Targeting Environmental Neurodevelopmental Risks to Protect Children.
Ontology highlight
ABSTRACT:
SUBMITTER: Hirtz D
PROVIDER: S-EPMC9923610 | biostudies-literature | 2017 Feb
REPOSITORIES: biostudies-literature
Publications
Targeting Environmental Neurodevelopmental Risks to Protect Children.
Hirtz Deborah D Campbell Carla C Lanphear Bruce B
Pediatrics 20170201 2
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Project description:One might expect that children with varying genetic mutations or children raised in low socioeconomic status environments would display different deficits. Although this expectation may hold for phenotypic outcomes in older children and adults, cross-syndrome comparisons in infancy reveal many common neural and sociocognitive deficits. The challenge is to track dynamic trajectories over developmental time rather than focus on end states like in adult neuropsychological studies. We contrast the developmental and adult approaches with examples from the cognitive and social domains, and we conclude that static models of adult brain lesions cannot be used to account for the dynamics of change in genetic and environmentally induced disorders in children.
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Project description:BackgroundChronic exposure to enteropathogens may result in environmental enteric dysfunction (EED), a subclinical condition associated with poor child growth. Growth faltering is strongly associated with poor neurodevelopment, and occurs during sensitive periods of postnatal brain development. We investigated the role of novel EED biomarkers, systemic inflammation, and micronutrient status on neurodevelopment in Tanzanian children.MethodsNon-stunted subjects with 6-week and 6-month blood samples and neurodevelopmental measures (n = 107) were included in this study. Samples were tested for biomarkers of gastrointestinal function (citrulline, antibodies to lipopolysaccharide, and flagellin), micronutrient status (iron, retinol binding protein [RBP], and vitamin D), systemic inflammation (C-reactive protein [CRP] and alpha-1-acid glycoprotein), and growth (insulin-like growth factor and insulin-like growth factor binding protein 3).ResultsCognitive scores at 15 months were associated with higher concentrations of 6-month anti-lipopolysaccharide IgG (β = 1.95, P = 0.02), anti-flagellin IgA (β = 2.41, P = 0.04), and IgG (β = 2.99, P = 0.009). Higher receptive language scores were positively associated with anti-flagellin IgG (β = 0.95, P = 0.05), and receptive language and gross motor scores were positively associated with citrulline at 6 months (β = 0.09, P = 0.02; β = 0.10, P = 0.03, respectively). Gross motor scores were positively associated with RBP at 6 months (β = 1.70, P = 0.03). Markers of systemic inflammation were not significantly associated with neurodevelopment.ConclusionsPlasma citrulline, a marker of gastrointestinal mucosal surface area, and vitamin A status were associated with higher gross motor development scores. Novel markers for EED, but not inflammation, were positively associated with cognitive scores, suggesting a possible mechanistic pathway involving immune response and neuroprotection.
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Project description:BackgroundAlthough ozone-depleting methyl bromide was destined for phase-out by 2005, it is still widely applied as a consequence of various critical-use-exemptions and mandatory international regulations aiming to restrict the spread of pests and alien species (e.g. in globalized transport and storage). The withdrawal of methyl bromide because of its environmental risk could fortuitously help in the containment of its human toxicity.MethodsWe performed a systematic review of the literature, including in vitro toxicological and epidemiological studies of occupational and community exposure to the halogenated hydrocarbon pesticide methyl bromide. We focused on toxic (especially chronic) or carcinogenic effects from the use of methyl bromide, on biomonitoring data and reference values. Eligible epidemiological studies were subjected to meta-analysis.ResultsOut of the 542 peer reviewed publications between 1990-2011, we found only 91 referring to toxicity of methyl bromide and 29 using the term "carcinogenic", "neoplastic" or "mutagenic". Several studies provide new additional data pertaining to the mechanistic aspects of methyl bromide toxicity. Few studies have performed a detailed exposure assessment including biomonitoring. Three evaluated epidemiological studies assessed a possible association between cancer and methyl bromide. Overall, exposure to methyl bromide is associated with an increased risk of prostate cancer OR, 1.21; 95% CI (0,98-1.49), P = 0.076. Two epidemiological studies have analyzed environmental, non-occupational exposure to methyl bromide providing evidence for its health risk to the general public. None of the epidemiological studies addressed its use as a fumigant in freight containers, although recent field and case reports do refer to its toxic effects associated with its use in shipping and storage.ConclusionsBoth the epidemiological evidence and toxicological data suggest a possible link between methyl bromide exposure and serious health problems, including prostate cancer risk from occupational and community exposure. The environmental risks of methyl bromide are not in doubt, but also its health risks, especially for genetically predisposed subjects, should not be underestimated.
