EBC pH Research Articles

Acute effects of e‐cigarette vaping on pulmonary function and airway inflammation in healthy individuals and in patients with asthma

The acute effects of e-cigarettes have not been scientifically demonstrated yet. The aim of this study was to assess the acute changes in pulmonary function and airway inflammation in patients with asthma after vaping one e-cigarette. Twenty-five smokers suffering from stable moderate asthma according to GINA guidelines with no other comorbidities and 25 healthy smokers matched with the baseline characteristics of the asthmatic patients were recruited. PFT, IOS, FeNO and EBC were performed before and after vaping one e-cigarette with nicotine. pH and concentrations of IL-1β, IL-4, IL-5, IL-6, IL-8, IL-10, IL-13, IL-17A, TNF-α, ISO8 and LTB4 were measured in EBC. FFEV1/FVC ratio and PEF were reduced in asthmatic patients after e-cigarette. Z5Hz and R5Hz, R10Hz and R20Hz increased in both groups. FeNO and EBC pH increased by 3.60 ppb (P = 0.001) and 0.15 (P = 0.014) in asthmatic patients after e-cigarette, whereas they decreased in control group by 3.28 ppb (P < 0.001) and 0.12 (P = 0.064), respectively. The concentrations of IL-10, TNF-α and ISO8 in EBC increased in asthmatic patients after e-cigarette and the changes in concentrations of IL-1β and IL-4 differed significantly between the two groups. E-cigarette vaping resulted in acute alteration of both pulmonary function and airway inflammation in stable moderate asthmatic patients.

Association of air pollution sources and aldehydes with biomarkers of blood coagulation, pulmonary inflammation, and systemic oxidative stress.

Using data collected before, during, and after the 2008 Summer Olympic Games in Beijing, this study examines associations between biomarkers of blood coagulation (vWF, sCD62P and sCD40L), pulmonary inflammation (EBC pH, EBC nitrite, and eNO), and systemic oxidative stress (urinary 8-OHdG) with sources of air pollution identified utilizing principal component analysis and with concentrations of three aldehydes of health concern. Associations between the biomarkers and the air pollution source types and aldehydes were examined using a linear mixed effects model, regressing through seven lag days and controlling for ambient temperature, relative humidity, gender, and day of week for the biomarker measurements. The biomarkers for pulmonary inflammation, particularly EBC pH and eNO, were most consistently associated with vehicle and industrial combustion, oil combustion, and vegetative burning. The biomarkers for blood coagulation, particularly vWF and sCD62p, were most consistently associated with oil combustion. Systemic oxidative stress biomarker (8-OHdG) was most consistently associated with vehicle and industrial combustion. The associations of the biomarkers were generally not significant or consistent with secondary formation of pollutants and with the aldehydes. The findings support policies to control anthropogenic pollution sources rather than natural soil or road dust from a cardio-respiratory health standpoint.

A cross-sectional study of exhaled carbon monoxide as a biomarker of recent household air pollution exposure

RationaleHousehold air pollution causes 3.5 million deaths annually. Personal exposure assessments required for examining health associations are expensive and require technical expertize, limiting the quality of research in resource-poor settings ObjectivesTo assess the feasibility of exhaled carbon monoxide and its relationship to continuous personal carbon monoxide monitoring and markers of respiratory health in female cooks primarily cooking with biomass fuels in Araihazar, Bangladesh Methods and measureFor a 24-h period, exhaled carboxyhemoglobin (eCOHb) % saturation was measured before and after each cooking episode while simultaneous 24-h personal carbon monoxide monitoring was conducted. The Coburn–Forester–Kane (CFK) equation was used to convert continuous personal CO exposures to predicted COHb % saturation. Respiratory symptoms were assessed by St. George's Respiratory Questionnaire, airway inflammation measured by exhaled breath condensate pH, and lung function determined by spirometry. Spearman's correlation was used to examine the relationship between eCOHb and CKF-derived COHb, EBC pH, and lung function variables. eCOHb % saturation was dichotomized around the median and odds ratios calculated for each respiratory symptom Main resultsMeasurement of eCOHb % saturation is feasible in a resource-poor setting. eCOHb % saturation responds to cooking episodes and demonstrates consistency when measured at the same time point 24-h later, suggesting that eCOHb may be a sensitive biomarker of recent HAP exposures.

