Residual Oil Fly Ash Research Articles

Particle Size and Morphological Evaluation of Airborne Urban Dust Particles by Scanning Electron Microscopy and Bidimensional Empirical Mode Analysis

Airborne particles affect the health of the population. As particles decrease in size, they can penetrate deeper into the respiratory system, reaching the terminal bronchioles and alveoli. Particles as small as 0.1 µm in diameter may translocate into the bloodstream, potentially impacting various organs. Additionally, the smaller the particle size, the longer they remain suspended in the air, thereby increasing their deleterious damages. The aim of this work is to study the size distribution of airborne particles emitted from anthropogenic sources of air pollution, with a special emphasis on estimating the distribution of micro and nanoparticles considered the most harmful to health. The Bidimensional Empirical Mode Decomposition (BEMD) algorithm was used on micrographs of the particles obtained by Scanning Electron Microscopy (SEM). BEMD is a current empirical computational tool applied to image analysis that allows extracting non-linear heterogeneous oscillations of brightness. We studied ROFA (Residual Oil Fly Ash) from industrial sources and DEP (Diesel Exhaust Particles) from vehicular emissions as airborne particles. After collecting the particles on filters, micrographs were taken using SEM at different magnifications to which the BEMD algorithm was applied. Particle size and asymmetry distributions were obtained for each mode, allowing the identification of the most deleterious particles. The methodology employed herein is relatively simple and effective for inferring the impact of airborne particulate matter on health and the environment.

Air pollution induces morpho-functional, biochemical and biomechanical vascular dysfunction in undernourished rats

Air pollution (gases and particulate matter -PM) and child undernutrition are globally recognized stressors with significant consequences. PM and its components breach the respiratory alveolar-capillary barrier, entering the vasculature transporting not only harmful particles and its mediators but, altering vascular paracrine and autocrine functions.The aim of this study was to investigate the effects of Residual Oil Fly Ash (ROFA), on the vasculature of young animals with nutritional growth retardation (NGR). Weanling rats were fed a diet restricted 20% (NGR) compared to ad libitum intake (control-C) for 4 weeks. Rats were intranasally instilled with 1 mg/kg BW of ROFA. After 24h exposure, histological and immunohistochemical, biochemical and contractile response to NA/ACh were evaluated in aortas.ROFA induced changes in the tunica media of the aorta in all groups regarding thickness, muscular cells and expression of Connexin-43. ROFA increased TGF-β1 and decreased eNOs levels and calcium channels in C and NGR animals. An increment in cytokines IL-6 and IL-10 was observed in C, with no changes in NGR. ROFA exposure altered the vascular contractile capacity.In conclusion, ROFA exposure could increase the risk for CVD through the alteration of vascular biochemical parameters, a possible step of the endothelial dysfunction.

Decreased immune response in undernourished rats after air pollution exposure

Children are highly vulnerable subpopulation to malnutrition and air pollution. We investigate, in a rat nutritional growth retardation (NGR) model, the impact of Residual Oil Fly Ash (ROFA) on the lung immune response using in vitro and ex vivo methods. In vitro: Alveolar macrophages (AM) were isolated from Control (C) and NGR animals, cultured and treated with ROFA (1–100 µg/ml) for 24 h. Ex vivo: C and NGR rats were intranasally instilled with ROFA (1 mg/kg BW) or PBS. 24 h post-exposure AM were isolated and cultured. ROFA-treatment increased superoxide anion production and TNFα secretion in C-AM in vitro, though for NGR-AM this response was lower. A similar pattern was observed for TNFα and IL-6 secretion in ex vivo experiments. Regarding the antioxidant response, although NGR-AM showed increased Nrf2, after ROFA instillation an attenuated activation was observed. To conclude, chronic undernutrition altered AM response to ROFA affecting immune responsiveness to air pollutants.

