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Taste

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The three chemosensory systems, smell, taste, and the common chemical sense, require direct stimulation by chemicals for sensory perception. Their role is to monitor constantly both harmful and beneficial inhaled and ingested chemical substances. Irritating or tingling properties are detected by the common chemical sense. The taste system perceives only sweet, salty, sour, bitter and possibly metallic and monosodium glutamate (umami) tastes. The totality of the oral sensory experience is termed “flavour,” the interaction of smell, taste, irritation, texture and temperature. Because most flavour is derived from the smell, or aroma, of food and beverages, damage to the smell system is often reported as a problem with “taste”. Verifiable taste deficits are more likely present if specific losses to sweet, sour, salty and bitter sensations are described.

Chemosensory complaints are frequent in occupational settings and may result from a normal sensory system perceiving environmental chemicals. Conversely, they may also indicate an injured system: requisite contact with chemical substances renders these sensory systems uniquely vulnerable to damage (see table 1). In the occupational setting, these systems can also be damaged by trauma to the head as well as by agents other than chemicals (e.g., radiation). Taste disorders are either temporary or permanent: complete or partial taste loss (ageusia or hypogeusia), heightened taste (hypergeusia) and distorted or phantom tastes (dysgeusia) (Deems, Doty and Settle 1991; Mott, Grushka and Sessle 1993).

Table 1. Agents/processes reported to alter the taste system

Agent/process

Taste disturbance

Reference

Amalgam

Metallic taste

Siblerud 1990; see text

Dental restorations/appliances

Metallic taste

See text

Diving (dry saturation)

Sweet, bitter; salt, sour

See text

Diving and welding

Metallic taste

See text

Drugs/Medications

Varies

See text

Hydrazine

Sweet dysgeusia

Schweisfurth and Schottes 1993

Hydrocarbons

Hypogeusia, “glue” dysgeusia

Hotz et al. 1992

Lead poisoning

Sweet/metallic dysgeusia

Kachru et al. 1989

Metals and metal fumes
(also, some specific metals listed in chart)

Sweet/Metallic

See text; Shusterman and Sheedy 1992

Nickel

Metallic taste

Pfeiffer and Schwickerath 1991

Pesticides
(Organo-phosphates)

Bitter/metallic dysgeusia

+

Radiation

Increased DT & RT

*

Selenium

Metallic taste

Bedwal et al. 1993

Solvents

“Funny taste”, H

+

Sulphuric acid mists

“Bad taste”

Petersen and Gormsen 1991

Underwater welding

Metallic taste

See text

Vanadium

Metallic taste

Nemery 1990

DT = detection threshold, RT = recognition threshold, * = Mott & Leopold 1991, + = Schiffman & Nagle 1992
Specific taste disturbances are as stated in the articles referenced.

The taste system is sustained by regenerative capability and redundant innervation. Because of this, clinically notable taste disorders are less common than olfactory disorders. Taste distortions are more common than significant taste loss and, when present, are more likely to have secondary adverse effects such as anxiety and depression. Taste loss or distortion can interfere with occupational performance where keen taste acuity is required, such as culinary arts and blending of wines and spirits.

Anatomy and Physiology

Taste receptor cells, found throughout the oral cavity, the pharynx, the larynx and the oesophagus, are modified epithelial cells located within the taste buds. While on the tongue taste buds are grouped in superficial structures called papillae, extralingual taste buds are distributed within the epithelium. The superficial placement of taste cells makes them susceptible to injury. Damaging agents usually come in contact with the mouth through ingestion, although mouth breathing associated with nasal obstruction or other conditions (e.g., exercise, asthma) allows oral contact with airborne agents. The taste receptor cell’s average ten-day life span permits rapid recovery if superficial damage to receptor cells has occurred. Also, taste is innervated by four pairs of peripheral nerves: the front of the tongue by the chorda tympani branch of the seventh cranial nerve (CN VII); the posterior of the tongue and the pharynx by the glossopharyngeal nerve (CN IX); the soft palate by the greater superficial petrosal branch of CN VII; and the larynx/oesophagus by the vagus (CN X). Last, taste central pathways, although not completely mapped in humans (Ogawa 1994), appear more divergent than olfactory central pathways.

