IONIZING RADIATION

Classification | Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

Specific Substances

1) Acute radiation disease
2) Acute radiation syndrome
3) Ionizing radiation
4) Radiation
5) Radiation sickness
6) Radiation toxicity
7) Radiation, ionizing
8) Radioactive material
9) Radioactivity
10) Radioisotopes
11) Radionuclides
12) Positrons

Available Forms Sources

1) IONIZING RADIATION: Nuclear emissions that have sufficient energy to ionize atoms and remove one or more electrons from the orbit of other atoms (Hallenbeck, 1994).
2) Radiation exposure may occur in medical, industrial, and laboratory accidents in which individuals are exposed to unacceptably high doses of radiation (ICRP, 1977; Gains, 1989; Wagner et al, 1994). With increased use of radioactive materials, there is also an increased need for transport of such materials with the attendant risk of transport accidents and releases. In addition, there remains the possibility of exposure of large masses of people through detonation of nuclear weapons (Conklin et al, 1983).
3) Radiation injuries occur secondary to exposure to ionizing radiation (eg, alpha particles, beta particles, gamma rays, x-rays, and neutrons). The radioactive exposure may be due to external irradiation (source at some distance from the body) or internal contamination (ingestion, inhalation, absorption through skin or wounds). The most common radionuclides in the atmosphere are: radon-222, tritium, iodine-129, strontium-90, cesium-137, and krypton-85. Radioactive materials of military significance (Military Five) include: Tritium (3H), uranium (235U, 238U), plutonium (239Pu), and americium (241Am) (Radiation Emergency Assistance Center, 2011; Berger, 2003; Jarrett, 1999; Diffre, 1990).
4) Radiation is reported as being any one of 5 types: alpha particles, beta particles, gamma rays, X-rays, and neutrons (Radiation Emergency Assistance Center, 2011).

a) Alpha particles: Charged particles consisting of 2 protons and 2 neutrons that do not travel far (a few inches in the air) and that penetrate only a few micrometers into the skin. Alpha particles create ionization easily and can be blocked by thin clothing or paper. They are more of a concern when ingested or inhaled as opposed to simple contamination.
b) Beta particles: Electrons emitted from the nuclei of particular isotopes, especially tritium and strontium-90, that can travel a couple of meters in the air and a few millimeters in tissue. A thin layer of plastic is an effective shield. Deposited on the skin, beta particles damage the basal layer, and cause radiation burns.
c) Gamma rays: Electromagnetic radiation that is not particulate and is emitted by the nucleus. Gamma rays are very energetic and can easily pass through most matter, but they are not efficient at causing ionization. They are capable of causing internal organ damage, and can be shielded by lead or other dense materials.
d) X-rays: Differ from gamma rays only in that they are emitted outside of the nucleus.
e) Neutrons: Less commonly encountered, neutrons are uncharged particles that are capable of making another substance radioactive. They have a potential to cause future effects that is 3 to 20 times that of gamma rays.

5) SOURCES OF LARGE RADIOACTIVE DISCHARGES

a) REACTOR ACCIDENTS: Radioactive substances such as I-131 may be released from nuclear power reactors (Jarrett, 1999; Becker, 1987). Nuclear energy production carries the extremely small risk of radiation accidents and radiation exposure of the general population worldwide (Champlin et al, 1988).
b) WINDSCALE (Sellafield, England, 1957): 30,000 Ci of iodine-131, 12,000 Ci of tellurium-132, and 600 Ci of cesium-137 were released (Diffre, 1990). A curie (Ci) is a unit of activity equal to 3.61 x 10(10) disintegration per second.
c) KYSCHTYMSK (Urals, 1957): 1 x 10(6) Ci of strontium-90 were estimated to have contaminated an area of 100 to 1,000 square kilometers (Diffre, 1990).
d) THREE MILE ISLAND (USA, 1979): Approximately 6 x 10(11) Bq of iodine-131 was released (Diffre, 1990). A becquerel (Bq) is a unit of activity, with 1 Bq equal to 1 disintegration/second. 1 curie equals 3.61 x 10(10) Bq.
e) CHERNOBYL (Byelorussia/Ukraine, 1986): 10 x 10(7) Ci of strontium-90 was reported to have been released, causing 2000 to 3000 square kilometers of soil to be unfit for agriculture (Diffre, 1990).
f) 2011 EARTHQUAKE, TSUNAMI, and RADIATION RELEASE in JAPAN (March, 2011): On March 11, 2011, a 9.0 magnitude earthquake and a tsunami caused serious widespread damage to the Fukushima nuclear power plant. An ongoing leak of radiation from this facility has forced the evacuation of hundreds of thousands of residents within 12 miles of the power plant (http://wwwnc.cdc.gov/travel/content/travel-health-precaution/2011-earthquake-tsunami-radiation).

6) OTHER SOURCES

a) POLONIUM-210 POISONING: In November 2006, a Russian man who was poisoned with radionuclide polonium-210 in London, UK, died several weeks post-exposure. At that time, it was determined that more than 700 individuals were exposed to polonium-210 and were tested for radiation poisoning. As an alpha-emitting radionuclide, polonium-210 is not an external hazard. It can be extremely toxic when absorbed into the body via inhalation and ingestion. Patients may develop acute radiation syndrome, with nausea, vomiting, and diarrhea during the prodromal phase. Later signs include loss of hair, bleeding, and multiple organ failure resulting in death (Fraser et al, 2012).
b) MILK: Iodine-131 is concentrated in the milk of herbivorous animals.
c) RADIUM-226: Is absorbed by plants and animals and its concentration in the human body results from ingestion of food (Diffre, 1990).
d) RAINWATER: Usually contains beryllium, carbon-14, tritium, strontium-90, and cesium-137; total normal beta radioactivity is around 1 Bq/L (Diffre, 1990).
e) UNDERGROUND WATER: Contains uranium-238 and related products and radium-226. It also contains radon-222 which can be highly concentrated at the source of thermal springs (Diffre, 1990).
f) SEAWATER: Beta radioactivity, primarily from potassium-40, is around 10 Bq/L (Diffre, 1990).
g) BULLETS: Depleted uranium, "DU", used in armor-piercing shells contains 99.75% U-238; soldiers handling or shot with these bullets may be exposed (Christensen, 1993).
h) Common fission products from nuclear tests that have fallen onto the surface of the globe include: strontium-90, cesium-137, iodine-129, and iodine-131 (Diffre, 1990).

1) Strontium-90 has chemical properties similar to calcium and is deposited in bone.
2) Cesium-137 behaves similarly to potassium, but it remains in the human body 2 to 5 times longer.
3) Iodine-129 has an atmospheric half-life of 16 x 10(6) years. Radioactive iodine is stored by mammals in the thyroid gland; there its concentration is 3 to 4 times that of exposed grass.

1) AMERICIUM-241 is a decay daughter of plutonium and is an alpha emitter, readily detectable with a standard radiation detection instrument due to emission of a 60-kEv gamma ray. Its use includes smoke detectors and other instruments, and it is found in fallout from a nuclear weapon detonation. It is considered a heavy metal poison, but in large radioactive doses, can cause whole-body irradiation (Jarrett, 1999).
2) CESIUM-137 may be found in medical radiotherapy devices. It was reported to be used in the Chechen RDD threat against Moscow. Both gamma rays and beta radiation are emitted and can be readily detected by gamma instruments. Whole-body irradiation is the primary toxicity, with deaths due to acute radiation syndrome reported (Jarrett, 1999).
3) COBALT-60 is commonly used in medical radiotherapy devices and commercial food irradiators. Most commonly, contamination is discovered after improper disposal, or after destruction of a hospital or commercial facility. Generation of high-energy gamma rays and 0.31-MeV beta rays are produced. A gamma detector provides easy detection. Uses of cobalt include as a contaminant in an improvised nuclear device to make fallout more radioactive. Whole-body irradiation and acute radiation syndrome are its primary toxicities (Jarrett, 1999).
4) DEPLETED URANIUM (DU) emits limited alpha, beta, and some gamma radiation, but poses no significant radiation threat. It is found in armor-piercing munitions, armor, and aircraft counterweights and is readily detectable with a typical end-window G-M (Geiger-Mueller) counter. DU oxides may be inhaled during tank fires or by entering destroyed armored vehicles without a protective mask. If DU metal fragments become encapsulated in wounds, they are gradually metabolized, resulting in whole-body distribution, especially to bones and kidney. No renal toxicity has been documented to date. DU does cross the placenta (Jarrett, 1999).
5) IODINE-131, 132, 134, and 135 are found after reactor accidents and following the destruction of a nuclear reactor by hostile forces. Radioactive iodine (RAI), a normal fission product found in reactor fuel rods, is released by rupturing the reactor core and its containment vessel. Wind patterns at the time of destruction determine the fallout pattern. Most of its radiation is beta rays, with some gamma. Toxicity is primarily to the thyroid gland. RAI concentrates in the thyroid due to uptake by this gland, and allows local irradiation similar to therapeutic thyroid ablation. Following the Chernobyl disaster, an increased incidence of childhood thyroid carcinoma was reported (Jarrett, 1999).
6) PHOSPHORUS-32 is usually found in research laboratories and in medical facilities used as a tracer. It emits strong beta rays and can be detected with the beta shield open on a beta-gamma detector. It is completely absorbed from all sites and is deposited in the bone marrow and other rapidly replicating cells. Local irradiation results in cell damage (Jarrett, 1999).
7) PLUTONIUM-239, -238 are produced from uranium in reactors and is the primary fissionable material in nuclear weapons and is the predominant radioactive contaminant in nuclear weapons accidents. Its primary radiation is in the form of alpha particles, thus not presenting an external irradiation hazard. It is ALWAYS contaminated with americium, which is a fairly readily detectable x-ray by use of thin-walled gamma probe. Primary toxicity is via the inhalation route, with 5-micron or smaller particles remaining in the lung and metabolized based on its salt solubility. Local irradiation damage is caused by remaining particles in the lungs. The chemical state of plutonium determines its GI absorption, with the metal not being absorbed. After 24 hours, stool specimens are positive and after 2 weeks urine specimens are positive. Wound absorption is variable. Plutonium is able to be washed from intact skin (Jarrett, 1999).
8) RADIUM-226 has no military use, but may be found in FSU equipment as instrument illumination, in industrial applications, and in older medical equipment. Its primary radiation is due to alpha particles, but daughter products emit beta and gamma rays, which in quantity may present a serious external irradiation hazard. Exposures are usually by ingestion, with 30% absorption. Wound absorption is not known, but radium will follow calcium to bone deposition. Leukemia, aplastic anemia, and sarcomas are associated with chronic exposures (Jarrett, 1999).
9) STRONTIUM-90 is a direct fission product (daughter) of uranium, with it and its daughters emitting both beta and gamma rays which can be an external irradiation hazard if present in quantity. Strontium follows calcium and is readily absorbed via both respiratory and GI routes. Up to 50% of a radiation dose will be deposited in bone (Jarrett, 1999).
10) TRITIUM (hydrogen-3) is a hydrogen with a nucleus composed of two neutrons and one proton. It has found use in nuclear weapons and in the U.S. (and other Western countries) in luminescent gun sights and muzzle-velocity detectors. It is NOT likely to be a hazard except within a confined space. Tritium gas is rapidly diffused into the atmosphere. Since tritium is a beta emitter, it is NOT a significant irradiation hazard. Water formed from tritium (HTO) is completely absorbed and equilibrates with body water. Excretion is via the urine, with urine samples positive within an hour of significant exposure. A single acute exposure has NOT been reported to result in any significant health effects (Jarrett, 1999).
11) URANIUM-238, -235, -239 can be found, in increasing order of radioactivity, in depleted uranium (DU), natural uranium, fuel rods, and weapons-grade material. Alpha, beta, and gamma radiation are emitted from uranium and its daughters. Neither DU nor natural uranium present any serious irradiation threats. Significant levels of gamma particles are emitted from used fuel rods and weapons-grade (enriched) uranium containing fission products. Following placement of enough enriched uranium together, a critical mass may form and emit lethal levels of radiation. This scenario could occur in a fuel-reprocessing plant or melted reactor core. Following an acute exposure, uranium urine levels of 100 mcg/dL may cause renal failure (Jarrett, 1999).