Molecular mechanisms underlying NLRP3 inflammasome activation and IL-1β production in air pollution fine particulate matter (PM2.5)-primed macrophages

Exposure to air pollution fine particulate matter (PM2.5) aggravates respiratory and cardiovascular diseases. It has been proposed that PM2.5 uptake by alveolar macrophages promotes local inflammation that ignites a systemic response, but precise underlying mechanisms remain unclear. Here, we demonstrate that PM2.5 phagocytosis leads to NLRP3 inflammasome activation and subsequent release of the pro-inflammatory master cytokine IL-1β. Inflammasome priming and assembly was time- and dose-dependent in inflammasome-reporter THP-1-ASC-GFP cells, and consistent across PM2.5 samples of variable chemical composition. While inflammasome activation was promoted by different PM2.5 surrogates, significant IL-1β release could only be observed after stimulation with transition-metal rich Residual Oil Fly Ash (ROFA) particles. This effect was confirmed in primary human monocyte-derived macrophages and murine bone marrow-derived macrophages (BMDMs), and by confocal imaging of inflammasome-reporter ASC-Citrine BMDMs. IL-1β release by ROFA was dependent on the NLRP3 inflammasome, as indicated by lack of IL-1β production in ROFA-exposed NLRP3-deficient (Nlrp3−/−) BMDMs, and by specific NLRP3 inhibition with the pharmacological compound MCC950. In addition, while ROFA promoted the upregulation of pro-inflammatory gene expression and cytokines release, MCC950 reduced TNF-α, IL-6, and CCL2 production. Furthermore, inhibition of TNF-α with a neutralizing antibody decreased IL-1β release in ROFA-exposed BMDMs. Using electron tomography, ROFA particles were observed inside intracellular vesicles and mitochondria, which showed signs of ultrastructural damage. Mechanistically, we identified lysosomal rupture, K+ efflux, and impaired mitochondrial function as important prerequisites for ROFA-mediated IL-1β release. Interestingly, specific inhibition of superoxide anion production (O2•-) from mitochondrial respiratory Complex I, but not III, blunted IL-1β release in ROFA-exposed BMDMs. Our findings unravel the mechanism by which PM2.5 promotes IL-1β release in macrophages and provide a novel link between innate immune response and exposure to air pollution PM2.5.

Air pollution combined with high-fat feeding aggravates metabolic and cardiovascular diseases: A dangerous, oxidative, and immune-inflammatory association

Obesity and particulate air pollutant (PM2.5) are important risk factors for cardiometabolic diseases. PM2.5 exacerbates insulin resistance and lipid ectopic deposition in obese animals. The inorganic fraction of PM2.5, the Residual Oil Fly Ash (ROFA), is related to cardiovascular events, by enhancing the generation of reactive species, inflammatory cytokines, and leukocyte activation. However, the synergistic effects of ROFA and a high-fat diet (HFD) are still poorly described, and the studies were mainly conducted with males. AimsTo investigate if ROFA could potentiate the cardiometabolic effects of diet-induced obesity in female rats. Material and methodsWistar female rats were divided into four groups: Control (n = 6), Polluted (n = 6), HFD (n = 6), and HFD + Polluted (n = 6). HFD and HFD + Polluted received a high-fat diet (HFD) (58.3 % as fats), whilst Control and Polluted groups received a standard diet (Nuvilab CR-1). In addition, Polluted and HFD + Polluted groups received intranasal instillation of ROFA (250 μg/50 μL), while Control and HFD groups received saline solution (50 μL) daily, five days per week. Both interventions occurred 24 weeks after the animals were euthanized. Key findingsHFD combined with ROFA exposure impaired lipid profile challenged systemic and cardiac antioxidant defense, and presented a synergistic effect in inducing an immune-inflammatory condition. We found that the lipid profile disturbance is associated with HFD-induced hepatic, but not cardiac, deposition of triglycerides in female animals. SignificanceOur results support the hypothesis that ROFA exposure combined with bad feeding can exacerbate metabolic and cardiovascular diseases.

Moderate aerobic training is safe and improves glucose intolerance induced by the association of high fat diet and air pollution.

Obesity and exposure to fine particulate matter (PM2.5) are risk factors for insulin resistance, to which physical exercise is the most powerful non-pharmacological strategy. However, public concern over whether exercise could be protective in a polluted environment exists. Therefore, evaluating the possible benefits of exercise in polluted conditions in different contexts (age, gender, and cardiometabolic health) is imperative. In this sense, muscle plays a major role in maintaining glucose homeostasis, and its oxidative status is closely affected during exercise. This study tested whether moderate aerobic training could alleviate the metabolic and oxidative impairment in the gastrocnemius induced by the combination of a high-fat diet (HFD) and PM2.5 exposure. Female mice (B6129SF2/J) received HFD (58.3% of fat) or standard diet, intranasal instillation of 20μg residual oil fly ash (ROFA: inorganic portion of PM2.5), or saline seven times per week for 19weeks. In the 13th week, animals were submitted to moderate training or remained sedentary. Trained animals followed a progressive protocol for 6weeks, ending at swimming with 5% body weight of workload for 60min, while sedentary animals remained in shallow water. Aerobic moderate training attenuated weight gain and glucose intolerance and prevented muscle and pancreatic mass loss induced by a HFD plus ROFA exposure. Interestingly, a HFD combined with ROFA enhanced the catalase antioxidant activity, regardless of physical exercise. Therefore, our study highlights that, even in polluted conditions, moderate training is the most powerful non-pharmacological treatment for obesity and insulin resistance.

