Human Exposure to Radioactivity From Tobacco Smoke: Systematic Review.

INTRODUCTION: Tobacco has been known to contain radioactive polonium and lead for 50 years but the literature is divided as to the public health significance. I review the data on tobacco radioactivity and its internalization by smokers. METHODS: Data sources: Reports of lead-210 and polonium-210 content of tobacco leaf, cigarettes, cigarette smoke, and human respiratory tissues, published between 1964 and September 2017. Study selection: Any identified study that reported values for lead-210 and polonium-210 content. Data extraction: Data quality was addressed by comparative review of analytic methods. RESULTS: The data about radiation content of tobacco and smoke are robust. Early reports suggesting microsievert lifetime doses of inhaled radioactivity to smokers were not borne out. The results remain sensitive to pharmacological assumptions around absorption and redistribution of inhaled radionuclides, and radiobiological assumptions about interaction with human tissues. CONCLUSIONS: Literature on tobacco radioactivity has not fully contended with pharmacological and radiobiological uncertainty, and is therefore divided as to health significance. This does much to explain regulatory inaction over the last half century. Before radiation safety law can offer a vehicle for tobacco control, more must be learnt about the pharmacology and radiobiology of inhaled radionuclides in tobacco smoke. IMPLICATIONS: This work makes it apparent that the study of tobacco smoke radioactivity has been scientifically stagnant for the last 40 years. The field cannot advance until we improve understanding of the pharmacology and radiobiology of inhaled radionuclides in tobacco smoke. Despite this, a subset of contemporary authors is still suggesting individual health risks about 1000 times higher than can be supported by internationally accepted models.

A study on the effect of the internal exposure to (210)Po on the excretion of urinary proteins in rats.

This study was designed to assess the feasibility of a noninvasive urine specimen for the detection of proteins as indicators of internal exposure to ionizing radiation. Three groups of rats (five in each group) were intravenously injected with 1601 ± 376, 10,846 ± 591 and 48,467 ± 2812 Bq of (210)Po in citrate form. A sham-exposed control group of five rats was intravenously injected with sterile physiological saline. Daily urine samples were collected over 4 days following injection. Purification and pre-concentration of urinary proteins were carried out by ultrafiltration using a 3000 Da molecular weight cutoff membrane filter. The concentration of common urinary proteins, namely albumin, alpha-1-acid glycoprotein, immunoglobulins IgA and IgG, was measured by an enzyme-linked immunosorbent assay. Urinary excretion of albumin decreased dose-dependently (p < 0.05) 96 h post-injection relative to the control group. In contrast, no statistically significant effects were observed for other proteins tested. The dose-dependent decrease in urinary excretion of albumin observed in this study underscores the need for further research, which may lead to the discovery of new biomarkers that would reflect the changes in the primary target organs for deposition of (210)Po.

Mortality among mound workers exposed to polonium-210 and other sources of radiation, 1944-1979.

