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PubMed1982

Analysis and formation of nitrosamines in the human intestine.

The method employed for nitrosamine analysis gave high recovery values and did not produce artefactual nitrosamines. Nitrosation reactions are not catalysed by the microbial ecosystem of human feces. Rapid loss of nitrate and nitrite in feces also precludes nitrosamine formation, unless very high concentrations of precursors are present. These concentrations are not physiological and it is therefore unlikely that N-nitroso compounds form in the lower gastrointestinal tract of man.

Feces↗
PubMed1982

Chemical structural effects in carcinogenesis by nitrosamines.

The effects of changes on chemical structure among groups of closely related nitrosamines on their carcinogenic effectiveness, including both potency and target organ specificity, have been examined by chronic oral administration of the nitrosamines to rats. The effects of deuterium substitution for hydrogen at various positions supports the concept that oxidation at the alpha position to the nitroso function is usually a key step in activation of carcinogenic nitrosamines. Methyl substituents at the alpha position reduce carcinogenic potency, supporting the same idea. A large number of derivatives of nitrosopiperidine have shown a large variation in carcinogenicity, not simply explained by differences in the relative rates of alpha oxidation. The effects of methyl substitution on the carcinogenicity of nitrosomorpholine and nitrosooxazolidine were opposite, although the unsubstituted compounds were of almost identical carcinogenic activity. The variations in the response of rats to a large series of nitrosodialkylamines indicated that they might be metabolized similarly, giving one or more common products which are the proximate carcinogens, and these biological effects can be related to the results of studies of the metabolism of these compounds in rats.

Animals↗
PubMed1982

Transnitrosation by nitrosamines in vivo.

The significance of in vivo transnitrosation in carcinogenesis by the nitrosamines formed was studied by feeding mixtures of morpholine and nitrosamines to rats for most of their lifespan. In some groups, a transnitrosation catalyst (sodium thiocyanate) was fed simultaneously. None of the four nitrosamines induced a significant number of liver tumours when fed singly, although nitrosophenylbenzylamine induced tumours of the spleen and upper gastrointestinal tract and nitroso-N-methylpiperazine induced tumours of the nasal cavity. Nitrosoproline taken with morpholine did not give rise to tumours, except when given in combination with sodium thiocyanate, which gave rise to an even higher frequency of hepatic tumours when given alone. Nitrosohydroxyproline with morpholine induced liver carcinomas in 3 of 20 rats and in 9 of 20 rats in the presence of sodium thiocyanate. Rats given nitrosophenylbenzylamine plus morpholine lived less than 2 years and 4 of them had liver tumours. Most rats treated with nitrosomethylpiperazine died within a year, because of the tumours induced; the combination with morpholine hydrochloride led to the formation of liver carcinomas in 2 of 20 rats and in 5 of 20 when thiocyanate was given.

Animals↗
PubMed1980

Determination of volatile N-nitrosamines in foodstuffs: I. A new clean-up technique for confirmation by II. A continued survey of foods and beverages.

A clean-up technique has been developed which enables MS confirmation of the identity of a nitrosamine from a sample extract obtained by the mineral oil distillation method. A survey of fried bacons using this technique has confirmed the presence of NPYR at levels of 7-26 micrograms/kg in six of nine samples. NDMA has been found by GC-TEA in 62 of 64 beer samples. Five of the higher levels (from 5.8-7.7 micrograms/kg) have been confirmed by MS, following a direct distillation technique. A survey of 106 market samples of poultry products, Chinese foods and herring meals for volatile nitrosamines was conducted. GC-TEA analyses indicated low levels of several nitrosamines in these samples (less than or equal to 11 micrograms/kg), with the exception of two herring meal samples in which NDMA was confirmed by MS at 2.5 and 2.7 mg/kg.

Animals↗
PubMed1980

Formation of N-nitrosamine and N-nitrosamino acids from food products and nitrite under simulated gastric conditions.

