Content uploaded by Ganesh Jagetia
Author content
All content in this area was uploaded by Ganesh Jagetia on Oct 29, 2017
Content may be subject to copyright.
Full Terms & Conditions of access and use can be found at
http://www.tandfonline.com/action/journalInformation?journalCode=iebm20
Download by: [Mizoram University] Date: 08 August 2017, At: 02:12
Electromagnetic Biology and Medicine
ISSN: 1536-8378 (Print) 1536-8386 (Online) Journal homepage: http://www.tandfonline.com/loi/iebm20
Impact of radiofrequency radiation on DNA
damage and antioxidants in peripheral blood
lymphocytes of humans residing in the vicinity of
mobile phone base stations
Zothansiama, Mary Zosangzuali, Miriam Lalramdinpuii & Ganesh Chandra
Jagetia
To cite this article: Zothansiama, Mary Zosangzuali, Miriam Lalramdinpuii & Ganesh Chandra
Jagetia (2017): Impact of radiofrequency radiation on DNA damage and antioxidants in
peripheral blood lymphocytes of humans residing in the vicinity of mobile phone base stations,
Electromagnetic Biology and Medicine, DOI: 10.1080/15368378.2017.1350584
To link to this article: http://dx.doi.org/10.1080/15368378.2017.1350584
Published online: 04 Aug 2017.
Submit your article to this journal
View related articles
View Crossmark data
Impact of radiofrequency radiation on DNA damage and antioxidants in
peripheral blood lymphocytes of humans residing in the vicinity of mobile
phone base stations
Zothansiama, Mary Zosangzuali, Miriam Lalramdinpuii, and Ganesh Chandra Jagetia
Department of Zoology, Cancer and Radiation Biology Laboratory, Mizoram University, Aizawl, Mizoram, India
ABSTRACT
Radiofrequency radiations (RFRs) emitted by mobile phone base stations have raised concerns on
its adverse impact on humans residing in the vicinity of mobile phone base stations. Therefore,
the present study was envisaged to evaluate the effect of RFR on the DNA damage and
antioxidant status in cultured human peripheral blood lymphocytes (HPBLs) of individuals residing
in the vicinity of mobile phone base stations and comparing it with healthy controls. The study
groups matched for various demographic data including age, gender, dietary pattern, smoking
habit, alcohol consumption, duration of mobile phone use and average daily mobile phone use.
The RF power density of the exposed individuals was significantly higher (p< 0.0001) when
compared to the control group. The HPBLs were cultured and the DNA damage was assessed by
cytokinesis blocked micronucleus (MN) assay in the binucleate lymphocytes. The analyses of data from
the exposed group (n= 40), residing within a perimeter of 80 m of mobile base stations, showed
significantly (p< 0.0001) higher frequency of micronuclei when compared to the control group,
residing 300 m away from the mobile base station/s. The analysis of various antioxidants in the plasma
of exposed individuals revealed a significant attrition in glutathione (GSH) concentration (p<0.01),
activities of catalase (CAT) (p< 0.001) and superoxide dismutase (SOD) (p< 0.001) and rise in lipid
peroxidation (LOO) when compared to controls. Multiple linear regression analyses revealed a sig-
nificant association among reduced GSH concentration (p<0.05),CAT(p<0.001)andSOD(p<0.001)
activitiesand elevated MN frequency (p< 0.001) and LOO (p< 0.001) with increasing RF power densit y.
ARTICLE HISTORY
Received 27 April 2017
Accepted 30 June 2017
KEYWORDS
Antioxidants; genotoxicity;
humans; micronucleus;
power density
Introduction
The mobile phone base stations are one of the essential
parts of mobile telecommunication as they transmit the
signals in the form of radiofrequency radiations (RFRs)
that are received by the mobile phones, acting as a two-
way radio, i.e. transceiver (Kwan-Hoong, 2005), generally
operating in the frequency range of 900 MHz to 1.9 GHz
(Levitt and Lai, 2010). The ever-increasing subscription of
mobile phones has led to a phenomenal increase in the
mobile phone base stations required to cater to the needs
of increasing demand of the mobile subscribers. For dec-
ades, there has been an increasing concern on the possible
adverse effects of RFR on humans living near mobile
phone base stations despite the fact that RFR spectrum
are of low frequency (ARPANSA, 2011). There has been a
link between the RFR exposures and several human health
disorders including cancer, diabetes, cardiovascular and
neurological diseases (Bortkiewicz et al., 2004; Eger et al.,
2004;Havas,2013;Lerchletal.,2015; Wolf and Wolf,
2004). The International Agency for Research on Cancer
(IARC, 2011) has classified RFR as a possible carcinogen
to humans (group 2B), based on the increased risk for
glioma, a malignant type of brain cancer associated with
wireless phone use (Hardell et al., 2013).
RFR may change the fidelity of DNA as the increased
incidence of cancer has been reported among those resid-
ing near mobile phone base stations (Abdel-Rassonl et al.,
2007;Bortkiewiczetal.,2004;Cherry,2000; Eger et al.,
2004;Hardelletal.,1999; Hutter et al., 2006;Wolfand
Wolf, 2004). RFR emittedfrom mobile base stations is also
reported to increase the DNA strand breaks in lympho-
cytes of mobile phone users and individuals residing in the
vicinity of a mobile base station/s (Gandhi and Anita,
2005;Gandhietal.,2014). Exposure of human fibroblasts
and rat granulosa cells to RFR (1800 MHz, SAR 1.2 or 2
W/kg) has been reported to induce DNA single- and
double-strands breaks (Diem et al., 2005). Irreversible
DNA damage was also reported in cultured human lens
epithelial cells exposed to microwave generated by mobile
phones (Sun et al., 2006). The adverse health effects of
RFR are still debatable as many studies indicated above
have found a positive correlation between the DNA
CONTACT Ganesh Chandra Jagetia gc.jagetia@gmail.com Department of Zoology, Mizoram University, Aizawl 796 004, Mizoram, India.
ELECTROMAGNETIC BIOLOGY AND MEDICINE
https://doi.org/10.1080/15368378.2017.1350584
© 2017 Taylor & Francis
Downloaded by [Mizoram University] at 02:12 08 August 2017
damage and RFR exposure; however, several studies
reported no significant effect of RFR on DNA strand
breaks and micronuclei formation in different study sys-
tems (Li et al., 2001;Ticeetal.,2002; McNamee et al.,
2003; Maes et al., 2006). The potential genotoxicity of RFR
emitted by mobile phone base stations can be determined
by micronucleus (MN) assay, which is an effective tool to
evaluate the genotoxic or clastogenic effects of physical
and chemical agents. This technique has also been used to
quantify the frequencies of radiation-induced MN in
human peripheral blood lymphocytes (HPBLs) (Fenech
and Morley, 1985; Jagetia and Venkatesha, 2005; Prosser
et al., 1988; Yildirim et al., 2010).
Besides its effect on DNA damage and association of
cancer in individuals living near mobile phone base sta-
tion, the deep penetration of RFR within the living cells
may cause overproduction of free radicals particularly
reactive oxygen species (ROS), thereby inducing adverse
effects in living cells (Yakymenko et al., 2015). ROS
amount is also reported to increase during infections,
exercise, exposure to pollutants, UV light, ionizing radia-
tions, etc. (Kunwar and Priyadarsini, 2011). Uncontrolled
generations of ROS can lead to their accumulation caus-
ing oxidative stress in the cells. Any chronic exposure to
conditions that increase the oxidative stress leads to an
increased risk of cancer, and elevated levels of cancer have
been demonstrated in populations with increased resi-
dential exposure to RFR (Dart et al., 2013; IARC, 2011).
