Comparative toxicity of coal and coal ash: Assessing biological impacts and potential mechanisms through in vitro and in vivo testing.

BACKGROUND: Coal and coal ash present inorganic elements associated with negative impacts on environment and human health. The objective of this study was to compare the toxicity of coal and coal ash from a power plant, assess their inorganic components, and investigate the biological impacts and potential mechanisms through in vitro and in vivo testing. METHODS: Particle-Induced X-ray Emission method was used to quantify inorganic elements and the toxicity was evaluated in Caenorhabditis elegans and Daphnia magna in acute and chronic procedures. The genotoxic potential was assessed using alkaline and FPG-modified Comet assay in HepG2 cells and mutagenicity was evaluated using Salmonella/microsome assay in TA97a, TA100, and TA102 strains. RESULTS: Inorganic elements such as aluminum (Al) and chromium (Cr) were detected at higher concentrations in coal ash compared to coal. These elements were found to be associated with increased toxicity of coal ash in both Caenorhabditis elegans and Daphnia magna. Coal and coal ash did not induce gene mutations, but showed genotoxic effects in HepG2 cells, which were increased using the FPG enzyme, indicating DNA oxidative damage. CONCLUSIONS: The combined findings from bioassays using C. elegans and D. magna support the higher toxicity of coal ash, which can be attributed to its elevated levels of inorganic elements. The genotoxicity observed in HepG2 cells confirms these results. This study highlights the need for continuous monitoring in areas affected by environmental degradation caused by coal power plants. Additionally, the analysis reveals significantly higher concentrations of various inorganic elements in coal ash compared to coal, providing insight into the specific elemental composition contributing to its increased toxicity.

Environmental impacts of Indian coal thermal power plants and associated human health risk to the nearby residential communities: A potential review.

Worldwide, harmful emissions from coal power plants cause many illnesses contribute to premature deaths burden. Despite its high impact on human health and being a major source of toxic pollutants, coal has been considered a component of global energy for decades. Hence, this work was envisaged to understand the rising environmental and multiple health issues from coal power plants. Studies on the adverse impacts of coal power plants on the environment, including soil, surface water, groundwater and air, were critically evaluated. The health risk from exposure to different pollutants and toxic metals released from the power plant was also demonstrated. The study also highlighted the government initiatives and policies regarding coal power operation and generation. Lastly, the study focused on guiding coal power plant owners and policymakers in identifying the essential cues for the risk assessment and management. The current study found an association between environmental and human health risks due to power generation, which needs intervention from the scientific and medical fields to jointly address public concerns. It is also suggested that future research should concentrate on exposure assessment techniques by integrating source-identification and geographic information systems to assess the health effects of different contaminants from power plants and to mitigate their adverse impact.

Assessing the health risks of coal-burning arsenic-induced skin damage: A 22-year follow-up study in Guizhou, China.

Risk assessment of arsenic-induced skin damage has always received significant global attention. Theories derived from arsenic exposure in drinking water may not be applicable to the coal-burning type to arsenic-exposed area. Furthermore, very few studies have successfully determined the reference value of cumulative arsenic (CA) exposure that leads to specific skin lesions. In this study, we conducted a 22-year follow-up investigation to assess the risk of skin lesions and cancer resulting from long-term, multi-channel arsenic exposure from hazard identification, dose-response assessment, exposure assessment, and risk characterization. The results show that the arsenic exposure can significantly increase the prevalence of skin lesions. For each interquartile range increase of hair arsenic (HA) and CA, the risk of skin damage increased by 1.91 and 3.90 times, respectively. The lower confidence limit of the benchmark dose of HA of arsenic-induced various skin lesions ranged from 0.07 to 0.12 µg·g-1, and 932.57 to 1368.92 mg for CA. The chronic daily intake, lifetime average daily dose in the arsenic-exposed area after the comprehensive prevention and control measures have decreased significantly, but remained higher than the daily baseline level of 3.0 µg·kg-1·d-1. Even as recently as 2020, the hazard quotients and hazard index still exceeded 1, measuring 155.33 and 55.20, and the lifetime excess risk of skin cancer (2.80 × 10-3) remains significantly higher than the acceptable level of 10-6. Our study underscores the effectiveness of comprehensive prevention and control measures in managing high arsenic exposure in coal-burning arsenic poisoning areas. However, it is crucial to acknowledge that the risk of both non-carcinogenic and carcinogenic effects on the skin remains substantially higher than the acceptable level. We recommend setting reference limits for monitoring skin damage among individuals exposed to arsenic, with a recommended upper limit of 0.07 µg·g-1 for HA and a maximum acceptable level of 935.57 mg for CA.

