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Chinese Journal of Pediatrics ; (12): 302-306, 2022.
Article in Chinese | WPRIM | ID: wpr-935691


Objective: To investigate the effect of maternal exposure to lipopolysaccharide during pregnancy on allergic asthma in offspring in mice. Methods: Animal experimental research was carried out from June 2019 to June 2021.Pregnant C57BL/6J mice were randomly divided into 2 groups by intraperitoneal injection with 7 μg/kg lipopolysaccharide (LPS) or phosphate buffered saline (PBS) at day 15.5 of gestation. After birth, 6 offspring were randomly chosen from each group at the age of 4 weeks, and stimulated with house dust mites (HDM) or PBS, further divided into 4 groups, such as LPS+PBS group, LPS+HDM group, PBS+PBS group, PBS+HDM group, with 3 mice in each group. The cough and wheezing were observed, the histological changes in lung tissue were examined after HE staining, and the expression of inflammatory factors including interleukin (IL)-4, IL-6, IL-17A, IL-23, interferon (IFN)-α and IFN-β in the lung tissue were detected by high-throughput liquid protein chip detection. T test or rank sum test was used for the comparison among these groups. Results: The asthma-like airway inflammation was more obvious in PBS+HDM group after stimulated by HDM than that in PBS+PBS group, nevertheless, this manifestation in LPS+HDM group was milder than that in PBS+HDM group. HE staining showed that inflammatory cell aggregation in the lung tissue in PBS+HDM group was significantly higher than that in PBS+PBS group (4.0 (3.5, 4.0) vs. 0 (0, 0.5), Z=2.02, P=0.043), while it was much lower in LPS+HDM group compared to PBS+HDM group (1.0 (0.5, 1.5) vs. 4.0 (3.5, 4.0), Z=1.99, P=0.046). High-throughput liquid protein chip detection of lung tissue showed that IL-6, IL-23 and IFN-β levels were significantly higher in PBS+HDM group when compared to those in PBS+PBS group ((114±3) vs. (94±4) ng/L, (210±4) vs. (173±7) ng/L, (113±2) vs. (94±4) ng/L, t=4.37, 4.84, 3.96, all P<0.05), while the levels of IL-6, IL-23, IFN-α, IFN-β in LPS+HDM group were significantly lower than those in PBS+HDM group ((87±5) vs. (114±3) ng/L, (171±7) vs. (210±4) ng/L, (16.1±0.6) vs. (20.9±0.3) ng/L, (95±1) vs. (113±2) ng/L, t=5.07, 5.07, 7.28, 7.47, all P<0.05). Conclusions: Prenatal low dose LPS exposure can reduce offspring's airway inflammatory reactions and prevent the development of allergic disease. Maternal infection during pregnancy may affect the occurrence and development of allergic asthma in offspring.

Animals , Asthma/etiology , Disease Models, Animal , Female , Humans , Inflammation , Interleukin-23 , Interleukin-6 , Lipopolysaccharides , Lung , Maternal Exposure/adverse effects , Mice , Mice, Inbred C57BL , Pregnancy , Pyroglyphidae
Article in Chinese | WPRIM | ID: wpr-935281


Objective: To investigate the influence and critical windows of prenatal exposure to pyrethroid pesticides (PYRs) on neurodevelopment of 2-year-old children. Methods: The subjects of this study were derived from the Xuanwei Birth Cohort. A total of 482 pregnant women who participated in the rural district of Xuanwei birth cohort from January 2016 to December 2018 were included. Maternal urinary concentrations of PYRs metabolites during 8-12 gestational weeks, 20-23 gestational weeks and 32-35 gestational weeks were measured with ultra high performance liquid chromatography system coupled with a tandem mass spectrometry detector. Child neurodevelopment was evaluated with the Bayley Scales of Infant and Toddler Development-Third Edition at 2 years of age. Multivariate linear regression models and binary logistic regression models were used to assess the association between PYRs exposure during pregnancy and children's neurodevelopment. Results: A total of 360 mother-child pairs had complete data on maternal urinary PYRs metabolites detection and children's neurodevelopment assessment. The detection rate of any one PYRs metabolites during the first, second and third trimester were 93.6% (337/360), 90.8% (327/360) and 94.2% (339/360), respectively. The neurodevelopmental scores of Cognitive, Language, Motor, Social-Emotional, and Adaptive Behavior of 2-year-old children were (102.3±18.9), (100.2±16.3), (102.0±20.3), (107.8±23.3) and (85.8±18.6) points, respectively. After controlling for confounding factors, 4-fluoro-3-phenoxybenzoic acid (4F3PBA, one of PYRs metabolites) exposure in the first trimester reduced Motor (β=-5.02, 95%CI: -9.08, -0.97) and Adaptive Behavior (β=-4.12, 95%CI:-7.92, -0.32) scores of 2-year-old children, and increased risk of developmental delay of adaptive behavior (OR=2.07, 95%CI:1.13-3.82). Conclusion: PYRs exposure during the first trimester of pregnancy may affect neurodevelopment of 2-year-old children, and the first trimester may be the critical window.

Birth Cohort , Child Development , Child, Preschool , Cohort Studies , Female , Humans , Infant , Maternal Exposure/adverse effects , Pesticides/adverse effects , Pregnancy , Pregnancy Trimester, Third , Prenatal Exposure Delayed Effects/chemically induced , Pyrethrins/metabolism
Article in English | WPRIM | ID: wpr-928842


BACKGROUND@#There are only limited numbers of reviews on the association of maternal-child genetic polymorphisms and environmental and lifestyle-related chemical exposure during pregnancy with adverse fetal growth. Thus, this article aims to review: (1) the effect of associations between the above highlighted factors on adverse fetal growth and (2) recent birth cohort studies regarding environmental health risks.@*METHODS@#Based on a search of the PubMed database through August 2021, 68 epidemiological studies on gene-environment interactions, focusing on the association between environmental and lifestyle-related chemical exposure and adverse fetal growth was identified. Moreover, we also reviewed recent worldwide birth cohort studies regarding environmental health risks.@*RESULTS@#Thirty studies examined gene-smoking associations with adverse fetal growth. Sixteen maternal genes significantly modified the association between maternal smoking and adverse fetal growth. Two genes significantly related with this association were detected in infants. Moreover, the maternal genes that significantly interacted with maternal smoking during pregnancy were cytochrome P450 1A1 (CYP1A1), X-ray repair cross-complementing protein 3 (XRCC3), interleukin 6 (IL6), interleukin 1 beta (IL1B), human leukocyte antigen (HLA) DQ alpha 1 (HLA-DQA1), HLA DQ beta 1 (HLA-DQB1), and nicotinic acetylcholine receptor. Fetal genes that had significant interactions with maternal smoking during pregnancy were glutathione S-transferase theta 1 (GSTT1) and fat mass and obesity-associated protein (FTO). Thirty-eight studies examined the association between chemical exposures and adverse fetal growth. In 62 of the 68 epidemiological studies (91.2%), a significant association was found with adverse fetal growth. Across the studies, there was a wide variation in the analytical methods used, especially with respect to the genetic polymorphisms of interest, environmental and lifestyle-related chemicals examined, and the study design used to estimate the gene-environment interactions. It was also found that a consistently increasing number of European and worldwide large-scale birth cohort studies on environmental health risks have been conducted since approximately 1996.@*CONCLUSION@#There is some evidence to suggest the importance of gene-environment interactions on adverse fetal growth. The current knowledge on gene-environment interactions will help guide future studies on the combined effects of maternal-child genetic polymorphisms and exposure to environmental and lifestyle-related chemicals during pregnancy.