The change in the activities of antioxidants such as glu-
tathione (GSH), superoxide dismutase (SOD) and cata-
lase (CAT) may be regarded as an indicator of increased
oxidative stress (Kerman and Senol, 2012). Since lipid
peroxidation (LOO) is a free-radical oxidation product
of polysaturated fatty acids, detection and measurement
of LOO is the evidence which is frequently cited to sup-
port the involvement of free-radical reactions in toxicity
and disease progression (Gutteridge, 1995). The increas-
ing use of mobile phones and installation of more mobile
base stations stimulated us to obtain an insight into the
genotoxic effects of RFR using MN assay and alteration in
the antioxidant status in the PBLs of the individuals
residing in the vicinity of the mobile phone base stations.
Methods
Chemicals
RPMI-1640 medium, phytohemagglutinin, acridine
orange, bovine serum albumin (BSA), GSH reduced, nico-
tinamide adenosine dinucleotide (NADH), nitrobluete-
trazolium (NBT) and n-butanol were purchased from
HiMedia laboratories Pvt Ltd. (Mumbai, Maharashtra,
India). Methanol, acetic acid, Folin–Ciocalteu reagent,
potassium tartarate, hydrogen peroxide (H
2
O
2
), trichlor-
oacetic acid (TCA), hydrochloric acid (HCl) and potas-
sium chloride (KCl) were purchased from MERCK
(Mumbai, Maharashtra, India). Cytochalasin B, thiobar-
baturic acid (TBA) and phenazinemethosulphate (PMS)
were purchased from Sigma Aldrich Chemical Co
(Bangalore, Karnataka, India) and 5,5ˊ-dithio-2-nitroben-
zoic acid (DTNB) was procured from Tokyo Chemical
Industry (Tokyo, Japan).
Power density measurement from mobile phone
base stations
Six mobile phone base stations, operating in the frequency
range of 900 MHz (N= 2) and1800 MHz (N=4),erected
in the thickly populated areas of Aizawl city were selected
for the present study. Both dish and sectored antennas of
each base station are arranged equilaterally that provide
360° network coverage. The power output of all the base
stations is 20 W, with their primary beam emitting radia-
tion at an angle of 20°. Power density measurements
(using HF-60105V4, Germany) were carried out in the
bedroom of each participant where they spent most of the
time and hence have the longest constant level of electro-
magnetic field exposure. Power density measurement was
carried out three times (morning, midday and evening),
and the average was calculated for each residence around
each base station. The main purpose of the measurement
of power density was to ensure that RFR emission from
each site did not exceed the safe public limits and to
determine any difference in power density between
selected households that were close to (within 80 m) and
far (>300 m) from the mobile phone base stations. The
safety limits for public exposure from mobile phone base
stations are 0.45 W/m
2
for 900 MHz and 0.92 W/m
2
for
1800 MHz frequency as per Department of
Telecommunications, Ministry of Communications,
Government of India, New Delhi guidelines (DoT, 2012).
Selection of subjects
The study was carried out in Aizawl city (23°43ˊ37.58ˊˊN
and 92°43ˊ3.49ˊˊE), Mizoram, India, during 2015 and
2016. Since the city is located in the hilly region, some
residences are located horizontally with the top of the
towers from which RFR are emitted, making it possible
to get an exposure at a short distance of 1–20 m, despite
being erected on the rooftop or in the ground. A mini-
mum of two individuals were sampled from each house-
hold and at least five individuals were sampled around
each mobile base station. Individuals sampled around
each base station were matched for their age and gender
(Table 1). The exposed group consisted of 40 healthy
2Z. SIAMA ET AL.
Downloaded by [Mizoram University] at 02:12 08 August 2017
individuals who fulfilled the inclusion criteria of being
above 18 years of age and residing in the vicinity of
mobile phone base stations (within 80 m radius). The
control group comprised of 40 healthy individuals
matched for age and gender who had been living at
least 300 m away from any mobile phone base stations.
None of the participants have occupational exposure to
RFR, and there were no electric transformer, high ten-
sion electric power line and radio and television trans-
mitters close to (at least 500 m) their residences.
Sampling was also done only from those residences
who did not use microwave oven for cooking, Wifi
devices and any other major source of electromagnetic
field as they are known to cause adverse effects (Atasoy
et al., 2013; Avendaño et al., 2012). The study was
approved by the Human Ethics Committee, Mizoram
University, Aizawl, India, and only those individuals
who gave their voluntary written consent were included
in the study.
Questionnaire used
A questionnaire was prepared to collect information on
demographic data such as family and exposure his-
tories, lifestyle such as smoking habit (≤10 cigarette in
a day), alcohol consumption (three to four times a
week) and dietary pattern, duration of stay near mobile
phone base stations, duration of mobile phone use and
average daily mobile phone use.
Blood sample collection and lymphocyte culture
The blood samples were collected by venipuncture from
each volunteer of both groups in individual heparinized
tubes. The lymphocyte culture was carried out according
to the method described earlier (Jagetia et al., 2001).
Briefly, the blood was allowed to sediment and the buffy
coat containing nucleated cells was collected in individual
sterile glass tubes. Usually 10
6
nucleated cells were inocu-
lated into sterile glass tubes containing RPMI-1640 med-
ium, supplemented with 10% fetal calf serum and
phytohemagglutinin as the mitogen. The cells were allowed
to grow for the next 44 h and cytochalasin B was added at a
final concentration of 5 µg/ml to block the cytokinesis
(Fenech and Morley, 1985). The cells were harvested at
the end of 72 h after initiation of lymphocyte culture by
centrifugation. The cell pellet was subjected to mild hypo-
tonic treatment so as to retain the cell membrane and fixed
in freshly prepared Carnoy’s fixative (methanol: acetic acid,
3:1). The cell suspension was dropped onto precleaned
coded slides to avoid observer’s bias and stained with acri-
dine orange. Usually a total of 1000 binucleate cells (BNCs)
with well-preserved cytoplasm were scored from each indi-
vidual using a fluorescence microscope (DM 2500, Leica
MikrosystemeVertrieb GmbH, Wetzlar, Germany).
Scoring of MN frequencies was performed based on the
criteria of Fenech et al. (2003).
Biochemical estimations
The antioxidants were measured in the plasma of the
study groups. Protein contents were measured by the
method of Lowry et al. (1951) using BSA as the standard.
Glutathione
GSH contents were measured using the method given
by Moron et al. (1979). Briefly, 80 µl of plasma was
mixed with 900 µl of 0.02 M sodium phosphate buffer
and 20 µl of 10 mM DTNB and incubated for 2 min at
room temperature. The absorbance of the sample was
read against blank at 412 nm in a UV-Visible spectro-
photometer (SW 3.5.1.0. Biospectrometer, Eppendorf
India Ltd., Chennai), and the GSH concentration was
calculated from the standard curve and expressed in
µmol/mg protein.
Superoxide dismutase
The SOD activity was measured by the method of Fried
(1975). Briefly, 100 µl each of plasma and 186 µM PMS
were mixed with 300 µl of 3 mM NBT and 200 µl of 780
µM NADH. The mixture was incubated for 90 s at 30°C
and 1 ml of acetic acid and 4 ml of n-butanol were
added to stop the reaction. The blank consisted of all
the reagents, and distilled H
2
O was added instead of
plasma. The absorbance of test and blank was measured
at 560 nm using a UV-VIS spectrophotometer, and the
Table 1. Composition of base stations and the demographic characteristics of the exposed group.
