Alex P Carll

Alex P Carll
University of Louisville | UL · Department of Physiology and Biophysics

Ph.D., M.S.P.H.

About

34
Publications
4,539
Reads
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539
Citations
Introduction
Alex P Carll is an Assistant Professor in the Department of Physiology, at the University of Louisville School of Medicine. Dr. Carll researches the mechanisms of air pollution-induced cardiovascular injury and dysfunction.
Additional affiliations
October 2015 - present
University of Louisville
Position
  • Professor (Assistant)
January 2013 - October 2015
Harvard University
Position
  • PostDoc Position
January 2006 - December 2012
University of North Carolina at Chapel Hill
Position
  • US EPA pre-doctoral fellow
Education
June 2008 - August 2012
University of North Carolina at Chapel Hill
Field of study
  • Environmental Health Sciences, Public Health
January 2006 - May 2008
August 2000 - May 2004
Duke University
Field of study
  • Environmental Science & Policy

Publications

Publications (34)
Article
Full-text available
Background: In mechanically ventilated subjects, intra-tracheal secretions can be aspirated with either open suction systems (OSS) or closed suction systems (CSS). In contrast to CSS, conventional OSS require temporarily disconnecting the patient from the ventilator, which briefly diminishes PEEP and oxygen supply. On the other hand, CSS are more...
Article
Full-text available
Smoking is associated with cardiac arrhythmia, stroke, heart failure, and sudden cardiac arrest, all of which may derive from increased sympathetic influence on cardiac conduction system and altered ventricular repolarization. However, knowledge of the effects of smoking on supraventricular conduction, and the role of the sympathetic nervous system...
Article
Background: E-cigarette (e-cig) use has rapidly increased, especially among youth. Vaping has been linked to adverse cardiopulmonary effects, but the full extent of effects remains unknown. Several constituents in e-cigs may increase cardiac risk partly by disturbing cardiac electrophysiology and the autonomic nervous system. Hypothesis: E-cig aero...
Article
Full-text available
Background: Using engineered nanomaterial-based toners, laser printers generate aerosols with alarming levels of nanoparticles that bear high bioactivity and potential health risks. Yet, the cardiac impacts of printer-emitted particles (PEPs) are unknown. Inhalation of particulate matter (PM) promotes cardiovascular morbidity and mortality, and ul...
Article
Background: Smoking and exposure to environmental tobacco smoke are associated with sympathetic nervous system activation, a leading putative mechanism of adverse cardiovascular events. However, the role of nicotine in cigarette smoke’s sympathomimetic effects remains unknown. Methods: Healthy young smokers were recruited and fasted from food and n...
Article
Although substantial evidence shows that smoking is positively and robustly associated with cardiovascular disease (CVD), the CVD risk associated with the use of new and emerging tobacco products, such as electronic cigarettes, hookah, and heat-not-burn products, remains unclear. This uncertainty stems from lack of knowledge on how the use of these...
Article
Full-text available
Duchenne muscular dystrophy (DMD) is a genetic recessive disorder with progressive muscle weakness. Despite the general muscle wasting, degeneration and necrosis of cardiomyocytes have been the main causes of morbidity and death in individuals with DMD. Cardiac failure is generally preceded by disturbances in heart rate variability (HRV), and non-i...
Chapter
The autonomic nervous system (ANS) is critical for maintaining homeostasis in the cardiovascular system, but dysfunction in its regulatory role promotes cardiovascular morbidity and mortality. This article details the neural, molecular, and physical foundations by which the ANS may confer toxicity to cardiovascular tissue. For context, the basics o...
Article
Full-text available
Background Epidemiological studies have linked exposures to ambient fine particulate matter (PM2.5) and traffic with autonomic nervous system imbalance (ANS) and cardiac pathophysiology, especially in individuals with preexisting disease. It is unclear whether metabolic syndrome (MetS) increases susceptibility to the effects of PM2.5. We hypothesiz...
Article
Full-text available
Acute exposure to ambient fine particulate matter (PM2.5) is tied to cardiovascular morbidity and mortality, especially among those with prior cardiac injury. The mechanisms and pathophysiological events precipitating these outcomes remain poorly understood but may involve inflammation, oxidative stress, arrhythmia and autonomic nervous system imba...
Article
Full-text available
Abstract Context: Air pollution exposure affects autonomic function, heart rate, blood pressure and left ventricular function. While the mechanism for these effects is uncertain, several studies have reported that air pollution exposure modifies activity of the carotid body, the major organ that senses changes in arterial oxygen and carbon dioxide...
Article
Full-text available
Background: Cardiac disease exacerbation is associated with short-term exposure to vehicular emissions. Diesel exhaust (DE) might impair cardiac performance in part through perturbing efferent sympathetic and parasympathetic autonomic nervous system (ANS) input to the heart.Objective: We hypothesized that acute changes in ANS balance mediate decrea...
Article
Full-text available
Exposure to air pollution increases the risk of cardiovascular morbidity and mortality, especially in susceptible populations with cardiovascular disease. Despite increased risk, adverse responses are often delayed and require additional stress tests to reveal latent effects of exposure. The goal of this study was to use an episode of "transient hy...
Article
Full-text available
Acute air pollutant inhalation is linked to adverse cardiac events and death, and hospitalizations for heart failure. Diesel exhaust (DE) is a major air pollutant suspected to exacerbate preexisting cardiac conditions, in part, through autonomic and electrophysiologic disturbance of normal cardiac function. To explore this putative mechanism, we ex...
Article
Full-text available
Epidemiological studies strongly link short-term exposures to vehicular traffic and particulate matter (PM) air pollution with adverse cardiovascular (CV) events, especially in those with preexisting CV disease. Diesel engine exhaust is a key contributor to urban ambient PM and gaseous pollutants. To determine the role of gaseous and particulate co...
Article
Full-text available
Ozone (O₃) is a well-documented respiratory oxidant, but increasing epidemiological evidence points to extrapulmonary effects, including positive associations between ambient O₃ concentrations and cardiovascular morbidity and mortality. With preliminary reports linking O₃ exposure with changes in heart rate (HR), we investigated the hypothesis that...
Article
Full-text available
Diesel exhaust (DE) is a major contributor to traffic-related fine particulate matter (PM)2.5. Although inroads have been made in understanding the mechanisms of PM-related health effects, DE’s complex mixture of PM, gases, and volatile organics makes it difficult to determine how the constituents contribute to DE’s effects. We hypothesized that ex...
Article
Full-text available
Spontaneously hypertensive heart failure rats (SHHFs) take longer to develop compensated heart failure (HF) and congestive decompensation than common surgical models of HF. Isoproterenol (ISO) infusion can accelerate cardiomyopathy in young SHHFs, while dietary salt loading in hypertensive rats induces cardiac fibrosis, hypertrophy, and--in a minor...
Article
Full-text available
Heart failure (HF) is characterized as a limitation to cardiac output that prevents the heart from supplying tissues with adequate oxygen and predisposes individuals to pulmonary edema. Impaired cardiac function is secondary to either decreased contractility reducing ejection (systolic failure), diminished ventricular compliance preventing filling...
Article
Epidemiological studies demonstrate a significant association between arrhythmias and air pollution exposure. Sensitivity to aconitine-induced arrhythmia has been employed to examine the factors that increase the risk of such dysfunction. We used aconitine to test whether a single exposure to diesel exhaust (DE) would increase the risk of arrhythmi...
Article
Full-text available
Ambient particulate matter (PM) exposure is linked to cardiovascular events and death, especially among individuals with heart disease. A model of toxic cardiomyopathy was developed in Spontaneously Hypertensive Heart Failure (SHHF) rats to explore potential mechanisms. Rats were infused with isoproterenol (ISO; 2.5 mg/kg/day subcutaneous [sc]), a...
Article
Full-text available
Recently, investigators demonstrated associations between fine particulate matter (PM)-associated metals and adverse health effects. Residual oil fly ash (ROFA), a waste product of fossil fuel combustion from boilers, is rich in the transition metals Fe, Ni, and V, and when released as a fugitive particle, is an important contributor to ambient fin...
Article
Full-text available
Exposure to combustion-derived fine particulate matter (PM) is associated with increased cardiovascular morbidity and mortality especially in individuals with cardiovascular disease, including hypertension. PM inhalation causes several adverse changes in cardiac function that are reflected in the electrocardiogram (ECG), including altered cardiac r...
Article
This study ascertains the effects of zinc, a major component of particulate matter, on pulmonary and systemic endpoints using hyperlipidemic rabbits to model diet-induced human atherosclerosis. New Zealand White rabbits were fed a normal or cholesterol-enriched diet and then were intratracheally instilled 1x/week for 4 weeks with saline or 16 micro...

