Wood smoke in a controlled exposure experiment with human volunteers.

Exposure to wood smoke in the general population is increasing and concurrently, also our awareness. This article describes a wood-smoke generating system for studying human exposure to wood smoke and symptoms related to this exposure. Twenty nonsmoking atopic human participants with normal lung function and normal bronchial reactivity were randomly exposed for 3 h at three different exposure conditions; clean filtered air (control exposure) and wood smoke with a characteristic particulate matter (PM) concentration of 200 µg/m³ (low) and 400 µg/m³ (high) under controlled environmental conditions. The range for PM2.5 load observed for single experiments was 165-303 µg/m³ for the low exposure and 205-662 µg/m³ for the high exposure, whereas particle loads during clean air exposure most often were below the detection limit (< 20 µg/m³). Health effects were evaluated in relation to rated changes in symptoms and environmental perception using a computerized questionnaire and a potentiometer. Subjective symptoms were generally weak, but when combining the effect of each of the symptoms into categorical symptom indices, significant effects were found for "environmental perception" (p = 0.0007), "irritative body perceptions" (p = 0.0127), "psychological/neurological effects" (p = 0.0075) and "weak inflammatory responses" (p = 0.0003). Furthermore, significant effects (p = 0.0192) on self-reported general mucosa irritation were found. In conclusion, exposure to wood smoke affected symptom rating and caused irritated mucosas in humans. The knowledge gained in this study on subjective-rated symptoms may be important for understanding human response to wood-smoke exposure.

Immunobiological effects of glucosamine in vitro.

Glucosamine (GlcN) and N-acetyl-d-glucosamine (GlcNAc) were assayed in vitro for their effects on proliferation, cytotoxicity and cytokine secretion in primary and secondary mixed lymphocyte cultures (MLCs). In addition, we studied the effect of GlcN and GlcNAc on the proliferation of purified CD4+ T cells exposed to immobilized anti-CD3 antibody. The present data show that GlcN, but not GlcNAc, inhibits CD4+ T-cell proliferation, the generation of alloreactive cytotoxic T lymphocytes (CTLs) and the secretion of interferon-gamma (IFN-gamma) and interleukin-5 (IL-5) in primary MLC. In secondary T helper-2 (Th2)-polarized MLC, GlcN, but not GlcNAc, inhibits IL-4 and IL-5 secretion, whereas no effect was found on IFN-gamma secretion in Th1-polarized MLC. Dendritic cells treated with GlcN showed a 75-80% decreased capacity for antigen cross-presentation and allostimulation. In cellular bioassays, GlcN was shown to inhibit the stimulatory activity of IL-4 and IL-2, as well as the cytotoxic activity of tumour necrosis factor-alpha (TNF-alpha). In conclusion, GlcN suppresses unprimed T-cell responses by interfering with antigen-presenting cell functions and by a direct inhibitory effect on T-cell proliferation. In addition, GlcN inhibits the secretion of cytokines in antigen-stimulated unprimed T cells and primed Th2-polarized cells.