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Abstract

Exposure to pollution can cause oxidative stress, premature ageing, inflammation, and diseases. Since most of us are exposed to pollution, protection is important. This can be achieved through skin protection or through protection with respect to food and food supplements. There is a wide range of products on the market with anti-pollution claims. However, it is important that these claims are thoroughly validated by proper efficacy testing. When skin cells are exposed to pollution factors, changes in a number of skin properties can be observed, such as lipid composition, lipid and protein oxidation, pH, sebum secretion rate, oxidative stress, inflammation markers, and collagen and elastin levels. These can be measured and used as markers to verify anti-pollution claims. In the present review, we summarize some of the most important in vitro and in vivo tests that are used to determine if an ingredient or formulation has anti-pollution efficacy.
cosmetics
Review
The Impact of Pollution on Skin and Proper Efficacy
Testing for Anti-Pollution Claims
Jadwiga Rembiesa 1,2,3,*, Tautgirdas Ruzgas 2,3, Johan Engblom 2,3 and Anna Holefors 1ID
1In vitro Plant-tech AB, SE-216 18 Limhamn, Sweden; holefors@invitroplanttech.se
2Department of Biomedical Sciences, Faculty of Health and Society, Malmö University,
SE-205 06 Malmö, Sweden; tautgirdas.ruzgas@mah.se (T.R.); johan.engblom@mah.se (J.E.)
3Biofilms—Research Center for Biointerfaces, Malmö University, SE-205 06 Malmö, Sweden
*Correspondence: rembiesa@invitroplanttech.se
Received: 30 November 2017; Accepted: 26 December 2017; Published: 2 January 2018
Abstract:
Exposure to pollution can cause oxidative stress, premature ageing, inflammation,
and diseases. Since most of us are exposed to pollution, protection is important. This can be achieved
through skin protection or through protection with respect to food and food supplements. There is
a wide range of products on the market with anti-pollution claims. However, it is important that these
claims are thoroughly validated by proper efficacy testing. When skin cells are exposed to pollution
factors, changes in a number of skin properties can be observed, such as lipid composition, lipid and
protein oxidation, pH, sebum secretion rate, oxidative stress, inflammation markers, and collagen
and elastin levels. These can be measured and used as markers to verify anti-pollution claims. In the
present review, we summarize some of the most important
in vitro
and
in vivo
tests that are used to
determine if an ingredient or formulation has anti-pollution efficacy.
Keywords: pollution; mechanisms of action; skin cells; in vivo and in vitro anti-pollution efficacy
1. Introduction
The levels of air pollutants are constantly increasing worldwide, causing major concerns and
health-related problems. The WHO report from 2016 states that over 3 million people die annually due
to pollution, and about 90% of people live in an area that does not comply with the WHO Air Quality
Guidelines [
1
]. The main sources of pollutions are particulate matter, polycyclic aromatic hydrocarbons
(PAHs), volatile organic compounds (VOCs), nitrogen and sulfur oxides, carbon monoxide, ozone,
and heavy metals [
2
,
3
]. These are generated mainly by industry and car exhaust. The quality of
indoor air is crucial as well. North Americans spend about 90% of time indoors, where they are highly
exposed to such pollutions as carbon monoxide, nitrogen dioxide, or VOCs coming from tobacco
smoke, paints, varnishes, or air deodorizers. Dust, fungi or pets, and pest allergens also influence the
quality of indoor air [46].
It is well-known that environmental pollutants have a negative impact on human health.
Excessive exposure to pollutants can lead to various health-related problems, including cardiovascular
and pulmonary diseases and increased risk of microbial and viral infections [
7
]. Environmental
contaminants also have a negative impact on the skin, which is the largest organ in the human body and
one of the most important barriers against pollution. Exposure to contaminants can cause premature
skin ageing, pigmentation spots, or acne. Exposure can also lead to more serious dermatological issues
such as atopic dermatitis, psoriasis, and even skin cancer. Pollutants can also weaken the skin barrier
function and penetrate through the skin, causing systemic toxicity in other organs [811].
In recent years, there has been an increasing interest in products that protect us from the negative
impact of pollutants and that help to restore the skin barrier function. It is important to carry out
Cosmetics 2018,5, 4; doi:10.3390/cosmetics5010004 www.mdpi.com/journal/cosmetics
Cosmetics 2018,5, 4 2 of 9
proper efficacy testing for this kind of products, and most of the available methods have not yet been
standardized. The aim of this review article is therefore to sum up the existing
in vitro
and
in vivo
tests
for anti-pollution claims regarding the mechanisms of skin toxicity.
2. Effect of Pollutants on the Skin and Its Mechanism of Action
Pollution has a great impact on skin cells, as presented schematically in Figure 1. The negative
impact can be observed at the skin surface, the stratum corneum, which is normally colonized with
residual microorganisms. In the presence of pollutants, the skin microbiome changes for the benefit of
pathogenic bacteria [
12
]. Moreover, environmental contamination enhances the production of reactive
oxygen species (ROS), which depletes the content of antioxidants in the skin. This causes disturbance in
the redox balance, causing stress to the cells. Some pollutants also tend to permeate through the stratum
corneum into deeper skin layers. There, they act as a ligand for the Aryl hydrocarbon receptor (AhR),
which takes part in mediating toxic effects of pollutants. The alterations of microflora, oxidative stress,
and the activation of AhR cause the induction of an inflammatory cascade in the skin. The increased
production of pro-inflammatory cytokines, such as interleukin1
β
or interleukin 8, greatly impacts the
biological function of the cells, resulting in skin lesions and deterioration of skin appearance [13].
Cosmetics 2017, 5, 4 2 of 9
In recent years, there has been an increasing interest in products that protect us from the
negative impact of pollutants and that help to restore the skin barrier function. It is important to
carry out proper efficacy testing for this kind of products, and most of the available methods have
not yet been standardized. The aim of this review article is therefore to sum up the existing in vitro
and in vivo tests for anti-pollution claims regarding the mechanisms of skin toxicity.