The dangerous link between coal dust exposure and DNA damage: unraveling the role of some of the chemical agents and oxidative stress.

Exposure to coal mining dust poses a substantial health hazard to individuals due to the complex mixture of components released during the extraction process. This study aimed to assess the oxidative potential of residual coal mining dust on human lymphocyte DNA and telomeres and to perform a chemical characterization of coal dust and urine samples. The study included 150 individuals exposed to coal dust for over ten years, along with 120 control individuals. The results revealed significantly higher levels of DNA damage in the exposed group, as indicated by the standard comet assay, and oxidative damage, as determined by the FPG-modified comet assay. Moreover, the exposed individuals exhibited significantly shorter telomeres compared to the control group, and a significant correlation was found between telomere length and oxidative DNA damage. Using the PIXE method on urine samples, significantly higher concentrations of sodium (Na), phosphorus (P), sulfur (S), chlorine (Cl), potassium (K), iron (Fe), zinc (Zn), and bromine (Br) were observed in the exposed group compared to the control group. Furthermore, men showed shorter telomeres, greater DNA damage, and higher concentrations of nickel (Ni), calcium (Ca), and chromium (Cr) compared to exposed women. Additionally, the study characterized the particles released into the environment through GC-MS analysis, identifying several compounds, including polycyclic aromatic hydrocarbons (PAHs) such as fluoranthene, naphthalene, anthracene, 7H-benzo[c]fluorene, phenanthrene, pyrene, benz[a]anthracene, chrysene, and some alkyl derivatives. These findings underscore the significant health risks associated with exposure to coal mining dust, emphasizing the importance of further research and the implementation of regulatory measures to safeguard the health of individuals in affected populations.

The impact of coal mine dust characteristics on pathways to respiratory harm: investigating the pneumoconiotic potency of coals.

Exposure to dust from the mining environment has historically resulted in epidemic levels of mortality and morbidity from pneumoconiotic diseases such as silicosis, coal workers' pneumoconiosis (CWP), and asbestosis. Studies have shown that CWP remains a critical issue at collieries across the globe, with some countries facing resurgent patterns of the disease and additional pathologies from long-term exposure. Compliance measures to reduce dust exposure rely primarily on the assumption that all "fine" particles are equally toxic irrespective of source or chemical composition. For several ore types, but more specifically coal, such an assumption is not practical due to the complex and highly variable nature of the material. Additionally, several studies have identified possible mechanisms of pathogenesis from the minerals and deleterious metals in coal. The purpose of this review was to provide a reassessment of the perspectives and strategies used to evaluate the pneumoconiotic potency of coal mine dust. Emphasis is on the physicochemical characteristics of coal mine dust such as mineralogy/mineral chemistry, particle shape, size, specific surface area, and free surface area-all of which have been highlighted as contributing factors to the expression of pro-inflammatory responses in the lung. The review also highlights the potential opportunity for more holistic risk characterisation strategies for coal mine dust, which consider the mineralogical and physicochemical aspects of the dust as variables relevant to the current proposed mechanisms for CWP pathogenesis.

Toxicity evaluation of polycyclic aromatic hydrocarbons (PAHs) in soils of coal chemical industry areas, North China.

