Smoke Species Research Articles

Modeling dispersion and deposition of smoke generated from chemical fires

AbstractSmoke is a mixture of toxic gases and suspended particulate matter of solids and liquids that evolves from a fire of flammable materials. This article presents real‐time consequence modeling to track the concentration of individual species in smoke as well as its soot deposition. In the modeling process presented, the burning rate or vapor mass is fed into a combustion model in which the combustion of products has been identified and quantified along with the temperature of the fire. The output of the combustion model is the smoke that will be dispersed into the ambient. The fire geometry, which depends on the type of fire (e.g., pool or flare), is identified. A dispersion model with the capability of determining particulate deposition is then used for tracking the smoke plume. The combustion model provides the composition of the toxic species present in the smoke: carbon monoxide, halogen acids, organic and inorganic irritants, and soot, and their quantities as the air‐to fuel ratio is changed. The end product is an excellent what‐if analysis tool for responders. For example, it provides the ability to determine whether to ignite or when to ignite a flammable, toxic release by comparing their consequences. © 2011 American Institute of Chemical Engineers Process Saf Prog, 2011

Evidence for Peroxynitrite and Cognates in Whole Smoke

Abstract The peroxynitrite anion (ONOO-), a major product of the gas-phase interaction between the superoxide radical and nitric oxide, has been detected by ion chromatography (IC) for the first time. IC analyses of cigarette whole mainstream smoke collected in deionized water (DiW), using a Dionex 4500i IC, a Dionex AS11 column, an aqueous sodium hydroxide linear gradient with conductivity suppression from 1-20 mMNaOH, and conductivity coupled with diode array detection, revealed an unknown singly charged anion I incompletely resolved from nitrite. Gradient modification produced baseline resolution of I from nitrite and from a number of additional, previously undetected anions associated with smoke samples. Possible candidates for the unexpected smoke sample anion, including bromide, cyanide, and hydrogen hyponitrite were rejected for possible correspondence with the new smoke species on the basis of concentration range and chemical behavior. Chemical, chromatographic, and spectroscopic evidence supported the assignment of this smoke component as ONOO-. Mineral acid immediately destroyed I in the collected aqueous smoke medium. Both the retention time and the ultraviolet spectrum (UV) maximum at 302 nm for I were identical to those for synthetic peroxynitrite. The smoke from full flavor [28.5-30.4 mg total particulate matter (TPM)] filter cigarettes contained 2.4-3.3 µg/cig of this species. Levels were 4 to 5 times higher, up to 13 µg/cig, in cigarettes with the filters removed.

Oxidation of glutathione and cysteine in human plasma associated with smoking

Cigarette smoking contributes to the development or progression of numerous chronic and age-related disease processes, but detailed mechanisms remain elusive. In the present study, we examined the redox states of the GSH/GSSG and Cys/CySS couples in plasma of smokers and nonsmokers between the ages of 44 and 85 years ( n = 78 nonsmokers, n = 43 smokers). The Cys/CySS redox in smokers (−64 ± 16 mV) was more oxidized than nonsmokers (− 76 ± 11 mV; p < .001), with decreased Cys in smokers (9 ± 5 μM) compared to nonsmokers (13 ± 6 μM; p < .001). The GSH/GSSG redox was also more oxidized in smokers (−128 ± 18 mV) than in nonsmokers (−137 ± 17 mV; p = .01) and GSH was lower in smokers (1.8 ± 1.3 μM) than in nonsmokers (2.4 ± 1.0; p < .005). Although the oxidation of GSH/GSSG can be explained by the role of GSH in detoxification of reactive species in smoke, the more extensive oxidation of the Cys pool shows that smoking has additional effects on sulfur amino acid metabolism. Cys availability and Cys/CySS redox are known to affect cell proliferation, immune function, and expression of death receptor systems for apoptosis, suggesting that oxidation of Cys/CySS redox or other perturbations of cysteine metabolism may have a key role in chronic diseases associated with cigarette smoking.

Loss of Glutathione, Ascorbate Recycling, and Free Radical Scavenging in Human Erythrocytes Exposed to Filtered Cigarette Smoke

Exposure of human erythrocytes to filtered cigarette smokein vitroinhibited their capacity to reduce dehydroascorbic acid (ascorbate recycling activity). Glucose uptake was not affected, implying that dehydroascorbic acid transport was not inhibited by the smoke treatment. The intracellular reduction of cationic nitroxide free radicals, which provides a measure of ascorbate recycling, was also inhibited by cigarette smoke. A major factor in the inhibition of free radical reduction was glutathione depletion. However, glutathione depletion alone could not account for the inhibition of free radical reduction because a restoration of the glutathione pool in hemolyzed cells only partially restored free radical reduction activity. Another factor inhibiting free radical reduction was a lowering of pH, which was attributed mainly to the uptake of CO2and was reversible by restoring the physiological pH. Exogenous glutathione spared both intracellular glutathione and free radical reduction activity. The rate of depletion of intracellular glutathione was similar to that of extracellular glutathione, indicating that the erythrocyte membrane did not significantly attenuate thiol-reactive species in smoke. Protein thiols were also depleted by cigarette smoke, but to a much lesser extent than was glutathione. Ascorbate was relatively unaffected by cigarette smoke; significant intracellular ascorbate levels remained after glutathione was barely detectable. Autooxidizable reducing agents, capable of reducing both reduced piperidinyl (Tempo) and pyrrolidinyl (Proxyl) nitroxides partitioned from filtered cigarette smoke into aqueous solutions. Attempts to detect cigarette smoke-derived oxidants in buffer solutions or in cell suspensions with a prereduced Tempo nitroxide, whose oxidation properties resemble those of ascorbate, were unsuccessful. The results of this study suggest that chemical modification of glutathione is a major damage mechanism of filtered cigarette smoke, whereas free radical oxidations are relatively insignificant.