Assessment of genotoxicity biomarkers in gasoline station attendants due to occupational exposure.

Gasoline station attendants are exposed to numerous chemicals that might have genotoxic and carcinogenic potential, such as benzene in fuel vapor and particulate matter and polycyclic aromatic hydrocarbons in vehicle exhaust emission. According to IARC, benzene and diesel particulates are Group 1 human carcinogens, and gasoline has been classified as Group 2A "possibly carcinogenic to humans." At gas stations, self-service is not implemented in Turkey; fuel-filling service is provided entirely by employees, and therefore they are exposed to those chemicals in the workplace during all working hours. Genetic monitoring of workers with occupational exposure to possible genotoxic agents allows early detection of cancer. We aimed to investigate the genotoxic damage due to exposures in gasoline station attendants in Turkey. Genotoxicity was evaluated by the Comet, chromosomal aberration, and cytokinesis-block micronucleus assays in peripheral blood lymphocytes. Gasoline station attendants (n = 53) had higher tail length, tail intensity, and tail moment values than controls (n = 61). In gasoline station attendants (n = 46), the frequencies of chromatid gaps, chromosome gaps, and total aberrations were higher compared with controls (n = 59). Increased frequencies of micronuclei and nucleoplasmic bridges were determined in gasoline station attendants (n = 47) compared with controls (n = 40). Factors such as age, duration of working, and smoking did not have any significant impact on genotoxic endpoints. Only exposure increased genotoxic damage in gasoline station attendants independently from demographic and clinical characteristics. Occupational exposure-related genotoxicity risk may increase in gasoline station attendants who are chronically exposed to gasoline and various chemicals in vehicle exhaust emissions.

A yearlong monitoring campaign of polycyclic aromatic compounds and other air pollutants at three sites in Sweden: Source identification, in vitro toxicity and human health risk assessment.

Air pollution is a complex mixture of gases and particulate matter (PM) with local and non-local emission sources, resulting in spatiotemporal variability in concentrations and composition, and thus associated health risks. To study this in the greater Stockholm area, a yearlong monitoring campaign with in situ measurements of PM10, PM1, black carbon, NOx, O3, and PM10-sampling was performed. The locations included an Urban and a Rural background site and a Highway site. Chemical analysis of PM10 was performed to quantify monthly levels of polycyclic aromatic compounds (PACs), which together with other air pollution data were used for source apportionment and health risk assessment. Organic extracts from PM10 were tested for oxidative potential in human bronchial epithelial cells. Strong seasonal patterns were found for most air pollutants including PACs, with higher levels during the winter months than summer e.g., highest levels of PM10 were detected in March at the Highway site (33.2 µg/m3) and lowest in May at the Rural site (3.6 µg/m3). In general, air pollutant levels at the sites were in the order Highway > Urban > Rural. Multivariate analysis identified several polar PACs, including 6H-Benzo[cd]pyren-6-one, as possible discriminatory markers for these sites. The main sources of particulate pollution for all sites were vehicle exhaust and biomass burning emissions, although diesel exhaust was an important source at the Highway site. In vitro results agreed with air pollutant levels, with higher oxidative potential from the winter samples. Estimated lung cancer cases were in the order PM10 > NO2 > PACs for all sites, and with less evident seasonal differences than in vitro results. In conclusion, our study presents novel seasonal data for many PACs together with air pollutants more traditionally included in air quality monitoring. Moreover, seasonal differences in air pollutant levels correlated with differences in toxicity in vitro.

Assessment of the Actual Toxicity of Engine Exhaust Gas Emissions from Euro 3 and Euro 6 Compliant Vehicles with the BAT-CELL Method Using In Vitro Tests.

Legal restrictions on vehicle engine exhaust gas emission control do not always go hand in hand with an actual reduction in the emissions of toxins into the atmosphere. Moreover, the methods currently used to measure exhaust gas emissions do not give unambiguous results on the impact of the tested gases on living organisms. The method used to assess the actual toxicity of gases, BAT-CELL Bio-Ambient-Tests using in vitro tests, takes into account synergistic interactions of individual components of a mixture of gases without the need to know its qualitative and quantitative composition and allows for determination of the actual toxicity of the gas composition. Using the BAT-CELL method, exhaust gases from passenger vehicles equipped with spark-ignition engines complying with the Euro 3 and Euro 6 emission standards were tested. The results of toxicological tests were correlated with the results of chromatographic analysis. It was shown that diverse qualitative composition of the mixture of hydrocarbons determining the exhaust gases toxicity may decrease the percentage value of cell survival. Additionally, it was proven that the average survival of cells after exposure to exhaust gases from tested vehicles meeting the more restrictive Euro 6 standard was lower than for vehicles meeting the Euro 3 standard thus indicating the higher toxicity of exhaust gases from newer vehicles.

