Condensate pH Research Articles

Exhaled Breath Condensate pH Does Not Discriminate Asymptomatic Gastroesophageal Reflux or the Response to Lansoprazole Treatment in Children with Poorly Controlled Asthma

Although exhaled breath condensate (EBC) pH has been identified as an "emerging" biomarker of interest for asthma clinical trials, the clinical determinants of EBC pH remain poorly understood. Other studies have associated acid reflux-induced respiratory symptoms, for example, cough, with transient acidification of EBC. We sought to determine the clinical and physiologic correlates of EBC acidification in a highly characterized sample of children with poorly controlled asthma. We hypothesized that (1) children with asymptomatic gastroesophageal reflux determined by 24-hour esophageal pH monitoring would have a lower EBC pH than children without gastroesophageal reflux, (2) treatment with lansoprazole would alter EBC pH in those children, and (3) EBC acidification would be associated with increased asthma symptoms, poorer asthma control and quality of life, and increased formation of breath nitrogen oxides (NOx). A total of 110 children, age range 6 to 17 years, with poor asthma control and esophageal pH data enrolled in the Study of Acid Reflux in Children with Asthma (NCT00442013) were included. Children submitted EBC samples for pH and NOx measurement at randomization and at study weeks 8, 16, and 24. Serial EBC pH measurements failed to distinguish asymptomatic gastroesophageal reflux and was not associated with breath NOx formation. EBC pH also did not discriminate asthma characteristics such as medication and health care utilization, pulmonary function, and asthma control and quality of life both at baseline and across the study period. Despite the relative ease of EBC collection, EBC pH as a biomarker does not provide useful information of children with asthma who were enrolled in asthma clinical trials.

Young “Healthy” Smokers Have Functional and Inflammatory Changes in the Nasal and the Lower Airways

Smoking is responsible for most COPD. Although people with COPD often have concomitant nasal disease, there are few studies that report physiologic or inflammatory changes in the upper airways in young asymptomatic smokers. We investigated physiologic and inflammatory changes in the nasal and lower airways of young smokers and if these changes were related to smoking history. Seventy-two subjects aged between 18 and 35 years (32 healthy nonsmokers and 40 young smokers) participated in this study. We measured nasal mucociliary clearance (MCC), nasal mucus surface contact angle, cell counts, myeloperoxidase and cytokine concentrations in nasal lavage fluid, exhaled breath condensate (EBC) pH, and lung function. Smokers had faster MCC, an increased number of cells (macrophages, ciliated cells, and goblet cells), increased lavage myeloperoxidase concentration, and decreased EBC pH compared with nonsmokers. There was a significant inverse relationship between pack-year smoking history and EBC pH. There were no differences in lung function or mucus surface properties comparing smokers to nonsmokers. Young adult smokers have functional and inflammatory changes in the nasal and lower airways and these correlate with smoking history. However, in these young smokers, smoking history was not associated with pulmonary function decline, probably because it is unlikely that spirometry detects early physiologic changes in the airways. ClinicalTrials.gov; No.: NCT01877291; URL: www.clinicaltrials.gov.

Airway acidification in childhood asthma exacerbations.

Exhaled breath condensate (EBC) is being used increasingly to sample airway lining fluid. In asthmatic patients, the concentration of pH in EBC has been found to be decreased and to be related to airway inflammation. The aim of this study was to determine exhaled pH levels during acute asthma exacerbations in relation to pharmacologic treatment in asthmatic children and compare these with control subjects. Twelve asthmatic children with asthma exacerbation and 27 healthy children were enrolled. Clinical observations and pH in EBC before and after standard treatment for asthma attack, based administration of inhaled beta2-agonist, and corticosteroid, according to international Global Initiative for Asthma guidelines, were compared with those in healthy subjects. All children performed skin-prick tests to aeroallergens. Asthmatic children underwent spirometry. Exhaled pH levels were significantly lower in children with asthma exacerbation before treatment (mean ± SD = 7.87 ± 0.66; p = 0.03) but not after treatment (8.11 ± 0.06; p = 0.40) compared with controls (8.12 + 0.19). Intragroup analyses found that condensate pH levels in asthmatic children before treatment were lower, but not significantly, than those after treatment. No correlation was found between pH values and treatment with systemic corticosteroids or lung function. Asthmatic children were atopic in 75% of cases. Levels of pH are decreased in EBC of asthmatic children with exacerbation before treatment. Larger studies are required to determine whether EBC pH levels may be a useful noninvasive biomarker to guide treatment of asthma exacerbations in childhood.

