Anna-Carin Olin

Air pollution, airway inflammation, and lung function in a cohort study of Mexico City schoolchildren.

Background The biological mechanisms involved in inflammatory response to air pollution are not clearly understood. Objective In this study we assessed the association of short-term air pollutant exposure with inflammatory markers and lung function. Methods We studied a cohort of 158 asthmatic and 50 nonasthmatic school-age children, followed an average of 22 weeks. We conducted spirometric tests, measurements of fractional exhaled nitric oxide (FeNO), interleukin-8 (IL-8) in nasal lavage, and pH of exhaled breath condensate every 15 days during follow-up. Data were analyzed using linear mixed-effects models. Results An increase of 17.5 μg/m3 in the 8-hr moving average of PM2.5 levels (interquartile range) was associated with a 1.08-ppb increase in FeNO [95% confidence interval (CI), 1.01–1.16] and a 1.07-pg/mL increase in IL-8 (95% CI 0.98–1.19) in asthmatic children and a 1.16 pg/ml increase in IL-8 (95% CI, 1.00–1.36) in nonasthmatic children. The 5-day accumulated average of exposure to particulate matter < 2.5 μm in aerodynamic diamter (PM2.5) was significantly inversely associated with forced expiratory volume in 1 sec (FEV1) (p = 0.048) and forced vital capacity (FVC) (p = 0.012) in asthmatic children and with FVC (p = 0.021) in nonasthmatic children. FeNO and FEV1 were inversely associated (p = 0.005) in asthmatic children. Conclusions Exposure to PM2.5 resulted in acute airway inflammation and decrease in lung function in both asthmatic and nonasthmatic children.

Exhaled breath malondialdehyde as a marker of effect of exposure to air pollution in children with asthma

BACKGROUNDnAssessment of the adverse effects of oxidative stress related to air pollution is limited by the lack of biological markers of dose to the lungs.nnnOBJECTIVEnWe evaluated the use of exhaled breath condensate (EBC) malondialdehyde as a biomarker of exposure to traffic-related pollution in children with asthma as part of a panel study in Mexico City.nnnMETHODSnStandard spirometry and collection of EBC and nasal lavage were performed. Environmental monitoring sites were located within 5 km of the childrens homes and schools. Data were analyzed by using generalized estimating equations.nnnRESULTSnA total of 480 samples of malondialdehyde were obtained from 107 patients with asthma, with a median level of 18.7 (interquartile range [IQR], 12.4-28.7) nmol. Ambient particulates less than 2.5 microg/m(3) and ozone levels on the day of sampling were significantly associated with higher malondialdehyde levels. A 14.2-microg/m(3) (IQR) increase in 8-hour moving average particulates less than 2.5 microg/m(3) in size was associated with a 1.12-nmol increase in malondialdehyde and a 15.9-ppb (IQR) increase in 8-hour moving average ozone with a 1.16-nmol increase in malondialdehyde. Malondialdehyde levels were inversely associated with forced vital capacity and FEV(1) and positively associated with IL-8 levels in nasal lavage.nnnCONCLUSIONnExhaled breath condensate malondialdehyde was related to both air pollution exposure and changes in lung function and inflammatory markers.

Exhaled nitric oxide: relation to sensitization and respiratory symptoms

Background Conflicting data have been presented as to whether nitric oxide (NO) in exhaled air is merely reflecting atopy rather than airway inflammation.

Prevalence of asthma and exhaled nitric oxide are increased in bleachery workers exposed to ozone.

The aims of the present study were to determine whether exposure to high peaks of ozone resulted in an increased prevalence of asthma or respiratory symptoms among bleachery workers and whether nitric oxide (NO) was elevated in the exhaled air of these workers. Bleachery workers (n=228) from three Swedish pulp mills who had been exposed to ozone, together with 63 unexposed control subjects, were investigated by means of spirometry, Phadiatop®, exhaled and nasal NO and answers to a questionnaire concerning respiratory symptoms and exposure. Exposure to an ozone peak that gave rise to respiratory symptoms was defined as a “gassing”. Bleachery workers reporting four or more gassings involving ozone had an increased prevalence of adult-onset asthma, wheeze, and current asthma symptoms. They also had a higher median concentration of exhaled NO in comparison with those who reported no such gassings (19.2 versus 15.7 parts per billion). No such associations were found in respect of nasal NO. The results from this study show that bleachery workers who have been repeatedly exposed to ozone gassings have an increased prevalence of adult-onset asthma. The results also indicate exhaled nitric oxide may be a marker of airway inflammation in bleachery workers who have been exposed to high peaks of ozone.

