Effect of Natural Gas Fuel Addition on the Oxidation of Fuel Cell Anode Gas

The anode exhaust gas from a fuel cell commonly has a fuel energy density between 15 and 25% that of the fuel supply, due to the incomplete oxidation of the input fuel. This exhaust gas is subsequently oxidized (catalytically or non-catalytically), and the resultant thermal energy is often used elsewhere in the fuel cell process. Alternatively, additional fuel can be added to this stream to enhance the oxidation of the stream, for improved thermal control of the power plant, or to adjust the temperature of the exhaust gas as may be required in other specialty co-generation applications. Regardless of the application, the cost of a fuel cell system can be reduced if the exhaust gas oxidation can be accomplished through direct gas phase oxidation, rather than the usual catalytic oxidation approach. Before gas phase oxidation can be relied upon however, combustor design requirements need to be understood. The work reported here examines the issue of fuel addition, primarily as related to molten-carbonate fuel cell technology. It is shown experimentally that without proper combustor design, the addition of natural gas can readily quench the anode gas oxidation. The Chemkin software routines were used to resolve the mechanisms controlling the chemical quenching. It is found that addition of natural gas to the anode exhaust increases the amount of CH3 radicals, which reduces the concentration of H and O radicals and results in decreased rates of overall fuel oxidation

Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead.

Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead

Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety ‘Mode of Action’ framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology

Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead

Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/ mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety ‘Mode of Action’ framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology

A Partial Oxidation Technique for Fuel-Cell Anode Exhaust-Gas Synthesis

This paper describes the performance of a gas generator used to synthesize the exhaust gas from the anode of a molten-carbonate fuel cell. The composition of this gas is estimated to be that of equilibrium at 1,250 ° F and 1 atm: 48% CO2 , 39% H2O, 5% CO, and 8% H2, with an energy content of approximately 39 Btu/scf (higher heating value). To synthesize a range of gas compositions around this point, the gas generator partially oxidizes a mixture of CH4 , O2 , and CO2 to generate energy densities between 20 and 60 Btu/scf at temperatures between 1,198 and 1,350 ° F. Results show that the technique provides a relatively high ratio of CO to H2 concentrations compared with the target composition (CO:H2 of 2, versus 0.71). A detailed chemical model shows that the likely cause is quenching of the CO and H2 chemistry below 2,000 ° F

A Partial Oxidation Technique for Fuel-Cell Anode Exhaust-Gas Synthesis

This paper describes the performance of a gas generator used to synthesize the exhaust gas from the anode of a molten-carbonate fuel cell. The composition of this gas is estimated to be that of equilibrium at 1,250 ° F and 1 atm: 48% CO₂ , 39% H₂O, 5% CO, and 8% H₂, with an energy content of approximately 39 Btu/scf (higher heating value). To synthesize a range of gas compositions around this point, the gas generator partially oxidizes a mixture of CH₄ , O₂ , and CO₂ to generate energy densities between 20 and 60 Btu/scf at temperatures between 1,198 and 1,350 ° F. Results show that the technique provides a relatively high ratio of CO to H2 concentrations compared with the target composition (CO:H₂ of 2, versus 0.71). A detailed chemical model shows that the likely cause is quenching of the CO and H₂ chemistry below 2,000 ° F

Acoustic energy-driven fluid pump and method

Bulk fluid motion is promoted in a gaseous fluid contained within a conduit system provided with a diffuser without the need for a mean pressure differential across the conduit system. The contacting of the gaseous fluid with unsteady energy at a selected frequency and pressure amplitude induces fluid flow through the conical diffuser. The unsteady energy can be provided by pulse combustors, thermoacoustic engines, or acoustic energy generators such as acoustic speakers