Dietary Nitrite Intake Research Articles

Exposure to Phosphates and Nitrites through Meat Products: Estimation of the Potential Risk to Pregnant Women.

Diet during pregnancy is one of the most important nutritional challenges associated with some risks for the mother and the fetus. For the first time, the study aims to estimate long-term (2018-2022) exposure to nitrate and phosphates in Serbian pregnant women, based on individual consumption data and accurate values measured in frequently consumed meat products. For this purpose, seven types of meat products, consisting of 3047 and 1943 samples, were collected from retail markets across Serbia, to analyze nitrites and phosphorus content, respectively. These data were combined with meat product consumption data from the Serbian National Food Consumption Survey to assess dietary intake of nitrites and phosphate. The results were compared with the acceptable daily intake (ADI) proposed by the European Food Safety Authority. The average dietary exposure (EDI) to phosphorus ranged from 0.733 mg/kg bw/day (liver sausage and pate) to 2.441 mg/kg bw/day (finely minced cooked sausages). Considering nitrite intake, the major sources were bacon (0.030 mg/kg bw/day) and coarsely minced cooked sausages (0.0189 mg/kg bw/day). In our study, average nitrite and phosphorus exposure in the Serbian pregnant women population are far below the EFSA recommendations (ADI 0.07 mg/kg bw/day and 40 mg/kg bw/day, respectively).

Nitrite and nitrate intake from processed meat is associated with elevated diastolic blood pressure (DBP)

Processed meat consumption has been linked to high blood pressure (BP), a key risk factor for cardiovascular disease (CVD), but gaps remain with regards to the ingredients which contribute to this association. This study, therefore, aimed to examine the association between nitrite and nitrate intake from processed meat with diastolic (DBP) and systolic (SBP) blood pressure, while accounting for sodium intake. Dietary nitrite and nitrate intake from processed meat, assessed as total nitrite equivalent, was estimated for 1774 adult, processed meat consumers (≥18 years, 55.1% females) who had enrolled in the Hellenic National Nutrition and Health Survey (HNNHS). To avoid selection and reverse causality bias, associations with measured DBP and SBP were considered instead of self-reported data of hypertension presence. Participants were divided by tertile of dietary nitrite intake and by level of dietary guideline adherence for sodium (<1500; 1500-2300; ≥2300). Multiple regression models were used to examine associations with SBP and DBP, including an interaction term of nitrite with dietary sodium intake, for potential synergy. Overall, DBP increased by 3.05mmHg (95% CI: 0, 6.06), per tertile increase in nitrite intake and 4.41mmHg (95% CI: 0.17, 8.64) per level increase in sodium intake, when the interaction effect between nitrite and total sodium intakes was accounted for. By considering the significant synergistic effect of the two factors, DBP finally increased by 0.94 mgHg overall and 2.24 mgHg for subjects in the third tertile compared to those in the first. Also, a rise in total sodium intake of approximately 800mg, above 1500mg, caused a 2.30 mgHg increase in DBP. No significant correlations were found with SBP. Higher nitrite and nitrate intake from processed meats contributed to the increase of DBP, but the interaction effect with total sodium intake levels should be accounted for to properly interpret the findings.

Association of Dietary Nitrate, Nitrite, and N-Nitroso Compounds Intake and Gastrointestinal Cancers: A Systematic Review and Meta-Analysis.

