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Parabens are preservatives widely used in consumer products including cosmetics and food. Whether low-dose paraben exposure may cause adverse health effects has been discussed controversially in recent years. Here we investigate the effect of prenatal paraben exposure on childhood overweight by combining epidemiological data from a mother-child cohort with experimental approaches. Mothers reporting the use of paraben-containing cosmetic products have elevated urinary paraben concentrations. For butyl paraben (BuP) a positive association is observed to overweight within the first eight years of life with a stronger trend in girls. Consistently, maternal BuP exposure of mice induces a higher food intake and weight gain in female offspring. The effect is accompanied by an epigenetic modification in the neuronal Pro-opiomelanocortin (POMC) enhancer 1 leading to a reduced hypothalamic POMC expression. Here we report that maternal paraben exposure may contribute to childhood overweight development by altered POMC-mediated neuronal appetite regulation.
Selective serotonin reuptake inhibitors (SSRIs) are the most widely used treatment by women experiencing depression during pregnancy. However, the effects of maternal SSRI use on early offspring development remain poorly understood. Recent studies suggest that SSRIs can modify the gut microbiota and interact directly with particular gut bacteria, raising the question of whether the gut microbiome impacts host responses to SSRIs. In this study, we investigate effects of prenatal SSRI exposure on fetal neurodevelopment and further evaluate potential modulatory influences of the maternal gut microbiome. We demonstrate that maternal treatment with the SSRI fluoxetine induces widespread alterations in the fetal brain transcriptome during midgestation, including increases in the expression of genes relevant to synaptic organization and neuronal signaling and decreases in the expression of genes related to DNA replication and mitosis. Notably, maternal fluoxetine treatment from E7.5 to E14.5 has no overt effects on the composition of the maternal gut microbiota. However, maternal pretreatment with antibiotics to deplete the gut microbiome substantially modifies transcriptional responses of the fetal brain to maternal fluoxetine treatment. In particular, maternal fluoxetine treatment elevates localized expression of the opioid binding protein/cell adhesion molecule like gene Opcml in the fetal thalamus and lateral ganglionic eminence, which is prevented by maternal antibiotic treatment. Together, these findings reveal that maternal fluoxetine treatment alters gene expression in the fetal brain through pathways that are impacted, at least in part, by the presence of the maternal gut microbiota.
Arsenic exposure is a significant public health issue, with harmful effects caused by its use in commercial products such as car batteries, pesticides, and herbicides. Arsenic has three main compounds: inorganic, organic, and arsine gas. Inorganic arsenic compounds in water are highly toxic. The daily intake of arsenic from food and beverages is between 20 and 300 mcg/day. Arsenic is known for its carcinogenic properties and is classified as a human carcinogen by different institutions. Exposure can lead to oxidative stress, DNA damage, and epigenetic deregulation, which can cause endocrine disorders, altered signal transduction pathways, and cell proliferation. In addition, arsenic can easily cross the placenta, making it a critical concern for maternal and fetal health. Exposure can lead to complications such as gestational diabetes, anemia, low birth weight, miscarriage, and congenital anomalies. Female babies are particularly vulnerable to the negative impact of arsenic exposure, with a higher risk of low weight for gestational age and congenital cardiac anomalies. Therefore, it is crucial to monitor and regulate the levels of arsenic in drinking water and food sources to prevent these adverse health outcomes. Further research is necessary to fully understand the impact of arsenic exposure on human health, especially during pregnancy and infancy, by implementing preventative measures and monitoring the levels of arsenic in the environment.
Conditions during fetal development influence health and disease in adulthood, especially during critical windows of organogenesis. Fetal exposure to the endocrine disrupting chemical, bisphenol A (BPA) affects the development of multiple organ systems in rodents and monkeys. However, effects of BPA exposure on cardiac development have not been assessed. With evidence that maternal BPA is transplacentally delivered to the developing fetus, it becomes imperative to examine the physiological consequences of gestational exposure during primate development. Herein, we evaluate the effects of daily, oral BPA exposure of pregnant rhesus monkeys (Macaca mulatta) on the fetal heart transcriptome. Pregnant monkeys were given daily oral doses (400 µg/kg body weight) of BPA during early (50-100 ± 2 days post conception, dpc) or late (100 ± 2 dpc--term), gestation. At the end of treatment, fetal heart tissues were collected and chamber specific transcriptome expression was assessed using genome-wide microarray. Quantitative real-time PCR was conducted on select genes and ventricular tissue glycogen content was quantified. Our results show that BPA exposure alters transcription of genes that are recognized for their role in cardiac pathophysiologies. Importantly, myosin heavy chain, cardiac isoform alpha (Myh6) was down-regulated in the left ventricle, and 'A Disintegrin and Metalloprotease 12', long isoform (Adam12-l) was up-regulated in both ventricles, and the right atrium of the heart in BPA exposed fetuses. BPA induced alteration of these genes supports the hypothesis that exposure to BPA during fetal development may impact cardiovascular fitness. Our results intensify concerns about the role of BPA in the genesis of human metabolic and cardiovascular diseases.
