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BACKGROUND: While ambient air pollution has been associated with fetal growth in singletons, its correlation among twins is not well-established due to limited research in this area. METHODS: The effects of exposure to PM2.5 particulate matter and its main components during pregnancy on birth weight and the incidence of large for gestational age (LGA) were investigated in 6177 twins born after in vitro fertilization at the Center for Reproductive Medicine of Shanghai Ninth People's Hospital (Shanghai, China) between 2007 and 2021. Other birth weight-related outcomes included macrosomia, low birth weight, very low birth weight, and small for gestational age (SGA). The associations of PM2.5 exposure with birth weight outcomes were analyzed using linear mixed-effect models and random-effect logistic regression models. Distributed lag models were incorporated to estimate the time-varying associations. RESULTS: The findings revealed that an interquartile range (IQR) increase (18 µg/m3) in PM2.5 exposure over the entire pregnancy was associated with a significant increase (57.06 g, 95 % confidence interval [CI]: 30.91, 83.22) in the total birth weight of twins. The effect was more pronounced in larger fetuses (34.93 g, 95 % CI: 21.13, 48.72) compared to smaller fetuses (21.77 g, 95 % CI: 6.94, 36.60) within twin pregnancies. Additionally, an IQR increase in PM2.5 exposure over the entire pregnancy was associated with a 34 % increase in the risk of LGA (95 % CI: 11 %, 63 %). Furthermore, specific chemical components of PM2.5, such as sulfate (SO42-), exhibited effect estimates comparable to the PM2.5 total mass. CONCLUSION: Overall, the findings indicate that exposures to PM2.5 and its specific components are associated with fetal overgrowth in twins.

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The human immunodeficiency virus (HIV) heavily affects women from resource-limited settings who are vulnerable to potentially harmful mycotoxins including aflatoxin B1 (AFB1), fumonisin B1 (FB1) and ochratoxin A (OTA). We aimed to conduct biomonitoring and ascertain the determinants of maternal mycotoxin exposure in pregnancy, lactation and post-lactation periods. We conducted a retrospective longitudinal study in HIV-infected and HIV-uninfected women from Harare, Zimbabwe. 175 and 125 random urine samples in pregnancy and 24 months after delivery (post-lactation) respectively were analysed for aflatoxin M1 (AFM1) and FB1 by ELISA. 6 weeks after delivery (lactation), 226 and 262 breast milk (BM) samples were analysed for AFM1 and OTA respectively by ELISA. The association of demographics and food consumption with mycotoxins was evaluated using multivariable logistic regression. In HIV-infected, urinary AFM1 was detected in 46/94 (Median: 0.05; Range: 0.04-0.46 ng mL-1) in pregnancy and 47/66 (Median: 0.05; Range: 0.04-1.01 ng mL-1) post-lactation. Urinary FB1 was detected in 86/94 (Median: 1.39; Range: 0.17-6.02 ng mL-1) in pregnancy and 56/66 (Median: 0.72; Range: 0.20-3.81 ng mL-1) post-lactation. BM AFM1 was detected in 28/110 (Median: 7.24; Range: 5.96-29.80 pg mL-1) and OTA in 11/129 (Median: 0.20; Range: 0.14-0.65 ng mL-1). In HIV-uninfected, urinary AFM1 was detected in 48/81 (Median: 0.05; Range: 0.04-1.06 ng mL-1) in pregnancy and 41/59 (Median: 0.05; Range: 0.04-0.52 ng mL-1) post-lactation. Urinary FB1 was detected in 74/81 (Median: 1.15; Range: 0.17-6.16 ng mL-1) in pregnancy and 55/59 (Median: 0.96; Range: 0.20-2.82 ng mL-1) post-lactation. BM AFM1 was detected in 38/116 (Median: 7.70; Range: 6.07-31.75 pg mL-1) and OTA in 4/133 (Median: 0.24; Range: 0.18-0.83 ng mL-1). Location, wealth, and peanut butter consumption were determinants of AFB1 exposure. HIV infection, BMI, location, rainy season, unemployment, and age were determinants of FB1 exposure. Women especially those pregnant and/or HIV-infected are at risk of adverse effects of mycotoxins.