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Projects

Projects (3)
Project
Examine in rat models of cardiomyopathy and metabolic syndrome the impact of airborne particulates inhalation on ECG endpoints, including HRV, arrhythmia, and ECG morphology. Test for effects of particulates on blood pressure and baroreflexes. Unveil associations between electrophysiologic and hemodynamic endpoints that suggest autonomic mediation of PM-induced cardiac toxicity.
Archived project
Test role of autonomic nervous system in acute diesel exhaust exposure-induced cardiac performance decline and electrophysiological dysfunction. Incorporate treadmill exercise in young adult heart failure-prone rats after diesel exhaust exposure to unmask latent autonomic imbalance and systolic dysfunction. Examine cardiac performance and autonomic imbalance after acute diesel exhaust exposure in aged heart failure-prone rats.
Project
The EPIMOV Study is a prospective follow-up study started at the end of 2013 in the city of Santos, São Paulo, Brazil. The primary goal of the EPIMOV Study is to assess the longitudinal association between objectively measured sedentary behavior and the occurrence of hypokinetic diseases. We emphasize cardiorespiratory and locomotor health problems, especially pulmonary function decline (COPD), coronary heart disease and myocardial infarction and frailty and falls. We also aim to identify mediators between sedentary behavior and the incident cardiorespiratory diseases and locomotor disturbances, e.g., moderate-to-vigorous physical activity and cardiorespiratory fitness.