Comparisons of Ultrafine and Fine Particles in Their Associations with Biomarkers Reflecting Physiological Pathways

Using a quasi-experimental opportunity offered by greatly restricted air pollution emissions during the Beijing Olympics compared to before and after the Olympics, we conducted the current study to compare ultrafine particles (UFPs) and fine particles (PM2.5) in their associations with biomarkers reflecting multiple pathophysiological pathways linking exposure and cardiorespiratory events. Number concentrations of particles (13.0–764.7 nm) and mass concentrations of PM2.5 were measured at two locations within 9 km from the residence and workplace of 125 participating Beijing residents. Each participant was measured 6 times for biomarkers of autonomic function (heart rate, systolic and diastolic blood pressures), hemostasis (von Willebrand factor, soluble CD40 ligand, and P-selectin), pulmonary inflammation and oxidative stress (exhaled nitric oxide and exhaled breath condensate pH, malondialdehyde, and nitrite), and systemic inflammation and oxidative stress (urinary malondialdehyde and 8-hydroxy-2′-deoxyguanosine, plasma fibrinogen, and white blood cells). Linear mixed models were used to estimate associations of biomarkers with UFPs and PM2.5 measured 1–7 days prior to biomarker measurements (lags). We found that the correlation coefficient for UFPs at two locations (∼9 km apart) was 0.45, and at the same location, the correlation coefficient for PM2.5 vs UFPs was −0.18. Changes in biomarker levels associated with increases in UFPs and PM2.5 were comparable in magnitude. However, associations of certain biomarkers with UFPs had different lag patterns compared to those with PM2.5, suggesting that the ultrafine size fraction (≤100 nm) and the fine size fraction (∼100 nm to 2.5 μm) of PM2.5 are likely to affect PM-induced pathophysiological pathways independently.

Lung function, airway inflammation, and polycyclic aromatic hydrocarbons exposure in mexican schoolchildren: a pilot study.

To determine the association of exposure to polycyclic aromatic hydrocarbons (PAHs) with lung function and pH of exhaled breath condensate (EBC) in Mexican schoolchildren. A pilot study was performed in a subsample of 64 schoolchildren from Mexico City. Lung function and pH of EBC were measured and metabolites of PAHs in urine samples were determined. The association was analyzed using robust regression models. A 10% increase in the concentrations of 2-hydroxyfluorene was significantly negatively associated with forced expiratory volume in 1 second (-11.2 mL, 95% CI: -22.2 to -0.02), forced vital capacity (-11.6 mL, 95% CI: -22.9 to -0.2), and pH of EBC (-0.035, 95% CI: -0.066 to -0.005). Biomarkers of PAHs exposure were inversely associated with lung function and decrease of ph of EBC as a marker of airway inflammation in Mexican schoolchildren.

Exhaled breath condensate pH decreases during exercise‐induced bronchoconstriction

Exercise-induced bronchoconstriction (EIB) is the temporary narrowing of the airways caused by physical exercise. Its exact pathophysiology is unclear; however, acute changes in airways pH may play a role. Exhaled breath condensate (EBC) pH was suggested as a surrogate indicator for airway acid-base status, but its value is also affected by volatile molecules and respiratory droplet dilution. The aim of the study was to assess changes in EBC pH during EIB. Twenty-two asthmatics who reported breathlessness following exercise and 16 healthy individuals participated in the study. Lung function test was performed and exhaled breath samples were collected for pH, dilution factor and volatile compound pattern measurements (Cyranose 320) pre-exercise and at 0, 10, 20 and 30 min after physical exercise challenge. Fractional exhaled nitric oxide was measured before exercise. EIB developed in 13 asthmatic subjects. In these participants, but not in the EIB-negative asthmatics (P = 0.51), EBC pH reduced significantly during exercise (P = 0.01). In addition, changes in EBC pH were related to the degree of bronchospasm in the EIB-positive group (P = 0.01, r = 0.68). Exhaled volatile pattern became altered (P < 0.05) during exercise in all subjects (asthmatics and controls). EBC pH changes were not related to EBC dilution or volatile compound pattern alterations (P > 0.05). The development of EIB was related to acute changes of EBC pH, which suggest the role of airway pH decrease in the pathophysiology of EIB. Exercise-induced changes in exhaled biomarkers suggest methodological precautions to avoid physical exercise before performing exhaled breath tests.

