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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 12  |  Issue : 4  |  Page : 139-146

222Radon carcinogenesis: Risk estimation in different working environments


1 Department of Mathematics and Physics, “Ennio De Giorgi”, University of Salento, Lecce, Italy
2 Università Cattolica del Sacro Cuore, Rome, Italy
3 Local Health Authority, Health Unit of Occupational Prevention and Protection, Lecce, Italy

Date of Submission03-May-2021
Date of Acceptance07-Jul-2021
Date of Web Publication21-Oct-2021

Correspondence Address:
Dr. Mauro Mazzotta
Departments of Mathematics and Physics, “Ennio De Giorgi”, University of Salento, Lecce
Italy
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jrcr.jrcr_10_21

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  Abstract 


Background: Occupational exposure to radon in working environments should be considered as chronic because the subjects involved undergo the effect due to the ionizing radiation from the same gas and decay products. The exposure characteristics create conditions for toxicological, radio-toxicological cellular, subcellular, and molecular mechanisms that lead to lung cancer. Aim: Our aim is to clarify the prediction of probable cases of lung cancer in 222Radon-exposed subjects in order to point out an obvious risk that should not be underestimated, particularly in subjects with an accumulated dose in many years of activity and for the previously underestimated gamma radiation (214Bi). Materials and Methods: A total of 168 electret sensors were set in couples for 84 surveys in working environments; also a further pair of them was used in order to determine the background γ generated by cosmic rays and we considered four group: general population, never smokers, former smokers, and current smokers. Results: Results are expressed in terms of mean and standard deviation, standard error, geometric mean with statistical significance (P < 0.01 [t-test]), and excess lifetime cancer risk (ELCR). They demonstrate an increase of both mean concentrations (P < 0.01 [t-test]) and ELCR. This happens with multiple values of the allowed limits >150 Bq m3 (U.S. Environmental Protection Agency, EPA) or >300 Bq m3 (international commission radiation protection), until to an individual accumulated dose as 90–95 work level month. We have detected the environmental variability associated with the structural characteristics of the buildings and their construction. Conclusion: The results showed that exposure in underground environments is significant although generally these environments are used as archives. Surprisingly, data greater than expected are also evident on the ground floor and first floor of historic buildings with solid and compact walls, with other factors playing a role as reduced or absent air changes during the night and activation of heating when work is resumed after renovation.

Keywords: 222Radon, 222Radon daughters, indoor environments, WLM, lung cancer, incremental cancer risk, electrets, radon ionization chambers


How to cite this article:
Mazzotta M, Mazzotta AD, Fernández M, Cazzato RG, D'Ettorre G. 222Radon carcinogenesis: Risk estimation in different working environments. J Radiat Cancer Res 2021;12:139-46

How to cite this URL:
Mazzotta M, Mazzotta AD, Fernández M, Cazzato RG, D'Ettorre G. 222Radon carcinogenesis: Risk estimation in different working environments. J Radiat Cancer Res [serial online] 2021 [cited 2022 Jun 26];12:139-46. Available from: https://www.journalrcr.org/text.asp?2021/12/4/139/328799




  Introduction Top


In working environments, exposure to radon is considered chronic because the subjects involved undergo the effect due to the ionizing radiation from both the same gas and decay products.

The exposure characteristics create conditions for toxicological, radio-toxicological cellular, subcellular, and molecular mechanisms that lead to lung cancer. Recent international indications[1] draw attention to the exposure dose values producing carcinogenic effects on the lung,[2] with the recommendation to maintain the 300 Bq/m3 levels in the indoor phase, which were reviewed in 2014 at the lower level reasonably achievable in the range 100–300 Bq/m3.[3] In application of the “New radon dose coefficients” published by international commission radiation protection (ICRP)[2],[4] with standard assumptions, exposure to radon at the upper end of the recommended range for a national reference level of 300 Bq/m3 corresponds to an effective annual dose of 4 mSv at work and 14 mSv at home. The daughter 214Bi mainly contributes to increasing the gamma radiation dose in 222Radon exposure [Table 1] to a bigger extent than the rest of the progeny.[5]
Table 1: Precise measurement of the 222Rn half-life gives us the opportunity to monitor the stability of radioactivity[5] 214Bi mainly contributes to increasing the gamma radiation dose in 222Rn exposure to a largely extent than the rest of the progeny

