Respiratory effects caused by exposure to diesel exhaust particles during moderate exercise: a murine model.

Aerobic exercise is an increasing trend worldwide. However, people are increasingly exercising outdoors, alongside roadways where heavy vehicles release diesel exhaust. We analyzed respiratory effects caused by inhaled diesel particulate emitted by vehicles adhering to Brazilian legislation, PROCONVE Phase P7 (equivalent to EURO 5), as well the effects of exposure during moderate-intensity aerobic exercise. Male C57BL/6 mice were divided into four groups for a 4-wk treadmill protocol: CE (n = 8) received intranasal sterile physiological saline and then performed moderate-intensity exercise (control), CS (n = 10) received saline and then remained stationary on the treadmill (control), DS (n = 9) received intranasal diesel exhaust particles and then remained stationary, and DE (n = 10) was exposed to diesel exhaust and then exercised at moderate intensity. Mice were subsequently connected to a mechanical ventilator (SCIREQ flexiVent, Canada) to analyze the following respiratory mechanics parameters: tissue resistance, elastance, inspiratory capacity, static compliance, Newtonian resistance, and pressure-volume loop area. After euthanasia, peripheral pulmonary tissue strips were extracted and subjected to force-length tests to evaluate parenchymal elastic and mechanical properties, using oscillations applied by a computer-controlled force transducer system; parameters obtained were tissue resistance, elastance, and hysteresivity. DS displayed impaired respiratory mechanics for all parameters, in comparison with CS. DE exhibited significantly reduced inspiratory capacity and static compliance, and increased Newtonian resistance when compared with CE. Exposure to diesel exhaust, both during exercise and rest, still exerts harmful pulmonary effects, even at current legislation limits. These results justify further changes in environmental standards, to reduce the health risks caused by traffic-related pollution.NEW & NOTEWORTHY Exercise, while beneficial, is often performed in areas of greater inhaled particulates. Here we show this effect using mice exposed to controlled diesel particle inhalation and moderate aerobic exercise. Diesel particle inhalation, without or with exercise, worsened both respiratory mechanical properties associated with changes in lung tissue mechanics and morphometry.

Biomonitoring of air quality in the Bodoquena microregion, Mato Grosso Do Sul: mutagenic and morphoanatomical alterations in Tradescantia pallida (rose) D.R. Hunt var. purpurea.

The objective of this study was to assess air quality in relation to vehicular traffic flow in cities located at different elevations in the Bodoquena microregion, state of Mato Grosso do Sul, Brazil. To do so, a micronucleus test was carried out using the TRAD-MCN bioassay on young Tradescantia buds collected from February to November 2018 in seven cities of the microregion with different traffic flow intensities. Meteorological parameters were evaluated, and vehicular traffic was counted to determine traffic flow in each city. With data from the Shuttle Radar Topography Mission (SRTM) and processing in Esri ArcGIS® software version 10.5.1, the regions was mapped based on an Elevation Model. Morphoanatomical analyses were performed according to standard methodology. Measurements were taken of thickness, length and width of tissues and structures, including the upper and lower cuticle, upper and lower epidermis, hypodermis and mesophyll. The greatest traffic flow was found in the cities of Bodoquena, Guia Lopes da Laguna, Jardim, and Porto Murtinho, with the period from 5:00 to 6:00 p.m. showing the highest traffic flow. The greatest frequency of mutagenic alterations was found in the city of Guia Lopes da Laguna, although the results did not differ significantly from Bonito, Caracol, and Jardim. Throughout the biomonitoring, the summer and autumn seasons showed the greatest micronuclei frequencies in all evaluated cities. Variations in the tissue/structure thickness was observed across cities and seasons, but with a decrease in thickness during autumn. In general, the tissues/structures were smaller for the cities of Nioaque and Porto Murtinho, while the anatomical and morphological characteristics of leaf length and thickness showed no differences among cities. We found limited correlation between micronuclei frequency and traffic flow, supporting the hypothesis that although mutagenic alterations are observed in T. pallida, in this microregion the changes are numerically lower when compared to other regions of the state. In light of the genotoxic and morphoanatomical factors assessed herein, the Bodoquena microregion appears to be well preserved in terms of air quality, presenting low micronuclei frequency and a limited reduction in tissues and leaf structures, regardless of the season.