Components Gender of volunteers
Base station Disc antenna Sectored antenna Power density (mW/m
2
) Average age (years) of volunteers Male Female
1 3 10 3.90–6.52 28.8 3 4
2 6 10 5.12–7.32 30.0 3 3
3 3 9 2.80–6.55 28.2 4 4
4 11 6 3.58–7.52 28.9 2 4
5 6 4 4.56–5.43 28.6 3 2
6 6 4 3.58–6.53 27.6 3 5
ELECTROMAGNETIC BIOLOGY AND MEDICINE 3
Downloaded by [Mizoram University] at 02:12 08 August 2017
enzyme activity has been expressed in units (1U = 50%
inhibition of NBT reduction)/mg protein.
% inhibition ¼OD of blank OD of test=OD of blankðÞ100
SOD unit ¼1=50 % inhibition:
Catalase
The CAT activity was determined using the modified
protocol of Aebi (1984). Briefly, 200 µl of 3% H
2
O
2
was
mixed with 50 µl each of plasma and 150 µl of 50 mM
phosphate buffer (pH 7.0). The absorbance was
recorded at 240 nm in a UV-VIS spectrophotometer.
The decomposition of H
2
O
2
can be followed directly by
the decrease in absorbance. The enzyme activity has
been expressed in units/mg protein. The catalytic activ-
ity of CAT at a time interval of 15 s was calculated by
the following formula,
K¼0:153 log A0=A1
ðÞ
where A
0
is the absorbance at 0 s and A
1
is the absor-
bance at 15 s.
Lipid peroxidation
The LOO was estimated by the method of Beuege
and Aust (1978). Briefly, plasma was mixed with 10%
TCA, 0.8% TBA and 0.025 N HCl in a 1:2 ratio. The
mixturewasboiledfor10mininaboilingwater
bath. After centrifugation, the absorbance of the
supernatant was recorded at 540 nm UV-VIS
spectrophotometer.
Statistical analyses
The data are expressed as mean ± standard error of the
mean. Student’s“t”and Chi-square tests were used for
comparison of demographic variables of the exposed and
control groups. Pearson`s correlation analysis was per-
formed to determine the relationship between power
density and the distance of residences from the base
stations. Mann Whitney Utest was applied to determine
the significance between the control and exposed group
for MN frequencies. Student’s“t”test was performed to
determine the significance between the groups for anti-
oxidants. Multiple linear regression analyses were carried
out for the prediction of MN frequency and antioxidants
status separately from the demographic characteristics.
SPSS Ver.16.0 software (SPSS Inc, Chicago, IL, USA)
was used for statistical analyses. A p-value of less than
0.05 was considered statistically significant.
Results
The demographic characteristics of both exposed and
control groups are depicted in Table 2. The groups
matched for most of the demographic data such as
age, gender, dietary pattern, smoking habit, alcohol
consumption, mobile phone usage, duration of mobile
phone use and average daily mobile phone use
(Table 2). A highly significant variation (p< 0.0001)
was observed for the distance of household from the
base station (40.10 ± 3.02 vs. 403.17 ± 7.98 in m)
between exposed and control groups. The data of RF
Table 2. Demographic data of the exposed and control groups.
Exposed group Control group p-value
Characteristics Category N(%) M±SEM N(%) M±SEM t/χ
2
-value (t/χ
2
-value)
Age (years) 20–30 26 (65) 28.6 ± 0.85 29 (72.5) 28.6 ± 0.85 1.074/–0.286/–
31–40 14 (35) 11 (27.5)
Gender Male 18 (45) 21 (52.5) –/0.450 –/0.502
Female 22 (55) 19 (47.5)
Diet Vegetarian 5 (12.5) 7 (17.5) –/0.392 –/0.531
Nonvegetarian 35 (87.5) 33 (82.5)
Smoking habit Yes 16 (40) 14 (35) –/0.213 –/0.644
No 24 (60) 26 (65)
Alcohol consumption Yes 7 (17.5) 9 (22.5) –/0.312 –/0.576
No 33 (82.5) 31 (77.5)
Mobile phone usage User 37 (92.5) 35 (87.5) –/0.556 –/0.456
Nonuser 3 (7.5) 5 (12.5)
Duration of mobile
phone use (years)
≤5 9 (24.32) 6.32 ± 0.265 11 (31.42) 5.91 ± 0.296 1.032/–0.306/–
>5 28 (75.68) 24 (68.58)
Daily mobile phone use
(hours)
≤3 24 (64.86) 3.054 ± 0.229 25 (71.42) 2.800 ± 0.156 1.145/–0.256/–
>3 13 (35.13) 10 (28.58)
Distance from the base
station (m)
1–20 8 (20) 40.10 ± 3.02 403.17 ± 7.98 42.046/–0.0001/–
21–40 12 (30)
41–60 13 (32.5)
61–80 7 (17.5)
Power density (mW/m
2
) Range 2.80–7.52 5.002 ± 0.182 0.014–0.065 0.035 ± 0.002 27.247/–0.0001/–
Duration of residing
near the base station
(years)
5–10 33 (82.5) 7.85 ± 0.419 ––––
11–15 7 (17.5)
4Z. SIAMA ET AL.
Downloaded by [Mizoram University] at 02:12 08 August 2017
power density were collected from 23 houses, each of
the exposed group staying within a perimeter of 80 m
and those of control group staying at least 300 m away
from mobile phone base stations. The RF power density
of the exposed group (2.80–7.52 mW/m
2
; average
5.002 ± 0.182 mW/m
2
) was significantly higher
(p< 0.0001) when compared to the control group
(0.014–0.065 mW/m
2
; average 0.035 ± 0.002 mW/m
2
).
The highest power density was recorded at a distance of
1–20 m (6.44 ± 0.31 mW/m
2
), which is significantly
higher (p< 0.0001) than those at a distance of 21–40 m
(4.79 ± 0.33), 41–60 m (4.48 ± 0.22) and 61–80 m
(4.61 ± 0.10). No significant variation was observed
for the RFR power density among the distance ranges
of 21–40 m, 41–60 m and 61–80 m (Table 1).
Nevertheless, there was a highly significant negative
correlation between distance from the base station
and the power density (r=−0.509, p< 0.0001).
The MN frequency and LOO were significantly
(p< 0.0001 for MN and LOO) higher in the exposed
group as compared to that of control group, while
antioxidants were significantly (p< 0.01 for GSH;
p< 0.001 for CAT and SOD) lower for the exposed
group compared to controls irrespective of their demo-
graphic characteristics (Tables 3 and 4). On considera-
tion of the demographic characteristics, smokers had
significantly higher MN frequency (p< 0.001) and LOO
(p< 0.01) and significantly lower GSH (p< 0.01) and
SOD (p< 0.01) than nonsmokers within each study
group. Similarly, alcoholics compared to nonalcoholics
had significantly higher MN frequency (p< 0.01) and
significantly lower GSH (p< 0.01) within the exposed
group and significantly higher MN frequency
(p< 0.001) and LOO (p< 0.01) within the control
group. The smokers of the exposed group had signifi-
cantly higher MN frequency (p< 0.001) and LOO
(p< 0.01) and significantly lower CAT (p< 0.001)
and SOD (p< 0.05) activities than the smokers of
control group. Alcoholic among exposed group also
had significantly higher MN frequency (p< 0.05) and
significantly lower GSH (p< 0.05) concentration and
CAT (p< 0.01) and SOD (p< 0.05) activities than the
alcoholic of control group. MN frequency and antiox-
idant status with LOO showed no significant variations
between the ages, genders and dietary pattern within
the exposed group. Among controls, males compared
to females had significantly (p< 0.05) higher MN
frequency (Table 3).
There was no significant variation in the MN fre-
quency and antioxidant status between mobile phone
user and nonuser of exposed group, while individuals
who have been using mobile phone for more than 5
years had significantly higher MN frequency (p< 0.01)
and lower GSH (p< 0.05) than those using for less than
5 years. Similarly, exposed group with average daily
mobile phone use of above 3 h showed a higher MN
frequency (p< 0.05) than those having the average daily
use of less than 3 h (Table 4). Among the control
group, features of mobile phone usage showed no var-
iation in MN frequency and antioxidant status.
