Dose to bone from strontium-90: implications for the setting of the maximum permissible body burden.
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Bone Marrow↗
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Cesium-137 body burdens in man: January 1956 to December 1966.
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Adult↗
Does smoking influence the lead body burden in workers?
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Adult↗
[Relation between environmental concentration, urinary elimination and body burden of chromium in occupationally exposed workers].
Biological and environmental monitoring of chromium exposure was carried out on 20 welders working with special electrodes in the manufacture of tank-cars. The workers were divided in groups, according to the different degree of chromium accumulation, which was determined by renal clearance of diffusible chromium. A closed linear relationship between TWA concentration of hydrosoluble chromium in air and urinary excretion of the metal at the end of exposure was observed. The parameters of regression lines in welders with more (clearance 10 ml/min) or less (clearance 5 ml/min) accumulation of chromium suggest that the renal burden influences not only the basal excretion, but also the excretion at the end of exposure. We underline the difficulty in the determination of correct biological limits if we take them from TLV in air. We must at least consider the degree of accumulation in exposed workers too.
Air Pollutants↗
[Comparison of the body burden of the population of Leipzig and Munich with the heavy metals cadmium, lead and mercury--a study of human organ samples].
In the former GDR it was almost impossible to perform studies on environmental pollution. Therefore, a short time after the opening of the German interior border the authors started an investigation on the heavy metal burden of humans in the former District of Leipzig (Saxonia). In 1990/91 tissues from 57 deceased were collected from this region. The concentrations of cadmium were determined in specimens from the liver and renal cortex, of mercury in liver, renal cortex and grey matter of the cerebrum and of lead in samples of the pelvic bone and the cortical part of the femur. After sample pretreatment, the heavy metal concentrations were determined by GF-AAS or CV-AAS. The results were compared with studies recently performed by the authors in the region of Munich (southern Bavaria, FRG) and with values from the literature. It was found that the burden with cadmium was similar in both regions, whereas on the average, the bone lead concentrations in Leipzig were 10 times (!) higher than in Munich. Considering dental amalgam as main factor for the burdening with inorganic mercury, the mercury concentrations in the liver and the renal cortex were of the same order of magnitude in both regions. In contrast to this, significantly higher mercury concentrations were found in the brain samples from Leipzig than from Munich. Possible negative health effects of these elevated lead and mercury burden in the Leipzig area are discussed.
Adolescent↗
Effects of exposure to a combination of zinc- and lead-spiked sediments on mouthpart development and growth in Chironomus tentans.
Exposures to either zinc or lead in contaminated sediments have been shown to induce characteristic deformities in larval chironomids. This study examined the effects of exposure to lead and zinc in combination on Chironomus tentans larvae. Proportions of mouthpart deformities in populations of larvae reared in sediments containing nominal combinations of lead and zinc were tested for additive, synergistic, and antagonistic interactions using logistic regression. Metal body burdens, body size measurements, and survival were used to evaluate toxicity and developmental impacts. Results demonstrate zinc and lead mixtures produce fewer deformities than the individual metal, so their interaction may be characterized as antagonistic. However, exposure to the metal mixtures also caused delayed development and failure to hatch. The apparent decline in deformities may be an artifact of higher mortalities or developmental effects. This research provides better understanding of some of the problems and considerations for use of chironomid population deformity proportions in bioassessments for sediment metal contamination.
Animals↗
Weight and salinity effects on zinc uptake and accumulation for the American oyster (Crassostrea virginica Gmelin).
The power relationships of short-term net uptake and of in-situ body burden with body weight were examined. The accumulation of soft tissue zinc in the American oyster (Crassostrea virginica) was related to time integration of uptake. Short term uptake of (65)Zn was measured in the laboratory. It was (i) a function of the (dry soft-tissue) weight of the oyster, (ii) inversely related to the salinity of the ambient water, and (iii) increased linearly with ambient concentrations. When in-situ soft-tissue zinc body burdens of oysters from the James River and the Rappahannock River were fit to power functions of body weights (y = aWb), the values of b for all sites were larger by 1 than the powers for (65)Zn uptake when b was adjusted for the oyster-bed salinities. The soft-tissue zinc concentration (y/W) of an oyster increased continuously, but the rate of the increase was reduced as the oyster grows larger. Both short-term uptake and in-situ body burden varied with salinity. The soft-tissue zinc concentrations of hooked mussels (Ischadium recurvum) from the Rappahannock River oyster beds, contrary to the oysters, appeared to be in equilibrium with ambient concentrations.
