Upper airway inflammation in children exposed to ambient ozone and potential signs of adaptation

Abstract

In order to investigate nasal inflammation and subsequent adaptation after ambient ozone exposure, nasal lavage (NL) fluid was collected from 170 schoolchildren on 11 occasions (time points) between March and October.Eosinophil cationic protein (ECP), albumin and leukocytes were quantified as markers of nasal inflammation. The highest half-hour outdoor O 3 concentration for each individual on the day prior to the NL was used as a measure of exposure (O 3 indiv). To avoid confounding with exposure to common environmental allergens, the study population was restricted to children without sensitization to inhalant allergens.In the initial period of increased O 3 levels in May (time point 4), with a median O 3 indiv of 135 mg . m -3 (5th ±95th percentile 100±184 mg . m ). Cross-sectional analysis of all 11 time points revealed no significant association of O 3 indiv on the one hand and ECP, albumin and leukocyte levels on the other. A multivariable model estimated using generalized estimating equations showed a statistically significant association of O 3 indiv and leukocytes and ECP as the dependent variable, when time points 1±4 were analysed (p<0.05). In the same model, this association diminished continuously when time points 5±11 were added stepwise, in spite of high O 3 exposure. Not even a tendency towards an O 3 effect could be recognized when time points 1±8 were considered.The results indicate: 1) acute inflammation of the nasal mucosa after the first increase in ambient ozone levels, with 2) a significant dose-dependent increase in leukocyte and eosinophil cationic protein levels, and 3) possible adaptation of the nasal mucosa in spite of constant high levels of ozone exposure in children during the summer season.

Nasal inflammation and personal exposure to fine particles PM2.5 in asthmatic children

“…Previous epidemiologic works have found that NALF inflammatory mediators are related to ETS exposure in children 42 and to ozone levels, 43 but none of them demonstrated leukocyte increase in relation to ambient PM10 exposures. 17,18,26,27 When PM10 concentrations were introduced in our multivariate models, we also failed to evidence any association between outdoor PM10 levels and nasal mediators (data not shown). These results indicate that environmental measurements of PM10 might not be relevant for study of respiratory inflammation.…”

“…In all previous works, assessment of PM exposure has been based on fixed-site measurements of particulate matter with a diameter of less than 10 mm (PM10), 17,18,26,27 which reflect only a part of the true exposure. In this work PM2.5 exposure, now regarded as the state of the art in the field of environmental epidemiology, [28][29][30] was measured in a personal manner to limit misclassifications.…”

Selected Contribution: Neuroplasticity in nucleus tractus solitarius neurons after episodic ozone exposure in infant primates

“…In rats, the respiratory responses (rapid shallow breathing and decreased lung function) adapt despite the continued presence of lung epithelial damage, inflammation, increased concentrations of lavagable proteins (24), and increased sensory nerve excitability (30,32), suggesting that lung-CNS reflexes might be involved in the adaptation. Of direct relevance to the present study is that the adaptation is not just limited to adults but also occurs earlier in life (37,38).…”

Postnatal episodic ozone results in persistent attenuation of pulmonary and peripheral blood responses to LPS challenge

“…27). The airway inflammatory cell profile of ozone is predominantly neutrophilic in adult humans and most animal models; however, there is evidence that children develop an eosinophilic response to ambient levels of exposure (14,35,36). Because of the nonantigenic nature of ozone, there is currently no evidence that an adaptive immune response leading to establishment of immunological memory and antibody production is induced by exposure alone.…”