The first step in taste perception involves interaction between chemicals and taste receptor cells. The four taste qualities, sweet, sour, salty and bitter, enlist different mechanisms at the level of the receptor (Kinnamon and Getchell 1991), ultimately generating action potentials in taste neurons (transduction).

Tastants diffuse through salivary secretions and also mucus secreted around taste cells to interact with the surface of taste cells. Saliva ensures that tastants are carried to the buds, and provides an optimal ionic environment for perception (Spielman 1990). Alterations in taste can be demonstrated with changes in the inorganic constituents of saliva. Most taste stimuli are water soluble and diffuse easily; others require soluble carrier proteins for transport to the receptor. Salivary output and composition, therefore, play an essential role in taste function.

Salt taste is stimulated by cations such as Na+, K+ or NH4+. Most salty stimuli are transduced when ions travel through a specific type of sodium channel (Gilbertson 1993), although other mechanisms may also be involved. Changes in the composition of taste pore mucus or the taste cell’s environment could alter salt taste. Also, structural changes in nearby receptor proteins could modify receptor membrane function. Sour taste corresponds to acidity. Blockade of specific sodium channels by hydrogen ions elicits sour taste. As with salt taste, however, other mechanisms are thought to exist. Many chemical compounds are perceived as bitter, including cations, amino acids, peptides and larger compounds. Detection of bitter stimuli appears to involve more diverse mechanisms that include transport proteins, cation channels, G proteins and second messenger mediated pathways (Margolskee 1993). Salivary proteins may be essential in transporting lipophilic bitter stimuli to the receptor membranes. Sweet stimuli bind to specific receptors linked to G protein-activated second-messenger systems. There is also some evidence in mammals that sweet stimuli can gate ion channels directly (Gilbertson 1993).

Taste Disorders

General Concepts

The anatomic diversity and redundancy of the taste system is sufficiently protective to prevent total, permanent taste loss. Loss of a few peripheral taste fields, for example, would not be expected to affect whole mouth taste ability (Mott, Grushka and Sessle 1993). The taste system may be far more vulnerable to taste distortion or phantom tastes. For example, dysgeusias appear to be more common in occupational exposures than taste losses per se. Although taste is thought to be more robust than smell with respect to the ageing process, losses in taste perception with ageing have been documented.

Temporary taste losses can occur when the oral mucosa has been irritated. Theoretically, this can result in inflammation of the taste cells, closure of taste pores or altered function at the surface of taste cells. Inflammation can alter blood flow to the tongue, thereby affecting taste. Salivary flow can also be compromised. Irritants can cause swelling and obstruct salivary ducts. Toxicants absorbed and excreted through salivary glands, could damage ductal tissue during excretion. Either of these processes could cause long-term oral dryness with resultant taste effects. Exposure to toxicants could alter the turnover rate of taste cells, modify the taste channels at the surface of the taste cell, or change the internal or external chemical environments of the cells. Many substances are known to be neurotoxic and could injure peripheral taste nerves directly, or damage higher taste pathways in the brain.

