To determine the tobacco industry's policy and action with respect to radioactive polonium 210 (210Po) in cigarette smoke and to assess the long-term risk of lung cancer caused by alpha particle deposits in the lungs of regular smokers.
Analysis of major tobacco industries’ internal secret documents on cigarette radioactivity made available online by the Master Settlement Agreement in 1998.
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 210Po 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.
The evidence of lung cancer risk caused by cigarette smoke radioactivity is compelling enough to warrant its removal.
The 1998, court-ordered, Master Settlement Agreement placed much of the internal tobacco industry research findings and correspondences online that had remained secret and inaccessible to the public for over a half a century (Schroeder, 2004; Sloan & Trogdon, 2004). The number of these internal secret documents posted online is constantly increasing and currently more than 13 million documents (more than 70 million pages) are available online. The availability of this novel source of information provided an opportunity to visit the often unappreciated issue of the potential ill-effects of polonium 210 (210Po) present in all commercially available domestic and foreign cigarette brands. In these industry documents, two previous studies have uncovered that cigarette radioactivity was common knowledge as early as 1964 among top executives, who were aware of the potential lung cancer risk of cigarette smoke radioactivity caused by 210Po (Muggli, Ebbert, Robertson, & Hurt, 2008; Rego, 2009). These studies also pointed out that the industry not only failed to act on its knowledge to inform consumers but also adamantly resisted efforts to remove the radionuclide from tobacco leaves and banned any and all publications related to tobacco smoke radioactivity (Muggli et al., 2008; Rego, 2009; 2011). These insightful studies, however, neither provided an explanation of the industry's resistance to remove alpha particles from tobacco leaves with acid treatment nor unveiled the industry's deep knowledge of lung radiation absorption dose (rad) of ionizing alpha particles and the risk of lung cancer in regular smokers. Furthermore, our research shows that the industry knew about tobacco smoke radioactivity even before 1964, the year when Radford and Hunt (1964) reported for the first time, in Science, the discovery of ionizing alpha particle emitting radionuclide 210Po in cigarettes. We were also surprised to discover that the industry's scientists had actually made, as early as the 1960s, quantitative and realistic radiobiological calculations of the long-term rad of ionizing alpha particles and reached the conclusion that the alpha particles in cigarette smoke in promoting “cancerous growth” in the lungs of smokers was “not an unlikely event.”
Here we present and analyze industry documents by focusing on these previously unaddressed issues. Specifically, we show that the industry used misleading statements to obfuscate the hazard of ionizing alpha particles to the lungs of smokers; we then show the industry's own estimates of the long-term (25 years) lung rad of alpha particles in regular smokers, an estimate that corroborates very well with our own calculations of the lung dose of radioactive polonium. We then used lung cancer death rate charts prepared by the U.S. Environmental Protection Agency (EPA) to estimate long-term lung cancer death rates in regular smokers. Finally, we provide an explanation for the industry’s reasons not to use acid wash to eliminate radionuclides from tobacco leaves. It is of historical interest to discover that the first attempt by a U.S. federal agent to regulate tobacco as “radioactive substance” was made in 1959 exactly 50 years before the Tobacco Control Act was finally signed into law by President Obama in 2009 providing for the first time the Food and Drug Administration (FDA) broad authority to regulate tobacco and tobacco harmful constituents hopefully paving the way for the total elimination of alpha particles from tobacco leaves.
Provision of answers to our proposed aims of this research was achieved by searching for the following terms in industry documents: atmospheric fallout, biological effects, bronchial epithelium, calcium phosphate, exudates, hot spots, hot particle, irradiat*, ion-exchange resin, lead and lung cancer, lead 210Pb, lead and hot spots, lead and smoke, polonium 210Po, alpha particles, radioact*, rem (Roentgen Equivalent in Man), relative biological effectiveness (RBE), radium isotopes, radiotracer, strontium, super-phosphate fertilizer, trichomes, uranium, potassium, acid treatment, fertilizer, picocurie or Curie, high phosphate, and Becquerel (Bq). We searched the internal documents of the following tobacco companies Philip Morris, R.J. Reynolds, Lorillard, Brown & Williamson (B&W), The American Tobacco Company, The Tobacco Institute, The Bliley Documents, and The Council for Tobacco Research. All of these documents are now available and accessible in the University of California San Francisco depository, http://legacy.library.ucsf.edu, and the UCSF Tobacco Control Archives, http://www.library.ucsf.edu/tobacco.
Using open literature and industry radiobiological data on 210Po and 210Pb, detailed below in the Results section, we determined lung dose of 210Po in regular smokers. Briefly, we first determined the fraction of 210Po absorbed from smoking cigarettes that becomes deposited preferentially at bronchial bifurcations of the lung. We then converted alpha particle emission to rad in regular smokers over a period of 25 years, taking into account the relatively long retention time of the radionuclide in the lungs of the smokers. We then compared this rad with an equivalent dose absorbed by inhabitants in dwellings infested with alpha particle emitting radon gas to estimate lung cancer risk from lung cancer death charts prepared by the EPA.
In the present paper, we analyzed 27 previously unprocessed documents that shed new light on industry's knowledge, policy, and realistic radiobiological calculations of the increased lung dose of ionizing alpha particles. We then present documents that uncover the true motives of the industry's adamant refusal to remove alpha particles from cigarettes using the method of acid wash, found to be highly effective in removing alpha particles from tobacco leaves.