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.

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.

Respiratory health and breath condensate acidity in sawmill workers

The aim of the study was to evaluate exhaled breath condensate acidity (EBC pH) as a biomarker of airway response to occupational respiratory hazards present in sawmill. Sixty-one sawmill workers in total (26 from Sawmill 1 and 35 from Sawmill 2) provided EBC samples at the beginning and at the end of the working week. Respiratory symptoms, lung function, bronchodilator test and atopy status were assessed. Occupational environment was checked for the levels of respiratory hazards. Airborne dust concentrations were below threshold limit value. Endotoxin in Sawmill 1 and Sawmill 2, and moulds in Sawmill 1 were at the levels able to induce inflammatory response in the airways. Mould levels were 2.5 times higher in Sawmill 1 than in Sawmill 2. Compared to Sawmill 2 workers, lower spirometry values, higher prevalence of dry cough and positive bronchodilator test were found in Sawmill 1 workers. Monday EBC pH values did not differ between sawmills, but declined after one working week in Sawmill 1 workers (from 7.88 to 7.49, P = 0.012) and not in Sawmill 2 workers. Similar results were obtained when only respiratory healthy non-smokers were analysed. Monday-to-Friday change of other respiratory parameters was not observed. The results suggest EBC pH as a biomarker of acute respiratory effects related to occupational exposure to respiratory hazards in sawmills, presumably increased mould levels. The effect was present even at subclinical level, namely in respiratory healthy subjects. The long-term health implications remain unclear and should be evaluated in a follow-up study.

Exhaled breath condensate pH is influenced by respiratory droplet dilution

Several studies support that airway acid stress plays a role in the pathophysiology of asthma. Exhaled breath condensate pH (EBC pH) was suggested as a surrogate marker of airway acidification. The dilution of airway lining fluid (ALF) acids and bases by alveolar water may influence condensate pH, but it has not been studied yet. The aim of our study was to investigate the relationship between EBC pH and ALF dilution in EBC samples obtained from asthmatic and healthy subjects. EBC was collected from 55 asthmatic and 57 healthy subjects for pH and conductivity measurements. Fractional exhaled nitric oxide (FENO) and lung function tests were also performed in asthmatic patients. EBC pH was determined after 10 min of argon deareation and the dilution was estimated by the measurement of conductivity in vacuum-treated samples. There was no difference either in EBC pH or dilution between the two groups. However, a significant relationship was found between EBC pH and dilution in both groups (p < 0.05, r = −0.35 and r = −0.29, asthmatic and healthy groups, respectively). Our results suggest important methodological aspect indicating that EBC pH is affected by respiratory droplet dilution, and this effect should be taken into consideration when interpreting EBC pH data.

Relationship between Exhaled Nitric Oxide and Exposure to Low-Level Environmental Tobacco Smoke in Children with Asthma on Inhaled Corticosteroids

Objectives. The relationship between exhaled nitric oxide (FeNO) and asthma severity or control is inconsistent. Active smoking lowers FeNO, but the relationship between passive smoking and FeNO is less clear. Children may be exposed to low-level environmental tobacco smoke (ETS) or thirdhand smoke, even if parents avoid smoking in the presence of their children. Our hypothesis was that FeNO is lower in children with asthma exposed to low-level ETS when compared with those who are not exposed. Methods. Children with stable asthma, 8–18 years of age, on low- or medium-dose inhaled corticosteroids (ICS) were enrolled. Spirometry, Asthma Control Questionnaire (ACQ), FeNO, exhaled breath condensate pH (EBC pH), and EBC ammonia were compared between children with and without ETS exposure as determined by urinary cotinine. Results. Thirty-three subjects were enrolled, of which 10 (30%) had urinary cotinine levels ≥1 ng/ml. There were no significant differences between the two groups in age, sex, BMI percentile, atopy status, FEV1, EBC pH, or EBC ammonia. Median ACQ was 0.29 (IQR: 0.22–0.57) for those with cotinine levels <1 ng/ml and 0.64 (IQR: 0.57–1.1) for those with cotinine levels of ≥1 ng/ml, p = .02. Median FeNO (ppb) was 23.9 (IQR: 15.2–34.5) for unexposed subjects and 9.6 (IQR: 5.1–15.8) for exposed subjects, p = .008. Conclusions: Children with asthma on low to medium doses of ICS and recent low-level ETS exposure have lower FeNO levels when compared with non-ETS-exposed subjects. Exposure to low-level ETS or thirdhand smoke may be an important variable to consider when interpreting FeNO as a biomarker for airway inflammation.

