" DISCLAIMER: The ILO does not take responsibility for content presented on this web portal that is presented in any language other than English, which is the language used for the initial production and peer-review of original content. Certain statistics have not been updated since the production of the 4th edition of the Encyclopaedia (1998)."

Monday, 07 March 2011 15:31

Smell

Written by
Rate this item
(0 votes)

Three sensory systems are uniquely constructed to monitor contact with environmental substances: olfaction (smell), taste (sweet, salty, sour, and bitter perception), and the common chemical sense (detection of irritation or pungency). Because they require stimulation by chemicals, they are termed “chemosensory” systems. Olfactory disorders consist of temporary or permanent: complete or partial smell loss (anosmia or hyposmia) and parosmias (perverted smells dysosmia or phantom smells phantosmia) (Mott and Leopold 1991; Mott, Grushka and Sessle 1993). After chemical exposures, some individuals describe a heightened sensitivity to chemical stimuli (hyperosmia). Flavour is the sensory experience generated by the interaction of the smell, taste and irritating components of food and beverages, as well as texture and temperature. Because most flavour is derived from the smell, or aroma, of ingestants, damage to the smell system is often reported as a problem with “taste”.

Chemosensory complaints are frequent in occupational settings and may result from a normal sensory system’s perceiving environmental chemicals. Conversely, they may also indicate an injured system: requisite contact with chemical substances renders these sensory systems uniquely vulnerable to damage. In the occupational setting, these systems can also be damaged by trauma to the head and agents other than chemicals (e.g., radiation). Pollutant-related environmental odours can exacerbate underlying medical conditions (e.g., asthma, rhinitis), precipitate development of odour aversions, or cause a stress-related type of illness. Malodors have been demonstrated to decrease complex task performance (Shusterman 1992).

Early identification of workers with olfactory loss is essential. Certain occupations, such as the culinary arts, wine making and the perfume industry, require a good sense of smell as a prerequisite. Many other occupations require normal olfaction for either good job performance or self-protection. For example, parents or day care workers generally rely on smell to determine children’s hygiene needs. Firefighters need to detect chemicals and smoke. Any worker with ongoing exposure to chemicals is at increased risk if olfactory ability is poor.

Olfaction provides an early warning system to many harmful environmental substances. Once this ability is lost, workers may not be aware of dangerous exposures until the concentration of the agent is high enough to be irritating, damaging to respiratory tissues or lethal. Prompt detection can prevent further olfactory damage through treatment of inflammation and reduction of subsequent exposure. Lastly, if loss is permanent and severe, it may be considered a disability requiring new job training and/or compensation.

Anatomy and Physiology

Olfaction

The primary olfactory receptors are located in patches of tissue, termed olfactory neuroepithelium, at the most superior portion of the nasal cavities (Mott and Leopold 1991). Unlike other sensory systems, the receptor is the nerve. One portion of an olfactory receptor cell is sent to the surface of the nasal lining, and the other end connects directly via a long axon to one of two olfactory bulbs in the brain. From here, the information travels to many other areas of the brain. Odorants are volatile chemicals that must contact the olfactory receptor for smell perception to occur. Odorant molecules are trapped by and then diffuse through mucus to attach to cilia at the ends of the olfactory receptor cells. It is not yet known how we are able to detect more than ten thousand odorants, discriminate from as many as 5,000, and judge varying odorant intensities. Recently, a multigene family was discovered that codes for odorant receptors on primary olfactory nerves (Ressler, Sullivan and Buck 1994). This has allowed investigation of how odours are detected and how the smell system is organized. Each neuron may respond broadly to high concentrations of a variety of odorants, but will respond to only one or a few odorants at low concentrations. Once stimulated, surface receptor proteins activate intracellular processes that translate sensory information into an electrical signal (transduction). It is not known what terminates the sensory signal despite continued odorant exposure. Soluble odorant binding proteins have been found, but their role is undetermined. Proteins that metabolize odorants may be involved or carrier proteins may transport odorants either away from the olfactory cilia or toward a catalytic site within the olfactory cells.

The portions of the olfactory receptors connecting directly to the brain are fine nerve filaments that travel through a plate of bone. The location and delicate structure of these filaments render them vulnerable to shear injury from blows to the head. Also, because the olfactory receptor is a nerve, physically contacts odorants, and connects directly to the brain, substances entering the olfactory cells can travel along the axon into the brain. Because of continued exposure to agents damaging to the olfactory receptor cells, olfactory ability might be lost early in the lifespan if it were not for a critical attribute: olfactory receptor nerves are capable of regeneration and may be replaced, provided the tissue has not been completely destroyed. If the damage to the system is more centrally located, however, the nerves can not be restored.

Common chemical sense

The common chemical sense is initiated by stimulation of mucosal, multiple, free nerve endings of the fifth (trigeminal) cranial nerve. It perceives the irritating properties of inhaled substances and triggers reflexes designed to limit exposure to dangerous agents: sneezing, mucus secretion, reduction of breathing rate or even breath-holding. Strong warning cues compel removal from the irritation as soon as possible. Although the pungency of substances vary, generally the odour of the substance is detected before irritation becomes apparent (Ruth 1986). Once irritation is detected, however, small increases in concentration enhance irritation more than odorant appreciation. Pungency may be evoked through either physical or chemical interactions with receptors (Cometto-Muñiz and Cain 1991). The warning properties of gases or vapours tend to correlate with their water solubilities (Shusterman 1992). Anosmics appear to require higher concentrations of pungent chemicals for detection (Cometto-Muñiz and Cain 1994), but thresholds of detection are not elevated as one ages (Stevens and Cain 1986).

Tolerance and adaptation

Perception of chemicals can be altered by previous encounters. Tolerance develops when exposure reduces the response to subsequent exposures. Adaptation occurs when a constant or rapidly repeated stimulus elicits a diminishing response. For example, short-term solvent exposure markedly, but temporarily, reduces solvent detection ability (Gagnon, Mergler and Lapare 1994). Adaptation can also occur when there has been prolonged exposure at low concentrations or rapidly, with some chemicals, when extremely high concentrations are present. The latter can lead to rapid and reversible olfactory “paralysis”. Nasal pungency typically shows less adaptation and development of tolerance than olfactory sensations. Mixtures of chemicals can also alter perceived intensities. Generally, when odorants are mixed, perceived odorant intensity is less than would be expected from adding the two intensities together (hypoadditivity). Nasal pungency, however, generally shows additivity with exposure to multiple chemicals, and summation of irritation over time (Cometto-Muñiz and Cain 1994). With odorants and irritants in the same mixture, the odour is always perceived as less intense. Because of tolerance, adaptation, and hypoadditivity, one must be careful to avoid relying on these sensory systems to gauge the concentration of chemicals in the environment.

