Article

Toxicology and Industrial Health

1–8
The effect of noise and dust exposure © The Author(s) 2020
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on oxidative stress among livestock DOI: 10.1177/0748233720962253
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and poultry feed industry workers

Seyedtaghi Mirmohammadi1, Narges Khanjani2,

Fereshteh Nazarkhani1 , Saeid Abediankenari3,
Jamshid Yazdani4 and Ramazan Ali Dianati Tilaki5

Abstract
Introduction: Simultaneous exposure to noise and dust may have detrimental health effects. This study was
conducted to determine the effect of exposure to noise and dust on oxidative stress.
Methods: In this cross-sectional study, 82 employees of two livestock and poultry feed factories in Golestan
Province, Iran, were selected as the exposed group and 82 office workers were selected as the control group.
Occupational noise and dust exposure were measured using a dosimeter, sampling pump, and vinyl chloride
filter. Oxidative stress was determined by measuring the levels of malondialdehyde (MDA) and superoxide
dismutase (SOD) in blood samples. T-tests, one-way analysis of variance, and multivariate linear regression
were used to analyze the data.
Results: The levels of MDA and SOD in the exposed group were significantly higher and lower than the
control group (p < 0.001), respectively. The results showed the subgroup with both over the threshold dust
and noise exposure had the highest MDA levels. The SOD level among those exposed to noise more than the
recommended level, in the subgroup with more dust exposure, was significantly less than the subgroup with
low noise exposure (p ¼ 0.017).
Conclusion: Noise and dust exposure probably increase the level of oxidative stress by increasing the level of
lipid peroxidation (MDA) and reducing the level of antioxidant enzymes (SOD).

Keywords
Oxidative stress, malondialdehyde, dust, superoxide dismutase, noise, reactive oxygen species

Received 27 April 2020; Revised 25 August 2020; Accepted 4 September 2020

Introduction
Noise is considered as one of the most significant risk
factors affecting workers’ health, because many
workers in various industries face noise exposure
(Bagheri Hosseinabadi et al., 2019a). Excessive noise
exposure can have a devastating effect on the function
of various systems in the body, such as the auditory
system, and can lead to heart disease, high blood
pressure, anxiety, stress, and hormonal disorders
(Fouladi et al., 2012). Some researchers think that
noise is a preliminary physiological stressor (Prasher,
2009) and can stimulate the central nervous system
and affect emotions. It may also stimulate the immune
1
Department of Occupational Health, Faculty of Health,
Mazandaran University of Medical Sciences, Sari, Iran
2
Environmental Health Engineering Research Center, Kerman
University of Medical Sciences, Kerman, Iran
3
Immunogenetic Research Center, Mazandaran University of
Medical Sciences, Sari, Iran
4
Department of Biostatistics, Faculty of Health, Mazandaran
University of Medical Sciences, Sari, Iran
5
Department of Environmental Health, Faculty of Health,
Mazandaran University of Medical Sciences, Sari, Iran
Corresponding author:
Fereshteh Nazarkhani, Department of occupational health, faculty
of health, Mazandaran University of Medical Sciences, Sari, Iran.
Email: Nazarkhani_f71@yahoo.com
2 Toxicology and Industrial Health XX(X)

