ライフサイエンスコーパス: nitrosamine

1 play a role in lung tumor initiation by this nitrosamine.

2 y the carcinogen, N-butyl-N-(4-hydroxybutyl) nitrosamine.

3 to the high cancer-causing potential of this nitrosamine.

4 d chemical structure of the parent amine and nitrosamine.

5 ion that it is the main source of endogenous nitrosamines.

6 in all amine solvents can form carcinogenic nitrosamines.

7 e desorber, forming potentially carcinogenic nitrosamines.

8 to cancer, because of their ability to form nitrosamines.

9 rosamines were more recalcitrant than linear nitrosamines.

10 ecursors of carcinogenic tobacco specific N'-nitrosamines.

11 examined due to the low thermal stability of nitrosamines.

12 ramine in feedwater led to the production of nitrosamines.

13 as duration of exposure to ethanolamines and nitrosamines.

14 ther with NO byproducts, such as nitrite and nitrosamines.

15 -glucuronidation of several tobacco-specific nitrosamines.

16 coumarin, indole, nicotine, and carcinogenic nitrosamines.

17 hydrocarbons (PAH) and the nicotine-derived nitrosamines.

18 a major role in the metabolic activation of nitrosamines.

19 high doses, but formed significantly less N-nitrosamines.

20 e primary amines, and that can form stable N-nitrosamines.

21 2.7 ng/L and recoveries of 53-93% for the 14 nitrosamines.

22 9% of precursors for other uncharacterized N-nitrosamines.

23 4 weekly doses of carcinogen (methyl-n-amyl nitrosamine, 25 mg/kg intraperitoneally), and survivors

24 N-methylaniline 2, N-butyl-N-(4-hydroxybutyl)nitrosamine 3, and N-nitrosodiethylamine 4) with ultravi

25 In contrast, nitrosamines 3 and 4 do not exchange the (18)O label and

26 ssue of mice exposed to the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

27 Exposure of cells to nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

28 The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

29 Exposure of cells to nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

30 (HPLD1), in response to the nicotine-derived nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

31 Nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

32 luate susceptibility to the nicotine-derived nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

33 The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

34 Nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

35 Nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

36 Nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

37 The nicotine-derived nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

38 rats were treated with the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butano

39 Tobacco-specific nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butan

40 Tobacco-specific nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butan

41 The nicotine-derived tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butan

42 Tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butan

43 bolism of low levels of one tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butan

44 The tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butan

45 nd the tar component, the tobacco-specific N-nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butan

46 The tobacco-specific nitrosamine, 4-(methylnitrosoamino)-1-(3-pyridyl)-1-buta

47 ogens: cigarette smoke condensate (CSC) or N-nitrosamine-4-(methylnitrosamino)-1-(3 pyridyl)-1-butano

48 nes 1-3 are converted to the alpha-hydroxy-N-nitrosamines 7-9 via the N-nitrosoiminium ions 4-6.

49 UV treatment converts the time dependence of nitrosamine accumulation from a quadratic to a linear fu

50 ng inhibitors and other strategies to reduce nitrosamine accumulation in CO2 capture by scrubbing wit

51 Flue gas humidity did not affect nitrosamine accumulation in either the absorber or the w

52 ively decompose NHeGly and NDELA to mitigate nitrosamine accumulation in MEA.

53 ile modeling indicated that more than 80% of nitrosamine accumulation in the washwater was associated

54 For alkanolamines, however, total N-nitrosamine accumulation in the washwater was similar re

55 results provide a useful tool for estimating nitrosamine accumulation over a range of amine solvents.

56 ter amines with residual NOx, a reduction in nitrosamine accumulation rates due to ozone oxidation of

57 While total N-nitrosamine accumulation rates in washwaters were genera

58 For diamines and amino acids, total N-nitrosamine accumulation rates in washwaters were lowest

59 hysical properties of the carbon sorbents on nitrosamine adsorption was examined.

60 in undesired photochemistry-the formation of nitrosamine and an oxynitrene intermediate with very lit

61 rifying influent water led to increases in N-nitrosamine and halogenated DBP formation, suggesting th

62 ating the effects of flue gas composition on nitrosamine and nitramine accumulation in postcombustion

63 egarding the formation and emission of toxic nitrosamine and nitramine byproducts from amine-based sy

64 The focus is on amine, nitrosamine and nitramine degradation, and nitrosamine a

65 In the absorber, flue gas NOx drives nitrosamine and nitramine formation after its dissolutio

66 , nitrosamine and nitramine degradation, and nitrosamine and nitramine formation processes.