Olfactory Disorders

General concepts

Olfaction is disrupted when odorants can not reach olfactory receptors, or when olfactory tissue is damaged. Swelling within the nose from rhinitis, sinusitis or polyps can preclude odorant accessibility. Damage can occur with: inflammation in the nasal cavities; destruction of the olfactory neuroepithelium by various agents; trauma to the head; and transmittal of agents via the olfactory nerves to the brain with subsequent injury to the smell portion of the central nervous system. Occupational settings contain varying amounts of potentially damaging agents and conditions (Amoore 1986; Cometto-Muñiz and Cain 1991; Shusterman 1992; Schiffman and Nagle 1992). Recently published data from 712,000 National Geographic Smell Survey respondents suggests that factory work impairs smell; male and female factory workers reported poorer senses of smell and demonstrated decreased olfaction on testing (Corwin, Loury and Gilbert 1995). Specifically, chemical exposures and head trauma were more frequently reported than by workers in other occupational settings.

When an occupational olfactory disorder is suspected, identification of the offending agent can be difficult. Current knowledge is largely derived from small series and case reports. It is of importance that few studies mention examination of the nose and sinuses. Most rely on patient history for olfactory status, rather than testing of the olfactory system. An additional complicating factor is the high prevalence of non-occupationally related olfactory disturbances in the general population, mostly due to viral infections, allergies, nasal polyps, sinusitis or head trauma. Some of these, however, are also more common in the work environment and will be discussed in detail here.

Rhinitis, sinusitis and polyposis

Individuals with olfactory disturbance must first be assessed for rhinitis, nasal polyps and sinusitis. It is estimated that 20% of the United States population, for example, has upper airway allergies. Environmental exposures can be unrelated, cause inflammation or exacerbate an underlying disorder. Rhinitis is associated with olfactory loss in occupational settings (Welch, Birchall and Stafford 1995). Some chemicals, such as isocyanates, acid anhydrides, platinum salts and reactive dyes (Coleman, Holliday and Dearman 1994), and metals (Nemery 1990) can be allergenic. There is also considerable evidence that chemicals and particles increase sensitivity to nonchemical allergens (Rusznak, Devalia and Davies 1994). Toxic agents alter the permeability of the nasal mucosa and allow greater penetration of allergens and enhanced symptoms, making it difficult to discriminate between rhinitis due to allergies and that due to exposure to toxic or particulate substances. If inflammation and/or obstruction in the nose or sinuses is demonstrated, return of normal olfactory function is possible with treatment. Options include topical corticosteroid sprays, systemic antihistamines and decongestants, antibiotics and polypectomy/sinus surgery. If inflammation or obstruction is not present or treatment does not secure improvement in olfactory function, olfactory tissue may have sustained permanent damage. Irrespective of cause, the individual must be protected from future contact with the offending substance or further injury to the olfactory system could occur.

Head trauma

Head trauma can alter olfaction through (1) nasal injury with scarring of the olfactory neuroepithelium, (2) nasal injury with mechanical obstruction to odours, (3) shearing of the olfactory filaments, and (4) bruising or destruction of the part of the brain responsible for smell sensations (Mott and Leopold 1991). Although trauma is a risk in many occupational settings (Corwin, Loury and Gilbert 1995), exposure to certain chemicals can increase this risk.

Smell loss occurs in 5% to 30% of head trauma patients and may ensue without any other nervous system abnormalities. Nasal obstruction to odorants may be surgically correctable, unless significant intranasal scarring has occurred. Otherwise, no treatment is available for smell disorders resulting from head trauma, although spontaneous improvement is possible. Rapid initial improvement may occur as swelling subsides in the area of injury. If olfactory filaments have been sheared, regrowth and gradual improvement of smell may also occur. Although this occurs in animals within 60 days, improvements in humans have been reported as long as seven years after injury. Parosmias developing as the patient recovers from injury may indicate regrowth of olfactory tissue and herald return of some normal smell function. Parosmias occurring at the time of injury or shortly thereafter are more likely due to brain tissue damage. Damage to the brain will not repair itself and improvement in smell ability would not be expected. Injury to the frontal lobe, the portion of the brain integral to emotion and thinking, may be more frequent in head trauma patients with smell loss. The resultant changes in socialization or thinking patterns may be subtle, though harmful to family and career. Formal neuropsychiatric testing and treatment may, therefore, be indicated in some patients.

Environmental agents

Environmental agents can gain access to the olfactory system through either the bloodstream or inspired air and have been reported to cause smell loss, parosmia and hyperosmia. Responsible agents include metallic compounds, metal dusts, nonmetallic inorganic compounds, organic compounds, wood dusts and substances present in various occupational environments, such as metallurgical and manufacturing processes (Amoore 1986; Schiffman and Nagle 1992 (table 1). Injury can occur both after acute and chronic exposures and can be either reversible or irreversible, depending on the interaction between host susceptibility and the damaging agent. Important substance attributes include bioactivity, concentration, irritant capacity, length of exposure, rate of clearance and potential synergism with other chemicals. Host susceptibility varies with genetic background and age. There are gender differences in olfaction, hormonal modulation of odorant metabolism and differences in specific anosmias. Tobacco use, allergies, asthma, nutritional status, pre-existing disease (e.g., Sjogren’s syndrome), physical exertion at time of exposure, nasal airflow patterns and possibly psychosocial factors influence individual differences (Brooks 1994). Resistance of the peripheral tissue to injury and presence of functioning olfactory nerves can alter susceptibility. For example, acute, severe exposure could decimate the olfactory neuroepithelium, effectively preventing spread of the toxin centrally. Conversely, long-term, low-level exposure might allow preservation of functioning peripheral tissue and slow, but steady-transit of damaging substances into the brain. Cadmium, for example, has a half-life of 15 to 30 years in humans, and its effects might not be apparent until years after exposure (Hastings 1990).

