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Induction of ferritin and lipid peroxidation by coal samples with different prevalence of coal workers' pneumoconiosis: role of iron in the coals.

BACKGROUND: Differences in levels of bioavailable iron (BAI) in coal may be responsible for the observed regional differences in the prevalence and severity of coal workers' pneumoconiosis (CWP). METHODS: Twenty-nine coal samples from three coal mine regions were tested in human lung epithelial Type II A549 cells. They were from Utah (UT), West Virginia (WV), and Pennsylvania (PA) with a prevalence of CWP of 4, 10, and 26%, respectively. RESULTS: Low molecular weight (LMW) chelators bound iron, a fraction of BAI in the cells released from coals, ferritin, and lipid peroxidation were significantly higher in cells treated with various coals than in control cells, with an increasing order of UT < WV < PA, in parallel to the prevalence of CWP in these coal mine regions. Deferoxamine (DFO), a specific iron chelator, was used to distinguish effects of BAI from those of other transition metals. Our results indicate that BAI in the coals of WV and UT is the main metal species in inducing ferritin and lipid peroxidation. In contrast, biological effects of PA coals are not only from BAI, but from other transition metals as well. CONCLUSIONS: Based on a large number of coal samples from various seams, the findings of this study provide further evidence that metals, particularly iron, play important roles in coal dust-induced cellular damage, ultimately leading to the development of CWP and contributing to the regional differences in the prevalence of the disease.

Cells, Cultured↗

Presence of stable coal radicals in autopsied coal miners' lungs and its possible correlation to coal workers' pneumoconiosis.

Stable coal radicals (SCRs) were detected by electron spin resonance (ESR) spectroscopy in the lung tissue of autopsied coal miners. The SCR concentrations were measured in the lung tissues from 98 coal miners with and without (a) coal workers' pneumoconiosis (CWP), (b) cancer, and (c) a history of cigarette smoking. Concentrations of SCRs were also determined in the lungs of nonminer controls. The SCR concentration was related to longer mining tenure, CWP disease severity, lung cancer, and cigarette smoking. The mean concentration of SCRs in the lung tissues of miners with 30 +/- 1.4 y of coal mining exposure was 5.3 +/- 1.3 x 10(17) spins/g versus controls who had a nondetectable level (less than 10(15) spins/g). An increase in disease severity was accompanied by a progressive increase in SCR concentration. A SCR concentration of 4.8 +/- 0.7 x 10(17) spins/g was found for simple CWP (with moderate coal macules) versus 7.8 +/- 4.6 spins/g lung tissue for complicated CWP (with progressive massive fibrosis). Significantly higher (i.e., 10 x 10(17] concentrations of SCR in the coal miners' lung tissues were associated with an exposure history in the anthracite regions of northeastern Pennsylvania. These results indicate a possible role for SCRs in the disease process. Furthermore, ESR appears to be an adequate methodology for the quantitation of coal dust retained in the lung and for distinguishing exposures to anthracite and/or bituminous coal.

Aged↗

Mobilization of iron from coal fly ash was dependent upon the particle size and the source of coal.

