Personal Exposure to Ambient Particulate Matter (pm2.5) Is Associated with Nasal Inflammation in Asthmatic Children Living in Paris

Allergic respiratory diseases have recently become a major public and political concern in most industrialized countries over the world. The increased incidence in allergic asthma and allergic rhinitis has paralleled the motor vehicle traffic booming, suggesting a potential role of air pollutants in this major rise. Epidemiological studies have revealed a consistent association between outdoor ambient air pollution (to which ozone, nitrogen dioxide and particulate matter (PM) are major contributors) and various health respiratory outcomes [Lebowitz, 1996]. They have shown an association between small short-term increases in PM levels and increases in daily mortality and morbidity due to cardiovascular and respiratory diseases [Katsouyanni et al., 1990; Dockery and Pope, 1994; Schwartz, 1994]. The role of diesel exhaust particles (DEP) is questioned because DEP is one of the major components of particulate matter pollution in urban environments, accounting for up to 90% of the ultra fine particulate mass [United Nations Environment Program, 1994]. The existence of plausible and reliable underlying mechanisms supports these epidemiological observations. Many studies have thus focused on the biological events that occur after diesel exhaust particles (DEP) exposure. Paralleling observations in the lung, in the nose, short-term DEP exposure results in common qualitative alterations characterized by immediate nasal hyper responsiveness, antioxidant response, marked epithelial inflammation, and a specific humoral response. In addition, studies on combined DEP/allergen challenge report that, beside their intrinsic deleterious properties, DEP have an adjuvant-like effect on the immediate and late-phase response to allergen challenge, since they are able to mimic effects occurring after allergen challenge (for a review, see [Nikasinovic et al., 2003]). The nose is an easily assessable mucosal surface, compared to lung. It is an interesting area for assessing upper airway inflammatory status, as it is the first region of the respiratory tract in contact with airborne pollutants. The nasal lavage (NAL) fluid (NALF) is rich in inflammatory biomarkers, as Naclerio and co-workers demonstrated in 1986 in allergic subjects [Naclerio et al., 1986]. NAL is a useful method for epidemiological studies since it fulfils conditions for large-scale use: it is simple to perform, non-invasive, and atraumatic. However, the rare epidemiological studies dealing with air pollution and nasal inflammation failed to demonstrate a significant effect of PM on NALF inflammatory biomarkers. In that context, the aim of this study was to determine the impact of personal exposure to fine particles (PM < 2.5 μm diameter, PM2.5) and to another major indicator of traffic air pollutants, NOx, on nasal inflammation in children with allergic asthma and in healthy children living in Paris area.