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The Effect of Aerobic Exercise in Ambient Particulate Matter on Lung Tissue Inflammation and Lung Cancer


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Background: Exposure to Air pollution PM10 results in lung inflammation increased risk of lung cancer. Regular aerobic exercise improves the inflammatory status in different lung diseases. However, the effects of long-term aerobic exercise on the pulmonary response to PM10 have not been investigated. Objectives: The present study evaluated the effect of aerobic exercise on the lung inflammatory and risk of lung cancer of rat exposed to PM10 carbon black. Materials and methods: Twenty four adult male Wistar rats were divided into 4 groups: A: control (without exposure PM10 and aerobic exercise; n = 6), B: aerobic exercise (five times per week for 4 weeks; n = 6), C: exposure to PM10 carbon black (5 mg/m(3); per rat; n = 6), D: and aerobic exercise concomitantly with exposure to PM10 carbon black (n = 6). The gene expression of TLR4, NF-κB and TNF-α were analyzed in lung tissue by Real time-PCR. In order to determine the significant differences between groups, one way ANOVA and LSD post hoc and Kruskal-Vallis test were used. Results: Aerobic exercise inhibited the PM10 -induced increase in the gene expression of TLR4, NF-κB and TNF-α. But there was significant different only between B and C groups for TNF-α and NF-κB (P = 0.047, 0.014, respectively). Conclusions: We conclude that four week aerobic exercise presents protective effects in a rat model of PM10 carbon black-induced lung inflammation and risk of lung cancer. Our results indicate a need for human studies that evaluate the lung Responses to aerobic exercise chronically performed in polluted areas.
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Iran J Cancer Preven. 2015 June; 8(3):e2333.
Published online 2015 June 22. Research Article
The Effect of Aerobic Exercise in Ambient Particulate Matter on Lung Tissue
Inflammation and Lung Cancer
Mohamad Fashi
; Hamid Agha Alinejad
; Hasan Asilian Mahabadi
Department of Physical Education and Sports Sciences, Tarbiat Modares University, Tehran, IR Iran
Deptartment of Occupational Health Engineering, Tarbiat Modares University, Tehran, IR Iran
*Corresponding author: Hamid Agha Alinejad, Department of Physical Education and Sports Sciences, Tarbiat Modares University, Tehran, IR Iran. Tel: +98-9124946181,
Received: January 14, 2015; Revised: January 20, 2015; Accepted: January 28, 2015
Background: Exposure to Air pollution PM10 results in lung inflammation increased risk of lung cancer. Regular aerobic exercise improves
the inflammatory status in different lung diseases. However, the effects of long-term aerobic exercise on the pulmonary response to PM10
have not been investigated.
Objectives: The present study evaluated the effect of aerobic exercise on the lung inflammatory and risk of lung cancer of rat exposed to
PM10 carbon black.
Materials and Methods: Twenty four adult male Wistar rats were divided into 4 groups: A: control (without exposure PM10 and aerobic
exercise; n = 6), B: aerobic exercise (five times per week for 4 weeks; n = 6), C: exposure to PM10 carbon black (5 mg/m
; per rat; n = 6), D: and
aerobic exercise concomitantly with exposure to PM10 carbon black (n = 6). The gene expression of TLR4, NF-κB and TNF-α were analyzed
in lung tissue by Real time-PCR. In order to determine the significant differences between groups, one way ANOVA and LSD post hoc and
Kruskal-Vallis test were used.
Results: Aerobic exercise inhibited the PM10 -induced increase in the gene expression of TLR4, NF-κB and TNF-α. But there was significant
different only between B and C groups for TNF-α and NF-κB (P = 0.047, 0.014 respectively).
Conclusions: We conclude that four week aerobic exercise presents protective effects in a rat model of PM10 carbon black-induced lung
inflammation and risk of lung cancer. Our results indicate a need for human studies that evaluate the lung Responses to aerobic exercise
chronically performed in polluted areas.
Keywords: Lung Neoplasms; Inflammation; Aerobic Exercise; PM10
Copyright © 2015, Iranian Journal of Cancer Prevention. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCom-
mercial 4.0 International License ( which permits copy and redistribute the material just in noncommercial us-
ages, provided the original work is properly cited.
1. Background
Inhalation of particulate matter (PM) from fossil fuel
combustion is associated with adverse health effects, in-
cluding reduced lung function (1) and increased mortal-
ity (2). Although the mechanism for PM-induced health
effects is not fully defined, animal models and in vitro
studies suggest that pro-inflammatory cytokine release
from airway cells is an important factor (3). Inflamma-
tion may play a role in the etiology of lung cancer. Envi-
ronmental agents associated with elevated lung cancer
risk, such as ambient particulate matter, may damage
the lung by inducing chronic inflammation. Lung can-
cer risk is elevated in individuals with emphysema (4, 5),
interstitial lung disease (6), and asthma (7), which could
similarly reflect effects of the underlying inflammatory
Induction of pro-inflammatory mediators by alveolar
macrophages exposed to ambient air particulate matter
has been suggested to be a key factor in the pathogene-
sis of inflammatory and diseases in the lungs. However,
receptors and mechanisms underlying these responses
have not been fully elucidated. Different contributing
physiological and psychosocial factors have been pro-
posed (8). A few prior studies have examined lung cancer
risk in relation to polymorphisms in the genes coding for
inflammation pathway signaling molecules, such as In-
terleukin 1β (IL1β) (9-11), IL1 receptor antagonist (IL1RN) (12,
13), IL6 (10, 14), IL10 (15), cyclooxygenase 2 (14), and tumor
necrosis factor α (16). These inflammatory cytokines are
regulated by the pro-inflammatory transcription factor,
nuclear factor NF-κB (8).
