Assessing Lead Screening Rates at a Rural Tertiary Teaching Hospital

Background Childhood obesity can result in adverse health outcomes. Objectives Objectives were to describe the prevalence of obesity and determine the association between obesity at cancer diagnosis and event-free survival (EFS) and overall survival (OS) in children diagnosed with cancer in Canada. Design/Methods We conducted a retrospective cohort study using the Cancer in Young People in Canada database, a population-based surveillance program collecting data from all paediatric cancer patients. This study included all children with newly diagnosed cancer aged 2 to 18 years across Canada from 2001 to 2020. Obesity was defined as age and sex-adjusted body mass index ≥ 95th percentile. EFS was defined as the time from diagnosis to first event (relapse, progression, secondary malignancies, or death). Univariate and multivariable Cox proportional hazards models compared EFS and OS between patients with and without obesity. Results A total of 11,291 patients were included (37.1% leukemias, 14.5% lymphomas, 21.8% central nervous system (CNS) tumors, 26.6% non-CNS solid tumors). At diagnosis, 10.5% were obese and the prevalence of obesity was significantly higher at 1 year (15.7%, p<0.001) and 2 years (20.1%, p<0.001) after diagnosis. The prevalence of obesity was higher in the leukemia and lymphoma cohort compared to other cancer categories (11.4% vs. 9.5%, p=0.001). In multivariable models controlling for age at diagnosis, sex, ethnicity, neighborhood income quintile, treatment era and cancer categories, obesity at diagnosis remained significantly associated with inferior EFS [adjusted HR (aHR) 1.16, 95% CI 1.02–1.32] and OS [aHR 1.29, 95% CI 1.11–1.49]. In children with acute lymphoblastic leukemia (ALL) (n=3458, 82.5% of all leukemias), after adjusting for high-risk features such as age, white blood cell count and CNS status, obesity at diagnosis remained significantly associated with inferior EFS [aHR 1.55, 95% CI 1.17–2.04] and OS [aHR 1.75, 95% CI 1.23–2.49]. In patients with CNS tumors, obesity at diagnosis was also independently associated with inferior EFS [aHR 1.38, 95% CI 1.09–1.76] and OS [aHR 1.47, 95% CI 1.13–1.91]. Conclusion In this population-based study of children with cancer, the prevalence of obesity was 11% at diagnosis and continued to increase in the following 2 years. Obesity at cancer diagnosis was independently associated with inferior survival across the entire cohort, especially in children with ALL and CNS tumors. Prevention of childhood obesity should be emphasized as it can lead to several adverse health outcomes in children with cancer.

IntroductionPrenatal negative life events (NLEs) have been linked to adverse health outcomes in children. However, few studies examine this relationship during late childhood using trajectory analyses. Additionally, the impact of specific NLEs domains on child development remains unclear. This study aims to longitudinally explore the association between NLEs (cumulative score and specific NLEs domains) and child outcomes from birth to late childhood. Methods1135 mother-child pairs from the French EDEN cohort were followed from 24 to 28 weeks of pregnancy up to 11 years of age. Maternal self-reports of prenatal NLEs were collected immediately after birth, then analyzed as a cumulative score and by NLEs domain. Children's emotional and behavioral symptoms were assessed at 4 timepoints through the Strengths and Difficulties Questionnaire. ResultsChildren of mothers exposed to ≥3 NLEs were more likely to follow trajectories of high levels of peer relationship problems (aOR [95 % CI] = 5.69 [1.74–18.69]), emotional symptoms (aOR [95 % CI] = 3.05 [1.08–8.63]), and conduct problems (aOR [95 %] = 3.53 [1.20–10.42]). Among the domains of NLEs, only events related to housing, finance, and living conditions were significantly associated with high emotional and behavioral difficulties trajectories (aOR [95%CI] = 2.71[1.26–5.81]). LimitationsPotential attrition bias due to a higher dropout rate for children experiencing early indications of emotional and behavioral difficulties. ConclusionFindings support the relationship between prenatal NLEs and child outcomes, underscoring the importance of assessing prenatal stressors across life domains to identify mothers who might be in need of support.