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While the measurement methods and the evaluation of the individual dose are known, it is important now to study the effects of the radon itself (alpha particles) and its decay products that are responsible of cellular damage including DNA breakage, inaccurate repair, apoptosis, gene mutations, chromosomal change and genetic instability, mutations, aberrations, generation of reactive oxygen species, and new synthesis of cytokines and proteins related to carcinogenesis.[6]

Toxicology

Aerosol and environmental pollutant particles, some of which are powerful environmental irritants that cause wheezing and pathologies of the nose and mouth, are recognized as important vehicles for radioactive materials and products of decay of 222Radon. The transformed and subsequent decay product atoms easily aggregate, cluster, and attach to aerosol particles that can subsequently settle in the tracheobronchial tree and repeatedly irradiate the neighboring cells with alpha particles, the associated fraction being much higher in environments with smokers than those with nonsmokers, and in those dusty compared to the well ventilated. Size, surface, and shape of the particles are the action key of a mechanism that applies to three levels of particle solubility, a wide range of particle sizes 0.0005–100 μm in diameter[7] that are inhaled can be distinguished based on the activity median aerodynamic diameter-mean aerodynamic diameter. After a particle has been deposited, its retention will depend on the physical and chemical properties of the powder and the physiological state of the lung.

While the particles containing the products of the decay undergo the ciliary clearance action in the upper respiratory tract, when they reach a deep layer of the lung, they are phagocytized by macrophages or absorbed by the lymphatic system or transported if soluble from the blood in various organs and tissues. The alpha particles are characterized by a linear energy transfer (LET) higher than beta or gamma radiation, react with DNA, and create oxidative stress and radiolysis. Tissue layers that can be crossed by the alpha generated by 214Polonium (6.0 MeV) and 218Polonium (7.69 MeV), have penetration depths of 47 μm and 70 μm, respectively,[1] suggesting high levels of irradiation, in particular, bronchial epithelium and bifurcation sites.[8]


  Materials and Methods Top


In order to determine radon concentration, two different methods were used: passive electret sensors and active ionization chambers.

Electrets are made of:

  • Charged teflon disks. The voltage of the surface at the beginning is generally of 700–800 V and reduces when α particles coming from radon decay strike the disk surface
  • A surrounding plastic chamber with a little filter which allows only radon to get inside, while it blocks any solid particle, including radon decay products.


Depending on the type of Teflon disks and on the volume of the chamber, it is possible to make measurements in times that are meaningful from 1 week up to 1 year. We used electrets in LLT configuration (large chamber and long term electrets), i.e. long-time disks and long-time chambers. The reading of the dosimeters was made when they were positioned in the rooms, after 6 months and after 1 year. Hence, we were able to take into account the mean value of the radon concentration over all the year. Before and after any set of measurements, the correct operation of our SPER-1 reader was verified with two reference electrets, which are very stable ones and normally reduce their voltage not more than 1 V/year. The device is calibrated regularly together with the reference electrets into the range 200 V–700 V. The sensitivity on radon concentration in the most critical conditions is about ~ 6%. To further check our instrumentation, we also participated to an interlaboratory comparison on indoor radon measurements under field conditions[9] for exposures of 242 ± 38 kBq/m3 h, 742 ± 99 kBq/m3 h, and 1573 ± 214 kBq/m3 h.

Electrets were positioned in 84 different workplaces, generally in couples to prevent any malfunction of one of them. The choice of environments was made in order to cover all the offices regularly used including also archives and library warehouses. Most of the dosimeters were set in ground floor rooms having no crawl space. Some were also positioned in underground environments. Two radon electret sensors were sealed in a Mylar envelope in order to determine the background γ generated by cosmic rays. The results of measurements are expressed in terms of mean and standard deviation, standard error, and geometric mean with statistical significance (P < 0.01 [t-test]).

