Annika Hagenbjörk-Gustafsson

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 µg·L−1) and 4 h postexposure (11.7±5.0 versus 7.9±2.6 µg·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 µg·L−1) with concentrations returning to baseline by 18 h (7.7±2.9 versus 6.6±1.7 µg·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.

Lung function in volunteers before and after exposure to trichloramine in indoor pool environments and asthma in a cohort of pool workers.

Objectives Exposure to trichloramine (NCl3) in indoor swimming-pool environments is known to cause mucous membrane irritation, but if it gives rise to changes in lung function or asthma in adults is not known. (1) We determined lung function in volunteers before and after exposure to indoor pool environments. (2) We studied the occurrence of respiratory symptoms and asthma in a cohort of pool workers. Design/methods/participants (1) We studied two groups of volunteers, 37 previously non-exposed healthy persons and 14 pool workers, who performed exercise for 2 h in an indoor pool environment. NCl3 in air was measured during pool exposures and in 10 other pool environments. Filtered air exposures were used as controls. Lung function and biomarkers of pulmonary epithelial integrity were measured before and after exposure. (2) We mailed a questionnaire to 1741 persons who indicated in the Swedish census 1990 that they worked at indoor swimming-pools. Results (1) In previously non-exposed volunteers, statistically significant decreases in FEV1 (forced expiratory volume) and FEV% (p=0.01 and 0.05, respectively) were found after exposure to pool air (0.23 mg/m3 of NCl3). In pool workers, a statistically significant decrease in FEV% (p=0.003) was seen (but no significant change of FEV1). In the 10 other pool environments the median NCl3 concentration was 0.18 mg/m3. (2) Our nested case/control study in pool workers found an OR for asthma of 2.31 (95% CI 0.79 to 6.74) among those with the highest exposure. Exposure-related acute mucous membrane and respiratory symptoms were also found. Conclusions This is the first study in adults showing statistically significant decreases in lung function after exposure to NCl3. An increased OR for asthma among highly exposed pool workers did not reach statistical significance, but the combined evidence supports the notion that current workroom exposures may contribute to asthma development. Further research on sensitive groups is warranted.

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.

Field validation of the Ogawa diffusive sampler for NO2 and NOx in a cold climate

A small-scale field trial in Umeå, Sweden with Ogawa samplers and a chemiluminescence instrument indicated that the NO(2) concentration was underestimated with respect to the reference monitor, if calculated according to the manufacturers Ogawa sampling protocol. By co-locating Ogawa samplers and reference monitors at six sites in two Swedish cities, uptake rates were determined for NO(2) and NO(x) better applicable to the Swedish conditions and climate. The concentrations of NO(2) and NO(x) calculated according to the instruction manual of the sampler and using the field-determined uptake rates were compared with values derived from chemiluminescence monitors for each week over which samples were taken. When calculated according to the manufacturers suggested protocol, the Ogawa sampler underestimated the NO(2) concentrations by 9.1% on average for all samples (N = 53), with respect to the reference monitor. In contrast, NO(x) concentrations were overestimated by a mean value of 15% for all samples (N = 45). By using the field determined uptake rates for the calculation of NO(2) and NO(x) a better estimation of the concentrations was obtained. The ratio between concentrations determined with the Ogawa samplers and chemiluminescence monitors was then 1.02 for all measurements of NO(2) and 1.00 for NO(x). Precision, expressed as the mean coefficient of variation, was 6.4% for six, 6-replicate measurements of NO(2) and 3.7% for five, 6-replicate measurements of NO(x).

Can NO(2) be used to indicate ambient and personal levels of benzene and 1,3-butadiene in air?

The aim of this study was to investigate the relation between two toxic volatile organic compounds, 1,3-butadiene and benzene, and a commonly used indicator of vehicle exhaust fumes, NO(2). This was to see if NO(2) can be used to indicate personal exposure to carcinogenic substances or at least estimate ambient levels measured at a stationary point. During the winter of 2001, 40 randomly selected persons living in the City of Umea (in the north of Sweden) were recruited to the study. Personal measurements of 1,3-butadiene, benzene and NO(2) were performed for one week, and were repeated for 20 of the 40 participants. Additional information was gathered using a diary kept by each participant. During the same time period weekly stationary measurements were performed at one urban background station and one street station in the city centre. The results from the personal measurements showed a negligible association of NO(2) with 1,3-butadiene (r= 0.06) as well as with benzene (r= 0.10), while the correlation coefficient between 1,3-butadiene and benzene was high and significant (r= 0.67). In contrast to the personal measurements, the stationary measurements showed strong relations between 1,3-butadiene, benzene and NO(2) both within and in-between the street and urban background station. This study supports NO(2) as a potential indicator for 1,3-butadiene and benzene levels in streets or urban background air, while the weak relations found for the personal measurements do not support the use of NO(2) as an indicator for personal 1,3-butadiene and benzene exposure.

Potential dermal exposure to methyl methacrylate among dental technicians; variability and determinants in a field study.

Methyl methacrylate (MMA) is a commonly used chemical in dental work that can cause dermatitis. Nineteen dental technicians participated in a field study in which potential dermal exposure to MMA and exposure determinants, including glove use and MMA vapour in the breathing zone, were repeatedly monitored during three consecutive days. Using patches placed on various parts of their hands we observed that the fingers and palms of the dental technicians were exposed to MMA, and their forefingers were significantly more exposed than their ring fingers; this is based on pooled data for both left and right hands (p = 0.04). The exposure variability was greater between workers than within worker (i.e. day-to-day variability), but the between worker variability was to some extent explained by a model which included the tested determinants. Neither the amount of MMA vapours in the breathing zone nor glove use was consistently correlated with the dermal exposure. Thus, the effects of glove use and the distribution of exposure to MMA on the hands in working environments needs to be further investigated.

Determinants of personal exposure to some carcinogenic substances and nitrogen dioxide among the general population in five Swedish cities

Environmental levels of airborne carcinogenic and related substances are comparatively better known than individual exposure and its determinants. We report on a personal monitoring program involving five Swedish urban populations. The aim of the program was to investigate personal exposure to benzene, 1,3-butadiene, formaldehyde, and nitrogen dioxide (NO2). The measurements were performed among 40 inhabitants during seven consecutive days, in one urban area each year, during 2000–2008. The estimated population exposure levels were 1.95 μg/m3 for benzene, 0.56 μg/m3 for 1,3-butadiene, 19.4 μg/m3 for formaldehyde, and 14.1 μg/m3 for NO2. Statistical analysis using a mixed-effects model revealed that time spent in traffic and time outdoors contributed to benzene and 1,3- butadiene exposure. For benzene, refueling a car was an additional determinant influencing the exposure level. Smoking or environmental tobacco smoke were significant determinants of exposure to NO2, benzene, and 1,3-butadiene. Those with a gas stove had higher NO2 exposure. Living in a single-family house increased the exposure to formaldehyde significantly. In a variance component model, the between-subject variance dominated for 1,3-butadiene and formaldehyde, whereas the between-city variance dominated for NO2. For benzene, the between-subject and between-cities variances were similar.