Air traffic is rapidly growing, raising concerns about the air pollution in the surroundings of airports and its impact on public health. However, little is known about the impact of air pollution ...sources on air quality and health in the vicinity of airports. In this study, the sources and adverse health effects of airport-related particulate matter (PM) were investigated and compared to those of urban traffic emissions. Ambient PM0.25 were collected at the Los Angeles International Airport (LAX) and at a central Los Angeles site (USC campus), along with PM2.5 collected directly from turbine and diesel engines. The particle chemical composition, oxidative potential (OP) (ascorbic acid (AA), and electron spin resonance (ESR) assay) as well as their reactive oxygen species (ROS) activity, inflammatory potential (interleukin (IL) 6 and 8 and tumor necrosis factor (TNF)–α) and cytotoxicity on human bronchial epithelial (16HBE) cells were assessed. Chemical composition measurements confirmed that aircraft emissions were the major source to LAX PM0.25, while the sources of the USC samples were more complex, including traffic emissions, suspended road and soil dust, and secondary aerosols. The traffic-related transition metals (Fe and Cu) in LAX and USC samples mainly affected OP values of particles, while multiple factors such as composition, size distribution and internalized amount of particles contributed to the promotion of ROS generation in 16HBE cells during 4 h exposure. Internalized particles in cells might also play an important role in activating inflammatory responses during cell recovery period, with LAX particles being more potent. Our results demonstrated considerable toxicity of airport-related particles, even at low exposure concentrations, suggesting that airport emission as source of PM0.25 may also contribute to the adverse effects on public health attributable to PM. The potency of such particles is in the same range as those collected at a site in urban area impacted heavily by traffic emissions.
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•Aviation emission was the main contributor to PM0.25 from a major airport.•Urban area PM0.25 was dominated by road traffic (traffic emission and road dust).•Airport-related PM0.25 exerts similar toxicity compared to PM0.25 from urban traffic.
Oxidative potential (OP) has been suggested to be a more health-relevant metric than particulate matter (PM) mass. Land use regression (LUR) models can estimate long-term exposure to air pollution in ...epidemiological studies, but few have been developed for OP.
We aimed to characterize the spatial contrasts of two OP methods and to develop and evaluate LUR models to assess long-term exposure to the OP of PM2.5.
Three 2-week PM2.5 samples were collected at 10 regional background, 12 urban background, and 18 street sites spread over the Netherlands/Belgium in 1 year and analyzed for OP using electron spin resonance (OP(ESR)) and dithiothreitol (OP(DTT)). LUR models were developed using temporally adjusted annual averages and a range of land-use and traffic-related GIS variables.
Street/urban background site ratio was 1.2 for OP(DTT) and 1.4 for OP(ESR), whereas regional/urban background ratio was 0.8 for both. OP(ESR) correlated moderately with OP(DTT) (R2 = 0.35). The LUR models included estimated regional background OP, local traffic, and large-scale urbanity with explained variance (R2) of 0.60 for OP(DTT) and 0.67 for OP(ESR). OP(DTT) and OP(ESR) model predictions were moderately correlated (R2 = 0.44). OP model predictions were moderately to highly correlated with predictions from a previously published PM2.5 model (R2 = 0.37-0.52), and highly correlated with predictions from previously published models of traffic components (R2 > 0.50).
LUR models explained a large fraction of the spatial variation of the two OP metrics. The moderate correlations among the predictions of OP(DTT), OP(ESR), and PM2.5 models offer the potential to investigate which metric is the strongest predictor of health effects.
Yang A, Wang M, Eeftens M, Beelen R, Dons E, Leseman DL, Brunekreef B, Cassee FR, Janssen NA, Hoek G. 2015. Spatial variation and land use regression modeling of the oxidative potential of fine particles. Environ Health Perspect 123:1187-1192; http://dx.doi.org/10.1289/ehp.1408916.
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Dostopno za:
CEKLJ, DOBA, IZUM, KILJ, NUK, OILJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
Copper oxide (CuO) nanoparticles (NPs) and copper carbonate nanoparticles (Cu
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NPs have applications as antimicrobial agents and wood preservatives: an application that may lead to oral ...ingestion via hand to mouth transfer. Rats were exposed by oral gavage to CuO NPs and Cu
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NPs for five consecutive days with doses from 1 to 512 mg/kg and 4 to 128 mg/kg per day, respectively, and toxicity was evaluated at days 6 and 26. Both CuO NPs and Cu
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NPs induced changes in hematology parameters, as well as clinical chemistry markers (e.g. increased alanine aminotransferase, ALT) indicative of liver damage For CuO NPs histopathological alterations were observed in bone marrow, stomach and liver mainly consisting of an inflammatory response, ulceration, and degeneration. Cu
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NPs induced morphological alterations in the stomach, liver, intestines, spleen, thymus, kidneys, and bone marrow. In spleen and thymus lymphoid, depletion was noted that warrants further immunotoxicological evaluation. The NPs showed partial dissolution in artificial simulated stomach fluids, while in intestinal conditions, the primary particles simultaneously shrank and agglomerated into large structures. This means that both copper ions and the particulate nanoforms should be considered as potential causal agents for the observed toxicity. For risk assessment, the lowest bench mark dose (BMD) was similar for both NPs for the serum liver enzyme AST (an indication of liver toxicity), being 26.2 mg/kg for CuO NPs and 30.8 mg/kg for Cu
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NPs. This was surprising since the histopathology evidence demonstrates more severe organ damage for Cu
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NPs than for CuO NPs.
