POLLUTIE: wat ademen we in? - BVPV-SBIP

POLLUTIE: wat ademen
we in?
Prof. Dr. W. De Backer
UZA/UA
Klinische betekenis blootstelling
aan polluenten
1
Astma kinderen voor en na
blootstelling polluenten
Renzetti G. et al. Pediatrics 2009;123:1051-1058
2
Astma kinderen voor en na
blootstelling polluenten
Renzetti G. et al. Pediatrics 2009;123:1051-1058
3
Astma kinderen voor en na
blootstelling polluenten
Renzetti G. et al. Pediatrics 2009;123:1051-1058
4
Astma kinderen voor en na
blootstelling polluenten
Renzetti G. et al. Pediatrics 2009;123:1051-1058
5
Astma kinderen voor en na
blootstelling polluenten
Renzetti G. et al. Pediatrics 2009;123:1051-1058
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Verband tussen polluenten en
luchtweg inflammatie
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Studies in celculturen (1)
Bayram H. Et al. AJRCMB 1998;18:441-448
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Studies in celculturen (2)
Bayram H. Et al. AJRCMB 1998;18:441-44!
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Studies in celculturen (3)
Bayram H. Et al. AJRCMB 1998;18:441-44!
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Verband verkeer en blootstelling
Roselund M. et al. Thorax 2009;64:573-580
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Verband verkeer en blootstelling (2)
Roselund M. et al. Thorax 2009;64:573-580
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Afstand tot bron (weg)
Bayer-Oglesby Am J Epidemiol 2006;1190-119
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1=0-23m
2=24-58m
3=59-117m
4=>118m-2684
Bayer-Oglesby Am J Epidemiol 2006;1190-1198
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Impact infrastructuur op
blootstelling polluenten
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DISPERSIEMODELLEN
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20
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Integrale benadering als oplossing
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Dispersie via CFD toegepast op
dispersie van polluenten in steden
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IN-PATIENT MODELING
Particulate deposition in the different airway regions
De Backer et al. Radiology 257 (2010) 854–862
Vinchurkar et al. Inhalation Toxicology 2011
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Particle deposition in asthmatics
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Case studies (1)
Craeybeckxtunnel
• Metingen in Craeybeckxtunnel in Antwerpen
van 23 Juni 2010 tot 7 Juli 2010
• Consortium met VITO, Von Karmann, KUL, UA
• Metingen PM en UFP in aantal & samenstelling
• Metingen luchtstroom
• Metingen depositie in proefdieren (muizen)
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1,60E+06
Drive through 1 (05/07/10)
1,40E+06
1,20E+06
12:49:38
dN/dlogDp
1,00E+06
12:49:48
12:49:58
12:50:08
8,00E+05
12:50:18
12:50:28
12:50:38
6,00E+05
12:50:48
12:50:58
12:51:08
4,00E+05
2,00E+05
0,00E+00
1
10
Size
100
1000
Figure 5:
Sizecar
distribution
during
(right)
size distribution
6: (left)
(left)VKI
standing measured
behind VITO
car;mobile
(right)measurements;
sonic anemometer
mounted
on VKI carmeasured
showing increasing particle number concentration in the mode around 60 nm
performed in the middle of the tunnel whereas mice were exposed at the end of the tunnel. However,
UFP measurements and animal exposure were performed simultaneously. Moreover, measurements in
the cage were performed during a short time (hours) using handheld CPCs (Condensation Particle
Counter) measuring number concentrations in the size range 20 nm – 1000 nm. The results showed no
significant difference in concentrations in the cage ((129 ± 16) 103 cm-3) as compared to the tunnel
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environment ((150 ± 25) 103 cm-3). Also in the cages with filter, similar concentrations were found
through the tunnel in both directions at about 100 km/hr. The purpose was to check whether the air
velocity on the middle lanes is different from the value on the emergency lane. Figure 8 shows the air
velocity measured, as starting at the Carpool Kontich, then in the tunnel section from Brussels to
Antwerp, turning 180° at the first traffic light and subsequently taking the tunnel section towards
Brussels. The air velocity in the tunnel equals the car speed minus the measured value by the sonic
anemometer on top of the moving car. The air velocity appeared to be 15-35% of the car velocity on
the middle lane, thus only slightly higher than on the emergency lane, underlining the piston concept.
It is interesting to note that before the tunnel section from Brussels to Antwerp, while driving closely
behind trucks, the air velocity in the truck’s slip stream (red curve) is similar to the air velocity in
tunnel.
Figure 8: Air velocity measurement on top of VKI car, driving at 100 km/hr through the Craeybeckx
tunnel.
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Dispersion Models
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Ultra Fine Particles
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Figure 10: Alveolar macrophages obtained by bronchoalveolar lavage from mice that remained for 5 days in the
tunnel in a cage without filter cap (LEFT panels, test group) or with “ reinforced” (2x3 layers) filter cap (RIGHT panels, control group). The macrophages from the test group contain abundant black PM, that is not
seen in the macrophages from the control group
However, no adverse effects could be detected in the most exposed group: body weights increased in a
similar way in all groups and there were no signs of pulmonary inflammation in the group exposed to
tunnel air compared to the control groups (Figure 11). Surprisingly, the group that stayed in the tunnel
in a cage with reinforced filter exhibited fewer leukocytes (mainly lymphocytes) in blood than all the
other groups. The reasons for this finding remain to be clarified.
