“…The importance of understanding the biological consequences of high-LET radiation is clear, given the scope of human IR exposure as a terrestrial environmental hazard, cosmic radiation, as well as in cancer treatment ( Darby et al, 2005 ; Krewski et al, 2005 ; Cucinotta et al, 2006 ; Mohamad et al, 2017 ; Gaskin et al, 2018 ; Nelson, Andersson, and Wuest 2021 ; Pearson et al, 2021 ). In this review, we have summarized the current understanding of lesions generated by high-LET IR exposure, how the cell repairs them in a chromatinized context, and the consequences of persistent or misrepaired damage.…”
Section: Discussionmentioning
confidence: 99%
“…The terms “damage” and “lesions” will hereafter refer specifically to damage caused to DNA. The most potentially deleterious form of damage induced by IR is the DNA double strand break (DSB) (reviewed in Pearson et al, 2021 ). For 1 Gy of photon IR exposure, human G 0 /G 1 phase cells accumulate roughly 20 DSBs, which increases to around 40 DSBs in G 2 phase as there is twice as much DNA present ( Asaithamby and Chen 2011 ; Bee et al, 2013 ).…”
Exposure to environmental ionizing radiation is prevalent, with greatest lifetime doses typically from high Linear Energy Transfer (high-LET) alpha particles via the radioactive decay of radon gas in indoor air. Particle radiation is highly genotoxic, inducing DNA damage including oxidative base lesions and DNA double strand breaks. Due to the ionization density of high-LET radiation, the consequent damage is highly clustered wherein ≥2 distinct DNA lesions occur within 1–2 helical turns of one another. These multiply-damaged sites are difficult for eukaryotic cells to resolve either quickly or accurately, resulting in the persistence of DNA damage and/or the accumulation of mutations at a greater rate per absorbed dose, relative to lower LET radiation types. The proximity of the same and different types of DNA lesions to one another is challenging for DNA repair processes, with diverse pathways often confounding or interplaying with one another in complex ways. In this context, understanding the state of the higher order chromatin compaction and arrangements is essential, as it influences the density of damage produced by high-LET radiation and regulates the recruitment and activity of DNA repair factors. This review will summarize the latest research exploring the processes by which clustered DNA damage sites are induced, detected, and repaired in the context of chromatin.
“…The importance of understanding the biological consequences of high-LET radiation is clear, given the scope of human IR exposure as a terrestrial environmental hazard, cosmic radiation, as well as in cancer treatment ( Darby et al, 2005 ; Krewski et al, 2005 ; Cucinotta et al, 2006 ; Mohamad et al, 2017 ; Gaskin et al, 2018 ; Nelson, Andersson, and Wuest 2021 ; Pearson et al, 2021 ). In this review, we have summarized the current understanding of lesions generated by high-LET IR exposure, how the cell repairs them in a chromatinized context, and the consequences of persistent or misrepaired damage.…”
Section: Discussionmentioning
confidence: 99%
“…The terms “damage” and “lesions” will hereafter refer specifically to damage caused to DNA. The most potentially deleterious form of damage induced by IR is the DNA double strand break (DSB) (reviewed in Pearson et al, 2021 ). For 1 Gy of photon IR exposure, human G 0 /G 1 phase cells accumulate roughly 20 DSBs, which increases to around 40 DSBs in G 2 phase as there is twice as much DNA present ( Asaithamby and Chen 2011 ; Bee et al, 2013 ).…”
Exposure to environmental ionizing radiation is prevalent, with greatest lifetime doses typically from high Linear Energy Transfer (high-LET) alpha particles via the radioactive decay of radon gas in indoor air. Particle radiation is highly genotoxic, inducing DNA damage including oxidative base lesions and DNA double strand breaks. Due to the ionization density of high-LET radiation, the consequent damage is highly clustered wherein ≥2 distinct DNA lesions occur within 1–2 helical turns of one another. These multiply-damaged sites are difficult for eukaryotic cells to resolve either quickly or accurately, resulting in the persistence of DNA damage and/or the accumulation of mutations at a greater rate per absorbed dose, relative to lower LET radiation types. The proximity of the same and different types of DNA lesions to one another is challenging for DNA repair processes, with diverse pathways often confounding or interplaying with one another in complex ways. In this context, understanding the state of the higher order chromatin compaction and arrangements is essential, as it influences the density of damage produced by high-LET radiation and regulates the recruitment and activity of DNA repair factors. This review will summarize the latest research exploring the processes by which clustered DNA damage sites are induced, detected, and repaired in the context of chromatin.
