Methyl-nitrophenols

Figure 6.2 Methyl nitrophenol dissolved in 10 mMTris buffer at pHs ranging from 2 (far left) to 12 (far right). The colorless protonated methylnitrophenol turns yellow when the pH increases. Reproduced in Color plate 6.2.

Photolysis of methylated nitrophenols is a potential source of OH radicals and thus also a potential source of error in the determination of the correction for photolysis in the kinetic analysis. To obtain the true values of toe photolysis rates for the compounds it was necessary to perform separate experiments in which the OH radicals were scavenged. Using isoprene as scavenger it was possible to calculate the OH radical concentration and thus calculate toe overestimation in the measured photolysis rate due to reaction with OH. The calculated concenfrations of OH radicals produced in the photolysis of the various nitrophenols are presented in Table 2. 

The magnitude of the photolysis rates for methylated nitrophenols under atmospheric conditions can be roughly estimated from the experiments using the superactinic lamps. This is accomplished by adjusting the values obtained in the reactor and presented in Table 2, with a factor comprised of the ratio of NO2 photolysis measured in the atmosphere and that measured in the reactor. For example, a factor of Jno2 (atmosphere)/ Jncu (in the reactor) = (8.5 0.5) X 10 s V (2.0 0.2) x 10 s = 4.25 is obtained when using an atmospheric noontime photolysis frequency of NO2 typical for clear sky conditions at a latitude of 40 N for July 1 (Klotz et al, 1997). 

This work represents the first reported experimental kinetic study of the reaction of OH radicals with methylated nitrophenols, therefore, a comparison with other experimentally obtained values is not possible. Because of the difficulties in handling the compounds the measured rate constants should be used with caution. The measured values presented here need verification by further experiments and also a reference hydrocarbon other than ethene. Validation by an independent absolute kinetic method is also desirable. 

COj liberated. All acids esters which hydrolyse easily, e.g., methyl oxalate (p. 357) salts of amines nitrophenols. 

The operation of the nitronium ion in these media was later proved conclusively. "- The rates of nitration of 2-phenylethanesulphonate anion ([Aromatic] < c. 0-5 mol l i), toluene-(U-sulphonate anion, p-nitrophenol, A(-methyl-2,4-dinitroaniline and A(-methyl-iV,2,4-trinitro-aniline in aqueous solutions of nitric acid depend on the first power of the concentration of the aromatic. The dependence on acidity of the rate of 0-exchange between nitric acid and water was measured, " and formal first-order rate constants for oxygen exchange were defined by dividing the rates of exchange by the concentration of water. Comparison of these constants with the corresponding results for the reactions of the aromatic compounds yielded the scale of relative reactivities sho-wn in table 2.1. 

An ipso attack on the fluorine carbon position of 4-fIuorophenol at -40 °C affords 4-fluoro-4-nitrocyclohexa-2 5-dienone in addtion to 2-nitrophenol The cyclodienone slowly isomenzes to the 2-nitrophenol Although ipso nitration on 4-fluorophenyl acetate furnishes the same cyclodienone the major by-product is 4 fluoro-2,6-dinitrophenol [25] Under similar conditions, 4-fluoroanisole pnmar ily yields the 2-nitro isomer and 6% of the cyclodienone The isolated 2 nitro isomer IS postulated to form by attack of the nitromum ion ipso to the fluorine with concomitant capture of the incipient carbocation by acetic acid Loss of the elements of methyl acetate follows The nitrodienone, being the keto tautomer of the nitrophenol, aromatizes to the isolated product [26] (equation 20) Intramolecular capture of the intermediate carbocation occurs in nitration of 2-(4-fluorophenoxy)-2-methyIpropanoic acid at low temperature to give the spiro products 3 3-di-methyl-8 fluoro 8 nitro-1,4 dioxaspiro[4 5]deca 6,9 dien 2 one and the 10-nitro isomer [2d] (equation 21)... 

Naphthalene, 216 Naphthalene picrate, 217 Naphthalene sulphonaie ofsodiiim, 218-/ J-Naphthol, 219 Naphthol yellow, 224 /i Naphthyl acetate, 222 /j-Naphthyl methyl ether, 220 /-Nitracetanilide, 153 w-Nitraniline, 154 /-Nitraniline, 153 Nitric acid (fuming), 22 NitroVienzene, 142 w-Nitrobenzoic acid, 200 Nitrogen, qualitative e rimation, 2 quantitative estimation, 13 Nitrophenol, 183 Nitrosohenzene, 146 /-Nitrosodimethylaniline, 157 Niirosoplienol, 159... 

Swain and Eddy have queried the wide applicability of the S l and Sif2 mechanisms and favored a push-pull termolecular process for the reaction of pyridine with methyl bromide in benzene solution for example, they have suggested that the effects observed on the addition of methanol, phenol, p-nitrophenol, and mercuric bromide to the reaction mixture can be explained by an intermediate of type 168. ... 

Several medical tests can determine whether you have been exposed to methyl parathion. The first medical test measures methyl parathion in your blood or measures 4-nitrophenol, which is a breakdown product of methyl parathion, in your urine. These tests are only reliable for about 24 hours after you are exposed because methyl parathion breaks down quickly and leaves your body. These tests cannot tell whether you will have harmful health effects or what those effects may be. The next medical test measures the levels of a substance called cholinesterase in your blood. If cholinesterase levels are less than half of what they should be and you have been exposed to methyl parathion, then you may get symptoms of poisoning. However, lower cholinesterase levels may also only indicate exposure and not necessarily harmful effects. The action of methyl parathion may cause lower cholinesterase levels in your red blood cells or your blood plasma. Such lowering, however, can also be caused by factors other than methyl parathion. For example, cholinesterase values may already be low in some people, because of heredity or disease. However, a lowering of cholinesterase levels can often show whether methyl parathion or similar compounds have acted on your nerves. Cholinesterase levels in red blood cells can stay low for more than a month after you have been exposed to methyl parathion or similar chemicals. For more information, see Chapters 3 and 7. 

