Lead in feces

Lead acetate administered at 100 pg lead/g in the drinking water of fasting rats for 3 days resulted in a 2-fold increase in the total mass of lead excreted in feces and urine compared with the same dose rate for fed rats (Hayashi et al. 1993). In addition, the total mass of lead in feces of control animals that were fasted for 3 days resulted in an increase in the mass of lead excreted, suggesting that excretion of lead from other tissues is enhanced during short periods of fasting. 

Riner, J.C., Wright, W.C. and McBeth, C.A. (1974). A technique for determining lead in feces of cattle by flameless atomic absorption spectrophotometry. At. Absorpt. Newsl. 13. 129-130... 

Lead is excreted in both urine and feces. However, true alimentary excretion is small and most of the lead in feces represents unabsorbed lead, while most absorbed lead is excreted by the kidneys. In normal individuals (no known exposure) the daily urinary excretion is 10-75 ng of lead, with the borderline at 80-100 /Ag/day (R4). Concentrations of 50 /ig/liter or greater generally indicate lead poisoning. Kehoe and co-workers have studied the excretion of lead in normal and lead-intoxi--cated individuals (K4-K6). Lead affects porphyrin metabolism (G7). 

In 1983-1984 blood of male teachers (age 25-50 years, nonsmokers) was collected in Malta, Mexico, Belgium, and Sweden. The choice of teachers was done to ensure comparable socioeconomic status [29]. Considerable differences in Pb-B levels are revealed between the countries, with the blood lead levels of Maltese teachers four times higher than those of Swedish teachers. The daily oral intake of lead was estimated from measurements of lead in feces to be around 1.9 p,mol in Malta, 0.86 p,mol in Mexico, 0.44 ixmol in Belgium, and 0.12 p,mol in Sweden, but no specific source to the high intake in Malta was pinpointed. This study and a few others indicate the reality of between-country differences in Pb-B levels [30] and also demonstrate the difficulties in establishing reliable reference values. 

The feces represents the major route of organic and inorganic lead elimination in man. The rate of fecal lead elimination is about 100 times the rate of elimination in urine, although most of the lead in feces represents metal that was not absorbed in the digestive tract. The characteristics of urinary lead excretion may be affected by the chemical form of the lead. Onyl one-third to two-thirds of the lead in the urine of lead workers is available for precipitation, indicating the presence of a stable lead complex. The lead concentration of sweat has also been found proportional to the dose. Although lead excretion appears to be disproportionally low in cases of high-level exposure, there is not yet a predictable relationship between increases in lead exposure and in lead excretion [73, 77]. 

The absorption, distribution, and accumulation of lead in the human body may be represented by a three-part model (6). The first part consists of red blood cells, which move the lead to the other two parts, soft tissue and bone. The blood cells and soft tissue, represented by the liver and kidney, constitute the mobile part of the lead body burden, which can fluctuate depending on the length of exposure to the pollutant. Lead accumulation over a long period of time occurs in the bones, which store up to 95% of the total body burden. However, the lead in soft tissue represents a potentially greater toxicological hazard and is the more important component of the lead body burden. Lead measured in the urine has been found to be a good index of the amount of mobile lead in the body. The majority of lead is eliminated from the body in the urine and feces, with smaller amounts removed by sweat, hair, and nails. 

Your body does not change lead into any other form. Once it is taken in and distributed to your organs, the lead that is not stored in your bones leaves your body in your urine or your feces. About 99% of the amount of lead taken into the body of an adult will leave in the waste within a couple of weeks, but only about 32% of the lead taken into the body of a child will leave in the waste. Under conditions of continued exposure, not all the lead that enters the body will be eliminated, and this may result in accumulation of lead in body tissues, notably bone. For more information on how lead can enter and leave your body, please refer to Chapter 2. 

Lead is also eliminated in the bile (Klaassen and Shoeman 1974). In the rat, excretion occurs in the urine, with greater excretion in the feces following intravenous administration (Castellino and Aloj 1964 Klaassen and Shoeman 1974 Morgan et al. 1977). As the dose increases, the proportion of the lead excreted into the gut via bile increases, then plateaus at 3 and 10 mg/kg (Klaassen and Shoeman 1974). Biliary excretion of lead is suggested to be a saturable process (Gregus and Klaassen 1986). Excretion of lead in the bile by dogs amounted to approximately 2% of that by rats, and biliary excretion of lead by rabbits amounted to approximately 40% of that by rats (Klaassen and Shoeman 1974). 

