RESUMO
BACKGROUND: Previous studies have shown that prenatal maternal smoking and maternal secondhand smoke exposure during pregnancy were associated with an increased risk of wheezing and asthma development. However, few studies have examined the influence of different sources of tobacco exposure in different perinatal timeframes (preconception, prenatal, and postnatal) on wheezing phenotypes in children. Using national survey data from Japan, we investigated the effects of exposure to tobacco smoke during pregnancy on wheezing phenotypes in children before the age of 3 years. METHODS: Pregnant women who lived in the 15 regional centers in the Japan Environment and Children's Study were recruited. We obtained information on prenatal and postnatal exposure to active and secondhand smoke (SHS) and wheeze development up to 3 years of age. Multiple logistic regression analysis was performed to determine the association between tobacco smoke exposure and wheezing phenotypes in children. RESULTS: We analyzed 73,057 singleton births and identified four longitudinal wheezing phenotypes: never wheezing; early transient wheezing (wheezing by age 1 year but not thereafter); late-onset wheezing (wheezing by age 2-3 years but not beforehand); and persistent wheezing. Maternal smoking during pregnancy was significantly associated with early transient and persistent wheezing in children compared with no maternal smoking [early transient wheezing: 1-10 cigarettes per day, adjusted odds ratio (aOR) 1.43, 95% confidence interval (CI) 1.23-1.66; ≥ 11 cigarettes per day, aOR 1.67, 95% CI 1.27-2.20; persistent wheezing: 1-10 cigarettes per day, aOR 1.64, 95% CI 1.37-1.97; ≥ 11 cigarettes per day, aOR 2.32, 95% CI 1.70-3.19]. Smoking cessation even before pregnancy was also significantly associated with increased risk of early transient wheezing, late-onset wheezing, and persistent wheezing in children. Moreover, maternal exposure to SHS during pregnancy was significantly associated with increased risk of early transient and persistent wheezing compared with no such exposure. CONCLUSIONS: Maternal smoking before and throughout pregnancy was associated with wheeze development in children up to 3 years of age. It appears that smoking is detrimental compared to never smoking, regardless of whether individuals quit smoking before or after becoming aware of the pregnancy.
Assuntos
Exposição Materna , Fenótipo , Efeitos Tardios da Exposição Pré-Natal , Sons Respiratórios , Poluição por Fumaça de Tabaco , Humanos , Feminino , Sons Respiratórios/etiologia , Gravidez , Japão/epidemiologia , Poluição por Fumaça de Tabaco/efeitos adversos , Pré-Escolar , Lactente , Masculino , Exposição Materna/efeitos adversos , Fumar/efeitos adversos , Adulto , Recém-Nascido , Estudos de Coortes , Fatores de RiscoRESUMO
BACKGROUND: Although recent in vitro experimental results have raised the question of whether maternal exposure to per- and polyfluoroalkyl substances (PFAS) may be a potential environmental risk factor for chromosomal abnormalities, epidemiological studies investigating these associations are lacking. OBJECTIVES: This study examined whether prenatal PFAS exposure is associated with a higher prevalence of chromosomal abnormalities among offspring. METHODS: We used data from the Japan Environment and Children's Study, a nationwide birth cohort study, and employed logistic regression models to examine the associations between maternal plasma PFAS concentrations in the first trimester and the diagnosis of chromosomal abnormalities in all births (artificial abortions, miscarriages, stillbirths, and live births) up to 2 years of age. In addition, we examined associations with mixtures of PFAS using multipollutant models. RESULTS: The final sample consisted of 24,724 births with singleton pregnancies, of which 44 confirmed cases of chromosomal abnormalities were identified (prevalence: 17.8/10,000 births). When examined individually, exposure to perfluorononanoic acid (PFNA) and perfluorooctane sulfonic acid (PFOS) showed positive associations with any chromosomal abnormalities with age-adjusted odds ratios of 1.81 (95% CI: 1.26, 2.61) and 2.08 (95% CI: 1.41, 3.07) per doubling in concentration, respectively. These associations remained significant after Bonferroni correction, although they did not reach the adjusted significance threshold in certain sensitivity analyses. Furthermore, the doubling in all PFAS included as a mixture was associated with chromosomal abnormalities, indicating an age-adjusted odds ratio of 2.25 (95% CI: 1.34, 3.80), with PFOS as the predominant contributor, followed by PFNA, perfluoroundecanoic acid (PFUnA), and perfluorooctanoic acid (PFOA). DISCUSSION: The study findings suggested a potential association between maternal exposure to PFAS, particularly PFOS, and chromosomal abnormalities in offspring. However, the results should be interpreted cautiously, because selection bias arising from the recruitment of women in early pregnancy may explain the associations. https://doi.org/10.1289/EHP13617.
