Effect of thyroid disruption on ovarian development following maternal exposure to Bisphenol S.

Thyroid hormones play a crucial role in numerous physiological processes, including reproduction. Bisphenol S (BPS) is a structural analog of Bisphenol A known for its toxic effects. Interference of this substitute with normal thyroid function has been described. To investigate the effect of thyroid disruption on ovarian development following maternal exposure to BPS, female rats were exposed, daily, to either AT 1-850 (a thyroid hormone receptor antagonist) (10 nmol/rat) or BPS (0.2 mg/kg) during gestation and lactation. The effects on reproductive outcome, offspring development, histological structures, hormone levels, oxidative status, cytoskeleton proteins expression, and oocyte development gene expression were examined. Our results are in favor of offspring ovarian development disruption due to thyroid disturbance in adult pregnant females. During both fetal and postnatal stages, BPS considerably altered the histological structure of the thyroid tissue as well as oocyte and follicular development, which led to premature ovarian failure and stimulation of oocyte atresia, being accompanied with oxidative stress, hypothalamic-pituitary-ovarian axis disorders, and cytoskeletal dynamic disturbance. Crucially, our study underscores that BPS may induce reproductive toxicity by blocking nuclear thyroid hormone receptors, evidenced by the parallelism and the perfect meshing between the data obtained following exposure to AT 1-850 and those after the treatment by this substitute.

The Effect of Various Environmental Pollutants on the Reproductive Health in Children: A Brief Review of the Literature.

PURPOSE OF REVIEW: Environmental pollutants in air, water, soil, and food are a significant concern due to their potential adverse effects on fetuses, newborns, babies, and children. These chemicals, which pass to fetuses and babies through trans-placental transfer, breast milk, infant formula, dermal transfer, and non-nutritive ingestion, can cause health problems during childhood. This review aims to discuss how exposure to various environmental pollutants in early life stages can disrupt reproductive health in children. RECENT FINDINGS: Environmental pollutants can affect Leydig cell proliferation and differentiation, decreasing testosterone production throughout life. This may result in cryptorchidism, hypospadias, impaired semen parameters, and reduced fertility. Although many studies on female reproductive health cannot be interpreted to support causal relationships, exposure to pollutants during critical windows may subsequently induce female reproductive diseases, including early or delayed puberty, polycystic ovary syndrome, endometriosis, and cancers. There is growing evidence that fetal and early-life exposure to environmental pollutants could affect reproductive health in childhood. Although diet is thought to be the primary route by which humans are exposed to various pollutants, there are no adopted nutritional interventions to reduce the harmful effects of pollutants on children's health. Therefore, understanding the impact of environmental contaminants on various health outcomes may inform the design of future human nutritional studies.

Postnatal Exposure to the Endocrine Disruptor Dichlorodiphenyltrichloroethane Affects Adrenomedullary Chromaffin Cell Physiology and Alters the Balance of Mechanisms Underlying Cell Renewal.

Dichlorodiphenyltrichloroethane (DDT) is a wide-spread systemic pollutant with endocrine disrupting properties. Prenatal exposure to low doses of DDT has been shown to affect adrenal medulla growth and function. The role of postnatal exposure to DDT in developmental disorders remains unclear. The aim of the present investigation is to assess growth parameters and the expression of factors mediating the function and renewal of chromaffin cells in the adult adrenal medulla of male Wistar rats exposed to the endocrine disruptor o,p'-DDT since birth until sexual maturation. The DDT-exposed rats exhibited normal growth of the adrenal medulla but significantly decreased tyrosine hydroxylase production by chromaffin cells during postnatal period. Unlike the control, the exposed rats showed enhanced proliferation and reduced expression of nuclear ß-catenin, transcription factor Oct4, and ligand of Sonic hedgehog after termination of the adrenal growth period. No expression of pluripotency marker Sox2 and absence of Ascl 1-positive progenitors were found in the adrenal medulla during postnatal ontogeny of the exposed and the control rats. The present findings indicate that an increase in proliferative activity and inhibition of the formation of reserve for chromaffin cell renewal, two main mechanisms for cell maintenance in adrenal medulla, in the adult DDT-exposed rats may reflect a compensatory reaction aimed at the restoration of catecholamine production levels. The increased proliferation of chromaffin cells in adults suggests excessive growth of the adrenal medulla. Thus, postnatal exposure to DDT alters cell physiology and increases the risk of functional insufficiency and hyperplasia of the adrenal medulla.