Given the close interaction between the external en-
vironment and the lung, TLRs have been implicated in
lung-associated immune responses, including airway
hyper responsiveness (AHR) and allergic asthma (17). Dys-
function and unregulated activation of the TLR pathway
can contribute to decreased lung function and the patho-
genesis of acute and chronic lung inflammatory diseases
(18). TLR activation, can occur via two pathways: 1- the
Myeloid Differentiation primary-response protein 88
(MyD88)-dependent pathway, and 2- the MyD88-indepen-
dent pathway. These two pathways correspond to early
and late-phase NF-κB signaling and pathway-specific in-
Fashi M et al.
Iran J Cancer Preven. 2015;8(3):e23332
duction of pro-inflammatory cytokines and chemokines
(19, 20). Inflammation play an important role in the etiol-
ogy of lung cancer.
Regular aerobic exercise results in multiple health ben-
efits, including improvement of cardiorespiratory fitness
and quality of life, reduction of obesity and blood pres-
sure, and increased longevity (21, 22). When performed
chronically on a regular basis, aerobic exercise also re-
duces oxidative stress systemically (23) in different dis-
eases, such as heart diseases, type 2 diabetes, rheumatic
arthritis, and alzheimer and parkinson diseases (23) , as
well as in the airway epithelial cells of animals with long-
term allergic lung inflammation (24). Chronic practice
of regular exercise exerts a marked anti-inflammatory
effect in different models of pulmonary diseases, such
as in asthma models (25-28), acute respiratory distress
syndrome (29, 30), and chronic obstructive pulmonary
disease (31).
Studies that have investigated the effects of exposure to
air pollutants during exercise have suggested that peo-
ple exercising in polluted environments are at increased
risk of respiratory and cardiovascular morbidity related
to air pollution owing to an exercise-induced amplifica-
tion in respiratory uptake, lung deposition, and toxicity
of inhaled pollutants (32-35). Exercise may increase the
likelihood of an adverse effect by increasing the dose of
pollutants delivered to target sites in the lungs as venti-
lation increases to meet metabolic demands (36). How-
ever, these studies do not take into account the potential
anti-inflammatory and health effects of exercising in air
pollution (37), which could inhibit the pro-inflammatory
events induced by air pollution.
2. Objectives
Therefore, the aim of this study was to investigate the
effects of 4 weeks of aerobic exercise performed in asso-
ciation with carbon black PM10 exposure on lung tissue
inflammation and lung cancer.
3. Materials and Methods
In all experiments, the Tarbiat Modares university
guidelines for animal care was followed. This study was
approved by the Tarbiat Modares University of Tehran
(code number: 62.2987).
3.1. Animals
Twenty four adult male Wistar rats aged 8 weeks were
obtained from Pasteur Institute of Iran and randomly di-
vided into the 4 groups: A; control (without exposure car-
bon black PM10 and aerobic exercise; n = 6), B; aerobic ex-
ercise (five times per week for 4 weeks; n = 6), C; exposure
to carbon black PM10 (5 mg/m
; per rat; n = 6), D; aerobic
exercise concomitantly with exposure to carbon black
PM10 (n = 6). Rats were housed in cages under controlled
environment (23°C and 12 hour light-dark cycle) with free
access to normal chow and tap water.
3.2. Exposure to Carbon Black PM10
Figure 1 shows the inhalation chamber at the labora-
tory of Tarbiat Modares university (Falonak) where inha-
lation exposure was carried out. Carbon black dust (38)
obtained from Iran-carbon factory. Rats in groups of C
and D were exposed to carbon black in the inhalation
chamber at nominal concentrations of 5 mg/m
for 2 h/
day, 5 days per week for a total of 4 weeks. The control rats
were exposed to clean, filtered air containing no carbon
black for the same period. The concentrations, size and
shape of CB particle were monitored once time weekly by
Grimm Aerosol Technique (GmbH and Co. KG. Dorfstraße
9 - 83404 Ainring-Germany (and light microscope (Acc.V-
Spot magn. 25.0 KV 3.4. 5000 x) respectively.
3.3. Exercise Treadmill Test and Training
Animals in B and D groups were adapted to the tread-
mill for rat (will running treadmill, Lafayette American)
training for 3 days (15 minutes, 20 m/min). On the fourth
day, the individual maximal exercise capacity test was
performed with a 5-minute warm-up (6 m/min) and fol-
lowed by an increase in treadmill speed (3 m/min every
3 minutes) until animal exhaustion (i.e., when they were
not able to run voluntarily after 3 mechanical stimuli)
(24, 27, 28). The maximal exercise capacity (100%) was
defined as the maximum speed reached by each animal.
The physical test was performed for each rat individually.
The speed average of each group was calculated, and then
the rats were submitted to treadmill training as a mean
speed of the group workload. rats were trained at low
intensity, corresponding to 50% of the initial maximal
speed obtained in the exercise test, for 60 minutes, five
times per week, as previously described (24, 27, 28).
3.4. Analysis of mRNA Expression TLR4, NF-κB and
After sacrificed rat and total lung tissue, RNA was isolat-
ed using Trizolereagent (Qiagen, Germany), according to
Figure 1. Inhalation Chamber Used for Whole-Body Inhalation Exposure
to Carbon Black PM10
Fashi M et al.
Iran J Cancer Preven. 2015;8(3):e2333
the manufacturer’s instructions. The RNA samples were-
subjected to reverse transcription using thermo scien-
tific revert aid first strand cDNA synthesis kit (Feremen-
tase). In the subsequent step, the cDNAs were used as
templates to perform real-time PCR using SYBR green PCR
master mix (SYBR green I,) by step one ABI system (Ap-
plied Biosystem).The crossing threshold values assessed
by the real-time PCR were evaluated for the transcripts
and normalized to the results for GAPDH mRNA. The cor-
responding primer pairs for TLR4, NF-κB, and TNF-α and
GAPDH (housekeeping gene) were listed in Table 1.
3.5. Real-Time PCR
All of the tests were repeated two times in each group.
The threshold cycle (Ct) for each specific gene, corre-
sponding housekeeping gene (GAPDH) and their differ-
ences (ΔCt) were determined and then evaluated gene
expression changes using ∆∆CT formula.
