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Environ Geochem Health (2007) 29:249–255 DOI 10.1007/s10653-007-9082-4

ORIGINAL PAPER

Enhancement of radon exposure in smoking areas Hayam A. Abdel Ghany

Received: 13 January 2006 / Accepted: 19 January 2007 / Published online: 7 March 2007  Springer Science+Business Media B.V. 2007

Abstract Radium-226 is a significant source of radon-222 which enters buildings through soil, construction materials or water supply. When cigarette smoke is present, the radon daughters attach to smoke particles. Thus, the alpha radiation to a smoker’s lungs from the natural radon daughters is increased because of smoking. To investigate whether the cigarette tobacco itself is a potential source of indoor radon, the a potential energy exposure level contents of radon (222Rn, 3.82d) and Thoron (220Rn, 55.60s) were measured in 10 different cigarette tobacco samples using CR-39 solid-state nuclear track detectors (SSNTDs). The results showed that the 222, 220 Rn concentrations in these samples ranged from 128 to 266 and 49 to 148 Bqm–3, respectively. The radon concentrations emerged from all investigated samples were significantly higher than the background level. Also, the annual equivalent doses from the samples were determined. The mean values of the equivalent dose were 3.51 (0.89) and 1.44 (0.08) mSvy–1, respectively. Measurement of the average indoor radon concentrations in 20 cafe´ rooms was, significantly, higher than 20 smoking-free residential houses. The result refers to the dual (chemical and H. A. Abdel Ghany (&) Physics Department, Faculty of Girls for Art, Science and Education, Ain-Shams University, Cairo, Egypt e-mail: [email protected]

radioactive) effect of smoking as a risk factor for lung cancer. Keywords detectors

220, 222

Rn  Tobacco  Nuclear track

Introduction Radon and the isotopes of its short-lived decay products represent the main source of public exposure from natural radiation. They contribute nearly 50% of the global effective dose to population (UNSCEAR, 1993; Choubey et al., 2004a). Indoor radon and its decay products usually come from soil, building materials, and water supply. The radioactive decay products of radon, charged ions, have a static charge that enables easy attachment to water vapor, dust, and smoke particles in the air (Kilthau, 1996; Choubey et al., 2004b). Considering the chemical composition of tobacco smoke as carbon dioxide (CO2), the attachment of radon and its daughters is probable. Numerous studies on the attachment of radon progeny to ambient aerosol particles have been carried out. The major attachment theory basically consists of a diffusion theory and a kinetic theory. The attachment is proportional to the particle size for particles >1 lm and to the particle surface area for particles <0.1 lm (Porstendorfer & Mercer, 1978). The inhalation of

123

250

radon and its short-lived decay products is considered an etiological factor of lung cancer. Indoor cigarette smoking enhances the air concentration of submicron particles, which trap radon decay products. It has been reported that radon decay products that pass from room air through burning cigarettes into mainstream smoke are present in large, insoluble smoke particles that selectively deposited at bronchial bifurcation of the inhabitant (Romola & Choubey, 2003), where the attached radon progeny undergo substantial radioactive decay before clearance. Also, for over 20 years it has been known that all types of tobacco contain radioactive 210Po (138.38d), which emits alpha particles and radioactive 210Pb (22.3y), which emits beta particles and is a precursor of 210Po. There is a degree of consensus about how tobacco becomes radioactive (Martell, 1974). Most soils contain radioactive elements such as radium, which decays into 210Pb and 210Po. In addition, Phosphate ore used as a fertilizer in tobacco fields may contain such isotopes in relatively high concentrations. Thus it was anticipated that tobacco plants can absorb 210Pb and 210Po through their roots (Cross, 1984). During tobacco processing, the radiation is not completely removed. Consequently, in addition to the traditional implication of smoking cigarette in lung cancer, the high incidence of lung cancer in cigarette smokers and nonsmokers may be attributed to the cumulative effect of a-radiation dose from indoor radon and thoron progeny generated and/or trapped by tobacco and its smoke (Radford & Hunt 1964). This triggers the interest of measuring 220,222Rn and their progenies in different samples of tobacco, which is widely consumed by smokers in Egypt and to investigate the difference between indoor radon concentration in smokefree and smoke-rich environments (Little, Radford, McCombs, & Hunt, 1965).