Síntomas respiratorios en agentes civiles de tránsito expuestos a smog en Quito en el año 2021 / Respiratory symptoms in civil traffic police agents exposed to smog in Quito in 2021

INTRODUCCIÓN. Existe relación entre la exposición de contaminantes en el aire y problemas respiratorios que van desde síntomas leves en vías respiratorias altas hasta enfermedades que pueden comprometer la vida de los pacientes como: neumonía, enfermedad pulmonar obstructiva crónica y cáncer pulmonar. OBJETIVO. Registrar los síntomas respiratorios presentados por agentes civiles de tránsito expuestos a smog. MATERIALES Y MÉTODOS. Estudio analítico transversal. Población de 3 458 y muestra de 454 participantes entre agentes civiles de tránsito, fiscalizadores de tránsito y personal administrativo de la Agencia Metropolitana de Tránsito en el año 2021, seleccionados por muestreo aleatorio simple estratificado para los dos grupos de participantes; se aplicó un sondeo digital basado en las encuestas: European Community Respiratory Health Survey y condiciones de trabajo. Para el análisis de datos se utilizó la herramienta EPI INFO, donde se realizó pruebas estadísticas bivariadas de Chi2 y análisis multivariado como regresiones logísticas crudas y ajustadas. RESULTADOS. Se observó que la población de trabajadores operativos en vía tuvo alrededor de dos veces más riesgo de desarrollar sibilancias en comparación a la población administrativa OR=2,1 (IC 95% 1,01­4,39); el personal operativo tuvo más del doble de riesgo de desarrollar bronquitis crónica versus la población administrativa OR=2,5 (IC 95% 1,14­5,73). Los resultados fueron ajustados mediante regresión logística con variables de condiciones de trabajo y salud (p=<0,05). CONCLUSIÓN. Se registró una relación significativa entre la contaminación ambiental por smog y enfermedades respiratorias a largo plazo.

INTRODUCTION. There is a relationship between exposure to air pollutants and respiratory problems ranging from mild upper respiratory symptoms to life-threatening diseases such as pneumonia, chronic obstructive pulmonary disease and lung cancer is evident. OBJECTIVE. To record the respiratory symptoms presented by civilian traffic officers exposed to smog. MATERIALS AND METHODS. Cross-sectional analytical study. Population of 3 458 and sample of 454 participants among civilian traffic agents, traffic inspectors and administrative personnel of the Metropolitan Traffic Agency in the year 2021, selected by simple stratified random sampling for the two groups of participants; a digital survey was applied based on the European Community Respiratory Health Survey and working conditions. For data analysis, the EPI INFO tool was used, where bivariate Chi2 statistical tests and multivariate analysis such as crude and adjusted logistic regressions were performed. RESULTS. It was observed that the population of operational track workers had about twice the risk of developing wheezing compared to the administrative population OR=2,1 (95% CI 1,01-4,39); operational personnel had more than twice the risk of developing chronic bronchitis versus the administrative population OR=2,5 (95% CI 1,14­5,73). Results were adjusted by logist regression with working conditions and health variables (p=<0,05). CONCLUSION. There was a significant relationship between smog pollution and long-term respiratory diseases.

Palm oil biodiesel: An assessment of PAH emissions, oxidative potential and ecotoxicity of particulate matter.

This work assessed the impact of fuelling an automotive engine with palm biodiesel (pure, and two blends of 10% and 20% with diesel, B100, B10 and B20, respectively) operating under representative urban driving conditions on 17 priority polycyclic aromatic hydrocarbon (PAH) compounds, oxidative potential of ascorbic acid (OPAA), and ecotoxicity through Daphnia pulex mortality test. PM diluted with filtered fresh air (WD) gathered in a minitunel, and particulate matter (PM) collected directly from the exhaust gas stream (W/oD) were used for comparison. Results showed that PM collecting method significantly impact PAH concentration. Although all PAH appeared in both, WD and W/oD, higher concentrations were obtained in the last case. Increasing biodiesel concentration in the fuel blend decreased all PAH compounds, and those with 3 and 5 aromatic rings were the most abundant. Palm biodiesel affected both OPAA and ecotoxicity. While B10 and B20 exhibited the same rate of ascorbic acid (AA) depletion, B100 showed significant faster oxidation rate during the first four minutes and oxidized 10% more AA at the end of the test. B100 and B20 were significantly more ecotoxic than B10. The lethal concentration LC50 for B10 was 6.13 mg/L. It was concluded that palm biodiesel decreased PAH compounds, but increased the oxidative potential and ecotoxicity.

Dimethyl Fumarate Attenuates Lung Inflammation and Oxidative Stress Induced by Chronic Exposure to Diesel Exhaust Particles in Mice.

