Sandra Johannesson

Experimental Wood Smoke Exposure in Humans

Experimental studies are used to evaluate effects of human exposure to diesel exhaust and concentrated ambient particles. This article describes a system for studying exposure of humans to wood smoke. Wood smoke was generated using a wood stove placed outside an exposure chamber that can hold at least 10 subjects. A partial flow of the generated wood smoke from the stove was mixed with filtered indoor air. Personal and stationary measurements were performed of PM2.5 and PM1 mass concentrations and various volatile organic compounds (VOCs): 1,3-butadiene, benzene, and aldehydes. In addition, particulate matter (PM) mass, number concentrations, and size distributions of particles (0.007–6.7 μm), as well as nitrous oxides, CO2, and CO, were measured online. Filters were analyzed for trace elements and black smoke. Polycyclic aromatic compounds, toluene, and xylenes were determined in stationary samples. Results of the first experiment showed no differences between personal and stationary measurements for particles or VOCs. Consequently, stationary measurements can be used to predict personal exposure. All PM mass (about 250 μg/m3) was in the PM1 fraction. Subjective symptoms were generally weak, while clear objective signs were found, for example, in biomarkers of inflammation. With careful control of the combustion process, relatively constant mass and number concentrations were obtained over each exposure session. By varying the combustion and dilution of the wood smoke, different exposure scenarios can be achieved and thus, knowledge about which of the properties of particles and gaseous compounds are crucial for the effects.

Exposure to fine particles (PM2.5 and PM1) and black smoke in the general population: personal, indoor, and outdoor levels.

Personal exposure to PM2.5 and PM1, together with indoor and residential outdoor levels, was measured in the general adult population (30 subjects, 23–51 years of age) of Gothenburg, Sweden. Simultaneously, urban background concentrations of PM2.5 were monitored with an EPA WINS impactor. The 24-h samples were gravimetrically analyzed for mass concentration and black smoke (BS) using a smokestain reflectometer. Median levels of PM2.5 were 8.4 μg/m3 (personal), 8.6 μg/m3 (indoor), 6.4 μg/m3 (residential outdoor), and 5.6 μg/m3 (urban background). Personal exposure to PM1 was 5.4 μg/m3, while PM1 indoor and outdoor levels were 6.2 and 5.2 μg/m3, respectively. In non-smokers, personal exposure to PM2.5 was significantly higher than were residential outdoor levels. BS absorption coefficients were fairly similar for all microenvironments (0.4–0.5 10−5 m−1). Personal exposure to particulate matter (PM) and BS was well correlated with indoor levels, and there was an acceptable agreement between personal exposure and urban background concentrations for PM2.5 and BS2.5 (rs=0.61 and 0.65, respectively). PM1 made up a considerable amount (70–80%) of PM2.5 in all microenvironments. Levels of BS were higher outdoors than indoors and higher during the fall compared with spring. The correlations between particle mass and BS for both PM2.5 vs. BS2.5 and PM1 versus BS1 were weak for all microenvironments including personal exposure. The urban background station provided a good estimate of residential outdoor levels of PM2.5 and BS2.5 within the city (rs=0.90 and 0.77, respectively). Outdoor levels were considerably affected by long-range transported air pollution, which was not found for personal exposure or indoor levels. The within-individual (day-to-day) variability dominated for personal exposure to both PM2.5 and BS2.5 in non-smokers.

Personal exposures and indoor, residential outdoor, and urban background levels of fine particle trace elements in the general population