Particulate air pollution, including coal fly ash, contains iron, and some of the pathological effects after inhalation may be due to reactive oxygen species produced by iron-catalyzed reactions. The objective of this study was to determine whether iron, present in coal fly ash, was mobilized, leading to ferritin induction in human airway epithelial cells, and whether the size of the particles affected the amount of iron mobilized. Three types of coal were used to generate the three size fractions of fly ash collected. The Utah coal fly ash was generated from a bituminous b coal, the Illinois coal fly ash from a bituminous c coal, and the North Dakota coal fly ash from a lignite a coal. Three size fractions were studied to compare the amount of iron mobilized in human airway epithelial (A549) cells and by citrate in cell-free suspensions. The size fractions selected were fine (<2.5 microm) and coarse (2.5-10 microm) components of PM10, airborne particulate matter <10 microm in diameter, and the fraction greater than 10 microm. Coal fly ash samples were incubated with 1 mM citrate to determine if iron associated with coal fly ash could be mobilized. Iron was mobilized by citrate from all three size fractions of all three coal types to levels as high as 56.7 nmol of Fe/mg of coal fly ash after 24 h. With all three coal types, more iron was mobilized by citrate from the <2.5 microm fraction than from the >2.5 microm fractions. Further, the mobilized iron was in the Fe(III) form. To determine if iron associated with the coal fly ash could be mobilized by A549 cells, cells were treated with coal fly ash, and the amount of the iron storage protein ferritin was determined after 24 h. Ferritin levels were increased by as much as 11.9-fold in cells treated with coal fly ash. With two of the three types of coal studied, more ferritin was induced in cells treated with the <2.5 microm fraction than with the >2.5 microm fractions. Further, inhibition of the endocytosis of the coal fly ash by the cells resulted in ferritin levels that were near that of the untreated cells, suggesting that iron was mobilized intracellularly, not in the culture medium. The results of this study suggest that differences in particle size and speciation of iron may affect the release of iron in human airway epithelial cells.

Air Pollutants, Occupational↗

Chemical reactivity of the carbon-centered free radicals and ferrous iron in coals: role of bioavailable Fe2+ in coal workers pneumoconiosis.

Striking differences in the prevalence of coal workers' pneumoconiosis (CWP) exist between different coal mine regions. The major factors responsible for the observed regional differences in CWP have not yet been identified. In the present study, chemical reactivity of the carbon-centered free radicals in coals and lung tissues, as well as ferrous iron in the coals, were studied by ESR techniques. The ESR spectra clearly demonstrated the presence of at least two types of carbon-centered free radical species, which might respectively attribute to the macromolecular phase and the molecular phase of coal. Grinding produced free radicals in coals. Exposure of freshly ground coal to air for 28 h induced a slight increase of free radicals for most of the coals, and a slight decrease after 4 months' exposure. The lung tissue samples of coal workers deceased of CWP showed similar ESR spectra as coal samples, and these radicals were highly stable in the lung. After incubation of coals with glutathione, hydrogen peroxide, sodium formate or oxygen, the coal sample from the Gardanne mine which has never induced CWP, and thus is the least hazardous coal, showed the most significant change in the carbon-centered free radical concentration. No significant changes were observed among other coals reported to induce CWP. On the other hand, we found that the coals released different amounts of Fe2+ in an acidic medium. Interestingly, the prevalence of CWP correlates positively with the released Fe2+ content in these coals and with the amount of oxygen radicals produced by the interaction of Fe2+ with O2 in the acidified coal filtrates. Our studies indicate that the carbon-centered free radicals may not be biologically relevant to coal dust-induced pneumoconiosis, whereas the acid soluble Fe2+, which may be dissolved in the phagolysosomes of macrophages, can then lead to Fe2+-induced oxidative stress and eventual CWP development.

Adult↗

Double-blind, randomised, multicentre, parallel group study comparing a 1% coal tar preparation (Exorex) with a 5% coal tar preparation (Alphosyl) in chronic plaque psoriasis.

