Radionuclide injury to the lung.

Dagle, G.E.; Sanders, C.L.

doi:10.1289/ehp.8455129

Cited by 29 publications

(14 citation statements)

References 49 publications

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“…Whether these initial pathological changes lead to any long-term lesions should be investigated in the future. Previous studies investigating the effects of inhaled radioactive plutonium, an α-emitter, showed that rats died with severe pulmonary edema at higher radiation doses, while radiation pneumonitis and emphysema developed at lower doses (Lundgren et al 1981 ; Dagle and Sanders 1984 ; Scott et al 1990 ). In the present study, occasional inflammations were observed in the lung in control group.…”

Section: Discussionmentioning

confidence: 99%

Internal exposure to neutron-activated 56Mn dioxide powder in Wistar rats—Part 2: pathological effects

Shichijo

Fujimoto

Uzbekov

et al. 2017

Radiat Environ Biophys

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To fully understand the radiation effects of the atomic bombing of Hiroshima and Nagasaki among the survivors, radiation from neutron-induced radioisotopes in soil and other materials should be considered in addition to the initial radiation directly received from the bombs. This might be important for evaluating the radiation risks to the people who moved to these cities soon after the detonations and probably inhaled activated radioactive “dust.” Manganese-56 is known to be one of the dominant radioisotopes produced in soil by neutrons. Due to its short physical half-life, 56Mn emits residual radiation during the first hours after explosion. Hence, the biological effects of internal exposure of Wistar rats to 56Mn were investigated in the present study. MnO2 powder was activated by a neutron beam to produce radioactive 56Mn. Rats were divided into four groups: those exposed to 56Mn, to non-radioactive Mn, to 60Co γ rays (2 Gy, whole body), and those not exposed to any additional radiation (control). On days 3, 14, and 60 after exposure, the animals were killed and major organs were dissected and subjected to histopathological analysis. As described in more detail by an accompanying publication, the highest internal radiation dose was observed in the digestive system of the rats, followed by the lungs. It was found that the number of mitotic cells increased in the small intestine on day 3 after 56Mn and 60Co exposure, and this change persisted only in 56Mn-exposed animals. Lung tissue was severely damaged only by exposure to 56Mn, despite a rather low radiation dose (less than 0.1 Gy). These data suggest that internal exposure to 56Mn has a significant biological impact on the lungs and small intestine.

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Section: Discussionmentioning

confidence: 99%

Internal exposure to neutron-activated 56Mn dioxide powder in Wistar rats—Part 2: pathological effects

Shichijo

Fujimoto

Uzbekov

et al. 2017

Radiat Environ Biophys

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“…As a result, researchers have tried for decades to dissect the mechanisms that underlie the initiation and progression of these events in the hope of identifying potential targets for prevention and mitigation, with the majority of this work making use of rodent (mainly murine) models that have been subjected to localized high dose, single exposures followed by tissue analysis of the subsequent molecular, biochemical, and pathologic changes (Rubin et al 1992, Hong et al 2003, Dagle & Sanders 1984, Calveley et al 2010). A consistent finding in such studies has been a chronically dysregulated lung environment, characterized by cyclical “waves” of cytokine expression in the irradiated tissue, principally proinflammatory in nature; these “waves” have been shown to appear at the time of injury, persist through the initiation of pneumonitis and continuing until the appearance of tissue remodeling and fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Effect of total body irradiation on late lung effects: Hidden dangers

Johnston

Manning²,

Hernady

et al. 2011

International Journal of Radiation Biology

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Purpose In our ongoing investigation into the consequences of a radiological terrorism event, we assessed whether a dose range that is believed to be subthreshold for the development of lung endpoints results in late pathological changes and, secondarily, whether those late changes affect the lung’s ability to respond to subsequent challenge. Materials and methods C57BL/6J mice received total body irradiation (0.5-10 Gy) and were followed for 6-18 months after irradiation. At 12 and 15 months, a subset of mice was exposed to a second challenge (aerosolized lipopolysaccharide [LPS]). Results Cytokines shown to be upregulated early (hours) following irradiation (interleukin [IL]6,keratinocyte chemoattractant [KC], IL1B, and IL1R2) demonstrated increases in messenger ribose nucleic acid (mRNA) expression at late time points, beginning at 9 months. Although persistent, dose-dependent increases in T cell counts were seen, no other overt changes in pathophysiology were observed. Nonetheless, animals that were exposed to a secondary challenge at late time points demonstrated an increased inflammatory cell recruitment and persistence in response relative to controls. Conclusions We propose that, following doses that elicit little change in pathophysiology, sub-clinical radiation-induced injury increases the lungs’ susceptibility to a secondary challenge, possibly through a radiation-induced alteration in the immune defense system.