3.6. Statistical Analysis
Results are expressed as Mean ± SD. Differences in body
weight between pre and post interventions were exam-
ined by 2-tailed t-test. In order to determine the significant
differences between groups one way ANOVA and LSD post
hoc test and Kruskal-Vallis test after examined normal dis-
tribution of data by Kolmogorov-Smirnov test were used. P
< 0.05 were considered statistically significant.
4. Results
Body weight: There were significant differences among
the A (control) and C (PM10 exposure only) groups in
body weight pre and post interventions. The mean of in-
crease in body weight in C group was higher than A, B and
D groups (Table 2).
4.1. Effects of Aerobic Exercise and Carbon Black
PM10 Exposure on Gene Expression TLR4. NF-κB
and TNF-α
Presented data in Figure 2 demonstrate that PM10 car-
bon black exposure increased the gene expression TLR4,
NF-κB and TNF-α in lung tissue compared with all of the
other groups (P ≤ 0.05) and that aerobic exercise in
carbon black PM10 exposure decreased the expression
of these cytokine compared with the carbon black PM10
exposure group (P ≤ 0.05). 0ne way ANOVA also dem-
onstrated that carbon black PM10 exposure presented a
significant effect on the TNF-α (P = 0.047) and NF-κB (P =
0.014). No significant effect was observed on the gene ex-
pression TLR4 by Kruskal-Vallis test (P = 0.325).
Table 1. Primer Sequences Used in Real-Time PCR
Gene Primer Sequence
Table 2. Body Weight of Animal’s Pre and Post Intervention
Groups Initial Test Final Test Final-Initial Test P Value
A, Control 285.83 ± 25.55 324.33 ± 27.12 38.50 ± 1.57 0.045
B, Exercise 279.17 ± 32.55 304.33 ± 43.31 25.16 ± 10.76 0.090
C, PM10 270.50 ± 27.12 311.17 ± 36.66 40.67 ± 9.54 0.023
D, exe+PM10 281.67 ± 22.73 315.67 ± 33.23 34.00 ± 10.50 0.101
Data are presented as mean ± SD.
Significantly Different at P ≤ 0.05.
Figure 2. Effects of Aerobic Exercise and Carbon Black PM10 Exposure on Gene Expression TLR4, NF- κB and TNF-α
Asterisk Indicates Treatments That are Significantly Different at P ≤ 0.05 Compared With all of the Groups.
Fashi M et al.
Iran J Cancer Preven. 2015;8(3):e23334
5. Discussion
In the present study, we demonstrated that aerobic ex-
ercise inhibits lung inflammation and pro-inflammatory
cytokine release in lung tissue in an experimental model
of PM10 carbon black-induced lung inflammation.
Considerable epidemiological and toxicological stud-
ies have established a clear link between exposure to air
pollution particles and adverse pulmonary health effects.
Several experimental and human studies have demon-
strated that increased levels of air pollution associated
with pulmonary inflammation (37, 38). The association
between ambient air pollution particles exposure and
lung cancer risk has been investigated in prospective
studies and the results are generally consistent, indicat-
ing that long-term exposure to air pollution may cause
lung cancer.
Gene expression analysis identified the association
with the effect of PM10 carbon black on the innate im-
mune response. PM10 carbon black exposure increased
the gene expression TLR4, NF-κB and TNF-α in lung tissue.
TLR4 activation is corresponded to NF-κB signaling and
pathway-specific induction of pro-inflammatory cyto-
kines and chemokines or interferon signaling (39).
An extensive research in recent years has been indicated
that chronic inflammation leads to various chronic dis-
orders associated with cancer (40-42). A central role in
the induction of chronic inflammation is played by a set
of genes encoding pro-inflammatory cytokines such as
IL-1, IL-2, IL-6, and TNF-α and monocyte chemotactic Pro-
tein 1 that are regulated by the transcription factor (NF-
κB) (43-45).
Particulate matter exposure could effect on Obesity
(46). These conditions are associated with derangements
in the interplay between metabolic and immune process-
es and inflammation (47). The authors observed signifi-
cant increase in body weight with PM10 carbon black ex-
posure which could explain the increased inflammation
can be caused by PM10 exposure.
Studies have suggested that potential anti-inflamma-
tory effects of aerobic exercise could inhibit the pro-
inflammatory events induced by air pollution. The anti-
inflammatory effects of exercise (48-50) have focused on
three possible mechanisms: the reduction in visceral fat
mass; increased production and release of anti-inflam-
matory cytokines from contracting skeletal muscle (such
molecules are termed myokines (48-51); and reduced ex-
pression of Toll-like receptors (TLRs) on monocytes and
macrophages (52). In the present study, aerobic exercise
in PM10 carbon black exposure decreased the gene ex-
pression TLR4, NF-κB and TNF-α in lung tissue and also
body weight of animals. Although this change in gene ex-
pression was slight, however this result can be clinically
We conclude that low-intensity aerobic exercise pres-
ents protective effects from PM10 carbon black-induced
lung inflammation. Future studies should therefore
be directed towards better defining the mechanism in-
volved in the induction of symptoms by inflammatory
molecules and risk of cancer in exposure to air pollution
We would like to thank the members of this research for
their assistance in conducting this study. Special thanks
to Amir Abbas Mofidi for assistance in construct chamber
and PM10 simulator system.
Authors’ Contributions
Mohamad Fashi designed and wrote this article and col-
lected and analyzed the data, with Dr. Hamid Agha Aline-
jad and Dr. Hasan Asilian Mahabadi. All authors read and
approved the final manuscript.
Financial Disclosure
The authors have no conflict of interest in this study.
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... One week before each handling, rats belonging to the groups Grp_Non Exposed_Trained; Grp_Exposed_Trained were subjected to a 5-day treadmill habituation protocol. For aerobic training, we therefore used and adapted the protocol of another [27]. Rats in these different groups were accustomed to running on a treadmill for 15 minutes per day at a speed of 20 meters per minute (20 m/min) over three days. ...