Air pollution is mainly caused by burning of fossil fuels, such as diesel, and is associated with increased morbidity and mortality due to adverse health effects induced by inflammation and oxidative stress. Dimethyl fumarate (DMF) is a fumaric acid ester and acts as an antioxidant and anti-inflammatory agent. We investigated the potential therapeutic effects of DMF on pulmonary damage caused by chronic exposure to diesel exhaust particles (DEPs). Mice were challenged with DEPs (30 µg per mice) by intranasal instillation for 60 consecutive days. After the first 30 days, the animals were treated daily with 30 mg/kg of DMF by gavage for the remainder of the experimental period. We demonstrated a reduction in total inflammatory cell number in the bronchoalveolar lavage (BAL) of mice subjected to DEP + DMF as compared to those exposed to DEPs alone. Importantly, DMF treatment was able to reduce lung injury caused by DEP exposure. Intracellular total reactive oxygen species (ROS), peroxynitrite (OONO), and nitric oxide (NO) levels were significantly lower in the DEP + DMF than in the DEP group. In addition, DMF treatment reduced the protein expression of kelch-like ECH-associated protein 1 (Keap-1) in lung lysates from DEP-exposed mice, whereas total nuclear factor κB (NF-κB) p65 expression was decreased below baseline in the DEP + DMF group compared to both the control and DEP groups. Lastly, DMF markedly reduced DEP-induced expression of nitrotyrosine, glutathione peroxidase-1/2 (Gpx-1/2), and catalase in mouse lungs. In summary, DMF treatment effectively reduced lung injury, inflammation, and oxidative and nitrosative stress induced by chronic DEP exposure. Consequently, it may lead to new therapies to diminish lung injury caused by air pollutants.

Nrf2 positively regulates autophagy antioxidant response in human bronchial epithelial cells exposed to diesel exhaust particles.

Diesel exhaust particles (DEP) are known to generate reactive oxygen species in the respiratory system, triggering cells to activate antioxidant defence mechanisms, such as Keap1-Nrf2 signalling and autophagy. The aim of this study was to investigate the relationship between the Keap1-Nrf2 signalling and autophagy pathways after DEP exposure. BEAS-2B cells were transfected with silencing RNA (siRNA) specific to Nrf2 and exposed to DEP. The relative levels of mRNA for Nrf2, NQO1, HO-1, LC3B, p62 and Atg5 were determined using RT-PCR, while the levels of LCB3, Nrf2, and p62 protein were determined using Western blotting. The autophagy inhibitor bafilomycin caused a significant decrease in the production of Nrf2, HO-1 and NQO1 compared to DEPs treatment, whereas the Nrf2 activator sulforaphane increased the LC3B (p = 0.020) levels. BEAS-2B cells exposed to DEP at a concentration of 50 µg/mL for 2 h showed a significant increase in the expression of LC3B (p = 0.001), p62 (p = 0.008), Nrf2 (p = 0.003), HO-1 (p = 0.001) and NQO1 (p = 0.015) genes compared to control. In siRNA-transfected cells, the LC3B (p < 0.001), p62 (p = 0.001) and Atg5 (p = 0.024) mRNA levels and the p62 and LC3II protein levels were decreased, indicating that Nrf2 modulated the expression of autophagy markers (R < 1). These results imply that, in bronchial cells exposed to DEP, the Nrf2 system positively regulates autophagy to maintain cellular homeostasis.

Chronic exposure to diesel particles worsened emphysema and increased M2-like phenotype macrophages in a PPE-induced model.

Chronic exposure to ambient levels of air pollution induces respiratory illness exacerbation by increasing inflammatory responses and apoptotic cells in pulmonary tissues. The ineffective phagocytosis of these apoptotic cells (efferocytosis) by macrophages has been considered an important factor in these pathological mechanisms. Depending on microenvironmental stimuli, macrophages can assume different phenotypes with different functional actions. M1 macrophages are recognized by their proinflammatory activity, whereas M2 macrophages play pivotal roles in responding to microorganisms and in efferocytosis to avoid the progression of inflammatory conditions. To verify how exposure to air pollutants interferes with macrophage polarization in emphysema development, we evaluated the different macrophage phenotypes in a PPE- induced model with the exposure to diesel exhaust particles. C57BL/6 mice received intranasal instillation of porcine pancreatic elastase (PPE) to induce emphysema, and the control groups received saline. Both groups were exposed to diesel exhaust particles or filtered air for 60 days according to the groups. We observed that both the diesel and PPE groups had an increase in alveolar enlargement, collagen and elastic fibers in the parenchyma and the number of macrophages, lymphocytes and epithelial cells in BAL, and these responses were exacerbated in animals that received PPE instillation prior to exposure to diesel exhaust particles. The same response pattern was found inCaspase-3 positive cell analysis, attesting to an increase in cell apoptosis, which is in agreement with the increase in M2 phenotype markers, measured by RT-PCR and flow cytometry analysis. We did not verify differences among the groups for the M1 phenotype. In conclusion, our results showed that both chronic exposure to diesel exhaust particles and PPE instillation induced inflammatory conditions, cell apoptosis and emphysema development, as well as an increase in M2 phenotype macrophages, and the combination of these two factors exacerbated these responses. The predominance of the M2-like phenotype likely occurred due to the increased demand for efferocytosis. However, M2 macrophage activity was ineffective, resulting in emphysema development and worsening of symptoms.

