How does plutonium affect the environment

The major type of radiation from Pu Is alpha radiation, which Is assigned a Q value of The International unit 1s the Sv, which equals rem. The number of rads In an organ following a single exposure to a certain amount of C1 of plutonlum deposited 1n that organ Increases with time as the plutonlum remains In that organ and decreases as the plutonlum 1s translocated out of the organ.

The mor- tality rates of the workers were lower than for the standard U. This means that the animal Is chronically exposed to alpha particle radiation, which Is the primary cause of adverse health effects following exposure to Pu.

Since the animals continue to be exposed to alpha radiation throughout their lifetime, these experiments can be considered chronic. The primary health risk from Inhaled "'PuO- 1n animals 1s death from diseases of the respiratory system. The early effects Include flbrosls, which can lead to respiratory failure.

If the animal survives the flbrosls, radiation pneumonltls can develop. A reduction 1n the number of circulating lymphocytes Is also a major effect of Inhaled PuO». Even- tually, lung or bone tumors will develop, which will also lead to early death.

Data on tumors are presented In Section 6. Mean survival was years In the four lower dose. Cause of death was usually radia- tion pneumonltls or lung tumors. No consistent changes were noted In serum chem- istry. The radiation pneumonltls was characterized by focal Interstitial and subpleural flbrosls, Increased numbers of alveolar macrophages, alveolar epithelial hyperplasla and fod of squamous metaplasia.

One month postexposure, lymphopenla occurred 1n dogs at the two highest doses. At the highest dose level, all dogs died from radiation pneumonltls months postexposure. The other dogs are presumably still alive. No bone cancer was observed. The primary cancer effect associated with Inhalation exposure to Pu 1s lung cancer, which was seen 1n the experiments In dogs, monkeys and rats. Exposure to Pu nitrate also Induced bone sarcomas.

These studies were described 1n Section 6. In the Park et al. Cause of death was usually radiation pneumonltls or lung tumors. Incidences of lung tumors 1n dogs reclevlng IADs of 0, 3. The lung tumors were primarily bronchlolar-alveolar carcinomas or adenomas.

Doses In rads were not calculated for Individual animals. The most common tumors were. Of the 35 animals that died, 22 died of primary lung neoplasla. Two dogs with pulmonary carcinomas exposed once to PuO?

Deaths occurred years postexposure. No cancer deaths were found 1n the controls. Other Investigators also found that lung carcinomas are a frequent cause of death In beagles exposed to 2a9Pu aerosols Gullmette et a!. Dagle exposed beagle dogs once to Pu nitrate, resulting In doses of 0, 2, 8, 56, , or nC1 and corresponding to 0, 0.

At the and nC1 levels, the primary cause of death was osteosarcomas occurring months post- exposure In the nC1 group and months postexposure 1n the nCI group. Lung tumors were also seen In these animals. Sanders et al. The IAD was calcu- lated as the sum of the plutonlum In the body and excreta days post- exposure. Control groups were always used, and additional rats were sacrificed for metabolic studies.

The IAD was 9. The low-dose group d. The controls. When the exposure was expressed In rads, the Inci- dence of lung tumors was significantly Increased at doses of , rads to the lung, but tumor Incidences did not occur In a dose-related manner.

The most prevalent tumor types were adenocardnomas, followed by squamous cell carcinomas. Nonpulmonary tumors, especially mammary gland tumors, were seen 1n all groups Including controls.

More adenocarclnomas were observed at lower doses of «»Pu than with 23BPu. Dose-related relationships were found In the Incidence of pulmonary metaplasia and tumors. The most common types of lung tumors were squamous cell carcinomas followed by adenocarclnomas.

Tumors were not found at other sites. Lung tumor Incidences were 0. The long-term lung burdens were equal to 0, 40 and nC1. Survival was longer for the low-dose groups than for the controls, and slightly shorter for the high-dose group.