Effectiveness of interventions to reduce exposure to lead through consumer products and drinking water: A systematic review

<div>Abstract<p><b>Background:</b> Maternal smoking in pregnancy is associated with adverse health outcomes in children, including cancers; underlying mechanisms may include epigenetic modifications. Using Illumina's 450K array, we previously identified differential DNA methylation related to maternal smoking during pregnancy at 26 CpG sites (CpGs) in 10 genes in newborn cord bloods from the Norwegian Mother and Child Cohort Study (MoBa). Whether these methylation signals in newborns reflect <i>in utero</i> exposure only or possibly epigenetic inheritance of smoking-related modifications is unclear.</p><p><b>Methods:</b> We therefore evaluated the impact of the timing of mother's smoking (before or during pregnancy using cotinine measured at 18 weeks gestation), the father's smoking before conception, and the grandmother's smoking during her pregnancy with the mother on methylation at these 26 CpGs in 1,042 MoBa newborns. We used robust linear regression, adjusting for covariates, applying Bonferroni correction.</p><p><b>Results:</b> The strongest and only statistically significant associations were observed for sustained smoking by the mother during pregnancy through at least gestational week 18 (<i>P</i> < 1.6 × 10<sup>−5</sup> for all 26 CpGs). We observed no statistically significant differential methylation due to smoking by the mother before pregnancy or that ceased by week 18, father's smoking before conception, or grandmother's smoking while pregnant with the mother.</p><p><b>Conclusions:</b> Differential methylation at these CpGs in newborns seems to reflect sustained <i>in utero</i> exposure rather than epigenetic inheritance.</p><p><b>Impact:</b> Smoking cessation in early pregnancy may negate effects on methylation. Analyses of maternal smoking during pregnancy and offspring health outcomes, including cancer, limited to ever smoking might miss true associations. <i>Cancer Epidemiol Biomarkers Prev; 23(6); 1007–17. ©2014 AACR</i>.</p></div>

Introduction: Air pollution exposure has been increasingly associated with adverse health outcomes in children, including airway disease. Underlying mechanisms may involve epigenetic modifications such as DNA methylation. A few studies have reported differential methylation at specific loci in relation to ambient air pollution exposure, whereas studies based on epigenome-wide methylation data are limited. Methods: Within the framework of Mechanisms of the Development of ALLergy (MeDALL) Consortium, we investigated exposure to traffic-related nitrogen dioxide (NO2), in relation to blood DNA methylation by pooling data from four European birth cohorts (N=766) in which DNA methylation was measured in paired samples (either at 0 and 4/5 years or at 4 and 8 years), using the Infinium HumanMethylation450 BeadChip. All participating cohorts assessed NO2 exposure at birth address by means of land-use regression modelling according to a uniform exposure protocol (within the ESCAPE project). The associations were analyzed with robust linear regression. Results: In the analysis of the association between NO2 exposure at birth and cord blood DNA methylation levels (N=286), 4 CpGs mapped to 3 genes (CYP7B1, ANO1, LIN7A) appeared below the Bonferroni adjusted significance threshold and 18 CpGs below the false discovery rate (FDR), located within 11 gene regions, none of which have previously been implicated in relation to air pollution exposure. These associations were largely robust to estimated cell type adjustment using Houseman's method. NO2 exposure at birth was also associated with differentially methylated CpGs in 4-year-olds (N=766), although without clear overlap with those found in cord blood. Discussion: Our analysis revealed a set of genes which represent novel associations of methylation changes in relation to NO2 exposure. We will further update the current results with analyses based on additional datasets including older children, and different exposure windows.