Pregnant women of advanced maternal age (AMA) are vulnerable to exposure to the surrounding environment. Assessment of trace elements in pregnant women living in specific areas is important for biomonitoring. However, exposure levels and variation patterns during pregnancy remains controversial and attracts extensive public concern. Therefore, we aimed to evaluate exposure of 18 toxic and/or essential trace elements in maternal plasma and in paired cord plasma during pregnancy at AMA. A total of 48 pregnant women of AMA were recruited in Peking University Third Hospital from 2018 to 2021. Eighteen elements found in maternal plasma during the 1st, 2nd, or 3rd trimester of pregnancy and paired cord plasma were measured by 7700x ICP-MS (Agilent Technologies, Palo Alto, CA, USA) and Elan DRC type II ICP-MS (The Perkin-Elmer Corporation, Waltham, MA USA). Concentrations of Pb, Se, Fe, Zn, and Mo all decreased during pregnancy, while Cu increased. Interestingly, concentrations of Rb decreased initially but then increased. Elements as Al, Co, Se, Cu, and Ni showed significantly lower levels in cord than in maternal plasma, while elements as Sr, Fe, Rb, Mn and Zn displayed significantly higher levels in cord than in maternal plasma. Moreover, positively- interacted clusters were found in Ni-Co-Cu-Al-Rb-Zn and Zn-Mn-Al-Pb in maternal blood. Similar positively-interacted clusters were found in Zn-Ni-Co, Zn-Ni-Fe, Mn-Al-Pb, Fe-Pb-Mn, Fe-Ni-Cu, and Rb-Cu-Sb-Fe-Mn in cord plasma. Furthermore, correlations between paired maternal and cord blood samples for As, Sr, and Mo were statistically significant, indicating that the fetus burden may reflect maternal exposure to some extent. Admittedly, levels of toxic and essential elements in our cohort study were comparatively lower than those in the scientific literature.
Prenatal exposure to ambient air pollution has been associated with preterm birth in several studies. Associations between air pollution and gestational or pre-existing diabetes have been hypothesized but are not well established. We examined the association between air pollution exposure in pregnancy and gestational diabetes and whether the association between air pollution and preterm birth is modified by diabetes (gestational or pre-existing) in a highly polluted area of California. Birth certificates and hospital discharge data from all singleton births from 2000 to 2006 to women living in four counties in the San Joaquin Valley of California were linked to criteria air pollution and traffic density measurements at the geocoded maternal residence. Air pollutants were dichotomized at the highest quartile and compared to the lower three quartiles. Logistic regression models were adjusted for maternal race-ethnicity, age, education, payment of birth expenses, and prenatal care. There were consistent inverse associations between exposure to air pollution during the first two trimesters and gestational diabetes (statistically significant odds ratios (OR) less than 1). When stratified by any diabetes (gestational or pre-existing), associations between air pollution exposure during pregnancy and categories of preterm birth (20-27, 28-31, 32-33, 34-36 weeks) were generally similar with few exceptions of exposures to carbon monoxide (CO) and particulate matter < 2.5 µm (PM2.5). Those with diabetes and exposure higher levels of CO (in first trimester or entire pregnancy) or PM2.5 (in first trimester) had higher risk of extremely preterm birth (20-27 weeks) compared with those without diabetes. The associations between traffic-related air pollution and gestational diabetes were in the unexpected ("protective") direction. Among those with any diabetes, associations were stronger between CO and PM2.5 and extremely preterm birth.