The ionization chamber we used was an AlphaGuard P2000 explicitly designed for revealing real time radon concentration. This instrument allows taking mean value measurements from 10-min to 1-h ranges, both in diffusion or airflow operation. The chamber has a measuring range of 222Radon from 20 Bq/m3 up to 2 MBq/m3. The system linearity error is <3% within the total range, while the instrumentation calibration error for 222Radon is ±3%. We put the lowest time step (10 min) and made data acquisition over some days in some fixed and significant environments changing microclimatic conditions. In this way, it was also possible to analyze the different behavior during night and daytime.


  Results Top


In this work, we want to make a dose-proportional quantitative prediction estimate of lung cancer in exposed subjects in order to indicate an obvious risk that should not be underestimated, particularly in subjects with a dose accumulated in high work level month (WLM) in relation to years of activity carried out. Our reference samples are representative of the total population, never smokers (NS), former smokers, and smokers [Figure 1].
Figure 1: Cases of lung cancer expected at the highlighted concentrations × 10−4

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The data [Table 2] show that the exposure in underground environments is greater although fortunately these environments are generally used as archives.[2],[10],[11],[12],[13] However, the radon due to its radiotoxicological behavior has a peculiarity absorption, distribution, and kinetics of its decay products and consequently accumulation.
Table 2: Activity concentration 222Radon and 222Radon progeny (in Bq/m3), 222Radon individual dose cumulative (work level months), excess lifetime cancer risk, International Commission radiation protection biological effects of ionizing radiation (National Research Council) VI – total group of population in occupational exposure, never smokers, exsmokers, and smokers[2],[10],[11],[12],[13]

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Our aim consists in identifying the probability of clinical evidence such as lung cancer, suggest a predictive method to protect subjects exposed to 222Radon and its effects, and identify through environmental data of those with accumulated doses beyond the danger limits.[10],[11],[14]

EPA estimates that out of a total of 157,400 lung cancer deaths detected in 1995, 21,100 (13.4%) were radon related. Among NS, an estimated 26% were radon related. Estimates of risk per unit exposure are are 5.38 × 10-4 for WLM representing the US population, 9.68 ×10-4 for WLM the ever smokers (ES) and 1.67 ×10-4 for WLM the never smokers (NS). The estimated risks from lifetime exposure at 4 pCi/L (148 Bq/m3) action level are 2.3% for the entire population, 4.1% for ES, and 0.73% for NS.[11],[15]

In November 24, 2011, ICRP announced the availability of publication 115[2] revising the 222Radon risk coefficient according to its previous November 2009 statement:

“Based on recent results from combined analyses of epidemiological studies of miners, a lifetime excess absolute risk of 5 × 10−4 for WLM (14 × 10−5 per mJ h/m3) should now be used as the nominal probability coefficient for 222Radon and 222Radon progeny-induced lung cancer, replacing the previous ICRP publication 65 value of 2.8 × 10−4 for WLM (8 × 10−5 per mJ h/m3).”[2]

The data on lung tumors expected at the actual concentrations found in working environments are indicative and useful for protective purposes, making also clear that the synergistic action of smoking greatly increases the risk of exposed subjects and the prohibition of smoking is fundamental in environments with radon pollution. This is evident in [Table 1] where the expressed data are then recalculated and plotted in [Figure 1] for the purpose of tumor prediction.[11],[14],[16]

In [Figure 2] and [Figure 3], it is shown that the exposure determines a significant dose in mSv according to the usual conversion from WLM.[2],[4]
Figure 2: Conversion Bq– work level month/year (WL = 101.3 pCi/l = 3748.1 Bqm− 3) – work environment

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Figure 3: Concentrations in terms of confidence limits for the mean in buildings orphanage 19th century-unmodified offices