system and cause systematic inflammation and oxida- stress among workers, which can lead to respiratory
tive stress (Recio et al., 2016; Shukla et al., 2020). disorders such as asthma (Rémen et al., 2010). Usually
Researchers think oxidative stress plays an important occupational environments include many risk factors,
role in inducing noise-related health diseases (Bagheri and employees typically encounter several risk factors
and Rashedi, 2020; Thomas et al., 2016). Active oxy- simultaneously. However, most studies have evaluated
gen species, oxidative stress, and antioxidant protec- the effects of risk factors separately. There is a huge
tion mechanisms have recently been the focus of number of livestock and poultry feed factories in Iran
studies about the harmful effects of noise exposure which have employed a large number of workers.
(Henderson et al., 2006). Active species of oxygen These workers are exposed to both high noise and
are naturally produced in the physiological process organic dust, but there are not sufficient studies about
of aerobic living cells. In normal physiological con- the combined effects of noise and dust exposure and
ditions, there is always a balance in the body between their relation with oxidative stress. In this study, the
the various antioxidant mechanisms and internal oxi- combined effect of noise and dust exposure was
dants. Oxidative damage happens when an imbalance evaluated.
occurs (Nawaz and Hasnain, 2013). Excessive
increase in active oxygen species may cause oxidative Materials and methods
damage to proteins, lipid membranes, and DNA
This was a descriptive and analytical cross-sectional
(Valavanidis et al., 2009). The increased levels of
study. The study participants included all employees
oxidative stress is a possible mechanism for the non-
working in two factories that made livestock and poul-
auditory effects of noise exposure, such as cardiovas-
try feed in Golestan Province, Iran, and their workers
cular disorders, because even after short-term
were exposed to both noise and dust. The total number
exposure, endothelial dysfunction related to oxidative
of employees in the two factories was 164, of whom 82
stress has been observed (Schmidt et al., 2013). Baha-
employees were working in the production process, in
loo et al. (2020) showed that exposure to 100 dB for
two different working shifts and were selected as the
10 days and 1 h a day can cause oxidative stress,
exposed group. In addition, 82 office workers who had
increase malondialdehyde (MDA) levels, and
similar conditions, but were exposed to less than the
decrease SOD levels in rats. (Bahaloo et al.,
permissible WHO recommended noise level for office
2020).Workers at grain elevators and animal feed
environments (50–40 dB) and their dust exposure was
mills are exposed to grain dust containing a complex
insignificant, were chosen as the control group. The
mixture of organic and inorganic particles from
inclusion criteria were at least 2 years of work experi-
plants, soil, insects, and microorganisms. Organic
ence, 8 h of daily work, and no cardiovascular disease.
dust exposure increases the risk of occupational
Individuals with hearing loss and those who used drugs
respiratory diseases, including chronic obstructive
that stimulated or suppressed the antioxidant system
pulmonary disease, asthma, hypersensitivity pneumo-
were excluded from the study. All participants signed a
nitis, and organic dust toxic syndrome (Zamani et al.,
consent form. None of the workers in the exposed
2019). Recent studies have shown that Chronic
group received training about the use of personal pro-
Obstructive Pulmonary Disease is associated with sys-
tective equipment and none of them used personal pro-
temic inflammation including oxidative stress, activa-
tective equipment. The effect of each factor was
tion of circulatory inflammatory cells, and increased
determined separately and then together to achieve
circulating cytotoxins (Agusti et al., 2003) and the use
better results. Thus, there were three exposure groups,
of antioxidants such as vitamins C and E and avoiding
which included the high noise exposed group, the high
contact with oxidant compounds such as environmen-
dust exposed group, and the high combined exposure
tal contaminants and cigarettes can alleviate the dis-
group. All participants were asked to complete a ques-
ease (Pandey et al., in press; Ratna et al., 2020;
tionnaire including questions about age, marital status,
Rondanelli et al., 2020). Remen et al. (2010) examined
weight, height, work shift, work history, smoking, and
the initial prevalence of occupational asthma among
the use of personal protective equipment.
young bakers, confectioners, and hairdressers. They