2. Effect of Pollutants on the Skin and Its Mechanism of Action
Pollution has a great impact on skin cells, as presented schematically in Figure 1. The negative
impact can be observed at the skin surface, the stratum corneum, which is normally colonized with
residual microorganisms. In the presence of pollutants, the skin microbiome changes for the benefit
of pathogenic bacteria [12]. Moreover, environmental contamination enhances the production of
reactive oxygen species (ROS), which depletes the content of antioxidants in the skin. This causes
disturbance in the redox balance, causing stress to the cells. Some pollutants also tend to permeate
through the stratum corneum into deeper skin layers. There, they act as a ligand for the Aryl
hydrocarbon receptor (AhR), which takes part in mediating toxic effects of pollutants. The
alterations of microflora, oxidative stress, and the activation of AhR cause the induction of an
inflammatory cascade in the skin. The increased production of pro-inflammatory cytokines, such as
interleukin1β or interleukin 8, greatly impacts the biological function of the cells, resulting in skin
lesions and deterioration of skin appearance [13].
Figure 1. Main mechanisms of pollutant action on the skin.
Pollution also causes a negative impact on other skin properties, which are necessary for proper
skin function and health. Most importantly, the environmental contaminations influence
composition of skin lipids: the ratio of lipids is disturbed, the cholesterol content is decreased, while
the sebum secretion rate is higher. Oxidation of lipids and proteins in the skin also occurs. After
exposure to pollution, the skin is characterized with increased pH and lactic acid content. These are
only a few examples which, if properly monitored, could be regarded as chemical markers to
determine anti-pollution efficacy [14].
The impact of various pollutants on skin health and protection systems against environmental
contaminants have been nicely reviewed by other authors [7,8,15]. In the following paragraphs of
this review, we will therefore focus on the main routes of action on the skin caused by pollutants.
Figure 1. Main mechanisms of pollutant action on the skin.
Pollution also causes a negative impact on other skin properties, which are necessary for proper
skin function and health. Most importantly, the environmental contaminations influence composition
of skin lipids: the ratio of lipids is disturbed, the cholesterol content is decreased, while the sebum
secretion rate is higher. Oxidation of lipids and proteins in the skin also occurs. After exposure
to pollution, the skin is characterized with increased pH and lactic acid content. These are only
a few examples which, if properly monitored, could be regarded as chemical markers to determine
anti-pollution efficacy [14].
The impact of various pollutants on skin health and protection systems against environmental
contaminants have been nicely reviewed by other authors [
7
,
8
,
15
]. In the following paragraphs of this
review, we will therefore focus on the main routes of action on the skin caused by pollutants.
Cosmetics 2018,5, 4 3 of 9
2.1. Impact on Skin Microflora
The skin is colonialized by various types of microbiota, which form the residual skin microbiome.
Its composition varies slightly between individuals and body parts, it is dependent on age, diet, lifestyle,
and environment [
16
18
]. It is known that the skin ecosystem is linked with the human immune system,
supports the proper skin barrier function, and influences overall human health [
19
]. Air pollutants have
a negative impact on skin microflora. He et al. observed a decrease in residual skin microflora of about
50% in the presence of ozone [
20
]. These alterations can cause colonization of the stratum corneum
with pathogenic strains of bacteria, such as certain strains of Staphylococcus spp. and Streptococcus spp.,
which have been implicated to promote serious skin problems, such as cellulitis [
21
]. The relation
between ambient air pollution and acne has also been confirmed. Pollution particles settle on the
skin, blocking pores and therefore creating an anaerobic environment—ideal conditions for growth of
Propionibacterium acnes, the main bacteria strain responsible for acne. Moreover, pollutions increase
the sebum secretion rate, decrease the content of vitamin E in the skin, and promote inflammation,
which worsens the skin condition [22].
2.2. Generation of Reactive Oxygen Species (ROS)
Reactive oxygen species (ROSs) are formed in each living cell, mainly during mitochondrial
reactions, but are also formed under the influence of exogenous factors such as UV-light,
toxic chemicals, and other pollutants. At low concentrations, ROSs play an important role in regulating
cellular signaling pathways related to cell proliferation and survival [
23
]. However, ROSs are unstable,
so they can easily react with other molecules in the cell, causing damage. Each living cell also
has defense mechanisms to neutralize the negative impact of ROS, such as antioxidant enzymes:
catalase, superoxide dismutase, or glutathione peroxidase [
24
,
25
]. Air pollutants are known to
deplete the antioxidant enzymes in epidermis. They also reduce the content of other antioxidants
substances such as ascorbic acid, tocopherol, or glutathione. As a result, the redox balance is disturbed,
causing oxidative stress and major damage to the skin cells. Accumulated ROSs react with the
skin lipids, initiating the lipid peroxidation, due to which the permeability of the skin barrier is
disrupted [
15
,
22
,
26
,
27
]. This can cause disorders in defense mechanisms against environmental toxins,
allergens, pathogens, and UV radiation [
28
]. Isik et al. showed that pollutants contained in the cigarette
smoke cause oxidative damage of lipids with production of malondialdehyde (MDA) in skin epithelial
cells and inhibition of paraoxonase enzyme (PON1) [
29
]. PON1 has been shown to protect lipoproteins
from oxidation. Thus, increased serum MDA and decreased activity of PON1 are possible markers of
oxidative stress caused by pollutions.
2.3. Activation of the Aryl Hydrocarbon Receptor (AhR)
AhR is a ligand activated receptor, which is expressed in all types of cells in the skin and other
tissues which are in contact with environmental factors, such as lungs or liver [
30
]. Its function is
to support a cellular response for exogenous signals by regulation of cell homeostasis, activation
of immune cells, and induction of xenobiotic metabolizing enzymes [
30
,
31
]. AhR is activated for
example by environmental pollutants, mainly dioxins and PAHs, and takes part in the biochemical
signaling cascade and toxic effects of these pollutants. It is also involved in processes such as
cell growth, proliferation, and differentiation [
13
,
30
]. Tauchi et al (2005) showed that activation
of the AhR in keratinocytes in transgenic mice caused inflammatory skin lesions and immunological
imbalance, revealed as skin rashes and itches similar to those observed during atopic dermatitis [
32
].
