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PubMed1986

The correlation between certain tryptophan metabolites and the N-nitrosamine content in the urine of bilharzial bladder cancer patients.

The present work is an up-to-date approach to study the correlation between the excretion pattern of tryptophan metabolites along the kynurenine pathway (after loading with 2 gm. L-tryptophan), and the N-nitrosamine content in urine of bilharzial bladder cancer patients. The control group was composed of healthy subjects who had no reported history of S. haematobium infection and no current bacterial cystitis. The N-nitrosamine content was determined by the colorimetric method of Eisebrand and Preussmann (1970). It was demonstrated that 64 per cent of the patients metabolized the tryptophan load abnormally and the others metabolized it almost normally. Moreover, the N-nitrosamines were present in 43 per cent of controls and 93 per cent of patients have these derivatives in higher values. The presence of an inverse correlation between certain tryptophan metabolites, shown previously to be bladder carcinogens, and the N-nitrosamine content, especially after loading, was interpreted in view of the possible conversion of some tryptophan metabolites into N-nitrosamines either under endovesical conditions or during the execution of the colorimetric determination of these compounds. Therefore, thorough investigation is urgently needed to study the origin of these urinary N-nitrosamines. Moreover, improved method(s) for their colorimetric determination are also urgently needed.

3-Hydroxyanthranilic Acid↗
PubMed2004

Detecting N-nitrosamines in drinking water at nanogram per liter levels using ammonia positive chemical ionization.

Detection of N-nitrosamines in water supplies is an environmental and public health issue because many N-nitrosamines are classified as probable human carcinogens. Some analytical methods are inadequate for detecting N-nitrosodimethylamine (NDMA) at low ng/L concentrations in water due to poor extraction efficiencies and nonselective and nondistinctive GC/MS electron ionization techniques. Development of a selective, sensitive, and affordable benchtop analytical method for eight N-nitrosamines, at relevant drinking water concentrations was the primary objective of this project. A solid-phase extraction method using Ambersorb 572 and LiChrolut EN was developed in conjunction with GC/MS ammonia positive chemical ionization (PCI). Ammonia PCI shows excellent sensitivity and selectivity for N-nitrosamines, which were quantified using both isotope dilution/surrogate standard and internal standard procedures. Method detection limits for all investigated N-nitrosamines ranged from 0.4 to 1.6 ng/L. Applying our extraction method to authentic drinking water samples with dissolved organic carbon concentrations of 9 mg/L, we were able to detect N-nitrosodimethylamine (2-180 ng/L) as well as N-nitrosopyrrolidine (2-4 ng/L) and N-nitrosomorpholine (1 ng/L), two N-nitrosamines that have not been reported in drinking water to date. With high recoveries of standards and analytes, the described internal standard method offers a valuable new approach for investigating several N-nitroso compounds at ultratrace levels in drinking water.

Alberta↗
PubMed2006

Nitrosamine formation pathway revisited: the importance of chloramine speciation and dissolved oxygen.

Nitrosamine formation during chloramination previously has been linked to a reaction between monochloramine and organic nitrogen precursors via unsymmetrical dialkylhydrazine intermediates. Our results demonstrate the critical importance of dichloramine and dissolved oxygen. We propose a new nitrosamine formation pathway in which dichloramine reacts with secondary amine precursors to form chlorinated unsymmetrical dialkylhydrazine intermediates. Oxidation of these intermediates by dissolved oxygen to form nitrosamines competes with their oxidation by chloramines. Even when preformed monochloramine was applied, our model explained nearly all N-nitrosodimethylamine formation from the traces of dichloramine formed via monochloramine disproportionation. We suggest that, in contrast to unsymmetrical dialkylhydrazines, the weak, nonpolar nature of the N-Cl linkage in chlorinated unsymmetrical dialkylhydrazine intermediates enables incorporation of dissolved oxygen to form nitrosamines. With the improved understanding of the nitrosamine formation pathway, strategies are suggested that could significantly reduce nitrosamine formation during chloramination.

