Search Results (60)

Allergic sensitization (AS) to pets is a notable health concern, with a 10–30% prevalence in developed countries, significantly higher than in developing nations; however, the critical exposure windows and reasons for this global disparity remain unclear. This study aimed to investigate associations between perinatal and current animal exposure and childhood AS among 2598 preschoolers (aged 3–6) in Changsha, China. Data on AS and pet exposure were gathered via questionnaires, while children’s prenatal and current exposure to outdoor air pollutants (PM₁₀, NO₂) was estimated from monitoring stations. Multiple logistic regression models revealed an overall AS prevalence of 1.8%. Current animal or pet exposure was significantly associated with childhood AS (adjusted OR 2.40, 95% CI 1.12–4.29). Conversely, no significant association was found for perinatal exposure. Intriguingly, a stratified analysis showed that the association with current exposure was significant only in children exposed to low levels of outdoor PM₁₀ (adj. OR 2.97, 95% CI 1.21–7.27) and NO₂ (adj. OR 3.01, 95% CI 1.23–7.37). The study concludes that current exposure to pets significantly increases childhood AS risk. This effect is unexpectedly magnified in environments with low outdoor air pollution. This novel finding not only may explain the higher prevalence of pet allergies in developed countries but also suggests that as air quality improves alongside rising pet ownership, developing nations like China could face a significant future increase in pet sensitization, highlighting a critical emerging public health challenge. Full article

In regions with sustained air pollution, the adoption of protective health behaviors is critical, particularly among pregnant women—a population marked by physiological vulnerability and heightened receptivity to preventive guidance. Understanding and supporting patient-driven behavioral change requires attention to individual perception and awareness, which are shaped by socio-economic and spatial factors, as well as access to credible information. Objectives: This study investigates how pregnant women in Serbia perceive air quality, identifies determinants that influence these perceptions, and evaluates the extent and nature of behavioral adaptations undertaken to mitigate exposure-related risks. Methods: A cross-sectional survey was conducted among 279 pregnant women using a structured, researcher-administered questionnaire. Collected data included demographic and psychosocial variables, air quality perceptions, self-reported health effects, and behavioral responses. Residential proximity to land-use attributes was assessed using GIS-based spatial analysis. Results: Most participants perceived air quality as poor (68.8%), primarily informed by unofficial sources such as mobile applications and social media. Living close to continuous urban fabric (OR = 0.180, 95% CI: 0.059–0.558, p = 0.003) and water (OR = 0.306, 95% CI: 0.127–0.738, p = 0.008) was associated with poorer perceptions, while proximity to forests (OR = 2.938, 95% CI: 1.323–6.525, p = 0.008) correlated with more favorable assessments. Despite prevalent concern, around half of respondents (50.2%) reported no behavioral modifications. Importantly, none had received guidance from healthcare professionals on the topic. Conclusions: These findings highlight critical gaps in environmental health literacy and provider engagement. Integrating tailored communication and behavioral support in existing prenatal counseling could advance health-related quality of life in this vulnerable population. Full article

Rapid industrialization has introduced a range of chemicals into the environment, posing significant risks to fetal and child brain development. Using the Comparative Toxicogenomics Database (CTD), we constructed chemical exposome frameworks for seven neurodevelopmental disorders (NDDs) and identified chemical pollutants of epidemiological concern, including air pollutants (n = 8), toxic elements (n = 14), pesticides and related compounds (n = 18), synthetic organic chemicals (n = 16), and solvents (n = 5). Gene set enrichment analysis validated and revealed significant toxicogenomic associations between these chemical pollutants and NDDs, including autism spectrum disorder (ASD) (12 pollutants, proportional reporting ratio (PRR) 3.56–7.21) and intellectual disability (ID) (9 pollutants, PRR 3.13–5.59). Functional annotation of pollutant-specific gene sets highlighted shared biological processes, such as metabolic processes (e.g., xenobiotic metabolic process, xenobiotic catabolic process, and cytochrome P450 pathway) for ASD and cognitive processes (e.g., cognition, social behavior, and synapse assembly) for ID (Bonferroni-corrected p-values < 0.05). Time trajectory analysis of developmental transcriptomic data from the BrainSpan database for ASD (275 genes) and ID (93 genes) revealed three distinct expression patterns of chemical-pollutant-associated genes—higher prenatal, postnatal, and perinatal expression—indicating common and divergent underlying mechanisms across critical windows of chemical pollutant exposure. Full article

