Acetaldehyde contributes to pathologies ranging from cancer to asthma. It affects the whole body, the architecture of the cell and molecular control mechanisms. The origins of acetaldehyde vary from bacteria in the oral cavity and intestinal tract to atmospheric acetaldehyde as an environmental pollutant. Significant amounts of acetaldehyde are also derived from cigarette smoke and alcohol, both of which are major contributors to disease globally. Acetaldehyde has deleterious effects in the liver, brain and skeletal muscle. It has also been shown that bacteria can generate significant amounts of acetaldehyde in the gastrointestinal tract, thus contributing to carcinogenesis in this tissue. Many of the toxic effects of ethanol ingestion are mediated through acetaldehyde and there is increasing awareness that acetaldehyde is a principal disease-forming agent in tobacco-related illnesses. Alcohol is metabolized by conversion to acetaldehyde, which in turn is converted to acetate by aldehyde dehydrogenase (ALDH). There are a number of forms of ALDH of which the mitochondrial isoform (ALDH2) is particularly important. The ALDH2 gene has a functional polymorphism: homozygous subjects have little or no ALDH2 activity compared to their wild-type counterparts. Heterozygotes generally also have low ALDH2 activity. Epidemiological studies have found increased risk of certain diseases, including cancer of the gastrointestinal tract, alcoholic liver disease and late-onset Alzheimer's disease in subjects with ALDH2 deficiency. This book features contributions from researchers working on all aspects of acetaldehyde-related pathology. From their expert accounts and the lively discussions accompanying each chapter, we can derive a better understanding of the pathogenesis of diseases in which acetaldehyde, from whichever source, is implicated.