Environ Geochem Health (2007) 29:249–255

cigarette samples coded T1-T10. A fixed amount of tobacco sample (10 gm, which corresponds to 15 cigarettes) was placed in plastic containers. The container was 7 cm height and 5.2 cm in diameter. A piece of CR-39 detector with area 1 · 1 cm2 was embedded in the sample in each container. At the same time a second piece of CR-39 detector was held at the top of the container (Fig. 1). Measurements were carried out four times for each sample. The cups were left at room temperature for two months exposure time. During this time aparticles from the decay of radon, thoron and their daughters bombard the CR-39 nuclear track detectors in the air volume of the cup. After exposure the detectors were etched chemically with 6 N NaOH solution at 70C for 6 h. The tracks were counted using an optical microscope. This arrangement ensures that the lower detector recorded alpha particles from radon, thoron and their daughter products present in the Tobacco samples. The upper detector, however records only the 222Rn component. Consequently, the difference in the track densities of the two detectors represents the content of 220Rn and their daughters in the sample. The density of tracks counted was assumed to be proportional to the 220,222Rn exposure (Hafez, Hussein, & Rasheed, 2000). The track density (q) recorded on the detector, attenuation factor of 222Rn (k), calibration coefficient of measuring system in terms of cm2 d–1 Bqm–3 (g), and exposure time (t) have been applied to determine the 222Rn concentration (C). Using formula 1: C ¼

q kgt

ð1Þ

The potential of energy alpha concentration (PEAC) of 222Rn and 220Rn daughters in terms of working level (WL) units was calculated using formula 2: Wl ¼ F  CRn=3700

ð2Þ

Experimental procedure A CR-39 (Intercast, Italy) nuclear track detector with a thickness of 500 lm was used in this work. Measurements were made in 10 different tobacco

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where F is the equilibrium factor of 0.4 (Ali, Taha, El-Hussein, Ahamed, & Gommaa, 2001). The annual effective dose equivalent, D, (in unit of mSvy–1) is computed from the integrated

Environ Geochem Health (2007) 29:249–255

251

Fig. 1 Schematic of the sealed-cup technique

CR-39 detector (1x1cm)

Cover

222Rn Cup height (7cm) 222Rn + 220Rn

CR-39 detector (1x1cm) Tobacco sample

222

Rn concentration using the following formula International commission on radiological protection (ICRP-65, 1993). D ¼ 0:4Rð3:88Þ 700 = 3700  170

where, R is the integrated 222Rn—concentration in Bqm–3 and 3.88 mSv WLM–1 is the ICRP conversion factor. The other factors are to take account of the house occupancy factor (ICRP-65, 1993). Radon and thoron were measured in 20 residential houses and 20 cafe´ rooms using CR-39 plastic track detectors. The selected houses were occupied with nonsmoking inhabitants and the detectors were placed in totally smoke-free areas. Four small pieces of detector 1 · 1 cm2 were fixed in every cane for each house or cafe´ room. The dosimeters were suspended inside the 20 houses and 20 cafe´ rooms. The detectors were exposed for two months and, after retrieval, were etched and scanned as described above. Results and discussion Although a significant portion of lung cancer occurs in nonsmokers, tobacco smoking is the most common risk factor for lung cancer (Behera & Balamugesh, 2005). Darby et al. (2005) provided compelling evidence that indoor 222Rn is an important contributor to the risk of lung cancer. However, the derived estimate of 222Rnattributable lung cancers may have a low bias. The authors estimated an increase in lung cancer risk of 16% for each incremental 100 Bqm–3 of 222Rn from a pooling of the