Adenoma- tous metaplasia occurred 1n control and exposed animals, but lung tumor Incidence did not differ from controls. Similar results were reported by Hobbs et al. Pertinent data regarding the carcinogenic effects of oral exposure to piuton1 urn were not located 1n the available literature cited 1n Appendix A. Other Relevant Information". Numerous reports show that Intra- venous Injections of Pu cause bone cancer In animals.

Representative studies are reviewed below. Beagle dogs given Intravenous Injections of Pu citrate developed osteogenlc sarcomas Jee et al. Dogs receiving 0, 0. Dogs that developed tumors survived an average of years postexposure. These dogs died years postlnjectlon, while the controls lived an average of 13 years.

The average rads before death were and for the two highest groups, respectively. In cultured human dlplold flbroblasts, alpha particles from Pu Induced mutation at the hypoxanthlne-guanlne phosphorlbosyl transferase locus Chen et al. In Intravenous Injection and Inhalation tests, pluton. Increased Incidence of chromosomal aberrations was not observed 1n rhesus monkeys treated by the same routes of exposure.

There was a significant Increase In lymphocytlc chromosomal aberra- tions 1n monkeys exposed to the highest lung burden. Male mice Injected Intravenously with «»Pu citrate Fetal body weights were slightly but statistically significantly reduced at the high dose.

The apparent reduction 1n fetal body weights In groups 2 and 4 were not attributed to treatment. Severely malformed fetuses Involved one litter In group 1 one fetus , one litter In group 6 three fetuses and one litter 1n group 7 one fetus. The Investigators did not attribute the malformations to treatment.

A significantly Increased Incidence of minor skeletal variations was reported In the ribs, sternebrae or fontanelles of fetuses In groups 5, 6 and 7.

Generalized retardation of development was reported 1n group 7. Matlngs occurred 6 days af-ter the low dose was given, and 3, 6 or 12 weeks after the high dose. Fewer mice became pregnant after the 6- or week exposure periods, and this prelmplantatlon loss probably represented oocyte damage. The number of alpha particles emitted by the plutonlum 1s measured 1n C1, and the amount of radiation Imparted to cells 1s measured In rads.

As the plutonlum remains In the tissue, the number of rads 1n the tissue Increases. Since plutonlum can remain In tissues for many years, a single Inhalation exposure provides chronic radiation exposure.

Ep1dem1olog1cal studies and studies of workers exposed to plutonlum have not shown any adverse health effects 1n humans from Pu. Intravenous Injections of Pu citrate led to bone sarcomas In dogs Jee et al. Oral administration Is not associated with adverse health effects, probably because so Uttle 1s absorbed by this route. Mutagenldty tests performed In vivo showed that plutonlum causes chromosomal aberrations Brooks et al. The only evidence of effects on repro- duction and development 1s that Intravenous Injections of plutonlum caused fetal mortality 1n rabbits and mice.

HUMAN Host national and International regulatory and advisory agencies set protective limits for public exposure at mrems. The mrem limit Is a dose equivalent for the weighted mean. The limit concerns man-made radiation only, not background radiation levels or medical exposures. The limit should protect against nonstocastlc effects such as radiation sickness syndrome and effects on unborn children and provide an acceptable risk for stocastlc effects such as cancer and hereditary effects.

It was originally based on effects observed after gamma radiation. The Nuclear Regulatory Commission regulations for cumulative annual dose limits for the general population from nuclear power plant operations Is mrem NRC, The Federal Radiation Protection Guidance Is mrem as an upper limit for exposure of Individual members of the general 'public.

Based on this, the RQ for Pu 1s 0. EPA, a. The radiation protection guidance to Federal agencies for protection against occupational exposure Is 5 rems, or 10 times greater than the general population exposure limits- U. EPA7 b. The occupational DAC for these compounds 1s 0.

EPA, Ihe NRC. EPA, b. Ep1dem1olog1cal studies of humans exposed to Plutonium 1n the workplace showed no Increase In deaths from cancer Crump et al.

