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Biomedical subjects

R D Kimbrough

Publications and source records attributed to R D Kimbrough.

At least 19 recordsLinked to original sources
PubMed1991

Consumption of fish: benefits and perceived risk.

Fish, a useful source of protein, may be polluted by microbes, natural toxins, and/or synthetic chemicals. However, based on a review of the U.S. General Accounting Office, "There does not appear to be a compelling case to implement a mandatory comprehensive federal seafood inspection program." Although earlier studies showed higher body burdens of polychlorinated biphenyls (PCBs) in populations who consumed a lot of fish from polluted waterways, a recent study refutes these observations. No information is available in the United States on the levels of polychlorinated dibenzodioxins (PCDDs) and dibenzofurans (PCDFs) in anglers who consume a great deal of fish presumed to be contaminated by these chemicals.

Animals↗
PubMed1991

Non-specificity of clinical signs and symptoms caused by environmental chemicals.

1. A review of the scientific literature revealed that 220 environmental chemicals had caused documented systemic toxicity in humans. This number is relatively small compared to the large number of industrial chemicals in the environment. 2. A total of 149 of these chemicals were verified as neurotoxins, thus emphasizing the sensitivity of this target organ. Despite the exclusion of chemicals that cause airway irritation only, 99 chemicals caused adverse effects on the respiratory system. Toxicity to the liver, kidneys and blood forming organs was less frequent. 3. Most of the individual clinical effects had a very low specificity in cases of human intoxication. Of 80 major signs and symptoms, 17 had only a single documented chemical aetiology. However, the combination of two or more signs or symptoms was found to provide an improved guidance to aetiological diagnosis. The paucity of specific signs and symptoms is probably one of the reasons that only 220 environmental chemicals have been documented as causes of human disease.

Environmental Exposure↗
PubMed1990

Kashin-Beck disease: a cross-sectional study in seven villages in the People's Republic of China.

Kashin-Beck disease (KBD) is an endemic disease that occurs in certain parts of the People's Republic of China and in Russia. The etiology of the disease is unknown. Selenium deficiency, mycotoxins, and chelating agents such as humic acid and decaying plant material from walnut tree forests have been suggested as causal agents. The primary lesion of this disease is the selective coagulative necrosis of the hypertrophic chondrocytes at the base of the articular and growth plate cartilages. A cross-sectional study was performed in the People's Republic of China in 7 villages, to focus on information about life styles, food consumption, and environmental factors from the village population where the disease is endemic. A total of 425 children were examined, of which 71 children had KBD. Results of detailed food consumption data analyses showed that certain combinations of food substances high in protein had a protective effect. It was also found that the disease was twice as prevalent in onset in boys as in girls, in the 12-yr-old age group. The overall onset of illness in this group of children ranged from 4 to 13 yr. Either the joints of the fingers or one ankle was affected first. Many of these children also had discolored teeth. However, this finding was unrelated to KBD.

Adolescent↗
PubMed1990

How toxic is 2,3,7,8-tetrachlorodibenzodioxin to humans?

The tissue levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) measured in different species are reviewed. Based on the correlation of tissue levels and a toxic response in different species, humans are less or no more susceptible to the toxic effects of TCDD than most of the laboratory animals that have been studied. Thus, the present exposure of the general population to environmental levels of TCDD are related compounds should not be of concern.

Animals↗
PubMed1987

Porphyrins and hepatotoxicity.

Human porphyrias are rare inborn disorders of porphyrin metabolism. Porphyria cutanea tarda is one such disorder, which may occur spontaneously after the ingestion of drugs and alcohol. This is the "constitutional" type and is associated with a deficiency of uroporphyrinogen decarboxylase in the liver. This constitutional type must be differentiated from the "acquired" type, which occurred in hundreds of people poisoned by hexachlorobenzene in Turkey. Morphological changes observed in the livers of animals and humans vary greatly. Porphyria cutanea tarda may be associated with very little liver pathology or with very pronounced changes, depending on the agent causing the porphyria. Usually, the liver has an increased iron load, and mitochondria contain a crystalline material.

Animals↗
PubMed1986

Characterization of pancreatic-type tissue in the liver of rat induced by polychlorinated biphenyls.

Pancreatic-type tissue induced in the livers of rats treated with polychlorinated biphenyls was characterized by transmission electron microscopy and high-resolution immunocytochemistry. The cells of pancreatic-type tissue were arranged as acini and in small groups. By electron microscopy the pancreatic-type tissue showed features very similar to normal pancreatic acinar tissue, such as well developed rough endoplasmic reticulum (RER), large numbers of mature zymogen granules, and a basally located nucleus. Protein A-gold imunocytochemical technique showed localization of amylase and trypsinogen over the zymogen granules and RER. These findings confirm that this tissue in the liver is morphologically and functionally identical to pancreatic acinar tissue.

Amylases↗
PubMed1985

Trichloroethylene: an update.

The toxicity of tricholoroethylene (TCE) has been summarized in a number of reviews. In this particular update, only the more recent studies that deal with metabolism and carcinogenicity have been examined. In reviewing the more recent publications on metabolism of TCE, we determined that differences exist in its metabolism if low doses are compared with high doses in animals. There may also be a difference in the metabolism of TCE between different species--namely mice, rats, and humans. TCE has not been shown to be a potent carcinogen in rats and it only seems to be a potent carcinogen in one specific strain of mice, namely the B6C3F1 mouse. Epidemiology studies have been rather limited. The number of persons examined so far for chronic toxic effects is small, compared with the enormous size of the work force that is exposed to TCE over prolonged periods. On an empirical basis, the occupational experience with TCE does not suggest that this compound is a potent carcinogen. The risk associated with exposure to trace amount (ppb) concentrations of TCE in water appear to be minimal or perhaps negligible. Because there are differences in metabolism of TCE, it is important that theoretical risks attributed to TCE in the past be reexamined. It is highly possible that in humans, the metabolic pathway leading to the formation of the proximate carcinogen is not activated at low doses, where TCE is excreted by first-order kinetics.