Overview

Life Support

Clinical Effects

0.2.1)

A) SOURCES: IONIZING RADIATION: Nuclear emissions that have sufficient energy to ionize atoms and remove one or more electrons from the orbit of other atoms. Radiation injuries occur secondary to exposure to ionizing radiation (eg, alpha particles, beta particles, gamma rays, x-rays, and neutrons). The radioactive exposure may be due to external irradiation (source at some distance from the body) or internal contamination (ingestion, inhalation, absorption through skin or wounds). Acute radiation syndrome may occur after total or near total body irradiation with a high dose of ionizing radiation over a short period of time. The most common radionuclides in the atmosphere are: radon-222, tritium, iodine-129, strontium-90, cesium-137, and krypton-85. Radioactive materials of military significance (Military Five) include: Tritium (3H), uranium (235U, 238U), plutonium (239Pu), and americium (241Am).
B) TOXICOLOGY: The response to exposure to ionizing radiation varies by cell type and is largely a function of the rate of cell replication or the cell cycle length. Cells are most vulnerable to the effects of radiation during mitosis; therefore, the tissue with the most mitotically active cells will be the most damaged. Spermatogonia, the cells of the gastrointestinal tract, and hematopoietic cells such as lymphocytes and erythroblasts are the most sensitive, while collagen-producing cells, muscle cells, and bone cells are less affected since they are not as mitotically active. Thus, the 3 syndromes that result are hematopoietic, gastrointestinal, and neurovascular, based on these decreasing radiation sensitivities. Increasing doses of ionizing radiation lead to increasing damage to the cells that are more radioresistant.
C) EPIDEMIOLOGY: Radiation exposures are rare, but can be life-threatening.
D) WITH POISONING/EXPOSURE

1) The clinical syndromes described for acute radiation syndrome (ARS) follow 4 clinical phases: prodromal, latent, manifest illness, and recovery (or death).

a) HEMATOPOIETIC SYNDROME: Dose (gamma equivalent values): Greater than 0.7 Gy (greater than 70 rads); mild symptoms may develop following doses as low as at 0.3 Gy (30 rads).

1) Prodromal stage: Anorexia, nausea, vomiting; onset 1 hour to 2 days postexposure; lasts minutes to days
2) Latent stage: Patients may appear well; stem cells are dying; lasts 1 to 6 weeks
3) Manifest illness stage: Anorexia, fever, malaise. All blood cell counts decrease for weeks. Death from infection or hemorrhage. Increasing dose decreases survival. Most deaths within few months.
4) Recovery: Bone marrow cells begin to repopulate the marrow. Large proportion will recover from few weeks up to 2 years. Death may occur at 1.2 Gy (120 rads). LD50/60 approximately 2.5 to 5 Gy (250 to 500 rads).

b) GASTROINTESTINAL SYNDROME: Dose (gamma equivalent values): Greater than 10 Gy (greater than 1000 rads); some symptoms may develop following doses as low as 6 Gy (600 rads).

1) Prodromal stage: Anorexia, severe nausea, vomiting, cramps, diarrhea. Onset within few hours; lasts 2 days.
2) Latent stage: Patients may appear well. Stem cells and gastrointestinal lining cells are dying; lasts less than 1 week.
3) Manifest illness stage: Malaise, anorexia, severe diarrhea, fever, dehydration, electrolyte imbalance. Death from infection, dehydration, and electrolyte imbalance. Death may occur within 2 weeks.
4) Recovery: LD100 is about 10 Gy (1000 rads).

c) CNS/CARDIOVASCULAR SYNDROME: Dose (gamma equivalent values): Greater than 50 Gy (greater than 5000 rads). Some symptoms may develop following doses as low as 20 Gy (2000 rads).

1) Prodromal stage: Extreme nervousness, confusion, severe nausea, vomiting, watery diarrhea, loss of consciousness, burning skin sensation. Onset within minutes; lasts minutes to hours.
2) Latent stage: Partial functionality may return. May last for hours but usually less.
3) Manifest illness stage: Return of watery diarrhea, seizures, coma. Onset 5 to 6 hours postexposure. Death within 3 days.
4) Recovery: No recovery expected.

2) CUTANEOUS RADIATION SYNDROME (CRS): Exposure to radiation can damage the basal cell layer of skin, resulting in inflammation, erythema, and dry or moist desquamation. Epilation may occur when hair follicles are damaged. A transient and inconsistent erythema and pruritus may occur within a few hours of exposure. Patients may develop intense reddening, blistering, and ulceration of the irradiated site during a latent phase that lasts from a few days up to several weeks. Although healing can occur, very large doses can cause permanent hair loss, damage sebaceous and sweat glands, atrophy, fibrosis, decreased or increased skin pigmentation, and ulceration or necrosis of the tissue. Patients may develop skin damage without ARS following radiation dose to the skin, especially after acute exposures to beta radiation or X-rays.
3) Hypothyroidism or hyperthyroidism may occur. Both benign and malignant thyroid tumors have been associated with ionizing radiation exposure.
4) COMBINED INJURY: Patients with combined injuries (trauma, thermal, chemical injury, and radiation exposure) may develop immunosuppression, delayed healing, pancytopenia, and other symptoms.

0.2.20)

A) Four major effects of ionizing radiation on the fetus include: growth retardation; severe congenital malformations (including errors of metabolism); embryonic, fetal, or neonatal death; and carcinogenesis. Fetal risk is noted at exposures above 10 rem. In early pregnancy, fetal death may occur. Later in pregnancy, radiation exposure may be teratogenic or may cause fetal growth retardation.
B) Occupational limits: Fetal dose (declared pregnancy): 0.5 rem (5 mSv). Although radiation doses to the embryo or fetus in the uterus is lower than the doses to its mother, health effects of exposure to ionizing radiation in human embryo and fetus can be severe, even at radiation doses too low to immediately affect the mother. Low-level ionizing radiation does not appear to increase the risk of teratogenicity. Consider doses of radioactive materials in specific fetal organs or tissues (eg, iodine-131 or iodine-123 in thyroid; iron-59 in the liver; gallium-67 in the spleen, strontium-90 and yttrium-90 in the skeleton). Approximately 5 Gy (500 rads) dose before 18 weeks' gestation can kill 100% of human embryos or fetuses; 50% of embryos may die with a fetal dose of 1Gy (100 rads).
C) Cesium has been shown to penetrate the human placenta and be present in breast milk in mothers following exposures.
D) Impaired fertility, including abnormal sperm production and impaired sexual function, has been reported in men. It is possible that radiation exposure in women may affect the viability of the ova and the function of the endocrine system which is responsible for production of some female sex hormones.

0.2.21)

A) Ionizing radiation has carcinogenic effects in many tissues. The major toxicity of low- and moderate-dose ionizing radiation is cancer induction. Acute ionizing radiation exposure survivors have increased long-term cancer risks. A dose-response relationship exists between exposure to ionizing radiation and the risk for the subsequent development of cancer.