Chloramines↗
PubMedDate not supplied

The nitrosation of hexetidine and hexedine: characterization of the major nitrosamine from common antimicrobial agents.

The acidic nitrosation of hexetidine and hexedine, common antimicrobial agents and drug constituents, leads to a mixture of nitrosamines. The major nitrosamine product, "HEXNO", forms rapidly in yields as high as 60% over the pH range 1-4.8 at incubation times of 1 h at 37 degrees C with 40 mM NO2- and 10 mM hexetidine. On the basis of extensive spectroscopic characterization and independent synthesis HEXNO has been assigned the structure of 1-(2-ethylhexyl)-3-nitroso-4-methyl-4-[[N-(2-ethylhexyl)-N- nitrosoamino]methyl]imidazolidine (7). The synthesis of HEXNO involves the novel interception by potassium nitrite in ether/18-crown-6 of an imminium ion produced from the reaction of hexedine with benzyl chloroformate. Collapse of the alpha-amino nitrous ester produced by this reaction yields the nitrosamine containing carbamate 8, which yields HEXNO after removal of the carbamate with trimethylsilyl iodide and subsequent nitrosation. The rapid formation of HEXNO from hexetidine and hexedine supports the hypothesis that tertiary geminal diamines will produce nitrosamines rapidly by a mechanism which involves the cleavage of a nitrosammonium ion with the assistance of the neighboring nitrogen atom. This process is deemed to be of possible importance in the endogenous production of potentially carcinogenic nitrosamines because of its low nitrite requirement and high nitrosation rate. The available data suggest the probable formation of HEXNO and other nitrosamines from hexetidine under conditions of its use.

Chromatography, High Pressure Liquid↗
PubMed1999

Stereoselective metabolism of nicotine and tobacco-specific N-nitrosamines to 4-hydroxy-4-(3-pyridyl)butanoic acid in rats.

The carcinogenic tobacco-specific nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N'-nitrosonornicotine (NNN) are believed to play a role in cancers associated with the use of tobacco products. Urinary metabolites of NNK and NNN could be used as biomarkers for an individual's ability to metabolically activate or detoxify these nitrosamines. While several metabolites of NNK can be quantified in human urine, no assay is available to determine human urinary levels of NNK and NNN metabolites resulting from the critical alpha-hydroxylation metabolic activation pathways. The major urinary metabolites resulting from alpha-hydroxylation of NNK and NNN in rodents are 4-oxo-4-(3-pyridyl)butanoic acid (keto acid) and 4-hydroxy-4-(3-pyridyl)butanoic acid (hydroxy acid). The major obstacle to the use of these metabolites as biomarkers of metabolic activation is the fact that they are also metabolites of nicotine, which is present at levels 1400-13000 times greater than those of the nitrosamines in cigarette smoke. However, the chirality of hydroxy acid could be useful in overcoming this problem. If different enantiomers of hydroxy acid were formed from nicotine versus the nitrosamines, and if the overall yield of hydroxy acid from nicotine were substantially smaller than that from the nitrosamines, then hydroxy acid might be useful as a urinary biomarker of NNK and NNN alpha-hydroxylation. To these ends, F-344 rats were administered either [5-3H]NNK, [5-3H]NNN, [5-3H]keto acid, or [2'-14C]nicotine. The levels of urinary hydroxy acid were determined by HPLC analysis. Its stereochemistry was determined by conversion to its methyl ester, reaction with (S)-(-)-alpha-methylbenzyl isocyanate, and separation and quantitation of the resulting diastereomers by HPLC. Urinary hydroxy acid accounted for 12% of the NNK dose and 31% of the NNN dose, but only 1 and 0.1% of the dose of keto acid and nicotine, respectively. Furthermore, metabolism of NNK produced mainly (S)-hydroxy acid in the urine, while metabolism of keto acid and nicotine gave predominantly (R)-hydroxy acid. Both enantiomers were present in the urine of NNN-treated rats. Therefore, in the rat, it is possible to distinguish the hydroxy acid derived from nicotine from that derived from the nitrosamines. If similar pathways occur in humans, (S)-hydroxy acid could potentially be developed as a urinary biomarker of NNK and NNN alpha-hydroxylation in smokers.

