Effects Of Airborne Particulate Matter Research Articles

Exposure of trophoblast cells to fine particulate matter air pollution leads to growth inhibition, inflammation and ER stress.

Ambient air pollution is considered a major environmental health threat to pregnant women. Our previous work has shown an association between exposure to airborne particulate matter (PM) and an increased risk of developing pre-eclamspia. It is now recognized that many pregnancy complications are due to underlying placental dysfunction, and this tissue plays a pivotal role in pre-eclamspia. Recent studies have shown that PM can enter the circulation and reach the human placenta but the effects of PM on human placental function are still largely unknown. In this work we investigated the effects of airborne PM on trophoblast cells. Human, first trimester trophoblast cells (HTR-8/SV) were exposed to urban pollution particles (Malmö PM2.5; Prague PM10) for up to seven days in vitro and were analysed for uptake, levels of hCGβ and IL-6 secretion and proteomic analysis. HTR-8/SVneo cells rapidly endocytose PM within 30 min of exposure and particles accumulate in the cell in perinuclear vesicles. High doses of Prague and Malmö PM (500–5000 ng/ml) significantly decreased hCGβ secretion and increased IL-6 secretion after 48 h exposure. Exposure to PM (50 ng/ml) for 48h or seven days led to reduced cellular growth and altered protein expression. The differentially expressed proteins are involved in networks that regulate cellular processes such as inflammation, endoplasmic reticulum stress, cellular survival and molecular transport pathways. Our studies suggest that trophoblast cells exposed to low levels of urban PM respond with reduced growth, oxidative stress, inflammation and endoplasmic reticulum stress after taking up the particles by endocytosis. Many of the dysfunctional cellular processes ascribed to the differentially expressed proteins in this study, are similar to those described in PE, suggesting that low levels of urban PM may disrupt cellular processes in trophoblast cells. Many of the differentially expressed proteins identified in this study are involved in inflammation and may be potential biomarkers for PE.

Marine Alga Ecklonia cava Extract and Dieckol Attenuate Prostaglandin E2 Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter.

Atmospheric particulate matter (PM) is an important cause of skin damage, and an increasing number of studies have been conducted to discover safe, natural materials that can alleviate the oxidative stress and inflammation caused by PM. It has been previously shown that the extract of Ecklonia cava Kjellman, a perennial brown macroalga, can alleviate oxidative stress in epidermal keratinocytes exposed to PM less than 10 microns in diameter (PM10). The present study was undertaken to further examine the anti-inflammatory effects of E. cava extract and its major polyphenolic constituent, dieckol. HaCaT keratinocytes were exposed to PM10 in the presence or absence of E. cava extract or dieckol and analyzed for their viability, prostaglandin E2 (PGE2) release, and gene expression of cyclooxygenase (COX)-1, COX-2, microsomal prostaglandin E2 synthase (mPGES)-1, mPGES-2, and cytosolic prostaglandin E2 synthase (cPGES). PM10 treatment decreased cell viability and increased the production of PGE2, and these changes were partially abrogated by E. cava extract. E. cava extract also attenuated the expression of COX-1, COX-2, and mPGES-2 stimulated by PM10. Dieckol attenuated PGE2 production and the gene expression of COX-1, COX-2, and mPGES-1 stimulated by PM10. This study demonstrates that E. cava extract and dieckol alleviate airborne PM10-induced PGE2 production in keratinocytes through the inhibition of gene expression of COX-1, COX-2, mPGES-1, and/or mPGES-2. Thus, E. cava extract and dieckol are potentially useful natural cosmetic ingredients for counteracting the pro-inflammatory effects of airborne PM.

Airborne Fine Particles Induce Hematological Effects through Regulating the Crosstalk of the Kallikrein-Kinin, Complement, and Coagulation Systems.

