Formaldehyde exposure and asthma in children: a systematic review.
ABSTRACT Despite multiple published studies regarding the association between formaldehyde exposure and childhood asthma, a consistent association has not been identified. Here we report the results of a systematic review of published literature in order to provide a more comprehensive picture of this relationship. After a literature search, we identified seven studies providing quantitative results regarding the association between formaldehyde exposure and asthma in children. Studies were heterogeneous with respect to the definition of asthma. For each study, an odds ratio (OR) and 95% confidence interval (CI) for asthma were abstracted from published results or calculated based on the data provided. We used fixed- and random-effects models to calculate pooled ORs and 95% CIs; measures of heterogeneity were also calculated. A fixed-effects model produced an OR of 1.03 (95% CI, 1.021.04), and random effects model produced an OR of 1.17 (95% CI, 1.011.36), both reflecting an increase of 10 mg/m3 of formaldehyde. Both the Q and I2 statistics indicated a moderate amount of heterogeneity. Results indicate a positive association between formaldehyde exposure and childhood asthma. Given the largely cross-sectional nature of the studies underlying this meta-analysis, further well-designed prospective epidemiologic studies are needed.
- SourceAvailable from: Raffaella Degan
Dataset: Stoten 2012
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ABSTRACT: Formaldehyde is a colorless, pungent gas commonly found in homes and is a respiratory irritant, sensitizer, carcinogen and asthma trigger. Typical household sources include plywood and particleboard, cleaners, cosmetics, pesticides, and others. Development of a fast and simple measurement technique could facilitate continued research on this important chemical. The goal of this research is to apply an inexpensive short-term measurement method to find correlations between formaldehyde sources and concentration, and formaldehyde concentration and asthma control. Formaldehyde was measured using 30-minute grab samples in length-of-stain detector tubes in homes (n=70) of asthmatics in the Boston, MA area. Clinical status and potential formaldehyde sources were determined. The geometric mean formaldehyde level was 35.1 ppb and ranged from 5-132 ppb. Based on one-way ANOVA, t-tests, and linear regression, predictors of log-transformed formaldehyde concentration included absolute humidity, season, and the presence of decorative laminates, fiberglass, or permanent press fabrics (p<0.05), as well as temperature and household cleaner use (p<0.10). The geometric mean formaldehyde concentration was 57% higher in homes of children with very poorly controlled asthma compared to homes of other asthmatic children (p=0.078). This study provides a simple method for measuring household formaldehyde and suggests that exposure is related to poorly controlled asthma. © 2012 John Wiley & Sons A/S. Published by Blackwell Publishing Ltd.Indoor Air 12/2012; · 3.30 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. · 3.73 Impact Factor