Table 1. Agents/processes associated with olfactory abnormalities

Agent

Smell disturbance

Reference

Acetaldehyde
Acetates, butyl and ethyl
Acetic acid
Acetone
Acetophenone
Acid chloride
Acids (organic and inorganic)
Acrylate, methacrylate vapours
Alum
Aluminium fumes
Ammonia
Anginine
Arsenic
Ashes (incinerator)
Asphalt (oxidized)

H
H or A
H
H, P
Low normal
H
H
Decreased odour ID
H
H
H
H
H
H
Low normal

2
3
2
2
2
2
2
1
2
2
1, 2
1
2
4
2

Benzaldehyde
Benzene
Benzine
Benzoic acid
Benzol
Blasting powder
Bromine
Butyl acetate
Butylene glycol

H
Below average
H/A
H
H/A
H
H
H/A
H

2
2
1
2
1
2
2
1
2

Cadmium compounds, dust, oxides


Carbon disulphide
Carbon monoxide
Carbon tetrachloride
Cement
Chalk dust
Chestnut wood dust
Chlorine
Chloromethanes
Chlorovinylarsine chlorides
Chromium (salts and plating)
Chromate
Chromate salts
Chromic acid
Chromium fumes
Cigarette smoking
Coal (coal-bunker)
Coal tar fumes
Coke
Copper (and sulphuric acid)
Copper arsenite
Copper fumes
Cotton, knitting factory
Creosote fumes
Cutting oils (machining)
Cyanides

H/A


H/A
A
H
H
H
A
H
Low normal
H
H
Olfactory disorder
A
H
H
Decreased ID
H
H
H or A
Olfactory disturbance
H
H
H
Abnormal UPSIT
Below average
H

1 ; Bar-Sela et al. 1992; Rose, Heywood and Costanzo 1992
1
2
2
4
1
1
2
2
2
2 ;4
1
2
2
2
1
4
2
4
Savov 1991
2
2
4
5
2
2

Dichromates

H

2

Ethyl acetate

Ethyl ether

Ethylene oxide

H/A
H
Decreased smell

1
2
Gosselin, Smith and
Hodge 1984

Flax
Flour, flour mill
Fluorides
Fluorine compounds
Formaldehyde
Fragrances
Furfural

H
H
H or A
H
H
Below average
H

2
4
3
2
1, 2 ; Chia et al. 1992
2
2

Grain

H or A

4

Halogen compounds
Hard woods
Hydrazine
Aromatic hydrocarbon solvent
combinations (e.g., toluene, xylene, ethyl
benzene)
Hydrogen chloride
Hydrogen cyanide
Hydrogen fluoride
Hydrogen selenide
Hydrogen sulphide

H
A
H/A
Decreased UPSIT, H


H
A
H
H/A
H or A

2
2
1
5 ; Hotz et al. 1992


2
2
2
1
5; Guidotti 1994

Iodoform
Iron carbonyl
Isocyanates

H
H
H

2
1
2

Lead
Lime
Lye

H
H
H

4
2
2

Magnet production
Manganese fumes
Menthol
Mercury
N-Methylformimino-methyl ester

H
H
H
Low normal
A

2
2
2 ; Naus 1968
2
2

Nickel dust, hydroxide, plating and refining
Nickel hydroxide
Nickel plating
Nickel refining (electrolytic)
Nitric acid
Nitro compounds
Nitrogen dioxide

H/A
A
Low normal
A
H
H
H

1;4; Bar-Sela et al. 1992
2
2
2
2
2
2

Oil of peppermint
Organophosphates
Osmium tetroxide
Ozone

H/A
Garlic odour; H or A
H
Temporary H

1
3 ; 5
2
3

Paint (lead)
Paint (solvent based)

Paper, packing factory
Paprika
Pavinol (sewing)
Pentachlorophenol
Pepper and creosol mixture
Peppermint
Perfumes (concentrated)
Pesticides
Petroleum
Phenylenediamine
Phosgene
Phosphorous oxychloride
Potash
Printing

Low normal
H or A

Possible H
H
Low normal
A
H/A
H or A
H

H or A
H or A
H
H
H/A
H
Low normal

2
Wieslander, Norbäck
and Edling 1994
4
2
2
2
1
3
2
5
3
2
2
1
1
2

Rubber vulcanization

H

2

Selenium compounds (volatile)
Selenium dioxide
Silicone dioxide
Silver nitrate
Silver plating
Solvents


Spices
Steel production
Sulphur compounds
Sulphur dioxide
Sulphuric acid

H
H
H
H
Below normal
H, P, Low normal


H
Low normal
H
H
H

2
2
4
2
2
1; Ahlström, Berglund and Berglund 1986; Schwartz et al. 1991; Bolla et al. 1995
4
2
2
2
1; Petersen and Gormsen 1991

Tanning
Tetrabromoethane
Tetrachloroethane
Tin fumes
Tobacco
Trichloroethane
Trichloroethylene

H
Parosmia, H or A
H
H
H
H
H/A

2
5
2
2
2; 4
2
2

Vanadium fumes
Varnishes

H
H

2
2

Wastewater

Low normal

2

Zinc (fumes, chromate) and production

Low normal

2

H = hyposmia; A = anosmia; P = parosmia; ID = odour identification ability

1 = Mott and Leopold 1991. 2 = Amoore 1986. 3 = Schiffman and Nagle 1992. 4 = Naus 1985. 5 = Callendar et al. 1993.

Specific smell disturbances are as stated in the articles referenced.

 

Nasal passages are ventilated by 10,000 to 20,000 litres of air per day, containing varying amounts of potentially harmful agents. The upper airways almost totally absorb or clear highly reactive or soluble gases, and particles larger than 2 mm (Evans and Hastings 1992). Fortunately, a number of mechanisms exist to protect tissue damage. Nasal tissues are enriched with blood vessels, nerves, specialized cells with cilia capable of synchronous movement, and mucus-producing glands. Defensive functions include filtration and clearing of particles, scrubbing of water soluble gases, and early identification of harmful agents through olfaction and mucosal detection of irritants that can initiate an alarm and removal of the individual from further exposure (Witek 1993). Low levels of chemicals are absorbed by the mucus layer, swept away by functioning cilia (mucociliary clearance) and swallowed. Chemicals can bind to proteins or be rapidly metabolized to less damaging products. Many metabolizing enzymes reside in the nasal mucosa and olfactory tissues (Bonnefoi, Monticello and Morgan 1991; Schiffman and Nagle 1992; Evans et al. 1995). Olfactory neuroepithelium, for example, contains cytochrome P-450 enzymes which play a major role in the detoxification of foreign substances (Gresham, Molgaard and Smith 1993). This system may protect the primary olfactory cells and also detoxify substances that would otherwise enter the central nervous system through olfactory nerves. There is also some evidence that intact olfactory neuroepithelium can prevent invasion by some organisms (e.g., cryptococcus; see Lima and Vital 1994). At the level of the olfactory bulb, there may also be protective mechanisms preventing transport of toxic substances centrally. For example, it has been recently shown that the olfactory bulb contains metallothioneins, proteins which have a protective effect against toxins (Choudhuri et al. 1995).