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[Table 3] is expressive of the stationary nature of the radon accumulation in environments where no provision and remediation has been adopted and with values substantially >300 Bq/m3.
Table 3: Concentrations in terms of mean±standard deviation in buildings orphanage 19th century-unmodified offices

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[Table 4], on the other hand, shows the values obtained in rooms with environmental preventive measures as an aspiration system, increasing the air exchange, resulting in a significant reduction during the day and even more with windows always open during the night.
Table 4: Concentrations in terms of mean±standard deviation in buildings “Orphanage 19th century” restructured and clean office before working hours start. Monitor resulting a significant reduction during the day and even more with windows always open during the night

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However, the data also show that radon pollution is also confirmed on the first floor due to the continuity of the walls with the subsoil, going up along the capillaries of stone structure of the building.

Higher evidence of the phenomenon is given using environmental heating as well as closing the windows two factors that accelerate the emission and accumulation of radon, respectively, from the underground as shown in [Table 5] and [Figure 4],[Figure 5],[Figure 6].
Figure 4: Data behavior in different buildings unmodified offices

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Figure 5: Data behavior in restructured and clean offices – Ground and first floor – after start of working hours-day time and night 15 h ventilation effect

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Figure 6: Data behavior in restructured and clean offices – Ground and first floor – after start of working hours-day time and night-heating and fans: increase with heating activation effect and reduction with the turning on of the fans

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Table 5: Data behavior in restructured and clean offices: Ground and first floor - after start of working hours

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Finally, it is to note that the increase in concentrations of 222Radon depends also on the porosity and graininess of the soil, temperature, humidity, and atmospheric pressure; in addition to rainfall and weather conditions and season.[2]


  Discussion Top


We have verified how much exposure for reasons of work can be estimated in environments of old construction with compact stone building used for high school activities. Our first purpose and concern is to understand the effects of exposure to Radon and its decay products for long-lived to short-lived 222Radon-progeny concentrations due to α radiation, with little penetrating power, β radiation, and γ that can pass through the skin and without mass can cross the whole body.

Precise measurement of the 222Radon half-life gives us the opportunity to monitor the stability of radioactivity.[5],[17] If the data on lung tumors expected at different concentrations found in working environments give the greatest alarm, even more alarm rise cases of uranium miners who are affected by pulmonary fibrosis with impaired lung function as described in the literature. In these cases, it was suspected that diffuse interstitial pulmonary fibrosis was induced by radiation due to inhalation of radon decay products. Moreover, a selection of 22 cases with serious respiratory diseases showed a “honeycomb lung” on the chest radiograph, while other cases with small nodules attributable to silicosis were not attributed to the predominant respiratory evolutionary processes due to the toxic action of α-particles from radon progeny. The very long latency time necessary for the appearance of these respiratory pathologies leads to an etiological uncertainty on the origin of the pathology even if pulmonary hypertension, hypoxygenation, and heart and lung damage predominate.[17]

Other indications show that there is a biointeraction respiratory infections and chronic obstructive pulmonary disease (COPD) in lung cancer and 222Radon exposure and decay product.[18]

It should be noted that the association between residential radon and mortality from nonmalignant respiratory illnesses is to be further studied. The Cancer Prevention Study-II is a large prospective cohort study of about 1.2 million Americans recruited in 1982 with radon inhalation equal to 53.5 ± 38.0 Bq/m3. For this sample and according to Cox proportional risk regression models for adjusted risk ratios (hazard ratio [HR]), adopting the 95% confidence intervals (CIs) for mortality of nonmalignant respiratory disease associated with radon concentrations, the analysis carried out on 811,961 participants in 2754 countries has shown that, up to the year 2006, there were a total of 28,300 deaths from nonmalignant respiratory diseases. Radon was significantly associated with mortality from COPD (HR for 100 Bq/m3 1.13, 95% CI: 1.05–1.21). There was a significant positive linear trend in COPD mortality with increasing categories of radon concentrations (P < 0.05). The results suggest that residential radon may increase COPD mortality. Of course, further research is needed to confirm this result and to better understand possible complex interrelations between 222Radon, COPD, cancer, sex differences between incidence and mortality[6],[19],[20],[21] and why non-smokers had increased odds of molecular mutations (GSTM1 or GSTT1 gene deletions), defective DNA mismatch repair with tumor mutation burden,[2],[22] and unlikelihood of epidermal growth factor receptor mutation status.[20]