67 eir loadings of ambient specific and total N-nitrosamines and chloramine-reactive and ozone-reactive

68 ng waters were adapted to measure specific N-nitrosamines and N-nitramines and total N-nitrosamines i

69 bout the potential release of carcinogenic N-nitrosamines and N-nitramines formed by reaction of exha

70 the formation of potentially carcinogenic N-nitrosamines and N-nitramines from reactions of flue gas

71 plies downwind by potentially carcinogenic N-nitrosamines and N-nitramines released following their f

72 cells to compare the toxicity of analogous N-nitrosamines and N-nitramines relevant to CO2 capture.

73 eeded for 90% removal of a series of model N-nitrosamines and N-nitramines, 280-1000 mJ/cm(2) average

74 ultraviolet (UV) light for destruction of N-nitrosamines and N-nitramines, and with ozone or hydroxy

75 s of this work on the potential formation of nitrosamines and nitramines are briefly discussed.

76 nt fluence alone reduced the accumulation of nitrosamines and nitramines by approximately an order of

77 also capture amines, preventing formation of nitrosamines and nitramines downwind by amine reactions

78 Formation of nitrosamines and nitramines from reactions between flue

79 o evaluate their effects on the formation of nitrosamines and nitramines in a lab-scale CO2 capture r

80 of the various atmospheric sinks for amines, nitrosamines and nitramines is presented.

81 dation products, such as ammonia, aldehydes, nitrosamines and nitramines, to the atmosphere from comm

82 d CO2 capture associated with the release of nitrosamines and nitramines, which are byproducts from t

83 ely predict the accumulation and emission of nitrosamines and nitramines.

84 Washwater scrubbers can capture nitrosamines and nitramines.

85 r groups of procarcinogens, tobacco-specific nitrosamines and polycyclic aromatic hydrocarbons, are p

86 Resins released different nitrosamines and precursors depending on their functiona

87 , consumer products contributed additional N-nitrosamines and precursors, but the remarkable uniformi

88 N-nitrosamines and their precursors are significant concer

89 A comparison of loadings of N-nitrosamines and their precursors from different source

90 N-Nitrosamines and their precursors were negligible in pri

91 represented the most significant source of N-nitrosamines and their precursors, followed by shower wa

92 resins releasing as many as three different nitrosamines and their precursors.

93 (nAChRs) bind nicotine and nicotine-derived nitrosamines and thus mediate many of the tobacco-relate

94 A clear relationship between ambient nitrosamines and total PM2.5 was observed with 1.9 ng m(

95 (i.e., halogenated organics, oxyanions, and nitrosamines), and identifies key research areas that sh

96 l groups), protein nitrosation (by measuring nitrosamines), and proteolysis.

97 species, such as nitrite, nitrated lipids, N-nitrosamine, and iron-nitrosyl complexes, may contribute

98 ogenated disinfection byproducts (DBPs), 8 N-nitrosamines, and bromate.

99 accelerated by exposure to bile acids and/or nitrosamines, and inhibited by IL-6 deficiency.

100 ivo leads to concomitant formation of RSNOs, nitrosamines, and nitrosylhemes with considerable variat

101 xidizable products such as hydroxlamines and nitrosamines, and these products react readily with Ru-(

102 e carcinogen BBN [N-butyl-N-(4-hydroxybutyl)-nitrosamine] and found that Uro-AR(-/y) mice had a lower

103 Nitrosamines are a class of ON compounds known to be hig

104 In the desorber, nitrosamines are formed under high temperatures by amine

105 N-Nitrosamines are potent mutagens and carcinogens that ca

106 yguanine adducts induced by tobacco-specific nitrosamines are repaired by O(6)-alkylguanine DNA alkyl

107 The results suggest that N-nitrosamines as a class may be more prevalent than sugge

108 e U.S. EPA considers limiting exposures to N-nitrosamines as a group, a critical question is whether

109 en linked to the formation of carcinogenic N-nitrosamines as byproducts during chloramine-based drink

110 are loadings of ambient specific and total N-nitrosamines as well as chloramine-reactive and ozone-re

111 enable the efficient syntheses of individual nitrosamines as well as mixture-based nitrosamine librar

112 ntly causes lung SCCs, and susceptibility to nitrosamines, as determined by polymorphisms in CYP2E1,

113 A total N-nitrosamine assay was developed and applied to 36 drinki

114 itroalkanes, halonitriles, haloamides, and N-nitrosamines associated with chlorine, ozone, chlorine d

115 cid that exhibited specific UV absorbance of nitrosamines at 335nm, supporting the assumption that it

116 135 degrees C indicated the decomposition of nitrosamines at the rate of 1 mug/(g h) with activation

117 furthers our understanding of environmental nitrosamine attenuation by revealing an enzymatic mechan

118 ure, mostly from the endogenous formation of nitrosamines based on intake of nitrite and nitrate.