Different Patterns in Changes of Exhaled Breath Condensate pH and Exhaled Nitric Oxide After Ozone Exposure.

Study objective was the evaluation of pH in exhaled breath condensate (EBC-pH) and nitric oxide in exhaled breath (FeNO) as biomarkers of ozone induced inflammation. We recently demonstrated that an ozone exposure of 240 ppb is sufficient to reduce lung function indices. We enrolled ten healthy subjects exposed in an intermittent exercise protocol to ozone concentrations of 240 ppb and 40 ppb (sham exposure). EBC-pH and FeNO were assessed before (pre), immediately post (post), and 16 h after exposure (16 h). Findings are that compared to baseline, EBC-pH was significantly higher immediately after sham and ozone exposures, but not 16 h later. There was a negative net change in EBC-pH after adjusting for effects after sham exposure (net-ΔpHpost -0.38%, net-ΔpH16h -0.23%). Concerning FeNO, we observed no changes of values after sham exposure compared to baseline, but measured a significant lower net response at the end of exposure (net-ΔFeNOpost -17.5%) which was transient within 16 h (net-ΔFeNO16h -9.4%). We conclude that exercise known to enhance EBC-pH may compensate for EBC acidification associated with inflammation resulting in diminished change of this biomarker. Ozone imposes an oxidative burden and reactions between reactive oxygen species and NO might be an explanation for reduced FeNO levels.

Acute effects of summer air pollution on pulmonary function and airway inflammation in healthy young women.

BackgroundExposure to air pollution has been reported to be associated with asthma exacerbation. However, little is known about the effects of air pollutant exposure in healthy people. A panel study was conducted to evaluate the acute effects of air pollutants on pulmonary function and airway inflammation in healthy subjects.MethodsExhaled breath condensate (EBC) pH, fractional concentration of exhaled nitric oxide (FeNO), and pulmonary function were measured in 21 healthy young women repeatedly for two weeks in the summer in Tokyo, Japan. The concentrations of air pollutants were obtained from the monitoring stations in the neighborhoods where the subjects lived. Statistical analyses were performed using generalized estimating equations.ResultsEBC pH decreased significantly with a 10-ppb increase in the 4-day average ozone (O3) concentration and a 10-µg/m3 increase in the 4-day average suspended particulate matter (SPM) concentration (−0.07 [95% confidence interval {CI} −0.11 to −0.03] and −0.08 [95% CI −0.12 to −0.03], respectively). Subjects with a history of rhinitis showed marked decreases in EBC pH associated with increases in O3 and SPM. The changes in forced expiratory volume in 1 second (FEV1) were also significantly associated with a 10-µg/m3 increase in the 3-day average concentration of SPM (−0.09 L [95% CI −0.17 to −0.01]). FeNO increased significantly in relation to the increase in O3 and SPM among only subjects with a history of asthma.ConclusionsOver the course of the study, EBC became significantly acidic with increases in O3 and SPM concentrations. Furthermore, higher SPM concentrations were associated with decreased FEV1. Subjects with a history of rhinitis or asthma are considered to be more susceptible to air pollutants.

Effect of Simvastatin on Physiological and Biological Outcomes in Patients Undergoing Esophagectomy

