The relationship between air pollution from heavy traffic and allergic sensitization, bronchial hyperresponsiveness, and respiratory symptoms in Dutch schoolchildren - Children's Health

Environmental Health Perspectives, Sept, 2003 by Nicole A.H. Janssen, Bert Brunekreef, Patricia van Vliet, Francee Aarts, Kees Meliefste, Hendrik Harssema, Paul Fischer

Few studies have included measurements of BHR in relation to traffic-related pollution. A recent study from Germany (Nicolai et al. 2003) found no relation between various measures of exposure to traffic-related air pollution and BHR, which was measured using the same technique as in our study. There was no relationship with lung function level, either.

A striking finding was the strong effect modification by BHR as well as sensitization. In this population, about 37% of the children had either a positive SPT or BHR test, or both, and it was in this group of children that the associations between air pollution exposure variables and chronic respiratory symptoms were almost exclusively found. Such effect modification has nor often been investigated. The German study (Nicolai et al. 2003) reported that associations between exposure to traffic-related air pollution were significant only in the atopic children, as in our study, but commented that the percentage of symptomatic children in the nonatopic subgroup was low, so statistical significance was hard to reach. No comparison of effect estimates was given.

Experimental evidence obtained in studies on human volunteers, animals, and in vitro test systems suggests that diesel exhaust particles have the capability to enhance immunologic responses to allergens and to elicit inflammatory reactions in the airways at relatively low concentrations and short exposure durations (Diaz-Sanchez 1997; Diaz-Sanchez et al. 2000; Miyabara et al. 1998; Muranaka et al. 1986; Nordenhall et al. 2001; Rudell et al. 1996, 1999; van Zijverden and Granum 2000). Against this background, it seems reasonable to interpret our findings as showing increased airway inflammation, in particular, in subjects who already are sensitized to common allergens or have BHR. At the same time, there was little evidence that the prevalence of these conditions was increased by exposure to (heavy,) traffic-related air pollution. In an earlier study on acute effects of air pollution, we also observed that children with BHR and high serum IgE responded more strongly to various measures of ambient air pollution, including black smoke, which may act as surrogate for diesel exhaust (Boezen et al. 1999).

The use of GIS to obtain more accurate measures of exposure to traffic-related air pollution has increased. The power of such systems was nicely illustrated by two subsequent analyses from Nottingham, the first one finding no relationship between traffic activity and wheeze in schoolchildren when analyzing traffic activity in the living area in tertiles (Venn et al. 2000). When the same material was analyzed for children living within short distances of major roads, a clear relationship with wheeze was observed (Venn et al. 2001). Similarly, the use of data on location of home with respect to roads and of data on traffic density on those roads resulted in observations of significant relationships with specific respiratory hospital admission rates in Toronto (Buckeridge et al. 2002), with childhood asthma hospitalization rates in Erie County, New York (Lin et al. 2002), and with childhood asthma medical care visits in San Diego County, California (English et al. 1999). These and other studies suggest that improvement of accuracy and precision of exposure classification helps to detect associations between adverse respiratory outcomes in children and (in a few studies) adults.