measured markers of oxidative stress including ery-
throcyte SOD1, glutathione peroxidase, glutathione Noise dosimeter
reductase, 4-hydroxynonenal, and malondialdehyde The TES1350 device was used for dosimetry. The
and concluded that exposure to dust causes oxidative microphone of the device was installed at a distance
Mirmohammadi et al.
of 10 to 30 cm from the external ear canal of partici-
pants, on their collar, shoulder, or protective helmet
(Yildirim et al., 2007). The device was calibrated
using a Cirrus CR514 Calibrator (Cirrus Research plc,
United Kingdom) at a frequency of 1000 and the
sound pressure of 94 dB before and after each mea-
surement to ensure proper functioning of the dosi-
meter. All dosimeters remained at the acceptable
calibration level of + 0.3 dB. This device can mea-
sure sound (noise) at temperatures between 20 C
and þ50 C with an accuracy of + 0.5 dB. Dosimetry
was performed in a short period of time (15 min); and
the total exposure during the whole period was calcu-
lated using the following ratio:
T2 D2
¼ :
T1 D1
In this equation, T2 is the working time of the indi-
vidual, T1 represents the measurement time, D1 rep-
resents the measured dose, and D2 represents the
calculated dose for the entire work shift. Then, using
the following equation, the received sound pressure
level was calculated:
Xn ! the last night shift in that week. Blood samples were
SPLi 85
Dð%Þ ¼ 12:5  t  10ð 10 Þ :
i
i¼1
In this equation, SPL is the noise pressure level
encountered, D is the received dose of noise, t repre-
sents the duration of noise exposure, SPLstd is the
standard threshold of noise exposure, which based
on the occupational standards in Iran is 85 dB.
Respirable dust measurement
The NIOSH0600 method was used for measuring the
amount of individual exposure with respirable parti-
cles. The average cutting point of the particles col-
lected using this method is 4 mm. In this method,
nylon cyclone was used to sample air particles in the
workers respiratory zone, in the sampler equipped
with a polyvinyl chloride filter with a diameter of 2
mm and an AirChek 3000 pump, which sampled at a
flow rate of 1.7 l per minute. The sampling pump was
calibrated in the workplace using an SKC (US-UK)
Rotameter. Also, 10 filters were used as control sam-
ples. Ultimately, after sampling and weighing the
exposed and control filters with the Japanese A&D
digital scale, which had an accuracy of 0.01 mg, and
placing it in the desiccator for 24 h to remove
3
moisture, the individual exposure in milligrams per
cubic meter was calculated using the following
formula:
ðW2  W1 Þ  ðB2  B1 Þ
C¼  10;
V
where W1 is the net filter weight before sampling
(mg), W 2 is the net filter weight after sampling
(mg), B1 is the average net weight of control filters
(mg), B2 is the average weight of control filters after
sampling (mg), and V is sampled air volume (m3).
Oxidative stress indicators measurements
In this study, MDA was measured as a lipid peroxida-
tion index and the main biomarker of oxidative stress
(Abdel-Salam et al., 2011); and antioxidant enzyme
activity was measured by SOD. Superoxide dismutase
and catalase play a critical role in the first line of anti-
oxidant defense which prevents the cellular and tissue
damage caused by reactive oxygen species (ROS)
(Fattman et al., 2003). 5cc blood was taken by a trained
laboratory assistant from all participants between 7 am
and 11 am and in the afternoon before the beginning of
collected in sterile laboratory tubes. Then, they were
centrifuged at 5000 r min1 for 10 min and the serum
was separated and stored in a freezer at 80 C, until
the laboratory experiments were performed. Oxidative
stress measurements were performed using the Teb
Pazhoohan Razi Company kits, by ELISA (DAS)
double-antibody sandwich method.
Statistical analysis
Data were statistically analyzed using SPSS v.24.0 soft-
ware. Descriptive statistics including mean (standard
deviation) and frequency (percentage) were used to
summarize demographic variables, noise exposure,
dust, lipid peroxidation, and antioxidant enzyme activ-
ity. The K-S and Levene’s tests were used to check the
normality and equality of variances. To compare the
demographic variables between the case and control
groups, 2, independent t-test, and one-way analysis
of variance were used. Comparisons between dust expo-
sure, noise, lipid peroxidation levels, and antioxidant
enzyme activity between the case and control groups
were made with independent t-tests. Multivariate linear
regression was used to estimate the effect of predictor
variables, adjusted for other variables. Abnormal data
were normalized before entering the model using the
method proposed by Templeton (2011).
4 Toxicology and Industrial Health XX(X)

