Examining the association between prenatal cannabis exposure and child autism traits: A multi-cohort investigation in the environmental influences on child health outcome program.

This study examined the association between prenatal cannabis exposure and autism spectrum disorder (ASD) diagnoses and traits. A total sample of 11,570 children (ages 1-18; 53% male; 25% Hispanic; 60% White) from 34 cohorts of the National Institutes of Health-funded environmental influences on child health outcomes consortium were included in analyses. Results from generalized linear mixed models replicated previous studies showing that associations between prenatal cannabis exposure and ASD traits in children are not significant when controlling for relevant covariates, particularly tobacco exposure. Child biological sex did not moderate the association between prenatal cannabis exposure and ASD. In a large sample and measuring ASD traits continuously, there was no evidence that prenatal cannabis exposure increases the risk for ASD. This work helps to clarify previous mixed findings by addressing concerns about statistical power and ASD measurement.

Setting a research agenda for examining early risk for elevated cognitive disengagement syndrome symptoms using data from the ABCD cohort.

Background: Little research has examined early life risk for symptoms of cognitive disengagement syndrome (CDS) despite a well-established literature regarding co-occurring outcomes (e.g., attention-deficit/hyperactivity disorder). The current study estimated bivariate associations between early life risk factors and CDS in a large and representative sample of U.S. children. Methods: We conducted secondary analyses of baseline data from the Adolescent Brain Cognitive Development (ABCD) study (N = 8,096 children, 9-10 years old). Birthing parents reported early life risk factors on a developmental history questionnaire, including parental, prenatal, delivery and birth, and developmental milestone information. They also completed the Child Behavior Checklist, which includes a CDS subscale that was dichotomized to estimate the odds of elevated CDS symptoms (i.e., T-score > 70) in children related to risk indices. Results: We observed significantly elevated odds of CDS related to parental risk factors (i.e., unplanned pregnancy, pregnancy awareness after 6 weeks, teenage parenthood), birthing parent illnesses in pregnancy (i.e., severe nausea, proteinuria, pre-eclampsia/toxemia, severe anemia, urinary tract infection), pregnancy complications (i.e., bleeding), prenatal substance exposures (i.e., prescription medication, tobacco, illicit drugs), delivery and birth risk factors (i.e., child blue at delivery, child not breathing, jaundice, incubation after delivery), and late motor and speech milestones in children. Conclusions: Several early-life risk factors were associated with elevated odds of CDS at ages 9-10 years; study design prevents the determination of causality. Further investigation is warranted regarding early life origins of CDS with priority given to risk indices that have upstream commonalities (i.e., that restrict fetal growth, nutrients, and oxygen).

Absence of association between maternal adverse events and long-term gut microbiome outcomes in the Australian autism biobank.

Introduction: Maternal immune activation (MIA) and prenatal maternal stress (MatS) are well-studied risk factors for psychiatric conditions such as autism and schizophrenia. Animal studies have proposed the gut microbiome as a mechanism underlying this association and have found that risk factor-related gut microbiome alterations persist in the adult offspring. In this cross-sectional study, we assessed whether maternal immune activation and prenatal maternal stress were associated with long-term gut microbiome alterations in children using shotgun metagenomics. Methods: This cross-sectional study included children diagnosed with autism (N = 92), siblings without a diagnosis (N = 42), and unrelated children (N = 40) without a diagnosis who were recruited into the Australian Autism Biobank and provided a faecal sample. MIA exposure was inferred from self-reported data and included asthma/allergies, complications during pregnancy triggering an immune response, auto-immune conditions, and acute inflammation. Maternal stress included any of up to 9 stressful life events during pregnancy, such as divorce, job loss, and money problems. Data were analysed for a total of 174 children, of whom 63 (36%) were born to mothers with MIA and 84 (48%) were born to mothers who experienced maternal stress during pregnancy (where 33 [19%] experienced both). Gut microbiome data was assessed using shotgun metagenomic sequencing of the children's faecal samples. Results: In our cohort, MIA, but not MatS, was associated with ASD. Variance component analysis revealed no associations between any of the gut microbiome datasets and neither MIA nor MatS. After adjusting for age, sex, diet and autism diagnosis, there was no significant difference between groups for bacterial richness, α-diversity or ß-diversity. We found no significant differences in species abundance in the main analyses. However, when stratifying the cohort by age, we found that Faecalibacterium prausnitzii E was significantly decreased in MIA children aged 11-17. Discussion: Consistent with previous findings, we found that children who were born to mothers with MIA were more likely to be diagnosed with autism. Unlike within animal studies, we found negligible microbiome differences associated with MIA and maternal stress. Given the current interest in the microbiome-gut-brain axis, researchers should exercise caution in translating microbiome findings from animal models to human contexts and the clinical setting.

