淄博市主要建筑材料所致室内γ辐射水平与管理

目的：加强对建筑材料的放射卫生管理。方法：测定不同建筑材料建造的房屋室内γ辐射水平。结果：室内γ辐射水平按建材依次为煤矸石砖＞半煤矸石砖＞土砖＞混凝土板块。结论：室内γ辐射水平决定于建筑材料，要严格对建筑材料进行监督管理。     

煤矸石砖γ辐射水平简易测量方法的探讨

目的　探索建筑材料γ辐射水平简易的测量评价方法。方法　选择煤矸石砖 ,按标准测量要求质量厚度 ( >15 0g/cm2 )与传统堆放高度 ( 16 0cm)对比测量。结果　砖标准测量厚度与砖垛顶部测量的结果比较 ,差异无显著性 (P >0 .0 5 )。结论　测量砖垛顶部的γ辐射水平可代表标准质量厚度的γ辐射水平。     

建筑材料花岗岩γ射线剂量率调查研究

花岗岩是从地亮开来后只经形状加工而成的产品，含有较高的辐射物［’］，如果用它作室内装修，会人为地增加室内的辐射水平，到一定高度时，给居民健康带来一定影响【’］。为此，我们对本市115间有花岗岩的住宅进行Y射线剂量率的检测调查，结果分析如下：l材料与方法1．l对象选择近代建造的钢筋混凝土框架结构，用砖（不包括煤渣砖，下同）砌墙的楼房（从首层到顶层都有，有楼群式住宅，也有独立式别墅住宅）中，选取有花岗岩的住宅共】匕间，在有花岗岩处取点检测，并在上述每一间住宅内没有花岗岩的地方作空白对照。l．2检测方法采用北…     

2016—2018年内蒙古自治区辐射环境水平分析

目的 为核与辐射安全监管和辐射环境保护工作提供科学依据,确保公众健康和辐射环境安全。方法 通过现场监测、实验室分析等方法,对2016—2018年内蒙古自治区辖区内陆地γ辐射空气吸收剂量率、地表水、土壤、生物样品中放射性水平进行监测。结果 陆地γ辐射空气吸收剂量率、地表水、土壤样品中放射性水平均处于1983—1990年内蒙古自治区环境天然放射性水平范围内。结论 2016—2018年内蒙古自治区辐射环境质量总体良好,处于本底涨落范围内,建议逐渐增加辐射环境质量监测点位,覆盖至旗县一级,并强化各级辐射环境监测机构人员、设备及专业技术培训。     

巴中市室外γ辐射水平调查及其相关因素分析

目的 了解巴中市室外γ辐射剂量水平,探索室外地表γ辐射剂量率相关因素。方法 按照《环境地表γ辐射剂量率测定规范》（GB/T14583—1993）布点和检测,使用RStudio 1.2.5033软件进行统计分析,多组均数的比较使用单因素方差分析,相关因素分析使用多重线性回归。结果 本次调查对巴中市辖区432个点的室外地表γ辐射剂量率进行巡测。巴中市室外地表γ辐射剂量率均值为113.04nGy/h,室外天然γ辐射所致居民人均年有效剂量当量为0.14mSv。不同县区、不同地点类型室外地表γ辐射剂量率分析结果显示巴州区（120.72nGy/h）、平昌县（119.65nGy/h）和通江县（121.45nGy/h）地表γ辐射剂量率均值高于南江县（98.08nGy/h）和恩阳区（103.74nGy/h）,一般道路γ辐射剂量率均值（115.57nGy/h）大于荒地（109.98nGy/h）。多重线性回归结果显示室外地表γ辐射剂量率可能的相关因素有县区和道路类型。结论 巴中市室外地表γ辐射属于正常本底水平。     

甲状腺癌131I清甲治疗病房环境辐射安全性探讨

目的 监测大剂量131I治疗后病房及病区内环境γ射线的辐射剂量率水平,评价医疗活动过程的辐射安全性,明确大剂量131I治疗后对环境的影响.方法 分别用γ辐射仪测量的17次患者治疗后24 h病房内距离患者1 m处及病区环境的γ辐射剂量率水平.结果 γ辐射仪测得的病房内距离患者1 m处γ辐射剂量率水平最大为21.71 μSv/h,根据我国〈电离辐射防护与辐射源安全基本标准〉计算,笔者所在科室工作人员每日可在此辐射环境下工作3.8小时;病区环境中走廊剂量率水平最大为0.58μSv/h,计算得一般公众每日可在此辐射环境下停留7.17小时.结论 实施大剂量131I治疗后,采取恰当防护措施,完全能保证核医学科工作者处于电离辐射容许剂量范围之内,病区环境电离辐射水平相对安全.     

