The hypothesis that chronic exposure to alcohol over many years could increase the risk of breast cancer in women is mechanistically plausible. Alcohol is metabolized by alcohol dehydrogenase (ADH) into acetaldehyde, a known genotoxin, and carcinogen which could increase breast cancer risk via multiple mechanisms (Seitz and Stickel, 2007). Both the ADHIB and ADH1C genes are expressed in the human breast, encoding alcohol dehydrogenases that are active at ethanol concentration that can be generated in the blood during social drinking. Consistent with these data, direct biochemical studies have shown that normal human breast tissue has the capacity to metabolize ethanol at low concentrations, and ADH immunoreactivity is also detectable in breast epithelial cells (Triano et al., 2003). Also, rodent mammary tissue can metabolize ethanol into acetaldehyde (Castro et al., 2006), providing a potential explanation for animal studies showing that chronic alcohol drinking causes mammary tumors in female mice (Watabiki et al., 2000).
