Application of ICP-OES for evaluating energy extraction and production wastewater discharge impacts on surface waters in Western Pennsylvania.

Oil and gas extraction and coal-fired electrical power generating stations produce wastewaters that are treated and discharged to rivers in Western Pennsylvania with public drinking water system (PDWS) intakes. Inductively coupled plasma optical emission spectroscopy (ICP-OES) was used to quantify inorganic species in wastewater and river samples using a method based on EPA Method 200.7 rev4.4. A total of 53 emission lines from 30 elements (Al, As, B, Ba, Ca, Cd, Ce, Co, Cr, Cu, Fe, K, Li, Mg, Mn, Mo, Na, Ni, P, Pb, S, Sb, Se, Si, Sn, Sr, Ti, Tl, V, and Zn) were investigated. Samples were prepared by microwave-assisted acid digestion using a mixture of 2% HNO3 and 0.5% HCl. Lower interferences and better detection characteristics resulted in selection of alternative wavelengths for Al, As, Sb, Mg, Mo, and Na. Radial view measurements offered accurate determinations of Al, Ba, K, Li, Na, and Sr in high-brine samples. Spike recovery studies and analyses of reference materials showed 80-105% recoveries for most analytes. This method was used to quantify species in samples with high to low brine concentrations with method detection limits a factor of 2 below the maximum contaminant limit concentrations of national drinking water standards. Elements B, Ca, K, Li, Mg, Na, and Sr were identified as potential tracers for the sources impacting PDWS intakes. Usability of the ICP-OES derived data for factor analytic model applications was also demonstrated.

Diesel and biodiesel exhaust particle effects on rat alveolar macrophages with in vitro exposure.

Combustion emissions from diesel engines emit particulate matter which deposits within the lungs. Alveolar macrophages (AMs) encounter the particles and attempt to engulf the particles. Emissions particles from diesel combustion engines have been found to contain diverse biologically active components including metals and polyaromatic hydrocarbons which cause adverse health effects. However little is known about AM response to particles from the incorporation of biodiesel. The objective of this study was to examine the toxicity in Wistar Kyoto rat AM of biodiesel blend (B20) and low sulfur petroleum diesel (PDEP) exhaust particles. Particles were independently suspended in media at a range of 1-500µgmL(-1). Results indicated B20 and PDEP initiated a dose dependent increase of inflammatory signals from AM after exposure. After 24h exposure to B20 and PDEP gene expression of cyclooxygenase-2 (COX-2) and macrophage inflammatory protein 2 (MIP-2) increased. B20 exposure resulted in elevated prostaglandin E2 (PGE2) release at lower particle concentrations compared to PDEP. B20 and PDEP demonstrated similar affinity for sequestration of PGE2 at high concentrations, suggesting detection is not impaired. Our data suggests PGE2 release from AM is dependent on the chemical composition of the particles. Particle analysis including measurements of metals and ions indicate B20 contains more of select metals than PDEP. Other particle components generally reduced by 20% with 20% incorporation of biodiesel into original diesel. This study shows AM exposure to B20 results in increased production of PGE2in vitro relative to diesel.

Systemic imbalance of essential metals and cardiac gene expression in rats following acute pulmonary zinc exposure.

