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Arboricultural Journal
The International Journal of Urban Forestry
ISSN: (Print) (Online) Journal homepage: https://www.tandfonline.com/loi/tarb20
Air pollution, human health and the benefits of
trees: a biomolecular and physiologic perspective
Patrick Mei , Vaishali Malik , Richard W. Harper & Juan M. Jiménez
To cite this article: Patrick Mei , Vaishali Malik , Richard W. Harper & Juan M. Jiménez (2021):
Air pollution, human health and the benefits of trees: a biomolecular and physiologic perspective,
Arboricultural Journal, DOI: 10.1080/03071375.2020.1854995
To link to this article: https://doi.org/10.1080/03071375.2020.1854995
Published online: 28 Jan 2021.
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Research Article
Air pollution, human health and the benets of trees: a
biomolecular and physiologic perspective
Patrick Mei
a
, Vaishali Malik
a
, Richard W. Harper
b
and Juan M. Jiménez
c,d
a
Department of Biochemistry and Molecular Biology, University of Massachusetts, Amherst, MA, USA;
b
Department of Environmental Conservation, University of Massachusetts, Amherst, MA, USA;
c
Department
of Mechanical and Industrial Engineering, University of Massachusetts, Amherst, MA, USA;
d
Department of
Biomedical Engineering, University of Massachusetts, Amherst, MA, USA
ABSTRACT
It is well accepted that particulate matter (PM) can aect human
health detrimentally. Chronic and prolonged exposures to particu-
late matter with an aerodynamic diameter ranging between 2.5
and 10 microns (PM
10
), 0.1 and 2.5 microns (PM
2.5
) and less than
0.1 microns in size (UFPM), have been associated with cardiopul-
monary diseases. PM is ubiquitously present in urban settings,
while primarily absent in forest environments primarily due to
the direct interception of airborne pollution particles by trees.
Both short- and long-term exposure to trees in forested environ-
ments is associated with lower blood pressure and inammation,
as well as enhanced immune function. Additionally, exposure to
volatile organic compounds (VOCs) actively released by trees is
associated with improved health through enhanced natural killer
cell activity, reduced inammatory responses, and reduced psy-
chological stress. This article presents the results of a literature
review on the harmful health eects of air pollution in urban
environments, and the potential of forested environments to pro-
mote health and disease prevention.
KEYWORDS
Cardiovascular Health;
Forest Bathing; Green
Spaces; PM; VOC
Introduction
According to the United Nations State of World Population Report, the year 2008 was
the turning point when more humans lived in urban settings than rural environments.
This shift has accelerated the need to understand the eects on human health due to
living in urban environments in comparison to rural settings, which may be more
forested. Forested environments contain relatively less particulate matter due to active
reduction of ozone, PM
2.5
, and PM
10
levels by trees (Nowak, Hirabayashi, Bodine, &
Greeneld, 2014). The number of cases of cardiovascular disease, inammation, and
psychological health problems is less frequent for individuals living in or near forest
environments (Maas et al., 2009, ; Nowak et al., 2014; Nowak, Hirabayashi, Bodine, &
Hoehn, 2013). Forest environments have also been associated with other health benets
ranging from changes in mood to feelings of well-being (Beute & de Kort, 2014; Oh et al.,
2017; Stigsdotter, Corazon, Sidenius, Kristiansen, & Grahn, 2017). In contrast, allergic,
CONTACT Richard W. Harper rharper@eco.umass.edu
ARBORICULTURAL JOURNAL, 2021
https://doi.org/10.1080/03071375.2020.1854995
© 2021 International Review of Finance Ltd.
auto-immune, inammatory and infectious diseases are associated with air pollution,
which is more prevalent in urbanised environments (Flies et al., 2019). Given the
interconnectedness of physiological and psychological health, this article reviews studies
that explore air quality, its eects on cardiopulmonary, immunological, neurological, and
psychological human health in the urban environment, and also explores the functions
that trees and forested settings may play in mitigating these impacts.
Methods
An initial literature search was conducted with the intention of identifying publications
that oered signicant insight into human physiological (i.e. cardiovascular, cerebro-
vascular, respiratory) and psychological health eects associated with exposure to
trees and forests. Such publications included elements like various populations, sam-
ple sizes, and geographic locales, evidence-based practices, and measurable physiolo-
gical and psychological eect parameters. These multiple studies expounded upon
practical frameworks and methodologies for the preparation of experimentation in
forest environments. Databases searched included PubMed Central, PubMed, NCBI,
ScienceDirect, and journals in the elds of cardiovascular, nervous system, pulmonary
system, and psychology (Table 1). Examination of bibliographies and reference lists
from seminal researchers of cardiovascular, neurologic, pulmonary, and psychological
conditions were also applied to the initial selection of publications. Keywords and
Boolean operators AND/OR were used for each database during snowball searches.
These terms were chosen from careful analyses of supporting literature.
Diseases and air pollution
Air pollution is one of the most pervasive health stressors in urban environments. It is
unquestionably not a new problem, but the composition of air pollution has changed
throughout the centuries. During the industrial revolution, coal was one of the main
contributors to air pollution, but this changed as cities evolved and sources of pollutants
expanded to include other types such as vehicular exhaust. Urban air pollution now
primarily consists of diverse molecules, such as ground-level ozone, lead, carbon mon-
oxide, sulphur dioxide, nitrogen dioxide, and particulate matter (PM), all of which have
been classied as harmful pollutants (Brook et al., 2002; Burnett, Dales, Brook, Raizenne,
& Krewski, 1997; Chen, Kuschner, Gokhale, & Shofer, 2007; Gojova et al., 2007; Gryparis
et al., 2004). PM can oat in the air for an extended period and can be easily inhaled due
to their small sizes. PM pollution has been associated with adverse eects in respiratory
and pulmonary functions directly linking health risks with particulate matter (Pope, 2002;
Pope et al., 2004). Cardiovascular morbidity and mortality increases with prolonged
exposure to PM (Pope et al., 2004; Tsao et al., 2014). Clinical data correlates low levels
of PM with decreased blood pressure, serum cortisol levels, inammatory cytokines, and
sympathetic nervous activity (Kobayashi et al., 2017; Kuo, 2015; Li et al., 2011; Mao et al.,
2017; Sung, Woo, Kim, Lim, & Chung, 2012; Tsao et al., 2014). Markers of neurodegen-
erative disease have also been observed to correlate with PM
2.5
exposure (Chen et al.,
2015; Wilker et al., 2015). The broad harmful health eects of PM exposure were
2Arboricultural Journal
Table 1. Health benefits associated with trees (selected articles).