Biological toxicity risk assessment of two potential neutral carbon diesel fuel substitutes.

We investigated the biological response of soluble organic fraction (SOF) and water-soluble fraction (WSF) extracted from particulate matter (PM) emitted by an automotive diesel engine operating in a representative urban driving condition. The engine was fueled with ultra-low sulfur diesel (ULSD), and its binary blends by volume with 13% of butanol (Bu13), and with hydrotreated vegetable oil (HVO) at 13% (HVO13) and 20% (HVO20). Cytotoxicity, genotoxicity, oxidative DNA damage and ecotoxicity tests were carried out, and 16 polycyclic aromatic hydrocarbons (PAH) expressed as tbenzo(a)pyrene total toxicity equivalent (BaP-TEQ) were also analyzed. The Hepatocarcinoma epithelial cell line (HepG2) was exposed to SOF for 24 h and analyzed using comet assay, with the inclusion of formamidopyrimidine DNA glycosylase (FPG) and endonuclease III (Endo III) to recognize oxidized DNA bases. The WSF was evaluated through acute ecotoxicity tests with the aquatic microcrustacean Daphnia pulex (D. Pulex). Results showed that there was no cytotoxic activity for all tested SOF concentrations. Genotoxic responses by all the SOF samples were at same level, except for the HVO13 which was weaker in the absence of the enzymes. The addition of the FPG and Endo III enzymes resulted in a significant increase in the comet tail, indicating that the DNA damage from SOF for all tested fuel blends involves oxidative damage including a higher level of oxidized purines for ULSD and Bu13 in comparison with HVO blends, but the oxidized pyrimidines for HVO blends were slightly higher compared to Bu13. The WSF did not show acute ecotoxicity for any of the fuels. Unlike other samples, Bu13-derived particles significantly increase the BaP-TEQ. The contribution to the genotoxic activity and oxidative DNA from SOF was not correlated to BaP-TEQ, which means that the biological activity of PM might be affected also by other toxic compounds present in particulate phase.

Mechanistic toxicity assessment of fine particulate matter emitted from fuel combustion via pathway-based approaches in human cells.

Fuel exhaust particulate matter (FEPM) is an important source of air pollution worldwide. However, the comparative and mechanistic toxicity of FEPMs emitted from combustion of different fuels is still not fully understood. This study employed pathway-based approaches via human cells to evaluate mechanistic toxicity of FEPMs. The results showed that FEPMs caused concentration-dependent (0.1-200 µg/mL) cytotoxicity and oxidative stress. FEPMs at low concentration (10 µg/mL) induced cell cycle arrest in S and G2 phases, while high level of FEPMs (200 µg/mL) caused cell cycle arrest in G1 phase. Different FEPMs induced distinct expression profiles of toxicity-related genes, illustrating different toxic mechanisms. Furthermore, FEPMs inhibited the phosphorylation of protein kinase A (PKA), which related with reproductive toxicity. Spearman rank correlations among the chemicals carried by FEPMs and the toxic effects revealed that PAHs and metals promoted cell cycle arrest in the G1 phase and suppressed PKA activity. Furthermore, PAHs (Nap and Acy) and metals (Al and Pb) in FEPMs were highly and positively correlated with the expression of genes involved in apoptosis, ER stress, metal stress and inflammation. Our findings offered more mechanistic information of FEPMs at the level of subcellular toxicity and help to better understand their potential health effects.

Potentially toxic elements and polycyclic aromatic hydrocarbons in street dust of Yazd, a central capital city in Iran: contamination level, source identification, and ecological-health risk assessment.