Table 1. The demographic characteristics and oxidative stress indices in the exposed (n ¼ 82) and unexposed groups (n
¼ 82).a
Variable Category Frequency (%) Exposed (n ¼ 82) Unexposed (n ¼ 82) p-Value
Age (years) >30 55 (33.6) 31 (37.8) 24 (29.3) 0.447b
30–40 85 (51.8) 40 (48.8) 45 (54.9)
<40 24 (14.6) 11 (13.4) 13 (15.8)
BMI Underweight 5 (3.1) 2 (2.4) 3 (3.6) 0.701b
Normal 93 (56.7) 49 (59.8) 44 (53.7)
Obese 66 (40.2) 31 (37.8) 35 (42.7)
Work experience 5 110 (67.1) 59 (71.9) 51 (62.2) 0.184b
<5 54 (32.9) 23 (28.1) 31 (37.8)
Work shift Fixed 95 (57.9) 51 (62.2) 44 (53.7) 0.268b
Rotating 69 (42.1) 31 (37.8) 38 (46.3)
Marital status Single 27 (16.5) 16 (19.5) 11 (13.4) 0.292b
Married 137 (83.5) 66 (80.5) 71 (86.6)
Smoking Yes 21 (12.8) 14 (17.1) 7 (8.5) 0.254b
No 136 (82.9) 65 (79.3) 71 (86.6)
Former 7 (4.3) 3 (3.6) 4 (4.9)
Mean + SD Exposed Unexposed p-value

