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Exposure to coal and coal ashes can cause harmful effects in in vitro and in vivo systems, mainly by the induction of oxidative damage. The aim of this work was to assess cytotoxic and genotoxic effects using the V79 cell line treated with coal and coal fly ash particles derived from a coal power plant located in Santa Catarina, Brazil. Two coal samples (COAL11 and COAL16) and two coal fly ash samples (CFA11 and CFA16) were included in this study. COAL16 was co-firing with a mixture of fuel oil and diesel oil. The comet assay data showed that exposure of V79 cells to coal and coal fly ash particles induced primary DNA lesions. Application of lesion-specific endonucleases (FPG and ENDO III) demonstrated increased DNA effects indicating the presence of high amounts of oxidative DNA lesions. The cytokinesis-block micronucleus cytome assay analysis showed that exposure of V79 cells to high concentrations of coal and coal fly ash particles induced cytotoxic effects (apoptosis and necrosis) and chromosomal instability (nucleoplasmic bridges, nuclear buds, and micronucleus (MN) formation). These results may be associated with compounds contained in the surface of the particles as hazardous elements, ultrafine/nanoparticles, and polycyclic aromatic hydrocarbons (PAHs) which were detected in the samples. Graphical abstract ᅟ

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 ‘hierarchy’ 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.

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.

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.

BackgroundCoal-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.ObjectiveThis community-based study collected primary data to investigate the relationships of residential proximity to power plants and neurobehavioral problems in children.Methods235 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.ResultsA 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.SignificanceResults 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.

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.

Background: Environmental pollutants such as polycyclic aromatic hydrocarbons (PAHs), lead, and mercury are released by combustion of coal and other fossil fuels. Objectives: In the present study we evaluated the association between prenatal exposure to these pollutants and child development measured by the Gesell Developmental Schedules at 2 years of age. Methods: The study was conducted in Tongliang, Chongqing, Chongqing, China, where a seasonally operated coal-fired power plant was the major source of ambient PAHs and also contributed lead and mercury to the air. In a cohort of nonsmoking women and their newborns enrolled between March 2002 and June 2002, we measured levels of PAH-DNA adducts, lead, and mercury in umbilical cord blood. PAH-DNA adducts (specifically benzo[a]pyrene adducts) provided a biologically relevant measure of PAH exposure. We also obtained developmental quotients (DQs) in motor, adaptive, language, and social areas. Results: Decrements in one or more DQs were significantly associated with cord blood levels of PAH-DNA adducts and lead, but not mercury. Increased adduct levels were associated with decreased motor area DQ (p = 0.043), language area DQ (p = 0.059), and average DQ (p = 0.047) after adjusting for cord lead level, environmental tobacco smoke, sex, gestational age, and maternal education. In the same model, high cord blood lead level was significantly associated with decreased social area DQ (p = 0.009) and average DQ (p = 0.038). Conclusion: The findings indicate that exposure to pollutants from the power plant adversely affected the development of children living in Tongliang; these findings have implications for environmental health policy.

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.

Objective: Nearly all China's rural residents and a shrinking fraction of urban residents use solid fuels (biomass and coal) for household cooking and/or heating. Consequently, global meta-analyses of epidemiologic studies indicate that indoor air pollution from solid fuel use in China is responsible for approximately 420,000 premature deaths annually, more than the approximately 300,000 attributed to urban outdoor air pollution in the country. Our objective in this review was to help elucidate the extent of this indoor air pollution health hazard. Data Sources: We reviewed approximately 200 publications in both Chinese- and English-language journals that reported health effects, exposure characteristics, and fuel/stove intervention options. Conclusions: Observed health effects include respiratory illnesses, lung cancer, chronic obstructive pulmonary disease, weakening of the immune system, and reduction in lung function. Arsenic poisoning and fluorosis resulting from the use of \"poisonous\" coal have been observed in certain regions of China. Although attempts have been made in a few studies to identify specific coal smoke constituents responsible for specific adverse health effects, the majority of indoor air measurements include those of only particulate matter, carbon monoxide, sulfur dioxide, and/or nitrogen dioxide. These measurements indicate that pollution levels in households using solid fuel generally exceed China's indoor air quality standards. Intervention technologies ranging from simply adding a chimney to the more complex modernized bioenergy program are available, but they can be viable only with coordinated support from the government and the commercial sector.

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.