天津市氡辐射状况与肺癌发病率的关系

目的　探讨地质断裂带及非断裂带之间氡辐射状况与肺癌发病率的关系。方法　采取单纯随机抽样的方法 ,对 6 9户断裂带及 135户非断裂带居民居室内氡及子体的浓度进行了测定 ,并应用单因素方差分析和 t-检验分析其与天津市肺癌发病率的关系。结果　断裂带肺癌发病率明显高于非断裂带 ,t=10 .85 ,P<0 .0 1;且断裂带与非断裂带居民居室内氡及子体的浓度比较 ,差异有显著性 ,t=2 7.0 9,P<0 .0 1。结论　肺癌发病率与居民居室内氡及子体的浓度有相关性。     

非铀矿山氡与矿工肺癌关系的探讨

氡及其子体是一种职业危害因素,关于氡及其子体的危害国内外已有报道。1984～1986年我们对本地区十三个非铀矿矿井氡及其子体浓度与1970～1984年的矿工肺癌发病情况进行了调查。结果发现:     

浙江省室内外氡和氡子体水平及所致居民剂量的研究

测量全省11个地区217个居室和83个室外点结果X为16.4和11.6。Bg/m~3,Xg为13.4和9.7BgXg;335个后室和165个室外点的氡子体的X为41.7×10~(-9)和32.6×10~(-9)J/m~3,Xg为32.s×10~(-9)和25.7×10~(-9)J/m~3。室内外氡子体平衡团子的X为0.46和0.49。室内外氡子体所致测区范围居民平均年有效剂量当量为0.636mSv,其中室内所致的占172％。对全省可归因于室内外氡子体所致居民肺癌死亡数进行了探讨。室内氡和氡子体对居民健康影响的问题,愈来愈引起人们的关注。为了解本省室内外氡和氡子体水平及其特点,我们对全省各地区住宅室内外空气中氡和氡子体浓度进行了调查,并估算了所致居民剂量当量。     

影响室内氡的因素

影响室内氡的因素苏州医学院张友九天然辐射的５０％以上来源于氢及其子体（１）。氡及其子体的照射不但大大增加了矿工的肺癌发生率（２）（３），而且也是导致居民肺癌发生的主要原因之一（４）。美国环保局认为８～２５％的肺癌来源于氡的照射（５）。因此，环境中的氡...     

某输水隧洞作业人员氡累积暴露量与致肺癌关系的初步研究

目的通过测算某输水隧洞作业人员氡子体的累积暴露量,探讨氡引起的职业照射水平与致肺癌的关系。方法分别采用氡和氡子体测量仪器,对现场关注点的氡及其子体水平进行了测量,采用被动式累积探测器对隧洞内氡、钍射气浓度水平进行了检测及数据分析。结果隧洞内关注点氡及平衡氡浓度分布呈现了凌晨高于午后的特点,初步分析了隧洞中氡及钍射气来源,氡子体总暴露量约为49.7 WLM,估算有效剂量约为497 mSv。结论从氡及其子体暴露的个案角度分析,在较短的时间内,作业人员接受氡及其子体暴露量的迅速增加。考虑到同时处于恶劣的隧洞施工条件下(单向掘进通风不良,生产性粉尘暴露量高,隧洞内未采用防氡、降氡措施,引水隧洞内气溶胶水平居高不下等),高氡子体暴露和生产性粉尘(游离SiO_2和ThO_2)对职业性肺癌可能具有协同作用,亟需开展职业性肺癌危害的进一步研究。     

氡及其子体的辐射效应和对居民的健康影响

目的 评价居室内氡及其子体的辐射效应和对居民的健康影响。方法 观察和检测吸入较高浓度氡及其子体时雄性大鼠的辐射效应。结果 吸入氡及其子体累积剂量达50 mSv时会使血淋巴细胞转化能力降低,DNA合成受到抑制,累积剂量达150 mSv时会出现骨髓PEC细胞微核率和肺细胞周期进程的明显变化,其远期效应是肺癌。结论 居室内氡及其子体浓度处于天然本底水平,因此对居民的健康危害很小,一般不会发生确定性效应,随机效应的发生率也很低。     

