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Corresponding Author Prof. Valentina M. Drozd, MD, PhD. In recent decades, differentiated thyroid cancer DTC incidence has been increasing worldwide. Less well understood is the role of nitrates — as environmental pollutants, in diet, and in medication — in thyroid carcinogenesis. Increasing exposure to nitrates is associated with rising incidence of esophageal, stomach, bladder, and colon cancers. Recent data suggest that in agricultural areas with higher mean nitrate levels in groundwater, DTC risk is also elevated.

ATSDR - Public Health Statement: Nitrate and Nitrite

Our work in Belarus after Chernobyl has shown that children in districts with high nitrate concentrations in drinking water had significantly higher thyroid cancer incidence after irradiation than did their counterparts in areas with lower nitrate concentrations. Notwithstanding thyroid shielding, increasing use of computed tomography and dental X-rays heightens radiation exposure of the salivary glands in the general population, especially in children and adolescents.

When nitrate intake is increased, salivary gland irradiation may potentially result in carcinogenic elevations in plasma nitric oxide concentrations. In conclusion, excess nitrate intake seems to be an independent risk factor for DTC. Additionally, we hypothesize from our data that high nitrate levels modulate the carcinogenic effect of radiation on the thyroid.

Cohort studies, case-control studies, or both, are needed to quantify the effects of nitrates on DTC risk in the presence or absence of radiation exposure, e. In the USA, DTC incidence is rising more rapidly than that of any other malignancy except liver cancer [ 1 ], with the annual percent change both genders increasing from 2.

In Europe, the increase in the last 2—3 decades has ranged from 5. In Belarus and Ukraine, DTC incidence has also substantially increased in the past 25 years; there is strong evidence that this increase was mainly due to radiation exposure of children and adolescents after the Chernobyl accident [ 9 - 11 ]. Nonetheless, an appreciable proportion of thyroid cancers diagnosed in young people in these countries may be related to screening or other confounders [ 10 , 12 ].

The main factors contributing to the worldwide increase in the incidence of DTC continue to be debated. Today, it is generally accepted that the widespread use of ultrasound, introduced in the s to diagnose structural thyroid diseases, has led to earlier, more frequent detection of this neoplasm.

Consistent with these estimates, small thyroid cancers that are best discovered using new technologies ultrasound and fine-needle aspiration biopsy have shown a sharply increased incidence [ 14 ]. Also well accepted as an explanation for greater frequency of DTC diagnoses is radiation exposure. External radiotherapy in childhood for cancer, tinea capitis, or an enlarged thymus or tonsils has been long known to be associated with an elevated risk of DTC [ 19 - 21 ]. Additionally, DTC was the first solid tumor to be found in excess among atomic bomb survivors in Japan [ 22 ].

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An updated pooled analysis of 12 studies [ 23 ] identified a consistent risk model across the full range of external radiation doses to the thyroid, with relative risk RR increasing approximately supralinearly through 2—4 Gy, and then leveling and declining above approximately 30 Gy, although RRs remained elevated. Radiogenic effects occurred for both PTC and nonpapillary thyroid tumors.


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The excess relative risk ERR estimate per Gy was significant within 10 years of radiation exposure at 2. In several other studies, dental radiography was associated with an increased risk of thyroid cancer [ 24 , 25 ] and parotid gland tumors [ 26 ]. One case-control study [ 24 ] found a significant association between self-reported dental X-ray exposure, particularly multiple exposures, and DTC risk odds ratio [OR]: 2. American Dental Association recommendations stress the need to shield the thyroid during dental X-ray examination [ 27 ].

Aquarium Nitrate Reduction - Ammonia Nitrite Nitrate

Pediatric DTC rates in Belarus began to increase as early as 4 years after the Chernobyl accident [ 28 , 29 ]. Cohort studies with measurement-based individual thyroid dose estimates reported ERRs per Gy of 5. Beyond diagnostic activity and radiation exposure, additional factors may contribute to increased DTC incidence, and require further investigation. In particular, nutritional exposure to chemical pollutants such as nitrates in drinking water, specifically during intrauterine life and early childhood, might affect thyroid cell propensity to mutagenesis.

