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Cigarette Smoke Radioactivity and Lung Cancer Risk
Abstract
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.
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 (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.
The evidence of lung cancer risk caused by cigarette smoke radioactivity is compelling enough to warrant its removal.
... It has been estimated that a burning cigarette emits into the air about 50% of its radioactive materials and its smoke, inhaled by the smoker, delivers about 32% of the 210 Po to the lungs. Furthermore, radioactive materials can be inhaled by non-smokers, and are retained in cigarette butts and ashes [5]. ...
... Since the discovery that the presence of radioactivity in tobacco leaves was higher than background levels, tobacco industries tried to remove 210 Pb and 210 Po in tobacco through washing tobacco leaves with acid treatments, measuring the radioactivity prior to manufacturing, filtering mainstream smoke, and employing genetic engineering techniques in order to reduce radioactivity in the leaves. As the results were not satisfactory or could compromise the optimal absorption of nicotine into the brain, they decided to stop research in this area and eliminate any evidence that might put their companies at risk for smoking and health litigation [5,7]. ...
... Indeed, since high concentrations of polonium have been found in bronchial epithelium of smokers, it was hypothesized that polonium may be implicated in the initiation of lung cancer [5,8]. Actually, 210 Pb and 210 Po might be implicated also in the initiation of other tumors, since the radioactive particles from the bronchopulmonary system might spread throughout the body and reach various organs and tissues. ...
Few studies have reported on polonium-210, a decay breakdown product of radon-222 and lead-210, in human lungs and there has been no study in patients with suspected lung cancer. The main aim of this “Polonium in vivo” study was to evaluate polonium-210 radioactivity in bronchopulmonary systems of smoker, ex-smoker and never smoker patients with suspected lung cancer. Alpha-spectrometric analyses were performed on bronchial lavage (BL) fluids from two Italian hospitals in 2013–2016. Socio-demographic, smoking, occupational and spirometric characteristics, lung cancer confirmation and histologic type and radon-222 concentration in patients’ homes were collected. Seventy BL samples from never (n = 13), former (n = 35) and current smokers (n = 22) were analyzed; polonium-210 was detected in all samples from current and former smokers and in 54% of samples from never smokers (p < 0.001; median values: 1.20, 1.43 and 0.40 mBq, respectively). Polonium-210 levels were significantly higher in COPD versus no COPD patients (median value: 3.60 vs. 0.97 mBq; p = 0.007); former and current smokers, without and with COPD, had significantly increased polonium-210 levels (p = 0.012); 96% of confirmed versus 69% of non-confirmed lung cancer patients recorded detectable polonium-210 levels (p = 0.018). A polonium-210 detectable activity was measured in BL samples from all current and former smokers. Polonium-210 in the lungs could be the result of lead-210 entrapment, which, with its half-life of 22 years, could provide a continuous emission of alpha radioactivity, even many years after quitting, thus proposing a possible explanation for the onset of lung cancer, particularly in former smokers.
... 5,13 Despite studies documenting the appearance of lung cancer in animals exposed to low dose of 210 Po, 12 the tobacco industry made no successful effort to remove 210 Po and 210 Pb from tobacco. 7,14,15 Studies on the role of 222 Rn and its progeny as a cause of lung cancer have demonstrated a synergetic effect with tobacco smoke, with efforts to reduce in-house 222 Rn bene ciating more to smokers. [16][17][18] In this respect, it appears that 210 Po present in tobacco smoke could be responsible of some lung cancers otherwise attributed to radon. ...
210Po is a radioactive component of conventional cigarette tobacco smoke and is a recognized carcinogen. Despite the expanding market of heated tobacco products, no data are available on the activity of 210Po in the smoke of IQOS Heets® cigarette. We determined the 210Po activity in the mainstream smoke of thirteen cigarette brands available on the Swiss market using a smoking machine and compared the results to the 210Po activity measured in the mainstream smoke of the IQOS® system. In addition, we measured the 210Po and 210Pb loss on heating after uniform heating from 50 to 600°C for several cigarette brands and the Heets® cigarettes. 13.6 ± 4.1% of 210Po activity was found in the mainstream smoke in conventional cigarette smoking (7% for 210Pb). This dropped to 1.8 ± 0.3% in the mainstream smoke of IQOS Heets®. Conversely, when the tobacco was heated uniformly at 330°C, a loss of 210Po of more than 80% was observed for all type of cigarettes. Apparently, IQOS® significantly reduced the 210Po and 210Pb activities in the mainstream smoke. However, our results show that only 15% of the Heets® tobacco reaches 330°C with IQOS®. While IQOS® reduces the 210Po and 210Pb activities in the mainstream smoke compared to conventional cigarettes, it only heats a marginal fraction of the tobacco present in the Heets® cigarette. Because smoking is an addiction (mostly due to nicotine), IQOS® could possibly deliver an unsatisfactory dose of nicotine to a Heets® cigarette smoker, as most of the tobacco is left unaltered.
... Tobacco is the leading preventable cause of cancer, with 30% of cancer deaths caused by tobacco products. [9][10][11] While nicotine itself is not a carcinogen, its addictive properties make it difficult for tobacco users to quit, increasing their exposure to carcinogens over time. ...
Introduction:
Tobacco cessation is a critical but challenging intervention for cancer patients. Our National Cancer Institute-designated Comprehensive Cancer Center instituted a tobacco cessation program in 2019. This manuscript reports on the first 2 years of our experience.
Methods:
Patients were referred to the program by their care team, and a certified tobacco treatment specialist contacted patients remotely and provided behavioral therapy and coordinated pharmacotherapy. We retrospectively captured data from patients with a cancer diagnosis referred to the tobacco cessation program. Univariate and multivariable logistic regression analyses with the backward elimination approach were performed to determine factors associated with patient acceptance of referral to the tobacco cessation program. Tobacco cessation rates after referral to the program were also captured.
Results:
Between July 2019 and August 2021, 194 patients were referred to the tobacco cessation program. Of the 194 patients referred, 93 agreed to enroll in the tobacco cessation program (47.9%), of which 84 requested pharmacotherapy (90.3%). Twenty-four were able to cease tobacco use (25.8%). Only 7 patients out of the 101 patients (6.9%) who declined cessation services were successful (p < 0.001). On univariate logistic regression, race (p = 0.027) and marital status (p = 0.020) were associated with referral acceptance. On multivariable analysis, single patients (odds ratio [OR] = 0.33) and Caucasian patients (OR = 0.43) were less likely to accept a referral.
Conclusions:
Access to tobacco cessation services is a critical component of comprehensive cancer care. Our experience highlights the need to understand patient-specific factors associated with engagement with a tobacco cessation program during cancer treatment. The use of pharmacotherapy is also a critical component of successful tobacco cessation.
... In males, lung cancer has the highest incidence and mortality rate, whereas in females, tumor has the second highest incidence and mortality rate [3]. Despite the fact that the specific causation of lung cancer is unknown, a large body of research supports a strong relationship between long-term smoking and lung cancer [4]. Long-term cigarette smokers have such a 10-to 20-fold higher risk of lung carcinoma compared to nonsmokers, according to existing studies, and the earlier the age of smoke, the greater the incidence of cancer. ...
Background:
One of the most frequent malignancies is lung carcinoma which poses heavy burden on the global health. The link among differentially expressed genes (DEGs) and lung cancer patients' clinical outcomes was still missing. In this study, we integrated transcriptome data with clinical data to investigate the relationship between them in lung carcinoma patients.
Methods:
To begin, DEGs were identified using the Gene Expression Omnibus (GEO) gene expression pattern (GSE180347). Then, these DEGs are being searched in the TCGA database using the DEGs collected in the preceding phase. The Kaplan-Meier plotter was then used to assess the predictive value of these DEGs in patients with lung cancer.
Results:
Our study revealed a total of 45 DEGs, 15 of which were up-regulated and 30 of which were down-regulated. These DEGs were mostly enriched in cytokine receptor binding and cytokine activity, according to GO enrichment analysis. These DEGs were mostly enriched in cytokine-cytokine receptor interaction, according to KEGG enrichment analysis. Based on the PPI network, which comprises of 12 DEGs, a major module was discovered. They are mostly interested in cytotoxicity mediated by natural killer cells. Among all 45 DEGs, the mutations of NCAM1 account for the most cases in TCGA database with a percentage above 15%. Among the 12 DEGs in the significant module, higher expression of FAS, GPR29, HAVCR2, and NCAM1 exhibits longer survival time with hazard ratio and 95% confident interval of 0.79 (0.69-0.89), 0.80 (0.70-0.90), 0.71 (0.60-0.84), and 0.73 (0.62-0.86), respectively. However, higher expression of FCGR3A and IFNG exhibits shorter survival time with hazard ratio and 95% confident interval of 1.50 (1.32-1.71) and 1.15 (1.02-1.31), respectively.
