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Triclosan (TCS) is a lipophilic antimicrobial agent present in commercial and healthcare products. Despite its beneficial properties, TCS disrupts thyroid hormone homeostasis and may be linked to metabolic disorders, cardiotoxicity, and increased cancer risk. Evidence on prenatal TCS exposure and adverse neurobehavioral outcomes is limited. This systematic review aimed to verify whether prenatal exposure to TCS is associated with neurobehavioral impairments. Observational studies with pregnant women exposed to TCS during pregnancy were included. The MEDLINE, EMBASE, Scopus, Web of Science, and LILACS databases were searched for studies up to February 27, 2024. Titles and abstracts were first screened, followed by full-text readings by two independent reviewers. Data extraction was performed independently, with conflicts resolved by consensus with a third reviewer. The included studies were assessed using an adapted Downs and Black tool and qualitatively synthesized. Certainty of evidence was assessed by GRADE. The study protocol was registered with PROSPERO (CRD42024526426). Among 17 studies, 14 cohort studies met the inclusion criteria. The sample size ranged from 193 to 794 pairs of pregnant women and children. Exposure to TCS throughout pregnancy resulted in median concentrations from 0.40 ng/mL to 28.2 ng/mL. Four studies suggested a potential association between prenatal TCS exposure and neurodevelopmental deficits, such as externalizing problems, attention issues, hyperactivity, somatization, emotional symptoms, social awareness, and communication; in contrast, eight studies found no significant effect. The studies had low certainty of evidence. Considering the heterogeneity and confounding factors, further investigation is required to confirm that prenatal TCS exposure leads to neurobehavioral disorders.

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Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental contaminants produced through the combustion of organic matter, with sources ranging from traffic pollution to diet. Although PAH exposure has been associated with adverse health effects, few studies have examined its impact on neurodevelopmental delay (NDD). Thus, our study aims to investigate the effect of prenatal PAH exposure on the odds of NDD. We measured 7 hydroxylated PAH metabolites in spot urine samples collected up to three times during pregnancy in the PROTECT birth cohort. NDD was identified using score cutoffs from the Ages and Stages Questionnaire, 3rd edition offered in Spanish, across five domains at 12, 24, 36, and 48 months. We utilized logistic regression and mixed effects logistic regression models to assess associations between prenatal PAH concentrations and NDD. Our results showed mostly lower odds of NDD with higher PAH exposure (p < 0.05). However, male children showed higher odds of NDD in relation to PAH exposure, particularly in the Fine Motor domain. For example, 1-hydroxypyrene was associated with 1.11 (1.01, 1.23) times odds of delay in fine motor function in male children versus 0.91 (0.82, 1.00) times odds in female children. Our preliminary sex-specific results suggest that PAH exposure may impact neurodevelopment in male children and prompt further investigation into the potential sex-specific mechanisms of PAHs on motor function.

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The potential neurotoxicity of environmental contaminants, such as pesticides, is implicated in the etiology of neurodevelopmental disorders, particularly given the heightened vulnerability of the developing brain. Among these contaminants, glyphosate, a widely used herbicide, has been linked to alterations in neurodevelopment, though its precise neurotoxic mechanisms are not fully elucidated. In this context, our systematic review evaluates the impact of maternal exposure to glyphosate alone (GLY) or glyphosate-based-herbicide (GBH) on neurodevelopmental and behavioral outcomes in rodent offspring. This assessment encompasses a comprehensive examination of behavioral, biochemical, morphological, and genetic alterations resulting from perinatal glyphosate exposure. The Systematic review protocol was registered in the platform Open Science Framework (OSF) following the guidelines of the Systematic Review Center for Laboratory Animal Experimentation (SYRCLE). Our analysis demonstrate that glyphosate disrupts redox signaling, metabolic pathways, and neurotransmitter systems, thereby affecting brain architecture and function across genders and developmental stages in rodents. The results of this review elucidate the extensive neurochemical and behavioral disruptions attributed to glyphosate, highlighting the critical need for advanced neurodevelopmental risk assessment methodologies. Such refined evaluations are vital to inform targeted prevention and intervention strategies in the context of environmental neurotoxicants.