Alpha-Ketoglutarate-Dependent Dioxygenase FTO , Female , Fetal Development , Gene-Environment Interaction , Humans , Life Style , Maternal Exposure/adverse effects , Polymorphism, Genetic , Pregnancy
Article in English | WPRIM | ID: wpr-880358


BACKGROUND@#The majority of studies linking exposure to metals with certain health outcomes focus on known toxic metals. Alternatively, this study assesses the extent to which exposure to a wider range of metals during gestation is associated with childhood morbidity.@*METHODS@#We analyzed the concentrations of 25 metals found in urine samples of 111 pregnant women of Arab-Bedouin origin collected prior to birth. In addition, we collected medical records on their offspring for six years following birth, including every interaction with HMOs, local hospitals, and pharmacies.@*RESULTS@#The main types of morbidities diagnosed and treated during this period were preterm births, malformations, asthma-like morbidity, cardiovascular and behavioral problems, and obesity. Multivariable analysis showed that offspring born before term were more likely to have been exposed to elevated maternal concentrations of zinc, thallium, aluminum, manganese, and uranium, all with adjusted relative risk above 1.40 for an increase by each quintile. Likewise, children with asthma had been exposed to higher levels of magnesium, strontium, and barium at gestation, while behavioral outcomes were associated with elevated biometals, i.e., sodium, magnesium, calcium, selenium, and zinc, as well as higher levels of lithium, cobalt, nickel, strontium, cadmium, vanadium, arsenic, and molybdenum. A heatmap of adjusted relative risk estimates indicates the considerable implications that exposure to metals may have for preterm birth and developmental outcomes.@*CONCLUSIONS@#The current study shows that perinatal exposure to metals is adversely associated with pediatric morbidity. Further such analyses on additional samples are warranted.

Adult , Arabs/statistics & numerical data , Child , Child, Preschool , Environmental Pollutants/urine , Female , Humans , Israel , Male , Maternal Exposure/adverse effects , Metals/urine , Morbidity , Pregnancy , Prenatal Exposure Delayed Effects/epidemiology , Young Adult
Article in English | WPRIM | ID: wpr-880352


BACKGROUND@#Arsenic is a developmental neurotoxicant. It means that its neurotoxic effect could occur in offspring by maternal arsenic exposure. Our previous study showed that developmental arsenic exposure impaired social behavior and serotonergic system in C3H adult male mice. These effects might affect the next generation with no direct exposure to arsenic. This study aimed to detect the social behavior and related gene expression changes in F2 male mice born to gestationally arsenite-exposed F1 mice.@*METHODS@#Pregnant C3H/HeN mice (F0) were given free access to tap water (control mice) or tap water containing 85 ppm sodium arsenite from days 8 to 18 of gestation. Arsenite was not given to F1 or F2 mice. The F2 mice were generated by mating among control F1 males and females, and arsenite-F1 males and females at the age of 10 weeks. At 41 weeks and 74 weeks of age respectively, F2 males were used for the assessment of social behavior by a three-chamber social behavior apparatus. Histological features of the prefrontal cortex were studied by ordinary light microscope. Social behavior-related gene expressions were determined in the prefrontal cortex by real time RT-PCR method.@*RESULTS@#The arsenite-F2 male mice showed significantly poor sociability and social novelty preference in both 41-week-old group and 74-week-old group. There was no significant histological difference between the control mice and the arsenite-F2 mice. Regarding gene expression, serotonin receptor 5B (5-HT 5B) mRNA expression was significantly decreased (p < 0.05) in the arsenite-F2 male mice compared to the control F2 male mice in both groups. Brain-derived neurotrophic factor (BDNF) and dopamine receptor D1a (Drd1a) gene expressions were significantly decreased (p < 0.05) only in the arsenite-F2 male mice of the 74-week-old group. Heme oxygenase-1 (HO-1) gene expression was significantly increased (p < 0.001) in the arsenite-F2 male mice of both groups, but plasma 8-hydroxy-2'-deoxyguanosine (8-OHdG) and cyclooxygenase-2 (COX-2) gene expression were not significantly different. Interleukin-1β (IL-1β) mRNA expression was significantly increased only in 41-week-old arsenite-F2 mice.@*CONCLUSIONS@#These findings suggest that maternal arsenic exposure affects social behavior in F2 male mice via serotonergic system in the prefrontal cortex. In this study, COX-2 were not increased although oxidative stress marker (HO-1) was increased significantly in arsnite-F2 male mice.

Animals , Arsenic/toxicity , Arsenites/toxicity , Behavior, Animal/drug effects , Environmental Pollutants/toxicity , Female , Gene Expression/drug effects , Genetic Markers , Male , Maternal Exposure/adverse effects , Mice , Mice, Inbred C3H , Oxidative Stress/genetics , Prefrontal Cortex/drug effects , Pregnancy , Prenatal Exposure Delayed Effects/psychology , Reverse Transcriptase Polymerase Chain Reaction , Serotonin/metabolism , Social Behavior , Sodium Compounds/toxicity
Article in English | WPRIM | ID: wpr-888606


BACKGROUND@#Particulate matter (PM), a major component of ambient air pollution, accounts for a substantial burden of diseases and fatality worldwide. Maternal exposure to PM during pregnancy is particularly harmful to children's health since this is a phase of rapid human growth and development.@*METHOD@#In this review, we synthesize the scientific evidence on adverse health outcomes in children following prenatal exposure to the smallest toxic components, fine (PM@*RESULTS@#Maternal exposure to fine and ultrafine PM directly and indirectly yields numerous adverse birth outcomes and impacts on children's respiratory systems, immune status, brain development, and cardiometabolic health. The biological mechanisms underlying adverse effects include direct placental translocation of ultrafine particles, placental and systemic maternal oxidative stress and inflammation elicited by both fine and ultrafine PM, epigenetic changes, and potential endocrine effects that influence long-term health.@*CONCLUSION@#Policies to reduce maternal exposure and health consequences in children should be a high priority. PM

Adult , Air Pollutants/adverse effects , Air Pollution/prevention & control , Animals , Cardiovascular Diseases/chemically induced , Child Health , Child, Preschool , Disease Models, Animal , Endocrine System Diseases/chemically induced , Epigenomics , Female , Humans , Immune System Diseases/chemically induced , Infant , Infant, Newborn , Male , Maternal Exposure/adverse effects , Nervous System Diseases/chemically induced , Oxidative Stress , Particle Size , Particulate Matter/adverse effects , Placenta , Pregnancy , Pregnancy Outcome/epidemiology , Prenatal Exposure Delayed Effects/epidemiology , Respiratory Tract Diseases/chemically induced , Young Adult
Article in English | WPRIM | ID: wpr-888503


To investigate the effects of maternal exposure to 13 chemicals mixture (CM) during pregnancy on pregnancy outcome and health status of maternal/offspring mice. C57BL/6 pregnant mice were given drinking water containing carbaryl dimethoate glyphosate methomyl methyl parathion triadimefon aspartame sodium benzoate calcium disodium ethylene diamine tetra-acetate ethylparaben butylparaben bisphenol A and acacia gum The effects of CM exposure on pregnancy outcome, health status of dams/offspring, levels of circulating inflammatory cytokines in dams/offspring and emotional related behaviors of offspring were evaluated. CM exposure during pregnancy had no significant effect on pregnancy outcome, liver function, body weight of the dams in late pregnancy and uterine/ovarian weight after delivery, however, it led to an increase in maternal serum IFN-γ level (<0.05). CM exposure during pregnancy had no significant effect on the liver function of offspring, but increased the serum IFN-γ, prefrontal cortex IFN-γ, and TNF-α and hippocampus IFN-γ levels in the offspring(all <0.01). In addition, the offspring of CM group showed significant abnormal emotion-related (autism-like) behaviors in adulthood, especially in male offspring. Low dose CM exposure during pregnancy may induce inflammation status in dams/offspring, and lead to autism-like behaviors in offspring, indicating the potential effects of low dose CM exposure on human maternal and infant health.