Early Developmental Exposure to Triclosan Impacts Fecal Microbial Populations, IgA and Functional Activities of the Rat Microbiome.

Triclosan (TCS), a broad-spectrum antibacterial chemical, is detected in human urine, breast milk, amniotic fluid, and feces; however, little is known about its impact on the intestinal microbiome and host mucosal immunity during pregnancy and early development. Pregnant female rats were orally gavaged with TCS from gestation day (GD) 6 to postpartum (PP) day 28. Offspring were administered TCS from postnatal day (PND) 12 to 28. Studies were conducted to assess changes in the intestinal microbial population (16S-rRNA sequencing) and functional analysis of microbial genes in animals exposed to TCS during pregnancy (GD18), and at PP7, PP28 and PND28. Microbial abundance was compared with the amounts of TCS excreted in feces and IgA levels in feces. The results reveal that TCS decreases the abundance of Bacteroidetes and Firmicutes with a significant increase in Proteobacteria. At PND28, total Operational Taxonomic Units (OTUs) were higher in females and showed correlation with the levels of TCS and unbound IgA in feces. The significant increase in Proteobacteria in all TCS-treated rats along with the increased abundance in OTUs that belong to pathogenic bacterial communities could serve as a signature of TCS-induced dysbiosis. In conclusion, TCS can perturb the microbiome, the functional activities of the microbiome, and activate mucosal immunity during pregnancy and early development.

Exposure to chlorpyrifos and pyrethroid insecticides and symptoms of Attention Deficit Hyperactivity Disorder (ADHD) in preschool children from the Odense Child Cohort.

BACKGROUND: Attention Deficit Hyperactivity Disorder (ADHD) is a common childhood psychiatric disorder with severe and lifelong impact on mental health and socioeconomic achievements. Environmental factors may play a role in the increasing incidens rates. Previous studies on associations between prenatal and childhood exposure to organophosphate and pyrethroid insecticides and ADHD symptoms have yielded mixed findings. OBJECTIVES: To investigate associations between prenatal and childhood exposure to chlorpyrifos and pyrethroids and ADHD symptoms in 5-year-old children from the Odense Child Cohort. METHODS: Spot urine samples from pregnant women in gestational week 28 (n = 614) and offspring at 5 years of age (n = 814) were collected and analyzed for the specific metabolite of chlorpyrifos, TCPY (3,5,6-trichloro-2-pyridinol), as well as the generic pyrethroid metabolite, 3-PBA (3-phenoxybenzoic acid). Offspring ADHD symptoms were assessed at age 5 years using the parent reported "ADHD scale" from the "Child Behavior Checklist 1½-5" (n = 1114). Associations between insecticide exposure variables and an ADHD score ≥90th percentile were analyzed using logistic regression for all children and stratified by sex. RESULTS: Most pregnant women had detectable concentrations of 3-PBA (93%) and TCPY (91%) with median concentrations of 0.20 µg/L and 1.62 µg/L, respectively. In children, 3-PBA and TCPY concentrations were detectable in 88% and 82% of the samples, and the median concentrations were 0.17 and 1.16 µg/L. No statistically significant associations were observed between insecticide metabolites and an ADHD score ≥90th percentile at age 5. CONCLUSION: In this relatively large Danish birth cohort study with mainly low dietary insecticide exposure, we found no statistically significant associations between prenatal or childhood exposure to chlorpyrifos or pyrethroids, and excess ADHD-symptom load, in 5-year-old children. Prospective studies with multiple urine samples across vulnerable windows of neurodevelopment is warranted to improve assessment of safe exposure levels, which is particularly relevant for pyrethroids, since their use is increasing.

Early-Life Exposure to Perfluoroalkyl Substances (PFAS) and Child Language and Communication Development: A Systematic Review.