Significantly lower levels of antioxidants (p< 0.05 for
GSH; p< 0.001 for CAT; p< 0.01 for SOD) and higher
Table 3. Function of the demographic characteristics on MN frequencies and the antioxidant status of exposed and control groups.
GSH CAT SOD LOO MN/1000 BNC
Characteristics Category N(M±SEM) (M±SEM) (M±SEM) (M±SEM) (M±SEM)
EXPOSED GROUP Age (years) 20–30 26 4.604 ± 2.68** 0.022 ± 0.001*** 1.832 ± 0.11*** 0.646 ± 0.064*** 38.15 ± 1.65**
31–40 14 3.882 ± 2.09 0.021 ± 0.001*** 1.791 ± 0.11** 0.755 ± 0.101* 43.71 ± 2.64**
Total 40 4.351 ± 1.95** 0.021 ± 0.001*** 1.823 ± 0.08*** 0.677 ± 0.054*** 40.10 ± 1.46***
Gender Male 18 4.209 ± 3.08* 0.020 ± 0.001*** 1.802 ± 0.12** 0.667 ± 0.072** 40.77 ± 2.71*
Female 22 4.467 ± 2.54 0.023 ± 0.001*** 1.834 ± 0.11*** 0.686 ± 0.080** 39.54 ± 1.51***
Dietary pattern Vegetarian 5 4.360 ± 4.26* 0.019 ± 0.001** 1.913 ± 0.18** 0.650 ± 0.040*** 40.20 ± 2.87***
Nonvegetarian 35 4.350 ± 2.17* 0.022 ± 0.001*** 1.807 ± 0.09*** 0.682 ± 0.053*** 40.08 ± 1.63***
Smoking habit Yes 16 3.713 ± 2.28
a
0.022 ± 0.001*** 1.645 ± 0.11* 0.892 ± 0.102
a
** 46.50 ± 1.65
a
***
No 24 4.777 ± 2.56** 0.021 ± 0.001*** 1.932 ± 0.11*** 0.535 ± 0.039** 35.83 ± 1.69***
Alcohol consumption Yes 7 3.394 ± 2.35
a
* 0.021 ± 0.001** 1.792 ± 0.22* 0.683 ± 0.119 49.71 ± 3.12
a
*
No 33 4.554 ± 2.16* 0.022 ± 0.001*** 1.823 ± 0.08*** 0.676 ± 0.061** 38.27 ± 1.47***
CONTROL GROUP Age (years) 20–30 29 5.380 ± 1.54 0.038 ± 0.001 2.534 ± 0.09 0.389 ± 0.037 31.89 ± 1.64
31–40 11 4.023 ± 3.82 0.036 ± 0,002 2.492 ± 0.21 0.482 ± 0.062 35.09 ± 1.96
Total 40 5.007 ± 1.79 0.037 ± 0.001 2.526 ± 0.09 0.415 ± 0.032 32.77 ± 1.31
Gender Male 21 5.067 ± 2.70 0.038 ± 0.002 2.434 ± 0.11 0.385 ± 0.049 35.23 ± 1.99
a
Female 19 4.940 ± 2.38 0.037 ± 0.001 2.622 ± 0.14 0.447 ± 0.040 30.05 ± 1.49
Dietary pattern Vegetarian 7 5.473 ± 2.53 0.039 ± 0.003 2.845 ± 0.17 0.378 ± 0.066 29.85 ± 1.95
Nonvegetarian 33 4.908 ± 1.08 0.037 ± 0.001 2.453 ± 0.10 0.423 ± 0.038 33.39 ± 1.52
Smoking habit Yes 14 3.996 ± 2.66
a
0.036 ± 0.002 2.181 ± 0.17
a
0.522 ± 0.055
a
39.78 ± 1.70
a
No 26 5.551 ± 1.53 0.040 ± 0.001 2.717 ± 0.08 0.356 ± 0.036 29.00 ± 1.30
Alcohol consumption Yes 9 4.416 ± 2.91 0.036 ± 0.002 2.212 ± 0.23 0.546 ± 0.073
a
42.44 ± 2.29
a
No 31 5.178 ± 2.07 0.038 ± 0.001 2.616 ± 0.09 0.376 ± 0.033 29.96 ± 1.15
*Significant (p≤0.05) between the exposed and control groups.
**Highly significant (p≤0.01) between the exposed and control groups.
***Very highly significant (p≤0.001) between the exposed and control groups.
a
Significant (p≤0.05) along the demographic characteristics within group.
ELECTROMAGNETIC BIOLOGY AND MEDICINE 5
Downloaded by [Mizoram University] at 02:12 08 August 2017
MN frequency (p< 0.001) and LOO (p< 0.001) were
observed in the exposed group residing in the vicinity
of the base stations for 5–10 years and 11–15 years
when compared to the control group. None of the
parameters showed a significant variation among the
exposed group residing for 5–10 years and 11–15 years
in the vicinity of the base stations (Table 4).
As a function of distance from the base stations, MN
frequency and LOO within the distance of 1–20 m
(p< 0.01 for MN and LOO), 21–40 m (p< 0.01 for
MN and LOO) and 41–60 m (p< 0.05 for MN and
LOO) were significantly higher in the exposed group
than that of the control group. There were no signifi-
cant variation in MN frequency and LOO between the
exposed group residing within 61–80 m away from
mobile stations and the control group. GSH, CAT and
SOD were significantly lower in the exposed group
residing within a distance range of 1–20 m (p< 0.01
for GSH; p< 0.001 for CAT; p< 0.001 for SOD), 21–40
m(p< 0.05 for GSH; p< 0.001 for CAT; p< 0.001 for
SOD), 41–60 m (p< 0.001 for CAT; p< 0.01 for SOD)
and 61–80 m (p< 0.01 for CAT; p< 0.05 for SOD) than
individuals residing at least 300 m away from the base
stations. However, GSH contents did not differ between
the exposed group residing between 41 and 80 m from
the base stations and controls (Table 4). The indivi-
duals exposed to a power density of ≤4 mW/m
2
and >4
mW/m
2
showed a higher MN frequency (p< 0.05 for
≤4 mW/m
2
;p< 0.001 for >4 mW/m
2
) and LOO
(p< 0.01 for ≤4 mW/m
2
;p< 0.001 for >4 mW/m
2
)
and lower GSH (p< 0.05 for ≤4 mW/m
2
;p< 0.01 for
>4 mW/m
2
), CAT (p< 0.01 for ≤4mW/m
2
;p< 0.001
for >4 mW/m
2
) and SOD (p< 0.05 for ≤4 mW/m
2
;
p< 0.001 for >4 mW/m
2
)(Table 4).
Multiple linear regression analyses revealed a signif-
icant association with low GSH concentration and age
(p< 0.05), smoking habit (p< 0.001), daily mobile
phone use (p< 0.05) and increasing power density
(p< 0.05). A similar association has been reported
with reduced CAT activity with increasing power den-
sity (p< 0.001) and alleviated SOD activity with smok-
ing habit (p< 0.05) and increasing power density
(p< 0.001) (Table 5). The analyses also showed a
significant relationship between higher MN frequency
with smoking habit (p< 0.001) and increasing power
density (p< 0.001) and higher LOO with smoking habit
(p< 0.001), alcohol consumption (p< 0.05) and
increasing power density (p< 0.001) (Table 5). The
parameter of mobile phone usage was not included in
the multiple linear regression analysis due to multi-
collinearity with the duration of mobile phone use
and average daily mobile phone use. Similarly, distance
from the base stations showed multicollinearity with
power density in the preliminary analysis; therefore,
the former is also excluded in the multiple linear
regression analysis.
