Expert Review of Respiratory Medicine

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Impact of long-term exposure wildfire smog on

respiratory health outcomes

Atcharaporn Ontawong, Surasak Saokaew, Busabong Jamroendararasame &

Acharaporn Duangjai

To cite this article: Atcharaporn Ontawong, Surasak Saokaew, Busabong Jamroendararasame

& Acharaporn Duangjai (2020): Impact of long-term exposure wildfire smog on respiratory health
outcomes, Expert Review of Respiratory Medicine, DOI: 10.1080/17476348.2020.1740089

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Published online: 10 Mar 2020.

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EXPERT REVIEW OF RESPIRATORY MEDICINE
https://doi.org/10.1080/17476348.2020.1740089

ORIGINAL RESEARCH

Impact of long-term exposure wildfire smog on respiratory health outcomes

Atcharaporn Ontawonga,b, Surasak Saokaewc,d,e,f,g,h, Busabong Jamroendararasameh,i and Acharaporn Duangjaia,b
a
Division of Physiology, School of Medical Sciences, University of Phayao, Phayao, Thailand; bUnit of Excellent in Research and Product
Development of Coffee and Division of Physiology, School of Medical Sciences, University of Phayao, Phayao, Thailand; cCenter of Health
Outcomes Research and Therapeutic Safety (Cohorts), School of Pharmaceutical Sciences, University of Phayao, Phayao, Thailand; dUnit of
Excellence on Clinical Outcomes Research and IntegratioN (UNICORN), School of Pharmaceutical Sciences, University of Phayao, Phayao, Thailand;
e
Unit of Excellence on Herbal Medicine, School of Pharmaceutical Sciences, University of Phayao, Phayao, Thailand; fBiofunctional Molecule
Exploratory Research Group, Biomedicine Research Advancement Centre, School of Pharmacy, Monash University Malaysia, Bandar Sunway,
Malaysia; gNovel Bacteria and Drug Discovery Research Group, Microbiome and Bioresource Research Strength, Jeffrey Cheah School of Medicine
and Health Sciences, Monash University Malaysia, Bandar Sunway, Malaysia; hSchool of Pharmaceutical Sciences, University of Phayao, Phayao,
Thailand; iUniversity of Phayao Medical Center and Hospital, University of Phayao, Phayao, Thailand

ABSTRACT ARTICLE HISTORY

Background: Air pollution is a global problem and also linked to respiratory diseases. Wildfire smog is Received 15 November 2019
a major cause of air pollution in the upper northern area of Thailand. Thus, in the current study, we Accepted 5 March 2020
examined whether long-term exposure to wildfire smog induces lung function changes in a population KEYWORDS
from the upper northern area of Thailand. Forest fire; pulmonary
Methods: The lung function of 115 participants with long-term exposure smog was determined using function; wildfire smog
peak flow meter.
Results: Long-term smoke exposure participants decreased FEV1 (forced expiratory volume in 1 second)/
FVC (forced vital capacity) ratio (56.49 ± 23.88 in males and 56.29 ± 28.23 in females) compared with
general Thai population. Moreover, the reduction of FVC, FEV1, and peak expiratory flow rate (PEFR) values
also showed in both male and female subjects. These results suggest that long-term smoke exposure
induces obstructive lung abnormality. Moreover, itchy/watery nose, cough, phlegm, and chest pain also
reported in these subjects.
Conclusion: Wildfire smog could be induced respiratory pathway inflammation and easily collapsible
respiratory airways.

