Particulate matter (PM) exposure is related to various health effects which may involve respiratory and cardiovascular diseases, as well as cancer induction; such different effects are produced by variable PM characteristics. We have previously reported that Milan PM composition is related to the sampling season and the particles size, and these properties are responsible for different effects on in vitro systems1. PM2.5 is dominated by combustion derived particles consisting of a carbonaceous core with organic and inorganic compounds adsorbed on its surface. Organic components of this fraction are mostly present in winter and they are responsible for inducing high level of ROS formation and DNA damage2. PM10 derives from abrasion and resuspension processes, and is enriched in crustal materials (metals) and biological components (endotoxins), especially during summer season; thus this fraction induces pro‐inflammatory responses on human cells. The mechanisms underlying PM‐induced effects are not completely understood and investigations on the cellular gene expression patterns, modulated after particles exposure, might greatly help this knowledge, elucidating the main molecular pathway involved. Aim: The genome wide expression profiles and the molecular changes associated with urban PM fractions have been investigated to individuate the pathways activated.

Gene expression profiling of human bronchial epithelial cells exposed to seasonal Milan particulate matter / E. Longhin, L. Capasso, C. Battaglia, C. Cosentino, M.C. Proverbio, I. Cifola, E. Mangano, M. Camatini, M. Gualtieri. ((Intervento presentato al 50. convegno Eurotox Congress of the European Societies of Toxicology tenutosi a Edinburgh nel 2014.

Gene expression profiling of human bronchial epithelial cells exposed to seasonal Milan particulate matter

C. Battaglia;C. Cosentino;M.C. Proverbio;
2014

Abstract

Particulate matter (PM) exposure is related to various health effects which may involve respiratory and cardiovascular diseases, as well as cancer induction; such different effects are produced by variable PM characteristics. We have previously reported that Milan PM composition is related to the sampling season and the particles size, and these properties are responsible for different effects on in vitro systems1. PM2.5 is dominated by combustion derived particles consisting of a carbonaceous core with organic and inorganic compounds adsorbed on its surface. Organic components of this fraction are mostly present in winter and they are responsible for inducing high level of ROS formation and DNA damage2. PM10 derives from abrasion and resuspension processes, and is enriched in crustal materials (metals) and biological components (endotoxins), especially during summer season; thus this fraction induces pro‐inflammatory responses on human cells. The mechanisms underlying PM‐induced effects are not completely understood and investigations on the cellular gene expression patterns, modulated after particles exposure, might greatly help this knowledge, elucidating the main molecular pathway involved. Aim: The genome wide expression profiles and the molecular changes associated with urban PM fractions have been investigated to individuate the pathways activated.
gene expression; pollution; BEAS; particulate matter; genomics
Settore BIO/10 - Biochimica
Settore BIO/11 - Biologia Molecolare
http://www.eurotox2014.com/
Gene expression profiling of human bronchial epithelial cells exposed to seasonal Milan particulate matter / E. Longhin, L. Capasso, C. Battaglia, C. Cosentino, M.C. Proverbio, I. Cifola, E. Mangano, M. Camatini, M. Gualtieri. ((Intervento presentato al 50. convegno Eurotox Congress of the European Societies of Toxicology tenutosi a Edinburgh nel 2014.
Conference Object
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/252611
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact