Uncovering the Effects of the Environment on CV Health: An Interview with Robert D. Brook, MD
Clinical Innovators | Interview by Katlyn Nemani, MD
Robert 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.
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 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.
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 numerous human and animal experiments. Inhalation of PM2.5 acutely instigates autonomic nervous system imbalance favoring sympathetic activity. This occurs by particles interacting with a wide array of receptors throughout the pulmonary tree. Heightened sympathetic tone can raise blood pressure, cause vasoconstriction, increase heart rate and myocardial demand, and increase arrhythmia potential. A second pathway is via the generation of systemic inflammation. Lung and immune cells interacting with inhaled PM2.5 and/or the associated chemicals triggers a localized inflammatory response such as the release of cytokines and reactive oxygen species. Many studies have shown that this response can “spill-over” into the systemic circulation and thereafter adversely impact cardiovascular tissues, for example by promoting endothelial dysfunction and the potentiation of atherosclerosis or plaque instability. Other experiments have shown that coagulation and thrombosis potential are enhanced following PM2.5 exposures. Finally, the very smallest nanometer-sized particles or chemicals may even be directly transmitted into the systemic circulation and thereby have a direct negative impact on cardiovascular tissues.
Is the effect of fine particulate matter on cardiovascular disease preventable?
Yes. The decreases in PM2.5 levels in the U.S. due to air quality regulations from 1980 have been associated with reductions in cardio-pulmonary morbidity and mortality. Other studies have shown that some personal-level actions such as wearing facemasks and indoor air filters in highly polluted regions can reduce exposures and prevent adverse cardiovascular responses. More local or city-wide ordinances to reduce emissions have also been linked to improved public health. A very high profile regulatory action taken before the Beijing Olympics resulted in reductions in various air pollutants and improvement in several biomarkers of cardiovascular health in several studies.
It’s fascinating that air quality regulations have such potential to effect cardiovascular health. You seem to be interested in many less conventional problems and solutions to addressing cardiovascular disease. In your recently published study in the American Journal of Medicine (“When and How to Recommend ‘Alternative Approaches’ in the Management of High Blood Pressure”) you offer some advice on providing alternative ways of managing hypertension. What are some examples of these approaches and what is the evidence supporting them?
One of the most common questions I am asked by patients is how can I control my high blood pressure without (or with the least possible number of) medications. I was the chairperson for an AHA scientific statement that examined the level of evidence regarding various alternative approaches to treat hypertension that are beyond the usual dietary (low sodium) and drug therapies. We found evidence to support several techniques. The most notable examples that I recommend to my patients are Transcendental Meditation, device-guided slow breathing, aerobic exercise (e.g., running), and isometric exercise (sustained handgrip for 2 minutes). The latter approach was somewhat surprising as isometrics are often associated with an increase in blood pressure during the exercise. While that is true, there is a sustained reduction in high blood pressure with 8-12 weeks of treatment. Most of the techniques produced on-average only a modest reduction in blood pressure (3-6 mm Hg). However, this can be helpful to patients who have borderline blood pressure values or mild hypertension. It may also help individuals to lower the dosages or number of pills required to control hypertension.
You have also discussed offering “medical nutrition therapy” to patients. What is it and what can it be used to treat?
This generally refers to dietary approaches to help control cardiovascular risk factors, including the Dietary Approaches to Stop Hypertension (DASH) diet and appropriate nutrition-recommended diets aiming to improve high cholesterol, triglycerides, or blood sugar. We work closely with expert registered dieticians in our prevention and hypertension clinic in order to help patients maximize their capacity to take control of their risk factors.
You have been on the forefront of a progressive approach to treating patients and understanding poorly understood environmental risk factors. What does the future of the field of environmental cardiology look like?
My belief is that the field is expanding from focusing on the short-term (days to months) adverse impacts of exposures to environmental pollutants (i.e., acting as an acute trigger for a heart attack or stroke), into looking at the long-term health effects. For example, we and others are showing more evidence that chronic exposures to air pollutants can promote the development of obesity, hypertension, diabetes, and atherosclerosis over several years. I also feel that more studies are being done, and rightly so, in the developing world (India and China) where air pollution levels are extremely high (10-50 fold higher than in North America) to assess the health impacts. Finally, more attention should be paid to effective measures that individual people and local governments can do in order to reduce exposures to pollutants and other environmental harmful factors (e.g., excessive noise, contaminated water).
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