Nitrate

Nitrate compounds (eg sodium nitrate) are found naturally on earth as large deposits. Nitrate (NO3−) naturally results from the breakdown of animal (or human) waste, but nitrate in groundwater mainly comes from fertilizers (eg ammonium nitrate) used in agriculture. Nitrate is much less toxic than ammonia. Nitrate is naturally consumed by growing plants, including fruit trees. The bioavailability of dietary nitrate is extremely high; almost 100%. van Velzen AG et al. Particularly vegetables may contain high levels of nitrate due to (besides nitrate fertilization) reduced sunlight exposure, undersupply of molybdenum and iron, and/or reduced assimilation of nitrate in the plant. Dietary nitrate inhibits iodide uptake, which may disrupt thyroid functioning De Groef B et al. A few studies found associations between dietary nitrate and hypothyroidism Ward MH et alAschebrook-Kilfoy B et alMukhopadhyay S et al or even thyroid cancer Kilfoy BA et alWard MH et al

"The overall results indicated the development of a relative state of functional hypothyroidism with enlarged thyroid after nitrate exposure." Mukhopadhyay S et alRRM Administrator

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Nitrite (NO2−)

The salivary glands extract and concentrate plasma nitrate. Bacteria in the mouth convert nitrate to nitrite. It is claimed that nitrite increases vascular health because it enhances athletic performance in athletes.

Nitric Oxide (NO)

Gastric juices convert nitrite to nitrous acid (HNO2, a powerful free radical), which decomposes into nitrate, NO and water. NO is also a powerful free radical; exhaust fumes are loaded with free radicals such as NO. More NO means more oxidative damage. Antioxidants such as the glutathione system regulate NO and HNO2 levels. NO has various properties (in various tissues), including anti-hypertensive, anti-inflammatory and anti-artherosclerotic. Therefore, in specific conditions, additional NO may be beneficial (eg myointimal hyperplasia). The nitrate to NO pathway influences blood flow, cell metabolism, signaling, and protects the gastric mucosa and protects tissue during hypoxia. Nitrite is also converted to NO by XOR and other enzymes, and eventually to ammonium and ureum.

Methemoglobinemia

Methemoglobinemia is characterized by elevated levels of oxidized hemoglobin (= methemoglobin = metHb). Normally, metHb levels are below 1% (of total Hb). Only when oxidative stress cannot sufficiently be prevented, the normal Fe2+ in hemoglobin (Hb) is oxidized to Fe3+ (in metHb). This results in a decreased capacity to release oxygen to tissues. The higher the level of metHb, the less oxygen released, which may lead to hypoxia. Normally, spontaneously formed metHb is reduced to Hb by mainly NADH metHb reductase, but also the vitamin C and glutathione enzyme systems. Exposure to nitrates may accelerate the rate of formation of metHb up to one-thousandfold, overwhelming the protective enzyme systems and acutely increasing metHb levels. One study found a direct proportionate relationship between nitrate ingestion and serum metHb level Zeman C et al. Another study found a direct correlation between nitrate levels in water samples and serum metHb level Niţuc E et al.

Infants are particularly vulnerable to methemoglobinemia due to nitrate metabolizing triglycerides present at higher concentrations than at other stages of development. Children drinking high-nitrate water are more likely to have methemoglobinemia Sadeq M et al. Young children may also get severe methemoglobinemia from consuming high-nitrate vegetables Savino F et al

Other causes/contributing factors of methemoglobinaemia include dehydration caused by diarrhea, sepsis, the use of antibiotics (trimethoprim, sulfonamides and dapsone Zosel A et al), local anesthetics (especially articaine and prilocaine Adams V et al), and others such as aniline dyes, metoclopramide, chlorates and bromates.