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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., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

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., (© 2023. The Author(s).)

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., (© 2023. The Author(s).)

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 (∑ 16 PAHs) ranged from 3.87 × 10 3 to 116 × 10 3  µg kg -1 and that the total carcinogenicity PAHs (∑BPAHs) ranged from 3.11 × 10 3 to 94.2 × 10 3  µg kg -1 , with the highest concentration of ∑ 16 PAHs noted in the RS samples, followed by PS and AS. The entire risk quotient of all PAH maximum permissible concentrations (RQ∑PAH MPCi ) was greater than 1.0, and the minimum concentration entire risk quotient (RQ∑PAH NCi ) 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., (© 2022. The Author(s), under exclusive licence to Springer Nature B.V.)

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.

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 qRT‑PCR 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., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

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-1β, TNFα) and profibrotic cytokines (CXCL2, TGFβ1), mitochondrial damage (reactive oxygen species and Ca 2+ 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, TGFβ1, 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., (© 2022. The Author(s).)

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., (© 2022. The Author(s), under exclusive licence to Springer Nature B.V.)

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. Fe II GSH and GS • produced from the interaction between ferric Fe and GSH facilitated the production of O 2 • - 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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

The objective of this study was to estimate the association between residence in coal mining environments and low birth weight. We conducted a cross-sectional, retrospective analysis of the association between low birth weight and mother's residence in coal mining areas in West Virginia. Birth data were obtained from the West Virginia Birthscore Dataset, 2005-2007 ( n = 42,770). Data on coal mining were from the US Department of Energy. Covariates regarding mothers' demographics, behaviors, and insurance coverage were included. We used nested logistic regression (SUDAAN Proc Multilog) to conduct the study. Mothers who were older, unmarried, less educated, smoked, did not receive prenatal care, were on Medicaid, and had recorded medical risks had a greater risk of low birth weight. After controlling for covariates, residence in coal mining areas of West Virginia posed an independent risk of low birth weight. Odds ratios for both unadjusted and adjusted findings suggest a dose-response effect. Adjusted findings show that living in areas with high levels of coal mining elevates the odds of a low-birth-weight infant by 16%, and by 14% in areas with lower mining levels, relative to counties with no coal mining. After covariate adjustment, the persistence of a mining effect on low-birth-weight outcomes suggests an environmental effect resulting from pollution from mining activities. Air and water quality assessments have been largely missing from mining communities, but the need for them is indicated by these findings. [ABSTRACT FROM AUTHOR]

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 (PM 2.5 ). The long-term health consequences are unknown and are being evaluated as part of the Hazelwood Health Study. Objectives: To explore the association between PM 2.5 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 PM 2.5 exposure was modeled. Multivariate linear regression and logistic models were fitted to analyze associations between mean and peak PM 2.5 exposure and clinical outcomes, stratified by smoking status. Results: A 10 μg/m 3 increase in mean PM 2.5 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 PM 2.5 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 PM 2.5 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.

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-β1 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., (© 2022. The Author(s).)

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 (PM 10 ) 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., (© 2021. The Author(s), under exclusive licence to Springer Nature America, Inc.)

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.

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., (Copyright © 2021 Elsevier B.V. All rights reserved.)

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., (Copyright © 2021. Published by Elsevier B.V.)

Although coal tar pitch (CTP) has a large yield in China, its large-scale and effective utilization is significantly hindered because of existing and possibly releasing polycyclic aromatic hydrocarbons (PAHs). Therefore, it is an imminent problem how to prepare an environmentally friendly CTP by detoxification modification. In the investigation, a typical CTP was subjected to structural characterization via solid-state 13 C NMR and gas chromatograph/mass spectrometer, which confirmed the existence of dominant PAHs such as fluoranthene, pyrene, as well as benzo[a]pyrene, and few heterocyclic compounds. Subsequently, the CTP was modified using 10-undecenal via alkylation reaction enhanced by ultraviolet & microwave radiation. Compared with the original CTP, the total content of 16 toxic PAHs in the modified CTP decreased with a reduction efficiency of above 90%. According to different environmental standards, toxic equivalent quotient of CTP after modification was reduced by above 90%. In order to veritably and fully evaluate the toxicity of CTP, a living vascular smooth muscle cell (A-10 cell) in vitro was used in the cell counting kit-8 assay. The viability of A-10 cell was always higher when exposed to modified CTP than the original CTP. These results powerfully indicated that the enhanced modification was actually effective and efficient for reducing the toxicity of CTP., (Copyright © 2020. Published by Elsevier B.V.)

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.

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-Br 2 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.

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., (© 2021. The Author(s), under exclusive license to Springer Nature Switzerland AG.)

The exploitation of coal is an important resource to generate energy worldwide. However, during the processes of coal extraction, transport, and cargo, dust particles are released into the environment. The aim of this study was to determine the toxicological effects of bituminous coal dust (<38 µm), obtained from a sample collected in a coal mine in Colombia, on the annelid Eisenia fetida. The earthworm culture was standardized under laboratory conditions to evaluate mortality, as well as morphological, physiological and histological changes using concentrations varying from 1 to 4% w/w coal dust in artificial soil, after 7, 14, and 28 days of exposure. In addition, an avoidance assay was carried out after 48-h treatment. Histopathological analysis was performed at the end of the experiment. After the sub-chronic exposure, an increase in mortality was observed at the highest coal dust concentration compared to the untreated group. Alterations in morphology and physiology of the exposed annelids were mostly evidenced at the greatest tested concentrations (3-4%) and exposure times (≥14 days). Changes included loss of weight and color, abundant mucus production, constriction, peeling of the epidermis, clitellum involution, violent movements and lethargy. Avoidance of coal dust-polluted soil followed a concentration-response relationship. Histopathological findings revealed changes on the cuticle, as well as in the circular and longitudinal muscle layers in animals living in soils containing 3 and 4% coal particles. In short, E. fetida exposed to coal dust experienced several pathological changes, suggesting that this pollutant may induce population problems in macroinvertebrates present in coal mining areas.

