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Page 8 of 16 Burke. Plast Aesthet Res 2020;7:59 I http://dx.doi.org/10.20517/2347-9264.2020.154

incinerators as well as smaller ultrafine particles (UFPs) (≤ 100 nm, 0.1 μm, diameter) from traffic. Up to
[28]
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475 kg/km are spewed into urban air each year . Even rural dwellers suffer from nearby highways and
inside furnaces and fireplaces as well as from forest fires and wind-blown dust. Polluting compounds (PAHs,
NO , SO , and trace minerals) cover the surfaces and are incorporated into the cores of the PMs [29,30] . These
2
2
PMs contacting skin are absorbed to the mid-stratum corneum, as shown by tape-stripping chimney
sweeps . UFPs not only penetrate the skin transdermally and through hair follicles [32,33] , but also are
[31]
inhaled through the lung to enter pulmonary circulation; PM contaminants can be measured in the blood
[34]
within one hour and can remain for weeks .
Direct damage to the skin by larger PMs was shown by exposing reconstituted human epidermis in vitro
to concentrated PM 2.5 [35] . Oxidation of surface lipids and apoptosis correlated with increasing dose and
exposure time. The impact of larger PM pollution has been demonstrated by in vitro exposure of human
10
[36]
dermal fibroblasts to PM for 24 h . Surprisingly, 1,977 genes were expressed, most significantly pro-
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inflammatory genes for interleukins (Iℓ) Iℓ-1β, Iℓ-6, Iℓ-8, and Iℓ-33, resulting in increases especially in Iℓ-6
and -8, cytochrome (CYP) P450 (CYP1A1, CYP1B1), and MMP-1 and -3, and accompanied by substantial
decreases in transforming growth factor-β (TGF-β) and in collagen I and elastin mRNA. All of these factors
directly result in the crepe-like, wrinkled, and sagging quality of extrinsic aging.

The mechanism of PM cutaneous insult is by oxidation of surface lipids with resultant ROS that activate
inflammation through transcription factors such as NF-κB, turning on gene transcription for cytokines
and Iℓ-1α, Iℓ-8, COX-1 and -2 [37,38] . In particular, PMs containing quinones or trace metals localize in
keratinocyte mitochondria, altering the mitochondrial ultrastructure with first dilation and vacuolization
[39]
and loss of cristae, then thickening and shrinking .
VOCS
VOCs such as car exhaust with benzene and industrial emissions (mainly tetrachloroethylene) pollute the
outdoor environment, while organic solvents in paints, varnishes, refinishing chemicals, glues, cleaning
agents, cosmetics (especially nail polish) such as aliphatic hydrocarbons (formaldehyde and acetone) fill
indoor closed spaces. Indoor pollution is particularly exacerbated in all homes in winter when windows are
kept closed, and throughout the year in cities where skyscrapers and other buildings have sealed windows
to maintain energy conservation. This VOC-contaminated air is recirculated, leading to “sick building
syndrome.” Workers experience conjunctivitis, rhinitis, atopic dermatitis, eczema, and other contact or
irritant dermatitis, particularly after reconstruction, painting, installation of new rugs and draperies, and
after thorough cleaning. These airborne irritants contribute to extrinsic aging of exposed skin, particularly
on the hands, neck, and face.

TOBACCO SMOKE
A major indoor pollutant is cigarette (and cigar and pipe) smoke which exposes not only the smoker but
also others to the “sidestream” smoke. In the closed environments of our modern world - with urban
skyscrapers and airplanes and mass transit of subways - the VOCs and tobacco contaminants linger. In
a cinema which had been designated “nonsmoking” for over 5 years, 35 tobacco-related chemicals were
measured, carried inside by smokers’ hair, skin, and clothes - leading to “third-hand exposure” .
[40]
More than 4,700 different chemicals are released by burning tobacco , some as PM (including nicotine,
[41]
quinone, and benzopyrenes), some as VOCs (PAHs, CO , CO, formaldehyde, nitrosamine and many
2
others). One dominant component of tobacco smoke, 4-aminobiphenyl, is particularly dangerous because
[42]
it forms adducts on hemoglobin, albumin, and collagen . These adducts remain for the “lifetime” of
each component: On hemoglobin, adducts remain for 120 days at levels 5.5 times higher in smokers than