It is important for the mechanism of carcinogenic action to clarify how 222Radon alters the communication between cells and their microenvironment, because biophysical and molecular messages and induction processes are no longer recognized.[22],[23]

Because the presence and accumulation of 222Radon pollutants and his progeny is quite assessed in environments characterized by specific structure of the buildings, it is important to have a regular monitoring. Special categories of more exposed subjects have to be considered with particular attention, at the same time discouraging the habit of the active and passive smoking.

Clinic monitoring is essential, not only based on complex and invasive examination as the high resolution computed axial tomography (CAT), but in particular on sputum citohystological examination and evaluation of the respiratory physiology, by means of periodical spirometry, at the onset of allergic disease insurgence presence.

At the same time, also an environmental cleanup, by removing biological factors as fungi (Aspergillus, Micropolyspora, Alternaria, and Mucor) or bacteria (Staphylococcus, Micrococcus) is essential.

In this respect, the different stages related to the protracted risk exposure of the subjects involved in working activities are simplified.


  Conclusions Top


Due to the presence and accumulation of 222Radon pollutants and his progeny that is quite assessed in environments characterized by specific structure of the buildings and the level of floor, it is important to have a regular monitoring using not only passive dosimeters but also instrument as an ionization chamber in diffusion or airflow operation. In this way, analyzing the different situations during the day and night, it is possible to select particular categories of the most exposed subjects to be considered with particular attention. The results demonstrate increased mean values in both hypotheses: concentrations (P < 0.01 [t-test]) and excess lifetime cancer risk, with many values greater than the permitted limits <150 Bq/m3 (EPA) or <300 Bq/m3 (ICRP) and up to an individual accumulated dose in some cases of 90–95 WLM. However, it is important to have detected the environmental variability associated with the structural characteristics of the buildings and the construction/restoration techniques, smoke, heating/air conditioning spare parts, for the purpose of a preventive program, at the same time discouraging the habit of the active and passive smoking without forgetting the housing risk itself.

Acknowledgment

Authors express their thanks to Prof. Francesco Strafella for several enlighting discussions.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
ICRP Summary of ICRP Recommendations on Radon ref 4836- 9756-8598 January 26, 2018 1-6.  Back to cited text no. 1
    
2.
Tirmarche M, Harrison JD, Laurier D, Paquet F, Blanchardon E, Marsh JW, et al. ICRP publication 115, lung cancer risk from radon and progeny and statement on radon. Ann ICRP 2010;40:1-64.  Back to cited text no. 2
    
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Lecomte JF, Solomon S, Takala J, Jung T, Strand P, Murith C, et al. Janssens radiological protection against radon exposure. Ann ICRP 2014;43:5-73.  Back to cited text no. 3
    
4.
Paquet F, Bailey MR, Leggett RW, Lipsztein J, Marsh J, Fell TP, et al. ICRP Publication 137: Occupational intakes of radionuclides: Part 3. Ann ICRP 2017;46:1-486.  Back to cited text no. 4
    
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Bellotti E, Broggini C, Di Carlo G, Laubenstein M, Menegazzo R. Precise measurement of the 222Rn half-life: A probe to monitor the stability of radioactivity. Phys Lett B 2015;743:526-30.  Back to cited text no. 5
    
6.
Robertson A, Allen J, Laney R, Curnow A. The cellular and molecular carcinogenic effects of radon exposure: A review. Int J Mol Sci 2013;14:14024-63.  Back to cited text no. 6
    
7.
ICRP Publication 66. Human Respiratory Tract Model for Radiological Protection. Ann ICRP 1994;24:1-3.  Back to cited text no. 7
    