Journal Article↗
Acute administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in pregnant Long Evans rats: association of measured tissue concentrations with developmental effects.
Prenatal exposure to TCDD interferes with fetal development at doses lower than those causing overt toxicity in adult animals. Exposure to TCDD during development produces alterations in the reproductive system of the developing pups- delayed puberty and reduced sperm counts in males and malformations in the external genitalia of females. The objectives of this study were to determine maternal and fetal tissue concentrations of TCDD after acute exposure and whether these tissue concentrations can be used to estimate the intensity of the developmental abnormalities reported by other laboratories. Pregnant Long Evans rats received a single, oral dose of 0.05, 0.20, 0.80, or 1.0 microg [3H]-TCDD/kg on gestation day (GD) 15, and maternal and fetal tissue concentrations of TCDD were measured on GD16 and GD21. On GD16, maternal liver contained the greatest amount of TCDD (30-47% administered dose). One day after administration of 0.20 microg TCDD/kg on GD15, there were 13.2 pg TCDD/g present in an individual fetus. This concentration is associated with delayed puberty and decreased epididymal sperm counts in male pups as well as malformations in the external genitalia of females. For the responses studied, tissue concentration measured during a critical period of gestation adequately predicts the intensity of the response. In addition, there was a strong correlation between fetal body burden and maternal body burden on GD16. A dose of 0.05 microg TCDD/kg resulted in maternal body burdens of 30.6+/-3.1 and 26.6+/-3.1 ng TCDD/kg on GD16 and GD21, respectively. In conclusion, low-level TCDD exposure during the perinatal stage of life can produce adverse effects within the developing pups and that tissue concentration measured during a critical period is the appropriate dose metric to predict adverse reproductive and developmental effects.
Animals↗
Human response to dioxin: aryl hydrocarbon receptor (AhR) molecular structure, function, and dose-response data for enzyme induction indicate an impaired human AhR.
The aryl hydrocarbon receptor (AhR) mediates nearly all studied adverse effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and many related compounds. Binding of TCDD or related ligands to AhR is the key initiating event in downstream biochemical responses. The binding affinity of AhR for TCDD is specific to species and strain, and studies of human AhR demonstrate binding affinities approximately an order of magnitude or more lower than those observed in the most sensitive laboratory strains and species. Molecular genetic studies confirmed that human AhR shares key mutations with the DBA mouse strain that result in an "impaired" AhR (with respect to TCDD binding and responsiveness). Despite a number of polymorphisms in human AhR, the key "DBA-type" mutations appear to be a constant feature of the human AhR, and no polymorphisms have been identified that compensate for the impaired binding function conferred by these mutations. Consistent with the impaired binding status of the human AhR, human cells have consistently required approximately 10-fold higher concentrations of TCDD in vitro than rodent cells to respond with enzyme induction. Recent studies of in vivo enzyme induction-related endpoints in human populations with moderately and highly increased TCDD body burdens detected no relationship between these endpoints and TCDD body burdens at body-burden levels up to 250 ng TEQ/kg body weight, or approximately 25 times above the upper range of current general population background body burdens, while marked elevations in enzyme activity were observed in persons with body burdens above 750 ng TEQ/kg. In contrast, the more sensitive laboratory rodent strains and species exposed to TCDD exhibit significant enzyme induction at body burdens below 50 ng/kg. These interspecies data on the most sensitive and best understood response to binding of TCDD and related compounds to the AhR are consistent with the binding affinity and molecular structure data and support the hypothesis that the human AhR is less functional than the AhR of the more sensitive laboratory animals at a molecular level. Quantitative risk assessments involving interspecies extrapolation from sensitive laboratory species and strains should take these fundamental differences into account when margins of exposure and safety factors are considered.
Animals↗
Dermal uptake of solvents from the vapour phase: an experimental study in humans.
