Human exposure urine

Application to Human Exposure (Urine Samples). Vycudihk (1985, 1987) analyzed urine samples from multiple casualties of the Iran-Iraq War in the 1980s that were hospitalized for treatment of suspected sulfur mustard exposure. Urine samples from eight of the patients produced positive results for sulfur mustard using GC-MS. Concentrations found ranged from 1 to 30 ng/mL. The method could not distinguish between sulfur mustard and its hydroxyethyl metabohtes that were present in the urine samples. 

Application to Human Exposure (Urine and Blood). To date, there have been no reports of the collection of biomedical samples from individuals with suspected lewisite exposure. Samples from such an incident will be critical for confirming the validity of assaying for the biomarkers observed in animal models. Additionally, the biomarkers that have been investigated in animal studies to date have indicated a rapid clearance in urine and less so for blood. This will obviously create severe problems for the retrospective determination of lewisite exposure beyond a few days at most when analyzing urine samples. The blood assay for both bound and free CVAA will potentially provide a longer opportunity for retrospective confirmation of exposure (based on one animal study), but also indicates a substantial decrease (90%) in concentration levels observed over a 10 day period. 

Shafik TM, Bradway DE, Enos HR, et al. 1973a. Human exposure to organophosphorus pesticides A modified procedure for the gas-liquid chromatographic analysis of alkylphosphate metabolites in urine. J Agr Food Chem 21 625-629. 

Exposure Levels in Humans. Endosulfan and endosulfan sulfate can be measured in human blood, urine, and tissues following exposure to high levels in worlq)lace environments or following accidental or intentional ingestion of insechcides containing endosulfan (Coutselinis et al. 1978 Demeter and Heyndrickx 1978 Demeter et al. 1977). However, no monitoring studies are available in which human... 

GC/MS has been employed by Demeter et al. (1978) to quantitatively detect low-ppb levels of a- and P-endosulfan in human serum, urine, and liver. This technique could not separate a- and P-isomers, and limited sensitivity confined its use to toxicological analysis following exposures to high levels of endosulfan. More recently, Le Bel and Williams (1986) and Williams et al. (1988) employed GC/MS to confirm qualitatively the presence of a-endosulfan in adipose tissue previously analyzed quantitatively by GC/ECD. These studies indicate that GC/MS is not as sensitive as GC/ECD. Mariani et al. (1995) have used GC in conjunction with negative ion chemical ionization mass spectrometry to determine alpha- and beta-endosulfan in plasma and brain samples with limits of detection reported to be 5 ppb in each matrix. Details of commonly used analytical methods for several types of biological media are presented in Table 6-1. 

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. 

Unchanged compounds or metabolites in blood and urine can be used to monitor human exposure to some carbamates. Table 5 shows some biological indices of internal dose used to monitor carbamate exposure. Urine carbamate metabolites may provide a good estimate of the internal dose because the half-life of most compounds is very short, samples collected soon after the end of the exposure are preferable for analysis (WHO, 1986). 

Dithiocarbamates are chemically characterized by the presence of metals in the molecule (iron, manganese, zinc, etc.) therefore, the measurement of these metals in urine has been proposed as an alternative approach to monitor exposure. For instance, increased urinary excretion of manganese has been reported in workers exposed to mancozeb (Canossa et al., 1993). Available data are at present insufficient to confirm the possibility of using metals as biomarkers of human exposure to DTC. 

Catenacci, G., Maroni, M., Cottica, D., and Pozzoli, L. (1990) Assessment of human exposure to atrazine through the determination of free atrazine in urine, Bulletin of Environmental Contamination and Toxicology, 44 1-7. 

In environmental health studies conducted near four NPL sites (plus a comparison area for each), ATSDR collected lead concentration data from both environmental media and human body fluids to estimate low-level exposure risk and to document the magnitude of human exposure to lead near those sites. Environmental samples collected at participants homes included drinking water, yard soil, house dust, and house paint body fluids collected from participants included venous blood and urine specimens. For the four sites, mean concentrations of lead in soil ranged from 317 to 529 mg/kg, and mean concentrations of lead in dust ranged from 206 to 469 mg/kg (ATSDR 1995). 

Metabolism in the rat is qualitatively similar to that in humans. Four male and four female Wistar rats were exposed individually to 14C-labeled HFC134a at 10,000 ppm for 1 h (Ellis et al. 1993). Atmospheres were monitored with a gas chromatograph. After exposure, urine and feces were collected at 6 h intervals up to 24 h and every 24 h for up to 5 d thereafter. Approximately 1% of the inhaled dose was recovered in urine, feces, and expired air of that 1%, approximately two-thirds was exhaled within 1 h postexposure as unchanged HFC-134a. Exhaled C02 was the primary metabolite and accounted for approximately 0.22% and 0.27% of the inhaled dose in males and females, respectively. Excretion in the urine and feces occurred within 24 h and accounted for 0.09% and 0.04% of the inhaled dose, respectively. The only metabolite identified in urine was trifluoroacetic acid. At sacrifice, 5 d postexposure, radioactivity was uniformly distributed among tissues and accounted for 0.14-0.15% of the inhaled dose. The average total metabolized dose in male and female rats was 0.37% of the inhaled dose. 

Perbellini L, Mozzo P, Brugnone F, et al. 1986. Physiologicomathematical model for studying human exposure to organic solvents Kinetics of blood/tissue -hexane concentrations and of 2,5-hexanedione in urine. Brit J Ind Med 43(11) 760-768. 

