Actinides inhalation

LaFuma J, Nenot JC, Morin M, et al. 1974. Respiratory carcinogenesis in rats after inhalation of radioactive aerosols of actinides and lanthanides in various physicochemical forms. In Karbe E, Park JF, eds. Experimental lung cancer Carcinogenesis and bioassays, international symposium. New York Springer, 443-453. 

Muller HL, Taya A, Drosselmeyer E, et al. 1989. Cellular aspects of retention and transport of inhaled soluble and insoluble actinide compounds in the rat lung. Sci Total Environ 83 239-251. 

Stradling GN, Moody JC. 1995. Use of animal studies for assessing intakes of inhaled actinide-bearing dusts. J Radioanal Nucl Chem 197(2) 309-329. 

Preparation and handling of actinides are very difficult, because of their scarcity, radioactivity, toxicity and reactivity. The actinides isotopes are unstable and they transform spontaneously into other elements by a and (3 decay or by fission. The chemical toxicity of the actinides is similar to the toxicity of other heavy elements. The radio toxicity is extremely high giving radiation damage in cells. The safe handling of actinides samples needs hermetically closed containments (glove boxes) maintained under low pressure with respect to the laboratory to avoid the risk of dispersion and inhalation of the particles if a break of containment occurs. 

There are two principal routes by which the actinides can enter the body uptake can occur either via inhalation or by oral uptake as contaminants of food. However, as both routes of uptake require the actinides to cross a variety of cellular barriers it is necessary to be familiar with some of the chemistry of these elements. 

The two principal methods by which actinides may enter the body are inhalation and penetration through wounds. These two routes of entry are of obvious concern to those individuals working in nuclear fuel reprocessing plants. The principal route of entry by which most of the general public is likely to be exposed to the actinides could be expected to be via the food chain. However, Bennett (176) has indicated that inhalation of 239>(i) 240Pii is more important by a factor of 1000 compared to the uptake by ingestion in contributing to the body burden. 

Inhaled actinides deposit in the lung as a function of the size of the particle or size of the droplet of actinide salt solution. In the case of larger inhaled particles and... 

Because of their physiological property of concentrating primarily in bone and the low penetrating power of the a particle, internal deposition from ingestion and inhalation intakes are the most important exposure modes to man. Most of the actinides show low water solubilities and consequently drinking water typically will not dominate over diet with respect to ingestion. 

Modeling Conclusions. This exercise indicates that Th and U span the interface between the case where inhalation appears to dominate in the contribution of actinides in bone, and the case where ingestion is the more important pathway. The reasons for these differences lie in two important transfers The soil/sedi-ment to organism transfer (as it affects dietary concentrations) and the assimilation from the vertebrate GI tract. While terrestrial-derived foodstuffs dominate our diet, other components of the diet (i.e., aquatic-derived foods) may also make a contribution to intakes. Exceptions to the inhalation case may therefore occur in special populations where certain aquatic foods are consumed in greater amounts, i.e., shellfish (16). 

Figure 3. Enrichment of trivalent actinides over Pu(IV) across biological membranes. The assimilation of Am-241 and Cm-244 from the rat GI tract is greater than for plutonium. When plutonium nitrate is inhaled by dogs, daughter Am-241 is preferentially transported to the liver, resulting in depletion in lung and lymph nodes.

Pu(IV), which forms highly charged polymers, strongly sorbs to soils and sediments. Other actinide III and IV oxidation states also bind by ion exchange to clays. The uptake of these species by solids is in the same sequence as the order of hydrolysis Pu > Am(III) > U(VI) > Np(V). The uptake of these actinides by plants appears to be in the reverse order of hydrolysis Np(V) > U(VI) > Am(III) > Pu(IV), with plants showing little ability to assimilate the immobile hydrolyzed species. The further concentration of these species in the food chain with subsequent deposit in humans appears to be minor. Of the 4 tons of plutonium released to the environment in atmospheric testing of nuclear weapons, the total amount fixed in the world population is less than 1 g [of this amount, most (99.9%) was inhaled rather than ingested]. 