... To answer this question, data from the literature provide information on the effects of aerobic training in polluted environments. Indeed, the work of Fashi et al. [27] has shown that aerobic training five times a week for four weeks in an environment rich in particulate matter (PM10) has protective effects on rats following PM10-induced inflammation. Aerobic exercise, therefore, inhibits PM10-induced increases in NF-KB and TNF-α gene expression. ...
... But a significant decrease in the concentration of TNF-α was observed at D14. These results seem logical given that aerobic training in a less polluted environment reduces the levels of oxidative stress and inflammation on one hand, and on the other hand, aerobic training in a polluted environment inhibits the increase in stress-related gene expression and inflammation [27,51]. It is, therefore evident that aerobic training in less polluted environments inhibits the exacerbation of deleterious effects induced by exposure to CO and NO2. ...
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The objective of this study is to determine the effects of isolated exercise and those of repeated exercise on oxidative stress and the inflammatory process following exposure to carbon monoxide (CO) and nitrogen dioxide (NO2). Material and Method: 15 male Wistar rats, all eight weeks old, were randomly assigned to three groups. CO and NO2 were produced by the combustion of diesel fuel using a device contained in a sealed metal box and supplied with ambient air by a pump. The ranges of CO and NO2 concentrations to which the rats were exposed ranged from 35 to 45 ppm and 0.2 to 0.3 ppm, respectively. The aerobic workouts were performed on a rat treadmill. Blood samples were taken 24 hours after completion of handling at D4, D9 and D14. Variables studied were Malondialdehyde (MDA) and Tumor Necrosis Factor-alpha (TNF-α). Results: Aerobic endurance training after repeated exposure to CO and NO2 induces at the end of the first training block (D4) a significant increase (p ˂ 0.01) in MDA and TNF-α. On the other hand, the second block (D9) and the third training block (D14) induced a significant decrease (p ˂ 0.01) in these same parameters. Conclusion: Aerobic exercise practiced in isolation exacerbates the oxidative stress and inflammation induced by exposure to CO and NO2. On the other hand, regular aerobic exercise in a less polluted environment, following five days of recovery, significantly reduces the high levels of oxidative stress and inflammation caused by repeated exposure to automobile pollutants.
... Penelitian yang dilakukan Devlin et al., (1999) juga mengamati peningkatan yang signifikan dalam inflamasi IL-6 dan TNF-α setelah 4 jam terpapar nitrogen dioksida diikuti latihan treadmill dengan intensitas sedang. Selain itu, paparan Particulate Matter 10 dan black carbon terbukti mampu meningkatkan TNF-alpha dan Nuclear Factor-Kb pada tikus setelah melakukan latihan intensitas ringan selama 60 menit (Fashi et al., 2015). ...
... Hasil peneltian lain juga menunjukkan bahwa tidak terjadi peningkatan TNF-alpha pada sampel yang melakukan olahraga tanpa terpapar PM10 dan black carbon dibandingkan sampel yang melakukan olahraga dengan paparan PM10 dan black carbon (Fashi et al., 2015). Penelitian yang dilakukan De Paula juga menunjukkan bahwa penanda inflamasi IL-6 dan TNF-alpha terlihat lebih tinggi pada sampel yang melakukan olahraga daya tahan dengan paparan partikel knalpot diesel dibandingkan sampel yang melakukan olahraga tanpa paparan partikel knalpot diesel. ...
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Tujuan penelitian ini adalah untuk menganalisis pengaruh olahraga di ruang terbuka dengan paparan polusi dan olahraga di ruang terbuka hijau terhadap inflamasi paru. Metode true eksperiment dan desain The Randomized Posttest-Only Control Group Design digunakan dalam penelitian ini. 24 ekor tikus putih galur wistar jantan dewasa dengan berat 200-250 gram berusia 8-9 minggu dibagi secara acak menjadi empat kelompok, NE (Non Exercise) sebagai kontrol, NE+Pol (Non Exercise + polusi Particulate Matter 2.5 >75 ppm dan Carbon Monoxide Meter <100 ppm), Ex (Exercise 5 kali/minggu selama 4 minggu), Ex+Pol (Exercise + polusi). Penanda inflamasi Tumor Necrosis Factor-αlpha (TNF-α) dianalisis menggunakan Western Blotting. Untuk mengetahui perbedaan yang signifikan antar kelompok, analisis ANOVA satu jalur dan uji Post Hoc digunakan. Hasil penelitian menunjukkan bahwa kelompok eksperimen olahraga dengan paparan polusi memiliki kadar TNF-α yang signifikan lebih tinggi dibandingkan kelompok kontrol (Ex+Pol: 1,63 AU; NE: 0,54 AU; p=0,000). Tidak ada perbedaan yang signifikan antara kelompok eksperimen olahraga di ruang terbuka hijau dengan kelompok kontrol (Ex: 0,80 AU; NE: 0,54 AU; p=0,357). Dapat disimpulkan bahwa terdapat pengaruh olahraga di ruang terbuka dengan paparan polusi terhadap inflamasi paru. Dan hasil lain menunjukkan bahwa tidak terdapat pengaruh olahraga di ruang terbuka hijau terhadap inflamasi paru.The effect of exercise in open spaces and green open spaces on lung inflammationAbstractThe purpose of this study was to analyze the effect of exercise in open spaces with exposure to pollution and exercise in green open spaces on lung inflammation. True eksperiment and The Randomized Posttest-Only Control Group Design was used in this study. 24 adult male wistar white rats weighing 200-250 grams aged 8-9 weeks were randomly divided into four group, NE (Non Exercise) as control, NE+Pol (Non Exercise + exposure pollution Particulate Matter 2.5 <75 ppm and Carbon Monoxide Meter <100 ppm), Ex (Exercise 5 times/week for 4 weeks), and Ex+Pol (Exercise + exposure pollution). The inflammatory marker Tumor Necrosis Factor-αlpha (TNF-α) was analyzed using Western Blotting. To find out the significant differences between groups, one-way ANOVA and Post Hoc test were used. The results showed that the exercise + exposure to pollution had significantly higher levels of TNF-α than the control group (Ex+Pol: 1,63 AU; NE: 0,54 AU; p=0,000). There was no significant difference between the exercise in green open space and the control group (Ex: 0,80 AU; NE: 0,54 AU; p=0,357). It can be concluded that there is an effect of exercise in an open space with exposure to pollution on lung inflammation. And other results show there is no effect of exercise in green open spaces on lung inflammation.
