The acute toxic effects of particulate matter in mouse lung are related to size and season of collection.

The toxicity of size-fractionated particulate matter (PM10 and PM2.5) collected in Milano during two different seasons (summer and winter) has been evaluated in vivo. The focus is on time related (3 h, 24 h and 1 week) lung response following a single intratracheal aerosolization in BALB/c mice. The bronchoalveolar lavage fluid (BALf) and the lung parenchyma were screened for different markers of inflammation and cytotoxicity. Histology and immunohistochemistry were performed on excised fixed lungs to assess the effects produced by the different PM fractions. All the analyzed inflammatory markers (PMNs percentage, TNF-α, Hsp70 in the BALf, HO-1 in lung parenchyma), increased after summer PM10 administration; on the contrary winter PM10 and PM2.5 specifically increased the amount of the Cyp1B1, a protein putatively involved in the induction of pro-carcinogenic effect. Moreover, we detected an intensification of LDH activity in the BALf after the administration of winter PM10 and PM2.5, potentially related to an in progress necrotic process while after summer PM10 and PM2.5 administration, the initiation of the caspase cascade suggested a cytotoxic effect sustained by apoptosis. Our results evidenced the toxicity mechanisms elicited by size fractionated PM samples, collected in winter and summer seasons, which differs for dimensions, chemical and microbiological composition. PM10 has been indicated to elicit above all a pro-inflammatory response, linked to its specific biological components, while PM2.5 is supposed to be more harmful due to its smaller dimension and the ability to distribute into the lung alveolar districts. We hypothesized that adverse health effects observed after a single dose of winter PM2.5 is at least partly caused by specific winter PM components, i.e. PAH and transitional metals.