Exposure. Concentrations of cyanide and its metabolite thiocyanate can be measured in the blood, urine, and tissues. Since certain amounts of cyanide can always be found in the human tissues, urine, and expired air, only exposure to high doses can be detected by this way. Cyanide is metabolized in the body to thiocyanate in a reaction that is catalyzed by an enzyme rhodanese and mercaptopyruvate sulfur transferase (Ansell and Lewis 1970). 

Human exposure to low levels of phenol is widespread because it is contained in many consumer products including mouthwashes, gargles, tooth drops, throat lozenges, and ointments (Douglas 1972 EPA 1980). Phenol is a normal product of protein metabolism, and it is also a metabolite of benzene. In persons not exposed to phenol or benzene, the total phenol concentration in the urine generally does not exceed 20 mg/L and is usually <10 mg/L (ACGIH 1991). 

The changes in metabolite concentrations in human blood, urine, or other appropriate biological media over time may be useful in estimating phenol s rate of metabolism in humans. In some instances, the quantification of metabolites may be useful in correlating the exposure doses to the human body burden. Studies that correlate phenol exposure with levels of metabolites in human biological matrices are not available for this compound, although analytical methods for the quantification of the metabolites are available. 

Exposure Levels in Humans. 1,2-Dibromoethane can be measured in blood and metabolites can be detected in urine (Letz et al. 1984 Nachtomi et al. 1965). However, since the compound is rapidly and extensively metabolized in mammals, and 1,2-dibromoethane metabolites do not persist in tissues, these biomarkers have not been useful in identifying or quantifying human exposure to the compound. 

In recent years there has been an upsurge in efforts to move from indirect measures of human exposure (obtained by measurements of chemicals in environmental media and estimation of dose accrued from contact with those media) to direct measures of the concentrations of chemicals in the body, typically in blood and in elimination pathways such as urine and hair. The most significant effort in this direction in the United States has been undertaken as part of the CDC s National Health and Nutrition Examination Survey (NHANES). 

Analytical methods exist for measuring heptachlor, heptachlor epoxide, and/or their metabolites in various tissues (including adipose tissue), blood, human milk, urine, and feces. The common method used is gas chromatography (GC) coupled with electron capture detection (ECD) followed by identification using GC/mass spectrometry (MS). Since evidence indicates that heptachlor is metabolized to heptachlor epoxide in mammals, exposure to heptachlor is usually measured by determining levels of heptachlor epoxide in biological media. A summary of the detection methods used for various biological media is presented in Table 6-1. 

Abstract We have reviewed the human exposure to selected emerging organic contaminants, such new brominated flame retardants, organophosphate flame retardants, phthalate substitutes, triclosan, synthetic musks, bisphenol-A, perchlorate, and polycyclic siloxanes. Levels of these emerging contaminants in matrices relevant for human exposure (air, dust, food, water, etc.) and in human matrices (blood, urine, or tissues) have been reviewed, together with some of the relevant health effects reported recently. 

To evaluate human exposure to phthalates and their substitutes, the main approaches investigate either the levels of chemicals in matrices relevant for human exposure (indoor air, dust, food and packages, etc.) or the levels of parent and metabolite compounds in human samples (serum, urine, or breast milk). An overview of phthalate and nonphthalate plasticizers together with their metabolites commonly reported in literature is presented in Table 5. The half-lives for the most of these compounds are already established and therefore, by evaluating the levels of their metabolites in human urine, the levels of their parent compounds may be... 

Some studies showed already that the levels of phthalate substitute s metabolites measured in human s urine are usually lower when compared to DEHP metabolites (Table 7) [105, 135]. However, such comparison should be carefully addressed since it was shown through rats exposure to such plasticizers that a considerable portion (about 50%) of the orally dosed DINP is excreted via the feces while it is known that DEHP is mainly extracted in humans via urine [105, 141]. 

Exposure of humans to perchlorate via foodstuffs and drinking water has been documented [241]. Urine, breast milk, amniotic fluid, saliva, and blood have been used as matrices in biomonitoring of human exposures to perchlorate [233, 242-253] (Table 10). Assessment of human exposures to perchlorate is important, since this compound blocks iodine uptake in the thyroid gland, which can lead to a decrease in the production of thyroid hormones (T3 and T4) essential for neurodevelopment [260]. 

Urine Urine is the principal route by which nonlactating humans excrete perchlorate [261, 262]. Urinary perchlorate provides a reasonable measure of human exposure because 70-95% of perchlorate dose is excreted unchanged in the urine with a half-life of 8 h [261-263]. Creatinine (CR) adjustment is typically used to minimize the effects of variation of analyte concentration in urine either among samples produced by different individuals or among samples produced by the same individual. 

Guo Y, Wu Q, Kannan K (2011) Phthalate metabolites in urine from China, and implications for human exposures. Environ Int 37 893-898... 

Exposure Levels in Humans. 1,3-DNB and 1,3,5-TNB have not been detected in human blood, urine, fat, or breast milk however, 1,3-DNB has been detected in the urine and blood of rodents fed the compound (Bailey et al. 1988 McEuen and Miller 1991 Nystrom and Rickert 1987). Biological monitoring data for both 1,3-DNB and 1,3,5-TNB are needed for populations living near Army ammunition plants and for occupationally exposed populations. This information is necessary for assessing the need to conduct studies on these populations. 

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