Tracing the influence of prenatal risk factors on the offspring retina: Focus on development and putative long-term consequences.

BACKGROUND: Pregnancy represents a window of vulnerability to fetal development. Disruptions in the prenatal environment during this crucial period can increase the risk of the offspring developing diseases over the course of their lifetime. The central nervous system (CNS) has been shown to be particularly susceptible to changes during crucial developmental windows. To date, research focused on disruptions in the development of the CNS has predominantly centred on the brain, revealing a correlation between exposure to prenatal risk factors and the onset of neuropsychiatric disorders. Nevertheless, some studies indicate that the retina, which is part of the CNS, is also vulnerable to in utero alterations during pregnancy. Such changes may affect neuronal, glial and vascular components of the retina, compromising retinal structure and function and possibly impairing visual function. METHODS: A search in the PubMed database was performed, and any literature concerning prenatal risk factors (drugs, diabetes, unbalanced diet, infection, glucocorticoids) affecting the offspring retina were included. RESULTS: This review collects evidence on the cellular, structural and functional changes occurring in the retina triggered by maternal risk factors during pregnancy. We highlight the adverse impact on retinal development and its long-lasting effects, providing a critical analysis of the current knowledge while underlining areas for future research. CONCLUSIONS: Appropriate recognition of the prenatal risk factors that negatively impact the developing retina may provide critical clues for the design of preventive strategies and for early therapeutic intervention that could change retinal pathology in the progeny.

Electrophysiological correlates of inhibitory control in children: Relations with prenatal maternal risk factors and child psychopathology.

Inhibitory control plays an important role in children's cognitive and socioemotional development, including their psychopathology. It has been established that contextual factors such as socioeconomic status (SES) and parents' psychopathology are associated with children's inhibitory control. However, the relations between the neural correlates of inhibitory control and contextual factors have been rarely examined in longitudinal studies. In the present study, we used both event-related potential (ERP) components and time-frequency measures of inhibitory control to evaluate the neural pathways between contextual factors, including prenatal SES and maternal psychopathology, and children's behavioral and emotional problems in a large sample of children (N = 560; 51.75% females; Mage = 7.13 years; Rangeage = 4-11 years). Results showed that theta power, which was positively predicted by prenatal SES and was negatively related to children's externalizing problems, mediated the longitudinal and negative relation between them. ERP amplitudes and latencies did not mediate the longitudinal association between prenatal risk factors (i.e., prenatal SES and maternal psychopathology) and children's internalizing and externalizing problems. Our findings increase our understanding of the neural pathways linking early risk factors to children's psychopathology.

Role of the brain-sparing effect on retinopathy of prematurity in newborns with fetal growth restriction.

INTRODUCTION: This study aimed to investigate the role of the brain-sparing effect (BSE) on retinopathy of prematurity (ROP) in fetal growth restriction (FGR). METHODS: In this retrospective study, 127 pregnant women were divided into two groups considering the cerebroplacental ratio (CPR): FGR with abnormal CPR group (n = 74) and the appropriate for gestational age with normal Doppler group (n = 53). CPR was computed using the pulsatility index (PI) and resistance index (RI) to quantitate the waveforms [middle cerebral artery (MCA) PI/umbilical artery (UA) PI and MCA RI/UA RI: a result <1 was taken into account as abnormal]. ROP screening results of newborns were recorded from electronic files. RESULTS: After adjusting for co-variants, BSE was not related to ROP (adjusted odds ratio [aOR], 1.06; 95% confidence interval [CI], 0.23-4.95). Gestational age at delivery <30 weeks (aOR, 2.55; 95% CI, 1.04-6.93) and birth weight <1500 g (aOR, 5.15; 95% CI, 1.15-25.2) were independently associated with ROP. Preeclampsia, emergency cesarean section birth, or 48 h completion after the first steroid administration were not associated with ROP. CONCLUSIONS: Gestational age at delivery <30 weeks and birth weight <1500 g are independent risk factors for ROP in FGR whereas the BSE is not a risk factor.