Biomarkers of exposure, effect, and susceptibility in occupational exposure to traffic-related air pollution: A review.

There is a well-recognized association between environmental air pollution exposure and several human diseases. However, the relationship between diseases related to occupational air pollution exposure on roads and high levels of traffic-related air pollutants (TRAPs) is less substantiated. Biomarkers are essential tools in environmental and occupational toxicology, and studies on new biomarkers are increasingly relevant due to the need to determine early biomarkers to be assessed in exposure conditions. This review aimed to investigate the main advances in the biomonitoring of subjects occupationally exposed to air pollution, as well as to summarize the biomarkers of exposure, effect, and susceptibility. Furthermore, we discuss how biomarkers could be used to complement the current application of methods used to assess occupational exposures to xenobiotics present in air pollution. The databases used in the preparation of this review were PubMed, Scopus, and Science Direct. Considering the significant deleterious effects on health associated with chronic occupational exposure to xenobiotics, this topic deserves attention. As it is difficult to avoid occupational exposure to TRAPs, biomonitoring should be applied as a strategy to reduce the toxic effects of workplace exposure.

Cytotoxic and genotoxic effects in mechanics occupationally exposed to diesel engine exhaust.

Diesel engine exhaust (DEE), which is the product of diesel combustion, is considered carcinogenic in humans. It comprises toxic gases, polycyclic aromatic hydrocarbons (PAHs) and particulate matter which can reach the pulmonary parenchyma and trigger various diseases, including cancer. The aim of the present study was to evaluate the potential cytotoxic and genotoxic effects of DEE exposure on peripheral blood and buccal epithelial cells in mechanics occupationally exposed to DEE. We recruited 120 exposed mechanics and 100 non-exposed control individuals. Significant differences were observed between the two groups in terms of percentage of tail DNA and damage index (DI) in the alkaline comet assay; levels of biomarkers by cytokinesis-block micronucleus cytome (CBMN-Cyt) assay; frequency of micronucleus (MN), nucleoplasmic bridge (NPB), nuclear bud (NBUD) and apoptotic cells (APOP) and levels of biomarkers for micronucleus, karyorrhexis (KRX), karyolysis (KRL) and condensed chromatin (CC) by the buccal micronucleus cytome (BM-Cyt) assay. A significant and positive correlation was found between the frequency of MN in lymphocytes and buccal cells in the exposed group. Also, there was a significant correlation between age and percentage of tail DNA and DI in the comet assay, APOP and MN in the CBMN-Cyt assay and NBUD and MN in the BM-Cyt assay. Additionally, we found a positive and significant correlation of MN frequency in lymphocytes and buccal cells and age and MN frequency in lymphocytes with the time of service (years). Regarding lifestyle-related factors, a significant correlation was observed between meat and vitamin consumption and NBUD formation on CBMN-Cyt and between meat consumption and MN formation on CBMN-Cyt. Of the BM-Cyt biomarkers, there was a correlation between alcohol consumption and NBUD formation and between binucleated cell (BN), pyknosis (PYC), CC and KRL occurrence and family cancer history. These results are the first data in Colombia on the cytotoxic and genotoxic effects induced by continuous exposure to DEE and thus showed the usefulness of biomarkers of the comet, CBMN-Cyt and BM-Cyt assays for human biomonitoring and evaluation of cancer risk in the exposed populations.

Tradescantia as a biomonitor for genotoxicity evaluation of diesel and biodiesel exhaust emissions.