Pesticides

Pesticide use is widespread and contamination occurs as residues in meat, vegetables, milk, rain and drinking water. Although workers exposed during the manufacture or use of pesticides are at greatest risk, the general population is also exposed. Important pesticides include organochloride compounds, organophosphate pesticides, and carbamate pesticides. Organochloride compounds are highly stable and therefore exist in the environment for lengthy periods. Direct toxic effects on central neurons have been demonstrated. Organophosphate pesticides have more widespread use because they are not as persistent, but they are more toxic; inhibition of acetylcholinesterase can cause neurological and behavioural abnormalities. Carbamate pesticide toxicity is similar to that for the organophosphorus compounds and are often used when the latter fail. Pesticide exposures have been associated with persistent bitter or metallic tastes (Schiffman and Nagle 1992), unspecified dysgeusia (Ciesielski et al. 1994), and less commonly with taste loss. Pesticides can reach taste receptors via air, water and food and can be absorbed from the skin, gastrointestinal tract, conjunctiva, and respiratory tract. Because many pesticides are lipid soluble, they can easily penetrate lipid membranes within the body. Interference with taste can occur peripherally irrespective of route of initial exposure; in mice, binding to the tongue has been seen with certain insecticides after injection of pesticide material into the bloodstream. Alterations in taste bud morphology after pesticide exposure have been demonstrated. Degenerative changes in the sensory nerve terminations have been also noted and may account for reports of abnormalities of neural transmission. Metallic dysgeusia may be a sensory paresthesia caused by the impact of pesticides on taste buds and their afferent nerve endings. There is some evidence, however, that pesticides can interfere with neurotransmitters and therefore disrupt transmission of taste information more centrally (El-Etri et al. 1992). Workers exposed to organophosphate pesticides can demonstrate neurological abnormalities on electroencephalography and neuropsychological testing independent of cholinesterase depression in the blood stream. It is thought that these pesticides have a neurotoxic effect on the brain independent of the effect upon cholinesterase. Although increased salivary flow has been reported to be associated with pesticide exposure, it is unclear what effect this might have on taste.

Metals and metal fume fever

Alterations of taste have occurred after exposure to certain metals and metallic compounds including mercury, copper, selenium, tellurium, cyanide, vanadium, cadmium, chromium and antimony. Metallic taste has also been noted by workers exposed to the fumes of zinc or copper oxide, from the ingestion of copper salt in poisoning cases, or from exposure to emissions resulting from the use of torches for cutting of brass piping.

Exposure to freshly formed fumes of metal oxides can result in a syndrome known as metal fume fever (Gordon and Fine 1993). Although zinc oxide is most frequently cited, this disorder has also been reported after exposure to oxides of other metals, including copper, aluminium, cadmium, lead, iron, magnesium, manganese, nickel, selenium, silver, antimony and tin. The syndrome was first noted in brass foundry workers, but is now most common in welding of galvanized steel or during galvanization of steel. Within hours after exposure, throat irritation and a sweet or metallic dysgeusia may herald more generalized symptoms of fever, shaking chills, and myalgia. Other symptoms, such as cough or headache, may also occur. The syndrome is notable for both rapid resolution (within 48 hours) and development of tolerance upon repeated exposures to the metal oxide. A number of possible mechanisms have been suggested, including immune system reactions and a direct toxic effect on respiratory tissue, but it is now thought that lung exposure to metal fumes results in release of specific mediators into the blood stream, called cytokines, that cause the physical symptoms and findings (Blanc et al. 1993). A more severe, potentially fatal, variant of metal fume fever occurs after exposure to zinc chloride aerosol in military screening smoke bombs (Blount 1990). Polymer fume fever is similar to metal fume fever in presentation, with the exception of the absence of metallic taste complaints (Shusterman 1992).

In lead poisoning cases, sweet metallic tastes are often described. In one report, silver jewellery workers with confirmed lead toxicity exhibited taste alterations (Kachru et al. 1989). The workers were exposed to lead fumes by heating jewellers’ silver waste in workshops which had poor exhaust systems. The vapours condensed on the skin and hair of the workers and also contaminated their clothing, food and drinking water.

Underwater welding

Divers describe oral discomfort, loosening of dental fillings and metallic taste during electrical welding and cutting underwater. In a study by Örtendahl, Dahlen and Röckert (1985), 55% of 118 divers working under water with electrical equipment described metallic taste. Divers without this occupational history did not describe metallic taste. Forty divers were recruited into two groups for further evaluation; the group with underwater welding and cutting experience had significantly more evidence of dental amalgam breakdown. Initially, it was theorized that intraoral electrical currents erode dental amalgam, releasing metal ions which have direct effects on taste cells. Subsequent data, however, demonstrated intraoral electrical activity of insufficient magnitude to erode dental amalgam, but of sufficient magnitude to directly stimulate taste cells and cause metallic taste (Örtendahl 1987; Frank and Smith 1991). Divers may be vulnerable to taste changes without welding exposure; differential effects on taste quality perception have been documented, with decreased sensitivity to sweet and bitter and increased sensitivity to salty and sour tastants (O’Reilly et al. 1977).