Particulate air pollution caused by human activities has drawn global attention due to its potential health risks. Considering the inevitable contact of inhaled airborne fine particulate matter (PM) with plasma, the hematological effects of PM are worthy of study. In this study, the potential effect of PM on hematological homeostasis through triggering the crosstalk of the kallikrein-kinin system (KKS), complement, and coagulation systems in plasma was investigated. The ex vivo, in vitro, and in vivo KKS activation assays confirmed that PM samples could efficiently cause the cascade activation of key zymogens in the KKS, wherein the particles coupled with lipopolysaccharide attachment provided substantial contribution. The binding of Hageman factor XII (FXII) with PM samples and its subsequent autoactivation initiated this process. The crucial elements in the complement cascade, including complement 3 (C3) and complement 5 (C5), and coagulation system (prothrombin) were also found to be actively induced by PM exposure, which was regulated by the interplay of KKS activation. The data provided solid evidence on hematological effects of airborne PM through inducing the activation of the KKS, complement, and coagulation systems, which would be valuable in the risk assessment on air-pollution-related cardiovascular diseases.

Effect of airborne particulate matter of 2.5 μm or less on preterm birth: A national birth cohort study in China

BackgroundMost evidences regarding ambient PM2.5 or PM10 (particulate matter of median aerodynamic diameter ≤2.5 μm or ≤10 μm) and preterm birth (PTB) come from western countries which has relatively low PM pollution exposure, and the results are still inconsistent. This study aims to examine whether exposure to high concentrations of PM2.5 or PM10 was associated with PTB (<37 weeks) and near term birth (37–38 weeks). MethodWe established a birth cohort with 1,280,524 singleton pregnancies who delivered from Dec 1st, 2013 to Nov 30th, 2014 and matched their home address to PM2.5 and PM10 concentrations which were predicted with machine learning methods based satellite remote sensing, meteorological and land use information. Cox proportional hazard regression models were used to analyze the associations between PTB and exposure of PM2.5 or PM10, after controlling for individual level covariates. ResultsExposure to PM2.5 or PM10 during pregnancy increases the risk of PTB and near term birth [e.g., Hazard ratios: 1.09 (95% CI: 1.09, 1.10), 1.08 (95% CI: 1.07, 1.08), 1.01 (95% CI: 1.01, 1.02), and 1.09 (95% CI: 1.08, 1.10) for each 10 μg/m3 increase in PM2.5 for the 1st, 2nd, 3rd trimester and over the entire pregnancy, respectively]. The effects appeared to be stronger among women who come from rural areas, worked as farmers, were overweight before conception, whose mate was smoking during pregnancy, and conceived in autumn. ConclusionThis study provides clear evidence that exposure to PM2.5 or PM10 during pregnancy increases the risk of PTB and near term birth. Public policies regarding improvement of air quality would produce great health benefit by reducing the burden of preterm birth.

Effects of airborne particulate matter (PM10) from dust storm and thermal inversion on global DNA methylation in human peripheral blood mononuclear cells (PBMCs) in vitro

Scientists have considered epigenetic modifications as a possible mechanism to deal with adverse effects of air pollution. This study aimed to compare the effect of PM10 (PM with aerodynamic diameter ≤ 10 μm) from dust storm and inversion conditions on in vitro global methylation in human peripheral blood mononuclear cells (PBMCs). PM10 was sampled in Tehran, Iran, at a point impacted with dust storm and inversion. PM toxicity was determined using the MTT assay. PBMCs were extracted from whole blood of healthy males and treated separately with a mixture of pooled PM10 from inversion and dusty conditions at concentrations of 50–300 μg/mL for 4 h. Untreated cells were used as the negative control. Moreover, 5-methylsytosine (%5-mC) and 5-hydroxymethylcytosine (%5-hmC) were measured by the enzyme-linked immunosorbent assay (ELISA) method. Daily average PM10 concentrations in dusty and inversion days were 348.40 and 220.54 μg/m3, respectively. The mean of %5-mC (2.04 ± 1.49%) was estimated 12 times more than that of %5-hmC (0.17 ± 0.11%). PM10 resulting from the both sources caused DNA hypomethylation; however, this effect from inversion (median = 3%, IQR = 2.4%) was found to be significantly more than that from dust storm (median = 1.1%, IQR = 1.38%). Moreover, particles increased %5-hmC caused by PM10, which was significantly greater when resulting from inversion (0.23 ± 0.1%) than from dust storm (0.12 ± 0.09%). Furthermore, %5-mC and %5-hmC were significantly different at different PM10 concentrations (50–300 μg/mL) so that a significant difference was observed between %5-mC and %5-hmC at extreme concentrations. Results showed that PM10 from inversion caused a significantly more global methylation than that from dust storm. It can be concluded that measurement of 5-mC and 5-hmC as epigenetic modifications in environmental studies of DNA methylation can be a good procedure to determine health effects related to PM10 exposure.

