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The interaction between exposure to nanomaterials and existing inflammatory conditions has not been fully established. Multiwalled carbon nanotubes (MWCNT; Nanocyl NC 7000 CAS no. 7782-42-5; count median diameter in atmosphere 61 + 5 nm) were tested by inhalation in high Immunoglobulin E (IgE)-responding Brown Norway (BN) rats with trimellitic anhydride (TMA)-induced respiratory allergy. The rats were exposed 2 days/week over a 3.5-week period to a low (11 mg/m 3 ) or a high (22 mg/m 3 ) concentration of MWCNT. Nonallergic animals exposed to MWCNT and unexposed allergic and nonallergic rats served as controls. At the end of the exposure period, the allergic animals were rechallenged with TMA. Histopathological examination of the respiratory tract showed agglomerated/aggregated MWCNT in the lungs and in the lung-draining lymph nodes. Frustrated phagocytosis was observed as incomplete uptake of MWCNT by the alveolar macrophages and clustering of cells around MWCNT. Large MWCNT agglomerates/aggregates were found in granulomas in the allergic rats, suggesting decreased macrophage clearance in allergic rats. In allergic rats, MWCNT exposure decreased serum IgE levels and the number of lymphocytes in bronchoalveolar lavage. In conclusion, MWCNT did not aggravate the acute allergic reaction but modulated the allergy-associated immune response.

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Introduction: Comprehensive data on the carcinogenicity of airborne nanoparticles are lacking. CeO 2 and BaSO 4 are currently being tested in a chronic and carcinogenicity inhalation study (OECD TG 453), within the EU-project NanoREG. Materials and Methods: Rats were exposed to 0.1, 0.3, 1 and 3 mg/ m 3 CeO 2 and 50 mg/m 3 BaSO 4 for 6 h/day for 2 years. Interim results after 13 and 52 weeks and results of previous studies with 1 and 4 weeks of exposure to 0.5, 5 and 25 mg/m 3 CeO 2 are available. Examinations included burdens and histopathology of the respiratory tract and bronchoalveolar lavage fluid (BALF) analysis. Results: Inhaled CeO 2 is deposited in the lung and cleared with a half-time of 40 days; the clearance was retarded by exposure to higher concentrations (25 mg/m 3 ). Lung burden after 13 weeks of exposure to 3 mg/m 3 was 1.4 mg/lung. Pulmonary inflammation was observed with neutrophils in BALF after 1 and 4 weeks of exposure to 5 and 25 mg/m 3 and after 13 weeks of exposure to 1 and 3 mg/m 3 CeO 2 . The slope of the dose-response curve was steeper after shorter exposure times. Granulomatous inflammation was observed by histopathology after 4 weeks exposure to 5 and 25 mg/m 3 CeO 2 . BaSO 4 is rapidly cleared from the lung (half-time 7 days); lung burdens were 1.7 mg/lung after 13 weeks exposure. Neutrophils in BALF were not increased after 4, but slightly increased after 13 weeks. Conclusions: The time course of particle burdens and effects in the lung are described. A link between retarded clearance and inflammation in the lung driven by neutrophils and macrophages and subsequent granulomatous inflammation was observed.

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