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 radia-
tion 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, respec-
tively. The radon concentrations emerged from
all investigated samples were significantly higher
than the background level. Also, the annual
equivalent doses from the samples were deter-
mined. The mean values of the equivalent dose
were 3.51 (0.89) and 1.44 (0.08) mSvy–1, respec-
tively. Measurement of the average indoor radon
concentrations in 20 café 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: Hayam168@maktoob.com
radioactive) effect of smoking as a risk factor
for lung cancer.
220, 222
Keywords Rn
Tobacco
Nuclear track
detectors
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; Chou-
bey 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 (Por-
stendorfer & Mercer, 1978). The inhalation of
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250
radon and its short-lived decay products is con-
sidered an etiological factor of lung cancer.
Indoor cigarette smoking enhances the air con-
centration 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 & Chou-
bey, 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 radioac-
tive 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, Phos-
phate ore used as a fertilizer in tobacco fields may
contain such isotopes in relatively high concen-
trations. 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 smoke-
free and smoke-rich environments (Little, Rad-
ford, McCombs, & Hunt, 1965).
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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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 a-
particles 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 detec-
tor 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, & Ras-
heed, 2000). The track density (q) recorded on the
detector, attenuation factor of 222Rn (k), calibra-
tion coefficient of measuring system in terms of
cm2 d–1 Bqm–3 (g), and exposure time (t) have
been applied to determine the 222Rn concentra-
tion (C). Using formula 1:
q
C ¼ ð1Þ
kgt
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
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
Fig. 1 Schematic of the
sealed-cup technique
Cup height
(7cm)
222
Rn concentration using the following formula
International commission on radiological protec-
tion (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 resi-
dential houses and 20 café 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 café room.
The dosimeters were suspended inside the 20
houses and 20 café 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 (Be-
hera & 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 222Rn-
attributable 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
251
CR-39 detector
(1x1cm)
Cover
222Rn
222Rn + 220Rn CR-39 detector
(1x1cm)
Tobacco
sample
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 concen-
trations. 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 Environ Geochem Health (2007) 29:249–255

Fig. 2 Radon and thoron 300

concentrations in 10 222Rn

Radon Conc. (Bqm -3)

tobacco samples. An 250
asterisk refers to a 220Rn
200
significant difference
between the 150
corresponding sample and
the background level for 100
the same isotope using the
50
unpaired t test. BG is the
background value 0
T1 T2 T3 T4 T5 T6 T7 T8 T9 T10 BG
Samples

Fig. 3 PAE of radon and

P A E o f r a d o n a nd t h o r o n ( m / w l ) 35
thoron in ten tobacco PEA 222Rn
samples 30
PEA220 Rn
25

20

15

10

0
T1 T2 T3 T4 T5 T6 T7 T8 T9 T10
Samples

due to the 220Rn series for different investigated exhalation rates varies from 6.71 mBqm–3h–1 for
tobacco samples. This is due to the fact that the the T8 sample to 13.97 mBqm–3h–1 for the T5
corresponding tobacco material samples contain sample and 2.57 mBqm–3h–1 for the T2 sample to
more 238U(4.468 · 109 y) than 228Th (1.913 y). 7.76 mBqm–3h–1 for the T6 sample.
Also, note that the half-life of thoron (220Rn) is The concentrations of 222Rn and 220Rn proge-
too short (55.60 s) compared to the exposure time nies are shown in Fig. 5. The values of 222Rn
(two months) of the SSNTD films inside the progeny concentration were lower in T8
plastic container (Misdaq & Flata 2003). (51 Bqm–3) and higher in T5 (106 Bqm–3). Also,
Consequently, it is anticipated that smokers the values of 220Rn progeny were lower in the T2
consuming tobaccos T1, T2, T4, T5, T6 and T7 and T10 samples (19 Bqm–3) and higher in T6
samples are exposed to higher alpha doses. (59 Bqm–3) (Romola, Negy, & Choubey, 2005).
Previous studies (Lagarde et al., 2001) have indi- Indoor air quality is a contributing factor of lung
cated that in a smoker’s lungs the ciliary action to cancer, although the attributable lung cancer risk
clear the lungs is reduced to about half the normal. from 222Rn in homes may be low. Due to the
The average length of time during which the presence of dust, the 222Rn and 220Rn daughters
insoluble forms of 210Pb and 210Po remain at the (from building materials, soil, or underground
bronchial bifurcations is 3–5 months. Coinciden- water supply) mainly attach to room surfaces, but
tally, the surface tissue of smokers’ bronchi at the indoor smoking allows 222Rn daughters to attach
bifurcations is replaced by damaged abnormal to smoke particles. Thus, the alpha radiation to a
tissue. smoker’s lungs from the natural 222Rn daughters
The exhalation rates of both 222Rn and 220Rn is increased because of smoking.
in different tobacco samples have been deter- The resulting estimates of dose due to the
mined (Fig. 4). The value of radon and thoron presence of 222Rn, 220Rn and their daughters are

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Fig. 4 Radon and thoron

Exhalation Rates (mBqm h )

