Chronic traffic pollution exposure is associated with eosinophilic, but not neutrophilic inflammation in older adult asthmatics.
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ABSTRACT:
SUBMITTER: Epstein TG
PROVIDER: S-EPMC5638037 | biostudies-literature | 2013 Nov
REPOSITORIES: biostudies-literature
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Chronic traffic pollution exposure is associated with eosinophilic, but not neutrophilic inflammation in older adult asthmatics.
Epstein Tolly G TG Kesavalu Banurekha B Bernstein Cheryl K CK Ryan Patrick H PH Bernstein Jonathan A JA Zimmermann Nives N Lummus Zana Z Villareal Manuel S MS Smith Andrew M AM Lenz Peter H PH Bernstein David I DI
The Journal of asthma : official journal of the Association for the Care of Asthma 20131001 9
<h4>Objective</h4>Airway inflammatory patterns in older asthmatics are poorly understood despite high asthma-related morbidity and mortality. In this study, we sought to define the relationship between exposure to traffic pollutants, biomarkers in induced sputum, and asthma control in older adults.<h4>Methods</h4>Induced sputum was collected from 35 non-smoking adults ≥65 years with a physician's diagnosis of asthma and reversibility with a bronchodilator or a positive methacholine challenge. Pa ...[more]
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| S-EPMC7061157 | biostudies-literature
Project description:BACKGROUND: Exposure to traffic-related air pollution is a risk factor for cardiovascular events, probably involving mechanisms of inflammation and coagulation. Little is known about effects of the short exposures encountered while participating in traffic. OBJECTIVES: The objective of the study was to examine effects of exposure of commuters to air pollution on cardiovascular biomarkers. METHODS: Thirty-four healthy adult volunteers commuted for 2 hr by bus, car, or bicycle during the morning rush hour. During the commute, exposure to particle number, particulate matter (PM) ? 2.5 µm in aerodynamic diameter (PM2.5), PM ? 10 µm in diameter (PM10), and soot was measured. We estimated inhaled doses based on heart rate monitoring. Shortly before exposure and 6 hr after exposure, blood samples were taken and analyzed for CC16 (Clara cell protein 16), blood cell count, coagulation markers, and inflammation markers. Between June 2007 and June 2008, 352 pre- and postexposure blood samples were collected on 47 test days. We used mixed models to analyze the associations between exposure and changes in health parameters. RESULTS: We observed no consistent associations between the air pollution exposures and doses and the various biomarkers that we investigated. CONCLUSIONS: Air pollution exposure during commuting was not consistently associated with acute changes in inflammation markers, blood cell counts, or blood coagulation markers.
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Project description:Physical disability is common though not inevitable in older age and has direct bearing on a person's ability to perform activities essential for self-care and independent living. Air pollution appears to increase the risk of several chronic diseases that contribute to the progression of disability.We evaluated long-term exposure to traffic-related air pollution (TRAP) in relation to progression in physical disability.We conducted our investigation within the Chicago Health and Aging Project. We measured participants' exposures to TRAP using two surrogates: residential proximity to major roads (1993 onwards) and ambient concentrations of oxides of nitrogen (NOX; 1999 onwards), predicted via a geographic information systems-based spatiotemporal smoothing model (cross-validation R2 = 0.87) that incorporated community-based monitoring and resolved intraurban exposure gradients at a spatial scale of tens of meters. Participants' lower-extremity physical ability was assessed every 3 years (1993-2012) via tandem stand, chair stand, and timed walking speed.In multivariable-adjusted analyses (n = 5,708), higher long-term NOX exposure was associated with significantly faster progression in disability. Compared with the 5-year decline in physical ability score among participants in the lowest quartile of NOX exposure, decline among those in the highest exposure quartile was 1.14 units greater (95% confidence interval [CI]: -1.86, -0.42), equivalent to 3 additional years of decline among those in the lowest exposure quartile. The association was linear across the continuum of NOX exposure: per 10-ppb increment in exposure, the 5-year decline in physical ability score was 0.87 unit greater (95% CI: -1.35, -0.39). Proximity to a major road was not associated with disability progression (n = 9,994).These data join a growing body of evidence suggesting that TRAP exposures may accelerate aging-related declines in health.Weuve J, Kaufman JD, Szpiro AA, Curl C, Puett RC, Beck T, Evans DA, Mendes de Leon CF. 2016. Exposure to traffic-related air pollution in relation to progression in physical disability among older adults. Environ Health Perspect 124:1000-1008;?http://dx.doi.org/10.1289/ehp.1510089.