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Neurodevelopmental disorders, such as autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD), are characterized by persistent changes in communication and social interaction, as well as restricted and stereotyped patterns of behavior. The complex etiology of these disorders possibly combines the effects of multiple genes and environmental factors. Hence, exposure to insecticides such as imidacloprid (IMI) has been used to replicate the changes observed in these disorders. Lutein is known for its anti-inflammatory and antioxidant properties and is associated with neuroprotective effects. Therefore, the aim of this study was to evaluate the protective effect of lutein-loaded nanoparticles, along with their mechanisms of action, on Drosophila melanogaster offspring exposed to IMI-induced damage. To simulate the neurodevelopmental disorder model, flies were exposed to a diet containing IMI for 7 days. Posteriorly, their offspring were exposed to a diet containing lutein-loaded nanoparticles for a period of 24 h, and male and female flies were subjected to behavioral and biochemical evaluations. Treatment with lutein-loaded nanoparticles reversed the parameters of hyperactivity, aggressiveness, social interaction, repetitive movements, and anxiety in the offspring of flies exposed to IMI. It also protected markers of oxidative stress and cell viability, in addition to preventing the reduction of Nrf2 and Shank3 immunoreactivity. These results demonstrate that the damage induced by exposure to IMI was restored through treatment with lutein-loaded nanoparticles, elucidating lutein's mechanisms of action as a therapeutic agent, which, after further studies, can become a co-adjuvant in the treatment of neurodevelopmental disorders, such as ASD and ADHD.

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El mercurio es un metal tóxico que puede atravesar la placenta y la barrera hematoencefálica, y causar la interrupción de varios procesos celulares. Estudios han investigado la exposición al mercurio y trastornos en el neurodesarrollo, por lo que se requiere un análisis crítico y riguroso de esta evidencia. El objetivo de esta revisión fue evaluar la evidencia científica disponible sobre los efectos de la exposición al mercurio durante las etapas prenatal y posnatal, y su relación con el desarrollo de trastornos neuroconductuales. Se realizó una búsqueda sistemática en las bases de datos MEDLINE y ScienceDirect; los resultados se presentaron a través de tablas y síntesis narrativa. Solo 31 estudios cumplieron los criterios de elegibilidad. En general, la evidencia es limitada sobre los efectos de la exposición al mercurio y trastornos del neurodesarrollo en niños. Entre los posibles efectos reportados, se hallan problemas en el aprendizaje, autismo y trastorno por déficit de atención e hiperactividad.

Mercury is a toxic metal which can cross the placenta and the blood-brain barrier and cause the disruption of various cellular processes. Studies have investigated mercury exposure and neurodevelopmental disorders; therefore, a critical and rigorous analysis of this evidence is required. The objective of this review was to evaluate the available scientific evidence on the effects of mercury exposure during the prenatal and postnatal periods and its relationship with the development of neurobehavioral disorders. A systematic search of the MEDLINE and ScienceDirect databases was conducted; the results were presented in tables and narrative synthesis. Only 31 studies met the eligibility criteria. Overall, the evidence on the effects of mercury exposure and neurodevelopmental disorders in children is limited. Learning disabilities, autism, and attention deficit hyperactivity disorder were some of the reported potential effects.

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Mercury is a toxic metal which can cross the placenta and the blood-brain barrier and cause the disruption of various cellular processes. Studies have investigated mercury exposure and neurodevelopmental disorders; therefore, a critical and rigorous analysis of this evidence is required. The objective of this review was to evaluate the available scientific evidence on the effects of mercury exposure during the prenatal and postnatal periods and its relationship with the development of neurobehavioral disorders. A systematic search of the MEDLINE and ScienceDirect databases was conducted; the results were presented in tables and narrative synthesis. Only 31 studies met the eligibility criteria. Overall, the evidence on the effects of mercury exposure and neurodevelopmental disorders in children is limited. Learning disabilities, autism, and attention deficit hyperactivity disorder were some of the reported potential effects.