Polonium-210 is a naturally occurring radioactive element that decays by emitting an alpha particle. It is in the air we breathe and also a component of tobacco smoke. Polonium-210 is used as an anti-static device in printing presses and gained widespread notoriety in 2006 after the poisoning and subsequent death of a Russian citizen in London. More is known about the lethal effects of polonium-210 at high doses than about late effects from low doses. Cancer mortality was examined among 7,270 workers at the Mound nuclear facility near Dayton, OH where polonium-210 was used (1944-1972) in combination with beryllium as a source of neutrons for triggering nuclear weapons. Other exposures included external gamma radiation and to a lesser extent plutonium-238, tritium and neutrons. Vital status and cause of death was determined through 2009. Standardized mortality ratios (SMRs) were computed for comparisons with the general population. Lifetime occupational doses from all places of employment were sought and incorporated into the analysis. Over 200,000 urine samples were analyzed to estimate radiation doses to body organs from polonium and other internally deposited radionuclides. Cox proportional hazards models were used to evaluate dose-response relationships for specific organs and tissues. Vital status was determined for 98.7% of the workers of which 3,681 had died compared with 4,073.9 expected (SMR 0.90; 95% CI 0.88-0.93). The mean dose from external radiation was 26.1 mSv (maximum 939.1 mSv) and the mean lung dose from external and internal radiation combined was 100.1 mSv (maximum 17.5 Sv). Among the 4,977 radiation workers, all cancers taken together (SMR 0.86; 95% CI 0.79-0.93), lung cancer (SMR 0.85; 95% CI 0.74-0.98), and other types of cancer were not significantly elevated. Cox regression analysis revealed a significant positive dose-response trend for esophageal cancer [relative risk (RR) and 95% confidence interval at 100 mSv of 1.54 (1.15-2.07)] and a negative dose-response trend for liver cancer [RR (95% CI) at 100 mSv of 0.55 (0.23-1.32)]. For lung cancer the RR at 100 mSv was 1.00 (95% CI 0.97-1.04) and for all leukemias other than chronic lymphocytic leukemia (CLL) it was 1.04 (95% CI 0.63-1.71). There was no evidence that heart disease was associated with exposures [RR at 100 mSv of 1.06 (0.95-1.18)]. Assuming a relative biological effectiveness factor of either 10 or 20 for polonium and plutonium alpha particle emissions had little effect on the dose-response analyses. Polonium was the largest contributor to lung dose, and a relative risk of 1.04 for lung cancer at 100 mSv could be excluded with 95% confidence. A dose related increase in cancer of the esophagus was consistent with a radiation etiology but based on small numbers. A dose-related decrease in liver cancer suggests the presence of other modifying factors of risk and adds caution to interpretations. The absence of a detectable increase in total cancer deaths and lung cancer in particular associated with occupational exposures to polonium (mean lung dose 159.8 mSv), and to plutonium to a lesser extent (mean lung dose 13.7 mSv), is noteworthy but based on small numbers. Larger combined studies of U.S. workers are needed to clarify radiation risks following prolonged exposures and radionuclide intakes.

Cigarette smoke radioactivity and lung cancer risk.

INTRODUCTION: To determine the tobacco industry's policy and action with respect to radioactive polonium 210 ((210)Po) in cigarette smoke and to assess the long-term risk of lung cancer caused by alpha particle deposits in the lungs of regular smokers. METHODS: Analysis of major tobacco industries' internal secret documents on cigarette radioactivity made available online by the Master Settlement Agreement in 1998. RESULTS: The documents show that the industry was well aware of the presence of a radioactive substance in tobacco as early as 1959. Furthermore, the industry was not only cognizant of the potential "cancerous growth" in the lungs of regular smokers but also did quantitative radiobiological calculations to estimate the long-term (25 years) lung radiation absorption dose (rad) of ionizing alpha particles emitted from the cigarette smoke. Our own calculations of lung rad of alpha particles match closely the rad estimated by the industry. According to the Environmental Protection Agency, the industry's and our estimate of long-term lung rad of alpha particles causes 120-138 lung cancer deaths per year per 1,000 regular smokers. Acid wash was discovered in 1980 to be highly effectively in removing (210)Po from the tobacco leaves; however, the industry avoided its use for concerns that acid media would ionize nicotine converting it into a poorly absorbable form into the brain of smokers thus depriving them of the much sought after instant "nicotine kick" sensation. CONCLUSIONS: The evidence of lung cancer risk caused by cigarette smoke radioactivity is compelling enough to warrant its removal.

Room model based Monte Carlo simulation study of the relationship between the airborne dose rate and the surface-deposited radon progeny.

The quantitative relationships between radon gas concentration, the surface-deposited activities of various radon progeny, the airborne radon progeny dose rate, and various residential environmental factors were investigated through a Monte Carlo simulation study based on the extended Jacobi room model. Airborne dose rates were calculated from the unattached and attached potential alpha-energy concentrations (PAECs) using two dosimetric models. Surface-deposited (218)Po and (214)Po were significantly correlated with radon concentration, PAECs, and airborne dose rate (p-values <0.0001) in both non-smoking and smoking environments. However, in non-smoking environments, the deposited radon progeny were not highly correlated to the attached PAEC. In multiple linear regression analysis, natural logarithm transformation was performed for airborne dose rate as a dependent variable, as well as for radon and deposited (218)Po and (214)Po as predictors. In non-smoking environments, after adjusting for the effect of radon, deposited (214)Po was a significant positive predictor for one dose model (RR 1.46, 95% CI 1.27-1.67), while deposited (218)Po was a negative predictor for the other dose model (RR 0.90, 95% CI 0.83-0.98). In smoking environments, after adjusting for radon and room size, deposited (218)Po was a significant positive predictor for one dose model (RR 1.10, 95% CI 1.02-1.19), while a significant negative predictor for the other model (RR 0.90, 95% CI 0.85-0.95). After adjusting for radon and deposited (218)Po, significant increases of 1.14 (95% CI 1.03-1.27) and 1.13 (95% CI 1.05-1.22) in the mean dose rates were found for large room sizes relative to small room sizes in the different dose models.