Adult , Animals , Autistic Disorder/chemically induced , Female , Humans , Male , Maternal Exposure/adverse effects , Mice , Mice, Inbred C57BL , Phenotype , Pregnancy , Prenatal Exposure Delayed Effects/chemically induced
Rev. pediatr. electrón ; 17(3): 2-12, oct. 2020. tab
Article in Spanish | LILACS | ID: biblio-1367094


INTRODUCCIÓN: El Trastorno del Espectro Autista (TEA) afecta al 1% de los niños y se ha demostrado que una de sus principales causas se debe a factores ambientales prenatales que afectan al feto durante el periodo gestacional. El objetivo fue estimar la prevalencia de factores de riesgo (FR) prenatales en niños con TEA menores de 8 años que se controlan en un Hospital de niños. MÉTODOS: Se realizó un estudio transversal descriptivo. Se aplicó una encuesta a los padres o tutores de los niños durante la espera a su control. Se realizó un análisis descriptivo de los datos. RESULTADOS: Participaron 76 madres de niños con TEA. Entre los niños predominó el sexo masculino, mediana de edad de 5,4 años, la mayoría puede hablar sin dificultad (78%) y un 28% tenía diagnóstico de alguna enfermedad crónica. La prevalencia de FR prenatales encontrados en este estudio es similar a las reportadas en otros estudios especialmente la edad de los padres, los años de educación materna, los abortos previos y el diagnóstico de enfermedades en el embarazo. Sin embargo, la prevalencia de factores como el embarazo de alto riesgo, el consumo materno de fármacos durante el embarazo, el parto prematuro y el consumo de tabaco y drogas durante el embarazo, fueron muy superiores en este estudio comparado con otros estudios, y podrían estar relacionadas con el diagnóstico de TEA en la infancia. CONCLUSIÓN: A partir de estos hallazgos, se establece una base para realizar estudios comparativos en el futuro.

INTRODUCTION: Autistic Spectrum Disorder (ASD) affects 1% of children and it has been shown that one of its main causes is due to prenatal factors that affect the fetus during the gestational period. The objective was to estimate the prevalence of prenatal risk factors (RF) in children with ASD under 8 years of age who are monitored in a Children's Hospital. METHODS: A descriptive cross-sectional study was carried out. A survey was applied to the parents or guardians of the children during the wait for their control. A descriptive analysis of the data was carried out. RESULTS: 76 mothers of children with ASD participated. The male sex predominated, the average age was 5.4 years, the majority could speak without difficulty (78%) and 28% had a diagnosis of a chronic disease. The prevalence of prenatal RF found in this study is similar to that reported in other studies, especially the age of the parents, the years of maternal education, previous abortions and the diagnosis of diseases in pregnancy. However, the prevalence of factors such as high-risk pregnancy, maternal consumption of medicines during pregnancy, preterm delivery and tobacco and drug use during pregnancy were much higher in this study compared to other studies, and could be related to the diagnosis of ASD in childhood. CONCLUSION: Based on these findings, a basis for comparative studies in the future is established.

Humans , Male , Female , Pregnancy , Infant , Child, Preschool , Child , Adult , Parents/psychology , Maternal Exposure/adverse effects , Environmental Hazards , Autism Spectrum Disorder/epidemiology , Prenatal Exposure Delayed Effects , Prevalence , Cross-Sectional Studies , Surveys and Questionnaires , Risk Factors , Substance-Related Disorders , Tobacco Use , Hospitals, Pediatric
Int. j. morphol ; 38(5): 1250-1257, oct. 2020. tab, graf
Article in English | LILACS | ID: biblio-1134433


SUMMARY: Residential heating with wood is an important source of ambient air pollution. Evidence links air pollution to serious health effects such as respiratory and cardiovascular mortality and morbidity. We hypothesized that prenatal exposure to wood smoke pollution causes morphological changes in the development of the rat lung, leading to altered lung structure and function during later life. We presumed that analysis of the fetal lung stereology provides novel insights into the underlying processes mediating particulate matter associated developmental changes and damage. The objective of the study was to investigate the effects of exposure during gestational period to wood smoke pollution on lung fetal morphology. To test this, pregnant rats were exposed during pregestational and gestational periods to wood smoke pollution. Complete lungs samples were obtained from 24 fetus from healthy female G3 rats subjected to cesarean at 19 days post-fecundation. The lungs were prepared for histological and stereological analysis. The volume fraction of terminal bronchioles VV [tb, lung] and volume fraction of parenchyma VV [par, lung], surface density of terminal bronchioles SV [tb, lung] as well as numerical density of bronchiolar exocrinocytes NA [ec,lung] were calculated by light microscopy. Statistical analysis detected significant differences between groups in volume density VV [tb, lung; %] (p=0.0012) and surface density SV [tb, lung; mm2/mm3] (p<0.0001) of the terminal bronchioles. However, it did not show differences between groups in the stereological parameter volume density VV [par, lung; %] (p=0.0838) and numerical density of bronchiolar exocrinocytes NA [ec,lung; nº/mm2] (p=0.0705). The analysis of the evidence obtained indicates that exposure to environmental pollution was affects lung maturation, and particularly the proportion and area of terminal bronchioles in the fetal lung. In conclusion, maternal exposure to wood smoke pollution during pregnancy was associated with a decrease in the lower conducting airways of lungs, which, according to urban pollution studies, could be related to early childhood lower respiratory illness. The public health implications of this study are that reducing or avoiding exposure to wood smoke is important before and during pregnancy.

RESUMEN: La calefacción residencial con leña es una fuente importante de contaminación ambiental. La evidencia vincula la contaminación del aire con graves efectos sobre la salud, como la mortalidad y la morbilidad respiratoria y cardiovascular. Hipotetizamos que la exposición prenatal a la contaminación por humo de leña causa cambios en el desarrollo del pulmón de rata, lo que conduce a una morfo-función pulmonar alteradas durante la vida posterior, creemos que el análisis de la estereología pulmonar fetal proporcionará nuevos conocimientos sobre los procesos subyacentes que median esos cambios. El objetivo del estudio fue investigar los efectos de la exposición prenatal a la contaminación ambiental por humo de leña sobre la morfología pulmonar fetal. Ratas preñadas fueron expuestas durante los períodos pregestacional y gestacional a la contaminación por humo de leña. En fetos de 19 días post-fecundación fue obtenido el pulmón para análisis histológico y estereológico. Fue determinado la fracción de volumen de bronquiolos terminales VV [tb, pulmón], fracción de volumen del parénquima VV [par, pulmón], densidad superficial de los bronquiolos terminales SV [tb, pulmón] así como la densidad numérica de exocrinocitos NA [ec, pulmón]. El análisis estadístico detectó diferencias significativas entre grupos en la densidad de volumen V [tb, pulmón; %] (p=0,0012) y densidad superficial SV [tb, pulmón; mm2/mm3] (p<0,0001) de los bronquiolos terminales. Sin embargo, no demostró diferencias entre grupos en la densidad de volumen VV [par, pulmón; %] (p=0,0838) y numérica de exocrinocitos bronquiolares NA [ec, pulmón; nº / mm ] (p=0,0705). El análisis de la evidencia obtenida indica que la exposición a la contaminación ambiental afectó la maduración pulmonar, y particularmente la proporción y área de bronquiolos terminales en el pulmón fetal. En conclusión, la exposición materna a la contaminación por humo de leña durante la gestación se asoció a una disminución de las vías respiratorias conductoras de aire en pulmón, lo que, según estudios de contaminación urbana, podría estar relacionado con enfermedades de las vías respiratorias inferiores en la primera infancia. Las implicaciones para la salud pública de este estudio son que reducir o evitar la exposición al humo de leña es importante previo y durante la gestación. Por otro lado, la contaminación por humo de leña tiene un gran impacto en la salud pública que, en teoría, es posible prevenir.

