Carbon body burden

The effect of accumulation in various systems depends greatly on the quantity of pollutants involved. Many pollutants can be detected at concentrations lower than those necessary to affect human health. For pollutants which are eliminated slowly, individuals can be monitored over long periods of time to detect trends in body burden the results of these analyses can then be related to total pollutant exposure. Following are two examples of air pollutants that contribute to the total body burden for lead and carbon monoxide. 

The second example of an air pollutant that affects the total body burden is carbon monoxide (CO). In addihon to CO in ambient air, there are other sources for inhalation. People who smoke have an elevated CO body burden compared to nonsmokers. Individuals indoors may be exposed to elevated levels of CO from incomplete combustion in heating or cooking stoves. CO gas enters the human body by inhalation and is absorbed directly into the bloodstream the total body burden resides in the circulatory system. The human body also produces CO by breakdown of hemoglobin. Hemoglobin breakdown gives every individual a baseline level of CO in the circulatory system. As the result of these factors, the body burden can fluctuate over a time scale of hours. 

In studies of mice, rats, and dogs, diisopropyl methylphosphonate was rapidly absorbed into plasma (Hart 1976). The plasma data indicate that all three species rapidly absorbed diisopropyl methylphosphonate, although the exact rate was species specific. Although no studies were located regarding human absorption, diisopropyl methylphosphonate is also likely to be absorbed rapidly into the plasma of humans. The ability of porous polymeric sorbents, activated carbon, and dialysis to remove diisopropyl methylphosphonate from human plasma has been studied (McPhillips 1983). The grafted butyl-XAD-4 was found to be the most efficient sorbent for the removal of diisopropyl methylphosphonate from human plasma. Hemoperfusion of plasma over synthetic XAD-4 or butyl-XAD-4 sorbent resin was more efficient than dialysis/ultrafiltration for the removal of diisopropyl methylphosphonate from human plasma the smaller surface of the packed resins provided less area to minimize damage to molecular constituents of the plasma. These methods are useful in reducing diisopropyl methylphosphonate concentrations in the plasma. However, since diisopropyl methylphosphonate and its metabolites are not retained by the body, the need for methods to reduce body burden is uncertain. 

Methods for Reducing Toxic Effects. Little information is available regarding reducing the toxic effects of diisopropyl methylphosphonate following exposure. Recommended treatments include general hygienic procedures for rapid decontamination. The ability of porous polymeric sorbents, activated carbon, and dialysis to remove diisopropyl methylphosphonate from human plasma has been studied. However, since diisopropyl methylphosphonate and its metabolites are not retained by the body, the need for methods to reduce body burden is uncertain. 

In addition to tobacco smokers, individuals who have had previous exposure to materials containing methylene chloride, such as degreasers, solvents, paint removers, and furniture strippers, are at greater risk because of an existing body burden of carbon monoxide. Approximately one-fourth to one-third of inhaled methylene chloride vapor is metabolized in the liver to carbon monoxide. In addition, methylene chloride is readily stored in body tissue. This stored material is released over time and results in elevated levels of carbon monoxide for extended periods, in some cases more than twice as long as compared with direct carbon monoxide inhalation. 

A variety of laboratory studies conducted over the last decade have evaluated the bioavailability and toxicity of SPs in sediments. Maund et al. [25] studied the partitioning, bioavailability, and toxicity of cypermethrin to II. azteca and C. dilutus using three sediments with organic carbon contents of 1, 3, and 13%. Bioavailability was assessed by measuring the body burden in C. dilutus and results demonstrated that bioavailability decreased with increasing organic carbon content... 

Excretion. Chloroform is largely excreted either in the parent form or as the end metabolite (carbon dioxide, CO2) in the bodies of both laboratory animals and humans. Corley et al. (1990) demonstrated that mice exposed to 10 or 89 ppm of chloroform by inhalation excreted 99% of the chloroform body burden as CO2 in exhaled air. As the chloroform concentrations in the air rose however, the amount of chloroform metabolized to CO2 decreased and the amount of unchanged chloroform rose in the exhaled air, indicating that chloroform metabolism in mice is a saturable process. Rats exposed in a similar manner to 93, 356, and 1,041 ppm chloroform excreted 2, 20, and 42.5%, respectively, of the total body burden of chloroform as unchanged parent compound, indicating that chloroform is metabolized to CO2 in rats but to a lesser degree than in mice. 

Methods for Reducing Toxic Effects. The usefulness of methods and treatments for reducing peak absorption and reducing the body burden of carbon tetrachloride are rather limited due to the chemical s rapid rates of absorption and tissue disposition. On the other hand, investigations of antidotal therapy based on the mechanism of action has been limited to a few studies involving the administration of compounds to reduce free radical injury. Additional studies would be useful to better establish the effectiveness of both acute and prolonged antidotal therapy, since carbon tetrachloride is persistent in the body. 

