Lifetime exposure to traffic-related air pollution and symptoms of depression and anxiety at age 12 years.
ABSTRACT: BACKGROUND:While air pollution has been associated with depression and anxiety in adults, its impact on childhood mental health is understudied. OBJECTIVE:We examined lifetime exposure to traffic-related air pollution (TRAP) and symptoms of depression and anxiety at age 12 years in the Cincinnati Childhood Allergy and Air Pollution Study cohort. METHODS:We estimated exposure to elemental carbon attributable to traffic (ECAT), a surrogate of diesel exhaust, at birth, age 12 years, and average exposure throughout childhood, using a validated land use regression model. We assessed depression and anxiety at age 12 years by parent report with the Behavior Assessment System for Children-2, and by child report with the Child Depression Inventory-2 (CDI-2) and the Spence Children's Anxiety Scale (SCAS). Associations between TRAP at birth, age 12 years, and childhood average and mental health outcomes were estimated using linear regression models adjusting for covariates including parent depression, secondhand smoke exposure, race, household income, and others. RESULTS:Exposure to ECAT was not significantly associated with parent-reported depression or anxiety. However, exposure to ECAT at birth was associated with increased child-reported depression and anxiety. Each 0.25?µg/m3 increase in ECAT was associated with a 3.5 point increase (95% CI 1.6-5.5) in CDI-2 scores and 2.3 point increase (95% CI 0.8-3.9) in SCAS total anxiety scores. We observed similar associations between average childhood ECAT exposures but not for concurrent exposures at age 12. CONCLUSIONS:TRAP exposure during early life and across childhood was significantly associated with self-reported depression and anxiety symptoms in children. The negative impact of air pollution on mental health previously reported among adults may also be present during childhood.
Project description: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.
Project description:Background:Early-life exposure to traffic-related air pollution may decrease fetal growth and increase childhood obesity risk. Our objective was to evaluate the relationship of early-life exposure to traffic-related air pollution with birthweight in term newborns and obesity at age 7-8 years in two prospective birth cohorts in Cincinnati, OH (the Health Outcomes and Measures of the Environment (HOME) Study and Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS)). Methods:We estimated elemental carbon attributable to traffic (ECAT) exposure at residential addresses during pregnancy with a validated land use regression model. We assessed birthweight among term infants using birth records or parent report (HOME Study n= 333 and CCAAPS n=590). We measured children's weight and height at 7-8 years, and calculated age- and sex-specific BMI z-scores (HOME Study n= 198 and CCAAPS n=459). Using multivariable linear regression, we estimated the difference in term birthweight and BMI z-score per interquartile range (IQR) increase in ECAT concentrations in each cohort separately and in the pooled sample. Results:In adjusted models, ECAT exposure was not associated with lower birthweight (pooled sample ?: 30g; 95% CI: -6, 66), or with higher BMI z-score (pooled sample ?: -0.04; 95% CI: -0.15, 0.08). Infant sex modified the association between ECAT and birthweight (p=0.05). Among male newborns, higher ECAT concentrations were associated with higher birthweight (?: 61g; 95% CI: 9, 113), but we observed no association among female newborns (?: -9g; 95% CI: -58, 41). Conclusions:In contrast to some prior studies, early-life traffic-related air pollution exposure was not associated with lower birthweight or increased childhood adiposity in these two cohorts.
Project description:Air pollution is a worldwide environmental health issue. Increasingly, reports suggest that poor air quality may be associated with mental health problems, but these studies often use global measures and rarely focus on early development when psychopathology commonly emerges. To address this, we combined high-resolution air pollution exposure estimates and prospectively-collected phenotypic data to explore concurrent and longitudinal associations between air pollutants of major concern in urban areas and mental health problems in childhood and adolescence. Exploratory analyses were conducted on 284 London-based children from the Environmental Risk (E-Risk) Longitudinal Twin Study. Exposure to annualized PM2.5 and NO2 concentrations was estimated at address-level when children were aged 12. Symptoms of anxiety, depression, conduct disorder, and attention-deficit hyperactivity disorder were assessed at ages 12 and 18. Psychiatric diagnoses were ascertained from interviews with the participants at age 18. We found no associations between age-12 pollution exposure and concurrent mental health problems. However, age-12 pollution estimates were significantly associated with increased odds of major depressive disorder at age 18, even after controlling for common risk factors. This study demonstrates the potential utility of incorporating high-resolution pollution estimates into large epidemiological cohorts to robustly investigate associations between air pollution and youth mental health.