Objectives of this study were to investigate the concentrations, distributions, toxicities, and risk assessment of 16 polycyclic aromatic hydrocarbons in surface soils surrounding a coal chemical industrial zone in the southeast of Shanxi province, China. A total of 52 topsoil samples were collected from different land-use areas: cereal agriculture, roadsides, and parkland. Results show that the total PAHs (∑16PAHs) ranged from 3.87 × 103 to 116 × 103 µg kg-1 and that the total carcinogenicity PAHs (∑BPAHs) ranged from 3.11 × 103 to 94.2 × 103 µg kg-1, with the highest concentration of ∑16PAHs noted in the RS samples, followed by PS and AS. The entire risk quotient of all PAH maximum permissible concentrations (RQ∑PAHMPCi) was greater than 1.0, and the minimum concentration entire risk quotient (RQ∑PAHNCi) of 84.3% of all samples was higher than 800. The value of the total toxicity equivalent concentration of PAH (PAHBapeq) for areas surrounding the coal chemical industrial zone was higher than the value of the standard level, and the incremental lifetime cancer risk (ILCR) far exceeds the U.S. EPA's risk standard. The toxic properties of PAHs indicated that the soils in the survey areas have a high risk to human health and the environment.

Association between cooking fuel and folate insufficiency among pregnant women in Northern China.

This study explored whether using a coal or biomass stove for cooking was associated with a greater risk of red blood cell (RBC) folate insufficiency among pregnant women compared to using clean energy. A researcher-designed questionnaire was used to collect information on exposure-related factors and confounding factors. RBC folate concentrations were examined by microbiological assay. Binary logistic regression analysis was used to identify factors related to RBC folate insufficiency. The use of coal or firewood for cooking was associated with an increased risk of RBC folate insufficiency (<906 nmol/L) compared to gas. In subgroup analyses, associations between the use of polluting cooking fuels and folate insufficiency were positive for both urban and rural residents and statistically significant for rural women. Efforts to promote the use of clean energy and proper ventilation, especially in rural areas, are recommended to improve the health of pregnant women and their offspring.

Exosomal miRNAs contribute to coal dust particle-induced pulmonary fibrosis in rats.

Coal workers' pneumoconiosis (CWP) is a fatal occupational disease caused by inhalation of coal dust particles, which leads to progressive pulmonary fibrosis. Recently, as new signal carriers for intercellular communication, exosomal miRNAs have been validated in the pathogenesis of multiple diseases. However, the research on exosomal miRNAs in CWP is still in the preliminary stage. Here, using miRNA sequencing, exosomal miRNA profiles in bronchoalveolar lavage fluid (BALF) from rats with pulmonary fibrosis induced by coal dust particles were analyzed, and the underlying biological function of putative target genes was explored by GO term analysis and KEGG pathway enrichment analysis. According to the results, intratracheal instillation of coal dust particles can alter the exosomal miRNAs expression in the BALF of rats. Further bioinformatics analysis provided some clues to reveal their function in pathological process of pneumoconiosis. More importantly, we identified 4 differentially expressed exosomal miRNAs (miRNA-21-5p, miRNA-29a-3p, miRNA-26a-5p, and miRNA-34a-5p) by qRT­PCR and further verified the temporal changes in the expression of these exosomal miRNAs in animal models from 2 weeks to 16 weeks postexposure. In addition, we conducted a preliminary study on Smad7 as a potential target of miRNA-21-5p and found that exosomal miRNA 21-5p/Smad7 may contribute to the pulmonary fibrosis induced by coal dust particles. Our study confirmed the contribution of exosomal miRNAs to coal dust particle-induced pulmonary fibrosis and provided new insights into the pathogenesis of CWP.

Differences in the characteristics and pulmonary toxicity of nano- and micron-sized respirable coal dust.

