Fluorescent reconstitution on deposition of PM2.5 in lung and extrapulmonary organs.

The deposition of PM2.5 (fine particulate matter in air with diameter smaller than 2.5 µm) in lungs is harmful to human health. However, real-time observation on the deposition of particles in the acinar area of the lung is still a challenge in experiments. Here, a fluorescent imaging method is developed to visualize the deposition process with a high temporal and spatial resolution. The observations reveal that the deposition pattern is nonuniform, and the maximum deposition rate in the acinar area differs significantly from the prediction of the widely used average deposition model. The method is also used to find single particles in the kidney and liver, though such particles are commonly believed to be too large to enter the extrapulmonary organs.

Caloric restriction attenuates C57BL/6 J mouse lung injury and extra-pulmonary toxicity induced by real ambient particulate matter exposure.

BACKGROUND: Caloric restriction (CR) is known to improve health and extend lifespan in human beings. The effects of CR on adverse health outcomes in response to particulate matter (PM) exposure and the underlying mechanisms have yet to be defined. RESULTS: Male C57BL/6 J mice were fed with a CR diet or ad libitum (AL) and exposed to PM for 4 weeks in a real-ambient PM exposure system located at Shijiazhuang, China, with a daily mean concentration (95.77 µg/m3) of PM2.5. Compared to AL-fed mice, CR-fed mice showed attenuated PM-induced pulmonary injury and extra-pulmonary toxicity characterized by reduction in oxidative stress, DNA damage and inflammation. RNA sequence analysis revealed that several pulmonary pathways that were involved in production of reactive oxygen species (ROS), cytokine production, and inflammatory cell activation were inactivated, while those mediating antioxidant generation and DNA repair were activated in CR-fed mice upon PM exposure. In addition, transcriptome analysis of murine livers revealed that CR led to induction of xenobiotic metabolism and detoxification pathways, corroborated by increased levels of urinary metabolites of polycyclic aromatic hydrocarbons (PAHs) and decreased cytotoxicity measured in an ex vivo assay. CONCLUSION: These novel results demonstrate, for the first time, that CR in mice confers resistance against pulmonary injuries and extra-pulmonary toxicity induced by PM exposure. CR led to activation of xenobiotic metabolism and enhanced detoxification of PM-bound chemicals. These findings provide evidence that dietary intervention may afford therapeutic means to reduce the health risk associated with PM exposure.

Pulmonary and systemic toxicity in rats following inhalation exposure of 3-D printer emissions from acrylonitrile butadiene styrene (ABS) filament.

BACKGROUND: Fused filament fabrication 3-D printing with acrylonitrile butadiene styrene (ABS) filament emits ultrafine particulates (UFPs) and volatile organic compounds (VOCs). However, the toxicological implications of the emissions generated during 3-D printing have not been fully elucidated. AIM AND METHODS: The goal of this study was to investigate the in vivo toxicity of ABS-emissions from a commercial desktop 3-D printer. Male Sprague Dawley rats were exposed to a single concentration of ABS-emissions or air for 4 hours/day, 4 days/week for five exposure durations (1, 4, 8, 15, and 30 days). At 24 hours after the last exposure, rats were assessed for pulmonary injury, inflammation, and oxidative stress as well as systemic toxicity. RESULTS AND DISCUSSION: 3-D printing generated particulate with average particle mass concentration of 240 ± 90 µg/m³, with an average geometric mean particle mobility diameter of 85 nm (geometric standard deviation = 1.6). The number of macrophages increased significantly at day 15. In bronchoalveolar lavage, IFN-γ and IL-10 were significantly higher at days 1 and 4, with IL-10 levels reaching a peak at day 15 in ABS-exposed rats. Neither pulmonary oxidative stress responses nor histopathological changes of the lungs and nasal passages were found among the treatments. There was an increase in platelets and monocytes in the circulation at day 15. Several serum biomarkers of hepatic and kidney functions were significantly higher at day 1. CONCLUSIONS: At the current experimental conditions applied, it was concluded that the emissions from ABS filament caused minimal transient pulmonary and systemic toxicity.