Intratracheal instillation of respirable particulate matter elicits neuroendocrine activation

Objective Inhalation of ozone activates central sympathetic-adrenal-medullary and hypothalamic-pituitary-adrenal stress axes. While airway neural networks are known to communicate noxious stimuli to higher brain centers, it is not known to what extent responses generated from pulmonary airways contribute to neuroendocrine activation. Materials and Methods Unlike inhalational exposures that involve the entire respiratory tract, we employed intratracheal (IT) instillations to expose only pulmonary airways to either soluble metal-rich residual oil fly ash (ROFA) or compressor-generated diesel exhaust particles (C-DEP). Male Wistar–Kyoto rats (12–13 weeks) were IT instilled with either saline, C-DEP or ROFA (5 mg/kg) and necropsied at 4 or 24 hr to assess temporal effects. Results IT-instillation of particulate matter (PM) induced hyperglycemia as early as 30-min and glucose intolerance when measured at 2 hr post-exposure. We observed PM- and time-specific effects on markers of pulmonary injury/inflammation (ROFA>C-DEP; 24 hr>4hr) as corroborated by increases in lavage fluid injury markers, neutrophils (ROFA>C-DEP), and lymphocytes (ROFA). Increases in lavage fluid pro-inflammatory cytokines differed between C-DEP and ROFA in that C-DEP caused larger increases in TNF-α whereas ROFA caused larger increases in IL-6. No increases in circulating cytokines occurred. At 4 hr, PM impacts on neuroendocrine activation were observed through depletion of circulating leukocytes, increases in adrenaline (ROFA), and decreases in thyroid-stimulating-hormone, T3, prolactin, luteinizing-hormone, and testosterone. C-DEP and ROFA both increased lung expression of genes involved in acute stress and inflammatory processes. Moreover, small increases occurred in hypothalamic Fkbp5, a glucocorticoid-sensitive gene. Conclusion Respiratory alterations differed between C-DEP and ROFA, with ROFA inducing greater overall lung injury/inflammation; however, both PM induced a similar degree of neuroendocrine activation. These findings demonstrate neuroendocrine activation after pulmonary-only PM exposure, and suggest the involvement of pituitary- and adrenal-derived hormones.

Ovariectomy reduces the cardiac cytoprotection in rats exposed to particulate air pollutant.

Fine particulate matter (PM2.5) has been considered a risk factor for cardiovascular diseases by inducing an oxidative and inflammatory phenotype. Besides, the reduction of 17β-estradiol (E2) levels during menopause is a natural risk for cardiovascular outcomes. During the E2 downfall, there is a high requirement of the 70-kDa heat shock proteins (HSP70), which present essential antioxidant, anti-inflammatory, and anti-senescence roles. We investigated if the ovariectomy, an animal model for menopause, could induce additional effects in cardiac health by impairing oxidative and heat shock response parameters of female rats chronically exposed to residual oil fly ash (ROFA; an inorganic fraction of PM2.5). Thus, ROFA was obtained from São Paulo (Brazil) and solubilized it in saline. Further, female Wistar rats were exposed to 50μL of saline (control group) or ROFA solution (250μg) (polluted) by intranasal instillation, 5days/week, 12weeks. At the 12th week, animals were subdivided into four groups (n = 6 p/group): control, OVX, polluted, and polluted + OVX. Control and polluted were submitted to false surgery, while OVX and polluted + OVX were ovariectomized. ROFA or saline exposure continued for 12weeks. Ovariectomy reduced the cardiac catalase activity and iHSP70 expression in female rats exposed to ROFA. Neither plasma eHSP72 levels nor H-index (eHSP72 to cardiac iHSP70 ratio) was affected. In conclusion, ovariectomy reduces the cardiac cytoprotection and antioxidant defense, and enhances the susceptibility to premature cellular senescence in rats exposed to ROFA.

