Dysfunction of Nrf2-regulated cellular defence system and JNK activation induced by high dose of fly Ash particles are associated with pulmonary injury in mouse lungs.

The mechanisms of the exposure to fine particulate matter (PM) as a risk factor for pulmonary injury are not fully understood. The transcription factor, NF-E2-related factor 2 (Nrf2), plays a key role in protection lung against PM insult and cancer chemoprevention. In this study, F3-S fly ash particles from a municipal waste incinerator were evaluated as a PM model. We found that F3-S triggered hierarchical oxidative stress responses involving the prolonged activation of the cytoprotective Nrf2 transcriptional program via Keap1 Cys151 modification, and c-Jun NH2-terminal kinase (JNK) phosphorylation at higher doses. In mouse lungs exposed to fly ash particles at a low dose (10-20 mg/kg), Nrf2 signalling was upregulated, while in those exposed to a high fly ash particle dose (40 mg/kg), there was significant activation of JNK, and this correlated with Nrf2 phosphorylation and the downregulation of antioxidant response element (ARE)-driven genes. The JNK inhibitor, SP600125, reversed Nrf2 phosphorylation, and downregulation of detoxifying enzymes. Silencing JNK expression in mouse lungs using adenoviral shRNA inhibited JNK activation and Nrf2 phosphorylation, promoted ARE-driven gene expression, and reduced pulmonary injury. Furthermore, we found that the 452-515 amino acid region within the Neh1 domain of Nrf2 was required for its interaction with P-JNK. We demonstrated that Nrf2 was an important P-JNK target in fly ash-induced pulmonary toxicity. JNK phosphorylated Nrf2, leading to a dysfunction of the Nrf2-mediated defence system.

Exposure to coal ash and depression in children aged 6-14 years old.

BACKGROUND: When coal is burned for energy, coal ash, a hazardous waste product, is generated. Throughout the world, over 1 billion tons of coal ash is produced yearly. In the United States, over 78 million tons of coal ash was produced in 2019. Fly ash, the main component of coal ash contains neurotoxic metal (loid)s that may affect children's neurodevelopment and mental health. The objective of this study was to investigate the association between fly ash and depressive problems in children aged 6-14 years old. METHODS: Children and their parents/guardians were recruited from 2015 to 2020. Tobit regression and logistic regression were used to assess the association between coal fly ash and depressive problems. To determine fly ash presence, Scanning Electron Microscopy was conducted on polycarbonate filters containing PM10 from the homes of the study participants. Depressive problems in children were measured using the Depressive Problems DSM and withdrawn/depressed syndromic problem scales of the Child Behavior Checklist. RESULTS: In covariate-adjusted Tobit regression models, children with fly ash on the filter had higher scores on the DSM Depressive Problems (3.13 points; 95% CI = 0.39, 5.88) compared with children who did not have fly ash on the filter. Logistic regression supported these findings. CONCLUSION: Coal ash is one of the largest waste streams in the U.S, but it is not classified as a hazardous waste by the Environmental Protection Agency. To our knowledge, no studies have assessed the impact of coal ash on children's mental health. This study highlights the need for further research into the effects of coal ash exposure on children's mental health, and improved regulations on release and storage of coal ash.

Isoleucilactucin Ameliorates Coal Fly Ash-Induced Inflammation through the NF-κB and MAPK Pathways in MH-S Cells.

We investigated whether isoleucilactucin, an active constituent of Ixeridium dentatum, reduces inflammation caused by coal fly ash (CFA) in alveolar macrophages (MH-S). The anti-inflammatory effects of isoleucilactucin were assessed by measuring the concentration of nitric oxide (NO) and the expression of pro-inflammatory mediators in MH-S cells exposed to CFA-induced inflammation. We found that isoleucilactucin reduced CFA-induced NO generation dose-dependently in MH-S cells. Moreover, isoleucilactucin suppressed CFA-activated proinflammatory mediators, including cyclooxygenase-2 (COX2) and inducible NO synthase (iNOS), and the proinflammatory cytokines such as interleukin-(IL)-1ß, IL-6, and tumor necrosis factor (TNF-α). The inhibiting properties of isoleucilactucin on the nuclear translocation of phosphorylated nuclear factor-kappa B (p-NF-κB) were observed. The effects of isoleucilactucin on the NF-κB and mitogen-activated protein kinase (MAPK) pathways were also measured in CFA-stimulated MH-S cells. These results indicate that isoleucilactucin suppressed CFA-stimulated inflammation in MH-S cells by inhibiting the NF-κB and MAPK pathways, which suggest it might exert anti-inflammatory properties in the lung.

