megavideolinks
Joined: 19 Nov 2011
Posts: 273
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 Posted: Sat Nov 26, 2011 11:24 am Post subject: AIR POLLUTION EFFECTS VASCULAR FUNCTION |
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peripheral circulation has been recently demonstrated (Nemmar
et al., 2001, 2002; Oberdorster et al., 1995). A rapid translocation of a substantial fraction of intratracheally instilled
99m
Tcalbumin nanocolloid particles from the lungs into the systemic
circulation has been observed in the hamster (Nemmar et al.,
2001) and in humans (Nemmar et al., 2002). Nemmar et al.
(2002) found that
99m
Tc ultrafine particles passed into the circulatory system within 1 min after inhalation, reached a peak concentration between 10 and 20 min, and remained at this level for
up to 60 min. These studies support the presence of a pathway
by which inhaled particles can have direct effects on vascular
endothelium.
Respiratory number deposition fraction of ultrafine particles
during exercise increases approximately 32% over resting values
and exceeds predicted values for exercise by approximately 22%
for 26-nm particles (Daigle et al., 2003). Total particle deposition increases approximately 4.5-fold for a 3.3-fold increase in
minute ventilation (Daigle et al., 2003), and prediction models of
particle deposition indicate that particles in the 30 nm size range
are predominately deposited in airway generations 19–22 during
exercise. Considering that greater than 90% of auto and truck
emission particle number is found in the 3–30 nm size range and
most of the particle mass is found in the 30–500 nm size range,
particle deposition in the alveolar region is most likely high for
individuals exercising in high auto emission conditions (ICRP,
1994). The probable high particle deposition in our high exposure treatment arm supports the observed PM-induced vascular
effects.
Although U.S. Environmental Protection Agency (EPA)
emission standards for particulate matter are based on mass metric, recent studies suggest that particle number and/or particle
surface area are better related to emission inhalation health effects (Kittelson et al., 2004; Ramachandran et al., 2005). In this
study, we chose to measure only particle number, since auto and
diesel emission number deposition efficiency is much greater
than on a mass basis (Daigle et al., 2003). Because we did not
obtain particle size distributions for our number counts, we were
unable to calculate a meaningful estimate of particle mass for
comparisons.
The 4% vasoconstriction of the brachial artery after exercise while breathing high [PM1] ambient air was consistent with
the ∼2.6% vasoconstriction reported by Brook et al. (2002).
The greater PM-induced vasoconstriction reported in the present
study could be due to differences in study populations; our subjects were a homogeneous group of fit college athletes who were
approximately 15 yr younger than subjects in the Brook et al.
(2002) study. Alternatively, particles in the Brook et al. (2002)
study were concentrated PM2.5, while the particles in our study
were freshly generated particles from auto/truck emissions with
a predominant size range in the ultrafine and nano fraction. We
have recently measured the rate of particle decay with distance
from a major highway (Rundell et al., 2006). We cannot rule
out the influence of ozone, as ozone exposure has been shown
to increase rate–pressure product and heart rate after inhalation
(Gong et al., 1998). Although it is clear that vasoconstriction
from particle inhalation occurs both in humans and in the animal model, it is not clear whether particles instill sympathetic
nervous system activation, or create an inflammatory response
with oxidative stress that causes an imbalance between vasoconstrictive and vasodilatory mediators. The acute 4% vasoconstriction does not seem large, and would be of little immediate
consequence to healthy individuals; however, those individuals
with cardiac risk factors could be more susceptible to myocardial
ischemia from this vasoreactive response.
Significant correlations have been made between endothelial
function and cardiovascular events, even after adjustment for
other cardiac risk factors (Schachinger & Zeiher, 2000) or in patients with no apparent obstructive coronary disease (Suwa et al.,
2002). Diesel exhaust PMhas been found to inhibit endotheliumdependent vasodilation via inhibition of NO release (Cheng &
Kang, 1999) and is cytotoxic to artery endothelial cells (Bai et al.,
2001). In the present study, the abolishment of a flow-mediated
dilatory response (0.3 ± 2.74%) following 4 min of upper arm
ischemia after high [PM1] exercise provides evidence for endothelial disruption in the conduit arteries from PM1 inhalation.
The 6.6 ± 4.06 and 6.8 ± 3.58% preexposure FMD values and
the postexposure 4.9 ± 4.42% low [PM1] FMD is in agreement
with other FMD measurements determined by upper arm occlusion. Agewall et al. (2001) reported greater dilation from upper
arm occlusion than from lower arm occlusion (6.4% vs. 3.9%);
likewise, Berry et al. (2000) found greater brachial artery dilation after upper arm occlusion than after lower arm occlusion
(9% vs. 5.9%). Incongruent with our results, Brook et al. (2002)
found no change in FMD after inhalation of concentrated ambient PM2.5. The mean percent FMD values reported in that study
were lower (range 3.57% to 4.52%, for control and exposed)
than our basal and low [PM1] exposure FMD values. It was not
reported whether upper or lower arm occlusion was used in the
Brook et al. (2002) study, but if lower arm occlusion was used,
then the basal FMD values would be in accord with our results.
The observation that motorcycle gas engine exhaust particles impaired vasorelaxation induced by acetylcholine (Cheng
& Kang, 1999) supports our results of impaired FMD, as
acetylcholine-induced vasoconstriction correlates highly with
FMD (Anderson et al., 1995; Kang et al., 2002). Nurkiewicz
et al. (2004) found that residual oil fly ash (ROFA) abolished both
NO-dependent and NO-independent systemic arteriolar dilation
in the spinotrapezius muscle of rats. That group showed that approximately 50% of the arteriole vasoresponsiveness was due to
NO-dependent factors. Since we did not evaluate nonendothelial
dilation using sublingual nitroglycerine, we cannot dismiss the
possibility that nonendothelial dilation contributed to our results.
In this study, the 55% reduction in NIRS reoxygenation slope
to baseline after high [PM1] exercise strongly suggests that the
microcirculation is affected by PM1 inhalation. The fact that
only 25% of the NIRS signal variability was accounted for by
brachial artery FMD supports a vasoconstrictive response in
the microcirculation from PM1 exposure. Since near- infrared
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