Individuals involved in rescue, recovery, demolition, and clean-up after the World Trade Center (WTC) disaster on September 11, 2001, were exposed to a complex mixture of airborne smoke, dust, combustion gases, acid mists, and metal fumes. The impact of this exposure on responders' upper and lower respiratory function has been well documented, but little is known about its impact on their sensitivity to odor and irritants. Researchers supported by NIDCD and the Monell Chemical Senses Center studied 102 individuals who worked or volunteered at the WTC site by administering a battery of tests to measure sensitivity to odors, which are perceived by the olfactory receptors high in the nasal cavity. They also measured irritants, which are perceived by the trigeminal nerve, a nerve in the head that senses touch, temperature, and pain. The researchers found that, even two years after exposure, the loss of olfactory and trigeminal sensitivity was significantly greater in the exposed group in comparison to individuals who weren't exposed. Thirty to 40 percent of the WTC group was significantly impaired in their ability to detect odors, while 75 percent were either partially or completely impaired in their ability to sense irritants. The most profound loss of sensitivity was found in people caught in the dust cloud after the buildings collapsed. The nose's ability to sense potentially harmful irritants in the air is part of an early warning system that protects the respiratory tract from toxic exposure.
The poster "Chemosensory Loss: Functional Consequences of the World Trade Center Disaster" (#249) takes place Saturday, April 24, 8:00 a.m. 12:00 p.m. ET in the Pavilion.
"Smounds" Delicious! Smell and Sound Converge in a Little-Known Part of the Brain
Recent NIDCD-sponsored research shows that cells in a part of the brain called the olfactory tubercle not only discriminate odors -- they also respond to sound. Scientists found that 65 percent of tubercle cells were activated by at least one of five odors. In the same area, about 20 percent of cells were activated by an audio tone. Further, 29 percent of the cells had either an enhanced or suppressed response to different mixes of odors and tones, depending on whether or not the tone was present with the odor. This discovery may provide the first neural evidence for a sensory crossover in the brain where smell and sound converge. It could also help explain clinical reports of sound-smell synesthesia (in which someone "smells" sounds), as well as the ability to relate auditory pitch with specific odors. It also brings to light a relatively unexplored area of the brain that could play a key role in conditions which are accompanied by disorders of sensory processing, such as schizophrenia and Alzheimer's disease.
The presentation "Smelling Sounds: Olfactory-Auditory Sensory Convergence in the Olfactory Tubercle" takes place as part of the Sensory Integration and Competition symposium, Friday, April 23, 8:15 10:20 p.m. ET in the Island Ballroom.
Cilia, Sensory Dysfunction, and Disease: Exploring the Role of an Ancient Cell Structure in a New Class of Genetic Disorders
Ciliopathies are a newly recognized class of human genetic disorders that are caused by defects in cilia, cell projections, like antennae, that receive signals in and between cells and are as ancient in origin as the whip-like flagella of single-celled algae. Nearly every cell in the body has one or more cilia. In the sensory systems they help us smell, see, and hear. The ciliopathies encompass disorders as different from each other as polycystic kidney disease and retinitis pigmentosa. Olfactory dysfunction is a newly recognized symptom that many of the ciliopathies share.
This NIDCD-sponsored symposium features presentations from researchers in olfaction and other disciplines who are exploring shared and distinct mechanisms that affect cilia in different systems of the body.
The symposium "Cilia, Sensory Dysfunction and Disease" takes place on Friday, April 23, from 8:00 to 10:40 a.m. ET in the Island Ballroom.
Are Clues for Neural Regeneration on the Tip of the Tongue?
One of the most critical problems in neuroscience is how to coerce neurons in the central nervous system to regenerate after injury. Fortunately, taste receptor cells-located in the taste buds of the tongue-are regularly replaced throughout life. Research sponsored by the NIDCD is using taste cells as a model in hopes that understanding how these cells successfully regenerate will show us ways to encourage similar kinds of regeneration in nerves that are less successful at repair, such as those severed by spinal cord injury. Building on the knowledge that aging impairs neural regeneration, researchers at the Medical College of Georgia explored whether aging could also impair taste cell regeneration in the tongue. Researchers severed the chorda tympani nerve on one side of the tongue of rats ranging from 3 to 24 months of age. They then observed what happened in the first days after injury and weeks later in recovery, focusing particularly on the role of immune system cells and their impact on taste response.
Previous work in young, healthy adult rats had shown a progression from one type of immune cell to another type immediately after injury. However, two days after cutting the nerve, the researchers observed higher and longer-lasting numbers of the early-arriving immune cells in old rats versus young rats. Further, taste responses in the older rats were absent until about 85 days post-injury, in spite of the presence of some functional taste buds, while younger rats recovered taste function at least 40 days sooner. The researchers plan to test methods to boost and control immune function in older rats to shorten recovery time after nerve injury.
The poster "Effects of aging on the injured peripheral taste system" (# 247) takes place Saturday, April 24, from 8:00 a.m. to 12:30 p.m. ET in the Pavilion.
|Contact: Robin Latham|
NIH/National Institute on Deafness and Other Communication Disorders