Biokinetic and dosimetric modelling in the estimation of radiation risks from internal emitters.

The International Commission on Radiological Protection (ICRP) has developed biokinetic and dosimetric models that enable the calculation of organ and tissue doses for a wide range of radionuclides. These are used to calculate equivalent and effective dose coefficients (dose in Sv Bq(-1) intake), considering occupational and environmental exposures. Dose coefficients have also been given for a range of radiopharmaceuticals used in diagnostic medicine. Using equivalent and effective dose, exposures from external sources and from different radionuclides can be summed for comparison with dose limits, constraints and reference levels that relate to risks from whole-body radiation exposure. Risk estimates are derived largely from follow-up studies of the survivors of the atomic bombings at Hiroshima and Nagasaki in 1945. New dose coefficients will be required following the publication in 2007 of new ICRP recommendations. ICRP biokinetic and dosimetric models are subject to continuing review and improvement, although it is arguable that the degree of sophistication of some of the most recent models is greater than required for the calculation of effective dose to a reference person for the purposes of regulatory control. However, the models are also used in the calculation of best estimates of doses and risks to individuals, in epidemiological studies and to determine probability of cancer causation. Models are then adjusted to best fit the characteristics of the individuals and population under consideration. For example, doses resulting from massive discharges of strontium-90 and other radionuclides to the Techa River from the Russian Mayak plutonium plant in the early years of its operation are being estimated using models adapted to take account of measurements on local residents and other population-specific data. Best estimates of doses to haemopoietic bone marrow, in utero and postnatally, are being used in epidemiological studies of radiation-induced leukaemia. Radon-222 is the one internal emitter for which control of exposure is based on direct information on cancer risks, with extensive information available on lung cancer induction by radon progeny in mines and consistent data on risks in homes. The dose per unit (222)Rn exposure can be calculated by comparing lung cancer risk estimates derived for (222)Rn exposure and for external exposure of the Japanese survivors. Remarkably similar values are obtained by this method and by calculations using the ICRP model of the respiratory tract, providing good support for model assumptions. Other informative comparisons with risks from external exposure can be made for Thorotrast-induced liver cancer and leukaemia, and radium-induced bone cancer. The bone-seeking alpha emitters, plutonium-239 and radium isotopes, are poorer leukaemogens than predicted by models. ICRP dose coefficients are published as single values without consideration of uncertainties. However, it is clear that full consideration of uncertainties is appropriate when considering best estimates of doses and risks to individuals or specific population groups. An understanding of the component uncertainties in the calculation of dose coefficients can be seen as an important goal and should help inform judgements on the control of exposures. The routine consideration of uncertainties in dose assessments, if achievable, would be of questionable value when doses are generally maintained at small fractions of limits.

Waking a sleeping giant: the tobacco industry's response to the polonium-210 issue.

The major tobacco manufacturers discovered that polonium was part of tobacco and tobacco smoke more than 40 years ago and attempted, but failed, to remove this radioactive substance from their products. Internal tobacco industry documents reveal that the companies suppressed publication of their own internal research to avoid heightening the public's awareness of radioactivity in cigarettes. Tobacco companies continue to minimize their knowledge about polonium-210 in cigarettes in smoking and health litigation. Cigarette packs should carry a radiation-exposure warning label.

Suspected radioactive contamination: evaluation of 45 Israeli citizens potentially exposed to polonium-210 in London.

The lethal poisoning of Alexander Litvinenco with the radioactive element polonium-210, and the risk that many civilians (including Israeli citizens) who were in the same location in London at the same time were exposed to radiation, was an unprecedented event in the western world. This was only the second known death due to 210Po, a natural alpha radiation-emitting element. A task team was created to handle the event. The team comprised representatives from the Ministry of Health's advisory committee for radiological events (which includes the Israel Defense Force, the Israeli Atomic Energy Commission and the Ministry of Environmental Protection), the Public Health Services Central District, and a public relations expert. Forty-seven people were located and underwent an epidemiological inquiry, and urine samples for detection of 210Po were sent abroad to a specialized laboratory. The radiotoxicological results were analyzed and evaluated by the expert team and follow-up recommendations were made. This unfamiliar and potentially stressful scenario was handled successfully by a multi-organizational multidisciplinary task team. The joint work of the task team was a real-life "exercise" simulating a radiological event in Israel. This team has recommended further evaluation of various vital missions in the event of any possible future radiological event, with special emphasis on a proactive communication approach to the media and the public.