Animals , Female , Pregnancy , Rats , Air Pollutants/toxicity , Air Pollution/adverse effects , Lung/drug effects , Smoke/adverse effects , Wood , Analysis of Variance , Maternal Exposure/adverse effects , Disease Models, Animal , Environmental Exposure , Particulate Matter/toxicity , Fetus/drug effects , Heating , Lung/pathology
Int. j. morphol ; 38(5): 1356-1364, oct. 2020. tab, graf
Article in English | LILACS | ID: biblio-1134448


SUMMARY: Studies in humans showed that prenatal exposure to urban air pollution (AP) influences fetal development, and increases the incidence of adverse pregnancy outcomes and some diseases in postnatal life. However, most of these were performed in environments where the main source of environmental particulate matters (PM) emission is diesel combustion by motor vehicles and industries, thereby ignoring the effects produced by wood smoke pollution. We hypothesized that morphological changes in the placenta could contribute to the reduction in fetal size associated with different periods of exposure to AP produced by wood smoke pollution prior to and during pregnancy. The objective of the study was to investigate the quantitative effects of long-term exposure to environmental levels of wood smoke pollution on the macroscopic and microscopic morphology of the placenta in rats. To test this, pregnant rats were exposed during pregestational and gestational periods to wood smoke pollution in indoor and outdoor environments. At 19 days of gestation, the placentas were obtained by caesarean and were prepared for histological, planimetric and stereological analysis. The volume and proportions of the placental compartments were estimated. In addition, stereological estimators in fetal capillaries were calculated in the labyrinth region. Crown rump length, fetus weight and litter weight were influenced by pregestational and gestational exposure periods. Exposure to wood smoke pollution during pregestational period has significant effect on the volume of the placenta, and consequently on fetal height. In conclusion, this study demonstrated that long-term outdoor exposure to wood smoke pollution from residential heating affects fetal health, decreasing the absolute volume of the entire placenta and the placental interface between the mother and fetus, decreasing the total volume of blood vessels present in the labyrinth region ofthe placenta and affecting the size of the fetus.

RESUMEN: Estudios en humanos demostraron que la exposición prenatal a la polución del aire urbano influye en el desarrollo fetal y aumenta la incidencia de resultados adversos de la gestación y algunas enfermedades postnatales. Sin embargo, la mayoría de ellos fueron realizados en entornos donde la principal fuente de emisión de material particulado, fue la combustión de petróleo por vehículos a motor e industrias, ignorando los efectos producidos por el humo de leña producido por la calefacción intradomiciliaria. Hipotetizamos respecto a que los cambios de la placenta contribuirían a la disminución del tamaño fetal relacionado a los períodos de exposición al humo de leña durante los periodos pregestacional y gestacional. El objetivo del estudio fue investigar los efectos cuantitativos de la exposición al humo de leña sobre la morfología macroscópica y microscópica en placenta de ratas. Para probar esto, ratas preñadas fueron expuestas durante los períodos pregestacional y gestacional a la contaminación por humo de leña en ambientes interiores y exteriores. A los 19 días de gestación, las placentas fueron obtenidas por cesárea y fueron preparadas para un análisis histológico, planimétrico y estereológico. Fue estimado el volumen absoluto y las proporciones de los compartimentos placentarios. Además, fueron calculados estimadores estereológicos en capilares fetales del laberinto y trofoblasto. La longitud, el peso del feto y el peso de la camada fueron influenciados por los períodos de exposición pregestacional y gestacional. La exposición a la contaminación por humo de leñá durante el período pregestacional tuvo un efecto significativo en el volumen de la placenta y, en consecuencia, en la altura del feto. En conclusión, este estudio demostró que la exposición a largo plazo al humo de leña afecta la salud del feto, disminuyendo el volumen absoluto de la placenta, además, afecta la interfaz placentaria entre la madre y feto, disminuyendo el volumen total de vasos sanguíneos presentes en la región del laberinto placentario y por consecuente afectando el tamaño del feto.

Animals , Female , Pregnancy , Rats , Placenta/drug effects , Smoke/adverse effects , Air Pollutants/toxicity , Fetus/drug effects , Wood , Rats, Sprague-Dawley , Maternal Exposure/adverse effects , Fires/adverse effects , Body Size , Fetal Development/drug effects , Environmental Pollution/adverse effects , Particulate Matter
Säo Paulo med. j ; 137(6): 486-490, Nov.-Dec. 2019. tab
Article in English | LILACS | ID: biblio-1094524


ABSTRACT BACKGROUND: Exposure to air pollutants has several effects on human health, including during pregnancy. OBJECTIVE: To identify whether exposure to benzene and toluene among pregnant women contributes to preterm delivery. DESIGN AND SETTING: Longitudinal study using data on newborns from mothers living in São José dos Campos (SP) in 2016, who had been exposed to benzene and toluene. METHODS: A logistic regression model with three hierarchical levels was constructed using maternal variables relating to newborns, and using benzene and toluene concentrations in quartiles. Occurrences of cesarean births, twins or malformations were excluded. Maternal exposure windows of 5, 10, 15, 30, 60 and 90 days prior to delivery were considered. RESULTS: Out of the 9,562 live births, 3,671 newborns were included and 343 newborns were born at less than 37 weeks of gestation (9.3%). The average birth weight was 3,167.2 g. Exposure to benzene and toluene was significantly associated (P = 0.04) with preterm delivery in the five-day window. There was no association in any of the other exposure windows. CONCLUSIONS: It was possible to identify that maternal exposure to benzene and toluene has an acute effect on preterm delivery.

Humans , Male , Female , Pregnancy , Infant, Newborn , Adult , Young Adult , Toluene/adverse effects , Benzene/adverse effects , Maternal Exposure/adverse effects , Premature Birth/chemically induced , Pregnancy Trimester, Third , Prenatal Care/statistics & numerical data , Odds Ratio , Risk , Longitudinal Studies , Air Pollutants/analysis
Rev. bras. ginecol. obstet ; 41(5): 333-347, May 2019. tab, graf
Article in English | LILACS | ID: biblio-1013618


Abstract Objective To investigate the relationship between maternal exposure to alcohol and low birthweight (LBW). Methods The literature search was performed in January 2017 using the following electronic databases: Medline, Embase, LILACS, SciELO, Web of Science, Scopus, CINHAL, Proquest, and PsychInfo. The search strategy used the following terms: alcohol drinking, binge drinking, alcohol-related disorders, alcoholism, alcohol addiction/ use/abuse/consumption, light/moderate/social/low drinking, low birthweight, case-control studies, retrospective studies, and cohort studies. No restrictions regarding language or publication date were considered. The literature search yielded 2,383 articles, and after screening and eligibility assessment, 39 articles were included in the systematic review, and 38 studies were included in the meta-analysis. Results Maternal alcohol consumption was associated with LBWamong retrospective cohort studies (relative risk [RR] = 1.37; 95%CI [confidence interval]:1.10-1.77; I2 = 98.4%; p < 0.01). Prospective cohort studies (RR = 1.11; 95%CI: 0.98-1.25; I2 = 81.5%; p < 0.01), and case-control studies (odds ration [OR] = 1.16; 95%CI: 0.68-1.97; I2 = 61.2%; p = 0.05) showed no association between alcohol and LBW.No publication bias was identified, and the meta-regression showed that the sample size influenced the high heterogeneity among retrospective cohort studies. The subgroup analysis showed differences in association between groups when compared by sample size, type of adjustment, or crude measures and publication year. Conclusions We have not found an association between alcohol consumption during gestation and LBW in the analysis in all of the subgroups. In addition, we have found a high heterogeneity between the primary studies, which is related to methodological differences in the conduction of these studies.