Sources of Cigarette Radioactivity
Two sources of tobacco radioactivity have been identified—the atmosphere and uptake from contaminated soil. Spread into the atmosphere of Radon 222 (222Rn), an inert but radioactive gas that forms in the soil, gets absorbed by submicron (<0.1 micron) dust particles in the air (i.e., Aitken particles). By means of diffusive deposition, these 222Rn loaded dust particles accumulate in the sticky, resinous, water insoluble, hair-like projections (trichome) on both sides of the tobacco leaves (Martell, 1974, 1983) reaching concentrations that are 10,000 times higher than the overall plant 222Rn concentration (Marmorstein, 1986; Martell, 1974, 1983). Most importantly, these 222Rn particles, with their decay products lead 210 (210Pb) and 210Po form insoluble complexes with the resin in the trichome that resist being washed off by precipitation or during the process of curing of the tobacco leaves (Marmorstein, 1986; Martell, 1974). The second source of tobacco radioactivity is the uptake from soil rich in calcium phosphate fertilizer contaminated with 210Po and 210Pb phosphates (Desideri, Meli, Feduzi, & Roselli, 2007; Hill, 1965; Holtzman & Ilcewicz, 1966; Khater, 2004; Martell, 1974; Papastefanou, 2007; Radford & Hunt, 1964; Savidou, Kehagia, & Eleftheriadis, 2006; Tso, Hallden, & Alexander, 1964; Tso, Harley, & Alexander, 1966). When the tobacco leaves are aged (cured) for as long as 2 years, the 210Pb (half-life of 22.3 years) in the tobacco leaves continues to convert to 210Po (half-life of 138 days) long after the cure period is over (Martell, 1974, 1983). When a cigarette is burnt, it is the 210Po formed from 210Pb decay and 210Pb that get vaporized by combustion and inhaled into the smoker's lungs (Cohen, Eisenbud, & Harley, 1980; Little, Radford, McCombs, & Hunt, 1965).
Cigarette Content of 210Po
We were surprised to discover that the Canadian Department of National Health and Welfare knew of the existence of higher than background levels of radioactivity in tobacco products as early as 1959. The levels of radioactivity were considered so high that the Department's scientist, Dr. Ash, in a “personal and not official” memorandum to Philip Morris dated April 4, 1959 and entitled “Smoke as a radioactive substance” contemplated to regulate tobacco as “Radioactive substance” by invoking the British Factories Act (Ash, 1959). To this end, Dr. Ash requested reducing the level of radioactivity by 33% and indicated “I can achieve this reduction without spoiling the smoking qualities of the tobacco but may alter the processing qualities and darken the colour [sic] somewhat” (Ash, 1959). Ash's request, however, was summarily dismissed by Philip Morris scientist Dr. Seligman who in a confidential memo to his colleagues and associates asserted:
Dr. Seligman then concluded “We feel Dr. Ash was prompted into action more from emotion rather than from a basis of scientific fact” (Seligman, 1959).
I have discussed this problem with several members of our staff, and all are of the opinion that we should not be concerned with the point raised by Dr. Ash. Dr. R.O. Simmons, our biochemist, points out that potassium (K) is an essential element for normal metabolism that normal human blood contains 17 mg per 100 ml, and that ingestion of a normal meal would add more radioactive K to the body than smoking a few cigarettes.
With this internal decision reached by the executives and scientists, the council of Philip Morris, Mr. Laporte then drafted a strenuous and a tough letter to Dr. Ash rejecting the proposed reduction of the level of radioactivity in the tobacco products and dismissing altogether the whole issue of tobacco radioactivity by stating:
The levels of activity of the smoke of cigarettes are even far below than your newly proposed ‘safe’ level of radioactivity, we are at a loss to understand your continued pursuit of this topic (Laporte, 1959).
Although the industry was aware of the presence of a radioactive substance in tobacco as early as 1959, however, the type of the isotope was not discovered until 1964 when Radford and Hunt (1964), in their January 17, 1964 Science paper, first showed that 210Po and its parent 210Pb were the major isotopes in tobacco and not potassium. Following the 1964 discovery of 210Po in tobacco, the industry became concerned about the potential lung cancer risk caused by the ionizing alpha particles that it issued a secret report suggesting that Radford and Hunt's discovery was “sufficiently provocative so to suggest that more thorough investigation of this possibility is warranted” (DNS, Jft, & JB, 1964). The secret report went even further indicating that “Over a 25-year period a sufficient exposure to this radioactive material could occur to produce cancerous growth” (DNS et al., 1964). Subsequent radiochemical analyses by the industry and universities have shown that indeed each cigarette, depending on the brand and the country of origin, contains from 8 to 32 mBq 210Po (mean of 16 ± 4 mBq; Desideri et al., 2007; Hill, 1964; Khater, 2004; Marmorstein, 1986; Martell, 1974; Radford & Hunt, 1964; Savidou et al., 2006; Skwarzec, Ulatowski, Struminska, & Borylo, 2001; Tahir & Alaamer, 2008; Tso et al., 1964)—with higher levels in the Brazilian (Peres & Hiromoto, 2002) and Chinese brands (Schayer, Nowak, Wang, Qu, & Cohen, 2009). At this juncture, Philip Morris hired a UK-based private company, Harwell, with expertise on radiation physics and radiobiology in late 1980s and 1990 to conduct a worldwide comprehensive literature search on cigarette content of radioactivity (Pritchard, Pattendon, & Gibson, 1990). The results of these worldwide findings remained strictly confidential until the 1998 Master Settlement Agreement (MSA). Harwell's findings showed that the cigarette content of 210Po in various brands reported in industry documents corroborated very well with open literature reports on cigarette content of 210Po (Pritchard et al., 1990).
Industry scientists not only had keen knowledge about cigarette smoke radioactivity but also had run sophisticated radiochemistry laboratories with remarkable insight into the dynamics and the nature of tobacco smoke radioactivity as early as in 1964. In a letter dated October 27, 1964 and referenced as “Polonium in Tobacco and Smoke,” an industry scientist (ajm) clarified to his colleagues Drs Bavley and Segura in no ambiguous terms the apparent dilemma of 210Po’s relatively short half-life (135 days) compared with the long periods of curing of the tobacco leaves that could cause considerable reduction of 210Po content in the cured leaves:
This should put to rest the contention that 210Po, with its half-life of 135 days, almost fully decays after a year or so of curing. The fact, however, is that the parent 210Pb with its half-life of 22 years remains the constant supplier of 210Po.
