstrate that the usual alcohol biomarkers are not effective in cord blood for identifying alcohol-exposed neonates.

Treatment With Selective Serotonin Reuptake Inhibitors During Pregnancy: Deceleration of Weight Gain Because of Depression or Drug?

Treatment With Selective Serotonin Reuptake Inhibitors During Pregnancy: Deceleration of Weight Gain Because of Depression or Drug?

A pilot study examining germline minisatellite mutations in the offspring of Danish childhood and adolescent cancer survivors treated with radiotherapy

Purpose:To investigate germline mutation rate at eight minisatellite loci in 24 Danish families, where one parent is the survivor of childhood or adolescent cancer treated with radiotherapy.Materials and methods:Parents and offspring were profiled for eight hypervariable minisatellite loci (B6.7, CEB1, CEB15, CEB25, CEB36, MS1, MS31, MS32) by Southern blotting.Results:Seven paternal mutations were observed for 130 informative alleles in 18 offspring from 11 radiation-exposed fathers (mean preconceptional dose for offspring 0.29 Gy, range <0.01 – 1.2 Gy), compared to six mutations for 146 informative alleles in 21 offspring from 13 unexposed fathers. No statistically significant difference between the total paternal mutation rates was observed (5.4% for exposed fathers and 4.1% for unexposed fathers). Three maternal mutations were observed for 148 informative alleles in 21 offspring from 13 radiation-exposed mothers (mean preconceptional dose for offspring 0.71 Gy, range <0.01 – 9.2 Gy), compared to one mutation for 130 informative alleles in 18 offspring from 11 unexposed mothers. Again, no statistically significant difference was observed between the total maternal mutation rates (2.0% for exposed mothers and 0.8% for unexposed mothers).Conclusions:The data from this pilot study demonstrate no statistically significant increase in germline minisatellite mutation rate associated with radiotherapy for childhood and adolescent cancer.