The connection between inflammatory skin diseases and AhR transcript levels has also been confirmed
on human volunteers [
33
]. Skin-biopsied samples were taken from patients diagnosed with atopic
dermatitis and psoriasis and compared to healthy volunteers concerning the AhR transcript levels
using quantitative real-time PCR analysis (qRT-PCR). Immunofluorescence staining was additionally
performed to visualize the expression of AhR in the skin samples. Increased transcript levels of AhR
were observed for affected skin samples as compared to healthy skin. Furthermore, an increased
Cosmetics 2018,5, 4 4 of 9
expression of inflammatory cytokines by the ELISA assay was found in epidermal keratinocytes of
patients with psoriasis and atopic dermatitis, which shows the correlation between AhR activation and
skin inflammation lesions [
33
]. Increased transcript levels of AhR were observed as well in normal
human melanocytes in response to dioxins. The AhR activation caused an increase in tyrosinase
activity and total melanin content, which are related to skin ageing, pigment spots, and skin cancer [
34
].
Moreover, the impact of AhR activation on matrix metalloproteinases (MMPs) was investigated after
exposure to cigarette smoke. MMPs are responsible for the degradation of collagen and elastin fibers.
They are as well engaged in the collagen biosynthesis. It was shown that AhR activation by cigarette
smoke is related to increased expression of MMP-1 and MMP-3 in the skin. This caused an increased
collagen degradation and reduced collagen biosynthesis, which resulted in premature skin ageing and
formation of wrinkles [35].
However, environmental pollutants are not the only ligands that bind to the AhR. Some natural
components, for example, certain plant constituents, are known to interact with AhR, thereby inhibiting
AhR signaling. Their binding will prevent the negative impact of AhR signaling in response to pollution.
These AhR antagonist belongs mainly to polyphenol class such as flavonoids or catechins [36,37].
2.4. Induction of Inflammatory Cascade
Exposure of skin cells to pollution will cause inflammation. Several studies have shown that
skin cell lines cultivated
in vitro
and treated with different pollutants are characterized by increased
production of pro-inflammatory compounds [
38
40
]. HaCaT (cultured human keratinocyte) cells in
the presence of particulate matter released increased amounts of transforming growth factor (TNF-
α
)
and interleukins (IL-1
α
and IL-8), which resulted in the accumulation of the inflammatory cells
causing an inflammatory response [
39
]. Similar results were obtained for normal human epidermal
keratinocytes (NHEKs) treated by pollution mixture consisting of heavy metals, particulate matter,
and ozone. Here, an overproduction of two inflammatory markers, IL-1
α
and prostaglandin E2
(PGE2), was observed [
40
]. An increased IL-8 amount and, in the human keratinocytes during
in vitro
conditions, after application of benzo(a)pyrene, a compound present in cigarette smoke was detected.
It was observed that benzo(a)pyrene binds to the AhR in the keratinocytes and increases CYP1A1
expression, which is a marker of oxidative stress. This cellular change was followed by the release of
IL-8 [
41
]. Overproduction of TNF
α
, IL1-
α
, IL-6, IL-8, and other pro-inflammatory factors are related to
inflammatory skin diseases, skin aging, and skin cancer [10].
3. Testing of Anti-Pollution Claims
As mentioned above, our environment is excessively polluted, which has a great impact on human
health. Since the skin is constantly exposed to external factors, such as pollutants, the development of
new products that protect the skin from the negative impact of pollution is needed. There is as well
a need for proper assays to evaluate their anti-pollution efficacy. It is very important that the study
design is trustworthy, reproducible, and performed in conditions that are similar to real conditions.
To confirm whether the product or ingredient has a significant anti-pollution effect, we need to know
the nature of pollutants, how they act on the skin, and how to measure their effect. We then need to be
sure that we are able to measure those changes and observe if they are significant or not. Several
in vivo
and
in vitro
anti-pollution study models have been proposed and tested [
42
]. In the present review,
we are going to discuss some of these.
3.1. In Vivo Efficacy Testing
In vivo
anti-pollution tests are performed directly on the skin of human volunteers. Therefore,
the real conditions are mimicked well and the obtained results are reliable. Although, in this kind of
study design, the mixture of pollutants needs to be applied to human skin, which can be an ethical
consideration concerning health hazards. In many tests, volunteers are selected based on their living
conditions and lifestyle, e.g., people who spend a high amount of time in highly polluted area or
Cosmetics 2018,5, 4 5 of 9
smokers—people who are already exposed to various types of pollutants. However, the study design
often requires an artificial pollution mixture to be applied to the skin of volunteers.
A mixture of sebum, soil, and pollutants, called Sebollution, was designed to test the cleaning
efficacy of cleansing formulation and devices. The Sebollution was applied to the cheeks of volunteers
and followed by a washing process. The non-invasive evaluation platform was performed based on the
photographs and image analysis before and after application of the pollution mixture and then again
after washing [
43
]. The photo imaging technique with the use of pollutant mixture based on carbon
particles is a fast and efficient way of evaluating the cleansing efficiency of products
in vivo
. However,
to confirm the anti-pollution effect, it is important as well to measure the skin barrier integrity and
protection against irritants. This can be done by monitoring the transepidermal water loss (TEWL) and
chromametry analysis of skin after treatment with known irritants such as sodium dodecyl sulfate
(SDS) or sodium hydroxide [44].
In another
in vivo
test, the protective effect of different formulations on the skin treated with
cigarette smoke was evaluated. Squalene monohydroperoxide (SQOOH) and malondialdehyde (MDA)
were chosen as markers to measure the oxidative stress in the skin, since the amount of both of these
substances tend to significantly increase during skin lipid oxidation. The skin of human volunteers
was first treated with the tested product, followed by exposure to the cigarette smoke. Thereafter,
lipid samples were collected from volunteers’ skin using a swabbing technique. The samples were
further freeze-dried and analyzed with chromatographic techniques to evaluate SQOOH and MDA
levels [
45
]. A similar study model was performed to assess the anti-pollution effect of baicaline [
46
].
There, the sebum samples were collected from volunteers’ skin prior the assay and the ex-vivo test was
performed to study the impact of baicaline on lipid peroxidation. Levels of squalene and SQOOH in
the sebum samples after exposure to the cigarette smoke were confirmed by chromatographic methods.
The
in vivo
methods for anti-pollution testing mimic real-life conditions, so some are perceived as
more reliable as compared to
in vitro
studies. However, the data interpretation might be complicated
because of the limited number of individuals in the examination group and high variability within
the group.