Reliable monitoring data for the levels of carbon tetrachloride in contaminated media at hazardous waste sites are needed so that the information obtained on levels of carbon tetrachloride in the environment can be used in combination with the known body burden of carbon tetrachloride to assess the potential risk of adverse health effects in populations living in the vicinity of hazardous waste sites. 

You are interested in the well-being of Ampelisca abdita, living in a harbor whose sediments are contaminated with 4-nonylphenol. You remember that the lethal volume fraction of narcotic chemicals in membranes is about 0.01 L compound L I lipid. If the sediment contains 2% organic carbon by weight, and the amphipod is assumed to accumulate body burdens up to equilibrium with the sediments on which it lives, what sediment concentration of 4-nonylphenol should be deemed acceptable with respect to baseline toxicity Assume a log ,lipsw = 5.5 for 4-nonylphenol. Use Eq. 9-26c (alkylated and chlorinated benzenes ) for estimating Kioc. Compare your result with the findings of Fay et al. (2000), who observed a die-off of half the amphipods when they were exposed to about 0.16 g 4-nonylphenol - kg-1 sediment. 

Further studies in the area of HOC accumulation in phytoplankton should concentrate on identifying and quantifying the mechanisms of uptake and depuration. Any descriptions of mechanisms are still speculative, although the data indicate that there are multiple uptake and loss processes. Furthermore, an understanding of the fate of HOCs within phytoplankton would be beneficial and would assist in determining the most accurate denominator for body burden (i.e., dry weight, organic carbon, or lipid fraction). 

Methods for Reducing Toxic Effects. There are no established methods for reducing absorption of DEHP or metabolites because the mechanism of absorption is not known. There have been no studies of compound-specific techniques for reducing DEHP body burden. External contact with DEHP can be treated by thoroughly washing the affected area. Activated carbon, possibly combined with a cathartic, will diminish absorption of ingested DEHP from the gastrointestinal tract (HSDB 2000). 

The secretion of and the subsequent reaction with H2PO4 allow the removal of one H without any significant decrease in urinary pH. As a result, the pH gradient is not greatly affected and more H" can be secreted into the tubules, whereas more Na is reabsorbed and conserved. The HCO3 formed by the action of carbonic anhydrase in the tubular cells in the process of H secretion reclaims the HCOJ lost in buffering the body burden of ingested or produced acid. 

In animal studies, the body burden of [ " C]2-butoxyethanol following 6-hour nose-only inhalation exposure of male Fischer 344 rats was determined at several inhaled concentrations (Sabourin et al. 1992a). The uptake (4.49 mol/ppm at 4.3 ppm 4.58 mol/ppm at 49 ppm 3.58 mol/ppm at 438 ppm) and metabolism (0.79 moFppm at 4.3 ppm 0.95 mol/ppm at 49 ppm 0.88 mol/ppm at 438 ppm) of 2-butoxyethanol, expressed as [ " C]2-butoxyethanol equivalents, were essentially linear up to 438 ppm. Most (greater than 80%) of the [ " C]2-butoxyethanol-derived material in blood was in the plasma. 2-Butoxyacetic acid was the major metabolite of 2-butoxyethanol in plasma. Ratios of ethylene glycol to 2-butoxyacetic acid in plasma were higher than those in urine. The 2-butoxyethanol-derived in plasma rapidly became associated with the acid-precipitable (protein) fraction, probably because of binding of metabolites to proteins or incorporation of the 2-butoxyethanol metabolites into the carbon pool. 

Chloroethanol, 2-butoxyethanol, carbon tetrachloride, 1,1,2-trichloroethane, DMF and dimethylsulfoxide gave rise to mortality in guinea pigs exposed percu-taneously (Wahlberg and Roman 1979). Fatalities in man have also been reported. An important aspect is thus that percutaneous absorption contributes to the total body burden, and there are strong motives to reduce percutaneous uptake as well as inhalation of solvents. 

Bioavailability and organism physiology are the two important variables that have a major effect on chemical contaminant body burden. Of the total environmental concentration, only the bioavailable fraction can enter the organism. Unlike that of metals and ionizable organics, the bioavailability of PAHs is affected by only a few environmental variables such as organic carbon and sediment surface area. Physiological factors, including lipid levels and the rates of uptake and elimination (metabolism, diffusion, and excretion), also determine contaminant body burden. 

Excretion. Excretion of toxic substances is a function of a critical balance between intake, body burden, and turnover in the storage tissues. Assuming repeated exposure to a substance, there is a steady increase of concentration until the storage tissues are saturated or at least until uptake and excretion are equal. For some toxic substances, such as carbon monoxide, the substance can be excreted completely between successive days of low-level exposure. 

Most chemicals have longer residence times in the body than carbon monoxide. The term used to denote the length of time that 50 percent of the body burden of a substance is excreted is the biological half-life. The biological half-life of a compound can vary from one tissue to another. Thus, the biological half-life of lead in bone is between ten to twenty years, but in blood and soft tissues it is in the 30-day range. 

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