Comparative Toxicity of Fly Ash: An In Vitro Study.

Fly ash produced during coal combustion is one of the major sources of air and water pollution, but the data on the impact of micrometer-size fly ash particles on human cells is still incomplete. Fly ash samples were collected from several electric power stations in the United States (Rockdale, TX; Dolet Hill, Mansfield, LA; Rockport, IN; Muskogee, OK) and from a metallurgic plant located in the Russian Federation (Chelyabinsk Electro-Metallurgical Works OJSC). The particles were characterized using dynamic light scattering, atomic force, and hyperspectral microscopy. According to chemical composition, the fly ash studied was ferro-alumino-silicate mineral containing substantial quantities of Ca, Mg, and a negligible concentration of K, Na, Mn, and Sr. The toxicity of the fly ash microparticles was assessed in vitro using HeLa cells (human cervical cancer cells) and Jurkat cells (immortalized human T lymphocytes). Incubation of cells with different concentrations of fly ash resulted in a dose-dependent decrease in cell viability for all fly ash variants. The most prominent cytotoxic effect in HeLa cells was produced by the ash particles from Rockdale, while the least was produced by the fly ash from Chelyabinsk. In Jurkat cells, the lowest toxicity was observed for fly ash collected from Rockport, Dolet Hill and Muscogee plants. The fly ash from Rockdale and Chelyabinsk induced DNA damage in HeLa cells, as revealed by the single cell electrophoresis, and disrupted the normal nuclear morphology. The interaction of fly ash microparticles of different origins with cells was visualized using dark-field microscopy and hyperspectral imaging. The size of ash particles appeared to be an important determinant of their toxicity, and the smallest fly ash particles from Chelyabinsk turned out to be the most cytotoxic to Jukart cells and the most genotoxic to HeLa cells.

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.

Evaluation of the phytotoxicity of coal ash on lettuce (Lactuca sativa L.) germination, growth and metal uptake.

Land application of coal ash is considered an environmentally friendly option to improve soil quality, but limited information exists on metal bioavailability and phytotoxicity of coal ash to sensitive plant species such as lettuce (Lactuca sativa L.). Germination and pot bioassay experiments were conducted at six coal application rates (0% (control), 5%, 15%, 25%, 50% and 75% v/v) to investigate the hypothesis that, coal ash will have a hormetic effect on germination, growth, metal uptake and biomass yield of lettuce, characterized by stimulatory and phytotoxicity effects at low and high application rates, respectively. Total concentrations (mg/kg) of metals in coal ash spanned several orders of magnitude, and decreased in the order: Fe (5150.5), Mn (326.0), Zn (102.6), Cu (94.7), Ni (74.7) and Pb (11.6). Bioavailable concentrations of metals were very low (0.0-14.1 mg/kg), accounting for less than 2% of the total concentrations. Coal ash had no significant effect on germination indices, but had hormetic effects on radicle elongation, evidenced by stimulatory and phytotoxicity effects at low (5-25%) and high (50-75%) application rates, respectively. Coal ash application at 50% and 75% significantly (p < 0.05) reduced lettuce growth and edible biomass yield, but lower application rates (5-25%) were similar to the unamended soil (control). Fe, Mn, Zn, Cu and Ni bioavailability and plant uptake generally decreased with increasing coal ash application rates particularly at 50% and 75%. Soil pH significantly increased (p < 0.05) from 6.5 for the control to about 8 for 75% coal ash, while electrical conductivity (EC) increased by 2-7 times to about 0.9 and 1.5 dS/m at 50% and 75% coal ash, respectively. Significant inverse linear relationship (p < 0.05; r2 = 0.80) were observed between edible and total biomass yields and EC, suggesting that increased salinity at high coal ash application rates could account for reduced growth and biomass. Partial elemental balances showed that plant uptake of metals was very low, accounting for just less than 2% of the bioavailable concentrations, while the bulk of the metals (98-99%) remained in the soil. In conclusion, the current findings show that coal ash may have hormetic and phytotoxic effects on sensitive plant species, an observation contrary to the bulk of earlier literature documenting beneficial effects of coal ash application to soils. Long-term field studies are required to confirm the current findings based on laboratory and pot bioassay experiments.