1. Introduction
Air pollution is a mixture of several components such as forest
fires, smoke from factories, vehicles, and construction and also
harmful to human health [1]. Wood smoke contains many
other air pollutants, including carbon monoxide (CO), alde-
hydes, volatile organic compounds, and polycyclic aromatic
hydrocarbons. Wildfire smog is a major problem in nine pro-
vinces of the upper northern region of Thailand. Bushfires or
open burning by humans between December and April of
each year are a one source of particulate matter (PM) pollution
[2]. PM can be used to assess air quality, consistently detecting
some association between forest fire smoke and people’s
health [3,4].
PM can be classified into three types according to their
diameters: coarse PM (particle size ranging from 2.5 to 10 µm,
PM10), fine PM (particle size ranging from 0.1 to 2.5 µm, PM2.5)
and ultrafine PM (particle size less than 0.1 µm, UFP) [5]. PM10
is deposited primarily in the primary bronchi and increased
pro-inflammatory cytokines such as interleukin (IL)-8, IL-1β,
granulocyte-macrophage colony-stimulating factor (GM-CSF),
and tumor necrosis factor-alpha (TNF-α) in nasal epithelial cells
[5,6]. PM2.5 can be reached and accumulated at the end of the
respiratory tract, resulting in damaging of gas exchange in the
lungs [7]. In addition, PMs with a diameter smaller than 10 µm
have a greater impact on human health and also induces
adverse effects such as lung irritation, coughing asthma,
chronic bronchitis, cancer, and finally death [8].
Similarly, long-term exposure to wildfire smog is linked with
respiratory diseases, especially among women and children [4].
Moreover, previous studies indicated that smog exposure could
induce inflammation [9,10] and lead to increased pro-
inflammatory cytokines in the blood serum of wildland firefigh-
ters [11]. Forest fires in Thailand annually occur during the dry
season from December to April. Phayao province is one of the
impact areas of wildfire events of Thailand. In addition, Pong
District has the highest amount of hotspot in Phayao province
(19 points from 15 points in 2017). Evidence shows an association
between PM2.5 and PM10 levels and health implications in the fire
season of Phayao province. During the smog period, the number
of patients who are hospitalized with cardiovascular disease,
respiratory diseases, and dermatitis in Phayao province has
increased from 219 (2018) to 325 (2019) [12].
Moreover, carbon monoxide (CO), sulfur dioxide (SO2),
nitrogen dioxide (NO2), and ozone (O3) levels were also
increased [13]. However, there is less information about the
effects of wildfire smog on the pulmonary function of people

CONTACT Acharaporn Duangjai achara.phso@gmail.com Division of Physiology, School of Medical Sciences, University of Phayao, Phayao 56000, Thailand
© 2020 Informa UK Limited, trading as Taylor & Francis Group
2 A. ONTAWONG ET AL.

5.73 ± 2.11 for calculation one mean to a reference value,

Article highlights the sample size needed is 7 subjects and vary based on out-
● The decrease of FCV, FEV1, and FEV1/FVC ratio indicates that long-
comes but less than 50 subjects. A total of 115 participants
term smoke exposure causes obstructive lung abnormality. residing in the Pong, Ngim, Oi, and Khuan districts were
● Long-term inhalation of wood smoke cause limited lung function and included in the study over 4 years. All study protocols were
airway obstruction.
● Smoke exposure caused lung function and diminished compliance of
approved by the Human Ethics Committee of the University of
the lungs. Phayao, Phayao, Thailand (Protocol number: 2/051/62).
● Wildfire smog is linked to respiratory airway disease and lead to
a deteriorating quality of life.
● Minimize risks from long-term exposure of wood smoke is necessary.
2.2. Borg scale
To measure the intensity or severity of participant breathlessness,
Borg scale was performed. The Borg scale was modified as pre-
viously described [15]. The modified Borg scale consists of
who have resided in upper northern Thailand for more than
a vertical scale from 0 to 10 with corresponding verbal expressions
4 years. Thus, in the current study, we examined whether
of progressively increasing sensation intensity. For measurements
long-term exposure to wildfire smog induces lung function
of respiratory discomfort, the subjects were instructed to rate the
changes in a population from the upper northern area of
degree of discomfort evoked by breathing, where 0 corresponded
Thailand.
to the sensation of normal breathing and 10 corresponded to the
subject’s maximum possible sensation of dyspnea.

2. Methodology
2.3. Lung function measurements
2.1. Study location and subjects
To clarify whether the subjects had any pulmonary problems, the
This study was conducted in the Pong District, Phayao
peak expiratory flow rate (PEFR) was determined for all partici-
Province, Thailand, which has the most serious problem with
pants using a peak flow meter. The test was performed by the
wildfire smog pollution due to intrusions and deforestation by
same experienced research staff. Each subject was instructed to
humans burning the forest or from bushfires. Participation in
maintain the mouthpiece horizontally, take a deep breath and
this study was voluntary. Each subject had the study explained
forcefully blow out for three times. The highest reading was
to them and signed a consent form agreeing to participate.
recorded. PEFR was calculated from the following formula:
The participant recruitment, inclusion, and exclusion criteria
are shown in Table 1. This study was calculated the sample PEFRðL=minÞ Male ¼ ð16:859 þ 0:307A þ 0:141H
size from the previous study by using an accidental sampling  0:0018A2  0:001AHÞx60
method. Previous study reported that long-term exposure of
wood smoke reduced FVC value (4540 ± 630 mL) [14]. The Female ¼ ð31:355 þ 0:162A þ 0:391H  0:00084A2
sample size was calculated from the following formula;  0:00099H2  0:00072AHÞ x60