Ovariectomy enhances female rats' susceptibility to metabolic, oxidative, and heat shock response effects induced by a high-fat diet and fine particulate matter.

Obesity and exposure to fine particulate matter (air pollutant PM2.5) are important risk factors for metabolic and cardiovascular diseases. They are also related to early menopause. The reduction of 17β-estradiol (E2) levels during female climacteric, marked by menopause, is of significant concern because of its imminent influence on metabolism, redox and inflammatory status. This complex homeostasis-threatening scenario may induce a heat shock response (HSR) in cells, enhancing the expression of the 70kDa heat shock protein (HSP70). A failure in this mechanism could predispose women to cardiovascular diseases. In this study, we evaluated if the climacteric could represent an additional risk among obese rats exposed to PM2.5 by worsening lipid, oxidative, and inflammatory parameters and HSP70 in cardiac tissue. We induced obesity in female Wistar rats using a high-fat diet (HFD) (58.3% as fats) and exposed them to 50μL of saline 0.9% (control, n=15) or 250μg residual oil fly ash (ROFA, the inorganic portion of PM2.5) (polluted, n=15) by intranasal instillation, 5days/w for 12weeks. At the 12th week, we subdivided these animals into four groups: control (n=6), OVX (n=9), polluted (n=6) and polluted+OVX (n=9). OVX and polluted+OVX were submitted to a bilateral ovariectomy (OVX), a surgical model for menopause, while control and polluted received a false surgery (sham). ROFA exposure and HFD consumption were continued for 12 additional weeks, after which the animals were euthanized. ROFA enhanced the susceptibility to ovariectomy-induced dyslipidemia, while ovariectomy predisposed female rats to the ROFA-induced decrease of cardiac iHSP70 expression. Ovariectomy also decreased the IL-6 levels and IL-6/IL-10 in obese animals, reinforcing a metabolic impairment and a failure to respond to unfavorable conditions. Our results support the hypothesis that obese ovariectomized animals are predisposed to a metabolic worsening under polluted conditions and are at higher risk of cardiovascular diseases.

P.191 The impact of physical activity and fitness on resilience to modern-life stress and the role of brain-derived neurotrophic factor (BDNF)

Although zinc is ubiquitous in ambient particulate matter (PM), exposure to size fractionated residual oil fly ash (ROFA) PM is of particular concern due to several studies implicating particle zinc in mortality, adverse respiratory and cardiac effects. The lack of zinc speciation data is an impediment to our understanding of the biological mechanism of Zn induced toxicity. ROFA PM2.5+ samples (i.e. particle with aerodynamic diameter >2.5 μm) are prepared in a small 732 kW practical fire tube boiler by combusting one No. 5 and three No. 6 residual oil(s) of varying sulfur and ash contents. The combined X-ray absorption spectroscopy and selective extraction method is used to determine the Zn speciation in PM2.5+ samples. The Zn speciation in ROFA PM2.5 (i.e. particle with aerodynamic diameter <2.5 μm) samples, reported earlier, is included here for comparison purposes. The data show that zinc sulfate is predominant in both fractions. In addition, an appreciable amount of zinc phosphate was detected in the PM2.5 fraction. The insoluble zinc forms in both the fractions are identified as Zn-sorbed-ferrihydrite and zinc sulphide. The variation of Zn speciation across different size fractions has implication on the bioavailability and toxicity of Zn. Such source specific speciation data are needed for developing source inventories, and for amending existing regulations/framing new regulations for different size fractions.

Maternal supplementation with Bifidobacterium breve M-16V prevents their offspring from allergic airway inflammation accelerated by the prenatal exposure to an air pollutant aerosol.