In vivo
assays allow one to detect and measure the changes occurring in the skin cells after
exposure to pollution. They also allow one to evaluate whether those changes are significant or not.
However, it is not possible to observe the molecular routes responsible for those changes, which is
necessary for proper prevention and treatment.
3.2. In Vitro Efficacy Testing
In vitro
anti-pollution tests are based on cell models that are set up to reflect the
in vivo
state under
laboratory conditions. Different types of skin cells can be used to observe the changes in a controlled
environment. This gives a strong advantage, because in this kind of study design it is much easier
to standardize the samples and conditions during treatments and measurements. It is also easier
to understand the mechanism for action of pollutants and anti-pollution products on specific cells.
However, cells grown
in vitro
are separated from their natural environment, which makes it difficult to
predict if the cell behavior will reproduce these in the living organism [42].
These
in vitro
studies are based on the cell lines grown under laboratory conditions. Such cell lines
can be keratinocyte cell lines, such as HaCaT or NHEK [
47
49
], or fibroblast cell lines, such as normal
human foreskin-derived dermal fibroblasts (NHDF) [
50
,
51
]. These cells can be formed in a single layer
or as a reconstructed skin model to create a more differentiated and accurate model of human skin
characterized inner alia in the presence of the stratum corneum [
40
]. Some studies use skin fragments
obtained from volunteers after treatments such as skin surgeries, followed by assays performed under
in vitro conditions [38,51].
The impact of different pollutants can be tested using the
in vitro
platform. Usually the cells
are treated with the pollutant mixture, which consists of, e.g., particulate matter, urban dust,
and heavy metals or cigarette smoke [
39
,
48
,
50
]. The impact of ozone or UV radiation can also be
evaluated [38,39,47].
Cosmetics 2018,5, 4 6 of 9
The impact of pollution on skin cells and the effect of the anti-pollution treatment are assessed
by the quantification of specific markers and cell parameters. The cell viability is often measured
by a mitochondrial activity (MTT) assay [
38
,
40
], by an evaluation of lactate dehydrogenase (LDH)
release, which is an indicator of cell damage [
47
], or by cell counting using microscopic techniques [
39
].
The microscopic images allow one to observe morphological changes in the epidermal and dermal cells
or the density and structure of the collagen network, after exposure to pollution [
39
,
51
]. Cell viability
in response to stress factors can be also estimated by caspase 3 activity, which is a marker for cell
apoptosis [38].
Important indicators of cell response to pollution are the inflammation markers such as
interleukins (IL-6, IL-8, IL-1
α
, and IL-1
β
), prostaglandins (PGE2), or transforming growth factor
(TNF-
α
). Concentration of those markers in the culture medium is measured using ELISA
assays [3840].
The negative impact of pollutants on cell culture can be observed by increased ROS accumulation.
This is measured using a prefluorescent probe, which is oxidized by ROS and gives a fluorescent
compound [
48
]. The effect of anti-pollution treatment is reflected in the antioxidant capacity of the
skin and the ability of antioxidants to neutralize harmful substances. The antioxidant capacity can be
assessed e.g., by the ferric reducing antioxidant power (FRAP) method [38,51].
The skin barrier integrity is crucial for proper function of the skin. Since pollutants highly influence
this integrity, some
in vitro
assays have been designed to measure these changes. Western blot analysis
is often implemented to determine the levels of proteins that support the skin barrier function [
39
].
Alternative assays are performed by measurement of transepidermal electrical resistance directly on
epidermal skin cells [
50
] or by estimating lipid peroxidation by MDA marker and heavy metal content
in the ex vivo stratum corneum samples obtained via skin stripping [
51
].
In vitro
anti-pollution tests
enable one to study changes in gene expression by qRT-PCR to quantify transcript levels of relevant
markers, such as interleukins and CYP1B1 [
52
]. CYP1B1 is linked to the AhR activation in response to
pollution. By qRT-PCR-based analysis, it is also possible to determine changes in gene expression for
genes related to skin firmness and integrity, such as those responsible for collagen, elastin, or matrix
metalloproteinases production [50].
Novel
in vitro
methods enable elucidation of different mechanisms related to cell response to
pollution in one single study system, which is designed in a more sustainable way, e.g., using very low
amounts of reagents. Microfluidic devices, integrated with a cell culture with a protein microarray
chip allows for a fast and reliable evaluation of the cell cytotoxicity and apoptosis in response to
pollution [49].
In vitro
anti-pollution tests provide a broad analysis platform, which focus on a deeper
understanding of changes occurring in the skin cells, including the molecular mechanisms and modes
of action. One of the biggest advantages of these assays is the control of specified conditions. However,
it is important to remember that results provided by
in vitro
analysis can significantly differ from those
observed in real situations. Therefore, it is recommended that such findings be supported by relevant
in vivo studies.
4. Summary
Environmental pollutants have a tremendous impact on the life quality and health of individuals.
There is no doubt that our protection from negative impact of pollutants is important. Research has
offered various assays to determine the mechanism of action of the pollutants on living cells and
to prove the protective efficacy of anti-pollution products.
In vivo
and
in vitro
assays have various
advantages but also limitations, so combining these two approaches is the best option to provide
reliable and trustworthy results.
Acknowledgments:
We gratefully acknowledge support from the Knowledge Foundation, Synergy project 20170058.
Conflicts of Interest: The authors declare no conflict of interest.
Cosmetics 2018,5, 4 7 of 9
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©
2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access
article distributed under the terms and conditions of the Creative Commons Attribution
(CC BY) license (http://creativecommons.org/licenses/by/4.0/).
... However, when pollutants stick or clog onto those pores, they do not let the skin do this function effectively [5]; so the sebum crystallises, the pores become clogged, they expand and deform; hence free radicals are created, resulting in aesthetic problems on the skin including; wrinkles, sagging, discoloration and sometimes skin diseases. Numerous studies used pollutants (e.g., dust, microparticles, and substances from cigarette *Address correspondence to this author at the School of Pharmacy and Biomolecular Sciences, Liverpool John Moores University, Liverpool L3 3AF, United Kingdom; Tel: (+44) 151 231 2736; E-mails: I.Khan@ljmu.ac.uk; iftikharkhans@yahoo.com smoke, etc.) to investigate the effectiveness of various active ingredients in detoxifying cells, fighting oxidative stress, and chronic inflammation [6][7][8]. Moreover, the aforementioned studies explored the effects of the active ingredients on activating genes that protect cells from environmental attacks and help them repair their damage. ...
