Exhaled Breath Condensate pH Assays

Hunt, J.F.

doi:10.1016/j.iac.2007.09.006

Cited by 33 publications

(31 citation statements)

References 20 publications

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“…The implication is that AH 2 , an otherwise efficient O 3 (g) scavenger under normal physiological conditions, should gradually lose its effectivity in ELF that become locally acidified by simultaneous inhalation of acidic airborne particles (35)(36)(37) or by preexistent pathologies such as asthma (38) or defective airway pH homeostasis (39). Secondary fine particulate matter (PM Ͻ2.5 ) should be particularly detrimental (2) because, by growing on sulfate/sulfuric acid nuclei, is essentially acidic and, because of its small size, can reach deeper into the airways to generate local acidic conditions (39)(40)(41). As a reference, the mean pH of exhaled breath condensates in healthy subjects is Ϸ7.8 but extends down to pH 4.5, particularly in younger individuals (38).…”

Section: Discussionmentioning

confidence: 99%

Acidity enhances the formation of a persistent ozonide at aqueous ascorbate/ozone gas interfaces

Enami

Hoffmann

Colussi

2008

Proc. Natl. Acad. Sci. U.S.A.

103

164

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The pulmonary epithelium, like most aerial biosurfaces, is naturally protected against atmospheric ozone (O3) by fluid films that contain ascorbic acid (AH 2) and related scavengers. This mechanism of protection will fail, however, if specific copollutants redirect AH2 and O3(g) to produce species that can transduce oxidative damage to underlying tissues. Here, the possibility that the synergistic adverse health effects of atmospheric O 3(g) and acidic particulate matter revealed by epidemiological studies could be mediated by hitherto unidentified species is investigated by electrospray mass spectrometry of aqueous AH 2 droplets exposed to O3(g). The products of AH2 ozonolysis at the relevant air-water interface shift from the innocuous dehydroascorbic acid at biological pH to a C 4-hydroxy acid plus a previously unreported ascorbate ozonide (m/z ‫؍‬ 223) below pH Ϸ5. The structure of this ozonide is confirmed by tandem mass spectrometry and its mechanism of formation delineated by kinetic studies. Present results imply enhanced production of a persistent ozonide in airway-lining fluids acidified by preexisting pathologies or inhaled particulate matter. Ozonides are known to generate cytotoxic free radicals in vivo and can, therefore, transduce oxidative damage.ascorbic acid ͉ oxidative damage ͉ particulate matter ͉ lung ͉ biosurfaces

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Section: Discussionmentioning

confidence: 99%

Acidity enhances the formation of a persistent ozonide at aqueous ascorbate/ozone gas interfaces

Enami

Hoffmann

Colussi

2008

Proc. Natl. Acad. Sci. U.S.A.

103

164

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“…Several issues of concern were shared by studying exhaled volatiles and EBC. Oral/upper airway/salivary contamination, expiratory flow, surface and temperature of the collecting device, sample storage, and mode of mediator determination have all been shown to influence the results of EBC studies [59][60][61][62][63][64][65][66][67][68][69][70][71][72][73][74][75][76]. One specific consideration in EBC research is the dilution of droplets by water vapour.…”

