How does radioactive contamination typically occur

Contamination vs. Minus Related Pages. Types of Contamination. More Information Infographic: What's the difference between radiation contamination and exposure? To receive email updates about this page, enter your email address: Email Address.

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Cancel Continue. Visit the U. Centers for Disease Control and Prevention CDC for more information about possible health effects of radiation exposure and contamination. A very high level of radiation exposure delivered over a short period of time can cause symptoms such as nausea and vomiting within hours and can sometimes result in death over the following days or weeks.

It takes a very high radiation exposure to cause acute radiation syndrome—more than 0. The U. One gray is equal to rads. The international equivalent is the Gray Gy. One hundred rads are equal to 1 Gray. This level of radiation would be like getting the radiation from 18, chest x-rays distributed over your entire body in this short period. Acute radiation syndrome is rare, and comes from extreme events like a nuclear explosion or accidental handling or rupture of a highly radioactive source.

Learn about protecting yourself from radiation. Exposure to low-levels of radiation does not cause immediate health effects, but can cause a small increase in the risk risk The probability of injury, disease or death from exposure to a hazard. Radiation risk may refer to all excess cancers caused by radiation exposure incidence risk or only excess fatal cancers mortality risk.

Risk may be expressed as a percent, a fraction, or a decimal value. There are studies that keep track of groups of people who have been exposed to radiation, including atomic bomb survivors and radiation industry workers. These studies show that radiation exposure increases the chance of getting cancer, and the risk increases as the dose increases: the higher the dose, the greater the risk.

Conversely, cancer risk from radiation exposure declines as the dose falls: the lower the dose, the lower the risk. Radiation doses are commonly expressed in millisieverts international units or rem rem The U.

Estimation of dose following internal contamination is dependent on understanding the nature and form of the radionuclide. Dose estimation is modelled using bioassay results and reference tables, manual and computer calculations. The tables and calculations utilise standard organ system models, such as the ICRP respiratory tract model.

Standard organ system models have limitations. It is difficult to determine precise aerosol aerodynamics, individual respiratory physiology and anatomy. Additionally, there is a range of variation within inhalation classes and absorption types. The estimates produced need to be interpreted with regard to specific individual criteria such as age, pregnancy, and pre-existing medical conditions. Toxicity The biological effects of incorporated radionuclides are dependent on the dose, route of entry, chemical form, and distribution within the body.

Susceptibility to the biological effects may be increased by host factors such as age and co-morbidities. Threshold and LD50 values for death due to radiation pneumonitis occur at dose rates of about 5 and 10 Gy respectively. Radiation pneumonitis may also develop following the deposition of sufficient radioactive particulates which are retained in the lung due to insolubility. Alpha emitting radionuclides are especially concerning because their high linear energy transfer LET increases the local tissue damage twenty-fold compared to gamma emissions.

Aerosol size is a major determinant of retention of particles in the respiratory tract. From the nasopharynx, they may be swallowed or expectorated. Swallowed particles contribute to ongoing gastrointestinal contamination.

Route of inhalation is another important determinant. Deeper penetration of larger particles occurs during mouth breathing. Once in the alveoli, the chemical form of the radionuclide determines its solubility. Soluble forms are absorbed into the alveolar capillaries. The rate of transfer is dependent on the precise chemical form. Insoluble forms may be retained for many years.

Small amounts may be phagocytosed, move into lymphatics and drain to regional lymph nodes. Following phagocytosis by alveolar macrophages, inhaled particulates may trigger a chronic inflammatory response with release of cytokines and leukotrienes, and proliferation of inflammatory cells. Stimulation of fibroblasts and deposition of extracellular collagen lead to pulmonary fibrosis.

The development of acute radiation pneumonia follows a latent period of 1 week to 7 months after radiation exposure. The onset may be insidious with non-productive cough dyspnoea, fever, pleuritic pain, malaise and weight loss. Auscultation may be normal. Atypical pneumonia and malignant change must be excluded. Fibrosis may follow radiation pneumonia or develop gradually without other clinical manifestations. There is no proven therapy for radiation fibrosis.