Exceeding protective capacities can precipitate a worsening cycle of injury. For example, loss of olfactory ability halts early warning of the hazard and allows continued exposure. Increase in nasal blood flow and blood vessel permeability causes swelling and odorant obstruction. Cilial function, necessary for both mucociliary clearance and normal smell, may be impaired. Change in clearance will increase contact time between injurious agents and nasal mucosa. Intranasal mucus abnormalities alter absorption of odorants or irritant molecules. Overpowering the ability to metabolize toxins allows tissue damage, increased absorption of toxins, and possibly enhanced systemic toxicity. Damaged epithelial tissue is more vulnerable to subsequent exposures. There are also more direct effects on olfactory receptors. Toxins can alter the turnover rate of olfactory receptor cells (normally 30 to 60 days), injure receptor cell membrane lipids, or change the internal or external environment of the receptor cells. Although regeneration can occur, damaged olfactory tissue can exhibit permanent changes of atrophy or replacement of olfactory tissue with nonsensory tissue.

The olfactory nerves provide a direct connection to the central nervous system and may serve as a route of entry for a variety of exogenous substances, including viruses, solvents and some metals (Evans and Hastings 1992). This mechanism may contribute to some of the olfactory-related dementias (Monteagudo, Cassidy and Folb 1989; Bonnefoi, Monticello and Morgan 1991) through, for example, transmittal of aluminium centrally. Intranasally, but not intraperitoneally or intracheally, applied cadmium can be detected in the ipsilateral olfactory bulb (Evans and Hastings 1992). There is further evidence that substances may be preferentially taken up by olfactory tissue irrespective of the site of initial exposure (e.g., systemic versus inhalation). Mercury, for example, has been found in high concentrations in the olfactory brain region in subjects with dental amalgams (Siblerud 1990). On electroencephalography, the olfactory bulb demonstrates sensitivity to many atmospheric pollutants, such as acetone, benzene, ammonia, formaldehyde and ozone (Bokina et al. 1976). Because of central nervous system effects of some hydrocarbon solvents, exposed individuals might not readily recognize and distance themselves from the danger, thereby prolonging exposure. Recently, Callender and colleagues (1993) obtained a 94% frequency of abnormal SPECT scans, which assess regional cerebral blood flow, in subjects with neurotoxin exposures and a high frequency of olfactory identification disorders. The location of abnormalities on SPECT scanning was consistent with distribution of toxin through olfactory pathways.

The site of injury within the olfactory system differs with various agents (Cometto-Muñiz and Cain 1991). For example, ethyl acrylate and nitroethane selectively damage olfactory tissue while the respiratory tissue within the nose is preserved (Miller et al. 1985). Formaldehyde alters the consistency, and sulphuric acid the pH of nasal mucus. Many gases, cadmium salts, dimethylamine and cigarette smoke alter ciliary function. Diethyl ether causes leakage of some molecules from the junctions between cells (Schiffman and Nagle 1992). Solvents, such as toluene, styrene and xylene change olfactory cilia; they also appear to be transmitted into the brain by the olfactory receptor (Hotz et al. 1992). Hydrogen sulphide is not only irritating to mucosa, but highly neurotoxic, effectively depriving cells of oxygen, and inducing rapid olfactory nerve paralysis (Guidotti 1994). Nickel directly damages cell membranes and also interferes with protective enzymes (Evans et al. 1995). Dissolved copper is thought to directly interfere with different stages of transduction at the olfactory receptor level (Winberg et al. 1992). Mercuric chloride selectively distributes to olfactory tissue, and may interfere with neuronal function through alteration of neurotransmitter levels (Lakshmana, Desiraju and Raju 1993). After injection into the bloodstream, pesticides are taken up by nasal mucosa (Brittebo, Hogman and Brandt 1987), and can cause nasal congestion. The garlic odour noted with organophosphorus pesticides is not due to damaged tissue, but to detection of butylmercaptan, however.

Although smoking can inflame the lining of the nose and reduce smell ability, it may also confer protection from other damaging agents. Chemicals within the smoke may induce microsomal cytochrome P450 enzyme systems (Gresham, Molgaard and Smith 1993), which would accelerate metabolism of toxic chemicals before they can injure the olfactory neuroepithelium. Conversely, some drugs, for example tricyclic antidepressants and antimalarial drugs, can inhibit cytochrome P450.

Olfactory loss after exposure to wood and fibre board dusts (Innocenti et al. 1985; Holmström, Rosén and Wilhelmsson 1991; Mott and Leopold 1991) may be due to diverse mechanisms. Allergic and nonallergic rhinitis can result in obstruction to odorants or inflammation. Mucosal changes can be severe, dysplasia has been documented (Boysen and Solberg 1982) and adenocarcinoma may result, especially in the area of the ethmoid sinuses near the olfactory neuroepithelium. Carcinoma associated with hard woods may be related to a high tannin content (Innocenti et al. 1985). Inability to effectively clear nasal mucus has been reported and may be related to an increased frequency of colds (Andersen, Andersen and Solgaard 1977); resultant viral infection could further damage the olfactory system. Olfactory loss may also be due to chemicals associated with woodworking, including varnishes and stains. Medium-density fibre board contains formaldehyde, a known respiratory tissue irritant that impairs mucociliary clearance, causes olfactory loss, and is associated with a high incidence of oral, nasal and pharyngeal cancer (Council on Scientific Affairs 1989), all of which could contribute to an understanding of formaldehyde-induced olfactory losses.

Radiation therapy has been reported to cause olfactory abnormalities (Mott and Leopold 1991), but little information is available about occupational exposures. Rapidly regenerating tissue, such as olfactory receptor cells, would be expected to be vulnerable. Mice exposed to radiation in a spaceflight demonstrated smell tissue abnormalities, while the rest of the nasal lining remained normal (Schiffman and Nagle 1992).

After chemical exposures, some individuals describe a heightened sensitivity to odorants. “Multiple chemical sensitivities” or “environmental illness” are labels used to describe disorders typified by “hypersensitivity” to diverse environmental chemicals, often in low concentrations (Cullen 1987; Miller 1992; Bell 1994). Thus far, however, lower thresholds to odorants have not been demonstrated.

Non-occupational causes of olfactory problems

Ageing and smoking decrease olfactory ability. Upper respiratory viral damage, idiopathic (“unknown”), head trauma, and diseases of the nose and sinuses appear to be the four leading causes of smell problems in the United States (Mott and Leopold 1991) and must be considered as part of the differential diagnosis in any individual presenting with possible environmental exposures. Congenital inabilities to detect certain substances are common. For example, 40 to 50% of the population can not detect androsterone, a steroid found in sweat.