Contamination level, source, and ecological-health risk of potentially toxic elements (PTEs) and polycyclic aromatic hydrocarbons (PAHs) in the street dust of Yazd, a central capital city in Iran, were investigated for the first time regarding samples collected from 21 sites. Geochemical indices pointed out an enrichment trend of [Formula: see text] and an ecological risk trend of [Formula: see text]. The ecological risk indices of PAHs reflected high ecological risk for pyrene (Pyr). The statistical approach along with the isomeric ratios of PAHs suggested that the traffic-related sources, such as wearing of tires and brake pads, and the vehicular exhaust emissions were greatly responsible for the elevated concentrations of Pb, Cu, Sb, and PAHs, while Al, Ni, Co, V, Mn, As, and, to a lesser extent, Fe, Zn, Mo, and Cr were mainly influenced by geogenic sources. The human health risk assessment of PTEs and PAHs reflected that As, Cr, and Pb pose the highest non-carcinogenic risk in adults and children, compared with other PTEs and also PAHs. The carcinogenic health risk of Pb in the children and PAHs in both subpopulations was high for cancer development.

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.

Health and economic consequences of applying the United States' PM2.5 automobile emission standards to other nations: a case study of France and Italy.

OBJECTIVES: The US has among the world's strictest automobile emission standards, but it is now loosening them. It is unclear where a nation should draw the line between the associated cost burden imposed by regulations and the broader societal benefits associated with having cleaner air. Our study examines the health benefits and cost-effectiveness of introducing stricter vehicle emission standards in France and Italy. STUDY DESIGN: Quasi-experimental study. METHODS: We used cost-effectiveness modeling to measure the incremental quality-adjusted life years (QALYs) and cost (Euros) of adopting more stringent US vehicle emission standards for PM2.5 in France and Italy. RESULTS: Adopting Obama era US vehicle emission standards would likely save money and lives for both the French and Italian populations. In France, adopting US emission standards would save €1000 and increase QALYs by 0.04 per capita. In Italy, the stricter standards would save €3000 and increase QALYs by 0.31. The results remain robust in both the sensitivity analysis and probabilistic Monte Carlo simulation model. CONCLUSIONS: Adopting more stringent emission standards in France and Italy would save money and lives.

Direct assessment of health impacts on hospital admission from traffic intensity in Madrid.

In this paper we establish the attributable risk on respiratory and cardiovascular disorders related to traffic intensity in Madrid. In contrast to previous related studies, the proposed approach directly associates road traffic counts to patient emergency admission rates instead of using primary air pollutants. By applying Shapley values over gradient boosting machines, a first selection step is performed among all traffic observation points based on their influence on patient emergency admissions at Gregorio Marañon hospital. A subsequent quantification of the relative risk associated to traffic intensity of the selected point is calculated via ARIMA and log-linear Poisson regression models. The results obtained show that 13% of respiratory cases are related to traffic intensity while, in the case of cardiovascular disorders, the percentage increases to 39%.

Quantitative assessment of exposure of heavy metals in groundwater and soil on human health in Reasi district, Jammu and Kashmir.

The assessment of heavy metal contents in environmental sectors is important to estimate the carcinogenic and non-carcinogenic doses and risks for the mankind associated with it. The present work deals with the assessment of the risk exposure related to heavy metal contents in groundwater and soil samples to two different age groups via three different transits, i.e., ingestion, inhalation and dermal. The concentrations of heavy metals (Zn, Cd, Cu, Pb and Cr) were measured in the villages of lower Himalayas of Reasi district by using microwave plasma atomic emission spectrometer. The calculated mean contamination factors of heavy metals in soil samples were as: Zn, 0.73; Cu, 0.70; Pb, 0.74; and Cr, 0.33; which led to pollution load index less than unity. The overall carcinogenic risks have been varied from 6.4E-08 to 5.1E-07 in soil samples and from 7.3E-06 to 1.1E-04 in ground water samples and were found to be well within the range prescribed by USEPA (Screening level ecological risk assessment protocol for hazardous waste combustion facilities, appendix E: toxicity reference values, US Environmental Protection Agency, Washington, D.C., 1999). The mean values of heavy metal contents except lead and chromium in water samples were found to be less than the values prescribed by various agencies. Geo-accumulation Index showed that Pb contribute to the highest contamination (0 < Igeo < 1) among the other heavy metals. Cluster analysis and principal component analysis identified that Zn, Cu, Pb and Cr had a relationship and the presence of these heavy metals could be related to vehicle emissions, traffic sources and industrial sources. The overall mean values of the non-carcinogenic doses and associated hazard risks in soil and water samples calculated for children were found to be higher than the adults which may be due to hand to mouth activities.

Toxicity assessment of particulate matter emitted from different types of vehicles on marine microalgae.