Objective: Acute lymphoblastic leukaemia (ALL) is the most frequent childhood cancer. Infant ALL (<1 year) is rare, but it captures a lot of interest due to its poor prognosis, especially in patients harbouring KMT2A rearrangements, which have been demonstrated to arise prenatally. However, epidemiological studies aimed at identifying specific risk factors in such cases are scarce, mainly due to sample-size limitations. We conducted a scoping review to elucidate the prenatal or perinatal factors associated with infant ALL. Methods: Original articles, letters, or conference abstracts published up to June 2022 were identified using the PubMed, Web of Science, and Embase databases, and 33 observational studies were selected. Results: The study reveals several well-established associations across the literature, such as maternal exposure to pesticides and high birth weight, and outlines suggestive associations, such as parental heavy smoking, parental use of several medications (e.g., dipyrone), and maternal exposure to air pollution during pregnancy. Conclusions: This scoping review summarizes the few observational studies that have analysed the prenatal and perinatal risk factors for ALL in infants diagnosed before the age of 1 year. The results of this review highlight the lack of research into this specific age group, which merits further research. Full article

Numerous epidemiologic studies have used remote sensing to quantify the contribution of greenness, air pollution, and wildfire smoke to asthma and other respiration outcomes. This is the first review paper to evaluate the influence of remote sensing exposures on specific outcome severity and risk factors in different ecological settings. Literature searches utilizing PubMed and Google Scholar identified 61 unique studies published between 2009 and 2023, with 198 specific outcomes. Respiration-specific outcomes were lower in greenness and higher in air pollution and wildfire ecological settings. Aerosol optical depth (AOD)-PM_2.5 readings and specific outcomes were higher in economically developing than in economically developed countries. Prospective studies found prenatal and infant exposure to higher ambient AOD-PM_2.5 concentration level readings contributed to higher childhood asthma incidence. Lung function was higher in greenness and lower in the other two ecological settings. Age, environment, gender, other, and total risk factors showed significant differences between health outcomes and ecological settings. Published studies utilized physiologic mechanisms of immune, inflammation, and oxidative stress to describe obtained results. Individual and total physiologic mechanisms differed between ecological settings. Study results were used to develop a descriptive physiologic asthma model and propose updated population-based asthma intervention program guidelines. Full article

This article uses machine learning techniques as fuzzy and neuro-fuzzy ANFISs, to develop and compare prediction models capable of relating pregnant women’s exposure to air pollutants, such as Nitrogen Dioxide and Particulate Matter, the mother’s age, and the number of prenatal consultations to the incidence of premature birth. In the current literature, studies can be found that relate prematurity to the exposure of pregnant women to NO₂, O₃, and PM₁₀; to Toluene and benzene, mainly in the window 5 to 10 days before birth; and to PM₁₀ in the week before birth. Both models used logistic regression to quantify the effects of pollutants as a result of premature birth. Datasets from Brazil—Departamento de Informatica do Sistema Único de Saúde (DATASUS) and Companhia Ambiental do Estado de São Paulo (CETESB)—were used, covering the period from 2016 to 2018 and comprising women living in the city of São José dos Campos (SP), Brazil. In order to evaluate and compare the different techniques used, evaluation metrics were calculated, such as correlation (r), coefficient of determination (R²), Root Mean Square Error (RMSE), Mean Absolute Percentage Error (MAPE), Mean Square Error (MSE), and Mean Absolute Error (MAE). These metrics are widely used in the literature due to their ability to evaluate the robustness and efficiency of prediction models. For the RMSE, MAPE, MSE, and MAE metrics, lower values indicate that prediction errors are smaller, demonstrating better model accuracy and confidence. In the case of (r) and R², a positive and strong result indicates alignment and better performance between the real and predicted data. The neuro-fuzzy ANFIS model showed superior performance, with a correlation (r) of 0.59, R² = 0.35, RMSE = 2.83, MAPE = 5.35%, MSE = 8.00, and MAE = 1.70, while the fuzzy model returned results of r = 0.20, R² = 0.04, RMSE = 3.29, MSE = 10.81, MAPE = 6.67%, and MAE = 2.01. Therefore, the results from the ANFIS neuro-fuzzy system indicate greater prediction capacity and precision in relation to the fuzzy system. This superiority can be explained by integration with neural networks, allowing data learning and, consequently, more efficient modeling. In addition, the findings obtained in this study have potential for the formulation of public health policies aimed at reducing the number of premature births and promoting improvements in maternal and neonatal health. Full article