N-nitroso compounds (NOCs) are a class of chemical carcinogens found in various environmental sources such as food, drinking water, cigarette smoke, the work environment, and the indoor air population. We conducted a systematic review and meta-analysis to investigate the links between nitrate, nitrite, and NOCs in food and water and the risk of gastrointestinal (GI) cancers, including esophageal cancer (EC), gastric cancer (GC), colorectal cancer (CRC), and pancreatic cancer (PC). A systematic search of the literature in Scopus, PubMed, Google Scholar, Web of Science, ScienceDirect, and Embase was performed for studies on the association between NOCs in drinking water and food sources and GI cancers. Forest plots of relative risk (RR) were constructed for all the cancer sites and the intake sources. The random-effects model was used to assess the heterogeneity between studies. Forty articles were included after removing duplicate and irrelevant articles. The meta-analysis indicated that the intake of high dose vs. low dose of these compounds was significantly associated with the overall GI cancer risk and nitrite (RR = 1.18, 95% CI = 1.07-1.29), and N-nitrosodimethylamine (NDMA) (RR = 1.32, 95% CI = 1.06-1.65). We found that dietary nitrite intake increased GC (RR = 1.33, 95% CI = 1.02-1.73), and EC (RR = 1.38, 95% CI = 1.01-1.89). Additionally, dietary NDMA intake increased the risk of CRC (RR = 1.36, 95% CI = 1.18-1.58). This meta-analysis provides some evidence that the intake of dietary and water nitrate, nitrite, and NOCs may be associated with GI cancers. In particular, dietary nitrite is linked to GC and EC risks and dietary NDMA intake is associated with CRC.

Daily intake of nitrate and nitrite via meat and poultry in Egypt

ABSTRACT Nitrate and nitrite are the most applied food additives to inhibit microbial growth. The main risk of nitrate and nitrite presence in food is the formation of nitrosamines during food preparation and digestion. However, dietary intake of nitrite and nitrate from food has potential cardiovascular benefits. Accordingly, 160 samples from meat and poultry were randomly collected to evaluate the level of occurrence nitrate and nitrite using an HPLC method and estimate the daily intake (EDI) of Egyptian adults and children. The levels of nitrate and nitrite ranged between 1.3–557 mg/kg and 6–812 mg/kg, respectively. The EDI was compared with the accepted daily intake (ADI) represented in the hazard index (HI) scale. The nitrite results clarify that all HI values were above 1 for all commodities, while for nitrate it exceeded 1 only for canned meat and basturma, when consumed by children.

Nitrite and nitrate content in meat products and estimated nitrite intake by the Estonian children

ABSTRACT Public interest in nitrate and nitrite content reduction in meat products has increased; therefore, the aim of the present study was to determine nitrate and nitrite levels in commercial meat products as the main source of added nitrites, and to estimate their dietary intake by children. The intake of nitrite from processed meat products and drinking water by Estonian children was estimated. Daily intake estimations were based on the food consumption data of the National Institute for Health Development. In addition, nitrite/nitrate concentrations of meat and processed meat products were measured using a liquid chromatographic method with UV detection. Mean nitrite intakes among 1087 studied children were 0.015 and 0.016 mg kg−1 b.w. day−1, respectively, among children aged 12–35 months and 3–10 years. Acceptable daily intake (ADI) of 0.07 mg nitrite kg−1 b.w. day−1 was exceeded in 3.1% of children, being more prevalent in the younger age group. Considering the consumption of processed meat and drinking water, mean nitrite intakes in the younger and the older age groups were, respectively, 21.9% and 22.9% of the ADI. Study results indicated that over a period of 10 years, children’s dietary nitrite intake from processed meat products has declined, which is probably caused by changes in food preferences and decreased usage of nitrite in cured meat products by meat industries.

Determination of dietary nitrite in patients with esophageal pre-cancerous lesion and normal people: a duplicate diet study

ABSTRACTThe goal of this study was to find the relationship between dietary nitrite and risk of esophageal cancer, and determine the amount of nitrite intake to establish the oral highest daily intake to prevent the occurrence of esophageal cancer. Duplicate portions of three-consecutive-day diets were collected from 100 patients with esophageal precancerous lesions and 100 controls. The average nitrite daily intakes for esophageal precancerous lesions and normal people were 15.72 mg/d and 11.11 mg/d. The median nitrite daily intakes for cases and controls were 8.76 mg/d and 5.33 mg/d. Positive association was observed between the risk of esophageal precancerous lesions and dietary nitrite intake (p = 0.035). An increased risk of esophageal precancerous lesions was observed for cases or controls in the highest intake quartile of nitrite (highest vs. lowest quartile odds ratio (OR) = 2.256, 95% confidence interval (CI): 1.012–5.026). These results suggest that dietary nitrite intake may influence the risk of esophageal cancer; populations with high incidence of esophageal cancer should take control of nitrite intake as one of the measures to prevent esophageal cancer.

