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Biomedical subjects

F Berglund

Publications and source records attributed to F Berglund.

At least 19 recordsLinked to original sources
PubMed1990

Does mercury from amalgam restorations constitute a health hazard?

Amalgam is the most extensively used implant material in dentistry. There have been no clinical trials of this substance and there are no epidemiological studies that allow any conclusions on the safety of amalgam fillings. Amalgam restorations continuously emit mercury vapour, which is absorbed in considerable quantities via the lungs. A comparison with dose-effect relationships, obtained in occupational studies, for certain effects on the kidneys and central nervous system (CNS), suggests that individuals with unusually high emission of mercury from amalgam fillings are at risk. It is unclear whether or not clinically significant effects could be expected. The limited sensitivity of available occupational studies, together with insufficient knowledge of possible host factors affecting resistance to mercury, implies that other more severe effects in susceptible individuals cannot be excluded. Information on long-term effects on organs other than brain or kidney is sparse. Animal studies suggest the possibility of immune system reactions to mercury, i.e. development of autoimmunity, that are not primarily dose-dependent, but rather depend on genetic susceptibility. From a toxicological point of view, amalgam is an unsuitable material for dental restorations.

Dental Amalgam↗
PubMed1984

Drug use during pregnancy and breast-feeding. A classification system for drug information.

Since 1978 the Swedish catalogue of registered pharmaceutical specialties (FASS) has carried a special section entitled "Pregnancy and breast-feeding" in each product presentation, intended to form an aid for the prescription of drugs to women during childbearing and lactation. After a brief review of transplacental transport and milk secretion, reproduction-toxicology studies in animals, and methods for clinical evaluation of drugs for use during pregnancy, the classification system is presented. On the basis of available data with regard to effects on early and late stages of pregnancy and labour, all the pharmaceutical specialties concerned are assigned to one of the following pregnancy categories: A, B 1, B 2, B 3, C or D. The letters refer to information based on findings in man, and the figures to information based on animal data. For drugs in categories B 3, C or D any harmful effects observed or likely to occur in man or animals are to be specified. The pregnancy categories are defined as follows: Category A. Drugs which may be assumed to have been used by a large number of pregnant women and women of child-bearing age, without any form of definite disturbance in the reproductive process having been noted so far, e.g. an increased incidence of malformations or other direct or indirect harmful effects on the fetus. Category B. Drugs which may be assumed to have been used by only a limited number of pregnant women and women of child-bearing age, without any form of definite disturbance in the reproduction process having been noted so far, e.g. an increased incidence of malformations or other direct or indirect harmful effects on the fetus. Category C. Drugs which by their pharmacological effects have caused, or must be suspected of causing disturbances in the reproduction process that may involve risk to the fetus without being directly teratogenic. Category D. Drugs which have caused an increased incidence of fetal malformations or other permanent damage in man or which on the basis of e.g. reproduction-toxicology studies must be suspected of doing so. This category comprises drugs with primary teratogenic effects. If the drug also has pharmacological effects that may directly or indirectly have a harmful effect on the fetus, this must also be stated. As experience of effects of drugs in Category B is limited, results of reproduction-toxicology studies in animals are indicated by allocation to one of three subgroups according to the following definitions: Category B 1.(ABSTRACT TRUNCATED AT 400 WORDS)

Abnormalities, Drug-Induced↗
PubMed1978

Food additives.

The use of additives to food fulfils many purposes, as shown by the index issued by the Codex Committee on Food Additives: Acids, bases and salts; Preservatives, Antioxidants and antioxidant synergists; Anticaking agents; Colours; Emulfifiers; Thickening agents; Flour-treatment agents; Extraction solvents; Carrier solvents; Flavours (synthetic); Flavour enhancers; Non-nutritive sweeteners; Processing aids; Enzyme preparations. Many additives occur naturally in foods, but this does not exclude toxicity at higher levels. Some food additives are nutrients, or even essential nutritents, e.g. NaCl. Examples are known of food additives causing toxicity in man even when used according to regulations, e.g. cobalt in beer. In other instances, poisoning has been due to carry-over, e.g. by nitrate in cheese whey - when used for artificial feed for infants. Poisonings also occur as the result of the permitted substance being added at too high levels, by accident or carelessness, e.g. nitrite in fish. Finally, there are examples of hypersensitivity to food additives, e.g. to tartrazine and other food colours. The toxicological evaluation, based on animal feeding studies, may be complicated by impurities, e.g. orthotoluene-sulfonamide in saccharin; by transformation or disappearance of the additive in food processing in storage, e.g. bisulfite in raisins; by reaction products with food constituents, e.g. formation of ethylurethane from diethyl pyrocarbonate; by metabolic transformation products, e.g. formation in the gut of cyclohexylamine from cyclamate. Metabolic end products may differ in experimental animals and in man: guanylic acid and inosinic acid are metabolized to allantoin in the rat but to uric acid in man. The magnitude of the safety margin in man of the Acceptable Daily Intake (ADI) is not identical to the "safety factor" used when calculating the ADI. The symptoms of Chinese Restaurant Syndrome, although not hazardous, furthermore illustrate that the whole ADI cannot always be ingested as a single dose on an empty stomach with impunity.

Animals↗
PubMed1975

Effect of trimethoprim-sulfamethoxazole on the renal excretion of creatinine in man.

Treatment with the chemotherapeutic combination of 160 mg. trimethoprim plus 800 mg. sulfamethoxazole twice daily increased the serum creatinine level by an average of 2 mg. per 1. in 21 patients. The effect was clearly reversible. The chemical analysis of creatinine was not affected by the addition of trimethoprim, sulfamethoxazole or their metabolites. In 2 subjects given the drug combination for 12 days renal excretion and 24-hour clearances of creatinine decreased but iothalamate 131I clearance was unchanged. Consequently, the rise in serum creatinine does not indicate any decrease in the glomerular filtration rate. The serum creatinine started to rise within 4 hours after oral administration of a single dose. The rise in serum creatinine could be produced with trimethoprim alone but not with sulfamethoxazole alone. When the plasma creatinine was raised to 100 mg. per l. in healthy subjects (by giving creatinine orally), trimethoprim increased the creatinine levels 10 times as much as at normal plasma levels. The effect was interpreted as a competitive inhibition of the mechanism for tubular secretion of creatinine through the base-secreting pathway.

Creatinine↗
PubMed1975

Electrocardiogram and renal concentrating capacity in rats fed a diet containing rapeseed oil.

The functional effects of a diet containing rapeseed oil (40% of total energy intake) were studied in rats, starting at age 28 days. There were no effects on the electrocardiogram in spite of morphological changes in the myocardium. In 10 female rats the urine osmolality following 16 hours of dehydration was approximately 20% lower than in 10 control rats during the 9th, 10th and 20th week of the experiment. It is suggested that erucic acid in the rapeseed oil inhibits beta-oxidation of fatty acids in the kidney, thereby depriving the kidney of energy involved in sodium transport.

Animals↗