The main route of contamination of the human body with airborne pollutants is through the upper air and food passages. Because of the delicate balance of the mucous membranes and special sensory organs of these passages with respect to mucociliary activity, local and recruited immune responses, rapid uptake of chemicals, and carcinogenic potential, the ingestion or inhalation of pollutants in the air can be harmful to these internal body barriers. The particular target organs for air pollution effects on the upper aerodigestive tract include the mucosa, olfactory epithelium, auditory receptor cells, glottic epithelium, and adjacent neural and muscular tissues. Hearing loss caused by noise exposure may be aggravated by the concomitant inhalation of solvents. The strongest evidence for the carcinogenic effect of occupational inhalants in the nasal cavity and paranasal sinuses is seen with exposure to hardwood dust, tobacco smoke, furniture making, and leather tanning. With the exception of tobacco smoke, which produces squamous cell carcinomas, the majority of the occupationally related cancers are adenocarcinomas, usually of the intestinal variety. Tobacco smoke, passive or active, may lead to end-artery obliteration at the level of the otic end organ, causing a progressive sensorineural hearing loss. Further environmental research in the upper aerodigestive tract should aim at developing biologic markers to determine early, premalignant tissue changes; identifying the effects of chronic, low-dose toxic exposure on mucous membranes and neurosensory organs; providing field-tested tools for the standardized screening of large at-risk populations.