Effects on airways of short-term exposure to two kinds of wood smoke in a chamber study of healthy humans

Introduction: Air pollution causes respiratory symptoms and pulmonary disease. Airway inflammation may be involved in the mechanism also for cardiovascular disease. Wood smoke is a significant contributor to air pollution, with complex and varying composition. We examined airway effects of two kinds of wood smoke in a chamber study. Materials and Methods: Thirteen subjects were exposed to filtered air and to wood smoke from the start-up phase and the burn-out phase of the wood-burning cycle. Levels of PM2.5 were 295 µg/m3 and 146 µg/m3, number concentrations 140 000/cm3 and 100 000/cm3. Biomarkers in blood, breath and urine were measured before and on several occasions after exposure. Effects of wood smoke exposure were assessed adjusting for results with filtered air. Results: After exposure to wood smoke from the start-up, but not the burn-out session, Clara cell protein 16 (CC16) increased in serum after 4 hours, and in urine the next morning. CC16 showed a clear diurnal variation. Fraction of exhaled nitric oxide (FENO) increased after wood smoke exposure from the burn-out phase, but partly due to a decrease after exposure to filtered air. No other airway markers increased. Conclusions: The results indicate that relatively low levels of wood smoke exposure induce effects on airways. Effects on airway epithelial permeability was shown for the start-up phase of wood burning, while FENO increased after the burn-out session. CC16 seems to be a sensitive marker of effects of air pollution both in serum and urine, but its function and the significance need to be clarified.

Effects of wood smoke particles from wood-burning stoves on the respiratory health of atopic humans.

BackgroundThere is growing evidence that particulate air pollution derived from wood stoves causes acute inflammation in the respiratory system, increases the incidence of asthma and other allergic diseases, and increases respiratory morbidity and mortality. The objective of this study was to evaluate acute respiratory effects from short-term wood smoke exposure in humans. Twenty non-smoking atopic volunteers with normal lung function and without bronchial responsiveness were monitored during three different experimental exposure sessions, aiming at particle concentrations of about 200u2009μg/m3, 400u2009μg/m3, and clean air as control exposure. A balanced cross-over design was used and participants were randomly allocated to exposure orders. Particles were generated in a wood-burning facility and added to a full-scale climate chamber where the participants were exposed for 3 hours under controlled environmental conditions. Health effects were evaluated in relation to: peak expiratory flow (PEF), forced expiratory volume in the first second (FEV1), and forced vital capacity (FVC). Furthermore, the effects were assessed in relation to changes in nasal patency and from markers of airway inflammation: fractional exhaled nitric oxide (FENO), exhaled breath condensate (EBC) and nasal lavage (NAL) samples were collected before, and at various intervals after exposure.ResultsNo statistically significant effect of wood smoke exposure was found for lung function, for FENO, for NAL or for the nasal patency. Limited signs of airway inflammation were found in EBC.ConclusionIn conclusion, short term exposure with wood smoke at a concentration normally found in a residential area with a high density of burning wood stoves causes only mild inflammatory response.

Diesel exhaust but not ozone increases fraction of exhaled nitric oxide in a randomized controlled experimental exposure study of healthy human subjects

BackgroundFraction of exhaled nitric oxide (FENO) is a promising non-invasive index of airway inflammation that may be used to assess respiratory effects of air pollution. We evaluated FENO as a measure of airway inflammation after controlled exposure to diesel exhaust or ozone.MethodsHealthy volunteers were exposed to either diesel exhaust (particle concentration 300 μg/m3) and filtered air for one hour, or ozone (300 ppb) and filtered air for 75 minutes. FENO was measured in duplicate at expiratory flow rates of 10, 50, 100 and 270 mL/s before, 6 and 24 hours after each exposure.ResultsExposure to diesel exhaust increased FENO at 6 hours compared with air at expiratory flow rates of 10 mL/s (pu2009=u20090.01) and at 50 mL/s (pu2009=u20090.011), but FENO did not differ significantly at higher flow rates. Increases in FENO following diesel exhaust were attenuated at 24 hours. Ozone did not affect FENO at any flow rate or time point.ConclusionsExposure to diesel exhaust, but not ozone, increased FENO concentrations in healthy subjects. Differences in the induction of airway inflammation may explain divergent responses to diesel exhaust and ozone, with implications for the use of FENO as an index of exposure to air pollution.

