Traffic-related air pollutants (TRAP-PM) promote neuronal amyloidogenesis through oxidative damage to lipid rafts.
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ABSTRACT:
SUBMITTER: Cacciottolo M
PROVIDER: S-EPMC7075030 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Motor vehicle traffic is an important source of particulate pollution in cities of the developing world, where rapid growth, coupled with a lack of effective transport and land use planning, may result in harmful levels of fine particles (PM(2.5)) in the air. However, a lack of air monitoring data hinders health impact assessments and the development of transportation and land use policies that could reduce health burdens due to outdoor air pollution. To address this important need, a study of traffic-related PM(2.5) was carried out in the city of Nairobi, Kenya, a model city for sub-Saharan Africa, in July 2009. Sampling was carried out using portable filter-based air samplers carried in backpacks by technicians on weekdays over two weeks at several sites in and around Nairobi ranging from high-traffic roadways to rural background. Mean daytime concentrations of PM(2.5) ranged from 10.7 at the rural background site to 98.1 ?g/m(3) on a sidewalk in the central business district. Horizontal dispersion measurements demonstrated a decrease in PM(2.5) concentration from 128.7 to 18.7 ?g/m(3) over 100 meters downwind of a major intersection in Nairobi. A vertical dispersion experiment revealed a decrease from 119.5 ?g/m(3) at street level to 42.8 ?g/m(3) on a third-floor rooftop in the central business district. Though not directly comparable to air quality guidelines, which are based on 24-hour or annual averages, the urban concentrations we observed raise concern with regard to public health and related policy. Taken together with survey data on commuting patterns within Nairobi, these results suggest that many Nairobi residents are exposed on a regular basis to elevated concentrations of fine particle air pollution, with potentially serious long-term implications for health.
| S-EPMC3138055 | biostudies-literature
Project description:Traffic-related air pollution (TRAP) is increasing worldwide. Habitual physical activity is known to prevent cardiorespiratory diseases and mortality, but whether exposure to TRAP during exercise affects respiratory health is still uncertain. Exercise causes inflammatory changes in the airways, and its interaction with the effects of TRAP or ozone might be detrimental, for both athletes exercising outdoor and urban active commuters. In this Mini-Review, we summarize the literature on the effects of exposure to TRAP and/or ozone during exercise on lung function, respiratory symptoms, performance, and biomarkers. Ozone negatively affected pulmonary function after exercise, especially after combined exposure to ozone and diesel exhaust (DE). Spirometric changes after exercise during exposure to particulate matter and ultrafine particles suggest a decrease in lung function, especially in patients with chronic obstructive pulmonary disease. Ozone frequently caused respiratory symptoms during exercise. Women showed decreased exercise performance and higher symptom prevalence than men during TRAP exposure. However, performance was analyzed in few studies. To date, research has not identified reliable biomarkers of TRAP-related lung damage useful for monitoring athletes' health, except in scarce studies on airway cells obtained by induced sputum or bronchoalveolar lavage. In conclusion, despite partly counteracted by the positive effects of habitual exercise, the negative effects of TRAP exposure to pollutants during exercise are hard to assess: outdoor exercise is a complex model, for multiple and variable exposures to air pollutants and pollutant concentrations. Further studies are needed to identify pollutant and/or time thresholds for performing safe outdoor exercise in cities.
| S-EPMC7793908 | biostudies-literature
Project description:BackgroundTraffic-related air pollution (TRAP) is one of the major sources of exposure in urban areas and has been associated with a wide range of adverse human health effects. Much of the Canadian population is regularly exposed to TRAP as a result of daily activities (e.g., commuting) and a significant portion of the population resides in close proximity to major roadways. The objective of this scoping review is to develop an evidence map of the epidemiological literature of the human health effects of exposure to TRAP, to support future reviews and assessments by Health Canada.MethodsLiterature searches will be conducted in Ovid EMBASE and Ovid MEDLINE database. DistillerSR will be used to manage the review process. Two reviewers will independently screen the studies in a two-part process (title and abstract; full text) for eligibility. Epidemiological studies and reviews will be included if they report on the human health effects of exposure to TRAP. Data collection will include study design parameters and human health outcomes evaluated in the study. A descriptive analysis will be used to provide a high-level summary of the number of studies evaluating the different types of health effects and cross-tabulations by study design parameters.DiscussionThe scoping review will be used to identify subject areas for more detailed review and evaluation of the human health effects of TRAP by the Air Health Effects Assessment Division of Health Canada.