Ingested nitrate and nitrite, disinfection by-products, and pancreatic cancer risk in postmenopausal women.

Nitrate and nitrite are precursors of N-nitroso compounds (NOC), probable human carcinogens that cause pancreatic tumors in animals. Disinfection by-products (DBP) exposures have also been linked with digestive system cancers, but few studies have evaluated relationships with pancreatic cancer. We investigated the association of pancreatic cancer with these drinking water contaminants and dietary nitrate/nitrite in a cohort of postmenopausal women in Iowa (1986-2011). We used historical monitoring and treatment data to estimate levels of long-term average nitrate and total trihalomethanes (TTHM; the sum of the most prevalent DBP class) and the duration exceeding one-half the maximum contaminant level (>½ MCL; 5 mg/L nitrate-nitrogen, 40 µg/L TTHM) among participants on public water supplies (PWS) >10 years. We estimated dietary nitrate and nitrite intakes using a food frequency questionnaire. We computed hazard ratios (HR) and 95% confidence intervals (CI) using Cox regression and evaluated nitrate interactions with smoking and vitamin C intake. We identified 313 cases among 34,242 women, including 152 with >10 years PWS use (N = 15,710). Multivariable models of average nitrate showed no association with pancreatic cancer (HRp95vs. Q1 = 1.16, 95% CI: 0.51-2.64). Associations with average TTHM levels were also null (HRQ4vs. Q1 = 0.70, 95% CI:0.42-1.18). We observed no trend with increasing years of exposure to either contaminant at levels >½ MCL. Positive associations were suggested in the highest dietary nitrite intake from processed meat (HRp95vs. Q1 = 1.66, 95% CI 1.00-2.75;ptrend = 0.05). We found no interactions of nitrate with known modifiers of endogenous NOC formation. Our results suggest that nitrite intake from processed meat may be a risk factor for pancreatic cancer.

Association between dietary nitrate and nitrite intake and sitespecific cancer risk: evidence from observational studies.

Epidemiological studies have reported inconsistent findings on the association between dietary nitrate and nitrite intake and cancer risk. We performed a meta-analysis of epidemiological studies to summarize available evidence on the association between dietary nitrate and nitrite intake and cancer risk from published prospective and case-control studies. PubMed database was searched to identify eligible publications through April 30th, 2016. Study-specific relative risks (RRs) with corresponding 95% confidence interval (CI) from individual studies were pooled by using random- or fixed- model, and heterogeneity and publication bias analyses were conducted.Data from 62 observational studies, 49 studies for nitrates and 51 studies for nitrites, including a total of 60,627 cancer cases were analyzed. Comparing the highest vs. lowest levels, dietary nitrate intake was inversely associated with gastric cancer risk (RR = 0.78; 95%CI = 0.67-0.91) with moderate heterogeneity (I2 = 42.3%). In contrast, dietary nitrite intake was positively associated with adult glioma and thyroid cancer risk with pooled RR of 1.21 (95%CI = 1.03-1.42) and 1.52 (95%CI = 1.12-2.05), respectively. No significant associations were found between dietary nitrate/nitrite and cancers of the breast, bladder, colorectal, esophagus, renal cell, non-Hodgkin lymphoma, ovarian, and pancreas. The present meta-analysis provided modest evidence that positive associations of dietary nitrate and negative associations of dietary nitrite with certain cancers.

Prenatal Exposure to Nitrosatable Drugs, Dietary Intake of Nitrites, and Preterm Birth.

