As mentioned on the Home Page, the Wold lab is interested in understanding the role of external triggers on cardiac disease, with emphasis on particulate matter less than 2.5µm in diameter (PM2.5). We are currently investigating several research projects based on this central theme:

Defining the Impact of E-Cigarettes on Cardiac Pathophysiology (NIH #5R01HL139348):

Within the last decade, the popularity of electronic cigarettes has increased as an artificial means of smoking nicotine, especially among young people. These e-cigarettes are a source of potentially toxic gases, fine particulates, and nicotine that could be linked with adverse cardiovascular (CV) outcomes, but it remains unknown if their usage increases inflammation and fibrosis long-term. Damage to the heart and vasculature could be at risk on a structural and functional level. Critical questions exploring these unknowns will be tested using data samples collected from mice and, for the first time, primary human myocytes, which are cells found in muscle tissue. We hypothesize that EC aerosol promotes both acute and chronic damage to multiple cardiac cell populations resulting in severe organ and organism dysfunction. The goals of this investigation are to define the impact of EC aerosol (in clinically-relevant concentrations) on animals and well-phenotyped human cardiac myocytes.


Mechanisms of Exposure-Induced Tissue Functional and Pathological Changes In A Mouse Model of Alzheimer’s Disease (NIH #5R01AG057046):

A post-mortem study reported evidence of accumulation of amyloid, a stark-like protein, among people living in cities with high levels of ambient pollution, which has been associated with both cognitive impairment and cardiac dysfunction. To further expand this study, we’ve proposed a 3 month controlled exposure experiment in Alzheimer’s Disease prone mice carrying a single or double mutation within their genes. Through this experiment, we hope to provide evidence that supports that Alzheimer’s prone mice exposed to high levels of air pollution will develop a greater quantity of aggregates in the specific regions of the brain and heart as functionality worsens. We also expect to see a worsen calcium balance in primary neurons and contractile function and calcium handling in isolated cardiac muscle cells.


Roles for World Trade Center Dust and DEP Co-Pollutant in First Responder Cardiovascular Ailments in Collaboration with Dr. Mitchell Cohen (NIH #5R01OH010921):

Cardiovascular (CV) diseases have increased among the first responders (FR) who were present at Ground Zero after the initial seventy-two (72) hours of which the World Trade Center (WTC) collapsed. Our previous analysis showed that rats exposed to relatively similar levels of the alkaline WTD dust led to persistent reductions in cell numbers that lined their airways. Accordingly, we hypothesize that entrained WTC dust may have acted as direct inducers of CV damage and/or caused enhanced diesel exhaust particles-induced CV injuries upon FR as a result of heavy breathing in an overwhelmingly stressful situation. This innovative study will clarify what role these co-pollutants may have had in changes seen in the CV health and ultimately help identify signs of CV problems before they become harmful.


Effect of Resident Microbes in the Development and Progression of PM2.5-Induced Cardiovascular Dysfunction:

Resident bacteria have been linked to the development and progression of numerous diseases, including cardiovascular disease and Alzheimer’s Disease. Our lab will be working to determine if PM2.5-induced changes to resident oral and gastrointestinal bacteria contribute to the development and progression of cardiovascular dysfunction and neurological dysfunction associated with Alzheimer’s Disease.


Can Probiotic Intervention Delay or Prevent Air Pollution-Enhanced Alzheimer’s Disease Development/Progression?

This week kicked off the beginning of a new project within our lab headed by junior faculty Amy Mackos. This study is part of a larger project working to decipher the involvement of resident bacteria on the development and progression of particulate matter (PM2.5) enhanced cardiovascular dysfunction and neurological dysfunction associated with Alzheimer’s disease. Resident bacteria live in a specific part of the human body and have been linked to the development and progression of numerous diseases, including cardiovascular disease and Alzheimer’s disease. We are currently focused on gut microbes, but in the future, we may also study oral and lung microbes.

In this current study, we are supplementing the mice with the probiotic bacteria Lactobacillus reuteri. Probiotic microbes are considered beneficial for health and are the “good” bacteria, but selecting the correct probiotic bacteria is crucial. According to, “Different types of probiotics may have different effects. For example, if a specific kind of Lactobacillus helps prevent an illness, that doesn’t necessarily mean that another kind of Lactobacillus probiotics would do the same thing.” It takes a deep understanding of microorganisms and diligent experience to select the proper probiotic bacteria for an experiment such as this one. 

Amy, being a brilliant professional, is optimistic about her experiment, and building upon her past discoveries. “I have worked with L. reuteri previously and it was able to reduced stressor-enhanced infectious colitis by reducing immune recruitment and inflammation in the colon.” She hypothesizes that PM2.5 leads to dysbiosis (microbial imbalance) in the gut and that this dysbiosis may lead to systemic changes with regard to immunity and inflammation which can contribute to the development and progression of Alzheimer’s disease.