Seasonal and spatial variations in the chemical components and the cellular effects of particulate matter collected in Northern China

The health effects of airborne particulate matter (PM) are likely to be strongly influenced by its components. The relationship between the composition of PM and its biological effects has been investigated in vitro/vivo, but more studies are needed to achieve a better understanding of the relationship. Such studies are limited in Northern China, where severe air pollution causes significant health impacts. In this study, we analyzed seasonal PM10 (PM, aerodynamic diameter less than 10μm) samples from five typical cities in Northern China for their physicochemical properties and their in vitro effects on A549 (human lung epithelial cell line) and RAW264.7 (murine monocyte macrophage) cells, including cytotoxicity, oxidative stress and inflammatory effects. Principal component analysis and multiple linear regressions were used to investigate the relationship between the PM components and the cellular responses. The cellular responses of A549 cells were more closely related to the endotoxin content and the levels of polycyclic aromatic hydrocarbons (PAHs) and their derivatives, while the cellular responses of RAW264.7 cells were largely related to PM10-bound metals, and the chalcophile elements (Pb, Cu, Zn, Cd) were more related to the PM-induced oxidative stress, whereas the lithophile and siderophile elements (Al, Fe, Mg, Co, V, Mn, Ca) were more related to PM-induced inflammation and cytotoxicity. As PM compositions changed seasonally, more intense cellular responses were seen when A549 cells were exposed to winter samples that contained higher levels of those components. The autumn and winter samples induced higher levels of oxidative stress in RAW264.7 cells, possibly due to higher contents of chalcophile elements, whereas the spring and/or summer samples were more cytotoxic and proinflammatory, possibly due to higher contents of lithophile and siderophile elements. The study suggests that the evaluation of health impacts induced by air pollution should take into account different physiochemical properties other than the mass concentration, and that public health would benefit greatly from effective, prioritized control of the sources that are the major producers of the central species.

From the air to the water phase: implication for toxicity testing of combustion-derived particles

The biological effects of airborne particulate matter (PM) in humans stimulated many research activities in recent years. One type of particles contributing to PM are those derived from combustion processes. By using in vitro test systems for assessing the toxic effects of those particles, the transfer into liquid media is necessary. Thus the question arises, how the transfer of airborne particles into liquid suspensions should be realized and how the exposure of test organisms/cells to the particles can be done and monitored with regard to concentration and stability. Further, the characterization of the airborne particles regarding their composition seems to be of importance in order to understand the induced biological effects. Hence, this review gathers and evaluates results from in vitro and ecotoxicity studies, where the introduction of airborne particles into liquids is required. The aim was to learn on the current practice and recommend on the design of toxicity studies in the future. In total, about 80 papers were retrieved by literature search that deal with the assessment of biological effects of combustion-derived particles or their constituents. The papers were evaluated in detail with regard to the methodology applied. From this evaluation and based on expert knowledge regarding nanoparticle testing, recommendations for the assessment of PM applying toxicological assays were developed. To provide guidance, essential criteria are developed that should help in preparation, testing, and during the evaluation phase of toxicological assays. We further advise whole particle testing, complemented by testing of particle extracts and washed particles.Graphical abstract