ðZα þ Zβ Þ2 x σ2 x ðr þ 1Þ n0 *A (Age in year) and H (Height in centimeters)

n1 ¼ when r ¼
ðμ1  μ0 Þ2 x r n1
The sample size from the calculation is 117.6 subjects.
However, the subjects that can be included in this study
area during study period were 115 subjects and this sample
size of 115 subjects are enough to effect size calculation. For
example, when this study used PEFR (L/sec) data which is
Table 1. Inclusion and exclusion criteria.
Inclusion criteria Exclusion criteria
- Ability to give informed consent. - Neurological disorder
- Age between 25–65 years old - Chronic health problems such as
- Ability to speak, read and write in high blood pressure, diabetes,
Thai chronic renal failure. Patients with
- Reside in Pong District, Phayao cardiovascular disease etc.
Province, Thailand for more than - Use of tobacco, including cigarettes,
4 years smokeless tobacco, cigars, and
- Normal breathing pipes.
- No visual defect - People with a body mass index of
more than 29.9 or less than
18 kilograms per square meter
- People who work with chemicals or
wood
- Pregnant
Subjects with a PEFR over 80% of the normal range were not
subjected to spirometry measurement. Spirometry is one of the
most common pulmonary function tests. This test was per-
formed using a Labscribe Systems spirometer (IWORX, New
Hampshire, USA). The research staff were explained spirometer
instruction before any measurement was taken. Measurements
of forced vital capacity (FVC), forced expiratory volume in
1 second (FEV1), PEFR and FEV1/FVC were done according to
the American Thoracic Society (ATS) requirements [12]. All data
were analyzed using Labscribe software (Version 2).
In this study, peak expiratory flow rate (PEFR), forced vital
capacity (FVC), forced expiratory volume in 1 second (FEV1) values
were compared with a normal range from The Thoracic Society of
Thailand under Royal Patronage guideline [16]. This guideline
measures the pulmonary function test from Thai people.
2.4. Questionnaire
A questionnaire was administered to obtain baseline informa-
tion regarding personal details, period of residence, congenital
disorder, smoking status of subjects, preexisting respiratory
illnesses, prescription medication. A daily questionnaire was
 EXPERT REVIEW OF RESPIRATORY MEDICINE 3

also administered to the subjects to obtained information
regarding inhalation incident, work-related respiratory symp-
toms and symptoms indicative of the presence of atopy and
bronchial hyper-responsiveness (BHR).
normal range (male: 2.65 ± 0.22 and female: 2.53 ± 0.14 L).
These lower FVC and FEV1 values lead to a decreased FEV1/FCV
ratio compared with normal range (male: 83.11 ± 1.44 and
female: 85.47 ± 1.25%), indicating that long-term exposure to
wildfire smog was able to reduce lung function.

