By Robert Fisch
Each year, an estimated 443,000 people die from exposure to either primary or secondhand tobacco smoke. An additional 8.6 million people have serious illnesses as a result of smoking. These illnesses come in the form of lung cancer, chronic pulmonary disease, heart disease, stroke, and various other medical complications.1 However, the side effects of exposure to tobacco smoke may be more harmful than previously thought, as smoking could also be quietly affecting people’s hearing.
Different research groups have recently found that smoking results in a decreased ability to hear high frequency sounds, and an increased degree of tinnitus, the constant ringing sound that lingers in a person’s ear, and hearing loss in adults.2,3,4,5
Research regarding the physical effect that nicotine has on the organs within the ear is sparse. However, Dr. Amel M. Abdel-Hafez and his team of doctors at Assiut University in Northern Egypt have found compelling visual evidence that nicotine can severely affect the size, shape, and health of cochlear hair cells that are imperative to hearing.6
Located deep inside the ear, the cochlea, a small, coiled, snail-like structure, is the primary organ for sound detection. Within the cochlea, hair cells are responsible for neuronal propagation of a detected sound to the auditory cortex of the brain. The auditory cortex then sends this information to other parts of the brain for processing. The cochlea’s essential hair cells have protrusions called cilia that bend upon sound detection, causing cell depolarization and adjacent neuronal firing.7 Complete hair cell ablation, or hair cell removal, fully wipes out the ability to hear, exemplifying these cells’ crucial role in hearing.8
To test how hair cells are physically affected by nicotine, Abdel-Hafez and his team took a closer look at hair cells and the surrounding cochlear support cells using modern microscopy techniques. These imaging techniques included standard light microscopy and two different types of high-magnification, high-resolution electron microscopy.
The team used cells belonging to guinea pigs, which share very similar auditory anatomy with humans.6 The cells that the researchers examined were exposed to different levels of nicotine and later compared.
Abdel-Hafez’s team used 15 guinea pigs to carry out their experiments. Five guinea pigs were given no nicotine as a control group, five guinea pigs were given a specific dose of nicotine every day for a month to mimic moderate tobacco users as an experimental group, and five guinea pigs were given double the dose of nicotine every day for a month to mimic heavy tobacco users as a second experimental group.
The guinea pigs were then anesthetized and euthanized, allowing the researchers to remove the cochleas and prepare samples for imaging. While imaging these different cells, the researchers looked at cochlear cell structure, organization, and size to determine the health of these vital cells. What they found in these images did not come as a surprise.
Hair cells and surrounding support cells within the cochlea of the non-nicotine group of guinea pigs were visibly healthy. They displayed appropriate spacing, were organized in the expected mosaic configuration, and were free from scars, growths, or any other disfigurations. The cilia attached to the hair cells were sturdy, smooth, evenly spread out, and neatly structured. This clean cell colony is an example of healthy hearing cells that should be able to properly detect sounds at frequencies and volumes normally audible to guinea pigs.
The cells of the two experimental groups did not exhibit these healthy characteristics. Hair cells and surrounding support cells of the low-dose nicotine guinea pigs were visibly not as healthy as their non-nicotine counterparts. Even at a moderately low dose, hair cells began to show signs of wrinkling and deterioration. The cells were organized relatively normally, but seemed to be squeezed toward the midline of the cell colony as a result of structural cells pushing in on the weakened hair cells. The nuclei within these hair cells became darker and there were large vacuoles – bubble-like membrane-bound organelles within a cell – that did not appear in the healthy cochlear cells. The cilia began bundling, bending, and showing signs of deformity and weakness.
The “heavy smoking” group of guinea pig ear cells displayed even worse signs of deterioration. Organization worsened and cells wrinkled. Support cells further encroached on the weakened hair cells. Discolored nuclei and large vacuoles were also visible. The cilia were even more bent, weak, and bundled than the low-dose nicotine cells. Growths protruded from the cells and scars were visible throughout the colony.
While this study itself did not test the hearing ability of the guinea pigs, tit provides evidence that nicotine is linked to deteriorating cochlear cell. These findings reinforce previous studies by adding visual evidence of physical damage to cochlear cell health caused by nicotine. Previous research showed significant hearing loss as a result of smoking, including a 2014 study that demonstrated that factory workers who smoked cigarettes had a noticeably weaker ability to hear high frequency sounds than non-smokers at the same factory.3,4 In tandem, these studies show that auditory cells are both physically and functionally affected when exposed to nicotine.
The results from Abdel-Hafez’s research are also in accordance with an earlier finding that the presence of low doses of nicotine on any cells that display nicotinic receptors induces degradation and apoptosis, the process of programmed cell death.9 Cochlear hair cells do in fact display nicotinic receptors and are therefore at risk of degradation and apoptosis when exposed to this tobacco constituent.10
A big challenge moving forward in research is obtaining hearing ability results and imaging from the same subject. If a single study could show decreased hearing ability and decreased hair cell health in the same subject, this would likely dispel any doubt about the negative effects of smoking on hearing. However, this is a challenge considering that live human cochlear cells cannot be harvested for research, as doing so would irreversibly damage the subject’s hearing.
Additionally, in animal-based experiments, it is difficult to mirror the exact conditions of human tobacco users, and to quantify cell health and degeneration. While qualitative imaging can show signs of cell health, it cannot directly compare the function of hair cells. Regardless, more research is necessary to uncover the direct effect that cigarette smoking can have on hearing.
For now, Abdel-Hafez and his research team have potentially quieted opposing studies, as there seems to be clear evidence of direct cochlear cell damage after exposure to nicotine. These findings may affirm tobacco as a true silent killer of hearing. ∎
1. CDC. (2011). Targeting the Nation’s Leading Killer at a Glance
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3. Vinay. (2010). Effect of smoking on transient evoked otoacoustic emissions and contralateral suppression. Auris Nasus Larynx 37:299-302.
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6. Abdel-Hafez, A. M. M., Elgayar, S. A. A., Husain, O. A., Thabet, H. S. A. (2014). Effect of nicotine on the structure of cochlea of guinea pigs. Anatomy and Cell Biology. 47:162-170
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8. Jones, J. E., Corwin, J. T. (1996). Regeneration of Sensory Cells after Laser Ablation in the Lateral Line System: Hair Cell Lineage and Macrophage Behavior Revealed by Time-Lapse Video Microscopy. The Journal of Neuroscience. 16(2):649-662.
9. Berger, F., Gage F.H., Vijayaraghavan, S. (1998) Nicotinic receptor-induced apoptotic cell death of hippocampal progenitor cells. J Neuroscience. 18:6871-81.
10. Matsunobu, T., Chung, J.W., Schacht, J. (2001). Acetylcholine-evoked calcium increases in Deiters’ cells of the guinea pig cochlea suggest alpha9-like receptors. Journal of Neuroscience Research. 63:252-6.