Body Dissatisfaction (BD) and low physical self-concept and exercise efficacy have been linked to poor physical fitness levels and adverse health outcomes in children. The purpose of this study was to examine the relationship between BD, physical fitness, exercise self-efficacy, and self-Perception of Physical Fitness (PFP) in Latina and Black female children. Twenty-eight Latina and Black children enrolled in an elementary afterschool program, aged 8–12, completed surveys evaluating body dissatisfaction, exercise efficacy, PFP, and measures of physical fitness. Subjects exhibited moderate but significant inverse relationships between BD and PFP in strength (r = −0.459), agility (r = −0.382), aerobic fitness (r = −0.354), and flexibility (r = −0.461) (p < 0.05 for all). There was a significant negative correlation between exercise efficacy and BD (r = −4.2; p < 0.05). Power (r = 0.51) and flexibility (r = 0.42) were the only physical fitness measures significantly and positively related to children’s PFP (p < 0.05). A significant medium inverse relationship was also found between BD and aerobic fitness scores (r = −0.381; p < 0.05). However, after controlling for exercise efficacy or perception of physical fitness, the relationship between BD and aerobic fitness was not significant (p > 0.05). Findings suggest that positive PFP and positive performance in several physical fitness measures are associated with lower levels of BD in minority female children. Furthermore, evidence suggests exercise efficacy and PFP can mediate the relationship body image and aerobic fitness. These findings suggest that PFP, more so than measured physical fitness, was associated with lower levels of BD in minority female children. These results have important implications for programs designed to improve physical fitness and mental health in minority children.

BackgroundLittle is known about the long-term safety of infant feeding interventions aimed at reducing breast milk HIV transmission in Africa.Methods and FindingsIn 2001–2005, HIV-infected pregnant women having received in Abidjan, Côte d'Ivoire, a peripartum antiretroviral prophylaxis were presented antenatally with infant feeding interventions: either artificial feeding, or exclusive breast-feeding and then early cessation from 4 mo of age. Nutritional counseling and clinical management were provided for 2 y. Breast-milk substitutes were provided for free. The primary outcome was the occurrence of adverse health outcomes in children, defined as validated morbid events (diarrhea, acute respiratory infections, or malnutrition) or severe events (hospitalization or death). Hazards ratios to compare formula-fed versus short-term breast-fed (reference) children were adjusted for confounders (baseline covariates and pediatric HIV status as a time-dependant covariate). The 18-mo mortality rates were also compared to those observed in the Ditrame historical trial, which was conducted at the same sites in 1995–1998, and in which long-term breast-feeding was practiced in the absence of any specific infant feeding intervention. Of the 557 live-born children, 262 (47%) were breast-fed for a median of 4 mo, whereas 295 were formula-fed. Over the 2-y follow-up period, 37% of the formula-fed and 34% of the short-term breast-fed children remained free from any adverse health outcome (adjusted hazard ratio [HR]: 1.10; 95% confidence interval [CI], 0.87–1.38; p = 0.43). The 2-y probability of presenting with a severe event was the same among formula-fed (14%) and short-term breast-fed children (15%) (adjusted HR, 1.19; 95% CI, 0.75–1.91; p = 0.44). An overall 18-mo probability of survival of 96% was observed among both HIV-uninfected short-term and formula-fed children, which was similar to the 95% probability observed in the long-term breast-fed ones of the Ditrame trial.ConclusionsThe 2-y rates of adverse health outcomes were similar among short-term breast-fed and formula-fed children. Mortality rates did not differ significantly between these two groups and, after adjustment for pediatric HIV status, were similar to those observed among long-term breast-fed children. Given appropriate nutritional counseling and care, access to clean water, and a supply of breast-milk substitutes, these alternatives to prolonged breast-feeding can be safe interventions to prevent mother-to-child transmission of HIV in urban African settings.