(1) Introduction: Epigenetic changes have been proposed as a biologic link between in-utero exposure to maternal smoking and health outcomes. Therefore, we examined if in-utero exposure to maternal smoking was associated with infant DNA methylation (DNAm) of cytosine-phosphate-guanine dinucleotides (CpG sites) in the arginine vasopressin receptor 1A AVPR1a gene. The AVPR1a gene encodes a receptor that interacts with the arginine vasopressin hormone and may influence physiological stress regulation, blood pressure, and child development. (2) Methods: Fifty-two infants were included in this cohort study. Multivariable linear models were used to examine the effect of in-utero exposure to maternal smoking on the mean DNAm of CpG sites located at AVPR1a. (3) Results: After adjusting the model for substance use, infants with in-utero exposure to maternal smoking had a reduction in DNAm at AVPR1a CpG sites by -0.02 (95% CI -0.03, -0.01) at one month of age. In conclusion, in-utero exposure to tobacco smoke can lead to differential patterns of DNAm of AVPR1a among infants. Conclusions: Future studies are needed to identify how gene expression in response to early environmental exposures contributes to health outcomes.
Interactions between air pollution and infectious agents are increasingly recognized and critical to identify, especially to protect vulnerable populations. Pregnancy represents a vulnerable period for influenza infection and air pollution exposure, yet interactions during pregnancy remain unclear. Maternal exposure to ultrafine particles (UFPs, [Formula: see text] 100 nm diameter), a class of particulate matter ubiquitous in urban environments, elicits unique pulmonary immune responses. We hypothesized that UFP exposure during pregnancy would lead to aberrant immune responses to influenza enhancing infection severity.
Mycotoxin exposure from food occurs globally but is more common in hot humid environments, especially in low-income settings, and might affect pregnancy outcomes. This study aimed to synthesize the evidence from epidemiological studies on the relationship between maternal or fetal exposure to different mycotoxins and the occurrence of adverse pregnancy outcomes. Multiple databases were systematically searched up to December 2018 to identify studies that assessed the association between mycotoxin exposure in pregnant women or fetuses and at least one pregnancy outcome. Studies were appraised and results were synthesized using standard methods for conducting systematic reviews. This review identified and included 17 relevant studies. There is some evidence to suggest that exposure to various Aspergillus mycotoxins (e.g., aflatoxin) during pregnancy may impair intrauterine fetal growth and promote neonatal jaundice. Findings were inconclusive concerning the influence of aflatoxin exposure on perinatal death and preterm birth. Only two studies assessed effects of maternal exposure to Fusarium mycotoxins (e.g., fumonisin) on adverse pregnancy outcomes. These studies found that maternal fumonisin exposure may be associated with hypertensive emergencies in pregnancy and with neural tube defects. Studies using grain farming and weather conditions as a proxy measure for mycotoxin exposure found that such exposure was associated with an increased risk of preterm birth and late-term miscarriage. In conclusion, there is already some evidence to suggest that exposure to mycotoxins during pregnancy may have detrimental effects on pregnancy outcomes. However, given the limited number of studies, especially on effects of Fusarium mycotoxins, more studies are needed for a more comprehensive understanding of the effects of different mycotoxins on maternal and fetal health and to guide public health policies and interventions.
A cardinal feature of the reaction to stress is the promotion of energy mobilization, enabling appropriate behavioural responses. Predator odours are naturalistic and ecologically relevant stressors present over evolutionary timescales. In this study, we asked whether maternal predator odour exposure could program long-term energy mobilization in C57BL/6 mice offspring. To test this hypothesis, we measured rates of oxygen consumption in prenatally predator odour exposed mice in adulthood while controlling for levels of locomotor activity at baseline and under stress. Circulating thyroid hormone levels and the transcript abundance of key regulators of the hypothalamic-pituitary-thyroid axis within the periventricular nucleus (PVN) of the hypothalamus and in the liver, including carriers and receptors and thyrotropin-releasing hormone, were measured as endocrine mediators facilitating energy availability. Prenatally predator odour exposed mice of both sexes mobilized more energy during lower energy demand periods of the day and under stressful conditions. Further, prenatally predator odour exposed mice displayed modifications of their hypothalamic-pituitary-thyroid axis through increased circulating thyroxine and thyroid hormone receptor α within the PVN and decreased transthyretin in the liver. Overall, these results suggest that maternal exposure to predator odour is sufficient to increase long-term energy mobilization in adult offspring.