Conclusion:
Our results demonstrate significant correlation between some DEGs and the survival outcome in lung adenocarcinomas patients, providing a comprehensive bioinformatics study in anticipation of future molecular mechanisms and biomarker studies.
... As early as 1964, Radford and Hunt hypothesized that the presence of 210 Po in tobacco smoke, and its preferential localization in the bronchial epithelium, would be a cause of lung cancer 5,13 . Despite studies documenting the appearance of lung cancer in animals exposed to low dose of 210 Po 12 , the tobacco industry made no successful effort to remove 210 Po and 210 Pb from tobacco 7,14,15 . Studies on the role of 222 Rn and its progeny as a cause of lung cancer have demonstrated a synergetic effect with tobacco smoke, with efforts to reduce in-house 222 Rn beneficiating more to smokers [16][17][18] . ...
210Po is a radioactive component of conventional cigarette tobacco smoke and is a recognized carcinogen. Despite the expanding market of heated tobacco products, no data are available on the activity of 210Po in the smoke of IQOS Heets cigarette. We determined the 210Po activity in the mainstream smoke of thirteen cigarette brands available on the Swiss market using a smoking machine and compared the results to the 210Po activity measured in the mainstream smoke of the IQOS system. In addition, we measured the 210Po and 210Pb loss on heating after uniform heating from 50 to 600 °C for several cigarette brands and the Heets cigarettes. 13.6 ± 4.1% of 210Po activity was found in the mainstream smoke in conventional cigarette smoking (7% for 210Pb). This dropped to 1.8 ± 0.3% in the mainstream smoke of IQOS Heets. Conversely, when the tobacco was heated uniformly at 330 °C, a loss of 210Po of more than 80% was observed for all type of cigarettes. Apparently, IQOS significantly reduced the 210Po and 210Pb activities in the mainstream smoke. However, our results show that only 15% of the Heets tobacco reaches 330 °C with IQOS. While IQOS reduces the 210Po and 210Pb activities in the mainstream smoke compared to conventional cigarettes, it only heats a marginal fraction of the tobacco present in the Heets cigarette. Because smoking is an addiction (mostly due to nicotine), IQOS could possibly deliver an unsatisfactory dose of nicotine to a Heets cigarette smoker, as most of the tobacco is left unaltered.
... Studies revealed that the presence of radioactive substances in the smoking tobacco results in the accumulation of insoluble radioactive particles in the respiratory system that acts as a significant factor for the increasing risk of cancers among smokers [5,6]. Among the toxic radionuclides present in tobacco 210 Po was the enhanced risk factor to cause lung cancer in smokers [7][8][9]. ...
... About 400 chemical compounds have been identified in tobacco and marijuana smoke, and it is probable that 70 of them are carcinogenic. The average smoker knows that the compounds contained in the dangerous substances in cigarettes, including dioxins, polycyclic aromatic hydrocarbons (PAH), volatile hydrocarbons and nicotine are probably the reason for the high incidence of cancer in smokers [21][22][23][24][25]. However, less is known of the harmfulness of radioactive isotopes 210 Po and 210 Pb contained in marijuana hash [11]. ...
This article contains and discusses the results of research on the source of polonium 210Po and radio-lead 210Pb in the human body of adults living in Poland. An adult inhabitant of Poland receives an effective annual radiation dose of 309 µSv from inhalation and absorption of 210Po and 210Pb. The main sources of both radionuclides in the body is cigarette and marijuana smoking. In terms of food, the consumption of fish, cereals, vegetables and fruit as well as mushrooms have the largest contribution to annual dose. This study highlights the importance of cigarette smoking and the growing importance of marijuana hash smoking as the main source of 210Po and 210Pb for adults living in Poland. The calculated dose that results from the decay of both radionuclides in body is 1/10 of the annual radiation dose received by a Polish inhabitant from natural sources (2.8 mSv) and is almost five times lower than the dose resulting from the inhalation of 222Rn.
... As the evidence for the lethal impact of tobacco products started mounting, the companies created uncertainty and dispute regarding health risks while putting filters on cigarettes and promised research into the health effects of smoking to address growing public concern. Further, there is strong evidence from the Master Settlement Agreement in 1998, which shows that the radioactivity of tobacco smoke and its potential to cause cancer were known to TI, but they purposefully concealed this information [62]. In another instance in the USA, a network of consultants was developed by TI to advocate ventilation as a "remedy" to second-hand smoke (SHS) [63]. ...
Background
The Tobacco Industry (henceforth TI) yearns to portray itself as being “socially responsible” and fights for the decision-making positions; that are it used to deter, delay or dilute tobacco control measures. There is little documented evidence of Tobacco Industry Interference (henceforth TII) from India, the scope of their interference and challenges faced by the experts for effective tobacco control. This research study seeks to cover this significant gap in the literature on the TI of India.
Methods
A cross-sectional qualitative research design, based upon in-depth interviews (N = 26), was used to explore the key stakeholders’ opinions regarding TII in India. The interviews used a set of questions to collect information about the participant’s roles and responsibilities in tobacco control, the nature of TII faced by the participants, means of influence by TI, barriers and challenges to tobacco control efforts.
Results
Most of the respondents were engaged in tobacco control, training, advocacy and awareness generation activities for 5–10 years or more. The respondents defined the TI and its scope as per their experience with the help of the power ranking methodology. Most of them perceived TI as ‘manufacturers’ while others consider them as ‘advertisers’, ‘public relation companies’, ‘wholesalers’, ‘vendors’, and ‘Government firms with TI stocks. The research team identified six significant domains: influencing the policy and administrative decisions, Interference in the implementation of tobacco control laws and activities, false propaganda and hiding the truth, manipulating front action groups (FAG), rampant tobacco advertising and promotion activities and others under which TII activities were classified. Most respondents believed that TI players were interfering in the policy decisions, implementing the tobacco control laws and activities and manipulating the FAG. A detailed taxonomic classification of the TII strategies that emerged from our analysis was linked to article 5.3 of FCTC.
Conclusions
The study documented a significant level of TII in different domains, with stakeholders acting at various hierarchical levels. Thus providing insight into the tactics of the TI in order to enable stakeholders to anticipate and pre-empt the kinds of alliances the TI may attempt to build; stimulating academicians and researchers to undertake in-depth analysis into various strategies and therefore underscoring the need to ensuring transparency in official interaction with the TI and its representatives.
... A number of studies have shown that smoking has a certain adverse effect on the development of lung cancer and is a prognostic factor for the treatment of lung cancer. [21][22][23] The data from this study also support this conclusion. The median PFS of patients who never smoked was significantly higher than that of patients with a smoking history (7.6 months vs 6.2 months). ...
Purpose:
This study was designed to assess the clinical efficacy and safety of anlotinib with immunotherapy in advanced non-small cell lung cancer as third-line therapy.
Patients and methods:
A total of 101 patients with advanced non-small cell lung cancer who were treated with anlotinib combined with immunotherapy were evaluated for progression-free survival, objective response rate, and disease control rate. Univariate and multivariate analyses were performed to determine the prognostic factors. The main adverse events were evaluated as per the Common Terminology Criteria for Adverse Events version 5.0.
Results:
Nineteen patients had partial response (18.8%), 61 had stable disease (60.4%), 31 had progressive disease (20.8%), and no patients achieved complete response (0%). The objective response rate was 18.8%, and the disease control rate was 79.2%. In all patients, the median progression-free survival was 6.7 months (95% confidence interval 6.13-7.24 months). In Cox regression analysis, the Eastern Cooperative Oncology Group performance status score, smoking history and age were predictive indicators for anlotinib treatment efficacy. Treatment-related adverse events were tolerated.
Conclusion:
This study demonstrated and confirmed the clinical effectiveness of anlotinib combined with immunotherapy in advanced non-small cell lung cancer as third-line therapy.
... As the evidence for lethal impact of tobacco products started mounting, the companies created uncertainty and dispute regarding health risks, whilst at the same time had put lters on cigarettes and promised research into health effects of smoking to address growing public concern. Further, there are strong evidence from the Master Settlement Agreement in 1998 which shows that the radioactivity of tobacco smoke and its potential to cause cancer were known to TI, but they purposefully concealed this information [37]. In another instance in the USA, a network of consultants was developed by TI to advocate ventilation as a "remedy" to second-hand smoke (SHS) [38]. ...
Background: Tobacco Industry (TI) strives to portray itself as being “socially responsible” and contest for pertinent decision-making positions, which it uses to deter, delay or dilute tobacco control measures. There is little documented evidence of Tobacco Industry Interference (TII) from India, the scope of their interference and challenges faced by the experts for effective tobacco control.
Methods: A cross-sectional qualitative research design, based upon in-depth interviews (N=26), was used to explore the opinion of key stakeholders regarding TII in India. The interview schedule collected information about the participant’s roles and responsibilities in tobacco control, the nature of TII faced by the participant, means of influence by TI, barriers and challenges to tobacco control efforts using a set of questions.