Air pollution caused by vehicle emissions remains a serious environmental threat in urban areas. Sedimentation of atmospheric aerosols, surface wash, drainage water, and urbane wastewater can bring vehicle particle emissions into the aquatic environment. However, the level of toxicity and mode of toxic action for this kind of particles are not fully understood. Here we explored the aquatic toxic effects of particulate matter emitted from different types of vehicles on marine microalgae Porphyridium purpureum and Heterosigma akashiwo. We used flow cytometry to evaluate growth rate inhibition, changes in the level of esterase activity, changes in membrane potential and size changes of microalgae cells under the influence of particulate matter emitted by motorcycles, cars and specialized vehicles with different types of engines and powered by different types of fuel. Both microalgae species were highly influenced by the particles emitted by diesel-powered vehicles. These particle samples had the highest impact on survival, esterase activity, and membrane potential of microalgae and caused the most significant increase in microalgae cell size compared to the particles produced by gasoline-powered vehicles. The results of the algae-bioassay strongly correlate with the data of laser granulometry analyses, which indicate that the most toxic samples had a significantly higher percentage of particles in the size range less than 1 µm. Visual observation with an optical microscope showed intensive agglomeration of the particles emitted by diesel-powered vehicles with microalgae cells. Moreover, within the scope of this research, we did not observe the direct influence of metal content in the particles to the level of their aquatic toxicity, and we can conclude that physical damage is the most probable mechanism of toxicity for vehicle emitted particles.

Assessment of genotoxic effects on elderly populations exposed to high traffic areas: Results for supporting public health surveillance.

In urban areas with intense vehicular traffic, particulate matter in suspension, especially the fraction of particles with ultra-fine diameter, has been regarded as the main problem of chronic diseases in susceptible populations, such as the elderly. This study aimed to determine the genotoxic effects of exposure to air pollution evaluating the association between the frequencies of micronuclei (MN) and binucleated (BN) cells in exfoliated oral mucosa cells of elderly population and exposure conditions, considering the influence of traffic and concentration of PM in different aerodynamic diameters. Traffic of passenger vehicles, heavy duty trucks and environmental concentrations of Particulate Matter were measured twice a day during 28 days before biological sampling of oral mucosa from 154 participants living in areas of distinct levels of urban traffic. Data from this study showed that the group of participants living near road traffic exhibited higher MN cell frequency, when compared to the other groups of subjects. In addition, a canonical correlation analysis between environmental and genotoxicity variables analysis revealed that high concentrations of the particulate matter were correlated with intense traffic and the genotoxicity in exfoliated oral cells.

Lichen as a Biomonitor for Vehicular Emission of Metals: A Risk Assessment of Lichen Consumption by the Sichuan Snub-Nosed Monkey (Rhinopithecus roxellana).

Two lichen species, Usnea aciculifera and Usnea luridorufa, were used as biomonitors for the deposition of traffic-related metals in China's Shennongjia National Nature Reserve. The suitability of the two lichen species for use as biomonitors was compared. The health threat to the Sichuan snub-nosed (aka golden) monkey (Rhinopithecus roxellana) from consuming lichen with elevated metal concentrations due to vehicular traffic was then assessed. Lichens, with large surface areas and neither roots nor stomata, efficiently absorb both particulate and gaseous air pollutants. The resulting data was used to assess the effect of heavy metal accumulation on the lichens as well as the health risk imposed on the monkeys as lichen is a primary food source. Lichen samples were collected in the core area of the reserve at three locations of varying traffic intensity. A forth site in the reserve, with no proximate traffic, was used as the control. Results show: (1) lichen from high traffic sites has significantly higher concentrations of Fe, Cd, Pb Zn, and Cr than lichen collected from the control site; (2) vehicular traffic is the primary source of metals in lichen; (3) U. luridorufa collected at high traffic sites displayed decreased photosynthetic efficiency, an indication of stress; (4) intake of Cd and Pb from vehicle emissions in the Shennongjia National Nature Reserve could adversely affect snub-nosed monkey health. This research advances the science of biomonitoring, contributes to environmental protection efforts in China's nature reserves and helps improve food safety for Sichuan snub-nosed monkey, a national treasure of China.

Risk of acute respiratory infection from crop burning in India: estimating disease burden and economic welfare from satellite and national health survey data for 250 000 persons.