Laboratory Monitoring

Treatment Overview

0.4.2)

A) MANAGEMENT OF TOXICITY

1) Stabilize all patients from their traumatic injuries prior to evaluating them for radiation injuries. Although high intensity external radiation can cause tissue damage (eg, skin burns or marrow depression), it does not make the patient radioactive. However, all staff should be in scrubs covered with a water resistant gown or a Tyvek(R) suit. A cap, mask, and shoe covers should be worn, and 2 pairs of plastic gloves worn with the first pair taped to the gown or suit. Dosimeters should be worn at the collar but under the protective clothing.
2) External decontamination should be performed, which is largely accomplished by removing and bagging the clothing, and washing the skin with warm water and soap. The history obtained at the scene is of great importance. The exact type of exposure (ie, internal versus external and partial versus whole body exposure) should be obtained. The main goals of therapy for acute radiation syndrome are prevention of neutropenia and sepsis. Examine the patient and repeat at 6 hours and 12 hours. Monitor vital signs, including temperature; the sooner the temperature rises, the greater the dose received. Trauma or other urgent medical or surgical situations should be managed prior to treatment for radiation exposure.
3) INGESTION: Patients who ingested any radioactive matter should receive aluminum hydroxide or magnesium carbonate antacids to reduce absorption. Treat patients with persistent nausea and vomiting with granisetron or ondansetron. Early oral feedings are recommended to maintain gut function. All emesis should be collected for the first few days, saving for later analysis. Antidiarrheals may be used to control diarrhea. Internal contamination may require treatment with radiation countermeasure agents such as potassium iodide (radioactive iodine exposure), prussian blue (cesium and thallium exposure), or chelating agents (plutonium, americium, curium exposure). However, these agents do not protect against external radiation absorption and acute radiation syndrome.
4) Colony-stimulating factor treatment should begin within 24 to 72 hours of exposure when granulocyte levels are falling, with daily therapy continued until the absolute neutrophil count increases to more than 1000 cells/mm(3). Patients who develop infection without neutropenia should have antibiotic therapy directed towards the source of infection and the most likely pathogen.
5) LOCALIZED RADIATION INJURY: Localized radiation injury may also occur in conjunction with acute radiation syndrome, usually presenting with delayed erythema and desquamation or blistering 12 to 20 days after exposure. Treatment includes pain management, infection prevention, and vasodilators.
6) PALLIATIVE CARE: Patients who vomited within a few minutes of exposure, with diarrhea developing in less than an hour, fever developing in less than 1 hour, severe headache, a possible history of loss of or altered consciousness, abdominal pain, parotid pain, erythema, and possible hypotension have likely received a lethal dose with poor prognosis. Palliative care should be started immediately, with initial treatment in the ICU if resources allow.
7) Further information is available from the CDC (http://www.bt.cdc.gov/radiation/) and the United States Department of Health and Human Services (http://www.remm.nlm.gov/). Emergency consultation services are also available through the Radiation Emergency Assistance Center/Training Site (REAC/TS) 24 hours a day, 7 days a week at 865-576-1005 (http://orise.orau.gov/reacts/).

B) DECONTAMINATION

1) DERMAL: Most decontamination (90%) is accomplished by removal of the outer clothing and shoes. A radiation detector passed over the body (held at a consistent distance from the body) can detect residual contamination. Further decontamination is accomplished by washing with warm soap and water, with gentle brushing while covering open wounds. Reduction of radiation to less than 2 times the background level is the goal of decontamination. Contaminated wounds require further effort. Abrasions are decontaminated with warm water and soap. Lacerations may require excision of contaminated tissue. Punctate lesions may be successfully cleaned using a water pick or oral irrigator. Shrapnel should be removed with forceps.
2) INGESTION: Patients who ingested any radioactive matter should receive aluminum hydroxide or magnesium carbonate antacids to reduce absorption. Gastric lavage may be used if ingestion occurred within 1 to 2 hours, and large ingestions may benefit from cathartics and enemas.
3) EYES: Obtain an x-ray to rule out presence of shrapnel in globe. If corneal contamination is present and globe is intact, carefully irrigate eyes with copious amounts of saline or water. Never irrigate a ruptured globe. To avoid contamination of nasolacrimal duct, direct irrigation stream away from inner canthus and toward outer canthus. Monitor the eyes for conjunctivitis after decontamination. The irrigation fluid should be tested frequently for residual radioactivity. Collect, store, and label irrigation fluid properly for forensic evaluation and proper disposal.

C) RADIATION INFORMATION

1) Several historical points should be quickly obtained when whole-body irradiation is a possibility: (1) location when the potential exposure occurred; (2) amount of possible shielding, including position inside a building; (3) amount of time outside away from shielding; and (4) occurrence of any vomiting or diarrhea. It should be documented whether any decontamination has occurred, and if any loss of consciousness was experienced. If trauma occurred, the mechanism of injury should be determined, and any medication use and allergy history recorded. MEASUREMENT OF RADIATION: In patients who have inhaled, ingested, or absorbed radioactive material through wound, direct measurement of radiation within the patient is a possible to guide therapy. Ingested radioactivity can be measured from collected urine. If inhalation may have occurred, nasal swabs should be taken as soon as possible in order to determine the approximate radiation exposure; combine the 2 measurements and divide by 0.1 to obtain the inhaled amount of radiation. Similar measurements may be taken from contaminated wounds. In all cases, the measurements can be converted into a measure of activity and compared with charts of known annual limits of intake to determine if the amount of radiation internally present is hazardous and requires treatment. Specific medical countermeasures may be employed to treat internal contamination, some of which depend on the specific radionuclide that has been ingested or inhaled.

D) AIRWAY MANAGEMENT

1) Administer 100% oxygen as needed for respiratory support. Endotracheal intubation and mechanical ventilation may rarely be required.

E) ANTIDOTES

1) DEFEROXAMINE

a) USES: Iron, manganese, neptunium, and plutonium.
b) DOSES: Not specified by age: 1 g IM or IV (2 ampules) slowly (15 mg/kg/hr); IM is preferred; repeat as indicated as 500 mg IM or IV every 4 hours for 2 doses; then 500 mg IM or IV every 12 hours for 3 days.

2) DIMERCAPROL

a) USES: Antimony, arsenic, bismuth, gold, lead, mercury, nickel, polonium-210.
b) DOSES: Not specified by age: 300 mg per vial for deep IM use, 2.5 mg/kg (or less) every 4 hours for 2 days, then twice daily for 1 day then once daily for days 5 to 10.

3) EDETATE CALCIUM DISODIUM

a) USES: Cadmium, chromium, cobalt, copper, iridium, lead, manganese, mercury, nickel, plutonium, ruthenium, yttrium, zinc, zirconium.
b) DOSES: Not specified by age: 1000 mg/m(2)/day added to 500 mL dextrose 5% normal saline over 8 to 12 hours.

4) DTPA, CALCIUM OR ZINC

a) USES: Plutonium-239, Americium-241, Curium-244.
b) DOSES: ADULTS: 1 g in 5 mL IV push over 3 to 4 minutes or IV infusion over 30 minutes diluted in 250 mL of 5% dextrose in water, Normal Saline (NS), or Ringers Lactate. Nebulized inhalation: 1 g in 1:1 dilution with water or NS. CHILDREN (age under 12 years): 14 mg/kg IV loading dose as soon as possible; MAX: 1 g.

5) PENICILLAMINE

a) USES: Antimony, bismuth, copper, gallium, gold, mercury, palladium, polonium.
b) DOSES: Not specified by age: 250 mg daily orally between meals and at bedtime; may increase to 4 or 5 g daily in divided doses.

6) POTASSIUM IODIDE

a) USES: radioactive iodine.
b) DOSES: ADULTS: 130 mg orally daily for ingestion of radioactive iodine. CHILDREN (age 12 to 18 years, weight greater than 150 pounds): 130 mg orally daily for ingestion of radioactive iodine. CHILDREN (age 12 to 18 years, weight less than 150 pounds): 65 mg orally daily for ingestion of radioactive iodine. CHILDREN (age 3 to 12 years): 65 mg orally daily for ingestion of radioactive iodine. CHILDREN (age 1 month to 3 years): 32.5 mg orally daily for ingestion of radioactive iodine. CHILDREN (birth to 1 month): 16.25 mg orally daily for ingestion of radioactive iodine.

7) PROPYLTHIOURACIL

a) USES: Iodine-131.
b) DOSES: Not specified by age: 2 tabs (50 mg each) 3 times daily for 8 days.

8) PRUSSIAN BLUE

a) USES: Cesium-137, thallium-201, rubidium.
b) DOSES: ADULTS: 3 g orally 3 times daily. CHILDREN (age 2 to 12 years): 1 g orally 3 times daily.

9) SUCCIMER

a) USES: Arsenic, bismuth, cadmium, cobalt, lead, mercury, polonium.
b) DOSES: CHILDREN: initial, 10 mg/kg or 350 mg/m(2) orally every 8 hours for 5 days. Reduce frequency of administration to 10 mg/kg or 350 mg/m(2) every 12 hours (two-thirds of initial daily dose) for an additional 2 weeks of therapy (course of therapy: 19 days).

F) NAUSEA AND VOMITING

1) Treat patients with persistent nausea and vomiting with granisetron or ondansetron. Early oral feedings are recommended to maintain gut function.

G) DIARRHEA

1) Antidiarrheals may be used for the control of diarrhea (eg, loperamide or diphenoxylate/atropine).