Language development starts during the fetal period when the brain is sensitive to endocrine disruptions from environmental contaminants. This systematic review aims to systematically summarize the existing literature on early-life exposure to PFAS and children's language and communication development, which is an indicator of neurocognitive development. A structured literature search was conducted using three databases, PubMed, Scopus, and CINAHL, last updated in April 2023. The population was defined as children and young adults. PFAS exposure was assessed pre- or postnatally. The outcome was defined as a language and communication ability assessed with validated instruments, parental self-reports, or clinical language disorder diagnoses. In total, 15 studies were identified for subsequent analyses. Thirteen were performed in background-exposed populations and two in highly exposed populations. There were some indications of potential adverse effects; however, these were not consistent across child sex, age of assessment, or PFAS exposure levels. No systematic effect of early-life PFAS exposure on language and communication development was found. These inconclusive findings may partly be explained by the use of general test instruments with limited validity as to children's language and communication development. Further studies over a wider exposure range using specific language test instruments are needed.

Association of prenatal and postnatal exposure to some endocrine-disrupting chemicals with birth and neurodevelopmental outcomes: an extensive review.

Endocrine-disrupting chemicals (EDCs) are natural or human-made chemicals that can mimic, block, or interfere with the body's hormones. The most common and well-studied EDCs are bisphenol A, phthalate, and persistent organic pollutants, including polychlorinated biphenyls, polybrominated diphenyl ethers, per- and polyfluoroalkyl substances, other brominated flame retardants, organochlorine pesticides, dioxins, and furans. Humans are constantly exposed to EDCs through air, diet, skin, and water starting from embryonic life. Fetuses and newborns set up crucial developmental processes allowing adaptation to the environment throughout life. They are extremely sensitive to very low doses of EDCs because they are developing organisms. Many EDCs can cross the placental barrier and reach the developing internal organs of the fetus during the prenatal period. Also, newborn babies can be exposed to EDCs through breastfeeding or infant formula feeding during the postnatal period. Prenatal and postnatal exposures to EDCs may increase the risk of childhood diseases by disrupting hormone-mediated processes that are critical for growth and development during gestation and infancy. This review discusses evidence examining the relationship between prenatal and postnatal exposure to several EDCs with children's birth and neurodevelopmental outcomes. The available evidence suggests that prenatal and postnatal exposure to some EDCs cause fetal growth restriction, preterm birth, low birth weight, and neurodevelopmental problems by a variety of mechanisms of action. Given the adverse effects of EDCs on child development, further studies are needed to clarify the overall association.

Sex-specific associations of maternal and childhood urinary arsenic levels with emotional problems among 6-year-age children: Evidence from a longitudinal cohort study in China.

BACKGROUND: Arsenic exposure has been linked to neurobehavior development disorders among children in cross-sectional studies, but there is little information on the effects of prenatal and childhood arsenic exposure on childhood behavior problem, especially emotional problems. OBJECTIVE: To explore the relationship between prenatal and childhood arsenic exposure and behavior problems among six-year-old children. METHODS: 389 mother-child pairs from a longitudinal birth cohort were enrolled in the study. The concentrations of arsenic in maternal and 6-year-old children's urine were measured using inductively coupled plasma mass spectrometry (ICP-MS). Neurobehavioral development in 6-year-old children was assessed by Child Behavior Checklist (CBCL). Generalized linear regression models were used to relate arsenic exposure to the score of different domains in CBCL. RESULTS: The median concentrations of maternal and 6-year-old children's urinary arsenic were 22.22 and 33.86 µg/L, respectively. After adjusting for potential covariates, natural logarithm transformed concurrent urinary arsenic levels were significantly associated with scores of anxious and depressed problems in 6-year-old girls (ß = 0.71, 95% CI: 0.12-1.31, p = 0.018). Furthermore, in terms of the trajectory of arsenic exposure, compared with the "consistently low" group, the "low to high" group (ß = 2.73, 95% CI: -3.99 to 9.45, p = 0.425) had a greater effect on total score of CBCL than "high to low" group (ß = -0.93, 95% CI: -7.22 to 5.36, p = 0.771) in girls, although insignificant. CONCLUSIONS: Our results suggested that concurrent arsenic exposure might have an adverse effect of emotional status in girls. Further studies are needed to verify the findings and explore the mechanisms of the sex-specific association.

Postnatal methylmercury exposure and neurodevelopmental outcomes at 7 years of age in the Seychelles Child Development Study Nutrition Cohort 2.