BACKGROUND: Respiratory infections are among the leading causes of death and disability globally. Respirable aerosol particles released by agricultural crop-residue burning (ACRB), practised by farmers in all global regions, are potentially harmful to human health. Our objective was to estimate the health and economic costs of ACRB in northern India. METHODS: The primary outcome was acute respiratory infection (ARI) from India's fourth District Level Health Survey (DLHS-4). DLHS-4 data were merged with Moderate-Resolution Imaging Spectroradiometer satellite data on fire occurrence. Mutually adjusted generalized linear models were used to generate risk ratios for risk factors of ARI. Overall disease burden due to ACRB was estimated in terms of disability-adjusted life years. RESULTS: Seeking medical treatment for ARI in the previous 2 weeks was reported by 5050 (2%) of 252 539 persons. Living in a district with intense ACRB-the top quintile of fires per day-was associated with a 3-fold higher risk of ARI (mutually adjusted risk ratio 2.99, 95% confidence interval 2.77 to 3.23) after adjustment for socio-demographic and household factors. Children under 5 years of age were particularly susceptible (3.65, 3.06 to 4.34 in this subgroup). Additional ARI risk factors included motor-vehicle congestion (1.96, 1.72 to 2.23), open drainage (1.91, 1.73 to 2.11), cooking with biomass (1.73, 1.58 to 1.90) and living in urban areas (1.35, 1.26 to 1.44). Eliminating ACRB would avert 14.9 million disability-adjusted life years lost per year, valued at US$152.9 billion over 5 years. CONCLUSIONS: Investments to stop crop burning and offer farmers alternative crop-residue disposal solutions are likely to improve population-level respiratory health and yield major economic returns.

Responsiveness assessment of a 3D tetra-culture alveolar model exposed to diesel exhaust particulate matter.

The aim of the current study was to evaluate the responses of a 3D tetra-culture alveolar model cultivated at the air-liquid-interface (ALI) after apical exposure to diesel exhaust particulate matter (DEPM) based on the three-tiered oxidative stress concept. The alveolar model exposed to increasing doses of DEPM (1.75-5 µg/cm2) responded with increasing activity of the anti-oxidant defense mechanisms (Nrf2 translocation, increased gene expression for anti-oxidant proteins and increased HMOX-1 synthesis) (tier 1). Higher exposure generated a proinflammatory response (NF-kB translocation, increased gene expression of pro-inflammatory cytokines and adhesion molecules, and increased IL-6 and IL-8 synthesis) (tier 2) and, finally, the highest doses applied resulted in a decrease of cell viability due to necrosis (extra-cellular release of LDH) or apoptosis (increased expression of the pro-apoptotic genes CASP7 and FAS) (tier 3). Overall, the results of our study demonstrate that the 3D tetra-culture model when directly exposed to DEPM potently generates a realistic response according to the three-tiered oxidative stress concept. Further evaluation and benchmarking against currently used in vivo rodent models is needed to show its suitability, and to serve in the future as an alternative for in vivo studies in the hazard evaluation of inhalable irritants.

Associations of Source-apportioned Fine Particles with Cause-specific Mortality in California.

BACKGROUND: Exposure to ambient fine particulate matter (PM2.5) has been linked with premature mortality, but sources of PM2.5 have been less studied. METHODS: We evaluated associations between source-specific PM2.5 exposures and cause-specific short-term mortality in eight California locations from 2002 to 2011. Speciated PM2.5 measurements were source-apportioned using Positive Matrix Factorization into eight sources and combined with death certificate data. We used time-stratified case-crossover analysis with conditional logistic regression by location and meta-analysis to calculate pooled estimates. RESULTS: Biomass burning was associated with all-cause mortality lagged 2 days after exposure (lag2) (% changelag2 in odds per interquartile range width increase in biomass burning PM2.5 = 0.8, 95% confidence interval [CI] = 0.2, 1.4), cardiovascular (% changelag2 = 1.3, 95% CI = 0.3, 2.4), and ischemic heart disease (% changelag2 = 2.0, 95% CI = 0.6, 3.5). Vehicular emissions were associated with increases in cardiovascular mortality (% changelag0 = 1.4, 95% CI = 0.0, 2.9). Several other sources exhibited positive associations as well. Many findings persisted during the cool season. Warm season biomass burning was associated with respiratory/thoracic cancer mortality (% changelag1 = 5.9, 95% CI = 0.7, 11.3), and warm season traffic was associated with all-cause (% changelag0 = 1.9, 95% CI = 0.1, 3.6) and cardiovascular (% changelag0 = 2.9, 95% CI = 0.1, 5.7) mortality. CONCLUSIONS: Our results suggest that acute exposures to biomass burning and vehicular emissions are linked with cardiovascular mortality, with additional sources (i.e., soil, secondary nitrate, secondary sulfate, aged sea salt, and chlorine sources) showing associations with other specific mortality types.