Airport emission particles: exposure characterization and toxicity following intratracheal instillation in mice.

BACKGROUND: Little is known about the exposure levels and adverse health effects of occupational exposure to airplane emissions. Diesel exhaust particles are classified as carcinogenic to humans and jet engines produce potentially similar soot particles. Here, we evaluated the potential occupational exposure risk by analyzing particles from a non-commercial airfield and from the apron of a commercial airport. Toxicity of the collected particles was evaluated alongside NIST standard reference diesel exhaust particles (NIST2975) in terms of acute phase response, pulmonary inflammation, and genotoxicity after single intratracheal instillation in mice. RESULTS: Particle exposure levels were up to 1 mg/m3 at the non-commercial airfield. Particulate matter from the non-commercial airfield air consisted of primary and aggregated soot particles, whereas commercial airport sampling resulted in a more heterogeneous mixture of organic compounds including salt, pollen and soot, reflecting the complex occupational exposure at an apron. The particle contents of polycyclic aromatic hydrocarbons and metals were similar to the content in NIST2975. Mice were exposed to doses 6, 18 and 54 µg alongside carbon black (Printex 90) and NIST2975 and euthanized after 1, 28 or 90 days. Dose-dependent increases in total number of cells, neutrophils, and eosinophils in bronchoalveolar lavage fluid were observed on day 1 post-exposure for all particles. Lymphocytes were increased for all four particle types on 28 days post-exposure as well as for neutrophil influx for jet engine particles and carbon black nanoparticles. Increased Saa3 mRNA levels in lung tissue and increased SAA3 protein levels in plasma were observed on day 1 post-exposure. Increased levels of DNA strand breaks in bronchoalveolar lavage cells and liver tissue were observed for both particles, at single dose levels across doses and time points. CONCLUSIONS: Pulmonary exposure of mice to particles collected at two airports induced acute phase response, inflammation, and genotoxicity similar to standard diesel exhaust particles and carbon black nanoparticles, suggesting similar physicochemical properties and toxicity of jet engine particles and diesel exhaust particles. Given this resemblance as well as the dose-response relationship between diesel exhaust exposure and lung cancer, occupational exposure to jet engine emissions at the two airports should be minimized.

A review of the possible associations between ambient PM2.5 exposures and the development of Alzheimer's disease.

PM2.5 particles in air pollution have been widely considered associated with respiratory and cardiovascular diseases. Recent studies have shown that PM2.5 can also cause central nervous system (CNS) diseases, including a variety of neurodegenerative diseases, such as Alzheimer's disease (AD). Activation of microglia in the central nervous system can lead to inflammatory and neurological damage. PM2.5 will reduce the methylation level of DNA and affect epigenetics. PM2.5 enters the human body through a variety of pathways to have pathological effects on CNS. For example, PM2.5 can destroy the integrity of the blood-brain barrier (BBB), so peripheral systemic inflammation easily crosses BBB and reaches CNS. The olfactory nerve is another way for PM2.5 particles to enter the brain. Surprisingly, PM2.5 can also enter the gastrointestinal tract, causing imbalances in the intestinal microecology to affect central nervous system diseases. The current work collected and discuss the mechanisms of PM2.5-induced CNS damage and PM2.5-induced neurodegenerative diseases.

Ambient fine particulate matter induces inflammatory responses of vascular endothelial cells through activating TLR-mediated pathway.

This study aims to investigate the role of Toll-like receptors (TLRs) on fine particulate matter (PM2.5)-induced inflammatory responses of vascular endothelial cells. Inflammatory factors and TLRs were examined in the aorta of mice after nonsurgical intratracheal instillation of PM2.5 as well as in the human umbilical vein endothelial cells (HUVECs) treated with PM2.5. In addition, the effects of TLR2 and TLR4 inhibitors in the secretion of interleukin 6 (IL-6) and IL-1ß and the expression of TLRs were determined in the HUVECs. The results showed that PM2.5 could increase the expression of IL-1ß, IL-6, TLR2, and TLR4 in vitro and in vivo. Anti-TLR2 IgG or TAK242, an inhibitor of TLR4, decreased the secretion of IL-1ß and IL-6 by HUVECs and reduced the expression of corresponding TLRs. In conclusion, we demonstrate that both TLR2 and TLR4 are involved in PM2.5-induced inflammatory responses of vascular endothelial cells. Inhibition of TLR2 and TLR4 expression has the potential to prevent PM2.5-induced cardiovascular diseases.