The overall mortality rates of workers were lower than for the overall U. Abundant evidence exists to show that dogs Park et al. Most of the studies used. AMADs of 0. For Inhalation of plutonlum nitrate, the more significant health effect 1s from bone tumors Dagle, This may be expected because Inhaled plutonlum nitrate 1s much more easily translocated out of the lungs Into the circulating blood and Into the bones than 1s plutonlum oxide.

Monkeys LaBauve et al. Pertinent' data regarding the carclnogenldty of oral exposure to plutonlum were not located 1n the available literature dted In Appendix A.

Other Routes. Data from mice and dogs Indicate that Pu citrate 1s carcinogenic when administered parenterally. Beagle dogs given d. The number of animals with tumors In these four experiments Increased with Increased exposure to plutonlum.

Height of Evidence. Data from epldemlologlcal studies have not shown any positive relationship between exposure to plutonlum and develop- ment of cancer 1n humans. However, the human studies have design limita- tions that render them Inadequate to definitively refute or demonstrate a carcinogenic effect.

Humans have developed cancers from exposure to other radlonuclldes, such as radium, radon and thorium, and, by analogy, may be expected to develop cancer from exposure to plutonlum. In animals, there 1s abundant evidence that Inhalation of plutonlum causes cancer In rats and dogs. Ionizing radiation of alpha particles produces Intense regions of 1on1zat1on and once the rad1onuc11de Is Ingested or Inhaled this radiation can be emitted within the body. The carcinogenic properties of Ionizing radiation have been extensively reported In detail since the beginning of the 20th century.

This overwhelming body of human epldemlologlcal data for other radlonuclldes and the unchanging physical properties of Ionizing radiation preclude accepting an alternate effect from the alpha particles of plutonlum U. Therefore, by analogy to the structure and activity of other radlonuclldes and Ionizing radiation 1n general, plutonlum can be placed 1n U. Quantitative Risk Estimates. Humans have not been shown to develop cancer from plutonlum by ep1dem1olbg1cal studies, but humans developed cancer from other radlonuclldes such as radon, radium and thorium BEIR, Animals, however, developed lung, bone and liver cancer from Inhaled plutonlum.

The various possible methods -that can be used to estimate cancer risks from plutonlum are as follows: 1. It Is difficult to account, for the differences In Hfespan, since humans will be exposed to the alpha radiation dose from a single exposure to Inhaled plutonlum for a much longer time than laboratory animals.

The shortcomings of this approach are that one cannot develop accurate human exposure equivalents from these data, and the route of exposure Is Irrelevant to environmentally exposed humans. Use data for development of bone cancer 1n humans by analogy to Ingested radium. Data from radium dial painters show that radium causes human bone tumors, and this method of risk assessment for plutonlum was suggested by Rowland Plutonium 1s known to emit a much higher dose of alpha radiation to bone cells than an equal amount of radium.

Using data from Induction of bone cancers In dogs from Injected or Inhaled plutonlum and radium, Muggenburg et al. One of the problems In using this approach 1s that Ingested radon may have a different distribution within the body than Inhaled plutonlum, particularly Pu02, which Is largely retained In the lungs.

Use an analogy to radon from data from miners who developed lung cancer. The shortcoming of this method 1s that the radon gas has different properties 1n the lung than do plutonlum particles. Use an analogy to thorium, as suggested by Hays Thorium, Injected Intravenously Into humans as Thorotrast, accumulates preferentially In the liver and causes liver tumors In humans.

Thus, there may be a risk to humans for developing liver cancer from absorbed 2a»Pu nitrate. One problem with this approach 1s that the Injected Thorotrast was bound to colloids, which were especially well absorbed and retained by the liver.

Also, liver tumors were not observed 1n animals exposed to Pu02 or Pu nitrate. This Is the method of risk assessment most consistent with that used by other International and national agencies. Federal agencies are required to follow this basic radiation protection guidance U. This value Is made with the additional policy that all radiation exposures should be made only with the expectation that benefits will occur and that all exposures should be "as low as reasonably achievable.

One of the problems with this approach 1s that the standard was originally designed to protect workers from adverse health effects associated with x-ray or gamma ray radiation from an external source. It may not be as useful 1n determining risks from an Internally deposited alpha emitter such as plutonlum.

