Prenatal exposure to social adversity and infant cortisol in the first year of life.

Exposure to social adversity has been associated with cortisol dysregulation during pregnancy and in later childhood; less is known about how prenatal exposure to social stressors affects postnatal cortisol of infants. In a secondary analysis of data from a longitudinal study, we tested whether a pregnant woman's reports of social adversity during the third trimester were associated with their infant's resting cortisol at 1, 6, and 12 months postnatal. Our hypothesis was that prenatal exposure to social adversity would be associated with elevation of infants' cortisol. Measures included prenatal survey reports of social stressors and economic hardship, and resting cortisol levels determined from infant saliva samples acquired at each postnatal timepoint. Data were analyzed using linear mixed effects models. The final sample included 189 women and their infants (46.56% assigned female sex at birth). Prenatal economic hardship was significantly associated with infant cortisol at 6 months postnatal; reports of social stressors were not significantly associated with cortisol at any time point. Factors associated with hardship, such as psychological distress or nutritional deficiencies, may alter fetal HPA axis development, resulting in elevated infant cortisol levels. Developmental changes unique to 6 months of age may explain effects at this timepoint. More work is needed to better comprehend the complex pre- and post-natal physiologic and behavioral factors that affect infant HPA axis development and function, and the modifying role of environmental exposures.

Maternal periodontitis potentiates monosodium glutamate-obesity damage on Wistar offspring's fast-glycolytic muscle.

OBJECTIVE: To evaluate the effects of magnifying the damage caused by obesity induced by monosodium glutamate, using a model of maternal periodontitis, on the structure of the anterior tibialis muscle of the offspring. MATERIALS AND METHODS: Twenty-four female Wistar rats were divided into four experimental groups: control (n = 6), obese (n = 6), control with periodontitis (n = 6) and obese with periodontitis (n = 6). At 78 days of life, the rats were mated with males without any experimental intervention. The offspring of these rats (n = 1/L), at 120 days of life, were weighed and measured, then euthanized. Plasma was collected for analysis of cytokines IL-6, IL-10, IL-17 and TNF-α. Adipose tissues were collected and weighed, and the anterior tibial muscle was designated for histomorphological analyses (n = 6/group). RESULTS: Monosodium glutamate offspring showed significant muscle changes, such as a reduction in the size of fibres and neuromuscular junctions, and an increase in the nucleus and capillaries. However, all these changes were more expressed in monosodium glutamate-obese with periodontitis offspring. CONCLUSION: This leads us to suggest a magnifying effect promoted by periodontitis to the damage already well described by monosodium glutamate-obesity, determined by low-intensity inflammation, causing greater muscle damage.

Prenatal exposure to environmental toxins and comprehensive dental findings in a population cohort of children.

Environmental toxins are known to have many impacts on growth and development in humans, starting in utero. Alterations in amelogenesis, caused by chemical and physical trauma that occur during the antenatal, perinatal and postnatal time periods, may result in developmental defects in deciduous and permanent tooth enamel, as demonstrated in animal studies. These defects can be clinically visible and result in a variety of morphological and functional problems in the dentition. Since enamel does not remodel after formation, it may serve as a permanent record of insults during organ development.Our primary purpose was to investigate any possible relationship between intrauterine exposure to endocrine disrupting chemicals (phenols and phthalates) and developmental defects in enamel in children, while also accounting for fluoride exposure. Our secondary purpose was to report descriptively on findings from comprehensive dental examinations performed on 356 children that were drawn from the general paediatric population. A cohort of children from the Utah Children's Project (N = 356) that had full medical exams, comprehensive medical and family histories and available biospecimens were given extraoral and intraoral examinations. They also completed an oral health questionnaire. Standardized intraoral photographs were taken of the teeth and viewed by standardised examiners and the dental observations were recorded for a full inventory of findings, including: tooth morphology, caries, restorations, colorations, attrition, erosion, fractures and hypomineralization. Perinatal maternal urine samples were assessed for the concentration of fluoride, phenols and phthalates, including bisphenol A (BPA).Pairwise statistical analyses were done to correlate the dental findings with one another and with the presence of environment chemicals found in the urine samples. Hypomineralization was the most common finding (96% of children; 37% of deciduous teeth, 42% of permanent teeth), consistent with molar incisor hypomineralization (MIH) described in other human populations. No consistent correlations were seen between dental findings and the presence of phenols and phthalates in prenatal urine, but the number of samples available for the assessment was limited (n = 35).In conclusion, we found a high proportion of dental hypomineralization in a population based paediatric cohort, but did not find an association with prenatal exposure to phenols and phthalates.

