Aldehydes are ubiquitous carbonyl-containing compounds and toxic levels are reached in the environment as a primary result of anthropogenic input. Combustion of organic substrates generates high levels of a number of diverse aldehydes, in part, as a function of combustion temperature or pyrolysis. Burning of fuels (e.g., coal diesel, and gasoline) generates reactive aldehydes in the environment, and likewise, aldehydes are made during cooking especially in the presence of overheated cooking oils. Human exposure to environmental aldehydes encompasses air, water and food sources. Many studies show that the cardiovascular system is exquisitely sensitive to aldehyde exposure, especially exposure to α-βunsaturated aldehydes, such as acrolein and 4-hydroxy-trans-2-nonenal (HNE). Interestingly, these aldehydes also are generated endogenously during lipid peroxidation and inflammation, and are associated with pathogenesis in chronic diseases (e.g., atherosclerosis, Alzheimer's disease). Fortunately not all environmental aldehydes appear to be toxic in the cardiovascular system and several could be beneficial, such as aromatic aldehydes ppresent in foods and flavorings including benzaldehyde (oil of almond) and cinnamaldehyde (cinnamon). These food-derived aldehydes have low toxicity in cardiovascular tissues, directly stimulate blood vessel relaxation, and are anti-inflammatory, which perhaps promotes decreased cardiovascular disease risk. While many of the mechanisms by which aldehydes exert effects in cardiovascular tissues remain unknown, studies indicate unsaturated aldehydes have proclivity to form protein-acrolein adducts via cysteine and lysine residues. Could this mechanism (e.g., protein-aldehyde adducts→ER stress→unfolded protein response) account for the association between environmental aldehyde exposure and increased cardiovascular disease risk? Alternatively, unsaturated aldehydes can stimulate the transient receptor potential channel (e.g., TRPA1) leading to increased cellular calcium. Collectively, the cardiovascular system possesses a large cadre of enzymes designed to metabolize and detoxify aldehydes for rapid clearance. Alterations in the level or efficiency of metabolite removal (e.g., GST gene polymorphisms) similarly provide a mechanistic explanation for altered individual susceptibility to aldehyde exposure. Future studies will endeavor to explore the role of aldehyde action and metabolism in human cardiovascular health.