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

  • 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
Published Article
Particle and Fibre Toxicology
BioMed Central
Publication Date
May 15, 2006
DOI: 10.1186/1743-8977-3-7
Springer Nature


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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