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People in Central Europe spend most of their time in private dwellings, offices, education centres or other public buildings. In these indoor places, they are exposed to a variety of gaseous or particulate pollutants that potentially exert adverse health effects. This work compiles current fields of action that are discussed in the public, among expert panels, and in the scientific community. These address ventilation in buildings, the impact of building product emissions and particulate matter sources on indoor air quality, the detection and prevention of mould as well as the assessment of indoor air quality using guidance values and the determination of the internal exposure by human biomonitoring. Indoor air quality appears as a dynamic field of action that has become more complex due to the interaction between new chemicals introduced into the indoor environment through a variety of products and the observed reduction of ventilation rates. Implications for human health have thus become less predictable.

Die von der Gesellschaft fur Hygiene, Umweltmedizin und Praventivmedizin (GHUP) federfuhrend erstellte Leitlinie „Medizinisch klinische Diagnostik bei Schimmelpilzexposition in Innenraumen“ ist Gegenstand des vorliegenden Abschnitts. Schimmelpilzwachstum im Innenraum ist als ein potenzielles Gesundheitsrisiko zu betrachten, auch ohne dass ein quantitativer und/oder kausaler Zusammenhang zwischen dem Vorkommen einzelner Arten und Gesundheitsbeschwerden gesichert werden kann. Abgesehen von der Allergischen Bronchopulmonalen Aspergillose (ABPA) und den durch Schimmelpilze kausal verursachten Mykosen, liegen lediglich ausreichende Evidenzen fur folgende Assoziationen von Feuchte-/Schimmelpilzschaden und unterschiedlichen Gesundheitseffekten vor: allergische Atemwegserkrankungen, Asthma (Manifestation, Progression, Exazerbation), allergische Rhinitis, Exogen Allergische Alveolitis, Begunstigung von Atemwegsinfekten/Bronchitis. Dabei ist das sensibilisierende Potenzial von Schimmelpilzen im Vergleich zu anderen Umweltallergenen deutlich geringer einzuschatzen. Aktuelle Studien zeigen europaweit eine vergleichsweise geringe Sensibilisierungspravalenz von 3–10 % gemessen an der Gesamtbevolkerung. Eingeschrankte oder vermutete Evidenz fur eine Assoziation liegt vor hinsichtlich „mucous membrane irritation“ und Atopischen Ekzems (Manifestation, Progression, Exazerbation). Inadaquate oder unzureichende Evidenz fur eine Assoziation liegt vor fur COPD, akute idiopathische pulmonale Hamorrhagie bei Kindern, Rheuma/Arthritis, Sarkoidose und Krebserkrankungen. Das Infektionsrisiko von den in Innenraumen regelmasig vorkommenden Schimmelpilzarten ist fur gesunde Personen gering, die meisten Arten sind in die Risikogruppe 1 und wenige in 2 (Aspergillus fumigatus, A. flavus) der Biostoffverordnung eingestuft. Nur Schimmelpilze, die potenziell in der Lage sind, Toxine zu bilden, kommen als Ausloser einer Intoxikation in Betracht. Ob im Einzelfall eine Toxinbildung im Innenraum stattfindet, entscheiden die Umgebungs- und Wachstumsbedingungen und hier vor allem das Substrat. Von Geruchswirkungen und/oder Befindlichkeitsstorungen kann bei Feuchte-/Schimmelpilzschaden im Innenraum grundsatzlich jeder betroffen sein. Hierbei handelt es sich nicht um eine Gesundheitsgefahrdung. Pradisponierende Faktoren fur Geruchswirkungen konnen genetische und hormonelle Einflusse, Pragung, Kontext und Adaptationseffekte sein. Pradisponierende Faktoren fur Befindlichkeitsstorungen konnen Umweltbesorgnisse, -angste, -konditionierungen und -attributionen sowie eine Vielzahl von Erkrankungen sein. Besonders zu schutzende Risikogruppen bezuglich eines Infektionsrisikos sind Personen unter Immunsuppression nach der Einteilung der Kommission fur Krankenhaushygiene und Infektionspravention (KRINKO) beim Robert Koch-Institut (RKI) und Personen mit Mukoviszidose (Zystischer Fibrose), bezuglich eines allergischen Risikos Personen mit Mukoviszidose (Zystischer Fibrose) und Personen mit Asthma bronchiale. Die rationale Diagnostik beinhaltet die Anamnese, eine korperliche Untersuchung, eine konventionelle Allergiediagnostik einschlieslich gegebenenfalls Provokationstests, vereinzelt sind auch zellulare Testsysteme indiziert. Zum Vorgehen bei Schimmelpilzinfektionen wird auf die angemeldete AWMF-Leitlinie Diagnose und Therapie invasiver Aspergillus-Infektionen verwiesen. Hinsichtlich Mykotoxine existieren zurzeit keine brauchbaren und validierten Testverfahren, die in der klinischen Diagnostik eingesetzt werden konnten. Praventivmedizinisch ist wichtig, dass Schimmelpilzbefall in relevantem Ausmas aus Vorsorgegrunden nicht toleriert werden darf. Zur Beurteilung des Schadensausmases und zum Vorgehen wird auf den „Schimmelpilzleitfaden“ des Umweltbundesamtes verwiesen.