Authors and Publication Date Article Results and Conclusions
Tsao T-M., Tsai M-J., Wang Y-N., Lin
H-L., Wu C-F., et al. (2014)
The Health Effects of a Forest
Environment on Subclinical
Cardiovascular Disease and Health-
Related Quality of Life
Individuals located in forest
environments featured improved
subclinical CVD’s markers of
carotid IMT.
Nowak D., Hirabayashi S., Bodine A.,
Greenfield E. (2014)
Trees and forest effects on air quality
and human health in the United
States
Urban trees remove substantial
amounts of pollution (i.e. O
3
and
PM), providing human health
benefits.
Furuyashiki A., Tabuchi K., Norikoshi
K., Kobayashi T., Oriyama S. (2019)
A comparative study of the
physiological and psychological
effects of forest bathing (Shinrin-
yoku) on working age people with
and without depressive tendencies
A day long forest bathing session
lowered the blood pressure, heart
rate, and improved profile of
mood states emotional health
metrics in subjects with depressive
tendencies.
Mao G., Cao Y., Wang B., Wang S.,
Chen Z., et al. (2017)
The Salutary Influence of Forest Bathing
on Elderly Patients with Chronic
Heart Failure
Decreased level of inflammatory
cytokines and improved
antioxidant function observed in
the forest group. Negative
emotional mood state wall
alleviated after forest bathing.
A better air quality in the forest
site was observed according to the
detection of PM
2.5
and negative
ions.
Li Q., Otsuka T., Kobayashi M.,
Wakayama Y., Inagaki H., et al.
(2011)
Acute effects of walking in forest
environments on cardiovascular and
metabolic parameters
Habitual walking in forest
environments may lower blood
pressure by reducing sympathetic
nerve activity and improve blood
adiponectin and DHEA-S levels;
may also have beneficial effects
on blood NT-proBNP levels.
Li Q., Kobayashi M., Kumeda S.,
Ochiai T., Miura T., et al. (2016)
Effects of Forest Bathing on
Cardiovascular and Metabolic
Parameters in Middle-Aged Males.
Walking 2.6 km for 80 minutes
significantly reduced pulse rate
and significantly increased the
score for vigour and decreased the
scores for depression, fatigue,
anxiety, and confusion. Urinary
adrenaline after forest bathing
also showed a slight decrease.
Urinary dopamine after forest
bathing was significantly lower
than that after urban area
walking, suggesting the relaxing
effect of the forest bathing. Serum
adiponectin after the forest
bathing was significantly greater
than that after urban area
walking.
Ideno Y., Hayashi K., Abe Y., Ueda K.,
Iso H., Noda M., Lee S L., Suzuki
S. (2017)
Blood Pressure-Lowering Effect of
Shinrin-yoku (Forest Bathing):
A systematic review and meta-
analysis.
Systolic blood pressure of the forest
environment was significantly
lower than that of the non-forest
environment. Additionally,
diastolic blood pressure of the
forest environment was
significantly lower than that of the
non-forest environment.
Barton J., Rogerson M. (2017) The Importance of Greenspace for
Mental Health.
Research indicates that potential
mechanisms underpinning the
positive relationship between
greenspace and health are likely
to include sensory-perceptual and
immunological processes, air
quality, physical activity, stress
and social integration.
(Continued)
P. Mei et al. 3
highlighted in a 2016 World Health Organisation (WHO) report emphasising 4.6 million
premature deaths due to ambient air pollution (World Health Organization, 2016).
Mechanisms of PM-induced responses
To understand the relationship between PM exposure and cardiovascular diseases, it is
essential to consider the mechanisms and pathways involved in the disease. Although
the inammatory response pathway is commonly associated with a protective mechan-
ism that cells employ as a defence against injury and infection, it can also play
a detrimental role in some diseases, including cardiovascular disease. For example, in
the most common cardiovascular disease, atherosclerosis, the pro-inammatory pheno-
type in arteries can result in the growth of plaques in the arterial wall, leading to
morbidity and mortality. In the presence of PM, the pro-inammatory phenotype in
arteries is further exacerbated, potentially aggravating atherosclerotic lesions (Figure 1).
Air particulate matter of small size and diameter can enter the respiratory tract during
inhalation. Once in the lungs, PM can cross the pulmonary epithelial-endothelial barrier
into the bloodstream (Pope, 2002). In the bloodstream, PM can interact with endothelial
cells, the innermost layer of blood vessels, and promote permeability, which in turn
increases transport across endothelial cells into the wall of arteries – a distinctive
characteristic of inammation (Chuang, Chan, Su, Lee, & Tang, 2007; Gojova et al.,
2007; Hirota et al., 2012). To determine if PM truly causes inammation, multiple studies
have measured the concentration of inammation biomarkers in the blood of test
subjects, such as C-reactive protein and inammatory cytokines (Pope et al., 2004;
Chuang et al., 2007; Yin et al., 2017). Unequivocally, inammation biomarker concentra-
tion is markedly increased in the blood of subjects after exposure to air particulate
matter, metal oxides, sulphates, and ozone (Brook et al., 2002; Gryparis et al., 2004;
Gojova et al., 2007; Yin et al., 2017).
Respiratory diseases
Respiratory diseases aect the lungs potentially altering the capacity to breathe and
exchange gases. Air enters the lungs and travels to the smallest branches where gases
Table 1. (Continued).
Authors and Publication Date Article Results and Conclusions
Nowak D J., Hirabayashi S., Bodine A.,
Greenfield E. (2014)
Trees and Forest Effects on Air Quality
and Human Health in the United
States
Computer simulations with local
environment data reveal that trees
and forests in the conterminous
US removes 17.4 million tonnes (t)
of air pollution in 2010.