H) MYELOSUPPRESSION

1) Colony-stimulating factors (FILGRASTIM: ADULTS: 2.5 to 5 mcg/kg once daily subQ. SARGRAMOSTIM: ADULTS: 5 to 10 mcg/kg once daily subQ. PEGFILGRASTIM: ADULTS: 6 mg once subQ) should begin within 24 to 72 hours of exposure when granulocyte levels are falling, with daily therapy continued until the absolute neutrophil count increases to more than 1000 cells/mm(3). Patients who develop infection without neutropenia should have antibiotic therapy directed towards the source of infection and the most likely pathogen. If febrile neutropenia develops, consultation with infectious disease and hematology specialists should be obtained, and guidelines on febrile neutropenia from the Infectious Disease Society of America should be followed for appropriate antibiotic therapy. Patients who received doses of 7 to 10 Gy (700 to 1000 rads) should be considered for bone marrow stem cell transplants. The Radiation Injury Treatment Network was founded to assist in situations in which profound damage to the bone marrow has occurred, and it can be reached at: http://bloodcell.transplant.hrsa.gov/ABOUT/RITN/index.html. If transfusion of blood products is required, all products should leukoreduced and irradiated to 25 Gy in order to avoid a transfusion-related graft-vs-host reaction.

I) HYPOTENSION

1) Treat hypotension with intravenous fluids; if hypotension persists, administer vasopressors.

J) SEIZURES

1) IV benzodiazepines; barbiturates or propofol if seizures recur or persist.

K) ENHANCED ELIMINATION PROCEDURE

1) In one in vitro study, charcoal hemoperfusion was NOT effective in decreasing radioactivity in artificial media containing cesium-137.

L) PATIENT DISPOSITION

1) HOME CRITERIA: Any patient who is asymptomatic, totally decontaminated as indicated by survey, and has a normal CBC and platelet count may be safely discharged. Follow-up instructions should include a repeat CBC in 48 hours and reevaluation following the onset of any gastrointestinal symptoms (eg, nausea, vomiting, and diarrhea).
2) ADMISSION CRITERIA: Admission is required for fluid and electrolyte therapy if severe vomiting and diarrhea are present. Patients manifesting thrombocytopenia, granulocytopenia, and/or lymphopenia require hospital admission. Hospital admission is also necessary for standard indications for multiple trauma or burns associated with radiation exposure.
3) CONSULT CRITERIA: For patients with localized injury, referral may be required for plastic surgery, grafting, or amputation.
4) PATIENT-TRANSFER CRITERIA: Initially, patients should be field-triaged to a facility designated for handling radioactively-contaminated patients. Other conditions (eg, multiple trauma) may necessitate transporting patients to a trauma center. After stabilization, decontamination, and initial evaluation, patients with the hematopoietic syndrome should be transferred to a facility with expertise in the treatment of pancytopenia. If transfer is indicated, it should be undertaken on the first day or as soon as possible.

M) PITFALL

1) Early symptoms of radiation exposure may be delayed or not evident (eg, myelosuppression). Appropriate therapy may be delayed due to failure to contact a radiation specialist. Beware of secondary exposures that may come from rescuers who were also exposed. History of radiation exposure may be difficult to obtain in some settings.

N) KINETICS

1) Systemic contamination will occur following ingestion, inhalation, skin absorption, or wound contamination of radioactive material. Following absorption, a radionuclide crosses capillary membranes through passive and active diffusion mechanisms and then is distributed throughout the body. Rate of distribution to each organ is dependent on organ metabolism, ease of chemical transport, and the affinity of the radionuclide for chemicals within the organ. The organs with the highest capacities for binding radionuclides are the liver, kidney, adipose tissue, and bone due to their high protein and lipid makeup. Each radionuclide has a unique half-life, with half-lives ranging from extremely short (fraction of a second) to millions of years. Samples of some radionuclides and their half-lives are: Tc-99m: 6 hours; I-131: 8.05 days; Co-60: 5.26 years; Sr-90: 28.1 years; Pu-239: 24,400 years; U-238: 4,150,000,000 years.

O) DIFFERENTIAL DIAGNOSIS

1) Local injuries such as chemical or thermal burn, insect bite, skin disease or allergy, trauma; food poisoning, gastroenteritis; chemotherapeutic agents, or myelosuppression agents.

0.4.3)

A) In patients who have inhaled radioactive material, direct measurement of radiation within the patient is possible to guide therapy. Nasal swabs should be taken as soon as possible in order to determine the approximate radiation exposure; combine the 2 measurements and divide by 0.1 to obtain the inhaled amount of radiation. In all cases, the measurements can be converted into a measure of activity and compared with charts of known annual limits of intake to determine if the amount of radiation internally present is hazardous and requires treatment. Specific medical countermeasures may be employed to treat internal contamination, some of which depend on the specific radionuclide that has been inhaled.
B) Refer to ORAL OVERVIEW AND MAIN SECTIONS for specific treatment information.

0.4.5)

A) OVERVIEW

1) Most decontamination (90%) is accomplished by removal of the outer clothing and shoes. A radiation detector passed over the body (held at a consistent distance from the body) can detect residual contamination. Further decontamination is accomplished by washing with warm soap and water, with gentle brushing while covering open wounds. Reduction of radiation to less than 2 times the background level is the goal of decontamination. Contaminated wounds require further effort. Abrasions are decontaminated with warm water and soap. Lacerations may require excision of contaminated tissue. Punctate lesions may be successfully cleaned using a water pick or oral irrigator. Shrapnel should be removed with forceps.
2) Refer to ORAL OVERVIEW AND MAIN SECTIONS for specific treatment information.

Range Of Toxicity

1) HEMATOPOIETIC (BONE MARROW) SYNDROME: Dose (gamma equivalent values): Greater than 0.7 Gy (greater than 70 rads); mild symptoms may develop following doses as low as at 0.3 Gy (30 rads). GASTROINTESTINAL SYNDROME: Dose (gamma equivalent values): Greater than 10 Gy (greater than 1000 rads); some symptoms may develop following doses as low as 6 Gy (600 rads). NEUROVASCULAR/CARDIOVASCULAR SYNDROME: Dose (gamma equivalent values): Greater than 50 Gy (greater than 5000 rads). Some symptoms may develop following doses as low as 20 Gy (2000 rads). CUTANEOUS RADIATION SYNDROME: Presentation of Local Radiation Injury defined by dose received: 3 Gy: Epilation (hair loss) begins 14 to 21 days after exposure. 6 Gy: Erythema that may be transient soon after exposure (primary erythema), may again appear 14 to 21 days following exposure (secondary erythema). It may also occur from time to time. 0 to 15 Gy: Dry desquamation is the response of the germinal epidermal layer that is seen 20 days after exposure. Mitotic activity slows in the basal and parabasal layers, the epidermis thins, and large flakes of skin desquamate. 20 to 50 Gy: Wet desquamation occurs as a partial thickness injury. There is intracellular edema, a coalescence of vesicles forming macroscopic bullae, and fibrin coating a wet dermal surface. Radionecrosis may develop as the dose increases. Greater than 50 Gy: Damage to endothelial cells and fibrinoid necrosis of the vasculature cause radionecrosis and ulceration.

Clinical Effects

Summary Of Exposure

1) The clinical syndromes described for acute radiation syndrome (ARS) follow 4 clinical phases: prodromal, latent, manifest illness, and recovery (or death).

a) HEMATOPOIETIC SYNDROME: Dose (gamma equivalent values): Greater than 0.7 Gy (greater than 70 rads); mild symptoms may develop following doses as low as at 0.3 Gy (30 rads).

b) GASTROINTESTINAL SYNDROME: Dose (gamma equivalent values): Greater than 10 Gy (greater than 1000 rads); some symptoms may develop following doses as low as 6 Gy (600 rads).

c) CNS/CARDIOVASCULAR SYNDROME: Dose (gamma equivalent values): Greater than 50 Gy (greater than 5000 rads). Some symptoms may develop following doses as low as 20 Gy (2000 rads).

Vital Signs

3.3.3)

A) WITH POISONING/EXPOSURE

1) Fever is often noted during the prodromal phase of illness (Donnelly et al, 2010; Koenig et al, 2005), and the timing of fever onset is related to the dose of radiation absorbed; the earlier the rise in temperature, the greater the does of radiation received. Temperature elevation within the first 5 to 6 hours indicates a radiation dose of greater than 2.5 Gy (250 rads) (Berger, 2003)

Heent

3.4.3)

A) WITH POISONING/EXPOSURE

1) CONJUNCTIVITIS: May develop if the dose of radiation was near the eyes and may occur during the prodromal phase (Radiation Emergency Assistance Center, 2011; Donnelly et al, 2010).
2) BLINDNESS: Sudden exposure to high-intensity visible light and infrared radiation from detonation will result in eye injury of the chorioretinal areas. Using binoculars will increase the likelihood of damage. Eye injury is due to both infrared energy and photochemical reactions that occur within the retina with light wavelengths in the range of 400 to 500 micrometers (Jarrett, 1999).

a) Retinal burns will occur in persons looking directly at the flash. Night vision apparatus (NVA) does NOT amplify the infrared and damaging wavelengths NOR does it cause retinal injury (Jarrett, 1999).
b) Flashblindness occurs with peripheral observation of a brilliant flash of intense light energy and is a temporary condition due to depletion of photopigment from the retina. This may last for a few seconds (daytime) up to 30 minutes (night-time) (Jarrett, 1999).

3) CATARACTS: CASE SERIES: Cataracts developed in 8 of 15 patients studied 6 years after being exposed to large amounts of beta radiation during the Chernobyl accident (Peter et al, 1994).
4) NYSTAGMUS: A continuous rolling movement of the eyeballs has been noted in patients following radiation exposure (Natl Acad Sci, 1963).

3.4.5)

A) WITH POISONING/EXPOSURE

1) ABNORMAL SENSATIONS: Persons exposed to ionizing radiation may complain of abnormal sensations of taste and smell (Natl Acad Sci, 1963).