Resumo Objetivo Investigar a associação entre a exposição maternal ao álcool e o baixo peso ao nascer. Método A busca na literatura ocorreu em janeiro de 2017 nas seguintes bases de dados eletrônicas: Medline, Embase, LILACS, SciELO, Web of Science, Scopus, CINHAL, Proquest, e PsychInfo. A estratégia de busca utilizou os seguintes termos: alcohol drinking, binge drinking, alcohol-related disorders, alcoholism, alcohol addiction/use/ abuse/consumption, light/moderate/social/low drinking, low birthweight, case-control studies, retrospective studies, e cohort studies. Não houve restrição de idioma e ano de publicação. A busca na literatura identificou 2.383 artigos, e depois de analisados conforme os critério de elegibilidade, foram incluídos na revisão sistemática 39 estudos, e 38 estudos foram incluídos na metanálise. Resultados A amostra foi composta por 497.023 gestantes. O consumo materno de álcool foi associado ao baixo peso ao nascer entre os estudos de coorte retrospectiva (risco relativo [RR] = 1,37; IC [intervalo de confiança] 95%: 1,10-1,77; I2 = 98,4%; p < 0,01). Os estudos de coorte prospectiva (RR = 1,11; IC95%: 0,98-1,25; I2 = 81,5%; p < 0,01) e caso-controle (razão de chances [OR, na sigla em inglês] = 1,16; IC95%: 0,68-1,97; I2 = 61,2%; p = 0,05) não apresentaram associação entre o consumo e o desfecho. Não foi identificado viés de publicação, e a metarregressão mostrou que o tamanho da amostra influenciou a heterogeneidade entre os estudos de coorte prospectiva. Na análise por subgrupo, houve diferenças entre os grupos por tamanho de amostra, por tipo de ajuste e por ano de publicação. Conclusão Não encontramos associação entre o consumo e o baixo peso ao nascer em todas as análises por subgrupo. Além disso, encontramos alta heterogeneidade entre os estudos primários, e isto se deve possivelmente às diferenças metodológicas na condução destes estudos.

Humans , Female , Pregnancy , Alcohol Drinking/adverse effects , Infant, Low Birth Weight , Maternal Exposure/adverse effects , Prenatal Care , Birth Weight
Int. j. morphol ; 37(1): 87-92, 2019. tab, graf
Article in English | LILACS | ID: biblio-990010


SUMMARY: This study aimed to investigate the toxic effects of cigarette smoke exposure on lung and the protective role of Omega 3 and Vitamin D against these toxic effects biochemically and histologically. 28 pregnant Wistar Albino rats were divided into four groups. The first group was control group; the second group was exposed to smoke of 10 cigarette by puff device 2 hours/day after pregnancy; the third group was exposed to cigarette smoke together with Omega 3 (0.5 mg/kg/day) and the fourth group was exposed to cigarette smoke together with vitamin D (42 microgram/kg/day). Finally, lung tissue sections of the newborn rats were stained with Hemotoxilen eosine and Masson tricromite. Malondialdehyde (MDA) and Fluorescent Oxidation Products (FOU) levels were measured. Fetal weights and the number of fetuses were significantly lower in the group received only cigarette smoke (both p<0.001). Histopathologically, pulmonary volume, number of developed alveols and parenchyma elasticity decreased significantly, meanwhile interstitial tissue increased, elastin and collagen did not develop adequately. Histopathologic changes significantly decreased in the group given Omega 3 and Vitamin D. Statistically, MDA and FOU levels were found to be higher in the group exposed to cigarette smoke compared to the control group, and MDA and FOU levels were lower in the group given Omega 3 along with cigarette smoke (p<0.001). Cigarette smoke caused histologically significant damage to fetal lung tissue, oxidative stress and increased MDA and FOU levels. This damage was significantly reduced with Omega 3 and Vitamine D supplementation. Omega 3 is an important antioxidant; vitamin D has no significant antioxidant effect.

RESUMEN: Este estudio tuvo como objetivo investigar los efectos tóxicos de la exposición al humo de cigarrillo en el pulmón, y el papel protector de Omega 3 y la Vitamina D contra esos efectos. 28 ratas Wistar albino preñadas fueron separadas en cuatro grupos. El primer grupo grupo control; el segundo grupo estuvo expuesto al humo de 10 cigarrillos por dispositivo de inhalación 2 horas / día después de la preñez; el tercer grupo se expuso al humo del cigarrillo junto con Omega 3 (0,5 mg / kg / día) y el cuarto grupo se expuso al humo del cigarrillo junto con vitamina D (42 microgramos / kg / día). Secciones de tejido pulmonar de las ratas recién nacidas se tiñeron con Hematoxilina Eosina y tricrómico de Masson. Se midieron los niveles de malondialdehído (MDA) y productos de oxidación fluorescente (POF). Los pesos fetales y el número de fetos fueron significativamente más bajos en el grupo que recibió solamente humo de cigarrillo (ambos p <0,001). Histopatológicamente, el volumen pulmonar, el número de alveolos desarrollados y la elasticidad del parénquima disminuyeron significativamente; mientras que el tejido intersticial aumentó y la elastina y el colágeno no se desarrollaron adecuadamente. Los cambios histopatológicos disminuyeron significativamente en el grupo que recibió Omega 3 y Vitamina D. Estadísticamente, se encontró que los niveles de MDA y POF eran más altos en el grupo expuesto al humo de cigarrillo en comparación con el grupo control, además los niveles de MDA y POF fueron más bajos en el grupo que recibió Omega 3 junto con el humo del cigarrillo (p <0,001). El humo del cigarrillo causó daños histológicamente significativos en el tejido pulmonar fetal, el estrés oxidativo y el aumento de los niveles de MDA y FOU. Este daño se redujo significativamente con los suplementos de Omega 3 y Vitamina D. El omega 3 es un importante antioxidante; la vitamina D no tiene ningún efecto antioxidante significativo.

Animals , Female , Pregnancy , Rats , Vitamin D/administration & dosage , Fatty Acids, Omega-3/administration & dosage , Maternal Exposure/adverse effects , Lung Injury/prevention & control , Nicotine/toxicity , Smoke/adverse effects , Analysis of Variance , Rats, Wistar , Oxidative Stress , Lung Injury/chemically induced , Lung Injury/pathology , Fetus/drug effects , Fluorescence , Animals, Newborn , Malondialdehyde/analysis
Cad. Saúde Pública (Online) ; 35(2): e00041018, 2019. tab
Article in Portuguese | LILACS | ID: biblio-1039414


O objetivo deste artigo foi avaliar a conformidade entre as recomendações de uso de medicamentos antidepressivos durante a amamentação, presentes em bulas, e as recomendações de fontes bibliográficas baseadas em evidências científicas. Foram avaliadas as bulas padrão de 23 antidepressivos com registro ativo no Brasil. A presença de contraindicação do uso do antidepressivo durante a amamentação foi comparada com as informações presentes no manual técnico do Ministério da Saúde, no livro Medications and Mothers' Milk e nas bases de dados LactMed, Micromedex e UpToDate. Na maioria das bulas (62,5%), o antidepressivo é contraindicado na amamentação. Entre as fontes bibliográficas, esse percentual variou de 0% a 25%. O estudo aponta para baixa conformidade entre bulas e fontes bibliográficas, alertando sobre a necessidade de revisão do conteúdo e forma de apresentação das informações presentes nas bulas dos antidepressivos no Brasil.

