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BACKGROUND: There is insufficient knowledge about the systemic health effects of exposure to fine (PM2.5) and ultrafine particles emitted from typical indoor sources, including cooking and candlelight burning. We examined whether short-term exposure to emissions from cooking and burning candles cause inflammatory changes in young individuals with mild asthma. Thirty-six non-smoking asthmatics participated in a randomized controlled double-blind crossover study attending three exposure sessions (mean PM2.5 µg/m3; polycyclic aromatic hydrocarbons ng/m3): (a) air mixed with emissions from cooking (96.1; 1.1), (b) air mixed with emissions from candles (89.8; 10), and (c) clean filtered air (5.8; 1.0). Emissions were generated in an adjacent chamber and let into a full-scale exposure chamber where participants were exposed for five hours. Several biomarkers were assessed in relation to airway and systemic inflammatory changes; the primary outcomes of interest were surfactant Protein-A (SP-A) and albumin in droplets in exhaled air - novel biomarkers for changes in the surfactant composition of small airways. Secondary outcomes included cytokines in nasal lavage, cytokines, C-reactive protein (CRP), epithelial progenitor cells (EPCs), genotoxicity, gene expression related to DNA-repair, oxidative stress, and inflammation, as well as metabolites in blood. Samples were collected before exposure start, right after exposure and the next morning.RESULTS: SP-A in droplets in exhaled air showed stable concentrations following candle exposure, while concentrations decreased following cooking and clean air exposure. Albumin in droplets in exhaled air increased following exposure to cooking and candles compared to clean air exposure, although not significant. Oxidatively damaged DNA and concentrations of some lipids and lipoproteins in the blood increased significantly following exposure to cooking. We found no or weak associations between cooking and candle exposure and systemic inflammation biomarkers including cytokines, CRP, and EPCs.CONCLUSIONS: Cooking and candle emissions induced effects on some of the examined health-related biomarkers, while no effect was observed in others; Oxidatively damaged DNA and concentrations of lipids and lipoproteins were increased in blood after exposure to cooking, while both cooking and candle emissions slightly affected the small airways including the primary outcomes SP-A and albumin. We found only weak associations between the exposures and systemic inflammatory biomarkers. Together, the results show the existence of mild inflammation following cooking and candle exposure.

Supplementary Material 1

Background Chronic cough is a common condition but disease mechanisms are not fully understood. Our aim was to study respiratory biomarkers from the small airways in individuals with non-productive cough. Methods A cohort of 107 participants answered detailed questionnaires, performed spirometry, exhaled NO measurement, impulse oscillometry, gave blood samples and particles in exhaled air (PEx) samples. Current smokers (N = 38) were excluded. A total of 14 participants reported non-productive cough (cases). A total of 55 participants reported no cough (control group). PEx samples, containing exhaled particles derived from small airways, were collected and analysed with the SOMAscan proteomics platform. Results Participants with non-productive cough had similar age, sex, BMI, and inflammation markers in blood tests, as participants without cough. The proteomics analysis found 75 proteins significantly altered among participants with chronic cough compared to controls, after adjusting for sex and investigator performing the PExA measurement (all with p-value Conclusions This exploratory study on proteomics of exhaled particles among individuals with chronic cough found alterations in relative abundance of 75 proteins. The proteins identified are implicated in both pathways known to be implicated in cough, but also potentially new pathways. Further studies are needed to explore the importance of these findings.

Additional file 1: Table S1. Proteins considered being detected in PEx samples using the SOMAscan 1.3 K platform. Table S2. Result from differential abundance analysis. Table S3. Result from manual reviewing the scientific literature on proteins found to be differentially abundant in A-hLCI as compared to NA group. Table S4. Demographic and clinical characteristics of groups based on smoking history.

Additional file 1.

Respiratory tract lining fluid (RTLF) is an important component of the lung epithelial barrier. Pathological changes in RTLF may cause increased permeability of the epithelial barrier, but changes within RTLF are difficult to assess non-invasively. The aim of this study was to explore if the use of the non-invasive measurement technique, Particles in Exhaled Air (PEx) and blood test were useful in assessing epithelial barrier, and if cigarette smoking affects the relationship. In a general population subcohort from the European Community Respiratory Health Survey III in Iceland (n = 112), we collected RTLF droplets using the PEx technique, in conjunction with blood samples and questionnaire data. We measured surfactant protein A (SP-A) in the collected plasma and PEx samples. Participants were defined as healthy if they did not currently have asthma, were non-smokers and had forced expiratory volume in one second & GE; 80% of predicted value. Of the 112 participants, 97 were healthy and 15 were current smokers. There was no correlation between plasma and PEx SP-A levels. However, the ratio of plasma to PEx SP-A was significantly higher in smokers compared to healthy subjects. The lack of correlation between PEx and plasma SP-A in healthy participants, indicates that SP-A in plasma does not diffuse freely over the lung epithelial barrier. However, the lung epithelial barrier may be injured by smoking, leading to diffusion of SP-A across the barrier into the bloodstream, causing an increased ratio of plasma to PEx SP-A.