BACKGROUND: Exorex lotion is a novel formulation of prepared coal tar indicated for the treatment of psoriasis. OBJECTIVES: To compare the efficacy and tolerability of 1% prepared coal tar lotion versus 5% coal tar extract in patients with mild to moderate plaque psoriasis. PATIENTS AND METHODS: This was a double-blind, randomised controlled study. Patients initially entered a 7-day washout period, during which they applied a yellow soft paraffin plus emulsifying wax ointment used as an emollient three times a day to their plaques. They were then randomised to receive treatment with 1% coal tar (Exorex) lotion or 5% conventional coal tar lotion (Alphosyl), three times a day for 12 weeks. Both treatment groups continued to apply the emollient throughout the duration of the study. Two target plaques were selected at entry for assessment. The clinical measures used were: 1) Total Sign Score (TSS), the sum of 5-point rating scores for erythema, induration and scaling averaged for the two target plaques (range 0-12), 2) the Psoriasis Area and Severity Index (PASI), and 3) patient and investigator 7-point global assessments of improvement at 12 weeks. Patients were assessed at 0, 4, 8 and 12 weeks during the treatment period or at the point of withdrawal. Spontaneously reported and observed adverse events were noted. RESULTS: Three hundred and twenty four of 338 randomised patients were evaluable (ITT analysis): 158 patients received 1% coal tar lotion and 166 patients received conventional coal tar. Both groups showed decreases from baseline to end of treatment in mean TSS (decrease of 2.4 points from 5.6 to 3.2 with 1% coal tar lotion and 1.8 points from 5.5 to 3.7 with conventional coal tar), and mean PASI (decrease of 2.4 points with 1% coal tar lotion and 1.5 points with conventional coal tar). Two hundred and twenty eight patients completed the full course of treatment. There was a statistically significant treatment difference in the percentage change in mean TSS at week 12, in favour of 1% coal tar lotion (-10.6%, 95% CI -20.6% to -0.5%, p=0.04). There was also a difference between treatments in the change in mean PASI in favour of 1% coal tar that was of borderline statistical significance (-11.7%, 95% CI -23.8% to 0.4%, p=0.06). Investigator global assessments also favoured 1% coal tar lotion (38% vs. 27% of patients showed clearance or marked improvement). The 1% coal tar lotion had a similar safety profile to 5% conventional coal tar lotion with the majority of treatment-related events being mild to moderate in severity. CONCLUSIONS: 1% coal tar lotion is more effective than a conventional coal tar lotion in mild to moderate psoriasis and may be preferred for first-line topical treatment.

Adolescent↗

Buffering capacity of coal and its acid-soluble Fe2+ content: possible role in coal workers' pneumoconiosis.

Epidemiological studies have shown that the prevalence of coal workers' pneumoconiosis (CWP) differed remarkably between different coal mine regions despite comparable exposures to respirable dust. In the United States, CWP was found to be most common in Pennsylvania coal miners and least common in miners from Utah. The active component(s) responsible for the regional differences in CWP has not yet been identified. In the present study, we found that coals from Pennsylvania, compared with Utah coals, showed a much lower buffering capacity as determined by the amount of acid consumed in order to reach pH 4.5, which is the pH of the phagolysosomes of macrophages. Moreover, the coals from Pennsylvania released large amounts of Fe2+ in the acidified extract, whereas the coals from Utah released little Fe2+. Using electron spin resonance (ESR), we found that the coals from Pennsylvania, but not from Utah, were effective in oxidizing formate by a radical pathway. Two coals, one from Utah with high buffering capacity and low acid-soluble Fe2+ and the other from Pennsylvania with low buffering capacity and high acid-soluble Fe2+, were then selected for cell treatment. We found that human tracheal epithelial (HTE) cells treated with the coal from Pennsylvania (10 microg/cm2) showed a 36% increase in oxidant formation over the control as detected by dichlorofluorescein assay, whereas the coal from Utah had no effect. An electrophoretic mobility shift assay was used to test the binding affinity of nuclear proteins extracted from the coal-treated HTE cells to an oxidative stress-responsive transcription factor activator protein-1 (AP-1) element. The coal from Pennsylvania with high acid-soluble Fe2+ (1 microg/cm2) activated AP-1 to the same extent as 10 microM H2O2, while the coal from Utah without acid-soluble Fe2+ had no effect. These results support our hypothesis that the prevalence of CWP may be higher in coal workers exposed to coal with high acid-soluble Fe2+ and low buffering capacity than in workers exposed to coal with low acid-soluble Fe2+ and high buffering capacity.

Buffers↗

Comparative chemical and biological analysis of coal tar-based therapeutic agents to other coal-derived materials.

