Clinical and epidemiological studies have determined that air pollution significantly increases the risk of premature deaths, especially in people with underlying cardiovascular disease.
For healthy individuals inhaling ozone or particle pollution triggers a defensive lung-heart reflex (pulmonary-cardiac reflex) that automatically slows heart rate to accommodate oxygen deficiency and help slow distribution of pollutants throughout the body. However, when patients with cardiovascular disease breathe pollutants that same protective mechanism does not kick in. Instead, their heart rates intermittently speed up, known as tachycardia, and can evoke a potentially deadly irregular heart rhythm, know as premature ventricular contractions.
Researchers at the University of South Florida who study the role of sensory airway nerves in protective behaviors wanted to know, and they have investigated what accounts for the difference. They published their findings in The Journal of Physiology, and these outcomes explain the altered physiological responses to air pollution in patients with pre-existing cardiovascular disease.
The team at USF Health used a rat model for high blood pressure (hypertension), a common chronic cardiovascular condition and discovered that pre-existing hypertension altered normal reflexes in the lungs to affect autonomic regulation of the heart when an irritant mimicking air pollution was inhaled.
Hypertension, especially, appeared to shift the reflex response from the parasympathetic nervous system to the sympathetic nervous system. In the sympathetic nervous system, it mobilizes the body's defensive "fight-or-flight" response to a threat, including releasing adrenaline that increases heart rate. The parasympathetic nervous system, in contrast, controls involuntary responses, including breathing and heart rate, while the body is at rest and maintains a state of calm.
The team used allyl isothiocyanate, the pungent ingredient in wasabi, and horseradish to stimulate effects of air pollution inhaled into the lungs, challenging to recreate in a laboratory setting. When healthy rats with normal blood pressure inhaled this irritant, their heart rates slowed as expected. But in the rats with chronic hypertension, inhaling the same irritant stimulated an increased heart rate accompanied by premature ventricular contractions.
The USF study suggests that chronic hypertension may remodel airway sensory nerves controlling the pulmonary-cardiac reflex that helps defend the body against physical damage from air pollution. According to Dr. Thomas-Taylor, the remodeling may happen in the development stages of hypertension, and it could turn on inappropriate sympathetic nervous system excitation of the heart.
Explaining further, Dr. Thomas-Taylor noted that their goal is to add another piece of information that clinicians could consider when selecting the best treatment for hypertension. In addition to the patient's age, ethnicity, and race, that might include whether the person lives in an area with high pollution levels. In the long-term, if scientists can identify the nervous system mechanisms involved in remodeling the pulmonary-cardiac reflex, they can target those to develop new blood pressure drugs.