Prenatal exposure to nitrosatable drugs, including secondary or tertiary amines, has been associated with preterm birth. Associations may be accentuated by higher intakes of dietary nitrites because of the increased formation of N-nitroso compounds. Using data from mothers of babies without major birth defects (controls) from the National Birth Defects Prevention Study, we examined the relationship between nitrosatable drug exposure in conjunction with dietary nitrite intake and preterm birth among 496 mothers of preterm infants and 5,398 mothers with full-term deliveries in 1997-2005. A protective association was observed with a high intake of plant nitrites (adjusted hazard ratio (AHR) = 0.72, 95% confidence interval (CI): 0.53, 0.97). Secondary amines in conjunction with high nitrite intake were associated with preterm birth during the first (AHR = 1.84, 95% CI: 1.14, 2.98), second (AHR = 1.89, 95% CI: 1.17, 3.07), and third (AHR = 2.00, 95% CI: 1.22, 3.29) trimesters. The adjusted hazard ratios for tertiary amine use in the third trimester by increasing tertiles of nitrite intake were 0.67 (95% CI: 0.35, 1.31), 1.25 (95% CI: 0.71, 2.19), and 2.02 (95% CI: 1.17, 3.49). Prenatal exposure to nitrosatable drugs, particularly secondary and tertiary amines, in conjunction with higher levels of dietary nitrite intake may increase the risk of preterm birth.

Nitrosatable drug exposure during the first trimester of pregnancy and selected congenital malformations.

Nitrosatable drugs can react with nitrite in the stomach to form N-nitroso compounds, and results from animal studies suggest that N-nitroso compounds are teratogens. With data from the National Birth Defects Prevention Study, the relation between prenatal exposure to nitrosatable drugs and limb deficiencies, oral cleft, and heart malformations in offspring was examined. Maternal reports of drugs taken during the first trimester of pregnancy were classified with respect to nitrosatability for mothers of 741 babies with limb deficiencies, 2774 with oral cleft malformations, 8091 with congenital heart malformations, and 6807 without major congenital malformations. Nitrite intake was estimated from maternal responses to a food frequency questionnaire. Isolated transverse limb deficiencies and atrioventricular septal defects were associated with secondary amine drug exposures (adjusted odds ratios [aORs], 1.51; 95% confidence limit [CI], 1.11-2.06 and aOR, 1.97; 95% CI, 1.19-3.26, respectively). Tertiary amines were associated with hypoplastic left heart syndrome (aOR, 1.50; 95% CI, 1.10-2.04) and single ventricle (aOR, 1.61; 95% CI, 1.06-2.45). These two malformations were also significantly associated with amide drugs. For several malformations, the strongest associations with nitrosatable drug use occurred among mothers with the highest estimated dietary nitrite intake, especially for secondary amines and atrioventricular septal defects (highest tertile of nitrite, aOR, 3.30; 95% CI, 1.44-7.58). Prenatal exposure to nitrosatable drugs may be associated with several congenital malformations, especially with higher nitrite intake. The possible interaction between nitrosatable drugs and dietary nitrite on risk of congenital malformations warrants further attention.

Thyroid cancer risk and dietary nitrate and nitrite intake in the Shanghai women's health study.

Nitrate and nitrite are precursors in the endogenous formation of N-nitroso compounds and nitrate can disrupt thyroid homeostasis by inhibiting iodide uptake. We evaluated nitrate and nitrite intake and risk of thyroid cancer in the Shanghai Women's Health Study that included 73,317 women, aged 40-70 years enrolled in 1996-2000. Dietary intake was assessed at baseline using a food frequency questionnaire. During approximately 11 years of follow-up, 164 incident thyroid cancer cases with complete dietary information were identified. We used Cox proportional hazards regression to estimate relative risks (RRs). We determined the nitrate and nitrite contents of foods using values from the published literature and focusing on regional values for Chinese foods. Nitrate intake was not associated with thyroid cancer risk [RR(Q4) = 0.93; 95% confidence interval (CI): 0.42-2.07; p for trend = 0.40]. Compared to the lowest quartile, women with the highest dietary nitrite intake had about a twofold risk of thyroid cancer (RR(Q4) = 2.05; 95%CI: 1.20-3.51), but there was not a monotonic trend with increasing intake (p for trend = 0.36). The trend with increasing nitrite intake from animal sources was significant (p for trend = 0.02) and was stronger for nitrite from processed meats (RR(Q4) = 1.96; 95%CI: 1.28-2.99; p for trend < 0.01). Although we did not observe an association for nitrate as hypothesized, our results suggest that women consuming higher levels of nitrite from animal sources, particularly from processed meat, may have an increased risk of thyroid cancer.

