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Similarities between histological features of alcoholic hepatitis and obesity-related liver disease suggest a common pathogenic mechanism. Because intestinal bacteria can produce ethanol, it is conceivable that intestinally derived alcohol may contribute to fatty liver disease. An indirect way of measuring endogenous ethanol is to measure the breath ethanol concentration. In a previous study in ob/ob mice, breath ethanol decreased with a course of non-absorbable antibiotics, suggesting that the ethanol is derived from intestinal bacterial flora. The aims of this study were 1) to determine whether alcohol can be detected in the breath of human subjects, and 2) to assess whether there is any correlation between ethanol and obesity in patients with nonalcoholic steatohepatits (NASH) and control subjects without known liver disease.Breath ethanol concentration was determined in 21 patients with biopsy-proven NASH and in 10 control subjects by gas chromatography. An abnormal breath ethanol level was defined as two standard deviations above the mean value of the breath ethanol of lean controls.Minute quantities of ethanol were detected in the breath of human subjects who had not consumed alcohol in the recent past. Patients who were obese were more likely to have higher breath ethanol concentrations. Women also had higher breath alcohol than men. However, there was no difference between patients with NASH and controls. Severity of liver disease, as evidenced by cirrhosis, did not influence the breath ethanol concentration.Higher breath ethanol concentrations are observed in obese subjects than in leaner ones. It is possible that intestinally derived ethanol may contribute to the pathogenesis of NASH.

Generation of toxic oxygen metabolites at reperfusion may contribute to the injury sustained as a consequence of harvest and ischemic preservation of organ allografts. Because there is a paucity of evidence that this mechanism is operative in human beings, we measured the generation of ethane into the exhaled breath as a biomarker of free radical-mediated lipid peroxidation in human liver transplantation.A novel technique that increased the previous standard of sensitivity 100-fold was used to measure picomole quantities of ethane in exhaled breath of eight recipients undergoing human orthotopic liver transplantation.Ethane production correlated closely with the specific events of liver transplantation including the initial reperfusion of the allografts. In every case a twofold to threefold increase in ethane production was superimposed on a stable baseline immediately after reestablishment of portal vein blood flow through the donor liver.Ethane production was interpreted as evidence of hepatic lipid peroxidation, presumably mediated by toxic metabolites of oxygen occurring at reperfusion. This noninvasive approach allowed localization of the time point at which lipid peroxidation occurred and may facilitate quantification of lipid peroxidation mediated by free radicals and other toxic oxygen metabolites during operation.

Knowledge about the health effects of exposure to formaldehyde associated with automotive emissions is of pivotal importance in the risk assessment of this agent. Mobile sources emit many combustion-derived pollutants, including formaldehyde, in association with respirable carbon particles. Because it is hydrophilic, most of the inhaled formaldehyde is absorbed in the upper respiratory tract. However, if the organic vapor is adsorbed on respirable particles, formaldehyde may be deposited in the deep lung with the inhaled particles and may be available to interact adversely with cells along the lung parenchyma. On the respiratory surface, the alveolar macrophage phagocytic system plays the pivotal role in defending the lung against infectious agents. Susceptibility to respiratory infections is a relevant and sensitive indicator of the adverse effects of air pollution because acute and chronic exposures to a variety of air pollutants have been shown to decrease pulmonary antibacterial defenses. The goal of this research was to investigate whether exposure to formaldehyde decreases resistance to respiratory infections through dysfunctions of the alveolar macrophage phagocytic system. The study also explored whether interactions between formaldehyde and respirable carbon black particles alter susceptibility to respiratory infections and impairment of alveolar macrophage phagocytosis by delivering adsorbed formaldehyde to the deep lung with the inhaled particles. A carbon black, Regal GR, was used in these studies as a surrogate for the carbonaceous core of Diesel particulate matter. This material was selected to represent the worst-case scenario because the carbon black was expected to adsorb formaldehyde strongly. To accomplish this goal, mice were exposed to formaldehyde and to carbon black and formaldehyde combinations; increased susceptibility to respiratory infections was quantified by alveolar macrophage-dependent intrapulmonary killing of Staphylococcus aureus after an inhalation challenge with the bacterium. The salient findings of the bactericidal studies are as follows: Fifteen parts per million (ppm)* formaldehyde impaired the intrapulmonary killing of S. aureus when exposure followed the bacterial challenge. One ppm formaldehyde impaired the intrapulmonary killing of S. aureus when exposure preceded and was continued after the bacterial challenge. Coexposures to target concentrations of 3.5 mg/m3 carbon black and 2.5 ppm formaldehyde, or 10 mg/m3 carbon black and 5 ppm formaldehyde after the bacterial challenge had no effect on the intrapulmonary killing of S. aureus. Preexposure for four hours per day for four days to target concentrations of 3.5 mg/m3 carbon black and 2.5 ppm formaldehyde had no effect on the intrapulmonary killing of S. aureus when the assay was performed one day after the cessation of exposure.(ABSTRACT TRUNCATED AT 400 WORDS)

