Excretion estimation

Information on the excretion of americium after dermal exposure in humans or animals is extremely limited. Some qualitative information is available from an accidental exposure in which a worker received facial wounds from projectile debris and nitric acid during an explosion of a vessel containing 241 Am (McMurray 1983). The subject also inhaled 241Am released to the air as dust and nitric acid aerosols, which was evident from external chest measurements of internal radioactivity thus, excretion estimates reflect combined inhalation, dermal, and wound penetration exposures (Palmer et al. 1983). Measurements of cumulative fecal and urinary excretion of241 Am during the first years after the accident, and periodic measurements made from day 10 to 11 years post accident indicated a fecal urine excretion ratio of approximately 0.2-0.3, although the ratio was approximately 1 on day 3 post accident (Breitenstein and... 

An ecological study showed a strong association between the iodine content of tap water in 41 towns and the iodine excretion estimated from more than four thousand 24 h urine samples collected 30 years apart (Figure 13.10) (Pedersen 1999). 

Figure 44.5 Variation in urinary iodine excretion expressed as crude urinary iodine content ( rg/l) and as 24 h urinary iodine excretion estimated from creatinine excretion in an age- and gender-matched group ( rg/24h).

P. M. % excreted Estimated blood level globin levels... 

Toxicology. Inorganic tin and its compounds are generally of a low order of toxicity, largely because of the poor absorption and rapid excretion from the tissues of the metal (42—49). The acidity and alkalinity of their solutions make assessment of their parenteral toxicity difficult. The oral LD q values for selected inorganic tin compounds are Hsted in Table 2. It is estimated that the average U.S. daily intake of tin, which is mostly from processed foods, is 4 mg (see Food processing). 

Relatively Httie is known about the bioavailabiUty of pantothenic acid in human beings, and only approximately 50% of pantothenic acid present in the diet is actually absorbed (10). Liver, adrenal glands, kidneys, brain, and testes contain high concentrations of pantothenic acid. In healthy adults, the total amount of pantothenic acid present in whole blood is estimated to be 1 mg/L. A significant (2—7 mg/d) difference is observed among different age-group individuals with respect to pantothenic acid intake and urinary excretion, indicating differences in the rate of metaboHsm of pantothenic acid. 

Approximately 0.05 to 0.2% of vitamin > 2 stores are turned over daily, amounting to 0.5—8.0 )J.g, depending on the body pool size. The half-life of the body pool is estimated to be between 480 and 1360 days with a daily loss of vitamin > 2 of about 1 )J.g. Consequentiy, the daily minimum requirement for vitamin B22 is 1 fig. Three micrograms (3.0 J.g) vitamin B22 are excreted in the bile each day, but an efficient enterohepatic circulation salvages the vitamin from the bile and other intestinal secretions. This effective recycling of the vitamin contributes to the long half-life. Absence of the intrinsic factor intermpts the enterohepatic circulation. Vitamin > 2 is not catabolized by the body and is, therefore, excreted unchanged. About one-half of the vitamin is excreted in the urine and the other half in the bile. 

The GI absorption of the dmg after po adrninistration is slow and variable with estimates ranging from 20—55%. Once absorbed, 96% of the dmg is bound to plasma proteins and other tissues on the body. Whereas peak plasma concentrations may be achieved in 3—7 h, the onset of antiarrhythmic action may occur in 2—3 days or more. This may result, in part, from distribution to and concentration of the dmg in adipose tissue, Hver, spleen, and lungs. Therapeutic plasma concentrations are 1—2 p.g/mL, although there appears to be no correlation between plasma concentration and antiarrhythmic activity. The plasma half-life after discontinuation of the dmg varies from 13—103 days. The dmg is metabolized in the Hver and the principal metaboHte is desethylamiodarone. The primary route of elimination is through the bile. Less than 1% of the unchanged dmg is excreted in the urine. The dmg can also be eliminated in breast milk and through the skin (1,2). 

The body excretes tritium with a biological half-life of 8—14 d (10.5 d average) (75), which can be reduced significantly with forced fluid intake. For humans, the estimated maximum permissible total body burden is 37 MBq (1 mCi). The median lethal dose (LD q) of tritium assimilated by the body is estimated to be 370 GBq (10 Ci). Higher doses can be tolerated with forced fluid intake to reduce the biological half-life. 

One of six workers died 12 days after exposure to a mixture of half dimethyltin dichloride and half trimeth-yltin chloride vapour during cleaning of a cauldron at a chemical plant in Germany in 1981. Maximum exposure time was 1.5 h over a 3-day period no estimates of exposure concentration were made. Symptoms preceding death included excretion of high levels of tin in the urine, respiratory depression, and coma (Rey et al.,... 

Nitrogen isotope ratios ( N/ " N) inerease from plants to herbivores to eami-vores and ean be used to estimate the degree of camivory in human diets. Some field studies observe a greater differenee in 5 N between trophie levels in dry, hot habitats than in wet, cool ones. Two hypotheses have been proposed to explain this variation in difference in 8 N between trophic levels. (1) Elevated excretion of -depleted urea in heat/water-stressed animals (2) recycling of nitrogen on protein-deficient diets. Both predict increased diet-tissue 8 N difference under stress. 

Renal excretion is the most important endosulfan elimination route in humans and animals. Biliary excretion has also been demonstrated to be important in animals. Estimated elimination half-lives ranged between approximately 1 and 7 days in adult humans and animals. Endosulfan can also be eliminated via the breast milk in lactating women and animals, although this is probably a relatively minor elimination route. No studies were located regarding known or suspected differences between children and adults with respect to endosulfan excretion. 

The cause of Wilson disease was also revealed in 1993, when it was reported that a variety of mutations in a gene encoding a copper-binding P-type ATPase were responsible. The gene is estimated to encode a protein of 1411 amino acids, which is highly homologous to the product of the gene affected in Menkes disease. In a manner not yet fully explained, a nonfunctional ATPase causes defective excretion of copper into the bile, a reduction of incorporation of copper into... 

Buhl, M.R. and Jorgensen, S. (1975). Breakdown of 5 -adenine nucleotides in ischaemic renal cortex estimated by oxypurine excretion during perfusion. Scand. J. Clin. Lab. Invest. 35, 211-217. 

Loft, S., Vistisen, K., Ewertz, M., Tjonneland, A., Overvad, K. and Poulsen, H.E. (1992). Oxidative DNA damage estimated by 8-hydroxydeoxyguanosine excretion in humans influence of smoking, gender and body mass index. Carcinogenesis 13, 2441-2447. 

Enhanced nutrient cycling in both the rhizosphere and bulk soil may depend on the bacterial grazing by protozoa or nematodes with release of inorganic N. Nematodes appear to be the primary consumers of bacteria in the rhizosphere, whereas protozoa are equally prevalent in rhizosphere and bulk soil (41,97). Estimated C-to-N ratios of bacterial-feeding nematodes range from 5 1 to 10 1 (98,99) and are generally higher than those of their bacterial food source thus the excess N is excreted as ammonia (100,101) by nematodes. The estimated... 

Applicators, mixers, loaders, and others who mix, spray, or apply pesticides to crops face potential dermal and/or inhalation exposure when handling bulk quantities of the formulated active ingredients. Although the exposure periods are short and occur only a few times annually, an estimate of this exposure can be obtained by quantifying the excreted polar urinary metabolites. Atrazine is the most studied triazine for potential human exposure purposes, and, therefore, most of the reported methods address the determination of atrazine or atrazine and its metabolites in urine. To a lesser extent, methods are also reported for the analysis of atrazine in blood plasma and serum. 

---