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Inhalation Toxicology
International Forum for Respiratory Research
Volume 24, 2012 - Issue 8
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Research Article

Impact of emerging pollutants on pulmonary inflammation in asthmatic rats: ethanol vapors and agglomerated TiO2 nanoparticles

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Pages 528-538 | Received 13 Feb 2012, Accepted 21 May 2012, Published online: 02 Jul 2012
 

Abstract

Context: Titanium dioxide nanoparticles (nano-TiO2) and ethanol vapors are air contaminants with increasing importance. The presence of a pathological pulmonary condition, such as asthma, may increase lung susceptibility to such contaminants.

Objective: This study aimed to investigate if exposure to inhaled ethanol vapors or nano-TiO2 can modulate the rat pulmonary inflammatory response resulting from an allergic asthmatic reaction.

Materials and methods: Brown Norway rats were sensitized (sc) and challenged (15 min inhalation, 14 days later) with chicken egg ovalbumin (OVA). Leukocytes were counted in bronchoalveolar lavages (BAL) performed at 6, 24, 36, 48 and 72 h following the challenge and either after ethanol exposures (3000 ppm, 6 h/day, daily) or at 48 h (peak inflammation) for nano-TiO2 exposures (9.35 mg/m3 aerosol for 6 and 42 h after the OVA challenge). For the nano-TiO2 exposures, plasma and BAL cytokines were measured and lung histological analyzes were performed.

Results: Exposure to ethanol did not significantly affect BAL leukocytes after OVA challenge. Exposure to nano-TiO2 significantly decreased BAL leukocytes compared to OVA-challenged controls. Plasma and BAL IL-4, IL-6, and INF-γ levels were also decreased in the nano-TiO2 group.

Discussion: While ethanol vapors do not modify the pulmonary inflammation in rats during an asthmatic response, a surprising protective effect for agglomerated nano-TiO2 was observed. A putative mechanistic basis involving a decrease in the Th2 response caused by OVA is proposed.

Conclusion: Allergic pulmonary inflammation is not up-regulated by inhalation of the pollutants ethanol and nano-TiO2. On the contrary, nano-TiO2 decreases lung inflammation in asthmatic rats.

Acknowledgments

The authors wish to acknowledge the technical contribution of Guylaine Lassonde, Ginette Charest-Tardif, and the team at Topigen Pharmaceuticals Inc. We thank the Agence française de sécurité sanitaire de l’environnement et du travail (AFSSET) and the Réseau de recherche en santé environnementale (RRSE) for their financial support.

Declaration of interest

There are no conflicts of interest for all authors included in this manuscript.

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