Bifidobacterium breve M-16V is a probiotic bacterial strain with efficacy in infants achieved by suppressing T-helper type (Th) 2 immune responses and modulating the systemic Th1/Th2 balance. Exposure to air pollution during pregnancy increases asthma susceptibility in offspring. The aim of this study was to investigate the effects of the maternal intake of B. breve M-16V on susceptibility to asthma accelerated by prenatal exposure to air pollution. The intake of B. breve M-16V in residual oil fly ash (ROFA)-exposed pregnant mice resulted in fewer eosinophils in the bronchoalveolar lavage fluid of neonatal mice and reduced allergic lung inflammation. The expressions of Th2 cytokines including IL-5 and IL-13 were decreased in neonatal mice from ROFA-exposed mothers fed B. breve M-16V. The analysis of fecal microbiota from neonatal mice revealed that the intake of B. breve M-16V by mothers changed the composition of fecal microbiota in neonatal mice, which resulted in a decreased population of Firmicutes. Moreover, several bacterial strains of fecal microbiota from neonatal mice had a strong correlation with Th2 cytokines and histological score. These results suggest that the maternal intake of M-16V might have beneficial effects in neonates by preventing and/or alleviating allergic reactions accelerated by prenatal exposure to air pollution.

NADPH oxidase and mitochondria are relevant sources of superoxide anion in the oxinflammatory response of macrophages exposed to airborne particulate matter

Exposure to ambient air particulate matter (PM) is associated with increased cardiorespiratory morbidity and mortality. In this context, alveolar macrophages exhibit proinflammatory and oxidative responses as a result of the clearance of particles, thus contributing to lung injury. However, the mechanisms linking these pathways are not completely clarified. Therefore, the oxinflammation phenomenon was studied in RAW 264.7 macrophages exposed to Residual Oil Fly Ash (ROFA), a PM surrogate rich in transition metals. While cell viability was not compromised under the experimental conditions, a proinflammatory phenotype was observed in cells incubated with ROFA 100 μg/mL, characterized by increased levels of TNF-α and NO production, together with PM uptake. This inflammatory response seems to precede alterations in redox metabolism, characterized by augmented levels of H2O2, diminished GSH/GSSG ratio, and increased SOD activity. This scenario resulted in increased oxidative damage to phospholipids. Moreover, alterations in mitochondrial respiration were observed following ROFA incubation, such as diminished coupling efficiency and spare respiratory capacity, together with augmented proton leak. These findings were accompanied by a decrease in mitochondrial membrane potential. Finally, NADPH oxidase (NOX) and mitochondria were identified as the main sources of superoxide anion (▪) in our model. These results indicate that PM exposure induces direct activation of macrophages, leading to inflammation and increased reactive oxygen species production through NOX and mitochondria, which impairs antioxidant defense and may cause mitochondrial dysfunction.

Hazardous effects of urban air particulate matter acute exposure on lung and extrapulmonary organs in mice

Air particulate matter (PM) can lead to extrapulmonary adverse reactions in organs such as liver and heart either by particle translocation from the lung to the systemic circulation or by the release of lung mediators. Young BALB/c mice were intranasal instilled with 1mg/BW of Urban Air Particles from Buenos Aires or Residual Oil Fly Ash. Histopathology, oxidative metabolism and inflammation on lungs and extrapulmonary organs and the systemic response were evaluated. Lung histophatological analysis supported the rise in the number of inflammatory cells in the bronchoalveolar lavage from PM-exposed animals. Also, both PM caused recruitment of inflammatory cells in the liver and heart parenchyma and IL-6 and transaminases augmentation in serum. We have shown that despite morphochemical differences, both urban air PM altered the lung and extrapulmonary organs. Therefore, exposure to urban air PM may distress body metabolism which, in turn could lead to the development and progression of multifactorial diseases.

Chemical nature of zinc in size fractionated particulate matter from residual oil combustion - A comparative study

Although zinc is ubiquitous in ambient particulate matter (PM), exposure to size fractionated residual oil fly ash (ROFA) PM is of particular concern due to several studies implicating particle zinc in mortality, adverse respiratory and cardiac effects. The lack of zinc speciation data is an impediment to our understanding of the biological mechanism of Zn induced toxicity. ROFA PM2.5+ samples (i.e. particle with aerodynamic diameter >2.5 μm) are prepared in a small 732 kW practical fire tube boiler by combusting one No. 5 and three No. 6 residual oil(s) of varying sulfur and ash contents. The combined X-ray absorption spectroscopy and selective extraction method is used to determine the Zn speciation in PM2.5+ samples. The Zn speciation in ROFA PM2.5 (i.e. particle with aerodynamic diameter <2.5 μm) samples, reported earlier, is included here for comparison purposes. The data show that zinc sulfate is predominant in both fractions. In addition, an appreciable amount of zinc phosphate was detected in the PM2.5 fraction. The insoluble zinc forms in both the fractions are identified as Zn-sorbed-ferrihydrite and zinc sulphide. The variation of Zn speciation across different size fractions has implication on the bioavailability and toxicity of Zn. Such source specific speciation data are needed for developing source inventories, and for amending existing regulations/framing new regulations for different size fractions.