Wilker E., Preis S., Beiser A., Wolf P.,
Au R., Kloog I., Li W., Schwartz J.,
Koutrakis P., Decarli C., Seshadri S.,
Mittleman M. (2015)
Long-Term Exposure to Fine Particulate
Matter, Residential Proximity to
Major Roads and Measures of Brain
Structure
Exposure to fine particulate matter
associates with total brain white
matter volume reduction and
higher probability of brain infarcts.
Pope C., Burnett R., Thun M., Calle E.,
Krewski D., Ito K., Thurston
G. (2004)
Lung cancer, cardiopulmonary
mortality, and long-term exposure to
fine particulate air pollution
Fine particulate and sulphur oxide-
related pollution increases the risk
of cardiopulmonary morbidity and
mortality.
4Arboricultural Journal
are exchanged at the epithelial-endothelial cell interface. Epithelial cells make up the
inner layer of the lungs, while the endothelial cells compose the inner layer of blood
vessels. Dierent respiratory diseases can aect gas exchange in the lungs increasing
breathing diculties. Of the dierent types of respiratory diseases, obstructive lung
diseases, chronic respiratory diseases, respiratory tract infections, and cancers are
strongly aected by PM (Karakatsani et al., 2012; Kelly & Fussell, 2011; Sax, Zu, &
Goodman, 2013; Vineis et al., 2006). The impact of PM
10
and nitrogen dioxide (NO
2
)
on human health was assessed in an Italian study using air pollution data from regional
environmental agencies (Faustini et al., 2013). Increases in chronic obstructive pulmon-
ary disease (COPD) related emergency hospitalisations were associated with increased
exposure to PM
10
and NO
2
. These patients tended to be aected more severely due to
lower respiratory tract infections (LRTI). A meta-analysis of more than one million COPD-
related acute events linked COPD emergency department visits and hospital admissions
with an increase in PM
2.5
, NO
2
, and sulphur dioxide (SO
2
). To address the question if
COPD patients suer from PM-induced chronic inammation, a 2-year observational
cohort study of COPD patients was conducted (Gao et al., 2020). During regular follow-
ups, blood serum levels of 20 cytokines and small secreted proteins released by cells
were measured and correlated with the geocoded residential address of the participants
to estimate the daily exposure to air pollutants. Increased systemic inammation on
COPD patients correlated with short-term exposure to air pollutants. Furthermore,
forced vital capacity (FVC), a metric for lung function due to the total amount of air
exhaled, was reduced in COPD patients after acute exposure to PM
2.5
, NO
2
, SO
2
, and
Figure 1. Particulate matter sources vary from a wide range of both human and natural origins,
including industrial processes, transport usage and natural causes such as volcanic eruptions. (a) PM
enters the body through the nasal passages and mouth. (b) These molecules travel down the
trachea and into the bronchi. (c) PM travel from the bronchi into the alveoli. (d) Within the alveoli
gas exchange occurs crossing the epithelial-endothelial cell interface and into the blood capillaries.
Once in the blood, PM can travel throughout the circulatory system.
P. Mei et al. 5
carbon monoxide (CO). Prolonged exposure to PM may promote chronic inammation
and contribute to remodelling of pulmonary airways and decrease airow in the lungs.
During the 1996 Summer Olympic Games in Atlanta, Georgia, USA, vehicular trac
decreased in the city of Atlanta resulting in decreases in peak daily ozone levels that
strongly associated with signicantly lower rates of childhood asthma (Friedman, 2001).
In a separate study, asthmatic children in urban settings exposed to higher concentra-
tion of NO
2
, sulphur dioxide, and PM
2.5
experienced signicantly lower pulmonary
function (O’Connor et al., 2008). A meta-analysis, focused on short-term air pollution
exposure, found an association between PM
10
and asthma episodes (Weinmayr, Romeo,
De Sario, Weiland, & Forastiere, 2010). Although air pollutants are responsible for asthma
exacerbation, they have also been suggested to cause new-onset asthma (Dong et al.,
2011). Suggested mechanisms for asthma exacerbation due to air pollution are oxidative
injuries in the pulmonary airways that promote inammation, remodelling of the air-
ways, and increased sensitisation (Guarnieri & Balmes, 2014). Chronic inammation is
characteristic of asthma patients accompanied by airway hyper-responsiveness and
tissue remodelling of the airway structure (Murdoch & Lloyd, 2010). Given that the
immune system of asthma patients reacts to non-pathogenic stimuli that can lead to
chronic inammation, air pollution is a risk factor for asthma patients (HOLGATE, 2008).
Fine particulate and sulphur oxide-related pollution has been linked to lung cancer
(Pope, 2002). In a nine country European analysis of 17-study cohorts, geocoded air
pollution showed a statistically signicant association between increased risk for lung
cancer and PM (Raaschou-Nielsen et al., 2013). Given the functions of the lungs and its
physical interaction with the air and potentially accompanying air pollution, it is reason-
able to expect an increased risk of lung cancer due to exposure to air pollution.
However, the Cancer Prevention Study II demonstrated an association between expo-
sure to air pollutants and increased risks of other cancer types as well (Pope, 2002). An
analysis of more than 600,000 participants in the Cancer Prevention Study II showed
signicantly positive association between outdoor air pollution and kidney and color-
ectal cancers (Turner et al., 2017).
Arguably, air pollution plays an important role in the onset and exacerbation of
respiratory diseases, including cancer.
Cardiovascular diseases
Atherosclerosis is one of the leading cardiovascular diseases worldwide and involves an
active inammatory response leading to blood vessel narrowing and restricted blood
ow (Libby, Ridker, & Maseri, 2002). With increased plaque build-up inside the blood
vessel wall, arteries are aected by arterial stiening where the blood vessels thicken
and are unable to constrict and dilate properly. Increased arterial stiening can impose
increased strain on the heart and lead to heart failure (Pandey et al., 2017).
