Conditions include:

Hypervitaminosis A
Hypervitaminosis D
Vitamin B3 § Toxicity
Megavitamin-B6 syndrome

Prevention
Prevention in healthy individuals not having any periods of avitaminosis or vitamin (vegetables) lack for 2 years at least is by not taking more than the expected normal or recommended amount of vitamin supplements. Epidemiology
In the United States, overdose exposure to all formulations of "vitamins" (which includes multi-vitamin/mineral products) was reported by 62,562 individuals in 2004 with nearly 80% of these exposures in children under the age of 6, leading to 53 "major" life-threatening outcomes and 3 deaths (2 from vitamins D and E; 1 from a multivitamin with iron). This may be compared to the 19,250 people who died of unintentional poisoning of all kinds in the U.S. in the same year (2004). In 2016, overdose exposure to all formulations of vitamins and multi-vitamin/mineral formulations was reported by 63,931 individuals to the American Association of Poison Control Centers with 72% of these exposures in children under the age of five. No deaths were reported. See also
Avitaminosis
Megavitamin therapy
Vitamin C megadosage

References
External links

Dietary reference intakes, official website.
Elevated levels of methemoglobin in the blood are caused when the mechanisms that defend against oxidative stress within the red blood cell are overwhelmed and the oxygen carrying ferrous ion (Fe2+) of the heme group of the hemoglobin molecule is oxidized to the ferric state (Fe3+). This converts hemoglobin to methemoglobin, resulting in a reduced ability to release oxygen to tissues and thereby hypoxia. This can give the blood a bluish or chocolate-brown color. Spontaneously formed methemoglobin is normally reduced (regenerating normal hemoglobin) by protective enzyme systems, e.g., NADH methemoglobin reductase (cytochrome-b5 reductase) (major pathway), NADPH methemoglobin reductase (minor pathway) and to a lesser extent the ascorbic acid and glutathione enzyme systems. Disruptions with these enzyme systems lead to methemoglobinemia. Hypoxia occurs due to the decreased oxygen-binding capacity of methemoglobin, as well as the increased oxygen-binding affinity of other subunits in the same hemoglobin molecule, which prevents them from releasing oxygen at normal tissue oxygen levels. Diagnosis
The diagnosis of methemoglobinemia is made with the typical symptoms, a suggestive history, low oxygen saturation on pulse oximetry measurements (SpO2) and these symptoms (cyanosis and hypoxia) failing to improve on oxygen treatment. The definitive test would be obtaining either CO-oximeter or a methemoglobin level on an arterial blood gas test.