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Introduction: Nitrate and nitrite are naturally occurring in both plant- and animal-sourced foods, are used as additives in the processing of meat, and are found in water. There is growing evidence that they exhibit a spectrum of health effects, depending on the dietary source. The aim of the study was to examine source-dependent associations between dietary intakes of nitrate/nitrite and both all-cause and cause-specific mortality., Methods: In 52,247 participants of the Danish Diet, Cancer and Health Study, associations between source-dependent nitrate and nitrite intakes--calculated using comprehensive food composition and national drinking water quality monitoring databases--and all-cause, cardiovascular disease (CVD)-related, and cancer-related mortality over 27 years were examined using restricted cubic splines within Cox proportional hazards models adjusting for demographic, lifestyle, and dietary confounders. Analyses were stratified by factors hypothesised to influence the formation of carcinogenic N-nitroso compounds (namely, smoking and dietary intakes of vitamin C, vitamin E, folate, and polyphenols)., Results: Plant-sourced nitrate intake was inversely associated with all-cause mortality [HR Q5vsQ1 : 0.83 (0.80, 0.87)] while higher risks of all-cause mortality were seen for higher intakes of naturally occurring animal-sourced nitrate [1.09 (1.04, 1.14)], additive permitted meat-sourced nitrate [1.19 (1.14, 1.25)], and tap water-sourced nitrate [1.19 (1.14, 1.25)]. Similar source-dependent associations were seen for nitrite and for CVD-related and cancer-related mortality except that naturally occurring animal-sourced nitrate and tap water-sourced nitrate were not associated with cancer-related mortality and additive permitted meat-sourced nitrate was not associated with CVD-related mortality. No clear patterns emerged in stratified analyses., Conclusion: Nitrate/nitrite from plant sources are inversely associated while those from naturally occurring animal-sources, additive-permitted meat sources, and tap water-sources are positively associated with mortality., (© 2024. The Author(s).)

Phenylalanine ammonia-lyase (PAL) is one of the principle enzymes involved in plant's secondary metabolism. Expression of individual isogene from the PAL gene family is variable with species of plants in responses to different stresses. In this study, transcriptome analysis of the PAL gene family in rice seedlings exposed to potassium chromate Cr(VI) or chromium nitrate Cr(III) was conducted using Agilent 44K rice microarray and real-time quantitative RT-PCR. Uptake and accumulation of both Cr species by rice seedlings and their effect on PAL activity were also determined. Three days of Cr exposure led to significant accumulation of Cr in plant tissues, but majority being in roots rather than shoots. Changes of PAL activities in rice tissues were evident from both Cr treatments. Individual isogene from the rice PAL gene family was expressed differentially in response to both Cr variants. Comparing gene expression between two Cr treatments, only osPAL2 and osPAL4 genes were expressed in similar patterns. Also, gene expression pattern was inconsistent in both plant tissues. Results indicated that expression of individual isoform from the rice PAL gene family is tissue, and stimulus specific under different Cr exposure, suggesting their different detoxification strategies for decreasing or eliminating Cr stresses.

Groundwater nitrate contamination from agriculture is of paramount environmental interest. A continuous consumption of polluted water as drinking water or for culinary purposes is by no means a minor hazard for people's health that must be studied. This research presents a new methodology for the spatial analysis of health risk rate from intake of nitrate-polluted groundwater. The method is illustrated through its application to a water quality sampling campaign performed in the south of Spain in 2003. The probability risk model used by the US Environmental Protection Agency has been applied, considering a residential intake framework and three representative population age groups (10, 40 and 65 years).The method was based upon coupling Monte Carlo simulations and geostatistics, which allowed mapping of the health risk coefficient (RC). The maps obtained were interpreted in the framework of water resources management and user's health protection (municipalities). The results showed waterborne health risk caused by nitrate-polluted water is moderately low for the region. The observed risk was larger for the elderly and children, although no significant differences were found among the three age groups (RC average values of 95th percentile for age of 0.37, 0.33 and 0.37, respectively). Significant risk values of RC > 1 were obtained for 10 % of the surface in the NW site of the study area, where the municipalities with the highest contamination thresholds are located (agricultural activity). Nitrate concentration and intake rate stood out as the main explanatory variables of the RC.

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.