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Project description:BackgroundNitrogen dioxide (NO2), a ubiquitous atmospheric pollutant, may enhance the asthmatic response to allergens through eosinophilic activation in the airways. However, the effect of NO2 on inflammation without allergen exposure is poorly studied.ObjectivesWe investigated whether repeated peaks of NO2, at various realistic concentrations, induce changes in airway inflammation in asthmatics.MethodsNineteen nonsmokers with asthma were exposed at rest in a double-blind, crossover study, in randomized order, to 200 ppb NO2, 600 ppb NO2, or clean air once for 30 min on day 1 and twice for 30 min on day 2. The three series of exposures were separated by 2 weeks. The inflammatory response in sputum was measured 6 hr (day 1), 32 hr (day 2), and 48 hr (day 3) after the first exposure, and compared with baseline values measured twice 10-30 days before the first exposure.ResultsCompared with baseline measurements, the percentage of eosinophils in sputum increased by 57% after exposure to 600 ppb NO2 (p = 0.003) but did not change significantly after exposure to 200 ppb. The slope of the association between the percentage of eosinophils and NO2 exposure level was significant (p = 0.04). Eosinophil cationic protein in sputum was highly correlated with eosinophil count and increased significantly after exposure to 600 ppb NO2 (p = 0.001). Lung function, which was assessed daily, was not affected by NO2 exposure.ConclusionsWe observed that repeated peak exposures of NO2 performed without allergen exposure were associated with airway eosinophilic inflammation in asthmatics in a dose-related manner.
| S-EPMC4123022 | biostudies-literature
Project description:BackgroundMitochondria are the main source of reactive oxygen species (ROS). Human mitochondrial haplogroups are linked to differences in ROS production and oxidative-stress induced inflammation that may influence disease pathogenesis, including coronary artery disease (CAD). We previously showed that traffic-related air pollutants were associated with biomarkers of systemic inflammation in a cohort panel of subjects with CAD in the Los Angeles air basin.ObjectiveWe tested whether air pollutant exposure-associated inflammation was stronger in mitochondrial haplogroup H than U (high versus low ROS production) in this panel (38 subjects and 417 observations).MethodsInflammation biomarkers were measured weekly in each subject (? 12 weeks), including interleukin-6 (IL-6), tumor necrosis factor-? (TNF-?), C-reactive protein, interleukin-6 soluble receptor and tumor necrosis factor-soluble receptor II. We determined haplogroup by restriction fragment length polymorphism analysis. Air pollutants included nitrogen oxides (NOx), carbon monoxide (CO), organic carbon, elemental and black carbon (EC, BC); and particulate matter mass, three size fractions (<0.25 µm, 0.25-2.5 µm, and 2.5-10 µm in aerodynamic diameter). Particulate matter extracts were analyzed for organic compounds, including polycyclic aromatic hydrocarbons (PAH), and in vitro oxidative potential of aqueous extracts. Associations between exposures and biomarkers, stratified by haplogroup, were analyzed by mixed-effects models.ResultsIL-6 and TNF-? were associated with traffic-related air pollutants (BC, CO, NOx and PAH), and with mass and oxidative potential of quasi-ultrafine particles <0.25 µm. These associations were stronger for haplogroup H than haplogroup U.ConclusionsResults suggest that mitochondrial haplogroup U is a novel protective factor for air pollution-related systemic inflammation in this small group of subjects.
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Project description:BACKGROUND:Effects of air pollution on neurotoxicity and behavioral alterations have been reported. The objective of this study was to investigate the pathophysiology caused by particulate matter (PM) in the brain. We examined the effects of traffic-related particulate matter with an aerodynamic diameter of <?1 ?m (PM1), high-efficiency particulate air (HEPA)-filtered air, and clean air on the brain structure, behavioral changes, brainwaves, and bioreactivity of the brain (cortex, cerebellum, and hippocampus), olfactory bulb, and serum after 3 and 6 months of whole-body exposure in 6-month-old Sprague Dawley rats. RESULTS:The rats were exposed to 16.3?±?8.2 (4.7~?68.8) ?g/m3 of PM1 during the study period. An MRI analysis showed that whole-brain and hippocampal volumes increased with 3 and 6 months of PM1 exposure. A short-term memory deficiency occurred with 3 months of exposure to PM1 as determined by a novel object recognition (NOR) task, but there were no significant changes in motor functions. There were no changes in frequency bands or multiscale entropy of brainwaves. Exposure to 3 months of PM1 increased 8-isoporstance in the cortex, cerebellum, and hippocampus as well as hippocampal inflammation (interleukin (IL)-6), but not in the olfactory bulb. Systemic CCL11 (at 3 and 6 months) and IL-4 (at 6 months) increased after PM1 exposure. Light chain 3 (LC3) expression increased in the hippocampus after 6 months of exposure. Spongiosis and neuronal shrinkage were observed in the cortex, cerebellum, and hippocampus (neuronal shrinkage) after exposure to air pollution. Additionally, microabscesses were observed in the cortex after 6 months of PM1 exposure. CONCLUSIONS:Our study first observed cerebral edema and brain impairment in adult rats after chronic exposure to traffic-related air pollution.