Assuntos
Ácidos Alcanossulfônicos , Aberrações Cromossômicas , Fluorocarbonos , Exposição Materna , Humanos , Feminino , Japão/epidemiologia , Fluorocarbonos/sangue , Fluorocarbonos/toxicidade , Gravidez , Exposição Materna/estatística & dados numéricos , Exposição Materna/efeitos adversos , Aberrações Cromossômicas/induzido quimicamente , Aberrações Cromossômicas/estatística & dados numéricos , Ácidos Alcanossulfônicos/sangue , Ácidos Alcanossulfônicos/toxicidade , Adulto , Poluentes Ambientais/toxicidade , Poluentes Ambientais/sangue , Masculino , Lactente , Recém-Nascido , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Estudos de Coortes , Pré-Escolar , Coorte de Nascimento , Caprilatos/toxicidade , Caprilatos/sangueRESUMO
OBJECTIVE: To probe into the protective effect of different dose of secoisolariciresinol diglucoside(SDG) on brain of offspring of mice anainst oxidative damage and inflammatory reaction induced by maternal exposure to trans fatty acids(TFA) during gestation, and observe the the changes of regulating Nrf2/Keap1 pathway in the course. METHODS: 30 healthy female mice(C57BL/6) were divided into 5 groups randomly, they are respectively control group, TFA-exposed group, and three SDG-intervention groups(low-(TFA+LSDG), medium-(TFA+MSDG) and high-(TFA+HSDG)). The pregnancy mice of control group and TFA group were treated with distilled water and 60 mg/kg·d TFA by gavage, in the same time, the mice of three SDG-intervention groups were treated with 60 mg/kg·d TFA by gavage and fed with feed included SDG(10, 20 and 30 mg/kg). The treatment to pregnancy mice continued to birth of offspring. After 21 days of lactation, the offspring were killed under anesthesia and the experiment was ended. The coefficient of brain was calculated. The levels of superoxide dismutase(SOD), glutathione peroxidase(GSH-Px), malondialdehyde(MDA), tumor necrosis factor-α(TNF-α), interferon-γ(IFN-γ) and amyloid-ß(Aß)of brain were detected. RT-PCR and Western Blot was used to detected gene expression and protein levels of nuclear factor erythroid-2 related factor 2(Nrf2), kelch-like ECH-associated protein 1(Keap1), quinone oxidoreductase 1(NQO1) and hemeoxygenase-l(HO-1). RESULTS: Compared with control group, the brain coefficient and Aß1-40 of offspring of TFA-group had no significant changes(P>0.05), the activity of SOD and GSH-Px reduced, the content of MDA, IFN-γ, TNF-α and Aß1-42 increased, the level of mRNA and protein expression of Nrf2, NQO1 and HO-1 decreased and the level of mRNA and protein expression of Keap1 increase because of the exposion to TFA during gestation and all the differences were statistically significant(P<0.05). Compared with TFA-group, the brain coefficient, Aß1-40 and the level of NQO1 mRNA of offspring of three SDG-intervention groups had no significant changes(P>0.05), the activity of SOD(the middle and high dose SDG intervention groups) and GSH-Px(three SDG-intervention groups) increased, the content of MDA(the middle and high dose SDG intervention groups), IFN-γ(the middle and high dose SDG intervention groups), TNF-α(three SDG-intervention groups) and Aß1-42(the middle and high dose SDG intervention groups) decreased, the mRNA expression of Nrf2 and HO-1(the middle and high dose SDG intervention groups) was up-regulated, the mRNA expression of Keap1(the middle and high dose SDG intervention group) decreased, proteic expression of Nrf2, NQO1 and HO-1 of three SDG-intervention groups increase and the level of protein of Keap1 decreased because of the intervention of SDG during gestation(P<0.05). CONCLUSION: These result suggest that maternal TFA exposure during gestation can result in oxidative stress and inflammation to brain of offspring in a way. SDG can protect brain of mice of offspring from TFA-induced oxidative injury by up-regulating the expression of mRNA and protein of Nrf2, down-regulating the expression of Keap1, accelerating expression of protein of NQO1 and HO-1 which are antioxidant protein lying downstream of pathway of Nrf2/Keap1.
Assuntos
Encéfalo , Butileno Glicóis , Glucosídeos , Proteína 1 Associada a ECH Semelhante a Kelch , Camundongos Endogâmicos C57BL , Fator 2 Relacionado a NF-E2 , Estresse Oxidativo , Ácidos Graxos trans , Animais , Feminino , Camundongos , Glucosídeos/farmacologia , Gravidez , Fator 2 Relacionado a NF-E2/metabolismo , Encéfalo/metabolismo , Encéfalo/efeitos dos fármacos , Proteína 1 Associada a ECH Semelhante a Kelch/metabolismo , Proteína 1 Associada a ECH Semelhante a Kelch/genética , Estresse Oxidativo/efeitos dos fármacos , Butileno Glicóis/farmacologia , Ácidos Graxos trans/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Inflamação/metabolismo , Inflamação/induzido quimicamente , Exposição Materna/efeitos adversos , Heme Oxigenase-1/metabolismo , Heme Oxigenase-1/genética , Superóxido Dismutase/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , Fator de Necrose Tumoral alfa/genética , Malondialdeído/metabolismo , NAD(P)H Desidrogenase (Quinona)/metabolismo , NAD(P)H Desidrogenase (Quinona)/genéticaRESUMO
Infertility has gradually become a global health concern, and evidence suggests that exposure to environmental endocrine-disrupting chemicals (EDCs) represent one of the key causes of infertility. Benzo(a)pyrene (BaP) is a typical EDC that is widespread in the environment. Previous studies have detected BaP in human urine, semen, cervical mucus, oocytes and follicular fluid, resulting in reduced fertility and irreversible reproductive damage. However, the mechanisms underlying the effects of gestational BaP exposure on offspring fertility in male mice have not been fully explored. In this study, pregnant mice were administered BaP at doses of 0, 5, 10 and 20 mg/kg/day via gavage from Days 7.5 to 12.5 of gestation. The results revealed that BaP exposure during pregnancy disrupted the structural integrity of testicular tissue, causing a disorganized arrangement of spermatogenic cells, compromised sperm quality, elevated levels of histone modifications and increased apoptosis in the testicular tissue of F1 male mice. Furthermore, oxidative stress was also increased in the testicular tissue of F1 male mice. BaP activated the AhR/ERα signaling pathway, affected H3K4me3 expression and induced apoptosis in testicular tissue. AhR and Cyp1a1 were overexpressed, and the expression of key molecules in the antioxidant pathway, including Keap1 and Nrf2, was reduced. The combined effects of these molecules led to apoptosis in testicular tissues, damaging and compromising sperm quality. This impairment in testicular cells further contributed to compromised testicular tissues, ultimately impacting the reproductive health of F1 male mice.
