Clara cell protein as a biomarker for ozone-induced lung injury in humans.

Exposure to ozone (O3) impairs lung function, induces airway inflammation and alters epithelial permeability. Whilst impaired lung function and neutrophilia have been observed at relatively low concentrations, altered lung epithelial permeability is only seen after high-dose challenges. The appearance of Clara cell protein (CC16) in serum has been proposed as a sensitive marker of lung epithelial injury. Here, the use of CC16 as an injury biomarker was evaluated under a controlled exposure to O3 and the relationship between this marker of lung injury and early lung function decrements was investigated. Subjects (n=22) were exposed on two separate occasions to 0.2 parts per million O3 and filtered air for 2 h. Blood samples were drawn and lung function assessed at 2 h pre-exposure, immediately before and immediately after exposure as well as 2 and 4 h postexposure. O3 increased CC16 serum concentrations at 2 h (12.0+/-4.5 versus 8.4+/-3.1 microg x L(-1)) and 4 h postexposure (11.7+/-5.0 versus 7.9+/-2.6 microg x L(-1)) compared with air concentrations. Archived samples from O3 studies utilising the same design indicated that this increase was sustained for up to 6 h postexposure (9.1+/-2.6 versus 7.1+/-1.7 microg x L(-1)) with concentrations returning to baseline by 18 h (7.7+/-2.9 versus 6.6+/-1.7 microg x L(-1)). In these studies, the increased plasma CC16 concentration was noted in the absence of increases in traditional markers of epithelial permeability. No association was observed between increased CC16 concentrations and lung function changes. To conclude, Clara cell protein represents a sensitive and noninvasive biomarker for ozone-induced lung epithelial damage that may have important uses in assessing the health effects of air pollutants in future epidemiological and field studies.

Validation of a diffusive sampler for NO2.

A diffusive sampler for NO2, Willems badge, was validated in laboratory experiments and field tests. The collecting reagent for NO2 in the sampler is triethanolamine, and the analysis is based on a modified colorimetric method, the Saltzman method. The analysis was performed by a flow injection analysis (FIA) technique. The sampling rate for the sampler was determined to be 40.0 ml min-1. There was no effect of NO2 concentration or relative humidity on sampling rate, and the influence of sampling time was found to be small. The detection limit was 4 micrograms m-3 for a 24 h sample. The capacity is high enough to allow sampling of 150 micrograms m-3 for 7 days, which is twice the recommended Swedish short-term (24 h) guideline value as a 98-percentile over 6 months. In field tests, the sampler performed well, even at wind speeds higher than 2 m s-1, and at low temperatures. The overall uncertainty of the method was 24%. The sensitivity and capacity of the method also make it suitable for personal sampling for 2-8 h in working environments.

Measurements of indoor and outdoor nitrogen dioxide concentrations using a diffusive sampler.

The Willems badge, a short-term diffusion sampler, was used to measure nitrogen dioxide concentrations inside and outside the homes of participants in the European study "PEACE' (Pollution Effects on Asthmatic Children in Europe). The main aim of the study was to determine levels of nitrogen dioxide concentrations both outside and inside children's homes, and to estimate the indoor/outdoor ratios for nitrogen dioxide in an urban area, in comparison with a less urbanized control area. We conducted measurements in 23 homes in Umeå, a city of about 100,000 inhabitants in the northern part of Sweden, in addition to 20 homes in a less urbanized control area situated about 20 km from Umeå. Measurements were made on two different occasions in each home during the period January-March, 1994. The houses were not equipped with any gas appliances. The mean outdoor 24-h concentration in Umeå was 28 micrograms m-3 and the mean indoor concentration was 11 micrograms m-3. The mean indoor: outdoor ratio was 0.44 (s = 0.23). The highest outdoor value, measured in the city centre of Umeå, was 54 micrograms m-3. In the control area the mean ambient 24-h concentration was 12 micrograms m-3, approximately half as high as in the urban area, and the mean indoor concentration was 6 micrograms m-3. The mean indoor: outdoor ratio was 0.67 (s = 0.55). The correlation coefficient between indoor and outdoor concentrations was higher in the control area, r = 0.79 (p < 0.001), in comparison with the urban area, r = 0.43 (p < 0.01). It is concluded that the outdoor as well as the indoor concentrations of nitrogen dioxide were approximately twice as high in Umeå as in the control area. This could be explained by heavier traffic density in Umeå. The mean 24-h concentration outside homes in Umeå was, however, below the 24-h national standard level of 75 micrograms m-3. The higher correlation between indoor and outdoor concentrations, combined with higher indoor: outdoor ratio, in the control area is interpreted as a sign of a lower level of penetration of outdoor air into the houses in the urban area. This was not explained by differences in types of buildings between the two areas, but possibly by differences in air-exchange rates and in habits of ventilating rooms with open windows.