Cytotoxicity induced by the mixture components of nickel and poly aromatic hydrocarbons.

Although particulate matter (PM) is composed of various chemicals, investigations regarding the toxicity that results from mixing the substances in PM are insufficient. In this study, the effects of low levels of three PAHs (benz[a]anthracene, benzo[a]pyrene, and dibenz[a,h]anthracene) on Ni toxicity were investigated to assess the combined effect of Ni-PAHs on the environment. We compared the difference in cell mortality and total glutathione (tGSH) reduction between single Ni and Ni-PAHs co-exposure using A549 (human alveolar carcinoma). In addition, we measured the change in Ni solubility in chloroform that was triggered by PAHs to confirm the existence of cation-π interactions between Ni and PAHs. In the single Ni exposure, the dose-response curve of cell mortality and tGSH reduction were very similar, indicating that cell death was mediated by the oxidative stress. However, 10 µM PAHs induced a depleted tGSH reduction compared to single Ni without a change in cell mortality. The solubility of Ni in chloroform was greatly enhanced by the addition of benz[a]anthracene, which demonstrates the cation-π interactions between Ni and PAHs. Ni-PAH complexes can change the toxicity mechanisms of Ni from oxidative stress to others due to the reduction of Ni2+ bioavailability and the accumulation of Ni-PAH complexes on cell membranes. The abundant PAHs contained in PM have strong potential to interact with metals, which can affect the toxicity of the metal. Therefore, the mixture toxicity and interactions between diverse metals and PAHs in PM should be investigated in the future.

Mechanisms of pollutant-induced toxicity in skin and detoxification: Anti-pollution strategies and perspectives for cosmetic products.

With the development of industry and increase in road traffic, atmospheric pollution has reached unprecedented levels in many regions of the world. Concentrations of pollutants are often far beyond the recommendations of the World Health Organization. Skin, as the first interface between the human body and its environment, is one of the main organs exposed to pollutants and to other environmental factors such as UV irradiation. As much as the effects of pollution and UV irradiation on human skin have been described, the underlying mechanisms remain to be elucidated. This state of the art study aims at exposing the numerous adverse effects of UV and pollution as well as their mode of action on skin. We summarize how these environmental factors negatively impact skin cells: by upregulating xenobiotic metabolism (and bioactivation) and inducing oxidative stress and inflammation, leading to premature aging and a disrupted barrier function. Consequently, we suggest adapted protective measures for the cosmetic industry to support anti-pollution claims.

Carbon load in airway macrophages as a biomarker of exposure to particulate air pollution; a longitudinal study of an international Panel.

BACKGROUND: Carbon load in airway macrophages (AM) has been proposed as an internal marker to assess long-term exposure to combustion-derived pollutant particles. However, it is not known how this biomarker is affected by changes in exposure. We studied the clearance kinetics of black carbon (BC) in AM, obtained by sputum induction, in a one-year panel study. METHODS: AM BC was measured 8 times with 6 weeks intervals in healthy young subjects: 15 long-term residents in Leuven, Belgium (BE, mean annual PM10 20-30 µg/m3) and 30 newcomers having arrived recently (< 3 weeks) in Leuven from highly polluted cities (mean annual PM10 > 50 µg/m3) in low and middle-income countries (LMIC, n = 15), or from low to moderately polluted cities in high-income countries (HIC, n = 15). The median and 90th percentile values of AM BC were quantified by image analysis of 25 macrophages per sputum sample; the carbonaceous nature of the black inclusions in AM was verified by Femtosecond Pulsed Laser Microscopy in 30 macrophages. We used a Bayesian hierarchical single-exponential decay model to describe the evolution of AM BC. RESULTS: In the LMIC group, the mean (95% credible interval) initial quantity (R0) of median AM BC [1.122 (0.750-1.509) µm2] was higher than in the HIC group [0.387 (0.168-0.613) µm2] and BE group [0.275 (0.147-0.404) µm2]. Median AM BC content decreased in the LMIC group (decay constant 0.013 µm2/day), but remained stable over one year in the other two groups. In the LMIC group, clearance half-lives of 53 (30-99) and 116 (63-231) days, were calculated for median and 90th percentile AM BC, respectively. CONCLUSIONS: In this real-life study of an international panel of healthy young subjects, we demonstrated that carbon load in airway macrophages obtained by induced sputum reflects past long-term exposure to particulate air pollution. Values of AM BC do not change over one year when exposure remains stable, but AM BC decreases upon moving from high to moderate exposure, with average half-lives of 53 and 116 days depending on the carbon load.