Physicochemical characterization of aerosol particles emitted by electrical appliances

Adverse health effects of airborne particulate matter depend on parameters like particle size, particle surface and chemical composition. Major emission of indoor particles is caused by combustion processes like tobacco smoking and cooking. Nevertheless, the use of household electrical appliances, such as vacuum cleaners, flat irons or hair dryers, can produce particles as well.In this study the emissions of different hair dryers and flat irons were investigated using a test chamber. The particle number concentrations, particle volume concentrations, as well as the size distributions were measured. Particles were sampled and analyzed by electron microscopy, inductively coupled plasma mass spectrometry and gas chromatography mass spectrometry. Moreover different volatile organic compounds (VOCs) were measured.Each tested appliance, especially flat irons produced small particles with diameters far below 100nm and might be a nonnegligible source for indoor particles. Copper was the main identified element in most of the particles emitted from hair dryers, but in the emission of two hair dryers silver-containing nanoparticles were found as well. Various VOCs were observed in the emission of both flat irons and hair dryers, while cyclic siloxanes were detected only in the emission of flat irons. The use of flat irons or hair dryers may significantly contribute to the personal particle exposure.

Effects of Airborne Particulate Matter on Respiratory Health in a Community near a Cement Factory in Chilanga, Zambia: Results from a Panel Study.

We conducted a panel study to investigate seasonal variations in concentrations of airborne PM2.5 and PM10 and the effects on respiratory health in a community near a cement factory; in Chilanga; Zambia. A panel of 63 and 55 participants aged 21 to 59 years from a community located at the edge of the factory within 1 km and a control community located 18 km from the factory respectively; were followed up for three climatic seasons July 2015 to February 2016. Symptom diary questionnaires were completed and lung function measurements taken daily for 14 days in each of the three climatic seasons. Simultaneously, PM2.5 and PM10 concentrations in ambient air were monitored at a fixed site for each community. Mean seasonal concentrations of PM2.5 and PM10 ranged from 2.39–24.93 μg/m3 and 7.03–68.28 μg/m3 respectively in the exposed compared to the control community 1.69–6.03 μg/m3 and 2.26–8.86 μg/m3. The incident rates of reported respiratory symptoms were higher in the exposed compared to the control community: 46.3 vs. 13.8 for cough; 41.2 vs. 9.6 for phlegm; 49.0 vs.12.5 for nose; and 13.9 vs. 3.9 for wheeze per 100 person-days. There was a lower performance on all lung indices in the exposed community compared to the control; overall the mean FEV1 (forced expiratory volume in one second) and FVC (forced vital capacity) predicted percentage for the exposed was six and four percentage points lower than the control. Restriction of industrial emissions coupled with on-going monitoring and regulatory enforcement are needed to ensure that PM (airborne particulate matter) levels in the ambient air are kept within recommended levels to safeguard the respiratory health of nearby community residents.

Investigation of Heavy Metals Content in Airborne Particles from Ploiesti, Romania

This study aims to evaluate the concentrations of heavy metals in airborne particulate matter (PM) collected in Ploiesti city (Romania) during the monitoring campaigns performed in 2015. Various health effects of airborne PM, from less serious to very serious ones, are often associated with its chemical speciation. The heavy metals bounded on PM may accumulate in human body by inhalation and can produce both short-term and long-term negative health effects especially in children and sensitive people. We investigated several heavy metals associated with PM2.5 collected in 12 relevant sampling points to estimate their potential impact on urban population health. PM samples were collected on 37 mm quartz fiberglass filters using a precision optical instrument i.e., DustTrak DRX8533EP. The deposition of elements on the surface of samples was determined using a scanning electron microscope (SEM). The analysis and quantification of trace elements were performed using Inductively Coupled Plasma-Mass Spectrometry (ICP-MS). The experiments indicated that samples of PM contained heavy metals in the following order Zn ] Ni ] Cr ] Pb ] As ] Cd. Monitoring of elemental composition in atmospheric particles can contribute to a better air quality management.