119 r via the formation of intermediates such as nitrosamines, but can also inhibit some DNA repair proce

120 ovel method for the determination of total N-nitrosamines by UV-photolysis and subsequent chemilumine

121 the formation of potentially carcinogenic N-nitrosamine byproducts from reactions between flue gas N

122 rom metabolically activated tobacco-specific nitrosamines can covalently modify guanine bases in DNA

123 This study suggests that stabilized primary nitrosamines can indeed form in the photochemical oxidat

124 Nitrosamines, caused by ammonia oxidation, were formed i

125 y-stable, consistent with iron-nitrosyl or N-nitrosamine complex.

126 reptozotocin, an antibiotic and diabetogenic nitrosamine compound derived from Streptomyces achromoge

127 o determine the potential cooperation of the nitrosamine compound N-nitrosomethylbenzylamine (NMBA),

128 of nitrosamines, including cancer-associated nitrosamines, compounds that are difficult to recognize.

129 washwater samples indicated a 59 muM total N-nitrosamine concentration for a system operated with a 2

130 The average total nitrosamine concentration was 5.2 ng m(-3), substantiall

131 At a 0.73 muM total N-nitrosamine concentration, a ~25000-fold reduction in co

132 Similar to NDMA, total N-nitrosamine concentrations in source waters increased af

133 response to the chemical carcinogen diethyl nitrosamine (DEN) than wild-type animals.

134 iliary carcinoma after initiation by diethyl-nitrosamine (DEN).

135 Because the carcinogenicity of N-nitrosamines depends on formation of O6-alkylguanine in

136 quantify putative protein nitrosothiol and N-nitrosamine derivatives.

137 rats were intraperitoneally given dimethyl n-nitrosamine (DMN) (10mg/kg) 3 days per week for 4 weeks.

138 ed a risk for the artifactual formation of N-nitrosamines during sample storage or analysis.

139 n of DNA lesions induced by tobacco-specific nitrosamines, e.g., 4-(methylnitrosamino)-1-(3-pyridyl)-

140 Nitrosamine emission control strategies are critical for

141 ples but was the most prevalent of the six N-nitrosamines evaluated using U.S. Environmental Protecti

142 The hypothesis that nitrosamine exposure may increase the risk of glioma has

143 udies because it can substantially influence nitrosamine exposure, mostly from the endogenous formati

144 ifficult because of the ubiquitous nature of nitrosamine exposure.

145 smoke PAHs for lung SCC and tobacco-specific nitrosamines for lung ACs.

146 n amine degradation (operational cost) and N-nitrosamine formation (health hazards), all of which are

147 f amine structure, primarily amine order, on nitrosamine formation and the corresponding mechanisms a

148 Among them, nitrosamine formation and their emissions are of particu

149 l chain length) indicated that Cu promotes N-nitrosamine formation from primary amines with hydroxyl

150 NO and NO(2) concentrations indicated that N-nitrosamine formation generally exceeds N-nitramine form

151 ors in municipal wastewater accounting for N-nitrosamine formation have met with limited success.

152 olamine (MEA), dissolved Cu promoted total N-nitrosamine formation in the absorber unit at concentrat

153 amine was the primary determinant of total N-nitrosamine formation in the absorber unit, with total N

154 formation in the absorber unit, with total N-nitrosamine formation in the order: secondary amines app

155 f this method for the determination of the N-nitrosamine formation potential of personal care product

156 The total N-nitrosamine formation rate was at least an order of magn

157 For secondary and tertiary amines, total N-nitrosamine formation under these desorber-like conditio

158 m the absorber, can contribute to additional nitrosamine formation when accumulated amines react with

159 o modify polyDADMAC and Epi-DMA to inhibit N-nitrosamine formation.