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BACKGROUND: Previous studies indicated that excessive engagement in digital devices could lead to negative psychological impacts in general population. We aimed to determine the association of electronic screen exposure with depression among women in early pregnancy. METHODS: A cross-sectional study was conducted from June 2021 to June 2022. A total of 665 women in early pregnancy were recruited and the information included socio-demographic characteristics, screen exposure and Patient Health Questionnaire - 9 depression scale. RESULTS: Among the women in early pregnancy, the total daily smartphone viewing time was the longest (median [P25-P75], 5 [3-6] hours/day) in the three types of electronic screen exposure. The total daily smartphone viewing time (P = 0.015, OR[95%CI] = 1.09[1.11-1.18]), smartphone (P = 0.016, OR[95%CI] = 1.24[1.04-1.47]) and television viewing time (P = 0.006, OR[95%CI] = 1.35[1.09-1.67]) before nocturnal sleep were significantly associated with depression among women in early pregnancy. The thresholds calculated by receiver operator characteristic curves were 7.5 h/day, 1.5 h/day and 1.5 h/day, respectively. In addition, women with higher scores of smartphone addiction were more susceptible to depression (P<0.001, OR[95%CI] = 1.11[1.07-1.16]). The top three smartphone usages in women with depression were watching videos (22.0%), listening to music (20.9%) and playing games (16.7%). CONCLUSIONS: In conclusion, electronic screen exposure, including screen viewing time, smartphone addiction and problematic smartphone use was associated with depression among women in early pregnancy. Further studies are warranted to verify the conclusions.

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BACKGROUND: Alkylphenols can originate from numerous products containing alkylphenol ethoxylates, including cleaning products, household items, and cosmetics. Some phenols, such as nonylphenol, are known to be endocrine disruptors, and exposure to them is thought to have contributed to the recent increase in allergic diseases such as asthma. However, the impacts of prenatal phenol exposure on asthma development in children are still unclear. METHODS: We analyzed the association between maternal urinary phenol concentrations during early pregnancy and the development of asthma in children at the age of 4, using data from the Japan Environment and Children's Study (JECS), a large-scale nationwide birth cohort study. RESULTS: We recruited 3,513 pairs of mothers and children participating in the Sub-Cohort Study of JECS. We measured 24 phenols, including nitrophenol, parabens, bisphenol, octylphenol, and nonylphenol, in urine samples taken during the first trimester of pregnancy. The urinary levels of these phenols differed markedly, and some showed a broad spectrum of distribution. Methylparaben was detected at high levels in almost every participant (267.7 ng/ml, standard deviation 433.78). Logistic regression analysis revealed that the odds ratio of asthma onset for high exposure to butylparaben was 1.54 (95% confidence interval: 1.11-2.15). Additionally, logistic regression analysis by gender revealed an asthma development odds ratio of 2.09 (95% confidence interval: 1.20-3.65) for males and 0.65 (95% confidence interval: 0.25-1.70) for females born to mothers in whom 4-nonylphenol was detected, suggesting a gender difference. CONCLUSION: Our current analysis using large cohort data suggests that high exposure to butylparaben and low exposure to 4-nonylphenol during pregnancy are risk factors for asthma development in children. These findings establish a valuable foundation for formulating recommendations about prenatal phenol exposure.