BACKGROUND: Consumption of fish yields many nutritional benefits, but also results in exposure to methylmercury (MeHg). The developing brain is known to be particularly susceptible to MeHg toxicity in high doses. However, the potential impact of low-level environmental exposure from fish consumption on children's neurodevelopment remains unclear. METHODS: We investigated postnatal MeHg exposure at 7 years and its association with a battery of 17 neurodevelopmental outcomes in a subset of children (n = 376) from 1535 enrolled mother-child pairs in Nutrition Cohort 2 of the Seychelles Child Development Study (SCDS NC2). Each outcome was modeled in relation to postnatal MeHg exposure using linear regression, adjusting for prenatal MeHg exposure, levels of maternal polyunsaturated fatty acids (PUFA), and several other covariates known to be associated with neurodevelopmental outcomes. RESULTS: Median postnatal MeHg exposure at 7 years was 2.5 ppm, while the median prenatal MeHg exposure was 3.5 ppm. We found no statistically significant associations between postnatal MeHg exposure and any of the 17 neurodevelopmental outcomes after adjusting for prenatal MeHg exposure and other covariates. CONCLUSIONS: These findings are consistent with previous cross-sectional analyses of the SCDS Main Cohort. Continued follow-up of the entire NC2 cohort at later ages with repeated exposure measures is needed to further confirm these findings.

Relationship between prenatal and postnatal exposure to BPA and its analogues (BPS, BPF) and allergic diseases.

Bisphenols, endocrine disrupting chemicals, are widely used in daily life. Continued exposure during key developmental periods of life (pregnancy, infancy and early childhood) can contribute to adverse health consequences such as decreased lung function, wheezing/asthma, the occurrence of allergies or changes in immune system responses. The purpose of this review is to present the current state of knowledge on the effects of prenatal or postnatal exposure to bisphenol A (BPA), bisphenol S (BPS) and bisphenol F (BPF) on the development of allergic diseases in childhood. A com- prehensive and systematic search of PubMed, Scopus and Web of Science databases was conducted. The review is restricted to studies published since 2015, in English in peer-reviewed journals. Based on keywords, 2648 studies were identified and reviewed for eligibility. Finally, 8 epidemio- logical studies were found to be appropriate for inclusion in this publication. The data collected in this review suggests that there is an associa- tion between maternal exposure during pregnancy or childhood to BPA and the development of allergic diseases. Most studies reported positive relationships between BPA exposure and at least one of the types of allergic disease. The paucity of studies and the observed differences in findings regarding the association between prenatal/postnatal exposure to BPS and/or BPF do not allow firm conclusions to be drawn. Further research is needed to identify the vulnerable population and the mechanisms responsible for the development of undesirable health consequences. Int J Occup Med Environ Health. 2023;36(5):575-86.

The influence of environmental particulate matter exposure during late gestation and early life on the risk of neurodevelopmental disorders: A systematic review of experimental evidences.

Particulate matter (PM) is a major component of ambient air pollution (AAP), being widely associated with adverse health effects. Epidemiological and experimental studies point towards a clear implication of AAP on the development of central nervous system (CNS) diseases. In this sense, the period of most CNS susceptibility is early life, when the CNS is maturing. In humans the last trimester of gestation is crucial for brain maturation while in rodents, due to the shorter gestational period, the brain is still immature at birth, and early postnatal development plays a significant role. The present systematic review provides an updated overview and discusses the existing literature on the relationship between early exposure to PM and neurodevelopmental outcomes in experimental studies. We included 11 studies with postnatal exposure and 9 studies with both prenatal and postnatal exposure. Consistent results between studies suggest that PM exposure could alter normal development, triggering impairments in short-term memory, sociability, and impulsive-like behavior. This is also associated with alterations in synaptic plasticity and in the immune system. Interestingly, differences have been observed between sexes, although not all studies included females. Furthermore, the developmental window of exposure seems to be crucial for effects to be observed in the future. In summary, air pollution exposure during development affects subjects in a time- and sex-dependent manner, the postnatal period being more important and being males apparently more sensitive to exposure than females. Nevertheless, additional experimental investigations should prioritize the examination of learning, impulsivity, and biochemical parameters, with particular attention provided to disparities between sexes.