Average-sized portions of a variety of food products were reacted with nitrite under realistically simulated gastric conditions. The aqueous incubation medium contained sodium nitrite (10 mg/l) and potassium thiocyanate to mimic the incoming flux of saliva, as well as pepsin, sodium chloride and hydrochloric acid, reflecting the composition of gastric juice. After incubation for 2 hr at 37 degrees C, volatile N-nitrosamines and N-nitrosamino acids were determined in the reaction mixtures. Nitrosodimethylamine (NDMA) was present in the incubation mixtures of smoked mackerel (8.5 micrograms per portion), canned herring (0.66 micrograms per portion) and beer (0.70 micrograms per 'portion'). Smaller amounts per portion, sometimes of other nitrosamines as well, were observed with canned salmon and anchovy, mustard, yoghurt and coffee brew. Negative results were obtained for canned tuna, soya sauce, ketchup, white bread, 'nasi goreng', tea brew and cocoa milk. Nitrosamino acids were detected in the reaction mixtures of smoked mackerel (58 micrograms per portion), soya sauce (24 micrograms per portion) and canned salmon (6.9 micrograms per portion) and in smaller amounts in those of canned herring, anchovy and cocoa milk. In order to reduce the number of analyses to be performed, most products have been studied only after incubation, so that the nitrosamines and nitrosamino acids found may already have been present -- wholly or partly -- in the original products, before incubation. Such is the case for part of the NDMA in the reaction mixture of smoked mackerel and for all the NDMA in beer. The toxicological implications of these findings remain to be established.

Amino Acids↗
PubMed1980

New pathways for the rapid formation of N-nitrosamines under neutral and alkaline conditions.

Ethylene glycol, several carbohydrates (sugars) and alkanolamines influence the formation of carcinogenic N-nitrosamines in neutral and alkaline aqueous solutions at 25 degrees C in presence of dissolved nitrosyl gases. These compounds either catalyse or inhibit the reactions (depending on the experimental conditions and reagent reactivities) by forming a nitrite ester intermediate, which reacts readily with secondary amines. The reactions may explain the origin of some N-nitrosamines in vivo and in consumer products, particularly those originating from NOX pollutants. N-Nitrosamines are also formed at ambient temperatures by the gamma-radiolysis of neutral aqueous solutions of either NaNO2 or NaNO3 and secondary amines. With NaNO3, N-nitroamines are in accompanying product. These reactions are considered to proceed via N2O3 and N2O4 intermediates, generated from NaNO2 and NaNO3, respectively.

Hydrogen-Ion Concentration↗
PubMed1980

N-Nitrosamines in the factory environment.

Under the NIOSH-sponsored contract, a total of 40 surveys were conducted at 28 manufacturing plants. The industries investigated were the fish, dye, leather, rubber and manufacturers and users of cutting fluids. NDELA, NMOR, NDMA and NDPhA were found in the air of several factories. In a chrome tannery, NDMA was identified at levels as high as 47 micrograms/m3 and NMOR was found at 27 micrograms/m3 in a rubber tire plant. This study has resulted in an increased understanding of man's exposure to exogenous N-nitrosamines. It is conceivable, from the information obtained in this study, that nitrosamine exposure comparable to that in the tire and rubber industry exists in other industries not yet surveyed. NIOSH is continuing its research on nitrosamines in the industrial environment. A full, industry-wide report on the 40 plant surveys is being compiled for publication.

Air↗
PubMed1980

Occurrence and formation of nitrosamines in animal feeds.