Neurological effects related to cholinesterase depression occurred in seven children acutely exposed to methyl parathion by inhalation as well as orally and dermally (Dean et al. 1984). The children were admitted to a local hospital with signs and symptoms of lethargy, increased salivation, increased respiratory secretions, and miosis. Two of the children were in respiratory arrest. Two children died within several days of each other. All of the children had depressed plasma and erythrocyte cholinesterase levels (Table 3-2). These effects are similar to those occurring in methyl parathion intoxication by other routes (see Sections 3.2.2.4 and 3.2.3.4). Three adults exposed in the same incident had normal plasma (apart from one female) and red blood cell cholinesterase, and urinary levels of 4-nitrophenol (0.46-12.7 ppm) as high as some of the ill children. 

Often, absorption occurs by multiple routes in humans. Dean et al. (1984) reported deaths and toxic effects as well as lowered blood cholinesterase levels and excretion of urinary 4-nitrophenol in several children who were exposed by inhalation, oral, and possibly dermal routes after the spraying of methyl parathion in a house. In the same incident (Dean et al. 1984), absorption was indicated in adults who also excreted 4-nitrophenol in the urine, though at lower levels than some of the children, and in the absence of other evidence of methyl parathion exposure. In this study, the potential for age-related differences in absorption rates could not be assessed because exposure levels were not known and the children may have been more highly exposed than the adults. Health effects from multiple routes are discussed in detail in Section 3.2. 

Nitrophenol and 4-nitrophenol glucuronide are excreted in urine. The studies of urinary excretion of methyl parathion metabolites, including those reported in this section, generally hydrolyze the glucuronide prior to analysis and report the resulting total 4-nitrophenol values. 

Most of the toxic effects caused by methyl parathion resulted from exposure by multiple routes, especially for workers in sprayed fields or formulating facilities, or people in homes. Dean et al. (1984) reported deaths and toxic effects in several children as well as lowered blood cholinesterase levels and excretion of urinary 4-nitrophenol (adults showing no adverse effects also excreted 4-nitrophenol). 

Only two studies were available that reported detection of a metabolite of methyl parathion in the urine of persons dermally exposed to methyl parathion (Ware et al. 1974, 1975). Four subjects were exposed for 5 hours to a methyl parathion formulation in a field that had been sprayed 24 hours prior to exposure (Ware et al. 1974). At 48 hours, an average of 0.5 mg 4-nitrophenol was found in the urine, but... 

Urinary 4-nitrophenol was detected in intoxicated children and clinically normal adults in a household where there had been exposure to methyl parathion (Dean et al. 1984). 

Associations between urinary 4-nitrophenol and indoor residential air and surface-wipe concentrations of methyl parathion have been studied in 142 residents of 64 contaminated homes in Uorain, Ohio (Esteban et al. 1996). The homes were contaminated through illegal spraying. A mathematic model was developed to evaluate the association between residential contamination and urinary 4-nitrophenol. There were significant positive correlations between air concentration and urinary 4-nitrophenol, and between maximum surface-wipe concentrations and urinary 4-nitrophenol. The final model includes the following variables number of days between spraying and sample collection, air and maximum surface wipe concentration, and age, and could be used to predict urinary 4-nitrophenol. 

Methyl parathion is an organophosphorus insecticide that is commercially produced in the United States and abroad. Methyl parathion, 0,0-dimethyl 0-(4-nitrophenyl) phosphorothioate, is not known to occur as a natural substance (lARC 1983). It is commercially produced by the reaction of 0,0-dimethyl phos-phorochloridothionate and the sodium salt of 4-nitrophenol in acetone solvent (EPA 1974b HSDB 1999 NIOSH 1976 NRC 1977 Worthing 1979). 

In freshwater systems, the only biodegradation product detected was 4-nitrophenol, which was rapidly utilized and transformed to undetectable metabolites by the microorganisms present. In seawater, the main initial product was methyl aminoparathion, formed by reduction of the nitro group (Badawy and El-Dib 1984). Studies in raw river water showed that 4-nitrophenol and dimethyl thiophosphoric acid are the main degradation products (Eichelberger and Lichtenberg 1971). 

In a study of 135 workers in the ehemical industry who handle methyl parathion, the methyl parathion concentration in plasma, the 4-nitrophenol concentration in urine, and the cholinesterase and acetylcholinesterase activities were determined to assess the pesticide burden in such workers (Leng and Lewalter 1999). The mean concentration of methyl parathion in the plasma of the workers was 233 pg/L no clinical symptoms were reported by the workers. In an additional group of 19 workers handling methyl parathion, who were also exposed to the pyrethroid cyfluthrin, the mean concentrations of methyl parathion in plasma were 269 and 241 pg/L (for groups without and with clinical S5miptoms, respectively), and 7 of the workers exhibited skin paraesthesia, while none of the 427 workers exposed only to the pyrethroid experienced the symptom (Leng and Lewalter 1999). 

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. 

A recent method, still in development, for determining total 4-nitrophenol in the urine of persons exposed to methyl parathion is based on solid phase microextraction (SPME) and GC/MS previously, the method... 

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