Lung cancer is the leading cause of cancer death worldwide. The Xuanwei-Fuyuan (XF) region of Yunnan, China has a high incidence of lung cancer from coal-related pollution. Effort to raise public awareness screening for lung cancer has been ongoing. We retrospectively analyzed overall survival (OS) of lung cancer patients of a tertiary cancer center in Yunnan to investigate screening and regional residential status as predictive factors. Consecutive cases of newly diagnosed lung cancer were reviewed. The lung cancer cases diagnosed by screening were more likely to be early-staged and treated by surgery than those diagnosed not by screening. In patients diagnosed not by screening, XF residential status was a significant predictor of improved OS. Frailty model detected significant heterogeneity associated with region of residence in unscreened patients. Potential biases associated with screening were examined by Monte Carlo simulations and sensitivity analyses. Focused effort in cancer screening and increased public awareness of pollution-related lung cancer in XF might have led to early diagnosis and improved OS, and increased investment in health care resources in high risk areas may have produced additional unobserved factors that underlay the association of XF residential status with improved OS in patients diagnosed not by screening.

Outdoor air pollution is a growing public health concern, particularly in urban settings. However, there are limited epidemiological data on outdoor air pollution in rural areas with substantial levels of air pollution attributed to solid fuel burning for household cooking and heating. Xuanwei and Fuyuan are rural counties in China where the domestic combustion of locally sourced bituminous ("smoky") coal has been associated with the highest lung cancer rates in China. We previously assessed indoor and personal air pollution exposures in this area; however, the influence of indoor coal combustion and household ventilation on outdoor air pollution has not been assessed. Therefore, we measured outdoor fine particulate matter (PM 2.5 ), species of polycyclic aromatic hydrocarbons (PAHs) including naphthalene (NAP) and the known carcinogen benzo(a)pyrene (BaP), sulfur dioxide (SO 2 ), and nitrogen dioxide (NO 2 ) over two consecutive 24-h sampling periods in 29 villages. Just over half of the villages were revisited two to nine months after the initial sampling period to repeat all measurements. The overall geometric mean (GM) of outdoor PM 2.5 , BaP, NAP, and NO 2 were 45.3 µg/m 3 , 9.7 ng/m 3 , 707.7 ng/m 3 , and 91.5 µg/m 3 , respectively. Using linear mixed effects models, we found that burning smoky coal was associated with higher outdoor BaP concentrations [GM ratio (GMR) = 2.79] and lower outdoor SO 2 detection rates (GMR = 0.43), compared to areas burning smokeless coal. Areas with predominantly ventilated stoves (> 50% of stoves) had higher outdoor BaP (GMR = 1.49) compared to areas with fewer ventilated stoves. These results show that outdoor air pollution in a rural region of China was associated with the type of coal used for cooking and heating indoors and the presence of stove ventilation. Our findings suggest that efforts of household stove improvement to reduce indoor air pollution have resulted in higher outdoor air pollution levels. Further reducing adverse health effects in rural villages from household coal combustion will require the use of cleaner fuel types.

Objective: To evaluate whether vascular health in young children was associated with exposure to a 6-week episode of coal mine fire smoke or environmental tobacco smoke (ETS) in a retrospective cohort study., Methods: Three years after a coal mine fire in Victoria, Australia, we investigated the vascular health of children either in utero (n=75) or aged <2 years (postnatal exposure, n=96) at the time of the fire. The outcomes were the carotid intima-media thickness (IMT) and pulse wave velocity (PWV). The mean and peak daily particulate matter <2.5 µm in diameter (PM 2.5 ) exposures were estimated based on their daily locations throughout the fire period. Multivariable linear regression models were used to test for associations between the fire-related PM 2.5 and outcomes adjusted for relevant covariates including ETS., Results: In the postnatal-exposure group, each 10 µg/m³ increase in mean PM 2.5 level was independently positively associated with PWV (β=0.116, p=0.028). When these two groups were combined, there was an association between mean PM 2.5 and increased PWV in those children who had ETS exposure (β=0.148, p=0.033) or whose mothers smoked (β=0.151, p=0.011), but not in those not exposed to ETS or maternal smoking., Conclusions: Three years after a coal mine fire, infants aged up to 2 years at the time of exposure have increases in vascular stiffness. Although no adverse effects were observed in the in uterus exposure group, further follow-up study is needed to elucidate the long-term effects of coal mine fire smoke exposure., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