Detailed deposition analysis of inertial and diffusive particles in a rat nasal passage.

Rats have been widely used as surrogates for evaluating the health effects of inhaled airborne particulate matter. To provide a thorough understanding of particle transport and deposition mechanisms in the rat nasal airway, this article presents a computational fluid dynamics (CFD) study of particle exposure in a realistic rat nasal passage under a resting flow condition. Particles covering a diameter range from 1 nm to 4 µm were passively released in front of the rat's breathing zone, and the Lagrangian particle tracking approach was used to calculate individual particle trajectories. Detailed particle deposition analysis shows the deposition of inertial particles >2 µm is high in the rat nasal vestibule and more than 70% of all inhaled inertial particles were trapped in this region. While for diffusive nanoparticles, the vestibule filtration effect is reduced, only less than 60% of inhaled nanoparticles were blocked by the anterior nasal structures. The particle exposure in the olfactory region only shows notable deposition for diffusive nanoparticles, which peaks at 9.4% for 5 nm particles. Despite the olfactory deposition remains at a low level, the ratio between the olfactory and the main passage is kept around 30-40% for 10-800 nm particles, which indicates a particle-size-independent distribution pattern in the main nasal passage and olfactory. This study provides a deep understanding of particles deposition features in a rat nasal passage, and the research findings can aid toxicologist in inter-species exposure-response extrapolation study.

Influence of airborne particulates on respiratory tract deposition of inhaled toluene and naphthalene in the rat.

OBJECTIVE: Most studies report that inhaled volatile and semivolatile organic compounds (VOCs/SVOCs) tend to deposit in the upper respiratory tract, while ultrafine (or near ultrafine) particulate matter (PM) (∼100 nm) reaches the lower airways. The objective of this study was to determine whether carbon particle co-exposure carries VOCs/SVOCs deeper into the lungs where they are deposited. MATERIALS AND METHODS: Male Sprague-Dawley rats were exposed by inhalation (nose-only) to radiolabeled toluene (20 ppm) or naphthalene (20 ppm) on a single occasion for 1 h, with or without concurrent carbon particle exposure (∼5 mg/m3). The distribution of radiolabel deposited within the respiratory tract of each animal was determined after sacrifice. The extent of adsorption of toluene and naphthalene to airborne carbon particles under the exposure conditions of the study was also assessed. RESULTS: We found that in the absence of particles, the highest deposition of both naphthalene and toluene was observed in the upper respiratory tract. Co-exposure with carbon particles tended to increase naphthalene deposition slightly throughout the respiratory tract, whereas slight decreases in toluene deposition were observed. Few differences were statistically significant. Naphthalene showed greater adsorption to the particles compared to toluene, but overall the particle-adsorbed concentration of each of these compounds was a small fraction of the total inspired concentration. CONCLUSIONS: These studies imply that at the concentrations used for the exposures in this study, inhaled carbon particles do not substantially alter the deposition of naphthalene and toluene within the respiratory tract.

Particle and inhalation exposure in human and monkey computational airway models.