Dietary Nitrate and Nitrite Intake and Non-Hodgkin Lymphoma Survival

Nitrate and nitrite are precursors in the formation of N-nitroso compounds. We recently found a 40% increased risk of NHL with higher dietary nitrite intake and significant increases in risk for follicular and T-cell lymphoma. It is possible that these compounds also affect NHL prognosis by enhancing cancer progression in addition to development by further impairing immune system function. To test the hypothesis that nitrate and nitrite intake affects NHL survival, we evaluated the association in study participants that have been followed post-disease diagnosis in a population-based case-control study among women in Connecticut. We did not observe a significant increasing trend of mortality for NHL overall or by subtype for nitrate or nitrite intake for deaths from NHL or death from any cause, although a borderline significant protective trend was observed for follicular lymphoma with increasing nitrate intake. We did not identify a difference in overall survival for nitrate (P = 0.39) or for nitrite (P = 0.66) or for NHL specific survival for nitrate (P = 0.96) or nitrite (P = 0.17). Thus, our null findings do not confer support for the possibility that dietary nitrate and nitrite intake impacts NHL survival by promoting immune unresponsiveness.

Nitrosatable Drug Exposure During Early Pregnancy and Neural Tube Defects in Offspring

Nitrosatable drugs, such as secondary or tertiary amines and amides, form N-nitroso compounds in the presence of nitrite. Various N-nitroso compounds have been associated with neural tube defects in animal models. Using data from the National Birth Defects Prevention Study, the authors examined nitrosatable drug exposure 1 month before and 1 month after conception in 1,223 case mothers with neural tube defect-affected pregnancies and 6,807 control mothers who delivered babies without major congenital anomalies from 1997 to 2005. Nitrite intakes were estimated from mothers' responses to a food frequency questionnaire. After adjustment for maternal race/ethnicity, educational level, and folic acid supplementation, case women were more likely than were control women to have taken tertiary amines (odds ratio = 1.60, 95% confidence interval (CI): 1.31, 1.95). This association was strongest with anencephalic births (odds ratio = 1.96, 95% CI: 1.40, 2.73); odds ratios associated with tertiary amines from the lowest tertile of nitrite intake to the highest tertile were 1.16 (95% CI: 0.59, 2.29), 2.19 (95% CI: 1.25, 3.86), and 2.51 (95% CI: 1.45, 4.37), respectively. Odds ratios for anencephaly with nitrosatable drug exposure were reduced among women who also took daily vitamin supplements that contained vitamin C. Prenatal exposure to nitrosatable drugs may increase the risk of neural tube defects, especially in conjunction with a mother's higher dietary intake of nitrites, but vitamin C might modulate this association.

Estimated dietary intake of nitrite and nitrate in Swedish children

This study examines the intake of nitrate and nitrite in Swedish children. Daily intake estimates were based on a nationwide food consumption survey (4-day food diary) and nitrite/nitrate content in various foodstuffs. The mean intake of nitrite from cured meat among 2259 children studied was 0.013, 0.010 and 0.007 mg kg−1 body weight day−1 in age groups 4, 8–9 and 11–12 years, respectively. Among these age groups, three individuals (0.1% of the studied children) exceeded the acceptable daily intake (ADI) of 0.07 mg nitrite kg−1 body weight day−1. The mean intake of nitrate from vegetables, fruit, cured meat and water was 0.84, 0.68 and 0.45 mg kg−1 body weight day−1 for children aged 4, 8–9 and 11–12 years, respectively. No individual exceeded the ADI of 3.7 mg nitrate kg−1 body weight day−1. However, when the total nitrite intake was estimated, including an estimated 5% endogenous conversion of nitrate to nitrite, approximately 12% of the 4-year-old children exceeded the nitrite ADI. Thus, the intake of nitrite in Swedish children may be a concern for young age groups when endogenous nitrite conversion is included in the intake estimates.