| S-EPMC6714303 | biostudies-literature
Project description:Exposure to traffic-related air pollutants (TRAP) remains a key public health issue, and improved exposure measures are needed to support health impact and epidemiologic studies and inform regulatory responses. The recently developed Research LINE source model (RLINE), a Gaussian line source dispersion model, has been used in several epidemiologic studies of TRAP exposure, but evaluations of RLINE's performance in such applications have been limited. This study provides an operational evaluation of RLINE in which predictions of NOx, CO and PM2.5 are compared to observations at air quality monitoring stations located near high traffic roads in Detroit, MI. For CO and NOx, model performance was best at sites close to major roads, during downwind conditions, during weekdays, and during certain seasons. For PM2.5, the ability to discern local and particularly the traffic-related portion was limited, a result of high background levels, the sparseness of the monitoring network, and large uncertainties for certain processes (e.g., formation of secondary aerosols) and non-mobile sources (e.g., area, fugitive). Overall, RLINE's performance in near-road environments suggests its usefulness for estimating spatially- and temporally-resolved exposures. The study highlights considerations relevant to health impact and epidemiologic applications, including the importance of selecting appropriate pollutants, using appropriate monitoring approaches, considering prevailing wind directions during study design, and accounting for uncertainty.
| S-EPMC8064696 | biostudies-literature
Project description:Exposure to particulate matter (PM) in the ambient air and its interactions with APOE alleles may contribute to the acceleration of brain aging and the pathogenesis of Alzheimer's disease (AD). Neurodegenerative effects of particulate air pollutants were examined in a US-wide cohort of older women from the Women's Health Initiative Memory Study (WHIMS) and in experimental mouse models. Residing in places with fine PM exceeding EPA standards increased the risks for global cognitive decline and all-cause dementia respectively by 81 and 92%, with stronger adverse effects in APOE ?4/4 carriers. Female EFAD transgenic mice (5xFAD+/-/human APOE ?3 or ?4+/+) with 225?h exposure to urban nanosized PM (nPM) over 15 weeks showed increased cerebral ?-amyloid by thioflavin S for fibrillary amyloid and by immunocytochemistry for A? deposits, both exacerbated by APOE ?4. Moreover, nPM exposure increased A? oligomers, caused selective atrophy of hippocampal CA1 neurites, and decreased the glutamate GluR1 subunit. Wildtype C57BL/6 female mice also showed nPM-induced CA1 atrophy and GluR1 decrease. In vitro nPM exposure of neuroblastoma cells (N2a-APP/swe) increased the pro-amyloidogenic processing of the amyloid precursor protein (APP). We suggest that airborne PM exposure promotes pathological brain aging in older women, with potentially a greater impact in ?4 carriers. The underlying mechanisms may involve increased cerebral A? production and selective changes in hippocampal CA1 neurons and glutamate receptor subunits.