A total of 465 samples of ingredients of animal feeds (fish meal, antarctic krill meal, experimental silage containing 40% dried animal wastes) and complete mixed feeds and protein concentrates were analysed for nitrate and nitrite content in the period 1973-78. Over 62% of the samples contained nitrates in concentrations ranging from 1 to 1020 mg/kg, and 6% contained 1-15 mg/kg of nitrites. After a preliminary survey, the samples having the highest levels of nitrate, nitrite and amines were selected and analysed for volatile N-nitrosamines. Of 171 selected samples, 40% were found to contain N-nitrosodimethylamine in the range of 0.003 to 0.417 mg/kg. No statistically confirmed correlation between concentrations of nitrates or nitrites and nitrosamines could be demonstrated. Large amounts of dimethylamine, ranging from 110 to 1765 mg/kg, were found in all samples of krill meal. Incubation of krill meal and fish meal with nitrite, under conditions similar to those existing in the animal stomach, resulted in the formation of substantial amounts of NDMA. The occurrence of N-nitrosamines in feeds and their possible formation in vivo from precursors present in feeds seems to be an important problem from the hygienic standpoint, because of possible "carry-over" to tissues, milk and eggs.

Animal Feed↗
PubMed1980

Confirmation of low microgram/kg amounts of volatile N-nitrosamines in foods by low resolution mass spectrometry.

Volatile N-nitrosamines were confirmed in foods at concentrations of less than 10 micrograms/kg by full scan low resolution mass spectrometry. Ground samples were vacuum-distilled from mineral oil and condensed in liquid nitrogen-cooled vapor traps. The thawed distillate was extracted, the extract was cleaned up and concentrated, and the N-nitrosamine content was determined by combined gas chromatograph-thermal energy analysis. Positive samples were further cleaned up, trapped from a gas chromatographic column, and purged into a gas chromatograph-mass spectrometer for qualitative confirmation by full scan low resolution mass spectrometry. This procedure was applied to foods spiked at 1 microgram/kg and to fried commercial bacons with volatile N-nitrosamine contents of 2 to 5 micrograms/kg.

Animals↗
PubMedDate not supplied

Evaluation of a degradation method for nitrosamine wastes.

Nitrosamines are being used with increasing frequency in biomedical laboratories. Disposal of these potentially carcinogenic compounds requires a decontamination procedure that is simple, efficient, and economical. Degradation of nitrosamine wastes by alkaline reduction and the analytical techniques for evaluating this method have been explored. Efficiencies of degradation vary from 9.0 to greater than 99.9 percent of a group of ten nitrosamines.

Chromatography, Gas↗
PubMed1980

Lack of enhancing effect of mucosal regeneration following ulceration of the urinary bladder on N-butyl-N-(4-hydroxybutyl)nitrosamine carcinogenesis in rats.

The potential enhancing effects of the regeneration response of the urothelium following ulceration of the bladder mucosa on N-butyl-N-(4-hydroxybutyl)nitrosamine carcinogenesis were examined in male Fischer rats. The carcinogen was administered in the drinking water at a concentration of 0.05% for 2 weeks. Ulceration was performed by a freezing technique 24 hr before the administration or 24 hr or 8 weeks after the discontinuation of N-butyl-N-(4-hydroxybutyl)nitrosamine. No enhancing effects by ulceration were observed. Ulceration prior to carcinogen treatment decreased rather than increased the induction of bladder tumors to approximatley one-half the incidence of the control. Ulceration after N-butyl-N-(4-hydroxybutyl)nitrosamine did not change the frequency of tumor induction. While the inhibitory effect of the prior ulceration may result from the exposure of fewer mature mucosal cells that are capable of activating the carcinogen, the ineffectiveness of the subsequent ulcerations suggests that a single wave of regeneration does not enhance the tumorigenic response of bladder mucosa.

Animals↗
PubMed1980

Theoretical study of N-nitrosamines and their presumed proximate carcinogens.

Quantum mechanical calculations in the MINDO/3 and CNDO/2 approximations have been used to study possible mechanisms of action of the carcinogenic N-nitrosamines. Calculated reaction path profiles show that hydroxylation at either the C-H bonds or the amino nitrogen of the nitrosamine may result in the formation of an alpha-hydroxynitrosamine with some interesting structural and stereochemical constraints. Dissociation of the alpha-hydroxynitrosamine, along a concerted pathway or two-step mechanism, releases the alkyldiazohydroxide which subsequently decomposes to the alkylating agents responsible for cancer induction. On the basis of the results obtained for the decomposition of the alkyldiazohydroxide, the alkylation mechanism of N-nitrosamines does not appear to involve carbocation intermediates or diazomethane. The most likely alternative for the alkylation reaction is, then, direct nucleophilic attack (SN2) on the alkyldiazonium ion by basic sites on the DNA molecule.