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OBJECTIVE: We review the prevalence of allergic diseases in children across prenatal exposures to heavy metals. METHODS: This systematic review and meta-analysis is registered in the PROSPERO database (CRD42023478471). A comprehensive search of PubMed, Web of Science, Medline and Cochrane library was conducted from the database inception until 31 October 2023. The Newcastle-Ottawa Quality Assessment Scale (NOS) was used to assess the quality of included studies. We used a random-effects model to summarize the effects from the studies. RESULTS: A total of 16 studies were included, 120,065 mother-child pairs enrolled. The NOS scores indicated that the quality of the literature included in the study was of a high standard. CONCLUSION: The final results indicate that prenatal exposure to Pb increased the incidence of wheeze and Eczema in infants, and exposure to Ni and CD increased the incidence of AD in infants.

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Bisphenol A (BPA) is a phenolic chemical that has been found to be associated with human health outcomes. It is one of the risk factors for thyroid function. Pregnancy is a vulnerable window for thyroid problems, because of the fluctuations in hormone levels. This review aimed to evaluate the association between BPA exposure and thyroid function during pregnancy. We conducted a comprehensive search of relevant databases, including PubMed, Scopus, Embase, Web of Science, and the Cochrane Library, for original studies published in English that reported data on BPA levels and thyroid-related hormone levels in pregnant women. We used the Newcastle-Ottawa Scale (NOS) to assess the methodological quality of the studies and the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) method to evaluate the quality of evidence. In total, 11 studies involving 6526 individuals were included in this systematic review. These studies explored fluctuations in thyroid-related hormones, including TSH, TT3, TT4, FT3, and FT4 levels, as well as the TT4/TT3 and FT4/FT3 ratios. The systematic review is to evaluate the evidences between bisphenol A exposure and thyroid-related hormones in pregnant women. We found that BPA exposure in pregnancy might disturb the homeostasis of maternal thyroid-related hormones and suggest an increased risk of hyperthyroidism. Further studies based on the findings are required to explore the underlying mechanisms and determine the potential effects of BPA exposure on thyroid function during pregnancy.

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Nanoplastics (NPs) have been commonly detected in aquatic ecosystems, and their negative effects on aquatic organisms have raised concerns in the scientific community and general public. The acute toxicity, neurotoxicity, and metabolic toxicity induced by NPs on fishes have been reported by many studies, although less attention has been focused on how mother exposed to NPs affected their offspring in aquatic organisms. Here, female zebrafish (F0) were exposed to 0, 200 and 2000 µg/L polystyrene nanoplastics (PS-NPs) for 42 d, with their offspring (F1) reared in clear water until sexual maturity. The results showed that PS-NPs were detected in various organs of F0 and F1. PS-NPs exposure significantly decreased gonadal 17-estradiol (E2), while increasing testosterone (T) contents. Lower levels of cyp19a1a, lhr and erα expressions in the 2000 µg/L group were consistent with a reduced number of mature oocytes (MO), but an increase in perinucleolar oocytes (PO). Interestingly, the expression of vtg was only up-regulated by 200 µg/L PS-NPs. After exposure, the egg production was dramatically reduced, but the hatching rate and heartbeat of F1 embryos from treated females were significantly higher than those observed in females from the control group. Maternal PS-NPs exposure significantly decreased the E2 and T levels in F1 adults, while PS-NPs exposure significantly up-regulated the sox9a but down-regulated the foxl2a in F1 larvae of 30 days post fertilization (dpf). This study showed that PS-NPs caused reproductive toxicity by changing the hypothalamic-pituitary-gonadal (HPG) axis-related genes, impairing the reproductive capacity of female zebrafish, affecting the development and disrupting the endocrine function of F1. These results suggested that PS-NPs had adverse effects on fish reproductive system both in the directly exposed generation and in their unexposed offspring.