3.4.6)

A) WITH POISONING/EXPOSURE

1) ABNORMAL SENSATIONS: Persons exposed to ionizing radiation may complain of abnormal sensations of taste and smell (Natl Acad Sci, 1963).

Cardiovascular

3.5.2)

A) HYPOTENSIVE EPISODE

1) WITH POISONING/EXPOSURE

a) Hypotension is noted during the prodromal phase and may occur during the neurovascular syndrome or as a result of hypovolemia (Donnelly et al, 2010; Jarrett, 1999).

Respiratory

3.6.2)

A) PNEUMONITIS

1) Early radiation-induced lung injury with diffuse alveolar damage has been reported in patients after inhalational exposure to greater than 8 to 10 Gy (800 to 1000 rads) (Radiation Emergency Assistance Center, 2011).
2) Radiation pneumonitis is a well-recognized syndrome associated with pulmonary radiation injury (secondary to radiation therapy) (Radiation Emergency Assistance Center, 2011; Gibson et al, 1988) and as an effect from exposure to elevated levels of airborne radioactive particles (dust) from reactor halls of nuclear power plants (Salovsky et al, 2000).
3) A latent period between radiation exposure and development of acute pulmonary reactions is common. Dyspnea (in 93 percent of patients) and cough (in 58 percent of patients) are the most common symptoms. Routine chest examinations usually reveal normal physical findings. Skin changes due to radiation exposure do not correlate well with pulmonary changes. Early onset of symptoms may indicate a more serious clinical course (Movsas et al, 1997).

B) FIBROSIS OF LUNG

1) Radiation pulmonary fibrosis resulting from chronic lung damage is another well-recognized syndrome associated with pulmonary radiation injury (secondary to radiation therapy) (Radiation Emergency Assistance Center, 2011; Movsas et al, 1997). Evolution of permanent fibrotic changes usually occurs over 6 to 24 months, then remains stable after 2 years. Patients may have no previous pneumonitis and may be asymptomatic or have varying degrees of dyspnea. If a large volume of lung is irradiated, chronic pulmonary insufficiency may evolve and may progress to pulmonary hypertension and cor pulmonale (Movsas et al, 1997).

Neurologic

3.7.2)

A) CENTRAL NERVOUS SYSTEM FINDING

1) WITH POISONING/EXPOSURE

a) NEUROVASCULAR/CARDIOVASCULAR SYNDROME

1) The nervous system is the target organ system that is the least sensitive to radiation, compared with the other 2 organ systems involved in ARS (Donnelly et al, 2010).
2) CDC has provided the following information: Dose (gamma equivalent values): Greater than 50 Gy (greater than 5000 rads). Some symptoms may develop following doses as low as 20 Gy (2000 rads) (Centers for Disease Control and Prevention, 2005).

a) Prodromal stage: Extreme nervousness, confusion, severe nausea, vomiting, watery diarrhea, loss of consciousness, burning skin sensation. Onset within minutes; lasts minutes to hours.
b) Latent stage: Partial functionality may return. May last for hours but usually less.
c) Manifest illness stage: Return of watery diarrhea, seizures, coma. Onset 5 to 6 hours postexposure. Death within 3 days.
d) Recovery: No recovery expected.

3) With exposures over 10 Gy (1000 rads), vomiting is suppressed, but patients are more generally fatigued (known as the 'fatigue syndrome'). Further features include headache, fever, altered reflexes, confusion, disorientation, dizziness, ataxia, and loss of consciousness (Donnelly et al, 2010).
4) When exposure exceeds 35 Gy (3500 rads), larger blood vessels are damaged, which may cause circulatory collapse and may be associated with increased intracerebral pressure, vasculitis, and meningitis (Donnelly et al, 2010; Koenig et al, 2005). Patients will also experience nausea, vomiting, prostration, hypotension, ataxia, and seizures (Koenig et al, 2005). Exposure to over 50 Gy (5000 rads) will result in death within 48 hours (Donnelly et al, 2010).

B) HEADACHE

1) A headache occurring early (within a few minutes of exposure) indicates exposure to a supralethal dose (greater than 12 Gy) (Andrews & Cloutier, 1965).
2) Headache is part of the 'fatigue syndrome' that can occur with exposures that exceed 10 Gy (1000 rads) (Donnelly et al, 2010).
3) Transient headache may be present after a low-dose exposure of 0.35 Gy (35 rads) that does not represent acute radiation syndrome. However, headache is also reported in patients with much higher exposure, associated with other symptoms, depending on the dose received (Donnelly et al, 2010).

C) CLOUDED CONSCIOUSNESS

1) WITH POISONING/EXPOSURE

a) Disorientation and confusion are part of the 'fatigue syndrome' that can occur with exposures that exceed 10 Gy (1000 rads) (Donnelly et al, 2010).

D) LOSS OF CONSCIOUSNESS

1) WITH POISONING/EXPOSURE

a) Loss of consciousness is part of the 'fatigue syndrome' that can occur with exposures that exceed 10 Gy (1000 rads) (Donnelly et al, 2010).

E) PAROTITIS

1) WITH POISONING/EXPOSURE

a) The cells of the parotid gland are very sensitive to ionizing radiation; therefore, the development of parotitis, noted typically during the prodromal phase of illness, indicates radiation exposure (Berger, 2003).

F) FATIGUE

1) WITH POISONING/EXPOSURE

a) Fatigue is part of the 'fatigue syndrome' that results from exposures above 10 Gy (1000 rads), and is associated with headache, fever, altered reflexes, confusion, disorientation, ataxia, and loss of consciousness (Donnelly et al, 2010).

G) DIZZINESS

1) Patients may experience vertigo following radiation exposure (Natl Acad Sci, 1963).

H) ATAXIA

1) Ataxia may be noted in patients exposed to high doses of radiation (Natl Acad Sci, 1963).

I) SEIZURE

1) Seizures will occur within a few minutes of exposure to a supralethal dose (greater than 12 Gy) but are rare (Andrews & Cloutier, 1965). One source reported that very high acute radiation doses associated with an early transient syndrome (lower limit of exposure, 20 to 40 Gy) are followed by a deteriorating state of consciousness with vascular instability, and seizures; increased intracranial pressure may or may not occur (Jarrett, 1999).
2) In the children of pregnant Japanese atomic bomb survivors, the incidence of seizure was highest following irradiation at the 8th through 15th weeks after fertilization (Dunn et al, 1990).

J) NEUROLOGICAL DEFICIT

1) In a cohort of 888 children whose mothers were exposed to ionizing radiation from atom bomb detonations, those who were exposed at 8 to 15 weeks postovulation had significantly worse scores on repetitive action tests. Those exposed at 0 to 7 weeks postovulation had decreased IQ's. These effects were not seen in children whose mothers were exposed at weeks 16 to 25 postovulation (Yoshimaru et al, 1995).

Gastrointestinal

3.8.2)

A) GASTROINTESTINAL TRACT FINDING

1) WITH POISONING/EXPOSURE

a) GASTROINTESTINAL SYNDROME

1) CDC has provided the following information: Dose (gamma equivalent values): Greater than 10 Gy (greater than 1000 rads); some symptoms may develop following doses as low as 6 Gy (600 rads) (Centers for Disease Control and Prevention, 2005).

a) Prodromal stage: Anorexia, severe nausea, vomiting, cramps, diarrhea. Onset within few hours; lasts 2 days .
b) Latent stage: Patients may appear well. Stem cells and gastrointestinal lining cells are dying; lasts less than 1 week.
c) Manifest illness stage: Malaise, anorexia, severe diarrhea, fever, dehydration, electrolyte imbalance. Death from infection, dehydration, and electrolyte imbalance. Death may occur within 2 weeks.
d) Recovery: LD100 is about 10 Gy (1000 rads).

2) Nausea, vomiting (sometimes severe), anorexia, and crampy abdominal pain occur within 1 to 2 hours of radiation exposure. Diarrhea early in the course is considered an ominous sign. Exposures over 10 Gy (1000 rads) may actually suppress vomiting. Death usually occurs within weeks of radiation exposure, resulting from multisystem organ failure, sepsis, or bleeding (Donnelly et al, 2010). Survival is considered highly unlikely with this syndrome (Centers for Disease Control and Prevention, 2005).
3) MECHANISM: Because they have a rapid turnover rate, the cells of the gastrointestinal tract, particularly the small intestinal villi, are affected earliest by exposure to ionizing radiation. Shrinkage of villi and morphological changes in mucosal cells occur as new cell production is diminished. Denudation of the intestinal mucosa occurs. Concomitant injury to the microvasculature of the mucosa results in hemorrhage and marked fluid and electrolyte loss leading to shock. These events generally occur within 1 to 2 weeks following irradiation. Direct radiation exposure of the vomiting center in the medulla oblongata will also cause nausea and vomiting (Jarrett, 1999).

B) NAUSEA

1) WITH POISONING/EXPOSURE

a) Mild nausea may be present after a low-dose exposure of 0.35 Gy (35 rads) that does not represent acute radiation syndrome (Donnelly et al, 2010).
b) Nausea is present following exposure to ionizing radiation at levels great enough to cause acute radiation sickness, and is typically present during the prodromal phase (Donnelly et al, 2010).
c) POLONIUM-210 POISONING: As an alpha-emitting radionuclide, polonium-210 is not an external hazard. It can be extremely toxic when absorbed into the body via inhalation and ingestion. Patients may develop acute radiation syndrome, with nausea, vomiting, and diarrhea during the prodromal phase. Later signs include loss of hair, bleeding, and multiple organ failure resulting in death (Fraser et al, 2012).