This study aimed to verify possible alterations involving histological and oxidative stress parameters in the lungs of wild bats in the Carboniferous Basin of Santa Catarina (CBSC) state, Southern Brazil, as a means to evaluate the impact of coal dust on the health of wildlife. Specimens of frugivorous bat species Artibeus lituratus and Sturnira lilium were collected from an area free of coal dust contamination and from coal mining areas. Chemical composition, histological parameters, synthesis of oxidants and antioxidant enzymes, and oxidative damage in the lungs of bats were analyzed. Levels of Na, Cl, Cu, and Br were higher in both species collected in the CBSC than in the controls. Levels of K and Rb were higher in A. lituratus, and levels of Si, Ca, and Fe were higher in S. lilium collected in the carboniferous basin. Both bat species inhabiting the CBSC areas exhibited an increase in the degree of pulmonary emphysema compared to their counterparts collected from control areas. Sturnira lilium showed increased reactive oxygen species (ROS) and 2',7'-dichlorofluorescein (DCF) levels, while A. lituratus showed a significant decrease in nitrite levels in the CBSC samples. Superoxide dismutase (SOD) activity did not change significantly; however, the activity of catalase (CAT) and levels of glutathione (GSH) decreased in the A. lituratus group from CBSC compared to those in the controls. There were no differences in NAD(P)H quinone dehydrogenase 1 protein (NQO1) abundance or nitrotyrosine expression among the different groups of bats. Total thiol levels showed a significant reduction in A. lituratus from CBSC, while the amount of malondialdehyde (MDA) was higher in both A. lituratus and S. lilium groups from coal mining areas. Our results suggested that bats, especially A. lituratus, living in the CBSC could be used as sentinel species for harmful effects of coal dust on the lungs., Competing Interests: Declaration of competing interest The authors declare that there are no conflicts of interest., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Coal dust is a primary air contaminant from coal mining operations that produces harmful health effects. However, it is unclear to what extent its detrimental properties would impact future generations, and whether alterations in the progenies might be concentration-dependent. The aim of this study was to determine the intergenerational effects of chronic exposure to coal dust on the red flour beetle, Tribolium castaneum (Herbst) (Coleoptera: Tenebrionidae), at three life stages. Groups of fifty adult insects were exposed during 30 days at different concentrations of coal dust mixed with ground oats as food substrate (0, 0.25, 0.5, 1.0 and 2.0% weight/weight), both with a particle size <38 μm. The LC 50 for F0 insects was 1.07%, whereas for larvae and adults from F1, values were 0.53 and 0.89%, respectively. Pathological findings assessed at F1 revealed a coal dust concentration-dependent frequency of several morphological abnormalities, including larvae without antenna or extremities, lack of T1, T2, T3 legs, loss of urogomphi, and the presence of abnormal protuberances. It was found that a considerable number of F1 larvae derived from parental beetles did not achieve a complete conversion into the next growth stage. Pupae with undeveloped eyes and adults with malformed elytra, as well as necrosis, were recurrently observed at high concentrations. Finally, adults exposed to 1% coal dust overexpressed genes related to oxidative stress (nuclear factor erythroid 2-related factor 2, Nrf2) and synaptic transmission (GABA-gated ion channel, Grd). In short, coal dust particles induced intergenerational effects on T. castaneum, highlighting the need to further study the impact of this airborne pollutant on wildlife and human populations., Competing Interests: Declaration of competing interest The authors have no conflicts of interest to disclose., (Copyright © 2019. Published by Elsevier Inc.)

Coal plants represent one of the main sources of environmental pollution due to the combustion process of this mineral and the consequent release of gases and particles which, in significant quantities, can lead to a potential risk to health and the environment. The susceptibility of individuals to the genotoxic effects of coal mining can be modulated by genetic variations in the xenobiotic detoxification and DNA repair processes. The aim of this study was to evaluate if xenobiotic metabolism polymorphism, base excision repair polymorphisms and non-homologous end joining repair polymorphism, could modify individual susceptibility to genomic instability and epigenetic alterations induced in workers by occupational exposure to coal. In this study, polymerase chain reaction was used to examine the polymorphic sites. The sample population comprising 70 coal mine workers and 71 workers non-exposed to coal. Our results demonstrated the effect of individual genotypes on different biomarkers evaluated. Significant decrease in % of global DNA methylation were observed in CYP1A1 Val/- exposed individuals compared to CYP1A1 Ile/Ile individuals. Coal workers who carried the XRCC4 Ile/Ile genotype showed decrease NBUD frequencies, while the XRCC4 Thr/- genotype was associated with decrease in Buccal micronucleus cells for the group not exposed. No influence of GSTM1 null, GSTT1 null, GSTP1 Ile105Val, hOGG1 Ser326Cys, XRCC1 Arg194Trp polymorphisms was observed. Thus, the current study reinforces the importance of considering the effect of metabolizing and repair variant genotypes on the individual susceptibility to incorporate DNA damage, as these processes act in a coordinated manner to determine the final response to coal exposure., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: Gestational cadmium exposure may impair fetal growth. Coal smoke has largely been unexplored as a source of cadmium exposure. We investigated the relationship between gestational cadmium exposure and fetal growth, and assessed coal smoke as a potential source of airborne cadmium, among non-smoking pregnant women in Ulaanbaatar, Mongolia, where coal combustion in home heating stoves is a major source of outdoor and indoor air pollution., Methods: This observational study was nested within the Ulaanbaatar Gestation and Air Pollution Research (UGAAR) study, a randomized controlled trial of portable high efficiency particulate air (HEPA) filter air cleaner use during pregnancy, fetal growth, and early childhood development. We measured third trimester blood cadmium concentrations in 374 out of 465 participants who had a live birth. We used multiple linear and logistic regression to assess the relationships between log 2 -transformed maternal blood cadmium concentrations and birth weight, length, head circumference, ponderal index, low birth weight, small for gestational age, and preterm birth in crude and adjusted models. We also evaluated the relationships between log 2 -transformed blood cadmium concentrations and the density of coal-burning stoves within 5000 m of each participant's apartment as a proxy of coal smoke emissions from home heating stoves., Results: The median (25th,75th percentile) blood cadmium concentration was 0.20 (0.15, 0.29) μg/L. A doubling of blood cadmium was associated with a 95 g (95% CI: 34, 155 g) reduction in birth weight in adjusted models. An interquartile range increase in coal stove density (from 3.4 to 4.9 gers/hectare) surrounding participants' apartments was associated with a 12.2% (95% CI: 0.3, 25.6%) increase in blood cadmium concentrations., Conclusions: Gestational cadmium exposure was associated with reduced birth weight. In settings where coal is a widely used fuel, cadmium may play a role in the putative association between air pollution and impaired fetal growth., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