8.
Deshpande A, Goodwin EH, Bailey SM, Marrone BL, Lehnert BE. Alpha-particle-induced sister chromatid exchange in normal human lung fibroblasts: Evidence for an extranuclear target. Radiat Res1996;145:260-7.  Back to cited text no. 8
    
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Gutierrez-Villanueva JL, Sainz Fernández C, Fuente M, Quindos López L, Quindos López J, Fernández Villar A, et al. Inter-Laboratory Comparison on Indoor Radon Measurements under Field Conditions; 16th March 2015, Editorial de la Universidad de Cantabria (ISBN:9788486116910).  Back to cited text no. 9
    
10.
National Academy of Sciences. Biological Effects of Ionizing Radiation (BEIR) VI Report: The Health Effects of Exposure to Indoor Radon. Washington, D.C: National Academy of Sciences; 1998. p. 514.  Back to cited text no. 10
    
11.
U.S. Environmental Protection Agency Office of Radiation and Indoor Air. EPA Assessment of Risks from Radon in Homes. Washington, DC, USA: United States Environmental Protection Agency; 2003.  Back to cited text no. 11
    
12.
Lim SM, Choi JW, Hong MH, Jung D, Lee CY, Park SY, et al. Indoor radon exposure increases tumor mutation burden in never-smoker patients with lung adenocarcinoma. Lung Cancer 2019;131:139-46.  Back to cited text no. 12
    
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Méndez D, Alshanqeety O, Warner KE, Lantz PM, Courant PN. The impact of declining smoking on radon-related lung cancer in the United States. Am J Public Health 2011;101:310-4.  Back to cited text no. 13
    
14.
Hunter N, Muirhead CR, Bochicchio F, Haylock RG. Calculation of lifetime lung cancer risks associated with radon exposure, based on various models and exposure scenarios. J Radiol Prot 2015;35:539-55.  Back to cited text no. 14
    
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Melloni BB. Lung cancer in never-smokers: Radon exposure and environmental tobacco smoke. Eur Respir J 2014;44:850-2.  Back to cited text no. 15
    
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Kendall GM, Smith TJ. Doses to organs and tissues from radon and its decay products. J Radiol Prot 2002;22:389-406.  Back to cited text no. 16
    
17.
Archer VE, Renzetti AD, Doggett RS, Jarvis JQ, Colby TV. Chronic diffuse interstitial fibrosis of the lung in uranium miners. J Occup Environ Med 1998;40:460-74.  Back to cited text no. 17
    
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Levy BS, Wegman DH, Baron SL, Sokas RK. Occupational and Environmental Health: Recognizing and Preventing Disease and Injury 2017, Oxford University Press, p 784 (ISBN: 9780190662677).  Back to cited text no. 18
    
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Donington JS, Le QT, Wakelee HA. Lung cancer in women: Exploring sex differences in susceptibility, biology, and therapeutic response. Clin Lung Cancer 2006;8:22-9.  Back to cited text no. 19
    
20.
Ruano-Ravina A, Torres-Durán M, Kelsey KT, Parente-Lamelas I, Leiro-Fernández V, Abdulkader I, et al. Residential radon, EGFR mutations and ALK alterations in never-smoking lung cancer cases. Eur Respir J 2016;48;1462-70.  Back to cited text no. 20
    
21.
Turner MC, Krewski D, Chen Y, Pope CA 3rd, Gapstur SM, Thun MJ. Radon and COPD mortality in the American Cancer Society Cohort. Eur Respir J 2012;39:1113-9.  Back to cited text no. 21
    
22.
Sonnenschein C, Soto AM. Theories of carcinogenesis: An emerging perspective. Semin Cancer Biol 2008;18:372-7.  Back to cited text no. 22
    
23.
Bizzarri M, Cucina A. Tumor and the microenvironment: A chance to reframe the paradigm of carcinogenesis? Biomed Res Int 2014;2014:934038.  Back to cited text no. 23
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

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