160 carcinogen and also a representative of some nitrosamines formed endogenously.

161 ure facilities by potentially carcinogenic N-nitrosamines formed from reactions between flue gas NOx

162 st-effective method for selectively removing nitrosamines from the absorber waterwash effluent with a

163 ol volatile and aerosol emissions, including nitrosamines, from carbon-capture plants, but it is stil

164 Nitrosamines generated in the amine solvent loop of post

165 nd NDELA decomposition is first order in the nitrosamine, half order in base concentration, and base-

166 ification and reduced precursor levels for N-nitrosamines, HANs, and HAMs, as reflected by lower conc

167 Nicotine and tobacco-derived nitrosamines have been shown to exhibit their pathobiolo

168 polymer that efficiently concentrated the 14 nitrosamines in 100 mL of water (in contrast to 500 mL i

169 ne, and 8 nonspecific and 4 tobacco-specific nitrosamines in ambient PM from central London over two

170 The occurrence of eight carcinogenic N-nitrosamines in biosolids from 74 wastewater treatment p

171 The DF and sum of mean concentrations of nitrosamines in biosolids increased with the treatment c

172 The DF of nitrosamines in biosolids was positively correlated with

173 ore research into the occurrence and fate of nitrosamines in biosolids-amended soils in the context o

174 unds, as occurs with acetaminophen overdose, nitrosamines in cigarette smoke, and reactive oxygen spe

175 Nitramines are much less studied than nitrosamines in CO2 capture systems.

176 determine the presence or absence of the 14 nitrosamines in drinking water systems (eight were evalu

177 uman exposure and health risk assessments of nitrosamines in drinking water.

178 Analytical methods for N-nitrosamines in drinking waters were adapted to measure

179 ic hydrocarbons (PAHs) and the increase in N-nitrosamines in inhaled smoke from filtered low-yield ci

180 cation and identification of low levels of N-nitrosamines in meat products (limits of quantitation (L

181 nd validated for the determination of nine N-nitrosamines in meat products.

182 Tertiary amidines also produce nitrosamines in minor, but significant, yields.

183 luence was needed for 90% removal of total N-nitrosamines in pilot washwaters associated with two dif

184 The presence of N-nitrosamines in samples was quantified by isotope diluti

185 N-nitrosamines and N-nitramines and total N-nitrosamines in solvent and washwater samples.

186 t it is still necessary to remove or destroy nitrosamines in the circulating waterwash to prevent the

187 lved metals on the potential to form total N-nitrosamines in the solvent within the absorber unit and

188 marker of human exposure to the carcinogenic nitrosamines in tobacco and tobacco smoke, but its prese

189 been linked to the presence of carcinogenic nitrosamines in treated drinking water.

190 The lifetime cancer risk from nitrosamines in urban PM exceeded the U.S. Environmental

191 hat TSNAs have a minor contribution to total nitrosamines in water.

192 otects against the formation of carcinogenic nitrosamines, in gastric juice.

193 rder kinetics was not observed for the other nitrosamines included in this study over a concentration

194 nables the recognition and quantification of nitrosamines, including cancer-associated nitrosamines,

195 Cytochrome P450 (P450) 2A6 activates nitrosamines, including N,N-dimethylnitrosamine (DMN) an

196 ith a carcinogen, N-butyl-N-(4-hydroxybutyl) nitrosamine, increases the susceptibility to N-butyl-N-(

197 mouse model after a N-butyl-N-4-hydroxybutyl Nitrosamine induced bladder carcinogenesis.

198 ion of dHGF dramatically accelerates diethyl-nitrosamine induced HCC tumorigenesis.

199 susceptibility to N-butyl-N-(4-hydroxybutyl) nitrosamine-induced bladder carcinoma development.

200 t POH has a weakly promoting effect early in nitrosamine-induced esophageal tumorigenesis and suggest

201 eased proliferation and delay in the diethyl-nitrosamine-induced inflammatory process.

202 showed a delay in the appearance of diethyl-nitrosamine-induced tumors, which correlated with decrea

203 Using N-butyl-N-(4-hydroxybutyl) nitrosamine induction of invasive and metastatic bladder

204 oceeds via exothermic formation of a primary nitrosamine intermediate, CH3NHNO, which can isomerize t

205 les were spiked with (2)H isotope-labelled N-nitrosamine internal standard prior to extraction.