Assuntos
Apoptose , Benzo(a)pireno , Estresse Oxidativo , Animais , Benzo(a)pireno/toxicidade , Masculino , Feminino , Camundongos , Estresse Oxidativo/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Gravidez , Testículo/efeitos dos fármacos , Testículo/metabolismo , Disruptores Endócrinos/toxicidade , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Células Germinativas/efeitos dos fármacos , Espermatozoides/efeitos dos fármacos , Exposição Materna/efeitos adversos , Histonas/metabolismo , Código das Histonas/efeitos dos fármacosRESUMO
The prevalence of allergies has been globally escalating. While allergies could appear at any age, they often develop in early life. However, the significant knowledge gap in the field is the mechanisms by which allergies affect certain people but not others. Investigating early factors and events in neonatal life that have a lasting impact on determining the susceptibilities of children to develop allergies is a significant area of the investigation as it promotes the understanding of neonatal immune system that mediates tolerance versus allergies. This review focuses on the research over the recent 10 years regarding the potential maternal factors that influence offspring allergies with a view to food allergy, a potentially life-threatening cause of anaphylaxis. The role of breast milk, maternal diet, maternal antibodies, and microbiota that have been suggested as key maternal factors regulating offspring allergies are discussed here. We also suggest future research area to expand our knowledge of maternal-offspring interactions on the pathogenesis of food allergy.
Assuntos
Hipersensibilidade Alimentar , Humanos , Hipersensibilidade Alimentar/imunologia , Feminino , Gravidez , Animais , Leite Humano/imunologia , Efeitos Tardios da Exposição Pré-Natal/imunologia , Tolerância Imunológica , Microbiota/imunologia , Anafilaxia/imunologia , Anafilaxia/etiologia , Exposição Materna/efeitos adversos , Recém-Nascido , Alérgenos/imunologiaRESUMO
Objective: To explore the relationship between the exposure level of particulate matter 2.5 (PM2.5) and particulate matter 10 (PM10) in the air of pregnant women during preconception and first trimester of pregnancy and the risk of gestational diabetes mellitus (GDM). Methods: The data of pregnant women delivered in 22 monitoring hospitals in Hebei Province from 2019 to 2021 were collected, and the daily air quality data of their cities were used to calculate the exposure levels of PM2.5 and PM10 in different pregnancy stages, and logistic regression model was used to analyze the impact of exposure levels of PM2.5 and PM10 on GDM during preconception and first trimester of pregnancy. Results: 108,429 singleton live deliveries were included in the study, of which 12,967 (12.0%) women had a GDM diagnosis. The prevalence of GDM increased over the course of the study from 10.2% (2019) to 14.9% (2021). From 2019 to 2021, the average exposure of PM2.5 and PM10 was relatively 56.67 and 103.08µg/m3 during the period of preconception and first trimester of pregnancy in Hebei Province. Handan, Shijiazhuang, and Xingtai regions had the most severe exposure to PM2.5 and PM10, while Zhangjiakou, Chengde, and Qinhuangdao had significantly lower exposure levels than other regions. The GDM group had statistically higher exposure concentrations of PM2.5 and PM10 during the period of preconception, first trimester, preconception and first trimester (P<0.05). Multivariate logistic regression analysis showed that the risk of GDM increases by 4.5%, 6.0%, and 10.6% for every 10ug/m3 increase in the average exposure value of PM2.5 in preconception, first trimester, preconception and first trimester, and 1.7%, 2.1%, and 3.9% for PM10. Moreover, High exposure to PM2.5 in the first, second, and third months of preconception and first trimester is associated with the risk of GDM. And high exposure to PM10 in the first, second, and third months of first trimester and the first, and third months of preconception is associated with the risk of GDM. Conclusion: Exposure to high concentrations of PM2.5 and PM10 during preconception and first trimester of pregnancy can significantly increase the risk of GDM. It is important to take precautions to prevent exposure to pollutants, reduce the risk of GDM, and improve maternal and fetal outcomes.
Assuntos
Poluição do Ar , Diabetes Gestacional , Exposição Materna , Material Particulado , Primeiro Trimestre da Gravidez , Humanos , Feminino , Gravidez , Diabetes Gestacional/epidemiologia , China/epidemiologia , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Adulto , Material Particulado/análise , Material Particulado/efeitos adversos , Exposição Materna/efeitos adversos , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/efeitos adversos , Estudos de Coortes , Exposição Ambiental/efeitos adversos , Adulto JovemRESUMO
BACKGROUND: Exposure to fine or respirable particulate matter has been linked to an elevated risk of gestational diabetes mellitus (GDM). However, the association between exposure to particulate matter with an aerodynamic diameter ≤ 1 µm (PM1) and GDM has not been explored. METHODS: We conducted a cohort study involving 60,173 pregnant women from nine hospitals in Beijing, China, from February 2015 to April 2021. Daily concentrations of PM1 and ozone were obtained from a validated spatiotemporal artificial intelligence model. We used a modified Poisson regression combined with distributed lag models to estimate the association between weekly-specific PM1 exposure and the risk of GDM after adjusting for individual-level covariates. RESULTS: Among the 51,299 pregnant women included in the final analysis, 4008 were diagnosed with GDM. Maternal exposure to PM1 during preconception and gestational periods was generally associated with an increased risk of GDM. The most pronounced associations were identified during the 12th week before pregnancy, the 5th-8th weeks of the first trimester, and the 23rd-24th weeks of the second trimester. Each 10⯵g/m3 increase in PM1 was associated with a relative risk of GDM of 1.65 (95â¯% CI: 1.59, 1.72) during the preconception period, 1.67 (95â¯% CI: 1.61, 1.73) in the first trimester, 1.52 (95â¯% CI: 1.47, 1.58) in the second trimester, and 2.54 (95â¯% CI: 2.45, 2.63) when considering the first and second trimester combined. CONCLUSIONS: Exposure to PM1 before and during pregnancy was associated with an increased risk of GDM, particularly during the 12 weeks before pregnancy and gestational weeks 5-8 and 23-24.