Project description:Traffic-related air and noise pollution may increase the risk for cardiovascular disorders, especially among susceptible populations like pregnant women. The objective of this study was to evaluate the association of exposure to traffic-related air pollution and traffic noise with blood pressure in pregnant women. We extracted systolic blood pressure (SBP) and diastolic blood pressure (DBP) at ?20?weeks gestation, as well as hypertensive disorders of pregnancy from medical records in the HOME Study, a prospective pregnancy and birth cohort from Cincinnati, OH (n?=?370). We estimated exposure to elemental carbon attributable to traffic (ECAT),1 a marker of traffic-related air pollution, at women's residences at ~20?weeks gestation using a validated land use regression model and traffic noise using a publicly available transportation noise model. We used linear mixed models and modified Poisson regression adjusted for covariates to examine associations of ECAT and traffic noise with blood pressure and hypertensive disorders of pregnancy risk, respectively. In adjusted models, we found a 1.6 (95% CI?=?0.02, 3.3; p?=?0.048) mm?Hg increase in SBP associated with an interquartile range increase in ECAT concentration; the association was stronger after adjusting for traffic noise (1.9?mm?Hg, 95%?=?0.1, 3.7; p?=?0.035). ECAT concentrations were not significantly associated with DBP or hypertensive disorders of pregnancy, and traffic noise was not associated with SBP, DBP, or hypertensive disorders of pregnancy. There was no evidence of a joint effect of traffic noise and ECAT on any outcome. In this cohort, higher residential traffic-related air pollution exposure at ~20?weeks gestation was associated with higher SBP in late pregnancy. It is important for future studies of traffic-related air or noise pollution to jointly consider both exposures and neighborhood characteristics given their correlation and potential cumulative impact on cardiovascular health.
Project description:Introduction:Traffic related air pollution (TRAP) has long been associated with the onset of childhood asthma. The relationship between TRAP exposure and the development of childhood asthma phenotypes is less understood. To better understand this relationship, we performed a systematic review of the literature studying childhood TRAP exposure and the development of childhood asthma and wheezing phenotypes (transient, persistent, and late-onset asthma/wheezing phenotypes). Methods:A literature search was performed in PubMed, Embase, and Scopus databases for current literature, returning 1706 unique articles. After screening and selection, 7 articles were included in the final review. Due to the low number of articles, no meta-analysis was performed. Results:TRAP exposure appears to be associated with both transient and persistent asthma/wheezing phenotypes. However, there was little evidence to suggest a relationship between TRAP exposure and late-onset asthma/wheezing. The differing results may be in part due to the heterogeneity in study methods and asthma/wheezing phenotype definitions, in addition to other factors such as genetics. Conclusion:TRAP exposure may be associated with transient and persistent asthma/wheezing phenotypes in children. The low number of studies and differing results suggest that further studies are warranted.
Project description:Early life exposure to air pollution poses a significant risk to brain development from direct exposure to toxicants or via indirect mechanisms involving the circulatory, pulmonary or gastrointestinal systems. In children, exposure to traffic related air pollution has been associated with adverse effects on cognitive, behavioral and psychomotor development. We aimed to determine whether childhood exposure to traffic related air pollution is associated with regional differences in brain volume and cortical thickness among children enrolled in a longitudinal cohort study of traffic related air pollution and child health. We used magnetic resonance imaging to obtain anatomical brain images from a nested subset of 12 year old participants characterized with either high or low levels of traffic related air pollution exposure during their first year of life. We employed voxel-based morphometry to examine group differences in regional brain volume, and with separate analyses, changes in cortical thickness. Smaller regional gray matter volumes were determined in the left pre- and post-central gyri, the cerebellum, and inferior parietal lobe of participants in the high traffic related air pollution exposure group relative to participants with low exposure. Reduced cortical thickness was observed in participants with high exposure relative to those with low exposure, primarily in sensorimotor regions of the brain including the pre- and post-central gyri and the paracentral lobule, but also within the frontal and limbic regions. These results suggest that significant childhood exposure to traffic related air pollution is associated with structural alterations in brain.