To study source-specific carcinogenicity and mutagenicity of polycyclic aromatic hydrocarbons (PAHs) under diverse anthropogenic activities, PM 2.5 -bound PAHs were detected in Beijing in four periods. PAHs in Asia-Pacific Economic Cooperation meeting (APEC) was much lower than that in after-APEC period. The highest PAHs concentration was in heating period (303 ng/m 3 ). Sources were quantified by Positive Matrix Factorization (PMF). In heating period, due to high emissions, weak diffusion, low degradation and evaporation, high contributions of all sources were observed, and both absolute and relative contributions of coal combustion increased. Changed contributions in during-APEC and after-APEC periods implied effectiveness of reinforced emission control, especially for coal combustion and vehicles. Furthermore, variations of sources-specific carcinogenicity and mutagenicity were investigated. In non-heating period, contributions of gasoline exhaust (38.4% TEQ: Toxic Equivalent Quantity, 33.7% MEQ: Mutagenic Equivalent Quantity) and diesel exhaust (53.8% TEQ, 57.9% MEQ) dominated both carcinogenic and mutagenic risks. Coal combustion sharply increased in heating period, attributing 27.5% TEQ and 21.7% MEQ. In during-APEC period, all contributions to carcinogenicity and mutagenicity were lower than those in after-APEC period, but "others" linked with regional transport contributed increased fractions (above 20%). Sources-specific carcinogenicity and mutagenicity under diverse anthropogenic activities, especially for APEC meeting with reinforced control, gave a new insight into assessment of control measures based on health risks., (Copyright © 2019 Elsevier Inc. All rights reserved.)

PM 2.5 -bound toxic metals (TMs) are derived from various sources, and they can cause many adverse health effects on the human body. To effectively reduce the disease burden of TMs by controlling the relative sources, an integrated approach of quality-adjusted life years (QALYs) and source-apportionment (positive matrix factorization, PMF) was proposed and applied to some typical diseases induced by TMs in 2017 in Beijing. The estimation included two parts; first, the number of potentially affected people was calculated based on the source mass contribution from PMF and the inhalation unit risk of TMs; second, the QALYs lost per affected person was calculated based on the disease duration, expected years of life lost (EYLL) and quality of life (QoL) for both affected people and the general population. The results showed that QALYs lost per person for renal cancer (17.3 QALYs), pneumonia (14.4 QALYs), lung cancer (14.2 QALYs), skin cancer (12.7 QALYs) and diabetes mellitus (12.6 QALYs) were higher than those for other diseases. Combined with PMF, the source contributions to the overall burden of typical diseases from the TMs followed the order of coal combustion (50.2%) > vehicle emissions (24.4%) > fuel oil combustion (11.4%) > Cr-related industry (10.9%) > resuspended dust (3.0%). The rank was further compared with that assessed for noncancer and cancer risks, and we verified the reasonability of the QALYs method. For seasonal contributions to coal combustion, winter and spring had the highest contributions, which coincided with the fact that coal was the main fuel for heating in Beijing. The QALYs lost attributed to TMs for coal combustion decreased by 49.1% from 2016 to 2017, which may indicate an effective policy associated with coal control. Overall, the integrated approach was successfully employed for estimating the disease burden induced by TMs from each source and was an effective solution to identify the control rank of sources for TM reduction., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Coal dust is a contaminant that impacts the terrestrial and aquatic environment with a complex mixture of chemicals, including PAHs and metals. This study aims to evaluate the toxic effect of a methanolic coal dust extract on a fish early life stage by analyzing phenotypic alterations, transcriptome changes, and mortality in zebrafish (ZF) embryos. ZF embryos were exposed to methanolic coal dust extract at 1-5000 mg·L-1 and monitored using bright field microscopy 24 and 48 hpf to determine malformations and mortality. In situ hybridization, RNA sequencing, and qRT-PCR were employed to identify transcriptome changes in malformed embryos. Three malformed phenotypes were generated in a dose-dependent manner. In situ hybridization analysis revealed brain, somite, dorsal cord, and heart tube development biomarker alterations. Gene expression profile analysis identified changes in genes related to structural constituent of muscle, calcium ion binding, actin binding, melanin metabolic process, muscle contraction, sarcomere organization, cardiac myofibril assembly, oxidation-reduction process, pore complex, supramolecular fiber, striated muscle thin filament, Z disc, and intermediate filament. This study shows, for the first time, the malformations generated by a mixture of pollutants from a methanolic coal dust extract on a fish early life stage, constituting a potential risk for normal embryonic development of other aquatic vertebrate organisms. Furthermore, we establish that phenotypes and changes in gene expression induced by the extract constitute a target for future studies about mechanical toxicity and their utility as sensitive tools in environmental risk assessments for biota and humans exposed to coal mining activities., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Pneumoconiosis is a serious occupational disease that often occurs to coal workers with no early diagnosis and effective treatment at present. Diffuse pulmonary fibrosis is the major pathological change of pneumoconiosis, and its mechanism is still unclear. Epigenetics is involved in the development of many diseases, and it is closely associated with fibrosis. In this study, we investigated whether DNA methylation contributes to the pathogenesis of pulmonary fibrosis in pneumoconiosis. By exposure to coal dust or silica dust, we established the models of coal worker's pneumoconiosis (CWP), which showed an increased expression of COL-I, COL-III. We further found that DNMT1, DNMT3a, DNMT3b, MBD2, MeCP2 protein expression changed. Pretreatment with DNMT inhibitor 5-aza-dC reduced expression of COL-I, COL-III, and reduced pulmonary fibrosis. In summary, our results showed that DNA methylation contributes to dust-induced pulmonary fibrosis and that it may serve as a theoretical basis for testing DNA methyltransferase inhibitors in the treatment of CWP., (© 2019 Wiley Periodicals, Inc.)