... Studies frequently indicate that the proinflammatory impact of environmental exposure may be limited by physical activity. In mice regular aerobic exercise limited the increase in proinflammatory cytokines like TNF-α and IL-6, leukocytes and FeNO, caused by long-term exposure to particulate matter (34)(35). This is confirmed by the study of Silva-Renno et al. ...
... Często wskazuje się na ograniczenie prozapalnego oddziaływania narażenia środowiskowego przez aktywność fizyczną. U myszy regularny aerobowy wysiłek fizyczny wiązał się z ograniczeniem powodowanego przez długotrwałe narażenie na pył zwieszony wzrostu stężenia cytokin prozapalnych, takich jak TNF-α i IL-6, leukocytów i stężenia tlenku azotu w wydychanym powietrzu (34)(35). Opisane efekty znajdują potwierdzenie w badaniu Silva--Renno i wsp., które wykazało, że kontrolowany wysiłek fizyczny w warunkach narażenia na pył zawieszony w powietrzu wiąże się z ograniczeniem indukowanego przez pył wzrostu stężenia leukocytów i cytokin prozapalnych IL-1 i TNF-α oraz podwyższeniem stężenia antyzapalnej IL-10 w popłuczynach oskrzelowo-płucnych (BAL) (32). ...
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Studies reveal the negative impact of exposure to particulate air pollution on human health, especially on respiratory and circulatory systems. At the same time the beneficial effects of maintaining adequate level of physical activity are well known. In this review author presents analysis of chosen current articles about health effects of recreational physical activity in the environment of high level of ambient particulate matter air pollution. Available data suggests that there are complex relations between physical activity and exposure to air pollution. The direct positive effects of recreational physical activity include decrease of diastolic blood pressure and bronchial dilatation. It is proven that particulate air pollution show contrary impact on respiratory and cardiovascular systems. The mechanisms of this influence consist of induction of inflammation in respiratory epithelial cells, increase of oxidative stress and alterations in autonomic nervous system regulation. Changes induced by air pollution, expressed by the decrease of spirometry parameters (most commonly FEV1 decrease) were observed even in young and healthy adults doing recreational physical activity. Nevertheless, several studies suggest modulatory impact of physical exercises, which may limit the pro-inflammatory influence of particulate air pollution. Less expressed short-term negative effects of exposure have been observed in people doing physical exercise in comparison to those being inactive at the same time. In addition, apart from direct health effects, air pollution may also discourage exposed people from doing physical activity. Therefore, balanced choices regarding physical activity are needed, in order to decrease the negative impact of exposure to air pollution, without limiting the positive impact of physical activity. Still, new research is needed in order to fully explain relations between physical activity and exposure to air pollution. This will allow to elaborate physical activity guidelines including current air pollution level, better risk communication and promotion of safe ways of exercise.
... (Banerjee et al., 2003) In addition, some studies indicate that the generation of reactive oxygen species is increased when individuals regularly perform an aerobic exercise (training) in environments with atmospheric pollution, due to the amplification of minute ventilation (MV); pulmonary deposition; and toxicity of inhaled pollutants. (Strak et al., 2010) Besides the increase in inhalable particles, physical exercise is also related to the oxidative stress in two manners: on the one hand it is capable of increasing the oxidative metabolism which generates the greater formation of free radicals, and on the other hand it is capable of producing an antioxidant protective effect, promoted by regular sessions (training) (Coelho et al., 2010;Silva et al., 2010;Fashi et al., 2015). ...
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Introduction: Particulate matter (PM) is an atmospheric pollutant associated with many deleterious health effects. Oxidative stress is among these effects, that can result from a local inflammatory response to systemic damage to the organism. Studies indicate that when an individual is submitted to aerobic physical training, it generates an antioxidant protective effect that overcomes the damages caused by PM. Objective: Therefore, the aim of this study was to evaluate the influence of the particulate matter PM2.5 and PM10 on the oxidative stress parameters. Methods: The evaluation of the influence of PM on oxidative stress parameters was performed by the dosages of superoxide dismutase, catalase, glutathione peroxidase, and total antioxidant power in male Wistar rats not exposed to the particulate matter, with and without aerobic physical training, and exposed to PM2.5 and PM10, with and without aerobic physical training. This protocol lasted five weeks. Results: The antioxidant enzymes analyzed that presented significant differences were catalase, and glutathione peroxidase. Conclusions: From this research, it was possible to perceive that PM influences negatively on the oxidative stress and in the weight of the rats and that the aerobic exercise generates a protective effect against these damages.
... The health benefits of exercise are well established. Exercise can attenuate the adverse effects of air pollution, a finding that has been corroborated by experimental animal studies 178,179 . However, the degree, duration and location of exercise (such as a high-pollution versus a low-pollution environment) are variables that might have opposing outcomes, given the potential effects of these factors on either decreasing or increasing exposure with the magnitude of exercise. ...
Air pollution is well recognized as a major risk factor for chronic non-communicable diseases and has been estimated to contribute more to global morbidity and mortality than all other known environmental risk factors combined. Although air pollution contains a heterogeneous mixture of gases, the most robust evidence for detrimental effects on health is for fine particulate matter (particles ≤2.5 µm in diameter (PM2.5)) and ozone gas and, therefore, these species have been the main focus of environmental health research and regulatory standards. The evidence to date supports a strong link between the risk of cardiovascular events and all-cause mortality with PM2.5 across a range of exposure levels, including to levels below current regulatory standards, with no ‘safe’ lower exposure levels at the population level. In this comprehensive Review, the empirical evidence supporting the effects of air pollution on cardiovascular health are examined, potential mechanisms that lead to increased cardiovascular risk are described, and measures to reduce this risk and identify key gaps in our knowledge that could help address the increasing cardiovascular morbidity and mortality associated with air pollution are discussed.