To test whether simvastatin improves physiological and biological outcomes in patients undergoing esophagectomy. One-lung ventilation during esophagectomy is associated with inflammation, alveolar epithelial and systemic endothelial injury, and the development of acute lung injury (ALI). Statins that modify many of the underlying processes are a potential therapy to prevent ALI. We conducted a randomized double-blind placebo-controlled trial in patients undergoing esophagectomy. Patients received simvastatin 80 mg or placebo enterally for 4 days preoperatively and 7 days postoperatively. The primary end point was pulmonary dead space (Vd/Vt) at 6 hours after esophagectomy or before extubation. Inflammation was assessed by plasma cytokines and intraoperative exhaled breath condensate pH; alveolar type 1 epithelial injury was assessed by plasma receptor for advanced glycation end products and systemic endothelial injury by the urine albumin-creatinine ratio. Thirty-nine patients were randomized; 8 patients did not undergo surgery and were excluded. Fifteen patients received simvastatin and 16 received placebo. There was no difference in Vd/Vt or other physiological outcomes. Simvastatin resulted in a significant decrease in plasma MCP-1 on day 3 and reduced exhaled breath condensate acidification. Plasma receptor for advanced glycation end products was significantly lower in the simvastatin-treated group, as was the urine albumin-creatinine ratio on day 7 postsurgery. ALI developed in 4 patients in the placebo group and no patients in the simvastatin group although this difference was not statistically significant (P=0.1). In this proof of concept study, pretreatment with simvastatin in esophagectomy decreased biomarkers of inflammation as well as pulmonary epithelial and systemic endothelial injury.

Exhaled breath condensate pH in mechanically ventilated patients

Exhaled breath condensate pH in mechanically ventilated patients

Increase of pro-oxidants with no evidence of lipid peroxidation in exhaled breath condensate after a 10-km race in non-athletes

It is a well-established fact that exercise increases pro-oxidants and favors oxidative stress; however, this phenomenon has been poorly studied in human lungs. Pro-oxidative generation (H(2)O(2), NO(2) (-)), lipid peroxidation markers (MDA), and inflammation (pH) in exhaled breath condensate (EBC) have been determined through data from 10 active subjects who ran 10 km; samples were obtained immediately before, at 20, and at 80 min post-exertion. In EBC, the concentration of H(2)O(2) at 80 min post-exertion was increased. NO(2) (-) concentration showed a tendency to increase at 80 min post-exertion, with no variations in MDA and pH. No variations of NO(2) (-) were found in plasma, while there was an increase of NO(2) (-) at 80 min post-exertion in the relation between EBC and plasma. NO(2) (-) in EBC did not correlate to plasmatic NO(2) (-), while it did correlate directly with H(2)O(2) in EBC, suggesting a localized origin for the exercise-related NO(2) (-) increase in EBC. MDA in plasma did not increase nor correlate with MDA in EBC. In conclusion, high-intensity exercise increases lung-originated pro-oxidants in non-athlete subjects with no evidence of early lipid peroxidation and changes in the pH value in EBC.

Seasonal Changes in Endotoxin Exposure and Its Relationship to Exhaled Nitric Oxide and Exhaled Breath Condensate pH Levels in Atopic and Healthy Children

Endotoxin, a component of the cell walls of gram-negative bacteria, is a contaminant in organic dusts (house dust) and aerosols. In humans, small amounts of endotoxin may cause a local inflammatory response. Exhaled nitric oxide (eNO) levels, an inflammation indicator, are associated with the pH values of exhaled breath condensate (EBC). This study evaluated seasonal changes on indoor endotoxin concentrations in homes and the relationships between endotoxin exposure and eNO/EBC pH levels for healthy children and children with allergy-related respiratory diseases. In total, 34 children with allergy-related respiratory diseases and 24 healthy children were enrolled. Indoor air quality measurements and dust sample analysis for endotoxin were conducted once each season inside 58 surveyed homes. The eNO, EBC pH levels, and pulmonary function of the children were also determined. The highest endotoxin concentrations were on kitchen floors of homes of children with allergy-related respiratory diseases and healthy children, and on bedroom floors of homes of asthmatic children and healthy children. Seasonal changes existed in endotoxin concentrations in dust samples from homes of children with allergic rhinitis, with or without asthma, and in EBC pH values among healthy children and those with allergy-related respiratory diseases. Strong relationships existed between endotoxin exposure and EBC pH values in children with allergic rhinitis.