MDA 27.37 + 14.26 29.81 + 9.58 24.91 + 17.51 <0.001c

SOD 3.35 + 2.08 3.02 + 2.53 3.68 + 1.45 <0.001c
BMI: body mass index; SD: standard deviation; MDA: malondialdehyde; SOD: superoxide dismutase.
a
Normal: 18.5–24.9; abnormal: <18.5 and 25. There were only two people in the <18.5 group.
b 2
 test.
c
Mann–Whitney U test.

Table 2. The predictors of oxidative stress indices (MDA and SOD levels) according to backward multiple linear
regression.a
Confidence interval
Variable Category  t Upper Lower p-value
MDA level
Work Experience 5 to<5 3.99 1.84 8.31 0.31 0.069
Work shift Rotating vs fixed 3.62 1.83 7.56 0.31 0.07
Respirable dust 1.76 2.16 3.39 0.14 0.034
Noise 0.56 3.44 0.88 0.23 0.001
SOD level
BMI Underweight vs normal 3.45 2.25 0.39 6.51 0.027
Work shift Rotating vs fixed 1.92 3.9 2.89 0.94 <0.001
Respirable dust 0.44 2.19 0.84 0.04 0.031
MDA: malondialdehyde; SOD: superoxide dismutase; BMI: body mass index.
a
Normal: 18.5–24.9; abnormal: <18.5 and 25. There were only two people in the <18.5 group.

found between the demographic variables of the case

Results
The demographic information of the study partici-
pants is shown in Table 1. Most individuals were in
the 30–40 age group and their body mass index was in
the normal range. Only 16.5% of them smoked and
12.8% were single. No significant difference was
and control groups. In addition, the levels of MDA
and SOD in the control group were, respectively, sig-
nificantly higher and lower than the control group.
The results of backward linear regression are shown
in Table 2. Among the demographic variables, only
working shift and body mass index remained in the
Mirmohammadi et al. 5

Table 3. The mean MDA level in the noise and dust exposure subgroups.
Variable Dust exposure
Less or equal the threshold Over the threshold
Noise exposure 4 mg m3 (n ¼ 47) >4 mg m3 (n ¼ 35) p-Valuea
Less the threshold 85 dB (n ¼ 28) 23.72 + 8.85 27.53 + 6.03 0.275
Over the threshold >85 dB (n ¼ 54) 27.93 + 8.56 36.87 + 7.78 <0.001
p-Valuea 0.107 0.004 —
MDA: malondialdehyde.
a
Independent T-test.