Maternal smoking during pregnancy and early childhood dental caries in children: a systematic review and meta-analysis.

BACKGROUND: Early childhood dental caries, or ECC, is a significant global oral health concern associated with various adverse outcomes. This systematic review and meta-analysis aimed to investigate the potential link between maternal smoking during pregnancy and the occurrence of dental caries in children. METHOD: Through a comprehensive search of PubMed, Scopus, and Google Scholar databases for studies examining the correlation between maternal smoking during pregnancy and childhood caries, we identified 609 relevant articles up to October 2023. Studies were selected, and data extraction was based on the pre-established eligibility criteria and items. Meta-analysis was executed utilizing Comprehensive Meta-analysis (CMA) with a random effects model, ensuring a robust synthesis of the gathered evidence. RESULT: 7 cohorts and five cross-sectional studies, totaling 12 studies, were included in our analysis. The combined results from the studies revealed a significant association between maternal smoking during pregnancy and an increased risk of dental caries in children (OR = 1.78, 95% CI = 1.55-2.05, I2 = 68.53). Sensitivity analyses confirmed the reliability of our results. However, there were indications of publication bias, as suggested by the funnel plot and Egger's test (P = 0.011) concerning the connection between prenatal smoking and childhood caries. CONCLUSION: This review underscores the association between maternal smoking during pregnancy and childhood dental caries. Nevertheless, confounding variables influence this link, necessitating more large-scale, longitudinal studies with adjusted factors. Additional randomized control trials are needed to validate these findings due to the observed heterogeneity. Future research should investigate the precise reasons behind this association. It is essential to raise awareness among pregnant women about the risks of smoking through educational programs.

Prenatal exposure to persistent organic pollutants and molar-incisor hypomineralization among 12-year-old children in the French mother-child cohort PELAGIE.

BACKGROUND: Exceptional episodes of exposure to high levels of persistent organic pollutants have already been associated with developmental defects of enamel among children, but knowledge is still scarce concerning the contribution of background levels of environmental contamination. METHODS: Children of the French PELAGIE mother-child cohort were followed from birth, with collection of medical data and cord blood samples that were used to measure polychlorinated biphenyls (PCBs), organochlorine pesticides (OCs), and perfluorinated alkyl substances (PFASs). At 12 years of age, molar-incisor hypomineralization (MIH) and other enamel defects (EDs) were recorded for 498 children. Associations were studied using logistic regression models adjusted for potential prenatal confounders. RESULTS: An increasing log-concentration of ß-HCH was associated with a reduced risk of MIH and EDs (OR = 0.55; 95% CI, 0.32-0.95, and OR = 0.65; 95% CI, 0.43-0.98, respectively). Among girls, intermediate levels of p,p'-DDE were associated with a reduced risk of MIH. Among boys, we observed an increased risk of EDs in association with intermediate levels of PCB 138, PCB 153, PCB 187, and an increased risk of MIH with intermediate levels of PFOA and PFOS. CONCLUSIONS: Two OCs were associated with a reduced risk of dental defects, whereas the associations between PCBs and PFASs and EDs or MIH were generally close to null or sex-specific, with an increased risk of dental defects in boys. These results suggest that POPs could impact amelogenesis. Replication of this study is required and the possible underlying mechanisms need to be explored.

Prenatal serotonin reuptake inhibitor antidepressant exposure, SLC6A4 genetic variations, and cortisol activity in 6-year-old children of depressed mothers: A cohort study.