Several negative health effects have been associated with environmental pollution. Coal mining activities are related to DNA damage. However, the impact of lifestyle as well as environmental exposure must be considered when evaluating the extent of DNA damage. The aim of this cross-sectional study was to analyze nutritional status, dietary patterns, and the prevalence of non-communicable diseases (CNCDs) among coal miners as well as to investigate the correlation of these variables with DNA damage. We used a questionnaire to assess demographics, health, and dietary habits. The nutritional status was measured in terms of BMI (body mass index) and DNA damage was assessed by the comet assay. The sample population was composed of 158 coal miners from the largest coal mining company in South of Brazil, and majority of them were classified as overweight (51.3%) or obese (28.5%). Hypertension was the most common CNCD (50.6%) and a majority of these workers consumed all groups of foods three or more times a week. There was a significant positive correlation between BMI and DNA damage (r = 0.1646, p = 0.04) and this association was stronger (r = 0.2556, p = 0.04) in coal miners with some CNCD. There was no significant correlation between dietary patterns and DNA damage in coal miners. These results suggest that the nutritional status and CNCD increase the extent of DNA damage in coal miners. Since this population is at high occupational risk, specific strategies should be designed to improve the health of these workers, aiming to achieve health equity.

Carbon capture and storage (CCS) could be an effective measurement for carbon emission reduction in China. This paper summarizes the development of power sector in 2020, 2030, and 2050, and it classifies 18 scenarios including with and without CCS, respectively, in G1:low, G2:middle, and G3:high in 2020, 2030, and 2050. It adopts China's input-output table (IO table) and analyzes the different mitigation strategies for power sector. In particular, this paper builds a new China's input-output table based on aggregating the sectors in IO table and disaggregating the power sector into 11 different technologies which are coal-fire power, coal-fire power with CCS, natural gas power, natural gas power with CCS, hydropower, nuclear power, wind power, solar power, biomass power, geothermal power, and ocean power. Through input-output model, this paper estimates gross value added (GVA) and employment effects of different scenarios of different technologies in power sector in China. It finds that the differences of GVA and employment effects among different scenarios are large. In CCS scenarios, the coal-fire power with CCS contribute 1.48-1.63 × 10 10 RMB in 2020, 1.09-1.55 × 10 10 RMB in 2030, and 0.85-1.20 × 10 10 RMB in 2050 for gross value added. Meanwhile, the employments of coal-fire power with CCS can add the jobs of 11,966-17,159 in 2020; 10,419-16,228 in 2030; and 8977-12,571 in 2050. CCS sector contributes the higher employment than in the renewable power sectors. Meanwhile, coal mining industry, equipment manufacturing industry, and metallic industry take main contribution to the employment of CCS sector.

An assortment of organic material can leach from lignite (low-rank coal) in water, and the water-soluble fraction from lignite has been associated with adverse health effects in areas of the Balkans. Recent efforts have been made to evaluate this hypothesis in other areas where lignite is in contact with groundwater like in the U.S. Gulf Coast region. In this study, five Gulf Coast lignite samples were extracted with water, and the water-soluble portion of the coal was then characterized by total organic carbon, UV-Vis spectroscopy, and gas chromatography/mass spectrometry. Additionally, human kidney cells (HK-2) were exposed to water-soluble extracts of Gulf Coast lignite to assess toxicity. Cell viability was measured, and a dose-response curve was used to generate IC 50 values that ranged from 490 to 3000 ppm. The most toxic extract (Dolet Hills) was from Louisiana where lignite-derived organic material has been previously linked to high incidence of renal pelvic cancer. Concentrations of nephrotoxic metals (As, Cd, Co, Cu, Hg, Pb, V, Zn) were screened and were below those considered toxic to renal cells. We conclude that leachates from lignite do indeed have toxic affects on cultured human renal cells. Although the IC 50 values are higher than the concentration of organic matter in the local groundwater, typically < 5 ppm, the effects of long-term low-level exposure is not known.