Evaluation of exhaled breath condensate pH as a biomarker for COPD

We assessed the utility of EBC pH as a biomarker in COPD in a large cohort of well-characterised individuals with COPD and control subjects from the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) study. We also determined short term reproducibility and the response of EBC to oral prednisolone. EBC was collected with R-Tubes(TM), using techniques for sampling and measurement that have been shown to be reproducible. EBC pH was lower in COPD (n = 676, 7.29 ± SD 0.60) and in smoking controls (n = 31, 7.18 ± 0.85), compared with non-smoking controls (n = 50, 7.59 ± 0.44, p = 0.0008 and 0.0033 respectively), but was not different between COPD and smoking controls. There was no relationship between EBC pH and disease severity, as assessed by the percent predicted FEV(1), nor with airway inflammation as assessed by sputum leukocyte counts. Treatment with 20 mg.day-1 prednisolone for 4 weeks did not change EBC pH. EBC pH is lower in COPD than in healthy control non-smokers, but does not differentiate COPD from smokers without COPD, relate to disease severity or to airway inflammation, and does not respond to corticosteroids. EBC pH therefore does not appear to be a useful biomarker in COPD.

Identification of Intrinsic Airway Acidification in Pulmonary Tuberculosis

Exhaled breath condensate acidification reflects the presence of airway acidification. Mycobacterium tuberculosis is an organism particularly sensitive to acidity. We aimed to determine if there is evidence of airway acidification in a cross section of patients with active tuberculosis.We enrolled 51 subjects with active tuberculosis in Ghana and Thailand, and compared them to control subjects. We collected exhaled breath condensate, and assayed for pH after gas standardization.Exhaled breath condensate pH from the control group revealed a median of 7.9 (7.7 - 8.0, n = 21), significantly higher than the active pulmonary tuberculosis patients who had a median pH of 7.4 (7.0 - 7.7; n = 51; p=0.002). Presence or absence of antibiotic therapy did not affect EBC pH values.These exhaled breath condensate data support the theory that airways become acidic in active tuberculosis infection. This may be a mechanism of immune response and pathology not previously considered.

The Effects of Mometasone DPI on Airway Hyperresponsiveness and Markers of Airway Inflammation

RATIONALE: Exhaled nitric oxide (eNO) and exhaled breath condensate pH (EBC pH) may be useful markers of airway inflammation, a cardinal feature of asthma. The ability of inhaled corticosteroids to influence these parameters concomitantly with FEV1 and methacholine responsiveness has not been elucidated. This study examines the effects of mometasone DPI on these markers of airway inflammation in asthma. METHODS: Twelve adult steroid naïve patients with mild to moderate persistent asthma (FEV1 ≥60% predicted and PC20 methacholine <8 mg/mL) were treated with mometasone furoate DPI 400 mcg daily for 8 weeks, followed by a 4-week washout. FEV1, methacholine PC20, eNO and EBC pH were measured at baseline, during active treatment (weeks 1, 4 and 8) and during mometasone washout (post-treatment weeks 1 and 4). RESULTS: Median FEV1 at baseline was 2.99 L (89% of predicted), and was unaffected during the study. Methacholine PC20 increased by 4.1 doubling doses by treatment week 4, and remained higher throughout post-treatment week 4 (p = 0.01). Median eNO decreased from 24.6 ppb to 15.1 ppb by treatment week 1 and remained significantly lower through week 8 (p = 0.05), reverting to baseline by post-treatment week 4. Median EBC pH increased from 7.81 to 8.02 by treatment week 4, and then plateaued, although statistical significance was not achieved. CONCLUSIONS: Treatment of asthma with mometasone DPI is associated with significant improvements in methacholine responsiveness and eNO, and a trend towards increased EBC pH. These data suggest that inhaled corticosteroids affect eNO more rapidly and transiently, but airway hyperresponsiveness more slowly and persistently.