Search Results (87)

Background: Gestational tobacco exposure is a major modifiable risk factor for adverse pregnancy outcomes; how smoking-induced redox perturbations transmit across the placental barrier to the fetal compartment, and mediate neonatal outcomes, remains incompletely understood. Methods: In a prospective cohort of 66 maternal-neonatal dyads (24 smokers, 42 non-smokers) from Târgu-Mures, six redox biomarkers (nitrite, nitrate, malondialdehyde, reduced, oxidized glutathione (GSH, GSSG) and GSH/GSSG ratio) were quantified in paired maternal and cord blood and converted to SI units, and pathway-specific composite indices (oxidative and nitrosative stress index–OSI, NSI, global redox index–GRI) were derived via standardized Z-scores of natural-log-transformed concentrations. Associations with preterm birth (PTB) and low birth weight (LBW) were assessed via multivariable regression. Benjamini–Hochberg false discovery rate (FDR) correction was applied within predefined test families. Results: Tobacco exposure was associated with nominally significant depletion of the Neonatal NSI (mean difference = −0.842; 95% CI: −1.567 to −0.117; p = 0.024; FDR-adjusted p = 0.142), while maternal indices showed no significant group differences. Lower Maternal GRI and Neonatal NSI were independently associated with lower birth weight and higher odds of preterm birth (aOR = 0.35 and 0.52, respectively; both p < 0.05). Maternal and neonatal nitrite concentrations were positively correlated (FDR-adjusted p = 0.002) and oxidized glutathione showed an inverse maternal-neonatal correlation (FDR-adjusted p = 0.001), whereas the maternal and neonatal NSI was not significant after FDR-correction (FDR-adjusted p = 0.078) Conclusions: Gestational tobacco exposure was associated with depletion of the neonatal nitrosative stress index. Independently, lower maternal and neonatal composite redox indices were associated with lower birth weight and higher odds of preterm birth. Composite indices may offer an integrated assessment of perinatal redox status, but without external validation warrant confirmation in larger cohorts. Full article

Indigenous women experience a disproportionate burden of adverse perinatal health outcomes, yet the extent and nature of health promotion interventions addressing modifiable behavioural and social determinants remain poorly synthesised. This scoping review mapped smoking, nutrition, alcohol, physical exercise, and social and emotional wellbeing (SNAPS(o))-related perinatal health promotion programs delivered through Australian Aboriginal Community Controlled Health Organisations (ACCHOs), supplemented by relevant peer-reviewed evidence identified across Australia, Aotearoa New Zealand, Canada, and the United States. A two-phase design looked at peer-reviewed literature from January 2010 to January 2025 across PubMed, CINAHL, and the Cochrane Library, followed by a structured review of Aboriginal Community Controlled Health Organisation (ACCHO) websites in Australia (n = 145). Data were extracted on program characteristics, SNAPS(o) components, implementation models, and evaluation outcomes. Findings were synthesised using content analysis. Thirty-four programs were identified in total, most delivered through ACCHOs (n = 26) and predominantly implemented in Australia (n = 29). Smoking was the most frequently addressed component (n = 18, 55%), while nutrition and social and emotional wellbeing were each included in 27% of programs (n = 9), physical exercise in 18% (n = 6), and alcohol in 15% (n = 5). Grey-literature programs more commonly reflected multi-component, holistic models compared with peer-reviewed studies and formal evaluations. Only 10 programs had identifiable formal evaluation evidence, including published or publicly reported evaluations, almost all of which were identified through academic sources. Evaluations focused primarily on tobacco-related behavioural outcomes, with limited reporting of sustained maternal or infant health endpoints. The perinatal SNAPS(o) intervention landscape for Indigenous women is characterised by strong community-controlled delivery but limited published evaluation, particularly of integrated models implemented within ACCHOs. The concentration of evidence on smoking cessation highlights a need to expand evaluation across broader domains of maternal wellbeing. Strengthening Indigenous-led evaluation frameworks and outcome measures that reflect holistic models of care is essential to advancing equitable and culturally grounded perinatal health systems. Full article