In present study, the volatilization of arsenic (As), cadmium (Cd), mercury (Hg) and lead (Pb) by the burning of coal samples in the electric furnace was evaluated. The coal samples were obtained from different blocks of newly developed Thar coal field, Pakistan. The replicate coal samples were heated/burned in an electric furnace at laboratory scale for three temperature intervals (200, 400 and 900 °C). The ash obtained after each temperature intervals were analyzed for selected toxic elements. The resulted data indicated that the total contents of As, Cd, and Pb in coal samples of block X and XI were found in the range of 16.8-18.5, 4.21-4.72, and 14.2-18.8 mg/kg, respectively. Whereas, 67.8-79.7%, 34.3-36.8% and 9.89-10.8% of As, Cd, and Pb, respectively, were volatized out after combustion of coal samples at 900 °C. The total contents of Hg in selected coal samples of block X and XI were observed in the range of 0.985-1.46 and 0.992-1.41 mg/kg, respectively. The contents of Hg volatilized out via burning in a furnace at 200 °C and 400 °C, were observed in the range of 32.0-36.5% and >91.0% of its total contents, respectively, whereas at 900 °C, it was not detected in ash. The partitioning and mobility of studied toxic elements in residue termed as (laboratory made ash) obtained after burning at 900 °C, was carried out by three-step sequential extraction scheme. The resulted data of present study will give a better knowledge about the quality of coal and its burning product, which may help to take measure to reduce the adverse effects on the environment in future., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

The aim of the present study was to evaluate the genotoxic effect of lettuce ( Lactuca sativa L.), beet ( Beta vulgaris L.), broccoli ( Brassica oleracea var. italica ), and kale ( Brassica oleracea var. acephala ) grown in vegetable garden built on the deposits of coal tailings. For this, we used 72 healthy male Swiss albino mice that received juice from the vegetables in an acute or chronic treatment. Using comet assay, we determined that acute administration of the juices of all vegetables from the coal-mining area was genotoxic, and increased the DNA damage in the blood, liver, and cerebral cortex of mice. Therefore, the present data suggest that intake of vegetables cultivated over coal waste results in an increase in DNA damage in some organs; this situation may pose a risk to health.

Obesity is an important nutritional disorder worldwide. Its association with environmental pollution may trigger an increase in oxidative stress and inflammatory parameters. Coal is a resource used throughout the world as an important fuel source for generating electricity. The ashes released by the coal combustion cause serious problems for human health due to their high toxicity and their capacity to bioaccumulate. The aim of this work was to investigate the effects of coal dust inhalation in the organs of obese and non-obese Wistar rats. Pro-inflammatory cytokines, oxidative stress, oxidative damage, histological analysis, comet assay, and micronuclei were investigated. Both obesity and coal dust inhalation increased the pro-inflammatory cytokines IL-1β and TNF-α and decreased HSP70 levels in serum, however, in obese animals that inhaled coal dust these changes were more pronounced. Liver histological analysis showed severe microvesicular steatosis in obese animals that inhaled coal dust. Lung histologic investigation showed abnormalities in lung structure of animals exposed to coal dust and showed severe lung distensibility in obese animals exposed to coal dust. The comet assay showed DNA damage in animals subjected to coal. In addition, there were modulations in enzymatic activities and damage to protein and lipids. Based on our results, the coal dust inhalation can potentiate the pro-inflammatory profile present in obese rats. We also observed an increase in the protein oxidative damage in obese rats that inhaled coal dust. Taken together, our results suggest that the combination of obesity and coal inhalation increased the risks of the development of diseases related to oxidative stress and inflammation., (Copyright © 2018 Elsevier Inc. All rights reserved.)

This paper originally investigated toxicity discrimination of typical cyclic compounds and bioassays selection on toxicity evaluation for coal gasification wastewater (CGW) effluent with mechanism-oriented investigation. Initially, representative cyclic toxicants were selected and classified with quantitative structure-toxicity relationship (QSTR). Nitrogen heterocyclic compounds (NHCs) and polycyclic aromatic hydrocarbons (PAHs) were basically discriminated as nonpolar narcotics with significant correlation to hydrophobicity (p < 0.05, R 2  = 0.8668-0.9635), while phenols were regarded as polar narcotics and reactive compounds due to slight correlation to hydrophobicity (p > 0.05, R 2  < 0.5). Furthermore, specific mechanism of actions (MOAs) to various organisms revealed that phenols were discriminated as critical source of acute toxicity in CGW, with short-term visible and irreversible damage. However, NHCs and PAHs, which exerted accumulation toxicity rather than acute toxicity, might result in potential mutagenicity and unpredictable risk along the food chain. Afterwards, based on species sensitivity to typical toxicants and application in real CGW effluent, non-applicability of Chlorella vulgaris (C. vulgaris) was validated in toxicity evaluation. While Daphnia magna (D. magna) was suggested as a toxicity bioassay in entire effluent due to the highest sensitivity and applicability. Tetrahymena thermophile (T. pyriformis) might be applicable in effluent with low biodegradability due to similar evaluation results (TU = 8.90) to D. magna (TU = 6.67) in aerobic effluent. Finally, the relationship between toxicity and bioavailability based on typical pollutants and model species illustrated necessity for dualism toxicity-biodegradability investigation on CGW., (Copyright © 2018. Published by Elsevier B.V.)

