Analytical and biological analyses of test materials from the synthetic fuel technologies

Ho, C.-H.; Clark, Bruce R.; Guerin, M.R.; Barkenbus, B.D.; Rao, T.K.; Epler, J.L.

doi:10.1016/0165-1161(81)90224-7

Cited by 107 publications

(5 citation statements)

References 7 publications

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“…Among pyridine analogs, 3-trifluoromethylpyridine (Figure 15) was toxic to the NM (see above). A large number of pyridine monomethyl- and dimethyl-substituted derivatives were not mutagenic in bacteria (Ho et al, 1981). 3-(Chloromethyl)pyridine was mutagenic in the presence of a bioactivation system, although its 2-analog was not.…”

Section: Rodent Nasal Carcinogensmentioning

confidence: 99%

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

2006

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Toxicity and carcinogenicity in the mucosa of the nasal passages in rodents has been produced by a variety of organic chemicals which are systemically distributed. In this review, 14 such chemicals or classes were identified that produced rodent nasal cytotoxicity, but not carcinogenicity, and 11 were identified that produced nasal carcinogenicity. Most chemicals that affect the nasal mucosa were either concentrated in that tissue or readily activated there, or both. All chemicals with effects in the nasal mucosa that were DNA-reactive, were also carcinogenic, if adequately tested. None of the rodent nasal cytotoxins has been identified as a human systemic nasal toxin. This may reflect the lesser biotransformation activity of human nasal mucosa compared to rodent and the much lower levels of human exposures. None of the rodent carcinogens lacking DNA reactivity has been identified as a nasal carcinogen or other cancer hazard to humans. Some DNA-reactive rodent carcinogens that affect the nasal mucosa, as well as other tissues, have been associated with cancer at various sites in humans, but not the nasal cavity. Thus, findings in only the rodent nasal mucosa do not necessarily predict either a toxic or carcinogenic hazard to that tissue in humans.

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Section: Rodent Nasal Carcinogensmentioning

confidence: 99%

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

2006

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“…They can damage the environment or pose a threat to human population [1]. This causes increasing demand for methods suitable for the determination of trace amounts of dangerous compounds in complex environmental or biological matrices.…”

Section: Introductionmentioning

confidence: 99%

Polarographic and voltammetric determination of genotoxic 4-nitroindane at mercury electrodes

2015

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Determination and electrochemical investigation of genotoxic nitrated polycyclic aromatic hydrocarbon 4-nitroindane (4-NI) were carried out using direct current tast polarography (DCTP) and differential pulse polarography (DPP) at a classical dropping mercury electrode (DME) and using direct current voltammetry (DCV), differential pulse voltammetry (DPV), and cyclic voltammetry (CV) at a hanging mercury drop minielectrode (HMDmE). The following optimal media for the determination of 4-NI were found: methanol-BrittonRobinson (BR) buffer of pH 12.0 (1:1) for DCTP and DPP, methanol-BR buffer of pH 9.0 (1:9) for DCV, and methanol-BR buffer of pH 8.0 (1:9) for DPV. For CV investigation, mixtures of methanol-BR buffer of pH 3.0, 8.0, and 12.0 (1:1) were used. The limits of quantification were: 0.65 lmol dm -3 (DCTP at the DME), 0.10 lmol dm -3 (DPP at the DME), 0.075 lmol dm -3 (DCV at the HMDmE), and 0.070 lmol dm -3 (DPV at the HMDmE). An attempt to increase the determination sensitivity using adsorptive accumulation of 4-NI on the HMDmE surface was not successful. The newly developed polarographic and voltammetric methods were successfully applied for the determination of 4-NI in model samples of drinking and river water. Graphical abstract -300 -400 -500 -600 -700 -800 -10 -15 -20 -25 -30 NO 2 I / nA E / mV 0 . 0 0 . 4 0 . 8 1 . 2 0 -4 -8 -12 c / µmol dm -3

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“…In mehreren Untersuchungen an Bakterien erwies sich N-Methylanilin mit und ohne Zusatz eines metabolischen Aktivierungssystems als nicht mutagen (NLM 2006;Ho et al 1981;Le et al 1985; NIHS Japan ohne Jahresangabe a, d; Wakabaya shi et al 1982;Zeiger et al 1988;Begründung 1987). Nur in Anwesenheit von Norharman führte die Substanz zu einer mutagenen Wirkung (Wakabayashi et al 1982;Begründung 1987).…”

Section: N-methylanilin 659unclassified

“…N-Methylanilin erwies sich mit und ohne Zusatz eines metabolischen Aktivierungssystems als nicht mutagen in Bakterien (Ho et al 1981;Le et al 1985; NIHS Japan ohne Jahresangabe a, d; NLM 2006; Wakabayashi et al 1982;Zeiger et al 1988;Begründung 1987). An Lungenzellen des Chinesischen Hamsters führte N-Methylanilin mit und ohne Zusatz eines metabolischen Aktivierungssystems zu strukturellen Chromosomenaberrationen wie Chromatidenbrüchen und Chromatidenaustauschen (NIHS Japan ohne Jahresangabe a, e).…”

Section: Fazitunclassified

N‐Methylanilin [MAK Value Documentation in German language, 2017]

Hartwig

2017

The MAK‐Collection for Occupational Health and Safety

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The German Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area has re‐evaluated the maximum concentration at the workplace (MAK value) of N‐methylaniline [ 100‐61‐8 ] considering all toxicity endpoints. Available publications and unpublished study reports are described in detail. Critical effect is the formation of methaemoglobin (MetHb). Adequate data in humans to derive a MAK value are not available; thus, data with rats are used. In rats, N‐methylaniline forms MetHb 2.7 times more efficiently than aniline. Based on the MAK value for aniline of 2 ml/m 3 , the MAK value for N‐methylaniline of 0.5 ml/m 3 is confirmed. As the critical effect is systemic, Peak Limitation Category II is retained; as the half‐life in blood is unknown, the default excursion factor of 2 is also retained. N‐Methylaniline remains in Pregnancy Risk Group D because developmental toxicity studies are lacking. The substance does not induce mutations in bacteria, but is clastogenic in mammalian cells. Studies on genotoxicity in vivo have not been performed. Adequate data to assess the carcinogenic potential of N‐methylaniline are not available. Data for the metabolite aniline are used to assess the carcinogenic potential of N‐methylaniline. Aniline induces spleen tumours in rats, but not in mice. The putative mode of action is an indirect tumour development by induction of MetHb and haemolytic effects which result in erythrocyte toxicity and its consequences, perturbations in iron metabolism in the spleen. The metabolites phenylhydroxylamine and nitrosobenzene are mainly responsible for the erythrocyte toxicity of aniline. As nitrosobenzene is also a metabolite of N‐methylaniline, a similar mode of action has to be assumed for N‐methylaniline. Therefore, a non‐genotoxic mode of action is of prime importance and genotoxic effects play at most a minor part provided the MAK and BAT values are observed. Thus, N‐methylaniline is classified as a suspected carcinogen in Carcinogen Category 3B. Skin contact may contribute significantly to systemic toxicity and the “H” notation is retained. There are no clinical data concerning the sensitizing activity of the substance. Results of a local lymph node assay in mice were negative.

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Analytical and biological analyses of test materials from the synthetic fuel technologies

Cited by 107 publications

References 7 publications

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

Polarographic and voltammetric determination of genotoxic 4-nitroindane at mercury electrodes

N‐Methylanilin [MAK Value Documentation in German language, 2017]

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