Atherosclerotic plaques can rupture and cause a fatal heart attack (Herrington, Lacey,
Sherliker, Armitage, & Lewington, 2016). Initiation of atherosclerosis starts with the
dysfunction of the endothelial cells that line the inner layer of blood vessels. High LDL
cholesterol, diabetes, high blood pressure, sex hormone imbalance, ageing, inamma-
tion, infectious agents, disturbed blood ow and environmental toxins, such as air
6Arboricultural Journal
pollutants, have been identied as risk factors for endothelial cell dysfunction and
initiation of atherosclerosis (Gimbrone & García-Cardeña, 2016).
A population study in 2003 suggested that, out of all data obtained from a Cancer
Prevention Study (CPS) from the American Cancer Society (ACS), 45% of deaths had
been attributable to cardiovascular disease. The empirical data analysed revealed spe-
cic relationships between ne air particulate matter and accelerated atherosclerosis,
pulmonary and systemic inammation, and altered cardiac autonomic function (Gojova
et al., 2007; Pope, 2002; Pope et al., 2004). The eects of long-term exposure to air
particulate matter and sulphur dioxide-related pollution, as well as ambient air pollution,
directly correlated with symptoms of poor cardiovascular health and exacerbation of
existing cardiovascular or cardiopulmonary diseases (Burnett et al., 1997; Chen et al.,
2007; Künzli et al., 2010; Pope, 2002; Pope et al., 2004). Tsao et al. (2014) noted that
short-term exposure to PM
10
, PM
2.5
, and nitric oxides contribute to an increased risk of
cardiovascular diseases. Many studies converge on the harmful eects of air pollutants
on cardiovascular and cardiopulmonary health (Block & Calderón-Garcidueñas, 2009;
L. Calderón-Garcidueñas et al., 2008; Chuang et al., 2007; Lawal, 2017; Li, Guan, Tao,
Wang, & He, 2018; Pope et al., 2004; Suwa et al., 2002; Tsao et al., 2014).
Exposure to particulate matter increases the concentration of C-reactive protein and
other inammatory markers circulating in the blood (Chuang et al., 2007; Yin et al., 2017
; Pope et al., 2004). At the biochemical and molecular level, particulate matter induces
various responses such as programmed cell death of the vascular endothelial cells, and
the increase of inammatory cytokines, causing inammation in the endothelial cells
(Hirota et al., 2012; Tsao et al., 2014; Yin et al., 2017). In vivo experiments have shown
that inhalation of nanoparticles leads to impaired endothelial cell-dependent vasodila-
tion in cardiac vessels (LeBlanc et al., 2009, 2010). In healthy volunteers devoid of
cardiovascular risk factors, endothelial cell dysfunction was correlated with exposition
to ambient air pollution in a large artery and an exaggerated dilatory response in small
arteries (Briet et al., 2007). Long-term exposure to ambient air pollution was linked to
increased inammatory markers in the blood of a multi-ethnic cohort (Hajat et al., 2015).
Increased inammatory markers in the blood increase the risk of endothelial dysfunction
and atherosclerosis (Gimbrone & García-Cardeña, 2016). The eects of air pollution
extend to epigenetic modication of cellular DNA where exposure to increased NO
2
,
PM
10
, PM
2.5
, and O
3
decreased global DNA methylation in non-smoking adults (De Prins
et al., 2013).
Air pollution found in urbanised areas promotes inammation, which contributes to
cardiovascular disease, including atherosclerosis.
Cerebrovascular disease, cognitive impairment, and mental illness
It is well known that long-term exposure to air PM correlates with cerebrovascular
disease and cognitive impairment (Ljungman & Mittleman, 2014; Power et al., 2011;
Weuve, 2012). More recently, it has been shown that exposure to PM
2.5
is associated
with a smaller total cerebral brain volume, a common feature of age-associated brain
atrophy (Wilker et al., 2015). In a separate study focusing on women, white matter loss in
older women was associated with PM
2.5
exposure (Chen et al., 2015). White matter
changes are linked to decreased memory, processing speed, and executive function
P. Mei et al. 7
(Gunning-Dixon & Raz, 2000). Air pollution has also been associated with other neuro-
degenerative diseases. An 11 year-long correlative study of 9.8 million patients in 50
north-eastern U.S. cities observed signicant association between long-term PM
2.5
expo-
sure and increased risk for dementia, Alzheimer’s disease, and Parkinson’s disease
(Kioumourtzoglou et al., 2016). In addition to long-term exposure to ne particles
(PM
2.5
), a Taiwanese study suggested that long-term exposure to ozone (O
3
), created
when by-products of combustion and sunlight interact, is associated with increased risk
of Alzheimer’s disease (Jung, Lin, & Hwang, 2015).
Given that brain morphometric changes are associated with long-term exposure to
air pollution, it is expected that air pollution causes phenotypic changes at the cellular
level. In vivo experiments have demonstrated that exposure to particles, ozone, or
combinations of particles and ozone changed the mRNA synthesis levels of genes
involved in vasoregulation in the cerebral hemisphere and the pituitary gland
(Thomson, Kumarathasan, Calderón-Garcidueñas, & Vincent, 2007). The olfactory and
respiratory nasal mucosae, olfactory bulb, and cortical and subcortical structures from
mongrel dogs living in Mexican cities with diering levels of air pollution were
evaluated to elucidate the eects of air pollutants on the upper and lower respiratory
tract (Calderón-Garcidueñas et al., 2002). Changes in the inammation-related genes
nuclear neuronal NF-kappaB and iNOS were observed in cortical endothelial cells.
Further detrimental changes due to air pollution included remodelling of the blood-
brain barrier, degeneration of cortical neurons, apoptotic glial white matter cells,
deposition of apolipoprotein E (apoE)-positive lipid droplets in smooth muscle cells
and pericytes, nonneuritic plaques, and neurobrillary tangles. In dogs exposed to air
pollution, a similar study showed via immunohistochemistry increased nuclear neuro-
nal NFkappaB p65, a critical step in inammation (Calderón-Garcidueñas et al., 2003).