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Project description:There are an estimated 5 million children working in artisanal and small-scale gold mines worldwide; however, the hazards are poorly characterized and often underreported. We systematically reviewed the literature on reports of hazards among children as a consequence of such activities through PubMed database using pre-defined search terms. We identified 113 articles published between 1984 and 2021 from 31 countries. Toxicological hazards were reported in 91 articles, including mercury, lead, and arsenic. Infectious hazards, noted in 18 articles, included malaria, cholera, and hepatitis. Six articles reported occupational hazards, including malnutrition, heat stroke, and reactive airway disease. Three articles reported traumatic hazards, including cave-ins, burns, animal attacks, falls, and weapon-inflected wounds. Those findings likely indicate a profound underreporting of the prevalence and consequences of such hazards among children. More work is needed both to characterize the burdens of those hazards and to address the underlying drivers of child labor in those settings.
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Project description:Many children participate in organized sports each year as a means of socialization, and physical skill building. Sports participation is dependent on physical growth, and neurodevelopmental readiness of the child. It is important to be aware of a child's level across the various streams of development and engage in specific strategies to optimize their ability at each age group. This article first outlines developmental skills across various age groups in childhood, and makes suggestions for such strategies.
| S-EPMC5532195 | biostudies-other
Project description:BackgroundAlthough studies show that maternal smoking during pregnancy increases the risks of respiratory outcomes in childhood, evidence concerning the effects of household environmental tobacco smoke (ETS) exposure remains inconsistent.MethodsWe conducted a population-based study comprised of 5,019 seventh and eighth-grade children in 14 Taiwanese communities. Questionnaire responses by parents were used to ascertain children's exposure and disease status. Logistic regression models were fitted to estimate the effects of ETS exposures on the prevalence of asthma, wheeze, and bronchitic symptoms.ResultsThe lifetime prevalence of wheeze was 11.6% and physician-diagnosed asthma was 7.5% in our population. After adjustment for potential confounders, in utero exposure showed the strongest effect on all respiratory outcomes. Current household ETS exposure was significantly associated with increased prevalence of active asthma, ever wheeze, wheeze with nighttime awakening, and bronchitis. Maternal smoking was associated with the increased prevalence of a wide range of wheeze subcategories, serious asthma, and chronic cough, but paternal smoking had no significant effects. Although maternal smoking alone and paternal smoking alone were not independently associated with respiratory outcomes, joint exposure appeared to increase the effects. Furthermore, joint exposure to parental smoking showed a significant effect on early-onset asthma (OR, 2.01; 95% CI, 1.00-4.02), but did not show a significant effect on late-onset asthma (OR, 1.17; 95% CI, 0.36-3.87).ConclusionWe concluded that prenatal and household ETS exposure had significant adverse effects on respiratory health in Taiwanese children.
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Project description:Epigenetics is a gene regulation mechanism that does not depend on genomic DNA sequences but depends on chemical modification of genomic DNA and histone proteins around which DNA is wrapped. The failure of epigenetic mechanisms is known to cause various congenital disorders. It is also known that the failures of epigenetic mechanisms causes various acquired disorders since epigenetic modifications of the genome (i.e., "epigenome") are more vulnerable to environmental stress, such as malnutrition, environmental chemicals, and mental stress, than the "genome," especially during the early period of life. However, the epigenome has a reversible property since it is based on removable residues on genomic DNA. Thus, environmentally induced epigenomic alterations can be potentially restored. In fact, some medicines, especially for psychiatric diseases, are known to restore an altered epigenome, resulting in the correction of gene expression. Several lines of evidence suggest that environmentally induced epigenomic alterations are not erased completely during gametogenesis, but are transmitted to subsequent generations with disease phenotypes. In accordance with these understandings, I would like to propose the development of epigenomic-based preemptive medicine that consists of the early detection of the developmental origins of diseases using epigenomic signatures and the early intervention that take advantages of the use of epigenomic reversibility.
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Project description:Complex neurodevelopmental disorders, such as schizophrenia, autism, attention deficit (hyperactivity) disorder, (manic) depressive illness and addiction, are thought to result from an interaction between genetic and environmental factors. Association studies on candidate genes and genome-wide linkage analyses have identified many susceptibility chromosomal regions and genes, but considerable efforts to replicate association have been surprisingly often disappointing. Here, we summarize the current knowledge of the genetic contribution to complex neurodevelopmental disorders, focusing on the findings from association and linkage studies. Furthermore, the contribution of the interaction of the genetic with environmental and epigenetic factors to the aetiology of complex neurodevelopmental disorders as well as suggestions for future research are discussed.
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Project description: Not available
| ST000877 | MetabolomicsWorkbench