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.
In the treatment of angina pectoris; in the manufacture of inorganic and organic nitrates and nitro
compounds for fertilizers, dye intermediates, explosives, and many different organic chemicals.
Nitrate is used in fertilizers; in the manufacture of nitrites,
nitrous oxide, explosives, pyrotechnics, matches, freezing
mixtures, and special cements; as a coloring agent and
preserving additive in food; for coagulation of latexes; in the
nuclear industry; and for odor (sulfide) and corrosion control
in aqueous systems.
Nitrate is the salt of nitric acid. it is used in meat curing to develop
and stabilize the pink color associated with cured meat. by itself, it
is not effective in producing the curing reaction until it is chemi-
cally reduced to nitrite. it has an effect on flavor and also functions
as an antioxidant. it is available as sodium and potassium nitrate,
with the sodium form being more common.
A salt or ester of nitric
acid.
ChEBI: A nitrogen oxoanion formed by loss of a proton from nitric acid. Principal species present at pH 7.3.
nitrate: A salt or ester of nitric acid.
Crystalline solids. Salts of nitrate, such as ammonium nitrate, potassium nitrate, and sodium nitrate.
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.
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.