El mercurio es un metal tóxico que puede atravesar la placenta y la barrera hematoencefálica, y causar la interrupción de varios procesos celulares. Estudios han investigado la exposición al mercurio y trastornos en el neurodesarrollo, por lo que se requiere un análisis crítico y riguroso de esta evidencia. El objetivo de esta revisión fue evaluar la evidencia científica disponible sobre los efectos de la exposición al mercurio durante las etapas prenatal y posnatal, y su relación con el desarrollo de trastornos neuroconductuales. Se realizó una búsqueda sistemática en las bases de datos MEDLINE y ScienceDirect; los resultados se presentaron a través de tablas y síntesis narrativa. Solo 31 estudios cumplieron los criterios de elegibilidad. En general, la evidencia es limitada sobre los efectos de la exposición al mercurio y trastornos del neurodesarrollo en niños. Entre los posibles efectos reportados, se hallan problemas en el aprendizaje, autismo y trastorno por déficit de atención e hiperactividad.

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Numerosas guías clínicas apoyan el uso de corticoides antenatales en embarazos menores de 34 semanas con riesgo de parto prematuro, ya que se asocian a menor morbimortalidad en este grupo al acelerar la maduración pulmonar y disminuir la incidencia de síndrome de distrés respiratorio. Sin embargo, existe menor evidencia del riesgo versus beneficio de esta medida en partos prematuros tardíos. El objetivo de este trabajo es realizar una revisión de la literatura actual con respecto al uso de corticoides antenatales en embarazos con riesgo de parto prematuro entre las 34 y 36+6 semanas. Métodos: Se realizó una revisión de la literatura relevante en PubMed, tanto en inglés como en español, desde 1997. Resultados: Se presentan estudios que demuestran beneficios a corto plazo relacionados con una disminución de la morbilidad respiratoria en los recién nacidos prematuros tardíos que recibieron corticoides antenatales. Pese a esto, es preocupante la mayor incidencia de hipoglicemia neonatal. Por otro lado, se presentan estudios que describen efectos neurocognitivos negativos a largo plazo en el mismo grupo poblacional. Finalmente, se describen las recomendaciones actuales de diversas guías clínicas en cuanto al uso de corticoides antenatales en este grupo. Conclusión: Actualmente, el uso de corticoides antenatales en prematuros tardíos no es una recomendación estándar para toda la población. Existen estudios recientes que muestran, beneficios a corto plazo de su uso en este grupo de pacientes, sin embargo, persisten dudas sobre el riesgo hipoglicemia neonatal y posibles efectos adversos a largo plazo en la esfera neuropsiquiátrica.

Introduction: Numerous clinical guidelines support the use of antenatal corticosteroids in pregnancies under 34 weeks at risk of premature delivery, since they are associated with lower morbidity and mortality in this group by accelerating lung maturation and reducing the incidence of respiratory distress syndrome. However, there is less evidence of the benefit of antenatal corticosteroids in late preterm deliveries. The objective of this work is to review the current literature regarding the use of antenatal corticosteroids in pregnancies at risk of preterm birth between 34 and 36+6 weeks. Methods: A review of the relevant literature was conducted in PubMed, both in English and Spanish, since 1997. Results: We present studies that demonstrate short-term benefits related to respiratory morbidity in late preterm infants who received antenatal corticosteroids. Nevertheless, some studies show an increased incidence of neonatal hypoglycemia. On the other hand, some studies show long-term negative neurocognitive effects in the same population group. Finally, the current recommendations of various clinical guidelines regarding the use of antenatal corticosteroids in this group are described. Conclusions: Currently, the use of antenatal corticosteroids in late preterm infants is not a standard recommendation for the entire population. There are recent studies that show short-term benefits of its use in this group of patients, however, doubts remain about the risk of neonatal hypoglycemia and possible long-term adverse effects in the neuropsychiatric sphere.