The control of exposure to hazardous substances in the workplace has traditionally focused on uptake via the inhalation route. Control of skin uptake has generally been considered for solids and liquids but the potential for uptake from vapours and gases has received relatively little attention. The current work was undertaken to establish a methodology to study the dermal uptake from vapours and to provide new and comparative information on a range of substance vapours. Groups of human volunteers were exposed to a small range of substances either 'whole body' or via the skin only. Substances (xylene, toluene, tetrahydrofuran [THF], methyl ethyl ketone [MEK] and 1-methoxypropan-2-ol [M2P]) were selected on the basis of their predicted dermal uptake from the vapour phase; their industrial use and potential for occupational exposure; the existence of a health-based occupational exposure limit; the availability of an analytical technique(s) for the substance and/or metabolite(s); and as representatives of chemical classes. Exposures were for four hours generally at the level of the UK Occupational Exposure Standard. Uptake was assessed by monitoring of parent or metabolite in blood, single breath or urine following exposure. Uptake of xylene, toluene and THF vapours via the skin under the conditions of this study was estimated to contribute around 1-2% of the body burden received following whole body (including inhalation) exposure. MEK showed more uptake via the skin, contributing around 3-3.5% of the body burden. Most dermal uptake was seen for the glycol ether M2P for which estimates of between 5-10% of whole body exposure body burden were obtained. The results of this and other studies indicate that uptake of vapours across the skin can occur but that for some substances (e.g., xylene, toluene, THF) this is likely to contribute little to the body burden. For other substances, such as the glycol ethers, skin uptake from vapours may be an important contributor to total uptake, particularly in situations where respiratory protective equipment is used to control inhalation exposure.
Administration, Cutaneous↗
Subchronic Exposure of [3H]- 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in female B6C3F1 mice: relationship of steady-state levels to disposition and metabolism.
The present study of subchronic low exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) at or near steady-state levels tries to emulate the most probable mode for human exposure, dietary consumption. This study is the first and most intensive pharmacokinetic study to be reported with repeated dosing, multiple times, and multiple doses examining disposition of TCDD-derived radioactivity and CYP1A activities in mice. For time-course relationships, animals were dosed (daily, Monday-Friday) with 0, 1.5, or 150 ng [3H]TCDD/kg for 4, 8, 13, or 17 weeks and also for 13 weeks followed by 4 weeks with no dosing. For dose-response relationships, animals were dosed for 13 weeks (daily, Monday-Friday) with 0, 0.15, 0.45, 1.5, 4.5, 15, 45, 150, or 450 ng [3H]TCDD/kg. Additional animals dosed for 13 weeks (daily, Monday-Friday) with 1.5 or 150 ng [(3)H]TCDD/kg were housed in metabolism cages. Time- and dose-dependencies of TCDD were confirmed in all measured tissues. Liver/fat (L/F) concentration ratios ranged from 0.2-3.4 (low to high dose). Hepatic CYP1A1 enzymatic activity increased (p < 0.05) starting at 0.15 ng/kg/day with L/F of 0.2 and body burden of 2.8 ng TCDD/kg body weight. By examining TCDD exposures at or near steady state, this study reports for the first time and provides direct evidence of low-dose effects on a measured reversible response at body burdens that are within background levels of the general human population. In addition, this study emphasizes cumulative effects of daily dosing and suggests the importance of tissue dosimetry or body burden for a persistent chemical such as TCDD.
Adipose Tissue↗
A comparison of the transport and fate of polychlorinated biphenyl congeners in three Great Lakes food webs.
A food web bioaccumulation model was used to compare transport and fate of polychorinated biphenyls (PCB) congeners in three food webs in the Laurentian Great Lakes of North America. The model was used to quantify the contribution of sediment-derived and freely dissolved PCBs to the body burden of aquatic biota. In eastern Lake Erie (OH, USA), almost 100% of the chemical body burden of biota originates from sediment. In western Lake Erie, benthic invertebrates accumulated slightly more than half of their PCB body burden from sediment while fish accumulated less than half of their chemical body burden from sediment. Fish from Lake Ontario, Canada, accumulated less than 30% of their body burden of PCB congeners with log Kow < 6.4 from sediment and approximately half of their body burden of PCB congeners with log Kow > or = 6.4 from sediment. Field data and the model were also used to determine the effects of declining concentrations of PCBs in water and sediment on concentrations of PCBs in aquatic biota. Results indicate that, as concentrations of PCB congeners in the ecosystem decline, the role of sediment as the source of contaminant to aquatic biota increases. Furthermore, as sediment becomes the predominant source of contaminant to aquatic biota. the concentration of PCB congeners in biota tends to equilibrium with bottom sediment.
Animals↗
Biological effects of 137CsCl injected in beagle dogs.