Project description:Studies of potential adverse effects of traffic related air pollution (TRAP) on allergic disease have had mixed findings. Nutritional studies to examine whether fish oil supplementation may protect against development of allergic disease through their anti-inflammatory actions have also had mixed findings. Extremely few studies to date have considered whether air pollution and dietary factors such as fish oil intake may interact, which was the rationale for this study.We conducted a secondary analysis of the Childhood Asthma Prevention Study (CAPS) birth cohort, where children were randomised to fish oil supplementation or placebo from early life to age 5 years. We examined interactions between supplementation and TRAP (using weighted road density at place of residence as our measure of traffic related air pollution exposure) with allergic disease and lung function outcomes at age 5 and 8 years.Outcome information was available on approximately 400 children (~?70% of the original birth cohort). Statistically significant interactions between fish oil supplementation and TRAP were seen for house dust mite (HDM), inhalant and all-allergen skin prick tests (SPTs) and for HDM-specific interleukin-5 response at age 5. Adjusting for relevant confounders, relative risks (RRs) for positive HDM SPT were RR 1.74 (95% CI 1.22-2.48) per 100 m local road or 33.3 m of motorway within 50 m of the home for those randomised to the control group and 1.03 (0.76-1.41) for those randomised to receive the fish oil supplement. The risk differential was highest in an analysis restricted to those who did not change address between ages 5 and 8 years. In this sub-group, supplementation also protected against the effect of traffic exposure on pre-bronchodilator FEV1/FVC ratio.Results suggest that fish oil supplementation may protect against pro-allergic sensitisation effects of TRAP exposure. Strengths of this analysis are that supplementation was randomised and independent of TRAP exposure, however, findings need to be confirmed in a larger experimental study with the interaction investigated as a primary hypothesis, potentially also exploring epigenetic mechanisms. More generally, studies of adverse health effects of air pollution may benefit from considering potential effect modification by diet and other factors.Australia New Zealand Clinical Trial Registry. www.anzctr.org.au Registration: ACTRN12605000042640 , Date: 26th July 2005. Retrospectively registered, trial commenced prior to registry availability.
Project description:Background: Current levels of traffic-related air pollution (TRAP) are associated with the development of childhood asthma, although some inconsistencies and heterogeneity remain. An important part of the uncertainty in studies of TRAP-associated asthma originates from uncertainties in the TRAP exposure assessment and assignment methods. In this work, we aim to systematically review the exposure assessment methods used in the epidemiology of TRAP and childhood asthma, highlight recent advances, remaining research gaps and make suggestions for further research. Methods: We systematically reviewed epidemiological studies published up until 8 September 2016 and available in Embase, Ovid MEDLINE (R), and "Transport database". We included studies which examined the association between children's exposure to TRAP metrics and their risk of "asthma" incidence or lifetime prevalence, from birth to the age of 18 years old. Results: We found 42 studies which examined the associations between TRAP and subsequent childhood asthma incidence or lifetime prevalence, published since 1999. Land-use regression modelling was the most commonly used method and nitrogen dioxide (NO?) was the most commonly used pollutant in the exposure assessments. Most studies estimated TRAP exposure at the residential address and only a few considered the participants' mobility. TRAP exposure was mostly assessed at the birth year and only a few studies considered different and/or multiple exposure time windows. We recommend that further work is needed including e.g., the use of new exposure metrics such as the composition of particulate matter, oxidative potential and ultra-fine particles, improved modelling e.g., by combining different exposure assessment models, including mobility of the participants, and systematically investigating different exposure time windows. Conclusions: Although our previous meta-analysis found statistically significant associations for various TRAP exposures and subsequent childhood asthma, further refinement of the exposure assessment may improve the risk estimates, and shed light on critical exposure time windows, putative agents, underlying mechanisms and drivers of heterogeneity.