This article sought to evaluate the conformity between recommendations regarding antidepressant use during breastfeeding found in drug package inserts with recommendations from science-based bibliographic sources. We evaluated the standard drug package inserts of 23 antidepressants with active registration in Brazil. The presence of contraindications of antidepressant use during breastfeeding was compared with information present in the Brazilian Ministry of Health technical manual, the book Medications and Mothers' Milk and on the databases LactMed, Micromedex and UpToDate. In most drug package inserts (62.5%), antidepressants are contraindicated during breastfeeding. Among bibliographical sources, that percentage varied between 0% and 25%. The study shows a low conformity between drug package inserts and bibliographical sources, alerting to the need for revising the content and presentation of information present in antidepressant drug package inserts in Brazil.

El objetivo de este artículo fue evaluar la conformidad entre las recomendaciones de uso de medicamentos antidepresivos durante la lactancia, presentes en prospectos, y las recomendaciones de fuentes bibliográficas, basadas en evidencias científicas. Se evaluaron los prospectos estándar de 23 antidepresivos con registro activo en Brasil. La presencia de contraindicaciones en el consumo de antidepresivos durante la lactancia se comparó con la información presente en el manual técnico del Ministerio de la Salud, en el libro Medications and Mothers' Milk, y en las bases de datos LactMed, Micromedex y UpToDate. En la mayoría de los prospectos (62,5%), el antidepresivo está contraindicado durante la lactancia. Entre las fuentes bibliográficas el porcentaje varió de 0% a 25%. El estudio señala la escasa conformidad entre prospectos y fuentes bibliográficas, alertando sobre la necesidad de revisión del contenido, así como de la forma de presentación de la información que aparece en los prospectos de los antidepresivos en Brasil.

Humans , Female , Breast Feeding/adverse effects , Evidence-Based Medicine , Drug Industry/standards , Drug Labeling/standards , Antidepressive Agents/adverse effects , Brazil , Lactation/metabolism , Risk Factors , Drug Monitoring , Maternal Exposure/adverse effects , Drug Information Services/standards , Antidepressive Agents/administration & dosage
Rev. chil. pediatr ; 89(6): 761-765, dic. 2018.
Article in Spanish | LILACS | ID: biblio-978152


Resumen: En el presente articulo se revisan los mecanismos del imprinting epigenético mediante el cual se producen los efectos diferidos generados por la exposición prenatal o infantil temprana a agentes químicos contaminantes. Se revisaron las bases de datos Pubmed y Embase para identificar estudios publicados entre 2005 y 2018, junto a artículos considerados pioneros en este ámbito. Se incluyeron además, datos generados en nuestro Laboratorio. Como fuente de información secundaria se citan normas chilenas de concentraciones de algunos contaminantes en agua potable publicados por el Ministerio de Salud de Chile. Se describen cambios en la metilación de diversos genes causados por exposición prenatal o infantil temprana a algunos contaminantes ambientales relevantes en Chile: arsénico, plomo, ftalatos y fenoles, y se mencionan algunas de las enfermedades orgánicas y cambios neuroconductuales que se desarrollan más tarde en la vida como consecuencia de dichas exposi ciones. Se sugiere que un mayor conocimiento de los factores ambientales y una mejor educación de la población, permitirían una protección más adecuada de embarazadas y lactantes, en especial durante las ventanas de susceptibilidad y que los pediatras y obstetras, serían los profesionales mejor indicados para desarrollar estas acciones. Se sugiere además la necesidad de adecuar normas am bientales y aumentar la fiscalización de contaminantes y sus fuentes, para prevenir el deterioro de la salud de las futuras generaciones.

Abstract: This review explains the epigenetic imprinting mechanisms by which the delayed effects generated by prenatal or early childhood exposure to chemical pollutants are produced. Pubmed and Embase databases were reviewed to identify studies published between 2005 and 2018, along with articles considered pioneers in this field. We also included data generated in our Laboratory. As a source of secondary information, Chilean standards on concentrations of some pollutants in drinking water published by the Ministry of Health of Chile are cited. Changes are described in the methylation of diverse genes caused by prenatal or early childhood exposure to some relevant environmental po llutants in Chile such as arsenic, lead, phenols, and phthalates, and some of the organic diseases and neurobehavioral changes that occur later in life as a consequence of these exposures are mentioned. We suggest that a wider knowledge of environmental factors and better education of the population would allow a more adequate protection of pregnant women and infants especially during the win dows of susceptibility, and that pediatricians and obstetricians would be in the best position to deve lop these actions. We also suggest the need to adapt environmental standards and increase the control of pollutants and their sources to prevent health deterioration of future generations.

Humans , Female , Pregnancy , Adult , Prenatal Exposure Delayed Effects/etiology , Maternal Exposure/adverse effects , Epigenesis, Genetic , Environmental Pollutants/toxicity , Prenatal Exposure Delayed Effects/genetics
Ciênc. Saúde Colet. (Impr.) ; 23(11): 3535-3545, Oct. 2018. tab
Article in English | LILACS | ID: biblio-974741


Abstract The gold rush in the Amazon Region caused an increase of mercury (Hg) levels in the environment, and, consequently, raised human exposure. Once released into aquatic systems, Hg could generate methylmercury (MeHg), an extremely toxic compound, which is accumulated through trophic chains. Several studies have provided evidences of the brain sensitivity to MeHg, as well as, of the fetus vulnerability during pregnancy. The main objective of this study was to estimate the Mild Mental Retardation (MMR) in Amazonian populations, caused by prenatal exposure to MeHg, using the methodology proposed by Poulin (2008), which quantifies the environmental burden of disease. The estimates of the MMR burden, attributed to prenatal MeHg exposure, were based on the calculation of Disability-Adjusted Life Years (DALY), which were obtained from MMR incidence rate in the studied populations. At the local level, the MMR incidence rate calculations were based on primary data of MeHg exposure of riverine women at childbearing age. The MMR incidence rate was equal to 5.96/1,000 infants, which would result in 2.0 IQ points loss in 34.31% of the newborns. The estimated DALY/1,000 infants was equal to 71.2, while the DALY was 576. For the regional estimates, different exposure scenarios were created. The calculated DALY varied from 3,256 to 65,952 per year.

Resumo A corrida pelo ouro na Amazônia elevou os níveis de mercúrio (Hg) no ambiente e, consequentemente, aumentou a exposição humana. Uma vez liberado em sistemas aquáticos, o Hg pode gerar metilmercúrio (MeHg), um composto tóxico que se acumula ao longo de cadeias tróficas. Vários estudos têm gerado evidências sobre a sensibilidade do cérebro ao MeHg, bem como sobre a vulnerabilidade do feto durante a gravidez. O principal objetivo deste trabalho foi estimar a carga de Retardo Mental Leve (RML) em populações amazônicas, causada pela exposição pré-natal ao MeHg, utilizando a metodologia proposta por Poulin (2008). As estimativas de RML, atribuída à exposição ao MeHg pré-natal, foram baseadas no cálculo dos Anos de Vida Ajustados por Incapacidade (DALY), que foi desenvolvido a partir de taxa de incidência RML nas populações estudadas. Em nível local, o cálculo da taxa de incidência RML baseou-se em dados primários sobre a exposição ao MeHg em mulheres ribeirinhas em idade fértil. A taxa de incidência RML foi igual a 5,96/1.000 nascidos, o que resulta na perda de 2,0 pontos de QI em 34,31% dos nascidos. A estimativa de DALY/1.000 nascidos foi igual a 71,2, enquanto o DALY foi de 576. Para as estimativas regionais, foram criados diferentes cenários de exposição. Os DALYs calculados variaram de 3.256 a 65.952 por ano.