Prenatal exposure to maternal depression and serotonin reuptake inhibitor (SRI) antidepressants both affect the development of the hypothalamic-pituitary-adrenal (HPA) system, possibly via the neurotransmitter serotonin (5HT). In a community cohort, we investigated the impact of two factors that shape prenatal 5HT signaling (prenatal SRI [pSRI] exposure and child SLC6A4 genotype) on HPA activity at age 6 years. Generalized estimating equation (GEE) models were used to study associations between cortisol reactivity, pSRI exposure, and child SLC6A4 genotype, controlling for maternal depression, child age, and sex (48 pSRI exposed, 74 nonexposed). Salivary cortisol levels were obtained at five time points during a laboratory stress challenge: arrival at the laboratory, following two sequential developmental assessments, and then 20 and 40 min following the onset of a stress-inducing cognitive/social task. Cortisol decreased from arrival across both developmental assessments, and then increased across both time points following the stress challenge in both groups. pSRI-exposed children had lower cortisol levels across all time points. In a separate GEE model, we observed a lower cortisol stress response among children with LG /S alleles compared with children with La/La alleles, and this was particularly evident among children of mothers reporting greater third trimester depressed mood. Our findings suggest that pSRI exposure and a genetic factor associated with modulating 5HT signaling shaped HPA reactivity to a laboratory stress challenge at school age.

Ontogeny of the Dyad: the Relationship Between Maternal and Offspring Neuroendocrine Function.

PURPOSE OF REVIEW: We review ontogeny of the maternal-offspring neuroendocrine relationship in human pregnancy. We present bidirectional genetic, physiological, and behavioral influences that enhance or disrupt HPA activity and its end product cortisol at the individual level and within the dyad. RECENT FINDINGS: Consistent evidence supports that maternal mood and caregiving behavior are associated with maternal and offspring cortisol levels. Select studies support the buffering effects of antidepressant use and maternal positive affect on offspring cortisol. Growing research highlights evocative effects of fetal neuroendocrine activity, antenatal gene transfer, and infant behavioral distress and risk characteristics on maternal cortisol levels and dyadic attunement. There is potential to advance our understanding of the mother-offspring neuroendocrine relationship by consideration of other neuroactive steroids in addition to cortisol, and to consider developmental timing and measurement source in study design. Future study should emphasize in what context or for whom neuroendocrine attunement is adaptive versus maladaptive for mother and child.

Prenatal lead exposure and childhood lung function: Influence of maternal cortisol and child sex.

INTRODUCTION: Maternal hypothalamic-pituitary-adrenal (HPA) axis disruption in pregnancy may contribute to the programming of childhood respiratory disease and may modify the effect of chemical toxins, like lead (Pb), on lung development. Child sex may further modify these effects. We sought to prospectively examine associations between maternal HPA axis disruption, prenatal Pb and childhood lung function and explore potential effect modification by maternal cortisol and child sex on the association between prenatal Pb and lung function outcomes. MATERIALS AND METHODS: Analyses included 222 mothers and children enrolled in a longitudinal birth cohort study in Mexico City. Maternal diurnal salivary cortisol was assessed in pregnancy; cortisol awakening response (CAR) and diurnal slope were calculated. Blood Pb was measured during the second trimester of pregnancy. Post-bronchodilator lung function was tested at ages 8-11 years. Associations were modeled using generalized linear models with interaction terms, adjusting for covariates. RESULTS: A higher (flatter) diurnal slope was associated with lower FEV1/FVC ratio (ß: 0.433, 95%CI [-0.766, -0.101]). We did not find any main effect associations between prenatal Pb and lung function outcomes. We report an interaction between Pb and cortisol in relation to FEV1/FVC and FEF25-75% (pinteraction<0.05 for all). Higher prenatal Pb was associated with reduced FEV1/FVC only in children whose mothers had a high CAR. Higher prenatal Pb was also associated with reduced FEV1/FVC and FEF25-75% in mothers with a flatter diurnal slope. A 3-way interaction between prenatal Pb, CAR and sex on FEV1/FVC, indicated that boys born to women with high CAR and higher prenatal Pb levels had lower FEV1/FVC ratios (pinteraction = 0.067). CONCLUSIONS: Associations between prenatal Pb and childhood lung function were modified by disrupted maternal cortisol in pregnancy and child sex. These findings underscore the need to consider complex interactions to fully elucidate effects of prenatal Pb exposure on childhood lung function.