Coal combustion is a major energy source in the US. The solid waste product of coal combustion, coal combustion residue (CCR), contains potentially toxic trace elements. Before 1980, the US primarily disposed of CCR in aquatic settling basins. Animals use these basins as habitat and can be exposed to CCR, potentially affecting their physiology. To investigate the effects of CCR on eastern mud turtles (Kinosternon subrubrum), we sampled 30 turtles exposed to CCRs and 17 unexposed turtles captured in 2015-2016 from the Savannah River Site (Aiken, SC, USA). For captured turtles, we (1) quantified accumulation of CCR in claw and blood samples, (2) used bacterial killing assays to assess influences of CCR on immune responses, (3) compared hemogregarine parasite loads, and (4) compared metabolic rates via flow-through respirometry between CCR-exposed and unexposed turtles when increased temperature was introduced as an added stressor. Turtles exposed to CCR accumulated CCR-associated trace elements, corroborating previous studies. Blood Se and Sr levels and claw As, Se, and Sr levels were significantly higher in turtles from contaminated sites. Average bacterial killing efficiency was not significantly different between groups. Neither prevalence nor average parasite load significantly differed between CCR-exposed and reference turtles, although parasite load increased with turtle size. Regardless of site, temperature had a significant impact on turtle metabolic rates; as temperature increased, turtle metabolic rates increased. The effect of temperature on turtle metabolic rates was less pronounced for CCR-exposed turtles, which resulted in CCR-exposed turtles having lower metabolic rates than reference turtles at 30 and 35 °C. Our results demonstrate that turtles accumulate CCR from their environment and that accumulation of CCR is associated with changes in turtle physiological functions when additional stressors are present., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

The mining production process is exposed to a series of different hazards. One of them is the accumulation of dust which can pose a serious threat to the life and health of mine workers. The analysis of dust hazard in hard coal mining should include two aspects. One is the risk of coal dust explosions, which poses a direct risk of injury or even loss of life, the second is the risk of harmful dust, associated with the possibility of negative health effects as a result of long-term exposure to dust in the worker's body. The technologies currently applied in underground mining produce large amounts of coal and stone dust. Long-term exposure to dust and crystalline silica may cause chronic respiratory disease. The article presents the results of tests on the dust levels in the area of a fully-powered longwall. The tests were conducted for five longwalls from different hard coal mines. In each of them, the average values of inhalable and respirable dust as well as the percentage content of free silica in the dust were determined in ten selected working positions. Additionally, for the longwall with the highest dust concentration, the levels of dust were determined for the basic activities related to the phases of the technological cycle. The comparative analysis conducted and the results obtained demonstrate large variations in the dust levels in the different areas. The permissible values were significantly exceeded in a number of cases. This poses a great threat to the health of Polish miners. The results obtained indicate that it is necessary to undertake more effective measures in order to improve the working environment of the crew in hard coal mines.

This article briefly reviews evidence of health effects associated with exposure to particulate matter (PM) air pollution from five common outdoor emission sources: traffic, coal-fired power stations, diesel exhaust, domestic wood combustion heaters, and crustal dust. The principal purpose of this review is to compare the evidence of health effects associated with these different sources with a view to answering the question: Is exposure to PM from some emission sources associated with worse health outcomes than exposure to PM from other sources? Answering this question will help inform development of air pollution regulations and environmental policy that maximises health benefits. Understanding the health effects of exposure to components of PM and source-specific PM are active fields of investigation. However, the different methods that have been used in epidemiological studies, along with the differences in populations, emission sources, and ambient air pollution mixtures between studies, make the comparison of results between studies problematic. While there is some evidence that PM from traffic and coal-fired power station emissions may elicit greater health effects compared to PM from other sources, overall the evidence to date does not indicate a clear &lsquo;hierarchy&rsquo; of harmfulness for PM from different emission sources. Further investigations of the health effects of source-specific PM with more advanced approaches to exposure modeling, measurement, and statistics, are required before changing the current public health protection approach of minimising exposure to total PM mass.

Continuous exposure to coal mining particles can cause a variety of lung diseases. We aimed to evaluate the outcomes of exposure to detailed characterized coal and coal fly ash (CFA) particles on DNA, lung and extrapulmonary tissues. Coal samples (COAL11 and COAL16) and CFA samples (CFA11 and CFA16) were included in this study. Intending to enhance the combustion process COAL16 was co-fired with a mixture of fuel oil and diesel oil, producing CFA16. Male BALB/c mice were intratracheally instilled with coal and CFA particles. Measurements were done 24h later. Results showed significant rigidity and obstruction of the central airways only for animals acutely exposed to coal particles. The COAL16 group also showed obstruction of the peripheral airways. Mononuclear cells were recruited in all treatment groups and expression of cytokines, particularly TNF-α and IL-1β, was observed. Only animals exposed to COAL16 showed a significant expression of IL-6 and recruitment of polymorphonuclear cells. DNA damage was demonstrated by Comet assay for all groups. Cr, Fe and Ni were detected in liver, spleen and brain, showing the efficient translocation of metals from the bloodstream to extrapulmonary organs. These effects were associated with particle composition (oxides, hydroxides, phosphates, sulfides, sulphates, silciates, organic-metalic compounds, and polycyclic aromatic hidrocarbons) rather than their size. This work provides state of knowledge on the effects of acute exposure to coal and CFA particles on respiratory mechanics, DNA damage, translocation of metals to other organs and related inflammatory processes., (Copyright © 2018 Elsevier B.V. All rights reserved.)