... However, other components of PM are responsible for inflammatory responses, including PAHs [26], activation of AHR [46], upregulation of CYP1A1 and CYP1B1 genes [66], hypomethylation in genes linked to cytokine and immune responses [45], upregulation of miR-146a [67], and suppression of a long non-coding RNA (lnc-PCK1-2:1) [68]. The inflammatory response induced by PM or by some PM components has been well demonstrated in several cell linages including blood mononuclear cells [69], natural killer cells [70], T cells [71], human pulmonary fibroblasts [72], but also in lung tissue of rats exposed to PM 10 [73] and circulating monocytes and T lymphocytes from humans environmentally exposed [74], as well as in BALB/c mice [75]. ...
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Air pollution has been recognized as a global health problem, causing around 7 million deaths worldwide and representing one of the highest environmental crises that we are now facing. Close to 30% of new lung cancer cases are associated with air pollution, and the impact is more evident in major cities. In this review, we summarize and discuss the evidence regarding the effect of particulate matter (PM) and its impact in carcinogenesis, considering the “hallmarks of cancer” described by Hanahan and Weinberg in 2000 and 2011 as a guide to describing the findings that support the impact of particulate matter during the cancer continuum.
... Instead, one can opt for a much more filling (and cheaper) meal with bad proteins, bad fat and 100% artificially flavored drinks. Equally the experts seem to ignore that mineral water costs substantially more than addictive drinks and that the recommended 30 min of daily exercise or 10,000 steps per day (Tudor-Locke et al., 2011) in a heavily polluted city is more likely to cause lung cancer (Fashi et al., 2015;Guillerm and Cesari, 2015;Kantipudi et al., 2016;Bhopal et al., 2019) ( cities/2017/feb/13/tipping-point-cities-exercise-more-harmthan-good) than generate a better control of blood glucose. ...
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“Quisquis amat valeat; pereat qui non-scit amare; bis tanti pereat, quisquis amare vetat”—(Whoever loves, may he be well; may he perish who does not know how to love; may he perish twice as much whoever forbids loving). This graffiti was found in the old city of Pompei. The author is unknown. Possibly a poet but quite possibly an ordinary citizen who in the spur of their passion wanted to share with everyone a pearl of wisdom. Amare in Latin is “to love” and, as in English, it is not just about sex or romance, but also about passion for a cause or an ideal. The Latins knew that to be in love, to have a passion, is to be healthy in the body and as well as in the mind. In this article, I hypothesize that the lack of passion and love in life is one of the main causes of modern diseases and specifically immune/inflammatory diseases. I will explore in layman terms the limitations of specifically focusing on controlling bodily functions without considering the social and emotional dimensions of one’s life. Lastly, I will highlight the importance of cooperative research, engagement with the public and education as the way forward for a more effective and democratic model for new socially inclusive therapies.
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(1) Background: No association between air pollution and periodontitis has yet been shown. Thus, we merged two nationwide databases to evaluate the risk of periodontitis in Taiwanese residents with long-term exposure to air pollution. (2) Methods: We conducted a nationwide retrospective cohort study using the Longitudinal Generation Tracking Database and the Taiwan Air Quality-Monitoring Database. The daily average air pollutant concentrations were categorized into quartiles (Q1, Q2, Q3, and Q4). We carried out Cox proportional hazards models to compute the hazard ratios of periodontitis, with 95% confidence intervals, in Q2–Q4 of the daily average air pollutant concentrations, compared with Q1. (3) Results: the adjusted HR (95 CI%) for periodontitis in Q2–Q4 increased with increased exposure to SO2, CO, NO, NO2, NOX, PM2.5, and PM10 from 1.72 (1.70, 1.76) to 4.86 (4.78–4.94); from 1.89 (1.85–1.93) to 2.64 (2.59–2.70); from 1.04 (1.02–1.06) to 1.52 (1.49–1.55); from 1.61 (1.58–1.64) to 2.51 (2.47–2.56); from 1.48 (1.45–1.51) to 2.11 (2.07–2.15); from 2.02 (1.98–2.06) to 22.9 (22.4–23.4, and from 2.71 (2.66–2.77) to 17.2 (16.8–17.6), respectively, compared to Q1. (4) Conclusions: Residents in Taiwan with long-term exposure to higher levels of air pollutants had a greater risk of periodontitis.
Particulate matter 2.5 (PM2.5) is an inflammatory-inducing factor that is considered to be related to many adverse respiratory problems, especially in the elderly. This study aimed to examine whether pre-exercise training could prevent pulmonary injury induced by urban PM2.5 in aging rats and investigate its relationship with inflammatory pathways. Male Wistar rats (aged 16 months) were randomly divided into four groups: sedentary, exercise, sedentary+ PM2.5 exposure, and exercise+ PM2.5 exposure. All rats in exercise-related groups were treadmill-trained for 8 weeks (65%–75% VO2max for 30 min every other day). Sedentary groups’ rats lived freely in cages without exercise intervention. Rats in the PM-related groups were exposed to ambient PM2.5 (4 h day⁻¹) for 2 weeks after an 8-week exercise intervention or sedentary treatment. Finally, all rats’ pulmonary function, lung morphology, degree of inflammation, and relevant protein and mRNA transcript expression levels were examined. The results indicated that PM2.5 exposure induced lung injury in the sedentary+PM2.5 exposure group, as evidenced by the deterioration of pulmonary function, histopathological characteristics, and inflammatory changes. Aerobic exercise alleviated PM2.5-induced airway obstruction, deterioration of pulmonary function, bronchial mucosal exfoliation, and inflammatory responses in aging rats. These effects in exercise groups were associated with the increased expression of intracellular 70 kDa heat shock protein (iHSP70) and the suppression of nuclear transcription factor-κB (NF-κB) activation, as confirmed by increased expression of inhibitor of NF-κB (IκBα) and a reduction in phospho-IKBα (p-IκBα), which is regulated by inhibiting kappa B kinase beta (IKKβ). Taken together, aerobic pre-exercise had protective effects on lung injury and reduced vulnerability to inflammation induced by PM2.5 exposure, possibly through the toll-like receptor 4 (TLR4)/NF-κB signaling pathways mediated by the extracellular-to-intracellular HSP70 ratio. Pre-exercise training may be an effective way to protect against PM2.5-induced lung toxicity in aging individuals.