Radiation dose and dose equivalent, expressed In rads and rems,-Indicate "the level of radiation absorbed by bodily tissues. The conver- sions from pC1 to rads need to take Into account the following factors: the Initial amount of radlonucUde 1n the tissue of Interest; biological half-life 1n the tissue; mass of the organ Involved; and the radiological half-life of the nucllde.

The risk factors for «'Pu are 0. These are lifetime risk assessments for lifetime Intake based on year committed dose equivalents.

They are calculated from a modeling scheme that uses the least mean squares method, based on a linear model, rather than the linearized multistage model. For pluton1um, the risk factors assume an Inhala- tion Class of Y clears from the lung over a period of years and an Ingestlon absorption factor of IxlO"4.

Absolute risk projection models were used for bone cancer and leukemia; relative risk projec- tions were used for lung and other cancers. However, the risk factor proposed by the U. EPA of 3. Ep1dem1olog1cal studies of humans exposed to Plutonium In the workplace have shown no adverse health effects or Increased mortality from exposure to this radlonucllde Crump et al.

The mor- tality rates of the workers were lower than those of average U. The early effects Include flbrosls, which can lead to respiratory failure and death. If the animal survives the flbrosls, radiation pneumonltis can develop. Eventually, lung tumors will develop.

Many of the studies attempted to convert the doses from IADs calculated In C1 to rad units, which account for the time that the plutonlum remains 1n the tissues. As discussed previously, 1t would be very difficult to convert the rad doses calculated 1n these animal studies Into rad doses In human lungs.

No acceptable model for Interspedes extrapolation exists. For these two reasons, no RfD for Inhalation exposure to plutonlum has been calculated. Oral Exposure.

Insufficient data are available from which to derive RfD values for oral exposure to plutonlum. Although the Initial lung deposition can be calculated In animals, as well as the absorbed dose In rads, there Is no model to estimate the human equivalent dose from these animal data.

An RQ based on systemic toxlclty 1s not derived. EPA, c. The commonly used units for radiation protection are rad and rem, which Indicate the amount of tissue damage from radiation, or C1, which Indicates the rate of radioactive decay. EPA a set standards measured 1n C1 and based on the Federal Radiation Protection Guidance, which recommends mrem as an upper limit on exposure of Individual members of the general public.

Accordingly, the RQ for 23«pu is 0. No new Information 1s available that would suggest that this RQ should be changed. Cincinnati, OH. Adrlano, D. McLeod and T. Plutonium, curium and other radlonucUde uptake by the rice plant from a naturally weathered, contaminated soil. Soil Sd. Alberts, J. Concentrations of , Pu and Am 1n drinking water and organic fertilizer, Health Phys.

Wahlgren D. Nelson and P. Submlcron particle size and charge characteristics of , Pu In natural waters. Bobula III and D. A comparison of the distribution of Industrially released pluton1um and fallout and pluton1um 1n temperate, northern United States soils.

Andersen, B. Plutonium aerosol particle size distributions In room air. Health Physics. Arthur W. RadlonucUde concentrations In vegetation at a solid radioactive waste disposal area In Southeastern Idaho.

Plutonium Inhalation studies. Mortality In dogs after Inhalation of aa»Pu Balr, H. Wlllard and L. Plutonium Inhalation studies - I. The retention and translocatlon of Inhaled Pu02 particles 1n mice. Health Phys. Ballestra S, M. Theln and R. Distribution of transuranlc nuclldes 1n the coastal ecosystems of the northwestern Mediterranean. Ballou, J. Effects of age and mode of 1ngest1on on absorption of Plutonium.

Biliary plutonlum excretion In the rat. Park and W. On the metabolic equiva- lence on Ingested, Injected and Inhaled 2a9Pu citrate. Beasley, T. Plutonium and amerlclum: Uptake from contaminated sediments by the polychaete Nereis dlverslcolor. Ball, J. Andrews III and J. Hanford derived plutonlum 1n Columbia River sediments. Beechey, C. Green, E. Humphreys and A. Cytonenetlc effects of pluton1um 1n male mice.