Results: Most of the respondents were engaged in tobacco control, training, advocacy, and awareness generation activities from the last 5-10 years or more. The respondents defined the TI and its scope as per their experience with the help of power ranking methodology. Most of them perceived TI as ‘Manufacturers’ while others consider them as ‘advertisers’, ‘public relation companies’, ‘wholesalers’, ‘vendors’, and ‘Government firms having TI stocks’ as TI. We identified six major domains (Influencing the policy and administrative decisions, Interference with implementation of tobacco control laws and activities, False propaganda and hiding the truth, manipulating front action groups (FAG), Rampant tobacco advertising and promotion activities, and others) under which TII activities were classified. Most respondents were of opinion that TI players were interfering in the policy decisions, implementation of the tobacco control laws and activities, and manipulating the FAG. A detailed taxonomic classification of the TII strategies that emerged from our analysis were linked to article 5.3 of FCTC.
Conclusions: The activity documented a significant level of TII in different domains with stakeholders acting at various hierarchical levels. The study provide insights about the nefarious tactics of TI, enable stakeholders to anticipate and pre-empt the kinds of alliances the TI may attempt to build, stimulate academicians and researchers to undertake in-depth analysis into various strategies and underscore the need for ensuring transparency in official interactions with the TI and their representatives.
... As the evidence for lethal impact of tobacco products started mounting, the companies created uncertainty and dispute regarding health risks, whilst at the same time had put lters on cigarettes and promised research into health effects of smoking to address growing public concern. Further, there are strong evidence from the Master Settlement Agreement in 1998 which shows that the radioactivity of tobacco smoke and its potential to cause cancer were known to TI, but they purposefully concealed this information [31]. In another instance in the USA, a network of consultants was developed by TI to advocate ventilation as a "remedy" to second-hand smoke (SHS) [32]. ...
Background: Tobacco Industry (TI) strives to portray itself as being “socially responsible” and contest for pertinent decision-making positions, which it uses to deter, delay or dilute tobacco control measures. There is little documented evidence of Tobacco Industry Interference (TII) from India, the scope of their interference and challenges faced by the experts for effective tobacco control.
Methods: A cross-sectional qualitative research design, based upon in-depth interviews (N=26), was used to explore the opinion of key stakeholders regarding TII in India. The interview schedule collected information about the socio-demographic information of the study participant, the participant’s roles and responsibilities in tobacco control, the nature of TII faced by the participant, means of influence by TI, barriers and challenges to tobacco control efforts using a set of questions. Principles of the ‘grounded theory’ were used to understand beliefs and thoughts of key-experts about TII in India, its interactions and interference at various levels.
Results: Most of the respondents were engaged in tobacco control, training, advocacy, and awareness generation activities from the last 5-10 years or more. The respondents defined the TI and its scope as per their experience. We identified six major domains (Influencing the policy and administrative decisions, Interference with implementation of tobacco control laws and activities, False propaganda and hiding the truth, manipulating front action groups, Rampant tobacco advertising and promotion activities, and others) under which TII activities can be classified comprehensively.
Conclusions: The activity documented a significant level of TII in different domains with stakeholders acting at various hierarchical levels. This can help to provide insights about the nefarious tactics of TI, enable stakeholders to anticipate and pre-empt the kinds of alliances the TI may attempt to build, stimulate academicians and researchers to undertake in-depth analysis into various strategies and underscore the need for ensuring transparency in official interactions with the TI and their representatives.
... ETS exposure was associated consistently with higher lung cancer risk in all the strata considered. The adjusted odds ratios (AOR) evaluating the association between ETS and lung cancer risk for the different strata were: nonsmokers ( 58) and participants who had <15 packyears and nonsmokers (GSTP1 GG AOR = 1.93; 95% CI = 0.54-6.97; GSTP1 AA AOR = 1.58; 95% CI = 0.83-3.01). ...
Cancer is the general name for a group of more than 100 diseases. Although there are many kinds of cancer, all cancers start because abnormal cells grow out of control. Untreated cancers can cause serious illness and death. The body is made up of trillions of living cells. Normal body cells grow, divide, and die in an orderly fashion. During the early years of a person's life, normal cells divide faster to allow the person to grow. After the person becomes an adult, most cells divide only to replace worn-out or dying cells or to repair injuries. This article introduces recent research reports as references in the cancer and smoke related studies.
... Uranium occurs naturally in soil but in much Higher, concentration in phosphate rock from which fertilizer is made. There are two pathways leading from Uranium to Polonium in tobacco: through the air and through the roots [3].The plants roots are naturally related to microorganisms, and these associations can have direct or indirect impacts on the mobility, availability and acquisition of elements by plants [4][5][6][7]. The radiological effect of the uses of fertilizers in soil is due to the internal irradiation of the respiratory organ by the alpha particles, short lived radon-thoron progeny and the external irradiation of the body by gamma rays emitted from the radionuclides. ...
In present work, radon gas concentrations were measured for (48) samples of cigarette that it was collected from market of Iraq, using plastic nuclear track detectors CR-39.The annual effective dose from use of these cigarette were determined. The results show that, Radon concentration ranges from (0.868 to 624.576) Bq/m 3 with average value (123.375) Bq/m 3 .The radon concentrations emerged from most investigated samples was significantly higher than the background level.
... Studies revealed that the presence of radioactive substances in the smoking tobacco results in the accumulation of insoluble radioactive particles in the respiratory system that acts as a significant factor for the increasing risk of cancers among smokers [5,6]. Among the toxic radionuclides present in tobacco 210 Po was the enhanced risk factor to cause lung cancer in smokers [7][8][9]. ...
The present study has carried out with an objective of determining the activity concentrations of two radionuclides namely polonium-210 (²¹⁰Po) and lead-210 (²¹⁰Pb) in smoke tobacco products (cigarette, bidi and cigar) and smokeless tobacco products (chewing tobacco and snuff) consumed in Tiruchirappalli District, Tamil Nadu (India) and their annual committed effective dose to tobacco consumers. The concentration of ²¹⁰Po was always higher than that of ²¹⁰Pb in all the analyzed tobacco products. It also revealed that 79% of Annual committed effective dose comes from ²¹⁰Po and about 21% from ²¹⁰Pb. Maximum concentration (13.2 mBq g⁻¹) of ²¹⁰Po recorded in cigarette and lowest concentration was observed in snuff (6.4 mBq g⁻¹). The highest mean committed effective dose of ²¹⁰Po and ²¹⁰Pb in various tobacco products were found in cigarette followed by bidi, cigar, chewing tobacco and snuff. The study revealed that the tobacco products available in Tiruchirappalli District contain a relatively lower concentration of radionuclides when compared to other regional studies. Since this kind of study in India is fragmentary, the present study has generated a base data for the first time for entire Tiruchirappalli District.
... Long-term smoking, therefore, may cause radiation-induced damages in perennial oral mucosa. [28] Thus, smokers are more likely to have severe radiation induced oral mucosal reactions during radiotherapy. The results in our study that smoking history is a significant correlated factor for oral mucosal reaction were consistent with the previous findings. ...
To investigate risk factors for acute oral mucosal reaction during head and neck squamous cell carcinoma radiotherapy.
A retrospective study of patients with head and neck squamous cell carcinoma who underwent radiotherapy from November 2013 to May 2016 in Anhui Provincial Cancer Hospital was conducted. Data on the occurrence and severity of acute oral mucositis were extracted from clinical records. Based on the Radiation Therapy Oncology Group (RTOG) grading of acute radiation mucosal injury, the patients were assigned into acute reaction (grades 2–4) and minimum reaction (grades 0–1) groups. Preradiotherapy characteristics and treatment factors were compared between the 2 groups. Multivariate logistic regression analysis was used to detect the independent factors associated with acute oral mucosal reactions.
Eighty patients completed radiotherapy during the study period. Oral mucosal reactions were recorded as 25, 31, and 24 cases of grades 1, 2, and 3 injuries, respectively. Significant differences between acute reaction and minimum reaction groups were detected in cancer lymph node (N) staging, smoking and diabetes history, pretreatment platelet count and T-Helper/T-Suppressor lymphocyte (Th/Ts) ratio, concurrent chemotherapy, and total and single irradiation doses.
Multivariate analysis showed that N stage, smoking history, single dose parapharyngeal irradiation, and pretreatment platelet count were independent risk factors for acute radiation induced oral mucosal reaction. Smoking history, higher grading of N stage, higher single dose irradiation, and lower preirradiation platelet count may increase the risk and severity of acute radiation oral mucosal reaction in radiotherapy of head and neck cancer patients.
... Asap rokok merupakan campuran kompleks yang terdiri dari lebih 100 zat karsinogen [1,2], dan Tar ...