Dental restorations and oral galvanism

In a large prospective, longitudinal study of dental restorations and appliances, approximately 5% of subjects reported a metallic taste at any given time (Participants of SCP Nos. 147/242 & Morris 1990). Frequency of metallic taste was higher with a history of teeth grinding; with fixed partial dentures than with crowns; and with an increased number of fixed partial dentures. Interactions between dental amalgams and the oral environment are complex (Marek 1992) and could affect taste through a variety of mechanisms. Metals that bind to proteins can acquire antigenicity (Nemery 1990) and might cause allergic reactions with subsequent taste alterations. Soluble metal ions and debris are released and may interact with soft tissues in the oral cavity. Metallic taste has been reported to correlate with nickel solubility in saliva from dental appliances (Pfeiffer and Schwickerath 1991). Metallic taste was reported by 16% of subjects with dental fillings and none of subjects without fillings (Siblerud 1990). In a related study of subjects who had amalgam removed, metallic taste improved or abated in 94% (Siblerud 1990).

Oral galvanism, a controversial diagnosis (Council on Dental Materials report 1987), describes the generation of oral currents from either corrosion of dental amalgam restorations or electrochemical differences between dissimilar intraoral metals. Patients considered to have oral galvanism appear to have a high frequency of dysgeusia (63%) described as metallic, battery, unpleasant or salty tastes (Johansson, Stenman and Bergman 1984). Theoretically, taste cells could be directly stimulated by intraoral electric currents and generate dysgeusia. Subjects with symptoms of oral burning, battery taste, metallic taste and/or oral galvanism were determined to have lower electrogustometric thresholds (i.e. more sensitive taste) on taste testing than control subjects (Axéll, Nilner and Nilsson 1983). Whether galvanic currents related to dental materials are causative is debatable, however. A brief tin-foil taste shortly after restorative work is thought to be possible, but more permanent effects are probably unlikely (Council on Dental Materials 1987). Yontchev, Carlsson and Hedegård (1987) found similar frequencies of metallic taste or oral burning in subjects with these symptoms whether or not there was contact between dental restorations. Alternative explanations for taste complaints in patients with restorations or appliances are sensitivity to mercury, cobalt, chrome, nickel or other metals (Council on Dental Materials 1987), other intraoral processes (e.g., periodontal disease), xerostomia, mucosal abnormalities, medical illnesses, and medication side effects.

Drugs and medications

Many drugs and medications have been linked to taste alterations (Frank, Hettinger and Mott 1992; Mott, Grushka and Sessle 1993; Della Fera, Mott and Frank 1995; Smith and Burtner 1994) and are mentioned here because of possible occupational exposures during the manufacture of these drugs. Antibiotics, anticonvulsants, antilipidemics, antineoplastics, psychiatric, antiparkinsonism, antithyroid, arthritis, cardiovascular, and dental hygiene drugs are broad classes reported to affect taste.

The presumed site of action of drugs on the taste system varies. Often the drug is tasted directly during oral administration of the drug or the drug or its metabolites are tasted after being excreted in saliva. Many drugs, for example anticholinergics or some antidepressants, cause oral dryness and affect taste through inadequate presentation of the tastant to the taste cells via saliva. Some drugs may affect taste cells directly. Because taste cells have a high turnover rate, they are especially vulnerable to drugs that interrupt protein synthesis, such as antineoplastic drugs. It has also been thought that there may be an effect on impulse transmission through the taste nerves or in the ganglion cells, or a change in the processing of the stimuli in higher taste centres. Metallic dysgeusia has been reported with lithium, possibly through transformations in receptor ion channels. Anti-thyroid drugs and angiotensin converting enzyme inhibitors (e.g., captopril and enalapril) are well known causes of taste alterations, possibly because of the presence of a sulphydryl (-SH) group (Mott, Grushka and Sessle 1993). Other drugs with -SH groups (e.g., methimazole, penicillamine) also cause taste abnormalities. Drugs that affect neurotransmitters could potentially alter taste perception.