Carbon black nanoparticle (CBNP) is a core constituent of air pollutants like fine particulate matter (PM2.5) as well as a common manufactural material. It was proved to pose adverse effects on lung function and even provoke pulmonary fibrosis. However, the underlying mechanisms of CBNPs-induced pulmonary fibrosis remain unclear. The present study aimed to investigate the mechanism of fibrotic effects caused by CBNPs in rat lung and human bronchial epithelial (16HBE) cells. Forty-nine male rats were randomly subjected to 7 groups, means the 14-day exposure group (30 mg/m3), the 28-day exposure groups (5 mg/m3 and 30 mg/m3), the 90-day exposure group (30 mg/m3) and their respective controls. Rats were nose-only-inhaled CBNPs. 16HBE cells were treated with 0, 50, 100 and 200 μg/mL CBNPs respectively for 24 h. Besides, Forkhead transcription factor class O (FOXO)3a and miR-96 overexpression or suppression 16HBE cells were established to reveal relative mechanisms. Our results suggested CBNPs induced pulmonary fibrosis in time- and dose-dependent manners. CBNPs induced persisting inflammation in rat lung as observed by histopathology and cytology analyses in whole lung lavage fluid (WLL). Both in vivo and in vitro, CBNPs exposure significantly increased the expression of NLRP3 inflammasome, accompanied by the increased reactive oxygen species (ROS), decreased miR-96 and increased FOXO3a expressions dose -and time-dependently. MiR-96 overexpression or FOXO3a suppression could partially rescue the fibrotic effects through inhibiting NLRP3 inflammasome. Conclusively, our research show that CBNPs-induced pulmonary fibrosis was at least partially depended on activation of NLRP3 inflammasome which modulated by miR-96 targeting FOXO3a.
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It has recently been suggested that regular exercise reduces lung function decline and risk of chronic obstructive pulmonary disease (COPD) among active smokers; however, the mechanisms involved in this effect remain poorly understood. The present study evaluated the effects of regular exercise training in an experimental mouse model of chronic cigarette smoke exposure. Male C57BL/6 mice were divided into four groups (control, exercise, smoke and smoke+exercise). For 24 weeks, we measured respiratory mechanics, mean linear intercept, inflammatory cells and reactive oxygen species (ROS) in bronchoalveolar lavage (BAL) fluid, collagen deposition in alveolar walls, and the expression of antioxidant enzymes, matrix metalloproteinase 9, tissue inhibitor of metalloproteinase (TIMP)1, interleukin (IL)-10 and 8-isoprostane in alveolar walls. Exercise attenuated the decrease in pulmonary elastance (p<0.01) and the increase in mean linear intercept (p=0.003) induced by cigarette smoke exposure. Exercise substantially inhibited the increase in ROS in BAL fluid and 8-isoprostane expression in lung tissue induced by cigarette smoke. In addition, exercise significantly inhibited the decreases in IL-10, TIMP1 and CuZn superoxide dismutase induced by exposure to cigarette smoke. Exercise also increased the number of cells expressing glutathione peroxidase. Our results suggest that regular aerobic physical training of moderate intensity attenuates the development of pulmonary disease induced by cigarette smoke exposure.
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Cancer is a disease characterized by dysregulation of multiple genes and is associated with symptoms such as cachexia, anorexia, fatigue, depression, neuropathic pain, anxiety, cognitive impairment, sleep disorders and delirium (acute confusion state) in medically ill patients. These symptoms are caused by either the cancer itself or the cancer treatment. During the past decade, increasing evidence has shown that the dysregulation of inflammatory pathways contributes to the expression of these symptoms. Cancer patients have been found to have higher levels of proinflammatory cytokines such as interleukin-6. The nuclear factor (NF)-κB is a major mediator of inflammatory pathways. Therefore, anti-inflammatory agents that can modulate the NF-κB activation and inflammatory pathways may have potential in improving cancer-related symptoms in patients. Because of their multitargeting properties, low cost, low toxicity and immediate availability, natural agents have gained considerable attention for prevention and treatment of cancer-related symptoms. How NF-κB and inflammatory pathways contribute to cancer-related symptoms is the focus of this review. We will also discuss how nutritional agents such as curcumin, genistein, resveratrol, epigallocatechin gallate and lycopene can modulate inflammatory pathways and thereby reduce cancer-related symptoms in patients.
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Airway epithelium plays an important role in the asthma physiopathology. Aerobic exercise decreases Th2 response in murine models of allergic asthma, but its effects on the structure and activation of airway epithelium in asthma are unknown. BALB/c mice were divided into control, aerobic exercise, ovalbumin-sensitized and ovalbumin-sensitized plus aerobic exercise groups. Ovalbumin sensitization occurred on days 0, 14, 28, 42, and aerosol challenge from day 21 to day 50. Aerobic exercise started on day 22 and ended on day 50. Total cells and eosinophils were reduced in ovalbumin-sensitized group submitted to aerobic exercise. Aerobic exercise also reduced the oxidative and nitrosative stress and the epithelial expression of Th2 cytokines, chemokines, adhesion molecules, growth factors and NF-kB and P2X7 receptor. Additionally, aerobic exercise increased the epithelial expression of IL-10 in non-sensitized and sensitized animals. These findings contribute to the understanding of the beneficial effects of aerobic exercise for chronic allergic airway inflammation, suggesting an immune-regulatory role of exercise on airway epithelium.