The charge exchange mass spectrum of nickel carbonyl has been reported using a typical gasoline engine exhaust gas as the reactant gas. Various positive ions which can be attributed to nickel carbonyl and its fragments were observed in this mass spectrum. The effect of pressure on the intensity of both the reactant gas ions and the nickel carbonyl was studied in an attempt to find the optimum condition for the quantification of nickel carbonyl. Using these data, the minimum detectable limit was found to be 10 ppb for nickel carbonyl. This methodology was used to monitor nickel carbonyl in the effluent from a model reactor for a catalytic controlled automobile. Based on these studies, no measureable quantities of nickel carbonyl can be expected from catalytic controlled automobiles. 4 figures, 1 table.

Studies involving the Ames Salmonella mutagenicity test and the Bacillus subtilis comptest have demonstrated that the soluble organic fraction of diesel particulate is potentially mutagenic and DNA damaging. The soluble organic fraction was extracted from exhaust particulate samples collected from four different diesel engines operated at specified conditions. For each fraction collected, an increase in the concentration of the organic material resulted in a subsequent increase in the number of histidine prototrophs obtained when this material was added to the histidine auxotrophic strains that comprise the Ames Salmonella test. Specifically, the number of induced revertants, for strains TA98 and TA100, ranged from less than one revertant per microgram of sample to 29 revertants per microgram of sample. The ability of these organic fractions to induce bacterial SOS functions also was determined by exposing competent cultures of Bacillus subtilis strain RUB827 to increasing concentrations of these extracts. With varying efficiencies, these samples were positive in their ability to induce the SOS system of B subtilis. Significantly, the toxicity of these mutagenic and DNA damaging samples never resulted in more than 95% killing, even for the highest concentrations tested in the Salmonella and B subtilis assay.

An account is given of the preparation, separation and detection of volatile fluorides. These fluorides are formed by the reaction of chlorine trifluoride with the elements in a specially designed PTFE reaction vessel enclosed in an HF coil. A comparison is also made of a spectroscopic detector with a katharometer for the detection of the fluorides. The separation of volatile fluorides has been reported to be partially successful on perfluorinated materials such as Kel-F oils or waxes on PTFE supports.1–3 The present communication describes a more detailed investigation of these separations and also compares the performance of a newly developed spectroscopic detector4 with a conventional katharometer detector.

The design and construction of a reactor injection assembly for the formation of volatile metal fluorides is described. The sample, in a chlorine trifluoride atmosphere, is heated with a radio-frequency induction heater and the volatile products passed into a hydrogen diffusion flame emission detector. Although this device is primarily intended for use in gas chromatography, this preliminary evaluation is concerned with its application to atomic spectroscopy.

A new methodology has been applied to the analysis of human white blood cells obtained both from donors with normal white cells and from donors having one of several cytologically identified leukemias. The analytical process makes use of evolution patterns of molecular fragments generated during the well controlled degradation of the cells. The process has been shown to be effective both in grouping together malignant cells that originate from the same diseases and in distinguishing between malignant cells originating from different diseases. The reproducibility of the method has been demonstrated.