Assuntos
Poluentes Atmosféricos , Diabetes Gestacional , Exposição Materna , Material Particulado , Gravidez , Feminino , Diabetes Gestacional/epidemiologia , Diabetes Gestacional/induzido quimicamente , Humanos , Material Particulado/análise , Adulto , Poluentes Atmosféricos/toxicidade , Poluentes Atmosféricos/análise , Exposição Materna/estatística & dados numéricos , Exposição Materna/efeitos adversos , Estudos de Coortes , Pequim/epidemiologia , Ozônio/análise , Adulto Jovem , Poluição do Ar/estatística & dados numéricos , Poluição do Ar/efeitos adversos , Tamanho da PartículaRESUMO
BACKGROUNDS AND AIM: Exposure to pesticides has been proposed as a potential contributor to adverse pregnancy outcomes, possibly through the induction of inflammation, oxidative stress, and disruption of endocrine functions. Nevertheless, the definitive link between prenatal pesticide exposure and the risk of Spontaneous Abortion (SAB) remains uncertain. The objective of this systematic review is to explore and analyze the existing evidence regarding the link between pesticide exposure and the risk of SAB. METHODS: A comprehensive systematic literature search was carried out on PubMed, Web of Science, and Scopus from their inception until February 2024 to identify relevant studies exploring the potential link between pesticide exposure and SAB. The frequency of SAB events and the total number of patients in each group were used to calculate the Relative Risk (RR) using the Mantel-Haenszel random-effects model. Heterogeneity among the studies was evaluated by visually inspecting the forest plot and performing the Chi-square test and I2 tests. We also used RevMan version 5.4 for Windows for the analysis. We also used the NIH tool to assess the quality of the included studies. RESULTS: The initial database search yielded 2121 results, with 1525 articles remaining after removing duplicates. After screening, 29 articles were eligible for full-text review, and 18 studies (Four case-control, eleven cohorts, three cross-sectional) were included in the meta-analysis, comprising 439,097 participants. All included studies evaluated the primary outcome, SAB. Most of the included studies were cross-sectional in design, and pesticide exposure was primarily assessed through questionnaires administered to patients. We found that most of our observational studies, precisely 12 out of the total, were deemed fair quality. Four studies were rated poor quality, while only two received a good quality rating. The analysis demonstrated a significant 41â¯% increase in SAB risk among pregnant women exposed to pesticides compared to pregnant women without exposure to pesticides (RR= 1.41, 95â¯% CI; [1.10, 1.80], P= 0.006). CONCLUSION: Our systematic review and meta-analysis revealed a significant 41â¯% increase in the risk of SAB among pregnant women exposed to pesticides. However, it is essential to acknowledge the limitations of the current evidence: potential publication bias and the inability to establish causality. Moving forward, future research should focus on longitudinal studies, mechanistic insights, and risk reduction strategies. In summary, our findings underscore the urgency of public health measures to protect maternal and fetal health in pesticide-exposed areas. Rigorous research and preventive strategies are crucial to mitigate adverse outcomes.
Assuntos
Aborto Espontâneo , Exposição Materna , Praguicidas , Praguicidas/toxicidade , Humanos , Feminino , Gravidez , Aborto Espontâneo/induzido quimicamente , Aborto Espontâneo/epidemiologia , Exposição Materna/efeitos adversos , Exposição Materna/estatística & dados numéricosRESUMO
Fetal exposures can induce epigenetic modifications, particularly DNA methylation, potentially predisposing individuals to later health issues. Cord blood (CB) DNA methylation provides a unique window into the fetal epigenome, reflecting the intrauterine environment's impact. Maternal factors, including nutrition, smoking and toxin exposure, can alter CB DNA methylation patterns, associated with conditions from obesity to neurodevelopmental disorders. These epigenetic changes underscore prenatal exposures' enduring effects on health trajectories. Technical challenges include tissue specificity issues, limited coverage of current methylation arrays and confounding factors like cell composition variability. Emerging technologies, such as single-cell sequencing, promise to overcome some of these limitations. Longitudinal studies are crucial to elucidate exposure-epigenome interactions and develop prevention strategies. Future research should address these challenges, advance public health initiatives to reduce teratogen exposure and consider ethical implications of epigenetic profiling. Progress in CB epigenetics research promises personalized medicine approaches, potentially transforming our understanding of developmental programming and offering novel interventions to promote lifelong health from the earliest stages of life.
[Box: see text].