Testing of chemosensation

Psychophysics is the measurement of a response to an applied sensory stimulus. “Threshold” tests, tests that determine the minimum concentration that can be reliably perceived, are frequently used. Separate thresholds can be obtained for detection of odorants and identification of odorants. Suprathreshold tests assess ability of the system to function at levels above threshold and also provide useful information. 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 odorants at usual threshold levels, but may not be able to identify common odorants.

Summary

The nasal passages are ventilated by 10,000 to 20,000 litres of air per day, which may be contaminated by possibly hazardous materials in varying degrees. The olfactory system is especially vulnerable to damage because of requisite direct contact with volatile chemicals for odorant perception. Olfactory loss, tolerance and adaptation prevent recognition of the proximity of dangerous chemicals and may contribute to local injury or systemic toxicity. Early identification of olfactory disorders can prompt protective strategies, ensure appropriate treatment and prevent further damage. Occupational smell disorders can manifest themselves as temporary or permanent anosmia or hyposmia, as well as distorted smell perception. Identifiable causes to be considered in the occupational setting include rhinitis, sinusitis, head trauma, radiation exposure and tissue injury from metallic compounds, metal dusts, nonmetallic inorganic compounds, organic compounds, wood dusts, and substances present in metallurgical and manufacturing processes. Substances differ in their site of interference with the olfactory system. Powerful mechanisms for trapping, removing and detoxifying foreign nasal substances serve to protect olfactory function and also prevent spread of damaging agents into the brain from the olfactory system. Exceeding protective capacities can precipitate a worsening cycle of injury, ultimately leading to greater severity of impairment and extension of sites of injury, and converting temporary reversible effects into permanent damage.

 

Back

Read 5403 times Last modified on Tuesday, 11 October 2011 21:04
More in this category: « Taste Cutaneous Receptors »

Contents

Preface
Part I. The Body
Blood
Cancer
Cardiovascular System
Digestive System
Mental Health
Musculoskeletal System
Nervous System
Renal-Urinary System
Reproductive System
Respiratory System
Sensory Systems
Resources
Skin Diseases
Systematic Conditions
Part II. Health Care
Part III. Management & Policy
Part IV. Tools and Approaches
Part V. Psychosocial and Organizational Factors
Part VI. General Hazards
Part VII. The Environment
Part VIII. Accidents and Safety Management
Part IX. Chemicals
Part X. Industries Based on Biological Resources
Part XI. Industries Based on Natural Resources
Part XII. Chemical Industries
Part XIII. Manufacturing Industries
Part XIV. Textile and Apparel Industries
Part XV. Transport Industries
Part XVI. Construction
Part XVII. Services and Trade
Part XVIII. Guides

Sensory Systems Additional Resources

Click the Button below to view additional resources for this topic.

button

Sensory Systems References

Adler, FH. 1992. Physiology of the Eye: Clinical Application. St. Louis: Mosby New York Books.

Adrian, WK. 1993. Visual Performance, Acuity and Age: Lux Europa Proceedings of the VIIth European Lighting Conference. London: CIBSE.

Ahlström, R, B Berglund, and U Berblund. 1986. Impaired odor perception in tank cleaners. Scand J Work Environ Health 12:574-581.

Amoore, JE. 1986. Effects of chemical exposure on olfaction in humans. In Toxicology of the Nasal Passages, edited by CS Barrow. Washington, DC: Hemisphere Publishing.

Andersen, HC, I Andersen, and J Solgard. 1977. Nasal cancers, symptoms and upper airway function in woodworkers. Br J Ind Med 34:201-207.

—. 1993. Otolaryngol Clin N Am 5(26).

Axéll, T, K Nilner, and B Nilsson. 1983. Clinical evaluation of patients referred with symptoms related to oral galvanism. Scand Dent J 7:169-178.

Ballantyne, JC and JM Ajodhia. 1984. Iatrogenic dizziness. In Vertigo, edited by MR Dix and JD Hood. Chichester: Wiley.

Bar-Sela, S, M Levy, JB Westin, R Laster, and ED Richter. 1992. Medical findings in nickel-cadmium battery workers. Israel J Med Sci 28:578-583.

Bedwal, RS, N Nair, and MP Sharma. 1993. Selenium-its biological perspectives. Med Hypoth 41:150-159.

Bell, IR. 1994. White paper: Neuropsychiatric aspects of sensitivity to low-level chemicals: A neural sensitization model. Toxicol Ind Health 10:277-312.

Besser, R, G Krämer, R Thümler, J Bohl, L Gutmann, and HC Hopf. 1987. Acute trimethyltin limbic cerebellar syndrome. Neurology 37:945-950.

Beyts, JP. 1987. Vestibular rehabilitation. In Adult Audiology, Scott-Brown’s Otolaryngology, edited by D Stephens. London: Butterworths.

Blanc, PD, HA Boushey, H Wong, SF Wintermeyer and MS Bernstein. 1993. Cytokines in metal fume fever. Am Rev Respir Dis 147:134-138.

Blount, BW. 1990. Two types of metal fume fever: mild vs. serious. Mil Med (Aug) 155(8):372-7

Bokina, AI, ND Eksler, and AD Semenenko. 1976. Investigation of the mechanism of action of atmospheric pollutants on the cenral nervous system and comparative evaluation of methods of study. Environ Health Persp 13:37-42.

Bolla, KI, BS Schwartz, and W Stewart. 1995. Comparison of neurobehavioral function in workers exposed to a mixture of organic and inorganic lead and in workers exposed to solvents. Am J Ind Med 27:231-246.

Bonnefoi, M, TM Monticello, and KT Morgan. 1991. Toxic and neoplastic responses in the nasal passages: Future research needs. Exp Lung Res 17:853-868.

Boysen, M and Solberg. 1982. Changes in the nasal mucosa of furniture workers. Scand J Work Environ Health :273-282.

Brittebo, EB, PG Hogman, and I Brandt. 1987. Epithelial binding of hexachlorocyclohexanes in the respiratory and upper alimentary tracts: A comparison between the alpha-, beta-, and gamma-isomers in mice. Food Chem Toxicol 25:773-780.

Brooks, SM. 1994. Host susceptibility to indoor air pollution. J Allergy Clin Immunol 94:344-351.

