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Myo-inositol mediates the effects of traffic-related air pollution on generalized anxiety symptoms at age 12?years.

ABSTRACT: BACKGROUND:Exposure to traffic-related air pollution (TRAP) has been linked to childhood anxiety symptoms. Neuroimaging in patients with anxiety disorders indicate altered neurochemistry. OBJECTIVES:Evaluate the impact of TRAP on brain metabolism and its relation to childhood anxiety symptoms in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS). METHODS:Adolescents (n?=?145) underwent magnetic resonance spectroscopy. Brain metabolites, including myo-inositol, N-acetylaspartate, creatine, choline, glutamate, glutamate plus glutamine, and glutathione were measured in the anterior cingulate cortex. Anxiety symptoms were assessed using the Spence Children's Anxiety Scale. TRAP exposure in early-life, averaged over childhood, and during the 12 months prior to imaging was estimated using a validated land use regression model. Associations between TRAP exposure, brain metabolism, and anxiety symptoms were estimated using linear regression and a bootstrapping approach for testing mediation by brain metabolite levels. RESULTS:Recent exposure to high levels of TRAP was associated with significant increases in myo-inositol (??=?0.26; 95%CI 0.01, 0.51) compared to low TRAP exposure. Recent elevated TRAP exposure (??=?4.71; 95% CI 0.95, 8.45) and increased myo-inositol levels (??=?2.98; 95% CI 0.43, 5.52) were also significantly associated with increased generalized anxiety symptoms with 12% of the total effect between TRAP and generalized anxiety symptoms being mediated by myo-inositol levels. CONCLUSIONS:This is the first study of children to utilize neuroimaging to link TRAP exposure, metabolite dysregulation in the brain, and generalized anxiety symptoms among otherwise healthy children. TRAP may elicit atypical excitatory neurotransmission and glial inflammatory responses leading to increased metabolite levels and subsequent anxiety symptoms.

SUBMITTER: Brunst KJ

PROVIDER: S-EPMC6571158 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Myo-inositol mediates the effects of traffic-related air pollution on generalized anxiety symptoms at age 12 years.

Brunst Kelly J KJ Ryan Patrick H PH Altaye Mekibib M Yolton Kimberly K Maloney Thomas T Beckwith Travis T LeMasters Grace G Cecil Kim M KM

Environmental research 20190511

<h4>Background</h4>Exposure to traffic-related air pollution (TRAP) has been linked to childhood anxiety symptoms. Neuroimaging in patients with anxiety disorders indicate altered neurochemistry.<h4>Objectives</h4>Evaluate the impact of TRAP on brain metabolism and its relation to childhood anxiety symptoms in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS).<h4>Methods</h4>Adolescents (n = 145) underwent magnetic resonance spectroscopy. Brain metabolites, including myo-inositol ...[more]

PMID: 31103795

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Project description:Health effects of traffic-related air pollution (TRAP) concentrations in densely populated areas are previously described. However, there is still a lack of knowledge of the health effects of moderate TRAP levels. The aim of the current study, a population-based survey including 16?099 adults (response rate 33%), was to assess the relationship between TRAP estimates and respiratory symptoms in an area with modest levels of traffic; Telemark County, Norway. Respondents reported respiratory symptoms the past 12 months and two TRAP exposure estimates: amount of traffic outside their bedroom window and time spent by foot daily along a moderate to heavy traffic road. Females reported on average more symptoms than males. Significant relationships between traffic outside their bedroom window and number of symptoms were only found among females, with the strongest associations among female occasional smokers (incidence rate ratio [IRR], 1.75, 95% confidence interval (CI) [1.16-2.62] for moderate or heavy traffic compared to no traffic). Significant relationship between time spent daily by foot along a moderate to heavy traffic road and number of symptoms was found among male daily smokers (IRR 1.09, 95% CI [1.04-1.15] per hour increase). Associations between traffic outside bedroom window and each respiratory symptom were found. Significant associations were primarily detected among females, both among smokers and non-smokers. Significant associations between time spent by foot daily along a moderate to heavy traffic road (per hour) and nocturnal dyspnoea (odds ratio (OR) 1.20, 95% CI [1.05-1.38]), nocturnal chest tightness (OR 1.13 [1.00-1.28]) and wheezing (OR 1.14 [1.02-1.29]) were found among daily smokers, primarily men. Overall, we found significant associations between self-reported TRAP exposures and respiratory symptoms. Differences between genders and smoking status were identified. The findings indicate an association between TRAP and respiratory symptoms even in populations exposed to modest levels of TRAP.