Assuntos
Metilação de DNA , Exposição Ambiental , Epigênese Genética , Sangue Fetal , Efeitos Tardios da Exposição Pré-Natal , Humanos , Sangue Fetal/metabolismo , Gravidez , Feminino , Exposição Ambiental/efeitos adversos , Exposição Materna/efeitos adversos , Epigenômica/métodosRESUMO
BACKGROUND: Exposure to ambient air pollution is a top risk factor contributing to the global burden of disease. Pregnant persons and their developing fetuses are particularly susceptible to adverse health outcomes associated with air pollution exposures. During pregnancy, the thyroid plays a critical role in fetal development, producing thyroid hormones that are associated with brain development. Our objective is to systematically review recent literature that investigates how prenatal exposure to air pollution affects maternal and fetal thyroid function. METHODS: Following the Navigation Guide Framework, we systematically reviewed peer-reviewed journal articles that examined prenatal exposures to air pollution and outcomes related to maternal and fetal thyroid function, evaluated the risk of bias for individual studies, and synthesized the overall quality and strength of the evidence. RESULTS: We found 19 studies that collected data on pregnancy exposure windows spanning preconception to full term from 1999 to 2020 across nine countries. Exposure to fine particulate matter (PM2.5) was most frequently and significantly positively associated with fetal/neonatal thyroid hormone concentrations, and inversely associated with maternal thyroid hormone concentrations. To a lesser extent, traffic-related air pollutants, such as nitrogen dioxide (NO2) had significant effects on fetal/neonatal thyroid function but no significant effects on maternal thyroid function. However, the body of literature is challenged by risk of bias in exposure assessment methods and in the evaluation of confounding variables, and there is an inconsistency amongst effect estimates. Thus, using the definitions provided by the objective Navigation Guide Framework, we have concluded that there is limited, low quality evidence pertaining to the effects of prenatal air pollution exposure on maternal and fetal thyroid function. CONCLUSION: To improve the quality of the body of evidence, future research should seek to enhance exposure assessment methods by integrating personal monitoring and high-quality exposure data (e.g., using spatiotemporally resolved satellite observations and statistical modeling) and outcome assessment methods by measuring a range of thyroid hormones throughout the course of pregnancy.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Exposição Materna , Efeitos Tardios da Exposição Pré-Natal , Glândula Tireoide , Humanos , Gravidez , Feminino , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Materna/efeitos adversos , Glândula Tireoide/efeitos dos fármacos , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Poluentes Atmosféricos/efeitos adversos , Material Particulado/análise , Material Particulado/efeitos adversos , Hormônios Tireóideos/sangue , Feto/efeitos dos fármacosRESUMO
Phthalates are ubiquitous in diverse environments and have been linked to a myriad of detrimental health outcomes. However, the association between phthalate exposure and allergic rhinitis (AR) remains unclear. To address this knowledge gap, we conducted a systematic review and meta-analysis to comprehensively evaluate the relationship between phthalate exposure and childhood AR risk. We searched the Cumulative Index to Nursing and Allied Health Literature, Excerpta Medica Database, and PubMed to collect relevant studies and estimated pooled odds ratios (OR) and 95% confidence intervals (CI) for risk estimation. Ultimately, 18 articles, including seven cross-sectional, seven case-control, and four prospective cohort studies, were selected for our systematic review and meta-analysis. Our pooled data revealed a significant association between di-2-ethylhexyl phthalate (DEHP) exposure in children's urine and AR risk (OR = 1.188; 95% CI = 1.016-1.389). Additionally, prenatal exposure to combined phthalates and their metabolites in maternal urine was significantly associated with the risk of childhood AR (OR = 1.041; 95% CI = 1.003-1.081), although specific types of phthalates and their metabolites were not significant. Furthermore, we examined environmental phthalate exposure in household dust and found no significant association with AR risk (OR = 1.021; 95% CI = 0.980-1.065). Our findings underscore the potential hazardous effects of phthalates on childhood AR and offer valuable insights into its pathogenesis and prevention.
Assuntos
Exposição Ambiental , Ácidos Ftálicos , Rinite Alérgica , Humanos , Rinite Alérgica/epidemiologia , Ácidos Ftálicos/efeitos adversos , Ácidos Ftálicos/urina , Criança , Exposição Ambiental/efeitos adversos , Feminino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Risco , Exposição Materna/efeitos adversos , Pré-EscolarRESUMO
Although emerging evidence on the association between per- and polyfluoroalkyl substances (PFASs) and neurodevelopment have been investigated, there is no consensus on the effect of maternal PFASs on neurodevelopment in offspring. Here, we assessed the risk of maternal PFASs exposure on the neurodevelopment of offspring using a novel Targeted Risk Assessment of Environmental Chemicals (TRAEC) strategy based on multiple evidence. The evidence from five online databases were analyzed the effect of PFASs on neurodevelopment. The potential neurodevelopment risk of PFASs was evaluated by the TRAEC strategy, which was conducted on a comprehensive scoring system with reliability, correlation, outcome fitness and integrity. The studies from five databases and additional researchers' experiments were included the present study to proceed following risk assessment. Based on the framework with TRAEC strategy, the comprehensive evaluation of health risks was classified as low (absolute value 0-4), medium (absolute value 4-8), high (absolute value 8-10). In the present study, the effect of PFASs exposure on neurodevelopment was a medium-risk level with 5.61 overall risk-score. The population-attributable risk (PAR) was 8.26 % for maternal PFASs exposure. The study identified a low-risk effect of prenatal PFASs exposure on ASD and behavioral disabilities. The chain length, type of PFASs and neurodevelopmental trajectories contributed to the risk of maternal PFASs on the neurodevelopment of offspring. Consistent with results of four criteria-based tools (ToxRTool, SciRAP, OHAT and IRIS), health risk assessment based on the TRAEC strategy demonstrated robustness and reliability in the present study. These results illustrated a medium-risk effect of maternal PFASs exposure on neurodevelopmental disorders of offspring. In addition, the TRAEC strategy provided a scientific and structured method for effect evaluation between prenatal PFASs and neurodevelopmental disorders, promoting the consistency and validation in risk assessment.