Callender, TJ, L Morrow, K Subramanian, D Duhon, and M Ristovv. 1993. Three-dimensional brain metabolic imaging in patients with toxic encephalopathy. Environmental Research 60:295-319.

Chia, SE, CN Ong, SC Foo, and HP Lee. 1992. Medical student’s exposure to formaldehyde in a gross anatomy dissection laboratory. J Am Coll Health 41:115-119.

Choudhuri, S, KK Kramer, and NE Berman. 1995. Constitutive expression of metallothionein genes in mouse brain. Toxicol Appl Pharmacol 131:144-154.

Ciesielski, S, DP Loomis, SR Mims, and A Auer. 1994. Pesticide exposures, cholinesterase depression, and symptoms among North Carolina migrant farmworkers. Am J Public Health 84:446-451.

Clerisi, WJ, B Ross, and LD Fechter. 1991. Acute ototoxicity of trialkyltins in the guinea pig. Toxicol Appl Pharmacol :547-566.

Coleman, JW, MR Holliday, and RJ Dearman. 1994. Cytokine-mast cell interactions: Relevance to IgE-mediated chemical allergy. Toxicology 88:225-235.

Cometto-Muñiz, JE and WS Cain. 1991. Influence of airborne contaminants on olfaction and the common chemical sense. In Smell and Taste in Health and Disease, edited by TV Getchell. New York: Raven Press.

—. 1994. Sensory reactions of nasal pungency and odor to volatile organic compounds: The alkylbenzenes. Am Ind Hyg Assoc J 55:811-817.

Corwin, J, M Loury, and AN Gilbert. 1995. Workplace, age, and sex as mediators of olfactory function: Data from the National Geographic Smell Survey. Journal of Gerontolgy: Psychiol Sci 50B:P179-P186.

Council on Dental Materials, Instruments and Equipment. 1987. American Dental Association status report on the occurence of galvanic corrosion in the mouth and its potential effects. J Am Dental Assoc 115:783-787.

Council on Scientific Affairs. 1989. Council report: Formaldehyde. JAMA 261:1183-1187.

Crampton, GH. 1990. Motion and Space Sickness. Boca Raton: CRC Press.

Cullen, MR. 1987. Workers with multiple chemical sensitivities. Occup Med: State Art Rev 2(4).

Deems, DA, RL Doty, and RG Settle. 1991. Smell and taste disorders, a study of 750 patients from the University of Pennsylvania Smell and Taste Center. Arch Otolaryngol Head Neck Surg 117:519-528.

Della Fera, MA, AE Mott, and ME Frank. 1995. Iatrogenic causes of taste disturbances: Radiation therapy, surgery, and medication. In Handbook of Olfaction and Gustation, edited by RL Doty. New York: Marcel Dekker.

Dellon, AL. 1981. Evaluation of Sensibility and Re-Education of Sensation in the Hand. Baltimore: Williams & Wilkins.

Dykes, RW. 1977. Sensory receptors. In Reconstructive Microsurgery, edited by RK Daniel and JK Terzis. Boston: Little Brown & Co.

El-Etri, MM, WT Nickell, M Ennis, KA Skau, and MT Shipley. 1992. Brain norepinephrine reductions in soman-intoxicated rats: Association with convulsions and AchE inhibition, time course, and relation to other monoamines. Experimental Neurology 118:153-163.

Evans, J and L Hastings. 1992. Accumulation of Cd(II) in the CNS depending on the route of administration: Intraperitoneal, intratracheal, or intranasal. Fund Appl Toxicol 19:275-278.

Evans, JE, ML Miller, A Andringa, and L Hastings. 1995. Behavioral, histological, and neurochemical effets of nickel(II) on the rat olfactory system. Toxicol Appl Pharmacol 130:209-220.

Fechter, LD, JS Young, and L Carlisle. 1988. Potentiation of noise induced threshold shifts and hair cell loss by carbon monoxide. Hearing Res 34:39-48.
Fox, SL. 1973. Industrial and Occupational Opthalmology. Springfield: Charles C. Thomas.

Frank, ME, TP Hettinger, and AE Mott. 1992. The sense of taste: Neurobiology, aging, and medication effects. Critical Reviews in Oral Biology Medicine 3:371-393.

Frank, ME and DV Smith. 1991. Electrogustometry: A simple way to test taste. In Smell and Taste in Health and Disease, edited by TV Getchell, RL Doty, and LM Bartoshuk. New York: Raven Press.

Gagnon, P, D Mergler, and S Lapare. 1994. Olfactory adaptation, threshold shift and recovery at low levels of exposure to methyl isobutyl ketone (MIBK). Neurotoxicology 15:637-642.

Gilbertson, TA. 1993. The physiology of vertebrate taste reception. Curr Opin Neurobiol 3:532-539.

Gordon, T and JM Fine. 1993. Metal fume fever. Occup Med: State Art Rev 8:505-517.

Gosselin, RE, RP Smith, and HC Hodge. 1984. Clinical Toxicology of Commercial Products. Baltimore: Williams & Wilkins.

Graham, CH, NR Barlett, JL Brown, Y Hsia, CG Mueller, and LA Riggs. 1965. Vision and Visual Perception. New York: John Wiley and Sons, Inc.

Grandjean, E. 1987. Ergonomics in Computerized Offices. London: Taylor & Francis.

Grant, A. 1979. Optical danger of fiberglass hardener. Med J Austral 1:23.

Gresham, LS, CA Molgaard, and RA Smith. 1993. Induction of cytochrome P-450 enzymes via tobacco smoke: A potential mechanism for developing resistance to environmental toxins as related to Parkinsonism and other neurologic disease. Neuroepidemiol 12:114-116.

Guidotti, TL. 1994. Occupational exposure to hydrogen sulfide in the sour gas industry: Some unresolved issues. Int Arch Occup Environ Health 66:153-160.

Gyntelberg, F, S Vesterhauge, P Fog, H Isager, and K Zillstorff. 1986. Acquired intolerance to organic solvents and results of vestibular testing. Am J Ind Med 9:363-370.

Hastings, L. 1990. Sensory neurotoxicology: use of the olfactory system in the assessment of toxicity. Neurotoxicology and Teratology 12:455-459.

Head, PW. 1984. Vertigo and barotrauma. In Vertigo, edited by MR Dix and JD Hood. Chichester: Wiley.

Hohmann, B and F Schmuckli. 1989. Dangers du bruit pour l’ouië et l’emplacement de travail. Lucerne: CNA.

Holmström, M, G Rosén, and B Wilhelmsson. 1991. Symptoms, airway physiology and histology of workers exposed to medium-density fiber board. Scand J Work Environ Health 17:409-413.