Regional deposition of inhaled aerosols is essential for assessing health risks from toxic exposure. Upper airway physiology plays a significant role in respiratory defense by filtering micrometer particles, whose deposition mechanism is predominantly inertial impaction and is mainly controlled by airflow characteristics. The monkey is commonly used in tests that study inhalation toxicity as well as in preclinical tests as human surrogates due to their anatomical similarities to humans. Therefore, accurate predictions and an understanding of the inhaled particles and their distribution in monkeys are essential for extrapolating laboratory animal data to humans. The study goals were as follows: (1) to predict the particle deposition based on aerodynamic diameters (1-10 µm) and various steady inspiratory flow rates in computational models of monkey and human upper airways; and (2) to investigate potential differences in inhalation flow and particle deposition between humans and monkeys by comparing numerical simulation results with similar in-vitro and in-vivo measurements from recent literature. The deposition fractions of the monkey's numerical airway model agreed well with in-vitro and human model data when equivalent Stokes numbers were compared, based on the minimum cross-sectional area as representative of length scale. Vestibule removal efficiencies were predicted to be higher in the monkey model compared with the human model. Our results revealed that the particle transportations were sensitive to the anatomical structure, airway geometry, airflow rates, inflow boundary conditions and particle size.

Online measurement of phthalate-particulate matter interactions by membrane introduction mass spectrometry (MIMS).

To enable further study and assessment of indoor inhalation exposure risk, an online apparatus enabling measurement of semi-volatile compound partitioning on household particulates was developed. An example for use of the apparatus is described using dimethyl phthalate (DMP). The system employs direct measurement by membrane introduction mass spectrometry (MIMS). The MIMS system was calibrated using known gas phase DMP concentrations produced by gravimetrically calibrated permeation devices. The quantity of DMP sorbed by particles is described first using a model particle type, a reverse-phase liquid chromatography packing material, and then with a household dust sample. In addition, the desorption of semi-volatile compounds from a household dust sample was monitored using the apparatus, and characteristic fragment ion signals for phthalate compounds were observed.

A tissue dose-based comparative exposure assessment of manganese using physiologically based pharmacokinetic modeling-The importance of homeostatic control for an essential metal.

A physiologically-based pharmacokinetic (PBPK) model (Schroeter et al., 2011) was applied to simulate target tissue manganese (Mn) concentrations following occupational and environmental exposures. These estimates of target tissue Mn concentrations were compared to determine margins of safety (MOS) and to evaluate the biological relevance of applying safety factors to derive acceptable Mn air concentrations. Mn blood concentrations measured in occupational studies permitted verification of the human PBPK models, increasing confidence in the resulting estimates. Mn exposure was determined based on measured ambient air Mn concentrations and dietary data in Canada and the United States (US). Incorporating dietary and inhalation exposures into the models indicated that increases in target tissue concentrations above endogenous levels only begin to occur when humans are exposed to levels of Mn in ambient air (i.e. >10µg/m3) that are far higher than those currently measured in Canada or the US. A MOS greater than three orders of magnitude was observed, indicating that current Mn air concentrations are far below concentrations that would be required to produce the target tissue Mn concentrations associated with subclinical neurological effects. This application of PBPK modeling for an essential element clearly demonstrates that the conventional application of default factors to "convert" an occupational exposure to an equivalent continuous environmental exposure, followed by the application of safety factors, is not appropriate in the case of Mn. PBPK modeling demonstrates that the relationship between ambient Mn exposures and dose-to-target tissue is not linear due to normal tissue background levels and homeostatic controls.

Deposition efficiency of inhaled particles (15-5000 nm) related to breathing pattern and lung function: an experimental study in healthy children and adults.