CONTROL GROUP
empty cage
TEST GROUP
empty cage
Figure 11: (left) Comparison of the body weight before and after the exposure time in different experimental
groups; (right) the view of the experimental design in the tunnel with the zoom on the animal test cages
This pilot study has demonstrated that it is feasible to expose mice to a tunnel environment for several
days and that these animals clearly get exposed to PM. However, this pilot experiment also indicates
that the duration of exposure needs probably to be longer before significant adverse effects
(pulmonary inflammation) manifest themselves. We propose to establish dose-response relationships
by appropriate combinations of duration and intensity of exposure. This should allow us to determine
threshold doses of PM (“points of departure”) at which inflammatory changes become detectable in
experimental animals.
The further histological evaluation of the lungs tissues was performed without knowledge of the group
from which the tissues were sampled. General appearance of the lung tissue was evaluated. In
addition, the lung tissues were checked for infiltration by alveolar macrophages and other
inflammatory cells (e.g. neutrophils) and for signs of edema (i.e. increase of interstitial tissue). The
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Figure 10: Alveolar macrophages obtained by bronchoalveolar lavage from mice that remained for 5 days in the
tunnel in a cage without filter cap (LEFT panels, test group) or with “ reinforced” (2x3 layers) filter cap (RIGHT panels, control group). The macrophages from the test group contain abundant black PM, that is not
seen in the macrophages from the control group
However, no adverse effects could be detected in the most exposed group: body weights increased in a
similar way in all groups and there were no signs of pulmonary inflammation in the group exposed to
tunnel air compared to the control groups (Figure 11). Surprisingly, the group that stayed in the tunnel
in a cage with reinforced filter exhibited fewer leukocytes (mainly lymphocytes) in blood than all the
other groups. The reasons for this finding remain to be clarified.
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Figure 13: (A) - Section through a capillary and type 2 alveolar cell; (B) - Detail of the multilamellar body from
the type II cell depicted in A. This structure contains several particles; (C) - STEM-EDX spectrum of the region
shown in B; (D) - Capillary with red blood cells and a leukocyte.
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Toegenomen gen expressie voor
inflammatoire mediatoren
in de hippocampus
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Case studie (2)
Stedelijke lokatie met intens
verkeer versus lokatie met weinig
verkeer
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AIR QUALITY SURVEY
Quantitative analysis of
PM mass and composition
Qualitative analysis of
individual particle composition
Collection on filter: PM1, PM2.5
Collection in six size fractions
Chemical characterization
Chemical characterization
Gravimetry
XRF
Aethalometry
IC
Mass
Elements
BC
Salts
SEM-EDX
Elemental composition
µ-Raman
Molecular structure
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hey are not
missions on
cles were
total size
ticle group
rbonaceous
micrometer
deposition
er than the
oofed these
all airway
ng segment
(Table 1).
articles was
s (Pearson
O2 and SO2
p < 0.05).
uthwesterly
or the quick
ys with low
particulate
definitely affect its deposition efficiency in human airways.
Simulated median particle deposition rates in the lung
segment of CRP are shown in Table 2, asif they were breathing
Table 2. Particle Deposition Rates in the Lungs of Chronic
Respiratory Patients by Date
median (range), μg · h−1
particle typea
date
heavy traffic
moderate traffic
pb
all
15/ 7
25/ 7
15/ 7
25/ 7
15/ 7
25/ 7
9.5 (3.1− 13)
5.8 (2.0− 8.4)
5.5 (1.8− 8.0)
4.0 (1.4− 5.9)
2.6 (0.88−3.8)
0.79 (0.26−1.1)
9.0 (3.1− 13)
5.0 (1.8− 7.5)
5.8 (2.2− 9.1)
3.5 (1.4− 5.9)
1.5 (0.51− 2.2)
0.30 (0.09− 0.42)
0.753
0.917
0.753
0.917
0.028
0.028
toxic
anthropogenic
a
All: Carbonaceous, iron-rich, minerals, ammonium salts and sea salts;
Toxic: Carbonaceous, iron-rich and minerals; Anthropogenic:
Carbonaceous and iron-rich (refer to text). bSignificance (bold: p <
0.05) of a Wilcoxon signed rank test; H0: no median difference (n =
6).
the air at the heavy and moderate traffic sites during two daysof
the air quality survey. Differences in the particle doses received
at the moderate and heavy traffic site did not manifest through
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Lung deposition (µg/h)
15th July
2011
25th July
2011
Regat
ta
City
Regat
ta
Wilrij
k
Patient Severe
1
asthma
7.54
7.11
4.61
4.01
Patient Asthma
2
child
9.94
9.57
6.12
5.42
13.03
12.95
8.16
7.38
Patient Asthma
4
child
9.00
8.44
5.50
4.68
Patient Severe
5
COPD
3.13
3.15
1.98
1.78
13.24
13.37
8.42
7.49
Patient Mild asthma
3
Patient COPD
6
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Besluit
• Invloed polluenten op volksgezondheid
bewezen (vb astma)
• Polluenten zijn vaak afkomstig van
verkeersemissies
• Metingen van de polluenten in de omgeving
volstaat niet om impact op de luchtwegen te
kennen
• Hiervoor is een integrale benadering nodig
• Cases die deze integrale benadering gebruiken
tonen verrassend veel blootstelling in
bepaalde omstandigheden
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