“…In North America, residential radon levels have increased over time, with new properties typically being constructed with 72% greater radon levels compared to early to mid twentieth century equivalents [5][6][7][8] . Repeated, long term radon inhalation is a primary cause of lung cancer amongst people who have never smoked tobacco 2,3,5,6,[9][10][11][12][13][14][15] , a disease that is now the 7 th leading cause of cancer-linked death globally 9,[16][17][18][19] . The inhalation of radon and its progeny can increase lung cancer risk as they emit alpha particle radiation within the lungs, which damages lung epithelial cell DNA and thereby increases the risk of cancer-causing mutations 2,[20][21][22][23] .…”
mentioning
confidence: 99%
“…Repeated, long term radon inhalation is a primary cause of lung cancer amongst people who have never smoked tobacco 2,3,5,6,[9][10][11][12][13][14][15] , a disease that is now the 7 th leading cause of cancer-linked death globally 9,[16][17][18][19] . The inhalation of radon and its progeny can increase lung cancer risk as they emit alpha particle radiation within the lungs, which damages lung epithelial cell DNA and thereby increases the risk of cancer-causing mutations 2,[20][21][22][23] . Radioactivity levels from radon in air are measured in Becquerels (Bq) per cubic meter (m 3 ), equal to one alpha particle (radioactive) emission per second per cubic metre of air 2 .…”
mentioning
confidence: 99%
“…The inhalation of radon and its progeny can increase lung cancer risk as they emit alpha particle radiation within the lungs, which damages lung epithelial cell DNA and thereby increases the risk of cancer-causing mutations 2,[20][21][22][23] . Radioactivity levels from radon in air are measured in Becquerels (Bq) per cubic meter (m 3 ), equal to one alpha particle (radioactive) emission per second per cubic metre of air 2 . Calculating the absorbed radiation doses from radon for an individual involves combining a quantitative measure of Bq/m 3 radon levels with so-called 'activity pattern' data, meaning the amount of time per year a person spends within in a given environment, then deriving Sievert (Sv) doses of absorbed energy per mass.…”
The COVID-19 pandemic has produced widespread behaviour changes that shifted how people split their time between different environments, altering health risks. Here, we report an update of North American activity patterns before and after pandemic onset, and implications to radioactive radon gas exposure, a leading cause of lung cancer. We surveyed 4009 Canadian households home to people of varied age, gender, employment, community, and income. Whilst overall time spent indoors remained unchanged, time in primary residence increased from 66.4 to 77% of life (+ 1062 h/y) after pandemic onset, increasing annual radiation doses from residential radon by 19.2% (0.97 mSv/y). Disproportionately greater changes were experienced by younger people in newer urban or suburban properties with more occupants, and/or those employed in managerial, administrative, or professional roles excluding medicine. Microinfluencer-based public health messaging stimulated health-seeking behaviour amongst highly impacted, younger groups by > 50%. This work supports re-evaluating environmental health risks modified by still-changing activity patterns.
Background
The general practice for all radiographic procedures is to use Lead Shielding to optimise radiation dose to the patient. The American Association of Physicists (AAPM) in Medicine in 2019 however, made a recommendation on the use of gonad and foetal shielding. The authors have noticed that very few papers on this topic come from developing countries, hence this study embarked on. The aim of our study was to evaluate internal scatter with Lead and without Lead Shielding in an anthropomorphic phantom during Computed Tomography of the brain, chest, abdomen, and pelvis.
Methods
The methodology was based on examinations of a RANDO phantom brain, chest, abdomen and pelvis on a General Electric Optima 660 scanner; which had a 128-channel multidetector row. Examinations were performed with Lead and without Lead Shielding equivalence of 0.35 mm, and the internal scatter measured using Thermoluminescent Dosimeters. The collected data was analysed descriptively to determine the mean and standard deviation. The T-tests and two-way analysis of variance (ANOVA) were used to compare the means.
Results
The findings of this study revealed that internal scatter was highest closest to the exposed area with higher internal scatter observed for thicker areas of the phantom. Although slightly higher readings were recorded without Pb shielding, a non-statistical significance was observed for all internal scatter measurements regardless of whether Lead Shielding was used or not.
Conclusions
A non-statistical significance for Computed Tomography examinations with and without Lead Shielding in confirmation with the AAPM positional statement.
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