2.5. Statistical analysis

Results are presented as mean ± standard error. Data were
considered statistically significant at p < 0.05.
3. Results
3.1. General characteristics
The initial study subjects included 33 men (28.7%) and 82
women (71.3%) aged 25–65 years as shown by mean ± stan-
dard error values (men: 55.70 ± 4.68; women: 51.62 ± 9.20)
(Table 2). The subjects were resident in Pong (72.2%), Ngim
(19.1%), Oi (3.5%), and Khuan (5.2%) for more than 4 years.
Moreover, the Borg scale values for male and female subjects
were 0 and 3, respectively. This scale is a subjective measure
with the potential to provide rapid information about
a patient’s subjective state of dyspnea [15].
3.2. The effects of wildfire smog on pulmonary function
The results show that the peak expiratory flow rate (PEFR) in
both male and female was lower than the normal range (male:
8.52 ± 0.59; female: 10.83 ± 0.81 L/sec) [17] (Table 3), indicat-
ing that long-term exposure to wildfire smog has led to airway
obstruction or other pulmonary conditions in our subjects.
To determine the pulmonary function of the subjects after
long-term exposure to wildfire smog, spirometry measurements
were performed (Table 3). Result showed that forced vital capa-
city (FVC) value was decreased for both male and female subjects
compared with the normal range (male: 2.12 ± 0.62 and female:
1.49 ± 0.43 L) [16]. Taken together, this data implied long-term
exposure of smog reduced lung volume.
Similarly, forced expiratory volume in 1 second (FEV1) value
was reduced in both male and female subjects compared to
Table 2. General characteristics of subjects.
Male
Age (year) 55.70 ± 4.68
Height (cm) 163.72 ± 6.05
Borg scale 0 3
Duration of residence (years) 4 4
Data are presented as mean ± standard error (male n = 33, female n = 82).
3.3. Prolonged exposure to wildfire smog linked to
respiratory diseases
The Thoracic Society of Thailand under Royal Patronage sug-
gests that decreased FVC, FEV1, and FEV1/FCV values can be
used to diagnose obstructive or restrictive lung defects in
patients [18]. An FEV1/FVC ratio of <70% indicates airflow
obstruction. In obstructive lung disorder FEV1 is usually
decreased, FVC is normal and the FEV1/FVC ratio is decreased,
whereas in restrictive disorders both FEV1 and FVC are
decreased and the FEV1/FVC ratio is normal. Therefore, these
parameters were used to clarify whether our subjects had
obstructive or restrictive lung defects. Results show that 43%
of subjects had an FEV1/FVC ratio of <70%, indicating that
wildfire smog exposure has led to obstructive lung disease.
The FVC and FEV1 values for male and female subjects were
significantly decreased compared to the normal range how-
ever the FEV1/FCV ratios were low and normal, respectively.
These data show that prolonged exposure to wood smoke can
cause obstructive pulmonary defects (in about 14.5% of males
and 47.83% of females) of various levels of severity. Moreover,
10.15% of males and 27.54% of females had restrictive lung
abnormality of mild, moderate, and severe levels (Table 4).
Thus, our data suggest that prolonged exposure to wildfire
smog is linked to respiratory airway disease or diminished
compliance of the lungs.
3.4. The adverse effects of wildfire smog
The main results are summarized in Figure 1. Itchy/watery nose,
cough, phlegm, and chest pain were more frequently reported
(25.17%, 21.09%, 14.29%, and 13.61%, respectively). Moreover,
our subjects also experienced wheezing and dry skin. Thus,
being subjected to fire smoke every day during the fire season
(December to April of each year) is associated with these
symptoms and leads to a deteriorating quality of life.
Female
51.62 ± 9.20
153.86 ± 5.44
4. Discussion
Wildfire smog is a major problem in the upper northern area of
Thailand and a previous study has reported an association
between occupational wood smoke exposure and respiratory