Direct and Indirect Effect of Air Particles Exposure Induce Nrf2-Dependent Cardiomyocyte Cellular Response In Vitro.

Air particulate matter has been associated with adverse effects in the cardiorespiratory system leading to cytotoxic and pro-inflammatory effects. Particulate matter-associated cardiac effects may be direct or indirect. While direct interactions may occur when inhaled ultrafine particles and/or particle components cross the air-blood barrier reaching the cardiac tissue, indirect interactions may occur as the result of pulmonary inflammation and consequently the release of inflammatory and oxidative mediators into the blood circulation. The aim of the study is to investigate the direct or indirectly the effect of Urban Air particles from downtown Buenos Aires (UAP-BA) and residual oil fly ash (ROFA), a surrogate of ambient air pollution, on cardiomyocytes (HL-1 cells). HL-1 cultured cells were directly exposed to particulate matter [UAP-BA (10-200µg/ml), ROFA (1-100µg/ml)] or indirectly exposed to conditioned media (CM) from particle-exposed alveolar macrophages (AM). Metabolic activity, reactive oxygen species (ROS), and Nrf2 expression were assessed by MTT, DHR 123, and immunocytochemistry techniques, respectively. We found that direct exposure of cardiomyocytes to UAP-BA or ROFA increased ROS generation but the oxidative damage did not alter metabolic activity likely by a concomitant increase in the cytoplasmic and nuclear Nrf2 expression. However, indirect exposure through CM caused a marked reduction on cardiac metabolic activity probably due to the rise in ROS generation without Nrf2 translocation into the cell nuclei. In this in vitro model, our results indicate both direct and indirect PM effects on cardiomyocytes cells in culture. Our findings employing lung and cardiomyocytes cells provide support to the hypothesis that particle-induced cardiac alteration may possibly involve lung-derived mediators.

INOS Inhibition Reduces Lung Mechanical Alterations and Remodeling Induced by Particulate Matter in Mice.

Background. The epidemiologic association between pulmonary exposure to ambient particulate matter (PM) and acute lung damage is well known. However, the mechanism involved in the effects of repeated exposures of PM in the lung injury is poorly documented. This study tested the hypotheses that chronic nasal instillation of residual oil fly ash (ROFA) induced not only distal lung and airway inflammation but also remodeling. In addition, we evaluated the effects of inducible nitric oxide inhibition in these responses. For this purpose, airway and lung parenchyma were evaluated by quantitative analysis of collagen and elastic fibers, immunohistochemistry for macrophages, neutrophils, inducible nitric oxide synthase (iNOS), neuronal nitric oxide synthase (nNOS), and alveolar septa 8-iso prostaglandin F2α (8-iso-PGF-2α) detection. Anesthetized in vivo (airway resistance, elastance, H, G, and Raw) respiratory mechanics were also analyzed. C57BL6 mice received daily 60ul of ROFA (intranasal) for five (ROFA-5d) or fifteen days (ROFA-15d). Controls have received saline (SAL). Part of the animals has received 1400W (SAL+1400W and ROFA-15d+1400W), an iNOS inhibitor, for four days before the end of the protocol. A marked neutrophil and macrophage infiltration and an increase in the iNOS, nNOS, and 8-iso-PGF2 α expression was observed in peribronchiolar and alveolar wall both in ROFA-5d and in ROFA-15d groups. There was an increment of the collagen and elastic fibers in alveolar and airway walls in ROFA-15d group. The iNOS inhibition reduced all alterations induced by ROFA, except for the 8-iso-PGF2 α expression. In conclusion, repeated particulate matter exposures induce extracellular matrix remodeling of airway and alveolar walls, which could contribute to the pulmonary mechanical changes observed. The mechanism involved is, at least, dependent on the inducible nitric oxide activation.