Using Nrf2/antioxidant response element-dependent signaling to assess the toxicity potential of fly ash particles.

Epidemiological studies have demonstrated an association between ambient particulate pollution and adverse health effects in humans. The antioxidant-responsive element (ARE) cytoprotective system mediated by the transcription factor NF-E2 p45-related factor 2 (Nrf2) serves as a primary defense against the oxidative stress triggered by particulate matter. In this study, using a cell-based ARE-reporter assay, the fine fractions of the fly ash collected from the municipal solid waste incinerators at four cities in China were examined for their ability to activate Nrf2/ARE signaling. We found that, at a non-lethal dose, all the fly ash samples were able to activate the ARE-reporter gene in a dose- and redox-dependent manner, and this was correlated with their cytotoxicity and their ability to induce DNA damage. Study of the kinetics revealed that fly ash particles elicited a prolonged activation of the ARE-reporter activity. Upon exposure to the particles, the ARE-luciferase activity significantly increased in 2 h, reached a peak at 24 h, and remained high level at 72 h. This was in contrast to the transient activation of the ARE-reporter gene triggered by the Nrf2 activators tert-butylhydroquinone and sulforaphane, while ARE-luciferase activity dropped to the basal level at 72 h from the peak at 24 h. These results demonstrate the robustness of using cell-based ARE-reporter assays to evaluate the oxidative potential of fly ash. Our novel findings suggest that the sustained activation of the Nrf2/ARE signaling pathway induced by fly ash particles perturbs cellular redox homeostasis, which in turn contributes to toxicity.

Effect of collection methods on combustion particle physicochemical properties and their biological response in a human macrophage-like cell line.

In vitro studies are a first step toward understanding the biological effects of combustion-derived particulate matter (cdPM). A vast majority of studies expose cells to cdPM suspensions, which requires a method to collect cdPM and suspend it in an aqueous media. The consequences of different particle collection methods on particle physiochemical properties and resulting biological responses are not fully understood. This study investigated the effect of two common approaches (collection on a filter and a cold plate) and one relatively new (direct bubbling in DI water) approach to particle collection. The three approaches yielded cdPM with differences in particle size distribution, surface area, composition, and oxidative potential. The directly bubbled sample retained the smallest sized particles and the bimodal distribution observed in the gas-phase. The bubbled sample contained ∼50% of its mass as dissolved species and lower molecular weight compounds, not found in the other two samples. These differences in the cdPM properties affected the biological responses in THP-1 cells. The bubbled sample showed greater oxidative potential and cellular reactive oxygen species. The scraped sample induced the greatest TNFα secretion. These findings have implications for in vitro studies of air pollution and for efforts to better understand the underlying mechanisms.

Toxic effects of coal fly ash on wheat seedlings.

We studied heavy metal (HM) stress on wheat seedlings (AK-58) with and without coal fly ash (CFA) exposure. Three CFA spray rates were used to simulate air quality of the second level. Results show airborne particulates can directly enter plant leaves, affecting the whole plant. HM deposition decreases seedling size and mass and reduces activities of the chlorophyll family, photosynthesis enzymes (RuBP and PEPC), and photosynthesis efficiency. In leaves, HM deposition increases with the CFA spray rate. In roots, however, CFA exposure seems to reduce HM deposition, compared with the control without CFA exposure. A possible reason is that HM deposition in leaves from airborne particulates hinders photosynthesis, weakens the whole physiology of the seedlings, and consequently reduces root absorption of HMs from soil. CFA leads to chloroplast expansion, layer-stack disorder of grana, plastoglobule increase, and even chlorophyll membrane damage.

Activation of Human Transient Receptor Potential Melastatin-8 (TRPM8) by Calcium-Rich Particulate Materials and Effects on Human Lung Cells.