... PAHs and especially PAH benzopyrenes are well-known pollutants [6], which usually derive from anthropogenic activities, like the combustion of organic matter and smoke, including cigarettes, wood-burning, fuels, and exhaust fumes [33]. They can make bonds on the surface of PM and be suspended in the air along with them [34]. ...
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Urban pollution is one of the main problems encountered worldwide with major impact on public health as well as the environment. Health impact of urban pollution is not limited to respiratory conditions but also encompasses major skin problems including irritation, skin ageing, and skin cancer. Toxic gases and particulate matter are the main pollutants and exhibit extensive local variability. The aforementioned pollutants are small particles that attach to the skin or penetrate into it, enhancing free radicals’ production inside the inner skin layers. This urges the need to propose cosmetic products that help prevent and/or minimise pollutants’ effects on the skin whether irritation, ageing and cancer. Furthermore, intrinsic and extrinsic factors contributed to skin irritation and ageing. Intrinsic factors are within skin factors and include genetic and physiological characteristics of individuals. Moreover, extrinsic factors comprise environmental factors such as humidity, temperature, and smoke. Subsequently active ingredients with antipollutant properties addressed the intrinsic and extrinsic factors by four mechanisms being: free radical neutralisation, film-forming ability, skin barrier enhancement and fortification. Such ingredients include vitamin A derivatives, vitamin C derivatives, carbohydrates, and plant-based products. Yet, very limited studies have evaluated the effectiveness of the aforementioned active ingredients against irritation or ageing and this should be considered in future work.
... This strengthens the effort towards caring about raw materials and waste, positioning biotechnology as a promising science to impact the production of beauty ingredients and/or final products [143]. Renewable raw materials may protect the skin from contaminants, as well as modulate the skin's microbiota, namely the ecological community of microorganisms that colonize our body, adding to the ease of biodegradability and skin biocompatibility [144]. Also, it can be commercialized in a dry state without requiring preservatives [145]. ...
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Polyhydroxyalkanoate (PHA), a biodegradable polymer obtained from microorganisms and plants, have been widely used in biomedical applications and devices, such as sutures, cardiac valves, bone scaffold, and drug delivery of compounds with pharmaceutical interests, as well as in food packaging. This review focuses on the use of polyhydroxyalkanoates beyond the most common uses, aiming to inform about the potential uses of the biopolymer as a biosensor, cosmetics, drug delivery, flame retardancy, and electrospinning, among other interesting uses. The novel applications are based on the production and composition of the polymer, which can be modified by genetic engineering, a semi-synthetic approach, by changing feeding carbon sources and/or supplement addition, among others. The future of PHA is promising, and despite its production costs being higher than petroleum-based plastics, tools given by synthetic biology, bioinformatics, and machine learning, among others, have allowed for great production yields, monomer and polymer functionalization, stability, and versatility, a key feature to increase the uses of this interesting family of polymers.
... A skinsurface sampling and analysis method could be added that measures target condensed phase species, such as squalene hydroperoxides, to determine if gas-phase measurements are suitable for cosmetic product testing. Combined, these techniques can help test the antipollution claims of cosmetics [27,28]. ...
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Personal care products are increasingly being marketed to protect skin from the potentially harmful effects of air pollution. Here, we experimentally measure ozone deposition rates to skin and the generation rates and yields of oxidized products from bare skin and skin coated with various lotion formulations. Lotions reduced the ozone flux to the skin surface by 12% to 25%; this may be due to dilution of reactive skin lipids with inert lotion compounds or by reducing ozone diffusivity within the resulting mixture. The yields of volatile squalene oxidation products were 25% to 70% lower for a commercial sunscreen and for a base lotion with an added polymer or with antioxidants. Lower yields are likely due to competitive reactions of ozone with lotion ingredients including some ingredients that are not intended to be ozone sinks. The dynamics of the emissions of squalene ozonation product 6 methyl-2-heptenone (6MHO) suggest that lotions can dramatically reduce the solubility of products in the skin film. While some lotions appear to reduce the rate of oxidation of squalene by ozone, this evidence does not yet demonstrate that the lotions reduce the impact of air pollution on skin health.
... O 3 , in combination with UV light, can potentiate UV-induced depletion of vitamin E, which is essential for skin health [99,100]. The oxinflammatory damage induced by pollutants can then culminate in the alteration of skin functionality by affecting the main components of the stratum corneum (SC), the cornified envelope, which is the primary barrier of the skin [101]. PM, O 3 and UV are all able to modulate cutaneous proteins that are essential for skin differentiation and proper barrier function, such as involucrin, filaggrin, and keratins [102][103][104], potentiating the damage when acting together [42,105]. ...
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Our current understanding of the pathogenesis of skin aging includes the role of ultraviolet light, visible light, infrared, pollution, cigarette smoke and other environmental exposures. The mechanism of action common to these exposures is the disruption of the cellular redox balance by the directly or indirectly increased formation of reactive oxygen species that overwhelm the intrinsic antioxidant defense system, resulting in an oxidative stress condition. Altered redox homeostasis triggers downstream pathways that contribute to tissue oxinflammation (cross-talk between inflammation and altered redox status) and accelerate skin aging. In addition, both ultraviolet light and pollution increase intracellular free iron that catalyzes reactive oxygen species generation via the Fenton reaction. This disruption of iron homeostasis within the cell further promotes oxidative stress and contributes to extrinsic skin aging. More recent studies have demonstrated that iron chelators can be used topically and can enhance the benefits of topically applied antioxidants. Thus, an updated, more comprehensive approach to environmental or atmospheric aging protection should include sun protective measures, broad spectrum sunscreens, antioxidants, chelating agents, and DNA repair enzymes.
... Furthermore, SHE reduced the expression of the sebum production-related biomarkers in the cultured sebocytes. Increased exposure to PM2.5 was associated with an increased sebum secretion in human skin 16 . Some studies revealed that the prevalence of oily skin was considerably higher in areas with a high level of air pollution in China and Mexico 17 . ...