Aging and airway inflammation

Since little is known of airways inflammation in the elderly, we have carried out a study to explore the presence of some inflammatory markers in the airways of healthy subjects of different ages using a non-invasive method which is particularly suitable for aged people. The aim of this work was to investigate whether parameters, including (1) pH, IL-8 and TNF-α in exhaled breath condensate (EBC), (2) exhaled nitric oxide levels (NO), and (3) inflammatory cell profile in induced sputum, are age-related. Thirty healthy adults (10 subjects below the age of 30 [A], 10 subjects between 30 and 60years [B], and 10 subjects over 60years of age [C]), were enrolled in the study. IL-8 and TNF-α levels were measured in breath condensate. Exhaled pH was measured after deaeration/decarbonation by means of a pH-meter. A rapid-response chemiluminescence NO analyzer was used to quantify NO. Induced sputum was collected, homogenized with dithiothreitol, and cytospins for differential cell were produced. The levels of IL-8 and TNF-α in EBC, the levels of exhaled NO, and the percentage of neutrophils in induced sputum were significantly elevated in C and B compared with A; the EBC pH level was significantly reduced in C and B compared with A. The EBC levels of IL-8, TNF-α, pH, the level of exhaled NO, and the percentage of neutrophils correlated significantly with age. This study has shown the presence of age-related airways inflammation in healthy subjects.

Marine lipid fraction PCSO-524™ (lyprinol®/omega XL®) of the New Zealand green lipped mussel attenuates hyperpnea-induced bronchoconstriction in asthma

Evaluate the effect of the marine lipid fraction of the New Zealand green-lipped mussel (Perna canaliculus) PCSO-524 (Lyprinol/Omega XL), rich in omega-3 fatty acids, on airway inflammation and the bronchoconstrictor response to eucapnic voluntary hyperpnea (EVH) in asthmatics. Twenty asthmatic subjects, with documented HIB, participated in a placebo controlled double-blind randomized crossover trial. Subjects entered the study on their usual diet and were then placed on 3 weeks of PCSO-524 or placebo supplementation, followed by a 2 week washout period, before crossing over to the alternative diet. Pre- and post-eucapnic voluntary hyperpnea (EVH) pulmonary function, fraction of exhaled nitric oxide (FENO), asthma symptom scores, medication use, exhaled breath condensate (EBC) pH, cysteinyl leukotrienes (cyst-LT), 8-isoprostane and urinary 9α, 11β-prostaglandin (PG)F2 and Clara (CC16) protein concentrations were assessed at the beginning of the trial and at the end of each treatment period. The PCSO-524 diet significantly reduced (p < 0.05) the maximum fall in post-EVH FEV1 (-8.4 ± 3.2%) compared to usual (-19.3 ± 5.4%) and placebo diet (-22.5 ± 13.7%). Pre- and post- EVH EBC cyst-LT and 8-isoprostane, and urinary 9α, 11β-PGF2 and CC16 concentrations were significantly reduced (p < 0.05) on the PCSO-524 diet compared to the usual and placebo diet. EBC pH and asthma symptom scores were significantly improved (p < 0.05) and rescue medication use significantly reduced (p < 0.05) on the PCSO-524 diet compared to the usual and placebo diet. PCSO-524 (Lyprinol)/Omega XL) may have beneficial effects in HIB and asthma by serving as a pro-resolving agonist and/or inflammatory antagonist.

Changes in exhaled breath condensate pH in healthy and asthmatic pregnant women

Asthma is a common chronic disease complicating pregnancy with a risk for perinatal complications. Control of airway inflammation in the asthmatic pregnancy improves pregnancy outcomes. Our aim was to evaluate pH of exhaled breath condensate (EBC), a non-invasive method for the assessment of asthmatic airway inflammation, in healthy and asthmatic pregnancies. Cross-sectional study. Hungarian university clinics. Seventeen healthy pregnant women, 21 asthmatic pregnant women, 23 healthy non-pregnant women and 22 asthmatic non-pregnant women. EBC samples were collected using a portable condenser, EBC pH was measured after argon deaeration. EBC pH. EBC pH (mean±SD) of healthy non-pregnant and asthmatic non-pregnant women was similar (7.75±0.27 vs. 7.54±0.57; p=0.118), probably indicating an optimal control of airway inflammation in asthmatic women. On the other hand, EBC pH was higher in healthy pregnant women compared with healthy non-pregnant women (8.02±0.43 vs. 7.75±0.27; p=0.017). Higher EBC pH accompanying healthy pregnancy was absent in asthmatic pregnant patients whose EBC pH was lower (7.65±0.38) than that of healthy pregnant women (p=0.006), and it was similar to that in asthmatic and healthy non-pregnant women (p=0.470 and p=0.300, respectively). The EBC pH in asthmatic pregnant women correlated positively with birthweight (r=0.49, p=0.047) and negatively with forced vital capacity (r=0.45, p=0.039). EBC pH was not related to blood pH. EBC pH is higher in healthy pregnant women but not in asthmatic pregnant women compared with data from healthy non-pregnant women, indicating that oxidative inflammatory processes induced by asthma may compromise the regulatory mechanisms causing alkaline pH in the airways during pregnancy.