How prenatal environmental factors affect rat molar enamel formation?

Amelogenin (AMELX) and ameloblastin (AMBN) are crucial for enamel formation, and interruptions in the production of these proteins may cause enamel defects. We investigated how prenatal environmental factors (chronic stress, bisphenol A (BPA), amoxicillin, and lipopolysaccharide (LPS)) affect AMELX and AMBN production of ameloblasts. Fifteen pregnant Sprague-Dawley rats were divided into four experimental groups and a control group. Chronic-stress group rats were exposed to a 12:12 light/light cycle (LL) from day E18 until delivery. BPA group rats were orally administered 5 µg/kg BPA daily from day E1 until delivery. Amoxicillin group rats were injected 100 mg/kg amoxicillin daily from day E18 until delivery. LPS-infection group rats were injected 125 µg/kg bacterial LPS once on day E18. Seven pups from the control group and ten pups from the experimental groups were euthanized on P10. Sections were stained with hematoxylin and eosin (H&E) and Gomori's one-step trichrome staining (GT) and incubated with rabbit polyclonal antibodies to AMELX and AMBN, to evaluate staining intensity at ameloblast stages. The surface morphology was evaluated with a stereomicroscope. AMELX (p = 0.008, p = 0.0001, p = 0.009) and AMBN (p = 0.002, p = 0.001, p = 0.0001) staining of all groups were significantly lower than that of the control group in the secretory, transitional, and maturation stages. Abnormal enamel matrix formation was observed in the H&E and GT staining sections of all experimental groups. Yellowish coloration of the amoxicillin group was observed in morphologic evaluation.

The effects of prenatal and lactational bisphenol A and/or di(2-ethylhexyl) phthalate exposure on female reproductive system.

Bisphenol A (BPA) and di(2-ethylhexyl) phthalate (DEHP) are endocrine disrupting chemicals (EDCs) that are abundantly used in polyvinyl chloride plastics, polycarbonates and epoxy resins. Prenatal and early postnatal exposures to EDCs are suggested to be more critical. Such exposures can lead to reprotoxic effects, hormonal and metabolic consequences in adulthood. Moreover, combined exposure to different EDCs can lead to more serious adverse effects, some of which cannot be predicted by examining their individual toxicity profiles. This study aimed to evaluate effects of single and combined prenatal and lactational exposures to BPA and/or DEHP on female reproductive hormones and ovarian follicle development. Pregnant Sprague-Dawley rats were divided randomly to four groups (n = 3/group): Control (received vehicle only); DEHP (30 mg/kg/day); BPA (50 mg/kg/day) and BPA + DEHP (30 mg/kg/day DEHP; 50 mg/kg/day BPA) through 6-21 gestational days and lactation by intra-gastric lavage. Female offspring (n = 6/group) were fed until the end of twelfth postnatal week and then euthanized. Reproductive hormones, ovarian follicle numbers and ovarian development were determined. Plasma testosterone and estradiol levels of BPA and BPA + DEHP groups were significantly lower than control. In BPA group, the number of tertiary ovarian follicles decreased significantly compared to control. In the combined exposure group, the number of corpus luteum (29%), as well as the number of primordial follicles (36%), showed marked decreases compared to control group. It can be suggested that early life exposure to BPA and DEHP may cause late life adverse effects in female reproductive system, especially after combined exposure.

Can Maternal Prenatal Self-Reported and Physiological Distress Predict Postnatal Caregiving Practices?