To better understand how adverse health effects are caused by exposure to particulate materials, and to develop preventative measures, it is important to identify the properties of particles and molecular targets that link exposure with specific biologic outcomes. Coal fly ash (CFA) is a by-product of coal combustion that can affect human health. We report that human transient receptor potential melastatin-8 (TRPM8) and an N-terminally truncated TRPM8 variant (TRPM8-Δ801) are activated by CFA and calcium-rich nanoparticles and/or soluble salts within CFA. TRPM8 activation by CFA was potentiated by cold temperature involving the phosphatidylinositol 4,5-bisphosphate binding residue (L1008), but was independent of the icilin and menthol binding site residue Y745 and, essentially, the N-terminal amino acids 1-800. CFA, calcium nanoparticles, and calcium salts also activated transient receptor potential vanilloid-1 (TRPV1) and transient receptor potential ankyrin-1 (TRPA1), but not TRPV4. CFA treatment induced CXCL1 and interleukin-8 mRNA in BEAS-2B and primary human bronchial epithelial cells through activation of both TRPM8 and TRPV1. However, neither mouse nor rat TRPM8 was activated by these materials, and Trpm8 knockout had no effect on cytokine induction in the lungs of CFA-instilled mice. Amino acids S921 and S927 in mouse Trpm8 were identified as important for the lack of response to CFA. These results imply that TRPM8, in conjunction with TRPV1 and TRPA1, might sense selected forms of inhaled particulate materials in human airways, shaping cellular responses to these materials, and improving our understanding of how and why certain particulate materials elicit different responses in biologic systems, affecting human health.

Characterization of Transient Receptor Potential Vanilloid-1 (TRPV1) Variant Activation by Coal Fly Ash Particles and Associations with Altered Transient Receptor Potential Ankyrin-1 (TRPA1) Expression and Asthma.

Transient receptor potential (TRP) channels are activated by environmental particulate materials. We hypothesized that polymorphic variants of transient receptor potential vanilloid-1 (TRPV1) would be uniquely responsive to insoluble coal fly ash compared with the prototypical soluble agonist capsaicin. Furthermore, these changes would manifest as differences in lung cell responses to these agonists and perhaps correlate with changes in asthma symptom control. The TRPV1-I315M and -T469I variants were more responsive to capsaicin and coal fly ash. The I585V variant was less responsive to coal fly ash particles due to reduced translation of protein and an apparent role for Ile-585 in activation by particles. In HEK-293 cells, I585V had an inhibitory effect on wild-type TRPV1 expression, activation, and internalization/agonist-induced desensitization. In normal human bronchial epithelial cells, IL-8 secretion in response to coal fly ash treatment was reduced for cells heterozygous for TRPV1-I585V. Finally, both the I315M and I585V variants were associated with worse asthma symptom control with the effects of I315M manifesting in mild asthma and those of the I585V variant manifesting in severe, steroid-insensitive individuals. This effect may be due in part to increased transient receptor potential ankyrin-1 (TRPA1) expression by lung epithelial cells expressing the TRPV1-I585V variant. These findings suggest that specific molecular interactions control TRPV1 activation by particles, differential activation, and desensitization of TRPV1 by particles and/or other agonists, and cellular changes in the expression of TRPA1 as a result of I585V expression could contribute to variations in asthma symptom control.

Toxicity of coal fly ash (CFA) and toxicological response of switchgrass in mycorrhiza-mediated CFA-soil admixtures.