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| S-EPMC8718617 | biostudies-literature
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.
| S-EPMC7461703 | biostudies-literature
Project description:BACKGROUND:Maternal exposure to traffic-related air pollution during pregnancy has been shown to increase the risk of adverse birth outcomes and neurodevelopmental disorders. By utilizing high-resolution metabolomics (HRM), we investigated perturbations of the maternal serum metabolome in response to traffic-related air pollution to identify biological mechanisms. METHODS:We retrieved stored mid-pregnancy serum samples from 160 mothers who lived in the Central Valley of California known for high air particulate levels. We estimated prenatal traffic-related air pollution exposure (carbon monoxide, nitric oxides, and particulate matter <2.5??m) during first-trimester using the California Line Source Dispersion Model, version 4 (CALINE4) based on residential addresses recorded at birth. We used liquid chromatography-high resolution mass spectrometry to obtain untargeted metabolic profiles and partial least squares discriminant analysis (PLS-DA) to select metabolic features associated with air pollution exposure. Pathway analyses were employed to identify biologic pathways related to air pollution exposure. As potential confounders we included maternal age, maternal race/ethnicity, and maternal education. RESULTS:In total we extracted 4038 and 4957 metabolic features from maternal serum samples in hydrophilic interaction (HILIC) chromatography (positive ion mode) and C18 (negative ion mode) columns, respectively. After controlling for confounding factors, PLS-DA (Variable Importance in Projection (VIP) ?2) yielded 181 and 251 metabolic features (HILIC and C18, respectively) that discriminated between the high (n?=?98) and low exposed (n?=?62). Pathway enrichment analysis for discriminatory features associated with air pollution indicated that in maternal serum oxidative stress and inflammation related pathways were altered, including linoleate, leukotriene, and prostaglandin pathways. CONCLUSION:The metabolomic features and pathways we found to be associated with air pollution exposure suggest that maternal exposure during pregnancy induces oxidative stress and inflammation pathways previously implicated in pregnancy complications and adverse outcomes.
| S-EPMC7017857 | biostudies-literature
Project description:Background: Limited evidence suggests an association between prenatal exposure to traffic pollution and greater adiposity in childhood, but the time window during which growth may be most affected is not known. Methods: We studied 1,649 children in Project Viva, a Boston-area pre-birth cohort. We used spatiotemporal models to estimate prenatal residential air pollution exposures and geographic information systems to estimate neighborhood traffic density and roadway proximity. We used weight and stature measurements at clinical and research visits to estimate a BMI trajectory for each child with mixed-effects natural cubic spline models. In primary analyses, we examined associations of residential PM2.5 and black carbon (BC) exposures during the third trimester and neighborhood traffic density and home roadway proximity at birth address with (1) estimated BMI at 6 month intervals through 10 years of age, (2) magnitude and timing of BMI peak and rebound, and (3) overall BMI trajectory. In secondary analyses, we examined associations of residential PM2.5 and BC exposures during the first and second trimesters with BMI outcomes. Results: Median (interquartile range; IQR) concentration of residential air pollution during the third trimester was 11.4 (1.7) ?g/m3 for PM2.5 and 0.7 (0.3) ?g/m3 for BC. Participants had a median (IQR) of 13 (7) clinical or research BMI measures from 0 to 10 years of age. None of the traffic pollution exposures were significantly associated with any of the BMI outcomes in covariate-adjusted models, although effect estimates were in the hypothesized direction for neighborhood traffic density and home roadway proximity. For example, greater neighborhood traffic density [median (IQR) 857 (1,452) vehicles/day x km of road within 100 m of residential address at delivery] was associated with a higher BMI throughout childhood, with the strongest associations in early childhood [e.g., per IQR increment natural log-transformed neighborhood traffic density, BMI at 12 months of age was 0.05 (-0.03, 0.13) kg/m2 higher and infancy peak BMI was 0.05 (-0.03, 0.14) kg/m2 higher]. Conclusions: We found no evidence for a persistent effect of prenatal exposure to traffic pollution on BMI trajectory from birth through mid-childhood in a population exposed to modest levels of air pollution.
| S-EPMC6330299 | biostudies-literature