To characterize the impact of the October 2007 wildfires on the air quality of Los Angeles, integrated ambient particulate matter (PM) samples were collected near the University of Southern ...California between October 24 and November 14, 2007. Samples were analyzed for different chemical species (i.e., water-soluble organic carbon, water-soluble elements, and several organic compounds), and the redox activity of PM was evaluated using two different assays: the dithiothreitol (DTT) and macrophage reactive oxygen species (ROS) assays. Tracers of biomass burning such as potassium and levoglucosan were elevated by 2-fold during the fire period (October 24−28), compared to the postfire period (November 1−14). Water-soluble organic carbon (WSOC) concentrations were also higher during the fire event (170 and 78 μg/mg of PM, during fire and postfire, respectively). While the DTT activity (on a per PM mass basis) increased for samples collected during the fire event (0.024 nmol DTT/min × μg on October 24) compared to the postfire samples (0.005 nmol DTT/min × μg on November 14), the ROS activity appears to be unaffected by the wildfires, probably because these two assays are driven by different PM species. While the DTT assay reflected the redox potential of polar organic compounds, which are abundant in wood-smoke, the ROS assay was mainly influenced by transition metals (e.g., Fe, Cu, Cr, Zn, Ni, and V), emitted mostly by vehicular traffic and other combustion sources, but not by the wildfires.
Increasing evidence from toxicological and epidemiological studies indicates that the central nervous system is an important target for ambient air pollutants. We have investigated whether long-term ...inhalation exposure to diesel engine exhaust (DEE), a dominant contributor to particulate air pollution in urban environments, can aggravate Alzheimer's Disease (AD)-like effects in female 5X Familial AD (5XFAD) mice and their wild-type female littermates. Following 3 and 13 weeks exposures to diluted DEE (0.95 mg/m
, 6 h/day, 5 days/week) or clean air (controls) behaviour tests were performed and amyloid-β (Aβ) plaque formation, pulmonary histopathology and systemic inflammation were evaluated.
In a string suspension task, assessing for grip strength and motor coordination, 13 weeks exposed 5XFAD mice performed significantly less than the 5XFAD controls. Spatial working memory deficits, assessed by Y-maze and X-maze tasks, were not observed in association with the DEE exposures. Brains of the 3 weeks DEE-exposed 5XFAD mice showed significantly higher cortical Aβ plaque load and higher whole brain homogenate Aβ42 levels than the clean air-exposed 5XFAD littermate controls. After the 13 weeks exposures, with increasing age and progression of the AD-phenotype of the 5XFAD mice, DEE-related differences in amyloid pathology were no longer present. Immunohistochemical evaluation of lungs of the mice revealed no obvious genetic background-related differences in tissue structure, and the DEE exposure did not cause histopathological changes in the mice of both backgrounds. Luminex analysis of plasma cytokines demonstrated absence of sustained systemic inflammation upon DEE exposure.
Inhalation exposure to DEE causes accelerated plaque formation and motor function impairment in 5XFAD transgenic mice. Our study provides further support that the brain is a relevant target for the effects of inhaled DEE and suggests that long-term exposure to this ubiquitous air pollution mixture may promote the development of Alzheimer's disease.
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•“Mini-BACS + AES” setup can be used for in vitro hazard characterization of simulated fume events.•Aircraft hydraulic fluid fumes are more harmful than engine oil fumes.•Higher OP ...level and smaller particle size may contribute to higher toxicity of hydraulic fluid fumes.•Our results clearly reflect potential health risks associated with fume events in aircraft cabins.