Personal exposures and indoor, residential outdoor, and urban background levels of PM(2.5) and PM(1) were measured simultaneously in Göteborg, Sweden. A total of 270 24 hour samples from 30 subjects were analyzed for elemental concentrations using X-ray fluorescence (XRF) spectroscopy. Personal exposures to PM(2.5) were significantly higher for Cl, Ca, Ti, and Fe compared with the other locations. For most elements, residential outdoor levels were significantly higher than urban background levels. Correlations between personal exposure and stationary measurements were moderate to high for Zn, Br, and Pb (r(s)= 0.47-0.81), while Ca and Cu showed low correlations. The penetration indoors from outdoors was 0.7, as calculated from S and Pb ratios. For the pairs of parallel PM(1) and PM(2.5) measurements, only Ca and Fe levels were significantly lower for PM(1) at all sites. Significant correlations were found between urban background mass concentrations and personal exposure levels for elements attributed to combustion processes (S, V, and Pb) and resuspended dust (Ti, Fe, and Zn), indicating that both sources could be relevant to health effects related to urban background mass. Air mass origin strongly affected the measured urban background concentrations of some elements (S, Cl, V, Ni, Br, and Pb). These findings were also seen for personal exposure (S, Cl, V, and Pb) and indoor levels (S, Cl, V, Ni, and Pb). No differences were seen for crustal elements. Air mass origin should be taken into account in the description and interpretation of time series studies of air pollution and health.

Effects on airways of short-term exposure to two kinds of wood smoke in a chamber study of healthy humans

Introduction: Air pollution causes respiratory symptoms and pulmonary disease. Airway inflammation may be involved in the mechanism also for cardiovascular disease. Wood smoke is a significant contributor to air pollution, with complex and varying composition. We examined airway effects of two kinds of wood smoke in a chamber study. Materials and Methods: Thirteen subjects were exposed to filtered air and to wood smoke from the start-up phase and the burn-out phase of the wood-burning cycle. Levels of PM2.5 were 295 µg/m3 and 146 µg/m3, number concentrations 140 000/cm3 and 100 000/cm3. Biomarkers in blood, breath and urine were measured before and on several occasions after exposure. Effects of wood smoke exposure were assessed adjusting for results with filtered air. Results: After exposure to wood smoke from the start-up, but not the burn-out session, Clara cell protein 16 (CC16) increased in serum after 4 hours, and in urine the next morning. CC16 showed a clear diurnal variation. Fraction of exhaled nitric oxide (FENO) increased after wood smoke exposure from the burn-out phase, but partly due to a decrease after exposure to filtered air. No other airway markers increased. Conclusions: The results indicate that relatively low levels of wood smoke exposure induce effects on airways. Effects on airway epithelial permeability was shown for the start-up phase of wood burning, while FENO increased after the burn-out session. CC16 seems to be a sensitive marker of effects of air pollution both in serum and urine, but its function and the significance need to be clarified.

Variability of environmental exposure to fine particles, black smoke, and trace elements among a Swedish population

Mixed-effects models were used to estimate within-person and between-person variance components, and some determinants of environmental exposure to particulate matter (PM2.5), black smoke (BS) and trace elements (Cl, K, Ca, Ti, Fe, Ni, Cu, Zn, and Pb) for personal measurements from 30 adult subjects in Gothenburg, Sweden. The within-person variance component dominated the total variability for all investigated compounds except for PM2.5 and Zn (in which the variance components were about equal). Expressed as fold ranges containing 95% of the underlying distributions, the within-person variance component ranged between 5-fold and 39-fold (median: sixfold), whereas the between-person variance component was always <sixfold (median: threefold). The relatively large within-person variance components can lead to attenuation bias in exposure–response relationships and point to the importance of obtaining repeated samples of PM exposure from study subjects in epidemiological investigations of urban air pollution. On the basis of the variance components estimated for the various particulate species, between 3 and 39 repeated measurements per subject would be required to limit attenuation bias to 20%. Significant determinants for personal exposure levels were urban background air concentrations (PM2.5, BS, Cl, Zn, and Pb), cigarette smoking (PM2.5, BS, K, and Ti), season (PM2.5, Fe, and Pb), and the time spent outdoors or in traffic (Fe).

Indoor concentrations of fine particles and particle-bound PAHs in Gothenburg, Sweden

Fine particles are formed in a variety of processes, both natural and anthropogenic. Epidemiological studies have shown an association between exposure to particulate matter and adverse health effects. Airborne particles contain a variety of compounds, including polycyclic aromatic hydrocarbons (PAHs), and several of the PAHs are known or suspected carcinogens. In this study, stationary measurements of PM2.5 were performed in the residences of 20 study participants along with simultaneous monitoring at an urban background site. The collected particle mass was then analyzed for its content of some particle-bound PAHs using GC-MS. The median level of PM2.5 indoors was 7.3 μg/m3 and in urban background 5.3 μg/m3. For benzo(a)pyrene (B(a)P) the corresponding results were 10 pg/m3 and 35 pg/m3, respectively. There were significant correlations between indoor and ambient levels for both PM2.5 (rs=0.58, p=0.02) and B(a)P (rs=0.67, p=0.007). No significant correlation was, however, found between the concentration of PM2.5 and the associated levels of the investigated PAH compounds. This finding implies that exposure to B(a)P or other particle-bound PAH components needs to be separately assessed.