Evaluation of the Effects of Airborne Particulate Matter on Bone Marrow-Mesenchymal Stem Cells (BM-MSCs): Cellular, Molecular and Systems Biological Approaches.

Particulate matter (PM) contains heavy metals that affect various cellular functions and gene expression associated with a range of acute and chronic diseases in humans. However, the specific effects they exert on the stem cells remain unclear. Here, we report the effects of PM collected from the city of Jeddah on proliferation, cell death, related gene expression and systems of biological analysis in bone marrow mesenchymal stem cells (BM-MSCs), with the aim of understanding the underlying mechanisms. PM2.5 and PM10 were tested in vitro at various concentrations (15 to 300 µg/mL) and durations (24 to 72 h). PMs induced cellular stress including membrane damage, shrinkage and death. Lower concentrations of PM2.5 increased proliferation of BM-MSCs, while higher concentrations served to decrease it. PM10 decreased BM-MSCs proliferation in a concentration-dependent manner. The X-ray fluorescence spectrometric analysis showed that PM contains high levels of heavy metals. Ingenuity Pathway Analysis (IPA) and hierarchical clustering analyses demonstrated that heavy metals were associated with signaling pathways involving cell stress/death, cancer and chronic diseases. qRT-PCR results showed differential expression of the apoptosis genes (BCL2, BAX); inflammation associated genes (TNF-α and IL-6) and the cell cycle regulation gene (p53). We conclude that PM causes inflammation and cell death, and thereby predisposes to chronic debilitating diseases.

Immunity-Related Protein Expression and Pathological Lung Damage in Mice Poststimulation with Ambient Particulate Matter from Live Bird Markets

The objective of this study was to obtain insight into the adverse health effects of airborne particulate matter (PM) collected from live bird markets and to determine whether biological material in PM accounts for immune-related inflammatory response. Mice were exposed to a single or repeated dose of PM, after which the expression of toll-like receptors (TLRs), cytokines, and chemokines in the lungs of infected mice were examined by enzyme-linked immunosorbent assay and histopathological analysis. Results after single and repeated PM stimulation with indicated that TLR2 and TLR4 played a dominant role in the inflammatory responses of the lung. Further analysis demonstrated that the expression levels of IL-1β, TNF-α, IFN-γ, IL-8, IP-10, and MCP-1 increased significantly, which could eventually contribute to lung injury. Moreover, biological components in PM were critical in mediating immune-related inflammatory responses and should therefore not be overlooked.

Assessment of DNA Damage and Cell Senescence in Corneal Epithelial Cells Exposed to Airborne Particulate Matter (PM2.5) Collected in Guangzhou, China.

To assess the genotoxic effect of airborne particulate matter on corneal epithelial cells and investigate the role of reactive oxygen species (ROS) formation in this process. Immortalized human corneal epithelial cells (HCECs) and primary bovine corneal epithelial cells were exposed to airborne particulate matter collected from Guangzhou for 24 hours. The cell viability and toxicity were measured by the CCK-8 test and lactate dehydrogenase (LDH) release, respectively. The DNA breaks and DNA repair were examined by alkaline comet assay and by immunofluorescence staining of the phosphorylated histone variant H2AX (γH2AX), respectively. Reactive oxygen species production was assessed by the fluorescent probe, CM-H2DCFDA. Cell senescence was evaluated with senescence-associated β-Galactosidase staining, and cell ultrastructure was observed with transmission electron microscopy. Exposure to PM2.5 at the concentration of 20 μg/mL to 200 μg/mL decreased cell viability and increased LDH release. Remarkably increased DNA double-stand breaks, increased expression of DNA repair-related protein γH2AX, elevated ROS formation, and altered cell ultrastructure were observed in HCECs after treatment with PM2.5. The genotoxic effect of PM2.5 was attenuated by the ROS inhibitor N-acetyl-l-cysteine (NAC). Particulate matter 2.5 could induce DNA damage and cell senescence in corneal epithelial cells, probably by promoting ROS formation. Thus, whether long-term exposure of PM2.5 might be related to potential risk of abnormality in corneal epithelium renewal and regeneration should be further investigated.