BACKGROUND: The characteristics of coal dust (CD) particles affect the inhalation of CD, which causes coal worker's pneumoconiosis (CWP). CD nanoparticles (CD-NPs, < 500 nm) and micron particles (CD-MPs, < 5 µm) are components of the respirable CD. However, the differences in physicochemical properties and pulmonary toxicity between CD-NPs and CD-MPs remain unclear. METHODS: CD was analyzed by scanning electron microscopy, Malvern nanoparticle size potentiometer, energy dispersive spectroscopy, infrared spectroscopy, and electron paramagnetic resonance spectroscopy. CCK-8 assay, ELISA, transmission electron microscope, JC-1 staining, reactive oxygen species activity probe, calcium ion fluorescent probe, AO/EB staining, flow cytometry, and western blot were used to determine the differences between CD-NPs and CD-MPs on acute pulmonary toxicity. CCK-8, scratch healing and Transwell assay, hematoxylin-eosin and Masson staining, immunohistochemistry, immunofluorescence, and western blot were applied to examine the effects of CD-NPs and CD-MPs on pneumoconiosis. RESULTS: Analysis of the size distribution of CD revealed that the samples had been size segregated. The carbon content of CD-NPs was greater than that of CD-MPs, and the oxygen, aluminum, and silicon contents were less. In in vitro experiments with A549 and BEAS-2B cells, CD-NPs, compared with CD-MPs, had more inflammatory vacuoles, release of pro-inflammatory cytokines (IL-6, IL-1ß, TNFα) and profibrotic cytokines (CXCL2, TGFß1), mitochondrial damage (reactive oxygen species and Ca2+ levels and decreased mitochondrial membrane potential), and cell death (apoptosis, pyroptosis, and necrosis). CD-NPs-induced fibrosis model cells had stronger proliferation, migration, and invasion than did CD-MPs. In in vivo experiments, lung coefficient, alveolar inflammation score, and lung tissue fibrosis score (mean: 1.1%, 1.33, 1.33) of CD-NPs were higher than those of CD-MPs (mean: 1.3%, 2.67, 2.67). CD-NPs accelerated the progression of pulmonary fibrosis by upregulating the expression of pro-fibrotic proteins and promoting epithelial-mesenchymal transition. The regulatory molecules involved were E-cadherin, N-cadherin, COL-1, COL-3, ZO-1, ZEB1, Slug, α-SMA, TGFß1, and Vimentin. CONCLUSIONS: Stimulation with CD-NPs resulted in more pronounced acute and chronic lung toxicity than did stimulation with CD-MPs. These effects included acute inflammatory response, mitochondrial damage, pyroptosis, and necrosis, and more pulmonary fibrosis induced by epithelial-mesenchymal transition.

Oxidative stress and alterations in the expression of genes related to inflammation, DNA damage, and metal exposure in lung cells exposed to a hydroethanolic coal dust extract.

BACKGROUND: Open cast mining is well known as a concerning source of environmental and public health problems. This work aimed to obtain a hydroethanolic coal dust extract (≤ 38 µm) and to characterize its composition with particular regard to content of organic compounds by GC/MS, as well as describe its toxicity in vitro on Calu-1 after exposure to several concentrations (0-500 µg/mL). MATERIALS AND RESULTS: Cytotoxicity was measured with MTT assay and DCFH-DA probe was employed to estimate the amount of reactive oxygen species (ROS) in Calu-1 cells. RT-PCR was employed to quantify relative expression of genes associated with inflammation, oxidative stress, as well as metals, and lipid metabolism. Seventeen organic compounds were identified in the extract, highlighting undecane, dodecane, pentadecane and benzo[a]anthracene, 6,12-dimethyl-1,2,3,4-tetrahydro-. Cytotoxicity test showed a decrease trend in the cell viability after 24 h hours from the concentration of 62.5 µg/mL. Further, the extract raised intracellular ROS when compared with control. Expression levels of CYP1A1, IL-8, IL-6, MT1X, and NQO1 were up-regulated when cells were exposed to 125 µg/mL of coal dust, whereas PPAR-α was down-regulated, likely involving aryl hydrocarbon receptor regulation. CONCLUSIONS: In short, this study shows that despite hydroethanolic coal dust extract is not cytotoxic to Calu-1 cells, it produces an elevation of intracellular ROS and alters the expression in marker genes of oxidative stress, inflammation, metal transport, xenobiotic and lipid metabolism. These findings suggest that chemicals present in coal dust are biologically active and may interfere key biochemical process in the living organisms.