In this study, methodologies developed for the analysis of synthetic fuel products were applied to the coal tar fractions isolated from coal tar-based pharmaceutical products. A pharmaceutical stock solution of 20% coal tar in alcohol, a 50% coal tar bath emulsion and a 4.3% coal tar shampoo were studied. The toxicology and chemical composition of the coal tar fractions isolated from these materials were compared with an industrial coal tar and with a direct-liquefaction coal liquid product. The coal tars and coal liquid product were fractionated into chemical classes by alumina column chromatography and individual components were identified and quantitated by high-resolution gas chromatography. The microbial mutagenicity of these materials was measured against S. typhimurium, TA 98. In addition, the industrial coal tar, coal-liquid product, and coal tar isolate from the 20% coal tar in alcohol solution were tested for initiating activity in an initiation/promotion mouse skin painting assay for carcinogenicity. The chemical compositions of the coal tar-based therapeutic agents, the industrial coal tar and direct-liquefaction coal liquid were similar. With the exception of the 50% bath emulsion, the microbial mutagenicity and tumor-initiating activity in mouse skin for those materials tested were also similar.

Animals↗

Emissions of air pollutants from household stoves: honeycomb coal versus coal cake.

Domestic coal combustion can emit various air pollutants. In the present study, we measured emissions of particulate matter (PM) and gaseous pollutants from burning a specially formulated honeycomb coal (H-coal) and a coal cake (C-coal). Flue gas samples for PM2.5, PM coarse (PM2.5-10), and TSP were collected isokinetically using a cascade impactor; PM mass concentrations were determined gravimetrically. Concentrations of SO2, NOx, and ionic Cr(VI) in PM were analyzed using spectrometric methods. Fluoride concentrations were measured using a specific ion electrode method. PM elemental components were analyzed using an X-ray fluorescence technique. Total (gas and particle phase) benzo[a]pyrene (BaP) concentration was determined using an HPLC/fluorescence method. Elemental and organic carbon contents of PM were analyzed using a thermal/optical reflectance technique. The compositional and structural differences between the H-coal and C-coal resulted in different emission characteristics. In generating 1 MJ of delivered energy, the H-coal resulted in a significant reduction in emissions of SO2 (by 68%), NOx (by 47%), and TSP (by 56%) as compared to the C-coal, whereas the emissions of PM2.5 and total BaP from the H-coal combustion were 2-3-fold higher, indicating that improvements are needed to further reduce emissions of these pollutants in developing future honeycomb coals. Although the H-coal and the C-coal had similar emission factors for gas-phase fluoride, the H-coal had a particle-phase fluoride emission factor that was only half that of the C-coal. The H-coal had lower energy-based emissions of all the measured toxic elements in TSP but higher emissions of Cd and Ni in PM2.5.

Air Pollutants↗

Inactivation of alpha 1-antitrypsin by aqueous coal solutions: possible relation to the emphysema of coal workers.

Increasing evidence demonstrates that emphysema in coal workers may be related to their exposure to coal dusts. The hypothesis that emphysema could be related to the production of reactive oxygen species (ROS) generated by inhaled coal dusts was examined in the present study. Using ESR, we investigated whether the interaction of different coals with dissolved oxygen in aqueous medium could generate ROS. Indeed, we found that one of the five examined French coal samples, Vouters coal, was effective in oxidizing formate anions or ethanol by a radical pathway. Inactivation of alpha 1-antitrypsin (alpha 1-AT) in vitro was then examined for all five coal filtrates. The Vouters coal filtrate, which exhibits oxidative activity, can also inactivate alpha 1-AT. When this coal filtrate was crystallized and redissolved, its oxidative activity was found to be conserved. By use of various analytical techniques, the active component of this coal filtrate was identified to be primarily ferrous sulfate. We confirmed that pure ferrous sulfate can effectively reduce oxygen to produce ROS in aqueous medium in vitro and can also inactivate alpha 1-AT. In this report, the nature of the coal-generated oxidative species, the origin of ferrous sulfate, and the stability of ferrous sulfate in the different coal samples are discussed. These results offer evidence that some inhaled coal dusts are capable of producing ROS, which may play an important role in the development of coal workers' emphysema.

