Which industrial chemicals cause toxic neuropathy?

Updated: Dec 06, 2017
  • Author: Jonathan S Rutchik, MD, MPH, FACOEM; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS  more...
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Answer

Industrial chemicals causing toxic axonal neuropathy also are listed by Kimura; they include the following [6, 7] :

  • Acrylamide

  • Carbon disulfide

  • Inorganic mercury

  • Methyl n -butyl ketone

  • Parathion

  • Polychlorinated biphenyl

  • Thallium

  • Triorthocresyl phosphate

  • Vinyl chloride

In 1999, Feldman added the heavy metals arsenic and lead, as well as the solvents n -hexane, perchloroethylene (PERC), and TCE to this list. [10] In 1995, Albers and Bromberg summarized the literature on toxic neuropathy caused by the solvents ethylene oxide (EtO), styrene, toluene, and mixed solvents. [11]

Spencer and Schaumberg listed agents that commonly are associated with peripheral neuropathy (see Table 2 in Schaumberg, 2000 [12] ).

Toxic neuropathy may be the result of exposure to numerous agents and is related to dose and duration of exposures and to host factors. Most syndromes are subacute, progressing to chronic as already described. Chemicals such as thallium, dimethylaminopropionitrile (DMAP), and organophosphates (eg, parathion) produce specific syndromes associated with peripheral neuropathy; however, all of these may lead to systemic abnormalities as well.

Thallium is used in glass and in metal alloys. It had been used therapeutically to treat venereal disease, tuberculosis, and ringworm. It has also been used as a rodenticide. Accidental or homicidal abuse is a common reason for toxicity.

Acute thallium intoxication leads to pain and paresthesias in the distal extremities followed by weakness and eventual atrophy. Preservation of peripheral reflexes is a useful physical finding to differentiate thallium toxicity from Guillain-Barré syndrome. Alopecia is a clinical hallmark of thallium toxicity that may develop weeks after intoxication. Mee lines, nephropathy, anemia, and hepatotoxicity are systemic manifestations. Autonomic dysfunction also may be a part of the clinical syndrome. Thallium toxicity may be mistaken for porphyria, arsenic toxicity, or botulism. Serum thallium levels typically are elevated.

DMAP is used as a catalyst in the manufacture of polyurethane foam and in an acrylamide grouting compound. It is used as a waterproofing agent in tunnels and sewer lines. Industrial exposure has led to prominent urinary and sexual dysfunction as well as to distal sensory neuropathy.

Alcohol, by itself, is toxic to the PNS. Individuals who consume alcohol also may become nutritionally compromised. Studies have found that alcohol impairs axonal transport and that this can occur in the setting of normal nutrition. Since it may affect both the cerebellum and the autonomic nervous system, ataxia and other systemic symptoms may accompany symptoms of dysesthesia and weakness of the lower extremities. In the patient with occupational exposure to other peripheral neurotoxic agents, alcohol may act either to slow metabolism and increase toxicity or, in the case of a habitual alcohol user, promote metabolism and reduce toxicity from the agent. This is observed most clearly with toluene exposure.

A number of studies have attempted to address the type of neuropathy that occurs with alcohol exposure, as well as what amount of exposure is required before neuropathy occurs. A sensorimotor axonopathy with secondary demyelination that was not necessarily related to a deficit in thiamine was described by Mellion et al in 2011. [13] Ten ounces of whiskey per day in a 70-kg man for several years was mentioned to cause alcohol neuropathy. [14] Three liters of beer per day for 3 years was described as another threshold. [15] Wine in combination with other forms of ethanol was deemed worse, possibly due to impurities with lead. [16]

Other organic solvents have been associated with peripheral neuropathy on the basis of cross-sectional studies and animal data. Prospective data are unavailable. Solvent mixtures have been noted to be responsible for toxic neuropathies in many studies. Identifying the culpable agent has been difficult. Often, no chemical with a clear association with neuropathy is listed, suggesting that organic solvents themselves, either in mixture or individually, may cause neuropathy. Studies that have found subclinical abnormalities further support this hypothesis.

Often, study designs have been criticized for their definition of neuropathy. NCV and EMG findings in many of these studies are difficult to categorize. To ascertain whether a toxic etiology is a possibility for a patient, a clinician may need to search the literature for the agent as well as the industry. Many agents are used in many different industries. The industrial agents and some of the industries that utilize them are listed in Table 3. For information on toxic neuropathy caused by organophosphates, refer to the article Organophosphates.


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