The pivotal risk of smoking and alcohol in laryngeal cancer has meant that evidence for alternate cofactors has been indicative to date. A number of case series, however, contain a few patients who are life-long nondrinkers and nonsmokers and question what other cofactors may contribute. Gastroesophageal reflux disease makes a small but significant contribution to the causal development of laryngeal cancer; however, what remains to be understood is the mechanism of its action. Bile reflux appears to be an additional causative factor in achlorhydrics. After controlling for the effects of alcohol and tobacco, exposure to oncogenic types of human papilloma virus is associated with an increased risk of laryngeal carcinoma. Evidence does not support asbestos exposure itself as increasing the relative risk of laryngeal cancer. A dietary increase in vegetables and fruit may confer an advantage in reducing the laryngeal cancer incidence. Inherited differences in cell cycle control systems, DNA repair systems, and carcinogen-metabolizing enzymes can increase the risk for laryngeal cancer, but as yet, no causal mechanism has been demonstrated.