氡及其子体监测方法简介

氡是广泛存在的天然辐射源。有关氡及其子体对人的危害是近几十年才逐渐被认识并广泛深入地开展研究的。从流行病学调查表明,吸入氡及其子体造成的辐射危害,不但大大地增加了铀矿工肺癌发生率,而且也是居民肺癌发生的有关原因之一,尤其当前一些国家为了节能,采用房屋密闭并减少了通风率,致使室     

氡及其子体的健康危害效应

地下矿工的队列研究和室内氡暴露的病例对照研究都证明氡及其子体是肺癌发生的危险因子,动物实验也证实了这样的危险增加。近年来地下矿工和室内氡暴露与肺癌关系的合并分析更有力地说明肺癌危险与氡及其子体暴露的相关性。氡致肺癌的细胞和分子机制的研究,包括抑癌基因和癌基因,以及常用的生物标志物或生物剂量计,如染色体畸变、红细胞血红糖蛋白A(GPA)、次黄嘌呤鸟嘌呤磷酸核糖转移酶基因(HPRT)的研究,有助于阐明氡致肺癌的机制,提出氡暴露危险评估的细胞和分子生物学依据。同时,进入呼吸道的氡的三分之一左右能进入血液分布至全身、血液和骨髓可能是肺之外氡及其子体作用的另一个靶器官,氡诱发白血病的危险也值得关注。     

氡暴露致肿瘤的研究进展

氡是一种分布广泛的惰性气体,在衰变过程中放出α、β、γ粒子后,衰变为氡子体,氡及氡子体对人类有明显的致癌效应,尤其氡在致肺癌和白血病方面日益受到人们的重视。对氡及其子体对人类辐射危害的研究成果进行综述。     

谈谈氡子体的危害及其防护

矿工吸入氡子体可诱发肺癌的结论,已为国内外多数研究者所公认。提高对吸入氡子体的辐射危害的认识,加强辐射防护和监测管理,是放射卫生及矿山劳动保护的当务之急。现围绕氡子体的危害及其防护措施,介绍国内外有关的资料。 一、矿井氡子体的水平与来源 据联合国原子辐射效应科学委员会(UNSC-EAR)于1982年报道,假如平衡因子为0.7,非     

Age-dependent lung doses from ingested 222Rn in drinking water

The U.S. Environmental Protection Agency currently is considering regulatory standards limiting the concentration of 222Rn in public drinking water supplies. As part of this effort, a criteria document has been prepared detailing the health risks expected to occur from the presence of 222Rn in water used in homes. The present report examines the dose equivalent delivered to lung tissue following direct ingestion of 222Rn in water. Irradiation from both in-situ decay of 222Rn in lung tissue and the decay of 222Rn in lung air passages following exhalation are examined and results presented for ages from neonate through adult. These results indicate that the risk of lung cancer from inhalation of airborne progeny following emanation of 222Rn from water into home air is significantly greater than the risk from both irradiation pathways considered in ingestion at all ages.     

Expected indoor 222Rn levels in counties with very high and very low lung cancer rates

Counties in the U.S. with high lung cancer rates should have higher average 222Rn levels than counties with low lung cancer rates, assuming the average 222Rn level in a county is not correlated with other factors that cause lung cancer. The magnitude of this effect was calculated, using the absolute risk model, the relative risk model, and an intermediate model, for females who died in 1950-1969. The results were similar for all three models. We concluded that, ignoring migration, the average Rn level in the highest lung cancer counties should be about three times higher than in the lowest lung cancer counties according to the theory. Preliminary data are presented indicating that the situation is quite the opposite: The average Rn level in the highest lung cancer counties was only about one-half that in the lowest lung cancer counties.     