Contamination of aircraft cabin air can result from leakage of engine oils and hydraulic fluids into bleed air. This may cause adverse health effects in cabin crews and passengers. To realistically mimic inhalation exposure to aircraft cabin bleed-air contaminants, a mini bleed-air contaminants simulator (Mini-BACS) was constructed and connected to an air-liquid interface (ALI) aerosol exposure system (AES). This unique “Mini-BACS + AES” setup provides steady conditions to perform ALI exposure of the mono- and co-culture lung models to fumes from pyrolysis of aircraft engine oils and hydraulic fluids at respectively 200 °C and 350 °C. Meanwhile, physicochemical characteristics of test atmospheres were continuously monitored during the entire ALI exposure, including chemical composition, particle number concentration (PNC) and particles size distribution (PSD). Additional off-line chemical characterization was also performed for the generated fume. We started with submerged exposure to fumes generated from 4 types of engine oil (Fume A, B, C, and D) and 2 types of hydraulic fluid (Fume E and F). Following submerged exposures, Fume E and F as well as Fume A and B exerted the highest toxicity, which were therefore further tested under ALI exposure conditions. ALI exposures reveal that these selected engine oil (0–100 mg/m3) and hydraulic fluid (0–90 mg/m3) fumes at tested dose-ranges can impair epithelial barrier functions, induce cytotoxicity, produce pro-inflammatory responses, and reduce cell viability. Hydraulic fluid fumes are more toxic than engine oil fumes on the mass concentration basis. This may be related to higher abundance of organophosphates (OPs, ≈2800 µg/m3) and smaller particle size (≈50 nm) of hydraulic fluid fumes. Our results suggest that exposure to engine oil and hydraulic fluid fumes can induce considerable lung toxicity, clearly reflecting the potential health risks of contaminated aircraft cabin air.
The ceramic industry is an industrial sector of great impact in the global economy that has been benefiting from advances in materials and processing technologies. Ceramic manufacturing has a strong ...potential for airborne particle formation and emission, namely of ultrafine particles (UFP) and nanoparticles (NP), meaning that workers of those industries are at risk of potential exposure to these particles. At present, little is known on the impact of engineered nanoparticles (ENP) on the environment and human health and no established Occupational Exposure Limits (OEL) or specific regulations to airborne nanoparticles (ANP) exposure exist raising concerns about the possible consequences of such exposure.
In this paper, we provide an overview of the current knowledge on occupational exposure to NP in the ceramic industry and their impact on human health. Possible sources and exposure scenarios, a summary of the existing methods for evaluation and monitoring of ANP in the workplace environment and proposed Nano Reference Values (NRV) for different classes of NP are presented. Case studies on occupational exposure to ANP generated at different stages of the ceramic manufacturing process are described. Finally, the toxicological potential of intentional and unintentional ANP that have been identified in the ceramic industry workplace environment is discussed based on the existing evidence from in vitro and in vivo inhalation toxicity studies.
ENPRA was one of the earlier multidisciplinary European Commission FP7-funded projects aiming to evaluate the risks associated with nanomaterial (NM) exposure on human health across pulmonary, ...cardiovascular, hepatic, renal, and developmental systems. The outputs from this project have formed the basis of this review. A retrospective interpretation of the findings across a wide range of in vitro and in vivo studies was performed to identify the main highlights from the project. In particular, focus was placed on informing what advances were made in the hazard assessment of NM, as well as offering some suggestions on the future of "nanotoxicology research" based on these observations, shortcomings, and lessons learned from the project. A number of issues related to the hazard assessment of NM are discussed in detail and include use of appropriate NM for nanotoxicology investigations; characterization and dispersion of NM; use of appropriate doses for all related investigations; need for the correct choice of experimental models for risk assessment purposes; and full understanding of the test systems and correct interpretation of data generated from in vitro and in vivo systems. It is hoped that this review may assist in providing information in the implementation of guidelines, model systems, validation of assessment methodology, and integrated testing approaches for risk assessment of NM. It is vital to learn from ongoing and/or completed studies to avoid unnecessary duplication and offer suggestions that might improve different aspects of experimental design.
Intensive discussions are ongoing about the interpretation of pulmonary effects observed in rats exposed to poorly soluble particles. Alveolar clearance differs between rats and humans and becomes ...impaired in rats at higher exposure concentrations. Some have doubted the human relevance of toxic effects observed in rats under impaired clearance conditions and have suggested that experimental exposures should stay below concentrations inducing impaired clearance. However, for regulatory purposes, insight in potential health effects at relatively high concentrations is needed to fully understand the hazard. Many aspects of impaired particle clearance remain unclear, hampering human health hazard and risk assessment. For an adequate evaluation of the impact of impaired clearance on pulmonary toxicity, a clear definition of alveolar clearance is needed that enables to quantitatively relate the level of impairment to the induction of adverse pulmonary health effects. Also, information is needed on the mechanism of action and the appropriate dose metric for the pulmonary effects observed. In absence of these data, human hazard and risk assessment can only be performed in a pragmatic way. Unless available data clearly point out otherwise, rat pulmonary toxicity including lung inflammation and tumour formation, needs to be considered relevant for human hazard and risk assessment.
•Evaluation of PSP-induced pulmonary effects should be based on mechanism of action.•Extrapolation of PSP-induced toxicity on an appropriate dose metric is preferred.•Test concentrations need to include conditions of impaired clearance.•Human risk for PSP-induced lung lesions is to be assessed on a case-by-case basis.
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