Animals↗
PubMed2001

Intragastric volatile N-nitrosamines, nitrite, pH, and Helicobacter pylori during long-term treatment with omeprazole.

BACKGROUND & AIMS: This study evaluated the effect of long-term gastric acid suppressive therapy with omeprazole on intragastric levels of carcinogenic N-nitrosamines and related parameters. METHODS: Forty-five patients on long-term omeprazole medication (mean, 35 months) and 13 healthy subjects without medication participated. Volatile N-nitrosamines were determined in gastric juice and urine. Intragastric pH, nitrite, nitrate, and H. pylori status were determined. DNA isolated from gastric biopsy specimens was analyzed for precarcinogenic alkyl-DNA adducts. RESULTS: The intragastric pH in patients was significantly higher compared with controls (P = 0.0001). Gastric nitrite levels in patients were nonsignificantly higher. There was no difference in total levels of intragastric volatile N-nitrosamines between patients and controls, however, urinary N-nitrosodimethylamine excretion was higher in patients (P = 0.001). On omeprazole, Helicobacter pylori-positive vs. -negative patients had a nonsignificantly higher intragastric nitrite level and higher urinary N-nitrosodimethylamine excretion. No alkyl-DNA adducts could be detected in gastric epithelium. CONCLUSIONS: Increased intragastric pH caused by long-term treatment with omeprazole does not result in increased intragastric levels of nitrite and volatile N-nitrosamines. The significantly higher urinary N-nitrosamine excretion implies the risk of increased endogenous formation of N-nitrosamines during long-term omeprazole treatment. This risk may be higher in H. pylori-positive patients.

Adult↗
PubMedDate not supplied

Ingestion of carcinogenic N-nitrosamines by infants and children.

Volatile N-nitrosamines are very potent carcinogens. They can be approximately 5 million times more powerful than saccharin. One of two principal methods is generally used when assaying rubber products for nitrosamine content: (1) the German method (aqueous extraction) or (2) the U.S. method (dichloromethane extraction). When 16 types of baby-bottle nipples and children's pacifiers were tested recently, relatively high levels of nitramines, nitrosamines, and nitrosatable precursors were found. Eighty-one percent failed to meet the strict Dutch standards (based on the German method), but only 37.5% would have been banned according to U.S. regulations, which ignore nitrosatable-precursor content. Up to one-third of the nitrosamines present in a rubber nipple may migrate into the milk in the bottle within a few hours. Transfer into infant formula may exceed 40%, and transfer into saliva may be even higher. Thus, a highly contaminated nipple may cause a 5-kg infant who drinks 1 l/d to ingest approximately 2 micrograms/kg body weight.d of nitrosamines. To this, add any exposure resulting from pacifier use or from in vivo nitrosation of precursors. Therefore, daily exposure of infants may, in the worst case, conceivably reach 4-5 micrograms/kg body weight.d. Entire average daily exposure of an American adult to volatile nitrosamines from major sources is estimated to be less than 0.05 micrograms/kg body weight.d. Infants who use products like those tested may, therefore, be exposed daily to less than or equal to 100 times more of these carcinogens than are adults.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Worker exposures to nitrosamines in a rubber vehicle sealing plant.

Occupational nitrosamine exposures were measured during a National Institute for Occupational Safety and Health (NIOSH) health hazard evaluation at a rubber vehicle sealing plant. All of the 28 personal breathing zone samples had detectable concentrations of nitrosodimethylamine (NDMA), nitrosodiethylamine, nitrosopiperidine (NPIP), and nitrosomorpholine; and 27 of the 28 samples had detectable concentrations of nitrosopyrrolidine. The NDMA exposures were the highest, ranging from 0.47 to 11.44 micrograms/m3. The next highest exposures were to NPIP, ranging from 0.20 to 4.39 micrograms/m3. Several general area air samples were also collected, which revealed concentrations of NDMA ranging from 2.29 to 88.47 micrograms/m3 at the drills along the salt bath lines. The salt bath curing process appears to be the primary source of nitrosamine formation, and personal exposures were highest for the salt bath line operators and assistant operators. Although there are no numerical occupational nitrosamine standards in the United States to reference, the exposures in this plant were much higher than the German standard of 1 micrograms/m3 total nitrosamines for general industry and 2.5 micrograms/m3 total nitrosamines for certain processes such as vulcanization. NIOSH investigators recommended that the ventilation systems be improved to reduce the exposures to the lowest feasible concentrations until the process can be redesigned so that nitrosamines are not formed.