Further observed changes were observed in endothelial, glial, and neuronal iNOS, in
addition to endothelial and glial cyclooxygenase-2 (COX2). ApoE was observed in
neuronal, glial, and vascular cells, which has been suggested as a risk factor of
Alzheimer’s disease. Amyloid precursor protein and beta-amyloid (1–42) in neurons,
diuse plaques, and in subarachnoid blood vessels were also observed, even in dogs
as young as 11 months old. Occasionally experimental animal results do not translate
to human health. To address this concern, brain autopsy samples from lifelong resi-
dents of cities with varying pollution levels were assessed for protein synthesis levels
of the inammatory mediator COX2 and accumulation of the 42-amino acid form of
beta-amyloid (Aβ 42), which causes neuronal dysfunction (Calderón-Garcidueñas et al.,
2004). In contrast to residents of lower air pollution cities, residents of cities with
higher air pollution burden showed signicantly higher COX2 accumulation in the
frontal cortex and hippocampus. Similarly, higher air pollution correlated with greater
neuronal and astrocytic accumulation of the 42-amino acid form of beta-amyloid. The
ndings suggest an association of long-term exposure to air pollution with brain
inammation and Aβ 42 accumulation in neural tissue, a risk factor for Alzheimer’s
disease.
The previously highlighted studies demonstrate the impact of PM on inammation of
the central nervous system. Consequently, eects to the central nervous system (CNS)
are expected to aect mental health. Accumulating evidence of human and animal
studies point to the potential role of PM-induced CNS inammation in increased risk for
8Arboricultural Journal
depressed mood, anxiety disorders, bipolar disorder, and other mental health problems
(Barron, Hazi, Andreazza, & Mizrahi, 2017). Although harder to assess, dierent studies
have attempted to elucidate the role of PM on mental illness. In a Northern California
study, 144 adolescents participated in a modied Trier Social Stress Test with heart rate
and skin conductance as the physiologic metrics of stress (Miller, Gillette, Manczak,
Kircanski, & Gotlib, 2019). Greater levels of stress were associated with adolescents
residing in higher PM
2.5
concentration neighbourhoods. A nationally representative
panel data from the USA’s Environmental Protection Agency Air Quality System was
used to determine if a relationship between psychological distress and air pollution
existed. When controlling for demographic, socioeconomic, and health-related covari-
ates, higher concentrations of PM
2.5
positively associated with psychological distress
(Sass et al., 2017). A recent meta-analysis determined that long-term PM
2.5
exposure
associates with depression, and a potential association with short-term PM
10
exposure
and suicide (Braithwaite, Zhang, Kirkbride, Osborn, & Hayes, 2019).
Particulate matter reduction strategies for health improvement
There has been an increase in the use of face masks due to increased awareness of the
negative impact of particulate matter on human health. A study in 2012 assessed
cardiovascular health metric changes in coronary artery disease patients due to air
pollution exposure reduction through the use of a face mask (Langrish et al., 2012).
The study reported an improvement in heart rate variability and function, as well as
reduction in systolic blood pressure. It has been further postulated that individuals with
a history of chronic air pollution exposure and those with pre-existing cardiovascular
diseases can benet from reduced exposure resulting in an overall improvement in
health (Langrish et al., 2012). A study performed on the eectiveness of N95 face masks
in China determined that 48–75% concentration of ambient air particles between 5.6
and 560 nm in diameter were prevented from entering the airways (Guan, Hu, Han, &
Zhu, 2018). Although the N95 face masks partially reduced acute particle-associated
airway inammation, it did little in reducing oxidative stress and endothelial dysfunction.
There is a greater need to determine long-term signicance of these tests, since ltration
eciency of masks is strongly dependent on proper usage and proper face seal (Qian,
Willeke, Grinshpun, Donnelly, & Coey, 1998).
Trees: particulate matter sinks and benecial volatile organic compounds sources
Forested environments have lower air PM concentration than urban settings since trees
act as biological lters that remove and intercept air particles. A direct result of this
biological ltering is lower levels of gaseous pollutants, such as NO
2
, SO
2
, PM
2.5
, and
ozone (Nowak et al., 2013; Yang, McBride, Zhou, & Sun, 2005). Lowering of gaseous
pollutants is not limited to forests, but also relevant in inner cities where forested
patches have demonstrated signicant removal of gaseous pollutants (Cavanagh, Zawar-
Reza, & Wilson, 2009; Nowak et al., 2014). Although it is known that gaseous pollutants
such as SO
2
, NO
2
, and ozone are absorbed by the tree leaf stomata, it is not trivial to
quantify pollution removal by trees. In one study, dierent analyses were conducted to
try to determine the magnitude to which trees aect air quality in the United States of
P. Mei et al. 9
America. The rst analysis focused on determining tree cover and leaf area index using
data from the National Land Cover Database (NLCD). A separate analysis focused on
health incidence eects and monetary value of NO
2
, SO
2
, ozone, and PM
2.5
as estimated
from the USA Environmental Protection Agency BenMAP programme. Lastly, the hourly
pollution removal by trees and the change in pollution concentration were calculated to
determine the eect of trees on air quality. A positive correlation between the amount
of tree cover and the removal of air pollutants was revealed. The trees substantially
improved air quality because of the signicant removal of ozone and PM
2.5
(Nowak et al.,
2014). Similarly, another study conducted in Beijing, China involved the analysis of
satellite images and eld surveys to determine the inuence of an urban forest patch
on air quality. Considering the high concentration of air pollution within the inner city,
2.4 million trees had removed 1261.4 tons of pollutants, namely PM
10
, substantially
improving air quality (Yang et al., 2005). However, not all trees have the same capacity to
lter the air, as shown by a recent analysis to determine optimal foliar traits for eective
PM
2.5
capture. Trees like conifers, with acicular needle shapes were more ecient at
PM
2.5
capture than broadleaved species (L. Chen, Liu, Zhang, Zou, & Zhang, 2017). This is
an important consideration when PM removal is the goal.
Trees act as biological lters of pollutants through the interception of particles and
gaseous absorption, resulting in reduced particulate matter and improved air quality (Q.
Li et al., 2008; Nowak et al., 2013; Yang et al., 2005). However, it is not just the absence of
PM in forest environments that may be playing a role in health benets, but also what
trees may be releasing. The combined release of phytoncides, a class of volatile organic
compounds (VOCs) that act as microbicides, from trees have been suggested to play
a potential role in improving the air quality and enhancing bodily immune function by
increasing natural killer cell function and activity (Li et al., 2009). These organic com-
pounds may also be involved in an elevated positive emotional state and increased
parasympathetic nervous activity (Li et al., 2011).