广西糖厂放射源应用辐射环境影响监测与评价

目的 掌握广西辖区内糖厂密封放射源的使用分布情况,评价密封放射源对周围环境、职业人员、公众成员产生的辐射影响,为今后糖厂放射源的使用管理提供科学依据。方法 按监测规范合理布点,利用γ辐射剂量率仪对广西区内所有使用密封放射源的糖厂开展辐射环境现场测量,根据监测结果进行估算,并结合个人剂量监测结果进行分析。结果 密封放射源使用场所周围辐射剂量率高于环境本底水平,职业人员、公众成员会受到一定的辐射剂量。结论 职业人员及公众成员年有效剂量结果符合相关要求。     

某公司放射线作业现场调查

对某公司生产中的放射线装置、放射源进行了现场调查，为射线作业场所卫生防护提供依据。用辐射剂量仪和热释光剂量方法（TLD）分别检测放射线作业现场的剂量率和累积剂量。结果表明，室外探伤多数情况下作业人员操作及躲避处的辐射剂量率在5-30цGy/h，室内探伤操作室内辐射水平接近本底值，基本符合工业探伤放射卫生防护标准；核子计车间的距源容器表面1m左右处的辐射剂量率多数在2цGy/h以下，个别仪表超过2.5Gy/h。提示，该公司探伤作业场所及放置核子计车间的事射剂量率水平基本符合国家有关规定，应注意薄弱环节，加强防护。     

苏南某煤电厂环境γ辐射水平调查

目的了解苏南某煤电厂环境γ辐射水平。方法于2009年7月用BH3103B型便携式χ-γ剂量率仪对厂区室内外的环境陆地γ辐射剂量率进行监测。结果室内外的陆地γ辐射剂量率水平按测点平均分别为119.4 nGy/h和103.4 nGy/h。厂区室内外陆地γ外照射对人体产生的年有效剂量为0.72 mSv/a。结论厂区γ外照射的年有效剂量偏高,主要原因是室外的陆地γ辐射剂量率较高。     

福清核电站运行前环境γ辐射水平及所致居民剂量估算

目的 调查福清核电站运行前环境地表γ辐射剂量率及其所致居民暴露剂量。方法 按照《环境地表γ辐射剂量率测定规范》(GB/T 14583-1993)和《辐射环境监测技术规范》(HJ/T 61-2001)的要求,用GPS全球定位器确定监测点位置,选择17个监测点作为调查区,用Radalert 100 Nuclear放射性检测仪测量环境γ辐射空气吸收剂量率,估算居民暴露剂量。结果 核电站周围17个监测点的环境地表γ辐射空气吸收剂量率居室内变化范围为96~238nGy/h,平均值为191 nGy/h,居室外变化范围为73~177 nGy/h,平均值为144 nGy/h,由环境辐射外照射致福清市居民人均年有效剂量为1113.6 μSv,集体年有效剂量为1375.1 man·Sv。结论 福清核电站周围地表γ辐射空气吸收剂量率水平属于福建省正常环境放射性本底水平。     

Role of DNA double-strand break repair genes in cell proliferation under low dose-rate irradiation conditions

Radiation-induced DNA double-stand breaks (DSBs) lead to numerous biological effects. To elucidate the molecular mechanisms involved in cellular responses to low dose and low dose-rate radiation, it is informative to clarify the roles of DSB repair related genes. In higher vertebrate cells, there are at least two major DSB repair pathways, namely non-homologous end-joining (NHEJ) and homologous recombination (HR). Here, it is shown that in chicken DT40 cells irradiated with gamma-rays at a low dose-rate (2.4 cGy/day), the growth delay in NHEJ-related KU70- and PRKDC (encoding DNA-PKcs)-defective cells were remarkably higher than in cells defective for the HR-related RAD51B and RAD54 genes. DNA-PKcs- defective human M059J cells also showed an obvious growth delay when compared to control M059K cells. RAD54(-/-)KU70(-/-) cells demonstrated their highest degree of growth delay after an X-irradiation with a high dose-rate of 0.9 Gy/min. However they showed a lower degree of growth delay than that seen in KU70(-/-) and PRKDC(-/-/-) cells exposed to low dose-rate irradiation. These findings indicate that cellular responses to low dose-rate radiation are remarkably different from those to high dose-rate radiation. The fact that both DT40 and mammalian NHEJ-defective cells were highly sensitive to low dose-rate radiation, provide a foundation for the concept that NHEJ-related factors may be useful as molecular markers to predict the sensitivity of humans to low dose-rate radiation.     