Kandungan 226Ra, 210Pb, 210Po dan 40K pada beberapa tembakau rokok di Indonesia. Pada penelitian ini telah dilakukan pengukuran radionuklida alam 226Ra, 210Pb, 210Po dan 40K yang terkandung didalam tembakau rokok, tujuannya untuk memperkirakan dosis efektif yang diterima oleh orang yang menghisap asap rokok. Sampel tembakau yang telah diukur meliputi 14 merek rokok yang umum dijual dan dikonsumsi di Indonesia. Konsentrasi 226Ra, 210Pb dan 40K diukur menggunakan spektrometri sinar γ, didapat konsentrasi 226Ra bervariasi dari 2,86 hingga 6,04 Bq/kg, rata-rata 4,18 ± 0.67 Bq/kg, untuk 210Pb bervariasi dari 3,04 hingga 6,76 Bq/kg rata-rata 4,71 ± 0.82 Bq/kg, sedangkan konsentrasi 40K bervariasi dari 23,57 hingga 32,69 Bq/kg rata-rata 26,50 ± 2,08 Bq/kg. 210Po dihitung berdasarkan kesetimbangan radioaktif, hasilnya bervariasi dari 2,65 hingga 5,88 Bq/kg rata-rata 4,09 ± 0,71 Bq/kg. Dengan menggunakan koefisen dosis efektif yang diberikan oleh ICRP, dapat dilakukan estimasi dosis efektif tahunan yang diterima oleh perokok. Rata-rata dosis efektif tahunan untuk 226Ra adalah 80,46 ± 12,93 µSv/tahun, untuk 210Pb rata-rata 28,47 ± 4,96 µSv/tahun, dan 210Po rata-rata 74,31 ± 12,96 µSv/tahun. Dengan menjumlahkan dosis rata-rata dari 226Ra, 210Pb dan 210Po, didapat total estimasi dosis efektif rata-rata pertahun 183,24 µSv/tahun atau sekitar 14,5% dari batas dosis paparan radiasi secara inhalasi di dunia 1260 µSv/tahun. Estimasi dosis efektif radionuklida 40K tidak dapat dilakukan karena koefisien dosis untuk 40K tidak tersedia di ICRP 71.
... Bretthauer e Black (1967) sugeriam a utilização de uma resina de troca iônica mista como um filtro para cigarros, na intenção de minimizar os efeitos do 210 Po para os tabagistas. A lavagem ácida foi descoberta em 1980 para ser altamente eficaz na remoção de 210 Po a partir das folhas do tabaco porém, assim como a alternativa anterior, não é aplicada porque a indústria tabagista considera prejudicial tal procedimento por ocasionar perda da chamada "nicotina kick", uma má absorção de nicotina no cérebro dos fumantes (KARAGUEUZIAN et al., 2011). ...
Este trabalho teve por finalidade revisar os estudos na literatura envolvendo o Polônio-210 (210Po) de forma geral e relacionado com o tabagismo. A pesquisa ocorreu em artigos científicos publicados no portal BIREME e suas respectivas bases de dados (MEDLINE, LILACS, DECS, HISA e IBECS), somando 944 publicações internacionais envolvendo o 210Po. Destas referências, 239 artigos foram selecionados por possuírem texto completo disponível, sendo utilizados 53 efetivamente. Considerados os estudos já realizados, torna-se necessária a realização de novas pesquisas laboratoriais e populacionais envolvendo a presença do Polônio-210 no tabaco. Mesmo que comprovada esta presença, não houve uma padronização referente ao método de pesquisa e detecção deste elemento químico radioativo.
... It accounts for 28% of all cancer related deaths and 14% of all new cancer cases annually [1]. Increasing amounts of epidemiologic data have indicated that cigarette smoking is the major cause of lung cancer [2][3][4]. Cigarette smoke is estimated to contain as many as 4000 chemicals [5,6]. Of these chemicals, B[a]P, a prototypical polycyclic aromatic hydrocarbon (PAH) found at high concentrations in cigarette smoke, is the most important and strongest lung carcinogen [7][8][9][10]. ...
Benzo[a]pyrene (B[a]P) is a carcinogen in cigarette smoke. We found that B[a]P
induced SIRT1 in human bronchial epithelial BEAS-2B cell. SIRT1 was overexpressed
in the lung of B[a]P-exposed mice and in human lung cancer biopsies. SIRT1
up-regulated TNF-α and β-catenin and down-regulated the membrane fraction of
E-cadherin. In addition, SIRT1 promoted invasion, migration and tumorigenesis
of BEAS-2B cells in nude mice upon B[a]P exposure. Thus, SIRT1 is involved in
B[a]P-induced transformation associated with activation of the TNF-α/β-catenin axis
and is as a potential therapeutic target for lung cancer.
... [1] Moreover, the incidence rate for lung cancer is still on the rise in the developing countries such as China. [2] The main reason for the increasing incidence rate was cigarette smoking and air pollution [3] . About 75-80% lung cancer was nonsmall lung cancer and other 25-20% was small cell lung carcinoma. ...
The purpose of this retrospective study was to evaluate the clinical value of serum cytokeratin-19-fragment (cyfra21-1) as a biomarker in nonsmall cell lung cancer (NSCLC).
Sixty-six patients with NSCLC and 48 cases with benign lung disease were retrospectively analyzed in the department of thoracic surgery in our hospital. The serum level of cyfra21-1 was detected in the above patients. The diagnosis sensitivity, specificity and the receiver operating characteristic curve were calculated by using the stata11.0 statistical software to evaluate the clinical diagnosis value of serum Cyfra21-1 as NSCLC serologic biomarker.
The mean of serum cyfra21-1 were 8.95 eat. 01 μ/L and 4.28 eat. 89 μ/L in NSCLC patient and control groups respectively, which indicated that the NSCLC group were much higher (P < 0.05). The diagnosis sensitivity and specificity were 77.08% and 63.64% at the threshold of 6.32 μ/L respectively. Moreover, the area under the curve was 0.78 (95% confidence interval: 0.70-0.87).
Serum cyfra21-1 can be a potential serologic biomarker in evaluation of NSCLC.
Lifetime lung cancer risks were computed using EPA/BEIR-VI models employing recent North Cyprus statistics (4-year averages from 2012 to 2016) to address public concerns about radon risk. The excess relative risk, the lifetime risk of lung cancer (Re), and lifetime relative risk were estimated in the Nicosia population for both genders of non-smoker and smokers. The excess relative risk average value for age < 55 y, 55 y ≤ age ≤ 64 y, 65 y ≤ age ≤ 74 y, and age ≥ 75 y groups were 0.38, 0.23, 0.13, and 0.04, respectively.
The purpose of this study is to find out the results of the “TITANEON” degradation power test on hazardous CO (carbon monoxide) compounds qualitatively and quantitatively and to explain the working system of the lamp. The research methods used in this study are (a) preparation: tools and materials, design testing tools; (b) conducting research: TiO2/Co synthesis, coating, tool performance test and data processing and analysis; (c) evaluation. The test results in this study were divided into two, namely qualitative and quantitative. In the qualitative test results, the “TITANEON” lamp is able to degrade CO compounds for 20 minutes. The quantitative results from 0 minutes amounted to 15526.24 ppm, 5 minutes later the CO concentration was 6202.82, in the next 15 minutes CO concentration was 2549.98 ppm and in the last 20 minutes the CO concentration was 1871.89 ppm. The system works, namely the first light that involves TiO2 nanoparticles will excite electrons from the valence band to the conduction band while producing positive holes in the valence band and negatively charged electron pairs. After that, TiO2 nanoparticles are transformed into super oxide compounds which release active oxygen species (O2 radicals and OH radicals), these compounds will degrade cigarette smoke compounds into CO2 and H2O compounds through photocatalytic mechanisms.
Cigarette smoking is a strong risk factor for bladder cancer. It has been shown that the duration of smoking is associated with a poor prognosis and a higher risk of recurrence. This is due to tobacco carcinogens forming adducts with DNA and proteins that participate in the DNA repair mechanisms. Additionally, polymorphisms of genes responsible for methyl group transfer in the methionine cycle and dosages of vitamins (from diet and supplements) can cause an increased risk of bladder cancer. Upregulated DNA methyltransferase 1 expression and activity results in a high level of methylated products of metabolism, as well as hypermethylation of tumor suppressor genes. The development of a market that provides new inhibitors of DNA methyltransferase or alternatives for current smokers is essential not only for patients but also for people who are under the danger of secondhand smoking and can experience its long-term exposure consequences.
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.
Objective:
To review current risk factors for lung cancer, identify screening and early detection guidelines while describing new approaches that use genomic technologies.
Data sources:
Published scientific literature, clinical literature, and published lung cancer screening guidelines from the United States and Canada.
Conclusion:
Nurses are caring for lung cancer patients who, historically, do not live for long periods after diagnosis. Research is revealing promising screening methodologies that can detect lung cancer 1 to 4 years earlier than the current approaches.
Implications for nursing practice:
Current knowledge about screening for lung cancer is a vital tool for nurses working with persons at high risk for this potentially aggressive and life-threatening malignancy. While old methods remain the standard of care, new detection methods use a variety of genomic-based technologies. These developing approaches emphasize the need for nurses at all levels of practice to have a working knowledge of genetics to educate patients and conference with colleagues.