Project description:Autism is a heterogeneous disorder with genetic and environmental factors likely contributing to its origins. Examination of hazardous pollutants has suggested the importance of air toxics in the etiology of autism, yet little research has examined its association with local levels of air pollution using residence-specific exposure assignments.To examine the relationship between traffic-related air pollution, air quality, and autism.This population-based case-control study includes data obtained from children with autism and control children with typical development who were enrolled in the Childhood Autism Risks from Genetics and the Environment study in California. The mother's address from the birth certificate and addresses reported from a residential history questionnaire were used to estimate exposure for each trimester of pregnancy and first year of life. Traffic-related air pollution was assigned to each location using a line-source air-quality dispersion model. Regional air pollutant measures were based on the Environmental Protection Agency's Air Quality System data. Logistic regression models compared estimated and measured pollutant levels for children with autism and for control children with typical development.Case-control study from California.A total of 279 children with autism and a total of 245 control children with typical development.Crude and multivariable adjusted odds ratios (AORs) for autism.Children with autism were more likely to live at residences that had the highest quartile of exposure to traffic-related air pollution, during gestation (AOR, 1.98 [95% CI, 1.20-3.31]) and during the first year of life (AOR, 3.10 [95% CI, 1.76-5.57]), compared with control children. Regional exposure measures of nitrogen dioxide and particulate matter less than 2.5 and 10 ?m in diameter (PM2.5 and PM10) were also associated with autism during gestation (exposure to nitrogen dioxide: AOR, 1.81 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.08 [95% CI, 1.93-2.25]; exposure to PM10: AOR, 2.17 [95% CI, 1.49-3.16) and during the first year of life (exposure to nitrogen dioxide: AOR, 2.06 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.12 [95% CI, 1.45-3.10]; exposure to PM10: AOR, 2.14 [95% CI, 1.46-3.12]). All regional pollutant estimates were scaled to twice the standard deviation of the distribution for all pregnancy estimates.Exposure to traffic-related air pollution, nitrogen dioxide, PM2.5, and PM10 during pregnancy and during the first year of life was associated with autism. Further epidemiological and toxicological examinations of likely biological pathways will help determine whether these associations are causal.

Project description:BackgroundA recent meta-analysis suggested evidence for an effect of exposure to ambient air pollutants on risk of certain congenital heart defects. However, few studies have investigated the effects of traffic-related air pollutants with sufficient spatial accuracy.ObjectivesWe estimated associations between congenital anomalies and exposure to traffic-related air pollution in Barcelona, Spain.MethodCases with nonchromosomal anomalies (n = 2,247) and controls (n = 2,991) were selected from the Barcelona congenital anomaly register during 1994-2006. Land use regression models from the European Study of Cohorts for Air Pollution Effects (ESCAPE), were applied to residential addresses at birth to estimate spatial exposure to nitrogen oxides and dioxide (NOx, NO2), particulate matter with diameter ? 10 ?m (PM10), 10-2.5 ?m (PMcoarse), ? 2.5 ?m (PM2.5), and PM2.5 absorbance. Spatial estimates were adjusted for temporal trends using data from routine monitoring stations for weeks 3-8 of each pregnancy. Logistic regression models were used to calculate odds ratios (ORs) for 18 congenital anomaly groups associated with an interquartile-range (IQR) increase in exposure estimates.ResultsIn spatial and spatiotemporal exposure models, we estimated statistically significant associations between an IQR increase in NO2 (12.2 ?g/m3) and coarctation of the aorta (ORspatiotemporal = 1.15; 95% CI: 1.01, 1.31) and digestive system defects (ORspatiotemporal = 1.11; 95% CI: 1.00, 1.23), and between an IQR increase in PMcoarse (3.6 ?g/m3) and abdominal wall defects (ORspatiotemporal = 1.93; 95% CI: 1.37, 2.73). Other statistically significant increased and decreased ORs were estimated based on the spatial model only or the spatiotemporal model only, but not both.ConclusionsOur results overall do not indicate an association between traffic-related air pollution and most groups of congenital anomalies. Findings for coarctation of the aorta are consistent with those of the previous meta-analysis.CitationSchembari A, Nieuwenhuijsen MJ, Salvador J, de Nazelle A, Cirach M, Dadvand P, Beelen R, Hoek G, Basagaña X, Vrijheid M. 2014. Traffic-related air pollution and congenital anomalies in Barcelona. Environ Health Perspect 122:317-323;?http://dx.doi.org/10.1289/ehp.1306802.

