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Preexposure to amorphous silica particles attenuates but also enhances allergic reactions in trimellitic anhydride-sensitized brown Norway rats

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Author: Arts, J.H.E. · Schijf, M.A. · Kuper, C.F.
Institution: TNO Kwaliteit van Leven
Source:Inhalation Toxicology, 10, 20, 935-948
Identifier: 240930
doi: doi:10.1080/08958370802105371
Keywords: Biology · Toxicology and Applied Pharmacology · silicon dioxide · trimellitic anhydride · animal experiment · animal model · animal tissue · article · biochemistry · breathing pattern · brown Norway rat · cell infiltration · controlled study · eosinophil · female · histopathology · inflammation · laryngeal inflammation · laryngeal ulceration · larynx disorder · liver weight · lung edema · lung function · lung lavage · lung weight · lymph node · lymphocyte count · macrophage · neutrophil · nonhuman · priority journal · rat · respiratory tract allergy · squamous cell metaplasia · tidal volume · Allergens · Animals · Body Weight · Drug Administration Schedule · Female · Immunoglobulin E · Liver · Lung · Lymph Nodes · Organ Size · Phthalic Anhydrides · Rats · Respiratory Function Tests · Silicon Dioxide · Animalia · Rattus norvegicus


Irritant-induced inflammation of the airways may aggravate respiratory allergy induced by chemical respiratory allergens. Therefore, the effect of airway irritation by synthetic amorphous silica (SAS) on respiratory allergy to trimellitic anhydride (TMA) was studied. Brown Norway (BN) rats were topically sensitized on day 0 and on day 7, subsequently exposed for 6 h/day for 6 days to 27 mg/m3 SAS, and challenged by inhalation to a minimally irritating concentration of 12 mg/m3 TMA, 24 h after the last SAS exposure. An additional group was exposed to SAS before a second challenge to TMA. Control groups were treated with vehicle, and/or did not receive SAS exposure. Breathing parameters, cellular and biochemical changes in bronchoalveolar lavage (BAL) fluid, and histopathological airway changes 24 h after challenge were the main parameters studied. Exposure to SAS alone resulted in transient changes in breathing parameters during exposure, and in nasal and alveolar inflammation with neutrophils and macrophages. Exposure to SAS before a single TMA challenge resulted in a slightly irregular breathing pattern during TMA challenge. SAS also diminished the effect of TMA on tidal volume, laryngeal ulceration, laryngeal inflammation, and the number of BAL (lung) eosinophils in most animals, but aggravated laryngeal squamous metaplasia and inflammation in a single animal. The pulmonary eosinophilic infiltrate and edema induced by a second TMA challenge was diminished by the preceding SAS exposure, but the number of lymphocytes in BAL was increased. Thus, a respiratory particulate irritant like SAS can reduce as well as aggravate certain aspects of TMA-induced respiratory allergy. Copyright © Informa UK Ltd.