Discussion
Mobile phone base stations have become an integral part
of telecommunication, which use RFR to transmit the
signals. These electromagnetic waves are generated by
Table 4. Function of mobile phone usage and residence near base stations on MN frequencies and antioxidants status on exposed
and control groups.
GSH CAT SOD LOO MN/1000 BNC
Characteristics Category N(M±SEM) (M±SEM) (M±SEM) (M±SEM) (M±SEM)
EXPOSED GROUP Mobile phone usage User 37 4.336 ± 2.07** 0.020 ± 0.002*** 1.852 ± 0.08*** 0.66 ± 0.051*** 40.21 ± 1.55***
Nonuser 3 4.534 ± 6.04 0.022 ± 0.001*** 1.394 ± 0.10* 0.890 ± 0.205* 38.66± 1.37**
Duration of mobile
phone use (years)
≤5 9 5.006 ± 3.26
a
0.023 ± 0.002** 1.834 ± 0.23** 0.673 ± 0.109* 34.77 ±3.23
a
>5 28 4.145 ± 2.24** 0.021 ± 0.001*** 1.863 ± 0.08*** 0.656 ± 0.058** 41.96 ±1.66***
Daily mobile phone use
(hours)
≤3 24 4.410 ± 1.26* 0.023 ± 0.001*** 1.902 ± 0.11*** 0.653 ± 0.068** 37.87 ±1.99
a*
>3 13 4.233 ± 1.73* 0.020 ± 0.001*** 1.765 ± 0.13*** 0.674 ± 0.073** 44.53 ±2.02***
Distance from the base
station (m)
1–20 8 3.884 ± 2.20** 0.018 ± 0.002*** 1.654 ± 0.18*** 0.720 ± 0.154** 43.00 ± 3.94**
21–40 12 4.174 ± 3.72* 0.020 ± 0.001*** 1.762 ± 0.13*** 0.674 ± 0.106** 41.69 ± 2.49**
41–60 13 4.692 ± 3.23 0.022 ± 0.001*** 1.903 ± 0.15** 0.600 ± 0.069* 39.00 ± 1.24*
61–80 7 4.631 ± 6.44 0.025 ± 0.002** 2.016 ± 0.17* 0.494 ± 0.084 36.71 ± 2.57
Duration of residence near
the base station (years)
5–10 33 4.406 ± 2.25* 0.024 ± 0.001*** 1.872 ± 0.08** 0.642 ± 0.055*** 40.03 ± 3.13**
11–15 7 4.092 ± 2.54* 0.021 ± 0.001*** 1.814 ± 0.12** 0.781 ± 0.170*** 40.42 ± 1.66**
Power density (mW/m
2
)≤4 mW/m
2
7 4.554 ± 2.22* 0.025 ± 0.002** 1.915 ± 0.16* 0.660 ± 0.122** 39.14 ±0.21*
>4 mW/m
2
33 4.308 ± 2.32** 0.021 ± 0.001*** 1.807 ± 0.09*** 0.681 ± 0.061*** 40.30 ± 1.59***
CONTROL GROUP Mobile phone usage User 35 5.145 ± 1.86 0.037 ± 0.001 2.550 ± 0.09 0.417 ± 0.035 32.28 ± 1.40
Nonuser 5 4.038 ± 4.21 0.041 ± 0.004 2.282 ± 0.25 0.456 ± 0.022 31.80± 1.22
Duration of mobile
phone use (years)
≤5 11 5.528 ± 2.24 0.036 ± 0.003 2.553 ± 0.10 0.372 ± 0.062 31.09 ± 1.88
>5 24 5.039 ± 2.31 0.037 ± 0.001 2.568 ± 0.13 0.438 ± 0.043 32.83 ± 1.87
Daily mobile phone use
(hours)
≤3 25 5.258 ± 1.99 0.038 ± 0.001 2.524 ± 0.11 0.436 ± 0.041 30.10± 2.46
>3 10 5.027 ± 3.75 0.036 ± 0.001 2.655 ± 0.19 0.371 ± 0.070 33.16 ± 1.70
*Significant (p≤0.05) between the exposed and control groups.
**Highly significant (p≤0.01) between the exposed and control groups.
***Very highly significant (p≤0.001) between the exposed and control groups.
a
Significant (p≤0.05) along the demographic characteristics within group.
6Z. SIAMA ET AL.
Downloaded by [Mizoram University] at 02:12 08 August 2017
electric charges that are rapidly accelerated to and fro in
the transmitting antenna. Although RFR are nonionizing
electromagnetic radiations, yet there has been a great
concern about their deleterious effects on the human
body as it is assumed that RFR could produce some of
the biological effects akin to those produced by ionizing
radiations such as X or γ-rays. Because of its adverse
health effects reported worldwide, the presence of mobile
base stations in the residential areas could be an electro-
magnetic threat, which is silently creeping in the lives of
residents staying near the mobile base stations. We have
therefore attempted to obtain an insight into the adverse
effects of RFR in the inhabitants residing in the vicinity
(within 80 m) of mobile base stations emitting RFR for
mobile connectivity.
The frequency of nonspecific health symptoms such as
nausea, loss of appetite, visual disturbance, irritability and
depression were found to be significantly higher in the
population living close (within 100 m) to mobile phone
base stations as compared to those living away from these
stations (Santini et al., 2002,2003). Besides the nonspe-
cific health symptoms of fatigue, headache, dizziness and
muscle pain self-reported by the volunteers in the earlier
study (Pachuau et al., 2015), the present study showed a
significant increase in MN frequency and decreased anti-
oxidants among inhabitants residing close to the base
station/s when compared to controls. A number of studies
have reported an increase in the DNA damage/micronu-
clei in different study systems. The human PBLs exposed
to RFR have shown an increased frequency of micronuclei
earlier (d’Ambrosio et al., 2002; Garaj-Vrhovac et al.,
1992; El-Abd and Eltoweissy, 2012;Ticeetal.,2002;
Zotti-Martelli et al., 2000). Various studies conducted in
other systems have also revealed an increased micronuclei
frequency after exposure to RFR (Balode, 1996; Busljeta
et al., 2004; Gandhi and Singh, 2005; Trosic et al., 2002,
2004). Our results are in agreement with a recent study
where buccal mucosa cells showed increased micronuclei
in mobile phone users (Banerjee et al., 2016). However,
some of the studies did not find any increase in the MN
frequency after RFR exposure both in vitro and in vivo
(Bisht et al., 2002; Scarfi et al., 2006; Vijayalaxmi et al.,
1997,1999,2001;Zenietal.,2003,2008), and such reports
emphasized on the lack of thermal effects from RFR
Table 5. Multiple linear regression in the exposed and control groups.
