Effect of oral hygiene instructions given by paraprofessional personnel.

A study was undertaken in order to test the effect of hygiene instructions given by specially trained chair-side assistants and to test the value of depuration prior to instructions. Chair-side assistants were trained to motivate and instruct patients in oral hygiene methods. The 71 participants (12 female and 59 male employees of the same industrial firm) were divided into three groups. Group C received depuration (one visit) prior to oral hygiene instruction, Group B hygiene instructions only, and Group A depuration only. Following instructions, the participants were examined after 4, 12 and 24 weeks with respect to: DMFT, Gingival Index, Retention Index, plaque surface and periodontal pockets greater than or equal to 4 mm. The results showed a reduction in plaque surfaces from baseline to 24 weeks in Groups B and C of 67% and 70% (difference not significant). Slight improvement was noted in Group A. Significant improvement was also observed in Gingival Index scores and pocket depths. Significant differences were not found between the groups with respect to Retention Index scores. Smoking did not influence the program. The effects of instructions were retained after 6 months. It is concluded that the use of this kind of personnel is highly effective and expedient, and that the present model can be useful in preventive dental health work.

Biotransformation of n-hexane and methyl n-butyl ketone in guinea pigs and mice.

Peripheral neuropathies caused by exposures to the industrial solvents n-hexane and MBK exhibit strinkingly similar characteristics. In in vivo studies, the metabolites of MBK and n-hexane identified in blood and urine of guinea pigs were 2-hexanol (partly as glucuronide in urine); and 2,5-hexanedione which was detected only in MBK treated groups. Phenobarbital pretreatment increased 2-hexanol urinary excretion in both solvent treatment groups. In in vitro studies, hepatic reduction of MBK required the cytosol fraction to form 2-hexanol; whereas the oxidation of MBK and n-hexane required the microsomal fraction to form 2,5-hexanedione and 2-hexanol, respectively. The in vivo and in vitro biotransformation of MBK and n-hexane to a common metabolite (2-hexanol) suggests that the neurotoxic action of these solvents may be metabolite related.

Toxicity and metabolism of methyl n-butyl ketone.

MEK (2-butanone) when combined with MBK (2-hexanone) markedly enhanced MBK neurotoxicity. MBK in rat plasma after exposure to MBK/MEK increased with time. Metabolites of MBK identified in blood and urine of rats and guinea pigs were 2-hexanol and 2,5-hexanedione.

Toxic polyneuropathy produced by methyl N-butyl ketone.

A polyneuropathy affecting a large number of workers was recently observed at a plant producing plastic-coated and color-printed fabrics. Epidemiological data suggested strongly that methyl N-butyl ketone (MBK) was responsible for the outbreak. This hypothesis is now supported by the development of a peripheral neuropathy in chickens, rats, and cats exposed to MBK at atmospheric concentrations of 200 to 600 parts per million, 24 hours per day, 7 days per week. Although the animals were exposed continuously and the affected workers were exposed intermittently, the averages of the total number of hours of exposure for development of the peripheral neutropathy in the animals and workers were remarkably close.