Variability and correlations of synthetic chemicals in urine from a New York City-based cohort of pregnant women

Background: Epigenetic modifications, such as DNA methylation, due to in utero exposures may play a critical role in early programming for childhood and adult illness. Maternal smoking is a major risk factor for multiple adverse health outcomes in children, but the underlying mechanisms are unclear.Objective: We investigated epigenome-wide methylation in cord blood of newborns in relation to maternal smoking during pregnancy.Methods: We examined maternal plasma cotinine (an objective biomarker of smoking) measured during pregnancy in relation to DNA methylation at 473,844 CpG sites (CpGs) in 1,062 newborn cord blood samples from the Norwegian Mother and Child Cohort Study (MoBa) using the Infinium HumanMethylation450 BeadChip (450K).Results: We found differential DNA methylation at epigenome-wide statistical significance (p-value < 1.06 × 10–7) for 26 CpGs mapped to 10 genes. We replicated findings for CpGs in AHRR, CYP1A1, and GFI1 at strict Bonferroni-corrected statistical significance in a U.S. birth cohort. AHRR and CYP1A1 play a key role in the aryl hydrocarbon receptor signaling pathway, which mediates the detoxification of the components of tobacco smoke. GFI1 is involved in diverse developmental processes but has not previously been implicated in responses to tobacco smoke.Conclusions: We identified a set of genes with methylation changes present at birth in children whose mothers smoked during pregnancy. This is the first study of differential methylation across the genome in relation to maternal smoking during pregnancy using the 450K platform. Our findings implicate epigenetic mechanisms in the pathogenesis of the adverse health outcomes associated with this important in utero exposure.

Excessive use of screen-based devices may be associated with a higher risk of various adverse health outcomes in children and adolescents. The aim of this study was to examine the associations between smartphone, computer, and television use and insufficient sleep duration and overweight/obesity among Lithuanian children and adolescents aged 11–18 years. Data on self-reported smartphone, computer, and television use, as well as sleep duration on weekdays, were collected from 1,350 schoolchildren aged 11 to 18 who participated in a cross-sectional study conducted in Lithuania between November 2019 and March 2020. Use of smartphone, computer, and television was categorised into two groups: <2 h/day and ≥ 2 h/day for each device. Overall, 54.5% of the participants reported using a smartphone for ≥ 2 h/day, 28.1% reported using a computer for ≥ 2 h/day, and 7.8% reported watching television for ≥ 2 h/day. After adjusting for age, BMI, and physical activity, participants who used a smartphone ≥ 2 h/day had significantly higher odds of insufficient sleep duration (boys: aOR = 2.49 (95% CI 1.81–3.44) and girls: aOR = 2.57 (95% CI 1.80–3.66). Participants who used a computer ≥ 2 h/day had also significantly greater odds of insufficient sleep duration (boys: aOR = 1.94 (95% CI 1.41–2.67) and girls: aOR = 1.92 (95% CI 1.25–2.94). After adjusting for age, sleep duration, and physical activity, computer use ≥ 2 h/day was associated with increased odds of overweight/obesity only among boys (aOR = 1.45 (95% CI 1.03–2.05)). Our study revealed significant associations between prolonged smartphone and computer use with insufficient sleep duration among Lithuanian schoolchildren. Additionally, greater computer use was associated with increased odds of overweight/obesity, specifically in boys.Supplementary InformationThe online version contains supplementary material available at 10.1038/s41598-025-29544-8.

Investigators examined 5,654 children enrolled in the El Paso, Texas, public school district by questionnaire in 2001. Exposure measurements were first collected in the late fall of 1999. School-level and residence-level exposures to traffic-related air pollutants were estimated using a land use regression model. For 1,529 children with spirometry, overall geographic information system (GIS)-modeled residential levels of traffic-related ambient air pollution (calibrated to a 10-ppb increment in nitrogen dioxide levels) were associated with a 2.4% decrement in forced vital capacity (95% confidence interval (CI): -4.0, -0.7) after adjustment for demographic, anthropomorphic, and socioeconomic factors and spirometer/technician effects. After adjustment for these potential covariates, overall GIS-modeled residential levels of traffic-related ambient air pollution (calibrated to a 10-ppb increment in nitrogen dioxide levels) were associated with pulmonary function levels below 85% of those predicted for both forced vital capacity (odds ratio (OR) = 3.10, 95% CI: 1.65, 5.78) and forced expiratory volume in 1 second (OR = 2.35, 95% CI: 1.38, 4.01). For children attending schools at elevations above 1,170 m, a 10-ppb increment in modeled nitrogen dioxide levels was associated with current asthma (OR = 1.56, 95% CI: 1.08, 2.50) after adjustment for demographic, socioeconomic, and parental factors and random school effects. These results are consistent with previous studies in Europe and California that found adverse health outcomes in children associated with modeled traffic-related air pollutants.