Table 3. The effects of wildfire smog on pulmonary function. Table 4. The effects of wildfire smog on the severity of respiratory defect.
Pulmonary function test, PFT Percentage of obstructive Percentage of restrictive
lung abnormality lung abnormality
Male Female
PEFR (L/sec) 5.73 ± 2.11 4.15 ± 1.25 Severity level Male Female Male Female
FVC (L) 2.12 ± 0.62 1.49 ± 0.43 Mild 1.45 - - 1.45
FEV1 (L) 1.07 ± 0.32 0.82 ± 0.45 Moderate - - - 1.45
FEV1/FVC (%) 56.49 ± 23.88 56.29 ± 28.23 Moderately severe - 1.45 4.35 8.70
Severe 7.25 2.90 4.35 13.04
Data are presented as mean ± standard error (male n = 17, female n = 52) Peak
Very severe 5.80 43.48 1.45 2.90
expiratory flow rate (PEFR), Forced vital capacity (FVC), Forced expiratory
volume in 1 second (FEV1). Data are presented as mean ± standard error (male n = 17, female n = 52).
4 A. ONTAWONG ET AL.
Figure 1. The adverse health effects associated with air pollution. Data are presented as percentage of subjects (male n = 17, female n = 52).
disease [18]. Wood smoke contains many air pollutants, including
carbon monoxide (CO), aldehydes, volatile organic compounds,
and polycyclic aromatic hydrocarbons [1], but the tiny particles
known as particulate matter (PM) are the main source of pollution.
PM data have been used to assess air quality in order to estimate
population exposure; moreover, a significant association was
observed between PM pollution from forest fires and hospitaliza-
tions [19]. Annual average PM of diameter <2.5 µm (PM2.5) and PM
of diameter <10 µm (PM10) from Phayao Knowledge Park stations
varied in the range 14–82 µg/m3 and 15–119 µg/m3 in October–
March, respectively. The report shows that during the fire season
PM2.5 and PM10 levels in the Phayao atmosphere are very high,
leading to significant health implications. However, this study
has no wildfire pollutants exposure data and this limitation should
be noted.
The levels of carbon monoxide (CO), sulfur dioxide (SO2), nitro-
gen dioxide (NO2) and ozone (O3) were also increased. A previous
study reported that PM2.5 was related to an increased mortality
rate in humans [20]. Furthermore, PM2.5 causes several respiratory
diseases, such as asthma, respiratory inflammation, and decreased
lung function, and also promotes cancer [21,22]. In addition, long-
term exposure to PM10 levels of 150 µg/m3 is associated with an
increase in the risk of respiratory mortality and an approximately
3–6% decline in lung function, as measured by the PEFR [23].
As shown in Table 3, significant decreases in PEFR were
exhibited in both males and females, suggesting that long-
term inhalation of PM10 and PM2.5 cause limited lung function
in our subjects; similarly, Luke et al. have shown that PM10 causes
decreased PEFR in children with airway hyperreactivity [24]. In
addition, PM induces pulmonary oxidative stress and inflamma-
tion by releasing systemic inflammatory cytokines, leading to the
accumulation of plaques, blood clotting and, finally, atherogen-
esis [25,26]. Particle interactions with the lung receptors may also
affect the autonomic nervous system, leading to the risk of
arrhythmias [27,28]. Moreover, the marked decreases of FVC,
FEV1, and FEV1/FVC ratio found here are in agreement with
a previous study showing that cumulative wildfire exposure is
associated with decreased FVC and FEV1 levels [29].
Furthermore, a lung morphological study of rabbits inhaling
wood smoke exhibited reproducible, necrotizing tracheobron-
chial epithelial cell damage [30]. Similar to this study, long-term
exposure to the irritants in wood smoke causes airway obstruc-
tion at a very severe level and 17.39% of subjects had severe
restricted lung expansion (Table 4). At present, several studies
have shown that prolonged inhalation of wood smoke is asso-
ciated with respiratory symptoms. In agreement with our data,
itchy/watery nose, cough, phlegm, and chest pain were more
frequently reported. All these symptoms are a sign of respiratory
disease, including chronic bronchitis, interstitial lung disease,
pulmonary arterial hypertension, cor pulmonale, and altered
pulmonary immune defense mechanisms [31–33].
5. Conclusion
Long-term exposure to wildfire smog being linked to respiratory
diseases. The decreased values found here for FCV, FEV1, and FEV1
/FVC ratio indicate that long-term smoke exposure causes obstruc-
tive lung abnormality. Moreover, itchy/watery nose, cough,
phlegm, and chest pain were more frequently reported. It is
concluded that wildfire smog perhaps caused the respiratory
diseases in residents in the upper northern area of Thailand.
Although this study is a descriptive study, however, all results
could be utilized to prevent the adverse effects of wildfire smog
exposure.
Funding
This research was supported by Unit of Excellent in Research and Product
Development of Coffee (no. UoE62007 to AO, AD) and Unit of Excellence
on Clinical Outcomes Research and IntegratioN (UNICORN) (no. UoE62003
to AD, SS).
Declaration of Interest
The authors have no relevant affiliations or financial involvement with any
organization or entity with a financial interest in or financial conflict with
the subject matter or materials discussed in the manuscript. This includes

employment, consultancies, honoraria, stock ownership or options, expert
testimony, grants or patents received or pending, or royalties.
Reviewer Disclosures
Peer reviewers on this manuscript have no relevant financial or other
relationships to disclose.
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