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  • Title: [Asthma and household chemical pollutants (with the exception of tobacco)].
    Author: Krieger P, de Blay F, Pauli G, Kopferschmitt MC.
    Journal: Rev Mal Respir; 1998 Feb; 15(1):11-24. PubMed ID: 9551510.
    Abstract:
    The relationship between allergens in a domestic environment and asthma has been extensively studied and it is only recently that studies have suggested the possibility of the role of chemical pollutants in the internal environment in the genesis of asthma. The pollutants studied are oxides of nitrogen (nitrogen dioxide NO2), volatile organic components (COV), formaldehyde, ozone (O3) and sulphur dioxide (SO2). The level of nitrogen dioxide in the interior of houses may be greater than those met outside. Normal values are 400 mcg per metre3 per hour and 150 mcg per metre3 in twenty four hours. In asthmatics challenge test to nitrogen dioxide and epidemiological studies suggest that internal nitrogen dioxide is capable of provoking asthmatic crises either by a direct pollutant effect or by potentialising the allergenic crises either by a direct pollutant effect or by potentialising the allergenic response of the bronchi. COV and formaldehyde are liberated by urea formaldehyde foams and by chipboard furniture. The levels of COV and formaldehyde inside a house may be up to 10 times higher than those outside. COV and formaldehyde perhaps would have an effect on the bronchi in asthmatics at significant levels which are rarely found in the domestic environment. Ozone is an external pollutant. However, from 5-80% of the external concentrations may be found inside some locations. Thus, in certain conditions which are relatively rare, the interior concentrations of dwelling places may attain levels which are capable of inducing, in healthy subjects who are sensitive to ozone, a drop in the FEV1. As regards asthmatics, only experimental work has been able to show any bronchospastic effect of ozone, either by a direct effect on the bronchi or by the potentiation of a bronchial response to allergens. It would be convenient to perform some epidemiological studies to determine if there is a relationship between exposure to ozone internally and to bronchial changes. The concentrations of SO2 inside houses increases when coal is burnt. The levels provoking a bronchial reaction are much greater than those found inside houses. The data and the literature which is mostly recent seems to stress the role of NO2 ozone and SO2 as a factor which might favour asthmatic crises induced by allergens in atopic subjects. However, other studies will be necessary to confirm the initial data.
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