Association between antibiotic exposure and adverse outcomes of children and pregnant women: evidence from an umbrella review.

BACKGROUND: Antibiotics are widely prescribed among children and pregnant women, but their safety profile is controversial. This study aimed to summarize and appraise current evidence for the potential impact of antibiotic exposure on pregnancy outcomes and children's health. METHODS: PubMed, Embase, Web of Science and the Cochrane Database of Systematic Reviews were searched from inception to June 2022. Meta-analyses of any study design comparing the impact of antibiotic exposure with nonexposure among children, pregnant women and prepregnant women on adverse health outcomes of children and pregnancy were retrieved. The quality of evidence was assessed by a Measurement Tool to Assess Systematic Reviews 2 (AMSTAR2) and the Grading of Recommendations, Assessment, Development and Evaluation (GRADE). Data were reanalyzed, and the credibility of the evidence was determined. RESULTS: Out of 2956 studies identified, 19 articles with 39 associations were included. Totally 19 of the associations (48.72%) were statistically significant with a P value ≤ 0.05, while only six were supported by highly suggestive evidence. Children with postnatal antibiotic exposure had a higher risk of developing asthma odds ratio (OR): 1.95, 95% confidence interval (CI): 1.76-2.17, wheezing (OR: 1.81, 95% CI 1.65-1.97) and allergic rhinoconjunctivitis (OR: 1.66, 95% CI 1.51-1.83), with prediction intervals excluding the nulls. Quality assessed by both AMSTAR2 and GRADE of included meta-analyses were very low in general. CONCLUSIONS: Antibiotic exposure in early life was associated with children's long-term health, especially in cases of allergic diseases. Prenatal exposure might also influence children's health in some aspects but requires more high-quality evidence. Potential adverse effects of antibiotics on pregnancy outcomes were not observed in our study. Studies with higher quality and better quantification of antibiotic exposure are needed in the future.

Early-life exposure to Saharan dust storms and adolescence functional disability: Evidence from Cameroon.

The direct link between early-life dust storm exposure and later-in-life outcomes is not fully understood. This study examines the association of functional disability in a large sample of adolescent Cameroonians (N = 112,855) with in-utero and early childhood exposure to Saharan dust storms. Adjusting all estimations for temperature, precipitation, time and location fixed-effects, and person and family sociodemographic characteristics, we documented adverse effects on functional disability in female adolescents due to exposure to dense dust storms during the third gestation trimester and the second postnatal trimester. We also found suggestive evidence that an effect exists for the first as well as the third through fifth postnatal trimesters. In the third trimester of gestation and the second postnatal trimester, exposure to an average length dust storm with PM10 levels beyond 190 µg/m3 increased the likelihood of disability among female adolescents by approximately 229 (95 % CI: 10-464) in 100,000. The size of the adverse effects for the other periods followed similar patterns. These results show the value of creating infrastructures to mitigate or adapt to the effects of dust storms. These endeavors should focus on communities and populations in and around the Sahara where international organizations can play a role. In addition, establishing health data infrastructures not only improves public health but also advances our understanding of the long-term effects of dust storms. This study demonstrates the importance of research on the long-term effects of early-life exposure to dust storms and the need for additional work on this topic.

Postnatal exposure to organic pollutants in maternal milk in north-western Spain.

Evaluation of postnatal exposure to organic pollutants is especially important for suckling infants during breastfeeding, a crucial perinatal growth period when organs and hormonal systems develop. We determined levels of 60 pollutants, including organochlorine pesticides (OCPs), organophosphorus pesticides (OPPs), pyrethroids (PYRs), polychlorinated biphenyls (PCBs), polycyclic aromatic hydrocarbons (PAHs), and polybrominated diphenyl ethers (PBDEs), in 81 breast milk samples from breastfeeding mothers from Santiago de Compostela (north-western Spain). For most detected organic pollutants, levels were correlated with the season of milk sampling, maternal age at delivery, and place of residence. Dietary consumption habits (eggs, molluscs, and vegetable oils) were also correlated with OCP, OPP, PCB, PBDE and PYR levels. We also assessed the risk to infant health of exposure to organic pollutants in breast milk. PAHs, OCPs, OPPs, and PYRs accounted for almost 95% of the targeted organic pollutants in the samples analysed.

