Detection in urine

Opioids are easily absorbed subcutaneously and intramuscularly, as well as from the gastrointestinal tract, nasal mucosa (e.g., when heroin is used as snuff), and lung (e.g., when opium is smoked). About 90% of the excretion of morphine occurs during the first 24 hours, but traces are detectable in urine for more than 48 hours. Heroin (diacetyhnorphine) is hydrolyzed to monoacetylmorphine, which is then hydrolyzed to morphine. Morphine and monoacetylmorphine are responsible for the pharmacologic effects of heroin. Heroin produces effects more rapidly than morphine because it is more lipid soluble and therefore crosses the blood-brain barrier faster. In the urine, heroin is detected as free morphine and morphine glucuronide (Gutstein and Akil 2001 Jaffe et al. 2004). 

Exposure Levels in Humans. Methyl parathion has been detected in serum and tissue shortly after acute exposure (EPA 1978e Ware et al. 1975). It is rapidly metabolized and does not persist in serum and tissues for long (Braeckman et al. 1983). Two metabolites of methyl parathion, 4-nitrophenol and dimethyl phosphate, can be detected in urine and tissues for up to 2 days following exposure (Morgan et al. 1977). These compounds are specific for methyl parathion when there is a history of exposure. 

Endosulfan and metabolites were observed in the urine of workers who had prepared and applied endosulfan for 2-5 hours either 1 day or 1 week prior to sampling, without using protective clothing or face mask (thus, exposure was probably both dermal and inhalation) (Vidal et al. 1998). Unchanged a-and P-endosulfan and endosulfan ether were the predominant chemicals excreted 1 day following exposure. One week after exposure, a-endosulfan was detected in urine of four of five workers, but P-endosulfan was detected in only one of five samples and endosulfan ether was not detected at all. Endosulfan sulfate was detected in only one of five samples at 1 week after exposure and in none of the four samples at 1 day postexposure. Endosulfan lactone was detected in one of four and one of five samples at 1 day and 1 week after exposure, respectively. 

Urinary excretion of radioactivity was measured in human volunteers during and after a 3.5-hour period of dermal exposure to 0.11 or 0.22 g 32P-labeled TOCP (Hodge and Sterner 1943). The specific activity of the test substance was not reported. Radioactivity in urine was measured with a Geiger-Muller counter, but the limits of detection were not reported. Maximum estimated excretion rates, 10 and 43 pg TOCP/hour for the respective dosage levels, were measured within 24 hours of initiation of exposure. Radioactivity was not detected 48 or 72 hours after dosing ceased. Cumulative radioactivity detected in urine accounted for 0.13% and 0.36% of the dermally applied radioactivity. 

Table 3 Alkylphosphates Detectable in Urine as Metabolites of Some Organophosphorus Pesticides...

Pentachlorophenol concentrations in urine and serum can be used as biomarkers of internal dose (Colosio et al., 1993a). PCP concentrations up to about 30 mg/L were detected in urine samples of exposed workers, while concentrations lower than 0.3 mg/L were detected in the general population. The presence of PCP in biological samples of the general population is attributable to indoor exposure to the compound released from treated materials (furniture, leather, paints, etc.). 

A case in which the toxin or appropriate metabolite is detected in urine, serum, or plasma, or detection of the specific toxin in environmental samples unless there could be a local source of the toxin (e.g., the molds that produce mycotoxins have been found in some residential and industrial settings, and the toxins have been implicated in some cases of "sick building" syndrome). 

The pantothenate in blood and cerebrospinal fluid is conjugated without enzymatic hydrolysis no pantothenate activity is detected. In urine, pantothenate activity did not increase with enzymatic treatment. 

Further studies in humans indicate that a large proportion of the 2,5-hexanedione detected in urine after M-hexane exposure is the result of an artifact resulting from treatment with acid to hydrolyze urinary conjugates (Fedtke and Bolt 1987). When urine from a male volunteer exposed to 217 ppm -hexanc for 4 hours was hydrolyzed enzymatically with -glucuronidase, excretion of 4,5-dihydroxy-2-hexanone was approximately 4 times higher than that of 2,5-hexanedione. When the urine was hydrolyzed with acid,... 

The chelated square-planar metabolite [Pt(Met)2)l has been detected in urine of patients treated with cisplatin (89). It is a relatively unreactive complex, existing in solution as a mixture of three diaster-eoisomers of each of the two geometrical isomers (90). The cis isomer predominates over the trans isomer by 87 13, and interconversion is slow (half-lives for conversion of cis to trans 22.4 h and of trans to cis 3.2 h at 310 K). 

In rabbits administered radio-labeled endrin, 50% of the radioactivity was excreted in the urine over a 50-day period (Bedford et al. 1975b). Excretion of the label was 87% complete within 13 days. The major compounds detected in urine were anti-12-hydroxyendrin sulfate and 3-hydroxyendrin sulfate (14%). 

