xRead - Olfactory Disorders (September 2023)

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INTERNATIONAL CONSENSUS ON OLFACTION

for patients presenting with idiopathic smell disorders. 319 Agents that have been associated with OD include met als (cadmium, manganese, chromium, arsenic, lead, mer cury, aluminum, and nickel), organic compounds (butyl acetate, benzene, and benzyl acetate), industrial agents (paint solvents, styrene, and toluene), dusts (cement and hardwood), and nonmetal inorganic compounds (methyl bromide, hydrogen sulfide, and chlorine). 320 Metal exposure occurs in the form of metal dust or vapors. 321 Of the metals, cadmium is the most commonly known to cause olfactory impairment, as this metal targets the first olfactory neuron. 320,322 Cadmium is used in the production of storage batteries and can be present in the environment through waste incineration, sewage, and fertilizers. 323 Previous studies have found a higher prevalence of smell loss and higher olfactory thresholds in cadmium-exposed workers compared with controls, which is directly related with the years of exposure. 322,324–330 Exposure to manganese, another metal, is also asso ciated with OD. 331–335 Inhaled manganese is absorbed by the olfactory neurons and transported from the OB to the olfactory cortex. 336 In manganese-exposed ferroal loy plant workers, high urinary manganese was associ ated with worsened odor detection thresholds. 335 How ever, in professional welders exposed to manganese, work ers with the highest manganese blood levels exhibited bet ter OF than those with the lowest levels. 326 Whether this effect is transitory before decompensation of the OF is unknown. 333 Styrene is a solvent used in the plastic industry that has been associated with atrophy of the OE in mice. 337 How ever, in humans, a study of chronically exposed workers to styrene showed no differences in the phenylethyl alco hol detection threshold and odor identification compared with controls. 338 Interestingly, the exposed workers did have exposure-induced olfactory adaptation with elevated thresholds to the exposed odor, which is known as “indus trial anosmia.” A variety of industrial solvents and solvent mixtures that contain hydrocarbons have been associated with olfactory impairment. Hydrocarbons can be present in cleaning products, paints, and in printing and plastic manufacturing, among other products. 339–344 In a cross sectional study, respondents with exposure to vapors such as paints, cleaning products, glues, solvents, acids, and welding/soldering fumes were more likely to have experi enced olfactory disturbance in the previous 12 months. 333 In past studies, workers in plastic manufacturing had decreased olfactory threshold scores but not in odor iden tification scores. 345 In a cross-sectional study of Korean workers in automobile repair, printing, shoemaking, and plating industries, all had a higher prevalence of OD com pared with office workers. 346

Trauma to the nasal passages and conductive path ways can block airflow and impair OF. Biopsy findings of patients with trauma-related anosmia have revealed injury to the OR cells and cilia. 304 Fractures including fronto orbital and Le Fort fractures have been associated with posttraumatic smell loss. In a study of 5000 patients with injuries to the head or face, 305 olfactory impairment was found in 44.8% of those with facial or skull fractures and 11.3% of those with fractures of the nasal bones. A common sequela of head injury is damage to the olfac tory nerves, even in mild cases of head injury. 306 Backand forth movement of the brain (coup-contrecoup forces) gen erated in blows to the head can tear or cause injury to the delicate olfactory nerve fibers as they pass through the crib riform plate and connect with the OBs. 307,308 Cortical injuries resulting from head trauma, including contusions and bleeding, may result in anosmia, hypos mia, parosmia, or phantosmia. The type of smell loss depends on the brain regions involved. 309 Yousem et al 310 studied primary sites of injury in patients with posttrau matic anosmia and hyposmia. Using MRI they found the highest incidence of posttraumatic encephalomalacia was in the OB and olfactory tracts, subfrontal lobes, and tem poral lobes. In a study of 176 combat-blast injuries, 35% of patients with olfactory loss had abnormal findings on brain imaging. 311 Skull base fractures are likely to injure the olfactory nerves and result in complete anosmia. 301 Blows to the back of the head are more likely to result in olfactory loss than blows to the front. 305,312,313 Sports injuries also play a role in olfactory loss. In a study com paring American football players and controls, 17% of the football players had olfactory losses attributed to either a single traumatic brain injury or multiple traumatic brain injuries. 314 Olfactory loss increases with severity of injury, defined by posttraumatic amnesia, 313 Glasgow Coma Scale (GCS), or mild, moderate or severe head injury. 302,315,316 Children with mild head trauma were found to have lower OF scores than an age matched control group. 317 Lower GCS scores in children also correlate with poor perfor mance on olfactory tests. 318 OD can be caused by head trauma. Aggregate grade of evidence : C (Level 3: one study; Level 4: 10 studies).

D Related to toxin exposure: environmental or work-related

The true prevalence of olfactory impairment related to occupational exposure to chemicals is unknown, with a likely frequency of 0.5% to 5% of all OD. 319 There is high likelihood that occupational exposure is underdiagnosed