Prenatal and postnatal exposure to PM2 .5 and the risk of tic disorders.

BACKGROUND: Tic disorders are common neurodevelopmental disorders during childhood. Whether prenatal and postnatal exposure to particulate matter with an aerodynamic diameter less than 2.5 µm (PM2.5 ) plays a role in the development of tic disorders remains unexplored. OBJECTIVES: To investigate the association of exposure between PM2.5 during the pregnancy and infancy periods and the risk of tic disorders. METHODS: This birth cohort study recruited singleton live births at term gestations in central Taiwan from the Taiwan Maternal and Child Health Database between 2004 and 2012 and followed up to the end of 2017. New cases of tic disorders were defined using the ICD-9-CM (307.2) and ICD-10-CM (F95), which include all tic spectrum disorders. We assigned daily PM2.5 concentrations derived from a satellite-based model to individuals based on maternal residential addresses at delivery. We fit Cox proportional hazard model and distributed lag non-linear model to estimate the associations between PM2.5 and tic disorders, with hazard ratio (HR) with 95% confidence interval (CI) as the effect measure. RESULTS: Of the 309,376 singleton live births at term gestations, we identified 5902 (1.9%) tic disorder cases. The HR of tic disorders was positively associated with a 10 µg/m3 increase in PM2.5 : during pregnancy HR 1.09, 95% CI 1.04, 1.15 and during infancy HR 1.12, 95% CI 1.06, 1.18. The vulnerable time window for infants with increased risk of tic disorders was 6-52 weeks after birth. We observed a nonlinear relationship between PM2.5 and the risk of tic disorders, with exposure to PM2.5 between 16 and 64 µg/m3 being associated with the risk of tic disorders. The association was restricted to Tourette's disorder group. Infant sex did not modify these associations. CONCLUSIONS: Infants delivered at term and exposed to PM2.5 are associated with an increased risk of tic disorders (6-52 weeks). Further studies are needed to confirm these associations.

Prenatal and postnatal exposure to polystyrene microplastics induces testis developmental disorder and affects male fertility in mice.

Polystyrene microplastics (PS-MPs) can threaten human health, especially male fertility. However, most existing studies have focused on the adulthood stage of male reproduction toxicity caused by relatively short-term PS-MP exposure. This study aimed to investigate the toxic effect of PS-MPs on testicular development and reproductive function upon prenatal and postnatal exposure. Pregnant mice and their offspring were exposed to 0, 0.5 mg/L, 5 mg/L, and 50 mg/L PS-MPs through their daily drinking water from gestational day 1 to postnatal day (PND) 35 or PND70. We found that PS-MP exposure induced testis development disorder by PND35 and spermatogenesis dysfunction by PND70. By combining RNA sequencing results and bioinformatics analysis, the hormone-mediated signaling pathway, G1/S transition of the mitotic cell cycle, coregulation of androgen receptor activity, and Hippo signaling pathway were shown to be involved in testis development on PND35. The meiotic cell cycle, regulation of the immune effector process, neutrophil degranulation, and inflammation mediated by chemokine and cytokine signaling pathways were associated with disturbed spermatogenesis on PND70. These findings show that prenatal and postnatal exposure to PS-MPs resulted in testis development disorder and male subfertility, which may be regulated by the Hippo signaling pathway and involve an immune reaction.

Changes in the histopathology and in the proteins related to the MAPK pathway in the brains of rats exposed to pre and postnatal radiofrequency radiation over four generations.