The toxicity of intravenously administered 137CsCl in the beagle dog was investigated as part of a program to evaluate the biological effects of internally deposited fission-product radionuclides. The intravenous route of exposure was chosen for simplicity and accuracy because it was known that after intravenous injection, inhalation or ingestion, internally deposited 137CsCl is rapidly absorbed and distributed throughout the body, exposing the whole body to beta-particle and gamma radiations. Fifty-four dogs were injected intravenously with 137Cs to provide one group of six dogs with mean initial body burdens of 141 MBq 137Cs/kg body mass and four groups of 12 dogs each with mean initial body burdens of 104, 72, 52 and 36 MBq 137Cs/kg. Twelve dogs were injected with isotonic saline as study controls. Because the number of study control dogs was small, data from an additional 49 control dogs from other studies at the Inhalation Toxicology Research Institute that were performed over a similar span of years were also used. There was a significant, dose-dependent decrease in survival of the 137Cs-injected dogs. Eleven 137Cs-injected dogs, including all six in the highest initial body burden group, died within 81 days after injection, primarily due to hematopoietic cell damage resulting in severe pancytopenia. An additional 25 dogs had transient hematological dyscrasia but survived for long times. All 137Cs-injected male dogs had marked damage to the germinal epithelium of the testicular seminiferous tubules with azoospermia in the long-term survivors. Benign and malignant neoplasms occurred in a variety of organs in 137Cs-injected dogs, rather than in a single target organ. When individual organs were considered, the incidence of malignant neoplasms was increased in the liver and in the nasal cavity and paranasal sinuses of the 137Cs-injected dogs. There was a 137Cs treatment effect in the incidence of malignant neoplasms (P < 0.001) in male dogs but no 137Cs-related treatment effect in female dogs. However, when malignant mammary neoplasms were excluded from the analysis, there was no gender difference, and there was a dose-related response (P < 0.001) in both males and females for the incidence of malignant neoplasms.
Animals↗
In situ quantification of aberrant p53 in colorectal neoplasia.
Aberrant p53 protein accumulation was measured immunohistologically in 342 colorectal paraffin-embedded tissue sections from 115 patients (24 with adenocarcinoma, 59 with adenoma and 32 'hospital controls'). Subjective scoring was compared with quantitative cell imaging, including dichotomous (p53+/p53-) status, ng p53mut mg(-1) enterocyte protein, and tumour burden and patient body 'burden' of aberrant p53. A total of 62.5% cancer patients, 23.7% adenoma patients and 3.1% hospital controls were accorded p53+ status on the basis of p53 quantification. Quantitative p53+/p53- assignment had a stronger inverse association with survival (chi2=6.17, p=0.013, Kaplan-Meier test) than subjective 'visual estimation' (chi2=0.57, p=0.449). There was a strong inverse relationship between the p53 'body burden' and the months of post-diagnosis survival (hazard ratio=1.42, p=0.0004, Cox proportional hazards). Absolute quantification for inactivated p53 permits objective and reproducible scoring, adjusts for intra-laboratory immunostaining 'batch effects', corrects for fixation artefacts, and standardizes for inter-laboratory differences in fixation, antibody selection and staining method. Clinically, in situ quantification of p53 will permit more accurate survival prognoses and will inform therapy selection and dose. Ultimately, accurate quantitative tissue/blood p53 correlations may provide a minimally invasive and systemic surrogate measure for these same clinical purposes.
Adenocarcinoma↗
[Lead and cadmium content in deciduous teeth of children of Stolberg and other cities of North-Rhine-Westphalia: a chronological trend 1968-1993].
The levels of lead and cadmium were determined in deciduous teeth (incisors only) of children living in Stolberg and some other cities located in North-Rhine-Westfalia, Germany. The Stolberg children were born in 1968-1973 (group 1; n = 103) and 1982/1983 (group 2; n = 103). The other children (n = 109) were born between 1979 and 1986. All teeth were analysed within the same analytical series by atomic absorption spectrometry (AAS). The results show that the average levels of lead and cadmium in milk teeth have decreased significantly in the time period from 1970 to 1990. Considering the Stolberg children the fall of tooth lead was about 50% and the fall of tooth cadmium was about 60%. Children from other cities show a comparable decrease of tooth lead and tooth cadmium. The results indicate that a significant decrease of the lead body burden and cadmium body burden of children and probably also of the general population of Germany has occurred during the last years.
Age Factors↗
A repository of bio-specimens from Mayak workers exposed to protracted radiation.