A panel study of airborne particulate matter composition versus concentration: Potential for inflammatory response and impaired pulmonary function in children

BackgroundThe relationship between airborne particulate matter (PM) and pulmonary function in children has not been consistent among studies, potentially owing to differences in the inflammatory response to PM, based on PM types and sources. The objective of this study was to investigate the effect of airborne PM on pulmonary function in schoolchildren and its potential for an inflammatory response. MethodsDaily morning peak expiratory flow (PEF) was measured in 339 schoolchildren in February 2015. Interleukin (IL)-8 production was assessed in THP1 cells stimulated by airborne PM collected every day during the study period, and these IL-8 concentrations are described as the daily IL-8 levels. A linear mixed model was used to estimate the association between PEF values and the daily levels of suspended PM (SPM), PM diameters smaller than 2.5 μm (PM2.5), and IL-8. ResultsThe daily IL-8 levels were significantly associated with those of SPM and PM2.5. A 0.83 μg/mL increase in IL-8 levels was significantly associated with a −1.07 L/min (95% confidence interval, −2.05 to −0.08) decrease in PEF. A 12.0 μg/m3 increase in SPM and a 10.0 μg/m3 increase in PM2.5 were associated with a −1.36 L/min (−2.93 to 0.22) and −1.72 L/min (−3.82 to 0.36) decreases in PEF, respectively. There were no significant relationships between PEF, SPM, and PM2.5. ConclusionsThese findings suggest that the effects of airborne PM on pulmonary function in schoolchildren might depend more on the pro-inflammatory response than the mass concentration of the PM.

Biomolecular Markers within the Core Axis of Aging and Particulate Air Pollution Exposure in the Elderly: A Cross-Sectional Study.

Background:Telomere length and mitochondrial DNA (mtDNA) content are markers of aging and aging-related diseases. There is inconclusive evidence concerning the mechanistic effects of airborne particulate matter (PM) exposure on biomolecular markers of aging.Objective:The present study examines the association between short- and long-term PM exposure with telomere length and mtDNA content in the elderly and investigates to what extent this association is mediated by expression of genes playing a role in the telomere–mitochondrial axis of aging.Methods:Among 166 nonsmoking elderly participants, we used qPCR to measure telomere length and mtDNA content in leukocytes and RNA from whole blood to measure expression of SIRT1, TP53, PPARGC1A, PPARGC1B, NRF1, and NFE2L2. Associations between PM exposure and markers of aging were estimated using multivariable linear regression models adjusted for sex, age, BMI, socioeconomic status, statin use, past smoking status, white blood cell count, and percentage of neutrophils. Mediation analysis was performed to explore the role of age-related markers between the association of PM exposure and outcome. Annual PM2.5 exposure was calculated for each participant’s home address using a high-resolution spatial–temporal interpolation model.Results:Annual PM2.5 concentrations ranged from 15 to 23 μg/m3. A 5-μg/m3 increment in annual PM2.5 concentration was associated with a relative decrease of 16.8% (95% CI: –26.0%, –7.4%, p = 0.0005) in telomere length and a relative decrease of 25.7% (95% CI: –35.2%, –16.2%, p < 0.0001) in mtDNA content. Assuming causality, results of the mediation analysis indicated that SIRT1 mediated 19.5% and 22.5% of the estimated effect of PM2.5 exposure on telomere length and mtDNA content, respectively.Conclusions:Our findings suggest that the estimated effects of PM2.5 exposure on the telomere–mitochondrial axis of aging may play an important role in chronic health effects of PM2.5.Citation:Pieters N, Janssen BG, Dewitte H, Cox B, Cuypers A, Lefebvre W, Smeets K, Vanpoucke C, Plusquin M, Nawrot TS. 2016. Biomolecular markers within the core axis of aging and particulate air pollution exposure in the elderly: a cross-sectional study. Environ Health Perspect 124:943–950; http://dx.doi.org/10.1289/ehp.1509728