Most radioactive particles and vapours, once deposited, are held rather firmly on surfaces, but resuspension does occur. A radioactive particle may be blown off the surface, or, more probably, the fragment of soil or vegetation to which it is attached may become airborne. This occurs most readily where soils and vegetation are dry and friable. Most nuclear bomb tests and experimental dispersions of fissile material have taken place in arid regions, but there is also the possibility of resuspension from agricultural and urban land, as an aftermath of accidental dispersion. This is particularly relevant to plutonium and other actinide elements, which are very toxic, and are absorbed slowly from the lung, but are poorly absorbed from the digestive tract. Inhalation of resuspended activity may be the most important route of human uptake for actinide elements, whereas entry into food chains is critical for fission products such as strontium and caesium. 

The purpose of this paper is to present data on the environmental behavior of selected actinide elements. Environmental chemistry factors that influence the mobility of these elements are discussed. Some of the variability of data on the uptake of actinide elements by plants is explained. The behavior of manmade actinides in a representative aquatic environment is also discussed. Except for general comparisons, exposure of man by the inhalation pathway is not considered in this paper, even though higher exposures are routinely calculated for this pathway relative to the ingestion pathway. 

It is difficult to distinguish between the fraction of contaminant retained on the surface of leaves and the fraction assimilated metabolically into internal tissues of foliage. Such distinction may not be important if only concentration of the element in the food consumed by man or livestock is the important factor. In any case, chronic anthopogenic release of Pu to the atmosphere followed by direct contamination of foliage would lead to the highest levels of Pu in plants. Thus, incorporation of actinides into foods by this pathway followed by ingestion and deposition of Pu in bone and liver of human populations may result in levels of Pu in these organs that approach those derived from inhalation. 

The ingestion toxicity indices of the actinides in the wastes are shown as a function of decay time in Fig. 8.9 [P2]. Because the actinides are nonvolatile and because the wastes are expected to be geologically isolated, ingestion toxicity is probably a more important measure than inhalation toxicity. During the first 600 years the total toxicity index is controlled by the fission products, mainly Sr. It is thereafter controlled by Am and Am, followed by... 

Inhalation of contaminated material or of actinide-compound aerosols and solids forms inhalation exposure). 

In the case of uptake via inhalation and/or wounds, and depending upon the initial chemical form the element(s), the lungs and/or wound site may be designated as a primary deposition site from which the actinide(s) will be transported to a secondary deposition site. 

The contribution of inhalation to the internal doses to the critical group is substantial for radioactive gases and vapours (e.g. radon or tritium oxide) and for radionuclides with low solubility and low mobility in food chains (e.g. actinides and transuranics), especially for persons working in the open air and in dusty conditions. The special case is that of long term residence in areas with elevated concentrations of natural uranium and radium resulting in the emanation of radon. 

The toxicity of the actinide elements which requires an absolute barrier between the experiment and the experimenter is dictated to only a small extent by external radiation hazards. Plutonium-239 is intensely radioactive, emitting 1.4 X 10 a particles per milligram per minute. However, the alpha radiation from plutonium-239 can easily be shielded by even a thin sheet of paper. It is the consequences of ingestion that make plutonium-239 and the other actinide elements such toxic substances. Plutonium-239, inhaled into the lungs as fine particulate matter, is translocated to the bone, and, over a period of time, may give rise to bone neoplasms (cf. Section 14.10). The biological properties of the actinide elements are discussed in more detail in Sections 14.9 and 14.10. 

This paper begins with a review of the behaviour of inhaled actinide aerosols, the affect of physicochemical factors, the bio kinetic model for limg dissolution and absorption and dissolution tests. The paper then presents a technique for doing new solubility measurements adapted from successful published methodologies. The results achieved using a pilot solubility test are then discussed along with proposals for further work. 

Table 1 Competing processes experienced by inhaled actinide aerosols ...

Table 3 indicates how actinide compounds should be assigned to each default absorption type. The parameter is the fraction of actinide absorbed by the gut following clearance from the respiratory tract. The dose per unit intake (DPUI) is for a 5g actinide aerosol inhalation, in gSv Bq. The armual limit on intake (ALI), on inhalation, is the activity (Bq) corresponding to the annual dose limit (20 mSv). For uranium the DPUI increased by a factor of ten between Type F and S materials, but for plutonimn the DPUI... 

Spitz HB, Robinson B. Deposition of plutonium in the lungs of a worker following an accidental inhalation exposure. In Proceedings of the Snowbird Actinide Workshop on Actinides in Man and Animal, October 15-17, 1979, Radiobiology Division. Salt Lake City University of Utah Press, 1981. 

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