Different animal species exhibit differences in GI absorption rates. The extent of GI absorption of lead in rats, for example, can be studied by feeding the animals known amounts of the metal and analyzing the unabsorbed amount that comes through in feces the difference is the amount absorbed. But because of possible species differences it is not possible to conclude that humans will absorb the same amount of lead as the rat. These types of differences complicate evaluation of toxic potential. At the same time, they help to explain why different species of animals respond differently to the same dose of a chemical. 

There are a large number of hereditary or acquired disturbances of porphyrin synthesis, known as porphyrias, some of which can cause severe clinical pictures. Several of these diseases lead to the excretion of heme precursors in feces or urine, giving them a dark red color. Accumulation of porphyrins in the skin can also occur, and exposure to light then causes disfiguring, poorly healing blisters. Neurological disturbances are also common in the porphyrias. 

Intoxication within 8 weeks most dead at day 105 Some deaths, mostly younger animals neurological signs. Lead levels, in mg/kg fresh weight, were 13.8 to 35.8 in blood, 6.9 to 96.5 in feces, 97 in liver, and 138 in kidney. Histopathology of liver and kidney Fatal in 8 to 22 days... 

Vinblastine is an alkaloid derived from the periwinkle plant Vinca rosea. Its mechanism of action involves inhibition of tubulin polymerization, which disrupts assembly of microtubules, an important part of the cytoskeleton and the mitotic spindle. This inhibitory effect results in mitotic arrest in metaphase, bringing cell division to a halt, which then leads to cell death. Vinblastine and other vinca alkaloids are metabolized by the liver P450 system, and the majority of the drug is excreted in feces via the biliary system. As such, dose modification is required in the setting of liver dysfunction. The main adverse effects are outlined in Table 54-4, and they include nausea and vomiting, bone marrow suppression, and alopecia. This agent is also a potent vesicant, and care must be taken in its administration. It has clinical activity in the treatment of Hodgkin s... 

Metabolism leads to their rapid deactivation in tire body and, hence, these compounds exhibit little oral activity. Thus, they have to be given parenterally. Most of the catabolism of these compounds occurs in liver, and enterohepatic circulation may then occur, with the metabolites exerting little if any biological activity. In cattle, most of these compounds are eliminated in feces where 60-90% of the metabolites are found in the free form. In conttast, metabolites occurring in urine are predominantly in conjugated forms. 

HCHs are readily absorbed through the gastrointestinal tract. Inhaling air contaminated with isomers of HCH can also lead to systemic absorption. HCHs can also be absorbed through the skin when used as a lotion, cream, or shampoo for the treatment or control of ectoparasites. In general, HCH isomers and their metabolites can be temporarily stored in body fat. Absorbed HCHs are mainly excreted via the urine. Lesser amounts are excreted in feces. In rats, the highest concentrations have been found in liver, kidneys, body fat, brain and muscles, with substantial deposition occurring in fatty tissue. 

In the healthy bowel, fecal protein is largely derived from enterocytes shed from the mucosal surface and from intestinal secretions. The normal Gl loss of albumin is less than 10% of albumin catabofism, representing a daily loss of less than 1% to 2% of the serum protein pool. " Protein loss may be greatly increased in disease. In studies using Cr-labeled proteins, 0.1% to 0.7% of an injected dose was excreted in feces over 4 days in healthy subjects in protein-losing enteropathies this may increase to 40%, leading to hypoal-buminemia and edema. 

The amount of secondary products of neutral steroids and bile acids in feces of patients with ulcerative colitis appears to be reduced as compared to normal subjects (88). Thus bacterial action on steroids is decreased, probably owing to enhanced colonic motility, and may lead to reduced absorption of primary and especially secondary bile acids from the colon. This may explain the absence or low level of lithocholic acid in serum (188,193) of these patients and does not support the concept that lithocholic acid causes the liver damage (212) found frequently in ulcerative colitis. 

CaNa2EDTA), and oral chelating agents, such as 2,3-dimercaptosuccinic acid (commonly referred to as DMSA) (Graziano et al. 1985). A much smaller proportion of absorbed lead is excreted in feces, sweat, breast milk, seminal fluid, and hair. 

The first step should preferably lead to a group separation of bile acids and to elimination of non-bile acid contaminants. In quantitative work it may be useful to add—at this stage or earlier—labeled compounds, which permit an estimation of recovery of bile acids of different polarities. Tauro-cholic and 3-ketocholanoic acids constitute suitable extremes in polarity. If specific bile acids are to be analyzed, one may add a suitable internal standard to the biological material. Thus, Rooversc/ r/. (36) used nordeoxy-cholic acid for gas chromatographic determination of bile acids in feces and plasma. 

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