Sensory neurotoxicology: use of the olfactory system in the assessment of toxicity.
Although many compounds are purported to cause olfactory dysfunction, little experimental research has been done in this area. The nasal epithelium, being one of the first "wet tissues" to come into contact with airborne compounds, should be a good indicator of toxic insult. The same general procedures used to measure visual or auditory function can be applied to the olfactory system, although olfactory stimuli are much more difficult to generate and control. Cadmium exposure, which is frequently cited as causing olfactory dysfunction in humans, did not produce anosmia (loss of smell) in rats, even though there was a large increase in cadmium levels in their olfactory bulbs. Rats exposed to methyl bromide showed a severe disruption in olfactory function as well as in morphology and neurochemical indices. However, functional recovery occurred even in the presence of continuing morphological and neurochemical evidence of damage. A nonsensory function of the olfactory system, transneuronal transport via the primary sensory neurons, may represent a mechanism of entry into the central nervous system for compounds that are normally excluded by the blood-brain barrier.
Hastings
L
L
Department of Environmental Health, University of Cincinnati Medical School, OH 45267-0056.
D000281:Administration, Intranasal; D000818:Animals; D002104:Cadmium / Q000633:toxicity; D003216:Conditioning, Operant / Q000187:drug effects; D004193:Discrimination Learning / Q000187:drug effects; D006842:Hydrocarbons, Brominated / Q000633:toxicity; D009420:Nervous System / Q000187:drug effects*; D009830:Olfactory Bulb / Q000187:drug effects; D051381:Rats; D012903:Smell / Q000187:drug effects*; D014116:Toxicology / Q000379:methods*
D006842:Hydrocarbons, Brominated; D002104:Cadmium; C005218:methyl bromide