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Background: Particulate matter (PM) is one of the air pollutants that can damage human skin; the recent increase in the amount of PM may be detrimental to skin health. Objective: We aimed to investigate the effects of PM on cultured human sebocytes and outer root sheath (ORS) cells and the effects of Siegesbeckia Herba extract (SHE) on PM-treated cultured cells. Methods: Sebocytes and ORS cells were cultured. The cultured cells were treated with various concentrations of PM of <10 µm in size (PM10) (10 µg/ml, 25 µg/ml, 50 µg/ml, and 100 µg/ml) for 24 h. Real-time polymerase chain reaction, measurement of reactive oxygen species (ROS), small interfering (si) RNA transfection, Oil Red O and Nile red staining, and immunofluorescence staining were performed to analyze the presence of inflammatory cytokines, matrix metalloproteinases (MMPs), aryl hydrocarbon receptor (AhR), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), ROS, and lipid production. In addition, PM10 (100 µg/ml)-treated cultured cells were treated with 10 mg/ml of SHE. Results: PM10 upregulates the expression of inflammatory cytokines, MMPs, AhR, NF-κB, and ROS in cultured human sebocytes and ORS cells. The production of ROS was dramatically reduced in AhR siRNA-transfected cells. In addition, PM10 upregulates sebum production in cultured sebocytes. SHE inhibited the upregulation of inflammatory cytokines, MMPs, AhR, NF-κB, ROS, and sebum production in cultured human sebocytes and/or ORS cells by PM10. Conclusion: Effects of PM10 on cultured human sebocytes and ORS cells can be regulated by SH.
... Besides these pollutants, cigarette smoke is a highly complex aerosol composed of a thousand chemicals, carcinogens and many oxygen-forming substances, such as catechol, known to interact with the skin. [122][123][124] The induction of oxidative stress by air pollution exceeds the skin's enzymatic and non-enzymatic antioxidant defences causing damage to cell lipid membranes and inducing the synthesis of proteolytic enzymes, such as matrix metalloproteinase, responsible for the breakdown of dermal proteins. 125 The ReAS also exacerbates the inflammatory response, activating important transcription factors and signalling pathways such as NF-kB, AP-1 and p38MAPK. ...
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... A second in vitro model was developed to study the impact of pollution on the skin and its ability to exacerbate the consequences of acne. Pollution can penetrate to the deeper layers of the skin inducing ROS production and antioxidant depletion, activation of aryl hydrocarbon receptors, and induction of inflammatory responses [44]. In our model, the application of PM10 pollutants induced morphological modifications resulting in impaired barrier function and an inflammatory response [45]. ...
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smoke contains all the important classes of documented indoor and outdoor pollutants. Furthermore, data derived from this type of study should correlate well with most in vitro or ex vivo findings, and add to the weight of evidence that is required to substantiate cosmetic claims. Skin produces sebum, and it is these sebum lipids which are in first contact with smoke exposure in the environment. It is well documented that sebum is oxidized by cigarette smoke (28, 31) to produce increased levels of squalene monohydroperoxide (SQOOH) and malondialdehyde (MDA). Furthermore skin barrier lipids of the stratum corneum are also oxidized by cigarette smoke with measurable increases in MDA (32). Increased levels of SQOOH have been reported to increase the likelihood of skin comedogenicity and the consequences of photo-oxidative stress (33). Malondialdehyde (MDA) is a good marker of oxidative stress and enzymes that limit free-radical formation (34, 35). As such, it is therefore a good indicator for measuring both oxidative damage and the efficiency of anti-oxidants. CHALLENGES Whilst our method is fairly straightforward to execute, we noted 3 key challenges in terms of: minimizing smoke inhalation by volunteers; the need for standardized and reproducible skin pollution exposure at a constant level for several minutes; and the requirement for "fresh" smoke since only fresh smoke contains the pollutants needed for "oxidation". To overcome these challenges, the method we have developed involves the use of a smoke-suction device (Figure 1) in which a pump produces negative pressure and transports smoke to the skin on a defined area of the back (3 cm diameter) for measuring sebum oxidation (Figure 2), or the volar forearm for barrier lipid oxidation. Free interaction of the skin with a constant stream of smoke is allowed for 15 minutes (approximately 8-9 cigarettes). This short intense application of smoke is akin to the use of intense UV light sources in routine SPF testing, which are 20 times stronger than natural sunlight. Cigarette smoke is also reported to be associated with psoriasis, the effects of which could be mediated by the ROS and in particular by the disturbed balance of oxidants and antioxidants-indicated with low levels of vitamin C and glutathione, and high levels of superoxide dismutase and malondialdehyde in cutaneous tissues (26, 27). Whilst the skin can be protected in order to help minimize the effects of pollution, complete avoidance of environmental pollution however, is impossible. There are 3 key protection approaches: good cleansing, neutralization of free-radicals and skin barriers. Products include moisturizers with barrier properties and/or formulated with free-radical scavenging properties; sunscreens to protect the skin from UV damage and those which also include technologies that might protect against other irradiation sources; and effective skin cleansing regimes. In addition vitamin based nutrition to help negate the effects of free-radical skin damage (29, 30). Such protection strategies for the skin against environmental pollution make good sense, yet their effectiveness in the marketplace requires robust evidence to support developing claims for such cosmetic products. A number of both in vitro ex-vivo methods are available to demonstrate antioxidant activity of pollution-treated skin models and explants. These testing methods are of limited clinical relevance and unreliable in correlating the antioxidant performance of a product to its efficacy in contending environmental impact. Furthermore extrapolation of their in vitro efficacy to physiological benefits is inconsistent and these assays are unable to capture a cosmetic formulations ability to penetrate the stratum corneum which is necessary for an antioxidant to counteract actual free radical production in the skin. In order to prove real consumer benefit(s) in terms of skin barrier protection and anti-oxidative damage however, human studies are required. Since environmental pollution is variable depending on its source and distribution, relevant pollutant models need to be chosen in studies in order to obtain meaningful data whilst also providing more general conclusions. This is easily achieved by exposing skin with combustion smoke-in this case cigarette smoke as the pollutant model-and measuring the degree of lipid and/or protein peroxidation in the stratum corneum when the skin is treated with test products. PRINCIPLE We have developed a new clinical method to assess pollution generated lipid peroxidation and its prevention and/or treatment by cosmetic products in human volunteers. The skin of the backs of human volunteers is treated with the product under test, exposed to smoke and then peroxidation of human sebum is assessed. Similarly, application on the volar forearm enables the assessment of the effects on skin barrier lipids. All assessments are performed using cigarette smoke as the combustion pollutant model. The rationale for using cigarette smoke as the pollution source is that many societies still accept smoking as a norm (though this is limited); most humans are in contact with varying degrees of cigarette smoke; cigarette smoke is easily handled in the laboratory as compared to other gaseous combustion pollutants; other smoke pollutants including diesel are classed as unethical in terms of their use as models in clinical studies; and cigarette Abstract Solar UVR, noxious gases, particulate matter, ozone, and cigarette smoke are key air pollutants with subsequent negative effects on the skin. Cigarette smoking is associated with skin aging (wrinkles, skin dryness, skin discoloration and so on), and the combination of smoking and solar UVR may even exacerbate the skin aging processes. In this paper we describe a new validated clinical method to evaluate the "protective" effects of specific cosmetic products against gaseous pollution exposure based on cigarette smoke as a pollutant model. The skin of human volunteers is treated with the product under test, exposed to cigarette smoke and then peroxidation of human sebum or skin barrier lipids is assessed using GC-MS/ LC-MS. Key advantages of this method is the small number of volunteers required, and the reproducibility and sensitivity of the method to detect protective and anti-oxidative properties of cosmetic active ingredients and cosmetic formulations. Pollutant cigarette smoke is a suitable substance containing all key pollution components that can be used in human volunteers without ethical issues as compared to other pollution sources. Furthermore, our method enables us to induce under standardized clinical laboratory conditions a pollution stress on "living skin".
