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We can hypothesize that metal and organic-enriched PM may cause greater tissue damage than particles having low overall metal organic mass because concentration of these causative components may reach high at the site of their deposition in the microenvironment of airways.
However, this will not allow us to identify causative components or the role of atmospheric aging of DE.
Exposure to particulate matter (PM) has been associated with increased cardiovascular morbidity; however, causative components are unknown.
Thus, PM-associated zinc may be one of the causative components of ambient PM responsible for cardiac effects.
Although human exposure to airborne particulate matter (PM) is associated with adverse cardiovascular effects (Pope et al. 2004), the specific causative components or sources have not been identified.
Moreover, there is a lack of correlation between health end points and PM mass or its causative components (Clarke et al. 2000; Gordon et al. 2000; Kodavanti et al. 2000a; Saldiva et al. 2002; Smith et al. 2003).
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Should symptoms persist, the causative component may remain elusive.
Although earlier diagnosis may contribute to a better clinical outcome, it is not clear from our data what is the main causative component of that better outcome.
These results are consistent with the reports showing that oxyhemoglobin is a major causative component of blood clot for cerebral vasospasm following SAH [ 30, 31] and that ET-1 potentiates the oxyhemoglobin-induced cerebrovascular smooth muscle contraction via the rhoA/rho kinase and PKC pathways [ 11].
These results consisted with the reports showing that oxyhemoglobin is a major causative component of blood clot for cerebral vasospasm following SAH [ 26] and that ET-1 potentiates the oxyhemoglobin-induced cerebrovascular smooth muscle contraction via the rhoA/rho kinase and PKC pathways [ 28, 29].
It has been shown that ET-1 potentiates the contraction of cerebrovascular smooth muscles induced by oxyhemoglobin, a blood clot component and major causative factor in cerebral vasospasm, via the protein kinase C (PKC) and rhoA/rho kinase pathways [ 11].
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