Risk of non-Hodgkin lymphoma and nitrate and nitrite from the diet in Connecticut women

It has been estimated that 65,980 individuals were diagnosed with non-Hodgkin lymphoma (NHL) and 19,500 died from NHL in the United States in 2009. Although established risk factors such as immunodeficiency and viral infections may be responsible for a portion of the cases, the majority of NHL cases remain unexplained. Dietary nitrate and nitrite intake are exposures of particular interest for NHL risk as they are precursors in the endogenous formation of N-nitroso compounds, which cause lymphomas in animal studies. We investigated NHL risk overall and by histologic type in relation to dietary nitrate and nitrite intake in a population-based case-control study of 1,304 women in Connecticut. Nitrate and nitrite intake were assessed using a 120-item food frequency questionnaire. We found no association between risk of NHL overall and dietary nitrate and a slightly increased risk of NHL with higher dietary nitrite intake (highest vs. lowest intake quartile OR = 1.4; 95% CI: 0.9-2.2). When we evaluated intake by subtype, a significant positive trend was observed for follicular lymphoma and nitrate (p-trend = 0.04) and nitrite (p-trend < 0.01) with an over twofold risk in the highest nitrite intake quartile (OR = 2.3; 95% CI: 1.1-4.9). An increased risk in the highest quartile of nitrite intake was also observed for T-cell lymphoma (OR = 3.4; 95% CI: 1.0-11.9). Animal products containing nitrite were more strongly associated with risk of follicular lymphoma; whereas, both animal and plant sources of nitrite were associated with elevated ORs for T-cell lymphoma. Our results confirm a previous finding for nitrite intake and NHL risk and highlight the importance of evaluating histologic type. We conclude that these results should be replicated in a larger study with data on drinking water as well as dietary sources of nitrate intake.

Evidence by gas chromatography–mass spectrometry of ex vivo nitrite and nitrate formation from air nitrogen oxides in human plasma, serum, and urine samples

Nitrite and nitrate in body fluids and tissues result from dietary source, endogenous nitric oxide (NO) production and from NO and its higher oxides (NO x) present as pollutants in the atmosphere. Nitrite and nitrate in human blood serum and plasma or urine are commonly used as biomarkers and measures of endogenous NO synthesis. In addition to dietary intake of nitrite and nitrate, our study indicates that NO x naturally present in the laboratory air may be an abundant source for nitrite and nitrate in human serum, plasma, and urine ex vivo. These artifacts can be effectively reduced by closing sample-containing vials during sample treatment.

Dietary nitrite restores NO homeostasis and is cardioprotective in endothelial nitric oxide synthase-deficient mice

Endothelial production of nitric oxide (NO) is critical for vascular homeostasis. Nitrite and nitrate are formed endogenously by the stepwise oxidation of NO and have, for years, been regarded as inactive degradation products. As a result, both anions are routinely used as surrogate markers of NO production, with nitrite as a more sensitive marker. However, both nitrite and nitrate are derived from dietary sources. We sought to determine how exogenous nitrite affects steady-state concentrations of NO metabolites thought to originate from nitric oxide synthase (NOS)-derived NO as well as blood pressure and myocardial ischemia–reperfusion (I/R) injury. Mice deficient in endothelial nitric oxide synthase (eNOS –/–) demonstrated decreased blood and tissue nitrite, nitrate, and nitroso proteins, which were further reduced by low-nitrite (NOx) diet for 1 week. Nitrite supplementation (50 mg/L) in the drinking water for 1 week restored NO homeostasis in eNOS –/– mice and protected against I/R injury. Nitrite failed to alter heart rate or mean arterial blood pressure at the protective dose. These data demonstrate the significant influence of dietary nitrite intake on the maintenance of steady-state NO levels. Dietary nitrite and nitrate may serve as essential nutrients for optimal cardiovascular health and may provide a novel prevention/treatment modality for disease associated with NO insufficiency.