In Utero Origins of Acute Leukemia in Children.

Acute leukemias, mainly consisting of acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML), comprise a major diagnostic group among hematologic cancers. Due to the early age at onset of ALL, particularly, it has long been suspected that acute leukemias of childhood may have an in utero origin. This supposition has motivated many investigations seeking direct proof of prenatal leukemogenesis, in particular, twin and "backtracking studies". The suspected in utero origin has also focused on gestation as a critical window of risk, resulting in a rich literature on prenatal risk factors for pediatric acute leukemias. In this narrative review, we recount the circumstantial and direct evidence for an in utero origin of childhood acute leukemias.

Cumulative Prenatal Risk Factors and Developmental Coordination Disorder in Young Children.

OBJECTIVES: To examine the effect of cumulative prenatal risk factors (RFs) on the presence of Developmental Coordination Disorder (DCD) in young children. METHODS: Participants (N = 589, 338 boys, Mage = 4.5 ± 0.5 years) were from a larger cohort study, the Coordination and Activity Tracking in Children (CATCH). Motor coordination was assessed using the Movement Assessment Battery for Children- 2nd Edition. Children were classified as at risk for DCD (DCDr) based on European Academy of Childhood Disability guidelines. RFs were obtained through a parent-completed survey. A multiple logistic regression was conducted to examine the effect of the RFs on DCD. RESULTS: Results showed that the odds of a child having DCDr are significantly higher with a greater total number of prenatal RFs, after adjustment for mother's age at child's birth, child's sex, child's age, marital status and total annual household income (OR = 1.48, p < 0.01). CONCLUSIONS: These findings warrant further investigation into the cumulative impact of multiple prenatal RFs and whether specific combinations of RFs might be more strongly linked to DCD than others. These results provide additional insight into possible causes and prevention of DCD.

Multiple Risk in Pregnancy- Prenatal Risk Constellations and Mother-Infant Interactions, Parenting Stress, and Child Externalizing and Internalizing Behaviors: A Prospective Longitudinal Cohort Study from Pregnancy to 18 Months Postpartum.

Multiple risk is associated with adverse developmental outcomes across domains. However, as risk factors tend to cluster, it is important to investigate formation of risk constellations, and how they relate to child and parental outcomes. By means of latent class analysis patterns of prenatal risk factors were identified, and relations to interactional quality, parenting stress, and child internalizing and externalizing behaviors were investigated. An array of prenatal risk factors was assessed in 1036 Norwegian pregnant women participating in a prospective longitudinal community-based study, Little in Norway. Mother-infant interactions were videotaped and scored with the Early Relational Health Screen (ERHS) at 12 months. The Parenting Stress Index (PSI) and Infant-Toddler Social and Emotional Assessment (ITSEA) were administered at 18 months. First, we analyzed response patterns to prenatal risks to identify number and characteristics of latent classes. Second, we investigated whether latent class membership could predict mother-child interactional quality, parenting stress, and child internalizing and externalizing behavior after the child was born. Results revealed three prenatal risk constellations: broad risk (7.52%), mental health risk (21.62%) and low-risk (70.86%). Membership in the broad risk group predicted lower scores on interactional quality, while membership in the mental health risk group predicted less favorable scores on all outcome measures. Prenatal risks clustered together in specific risk constellations that differentially related to parent, child and interactional outcomes.

Disentangling the trajectories of maternal depressive symptoms and partnership problems in the transition to parenthood and their impact on child adjustment difficulties.