A Bayesian analysis or scientific judgment of uncertainties in estimating risk due to 222Rn in U.S. public drinking water supplies

The elements which contribute to the range of values or uncertainties for the lifetime risk and dose equivalent due to 222Rn in U.S. public drinking water supplies are estimated and discussed here. From imperfect scientific knowledge, reasonable upper and lower bounds are placed on these estimates through the use of a semiquantitative Bayesian approach to uncertainty analysis. The factors considered are: occurrence of 222Rn in drinking water, indoor air 222Rn concentrations as a function of drinking water concentration, equilibrium state of the progeny, fraction of daughter products attached to aerosol particles, anatomical and dosimetric variables, epidemiological studies and choice of latency period, plateau period and effects of age. For Rn in U.S. public drinking water supplies, it is estimated that the best estimate for the lifetime lung cancer risk factor is 5 X 10(-9) excess cases of lung cancer per becquerel of Rn per m3 of water (2 X 10(-7) excess cases of lung cancer per picocurie of Rn per liter of water), with an estimated range between 2 X 10(-9) and 2 X 10(-8) excess cases per becquerel of Rn per m3 of water (5 X 10(-8) and 7 X 10(-7) excess cases per picocurie of Rn per liter). The best estimate of the lifetime population risk due to 222Rn in U.S. public drinking water supplies is estimated to be 6,000 excess lung cancers, with a reasonable range of 1,000 to 30,000.     

Interaction of alpha particles with bronchial cells

The alpha-activity on the bronchial airways has been calculated for 222Rn daughter exposures producing observable excess bronchogenic lung cancer in underground miners. The activity distribution of aerosol particles with attached 222Rn daughters on the bronchial tree is truly diffuse because of the short half-life of the daughters and the large number of particles in the ambient aerosol. From the bronchial airway activity and the minor epidemiology, it can be shown that it requires, on average, 4 X 10(9) stem cells in bronchial epithelium to be hit in order to produce an observed lung cancer. For very high 222Rn daughter exposures of miners, multiply hit cells are highly probable; yet the lung cancer response is lower per unit exposure at high exposures than for mining exposures--near those sustained in the environment probably due to stem cell death. A knowledge of the number of multiply hit cells in miners permits some infererences to be made about the effectiveness of particulate versus diffusely distributed alpha emitters in the lung, namely, that particulates should not be significantly more effective in lung cancer induction than a diffuse distribution.     

Lung cancer risk at low doses of alpha particles

A survey of inhabitant exposures arising from the inhalation of 222Rn and 220Rn progeny, and lung cancer mortality has been carried out in two adjacent areas in Guangdong Province, People's Republic of China, designated as the "high background" and the "control" area. Annual exposure rates are 0.38 working level months (WLM) per year in the high background, and 0.16 WLM/yr in the control area. In 14 yr of continuous study, from 1970 to 1983, age-adjusted mortality rates were found to be 2.7 per 10(5) living persons of all ages in the high background area, and 2.9 per 10(5) living persons in the control area. From this data, we conclude that we are unable to determine excess lung cancers over the normal fluctuations below a cumulative exposure of 15 WLM. This conclusion is supported by lung cancer mortality data from Austrian and Finnish high-background areas. A theoretical analysis of epidemiological data on human lung cancer incidence from inhaled 222Rn and 220Rn progeny, which takes into account cell killing as competitive with malignant transformation, leads to the evaluation of a risk factor which is either a linear-exponential or a quadratic-exponential function of the alpha-particle dose. Animal lung cancer data and theoretical considerations can be supplied to support either hypothesis. Thus we conclude that at our current stage of knowledge both the linear-exponential and the quadratic-exponential extrapolation to low doses seem to be equally acceptable for Rn-induced lung cancer risk, possibly suggesting a linear-quadratic transformation function with an exponential cell-killing term, or the influence of risk-modifying factors such as repair or proliferation stimuli.     

Environmental radon daughter alpha dose factors in a five-lobed human lung

The alpha dose from 222Rn daughters per unit exposure (rad per WLM or rad per year per pCi 222Rn/m3) to basal cells in bronchial epithelium in a five-lobed human male lung is calculated. These factors are then derived for women, children and infants by scaling the dimensions of the male lung. The 222Rn daughter characteristics chosen are those typical of environmental atmospheres. Both active and resting breathing patterns are utilized in the calculations to yield the overall dose per unit exposure in typical population exposures.     