Maternal Smoking During Pregnancy (MSDP) remains a major source of fetal toxicant exposure. We applied adductomics to profile reactive adducts at the human serum albumin cysteine-34 (HSA-Cys³⁴) locus, which integrates longer-term exposures. HSA-Cys³⁴ adducts formed by acrylonitrile and ethylene oxide, two tobacco-related toxicants previously linked to smoking in adults, were quantified and compared with cotinine and MSDP status. Their relationships with other reactive adducts were also examined. Neonatal dried blood spots (DBS) from 110 children were analyzed. Cotinine and 55 Cys³⁴ adducts were measured by Liquid Chromatography–Tandem Mass Spectrometry (LC-MS/MS). Associations were evaluated using linear regression, chi-square tests, and principal component analysis. Eighteen adducts differed significantly by MSDP status after Bonferroni correction (p ≤ 9.1 × 10⁻⁴). S-acrylonitrile was markedly elevated in exposed newborns, including those whose mothers reported smoking cessation after early pregnancy (p < 0.001). S-acrylonitrile correlated with 31 adducts related to oxidative stress and thiol metabolism, whereas cotinine correlated with eight. S-ethylene oxide, though detectable in DBS, showed no consistent association with MSDP. Adductomics analysis of newborn DBS sensitively captures molecular signatures of prenatal tobacco exposure and related oxidative stress. Acrylonitrile adducts appear to better reflect cumulative MSDP exposure than cotinine, highlighting the utility of adductomics for improved exposure assessment and mechanistic insight. Full article

Background: Vitamin D (VD) plays a central role in calcium homeostasis during pregnancy and has been implicated in redox-related biological processes. While VD deficiency (VDD) has been consistently associated with adverse pregnancy outcomes, the relationships between VD insufficiency (VDI), maternal antioxidant-related biomarkers, and neonatal outcomes remain incompletely characterized, particularly during the third trimester. Objective: To determines the prevalence of VDI in third-trimester pregnant women and to examine its associations with antioxidant-related markers and selected neonatal outcomes. Methods: A cross-sectional study was conducted among pregnant women in the third trimester attending a tertiary referral hospital in Mexico City. Maternal serum 25-hydroxyvitamin D (25-OHD) concentrations were measured, along with a panel of redox-related markers, including 2,2-diphenyl-2-2picrylhydrazyl (DPPH) radical scavenging activity, reduced glutathione (GSH), glutathione S-transferase (GST), glutathione peroxidase (GPx), and oxygen radical absorbance capacity (ORAC). Neonatal anthropometric parameters were recorded at birth. Associations between maternal VD status, redox-related markers, environmental factors, and neonatal outcomes were evaluated using appropriate statistical analyses. Results: A high prevalence of VDI was observed in the study population. Maternal VDI was associated with lower activities of GSH, GST, and GPx. Passive exposure to tobacco smoke and season of sampling were also associated with lower VD concentrations. Neonates born to women with VDI had higher birth weight compared with those born to women with sufficient VD concentrations. Maternal serum 25-OHD concentrations correlated positively with selected antioxidant enzyme activities. Conclusions: In this cohort of third-trimester pregnant women, VDI co-occurred with environmental factors, differences in maternal redox-related markers, and selected neonatal outcomes. These findings support an associative framework in which suboptimal VD status during the third trimester is accompanied by variations in redox-related markers. Longitudinal and mechanistic studies are needed to clarify the temporal sequence and biological relevance of these associations. Full article

Developmental programming, shaped by environmental and lifestyle stressors during prenatal life, is increasingly recognized as a major contributor to non-communicable diseases (NCDs) later in life. Oxidative stress, one of key mechanisms linking these stressors to fetal metabolomic reprogramming and disease pathogenesis, leaves measurable metabolomic signatures that reflect disrupted redox balance. Alterations in glucose, lipid, and amino acid metabolism and antioxidant response could reveal the main pathways driving NCD development. This review summarizes epidemiological studies that have investigated biochemical responses of the prenatal exposure to metals, air pollution, and tobacco smoke and e-cigarette vapor in maternal–placental–fetal compartments using a metabolomic approach. Summarized studies indicate that maternal exposure to metals primarily disrupts amino acid pathways related to one-carbon metabolism, glutathione synthesis, and oxidative stress defense, while air pollution, particularly fine particulate matter, mainly affects lipid oxidation, fatty acid β-oxidation, and amino acid and carbohydrate metabolism. Tobacco smoke and e-cigarette vapor induce widespread disturbances involving reduced citric acid cycle intermediates, altered acylcarnitines and phospholipids, and impaired antioxidant capacity, collectively promoting oxidative damage and inflammatory signaling. The identification of these metabolome alterations might contribute to a deeper understanding of the toxicity and biological impact of environmental stressors on offspring health. These results may eventually lead to the identification of early biomarkers and to the development of therapeutic strategies aimed at reducing NCD risk. Full article