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By virtue of its direct contact with the environment, the lung is constantly challenged by infectious and non-infectious stimuli that necessitate a robust yet highly controlled host response coordinated by the innate and adaptive arms of the immune system. Mammalian Toll-like receptors (TLRs) function as crucial sentinels of microbial and non-infectious antigens throughout the respiratory tract and mediate host innate immunity. Selective induction of inflammatory responses to harmful environmental exposures and tolerance to innocuous antigens are required to maintain tissue homeostasis and integrity. Conversely, dysregulated innate immune responses manifest as sustained and self-perpetuating tissue damage rather than controlled tissue repair. In this article we review aspects of Toll-like receptor function that are relevant to the development of acute lung injury and chronic obstructive lung diseases as well as resistance to frequently associated microbial infections.
Background Although running is a popular leisure-time physical activity, little is known about the long-term effects of running on mortality. The dose-response relations between running, as well as the change in running behaviors over time, and mortality remain uncertain. Objectives We examined the associations of running with all-cause and cardiovascular mortality risks in 55,137 adults, 18 to 100 years of age (mean age 44 years). Methods Running was assessed on a medical history questionnaire by leisure-time activity. Results During a mean follow-up of 15 years, 3,413 all-cause and 1,217 cardiovascular deaths occurred. Approximately 24% of adults participated in running in this population. Compared with nonrunners, runners had 30% and 45% lower adjusted risks of all-cause and cardiovascular mortality, respectively, with a 3-year life expectancy benefit. In dose-response analyses, the mortality benefits in runners were similar across quintiles of running time, distance, frequency, amount, and speed, compared with nonrunners. Weekly running even <51 min, <6 miles, 1 to 2 times, <506 metabolic equivalent-minutes, or <6 miles/h was sufficient to reduce risk of mortality, compared with not running. In the analyses of change in running behaviors and mortality, persistent runners had the most significant benefits, with 29% and 50% lower risks of all-cause and cardiovascular mortality, respectively, compared with never-runners. Conclusions Running, even 5 to 10 min/day and at slow speeds <6 miles/h, is associated with markedly reduced risks of death from all causes and cardiovascular disease. This study may motivate healthy but sedentary individuals to begin and continue running for substantial and attainable mortality benefits.
The health benefits of exercise are well known. Many of the most accessible forms of exercise, such as walking, cycling, and running often occur outdoors. This means that exercising outdoors may increase exposure to urban air pollution. Regular exercise plays a key role in improving some of the physiologic mechanisms and health outcomes that air pollution exposure may exacerbate. This problem presents an interesting challenge of balancing the beneficial effects of exercise along with the detrimental effects of air pollution upon health. This article summarizes the pulmonary, cardiovascular, cognitive, and systemic health effects of exposure to particulate matter, ozone, and carbon monoxide during exercise. It also summarizes how air pollution exposure affects maximal oxygen consumption and exercise performance. This article highlights ways in which exercisers could mitigate the adverse health effects of air pollution exposure during exercise and draws attention to the potential importance of land use planning in selecting exercise facilities.
Epithelia lining the respiratory tract represent a major portal of entry for microorganisms and allergens and are equipped with innate and adaptive immune signaling receptors for host protection. These include Toll-like receptors (TLRs) that recognize microbial components and evoke diverse responses in cells of the respiratory system. TLR stimulation by microorganism-derived molecules activates antigen presenting cells, control T helper (Th) 1, Th2, and Th17 immune cell differentiation, cytokine production by mast cells, and activation of eosinophils. It is clear that TLR are involved in the pathophysiology of allergic airway diseases such as asthma. Dendritic cells (DCs), a kind of antigen presenting cells, which play a key role in the induction of allergic airway inflammation, are privileged targets for pathogen associated molecular patterns (PAMPs). During the allergic responses, engagement of TLRs on DCs determines the Th2 polarization of the T cells. TLR signaling in mast cells increases the release of IL-5, and TLR activation of airway epithelial cells forces the generation of proallergic Th2 type of cytokines. Although these responses aim to protect the host, they may also result in inflammatory tissue damage in the airway. Under certain conditions, stimulation of TLRs, in particular, TLR9, may reduce Th2-dependent allergic inflammation by induction of Th1 responses. Therefore, understanding the complex regulatory roles of TLRs in the pathogenesis of allergic airway inflammation should facilitate the development of preventive and therapeutic measures for asthmatic patients.
Recent genome-wide association studies have identified common variants associated with high-density lipoprotein cholesterol (HDL-C). Whether these associations are modified by physical activity, which increases HDL-C levels and reduces the risk of cardiovascular disease, is uncertain. In a prospective cohort study of 22 939 apparently healthy US women of European ancestry, we selected 58 single nucleotide polymorphisms (SNPs) in 9 genes that demonstrated genome-wide association (P<5×10(-8)) with HDL-C levels and sought evidence of effect modification according to levels of physical activity. Physical activity modified the effects on HDL-C of 7 SNPs at 3 loci, and the strongest evidence of effect was observed for rs10096633 at lipoprotein lipase (LPL), rs1800588 at hepatic lipase (LIPC), and rs1532624 at cholesteryl ester transfer protein (CETP) (each P-interaction<0.05). The per-minor-allele increase in HDL-C for rs1800588 at LIPC and rs1532624 at CETP was greater in active than inactive women, whereas the reverse was observed for rs10096633 at LPL. Minor-allele carrier status at the LPL SNP was associated with a reduced risk of myocardial infarction in active (hazard ratio, 0.51; 95% confidence interval 0.30-0.86) but not among inactive women (hazard ratio 1.13; 95% confidence interval 0.79 to 1.61; P-interaction=0.007). By contrast, carrier status at the CETP SNP was associated with a reduced risk of myocardial infarction regardless of activity level (hazard ratio, 0.72; 95% confidence interval, 0.57 to 0.92; P-interaction=0.71). No association between LIPC SNP carrier status and myocardial infarction risk was noted. The effects of common variants in the LPL, LIPC, and CETP genes on HDL-C levels are modified by physical activity. For a common variant in LPL, the impact on myocardial infarction varied by activity level, whereas the effects of a common variant in CETP on myocardial infarction risk did not.