Design issues in epidemiologic studies of indoor exposure to Rn and risk of lung cancer

Recent data on indoor air quality have indicated that Rn (222Rn) and its decay products are frequently present in domestic environments. Since studies of Rn-exposed miners have established that Rn decay products are a lung carcinogen, their presence in indoor air raises concerns about an increase in lung cancer risk for the general population. To directly evaluate lung cancer risk from domestic exposure to Rn and its decay products, as well as to evaluate risk assessments derived from studies of Rn-exposed underground miners, several epidemiologic studies of indoor Rn exposure have been initiated or are planned. This paper calculates sample sizes required for a hypothetical case-control study to address several important hypotheses and shows the impact of several difficult problems associated with estimating a subject's Rn exposure. We consider the effects of subject mobility, choice of the exposure response trend which is used to characterize an alternative hypothesis, and errors in the estimation of exposure. Imprecise estimation of Rn exposure arises from errors in the measurement device, exposure to Rn decay products from sources outside the home, inability to measure exposures over time in current as well as previous residences, and the unknown relationship between measured concentration and lung dose of alpha energy from the decay of Rn and its progeny. These methodological problems can result in large discrepancies between computed and actual study power. Failure to anticipate these problems in the design of a study can result in inaccurate estimates of power. We conclude that case-control studies of indoor Rn and lung cancer may require substantial numbers of subjects in order to address the many questions of importance that burden current risk assessments with uncertainty. We suggest pooling data from studies with the largest numbers of cases and with the most precise estimates of Rn exposure as the best approach for meeting present research needs.     

Radon-222 concentrations and decay-product equilibrium in dwellings and in the open air

Results are presented of measurements of the activity concentrations of 222Rn and its short-lived decay products and the 212Pb/212Bi concentrations in more than 200 dwellings in West Germany and in the open air. For more than 130 measurements of the equilibrium factor F in dwellings the median value was found to be 0.3. Measurements of F in the open air under various conditions resulted in a mean value of about 0.4. The results of the investigations showed that indoors F depends only slightly on ventilation, indoor 222Rn concentration and other parameters. The equilibrium factor F in the open air, however, was found to depend on meteorological conditions. Empirical correlations from the data obtained for the daughter/222Rn concentration ratios were derived to provide relations for the prediction of the individual daughter product concentrations at a measured 222Rn level. It was established that the daughter/222Rn concentration ratios for indoor air do not change within the range of 222Rn concentrations investigated (1-370 Bq X m-3). These relations, however, are not valid for the daughter/222Rn concentration ratios in outdoor air. The correlations derived further suggest that the individual daughter product concentrations may be assessed with sufficient accuracy by only measuring the 222Rn concentrations. Thus the daughter ratios obtained in this way should enable good estimates of the lung dose for members of the public due to inhalation of the short-lived 222Rn daughters and the dose contribution of the individual 222Rn-daughter products.     

Relationship of 220Rn and 222Rn progeny levels in Canadian underground U mines

Radon-222 and 220Rn progeny are found in some Canadian underground U mines. Because both can contribute to lung dose, their experimental determinations are important. The relationship between 222Rn progeny Working Level [WL(Rn)] and 220Rn progeny Working Level [WL(Tn)] has been investigated in U mines. Experimental measurements extended from 1981 to 1986 and consisted of about 700 measurements of each WL(Rn) and WL(Tn). The data were analyzed by standard linear and power-function regression analysis. A power-function relationship between WL(Rn) and WL(Tn) seemed to fit the experimental data best. The relationship obtained permits the calculation of WL(Tn) from experimental values of WL(Rn). The relationship is useful for lung-dose-calculation purposes and in mine-ventilation-engineering calculations.     

A simple two-count method for routine monitoring of 222Rn and 220Rn progeny working levels in U mines

In the case of U mines containing Th, the total alpha energy will contain contributions from both 222Rn progeny and 220Rn progeny. A simple routine grab sampling monitoring scheme is therefore needed for separate measurement of the working levels of 222Rn and 220Rn progeny. The scheme presented here is based on a short delay period after sampling (2 min) for 222Rn progeny and a long delay period (340 min) before counting 220Rn progeny. An advantage of this scheme is that no corrections need to be made to the 222Rn progeny working level for the presence of 220Rn progeny. Such corrections must be made in the commonly used Kusnetz scheme.