Air Pollutants, Occupational↗
PubMed1992

Cytochrome P450 2E1 and 2A6 enzymes as major catalysts for metabolic activation of N-nitrosodialkylamines and tobacco-related nitrosamines in human liver microsomes.

An acetyltransferase-overexpressing strain of Salmonella typhimurium (NM2009) has been used to investigate roles of human liver microsomal cytochrome P450 (P450) enzymes in the activation of carcinogenic nitrosamine derivatives, including N-nitrosodialkylamines and tobacco-smoke-related nitrosamines, to genotoxic products. Studies employing correlation of activities with several P450-dependent monooxygenase reactions in different human liver samples, inhibition of microsomal activities by antibodies raised against human P450 enzymes and by specific P450 inhibitors, and reconstitution of activities with purified P450 enzymes suggest that the tobacco-smoke-related nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and N-nitrosonornicotine (NNN) as well as N-nitrosodimethylamine (NDMA) and N-nitrosodiethylamine (NDEA) are oxidized to genotoxic products by different P450 enzymes, particularly P450 2E1 and 2A6. The activation of NDMA and NNN by liver microsomes was suggested to be catalyzed more actively by P450 2E1 than by other P450 enzymes because the activities were well correlated with NDMA N-demethylation and aniline p-hydroxylation in different human samples, and purified P450 2E1 had the highest activities in reconstituted monooxygenase systems. The relatively high contribution of P450 2A6 to the activation of NDEA and NNK was supported by the correlation seen with coumarin 7-hydroxylation in human liver microsomes, and antibodies raised against P450 2A6 inhibited both activities by approximately 50%. P450 3A4, 2D6 and 2C enzymes appear not to be extensively involved in the activation of these nitrosamines as judged by several criteria examined. Thus, this work indicates that several P450 enzymes, particularly P450 2E1 and 2A6, catalyze metabolic activation of nitrosamine derivatives including N-nitrosodialkylamines and tobacco-smoke-related nitrosamines in human liver microsomes.

Animals↗
PubMed1993

Metabolism and activation of pancreas specific nitrosamines by pancreatic ductal cells in culture.

Metabolism of 14C labeled N-nitrosobis(2-oxopropyl)amine (BOP), N-nitroso(2-hydroxypropyl)(2-oxopropyl)amine (HPOP) and N-nitrosobis(2-hydroxypropyl)amine (BHP) by pancreatic duct cells in culture involves the following two pathways: reduction or oxidation reactions at the beta-carbon which result in the inter-conversion of these nitrosamines and activation reactions which result in the decomposition of the nitrosamine, the evolution of 14CO2 and the labeling of macromolecules. Reduction of BOP to HPOP seems to contribute significantly to the metabolism of the former nitrosamine by pancreatic duct cells, however, redox reactions at the beta-carbon of HPOP or BHP are not extensive. In terms of DNA damage, all three nitrosamines yield methyl and hydroxypropyl adducts. As expected, HPOP and BHP yield higher levels of O6-hydroxypropylguanine than BOP, while the latter yields higher levels of O6-methylguanine. There is no correlation between the ability of these nitrosamines to alkylate duct cell DNA in vitro and their carcinogenic potency in vivo. Concentrations of DNA adducts induced by pancreas specific nitrosamines (PSNs) in cultured duct cells at concentrations comparable to those found in the pancreatic juice of animals treated with BOP, are almost an order of magnitude lower than those induced in the pancreas of such animals. Discrepancies between in vitro and in vivo formation of active metabolites and DNA adducts may be attributed to the decline of the cells' ability to activate PSNs during culturing. In the same vein, the ductal cell may not be the main source of active metabolites targeting its DNA in the animal model.