Humans , Female , Pregnancy , Infant, Newborn , Infant , Adolescent , Adult , Young Adult , Maternal Exposure/adverse effects , Environmental Exposure/adverse effects , Intellectual Disability/epidemiology , Methylmercury Compounds/toxicity , Prenatal Exposure Delayed Effects/epidemiology , Brazil , Cost of Illness , Disabled Persons , Quality-Adjusted Life Years , Intellectual Disability/etiology , Middle Aged
J. pediatr. (Rio J.) ; 93(6): 610-618, Nov.-Dec. 2017. tab, graf
Article in English | LILACS | ID: biblio-894070


Abstract Objective: The population-based cancer registries (PBCR) and the Information System on Live Births in Brazil (Sistema de Informações sobre Nascidos Vivos [SINASC]) have information that enables the test for risk factors associated with leukemia at an early age. The aim of this study was to identify maternal and birth characteristics associated with early-age acute leukemia (EAL) in Brazil. Methods: A case-cohort study was performed using secondary dataset information of PBCR and SINASC. The risk association variables were grouped into (i) characteristics of the child at birth and (ii) characteristics of maternal exposure during pregnancy. The case-control ratio was 1:4. Linkage was performed using R software; odds ratio (OR) and 95% confidence interval (CI) were calculated by logistic regression models. Results: EAL was associated with maternal occupational exposure to chemicals (agricultural, chemical, and petrochemical industry; adjOR: 2.18, 95% CI: 1.16-4.10) and with birth defects (adjOR: 3.62, 95% CI: 1.19-11.00). Conclusions: The results of this study, with the identification of EAL risk factors in population-based case-cohort study, strengthen the knowledge and improve databases, contributing to investigations on risk factors associated with childhood leukemia worldwide.

Resumo Objetivos: Os registros de câncer de base populacional (RCBP) e o Sistema Nacional de Nascidos Vivos (SINASC) possuem informações que possibilitam testar hipóteses sobre fatores de riscos associados às leucemias. O objetivo principal deste projeto é identificar quais as características ao nascimento das crianças que estariam associadas ao risco de desenvolver Leucemia Aguda (LA) na primeira infância. Métodos: Foram utilizadas informações de 12 RCBP e do Sistema de Informação de Nascidos Vivos das mesmas localidades. Foram elegíveis 272 casos e 1.088 controles no período de 1996 a 2010. As associações de riscos de LA foram agrupadas em, (i) características da criança ao nascer, e (ii) características de exposição materna durante a gestação da criança. A relação de casos e controles foi de 1:4. As análises para padronização, estruturação do banco de dados e análises estatísticas foram realizadas através dos aplicativos Excel, R-Studio e SPSS 21. Resultados: Houve associação entre anomalias congênitas (RC 3,62, IC95% 1,19-11,00) e exposição ocupacional materna a produtos químicos (OR 2,18, p 0,002) com o risco do desenvolvimento de LA. Conclusão: A utilização de banco de dados secundários populacionais para a identificação de fatores de risco para LA fortaleceu o intercâmbio de conhecimentos e melhoria das bases de dados, e contribuiu para investigações sobre as associações de riscos nas leucemias agudas em contexto mundial.

Humans , Female , Child , Leukemia/etiology , Occupational Exposure/adverse effects , Maternal Exposure/adverse effects , Brazil , Information Systems , Birth Certificates , Case-Control Studies , Risk Factors , Cohort Studies
Säo Paulo med. j ; 135(4): 347-354, July-Aug. 2017. tab
Article in English | LILACS | ID: biblio-904097


ABSTRACT CONTEXT AND OBJECTIVE: Several effects of exposure to air pollutants on human health are known. The aim of this study was to identify whether exposure of pregnant women to air pollutants contributes towards low birth weight and which sex is more affected. DESIGN AND SETTING: Longitudinal study using data on newborns from mothers living in São José do Rio Preto (SP) who were exposed to air pollutants in 2012-2013. METHODS: A hierarchical model on three levels was built using maternal and newborn variables and environmental concentrations of particulate matter, ozone and nitrogen dioxide in quartiles. Preterm new-borns, twins and newborns with birth defects were excluded and exposure windows of 30, 60 and 90 days before delivery were considered. RESULTS: 8,948 newborns were included: 4,491 males (50.2%) and 4,457 females (49.8%); 301 newborns presented low birth weight (3.4%). The mean weight differed between males (3281.0 g) and females (3146.4 g) (P < 0.001). Exposure to ozone was significantly associated with low birth weight in both sexes in the 30-day window (odds ratio, OR = 1.38) and 90-day window (OR = 1.48); and among females, in the 30-day window (OR = 1.58) and 90-day window (OR = 1.59). Exposure to particulate matter had a paradoxical protective effect. No association was found among male newborns. CONCLUSIONS: Female newborns showed greater susceptibility to maternal exposure to air pollutants. Studies on low birth weight in relation to maternal exposure to air pollutants should deal with males and females separately.

RESUMO CONTEXTO E OBJETIVO: São vários os efeitos da exposição a poluentes do ar na saúde humana. O objetivo deste estudo foi identificar se a exposição da gestante contribui para o baixo peso ao nascer e qual o sexo mais acometido. TIPO DE ESTUDO: Estudo longitudinal com dados de recém-nascidos de mães residentes em São José do Rio Preto (SP) com exposição a poluentes do ar em 2012 e 2013. MÉTODOS: Foi construído modelo hierarquizado em três níveis com variáveis maternas, do recém-nascido e concentrações de material particulado, ozônio e dióxido de nitrogênio, em quartis. Foram excluídos recém-nascidos prematuros, gemelares ou com malformações e consideradas janelas de exposição de 30, 60 e 90 dias anteriores ao parto. RESULTADOS: Foram incluídos 8.948 recém-nascidos, 4.491 do sexo masculino (50,2%) e 4.457 do feminino (49,8%), e identificados 301 recém-nascidos com baixo peso (3,4%). Os pesos médios foram diferentes entre o sexo masculino (3.281,0 g) e o feminino (3.146,4 g) (P < 0,001). Exposição ao ozônio esteve associada significativamente ao baixo peso ao nascer em ambos os sexos nas janelas de 30 dias (odds ratio, OR = 1,38) e 90 dias (OR = 1,48) e, no sexo feminino, nas janelas de 30 dias (OR = 1,58) e 90 dias (OR =1,59). Exposição ao material particulado teve efeito protetor paradoxal. Não houve associação no sexo masculino. CONCLUSÕES: Houve maior susceptibilidade do sexo feminino aos poluentes a partir da exposição materna. Estudos sobre baixo peso ao nascer segundo exposição materna a poluentes do ar devem separar sexo masculino e feminino.