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Skin barrier structure and function is essential to human health. Hitherto unrecognized functions of epidermal keratinocytes show that the skin plays an important role in adapting whole-body physiology to changing environments, including the capacity to produce a wide variety of hormones, neurotransmitters and cytokine that can potentially influence whole-body states, and quite possibly, even emotions. Skin microbiota play an integral role in the maturation and homeostatic regulation of keratinocytes and host immune networks with systemic implications. As our primary interface with the external environment, the biodiversity of skin habitats is heavily influenced by the biodiversity of the ecosystems in which we reside. Thus, factors which alter the establishment and health of the skin microbiome have the potential to predispose to not only cutaneous disease, but also other inflammatory non-communicable diseases (NCDs). Indeed, disturbances of the stratum corneum have been noted in allergic diseases (eczema and food allergy), psoriasis, rosacea, acne vulgaris and with the skin aging process. The built environment, global biodiversity losses and declining nature relatedness are contributing to erosion of diversity at a micro-ecological level, including our own microbial habitats. This emphasises the importance of ecological perspectives in overcoming the factors that drive dysbiosis and the risk of inflammatory diseases across the life course.
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Jean Krutmann,1 Dominique Moyal,2 Wei Liu,3 Sanjiv Kandahari,4 Geun-Soo Lee,5 Noppakun Nopadon,6 Leihong Flora Xiang,7 Sophie Seité2 1IUF – Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany; 2La Roche Posay Dermatological Laboratories, Asnières, France; 3Department of Dermatology, The General Hospital of Air Force, PLA, Beijing, People’s Republic of China; 4Dr. Kandhari’s Skin & Dental Clinic, New Delhi, India; 5Drs. Woo and Hann Skin Center, Yongsan-gu, Seoul, Korea; 6Division of Dermatology, Faculty of Medicine, Department of Medicine, Chulalongkorn University, Bangkok, Thailand; 7Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, People’s Republic of China Abstract: In recent years, the critical role that inflammation may play in the development and progression of acne has become increasingly recognized. The prevalence of acne is similar between Asian and Caucasian women, but Asian women have a higher prevalence of inflammatory acne. They also report their symptoms exacerbate during periods of high air pollution. The objective of this study was to review the current evidence that links air pollution to worsening of acne symptoms. Firstly, a group of five Asian and three European scientists with expertise in Dermatology reviewed the current literature and described current acne treatment practices in their countries. During this activity, they identified the need for further epidemiological and clinical research. Secondly, additional studies ensued which provided evidence that acne symptoms might exacerbate in regions of high ambient air pollution. Based on these findings, the authors suggest that people with acne should protect the natural barrier function of their skin with emollients and ultraviolet (UV)A/UVB protection. Keywords: pollution, acne, Asia, epidemiology, pathophysiology
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Background Urban pollution is a major source of concern for human health and is a complex of many environmental factors. The topical exposure to pollution activates cutaneous stress. Objective In this study, we tested the antipollution protection of two active components: Dead Sea minerals (Dead Sea mineral-rich water [DSW]) and anionic polysaccharide (PolluStop® [PS]). Materials and methods Two representative pollution models were studied using reconstructed epidermis: 1) mixture of pollutants (MOP) containing heavy metals and atmospheric particulate matter and 2) ozone exposure. DSW and PS were topically applied alone or in combination, and their protection against pollution was assessed by testing the levels of the inflammation markers interleukin 1α (IL-1α) and prostaglandin E2 (PGE2). Results MOP exposure induced IL-1α release, which was attenuated following pre-application with DSW and PS alone or in combination. Ozone exposure induced IL-1α and PGE2 release. Pre-application with DSW or PS alone did not inhibit IL-1α and PGE2 overproduction. Only when DSW and PS were mixed together, inhibition of these inflammatory markers was observed. Conclusion The observations reveal the potential use of active agents in combination for a selective mode of protection from urban pollution. This is because many active materials cannot solely provide a broad protection against different types of pollutants. This strategy might be beneficial for future antipollution regimen formulated in both pharmaceutical and cosmetic products.