Background and objective: The association between air pollution and poor respiratory health outcomes is well established. Children are particularly at risk from air pollution, especially during the prenatal period as their organs and systems are still undergoing crucial development. This study investigated maternal exposure to air pollution during pregnancy and oxidative stress (OS), inflammation, and infant lung function at 4 weeks of age. Methods: Data from the Barwon Infant Study were available for 314 infants. The exposure to NO₂ and PM_2.5 were estimated. Infant lung function (4 weeks) was measured by multiple-breath washout. Glycoprotein acetyls (GlycA) (36 weeks prenatal), cord blood, and OS biomarkers were measured in maternal urine (28 weeks). A genetic pathway score for OS (gPFSox) was calculated. Linear regression was used and potential modification by the OS genotype was tested. Results: There was no relationship between maternal exposure to air pollution and infant lung function, or with GlycA or OS during pregnancy. We found an association in children with a genetic propensity to OS between NO₂ and a lower functional residual capacity (FRC) (β = −5.3 mls, 95% CI (−9.3, −1.3), p = 0.01) and lung clearance index (LCI) score (β = 0.46 turnovers, (95% CI 0.10, 0.82), p = 0.01). Conclusion: High prenatal exposure to ambient NO₂ is associated with a lower FRC and a higher LCI score in infants with a genetic propensity to oxidative stress. There was no relationship between maternal exposure to air pollution with maternal and cord blood inflammation or OS biomarkers. Full article

An understanding of the molecular mechanism whereby an environmental chemical causes a disease is important for the purposes of future applications. In this study, a multiomics workflow was designed to combine several publicly available datasets in order to identify CpG sites and genes that mediate the impact of exposure to environmental chemicals on cardiometabolic traits. Organophosphate and prenatal lead exposure were previously reported to change methylation level at the cg23627948 site. The outcome of the analyses conducted in this study revealed that, as the cg23627948 site becomes methylated, the expression of the GNA12 gene decreases, which leads to a higher body fat percentage. Prenatal perfluorooctane sulfonate exposure was reported to increase the methylation level at the cg21153102 site. Findings of this study revealed that higher methylation at this site contributes to higher diastolic blood pressure by changing the expression of CHP1 and GCHFR genes. Moreover, HKR1 mediates the impact of B12 supplementation → cg05280698 hypermethylation on higher kidney function, while CTDNEP1 mediates the impact of air pollution → cg03186999 hypomethylation on higher systolic blood pressure. This study investigates CpG sites and genes that mediate the impact of environmental chemicals on cardiometabolic traits. Furthermore, the multiomics approach described in this study provides a convenient workflow with which to investigate the impact of an environmental factor on the body’s biomarkers, and, consequently, on health conditions, using publicly available data. Full article

Exposure to PM_2.5 while pregnant is associated with negative effects on low birth weight (LBW). This study employed a systematic review and meta-analysis to investigate the impact of PM_2.5 exposure during pregnancy on LBW. A search of databases such as Scopus, ScienceDirect, and PubMed identified thirteen appropriate studies. This study used a random-effects model to calculate pooled odds ratios (ORs) and 95% confidence intervals (CIs) for each trimester. The findings revealed a significant relationship between PM_2.5 exposure and LBW in both the first and second trimesters (OR 1.05, 95% CI 1.00–1.09, p < 0.001). There was no significant difference between trimesters (p = 0.704). The results emphasize the persistent influence of PM_2.5 on fetal development throughout all stages of pregnancy. Reducing air pollution is critical for improving pregnancy outcomes and decreasing the incidence of LBW. Further study is needed to improve exposure assessments and investigate the underlying biological pathways. Full article

