[Health effects of formaldehyde, as an indoor air pollutant].
ABSTRACT Formaldehyde is an important chemical used widely by industry in numerous household products. Therefore, when room ventilation is inadequate, formaldehyde may stagnate in rooms and adversely affect the health of inhabitants. Exposure to formaldehyde in living space has been found to be associated with asthma and 'sick house syndrome' (health disturbances induced by chemical contaminants in domestic environments). In addition, formaldehyde exposure among medical students and teachers who dissect cadavers in the gross anatomy laboratory likely causes a health problem. Avoidance of formaldehyde exposure can reduce the incidence and severity of ill-health conditions, although the ability of low concentrations of formaldehyde to trigger mechanisms contributing to them is still debated. Setting appropriate exposure limits for formaldehyde as an indoor environmental pollutant requires further quantitative and predictive evaluation of its health effects.
SourceAvailable from: Caterina Ledda[Show abstract] [Hide abstract]
ABSTRACT: A literature review was conducted in order to give an update on data regarding the various factors involved in the pathogenesis of allergic rhinitis and asthma. Preventive strategies are also discussed.Igiene e sanita pubblica 01/2011; 67(4):467-80.
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ABSTRACT: Formaldehyde (FA) has been known to be associated with development of asthma (AS) and atopic dermatitis (AD). In this study, we investigated whether FA inhalation would affect the provocation or exacerbation of AD-like symptoms. Atopic-prone NC/Nga mice were exposed to low (0.2 ppm) and high (1.0 ppm) concentration of FA by inhalation. Combined exposure to low concentration of FA inhalation and topical house dust mite (HDM) stimulation significantly upregulated HDM-induced total plasma IgE and IgG2a production, Th1-, Th2-, Th17-related cytokine as well as COX-2 mRNA expressions in the skin. Interestingly, independent FA inhalation, especially at low concentration (0.2 ppm), increased the skin mRNA expressions of IL-13, IL-17E/IL-25 and COX-2, even though it failed to induce AD-like skin inflammation. In conclusion, we suggest that increased skin mRNA expressions of IL-13, IL-25/IL-17E and COX-2 by independent low concentration of FA exposure might be a key factor to exacerbate HDM-mediated AD-like skin inflammation.Experimental Dermatology 01/2013; DOI:10.1111/exd.12092 · 4.12 Impact Factor
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ABSTRACT: BACKGROUND: Recent studies suggest that formaldehyde (FA) could be synthesized endogeneously and transient receptor potential (TRP) channel might be the sensor of FA. However, the physiological significance is still unclear. METHODOLOGY/PRINCIPAL FINDINGS: The present study investigated the FA induced epithelial Cl(-) secretion by activation of TRPV-1 channel located in the nerve ending fiber. Exogenously applied FA induced an increase of I(SC) in intact rat trachea tissue but not in the primary cultured epithelial cells. Western blot and immunofluorescence analysis identified TRPV-1 expression in rat tracheal nerve ending. Capsazepine (CAZ), a TRPV-1 specific antagonist significantly blocked the I(SC) induced by FA. The TRPV-1 agonist capsaicin (Cap) induced an increase of I(SC), which was similar to the I(SC) induced by FA. L-703606, an NK-1 specific inhibitor and propranolol, an adrenalin β receptor inhibitor significantly abolished the I(SC) induced by FA or Cap. In the ion substitute analysis, FA could not induce I(SC) in the absence of extracelluar Cl(-). The I(SC) induced by FA could be blocked by the non-specific Cl(-) channel inhibitor DPC and the CFTR specific inhibitor CFTR(i-172), but not by the Ca(2+)-activated Cl(-) channel inhibitor DIDS. Furthermore, both forskolin, an agonist of adenylate cyclase (AC) and MDL-12330A, an antagonist of AC could block FA-induced I(SC). CONCLUSION: Our results suggest that FA-induced epithelial I(SC) response is mediated by nerve, involving the activation of TRPV-1 and release of adrenalin as well as substance P.PLoS ONE 01/2013; 8(1):e54494. DOI:10.1371/journal.pone.0054494 · 3.53 Impact Factor