Journal of environmental pathology and toxicology最新文献

Juvenile and adult mice (4 and 7 weeks old, respectively) were fed various levels of 2, 3, 7, 8-tetracholorodibenzo-p-dioxin (TCDD) incorporated in mouse feed for five weeks or more. Animal parameters monitored included body weight, organ weights, white blood counts, hematocrits, certain serum protein levels (see below), symptoms of overt toxicity and mortality. High exposure levels (100 ppb) produced marked suppression in total serum protein, gamma globulin and albumin, but an increase in the beta-globulins. Feeding levels of 10 ppb TCDD or more reduced the primary and secondary antibody response to both tetanus toxoid and sheep erythrocytes. The amount of suppression appeared to be dose related, with juvenile animals showing greater suppression than adults. Antibody suppression from the 10 ppb feed level was roughly equivalent to that observed from a single high dose (200 mg/kg) of cyclophosphamide (CY). No evidence of enhanced IgE synthesis was obtained from TCDD exposed animals. TCDD feeding also lowered contact sensitization to dinitrofluorobenzene and resistance to challenge with either Salmonella typhimurium or Listeria monocytogenes.

Because of excessive reliance on the method of ecological correlation, in which the units of study are entire communities, there have been few agreed conclusions concerning the relation between mineral quality of water and health. However, in recent years there have been attempts to relate water exposure to health outcome in statistical series of individual subjects. Studies in Kitchener, Ontario and Regina, Saskatchewan found that households having domestic water softeners experience lower death rates than others. Kitchener data clearly implied an association between copper piping and mortality rate but this was not confirmed in Regina. Comparison of myocardial tissue between residents of soft and hard water areas has confirmed that insufficient magnesium intake is a likely cause of higher mortality in soft water areas. Within the 'normal' range of myocardial magnesium concentration the risk of IHD death appears to vary by at least one and possibility two orders of magnitude.

The increasing use of new sources of energy may result in additional contamination of the human environment with inorganic and organic pollutants which are not yet adequately investigated with regard to their potential impact on human health. However, some evidence exists that several trace inorganic and organic contaminants found in coal processing residues may constitute potential health problems. Therefore, the comparative biological hazards of solid wastes and effluents from a Lurgi coal gasification plant were initially evaluated using acute and chronic feeding experiments in male and female rats. In the subchronic experiment, six-week old animals were fed diets wih various levels of ash (slag) additive (0.5%, 1%, and 5%) for period of 16 weeks. Following exposure, blood samples were taken and 22-hour urine samples were collected. Livers and kidneys, and testicles in males, were taken for trace element analysis or histologic examination. The urinary values, erythrocyte and leucocyte count, hemoglobin, packed cell volume, and concentration of trace elements in exposed animals were determined. The addition of ash (slag) to the diet in concentrations much higher than expected in conditions of environmental contamination had no measurable health effects. Although these initial results obtained in relatively short-term experiments cannot be directly extrapolated to human health effects, particularly not for carcinogenic assessment, there is an indication that exposure to solid wastes from the coal gasification plant may not be toxic.

Heart, kidney, liver, hair, and toenails were analysed for Cd, Cr, Cu, Se and Zn in male subjects who died with myocardial infarction or hypertension, as compared to subjects who died a non-cardiovascular death. Autopsy collection was made according to a WHO protocol using a titanium knife. Tissues were immediately frozen and subsequently shipped by air to the analytical laboratory. Analysis was usually by neutron activation according to an IAEA protocol. Pathology and analytical data were reported according to standard formats. Institutions in many countries, both developed and developing, collaborated in this programme.

Plasma, erythrocyte and home tap water samples were taken from life-long residents of two counties (Evans-rural and Chatham-urban) in the high cardiovascular disease (CVD) belt of southeastern Georgia and from Habersham County, a rural county of North Georgia which is outside of the CVD belt. One-half of the subjects from each cohort had a serious CVD problem and the remaining half were healthy controls. Water samples were analyzed for hardness, total dissolved solids, pH and selenium (Se) content. Blood samples were analyzed for Se (by neutron activation analysis) and glutathione peroxidase (GSHPx). Se levels in all water samples were less than 0.01 ppb. Water hardness and total dissolved solids levels were higher in the CVD belt counties. There were no significant differences (P greater than 0.05), but water hardness and total dissolved solid levels were inversely correlated (p greater than 0.01) with the activity of erythrocyte GSHPx, a selenium containing enzyme which detoxifies oxidized fats.

Epidemiologic studies have suggested factors in drinking water influence on the human cardiovascular system. A clear identification of the factors involved requires more invasive techniques and more strict experimental controls than can usually be applied in epidemiologic studies. Consequently laboratory animals are often used to expand and support epidemiologic data. For laboratory purposes cardiovascular toxicology must be broken down to effects on the myocardium, the vasculature and the kidney. Further division may be necessary to take into account the influence of the neuroendocrine system or other systems that influence the function of the cardiovascular system. Since environmental influences upon the cardiovascular disease are relatively subtle (versus the acute effects of some drugs) it is assumed that major difficulties are chronic in nature. Accordingly, it is suggested that laboratory experimentation focus on either chronic toxin exposure or short-term exposure to stressed or genetically susceptible animals. A variety of in vivo and in vitro tests may be necessary to relate the toxicity realized in animals to what might be expected in man. Wide species differences with respect to the susceptibility of particular target tissues must be taken into account to clearly apply the results to man. Similarly, special characteristics of stressed and genetically susceptible animals must be understood to avoid deceptive results.

Dichloroacetylene (DCA) shows pronounced nephrotoxic effects in several animal species and is neurotoxic in humans. It is a chemically highly reactive compound that decomposes spontaneously in the presence of oxygen. The chemical decomposition of DCA has been studied in order to understand the role of the decomposition products for the toxic effects of DCA. Seven compounds were identified by their mass spectra and by comparison with authentic reference materials. Among these were phosgene, hexachlorobutadiene, and other reactive products (e.g., trichloroacetyl chloride and trichloroacryloyl chloride), which may explain, in part, the toxicity of DCA.

A program suitable for terminal, conversational-mode usage was developed in the BASIC language to compute the median effective dose (LD50), various error terms, and confidence intervals. The overall algorithm used in the program was based on a method described by Finney. The accuracy, speed and flexibility of the program makes the terminal approach an efficient alternative to simple graphic methods.