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Foods and beverages provide a source of fluoride exposure in Mexico. While high fluoride concentrations are neurotoxic, recent research suggests that exposures within the optimal range may also pose a risk to the developing brain. This prospective study examined whether dietary fluoride intake during pregnancy is associated with toddlers' neurodevelopment in 103 mother-child pairs from the PROGRESS cohort in Mexico City. Food and beverage fluoride intake was assessed in trimesters 2 and 3 using a food frequency questionnaire and Mexican tables of fluoride content. We used the Bayley-III to evaluate cognitive, motor, and language outcomes at 12 and 24 months of age. Adjusted linear regression models were generated for each neurodevelopment assessment time point (12 and 24 months). Mixed-effects models were used to consider a repeated measurement approach. Interactions between maternal fluoride intake and child sex on neurodevelopmental outcomes were tested. Median (IQR) dietary fluoride intake during pregnancy was 1.01 mg/d (0.73, 1.32). Maternal fluoride intake was not associated with cognitive, language, or motor outcomes collapsing across boys and girls. However, child sex modified the association between maternal fluoride intake and cognitive outcome (p interaction term = 0.06). A 0.5 mg/day increase in overall dietary fluoride intake was associated with a 3.50-point lower cognitive outcome in 24-month old boys (95 % CI: -6.58, -0.42); there was no statistical association with girls (ß = 0.07, 95 % CI: -2.37, 2.51), nor on the cognitive outcome at 12-months of age. Averaging across the 12- and 24-month cognitive outcomes using mixed-effects models revealed a similar association: a 0.5 mg/day increase in overall dietary fluoride intake was associated with a 3.46-point lower cognitive outcome in boys (95 % CI: -6.23, -0.70). These findings suggest that the development of nonverbal abilities in males may be more vulnerable to prenatal fluoride exposure than language or motor abilities, even at levels within the recommended intake range.

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Paracetamol (PAR) has been employed worldwide for pain and fever treatment during pregnancy and lactation. Epidemiologic studies have shown that exposure to PAR can increase the risk for developmental disorders, such as attention-deficit hyperactive disorder and autism spectrum disorder. This study aimed to investigate if gestational and lactational exposure to human-relevant doses of PAR could alter behavioural and brain oxidative stress parameters in the rat`s offspring. Wistar dams were gavaged daily with water or PAR (35 mg/kg/ or 350 mg/kg) during gestational day 6 to weaning (postnatal day 21). Behavioural assessments occurred at post-natal days 10 (nest seeking test), 27 (behavioural stereotypy) and 28 (three chamber sociability test and open field). Concentration of advanced oxidation protein products (AOPP), reduced glutathione (GSH), lipid hydroperoxides (LOOH) and activity of superoxide dismutase (SOD) were estimate in prefrontal cortex, hippocampus, striatum and cerebellum of 22-day-old rats. Compared to CON animals, males exposed to PAR during pregnancy and lactation augmented apomorphine-induced stereotyped behaviour (350 mg/kg) and ambulation in open-field test (35 mg/kg). Reduced exploratory behaviour in three chamber sociability test was observed in pups exposed to PAR at 350 mg/kg in both sexes. PAR treatment decreased hippocampal GSH level and striatal SOD activity in males exposed to 35 mg/kg, suggesting the vulnerability of these areas in PAR-induced developmental neurotoxicity. Findings suggest PAR use during pregnancy and lactation as a potential risk factor for neurodevelopmental disorders with males being more susceptible.

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Bisphenol A (BPA), a compound used in the manufacturing of plastics and epoxy resins, is an endocrine disruptor with significant adverse impact on the human's health. Here, we review the animal models and clinical studies as well as the molecular and cellular mechanisms that show that BPA alters the normal function of the reproductive system, metabolism, brain function and behavior and contributes to the development of certain neurodevelopmental disorders including autism spectrum and attention-deficit and hyperactivity disorders. BPA also causes aberrant cognitive function, behavioral disturbances, and neurodegenerative diseases, including Parkinson's disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis. It has recently been proposed that exposure to BPA may be associated with the development of certain neurodegenerative diseases and neurodevelopmental disorders; however, it is a line of research that is just emerging. This work aims to review the available information about the association between exposure to BPA and cognitive function, behavioral disturbances, neurodegenerative diseases (Parkinson�s Disease, Amyotrophic lateral sclerosis, Multiple Sclerosis), and neurodevelopmental disorders (Autism Spectrum and Attention-Deficit/Hyperactivity Disorders). Likewise, the molecular and cellular mechanisms that may be involved with these pathological conditions will be analyzed.