Oxidative stress response to air particle pollution in a rat nutritional growth retardation model

ABSTRACTAir pollution consisting of gases and particulate matter-(PM) represents a health problem in cities worldwide. However, air pollution does not impact equally all individuals, as children appear to be more vulnerable subpopulations. Air pollution and malnutrition are two distinct factors that have been associated with oxidative damage. Therefore, the interaction between environmental exposure and nutritional status in populations at risk needs to be explored. The aim of this study was to examine oxidative metabolism in lung, heart and liver in malnourished young rats exposed to residual oil fly ash (ROFA). A Nutritional Growth Retardation (NGR) model was developed in weanling male rats placed on a 20% restricted balanced diet for 4 weeks. Then, NGR and control rats were intranasally instilled with either ROFA (1mg/kg BW) or phosphate buffered saline (PBS). Twenty-four hr post-exposure lung, heart and liver were excised, and serum collected. ROFA induced lung and liver inflammation in control and NGR animals as evidenced by lung polymorphonuclear neutrophil (PMN) recruitment and alveolar space reduction accompanied by liver lymphocyte and binucleated hepatocyte level increase. In lung and liver, antioxidant defense mechanisms reduced lipoperoxidation. In contrast, only in NGR animals did ROFA exposure alter heart oxidative metabolism leading to lipid peroxidation. Although histological and biochemical tissue alterations were detected, no marked changes in serum liver and heart systemic biomarkers were observed. In conclusion, NGR animals responded differently to PM exposure than controls suggesting that nutritional status plays a key role in responsiveness to ambient air contaminants.

Effects of Residual Oil Fly Ash (ROFA) on the Development of Lung Cancer in Mice

Relationship between environmental pollution and lung cancer has not been fully clarified. There are particles with aerodynamic mass below 2.5 m, capable of directly injuring the lung due to their small size. The majority arise from the burning of fossil combustibles, and are called residual oil fly ash (ROFA).

Subacute exposure to residual oil fly ash (ROFA) increases eHSP70 content and extracellular-to-intracellular HSP70 ratio: a relation with oxidative stress markers.

The purpose of this study was to evaluate whether exposure to particles induces an imbalance in 70-kDa heat shock proteins (HSP70). Since intracellularly (iHSP70) it has anti-inflammatory roles whereas extracellularly (eHSP70) it has pro-inflammatory roles, we evaluate the effect of residual oil fly ash (ROFA) exposure on eHSP70-to-iHSP70 ratio (H index), a biomarker of inflammatory status that is related to oxidative stress in plasma and lymphoid tissue. Wistar rats that received ROFA suspension for three consecutive days (750μg) showed an increase in plasma eHSP70 levels (mainly the 72-kDa inducible form). Also, ROFA promoted alterations on plasma oxidative stress (increased protein carbonyl groups and superoxide dismutase activity, and decrease sulfhydryl groups). There was an increase in H index of the plasma/thymus with no changes in circulating leukocyte level, iHSP70, or oxidative stress markers in lymphoid tissues. Our results support the hypothesis that eHSP70 content and H index represent inflammatory and oxidative biomarkers.

Variability of zinc speciation in fine particulate matter emitted from a boiler and a combustor using residual oils

Zinc emission into the atmosphere from residual oil combustion is of significant concern due to its higher concentration, solubility and bioavailability. Exposure to zinc laden residual oil fly ash fine particulate matter with aerodynamic diameter ≤2.5 μm (ROFA PM2.5) induces pulmonary and cardiac effects. These effects are closely linked to the concentration and bonding environment of zinc in ROFA PM2.5. Four ROFA PM2.5 samples were prepared in a 732 kW practical fire tube boiler (FTB) by burning one No. 5 and three No. 6 residual oil(s) of varying sulfur and ash contents. For comparison, one ROFA PM2.5 sample was prepared in a 82 kW small refractory line combustor (RLC) by burning one of the No. 6 oils. The X-ray absorption spectroscopy data of FTB PM2.5 samples reveal that zinc sulfate hydrate (ZnSO4.7H2O) is the dominant zinc form, with the remainder Zn in zinc phosphate hydrate (Zn3(PO4)2.4H2O) form. Following dissolution of zinc sulfate from FTB PM2.5, a minor Zn-sorbed ferrihydrite form was detected in the residue. In the RLC PM2.5, zinc phosphate hydrate is predominant. The study shows that zinc solubility is dependent on its speciation, grade and composition of oils, combustion condition, and mode of Zn incorporation into particle's carbonaceous matrix. Speciation data provide valuable input to source attribution and health effect studies, and establish a link between the two.