Assuntos
Poluentes Ambientais , Fluorocarbonos , Exposição Materna , Efeitos Tardios da Exposição Pré-Natal , Medição de Risco , Humanos , Fluorocarbonos/toxicidade , Gravidez , Feminino , Poluentes Ambientais/toxicidade , Exposição Materna/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Transtornos do Neurodesenvolvimento/induzido quimicamenteRESUMO
Autism spectrum disorder (ASD) is a neurodevelopmental disorder that is globally increasing in prevalence. The rise of ASD can be partially attributed to diagnostic expansion and advocacy efforts; however, the interplay between genetic predisposition and modern environmental exposures is likely driving a true increase in incidence. A range of evidence indicates that prenatal exposures are critical. Infection during pregnancy, gestational diabetes, and maternal obesity are established risk factors for ASD. Emerging areas of research include the effects of maternal use of selective serotonin reuptake inhibitors, antibiotics, and exposure to toxicants during pregnancy on brain development and subsequent ASD. The underlying pathways of these risk factors remain uncertain, with varying levels of evidence implicating immune dysregulation, mitochondrial dysfunction, oxidative stress, gut microbiome alterations, and hormonal disruptions. This narrative review assesses the evidence of contributing prenatal environmental factors for ASD and associated mechanisms as potential targets for novel prevention strategies.
Assuntos
Transtorno do Espectro Autista , Efeitos Tardios da Exposição Pré-Natal , Humanos , Transtorno do Espectro Autista/etiologia , Transtorno do Espectro Autista/epidemiologia , Gravidez , Fatores de Risco , Feminino , Exposição Ambiental/efeitos adversos , Exposição Materna/efeitos adversosRESUMO
BACKGROUND: Both interpregnancy intervals (IPI) and environmental factors might contribute to low birth weight (LBW). However, the extent to which air pollution influences the effect of IPIs on LBW remains unclear. We aimed to investigate whether IPI and air pollution jointly affect LBW. METHODS: A retrospective cohort study was designed in this study. The data of birth records was collected from the Jiangsu Maternal Child Information System, covering January 2020 to June 2021 in Nantong city, China. IPI was defined as the duration between the delivery date for last live birth and date of LMP for the subsequent birth. The maternal exposure to ambient air pollutants during pregnancy-including particulate matter (PM) with an aerodynamic diameter of ≤ 2.5 µm (PM2.5), PM10, ozone (O3), nitrogen dioxide (NO2), sulfur dioxide (SO2) and carbon monoxide (CO)-was estimated using a hybrid kriging-LUR-RF model. A novel air pollution score was proposed, assessing combined exposure to five pollutants (excluding CO) by summing their concentrations, weighted by LBW regression coefficients. Multivariate logistic regression models were used to estimate the effects of IPI, air pollution and their interactions on LBW. Relative excess risk due to interaction (RERI), attributable proportion of interaction (AP) and synergy index (S) were utilized to assess the additive interaction. RESULTS: Among 10, 512 singleton live births, the LBW rate was 3.7%. The IPI-LBW risk curve exhibited an L-shaped pattern. The odds ratios (ORs) for LBW for each interquartile range increase in PM2.5, PM10, O3 and the air pollution score were 1.16 (95% CI: 1.01-1.32), 1.30 (1.06-1.59), 1.22 (1.06-1.41), and 1.32 (1.10-1.60) during the entire pregnancy, respectively. An additive interaction between IPI and PM2.5 was noted during the first trimester. Compared to records with normal IPI and low PM2.5 exposure, those with short IPI and high PM2.5 exposure had the highest risk of LBW (relative risk = 3.53, 95% CI: 1.85-6.49, first trimester). CONCLUSION: The study demonstrates a synergistic effect of interpregnancy interval and air pollution on LBW, indicating that rational birth spacing and air pollution control can jointly improve LBW outcomes.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Intervalo entre Nascimentos , Recém-Nascido de Baixo Peso , Exposição Materna , Humanos , Estudos Retrospectivos , China/epidemiologia , Feminino , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Gravidez , Adulto , Recém-Nascido , Intervalo entre Nascimentos/estatística & dados numéricos , Exposição Materna/efeitos adversos , Exposição Materna/estatística & dados numéricos , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/efeitos adversos , Fatores de Risco , Material Particulado/análise , Material Particulado/efeitos adversos , Masculino , Adulto JovemRESUMO
BACKGROUND: The Australian National Perinatal Data Collection collates all live and stillbirths from States and Territories in Australia. In that database, maternal cigarette smoking is noted twice (smoking <20 weeks gestation; smoking >20 weeks gestation). Cannabis use and other forms of nicotine use, for example vaping and nicotine replacement therapy, are nor reported. The 2021 report shows the rate of smoking for Australian Indigenous mothers was 42% compared with 11% for Australian non-Indigenous mothers. Evidence shows that Indigenous babies exposed to maternal smoking have a higher rate of adverse outcomes compared to non-Indigenous babies exposed to maternal smoking (S1 File). OBJECTIVES: The reasons for the differences in health outcome between Indigenous and non-Indigenous pregnancies exposed to tobacco and nicotine is unknown but will be explored in this project through a number of activities. Firstly, the patterns of parental and household tobacco, nicotine and cannabis use and exposure will be mapped during pregnancy. Secondly, a range of biological samples will be collected to enable the first determination of Australian Indigenous people's nicotine and cannabis metabolism during pregnancy; this assessment will be informed by pharmacogenomic analysis. Thirdly, the pharmacokinetic and pharmacogenomic findings will be considered against maternal, placental, foetal and neonatal outcomes. Lastly, an assessment of population health literacy and risk perception related to tobacco, nicotine and cannabis products peri-pregnancy will be undertaken. METHODS: This is a community-driven, co-designed, prospective, mixed-method observational study with regional Queensland parents expecting an Australian Indigenous baby and their close house-hold contacts during the peri-gestational period. The research utilises a multi-pronged and multi-disciplinary approach to explore interlinked objectives. RESULTS: A sample of 80 mothers expecting an Australian Indigenous baby will be recruited. This sample size will allow estimation of at least 90% sensitivity and specificity for the screening tool which maps the patterns of tobacco and nicotine use and exposure versus urinary cotinine with 95% CI within ±7% of the point estimate. The sample size required for other aspects of the research is less (pharmacokinetic and genomic n = 50, and the placental aspects n = 40), however from all 80 mothers, all samples will be collected. CONCLUSIONS: Results will be reported using the STROBE guidelines for observational studies. FORWARD: We acknowledge the Traditional Custodians, the Butchulla people, of the lands and waters upon which this research is conducted. We acknowledge their continuing connections to country and pay our respects to Elders past, present and emerging. Notation: In this document, the terms Aboriginal and Torres Strait Islander and Indigenous are used interchangeably for Australia's First Nations People. No disrespect is intended, and we acknowledge the rich cultural diversity of the groups of peoples that are the Traditional Custodians of the land with which they identify and with whom they share a connection and ancestry.
