e recent studies have investigated environmental exposure to PAHs, including via vehicle emissions or indoor sources such as coal burning stoves and tobacco smoke [21, 22]. The current study is the first to investigate the utility of 1-OHP for assessing environmental exposure to PAHs suggested to be primarily derived from wood-burning for home-heating. PAH concentrations are highly correlated with particulate air pollution in Christchurch . The potential use of 1-OHP as a biomarker of pollution exposure in this population is explored in more detail elsewhere .
Small effects of peak air pollution levels on some lung function measurements were detected in the asthmatic subjects. The effects on afternoon peak flow and decreased variability between morning and evening FEV1 might represent a 1/2–1 day lag effect of pollution on lung function in this group. Generally, the effect sizes were small. No significant independent effect of air pollution on lung function was detected in the population as a whole. It is unlikely that reliever use in the asthmatic children significantly reduced any effect size seen, since reliever use was generally very low, and the variable used for any reliever use was only retained in one model in the multivariate analysis. Even attempting to force the variable into the multivariate models did not alter the analyses. The effects in asthmatic students were only seen associated with peak pollution levels, as averaged over a 10 minute period. No association was seen between lung function and 24 hour average pollution levels in the multivariate analyses. This contrasts with the study of Trenga and co-workers who identified a relationship between 24 hour mean pollution levels and lung function in children with asthma .
This study also demonstrated small but statistically significant effects of pollution on ear, nose and throat symptoms in this population. This is consistent with previous studies of wood-smoke air pollution .
The power of the study may have been reduced by relatively low pollution levels during the winter of 2004, especially during the school terms, when children were collecting lung function data. A systematic review of air pollution and panel studies in children has however suggested publication bias towards adverse effects of particulate air pollution on lung function and lower respiratory symptoms .
More recently, researchers have explored the utility of studying airway inflammation in the context of pollution exposure. A number of studies have recently been published describing the relationship of exhaled nitric oxide levels to pollution exposure [26, 27]. Nitric oxide was not measured in this current study, due to the lack of portable equipment in 2004. However, exhaled breath condensate has been proposed as another simple non-invasive tool for measurement of airway inflammation . Whilst nitric oxide measurement only provides information about eosinophilic airway inflammation, other markers of airway inflammation such as pH and hydrogen peroxide can be studied in EBC. EBC pH has been shown to vary between individuals and in respiratory conditions such as bronchial asthma, bronchiectasis and chronic obstructive pulmonary disease , and EBC H2O2 is increased in a number of inflammatory conditions such as asthma, chronic obstructive pulmonary disease and community acquired pneumonia [30–33]. Measurement of such "biomarkers of effect" in EBC has been proposed as a way of exploring health effects of air pollution in exposed populations .
No demonstrable effect of pollution on EBC pH or H2O2 was demonstrated in this study, either in healthy children, or children with asthma. The ranges of results for both tests were broad, with no correlations between EBC levels of hydrogen peroxide, and pH, and no correlation with either of these measurements and urine 1-OHP.
Similar issues are described by Doniec and co-workers who studied effects of passive smoking on EBC H2O2 in 9 year old children . They were unable to demonstrate a difference in EBC H2O2 between exposed and non-exposed children, thoug