C) VOMITING

1) WITH POISONING/EXPOSURE

a) Vomiting is present following exposure to ionizing radiation at levels great enough to cause acute radiation sickness, and this symptom is typically present during the prodromal phase. The time to the onset of vomiting following total body irradiation is an indication of the dose received up to approximately 10 Gy (1000 rads), at which point vomiting is suppressed (Donnelly et al, 2010).
b) Fewer than 50% of patients will vomit after an exposure of 2 to 3 Gy (200 to 300 rads), and at doses of 5 to 6 Gy (500 to 600 rads), up to 90% will vomit (Donnelly et al, 2010).

1) Estimation of dose received based on time to onset of vomiting after single acute exposure: Less than 10 minutes: greater than 8 Gy (800 rads); less than 30 minutes: 6 to 8 Gy (600 to 800 rads); less than 1 hour: 4 to 6 Gy (400 to 600 rads); 1 to 2 hours: 2 to 4 Gy (200 to 400 rads); more than 2 hours or no vomiting: less than 2 Gy (200 rads) (Donnelly et al, 2010)

c) Bloody vomiting may occur secondary to exposure to higher doses (Finch, 1987).
d) POLONIUM-210 POISONING: As an alpha-emitting radionuclide, polonium-210 is not an external hazard. It can be extremely toxic when absorbed into the body via inhalation and ingestion. Patients may develop acute radiation syndrome, with nausea, vomiting, and diarrhea during the prodromal phase. Later signs include loss of hair, bleeding, and multiple organ failure resulting in death (Fraser et al, 2012).

D) ABDOMINAL PAIN

1) WITH POISONING/EXPOSURE

a) Crampy abdominal pain is a typical finding in patients exposed to 6 to 10 Gy (600 to 1000 rads), occurring within 1 to 2 hours of exposure (Donnelly et al, 2010).

E) DIARRHEA

1) WITH POISONING/EXPOSURE

a) The early occurrence of diarrhea is an ominous finding in patients exposed to more than 6 Gy (600 rads) (Donnelly et al, 2010). Acute onset of diarrhea is associated with an exposure to more than 9 Gy (900 rads) (Berger, 2003).
b) Persistent diarrhea may be bloody. The presence of high fever and persistent bloody diarrhea secondary to high doses is an ominous sign (Andrews & Cloutier, 1965). Immediate explosive bloody diarrhea indicates a potentially lethal dose (Conklin et al, 1983).
c) POLONIUM-210 POISONING: As an alpha-emitting radionuclide, polonium-210 is not an external hazard. It can be extremely toxic when absorbed into the body via inhalation and ingestion. Patients may develop acute radiation syndrome, with nausea, vomiting, and diarrhea during the prodromal phase. Later signs include loss of hair, bleeding, and multiple organ failure resulting in death (Fraser et al, 2012).

F) SERUM AMYLASE RAISED

1) WITH POISONING/EXPOSURE

a) Exposures above 0.5 Gy (50 rads) will result in a significant elevation of serum amylase. Maximum amylase levels are seen with exposures between 4 to 10 Gy (400 and 1000 rads) (Berger, 2003).

G) LOSS OF APPETITE

1) WITH POISONING/EXPOSURE

a) Anorexia is generally present during the prodromal phase for most patients with acute radiation exposure (Centers for Disease Control and Prevention, 2005).

H) ESOPHAGEAL INJURY

1) RADIATION-INDUCED ESOPHAGEAL INJURY: Although the esophagus is a relatively radiation-tolerant organ, development of acute radiation esophagitis during treatment of a number of cancers may be common and chronic radiation esophagitis and perhaps radiation-induced esophageal cancer may also occur (Vanagunas et al, 1990).

Hematologic

3.13.2)

A) MYELOSUPPRESSION

1) WITH POISONING/EXPOSURE

a) HEMATOPOIETIC (BONE MARROW) SYNDROME

1) CDC has provided the following information: Dose (gamma equivalent values): Greater than 0.7 Gy (greater than 70 rads); mild symptoms may develop following doses as low as at 0.3 Gy (30 rads).(Centers for Disease Control and Prevention, 2005).

a) Prodromal stage: Anorexia, nausea, vomiting; onset 1 hour to 2 days postexposure; lasts minutes to days
b) Latent stage: Patients may appear well; stem cells are dying; lasts 1 to 6 weeks
c) Manifest illness stage: Anorexia, fever, malaise. All blood cell counts decrease for weeks. Death from infection or hemorrhage. Increasing dose decreases survival. Most deaths within few months.
d) Recovery: Bone marrow cells begin to repopulate the marrow. Large proportion will recover from few weeks up to 2 years. Death may occur at 1.2 Gy (120 rads). LD50/60 approximately 2.5 to 5 Gy (250 to 500 rads).

2) Lymphocytes are the most radiosensitive blood cell line and are the first to be depleted, followed by granulocytes and platelets. Mature erythrocytes are depleted at a much slower rate (Donnelly et al, 2010).
3) Early effects of radiation exposure noted in the hematopoietic syndrome are not the result of hematopoietic stem cell loss, but early onset of symptoms reflects the severity of exposure; the earlier symptoms occur and the more severe the symptoms, the greater the radiation exposure received (Donnelly et al, 2010).
4) Later effects of exposure are due to hematopoietic stem cell loss and reflect the impact on immunity and blood cell production. Infections develop, bleeding occurs, and wound healing is poor; death may occur from weeks to months following radiation exposure (Donnelly et al, 2010).

b) COMBINED INJURY: Patients with combined injuries (trauma, thermal, chemical injury, and radiation exposure) may develop immunosuppression, delayed healing, and pancytopenia (Berger, 2003).
c) INFECTION: An infection may occur secondary to pancytopenia. The patient becomes most susceptible to infection in the second to third week postexposure when the maximum decrease in the WBC count occurs.

1) For patients with multiple injuries who have survived more than five days, infection is the second most common cause of death. Gram-negative bacteria or endotoxin is most commonly responsible (Conklin et al, 1983).

B) THROMBOCYTOPENIC DISORDER

1) Thrombocytopenia generally occurs by 3 to 4 weeks after midlethal-range doses and results from the killing of stem cells and immature megakaryocyte stages, with subsequent maturational depletion of functional megakaryocytes. After sublethal radiation, regeneration of thrombocytopoiesis usually lags behind both erythropoiesis and myelopoiesis (Jarrett, 1999). The platelet count is of little value in the first few days postexposure; however, it should be followed to plan supportive therapy over several weeks to two months postexposure (Natl Acad Sci, 1963; Andrews & Cloutier, 1965).

C) RETICULOCYTE COUNT ABNORMAL

1) RETICULOCYTOPENIA: The absence of reticulocytes in the first 3 to 5 days postexposure indicates the patient received a high dose (Natl Acad Sci, 1963; Andrews & Cloutier, 1965).

Dermatologic

3.14.2)

A) SKIN FINDING

1) WITH POISONING/EXPOSURE

a) CUTANEOUS RADIATION SYNDROME (CRS): Exposure to radiation can damage the basal cell layer of skin, resulting in inflammation, erythema, and dry or moist desquamation. Epilation may occur when hair follicles are damaged. A transient and inconsistent erythema and pruritus may occur within a few hours of exposure. Patients may develop intense reddening, blistering, and ulceration of the irradiated site during a latent phase that lasts from a few days up to several weeks. Although healing can occur, very large doses can cause permanent hair loss, damage sebaceous and sweat glands, atrophy, fibrosis, decreased or increased skin pigmentation, and ulceration or necrosis of the tissue. Patients may develop skin damage without ARS following radiation dose to the skin, especially after acute exposures to beta radiation or X-rays (Centers for Disease Control and Prevention, 2005; Gottlober et al, 2000).
b) The guideline for grading cutaneous radiation injury from the US CDC: Grade I: greater than 2 Gy; Grade II: greater than 15 Gy; Grade III: greater than 40 Gy (Radiation Emergency Assistance Center, 2011).
c) LOCAL RADIATION INJURY

1) Presentation of local radiation injury defined by dose received (Radiation Emergency Assistance Center, 2011):

a) 3 Gy: Epilation (hair loss) begins 14 to 21 days after exposure.
b) 6 Gy: Erythema that may be transient soon after exposure (primary erythema), may again appear 14 to 21 days following exposure (secondary erythema). It may also occur from time to time.
c) 10 to 15 Gy: Dry desquamation is the response of the germinal epidermal layer that is seen 20 days after exposure. Mitotic activity slows in the basal and parabasal layers, the epidermis thins, and large flakes of skin desquamate.
d) 20 to 50 Gy: Wet desquamation occurs as a partial thickness injury. There is intracellular edema, a coalescence of vesicles forming macroscopic bullae, and fibrin coating a wet dermal surface. Radionecrosis may develop as the dose increases.
e) Greater than 50 Gy: Damage to endothelial cells and fibrinoid necrosis of the vasculature cause radionecrosis and ulceration.

d) Partial body exposure to beta- and gamma-radiation, as often happens in accidents, can involve up to 50% of total body surface area with lesions including telangiectasias, hemangiomas, radiation ulcers and keratoses, splinter hemorrhages, hematolymphangiomas, hyperpigmentation, and fibrosis (Peter et al, 1994).
e) CASE REPORT: A male industrial radiographer, exposed to iridium-192 sources ranging from 10 to 25 Ci in torch type containers from 1974 to 1983, then exposed to iridium-192 from wind-out remotely operated sources through 1988, initially complained of dermatitis of the right index finger in 1984. By 1988, the finger was noted to be sclerotic with telangiectasia and ulcerations of the fingernail. The remaining fingernails were abnormal with linear streaks and a ragged free margin. Skin biopsy of the right index finger revealed keratin thickening with parakeratosis and acanthosis with irregular downgrowths of the basal layer. Amputation of the finger was necessary. It was estimated that this worker was exposed to a total average whole body dose of at least 10 Gy over several years of gamma radiation. Myelodysplasia progressing to acute myeloid leukemia was the eventual cause of death (Lloyd et al, 1994).
f) Physicians occupationally exposed to low-dose ionizing radiation had morphological and function alterations of the fingernail-fold dermal microcirculation as compared to unexposed controls (Tomei et al, 1996).
g) Iridium-192 exposure in industrial radiologists may cause radiodermatitis with epidermal necrosis, erythema, nail plate loss, intense local pain with a burning sensation, ulcerations, keratotic lesions, and in rare cases the need for digit amputation (Conde-Salazar et al, 1986).