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BACKGROUND: Several studies have reported that there is an association between developmental and emotional/behavioural problems in children exposed to acetaminophen during foetal development. However, few studies have focused on development and behavioural outcomes in early life. OBJECTIVES: To test the association between prenatal exposure to acetaminophen and low neurodevelopmental performance at 24 months and behavioural/emotional problems at 48 months of life. METHODS: We used data from the 2004 Pelotas Birth Cohort, a population-based longitudinal prospective study. Neurodevelopment was evaluated at 24 months using Battelle's Developmental Inventory (BDI) (n = 3737). We assessed global function as well as each domain (personal-social, adaptative, motor, cognitive, and communication). Behavioural/emotional problems were assessed at 48 months using the Child Behaviour Checklist (CBCL) (n = 3624). We used the CBCL total, externalising, and internalising symptomatology and individual subscales (withdrawn, somatic complaints, anxious/depressed, social problems, cognitive problems, attention problems, aggressive behaviour, and rule-breaking behaviour). Acetaminophen use during pregnancy was retrospectively assessed at the perinatal follow-up. Poisson regression and multiple linear regression analyses were used to test the association, adjusting for several family and maternal sociodemographic and health factors, medication use during pregnancy, and the sex of the child. RESULTS: Acetaminophen exposure during prenatal development was not associated with low neurodevelopmental performance at 24 months assessed using the BDI or to emotional and behavioural problems assessed at 48 months using the CBCL in the adjusted models. CONCLUSIONS: We cannot confirm the existence of an association between acetaminophen used during pregnancy and low neurodevelopmental performance at 24 months and emotional/behavioural problems at 48 months of life based on the present results.

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BACKGROUND: Over-the-counter analgesic use during pregnancy, particularly acetaminophen, may be associated with negative developmental outcomes in children. OBJECTIVE: Estimate associations of prenatal and early-life exposure to acetaminophen in early childhood with cognitive, motor, and language skills in two birth cohorts. METHODS: The American Project Viva cohort (1217 mother-child pairs enrolled 1999-2002) assessed cognition at approximately 3 years using the Peabody Picture Vocabulary Test and the Wide Range Achievement of Visual Motor Abilities (WRAVMA). The Brazilian 2015 Pelotas Birth Cohort (3818 mother-child pairs) assessed cognition at 2 years using the INTERGROWTH-21st Neurodevelopment Assessment. We used linear regression to estimate associations of acetaminophen use during pregnancy (Project Viva and Pelotas) and infancy (Project Viva) with children's cognitive scores adjusted for maternal age, pre-pregnancy body mass index, education, parity, race/ethnicity, smoking and alcohol use during pregnancy, depression during pregnancy, antibiotic and ibuprofen use during pregnancy, household income, and child's sex. RESULTS: In Project Viva, exposure to acetaminophen in both the 1st and 2nd trimester of pregnancy was associated with lower WRAVMA drawing scores (ß -1.51, 95% CI -2.92, -0.10). However, in Pelotas, exposure to acetaminophen in both the 1st and 2nd trimester of pregnancy was not associated with INTER-NDA motor scores (ß 0.02; 95% CI -0.05, 0.09) and was associated with higher INTER-NDA total scores (ß 0.08, 95% CI 0.01, 0.16). Other comparisons did not show evidence for any associations. CONCLUSIONS: Inconsistencies and lack of specificity of the findings did not clarify the research question considering that we still have a large variability and uncertainty to define the risk or safety in the use of acetaminophen related to cognition in early childhood. More studies using better exposure assessment and better confounding variables are needed to clarify these associations.

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High-fat diets (HFDs) during pregnancy may damage the neural development and emotional behavior of rat offspring. Therefore, we investigated the neurobehavioral development of rat offspring who were fed a control diet (CD) or an HFD with lard (HFD-lard) or canola oil (HFD-canola oil), during pregnancy. Offspring's neurodevelopment (somatic growth, physical maturation, and ontogenesis reflex) was assessed while they were suckling. The rat's levels of depression, anxiety, and aggression were assessed through forced swimming, elevation plus a maze or open field test, and a foot-shock test on postnatal days 60, 80, and 110, respectively. Maternal HFDs with lard or canola oil promoted rats' offspring during suckling. They had reduced body weight and growth, physical maturation delay (auditory conduit and eyes opening to both groups HFDs-lard and canola oil; ear unfolding and incisor eruption only HFD-lard) and an ontogenesis reflex (palm grasp/vibrissa placing to both groups HFDs-lard and canola oil, and free-fall righting only in HFD-lard). Negative geotaxis resulted in the faster development of the HFD-lard offspring. Furthermore, in adulthood, the HDFs-offspring were more likely to be overweight, have shorter swimming times in the swim test, greater susceptibility to anxiety with an increased time spent in the closed arm in the elevated plus-maze while spending less time in the open arm, and having a decreased number of crossings and rearing in the open field. On the other hand, aggressive-like behavior was not affected. Therefore, these findings indicate that maternal HFDs enriched with lard or canola oil during pregnancy can impair the neurodevelopment of rat offspring and can perhaps be associated with possible changes to the emotional behavior of adult offspring.

