The largest cause of iron poisoning in children less than 6 years of age is accidental overdose of iron-containing products. Although the oral lethal dose of elemental iron is approximately 200–250 mg/kg of body weight, considerably less has been fatal.
Acute toxicity may occur with iron doses of 20–60 mg/kg of body weight, producing symptoms in four stages (11, 26).
Adverse effects at therapeutic levels of iron supplements may include gastrointestinal irritation, nausea, vomiting, diarrhea, or constipation. Stools will often appear darker in color. Iron-containing liquids can temporarily stain teeth, but diluting the liquid helps to prevent this effect. Taking iron supplements with food instead of on an empty stomach may relieve gastrointestinal effects (26).
Diseases associated with iron excess
Cardiovascular disease
While animal studies suggest a role for iron-induced oxidative stress in the pathology of atherosclerosis and heart attack ('myocardial infarction') (27), epidemiological studies of iron nutritional status and cardiovascular diseases in humans have yielded conflicting results.
A systematic review of 12 prospective cohort studies including 7,800 cases of coronary heart disease (CHD) did not find good evidence to support the existence of strong associations between a number of different measures of iron status and CHD (28). Two large prospective studies found increased dietary heme iron, but not total dietary iron, to be associated with increased risk of myocardial infarction (29, 30).
Although the relationship between iron stores and CHD requires further clarification, it would be prudent for those who are not at risk of iron deficiency (e.g., adult men and postmenopausal women) to avoid excess iron intake.
Cancer
A dramatically increased risk of liver cancer in individuals with abnormal liver function ('cirrhosis') due to hereditary conditions of iron overload (e.g., 'hemochromatosis') has been well documented. However, the relationship between dietary iron and cancer risk in individuals without hemochromatosis is less clear (11).
Several epidemiological studies reported associations between measures of increased iron status and the incidence of colorectal cancer or the occurrence of precancerous polyps ('adenomas'), but the associations were not consistent.
Dietary iron intake appears to be more consistently related to the risk of colorectal cancer than measures of iron status or iron stores (31, 32). Increased red meat consumption has been associated with an increased risk of colorectal cancer, but there are a number of potential mechanisms by which increased meat consumption could affect cancer risk other than increasing iron intake (e.g., increased secretion of bile acids and increased exposure to carcinogenic compounds generated when meat is cooked) (33). Increased iron in the contents of the colon, rather than increased body iron stores, could increase the risk of colon cancer by exposing colonic cells to potentially damaging reactive oxygen species derived from iron-catalyzed reactions, especially in the presence of a high-fat diet.
However, the relationship between dietary iron intake, iron stores, and the risk of colorectal cancer remains unclear.
Neurodegenerative disease
Accumulation of excess iron can result in increased oxidative stress, potentially damaging nerve cells in the brain and contributing to a number of degenerating ('neurodegenerative') diseases such as Alzheimer's disease and Parkinson's disease (34). The abnormal accumulation of iron in the brain does not appear to be a result of increased dietary iron, but rather a disruption in the complex process of cellular iron regulation.
However, the mechanisms for this disruption in iron regulation are not yet known (35).
Hereditary hemochromatosis and anemia
Several genetic disorders may lead to disease-causing accumulation of iron in the body despite normal iron intake. 'Hereditary hemochromatosis' is characterized by iron deposition in the liver and other tissues as a result of a small increase in intestinal iron absorption over many years (36, 37). If untreated, tissue iron accumulation may lead to abnormal liver function ('cirrhosis'), diabetes, heart muscle damage, or joint damage ('arthritis').
Unlike hereditary hemochromatosis, 'Sub-Saharan African hemochromatosis' appears to require high iron intake in association with a genetic factor that has not yet been identified (1, 38, 39).
Iron overload may also occur in individuals with severe hereditary 'anemias' that are not caused by iron deficiency. Excessive dietary absorption of iron may occur in response to the body's continued efforts to form red blood cells (1).
Tolerable upper intake level
The European Food Safety Authority has decided that the available data are not sufficient to establish an upper level for iron from dietary sources (23).
The U.S. Food and Nutrition Board has based its tolerable upper intake level (UL) for iron on the prevention of gastrointestinal distress (11):
| Age Group | UL (mg/day) |
| Infants 0-12 months | not possible to establish* |
| Children 1-13 years | 40 |
| Adolescents 14-18 years | 45 |
| Adults 19 years and older | 45 |
* The UL applies also to pregnant and breast-feeding women.
The UL is not meant to apply to individuals being treated with iron under close medical supervision.
Individuals with hereditary conditions of iron overload (e.g. 'hemochromatosis'), as well as individuals with alcoholic cirrhosis and other liver diseases, may experience adverse effects at iron intake levels below the UL (11).
Drug interactions
Please note:
Because of the potential for interactions, dietary supplements should not be taken with medication without first talking to an experienced healthcare provider.