Effects of airborne particulate matter on alternative pre-mRNA splicing in colon cancer cells

Alternative pre-mRNA splicing plays key roles in determining tissue- and species-specific cell differentiation as well as in the onset of hereditary disease and cancer, being controlled by multiple post- and co-transcriptional regulatory mechanisms. We report here that airborne particulate matter, resulting from industrial pollution, inhibits expression and specifically affects alternative splicing at the 5′ untranslated region of the mRNA encoding the bone morphogenetic protein BMP4 in human colon cells in culture. These effects are consistent with a previously reported role for BMP4 in preventing colon cancer development, suggesting that ingestion of particulate matter could contribute to the onset of colon cell proliferation. We also show that the underlying mechanism might involve changes in transcriptional elongation. This is the first study to demonstrate that particulate matter causes non-pleiotropic changes in alternative splicing.

Alternative Testing Methods for Predicting Health Risk from Environmental Exposures

Alternative methods to animal testing are considered as promising tools to support the prediction of toxicological risks from environmental exposure. Among the alternative testing methods, the cell transformation assay (CTA) appears to be one of the most appropriate approaches to predict the carcinogenic properties of single chemicals, complex mixtures and environmental pollutants. The BALB/c 3T3 CTA shows a good degree of concordance with the in vivo rodent carcinogenesis tests. Whole-genome transcriptomic profiling is performed to identify genes that are transcriptionally regulated by different kinds of exposures. Its use in cell models representative of target organs may help in understanding the mode of action and predicting the risk for human health. Aiming at associating the environmental exposure to health-adverse outcomes, we used an integrated approach including the 3T3 CTA and transcriptomics on target cells, in order to evaluate the effects of airborne particulate matter (PM) on toxicological complex endpoints. Organic extracts obtained from PM2.5 and PM1 samples were evaluated in the 3T3 CTA in order to identify effects possibly associated with different aerodynamic diameters or airborne chemical components. The effects of the PM2.5 extracts on human health were assessed by using whole-genome 44 K oligo-microarray slides. Statistical analysis by GeneSpring GX identified genes whose expression was modulated in response to the cell treatment. Then, modulated genes were associated with pathways, biological processes and diseases through an extensive biological analysis. Data derived from in vitro methods and omics techniques could be valuable for monitoring the exposure to toxicants, understanding the modes of action via exposure-associated gene expression patterns and to highlight the role of genes in key events related to adversity.

Global perspective on the oxidative potential of airborne particulate matter: a synthesis of research findings.

An emerging hypothesis in the field of air pollution is that oxidative stress is one of the important pathways leading to adverse health effects of airborne particulate matter (PM). To advance our understanding of sources and chemical elements contributing to aerosol oxidative potential and provide global comparative data, we report here on the biological oxidative potential associated with size-segregated airborne PM in different urban areas of the world, measured by a biological (cell-based) reactive oxygen species (ROS) assay. Our synthesis indicates a generally greater intrinsic PM oxidative potential as well as higher levels of exposure to redox-active PM in developing areas of the world. Moreover, on the basis of our observations, smaller size fractions are generally associated with higher intrinsic ROS activity compared with larger PM size fractions. Another important outcome of our study is the identification of major species and sources that are associated with ROS activity. Water-soluble transition metals (e.g., Fe, Ni, Cu, Cr, Mn, Zn and V) and water-soluble organic carbon (WSOC) showed consistent correlations with the oxidative potential of airborne PM across different urban areas and size ranges. The major PM sources associated with these chemical species include residual/fuel oil combustion, traffic emissions, and secondary organic aerosol formation, indicating that these sources are major drivers of PM-induced oxidative potential. Moreover, comparison of ROS activity levels across different seasons indicated that photochemical aging increases the intrinsic oxidative potential of airborne PM.