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Exposure to environmental mixtures can exert wide-ranging effects on child neurodevelopment. However, there is a lack of statistical methods that can accommodate the complex exposure-response relationship between mixtures and neurodevelopment while simultaneously estimating neurodevelopmental trajectories. We introduce Bayesian varying coefficient kernel machine regression (BVCKMR), a hierarchical model that estimates how mixture exposures at a given time point are associated with health outcome trajectories. The BVCKMR flexibly captures the exposure-response relationship, incorporates prior knowledge, and accounts for potentially nonlinear and nonadditive effects of individual exposures. This model assesses the directionality and relative importance of a mixture component on health outcome trajectories and predicts health effects for unobserved exposure profiles. Using contour plots and cross-sectional plots, BVCKMR also provides information about interactions between complex mixture components. The BVCKMR is applied to a subset of data from PROGRESS, a prospective birth cohort study in Mexico city on exposure to metal mixtures and temporal changes in neurodevelopment. The mixture include metals such as manganese, arsenic, cobalt, chromium, cesium, copper, lead, cadmium, and antimony. Results from a subset of Programming Research in Obesity, Growth, Environment and Social Stressors data provide evidence of significant positive associations between second trimester exposure to copper and Bayley Scales of Infant and Toddler Development cognition score at 24 months, and cognitive trajectories across 6-24 months. We also detect an interaction effect between second trimester copper and lead exposures for cognition at 24 months. In summary, BVCKMR provides a framework for estimating neurodevelopmental trajectories associated with exposure to complex mixtures.

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Abstract Objective To assess the relationship between the use of psychoactive substances during pregnancy and the occurrence of severe maternal morbidity (SMM), perinatal outcomes and repercussions on the neuropsychomotor development of exposed children. Methods A case-control study nested within a cohort of severe maternal morbidity (COMMAG) was performed. Women with SMM were considered cases. Controls were thosewith low-risk pregnancy,without SMMand admitted during the same time period as the cases. Cohort data were collected retrospectively in hospital records for childbirth. A face-to-face interview was also performed with 638 women (323 without SMM and 315 with SMM) and their children of the index pregnancy between 6 months and 5 years after childbirth. During the interview, substance abuse during pregnancy was assessed by a modified question from the Alcohol, Smoking and Substance Involvement Screening Test 2.0 (ASSIST) and the neuropsychomotor development in the children was assessed by the Denver Developmental Screening Test, 2nd edition. Results The prevalence of licit or illicit drug use during pregnancy was ~ 17%. Among drug users, 63.9% used alcohol, 58.3% used tobacco, 9.2% used cocaine/crack and 4.6% used marijuana. There was no association between drug use during pregnancy and SMM, although tobacco use during pregnancy was associated with bleeding, presence of near-miss clinical criteria (NMCC) and alteration in infant development; alcohol use was associated with neonatal asphyxia; and cocaine/crack use was associated with the occurrence of some clinical complications during pregnancy. Conclusion The use of psychoactive substances during pregnancy is frequent and associated with worse maternal, perinatal and child development outcomes.

Resumo Objetivo Avaliar a relação entre o uso de substâncias psicoativas na gestação e a ocorrência de morbidade materna grave (MMG), resultados perinatais e repercussões no desenvolvimento neuropsicomotor das crianças expostas. Métodos Estudo de caso-controle a partir de uma coorte de morbidade materna grave (COMMAG). Mulheres com MMG foram consideradas casos. Controles foram mulheres com gestação de baixo risco, admitidas no mesmo período que os casos. Os dados da coorte foram coletados retrospectivamente em prontuários de internação para o parto e entrevistas presenciais conduzidas com 638 mulheres e seus filhos da gestação-índice, entre 6 meses e 5 anos após o parto. Na entrevista, o uso de substâncias na gestação foi avaliado com uma pergunta modificada introduzida no questionário para triagem do uso de álcool, tabaco e outras substâncias 2.0 (ASSIST, na sigla em inglês) e o desenvolvimento neuropsicomotor das crianças foi avaliado pelo teste de triagem do desenvolvimento Denver II. Resultados A prevalência do uso de drogas lícitas ou ilícitas na gestação foi de cerca de 17%. Das usuárias, 63,9% usaram álcool, 58,3% usaram tabaco, 9,2% usaram cocaína/crack e 4,6% usaram maconha. Não houve associação entre o uso de drogas na gestação eMMG. Contudo, o uso de tabaco foi associado a hemorragia, presença de critérios clínicos de near miss e alteração no desenvolvimento infantil. O uso de álcool foi associado à asfixia neonatal e o uso de cocaína/crack à ocorrência de alguma complicação clínica na gestação. Conclusão O abuso de substâncias lícitas ou ilícitas na gestação é frequente e associado a piores desfechos maternos, perinatais e do desenvolvimento infantil.