Risk of Non-Hodgkin Lymphoma and Nitrate and Nitrite From Drinking Water and Diet

Nitrate and nitrite are precursors in the in vivo formation of N-nitroso compounds, potent animal carcinogens. We conducted a population-based case-control study of non-Hodgkin lymphoma (NHL) in 1998 to 2000 in Iowa, Detroit, Seattle, and Los Angeles. Because nitrate levels were elevated in many drinking water supplies in Iowa, but not in the other study centers, we evaluated water nitrate levels and risk of NHL in Iowa only. Monitoring data for public supplies were linked to water source histories from 1960 onward. Nitrate was measured at interview homes with private wells. We limited most analyses to those with nitrate estimates for > 70% of their person-years since 1960 (181 cases, 142 controls). For those in the diet arm of the study (458 cases, 383 controls from 4 centers) and for Iowa participants in both the diet and drinking water analyses, we estimated dietary nitrate and nitrite intake using a 117-item food-frequency questionnaire that included foods high in nitrate and nitrite. Odds ratios and 95% confidence intervals were calculated using logistic regression, adjusting for the study matching factors, education, and caloric intake (diet analyses only). We found no overall association with the highest quartile of average drinking water nitrate (> 2.90 mg/L nitrate-N: odds ratios = 1.2; 95% confidence interval = 0.6-2.2) or with years > or = 5 mg/L (10+ years: 1.4; 0.7-2.9). We observed no evidence of an interaction between drinking water nitrate exposure and either vitamin C or red meat intake, an inhibitor and precursor, respectively, of N-nitroso compound formation. Among those in the diet arm, dietary nitrate was inversely associated with risk of NHL (highest quartile: 0.54; 0.34-0.86). Dietary nitrite intake was associated with increasing risk (highest quartile: 3.1; 1.7-5.5) largely due to intakes of bread and cereal sources of nitrite. Average drinking water nitrate levels below 3 mg/L were not associated with NHL risk. Our study had limited power to evaluate higher levels that deserve further study.

Drinking Water and Dietary Sources of Nitrate and Nitrite and Risk of Glioma

Dietary nitrite has been associated with increased glioma risk; however, drinking water nitrate has not been extensively evaluated. We conducted a population-based case-control study of adult glioma in Nebraska. Water utility nitrate measurements were linked to residential water source histories. We computed average nitrate exposure over a 20-year period. A food frequency questionnaire was used to assess dietary nitrate and nitrite. Increasing quartiles of the average nitrate level in drinking water were not significantly associated with risk (adjusted odd ratios: 1.4, 1.2, 1.3). Risk was similar among those with both higher and lower intakes of vitamin C, an inhibitor of N-nitroso compound formation. Dietary nitrite intake was not associated with risk. Our study does not support a role for drinking water and dietary sources of nitrate and nitrite in risk of adult glioma.

Estimation of daily intake of food preservatives

The techniques that are available for estimating the intake of food preservatives are reviewed. These include per-capita, duplicate diet, diary records, food frequency, Total Diet and biomarker-based methods. Each approach has its merits and disadvantages and selection will depend upon a number of factors such as the reasons why the intake information is required, resource availability and the nature and extent of usage of the preservative. The application of these techniques is exemplified with reference to those that have been employed to estimate the dietary intake of nitrite and nitrate. It is concluded that such estimates are only as good as the analytical data upon which they are based and, in the case of nitrite, there is evidence to suggest that current data overestimate actual intake in the UK.