Biodiesel, an alternative energy source, is promoted as cleaner and safer than other fuel options due to its reported reduction of particulate and gaseous emissions (CO2, CO, and total hydrocarbons). However, its volatile organic compounds (VOCs) and polycyclic aromatic hydrocarbon (PAHs) emissions are key to understanding its toxic, mutagenic and carcinogenic risk factors. This research was developed to assess the genotoxic impact of exhaust emissions using biodiesel from animal fat, palm oil and soybean oil blended with diesel (B80). Diluted exhaust gases were analyzed simultaneously for pollutant emissions and for toxicity using an exposure chamber called the BioToxMonitor, where Tradescantia pallida and a KU-20 clone were exposed to exhaust following Trad-MCN and Trad-SH bioassays. The results show differences in the emission compositions and considerable mutagenic potential among the three biodiesels tested, with palm oil biodiesel emissions being the least harmful, based on its low pollutant concentrations and the negative response in the TradSH bioassay. In contrast, the animal fat biodiesel and soybean oil biodiesel emissions were as toxic as the diesel emissions, being positive in both Trad bioassays. This could be related to the PAH and carbonyl concentrations found in the vehicular exhaust. The genotoxicity of diesel emissions was related to PM1 and the concentrations of both gas and particle PAHs concentrations, which were two times higher compared to the highest concentrations observed for biodiesel. The data suggest that micronucleus assays in Tradescantia pallida are more sensitive for gaseous pollutant exposure. This is the first reported study of biodiesel exhaust biomonitoring in situ and under controlled conditions inside an exposure chamber.

Vesicular acetylcholine transport deficiency potentiates some inflammatory responses induced by diesel exhaust particles.

Endogenous acetylcholine (ACh), which depends of the levels of vesicular ACh transport (VAChT) to be released, is the central mediator of the cholinergic anti-inflammatory system. ACh controls the release of cytokine in different models of inflammation. Diesel exhaust particles (DEP) are one of the major environmental pollutants produced in large quantity by automotive engines in urban center. DEP bind the lung parenchyma and induce inflammation. We evaluated whether cholinergic dysfunction worsens DEP-induced lung inflammation. Male mice with decreased ACh release due to reduced expression of VAChT (VAChT-KD mice) were submitted to DEP exposure for 30 days (3 mg/mL of DEP, once a day, five days a week) or saline. Pulmonary function and inflammation as well as extracellular matrix fiber deposition were evaluated. Additionally, airway and nasal epithelial mucus production were quantified. We found that DEP instillation worsened lung function and increased lung inflammation. Higher levels of mononuclear cells were observed in the peripheral blood of both wild-type (WT) and VAChT-KD mice. Also, both wild-type (WT) and VAChT-KD mice showed an increase in macrophages in bronchoalveolar lavage fluid (BALF) as well as increased expression of IL-4, IL-6, IL-13, TNF-α, and NF-κB in lung cells. The collagen fiber content in alveolar septa was also increased in both genotypes. On the other hand, we observed that granulocytes were increased only in VAChT-KD peripheral blood. Likewise, increased BALF lymphocytes and neutrophils as well as increased elastic fibers in alveolar septa, airway neutral mucus, and nasal epithelia acid mucus were observed only in VAChT-KD mice. The cytokines IL-4 and TNF-α were also higher in VAChT-KD mice compared with WT mice. In conclusion, decreased ability to release ACh exacerbates some of the lung alterations induced by DEP in mice, suggesting that VAChT-KD animals are more vulnerable to the effects of DEP in the lung.

Acute Exposure to Diesel-Biodiesel Particulate Matter Promotes Murine Lung Oxidative Stress by Nrf2/HO-1 and Inflammation Through the NF-kB/TNF-α Pathways.

Air pollution caused by fuel burning contributes to respiratory impairments that may lead to death. We aimed to investigate the effects of biodiesel (DB) burning in mouse lungs. DB particulate matter was collected from the exhaust pipes of a bus engine. Mice were treated with 250 µg or 1000 µg of DB particulate matter by intranasal instillation over 5 consecutive days. We demonstrated that DB particulate matter penetrated the lung in the 250-µg and 1000-µg groups. In addition, the DB particulate matter number in pulmonary parenchyma was 175-fold higher in the 250-µg group and 300-fold higher in the 1000-µg group compared to control mice. The instillation of DB particulate matter increased the macrophage number and protein levels of TNF-alpha in murine lungs. DB particulate matter enhanced ROS production in both exposed groups and the malondialdehyde levels compared to the control group. The protein expression levels of Nrf2, p-NF-kB, and HO-1 were higher in the 250-µg group and lower in the 1000-µg group than in control mice and the 250-µg group. In conclusion, DB particulate matter instillation promotes oxidative stress by activating the Nrf2/HO-1 and inflammation by p-NF-kB/TNF-alpha pathways.