Drinking water and dietary sources of nitrate and nitrite can react in vivo with amines and amides to form N-nitroso compounds (NOC), potent animal carcinogens. Nitrate is a widespread contaminant of drinking water supplies especially in agricultural areas. We conducted a population-based case-control study of renal cell carcinoma in 1986-1989 in Iowa, a state with elevated levels in many public water supplies. We collected a lifetime water source history, but due to limited monitoring data, most analyses focused on the subpopulation, who used Iowa public supplies with nitrate measurements (actual or imputed data) for > or = 70% of their person-years since 1960 (201 cases, 1,244 controls). We computed the average nitrate level and years using a public supply with nitrate levels >5 and >10 mg/l. Dietary nitrate and nitrite were estimated from a 55-item food frequency questionnaire. There was no association of renal cell carcinoma with the average nitrate level and years using public supplies >5 and >10 mg/l nitrate-nitrogen (10+ years >5 mg/l odds ratio (OR) = 1.03, 95% confidence interval (CI) 0.66, 1.60). However, higher nitrate exposure was associated with an increased risk among subgroups with above the median red meat intake (10+ years >5 mg/l OR = 1.91, 95% CI 1.04-3.51) or below the median vitamin C intake (10+ years >5 mg/l OR = 1.90, 95% CI 1.01, 3.56), dietary factors that increase the endogenous formation of NOC. Exclusion of long-term Des Moines residents, a large proportion of the high exposure categories, attenuated the association. These findings deserve additional study in populations with high water nitrate intake and information on dietary intakes.

The carcinogenic feature of N-nitroso compounds has been well established. Similarly, the transformation of ingested nitrate to N-nitroso compounds in the stomach has been thoroughly documented, nevertheless nitrates' carcinogenic effect has not been proved convincingly in human. The present study was aimed to investigate a population of small villages provided by drinking water with high and widely variable nitrate content (72 mg/l median, 290.7 mg/l 95-percentile concentration). Empirical Bayes estimates for settlement-specific age-, sex-, and year-standardised mortality ratios of gastric cancer (GC) were related to the settlement level average nitrate concentrations in drinking water controlling for confounding effects of smoking, ethnicity and education. The log-transformed average nitrate concentration showed significant positive association with stomach cancer mortality in linear regression analysis (p = 0.014). The settlements were aggregated according to the nitrate concentration into 10-percentile groups and the standardised mortality ratios (SMRs) were calculated. Those groups with higher than 88 mg/l average nitrate concentration showed substantial risk elevation and the log-transformed exposure variables proved to be significant predictors of mortality (p = 0.032) at this level of aggregation also. The association seemed to be fairly strong (r2 = 0.46). Although this investigation constituting an ecological study has certain limitations, it supports the hypothesis that the high level of nitrate in drinking water is involved in the development of GC.

Objectives: This small-area ecologic study in Yorkshire, northern England, examines the hypothesis that exposure to higher levels of nitrate in drinking water increases the risk of stomach, esophageal, or brain cancer in adults., Methods: Nitrate levels over the period 1990-95 and numbers of incident cancers from 1975-94 were available for 148 water supply zones, geographically defined areas each supplying water of homogeneous chemical composition to an average population of around 20,000., Results: No relationship was found between nitrate concentrations and the incidence of stomach or esophageal cancers. The incidence of cancer of the brain and central nervous system was found to be higher in areas with higher nitrate levels, with a relative risk of 1.18 (95 percent confidence interval = 1.08-1.30) in the quartile of the population with the highest average levels (mean 29.8 mg/l) compared with the lowest quartile (mean 2.4 mg/l). The increase in risk remained statistically significant (P < 0.01) after allowing for other covariates and for extra-Poisson variation in a regression model., Conclusions: This study does not support the hypothesis of an increased risk of stomach or esophageal cancer associated with higher nitrate levels in drinking water. The observed relationship with brain cancer requires confirmation in other studies, including those involving data on individuals.