Alkylation↗
PubMed1996

[Urban air pollution by carcinogenic N-nitrosamines].

Moscow is used as an example to discuss the problem of urban atmospheric pollution by carcinogenic N-nitrosamines. An analytical method is proposed, which is based on the use of a Russian gas chromatograph compatible with a chemiluminescence detector, that is a TEA thermal energy analyzer (USA) having some modifications to reduce the time of analysis and loss during sample pretreatment. The minimal detected concentration is 3 ng/m3 for 2-hour sampling. The method identifies and quantifies 7 volatile N-nitrosamines: N-nitrosodimethylamine (NDMA), N-nitrosodiethylamine, N-nitrosodibutylamine, N-nitrosodipropylamine, N-nitrosopiperidine, N-nitrosopyrrolidine, N-nitrosomorpholine. The pollution of the Moscow air was evaluated in the center of Moscow (30-60 ng/m3 for NDMA), in the industrial emission area (as high as several hundred ng/m3, and in the heavy traffic area (100 ng/m3 or more). It is proposed to study the working area for rubber and tire industries, to establish nitrosamine tolerances for these industries and maximum allowable discharge concentrations in the urban air and to monitor these parameters.

Air Pollutants↗
PubMedDate not supplied

Nitrosamines, alcohol, and gastrointestinal tract cancer: recent epidemiology and experimentation.

Recent epidemiological and experimental data continues to implicate nitrosamines in causation of gastrointestinal cancers. The evidence is strong for pharynx, esophagus, and stomach, and more problematic for liver, pancreas, and colorectum. Substantial levels of the promutagenic DNA adduct, Ob-methylguanine, in DNA from these organs in patas monkeys after a low dose of N-nitrosodimethylamine confirms the capacity for activation of environmental nitrosamines in these primate tissues. Alcohol is both an independent and a tobacco-interactive risk factor, influencing cancer incidence for oropharynx and esophagus strongly, and for stomach, colorectum, and liver more moderately. In a tabulation of experimental effects of ethanol potentially related to cancer-enhancing effects, toxicokinetic inhibition of hepatic first-pass clearance of nitrosamines is quantitatively greatest, and may be a major part of the mechanism of alcohol's effect on cancer risk for oropharnx, esophagus, and colon. Other operative mechanisms supported by experimental data are induction of activating enzymes, inhibition of DNA repair, and tumor promotion.

Alcohol Drinking↗
PubMed1996

Risk factors for lower urinary tract cancer: the role of total fluid consumption, nitrites and nitrosamines, and selected foods.

Many cases of lower urinary tract cancer cannot be attributed to the known risk factors of cigarette smoking and certain occupational chemical exposures. Data from a case-control study conducted on Oahu, Hawaii, from 1979 to 1986 were used to determine the role of several additional exposures in the etiology of lower urinary tract cancer, such as total fluid intake and dietary nitrites and nitrosamines, as well as intake of selected foods. A total of 195 male and 66 female lower urinary tract cancer cases of Caucasian and Japanese ancestry were matched to two population-based controls on age, sex, and race. Total fluid intake, and tap water in particular, showed a strong inverse dose-response relationship to cancer risk among women (odds ratio (OR) for highest to lowest quartile of total fluid intake = 0.3; trend P < 0.01).. This association was stronger in smokers than nonsmokers. Although fluid intake showed no overall association among men, the findings among smokers were suggestive of an effect similar to that found in women. Intake of dietary nitrites and nitrosamines was positively associated with risk in Japanese men (for nitrites, OR for highest to lowest tertile = 2.0; trend P = 0.05; for nitrosamines, OR for highest to lowest tertile = 3.0; trend P = 0.01). Consumption of processed meats, in particular bacon, sausage, and ham, was also significantly associated with increased risk in Japanese men. No other ethnic sex group exhibited this association with processed meats, although an effect was suggested for sausage in Japanese females and for bacon in Caucasian females. Unfortunately, it was not possible to determine whether these elevated risks were due to the fat, nitrite, or sodium content of the processed meats, or to the fact that they may have been fried.