[Motorized mobility, environmental impact, alternatives and future prospects: considerations for the Área Metropolitana del Valle de Aburrá]. / Movilidad motorizada, impacto ambiental, alternativas y perspectivas futuras: consideraciones para el Área Metropolitana del Valle de Aburrá.

Motorized mobility is closely linked to liquid fuels such as gasoline and diésel and therefore, to the environment. Besides the problems associated with global warming, the use of these fuels also generates polluting compounds affecting the population health. Among all primary pollutants, particulate matter (PM) less than or equal to 2.5 microns (PM25) in size, is regarded as one of the most dangerous compounds because it can penetrate the region lung gas exchange. The records for the Área Metropolitana del Valle de Aburrá (AMVA) often show that the average levels of air quality were found to be harmful to the health of metropolitan habitants. This is mainly attributed to the high concentrations of PM25 generated by heavy-duty vehicles that use diésel fuel. Although the properties of diesel fuel have a direct effect on breathable PM, there are other strategies influencing both nature and amount of emissions. For example, the improvement of the technological level of the engines and the driving pattern, as well as the incorporation of electric vehicles. This paper shows some considerations in order to propose possible strategies to solve the environmental problem of the city and the country.

La movilidad motorizada está íntimamente ligada a los combustibles líquidos como la gasolina y el diésel; y en consecuencia, con el medio ambiente. Además de la problemática con el calentamiento global, la utilización de estos combustibles genera compuestos de carácter contaminante que afecta la salud de la población. Entre todos los contaminantes criterio, el material particulado (PM) de tamaño menor o igual a 2,5 micras (PM25) es considerado como uno de los compuestos de mayor peligrosidad debido a que puede penetrar hasta la región de intercambio de gases del pulmón. Los registros para el Área Metropolitana del Valle de Aburrá (AMVA) muestran eventualmente que los niveles promedio de calidad del aire resultan ser nocivos para la salud del habitante metropolitano. Lo anterior se debe principalmente a las altas concentraciones de PM25 generadas por vehículos pesados que usan combustible diésel. Si bien las propiedades de este combustible tienen un efecto directo en el PM respirable, existen otras estrategias que influyen en las características y la cantidad de las emisiones generadas. Por ejemplo, la mejora del nivel tecnológico de los motores a partir de planes de chatarrización y renovación, y de la pauta de conducción, así como la incorporación de vehículos eléctricos. Con todo lo anterior, este trabajo muestra una serie de consideraciones a fin de plantear posibles estrategias de solución a la problemática ambiental de la ciudad y el país.

Evaluation of vehicular pollution using the TRAD-MCN mutagenic bioassay with Tradescantia pallida (Commelinaceae).

Biomonitoring is one of the tools used to assess the mutagenic potential of the atmosphere. In this study, the mutagenicity of Tradescantia pallida, a species of plant largely present in urban environments, was investigated. The objectives of this study was to estimate the mutagenic potential of vehicular flow through the TRAD-MCN bioassay in cities located at different altitudes in the southwest mesoregion of Mato Grosso do Sul, Brazil, to infer possible abiotic agents that may contribute to the effects of atmospheric pollutants, and finally to map the cities with greater risks to the health of the local population. To achieve these objectives, the Tradescantia-micronucleus test was performed on young buds of T. pallida collected between August 2015 and August 2016 in nine cities of Mato Grosso do Sul. These buds were exposed to traffic flows of various intensities. The data collected consisted of measurements of meteorological parameters and vehicular traffic counts for each city. The variables considered were: mean ambient temperature; micronuclei frequency; vehicular flow; altitude; relative humidity; pluviosity. The application of the Trad-MCN bioassay, with the consideration of environmental variables and altitudes, and the use of the Kernel interpolation technique, allowed us to map the areas with significant pollution risks to the population. The highest frequency of exposure to mutagens occurred in the cities with the highest vehicular traffic intensity. The average ambient temperature failed to show a linear association with the frequency of the micronuclei in the samples analyzed (r = 0.11ns). A positive correlation was observed between micronuclei frequency and vehicular flow, (r = 0.67; p ≤ 0.001%) and between micronuclei frequency and altitude (r = 0.24; p ≤ 0.05). A negative correlation was found between relative humidity and micronuclei frequency (r = -0.19; p ≤ 0.05%). Thus, higher micronuclei frequency tended to be present in locations with low relative humidity and high altitudes and vehicular flow.

