Editing Nitrate (section)

== Toxicity and safety ==
The two areas of concerns about the toxicity of nitrate are the following: 
* nitrate reduced by the microbial activity of [[nitrate reducing bacteria]] is the precursor of [[nitrite]] in water and in the [[lower gastrointestinal tract]]. Nitrite is a precursor to [[carcinogenesis|carcinogenic]] [[nitrosamine]]s, and;
* via the formation of nitrite, nitrate is implicated in [[methemoglobinemia]], a disorder of [[hemoglobin]] in [[red blood cell]]s susceptible to especially affect infants and toddlers.<ref>{{cite journal | vauthors = Powlson DS, Addiscott TM, Benjamin N, Cassman KG, de Kok TM, van Grinsven H, L'Hirondel JL, Avery AA, van Kessel C | title = When does nitrate become a risk for humans? | journal = Journal of Environmental Quality | volume = 37 | issue = 2 | pages = 291–295 | year = 2008 | pmid = 18268290 | doi = 10.2134/jeq2007.0177 | s2cid = 14097832 | bibcode = 2008JEnvQ..37..291P | url = https://digitalcommons.unl.edu/agronomyfacpub/102 }}
</ref><ref>{{cite web|work=The Merck Veterinary Manual|title=Nitrate and Nitrite Poisoning: Introduction|url=http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/212300.htm|access-date=2008-12-27}}</ref>

=== Methemoglobinemia ===
{{Main Article|Blue baby syndrome|Methemoglobinemia}}
One of the most common cause of [[methemoglobinemia]] in infants is due to the ingestion of nitrates and nitrites through [[well water]] or foods. 

In fact, nitrates ({{Chem2|NO3-}}), often present at too high [[concentration]] in drinkwater, are only the precursor chemical species of [[nitrite]]s ({{Chem2|NO2-}}), the real culprits of methemoglobinemia. Nitrites produced by the [[Denitrification|microbial reduction of nitrate]] (directly in the drinkwater, or after ingestion by the infant, in his digestive system) are more powerful [[Oxidizing agent|oxidizers]] than nitrates and are the chemical agent really responsible for the [[Redox|oxidation]] of Fe<sup>2+</sup> into Fe<sup>3+</sup> in the [[tetrapyrrole]] [[heme]] of [[hemoglobin]]. Indeed, nitrate anions are too weak oxidizers in [[aqueous solution]] to be able to directly, or at least sufficiently rapidly, oxidize Fe<sup>2+</sup> into Fe<sup>3+</sup>, because of [[Chemical kinetics|kinetics]] limitations.

Infants younger than 4 months are at greater risk given that they drink more water per body weight, they have a lower [[Nicotinamide adenine dinucleotide|NADH]]-[[cytochrome b5 reductase]] activity, and they have a higher level of fetal hemoglobin which converts more easily to [[methemoglobin]]. Additionally, infants are at an increased risk after an episode of [[gastroenteritis]] due to the production of [[nitrite]]s by [[bacteria]].<ref>{{Cite book | vauthors = Smith-Whitley K, Kwiatkowski JL | chapter = Chapter 489: Hemoglobinopathies | veditors = Kliegman RM |title=Nelson Textbook of Pediatrics | edition = 21st | date = 2000 |publisher=Elsevier Inc.|pages=2540–2558 | isbn = 978-0-323-52950-1 }}</ref> 

However, other causes than nitrates can also affect infants and pregnant women.<ref>{{Cite journal | doi=10.1111/j.1475-2743.2004.tb00344.x|title = Nitrate and human health| journal=Soil Use and Management| volume=20| issue=2| pages=98–104|year = 2006| vauthors = Addiscott TM, Benjamin N | s2cid=96297102 }}</ref><ref name="pmid10379005">{{cite journal | vauthors = Avery AA | title = Infantile methemoglobinemia: reexamining the role of drinking water nitrates | journal = Environmental Health Perspectives | volume = 107 | issue = 7 | pages = 583–6 | date = July 1999 | pmid = 10379005 | pmc = 1566680 | doi = 10.1289/ehp.99107583 | bibcode = 1999EnvHP.107..583A }}</ref> Indeed, the [[blue baby syndrome]] can also be caused by a number of other factors such as the [[cyanotic heart disease]], a [[congenital heart defect]] resulting in low levels of oxygen in the blood,<ref name="MedlinePlusEncyclopedia Cyanotic heart disease">{{MedlinePlusEncyclopedia|001104|Cyanotic heart disease}}</ref> or by gastric upset, such as diarrheal infection, protein intolerance, heavy metal toxicity, etc.<ref>{{cite journal | vauthors = Manassaram DM, Backer LC, Messing R, Fleming LE, Luke B, Monteilh CP | title = Nitrates in drinking water and methemoglobin levels in pregnancy: a longitudinal study | language = En | journal = Environmental Health | volume = 9 | issue = 1 | pages = 60 | date = October 2010 | pmid = 20946657 | pmc = 2967503 | doi = 10.1186/1476-069x-9-60 | doi-access = free | bibcode = 2010EnvHe...9...60M }}</ref>