It has been known for a long time that cigarette tobacco contains naturally occurring radioactive nuclides such as Pb and Po. In this study, the concentrations of Pb and Po in the 10 most widely sold cigarette brands in Italy during the year 2010 were measured, and the effective dose to smokers has been calculated. The results of this study show that Pb concentration ranged from 11.6 to 20.0 mBq cig with an arithmetic mean of 14.6 mBq cig, while the activity concentration of Po ranged from 13.1 to 19.0 mBq cig with an arithmetic mean of 15.7 mBq cig, thus confirming previous results and showing that the radioactivity concentration was not reduced in the last few years. The annual effective dose for a typical smoker consuming 20 cigarettes per day ranged from an average of 55 μSv y to about 81 μSv y. It is finally put in evidence the need to improve the knowledge about crucial data needed for accurate dose assessment deriving from the inhalation of both radioisotopes contained in the cigarettes, namely the dose conversion coefficients, which strongly depend on several parameters such as the inhalation speed through the mouth, the real fraction of radionuclide transferred from cigarette to mainstream smoke, the lung absorption behavior of the radioisotopes inhaled with mainstream smoke, and the AMAD of particles inhaled by smokers.
The first scientific paper on polonium-210 in tobacco was published in 1964, and in the following decades there would be more research linking radioisotopes in cigarettes with lung cancer in smokers. While external scientists worked to determine whether polonium could be a cause of lung cancer, industry scientists silently pursued similar work with the goal of protecting business interests should the polonium problem ever become public. Despite forty years of research suggesting that polonium is a leading carcinogen in tobacco, the manufacturers have not made a definitive move to reduce the concentration of radioactive isotopes in cigarettes. The polonium story therefore presents yet another chapter in the long tradition of industry use of science and scientific authority in an effort to thwart disease prevention. The impressive extent to which tobacco manufacturers understood the hazards of polonium and the high executive level at which the problem and potential solutions were discussed within the industry are exposed here by means of internal documents made available through litigation.
Concerns over cancer development from exposure to environmental sources of densely ionizing, high linear energy transfer (LET) radiation, such as alpha-particles from radon, is a current public health issue. The study of tumors attributable to high LET irradiation would greatly augment our insights into the biological mechanisms of carcinogenesis. Chronic low-dose-rate internal exposure to alpha-radiation from thorium dioxide deposits following intravascular administration of the radiographic contrast agent Thorotrast is known to markedly increase the risk of cancer development, especially that of hepatic angiosarcomas and cholangiocarcinomas. Although the mechanism is hypothesized to be via cellular damage, DNA being a major target, wrought by the high LET alpha-particles, the specific genes and the actual sequence of events involved in the process of transforming a normal cell into a malignant one are largely unknown. To shed some light on the molecular mechanisms of cancer development during a lifetime exposure to alpha-radiation, we analyzed the most commonly affected tumor suppressor gene in humans, p53, in 20 Thorotrast recipients who developed cancer, mostly of hepatic bile duct and blood vessel origin. Of the 20 cases, 19 were found to harbor p53 point mutations. Moreover, the accompanying non-tumor tissues from these patients also had p53 mutations, albeit at lower frequency. The distribution pattern of the point mutations was significantly different between the non-tumor and tumor tissues, with most mutations in malignant tissues located in the highly conserved domains of the p53 gene. Our results support the idea that p53 mutations are important in the genesis of Thorotrast-induced tumors but that these point mutations are a secondary outcome of genomic instability induced by the irradiation. Additionally, non-tumor cells harboring p53 mutations may gain some survival advantage in situ but mutations in the domains responsible for the formation of structural elements critical in binding DNA may be necessary for a cell to reach full malignancy.
Due to the relatively high activity concentrations of ²¹⁰Po and ²¹⁰Pb that are found in tobacco and its products, cigarette smoking highly increases the internal intake of both radionuclides and their concentrations in the lung tissues. That might contribute significantly to an increase in the internal radiation dose and in the number of instances of lung cancer observed among smokers. Samples of most frequently smoked fine and popular brands of cigarettes were collected from those available on the Egyptian market. ²¹⁰Po activity concentrations were measured by alpha spectrometry, using surface barrier detectors, following the radiochemical separation of polonium. Samples of fresh tobacco, wrapping paper, fresh filters, ash and post-smoking filters were spiked with ²⁰⁸Po for chemical recovery calculation. The samples were dissolved using mineral acids (HNO3, HCl and HF). Polonium was spontaneously plated-out on stainless steel disks from diluted HCl solution. The ²¹⁰Po activity concentration in smoke was estimated on the basis of its activity in fresh tobacco and wrapping paper, fresh filter, ash and post-smoking filters. The percentages of ²¹⁰Po activity concentrations that were recovered from the cigarette tobacco to ash, post-smoking filters, and smokes were assessed. The results of this work indicate that the average (range) activity concentration of ²¹⁰Po in cigarette tobacco was 16.6 (9.7–22.5) mBq/cigarette. The average percentages of ²¹⁰Po content in fresh tobacco plus wrapping paper that were recovered by post-smoking filters, ash and smoke were 4.6, 20.7 and 74.7, respectively. Cigarette smokers, who are smoking one pack (20 cigarettes) per day, are inhaling on average 123 mBq/d of ²¹⁰Po and ²¹⁰Pb each. The annual effective doses were calculated on the basis of ²¹⁰Po and ²¹⁰Pb intake with the cigarette smoke. The mean values of the annual effective dose for smokers (one pack per day) were estimated to be 193 and 251 μSv from ²¹⁰Po and ²¹⁰Pb, respectively.
The present study assessed smokers' beliefs about the health risks of smoking and the benefits of smoking filtered and low-tar cigarettes, and their awareness of and interest in trying so-called reduced-risk tobacco products. Results were based on a nationally representative random-digit-dialed telephone survey of 1,046 adult (aged 18 years or older) current cigarette smokers. Data were gathered on demographic characteristics, tobacco use behaviors, awareness and use of nicotine medications, beliefs about the health risks of smoking, content of smoke and design features of cigarettes, and the safety and efficacy of nicotine medications. In addition, respondents were asked about their interest in and perceived ability to stop smoking and about their desire for more information about the health risks of smoking. Smokers were least knowledgeable about low-tar and filter cigarettes (65% of responses were incorrect or "don't know") and most knowledgeable about the health risks of smoking (39% of responses were incorrect or "don't know"). The smokers' characteristics most commonly associated with misinformation when all six indices were combined into a summary index were as follows: those aged 45 years or older, smokers of ultralight cigarettes, smokers who believe they will stop smoking before they experience a serious health problem caused by smoking, smokers who have never used a stop-smoking medication, and smokers with a lower education level. Those who believed they would stop smoking in the next year were more knowledgeable about smoking. Some 77% of respondents reported a desire for additional information from tobacco companies on the health dangers of smoking. The present findings demonstrate that smokers are misinformed about many aspects of the cigarettes they smoke and stop-smoking medications and that they want more information about ways to reduce their health risks.
Concerns over cancer development from exposure to environmental sources of densely ionizing, high linear energy transfer (LET) radiation, such as α-particles from radon, is a current public health issue. The study of tumors attributable to high LET irradiation would greatly augment our insights into the biological mechanisms of carcinogenesis. Chronic low-dose-rate internal exposure to α-radiation from thorium dioxide deposits following intravascular administration of the radiographic contrast agent Thorotrast is known to markedly increase the risk of cancer development, especially that of hepatic angiosarcomas and cholangiocarcinomas. Although the mechanism is hypothesized to be via cellular damage, DNA being a major target, wrought by the high LET α-particles, the specific genes and the actual sequence of events involved in the process of transforming a normal cell into a malignant one are largely unknown. To shed some light on the molecular mechanisms of cancer development during a lifetime exposure to α-radiation, we analyzed the most commonly affected tumor suppressor gene in humans, p53, in 20 Thorotrast recipients who developed cancer, mostly of hepatic bile duct and blood vessel origin. Of the 20 cases, 19 were found to harbor p53 point mutations. Moreover, the accompanying non-tumor tissues from these patients also had p53 mutations, albeit at lower frequency. The distribution pattern of the point mutations was significantly different between the non-tumor and tumor tissues, with most mutations in malignant tissues located in the highly conserved domains of the p53 gene. Our results support the idea that p53 mutations are important in the genesis of Thorotrast-induced tumors but that these point mutations are a secondary outcome of genomic instability induced by the irradiation. Additionally, non-tumor cells harboring p53 mutations may gain some survival advantage in situ but mutations in the domains responsible for the formation of structural elements critical in binding DNA may be necessary for a cell to reach full malignancy.
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.