Mechanisms of taste alterations vary, however, even within a class of drug. For example, taste alterations after treatment with tetracycline may be caused by oral mycosis. Alternatively, an increased blood urea nitrogen, associated with the catabolic effect of tetracycline, can sometimes result in a metallic or ammonia-like taste.

Side effects of metronidazole include alteration of taste, nausea, and a distinctive distortion of the taste of carbonated and alcoholic beverages. Peripheral neuropathy and paraesthesias can also sometimes occur. It is thought that the drug and its metabolites may have a direct affect upon taste receptor function, and also on the sensory cell.

Radiation exposure

Radiation treatment can cause taste dysfunction through (1) taste cell changes, (2) damage to taste nerves, (3) salivary gland dysfunction, and (4) opportunistic oral infection (Della Fera et al. 1995). There have been no studies of occupational radiation effects on the taste system.

Head trauma

Head trauma occurs in the occupational setting and can cause alterations in the taste system. Although perhaps only 0.5% of head trauma patients describe taste loss, the frequency of dysgeusia may be much higher (Mott, Grushka and Sessle 1993). Taste loss, when it occurs, is likely quality-specific or localized and may not even be subjectively apparent. The prognosis of subjectively noted taste loss appears better than that for olfactory loss.

Non-occupational causes

Other causes of taste abnormalities must be considered in the differential diagnosis, including congenital/genetic, endocrine/metabolic, or gastrointestinal disorders; hepatic disease; iatrogenic effects; infection; local oral conditions; cancer; neurological disorders; psychiatric disorders; renal disease; and dry mouth/Sjogren’s syndrome (Deems, Doty and Settle 1991; Mott and Leopold 1991; Mott, Grushka and Sessle 1993).

Taste testing

Psychophysics is the measurement of a response to an applied sensory stimulus. “Threshold” tasks, tests that determine the minimum concentration that can be reliably perceived, are less useful in taste than olfaction because of wider variability in the former in the general population. Separate thresholds can be obtained for detection of tastants and recognition of tastant quality. Suprathreshold tests assess the ability of the system to function at levels above threshold and may provide more information about “real world” taste experience. Discrimination tasks, telling the difference between substances, can elicit subtle changes in sensory ability. Identification tasks may yield different results than threshold tasks in the same individual. For example, a person with central nervous system injury may be able to detect and rank tastants, but may not be able to identify them. Taste testing can assess whole mouth taste through swishing of tastants throughout the oral cavity, or can test specific taste areas with targeted droplets of tastants or focally applied filter paper soaked with tastants.

Summary

The taste system is one of three chemosensory systems, together with olfaction and the common chemical sense, committed to monitoring harmful and beneficial inhaled and ingested substances. Taste cells are rapidly replaced, are innervated by pairs of four peripheral nerves, and appear to have divergent central pathways in the brain. The taste system is responsible for the appreciation of four basic taste qualities (sweet, sour, salty, and bitter) and, debatably, metallic and umami (monosodium glutamate) tastes. Clinically significant taste losses are rare, probably because of the redundancy and diversity of innervation. Distorted or abnormal tastes, however, are more common and can be more distressing. Toxic agents unable to destroy the taste system, or to halt transduction or transmission of taste information, nevertheless have ample opportunities to impede the perception of normal taste qualities. Irregularities or obstacles can occur through one or more of the following: suboptimal tastant transport, altered salivary composition, taste cell inflammation, blockage of taste cell ion pathways, alterations in the taste cell membrane or receptor proteins, and peripheral or central neurotoxicity. Alternatively, the taste system may be intact and functioning normally, but be subjected to disagreeable sensory stimulation through small intraoral galvanic currents or the perception of intraoral medications, drugs, pesticides or metal ions.

 

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