=== Drinking water standards ===
Through the [[Safe Drinking Water Act]], the [[United States Environmental Protection Agency]] has set a maximum contaminant level of 10&nbsp;mg/L or 10 ppm of nitrate in drinking water.<ref>{{Cite web|url=https://safewater.zendesk.com/hc/en-us/articles/211401718-4-What-are-EPA-s-drinking-water-regulations-for-nitrate-|title=4. What are EPA's drinking water regulations for nitrate?|website=Ground Water & Drinking Water|date=20 September 2016 |language=en-US|access-date=2018-11-13}}</ref>

An acceptable daily intake (ADI) for nitrate ions was established in the range of 0–3.7&nbsp;mg (kg body weight)<sup>−1</sup> day<sup>−1</sup> by the Joint FAO/WHO Expert Committee on Food Additives (JEFCA).<ref>{{cite journal | vauthors = Bagheri H, Hajian A, Rezaei M, Shirzadmehr A | title = Composite of Cu metal nanoparticles-multiwall carbon nanotubes-reduced graphene oxide as a novel and high performance platform of the electrochemical sensor for simultaneous determination of nitrite and nitrate | journal = Journal of Hazardous Materials | volume = 324 | issue = Pt B | pages = 762–772 | date = February 2017 | pmid = 27894754 | doi = 10.1016/j.jhazmat.2016.11.055 | bibcode = 2017JHzM..324..762B }}</ref>

=== Aquatic toxicity ===
[[File:Annual mean sea surface nitrate (World Ocean Atlas 2009).png|right|thumb|Sea surface nitrate from the [[World Ocean Atlas]]]]
In [[freshwater]] or [[estuary|estuarine]] systems close to land, nitrate can reach concentrations that are lethal to fish. While nitrate is much less toxic than ammonia,<ref>{{cite journal | vauthors = Romano N, Zeng C | title = Acute toxicity of sodium nitrate, potassium nitrate, and potassium chloride and their effects on the hemolymph composition and gill structure of early juvenile blue swimmer crabs(Portunus pelagicus Linnaeus, 1758) (Decapoda, Brachyura, Portunidae) | journal = Environmental Toxicology and Chemistry | volume = 26 | issue = 9 | pages = 1955–1962 | date = September 2007 | pmid = 17705664 | doi = 10.1897/07-144r.1 | bibcode = 2007EnvTC..26.1955R | s2cid = 19854591 }}</ref> levels over 30 ppm of nitrate can inhibit growth, impair the immune system and cause stress in some aquatic species.<ref>{{cite web | url=http://freshaquarium.about.com/od/watercare/a/nitrates.htm | title=Nitrates in the Aquarium | work=About.com | access-date=October 30, 2013 | author=Sharpe, Shirlie | archive-date=July 24, 2011 | archive-url=https://web.archive.org/web/20110724135608/http://freshaquarium.about.com/od/watercare/a/nitrates.htm | url-status=dead }}</ref> Nitrate toxicity remains a subject of debate.<ref>{{cite journal | vauthors = Romano N, Zeng C | title = Effects of potassium on nitrate mediated alterations of osmoregulation in marine crabs | journal = Aquatic Toxicology | volume = 85 | issue = 3 | pages = 202–208 | date = December 2007 | pmid = 17942166 | doi = 10.1016/j.aquatox.2007.09.004 | bibcode = 2007AqTox..85..202R }}</ref>

In most cases of excess nitrate concentrations in aquatic systems, the primary sources are wastewater discharges, as well as [[surface runoff]] from agricultural or [[landscape]]d areas that have received excess nitrate fertilizer. The resulting [[eutrophication]] and algae blooms result in [[Hypoxia (environmental)|anoxia]] and [[Dead zone (ecology)|dead zones]]. As a consequence, as nitrate forms a component of [[total dissolved solids]], they are widely used as an indicator of [[water quality]].