PH in exhaled breath condensate and nasal lavage as a biomarker of air pollution-related inflammation in street traffic-controllers and office-workers

OBJECTIVE:To utilize low-cost and simple methods to assess airway and lung inflammation biomarkers related to air pollution.METHODS:A total of 87 male, non-smoking, healthy subjects working as street traffic-controllers or office-workers were examined to determine carbon monoxide in exhaled breath and to measure the pH in nasal lavage fluid and exhaled breath condensate. Air pollution exposure was measured by particulate matter concentration, and data were obtained from fixed monitoring stations (8-h work intervals per day, during the 5 consecutive days prior to the study).RESULTS:Exhaled carbon monoxide was two-fold greater in traffic-controllers than in office-workers. The mean pH values were 8.12 in exhaled breath condensate and 7.99 in nasal lavage fluid in office-workers; these values were lower in traffic-controllers (7.80 and 7.30, respectively). Both groups presented similar cytokines concentrations in both substrates, however, IL-1β and IL-8 were elevated in nasal lavage fluid compared with exhaled breath condensate. The particulate matter concentration was greater at the workplace of traffic-controllers compared with that of office-workers.CONCLUSION:The pH values of nasal lavage fluid and exhaled breath condensate are important, robust, easy to measure and reproducible biomarkers that can be used to monitor occupational exposure to air pollution. Additionally, traffic-controllers are at an increased risk of airway and lung inflammation during their occupational activities compared with office-workers.

Safety of an Alkalinizing Buffer Designed for Inhaled Medications in Humans

Airway acidification plays a role in disorders of the pulmonary tract. We hypothesized that the inhalation of alkalinized glycine buffer would measurably alkalinize the airways without compromising lung function or causing adverse events. We evaluated the safety of an inhaled alkaline glycine buffer in both healthy subjects and in subjects with stable obstructive airway disease. This work includes 2 open-label safety studies. The healthy controls were part of a phase 1 safety study of multiple inhalations of low-dose alkaline glycine buffer; nebulized saline was used as a comparator in 8 of the healthy controls. Subsequently, a phase 2 study in subjects with stable obstructive airway disease was completed using a single nebulized higher-dose strategy of the alkaline inhalation. We studied 20 non-smoking adults (10 healthy controls and 10 subjects with obstructive airway disease), both at baseline and after inhalation of alkaline buffer. We used spirometry and vital signs as markers of clinical safety. We used changes in fraction of exhaled nitric oxide (NO) and exhaled breath condensate (EBC) pH as surrogate markers of airway pH modification. Alkaline glycine inhalation was tolerated by all subjects in both studies, with no adverse effects on spirometric parameters or vital signs. Airway alkalinization was confirmed by a median increase in EBC pH of 0.235 pH units (IQR 0.56-0.03, P = .03) in subjects after inhalation of the higher-dose alkaline buffer (2.5 mL of 100 mmol/L glycine). Alkalinization of airway lining fluid is accomplished with inhalation of alkaline glycine buffer and causes no adverse effects on pulmonary function or vital signs.

