The presence of Toxocara larva in the lungs at 60 days p.i. following a single infection could explain the persistent pulmonary inflammation, airway hyper-reactivity, eosinophilia and increased IgE production observed in T. canis-infected BALB/c mice.

During 2 months of the pollen season, the acute and putative adjuvant effect of traffic-related air pollution on respiratory health was investigated in children sensitised to grass pollen or house dust mite (HDM). Respiratory complaints were objectified via measurement of exhaled NO and inflammatory mediators in nasal lavage (NAL). During the study children, skin prick negative (n = 31) or positive to grass pollen (n = 22), HDM (n = 34) or grass pollen + HDM (n = 32), kept a daily diary on respiratory symptoms, and NAL and exhaled air was sampled twice a week. The level of air pollutants and pollen was monitored continuously. Like children sensitised to HDM, those sensitised to pollen reported respiratory complaints (shortness of breath, itchy eyes or blocked nose) more frequently than non-sensitised children during (but not before) the pollen season; the respiratory complaints of sensitised children were independent of the pollen level. In addition, exposure to increased levels of PM₁₀ induces ‘shortness of breath’ in pollen- and HDM-sensitised children, whereas ozone induces a blocked nose in HDM-sensitised children. Combined exposure to PM₁₀ + pollen and O₃ + pollen induces a blocked nose in both HDM-sensitised children and children sensitised to pollen + HDM. Significant positive associations were found between eNO and the levels of NO₂, CO, PM_2.5 and pollen in both sensitised and non-sensitised children. At the start of the pollen season, the NAL concentration of eosinophils and ECP in pollen-sensitised children was increased compared to winter, but their levels were not further affected by increased exposure to pollen or air pollution. In conclusion, during the pollen season, sensitised children continuously report a high prevalence of respiratory complaints which coincides with increased levels of upper and lower airway inflammatory markers. No additional pro-inflammatory effect of air pollution was observed, which indicates that air pollution does not facilitate allergen-induced inflammatory responses.

Objectives: This study investigates the upper and lower inflammatory response induced by natural exposure to grass pollen in atopic and non-atopic children. Methods: After children's atopic profile had been assessed, their nasal lavage fluid (NAL) and exhaled air was sampled once before and once during the pollen season. Level of nitric oxide (NO) was determined in exhaled air, and the following mediators were measured in NAL: ECP, IL-6, IL-8, albumin, uric acid, and urea. The number of eosinophils in NAL was determined after Giemsa staining. During the experiment ozone and pollen levels were measured continuously. Results: During the pollen season the level of grass pollen was 95 pollen grains per cubic metre. At baseline, 8.0% and 5.4% of total cells in NAL of children sensi-tive to, respectively, house dust mite (HDM) and pollen + HDM were eosinophils, whereas virtually no eosinophils were observed in NAL of non-atopic children. In contrast to the non-atopic and HDM groups, in children sensitive only to grass pollen, grass pollen induced a threefold increase in the percentage of NAL eosinophils and a 2.5-fold increase in the NAL level of ECP (P<0.05). In all groups, the NAL levels of albumin, uric acid, urea, IL-6 and IL-8 were not significantly increased by pollen exposure. At baseline, children sensitive to HDM showed significantly higher exhaled nitric oxide (eNO) values than non-atopic subjects and children sensitive only to pollen (79 to 141% increase). During pollen exposure eNO of children sensitive only to pollen increased from 35.8 to 64.5 ppb (P<0.05), whereas no increase in eNO was observed in the other children. Conclusion: Pollen-sensitive children show a seasondependent upper and lower airway inflammatory response, resembling the continuous inflammation in HDM-sensitive children.

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