The largest proportion of reactive nitrogen, i. The past 60 years have witnessed an exponential increase in the use of nitrogen-rich manure and reactive nitrogen as fertilizers [ 40 ]. Although they boost agricultural productivity, nitrogen-rich fertilizers let nitrates seep through the soil into both groundwater and surface water. There, these substances can accumulate for years until the concentration is adverse to human health. Because of water pollution, high amounts of nitrate might be present in fruits and vegetables, specifically those grown in greenhouses. Additionally, high nitrate levels may be found in cured and processed meats due to the addition of these chemicals as preservatives or color enhancers.

Medications, including antidiarrheals, diuretics, vasodilators, and the cytotoxic chemotherapy agent nitrosourea, also contribute to nitrate exposure in humans [ 39 , 41 ]. Groundwater from open wells is the main source of drinking water in rural Belarus. In the past 30 years, the roles of NO in physiology and pathophysiology have been extensively studied. Nitrate is metabolized by the nitrate-nitrite-NO pathway.

Beneficial effects of inorganic nitrate/nitrite in type 2 diabetes and its complications

As a gas in the pure state and under standard temperature and pressure conditions with an unshared electron, NO participates in various biological processes. In hypoxia, nitrite is reduced by a variety of reductases, including deoxyhemoglobin, to produce NO. Nitrate and NO are known to affect the iodine metabolism of the thyroid. Nitrate is a competitive inhibitor of the sodium-iodine symporter and prevents iodide uptake by the gland. Thyroid hormone synthesis is thereby compromised, leading to thyrotropin elevation.

The resultant chronic thyroid stimulation can lead to proliferative changes, including hypertrophy and hyperplasia as well as neoplasia [ 45 - 47 ]. There are other mechanisms by which ingested nitrate may produce detrimental effects on health. One is through formation of methemoglobin, which inhibits the oxygen-carrying capacity of blood; another is through endogenous formation of N-nitroso compounds that may act as carcinogens [ 41 , 46 ].

Nitrosamine synthesis depends on temperature and pH, and may be stimulated by low-level gamma radiation [ 48 - 50 ]. The salivary glands play a very important role in the metabolism of nitrate and the nitrate-nitrite-NO pathway [ 36 , 37 ]. Dietary nitrate is rapidly completely absorbed in the upper gastrointestinal tract. Sixty percent of ingested nitrate is excreted in the urine within 48 h [ 36 , 37 ].

Salivary nitrate concentrations are to fold above blood levels, and may reach several millimolars.


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This relatively effective process results in nitrite levels that are 1,fold higher in saliva than in plasma. Therapeutic irradiation increases NO levels in salivary gland tissue. NO produced in irradiated tissues mediates cellular regulation through posttranslational modification of a number of proteins [ 44 ].

Evidence exists for the role of NO as an intrinsic radiosensitizer [ 51 ]. On the other hand, administration of an NO synthesis inhibitor ameliorated the dysfunction of irradiated salivary glands, indicating that NO helps mediate the dry mouth symptoms occurring after irradiation [ 52 ]. Radiation-induced bystander effects may be modulated by NO [ 53 - 56 ]. NO synthase activation and NO overproduction after exposure to ionizing radiation not only affect bystander cells with activated NO synthase, but also can stimulate specific cell-signaling mechanisms.

Finally, the last section discusses nitric oxide-based therapeutics and how nitrite and nitrate biochemistry can be safely harnessed to improve human health. Each chapter provides a balanced, evidence-based view and heavily cites the most recent published literature.

Nitrate and Nitrite in Health and Disease

They follow a strict chapter format which includes keywords, key points, a conclusion highlighting major findings, and extensive references. The second edition contains new chapters on nitrite and nitrate in age medicine, nitrite and nitrate as a treatment for hypertension, and nitrite and nitrate in exercise performance. Additionally, the editors have expanded the biochemistry section to include chapters on nitrate reducing oral bacteria, nitrite mediated S-Nitrosation, epigenetics and the regulation of nitric oxide, and nitrite control of mitochondrial function.

Nitrate and Nitrite in Human Health and Disease , 2e, will be of interest to health professionals, nutritionists, dieticians, biomedical scientists, and food scientists.

Bibliographic Information

Add a Book Review. Author: Nathan S. Bryan Editor , Joseph Loscalzo Editor. Publish Date: Feb 03, Bryan Editor: Joseph Loscalzo.