Current evidence suggests that airborne pollutants have a detrimental effect on fetal growth through the emergence of small for gestational age (SGA) or term low birth weight (TLBW). The study’s objective was to critically evaluate the available literature on the association between environmental pollution and the incidence of SGA or TLBW occurrence. A comprehensive literature search was conducted across Pubmed/MEDLINE, Web of Science, Cochrane Library, EMBASE, and Google Scholar using predefined inclusion and exclusion criteria. The methodology adhered to the PRISMA guidelines. The systematic review protocol was registered in PROSPERO with ID number: CRD42022329624. As a result, 69 selected papers described the influence of environmental pollutants on SGA and TLBW occurrence with an Odds Ratios (ORs) of 1.138 for particulate matter ≤ 10 μm (PM₁₀), 1.338 for particulate matter ≤ 2.5 μm (PM_2.5), 1.173 for ozone (O₃), 1.287 for sulfur dioxide (SO₂), and 1.226 for carbon monoxide (CO). All eight studies analyzed validated that exposure to volatile organic compounds (VOCs) is a risk factor for SGA or TLBW. Pregnant women in the high-risk group of SGA occurrence, i.e., those living in urban areas or close to sources of pollution, are at an increased risk of complications. Understanding the exact exposure time of pregnant women could help improve prenatal care and timely intervention for fetuses with SGA. Nevertheless, the pervasive air pollution underscored in our findings suggests a pressing need for adaptive measures in everyday life to mitigate worldwide environmental pollution. Full article

Incense burning is a significant source of indoor air pollution in many Asian regions. There is emerging evidence that maternal prenatal exposure to incense-burning smoke may be a risk factor for childhood obesity. We aimed to extend this new line of research by investigating the independent and joint effect of incense-burning smoke exposure, and children’s outdoor activity in early life, on preschoolers’ obesity. A total of 69,637 mother–child dyads were recruited from all kindergartens in the Longhua District of Shenzhen, China. Information on sociodemographic characteristics, maternal exposure to incense-burning smoke (IBS) during pregnancy, and frequency and duration of outdoor activity at the age of 1–3 years was collected by a self-administered questionnaire. In addition, the heights and weights of the children were measured by the research team. Logistic regression models and cross-over analyses were conducted to investigate the independent and combined effects of maternal exposure to incense-burning smoke during pregnancy and children’s early outdoor activity on obesity in preschoolers. We found that prenatal exposure to incense-burning smoke increased the risk of the presence of obesity in preschoolers’ (AOR = 1.13, 95% CI = 1.03–1.23). Additionally, lower frequencies (<3 times/week) or shorter durations (<60 min/time) of outdoor activity from the age of 1–3 years were significantly associated with the presence of obesity, with AORs of 1.24 (95% CI =1.18–1.32) and 1.11 (95% CI = 1.05–1.17), respectively. Furthermore, the cross-over analysis showed that prenatal exposure to IBS combined with a lower frequency of early outdoor activity (AOR = 1.47, 95% CI = 1.31–1.66) or a shorter duration of outdoor activity during ages of 1–3 years (AOR = 1.22, 95% CI = 1.07–1.39) increased the risk of obesity in preschoolers. Finally, additive interactions between prenatal exposure to IBS and postnatal outdoor activity on obesity were identified. Our study indicates that maternal exposure to incense-burning smoke during pregnancy and early lower postanal outdoor activity may independently and jointly increase the risk of obesity among preschoolers. Full article

The long-term effects of environmental pollution have been of concern as several pollutants are carcinogenic, potentially inducing a variety of cancers, including childhood cancer, which is a leading cause of death around the world and, thus, is a public health issue. The present scoping review aimed to update and summarize the available literature to detect specific environmental pollutants and their association with certain types of childhood cancer. Studies published from 2013 to 2023 regarding environmental pollution and childhood cancer were retrieved from the PubMed database. A total of 174 studies were eligible for this review and were analyzed. Our search strategy brought up most of the articles that evaluated air pollution (29%) and pesticides (28%). Indoor exposure to chemicals (11%), alcohol and tobacco use during pregnancy (16%), electromagnetic fields (12%), and radon (4%) were the subjects of less research. We found a particularly high percentage of positive associations between prenatal and postnatal exposure to indoor (84%) and outdoor (79%) air pollution, as well as to pesticides (82%), and childhood cancer. Positive associations were found between leukemia and pesticides and air pollution (33% and 27%); CNS tumors and neuroblastoma and pesticides (53% and 43%); and Wilms tumor and other rare cancers were found in association with air pollution (50%). Indoor air pollution was mostly reported in studies assessing several types of cancer (26%). Further studies are needed to investigate the mechanisms underlying the potential associations between indoor/outdoor air pollution and pesticide exposure with childhood cancer risk as more preventable measures could be taken. Full article