放射性核素内照射诱发大鼠脾淋巴细胞的HPRT基因突变

目的探讨克隆法研究放射性核素内照射诱发大鼠脾淋巴细胞HPRT基因突变的可行性。方法大鼠尾静脉注入晚期混合裂变产物,克隆法检测不同累积剂量和不同剂量率的内照射诱发的脾淋巴细胞HPRT基因突变,拟合剂量-效应方程。结果随着累积剂量和剂量率的增加,HPRT基因突变频率随之上升,剂量-效应关系和剂量率-效应关系均符合线性平方模型,分别为：y=4．5060 0．5635D 0．0606D^2,y=2、6638 0．5177D-0．0008D^2。结论克隆法是一种敏感的检测辐射诱发HPRT基因突变的方法,脾淋巴细胞的HPRT基因突变对辐射敏感。     

Spatial and temporal distribution of energy

Studies of the spatial and temporal distribution of microscopic radiation doses lead to potentially important questions regarding conventional approaches to radiation protection. The short ranges of alpha-particle and Auger-electron emissions from radionuclides lead to uncertainties in assessing their hazards. The conventional extrapolations from intermediate doses to low doses and dose rates are questioned by observed dose-rate effects in the so-called "initial slope," by the total lack of data for single tracks in cells and by the possibility of multiple-cell effects. At all subcellular levels, even down to DNA, high linear-energy-transfer (LET) radiations can produce unique initial damage, different from that possible with low-LET radiations, and therefore may even, in principle, produce unique final biological effects. This questions simple extrapolations from low- to high-LET radiations and the application of universal quality factors to diverse effects. Further understanding of these questions could lead, in future, to substantial increases or decreases in estimations of risk.     

Effects of single-pulse (< or = 1 ps) X-rays from laser-produced plasmas on mammalian cells

The effects of low linear energy transfer (LET) radiation on mammalian cells have been studied at dose-rates as high as 10(9) Gy/sec delivered as a single 3-nanosecond pulse, and no increase in cytotoxicity was shown compared with delivery at a conventional dose-rate. There have been no observations on the effects of radiation delivered at even higher dose-rates on the picosecond time-scale. Here we examined, for the first time, the effects on cultured mouse L5178Y cells and its radiosensitive XRCC4-deficient mutant M10 cells of sub-picosecond X-rays emitted from laser-produced plasmas at the ultrahigh dose-rate of 10(12)-10(13) Gy/sec. No increase in the sensitivity to the X-rays was observed compared with gamma-rays at a conventional dose-rate. The increase in the sensitivity of L5178Y cells by labeling with 5-iododeoxyuridine was smaller than those irradiated with gamma-rays at a conventional dose-rate, while the difference was apparently the reverse in M10 cells. The D10 ratio between L5178Y cells and M10 cells produced by the X-rays at temporally dense ionization was the same as that produced by X(gamma)-rays at the conventional dose-rate, while the ratio is greatly reduced in the case of particle radiation. These results suggest that there is no increase in the cytotoxic effects of X-rays at dose-rates as high as 10(13) Gy/sec, and that the increased cytotoxicity of particle radiation is not attributable to temporally dense ionization. It is discussed that the mechanism for the induction of radiation damage responsible for cytotoxicity may be slightly modified at ultrahigh dose-rates.     

Checking the foundation: recent radiobiology and the linear no-threshold theory

The linear no-threshold (LNT) theory has been adopted as the foundation of radiation protection standards and risk estimation for several decades. The "microdosimetric argument" has been offered in support of the LNT theory. This argument postulates that energy is deposited in critical cellular targets by radiation in a linear fashion across all doses down to zero, and that this in turn implies a linear relationship between dose and biological effect across all doses. This paper examines whether the microdosimetric argument holds at the lowest levels of biological organization following low dose, low dose-rate exposures to ionizing radiation. The assumptions of the microdosimetric argument are evaluated in light of recent radiobiological studies on radiation damage in biological molecules and cellular and tissue level responses to radiation damage. There is strong evidence that radiation initially deposits energy in biological molecules (e.g., DNA) in a linear fashion, and that this energy deposition results in various forms of prompt DNA damage that may be produced in a pattern that is distinct from endogenous (e.g., oxidative) damage. However, a large and rapidly growing body of radiobiological evidence indicates that cell and tissue level responses to this damage, particularly at low doses and/or dose-rates, are nonlinear and may exhibit thresholds. To the extent that responses observed at lower levels of biological organization in vitro are predictive of carcinogenesis observed in vivo, this evidence directly contradicts the assumptions upon which the microdosimetric argument is based.     