Some experimental evidence indicates that the polonium-210 found in plants does not get there directly (if that were the case the activity would decrease after harvest with a half-life of 135 days). Instead, it seems that the plant picks up lead-210, a radium disintegration product, and that it is this lead-210 [half-life of 22 years] which then gives rise to the polonium (Polonium in Tobacco and Smoke, 1964).
Lung Content 210Po in Smokers
Due to the presence of elevated 210Po levels in cigarettes, a question arises as to whether the levels of radioactivity in the lungs of the smokers will also be higher than the levels of radioactivity in the lungs of nonsmokers. This question led to much research in the field of alpha particle inhalation via tobacco smoke, detailing how much of the cigarette radioactivity is actually delivered to the lungs of smokers, where in the lungs alpha particles distribute and accumulate, how long they stay in the lungs, and what possible deleterious effects they may cause. Open literature (Winters & Di Franza, 1983) and tobacco industry documents (Natural radioactivity in tobacco and tobacco smoke) show that over half of the radioactive materials emitted by burning a cigarette are released into the air (i.e., side stream smoke) where they can be inhaled by nonsmokers (secondhand smokers). The smoke inhaled by the smoker (i.e., mainstream smoke), with or without the presence of a filter tip, delivers about 32% of the 210Po from each cigarette to the lungs of the smoker. Only a negligible fraction of the 210Po (∼3%) is filtered by filter-tipped cigarettes and about 10% is retained in cigarette butts and ashes (Department of Health, 1979; Horsewell & Richardson, 1966; Rajewsky & Stahlhofen, 1966; Skwarzec et al., 2001). Because 210Pb and 210Po become attached to the insoluble trichome particles of the inhaled cigarette smoke (Martell, 1974), they get stuck at the bronchial bifurcations of the smokers’ lungs, resist being cleared rapidly thus staying at these bifurcations for a relatively long period of time. Radford and Martell determined the residence time of 210Po at these bronchial bifurcations by assuming that all of the 210Po in the cigarette arise from the 210Pb-enriched insoluble trichome particles. Using the 210Po/210Pb ratio, a mean residence time of 210Po in the lungs of smokers was determined to be about 120 days (Radford and Martell, 1975). According to open literature (Little et al., 1965; Martell, 1983) and tobacco industry documents (Polonium 210), 210Po concentration actually builds up at these bifurcation sites causing what is known as “hot spots.” A landmark study by Little et al. and Little and Radford (1967) systematically analyzed autopsy lung specimens from the lungs of smokers who died of lung cancer and the lungs of nonsmokers who died of car accidents. These authors found that the concentration of 210Po was significantly higher in the lungs of smokers compared with nonsmokers and that the highest level of radioactivity was selectively confined to the segmental bifurcation of the lower lobes of the lungs (hot spots)—where 210Po concentration reached up to 500 mBq/g (i.e., 13 pCi/g). Other sites in the lung parenchyma 210Po concentrations were less than 0.5 mBq/g or nondetectable known as “cold spots.” Similar lung deposits of 210Po were later reported in other studies (Holtzman & Ilcewicz, 1966; Little & Radford, 1967; Martell, 1974, 1983; Radford & Martell, 1975) and in the confidential industry reports (Polonium 210; Post-mortem concentrations of Po 210 in tissues of cigarette smokers and non-smokers). Most interestingly, and relevant to the issue of hot spots, the systematic and careful studies of Auerbach, Stout, Hammond, and Garfinkel (1961) carried out independently some 4 years earlier than the studies of Little et al. showed in the lung autopsies of 63 smokers who died of lung cancer that the highest incidence of malignant changes occurred at the bronchial bifurcations of the lungs of these smokers precisely at the same sites where Little et al. found the highest levels of 210Po accumulations in the lungs of smokers who died of lung cancer.
Industry's Own Calculation of Lung Dose and Lung Cancer Risk
The early discovery of elevated radioactivity at the bronchial bifurcations in the lungs of smokers, and the demonstrations of colocalization of malignant transformation in the lungs at sites with the highest level of 210Po accumulation, generated a great deal of concern among industry executives. Although this concern did not amount to action, the documents provide a glimpse of the industry's inner thoughts, tribulations, and attitudes since the early 1960s. For example, starting 1962 industry executives had already dubbed the presence of radionuclides in tobacco as an “issue,” a “problem,” or a “situation.” This concern was well articulated in a 1962 BATCO document when high-ranking executives requested their radiotracer laboratory scientists to more accurately clarify the issue of tobacco smoke radioactivity:
It is remarkable that industry executives were already contemplating a comparative lung cancer risk analyses between people inhaling alpha particles emitted from cigarette smoke and people breathing alpha particles emitted from air infested with radioactive radon gas. Interestingly, the EPA, as an independent agency of the U.S government, was founded 8 years after the industry's call for a comparative analysis.
Volatile radioactive materials may be retained in the smoke particles and trapped on the lung's surface, staying there until they disintegrate. Can you make a guess what this quantity is likely to be and compare it to that part inhaled by radon, which will decompose while it is actually within the lung? If the answer is that it is still negligible, the matter can rest, but if not, then we may have to take very seriously any raising of this issue of radioactivity in tobacco (Anderson, 1962).
The issue of radioactivity preoccupied BATCO scientist and executives in the ensuing years but no concrete action was taken to remove 210Po from tobacco smoke (Hughes, 1964).