Background: Growing evidence suggests that air pollution may influence fetal development, with potential consequences for later health. Alteration of telomere length (TL) is one possible mediating mechanism for the link between fetal exposure to air pollution and the development of disease. However, the few studies exploring associations between prenatal pollution and infant TL have assessed varied trimesters of pregnancy and shown mixed results. The aim of this study was to examine the differential relationships between prenatal exposure to air pollutant PM_2.5 during the first, second, and third trimesters of pregnancy with infant TL at one month of age. Methods: Women (n = 74) were recruited in obstetric clinics during their third trimester. Data on PM_2.5 exposure for each woman’s residential area during each trimester was acquired from the regional Air Quality Management District. At one month postnatal, a salivary sample was collected from the infant, which provided DNA for the telomere assay. Women completed questionnaires about stressors in their lives, perceived stress, depression, and sociodemographics for inclusion as covariates. Multiple linear regression was used to analyze the results. Results: PM_2.5 exposure during the second (β = 0.31, p = 0.003) and third (β = 0.24, p = 0.02) trimesters was associated with longer infant TL. Exposure in the first trimester was not related to TL. Covariates of maternal depression and age and infant female sex were also associated with longer TL. Variables in the model contributed to 34% of the variance in TL (F = 10.58, p = 0.000). Discussion: Fetal programming of longer telomeres in response to pollution may have adaptive value in preparing the neonate for a postnatal environment that is less than optimal in terms of air quality. Alternatively, longer telomeres may forecast later health risks, considering established links between longer TL and diseases such as cancer. Future research needs to address how prenatal pollution interacts with TL to influence health over time. Full article

Allergic diseases are one of the most common chronic conditions and their prevalence is on the rise. Environmental exposure, primarily prenatal and early life influences, affect the risk for the development and specific phenotypes of allergic diseases via epigenetic mechanisms. Exposure to pollutants, microorganisms and parasites, tobacco smoke and certain aspects of diet are known to drive epigenetic changes that are essential for immune regulation (e.g., the shift toward T helper 2-Th2 cell polarization and decrease in regulatory T-cell (Treg) differentiation). DNA methylation and histone modifications can modify immune programming related to either pro-allergic interleukin 4 (IL-4), interleukin 13 (IL-13) or counter-regulatory interferon γ (IFN-γ) production. Differential expression of small non-coding RNAs has also been linked to the risk for allergic diseases and associated with air pollution. Certain exposures and associated epigenetic mechanisms play a role in the susceptibility to allergic conditions and specific clinical manifestations of the disease, while others are thought to have a protective role against the development of allergic diseases, such as maternal and early postnatal microbial diversity, maternal helminth infections and dietary supplementation with polyunsaturated fatty acids and vitamin D. Epigenetic mechanisms are also known to be involved in mediating the response to common treatment in allergic diseases, for example, changes in histone acetylation of proinflammatory genes and in the expression of certain microRNAs are associated with the response to inhaled corticosteroids in asthma. Gaining better insight into the epigenetic regulation of allergic diseases may ultimately lead to significant improvements in the management of these conditions, earlier and more precise diagnostics, optimization of current treatment regimes, and the implementation of novel therapeutic options and prevention strategies in the near future. Full article

A growing body of evidence suggests that chemicals interfere with the age of onset of menarche. We conducted a review in order to demonstrate the relationship between several categories of chemicals and menarche. We searched for English language papers using the Medline/PubMed database until April 2023. The chemical factors found to affect menarche were prenatal and antenatal smoke, phthalates, phenols, organochlorines, perfluoroalkyls and polyfluoroalkyls, metals, air pollutants and polybrominated diphenyl ethers. Low or high exposure to each chemical compound could affect the age of menarche, leading to early or delayed menarche. Furthermore, the results show that intrauterine exposure may have a different impact from antenatal exposure. There is evidence that endocrine-disrupting chemicals affect the age of menarche, but more research needs to be conducted. Full article