Animals↗
PubMed2000

O(6)-methylguanine DNA adducts associated with occupational nitrosamine exposure.

Occupational nitrosamine exposures from a rubber vehicle seal (VS) curing operation were compared with the peripheral blood lymphocyte concentrations of two nitrosamine-related DNA adducts, N(7)-methylguanine (N(7)mdG) and O(6)-methylguanine (O(6)mdG), and with the activity of the enzyme that repairs O(6)mdG adducts, O(6)-alkylguanine-DNA alkyltransferase (AGT). The occupational personal breathing zone (PBZ) nitrosamine exposures ranged from 0.4 to 9.3 microg/m(3) in the VS area, from 0.1-2 microg/m(3) in an area remote from the VS and were not detected at a nearby rubber plant. Workers from all three of these locations had detectable concentrations of N(7)mdG adducts, ranging from 0.1 to 133.2 adducts/10(7) deoxyguanosine nucleosides. Although N(7)mdG concentrations were elevated for those who worked in the VS area (median 3.60 compared with 1.44), the difference was not statistically significant after controlling for confounding factors. The O(6)mdG adduct concentrations were much lower than those of N(7)mdG, ranging from non-detectable to 12.7 O(6)mdG adducts/10(7) deoxyguanosine nucleosides and many of the participants (40/78 successfully analyzed) did not have detectable amounts of these adducts (limit of detection 0.03 O(6)mdG adducts/10(7) deoxyguanosine nucleosides). Analysis of the ordinal exposure categories (high, medium/high, medium/low, low and no exposure) yielded a statistically significant association with having detectable O(6)mdG adducts (Kendall's taub = -0.253, asymptotic SE = 0.096). There was no significant association between AGT activity and nitrosamine exposure or exposure category (P > 0.30). Although no association was found between PBZ exposure and either the N(7)mdG adduct concentrations or AGT activity, the significant positive association between working in and near the VS department and the presence of O(6)mdG adducts, which have mutagenic potential, provides evidence to link nitrosamine exposure one step closer to human cancer by demonstrating an association between external nitrosamine exposures and cancer-related biological effects.

DNA Adducts↗
PubMed2006

Evaluation of occupational exposure to N-nitrosamines in a rubber-manufacturing industry.

OBJECTIVE: We sought to determine volatile N-nitrosamines levels in the air of a rubber-manufacturing industry and to measure urinary N-nitrosamines concentrations in exposed workers. METHODS: Personal monitoring of 34 workers was performed by sampling nine airborne N-nitrosamines in four factories that manufactured rubber drive belts for automotive engines. Urinary N-nitrosamine levels were determined in all workers and in a control group of 26 subjects. Analyses were conducted by capillary gas chromatography-thermal energy analyzer. RESULTS: Airborne and urinary N-nitrosamines levels were very low and, in most cases, below the limit of detection (0.06 microg/m and 0.1 microg/L, respectively). CONCLUSIONS: Although airborne and urinary N-nitrosamines levels were found to be very low, exposed workers should still be monitored constantly because some of these substances are known to be genotoxic and carcinogenic.

Adult↗
PubMed2000

Exposure to high concentrations of nitrosamines and cancer mortality among a cohort of rubber workers.