BACKGROUND: Exposure to airborne particles has a major impact on global health. The probability of these particles to deposit in the respiratory tract during breathing is essential for their toxic effects. Observations have shown that there is a substantial variability in deposition between subjects, not only due to respiratory diseases, but also among individuals with healthy lungs. The factors determining this variability are, however, not fully understood. METHOD: In this study we experimentally investigate factors that determine individual differences in the respiratory tract depositions of inhaled particles for healthy subjects at relaxed breathing. The study covers particles of diameters 15-5000 nm and includes 67 subjects aged 7-70 years. A comprehensive examination of lung function was performed for all subjects. Principal component analyses and multiple regression analyses were used to explore the relationships between subject characteristics and particle deposition. RESULTS: A large individual variability in respiratory tract deposition efficiency was found. Individuals with high deposition of a certain particle size generally had high deposition for all particles <3500 nm. The individual variability was explained by two factors: breathing pattern, and lung structural and functional properties. The most important predictors were found to be breathing frequency and anatomical airway dead space. We also present a linear regression model describing the deposition based on four variables: tidal volume, breathing frequency, anatomical dead space and resistance of the respiratory system (the latter measured with impulse oscillometry). CONCLUSIONS: To understand why some individuals are more susceptible to airborne particles we must understand, and take into account, the individual variability in the probability of particles to deposit in the respiratory tract by considering not only breathing patterns but also adequate measures of relevant structural and functional properties.

Toxicity of inhaled particulate matter on the central nervous system: neuroinflammation, neuropsychological effects and neurodegenerative disease.

Particulate matter (PM) combined with meteorological factors cause the haze, which brings inconvenience to people's daily life and deeply endanger people's health. Accumulating literature, to date, reported that PM are closely related to cardiopulmonary disease. Outpatient visits and admissions as a result of asthma and heart attacks gradually increase with an elevated concentration of PM. Owing to its special physicochemical property, the brain could be a potential target beyond the cardiopulmonary system. Possible routes of PM to the brain via a direct route or stimulation of pro-inflammatory cytokines have been reported in several documents concerning toxicity of engineered nanoparticles in rodents. Recent studies have demonstrated that PM have implications in oxidative stress, inflammation, dysfunction of cellular organelles, as well as the disturbance of protein homeostasis, promoting neuron loss and exaggerating the burden of central nervous system (CNS). Moreover, the smallest particles (nano-sized particles), which were involved in inflammation, reactive oxygen species (ROS), microglial activation and neuron loss, may accelerate the process of the neurodevelopmental disorder and neurodegenerative disease. Potential or other undiscovered mechanisms are not mutually exclusive but complementary aspects of each other. Epidemiology studies have shown that exposure to PM could bring about neurotoxicity and play a significant role in the etiology of CNS disease, which has been gradually corroborated by in vivo and in vitro studies. This review highlights research advances on the health effects of PM with an emphasis on neurotoxicity. With the hope of enhancing awareness in the public and calling for prevention and protective measures, it is a critical topic that requires proceeding exploration. Copyright © 2017 John Wiley & Sons, Ltd.

Modeling particle deposition in the Balb/c mouse respiratory tract.

The mouse lung has become increasingly important as a surrogate of the human lung for inhalation risk assessment. The main structural difference between the two lungs is that the airway branching of the human lung is relatively symmetric, while that of the mouse lung is distinctly asymmetric or monopodial. The objectives of this study were to develop a stochastic, asymmetric particle deposition model for the Balb/c mouse and to compare predicted deposition patterns with those in the human lung. The asymmetric bronchial airway geometry of the Balb/c mouse was based on a statistical analysis of several lung casts, while, in the absence of pertinent data, the asymmetric acinar airway geometry was represented by an allometrically scaled-down version of the rat acinar region, assuming structural similarity. Deposition of inhaled particles in nasal, bronchial and acinar airways for mouse-specific breathing conditions was computed with the Monte Carlo deposition model IDEAL-mouse. While total deposition for submicron particles decreases with increasing diameter in a fashion similar to that in the human lung, the effect of inhalability and nasal pre-filtration significantly reduces total deposition in the mouse lung for particles with diameters greater than about 3 µm. The most notable difference between submicron particle deposition in the mouse and human airways is the shift of the deposition distribution from distal airway generations in the human lung to upper airway generations in the mouse lung. However, if plotted as a function of airway diameter, both deposition distributions are quite similar, indicating that airway diameter may be a more appropriate morphometric parameter for extrapolation purposes than airway generation.

Predicting lung dosimetry of inhaled particleborne benzo[a]pyrene using physiologically based pharmacokinetic modeling.

