58 research outputs found

    Air Pollution and Acute Respiratory Response in a Panel of Asthmatic Children along the U.S.–Mexico Border

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    Background: Concerns regarding the health impact of urban air pollution on asthmatic children are pronounced along the U.S.–Mexico border because of rapid population growth near busy border highways and roads. Objectives: We conducted the first binational study of the impacts of air pollution on asthmatic children in Ciudad Juarez, Mexico, and El Paso, Texas, USA, and compared different exposure metrics to assess acute respiratory response. Methods: We recruited 58 asthmatic children from two schools in Ciudad Juarez and two schools in El Paso. A marker of airway inflammation [exhaled nitric oxide (eNO)], respiratory symptom surveys, and pollutant measurements (indoor and outdoor 48-hr size-fractionated particulate matter, 48-hr black carbon, and 96-hr nitrogen dioxide) were collected at each school for 16 weeks. We examined associations between the pollutants and respiratory response using generalized linear mixed models. Results: We observed small but consistent associations between eNO and numerous pollutant metrics, with estimated increases in eNO ranging from 1% to 3% per interquartile range increase in pollutant concentrations. Effect estimates from models using school-based concentrations were generally stronger than corresponding estimates based on concentrations from ambient air monitors. Both traffic-related and non–traffic-related particles were typically more robust predictors of eNO than was nitrogen dioxide, for which associations were highly sensitive to model specification. Associations differed significantly across the four school-based cohorts, consistent with heterogeneity in pollutant concentrations and cohort characteristics. Models examining respiratory symptoms were consistent with the null. Conclusions: The results indicate adverse effects of air pollution on the subclinical respiratory health of asthmatic children in this region and provide preliminary support for the use of air pollution monitors close to schools to track exposure and potential health risk in this population

    Air Pollution and Acute Respiratory Response in a Panel of Asthmatic Children along the U.S.–Mexico Border

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    Background: Concerns regarding the health impact of urban air pollution on asthmatic children are pronounced along the U.S.–Mexico border because of rapid population growth near busy border highways and roads

    Exposure to traffic pollution, acute inflammation and autonomic response in a panel of car commuters

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    Background Exposure to traffic pollution has been linked to numerous adverse health endpoints. Despite this, limited data examining traffic exposures during realistic commutes and acute response exists. Objectives: We conducted the Atlanta Commuters Exposures (ACE-1) Study, an extensive panel-based exposure and health study, to measure chemically-resolved in-vehicle exposures and corresponding changes in acute oxidative stress, lipid peroxidation, pulmonary and systemic inflammation and autonomic response. Methods We recruited 42 adults (21 with and 21 without asthma) to conduct two 2-h scripted highway commutes during morning rush hour in the metropolitan Atlanta area. A suite of in-vehicle particulate components were measured in the subjects’ private vehicles. Biomarker measurements were conducted before, during, and immediately after the commutes and in 3 hourly intervals after commutes. Results At measurement time points within 3 h after the commute, we observed mild to pronounced elevations relative to baseline in exhaled nitric oxide, C-reactive-protein, and exhaled malondialdehyde, indicative of pulmonary and systemic inflammation and oxidative stress initiation, as well as decreases relative to baseline levels in the time-domain heart-rate variability parameters, SDNN and rMSSD, indicative of autonomic dysfunction. We did not observe any detectable changes in lung function measurements (FEV1, FVC), the frequency-domain heart-rate variability parameter or other systemic biomarkers of vascular injury. Water soluble organic carbon was associated with changes in eNO at all post-commute time-points (p \u3c 0.0001). Conclusions Our results point to measureable changes in pulmonary and autonomic biomarkers following a scripted 2-h highway commute

    Modification of Traffic-related Respiratory Response by Asthma Control in a Population of Car Commuters

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    Background: Effects of traffic-related exposures on respiratory health are well documented, but little information is available about whether asthma control influences individual susceptibility. We analyzed data from the Atlanta Commuter Exposure study to evaluate modification of associations between rush-hour commuting, in- vehicle air pollution, and selected respiratory health outcomes by asthma control status. Methods: Between 2009 and 2011, 39 adults participated in Atlanta Commuter Exposure, and each conducted two scripted rush-hour highway commutes. In-vehicle particulate components were measured during all commutes. Among adults with asthma, we evaluated asthma control by questionnaire and spirometry. Exhaled nitric oxide, forced expiratory volume in 1 second (FEV1), and other metrics of respiratory health were measured precommute and 0, 1, 2, and 3 hours postcommute. We used mixed effects linear regression to evaluate associations between commute-related exposures and postcommute changes in metrics of respiratory health by level of asthma control. Results: We observed increased exhaled nitric oxide across all levels of asthma control compared with precommute measurements, with largest postcommute increases observed among participants with below-median asthma control (2 hours postcommute: 14.6% [95% confidence interval {CI} = 5.7, 24.2]; 3 hours postcommute: 19.5% [95% CI = 7.8, 32.5]). No associations between in-vehicle pollutants and percent of predicted FEV1 were observed, although higher PM2.5 was associated with lower FEV1 % predicted among participants with below-median asthma control (3 hours postcommute: -7.2 [95% CI = -11.8, -2.7]). Conclusions: Level of asthma control may influence respiratory response to in-vehicle exposures experienced during rush-hour commuting

    Source-specific pollution exposure and associations with pulmonary response in the Atlanta Commuters Exposure Studies