Maternal prenatal distress is associated with child outcomes, including health, neurocognitive, and socio-emotional development. Knowledge on underlying mechanisms is limited, yet relevant for prevention and intervention. This study investigated whether maternal prenatal distress predicts specific caregiving practices that are known for their effects on child outcomes. Caregiving practices studied were maternal caregiving quality and the initiation and course of breastfeeding and room-sharing. We hypothesized that more maternal prenatal distress would be associated with altered caregiving practices. Participants were 174 healthy mother-child dyads. During the 37th week of pregnancy maternal self-reported distress was assessed using questionnaires, and physiological stress by collecting saliva cortisol. Maternal caregiving quality was observed in postnatal week 5 during infant bathing. Weekly diaries on breastfeeding and daily diaries on room-sharing were completed during the first 6 postnatal months. In a regression analysis, no associations between maternal prenatal distress and caregiving quality were found. Multilevel analyses indicated that maternal prenatal evening cortisol was positively related to the initiation of breastfeeding and room-sharing. Replications are warranted, but these results suggest that breastfeeding and room-sharing initiation may be part of a mechanism underlying links between maternal prenatal physiological stress and child outcomes. As other prenatal cortisol markers and self-reported distress were not found to be related to the caregiving practices, it is likely that alternative mechanisms (co-)exist in explaining links between maternal prenatal distress and child outcomes. Future replication research including child outcomes and (other) potential mechanisms will inform prevention and intervention programs fostering healthy pregnancies and child development.

Integrated and diurnal indices of maternal pregnancy cortisol in relation to sex-specific parasympathetic responsivity to stress in infants.

Maternal hypothalamic-pituitary-adrenal axis activity may prenatally program sex-specific stress-response pathways. We investigated associations between maternal cortisol during pregnancy and infant parasympathetic responsivity to stress among 204 mother-infant pairs. Cortisol indices included 3rd trimester hair cortisol, as well as diurnal slope and area under the curve, derived from saliva samples collected during pregnancy. Mother-infant dyads participated in the Repeated Still-Face Paradigm (SFP-R) at age 6 months. We calculated respiration-adjusted respiratory sinus arrhythmia (RSAc ), an indicator of parasympathetic activation, from infant respiration and cardiac activity measured during the SFP-R. We used multivariable linear mixed models to examine each cortisol index in relation to infant RSAc and investigated sex differences using cross-product terms. Diurnal cortisol indices were not associated with RSAc . There was no association between hair cortisol and baseline RSAc . However, hair cortisol was associated with sex-specific changes in RSAc over the SFP-R such that, among girls, parasympathetic withdrawal was reduced with increasing prenatal exposure to cortisol. Consistently higher levels of prenatal cortisol exposure may lead to dampened parasympathetic responsivity to stress during infancy, particularly among girls. Maternal hair cortisol may be particularly valuable for studying the effects of prenatal cortisol exposure on infant autonomic reactivity.

Prenatal Octamethylcyclotetrasiloxane Exposure Impaired Proliferation of Neuronal Progenitor, Leading to Motor, Cognition, Social and Behavioral Functions.

Cyclic siloxane octamethylcyclotetrasiloxane (D4) has raised concerns as an endocrine-disrupting chemical (EDC). D4 is widely used in detergent products, cosmetics, and personal care products. Recently, robust toxicological data for D4 has been reported, but the adverse effects of D4 on brain development are unknown. Here, pregnant mice on gestational day 9.5 were treated daily with D4 to postnatal day 28, and the offspring mice were studied. The prenatal D4-treated mice exhibited cognitive dysfunction, limited memory, and motor learning defect. Moreover, prenatal D4 exposure reduced the proliferation of neuronal progenitors in the offspring mouse brain. Next, the mechanisms through which D4 regulated the cell cycle were investigated. Aberrant gene expression, such as cyclin-dependent kinases CDK6 and cyclin-dependent kinase inhibitor p27, were found in the prenatal D4-treated mice. Furthermore, the estrogen receptors ERa and ERb were increased in the brain of prenatal D4-treated mice. Overall, these findings suggest that D4 exerts estrogen activity that affects the cell cycle progression of neuronal progenitor cells during neurodevelopment, which may be associated with cognitive deficits in offspring.

