| Zinc toxicity | |
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| Zinc | |
| Specialty | Emergency medicine  |
Zinc toxicity is a medical condition involving an overdose on, or toxic overexposure to,zinc. Such toxicity levels have been seen to occur at ingestion of greater than 50 mg of zinc.[1][unreliable medical source?] Excessive absorption of zinc can suppress copper and iron absorption. The free zinc ion in solution is highly toxic to bacteria, plants, invertebrates, and even vertebrate fish.[2][3][4] Zinc is an essentialtrace metal with very low toxicity in humans.[1][5]
Following an oral intake of extremely high doses of zinc (where 300 mg Zn/d – 20 times the USRDA – is a "low intake" overdose[1]), nausea, vomiting, pain, cramps, and diarrhea may occur.[1] There is evidence of inducedcopper deficiency, alterations of blood lipoprotein levels, increased levels ofLDL, and decreased levels ofHDL at long-term intakes of 100 mg Zn/d.[1] The USDARDA is 15 mg Zn/d.[1] There is also a condition called the "zinc shakes", "zinc chills", ormetal fume fever that can be induced by the inhalation of freshly formedzinc oxide formed during thewelding ofgalvanized materials.[6]
Zinc has been used therapeutically at a dose of 150 mg/day for months, or in some cases for years, and in one case at a dose of up to 2000 mg/day zinc for months.[7][8][9][10][11] A decrease in copper levels and hematological changes have been reported; however, those changes were completely reversed with the cessation of zinc intake.[9]
Zinc has been popularly used aszinc gluconate orzinc acetate lozenges fortreating the common cold,[12] and therefore the safety of usage at about 100 mg/day level is a relevant question.
Unlikeiron, the elimination of zinc is concentration-dependent.[13]
Zinc toxicity is commonly fatal in dogs, where it causes a severehemolytic anemia.[14][verification needed] It is also highly toxic inpet parrots and can often be fatal.[15][better source needed]
Supplemental zinc can prevent iron absorption, leading to iron deficiency. Zinc and iron should be taken at different times of the day.[16]
Zinc concentrations are typically quantified using instrumental methods such as atomic absorption, emission, or mass spectroscopies; X-ray fluorescence; electro-analytical techniques (e.g., stripping voltammetry); or neutron activation analysis.Inductively coupled plasma atomic emission spectroscopy (ICP-AES) is used for zinc determinations in blood and tissue samples (NIOSH Method 8005) and in urine (NIOSH Method 8310). Detection limits in blood and tissue are 1 μg/100 g and 0.2 μg/g, respectively, with recoveries of 100% (NIOSH 1994). Sample preparation involves acid digestion using concentrated acids. Detection of zinc in urine samples requires extraction of the metals with apolydithiocarbamate resin prior to digestion and analysis (NIOSH 1984). Detection limits in urine are 0.1 μg/sample.
Treatment of zinc toxicity consists of eliminating exposure to zinc. However, no antidotes are available.[citation needed]
Homeostatic regulation of iron and zinc differ, with iron being regulated through absorption and zinc being regulated primarily through secretion. As the body does not have a means to eliminate excess iron, absorption from the small intestine is tightly regulated by hepcidin. Hepcidin is a peptide hormone that is present in higher concentrations when body iron is replete [52]. Higher concentrations of hepcidin prevent ingested iron from entering the bloodstream by trapping iron in enterocytes which are naturally shed every two days [112], thereby preventing body iron from escalating to dangerous levels. In comparison, endogenous (pancreatic, biliary and intestinal) secretions comprise the main route of zinc loss, with larger zinc intakes being balanced by larger zinc secretions [113, 114].
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