In the race to the South Pole, explorer Robert F. Scott refused to sacrifice his ambitious science agenda
The tobacco industry has known for decades how to remove a dangerous isotope from cigarettes but has done nothing about it. The government now has the power to force a change
The Family Smoking Prevention and Tobacco Control Act provides the FDA with the authority to regulate tobacco products. Drs. Lawrence Deyton, Joshua Sharfstein, and Margaret Hamburg from the FDA describe the implementation of this law.
The radon decay products lead-210 ((210)Pb) and polonium-210 ((210)Po) are known components of tobacco. China is the world's largest producer and consumer of cigarettes, yet no comprehensive published reports of the (210)Pb and (210)Po activity concentrations in Chinese cigarettes are available. Twelve brands of cigarettes that were commonly smoked within a group of 184 Chinese smokers were selected for (210)Pb and (210)Po activity analysis. For each brand, the tobacco from two cigarettes was isolated, dried, weighed, spiked with a (209)Po tracer for yield, and digested with concentrated HNO3, followed by HCl. The polonium in each digested solution was spontaneously deposited onto a nickel disc. The polonium activity was then counted using alpha spectroscopy. The mean (range) (210)Po activity for all brands was 23 (18-29) mBq cig(-1). The state of radioactive equilibrium between (210)Po and (210)Pb in each cigarette was verified in three brands of cigarettes. Cigarettes from two brands were smoked on a machine in order to estimate the fraction of (210)Pb and (210)Po inhaled. An average of 8% of the (210)Pb and 13% of the (210)Po in the tobacco of the cigarettes was transferred to the mainstream smoke. It is thus estimated that a person smoking 20 of these cigarettes per day in China would inhale a mean (range) of 37 (29-46) mBq d(-1) of (210)Pb and 60 (47-75) mBq d(-1) of (210)Po. Cigarette smoking in China may therefore be a large source of a person's daily intake of (210)Pb and (210)Po.
This paper presents clinical, experimental, and epidemiologic evidence to help explain the rapidly increasing incidence of primary lung cancer, with recently observed reversal in leading cell type from squamous cell to adenocarcinoma. It postulates that this may be due to changes in modern cigarettes, with or without filters, which allow inhalation of increased amounts of radioactive lead and polonium and decreased amounts of benzopyrene. This hypothesis is based upon measurements of increased concentrations of radioactive polonium in the lungs of cigarette smokers, in modern tobaccos grown since 1950, and in high-phosphate fertilizers used for tobacco farming in industrialized countries. Critical support for this thesis is based upon experimental animal studies in which lung cancers that resemble adenocarcinomas are induced with as little as 15 rads of radioactive polonium, equal to one fifth the dosage inhaled by cigarette smokers who average two packs a day during a 25-year period.
Airborne 210Pb is concentrated on small Aitken particles which accumulate on tobacco trichomes. Tobacco curing and the combustion of trichomes in burning cigarettes produce insoluble particles of high 210Pb radioactivity which are inhaled and deposited in the bronchi of smokers. The subsequent ingrowth of 210Po results in high local a irradiation which may account for bronchial cancer among smokers.
Use of a mixed ion-exchange resin as a filter for cigarettes markedly reduces both the total amount of polonium-210 in mainstream
smoke and the picocuries per milligram of smoke. This procedure effectively minimizes exposure of the lungs of smokers to
alpha irradiation.
Concentrations of the alpha-particle-emitting radioactive element polonium was measured in various pulmonary tissues of smokers and nonsmokers in order to determine 1) whether this radiation exposure is associated with the development of bronchial cancer in smokers; and 2) how smoke is absorbed and excreted in human lungs. Lung specimens from 25 current cigarette smokers, 2 current pipe smokers, 1 former cigarette smoker, and 8 nonsmokers ere analyzed. The average concentration of polonium in the peripheral parenchyma of current smokers was .0074 picocurie/gm and in nonsmokers was .0016. For smokers, the average concentration was doubled in more centrally located parenchyma and was greater in the upper than in the lower lobes. Polonium concentrations correlated with daily cigarette consumption but not with total cigarettes smoked. The concentrations in peribronchial lymph nodes of smokers were also higher than in nonsmokers. These values show no correlation with total or daily cigarette consumption. Polonium concentration was similiar in bronchial wall parenchyma as in lung parenchyma but was greater in bronchial epithelium than in parenchymal or lymph nodes. The patterns of distribution of polonium throughout the lung suggest that most inhaled smoke particles are rapidly cleared from the lung, and polonium is primarily cleared by mucus sheet. Since the highest local concentrations of polonium were found in bronchial epithelium from segmental bifurcations, leading to a high cumulative local radiation dose, polonium may be implicated in the initiation of bronchial cancer in humans.
The part played by polonium-210 in contributing to the biologically effective radiation dose received by humans in a variety of environments is described. The selection of data presented has been dictated to a large extent by the availability of post-mortem and other specimens and cannot be considered comprehensive. The correspondence both for grazing animals and humans between the levels of polonium-210 in the food of a community and in the tissues of its members clearly indicates that food ingestion is an important route for acquisition of body-burdens of the nuclide. The variations by an order of magnitude or more between polonium-210 body-burdens in "normal" United Kingdom and U.S. residents and in some Canadian Eskimos are probably due to the latter having a high dietary content of meat derived from animals grazing on poor slowly growing pasture. Cigarette smoking does not seem to lead to abnormal levels of polonium-210 in tissues other than lung and the levels here examined either as gross tissue concentrations or as localized concentrations are not such that would lead to abnormally high radiation dose rates. The question of the part played by physiological uptake of lead-210 in producing tissue concentrations of polonium-210 is still not completely resolved.
Test plants were grown within a chamber enriched with radon-222 in the atmosphere, in tobacco fields with different sources of phosphate-containing fertilizer, and in culture containing lead-210 in the nutrient solution. Harvested leaves were subjected to three curing conditions. The major portion of the lead-210 in the plant was probably absorbed through the roots. Airborne radon 222 and its daughters contributed much less to the plant's content of lead-210 and of polonium-210. The stage of leaf development and the methods used to cure the leaf affected the final amount of polonium-210 in tobacco leaf.
Concentrations of lead-210 and polonium-210 in rib bones taken from 13 cigarette smokers were about twice those in six nonsmokers, the polonium-210 being close to radioactive equilibrium with the lead-210. In alveolar lung tissue the concentration of lead-210 in smokers was about twice that in nonsmokers. These differences are attributed to additional intake by inhalation of lead-210.
Analyses of smokers pulmonary tissues that showed "hot spots" of 210-polonium at segmental bifurcations of bronchial epithelium (4.5 pc/g of wet tissue vs. .12 in the trachea 119 in the lobar bronchi and .004 in the bronchial wall and submucosa) are 100 times higher than some recently reported radiation dose estimates for these areas. However the results of the different studies are compatible when the type and quality of tissues used are taken into consideration. It is emphasized that bronchial epithelium samples deteriorate rapidly after death so they should be obtained quickly. As the concentration of 210-polonium is so much greater at these hot spots than in the bronchial wall and submucosa estimates of radiation dose should be based just on the measured concentrations in the bifurcations.
Synergistic interactions of indoor radon progeny with the cigarette smoking process have been evaluated experimentally. Smoking enhances the air concentration of submicron particles and attached radon decay products. Fractionation in burning cigarettes gives rise to the association of radon progeny with large particles in mainstream cigarette smoke, which are selectively deposited in "hot spots" at bronchial bifurcations. Because smoke tars are resistant to dissolution in lung fluid, attached radon progeny undergo substantial radioactive decay at bifurcations before clearance. Radon progeny inhaled during normal breathing between cigarettes make an even larger contribution to the alpha-radiation dose at bifurcations. Progressive chemical and radiation damage to the epithelium at bifurcations gives rise to prolonged retention of insoluble 210Pb-enriched smoke particles produced by tobacco trichome combustion. The high incidence of lung cancer in cigarette smokers is attributed to the cumulative alpha-radiation dose at bifurcations from indoor radon and thoron progeny--218Po, 214Po, 212Po, and 212Bi--plus that from 210Po in 210Pb-enriched smoke particles. It is estimated that a carcinogenic alpha-radiation dose of 80-100 rads (1 rad = 0.01 J/kg = 0.01 Gy) is delivered to approximately equal to 10(7) cells (approximately equal to 10(6) cells at individual bifurcations) of most smokers who die of lung cancer.
In a study in 29 health centre districts in Japan 91 540 non-smoking wives aged 40 and above were followed up for 14 years (1966-79), and standardised mortality rates for lung cancer were assessed according to the smoking habits of their husbands. Wives of heavy smokers were found to have a higher risk of developing lung cancer and a dose-response relation was observed. The relation between the husband's smoking and the wife's risk of developing lung cancer showed a similar pattern when analysed by age and occupation of the husband. The risk was particularly great in agricultural families when the husbands were aged 40-59 at enrolment. The husbands' smoking habit did not affect their wives' risk of dying from other disease such as stomach cancer, cervical cancer, and ischaemic heart disease. The risk of developing emphysema and asthma seemed to be higher in non-smoking wives of heavy smokers but the effect was not statistically significant. The husband's drinking habit seemed to have no effect on any causes of death in their wives, including lung cancer. These results indicate the possible importance of passive or indirect smoking as one of the causal factors of lung cancer. They also appear to explain the long-standing riddle of why many women develop lung cancer although they themselves are non-smokers. These results also cast doubt on the practice of assessing the relative risk of developing lung cancer in smokers by comparing them with non-smokers.
