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, though commented that low sensitivity of the assay, and wide spread of measured concentrations of H2O2 might mask subtle effects on airway inflammation. Similarly, Barregard and co-workers, though they describe statistically significant alterations in EBC malondialdehyde (another proposed biomarker of oxidative stress) after exposure to wood smoke, suggest that the results be interpreted with caution due to very low overall levels in EBC, with many measurements below detection limit of the assay . Assay variability when measuring H2O2 using fluorimetry and colorimetry is broad in the reported literature, with some studies reporting good agreement of results [36–38], while others show higher coefficients of variation [32, 39, 40].
EBS pH was measured immediately after collection, without argon degassing or standardisation for CO2 partial pressure. There continues to be vigorous debate about the merits of each of these approaches , however degassing is not a feasible approach when collecting and processing large numbers of samples in a short period.
The potential drawbacks of EBC analysis, including assay variability and very low biomarker concentration have been highlighted in a recent review article  and are addressed in the ATS/ERS taskforce position paper on EBC . At this stage, EBC collection and analysis appears to show utility in highly controlled research settings, but the current collection and analysis techniques are not suitable for application "in the field" for community assessment of effects of air pollution.
In summary, in this study we detected no significant effect of ambient wood-smoke particulate air pollution on lung function of healthy school-aged male students, but a small effect on cough. Small but significant effects of peak pollution levels were seen in students with asthma. Urinary 1-OHP shows potential as a biomarker of exposure to PAHs in wood smoke in this population; however measurement of EBC pH and hydrogen peroxide using current methods of collection and analysis appears not to be useful