This concern, however, did not subside, as more realistic predictions made by industry scientists led to discover that 210Po in the tobacco smoke may indeed be a cause lung cancer. In a confidential industry report discovered in the American Tobacco collection dated January 29, 1964 and entitled “Suggestions for research on Polonium-210 in tobacco,” the industry scientist admits with no ambiguity the carcinogenic potential of the ionizing alpha particles in cigarette smoke in a startling and scientifically accurate manner:
This early and scientifically accurate assessment of the potential ill-effects caused by inhalation of ionizing alpha particles clearly shows the deep and intimate knowledge by the industry of the sequence of pathobiological events in which the inhaled alpha particles might lead to lung cancer. The sequence of these events can be summarized as follows: (a) formation of complex radionuclide-resinous insoluble particles, (b) lodging of the insoluble complex particles at the bronchial bifurcations (hot spots), (c) ciliary paralysis of the affected bronchial bifurcations causing long retention time of the radionuclides, and finally (d) induction of metaplastic cellular transformations leading to cancerous growth at the hot spots.
Ionizing radiation can produce cancer in man. Polonium has been shown to be present in significant amounts in tobacco. When tobacco is burned polonium is vaporized, attaches to the smoke, and is carried into the lungs. Here much of it is retained, some reaching the alveolar capillary bed and being absorbed into the general circulation and some phagocytized and removed in the mucous and ciliary action of the tracheobronchial tree. It is possible for it to concentrate in certain areas in sufficient quantities to produce a metaplastic reaction. Cigarette smoking has been demonstrated to paralyze cilia and interfere with normal draining mechanism of the lungs. Over a 25-year period a sufficient exposure to this radioactive material could occur to produce cancerous growth (DNS et al., 1964).
This early and insightful knowledge was neither an isolated finding nor did it end here. In a 1967 confidential memo by Philip Morris, we found yet another level of sophisticated analyses and interpretation of the long-term deleterious consequences of alpha particle inhalation, and yet the industry chose to look the other way:
These early industry predictions of the potential ill-effects of alpha particles in cigarette smoke proved prophetic. The industry's and our own calculations (see below) of the long-term lung tissue absorption dose of alpha particles show comparable levels of rad in regular smokers over a 25-year period.
The implications of alpha-radiation in the induction of human lung cancer is very convincing with respect to cumulative exposure in the order of several hundred times as large as those experienced by steady two-pack-a-day smokers. We find general agreement among investigators of the cigarette-polonium hazard, however that too many uncertainties remain in the available epidemiological data to permit any definite conclusions to be drawn from them about the effect of the relatively minor 210Po alpha-radiation experienced by the cigarette smoking public. This is not to be taken as complete exoneration of 210Po as a causative factor in human lung cancer (Kensler, 1967).
Industry concern over cigarette smoke radioactivity lingered in the ensuing decades, with no concrete steps taken to eliminate the radionuclide. The industry kept insisting that the dose was “too small” to worry and that there were a great deal of “uncertainties” as to a cause and effect relationship between alpha particles and lung cancer. As a rebuttal to these early leads and while admitting in confidence a definite carcinogenic potential of inhaled alpha particles, Philip Morris prepared in 1980 the following report:
That issue of alpha particle absorption dose was directly addressed by a scientist working for the Brazilian Souza Cruz cigarette company (BATCO subsidiary). The scientist determined quantitatively the actual lung dose of alpha particles in regular smokers and provided an estimate of the rad over a 20-year period in regular smokers of two packs a day of a Brazilian brand of cigarettes. The BATCO scientist reached the following conclusion:
210Pb and 210Po are present in tobacco smoke and smoke ash. The Martell “Hot Particle Theory” has been addressed in the past and has apparently lost popularity in the scientific community (lack of recent publicity in this field). For α-particles from 210Po to be the cause of lung cancer is unlikely due to the amount of radioactivity of a particular energy necessary for induction. Evidence to date, however, does not allow one to state that this is an impossibility (Comes, 1980).
Basing on data of my studies, I estimate that a person smoking two packs of Brazilian cigarettes per day would have 1,000 rems in 20 years (de Siqueira, 1988).
rem (radiation equivalent in man) is numerically equal to the absorbed dose in rads multiplied by the RBE, which in the case of alpha particles is 20, so 1,000 rem is equivalent to 50 rads. A rad is a unit of absorbed dose equal to 100 ergs of energy absorbed per 1 g of tissue. Notice that 100 rem equals 1 sievert (Sv), the more commonly used unit.
The details of the calculations were not provided in this report; however, our own calculations using industry and academic published radiobiological data and kinetic parameters of alpha particle distribution and residence time in the lungs of smokers, we found that the lung burden of chronic two packs a day of smoking produced results comparable to those obtained by the industry.
Our Own Calculations of Lung Dose and Lung Cancer Risk
We repeated the lung dose calculations of alpha particles in regular smokers of two packs a day (40 cigarettes) over a 20- and 25-year period as the BATCO scientists did some 23 years ago. Using an average 210Po content of 16 mBq in each cigarette with an inhaled fraction of 0.32 per cigarette, smoking of 40 cigarettes/day will cause a total lung radiation burden of 16 × 0.32 × 40 x 120 days (retention time) = 24.5 Bq (1Bq = 1 disintegration/s).
Because the energy of an emitted alpha particle is 5.3 MeV (Hall, 1987), then the total energy available to the total lung volume per second will be 24.5/s × 5.3 MeV = 130 MeV/s.
This total alpha particle energy in the lungs, however, does not distribute uniformly in the 1 kg of human lung tissue mass. Instead, as we seen above, the alpha particles are selectively and exclusively concentrated at the small bronchial bifurcation of the lungs (hot spots) estimated to be about 4% of the total lung tissue mass or about 40-g tissue (40-ml volume). Consequently, the true lung dose per gram of lung tissue will be 130 MeV/s divided by 40 g equals 3.25 MeV/s g. Using 120 days as retention time of the radionuclides (Radford & Martell, 1975), the total lung dose in smokers over a 25-year period will be 3.25 MeV/s g × s/25 years, and using the value of 6.24 × 107 MeV/g as equivalent to 1 rad (Effects of pollution on health, 1972), we get a lung dose of 41 rads. So the rad over a 25-year period is 41 rads and for 20 years it is 33 rads. To convert rads to rem, we need to multiply the rad by the RBE which in the case of alpha particles is 20 (Committee on Health Risks of Exposure to Radon, 1999; Rego, 2009). Notice that for beta particles, x-rays, and gamma particles the RBE is around 1 (Hall, 1987).
