Showing papers by "Royal London Hospital published in 1974"

Handpiece sterilization in General Practice.

Abstract: The risk of transmitting serum hepatitis in dental practice is, of course, by no means confined to the problem of sterilizing instruments. Only minute quantities of blood are required to transmit the disease and in a large proportion of cases of serum hepatitis there is no history of parenteral exposure. In a study employing human volunteers (Barker et al. 1970) and using pooled plasma which had been preserved for 15 years at -20°C, it was found that 1 ml of a 1 in 10 000 dilution of the plasma caused icteric hepatitis and 1 ml of a 1 in 10 000 000 dilution caused a virnemia, but no illness, after the normal incubation period. This was despite the fact that the amount of virus in the pooled plasma was comparatively small, being undetectable by gel diffusion methods and having a titre of only 1 in 10 by complement fixation. In some sera as much as 1% of the serum protein consists of Australia antigen and 1 ml may contain 1013 particles (Almeida et al. 1969), enough to provide 20003000 particles for every human being. The situation, then, is that invisible amounts of blood may contain an infectious dose of serum hepatitis virus and there is hardly a dental procedure in which instruments do not become slightly contaminated with blood. In oral surgery the instruments, hands, gown, rinse bowl and occasionally the dental unit and surgery furniture may become grossly contaminated with blood. Serum hepatitis is clearly an occupational hazard and it is, perhaps, surprising that we do not all contract the disease early in our careers. About 0.1 % of people in the UK are believed to be carriers of Australia antigen and, if we assume that the 12 500 dentists engaged in private practice treat 20 patients per day then it appears that 250 carriers are treated each day. This increased exposure to serum hepatitis virus results in a higher carriage rate among dentists (Jones et al. 1972, Glenwright et al. 1974). In a recently reported study of a group of health workers (Lewis et al. 1973), of which dentists constituted 3%, it was found that 0.8% were positive for Australia antigen and 16.0% had antibody to the antigen, compared with rates of 0.4% and 8.7% respectively in the group of carefully matched controls. Applying these rates to the 18 756 dentists in the 1974 register we find that 150 would be expected to be carriers and 3000 to have antibody to serum hepatitis virus. I am sure we would all agree that one ought to be able to receive dental treatment without at the same time receiving a mini-transfusion from some previous patient, or the dentist, or one of his staff. To this end, not only must instruments be properly sterilized and pre-sterilized items correctly used, but blood must be regarded as the potentially infectious material it really is. The dentist should always wear gloves whenever he has a cut or other lesion of the hands. If there is a risk of blood being splashed on to the face a mask and spectacles, or visor, should be worn. A wash bottle containing fresh, strong hypochlorite solution (10 000 parts/106 available chlorine) should be available for treating areas which become contaminated with blood. A disadvantage with hypochlorite is that it may corrode metals other than stainless steel; a suitable alternative is 2% buffered glutaraldehyde. The dental nurse should be provided with heavy duty rubber gloves for handling bloody instruments, and the sink where these instruments are washed and items such as aspirator bottles and rinse bowls should be regularly washed down with hypochlorite or glutaraldehyde. Needles and other sharp disposable items should be placed in rigid containers and bloody swabs and similar materials in impermeable waste bags. The arrangements for final disposal of materials contaminated with blood are problematical and unsatisfactory in many dental practices. A little bleeding so commonly occurs during dental treatment that most dentists become indifferent to contamination with blood. The hazard inherent in this attitude must be appreciated and much greater care exercised.

Experimental Evidence of Etiology of Thyroid Cancer

Abstract: Experimental Evidence ofEtiology of Thyroid Cancer Maintenance of considerably raised endogenous secretion of TSH in experimental animals for half or more of their life-span leads to the development of thyroid follicle cell adenomas and carcinomas. The varied regimens used have been iodine deficient diets, goitrogenic drugs, subtotal thyroidectomy. The yield of tumours in rats is considerably enhanced by pretreatment with ionizing radiation to the thyroid, external X-radiation or radioactive iodine. Radiation on its own in doses of 1000 rad X-rays or 10-50 ,uCi of 1131 initiates neoplastic changes and, by diffuse radiation damage to the thyroid gland, leads to a rise in endogenous secretion of TSH that promotes tumour development. Occasional follicle cell tumours arise 1i to 2 years after small doses of radiation, 100 rad X-rays or 1 ,uCi of 1311, in the absence of any maintained rise in TSH.