Methyl n-Butyl Ketone

01/01/1991 - "Methyl n-butyl ketone (MBK) was considered rather harmless until an outbreak of peripheral neuropathy occurred in 1973 among workers exposed to MBK. "
11/15/1974 - "Peripheral neuropathy associated with inhalation of methyl-n-butyl ketone."
07/01/1989 - "2. Peripheral neuropathy is mainly associated with n-hexane and methyl n-butyl ketone. "
04/05/1976 - "It has been suggested that the solvent methyl N-butyl ketone (MBK) may cause peripheral neuropathy in humans. "
06/01/2014 - "Mercury, TCE, methyl n-butyl ketone, acrylamide, and arsenic were newly included in peripheral neuropathy. "

10/01/1976 - "Symmetrical polyneuropathy developed in two patients after they had been in contact with acrylamide and methyl n-butyl ketone, respectively. "
05/01/1976 - "Toxic polyneuropathy secondary to methyl n-butyl ketone."
04/01/1976 - "Letter: Toxic polyneuropathy due to methyl n-butyl ketone."
04/01/1975 - "Toxic polyneuropathy due to methyl n-butyl ketone. "
08/30/1974 - "Toxic polyneuropathy produced by methyl N-butyl ketone."

09/09/1977 - "Methyl n-butyl ketone (MBK) is known to produce a giant axonal neuropathy in man and experimental animals characterized pathologically by a gradual increase in the number of neurofilaments which become associated with focal areas of axonal swelling and thinning of the myelin sheath. "
11/01/1983 - "Axonal swellings associated with large aggregates of neurofilaments are characteristic of neuropathies caused by chemical neurotoxins (n-hexane, methyl n-butyl ketone, and acrylamide) or giant axonal neuropathy (GAN--an autosomal recessive genetic disease). "

11/01/1983 - "Axonal swellings associated with large aggregates of neurofilaments are characteristic of neuropathies caused by chemical neurotoxins (n-hexane, methyl n-butyl ketone, and acrylamide) or giant axonal neuropathy (GAN--an autosomal recessive genetic disease). "

01/01/2022 - "Specifically, knocking down individual palp odorant receptors (ORs) such as OR17, OR21, and OR22 attenuated the vomiting intensity evoked by E-2-hexenal and hexanal, while suppression of OR12 and OR22 augmented vomiting to E-2-hexenal and 2-hexanone, respectively. "