Subject(s)
Depressive Disorder/chemically induced , Methyl n-Butyl Ketone/poisoning , Occupational Diseases/chemically induced , Occupational Exposure , Substance-Related Disorders/physiopathology , Vitamin B 12/physiology , Adult , Depressive Disorder/physiopathology , Humans , Male , Occupational Diseases/physiopathologySubject(s)
Behavior/drug effects , Environmental Health , Toxicology , Air Pollutants/adverse effects , Animals , Carbon Disulfide/poisoning , Child, Preschool , Developmental Disabilities/chemically induced , Female , Humans , Infant , Lead Poisoning/psychology , Mercury Poisoning/diagnosis , Methyl n-Butyl Ketone/poisoning , Methylmercury Compounds/poisoning , Neuromuscular Diseases/chemically induced , Occupational Diseases/diagnosis , Pesticides/adverse effects , Pregnancy , Prenatal Exposure Delayed Effects , Psychology , Rats , Social Class , Substance-Related Disorders/physiopathology , TolueneABSTRACT
Human exposure to hexacarbon compounds is quite pervasive, including occupational exposures to industrial solvents as well as unintentional and sometimes deliberate exposures to hexacarbon solvents contained in innumerable commercial products. The exact mechanism of hexacarbon neurotoxicity has not yet been identified, but an interference with neuronal axoplasmic flow seems most likely. Metabolism of n-hexane and 2-hexanone to 2,5-hexanedione is a prominent feature which appears to be causally related to the neuropathologic syndrome, and mixed solvent effects have been noted in regard to potentiation of hexacarbon neurotoxicity. Continued effort in investigating the chemically induced peripheral neuropathy is essential not only to define the precise molecular mechanism, but to advance our basic understanding of other polyneuropathies as well. Ultimately, progress in these areas should yield such benefits as early diagnosis of potential neuropathology, better measures for the prevention of neurotoxicities, and more effective modalities of treatment. Indeed, sustained research efforts are imperative in maintaining human health and safety throughout our current era of advancing global technology.
Subject(s)
Hexanes/poisoning , Hexanones/poisoning , Ketones/poisoning , Methyl n-Butyl Ketone/poisoning , Nervous System Diseases/chemically induced , Occupational Diseases/chemically induced , Animals , Biotransformation , Drug Synergism , Hexanes/metabolism , Hexanones/metabolism , Humans , Lethal Dose 50 , Methyl n-Butyl Ketone/metabolism , Rats , Solvents/poisoningABSTRACT
In West Berlin in the autumn of 1975 through the following 5 months we observed 18 juvenile patients who had a toxic polyneuropathy and had sniffed a glue thinner. The neurological picture consisted of a symmetrical, progressive, ascending, mainly motor, polyneuropathy with pronounced muscle atrophy and characteristic vegetative alterations. The height of the disease was reached after 1 1/2-2 1/2 months and was characterized by tetraplegia in 7 patients. After 8 months all patients still had a motor deficit. Nerve biopsy showed paranodal axon swelling, dense masses of neurofilaments and secondary myelin retraction. The neurological and morphological data correspond to the "glue sniffer's neuropathy" and the n-hexane and MBK polyneuropathy after industrial exposure, as described in 10 cases to date. However, there was no MBK in the glue thinner. The polyneuropathies occurred in close time relation with the denaturation of the thinner with MEK (2-butanone). It is concluded from the data n-hexane and MBK have a common toxic mechanism with primary axonal changes and that there is an additional synergistic effect of MEK.