Project description:BACKGROUND:Long-term exposure to particulate matter (PM) air pollution is associated with all-cause mortality and adverse cognitive outcomes, but the association with developing depression remains inconsistent. OBJECTIVE:Our goal was to evaluate the prospective association between PM air pollution and developing depression assessed using the Center for Epidemiological Studies Depression (CES-D) scale. METHODS:Subjects were drawn from a prospective cohort study of 123,045 men and women free of depressive symptoms at baseline who attended regular screening exams in Seoul and Suwon, South Korea, from 2011 to 2015. Exposure to PM with an aerodynamic diameter of [Formula: see text] ([Formula: see text] and [Formula: see text], respectively) was estimated using a land-use regression model based on each subject's residential postal code. Incident depression was defined as a CES-D score [Formula: see text] during follow-up. As a sensitivity analyses, we defined incident depression using self-reports of doctor's diagnoses or use of antidepressant medications during follow-up. RESULTS:The mean baseline 12-month concentrations of [Formula: see text] and [Formula: see text] were 50.6 (4.5) and [Formula: see text], respectively. The hazard ratios (HRs) and 95% confidence intervals (CIs) for developing depression associated with a [Formula: see text] increase in 12- and 60-month [Formula: see text] exposure were 1.11 (95% CI: 1.06, 1.16) and 1.06 (95% CI: 1.01, 1.11), respectively. The corresponding HRs for 12-month [Formula: see text] exposure was 0.96 (95% CI: 0.64, 1.43). Similar results were obtained when incident depression was identified using self-reports of doctor's diagnoses or the use of antidepressant medications. CONCLUSION:In this large cohort study, we found a positive association between long-term exposure to outdoor [Formula: see text] air pollution and the developing depression. We did not find an association for outdoor [Formula: see text] air pollution; however, we had a much shorter follow-up for subjects' exposure to [Formula: see text]. https://doi.org/10.1289/EHP4094.
Project description:BACKGROUND:Ambient air pollution exposure has been associated with dementia. Additionally, epidemiologic evidence supports associations between air pollution and diabetes as well as diabetes and dementia. Thus, an indirect pathway between air pollution and dementia may exist through metabolic dysfunction. OBJECTIVE:To investigate whether local traffic-related air pollution (TRAP) influences incident dementia and cognitive impairment, non-dementia (CIND) in a cohort of older Mexican Americans. We also assess how much of this estimated effect might be mediated through type 2 diabetes (T2DM). METHODS:In a 10-year, prospective study of Latinos (n?=?1,564), we generated TRAP-NOx as a surrogate for pollution from local traffic sources at participants' residences during the year prior to enrollment. We used Cox proportional hazards modeling and mediation analysis to estimate the effects of TRAP-NOx on dementia and/or CIND and indirect pathways operating through T2DM. RESULTS:Higher TRAP-NOx was associated with incident dementia (HR?=?1.55 for the highest versus lower tertiles, 95% CI?=?1.04, 2.55). Higher TRAP-NOx was also associated with T2DM (OR?=?1.62, 95% CI?=?1.27, 2.05); furthermore, T2DM was associated with dementia (HR?=?1.94, 95% CI?=?1.42, 2.66). Mediation analysis indicated that 20% of the estimated effect of TRAP-NOx on dementia/CIND was mediated through T2DM. CONCLUSION:Our results suggest that exposure to local traffic-related air pollution is associated with incident dementia. We also estimated that 20% of this effect is mediated through T2DM. Thus, ambient air pollution might affect brain health via direct damage as well as through indirect pathways related to diabetes and metabolic dysfunction.