14797-55-8

A colorless liquid.

ChEBI: A nitrogen oxoanion formed by loss of a proton from nitric acid. Principal species present at pH 7.3.

Crystalline solids. Salts of nitrate, such as ammonium nitrate, potassium nitrate, and sodium nitrate.

Most are water soluble.

Mixtures of metal/nonmetal nitrates with alkyl esters may explode, owing to the formation of alkyl nitrates; mixtures a nitrate with phosphorus, tin (II) chloride, or other reducing agents may react explosively [Bretherick 1979. p. 108-109].

Inhalation, ingestion or contact (skin, eyes) with vapors or substance may cause severe injury, burns or death. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may cause pollution.

These substances will accelerate burning when involved in a fire. Some may decompose explosively when heated or involved in a fire. May explode from heat or contamination. Some will react explosively with hydrocarbons (fuels). May ignite combustibles (wood, paper, oil, clothing, etc.). Containers may explode when heated. Runoff may create fire or explosion hazard.

Moderately toxic.

Nitrate is commonly found in drinking water sources especially in agricultural areas where nitrogen fertilizer is used, and where unregulated shallow private wells are more at the risk of contamination. The World Health Organization (WHO) guideline of 50 ppm and the US maximum contaminant level (MCL) of 45 ppm for nitrate in drinking water have been established for protecting infants from methemoglobinemia, commonly known as blue baby syndrome. The health protective value continues to be a subject of public health interest for many years, with varying opinion on whether it is too high or too low. Evaluation of nitrate will need to include consideration of nitrite because both are closely related in the nitrogen cycle in the environment and the body, and nitrite plays a major role in inducing toxicity after its formation from nitrate. More recently, reports of nitrate in drinking water, especially at levels higher than 50 ppm, have been associated with other health effects other than methemoglobinemia. This toxicological review provides an update on the health effects of nitrate with a focus on methemoglobinemia, reproductive and developmental effects, potential carcinogenicity, and especially endocrine/thyroid effects.

Nitrate (NO3 -), a product of nitrogen oxidation, is a naturally occurring ion in the environment and integrated into complex organic molecules such as proteins and enzymes required by living systems. Nitrate is a more stable form of oxidized nitrogen than nitrite; however, it can be reduced by microbial action to nitrite, which, in turn, can be reduced to various compounds or oxidized to nitrate by chemical and biological processes. Nitrates occur naturally in soil from microbial oxidation of ammonia derived from organic nitrogenous materials such as plant proteins, animals, and animal excreta. Other source contributions are wastewater, septic tank runoffs, airborne nitrogen compounds emitted by industry and automobiles, nitrogen fertilizer, and manure from animal feeding. Nitrate in groundwater is generally found below 10 ppm, with higher levels in areas of high agricultural activities.

The acute oral LD50 values for sodium nitrate range from 2480 to 9000 mg kg-1 in rats, mice, and rabbits. Acute, subchronic, and chronic animal toxicity studies showed low toxicity for nitrate as sodium or potassium nitrate. A long-term study showed a slight depression in growth rate. Nitrite, but not nitrate, is capable of inducing methemoglobinemia (see Nitrites, for more details).
Nitrate has been reported to be associated with thyroid effects in experimental animals and humans. Possible mode of action includes inhibition of iodine uptake to thyroid, serum T3 and T4 changes, and tissue T3 changes. However, there is a lack of knowledge on the differences in the mode of action to permit animal-to-human extrapolation. While the data indicate humans and rats exhibit similar dose–response relationships in acute inhibition of thyroidal iodide uptake, they show differences in thyroid hormone response following iodide uptake inhibition. Comparative data are needed for serum and brain tissue levels of thyroid hormones and characterization of the dose–response relationship between changes of thyroid hormone levels and adverse effects.
Early experimental and field studies in mammals have found inorganic nitrate to be goitrogenic. The effects were observed in rats following oral and parenteral administration of potassium and sodium nitrate, whereas antithyroid effects were also reported in sheep and pigs administered potassium nitrate. Nitrate exposure through diet or drinking water caused functional and histological changes to the thyroid gland in rats and pigs. More recent investigations between 2000 and 2010 reported changes in thyroid and thyroid activity following exposure to nitrate. In these more recent studies, nitrate exposure has consistently resulted in increases in thyroid weight and/or changes to the follicle cell; however, the reported thyroidal hormone changes have not been as consistent. The studies reported increased thyroid weights with a decrease in thyroid hormones (i.e., T3 and T4) and/or decrease in thyroid stimulating hormone. However, not all the results are consistent with the expected outcome of a sodium–iodide symporter (NIS) inhibitor, which can be seen as supplementation of iodine in the diet that did not result in thyroid changes. Overall, the data support that nitrate impairs thyroid function involving the hypothalamic–pituitary–adrenal axis.