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Background Cigarette smoking is the single biggest preventable cause of death and disability in developed countries and is a significant public health concern. While known to be strongly associated with a number of cardiovascular and pulmonary diseases and cancers, smoking also leads to a variety of cutaneous manifestations. Objective This article reviews the effects of cigarette smoking on the skin and its appendages. Methods A literature review was based on a MEDLINE search (1966–2004) for English-language articles using the MeSH terms cutaneous, dermatology, tobacco, skin, and smoking. An additional search was subsequently undertaken for articles related to smoking and associated mucocutanous diseases, with the focus on pathogenesis and epidemiologic data. Articles presenting the highest level of evidence and latest reports were preferentially selected. Results Smoking is strongly associated with numerous dermatologic conditions including poor wound healing, wrinkling and premature skin aging, squamous cell carcinoma, psoriasis, hidradenitis suppurativa, hair loss, oral cancers, and other oral conditions. In addition, it has an impact on the skin lesions observed in diabetes, lupus, and AIDS. The evidence linking smoking and melanoma, eczema, and acne is inconclusive. Anecdotal data exist on the possible protective effects of smoking in oral/genital aphthosis of Behçet's disease, herpes labialis, pyoderma gangrenosum, acral melanoma, and Kaposi's sarcoma in AIDS patients. Conclusions An appreciation of the adverse cutaneous consequences of smoking is important. Dermatologists can play an integral role in promoting smoking cessation by providing expert opinion and educating the public on the deleterious effects of smoking on the skin.
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Human exposure to PM2.5 causes several adverse health effects. Skin is the first barrier against harmful environmental substances and can has direct contact with PM2.5, but there is no study about PM2.5-induced cytotoxicity in human skin cells on the molecular level partially due to the shortcomings of traditional research methods. In present study, we established a microfluidic system including a cell culture chip integrated with a high-throughput protein microarray chip to investigate the mechanism of PM2.5-mediated cytotoxicity in human HaCaT cells. We found that PM2.5 was lodged inside the cytoplasm, mitochondria and nucleus of HaCaT cells by TEM. Flow cytometry analysis indicated that the cell apoptosis rate increased from 0.49% to 53.4%. The results of protein microarray showed that NF-κB and NALP3 signal transductions were activated in HaCaT cells after PM2.5 stimulations, up-regulating the expression of IL-1β and IL-6, which resulted in inflammatory response in HaCaT cells. Our findings provide a molecular insight into PM2.5-induced skin injury.
Article
Background: Pollution, especially cigarette smoke, is a major cause of skin damage. Objectives: To assess the effects of the small molecule polyphenol, honokiol, on reversing cigarette smoke-induced damage in vitro to relevant skin cells. Methods: Keratinocytes (HaCat) cultures were exposed to cigarette smoke and, after 48 hours, IL-1α and IL-8 were measured in cell supernatants. Moreover, TIMP-2 production, apoptosis rate, and senescence β-galactosidase expression were evaluated in primary human foreskin fibroblasts (HFF-1) cultures. Results: Honokiol at 10 μm reduced IL-1α production by 3.4 folds (P < 0.05) and at 10 and 20 μm reduced IL-8 by 23.9% and 53.1% (P < 0.001), respectively, in HaCat keratinocytes. In HFF-1, honokiol restored TIMP-2 production by 96.9% and 91.9% (P < 0.001), respectively, at 10 and 20 μm, as well as reduced apoptosis by 47.1% (P < 0.001) and 41.3% (P < 0.01), respectively. Finally, honokiol reduced senescence-associated β-galactosidase expression in HFF-1. Conclusion: Honokiol protects both HFF-1 and HaCat against cigarette smoke-induced inflammation, collagenolysis, apoptosis, and senescence.
Article
The transcription factor AHR is highly expressed in all skin cells and an increasing body of evidence shows its involvement in immunity of barrier organds. The AHR is activated by many molecules found in the environment, both man-made and natural compounds, e.g., from dietary plants. Also endogenous activators of AHR were identified. We here review beneficial and adverse functions of activated AHR for skin integrity and skin health. We identify open questions, and hypothesize how concurrent inflammatory events can influence the outcome of physiological AHR signaling in the skin. AHR is a highly interesting therapeutic target, but different ligands can result in completely different immune effects. The underlying reasons, such as possible differences in ligand-induced conformational changes, are often unclear or speculative. This remains a challenge for therapeutic use. Also, long-term effects such as epigenetic changes need to come more into focus.
Article
The increase in air pollution over the years has had major effects on the human skin. Various air pollutants such as ultraviolet radiation, polycyclic aromatic hydrocarbons, volatile organic compounds, oxides, particulate matter, ozone and cigarette smoke affect the skin as it is the outermost barrier. Air pollutants damage the skin by inducing oxidative stress. Although human skin acts as a biological shield against pro­oxidative chemicals and physical air pollutants, prolonged or repetitive exposure to high levels of these pollutants may have profound negative effects on the skin. Exposure to ultraviolet radiation has been associated with extrinsic skin aging and skin cancers. Cigarette smoke contributes to premature aging and an increase in the incidence of psoriasis, acne and skin cancers. It is also implicated in allergic skin conditions such as atopic dermatitis and eczema. Polyaromatic hydrocarbons are associated with extrinsic skin aging, pigmentation, cancers and acneiform eruptions. Volatile organic compounds have been associated with atopic dermatitis. Given the increasing levels of air pollution and its detrimental effects on the skin, it is advisable to use strategies to decrease air pollution.
The current study was conducted to observe the effects of fine particulate matter (PM2.5) on human keratinocyte cell line (HaCaT) cells. The potential mechanism linking PM2.5 and skin was explored. HaCaT cells were cultured and then accessed in plate with PM2.5. Cell viability was tested by Cell Counting Kit-8. The mRNA and protein expression of Filaggrin, Loricrin, Involucrin, and Repetin were analyzed. The levels of Granulocyte-macrophage Colony Stimulating Factor, Thymic Stromal Lymphopoietin, Tumor Necrosis Factor-α, Interleukin-1α, and Interleukin-8 were detected in the supernatant of the HaCaT cell with enzyme-linked immunosorbent assay kits. Cell viability decreased with the increase in PM2.5. Compared with the control group, the protein expression of Filaggrin, Repetin, Involucrin, and Loricrin showed different expression patterns in PM2.5 treatment groups. The level of Tumor Necrosis Factor-α, Thymic Stromal Lymphopoietin, Interleukin-1α, and Interleukin-8 significantly increased in the cells treated with PM2.5. Ambient PM2.5 may increase the risk of eczema and other skin diseases. The relative mechanism may be associated with the impairment of the skin barrier and the elevation of inflammatory responses.