Smoking in pregnancy increases a woman's risk of preterm delivery resulting in serious neonatal health problems and chronic lifelong disabilities for the children (e.g., mental retardation, learning problems). To study the effects of tobacco smoke on the placental transcriptome, we performed gene expression profiling on placentas from women exposed to tobacco smoke in pregnancy (N = 12) and from those without significant exposure (N = 64). Gene expression profiles were determined by Illumina HumanRef-8 v2 Expression BeadChips with 18,216 gene probes. Microarray data were normalized by quantile method and filtered for a detection P-value <0.01. Differential gene expression was determined by moderated t-statistic. A linear model was fitted for each gene given a series of arrays using lmFit function. Multiple testing correction was performed using the Benjamini and Hochberg method. Abundant levels of transcripts were found for genes encoding placental hormones (CSH1, CSHL1), pregnancy-specific proteins (PSG3, PSG4, PAPPA), and hemoglobins (HBB, HBG, HBA). Comparative analysis of smokers vs nonsmokers revealed the differential expression of 241 genes (P < 0.05). In smoker cohort, we detected high up-regulation of xenobiotic genes (CYP1A1, CYP1B1, CYB5A, COX412), collagen genes (e.g., COL6A3, COL1A1, COL1A2), coagulation genes (F5, F13A1) as well as thrombosis-related genes (CD36, ADAMTS9, GAS6). In smokers, we identified deregulated genes that show tissue non-specific induction and may be considered as general biomarkers of tobacco smoke exposure. Further, we also found genes specifically deregulated in the exposed placentas. Functional annotation analysis suggested processes and pathways affected by tobacco smoke exposure that may represent molecular mechanisms of smoke-induced placental abnormalities.
The incidence of diabetes mellitus has significantly increased among women of childbearing age, and it has been shown that prenatal exposure to maternal diabetes increases the risk of associated congenital anomalies of the kidney. Congenital anomalies of the kidney are among the leading causes of chronic kidney disease in children. To better understand the effect of maternal diabetes on kidney development, we analyzed wild-type offspring (DM_Exp) of diabetic Ins2+/C96Y mice (Akita mice). DM_Exp mice at postnatal day 34 have a reduction of ~20% in the total nephron number compared with controls, using the gold standard physical dissector/fractionator method. At the molecular level, the expression of the nephron progenitor markers sine oculis homeobox homolog 2 and Cited1 was increased in DM_Exp kidneys at postnatal day 2. Conversely, the number of early developing nephrons was diminished in DM_Exp kidneys. This was associated with decreased expression of the intracellular domain of Notch1 and the canonical Wnt target lymphoid enhancer binding factor 1. Together, these data suggest that the diabetic intrauterine environment impairs the differentiation of nephron progenitors into nephrons, possibly by perturbing the Notch and Wnt/β-catenin signaling pathways.
Climate change will increasingly affect the health of vulnerable populations, including maternal and fetal health. This systematic review aims to identify recent literature that investigates increasing heat and extreme temperatures on pregnancy outcomes globally. We identify common research findings in order to create a comprehensive understanding of how immediate effects will be sustained in the next generation. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guide, we systematically reviewed articles from PubMed and Cochrane Reviews. We included articles that identify climate change-related exposures and adverse health effects for pregnant women. There is evidence that temperature extremes adversely impact birth outcomes, including, but not limited to: changes in length of gestation, birth weight, stillbirth, and neonatal stress in unusually hot temperature exposures. The studies included in this review indicate that not only is there a need for further research on the ways that climate change, and heat in particular, may affect maternal health and neonatal outcomes, but that uniform standards for assessing the effects of heat on maternal fetal health also need to be established.
Although nanoscale titanium dioxide (nano-TiO2) has been extensively used in industrial food applications and daily products for pregnant women, infants, and children, its potential toxicity on fetal development has been rarely studied. The main objective of this investigation was to establish the effects of maternal exposure of nano-TiO2 on developing embryos. Female imprinting control region mice were orally administered nano-TiO2 from gestational day 0 to 17. Our findings showed that Ti concentrations in maternal serum, placenta, and fetus were increased in nano-TiO2-exposed mice when compared to controls, which resulted in reductions in the contents of calcium and zinc in maternal serum, placenta, and fetus, maternal weight gain, placental weight, fetal weight, number of live fetuses, and fetal crown-rump length as well as cauda length, and caused an increase in the number of both dead fetuses and resorptions. Furthermore, maternal nano-TiO2 exposure inhibited development of the fetal skeleton, suggesting a significant absence of cartilage, reduced or absent ossification, and an increase in the number of fetuses with dysplasia, including exencephaly, spina bifida, coiled tail, scoliosis, rib absence, and sternum absence. These findings indicated that nano-TiO2 can cross the blood-fetal barrier and placental barrier, thereby delaying the development of fetal mice and inducing skeletal malformation. These factors may be associated with reductions in both calcium and zinc in maternal serum and the fetus, and both the placenta and embryos may be major targets of developmental toxicity following maternal exposure to nano-TiO2 during the prenatal period. Therefore, the application of nano-TiO2 should be carried out with caution.