Coal↗

Hydroxyl radical generation by coal mine dust: possible implication to coal workers' pneumoconiosis (CWP).

Occupational exposure to coal mine dust causes coal workers' pneumoconiosis (CWP) and other pulmonary diseases by mechanisms that remain unclear. Because the hydroxyl radicals (.OH) may play an important role in the pathogenesis of CWP, we studied the potential role of bituminous coal mine dust samples for catalyzing the generation of .OH from hydrogen peroxide (H2O2). These coal mine dusts evaluated represented two geographic areas with diversity in CWP prevalence. Electron spin resonance (ESR), with the aid of spin trapping techniques, was used to measure the .OH radical generation. Bituminous coal mine dusts representing the Pittsburgh seam in the eastern United States and Blind Canyon seam in the mid-western United States were used together with a standard coal dust obtained from the National Institute of Standards and Technology, Gaithersburg, MD. All the coal mine dust samples generated varying levels of .OH radicals from H2O2 in the presence of a .OH spin trap 5,5-dimethyl-l-pyrroline-N-oxide (DMPO). .OH radical generation by the coal from H2O2 was effectively inhibited by deferoxamine and catalase, but only partially inhibited by superoxide dismutase. Metal chelators DETAPAC and EDTA enhanced the radical generation. These results indicated that the Fenton reaction is predominantly involved in the generation of .OH radicals from H2O2. The .OH-generating potential of all the coal dusts showed a positive correlation with the surface iron content of coal mine dusts. In addition, the potential to induce lipid peroxidation by the coal samples exhibited a good correlation with the available surface iron. Based on the results presented here, we propose that higher concentrations of surface iron in coal mine dust may be involved in the generation of increased levels of .OH radicals and may play an important role in the development of CWP in different coal mining areas.

Chelating Agents↗

Roles of bioavailable iron and calcium in coal dust-induced oxidative stress: possible implications in coal workers' lung disease.

Marked regional differences in prevalence of pneumoconiosis are apparent in the US despite comparable dust exposure. In the present study, we examined the ability of 28 coal samples to release bioavailable iron (BAI) and calcium, as well as other metals such as Cr, Ni, Cu, and Co, from three coal mine regions in Utah (UT), West Virginia (WV), and Pennsylvania (PA), respectively. BAI is defined as iron (both Fe2+ and Fe3+) released by the coals in 10 mM phosphate solution, pH 4.5, which mimics conditions of the phagolysosomes in cells. We found that coals from the UT, WV, and PA regions released average levels of BAI of 9.6, 4658.8, and 12149 parts per million (ppm, w/w), respectively, which correlated well with the prevalence of pneumoconiosis from that region (correlation coefficient r = 0.92). The low levels of BAI in the UT coals were due to the presence of calcite (CaCO3), which was shown to be preferentially acid solubilized before iron compounds. Release of iron by two coal samples from the PA and UT regions was further examined in vitro in human lung epithelial A549 cells. We found that the coal from PA, with a high prevalence of pneumoconiosis, released BAI in a dose-dependent manner, both in tissue culture media and in A549 cells. At 2 microg/cm2, levels of lipid peroxidation induced by the PA coal were increased 112% over control cells at 24 h treatment, and were sustained at this level for 3 days. The coal from UT, with a low prevalence of pneumoconiosis, induced a marginal increase in cellular iron at 5 and 10 microg/cm2 treatments and had no effect on lipid peroxidation. Calcium levels in the cells treated with the PA and UT coals were 8.6 and 11.5 micromoles/10(6) cells, respectively, and were significantly higher than that in the controls (5.3 micromoles/10(6) cells) [corrected]. Our results suggest that the differences in the BAI content in the coals may be responsible for the observed regional differences in the prevalence of pneumoconiosis. Therefore, BAI may be a useful characteristic of coal for predicting coal's toxicity.

Biological Availability↗

Mapping and prediction of coal workers' pneumoconiosis with bioavailable iron content in the bituminous coals.