Consequently, the level of rems of smokers of two packs a day for 25 and 20 years will be 820 and 660 rems, respectively. Because the 210Po content of Brazilian cigarettes is >30 mBq/cigarette, then increasing alpha particle dose from 16 to 30 mBq/cigarette according to our own calculations will be 1,235 rems, a value not far from the industry's estimate of 1,000 rems. Interestingly, the industry's and our own estimates of long-term lung absorption dose of alpha particles are also comparable to three other estimates reported in the open literature by Radford and Hunt (1964) who found 50 rads (1,000 rem), by Little et al. (1965) who found 20 rads and by Martell (1983) who reported 60–140 rads.
The EPA estimated lung cancer risk as a function of home alpha emitting radon gas concentrations as pCi/L (1 pCi equals 37 mBq) and prepared Radon Risk Charts available on the EPA's Web site (www.epa.gov). The EPA found that exposure to 100 pCi/L of alpha particle emitting radon will result in a lung rad of 36 rads over a 25-year period. Such level of rad is comparable to the rad by smokers of two packs a day of cigarettes for 25 years. According to the EPA charts, 36 rads over a 25-year period will cause 120–138 lung cancer deaths per year per 1,000 people.
Industry's Policy on Tobacco Smoke Radioactivity
All major tobacco companies, including Philip Morris, BATCO, Brown & Williamson, R.J. Reynolds, and the Council on Tobacco Research, rallied around a common policy of silence and secrecy that spanned from 1959 to 1998 when the MSA ordered posting of most of the secret documents online. The policy of silence and secrecy was adopted by most industry executives and was achieved using four basic mechanisms that involved outright denial, total ban on publications, rebuttal and discrediting of scholarly publications on tobacco radioactivity, and finally use of language designed to obfuscate the true lung dose and the potential of cancerous growth caused by tobacco smoke alpha particles.
Perhaps, the most graphic example of denial of tobacco radioactivity comes from Philip Morris CEO, Geoffrey C. Bible, during his 1997 court deposition. After 38 years of research on the chemistry, kinetics, and dosimetry of tobacco smoke radioactivity, Mr. Bible categorically denied the presence of radioactivity in tobacco smoke. Here is the Q & A exchange that appeared in that deposition:
Question: Do you know when you smoke a Marlboro that you may be taking in radioactive substances in your body?
Answer: No, I didn’t know that.
Question: Have you ever heard of polonium 210?
Answer: I think I have, yes.
Question: Do you know that polonium 210 is a contaminant of tobacco?
Ban on publication
Industry executives sensed as early as in 1962 that any knowledge of cigarette radioactivity would cause serious harm to the tobacco business. The logic behind this reasoning was understandable. The general public remains mindful of the severe harm that radiation may cause to humans due to the graphic memory of the victims of nuclear bombs and nuclear plant disasters, and in particular the most recent disaster at the Fukushima Daiichi nuclear power plant in the aftermath of the March 11, 2011 earthquake and tsunami in northern Japan. As a result, the knowledge that one is actually inhaling a radioactive substance will most likely trigger a fear and outright abhorrence both by smokers and beginners alike. Consequently, the industry, based on such realistic reasoning, chose the path of absolute silence and secrecy, banning any and all publication on tobacco radioactivity that could clearly damage the industry's business and tarnish its image. In a 1962 letter with reference to “Alpha activity in tobacco,” Philip Morris executive Bavley instructed the company's scientist Wakeham not to publish his results on radioactivity for concerns that such knowledge could trigger a hostile and rejectionist attitude by the smokers. Here is part of that letter:
The policy of total ban on publications was very well articulated in a 1963 executive memo by Mr. Blackmore of Philip Morris who said:
Radioactivity in Australian made cigarettes and pipe tobacco is extremely low and by itself, represents no problem. However, information such as this is seized upon by those who zealously seek information to prove the harmful nature of tobacco (Bavley, 1962).
We assume that this paper was prepared as a rebuttal against some claims of radioactivity in tobacco or cigarettes. … We see no reason for publishing the paper at this time. People generally read articles of this nature by headlines only without digesting the contents of the publication. Thus, the paper might do more harm than good for the tobacco industry if people were to relate radioactivity with tobacco (Blackmore, 1963).
The policy of ban on publishing any and all information on tobacco radioactivity that was comprehensively adopted by the industry started as early as 1962 continued long after, as highlighted in this 1980 Philip Morris memo entitled “210 Polonium briefing”:
By 1967-68 the level of 210Po in tobacco and cigarette smoke were verified at R&D. This research was put into manuscript … but it was decided not to publish the paper (Charles, 1980).
It must be admitted that the policy of banning publications proved to be very successful in preventing the public at large and smokers as well from becoming aware of tobacco smoke radioactivity. A 2004 survey by Cummings et al. (2004) found that 86% of 1,046 adult smokers polled were unaware that there are radioactive isotopes in tobacco, let alone that that they were inhaling it. Rego (2009) in her survey considered 86% as an underestimation and suggested that the percent of people who still remain unaware of tobacco smoke radioactivity is much higher. These findings clearly indicate that the industry's total ban on publication was a highly successful venture for over 40 years, as not a single paper was ever published. Similarly, not a single piece of information regarding the presence of radioactivity in tobacco was ever communicated to the consumers or the public at large.
