Bone stores

In a review of data on occupational chemicals that may contaminate breast milk (Byczkowski et al. 1994), it is stated that lead may be excreted in milk in amounts lethal to the infant and that the metal may be mobilized from bone stores to milk during the lactation period. Even when the concentration of lead in mother s milk is low, the absorption of metals into the systemic circulation of infants is generally high when they are on a milk diet. To better understand the sensitivity of the nursing infant to chemicals, epidemiological studies, chemical monitoring, and model development and application are needed. 

Gulson BL, Mahaffey KR, Jameson CW, Patison N, Law AJ, Mizon KJ, Korsch MJ, Pederson D (1999) Impact of diet on lead in blood and urine in female adults and relevance to mobilization of lead from bone stores. Environ Health Perspect, 107(4) 257-263. 

Transfer of uranium across the placenta was investigated in an animal study, but no information is available for humans. In the animal study, only 0.01-0.03% of an intravenous dose of uranium to rat dams crossed the placenta (Sikov and Mahlum 1968) thus if an inhalation, oral, or dermal exposure was sufficient to raise the blood uranium level, a very limited amount of uranium might cross the placenta. No studies were located regarding uranium in breast milk. Based on the chemical properties of uranium, it seems unlikely that there would be preferential distribution from the blood to this high-fat compartment. It is not known if uranium has any effect on the active transport of calcium into breast milk. Most of the adult body burden of uranium is stored in bone (ICRP 1979, 1995, 1996). It is not known if maternal bone stores of uranium (like those of calcium and lead) are mobilized during pregnancy and lactation. 

Lead is measured in whole blood or in urine (Table 1). Excretion can be enhanced using any of the chelating agents NaCaEDTA. dimercaprol or N-acetyl-pcnicillamine. but may require to be prolonged in order to deplete bone stores. 

Blood lead monitoring during chelation. Obtain a blood lead measurement immediately prior to chelation and recheck the measurement within 24-48 hours after starting chelation to confirm that levels are declining. Recheck measurements 1 and 7 to 21 days postchelation to assess the extent of rebound in blood lead level associated with redistribution of lead from high bone stores, and/or the possibility of reexposure. Additional courses of treatment and further investigation of exposure sources may be warranted. 

A remaining issue with use of the traditional as well as the newer, outpatient chelants is the rebound phenomenon. Some insight about rebound biokinetics may be found in the Cory-Slechta et al. (1987) report discussed above and other citations there. They noted that alternate administrations across a serial dosing protocol, i.e., injections 1 and 3, produced bone Pb reductions but injections 2, 4, and 5 did not. They postulated return of mobilized Pb back to bone stores. If such redeposited Pb is more mobile than initially unmobilized Pb, this fraction s biokinetics of Pb movement to blood may differ from overall bone Pb mobility. 

PbP is the pathway by which Pb that is absorbed from receiving compartments or is resorbed from bone stores is transferred to target tissues or is excreted. Compared to the history of PbB as a widely accepted biomarker of Pb exposure, consensus acceptance of PbP as a potentially useful biomarker is relatively recent (NAS/NRC, 1993 U.S. EPA, 1986). There are two reasons for this. First, analytical methodological problems for measuring PbP on a routine basis are daunting. Second, while PbP is qualitatively assumed to be the more direct biomarker of dose in dose—toxic response relationships than PbB, quantitative expressions of these relationships are largely lacking. That is, what level of PbP is linked to what toxic expression(s) in dose—toxic response relationships ... 

Pb(II) binds strongly with phosphate group and forms insoluble lead phosphate PbjlPO ). Newly absorbed lead is retained in the body as lead phosphate in liver, kidneys, pancreas, and aorta. This results in a decrease of available phosphate level phosphate is one of the most important entities in the cell physiology. Pb(ll) happens to be similar in size to calcium, Ca(ll), and hence often replaces Ca(ll) in a bone mineral, which is essentially calcium phosphate Caj(PO )j. Bones store as much as 90% of the total body lead. It has been estimated that it takes 90 years for about half of the lead to be removed from the bone, assuming no new lead becomes incorporated in the bone meanwhile. That is, it is very slow. 

Studies show that the main sites of uranium deposition ate the renal cortex and the Hvet (8). Uranium is also stored in bones deposition in soft tissues is almost negligible. Utanium(VI) is deposited mostly in the kidneys and eliminated with the urine whereas, tetravalent uranium is preferentially deposited in the Hvet and eliminated in the feces. The elimination of uranium absorbed into the blood occurs via the kidneys in urine, and most, - 84%, of it is cleared within 4 to 24 hours (8). 

The concept of total body burden refers to the way a trace material accumulates in the human system. The components of the body that can store these materials are the blood, urine, soft tissue, hair, teeth, and bone. The blood and mine allow more rapid removal of trace materials than the soft tissue, hair, and bone (5). Accumulation results when trace materials are stored more rapidly than they can be eliminated. It can be reversed when the source of the material is reduced. The body may eliminate the trace material over a period of a few hours to days, or may take much longer— often years. 

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. 

Storage conditions in terms of air movement and humidity will be different to those used when initially chilling the carcase. Chilled meat on the bone is stored at about 0°C, up to the point of sale. The humidity of the surrounding air is also critical in the case of fresh meats - too dry and the meat will lose weight and discolour, too humid and a slime will form on the surface. 

Cut meats are usually wrapped or vacuum packed directly after cutting. The viscera, bones and other parts not going for human consumption have a byproduct value, and will probably need to be stored at chill temperature before disposal. 

The shift to the use of PBPCs over bone marrow for autologous HCT is primarily because of the more rapid engraftment and decreased health care resource use. Because the harvest occurs before administering the preparative regimen, autologous hematopoietic cells must be cryopreserved and stored for future use. 

Lymphatic system The tissues and organs that produce, store, and carry white blood cells that fight infection and disease. This system includes the bone marrow, spleen, thymus, and lymph nodes and a network of thin tubes that carry lymph and white blood cells. 

Exchanges between bone and soft tissue stores of americium would be expected to be more rapid during periods of active bone metabolism such as infancy and childhood, pregnancy, and menopause. Thus, it is possible that, in humans, some of the maternal bone americium stores may be transferred to the fetus during gestation and may be incorporated into fetal bone during the development of the fetal skeleton. 

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