Humans , Male , Female , Pregnancy , Infant, Newborn , Adult , Birth Weight/drug effects , Maternal Exposure/adverse effects , Air Pollutants/toxicity , Particulate Matter/toxicity , Prenatal Exposure Delayed Effects/etiology , Infant, Low Birth Weight , Sex Factors , Risk Factors , Longitudinal Studies , Maternal Exposure/statistics & numerical data
Rev. bras. epidemiol ; 20(2): 189-199, Abr.-Jun. 2017. tab, graf
Article in English | LILACS | ID: biblio-898592


ABSTRACT: Introduction: Birth weight is an important indicator of several conditions that manifest earlier (as fetal and neonatal mortality and morbidity, inhibited growth and cognitive development) and later in life such as chronic diseases. Air pollution has been associated with adverse pregnancy outcomes. Objective: Retrospective cohort study investigated the association between low birth weight (LBW) and maternal exposure to air pollutants in Volta Redonda city, Rio de Janeiro, Brazil, from 2003 to 2006. Methods: Birth data was obtained from Brazilian Information System. Exposure information (O3, PM10, temperature and humidity) was provided by Governmental Air Quality Monitoring System. Linear and Logistic models, adjusted for sex, type of pregnancy, prenatal care, place of birth, maternal age, parity, education, congenital anomalies and weather variables were employed. Results: Low birth weight (LBW) represented 9.1% of all newborns (13,660). For an interquartile range increase in PM10 it was found OR2 ndTrimester = 1.06 (95%CI 1.02 - 1.10), OR3 rdTrimester = 1.06 (95%CI 1.02 - 1.10) and, in O3 it was found OR2 ndTrimester = 1.03 (95%CI 1.01 - 1.04), OR3 rdTrimester = 1.03 (95%CI 1.02 - 1.04). The dose-response relationship and a reduction in birth weight of 31.11 g (95%CI -56.64 - -5.58) was observed in the third trimester of pregnancy due to an interquartile increase of O3. Conclusion: This study suggests that exposures to PM10 and O3, even being below the Brazilian air quality standards, contribute to risks of low birth weight.

RESUMO: Introdução: O peso de nascimento é considerado como um indicador importante de várias condições que se manifestam mais cedo (como mortalidade fetal e neonatal e morbidade, inibição do crescimento e desenvolvimento cognitivo) e mais tarde na vida, tais como as doenças crônicas. A poluição atmosférica tem sido associada a efeitos adversos da gestação. Objetivo: Estudo de coorte histórica que associa o baixo peso ao nascer (BPN) e a exposição materna aos poluentes do ar em Volta Redonda, Rio de Janeiro, Brasil, entre 2003 e 2006. Metodologia: Dados sobre nascidos vivos foram obtidos no sistema de informação Brasileiro, e os de exposição (O3, PM10, temperatura e umidade) na rede pública de monitoramento do ar. Foram utilizados modelos lineares e logísticos, ajustados por sexo, tipo de gravidez, assistência pré-natal, local de nascimento, idade materna, paridade, educação, anomalias congênitas e variáveis meteorológicas. Resultados: A prevalência de BPN foi de 9,1% sobre 13.660 nascimentos. Para o aumento de um interquartil no nível de PM10 (OR2 ºtrimestre = 1,06; IC95% 1,02 - 1,10; OR3 ºtrimestre = 1,06; IC95% 1,02 - 1,10) e no nível de O3 (OR2 ºtrimestre = 1,03; IC95% 1,01 - 1,04; OR3 ºtrimestre = 1,03; IC95% 1,02 - 1,04). Observou-se uma relação dose-resposta e uma redução do peso ao nascer de 31,11 g (95%IC -56,64 - -5,58) no terceiro trimestre da gravidez devido ao aumento de um interquartil de O3. Conclusão: Este estudo sugere que exposições ao PM10 e O3, mesmo abaixo de padrões de qualidade do ar, contribuem para os riscos de BPN.

Humans , Male , Female , Pregnancy , Adolescent , Adult , Young Adult , Infant, Low Birth Weight , Maternal Exposure/adverse effects , Air Pollution/adverse effects , Brazil , Urban Health , Retrospective Studies , Cohort Studies
J. pediatr. (Rio J.) ; 93(2): 111-119, Mar.-Apr. 2017. graf
Article in English | LILACS | ID: biblio-841331


Abstract Objective: Autism spectrum disorders are lifelong and often devastating conditions that severely affect social functioning and self-sufficiency. The etiopathogenesis is presumably multifactorial, resulting from a very complex interaction between genetic and environmental factors. The dramatic increase in autism spectrum disorder prevalence observed during the last decades has led to placing more emphasis on the role of environmental factors in the etiopathogenesis. The objective of this narrative biomedical review was to summarize and discuss the results of the most recent and relevant studies about the environmental factors hypothetically involved in autism spectrum disorder etiopathogenesis. Sources: A search was performed in PubMed (United States National Library of Medicine) about the environmental factors hypothetically involved in the non-syndromic autism spectrum disorder etiopathogenesis, including: air pollutants, pesticides and other endocrine-disrupting chemicals, electromagnetic pollution, vaccinations, and diet modifications. Summary of the findings: While the association between air pollutants, pesticides and other endocrine-disrupting chemicals, and risk for autism spectrum disorder is receiving increasing confirmation, the hypothesis of a real causal relation between them needs further data. The possible pathogenic mechanisms by which environmental factors can lead to autism spectrum disorder in genetically predisposed individuals were summarized, giving particular emphasis to the increasingly important role of epigenetics. Conclusions: Future research should investigate whether there is a significant difference in the prevalence of autism spectrum disorder among nations with high and low levels of the various types of pollution. A very important goal of the research concerning the interactions between genetic and environmental factors in autism spectrum disorder etiopathogenesis is the identification of vulnerable populations, also in view of proper prevention.

Resumo Objetivo: Os transtornos do espectro autista (TEAs) são vitalícios e normalmente são doenças devastadoras que afetam gravemente o funcionamento social e a autossuficiência. A etiopatogenia é presumivelmente multifatorial, resultante de uma interação muito complexa entre fatores genéticos e ambientais. O aumento drástico na prevalência de TEAs observado nas últimas décadas levou à maior ênfase no papel dos fatores ambientais na etiopatogenia. O objetivo desta análise da narrativa biomédica foi resumir e discutir os resultados dos estudos mais recentes e relevantes sobre os fatores ambientais hipoteticamente envolvidos na etiopatogenia dos TEAs. Fontes: Foi feita uma pesquisa na Biblioteca Nacional de Medicina dos Estados Unidos (PubMed) sobre os fatores ambientais hipoteticamente envolvidos na etiopatogenia dos TEAs não sindrômicos, inclusive poluentes atmosféricos, pesticidas e outros desreguladores endócrinos, poluição eletromagnética, vacinas e alterações na dieta. Resumo dos achados: Embora a associação entre poluentes atmosféricos, pesticidas e outros desreguladores endócrinos e o risco de TEA tenha recebido cada vez mais confirmações, a hipótese de uma relação causal real entre eles ainda precisa de mais dados. Os possíveis mecanismos patogênicos por meio dos quais os fatores ambientais podem causar TEA em indivíduos geneticamente predispostos foram resumidos, com ênfase especial no papel cada vez mais importante da epigenética. Conclusões: Futuras pesquisas devem investigar se há uma diferença significativa na prevalência de TEA entre nações com níveis altos e baixos de vários tipos de poluição. Um objetivo muito importante da pesquisa a respeito das interações entre fatores genéticos e ambientais na etiopatogenia do TEA é a identificação de populações vulneráveis, também em virtude da prevenção adequada.

Humans , Female , Pregnancy , Child , Autistic Disorder/etiology , Autistic Disorder/genetics , Environmental Pollutants/toxicity , Autism Spectrum Disorder/etiology , Autism Spectrum Disorder/genetics , Prenatal Exposure Delayed Effects , Risk Factors , Maternal Exposure/adverse effects , Genetic Predisposition to Disease