Review: Nasal toxicity, carcinogenicity, and olfactory uptake of metals

Occupational exposures to inhalation of certain metal dusts or aerosols can cause loss of olfactory acuity, atrophy of the nasal mucosa, mucosal ulcer s, perforated nasal septum, or sinonasal cancer. Anosmia and hyposmia have been observed in workers exposed to Ni- or Cd-containing dusts in alkaline battery factories, nickel refineries, and cadmium industries. Ulcers of the nasal mucosa and perforated nasal septum have been reported in workers exp osed to Cr(VI) in chromate production and chrome plating, or to As(III) in arsenic smelters. Atrophy of the olfactory epithelium has been observed in rodents following inhalation of NiSO4 or alpha Ni3S2. Cancers of the nose a nd nasal sinuses have been reported in workers exposed to Ni compounds in n ickel refining, cutlery factories, and alkaline battery manufacture, or to Cr(VI) in chromate production and chrome plating. III animals, several meta ls (eg, Al, Cd, Co, Hg, Mn, Ni, Zn) have been shown to pass via olfactory r eceptor neurons from the nasal lumen through the cribriform plate to the ol factory bulb. Some metals (eg. Mn, Ni, Zn) can cross synapses in the olfact ory bulb and migrate via secondary olfactory neurons to distant nuclei of t he brain. After nasal instillation of a metal-containing solution, transpor t of the metal via olfactory axons can occur rapidly within hours or a few days (eg, Mn), or slowly other days or weeks (eg, Ni). The olfactory bulb t ends to accumulate certain metals (eg, Al, Bi, Cu, Mn, Zn) with greater avi dity than other regions of the brain. The molecular mechanisms responsible for metal translocation in olfactory neurons and deposition in the olfactor y bulb are unclear, but complexation by metal-binding molecules such as car nosine (beta -alanyl-L-histidine) may be involved.