Although the policy of banning publications of all internal research findings on tobacco radioactivity was by all accounts was quite effective in keeping the public unaware of tobacco smoke radioactivity, the industry however had to resort to a different approach when dealing with published academic findings on tobacco smoke radioactivity. Here, the industry reasoned that an effective way to discredit the significance of the published data would be to raise serious doubts about the veracity, reproducibility, and the reliability of the academic findings. The 1992 example of a San Paulo University Professor's report on the presence of excess amounts of 210Po in the Brazilian brands of cigarettes (Souza Cruz, a subsidiary of BATCO) compared with other brands was strenuously challenged by the industry as can be seen in this 1992 memo marked “Secret”:
The industry's strategy to dismiss and repudiate academic finding was then coupled to a self-praise and assertion that only the industry is capable of conducting accurate measurements of 210Po and in particular by their own paid, private consultant, Harwell, whose findings remained confidential and out of reach to the public. Here is how the 1992 Souza Cruz memo described this self-asserted attitude in response to the academic findings:
The findings of this professor would have resulted from an adaptation of the radioactivity measuring methods to other materials in order to evaluate substances normally with low radioactivity, such as plants (in this case, the tobacco). This adaptation, developed by the professor, would have not yet been used in any part of the world, being a ‘novelty’, introduced by him (Cruz, 1992).
The results of our measurements [by Harwell] proved that no difference exists between Brazilian and foreign tobaccos. Likewise levels of radioactivity found in Souza Cruz brands … are irrelevant and do not significantly differ from other brands available in the Brazilian and foreign market. Souza Cruz systematically carries out at its Research Center rigorous quality control programs with object of assuring that its products are kept under permanent international standards (Cruz, 1992).
In addition of repudiating academic findings, the Souza Group bought journal advertisements asserting its scientific authority and competence in measuring tobacco radioactivity. Here is a section of an advertisement bought by Souza-Cruz:
Souza Cruz has on hand measurements carried out by the ‘Institute of Radioprotection and Dosimetry of the National Commission of Nuclear Energy’ in Brazil and by the Harwell Laboratory, linked to the United Kingdom Atomic Energy Authority (UKAEA) in England. These measurements carried out through methods internationally recognized as appropriate and reliable, place Souza Cruz's products absolutely in line with patterns and products worldwide (Cruz, 1992).
The policy of repudiation of academic publications goes back to 1974 in light of the pioneering findings by Radford and Martell on tobacco smoke radioactivity. The 1974 letter of Philip Morris’ scientist, Mr. Wakeham, further emphasizes the well-entrenched industry policy of repudiation and rejection of academic findings:
Both Martell and Radford have reported to the press to publicize their findings before presentations to their peers either at technical meetings or through publications. Under these circumstances, it is reasonable to question whether or not they are truly interested in an objective discovery of the facts as opposed to personal aggrandizement or antismoker missionary work (Wakeham, 1974).
This statement is odd as it is self-contradictory, considering the fact that at the beginning of his confidential memo Mr. Wakeham unambiguously states that:
It has been fairly well demonstrated that the radioactive polonium is on tobacco and that it is found in excess quantities at the bifurcation of the trachea in smokers (Wakeham, 1974).
In addition to denial, ban on publication, and repudiation of academic findings, the industry resorted to the use of language designed to obfuscate and conceal the potential lung tissue damage caused by alpha particles in cigarette smoke. Such misleading statements were found in BATCO documents
For example, yet another form of obfuscation was the way 210Po concentrations in postmortem human lung tissues were expressed. Because 210Po concentrates in a small lung tissue volume, estimated to be about 4% of the total lung mass), expressing 210Po content per 100 g of lung tissue (post-mortem concentrations of Po 210 in tissues of cigarette smokers and non-smokers) will artificially dilute the true dose of 210Po at the hot spots (i.e., ∼10 mg tissue) by as much as 100–10,000 times. Furthermore, because alpha particles do not penetrate more than 40-micron deep into tissue, expressing the dose of radiation as an “average” of alpha particles of hot spots + cold spots will be highly misleading (Hill, 1965; Little & Radford, 1967).
Polonium Removal, pH, and Nicotine
The reasons for the swift and adamant rejection by the industry were not clear at the time. With the 1980 discovery of a highly effective method for removing alpha particles from tobacco leaves using an acid wash technique (Campbell, 1980), the industry's motivation to reject acid wash became clear based on the industry's internal secret documents. Academic findings have shown that acid treatment (Bretthauer & Black, 1967; Campbell, 1980; Jenkins, 1985; Kensler, 1967) and resin-exchanger filters (Horsewell & Richardson, 1966; Kensler, 1967) were highly effective in removing up to 99% of the radionuclide from tobacco leaves. The industry rejected the use of acid treatment by citing “cost,” “impracticality,” and “unknown consequences to the environment” as reasons for inaction (Campbell, 1980; Jenkins, 1985). Here is a document prepared by Mr. Jenkins Philip Morris describing the alleged reasons for refusal to use acid wash to remove polonium from tobacco leaves despite its proven efficacy:
The irony is that none of the industry's cited concerns, damage to the environment, the negative economic impact, and the problem of disposing the radioactive waste derived from acid wash appear to be true reasons for industry's refusal to remove radionuclides from the tobacco leaves by acid wash. Accepting industry's logic will be tantamount to accepting that inhalation of the radionuclides by smokers is a safer way to dispose of excess tobacco radionuclides than dumping radionuclide-rich acid tobacco wash extracts to the soil. On closer examination of industry's documents related to the influence of pH on the speed and amount of nicotine delivery to the brain of smokers (i.e., “nicotine freebasing”; Stevenson and Proctor, 2008), we concluded that the reasons for rejecting acid wash were not the ones cited by the industry. In fact, Mr. Jenkins in his confidential memo provided a clear hint as to the main reason for not using acid:
The degree of practicality of this patent is another issue. Leaf washing with acid in the field is quite impractical as the farmer spends considerable money to keep his soil at a proper pH and adding acid is in a negative direction economically. Leaf washing after harvest, but prior to curing, appears more practical. The problem of waste water treatment is of concern, not only for the acid, but because this washing procedures would lead to an enrichment of the natural radionuclides and would require their proper disposal (Jenkins, 1985).
