5, personally monitored exposure showing the strongest associations followed by NVP-BEZ235 in vivo indoor PM exposure, and then outdoor and central-site measurements (Delfino et al., 2004). A 3-year panel study on children with asthma and adults with or without chronic obstructive pulmonary disease found inverse associations between lung function and exposure

to PM2.5 in both adults and children with lung disease and most consistently with respect to indoor exposures (Trenga et al., 2006). Most studies of healthy individuals have reported no associations between indoor PM2.5 and lung function (Ebelt et al., 2005, Jansen et al., 2005 and Yeatts et al., 2012). Two studies including both smokers and subjects who were exposed to environmental tobacco smoke, but otherwise healthy, have shown associations between lung function or symptoms with

indoor concentrations of PM2.5 in a panel study of elderly especially during winter (Simoni et al., 2003) and in an indoor air filtration crossover study with young adults (Weichenthal et al., 2013). By contrast, our investigation encompassed only non-smokers without asthma, living in non-smoking homes and lung function was not associated with PM2.5 only with PNC levels. Possibly specific effects of high outdoor PNC levels from traffic have been found in adults with asthma, showing decreased lung function after short-term exposure in traffic-dense environments INCB024360 cell line (McCreanor et al., 2007). An exposure contrast in PNC (9000–66,500 particles/cm3) else for 5 h while exercising intermittently at five different locations including two traffic sites, an urban background location, an underground train station and a farm in the Netherlands was associated with decreased lung function in young healthy subjects (Strak et al., 2012). However, in healthy young adults no effect on lung function was observed during 24 h of exposure to air from a busy street in Copenhagen, Denmark, with PNC of 6000–15,000 particles/cm3

(Brauner et al., 2009). Similarly, a 2-hour exposure to high PNC in a road tunnel (1.3 × 105 particles/mL) or concentrated ambient UFP (2.1 × 105 particles/cm3) were not associated with altered lung function in young and healthy subjects (Larsson et al., 2007 and Samet et al., 2009). Many studies on the associations between air pollution-mediated systemic inflammation and cardiovascular diseases have assessed CRP and leukocyte counts as markers of inflammation (Delfino et al., 2005). We found a significant positive association between indoor exposure to PM2.5 and elevated levels of CRP. We also found positive associations between outdoor particle levels and CRP, but they were not statistically significant. A 7-day intervention study with air filtration in the homes of a wood smoke impacted area found an association between the indoor concentration of PM2.5 and CRP (Allen et al.