16

- 3 -1
exhalation rates in 10 222Rn
14
tobacco samples

Radon and Thoron

12 220Rn
10
8
6
4
2
0
T1 T2 T3 T4 T5 T6 T7 T8 T9 T10
Samples

Fig. 5 Distribution of the Radon and Thoron Progenies (Bqm-3)

concentrations of radon
and thoron progenies in 222Rn
120
10 tobacco samples
100 220Rn

80

60

40

20

0
T1 T2 T3 T4 T5 T6 T7 T8 T9 T10
Samples

Fig. 6 Resulting dose due

e qu iv a len t D os e o f R a do n a nd T h or o n

to radon and thoron in 10 5 222Rn

tobacco samples 4.5
4 220Rn
3.5
(mSvy )

3
-1

2.5
2
1.5
1
0.5
0
T1 T2 T3 T4 T5 T6 T7 T8 T9 T10
Samples

shown in Fig. 6. Most of the values of radon and radiation playing the most important role in
thoron observed were, respectively, 2.21-4.59 causing lung cancer. These values correspond to
(mSvy–1) with high values in T5 and low values 2/3 of a pack of cigarette, which means these
in T8 samples, and 0.84–2.55 (mSvy–1) with high values will increase by 25% when a complete
values in T6 and low values in T2 and T10 pack is used (Abu-Jarad, 1997).
samples. However, the fact that these higher The measured values of both radon and thoron
doses of radiation are delivered to vulnerable in residential houses and café rooms (n = 20
tissue at the location where malignancy is most each) are shown in Table 1. Radon and thoron
frequently observed argues strongly for alpha concentrations, in most cases, were found to be

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Table 1 Radon and

Location no. Residential houses Café room
thoron concentrations in
residential houses and 222
Rn (Bqm–3) 220
Rn (Bqm–3) 222
Rn (Bqm–3) 220
Rn (Bqm–3)
café rooms 1 55 ± 3.44 15 ± 0.93 110 ± 6.88 25 ± 1.56
2 41 ± 2.56 13 ± 0.81 105 ± 6.56 29 ± 1.81
3 51 ± 3.18 11 ± 0.68 114 ± 7.13 30 ± 1.87
4 44 ± 2.75 12 ± 0.75 112 ± 7.00 27 ± 1.68
5 50 ± 3.12 14 ± 0.87 100 ± 6.25 24 ± 1.50
6 60 ± 3.75 11 ± 0.68 103 ± 6.44 29 ± 1.81
7 42 ± 2.62 14 ± 0.87 100 ± 6.25 26 ± 1.62
8 45 ± 2.81 15 ± 0.93 105 ± 6.56 28 ± 1.75
9 41 ± 2.56 13 ± 0.81 99 ± 6.19 30 ± 1.87
10 67 ± 4.19 14 ± 0.87 104 ± 6.50 30 ± 1.87
11 71 ± 4.44 12 ± 0.75 101 ± 6.31 26 ± 1.62
12 48 ± 3.00 14 ± 0.87 99 ± 6.19 31 ± 1.93
13 43 ± 2.68 11 ± 0.68 108 ± 6.75 29 ± 1.81
14 51 ± 3.18 16 ± 1.00 100 ± 6.25 25 ± 1.56
15 52 ± 3.25 15 ± 0.93 115 ± 7.19 30 ± 1.87
16 56 ± 3.50 13 ± 0.81 110 ± 6.88 28 ± 1.75
17 41 ± 2.56 11 ± 0.68 113 ± 7.06 31 ± 1.93
18 53 ± 3.31 14 ± 0.87 98 ± 6.12 27 ± 1.68
19 55 ± 3.44 10 ± 0.62 117 ± 7.31 24 ± 1.50
20 48 ± 3.00 12 ± 0.75 110 ± 6.88 28 ± 1.75
21 43 ± 2.68 11 ± 0.68 105 ± 6.56 30 ± 1.87
22 47 ± 2.93 13 ± 0.81 110 ± 6.88 33 ± 2.06
*222Rn and **220Rn were 23 63 ± 3.94 14 ± 0.87 100 ± 6.25 28 ± 1.75
significantly and highly 24 45 ± 2.81 10 ± 0.62 97 ± 6.06 31 ± 1.93
significant lower 25 53 ± 3.31 11 ± 0.68 106 ± 6.62 29 ± 1.81
(respectively) in 26 60 ± 3.75 15 ± 0.93 110 ± 6.88 27 ± 1.68
residential houses 27 70 ± 4.37 12 ± 0.75 99 ± 6.19 34 ± 2.12
compared with café 28 52 ± 3.25 11 ± 0.68 115 ± 7.19 26 ± 1.62
rooms (P \ 0.0001 29 49 ± 3.06 13 ± 0.81 111 ± 6.94 32 ± 2.00
and \ 0.0001, 30 73 ± 4.56 10 ± 0.62 97 ± 6.06 29 ± 1.81
respectively) (estimated Average ± SD 52.3 ± 3.27* 12.66 ± 0.79** 105.76 ± 6.61 28.53 ± 1.78
by unpaired t test).

higher in café rooms than residential houses. It is
probable that the smoke-rich air of the café room
enhances the presence of such elements com-
pared 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 lympho-
cytes 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
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,

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