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Sci Total Environ. 2013 Jan 15;443:256-66. doi: 10.1016/j.scitotenv.2012.11.004. Epub 2012 Nov 28.

Pulmonary inflammation and tissue damage in the mouse lung after exposure to PM samples from biomass heating appliances of old and modern technologies.

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  • 1Department of Environmental Science, University of Eastern Finland, Kuopio, FI-70211, Finland. mikko.happo@uef.fi

Abstract

Current levels of ambient air fine particulate matter (PM(2.5)) are associated with mortality and morbidity in urban populations worldwide. In residential areas wood combustion is one of the main sources of PM(2.5) emissions, especially during wintertime. However, the adverse health effects of particulate emissions from the modern heating appliances and fuels are poorly known. In this study, health related toxicological properties of PM(1) emissions from five modern and two old technology appliances were examined. The PM(1) samples were collected by using a Dekati® Gravimetric Impactor (DGI). The collected samples were weighed and extracted with methanol for chemical and toxicological analyses. Healthy C57BL/6J mice were intratracheally exposed to a single dose of 1, 3, 10 or 15 mg/kg of the particulate samples for 4, 18 or 24h. Thereafter, the lungs were lavaged and bronchoalveolar lavage fluid (BALF) was assayed for indicators of inflammation, cytotoxicity and genotoxicity. Lungs of 24h exposed mice were collected for inspection of pulmonary tissue damage. There were substantial differences in the combustion qualities of old and modern technology appliances. Modern technology appliances had the lowest PM(1) (mg/MJ) emissions, but they induced the highest inflammatory, cytotoxic and genotoxic activities. In contrast, old technology appliances had clearly the highest PM(1) (mg/MJ) emissions, but their effect in the mouse lungs were the lowest. Increased inflammatory activity was associated with ash related components of the emissions, whereas high PAH concentrations were correlating with the smallest detected responses, possibly due to their immunosuppressive effect.

Copyright © 2012 Elsevier B.V. All rights reserved.

PMID:
23201646
[PubMed - indexed for MEDLINE]
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