Hotz, P, A Tschopp, D Söderström, and J Holtz. 1992. Smell or taste disturbances, neurological symptoms, and hydrocarbon exposure. Int Arch Occup Environ Health 63:525-530.

Howard, IP. 1982. Human Visual Orientation. Chichester: Wiley.

Iggo, A and AR Muir. 1969. The structure and function of a slowly adapting touch corpuscle in hairy skin. J Physiol Lond 200(3):763-796.

Illuminating Engineering Society of North America (IESNA). 1993. Vision and perception. In Lighting Handbook: Reference and Application, edited by MS Rea and Fies. New York: IESNA.

Innocenti, A, M Valiani, G Vessio, M Tassini, M Gianelli, and S Fusi. 1985. Wood dust and nasal diseases: Exposure to chestnut wood dust and loss of smell (pilot study). Med Lavoro 4:317-320.

Jacobsen, P, HO Hein, P Suadicani, A Parving, and F Gyntelberg. 1993. Mixed solvent exposure and hearing impairment: An epidemiological study of 3284 men. The Copenhagen male study. Occup Med 43:180-184.

Johansson, B, E Stenman, and M Bergman. 1984. Clinical study of patients referred for investigation regarding so-called oral galvanism. Scand J Dent Res 92:469-475.

Johnson, A-C and PR Nylén. 1995. Effects of industrial solvents on hearing. Occup Med: State of the art reviews. 10:623-640.

Kachru, DM, SK Tandon, UK Misra, and D Nag. 1989. Occupational lead poisoning among silver jewelry workers. Indian Journal of Medical Sciences 43:89-91.

Keele, CA. 1964. Substances Producing Pain and Itch. London: Edward Arnold.

Kinnamon, SC and TV Getchell. 1991. Sensory transduction in olfactory receptor neurons and gustatory receptor cells. In Smell and Taste in Health and Disease, edited by TV Getchell, RL Doty, and LM Bartoshuk. New York: Raven Press.

Krueger, H. 1992. Exigences visuelles au poste de travail: Diagnostic et traitement. Cahiers
médico-sociaux 36:171-181.

Lakshmana, MK, T Desiraju, and TR Raju. 1993. Mercuric chloride-induced alterations of levels of noradrenaline, dopamine, serotonin and acetylcholine esterase activity in different regions of rat brain during postnatal development. Arch Toxicol 67:422-427.

Lima, C and JP Vital. 1994. Olfactory mucosa response in guinea pigs following intranasal instillation with Cryptococcus neoformans: A histological and immunocytochemical study. Mycopathologia 126:65-73.

Luxon, LM. 1984. The anatomy and physiology of the vestibular system. In Vertigo, edited by MR Dix and JD Hood. Chichester: Wiley.

MacKinnon, SE and AL Dellon. 1988. Surgery of the Peripheral Nerve. New York: Thieme Medical Publishers.

Marek, J-J. 1993. The molecular biology of taste transduction. Bioessays 15:645-650.

Marek, M. 1992. Interactions between dental amalgams and the oral environment. Adv Dental Res 6:100-109.

Margolskee, RF. 1993. The biochemistry and molecular biology of taste transduction. Curr Opin Neurobiol 3:526-531.

Martin, JH. 1985. Receptor physiology and submodality coding in the somatic sensory system. Principles of Neuroscience, edited by ER Kandel and JH Schwartz.

Meyer, J-J. 1990. Physiologie de la vision et ambiance lumineuse. Document de l’Aerospatiale, Paris.

Meyer, J-J, A Bousquet, L Zoganas and JC Schira. 1990. Discomfort and disability glare in VDT operators. In Work with Display Units 89, edited by L Berlinguet and D Berthelette. Amsterdam: Elsevier Science.

Meyer, J-J, P Rey, and A Bousquet. 1983. An automatic intermittent light stimulator to record flicker perceptive thresholds in patients with retinal disease. In Advances in Diagnostic Visual Optics, edited by GM Brenin and IM Siegel. Berlin: Springer-Verlag.

Meyer, J-J, P Rey, B Thorens, and A Beaumanoire. 1971. Examen de sujets atteints d’un traummatisme cranio-cérébral par un test perception visuelle: courbe de Lange. Swiss Arch of Neurol 108:213-221.

Meyer, J-J, A Bousquet, JC Schira, L Zoganas, and P Rey. 1986. Light sensitivity and visual strain when driving at night. In Vision in Vehicles, edited by AG Gale. Amsterdam: Elsevier Science Publisher.

Miller, CS. 1992. Possible models for multiple chemical sensitivity: conceptual issues and role of the limbic system. Toxicol Ind Health 8:181-202.

Miller, RR, JT Young, RJ Kociba, DG Keyes, KM Bodner, LL Calhoun, and JA Ayres. 1985. Chronic toxicity and oncogenicity bioassay of inhaled ethyl acrylate in fischer 344 rats and B6C3F1 mice. Drug Chem Toxicol 8:1-42.

Möller, C, L Ödkvist, B Larsby, R Tham, T Ledin, and L Bergholtz. 1990. Otoneurological finding among workers exposed to styrene. Scand J Work Environ Health 16:189-194.

Monteagudo, FSE, MJD Cassidy, and PI Folb. 1989. Recent developments in aluminum toxicology. Med Toxicol 4:1-16.

Morata, TC, DE Dunn, LW Kretschmer, GK Lemasters, and RW Keith. 1993. Effects of occupational exposure to organic solvents and noise on hearing. Scand J Work Environ Health 19:245-254.

Mott, AE, M Grushka, and BJ Sessle. 1993. Diagnosis and management of taste disorders and burning mouth syndrome. Dental Clinics of North America 37:33-71.

Mott, AE and DA Leopold. 1991. Disorders in taste and smell. Med Clin N Am 75:1321-1353.

Mountcastle, VB. 1974. Medical Physiology. St. Louis: CV Mosby.

Mountcastle, VB, WH Talbot, I Darian-Smith, and HH Kornhuber. 1967. Neural basis of the sense of flutter-vibration. Science :597-600.

Muijser, H, EMG Hoogendijk, and J Hoosima. 1988. The effects of occupational exposure to styrene on high-frequency hearing thresholds. Toxicology :331-340.

Nemery, B. 1990. Metal toxicity and the respiratory tract. Eur Respir J 3:202-219.

Naus, A. 1982. Alterations of the smell acuity caused by menthol. J Laryngol Otol 82:1009-1011.

Örtendahl, TW. 1987. Oral changes in divers working with electrical welding/cutting underwater. Swedish Dent J Suppl 43:1-53.