ABSTRACTEvolving evidence links maternal stress exposure to changes in placental DNA methylation of specific genes regulating placental function that may have implications for the programming of a host of chronic disorders. Few studies have implemented an epigenome-wide approach. Using the Infinium HumanMethylation450 BeadChip (450K), we investigated epigenome-wide placental DNA methylation in relation to maternal experiences of traumatic and non-traumatic stressors over her lifetime assessed using the Life Stressor Checklist-Revised (LSC-R) survey (n = 207). We found differential DNA methylation at epigenome-wide statistical significance (FDR = 0.05) for 112 CpGs. Additionally, we observed three clusters that exhibited differential methylation in response to high maternal lifetime stress. Enrichment analyses, conducted at an FDR = 0.20, revealed lysine degradation to be the most significant pathway associated with maternal lifetimes stress exposure. Targeted enrichment analyses of the three largest clusters of probes, identified using the gap statistic, were enriched for genes associated with endocytosis (i.e., SMAP1, ANKFY1), tight junctions (i.e., EPB41L4B), and metabolic pathways (i.e., INPP5E, EEF1B2). These pathways, also identified in the top 10 KEGG pathways associated with maternal lifetime stress exposure, play important roles in multiple physiological functions necessary for proper fetal development. Further, two genes were identified to exhibit multiple probes associated with maternal lifetime stress (i.e., ANKFY1, TM6SF1). The methylation status of the probes belonging to each cluster and/or genes exhibiting multiple hits, may play a role in the pathogenesis of adverse health outcomes in children born to mothers with increased lifetime stress exposure.

Background/Objectives: Vitamin D deficiencies are very common in pregnant women, raising concerns about adverse health outcomes in children. This issue has hardly been studied in multiple pregnancies, the prevalence of which has been steadily increasing. Therefore, our study investigated the relationship between newborns’ anthropometric parameters and the concentration of 25(OH)D in maternal blood of women with twin pregnancies and umbilical cord blood. Methods: The study included 50 women who gave birth after the 36th week of twin gestation. The concentration of 25(OH)D was determined in maternal blood collected during the antenatal period and in the umbilical cord blood of 100 newborns. Anthropometric parameters of the newborns (birth weight, length and head and chest circumference) were obtained from hospital records. Data on nutrition and lifestyle during pregnancy were collected from the patients during an interview conducted by a dietitian. Results: No relationship between maternal and neonatal cord blood vitamin D concentrations and any of the anthropometric parameters of the newborns was found. However, only 6% of the mothers and 13% of the newborns had vitamin D deficiency (≤20 ng/mL). The type of pregnancy and maternal height were the main factors associated with neonatal size. Newborns from dichorionic pregnancies were on average 202 g heavier (p &lt; 0.001) and 1 cm longer (p = 0.006) than newborns from monochorionic pregnancies. Newborns of mothers ≤160 cm in height had on average 206 g lower birth weight (p = 0.006) and were 3.5 cm shorter (p = 0.003) compared to newborns of taller mothers. Conclusions: Therefore, in our study, the neonatal size of twins was not related to the vitamin D status but to other factors such as the type of pregnancy and maternal height.