Maternal perinatal depression (PND) and partnership problems have been identified to influence the development of later child adjustment difficulties. However, PND and partnership problems are closely linked which makes it difficult to draw conclusions about the exact transmission pathways. The aim of the present study was to investigate to what extent PND symptoms and partnership problems influence each other longitudinally and to examine the influence of their trajectories on child adjustment difficulties at the age of three. Analyses were based on publicly available data from the German family panel "pairfam". N = 354 mothers were surveyed on depressive symptoms and partnership problems annually from pregnancy (T0) until child age three (T4). Child adjustment difficulties were assessed at age three. Results of latent change score modeling showed that partnership problems predicted change in PND symptoms at T0 and T3 while PND symptoms did not predict change in partnership problems. Child adjustment difficulties at age three were predicted by PND symptoms, but not by partnership problems. Partnership problems predicted externalizing, but not internalizing symptoms. Results underline the effects of family factors for the development of child adjustment difficulties and emphasize the importance of early interventions from pregnancy onwards.

Exposures during pregnancy and at birth are associated with the risk of offspring eating disorders.

BACKGROUND: Eating disorders (ED) are severe psychiatric disorders, commonly debuting early. Aberrances in the intrauterine environment and at birth have been associated with risk of ED. Here, we explore if, and at what effect size, a variety of such exposures associate with offspring ED, that is, anorexia nervosa (AN), bulimia nervosa (BN), and eating disorder not otherwise specified (EDNOS). METHODS: This population-based cohort study, conducted from September 2021 to August 2023, used Finnish national registries of all live births in 1996-2014 (N = 1,097,753). Cox proportional hazards modeling was used to compare ED risk in exposed versus unexposed offspring, adjusting for potential confounders and performing sex-stratified analyses. RESULTS: A total of 6614 offspring were diagnosed with an ED; 3668 AN, 666 BN, and 4248 EDNOS. Lower risk of offspring AN was seen with young mothers, continued smoking, and instrumental delivery, while higher risk was seen with older mothers, inflammatory disorders, prematurity, small for gestational age, and low Apgar. Offspring risk of BN was higher with continued smoking and prematurity, while lower with postmature birth. Offspring risk of EDNOS was lower with instrumental delivery, higher for older mothers, polycystic ovary syndrome, insulin-treated pregestational diabetes, antibacterial treatment, prematurity, and small for gestational age. Sex-specific associations were found. CONCLUSIONS: Several prenatal and at birth exposures are associated with offspring ED; however, we cannot exclude confounding by maternal BMI. Nevertheless, several exposures selectively associate with risk of either AN, BN, or EDNOS, and some are sex-specific, emphasizing the importance of subtype- and sex-stratified analyses of ED. PUBLIC SIGNIFICANCE: We define environmental factors involved in the development of different ED, of importance as preventive measure, but also in order to aid in defining the molecular pathways involved and thus in the longer perspective contribute to the development of pharmacological treatment of ED.

Sex-specific and sex-independent steroid-related biomarkers in early second trimester maternal serum associated with autism.

BACKGROUND: Prenatal exposure to maternal metabolic conditions associated with inflammation and steroid dysregulation has previously been linked to increased autism risk. Steroid-related maternal serum biomarkers have also provided insight into the in utero steroid environment for offspring who develop autism. OBJECTIVE: This study examines the link between autism among offspring and early second trimester maternal steroid-related serum biomarkers from pregnancies enriched for prenatal metabolic syndrome (PNMS) exposure. STUDY DESIGN: Early second trimester maternal steroid-related serum biomarkers (i.e., estradiol, free testosterone, total testosterone, and sex hormone binding globulin) were compared between pregnancies corresponding to offspring with (N = 68) and without (N = 68) autism. Multiple logistic regression analyses were stratified by sex and gestational duration. One-way ANCOVA with post hoc tests was performed for groups defined by autism status and PNMS exposure. RESULTS: Increased estradiol was significantly associated with autism only in males (AOR = 1.13 per 100 pg/ml, 95% CI 1.01-1.27, p = 0.036) and only term pregnancies (AOR = 1.17 per 100 pg/ml, 95% CI 1.04-1.32, p = 0.010). Autism status was significantly associated with decreased sex hormone binding globulin (AOR = 0.65 per 50 nmol/L, 95% CI 0.55-0.78, p < 0.001) overall and when stratified by sex and term pregnancy status. The inverse association between sex hormone binding globulin and autism was independent of PNMS exposure. LIMITATIONS: The relative racial and ethnic homogeneity of Utah's population limits the generalizability of study results. Although significant differences by autism status were identified in concentrations of sex hormone binding globulin overall and of estradiol in participant subgroups, differences by PNMS exposure failed to reach statistical significance, which may reflect insufficient statistical power. CONCLUSION: Both elevated maternal serum estradiol in males only and low maternal serum sex hormone binding globulin in both sexes are associated with increased autism risk. Further investigation is merited to identify how steroid, metabolic, and inflammatory processes can interact to influence neurodevelopment in early second trimester.