A repository of bio-specimens that includes organs from 700 deceased workers employed at the first nuclear weapons facility "Mayak" and donations of blood, buccal cells, and tissues removed at the time of surgery and/or biopsy from the members of the Mayak cohort undergoing medical treatment or diagnostic procedures has been established at the Southern Ural Biophysics Institute, in Ozyorsk, Russian Federation. The autopsied tissues include formaline-preserved organs, paraffin blocks, and histology slides. For all, occupational, dosimetry, and detailed medical information is available. For 359 individuals, information on malignant tumors, i.e., lung (171), stomach (51), liver (28), and intestine (19), as well as 32 cases of leukemia, are available. External gamma exposures are known for 95% of the 700 autopsies, of whom 560 were exposed to protracted doses exceeding 0.5 Gy, with known maximum annual doses ranging from 0.01-0.5 Gy for about 46%, and annual doses exceeding 0.5 Gy for 48%. Plutonium body burden is known for 73%, of which 40% had body burden greater than 1.5 kBq, and 15% of individuals had body burdens greater than 11.85 kBq. Newly collected specimens include frozen lymphocytes, EBV-immortalized B-cells, frozen erythrocytes, and DNA as well as frozen tumors. Donations were obtained to date from more than 1,600 individuals. For these donors external doses of exposure exceeded 0.5 Gy for 83%, and plutonium body burden exceeded 1.48 kBq for 30%. A Web site describing the Repository that also includes forms for tissue requests can be accessed at http://www.subi.ru/RHTR.
Autopsy↗
Elimination of PBBs in rats. Effect of mineral oil and/or feed restriction.
Rats were fed polybrominated biphenyls (PBBs) at 0.1 to 100.0 ppm for 14 d and then treated to hasten the removal of PBBs with 0, 5, or 10% mineral oil (MO) and/or 0, 15, 30, or 45% feed restriction (FR) for 21 d. PBB body burdens were determined at d 14 and expressed on a log-log basis by Y = 0.91X + 2.179 (r2 = 0.974), where X = log of PBB concentration in diet (ppm) and Y = log of PBB body burden (micrograms). After 21 d withdrawal, body burdens were expressed by the equation Y = 0.787X + 2.218 (r2 = 0.95). The most effective withdrawal treatment was 10% MO + 45% FR producing a reduction of body burdens inversely related to prior body burdens (69% at 0.1 ppm to 23% at 100 ppm). Body weights and fat content were significantly (p less than or equal to .05) reduced by feed restriction, with fat content only 39% of controls at 21 d off. Mortality averaged 0, 13.6, and 35.8% for rats fed 0, 5, or 10% MO, and 25, 15, 8.6, and 3.7% for rats feed restricted at 0, 15, 30, and 45%, respectively. Histopathology of the dead and moribund rats indicated that the clinical signs were not characteristic of PBB toxicity. In a second experiment, safflower oil at 3.5% or excess vitamins prevented the mortality and clinical signs associated with MO during withdrawal from 100 ppm PBBs. Based on these data and those in the literature, PBBs interfere with vitamin utilization.
Administration, Oral↗
The effects of dimercaptosuccinic acid on the excretion and distribution of mercury in rats and mice treated with mercuric chloride and methylmercury chloride.
1 All five rats in a group survived if dimercaptosuccinic acid (DMSA), a water soluble derivative of 2,3-dimercaptopropanol (BAL), was given in doses of 10-40 mg/kg intraperitoneally 30 min, 4 and 24 h after administration of 2.4 mg/kg Hg as HgCl2, whereas three out of a group of five died if DMSA was not given. DMSA 20 mg/kg increased urinary excretion and decreased the body burden significantly more than 10 mg/kg DMSA, but further doubling of the dose had only marginal effects. 2 DMSA was able to reduce body burden and increase urinary excretion of Hg when intraperitoneal treatment started eight days after the subcutaneous administration of HgCl2. 3 DMSA was effective in decreasing body burden and the brain concentration of Hg in rats dosed orally with methylmercury (MeHgCl) when intraperitoneal treatment started with 40 mg/kg DMSA 24 h after Hg. Increase in the urinary excretion of mercury was responsible for the decrease in body burden. 4 DMSA was effective when given in the drinking water of rats or mice both against inorganic Hg and MeHgCl. In mice treated intraperitoneally with MeHgCl, DMSA 19.5 mug/ml in the drinking water caused a significant decrease in the body burden and increase in the excretion of Hg. 5 DMSA was about four times more efficient than D-penicillamine in decreasing the body burden of Hg. As their toxicity is in the same range, the higher efficiency of DMSA offers a larger margin of safety for the mobilization of Hg.
Animals↗