Characteristics Durbin–Watson Model-FB-value t-value p-value
GSH Age 2.22 6.62*** −0.24 −2.10 0.043
Gender 0.11 1.09 0.283
Dietary pattern −0.10 −0.99 0.328
Smoking habit 0.44 −3.86 0.001
Alcohol consumption −0.06 −0.47 0.640
Duration of mobile phone use −0.09 −0.69 0.492
Daily mobile phone use 0.22 2.06 0.039
Power density −0.18 −1.97 0.041
CAT Age 2.10 11.19*** −0.09 −0.94 0.352
Gender 0.03 0.29 0.774
Dietary pattern 0.01 0.12 0.907
Smoking habit −0.01 −0.07 0.950
Alcohol consumption 0.03 0.29 0.771
Duration of mobile phone use 0.01 0.08 0.944
Daily mobile phone use −0.07 −0.77 0.447
Power density −0.72 −8.93 0.001
SOD Age 2.23 4.94*** 0.01 0.11 0.911
Gender 0.00 0.01 0.993
Dietary pattern −0.12 −1.22 0.237
Smoking habit −0.32 −2.70 0.012
Alcohol consumption 0.01 0.10 0.923
Duration of mobile phone use 0.11 0.81 0.426
Daily mobile phone use −0.07 −0.61 0.551
Power density −0.46 −4.74 0.001
LOO Age 1.82 6.53*** 0.22 1.96 0.052
Gender −0.13 −1.30 0.208
Dietary pattern 0.11 1.13 0.262
Smoking habit 0.47 4.12 0.001
Alcohol consumption −0.15 −1.25 0.210
Duration of mobile phone use −0.01 −0.05 0.965
Daily mobile phone use 0.02 0.15 0.886
Power density 0.37 3.99 0.001
MN Age 2.17 11.10*** 0.09 0.87 0.390
Gender −0.05 −0.58 0.572
Dietary pattern 0.03 0.38 0.718
Smoking habit 0.44 4.41 0.001
Alcohol consumption 0.28 2.62 0.013
Duration of mobile phone use −0.04 −0.34 0.733
Daily mobile phone use 0.06 0.58 0.562
Power density 0.36 4.45 0.001
Values in bold are significant (p< 0.05).
ELECTROMAGNETIC BIOLOGY AND MEDICINE 7
Downloaded by [Mizoram University] at 02:12 08 August 2017
(Vijaylaxmi and Obe, 2004), whereas the observed effect
in the present study may be due to the interaction of RFR
with various cellular macromolecules by producing ROS.
This contention is supported by the fact that RFR-exposed
individuals showed increased LOO and alleviated GSH
contents, CAT and SOD activities in the present study. A
similar effect has been observed earlier inthe CAT activity
in the rats exposed to low level of RFR (Achudume et al.,
2010). Also, RFR emitted from cell phones led to oxidative
stress in human semen (Agarwal et al., 2009). RFR (2.45
GHz) has been reported to cause a significant increase in
the LOO of exposed Wistar rats (Aweda et al., 2003). The
present study also revealed the induction of LOO by RF
radiation, which could possibly react with DNA and
produce lesions in it. The increased LOO has been
reported in the plasma of rats with a decline in GSH
and other antioxidants earlier (Aydin and Akar, 2011).
The highestmeasured power density was 7.52 mW/m
2
.
Most of the measured values close to base stations
(Table 1) are higher than that of the safe limits recom-
mended by Bioinitive Report 2012 (0.5 mW/m
2
), Salzburg
resolution 2000 (1 mW/m
2
) and EU (STOA) 2001 (0.1
mW/m
2
). However, all the recorded values were well
below the current ICNIRP safe level (4700 mW/m
2
)and
the current Indian Standard (450 mW/m
2
). Although
cigarette smoking increased the MN frequency and
decreased the antioxidants, the statistical analysis also
revealed a close correlation between the power density
and MN frequency and antioxidant status. Thus, the
effects of RF radiation cannot be ignored as unrepaired
DNA damage and oxidative stress are associated with
several diseases such as cancer and several age-related
diseases (Bernstein et al., 2013;Dartetal.,2013). The
persistence of low level of DNA damage could have nega-
tive effect on human health.
The exact mechanism of action of RFR in micronuclei
induction and reduced antioxidant status is not apparent.
The possible putative mechanism of generation of DNA
damage may be the production of endogenous free radi-
cals due to continuous exposure. RFR has been reported
to produce different free radicals earlier (Avci et al., 2009;
Burlaka et al., 2013; Barcal et al., 2014; Kazemi et al.,
2015). Cells possess a number of compensatory mechan-
isms to deal with ROS and its effects. Among these are the
induction of antioxidant proteins such as GSH, SOD and
CAT. Enzymatic antioxidant systems function by direct
or sequential removal of ROS, thereby terminating their
activities. An imbalance between the oxidative forces and
antioxidant defense systems causes oxidative injury,
which has been implicated in various diseases, such as
cancer, neurological disorders, atherosclerosis, diabetes,
liver cirrhosis, asthma, hypertension and ischemia
(Andreadis et al., 2003;Comhairetal.,2005; Dhalla
et al., 2000; Finkel and Holbrook, 2000; Kasparova et al.,
2005; Sayre et al., 2001;Sohaletal.,2002). Because of the
significant decrease in endogenous antioxidants and
increased LOO among the exposed group, the extra bur-
den of free radicals is unlikely to get neutralized, and these
surplus ROS may react with important cellular macro-
molecules including DNA forming either DNA adducts
or stand breaks, which may be later expressed as micro-
nuclei once the cell decides to divide. The decline in the
antioxidant status may be also due to the suppressed
activity of Nrf2 transcription factor which is involved in
maintaining the antioxidant status in the cells.
The present study has reported that RFR increased
the frequency of MN and LOO and reduced GSH con-
tents, CAT and SOD activities in the plasma of the
exposed individuals. The induction of MN may be due
to the increase in free-radical production. The present
study demonstrated that staying near the mobile base
stations and continuous use of mobile phones damage
the DNA, and it may have an adverse effect in the long
run. The persistence of DNA unrepaired damage leads
to genomic instability which may lead to several health
disorders including the induction of cancer.
Acknowledgements
The authors would like to acknowledge the cooperation
extended by the participants without which the study would
have not been completed. The authors are grateful to Prof. N.
Senthilkumar for allowing us to use the instrument facility in
the Department of Biotechnology, Mizoram University, State
Biotech Hub Programme, Government of India, New Delhi.
The authors wish to thank Dr. Lalrinthara Pachuau for his
valuable assistance in power density measurements. We are
grateful to Dr. C. Lalfamkima Varte for his assistance in
statistical analyses.
Declaration of interest
The authors report no declarations of interest.
Funding
This work was supported by University Grants Commission,
Govt. of India, New Delhi, vide grant number F.4-10/2010 (BSR).
References
Abdel-Rassoul, G., El-Fateh, O. A., Salem, M. A., et al. (2007).
Neurobehavioral effects among inhabitants around mobile
phone base stations. Neurotoxicology. 28:434–440.
Achudume, A., Onibere, B., Aina, F., et al. (2010). Induction
of oxidative stress in male rats subchronically exposed to
electromagnetic fields at non-thermal intensities. JEMAA.
2:482–487.
8Z. SIAMA ET AL.
Downloaded by [Mizoram University] at 02:12 08 August 2017
Aebi, H. (1984). Catalase in vitro. Methods. Enzymol.
105:121–126.
Agarwal, A., Desai, N. R., Makker, K., et al. (2009). Effects of
radiofrequency electromagnetic waves (RF-EMW) from
cellular phones on human ejaculated semen: an in vitro
pilot study. Fertil. Steril. 92:1318–1325.
Andreadis, A. A., Hazen, S. L., Comhair, S. A., et al. (2003).
Oxidative and nitrosative events in asthma. Free. Radic.
Biol. Med. 35:213–225.
Atasoy, H. I., Gunal, M. Y., Atasoy, P., et al. (2013).
Immunohistopathologic demonstration of deleterious
effects on growing rat testes of radiofrequency waves
emitted from conventional Wi-Fi devices. J. Pediatr. Urol.
9:223–229.
Australian Radiation Protection and Nuclear Safety Agency
(ARPANSA) Fact Sheet 3. (2011). Available from: www.
arpansa.gov.au (accessed 23 December 2016).
Avci, B., Akar, A., Bilgici, B., et al. (2009). Oxidative stress
induced by 1.8 GHz radio frequency electromagnetic
radiation and effects of garlic extract in rats. Int. J.
Radiat. Biol. 88:799–805.