Epidemiologic evidence on the relation between contaminants in drinking water and cancer is reviewed. The reviewed studies cover exposure to: disinfection byproducts; nitrate; arsenic and other metals; volatiles and contaminants from hazardous waste sites; asbestiform fibers; radionuclides; and fluoride. Most investigations are ecologic, with some confirmation of elevated risk from individual-based studies. In the case of waterborne arsenic, and possibly chlorination byproducts, there is a consistent but small body of epidemiologic evidence of an association with one or more types of cancer. Nitrate in groundwater has increased greatly over the years, and the demonstration of endogenous nitrosation among highly exposed subjects raises concern of elevated cancer risk. However, the epidemiologic data are not yet sufficient to draw a conclusion. There is a diversity of studies among populations exposed to water contaminated with pesticides, volatile organics, or mixtures from hazardous waste sites. Studies of asbestiform fibers and radionuclides in water are not conclusive, but there are suggested elevations of several cancer sites in highly exposed populations. There is no suggestion that fluoride in drinking water is linked with elevated risk of cancer. As topics for epidemiologic evaluation, drinking water contaminants pose methodologic problems common to studies designed to detect relatively small elevations in risk, with the added challenge of assessing exposures for many years in the past. Nevertheless, epidemiologic assessment is valuable and clearly warranted, given the potential public health impact of small risk elevations among very large exposed populations, and the limitations of toxicologic experiments in assessing carcinogenic risk of complex mixtures or of compounds for which appropriate animal models are not available.

Epidemiologic evidence on the relation between nutrition and stomach cancer is reviewed. Stomach cancer shows a distinct international variation and dramatic worldwide decline. These descriptive features suggest that dietary factors are important in determining the risk of stomach cancer. The authors assessed relevant data regarding specific dietary hypotheses in the etiology of stomach cancer. A negative association with fresh vegetables and fruits is highly consistent in numerous case-control studies in different populations. Both epidemiologic and experimental data suggest that vitamins C and carotenoids lower risk of stomach cancer. Evidence is sparse and inconsistent as to protective effects of vitamin E and selenium. Epidemiologic studies have not lent, and will not provide, supportive evidence for an etiologic role of nitrate intake. High salt intake has been associated with an increased risk in many case-control studies and limited cohort studies. Taken together with animal data, it is considered that high salt intake is a risk factor for stomach cancer. Both epidemiologic and experimental data are inconclusive as to whether high-starch diets confer an increased risk. Cohort studies using quantitative dietary assessment and biologic measurement of micronutrients are needed for further understanding of etiologic roles of dietary factors in the causation of stomach cancer.

A case-control study on gastric cancer and diet was conducted in Marseille (France). Ninety-two patients with histologically confirmed adenocarcinoma and 128 controls undergoing functional reeducation for injuries or trauma were interviewed by a trained dietician using a dietary history questionnaire on their usual diet during the year preceding the first symptoms for cases, or preceding interview for controls. Intake of nitrite, nitrate and pre-formed N-nitrosodimethylamine (NDMA) from food was estimated using a food composition table compiled ad hoc. Odds ratios (ORs) were calculated after adjustment for age, sex, occupation and calorie intake. The results indicated that high intake of NDMA was associated with increased risk for gastric cancer. The ORs for the second and third tertile of NDMA intake were: OR2 = 4.13 (95% CI = 0.93 18.27) and OR3 = 7.00 (95% CI = 1.85 to 26.46). Intake of nitrate and nitrite was not associated with increased risk of stomach cancer. Consumption of vegetables was protective in general and independent of their estimated nitrate content.

The concentrations of nitrates in public drinking water in the Mediterranean coastal province of Valencia are not only the highest in Spain but also in the whole of Europe. Intensive agricultural practices involve a traditional and growing use of nitrogen fertilizers. This and the terrain--poorly consolidated and porous in areas--favors the accumulation of nitrates in underground aquifers, thereby perhaps accounting for this contamination. The possible conversion of nitrates to nitrites under certain conditions of gastric achlorhydria, followed by their transformation to nitrosamines--substances known to be carcinogenic in experimental models--has led to a number of epidemiological studies of the possible relationship between high nitrate levels in public drinking water and mortality due to different cancers. The aim of the present study was to analyze the relationship between different levels of exposure to nitrates in the drinking water of the 258 municipalities in the province of Valencia and mortality due to cancer of the stomach, bladder, prostate and colon in this population. The cancer mortality rate was found to rise with increasing exposure to nitrates in the case of gastric cancer in both sexes, and in prostate cancer. These same results were obtained on calculating relative risk for the different age groups associated with the consumption of drinking water containing different levels of nitrates.(ABSTRACT TRUNCATED AT 250 WORDS)