Project description:Traffic congestion increases vehicle emissions and degrades ambient air quality, and recent studies have shown excess morbidity and mortality for drivers, commuters and individuals living near major roadways. Presently, our understanding of the air pollution impacts from congestion on roads is very limited. This study demonstrates an approach to characterize risks of traffic for on- and near-road populations. Simulation modeling was used to estimate on- and near-road NO2 concentrations and health risks for freeway and arterial scenarios attributable to traffic for different traffic volumes during rush hour periods. The modeling used emission factors from two different models (Comprehensive Modal Emissions Model and Motor Vehicle Emissions Factor Model version 6.2), an empirical traffic speed-volume relationship, the California Line Source Dispersion Model, an empirical NO2-NOx relationship, estimated travel time changes during congestion, and concentration-response relationships from the literature, which give emergency doctor visits, hospital admissions and mortality attributed to NO2 exposure. An incremental analysis, which expresses the change in health risks for small increases in traffic volume, showed non-linear effects. For a freeway, "U" shaped trends of incremental risks were predicted for on-road populations, and incremental risks are flat at low traffic volumes for near-road populations. For an arterial road, incremental risks increased sharply for both on- and near-road populations as traffic increased. These patterns result from changes in emission factors, the NO2-NOx relationship, the travel delay for the on-road population, and the extended duration of rush hour for the near-road population. This study suggests that health risks from congestion are potentially significant, and that additional traffic can significantly increase risks, depending on the type of road and other factors. Further, evaluations of risk associated with congestion must consider travel time, the duration of rush-hour, congestion-specific emission estimates, and uncertainties.

Project description:PurposeTo investigate the association between exposure to traffic-related air pollution and use of spectacles (as a surrogate measure for myopia) in schoolchildren.MethodsWe analyzed the impact of exposure to NO2 and PM2.5 light absorbance at home (predicted by land-use regression models) and exposure to NO2 and black carbon (BC) at school (measured by monitoring campaigns) on the use of spectacles in a cohort of 2727 schoolchildren (7-10 years old) in Barcelona (2012-2015). We conducted cross-sectional analyses based on lifelong exposure to air pollution and prevalent cases of spectacles at baseline data collection campaign as well as longitudinal analyses based on incident cases of spectacles use and exposure to air pollution during the three-year period between the baseline and last data collection campaigns. Logistic regression models were developed to quantify the association between spectacles use and each of air pollutants adjusted for relevant covariates.ResultsAn interquartile range increase in exposure to NO2 and PM2.5 absorbance at home was respectively associated with odds ratios (95% confidence intervals (CIs)) for spectacles use of 1.16 (1.03, 1.29) and 1.13 (0.99, 1.28) in cross-sectional analyses and 1.15 (1.00, 1.33) and 1.23 (1.03, 1.46) in longitudinal analyses. Similarly, odds ratio (95% CIs) of spectacles use associated with an interquartile range increase in exposures to NO2 and black carbon at school was respectively 1.32 (1.09, 1.59) and 1.13 (0.97, 1.32) in cross-sectional analyses and 1.12 (0.84, 1.50) and 1.27 (1.03, 1.56) in longitudinal analyses. These findings were robust to a range of sensitivity analyses that we conducted.ConclusionWe observed increased risk of spectacles use associated with exposure to traffic-related air pollution. These findings require further confirmation by future studies applying more refined outcome measures such as quantified visual acuity and separating different types of refractive errors.

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Myo-inositol mediates the effects of traffic-related air pollution on generalized anxiety symptoms at age 12?years.

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Myo-inositol mediates the effects of traffic-related air pollution on generalized anxiety symptoms at age 12 years.

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Myo-inositol mediates the effects of traffic-related air pollution on generalized anxiety symptoms at age 12?years.

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Myo-inositol mediates the effects of traffic-related air pollution on generalized anxiety symptoms at age 12 years.

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OmicsDI is part of the ELIXIR infrastructure

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Myo-inositol mediates the effects of traffic-related air pollution on generalized anxiety symptoms at age 12 years.