Prolonged treatment with corticosteroids is advised to mitigate against the chronic inflammatory reaction. The spectrum of radionuclide-induced cancers, in decreasing frequency of occurrence, is adenocarcinoma, bronchiolo-alveolar carcinoma, and combined epidermoid and adenocarcinoma. Mesothelioma and fibrosarcoma have been observed in some animal models. Gastrointestinal injury Many radionuclides are not absorbed from the gastrointestinal tract. Injury is limited to the combination of the amount ingested, the specific activity of the radionuclide, and the gastrointestinal transit time.

If the amount is significant or the activity of the substance is high, there is a likelihood of mucosal damage to the GIT, or whole body irradiation.

Ingestion in pelletised form or as a solid metal, such as iridium, may lead to localised gastrointestinal burns, with consequent perforation or stricture formation. Polonium has a propensity to form colloids, and will deposit on the mucosal surface of the intestine.

On autoradiographs, the polonium accumulates at the tips of villi but the alpha radiation does not reach the basal stem cells in the crypts. It is thought that this contributes to the earlier development of the gastrointestinal syndrome following polonium ingestion, than is accounted for by the whole body irradiation effect.

Target organ injury Some radionuclides are isotopes of essential elements normally absorbed by the body, such as iodine and cobalt. Others behave as analogues or substitutes for other elements. Strontium, radium and plutonium follow calcium metabolism pathways, and caesium behaves like potassium. The distribution of radionuclides following absorption into the bloodstream relates to the normal or analogous behaviour of that element.

Hence, the thyroid takes up radioiodine preferentially, leading to eventual hypothyroidism and thyroid tumours. The calcium analogues are distributed to the skeleton where they affect haematopoiesis bone marrow hypoplasia and aplasia, and leukaemia , bone turnover osteonecrosis and osteosarcoma and local soft tissue rhabdomyosarcoma. Radionuclides that are deposited in the reticuloendothelial system americium, polonium may cause local injury due to the biological effects of ionising radiation to the liver, spleen and kidneys manifesting as organ failure.

Uranium damages the kidneys where it precipitates in the renal tubules in acid urine, because of its chemical, rather than its radiological properties. Whole body irradiation Because of wide intracellular distribution, radioactive potassium analogues such as caesium cause whole body irradiation. This is also seen with any other radionuclide with distribution throughout the body, such as tritium, cobalt and polonium.

Contaminated wounds Intact skin is a barrier to most radionuclides. Absorption of contamination from wounds is dependent on the physicochemical properties of the radionuclide such as solubility, pH, reactivity and particle size. Solubility may be altered by prolonged contact with body fluids. The contaminant may: absorb into the bloodstream transfer to regional lymph nodes migrate along fascial planes, potentially making it difficult to localise incorporate into coagulated tissue following acid or caustic exposure incorporate into the eschar following full thickness burns incorporate into the scab over an abrasion remain in the wound causing local irradiation, and development of fibrotic nodules Treatment Options The clinical decision to undertake any specific treatment must consider the risks and benefits of the therapy in the specific clinical scenario.

Ideally, this is informed by evidence of effectiveness. Gastrointestinal decontamination The amount of a substance able to be removed from the stomach by emesis or gastric lavage is unreliable, and negligible if performed more than one hour after ingestion. The risks of pulmonary aspiration or physical injury with emesis or lavage are considerable. The benefit of these procedures for gastrointestinal decontamination of radionuclides is unproven. However, there are significant contraindications uncooperative patient, uncontrolled vomiting, inability to place a nasogastric tube, ileus or bowel obstruction, and potential impairment of conscious state or development of seizures and complications of therapy nausea, vomiting, abdominal distension, pulmonary aspiration, and metabolic acidosis.

It is unlikely to be tolerated by patients with injury or significant illness. The efficacy of whole bowel irrigation for radionuclide ingestions is unknown.

Catharsis is an ineffective means of reducing gastrointestinal transit time and not used in current clinical toxicological practice.

Enhanced Elimination Metals are poorly bound to activated charcoal. Therefore charcoal is not likely to be effective in reducing absorption of radionuclides. Alginates and antacids complex with a number of radionuclides polonium, radium, strontium, uranium and are relatively non-toxic, if oral therapy is not contraindicated. Prussian blue acts as an ion exchange resin to form non-absorbable complexes with Cs which are excreted in the faeces.

Urinary alkalinisation promotes the ionisation of uranium, preventing reabsorption across the renal tubular epithelium and promoting urinary excretion. The resultant metabolic alkalosis is usually well tolerated, however serum potassium may be lowered.