Maternal tobacco smoke exposure is associated with impaired fetal growth and long-term disease risk (DOHaD, Developmental Origins of Health and Disease). Whether placental steroid hormones are independently altered remains a matter of debate. We quantified six placental steroids (estradiol, estriol, estrone, progesterone, testosterone, and pregnanediol) using HPLC–Corona CAD in 70 deliveries (C = 30; PS = 20; AS = 20). Distributional differences were assessed with Kruskal–Wallis and pairwise Mann–Whitney tests with Benjamini–Hochberg (BH) control. Adjusted associations used log-linear OLS with HC3 robust SE: Model A (gestational age, maternal BMI, newborn sex) and Model B (Model A + birth weight), reported as percent change vs. controls, computed as (exp(β) − 1) × 100 with 95% CI. Secondary analyses tested (i) multiclass logistic classification of C/PS/AS from the steroid panel (5-fold stratified CV) and (ii) prediction of birth weight (OLS and 2-component PLS). All six steroids differed by group (BH-adjusted p ranging from 9.18 × 10⁻¹² to 6.66 × 10⁻⁸). In Model A, AS vs. C showed lower estrogens/progestins (estradiol, −46.2%; estriol, −24.7%; estrone, −25.9%; progesterone, −28.2%; pregnanediol, −31.4%) and higher testosterone (+40.8%); these effects persisted in Model B after adjusting for birth weight. The panel classified C/PS/AS with 0.900 cross-validated accuracy (weighted OvR AUC 0.994). Hormones poorly predicted birth weight (PLS CV R² = −0.777). Maternal active and passive smoking is associated with a coherent and independent disruption of placental steroidogenesis. A targeted placental steroid panel offers biologically meaningful early markers relevant to DOHaD. Full article

Background/Objectives: There is a need to search for risk factors of CL/P, which is the most common facial congenital deformity due to its multifactorial etiology. This study aimed to assess the possible external factors influencing the occurrence of non-syndromic CL/P. Methods: Retrospective–prospective case record analysis was performed with a sample of 224 consecutively treated patients. The data were obtained from medical records and questionnaires completed by children’s parents. Results: Factors that may have potentially increased the risk of CL/P were as follows: advanced paternal age (p = 0.014), mother experiencing an infection in the first trimester of pregnancy (p < 0.001), maternal passive smoking (p = 0.001) and stress during the first trimester of pregnancy (p = 0.003). Where mothers were treated with folic acid in the first trimester of pregnancy, in the whole sample the risk of a CL/P in newborns was reduced (p = 0.007). Advanced paternal age was unrelated to the occurrence of isolated CL, and stress did not increase the risk of isolated CP etiology. Maternal folic acid intake in the first trimester of pregnancy did not influence CLP occurrence. Conclusions: In a group of children from Southeastern Poland, the occurrence of CL/P was related to advanced maternal age and maternal external risk factors, such as infections, passive tobacco smoking and severe stress during the first trimester of pregnancy. Maternal folic acid intake during the first trimester reduced the risk of CL and CP. Due to the observational nature of the study, the above conclusions should be interpreted as a potential effect. Full article

Objectives: Parental exposure to tobacco smoke is a significant public health concern, with over 1.1 billion smokers worldwide. The aim of this systematic review was to evaluate the impact of maternal, paternal, and dual-parental cigarette smoke exposure on offspring reproductive health. Methods: Original human clinical and animal research studies were included; titles and abstracts were manually scanned for relevance to the effect of parental smoking on offspring reproductive outcomes (Date of search:18/03/2025). Results: This systematic review incorporates 30 studies identified from three databases (PubMed, Web of Science, and Scopus). The results indicate that male offspring exhibit reduced spermatogenic capacity, characterized by decreased testicular size, lower sperm count, and impaired hormonal biosynthesis, with reductions of 30–40% in sperm production. Dual-parental smoking exacerbates these effects, with sperm counts averaging 85 million per ml in human male offspring from dual-smoking households, compared to 111 million per ml in single-smoking households. Animal studies provide mechanistic insights, revealing reduced testis weight in nicotine-exposed male rats and increased oxidative stress in offspring. Conclusions: This review highlights the dose-dependent and sex-specific effects of smoking on the fertility of offspring and underscores the need for standardized protocols to enhance the consistency and comparability of future research in both human and animal studies. Full article