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While maternal exposure to high metal levels during pregnancy is an established risk factor for birth defects, the role of paternal exposure remains largely unknown. We aimed to assess the associations of prenatal paternal and maternal metal exposure and parental coexposure with birth defects in singletons. This study conducted within the Jiangsu Birth Cohort recruited couples in early pregnancy. We measured their urinary concentrations for 25 metals. A total of 1675 parent-offspring trios were included. The prevalence of any birth defects among infants by one year of age was 7.82%. Paternal-specific gravity-corrected urinary concentrations of titanium, vanadium, chromium, manganese, cobalt, nickel, copper, and selenium and maternal vanadium, chromium, nickel, copper, selenium, and antimony were associated with a 21-91% increased risk of birth defects after adjusting for covariates. These effects persisted after mutual adjustment for the spouse's exposure. Notably, when assessing the parental mixture effect by Bayesian kernel machine regression, paternal and maternal chromium exposure ranked the highest in relative importance. Parental coexposure to metal mixture showed a pronounced joint effect on the risk of overall birth defects, as well as for some specific subtypes. Our findings suggested a couple-based prevention strategy for metal exposure to reduce birth defects in offspring.

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PURPOSE: Considering that endocrine disruptors have certain effects on fetal growth, we conducted a systematic review of epidemiological literature to elucidate the correlation between exposure to endocrine-disrupting chemicals during pregnancy and the neurodevelopment of offspring. METHOD: We systematically explored PubMed, Web of Science, and CINAHL databases from inception to April 4, 2023. References from pertinent studies were reviewed, and data regarding the link between maternal prenatal EDC exposure and offspring neurological development were compiled. A domain-based approach was used to evaluate studies of neurodevelopmental effects in children ≤3 years old by two reviewers, including cognition, motor, behavior, language, and non-verbal ability. RESULTS: A comprehensive search yielded 45,373 articles, from which 48 articles, involving 26,005 mother-child pairs, met the criteria and were subsequently included in our analysis. The results revealed that EDC exposure during pregnancy had a significant impact on offspring neurobehavior development, especially in cognition, motor, and language. Our findings indicated adverse associations between prenatal exposure to metals and offspring cognition (before 12 months: ß coefficient: -0.28; 95 % CI, -0.50 to -0.06; 1-3 years old: ß coefficient: -0.55; 95 % CI: -1.08 to -0.02). Furthermore, metals (ß coefficient: -0.71; 95 % CI: -1.23 to -0.19) and phthalates (ß coefficient: -0.69; 95 % CI: -1.05 to -0.33) exposure exhibited detrimental effects on motor development from1-3 years old, while poly-fluoroalkyl substances were linked to the disruption of offspring language development (ß coefficient: -1.01; 95 % CI: -1.90 to -0.11) within this timeframe. Additionally, exposure to EDCs during pregnancy had a negative impact on cognition development among girls from 12 to 36 months of age (ß coefficient: -0.53; 95 % CI: -1.01 to -0.06). CONCLUSION: Prenatal exposure to EDCs, especially metals, phthalates and, poly-fluoroalkyl substances, was associated with disrupting the development of offspring neurobehavior in the short and long term. Additionally, cognitive development showed gender differences due to prenatal endocrine-disrupting chemicals exposure.