Based on the first National Study of Coal Workers' Pneumoconiosis (CWP) and the U.S. Geological Survey database of coal quality, we show that the prevalence of CWP in seven coal mine regions correlates with levels of bioavailable iron (BAI) in the coals from that particular region (correlation coefficient r = 0.94, p < 0.0015). CWP prevalence is also correlated with contents of pyritic sulfur (r = 0.91, p < 0.0048) or total iron (r = 0.85, p < 0.016) but not with coal rank (r = 0.59, p < 0.16) or silica (r = 0.28, p < 0.54). BAI was calculated using our model, taking into account chemical interactions of pyrite, sulfuric acid, calcite, and total iron. That is, iron present in coals can become bioavailable by pyrite oxidation, which produces ferrous sulfate and sulfuric acid. Calcite is the major component in coals that neutralizes the available acid and inhibits iron's bioavailability. Therefore, levels of BAI in the coals are determined by the available amounts of acid after neutralization of calcite and the amount of total iron in the coals. Using the linear fit of CWP prevalence and the calculated BAI in the seven coal mine regions, we have derived and mapped the pneumoconiotic potencies of 7,000 coal samples. Our studies indicate that levels of BAI in the coals may be used to predict coal's toxicity, even before large-scale mining.

Biological Availability↗

Role of bioavailable iron in coal dust-induced activation of activator protein-1 and nuclear factor of activated T cells: difference between Pennsylvania and Utah coal dusts.

Activator protein-1 (AP-1) and nuclear factor of activated T cells (NFAT) are two important transcription factors responsible for the regulation of cytokines, which are involved in cell proliferation and inflammation. Coal workers' pneumoconiosis (CWP) is an occupational lung disease that may be related to chronic inflammation caused by coal dust exposure. In the present study, we demonstrate that coal from the Pennsylvania (PA) coalmine region, which has a high prevalence of CWP, can activate both AP-1 and NFAT in JB6 mouse epidermal cells. In contrast, coal from the Utah (UT) coalmine region, which has a low prevalence of CWP, has no such effects. The PA coal stimulates mitogen-activated protein kinase (MAPK) family members of extracellular signal-regulated kinases (ERKs) and p38 MAPK but not c-Jun-NH(2)-terminal kinases, as determined by the phosphorylation assay. The increase in AP-1 by the PA coal was completely eliminated by the pretreatment of cells with PD98059, a specific MAPK kinase inhibitor, and SB202190, a p38 kinase inhibitor, further confirming that the PA coal-induced AP-1 activation is mediated through ERKs and p38 MAPK pathways. Deferoxamine (DFO), an iron chelator, synergistically enhanced the PA coal-induced AP-1 activity, but inhibited NFAT activity. For comparison, cells were treated with ferrous sulfate and/or DFO. We have found that iron transactivated both AP-1 and NFAT, and DFO further enhanced iron-induced AP-1 activation but inhibited NFAT. These results indicate that activation of AP-1 and NFAT by the PA coal is through bioavailable iron present in the coal. These data are in agreement with our previous findings that the prevalence of CWP correlates well with levels of bioavailable iron in coals from various mining regions.

Animals↗

Factors that influence the formation and stability of hydrated ferrous sulfate in coal dusts. Possible relation to the emphysema of coal miners.