| S-EPMC5299391 | biostudies-literature
Project description:Numerous studies have established that acute or chronic exposure to environmental pollutants like particulate matter (PM) leads to the development of accelerated aging related pathologies including pulmonary and cardiovascular diseases, and thus air pollution is one of the major global threats to human health. Air pollutant particulate matter 2.5 (PM2.5)-induced cellular dysfunction impairs tissue homeostasis and causes vascular and cardiopulmonary damage. To test a hypothesis that elevated plasminogen activator inhibitor-1 (PAI-1) levels play a pivotal role in air pollutant-induced cardiopulmonary pathologies, we examined the efficacy of a drug-like novel inhibitor of PAI-1, TM5614, in treating PM2.5-induced vascular and cardiopulmonary pathologies. Results from biochemical, histological, and immunohistochemical studies revealed that PM2.5 increases the circulating levels of PAI-1 and thrombin and that TM5614 treatment completely abrogates these effects in plasma. PM2.5 significantly augments the levels of pro-inflammatory cytokine interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF), and this also can be reversed by TM5614, indicating its efficacy in amelioration of PM2.5-induced increases in inflammatory and pro-thrombotic factors. TM5614 reduces PM2.5-induced increased levels of inflammatory markers cluster of differentiation 107 b (Mac3) and phospho-signal transducer and activator of transcription-3 (pSTAT3), adhesion molecule vascular cell adhesion molecule 1 (VCAM1), and apoptotic marker cleaved caspase 3. Longer exposure to PM2.5 induces pulmonary and cardiac thrombosis, but TM5614 significantly ameliorates PM2.5-induced vascular thrombosis. TM5614 also reduces PM2.5-induced increased blood pressure and heart weight. In vitro cell culture studies revealed that PM2.5 induces the levels of PAI-1, type I collagen, fibronectin (Millipore), and sterol regulatory element binding protein-1 and 2 (SREBP-1 and SREBP-2), transcription factors that mediate profibrogenic signaling, in cardiac fibroblasts. TM5614 abrogated that stimulation, indicating that it may block PM2.5-induced PAI-1 and profibrogenic signaling through suppression of SREBP-1 and 2. Furthermore, TM5614 blocked PM2.5-mediated suppression of nuclear factor erythroid related factor 2 (Nrf2), a major antioxidant regulator, in cardiac fibroblasts. Pharmacological inhibition of PAI-1 with TM5614 is a promising therapeutic approach to control air pollutant PM2.5-induced cardiopulmonary and vascular pathologies.
| S-EPMC8434953 | biostudies-literature
Project description:Vehicles are major sources of air pollutant emissions, and individuals living near large roads endure high exposures and health risks associated with traffic-related air pollutants. Air pollution epidemiology, health risk, environmental justice, and transportation planning studies would all benefit from an improved understanding of the key information and metrics needed to assess exposures, as well as the strengths and limitations of alternate exposure metrics. This study develops and evaluates several metrics for characterizing exposure to traffic-related air pollutants for the 218 residential locations of participants in the NEXUS epidemiology study conducted in Detroit (MI, USA). Exposure metrics included proximity to major roads, traffic volume, vehicle mix, traffic density, vehicle exhaust emissions density, and pollutant concentrations predicted by dispersion models. Results presented for each metric include comparisons of exposure distributions, spatial variability, intraclass correlation, concordance and discordance rates, and overall strengths and limitations. While showing some agreement, the simple categorical and proximity classifications (e.g., high diesel/low diesel traffic roads and distance from major roads) do not reflect the range and overlap of exposures seen in the other metrics. Information provided by the traffic density metric, defined as the number of kilometers traveled (VKT) per day within a 300 m buffer around each home, was reasonably consistent with the more sophisticated metrics. Dispersion modeling provided spatially- and temporally-resolved concentrations, along with apportionments that separated concentrations due to traffic emissions and other sources. While several of the exposure metrics showed broad agreement, including traffic density, emissions density and modeled concentrations, these alternatives still produced exposure classifications that differed for a substantial fraction of study participants, e.g., from 20% to 50% of homes, depending on the metric, would be incorrectly classified into "low", "medium" or "high" traffic exposure classes. These and other results suggest the potential for exposure misclassification and the need for refined and validated exposure metrics. While data and computational demands for dispersion modeling of traffic emissions are non-trivial concerns, once established, dispersion modeling systems can provide exposure information for both on- and near-road environments that would benefit future traffic-related assessments.