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STUDY QUESTION: What is the longitudinal association between gestational phthalate exposure and in vivo placental outcomes? SUMMARY ANSWER: Phthalates were adversely associated with placental microvasculature, stiffness, and presence of calcification, with different metabolites associated with different outcomes. WHAT IS KNOWN ALREADY: Phthalate exposure is ubiquitous and implicated as a contributor to adverse pregnancy outcomes, possibly through impacts on the placenta. STUDY DESIGN, SIZE, DURATION: A total of 303 women were recruited in early pregnancy and prospectively followed for up to eight visits across gestation in the Human Placenta and Phthalates study. PARTICIPANTS/MATERIALS, SETTING, METHODS: At each visit, women provided urine samples and underwent placental ultrasounds. Urine was analyzed for 18 metabolites of phthalates and replacements. We took the geometric mean of repeated measurements to reflect pregnancy-averaged phthalate or replacement exposure for each participant (n = 303). Placental microvasculature, stiffness, and microcalcification presence were quantified from ultrasounds at each visit. Higher scores reflected worse placental function for all measures. Generalized linear mixed models were created to estimate the association between pregnancy-averaged exposure biomarker concentrations and repeated outcome measurements for microvasculature and stiffness. Gestational age at the time of calcification detection was modeled using Cox proportional hazards models. MAIN RESULTS AND THE ROLE OF CHANCE: Monocarboxyisononyl phthalate and summed di(2-ethylhexyl) phthalate metabolites were associated with impaired microvasculature development, such that an interquartile range increase in concentration was associated with 0.11 standard deviation increase in the microvasculature ratio, indicating poorer vascularization (95% CI: 0.00, 0.22); 0.11 [95% CI: -0.01, 0.22], respectively. Monoethyl phthalate was associated with increased placental stiffness (0.09 [95% CI: -0.01, 0.19]) while summed di-iso-butyl phthalate metabolites and monobenzyl phthalate were associated with increased hazard of calcification detection (hazard ratios: 1.18 [95% CI: 0.98, 1.42]; 1.13 [95% CI: 0.96, 1.34]). LIMITATIONS, REASONS FOR CAUTION: Outcomes used in this study are novel and further investigation is needed to provide clinical context and relevance. WIDER IMPLICATIONS OF THE FINDINGS: We found evidence of associations between select phthalate biomarkers and various aspects of in vivo placental health, although we did not observe consistency across placental outcomes. These findings could illustrate heterogeneous effects of phthalate exposure on placental function. STUDY FUNDING/COMPETING INTEREST(S): This research was supported in part by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (ZIA ES103344), and NIEHS T32ES007018. The authors declare that they have no competing interests to disclose. The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention. Use of trade names is for identification only and does not imply endorsement by the CDC, the Public Health Service, or the US Department of Health and Human Services. TRIAL REGISTRATION NUMBER: N/A.

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In day-to-day living, individuals are exposed to various environmentally hazardous substances that have been associated with diverse diseases. Exposure to air pollutants can occur during breathing, posing a considerable risk to those with environmental health vulnerabilities. Among vulnerable individuals, maternal exposure can negatively impact the mother and child in utero. The developing fetus is particularly vulnerable to environmentally hazardous substances, with potentially greater implications. Among air pollutants, toluene is neurotoxic, and its effects have been widely explored. However, the impact of low-level toluene exposure in daily life remains unclear. Herein, we evaluated 194 mothers and infants from the Growing children's health and Evaluation of Environment (GREEN) cohort to determine the possible effects of early-life toluene exposure on the nervous system. Using Omics experiments, the effects of toluene were confirmed based on epigenetic changes and altered mRNA expression. Various epigenetic changes were identified, with upregulated expression potentially contributing to diseases such as glioblastoma and Alzheimer's, and downregulated expression being associated with structural neuronal abnormalities. These findings were detected in both maternal and infant groups, suggesting that maternal exposure to environmental hazardous substances can negatively impact the fetus. Our findings will facilitate the establishment of environmental health policies, including the management of environmentally hazardous substances for vulnerable groups.

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Dibutyl phthalate (DBP) is a widely-used plasticizer that is dispersed in various environments, causing significant pollution and health risks. The toxic mechanism of DBP has been discussed in recent years, while the susceptibility of mitochondrial DNA (mtDNA) to DBP exposure and the resulting damage remain unclear. In this study, maternal zebrafish were exposed to environmentally relevant concentration of DBP for 0, 2, 4, and 6 weeks. Results showed that DBP exposure impaired health status, leading to the reduced body length and weight, condition factor, hepatosomatic index, and gonadosomatic index. Furthermore, DBP exposure induced oxidative stress and ATP deficiency in the gill and liver in a time-dependent manner. The oxidized mtDNA (ox-mtDNA) levels in the D-loop and ND1 regions were assessed in different tissues, showing distinct response patterns. The high energy-consuming tissues such as heart, brain, gill, and liver exhibited elevated susceptibility to mitochondrial damage, with a rapid increase in ox-mtDNA levels in the short term. Conversely, in muscle, ovary, eggs, and offspring, ox-mtDNA gradually accumulated over the exposure period. Notably, the ox-mtDNA levels in the D-loop region of blood showed a prompt response to DBP exposure, making it convenient for evaluation. Additionally, decreased hatching rates, increased mortality, lipoperoxidation, and depressed swimming performance were observed in offspring following maternal DBP exposure, suggesting the inherited impairments of maternal mtDNA. These findings highlight the potential for ox-mtDNA to serve as a convenient biomarker for environmental contamination, aiding in ecological risk assessment and forewarning systems in aquatic environment.