Forested environments lower biomarkers of cardiovascular disease
Forest bathing, the practice of spending intentional time in natural-wooded settings for
the aliated health benets has been suggested as a treatment for diseases (Park,
Tsunetsugu, Kasetani, Kagawa, & Miyazaki, 2010). The motivation for forest bathing is
based on the theory of biophilia that attempts to describe the human appeal for water,
grass (savannah), trees, and other natural factors, as being rooted in a longstanding
relationship of humans and their surrounding environment (Wilson, 1992). Forest bath-
ing studies have explored the relationship of spending time exposed to forested
environments surrounded by vegetation and changes in the levels of cardiovascular
disease markers in the blood serum of participants. Imbalanced levels of these biomar-
kers may increase the risk of cardiovascular diseases. One such study asked participants
to exercise in an urban environment in the morning and afternoon for 2 hours, and
repeated the same routine exercise in a forest park a week later (Li et al., 2011). Blood
was drawn 24 hours before and after each exercise day. The results showed that many
well-known cardiovascular disease biomarkers, such as triglycerides, total cholesterol,
LDL, HDL, RPL and hs-CRP, were unchanged. However, two protective biomarkers,
adiponectin and DHEAS-S, had increased in the subjects after exercising in the forest
10 Arboricultural Journal
park, while remaining unchanged after exercise in the urban environment. Low levels of
both adiponectin and DHEAS-S are associated with higher risk of developing cardiovas-
cular diseases. A signicant decrease in the detrimental serum N-terminal pro-B-type
natriuretic peptide (NT-proBNP) was also observed after walking in the forest park. The
increase in blood serum levels of adiponectin and DHEAS-S and decrease of NT-proBNP,
suggested that not just exercising, but exercising in a forest park can have superior
benets relative to exercising in an urban setting (Li et al., 2011). Although promising,
this study focused only on healthy subjects and not on the elderly and inrmed.
A separate study addressed this dearth by assessing if forest bathing can be benecial
for elderly patients with chronic heart failure (Mao et al., 2017). Study subjects were
separated into two groups that visited either a forested or urbanised environment for
four days. Subjects visiting the forested environment experienced signicant reduction
in brain natriuretic peptide (BNP), a congestive heart failure biomarker, in comparison to
their initial levels and the initial and nal levels of the urban group. Blood serum levels
of other cardiovascular disease biomarkers, including endothelin-1 (ET-1), and constitu-
ents of the renin-angiotensin system (RAS), including renin, angiotensinogen (AGT),
angiotensin II (ANGII), and ANGII receptor type 1 or 2 (AT1 or AT2) were lower than
those of the urban group. Similarly, assessment of the prole of mood states (POMS)
showed improvements in emotional mood states after forest bathing. Forest bathing has
also shown improvements in the heart rate of both men and women alike (Ochiai et al.,
2015; Tsunetsugu et al., 2013).
Forested areas lower blood pressure
Blood pressure is an important metric in cardiovascular diseases, and potential eects of
forest environments on blood pressure regulation are of much interest. One study seeking
to elucidate a potential relationship between exposure to forested areas and blood
pressure enrolled subjects to exercise in a city environment and a week later in a forest
park. On both trips, the subjects walked for 2 hours in the morning and afternoon for
a total distance of about 6 km. Results found that blood pressure was signicantly lower
after the forest park visit than after the walk in an urban setting (Li et al., 2011). Other
studies have found similar blood pressure lowering results and improvements in other
health metrics by forest bathing. This suggests that although exercise itself can lower
blood pressure, exercise in a forest environment can have a greater blood pressure
lowering eect (Moreira, Cruz, Diniz, Albuquerque, & Carvalho, 2013; Lee & Lee, 2014; Li
et al., 2016a; Ideno et al., 2017; Lanki et al., 2017).
Volatile Organic Compounds Secreted by Trees Boost the Human Immune
System, Lower Stress Hormones, and Combat Inammation
Forest environments also inuence the immune system. Immune response has been
explored by focusing on natural killer (NK) cells, which are lymphocytes that target viral-
infected cells and tumours. A 2009 study looked at the immune activity of NK cells from
randomly selected subjects that visited a forest for 3 days and compared NK activity
from the same subjects on workdays and tourist excursions to an urban environment.
Only the forest bathing trip increased NK activity (Li et al., 2009). This and other studies
P. Mei et al. 11
prompted inquiries into what molecules in a forest environment may be boosting the
immune system (Q. Li et al., 2008; Li, 2010). One subset of molecules that has become of
interest are volatile organic compounds (VOCs) released by trees. It has been long
known that trees of many species emit phytoncides, allelochemic VOCs that protect the
trees against microbial, fungal, and insectile threats (Li et al., 2009). Could these VOCs
be responsible for the increase in NK cellular observed in other studies? To address this
question one study placed 12 healthy male subjects in a hotel room with heavy
concentrations of vaporised Japanese cedar (Cryptomeria japonica) and Hinoki cypress
(Chamaecyparis obtusa) for three consecutive nights. Blood and urinary samples were
monitored for a variety of immune system function markers including white blood cell
counts, natural killer cell activity, perforin levels, granzyme A levels, granulysin levels,
and adrenaline and noradrenaline concentrations. The study showed that oil extracts
from the Japanese cedar and Hinoki cypress inuenced natural killer cell activity and its
proliferation, as well as inuenced the intracellular perforin levels, granzyme A levels,
and granulysin levels within NK cells (Li et al., 2009). These eects are all desirable
immune system traits.
VOCs, such as α-pinene, d-limonene, and oils derived from various species of trees not
only have been shown to enhance natural killer cell activity, but also to reduce stress via
blood serum cortisol level reductions (Li et al., 2008). Cortisol is a stress hormone
released by the body under stressful conditions and increases blood pressure.
