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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.
Highlights
Many epidemiological studies have shown that mass concentrations of ambient particulate matter (PM) are associated with adverse health effects in the human population
The PM-associated adverse health effects have been found all over the world, a more closer look reveals that there seem to be heterogeneous across locations [4,5,6,7,8], which might be due to differences of anthropogenic sources such as traffic [9]
While alterations of biological endpoints were occasionally statistically significant and potentially biologically relevant, we found no convincing proof that ambient PM exposures can modify homeostasis
Summary
Many epidemiological studies have shown that mass concentrations of ambient particulate matter (PM) are associated with adverse health effects in the human population. 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. Epidemiological studies have shown that exposure to ambient particulate air pollution (particulate matter or PM) is associated with many health effects [1,2,3], which include premature death, increased hospitalization for cardiopulmonary diseases, airway complaints, and reduced lung function. Particulate matter consists of many chemicals, but it is not very likely that some of them The risk can be effectively reduced by reducing the PM fraction that is most likely to cause adverse health effects
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