Comparison of personal exposure to black carbon levels with fixed-site monitoring data and with dispersion modelling and the influence of activity patterns and environment.

BACKGROUND: Short-term studies of health effects from ambient air pollution usually rely on fixed site monitoring data or spatio-temporal models for exposure characterization, but the relation to personal exposure is often not known. OBJECTIVE: We aimed to explore this relation for black carbon (BC) in central Stockholm. METHODS: Families (n = 46) with an infant, one parent working and one parent on parental leave, carried battery-operated BC instruments for 7 days. Routine BC monitoring data were obtained from rural background (RB) and urban background (UB) sites. Outdoor levels of BC at home and work were estimated in 24 h periods by dispersion modelling based on hourly real-time meteorological data, and statistical meteorological data representing annual mean conditions. Global radiation, air pressure, precipitation, temperature, and wind speed data were obtained from the UB station. All families lived in the city centre, within 4 km of the UB station. RESULTS: The average level of 24 h personal BC was 425 (s.d. 181) ng/m3 for parents on leave, and 394 (s.d. 143) ng/m3 for working parents. The corresponding fixed-site monitoring observations were 148 (s.d. 139) at RB and 317 (s.d. 149) ng/m3 at UB. Modelled BC levels at home and at work were 493 (s.d. 228) and 331 (s.d. 173) ng/m3, respectively. UB, RB and air pressure explained only 21% of personal 24 h BC variability for parents on leave and 25% for working parents. Modelled home BC and observed air pressure explained 23% of personal BC, and adding modelled BC at work increased the explanation to 34% for the working parents. IMPACT: Short-term studies of health effects from ambient air pollution usually rely on fixed site monitoring data or spatio-temporal models for exposure characterization, but the relation to actual personal exposure is often not known. In this study we showed that both routine monitoring and modelled data explained less than 35% of variability in personal black carbon exposure. Hence, short-term health effects studies based on fixed site monitoring or spatio-temporal modelling are likely to be underpowered and subject to bias.

Personal exposure to black carbon in Stockholm, using different intra-urban transport modes.

The traffic microenvironment has been shown to be a major contributor to the total personal exposure of black carbon (BC), and is key to local actions aiming at reducing health risks associated with such exposure. The main aim of the study was to get a better understanding of the determinants of traffic-related personal exposure to BC in an urban environment. Personal exposure to ambient levels of BC was monitored while walking, cycling and traveling by bus or car along four streets and while cycling alternative routes simultaneously. Monitoring was performed during morning and afternoon peak hours and at midday, with a portable aethalometer recording one-minute mean values. In all, >4000 unique travel passages were performed. Stepwise Linear Regression was used to assess predictors to personal exposure levels of BC. The personal BC concentration ranged 0.03-37 µg/m3. The average concentrations were lowest while walking (1.7 µg/m3) and highest traveling by bus (2.7 µg/m3). However, only 22% of the variability could be explained by travel mode, urban background BC and wind speed. BC concentrations measured inside a car were on average 33% lower than measured simultaneously outside the car. Choosing an alternative bicycle route with less traffic resulted in up to 1.4 µg/m3 lower personal exposure concentrations. In conclusion, traveling by bus rendered the highest personal BC concentrations. But when taking travel time and inhalation rate into account, the travel-related exposure dose was predicted to be highest during walking and cycling. It is however probable that the benefits from physical activity outweigh health risks associated with this higher exposure dose. It is clear that road traffic makes an important contribution to personal exposure to BC regardless of mode of intra-urban transport. Our data suggest that commuting along routes with lower BC levels would substantially decrease commuter's exposure.

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/m(3) for benzene, 0.56 µg/m(3) for 1,3-butadiene, 19.4 µg/m(3) for formaldehyde, and 14.1 µg/m(3) 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.

Serum amyloid A opposes lipoxin A4 to mediate glucocorticoid refractory lung inflammation in chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) will soon be the third most common cause of death globally. Despite smoking cessation, neutrophilic mucosal inflammation persistently damages the airways and fails to protect from recurrent infections. This maladaptive and excess inflammation is also refractory to glucocorticosteroids (GC). Here, we identify serum amyloid A (SAA) as a candidate mediator of GC refractory inflammation in COPD. Extrahepatic SAA was detected locally in COPD bronchoalveolar lavage fluid, which correlated with IL-8 and neutrophil elastase, consistent with neutrophil recruitment and activation. Immunohistochemistry detected SAA was in close proximity to airway epithelium, and in vitro SAA triggered release of IL-8 and other proinflammatory mediators by airway epithelial cells in an ALX/FPR2 (formyl peptide receptor 2) receptor-dependent manner. Lipoxin A(4) (LXA(4)) can also interact with ALX/FPR2 receptors and lead to allosteric inhibition of SAA-initiated epithelial responses (pA(2) 13 nM). During acute exacerbation, peripheral blood SAA levels increased dramatically and were disproportionately increased relative to LXA(4). Human lung macrophages (CD68(+)) colocalized with SAA and GCs markedly increased SAA in vitro (THP-1, pEC(50) 43 nM). To determine its direct actions, SAA was administered into murine lung, leading to induction of CXC chemokine ligand 1/2 and a neutrophilic response that was inhibited by 15-epi-LXA(4) but not dexamethasone. Taken together, these findings identify SAA as a therapeutic target for inhibition and implicate SAA as a mediator of GC-resistant lung inflammation that can overwhelm organ protective signaling by lipoxins at ALX/FPR2 receptors.