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Children's mobility and environmental exposures in urban landscapes: A cross-sectional study of 10-11 year old Scottish children.

ABSTRACT: Research into how the environment affects health and related behaviour is typically limited in at least two ways: it represents the environment to which people are exposed using fixed areal units, and, it focuses on one or two environmental characteristics only. This study developed a methodology for describing children's mobility and the complexity of their environmental exposure across a 1934 km2 study area, including urban, suburban and rural zones. It conceptualised and modelled this area as a landscape, comprised of spatially discrete amenities, infrastructure features, differing land covers/use and broader environmental contexts. The model used a 25 m2 grid system (∼3 million cells). For each cell, there was detailed built-environment information. We joined data for 100 10/11-year-old children who had worn GPS trackers to provide individual-level mobility information for one week during 2015/16 to our model. Using negative binomial regression, we explored which landscape features were associated with a child visiting that space and time spent there. We examined whether relationships between the features across our study area and children's use of the space differed by their sociodemographic characteristics. We found that children often used specific amenities outside their home neighbourhood, even if they were also available close to home. They spent more time in cells containing roads/transportation stops, food/drink retail (Incidence rate ratio (IRR):4.02, 95%CI 2.33 to 6.94), places of worship (IRR:5.98, 95%CI 3.33 to 10.72) and libraries (IRR:7.40, 95%CI 2.13 to 25.68), independently of proximity to home. This has importance for the optimal location of place-based health interventions. If we want to target children, we need to understand that using fixed neighbourhood boundaries may not be the best way to do it. The variations we found in time spent in certain areas by sex and socio-economic position also raise the possibility that interventions which ignore these differences may exacerbate inequalities.

SUBMITTER: Olsen JR

PROVIDER: S-EPMC6411928 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Introduction: Prenatal environmental exposures have been associated with children's cognitive, behavioral, and mental health problems, and alterations in DNA methylation have been hypothesized as an underlying biological mechanism. However, when testing this hypothesis, it is often difficult to overcome the problem of multiple comparisons in statistical testing when evaluating a large number of developmental outcomes and DNA methylation sites as potential mediators. The objective of this study is to implement a 'meet-in-the-middle' approach with a sequential roadmap to address this concern. Methods: In the Columbia Center for Children's Environmental Health birth cohort study, we implemented a 5-step sequential process for identifying CpG sites that mediate associations between prenatal environmental exposures and cognitive, behavioral, and mental health problems as measured by the Wechsler Intelligence Scale for Children-Fourth Edition (WISC-IV) and the Child Behavior Checklist (CBCL). These steps include 1) the identification of biological pathways that are relevant to each outcome of interest; 2) selection of a set of genes and CpGs on genes that are significantly associated with the outcomes; 3) identification of exposures that are significantly associated with selected CpGs; 4) examination of exposure-outcome relationships among those where significant CpGs were identified; and 5) mediation analysis of the selected exposures and corresponding outcomes. In this study, we considered a spectrum of environmental exposure classes including environmental phenols, pesticides, phthalates, flame retardants and air pollutants. Results: Among all considered exposures and outcomes, we found one CpG site (cg27510182) on gene (DAB1) that potentially mediates the effect of exposure to PAH on CBCL social problems at children aged 7. Conclusion: This 'meet-in-the-middle' approach attenuates concerns regarding multiple comparisons by focusing on genes and pathways that are biologically relevant for the hypothesis.

Project description:BackgroundAnimal studies suggest that organophosphorus pesticides (OPs) may be environmental obesogens. While prenatal OP exposures have been associated with altered infant glucose metabolism, associations with pediatric adiposity remain unknown.MethodsWe summed concentrations of three dimethylphosphate (∑DMP) and three diethylphosphate (∑DEP) metabolites of OPs measured in third trimester spot urine samples collected from pregnant women enrolled in New York City, 1998-2002. We measured percent fat mass using bio-electrical impedance analysis and calculated age- and sex-standardized body mass index (BMI) z-scores from anthropometric measurements collected at approximately 4, 6, and 7-9 years of age (166 children, 333 observations). We assessed covariate-adjusted associations of OPs with repeated adiposity measures using linear mixed models and evaluated effect measure modification (EMM) by sex and paroxonase (PON) 1 -108C/T and Q192R polymorphisms measured in maternal peripheral blood samples.ResultsThe geometric mean urinary concentration of ∑DMP metabolites (29.9 nmol/L, IQR: 105.2 nmol/L) was higher than ∑DEP metabolites (8.8 nmol/L, IQR: 31.2 nmol/L). Adjusted associations were null, with differences in fat mass per 10-fold increase in prenatal ∑DMP and ∑DEP concentrations of 0.7% (95% CI: -0.6, 2.0) and 0.8% (95% CI: -0.4, 2.0), respectively. Maternal PON1-108C/T polymorphisms modified relationships of prenatal ∑DMP with percent fat mass (EMM p-value = 0.18) and ∑DEP with BMI z-scores (EMM p-value = 0.12). For example, ∑DMP was modestly associated with increased percent fat mass among children of mothers with the at-risk CT or TT genotype (β = 1.2%, 95% CI: -0.6, 3.0) but not among those whose mothers had the CC genotype (β = -0.4%, 95% CI: -2.4, 1.5). Associations were not modified by sex or maternal PON1 Q192R polymorphisms.ConclusionsWe observed little evidence of a relationship between prenatal OP exposures and child adiposity, although there was some suggestion of increased risk among offspring of mothers who were slow OP metabolizers. Larger studies are warranted to further evaluate possible associations of prenatal OP exposures with child adiposity and differences by maternal PON1 genotype, which regulates OP metabolism and may increase susceptibility to exposure.

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Children's mobility and environmental exposures in urban landscapes: A cross-sectional study of 10-11 year old Scottish children.

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