European residential case-control studies. They estimated that 222Rn may contribute to 9% of all lung cancers in those countries on the basis of an estimated average 222Rn concentration of 59 Bqm–3 for 29 European countries. Although a huge amount of data is available about the biological effect of tobacco smoking, here we investigate the possible involvement of 222Rn derived from tobacco as a risk factor of lung cancer. The study investigated the 222Rn and 220 Rn content of 10 different tobacco samples (coded T1–T10) used in cigarette manufacture. The data obtained revealed that sample T5 recorded the highest level of 222Rn whereas T6 contained the highest level of 220Rn. Compared to the background levels (106 ± 3 Bqm–3 and 20 Bqm–3) all samples had significantly higher 222 Rn and 220Rn values (Fig. 2). In descending order, the 222Rn concentrations among the investigated samples were those of T5, T1, T7, T2, T4, T6, T3, T9, T10 and T8. In terms of 220Rn concentrations the order was T6, T4, T7, T1, T9, T5, T3, T8, T2 and T10. The high 222Rn and/or 220Rn contents in the tobacco samples may be attributed to the escape of these elements from the soil, where most soils contain radium, a radioactive element, that decays into 210Pb and 210 Po. In addition, phosphate ore used to make fertilizers, which is used in tobacco fields, may contain these isotopes in relatively high concentrations. Tobacco plants can absorb 210Pb and 210 Po through their roots (Martell, 1974). The potential of energy alpha (PEA) of 222Rn and 220Rn concentrations were calculated (Fig. 3). The alpha activities due to the 222Rn columns were observed to be higher than those

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252 300

Radon Conc. (Bqm -3)

Fig. 2 Radon and thoron concentrations in 10 tobacco samples. An asterisk refers to a significant difference between the corresponding sample and the background level for the same isotope using the unpaired t test. BG is the background value

Environ Geochem Health (2007) 29:249–255

222Rn 250

220Rn 200 150 100 50 0

T1

T2

T3

T4

T5

T6

T7

T8

T9

T10

BG

Fig. 3 PAE of radon and thoron in ten tobacco samples

P A E o f r a d o n a nd t h o r o n ( m / w l )

Samples

35

PEA 222Rn

30 PEA220 Rn 25 20 15 10 5 0 T1

T2

T3

T4

T5

T6

T7

T8

T9

T10

Samples

due to the 220Rn series for different investigated tobacco samples. This is due to the fact that the corresponding tobacco material samples contain more 238U(4.468 · 109 y) than 228Th (1.913 y). Also, note that the half-life of thoron (220Rn) is too short (55.60 s) compared to the exposure time (two months) of the SSNTD films inside the plastic container (Misdaq & Flata 2003). Consequently, it is anticipated that smokers consuming tobaccos T1, T2, T4, T5, T6 and T7 samples are exposed to higher alpha doses. Previous studies (Lagarde et al., 2001) have indicated that in a smoker’s lungs the ciliary action to clear the lungs is reduced to about half the normal. The average length of time during which the insoluble forms of 210Pb and 210Po remain at the bronchial bifurcations is 3–5 months. Coincidentally, the surface tissue of smokers’ bronchi at the bifurcations is replaced by damaged abnormal tissue. The exhalation rates of both 222Rn and 220Rn in different tobacco samples have been determined (Fig. 4). The value of radon and thoron

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exhalation rates varies from 6.71 mBqm–3h–1 for the T8 sample to 13.97 mBqm–3h–1 for the T5 sample and 2.57 mBqm–3h–1 for the T2 sample to 7.76 mBqm–3h–1 for the T6 sample. The concentrations of 222Rn and 220Rn progenies are shown in Fig. 5. The values of 222Rn progeny concentration were lower in T8 (51 Bqm–3) and higher in T5 (106 Bqm–3). Also, the values of 220Rn progeny were lower in the T2 and T10 samples (19 Bqm–3) and higher in T6 (59 Bqm–3) (Romola, Negy, & Choubey, 2005). Indoor air quality is a contributing factor of lung cancer, although the attributable lung cancer risk from 222Rn in homes may be low. Due to the presence of dust, the 222Rn and 220Rn daughters (from building materials, soil, or underground water supply) mainly attach to room surfaces, but indoor smoking allows 222Rn daughters to attach to smoke particles. Thus, the alpha radiation to a smoker’s lungs from the natural 222Rn daughters is increased because of smoking. The resulting estimates of dose due to the presence of 222Rn, 220Rn and their daughters are

Radon and Thoron

- 3 -1

Fig. 4 Radon and thoron exhalation rates in 10 tobacco samples

253

Exhalation Rates (mBqm h )

Environ Geochem Health (2007) 29:249–255 16

222Rn

14

220Rn

12 10 8 6 4 2 0 T1

T2

T3

T5

T4

T6

T7

T8

T9

T10

Samples

e qu iv a len t D os e o f R a do n a nd T h or o n -1 (mSvy )