Disulfoton and its breakdown products can be measured in the blood, urine, feces, liver, kidney, or body fat of exposed people. In cases of occupational or accidental exposure to disulfoton, the breakdown products are often measured in the urine. The breakdown products are relatively specific for disulfoton and a few other similar organophosphate pesticides and can be detected in urine for up to one week after people were last exposed. Because disulfoton inhibits cholinesterase in blood and in blood cells, inhibition of this enzyme activity may also suggest exposure to disulfoton. Cholinesterase activity in blood and in blood cells may remain inhibited for as long as 1-2 weeks after the last exposure. Because other organophosphate pesticides also inhibit cholinesterase activity in blood and blood cells, this test is not specific for disulfoton. The measurement of cholinesterase in blood and blood cells and the amount of disulfoton breakdown products in the urine cannot always predict how much disulfoton you were exposed to. Your doctor can send samples of your blood or urine to special laboratories that perform these tests. Chapters 2 and 6 provide more information about medical tests. 

There are two common myths that are believed to increase the usage of Rohypnol among young people (1) it is a pharmaceutical pill sold in sealed bubble packaging, so it is safe and free of contaminants, and (2) it cannot be detected in urine samples. 

In rats administered 2-bromoethylamine, urinary aziridine accounted for 15-45% of the dose. The carbamate 11.135 was not detected in urine, whereas oxazolidin-2-one and a tertiary metabolite, 5-hydroxy oxazolidin-2-one, accounted for 0 - 20% and 2 - 12% of the dose, respectively [156], The innocuity of oxazolidin-2-one led to the suggestion that either aziridine or 2-bromoethylamine itself is responsible for mitochondrial toxicity. These studies show that the nephrotoxic 2-haloethylamines undergo two competitive cyclizations with halide elimination, one probably a reaction of toxification, the other clearly a reaction of detoxification. 

Once in the blood stream, cocaine levels quickly rise in the brain, faster than plasma levels, which then redistribute to other tissues. Cocaine is rapidly metabolized in the blood and liver, with a half-life of 30 to 90 minutes. The major metabolites have a half-life of approximately 8 hours. Although cocaine itself is detected in urine for only 12 hours, the metabolite benzoylecgonine can be detected in urine for at least 48 hours and sometimes up to 2 weeks. Concurrent use of cocaine and ethanol produces an ethyl ester of benzoylecgonine called cocaethylene. Cocaethylene is an active metabolite, blocking dopamine reuptake, and potentiating the effect of cocaine. Thus, concurrent use of cocaine and ethanol can further increase the additional effects of the drugs and the risk of dependency. 

The active constituents of amanita, and perhaps active metabolites as well, are excreted in urine. Because the mushrooms can be very expensive, many Siberian tribesmen drink their urine to prolong intoxication. Both ibotenic acid and muscimol are detected in urine. Up to 27% of muscimol injected into mice has been recovered from urine. 

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. 

Several small studies have also found measurable perchlorate levels in human urine. For 61 adults living in Georgia, USA, aU urine samples contained measurable levels of perchlorate, with a median of 3.2 pg/L and a log-normal distribution [256]. Similar background levels of perchlorate (median 5.5 pg/L) were detected in urine from 13 subjects in a Southern California study [257]. Similarly, detectable levels of perchlorate were also found in all urine samples provided ( = 273) in an urban community in New Jersey [253]. The range, mean SD, and median for all urine perchlorate samples were 0.18-18.3 pg/L, 3.19 3.64 pg/L, and 2.14 pg/L, respectively. 

Toxicokinetic data can also be used to make informed decisions on testing of chemical substances. In specific circumstances, valid toxicokinetic data may be used to support a decision to omit testing for systemic effects, e.g., in cases where the toxicokinetic data provide sufficient evidence that a substance is not absorbed and therefore not systemically available, i.e., no plasma/blood concentrations were measurable and no parent compound or metabolites could be detected in urine, bile, or exhaled air. For example, in vivo testing for mutagenicity, reproductive toxicity, or carcinogenicity may be omitted if toxicokinetic data or other data indicate a lack of systemic availability. 

The metabolism of an oral dose of 50-100 mg/kg "C-1,3-DNB was followed in rabbits (Parke 1961). Of the metabolites detected in urine, 30% were conjugated with glucuronic acid and 6% with sulfate. The major urinary metabolites of 1,3-DNB were 2,4-diaminophenol (31%), 1,3-phenylenediamine (25%), 1,3-nitroaniline (18%), and 2-amino-4-nitrophenol (14%). Other minor metabolites comprising about 20% of the label were oxidation and reduction products and azoxy dimers. 

Metabolism/Excretion-The drug is rapidly metabolized. Over 48 hours, 45% of the dose appeared in the urine as metabolites. Unchanged selegiline is not detected in urine. 

No information was located on the retention of hexachlorobutadiene or its metabolites in humans. In animals, the compound and its metabolites were detected in urine and areas extent in breath within 3 days after exposure. Adverse effects were seen within 24 hours, suggesting that the compound and its metabolites are toxic while retained in the body. 

Age can not be tested using urine. There is a rumor that approximate age can be detected in urine, and is tested in medical insurance exams. It s a myth. 

Gender cannot be tested either. As with age, there is a rumor that gender can be detected in urine, and is tested in medical insurance exams. This is another myth. It may be argued that a pregnancy test can be used to detect the gender of the urine provider, but the same test is used to detect prostate cancer in males. 

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