206 n end products in plasma, such as nitrite, N-nitrosamines, iron-nitrosyls, and nitrated lipids, shoul

207 ove reaction pathways and confirmed that the nitrosamine is a primary photoproduct.

208 usly proposed mechanism in which the primary nitrosamine is destroyed via isomerization to CH2NHNOH,

209 on that intake of meat, nitrate, nitrite, or nitrosamines is related to the risk of glioma.

210 of an oxygen-atom photoexchange process of N-nitrosamines is reported.

211 the metabolic activation of tobacco-specific nitrosamines, is selectively expressed in the respirator

212 garette smoke, nicotine and nicotine-derived nitrosamine ketone (NNK).

213 vidual nitrosamines as well as mixture-based nitrosamine libraries.

214 e in the solution phase to yield the desired nitrosamine library in good yield and purity.

215 ole in protecting human lung against tobacco nitrosamine-mediated DNA damage and that inefficient AGT

216 before cage escape to form triplet NO(-) and nitrosamine (minor process) or rapidly dissociates to fo

217 ve group were investigated as sources of the nitrosamines N-nitrosodimethylamine (NDMA), N-nitrosodie

218 The photolysis of four nitrosamines (N-nitrosodiphenylamine 1, N-nitroso-N-meth

219 romatography-tandem mass spectrometry, seven nitrosamines [(N-nitrosodimethylamine (NDMA), N-nitrosom

220 Literature on formation and mitigation of N-nitrosamine (NA) and especially non-volatile NA (NVNA) i

221 N-nitrosamines (NAms) are highly active carcinogens that h

222 imethylamine (NDMA) and other six volatile N-nitrosamines (NAms) from meat products.

223 monstrated using water samples spiked with N-nitrosamines (NAs) as model compounds.

224 ngerous levels of mutagenic and carcinogenic nitrosamines (NAs).

225 was evaluated to control the accumulation of nitrosamines, nitramines and amines in a laboratory-scal

226 en intakes of meats, nitrate, nitrite, and 2 nitrosamines [nitrosodimethylamine (NDMA) and nitrosopyr

227 = 2,4-dinitrophenyl, the contribution of the nitrosamine/O-nitrene-forming pathway was diminished.

228 itrosodimethylamine (NDMA) or other specific nitrosamines of current interest are dominant or minor c

229 try (HPLC-MS/MS) for the determination of 14 nitrosamines of health concern with widely differing pro

230 mice treated with N-butyl-N-(4-hydroxybutyl)-nitrosamine (OH-BBN) developed transitional and squamous

231 adder carcinogen, N-butyl-N-(4-hydroxybutyl) nitrosamine (OH-BBN), survivin transgenic animals exhibi

232 tion is whether NDMA is the most prevalent N-nitrosamine or whether significant concentrations occur

233 ether significant concentrations occur for N-nitrosamines other than those captured by EPA Method 521

234 ted have a high capacity and selectivity for nitrosamines over the parent solvent amines, with capaci

235 Thus, the processivity of dialkyl nitrosamine oxidation appears to be shared by a number o

236 exposure to a tobacco-specific carcinogenic nitrosamine per cigarette dose.

237 ed with 1.9 ng m(-3) +/- 2.6 ng m(-3) (total nitrosamine) per 10 mug m(-3) PM2.5.

238 use the ozonation products of amines reduced nitrosamine photolysis rates by competing for photons.

239 nor components, respectively, of the total N-nitrosamine pool in technical aquatic systems or biologi

240 ccounted for approximately 5% of the total N-nitrosamine pool on a median basis.

241 orination or ozonation destroyed most of the nitrosamine precursors in water.

242 and chloramine-reactive and ozone-reactive N-nitrosamine precursors to domestic sewage.

243 particularly important for ozone-reactive N-nitrosamine precursors, accounting for approximately 99%

244 Resins released similarly high levels of nitrosamine precursors, with spikes in precursor release

245 N-Nitrosamines, probable human carcinogens, are a group of

246 ochemical cleavage of the N=N bond to form a nitrosamine (R(2)NN=O) and an oxygen-substituted nitrene

247 The production of nitrosamine radical anion 5 upon photolysis of diazenium

248 The nitrosamine radical anion either undergoes electron tran

249 The detection limits for differing N-nitrosamines ranged between 0.07 muM (14 pmol injected)

250 standard NO(2) gas to better understand the nitrosamine reaction pathways under scrubber and strippe