Adult↗
PubMed1986

The effect of the trichothecene mycotoxin diacetoxyscirpenol on nitrosamine-induced esophageal cancer in the rat.

The fact that the only chemicals known to be potent carcinogens for the esophagus in animals are certain nitrosamines suggests that these environmental carcinogens could be a cause of human esophageal cancer. Epidemiological investigations support this concept. The level of exposure alone is not considered sufficient to account for the very high incidence of the disease in certain regions, but potentiating factors have been shown to have a dramatic effect on nitrosamine-induced esophageal cancer in animal experiments. A likely enhancing factor is consumption of food contaminated by molds, especially by Fusaria spp, a group known to produce trichothecene mycotoxins. The effect of simultaneous treatment with diacetoxyscirpenol (DS) on methyl-benzyl-nitrosamine (NMBzA)-induced esophageal cancer was studied. Feeding a diet containing DS at 10 ppm for 10 weeks caused thickening of the basal cell layer of the esophageal epithelium, but feeding DS (10 ppm) simultaneously with NMBzA (4, 8, 16 ppm) for 10 weeks, or feeding a lower dose of DS with NMBzA for a longer period, or administration of DS per os at intervals during NMBzA treatment, did not potentiate but possibly reduced esophageal tumors. Toxicity, revealed by reduced growth rate of DS-fed animals, may have inhibited carcinogenesis. In contrast to the rapid potentiating effect of zinc deficiency, DS does not appear to cause an early enhancement of esophageal cancer.

Animals↗
PubMed1996

Synthesis, Structure, and Conformational Dynamics of Bridgehead-Substituted Nitrosamines. Di-1-adamantylnitrosamine and Di-1-norbornylnitrosamine.

The synthesis of two bridgehead-substituted nitrosamines, di-1-adamantylnitrosamine (1) and di-1-norbornylnitrosamine (2), is described, and their solid state crystal structures are reported. Large bridgehead substituents increase the NNO angle of the nitrosamine (compared to that found for dimethylnitrosamine) without deconjugating the NNO pi system significantly. This structural change correlates with a red-shifted optical absorption, a diminished N,N rotational barrier, and a greater ease of oxidation of these hindered nitrosamines than is observed for dimethylnitrosamine. The electronic basis of these structure/function correlations is examined. It is concluded that 1 is more strained than N-nitroso-2,2,6,6-tetramethylpiperidine (3) which is more strained than 2 and that a raised (in energy) NO n orbital is primarily responsible for the extreme properties of the former.

Journal Article↗
PubMed1985

Formation of O6-methylguanine in rat liver DNA by nitrosamines does not predict initiation of preneoplastic foci.

Nitrosodimethylamine (NDMA) at 26 mumol/kg, and nitrosomethylbenzylamine (NMBzA) at 33.5 mumol/kg were equally potent in producing 7-methylguanine and O6-methylguanine in rat liver DNA. These doses were used to compare the abilities of the two nitrosamines to initiate production of putative preneoplastic foci in rat liver. Whereas NMBzA resulted in no increase above the background level of foci (0.9 +/- 0.1 foci/cm2), NDMA produced 7.5 +/- 0.6 foci/cm2. Co-administration of NDMA and NMBzA produced no more foci than NDMA alone, even though the combined effect of the two nitrosamines on DNA methylation was additive. The results suggest that methylation of hepatic DNA by nitrosamines does not predict initiation of preneoplastic foci.

Animals↗