For near thirty years, epidemiological studies have coped with the search of posible noxious consequences of an involuntary exposure of pregant women to environmental tobacco smoke on the gestation and the intrauterine development of embryo and foetus. These studies were mainly retrospectives ; a careful study of the methods used (questionnaires, evaluation of exposure, and so on...) gives evidence that they can rarely avoid serious criticims. As possible effects of intrauterine exposure to environmental tobacco smoke, low birth weight and impairing of other body parameters, perinatal mortality, frequency of abnormalities have been reviewed. As a potential cause, the role of the father tobacco smoking has been especially examined. As a whole, the consequences of a prenatal exposure to environmental tobacco smoke are an extremely controversial subject and no obvious effect has yet been universally recognized. The critical analysis of the studies has shown that, frequently, the epidemiological studies have been interpreted in order to find links between and involuntary exposure to tobacco smoke and some troubles of reproduction, particularly in offspring. As a matter of facts, fundamentally, the noted actually correlations, even if they are statistically significant, are not able to move such links. Thet are only able to indicate the existence of an association and only, if the eventual role of confounding factors has been properly treated. An interesting case is the potential effects of the father's tobacco smoking. The hypotheses emerging from these examined inquiries remain to be more precisely defined and thoroughly by new studies, preferentially prospective, and, when necessary, completed by animal experiments. It is suggested that a special effort shall be applied to the measurement of the exposure of pregnant women to defined toxic compounds originatring from environmental tobacco smoke. Presently, it is not possible to draw a conclusion on the noxious or innoxious influence of the involuntary exposure of pregnant women to environmental tobacco smoke, particularly as far as potential risks for foetus are concerned.
The authors report the history of 49 patients, admitted to an intensive care unit after a caustic or corrosive ingestion. This series follows a similar one, related in 1979. An update is made for early evaluation and management, based on patients classification in three groups: sever cases, moderate cases, mild cases. Clinical and biological data, treatment and outcome for the three groups are related. The frequency and gravity of these poisonings appear to be the same as in the first series, with poor prognosis for extreme emergencies and high risk of oesophageal or gastric stricture for important forms. In this population, 20 % of extreme emergencies have favorable outcome with early major surgical procedure.
After a chloroform intraperitoneal injection, lactate dehydrogenase, alanine aminotransferase and particularly aspartate aminotransferase serum activities are much more raised in deficients animals. Liver ornithine decarboxylase (ODC) activity normally decreases in rats between the 4th. and the 7th. month after the weaning. In vitamin A deficients animals, basal values of the enzyme activity are lower and the decrease is deaper. But even at month 7, liver sustains a partial capacity of ODC recovery if retinol is fed during 15 days. Chloroform administration strongly enhances liver ODC activity in normal rats. In the deficients, stimulation is lower in absolute value but relatively higher if refered to basal level. After retinol refeeding, chloroform stimulates enzyme activity to nearly normal values. Vitamin A deficiency impairs obviously liver ODC activity and its response to chloroform stimulation in rats, but the stroke is at least partially reversible in our conditions. Moreover, deficient animals maintain a non negligible capacity of ODC response under chloroform stimulation.
To provide a consistent teratogenic risk assessment from animals' data, the system described here suggests an evaluation by stages. Based on the expert system from Mattison, the toxic responses of commun species of experimental animals are scored. The scores are then multiplied by the ratio of the lowest adult toxic dose A, to the lowest developmental toxic dose D (A/D). The products form 3 categories. Based on the reversibility of the developmental effects, the categories are subdivided into classes A B C D. This system should permit an unbiased risk assessment and a comparaison of industrial chemicals' prenatal toxicity.
The embryotoxicity and teratogenicity of alpha-asarone were investigated in mice. The drug was dissolved in corn oil, and administered daily, by gavage, on days 6 to 15 of gestation, at 0 (controls), 5, 15, 30 and 60 mg/kg. Fetuses were removed on day 18 by caesarean section and examined using routine teratological methods. A significant maternal toxicity was observed in dams given 60 mg/kg, as indicated by a reduced weight gain. An embryolethality was observed in 15, 30 and 60 mg/kg treated groups. In addition, the highest dose induced fetal malformations, mainly represented by hydrocephaly, extraribs, clubfeet and cleft lips.
Acute renal failure and rhabdomyolysis are reported in a 33 year old man who had taken 6 g of amoxapine. Different possible levels for the toxic action of amoxapine are discussed and compared with literature data.
The authors present the results of a study on urinary excretion of caffeine, after a single oral intake of 100 mg of caffeine, in two populations of students at rest and during exercise. Whether expressed in mg/l or mg/g creatinine no significant difference in urinary excretion of caffeine was observed between the two populations and it proves to be lower than the limit level authorized by the IOC (12 mg/l).