Vanguards of paradigm shift in radiation biology: radiation-induced adaptive and bystander responses

The risks of exposure to low dose ionizing radiation (below 100 mSv) are estimated by extrapolating from data obtained after exposure to high dose radiation, using a linear no-threshold model (LNT model). However, the validity of using this dose-response model is controversial because evidence accumulated over the past decade has indicated that living organisms, including humans, respond differently to low dose/low dose-rate radiation than they do to high dose/high dose-rate radiation. In other words, there are accumulated findings which cannot be explained by the classical "target theory" of radiation biology. The radioadaptive response, radiation-induced bystander effects, low-dose radio-hypersensitivity, and genomic instability are specifically observed in response to low dose/low dose-rate radiation, and the mechanisms underlying these responses often involve biochemical/molecular signals that respond to targeted and non-targeted events. Recently, correlations between the radioadaptive and bystander responses have been increasingly reported. The present review focuses on the latter two phenomena by summarizing observations supporting their existence, and discussing the linkage between them from the aspect of production of reactive oxygen and nitrogen species.     

Diminished or inversed dose-rate effect on clonogenic ability in Ku-deficient rodent cells

The biological effects of ionizing radiation, especially those of sparsely ionizing radiations like X-ray and γ-ray, are generally reduced as the dose rate is reduced. This phenomenon is known as ‘the dose-rate effect’. The dose-rate effect is considered to be due to the repair of DNA damage during irradiation but the precise mechanisms for the dose-rate effect remain to be clarified. Ku70, Ku86 and DNA-dependent protein kinase catalytic subunit (DNA-PKcs) are thought to comprise the sensor for DNA double-strand break (DSB) repair through non-homologous end joining (NHEJ). In this study, we measured the clonogenic ability of Ku70-, Ku86- or DNA-PKcs-deficient rodent cells, in parallel with respective control cells, in response to high dose-rate (HDR) and low dose-rate (LDR) γ-ray radiation (~0.9 and ~1 mGy/min, respectively). Control cells and murine embryonic fibroblasts (MEF) from a severe combined immunodeficiency (scid) mouse, which is DNA-PKcs-deficient, showed higher cell survival after LDR irradiation than after HDR irradiation at the same dose. On the other hand, MEF from Ku70^−/− mice exhibited lower clonogenic cell survival after LDR irradiation than after HDR irradiation. XR-V15B and xrs-5 cells, which are Ku86-deficient, exhibited mostly identical clonogenic cell survival after LDR and HDR irradiation. Thus, the dose-rate effect in terms of clonogenic cell survival is diminished or even inversed in Ku-deficient rodent cells. These observations indicate the involvement of Ku in the dose-rate effect.     

Leukemia mortality among radiation-exposed workers

The qualitative leukemogenicity of ionizing radiation was firmly established by studies of medical workers and patients exposed to high radiation levels in the mid-1900s. Quantitative relationships were evaluated through extensive studies of atomic bomb survivors and patients who received therapeutic radiation, for whom the duration of exposure was brief. Although many studies have been conducted of nuclear workers and others exposed occupationally, uncertainty remains about quantitative aspects of the leukemia-radiation exposure relation for low dose-rate, fractionated exposures. Some studies have shown dose-related increases in leukemia risks for certain nuclear workers in the U.S. and Europe, although these findings are inconsistent across populations. Despite limitations in low-dose epidemiology, well-designed studies among nuclear workers should inform some controversial aspects of the relation between ionizing radiation exposure and leukemia risk.     

Radiation cancer risk at different dose rates: new dose-rate effectiveness factors derived from revised A-bomb radiation dosimetry data and non-tumor doses

The dose rate of atomic bomb (A-bomb) radiation to the survivors has still remained unclear, although the dose–response data of A-bomb cancers has been taken as a standard in estimating the cancer risk of radiation and the dose and dose-rate effectiveness factor (DDREF). Since the applicability of the currently used DDREF of 2 derived from A-bomb data is limited in a narrow dose-rate range, 0.25-75 Gy/min as estimated from analysis of DS86 dosimetry data in the present study, a non-tumor dose (D_nt) was applied in an attempt to gain a more universal dose-rate effectiveness factor (DREF), where D_nt is an empirical parameter defined as the highest dose at which no statistically significant tumor increase is observed above the control level and its magnitude depends on the dose rate. The new DREF values were expressed as a function of the dose rate at four exposure categories, i.e. partial body low LET, whole body low linear energy transfer (LET), partial body high LET and whole body high LET and provided a value of 14 for environmental level radiation at a dose rate of 10⁻⁹ Gy/min for whole body low LET.