title: No oxidative stress or DNA damage in peripheral blood mononuclear cells after exposure to particles from urban street air in overweight elderly.
abstract: Exposure to traffic-related particulate matter (PM) has been associated with increased risk of lung disease, cancer and cardiovascular disease especially in elderly and overweight subjects. The proposed mechanisms involve intracellular production of reactive oxygen species (ROS), inflammation and oxidation-induced DNA damage studied mainly in young normal-weight subjects. We performed a controlled cross-over, randomised, single-blinded, repeated-measure study where 60 healthy subjects (25 males and 35 females) with age 55-83 years and body mass index above 25 kg/m(2) were exposed for 5h to either particle-filtered or sham-filtered air from a busy street with number of concentrations and PM2.5 levels of 1800/cm(3) versus 23 000/cm(3) and 3 µg/m(3) versus 24 µg/m(3), respectively. Peripheral blood mononuclear cells (PBMCs) were collected and assayed for production of ROS with and without ex vivo exposure to nanosized carbon black as well as expression of genes related to inflammation (chemokine (C-C motif) ligand 2, interleukin-8 and tumour necrosis factor), oxidative stress response (heme oxygenase (decycling)-1) and DNA repair (oxoguanine DNA glycosylase). DNA strand breaks and oxidised purines were assayed by the alkaline comet assay. No statistically significant differences were found for any biomarker immediately after exposure to PM from urban street air although strand breaks and oxidised purines combined were significantly associated with the particle number concentration during exposure. In conclusion, 5h of controlled exposure to PM from urban traffic did not change the gene expression related to inflammation, oxidative stress or DNA repair, ROS production or oxidatively damaged DNA in PBMCs from elderly overweight human subjects.
authors.affiliation: Section of Environmental Health, Department of Public Health, Faculty of Health and Medical Sciences, University of Copenhagen, Øster Farimagsgade 5A, DK-1014 Copenhagen, Denmark.
authors.forename: Jette Gjerke
authors.initials: JG
authors.lastname: Hemmingsen
authors.affiliation: Section of Environmental Health, Department of Public Health, Faculty of Health and Medical Sciences, University of Copenhagen, Øster Farimagsgade 5A, DK-1014 Copenhagen, Denmark.
authors.forename: Kim
authors.initials: K
authors.lastname: Jantzen
authors.affiliation: Section of Environmental Health, Department of Public Health, Faculty of Health and Medical Sciences, University of Copenhagen, Øster Farimagsgade 5A, DK-1014 Copenhagen, Denmark.
authors.forename: Peter
authors.initials: P
authors.lastname: Møller
authors.affiliation: Section of Environmental Health, Department of Public Health, Faculty of Health and Medical Sciences, University of Copenhagen, Øster Farimagsgade 5A, DK-1014 Copenhagen, Denmark stl@sund.ku.dk.
authors.forename: Steffen
authors.initials: S
authors.lastname: Loft
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000393:Air Pollutants / Q000633:toxicity*; D002947:Cities; D018592:Cross-Over Studies; D004247:DNA / Q000187:drug effects; D004249:DNA Damage; D045647:DNA Glycosylases / Q000187:drug effects / Q000235:genetics; D005260:Female; D015870:Gene Expression; D006801:Humans; D007249:Inflammation / Q000235:genetics; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D050177:Overweight; D018384:Oxidative Stress / Q000187:drug effects* / Q000235:genetics; D052638:Particulate Matter / Q000633:toxicity*; D016037:Single-Blind Method
chemical_list: D000393:Air Pollutants; D052638:Particulate Matter; D004247:DNA; D045647:DNA Glycosylases; C479058:oxoguanine glycosylase 1, human