B) THERMAL BURN

1) THERMONUCLEAR DETONATION: Immediate onset of thermal burns of the skin will occur. Thermal radiation causes burns in two ways: by direct absorption of the thermal energy through exposed surfaces (flash burns) or by the indirect action of fires caused within the environment (flame burns). Exposed skin absorbs the infrared; light colors will reflect the infrared and dark colored clothing will absorb it and cause burn patterns. Loose, light colored clothing can reduce the effective range, producing partial thickness burns and giving significant protection against thermal flash burns (Jarrett, 1999). Mortality of thermal burns significantly increases with concomitant radiation doses as small as 1.5 Gy.
2) RADIATION EXPOSURE: The onset of skin burns from radiation devices or secondary to beta particle contamination is usually delayed for several days. The possibility of beta burns, which produce damage to the basal stratum of the skin, can be minimized by early vigorous decontamination procedures ((Anon, 2000); Andrews & Cloutier, 1965).

a) CASE REPORTS: A radiation accident occurred during a military exercise when 11 soldiers were accidentally exposed to cesium-137 and developed acute radiation syndrome. Sharply demarcated red macules in various body areas occurred during the prodromal stage. Two weeks later, ulcers, contaminated with bacteria, appeared in the regions of the initial erythema. Ulcers measured up to 10 cm in diameter. In 7 of the 11 patients, ulcers reached down to the muscles. Cutaneous radiation fibrosis was diagnosed in 1 patient. Dermal histologic examination revealed dermal necrosis and cellular detritus in all 11 patients (Gottlober et al, 2000).

C) DERMATITIS

1) WITH POISONING/EXPOSURE

a) Acute radiation dermatitis secondary to x- or gamma-ray exposure is most often seen after radiation therapy.
b) PEMPHIGUS: Pemphigus lesions may develop in patients treated for cancer with ionizing radiation (Correia et al, 1998).

Musculoskeletal

3.15.2)

A) TREMOR

1) Muscle tremor occurs following massive radiation exposure (Natl Acad Sci, 1963).

Endocrine

3.16.2)

A) FINDING OF THYROID FUNCTION

1) WITH POISONING/EXPOSURE

a) Radiation therapy-associated thyrotoxicosis of either the hypothyroid or hyperthyroid type can occur and may involve an organ-specific autoimmune mechanism (Katayama et al, 1986).
b) In survivors of the Nagasaki, Japan atomic bomb detonation, there was a significant dose-response relationship between ionizing radiation exposure and thyroid diseases including cancer, adenoma, adenomatous goiter, thyroid nodules, and antibody-positive spontaneous hypothyroidism (Nagataki et al, 1994).
c) A significant increase in thyroid autoimmunity was found 6 to 8 years after the Chernobyl accident in children (n=495) exposed to radioactive fallout. The autoimmune response was limited to an increased prevalence of circulating thyroid autoantibodies without evidence of significant thyroid dysfunction. No significant changes of serum FT-4, FT-3, or TSH were noted (Pacini et al, 1998).
d) Childhood thyroid carcinoma was reported with an increased incidence rate, especially in the youngest children, since the nuclear reactor accident at Chernobyl in 1986. One study analyzed the association between disease severity (TNM classification) and age at radiation exposure. They found the severity of disease was associated inversely with age at the time of radiation exposure (Farahati et al, 2000).

Reproductive

3.20.1)

3.20.2)

A) GENERAL INFORMATION

1) Four major effects of ionizing radiation on the fetus include: growth retardation; severe congenital malformations (including errors of metabolism); embryonic, fetal, or neonatal death; and carcinogenesis. The most pronounced permanent growth retardation occurs following irradiation in the fetal period. Functional impairment is also described in the literature. When the fetus is irradiated during organogenesis, the peak incidence of teratogenesis occurs. In humans, radiation-induced malformations of bodily structures other than the CNS are uncommon. The mechanism of neurological defects may involve radiation-induced cell death (Jarrett, 1999).
2) Although radiation doses to the embryo or fetus in the uterus is lower than the doses to its mother, health effects of exposure to ionizing radiation in human embryo and fetus can be severe, even at radiation doses too low to immediately affect the mother. Initially, all sources (external or internal) of radiation to the mother's body should be considered. The fetal radiation dose should be estimated. Ingested or inhaled radioactive substances can be absorbed in the mother's bloodstream (or entered through a contaminated wound) and pass the placental barrier. Certain substances, such as iodine which is needed for growth and development, can be found in larger concentrations in the fetus than in maternal tissues. Maternal tissues around the uterus may contain radioactive substances that can irradiate the fetus (Centers for Disease Control and Prevention, 2006).

B) ANNUAL REGULATORY LIMITS (US NRC)

1) US NRC: US Nuclear Regulatory Commission
2) Occupational limits: Fetal dose (declared pregnancy): 0.5 rem (5 mSv) (Radiation Emergency Assistance Center, 2011):

C) ICRP GENERAL RECOMMENDATIONS

1) ICRP: The International Commission on Radiological Protection
2) Occupational limits: Fetal dose (declared pregnancy - remainder of pregnancy): 0.1 rem (1 mSv) (Radiation Emergency Assistance Center, 2011):

D) FETAL DOSES

1) Consider doses of radioactive materials in specific fetal organs or tissues (eg, iodine-131 or iodine-123 in thyroid; iron-59 in the liver; gallium-67 in the spleen, strontium-90 and yttrium-90 in the skeleton) (Centers for Disease Control and Prevention, 2006).
2) To evaluate fetal doses from internal uptakes, you can refer to the National Council on Radiation Protection and Measurements (NCRP) Report No. 128. "Radionuclide Exposure of the Embryo/Fetus" (Centers for Disease Control and Prevention, 2006).
3) To estimate fetal dose from medical exposures to pregnant women, refer to "Publication 84: Pregnancy and Medical Radiation" from the International commission on Radiological Protection (ICRP) (Centers for Disease Control and Prevention, 2006).
4) Other sources are the Conference of Radiation Control Program Directors, Inc, (CRCPD), Radiation Control/Radiation Protection contact information (http://crcpd.org/Radon.asp) AND the Health Physics Society (HPS) to obtain a list of active certified Health Physicists (http://www.hps1.org/aahp/members/members.htm) (Centers for Disease Control and Prevention, 2006).
5) Prenatal radiation exposure can result in immediate effects (eg, fetal death or malformations) or increased risk for cancer later in life. The potential noncancer health risks of prenatal radiation exposure have been provided by CDC (Centers for Disease Control and Prevention, 2006):

a) ACUTE RADIATION DOSE TO THE EMBRYO OR FETUS: Less than 0.05 Gy (5 rads): Noncancer health effects not detectable.
b) ACUTE RADIATION DOSE TO THE EMBRYO OR FETUS: 0.05 to 0.5 Gy (5 to 50 rads):

1) Blastogenesis (up to 2 weeks): Incidence of failure to implant may increase slightly, but surviving embryos will probably have no significant (noncancer) health effects.
2) Organogenesis (2 to 7 weeks): Incidence of major malformations may increase slightly; possible growth retardation.
3) Fetogenesis (8 to 15 weeks): Possible growth retardation; reduction in IQ possible (up to 15 points, depending on dose); incidence of severe mental retardation up to 20%, depending on dose.
4) Fetogenesis (16 to 25 weeks): Noncancer health effects unlikely.
5) Fetogenesis (26 to 38 weeks): Noncancer health effects unlikely.

c) ACUTE RADIATION DOSE TO THE EMBRYO OR FETUS: Greater than 0.5 Gy (50 rads); acute radiation syndrome may develop in the mother with this dose:

1) Blastogenesis (up to 2 weeks): Incidence of failure to implant will likely be large depending on the dose, but surviving embryos will have no significant (noncancer) health effects.
2) Organogenesis (2 to 7 weeks): Incidence of miscarriage may increase; substantial risk of major malformations such as neurological and motor deficiencies; growth retardation likely.
3) Fetogenesis (8 to 15 weeks): Incidence of miscarriage probably will increase; growth retardation likely; reduction in IQ possible (greater than 15 points, depending on dose); incidence of severe mental retardation greater than 20%, depending on dose; incidence of major malformations will probably increase.
4) Fetogenesis (16 to 25 weeks): Incidence of miscarriage may increase; growth retardation possible; reduction in IQ possible, depending on dose; severe mental retardation possible; incidence of major malformations may increase.
5) Fetogenesis (26 to 38 weeks): Incidence of miscarriage and neonatal death will probably increase, depending on dose.

6) Approximately 5 Gy (500 rads) dose before 18 weeks' gestation can kill 100% of human embryos or fetuses; 50% of embryos may die with a fetal dose of 1Gy (100 rads) (Centers for Disease Control and Prevention, 2006).