This article has no abstract; the first 100 words appear below.
DEATHS Biron — Pierre Edouard Biron, M.D., of Beverly, died on October 12. He was in his 50th year. Dr. Biron received his degree from the University of Ottawa School of Medicine in 1957. He was a member of the American Medical Association and the American Academy of Orthopedic Surgeons. He is survived by his wife, two daughters and a son, his parents, and a sister. Denning — Walter Stephen Denning, M.D., of Brookline, died on December 23. He was in his 79th year. Dr. Denning received his degree from the University of Vermont College of Medicine in 1929. He . . .
The ..cap alpha.. activity of cigarette smoke tar deposited onto membrane filters was found to be associated with the relatively insoluble fraction. Perfusion of the tar with physiological saline resulted in no change in the mean measured activity, but there was more variability in the measured values for the perfused tar than for the initial tar samples. Analysis of cigarette smoke condensate shows that radium and thorium are present, but over 99% of the ..cap alpha.. activity results from ²¹°Po. Repeat measurements after a time lapse of 2 1/2 years indicate that the initial ²¹°Pb content of the tar is roughly 30 to 40% of the original ²¹°Po content for both unprocessed and perfused samples. An increase in the ..cap alpha.. activity concentration of smoke deposited in lung tissue may result from the lack of solubility of the radioactive material compared with other smoke constituents.
To examine the involvement of tobacco industry lawyers in the selection of tobacco industry scientific research projects and to examine how the research was used to influence public policy.
Documents from Brown and Williamson Tobacco Corporation, the British American Tobacco Company (BAT), and other tobacco interests provided by an anonymous source, obtained from Congress, and received from the private papers of a former BAT officer.
All available materials, including confidential reports regarding research and internal memoranda exchanged between tobacco industry lawyers.
The involvement of tobacco industry lawyers in the selection of scientific projects to be funded is in sharp contrast to the industry's public statements about its review process for its external research program. Scientific merit played little role in the selection of external research projects. The results of the projects were used to generate good publicity for the industry, to deflect attention away from tobacco use as a health danger, and to attempt, sometimes surreptitiously, to influence policymakers.
To understand how attorneys for the tobacco industry in general, and Brown and Williamson Tobacco Corporation (B&W) in particular, have responded to the threat of products liability litigation arising from smoking-induced diseases.
Documents from B&W, the British American Tobacco Company (BAT), and other tobacco interests provided by an anonymous source, obtained from Congress, or received from the private papers of a former BAT officer.
All available materials, including confidential reports regarding research and internal memoranda exchanged between tobacco industry lawyers.
The documents demonstrate that the tobacco industry in general, and B&W in particular, were very concerned about the threat of products liability lawsuits, and they illustrate some of the steps taken by lawyers at one company to avoid the discovery of documents that might be useful to a plaintiff in such a lawsuit. These steps included efforts to control the language of scientific discourse on issues related to smoking and health, to bring all potentially damaging internal scientific documents under attorney work product and attorney-client privilege to avoid discovery, to remove "deadwood" documents, and to insulate B&W from knowledge of potentially damaging scientific information from other BAT companies.
The carcinogenic etfect of 210Po and 210Pb with respect to lung cancer is an important problem in many countries with very high cigarette consumption. Poland has one of the highest consumptions of cigarettes in the world. The results of 210Po determination on the 14 most frequently smoked brands of cigarettes which constitute over 70% of the total cigarette consumption in Poland are presented and discussed. Moreover, the polonium content in cigarette smoke was estimated on the basis of its activity in fresh tobaccos, ash, fresh filters and post-smoking filters. The annual effective doses were calculated on the basis of 210Po and 210Pb inhalation with the cigarette smoke. The results of this work indicate that Polish smokers who smoke one pack (20 cigarettes) per day inhale from 20 to 215 mBq of 210Po and 210Pb each. The mean values of the annual effective dose for smokers were estimated to be 35 and 70 microSv from 210Po and 210Pb, respectively. For persons who smoke two packs of cigarettes with higher radionuclide concentrations, the effective dose is much higher (471 microSv yr(-1)) in comparison with the intake in diet. Therefore, cigarettes and the absorption through the respiratory system are the main sources and the principal pathway of 210Po and 210Pb intake of smokers in Poland.
Cigarette smoking is one of the pathways that might contribute significantly to the increase in the radiation dose reaching man, due to the relatively large concentrations of 210Pb and 210Po found in tobacco leaves. In the present study, the concentrations of these two radionuclides were determined in eight of the most frequently sold cigarette brands produced in Brazil. 210Pb was determined by counting the beta activity of 210Bi with a gas flow proportional detector after radiochemical separation and precipitation of PbCrO4. 210Po was determined by alpha spectrometry using a surface barrier detector after radiochemical separation and spontaneous deposition of Po on a copper disk. The results showed concentrations ranging from 11.9 to 30.2 mBq per gram of dry tobacco for 210Pb and from 10.9 to 27.4 mBq per gram of dry tobacco for 210Po. The collective committed effective dose resulting from the use of cigarettes produced in Brazil per year is estimated to be 1.5 x 10(4) man-Sv.
IN 1957 two of us (O.A. and A.P.S.), with several collaborators, presented a report of progress on a study of the relative frequency of carcinoma in situ, squamous metaplasia, stratification and basal-cell hyperplasia in the lungs of nonsmokers and light and heavy smokers of cigarettes.1 The study was carried out on the lungs of 117 male patients dying with and without lung cancer by means of step sections of the entire tracheobronchial tree, totaling 208 sections per case. This was done in conformity with a rigidly observed plan, the details of which are fully described in the preceding publication. . . .
Polonium-210, which emits alpha particles, is a natural contaminant of tobacco. For an individual smoking two packages of cigarettes a day, the radiation dose to bronchial epithelium from Po(210) inhaled in cigarette smoke probably is at least seven times that from background sources, and in localized areas may be up to 1000 rem or more in 25 years. Radiation from this source may, therefore, be significant in the genesis of bronchial cancer in smokers.
Contents of radium-226 and polonium-210 in leaf tobacco and tobacco-growing soils vary with the source. The differences may
result from production locality, culture, and curing. The polonium seems to be not entirely derived from the radium; plants
probably take it up from the soil or air.
This Special Report discusses the implications of the 1998 Master Settlement Agreement between the states and the tobacco industry. In the context of current state budget crises, a decreasing proportion of the settlement dollars is being spent on programs to reduce smoking. This report presents an overview of local, state, and federal tobacco-control policies and reviews recent developments focused on taxation, smoking cessation, bans on smoking in public areas, and international trade policies.
In 1998, 46 states and the four major tobacco companies signed the Master Settlement Agreement (MSA), which stipulated that the tobacco companies pay states $206 billion over 25 years and take steps to reduce youth smoking. The remaining states settled separately. We sought to determine the effect of the settlements on demand for cigarettes. Using a nationwide sample from 1990 to 2002, we estimated a model of the decision to smoke cigarettes. The settlements affected smoking primarily through price increases for cigarettes, although there was evidence that other policy instruments influenced smoking rates for younger smokers. By 2002, the settlements had reduced overall smoking rates by 13 percent for ages 18 to 20 and older than 65 and 5 percent for ages 21 to 64.
Tobacco leaves are large and have sticky exudates that retain the radon decay products once they deposit on the leaves. The study of 210Po in tobacco is required, because of the cumulative alpha-radiation dose delivered to humans from inhaled 210Po in cigarette smoke. 210Pb is the other element of interest since it is the 210Po precursor in the radioactive decay chain. In the present study, the concentrations of these two radionuclides were determined in tobacco samples from seven regions in Greece. 210Po was determined by alpha spectrometry using a surface barrier detector after radiochemical separation and spontaneous deposition of polonium on a nickel disk. The 210Pb activity in the samples was determined via the 210Po resulting from the decay of 210Pb. The results of the present study indicate that 210Po concentrations ranged from 3.6 to 17.0 mBqg(-1) (average 13.1 mBqg(-1)) of dry tobacco, while 210Pb concentrations ranged from 7.3 to 18.0 mBqg(-1) (average 13.4 mBqg(-1)). The mean value of the annual committed effective dose for smokers (20 cigarettes per day) of Greek tobacco was estimated to be 287 microSv (124 microSv from 210Po and 163 microSv from 210Pb). The inhalation dose for smokers is on average about 12 times higher than for non-smokers living in the mid-latitudes of the northern hemisphere.