Increasing support for the use of Coal fly ash (CFA) in agriculture has necessitated a better understanding of the effects of the CFA in various cropping schemes. Experiments were conducted to assess mutagenic response of a mutant strain of Salmonella enterica serovar Typhimurium (TA100) to varying concentrations of CFA-water extracts, determine oxidative stress in switchgrass (Panicum virgatum L.) at varying levels of CFA-soil admixtures, and evaluate mycorrhiza-mediated modulation of oxidative stress responses of CFA-grown switchgrass. The TA100 exposed to 0%, 5%, 10%, 15%, 20% and 25% (w/v) CFA-water extracts elicited significant (p < 0.05) mutagenic responses at 20% and 25% extract levels but not below the 15% level. In greenhouse pot experiment, CFA-soil admixtures at 7.5% and 15% (w/w) significantly (p < 0.05) decreased the activities of superoxide dismutase (SOD) by 19.1% and 28.3% respectively, compared to control soil (0% w/w CFA/soil). Under the same conditions, activities of glutathione peroxidase (GPx) decreased by 75.9% and 66.9%. In contrast to the antioxidant enzyme activities, levels of malondialdehyde (MDA) an indicator of lipid peroxidation increased significantly (p < 0.05) by 30.49% and 38.38%. Inoculation of 7.5% and 15% CFA-soil admixtures with arbuscular mycorrhizal fungi (AMF), Rhizophaga clarus enhanced the activities of both SOD and GPx in the switchgrass, while it significantly (p < 0.05) reduced the levels of MDA. The study demonstrated that incorporation of CFA (at concentrations considered to be non-mutagenic against TA100) as soil amendment produced concentration-dependent oxidative stress responses in switchgrass; however, inoculation of the CFA-soil admixtures with AMF significantly modulated the oxidative stress responses.

Acute exposure to air pollution particulate matter aggravates experimental myocardial infarction in mice by potentiating cytokine secretion from lung macrophages.

Clinical, but not experimental evidence has suggested that air pollution particulate matter (PM) aggravates myocardial infarction (MI). Here, we aimed to describe mechanisms and consequences of PM exposure in an experimental model of MI. C57BL/6J mice were challenged with a PM surrogate (Residual Oil Fly Ash, ROFA) by intranasal installation before MI was induced by permanent ligation of the left anterior descending coronary artery. Histological analysis of the myocardium 7 days after MI demonstrated an increase in infarct area and enhanced inflammatory cell recruitment in ROFA-exposed mice. Mechanistically, ROFA exposure increased the levels of the circulating pro-inflammatory cytokines TNF-α, IL-6, and MCP-1, activated myeloid and endothelial cells, and enhanced leukocyte recruitment to the peritoneal cavity and the vascular endothelium. Notably, these effects on endothelial cells and circulating leukocytes could be reversed by neutralizing anti-TNF-α treatment. We identified alveolar macrophages as the primary source of elevated cytokine production after PM exposure. Accordingly, in vivo depletion of alveolar macrophages by intranasal clodronate attenuated inflammation and cell recruitment to infarcted tissue of ROFA-exposed mice. Taken together, our data demonstrate that exposure to environmental PM induces the release of inflammatory cytokines from alveolar macrophages which directly worsens the course of MI in mice. These findings uncover a novel link between air pollution PM exposure and inflammatory pathways, highlighting the importance of environmental factors in cardiovascular disease.

Real-Time Cell-Electronic Sensing of Coal Fly Ash Particulate Matter for Toxicity-Based Air Quality Monitoring.

The development of a unique bioassay for cytotoxicity analysis of coal fly ash (CFA) particulate matter (PM) and its potential application for air quality monitoring is described. Using human cell lines, A549 and SK-MES-1, as live probes on microelectrode-embedded 96-well sensors, impedance changes over time are measured as cells are treated with varying concentrations (1 µg/mL-20 mg/mL) of CFA samples. A dose-dependent impedance change is determined for each CFA sample, from which an IC50 histogram is obtained. The assay was successfully applied to examine CFA samples collected from three coal-fired power plants (CFPs) in China. The samples were separated into three size fractions: PM2.5 (<2.5 µm), PM10-2.5 (2.5 µm < x < 10 µm), and PM10 (>10 µm). Dynamic cell-response profiles and temporal IC50 histograms of all samples show that CFA cytotoxicity depends on concentration, exposure time (0-60 h), and cell-type (SK-MES-1 > A549). The IC50 values differentiate the cytotoxicity of CFA samples based on size fraction (PM2.5 ≈ PM10-2.5 ≫ PM10) and the sampling location (CFP2 > CFP1 ≈ CFP3). Differential cytotoxicity measurements of particulates in human cell lines using cell-electronic sensing provide a useful tool for toxicity-based air quality monitoring and risk assessment.

Morphological and biochemical changes in Azadirachta indica from coal combustion fly ash dumping site from a thermal power plant in Delhi, India.