This study was aimed to investigate the potential harmful element (PHE) concentrations in coal dust and evaluate the human risk assessment and health effects near coal mining areas. For this purpose, dust samples were collected near various coal mines in Cherat, Pakistan, and analyzed for the PHE concentrations. Determined PHE concentrations were evaluated for the health risk assessment. Results revealed that ingestion was the major pathway as compared to others for PHE exposure. Individual chronic daily intake (CDI) of PHEs was higher than their respective permissible exposure limits set for oral exposure routes by the Agency for Toxic Substances and Disease Registry (ATSDR). Chronic risk or health index (HI) values were observed < 1 for all PHEs and in the order of Pb > Cr > Cd > Ni > Cu > Co > Zn. Higher HI values of Pb, Cr, and Cd could attribute to various chronic health problems as observed during the medical examination survey of this study. Cancer risk (CR) values for this study were observed within the US Environmental Protection Agency (EPA) limits. However, if current practices continued, the PHEs will cross these limits in a near future. Therefore, this study strongly recommends the provision of safety measures, rules, and regulation to avoid health hazards in the future.

Lung cancer mortality in Xuan Wei County (XWC) is among the highest in China. Lung cancer in XWC is associated with exposure, in poorly vented homes, to coal smoke containing high levels of polycyclic aromatic hydrocarbons (PAHs). We have previously investigated mutations in the p53 tumor suppressor gene and the K-ras oncogene in lung carcinomas and in sputum samples from individuals exposed to smoky coal emissions in XWC. This paper summarizes the results concerning p53 and K-ras mutations from these studies, in relation to mutations found in lung cancer patients not exposed to smoky coal emissions., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Coal mining is one of the economic activities with the greatest impact on environmental quality. At all stages contaminants are released as particulates such as coal dust. The first aim of this study was to obtain an aqueous coal dust extract and characterize its composition in terms of trace elements by ICP-MS. In addition, the developmental toxicity of the aqueous coal extract was evaluated using zebrafish (Danio rerio) after exposure to different concentrations (0-1000 ppm; μg mL -1 ) to establish acute toxicity, morphology and transcriptome changes. Trace elements within the aqueous coal dust extract present at the highest concentrations (>10 ppb) included Sr, Zn, Ba, As, Cu and Se. In addition, Cd and Pb were found in lower concentrations. No significant difference in mortality was observed (p > 0.05), but a delay in hatching was found at 0.1 and 1000 ppm (p < 0.05). No significant differences in morphological characteristics were observed in any of the treatment groups (p > 0.05). Transcriptomic results of zebrafish larvae revealed alterations in 77, 61 and 1376 genes in the 1, 10, and 100 ppm groups, respectively. Gene ontology analysis identified gene alterations associated with the development and function of connective tissue and the hematological system, as well as pathways associated with apoptosis, the cell cycle, transcription, and oxidative stress including the MAPK signaling pathway. In addition, altered genes were associated with cancer; connective tissue, muscular, and skeletal disorders; and immunological and inflammatory diseases. Overall, this is the first study to characterize gene expression alterations in response to developmental exposure to aqueous coal dust residue from coal mining with transcriptome results signifying functions and systems to target in future studies.

The objective of this researsh is to study the effects of Eminium Regelii phytopreparation (ERP) on immune status and free radical oxidation in the tissues of the adrenal glands and immunocompetent organs after combined exposure to 6 Gy dose of gamma irradiation and coal dust (remote period). The study was realized on 30 white laboratory male rats of the Wistar line, weighing 240±20g, that were divided into equal 3 groups: I group - intact, ІІ group - were exposured to combined effects of coal dust and gamma irradiation, III group - were exposured to combined effects and in parallel taking phytopreparation Eminium Regel. The animals of II and III groups were irradiated 90 days prior to the study at the TERAGAM 60Co radiotherapy unit ("ISOTREND spol. S.r.o.", Czech Republic) in dose of 6 Gy once. Experimental animals received phytopreparation of ER 2.5 mg/kg per day on calculate of body mass for 14 days. The results of the conducted studies showed that in the long-term period after the actions of the sublethal dose of gamma radiation and coal dust, significant changes were revealed that were characterized by a decrease in immunological reactivity, increased lipoperoxidation and inhibition of antioxidant defense activity of the organism. After exposure to ER, oxidative stress was alleviated, sufficient restoration of antioxidant protection and immune system indices, which were disrupted by the combined effects of a single high dose of radiation and a prolonged three-month inhalation of coal dust.

Ultrafine particles (UFPs, < 2.5 µm) in air pollutants have been identified as a major cause of respiratory diseases, since they can affect the lung alveoli through the bronchus. In particular, if toxicants such as heavy metals and polycyclic aromatic hydrocarbons (PAHs) are present in UFPs, they can cause diseases such as asthma, chronic obstructive pulmonary disease, and lung cancer. This study compared in vitro toxicity of various particulate matter including UFPs from combustion particles of diesel (diesel exhaust particles (DEP)), rice straw (RS), pine stem (PS) and coal (CC), and road dust particles from tunnel (TD) and roadside (RD). UFPs from combustion particles and road dust were collected with a glass fiber filter using burning systems and a solid aerosol generator. Cell viability was determined by neutral red uptake assay using Chinese hamster ovary strain K1 cells. Redox cycling activity and intracellular reactive oxygen species were measured using 1,4-dithiothreitol (DTT) and 2',7'-dichlorofluorescin diacetate (DCF-DA) assay, respectively. Our in vitro studies validated that combustion particles had high toxicological activity. PS demonstrated the highest activity in cytotoxicity but DEP had the highest activity in the DTT and DCF-DA assays. Overall, since the toxicological activity of particles generated by various means was different, risk assessment should be conducted through various toxicity evaluations rather than one toxicity evaluation.