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“…Once inhaled into the lungs, much of the radiation energy will get absorbed by cells, tissues, and organs. The association of radioactive exposure and lung cancer has been well documented in populations exposed to residential radon 14,15 , children in nuclear-contaminated areas 16 , Mayak workers 17,18 , fluorspar miners 19 , and workers in Uranium mines 20,21 , mills 22,23 , or enrichment 24 . The correlation between lung carcinoma and internally deposited radionuclides were reviewed by Bair 25 , Harrison and Stather 26 , Harrison and Muirhrad 27 , and Raabe 28 .…”

Section: Introductionmentioning

confidence: 99%

Radiation Dosimetry of Inhaled Radioactive Aerosols: CFPD and MCNP Transport Simulations of Radionuclides in the Lung

Talaat

Baldez

et al. 2019

Sci Rep

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Despite extensive efforts in studying radioactive aerosols, including the transmission of radionuclides in different chemical matrices throughout the body, the internal organ-specific radiation dose due to inhaled radioactive aerosols has largely relied on experimental deposition data and simplified human phantoms. Computational fluid-particle dynamics (CFPD) has proven to be a reliable tool in characterizing aerosol transport in the upper airways, while Monte Carlo based radiation codes allow accurate simulation of radiation transport. The objective of this study is to numerically assess the radiation dosimetry due to particles decaying in the respiratory tract from environmental radioactive exposures by coupling CFPD with Monte Carlo N-Particle code, version 6 (MCNP6). A physiologically realistic mouth-lung model extending to the bifurcation generation G9 was used to simulate airflow and particle transport within the respiratory tract. Polydisperse aerosols with different distributions were considered, and deposition distribution of the inhaled aerosols on the internal airway walls was quantified. The deposition mapping of radioactive aerosols was then registered to the respiratory tract of an image-based whole-body adult male model (VIP-Man) to simulate radiation transport and energy deposition. computer codes were developed for geometry visualization, spatial normalization, and source card definition in MCNP6. Spatial distributions of internal radiation dosimetry were compared for different radionuclides (131 i, 134,137 cs, 90 Sr-90 Y, 103 Ru and 239,240 Pu) in terms of the radiation fluence, energy deposition density, and dose per decay. Radioactive aerosols arise from various sources such as nuclear accidents, natural decay processes, and the decommissioning of nuclear reactors 1-3. Highly radioactive micro-particles were released to the surrounding environment in the Chernobyl and Fukushima Daiichi accidents 1,4. The aerosol particles released from accidents and natural decay processes may remain suspended in the air for extended periods, be incorporated into soil particles that can reenter the air, or be inhaled by humans or animals. When aerosol particles are inhaled, a fraction of the inhaled particles deposit in the respiratory tract, while the rest is exhaled out 5-9. The deposition fraction is dependent on many parameters such as the geometry of the respiratory airways, the particle size of the inhaled aerosol, and the breathing condition 10,11. Inhaled radioactive aerosols can expose internal organs to radiation for extended periods and may induce a spectrum of functional and morphological changes, such as genetic mutations and carcinogenesis 12,13. Their severity can be related to the absorbed radiation dose in the different specific tissues, which is further related to the number of radioactive particles inhaled, how long they stay, and the type of radiation they emit. Unlike fat and muscles being the main internal defense to external exposures, there is nothing to protect cells and tissues of sus...

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Radionuclide injury to the lung.

Cited by 29 publications

References 49 publications

Internal exposure to neutron-activated 56Mn dioxide powder in Wistar rats—Part 2: pathological effects

Internal exposure to neutron-activated 56Mn dioxide powder in Wistar rats—Part 2: pathological effects

Effect of total body irradiation on late lung effects: Hidden dangers

Radiation Dosimetry of Inhaled Radioactive Aerosols: CFPD and MCNP Transport Simulations of Radionuclides in the Lung

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