E) RISK OF CANCER FROM PRENATAL EXPOSURE

1) Radiation dose: No radiation exposure above background (Centers for Disease Control and Prevention, 2006):

a) Estimated childhood cancer incidence: 0.3%
b) Estimated lifetime cancer incidence (exposure at age 10): 38%

2) Radiation dose: 0 to 0.05 Gy (0 to 5 rads) (Centers for Disease Control and Prevention, 2006):

a) Estimated childhood cancer incidence: 0.3% to 1%
b) Estimated lifetime cancer incidence (exposure at age 10): 38% to 40%

3) Radiation dose: 0.05 to 0.5 Gy (5 to 50 rads)(Centers for Disease Control and Prevention, 2006):

a) Estimated childhood cancer incidence: 1% to 6%
b) Estimated lifetime cancer incidence (exposure at age 10): 40% to 55%

4) Radiation dose: Greater than 0.5 Gy (50 rads) (Centers for Disease Control and Prevention, 2006):

a) Estimated childhood cancer incidence: Greater than 6%
b) Estimated lifetime cancer incidence (exposure at age 10): Greater than 55%

5) Note: The estimated lifetime risks of cancer listed above have been obtained from Japanese males exposed at age 10 years (United Nations Scientific Committee on the Effects of Atomic Radiation published models). In animal studies, a strong sensitivity to carcinogenic effects was observed in late fetal development, but the stages of blastogenesis and organogenesis were not found to be susceptible (Centers for Disease Control and Prevention, 2006).

F) CONGENITAL ANOMALY

1) Prenatal exposure to ionizing radiation is well known to induce birth defects in humans, as documented in the children of pregnant atomic bomb detonation survivors (Otake & Schull, 1998; Brent, 1989).
2) CASE REPORT: Two children conceived while their mothers were undergoing I-131 therapy for thyroid cancer were born with fatal birth defects (Smith et al, 1994).

G) DOWN SYNDROME

1) An increased prevalence of Down syndrome (trisomy 21) has been suggested, but not confirmed, to be associated with periods of increased environmental ionizing radiation (Bound et al, 1995; Verger, 1997).
2) A cluster of DOWN SYNDROME (trisomy 21) cases was seen in the Lothian region of Scotland in 1987, temporally associated with the Chernobyl incident in April, 1986. This was unlikely to have been due to chance, but could not be readily explained by the documented low radiation exposure in that region (Ramsay et al, 1991). A significant increase in cases of Down syndrome was noted in Germany after the Chernobyl disaster, with the highest rates in the most contaminated regions (Sperling et al, 1991).

H) MENTAL DEFICIENCY

1) Exposures in the range of 0.01 to 0.1 gray (Gy) may produce mental retardation and increase the risk for childhood cancers. No gross malformations seem to occur at exposures less than about 0.05 Gy (REPROTOX , 1999). The developing central nervous system may be the most sensitive target for the effects of ionizing radiation, with the critical period being between weeks 10 and 17 of pregnancy (Mole, 1985; Cockerham & Prell, 1989).
2) Studies of the offspring of pregnant atomic bomb survivors have found mental retardation at exposures of less than 0.05 gray (Gy), with NO APPARENT THRESHOLD (Otake & Schull, 1998). The probability of mental retardation in this population was 40% per gray of fetal tissue dose (Otake & Schull, 1984). Expressed another way, there was a reduction of 21 to 29 IQ points per Gy of exposure (Miller, 1990). The frequency of mental retardation increased from a background of 0.8% to 46% with prenatal exposure to 1 Gy or greater in children of atom bomb detonation survivors (Ikenoue et al, 1993). Special note should be made of the fact that these were acute exposures, which in general have more severe biological effects than equivalent doses delivered over a longer period of time.
3) COHORT STUDY: In a cohort of 888 children whose mothers were exposed to ionizing radiation from atom bomb detonations, those who were exposed at 8 to 15 weeks postovulation had significantly worse scores on repetitive action tests. Those exposed at 0 to 7 weeks postovulation had decreased IQs. These effects were not seen in children whose mothers were exposed at weeks 16 to 25 postovulation. (Yoshimaru et al, 1995).
4) Severe mental retardation has been described in children exposed in utero to ionizing radiation from atomic bomb detonations at gestation ages 8 to 15 weeks (Mole, 1990).

I) MICROCEPHALY

1) Reports on atomic bomb survivors indicate that microcephaly may result from a free-in-air dose of 100 to 190 milliGrays (Jarrett, 1999).
2) Exposures greater than 2 gray (Gy) can cause microcephaly and severe mental retardation. The critical dose and period of exposure for microcephaly is at least 0.10 to 0.19 Gy at 4 to 17 weeks, and for mental retardation is at least 0.2 to 0.4 Gy at 8 to 15 weeks (Miller, 1990).

J) LACK OF EFFECT

1) LOW-LEVEL IONIZING RADIATION

a) Nuclear power industry workers exposed to low levels of ionizing radiation do not appear to have an increased risk of having a liveborn child with a congenital anomaly (Green et al, 1997).
b) Offspring of men and women occupationally exposed to low-level ionizing radiation were studied to determine any increased risk of congenital malformations. No evidence of a link between exposure before conception and increased risk of adverse reproductive outcome was noted in men (n=11,697) or women (n=1903) (Doyle et al, 2000).

K) ANIMAL STUDIES

1) Many similar effects in the offspring have been produced in laboratory animals, such as low birth weight and behavioral changes including hyperactivity (Norton, 1986). In experimental animal studies, induction of structural malformations has been seen, but these are lacking in exposed humans (Mole, 1987).
2) MICE: Fetal Swiss albino mice had different effects from a single 0.5 gray (Gy) dose of gamma radiation given at different times of gestation. Dosing during the preimplantation period increased prenatal mortality. Exposure between days 2 and 4 produced increased resorptions. Dosing between days 9 and 13 resulted in small heads, low brain weight, and microphthalmia (Devi & Baskar, 1996).
3) MICE: Prenatal exposure to ionizing radiation produced an increased risk of cancer and reproductive defects in mice. Female mice exposed to 1.0 and 2.7 gray (Gy) of Cf(252) and Co(60) in utero had an increased incidence of tumors of the pituitary gland, mammary gland, liver, and lung for up to two years; as well as dysfunctional ovaries (Nitta et al, 1992).
4) MICE: Maternal-mediated neonatal and developmental toxicity developed in mouse pups after maternal intake of cesium in drinking water (Messiha, 1994).

3.20.3)

A) FETAL RISK

1) Fetal risk is noted at exposures above 10 rem. In early pregnancy, fetal death may occur. Later in pregnancy, radiation exposure may be teratogenic or may cause fetal growth retardation (Medical Response Subcommittee of the National Health Physics Society Homeland Security Committee, 2009).

B) PATERNAL PRECONCEPTIONAL IRRADIATION STILLBIRTHS

1) In one study, stillbirths were reported among offspring of male radiation workers (paternal preconceptional irradiation) at a nuclear reprocessing plant. A point estimate range of 0 to 31.9 (95% confidence limits) stillbirths (n=130) was calculated. These estimates are stated to be qualitatively consistent with animal models (Parker et al, 1999). However, in a letter from another researcher who quantitatively compared animal studies to the radiation workers at the nuclear reprocessing plant, a point estimate of 0.1 stillbirth caused by paternal preconceptional irradiation is suggested (Selby, 2000).

C) SPONTANEOUS ABORTION

1) Increased incidences of spontaneous abortions and toxicosis of pregnancy have been seen following maternal radiation exposure, especially in women affected by the Chernobyl incident (Lieberman et al, 1990).

D) OTHER

1) Commercial and military flight crew members have exposure to cosmic radiation greater than that of the general public, which may be of concern during pregnancy (Geeze, 1998).

E) LACK OF EFFECT

1) The reproductive risk from therapeutic doses of I-131 are low: in 3 studies there were no excess malformations, stillbirths, or early deaths (Dottorini, 1996).

3.20.4)

A) BREAST MILK

1) Cesium has been shown to penetrate the human placenta and be present in breast milk in mothers following exposures (Messiha, 1994).

3.20.5)

A) SPERM PRODUCTION

1) At exposures less than 5 to 10 rads, effects on male reproduction are not well understood. X-rays at doses as low as 15 rads can temporarily depress sperm production. At doses of 50 rads, there is temporary elimination of sperm production, and at doses of 236 to 365 rads, damage to sperm production can persist for months. Exposure to greater than 400 rads can cause complete and permanent damage to sperm production.

B) IMPAIRED SEXUAL FUNCTION

1) Of twelve men with chronic radiation dermatitis after the Chernobyl incident, all had impaired sexual function including impotence, aspermia, azoospermia, abnormal sperm shapes, decreased plasma testosterone levels, increased follicle stimulating hormone (FSH) levels, and decreased luteinizing hormone (LH) levels (Birioukov et al, 1993).

C) REPRODUCTION EFFECTS

1) Female reproduction can be affected by ionizing radiation, which alters the viability of ova and can disrupt the function of the endocrine system which produces female sex hormones. Human oocytes may be more resistant to ionizing radiation than those of laboratory animals.

Carcinogenicity

3.21.2)

3.21.3)

A) RISK OF FUTURE CANCER

1) The risk of future fatal cancer is estimated as being approximately 4% per 100 rem of radiation absorbed. Therefore, a dose of 5 rems increases the risk by about 0.2% and a dose of 25 rems increases the risk by about 1%. The risk of a hereditary disorder per rem approximates 10% of the fatal cancer risk (Medical Response Subcommittee of the National Health Physics Society Homeland Security Committee, 2009). The risk of a hereditary disorder to a population that received high doses of radiation is approximately 0.4% per 100 rem or 4% per Sv (Medical Response Subcommittee of the National Health Physics Society Homeland Security Committee, 2009).
2) The increase in risk of childhood cancers is approximately 0.6% per 10 rem exposure (Medical Response Subcommittee of the National Health Physics Society Homeland Security Committee, 2009).

B) RISK OF CANCER FROM PRENATAL EXPOSURE