None of my comments address the subjective alterations of the tobacco which may take place due to the acid treatment (Jenkins, 1985).
Indeed, manipulating the pH of the tobacco so to cause “subjective alterations” in smokers was very much in the minds of the industry long before the method of acid treatment was discovered. Acid medium ionizes the nicotine molecules (protonation) by imparting a net positive charge. The positively charged nicotine molecules (ionized nicotine) cross biological membranes at a much slower rate than the noncharged nicotine molecules (i.e., nicotine free base) thus reducing the speed and the amount of nicotine delivery to the brain of smokers. Slowing of nicotine delivery to the brain of smokers causes loss of the much appreciated instant nicotine “kick” award. An explicit description of the consequences of acid wash was found in a 1971 Liggitt document that reads in part:
Increasing the pH of a medium in which nicotine is delivered increases the physiological effect of the nicotine by increasing the ratio of free base to acid salt form, the free base form being more readily transported across physiological membranes. We are pursuing this project with the eventual goal of lowering the total nicotine present in smoke while increasing the physiological effect of the nicotine which is present, so that no physiological effect is lost on nicotine reduction (Williams, 1971).
The link between acid wash and loss of “nicotine kick” was well articulated by the Assistant Director of Research at R.J. Reynolds, Claude E. Teague, Jr.’s poignant statement:
Tobacco products, uniquely, contain and deliver nicotine, a potent drug with a variety of physiological effects … if we meekly accept the allegations of our critics and move toward reduction or elimination of nicotine from our products, then we shall eventually liquidate our business. If we intend to remain in business and our business is the manufacture and sale of dosage forms of nicotine, then at some point we must make a stand (Teague, 1972).
Teague in a 1973 memo stated the huge sales of Marlboro realized by Philip Morris as a result of raising tobacco pH:
Stevenson and Proctor (2008) in their comprehensive study also exposed in great detail industry's manipulation of tobacco pH with ammonia designed to raise the pH to speed up nicotine delivery to the brain of smokers (free basing). However, the industry rejected the reason for raising the pH with ammonia as a means of promoting “nicotine freebasing” (i.e., quick nicotine delivery to the brain), instead it insisted that ammonia was used as a “flavorant” and “pectin releaser.” Clearly, with so much at stake, the industry attempted to cover up and deny its use of ammonia as a freebasing agent. In fact in the case of Iron Workers v. Philip Morris, Harold G. Burnle, Jr., the company's former vice president of operations, was asked:
As a result of its higher smoke pH, the current Marlboro, despite a two-thirds reduction in smoke “tar” and nicotine over the years, calculates to have essentially the same amount of ‘free’ nicotine in its smoke as did the early Winston [cigarette brand] (Stevenson & Proctor, 2008).
Is it true that Philip Morris uses ammonia for the purpose of increasing a nicotine kick?
His answer: No, sir … it was used really initially in blended leaf to hold together , and it was used as a flavorant in the reconstituted leaf (Stevenson & Proctor, 2008).
Over the years, as evidence gathered of the harmful effects of tobacco smoke, including the presence of elevated levels of alpha particles, along with the warnings by the Surgeon General on the harmful effects of smoking, the industry adopted a new and different strategy to protect itself form possible lawsuits. In anticipation of possible lawsuits, industry scientists and executives prepared a draft report of all their internal findings on radioactivity in tobacco and handed them to their lawyers in order to invoke the attorney-client privilege clause (Bero, Barnes, Hanauer, Slade, & Glantz, 1995; Hanauer, Slade, Barnes, Bero, & Glantz, 1995; Kensler, 1967). However, it was in the 1998 MSA that most of the internal documents were posted online by court order (Schroeder, 2004). Finally, it must be noted that the commonly used cigarette filters remove less than 5% of the polonium present in tobacco smoke (Horsewell & Richardson, 1966) and probably have very little or no nicotine filtering. It is important to realize that whatever amount of nicotine might be filtered, the smokers compensate for the “lost” nicotine by practicing more aggressive smoking patterns such as increase in the number of puffs per cigarette, more intense inhalation per puff, and by a greater number of cigarettes smoked. Ironically, these compensatory mechanisms while smoking the so-called “low tar, low nicotine” cigarettes actually increase and not decrease the amount of inhaled alpha particles (Russel, 1987). However, as we discuss below, the 2009 signing of the Tobacco Control Act into law by President Obama granted fairly broad authority to the FDA to regulate tobacco products and disclose and identify harmful substances in tobacco smoke. This may finally allow the public at large to learn that when they smoke they inhale ionizing alpha particles.
Industry scientists and executives knew of the presence of higher than background levels of radioactivity in tobacco leaves as early as 1959 at a time when a Canadian health official first suggested to Philip Morris executives to reduce the level of tobacco radioactivity (Ash, 1959).
The documents analyzed in this study further show that industry scientists actually made realistic radiobiological calculations and determined the long-term absorption dose of alpha particles by the lungs of regular smokers. Although the details as to how the value of 50 rads (i.e., 1,000 rem or 10 Sv) were calculated by industry scientists, our own calculations using combined academic–industry radiobiological and alpha particle distribution-kinetics data, we reached similar values of long-term lung absorption dose of 210Po. These estimates of lung rad levels were comparable to three previous academic estimates ranging between 40 and 160 rads (Little et al., 1965; Martell, 1983; Radford and Hunt, 1964). According to the EPA, such lung doses of alpha particles would over a 25-year period induce lung cancer causing 120–138 deaths per 1,000 smokers. The potential of causal association between alpha particles and cancerous growth seems quite convincing as rigorously stated in the National Academy of Sciences’ report on the biological effects of ionizing radiation (BEIR VI):
Based on BEIR's report, the probability of a single epithelial cell surviving a hit by one alpha particle in the hot spots of the lungs of regular smokers is not an unlikely event, considering the availability of two previous independent observations supporting the causal relationship between alpha particles and cancer. Perhaps, the earliest causal link between alpha particles and cancer was made beginning around 1920, when alpha particle emitting radium paint was used to paint luminescent numbers on watch dials. The painting was done by hand, with the common practice of using the lips to produce a point on the tip of the brush. Many workers accumulated significant burdens of alpha particles through ingestion and absorption of radium-226 into the bones causing cancer of the jawbone or the mouth that eventually led to the discontinuation of the practice (Frame, 1999). The second example is the induction of liver cancer in human patients exposed to chronic low-dose internal alpha particles emitted from the poorly soluble deposits of thorium dioxide following intravascular administration of the radiographic contrast agent Thorotrast. It has been hypothesized that the liver cancers in these patients result from point mutations of the tumor suppressor gene p53 by alpha particles (Iwamoto et al., 1999).