Epidemiological studies have shown that a causal relationship may exist between coal dust exposure and emphysema in coal miners. Emphysema can be considered as one of the human pathologies associated with oxidative stress, resulting from oxidant-induced alpha 1-antitrypsin (alpha 1-AT) inactivation and uncontrolled proteolysis of lung tissue. We have previously reported that certain coal dusts contained hydrated ferrous sulfate (FeSO4) that inactivated alpha 1-AT [Huang et al. (1993) Chem. Res. Toxicol. 6, 452-458]. In the present study, we have shown that the FeSO4 originated from oxidation of pyrite (FeS2), which is a typical contaminant of coal dusts. The relative humidity and microenvironment around individual pyrite particles influence the formation of FeSO4 in the coal. However, the subsequent human exposure to coal dust containing FeSO4 depends on the stability of the formed FeSO4. We found that pH played the most important role in stabilizing the FeSO4, such that a final pH < 4.5 after oxidation of pyrite stabilized FeSO4, whereas at high pH the conversion of reactive Fe2+ to Fe3+ was immediate. Sulfuric acid (H2SO4), which is also produced by the oxidation of pyrite, can lower the pH, but it can also be neutralized by other minerals in coal dusts, such as calcite (CaCO3). The stability of FeSO4 in coal dust can also be influenced by the length of exposure to air. Our studies demonstrated that coal samples differed in their capacity to stabilize FeSO4. This current study strengthens our previous reported hypothesis that emphysema, which occurs irregularly in coal miners, could be directly related to exposure to coal dust containing FeSO4.

Coal↗

Gene expression of primary human bronchial epithelial cells in response to coal dusts with different prevalence of coal workers' pneumoconiosis.

Striking regional differences in the prevalence of coal workers' pneumoconiosis (CWP) have been observed but not fully understood. This study investigated the early biological responses of primary lung cells to treatment with coal dusts from various seams. High-density oligoarray technology (GeneChip, Affymetrix, Santa Clara, CA) was used to compile gene expression profiles of primary human bronchial epithelial cells to low concentrations (2 microg/cm(2)) of coals for 6 h or 24 h of treatment. Data showed that a total of 1050 out of 12,000 genes on the chip were altered by 2 coal dusts. The coal from the Pennsylvania (PA) coal-mine region with a high prevalence of CWP altered 908 genes, many more than the coal from Utah (UT) with a low prevalence of CWP, which affected 356 genes. Many genes decreased their expression levels in response to the PA coal at 6 h and/or 24 h of treatment. For example, transferrin receptor, a gene known to control cellular iron uptake, was downregulated in the cells treated with the iron-containing PA coal in order to protect cells from iron overload. The UT coal without bioavailable iron had no such effect. The downregulation patterns of genes were confirmed by reverse-transcription polymerase chain reaction (RT-PCR). This study is one of the first in profiling gene expressions of primary bronchial epithelial cells treated with coals from various seams, which may set stages for future studies on specific genes.

Cell Culture Techniques↗

Boiler briquette coal versus raw coal: Part I--Stack gas emissions.

Stack gas emissions were characterized for a steam-generating boiler commonly used in China. The boiler was tested when fired with a newly formulated boiler briquette coal (BB-coal) and when fired with conventional raw coal (R-coal). The stack gas emissions were analyzed to determine emission rates and emission factors and to develop chemical source profiles. A dilution source sampling system was used to collect PM on both Teflon membrane filters and quartz fiber filters. The Teflon filters were analyzed gravimetrically for PM10 and PM2.5 mass concentrations and by X-ray fluorescence (XRF) for trace elements. The quartz fiber filters were analyzed for organic carbon (OC) and elemental carbon (EC) using a thermal/optical reflectance technique. Sulfur dioxide was measured using the standard wet chemistry method. Carbon monoxide was measured using an Orsat combustion analyzer. The emission rates of the R-coal combustion (in kg/hr), determined using the measured stack gas concentrations and the stack gas emission rates, were 0.74 for PM10, 0.38 for PM2.5, 20.7 for SO2, and 6.8 for CO, while those of the BB-coal combustion were 0.95 for PM10, 0.30 for PM2.5, 7.5 for SO2, and 5.3 for CO. The fuel-mass-based emission factors (in g/kg) of the R-coal, determined using the emission rates and the fuel burn rates, were 1.68 for PM10, 0.87 for PM2.5, 46.7 for SO2, and 15 for CO, while those of the BB-coal were 2.51 for PM10, 0.79 for PM2.5, 19.9 for SO2, and 14 for CO. The task-based emission factors (in g/ton steam generated) of the R-coal, determined using the fuel-mass-based emission factors and the coal/steam conversion factors, were 0.23 for PM10, 0.12 for PM2.5, 6.4 for SO2, and 2.0 for CO, while those of the BB-coal were 0.30 for PM10, 0.094 for PM2.5, 2.4 for SO2, and 1.7 for CO. PM10 and PM2.5 elemental compositions are also presented for both types of coal tested in the study.

