My research laboratory for many years addressed the metabolic mechanisms through which the heart and the larger blood vessels, including the large elastic arteries such as the aorta, are injured by toxic chemicals in our environment. This work was funded for many years by the NIH RO1 mechanism, and by other funding mechanisms, including industrial sources such as the DOW and BASF chemical companies. The area of greatest concentration for this work was the muscular wall of blood vessels, or the "media." Experimental drugs and other chemicals that protect against injury - or predispose to injury – were defined in the hope that we may be able to manipulate the blood vessel wall to delay the commonest degenerative diseases, with the greatest human morbidity and mortality, including atherosclerosis and aneurysm. These studies were highly relevant in defining cellular and biochemical events that occur during vascular injury by toxic chemicals including cigarette smoke. The metabolism of vasculotoxic amines to aldehydes was explored, as well as how antioxidants and specific vascular glutathione-S-transferases act in the defense of vascular wall against reactive molecules. A small animal model of dissecting aortic aneurysm was discovered, and still serves researchers today.
As an adjunct professor I continue collaborative research efforts with scientists in our department into the adverse effects of chemicals on the liver and pancreas. I also have part time clinical and anatomic pathology duties as a cardiovascular consultant. This work continues to contribute to our understanding of heart and blood vessel pathology, as reflected in my list of recent publications.