There is good evidence that a single alpha particle can cause major genomic changes in a cell, including mutations & transformations. [T]he passage of a single alpha particle has the potential to cause irreparable damage in cells that are not killed. In addition there is convincing evidence that most cancers are of monoclonal origin, that is, they originate from damage of a single cell (Committee on Health Risks of Exposure to Radon, 1999).
The presence of tobacco radioactivity was of sufficient concern that as early as 1959 a Canadian health official proposed to the industry a method that could reduce the level of tobacco radioactivity by 35% (Ash, 1959). The industry, however, swiftly rejected this early and the subsequent very effective acid wash removal (99%) method discovered in 1980 by Campbell. Although the industry rejected the use of acid wash, citing, “economic costs to the farmers” and “unknown environmental consequences of acid dumping in the soil” as reasons (Jenkins, 1985), our discovered documents show that industry's true motives in resisting acid wash were unrelated to these cited “concerns” and were directly linked to the fact that in acid media nicotine molecules become ionized (i.e., protonated) a process that converts the basic form of nicotine molecule (i.e., nonprotonated form) to poorly absorbable charged form of nicotine molecules (i.e., protonated form). Because charged molecules cross biological membranes very slowly, acid treatment would therefore deprive the smokers of the much sought-after instant nicotine “kick” sensation (nicotine-free basing). The loss of the nicotine “kick” sensation was found unacceptable by industry executives. After all, the industry, according to its own admission, was in the business of dispensing nicotine, with the tobacco smoke serving as the delivery vehicle (Stevenson & Proctor, 2008; Teague, 1972).
The industry not only did not act on its knowledge but also remained silent on the issue of tobacco radioactivity. Moreover, the industry even denied the presence of radioactivity in cigarettes and banned any and all publications on tobacco and tobacco smoke radioactivity (Muggli et al., 2008; Rego, 2009). In addition, we discovered that the industry resorted to two additional mechanisms designed to cover up and minimize the potential harm of cigarette smoke radioactivity. First, it used pseudoscientific language to obfuscate and confuse the true lung burden of radioactivity, and secondly, it used rebuttals and repudiations in paid public ads to discredit the veracity and reliability of the academic findings on tobacco radioactivity. There remains no doubt that the industry was unshakable and adamant with respect to its policy of silence, denial, obfuscation, and rebuttal to any and all form of news about tobacco radioactivity. These led some to conclude that “The polonium story presents yet another chapter in the long tradition of industry use of science and scientific authority in an effort to thwart disease prevention” (Rego, 2009). Since the first 1959 attempt, it took exactly 50 years for the Family Smoking Prevention and Tobacco Control Act to be signed into law in 2009 finally granting the FDA broad authority to regulate harmful substances in tobacco products (with the exception of nicotine) in order to protect the public health (Deyton, Sharfstein, & Hamburg, 2010; Harris, 2010). Although it is understandable that it may not be easy for the industry to immediately submit to the new regulations, the case for alpha particles is serious enough that now is the time to regulate alpha particles in cigarettes and to bring their levels to near zero. Based on the findings in this study and complemented by two previous reports (Muggli et al., 2008; Rego, 2009) and the Tobacco Control Act's section 904(e) requiring the FDA to establish a list of “harmful” and “potentially harmful” constituents (Deyton et al., 2010), we strongly recommend that radioactive polonium should be on top of the list of harmful substances requiring regulations. Until this important corrective measure is made, warning labels be put on cigarette packs warning the consumers that “cigarette smoke contains radioactive substance” or “radioactivity in cigarette smoke increases the risk of lung cancer” or wording to these effects. It is also important to also add similar warning labels on cigarettes exported to other countries that may be considering the content of their warnings now or in the immediate future.
Cigarette smoking–related lung cancer death claims the lives of 160,000 Americans each year and remains responsible for most cancers of the larynx, oral cavity and pharynx, esophagus, and bladder (U.S. Department of Health and Human Services, 2004). It is believed that knowledge about cigarette radioactivity could raise anxiety, particularly within the younger population, that may deter them from starting to smoke and may also force chronic smokers to seriously consider quitting and freeing themselves from addiction. Radiation and radioactivity are bound to raise concern in most people's mind about the serious health consequences because they evoke graphic images of survivors of atomic bombs or nuclear power plant disasters. Anecdotal evidence suggests that this may indeed be the case (Di Franza & Winters, 1982; Winters & Di Franza, 1982).
Finally, it must be noted that the harmful effects of alpha particles could also affect secondhand smokers because some 50% of the cigarette smoke (i.e., 50% of cigarette radionuclide content) is discharged into the immediate environment of the smokers greatly increasing the risk of lung cancer in these secondhand smokers (Hirayama, 1981).
University of California Tobacco-Related Disease Research Program (UC-TRDRP, 141T-0001) to H.S.K.
Declaration of Interests
Professor Amos Norman died prior to the publication of the paper. We thank Dr. John DeMarco of the Department of Radiation Oncology and Dr. Alan Garfinkel of the Departments of Medicine and Physiological Sciences, David Geffen School of Medicine at UCLA, for reading the manuscript and for useful comments.