Elucidation of alveolar macrophage cell response to coal dusts: Role of ferroptosis in pathogenesis of coal workers' pneumoconiosis.

Causal factors underlying coal workers' pneumoconiosis (CWP) have been variously attributed to the presence of carbon, crystalline silica and reduced iron (Fe) minerals, especially pyrite and Fe/Si-amorphous compounds. The aim of this research was to assess the role of iron in CWP and, more specifically, the cytotoxicity of coal dusts with different elemental composition towards alveolar macrophages (AMs). Survival rate of AMs, alteration in the production of pro-inflammatory cytokine TNF-α, MDA (the lipid peroxidation product) and intracellular GSH were assessed using commercial assay kits. The quantitative interaction between iron and GSH was investigated by developing a numerical model. The presence of various reduced Fe minerals (viz. pyrite and siderite) in coal dusts exhibited a consistently acute adverse impact on the viability of AMs and enhanced the production of TNF-α. The presence of the clinically available Fe chelator deferiprone (DFP) and the cytosolic antioxidant glutathione (GSH) significantly increased the viability of AMs exposed to Fe bearing coal dusts, suggesting coal dusts containing reduced Fe minerals were likely contributors to the initial stages of AM cytotoxicity via a ferroptosis related pathway. Chemical kinetic modeling indicated that these results may be attributed to an enhanced consumption of GSH as a result of Fe redox cycling. FeIIGSH and GS• produced from the interaction between ferric Fe and GSH facilitated the production of O2•- which further oxidized GSH via a direct reaction between GSH and GS• or GSO•. These results suggest that coal dusts containing reduced Fe minerals and Fe compounds may elevate acute inflammation levels in AMs, indicating that crystalline silica may not be the only hazard of concern in mining environments.

Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies.

BACKGROUND: Coal dust particles (CDP), an inevitable by-product of coal mining for the environment, mainly causes coal workers' pneumoconiosis (CWP). Long-term exposure to coal dust leads to a complex alternation of biological processes during regeneration and repair in the healing lung. However, the cellular and complete molecular changes associated with pulmonary homeostasis caused by respiratory coal dust particles remain unclear. METHODS: This study mainly investigated the pulmonary toxicity of respirable-sized CDP in mice using unbiased single-cell RNA sequencing. CDP (< 5 µm) collected from the coal mine was analyzed by Scanning Electron Microscope (SEM) and Mass Spectrometer. In addition, western blotting, Elisa, QPCR was used to detect gene expression at mRNA or protein levels. Pathological analysis including HE staining, Masson staining, immunohistochemistry, and immunofluorescence staining were performed to characterize the structure and functional alternation in the pneumoconiosis mouse and verify the reliability of single-cell sequencing results. RESULTS: SEM image and Mass Spectrometer analysis showed that coal dust particles generated during coal mine production have been crushed and screened with a diameter of less than 5 µm and contained less than 10% silica. Alveolar structure and pulmonary microenvironment were destroyed, inflammatory and death (apoptosis, autophagy, and necrosis) pathways were activated, leading to pneumoconiosis in post 9 months coal dust stimulation. A distinct abnormally increased alveolar type 2 epithelial cell (AT2) were classified with a highly active state but reduced the antimicrobial-related protein expression of LYZ and Chia1 after CDP exposure. Beclin1, LC3B, LAMP2, TGF-ß, and MLPH were up-regulated induced by CDP, promoting autophagy and pulmonary fibrosis. A new subset of macrophages with M2-type polarization double expressed MLPH + /CD206 + was found in mice having pneumoconiosis but markedly decreased after the Vitamin D treatment. Activated MLPH + /CD206 + M2 macrophages secreted TGF-ß1 and are sensitive to Vitamin D treatment. CONCLUSIONS: This is the first study to reconstruct the pathologic progression and transcriptome pattern of coal pneumoconiosis in mice. Coal dust had obvious toxic effects on lung epithelial cells and macrophages and eventually induced pulmonary fibrosis. CDP-induced M2-type macrophages could be inhibited by VD, which may be related to the alleviation of the pulmonary fibrosis process.