Örtendahl, TW, G Dahlén, and HOE Röckert. 1985. The evaluation of oral problems in divers performing electrical welding and cutting under water. Undersea Biomed Res 12:55-62.

Ogawa, H. 1994. Gustatory cortex of primates: Anatomy and physiology. Neurosci Res 20:1-13.

O’Reilly, JP, BL Respicio, and FK Kurata. 1977. Hana Kai II: A 17-day dry saturation dive at 18.6 ATA. VII: Auditory, visual and gustatory sensations. Undersea Biomed Res 4:307-314.

Otto, D, G Robinson, S Bauman, S Schroeder, P Mushak, D Kleinbaum, and L Boone. 1985. %-years follow-up study of children with low-to-moderate lead absorption: Electrophysiological evaluation. Environ Research 38:168-186.

Oyanagi, K, E Ohama, and F Ikuta. 1989. The auditory system in methyl mercurial intoxication: A neuropathological investigation on 14 autopsy cases in Niigata, Japan. Acta Neuropathol 77:561-568.

Participants of SCP Nos. 147/242 and HF Morris. 1990. Veterans administration cooperative studies project no. 147: Association of metallic taste with metal ceramic alloys. J Prosthet Dent 63:124-129.

Petersen, PE and C Gormsen. 1991. Oral conditions among German battery factory workers. Community Dentistry and Oral Epidemiology 19:104-106.

Pfeiffer, P and H Schwickerath. 1991. Nickel solubility and metallic taste. Zwr 100:762-764,766,768-779.

Pompeiano, O and JHJ Allum. 1988. Vestibulospinal Control of Posture and Locomotion. Progress in Brain Research, no.76. Amsterdam: Elsevier.

Rees, T and L Duckert. 1994. Hearing loss and other otic disorders. In Textbook of Clinical, Occupational and Environmental Medicine, edited by C Rosenstock. Philadelphia: WB Saunders.

Ressler, KJ, SL Sullivan, and LB Buck. 1994. A molecular dissection of spatial patterning in the olfactory system. Curr Opin Neurobiol 4:588-596.

Rey, P. 1991. Précis De Medecine Du Travail. Geneva: Medicine et Hygiène.

Rey, P and A Bousquet. 1990. Medical eye examination strategies for VDT operators. In Work With Display Units 89, edited by L Berlinguet and D Berthelette. Amsterdam: Elsevier Science.

Rose, CS, PG Heywood, and RM Costanzo. 1934. Olfactory impairment after chronic occupational cadmium exposure. J Occup Med 34:600-605.

Rubino, GF. 1990. Epidemiologic survey of ocular disorders: The Italian multicentric research. In Work with Display Units 89, edited by L Berlinguet and D Berthelette. Amsterdam: Elsevier Science Publishers B.V.

Ruth, JH. 1986. Odor thresholds and irritation levels of several chemical substances: A review. Am Ind Hyg Assoc J 47:142-151.

Rusznak, C, JL Devalia, and RJ Davies. 1994. The impact of pollution on allergic disease. Allergy 49:21-27.

Ryback, LP. 1992. Hearing: The effects of chemicals. Otolaryngology-Head and Neck Surgery 106:677-686.

—. 1993. Ototoxicity. Otolaryngol Clin N Am 5(26).

Savov, A. 1991. Damages to the ears, nose and throat in copper production. Problemi na Khigienata 16:149-153.

—. 1994. Changes in taste and smell: Drug interactions and food preferences. Nutr Rev 52(II):S11-S14.

Schiffman, SS. 1994. Changes in taste and smell: Drug interactions and food preferences. Nutr Rev 52(II): S11-S14.

Schiffman, SS and HT Nagle. 1992. Effect of environmental pollutants on taste and smell. Otolaryngology-Head and Neck Surgery 106:693-700.

Schwartz, BS, DP Ford, KI Bolla, J Agnew, and ML Bleecker. 1991. Solvent-associated olfatory dysfunction: Not a predictor of deficits in learning and memory. Am J Psychiatr 148:751-756.

Schweisfurth, H and C Schottes. 1993. Acute intoxication of a hydrazine-like gas by 19 workers in a garbage dump. Zbl Hyg 195:46-54.

Shusterman, D. 1992. Critical review: The health significance of environmental odor pollution. Arch Environ Health 47:76-87.

Shusterman, DJ and JE Sheedy. 1992. Occupational and environmental disorders of the special senses. Occup Med: State Art Rev 7:515-542.

Siblerud, RL. 1990. The relationship between mercury from dental amalgam and oral cavity health. Ann Dent 49:6-10.

Sinclair. 1981. Mechanisms of Cutaneous Sensation. Oxford: Oxford Univ. Press.

Spielman, AI. 1990. Interaction of saliva and taste. J Dental Res 69:838.

Stevens, JC and WS Cain. 1986. Aging and the perception of nasal irritation. Physiol Behav 37:323-328.

van Dijk, FJH. 1986. Non-auditory effects of noise in industry. II A review of the literature. Int Arch Occup Environ Health 58.

Verriest, G and G Hermans. 1975. Les aptitudes visuelles professionnelles. Bruxelles: Imprimerie médicale et scientifique.

Welch, AR, JP Birchall, and FW Stafford. 1995. Occupational rhinitis - Possible mechanisms of pathogenesis. J Laryngol Otol 109:104-107.

Weymouth, FW. 1966. The eye as an optical instrument. In Physiology and Biophysics, edited by TC Ruch and HD Patton. London: Saunders.

Wieslander, G, D Norbäck, and C Edling. 1994. Occupational exposure to water based paint and symptoms from the skin and eyes. Occup Environ Med 51:181-186.

Winberg, S, R Bjerselius, E Baatrup, and KB Doving. 1992. The effect of Cu(II) on the electro-olfactogram (EOG) of the Atlantic salmon (Salmo salar L) in artificial freshwater of varying inorganic carbon concentrations. Ecotoxicology and Environmental Safety 24:167-178.

Witek, TJ. 1993. The nose as a target for adverse effects from the environment: Applying advances in nasal physiologic measurements and mechanisms. Am J Ind Med 24:649-657.

World Health Organization (WHO). 1981. Arsenic. Environmental Health Criteria, no.18. Geneva: WHO.

Yardley, L. 1994. Vertigo and Dizziness. London: Routledge.

Yontchev, E, GE Carlsson, and B Hedegård. 1987. Clinical findings in patients with orofacial discomfort complaints. Int J Oral Maxillofac Surg 16:36-44.