Table 4. The mean SOD level in the noise and dust exposure subgroups.
Variable Dust exposure
Less or equal the threshold Over the threshold
Noise exposure 4mg m3 (n ¼ 47) >4 mg m3 (n ¼ 35) p-Value
Less the threshold 85 dB (n ¼ 28) 3.61 + 4.88 2.81+0.71 0.94a
Over the threshold >85 dB (n ¼ 54) 3.17 + 1.03 2.51+0.91 0.017b
p-Value 0.59a 0.356b —
SOD: superoxide dismutase.
a
Mann–Whitney test.
b
Independent T-test.

model. In addition, only dust exposure was signifi-
cantly related to the increased levels of both biomar-
kers. The mean MDA level in the noise and dust
exposure subgroups is shown in Table 3. In the group
exposed to over the threshold dust levels, MDA levels
were significantly lower in the subgroup with less
noise exposure than the subgroup with high noise
exposure. In addition, in the group exposed to high
noise levels, MDA levels were significantly higher in
individuals exposed to over the threshold levels of
dust. The subgroup with the highest noise and dust
exposure had the highest MDA levels. These results
may show the synergistic effect of noise and dust
exposure on MDA levels. The mean SOD among
groups with different dust and noise exposure is
shown in Table 4. In the group that was exposed to
noise higher than the threshold, SOD levels were sig-
nificantly lower in the subgroup with over permissible
levels dust exposure.
Discussion
This study revealed a possible synergistic effect of
noise and dust exposure in increasing MDA and
decreasing SOD levels. Yildirim et al. (2007) showed
that noise exposure among textile workers increased
the level of MDA and decreased the level of catalase,
while there was no significant difference in the activity
of SOD between the case and control groups. The rea-
son might be that in Yildirim’s study, the control group
was chosen from hospital staff with an average noise
exposure of 68.5 dB, while in the present study, the
control group was chosen from office staff, and their
average noise exposure level was 40 to 50 dB (Yildirim
et al., 2007). In line with our results, a similar study by
Pinar et al. (2011) on 127 workers working in noisy
environments as the exposed group and 117 workers
working in quiet environments as the control group
showed that people who worked in high-noise envir-
onments, had lower levels of catalase and nitric oxide
and higher levels of MDA compared to those working
in less noisy environments. These authors also con-
cluded that oxidative stress, which results from high
noise exposure, may be a significant pathophysiologi-
cal pathway for hearing loss (Pinar et al., 2011).
Animal studies have also reported changes in the
levels of antioxidant enzymes and lipid peroxidation
due to noise exposure. A study conducted by Deh-
ghani et al. (2013) studied the effect of noise on oxi-
dative and antioxidant parameters in the blood and
liver tissue of mice. They showed that in mice
exposed to 100 dBs of noise for 8 h a day during
6 Toxicology and Industrial Health XX(X)
8 days, and mice exposed to the same noise level for 8
h a day during 14 days, MDA increased significantly
in the blood and liver, and glutathione increased sig-
nificantly in the serum (Dehghani et al., 2013). These
results are consistent with the results of the present
study that showed increase in serum levels of MDA
due to noise exposure. Bagheri Hosseinabadi et al.
studied the effect of chronic noise exposure on oxida-
tive stress indices, DNA damage, blood pressure, and
blood biochemistry. The exposed group included 109
individuals in three sections of a food factory, and the
control group was chosen from administrative staff
who were exposed to a 50 to 40 dB noise levels. They
reported that the mean of MDA, catalase, and total
antioxidant capacity was higher in the case group, but
SOD was not significantly different (Bagheri Hossei-
nabadi et al., 2019a). Furthermore, they found that
noise exposure may induce DNA damage in periph-
eral mononuclear lymphocytes (Bagheri Hosseina-
badi et al., 2019b). Amer et al. (2020) studied the
effect of noise exposure on a group of men working
in the textile industry and showed that malondialde-
hyde levels increased and total antioxidant capacity
levels decreased among these workers (Amer et al.,
2020). It is already known that dust exposure
increases the risk of respiratory diseases and exposure
to dust may increase the production of ROS. How-
ever, fewer studies have been done on the effect of
organic dust exposure in oxidative stress; further-
more, most studies are about other types of dust such
as silica, coal, and benzene. A study done by Saad-
Hussein et al. (2014) showed that the levels of MDA
and SOD in wheat mill workers were both signifi-
cantly greater than the control group. These authors
concluded that the oxidative stress of AFB1 increased
MDA and the liver enzymes and led to increased SOD
as an antioxidant to hinder the toxic oxidative effects
of AFB1 on the liver of the workers (Saad-Hussein
et al., 2014). A study by Yilmaz et al. (2020) showed
that MDA and glutathione-S-transferase and TP53
gene expressions were increased by exposure to afla-
toxins in rats. They stated that exposure to aflatoxins
can upset the balance of the antioxidant system and
cause liver damage (Yilmaz et al., 2020). Another
similar study was conducted by DA (2012) on oxida-
tive stress levels and immunoglobulins in workers of a
flax industry. In this study, the levels of oxidant bio-
markers (MDA, nitric oxide) and antioxidants (glu-
tathione peroxidase, catalase, SOD, and total
antioxidant) were, respectively, higher and lower
among the flax factory workers. In addition, they
found that total antioxidant levels significantly
decreased and oxidative biomarkers increased result-
ing from cotton dust exposure (DA, 2012). But, Man-
awil et al. (2013) measured MDA and SOD levels
among 52 bakery workers and did not find a signifi-
cant difference between MDA and SOD levels in the
exposure and control groups. The reason for not find-
ing a significant difference in this study may be their
small sample size and younger population compared
to our study (Manawil et al., 2013). Another study by
Suryakar et al. (2010), conducted among flax industry
workers with different working histories, showed that
the serum levels of MDA and nitric oxide were higher
in all flax industry employees compared to the control
group. These results confirm that dust can increase the
level of oxidative stress, and this may be the mechan-
ism of various diseases, such as lung diseases (Surya-
kar et al., 2010). Mordukhovich et al. (2015)
investigated oxidative stress and its relation with
long-term exposure to carbon black dust and changes
in pulmonary parameters and found that there was a
strong relation between long-term exposure to car-
bon black and decrease in pulmonary parameters.
They concluded that carbon black may cause its det-
rimental effects on pulmonary function by inducing
high levels of oxidative stress (Mordukhovich et al.,
2015). Exposure to high levels of noise and dust can
also stimulate the generation of free radicals through
processes such as energy catastrophy, mitochondrio-
pathy, Ca2þ dyshomeostasis, and anoxia/ischemia,
which may lead to cell damage, especially through
the lipid peroxidation pathway (Bagheri Hosseina-
badi et al., 2019a; Le Prell et al., 2007). However,
diet can influence oxidative stress, and a healthy diet
with high antioxidant capacity can improve oxidant
status. Epidemiological studies suggest that oxida-
tive stress increases as age and body mass index
increase (Wonisch et al., 2012).
Limitations
A limitation of this cross-sectional study is that it
cannot demonstrate a causal relation. Also, the results
might not be generalizable to other industries. In addi-
tion, the entire population was male, except for one
female; and we were not able to study gender differ-
ences. Ultimately, oxidative stress is a multifaceted
issue that in addition to noise and dust may be
affected by various factors. As another limitation, in
this study, workers’ diets were not evaluated.
Mirmohammadi et al.
Conclusion
The results of this study indicate that workers working
in the livestock and poultry feed factories are at risk of
the harmful effects of noise and dust through
increased oxidative stress.
Acknowledgements
All authors would like to thank all of the workers who
participated in this study.
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest
with respect to the research, authorship, and/or publication
of this article.
Ethical considerations
This study was approved by the Ethics Committee of
Mazandaran University of Medical Sciences
(IR.MAZUMS.REC.1398.5335).
Funding
The author(s) disclosed receipt of the following financial
support for the research, authorship, and/or publication of
this article: The study was financially supported by Mazan-
daran University of Medical Sciences (Grant No 5335).
ORCID iD
Fereshteh Nazarkhani https://orcid.org/0000-0002-
6828-3241
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