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OBJECTIVE: To assess the relationship between the use of psychoactive substances during pregnancy and the occurrence of severe maternal morbidity (SMM), perinatal outcomes and repercussions on the neuropsychomotor development of exposed children. METHODS: A case-control study nested within a cohort of severe maternal morbidity (COMMAG) was performed. Women with SMM were considered cases. Controls were those with low-risk pregnancy, without SMM and admitted during the same time period as the cases. Cohort data were collected retrospectively in hospital records for childbirth. A face-to-face interview was also performed with 638 women (323 without SMM and 315 with SMM) and their children of the index pregnancy between 6 months and 5 years after childbirth. During the interview, substance abuse during pregnancy was assessed by a modified question from the Alcohol, Smoking and Substance Involvement Screening Test 2.0 (ASSIST) and the neuropsychomotor development in the children was assessed by the Denver Developmental Screening Test, 2nd edition. RESULTS: The prevalence of licit or illicit drug use during pregnancy was ∼ 17%. Among drug users, 63.9% used alcohol, 58.3% used tobacco, 9.2% used cocaine/crack and 4.6% used marijuana. There was no association between drug use during pregnancy and SMM, although tobacco use during pregnancy was associated with bleeding, presence of near-miss clinical criteria (NMCC) and alteration in infant development; alcohol use was associated with neonatal asphyxia; and cocaine/crack use was associated with the occurrence of some clinical complications during pregnancy. CONCLUSION: The use of psychoactive substances during pregnancy is frequent and associated with worse maternal, perinatal and child development outcomes.

OBJETIVO: Avaliar a relação entre o uso de substâncias psicoativas na gestação e a ocorrência de morbidade materna grave (MMG), resultados perinatais e repercussões no desenvolvimento neuropsicomotor das crianças expostas. MéTODOS: Estudo de caso-controle a partir de uma coorte de morbidade materna grave (COMMAG). Mulheres com MMG foram consideradas casos. Controles foram mulheres com gestação de baixo risco, admitidas no mesmo período que os casos. Os dados da coorte foram coletados retrospectivamente em prontuários de internação para o parto e entrevistas presenciais conduzidas com 638 mulheres e seus filhos da gestação-índice, entre 6 meses e 5 anos após o parto. Na entrevista, o uso de substâncias na gestação foi avaliado com uma pergunta modificada introduzida no questionário para triagem do uso de álcool, tabaco e outras substâncias 2.0 (ASSIST, na sigla em inglês) e o desenvolvimento neuropsicomotor das crianças foi avaliado pelo teste de triagem do desenvolvimento Denver II. RESULTADOS: A prevalência do uso de drogas lícitas ou ilícitas na gestação foi de cerca de 17%. Das usuárias, 63,9% usaram álcool, 58,3% usaram tabaco, 9,2% usaram cocaína/crack e 4,6% usaram maconha. Não houve associação entre o uso de drogas na gestação e MMG. Contudo, o uso de tabaco foi associado a hemorragia, presença de critérios clínicos de near miss e alteração no desenvolvimento infantil. O uso de álcool foi associado à asfixia neonatal e o uso de cocaína/crack à ocorrência de alguma complicação clínica na gestação. CONCLUSãO: O abuso de substâncias lícitas ou ilícitas na gestação é frequente e associado a piores desfechos maternos, perinatais e do desenvolvimento infantil.

