Update on Airborne Pollution

and

Blood Pressure

Philippe van de Borne

Hôpital Erasme

Department of cardiology

Brussels - Belgium

10h30-11h00 Friday 4th March 2016

http://urgencesgrece.eu/fr

http://urgencesgrece.eu/fr

Health effects of pollution" by Mikael Häggström

Health effects of pollution" by Mikael Häggström

BMC Public Health 2014, 14:1137

Responses of aortas isolated from normotensive Wistarrats exposed in vitro to Diesel exhaust particles (DEP)

(DEP suspension and aqueous DEP extract).

In vivo experiments were performed on Wistar rats and spontaneously hypertensive rats (SHRs) exposed for 4

weeks via intratracheal instillation to either DEP or saline vehicle.

(1)

Diesel exhaust particles(DEP)

Acetylcholine(ACh)

(2)

In vitro:

Superoxide dismutase (SOD), a potent and specific inhibitor of superoxide anion, completely

abolished the vascular toxicity of DEP

In vivo:

.

L-NAME iontophoresis: a tool to assess NO-mediated

vasoreactivity duringthermal hyperemic

vasodilation in humans.

Dreyfuss C, Wauters A, Adamopoulos D, Pochet S,

Azarkan M, Berkenboom G, van de Borne P, Argacha JF.

J Cardiovasc Pharmacol. 2013 May;61(5):361-8.

HEATING

AMBIENT AIR

LNAME

SALINE

PanelA/C: Effect on skin local

vasodilation upon heating of

L-NAME (dotted line) compared

saline solution (continuous line)

iontophoresis (n=12) after

ambient (Panel A) and polluted

air exposure (Panel C).

Panel B/D: Late phase AUC’s

of heating-induced skin

vasodilation after L-NAME

(dotted line) compared saline

solution (continuous line)

iontophoresis (n=12)

in ambient

(Panel B) and polluted air

sessions (Panel D).

Acute exposure to diesel exhaust impairs nitric oxide-mediated endothelial vasomotor function by increasing

endothelial oxidative stress.

AMBIENT AIR

POLLUTED AIR

Wauters A, Dreyfuss C, Pochet S, Hendrick P,

Berkenboom G, van de Borne P, Argacha JF.

Hypertension. 2013 Aug;62(2):352-8

LNAME

SALINE

Panel A: Superoxide anion

production by HUVEC incubated

with sera from subjects exposed

to ambient air at rest, polluted

air at rest and polluted air during

exercise.

Panel B: Correlation analysis

between superoxide anion

production by HUVEC incubated

with sera from subjects exposed

to ambient air at rest, polluted

air at rest and polluted air during

exercise and total PM2.5 inhaled

during exercise.Hypertension. 2013 Aug;62(2):352-8.

Wauters A, Dreyfuss C, Pochet S, Hendrick P, Berkenboom G,

van de Borne P, Argacha JF.

(A) Long-term particulate matter <2.5 μm in aerodynamic diameter (PM2.5) concentrations estimated for the year 2000 annual average.

(B) Short-term PM 2.5 concentrations for 2 days before the brachial examination.

For every 3μg/m3 increase in annual average of PM2.5, FMD decreased by 0.3% (p = 0.03) adjusting for demographic characteristics, traditional

risk factors, sonographers, and 1/baseline arterial diameter.

Long-term PM 2.5 concentrations were estimated for the year 2000 at each participant’s residence (n = 3,040).

Women, nonsmokers, younger participants, and those with hypertension

seemed to show a greater association of PM2.5 with FMD.

FMD was not significantly associated with short-term variation in PM2.5

on the day before examination.

Exposition to lower temperatures

and, in man, to PM10 pollution:

Early pulse wave reflection and

increased central pulse pressure

1222 consecutive

patients,

Athens

Odds ratios (and 95% CIs) associated with a 10-µg/m3 increase in PM2.5 for ACS events for persons with coronary

artery disease compared across various models.

Filled squares: all ACS events, Filled circles represent STEMI events, Open circles represent non-STEMI events,

Open triangles represent unstable angina events, Filled diamonds represent non–ST-segment elevation ACS events.

A: Mean change in systolic blood pressure (SBP) from baseline. Mean difference between SBP at each time point and SBPpre-exposure for diesel exhaust (DE●) and filtered air (FA ).

B: Mean diesel exhaust effect on SBP.

The shaded area is the exposure

period.

45 nonsmoking subjects, 18 to 49 years of age in double-blinded, crossover exposure studies, randomized to order.

Each subject was exposed to diesel exhaust, maintained at 200 µg/m3 of fine particulate matter, and filtered air for 120 minutes on days separated by 2 weeks.

There was no significant effect on heart rate or diastolic pressure.

Children 6–12 years of age were recruited

at two primary schools in Antwerp, Belgium;

The first sampling period fell within the spring

season 2011, whereas the second period fell

within fall 2011.

After the children had rested for 5 min

in a sitting position, a study nurse measured

blood pressure by making five to seven

consecutive readings using an

automated blood pressure instrument

(Stabil-O-Graph, Stolberg, Germany)

with a pediatric cuff.

The first blood pressure measurement

was excluded. The mean of the remaining

blood pressure measurements

was used for analysis.

UFP fraction size: 20–30 nm