Section: Exhaled Monoxidesmentioning

confidence: 99%

Exhaled biomarkers in lung cancer

et al. 2009

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Lung cancer is the leading cause of cancer death. Results of therapeutic interventions are particularly discouraging when the disease is discovered in an advanced stage. Early diagnosis is limited by the fact that the disease usually develops asymptomatically and available screening methods do not fulfil the requirements for reliable discrimination between patients with lung cancer and subjects not suffering from the disease. Breath sampling is completely noninvasive and provides a potentially useful approach to screening lung cancer. Exhaled biomarkers contain both volatile and nonvolatile molecules. The profile of volatile organic compounds is different in patients with lung cancer than in control subjects. In exhaled breath condensate, the proteomic profile of breath from cancer patients differs from that of healthy smokers. We reviewed the scientific evidence demonstrating that a unique chemical signature can be detected in the breath of patients with lung cancer and that the exhaled breath biomarker profile could aid clinical decision making.KEYWORDS: Biomarker, electronic nose, exhaled breath, exhaled breath condensate, lung cancer, smell L ung cancer is the leading cause of global cancer death in both males and females. According to the most recent projection of global mortality, by 2030 it will emerge as the third and the fifth leading cause of death in highand middle-income countries, respectively [1,2]. Figures on disease outcome measures are very discouraging as even with the most advanced treatment strategies ,86% of lung cancer patients die within 5 yrs of diagnosis. With early detection and treatment, however, the 5-yr survival rate improves dramatically from 20% in patients with stage III lung cancer to 70% in patients with stage I disease [3]. Researchers, therefore, have sought out screening tests to detect lung cancer in the earliest stages and several promising new approaches have been proposed for this purpose, such as computer-assisted image analysis of chest radiographs, spiral computed tomography (CT) scanning, PCR-based assays of sputum and fluorescence bronchoscopy [4][5][6][7].Breath chemical tests have a broad spectrum of applications ranging from the US Food and Drug Administration-approved exhaled nitric oxide fraction (FeNO) measurement to monitor the effect of anti-inflammatory treatment in asthma, to volatile organic compound (VOC) determination and nonvolatile biomarker profiling in the cooled breath sample called exhaled breath condensate (EBC) [8][9][10][11]. Being completely noninvasive, sampling of the breath allows clinicians and researchers to assess different body functions in a flexible manner. Breath collection can be performed even in very severe patients and also repeated within short intervals. Therefore, breath testing is considered to be a potentially ideal candidate for screening purposes. Besides widely known constituents such as nitrogen, oxygen, carbon dioxide, inert gases and water vapour, exhaled breath also consists of thousands of volatile and nonv...

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“…For instance, urine pH in the collecting duct can vary from 4.5 to 8 in response to metabolic acidosis and alkalosis as well as with changes in diet and volume status (22). Normal airway surface liquid pH is slightly alkaline (pH 7.8 -8.1) (23) but can become highly acidic (pH 4 -6) with lung disease (24). Sweat pH can fall to Ͻ6 when the production rate is low but becomes neutral as production increases (25).…”

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confidence: 99%

Extracellular Protons Regulate Human ENaC by Modulating Na+ Self-inhibition

Collier

Snyder

2009

Journal of Biological Chemistry

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The epithelial Na ؉ channel, ENaC, is exposed to a wide range of proton concentrations in the kidney, lung, and sweat duct. We, therefore, tested whether pH alters ENaC activity. In Xenopus oocytes expressing human ␣-, ␤-, and ␥ENaC, amiloridesensitive current was altered by protons in the physiologically relevant range (pH 8.5-6.0). Compared with pH 7.4, acidic pH increased ENaC current, whereas alkaline pH decreased current (pH 50 ‫؍‬ 7.2). Acidic pH also increased ENaC current in H441 epithelia and in human primary airway epithelia. In contrast to human ENaC, pH did not alter rat ENaC current, indicating that there are species differences in ENaC regulation by protons. This resulted predominantly from species differences in ␥ENaC. Maneuvers that lock ENaC in a high open-probability state ("DEG" mutation, proteolytic cleavage) abolished the effect of pH on human ENaC, indicating that protons alter ENaC current by modulating channel gating. Previous work showed that ENaC gating is regulated in part by extracellular Na ؉ ("Na ؉ self-inhibition"). Based on several observations, we conclude that protons regulate ENaC by altering Na ؉ self-inhibition. First, protons reduced Na ؉ self-inhibition in a dose-dependent manner. Second, ENaC regulation by pH was abolished by removing Na ؉ from the extracellular bathing solution. Third, mutations that alter Na ؉ self-inhibition produced corresponding changes in ENaC regulation by pH. Together, the data support a model in which protons modulate ENaC gating by relieving Na ؉ self-inhibition. We speculate that this may be an important mechanism to facilitate epithelial Na ؉ transport under conditions of acidosis.

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Exhaled Breath Condensate pH Assays

Cited by 33 publications

References 20 publications

Acidity enhances the formation of a persistent ozonide at aqueous ascorbate/ozone gas interfaces

Acidity enhances the formation of a persistent ozonide at aqueous ascorbate/ozone gas interfaces

Exhaled biomarkers in lung cancer

Extracellular Protons Regulate Human ENaC by Modulating Na+ Self-inhibition

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