Multi-cellular human bronchial models exposed to diesel exhaust particles: assessment of inflammation, oxidative stress and macrophage polarization.

BACKGROUND: Diesel exhaust particles (DEP) are a major component of outdoor air pollution. DEP mediated pulmonary effects are plausibly linked to inflammatory and oxidative stress response in which macrophages (MQ), epithelial cells and their cell-cell interaction plays a crucial role. Therefore, in this study we aimed at studying the cellular crosstalk between airway epithelial cells with MQ and MQ polarization following exposure to aerosolized DEP by assessing inflammation, oxidative stress, and MQ polarization response markers. METHOD: Lung mucosa models including primary bronchial epithelial cells (PBEC) cultured at air-liquid interface (ALI) were co-cultured without (PBEC-ALI) and with MQ (PBEC-ALI/MQ). Cells were exposed to 12.7 µg/cm2 aerosolized DEP using XposeALI®. Control (sham) models were exposed to clean air. Cell viability was assessed. CXCL8 and IL-6 were measured in the basal medium by ELISA. The mRNA expression of inflammatory markers (CXCL8, IL6, TNFα), oxidative stress (NFKB, HMOX1, GPx) and MQ polarization markers (IL10, IL4, IL13, MRC1, MRC2 RETNLA, IL12 andIL23) were measured by qRT-PCR. The surface/mRNA expression of TLR2/TLR4 was detected by FACS and qRT-PCR. RESULTS: In PBEC-ALI exposure to DEP significantly increased the secretion of CXCL8, mRNA expression of inflammatory markers (CXCL8, TNFα) and oxidative stress markers (NFKB, HMOX1, GPx). However, mRNA expressions of these markers (CXCL8, IL6, NFKB, and HMOX1) were reduced in PBEC-ALI/MQ models after DEP exposure. TLR2 and TLR4 mRNA expression increased after DEP exposure in PBEC-ALI. The surface expression of TLR2 and TLR4 on PBEC was significantly reduced in sham-exposed PBEC-ALI/MQ compared to PBEC-ALI. After DEP exposure surface expression of TLR2 was increased on PBEC of PBEC-ALI/MQ, while TLR4 was decreased in both models. DEP exposure resulted in similar expression pattern of TLR2/TLR4 on MQ as in PBEC. In PBEC-ALI/MQ, DEP exposure increased the mRNA expression of anti-inflammatory M2 macrophage markers (IL10, IL4, IL13, MRC1, MRC2). CONCLUSION: The cellular interaction of PBEC with MQ in response to DEP plays a pivotal role for MQ phenotypic alteration towards M2-subtypes, thereby promoting an efficient resolution of the inflammation. Furthermore, this study highlighted the fact that cell-cell interaction using multicellular ALI-models combined with an in vivo-like inhalation exposure system is critical in better mimicking the airway physiology compared with traditional cell culture systems.

Burden of lung cancer attributable to occupational diesel engine exhaust exposure in Canada.

OBJECTIVE: To estimate the population attributable fraction (PAF) and number of incident and fatal lung cancers in Canada from occupational exposure to diesel engine exhaust (DEE). METHODS: DEE exposure prevalence and level estimates were used with Canadian Census and Labour Force Survey data to model the exposed population across the risk exposure period (REP, 1961-2001). Relative risks of lung cancer were calculated based on a meta-regression selected from the literature. PAFs were calculated using Levin's equation and applied to the 2011 lung cancer statistics obtained from the Canadian Cancer Registry. RESULTS: We estimated that 2.4% (95% CI 1.6% to 6.6%) of lung cancers in Canada are attributable to occupational DEE exposure, corresponding to approximately 560 (95% CI 380 to 1570) incident and 460 (95% CI 310 to 1270) fatal lung cancers in 2011. Overall, 1.6 million individuals alive in 2011 were occupationally exposed to DEE during the REP, 97% of whom were male. Occupations with the highest burden were underground miners, truck drivers and mechanics. Half of the attributable lung cancers occurred among workers with low exposure. CONCLUSIONS: This is the first study to quantify the burden of lung cancer attributable to occupational DEE exposure in Canada. Our results underscore a large potential for prevention, and a large public health impact from occupational exposure to low levels of DEE.

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.