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CASE REPORTS
JOURNAL ARTICLE
Severe neurotoxicity associated with exposure to the solvent 1-bromopropane (n-propyl bromide).
Clinical Toxicology 2007
BACKGROUND: 1-bromopropane was recently substituted for traditional ozone-depleting solvents in the industrial setting.
CASE SERIES: We report a cohort of six cases of 1-bromopropane neurotoxicity occurring in foam cushion gluers exposed to 1-bromopropane vapors from spray adhesives. Patients 1-5 were exposed 30-40 hours per week over three years; patient 6 had been employed for the previous three months. Exposure had peaked over the previous month when ventilatory fans were turned off. All patients complained of subacute onset of lower extremity pain or paresthesias. Five of six complained of difficulty walking and on examination had spastic paraparesis, distal sensory loss, and hyperreflexia. Three patients initially had nausea and headache. Serum bromide concentrations ranged from 44 to 170 mg/dL (reference 0-40 mg/dL). Apparent hyperchloremia was present with serum chloride concentrations of 105 to 139 mmol/L (reference 98-107 mmol/L). Air samples taken at the workplace during gluing operations revealed the mean air concentration of 1-bromopropane to be 130 ppm (range 91-176 ppm) with a seven hour time-weighted average of 108 ppm (range 92-127 ppm), well above the EPA-proposed limit of 25 ppm. Two years after exposure, the two most severely affected patients had minimal improvement of function and they, with a third patient, continued to experience chronic neuropathic pain.
CONCLUSION: This report supports the growing recognition of 1-bromopropane neurotoxicity in humans consisting most commonly of headache, nausea, and subacute spastic paraparesis with distal sensory loss. The pathogenesis of 1-BP neurotoxicity in humans has yet to be fully elucidated but may reflect a central distal axonopathy syndrome.
CASE SERIES: We report a cohort of six cases of 1-bromopropane neurotoxicity occurring in foam cushion gluers exposed to 1-bromopropane vapors from spray adhesives. Patients 1-5 were exposed 30-40 hours per week over three years; patient 6 had been employed for the previous three months. Exposure had peaked over the previous month when ventilatory fans were turned off. All patients complained of subacute onset of lower extremity pain or paresthesias. Five of six complained of difficulty walking and on examination had spastic paraparesis, distal sensory loss, and hyperreflexia. Three patients initially had nausea and headache. Serum bromide concentrations ranged from 44 to 170 mg/dL (reference 0-40 mg/dL). Apparent hyperchloremia was present with serum chloride concentrations of 105 to 139 mmol/L (reference 98-107 mmol/L). Air samples taken at the workplace during gluing operations revealed the mean air concentration of 1-bromopropane to be 130 ppm (range 91-176 ppm) with a seven hour time-weighted average of 108 ppm (range 92-127 ppm), well above the EPA-proposed limit of 25 ppm. Two years after exposure, the two most severely affected patients had minimal improvement of function and they, with a third patient, continued to experience chronic neuropathic pain.
CONCLUSION: This report supports the growing recognition of 1-bromopropane neurotoxicity in humans consisting most commonly of headache, nausea, and subacute spastic paraparesis with distal sensory loss. The pathogenesis of 1-BP neurotoxicity in humans has yet to be fully elucidated but may reflect a central distal axonopathy syndrome.
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