In utero and lactational exposure to triclocarban: Age-associated changes in reproductive parameters of male rat offspring.

Triclocarban (TCC) is an antimicrobial compound, widely used in personal care products, such as soaps, toothpaste, and shampoo. This agent is incompletely removed by wastewater treatment and represents an environmental contaminant. Studies show that TCC has been associated with some endocrine disruptions. In vitro, TCC demonstrated potent androgen-augmenting activity and aromatase inhibition. In this sense, exposure during critical periods of development (gestation and lactation) could lead to some adverse health outcomes in offspring. Therefore, the present study evaluated if maternal exposure to three different doses of TCC could interfere in the reproductive parameters of male offspring. Pregnant female Wistar rats were separated into four groups: vehicle Control (CTR); TCC 0.3 mg/kg (TCC 0.3); TCC 1.5 mg/kg (TCC 1.5); TCC 3.0 mg/kg (TCC 3.0). Dams were treated daily by oral gavage from gestational day 0 to lactational day 21. The males were evaluated in different timepoint: infancy (PND 21), puberty (PND 50) and adult life (PND 90-120). The histomorphometric analysis of testis and testosterone level were assessed on PND 21, 50, 120; sexual behavior and sperm parameters at adulthood. In the TCC 3.0 group, a decrease in the testis interstitial volume and an increase in testosterone levels were observed on PND 21. Moreover, there was a decrease in the diameter of the seminiferous tubules on PND 50, and a decrease in sexual competency in adulthood. These results suggest that exposure to a human relevant dose of TCC may interfere with reproduction and could have implications for human health.

Caries experience and oral health related quality of life in a cohort of Ugandan HIV-1 exposed uninfected children compared with a matched cohort of HIV unexposed uninfected children.

BACKGROUND: Very few studies consider the oral health status and quality of life in HIV-1 exposed uninfected (HEU) children. The aim of this study was to estimate the prevalence of caries in primary teeth and its oral health related quality of life impacts in HEU children compared to HIV-unexposed-uninfected (HUU) children, whilst adjusting for confounding covariates. METHODS: This study uses data from the Ugandan site of the ANRS 121741 PROMISE- PEP trial (ClinicalTrials.gov, number NCT00640263) conducted in 2009-2013 that recruited mothers with HIV-1 and their uninfected children. Of 244 HEU-children-caretaker pairs available at the end of the one-year trial, 166 were re-enrolled in the ANRS 12341 PROMISE-PEP M&S study at 5-7 years and 164 were included in this study. These were age and sex-matched with 181 HUU children-caretaker comparators. Caries experience was recorded using World Health Organization's Decayed, Missed and Filled teeth (dmft/DMFT) indices. The Early Childhood Oral health Impact Scale (ECOHIS) was used for assessment of oral health related quality of life. Mixed effects logistic regression was conducted with dmft and ECOHIS scores as outcomes and HIV-1 exposure status as the main exposure. RESULTS: Forty-eight percent of HEU children and 60% of HUU had dmft> 0. Corresponding figures for ECOHIS> 0 were 12% of HEU and 22% of HUU. The crude analysis showed differences related to HIV-1 exposure in caries experience and oral health related quality of life. Mixed effect logistic regression analyses were not significant when adjusted for use of dental care and toothache. If caregivers' DMFT> 0, the adjusted odds ratio for caries experience (dmft> 0) was 1.6 (95% CI: 1.0-2.8) while if dmft> 0 the adjusted odds ratio for quality of life impacts (ECOHIS> 0) was 4.6 (95% CI: 2.0-10.6). CONCLUSION: The prevalence of untreated caries in primary teeth and quality of life impacts was high in this study population. HIV-1 exposed uninfected children were not more likely than HUU children to experience dental caries or have impaired oral health related quality of life. Given the global expansion of the HEU child population, the present findings indicating no adverse effect of pre- and post-natal HIV-1 exposure on caries in deciduous teeth are reassuring.

Maternal Mental Disorders before Delivery and the Risk of Dental Caries in Children.

