CLINICAL INNOVATORS
Interview by
KATLYN NEMANI, MD
Uncovering the Effects of the
Environment on CV Health:
An Interview with Robert D.
Brook, MD
the help of colleagues at the University of Toronto to
investigate if brief exposure to concentrated ambient
PM2.5 impairs blood vessel function in a randomized double-blind filtered air controlled experiment.
We demonstrate that PM2.5 prompts acute arterial
vasoconstriction and raises blood pressure along
with heart rate within minutes-to-hours. I have been
investigating the mechanistic pathways (in addition
to other ill effects of PM2.5) ever since.
R
obert D. Brook is a Professor of Internal
Medicine at the University of Michigan.
Dr. Brook played a key role in helping to
create an independent research field examining the
biological actions of environmental pollutants—including air pollution—on the cardiovascular system,
termed “environmental cardiology.” He has served
as the chairperson for two American Heart Association (AHA) scientific statements on the cardiovascular effects of air pollution as well as on a third
AHA consensus statement regarding alternative
approaches for hypertension. He is currently the
director of the American Society of Hypertension
Comprehensive Hypertension Center and the Vascular Clinical Research Laboratory at the University
of Michigan. Dr. Brook completed his internal
medicine residency at Northwestern University and
a fellowship in Hypertension and Vascular Medicine
at the University of Michigan.
62 CardioSource WorldNews
How did you become interested in the effects of
the environment on cardiovascular health?
That is the fault of my oldest brother, Jeff Brook,
who is an atmospheric scientist working with Environment Canada. In the mid-1990s, he had a discussion with me while I was a fellow regarding some
interesting new epidemiological findings showing a
relationship between air pollution and cardiovascular
events. Until about that time, most researchers and
health care providers believed that the main pathway
whereby air pollutants have an adverse effect on human health was by worsening pulmonary diseases.
While it is true that air pollution, like fine particulate
matter (PM2.5), promotes asthma and COPD exacerbations, we now know that the largest portion of the
morbidity and mortality induced by exposure is actually the instigation of cardiovascular events – myocardial infarctions, strokes, heart failure, and sudden
death. We launched a pilot study at that time with
What exactly is fine particulate matter, and how
is it measured?
PM2.5 is an amalgam of solid and liquid particles
derived mostly from fossil fuel (coal, oil, diesel, gas)
combustion. These “fine” particles are less than 2.5
micrometers in diameter (1/20-1/30 the width of a
human hair). Primary soot particles from incomplete
combustion aggregate from a few nanometers up to
2.5 micrometers in diameter. Other chemicals including metals such as iron, nickel, and zinc attach to the
particles. Secondary species form from gases onto
the particle including sulfates and nitrates. Finally,
hundreds of various organic chemicals (hydrocarbons) accumulate in the particles as well. While
the chemistry is complicated and depends upon
many factors like sources and atmospheric conditions, PM2.5 is typically measured as the mass per
unit volume (micrograms/cubic meter). In the U.S.,
average levels range from 5 to 30 µg/m3; whereas in
developing nations (India, China), concentrations can
range from 50 to 500 µg/m3. PM2.5 ranks among
the top 10 leading risk factors for premature morbidity and mortality worldwide. It has been shown to
trigger numerous cardiovascular events (myocardial
infarctions, strokes, heart failure).
What is the mechanism by which PM2.5 affects
cardiovascular health?
The main mechanistic pathways whereby PM2.5
causes cardiovascular events have been studied in
nume &