Respiratory syncytial virus (RSV) is a major cause of acute lower respiratory infections (ALRIs) in young children, especially bronchiolitis, with significant global health and economic impact. Increasing evidence links early-life RSV infection to long-term respiratory complications, notably recurrent wheezing and asthma. This narrative review examines these associations, emphasizing predictive factors and emerging biomarkers for risk stratification. Early RSV infection can trigger persistent airway inflammation and immune dysregulation, increasing the likelihood of chronic respiratory outcomes. Risk factors include severity of the initial infection, age at exposure, genetic susceptibility, prematurity, air pollution, and tobacco smoke. Biomarkers such as cytokines and chemokines are showing promise in identifying children at higher risk, potentially guiding early interventions. RSV-related bronchiolitis may also induce airway remodeling and promote Th2/Th17-skewed immune responses, mechanisms closely linked to asthma development. Advances in molecular profiling are shedding light on these pathways, suggesting novel targets for early therapeutic strategies. Furthermore, passive immunization and maternal vaccination offer promising approaches to reducing both acute and long-term RSV-related morbidity. A deeper understanding of RSV’s prolonged impact is essential to develop targeted prevention, enhance risk prediction, and improve long-term respiratory health in children. Future studies should aim to validate biomarkers and refine immunoprophylactic strategies. Full article

Background: Exposure to secondhand smoke (SHS) during pregnancy has been linked to adverse maternal and perinatal outcomes. Preterm birth is one of the most critical complications. However, the evidence of an association between SHS exposure and preterm birth remains inconclusive. Objectives: our aim was to identify the prevalence of exposure to secondhand smoke among pregnant women and investigate the association between exposure to SHS and preterm birth. Methods: A cross-sectional study was conducted in Madinah, Saudi Arabia, from October to December 2024. A self-administered questionnaire was distributed among women in the postnatal ward to assess sociodemographic and pregnancy-related variables and exposure to SHS. Results: A total of 469 women were included in the study. About 33.7% of the women reported that their husbands currently smoked tobacco, with 51% smoking indoors; 21% of the women did not impose smoking restrictions at home. Pregnant women exposed to SHS had more than twice the odds of preterm birth compared to unexposed women (OR = 2.09; 95% CI: 1.06–4.13; p = 0.03). Conclusions: SHS exposure increased the risk of preterm birth among pregnant women in Madinah. These findings emphasize the essential need for preventive strategies to diminish SHS exposure in residential and public environments. Full article

Objectives: Attention deficit hyperactivity disorder (ADHD) is among the most common neurodevelopmental disorders affecting women of reproductive age. Previous data on this condition did not study its different symptom clusters separately. Our aim was to compare perinatal outcomes between women with hyperactivity cluster (ADHD) and those with the inattentive cluster (attention deficit disorder (ADD)). Methods: A retrospective population-based study utilizing data from the Healthcare Cost and Utilization Project–Nationwide Inpatient Sample (HCUP-NIS). All deliveries or maternal deaths from 2004 to 2014 were available for analysis, and perinatal outcomes were compared between participants with an ADD diagnosis and those with an ADHD diagnosis. A multivariate logistic regression was used to control for confounders. Results: During the study period, there were 9,096,788 deliveries. Of them, 7103 had an ADHD diagnosis, and 2928 had an ADD diagnosis. Women with ADHD, compared to those with ADD, were more likely to be younger than 25 years of age; to be Black; to be from a lower income quartile; to smoke tobacco during pregnancy; and to use illicit drugs (p < 0.001 for all). Using multivariate logistic regression, women with ADHD, compared to those with ADD, had a higher rate of hypertensive disorders of pregnancy (HDPs) (aOR 1.19, 95% CI 1.03–1.37, p = 0.02), preterm delivery (aOR 1.19, 95% CI 1.01–1.39, p = 0.038), maternal infection (aOR 1.39, 95% CI 1.04–1.85, p = 0.024), and small-for-gestational-age (SGA) neonates (aOR 1.33, 95% CI 1.04–1.69, p = 0.022). Conclusions: Women with an ADHD diagnosis, compared to those with ADD, had a higher incidence of various maternal and neonatal complications, including HDPs, preterm delivery, and SGA neonates. Full article

Objective: To examine trends in perinatal smoking across rural and urban areas and investigate whether structural and intermediary health factors explain rural-urban disparities. Methods: This cross-sectional study used data from the Pregnancy Risk Assessment Monitoring System (PRAMS) collected between 2009 and 2021 in the United States. Perinatal smoking patterns were based on self-reported smoking before, during, and after pregnancy. Weighted prevalence estimates with 95% confidence intervals (CIs) were calculated for persistent smoking and cessation, stratified by rural–urban residence. Temporal trends were analyzed using logistic regression. Multivariable weighted logistic regression was performed on Phase 8 data (2016–2021) to examine associations between rural–urban status and perinatal smoking patterns, adjusting for maternal age, year of delivery, region, and structural (e.g., education, Tobacco 21 policy) and intermediary (e.g., perinatal stressors) health determinants. All analyses accounted for the complex survey design. Results: Although perinatal smoking declined over time, prevalence remained consistently higher among rural mothers. From 2009 to 2021, persistent smoking decreased significantly in both rural and urban areas (p < 0.001). Smoking cessation rates remained stable (p = 0.087), with no significant difference by rural–urban status (p = 0.475). After adjustment, rural women were 45% more likely to smoke persistently than urban women (OR = 1.45, 95% CI: 1.35–1.56) and 26% less likely to quit smoking. Conclusions: While perinatal smoking declined overall, rural mothers remained more likely to smoke throughout pregnancy. Structural and intermediary determinants partially explained this persistent rural–urban disparity. Full article