This article is an abridged version of the AWMF mould guideline “Medical clinical diagnostics of indoor mould exposure” presented in April 2016 by the German Society of Hygiene, Environmental Medicine and Preventive Medicine (Gesellschaft für Hygiene, Umweltmedizin und Präventivmedizin, GHUP), in collaboration with the above-mentioned scientific medical societies, German and Austrian societies, medical associations and experts. Indoor mould growth is a potential health risk, even if a quantitative and/or causal relationship between the occurrence of individual mould species and health problems has yet to be established. Apart from allergic bronchopulmonary aspergillosis (ABPA) and mould-caused mycoses, only sufficient evidence for an association between moisture/mould damage and the following health effects has been established: allergic respiratory disease, asthma (manifestation, progression and exacerbation), allergic rhinitis, hypersensitivity pneumonitis (extrinsic allergic alveolitis), and increased likelihood of respiratory infections/bronchitis. In this context the sensitizing potential of moulds is obviously low compared to other environmental allergens. Recent studies show a comparatively low sensitizing prevalence of 3–10% in the general population across Europe. Limited or suspected evidence for an association exist with respect to mucous membrane irritation and atopic eczema (manifestation, progression and exacerbation). Inadequate or insufficient evidence for an association exist for chronic obstructive pulmonary disease, acute idiopathic pulmonary hemorrhage in children, rheumatism/arthritis, sarcoidosis and cancer. The risk of infection posed by moulds regularly occurring indoors is low for healthy persons; most species are in risk group 1 and a few in risk group 2 (Aspergillus fumigatus, A. flavus) of the German Biological Agents Act (Biostoffverordnung). Only moulds that are potentially able to form toxins can be triggers of toxic reactions. Whether or not toxin formation occurs in individual cases is determined by environmental and growth conditions, above all the substrate. In the case of indoor moisture/mould damage, everyone can be affected by odour effects and/or mood disorders. However, this is not a health hazard. Predisposing factors for odour effects can include genetic and hormonal influences, imprinting, context and adaptation effects. Predisposing factors for mood disorders may include environmental concerns, anxiety, condition, and attribution, as well as various diseases. Risk groups to be protected particularly with regard to an infection risk are persons on immunosuppression according to the classification of the German Commission for Hospital Hygiene and Infection Prevention (Kommission für Krankenhaushygiene und Infektionsprävention, KRINKO) at the Robert Koch- Institute (RKI) and persons with cystic fibrosis (mucoviscidosis); with regard to an allergic risk, persons with cystic fibrosis (mucoviscidosis) and patients with bronchial asthma should be protected. The rational diagnostics include the medical history, physical examination, and conventional allergy diagnostics including provocation tests if necessary; sometimes cellular test systems are indicated. In the case of mould infections the reader is referred to the AWMF guideline “Diagnosis and Therapy of Invasive Aspergillus Infections”. With regard to mycotoxins, there are currently no useful and validated test procedures for clinical diagnostics. From a preventive medicine standpoint it is important that indoor mould infestation in relevant dimension cannot be tolerated for precautionary reasons. With regard to evaluating the extent of damage and selecting a remedial procedure, the reader is referred to the revised version of the mould guideline issued by the German Federal Environment Agency (Umweltbundesamt, UBA).

To determine the exchange of nitrogen and carbon between ectomycorrhiza and host plant, young beech (Fagus sylvatica) trees from natural regeneration in intact soil cores were labelled for one growing season in a greenhouse with 13CO2 and 15NO3 15NH4. The specific enrichments of 15N and 13C were higher in ectomycorrhizas (EMs) than in any other tissue. The enrichments of 13C and 15N were also higher in the fine-root segments directly connected with the EM (mainly second-order roots) than that in bulk fine or coarse roots. A strict, positive correlation was found between the specific 15N enrichment in EM and the attached second-order roots. This finding indicates that strong N accumulators provide more N to their host than low N accumulators. A significant correlation was also found for the specific 13C enrichment in EM and the attached second-order roots. However, the specific enrichments for 15N and 13C in EM were unrelated showing that under long-term conditions, C and N exchange between host and EMs are uncoupled. These findings suggest that EM-mediated N flux to the plant is not the main control on carbon flux to the fungus, probably because EMs provide many different services to their hosts in addition to N provision in their natural assemblages.

Background At Holi festivals, originally celebrated in India but more recently all over the world, people throw coloured powder (Holi powder, Holi colour, Gulal powder) at each other. Adverse health effects, i.e. skin and ocular irritations as well as respiratory problems may be the consequences. The aim of this study was to uncover some of the underlying mechanisms. Methods We analysed four different Holi colours regarding particle size using an Electric field cell counting system. In addition, we incubated native human cells with different Holi colours and determined their potential to induce a pro-inflammatory response by quantifying the resulting cytokine production by means of ELISA (Enzyme Linked Immunosorbent Assay) and the resulting leukocyte oxidative burst by flow cytometric analysis. Moreover, we performed the XTT (2,3-Bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide) and Propidium iodide cytotoxicity tests and we measured the endotoxin content of the Holi colour samples by means of the Limulus Amebocyte Lysate test (LAL test). Results We show here that all tested Holi colours consist to more than 40 % of particles with an aerodynamic diameter smaller than 10 μm, so called PM10 particles (PM, particulate matter). Two of the analysed Holi powders contained even more than 75 % of PM10 particles. Furthermore we demonstrate in cell culture experiments that Holi colours can induce the production of the pro-inflammatory cytokines TNF-α (Tumor necrosis factor-α), IL-6 (Interleukine-6) and IL-1β (Interleukine-1β). Three out of the four analysed colours induced a significantly higher cytokine response in human PBMCs (Peripheral Blood Mononuclear Cells) and whole blood than corn starch, which is often used as carrier substance for Holi colours. Moreover we show that corn starch and two Holi colours contain endotoxin and that certain Holi colours display concentration dependent cytotoxic effects in higher concentration. Furthermore we reveal that in principle Holi colours and corn starch are able to generate an oxidative burst in human granulocytes and monocytes. In Holi colour 1 we detected a fungal contamination. Conclusions Some of the observed unwanted health effects of Holi colours might be explained by the high content of PM10 particles in conjunction with the possible induction of a pro-inflammatory response and an oxidative leukocyte burst.