Urban air pollution and effects on biomarkers of systemic inflammation and coagulation: a panel study in healthy adults

Abstract Context: Urban particulate air pollution is associated with cardiovascular diseases and mortality, possibly mediated through systemic inflammation and increased blood viscosity. Objectives: To examine short-term effects of exposure to urban air pollution on blood biomarkers for systemic inflammation and coagulation in a panel of healthy adults living in Gothenburg, Sweden. Materials and methods: The 16 volunteers, all non-smokers, median age 35 years, were called for blood sampling the morning after a day with high levels of urban particulate matter (PM10 > 30 µg/m3) or a day with low levels (PM10 < 15 µg/m3 and NO2 < 35 µg/m3). Associations between exposure to air pollution and each biomarker (C-reactive protein, fibrinogen, serum amyloid A, coagulation factor VIII, plasminogen activator inhibitor-1, p-selectin, soluble intercellular adhesion molecule-1, soluble vascular adhesion molecule-1, Clara cell protein 16 and surfactant protein D) were examined using a linear mixed-effects model. Results: In total, 12 sampling sessions were performed, six after high-pollution and six after low-pollution days, over 21 months. The ratio of air pollution levels between high- and low-pollution days was five for PM10 (median: 49 and 10 µg/m3) and two for NO2 (median: 47 and 24 µg/m3). No significant increase in blood levels of any of the biomarkers were seen after days with high air pollution levels compared with low levels. Conclusion: Biomarkers of inflammation and coagulation were not found to be significantly increased in the mornings after days with elevated levels of urban air pollution compared with low levels when performing repeated blood samplings in healthy volunteers.

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.

Exposure to Particles, Polycyclic Aromatic Hydrocarbons, and Nitrogen Dioxide in Swedish Restaurant Kitchen Workers

Aims The aim of this study was to measure the exposure to total dust, polycyclic aromatic hydrocarbons (PAHs), and nitrogen dioxide (NO2) of kitchen workers in four different types of restaurants in Sweden (Large scale, European, Fast food, and Asian). Methods One hundred full work-shift (8 h) personal exposure samples were taken from 36 workers in 21 commercial kitchens. Most workers were sampled three times. Mass concentration of total dust was determined using standard gravimetric methods; the filters were analyzed for their content of particulate PAHs. Gas-phase PAHs were sampled using adsorbent tubes (XAD-II) placed after the filter and analyzed with high-resolution gas chromatography/low-resolution mass spectrometry. NO2 was measured using passive dosimeters. Stationary measurements in the kitchen were made in parallel with the personal sampling. Results Group geometric mean concentrations for personal exposure to total dust ranged from 77 µg m-3 (Fast food) to 320 µg m-3 (European kitchens). Individual exposure samples of total dust ranged from ~40 to 3900 µg m-3. In the Large-scale and European kitchens, the time spent frying was identified as a determinant increasing personal exposure to total dust. The within-worker variance dominated the exposure variability of total dust in Large-scale and European kitchens, whereas between-worker variance dominated in Fast food and Asian kitchens. Exposure to total PAHs was statistically significantly higher for workers in the Asian kitchens. Also, exposure to NO2 was higher in the Asian kitchens, which all used gas stoves for cooking. The stationary measurements of total dust showed lower levels than personal exposures for most kitchens, whereas for PAHs, stationary levels were closer to personal exposure levels for all kitchen types. Conclusions The results of this study increase the knowledge about exposure to air pollutants for kitchen workers of restaurant types that are common in Sweden and the rest of Europe. Personal sampling is essential for an accurate exposure assessment, and the large day-to-day variability in exposure levels points to the importance of repeated sampling.