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BACKGROUND: Although growing evidence suggests that early-life excess manganese (Mn) impairs neurodevelopment, data on the neurodevelopmental effects of mancozeb, a fungicide containing Mn, and its main metabolite ethylenethiourea (ETU) are limited. OBJECTIVE: We examined whether prenatal mancozeb exposure and excess Mn were associated with neurodevelopment in 355 1-y-old infants living near banana plantations with frequent aerial mancozeb spraying in Costa Rica. METHODS: We measured urinary ETU, hair Mn, and blood Mn concentrations in samples collected 1-3 times during pregnancy from mothers enrolled in the Infants' Environmental Health (ISA) study. We then assessed neurodevelopment in their 1-y-old infants using the Bayley Scales of Infant and Toddler Development, 3rd edition (BSID-III). We estimated exposure-outcome associations using linear regression models adjusted for maternal education, parity, gestational age at birth, child age, Home Observation for Measurement of the Environment score, and location of neurodevelopmental assessment. RESULTS: Median (P25-P75) urinary ETU, hair Mn, and blood Mn measured during pregnancy were 3.3 µg/L (2.4-4.9; specific gravity-corrected), 1.7 µg/g (0.9-4.1), and 24.0 µg/L (20.3-28.0), respectively. Among girls, higher ETU was associated with lower social-emotional scores [ß per 10-fold increase=-7.4 points (95% CI: -15.2, 0.4)], whereas higher hair Mn was associated with lower cognitive scores [-3.0 (-6.1, 0.1)]. Among boys, higher hair Mn was associated with lower social-emotional scores [-4.6 (-8.5, -0.8)]. We observed null associations for blood Mn, language, and motor outcomes. CONCLUSIONS: Our findings indicate that maternal exposure to mancozeb and excess Mn during pregnancy may have adverse and sex-specific effects on infant neurodevelopment. https://doi.org/10.1289/EHP1955.

RESUMO

The decision to administer general anesthesia is childhood age remains controversial. East the issue has not only generated a high degree of concern in health professionals for Neonates and infants, but also, by the school age, being susceptible to alterations. during the consolidation process of earning and memory, where anesthetics They alter brain functioning, causing alterations in synaptogenesis and neurodegeneration in different areas such as. primary visual cortex, temporal cortices / sensory, the frontal cortex and the hippocampus. This is associated with some factors. of risk as the drugs and / or doses used for the procedure, exposure time, or own conditions of the patient.

La decisión de administrar anestesia general en la edad infantil sigue siendo controversial. Este tema no solo ha generado un alto grado de preocupación en los profesionales de la salud por los neonatos y lactantes, sino también, por la edad escolar, siendo susceptibles a alteraciones durante el proceso de consolidación del aprendizaje y memoria, donde los anestésicos alteran el funcionamiento cerebral, provocando alteraciónes en la sinaptogénesis y neurodegeneración en diferentes áreas como la corteza visual primaria, cortezas temporales / somato sensoriales, la corteza frontal y el hipocampo . Esto asociado a algunos factores de riesgo como los fármacos y/o dosis utilizadas para el procedimiento, tiempo de exposición, o condiciones propias del paciente.

RESUMO

BACKGROUND: Retinopathy of prematurity (ROP) is an eye disease caused by an alteration in retinal vasculogenesis that may lead to partial or complete vision loss with a harmful impact in terms of neurodevelopment. The purpose of the present study was to determine the neurodevelopment in patients with type i retinopathy of prematurity treated with intravitreal bevacizumab. MATERIAL AND METHODS: Case series. The inclusion criteria were: patients with type I ROP treated with a dose of 0.625mg/0.025ml of intravitreal bevacizumab. Demographic data and comorbidities were documented. Neurodevelopment was evaluated with the screening test of the Bayley Scale of Infant Development (BSID) in all patients between 11 and 28 weeks of age. RESULTS: Seven patients were included in the study. Four patients showed normal neurodevelopment according to the overall scores of the BSID scale. The distribution of high risk for neurodevelopmental delay in the different areas evaluated were as follows: 3 patients presented it in the cognitive area, one in the receptive communication area, one in the expressive area, one in the fine motor skills and 3 patients in the gross motor skills area. CONCLUSIONS: In these case series, the majority of patients treated with intravitreal bevacizumab for ROP showed normal neurodevelopment scores.