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Environmental factors have long been known to play a role in the pathogenesis of congenital heart disease (CHD), but this has not been a major focus of research in the modern era. Studies of human exposures and animal models demonstrate that demographics (age, race, socioeconomic status), diseases (e.g., diabetes, hypertension, obesity, stress, infection, high altitude), recreational and therapeutic drug use, and chemical exposures are associated with an increased risk for CHD. Unfortunately, although studies suggest that exposures to these factors may cause CHD, in most cases, the data are not strong, are inconclusive, or are contradictory. Although most studies concentrate on the effects of maternal exposure, paternal exposure to some agents can also modify this risk. From a mechanistic standpoint, recent delineation of signaling and genetic controls of cardiac development has revealed molecular pathways that may explain the effects of environmental signals on cardiac morphogenesis and may provide further tools to study the effects of environmental stimuli on cardiac development. For example, environmental factors likely regulate cellular signaling pathways, transcriptional and epigenetic regulation, proliferation, and physiologic processes that can control the development of the heart and other organs. However, understanding of the epidemiology and risk of these exposures and the mechanistic basis for any effects on cardiac development remains incomplete. Further studies defining the relationship between environmental exposures and human CHD and the mechanisms involved should reveal strategies to prevent, diagnose, and treat CHD induced by environmental signals.

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With the widespread use of bisphenol A (BPA) analogs, their health risks have attracted attention. The effects of maternal BPA analogs exposure on glucose homeostasis in adult offspring and the underlying fetal origins require further exploration. Herein, we exposed pregnant mice to two types of BPA analogs─BPB and BPAF; we evaluated glucose homeostasis in adult offspring and maternal-fetal glucose transport by testing intraperitoneal glucose tolerance, determining glucose and glycogen contents, conducting positron emission tomography (PET)/computed tomography (CT), detecting expression of placental nutrient transport factors, and assessing placental barrier status. We observed that adult female offspring maternally exposed to BPB and BPAF exhibited low fasting blood glucose in adulthood, with even abnormal glucose tolerance in the BPAF group. This phenomenon can be traced back to the elevated fetal glucose induced by the increased efficiency of placenta glucose transport in late pregnancy. On the other hand, the expression of genes associated with vascular development and glucose transport was significantly altered in the placenta in the BPAF group, potentially contributing to enhanced fetal glucose. These findings provide preliminary insights into potential mechanisms underlying the disturbance of glucose metabolism in adult female offspring mice induced by maternal exposure to BPA analogs.

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Research on the association between maternal PM2.5 exposure and hypospadias risk in male offspring, particularly in highly polluted areas, has been limited and inconsistent. This study leveraged data from China's National Population-based Birth Defects Surveillance System spanning the years 2013 to 2019, and employed sophisticated machine learning models to estimate daily PM2.5 levels and other pollutants for mothers at a 1-km resolution and a 6-km buffer surrounding maternal residences. Multivariate logistic regression analyses were performed to evaluate the relationship between PM2.5 exposure and hypospadias risk. For sensitivity analyses, stratification analysis was conducted, and models for one-pollutant and two-pollutants, as well as distributed lag nonlinear models, were constructed. Of the 1194,431 boys studied, 1153 cases of hypospadias were identified. A 10 µg/m3 increase in maternal PM2.5 exposure during preconception and the first trimester was associated with an elevated risk of isolated hypospadias, with Odds Ratios (ORs) of 1.102 (95% CI: 1.023-1.188) and 1.089 (95% CI: 1.007-1.177) at the 1-km grid, and 1.122 (95% CI: 1.034-1.218) and 1.143 (95% CI: 1.048-1.246) within the 6-km buffer. Higher quartiles of PM2.5 exposure were associated with increased odds ratios compared to the lowest quartile. These findings highlight a significant association between PM2.5 exposure during the critical conception period and an elevated risk of isolated hypospadias in children, emphasizing the need for targeted interventions to reduce PM2.5 exposure among expectant mothers.