Benzo[a]pyrene (BaP) is a by-product of incomplete combustion of fossil fuels and plant/wood products, including tobacco. A physiologically based pharmacokinetic (PBPK) model for BaP for the rat was extended to simulate inhalation exposures to BaP in rats and humans including particle deposition and dissolution of absorbed BaP and renal elimination of 3-hydroxy benzo[a]pyrene (3-OH BaP) in humans. The clearance of particle-associated BaP from lung based on existing data in rats and dogs suggest that the process is bi-phasic. An initial rapid clearance was represented by BaP released from particles followed by a slower first-order clearance that follows particle kinetics. Parameter values for BaP-particle dissociation were estimated using inhalation data from isolated/ventilated/perfused rat lungs and optimized in the extended inhalation model using available rat data. Simulations of acute inhalation exposures in rats identified specific data needs including systemic elimination of BaP metabolites, diffusion-limited transfer rates of BaP from lung tissue to blood and the quantitative role of macrophage-mediated and ciliated clearance mechanisms. The updated BaP model provides very good prediction of the urinary 3-OH BaP concentrations and the relative difference between measured 3-OH BaP in nonsmokers versus smokers. This PBPK model for inhaled BaP is a preliminary tool for quantifying lung BaP dosimetry in rat and humans and was used to prioritize data needs that would provide significant model refinement and robust internal dosimetry capabilities.

An approach to assess the Particulate Matter exposure for the population living around a cement plant: modelling indoor air and particle deposition in the respiratory tract.

In this paper we studied the exposure to three size fractions of outdoor particulate matter (PM10, PM2.5, and PM1) collected in an area influenced by a cement plant. For that purpose, three groups of population were evaluated (children, adults and retired) in two seasons (summer and winter). Outdoor measured PM concentrations, as well as physiological parameters and activity patterns of the three groups of population were used as input data in two different models. The first one was an indoor air quality model, used to elucidate indoor PM concentrations in different microenvironments. The second one was a dosimetry model, used to evaluate the internal exposure and the distribution of the different PM fractions in the respiratory tract. Results from the indoor air quality model showed that special attention must be paid to the finest particles, since they penetrate indoors in a greater degree. Highest pulmonary doses for the three PM sizes were reported for retired people, being this a result of the high amount of time in outdoor environments exercising lightly. For children, the exposure was mainly influenced by the time they also spend outdoors, but in this case due to heavy intensity activities. It was noticed that deposition of fine particles was more significant in the pulmonary regions of children and retired people in comparison with adults, which has implications in the expected adverse health effects for those vulnerable groups of population.

Bioaccessibility of trace elements in fine and ultrafine atmospheric particles in an industrial environment.

The lung bioaccessibility, i.e., the solubility in alveolar lung fluid of metals in particulate matter, has been recognized as an important parameter for health risk assessment, associated with the inhalation of airborne particles. The purpose of this study is to use an in vitro method to estimate the pulmonary bioaccessibility of toxic metals in different particle sizes, from a multi-influenced industrial emission area. The fine and ultrafine particles collected with cascade impactors in the chimneys and at different distances from a Fe-Mn smelter were extracted with a simulated alveolar fluid (Gamble solution). In addition, a four-step sequential extraction procedure was employed to approach the metal speciation. The bioaccessibility of metals ranged from almost insoluble for Fe (<1%) to extremely soluble for Rb (>80%). In terms of particle size, the trace element bioaccessibility is generally higher for the finer size fractions (submicron and ultrafine particles) than for the coarse one (>1 µm). These submicron particles have a very high number concentration and specific surface area, which confer them an important contact surface with the alveolar fluid, i.e., a higher bioaccessibility. Interestingly, the bioaccessibility of most metals clearly increases between the chimney stacks and the close environment of the studied Fe-Mn smelter, over a very short distance (800 m), possibly due to a mix with surrounding steelworks emissions. This increase is not observed over a greater distance from the smelter (2000 m), when industrial particles were mixed with urban aerosols, except for Fe, under more soluble forms in combustion particles.