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Response of spontaneously hypertensive rats to inhalation of fine and ultrafine particles from traffic: experimental controlled study

Authors
  • Kooter, Ingeborg M1
  • Boere, A John F1
  • Fokkens, Paul HB1
  • Leseman, Daan LAC1
  • Dormans, Jan AMA2
  • Cassee, Flemming R1
  • 1 National Institute for Public Health and the Environment, Centre for Environmental Health Research, Bilthoven, The Netherlands , Bilthoven
  • 2 National Institute for Public Health and the Environment, Laboratory of Toxicology, Pathology and Genetics, Bilthoven, The Netherlands , Bilthoven
Type
Published Article
Journal
Particle and Fibre Toxicology
Publisher
BioMed Central
Publication Date
May 15, 2006
Volume
3
Issue
1
Identifiers
DOI: 10.1186/1743-8977-3-7
Source
Springer Nature
Keywords
License
Yellow

Abstract

BackgroundMany epidemiological studies have shown that mass concentrations of ambient particulate matter (PM) are associated with adverse health effects in the human population. Since PM is still a very crude measure, this experimental study has explored the role of two distinct size fractions: ultrafine (<0.15 μm) and fine (0.15- 2.5 μm) PM. In a series of 2-day inhalation studies, spontaneously hypersensitive (SH) rats were exposed to fine, concentrated, ambient PM (fCAP) at a city background location or a combination of ultrafine and fine (u+fCAP) PM at a location dominated by traffic. We examined the effect on inflammation and both pathological and haematological indicators as markers of pulmonary and cardiovascular injury. Exposure concentrations ranged from 399 μg/m3 to 3613 μg/m3 for fCAP and from 269μg/m3 to 556 μg/m3 for u+fCAP.ResultsAmmonium, nitrate, and sulphate ions accounted for 56 ± 16% of the total fCAP mass concentrations, but only 17 ± 6% of the u+fCAP mass concentrations. Unambiguous particle uptake in alveolar macrophages was only seen after u+fCAP exposures. Neither fCAP nor u+fCAP induced significant changes of cytotoxicity or inflammation in the lung. However, markers of oxidative stress (heme oxygenase-1 and malondialdehyde) were affected by both fCAP and u+fCAP exposure, although not always significantly. Additional analysis revealed heme oxygenase-1 (HO-1) levels that followed a nonmonotonic function with an optimum at around 600 μg/m3 for fCAP. As a systemic response, exposure to u+fCAP and fCAP resulted in significant decreases of the white blood cell concentrations.ConclusionMinor pulmonary and systemic effects are observed after both fine and ultrafine + fine PM exposure. These effects do not linearly correlate with the CAP mass. A greater component of traffic CAP and/or a larger proportion ultrafine PM does not strengthen the absolute effects.

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