Animals↗
PubMed1985

Subchronic inhalation toxicity of isobutyl nitrite in BALB/c mice. I. Systemic toxicity.

The effects of subchronic inhalation exposure to isobutyl nitrite (IBN) on body weight, selected organ weights, hematology, and gross pathology and histopathology of BALB/c mice were evaluated. Mice of both sexes were exposed at 0, 20, 50, or 300 ppm IBN for 6.5 h/d, 5 d/wk for up to 18 wk. Most changes in measured indices occurred in mice exposed at 300 ppm IBN and included decreased thymus weight (females); decreased liver weight (males); decreased white blood cell counts (males); mild focal hyperplasia and vacuolization of the epithelium lining bronchi and bronchioles of the lungs (males and females). Organ weight and hematologic changes, however, were not accompanied by any observed histologic changes. In addition, elevated methemoglobin concentrations were detected in mice of both sexes exposed at 50 and 300 ppm IBN. Body weights were not adversely affected by exposure. These data suggest that mild tissue injury, restricted to the lung, and methemoglobinemia are the major toxic effects observed following exposures of mice to IBN at concentrations up to 300 ppm for 18 wk. No treatment-related effects were noted in mice exposed at 20 or 50 ppm IBN, except for slight elevations in methemoglobin concentrations in mice exposed at 50 ppm.

Animals↗
PubMed1985

Laboratory and human studies on polychlorinated biphenyls (PCBs) and related compounds.

Similar qualitative toxic effects have been observed in animals for a class of halogenated aromatic compounds, which include the halogenated biphenyls, naphthalenes, dibenzodioxins, and dibenzofurans. All of these compounds are lipid soluble and persist in the environment and in mammals. The polybrominated biphenyls (PBBs) are the most persistent. They are predominantly stored in fatty tissue; they pass the placenta and are excreted in milk. Some isomers of the halogenated biphenyls are more toxic than others. With some exceptions, the more toxic isomers are retained longer in tissues and are also the carcinogenic components of the mixture. Most of these chemicals seem to be promoters of carcinogenesis in animals rather than initiators. An array of toxic effects in laboratory animals has been ascribed to these compounds and numerous reviews summarizing this information are available. Less information is available on the human health effects of environmental and occupational exposure. Results of recent studies in animals to further elucidate the effects of these chemicals are presented, and results from some human studies conducted in the United States are reviewed.

Accidents↗
PubMed1984

Health implications of 2,3,7,8-tetrachlorodibenzodioxin (TCDD) contamination of residential soil.

Extrapolations from animal toxicity experiments (including carcinogenicity and reproductive effects) to possible human heath effects can be used to estimate a reasonable level of risk for 2,3,7,8-tetrachlorodibenzodioxin (2,3,7,8-TCDD). Extrapolations are derived from: (1) review of published studies, (2) a complex set of assumptions related to human exposure to contaminated soil, and (3) estimates of (a) a dose response curve, (b) appropriate margins of safety, and/or (c) applicable mechanisms of action. One ppb of 2,3,7,8-TCDD in soil is a reasonable level at which to begin consideration of action to limit human exposure for contaminated soil.

Animals↗
PubMed1984

Stunted growth, increased mortality, and liver tumors in offspring of polybrominated biphenyl (PBB) dosed sherman rats.

Firemaster FF-1, a polybrominated biphenyl (PBB) mixture, was dissolved in corn oil and given as a dose of 200 mg/kg body weight to Sherman rats on d 7 and 14 of pregnancy. Control rats received equivalent doses of corn oil alone. Selected pups and all dams were killed 1 mo after pups were weaned. A total of 50 male and 50 female offspring per group were followed until they were 2 yr old. The livers of offspring killed at the ages of 2 mo and 2 yr had PBB levels of 2,4 (SD 1.2) and 0.8 (SD 0.65) mg/kg for females and 3.0 (SD 1.6) and 0.6 (SD 0.37) mg/kg for males, respectively. The incidence of hepatocellular carcinomas was 3/51 (5.9%) and 4/41 (9.6%) after 2 yr in females and males, respectively. Hepatocellular carcinomas were not observed among the controls. Neoplastic (hyperplastic) nodules of the liver were present in 9/51 (17.6%) and 2/41 (4.9%) of exposed females and males, respectively, whereas only 2/48 (4.2%) of control females and no control males had neoplastic (hyperplastic) nodules. Body weights were lower in PBB-exposed rats at ages 1, 6, 12, and 24 mo. Survival rates from birth to weaning were lower in PBB-exposed pups (89%) than in controls (98%). Mortality was two times higher in PBB-exposed males (64%) than in control males (32%) after 2 yr. Transplacental PBB exposure and exposure through milk resulted in PBB body burdens in the offspring still measurable at the end of their lifespan. These offspring had increased mortality rates and lower body weights than controls, and they developed hepatocellular carcinomas.

Animals↗
PubMed1984

Relationship between dose and health effects.

The health effects produced by chemicals depend on the inherent toxicity of the chemical and the dose received by the exposed individual. Health effects are modified by genetic make-up, life style, nutrition, and interaction with other chemicals. In some situations it may be difficult to impossible to determine through epidemiologic studies whether exposure to chemicals (naturally occurring or synthetic) has caused harm. For all practical purposes, the risk associated with minuscule doses of most chemicals is negligible.

Adipose Tissue↗