Chronic Obstructive Pulmonary Disease in Adults Exposed to Fine Particles from a Coal Mine Fire.

Rationale: In 2014, the Hazelwood open-cut coal mine in southeastern Australia burned for 6 weeks, exposing nearby residents to high concentrations of fine particulate matter (PM2.5). The long-term health consequences are unknown and are being evaluated as part of the Hazelwood Health Study. Objectives: To explore the association between PM2.5 exposure and chronic obstructive pulmonary disease (COPD). Methods: A sample of 346 exposed and 173 unexposed adults participated in the longitudinal Respiratory Stream of the Hazelwood Health Study. Participants underwent spirometry and gas transfer measurements and answered validated respiratory questionnaires 3.5-4 years after the fire. Individual-level mine fire-related PM2.5 exposure was modeled. Multivariate linear regression and logistic models were fitted to analyze associations between mean and peak PM2.5 exposure and clinical outcomes, stratified by smoking status. Results: A 10 µg/m3 increase in mean PM2.5 exposure was associated with a 69% (95% confidence interval [CI], 11-158%) increase in odds of spirometry consistent with COPD among nonsmokers and increased odds of chest tightness (odds ratio [OR], 1.30; 95% CI, 1.03-1.64) and chronic cough (OR, 1.24; 95% CI, 1.02-1.51) in the previous 12 months in all participants. For current smokers, increments in mean PM2.5 exposure were associated with higher odds of chronic cough in the preceding 12 months (OR, 2.13; 95% CI, 1.24-3.65). Conclusions: Almost 4 years after a 6-week period of coal fire PM2.5 exposure, we identified a dose-response association between exposure and COPD in nonsmokers. With climate change a likely contributor to increased risk of landscape fires, the findings will inform policy decisions during future sustained smoke events.

Proximity to coal-fired power plants and neurobehavioral symptoms in children.

BACKGROUND: Coal-fired power plants are a major source of air pollution that can impact children's health. Limited research has explored if proximity to coal-fired power plants contributes to children's neurobehavioral disorders. OBJECTIVE: This community-based study collected primary data to investigate the relationships of residential proximity to power plants and neurobehavioral problems in children. METHODS: 235 participants aged 6-14 years who lived within 10 miles of two power plants were recruited. Exposure to particulate matter ≤10 µm (PM10) was measured in children's homes using personal modular impactors. Neurobehavioral symptoms were assessed using the Child Behavior Checklist (CBCL). Multiple regression models were performed to test the hypothesized associations between proximity/exposure and neurobehavioral symptoms. Geospatial statistical methods were used to map the spatial patterns of exposure and neurobehavioral symptoms. RESULTS: A small proportion of the variations of neurobehavioral problems (social problems, affective problems, and anxiety problems) were explained by the regression models in which distance to power plants, traffic proximity, and neighborhood poverty was statistically associated with the neurobehavioral health outcomes. Statistically significant hot spots of participants who had elevated levels of attention deficit hyperactivity disorder, anxiety, and social problems were observed in the vicinity of the two power plants. SIGNIFICANCE: Results of this study suggest an adverse impact of proximity to power plants on children's neurobehavioral health. Although coal-fired power plants are being phased out in the US, health concern about exposure from coal ash storage facilities remains. Furthermore, other countries in the world are increasing coal use and generating millions of tons of pollutants and coal ash. Findings from this study can inform public health policies to reduce children's risk of neurobehavioral symptoms in relation to proximity to power plants.

Review on Health Impacts from Domestic Coal Burning: Emphasis on Endemic Fluorosis in Guizhou Province, Southwest China.