Previous reviews and meta-analysis have not adequately explored the impact of specific parental adverse childhood experiences (ACEs) subtypes on offspring’s health. This updated systematic review and meta-analysis aimed to investigate the association between parental ACE subtypes and various offspring health outcomes. A comprehensive search was conducted in electronic databases including PubMed, Web of Science, the Cochrane Library, WANFANG, and China National Knowledge Infrastructure for studies published in English and Chinese from January 1, 1998, until July 18, 2023. Two independent reviewers screened studies, extracted data, and assessed study quality using the Newcastle-Ottawa Scale. A random-effects model was applied to generate pooled odds ratios (ORs) and 95% confidence interval (95% CI). A total of 47 eligible studies were included in the final analysis. Overall, parental ACEs were significantly associated with several offspring’s health outcomes, including preterm birth (PTB), low birth weight (LBW), total developmental delay, social-emotional problems, and behavioral problems (total, externalizing and internalizing behaviors), with ORs ranging from 1.06 to 3.02. Specific subtypes of parental ACEs, such as household dysfunction, sexual abuse, and physical abuse (but not emotional abuse) were significantly associated with PTB. Household dysfunction was notably linked to delayed cognition ability in offspring. Parental sexual abuse, physical abuse, emotional abuse, and emotional neglect were significantly correlated with social-emotion problems, with the expception of household dysfunction. Regarding total behavioral problems, parental household dysfunction, physical abuse, emotional abuse, physical neglect, and peer bullying were all significantly associated with children’s behavioral issues, except for emotional neglect. There is a positive correlation between parental household dysfunction, sexual abuse, physical abuse, emotional abuse, emotional neglect, physical neglect, peer bullying, and neighborhood-related adversity and their children’s externalizing behavior problems. These findings underscore the significant impacts of parental ACEs on multiple adverse health outcomes in children, with specific parental ACEs subtypes exerting unique effects. This highlight the significance of comprehending the intergenerational effects of different ACE subtypes, and emphasizes the urgency of interventions to address these issues.

BackgroundAflatoxins (AFs) are naturally occurring fungal metabolites produced by the Aspergilla species of fungi. The staple food grain, maize (Zea mays), is highly susceptible to AF contamination. In Kenya, contamination of maize supplies by AFs is a recognized public health problem which has resulted in over 600 human deaths. Human exposure to AFs can occur in utero, via breast milk, through weaning foods, and throughout an individual’s lifetime. Recent epidemiological studies have shown that exposure to AFs in early life through diet is a contributing factor to immune suppression, micronutrient deficiency, possible vaccine interference, and impaired growth in children. However, these results remain inconsistent and inconclusive due to lack of randomized controlled studies.MethodsA randomized school-based cross-sectional study was designed to study AF exposure levels and associated health effects in children between ages 6 and 12 years. Participants were recruited from primary schools within Siaya and Makueni Counties of Kenya, East Africa. The Joint Ethics Committee of the University of Nairobi and Kenyatta National Hospital in Kenya approved the research protocol and procedures for the study. Both parental consent and child assent were obtained before enrollment in the study. Parents were requested to provide household grain samples and fill out questionnaires detailing their sociodemographic information, household dietary patterns, farming practices, and knowledge of AF contamination. Blood samples were collected from children participants, and sera were prepared for analysis of AFB1-lysine which is one of the validated biomarkers for AF exposure.DiscussionThis protocol describes a school-based, cross-sectional study whose objective is to comparatively evaluate the role of AF exposure on adverse health outcomes in children. Specifically, effects of cumulative AF exposure on nutritional status, immune markers, and growth parameters will be assessed.Trial registrationThis study is not a clinical trial, rather a cross-sectional study aimed at providing baseline data on AF exposures in children who live in presumably high versus low AF exposure regions. Results from the study can be used to design interventions and/or prospective cohort studies aimed at studying adverse health effects associated with cumulative AF exposure through diets. The study reference number is P741/12/2017 and registered with KNH-UoN Ethics and Research Committee.