Prevention of Neurological Sequelae in Preterm Infants.

BACKGROUND: Preterm birth is one of the world's critical health problems, with an incidence of 5% to 18% of living newborns according to various countries. White matter injuries due to preoligodendrocytes deficits cause hypomyelination in children born preterm. Preterm infants also have multiple neurodevelopmental sequelae due to prenatal and perinatal risk factors for brain damage. The purpose of this work was to explore the effects of the brain risk factors and MRI volumes and abnormalities on the posterior motor and cognitive development at 3 years of age. METHODS: A total of 166 preterm infants were examined before 4 months and clinical and MRI evaluations were performed. MRI showed abnormal findings in 89% of the infants. Parents of all infants were invited to receive the Katona neurohabilitation treatment. The parents of 128 infants accepted and received Katona's neurohabilitation treatment. The remaining 38 infants did not receive treatment for a variety of reasons. At the three-year follow-up, Bayley's II Mental Developmental Index (MDI) and the Psychomotor Developmental Index (PDI) were compared between treated and untreated subjects. RESULTS: The treated children had higher values of both indices than the untreated. Linear regression showed that the antecedents of placenta disorders and sepsis as well as volumes of the corpus callosum and of the left lateral ventricle significantly predicted both MDI and PDI, while Apgar < 7 and volume of the right lateral ventricle predicted the PDI. CONCLUSIONS: (1) The results indicate that preterm infants who received Katona's neurohabilitation procedure exhibited significantly better outcomes at 3 years of age compared to those who did not receive the treatment. (2) The presence of sepsis and the volumes of the corpus callosum and lateral ventricles at 3-4 months were significant predictors of the outcome at 3 years of age.

Maternal rheumatoid arthritis and risk of autism in the offspring.

BACKGROUND: Maternal Rheumatoid Arthritis (RA) is suggested to increase the risk of Autism Spectrum Disorder (ASD) in the offspring, mainly through inflammation/autoimmunity, but the association is unclear. A prospective population-based cohort study was implemented to examine the association between maternal RA and offspring ASD. METHODS: We included all children born alive in Sweden from 1995 to 2015, followed up through 2017. Diagnoses of ASD and RA were clinically ascertained from National Patient Register. We quantified the association by hazard ratios (HR) and two-sided 95% confidence intervals (CI), from Cox regression after detailed adjustment for potential confounders. We examined RA serostatus, etiological subgroups and the timing of exposure. To closer examine the underlying mechanism for the association, we included a negative control group for RA, arthralgia, with similar symptomology as RA but free from inflammation/autoimmunity. RESULTS: Of 3629 children born to mothers with RA, 70 (1.94%) were diagnosed with ASD, compared to 28 892 (1.92%) of 1 503 908 children born to mothers without RA. Maternal RA before delivery was associated with an increased risk of offspring ASD (HR = 1.43, 95% CI 1.11-1.84), especially for seronegative RA (HR = 1.61, 95% CI 1.12-2.30). No similar association was observed for paternal RA, maternal sisters with RA, or RA diagnosed after delivery. Maternal arthralgia displayed as high risks for offspring ASD as did maternal RA (HR = 1.41, 95% CI 1.24-1.60). CONCLUSIONS: In Sweden, maternal RA before delivery was associated with an increased risk of offspring ASD. The comparable association between maternal arthralgia and ASD risk suggests other pathways of risk than autoimmunity/inflammation, acting jointly or independently of RA.

Prenatal Stress Exposure Amplifies Effect of Maternal Suicidal Ideation on Early Childhood Behavioral Trajectories.

