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G J van Esch

Publications and source records attributed to G J van Esch.

At least 19 recordsLinked to original sources
PubMed1986

Influence of exposure regimen on nitrogen dioxide-induced morphological changes in the rat lung.

Experiments were performed to study the influence of concentration, exposure pattern, and length of exposure on the degree and extent of morphological alterations in the NO2-exposed rat lung. Four weeks of continuous exposure to 20 mg NO2/m3 consecutively revealed damage and loss of cilia, replacement of desquamated type I pneumocytes by type II pneumocytes resulting in a cuboidal epithelial lining, an influx of alveolar macrophages, and hypertrophy and hyperplasia of the bronchiolar epithelium. The animals recovered almost completely from the induced lesions within 8 days. Continuous exposure to 1, 2.5, or 5 mg/m3 displayed minimal alterations in the 5 mg/m3 group. The effects increased with exposure time. Intermittent or continuous exposure to 20 mg NO2/m3 resulted in minor differences after 4 weeks. The onset of the lesions was delayed and the massive influx of alveolar macrophages in the continuously exposed animals failed to appear in the intermittently exposed animals. This work demonstrates that in subacute experiments: Concentration plays a more important role in inducing pulmonary lesions than exposure time when the product of concentration and time is kept constant. This effect is stronger during intermittent exposure than during continuous exposure. Continuous exposure seems to be a more important factor with regard to a macrophage response than intermittent exposure. The rat lung has a large capacity to repair almost completely from damage caused by short-term NO2 exposure.

Animals↗
PubMed1985

Carcinogenicity study in rats with a mixture of eleven volatile halogenated hydrocarbon drinking water contaminants.

A lifetime carcinogenicity study was carried out in Wistar rats, with a mixture of the following halogenated hydrocarbons: trichloromethane, tetrachloromethane, monobromodichloromethane, trichloroethylene, tetrachloroethylene, 1,2-dichlorobenzene, 1,3,-dichlorobenzene, 1,4,-dichlorobenzene, 1,2,3,-trichlorobenzene, 1,2,4,-trichlorobenzene, 1,3,5-trichlorobenzene. From this mixture 0.22, 2.2, or 22 mg was added per liter drinking water representing concentrations being three orders of magnitude higher than found in several water wells. Most of the changes found in body weight, hematology and pathology correlated with intercurrent diseases or were in accordance with background pathology. With respect to incidence and time of occurrence of tumors, no significant differences were found between the control and the high dose group when lifespan correction was applied. Thus it is concluded that in the present study no significant toxic or carcinogenic effects are induced by lifetime exposure of rats to a mixture of volatile halogenated hydrocarbons in the drinking water.

Animals↗
PubMed1977

Effect of food deprivation on low level hexachlorobenzene exposure in rats.

The purpose of the present study was to determine if food deprivation could modify the biological activity of hexachlorobenzene (HCB) in the rat. Male and female Wistar rats were divided into 6 groups containing 6 animals. Groups 1, 3 and 5 were fed standard control diet ad libitum for 2 weeks. For the next 4 weeks their respective diets contained 0, 20 and 100 ppm HCB. Groups 2, 4 and 6 were also fed a standard control diet for 2 weeks but at an intake of approximately 50% of those groups fed ad libitum. For the following 4 weeks food deprivation was continued but the control diets were replaced with diets containing 0, 40 or 200 ppm HCB. The parameters measured were food, body weight changes, changes in tissue weights, microsomal enzyme activity and histopathology of liver, kidneys, adrenals and pancreas. Tissue residue profiles were established for plasma, liver, brain and adrenals. Food deprivation augmented the induction of microsomal enzyme activity by HCB in both males and females at both dose levels. Liver hypertrophy was observed in both males and females fed 200 ppm HCB and subjected to food libitum. Food deprivation resulted in a higher plasma, liver, brain and adrenal accumulation of HCB in both males and females.

Adrenal Glands↗
PubMed1977

Short-term toxicity of strontium chloride in rats.

A range-finding experiment with strontium chloride hexahydrate (0, 3, 30, 300 and 3000 ppm in the diet) and subsequently a 90-day test with the same compound at dose levels of 0, 75, 300, 1200 and 4800 ppm in a semipurified diet was carried out with SPF-derived Wistar-rats. The diet contained adequate levels of Ca, Mg, P and Vit.D3. Growth, food intake, behaviour and mortality were measured, extensive haematology and clinical biochemistry carried out, organ weights determined, X-ray photographs of the bones taken and complete histopathological examination was performed. In addition Sr-content of blood, bone and muscles was determined. Thyroid weights were significantly increased in the males of the 1200 and 4800 ppm group. Histological evidence for increased thyroid activity was noticed in the males of the 4800 ppm group. Pituitary weights were significantly decreased in the females of the 300 ppm and 4800 ppm group, but not of the 1200 ppm group. A histologically confirmed glycogen depletion of the liver was noted biochemically in the highest dose group (4800 ppm). Sr-content in bone was increased at all dose levels having a constant level from 4 weeks onwards, thus indicating that a no effect level cannot be established. If the increased Sr-concentration in the bone can be considered a non-toxic effect, the non-toxic effect level appears to be 309 ppm.

Animals↗
PubMed1976

The short-term toxicity of some feed additives to different freshwater organisms.

The short-term toxicity (EC50 respectively LC50 after 2 or 4 days) of 13 feed additives was determined to 4 freshwater organisms of different trophical levels: Chlorella pyrenoidosa, Daphnia magna, Lebistes reticulatus and Salmo gairdneri. The most toxic (LC(EC)50 less than 1 mg/1) were robenidine (to all tested organisms) and stenorol (to Daphnia); moderately toxic (1 less than LC(EC)50 less than 10 mg/1) was pyrimethamine. Amprolium, ethopabate, furazolidone and zoalene proved to be little toxic (LC(EC)50 greater than 10 mg/1); whereas buquinolate, carbadox, clopidol, decoquinate, grofas and sulfaquinoxaline were under the experimental conditions not toxic for the tested organisms.

Animals↗
PubMed1976

Short-term toxicity of 1-naphthaleneacetic acid in rats.

In a 90-day feeding study, 4 groups of 10 male and 10 female rats received in the diet 0,200, 1000 and 5000 ppm 1-naphthaleneacetic acid (1-NAA). Growth and food intake was reduced significantly only in males on 5000 ppm. Haematological examination yielded essentially negative results except for a non-significant reduction at the 1000 and 5000 ppn levels in the leucocyte count, mainly due to a reduction in neutrophils. No significant effects were observed in the renal concentration test, urinalysis, renal histochemistry or histology of a wide range of organs at any level of 1-NAA tested. Increased relative weights of thyroid, testes, brain and liver were confined to the 5000 ppm level. The increase in relative liver weight was not accompanied by histological liver damage and was associated with elevated liver microsomal enzyme activity. The loss of glucose 6-phosphatase (G6Pase) and increase in glucose 6-phosphate dehydrogenase (G6PDH) seen histochemically in the centrilobular region of the liver in males on 5000 ppm, accompanied by glycogen depletion in the liver, could however be indicative of liver damage. On the basis of conventional criteria, a no-effect level of 1000 ppm would have been indicated by this study but in view of liver glycogen depletion at all levels tested a no-effect level was not established.

Animals↗