Avendaño, C., Mata, A., Sanchez Sarmiento, C. A., et al.
(2012). Use of laptop computers connected to internet
through Wi-Fi decreases human sperm motility and
increases sperm DNA fragmentation. Fertil. Steril.97:39–45.
Aweda, M. A., Gbenebitse, S., Meidinyo, R. O. (2003). Effects
of 2.45 GHz microwave exposures on the peroxidation
status in Wistar rats. Niger. Postgrad. Med. J. 10:243–246.
Aydin, B., Akar, A. (2011). Effects of a 900-MHz electromag-
netic field on oxidative stress parameters in rat lymphoid
organs, polymorphonuclear leukocytes and plasma. Arch
Med Res. 42(4):261–267.
Balode, Z. (1996). Assessment of radio-frequency electromag-
netic radiation by the micronucleus test in bovine periph-
eral erythrocytes. Sci. Total. Environ. 180:81–85.
Banerjee, S., Singh, N. N., Sreedhar, G., et al. (2016). Analysis
of the genotoxic effects of mobile phone radiation using
buccal micronucleus assay: A comparative evaluation. J.
Clin. Diagn. Res. 10:82–85.
Barcal, J., Stopka, P., Křížová, J., et al. (2014). High-frequency
electromagnetic radiation and the production of free radicals in
four mouse organs. Act.Nerv.Super.Rediviva. 56(1–2):9–14.
Bernstein, C., Nfonsam, V., Prasad, A. R., et al. (2013).
Epigenetic field defects in progression to cancer. World.
J. Gastrointest. Oncol. 5:43–49.
Beuege, J. A., Aust, S. D. (1978). Microsomal lipid peroxida-
tion. Method. Enzymol. 30:302–310.
Bisht, K. S., Moros, E. G., Straube, W. L., et al. (2002). The
effect of 835.62 MHz FDMA or 847.74 MHz CDMA
modulated radiofrequency radiation on the induction of
micronuclei in C3H 10T½ Cells. Radiat. Res. 157:506–515.
Bortkiewicz, A., Zmys’lony, M., Szyjkowska, A., et al. (2004).
Subjective symptoms reported by people living in the vici-
nity of cellular phone base stations: Review. Med. Pr.
55:345–351.
Burlaka, A., Tsybulin, O., Sidorik, E., et al. (2013).
Overproduction of free radical species in embryonal cells
exposed to low intensity radiofrequency radiation. Exp.
Oncol. 35(3):219–225.
Busljeta, I., Trosic, I., Milkovic-Kraus, S. (2004).
Erythropoietic changes in rats after 2.45 GHz nonthermal
irradiation. Int. J. Hyg. Environ. Health. 207:549–554.
Cherry, N. (2000). A new paradigm, the physical, biological
and health effects of radio-frequency/microwave radiation.
Available from: http://hdl.handle.net/10182/3973.
Comhair, S. A., Ricci, K. S., Arroliga, M., et al. (2005).
Correlation of systemic superoxide dismutase deficiency
to airflow obstruction in asthma. Am. J. Respir. Crit.
Care. Med. 172:306–313.
d’Ambrosio, G., Massa, R., Scarfi, M. R., et al. (2002). Cytogenetic
damage in human lymphocytes following GMSK phase modu-
lated microwave exposure. Bioelectromagnetics. 23:7–13.
Dart, P., Cordes, K., Elliott, A., et al. (2013). Biological and
health effects of microwave radiofrequency transmission.
A review of the research literature. A report to the staff
and directors of the Eugene water and electric board.
Available from: www.national-toxic-encephalopathy-foun
dation.org/
Department of Telecommunications (DoT). (2012).
Government of India Ministry of Communications &
Information Technology Report of the Departmental
Committee on BTS Towers. pp. 1–35. Available from:
www.dot.gov.in/sites/default/files/Committee Report on
BTS towers.
Dhalla, N. S., Temsah, R. M., Netticadan, T. (2000). Role of
oxidative stress in cardiovascular diseases. J. Hypertens.
18:655–673.
Diem, E., Schwarz, C., Adlkofer, F., et al. (2005). Non-ther-
mal DNA breakage by mobile-phone radiation (1800
MHz) in human fibroblasts and in transformed GFSH-
R17 rat granulosa cells in vitro. Mutat. Res. 583:178–183.
Eger, H., Hagen, K. U., Lucas, B., et al. (2004). The influence of
being physically near to a cell phone transmission mast on the
incidence of cancer. Umwelt. Medizin. Gesellschaft.17:1–7.
El-Abd, S. F., Eltoweissy, M. Y. (2012). Cytogenetic altera-
tions in human lymphocyte culture following exposure to
radiofrequency field of mobile phone. J. App. Pharm. Sci.
2:16–20.
Fenech, M., Morley, A. A. (1985). Measurement of micro-
nuclei in lymphocytes. Mutat. Res. 147:29–36.
Fenech, M., Chang, W. P., Kirsch-Volders, M., et al. (2003).
HUMN project: detailed description of the scoring criteria
for the cytokinesis-block micronucleus assay using isolated
human lymphocyte cultures. Mutat. Res. 534:65–75.
Finkel, T., Holbrook, N. J. (2000). Oxidants, oxidative stress
and the biology of aging. Nature. 408:239–247.
Fried, R. (1975). Enzymatic and non-enzymatic assay of
superoxide dismutase. Biochimie. 57:657–660.
Gandhi, G., Anita. (2005). Genetic damage in mobile phone
users: Some preliminary findings. Indian J. Hum. Genet.
11:99–104.
Gandhi, G., Kaur, G., Nisar, U. (2014). A cross-sectional case
control study on genetic damage in individuals residing in
the vicinity of a mobile phone base station. Electromagn.
Biol. Med. 4:344–354.
Gandhi, G., Singh, P. (2005). Cytogenetic damage in mobile
phone users: preliminary data. Int. J. Hum. Genet.5:259–265.
Garaj-Vrhovac, V., Fucic, A., Horvat, D. (1992). The correla-
tion between the frequency of micronuclei and specific
chromosome aberrations in human lymphocytes exposed
to microwave radiation in vitro. Mutat. Res. 281:181–186.
Gutteridge, J. M. C. (1995). Lipid peroxidation and antiox-
idant as biomarkers of tissue damage. Clin. Chem.
41:1819–1828.
ELECTROMAGNETIC BIOLOGY AND MEDICINE 9
Downloaded by [Mizoram University] at 02:12 08 August 2017
Hardell, L., Nasman, A., Pahlson, A., et al. (1999). Use of
cellular telephones and the risk for brain tumours: a case-
control study. Int. J. Oncol. 15:113–116.
Hardell, L., Carlberg, M., Mild, K. H. (2013). Use of mobile
phones and cordless phones is associated with increased
risk for glioma and acoustic neuroma. Pathophysiology.
20:85–110.
Havas, M. (2013). Radiation from wireless technology affects
the blood, the heart, and the autonomic nervous system.
Rev. Environ. Health. 28:75–84.
Hutter, H. P., Moshammer, H., Wallner, P., et al. (2006).
Subjective symptoms, sleeping problems, and cognitive
performance in subjects living near mobile phone base
stations. Occup. Environ. Med. 63:307–313.
International Agency for Research on Cancer (IARC). (2011).
World Health Organization. Available from: www.iarc.fr
(accessed 23 March 2017).
Jagetia, G. C., Jayakrishnan, A., Fernandes, D., et al. (2001).
Evaluation of micronuclei frequency in the cultured per-
ipheral blood lymphocytes of cancer patients before and
after radiation treatment. Mutat. Res. 491:9–16.
Jagetia, G. C., Venkatesha, V. A. (2005). Effect of mangiferin
on radiation-induced micronucleus formation in cultured
human peripheral blood lymphocytes. Environ. Mol.