Allergic Airway Inflammation by Nasal Inoculation of Particulate Matter (PM2.5) in NC/Nga Mice

To evaluate the effect of airborne particulate matter 2.5 (PM2.5) in winter on airway inflammation, water-soluble supernatant (Sup) and water-insoluble precipitate (Pre) in PM2.5 were inoculated in NC/Nga mice with high sensitivity to mite allergens. Sup with aluminum oxide was injected intraperitoneally for sensitization. Five days later, Sup, Pre or both Sup and Pre were inoculated via the nasal route five times for more sensitization and a challenge inoculation on the 11th day in NC/Nga mice. On the 12th day, mice were examined for airway hyperresponsiveness (AHR), BALF cell count and IL-1β concentration, mRNA expression of Th1 and Th2 cytokines, chemokines such as eotaxin 1 and eotaxin 2, inflammasomal complex molecules such as IL-1β, caspase 1 and the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) in lung tissue as well as histopathology. The synergistic effect of Sup and Pre was observed in terms of increases in AHR, BALF cells, the mRNA expression of IL-13, eotaxin1 and IL-1β, and the IL-1β concentration in BALF. Intracellular deposits of insoluble particulates were observed in macrophages around inflammatory granulation of the mouse group treated with Sup and Pre. These results suggest that PM2.5 can induce airway hyperresponsiveness in mice with genetically high sensitivity to mite allergens by an inflammasome-associated mechanism and synergistic action of insoluble particulates and soluble components.

Particulate Air Pollution, Ambulatory Heart Rate Variability, and Cardiac Arrhythmia in Retirement Community Residents with Coronary Artery Disease

Background: Decreased heart rate variability (HRV) has been associated with future cardiac morbidity and mortality and is often used as a marker of altered cardiac autonomic balance in studies of health effects of airborne particulate matter. Fewer studies have evaluated associations between air pollutants and cardiac arrhythmia.Objectives: We examined relationships between cardiac arrhythmias, HRV, and exposures to airborne particulate matter.Methods: We measured HRV and arrhythmia with ambulatory electrocardiograms in a cohort panel study for up to 235 hr per participant among 50 nonsmokers with coronary artery disease who were ≥ 71 years of age and living in four retirement communities in the Los Angeles, California, Air Basin. Exposures included hourly outdoor gases, hourly traffic-related and secondary organic aerosol markers, and daily size-fractionated particle mass. We used repeated measures analyses, adjusting for actigraph-derived physical activity and heart rate, temperature, day of week, season, and community location.Results: Ventricular tachycardia was significantly increased in association with increases in markers of traffic-related particles, secondary organic carbon, and ozone. Few consistent associations were observed for supraventricular tachycardia. Particulates were significantly associated with decreased ambulatory HRV only in the 20 participants using ACE (angiotensin I–converting enzyme) inhibitors.Conclusions: Although these data support the hypothesis that particulate exposures may increase the risk of ventricular tachycardia for elderly people with coronary artery disease, HRV was not associated with exposure in most of our participants. These results are consistent with previous findings in this cohort for systemic inflammation, blood pressure, and ST segment depression.Citation: Bartell SM, Longhurst J, Tjoa T, Sioutas C, Delfino RJ. 2013. Particulate air pollution, ambulatory heart rate variability, and cardiac arrhythmia in retirement community residents with coronary artery disease. Environ Health Perspect 121:1135–1141; http://dx.doi.org/10.1289/ehp.1205914