The in utero environment influences fetal development and may predispose to disease later in life. This study examines whether maternal suicidal ideation during pregnancy is associated with children's behavioral trajectories across early childhood, and whether prenatal maternal traumatic stress accelerates the trajectories. The study included mother-child dyads (N = 331, 51.1% boys) from the longitudinal Stress In Pregnancy study; 31.1% (n = 103) mothers were Exposed to Superstorm Sandy. During their second trimester, 12.4% (n = 41) women reported suicidal ideation during pregnancy. Mothers completed the Behavior Assessment Scale for Children-2 annually from ages 2- to 6-years-old to assess multiple behavioral domains. Hierarchical linear modeling estimated within-person longitudinal trajectories of clinical behaviors, and between-person effects of maternal suicidal ideation and disaster-related stress in utero on changes in child behavior. For children exposed to both risks, Atypical behaviors (i.e., unusual behaviors, social disconnection) increased linearly across early childhood. Exposure to Superstorm Sandy and maternal suicidal ideation were independently associated with non-linear increases in Anxiety severity and maternal suicidal ideation during pregnancy was associated with a linear increase in Attention problems across early childhood. Maternal suicidal ideation during pregnancy is associated with increased risk for a range of behavioral and emotional difficulties in early childhood and the trajectory of atypical behaviors was amplified by disaster-related traumatic stress. Findings highlight the need for health professionals to screen for suicidal ideation among their pregnant patients. Pregnant women who experience severe stress may require additional monitoring and support to reduce risk for poorer early childhood outcomes.

Neuroprotective Epigenetic Changes Induced by Maternal Treatment with an Inhibitor of Soluble Epoxide Hydrolase Prevents Early Alzheimer's Disease Neurodegeneration.

Modulation of Alzheimer's disease (AD) risk begins early in life. During embryo development and postnatal maturation, the brain receives maternal physiological influences and establishes epigenetic patterns that build its level of resilience to late-life diseases. The soluble epoxide hydrolase inhibitor N-[1-(1-oxopropyl)-4-piperidinyl]-N'-[4-(trifluoromethoxy)phenyl] urea (TPPU), reported as ant-inflammatory and neuroprotective against AD pathology in the adult 5XFAD mouse model of AD, was administered to wild-type (WT) female mice mated to heterozygous 5XFAD males during gestation and lactation. Two-month-old 5XFAD male and female offspring of vehicle-treated dams showed memory loss as expected. Remarkably, maternal treatment with TPPU fully prevented memory loss in 5XFAD. TPPU-induced brain epigenetic changes in both WT and 5XFAD mice, modulating global DNA methylation (5-mC) and hydroxymethylation (5-hmC) and reducing the gene expression of some histone deacetylase enzymes (Hdac1 and Hdac2), might be on the basis of the long-term neuroprotection against cognitive impairment and neurodegeneration. In the neuropathological analysis, both WT and 5XFAD offspring of TPPU-treated dams showed lower levels of AD biomarkers of tau hyperphosphorylation and microglia activation (Trem2) than the offspring of vehicle-treated dams. Regarding sex differences, males and females were similarly protected by maternal TPPU, but females showed higher levels of AD risk markers of gliosis and neurodegeneration. Taken together, our results reveal that maternal treatment with TPPU impacts in preventing or delaying memory loss and AD pathology by inducing long-term modifications in the epigenetic machinery and its marks.

Prenatal Education Intervention for Increasing Knowledge and Changing Attitude Toward Offspring Obesity Risk Factors.

This pre- and post-test quasi-experimental design study pilot tested an educational intervention designed to increase knowledge of and change attitudes toward prenatal factors that increase risk of childhood offspring obesity in 36 pregnant women. Educational intervention content included monitoring blood glucose, gestational weight gain in pregnancy, healthy lifestyle choices, and breastfeeding. Education intervention delivery method included: Verbal, written, and video. Participants' knowledge improved after the intervention for most topics (p = .03-.000). Their attitude score also differed before and after intervention (p = .002). Video delivery mode was the most useful, attractive, and most helpful method. This study showed an education intervention could potentially increase pregnant women's knowledge and attitudes toward offspring obesity risk factors.

Incidence of Eczema in Early Infancy and the Prenatal Risk Factors - Guangzhou, Guangdong, China, 2018-2019.