Fig. 6 Resulting dose due to radon and thoron in 10 tobacco samples

Radon and Thoron Progenies (Bqm-3)

Fig. 5 Distribution of the concentrations of radon and thoron progenies in 10 tobacco samples

222Rn

120

220Rn

100 80 60 40 20 0 T1

T2

T3

T4

T5 T6 Samples

T7

T8

T9

T10

222Rn

5 4.5 4 3.5 3 2.5 2 1.5 1 0.5 0

220Rn

T1

T2

T3

T4

T5

T6

T7

T8

T9

T10

Samples

shown in Fig. 6. Most of the values of radon and thoron observed were, respectively, 2.21-4.59 (mSvy–1) with high values in T5 and low values in T8 samples, and 0.84–2.55 (mSvy–1) with high values in T6 and low values in T2 and T10 samples. However, the fact that these higher doses of radiation are delivered to vulnerable tissue at the location where malignancy is most frequently observed argues strongly for alpha

radiation playing the most important role in causing lung cancer. These values correspond to 2/3 of a pack of cigarette, which means these values will increase by 25% when a complete pack is used (Abu-Jarad, 1997). The measured values of both radon and thoron in residential houses and cafe´ rooms (n = 20 each) are shown in Table 1. Radon and thoron concentrations, in most cases, were found to be

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254 Table 1 Radon and thoron concentrations in residential houses and cafe´ rooms

*222Rn and **220Rn were significantly and highly significant lower (respectively) in residential houses compared with cafe´ rooms (P \ 0.0001 and \ 0.0001, respectively) (estimated by unpaired t test).

Environ Geochem Health (2007) 29:249–255

Location no.

222

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 Average ± SD

Rn (Bqm–3) 55 ± 3.44 41 ± 2.56 51 ± 3.18 44 ± 2.75 50 ± 3.12 60 ± 3.75 42 ± 2.62 45 ± 2.81 41 ± 2.56 67 ± 4.19 71 ± 4.44 48 ± 3.00 43 ± 2.68 51 ± 3.18 52 ± 3.25 56 ± 3.50 41 ± 2.56 53 ± 3.31 55 ± 3.44 48 ± 3.00 43 ± 2.68 47 ± 2.93 63 ± 3.94 45 ± 2.81 53 ± 3.31 60 ± 3.75 70 ± 4.37 52 ± 3.25 49 ± 3.06 73 ± 4.56 52.3 ± 3.27*

higher in cafe´ rooms than residential houses. It is probable that the smoke-rich air of the cafe´ room enhances the presence of such elements compared to the relatively smoke-free environment. Smokers exposed to the higher indoor radon and thoron levels should experience the highest risk and the earliest incidence of lung cancer. This possibility was investigated cytogenetically by Brandom, Saccomanno, Archer, Archer, and Bloom (1987), who showed that chromosome aberrations in cultured peripheral blood lymphocytes are a sensitive measure of cumulative exposure to radon progeny. If most smokers who develop bronchial cancer are those with the highest cumulative radon progeny exposure, they should exhibit the highest prevalence of the indicator aberrations. Cigarette smokers exposed occupationally to inhalation of fibrous aerosols or toxic chemicals agents that damage the bronchial

123

Cafe´ room

Residential houses 220

Rn (Bqm–3) 15 ± 0.93 13 ± 0.81 11 ± 0.68 12 ± 0.75 14 ± 0.87 11 ± 0.68 14 ± 0.87 15 ± 0.93 13 ± 0.81 14 ± 0.87 12 ± 0.75 14 ± 0.87 11 ± 0.68 16 ± 1.00 15 ± 0.93 13 ± 0.81 11 ± 0.68 14 ± 0.87 10 ± 0.62 12 ± 0.75 11 ± 0.68 13 ± 0.81 14 ± 0.87 10 ± 0.62 11 ± 0.68 15 ± 0.93 12 ± 0.75 11 ± 0.68 13 ± 0.81 10 ± 0.62 12.66 ± 0.79**