Genotoxic effects following exposure to air pollution in street vendors from a high-traffic urban area.

Workers in several occupational environments are exposed to pollutants. Street vendors, for example, typically work in a high-traffic urban environment and are exposed to numerous air pollutants, including genotoxic substances emitted by motor vehicles. This study examined the genotoxic effects of exposure to air pollution. We conducted cytological analyses to assess frequencies of micronucleated (MN) and binucleated (BN) cells in a sample of exfoliated oral mucosa cells. We compared street vendors and control subjects in the city of Uberlândia, Minas Gerais, Brazil, and also collected quantitative information on exposure conditions of all test subjects, including concentrations of particulate matter. We found street vendors to exhibit higher frequencies of MN cells compared to the control group. We evaluated the effects of possible confounding variables on MN frequencies, namely the body mass index (BMI), age, as well as smoking and alcohol habits. Multiple linear regression analysis found no significant effects of any of those variables. Our results suggest that continued exposure to air pollution from traffic represents a major source of genotoxicity and raises concerns regarding disease prevention not only in street vendors but also other groups of people working in urban environments.

Respiratory hazard assessment of combined exposure to complete gasoline exhaust and respirable volcanic ash in a multicellular human lung model at the air-liquid interface.

Communities resident in urban areas located near active volcanoes can experience volcanic ash exposures during, and following, an eruption, in addition to sustained exposures to high concentrations of anthropogenic air pollutants (e.g., vehicle exhaust emissions). Inhalation of anthropogenic pollution is known to cause the onset of, or exacerbate, respiratory and cardiovascular diseases. It is further postulated similar exposure to volcanic ash can also affect such disease states. Understanding of the impact of combined exposure of volcanic ash and anthropogenic pollution to human health, however, remains limited. The aim of this study was to assess the biological impact of combined exposure to respirable volcanic ash (from Soufrière Hills volcano (SHV), Montserrat and Chaitén volcano (ChV), Chile; representing different magmatic compositions and eruption styles) and freshly-generated complete exhaust from a gasoline vehicle. A multicellular human lung model (an epithelial cell-layer composed of A549 alveolar type II-like cells complemented with human blood monocyte-derived macrophages and dendritic cells cultured at the air-liquid interface) was exposed to diluted exhaust (1:10) continuously for 6 h, followed by immediate exposure to the ash as a dry powder (0.54 ±â€¯0.19 µg/cm2 and 0.39 ±â€¯0.09 µg/cm2 for SHV and ChV ash, respectively). After an 18 h incubation, cells were exposed again for 6 h to diluted exhaust, and a final 18 h incubation (at 37 °C and 5% CO2). Cell cultures were then assessed for cytotoxic, oxidative stress and (pro-)inflammatory responses. Results indicate that, at all tested (sub-lethal) concentrations, co-exposures with both ash samples induced no significant expression of genes associated with oxidative stress (HMOX1, NQO1) or production of (pro-)inflammatory markers (IL-1ß, IL-8, TNF-α) at the gene and protein levels. In summary, considering the employed experimental conditions, combined exposure of volcanic ash and gasoline vehicle exhaust has a limited short-term biological impact to an advanced lung cell in vitro model.

Effects of organic and inorganic compounds of diesel exhaust particles on the mucociliary epithelium: An experimental study on the frog palate preparation.

The toxic actions of acute exposition to different diesel exhaust particles (DEPA) fractions on the mucociliary epithelium are not yet fully understood due to different concentrations of organic and inorganic elements. These chemicals elements produce damage to the respiratory epithelium and exacerbate pre-existent diseases. In our study we showed these differences in two experimental studies. Study I (dose-response curve - DRCS): Forty frog-palates were exposed to the following dilutions: frog ringer, intact DEPA diluted in frog-ringer at 3mg/L, 6mg/L and 12mg/L. Study II (DEPF) (DEPA fractions diluted at 12mg/L): Fifty palates - Frog ringer, intact DEPA, DEPA treated with hexane, nitric acid and methanol. Variables analyzed: relative time of mucociliary transport (MCT), ciliary beating frequency (CBF) and morphometric analysis for mucin profile (neutral/acid) and vacuolization. The Results of DRCS: Group DEPA-12mg/L presented a significant increase in the MCT (p<0.05), proportional volume of acid mucus (p<0.05) and decreased proportional volume of neutral mucus and vacuoles (p<0.05). In relation of DEPF: A significant increase in the MCT associated to a decrease in the proportional volume of neutral mucus was founded in nitric acid group. In addition, a significant increase in the proportional volume of acid mucus was found in methanol group. We concluded that: 1) Increasing concentrations of intact DEPA can progressively increase MCT and promote an acidification of intra-epithelial mucins associated to a depletion of neutral mucus. 2) Intact DEPA seem to act as secretagogue substance, promoting mucus extrusion and consequently reducing epithelial thickness. 3) Organic fraction of low polarity seems to play a pivotal role on the acute toxicity to the mucociliary epithelium, by promoting a significant increase in the MCT associated to changes in the chemical profile of the intracellular mucins.