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BACKGROUND: We previously conducted a case-control study and found that exposure to electronic screen before nocturnal sleep was associated with hypertensive disorders in pregnancy (HDP). Hence, we carried out this cohort study aiming to identify the effects of screen exposure time on the incidence rate and severity of HDP. METHODS: A retrospective cohort study was conducted from January 2022 and July 2022 from three hospitals in Wuxi and Changzhou cities. A total of 732 women were recruited and the information included socio-demographic characteristics, screen exposure and outcomes. Generalized estimating equations and binary non-conditional logistic models were applied to multivariate analysis, calculating the odds ratios (ORs) and 95% confidence intervals (CIs) of screen exposure time. RESULTS: The duration order of total screen time was smartphone > computer > television, while the duration order of screen time before nocturnal sleep was smartphone > television > computer. Multivariate analyses showed that the susceptibility of HDP among women who exposed to television before nocturnal sleep was 81.5% percent higher than those not exposed (P = 0.018, OR[95%CI] = 1.815[1.106-2.981]). In addition, total daily exposure time of television in the third trimester of pregnancy significantly increased the severity of HDP (P = 0.021, OR[95%CI] = 3.641[1.213-10.927]). CONCLUSIONS: Based on this preliminary study, we would suggest that pregnant women do not watch television before nocturnal sleep. While in the third trimester of pregnancy, total exposure time of television should be limited. Investigations from other areas and experimental studies should be conducted to verify the conclusion.

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BACKGROUND: Orofacial clefts (OFC) are the most common congenital malformation of the craniofacial skeleton. Attempts have been made to correlate the components of maternal diet as triggers for the development or prevention of OFC. OBJECTIVE: To analyze nutritional status as a predictive factor for the development of cleft lip and palate in an Amazonian population. METHODS: A total of 152 mothers within 3 months of delivery were interviewed for comparison: 51 mothers of children with nonsyndromic cleft lip and palate (CLP) (study group) and 101 mothers of children without OFC (control group). A food frequency questionnaire was used to assess maternal nutrition and to analyze the influence of macro- and micronutrients on the possible predisposition or protection for CLP. RESULTS: The study group showed higher percentage of lipid intake than did the control group (p = 0.01). Among the participants with no family history of OFC, the study group had a higher percentage of lipid intake (p = 0.002) and lower vegetable intake (p = 0.037). Maternal micronutrient intake among the participants with a positive family history was lower in the study group for vitamins B2 (p = 0.03), B5 (p = 0.036), E (p = 0.03), and folate (p = 0.022). CONCLUSIONS: Nutritional analysis indicated that higher maternal lipid intake increased the likelihood of having offsprings with nonsyndromic CLP. Moreover, families with a history of OFC and low maternal folate intake showed heightened risk of nonsyndromic CLP in their offsprings.