251 d chiral stationary phase-gas chromatography-nitrosamine-selective detection with confirmation by liq

252 rtunately, a greater fraction of the total N-nitrosamine signal was uncharacterized for the MEA-assoc

253 ts treated with the carcinogen methyl-n-amyl nitrosamine, squamous cancer of the esophagus develops i

254 When exposed to the carcinogen nitrosamine, Stat3-transgenic mice developed invasive ca

255 The chemical and physical properties of nitrosamines, the parent amine, and the influence of the

256 The toxicity of N-nitrosamines, their presence in drinking and environment

257 hanism for the biotransformation of multiple nitrosamines, their relative recalcitrance to transforma

258 ns of N-nitrosodimethylamine (NDMA), total N-nitrosamines (TONO), regulated trihalomethanes (THMs) an

259 Previously, we showed that nitrosamine treated rodents develop PNEC hyperplasia but

260 Nitrosamine-treated hamsters also demonstrate pulmonary

261 tially screened a chromosome 3 library using nitrosamine-treated versus normal hamster lung cDNAs and

262 When methyl-n-amyl nitrosamine treatment is preceded by an operation to ind

263 metabolic activation of the tobacco-specific nitrosamines (TSNA) 4-(methylnitrosamino)-1-(3-pyridyl)-

264 rmination of the four major tobacco-specific nitrosamines (TSNA) in mainstream cigarette smoke.

265 We report here that tobacco-specific nitrosamines (TSNAs) are produced from specific tobacco

266 Tobacco-specific nitrosamines (TSNAs) exist in environmental waters; howe

267 Tobacco-specific nitrosamines (TSNAs) have been previously implicated as

268 e trace levels of alkyl and tobacco-specific nitrosamines (TSNAs) of varying physical and chemical pr

269 A method for measuring four tobacco-specific nitrosamines (TSNAs), an important group of compounds in

270 r biomarkers of nicotine, tobacco-specific N-nitrosamines (TSNAs), and volatile organic compounds (VO

271 (HONO) to form carcinogenic tobacco-specific nitrosamines (TSNAs).

272 e above drinking water regulatory levels) of nitrosamines upon initial rinsing with lab-grade water,

273 Nitrate, nitrite, and nitrosamine values were calculated based on published va

274 ust could potentially serve as a source of N-nitrosamines via reactions of residual NO(x) with amines

275 Aliphatic or aromatic N,N-disubstituted nitrosamine was generated in fair to excellent yield fro

276 The most frequently detected nitrosamine was NDPhA (0.7-147 ng/g) with a DF of 79%, f

277 Denitrosation of N-nitrosamines was accomplished with a microphotochemical

278 The nitric oxide formation from selected N-nitrosamines was linear (R(2) = 0.98-0.99) from 0.1 to 1

279 ary amines, significant formation of total N-nitrosamines was only observed in the absorber.

280 chloropicrin, haloacetonitriles (HANs), and nitrosamines) was examined during the chlorination or ch

281 Overall, N-nitrosamines were approximately 15-fold more mutagenic t

282 aters, NDMA was detected once, while total N-nitrosamines were detected in five samples, suggesting t

283 Preexisting traces of carcinogenic nitrosamines were detected in some samples of diazeniumd

284 The N-nitrosamines were extracted with NaOH/methanol, partitio

285 and HPLC-MS/MS data show that (18)O-labeled nitrosamines were generated for 1 and 2.

286 groups scaled inversely with mass and cyclic nitrosamines were more recalcitrant than linear nitrosam

287 luent and polyDADMAC, high yields of total N-nitrosamines were observed from the algal exudate, the w

288 ably produced by secondary photolysis of the nitrosamine, were observed.

289 Nitrosamines, which are known bladder carcinogens, or th

290 es to meet potential future regulations on N-nitrosamines while maintaining polymer usage to meet exi

291 educed nicotine and reduced tobacco-specific nitrosamines with certified values for composition.

292 eroxy intermediates arising from reaction of nitrosamines with O2 is also presented.

293 e structure on the potential to form total N-nitrosamines within the absorber and washwater units of

294 A was the most prevalent of the Method 521 N-nitrosamines yet accounted for approximately 5% of the t

295 Nitrosamine yield was proportional to the concentration

296 ormation potential testing with chloramines, nitrosamine yields from IOM were measured for N-nitrosod

297 IOM was added to a natural water matrix, the nitrosamine yields were not realized likely due to compe