Prevention of childhood caries is an ongoing public health challenge, but the possibility of an association with maternal mental disorders has received limited attention. We estimated the extent to which maternal mental disorders are associated with an increased risk of hospitalization due to dental caries. We conducted a longitudinal cohort study of 790,758 infants born in Quebec, Canada between 2006 and 2016, with follow-up extending to 2018. We identified women with mental disorders before or during pregnancy and computed the incidence of dental caries in their children. We estimated HR and 95% CI for the association of maternal mental disorders with the risk of dental caries, adjusted for personal characteristics. Infants of women with mental disorders before or during pregnancy had a higher incidence of dental caries compared to children of women with no mental disorder (56.1 vs. 27.2 per 10,000 person-years). Maternal stress and anxiety disorders (HR = 1.73; 95% CI 1.60-1.86), depression (HR = 1.81; 95% CI 1.60-2.03), schizophrenia and delusional disorders (HR = 1.69; 95% CI 1.29-2.22), and personality disorders (HR = 1.89; 95% CI 1.70-2.11) were associated with the risk of dental caries. The associations were present throughout childhood, including after 7 years (HR = 1.65; 95% CI 1.38-1.96). Maternal mental disorders were associated with caries of the enamel, dentin, and cementum and caries that reached the dental pulp. Maternal mental disorders before or during pregnancy, especially stress and anxiety, depression, schizophrenia, and personality disorders, are associated with the risk of childhood caries. Women with a history of mental disorders may benefit from enhanced strategies for prevention of dental caries in their children.

In utero and lactational exposure to triclocarban: reproductive effects on female rat offspring.

Triclocarban (TCC) is an antimicrobial compound widely used in personal care products such as soaps, toothpaste, and shampoo. This agent is incompletely removed by wastewater treatment and represents an environmental contaminant. Recent studies have shown that TCC is associated with some endocrine disruptions. The aim of the present study was to evaluate if TCC exposure during critical periods of development (gestation and lactation) could lead to adverse effects on reproductive and behavior parameters of female offspring. Pregnant female Wistar rats were divided into four groups (n = 8-11/group): Control; TCC 0.3 mg/kg (TCC 0.3); TCC 1.5 mg/kg; TCC 3.0 mg/kg (TCC 3.0); and treated daily by oral gavage from gestational day 0 to lactational day 21. The female pups (F1 generation) were weaned on post-natal day 21 and included in the study. No litter-mates were used for the same group. There was a decrease in estradiol levels in the TCC 0.3 and TCC 3.0 groups. Moreover, there was a decrease in progesterone levels and an increase in pre-implantation loss in the TCC 3.0 group in adulthood. It is suggested, in this study, that the decrease in progesterone biosynthesis could interfere with implantation process. The exposure window to TCC is an important factor, as we found alterations only in the offspring.

Long-Term Associations Between Prenatal Maternal Cortisol and Child Neuroendocrine-Immune Regulation.

BACKGROUND: Advancing understanding of the developmental origins of neuroendocrine-immune (NEI) functioning is key to elucidating the biological mechanisms involved in health and disease risk across the lifespan. This study examined whether prenatal maternal hypothalamic-pituitary-adrenal (HPA) activity moderates child NEI relations and explored the consistency of this moderating effect across gestation. METHODS: Pregnant women participated in five prenatal study visits from 24 to 38 weeks gestation. At each visit, women provided a saliva sample. In a 5-year follow-up study, children (nfemale = 25, nmale=20) provided four saliva samples and participated in behavioral assessments and challenge tasks. Prenatal maternal saliva samples were assayed for cortisol. Child saliva samples were assayed for cortisol and cytokines (IL-1ß, IL-6, IL-8, TNFα) as indices of HPA and inflammatory activity. Multilevel mixed-effects models examined the moderation of child NEI relations by prenatal maternal cortisol. RESULTS: Among males, average prenatal maternal cortisol did not moderate child NEI relations. Among females, average prenatal maternal cortisol moderated some child NEI relations with higher prenatal cortisol associated with more positive cortisol-cytokine relations at age five. When examined by gestational time point, there were more significant NEI moderation effects by maternal cortisol from later gestation (≥ 30 weeks) than earlier. CONCLUSIONS: The findings suggest prenatal maternal HPA activity may moderate child NEI functioning. Additional research conducted with more heterogeneous and larger samples is needed to fully understand these relations. Furthering our knowledge of NEI development has important research and clinical implications, particularly for understanding and addressing conditions with inflammatory pathophysiologies, such as depression and cardiovascular disease.