The foliar and biochemical traits of Azadirachta indica A. Juss from fly ash (FA) dumping site in Badarpur thermal power plant (BTPP) New Delhi, India was studied. Three different experimental sites were selected at different distances from the thermal power plant. Ambient suspended particulate matter (SPM) and plant responses such as leaf pigments (chlorophyll a, chlorophyll b, and carotenoids), total chlorophyll, net photosynthetic rate, stomatal index (SI), stomatal conductance (SC), intercellular carbon dioxide concentration [CO2]i, net photosynthetic rate (NPR), nitrogen, nitrate, nitrate reductase activity, proline, protein, reducing sugar and sulphur content were measured. Considerable reduction in pigments (chlorophyll a, chlorophyll b and carotenoids), and total chlorophyll was observed at fly ash dumping site. Fly ash stress revealed the inhibitory effect on Nitrate reductase activity (NRA), Nitrate, soluble protein, and reducing sugar content, whereas stimulatory effect was found for the stomatal index, nitrogen, proline, antioxidants and sulphur content in the leaves. Under fly ash stress, stomatal conductance was low, leading to declining in photosynthetic rate and increase in the internal CO2 concentration of leaf. Single leaf area (SLA), leaf length and leaf width also showed a declining trend from control to the polluted site. Antioxidant enzymes increased in leaves reflecting stress and extenuation of reactive oxygen species (ROS).

Screening the toxicity of phosphorous-removal adsorbents using a bioluminescence inhibition test.

When found in excess, phosphorus (P) has been linked to surface water eutrophication. As a result, adsorbents are now used in P remediation efforts. However, possible secondary toxicological impacts on the use of new materials for P removal from surface water have not been reported. This study evaluated the toxicity of adsorbent materials used in the removal of P from surface water including: fly ash, bottom ash, alum sludge, a proprietary mix of adsorbents, and a proprietary engineered material. Toxicity screening was conducted by performing solid-liquid extractions (SLEs) followed by the bacterial bioluminescence inhibition test with a Microtox® M500. Of the materials tested, the samples extracted at lower pH levels demonstrated higher toxicity. The material exhibiting the most toxic response was the iron and aluminum oxide coated engineered material registering a 66-67% 15-min EC50 level for pH 4 and 5 SLEs, respectively. However, for SLEs prepared at pH 7, toxic effects were not detected for this engineered material. Fly ash and bottom ash demonstrated between 82 and 84% 15-min EC50 level, respectively, for pH 4 SLE conditions. Dried alum sludge and the proprietary mix of adsorbents were classified as having little to no toxicity.

The Cellular Toxicity of PM2.5 Emitted from Coal Combustion in Human Umbilical Vein Endothelial Cells.

OBJECTIVE: To explore the relationship between different components of fine particulate matter (PM2.5) emitted from coal combustion and their cytotoxic effect in the vascular endothelial cells. METHODS: Coal-fired PM(2.5) was sampled using a fixed-source dilution channel and flow sampler. The sample components were analyzed by ion chromatography and inductively coupled plasma atomic emission spectroscopy (ICP-AES). The PM(2.5) suspension was extracted using an ultrasonic water-bath method and then human umbilical vein endothelial cells (EA.hy926) were treated with various concentrations of the PM(2.5) suspension. Cell proliferation, oxidative DNA damage, and global DNA methylation levels were used to measure the cellular toxicity of PM(2.5) emitted from coal combustion. RESULTS: Compared to other types of coal-fired PM(2.5) preparations, the PM2.5 suspension from Yinchuan coal had the highest cytotoxicity. PM(2.5) suspension from Datong coal had the highest toxic effect while that from Yinchuan coal had the lowest. Exposure to coal-fired PM(2.5) from Jingxi coal resulted in lower 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels. At the same dose, PM(2.5) emitted from coal combustion could produce more severe DNA impairment compared to that produced by carbon black. Cell survival rate was negatively correlated with chloride and potassium ions content. The 5-methylcytosine (5-mC) level was positively correlated with Mn and negatively correlated with Zn levels. The 8 OHdG% level was positively correlated with both Mn and Fe. CONCLUSION: PM(2.5) emitted from coal combustion can decrease cell viability, increase global DNA methylation, and cause oxidative DNA damage in EA.hy926 cells. Metal components may be important factors that influence cellular toxicity.