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    Concentrations of traffic-related air pollutants are frequently higher within commuting vehicles than in ambient air. Pollutants found within vehicles may include those generated by tailpipe exhaust, brake wear, and road dust sources, as well as pollutants from in-cabin sources. Sourcespecific pollution, compared to total pollution, may represent regulation targets that can better protect human health. We estimated source-specific pollution exposures and corresponding pulmonary response in a panel study of commuters. We used constrained positive matrix factorization to estimate source-specific pollution factors and, subsequently, mixed effects models to estimate associations between source-specific pollution and pulmonary response. We identified four pollution factors that we named: crustal, primary tailpipe traffic, non-tailpipe traffic, and secondary. Among asthmatic subjects (N=48), interquartile range increases in crustal and secondary pollution were associated with changes in lung function of −1.33% (95% confidence interval (CI): −2.45, −0.22) and −2.19% (95% CI: −3.46, −0.92) relative to baseline, respectively. Among non-asthmatic subjects (N=51), non-tailpipe pollution was associated with pulmonary response only at 2.5 hours post-commute. We found no significant associations between pulmonary response and primary tailpipe pollution. Health effects associated with traffic-related pollution may vary by source, and therefore some traffic pollution sources may require targeted interventions to protect healt

    A State-of-the-Science Review on High-Resolution Metabolomics Application in Air Pollution Health Research: Current Progress, Analytical Challenges, and Recommendations for Future Direction

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    BACKGROUND: Understanding the mechanistic basis of air pollution toxicity is dependent on accurately characterizing both exposure and biological responses. Untargeted metabolomics, an analysis of small-molecule metabolic phenotypes, may offer improved estimation of exposures and corresponding health responses to complex environmental mixtures such as air pollution. The field remains nascent, however, with questions concerning the coherence and generalizability of findings across studies, study designs and analytical platforms. OBJECTIVES: We aimed to review the state of air pollution research from studies using untargeted high-resolution metabolomics (HRM), highlight the areas of concordance and dissimilarity in methodological approaches and reported findings, and discuss a path forward for future use of this analytical platform in air pollution research. METHODS: We conducted a state-of-the-science review to a) summarize recent research of air pollution studies using untargeted metabolomics and b) identify gaps in the peer-reviewed literature and opportunities for addressing these gaps in future designs. We screened articles published within Pubmed and Web of Science between 1 January 2005 and 31 March 2022. Two reviewers independently screened 2,065 abstracts, with discrepancies resolved by a third reviewer. RESULTS: We identified 47 articles that applied untargeted metabolomics on serum, plasma, whole blood, urine, saliva, or other biospecimens to investigate the impact of air pollution exposures on the human metabolome. Eight hundred sixteen unique features confirmed with level-1 or-2 evidence were reported to be associated with at least one or more air pollutants. Hypoxanthine, histidine, serine, aspartate, and glutamate were among the 35 metabolites consistently exhibiting associations with multiple air pollutants in at least 5 independent studies. Oxidative stress and inflammation-related pathways—including glycerophospholipid metabolism, pyrimidine metabolism, methionine and cysteine metabolism, tyrosine metabolism, and tryptophan metabolism—were the most commonly perturbed pathways reported in >70% of studies. More than 80% of the reported features were not chemically annotated, limiting the interpretability and generalizability of the findings. CONCLUSIONS: Numerous investigations have demonstrated the feasibility of using untargeted metabolomics as a platform linking exposure to internal dose and biological response. Our review of the 47 existing untargeted HRM–air pollution studies points to an underlying coherence and consistency across a range of sample analytical quantitation methods, extraction algorithms, and statistical modeling approaches. Future directions should focus on validation of these findings via hypothesis-driven protocols and technical advances in metabolic annotation and quantification. https://doi.org/10.1289/EHP11851

    Long-term exposure to PM\u3csub\u3e2.5\u3c/sub\u3e and incidence of disability in activities of daily living among oldest old

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    Currently the Chinese government has adopted World Health Organization interim target-1 values as the national ambient air quality standards values. However, the population-based evidence was insufficient, especially for the oldest old (aged 80+). We evaluated the association of fine particulate matters (PM2.5) exposure and incidence of disability in activities of daily living (ADL) in 15 453 oldest old in 886 counties/cities in China from 2002 to 2014 using Cox model with penalized splines and competing risk models to evaluate the linear or non-linear association. After adjusting for potential confounders, a J-shaped association existed between PM2.5 exposure with a threshold concentration of 33 μg/m3, and incident disability in ADL. Above this threshold, the risk magnitude significantly increased with increase of PM2.5 concentrations; compared to 33 μg/m3, the hazard ratio ranged from 1.03 (1.00–1.06) at 40 μg/m3 to 2.25 (1.54–3.29) at 110 μg/m3. The risk magnitude was not significantly changed below this threshold. Each 10 μg/m3 increase in PM2.5 exposure corresponded to a 7.7% increase in the risk of disability in ADL (hazard ratio 1.077, 95% CI 1.051–1.104). Men, smokers, and participants with cognitive impairment might be more vulnerable to PM2.5 exposure. The study provided limited population-based evidence for the oldest old and detected a threshold of 33 μg/m3, and supported that reduction to current World Health Organization interim target-1value (35 μg/m3) and Chinese national ambient air quality standards (35 μg/m3) or lower may be associated with lower risk of disability in ADL
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