Atrazine is a widely used herbicide applied to corn, sugar and other crops as a broad leaf weed inhibitor. Using the Balb/c mouse model, we have determined that prenatal/lactational exposure to atrazine alters adult immune function. Pregnant Balb/c dams were exposed subcutaneously for 21 days via time release pellets to 700 microg per day of atrazine beginning between days 10 and 12 of pregnancy. Prenatal/Lactational exposure caused no overt physical malformations in the offspring and had no effect on the number of litters carried to term or the litter size. Upon reaching early adulthood (approximately 3 months of age), the state of their immune system was evaluated. There were no changes in body weight or in the organ to body weight ratio of the spleen. Additionally, no changes were observed in the number of CD8+ T cell, CD4+ T cell, or B220+ B cell subpopulations in the spleen. T cell function was assessed by measuring proliferation and cytolytic activity after in vitro allogeneic stimulation. Male mice which had been prenatally/lactationally exposed to atrazine had an increase in both T cell proliferation and cytolytic activity. The humoral immune response was assessed after immunization with heat killed Streptococcus pneumoniae (HKSP). There was a significant increase in the number of HKSP-specific IgM secreting B cells in the spleen of prenatal/lactational exposed male mice. Inasmuch as atrazine is a widespread environmental contaminant, this immunopotentiation raises concerns that it may potentiate clinical diseases, such as autoimmune disease and hypersensitivity, and needs to be carefully monitored and studied.
Emerging evidence suggests that inhalation of particulate matter (PM) can have direct adverse effects on liver function. Early life is a time of particular vulnerability to the effects of air pollution. On that basis, we tested whether in utero exposure to residential PM has an impact on the developing liver. Pregnant mice (C57BL/6J) were intranasally administered 100 µg of PM sampled from residential roof spaces (~5 mg/kg) on gestational days 13.5, 15.5, and 17.5. The pups were euthanized at two weeks of age, and liver tissue was collected to analyse hepatic metabolism (glycogen storage and lipid level), cellular responses (oxidative stress, inflammation, and fibrosis), and genotoxicity using a range of biochemical assays, histological staining, ELISA, and qPCR. We did not observe pronounced effects of environmentally sampled PM on the developing liver when examining hepatic metabolism and cellular response. However, we did find evidence of liver genomic DNA damage in response to in utero exposure to PM. This effect varied depending on the PM sample. These data suggest that in utero exposure to real-world PM during mid-late pregnancy has limited impacts on post-natal liver development.
High maternal serum bile acid level is common and sometimes harmful to the gravida. This study aimed to confirm the bile acid phenotypic change caused by prenatal ethanol exposure (PEE) and elucidate its placental mechanism. Pregnant Wistar rats were administered intragastrically with ethanol 4 g/kg⋅d from gestational day 9-20. Total bile acids (TBA) were detected in maternal, fetal serum and placental tissues, increasing significantly in the serum but no significant change in the placental tissues. Meta-analysis was performed and verified the efficacy of the PEE-induced model based on published data from several relevant studies. Mining of microarray data from human and rat placental sources identified the involvement of bile acid metabolism and its significant genes, which were verified by RT-qPCR and western blotting on tissues and treated BeWo cells with the administration of FXR/PXR siRNAs or FXR/PXR agonists. Our examination, consistent with microarray data and wet experiments, showed that organic anion transporter polypeptide-related protein 2B1 (Oatp2b1), multidrug resistance-associated proteins 3 (Mrp3) and breast cancer resistance protein (Bcrp) expression were increased, while nuclear receptor farnesoid X receptor (Fxr) was decreased but pregnane X receptor (Pxr) was increased. Furthermore, the interventional experiments confirmed that FXR regulated Bcrp while PXR regulated Oatp2b1 and Mrp3. In summary, PEE could induce high bile acid level in maternal serum and its mechanism is associated with the high expression of BCRP/MRP3/OATP2B1 in the placenta through up-regulating PXR and down-regulating FXR, thereby leading to an excessive bile acid transport to maternal blood via the placenta. Our study provides a novel perspective in terms of placenta, explaining the increased maternal blood bile acids under the toxicity of PEE.
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