Prenatal Glucocorticoid Treatment Completeness and Steroid Hormonal Levels as Related to Infant and Maternal Health.

This study was conducted to confirm the negative associations between testosterone and cortisol levels and health and developmental outcomes in very low-birth weight (VLBW) infants after controlling for prenatal glucocorticoid (GC) treatment. Seventy-four VLBW infant-mother pairs were recruited from a neonatal intensive care unit in the Southeastern United States. We divided the pairs into the complete (n = 58) and incomplete (n = 16) GC treatment groups. Data on infants and mothers were obtained at birth, 40 weeks' postmenstrual age, and 3 and 6 months' corrected age. Salivary testosterone and cortisol levels of the pairs were determined at 40 weeks' postmenstrual age using enzyme immunoassay. Log-linear and general linear mixed models showed that gestational age and birth weight were lower when testosterone was 1 pg/mL higher. When cortisol was 1 µg/dL higher, technology dependence at discharge was higher and motor development at 6 months was lower. Mothers with complete GC treatment had greater parity and gravida, more prenatal visits, and more medical complications. The study outcomes supported our hypothesis that steroid hormonal levels are more predictive of infant health and development than GC treatment completeness. Single dose of GC treatment might be just as effective as 2 doses, although further study with more subjects would be needed to confirm. As the associations with steroid hormonal levels lasted longer than the GC treatment associations, we recommend confirming the predictive effects of testosterone and cortisol levels after 6 months.

Prospective Relations Between Prenatal Maternal Cortisol and Child Health Outcomes.

OBJECTIVE: The aim of the study was to investigate prospective, longitudinal associations between maternal prenatal cortisol response to an interpersonal stressor and child health for the subsequent 3 years. METHODS: One hundred twenty-three women expecting their first child provided salivary cortisol samples between 12 and 32 weeks of gestation (M (SD) = 22.4 (4.9) weeks) before and after a videotaped couple conflict discussion with their partner. Mothers reported on overall child health and several indicators of child illness (sick doctor visits, fevers, ear, and respiratory infections) when children were 6 months (n = 114), 1 (n = 116), and 3 (n = 105) years old. Associations between maternal prenatal cortisol reactivity and recovery and later child health at each of the three time points were analyzed using longitudinal regression models. RESULTS: Greater cortisol reactivity in response to the couple conflict discussion was associated with maternal self-report of better overall child health (p = .016, 95% CI = 0.06-1.30, Cohen's f = 0.045) across the study period. Greater cortisol reactivity was also associated with lower incidence rate ratios for maternal reports of sick doctor visits (incidence rate ratio 95% CI = 0.25-0.83, p = .006), fevers (95% CI = 0.25-0.73, p = .002), ear infections (95% CI = 0.25-0.58, p < .001), and respiratory infections (95% CI = 0.08-1.11, p = .073). Cortisol recovery was unrelated to study outcomes (all p's > 0.05). Maternal prenatal depressive symptoms moderated the association between cortisol reactivity and overall child health (p = .034, 95% CI = 0.07-1.87 for interaction term) but no other health outcomes (p's > 0.05). Among women with lower depressive symptoms, cortisol reactivity was not associated with overall child health; among women with higher levels of depressive symptoms, greater cortisol reactivity was associated with better overall child health. CONCLUSIONS: This study provides longitudinal evidence that greater maternal cortisol reactivity to a salient interpersonal stressor during pregnancy is associated with fewer child health problems and better maternal report of overall child health during infancy and into early childhood. TRIAL REGISTRATION: Clinicaltrials.gov ID NCT01901536.