Secondhand smoke exposure induces acutely airway acidification and oxidative stress

Previous studies have shown that secondhand smoke induces lung function impairment and increases proinflammatory cytokines. The aim of the present study was to evaluate the acute effects of secondhand smoke on airway acidification and airway oxidative stress in never-smokers. In a randomized controlled cross-over trial, 18 young healthy never-smokers were assessed at baseline and 0, 30, 60, 120, 180 and 240min after one-hour secondhand smoke exposure at bar/restaurant levels. Exhaled NO and CO measurements, exhaled breath condensate collection (for pH, H(2)O(2) and NO(2)(-)/NO(3)(-) measurements) and spirometry were performed at all time-points. Secondhand smoke exposure induced increases in serum cotinine and exhaled CO that persisted until 240min. Exhaled breath condensate pH decreased immediately after exposure (p<0.001) and returned to baseline by 180min, whereas H(2)O(2) increased at 120min and remained increased at 240min (p=0.001). No changes in exhaled NO and NO(2)/NO(3) were observed, while decreases in FEV(1) (p<0.001) and FEV(1)/FVC (p<0.001) were observed after exposure and returned to baseline by 180min. A 1-h exposure to secondhand smoke induced airway acidification and increased airway oxidative stress, accompanied by significant impairment of lung function. Despite the reversal in EBC pH and lung function, airway oxidative stress remained increased 4h after the exposure. Clinical trial registration number (EudraCT): 2009-013545-28.

Traffic-related air pollutants and exhaled markers of airway inflammation and oxidative stress in New York City adolescents

Exposures to ambient diesel exhaust particles have been associated with respiratory symptoms and asthma exacerbations in children; however, epidemiologic evidence linking short-term exposure to ambient diesel exhaust particles with airway inflammation is limited. We conducted a panel study with asthmatic and nonasthmatic adolescents to characterize associations between ambient diesel exhaust particle exposures and exhaled biological markers of airway inflammation and oxidative stress.Over four weeks, exhaled breath condensate was collected twice a week from 18 asthmatics and 18 nonasthmatics (ages 14–19 years) attending two New York City schools and analyzed for pH and 8-isoprostane as indicators of airway inflammation and oxidative stress, respectively. Air concentrations of black carbon, a diesel exhaust particle indicator, were measured outside schools. Air measurements of nitrogen dioxide, ozone, and fine particulate matter were obtained for the closest central monitoring sites. Relationships between ambient pollutants and exhaled biomarkers were characterized using mixed effects models.Among all subjects, increases in 1- to 5-day averages of black carbon were associated with decreases in exhaled breath condensate pH, indicating increased airway inflammation, and increases in 8-isoprostane, indicating increased oxidative stress. Increases in 1- to 5-day averages of nitrogen dioxide were associated with increases in 8-isoprostane. Ozone and fine particulate matter were inconsistently associated with exhaled biomarkers. Associations did not differ between asthmatics and nonasthmatics. The findings indicate that short-term exposure to traffic-related air pollutants may increase airway inflammation and/or oxidative stress in urban youth and provide mechanistic support for associations documented between traffic-related pollutant exposures and respiratory morbidity.

Exhaled breath condensate pH in mechanically ventilated patients

ObjectivesIn this prospective clinical trial we aimed to answer if spontaneous exhaled breath condensate (EBC) in the trap of the expiratory arm of the ventilator could replace EBC collected by coolant chamber standardized with Argon as an inert gas. Second, if EBC pH could predict ventilator associated pneumonia (VAP) and mortality. PatientsWe included 34 critically ill patients (males=26), aged=54.85±19.86 (mean±SD) yrs, that required mechanical ventilation due to non-pulmonary direct cause (APACHE II score=23.58±14.7; PaO2/FiO2=240.00±98.29). SettingICU with 9 beds from a regional teaching hospital. Intervention and ResultsThe patients were followed up until development of VAP, successful weaning or death. There were significant differences between mean EBC pH from the 4 procedures with the exception of spontaneous EBC de-aerated with Argon (n=79; 6.74±0.28) and coolant chamber deaerated with Argon (n=79; 6.70±0.36; p=NS by Tukey's Multiple Comparison Test). However, none of the procedures were extrapolated between each other according to Bland & Altman method. The mean EBC pH from the trap without Argon was 6.50±0.28. From the total of 34 patients, 22 survived and were discharged and 12 patients died in the ICU. ConclusionSpontaneous EBC pH could not be extrapolated to EBC pH from coolant chamber and it did not change in subjects who dead, neither subject with VAP in comparison with baseline data. The lack of other biomarker in EBC and the lack of a control group determinate the need for further studies in this setting.