Internal dose assessment of 210Po using biokinetic modeling and urinary excretion measurement.

The mysterious death of Mr. Alexander Litvinenko who was most possibly poisoned by Polonium-210 ((210)Po) in November 2006 in London attracted the attention of the public to the kinetics, dosimetry and the risk of this high radiotoxic isotope in the human body. In the present paper, the urinary excretion of seven persons who were possibly exposed to traces of (210)Po was monitored. The values measured in the GSF Radioanalytical Laboratory are in the range of natural background concentration. To assess the effective dose received by those persons, the time-dependence of the organ equivalent dose and the effective dose after acute ingestion and inhalation of (210)Po were calculated using the biokinetic model for polonium (Po) recommended by the International Commission on Radiological Protection (ICRP) and the one recently published by Leggett and Eckerman (L&E). The daily urinary excretion to effective dose conversion factors for ingestion and inhalation were evaluated based on the ICRP and L&E models for members of the public. The ingestion (inhalation) effective dose per unit intake integrated over one day is 1.7 x 10(-8) (1.4 x 10(-7)) Sv Bq(-1), 2.0 x 10(-7) (9.6 x 10(-7)) Sv Bq(-1) over 10 days, 5.2 x 10(-7) (2.0 x 10(-6)) Sv Bq(-1) over 30 days and 1.0 x 10(-6) (3.0 x 10(-6)) Sv Bq(-1) over 100 days. The daily urinary excretions after acute ingestion (inhalation) of 1 Bq of (210)Po are 1.1 x 10(-3) (1.0 x 10(-4)) on day 1, 2.0 x 10(-3) (1.9 x 10(-4)) on day 10, 1.3 x 10(-3) (1.7 x 10(-4)) on day 30 and 3.6 x 10(-4) (8.3 x 10(-5)) Bq d(-1) on day 100, respectively. The resulting committed effective doses range from 2.1 x 10(-3) to 1.7 x 10(-2) mSv by an assumption of ingestion and from 5.5 x 10(-2) to 4.5 x 10(-1) mSv by inhalation. For the case of Mr. Litvinenko, the mean organ absorbed dose as a function of time was calculated using both the above stated models. The red bone marrow, the kidneys and the liver were considered as the critical organs. Assuming a value of lethal absorbed dose of 5 Gy to the bone marrow, 6 Gy to the kidneys and 8 Gy to the liver, the amount of (210)Po which Mr. Litvinenko might have ingested is therefore estimated to range from 27 to 1,408 MBq, i.e 0.2-8.5 microg, depending on the modality of intake and on different assumptions about blood absorption.

[Polonium: the radioactive killer from tobacco smoke]. / Poloniul: ucigasul radioactiv din fumul de tutun.

Among all carcinogenic substances contained in tobacco smoke, Polonium 210 (Po-210), with a half-life of 138 days, is one of the most dangerous, by exerting a devastating, chronic, slow and progressive carcinogenesis activity. The main source of Po-210 in tobacco is represented by fertilizers (polyphosphates) containing radium-226 (Ra-222) which decades to plumb 210 (Pb-210). Through the thricomes Pb-210 is concentrated in the tobacco leaves, where it turns to Po-210, which at the cigarette combustion temperature (800-900 degrees C) reaches the gaseous state and it is absorbed by the micro particles released into tobacco smoke. Thus, smoke becomes radioactive in both its gaseous and corpuscular components and reaches the airways, where, particularly at the branches level and together with other substances, it exerts its carcinogenic activity, especially in those subjects with impaired respiratory mucosal clearance. The carcinogenic risk/one year lifetime of a smoker of 20 cigarettes per day is equivalent to that of undertaking 300 chest x-rays. It is calculated that Po-210 may be independently responsible of 4 lung cancers every 10,000 smokers. During cigarette's combustion, tobacco smoke is also released in the air, contributing to serious health risks for those exposed to passive smoke.

Relative biological effectiveness (RBE) of 210Po alpha-particles versus X-rays on lethality in bovine endothelial cells.

