Conventional and toxicogenomic assessment of the acute pulmonary damage induced by the instillation of Cardiff PM10 into the rat lung.

There is strong epidemiological evidence of association between PM10 (particulate matter with an aerodynamic diameter less than or equal to 10 microm) and adverse health outcomes including death and increased hospital admissions for cardiopulmonary conditions. Ambient PM10 surrogates such as diesel exhaust particles (DEP), a common component of UK PM10 have been shown to induce lung inflammation in both humans and rodents. To date, few studies have reported on the toxicological response of UK PM10 in experimental animals. This study examines the pulmonary toxicological responses in male Sprague Dawley rats following the intratracheal instillation of Cardiff urban PM10. A mild but significant change in lung permeability was observed in the lung post-instillation of a high (10 mg) dose of the whole PM10 as adjudged by increases in lung to body weight ratio and total acellular lavage protein. Such effects were less marked following instillation of a water-soluble fraction (80% of the total mass) but histological examination showed that lung capillaries were swollen in size with this treatment. In conclusion, conventional toxicological, histological and toxicogenomic studies have indicated that Cardiff PM10 exhibits low bioreactivity in the form of mild permeability changes. Differential gene expression was observed when the lung was treated with whole PM10, containing durable particles, in comparison with the water-soluble fraction of PM10 that was devoid of particles. Such changes were linked to different histopathological events within the lung.