The radioactivity in tobacco leaves collected from 15 different regions of Greece before cigarette production was studied
in order to estimate the effective dose from cigarette tobacco due to the naturally occurring primordial radionuclides, such
as 226Ra and 210Pb of the uranium series and 228Ra of the thorium series and or man-made radionuclides, such as 137Cs of Chernobyl origin. Gamma-ray spectrometry was applied using Ge planar and coaxial type detectors of high resolution and
high efficiency. It was concluded that the annual effective dose due to inhalation for adults (smokers) for 226Ra varied from 42.5 to 178.6 μSv y−1 (average 79.7 μSv y−1), while for 228Ra from 19.3 to 116.0 μSv y−1 (average 67.1 μSv y−1) and for 210Pb from 47.0 to 134.9 μSv y−1 (average 104.7 μSv y−1), that is the same order of magnitude for each radionuclide. The sum of the effective doses of the three natural radionuclides
varied from 151.9 to 401.3 μSv y−1 (average 251.5 μSv y−1). The annual effective dose from 137Cs of Chernobyl origin was three orders of magnitude lower as it varied from 70.4 to 410.4 nSv y−1 (average 199.3 nSv y−1).
210Po and its precursor 210Pb in cigarette smoke contribute a significant radiation dose to the lungs of smokers. In this work, the concentration of 210Po was determined in 17 of the most frequently smoked cigarette brands in Italy. Samples of tobacco, fresh filters, ash, and post-smoking filters were analyzed; 210Po was determined by alpha spectrometry after its spontaneous deposition on a silver disk. To verify the radioactive equilibrium between 210Po and 210Pb, lead was determined in one tobacco sample by counting the beta activity of its decay product 210Bi with a gas flow proportional detector after separation. The results of the present study show 210Po concentrations ranged from 6.84 to 17.49 mBq per cigarette. Based on these results, smokers who smoke 20 cigarettes per day inhale, on average, 79.53 +/- 28.65 mBq d(-1) of 210Po and 210Pb each. The mean value of the annual committed effective dose for Italian smokers, calculated by applying the dose conversion factor for adults of 4.3 microSv Bq(-1) for 210Po and 5.6 microSv Bq(-1) for 210Pb, was estimated to be 124.8 and 162.6 microSv y(-1) for 210Po and 210Pb, respectively. The lung dose from inhalation of cigarette smoke is much higher than the lung dose from inhalation of atmospheric 210Po and 210Pb.
Cigarette smoking is a source of radiation exposure due to the concentrations of natural radionuclides in the tobacco leaves. From the health point of view, measurement of (210)Pb and (210)Po contents in cigarette tobacco is important to assess the radiological effects associated with the tobacco smoking for the smokers. In the present study, activity concentrations of (210)Pb, which is a (210)Po precursor in the (238)U-decay series, were measured in cigarette tobaccos. Samples of nine different commonly sold brands of cigarette tobaccos were analysed by employing a planar high purity germanium (HPGe) low background detector. Activity concentrations of (210)Pb were measured from its gamma peak at 47 keV. Mean activity concentration of (210)Pb was measured to be 13 +/- 4 Bq kg(-1) from all samples analysed. The annual committed effective dose for a smoker and the collective committed effective dose corresponding to annual cigarettes production were estimated to be 64 +/- 20 microSv and 0.6 x 10(2) man-Sv, respectively.
Philip Morris and other tobacco companies have been using ammonia in their manufacturing for more than half a century, and for a variety of purposes: to highlight certain flavors, to expand or “puff up” the volume of tobacco, to prepare reconstituted tobacco sheet (“recon”), to denicotinize (reduce the amount of nicotine in) tobacco, and to remove carcinogens.
By the early 1960s, however, Philip Morris had also begun using ammonia to “freebase” the nicotine in cigarette smoke, creating low-yield (reduced-tar or -nicotine) cigarettes that still had the nicotine kick necessary to keep customers “satisfied” (i.e., addicted). We show that Philip Morris discovered the virtues of freebasing while analyzing the impact of the ammoniated recon used in Marlboro cigarettes.
We also show how Marlboro’s commercial success catalyzed efforts by the rest of the tobacco industry to discover its “secret,” eventually identified as ammonia technology, and how Philip Morris later exploited the myriad uses of ammonia (e.g., for flavoring and expanding tobacco volume) to defend itself against charges of manipulating the nicotine deliveries of its cigarettes.
210Po and 210Pb inhalation by cigarette smoking in Italy Radioactivity measurements on tobacco leaf & cigarettes. Souza Cruz Group. Bates numbers 400751698 to 1699 Tobacco product regulation—A public health approach Radioactivity in ciga-rette smoke
- D Desideri
- M A Meli
- L Feduzi
- C L Roselli
- J Sharfstein
- M Hamburg
Desideri, D., Meli, M. A., Feduzi, L., & Roselli, C. (2007). 210Po and 210Pb inhalation by cigarette smoking in Italy. Health Physics, 92, 58–63. doi:10.1097/01.HP.0000236597.72973.3c de Siqueira, C. J. P. (1988). Radioactivity measurements on tobacco leaf & cigarettes. Souza Cruz Group. Bates numbers 400751698 to 1699. Retrieved from http://legacy.library.ucsf.edu Deyton, L., Sharfstein, J., & Hamburg, M. (2010). Tobacco product regulation—A public health approach. New England Journal of Medicine, 362, 1753–1756. doi:10.1056/NEJMp1004152 Di Franza, J. R., & Winters, T. H. (1982). Radioactivity in ciga-rette smoke. New England Journal of Medicine, 307, 312–313.
Disease and radioactive polonium in tobacco smoke Bates numbers: 1004863883 to 10014863883 Retrieved from: http://legacy.library.ucsf Development of a cigarette with increased smoke pH. Trial exhibit 11903
- H Wakeham
- R L Williams
Wakeham, H. (1974). Disease and radioactive polonium in tobacco smoke. Bates numbers: 1004863883 to 10014863883. Retrieved from: http://legacy.library.ucsf.edu Williams, R. L. (1971). Development of a cigarette with increased smoke pH. Trial exhibit 11903. Liggett Company. Cited (1998) in Journal of the American Medical Association, 280., 1173-1181
To: Dr. Michael Ash. From: L.C. Laporte. Letter in reply to Dr
- L C Laporte
Laporte, L. C. (1959). To: Dr. Michael Ash. From: L.C. Laporte. Letter in reply to Dr. Ash. 11/16/1959. Bates numbers: 11276498–499.
Souza Group, Radioactivity in cigarettes
- G S Cruz
Cruz, G. S. (1992). Souza Group, Radioactivity in cigarettes, 3rd September 1992. (Secret). Bates numbers: 201816728–6729.
Radioactive material (radioisotopes proj-ect) Philip Morris Memo dated Bates number: 1000323899. Retrieved from: http://www.library.ucsf Radiation dose from cigarette tobacco. Radiation Protection and Dosimetry Evaluation of 210Pb and 210Po in cigarette tobacco produced in Brazil
- C Papastefanou
Retrieved from: http://www.library.ucsf.edu/tobacco/batco/ O'Keeffe, A.E. (1960). Radioactive material (radioisotopes proj-ect) Philip Morris Memo dated January 20, 1960. Bates number: 1000323899. Retrieved from: http://www.library.ucsf. edu/tobacco/batco/ Papastefanou, C. (2007). Radiation dose from cigarette tobacco. Radiation Protection and Dosimetry, 123, 68–73. doi:10.1093/ rpd/ncl033 Peres, A. C., & Hiromoto, G. (2002). Evaluation of 210Pb and 210Po in cigarette tobacco produced in Brazil. Journal of Environmental Radioactivity, 62, 115–119. doi:10.1016/S0265-931X(01)00146-1 Polonium 210. British American Tobacco Company, Bates numbers: 100180837–838.
Re: Prof. Philip Drinker's paper Studies of Radioactivity of Tobacco and Cigarette Smoke " . Bates number: 1001898298. Retrieved from: http://legacy.library.ucsf Polonium-210: Removal from smoke by resin filters
- R H Blackmore
- E W Bretthauer
- S C Black
Blackmore, R. H. (1963). To: Dr. A. Bavley. From: R.H. Black-more. Re: Prof. Philip Drinker's paper, " Studies of Radioactivity of Tobacco and Cigarette Smoke ". Bates number: 1001898298. Retrieved from: http://legacy.library.ucsf.edu Bretthauer, E. W., & Black, S. C. (1967). Polonium-210: Removal from smoke by resin filters. Science, 156, 1375–1376.
F.D.A. unveils graphic warn-ing labels for cigarettes
- G Harris
Harris, G. (2010, November 10). F.D.A. unveils graphic warn-ing labels for cigarettes. New York Times.
Radioactivity in tobacco and smoke (polonium 210)
- C R Hill
Hill, C. R. (1964). Radioactivity in tobacco and smoke (polonium 210). (Private and Confidential) 2/18/1964. British American Tobacco Document Collection. Bates numbers: 100152935– 937.