Endemic fluorosis in Guizhou Province, Southwest China was firstly reported by Lyth in 1946 and was extensively concerned since the early 1980s. Initially, the pathological cause of endemic fluorosis in Guizhou Province was instinctively ascribed to the drinking water. However, increasing evidences pointed that the major exposure route of fluorine for the local residents is via the roasted foodstuffs, especially the roasted pepper and corn. Source of fluorine in roasted foodstuffs was once blamed on the local coal and subsequently imputed to clay mixed in the coal. In fact, both are probably the source. Geogenic fluorine concentration in soil and clay is indeed high in Guizhou Province, but is not likely to be the direct cause for endemic fluorosis. The real culprit for endemic fluorosis in Guizhou Province is the unhealthy lifestyle of the local residents, who usually roasted their foodstuffs using local coal or briquettes (a mixture of coal and clay), resulting in the elevated fluorine in roasted foodstuffs. Nowadays, endemic fluorosis in Guizhou Province has substantially mitigated. Nevertheless, millions of confirmed cases of dental fluorosis remain left. In addition to endemic fluorosis, other health problems associated with domestic coal burning may also exist, because of the enrichment of toxic/harmful elements in the local coal. It is necessary to determine how serious the situation is and find out the possible solution. As people in other developing countries may suffer from similar health issues, same health issues around the world deserve more attention.

Pathomorphological Changes in the Brain in Dynamics of Long-Term Dust Exposure.

Histological and morphometric studies of brain autopsy material showed that the development of hypoxic changes in miners starts at the early stages of working in the dusty atmosphere. Edema of the pericellular and perivascular zones and the pia mater, degenerative changes in some nerve cells and even their loss and formation of gliosis foci were identified. The revealed changes in neurons progressed with increasing the duration of working under hazardous conditions.

Genetic damage in coal and uranium miners.

Mining has a direct impact on the environment and on the health of miners and is considered one of the most hazardous occupations worldwide. Miners are exposed to several occupational health risks, including genotoxic substances, which may cause adverse health effects, such as cancer. This review summarizes the relation between DNA damage and mining activities, focusing on coal and uranium miners. The search was performed using electronic databases, including original surveys reporting genetic damage in miners. Additionally, a temporal bibliometric analysis was performed using an electronic database to create a map of cooccurrence terms. The majority of studies were performed with regard to occupational exposure to coal, whereas genetic damage was assessed mainly through chromosomal aberrations (CAs), micronuclei (MNs) and comet assays. The bibliometric analysis demonstrated associations of coal exposure with silicosis and pneumoconiosis, uranium miners with lung cancer and tumors and some associated factors, such as age, smoking, working time and exposure to radiation. Significantly higher DNA damage in miners compared to nonexposed groups was observed in most of the studies. The timeline reveals that classic biomarkers (comet assay, micronucleus test and chromosomal aberrations) are still important tools to assess genotoxic/mutagenic damage in occupationally exposed miners; however, newer studies concerning genetic polymorphisms and epigenetic changes in miners are being conducted. A major challenge is to investigate further associations between miners and DNA damage and to encourage further studies with miners of other types of ores.

Evaluation of soils under the influence of coal mining and a thermoelectric plant in the city of Candiota and vicinity, Brazil.

Coal burning generates gases, particles, and condensation by-products that are harmful to soil, water, and to the atmosphere. The aim of this study was to characterize and identify the cytotoxic and mutagenic potential of soil samples from the cities of Aceguá, Bagé, Candiota and Pinheiro Machado, near a large coal-fired power plant. Our study describes soil characteristics and contributes to the evaluation of the genotoxic activity of coal mining and burning, using the Comet Assay and Micronucleus test in V79 cells, as well as mutagenicity assays with Salmonella typhimurium strains. Comet Assay results show that the winter soil samples of Candiota and Pinheiro Machado induced a significant increase of the Damage Index for cells, as well as for the Aceguá summer sample. The micronucleus test did not detect differences between cities and seasons. A component analysis indicates associations between results obtained in Comet Assay and Ti and phenanthene concentrations for Pinheiro Machado during the winter, and Al for Aceguá during the summer and Zn during the winter. Results of Salmonella/microsome assays were negative, only Candiota and Pinheiro Machado samples showed a statistical increase of his + colonies in TA102. Our work describes biological data on these cells exposed to coal-contaminated soil, confirming the sensitivity of the Comet Assay in V79 cells and Salmonella/microsome assay for the evaluation of the effects of complex mixtures. These findings help to understand the spatial distribution of contaminants in the local soil related to a power plant, which is important for planning public safety actions.