Perinatal depression is a leading cause of maternal morbidity worldwide, impacting about one-third of all pregnant individuals. The indoor home environment plays a critical role in the mental health of pregnant individuals, as they spend a substantial amount of their day inside their homes. We conducted a systematic review and meta-analysis to identify, synthesize, and evaluate the available scientific literature on the association between home environment attributes related to stability, quality, and indoor exposures and perinatal depression. Comprehensive electronic searches were conducted in four major bibliographic databases. Dual independent screening, data extraction, and quality assessment were completed. Weighted Z-meta-analysis was conducted to synthesize the available evidence. The review included 27 observational epidemiological studies published between 2003 and 2024, involving 174,914 pregnant and/or postpartum individuals, which investigated the role of at least one home environment attribute in relation to perinatal depression. We found very strong evidence linking indoor air pollutants, particularly household tobacco smoke, to perinatal depression. We found strong evidence for the impact of housing instability on perinatal depression. In contrast, the evidence for associations involving housing quality and residential noise was weak. Our findings underscore the significance of incorporating home environment-focused initiatives in public health efforts to improve perinatal mental health. Further research is needed to identify common household attributes associated with poor perinatal mental health to inform future public intervention and policies. Full article

Children’s tobacco smoke exposure (CTSE) is a public health concern, particularly in low-income and minority communities. Interventions to reduce CTSE have had modest success, and so research must identify mechanisms to improve intervention efficacy. This study investigated mediators of CTSE reduction in an intervention designed to facilitate CTSE protection and maternal smoking abstinence. We analyzed data from the Babies Living Safe and Smokefree (BLiSS) trial, which evaluated the efficacy of a multilevel behavioral smoking intervention initiated in community clinics serving low-income mothers. We estimated direct and indirect effects to evaluate the role of two mediators of the intervention on CTSE at post-intervention follow-up: mothers’ skills in managing smoking urges and their protective behaviors to shield children from TSE. CTSE was measured using mothers’ reports and child cotinine (a CTSE biomarker). The BLiSS intervention was linked to statistically significant lower longitudinal reported CTSE directly and indirectly by increasing mothers’ urge management skills and CTSE protection behaviors (p-values < 0.05). The intervention was not directly linked to child cotinine. However, evidence of a statistically significant indirect effect (p-value = 0.028) suggested that the intervention reduced longitudinal child cotinine levels by increasing CTSE protection behaviors. Two non-program factors, nicotine dependence and total smokers in the home, also increased child cotinine and reported CTSE (p-values < 0.001). Interventions that improve maternal smokers’ urge management skills and CTSE protections can mitigate CTSE. In addition, it is essential to target barriers to CTSE reduction, such as nicotine dependence levels and the presence of other smokers in the home. Full article

Background/Objectives: We investigated maternal and parent-of-origin (PoO) gene-environment interaction effects on the risk of nonsyndromic orofacial clefts for two maternal environmental factors: periconceptional smoking and folic acid supplementation. Methods: Genome-wide single nucleotide polymorphisms (SNPs) genotypes and TopMed-imputed genotypes were obtained for case-parent triads from the EUROCRAN and ITALCLEFT studies. Candidate regions were selected around target SNPs from a previous genome-wide association study, resulting in 12 (726 SNPs) and 11 regions (730 SNPs) for maternal and PoO effects, respectively. Log-linear models were used to analyze 404 case-parent triads and 40 case-parent dyads. p-values were combined across regions. Results: None of the interactions reached statistical significance after correction for the number of regions tested. Nominally significant (pooled p-values < 0.05) interactions pointed to regions in or close to genes LRRC7 (maternal gene-folate interaction), NCKAP5 (PoO-smoking interaction), and IFT43 and GPATCH2L (PoO-folate interaction). Conclusions: Our results suggested that the genetic effects in or around these genes were heightened under periconceptional exposure to tobacco or no folic acid supplementation. The involvement of these genes in orofacial cleft development, in conjunction with environmental exposures, should be further studied. Full article