OBJECTIVES: To examine if the occurrence of different cancers was increased among rubber workers, as the highest known exposures of humans to nitrosamines have occurred in the rubber industry. METHODS: A cohort of 8933 rubber workers (hired after 1 January 1950, still active or retired on 1 January 1981 and employed for at least 1 year in one of five study factories) was followed up for mortality from 1 January 1981 to 31 December 1991. Work histories were reconstructed with routinely documented cost centre codes, which allowed identification by employment in specific work areas. For each cost centre code time and factory specific, semi-quantitative exposures to nitrosamines (three levels: low, medium, high) and other compounds were estimated by industrial hygienists. Rate ratios for medium (RRm) and high (RRh) exposures and 95% confidence intervals (95% CIs) were calculated with Cox's proportional hazards models with the low exposure as reference. RESULTS: Exposure to nitrosamines was significantly associated with an increased mortality from cancers of the oesophagus (13 deaths: RRm 1.7, 95% CI 0.3 to 10.3; RRh 7.3, 95% CI 1.9 to 27.8) and of the oral cavity and pharynx (17 deaths: RRm 0.8, 95% CI 0.2 to 4.1; RRh 3.9, 95% CI 1.4 to 11.1). A non-significant trend of increasing mortality with exposure to higher concentrations of nitrosamines was found for mortality from cancer of the prostate (26 deaths: RRm 1.4, 95% CI 0.5 to 3.8; RRh 2.2, 95% CI 0.9 to 5.6), and the brain (six deaths: RRm 3.9, 95% CI 0.3 to 42.6; RRh 6.0, 95% CI 0.6 to 57.6). No association was found between exposure to nitrosamines and cancer of the stomach (RRm 0.8, 95% CI 0.4 to 1.8; RRh 1.2, 95% CI 0.5 to 2.5) or lung (RRm 1.0, 95% CI 0.6 to 1.5; RRh 1.0, 95% CI 0.7 to 1.6). CONCLUSIONS: Exposure to high concentrations of nitrosamines is associated with increased mortality from cancers of the oesophagus, oral cavity, and pharynx, but not with increased mortality from cancers of the stomach or lung.

Adult↗
PubMed1999

[N-nitrosamines and nitrites in meat and meat products].

Content of N-nitrosamines and nitrites in meat and meat products of Russian manufacture made on traditional and recently developed techniques was measured. The influence of conditions and duration of storage of meat products on changes in N-nitrosamines and nitrites was investigated. It is established that in observance of instruction of entering nitrites during manufacture their residual amounts in a ready product do not exceed hygienic levels accepted in Russian Federation. N-nitrosamines (N-nitrosodimethylamine and N-nitrosodiethylamine) were found in amounts from 0.1 up to 30 ppb. The least amount of N-nitrosamines was in canned meat (up to 0.7 ppb) and fresh meat (up to 0.4 ppb), greatest--in smoked products from pork. 8.6% tested samples of meat products contained N-nitrosamines in amounts exceeding the hygienic levels. The reasons of high contents of N-nitrosamines was infringement of conditions and terms of storage of ready meat products.

Carcinogens↗
PubMed1987

Comparison of induction of DNA single-strand breaks and initiation of rat hepatocarcinogenesis by different nitrosamines.

The capacities of nitrosamines to induce DNA single-strand breaks (SSB) and to initiate carcinogenesis in rat liver were compared. N-Nitrosodiethanolamine (NDELA), N-nitrosoethylhydroxyethylamine (NEHEA) and N-nitrosodiethylamine (NDEA) were equipotent in inducing DNA SSB when administered by gavage at doses of 0.35 mmol/kg, 0.015 mmol/kg and 0.37 mmol/kg, respectively. Male Wistar rats were injected with these nitrosamines and were then submitted to a selection procedure. Ten rats per group were sacrificed one week after the end of the selection to see the effects of the nitrosamines on the development of preneoplastic lesions. The numbers of gamma-glutamyl transferase (GGT)-positive lesions per cm2 were 0.8, 2.1, 5.2 and 40.1 in rats treated with saline, NDELA, NEHEA and NDEA, respectively. N-Nitrosobis(2,2,2-trifluorethyl)amine (6F-NDEA), a nongenotoxic and noncarcinogenic nitrosamine, induced 0.7 GGT-positive lesions per cm2. Ten rats per group also received 0.05% phenobarbital in their drinking-water and were killed six months after initiation in order to see the effect of the different nitrosamines on the incidence and yield of tumours. Two extrahepatic cancers were found after administration of NEHEA, whereas two hepatocellular carcinomas were detected after injection of NDEA. No cancer developed in the other groups. Although other factors may influence the process, these results indicate that no simple correlation can be established between induction of SSB in DNA and initiation of tumours by nitrosamines in rat liver.