| S-EPMC4199035 | biostudies-literature
Project description:Exposures to ambient diesel exhaust particles have been associated with respiratory symptoms and asthma exacerbations in children; however, epidemiologic evidence linking short-term exposure to ambient diesel exhaust particles with airway inflammation is limited. We conducted a panel study with asthmatic and nonasthmatic adolescents to characterize associations between ambient diesel exhaust particle exposures and exhaled biological markers of airway inflammation and oxidative stress. Over four weeks, exhaled breath condensate was collected twice a week from 18 asthmatics and 18 nonasthmatics (ages 14-19 years) attending two New York City schools and analyzed for pH and 8-isoprostane as indicators of airway inflammation and oxidative stress, respectively. Air concentrations of black carbon, a diesel exhaust particle indicator, were measured outside schools. Air measurements of nitrogen dioxide, ozone, and fine particulate matter were obtained for the closest central monitoring sites. Relationships between ambient pollutants and exhaled biomarkers were characterized using mixed effects models. Among all subjects, increases in 1- to 5-day averages of black carbon were associated with decreases in exhaled breath condensate pH, indicating increased airway inflammation, and increases in 8-isoprostane, indicating increased oxidative stress. Increases in 1- to 5-day averages of nitrogen dioxide were associated with increases in 8-isoprostane. Ozone and fine particulate matter were inconsistently associated with exhaled biomarkers. Associations did not differ between asthmatics and nonasthmatics. The findings indicate that short-term exposure to traffic-related air pollutants may increase airway inflammation and/or oxidative stress in urban youth and provide mechanistic support for associations documented between traffic-related pollutant exposures and respiratory morbidity.
| S-EPMC3577992 | biostudies-literature
Project description:Human exposure to air pollution in many studies is represented by ambient concentrations from space-time kriging of observed values. Space-time kriging techniques based on a limited number of ambient monitors may fail to capture the concentration from local sources. Further, because people spend more time indoors, using ambient concentration to represent exposure may cause error. To quantify the associated exposure error, we computed a series of six different hourly-based exposure metrics at 16,095 Census blocks of three Counties in North Carolina for CO, NO(x), PM(2.5), and elemental carbon (EC) during 2012. These metrics include ambient background concentration from space-time ordinary kriging (STOK), ambient on-road concentration from the Research LINE source dispersion model (R-LINE), a hybrid concentration combining STOK and R-LINE, and their associated indoor concentrations from an indoor infiltration mass balance model. Using a hybrid-based indoor concentration as the standard, the comparison showed that outdoor STOK metrics yielded large error at both population (67% to 93%) and individual level (average bias between -10% to 95%). For pollutants with significant contribution from on-road emission (EC and NO(x)), the on-road based indoor metric performs the best at the population level (error less than 52%). At the individual level, however, the STOK-based indoor concentration performs the best (average bias below 30%). For PM(2.5), due to the relatively low contribution from on-road emission (7%), STOK-based indoor metric performs the best at both population (error below 40%) and individual level (error below 25%). The results of the study will help future epidemiology studies to select appropriate exposure metric and reduce potential bias in exposure characterization.
| S-EPMC4690943 | biostudies-literature
Project description:BackgroundPrevious studies have shown inconsistent results regarding the impact of traffic pollution on the prevalence of chronic obstructive pulmonary disease (COPD). Therefore, using frequency matching and propensity scores, we explored the association between traffic pollution and COPD in a cohort of 8284 residents in a major agricultural county in Taiwan.MethodsAll subjects completed a structured questionnaire interview and health checkups. Subjects with COPD were identified using Taiwan National Health Insurance Research Databases. A hybrid kriging/LUR model was used to identify levels of traffic-related air pollutants (PM2.5 and O3). Multiple logistic regression models were used to calculate the prevalence ratios (PRs) of COPD and evaluate the role played by traffic-related indices between air pollutants and COPD. The distributed lag nonlinear model was applied in the analysis; we excluded current or ever smokers to perform the sensitivity analysis.ResultsIncreased PRs of COPD per SD increment of PM2.5 were 1.10 (95% CI 1.05-1.15) and 1.25 (95% CI 1.13-1.40) in the population with age and sex matching as well as propensity-score matching, respectively. The results of the sensitivity analysis were similar between the single and two pollutant models. PM2.5 concentrations were significantly associated with traffic flow including sedans, buses, and trucks (p < 0.01). The higher road area and the higher PM2.5 concentrations near the subject's residence correlated with a greater risk of developing COPD (p for interaction < 0.01).ConclusionsOur results suggest that long-term exposure to traffic-related air pollution may be positively associated with the prevalence of COPD.
| S-EPMC8336021 | biostudies-literature