WHAT IS ALREADY KNOWN ON THIS TOPIC?: Eczema is a common allergic disease in children, which seriously affects the quality of life of children and their families. WHAT IS ADDED BY THIS REPORT?: The results showed that the incidence of very-early-onset eczema was 12.4%. Primiparity was associated with a higher risk of eczema [risk ratio (95% confidence interval): 1.23 (1.06-1.42)]. WHAT ARE THE IMPLICATIONS FOR PUBLIC HEALTH PRACTICE?: Very-early-onset eczema is common. Given its adverse impact on children's health and life quality, this previously neglected public health issue needs to be prioritized. In addition, maternal parity could serve as an indicator in risk assessment and prediction for infant eczema.

Environmental Air Pollutants Inhaled during Pregnancy Are Associated with Altered Cord Blood Immune Cell Profiles.

Air pollution exposure during pregnancy may be a risk factor for altered immune maturation in the offspring. We investigated the association between ambient air pollutants during pregnancy and cell populations in cord blood from babies born to mothers with asthma enrolled in the Breathing for Life Trial. For each patient (n = 91), daily mean ambient air pollutant levels were extracted during their entire pregnancy for sulfur dioxide (SO2), nitric oxide, nitrogen dioxide, carbon monoxide, ozone, particulate matter <10 µm (PM10) or <2.5 µm (PM2.5), humidity, and temperature. Ninety-one cord blood samples were collected, stained, and assessed using fluorescence-activated cell sorting (FACS). Principal Component (PC) analyses of both air pollutants and cell types with linear regression were employed to define associations. Considering risk factors and correlations between PCs, only one PC from air pollutants and two from cell types were statistically significant. PCs from air pollutants were characterized by higher PM2.5 and lower SO2 levels. PCs from cell types were characterized by high numbers of CD8 T cells, low numbers of CD4 T cells, and by high numbers of plasmacytoid dendritic cells (pDC) and low numbers of myeloid DCs (mDCs). PM2.5 levels during pregnancy were significantly associated with high numbers of pDCs (p = 0.006), and SO2 with high numbers of CD8 T cells (p = 0.002) and low numbers of CD4 T cells (p = 0.011) and mDCs (p = 4.43 × 10-6) in cord blood. These data suggest that ambient SO2 and PM2.5 exposure are associated with shifts in cord blood cell types that are known to play significant roles in inflammatory respiratory disease in childhood.

Early diagnosis and treatment of infants with prenatal and perinatal risk factors for brain damage at the neurodevelopmental research unit in Mexico.

Prenatal and perinatal risk factors for perinatal brain damage frequently produce brain injuries in preterm and term infants. The early diagnosis and treatment of these infants, in the period of higher brain plasticity, may prevent the neurological and cognitive sequels that accompany these lesions. The Neurodevelopmental Research Unit at the Institute of Neurobiology of the National Autonomous University of Mexico has taken this endeavor. A multidisciplinary approach is followed. Pediatric, neurologic and rehabilitation clinical studies, MRI, EEG, visual and auditory evoked responses, and Bayley II evaluations are carried out initially. Infants are followed up to 8 years, with periodic appointments for evaluation and treatment. Katona's neurohabilitation method is used for initial diagnosis and treatment. Selective visual and auditory attention are explored from 3 months of age. This method was created in the Unit and, if deficiencies are observed, the method also describes the treatment to avoid subsequent alterations of these processes. Deficiencies in the acquisition of language are evaluated from 4 months of age, implementing treatment through instructions to parents on how they should teach their children to speak. This method has also been developed in the Unit and is in its validation process. In the MRI, we pay special attention to subtle and diffuse patterns, due to the high frequency with which they appear in contemporary cohorts at a national and international level. More than 80% of these infants showed abnormal MRI findings that should be taken into consideration. The outcome of children at 8 years old showed that 78%, 76% and 78% of extremely preterm, very preterm and late preterm, respectively, had a normal neurodevelopment. In term infants, only 69% had a normal neurodevelopment; in this group, the majority of infants had very severe brain lesions. Conclusions: It is necessary to evaluate, at an early age, all newborns with prenatal and perinatal risk factors for brain damage. Special attention should be payed to all premature newborns and those newborns who have been discharged from the intensive care unit.