Animals↗
PubMedDate not supplied

Volatile N-nitrosamines in infant pacifiers sold in the United States as determined by gas chromatography/thermal energy analysis.

Volatile N-nitrosamines in infant latex rubber pacifiers were determined using a modification of a previously described dichloromethane extraction procedure, followed by gas chromatography/thermal energy analysis. Under an interagency agreement between the National Center for Toxicological Research and the Consumer Product Safety Commission (CPSC), data were obtained on the baseline and compliance concentrations of volatile N-nitrosamines in infant pacifiers sold in the United States. Pacifiers made by 18 different manufacturers before and after the January 1, 1984 action level of 60 ppb was set by the CPSC were analyzed for volatile N-nitrosamines. N-Nitrosodibutylamine was the principal N-nitrosamine found, along with trace amounts of N-nitrosodimethylamine, N-nitrosodiethylamine, and N-nitrosopiperidine. Mean total volatile N-nitrosamine levels for baseline and compliance samples were 63.9 and 21.2 ppb, respectively. The pacifier lots sampled after January 1, 1984 showed a significant decrease in contamination levels, indicating that at least 98% of the market share is in compliance with the CPSC enforcement policy for N-nitrosamines in infant pacifiers sold in the United States.

Chromatography, Gas↗
PubMedDate not supplied

Nitrosamines in bacon: a case study of balancing risks.

Nitrite has been used for centuries to preserve, color, and flavor meat. Today, about 10 billion pounds of cured meat products are produced annually, accounting for some one-tenth of the American food supply. Regulators became concerned about the safety of using nitrite in the early 1960s when studies showed the presence of carcinogenic nitrosamines in cured meat products. In the early 1970s, a study at the Massachusetts Institute of Technology implicated nitrite itself as a carcinogen. As studies have raised concern over the safety of nitrite, regulators have had to weigh the potential risk from cancer against nitrite's proven role in protecting consumers from deadly food poisoning bacteria. Today there is little scientific support for the theory that nitrite is a direct carcinogen. To deal with the nitrosamine problem, the U.S. Department of Agriculture (USDA) lowered the permissible amount of nitrite in cured meats to that level considered necessary for botulism protection. Regulators, however, found it necessary to take additional steps with bacon because nitrosamines were found consistently in fried bacon samples. In addition to lowering the amount of nitrite that could be added to "pumped bacon" (cured by injecting liquid curing agents in the pork belly), USDA required the addition of nitrosamine inhibitors and began an intensive monitoring program in processing plants to ensure that fried bacon did not contain confirmable nitrosamines. The cooperative effort between Government and industry resulted in the virtual elimination of confirmable nitrosamines in pumped bacon by 1980. USDA is continuing its efforts to reduce nitrite in meats wherever possible. It is involved in active research programs in the Federal Government, academia, and industry.

Animals↗
PubMed1984

Epidemiological assessment of risk to humans from exposure to nitrosamines.

In order for epidemiologists to evaluate the 'nitrosamine hypothesis' it is necessary to develop measures of human exposure to N-nitrosamines - both exogenous and when formed internally through consumption precursors. Dissatisfied with indefinite findings using indirect indices of N-nitrosamine exposure, we have attempted to derive an index based on the known kinetics of N-nitrosamine formation. This has been applied in a case-control study of cerebral tumours and resulted in a suggestive finding of increased risk for exogenous but not total N-nitrosamine exposure. A potential difficulty with our index is doubt as to whether vegetable sources of nitrates and consequent endogenous formation of nitrites indeed result in N-nitrosamine exposure, in view of the possible presence of blocking agents or of vitamin C consumed at the same time as vegetables. Further work is necessary, but we hope to apply the index in a case-control study of gastric cancer currently under analysis.

Dimethylnitrosamine↗