Chronic Ingestion of Coal Fly-Ash Contaminated Prey and Its Effects on Health and Immune Parameters in Juvenile American Alligators (Alligator mississippiensis).

Coal-burning power plants supply approximately 37 % of the electricity in the United States. However, incomplete combustion produces ash wastes enriched with toxic trace elements that have historically been disposed of in aquatic basins. Organisms inhabiting such habitats may accumulate these trace elements; however, studies investigating the effects on biota have been primarily restricted to shorter-lived, lower-trophic organisms. The American alligator (Alligator mississippiensis), a long-lived, top-trophic carnivore, has been observed inhabiting these basins, yet the health or immune effects of chronic exposure and possible accumulation remains unknown. In this study, we investigated how chronic dietary ingestion of prey contaminated with coal combustion wastes (CCWs) for 25 months, and subsequent accumulation of trace elements present in CCWs, affected juvenile alligator immune function and health. Alligators were assigned to one of four dietary-treatment groups including controls and those fed prey contaminated with CCWs for one, two, or three times a week. However, no effect of Dietary Treatment (p > 0.05) was observed on any immune parameter or hematological or plasma analyte we tested. Our results suggest that neither exposure to nor accumulation of low doses of CCWs had a negative effect on certain aspects of the immune and hematological system. However, future studies are required to elucidate this further.

Eco-friendly porous concrete using bottom ash aggregate for marine ranch application.

This article presents the test results of an investigation carried out on the reuse of coal bottom ash aggregate as a substitute material for coarse aggregate in porous concrete production for marine ranch applications. The experimental parameters were the rate of bottom ash aggregate substitution (30%, 50% and 100%) and the target void ratio (15%, 20% and 25%). The cement-coated granular fertiliser was substituted into a bottom ash aggregate concrete mixture to improve marine ranch applications. The results of leaching tests revealed that the bottom ash aggregate has only a negligible amount of the ten deleterious substances specified in the Ministry of Environment - Enforcement Regulation of the Waste Management Act of Republic Korea. The large amount of bubbles/air gaps in the bottom ash aggregate increased the voids of the concrete mixtures in all target void ratios, and decreased the compressive strength of the porous concrete mixture; however, the mixture substituted with 30% and 10% of bottom ash aggregate and granular fertiliser, respectively, showed an equal strength to the control mixture. The sea water resistibility of the bottom ash aggregate substituted mixture was relatively equal to that of the control mixture, and also showed a great deal of improvement in the degree of marine organism adhesion compared with the control mixture. No fatality of fish was observed in the fish toxicity test, which suggested that bottom ash aggregate was a harmless material and that the combination of bottom ash aggregate and granular fertiliser with substitution rates of 30% and 10%, respectively, can be effectively used in porous concrete production for marine ranch application.

Sustainability assessment and prioritisation of bottom ash management in Macao.

In Macao, about 7200 t yr-1 of bottom ash (BA) is generated and conventionally landfilled with construction waste. Because the properties of BA are similar to those of natural aggregates, it is suitable to be recycled as construction material. However, pre-treatment processes for BA reuse may require more resource input and may generate additional environmental impacts. Life cycle assessment, multi-media transport model analysis, cost-benefit analysis and the analytical hierarchy process were conducted to evaluate the impacts of current and potential BA management scenarios regarding environmental, economic, social and regulatory aspects. The five analysed scenarios are as follows: (0) BA buried with construction and demolition waste (current system); (1) pre-treated BA used to replace 25% of the natural aggregate in asphalt concrete; (2) pre-treated BA used to replace 25% of the natural aggregate in cement concrete; (3) pre-treated BA used to replace 25% of cement in cement concrete; and (4) pre-treated BA sent to China, blended with municipal solid waste for landfill. The results reveal the following ranking of the scenarios: 3 > 2 > 0 > 1 > 4. Scenario 3 shows the best conditions for BA recycling, because the quantity of cement concrete output is the highest and this brings the greatest economic benefits. Our use of integrated analysis provides multi-aspect investigations for BA management systems, particularly in accounting for site-specific characteristics. This approach is suitable for application in other non-western regions.