Exposure to Mixtures of Pollutants in Mexican Children from Marginalized Urban Areas.

BACKGROUND: Exposure to contaminant mixtures in developing countries is an important public health issue. Children are identified as the most susceptible group to adverse health effects due to the exposure. OBJECTIVE: The aim of this study was to conduct a screening for mixture pollutants in Mexican children in urban marginalized communities. METHODS: We analyzed children (aged 6-12 years old) who resided in four urban marginalized communities in San Luis Potosi, Mexico: i) Bellas Lomas (BEL), a site with vehicular traffic; ii) Tercera Chica (TC), a site with brick kilns; Iii) Rincon de San Jose (SJR), a site with a hazardous waste landfill; and (iv) Morales (MOR) a metallurgical zone with copper-arsenic and electrolytic zinc smelters. Polycyclic Aromatic Hydrocarbons (1-hydroxypyrene (1-OHP)), benzene (trans, trans-muconic acid (t,t-MA), manganese, arsenic and fluoride were quantified in urine and lead in blood samples. FINDINGS: Our results indicate that median exposures to manganese were 4.4, 5.2, 5.8 and 6.3 µg/L for BEL, TC, SJR and MOR, respectively. For BEL, fluoride was present at a higher concentration with 2.3 mg/L followed by MOR, TC and SJR with 1.7, 1.5 and 1.2 mg/L respectively. The highest concentrations of arsenic that were found were 11 µg/L in MOR and lead concentration was reported between 4.2 and 6.8 µg/dL, in BEL, TC and MOR. 1-OHP and t,t-MA were higher in TC (0.23 µmol/mol creatinine (cr), 429.7 µg/g cr, respectively) followed by SJR (0.09 µmol/mol cr, 427.4 µg/g cr), MOR (0.03 µmol/mol cr, 258.6 µg/g cr) and BEL (0.06 µmol/mol cr, 220.6 µg/g cr). CONCLUSION: Considering the large number of people, especially children, exposed to multiple pollutants, it is important to design effective intervention programs that reduce exposure and the resultant risk in the numerous urban marginalized communities in Mexico.

Combustion-derived nanoparticles, the neuroenteric system, cervical vagus, hyperphosphorylated alpha synuclein and tau in young Mexico City residents.

Mexico City (MC) young residents are exposed to high levels of fine particulate matter (PM2.5), have high frontal concentrations of combustion-derived nanoparticles (CDNPs), accumulation of hyperphosphorylated aggregated α-synuclein (α-Syn) and early Parkinson's disease (PD). Swallowed CDNPs have easy access to epithelium and submucosa, damaging gastrointestinal (GI) barrier integrity and accessing the enteric nervous system (ENS). This study is focused on the ENS, vagus nerves and GI barrier in young MC v clean air controls. Electron microscopy of epithelial, endothelial and neural cells and immunoreactivity of stomach and vagus to phosphorylated ɑ-synuclein Ser129 and Hyperphosphorylated-Tau (Htau) were evaluated and CDNPs measured in ENS. CDNPs were abundant in erythrocytes, unmyelinated submucosal, perivascular and intramuscular nerve fibers, ganglionic neurons and vagus nerves and associated with organelle pathology. ɑSyn and Htau were present in 25/27 MC gastric,15/26 vagus and 18/27 gastric and 2/26 vagus samples respectively. We strongly suggest CDNPs are penetrating and damaging the GI barrier and reaching preganglionic parasympathetic fibers and the vagus nerve. This work highlights the potential role of CDNPs in the neuroenteric hyperphosphorylated ɑ-Syn and tau pathology as seen in Parkinson and Alzheimer's diseases. Highly oxidative, ubiquitous CDNPs constitute a biologically plausible path into Parkinson's and Alzheimer's pathogenesis.