222

Rn (Bqm–3) 110 ± 6.88 105 ± 6.56 114 ± 7.13 112 ± 7.00 100 ± 6.25 103 ± 6.44 100 ± 6.25 105 ± 6.56 99 ± 6.19 104 ± 6.50 101 ± 6.31 99 ± 6.19 108 ± 6.75 100 ± 6.25 115 ± 7.19 110 ± 6.88 113 ± 7.06 98 ± 6.12 117 ± 7.31 110 ± 6.88 105 ± 6.56 110 ± 6.88 100 ± 6.25 97 ± 6.06 106 ± 6.62 110 ± 6.88 99 ± 6.19 115 ± 7.19 111 ± 6.94 97 ± 6.06 105.76 ± 6.61

220

Rn (Bqm–3) 25 ± 1.56 29 ± 1.81 30 ± 1.87 27 ± 1.68 24 ± 1.50 29 ± 1.81 26 ± 1.62 28 ± 1.75 30 ± 1.87 30 ± 1.87 26 ± 1.62 31 ± 1.93 29 ± 1.81 25 ± 1.56 30 ± 1.87 28 ± 1.75 31 ± 1.93 27 ± 1.68 24 ± 1.50 28 ± 1.75 30 ± 1.87 33 ± 2.06 28 ± 1.75 31 ± 1.93 29 ± 1.81 27 ± 1.68 34 ± 2.12 26 ± 1.62 32 ± 2.00 29 ± 1.81 28.53 ± 1.78

epithelium and impair clearance may experience bronchial cancer at lower cumulative radon progeny exposures. Lung cancer is a serious chronic health effect of cigarette smoking and indoor radon progeny may be a factor in the etiology of some of the other cancers, in particular of the larynx, pharynx, and esophagus.

Conclusion Based on the results obtained from this study the concentrations of radon 222Rn and thoron 220Rn in 10 tobacco samples showed that the highest concentrations were observed in the T5 and T6 samples. This is mainly attributable to the soil and fertilizers, which are the source of the radioactive isotopes. Annual equivalent doses due to radon,

Environ Geochem Health (2007) 29:249–255

thoron and its short-lived daughters from the inhalation of various cigarette smokes have been evaluated. Acknowledgement I would like to thank Dr. M. A. ElKhosht Prof. of Radiation Physics, Faculty of Science, Tanta University, for his useful comments and assistance.

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255 of individual data from 13 European case-control studies. British Medical Journal, 330, 223–226. Hafez, A. F., Hussein, A. S., & Rasheed, N. M. (2000). Radon measurements in underground metro stations in Cairo City, Egypt. Seventh Conference of nuclear Sciences & Applications 6–10 February, Cairo, Egypt. ICRP publication 65 1993, 23 (2). Pergamon Press. Oxford, UK. Kilthau, G. F. (1996). Cancer risk in relation to radioactivity in tobacco. Radiologic Technology, 67(3), 217–222. Lagarde, F., Axelsson, G., & Damber, L., et al. 2001 Residential radon and lung cancer among neversmokers in Sweden. Epidemiology, 12, 396–404. Little, J. B., Radford, E. P. Jr, McCombs, H. L., & Hunt, V. R. (1965). Distribution of polonium-210 in pulmonary tissues of cigarette smokers. The New England Journal of Medicine, 273, 1343–1351. Martell, E. A. (1974). Radioactivity of tobacco trichomes and insoluble cigarette smoke particles. Nature, 249, 215–217. Misdaq, M. A., & Flata, K. (2003). Radon and daughters in cigarette smoke measured with SSNTD and corresponding committed equivalent dose to respiratory tract. Radiation Measurements, 37, 31–38. Porstendorfer, J., & Mercer, T. T. (1978). Adsorption probability of atoms and ions on particle surfaces in submicrometer size range. Journal of Aerosol Science, 9, 469–474 Radford E. P. Jr, & Hunt, V. R. (1964). Polonium-210: A volatile radioelement in cigarettes. Science, 143, 247– 249. Ramola, R. C., & Choubey, V. M. (2003). Measurement of radon exhalation rate fromsoil samples of Garhwal Himalaya, India. Journal of Radioanalytical and Nuclear Chemistry, 256(2), 219–222. Ramola, R. C., Negi, M. S., & Choubey, V. M. (2005). Radon and thoron monitoring, in the environment of Kumaun Himalayas: Survey and outcomes. Journal Environmental Radioactivity, 79(1), 85–92. UNSCEAR, (1993). Sources and effects of ionizing radiation. United Nations Publication E 94. IX. 2, pp. 33–89.

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