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Metformin use in pregnancy is increasing worldwide. Unlike insulin, metformin crosses the placenta. Consequently, maternal and fetal concentrations are comparable. Teratogenic effects are not reported, nor are adverse pregnancy outcomes. Reduced risk of hypertensive disorders, hypoglycemia, and macrosomia are potential benefits, together with lower gestational weight gain. Although metformin has been prescribed for pregnant women during the last 40 years, long-term data regarding offspring outcomes are still lacking. Independent of maternal glycemic control, recent meta-analyses report lower birthweight but accelerated postnatal growth and higher body mass index in metformin-exposed children. The longest follow-up study of placebo-controlled metformin exposure in utero found an increased prevalence of central adiposity and obesity among children 5-10 years old. Recently, a Danish study reported a threefold increased risk of genital anomalies in boys, whose fathers used metformin around the time of conception. This commentary addresses the current controversies on metformin use in pregnancy.

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BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) are endocrine disruptors resulting from incomplete combustion. Pregnancy represents a particularly vulnerable period to such exposures, given the significant influence of hormone physiology on fetal growth and pregnancy outcomes. Maternal thyroid hormones play crucial roles in fetal development and pregnancy outcomes. However, limited studies have examined gestational PAH exposure and maternal thyroid hormones during pregnancy. METHODS: Our study included 439 women enrolled in the LIFECODES birth cohort in Boston, aiming to explore the relationship between urinary PAH metabolites and thyroid hormones throughout pregnancy. Urine samples for PAH metabolite analysis and plasma samples for thyroid hormone were measured up to four visits throughout gestation. Single pollutant analyses employed linear mixed effect models to investigate individual associations between each PAH metabolite and thyroid hormone concentration. Sensitivity analyses were conducted to assess potential susceptibility windows and fetal-sex-specific effects of PAH exposure. Mixture analyses utilized quantile g-computation to evaluate the collective impact of eight PAH metabolites on thyroid hormone concentrations. Additionally, Bayesian kernel machine regression (BKMR) was employed to explore potential non-linear associations and interactions between PAH metabolites. Subject-specific random intercepts were incorporated to address intra-individual correlation of serial measurements over time in both single pollutant and mixture analyses. RESULTS: Our findings revealed positive trends in associations between PAH metabolites and thyroid hormones, both individually and collectively as a mixture. Sensitivity analyses indicated that these associations were influenced by the study visit and fetal sex. Mixture analyses suggested non-linear relationships and interactions between different PAH exposures. CONCLUSIONS: This comprehensive investigation underscores the critical importance of understanding the impact of PAH exposures on thyroid hormone physiology during pregnancy. The findings highlight the intricate interplay between environmental pollutants and human pregnancy physiology, emphasizing the need for targeted interventions and public health policies to mitigate adverse outcomes associated with prenatal PAH exposure.

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BACKGROUND: Maternal solvent exposure has been suspected to increase offspring cancer risk. The study aimed to evaluate the associations between maternal residential exposure to solvents from industrial pollution during pregnancy and childhood cancer. METHODS: The present study included 15,744 cancer cases (aged 0-19 years at diagnosis) identified from California Cancer Registry and 283,141 controls randomly selected from California Birth Registry (20:1 frequency-matched by birth year: 1998-2016). We examined industrial releases of tetrachloroethylene and 1,1,1-trichloroethane within 3 km of the birth address, while we used a 5 km buffer for carbon disulfide. We calculated the total exposure from all linked Toxic Release Inventory sites during each index pregnancy and assigned "ever/never" and "high/low exposed/unexposed" exposure, using median values. We performed quadratic decay models to estimate cancer risks associated with maternal solvent exposure in pregnancy. RESULTS: 1,1,1-Trichloroethane was associated with rhabdomyosarcoma (adjusted Odds Ratio (aOR): 1.96; 95% Confidence Interval (CI): 1.16, 3.32) in the "ever exposed" group. Ever exposure to carbon disulfide was associated with increased risks of medulloblastoma (OR = 1.85, 95% CI 1.01, 3.40) and ependymoma (OR = 1.63, 95% CI 0.97, 2.74). CONCLUSIONS: Overall, our findings suggested maternal residential exposure to solvents from industrial sources might be associated with elevated childhood cancer risks.

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