Assuntos
Uso da Maconha , Exposição Materna , Nicotina , Uso de Tabaco , Adulto , Feminino , Humanos , Gravidez , Austrália/epidemiologia , Cannabis/efeitos adversos , Exposição Materna/efeitos adversos , Nicotina/efeitos adversos , Resultado da Gravidez/epidemiologia , Efeitos Tardios da Exposição Pré-Natal , Povos Aborígenes Australianos e Ilhéus do Estreito de Torres , Uso de Tabaco/efeitos adversos , Uso da Maconha/efeitos adversosRESUMO
OBJECTIVE: To evaluate the association between wildfire exposure in pregnancy and spina bifida risk. METHODS: This retrospective cohort study used the California Office of Statewide Health Planning and Development Linked Birth File with hospital discharge data between 2007 and 2010. The Birth File data were merged with the California Department of Forestry and Fire Protection data of the same year. Spina bifida was identified by its corresponding ICD-9 code listed on the hospital discharge of the newborn. Wildfire exposure was determined based on the zip code of the woman's home address. Pregnancy was considered exposed to wildfire if the mother lived within 15 miles of a wildfire during the pregnancy or within 30 days prior to pregnancy. RESULTS: There were 2,093,185 births and 659 cases of spina bifida between 2007 and 2010. The births were analyzed using multivariable logistic regression models and adjusted for potential confounders. Exposure to wildfire in the first trimester was associated with higher odds of spina bifida (aOR= 1.43 [1.11-1.84], p-value = 0.01). Wildfire exposure 30 days before the last menstrual period and during the second and third trimesters were not associated with higher spina bifida risk. CONCLUSION: Wildfire exposure has shown an increased risk of spina bifida during the early stages of pregnancy.
Assuntos
Disrafismo Espinal , Incêndios Florestais , Humanos , Feminino , Disrafismo Espinal/epidemiologia , Gravidez , Estudos Retrospectivos , Adulto , California/epidemiologia , Incêndios Florestais/estatística & dados numéricos , Recém-Nascido , Adulto Jovem , Fatores de Risco , Exposição Materna/efeitos adversos , Exposição Materna/estatística & dados numéricos , Características de Residência/estatística & dados numéricosRESUMO
BACKGROUND: This study aimed to investigate the relationship between phthalates exposure and estrogen and progesterone levels, as well as their role in late-onset preeclampsia. METHODS: A total of 60 pregnant women who met the inclusion and exclusion criteria were recruited. Based on the diagnosis of preeclampsia, participants were divided into two groups: normotensive pregnant women (n = 30) and pregnant women with late-onset preeclampsia (n = 30). The major metabolites of phthalates (MMP, MEP, MiBP, MBP, MEHP, MEOHP, MEHHP) and sex steroid hormones (estrogen and progesterone) were quantified in urine samples of the participants. RESULTS: No significant differences were observed in the levels of MMP, MEP, MiBP, MBP, MEHP, MEOHP, and MEHHP between women with preeclampsia and normotensive pregnant women (P > 0.05). The urinary estrogen showed a negative correlation with systolic blood pressure (rs= -0.46, P < 0.001) and diastolic blood pressure (rs= -0.47, P < 0.001). Additionally, the urinary estrogen and progesterone levels were lower in women with preeclampsia compared to those in normotensive pregnant women (P < 0.05). After adjusting for confounding factors, we observed a significant association between reduced urinary estrogen levels and an increased risk of preeclampsia (aOR = 0.09, 95%CI = 0.02-0.46). Notably, in our decision tree model, urinary estrogen emerged as the most crucial variable for identifying pregnant women at a high risk of developing preeclampsia. A positive correlation was observed between urinary progesterone and MEHP (rs = 0.36, P < 0.05) in normotensive pregnant women. A negative correlation was observed between urinary estrogen and MEP in pregnant women with preeclampsia (rs= -0.42, P < 0.05). CONCLUSIONS: Phthalates exposure was similar in normotensive pregnant women and those with late-onset preeclampsia within the same region. Pregnant women with preeclampsia had lower levels of estrogen and progesterone in their urine, while maternal urinary estrogen was negatively correlated with the risk of preeclampsia and phthalate metabolites (MEP). TRIAL REGISTRATION: Registration ID in Clinical Trials: NCT04369313; registration date: 30/04/2020.