Air Pollution↗

Addition of calcite reduces iron's bioavailability in the Pennsylvania coals--potential use of calcite for the prevention of coal workers' lung diseases.

In the present study, a hypothesis was tested that the addition of calcite into the Pennsylvania coals may reduce levels of bioavailable iron (BAI), an important component in the mixed coal dust that may contribute to coal workers' lung diseases. Predetermined proportions of calcite (0, 1, 2, 5, 10% w/w) were added into three PA coals. After suspending the mixtures in an aqueous phosphate solution (10 mM, pH 4.5), which mimics the phagolysosomal conditions of the cells, levels of pH as well as calcium ions (Ca2+) in the coals were increased in a calcite concentration-dependent manner. In contrast, levels of BAI (both Fe2+ and Fe3+) were decreased. The inhibitory effects of calcite on the bioavailability of iron in human lung epithelial A549 cells and primary rat alveolar macrophages (AMs) were also examined. It was found that levels of low-molecular-weight (LMW) iron were significantly decreased in both A549 cells and AMs treated with the 10% calcite-PA coal mixture compared to those treated with the PA coal alone, while calcite itself had no effect on intracellular LMW iron. Calcite also showed a significant inhibitory effect on PA coal-induced ferritin synthesis in A549 cells. Reverse-transcription polymerase chain reaction (RT-PCR) studies revealed that the iron-containing PA coal downregulated levels of transferrin receptor (TfR) mRNA in A549 cells, which was partially restored by the addition of calcite. Our results indicate that calcite can inhibit the bioavailability of iron in the iron-containing PA coals.

Animals↗

Coal tar phototherapy for psoriasis reevaluated: erythemogenic versus suberythemogenic ultraviolet with a tar extract in oil and crude coal tar.

Recent studies have questioned the therapeutic value of coal tar versus ultraviolet (UV) radiation and their relative necessity in phototherapy for psoriasis. In this investigation, different aspects of tar phototherapy have been studied in single-blind bilateral paired comparison studies. The effects of 1% crude coal tar were compared with those of petrolatum in conjunction with erythemogenic and suberythemogenic doses of ultraviolet light (UVB) using a FS72 sunlamp tubed cabinet. Crude coal tar was clinically superior to petrolatum with suberythemogenic ultraviolet. With the erythemogenic UVB, petrolatum was equal in efficacy to crude coal tar. Suberythemogenic UVB was also used adjunctively to compare the effects of a 5% concentration of a tar extract in an oil base to 5% crude coal tar in petrolatum or the oil base without tar. The tar extract in oil plus suberythemogenic UVB produced significantly more rapid improvement than the oil base plus UVB. The direct bilateral comparison of equal concentrations of tar extract in oil base versus crude coal tar in petrolatum in a suberythemogenic UV photo regimen revealed no statistical differences between treatments. In a study comparing tar extract in oil and the oil base without ultraviolet radiation, the tar extract in oil side responded more rapidly. This demonstrates a direct effect of tar alone in therapy. We have also studied the effects of erythemogenic and suberythemogenic UVB with and without tar extract in oil in the hairless mouse epidermal deoxyribonucleic acid (DNA) synthesis suppression assay. It was found that erythemogenic dosages of UVB produced near maximal inhibition of DNA synthesis with or without coal tars. Suberythemogenic dosages of UVB produced submaximal suppression of DNA synthesis that was enhanced by adjunctive coal tar but not by vehicle, findings which are consistent with the above clinical results. These studies suggest that coal tars combined with suberythemogenic UVB therapy is a practical alternative (to more aggressive UVB therapy without coal tar) which reduces the UVB exposure to the patient.

Animals↗