Nature London. National Academy Press. Washington, DC. Bly, J. Plutonium concentrations In arthropods at a nuclear facility. Bondlettl E. Oxidation states of plutonlum and plutonlum 1n global fallout. Brooks, A. LaBauve, R. HcClellan and D. Chromo- some aberration frequency In blood lymphocytes of animals with pluton1um lung burdens. ERDA Symp. Dlel and R. The Influence of testlcular mlcroanatomy on the potential genet-lc dose from Internally deposited Pu citrate In Chinese hamster, mouse, and man.

Mewhlnney, H. Redman, R. Gullmette and R. Distribution, retention and ealty cytogenetlc damage In cynomolgus monkeys following Inahalatlon of 23'Pu N D1el, D. B1ce and B. Martinez, Ed. Brown, K. Pluton1um and amerlclum uptake by plants from soil. Buesseler K. Bulman, R. Johnson and A. An examination of new procedures for fractlonatlon of plutonlum and amerlclum bearing sediments.

Total Environ. Bunzl, K. Soil to plant transfer of plutonlum plus pluton1um amerlclum ceslum and strontlum from global fallout In flour and bran from wheat rye barley and oats as obtained by field measurements.

Beasley, D. Zahnle and B. Cycling of fallout plutonlum amerlclum ceslum and natural uranium thorium and lead radlonuclldes 1n Washington continental slope sediments. Chemical file for plutonlum. On-Hne February 28, Cataldo, 0. The role of soil and plant metabolic processes In controlling trace element behavior and b1oava1lab1l1ty to animals. Despite not being confined by external pressure as is required for a nuclear weapon, it will nevertheless heat itself and break whatever confining environment it is in.

Shape is relevant; compact shapes such as spheres are to be avoided. Plutonium could also be used to manufacture radiological weapons. The plutonium isotope Pu is an alpha emitter with a half life of 87 years. These characteristics make it well suited for electrical power generation for devices which must function without direct maintenance for timescales approximating a human life time.

Plutonium was used on the Apollo lunar flight in to power seismic devices and other equipment left on the Moon, and it was also the power supply of the two Voyager supercraft launched in Plutonium can also be used as a fuel in a new generation of fast-breeder nuclear weapons, which burn a mixed oxide MOX fuel consisting of uranium and plutonium.

Trace amounts of plutonium are found naturally in uranium-rich ores. Humans produce most of the existing plutonium, in special nuclear reactors. Besides being naturally present in very small amounts, plutonium may also enter the environment from releases of nuclear reactors, weapons production plants, and research facilities. A major source of plutonium release is nuclear weapons testing.

Annual world production of plutonium is probably in excess of 50 tonnes and there may be more than 1. Plutonium is sometimes described in media reports as the most toxic substance known to man, although there is general agreement among experts in the field that this is incorrect. As of , there has yet to be a single human death officially attributed to plutonium exposure. This chemical separation is called reprocessing. It is important to remember that this classification of plutonium according to grades is somewhat arbitrary.

The ability of countries to build nuclear arsenals from reactor grade plutonium is not just a theoretical construct. It is a proven fact. All grades of plutonium can be used as weapons of radiological warfare which involve weapons that disperse radioactivity without a nuclear explosion.

Posted on July, Last modified April, Download this page as a PDF. Table 1. C Boiling point: deg. Table 2. Chemical properties and hazards of plutonium. Table 3. Humid, elevated temperatures PuO2 readily reacts to form plutonium dioxide Important Plutonium Compounds and their Uses Plutonium combines with oxygen, carbon, and fluorine to form compounds which are used in the nuclear industry, either directly or as intermediates.

Table 4. Formation and Grades of Plutonium Plutonium is formed in both civilian and military reactors from uranium Table 5. Cochran, Thomas B. Arkin, and Milton M. Cambridge, Massachusetts: Ballinger Publishing Company, Notes: Source of neutrons causing added radiation dose to workers in nuclear facilities.

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