Inhalation and exposure to pine (Pinus spp.) oil and cypress (Cupressaceae spp.) oil
phytoncides reduces serum cortisol levels and consequently blood pressure (Nam &
Uhm, 2008). VOCs also decrease adrenaline and noradrenaline levels, hormones
involved in psychological distress (Calfapietra et al., 2013; Nam & Uhm, 2008).
Decreased adrenaline and noradrenaline levels may suggest that phytoncides inhibit
stress hormones, thereby potentially reducing the stress experienced by the individuals.
Studies that elucidated the eects of phytoncide derivatives on immunity found an
increase in intracellular perforin levels, granzyme A levels, and granulysin levels
(Li et al., 2009). However, the biochemical mechanisms by which VOCs secreted by
trees aect the immune system are not completely understood. Recently, insights into
the interaction of VOCs and the inammation biochemical pathway have been uncov-
ered. VOCs induce an anti-inammatory response and analgesic eect through the
inhibition of inammatory proteins and overexpression of cyclooxygenase-2 (COX-2),
an enzyme known for inducing pain relief through the production of prostanoids
(Li et al., 2016). Though this category of phytoncides exhibits a biochemical mechan-
ism for anti-inammation, other phytoncides and VOCs may exhibit an entirely dier-
ent mechanism.
Concentrations of phytoncides in urban environments are signicantly lower when
compared to forest environments positing why natural killer cell activity increases and
stress hormones decrease in forests (Li et al., 2008). Phytoncides present a natural
method of improving human immunity and mental health. With their essential roles in
immunological and inammatory responses, phytoncides and other VOCs may present
a viable approach in reducing the harmful eects felt by air particulate matter. Further
research and evidence are needed for a denitive conclusion on the clinical implications
of VOCs secreted by trees.
12 Arboricultural Journal
Psychological health and forested environments
Forested environments may prove potentially benecial to the mental health of indivi-
duals. The importance of nature and experiences around greenery and the natural world
continues to be recognised with increasing importance, by a medical sector that has
traditionally placed more of a curative, bio-pathological emphasis on human health (van
den Bosch, 2017). Visual perception and close proximity to these spaces have been
correlated with reduced levels of stress, thereby reducing the risks of developing mental
health illnesses and improving well-being (Dolling, Nilsson, & Lundell, 2017; Svendsen,
Northridge, & Metcalf, 2012 ; Wang, Rodiek, Wu, Chen, & Li, 2016). Associations with
nature, for example individuals viewing natural sceneries and selections can more
eectively reduce stress when compared to individuals observing scenes from the
built environment (Dadvand et al., 2016; Kuo, 2015). Although it may be advisable to
integrate green spaces into urban infrastructure to increase exposure to more natur-
alised environments and potentially reduce stress, assessing the positive eects of
spending time in forest environments to justify costs may be nontrivial. Traditionally,
mental health assessments after exposure to forested environments have relied on
subjective self-reporting questionnaires. In recent years, a greater emphasis has been
placed on coupling objective measurements of biomarkers that can serve as proxies for
stress levels with subjective self-reporting psychological questionnaires with the goal of
obtaining more impartial assessments. In a study by Lee, Park, Tsunetsugu, Kagawa, and
Miyazaki (2009) 12 subjects were randomly selected to visit an urban or forested
environment (Lee et al., 2009). Physiological and psychological data were collected
four times a day for each subject. Subjects in the forest environment experienced
signicantly lower salivary cortisol concentration, blood pressure and pulse rate, all
proxies for stress level measurements. The psychological results of the urban subjects
mirrored their physiological outcomes showing decreased positive emotions. Other
studies with relatively larger samples have shown similar trends where subjects exposed
to urban settings experience physiological changes associated with increased stress
levels, such as higher salivary cortisol concentration, blood pressure, and pulse rate
along with more negative self-reported emotions (J. Lee et al., 2011; Tsunetsugu et al.,
2013; Tyrväinen et al., 2014; Ward Thompson et al., 2012). Of note, these measurements
correspond to acute exposure in a specic environment. If the results hold for chronic
exposures, then it is likely that city dwellers experience prolonged increased stress
levels, which are a major factor not only in physiological symptoms such as chronic
fatigue and elevated stress hormones, but also various psychological consequences such
as mental exhaustion and stress-induced mental illnesses (Dolling et al., 2017). In
addition, urban dwellers are further exposed to physical environmental stressors com-
monly found in cities such as pollution, noise, and grey infrastructure, which may further
contribute to increased stress levels and negative mental health eects (Galea, Uddin, &
Koenen, 2011; Hartig et al., 2011; Park et al., 2011; Svendsen, Northridge, & Metcalf, 2012
; Tyrväinen et al., 2014; Wang et al., 2016). These observations may partially explain the
higher rates of major mental illnesses in urban environments where individuals are more
likely to suer from PTSD, distress, paranoia, schizophrenia, and depression (Galea et al.,
2011). There is also increasing awareness that an overarching nature-decit may be
contributing to the growing numbers of youth struggling with conditions like attention
P. Mei et al. 13
decit hyperactivity (ADHD) (van den Bosch, 2017). Increasingly, medical treatment
strategies include reconnecting youth with nature, supported by a growing body of
literature that reinforces the relationship between mental cognitive health and exposure
to green spaces (Amoly et al., 2014; Dadvand et al., 2016).
Eorts have been made to introduce green spaces as a part of urban infrastructure. It
is becoming more common for cities to incorporate green spaces through parks and
gardens to improve aesthetics and quality of life. These eorts have been propelled by
studies that suggest that people’s visual perception and closer proximity to nature and
green spaces is associated with reduced stress levels (Dolling et al., 2017; Svendsen,
Northridge, & Metcalf, 2012). Although the mechanisms remain elusive as to how and
why green spaces may promote mental health benets in humans, correlative studies
have suggested that green spaces in urban environments promote improved mental
health and well-being (Barton & Rogerson, 2017; Kuo, 2015). The restorative eects vary
with location and amount of natural green settings. However, even exposure to
a modest-sized urban park, has shown to correlate with improved psychological and
emotional well-being (Larson, Jennings, & Cloutier, 2016; Svendsen, Northridge, &
Metcalf, 2012 ; Wang et al., 2016; White, Pahl, Ashbullby, Herbert, & Depledge, 2013).
