Liubov Barbinova

Occupational airborne exposure, specific sensitization and the atopic status: evidence of a complex interrelationship

BackgroundWe have investigated the relationship between atopic status and long-term occupational exposure to latex proteins or methyl diethyl diisocyanate (MDI) as high and low molecular weight asthma-inducing agents, respectively.MethodsThis study is based on retrospective analyses of two groups of symptomatic outpatients: 184 healthcare workers with latex exposure and 156 workers with isocyanate (MDI) exposure. We analysed atopic and non-atopic subgroups according to exposure duration and the frequencies of specific sensitization.Results45% of the healthcare subgroup specifically sensitized to latex were atopic, whereas in the non-sensitized healthcare subgroup only 26% were atopic. On the other hand, subjects specifically sensitized to MDI were rarely atopic (only 15%), whereas in the subgroup non-sensitized to MDI atopy was present in 38%. After prolonged durations of exposure, the proportion of atopics was further elevated in most healthcare subgroups but it decreased in the MDI-exposed subjects.ConclusionsWe hypothesize that latex proteins as sensitizing agents might promote the development of atopy, whereas exposure to the low molecular weight MDI might inhibit the atopic status.

Stickstoffmonoxid in verschiedenen Kompartimenten des Atemtrakts – Vergleich der Daten von Nichtrauchern und Rauchern

Our aim was to determine by means of five exhaled flow rates differential parameters of FeNO and the relations between them in smokers and non-smokers. 34 smokers (without respiratory symptoms and medication) were examined. Compared to 43 healthy non-smokers, FeNO was significantly lower. The analysis of the differential NO parameters by means of the two-compartment model of NO production revealed a significant decrease in the bronchial NO concentration, but no significant changes of NO in alveolar fraction by smokers. The relations between differential parameters in non-smokers confirm the theoretical expectations of the two-compartment model. Conversely, smokers exhibit an abnormal remarkable correlation, namely, a high correlation between the reduced C(aw) und FeNO at all five flow rates. It may be assumed that the alveolar NO fraction in smokers is to some extent of bronchial origin. Such a preposition is in line with significantly decreases of FEV(1), FEF(50) and FEF(75) in smokers, which are associated with turbulences, flow inhomogeneity and a varied delay of expiration time from the peripheral airways. We hypothesize that the decreased NO concentration in the bronchial wall of smokers plays a pathophysiological role in the genesis of small airways disease.