Validity of a questionnaire-based diagnosis of chronic obstructive pulmonary disease in a general population-based study

BackgroundThe diagnosis of chronic obstructive pulmonary disease (COPD) is based on airflow obstruction. In epidemiological studies, spirometric data have often been lacking and researchers have had to rely almost solely on questionnaire answers. The aim of this study is to assess the diagnostic accuracy of questionnaire answers to detect COPD.MethodsA sample of the Swedish general population without physician-diagnosed asthma was randomly selected and interviewed using a respiratory questionnaire. All eligible subjects aged 25–75xa0years (nu2009=u20093892) performed spirometry for detection of airflow obstruction using Global Initiative for Chronic Obstructive Lung Disease (GOLD) or American Thoracic Society (ATS)/European Respiratory Society (ERS) criteria. Sensitivity, specificity, positive likelihood ratio (LR+), positive predictive values (PPVs), and negative predictive values (NPVs) were calculated to define diagnostic accuracy of questionnaire answers.ResultsThe sensitivity of the question “Have you been diagnosed by a physician as having COPD or emphysema?” in detecting airflow obstruction was 5.7% using GOLD, and 9.8% using ATS/ERS, criteria; specificity was 99.7% for GOLD and 99.5% for ATS/ERS. Sensitivity, specificity, and PPV were higher for the question compared to self-reported symptoms of chronic bronchitis in identifying subjects with airflow obstruction.ConclusionsThe high specificity and good PPV suggest that the question “Have you been diagnosed by a physician as having COPD or emphysema?” is more likely to identify those who do not have airflow obstruction, whereas the low sensitivity of this question could underestimate the real burden of COPD in the general population.

A physiologically based model for spirometric reference equations in adults

A spirometric reference equation consists of a mathematical model with constants and coefficients optimized to fit a specific data set from healthy individuals. Commonly applied models are selected on statistical rather than physiological considerations. A predetermined model with constants and coefficients optimized to various populations would enable interpretable and interesting comparisons between populations. Lubiński and Gólczewski recently presented a piecewise linear model with constants and coefficients claimed to be physiologically interpretable (Lubiński model). Three questions were addressed: Is the Lubiński model as useful clinically as other models: multiple linear, piecewise polynomial and exponential with splines? Will reference equations based on the Lubiński model and optimized to a Swedish and to a Polish population allow for interpretable comparisons? Are three well‐known reference equations clinically useful in the Swedish adult population? A recent Swedish random population sample with high‐quality spirometric measurements enabled the present analyses. When optimized to fit the Swedish population sample, the Lubiński model and two other models provided accurate predictive normal values. Interesting differences were demonstrated between the Polish and Swedish populations. The proportion of subjects below lower limit normal was adequate for the piecewise polynomial equations but too low and not clinically useful for the advocated exponential equations with splines. It is concluded that the Lubiński model is clinically as useful as other models, and it adds important value and is recommended for future spirometric reference equations for adults. The advocated exponential equations with splines are not recommended for Swedish adults because of too wide normal limits.

Increased risk of rhinitis symptoms in subjects with gastroesophageal reflux.

Abstract Conclusion: This study shows that gastroesophageal reflux and tobacco smoke are associated with adult-onset non-infectious rhinitis (NIR). The results support an association between gastroesophageal reflux and upper airway inflammation. Objectives: To examine the incidence of adult-onset NIR in relation to several risk factors. Methods: This is a follow-up study of 3307 randomly selected men and women aged 25–75 years from a general population-based sample. At baseline, the subjects were investigated with questionnaires, a pulmonary function test, blood samples, and FENO. At follow-up 4 years later, all the subjects were mailed a respiratory questionnaire. The incidence of NIR and associated risk factors, such as smoking, atopy, asthma, cough, obesity, and gastroesophageal reflux, was assessed. Results: The response rate at follow-up was 92%. The incidence of new-onset NIR was 14.9/1000 person-years (n = 247). In a regression model including age, gender, obesity, asthma, cough, and atopy, both current smoking (OR 1.7, 95% CI 1.2–2.5, p = 0.002) and gastroesophageal reflux (OR 2.5, 95% CI 1.4–3.1, p < 0.001) were significantly associated with adult-onset NIR.