The study was partly funded and carried out within the framework of the DEMOCOPHES (LIFE + Programme DG Environment—Life09 ENV/BE000410) and COPHES (7th Framework Programme DG Research — No. 244237) projects, which aimed to harmonize biomonitoring throughout Europe, and the Swedish National Environmental Monitoring Program, coordinated by Swedish EPA (NV-734-11/2151102). NLG919 datasheet We greatly acknowledge the participating women and children and the technical assistance of B Norrfors and L-M Lundmark. “
“Long-term exposure to particulate air pollution

from traffic and other combustion sources is associated with an increase in general mortality and morbidity from respiratory and cardiovascular diseases, especially among elderly and people with previous respiratory and cardiovascular diseases (Hoek et al., 2013). Short-term exposure to elevated levels of outdoor air pollution, lasting hours to several days, has been linked to increased mortality and hospital admissions due to heart and lung diseases (Ruckerl et al., 2011). Ambient

air particulate matter (PM) is usually assessed by mass concentration in terms of PM10 (aerodynamic diameter < 10 μm) or PM2.5, (aerodynamic diameter < 2.5 μm), whereas ultrafine particles (UFP, diameter < 0.1 μm), contributing only few percent to the total mass, are often characterized by particle number concentration Androgen Receptor Antagonist (PNC). The composition of ambient air PM varies widely and depends on the emission source, particle size, geographic location, atmospheric chemical transformations, and meteorology (Putaud et al., 2010). UFP, especially from combustion processes, are thought to be more harmful than larger particles due to their large reactive surface area, chemical composition, high alveolar deposition, Ribose-5-phosphate isomerase poor clearance and the potential for translocation to the systemic circulation (Franck et al., 2011). Nevertheless,

epidemiological evidence supporting the specific hazards of UFP is relatively scarce, possibly due to problems in exposure assessment, including high spatial variation (Ruckerl et al., 2011). The mechanisms involved in the health effects of PM include pulmonary and systemic inflammation, oxidative stress, altered cardiac autonomic function, altered balance between coagulation and fibrinolysis, endothelial and microvascular dysfunction, atherosclerosis progression and plaque instability, as studied in panel and cross-sectional studies with short-term exposure assessed from monitoring stations or after controlled exposure (Brook et al., 2010). However, results have shown less consistency for prognostic markers for cardiovascular risk, including blood markers reflecting inflammation such as C-reactive protein (CRP) and circulating leukocyte counts, cell expression of adhesion molecules and impaired endothelial function (Li et al., 2012, Pope et al., 2011 and Ruckerl et al., 2011).