Thesis (M.S.)--West Virginia University, 2009. / Title from document title page. Document formatted into pages; contains xii, 105 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 96-100).

The increase in environmental levels of platinum can in part be attributed to the introduction of motor vehicle catalytic converters. Quadrupole inductively coupled plasma mass spectrometry (Q-ICP-MS) has been evaluated as a analytical tool for the determination of platinum in environmental samples, such as vegetation, roadside dust, soil and sediment. Instrumental parameters were studied and a forward power of 1.4 kW and nebuliser flow rate of 0.95 1 min-1 were shown to give the optimum signal response for the 195Pt+ isotope. A detection limit of 0.12 ng ml-1 was achieved. Iridium was shown to be the most suitable choice for use as an internal standard with the 191Ir+ isotope being monitored. Various digestion methods were studied with aqua regia / hydrofluoric acid open vessel digestion being found to give good recovery for 2 certified reference materials, NIST 2556 (Used Autocatalyst, Pellets) and 2557 Used Autocatalyst, Monolith) with concentrations of 681 (38) mug g-1 and 1085 (32) mug g-1 respectively [certified values 697.4 (2.3) mug g-1 and 1131 (11) mug g-1]. Attention has been given to the problem of spectroscopic interference on 195Pt+ from hafnium oxide. Various correction methods were evaluated with a modification proposed to a previous method of mathematical correction being found to provide the best correction for the 179Hf16O+. An 'in-house' reference sample was prepared from a used catalytic converter and its platinum content of 3563 (176) ng g-1 established through inter-laboratory and inter-method procedures. Common rye grass (Lolium perenne) was shown to uptake platinum from both solid and liquid platinum-containing matrices. The methods developed were applied to a study of roadside dust samples taken from a busy section of the London M25 orbital motorway. The measured platinum levels of up to 194 ng g-1 agree with published literature from other European countries and represent a useful contribution to the knowledge concerning roadside platinum in the UK.

Many production technologies generate a variety of gas pollutants, which are unhealthy. The aim is therefore to minimize the content of such gas pollutants in the work environment. The highest capture efficiency of gas pollutants offers the local exhausting. Its disadvantage is the necessity to surround the source of pollutants, or to be as close as possible which is usually not technically or technologically possible. A possible alternative is to use a reinforced exhaust system that achieves greater capture distances. In the initial stage of the solution of the dissertation, a review of reinforced exhaust systems was carried out. Further, an existing measurement system was modified for measurements with the partition above the exhaust slot and the measurement system was partially automated. In order to investigate the case with pollutants having a lower density than the air, the workbench - the partition was moved above the exhaust slot. Based on of the literature review, a modification of the reinforced slot exhaust system was proposed. The modification consisted in the adjustment of the air inlet adjustment where a set of holes and a tube assembly were used instead of the slot. Such setup allowed for higher flow turbulence and thus for an increased exhaust efficiency. Subsequently, the inlet streams from the slot, holes and tubes were visualized by the smoke method. Further measurements were carried out by the tracer gas method for the determination of the exhaust efficiency. Measurements of velocity fields in front of the proposed configurations of the reinforced slot exhaust hood were also carried out. In conclusion, an energy performance assessment was carried out by means of the measurement of the electric power input to the fans with the determination of the electric loss power.

One of the most prevalent pollutants in urban cities is diesel exhaust particulate (DEP). Air pollution has been linked with increased risk of recurrent myocardial infarction (MI) and MI related death (Brook, 2008). This may be due, in part, to effects on atherosclerotic plaque stability and blood clotting tendency. Whether exposure to DEP changes the response of the heart to ischaemia, resulting in increased damage after MI is less well documented. The work described in this thesis was designed to investigate the hypothesis that pulmonary instillation of DEP would increase vulnerability of the heart to subsequent myocardial reperfusion injury secondary to activation of a systemic inflammatory response, endothelial dysfunction and triggering of transient receptor potential vanilloid 1 (TRPV1) mediated autonomic reflexes in the lung. Examination of bronchoalveolar lavage (BAL) fluid revealed pulmonary inflammation 6 h after exposure to DEP, characterised by neutrophil infiltration, raised levels of the inflammatory mediator interleukin-6 (IL-6) and an increase in alveolar permeability demonstrated by increased levels of protein in the lavage fluid. Pulmonary inflammation was largely resolved 24 h after exposure. While there was no indication of systemic inflammation at 6 h after DEP instillation, the levels of two inflammatory mediators, IL-6 and tumour necrosis factor alpha (TNFα) were increased in the plasma by 24 h after exposure. DEP had no affect on blood flow responses to the endothelium dependent dilator acetylcholine (ACh) in rat hind-limb vasculature in vivo at 6 or 24 h. In summary, while exposure of rats to DEP can induce both pulmonary and systemic inflammation, it does not modify endothelium-dependent vasodilatation. Ischaemia-reperfusion (I/R) was induced in vivo in anaesthetised rats and ex vivo in buffer perfused hearts from rats that had received DEP in vivo 6 h earlier. In both in vivo and ex vivo I/R models, infarct size (unstained by triphenyltetrazolium choride) was significantly increased in hearts from DEP-instilled rats relative to hearts from saline-instilled or non-instilled rats. Baseline oxidant stress, determined by electron paramagnetic spin resonance (EPR) in heart perfusate, was also significantly higher in perfusate of hearts from DEP-instilled rats. In summary, a single exposure of the lung to DEP leads to priming of the myocardium for I/R injury. As the results cited above illustrated, priming of hearts appeared unlikely to be due to either coronary vascular endothelial dysfunction or systemic inflammation. At 6 h post exposure, DEP was associated with increased blood pressure and myocardial hypersensitivity to ischaemia-induced arrhythmias, both suggestive of sympathetic activation. The beta 1 (β1) selective blocker metoprolol was used to investigate the role of the sympathetic nervous system (SNS) in transmitting the influence of DEP in the lung to the myocardium via β1 adrenoceptor activation. Administration of metoprolol (10 mg/kg, intraperotineal) at the time of DEP instillation into the lung was found to protect the heart from potentiation of ex vivo reperfusion injury. Metoprolol was also effective in reducing oxygen free radical generation from these hearts. The TRPV1 antagonist AMG 9810 was also used to study the role of TRPV1 receptors in mediating the priming influence of pulmonary DEP to the myocardium since activation of sensory receptors have been reported to modify sympathetic output via feedback to the central nervous system (Widdicombe et al., 2001). Coadministration of AMG 9810 (30 mg/kg) in vivo with DEP into the lung was found to prevent enhancement of ex vivo reperfusion injury associated with DEP instillation alone. Collectively these results have demonstrated that a single exposure of the lung to DEP leads to priming of the myocardium for I/R injury. Furthermore, this priming occurs via activation of a pulmonary sensory reflex that is likely to involve secondary activation of systemic β1 adrenoceptors.

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