It was recently demonstrated that particulate matter (PM) containing water-soluble zinc produces cardiac injury following pulmonary exposure. To investigate whether pulmonary zinc exposure produces systemic metal imbalance and direct cardiac effects, male Wistar Kyoto (WKY) rats (12-14 wk age) were intratracheally (IT) instilled with saline or 2 micromol/kg zinc sulfate. Temporal analysis was performed for systemic levels of essential metals (zinc, copper, and selenium), and induction of zinc transporter-2 (ZT-2) and metallothionein-1 (MT-1) mRNA in the lung, heart, and liver. Additionally, cardiac gene expression profile was evaluated using Affymetrix GeneChips (rat 230A) arrays to identify zinc-specific effects. Pulmonary zinc instillation produced an increase in plasma zinc to approximately 20% at 1 and 4 h postexposure with concomitant decline in the lung levels. At 24 and 48 h postexposure, zinc levels rose significantly (approximately 35%) in the liver. At these time points, plasma and liver levels of copper and selenium also increased significantly, suggesting systemic disturbance in essential metals. Zinc exposure was associated with marked induction of MT-1 and ZT-2 mRNA in lung, heart, and liver, suggesting systemic metal sequestration response. Given the functional role of zinc in hundreds of proteins, the gene expression profiles demonstrated changes that are expected based on its physiological role. Zinc exposure produced an increase in expression of kinases and inhibition of expression of phosphatases; up- or downregulation of genes involved in mitochondrial function; changes in calcium regulatory proteins suggestive of elevated intracellular free calcium and increases in sulfotransferases; upregulation of potassium channel genes; and changes in free radical-sensitive proteins. Some of these expression changes are reflective of a direct effect of zinc on myocardium following pulmonary exposure, which may result in impaired mitochondrial respiration, stimulated cell signaling, altered Ca2+ homeostasis, and increased transcription of sulfotransferases. Cardiotoxicity may be an outcome of acute zinc toxicosis and occupational exposures to metal fumes containing soluble zinc. Imbalance of systemic metal homeostasis as a result of pulmonary zinc exposure may underlie the cause of extrapulmonary effects.

Cardiovascular and blood coagulative effects of pulmonary zinc exposure.

Cardiovascular damage induced by pulmonary exposure to environmental chemicals can result from direct action or, secondarily from pulmonary injury. We have developed a rat model of pulmonary exposure to zinc to demonstrate cardiac, coagulative, and fibrinolytic alterations. Male Wistar Kyoto rats were instilled intratracheally with saline or zinc sulfate, 131 microg/kg (2 micromol/kg); the alterations were determined at 1, 4, 24, and 48 h postexposure. High-dose zinc enabled us to show changes in circulating levels of zinc above normal and induce significant pulmonary inflammation/injury such that cardiac impairments were likely. At 1-24 h postexposure, plasma levels of zinc increased to nearly 20% above the base line. Significant pulmonary inflammation and injury were determined by analysis of bronchoalveolar lavage fluid and histopathology in zinc-exposed rats at all time points. Starting at 4 h postexposure, pulmonary damage was accompanied by persistently increased gene expressions of tissue factor (TF) and plasminogen activator-inhibitor-1 (PAI-1), but not thrombomodulin (TM). Cardiac tissues demonstrated similar temporal increases in expressions of TF, PAI-1, and TM mRNA following pulmonary instillation of zinc. In contrast to extensive pulmonary edema and inflammation, only mild, and focal acute, myocardial lesions developed in a few zinc-exposed rats; no histological evidence showed increased deposition of fibrin or disappearance of troponin. At 24 and 48 h postexposure to zinc, increases occurred in levels of systemic fibrinogen and the activated partial thromboplastin time. These data suggest that cardiovascular blood coagulation impairments are likely following pulmonary zinc exposure and associated pulmonary injury and inflammation.

The role of soluble components in ambient fine particles-induced changes in human lungs and blood.

Normal individuals developed pulmonary neutrophilic inflammation and increased blood fibrinogen following inhalation of concentrated ambient particles (CAPS). In this study, we sought to determine how soluble components in CAPS contributed to these changes. We expanded and reanalyzed data from 37 young healthy volunteers from a previous study (Ghio et al., 2000) who were exposed to either filtered air or CAPS. Postexposure bronchoalveolar lavage (BAL) as well as pre- and postexposure venous blood samples was analyzed for cellular and acute inflammatory endpoints. Nine most abundant components in the water-soluble fraction of CAPS were correlated with these endpoints using principal component analysis. We found that a sulfate/Fe/Se factor was associated with increased BAL percentage of neutrophils and a Cu/Zn/V factor with increased blood fibrinogen. The concentrations of sulfate, Fe, and Se correlated highly with PM mass (R > 0.75) while the correlations between PM and Cu/Zn/V were modest (R = 0.2-0.6). These results from controlled human exposure linked specific PM components to pulmonary neutrolphil influx and blood fibrinogen increase, and indicated the soluble components of pollutant particles may differentially affect pulmonary and hematological systems in humans exposed to PM.