Mutagen. 46:12–21.
Kasparova, S., Brezova, V., Valko, M., et al. (2005). Study of
the oxidative stress in a rat of chronic brain hypoperfusion.
Neurochem. Int. 46:601–661.
Kazemi E., Mortazavi, S.M.J., Ali-Ghanbari A., et al. (2015).
Effect of 900 MHz electromagnetic radiation on the induc-
tion of ROS in human peripheral blood mononuclear cells.
J. Biomed. Phys. Eng. 5(3):105–114.
Kerman, M., Senol, N. (2012). Oxidative stress in hippocam-
pus induced by 900 MHz electromagnetic field emitting
mobile phone: Protection by melatonin. Biomed. Res.
23:147–151.
Kunwar, A., Priyadarsini, K. (2011). Free radicals, oxidative
stress and importance of antioxidants in human health. J.
Med. Allied. Sci. 1:53–60.
Kwan-Hoong, N. (2005). Radiation, mobile phones, base sta-
tions and your health. Malaysia: Malaysian Communications
and Multimedia Commission. (accessed 15 July 2016).
Lerchl, A., Klose, M., Grote, K., et al. (2015).Tumor promo-
tion by exposure to radiofrequency electromagnetic fields
below exposure limits for humans. Biochem. Biophys. Res.
Commun. 459:585–590.
Levitt, B. B., Lai, H. (2010). Biological effects from exposure to
electromagnetic radiation emitted by cell tower base stations
and other antenna arrays. Environ. Rev. 18:369–395.
Li, L., Bisht, K. S., LaGroye, I., et al. (2001). Measurement of
DNA damage in mammalian cells exposed in vitro to
radiofrequency fields at sars of 3–5 w/kg. Radiat. Res.
156:328–332.
Lowry, O. H., Rosebrough, N. J., Randall, R. J. (1951). Protein
measurement with the folin phenol reagent. J. Biochem.
193:265–275.
Maes, A., Van Gorp, U., Verschaeve, L. (2006). Cytogenetic
investigation of subjects professionally exposed to radio-
frequency radiation. Mutagenesis. 21:139–142.
McNamee, J. P., Bellier, P. V., Gajda, G. B., et al. (2003). No
evidence for genotoxic effects from 24 h exposure of
human leukocytes to 1.9 GHz radiofrequency fields.
Radiat. Res. 159(5):693–697.
Moron, M. S., Depierre, J. W., Mannervik, B. (1979). Levels
of glutathione, glutathione reductase and glutathione-s-
transferase activities in rat lung and liver. Biochim.
Biophys. Acta. 582:67–78.
Pachuau, L., Pachuau, Z., Zothansiama. (2015). Comparisons
of non specific health symptoms faced by inhabitants
exposed to high and low power density from mobile
phone tower radiation. Int. J. Recent. Innov. Trends.
Comp. Commun. 3:94–98.
Prosser, J. S., Moquet, J. E., Lloyd, D. C., et al. (1988).
Radiation induction of micronuclei in human lympho-
cytes. Mutat. Res. 199:37–45.
Santini, R., Santini, P., Danze, J. M., et al. (2002). Study of the
health of people living in the vicinity of mobile phone base
stations I: Influences of distance and sex. Pathol. Biol.
50:369–373.
Santini, R., Santini, P., Danze, J. M., et al. (2003). Symptoms
experienced by people in vicinity of base stations: II.
Incidences of age, duration of exposure, location of sub-
jects in relation to the antennas and other electromagnetic
factors. Pathol. Biol. 51:412–415.
Sayre, L. M., Smith, M. A., Perry, G. (2001). Chemistry and
biochemistry of oxidative stress in neurodegenerative dis-
ease. Curr. Med. Che. 8:721–738.
Scarfi, M. R., Fresegna, A. M., Villani, P., et al. (2006).
Exposure to radiofrequency radiation (900 MHz, GSM
signal) does not affect micronucleus frequency and cell
proliferation in human peripheral blood lymphocytes: an
interlaboratory study. Radiat. Res. 165:655–663.
Sohal, R. S., Mockett, R. J., Orr, W. C. (2002). Mechanisms of
aging: An appraisal of the oxidative stress hypothesis. Free.
Radic. Biol. Med. 33:575–586.
Sun, L. X., Yao, K., He, J. L., et al. (2006). DNA damage and
repair induced by acute exposure of microwave from
mobile phone on cultured human lens epithelial cells.
Zhonghua. Yan. Ke. Za. Zhi. 42:1084–1088.
Tice, R. R., Hook, G. G., Donner, M., et al. (2002).
Genotoxicity of radiofrequency signals. I. Investigation of
DNA damage and micronuclei induction in cultured
human blood cells. Bioelectromagnetics. 23:113–126.
Trosic, I., Busljeta, I., Kasuba, V., et al. (2002). Micronucleus
induction after whole-body microwave irradiation of rats.
Mutat. Res. 521:73–79.
Trosic, I., Busljeta, I., Modlic, B. (2004). Investigation of the
genotoxic effect of microwave irradiation in rat bone mar-
row cells: in vivo exposure. Mutagenesis. 19:361–364.
Vijayalaxmi Mohan, N., Meltz, M. L., et al. (1997).
Proliferation and cytogenetic studies in human blood lym-
phocytes exposed in vitro to 2450 MHz radiofrequency
radiation. Int. J. Radiat. Biol. 72:751–757.
Vijayalaxmi Seaman, R. L., Belt, M. L., et al. (1999).
Frequency of micronuclei in the blood and bone marrow
cells of mice exposed to ultra-wideband electromagnetic
radiation. Int. J. Radiat. Biol. 75(1):115–120.
V
ijayalaxmi,Pickard,W.F.,Bisht,K.S.,etal.(2001).
Cytogenetic studies in human blood lymphocyte exposed
invitrotoradiofrequencyradiationatacellulartele-
phone frequency (835.62 MHz, FDMA). Radat. Res.
155:113–121.
10 Z. SIAMA ET AL.
Downloaded by [Mizoram University] at 02:12 08 August 2017
Vijayalaxmi, Obe, G. (2004). Controversial cytogenetic obser-
vations in mammalian somatic cells exposed to radiofre-
quency radiation. Radiat. Res. 162:481–496.
Wolf, R., Wolf, D. (2004). Increased incidence of cancer near
a cellphone transmitter station. Int. J. Cancer. Prev. 1:1–19.
Yakymenko, I., Tsybulin, O., Sidorik, E., et al. (2015).
Oxidative mechanisms of biological activity of low-intensity
radiofrequency radiation. Electromagn. Biol. Med. 19:1–16.
Yildirim, M. S., Yildirim, A., Zamani, A. G., et al. (2010).
Effect of mobile phone station on micronucleus frequency
and chromosomal aberrations in human blood cells. Gen.
Couns. 21:243–251.
Zeni, O., Schiavoni, A., Sannino, A., et al. (2003). Lack of
genotoxic effects (micronucleus induction) in human lym-
phocytes exposed in vitro to 900 MHz electromagnetic
fields. Radiat. Res. 160:152–158.
Zeni, O., Schiavoni, A., Perrottam, A., et al. (2008).
Evaluation of genotoxic effects in human leukocytes after
in vitro exposure to 1950 MHz UMTS radiofrequency
field. Bioelectromagnetics. 29:177–184.
Zotti-Martelli, L., Peccatori, M., Scarpato, R., et al. (2000).
Induction of micronuclei in human lymphocytes
exposed in vitro to microwave radiation. Mutat. Res.
472:51–58.
ELECTROMAGNETIC BIOLOGY AND MEDICINE 11
Downloaded by [Mizoram University] at 02:12 08 August 2017