[Emission Characteristics and Toxicity Effects of Halogenated Polycyclic Aromatic Hydrocarbons from Coal-Fired and Waste Incineration Power Plants].

Coal-fired power plants (CFPPs) and waste incineration power plants (WIPPs) represent a large portion of polycyclic aromatic hydrocarbons (PAHs) sources in the environment, among which halogenated PAHs (HPAHs) are more toxic to the human body compared with their corresponding parent PAHs. In the current work, we investigated the occurrence, formation mechanism, and toxicity effects of HPAHs in the coal and waste combustion products from three CFPPs and one WIPP. The results indicate that the contents of chlorinated PAHs (Cl-PAHs) in the fly ash from the CFPPs and WIPP were 1.06-1.67 ng·g-1 and 2.76 ng·g-1, respectively, and the contents of brominated PAHs (Br-PAHs) in the fly ash from the CFPPs and WIPP were 26.4-44.2 ng·g-1 and 6.31 ng·g-1, respectively. The HPAH contents in the fly ash from the WIPP were significantly higher than those from the CFPPs primarily due to the abundant plastics in the domestic waste, represented by polyvinyl chloride, resulting in the formation of Cl-PAHs during combustion. The HPAH contents in the fly ash from the pulverized coal-fired (PC) boiler were significantly higher than those from the circulating fluidized bed (CFB) boiler mostly due to the higher combustion temperature operated in the PC boiler. The HPAHs in the fly ash from coal combustion were predominantly 7-BrBaA and 9-ClPhe, and those from domestic combustion were predominantly 9-BrPhe and 2-ClAnt. In addition, the contents of 7-BrBaA and 9,10-Br2 Ant in the coal combustion fly ash were significantly higher than those in domestic waste combustion fly ash, whereas 2-BrFle exhibited a contrasting profile. The content of Br-PAHs in the fly ash treated by semi-dry deacidification was twice that in dust removal fly ash but significantly increased in the chelating agent stabilization fly ash. The Pearson correlation analysis indicated the the formation mechanism of Cl-PAHs and Br-PAHs were the same but a secondary formation of HPAHs during the chelating agent stabilization of the fly ash was deduced. The TEQ values of the HPAHs in the fly ash (8.87×10-3-15.0×10-3 ng·g-1) from the WIPP were similar to those in the fly ash from the CFPPs (10.0×10-3 ng·g-1), which were significantly reduced in the fly ash treated by semi-dry deacidification due to the removal of 7-BrBaA. Moreover, the TEQ values of the HPAHs in the fly ash increased 5.4 times after the chelating agent stabilization. The ecological risk should be considered for the CFPP fly ash due to their massive amount of discharge and high TEQ values.

Public health impact of coal-fired power plants: a critical systematic review of the epidemiological literature.

Coal-based energy production is the most utilized method of electricity production worldwide and releases the highest concentration of gaseous, particulate, and metallic pollutants. Toxicological research has shown that coal combustion by-products are carcinogens, endocrine disruptors, and cardiorespiratory toxins. This article aims to systematically review the epidemiological literature on the impact emissions from coal-based power production has on morbidity and mortality worldwide. Two thousand one hundred and fifty-two articles were retrieved based on search criteria. Word search of abstract and article text filtered the results to 95 articles. Forty articles were included after screening. The literature indicates a significant adverse effect from particulate matter and polyaromatic hydrocarbon emissions on morbidity and mortality. There is a lack of consistency of exposure assessment and inadequate control of significant potential confounders such as social economic status. Future research should focus on improving exposure assessment models, specifically source-apportionment and geographic information system methods to model power plant-specific emissions.