As a result, suggestions have been made to study environmental biodiversity, air quality,
sensory perception, and social community in order to elucidate the underlying mechan-
isms that benet mental health and well-being (Barton & Rogerson, 2017; Svendsen,
Northridge, & Metcalf, 2012).
Does length of exposure to forested environments matter?
Whether it is short-term or long-term exposure, particulate air pollution remains a risk
factor for a variety of diseases. Long-term exposure to air particulate matter pollution
has been suggested as a health risk factor by invoking various physiological responses
such as inammatory lung injury, elevated blood plasma viscosity, endothelial dysfunc-
tion, and myocardial infarction (Calderón-Garcidueñas et al., 2008; Pope et al., 2004).
Ample evidence exists associating cardiovascular health with air quality, amongst other
diseases (Pope et al., 2004).
A recent short-term exposure study assessed the risk of cardiovascular diseases on
114 urban and 107 forest workers by collecting data in relation to blood pressure, pulse
rates, subjective Health-Related Quality of Life (HRQOL), as well as maximum intima-
media thickness (IMT) of the carotid artery (Tsao et al., 2014). IMT is an important metric
as it is an indicator of future progression of atherosclerosis and other cardiovascular
diseases (Kablak-Ziembicka, 2004; Su, Hwang, Shen, & Chan, 2015). From this study,
PM
10
, PM
2.5
, and nitric oxide were noted as contributing factors to cardiovascular
diseases. The subjects exposed to the forested environments demonstrated superior
health as evidenced by lower blood pressure, higher parasympathetic nervous activity
and lower IMT (Tsao et al., 2014). The forest workers are exposed to a natural environ-
ment for extended periods raising the question if time exposure plays a role. In
a separate study, individuals spending as little as 2 hours in forested environments
demonstrated lower blood pressure and lower blood levels of Nt-proBNP and BNP,
cardiac biomarkers associated with heart failure (Li et al., 2011). Additional data also
indicated an increase in levels of serum adiponectin and DHEA-S (Li et al., 2011).
14 Arboricultural Journal
Chronic heart failure patients beneted from lower inammatory markers, such as IL-6
TNF- α and C-reactive protein, after a four-day exposure to a forested environment
(Mao et al., 2017). These data suggest that relatively short exposures to forested
environments can decrease risk factors for heart disease, but can short exposures to
forested environments improve mental health? Decades of research have suggested an
interconnectedness between heart disease and mental illness (De Hert, Detraux, &
Vancampfort, 2018). It could be expected that decrease in heart disease risk factors
could improve mental health. A study including subjects with depressive tendencies
demonstrated that after a day-long session of forest bathing, subjects with depressive
tendencies demonstrated signicantly greater improvements in metrics of depression
in comparison to control subjects (Furuyashiki, Tabuchi, Norikoshi, Kobayashi, &
Oriyama, 2019). Furthermore, all participants showed signicant reduction in blood
pressure and pulse rate, which are metrics of not only mental illness, but also of heart
disease.
It can be reasonably expected that relatively short exposures to less air pollutants,
namely PM
2.5
and PM
10
, concomitant with forested environments may improve human
overall health.
Conclusion
The continuing mass migration of humans to urban environments has highlighted the
importance of understanding air quality and increased risk for diseases. Various risks in
human health and well-being have been associated with this change in environment.
Humans living in urban industrial environments are frequently exposed to PM
10
, PM
2.5
, and
other air pollutants that induce inammatory responses. Several physiological health risks
have been correlated with this increased exposure, including cardiovascular and pulmon-
ary diseases. Those already suering from these diseases may even be at more risk with
increased exposure to particulate matter. In contrast, forested environments can promote
superior health outcomes due to the improved air quality and biological role of trees.
Studies which compare the health outcomes of both environments indicate that forested
environments provide more health benets by releasing VOCs that boost the immune
system, lower stress hormones, and reduce inammation. Forested environments also
improve well-being and mental health by reducing stress, promoting a positive emotional
state, and eliciting feelings of well-being. Based on these ndings, forests may provide
a potential source of therapy in physiological and mental health for humans. From the
studies considered for this review, it can be concluded that the inuence of trees on the
environment is of great impact and implementing green spaces such as parks or green
indoor environments may positively inuence urban human health.
Acknowledgments
We thank Dr Melissa D. Sánchez for constructive criticism.
Disclosure statement
No potential conict of interest was reported by the author(s).
P. Mei et al. 15
Funding
This work was supported by NSF grant CAREER CMMI1842308 (to J.M. Jiménez) and the USDA
National Institute of Food and Agriculture – McIntire Stennis Project #34, Accession #1014171.
Notes on contributors
Patrick Mei completed a BS from the University of Massachusetts in Biochemistry and Molecular
Biology. He is currently enrolled in a Master’s degree in the Bioengineering programme at the
University of Pennsylvania in Philadelphia, PA. His current research interests include nanomedicine
and targeted drug delivery as treatments for various acute vascular and pulmonary diseases.
Vaishali Malik is a M.S. student in the Molecular Cellular Biology programme at the University of
Massachusetts Amherst. Her research interests focus on targeted drug delivery for immunomo-
dulation in cancer and atherosclerotic disease models.
Richard W. Harper, PhD., is an Extension Associate Professor of Urban and Community Forestry in
the Department of Environmental Conservation, University of Massachusetts Amherst. Rick teaches
courses and administers an applied integrated research and extension programme in urban
forestry. He is the recipient of the 2020 Early Career Scientist award from the International
Society of Arboriculture (ISA) and the 2020 Public Education Award from Tree Canada.
Dr. Juan M. Jiménez is a faculty member in the Departments of Mechanical & Industrial
Engineering and Biomedical Engineering at the University of Massachusetts, Amherst. He is also
a dual recipient of the prestigious NIH K25 Mentored Quantitative Research Career Development
and NSF CAREER awards, and has also been awarded the Biomedical Engineering Society
Innovation and Career Development Award. His research focuses on experimental cardiovascular
biomedicine; specically, addressing the interaction of uid ow in the blood vasculature and
lymphatic system.
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