PURPOSE: Alpha-radiation from polonium-210 ((210)Po) can elevate background radiation dose by an order of magnitude in people consuming large quantities of meat and seafood, particularly caribou and reindeer. Because up to 50% of the ingested (210)Po body burden is initially found in the blood, a primary target for the short range alpha-particles is the endothelial cells lining the blood vessels. This study examined the relative biological effectiveness (RBE) of (210)Po alpha-particles versus 250 kVp X-rays in producing injury to cultured bovine aortic endothelial cells. MATERIALS AND METHODS: Radiation effects on cells were measured in four different ways: the percentage viable cells by trypan blue dye exclusion, the number of live cells, the lactate dehydrogenase (LDH) release to medium and the ability to form colonies (clonogenic survival). RESULTS: Comparison of dose-response curves yielded RBE values of 13.1+/-2.5 (SEM) for cell viability, 10.3+/-1.0 for live cell number and 11.1+/-3.0 for LDH activity. The RBE values for clonogenic survival were 14.0+/-1.0 based on the ratio of the initial slopes of the dose-response curves and 13.1, 9.9 and 7.7 for 50, 10 and 1% survival rate, respectively. At X-ray doses <0.25 Gy, a pronounced stimulatory effect on proliferation was noted. CONCLUSIONS: Exposure to (210)Po alpha-particles was seven to 14 times more effective than X-ray exposure in causing endothelial cell damage.

Trace metals and 210Po (210Pb) concentrations in mussels (Mytilus galloprovincialis) consumed at western Anatolia.

The mussels (Mytilus galloprovincialis) have been evaluated for their bioavailability as biomonitors of trace and toxic elements in coastal water of western Anatolia. The levels of Fe, Cu, Zn, Pb, Br and Sr in the edible part of mussels were determined using X-ray fluorescence method during the period of September 1999-July 2000. Distribution of 210Po and 210Pb activities were measured by radiometric methods and their ratios were calculated. The activity concentrations of 210Po and 210Pb were found to vary between 52 +/- 6-1,344 +/- 108 and 6 +/- 2-167 +/- 10 Bqkg(-1) dry wt, respectively. The highest values for 210Po and 210Pb were measured in Foca mussels and also observed the highest Fe, Zn and Br concentrations in the same species. 210Po/210Pb activity ratio were derived as between 3.1 and 25.0.

Effects of wind and electric fields on 218Po deposition from the atmosphere.

PURPOSE: To estimate, under atmospheric conditions, 218Po deposition on a sphere representing the human head and compare with the effects of the maximum electric field to be found under a transmission line. METHOD: The effect of the wind in the absence of electric fields was calculated using the Reynolds Analogy between heat and mass transfer. The effect of the electric field was shown to be large compared with that of turbulence. A 'capture radius' due to the field was then estimated and charged 218Po particles blown into this region were assumed to be captured. RESULTS: The deposition ratio was proportional to gammaV0.4E0(0.67), where gamma = charged fraction of 218Po, V = velocity and E0 = surface electric field. With the charged fraction ranging from 0.9% to 3.2%, a surface field on 280 kV m(-1) and a wind speed of 3 m s(-1), the deposition ratio ranged from 3.4 to 9.3. The surface field is several orders of magnitude higher than the average personal exposures that have been measured in epidemiological studies and the effect does not appear to be of epidemiological significance. At low velocities, the predictions of this model are in agreement with the measurements of Henshaw et al. CONCLUSIONS: 218Po deposition by environmental AC fields cannot be advanced as an explanation for the reported associations between childhood leukaemia and electrical installations.

Cancer risk in relation to radioactivity in tobacco.

Leaf tobacco contains minute amounts of lead 210 (210Pb) and polonium 210 (210Po), both of which are radioactive carcinogens and both of which can be found in smoke from burning tobacco. Tobacco smoke also contains carcinogens that are nonradioactive. People who inhale tobacco smoke are exposed to higher concentrations of radioactivity than nonsmokers. Deposits of 210Pb and alpha particle-emitting 210Po form in the lungs of smokers, generating localized radiation doses far greater than the radiation exposures humans experience from natural sources. This radiation exposure, delivered to sensitive tissues for long periods of time, may induce cancer both alone and synergistically with nonradioactive carcinogens. This article explores the relationship between the radioactive and nonradioactive carcinogens in leaf tobacco and tobacco smoke and the risk of cancer in those who inhale tobacco smoke.