Assuntos
Estrogênios , Ácidos Ftálicos , Pré-Eclâmpsia , Progesterona , Humanos , Feminino , Pré-Eclâmpsia/urina , Pré-Eclâmpsia/epidemiologia , Gravidez , Estudos de Casos e Controles , Ácidos Ftálicos/urina , Ácidos Ftálicos/efeitos adversos , Adulto , Estrogênios/urina , Progesterona/urina , Pressão Sanguínea , Exposição Materna/efeitos adversosRESUMO
Exposure to mercury has been associated with adverse effects on pregnancy outcomes. However, there is limited literature on mercury exposure and pregnancy outcomes in Chinese pregnant women. Our study was to investigate the possible association between maternal mercury exposure and spontaneous preterm birth and birth weight. This study was a nested case-control study. The association between blood mercury concentration and both spontaneous preterm birth and birth weight was analyzed using conditional logistic regression and linear regression adjusted for the potential confounding factors, respectively. The dose-response relationship between mercury concentration and birth outcomes was estimated using restricted cubic spline regression. The mean concentration of mercury was 2.8 ± 2.2 µg/L. A positive relationship was observed between maternal blood mercury concentration and SPB when analyzed as a continuous variable. However, it was not found to be statistically significant (adjusted OR = 1.10, 95% CI = 0.95-1.26, P = 0.202). Moderate mercury exposure was associated with a higher risk of SPB (Q3 vs. Q1: crude OR = 2.50, 95% CI = 1.16-5.41, P = 0.02; adjusted OR = 3.49, 95% CI = 1.33-9.11, P = 0.011). After considering the combined effects of chemicals other than mercury exposure (including lead, selenium, and cadmium), the results remained consistent. There was no statistically significant association between blood mercury levels and birth weight (adjusted coefficient = 18.64, P-value = 0.075). There were no statistically significant dose-response associations between mercury concentration and birth outcomes (SPB: P = 0.076; birth weight: P = 0.885). Public health policies should focus on reducing environmental releases of mercury, improving food safety standards, and providing education to pregnant women about the risks of mercury exposure and preventive measures.
Assuntos
Peso ao Nascer , Exposição Materna , Mercúrio , Resultado da Gravidez , Primeiro Trimestre da Gravidez , Nascimento Prematuro , Humanos , Gravidez , Feminino , Mercúrio/sangue , Adulto , Nascimento Prematuro/sangue , Estudos de Casos e Controles , Primeiro Trimestre da Gravidez/sangue , Peso ao Nascer/efeitos dos fármacos , Exposição Materna/efeitos adversos , Recém-Nascido , ChinaRESUMO
BACKGROUND: Nephron number variability may hold significance in the Developmental Origins of Health and Disease hypothesis. We explore the impact of gestational particulate pollution exposure on cord blood cystatin C, a marker for glomerular function, as an indicator for glomerular health at birth. METHODS: From February 2010 onwards, the ENVIRONAGE cohort includes over 2200 mothers giving birth at the East-Limburg hospital in Genk, Belgium. Mothers without planned caesarean section who are able to fill out a Dutch questionnaire are eligible. Here, we evaluated cord blood cystatin C levels from 1484 mother-child pairs participating in the ENVIRONAGE cohort. We employed multiple linear regression models and distributed lag models to assess the association between cord blood cystatin C and gestational particulate air pollution exposure. FINDINGS: Average ± SD levels of cord blood cystatin C levels amounted to 2.16 ± 0.35 mg/L. Adjusting for covariates, every 0.5 µg/m³ and 5 µg/m³ increment in gestational exposure to black carbon (BC) and fine particulate matter (PM2.5) corresponded to increases of 0.04 mg/L (95% CI 0.01-0.07) and 0.07 mg/L (95% CI 0.03-0.11) in cord blood cystatin C levels (p < 0.01), respectively. Third-trimester exposure showed similar associations, with a 0.04 mg/L (95% CI 0.00-0.08) and 0.06 mg/L (95% CI 0.04-0.09) increase for BC and PM2.5 (p < 0.02). No significant associations were observed when considering only the first and second trimester exposure. INTERPRETATION: Our findings indicate that particulate air pollution during the entire pregnancy, with the strongest effect sizes from week 27 onwards, may affect newborn kidney function, with potential long-term implications for later health. FUNDING: Special Research Fund (Bijzonder Onderzoeksfonds, BOF), Flemish Scientific Research Fund (Fonds Wetenschappelijk Onderzoek, FWO), and Methusalem.
Assuntos
Poluição do Ar , Cistatina C , Sangue Fetal , Material Particulado , Humanos , Feminino , Gravidez , Material Particulado/efeitos adversos , Material Particulado/análise , Cistatina C/sangue , Recém-Nascido , Adulto , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Materna/efeitos adversos , Glomérulos Renais , Masculino , Bélgica/epidemiologia , Biomarcadores , Taxa de Filtração GlomerularRESUMO
The first 1000 days of life is a critical period of development in which adverse circumstances can have long-term consequences for the child's health. Maternal immune activation is associated with increased risk of neurodevelopmental disorders in the child. Aberrant immune responses have been reported in individuals with neurodevelopmental disorders. Moreover, lasting effects of maternal immune activation on the offspring's immune system have been reported. Taken together, this indicates that the effect of maternal immune activation is not limited to the central nervous system. Here, we explore the impact of maternal immune activation on the immune system of the offspring. We first describe the development of the immune system and provide an overview of reported alterations in the cytokine profiles, immune cell profiles, immune cell function, and immune induction in pre-clinical models. Additionally, we highlight recent research on the impact of maternal COVID-19 exposure on the neonatal immune system and the potential health consequences for the child. Our review shows that maternal immune activation alters the offspring's immune system under certain conditions, but the reported effects are conflicting and inconsistent. In general, epigenetic modifications are considered the mechanism for fetal programming. The available data was insufficient to identify specific pathways that may contribute to immune programming. As a consequence of the COVID-19 pandemic, more research now focuses on the possible health effects of maternal immune activation on the offspring. Future research addressing the offspring's immune response to maternal immune activation can elucidate specific pathways that contribute to fetal immune programming and the long-term health effects for the offspring.