[Health effects of formaldehyde, as an indoor air pollutant].

Hazard Evaluation & Epidemiology Research Group, National Institute of Occupational Safety and Health, Nagao 6-21-1, Tama-ku, Kawasaki 214-8585, Japan.
Kaibogaku Zasshi 03/2010; 85(1):35-41.
Source: PubMed

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.

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    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.
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    PLoS ONE 01/2013; 8(1):e54494. DOI:10.1371/journal.pone.0054494 · 3.53 Impact Factor