The development of new technologies and industry increases the number and variety of electromagnetic field (EMF) sources. Researcher are increasingly interested in the effects of EMF on brain health. The brain's function is largely dependent on electrical excitability, so it would be expected to be vulnerable to EMF. We therefore investigated the effects of brain development in the fetus, histopathological changes in female rats and the hippocampal level of MAPK proteins in male rats after exposed to pre and postnatal 2450 MHz continuous wave (CW) radiofrequency radiation (RFR) over four generations. Four groups; sham, irradiated female, irradiated male, irradiated male and female, with each consisting of four rats (one male and three females) were created. Rats in the exposure groups were whole-body exposed to 2450 MHz CW-RFR for 12 h/day during the experiment. Irradiation started one month before fertilization in the experimental group. On the 18th day of the gestational period, one pregnant rat from each group was decapitated under general anesthesia and the fetuses were taken. The remaining two pregnant rats completed the normal gestation period. When the offspring were two months old, four rats, one male and three female, were allocated for the second generation study. Next generation animals were also experienced the same processes as the first generation rats. This study were evaluated development of brain in fetuses and histopathological changes in brain of female rats using haematoxylin eosin staining, and the hippocampal level of MAPK proteins in brain of male rats by Western Bloting. We observed hemorrhagic areas, irregular cellular localization and vascular structures in the brain of fetal and adult female rat of exposed groups in the all generations. pERK, ptau, pJNK and pP38 were increased in the brain of adult male rat of exposed groups in the all generations (p < 0.005). Pre and postnatal 2450 MHz continuous wave radiofrequency radiation exposure may cause changes in the function of the MAPK pathway affecting cognitive processes such as learning and memory and may cause damage to both the fetus and adult brain tissue. Also, EMF may have potential to affect brain of future generations.

Evaluating postnatal exposure to six heavy metals in a Chinese e-waste recycling area.

This study is the first to assess postnatal exposure to heavy metals using breast milk in an electronic waste (e-waste) recycling area. From January to April 2021, 102 and 97 breastfeeding women were recruited from an e-waste recycling area and a control area, respectively. Four weeks after delivery, medical staff collected 20 mL of breast milk from each participant. The breast milk was tested for six heavy metals (lead, cadmium, chromium, arsenic, copper, and manganese) using inductively coupled plasma mass spectrometry (ICP-MS). The estimated daily intake (EDI) of infants during breastfeeding was calculated to assess the impact of postnatal exposure to heavy metals on infant health. The concentrations of chromium and lead in the breast milk were significantly higher in the e-waste recycling area than in the control area. Chromium concentrations in breast milk was 34.3%, exceeding the permissible limits set by the World Health Organization (WHO), in the e-waste recycling area, which is 16 times higher than that in the control areas. The EDIs of lead and chromium in the e-waste area were twice as those in the control area. This strongly indicates that the potential impact of postnatal exposure to lead and chromium on infant and child health in e-waste recycling areas cannot be ignored. Infants and children in e-waste recycling areas are at risk of long-term exposure to heavy metals. Therefore, ongoing health monitoring is necessary.

Sex-specific associations of early postnatal blood copper levels with neurodevelopment at 2 years of age.

Copper (Cu) is an essential trace element; however, it can be harmful in excess. Previous studies have shown that prenatal Cu levels may affect childhood neurodevelopment; however, studies focused on early postnatal Cu levels are limited. We studied 843 children born in Wuhan City and investigated the associations between early life Cu levels and neurodevelopment in 2-year-old children. Blood samples collected from children at 12 and 24 months of age were used to analyze Cu levels. Neurodevelopment was scored using the Bayley Scale of Children at 24 months of age. We found that a higher Cu level at 12 months of age was positively associated with mental development index (MDI) in boys (ß = 6.75, 95 %CI: 1.12, 12.38). Further non-linear analysis showed an inverted U-shape association between Cu level at 20 months and PDI in boys, indicating that Cu levels may have an optimal concentration for neurodevelopment (p for overall association = 0.01, p for non-linear association < 0.01). In addition, all meaningful results mentioned above were observed only in boys, and a statistically significant sex-related modifying effect was observed (p < 0.05). In conclusion, this study repeated measures early life Cu levels and suggested sex-specific associations between early life Cu levels and neurodevelopment in 2-year-old children.

The prenatal and postnatal effects of air pollution on asthma in children with atopic dermatitis.

OBJECTIVES: Air pollution is strongly associated with asthma, but has not been determined to induce new-onset asthma development in children with atopic dermatitis (AD). WORKING HYPOTHESIS: To assess whether prenatal/postnatal exposure to air pollutants triggers new-onset asthma development in children with AD. STUDY DESIGN: Retrospective cohort study. PATIENT-SUBJECT SELECTION: Data of patients 3% were significantly influenced by prenatal exposure to PM2.5 , especially SO2 , NO, and NO2 . CONCLUSIONS: Prenatal and postnatal exposure to air pollution have an association with asthma development in AD patients.